StemCell Therapy

Renal stem cells are self-renewing, multipotent stem cells which are able to give rise to all the cell types of the kidney. It is involved in the homeostasis and repair of the kidney, and holds therapeutic potential for treatment of kidney failure.[1]

Strong evidence suggests that renal stem cells are located in the renal papilla.[2] Using stain-retaining assay (with bromodeoxyuridine, or BrdU), a low-cycling cell population was found in the papillary region, which was able to divide rapidly to repair the damaged caused by transcient renal ischemia.[2] These cells are able to incorporate into other renal tissues, and was able to repeatedly form spheres in 3D cultures, and clonal analysis also exhibited its multipotency.[2]

Other reports have suggested the renal tubule and renal capsule to be the site of stem cells. The renal capsule contain stain-retaining cells which exhibited markers for mesenchymal stem cells; after their removal, recovery was significantly slower post-ischemic injury. These evidence suggests a stem cell population exists within the renal capsule.[3]

Using in vivo lineage tracing techniques, Lgr5+ cells were found to contribute to the nephron, specifically to the ascending limb of the loop of Henle and the distal convoluted tubule. Thus, Lgr5+ cells can potentially be a marker for renal stem and/or progenitor cells.[4]

There is much debate regarding the cells involved in repair after injury; while some suggests that stem cells are the sole driving force of repair, others suggests that cells dedifferentiate after damage to act like stem cells.[5] Alternately, it was also reported that differentiated tubular epithelial cells are the driving mechanism for regeneration after injury, using proliferative expansion as the mechanism.[6]

Multipotent mouse kidney progenitor cells (MKPC) were obtained from Myh9 targeted mutant mice. Injection of MKPC into mice post-ischemic injury saw the MKPC regenerating different cell lineages and was able to regenerate renal function and enhanced survival.[7]

It has been reported that endogenous kidney tubular renal epithelial cells can be dedifferentiated into induced pluripotent stem cells by the treatment of only two factors - Oct4 and Sox2.[8]

See the article here:
Renal stem cell - Wikipedia, the free encyclopedia

The mission of the Pan-American Association of Ophthalmology is the prevention of blindness through lifelong education and cultural exchange among ophthalmologists in the Western Hemisphere.

This Portal will provide a virtual meeting place for professionals from all over the world to gather as a Pan-American Community and focus on ways to standardize and improve ophthalmic knowledge and skills for the improvement of patient care.

The Pan-American Association of Ophthalmology (PAAO) was founded in 1939 by Moacyr E. Alvaro MD (Brazil), Conrad Berens MD (USA), and Harry S. Gradle MD (USA). The Pan-American Ophthalmological Foundation (PAOF) was founded in 1959 to support the PAAO and its educational programs. The Pan-American strives to provide continuing education for ophthalmologists, prevention of blindness programs, and cultural exchange.

Pan-American Ophthalmological Foundation

For over 70 years, the Association has been instrumental helping to restore sight in countless numbers of people and has been a leader in elevating the standards of practice of ophthalmology and quality of eye care in the Western Hemisphere.

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PAAO - Pan-American Association of Ophthalmology

The LonGenity research study builds upon the Longevity Genes Project, initiated in 1998 at the Albert Einstein College of Medicine by Dr. Nir Barzilai. Dr. Barzilai's early observations of the phenotypes of healthy, vital centenarians led him to ask a series of questions. The project'sprimary focus questioned why some people enjoy extremely long life spans, with physical health and brain function far better than expected in the 9th and 10th decades of life.

In 2006 Dr. Barzilai and his team increased their efforts to conduct a large program, "Roles of genes in exceptional longevity in humans" (LonGenity), funded by the National institute of Aging.

In the LonGenity program, genetic analysis (GWAS and candidate gene approach) is performed in an already established cohort (centenarians, their offspring, and age-match unrelated control to these offspring), and genetic findings are validated in a newly established cohort of offspring of parents with exceptional longevity (OPEL) vs. offspring of parents with usual survival (OPUS).

Over the pastten years Dr. Barzilai's team has assembled and characterized families with exceptional longevity and have identified several biological markers that may explain their longevity. Their hypothesis is that unique genotypes and phenotypes protect against age-related diseases (Figure 1). In order to comply with the steps to prove the causality suggested by the figure 1, novel genetic, epidemiologic, and statistical approaches are used to identify genetic markers in subjects with exceptional longevity, and test the impact of these markers on biological measurements and clinical out comes.The long-term objectives are to identify genes that contribute to exceptional longevity in humans, and assess associations among these genes with age-related diseases and longevity.

The LonGenity research study aims:

To date, a unique cohort of over 500 proband with exceptional longevity (~100 y/o), over 700 of their offspring (ages 60-85), and over 600 unrelated subjects ages 60-95 have been assembled and characterized.

Findings

Results of the research to date have been encouraging and enthusiastically received by the medical research community. Among the findings, the team has learned that longevity is:

Additionally,they have learned that:

Continue reading here:
LonGenity and Longevity Genes Project

Glycation is one of four key process which lead to aging by damaging cells. Addressing these four issues reduces aging.

Glycation is a process where sugar and protein molecules combine to form a tangled mess of tissue. Glycated tissue is tough and inflexible, leading to wrinkling not only of the skin, but also of important internal organs. Furthermore, glycated tissues then produce Aged Glycation End-products [AGEs], which further compound the problem by producing large numbers of damaging free radicals.

All in all, glycation is a nightmare process which degrades important body tissues. It must be dramatically reduced if aging is to be minimized.

Glycation causes tough, wrinkled connective tissue. This is most visible on the skin as wrinkles. However, it occurs all through the body. Tough, inelastic connective tissue is very damaging to organs where flexibility is vital. This is especially important in the heart, kidneys, brain, eyes and pancreas.

The lack of flexibility in the important organs leads to reduced functionality and early death. The reason diabetics suffer from organ ailments earlier than most people is that their raised blood sugar level produce greater glycation.

Glycation cannot be stopped completely; neither can it be reversed, currently. However, it can be reduced considerably by making changes in lifestyle and diet.

There are two main causes of glycation;

Continually high blood glucose promotes glycation, as well as other aging processes and degenerative diseases. If glycation is to be reduced, then so must the intake of sugar from the diet.

Sugar in the Diet

Dietary sugar comes from the obvious sugary sources including honey and maple syrup but it also comes from starchy food, many of which are close to 100% sugar, when they are broken down in the body.

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Aging and Longevity 3. Glycation - Living To 150

PKD News Headlinesonly PKD Foundation awards fellowships to promising PKD researchers

We have selected five outstanding researchers to receive the 2015 PKD Foundation Fellowships. These fellowships honor early-career scientists whose achievements and potential identify them as rising stars the next generation of scientific leaders in PKD research. Over two years, each fellow will receive $50,000 a year, totaling a half-million dollars. Initially, our goal was to fund three fellowships. However, thanks in large part to a highly successful response to this year's PKD Matching Gift Challenge (which raised $412,000), we were able to increase this to five.

Read more about the five PKD researchers

From Medical News Today

A new method that allows antibodies to penetrate cyst walls may open the door for already approved drugs to target the growth factors that drive polycystic kidney disease.

Read more

New Orleans Saintsations Kriste Lewis, along with others impacted by PKD, helps create awareness in this promotional video. Please help spread the word to people who may not know about this disease by sharing this video.

PKD affects thousands in the United States and millions worldwide and yet, many people have never heard of it. Watch this short video and learn more about this little-known disease.

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Home - PKD Foundation

What is a genetic disease?

A genetic disease is any disease that is caused by an abnormality in an individual's genome, the person's entire genetic makeup. The abnormality can range from minuscule to major -- from a discrete mutation in a single base in the DNA of a single gene to a gross chromosome abnormality involving the addition or subtraction of an entire chromosome or set of chromosomes. Some genetic disorders are inherited from the parents, while other genetic diseases are caused by acquired changes or mutations in a preexisting gene or group of genes. Mutations can occur either randomly or due to some environmental exposure.

There are a number of different types of genetic inheritance, including the following four modes:

Single gene inheritance, also called Mendelian or monogenetic inheritance. This type of inheritance is caused by changes or mutations that occur in the DNA sequence of a single gene. There are more than 6,000 known single-gene disorders, which occur in about 1 out of every 200 births. These disorders are known as monogenetic disorders (disorders of a single gene).

Some examples of monogenetic disorders include:

Single-gene disorders are inherited in recognizable patterns: autosomal dominant, autosomal recessive, and X-linked.

Medically Reviewed by a Doctor on 5/21/2015

Genetic Disease - Symptoms Question: What were the symptoms of a genetic disease in you or a relative?

Genetic Disease - Screening Question: Have you been screened for a genetic disease? Please share your story.

Genetic Disease - Personal Experience Question: Is there a genetic disease in your family? Please share your experience.

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Genetic Disease: Get the Definition of These Disorders

TREATMENT WITH Fat Stem Cell Therapy

Face Lift Procedure Avg. Rating: 4.5 out of 5 from 129 votes.

Women and men around the globe are seeking for alternatives to Surgical Face Lifts and expensive chemical injection namely Botox. And when celebs like legend pop-artist Madonna, choose the natural approach you know you are onto something really good.

Thanks to the local rejuvenating and toning effect of stem cells, now there is an alternative. An enriched Fat Stem Cell (FSC) Face Lift can leave you looking 10 - 15 years younger, all without surgical scars and long recovery period as well as that nonsense "pulled back look".

And don't forget, the neck and hands, which are a sure sign of "old age". Our procedure takes care of that too.

A detailed explanation of our procedure for a Fat Stem Cell (FSC) Face Lift with autologous adipose enriched Stem Cell Therapy is available on our procedure page.

Activated Stem Cells are returned to the patient by our Cosmetic Surgeon using surgical needles. Only a local anesthetic is used. Excess fat extracted during the Harvest phase of the procedure is mixed with activated stem cells and is used as filler to inject into the patient's Hands, Face and Neck to fill wrinkles and age lines.

The natural effects of the enriched stem cells smooth and tone the skin. The entire process takes about 4-5 hours to complete.

Here too, the results of this procedure speak for themselves. Cleaner, whiter, smoother, softer and wrinkle free, facial skin can be had within a week after the procedure. Acne dents and scars disappear, age spots fade quickly. In 2-3 weeks the full effects of the procedure will be evident. Your friends will be shocked by just how young you look and they will surely be looking for the scars.

The woman in the images above also had dents on both sides of her forehead. A trained cosmetic surgeon filled those dents with her own fat

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Face Lift Using Fat Stem Cell Therapy

The death of a woman after she was treated with stem cells at a private clinic in Thailand has reinforced warnings for desperate sick people to avoid stem-cell tourism the gamble of undergoing untested stem-cell treatments in unlicensed private clinics abroad.

Post-mortem results reported this week reveal that the stem-cell treatment almost certainly killed the woman, who had been suffering from kidney disease. She developed strange lumps in the kidney, liver and adrenal gland.

So what are the implications for stem cell research generally, and is it safe for clinical trials to continue? New Scientist has some answers.

What was wrong with the patient, and what treatment did she receive?

She had lupus nephritis, a condition in which the bodys own immune system mistakenly attacks and destroys the kidneys. Usually it can be kept in check with immunosuppressive steroids, but when these failed, the woman turned to a private stem-cell clinic in Bangkok.

How would stem cells help?

Bona-fide trials in European clinics about six years ago showed that some people with similar kidney disease benefited if stem cells from their own bone marrow were injected into their blood. The bodys immune system was first deliberately destroyed with powerful immunosuppressive drugs, then the reinjected stem cells helped to stop the attacks on the kidney by rebuilding and rebalancing the immune system. About a third of the 50 recipients relapsed after a year or so, and 12 of these people died. But around two-thirds saw benefits, with some going into remission.

So what happened with the woman who went to Bangkok?

Continue reading here:
Death revives warnings about rogue stem cell clinics - New ...

Hematological deficiencies increase with aging, including anemias, reduced responses to hematopoietic stress and myelodysplasias. This investigation tested the hypothesis that increased bone marrow (BM) fat content in humans with age was associated with decreased numbers of side population (SP) hematopoietic stem cells, and this decrease correlated with changes in cytokine levels. BM was obtained from the femoral head and trochanteric region of the femur removed at surgery for total hip replacement (N = 100 subjects). In addition, BM from cadavers (N = 36), with no evidence of hip disease, was evaluated for fat content. Whole trabecular marrow samples were ground in a sterile mortar and pestle, and cellularity and lipid content determined. Marrow cells were stained with Hoechst dye and SP profiles were acquired. Plasma levels of insulin-like growth factor (IGF)-1, stromal-derived factor (SDF)-1 and interleukin (IL)-6 were measured using ELISA. Fat content in the BM of human subjects and cadavers increased with age. The numbers of SP stem cells in BM as well as plasma IGF-1 and SDF-1 levels decreased in correlation with increased BM fat. IL-6 had no relationship to changes in marrow fat. These data suggest that increased BM fat may be associated with a decreased number of SP stem cells and IGF-1 and SDF-1 levels with aging. These data further raise a more general question as to the role of adipose cells in the regulation of tissue stem cells.

2011 The Authors. Journal of Anatomy 2011 Anatomical Society of Great Britain and Ireland.

Originally posted here:
Changes in human bone marrow fat content associated with ...

Genetics Practice Problems

You may type in your own answers, then check to see if you were right. If youre totally stumped, you can tell the computer to show you the answer to a particular question.

Monohybrid Cross:

In humans, brown eyes (B) are dominant over blue (b)*. A brown-eyed man marries a blue-eyed woman and they have three children, two of whom are brown-eyed and one of whom is blue-eyed. Draw the Punnett square that illustrates this marriage. What is the mans genotype? What are the genotypes of the children?

(* Actually, the situation is complicated by the fact that there is more than one gene involved in eye color, but for this example, well consider only this one gene.)

Testcross:

In dogs, there is an hereditary deafness caused by a recessive gene, d. A kennel owner has a male dog that she wants to use for breeding purposes if possible. The dog can hear, so the owner knows his genotype is either DD or Dd. If the dogs genotype is Dd, the owner does not wish to use him for breeding so that the deafness gene will not be passed on. This can be tested by breeding the dog to a deaf female (dd). Draw the Punnett squares to illustrate these two possible crosses. In each case, what percentage/how many of the offspring would be expected to be hearing? deaf? How could you tell the genotype of this male dog? Also, using Punnett square(s), show how two hearing dogs could produce deaf offspring.

Incomplete Dominance:

Note: at least one textbook Ive seen also uses this as an example of pleiotropy (one gene multiple effects), though to my mind, the malaria part of this is not a direct effect of the gene.

(For many genes, such as the two mentioned above, the dominant allele codes for the presence of some characteristic (like, B codes for make brown pigment in someones eyes), and the recessive allele codes for something along the lines of, I dont know how to make that, (like b codes for the absence of brown pigment in someones eyes, so by default, the eyes turn out blue). If someone is a heterozygote (Bb), that person has one set of instructions for make brown and one set of instructions for, I dont know how to make brown, with the result that the person ends up with brown eyes. There are, however, some genes where both alleles code for something. One classic example is that in many flowering plants such as roses, snapdragons, and hibiscus, there is a gene for flower color with two alleles: red and white. However, in that case, white is not merely the absence of red, but that allele actually codes for, make white pigment. Thus the flowers on a plant that is heterozygous have two sets of instructions: make red, and make white, with the result that the flowers turn out mid-way in between; theyre pink.)

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Genetics Practice Problems - Biology

Welcome to the Nicholas Institute of Sports Medicine and Athletic Trauma (NISMAT), a world-renowned research, teaching, and treatment center. Established at Lenox Hill Hospital in 1973, NISMAT was the worlds first hospital-based facility committed solely to the study of sports medicine, and has since played a key role in advancing the field, as well as redefining its focus. Once perceived as a discipline concerned only with repairing athletes' traumatic injuries, sports medicine is now recognized as a science that expands the understanding of the relationship between exercise and fitness at all levels, across every age group. Whether youre a medical practitioner or a patient, a professional athlete--or a weekend one, an occasional jogger or a marathon runner, woman or man,...

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Welcome to the Nicholas Institute of Sports Medicine and Athletic Trauma (NISMAT), a world-renowned research, teaching, and treatment center. Established at Lenox Hill Hospital in 1973, NISMAT was the worlds first hospital-based facility committed solely to the study of sports medicine, and has since played a key role in advancing the field, as well as redefining its focus. Once perceived as a discipline concerned only with repairing athletes' traumatic injuries, sports medicine is now recognized as a science that expands the understanding of the relationship between exercise and fitness at all levels, across every age group. Whether youre a medical practitioner or a patient, a professional athlete--or a weekend one, an occasional jogger or a marathon runner, woman or man, adolescent or octogenarian, NISMAT brings you the most comprehensive and current medical information and references available. Here, youll learn about injury treatment and prevention. Training tips and exercise programs. Physical therapy, sports physiology, nutrition, and so much more. Welcome to NISMAT.

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Nismat / Home

Alefacept Preserves Beta Cell Function in Some New-Onset Type 1 Diabetes Patients out to Two Years July 20, 2015 Individuals with new-onset type 1 diabetes who took two courses of alefacept (Amevive, Astellas Pharma Inc.) soon after diagnosis show preserved beta cell function after two years compared to those ... read more Antibiotic Exposure Could Increase the Risk of Juvenile Arthritis July 20, 2015 Taking antibiotics may increase the risk that a child will develop juvenile arthritis, according to a study. Researchers found that children who were prescribed antibiotics had twice the risk of ... read more Cholesterol Metabolism in Immune Cells Linked to HIV Progression July 17, 2015 Lower levels of cholesterol in certain immune cells -- a result of enhanced cholesterol metabolism within those cells -- may help explain why some HIV-infected people are able to naturally control ... read more July 17, 2015 A study in mice may identify new ways to treat immune thrombocytopenia. Immune thrombocytopenia, or ITP, is an autoimmune disease whereby the immune system sends antibodies to attack and destroy the ... read more July 16, 2015 In response to an infection, the immune system refines its defensive proteins, called antibodies, to better target an invader. New research has revealed two mechanisms that favor the selection of B ... read more July 16, 2015 Iron regulatory proteins play an important role in the body's immune system. Proteins responsible for controlling levels of iron in the body also play an important role in combating infection, ... read more HIV Uses Immune System's Own Tools to Suppress It July 15, 2015 A research team has made a significant discovery on how HIV escapes the body's antiviral responses. The team uncovered how an HIV viral protein known as Vpu tricks the immune system by using its ... read more Host Genetics Played a Role in Vaccine Efficacy in the RV144 HIV Vaccine Trial July 15, 2015 Host genetics played a role in protection against HIV infection in the landmark RV144 vaccine trial conducted in Thailand, research ... read more July 15, 2015 Immunologists have identified a distinct set of long-lived antibody-producing cells in the human bone marrow that function as an immune ... read more Magnetic Nanoparticles Could Be Key to Effective Immunotherapy July 15, 2015 In recent years, researchers have hotly pursued immunotherapy, a promising form of treatment that relies on harnessing and training the body's own immune system to better fight cancer and ... read more Why Does PTSD Increase the Risk of Cardiovascular Disease? July 15, 2015 A new review article finds that post-traumatic stress disorder (PTSD) leads to overactive nerve activity, dysfunctional immune response and activation of the hormone system that controls blood ... read more Scientific Curiosity and Preparedness for Emerging Pathogen Outbreaks July 14, 2015 An essay reflects on a career path that started with the study of a somewhat obscure mouse virus mice and ended up at the frontline of the SARS and MERS coronavirus ... read more Anti-Stress Hormone May Provide Indication of Breast Cancer Risk July 14, 2015 A new study shows that women with low levels of an anti-stress hormone have an increased risk of getting breast cancer. The study is the first of its kind on humans and confirms previous similar ... read more Aerosolized Vaccine Protects Primates Against Ebola July 13, 2015 Scientists have developed an inhalable vaccine that protects primates against ... read more Cancer Discovery Links Experimental Vaccine and Biological Treatment July 13, 2015 A new study has linked two seemingly unrelated cancer treatments that are both now being tested in clinical trials. One treatment is a vaccine that targets a structure on the outside of cancer cells, ... read more Skin Cancer Marker Plays Critical Role in Tumor Growth July 13, 2015 The protein keratin 17 -- the presence of which is used in the lab to detect and stage various types of cancers -- is not just a biomarker for the disease, but may play a critical role in tumor ... read more July 13, 2015 Immune cells that creep across blood vessels trigger potentially fatal bleeding in platelet-deficient mice, according to a new report. If the same is true in humans, blocking the passage of these ... read more Scientists Find Molecular Switch That Creates Long-Term Immunity July 13, 2015 Researchers have identified a protein responsible for preserving the antibody-producing cells that lead to long-term immunity after infection or ... read more July 10, 2015 The microbiota is involved in many mechanisms, including digestion, vitamin synthesis and host defense. It is well established that a loss of bacterial symbionts promotes the development of ... read more Multiple Myeloma Hides in Bones Like a Wolf in Sheep's Clothing July 9, 2015 Multiple myeloma uses a trick akin to a wolf in sheeps clothing to grow in and spread to new bone sites. By overexpressing Runx2, a gene that normally is a master regulator of bone formation, the ... read more

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Immune System News -- ScienceDaily

Fat transfer breast augmentation can give women fuller, more attractive breasts without the need for breast implants.

Many women are now choosing fat transfer breast augmentation as a natural alternative to enhance their breasts without getting breast implants. Fat transfer breast augmentation is considered a more natural approach to breast augmentation since it uses the patients own fat cells instead of unnatural materials. As an added benefit, liposuction is used to remove the fat that will be used in the fat transfer breast augmentation. The fat is removed from the thighs, abdomen, buttocks or another area with excess fat, offering the added benefit ofslimming and toning.

Fat cell transfers were first performed around 1896. The first fat transfers for facial rejuvenation as early as 1912. This is not anovel or new procedure, but has been perfected over the years.

In the last 20 years, surgeons have been documenting some long-term benefits found fromfat cell transfers, including the ability to maintain volume as well as regenerative evidence.

The BRAVA is an external bra which gently expands a womans breast tissue making this breakthrough procedure possible for natural breast augmentation and reconstruction.

It is the Brava that makes the Brava + Fat Cell transfer breast augmentation technique possible. For women who want cosmetic breast augmentation the options are no longer limited to the traditional methods of implants.

I have always wanted to have natural looking breast augmentation without implants because I just felt that I did not want a foreign object in my body

I did tons of research on fat transfer the breast and decided that that was the best option for me. In addition to that I was able to harvest the fat from my stomach and inner thighs which have always been my problem areas. The result has been beyond my wildest dream. Not only do my breasts look like Im back in High school I have gone down two dress sizes after surgery. I cannot be happier. Dr Bednar is an amazing doctor!

I cannot wait to show off my new body when I go on my anniversary cruise in April . My husband also cannot believe my transformation. Hes even thinking about Botox now!

Kindest regards to all the staff for taking such good care of me. I will send you tons of patients, trust me, Leslie

Read more here:
Breast Augmentation using Fat Stem Cell Transfer in ...

Although the word "arthritis" means joint inflammation, the term is used to describe around 200 rheumatic diseases and conditions that affect joints, the tissues that surround the joint, and other connective tissue.5

The most common form of arthritis is osteoarthritis. Other common rheumatic conditions include gout, fibromyalgia and rheumatoid arthritis.4

You will also see introductions at the end of some sections to any recent developments that have been covered by MNT's news stories. Also look out for links to information about related conditions.

Fast facts on arthritis

Here are some key points about arthritis. More detail and supporting information is in the main article.

Typically, pain, aching, stiffness and swelling in and around one or more joints characterize rheumatic conditions. The symptoms can develop gradually or suddenly. Certain rheumatic conditions can also involve the immune system and various internal organs of the body.6

Some forms of arthritis, such as rheumatoid arthritis and lupus, can affect multiple organs and cause widespread symptoms.

Arthritis is more common among adults aged 65 years or older, but people of all ages (including children) can be affected.

There are 52.5 million adults in the US, equating to 22.7% of the population, reported to have a form of arthritis, rheumatoid arthritis, gout, lupus or fibromyalgia.1

With people living longer in the US, the prevalence of doctor-diagnosed arthritis is expected to increase. It has been estimated that by the year 2030, 67 million, 25% of the projected total adult population aged 18 years and older, will have doctor-diagnosed arthritis.

Read the original:
Arthritis: Causes, Symptoms and Treatments

Arthritis Arthritis Overview

Arthritis is a joint disorder featuring inflammation. A joint is an area of the body where two bones meet. A joint functions to allow movement of the body parts it connects. Arthritis literally means inflammation of one or more joints. Arthritis is frequently accompanied by joint pain. Joint pain is referred to as arthralgia.

Arthritis is classified as one of the rheumatic diseases. These are conditions that are different individual illnesses, with differing features, treatments, complications, and prognosis. They are similar in that they have a tendency to affect the joints, muscles, ligaments, cartilage, and tendons, and many have the potential to affect internal body areas as well.

There are many forms of arthritis (over 100 have been described so far, and the number is growing). The forms range from those related to wear and tear of cartilage (such as osteoarthritis) to those associated with inflammation as a result of an overactive immune system (such as rheumatoid arthritis). Together, the many forms of arthritis make up the most common chronic illness in the United States.

Arthritis sufferers include men and women, children and adults. More than half of those with arthritis are under 65 years of age. A majority of Americans with arthritis are women.

Medically Reviewed by a Doctor on 5/23/2014

See original here:
Arthritis: Get the Facts About Symptoms and Diet

Hair follicle lineage and niche signals regulate hair follicle stem cells. (a) HFSCs can exist in two states. Quiescent bulge stem cells (Bu-SCs) are located in the outer layer of this niche and contribute to the generation of the outer root sheath. Primed stem cells reside in the hair germ, sandwiched between the bulge and a specialized dermal cluster known as the dermal papilla. They are responsible for generating the transit amplifying cell (TAC) matrix, which then gives rise to the hair shaft and its inner root sheath (IRS) channel. Although matrix and IRS are destroyed during catagen, many of the outer root sheath (ORS) cells are spared and generate a new bulge right next to the original one at the end of catagen. The upper ORS contributes to the outer layer of the new bulge, and the middle ORS contributes to the hair germ. Some of the lower ORS cells become the differentiated inner keratin 6+ (K6+) bulge cells, which provide inhibitory signals to Bu-SCs, raising their activation threshold for the next hair cycle. (b) During telogen, K6+ bulge cells produce BMP6 and FGF-18, dermal fibroblasts (DFs) produce BMP4 and subcutaneous adipocytes express BMP2. Together, these factors maintain Bu-SCs and hair germ in quiescence. At the transition to anagen, BMP2 and BMP4 are downregulated, whereas the expression of activation factors including noggin (NOG), FGF-7, FGF-10 and TGF-2 from dermal papillae and PDGF- from adipocyte precursor cells (APCs) is elevated. This, in turn, stimulates hair germ proliferation, and a new hair cycle is launched. Bu-SCs maintain their quiescent state until TAC matrix is generated and starts producing SHH.

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Emerging interactions between skin stem cells and their ...

IMAGE:Amir Toor, M.D., hematologist-oncologist and member of the Developmental Therapeutics research program at VCU Massey Cancer Center is pictured. view more

Credit: VCU Massey Cancer Center

Researchers at VCU Massey Cancer Center's Bone Marrow Transplant Program have recently published findings from a phase 2 clinical trial that demonstrate lymphocyte recovery in related and unrelated stem cell transplant recipients generally falls into three patterns that are significantly associated with survival. This first-of-its-kind research continues the efforts of principal investigator Amir Toor, M.D., to understand the immune system as a dynamical system that can be modeled to improve stem cell transplantation.

"We began considering lymphocyte reconstitution following stem cell transplantation as similar to population growth models. So, we graphed the lymphocyte counts of our patients at various times following their transplant as a logistic function and observed distinct patterns that correlated with clinical outcomes," says Toor, the lead investigator of the study and hematologist-oncologist and member of the Developmental Therapeutics research program at VCU Massey Cancer Center. "Our goal is to use this data to develop models that can predict complications from stem cell transplantation. Then, we may be able to intervene at key points in times with appropriate clinical treatments that will make the most positive impact on patients' outcomes."

The study, recently published in the journal Biology of Blood & Marrow Transplantation, retrospectively examined lymphocyte recovery and clinical outcome data from a recent phase 2 clinical trial (Clinical trials.gov identifier - NCT00709592) in which 41 patients received a stem cell transplant from related or unrelated donors. As part of the clinical trial protocol, the patients underwent low-dose radiation therapy and received one of two different doses of anti-thymocyte globulin (ATG), an immune-modulating drug given to guard against graft-versus-host-disease (GVHD) before transplantation. GVHD is a condition where the donor's immune system attacks the recipient's body. Following transplantation, the researchers observed that the patients' lymphocytes recovered in one of three general patterns that correlated significantly with survival, relapse, GVHD and the need for further donor immune cell infusions to treat the cancer.

Group A experienced fast, early lymphoid expansion, culminating in a high absolute lymphoid count (ALC) within two months of transplantation. Group B experienced a slower, but steady lymphoid expansion that peaked much later than group A with a lower ALC. Group C experienced very poor lymphocyte recovery that demonstrated an early, but brief lymphoid expansion with a very low ALC. Group B had the best clinical outcomes with a survival rate of 86 percent, followed by group A with a survival rate of 67 percent and group C with 30 percent survival. Relapse rates between groups A and B were similar at 33 and 29 percent, respectively, while group C experienced a 90 percent relapse rate. GVHD was observed in 67 percent of patients in group A, 43 percent of patients in group B and 10 percent of patients in group C. Finally, adoptive immunotherapy with donor cell infusions was required for 13 percent of patients in group A, 21 percent in group B and 70 percent in group C.

The discovery of these patterns in lymphocyte recovery build on prior research by Toor and his team that supports the concept of the immune system working as a dynamical system. In 2013, the Massey Bone Marrow Transplant Program's research team and Massey researcher Masoud Manjili*, D.V.M., Ph.D., sequenced DNA from the T cells of 10 stem cell transplant recipients and their donors and found a fractal, self-repeating pattern in the participants' T cell repertoires. This discovery suggested that physicians could potentially sequence the DNA of patients after they undergo stem cell transplantation and predict potential GVHD complications based on the pattern in which their T cell repertoire is developing. Another study of the same participants in 2014 also used whole exome sequencing and found significant variation in minor histocompatability antigens (mHA, which are receptors on the cellular surface of donated organs that are known to give an immunological response in some organ transplants) between the donor-recipient pairs. This variation represents a large and previously unmeasured potential for developing GVHD for which conventional human leucocyte antigen (HLA) testing, the test that matches stem cell transplants with donors, does not measure. This large library of immune targets, in turn, can serve to drive immune complications of transplantation such as GVHD or graft rejection.

Currently, physicians use stochastic models to determine the probability of a patient developing GVHD based on HLA test results. Stochastic models are not precise because they estimate probability by allowing for random variation in one or more variables. Dynamical system modeling, on the other hand, would account for the key variables influencing transplant outcomes and their evolution over time, allowing physicians to personalize therapy based on the extent of a patient's immune recovery following transplantation.

"We've uncovered order in the structure of the immune system, we've found new variables influencing GVHD and we've now shown patterns in lymphocyte reconstitution that identify at-risk patients," says Toor. "Now, we are working to put it all together and develop a model of immune system reconstruction following stem cell transplantation that will allow physicians to make more informed treatment decisions."

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Adult stem cells are undifferentiated cells, found throughout the body after development, that multiply by cell division to replenish dying cells and regenerate damaged tissues. Also known as somatic stem cells (from Greek , meaning of the body), they can be found in juvenile as well as adult animals and human bodies.

Scientific interest in adult stem cells is centered on their ability to divide or self-renew indefinitely, and generate all the cell types of the organ from which they originate, potentially regenerating the entire organ from a few cells. Unlike embryonic stem cells, the use of human adult stem cells in research and therapy is not considered to be controversial, as they are derived from adult tissue samples rather than human 5 day old embryos generated by IVF (in vitro fertility) clinics designated for scientific research. They have mainly been studied in humans and model organisms such as mice and rats.

A stem cell possesses two properties:

To ensure the safety of others, stem cells undergo two types of cell division (see Stem cell division and differentiation diagram). Symmetric division gives rise to two identical daughter cells, both endowed with stem cell properties, whereas asymmetric division produces only one of those stem cells and a progenitor cell with limited self-renewal potential. Progenitors can go through several rounds of cell division before finally differentiating into a mature cell. It is believed that the molecular distinction between symmetric and asymmetric divisions lies in differential segregation of cell membrane proteins (such as receptors) between the daughter cells.

Adult stem cells express transporters of the ATP-binding cassette family that actively pump a diversity of organic molecules out of the cell.[2] Many pharmaceuticals are exported by these transporters conferring multidrug resistance onto the cell. This complicates the design of drugs, for instance neural stem cell targeted therapies for the treatment of clinical depression.

Adult stem cell research has been focused on uncovering the general molecular mechanisms that control their self-renewal and differentiation.

Discoveries in recent years have suggested that adult stem cells might have the ability to differentiate into cell types from different germ layers. For instance, neural stem cells from the brain, which are derived from ectoderm, can differentiate into ectoderm, mesoderm, and endoderm.[5] Stem cells from the bone marrow, which is derived from mesoderm, can differentiate into liver, lung, GI tract and skin, which are derived from endoderm and mesoderm.[6] This phenomenon is referred to as stem cell transdifferentiation or plasticity. It can be induced by modifying the growth medium when stem cells are cultured in vitro or transplanting them to an organ of the body different from the one they were originally isolated from. There is yet no consensus among biologists on the prevalence and physiological and therapeutic relevance of stem cell plasticity. More recent findings suggest that pluripotent stem cells may reside in blood and adult tissues in a dormant state.[7] These cells are referred to as "Blastomere Like Stem Cells" (Am Surg. 2007 Nov;73:1106-10) and "very small embryonic like" - "VSEL" stem cells, and display pluripotency in vitro.[7] As BLSC's and VSEL cells are present in virtually all adult tissues, including lung, brain, kidneys, muscles, and pancreas[8] Co-purification of BLSC's and VSEL cells with other populations of adult stem cells may explain the apparent pluripotency of adult stem cell populations. However, recent studies have shown that both human and murine VSEL cells lack stem cell characteristics and are not pluripotent.[9][10][11][12]

Stem cell function becomes impaired with age, and this contributes to progressive deterioration of tissue maintenance and repair.[13] A likely important cause of increasing stem cell dysfunction is age-dependent accumulation of DNA damage in both stem cells and the cells that comprise the stem cell environment.[13] (See also DNA damage theory of aging.)

Hematopoietic stem cells are found in the bone marrow and give rise to all the blood cell types.

Mammary stem cells provide the source of cells for growth of the mammary gland during puberty and gestation and play an important role in carcinogenesis of the breast.[14] Mammary stem cells have been isolated from human and mouse tissue as well as from cell lines derived from the mammary gland. Single such cells can give rise to both the luminal and myoepithelial cell types of the gland, and have been shown to have the ability to regenerate the entire organ in mice.[14]

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Adult stem cell - Wikipedia, the free encyclopedia

This article is about the ageing of living things. For ageing specifically in humans, see ageing. For the study of ageing in humans, see gerontology. For the science of the care of the elderly, see geriatrics. For experimental gerontology, see life extension. For premature ageing disorders, see Progeroid syndromes.

Senescence () (from Latin: senescere, meaning "to grow old", from senex) or biological aging (also spelled biological ageing) is the gradual deterioration of function characteristic of most complex lifeforms, arguably found in all biological kingdoms, that on the level of the organism increases mortality after maturation. The word "senescence" can refer either to cellular senescence or to senescence of the whole organism. It is commonly believed that cellular senescence underlies organismal senescence. The science of biological aging is biogerontology.

Senescence is not the inevitable fate of all organisms. Organisms of some taxonomic groups (taxa), including some animals, even experience chronological decrease in mortality, for all or part of their life cycle.[1] On the other extreme are accelerated aging diseases, rare in humans. There is also the extremely rare and poorly understood "Syndrome X", whereby a person remains physically and mentally an infant or child throughout one's life.[2][3]

Even if environmental factors do not cause aging, they may affect it; in such a way, for example, overexposure to ultraviolet radiation accelerates skin aging. Different parts of the body may age at different rates. Two organisms of the same species can also age at different rates, so that biological aging and chronological aging are quite distinct concepts.

Albeit indirectly, senescence is by far the leading cause of death (other than in the trivially accurate sense that cerebral hypoxia, i.e., lack of oxygen to the brain, is the immediate cause of all human death). Of the roughly 150,000 people who die each day across the globe, about two thirds100,000 per daydie of age-related causes; in industrialized nations, moreover, the proportion is much higher, reaching 90%.[4]

There are a number of hypotheses as to why senescence occurs; for example, some posit it is programmed by gene expression changes, others that it is the cumulative damage caused by biological processes. Whether senescence as a biological process itself can be slowed down, halted or even reversed, is a subject of current scientific speculation and research.[5]

Cellular senescence is the phenomenon by which normal diploid cells cease to divide. In cell culture, fibroblasts can reach a maximum of 50 cell divisions before becoming senescent. This phenomenon is known as "replicative senescence", or the Hayflick limit in honour of Dr.Leonard Hayflick, co-author with Paul Moorhead, of the first paper describing it in 1961.[6] Replicative senescence is the result of telomere shortening that ultimately triggers a DNA damage response. Cells can also be induced to senesce via DNA damage in response to elevated reactive oxygen species (ROS), activation of oncogenes and cell-cell fusion, independent of telomere length. As such, cellular senescence represents a change in "cell state" rather than a cell becoming "aged" as the name confusingly suggests. Although senescent cells can no longer replicate, they remain metabolically active and commonly adopt an immunogenic phenotype consisting of a pro-inflammatory secretome, the up-regulation of immune ligands, a pro-survival response, promiscuous gene expression (pGE) and stain positive for senescence-associated -galactosidase activity.[7] The nucleus of senescent cells is characterized by senescence-associated heterochromatin foci (SAHF) and DNA segments with chromatin alterations reinforcing senescence (DNA-SCARS).[8] Senescent cells are known to play important physiological functions in tumour suppression, wound healing and possibly embryonic/placental development and paradoxically play a pathological role in age-related diseases.[9] The elimination of senescent cells using a transgenic mouse model led to greater resistance against aging-associated diseases,[10] suggesting that cellular senescence is a major driving force of ageing and its associated diseases.

Organismal senescence is the aging of whole organisms. In general, aging is characterized by the declining ability to respond to stress, increased homeostatic imbalance, and increased risk of aging-associated diseases. Death is the ultimate consequence of aging, though "old age" is not a scientifically recognized cause of death because there is always a specific proximal cause, such as cancer, heart disease, or liver failure. Aging of whole organisms is therefore a complex process that can be defined as "a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increase in vulnerability".[11]

Differences in maximum life span among species correspond to different "rates of aging". For example, inherited differences in the rate of aging make a mouse elderly at 3 years and a human elderly at 80 years.[12] These genetic differences affect a variety of physiological processes, including the efficiency of DNA repair, antioxidant enzymes, and rates of free radical production.

Senescence of the organism gives rise to the GompertzMakeham law of mortality, which says that mortality rate accelerates rapidly with age.

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Senescence - Wikipedia, the free encyclopedia

Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss in renal function over a period of months or years. The symptoms of worsening kidney function are not specific, and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with CKD. This disease may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia, or pericarditis.[1] It is differentiated from acute kidney disease in that the reduction in kidney function must be present for over 3 months.

Chronic kidney disease is identified by a blood test for creatinine, which is a breakdown product of muscle metabolism. Higher levels of creatinine indicate a lower glomerular filtration rate and as a result a decreased capability of the kidneys to excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis (testing of a urine sample) shows the kidney is allowing the loss of protein or red blood cells into the urine. To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests, and sometimes a renal biopsy (removing a small sample of kidney tissue) are employed to find out if a reversible cause for the kidney malfunction is present.[1]

Recent professional guidelines classify the severity of CKD in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is often called end-stage kidney disease, end-stage renal disease, or end-stage kidney failure, and is largely synonymous with the now outdated terms chronic renal failure or chronic kidney failure; and usually means the patient requires renal replacement therapy, which may involve a form of dialysis, but ideally constitutes a kidney transplant.

No specific treatment has been unequivocally shown to slow the worsening of CKD. If an underlying cause of CKD, such as vasculitis, or obstructive nephropathy (blockage to the drainage system of the kidneys) is found, it may be treated directly to slow the damage. In more advanced stages, treatments may be required for anemia and renal bone disease (also called renal osteodystrophy, secondary hyperparathyroidism or chronic kidney disease - mineral bone disorder (CKD-MBD)). Chronic kidney disease resulted in 956,000 deaths in 2013 up from 409,000 deaths in 1990.[2]

CKD is initially without specific symptoms and is generally only detected as an increase in serum creatinine or protein in the urine. As the kidney function decreases:

People with CKD suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with CKD and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter.[citation needed]

Sexual dysfunction is very common in both men and women with CKD. A majority of men have a reduced sex drive, difficulty obtaining an erection, and reaching orgasm, and the problems get worse with age. A majority of women have trouble with sexual arousal, and painful menstruation and problems with performing and enjoying sex are common.[8]

The most common recognised cause of CKD is diabetes mellitus. Others include idiopathic (ie unknown cause, often associated with small kidneys on renal ultrasound), hypertension, and glomerulonephritis.[9] Together, these cause about 75% of all adult cases.

Historically, kidney disease has been classified according to the part of the renal anatomy involved.[citation needed]

Diagnosis of CKD is largely based on the clinical picture combined with the measurement of the serum creatinine level (see above). In many CKD patients, previous renal disease or other underlying diseases are already known. A significant number present with CKD of unknown cause. In these patients, a cause is occasionally identified retrospectively.[citation needed]

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Chronic kidney disease - Wikipedia, the free encyclopedia