StemCell Therapy

June 30, 2017

Uncovering rare susceptibility variants that contribute to the causes of complex diseases requires large sample sizes and massively parallel sequencing technologies. These sample sizes, often made up of exome and genome data from tens to hundreds of thousands of individuals, are often too large for current analytical tools to process. A team at Baylor College of Medicine, led by Dr. Suzanne Leal, professor of molecular and human genetics, has developed new software called SEQSpark to overcome this processing obstacle. A study on the new technology appears in The American Journal of Human Genetics.

"To handle these large data sets, we built the SEQSpark tool based on the commonly used Spark program, which allows SEQSpark to utilize multiple processing platforms to increase the speed and efficiency of performing data quality control, annotation and rare variant association analysis," Leal said.

To test and validate the versatility and speed of SEQSpark, Leal and her team analyzed benchmarks from the whole genome sequence data from the UK10K, testing specifically for waist-to-hip ratios.

"The analysis and related tasks took about one and a half hours to complete, in total. This includes loading the data, annotation, principal components analysis and single and rare variant aggregate association analysis for the more than 9 million variants present in this sample set," explained Di Zhang, a postdoctoral associate in the Leal lab at Baylor and first author on the paper.

To evaluate SEQSpark's performance in a larger data set, Leal and the research team generated 50,000 simulated exomes. The SEQSprak program ran the analysis for a quantitative trait using several variant aggregate association methods in an hour and forty-five minutes.

When compared to other variant association tools, SEQSpark was consistently faster, reducing computation to a hundredth of the time in some cases.

"What is unique about SEQSpark is that it is scalable, and smaller labs can run it without super specific hardware, and it can also be run in a multi-server environment to increase its speed and capacity for large genetic data sets," Zhang said. "It is ideal for large-scale genetic epidemiological studies and is highly efficient from a computational standpoint."

"We see this software as being very useful as the demand for the analysis of massively parallel sequence data grows. SEQSpark is highly versatile, and as we analyze increasingly large sets of rare variant data, it has the potential to play a key role in furthering personalized medicine," Leal said.

In the future, Leal and her team will continue to test and increase SEQSpark's capabilities and will be analyzing soon data sets that have 500,000 samples or more.

Explore further: Genetic test for familial data improves detection genes causing complex diseases such as Alzheimer's

More information: Di Zhang et al. SEQSpark: A Complete Analysis Tool for Large-Scale Rare Variant Association Studies using Whole-Genome and Exome Sequence Data, The American Journal of Human Genetics (2017). DOI: 10.1016/j.ajhg.2017.05.017

A team of researchers at Baylor College of Medicine has developed a family-based association test that improves the detection in families of rare disease-causing variants of genes involved in complex conditions such as Alzheimer's. ...

Precision medicine, which utilizes genetic and molecular techniques to individually tailor treatments and preventative measures for chronic diseases, has become a major national project, with President Obama launching the ...

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Researchers build SEQSpark to analyze massive genetic data sets - Medical Xpress

June 26, 2017 Credit: CC0 Public Domain

Between 15 and 20 percent of black people carry a genetic mutation that puts them at risk for certain chronic kidney disease, but only about half of them develop the illness - a variance that long has puzzled researchers. Now a study has found that the gene mutation's toxic effects require higher than normal levels of a protein called suPAR to trigger the onset and progression of the disease.

The results of the study, published in a research article in the journal Nature Medicine today, could lead soon to new treatments for chronic kidney disease that target these risk factors, according to Dr. Jochen Reiser, the senior author of the paper. Reiser is the chairperson of the Department of Internal Medicine and Ralph C. Brown MD Professor of Medicine at Rush University Medical Center, Chicago.

Chronic kidney disease - or CKD for short - is a progressive failure of function that prevents kidneys from fulfilling their role filtering waste from the blood stream. Nearly 17 percent of people in the U.S. have chronic kidney disease, and approximately 4 percent require dialysis and/or a kidney transplant due to kidney failure. Currently, there are no drugs that can treat CKD in an effective way.

Study analyzed samples from more than 1,000 people with genetic risk for CKD

For the study recounted in the Nature Medicine paper, Reiser worked with a team that included researchers at Emory University, Harvard University, Johns Hopkins University, the National Institute of Health, Ruprecht Karls University of Heidelberg, the Israel Institute of Technology and others. Together, they looked at two well-known genetic risk factors for CKD in black people, the mutated G1 or G2 variations in the gene known as apolipoprotein L1 (APOL1). To be at risk for developing CKD, an individual must have inherited two of these gene variants, one from each parent.

The study analyzed blood samples for suPAR levels, screened for APOL1 gene mutations and measured kidney function from two separate cohorts of black patients - 487 people from the Emory Cardiovascular Biobank, 15 percent of whom had a high-risk APOL1 genotype; and 607 from the multi-center African American Study of Kidney Disease and Hypertension, including 24 percent with the high-risk mutation.

Using these two large, unrelated cohorts, the researchers found that plasma suPAR levelsindependently predict renal function decline in individuals with two copies of APOL1 risk variants. APOL1-related risk is reduced by lower levels of plasma suPAR and strengthened by higher levels.

The team then went on and used purified proteins to study if suPAR and APOL1 bind to each other. They found that the mutated G1 and G2 variant did so particularly well on what's known as a receptor on the surface of kidney cells, in this case the suPAR activated receptor alphavbeta3 integrin. "This binding appears to be a key step in the disease onset" adds Dr. Kwi Hye Ko, a scientist at Rush and the study's co-first author.

This binding causes kidney cells to change their structure and function, permitting disease onset. Using cell models and genetically engineered mice, the authors then could reproduce kidney disease changes upon expression of APOL1 gene variants, but the disease required the presence suPAR.

Without elevated suPAR levels, genetic mutation much less likely to trigger disease

Everybody has suPAR, which is produced by bone marrow cells, in their blood, with normal levels around 2400 picogram per milliliter (pg/ml). As levels of suPAR rise, risk for kidney disease rises in turn.

Patients with levels above 3000 picogram per milliliter carry a much higher risk for kidney disease in the general population. Black people are particularly at risk, given the study's finding that suPAR activates its receptor on kidney cells that then attract the APOL1 risk proteins. Over time, these assaults can damage and eventually destroy the kidney.

On the other hand, without high levels of suPAR, the ability of the genetic mutation of APOL1 to exert its damaging effects is impaired, which helps identify patients in most need of suPAR lowering or future anti-suPAR therapy.

"Patients with APOL1 mutations who don't get kidney disease have more commonly low suPAR levels," said Dr. Salim Hayek, co-first author of the paper and a cardiologist at Emory University School of Medicine. "The suPAR level needs to be high to activate the mechanism in the kidney that enables APOL1 proteins" and set off the chain of events the genetic mutation can trigger.

suPAR 'is to the kidneys as cholesterol is to the heart'

Like some other pathological gene mutations, the APOL1 variations may have persisted in the population, in this case in Africa, because they could protect people from infection with the parasites known as trypanosome. explained Sanja Sever, PhD, co-correspondent author of the paper and associate professor of medicine at Harvard Medical School. In the United States, however, fighting parasitic trypanosomes isn't a significant concern, while lifestyle and environmental pressures such as obesity promote the rise in suPAR levels. This scenario sets up people for high risk of kidney disease.

Reiser has spent his career studying a scarring type of chronic kidney disease, focal segmental glomerulosclerosis. In past studies, he discovered that suPAR not only is a marker for kidney disease, but also a likely cause.

"What we are learning today is that suPAR in a general way is to kidneys what cholesterol is to the heart, a substance that can cause damage if levels rise too high, or a substance that can likely make many forms of kidney disease worse," Reiser says. "Based on these fundamental insights, suPAR level testing may become a routine test at many institutions around the world."

Like cholesterol, suPAR levels vary from person to person. Some environmental factors can contribute significantly to elevated suPAR levels. "Lifestyle is a big factor, bigger than we thought," Reiser says.

Smoking, weight gain and even frequent infections can add up and send suPAR to dangerous heights. Weight loss and smoking cessation can help bring levels down, but once elevated, suPAR may not recede to a healthy level again, said Dr. Melissa Tracy, co-author of the study and an associate professor of cardiology at Rush. People at genetic risk for kidney disease should aim to live a healthy life to keep suPAR levels low.

Explore further: Circulating blood factor linked with a leading cause of kidney failure

More information: A tripartite complex of suPAR, APOL1 risk variants and v3 integrin on podocytes mediates chronic kidney disease, Nature Medicine (2017). DOI: 10.1038/nm.4362

Patients with a disease that is a leading cause of kidney failure tend to have high levels of a particular factor circulating in their blood, according to a study appearing in an upcoming issue of the Journal of the American ...

A protein known as suPAR has been identified in recent years as both a reliable marker for chronic kidney disease and a pathogen of the often deadly condition. Its place of origin in the human body, however, has been a mysteryuntil ...

Make room, cholesterol. A new disease marker is entering the medical lexicon: suPAR, or soluble urokinase-type plasminogen activator receptor. A study in the New England Journal of Medicine shows that suPAR, a circulating ...

African Americans have a heightened risk of developing chronic and end-stage kidney disease. This association has been attributed to two common genetic variants - named G1 and G2in APOL1, a gene that codes for a human-specific ...

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Catalyst for genetic kidney disease in black people identified - Medical Xpress

June 29, 2017 Micrograph showing prostatic acinar adenocarcinoma (the most common form of prostate cancer) Credit: Wikipedia

Scientists have had limited success at identifying specific inherited genes associated with prostate cancer, despite the fact that it is one of the most common non-skin cancers among men. Researchers at University of Utah Health studied prostate cancer patients with multiple cancer diagnoses, many who would not be recommended for genetic tests following current guidelines, to identify genetic mutations that may influence cancer treatment and cancer risk assessment for family members. Their findings are reported in the June issue of the journal Cancer.

"We commonly use a combination of a patient's personal and family cancer histories to identify those individuals who may have a mutation in a gene that predisposes that individual to developing cancers," said Patrick Pili, M.D., medical oncology fellow at the University of Texas MD Anderson Cancer Center. "Testing for hereditary cancers impacts not only the patient with cancer but also potentially the cancer screening and health outcomes of their entire family, but many prostate cancer patients do not meet the current guidelines to test for genetic cancer heritability."

Pili was part of a research team led by Kathleen Cooney, M.D., chair of the Department of Internal Medicine at U of U Health and a Huntsman Cancer Institute investigator, who proposed a strategy to identify germline mutations in men selected for the study based on their clinical history not their family history.

The study was highly selective, including 102 patients who had been diagnosed with prostate cancer and at least one additional primary cancer, like melanoma, pancreatic cancer, testicular cancer, or Hodgkin lymphoma.

The researchers examined the frequency of harmful germline mutations in this group of men. These mutations originate on either the egg or sperm and become incorporated into the DNA of every cell in the body of the resulting offspring.

Using next generation sequencing, the researchers found that 11 percent of the patients had a disease-causing mutation in at least one cancer-predisposing gene, which suggests these genetic variations contributed to their prostate cancer. Cooney found no difference in cancer aggressiveness or age of diagnosis compared to patients without these mutations.

In addition, a certified genetic counselor and co-investigator Elena Stoffel, M.D., University of Michigan Comprehensive Cancer Center, reviewed personal and family histories from each patient to determine whether they would meet clinical genetic testing guidelines. The majority of the men in the study, 64 percent, did not meet current criteria to test for hereditary cancer based on personal and/or family history.

The findings suggest that there are men with heritable prostate cancer-predisposing mutations that are not eligible for genetic screening under current guidelines.

"This is the first paper in which we can show the potential of using a clinical history of multiple cancers, including prostate cancer, in a single individual to identify inherited germline mutations," Cooney said.

The majority of harmful mutations identified were in genes involved in DNA repair.

"These mutations prevent the DNA from healing itself, which can lead to a predisposition for cancer," Cooney said.

This result is also beneficial because drugs like PARP [poly ADP ribose polymerase] inhibitors have a better success rate in treating cancers with the underlying gene mutation associated with DNA repair.

Cooney cautions that this is a small pilot study rather than a broader epidemiological survey, and it consists of a highly specific subset of patients.

"We cannot generalize these findings to the broader population, because we used highly selective criteria to tip us off to patients that may have mutations outside typical hereditary genetic patterns," she said.

The 102 patients included in the study were identified from the University of Michigan's Prostate Cancer Genetics Project, which registers patients who are diagnosed with prostate cancer before age 55 or who have a first- or second-degree relative with prostate cancer. In addition, the research team identified patients from the University of Michigan's Cancer Genetics Registry, which includes individuals with personal or family history suggestive of a hereditary risk of cancer.

"Our findings are in line with those of other studies, suggesting that approximately 1 in 10 men with advanced prostate cancer harbors a genetic variant associated with increased cancer risk," said Stoffel. "While family history is an important tool, there may be better ways to identify patients with genetic risk."

Future studies with larger sample sizes will include sequencing of tumors that will allow investigators to more carefully explore the different features associated with tumors that arise in individuals with germline mutations.

"This approach will help us identify patients at greater risk for aggressive prostate cancer so they can seek earlier screening while pre-symptomatic," Cooney said.

Explore further: Are men with a family history of prostate cancer eligible for active surveillance?

More information: Patrick G. Pili et al. Germline genetic variants in men with prostate cancer and one or more additional cancers, Cancer (2017). DOI: 10.1002/cncr.30817

Journal reference: Cancer

Provided by: University of Utah

Active surveillancecareful monitoring to determine if or when a cancer warrants treatmentis an increasingly prevalent choice for prostate cancer, but it's unclear if the strategy is appropriate for men with a family ...

Inherited mutations in genes that function to repair DNA may contribute to metastatic prostate cancer more than previously recognized, according to a study out today in the New England Journal of Medicine. Though infrequent ...

African-American men develop prostate cancer more often than other men, and it tends to be more deadly for this population. Some of the differences seem to be due to socioeconomic factors, but scientists wondered whether ...

(HealthDay)A man's risk of aggressive and fatal prostate cancer may be heavily influenced by gene mutations previously linked to breast and ovarian cancer in women, a trio of new studies suggests. Findings from the studies ...

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A form of genetic variation, called differential RNA splicing, may have a role in tumor aggressiveness and drug resistance in African American men with prostate cancer. Researchers at the George Washington University (GW) ...

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Researchers propose new approach to identify genetic mutations in ... - Medical Xpress

Born in August, Charlie Gard has a rare genetic disorder known as mitochondrial DNA depletion syndrome. Caused by a genetic mutation, it leads to weakened muscles and organ dysfunction, among other symptoms, with a poor prognosis for most patients.

Charlie is on life support and has been in the intensive care unit at the Great Ormond Street Hospital for Children in London since October. His doctors wish to take him off life support, but his parents disagree.

"The domestic courts concluded that it would be lawful for the hospital to withdraw life sustaining treatment because it was likely that Charlie would suffer significant harm if his present suffering was prolonged without any realistic prospect of improvement, and the experimental therapy would be of no effective benefit," a press release from the court announcing the decision said.

Charlie's parents appealed to the UK Supreme Court to decide the best interests of their child. After they lost that appeal, the 10-month-old was due to have his life support switched off at the end of the day June 13.

Gard and Yates then filed a request with the European Court of Human Rights, an international court based in Strasbourg, France, to consider the case.

The original ruling to provide life support until June 13 was extended by European Court of Human Rights initially for one week, until June 19. Rather than making a decision then, the court granted a three week-extension, until July 10, to allow for a more informed decision by the court. That extension ended Tuesday with the courts decision.

However, parental rights are not absolute, and in cases in which doctors and parents disagree, the courts may exercise objective judgment in a child's best interest.

In April, a judge tasked with ruling on the impasse between doctors and parents decided in favor of the Great Ormond Street Hospital doctors. In his decision, Justice Francis said life support treatment should end so Charlie could die with dignity.

The boy's parents challenged this ruling in May, yet it was upheld by a Court of Appeal. Three Supreme Court justices later dismissed another challenge from the couple.

Since Charlie's birth, "his condition has deteriorated seriously," the UK Supreme Court stated in a decision June 8; his brain is severely affected, and "he cannot move his arms or legs or breathe unaided."

On this basis, the court ruled that the child's life support should be switched off June 13, but the family appealed to the European court.

Charlie's parents argued that the UK courts gave insufficient weight to their own human rights, and some of Charlie's human rights, in their decision-making, Wilson said.

After the European court's ruling to extend the deadline while judges considered the case further, the Supreme Court told doctors it "would not be unlawful" to continue to provide life support.

After the extension, a Supreme Court hearing was requested by the government and the Great Ormond Street Hospital for Children, which did not know whether the Strasbourg court order was legally binding in the UK, Wilson explained.

"There was also a secondary issue, which was that (Great Ormond Street Hospital's) legal representatives were concerned that at present, doctors did not have sufficient legal clarity about what they can and can't do if Charlie's condition deteriorates," Wilson said. "So this court was also invited to consider whether any UK court, and if so which court, should handle that matter."

In fact, it has never been used to treat this form of mitochondrial DNA depletion syndrome, according to the British ruling, though it has proved beneficial to patients with a different form of the disease.

"He literally has nothing to lose but potentially a healthier, happier life to gain," they said.

Parents are rightly at the "heart" of decisions made about life-sustaining treatment for critically ill children, noted Dominic Wilkinson, director of medical ethics at the Oxford Uehiro Centre.

"Sadly, reluctantly, doctors and judges do sometimes conclude -- and are justified in concluding -- that slim chances of life are not always better than dying." Sometimes, the "best that medicine can do" -- and the most ethical decision -- is to provide comfort and to avoid painful and unhelpful medical treatments, he wrote.

The court said the decision was meticulous, noting that they spoke with Charlie's health care providers, independent experts, experts recommended by the family, and Charlie's parents to inform the ruling. In the end, the press released said they determined, "it was most likely Charlie was being exposed to continued pain, suffering and distress and that undergoing experimental treatment with no prospects of success would offer no benefit, and continue to cause him significant harm."

CNN's Stephanie Halasz, Debra Goldschmidt and Judith Vonberg contributed to this report.

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Court rules hospital can withdraw life support for sick baby Charlie Gard - CNN International

June 30, 2017 Size switchable nano-theranostics constructed with decomposable inorganic nanomaterials for acidic TME targeted cancer therapy. (a) A scheme showing the preparation of HSA-MnO2-Ce6&Pt (HMCP) nanoparticles, and (b) their tumor microenvironment responsive dissociation to enable efficient intra-tumoral penetration of therapeutic albumin complexes. (c) A scheme showing the preparation of Ce6(Mn)@CaCO3-PEG, and (d) its acidic TME responsive dissociation for enhanced MR imaging and synergistic cancer therapy. Credit: Science China Press

Cancer is one of leading causes of human mortality around the world. The current mainstream cancer treatment modalities (e.g. surgery, chemotherapy and radiotherapy) only show limited treatment outcomes, partly owing to the complexities and heterogeneity of tumor biology. In recent decades, with the rapid advance of nanotechnology, nanomedicine has attracted increasing attention as promising for personalized medicine to enable more efficient and reliable cancer diagnosis and treatment.

Unlike normal cells energized via oxidative phosphorylation, tumor cells utilize the energy produced from oxygen-independent glycolysis for survival by adapting to insufficient tumor oxygen supply resulting from the heterogeneously distributed tumor vasculatures (also known as the Warburg effect). Via such oncogenic metabolism, tumor cells would produce a large amount of lactate along with excess protons and carbon dioxide, which collectively contribute to enhanced acidification of the extracellular TME with pH, often in the range of 6.5 to 6.8, leading to increased tumor metastasis and treatment resistance.

With rapid advances in nanotechnology, several catalogs of nanomaterials have been widely explored for the design of cancer-targeted nano-theranostics. In a new overview published in the Beijing-based National Science Review, co-authors Liangzhu Feng, Ziliang Dong, Danlei Tao, Yicheng Zhang and Zhuang Liu at the Institute of Functional Nano & Soft Materials (FUNSOM), Soochow University in Suzhou, China present new developments in the design of novel multifunctional nano-theranostics for precision cancer nanomedicine by targeting the acidic TME and outline the potential development directions of future acidic tumor microenvironment-responsive nano-theranostics.

"Various types of pH-responsive nanoprobes have been developed to enable great signal amplification under slightly reduced pH within solid tumors. By taking the acidic TME as the target, smart imaging nanoprobes with excellent pH-responsive signal amplification would be promising to enable more sensitive and accurate tumor diagnosis," they state in the published study.

"As far as nano-therapeutics are concerned, it has been found that the acidic TME responsive surface charge reverse, PEG corona detachment and size shrinkage (or decomposition) of nanoparticles would facilitate the efficient tumor accumulation, intra-tumoral diffusion and tumor cellular uptake of therapeutics, leading to significantly improved cancer treatment. Therefore, the rational development of novel cancer-targeted nano-theranostics with sequential patterns of size switch from large to small, and surface charge reverse from neutral or slightly negative to positive within the tumor, would be more preferred for efficient tumor-targeted drug delivery."

The scientists also write, "For the translation of those interesting smart pH-responsive nano-therapeutics from bench to bedside, the formulation of those nanoscale systems should be relatively simple, reliable and with great biocompatibility, since many of those currently developed nano-theranostics were may be too complicated for clinical translation."

Explore further: Treatment with Alk5 inhibitor improves tumor uptake of imaging agents

More information: Liangzhu Feng et al, The acidic tumor microenvironment: a target for smart cancer nano-theranostics, National Science Review (2017). DOI: 10.1093/nsr/nwx062

A form of genetic variation, called differential RNA splicing, may have a role in tumor aggressiveness and drug resistance in African American men with prostate cancer. Researchers at the George Washington University (GW) ...

While mutations in protein-coding genes have held the limelight in cancer genomics, those in the noncoding genome (home to the regulatory elements that control gene activity) may also have powerful roles in driving tumor ...

A molecular test can pinpoint which patients will have a very low risk of death from breast cancer even 20 years after diagnosis and tumor removal, according to a new clinical study led by UC San Francisco in collaboration ...

Scientists have had limited success at identifying specific inherited genes associated with prostate cancer, despite the fact that it is one of the most common non-skin cancers among men. Researchers at University of Utah ...

Cancerous tumors are formidable enemies, recruiting blood vessels to aid their voracious growth, damaging nearby tissues, and deploying numerous strategies to evade the body's defense systems. But even more malicious are ...

Leukemia researchers led by Dr. John Dick have traced the origins of relapse in acute myeloid leukemia (AML) to rare therapy-resistant leukemia stem cells that are already present at diagnosis and before chemotherapy begins.

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Exploiting acidic tumor microenvironment for the development of novel cancer nano-theranostics - Medical Xpress

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5280 Stem Cell | Colorado Stem Cell Therapy

Regenerative medicine combines the latest advances in stem cell biology, embryology, tissue engineering and medicine to develop products for the replacement, restoration or regeneration of damaged or diseased cells and tissues. Tools used in regenerative medicine include biomaterials and extracellular matrices, lab-generated cells and tissues, and new biological molecules. These powerful technologies and tools are allowing clinical scientists to engineer and provide healthy cells, tissues and organs to patients with chronic degenerative diseases. This revolution in medical science changes the focus from treating symptoms of chronic and degenerative diseases to providing cures, and directly addresses costs that constitute approximately 83% of the 2.5 trillion dollar annual healthcare budget in the U.S. and are growing due to an aging population.

BioTime is led by Michael West, PhD., who pioneered the regenerative medicine industry. He founded Geron Corporation in the early 90s which funded the first studies of cultured hESC to realize their potential to cure intractable human degenerative diseases. Dr. West has since built BioTime around key technologies and intellectual property that constitute major pillars of regenerative medicine.

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Regenerative Medicine - BioTime, Inc.

A regenerative medicine startup led by a Mayo Clinic cardiologist is setting up shop in a downtown Rochesters Minnesota BioBusiness Center, according to newly filed city documents. The filing indicated Rion LLC, a Minnesota company registered to Dr. Atta Behfar of the Mayo Clinic Center for Regenerative Medicine, has signed a three-year lease for just over 2,000 square feet at the city-owned BioBusiness Center. The lease begins July 1. The nine-story BioBusiness Center opened in downtown Rochester in 2007 as a center for innovation in biotechnology, promoting the linkages between the researchers and practitioners at Mayo Clinic; instructors and students at the University of Minnesota Rochester, and the biotechnology business community. It houses the Mayo Clinic Business Accelerator among other tenants. Behfar is an assistant medical professor and leads a laboratory at Mayo concentrating on applying regenerative medicine the practice of using stem cells to regenerate damaged or missing tissue to prevent and cure chronic heart conditions. Specifically, his group focuses on development and use of both stem cells and protein-based therapies to reverse injury caused by lack of blood flow to the heart. The business direction of Rion, meanwhile, appears to be specifically geared toward a cutting-edge development in the field of regenerative medicine the use of extracellular vesicles (EVs) in speeding and directing the growth of regenerating tissues in the heart and elsewhere in the body. EVs, long brushed off by researchers as mere debris in the bloodstream, are membrane-enclosed spheres that break off from the surfaces of nearly all living cells when disturbed. They transport lipids, proteins and nucleic acids, and have now been found to be important players in cell-to-cell communication, influencing the behavior and even the identity of cells. Their emerging role in regenerative medicine could potentially be huge. For instance, by bioengineering them to transport protein payloads from stem cells, they can be used to signal the bodys own cells to regenerate tissue instead of transplanting the stem cells themselves, thus eliminating the chance of host immune system rejection. A patent application filed last year by Rion, Behfar, Mayo Center for Regenerative Medicine Director Dr. Andre Terzic and two other local inventors is aimed at adapting the healing properties of a specific type of EV into a unique kind of product that could have wide applications. It focuses on EVs derived from blood platelets, which are well known to stop bleeding, promote the growth of new tissues and blood vessels, relieve inflammation and provide a host of other benefits. The patent describes a system of encapsulating platelet EVs derived from human or animal blood into a platelet honey and delivering it to target areas of the body, such as damaged tissues or organs. Its purported effect is to regenerate, repair and restore damaged tissue, with possible uses including treating heart disease; healing damaged bones or joints; wound treatment; and cosmetic skin applications. A brief business description provided by Rion to Rochester city officials stated the company is focused on the delivery of cutting edge regenerative technologies to patients at low cost and in off-the-shelf fashion. Building on initial research at Mayo Clinic, Rion LLC aims to develop and bring to practice products in the space of wound healing, orthopedics and cardiac disease. The statement also added the company is an enthusiastic backer of Rochesters efforts to develop a local biotech business cluster, and is seeking to participate in the realization of the Destination Medical Center initiative.

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Mayo-Connected Regenerative Medicine Startup Inks Downtown Rochester Lease - Twin Cities Business Magazine

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The new finding could help scientists unlock the secrets to regenerative medicine in humans.

In the future, artificial and transplanted organs may be things of the past as regenerative medicine becomes so advancedthat a damaged heart or lung is simply regrown from cells already present.

That possibility is still far in the distance, but a new study out of the University of Floridacould help pave the way. While examining the genes of the starlet sea anemone an invertebrate capable of regenerating itself a research team led by Mark Martindale discovered genes that are known to grow heart cells in humans.

The finding was surprising in part because anemones dont have hearts or muscles, and yet Martindale knew they shared more in common with humans than might be expected.

A group of us sequenced the genome of the anemone about 10 years ago, he told Digital Trends. One of the super cool things we found was that this little sea anemone had more genes in common with human beings than all of the other so-called model systems that 99 percent of the people in my field work on.

Since these model systems including fruit flies and nematodes are nearer to humans on the evolutionary timescale, that finding suggested that theyve lost genes along the way.

It turns out that the number of genes you have does not seem to be a very good predictor of organismal complexity as we have traditionally interpreted it, Martindale said.

Rather of the number of genes, the deciding factor may be the way they communicate with each other.

One of the most important findings in this paper is not necessarily how many genes are involved in heart formation, but how they are wired-up. Martindale explained. Genes control other genes in very complicated networks. Many people focus on genes that are involved in cell division but not as many people have studied the differences in how these genes talk to each other in animals that can regenerate versus those that can not regenerate.

By understanding how genes communicate, the researchers hope that they can someday stimulate regenerative healing in the human body.

But theres a lot of work to be done first. One of the big challenges will be determining whether certain mechanisms are species-specific or if they can be adapted. In vertebrates, for example, heart genes create lockdown loops that require them to perform functions related to their location in the body. Anemone genes dont lockdown in such a way. Its unclear whether this feature is fixed to anemone or if it can be activated in humans as well.

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Sea anemone genes could spur advancements in regenerative medicine - Digital Trends

sea anemone heart gene regeneration regenerative medicine

In the future, artificial and transplanted organs may be things of the past as regenerative medicine becomes so advancedthat a damaged heart or lung is simply regrown from cells already present.

That possibility is still far in the distance, but a new study out of the University of Floridacould help pave the way. While examining the genes of the starlet sea anemone an invertebrate capable of regenerating itself a research team led by Mark Martindale discovered genes that are known to grow heart cells in humans.

The finding was surprising in part because anemones dont have hearts or muscles, and yet Martindale knew they shared more in common with humans than might be expected.

A group of us sequenced the genome of the anemone about 10 years ago, he told Digital Trends. One of the super cool things we found was that this little sea anemone had more genes in common with human beings than all of the other so-called model systems that 99 percent of the people in my field work on.

Since these model systems including fruit flies and nematodes are nearer to humans on the evolutionary timescale, that finding suggested that theyve lost genes along the way.

It turns out that the number of genes you have does not seem to be a very good predictor of organismal complexity as we have traditionally interpreted it, Martindale said.

Rather of the number of genes, the deciding factor may be the way they communicate with each other.

One of the most important findings in this paper is not necessarily how many genes are involved in heart formation, but how they are wired-up. Martindale explained. Genes control other genes in very complicated networks. Many people focus on genes that are involved in cell division but not as many people have studied the differences in how these genes talk to each other in animals that can regenerate versus those that can not regenerate.

By understanding how genes communicate, the researchers hope that they can someday stimulate regenerative healing in the human body.

But theres a lot of work to be done first. One of the big challenges will be determining whether certain mechanisms are species-specific or if they can be adapted. In vertebrates, for example, heart genes create lockdown loops that require them to perform functions related to their location in the body. Anemone genes dont lockdown in such a way. Its unclear whether this feature is fixed to anemone or if it can be activated in humans as well.

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New study on anemone genes could pave way for regenerative ... - Yahoo News

American Veterinary Medical Association

New Texas veterinary school plan still alive American Veterinary Medical Association Plans for a proposed Texas Tech University School of Veterinary Medicine in Amarillo got a boost this spring.

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New Texas veterinary school plan still alive - American Veterinary Medical Association

At Jacobs Island Dog Park on Wednesday afternoon, Laura Tonnessen threw a stick into the river for her dog Thor. He barked enthusiastically, retrieving and dropping the stick at her feet. But in a few days, on the Fourth of July, Tonnessen knows Thors demeanor will change. The loud fireworks frighten him.

Hell hide behind furniture and act weird and whine, Tonnessen said.

Last year, Tonnessens friends pitbull, Cracker, ran away and was lost for three days because he was spooked by loud fireworks. It was traumatic to lose him for so long, Tonnessen said, and she makes sure to keep Thor inside on the holiday to prevent him from running away, too.

Michael Edwards, a student at the University of Montana, said his 130-pound great Pyrenees, Snowy, climbs into the bathtub, pulls the shower curtain closed with her mouth, and howls until the thunder storm or fireworks end.

If shes outside, she runs. They once found her about seven miles from their house, trying to escape the source of the noise. Animal shelters report that July 4-5 are their busiest days of the year.

When dogs bark, flee or cower on the Fourth of July, they are exhibiting symptoms of a panic disorder called noise phobia.

Fireworks and other loud noises terrify a fraction of all dogs, and their reactions sometimes endanger their health. Dogs may jump through windows, climb fences or run away for days to try to escape the sounds of patriotic celebration.

This phobia, which is a symptom of underlying anxiety issues, has recently been linked to a certain gene in dogs, says Dr. Leticia Fanucchi, a veterinary behaviorist at Washington State University's College of Veterinary Medicine.

Some dogs are more genetically predisposed to anxiety disorders, Fanucchi said, just like humans.

The area that is activated in our brain for fear is the amygdala, and the amygdala can be triggered long before the prefrontal cortex can process information, Fanucchi said.

Its like people who suffer from arachnophobia even if you explain that the spider won't hurt them, it activates the amygdala and makes them panic.

The amygdala is where irrational fears trigger a fight, flight or freeze response, while the prefrontal cortex controls reason and rational decision-making. Dogs panic at the sound of fireworks because they think their lives are at risk, even if they are safe at home.

Fanucchi said not all breeds of dogs carry this anxiety gene, and some are more prone to it than others. Within one breed, a dog could have the anxiety gene while another might not. This explains why some dogs dont react at all to loud noises. Those that do are typically anxious about other things, as well.

What we do know is that a good chunk of the dogs that have noise phobia do have generalized anxiety as an underlying disease, Fanucchi said. About 40 percent of the dogs that have generalized anxiety have noise phobia. So noise phobia is a big red flag that something else is going on with that dog, and it needs to be diagnosed and treated appropriately.

For this Fourth of July, its too late to start a long-term medication regimen to treat anxiety because medications typically take a few weeks to become effective, Fanucchi said. But there are other, short-term practices that can minimize dogs anxiety and keep them safe.

Creating a quiet and distracting setting for dogs can help them stay calm, said Emily Adamson, director of Organizational Advancement at the Humane Society of Western Montana. Scent therapy, like lavender spray, is popular for calming dogs, Adamson said.

Food toys and soft music (they play classical at the shelter) help distract the dogs from the source of their fear. For people who do take their dogs outside, Adamson recommends double-checking their ID tags to make sure the information is current, in case the dogs run away.

And then, theres the Thundershirt.

Dr. Lindsey Rewinkel at Pruyn Veterinary Hospital in Missoula said Thundershirts are available at pet stores and some veterinary hospitals, and serve as a dog anxiety vest.

Its a heavy fabric fashioned into a shirt that you wrap them in, Rewinkel said. Its not quite as severe as a swaddle, but the goal is to make them feel comforted. That has helped an incredible amount of dogs cope with noise phobias if they're not as severe.

Finally, there are medications vets can prescribe that sedate dogs and minimize their anxiety symptoms on the Fourth of July if none of these other practices work. Rewinkel said she always urges people to also treat the underlying anxiety issue with long-term behavioral therapy, and not just resort to medication, which can serve as a Band-Aid solution to a larger problem.

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Why does your dog hate Fourth of July fireworks? It's genetic - The Missoulian

American Veterinary Medical Association

Zoo veterinarians, behind the scenes and in the field American Veterinary Medical Association For zoo veterinarians, their day-to-day work can encompass thousands of individual animals and a multitude of species. and more »

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Zoo veterinarians, behind the scenes and in the field - American Veterinary Medical Association

(Logo: http://photos.prnewswire.com/prnh/20150323/735844 )

An impact with a stone during a hunting trip: this is the reason why Tom had to be operated on the deep wound generated. The 4-year-old Italian Pointer, due to the wound position and poor post-surgery care of the owners, had to also deal with its subsequent reopening from the painful, non-secondary repercussions. Stumbling, instead, on a hooked piece of iron in the ground as he walked with his owners, Niki, a 9-year-old German shepherd, got a contused and lacerated wound that, though promptly sutured, created problems afterwards that eventually led to a surgical curettage and the removal of an already necrotic skin flap.

How to help the closure of the two wounds in a short time, without pain and contraindications? Laser therapy applied in the veterinary field turns out to be providential. Thanks to its anti-inflammatory, antiedemigenous, analgesic, and biostimulating effects, it results in a rapid healing and oedema resolution, an immediate improvement in local blood circulation, a fast recovery of the structural integrity of damaged tissues, and a significant reduction of pain in the short term. The speed of application of the treatment also has positive effects on its tolerability even for the more restless or sensitive animals.

The confirmation of the value of this therapeutic solution comes from the experience of some veterinary medicine specialists who have chosen it to treat frequent pathologies in everyday outpatient practice.

"Practicing physiotherapy in the veterinary field," explains Dr. Jane McNae of the Hong Kong Vet Clinic 'Paws in Motion.' "after careful research I chose MLS Laser Therapy by ASAlaser, because the benefits of this therapeutic laser are essential for the pain and inflammation management, and to improve the natural healing of the body in many post-operative cases in the orthopaedic and neurological fields, and in common disorders of old pets. I also practice acupuncture or acu-laser treatment using both the traditional points indicated by Chinese veterinary medicine as described in the TCVM texts, and the trigger points in the myofascial tissues of the individual animals. Even in this context, MLS is valid, allowing you to act quickly on the defined points."

The fields of use of laser therapy are many, and, besides injuries and wounds, it also speaks the language of potentially disabling pathologies.

On the subject, the words of Dr. Martha Matallana, a veterinary physician specialized in physical therapy and rehabilitation of small animals, chiropractic and ozone therapy, DMV at the Salle University of Bogot: 'The effective use of MLS Laser Therapy is extensive, and covers, for example, both patients who, after an orthopaedic operation, must be able to return to their activity in the shortest amount of time possible, and also animals that are unsuitable for surgery that have to live with acute pain coming from problems such as the infirmity of the intervertebral disc. In both cases, the time factor is crucial: MLS not only has short application times, but also offers fast recovery results ."

A non-secondary advantage that benefits pets like equine and exotic species. A comprehensive therapy already in its DNA.

SOURCE ASA Srl

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Laser Therapy: Amazing Results in Veterinary Medicine - PR Newswire (press release)

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Columns should be submitted to: wayne.greene@tulsaworld.com

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Letter to the editor: The eyes disprove evolution theory - Tulsa World

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NEW YORK Monty Capers says she desperately needs a pediatric wheelchair for her oldest son, 3-year-old Christopher.

"He makes me smile. He makes my heart skip a beat. He is suffering," said Capers.

Christopher Capers was born with cerebral palsy.

Right now, he is sharing a stroller with his baby sister, Malaysia, which is a tight fit for his long legs.

"He's very long for a child for his age. So it's uncomfortable for him to be positioned like this. He needs the chair for pre-school on July 7th," said Capers.

PIX11 News reached to a company with a generous spirit called Rehabco. Rehabco delivered Christopher's chair in 48 hours.

Jacqueline Kotschenrwurher is a survivor and a fighter. A domestic violence survivor, she says 10 years ago, during a fight with her husband, her husband shot her in the back. Kotschenrwurher survived the ordeal but became paralyzed.

"I'm angry. But I forgive him. Now I have make the best of my life," says Kotschenrwurher.

Now in a wheelchair, she says her home is now her world, and it's falling apart. Her bedroom walls are constantly dripping water.

"I can't sleep," said kotschenrwurher.

We reached out to the New York City Housing Authority for answers. NYCHAsays they first took care of the problem back in April.

A spokesperson for the New York City Housing Authority says,

All NYCHA residents deserve to live in well maintained homes. This reoccurring leak is unacceptable and we will find a permanent solution. A specialist will inspect the residents apartment tomorrow to find and resolve the underlying leak as quickly as possible."

NYCHA sent a team of workers to fix the wall.

Arianna Padilla, 25, from Central Islip says watching her 8-month-old son grow is her biggest joy. But Padilla was given bad news by her doctor.

She says in just a matter of months, she will lose her sight.

"I'm already experiencing problems with my vision. I can't drive and it scares me," said Padilla. Padilla needs cataract surgery in both eyes and suffers from severe diabetes.

The cost of treatment is $1500 an eye. Living paycheck to paycheck, she says she can't afford it.

"I don't have the money," said Padilla.

PIX11 News called her insurance companies and doctors and she got a call.

"Health First and my doctors will cover the surgery," said Padilla.

PIX11 News will follow Padilla every step of the way during her recovery.

If you would like to help, visit https://www.gofundme.com/arianas-eyesurgery

If you have a story reach out to Monica Morales on Facebook at monicamoralestv.

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Follow-up Friday: Toddler gets pediatric wheelchair, Islip mother's critical eye surgery will be covered - New York's PIX11 / WPIX-TV

Type 2 Diabetes is a serious condition for anyone, but area Latinos, men, and youth sometimes face extra barriers to early diagnosis and management.

People with Type 2 Diabetes make insulin, but not enough or their bodies become resistant to it. If not diagnosed early or properly managed, the condition can lead to irreversible damage to major body organs such as the kidneys, eyes, blood vessels and nerves.

Latinos, African Americans, Native Americans and Asian Americans are ethnically predisposed to higher rates of Type 2 Diabetes, said Amy Knights, registered nurse, Northwest Colorado Health Diabetes educator and community health manager.

In the past, language was a barrier for Spanish speaking Latinos, Knights said.

Last year Northwest Colorado Health started a number of programs, providing on-sight interpretation and education about prevention and management by people who speak the language.

Early diagnosis and management is important to preventing disease progression and avoiding irreversible damage.

"Men are usually less likely to seek preventative care. Men tend to wait until things are really bad. The biggest barrier in this group of patients is their own attitudes towards prevention," Knights said.

The American Diabetes Association reminds men that it's important to talk about their health with doctors and to seek early intervention to avoid complications that can include erectile dysfunction.

Type 2 diabetes isn't an adults only health problem.

"More and more kids are being diagnosed with it, some as young as 10 years old," according the Centers for Disease Control and Prevention update Thursday.

The increase is due to inactivity leading to weight gain.

"Weight is still the biggest precursor to diabetes," Knights said when explaining that she's seeing more local children tested.

She believes that management is extra challenging when youth are diagnosed with the disease because it often means life style changes for the entire family.

"If you have diabetes and you are trying to make those changes, it won't happen overnight," Knights said. "So give yourself enough time to make those life style changes so that you can succeed."

Contact Sasha Nelson at 970-875-1794 or snelson@CraigDailyPress.com or follow her on Twitter @CDP_Education

Link:
Latinos, men, youth face challenges in diabetes diagnosis, management - Craig Daily Press

News & Observer

'Smart' insulin patches developed at UNC, NCSU one step closer to market News & Observer Zhen Gu, whose team at the UNC-N.C. State Biomedical Engineering Program has been leading the effort to develop smart insulin patches for treating diabetes, co-founded a company based in Research Triangle Park two years ago with the idea of ... and more »

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'Smart' insulin patches developed at UNC, NCSU one step closer to market - News & Observer

FRIDAY, June 30, 2017 (HealthDay News) -- Almost half of people with type 1 diabetes are still producing some insulin more than a decade after being diagnosed with the disease.

The new findings challenge previous assumptions that people with type 1 diabetes lose the ability to produce any insulin -- a hormone that helps usher sugar to cells to be used as fuel -- over time.

Researchers at Sweden's Uppsala University, led by post-doctoral researcher Daniel Espes, reached their conclusions after studying more than 100 patients with type 1 diabetes.

The investigators found that people who still produced insulin despite their long-standing type 1 diabetes had higher levels of a protein called interleukin-35. This protein appears to play an important role in the immune system.

Past research had shown that both newly diagnosed people with type 1 diabetes and those who've had the disease for some time had lower average levels of interleukin-35 compared to healthy people.

Type 1 diabetes is an autoimmune disease that causes the body's immune system to mistakenly attack healthy cells in the pancreas that make insulin.

This leaves people without enough insulin to meet the body's daily needs. To survive, people with type 1 diabetes must replace that lost insulin through multiple daily injections or through a tiny tube inserted under the skin every few days and then attached to an insulin pump.

The Uppsala researchers have launched a new study to see if they may be able to boost insulin production in those people with type 1 diabetes who are still making insulin.

The study appears in the June issue of Diabetes Care.

For more about type 1 diabetes, visit JDRF.

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Many People With Type 1 Diabetes Still Make Some Insulin - Sioux City Journal

TheHorse.com

How Newborn Foals' Dental Pulp Can Help Heal Horses TheHorse.com It is the most primitive form of stem cell tissue and has the greatest potential for developing into bone, ligaments, blood vessels, and more. Bertone and colleagues recently tested the effectiveness of dental pulp treatment in 20 lame horses with ...

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How Newborn Foals' Dental Pulp Can Help Heal Horses - TheHorse.com