StemCell Therapy

Stem cells are the building blocks of your skin. They have a unique ability to replace damaged and diseased cells. As they divide, they can proliferate for long periods into millions of new skin cells.

As we age, our stem cells lose their potency. Your skins ability to repair itself just isnt what it used to be. The result can be fine lines, wrinkles, age spots, and sagging skin. But non-embryonic stem cells the same stem cells active early in life are highly potent.

Emerge Skin Cares Anti-Aging Stem Cell Skin Care Serum tap into the potency of these stem cells to renew skin.

Scientists at Emerge Labs Stem Cell Skin Care discovered that human non-embryonic stem cell extracts can renew skin by replacing old cells with healthy new ones. These stem cell extracts stimulate your own skins abilities to repair itself. And Emerge anti-aging stem cell serums were born. Where Stem Cells in Anti Aging Products Come From The first types of human stem cells to be studied by researchers were embryonic stem cells, donated from in vitro fertilization labs. But because creating embryonic stem cells involves the destruction of a fertilized human embryo, many people have ethical concerns about the use of such cells.

The non-embryonic stem cells in Lifeline stem cell serums are derived from unfertilized human oocytes (eggs) which are donated to ISCO from in vitro fertilization labs and clinics. Emerge Anti Aging Stem Cell Skin Care is Based On Proven Scientific Research Emerge Skin Cares exclusive anti-aging products are a combination of several discoveries and unique high-technology, patent-pending formulations.

PhytoCellTecMalus Domestica the first plant stem cell activefor skin stem cell protection with proven efficacy PhytoCellTec Malus Domestica is a liposomal preparation of apple stem cells developed by a novel, patent pending plant cell culture technology.

PhytoCellTec a novel plant cell culture technology has been invented to cultivate dedifferentiated callus cells from a rare Swiss apple. These apple stem cells are rich in epigenetic factors and metabolites, assuring the longevity of skin cells. PhytoCellTec Malus Domestica has been shown to protect skin stem cells and delay the senescence of hair follicles.

PhytoCellTec Malus Domestica provides a revolutionary anti-aging performance for real rejuvenation.

Claims with PhytoCellTec Malus Domestica Protects longevity of skin stem cells Delays senescence of essential cells Combats chronological aging

PhytoCellTec Solar Vitis is based on stem cells derived from a specific grape cultivar that has been obtained through our unique PhytoCellTec technology. As we all know UV radiation is responsible for 80% of skin aging. Despite the use of sun protection filters, toxins and free radicals are generated by UV in the skin. This affects sensitive cells such as the epidermal stem cells which are essential and most valuable. The activity of skin stem cells is the key factor in ensuring the vitality and regeneration capacity of the skin. PhytoCellTec Solar Vitis both protects and maintains the activity of epidermal stem cells even in cases of stress induced by UV.

Claims with PhytoCellTecTM Solar VitisProtects skin stem cells against UV stress Delays senescence of essential cells Fights photo-aging For a vital and healthy-looking skin

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Stem Cell Skin Care | Science Meets Beauty

Nanobiotechnology, bionanotechnology, and nanobiology are terms that refer to the intersection of nanotechnology and biology.[1] Given that the subject is one that has only emerged very recently, bionanotechnology and nanobiotechnology serve as blanket terms for various related technologies.

This discipline helps to indicate the merger of biological research with various fields of nanotechnology. Concepts that are enhanced through nanobiology include: nanodevices (such as biological machines), nanoparticles, and nanoscale phenomena that occurs within the discipline of nanotechnology. This technical approach to biology allows scientists to imagine and create systems that can be used for biological research. Biologically inspired nanotechnology uses biological systems as the inspirations for technologies not yet created.[2] However, as with nanotechnology and biotechnology, bionanotechnology does have many potential ethical issues associated with it.

The most important objectives that are frequently found in nanobiology involve applying nanotools to relevant medical/biological problems and refining these applications. Developing new tools, such as peptoid nanosheets, for medical and biological purposes is another primary objective in nanotechnology. New nanotools are often made by refining the applications of the nanotools that are already being used. The imaging of native biomolecules, biological membranes, and tissues is also a major topic for the nanobiology researchers. Other topics concerning nanobiology include the use of cantilever array sensors and the application of nanophotonics for manipulating molecular processes in living cells.[3]

Recently, the use of microorganisms to synthesize functional nanoparticles has been of great interest. Microorganisms can change the oxidation state of metals. These microbial processes have opened up new opportunities for us to explore novel applications, for example, the biosynthesis of metal nanomaterials. In contrast to chemical and physical methods, microbial processes for synthesizing nanomaterials can be achieved in aqueous phase under gentle and environmentally benign conditions. This approach has become an attractive focus in current green bionanotechnology research towards sustainable development.[4]

The terms are often used interchangeably. When a distinction is intended, though, it is based on whether the focus is on applying biological ideas or on studying biology with nanotechnology. Bionanotechnology generally refers to the study of how the goals of nanotechnology can be guided by studying how biological "machines" work and adapting these biological motifs into improving existing nanotechnologies or creating new ones.[5][6] Nanobiotechnology, on the other hand, refers to the ways that nanotechnology is used to create devices to study biological systems.[7]

In other words, nanobiotechnology is essentially miniaturized biotechnology, whereas bionanotechnology is a specific application of nanotechnology. For example, DNA nanotechnology or cellular engineering would be classified as bionanotechnology because they involve working with biomolecules on the nanoscale. Conversely, many new medical technologies involving nanoparticles as delivery systems or as sensors would be examples of nanobiotechnology since they involve using nanotechnology to advance the goals of biology.

The definitions enumerated above will be utilized whenever a distinction between nanobio and bionano is made in this article. However, given the overlapping usage of the terms in modern parlance, individual technologies may need to be evaluated to determine which term is more fitting. As such, they are best discussed in parallel.

Most of the scientific concepts in bionanotechnology are derived from other fields. Biochemical principles that are used to understand the material properties of biological systems are central in bionanotechnology because those same principles are to be used to create new technologies. Material properties and applications studied in bionanoscience include mechanical properties(e.g. deformation, adhesion, failure), electrical/electronic (e.g. electromechanical stimulation, capacitors, energy storage/batteries), optical (e.g. absorption, luminescence, photochemistry), thermal (e.g. thermomutability, thermal management), biological (e.g. how cells interact with nanomaterials, molecular flaws/defects, biosensing, biological mechanisms s.a. mechanosensing), nanoscience of disease (e.g. genetic disease, cancer, organ/tissue failure), as well as computing (e.g. DNA computing). The impact of bionanoscience, achieved through structural and mechanistic analyses of biological processes at nanoscale, is their translation into synthetic and technological applications through nanotechnology.

Nano-biotechnology takes most of its fundamentals from nanotechnology. Most of the devices designed for nano-biotechnological use are directly based on other existing nanotechnologies. Nano-biotechnology is often used to describe the overlapping multidisciplinary activities associated with biosensors, particularly where photonics, chemistry, biology, biophysics, nano-medicine, and engineering converge. Measurement in biology using wave guide techniques, such as dual polarization interferometry, are another example.

Applications of bionanotechnology are extremely widespread. Insofar as the distinction holds, nanobiotechnology is much more commonplace in that it simply provides more tools for the study of biology. Bionanotechnology, on the other hand, promises to recreate biological mechanisms and pathways in a form that is useful in other ways.

Nanomedicine is a field of medical science whose applications are increasing more and more thanks to nanorobots and biological machines, which constitute a very useful tool to develop this area of knowledge. In the past years, researchers have done many improvements in the different devices and systems required to develop nanorobots. This supposes a new way of treating and dealing with diseases such as cancer; thanks to nanorobots, side effects of chemotherapy have been controlled, reduced and even eliminated, so some years from now, cancer patients will be offered an alternative to treat this disease instead of chemotherapy, which causes secondary effects such as hair lose, fatigue or nausea killing not only cancerous cells but also the healthy ones. At a clinical level, cancer treatment with nanomedicine will consist on the supply of nanorobots to the patient through an injection that will seek for cancerous cells leaving untouched the healthy ones. Patients that will be treated through nanomedicine will not notice the presence of this nanomachines inside them; the only thing that is going to be noticeable is the progressive improvement of their health.[8]

Nanobiotechnology (sometimes referred to as nanobiology) is best described as helping modern medicine progress from treating symptoms to generating cures and regenerating biological tissues. Three American patients have received whole cultured bladders with the help of doctors who use nanobiology techniques in their practice. Also, it has been demonstrated in animal studies that a uterus can be grown outside the body and then placed in the body in order to produce a baby. Stem cell treatments have been used to fix diseases that are found in the human heart and are in clinical trials in the United States. There is also funding for research into allowing people to have new limbs without having to resort to prosthesis. Artificial proteins might also become available to manufacture without the need for harsh chemicals and expensive machines. It has even been surmised that by the year 2055, computers may be made out of biochemicals and organic salts.[9]

Another example of current nanobiotechnological research involves nanospheres coated with fluorescent polymers. Researchers are seeking to design polymers whose fluorescence is quenched when they encounter specific molecules. Different polymers would detect different metabolites. The polymer-coated spheres could become part of new biological assays, and the technology might someday lead to particles which could be introduced into the human body to track down metabolites associated with tumors and other health problems. Another example, from a different perspective, would be evaluation and therapy at the nanoscopic level, i.e. the treatment of Nanobacteria (25-200nm sized) as is done by NanoBiotech Pharma.

While nanobiology is in its infancy, there are a lot of promising methods that will rely on nanobiology in the future. Biological systems are inherently nano in scale; nanoscience must merge with biology in order to deliver biomacromolecules and molecular machines that are similar to nature. Controlling and mimicking the devices and processes that are constructed from molecules is a tremendous challenge to face the converging disciplines of nanotechnology.[10] All living things, including humans, can be considered to be nanofoundries. Natural evolution has optimized the "natural" form of nanobiology over millions of years. In the 21st century, humans have developed the technology to artificially tap into nanobiology. This process is best described as "organic merging with synthetic." Colonies of live neurons can live together on a biochip device; according to research from Dr. Gunther Gross at the University of North Texas. Self-assembling nanotubes have the ability to be used as a structural system. They would be composed together with rhodopsins; which would facilitate the optical computing process and help with the storage of biological materials. DNA (as the software for all living things) can be used as a structural proteomic system - a logical component for molecular computing. Ned Seeman - a researcher at New York University - along with other researchers are currently researching concepts that are similar to each other.[11]

DNA nanotechnology is one important example of bionanotechnology.[12] The utilization of the inherent properties of nucleic acids like DNA to create useful materials is a promising area of modern research. Another important area of research involves taking advantage of membrane properties to generate synthetic membranes. Proteins that self-assemble to generate functional materials could be used as a novel approach for the large-scale production of programmable nanomaterials. One example is the development of amyloids found in bacterial biofilms as engineered nanomaterials that can be programmed genetically to have different properties.[13]Protein folding studies provide a third important avenue of research, but one that has been largely inhibited by our inability to predict protein folding with a sufficiently high degree of accuracy. Given the myriad uses that biological systems have for proteins, though, research into understanding protein folding is of high importance and could prove fruitful for bionanotechnology in the future.

Lipid nanotechnology is another major area of research in bionanotechnology, where physico-chemical properties of lipids such as their antifouling and self-assembly is exploited to build nanodevices with applications in medicine and engineering.[14]

This field relies on a variety of research methods, including experimental tools (e.g. imaging, characterization via AFM/optical tweezers etc.), x-ray diffraction based tools, synthesis via self-assembly, characterization of self-assembly (using e.g. dual polarization interferometry, recombinant DNA methods, etc.), theory (e.g. statistical mechanics, nanomechanics, etc.), as well as computational approaches (bottom-up multi-scale simulation, supercomputing).

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Nanobiotechnology - Wikipedia, the free encyclopedia

Diabetes is a life-long disease that affects the way your body handles glucose, a kind of sugar, in your blood.

Most people with the condition have type 2. There are about 27 million people in the U.S. with it. Another 86 million have prediabetes: Their blood glucose is not normal, but not high enough to be diabetes yet.

Diabetes is a serious disease that can cause debilitating nerve pain.

Here's some helpful information:

2008 WebMD, LLC. All rights reserved.

Your pancreas makes a hormone called insulin. It's what lets your cells turn glucose from the food you eat into energy. People with type 2 diabetes make insulin, but their cells don't use it as well as they should. Doctors call this insulin resistance.

At first, the pancreas makes more insulin to try to get glucose into the cells. But eventually it can't keep up, and the sugar builds up in your blood instead.

Usually a combination of things cause type 2 diabetes, including:

Genes. Scientists have found different bits of DNA that affect how your body makes insulin.

Extra weight. Being overweight or obese can cause insulin resistance, especially if you carry your extra pounds around the middle. Now type 2 diabetes affects kids and teens as well as adults, mainly because of childhood obesity.

Metabolic syndrome. People with insulin resistance often have a group of conditions including high blood glucose, extra fat around the waist, high blood pressure, and high cholesterol and triglycerides.

Too much glucose from your liver. When your blood sugar is low, your liver makes and sends out glucose. After you eat, your blood sugar goes up, and usually the liver will slow down and store its glucose for later. But some people's livers don't. They keep cranking out sugar.

Bad communication between cells. Sometimes cells send the wrong signals or don't pick up messages correctly. When these problems affect how your cells make and use insulin or glucose, a chain reaction can lead to diabetes.

Broken beta cells. If the cells that make the insulin send out the wrong amount of insulin at the wrong time, your blood sugar gets thrown off. High blood glucose can damage these cells, too.

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Type 2 Diabetes: Causes, Symptoms, Prevention, and More

Date: 25 Aug 2015

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Circumcision is described as a cultural, medical, and religious process which states surgical removal of the foreskin either partly or fully. Cells isolated from the circumcised tissues are referred as foreskin cells. They have been thought as feeder cell lines for embryonic stem cells. Their fibroblastic properties were also utilized for several experiments. The waste tissues that remain after the circumcision thought to have stem cell properties. Therefore, there have been very few attempts to expose their stem cell properties without turning them into induced pluripotent stem cells. Although stem cell isolation from prepuce and their mesenchymal multilineage differentiation potential have been presented many times in the literature, the current study explored hematopoietical phenotype of newborn foreskin stem cells for the first time. According to the results, human newborn foreskin stem cells (hnFSSCs) were identified by their capability to turn into all three germ layer cell types under in vitro conditions. In addition, these cells have exhibited a stable phenotype and have remained as a monolayer in vitro. hnFSSCs suggested to carry different treatment potentials for bone damages, cartilage problems, nerve damages, lesion formations, and other diseases that are derive from mesodermal, endodermal, and ectodermal origins. Owing to the location of the tissue in the body and differentiation capabilities of hnFSSCs, these cells can be considered as easily obtainable and utilizable even better than the other stem cell sources. In addition, hnFSSCs offers a great potential for tissue engineering approaches due to exhibiting embryonic stem cell-like characteristics, not having any ethical issues, and teratoma induction as in embryonic stem cell applications.

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Characterization and Differentiation of Stem Cells ...

Fat processing in centrifuge

I recently heard a news video clip about fat derived stem cell injections to the breast. There were a lot of unsubstantiated claims made, and I thought I would try to clarify some issues regarding Breast Augmentation with fat derived stem cells.

There are two types of fat injection that are being confused in this debate. The first is injection of fat itself for breast augmentation. We will call this fat injection. The second is injection of fat which is supplemented with an ultra concentrated volume of fat. This ultra concentrate sample of fat has a high concentration of stem cells. We will call this stem cell enhanced fat injection.

The American Society of Plastic Surgeons has put out a position paper regarding fat transfer. In it the issue of breast cancer detection is addressed. To quote the ASPS text:

Concern regarding the interference of autologous fat grafts with breast cancer detection is not validated by the limited number of studies available on the topic.

In other words, at this point there is no evidence that fat injection interferes with breast cancer detection. As far as complications, lumps, or irregularities the position paper states:

Studies indicate that results of fat transfer remain dependent on a surgeons technique and expertise.

In other words, when an experienced surgeon uses the correct technique, the results are good. In more than four years of injecting massive volumes of fat to the buttocks, I have yet to encounter any significant complications. I use techniques described by Sidney Coleman which have stood the test of time.

Fat injections for breast augmentation have been done carefully, systematically, and succesfully in other countries as well as in the US. As long as proper technique is used, I dont see why results would be any different than fat injection to the buttocks, which already has an established track record.

There are no new types of cells injected in a stem cell enhanced fat cell injection. The stem cells come from the same place the rest of the fat cells come from, your own fat tissue. There are normally occurring stem cells mixed with other fat cells as within the blood vessels and connective tissue of the fat.

All that we are doing is concentrating those cells so they are injected in closer proximity to each other. This likely allows for greater interaction between the stem cells themselves and the surrounding tissues, so there is stimulation for the stem cells to differentiate and create new healthy tissues.

This is not theory, it has been shown to work in breast cancer patients who have had lumpectomies followed by irradiation of tissues. I have seen the positive results in my own lumpectomy patients. These are very difficult cases which up to now were treated with complicated tissue transfers that depended on taking large pieces of tissue from other parts of the body. Clinical studies in Italy, France, and the United states have shown the efficacy of stem cell enhanced fat transfers in helping these patients.

There is a theory that stem cells themselves pose a risk to the breast by somehow turning themselves into breast cancer cells. In order to do that the stem cells would have to differentiate first into breast duct cells. The breast duct cells develop as outgrowths from the areola after a long and complex series of signals highly dependent on specific surrounding tissues. That a stem cell injected into breast would follow this highly specific series of steps is unlikely, at best. Rather, stem cells injected into connective tissue, as they are in the breast, will follow local tissue signals and differentiate ito new connective tissue. This has been demonstrated clinically.

Stem cells injected into the breast are no more likely to turn cancerous than anywhere else in the body.

There is a lot of misinformation and confusion regarding stem cell therapy, as this is a new and exciting field. The FDA is even thinking of classifying stem cell therapy as drug therapy.This would be a tremendous mistake as it would bring progress in this extremely promising field to a screeching halt.

Adult stem cells are purified from your own fat. They are not a drug. I know that I will be discussing this more.

By Dr. Ricardo L Rodriguez Board Certified Plastic Surgeon Baltimore, Maryland Ricardo L Rodriguez on Google +

Posted in Breast Fat Stem Cells

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Fat Stem Cell injections to the breast- Risky ...

The term diabetes mellitus includes several different metabolic disorders that all, if left untreated, result in abnormally high concentration of a sugar called glucose in the blood. Diabetes mellitus type 1 results when the pancreas no longer produces significant amounts of the hormone insulin, usually owing to the autoimmune destruction of the insulin-producing beta cells of the pancreas. Diabetes mellitus type 2, in contrast, is now thought to result from autoimmune attacks on the pancreas and/or insulin resistance. The pancreas of a person with type 2 diabetes may be producing normal or even abnormally large amounts of insulin. Other forms of diabetes mellitus, such as the various forms of maturity onset diabetes of the young, may represent some combination of insufficient insulin production and insulin resistance. Some degree of insulin resistance may also be present in a person with type 1 diabetes.

The main goal of diabetes management is, as far as possible, to restore carbohydrate metabolism to a normal state. To achieve this goal, individuals with an absolute deficiency of insulin require insulin replacement therapy, which is given through injections or an insulin pump. Insulin resistance, in contrast, can be corrected by dietary modifications and exercise. Other goals of diabetes management are to prevent or treat the many complications that can result from the disease itself and from its treatment.

The treatment goals are related to effective control of blood glucose, blood pressure and lipids, to minimize the risk of long-term consequences associated with diabetes. They are suggested in clinical practice guidelines released by various national and international diabetes agencies.

The targets are:

Goals should be individualized based on:[3]

In older patients, clinical practice guidelines by the American Geriatrics Society states "for frail older adults, persons with life expectancy of less than 5 years, and others in whom the risks of intensive glycemic control appear to outweigh the benefits, a less stringent target such as HbA1c of 8% is appropriate".[4]

The primary issue requiring management is that of the glucose cycle. In this, glucose in the bloodstream is made available to cells in the body; a process dependent upon the twin cycles of glucose entering the bloodstream, and insulin allowing appropriate uptake into the body cells. Both aspects can require management.

The main complexities stem from the nature of the feedback loop of the glucose cycle, which is sought to be regulated:

As diabetes is a prime risk factor for cardiovascular disease, controlling other risk factors which may give rise to secondary conditions, as well as the diabetes itself, is one of the facets of diabetes management. Checking cholesterol, LDL, HDL and triglyceride levels may indicate hyperlipoproteinemia, which may warrant treatment with hypolipidemic drugs. Checking the blood pressure and keeping it within strict limits (using diet and antihypertensive treatment) protects against the retinal, renal and cardiovascular complications of diabetes. Regular follow-up by a podiatrist or other foot health specialists is encouraged to prevent the development of diabetic foot. Annual eye exams are suggested to monitor for progression of diabetic retinopathy.

Late in the 19th century, sugar in the urine (glycosuria) was associated with diabetes. Various doctors studied the connection. Frederick Madison Allen studied diabetes in 1909-12, then published a large volume, Studies Concerning Glycosuria and Diabetes, (Boston, 1913). He invented a fasting treatment for diabetes called the Allen treatment for diabetes. His diet was an early attempt at managing diabetes.

Modern approaches to diabetes primarily rely upon dietary and lifestyle management, often combined with regular ongoing blood glucose level monitoring.

Diet management allows control and awareness of the types of nutrients entering the digestive system, and hence allows indirectly, significant control over changes in blood glucose levels. Blood glucose monitoring allows verification of these, and closer control, especially important since some symptoms of diabetes are not easy for the patient to notice without actual measurement.

Other approaches include exercise and other lifestyle changes which impact the glucose cycle.

In addition, a strong partnership between the patient and the primary healthcare provider general practitioner or internist is an essential tool in the successful management of diabetes. Often the primary care doctor makes the initial diagnosis of diabetes and provides the basic tools to get the patient started on a management program. Regular appointments with the primary care physician and a certified diabetes educator are some of the best things a patient can do in the early weeks after a diagnosis of diabetes. Upon the diagnosis of diabetes, the primary care physician, specialist, or endocrinologist will conduct a full physical and medical examination. A thorough assessment covers topics such as:

Diabetes can be very complicated, and the physician needs to have as much information as possible to help the patient establish an effective management plan. Physicians may often experience data overload resulting from hundreds of blood-glucose readings, insulin dosages and other health factors occurring between regular office visits which must be deciphered during a relatively brief visit with the patient to determine patterns and establish or modify a treatment plan.[5]

The physician can also make referrals to a wide variety of professionals for additional health care support. In the UK a patient training course is available for newly diagnosed diabetics (see DESMOND). In big cities, there may be diabetes centers where several specialists, such as diabetes educators and dietitians, work together as a team. In smaller towns, the health care team may come together a little differently depending on the types of practitioners in the area. By working together, doctors and patients can optimize the healthcare team to successfully manage diabetes over the long term.

The 10 countries with the largest populations of diabetic patients are China, India, the U.S., Brazil, Russia, Mexico, Indonesia, Germany, Egypt and Japan.[6]

Blood sugar level is measured by means of a glucose meter, with the result either in mg/dL (milligrams per deciliter in the USA) or mmol/L (millimoles per litre in Canada and Europe) of blood. The average normal person should have a glucose level of around 4.5 to 7.0mmol/L (80 to 125mg/dL).

Optimal management of diabetes involves patients measuring and recording their own blood glucose levels. By keeping a diary of their own blood glucose measurements and noting the effect of food and exercise, patients can modify their lifestyle to better control their diabetes. For patients on insulin, patient involvement is important in achieving effective dosing and timing.

Some edible mushrooms are noted for the ability to lower blood sugar levels including Reishi,[7][8]Maitake[9][10][11][12][13][14]Agaricus blazei[15][16][17][18] as well as some others.

Levels which are significantly above or below this range are problematic and can in some cases be dangerous. A level of <3.8mmol/L (<70mg/dL) is usually described as a hypoglycemic attack (low blood sugar). Most diabetics know when they are going to "go hypo" and usually are able to eat some food or drink something sweet to raise levels. A patient who is hyperglycemic (high glucose) can also become temporarily hypoglycemic, under certain conditions (e.g. not eating regularly, or after strenuous exercise, followed by fatigue). Intensive efforts to achieve blood sugar levels close to normal have been shown to triple the risk of the most severe form of hypoglycemia, in which the patient requires assistance from by-standers in order to treat the episode.[19] In the United States, there were annually 48,500 hospitalizations for diabetic hypoglycemia and 13,100 for diabetic hypoglycemia resulting in coma in the period 1989 to 1991, before intensive blood sugar control was as widely recommended as today.[20] One study found that hospital admissions for diabetic hypoglycemia increased by 50% from 1990-1993 to 1997-2000, as strict blood sugar control efforts became more common.[21] Among intensively controlled type 1 diabetics, 55% of episodes of severe hypoglycemia occur during sleep, and 6% of all deaths in diabetics under the age of 40 are from nocturnal hypoglycemia in the so-called 'dead-in-bed syndrome,' while National Institute of Health statistics show that 2% to 4% of all deaths in diabetics are from hypoglycemia.[22] In children and adolescents following intensive blood sugar control, 21% of hypoglycemic episodes occurred without explanation.[23] In addition to the deaths caused by diabetic hypoglycemia, periods of severe low blood sugar can also cause permanent brain damage.[24] Interestingly, although diabetic nerve disease is usually associated with hyperglycemia, hypoglycemia as well can initiate or worsen neuropathy in diabetics intensively struggling to reduce their hyperglycemia.[25]

Levels greater than 13-15mmol/L (230270mg/dL) are considered high, and should be monitored closely to ensure that they reduce rather than continue to remain high. The patient is advised to seek urgent medical attention as soon as possible if blood sugar levels continue to rise after 2-3 tests. High blood sugar levels are known as hyperglycemia, which is not as easy to detect as hypoglycemia and usually happens over a period of days rather than hours or minutes. If left untreated, this can result in diabetic coma and death.

Prolonged and elevated levels of glucose in the blood, which is left unchecked and untreated, will, over time, result in serious diabetic complications in those susceptible and sometimes even death. There is currently no way of testing for susceptibility to complications. Diabetics are therefore recommended to check their blood sugar levels either daily or every few days. There is also diabetes management software available from blood testing manufacturers which can display results and trends over time. Type 1 diabetics normally check more often, due to insulin therapy.

A history of blood sugar level results is especially useful for the diabetic to present to their doctor or physician in the monitoring and control of the disease. Failure to maintain a strict regimen of testing can accelerate symptoms of the condition, and it is therefore imperative that any diabetic patient strictly monitor their glucose levels regularly.

Glycemic control is a medical term referring to the typical levels of blood sugar (glucose) in a person with diabetes mellitus. Much evidence suggests that many of the long-term complications of diabetes, especially the microvascular complications, result from many years of hyperglycemia (elevated levels of glucose in the blood). Good glycemic control, in the sense of a "target" for treatment, has become an important goal of diabetes care, although recent research suggests that the complications of diabetes may be caused by genetic factors[26] or, in type 1 diabetics, by the continuing effects of the autoimmune disease which first caused the pancreas to lose its insulin-producing ability.[27]

Because blood sugar levels fluctuate throughout the day and glucose records are imperfect indicators of these changes, the percentage of hemoglobin which is glycosylated is used as a proxy measure of long-term glycemic control in research trials and clinical care of people with diabetes. This test, the hemoglobin A1c or glycosylated hemoglobin reflects average glucoses over the preceding 23 months. In nondiabetic persons with normal glucose metabolism the glycosylated hemoglobin is usually 4-6% by the most common methods (normal ranges may vary by method).

"Perfect glycemic control" would mean that glucose levels were always normal (70130mg/dl, or 3.9-7.2mmol/L) and indistinguishable from a person without diabetes. In reality, because of the imperfections of treatment measures, even "good glycemic control" describes blood glucose levels that average somewhat higher than normal much of the time. In addition, one survey of type 2 diabetics found that they rated the harm to their quality of life from intensive interventions to control their blood sugar to be just as severe as the harm resulting from intermediate levels of diabetic complications.[28]

Accepted "target levels" of glucose and glycosylated hemoglobin that are considered good control have been lowered over the last 25 years, because of improvements in the tools of diabetes care, because of increasing evidence of the value of glycemic control in avoiding complications, and by the expectations of both patients and physicians. What is considered "good control" also varies by age and susceptibility of the patient to hypoglycemia.

In the 1990s the American Diabetes Association conducted a publicity campaign to persuade patients and physicians to strive for average glucose and hemoglobin A1c values below 200mg/dl (11mmol/l) and 8%. Currently many patients and physicians attempt to do better than that.

Poor glycemic control refers to persistently elevated blood glucose and glycosylated hemoglobin levels, which may range from 200500mg/dl (11-28mmol/L) and 9-15% or higher over months and years before severe complications occur. Meta-analysis of large studies done on the effects of tight vs. conventional, or more relaxed, glycemic control in type 2 diabetics have failed to demonstrate a difference in all-cause cardiovascular death, non-fatal stroke, or limb amputation, but decreased the risk of nonfatal heart attack by 15%. Additionally, tight glucose control decreased the risk of progression of retinopathy and nephropathy, and decreased the incidence peripheral neuropathy, but increased the risk of hypoglycemia 2.4 times.[29]

Relying on their own perceptions of symptoms of hyperglycemia or hypoglycemia is usually unsatisfactory as mild to moderate hyperglycemia causes no obvious symptoms in nearly all patients. Other considerations include the fact that, while food takes several hours to be digested and absorbed, insulin administration can have glucose lowering effects for as little as 2 hours or 24 hours or more (depending on the nature of the insulin preparation used and individual patient reaction). In addition, the onset and duration of the effects of oral hypoglycemic agents vary from type to type and from patient to patient.

Control and outcomes of both types 1 and 2 diabetes may be improved by patients using home glucose meters to regularly measure their glucose levels.[citation needed] Glucose monitoring is both expensive (largely due to the cost of the consumable test strips) and requires significant commitment on the part of the patient. The effort and expense may be worthwhile for patients when they use the values to sensibly adjust food, exercise, and oral medications or insulin. These adjustments are generally made by the patients themselves following training by a clinician.

Regular blood testing, especially in type 1 diabetics, is helpful to keep adequate control of glucose levels and to reduce the chance of long term side effects of the disease. There are many (at least 20+) different types of blood monitoring devices available on the market today; not every meter suits all patients and it is a specific matter of choice for the patient, in consultation with a physician or other experienced professional, to find a meter that they personally find comfortable to use. The principle of the devices is virtually the same: a small blood sample is collected and measured. In one type of meter, the electrochemical, a small blood sample is produced by the patient using a lancet (a sterile pointed needle). The blood droplet is usually collected at the bottom of a test strip, while the other end is inserted in the glucose meter. This test strip contains various chemicals so that when the blood is applied, a small electrical charge is created between two contacts. This charge will vary depending on the glucose levels within the blood. In older glucose meters, the drop of blood is placed on top of a strip. A chemical reaction occurs and the strip changes color. The meter then measures the color of the strip optically.

Self-testing is clearly important in type I diabetes where the use of insulin therapy risks episodes of hypoglycaemia and home-testing allows for adjustment of dosage on each administration.[30] However its benefit in type 2 diabetes is more controversial as there is much more variation in severity of type 2 cases.[31] It has been suggested that some type 2 patients might do as well with home urine-testing alone.[32] The best use of home blood-sugar monitoring is being researched.[33]

Benefits of control and reduced hospital admission have been reported.[34] However, patients on oral medication who do not self-adjust their drug dosage will miss many of the benefits of self-testing, and so it is questionable in this group. This is particularly so for patients taking monotherapy with metformin who are not at risk of hypoglycaemia. Regular 6 monthly laboratory testing of HbA1c (glycated haemoglobin) provides some assurance of long-term effective control and allows the adjustment of the patient's routine medication dosages in such cases. High frequency of self-testing in type 2 diabetes has not been shown to be associated with improved control.[35] The argument is made, though, that type 2 patients with poor long term control despite home blood glucose monitoring, either have not had this integrated into their overall management, or are long overdue for tighter control by a switch from oral medication to injected insulin.[36]

Continuous Glucose Monitoring (CGM) CGM technology has been rapidly developing to give people living with diabetes an idea about the speed and direction of their glucose changes. While it still requires calibration from SMBG and is not indicated for use in correction boluses, the accuracy of these monitors are increasing with every innovation.

A useful test that has usually been done in a laboratory is the measurement of blood HbA1c levels. This is the ratio of glycated hemoglobin in relation to the total hemoglobin. Persistent raised plasma glucose levels cause the proportion of these molecules to go up. This is a test that measures the average amount of diabetic control over a period originally thought to be about 3 months (the average red blood cell lifetime), but more recently[when?] thought to be more strongly weighted to the most recent 2 to 4 weeks. In the non-diabetic, the HbA1c level ranges from 4.0-6.0%; patients with diabetes mellitus who manage to keep their HbA1c level below 6.5% are considered to have good glycemic control. The HbA1c test is not appropriate if there has been changes to diet or treatment within shorter time periods than 6 weeks or there is disturbance of red cell aging (e.g. recent bleeding or hemolytic anemia) or a hemoglobinopathy (e.g. sickle cell disease). In such cases the alternative Fructosamine test is used to indicate average control in the preceding 2 to 3 weeks.

The first CGM device made available to consumers was the GlucoWatch biographer in 1999. This product is no longer sold. It was a retrospective device rather than live. Several live monitoring devices have subsequently been manufactured which provide ongoing monitoring of glucose levels on an automated basis during the day, for example:

For Type 1 diabetics there will always be a need for insulin injections throughout their life. However, both Type 1 and Type 2 diabetics can see dramatic effects on their blood sugars through controlling their diet, and some Type 2 diabetics can fully control the disease by dietary modification. As diabetes can lead to many other complications it is critical to maintain blood sugars as close to normal as possible and diet is the leading factor in this level of control.

The American Diabetes Association in 1994 recommended that 60-70% of caloric intake should be in the form of carbohydrates. This is somewhat controversial, with some researchers claiming that 40% is better,[37] while others claim benefits for a high-fiber, 75% carbohydrate diet.[38]

An article summarizing the view of the American Diabetes Association[39] gives many recommendations and references to the research. One of the conclusions is that caloric intake must be limited to that which is necessary for maintaining a healthy weight. The methodology of the dietary therapy has attracted lots of attentions from many scientific researchers and the protocols are ranging from nutritional balancing to ambulatory diet-care.[40][41][42]

Currently, one goal for diabetics is to avoid or minimize chronic diabetic complications, as well as to avoid acute problems of hyperglycemia or hypoglycemia. Adequate control of diabetes leads to lower risk of complications associated with unmonitored diabetes including kidney failure (requiring dialysis or transplant), blindness, heart disease and limb amputation. The most prevalent form of medication is hypoglycemic treatment through either oral hypoglycemics and/or insulin therapy. There is emerging evidence that full-blown diabetes mellitus type 2 can be evaded in those with only mildly impaired glucose tolerance.[43]

Patients with type 1 diabetes mellitus require direct injection of insulin as their bodies cannot produce enough (or even any) insulin. As of 2010, there is no other clinically available form of insulin administration other than injection for patients with type 1: injection can be done by insulin pump, by jet injector, or any of several forms of hypodermic needle. Non-injective methods of insulin administration have been unattainable as the insulin protein breaks down in the digestive tract. There are several insulin application mechanisms under experimental development as of 2004, including a capsule that passes to the liver and delivers insulin into the bloodstream.[44] There have also been proposed vaccines for type I using glutamic acid decarboxylase (GAD), but these are currently not being tested by the pharmaceutical companies that have sublicensed the patents to them.

For type 2 diabetics, diabetic management consists of a combination of diet, exercise, and weight loss, in any achievable combination depending on the patient. Obesity is very common in type 2 diabetes and contributes greatly to insulin resistance. Weight reduction and exercise improve tissue sensitivity to insulin and allow its proper use by target tissues.[45] Patients who have poor diabetic control after lifestyle modifications are typically placed on oral hypoglycemics. Some Type 2 diabetics eventually fail to respond to these and must proceed to insulin therapy. A study conducted in 2008 found that increasingly complex and costly diabetes treatments are being applied to an increasing population with type 2 diabetes. Data from 1994 to 2007 was analyzed and it was found that the mean number of diabetes medications per treated patient increased from 1.14 in 1994 to 1.63 in 2007.[46]

Patient education and compliance with treatment is very important in managing the disease. Improper use of medications and insulin can be very dangerous causing hypo- or hyper-glycemic episodes.

Insulin therapy requires close monitoring and a great deal of patient education, as improper administration is quite dangerous. For example, when food intake is reduced, less insulin is required. A previously satisfactory dosing may be too much if less food is consumed causing a hypoglycemic reaction if not intelligently adjusted. Exercise decreases insulin requirements as exercise increases glucose uptake by body cells whose glucose uptake is controlled by insulin, and vice versa. In addition, there are several types of insulin with varying times of onset and duration of action.

Insulin therapy creates risk because of the inability to continuously know a person's blood glucose level and adjust insulin infusion appropriately. New advances in technology have overcome much of this problem. Small, portable insulin infusion pumps are available from several manufacturers. They allow a continuous infusion of small amounts of insulin to be delivered through the skin around the clock, plus the ability to give bolus doses when a person eats or has elevated blood glucose levels. This is very similar to how the pancreas works, but these pumps lack a continuous "feed-back" mechanism. Thus, the user is still at risk of giving too much or too little insulin unless blood glucose measurements are made.

A further danger of insulin treatment is that while diabetic microangiopathy is usually explained as the result of hyperglycemia, studies in rats indicate that the higher than normal level of insulin diabetics inject to control their hyperglycemia may itself promote small blood vessel disease.[25] While there is no clear evidence that controlling hyperglycemia reduces diabetic macrovascular and cardiovascular disease, there are indications that intensive efforts to normalize blood glucose levels may worsen cardiovascular and cause diabetic mortality.[47]

Studies conducted in the United States[48] and Europe[49] showed that drivers with type 1 diabetes had twice as many collisions as their non-diabetic spouses, demonstrating the increased risk of driving collisions in the type 1 diabetes population. Diabetes can compromise driving safety in several ways. First, long-term complications of diabetes can interfere with the safe operation of a vehicle. For example, diabetic retinopathy (loss of peripheral vision or visual acuity), or peripheral neuropathy (loss of feeling in the feet) can impair a drivers ability to read street signs, control the speed of the vehicle, apply appropriate pressure to the brakes, etc.

Second, hypoglycemia can affect a persons thinking process, coordination, and state of consciousness.[50][51] This disruption in brain functioning is called neuroglycopenia. Studies have demonstrated that the effects of neuroglycopenia impair driving ability.[50][52] A study involving people with type 1 diabetes found that individuals reporting two or more hypoglycemia-related driving mishaps differ physiologically and behaviorally from their counterparts who report no such mishaps.[53] For example, during hypoglycemia, drivers who had two or more mishaps reported fewer warning symptoms, their driving was more impaired, and their body released less epinephrine (a hormone that helps raise BG). Additionally, individuals with a history of hypoglycemia-related driving mishaps appear to use sugar at a faster rate[54] and are relatively slower at processing information.[55] These findings indicate that although anyone with type 1 diabetes may be at some risk of experiencing disruptive hypoglycemia while driving, there is a subgroup of type 1 drivers who are more vulnerable to such events.

Given the above research findings, it is recommended that drivers with type 1 diabetes with a history of driving mishaps should never drive when their BG is less than 70mg/dl (3.9mmol/l). Instead, these drivers are advised to treat hypoglycemia and delay driving until their BG is above 90mg/dl (5mmol/l).[53] Such drivers should also learn as much as possible about what causes their hypoglycemia, and use this information to avoid future hypoglycemia while driving.

Studies funded by the National Institutes of Health (NIH) have demonstrated that face-to-face training programs designed to help individuals with type 1 diabetes better anticipate, detect, and prevent extreme BG can reduce the occurrence of future hypoglycemia-related driving mishaps.[56][57][58] An internet-version of this training has also been shown to have significant beneficial results.[59] Additional NIH funded research to develop internet interventions specifically to help improve driving safety in drivers with type 1 diabetes is currently underway.[60]

The U.S. Food and Drug Administration (FDA) has approved a treatment called Exenatide, based on the saliva of a Gila monster, to control blood sugar in patients with type 2 diabetes.

Artificial Intelligence researcher Dr. Cynthia Marling, of the Ohio University Russ College of Engineering and Technology, in collaboration with the Appalachian Rural Health Institute Diabetes Center, is developing a case based reasoning system to aid in diabetes management. The goal of the project is to provide automated intelligent decision support to diabetes patients and their professional care providers by interpreting the ever increasing quantities of data provided by current diabetes management technology and translating it into better care without time consuming manual effort on the part of an endocrinologist or diabetologist.[61] This type of Artificial Intelligence-based treatment shows some promise with initial testing of a prototype system producing best practice treatment advice which anaylizing physicians deemed to have some degree of benefit over 70% of the time and advice of neutral benefit another nearly 25% of the time.[5]

Use of a "Diabetes Coach" is becoming an increasingly popular way to manage diabetes. A Diabetes Coach is usually a Certified diabetes educator (CDE) who is trained to help people in all aspects of caring for their diabetes. The CDE can advise the patient on diet, medications, proper use of insulin injections and pumps, exercise, and other ways to manage diabetes while living a healthy and active lifestyle. CDEs can be found locally or by contacting a company which provides personalized diabetes care using CDEs. Diabetes Coaches can speak to a patient on a pay-per-call basis or via a monthly plan.

High blood glucose in diabetic people is a risk factor for developing gum and teeth problems, especially in post puberty and aging individuals. Diabetic patients have greater chances of developing oral health problems such as tooth decay, salivary gland dysfunction, fungal infections, inflammatory skin disease, periodontal disease or taste impairment and thrush of the mouth.[62] The oral problems in persons suffering from diabetes can be prevented with a good control of the blood sugar levels, regular check-ups and a very good oral hygiene. By maintaining a good oral status, diabetic persons prevent losing their teeth as a result of various periodontal conditions.

Diabetic persons must increase their awareness towards the oral infections as they have a double impact on one's health. Firstly, people with diabetes are more likely to develop periodontal disease which causes increased blood sugar levels, often leading to diabetes complications. Severe periodontal disease can increase blood sugar, contributing to increased periods of time when the body functions with a high blood sugar. This puts diabetics at increased risk for diabetic complications.[63]

The first symptoms of gum and teeth infections in diabetic persons are decreased salivary flow, burning mouth or tongue. Also, patients may experience signs as dry mouth which increases the incidence of decay. Poorly controlled diabetes usually leads to gum problems recession as plaque creates more harmful proteins in the gums.

Tooth decay and cavities are some of the first oral problems that individuals with diabetes are at risk for. Increased blood sugar levels translate into greater sugars and acids that attack the teeth and lead to gum diseases. Gingivitis can also occur as a result of increased blood sugar levels along with an inappropriate oral hygiene. Periodontitis is an oral disease caused by untreated gingivitis and which destroys the soft tissue and bone that support the teeth. This disease may cause the gums to pull away from the teeth which may eventually loosen and fall out. Diabetic people tend to experience more severe periodontitis because diabetes lowers the ability to resist infection[64] and also slows healing. At the same time, an oral infection such as periodontitis can make diabetes more difficult to control because it causes the blood sugar levels to rise.[65]

To prevent further diabetic complications as well as serious oral problems, diabetic persons must keep their blood sugar levels under control and have a proper oral hygiene. A study in the Journal of Periodontology found that poorly controlled type 2 diabetic patients are more likely to develop periodontal disease than well-controlled diabetics are.[63] At the same time, diabetic patients are recommended to have regular checkups with a dental care provider at least once in three to four months. Diabetics who receive good dental care and have good insulin control typically have a better chance at avoiding gum disease to help prevent tooth loss.[66]

Dental care is therefore even more important for diabetic patients than for healthy individuals. Maintaining the teeth and gum healthy is done by taking some preventing measures such as regular appointments at a dentist and a very good oral hygiene. Also, oral health problems can be avoided by closely monitoring the blood sugar levels. Patients who keep better under control their blood sugar levels and diabetes are less likely to develop oral health problems when compared to diabetic patients who control their disease moderately or poorly.

Poor oral hygiene is a great factor to take under consideration when it comes to oral problems and even more in people with diabetes. Diabetic people are advised to brush their teeth at least twice a day, and if possible, after all meals and snacks. However, brushing in the morning and at night is mandatory as well as flossing and using an anti-bacterial mouthwash. Individuals who suffer from diabetes are recommended to use toothpaste that contains fluoride as this has proved to be the most efficient in fighting oral infections and tooth decay. Flossing must be done at least once a day, as well because it is helpful in preventing oral problems by removing the plaque between the teeth, which is not removed when brushing.

Diabetic patients must get professional dental cleanings every six months. In cases when dental surgery is needed, it is necessary to take some special precautions such as adjusting diabetes medication or taking antibiotics to prevent infection. Looking for early signs of gum disease (redness, swelling, bleeding gums) and informing the dentist about them is also helpful in preventing further complications. Quitting smoking is recommended to avoid serious diabetes complications and oral diseases.

Diabetic persons are advised to make morning appointments to the dental care provider as during this time of the day the blood sugar levels tend to be better kept under control. Not least, individuals who suffer from diabetes must make sure both their physician and dental care provider are informed and aware of their condition, medical history and periodontal status.

Because many patients with diabetes have two or more comorbidities, they often require multiple medications. The prevalence of medication nonadherence is high among patients with chronic conditions, such as diabetes, and nonadherence is associated with public health issues and higher health care costs. One reason for nonadherence is the cost of medications. Being able to detect cost-related nonadherence is important for health care professionals, because this can lead to strategies to assist patients with problems paying for their medications. Some of these strategies are use of generic drugs or therapeutic alternatives, substituting a prescription drug with an over-the-counter medication, and pill-splitting. Interventions to improve adherence can achieve reductions in diabetes morbidity and mortality, as well as significant cost savings to the health care system.[67]

Diabetes type1 is caused by the destruction of enough beta cells to produce symptoms; these cells, which are found in the Islets of Langerhans in the pancreas, produce and secrete insulin, the single hormone responsible for allowing glucose to enter from the blood into cells (in addition to the hormone amylin, another hormone required for glucose homeostasis). Hence, the phrase "curing diabetes type1" means "causing a maintenance or restoration of the endogenous ability of the body to produce insulin in response to the level of blood glucose" and cooperative operation with counterregulatory hormones.

This section deals only with approaches for curing the underlying condition of diabetes type1, by enabling the body to endogenously, in vivo, produce insulin in response to the level of blood glucose. It does not cover other approaches, such as, for instance, closed-loop integrated glucometer/insulin pump products, which could potentially increase the quality-of-life for some who have diabetes type1, and may by some be termed "artificial pancreas".

A biological approach to the artificial pancreas is to implant bioengineered tissue containing islet cells, which would secrete the amounts of insulin, amylin and glucagon needed in response to sensed glucose.

When islet cells have been transplanted via the Edmonton protocol, insulin production (and glycemic control) was restored, but at the expense of continued immunosuppression drugs. Encapsulation of the islet cells in a protective coating has been developed to block the immune response to transplanted cells, which relieves the burden of immunosuppression and benefits the longevity of the transplant.[68]

Research is being done at several locations in which islet cells are developed from stem cells.

Stem cell research has also been suggested as a potential avenue for a cure since it may permit regrowth of Islet cells which are genetically part of the treated individual, thus perhaps eliminating the need for immuno-suppressants.[48] This new method autologous nonmyeloablative hematopoietic stem cell transplantation was developed by a research team composed by Brazilian and American scientists (Dr. Julio Voltarelli, Dr. Carlos Eduardo Couri, Dr Richard Burt, and colleagues) and it was the first study to use stem cell therapy in human diabetes mellitus This was initially tested in mice and in 2007 there was the first publication of stem cell therapy to treat this form of diabetes.[69] Until 2009, there was 23 patients included and followed for a mean period of 29.8 months (ranging from 7 to 58 months). In the trial, severe immunosuppression with high doses of cyclophosphamide and anti-thymocyte globulin is used with the aim of "turning off" the immunologic system", and then autologous hematopoietic stem cells are reinfused to regenerate a new one. In summary it is a kind of "immunologic reset" that blocks the autoimmune attack against residual pancreatic insulin-producing cells. Until December 2009, 12 patients remained continuously insulin-free for periods ranging from 14 to 52 months and 8 patients became transiently insulin-free for periods ranging from 6 to 47 months. Of these last 8 patients, 2 became insulin-free again after the use of sitagliptin, a DPP-4 inhibitor approved only to treat type 2 diabetic patients and this is also the first study to document the use and complete insulin-independendce in humans with type 1 diabetes with this medication. In parallel with insulin suspension, indirect measures of endogenous insulin secretion revealed that it significantly increased in the whole group of patients, regardless the need of daily exogenous insulin use.[70]

Technology for gene therapy is advancing rapidly such that there are multiple pathways possible to support endocrine function, with potential to practically cure diabetes.[71]

Type2 diabetes is usually first treated by increasing physical activity, and eliminating saturated fat and reducing sugar and carbohydrate intake with a goal of losing weight. These can restore insulin sensitivity even when the weight loss is modest, for example around 5kg (10 to 15lb), most especially when it is in abdominal fat deposits. Diets that are very low in saturated fats have been claimed to reverse insulin resistance.[75][76]

Testosterone replacement therapy may improve glucose tolerance and insulin sensitivity in diabetic hypogonadal men. The mechanisms by which testosterone decreases insulin resistance is under study.[77] Moreover, testosterone may have a protective effect on pancreatic beta cells, which is possibly exerted by androgen-receptor-mediated mechanisms and influence of inflammatory cytokines.[78]

Recently[when?] it has been suggested that a type of gastric bypass surgery may normalize blood glucose levels in 80-100% of severely obese patients with diabetes. The precise causal mechanisms are being intensively researched; its results may not simply be attributable to weight loss, as the improvement in blood sugars seems to precede any change in body mass. This approach may become a treatment for some people with type2 diabetes, but has not yet been studied in prospective clinical trials.[79] This surgery may have the additional benefit of reducing the death rate from all causes by up to 40% in severely obese people.[80] A small number of normal to moderately obese patients with type2 diabetes have successfully undergone similar operations.[81][82]

MODY is another classification of diabetes and it can be treated by early lifesyle management and medical management. it has to be treated in the early stage, so as to provide a good health.

Excerpt from:
Diabetes management - Wikipedia, the free encyclopedia

If you have been diagnosed with chronic kidney diseaseor have a family member or friend who hasyou probably have a lot of questions. What does it mean to have chronic kidney disease? How will it impact my health and my life? Will I need dialysis? What do I do now? We hope this site will provide some answers.

Kidney disease means that the kidneys are damaged and can't filter blood like they should. This damage can cause wastes to build up in the body. It can also cause other problems that can harm your health.

For most people, kidney damage occurs slowly over many years, often due to diabetes or high blood pressure. This is called chronic kidney disease. When someone has a sudden change in kidney functionbecause of illness, injury, or have taken certain medicationsthis is called acute kidney injury. This can occur in a person with normal kidneys or in someone who already has kidney problems.

People with kidney disease often have high blood pressure, and are more likely to have a stroke or heart attack. They can also develop anemia (low number of red blood cells), bone disease, and malnutrition. Kidney disease can get worse over time, and may lead to kidney failure. Learn about what your kidneys do.

Diabetes and high blood pressure are the most common causes of kidney disease. Other important causes include glomerulonephritis and polycystic kidney disease. Your provider will want to know why you have kidney disease so your treatment can also address the cause.

Treatment may help slow kidney disease and keep the kidneys healthier longer. Find out about medicines and diet and lifestyle changes that are important for people with kidney disease.

Take these steps to help keep your kidneys healthier longer:

Work with your health care team to figure out the treatment plan that makes the most sense for you. With proper management, you may never need dialysis or, at least, not for a very long time.

NIDDK conducts and supports research to improve the detection of kidney disease, as well as treatment for those with kidney disease and kidney failure. For example, the Chronic Renal Insufficiency Cohort (CRIC) Study, an NIDDK-funded study started in 2001, is working to better understand kidney disease and its link to heart disease. NIDDK also supports many clinical trials, which are research studies to determine how well a treatment works. To learn more about eligibility and how to get involved in a clinical trial, visit http://www.clinicaltrial.gov.

Your GFR and urine albumin results will help you and your provider keep track of your kidney health.

Treating kidney disease includes making changes to your diet and to other lifestyle choices.

Medicines may slow down kidney disease.

Your health care team may include your primary care provider, as well as a dietitian, a nephrologist, and others.

It's important to understand kidney failure treatment options and know the steps you can take early on to prepare for treatment if you need it.

Find Frequently Asked Questions for people with kidney disease.

Page last updated: September 17, 2014

Originally posted here:
Living with - National Kidney Disease Education Program

High blood pressure and kidney disease facts

*High blood pressure and kidney disease facts medically edited by: Charles Patrick Davis, MD, PhD

The kidneys play a key role in keeping a person's blood pressure in a healthy range, and blood pressure, in turn, can affect the health of the kidneys. High blood pressure, also called hypertension, can damage the kidneys and lead to chronic kidney disease (CKD).

Blood pressure measures the force of blood against the walls of the blood vessels. Extra fluid in the body increases the amount of fluid in blood vessels and makes blood pressure higher. Narrow, stiff, or clogged blood vessels also raise blood pressure.

People with high blood pressure should see their doctor regularly.

Medically Reviewed by a Doctor on 3/31/2014

Kidney Disease (HBP Related) - Symptoms Question: What were the symptoms of your kidney disease?

Hypertensive Kidney Disease - Experiences Question: Please share your experiences of hypertensive kidney disease.

Hypertensive Kidney Disease - Hypertension Symptoms Question: What symptoms of hypertension did you experience with hypertensive kidney disease?

Hypertensive Kidney Disease - Medications Question: What medications have been effective for treating hypertensive kidney disease?

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Many Americans know nothing about kidney diseaseuntil it's too late.

"Unlike many diseases, kidney disease often has no symptoms until it is very advanced," says Andrew Narva, M.D., Director of the National Kidney Disease Education Program (NKDEP) a part of the NIH's National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

"For this reason and others, it is important for people to not only become aware of their risk, but also to learn about the steps they can take to keep their kidneys healthier longer. An important step is to get tested."

That testing is even more important for populations that are at higher risk for kidney disease, such as African Americans, adds Dr. Narva.

Your doctor can do very simple tests to check for kidney disease:

How can you tell if you are at risk for kidney disease? Ask yourself these questions:

If you answered "yes" to any of these questions, you are at risk for kidney disease. Now is the time to get tested.

Your health care provider will order two simple tests to check your kidneysa blood test to check your glomerular filtration rate (GFR) and a urine test to check for protein.

Kidney disease is usually a progressive disease, which means that the damage in the kidneys tends to be permanent and can't be undone. So it is important to identify kidney disease early before the damage is done. The good news is that kidney disease can be treated very effectively if it is caught in the early stages. This is very important, since kidney disease also makes your risks for heart disease and stroke higher.

For people who have diabetes, monitoring blood glucose levels is very important. Your health care provider can help you find the right device for doing this if you are diagnosed with diabetes.

Controlling blood pressure is also very important for people with kidney disease. There are several types of medicine that help people keep their blood pressure in a healthy range. Two kinds of medicines, ACEi (angiotensin converting enzyme inhibitors) and ARBs (angiotensin receptor blockers) also help to protect the kidneys.

If one or both kidneys fail completely and the damage can't be reversed, the condition is called kidney failure or end-stage renal disease (ESRD). When this occurs, your kidneys can no longer filter wastes well enough to keep you healthy. The symptoms for ESRD include fatigue, weakness, nausea, vomiting, and itching.

Treatments for kidney failure include dialysis or transplantation. There are two major types of dialysis:

A kidney transplant is an operation that places a healthy kidney in your body. The transplanted kidney takes over the work of the two kidneys that failed, and you no longer need dialysis.

Many researchers are studying kidney disease. They are looking for ways to improve diagnosis, make treatments more effective, and make dialysis and transplantation work better. Several areas of research supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) hold great potential.

NIDDK is sponsoring a major studythe Chronic Renal Insufficiency Cohort (CRIC) studyto learn more about how kidney disease progresses. CRIC is following 3,000 adults for seven years. All study participants have mild to moderate kidney disease, and about half have diabetes.

Researchers think that some CRIC study participants' kidney function will decline more rapidly than others', and that some will develop cardiovascular disease while others won't. The goal of the study is to identify the factors linked to rapid decline of kidney function and development of cardiovascular disease.

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Kidney Disease: Early Detection and Treatment

David Wolfe Health, Eco, Nutrition, and Natural Beauty Expert

Today is the best day ever.

David Avocado Wolfe is the rock star and Indiana Jones of the superfoods and longevity universe. The worlds top CEOs, ambassadors, celebrities, athletes, artists, and the real superheroes of this planetMomsall look to David for expert advice in health, beauty, herbalism, nutrition, and chocolate!

David is the celebrity spokesperson for Americas #1 selling kitchen appliance: the NUTRiBULLET and for http://www.LongevityWarehouse.com. He is the co-founder of TheBestDayEver.com online health magazine and is the visionary founder and president of the non-profit The Fruit Tree Planting Foundation charity (www.ftpf.org) with a mission to plant 18 billion fruit, nut, and medicinal trees on planet Earth.

With over 20 years of dedicated experience and having hosted over 2750 live events, David has led the environmental charge for radiant health via a positive mental attitude, eco-community building, living spring water, and the best-ever quality organic foods and herbs.

David champions the ideals of spending time in nature, growing ones own food, and making today the best day ever. He teaches that inspiration is found in love, travel, natural beauty, vibrant health, and peak-performance.

David has circumnavigated the Earth for decades seeking out the worlds purest foods and waters and leading adventure retreats (please see http://www.davidwolfeadventures.com).

David is a gourmet chocolatier, organic farmer, beekeeper, and a vanilla grower. He is passionate about the beautifying, health giving and mystical qualities of dark organic chocolate.You may find his favorite chocolate at:www.sacredchocolate.com/DavidAvocadoWolfe.

David is the author of many best-selling books, including Eating for Beauty, The Sunfood Diet Success System, Naked Chocolate, Amazing Grace, Superfoods: The Food and Medicine of the Future, Chaga: King of the Medicinal Mushrooms and Longevity NOW. He has also appeared in numerous breakthrough documentaries and films including: Food Matters, Hungry for Change, and Discover the Gift.

Davids Facebook site (www.facebook.com/DavidAvocadoWolfe) daily touches people all over the globe by delivering succinct powerful inspiration, news, and education.

David is a highly sought after health and personal success speaker. He has shared the stage with success and business coaches like Anthony Robbins, Richard Branson, Brian Tracy, John DeMartini, as well as acclaimed doctors and health researchers including: Dr. Bruce Lipton, Dr. Joseph Mercola, Dr. Sara Gottfried, Dr. Lissa Rankin, Dr Dave Woynarowksi and many more.

David is a lead educator and presenter at the annual Longevity Conference, Institute of Integrative Nutrition, and the Body-Mind Institute, where he hosts his own course: http://www.bodymindinstitute.com/the-david-wolfe-nutrition-certification/

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Type 1 Diabetes

Understanding type 1 diabetes is the first step to managing it. Get information on type 1 diabetes causes, risk factors, warning signs, and prevention tips.

Normally, the body's immune system fights off foreign invaders like viruses or bacteria. But for unknown reasons, in people with type 1 diabetes, the immune system attacks various cells in the body.

Symptoms of type 1 diabetes usually develop quickly, over a few days to weeks, and are caused by blood sugar levels rising above the normal range (hyperglycemia).

You can inherit a tendency to develop type 1 diabetes, but most people who have the disease have no family history of it.

If a person is not in ketoacidosis, the American Diabetes Association's criteria for symptoms, a medical history, a physical exam, and blood tests are used to diagnose type 1 diabetes.

Type 1 diabetes requires lifelong treatment to keep blood sugar levels within a target range.

There are many forms of insulin to treat diabetes. They are classified by how fast they start to work and how long their effects last.

Currently there is no way to prevent type 1 diabetes, but ongoing studies are exploring ways to prevent diabetes in those who are most likely to develop it.

See animated illustrations of how type 1 diabetes works.

WebMD offers a pictorial overview of the symptoms, diagnosis, and treatment of type 1 diabetes.

This type 1 diabetes assessment was designed to explore and evaluate your personal health and lifestyle history to help you manage your health and your familys health better.

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At Washington Orthopaedic Center, our highly trained staff of orthopedic surgeons specialize ina wide range of services. If you are living with unwanted pain in your bones or joints, we can help you live a pain free life once again.Our office is conveniently located in Centralia, between Olympia and Longview, Washington.

Our skilled physicians have proven that they are some of the best in the industry. Some of their accomplishments includeteaching courses around the world, helping underprivileged patients in third world countries, andbeing an official provider of the U.S. Ski Team. We offermany servicesincluding sports medicine, joint replacement, foot and ankle surgery, arthroscopic surgery, arthritis care, and more. If your injury requires surgery, we have a surgery center that offers cost effective, same day surgery.

For larger scans, such as backs and hips, we schedule imaging at Washington Diagnostic MRI and Providence Centralia Hospital directly adjacent to our offices. Our patients also benefit from the latest technology in tele-radiology. This is where the image is sent electronically to specialists that read our patients results with expert accuracy. Todays MRI technology has virtually eliminated the need for invasive exploratory surgeries.

Bursitis/tendonitis, and various sprains and strains may also imitate arthritis. Accurate diagnosis requires a careful history and physical examination, as well as x-rays of the involved area.

Treatment is dictated by the proper diagnosis, location, and severity of the condition. Our orthopedic surgeons are specially trained to provide appropriate care including medications, techniques to protect the joint, and when appropriate; surgery for the afflicted area.

All of our orthopedists have broad, extensive training in caring for these injuries, some with special interest and extra training devoted to sports medicine.

Our physicians are specialists in this area of orthopedic surgery specializing in rapid return to normal life after total hip and total knee replacement. State-of-the-art computer navigation is an option for some total knee replacement surgeries. Total joint replacement surgeries are done at Providence Centralia Hospital. Patients begin physical rehabilitation therapy at the hospital under their orthopedic physicians care and continue rehabilitation in an appropriate setting for their condition and lifestyle.

In 2008, Dr. Keith Birchard of Washington Orthopaedic Center traveled to Kudjip Nazarene Hospital in Papua New Guinea to offer his medical expertise to the local residents. Dr. Birchard spent three weeks away from []

Job Summary The Medical Assistant (MA) operates in a team with other clinic healthcare providers and support staff. The assistant escorts patients to the exam rooms and assists providers while treating patients. The MA assists []

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Washington Orthopaedic Center - World Class Orthopedic Care

Induced pluripotent stem cells (also known as iPS cells or iPSCs) are a type of pluripotent stem cell that can be generated directly from adult cells. The iPSC technology was pioneered by Shinya Yamanakas lab in Kyoto, Japan, who showed in 2006 that the introduction of four specific genes encoding transcription factors could convert adult cells into pluripotent stem cells.[1] He was awarded the 2012 Nobel Prize along with Sir John Gurdon "for the discovery that mature cells can be reprogrammed to become pluripotent." [2]

Pluripotent stem cells hold great promise in the field of regenerative medicine. Because they can propagate indefinitely, as well as give rise to every other cell type in the body (such as neurons, heart, pancreatic, and liver cells), they represent a single source of cells that could be used to replace those lost to damage or disease.

The most well-known type of pluripotent stem cell is the embryonic stem cell. However, since the generation of embryonic stem cells involves destruction (or at least manipulation) [3] of the pre-implantation stage embryo, there has been much controversy surrounding their use. Further, because embryonic stem cells can only be derived from embryos, it has so far not been feasible to create patient-matched embryonic stem cell lines.

Since iPSCs can be derived directly from adult tissues, they not only bypass the need for embryos, but can be made in a patient-matched manner, which means that each individual could have their own pluripotent stem cell line. These unlimited supplies of autologous cells could be used to generate transplants without the risk of immune rejection. While the iPSC technology has not yet advanced to a stage where therapeutic transplants have been deemed safe, iPSCs are readily being used in personalized drug discovery efforts and understanding the patient-specific basis of disease.[citation needed]

Depending on the methods used, reprogramming of adult cells to obtain iPSCs may pose significant risks that could limit their use in humans. For example, if viruses are used to genomically alter the cells, the expression of oncogenes (cancer-causing genes) may potentially be triggered. In February 2008, scientists announced the discovery of a technique that could remove oncogenes after the induction of pluripotency, thereby increasing the potential use of iPS cells in human diseases.[4] In April 2009, it was demonstrated that generation of iPS cells is possible without any genetic alteration of the adult cell: a repeated treatment of the cells with certain proteins channeled into the cells via poly-arginine anchors was sufficient to induce pluripotency.[5] The acronym given for those iPSCs is piPSCs (protein-induced pluripotent stem cells).

iPSCs are typically derived by introducing a specific set of pluripotency-associated genes, or reprogramming factors, into a given cell type. The original set of reprogramming factors (also dubbed Yamanaka factors) are the genes Oct4 (Pou5f1), Sox2, cMyc, and Klf4. While this combination is most conventional in producing iPSCs, each of the factors can be functionally replaced by related transcription factors, miRNAs, small molecules, or even non-related genes such as lineage specifiers.

iPSC derivation is typically a slow and inefficient process, taking 12 weeks for mouse cells and 34 weeks for human cells, with efficiencies around 0.01%0.1%. However, considerable advances have been made in improving the efficiency and the time it takes to obtain iPSCs. Upon introduction of reprogramming factors, cells begin to form colonies that resemble pluripotent stem cells, which can be isolated based on their morphology, conditions that select for their growth, or through expression of surface markers or reporter genes.

Induced pluripotent stem cells were first generated by Shinya Yamanaka's team at Kyoto University, Japan, in 2006.[1] Their hypothesis was that genes important to embryonic stem cell function might be able to induce an embryonic state in adult cells. They began by choosing twenty-four genes that were previously identified as important in embryonic stem cells, and used retroviruses to deliver these genes to fibroblasts from mice. The mouse fibroblasts were engineered so that any cells that reactivated the ESC-specific gene, Fbx15, could be isolated using antibiotic selection.

Upon delivery of all twenty-four factors, colonies emerged that had reactivated the Fbx15 reporter, resembled ESCs, and could propagate indefinitely. They then narrowed their candidates by removing one factor at a time from the pool of twenty-four. By this process, they identified four factors, Oct4, Sox2, cMyc, and Klf4, which as a group were both necessary and sufficient to obtain ESC-like colonies under selection for reactivation of Fbx15.

Similar to ESCs, these first-generation iPSCs showed unlimited self-renewal and demonstrated pluripotency by contributing to lineages from all three germ layers in the context of embryoid bodies, teratomas, fetal chimeras. However, the molecular makeup of these cells, including gene expression and epigenetic marks, was somewhere between that of a fibroblast and an ESC, and the cells also failed to produce viable chimeras when injected into developing embryos.

In June 2007, the same group published a breakthrough study along with two other independent research groups from Harvard, MIT, and the University of California, Los Angeles, showing successful reprogramming of mouse fibroblasts into iPS cells. Unlike the first generation of iPS cells, these cells could produce viable chimeric mice and could contribute to the germline, the 'gold standard' for pluripotent stem cells. These cells were derived from mouse fibroblasts by retroviral-mediated expression of the same four transcription factors (Oct4, Sox2, cMyc, Klf4), but the researchers used a different marker to select for pluripotent cells. Instead of Fbx15, they used Nanog, a gene that is functionally important in ESCs. By using this different strategy, the researchers were able to create iPS cells that were more similar to ESCs than the first generation of iPS cells, and independently proved that it was possible to create iPS cells that are functionally identical to ESCs.[6][7][8][9]

Unfortunately, two of the four genes used (namely, c-Myc and KLF4) are oncogenic, and 20% of the chimeric mice developed cancer. In a later study, Yamanaka reported that one can create iPSCs even without c-Myc. The process takes longer and is not as efficient, but the resulting chimeras didn't develop cancer.[10]

Induced pluripotent cells have been made from adult stomach, liver, skin cells, blood cells, prostate cells and urinary tract cells.[11]

In November 2007, a milestone was achieved[12][13] by creating iPSCs from adult human cells; two independent research teams' studies were released one in Science by James Thomson at University of WisconsinMadison[14] and another in Cell by Shinya Yamanaka and colleagues at Kyoto University, Japan.[15] With the same principle used earlier in mouse models, Yamanaka had successfully transformed human fibroblasts into pluripotent stem cells using the same four pivotal genes: Oct3/4, Sox2, Klf4, and c-Myc with a retroviral system. Thomson and colleagues used OCT4, SOX2, NANOG, and a different gene LIN28 using a lentiviral system.

On 8 November 2012, researchers from Austria, Hong Kong and China presented a protocol for generating human iPSCs from exfoliated renal epithelial cells present in urine on Nature Protocols.[16] This method of acquiring donor cells is comparatively less invasive and simple. The team reported the induction procedure to take less time, around 2 weeks for the urinary cell culture and 3 to 4 weeks for the reprogramming; and higher yield, up to 4% using retroviral delivery of exogenous factors. Urinary iPSCs (UiPSCs) were found to show good differentiation potential, and thus represent an alternative choice for producing pluripotent cells from normal individuals or patients with genetic diseases, including those affecting the kidney.[16]

Although the methods pioneered by Yamanaka and others have demonstrated that adult cells can be reprogrammed to iPS cells, there are still challenges associated with this technology:

The table at right summarizes the key strategies and techniques used to develop iPS cells over the past half-decade. Rows of similar colors represents studies that used similar strategies for reprogramming.

One of the main strategies for avoiding problems (1) and (2) has been to use small compounds that can mimic the effects of transcription factors. These molecule compounds can compensate for a reprogramming factor that does not effectively target the genome or fails at reprogramming for another reason; thus they raise reprogramming efficiency. They also avoid the problem of genomic integration, which in some cases contributes to tumor genesis. Key studies using such strategy were conducted in 2008. Melton et al. studied the effects of histone deacetylase (HDAC) inhibitor valproic acid. They found that it increased reprogramming efficiency 100-fold (compared to Yamanakas traditional transcription factor method).[25] The researchers proposed that this compound was mimicking the signaling that is usually caused by the transcription factor c-Myc. A similar type of compensation mechanism was proposed to mimic the effects of Sox2. In 2008, Ding et al. used the inhibition of histone methyl transferase (HMT) with BIX-01294 in combination with the activation of calcium channels in the plasma membrane in order to increase reprogramming efficiency.[26] Deng et al. of Beijing University reported on July 2013 that induced pluripotent stem cells can be created without any genetic modification. They used a cocktail of seven small-molecule compounds including DZNep to induce the mouse somatic cells into stem cells which they called CiPS cells with the efficiency at 0.2% comparable to those using standard iPSC production techniques. The CiPS cells were introduced into developing mouse embryos and were found to contribute to all major cells types, proving its pluripotency.[27][28]

Ding et al. demonstrated an alternative to transcription factor reprogramming through the use of drug-like chemicals. By studying the MET (mesenchymal-epithelial transition) process in which fibroblasts are pushed to a stem-cell like state, Dings group identified two chemicals ALK5 inhibitor SB431412 and MEK (mitogen-activated protein kinase) inhibitor PD0325901 which was found to increase the efficiency of the classical genetic method by 100 fold. Adding a third compound known to be involved in the cell survival pathway, Thiazovivin further increases the efficiency by 200 fold. Using the combination of these three compounds also decreased the reprogramming process of the human fibroblasts from four weeks to two weeks. [29][30]

Another key strategy for avoiding problems such as tumor genesis and low throughput has been to use alternate forms of vectors: adenovirus, plasmids, and naked DNA and/or protein compounds.

In 2008, Hochedlinger et al. used an adenovirus to transport the requisite four transcription factors into the DNA of skin and liver cells of mice, resulting in cells identical to ESCs. The adenovirus is unique from other vectors like viruses and retroviruses because it does not incorporate any of its own genes into the targeted host and avoids the potential for insertional mutagenesis.[31] In 2009, Freed et al. demonstrated successful reprogramming of human fibroblasts to iPS cells.[32] Another advantage of using adenoviruses is that they only need to present for a brief amount of time in order for effective reprogramming to take place.

Also in 2008, Yamanaka et al. found that they could transfer the four necessary genes with a plasmid.[33] The Yamanaka group successfully reprogrammed mouse cells by transfection with two plasmid constructs carrying the reprogramming factors; the first plasmid expressed c-Myc, while the second expressed the other three factors (Oct4, Klf4, and Sox2). Although the plasmid methods avoid viruses, they still require cancer-promoting genes to accomplish reprogramming. The other main issue with these methods is that they tend to be much less efficient compared to retroviral methods. Furthermore, transfected plasmids have been shown to integrate into the host genome and therefore they still pose the risk of insertional mutagenesis. Because non-retroviral approaches have demonstrated such low efficiency levels, researchers have attempted to effectively rescue the technique with what is known as the piggyBac transposon system. The lifecycle of this system is shown below. Several studies have demonstrated that this system can effectively deliver the key reprogramming factors without leaving any footprint mutations in the host cell genome. As demonstrated in the figure, the piggyBac transposon system involves the re-excision of exogenous genes, which eliminates issues like insertional mutagenesis

In January 2014, two articles were published claiming that a type of pluripotent stem cell can be generated by subjecting the cells to certain types of stress (bacterial toxin, a low pH of 5.7, or physical squeezing); the resulting cells were called STAP cells, for stimulus-triggered acquisition of pluripotency.[34]

In light of difficulties that other labs had replicating the results of the surprising study, in March 2014, one of the co-authors has called for the articles to be retracted.[35] On 4 June 2014, the lead author, Obokata agreed to retract both the papers [36] after she was found to have committed research misconduct as concluded in an investigation by RIKEN on 1 April 2014.[37]

Studies by Blelloch et al. in 2009 demonstrated that expression of ES cell-specific microRNA molecules (such as miR-291, miR-294 and miR-295) enhances the efficiency of induced pluripotency by acting downstream of c-Myc .[38] More recently (in April 2011), Morrisey et al. demonstrated another method using microRNA that improved the efficiency of reprogramming to a rate similar to that demonstrated by Ding. MicroRNAs are short RNA molecules that bind to complementary sequences on messenger RNA and block expression of a gene. Morriseys team worked on microRNAs in lung development, and hypothesized that their microRNAs perhaps blocked expression of repressors of Yamanakas four transcription factors. Possible mechanisms by which microRNAs can induce reprogramming even in the absence of added exogenous transcription factors, and how variations in microRNA expression of iPS cells can predict their differentiation potential discussed by Xichen Bao et al.[39]

[citation needed]

The generation of iPS cells is crucially dependent on the genes used for the induction.

Oct-3/4 and certain members of the Sox gene family (Sox1, Sox2, Sox3, and Sox15) have been identified as crucial transcriptional regulators involved in the induction process whose absence makes induction impossible. Additional genes, however, including certain members of the Klf family (Klf1, Klf2, Klf4, and Klf5), the Myc family (c-myc, L-myc, and N-myc), Nanog, and LIN28, have been identified to increase the induction efficiency.

Induced pluripotent stem cells are similar to natural pluripotent stem cells, such as embryonic stem (ES) cells, in many aspects, such as the expression of certain stem cell genes and proteins, chromatin methylation patterns, doubling time, embryoid body formation, teratoma formation, viable chimera formation, and potency and differentiability, but the full extent of their relation to natural pluripotent stem cells is still being assessed.[42]

Gene expression and genome-wide H3K4me3 and H3K27me3 were found to be extremely similar between ES and iPS cells.[43][citation needed] The generated iPSCs were remarkably similar to naturally isolated pluripotent stem cells (such as mouse and human embryonic stem cells, mESCs and hESCs, respectively) in the following respects, thus confirming the identity, authenticity, and pluripotency of iPSCs to naturally isolated pluripotent stem cells:

Recent achievements and future tasks for safe iPSC-based cell therapy are collected in the review of Okano et al.[54]

The task of producing iPS cells continues to be challenging due to the six problems mentioned above. A key tradeoff to overcome is that between efficiency and genomic integration. Most methods that do not rely on the integration of transgenes are inefficient, while those that do rely on the integration of transgenes face the problems of incomplete reprogramming and tumor genesis, although a vast number of techniques and methods have been attempted. Another large set of strategies is to perform a proteomic characterization of iPS cells. The Wu group at Stanford University has made significant progress with this strategy.[55] Further studies and new strategies should generate optimal solutions to the five main challenges. One approach might attempt to combine the positive attributes of these strategies into an ultimately effective technique for reprogramming cells to iPS cells.

Another approach is the use of iPS cells derived from patients to identify therapeutic drugs able to rescue a phenotype. For instance, iPS cell lines derived from patients affected by ectodermal dysplasia syndrome (EEC), in which the p63 gene is mutated, display abnormal epithelial commitment that could be partially rescued by a small compound[56]

An attractive feature of human iPS cells is the ability to derive them from adult patients to study the cellular basis of human disease. Since iPS cells are self-renewing and pluripotent, they represent a theoretically unlimited source of patient-derived cells which can be turned into any type of cell in the body. This is particularly important because many other types of human cells derived from patients tend to stop growing after a few passages in laboratory culture. iPS cells have been generated for a wide variety of human genetic diseases, including common disorders such as Down syndrome and polycystic kidney disease.[57][58] In many instances, the patient-derived iPS cells exhibit cellular defects not observed in iPS cells from healthy patients, providing insight into the pathophysiology of the disease.[59] An international collaborated project, StemBANCC, was formed in 2012 to build a collection of iPS cell lines for drug screening for a variety of disease. Managed by the University of Oxford, the effort pooled funds and resources from 10 pharmaceutical companies and 23 universities. The goal is to generate a library of 1,500 iPS cell lines which will be used in early drug testing by providing a simulated human disease environment.[60]

A proof-of-concept of using induced pluripotent stem cells (iPSCs) to generate human organ for transplantation was reported by researchers from Japan. Human liver buds (iPSC-LBs) were grown from a mixture of three different kinds of stem cells: hepatocytes (for liver function) coaxed from iPSCs; endothelial stem cells (to form lining of blood vessels) from umbilical cord blood; and mesenchymal stem cells (to form connective tissue). This new approach allows different cell types to self-organize into a complex organ, mimicking the process in fetal development. After growing in vitro for a few days, the liver buds were transplanted into mice where the liver quickly connected with the host blood vessels and continued to grow. Most importantly, it performed regular liver functions including metabolizing drugs and producing liver-specific proteins. Further studies will monitor the longevity of the transplanted organ in the host body (ability to integrate or avoid rejection) and whether it will transform into tumors.[61][62] Using this method, cells from one mouse could be used to test 1,000 drug compounds to treat liver disease, and reduce animal use by up to 50,000.[63]

Embryonic cord-blood cells were induced into pluripotent stem cells using plasmid DNA. Using cell surface endothelial/pericytic markers CD31 and CD146, researchers identified 'vascular progenitor', the high-quality, multipotent vascular stem cells. After the iPS cells were injected directly into the vitreous of the damaged retina of mice, the stem cells engrafted into the retina, grew and repaired the vascular vessels.[64][65]

In a study conducted in China in 2013, Superparamagnetic iron oxide (SPIO) particles were used to label iPSCs-derived NSCs in vitro. Labeled NSCs were implanted into TBI rats and SCI monkeys 1 week after injury, and then imaged using gradient reflection echo (GRE) sequence by 3.0T magnetic resonance imaging (MRI) scanner. MRI analysis was performed at 1, 7, 14, 21, and 30 days, respectively, following cell transplantation. Pronounced hypointense signals were initially detected at the cell injection sites in rats and monkeys and were later found to extend progressively to the lesion regions, demonstrating that iPSCs-derived NSCs could migrate to the lesion area from the primary sites. The therapeutic efficacy of iPSCs-derived NSCs was examined concomitantly through functional recovery tests of the animals. In this study, we tracked iPSCs-derived NSCs migration in the CNS of TBI rats and SCI monkeys in vivo for the first time. Functional recovery tests showed obvious motor function improvement in transplanted animals. These data provide the necessary foundation for future clinical application of iPSCs for CNS injury.[66]

In 2014, type O red blood cells were synthesized at the Scottish National Blood Transfusion Service from iPSC. The cells were induced to become a mesoderm and then blood cells and then red blood cells. The final step was to make them eject their nuclei and mature properly. Type O can be transfused into all patients. Each pint of blood contains about two trillion red blood cells, while some 107 million blood donations are collected globally every year. Human transfusions were not expected to begin until 2016.[67]

The first human clinical trial using autologous iPSCs is approved by the Japan Ministry Health and will be conducted in 2014 in Kobe. iPSCs derived from skin cells from six patients suffering from wet age-related macular degeneration will be reprogrammed to differentiate into retinal pigment epithelial (RPE) cells. The cell sheet will be transplanted into the affected retina where the degenerated RPE tissue has been excised. Safety and vision restoration monitoring is expected to last one to three years.[68][69] The benefits of using autologous iPSCs are that there is theoretically no risk of rejection and it eliminates the need to use embryonic stem cells.[69]

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Induced pluripotent stem cell - Wikipedia, the free ...

What are the kidneys?

The kidneys play key roles in body function, not only by filtering the blood and getting rid of waste products, but also by balancing the electrolyte levels in the body, controlling blood pressure, and stimulating the production of red blood cells.

The kidneys are located in the abdomen toward the back, normally one on each side of the spine. They get their blood supply through the renal arteries directly from the aorta and send blood back to the heart via the renal veins to the vena cava. (The term "renal" is derived from the Latin name for kidney.)

The kidneys have the ability to monitor the amount of body fluid, the concentrations of electrolytes like sodium and potassium, and the acid-base balance of the body. They filter waste products of body metabolism, like urea from protein metabolism and uric acid from DNA breakdown. Two waste products in the blood usually are measured; 1) blood urea nitrogen (BUN), and 2) creatinine (Cr). Continue Reading

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Longo DL, et al. Harrisons Principles of Internal Medicine. 18th edition. McGraw Hill Professional. 2011.

Medscape. Renal Failure, Acute.

NIH. Amyloidosis and Kidney Disease. IMAGES:

1. iStock

2. Veer

3. MedicineNet

4. Bigstock

5. iStock

6. iStock

7. iStock

8. iStock

9. iStock

10. Veer

11. Bigstock

12. iStock

13. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH)

14. iStock

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Kidney Failure - MedicineNet

Graduate Medical Education (GME): Medical Genetics

Maximilian Muenke, MD

Eligibility CriteriaCandidates with the MD degree must have completed an accredited U.S. residency training program and have a valid U.S. license. Previous training is usually in, but not limited to, Pediatrics, Internal Medicine or Obstetrics and Gynecology.

OverviewThe NIH has joined forces with training programs at the Children's National Medical Center, George Washington University School of Medicine and Washington Hospital Center. The combined training program in Medical Genetics is called the Metropolitan Washington, DC Medical Genetics Program. This is a program of three years duration for MDs seeking broad exposure to both clinical and research experience in human genetics.

The NIH sponsor of the program is National Human Genome Research Institute (NHGRI). Other participating institutes include the National Cancer Institute (NCI), the National Eye Institute (NEI), the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), the National Institute of Child Health and Human Development (NICHD), the National Institute on Deafness and Other Communication Disorders (NIDCD), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and the National Institute of Mental Health (NIMH). Metropolitan area participants include Children's National Medical Center (George Washington University), Walter Reed Army Medical Center, and the Department of Pediatrics, and the Department of Obstetrics and Gynecology at Washington Hospital Center. The individual disciplines in the program include clinical genetics, biochemical genetics, clinical cytogenetics, and clinical molecular genetics.

The primary goal of the training program is to provide highly motivated physicians with broad exposure to both clinical and research experiences in medical genetics. We train candidates to become effective, independent medical geneticists, prepared to deliver a high standard of clinical genetics services, and to perform state-of-the-art research in the area of genetic disease.

Structure of the Clinical Training Program

RotationsThis three year program involves eighteen months devoted to learning in clinical genetics followed by eighteen months of clinical or laboratory research.

Year 1Six months will be spent on rotation at the NIH. Service will include time spent on different outpatient genetics clinics, including Cancer Genetics and Endocrine Disorders and Genetic Ophthalmology; on the inpatient metabolic disease and endocrinology ward; on inpatient wards for individuals involved in gene therapy trials; and on the NIH Genetics Consultation Service.

Three months will be spent at Children's National Medical Center and will be concentrated on pediatric genetics. Fellows will participate in outpatient clinics, satellite and outreach clinics. They will perform consults on inpatients and patients with metabolic disorders and on the neonatal service. Fellows will be expected to participate in the relevant diagnostic laboratory studies on patients for whom they have provided clinical care.

One month will be spent at Walter Reed Army Medical Center and will concentrate on adult and pediatric clinical genetics. One month will be spent at Washington Hospital Center on rotations in prenatal genetics and genetic counseling.

Year 2 Fellows will spend one month each in clinical cytogenetics, biochemical genetics, and molecular diagnostic laboratories. The remaining three months will be devoted to elective clinical rotations on any of the rotations previously mentioned. The second six months will be spent on laboratory or clinical research. The fellow will spend at least a half-day per week in clinic at any one of the three participating institutions.

Year 3This year will be devoted to research, with at least a half day per week in clinic.

NIH Genetics Clinic (Required)Fellows see patients on a variety of research protocols. The Genetics Clinic also selectively accepts referrals of patients requiring diagnostic assessment and genetic counseling. Areas of interest and expertise include: chromosomal abnormalities, congenital anomalies and malformation syndromes, biochemical defects, bone and connective tissue disorders, neurological disease, eye disorders, and familial cancers.

Inpatient Consultation Service (Required)Fellows are available twenty-four hours daily to respond to requests for genetics consultation throughout the 325-bed hospital. Written consultation procedures call for a prompt preliminary evaluation, a written response within twenty-four hours, and a subsequent presentation to a senior staff geneticist, with an addendum to the consult, as needed. The consultant service fellow presents the most interesting cases from the wards during the Post-Clinic Patient Conference on Wednesday afternoons during which Fellows present interesting clinical cases for critical review. Once a month the fellow presents relevant articles for journal club.

Metropolitan Area Genetics Clinics

Other Clinical Opportunities: Specialty Clinics at NIHThe specialty clinics of NIH treat a large number of patients with genetic diseases. We have negotiated a supervised experience for some of the fellows at various clinics; to date, fellows have participated in the Cystic Fibrosis Clinic, the Lipid Clinic, and the Endocrine Clinic.

Lectures, Courses and SeminarsThe fellowship program includes many lectures, courses and seminars. Among them are a journal club and seminars in medical genetics during which invited speakers discuss research and clinical topics of current interest. In addition, the following four courses have been specifically developed to meet the needs of the fellows:

Trainees are encouraged to pursue other opportunities for continuing education such as clinical and basic science conferences, tutorial seminars, and postgraduate courses, which are plentiful on the NIH campus.

Structure of the Research Training ProgramFellows in the Medical Genetics Program pursue state-of-the-art research related to genetic disorders. Descriptions of the diverse interests of participating faculty are provided in this catalog. The aim of this program is to provide fellows with research experiences of the highest caliber and to prepare them for careers as independent clinicians and investigators in medical genetics.

Fellows entering the program are required to select a research supervisor which may be from among those involved on the Genetics Fellowship Faculty Program. It is not required that this selection be made before coming to NIH.

In addition to being involved in research, all fellows attend and participate in weekly research seminars, journal clubs and laboratory conferences, which are required elements of each fellow's individual research experience.

Program Faculty and Research Interests

Examples of Papers Authored by Program Faculty

Program GraduatesThe following is a partial list of graduates including their current positions:

Application Information

The NIH/Metropolitan Washington Medical Genetics Residency Program is accredited by the ACGME and the American Board of Medical Genetics. Upon successful completion of the three year program, residents are eligible for board certification in Clinical Genetics. During the third residency year, residents may elect to complete either (a) the requirements for one of the ABMG laboratory subspecialties, such as Clinical Molecular Genetics, Clinical Biochemical Genetics or Clinical Cytogenetics, or (b) a second one year residency program (e.g., Medical Biochemical Genetics).

Candidates should apply through ERAS, beginning July 1 of the year prior to their anticipated start date. Candidates with the MD or MD and PhD degree must have completed a U.S. residency in a clinically related field. Previous training is usually in, but not limited to, Pediatrics, Internal Medicine or Obstetrics and Gynecology. Four new positions are available each year. Interviews are held during August and September.

Electronic Application The quickest and easiest way to find out more about this training program or to apply for consideration is to do it electronically.

The NIH is dedicated to building a diverse community in its training and employment programs.

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NIH Clinical Center: Graduate Medical Education (GME ...

FDA and Adipose Stem Cells

Several years ago we became fascinated with the potential of adipose stem cells for both cosmetic and medical purposes. However, we soon discovered that nothing in the written FDA guidelines specifically addressed the use of autologous adipose stem cells. Thus began our journey for an answer. In June 2009, we sent a letter to the FDA asking for a position statement on adipose stem cells. Our request focused specifically on autologous, freshly isolated, adipose stem cells for use in soft tissue reconstruction. These stem cells are from your own fat, for your own usage, and not culture expanded .

After a very long wait, we recently received a written response from the FDA. First, a little bit of background for any stem cell newbies.

Human cells and tissues intended for human transplant are regulated by the FDA. The FDA maintains two levels of classifications for cells and tissues: 1) HCT/P 361 and 2) HCT/P 351.

uncultured stem cells from my own fat. a tissue or a drug?

Category 361 is summarized as a tissue. A subset of category 361 includes procedures that take place in the same operative session . These same session operative procedures are exempt from FDA regulation. These procedures fall under the jurisdiction of practice of medicine. Surgeons follow guidelines and laws established by state medical boards and their professional societies, but are not controlled by the FDA. The other category, 351, is the drug/biologic category, which is completely regulated by the FDA. It is infinitely easier and faster to bring medical procedures which fall under 361 guidelines to a physicians practice compared to the 351 category.

Examples of tissues and cell types in each of the two FDA categories are as follows:

Our request simply asked the FDA if SVF (not culture expanded) adipose stem cells for autologous usage in soft tissue reconstruction in the same operative session fall under the tissue or the drug classification.

Last month we finally received a response from the FDA. Close your eyes and imagine a train coming to a screeching halt.It was not the answer we were hoping for.

Your own autologous adipose stem cells from the stromal vascular fraction (SVF) used for reconstruction and repair in the same operative session are considered by the FDA to be a DRUG.

What is interesting to us is that hematopoeitic stem cells and IVF procedures are both not classified as drugs, but uncultured fat stem cells are. The FDAs main consideration for classifying adipose stem cells as a drug was because the cells are more than minimally manipulated. So what about IVF procedures? Is creating a human from a sperm and an egg only a minimal manipulation?

To make a long story short, the drug classification will add several years to the equation for surgeons manually performing therapies with adipose stem cells. In our opinion, the FDAs new position on adipose stem cells will likely have two effects:

The new FDA position means that any surgeon who wishes to use the SVF fraction (centrifuged adipose tissue plus collagenase to yield higher numbers of stem cells) must now submit an IND (Investigational New Drug Application) to the FDA and have an approved IRB (Institutional Review Board) with a hospital. This submittal process is extremely time consuming, requires many resources, and is expensive. Some surgeons will simply move their trials, therapies, and clinics offshore.

This FDA position essentially takes surgeons performing manual processing with collagenase in their ORs out of the physician practice equation for the near future. Therefore, this FDA position likely benefits adipose stem cell device makers who process adipose tissue as they are much further along in the approval process with the FDA. Device makers will likely be first to market with their autologous stem cell processes.

No. But it is not out of the question that the FDA may put fat grafting under the magnifying glass in the future.

Fat grafting uses fat obtained from liposuction. The fat is harvested with a cannula, decanted, and processed via centrifugation techniques. A portion of the processed fat is then reinjected into areas for cosmetic enhancement. The enhancements primarily involve restoring volume and fullness.

Although fat grafting does not use collagenese to isolate the stem cells, the dirty little secret is that high density fat grafting does contain small numbers of stem cells. These stem cells are found in the fat pellet separated via centrifugation after the tumescent liposuction procedure. The mechanical forces of the liposuction procedure act to separate the mesenchymal stem cells from the blood vessels. This is all within the great science of stem cell activation. Plastic surgeons have recently come to understand that the small population of stem cells in the fat pellet provide more vascularity to fat grafts. High density fat grafting results in long lasting fat grafts and healthier looking skin.

by Leeza Rodriguez CosmeticSurg Staff Writer Leeza Rodriguez on Google +

Posted in Fat Stem Cells

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FDA: Stem Cells from Your Own Fat are a Drug ...

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People in the DMV region are increasingly feeling the effects of diabetes as thousands of people suffer from the disease, and many others may have diabetes and don't know it! It is estimated that one out of every three children born after 2000 in the United States will be directly affected by diabetes.

That is why the American Diabetes Association's Washington office is so committed to educating the public about how to stop diabetes and support those living with the disease.

We are here to help.

The American Diabetes Association has established a program to train volunteers to implement diabetes/wellness education workshops in the Washington DC Metro Area. The idea is to give people who are passionate about health promotion the resources they need to act by leading workshops on diabetes/wellness in their communities. These workshops will help get the word out about prevention strategies and the dangers of uncontrolled diabetes. The Association also hopes these workshops become places community members can exchange ideas about what they are doing to stay healthy. The ideal audience will be people that you know from your communities. Ambassador volunteers have the opportunity to motivate friends, family and members of the community to join the fight to Stop Diabetes!

If you, or someone you know, is interested in serving as an American Diabetes Association Ambassador, please contact Tiffany Ingram at 202-331-8303 ext. 4540 or tingram@diabetes.org.

We welcome your help.

Your involvement as an American Diabetes Association volunteer whether on a local or national level will help us expand our community outreach and impact, inspire healthy living, intensify our advocacy efforts, raise critical dollars to fund our mission, and uphold our reputation as the moving force and trusted leader in the diabetes community.

Find volunteer opportunities in our area through the Volunteer Center.

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Washington, DC - American Diabetes Association

Mr. Deven Patel President, CEO and Co-founder

Mr. Deven Patel is the President, CEO and Cofounder of GIOSTAR. He has also served as the CEO, President and Board of Directors in highly comprehensive environment of Healthcare Management, Architectural, General Construction, Alternative Energy and multifaceted Internet industries. Apart from serving as CEO and President, Mr. Patel has also served in a key positions of several public and private organizations such as Asian & Pacific American Coalition, Asian Outreach Committee Children Memorial Hospital San Diego, Federation of India Associations, National Federation of Indian American Association, CRY America, Global Organization of People of Indian Origin, Kelly Dean Citizens Awareness Circle, Phillip Redmond Foundation, Lockport Planning Commission.

During his early career, Mr. Patel was involved with the design and construction of several healthcare projects as an architect and a builder. He has also served as a partner for an assisted living and wellness center fostering care for senior citizens suffering from special conditions.

Dr. Anand Srivastava, M.S., Ph.D. Chairman, Cofounder and Chief Scientific Officer

Dr. Anand Srivastava has been associated with leading universities and research institutions of USA. In affiliation with University of California San Diego Medical College (UCSD), University of California Irvine Medical College (UCI), Salk Research Institute, San Diego, Burnham Institute For Medical Research, San Diego, University of California Los Angeles Medical College (UCLA), USA has developed several research collaborations and has an extensive research experience in the field of Embryonic Stem cell which is documented by several publications in revered scientific journals.

Dr. Anand Srivastava's success has its root in his unique background of expertise in Stem cell biology, protein biochemistry, molecular biology, immunology, in utero transplantation of stem cell, tissue targeting, gene therapy and clinical research. There are many scientists who can work in a narrowly defined field but few have broad and multidisciplinary experience to carry out clinical research in a field as challenging as Stem cell biology, cancer and gene therapy field. Dr. Anand Srivastava's wide-spectrum expertise is rare in clinical research and perfectly crafted to fit ideally with the GIOSTAR projects for Stem cell transplant, cancer and gene therapy research.

Dr. Anand Srivastava's research work has been presented in various national and international scientific meetings and conferences in India, Japan, Germany and USA. His research articles have been published in peer reviewed medical scientific journals and he has been cited extensively by other scientists. Dr. Anand Srivastava's expertise and scientific achievements were recognized by many scientific fellowships and by two consecutive award of highly prestigious and internationally recognized, JISTEC award from Science and Technology Agency, Government of Japan. Also, his research presentation was awarded with the excellent presentation award in the "Meeting of Clinical Chemistry and Medicine, Kyoto, Japan. He has also expertise in genetic engineering research, developmental biology, immunology, making the transgenic animals and his extraordinary expertise of searching and characterizing the new genes are ideal for our ongoing projects of developing the effective treatments for many degenerative diseases, genetic diseases and cancer. Based on his extraordinary scientific achievements his biography has been included in "WHO IS WHO IN AMERICA" data bank two times, first in 2005 and second in 2010.

Dr. Anand Srivastava's Long Profile

Dr. Anand Srivastava has been associated with leading universities and research institutions of USA. In affiliation with University of California San Diego Medical College (UCSD), University of California Irvine Medical College (UCI), Salk Research Institute, San Diego, Burnham Institute For Medical Research, San Diego, University of California Los Angeles Medical College (UCLA), USA has developed several research collaborations and has an extensive research experience in the field of Embryonic Stem cell which is documented by several publications in revered scientific journals.

Dr. Srivastava is a Chairman and Cofounder of California based Global Institute of Stem Cell Therapy and Research (GIOSTAR) headquartered in San Diego, California, (U.S.A.). The company was formed with the vision to provide stem cell based therapy to aid those suffering from degenerative or genetic diseases around the world such as Parkinson's, Alzheimer's, Autism, Diabetes, Heart Disease, Stroke, Spinal Cord Injuries, Paralysis, Blood Related Diseases, Cancer and Burns. GIOSTAR is a leader in developing most advance stem cell based technology, supported by leading scientists with the pioneering publications in the area of stem cell biology. Companys primary focus is to discover and develop a cure for human diseases with the state of the art unique stem cell based therapies and products. The Regenerative Medicine provides promise for treatments of diseases previously regarded as incurable.

Giostar is worlds leading Stem cell research company involved with stem cell research work for over a decade. It is headed by Dr Anand Srivastava, who is a world-renowned authority in the field of Stem cell biology, Cancer, Gene therapy. Several governments including USA, India, China, Turkey, Kuwait, Thailand and many others seek his advice and guidance on drafting their strategic & national policy formulations and program directions in the area of stem cell research, development and its regulations. Under his creative leadership a group of esteemed scientists and clinicians have developed and established Stem cell therapy for various types of Autoimmune diseases and blood disorders which are being offered to patients in USA and soon it will be offered on a regular clinical basis to the people around the globe. Giostar is already the official collaborator of Government of Gujarat, India by setting up a state of art stem cell treatment hospital in Surat civil hospital for the less fortunate tribal populace of the southern belt of Gujarat suffering from Sickle Cell Anemia. Several state Governments in India is looking for a collaborative efforts of GIOSTAR and Dr. Anand to develop stem cell transplant program in their respective states.

SUMMARY OF DR. SRIVASTAVAS WORK:

Dr. Anand Srivastavas success has its root in his unique background of expertise in Stem cell biology, protein biochemistry, molecular biology, immunology, in utero transplantation of stem cell, tissue targeting, gene therapy and clinical research. There are many scientists who can work in a narrowly defined field but few have broad and multidisciplinary experience to carry out clinical research in a field as challenging as Stem cell biology, cancer and gene therapy field. Dr. Anand Srivastavas wide-spectrum expertise is rare in clinical research and perfectly crafted to fit ideally with the GIOSTAR projects for Stem cell transplant, cancer and gene therapy research.

Dr. Anand Srivastavas research work has been presented in various national and international scientific meetings and conferences in India, Japan, Germany and USA. His research articles have been published in peer reviewed medical scientific journals and he has been cited extensively by other scientists. Dr. Anand Srivastavas expertise and scientific achievements were recognized by many scientific fellowships and by two consecutive award of highly prestigious and internationally recognized, JISTEC award from Science and Technology Agency, Government of Japan. Also, his research presentation was awarded with the excellent presentation award in the Meeting of Clinical Chemistry and Medicine, Kyoto, Japan. He has also expertise in genetic engineering research, developmental biology, immunology, making the transgenic animals and his extraordinary expertise of searching and characterizing the new genes are ideal for our ongoing projects of developing the effective treatments for many degenerative diseases, genetic diseases and cancer. Based on his extraordinary scientific achievements his biography has been included in WHO IS WHO IN AMERICA data bank two times, first in 2005 and second in 2010.

POSITIONS HELD BY DR. SRIVASTAVA (1997 to Date):

1. Chairman & Cofounder (2008-till date): Global Institute of Stem Cell Therapy and Research, San Diego, CA. USA. 2. Associate Professor: Department of Cellular and Molecular Biology, School of Medicine, University of California Los Angeles (UCLA), CA, USA. 3. Visiting Senior Scientist: Department of Stem Cell Biology, Burnham Research Institute for Medical Science, San Diego, CA, USA. 4. Senior Scientist: Stem Cell Core Facility, The Salk Research Institute, La Jolla, CA, USA. 5. Associate Professor: Department of Stem Cells and Neurology, School of Medicine, University of California Irvine (UCI), Irvine, CA, USA. 6. Assistant Professor: Cancer Center, School of Medicine, University of California San Diego (UCSD), La Jolla, CA, USA 7. Honorary Visiting Professor: National Research Institute, Nansei, Mie, JAPAN.

SPECIAL STEM ISSUES OF JOURNALS DEVOTED TO DR. SRIVASTAVA

1. Current Topics of Medicinal Chemistry among top five medicinal chemistry journal devoted its special issue of stem cell to Dr. Srivastava in 2010. 2. Stem Cell International devoted its special issue on stem cells to Dr. Srivastava in 2012.

EXPERT SCIENTIFIC REVIEWER FOR LEADING JOURNALS OF MEDICINE:

Dr. Srivastava is the member of the several scientific review committees and reviewing the research grants. He has written several review articles and scientific manuscripts. He is also the reviewer and editor of several scientific journals.

1. Advances in Stem Cells 2. Current pharmaceutical Design 3. Current Topics in Medicinal Chemistry 4. Stem Cells 5. Stem Cell International 6. Current in Cell Medicine 7. Journal of Stem Cell Research and Therapy 8. Conference Papers in Molecular Biology 9. Journal of Pharmaceutics 10. Current Pharmaceutical Biotechnology 11. Open Journal of Organ Transplant Surgery 12. Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry 13. Stem Cells and Cloning: Advances and Applications 14. Blood and Lymphatic Cancer: Targets and Therapy 15. Degenerative Neurological and Neuromuscular Disease 16. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 17. Immuno Targets and Therapy 18. Current Vascular Pharmacology 19. Gastrointestinal Cancer: Targets and Therapy 20. Journal of Bioengineering and Biomedical Sciences 21. The Application of Clinical Genetics 22. Journal of Tissue Science & Engineering 23. Neuropsychiatric Disease and Treatment 24. Current Tissue Engineering 25. Hepatic Medicine: Evidence and Research 26. Current Drug Discovery Technologies 27. Current Bioactive Compounds 28. Transplant Research and Risk Management 29. Biosimilars 30. Current Drug Delivery 31. Journal of Experimental Pharmacology 32. Open Journal of Regenerative Medicine 33. Current Diabetes Reviews 34. Journal of Fertilization: In Vitro 35. Clinical and Translational Medicine

FELLOWSHIPS/ AWARDS:

2003 Awarded with NIMA (National Integrated Medical Association) Outstanding Scientist award from NIMA, India. 2003 Awarded with Excellent Scientist Award from Bharat Vikas Parisad, India for continuous excellent performance in the life science research. The 18th International Congress of Clinical Chemistry and Laboratory Medicine Kyoto Excellent Poster Award, Kyoto, Japan. 2002 Best Scientist Award for excellent contribution in the field of life science research from Kayastha Maha Sabha, Varanasi, India. 1998-2000: Long-term STA/JISTEC Award (Science and Technology Agency/Japan International Science and Technology Exchange Center, JAPAN)- Fellowship award for two year from government of Japan. 1997-1998: Short-term STA/JISTEC Award (Science and Technology Agency/Japan International Science and Technology Exchange Center, JAPAN)- Fellowship Award for three months from government of Japan (October 1997- January 1998). 1997-1998: Awarded with Research Associate-ship award from CSIR (Council of Scientific and Industrial Research) Government of India. 1990-1995: CAS (Center of Advanced Study) Award in Zoology. A doctoral research fellowship award from Government of India.

THE FOLLOWING SUMMARIZES DR. SRIVASTAVAS MAJOR SCIENTIFIC ACHIEVEMENTS:

1. Dr. Srivastava developed the animal material free and serum free Human embryonic Stem cell culture condition to use the Human ES cells to treat the human diseases. 2. Dr. Srivastava for the first time showed that if the ES cell injected into developing fetuses in utero takes participation in development of all body of a living organism. 3. For the first time he showed that ES cell is better accepted by the transplanted animals in comparison to adult stem cells. 4. For the first time he showed the way to generate the high number of pre-erythrocytes using glucocorticoid hormone. Which may be use to treat several blood diseases. 5. For the first time Using ES cells he generated the high number of CD34+ expressing a kind of hematopoietic stem cell which can be used to treat several autoimmune diseases, immune reconstitution and blood diseases. 6. For the first time he showed the molecular mechanism behind the regulation of ES cell differentiation into hematopoietic cells. 7. For the first time he showed that ES cells automatically recognize the damage portion of the brain and can be used to repair the damage brain. 8. For the first time he showed that ES cell can be used to treat the Crohns disease a kind of colon cancer. 9. For the first time, he demonstrated that the mammalian fetuses can be programmed inside the mother uterus to face the challenges of the future possible infection. This finding is very important to develop the advanced therapy for any fatal disease such as cancer and AIDS. Utilizing these techniques, fetuses can be given information about all possible infections and the capability to counter those infections and disease. 10. He has demonstrated for the first time that it is easy to correct the genetic diseases in developing fetus in utero in comparison to adult animals. 11. He has shown for the first time that the lung cancer cells can be treated with the help of plant product curcumin and can be used as effective cancer therapeutic agent. He also demonstrated that how curcumin regulated the genes related to programmed death of cancerous cell. Finding help in development of non-toxic, less expensive, easily available drug for cancer. 12. The biggest problem in the treatment of cancer and other diseases is the non-specific distribution of medicine and toxic chemotherapeutic agents to healthy tissues. Dr. Srivastava for the first time developed a technique that can help in targeting the diseased tissues using the tissue receptor binding peptide ligands. These techniques can be used for targeted delivery of drugs and genes (in case of genetic disease) to the specific fetal tissues inside the mother uterus without harming the normal tissues of mother and fetus. 13. For the first time, He demonstrated the insertion of foreign pancreas enzyme specific gene promoter into the developing animals embryo and successfully shown the incorporation and regulation of pancreatic enzyme in the control of inserted gene. This is very important finding and proves that the defective genes can be replaced easily and effectively by the normal functional genes during the development of animals. This finding will help in the change of defective genes of insulin hormone, which is present in the pancreas of diabetic patients and many other genetic diseases also. 14. For the first time, He reported the gene sequence of all important pancreatic enzymes (three isoform of trypsinogen, two isoforms of chymotrypsinogen, four types of elastases, three forms of carboxypeptidases and lipase) and its evolutionary relationship with human. Also,he reported first time the regulation of digestion by these enzymes in the alimentary canal during digestion of proteins in the developing animals. 15. For the first time, He cloned and sequenced two types of human homologue of Vitamin D receptor gene from Japanese flounder, which is most important receptor, which help in the development of bone. Before my report, characters of this gene were not known in Japanese flounder. This finding helped in the understanding of the genetic evolution of mammals. 16. For the first time, he cloned and sequenced the homologue of human placental protein, PP11, and mouse T cell specific, Tcl-30, in pancreas of Japanese flounder, this study suggest that these genes evolved from the fish pancreas and in fish it helps in synthesizing the digestive enzymes but during the evolution its function got changed and work differently in the mammalian placenta. This was very important finding related to this rare gene. 17. For the first time, He has shown that the Hox and sonic hedgehog genes regulate the development of bones and respiratory organs. He also demonstrated that how these genes could be regulated artificially. This was very important finding because it gives the idea that how genes regulate the development of organs. 18. For the first time, He has purified and characterized the human homolog of AAT and ASPT enzymes, which is the basic clinical marker in all the infection and major marker of liver function test. 19. For the first time, he demonstrated the co-ordination of AAT and ASPT enzymes in the production of energy through the amino acids after aerobic respiration. 20. For the first time, he has shown that according to metabolic demand of the body AAT and ASPT genes synthesized additional forms of its isoform to cope up with the extra energy demand and work as an on and off switch.

DR. SRIVASTAVAS EXCELLENCE IN SEVERAL ADVANCED BIOLOGICAL TECHNIQUES:

Techniques related to Human Embryonic Stem Cell Human Embryonic Stem cell culture, Serum free and feeder free hES cell culture, in vitro differentiation of hES cells into neural cells, in vitro differentiation of hES into hematopoietic cells and red blood cells under the control of cytokines. Gene regulation studies using RT-PCR, Real time PCR, Northern blot, Southern blot and in situ hybridization, immunohistochemistry during the differentiation, Cell cycle regulation studies during differentiation of hES cells into hematopoietic and neural cells. Use of siRNA for blocking a specific cell cycle. FACS analysis of differentiated cells and cell shorting. ES cell transfection.

In vivo studies with ES cells Created a mouse model for study the effect of ES cells on damaged brain. Injection of ES cells into mouse brain, tail vein injection, in vivo tracking of ES cell migration. Used the ES cells for repair of damaged brain. Gene and protein regulation during neural cell differentiation. Studies on transcription factors. Histochemical analysis of transplanted ES cells using fluorescent, confocal microscopy and deconvolution microscopy. Created a mouse model for Crohns disease. In vivo migration of ES cells into diseased portion of intestine. Studies on inflammatory cytokines during the repair of Crohns disease with ES cell. Gene regulation studies during this process. Elisa assays for the cytokines. Stem cell niche interaction.

Created in utero mouse model for ES cells transplantation. Used this model to make chimeric animals. Distribution and differentiation of ES cells into developing mouse embryo. FACS and magnetic shorting of ES cells derived CD31+, CD34+, CD45+ cells from the transplanted animal tissues. Gene and protein regulation of in vivo differentiating cells.

Created immunocompromised mouse model to study the effect of in vivo immune component on T7 phage virus. In vivo selection of tissue specific receptor binding peptide using in vivo biopanning method. Tissue targeted gene delivery to correct the blood related genetic diseases. Gene cloning, gene sequencing, synthesis of RNA probes. Protein and enzyme biochemistry Protein assay, peptide structure and amino acid sequencing, Enzyme assay, Ultra centrifugation, Ion exchange chromatography, column chromatography, HPLC, Protein and gene regulation during the development. Enzyme kinetics, Enzyme inhibition, SDS gel electrophoresis, Protein characterization.

Selection of cell receptor binding peptide and Phage display technology

- Selection of tissue receptor binding peptides using T7 phage display system. - In vivo and in vitro biopanning for selection of receptor binding peptides sequences. - Characterization of targeted cells and tissues using histochemistry and gene expression analyses. - In vivo delivery of drugs and genes to targeted tissues using microinjection.

Cancer Research

- Studying the role of pharmaceutical agent curcumin as an anti-lung cancer drug and develop it as a non-toxic cancer drug. - Role of apoptotic genes on the lung cancer cell lines. - Development of tissue targeted delivery protocol of pharmaceuticals agents for cancer and genetic diseases

Fluorescence techniques for nucleic acid sequence detection: Clinical and diagnostic applications

- Fluorescent labeling of DNA and RNA probes. - Fluorescence resonance energy transfer (FRET) protocols for DNA and RNA sequence. detection in real time (Sequence Detection System 7700, ABI, Perkin Elmer) - FRET protocols for monitoring ribozyme reactions and kinetics in real time (TaqMan, SDS 7700, ABI, Perkin Elmer). - Accessibility studies for DNA and RNA target sequences using FRET. - Fluorescence polarization protocols for monitoring ribozyme reactions (POLARstar, BMG, GmbH) and for DNA and RNA sequence detection. - Sequence detection with Syber green dye in real time quantitative PCR by Light Cycler (Roche Diagnostics, USA). - Single nucleotide polymorphism detection in real time with LightCycler hybridization probes (Roche Diagnostics, USA).

Gene detection technology: Research and Clinical applications

- Preparation of radio labeled & fluorescent labeled RNAs (ribozymes and target substrates). - In vitro transcription of RNA. - Expression of ribozymes in yeast. - Isolation and purification of cellular RNA. - RNase Protection Assay. - Kinetic characterization of ribozymes & binding kinetics using fluorescence methods. - Designing, synthesis and characterization of allosteric ribozymes induced by small drug ligands (such as theophylline & caffeine).

In utero transplantation: Clinical Research to cure the fetal genetic diseases

- Developed in utero microinjection techniques to transplant the bone marrow and stem cells to cure blood related genetic disease. - Harvest the fetal liver, bone marrow and mouse embryonic stem cells for transplantation. - Culture mouse embryonic stem cell and in vitro differentiation into the blood cells. - Fractionation of cells using flow cytometry techniques.

Standard Molecular biology techniques - Standard and site directed mutagenesis polymerase chain reaction (PCR). - Preparation and purification of plasmids. - Transformations and Transfection of DNA. - Cloning of DNA. - Solid phase synthesis of DNA (Gene Assembler, Pharmacia). - DNA sequencing & fragment analyses (ABI 310 Gene Sequencer, Perkin Elmer). - Quantitation of DNA, RNA and proteins. - Mammalian cell culture and yeast culture. - Gel electrophoresis (polyacrylamide and agarose). - Capillary gel electrophoresis (ABI 310 Gene Sequencer, Perkin Elmer). - Column/ gel/ thin layer chromatography. - Autoradiography by phosphorimager (Storm, Molecular Dynamics, USA). - High Performance Liquid Chromatography (HPLC). - Preparation and purification of chemical reagents & solvents. - Enzyme/ Protein/ purification and characterization. - Isolation of Genomic DNA, Genomic library Construction. - Radioimmunoassay.

General molecular and biochemical techniques

mRNA preparation and purification, Primer designing, Real-time PCR, RT-PCR, DNA cloning, DNA sequencing, Isolation of Genomic DNA, Genomic library Construction, Transformation, Transfection, Cell culture, Plasmid purification, RNA probe making, Different kinds of microscopy, In situ hybridization, Southern blotting, Northern blotting, Western blotting, Spectrophotometery, In utero-microinjection, Column chromatography, HPLC, PAGE, Agarose gel-electrophoresis, Enzyme assay, Protein assay, Enzyme/ Protein/ DNA purification, Histology, Phage display for tissue targeting, Radio-immunoassay,

INVITED SPEAKER AND PRESENTATIONS OF DR. SRIVASTAVAS SCIENTIFIC FINDINGS IN NATIONAL AND INTERNATIONAL CONFERENCES:

1. Srivastava A.S. Invited Speaker, STEM 2013, 9 Th Annual Conference on Biotechnology - Focusing On Latest Trend in Stem Cells, Regenerative Medicine and Tissue Engineering Mumbai, India, January 2013.

2. Srivastava A.S. "International Conference on Regenerative and Functional Medicine" (Regenerative Medicine-2012), San Antonio, USA. November 2012.

3. Sriavstava A.S. 2nd International Congress on Neurology & Epidemiology; "Impact of drugs on the natural history of neurological diseases". Nice, France. November 2012.

4. Srivastava A.S. Invited Speaker, International Expo and Conference on Analytrix & HPLC, Chicago, USA. October 2012.

5. Srivastava A.S. Invited Speaker at "International Conference on Emerging Cell Therapies" (Cell Therapy-2012) Chicago, USA. October 2012.

6. Srivastava A.S. Invited Speaker, 6th Neurodegenerative Conditions Research and Development Conference San Francisco, CA, USA. September 2012.

7. Srivastava A.S. 8th International Congress on Mental Dysfunction & Other Non-Motor Features In Parkinson's Disease and Related Disorders, Berlin, Germany. May 2012.

8. Srivastava A.S. International Conference and Exhibition on Neurology & Therapeutics Las Vegas, USA. May 2012.

9. Srivastava A.S. Montreal International Biotechnology Forum, Montreal, Quebec, Canada. May 2012.

10. Srivastava A.S. Invited Speaker, International Association of Neurorestoratology (IANR) V and 9th Global College Neuroprotection and Neuroregeneration (GCNN) conference with the 4th International Spinal Cord Injury Treatment & Trial Symposium (ISCITT) Xian City, China. May 2012.

11. Srivastava A.S. International Forum on the Mediterranean Diet, Ravello - Amalfi Coast, Italy. March 2012

12. Srivastava A.S. Hong Kong international Stem Cell Forum 2012, Hong Kong. February 2012.

13. Srivastava A.S. 4th International Conference on Drug Discovery and Therapy" (4th ICDDT 2012) Dubai, UAE, February 2012.

14. Srivastava A.S. Evolving Strategies in Hematopoietic Stem Cell Transplantation- San Diego, USA. February 2012.

15. Srivastava A.S. Hebei International Biotechnology Forum; Shijiazhuang, Hebei, China. November 2011

16. Srivastava A.S. 3rd International Conference on Drug Discovery and Therapy. Regenerative Medicine. Dubai, UAE. February 2011.

17. Srivastava A.S. 3rd Annual Congress of Regenerative Medicine & Stem Cell-2010, Shanghai, China. December 2010.

18. Srivastava A.S. 1st Annual Tetra-Congress of MolMed-Personal Medicine Congress 2010, Shanghai, China. November 2010.

19. Srivastava A.S. International Association of Neurorestoratology(IANR), American Journal of Neuroprotection and Neuroregeneration, Beijing, China. October 2010.

20. Srivastava A.S. EPS Global International Neuroscience Forum. Nha Trang, Vietnam. October 2010.

21. Srivastava A.S. EPS Global International Neuroscience Forum, Guangzhou, China. September 2010.

22. Srivastava A.S. 4th Academic Congress of International Chinese Neurosurgical Sciences. Chengdu, China. June 2010.

23. Srivastava A.S. 1st Annual World Congress of Immunodiseases and Therapy (WCIT 2010). Beijing, China. May 2010.

24. Srivastava A.S. 3rd PepCon-2010 - Protein Misfolding and Neurodegeneration. Beijing, China. March 2010

25. Srivastava A.S. Potential use of ES cells in hematopoietic and neural diseases. City of Hope National Medical Center, Duarte, California, USA. January, 2009.

26. Srivastava A.S. Differentiation of Human Embryonic Stem cell into erythrocyte and neural precursor cells: Its potential application. Cleveland Clinic, Cleveland, Ohio, USA, December, 2008.

27. Srivastava A.S. Potential of ES cell in repair of Hematopoietic and neural diseases. International Conference in Stem cell, Kerala, India, August, 2008.

28. Srivastava A. S., Singh U. and Carrier E. Embryonic stem cell improve colitis and decrease IL- 12 levels in the colitis mice. BMRP Fourth Annual Investigator Meeting, Los Angeles, USA. 2006

29. Carrier E., Shermila Kausal and Srivastava A. S. Gene Regulation During the Erythrocytic Differentiation of Embryonic Stem Cells. Blood (ASH Meeting), 2005.

30. Carrier E., Shermila Kausal and Srivastava A. S. Differentiation of Human ES cell into the Hemangioblast. Blood (AHS Meeting), 2005.

31. Srivastava A.S., Zhongling F., Victor A., Kim H.S. and Carrier E. Repair of Crohns disease with embryonic stem cells. Broad Medical Research Program, Third Annual Investigator Meeting, Los Angeles, CA, USA, 2005.

32. Srivastava A.S., Shenouda S. and Carrier E. Damaged murine brain induces ES cells into migration and proliferation. Blood:104, 779a, 2004.

33. Srivastava A.S., Shenouda S. and Carrier E. Increased expression of OCT4,SOX2 and FGF4 genes following injection of embryonic stem cell into damaged murine brain. American Society of Gene Therapy, 2004.

34. Srivastava A.S. and Carrier E.; Distribution and stability of T7 phage in mouse blood and tissues. Molecular Therapy:7, 230, 2003.

35. Moustafa M., Srivastava A.S., Nedelcu E., Minev B., Carrier E.; Chimerism and tolerance post in utero transplantation with ontogenically different sources of stem cells. 32nd annual meeting of the international society for Experimental Hematology, 31, 274, 2003 (Paris, France).

36. Steve S., Srivastava A.S. Carrier E.; In vivo survival of hematopoietic stem cell in mouse brain.11th international symposium on recent advances in Stem cell transplantation, 89-90, 2003 (San Diego, USA).

37. Srivastava A.S., Carrier E.; Distribution and stability of T7 phage in mouse. 11th international symposium on recent advances in Stem cell transplantation, 93, 2003 (San Diego, USA).

38. Elena N., Srivastava A.S., Varki N.M., Assatourian G. and E. Carrier; Embryonic stem cells survive and proliferate after intraperitoneal In utero transplantation and produce teratocarcinomas. Blood:160b, 2002.

39. Srivastava A.S and E. Carrier; In utero targeting the fetal liver by using T7 phage display system. Blood:489b, 2002.

40. Srivastava A.S. and E. Carrier; Factor responsible for in vivo neutralization of T7 phage display vector in the blood of mice. Blood:489b, 2002.

41. Srivastava A.S. and E. Carrier; Distribution and stability of T7 phage in the mouse after intravenous administration. ICCC, Kyoto, Japan. (October 2002).

42. Srivastava A.S., T. Kaido and E. Carrier; Immunological factors that affect the in vivo fate of T7 phage in the mouse. Molecular Therapy:5, 713, 2002.

43. Srivastava A.S., E. Nedelcu and E. Carrier; Engraftment of murine embryonic stem cells after in utero transplantation. Molecular Therapy:5, 1132, 2003.

44. M. Rizzi, T. Kaido, M.Gerloni, K.Schuler, A. S. Srivastava, E.Carrier and M. Zanetti; Neonatal T cell immunity by in utero immunization. AAI 2002 annual meeting, April 20 - 24, New Orleans, Experimental Biology 2002 sponsored by 7 FASEB societies.

45. Srivastava A.S., T. Kaido and E. Carrier; Kinetics of T7 phage neutralization in the blood of normal and immunodeficient mice. Blood:407, 2001.

46. Hassan S., Jody D., Srivastava A.S., T.H. Lee, M.P. Busch, Carrier E.; Immunity without microchimerism after in utero transplantation of Hematopoietic stem cell. Blood:320, 2001.

47. Srivastava A.S., Felix Tinkov, T. Friedmann and E. Carrier; Detection of T7 phage in the fetus after Systemic administration to pregnant mice. Molecular Therapy:4, 760, 2001.

48. Pillai G.R., Srivastava A.S., Hassan S., Carrier E. Differential sensitivity of human lung cancer cell lines to curcumin. 9th Annual International Symposium on Recent Advances in Hematopoietic Stem cell Transplantation. USA. 2001.

49. Hassan S., Jody D., Srivastava A.S., Carrier E.; The role of I-E molecule on survival rate and tolerance after in utero transplantation. The 42 ASH meeting, San Francisco, USA. 2000.

50. Suzuki T., Srivastava A.S., Kurokawa T.; Identification of cDNA encoding two subtypes of vitamin D receptor in flounder, Paralichthys olivaceus. Meeting of the Japanese Society of Fisheries Science, April 2 - 4, 2000, Tokyo, JAPAN.

51. Srivastava A.S., Suzuki T., Kurokawa T., Kamimoto M., Nakatsuji T.; GFP expression in pancreas of developing fish embryo under control of Carboxypeptidase A promoter. Plant and Animal Genome-VIII (PAG-VIII), Conference, San Diego, California, USA. January 9th to 12th, 2000.

52. Srivastava A.S., Suzuki T., Kurokawa T.; Molecular cloning of serine protease cDNAs from pancreas of Japanese flounder, Paralichthys olivaceus. Meeting of the Japanese Society of Fisheries Science, Tokyo, JAPAN. 1999.

53. Suzuki T., Srivastava A.S., Kurokawa T.; Cloning of FGFRs from Flounder embryos, and their expression during axial skeletal development. 32nd Annual Meeting of the Japanese Society of Developmental Biologists. JAPAN. 1999.

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