Tisch MS researchers announce breakthrough in disease monitoring

Main Category: Multiple Sclerosis
Article Date: 01 Aug 2013 - 2:00 PDT Current ratings for:
Tisch MS researchers announce breakthrough in disease monitoring

A research team lead by Violaine Harris, Ph.D., at the Tisch MS Research Center of New York, has just published findings on a new method of measuring disease activity in patients with multiple sclerosis (MS).

This important biomarker discovery is based on spinal fluid measurement of Fetuin-A levels obtained over the course of several years of clinical and pathological studies of MS patients as well as experimental models of the disease. Dr. Harris's findings are likely to change the process for making treatment decisions in MS patients.

Current MS treatment is designed to stop disease activity in the brain and spinal cord with the goal of arresting disease progression and disability. According to Dr. Saud A. Sadiq, the senior author on the study, "these findings will provide a measurable method of monitoring the effectiveness of treatment much like determining blood sugar levels are assayed for diabetic patients. Many patients with MS on treatment report 'worsening' despite stable MRI findings. Addition of Fetuin-A measurement will help better evaluate disease activity in such patients."

The Tisch MS Research Team continues to study the underlying mechanisms of elevation of spinal fluid Fetuin-A to determine its exact role in multiple sclerosis.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our multiple sclerosis section for the latest news on this subject.

Cerebrospinal fluid fetuin-A is a biomarker of active multiple sclerosis, Multiple Sclerosis Journal, Epub: 2/25/2013 doi: 10.1177/1352458513477923 ahead of print.

The Tisch MS Research Center of New York

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

The Tisch MS Research Center of New York. "Tisch MS researchers announce breakthrough in disease monitoring." Medical News Today. MediLexicon, Intl., 1 Aug. 2013. Web.
1 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

posted by Dr Zinia Thomas on 1 Aug 2013 at 5:10 am

Fetuin-A levels is very much important to monitor a disease. It is important because if you can't properly monitor the disease treatment will goes wrong.

| post followup | alert a moderator |

'Tisch MS researchers announce breakthrough in disease monitoring'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Innovation in mouse model helps researchers distinguish disease mechanisms and biomarkers

Main Category: Urology / Nephrology
Article Date: 30 Jul 2013 - 2:00 PDT Current ratings for:
Innovation in mouse model helps researchers distinguish disease mechanisms and biomarkers

A team led by researchers at the National Institutes of Health has overcome a major biological hurdle in an effort to find improved treatments for patients with a rare disease called methylmalonic acidemia (MMA). Using genetically engineered mice created for their studies, the team identified a set of biomarkers of kidney damage - a hallmark of the disorder - and demonstrated that antioxidant therapy protected kidney function in the mice.

Researchers at the National Human Genome Research Institute (NHGRI), part of NIH, validated the same biomarkers in 46 patients with MMA seen at the NIH Clinical Center. The biomarkers offer new tools for monitoring disease progression and the effects of therapies, both of which will be valuable in the researchers' design of clinical trials for this disease.

The discovery, reported in the July 29, 2013, advance online issue of the Proceedings of the National Academy of Sciences, paves the way for use of antioxidant therapy in a clinical trial for patients with MMA. It also illustrates the mechanisms by which dysfunction of mitochondria - the power generators of the cell - affects kidney disease. Mitochondrial dysfunction is a factor not only in rare disorders, such as MMA, but also in a wide variety of common conditions, such as obesity, diabetes and cancer.

MMA affects as many as one in 67,000 children born in the United States. It can have several different causes, all involving loss of function of a metabolic pathway that moderates levels of an organic compound called methylmalonic acid. Affected children are unable to properly metabolize certain amino acids consumed in their diet, which damages a number of organs, most notably the kidneys.

"Metabolic disorders like MMA are extremely difficult to manage because they perturb the delicate balance of chemicals that our bodies need to sustain health," said Daniel Kastner, M.D., Ph.D., NHGRI scientific director. "Given that every newborn in the United States is screened for a number of inherited metabolic disorders, including MMA, there is a critical need for better understanding of the disease mechanisms and therapies to treat them."

MMA is the most common organic acid disorder and invariably impairs kidney function, which can lead to kidney failure. The most common therapy is a restrictive diet, but doctors must resort to dialysis or kidney transplantation when the disease progresses. MMA patients also suffer from severe metabolic instability, failure to thrive, intellectual and physical disabilities, pancreatitis, anemia, seizures, vision loss and strokes.

"There are no definitive treatments for the management of patients with MMA," said Charles Venditti, M.D., Ph.D., senior author and investigator in the Organic Acid Research Section of NHGRI's Genetics and Molecular Biology Branch. "This study is the culmination of collaboration with the patient community. It uses mouse modelling, coupled with innovations in genomics and biochemical analyses, to derive new insights into the causes of renal injury in MMA. Our studies have improved our understanding of the basic biology underlying MMA, created a novel animal model for testing interventions and, now, led us to the promise of a new therapy."

The researchers performed the studies using mice bred to carry gene alterations that disrupt the production of the same mitochondrial enzyme that is defective in patients with MMA. These are called transgenic mice. The enzyme, called methylmalonyl-CoA mutase (MUT), is an important component of the chemical process that metabolizes organic acids, specifically methylmalonic acid.

By measuring gene expression in the transgenic mice using DNA microarrays, researchers discovered 50 biomarkers of gene expression that each indicated declining kidney function. DNA microarrays are silicon chips with many spots to which a given molecule may bind. In this case, the DNA microarrays were used to precisely generate, with the aid of a computer program, a profile of gene expression in a kidney cell.

The researchers chose one of the biomarkers, called lipocalin-2, to test how it correlated with kidney function in 46 MMA patients. Plasma levels of this biomarker rose with kidney deterioration in patients with MMA, and may serve as a valuable indicator of MMA kidney disease progression in the clinic.

"The detection of biomarkers through microarray technology is immensely helpful in pointing to downstream pathways affected by the defective MUT activity," said Irini Manoli, M.D., Ph.D., lead author and a physician scientist and staff clinician in NHGRI's Genetics and Molecular Biology Branch. "The biomarkers provide new plasma or serum tests to follow disease progression in our patients."

Having discovered these important biomarkers of kidney function, the authors turned to kidney physiology experts on their team to explore the structural changes that occur in MMA disease. They analyzed the rate at which the kidneys filter waste from the blood. Co-author and renal physiology expert Jurgen Schnermann, M.D., and members of his laboratory at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), also part of NIH, demonstrated the early and significant decrease in this rate in MMA mice.

With further studies, the researchers identified increased production of free radicals in tissues from the mice, as well as in the MMA patients. Detection of free radicals indicates chemical instability in cells, which the researchers sought to remedy with antioxidant therapy. After treating the mice with two forms of dietary antioxidants, the researchers observed that the biomarkers of kidney damage diminished and the faltering kidney filtration rate tapered off. The findings demonstrated that readily available antioxidants can significantly affect the rate of decline of kidney function in transgenic mice, which replicate the kidney disease of MMA.

"The next step will be to translate these findings to the clinic," Dr. Venditti said. "With a progressive disorder like MMA, we are hopeful that we have achieved a laboratory success that our patients will benefit from in the near future."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our urology / nephrology section for the latest news on this subject.

Irini Manoli, Justin R. Sysol, Lingli Li, Pascal Houillier, Caterina Garone, Cindy Wang, Patricia M. Zerfas, Kristina Cusmano-Ozog, Sarah Young, Niraj S. Trivedi, Jun Cheng, Jennifer L. Sloan, Randy J. Chandler, Mones Abu-Asab, Maria Tsokos, Abdel G. Elkahloun, Seymour Rosen, Gregory M. Enns, Gerard T. Berry, Victoria Hoffmann, Salvatore DiMauro, Jurgen Schnermann, and Charles P. Venditti, "Targeting proximal tubule mitochondrial dysfunction attenuates the renal disease of methylmalonic acidemia", Published online before print July 29, 2013, doi: 10.1073/pnas.1302764110

For information about the MMA clinical trial, go to ClinicalTrials.gov and search with NCT00078078.

Learn more about the study

NIH/National Human Genome Research Institute

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

NIH/National Human Genome Research Institute. "Innovation in mouse model helps researchers distinguish disease mechanisms and biomarkers." Medical News Today. MediLexicon, Intl., 30 Jul. 2013. Web.
30 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Innovation in mouse model helps researchers distinguish disease mechanisms and biomarkers'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Women and heart disease: more deaths, less care

Featured Article
Academic Journal
Main Category: Cardiovascular / Cardiology
Also Included In: Preventive Medicine
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
Women and heart disease: more deaths, less care

Coronary artery disease (CAD) kills more women than men each year, yet women are still not receiving as many preventive recommendations as men, according to a paper published in Global Heart.

Researchers from Ohio State University wanted to analyze the risk for CAD in women, as well as its impact and female-specific strategies for treatment.

They found that the disease should be managed differently for women, based on varying risk factors related to pregnancy and autoimmune diseases.

According to the authors, 8.6 million women die each year around the world from heart-related diseases, making up a third of all deaths in women. Additionally, cardiovascular diseases are the number one cause of death for both males and females worldwide.

Although the researchers note that awareness about the impact of CAD on women is slowly increasing, it still has a long way to go. In 2004, a survey revealed that only one in five doctors acknowledged that more women die each year from CAD. In addition, women are 55% less likely to participate in cardiac rehabilitation activities than men.

The authors say:

"More women than men die of CAD and more women have died from CAD than of cancer (including breast cancer), chronic lower respiratory disease, Alzheimer's disease, and accidents combined."

Deaths from CAD in the US fell by 30% between 1998 and 2008, but rates are going up in younger women under 55 years of age.

A number of risk factors differ between men and women, the authors note:

Obesity raises risk of coronary artery disease by 64% in women, but by only 46% in men.Women who suffer a heart attack related to CAD at a younger age are twice as likely to die as their male counterparts.42% of women are likely to die within a year of suffering a heart attack versus 24% of men.Women are 20% more likely to suffer angina than men.

The researchers say that women have narrower coronary arteries than men, and so are more likely to suffer CAD as a result of microvascular disease - disease of the heart affecting its small arteries.

The danger, the researchers say, is that while women may not appear to have major blockages of the coronary artery, they do suffer blockages of the smaller vessels. They add that over half of symptomatic women who do not have obstructive CAD still have signs and symptoms of ischemia.

Conditions that affect women rather than men also raise their risk of CAD, including polycystic ovary syndrome, pre-eclampsia and gestational diabetes, the researchers say.

"Women are affected by CAD in large numbers and to a large degree," the researchers say. "CAD is the leading cause of mortality in women. The manifestation of CAD has unique characteristics in women. Increasing data demonstrate that some treatment strategies have sex-specific effectiveness."

The researchers add:

"Further research regarding the pathophysiology of CAD in women, diagnosis and treatment strategies specific to women is required.

CAD is not a 'man's only' disease, and we eagerly await future studies that examine its unique presence in women."

Written by Marie Ellis

Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today Visit our cardiovascular / cardiology section for the latest news on this subject.

“Coronary artery disease in women: A 2013 update,” Kavita Sharma, Martha Gulati, Global Heart, Volume 8, Issue 2, June 2013, Pages 105–112.

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Ellis, Marie. "Women and heart disease: more deaths, less care." Medical News Today. MediLexicon, Intl., 30 Jul. 2013. Web.
30 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Women and heart disease: more deaths, less care'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Finding may lead to new treatments for neurodegenerative disease and stroke

Main Category: Neurology / Neuroscience
Also Included In: Stroke;  Rehabilitation / Physical Therapy
Article Date: 25 Jul 2013 - 1:00 PDT Current ratings for:
Finding may lead to new treatments for neurodegenerative disease and stroke

In degenerative brain diseases and after stroke, nerve cells die while their support cells activate the brain's immune system to cause further damage. Now Jonathan Gilthorpe, Adrian Pini and Andrew Lumsden at the MRC Centre for Developmental Neurobiology at King's College London, have found that a single protein, histone H1, causes these distinct outcomes.

The research passed peer review within a week of being published in F1000Research, where Jan-Marino Ramirez, of the University of Washington, called the work "a very important contribution to our understanding of neurodegenerative disease and the response of the brain to injury" in his public referee report. He also noted that he is "confident that this study will be a much cited contribution to the field of traumatic brain injury".

The most unexpected finding in this study is that a histone protein is responsible for neuronal damage. "Histone H1 partners with DNA in the cell nucleus and has been thought of as harmless," explain the authors, "The surprise came when we discovered that it can be released from brain cells upon injury, killing healthy nerve cells and activating the damaging immune response".

The research team is now working on ways to suppress these harmful actions, which may lead to the development of new treatments for neurodegenerative disease and stroke.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our neurology / neuroscience section for the latest news on this subject.

Extracellular histone H1 is neurotoxic and drives a pro-inflammatory response in microglia [v1; ref status: indexed] F1000Research 2013, 2:148 (doi: 10.12688/f1000research.2-148.v1)

Faculty of 1000

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

1000, Faculty of. "Finding may lead to new treatments for neurodegenerative disease and stroke." Medical News Today. MediLexicon, Intl., 25 Jul. 2013. Web.
25 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Finding may lead to new treatments for neurodegenerative disease and stroke'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

New stem cell gene therapy gives hope to prevent Sanfilippo - an inherited neurological disease

Main Category: Neurology / Neuroscience
Also Included In: Stem Cell Research;  Genetics
Article Date: 25 Jul 2013 - 1:00 PDT Current ratings for:
New stem cell gene therapy gives hope to prevent Sanfilippo - an inherited neurological disease

Scientists from The University of Manchester have used stem cell gene therapy to treat a fatal genetic brain disease in mice for the first time.

The method was used to treat Sanfilippo - a fatal inherited condition which causes progressive dementia in children - but could also benefit several neurological, genetic diseases.

Researchers behind the study, published in the journal Molecular Therapy this month, are now hoping to bring a treatment to trial in patients within two years.

Sanfilippo, a currently untreatable mucopolysaccharide (MPS) disease, affects one in 89,000 children in the United Kingdom, with sufferers usually dying in their mid-twenties. It is caused by the lack of SGSH enzyme in the body which helps to breakdown and recycle long chain sugars, such as heparan sulphate (HS). Children with the condition build up and store excess HS throughout their body from birth which affects their brain and results in progressive dementia and hyperactivity, followed by losing the ability to walk and swallow.

Dr Brian Bigger, from the University of Manchester's Institute of Human Development who led the research, said bone marrow transplants had been used to correct similar HS storage diseases, such as Hurler syndrome, by transplanting normal cells with the missing enzyme but the technique did not work with Sanfilippo disease. This is because monocytes, a type of white blood cell, from the bone marrow, did not produce enough enzyme to correct the levels in the brain.

Dr Bigger said: "To increase SGSH enzyme from bone marrow transplants, and to target it to the cells that traffic into the brain, we have developed a stem cell gene therapy which overproduces the SGSH enzyme specifically in bone marrow white blood cells.

"We have shown that mice treated by this method produce five times the normal SGSH enzyme levels in the bone marrow and 11 per cent more compared to normal levels in the brain.

"The enzyme is taken up by affected brain cells and is enough to correct brain HS storage and neuro inflammation to near normal levels and completely corrects the hyperactive behaviour in mice with Sanfilippo.

"This is extremely exciting and could have huge implications for treatments. We now hope to work to a clinical trial in Manchester in 2015."

The University of Manchester team is now manufacturing a vector - a tool commonly used by molecular biologists to deliver genetic material into cells - for use in humans and hope to use this in a clinical trial with patients at Central Manchester University Hospital NHS Foundation Trust by 2015.

The stem cell gene therapy approach was recently shown by Italian scientists to improve conditions in patients with a similar genetic disease affecting the brain called metachromatic leukodystrophy, with results published in the journal Science earlier this month.

Manchester scientists refined the vector used by the Italian scientists. "This approach has the potential to treat several neurological genetic diseases," Dr Bigger added.

The research was funded by the UK MPS Society and the Sanfilippo Children's Research Foundation based in Canada.

Christine Lavery MBE, Chief Executive of the UK MPS Society, said: "Since 1970 over 130 children and young adults have lost their lives to Sanfilippo disease (MPS III) in the UK alone.

"Whilst new therapies for other MPS diseases are changing children's lives, parents of children with Sanfilippo disease can do no more than give the best possible care and live in hope that a treatment is around the corner. The positive results of Dr Brian Bigger's gene therapy programme in mice provides optimism for future generations of Sanfilippo children."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our neurology / neuroscience section for the latest news on this subject.

The research is published in the journal Molecular Therapy this month.

The University of Manchester

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

The University of Manchester. "New stem cell gene therapy gives hope to prevent Sanfilippo - an inherited neurological disease." Medical News Today. MediLexicon, Intl., 25 Jul. 2013. Web.
25 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'New stem cell gene therapy gives hope to prevent Sanfilippo - an inherited neurological disease'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Potential cause of Parkinson's disease discovered that points to a new therapeutic strategy

Main Category: Parkinson's Disease
Article Date: 27 Jul 2013 - 0:00 PDT Current ratings for:
Potential cause of Parkinson's disease discovered that points to a new therapeutic strategy

Biologists at The Scripps Research Institute (TSRI) have made a significant discovery that could lead to a new therapeutic strategy for Parkinson's disease.

The findings, recently published online ahead of print in the journal Molecular and Cell Biology, focus on an enzyme known as parkin, whose absence causes an early-onset form of Parkinson's disease. Precisely how the loss of this enzyme leads to the deaths of neurons has been unclear. But the TSRI researchers showed that parkin's loss sharply reduces the level of another protein that normally helps protect neurons from stress.

"We now have a good model for how parkin loss can lead to the deaths of neurons under stress," said TSRI Professor Steven I. Reed, who was senior author of the new study. "This also suggests a therapeutic strategy that might work against Parkinson's and other neurodegenerative diseases."

Genetic Clues

Parkinson's is the world's second-most common neurodegenerative disease, affecting about one million people in the United States alone. The disease is usually diagnosed after the appearance of the characteristic motor symptoms, which include tremor, muscle rigidity and slowness of movements. These symptoms are caused by the loss of neurons in the substantia nigra, a brain region that normally supplies the neurotransmitter dopamine to other regions that regulate muscle movements.

Most cases of Parkinson's are considered "sporadic" and are thought to be caused by a variable mix of factors including advanced age, subtle genetic influences, chronic neuroinflammation and exposure to pesticides and other toxins. But between 5 and 15 percent of cases arise specifically from inherited gene mutations. Among these, mutations to the parkin gene are relatively common. Patients who have no functional parkin gene typically develop Parkinson's-like symptoms before age 40.

Parkin belongs to a family of enzymes called ubiquitin ligases, whose main function is to regulate the levels of other proteins. They do so principally by "tagging" their protein targets with ubiquitin molecules, thus marking them for disposal by roving protein-breakers in cells known as proteasomes. Because parkin is a ubiquitin ligase, researchers have assumed that its absence allows some other protein or proteins to evade proteasomal destruction and thus accumulate abnormally and harm neurons. But since 1998, when parkin mutations were first identified as a cause of early-onset Parkinson's, consensus about the identity of this protein culprit has been elusive.

"There have been a lot of theories, but no one has come up with a truly satisfactory answer," Reed said.

Oxidative Stress

In 2005, Reed and his postdoctoral research associate (and wife) Susanna Ekholm-Reed decided to investigate a report that parkin associates with another ubiquitin ligase known as Fbw7. "We soon discovered that parkin regulates Fbw7 levels by tagging it with ubiquitin and thus targeting it for degradation by the proteasome," said Ekholm-Reed.

Loss of parkin, they found, leads to rises in Fbw7 levels, specifically for a form of the protein known as Fbw7ß. The scientists observed these elevated levels of Fbw7ß in embryonic mouse neurons from which parkin had been deleted, in transgenic mice that were born without the parkin gene, and even in autopsied brain tissue from Parkinson's patients who had parkin mutations.

Subsequent experiments showed that when neurons are exposed to harmful molecules known as reactive oxygen species, parkin appears to work harder at tagging Fbw7ß for destruction, so that Fbw7ß levels fall. Without the parkin-driven decrease in Fbw7ß levels, the neurons become more sensitive to this "oxidative stress" - so that more of them undergo a programmed self-destruction called apoptosis. Oxidative stress, to which dopamine-producing substantia nigra neurons may be particularly vulnerable, has long been considered a likely contributor to Parkinson's.

"We realized that there must be a downstream target of Fbw7ß that's important for neuronal survival during oxidative stress," said Ekholm-Reed.

A New Neuroprotective Strategy

The research slowed for a period due to a lack of funding. But then, in 2011, came a breakthrough. Other researchers who were investigating Fbw7's role in cancer reported that it normally tags a cell-survival protein called Mcl-1 for destruction. The loss of Fbw7 leads to rises in Mcl-1, which in turn makes cells more resistant to apoptosis. "We were very excited about that finding," said Ekholm-Reed. The TSRI lab's experiments quickly confirmed the chain of events in neurons: parkin keeps levels of Fbw7ß under control, and Fbw7ß keeps levels of Mcl-1 under control. Full silencing of Mcl-1 leaves neurons extremely sensitive to oxidative stress.

Members of the team suspect that this is the principal explanation for how parkin mutations lead to Parkinson's disease. But perhaps more importantly, they believe that their discovery points to a broad new "neuroprotective" strategy: reducing the Fbw7ß-mediated destruction of Mcl-1 in neurons, which should make neurons more resistant to oxidative and other stresses.

"If we can find a way to inhibit Fbw7ß in a way that specifically raises Mcl-1 levels, we might be able to prevent the progressive neuronal loss that's seen not only in Parkinson's but also in other major neurological diseases, such as Huntington's disease and ALS [amyotrophic lateral sclerosis]," said Reed.

Finding such an Mcl-1-boosting compound, he added, is now a major focus of his laboratory's work.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our parkinson's disease section for the latest news on this subject.

“Parkin-Dependent Degradation of the F-box protein Fbw7 ß Promotes Neuronal Survival in Response to Oxidative stress by Stabilizing Mcl-1,” Susanna Ekholm-Reed, Matthew S. Goldberg, Michael G. Schlossmacher and Steven I. Reed, Published ahead of print 15 July 2013, doi: 10.1128/MCB.00535-13

Funding for the study was provided in part by the National Institutes of Health (NS059904 and CA078343).

Scripps Research Institute

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Institute, Scripps Research. "Potential cause of Parkinson's disease discovered that points to a new therapeutic strategy." Medical News Today. MediLexicon, Intl., 27 Jul. 2013. Web.
27 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Potential cause of Parkinson's disease discovered that points to a new therapeutic strategy'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Research approach highlights potential therapeutic targets for Alzheimer's disease

Main Category: Alzheimer's / Dementia
Article Date: 26 Jul 2013 - 1:00 PDT Current ratings for:
Research approach highlights potential therapeutic targets for Alzheimer's disease

Key molecular pathways that ultimately lead to late-onset Alzheimer's disease, the most common form of the disorder, have been identified by researchers at Columbia University Medical Center (CUMC). The study, which used a combination of systems biology and cell biology tools, presents a new approach to Alzheimer's disease research and highlights several new potential drug targets. The paper was published in the journal Nature.

Much of what is known about Alzheimer's comes from laboratory studies of rare, early-onset, familial (inherited) forms of the disease. "Such studies have provided important clues as to the underlying disease process, but it's unclear how these rare familial forms of Alzheimer's relate to the common form of the disease," said study leader Asa Abeliovich, MD, PhD, associate professor of pathology and cell biology and of neurology in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at CUMC. "Most important, dozens of drugs that 'work' in mouse models of familial disease have ultimately failed when tested in patients with late-onset Alzheimer's. This has driven us, and other laboratories, to pursue mechanisms of the common form of the disease."

Non-familial Alzheimer's is complex; it is thought to be caused by a combination of genetic and environmental risk factors, each having a modest effect individually. Using so-called genome-wide association studies (GWAS), prior reports have identified a handful of common genetic variants that increase the likelihood of Alzheimer's. A key goal has been to understand how such common genetic variants function to impact the likelihood of Alzheimer's.

In the current study, the CUMC researchers identified key molecular pathways that link such genetic risk factors to Alzheimer's disease. The work combined cell biology studies with systems biology tools, which are based on computational analysis of the complex network of changes in the expression of genes in the at-risk human brain.

More specifically, the researchers first focused on the single most significant genetic factor that puts people at high risk for Alzheimer's, called APOE4 (found in about a third of all individuals). People with one copy of this genetic variant have a three-fold increased risk of developing late-onset Alzheimer's, while those with two copies have a ten-fold increased risk. "In this study," said Dr. Abeliovich, "we initially asked: If we look at autopsy brain tissue from individuals at high risk for Alzheimer's, is there a consistent pattern?"

Surprisingly, even in the absence of Alzheimer's disease, brain tissue from individuals at high risk (who carried APOE4 in their genes) harbored certain changes reminiscent of those seen in full-blown Alzheimer's disease," said Dr. Abeliovich. "We therefore focused on trying to understand these changes, which seem to put people at risk. The brain changes we considered were based on 'transcriptomics' - a broad molecular survey of the expression levels of the thousands of genes expressed in brain."

Using the network analysis tools mentioned above, the researchers then identified a dozen candidate "master regulator" factors that link APOE4 to the cascade of destructive events that culminates in Alzheimer's dementia. Subsequent cell biology studies revealed that a number of these master regulators are involved in the processing and trafficking of amyloid precursor protein (APP) within brain neurons. APP gives rise to amyloid beta, the protein that accumulates in the brain cells of patients with Alzheimer's. In sum, the work ultimately connected the dots between a common genetic factor that puts individuals at high risk for Alzheimer's, APOE4, and the disease pathology.

Among the candidate "master regulators" identified, the team further analyzed two genes, SV2A and RFN219. "We were particularly interested in SV2A, as it is the target of a commonly used anti-epileptic drug, levetiracetam. This suggested a therapeutic strategy. But more research is needed before we can develop clinical trials of levetiracetam for patients with signs of late-onset Alzheimer's disease."

The researchers evaluated the role of SV2A, using human-induced neurons that carry the APOE4 genetic variant. (The neurons were generated by directed conversion of skin fibroblasts from individuals at high risk for Alzheimer's, using a technology developed in the Abeliovich laboratory.) Treating neurons that harbor the APOE4 at-risk genetic variant with levetiracetam (which inhibits SV2A) led to reduced production of amyloid beta. The study also showed that RFN219 appears to play a role in APP-processing in cells with the APOE4 variant.

"Our findings suggest that both SV2A and RFN219 are candidate drug targets," said Dr. Abeliovich. "What's exciting to us is that these approaches may play a role in the development of drugs for the common non-familial form of Alzheimer's disease. This has been an enormous challenge."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our alzheimer's / dementia section for the latest news on this subject.

The paper is titled, "Integrative genomics identifies APOE ?4 effectors in Alzheimer's disease." The other contributors are all members of CUMC's Taub Institute for Research on Alzheimer's Disease and the Aging Brain: Herve Rhinn, Ryousuke Fujita, Liang Qiang, Rong Chen, and Joseph H. Lee. Dr. Lee is also a member of CUMC's Gertrude H. Sergievsky Center.

The authors declare no financial or other conflicts of interest. Subsequent to the acceptance of this paper, Dr. Abeliovich received a grant from UCB, Inc. for an unrelated study.

The study was supported by grants from the National Institutes of Health (R01AG042317 and RO1NS064433).

Columbia University Medical Center

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Columbia University Medical Center. "Research approach highlights potential therapeutic targets for Alzheimer's disease." Medical News Today. MediLexicon, Intl., 26 Jul. 2013. Web.
27 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Research approach highlights potential therapeutic targets for Alzheimer's disease'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Record incidence of hantavirus disease in Germany

Main Category: Infectious Diseases / Bacteria / Viruses
Article Date: 26 Jul 2013 - 1:00 PDT Current ratings for:
Record incidence of hantavirus disease in Germany

2824 new cases of hantavirus disease were reported in Germany in 2012, the highest number ever in a single year.

In the current issue of Deutsches Arzteblatt International, Detlev Kruger and coauthors present the main facts about this disease.

Every two to three years, large outbreaks of hantavirus disease are caused by Puumala virus, which is transmitted by bank voles and is endemic to southwestern and western Germany. In the north and east of the country, hantavirus infections are caused by the Dobrava-Belgrad virus, which is transmitted by striped field mice.

The manifestations that typically arise over the course of hantavirus disease come in several phases. The first sign is often an otherwise unexplained high fever; this may be followed by shock, renal failure, and pulmonary failure, depending on the severity of the disease. Thus, whenever persons living in high-risk areas present with fever of unknown origin or renal failure of unknown origin, physicians should consider the possibility of a hantavirus infection. Once the suspicion of hantavirus disease has been raised, special techniques can be used for precise viral diagnostic evaluation.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

International, Deutsches Aerzteblatt. "Record incidence of hantavirus disease in Germany." Medical News Today. MediLexicon, Intl., 26 Jul. 2013. Web.
27 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Record incidence of hantavirus disease in Germany'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

In patients with kidney disease, calcium linked to increased risk of heart disease and death

Main Category: Urology / Nephrology
Also Included In: Nutrition / Diet;  Heart Disease
Article Date: 24 Jul 2013 - 0:00 PDT Current ratings for:
In patients with kidney disease, calcium linked to increased risk of heart disease and death

Kidney patients who take calcium supplements to lower their phosphorous levels may be at a 22 per cent higher risk of death than those who take other non-calcium based treatments, according to a new study by Women's College Hospital's Dr. Sophie Jamal.

The study, published in the Lancet, calls into question the long-time practice of prescribing calcium to lower phosphate levels in patients with chronic kidney disease. The researchers suggest some of the calcium is absorbed into the blood stream and may expedite hardening of the arteries, leading to a higher risk of heart disease and even death. Cardiovascular disease is a leading cause of death for people with chronic kidney disease.

"Doctors commonly prescribe calcium supplements to prevent elevated phosphate levels, which can damage the body, but a growing number of studies have shown calcium supplements may actually increase the risk of heart disease," explains Dr. Sophie Jamal, a physician at Women's College Hospital and an associate professor of medicine at the University of Toronto. "Our study validates these claims and, for the first time, shows the long-term consequences of taking calcium supplements can be dangerous for patients with kidney disease."

As part of their analysis, researchers reviewed 11 randomized, controlled studies that included more than 4,600 patients. The researchers assessed the risk of heart disease, including heart attack, stroke, and hardening of the arteries, along with death among individuals prescribed the medication containing calcium and those prescribed the medication without calcium. They found:

A 22% reduction in death among patients who took non-calcium based treatments sevelamer and lanthanum. Less artery calcification (hardening) in patients who did not take calcium supplements.

"Some researchers and physicians have been saying for years that kidney disease patients need to get off calcium, now we think our review shows there is much more solid evidence to argue for that change to clinical practice," the study's senior author Ross Tsuyuki from the University of Alberta's faculty of medicine and dentistry.

In the meantime, given the study's findings, the researchers suggest non-calcium containing treatments be used as a first line of treatment to lower phosphate for patients with chronic kidney disease.

"The findings of our study provides the best evidence as to what doctors should be prescribing their patients, but further research is necessary to help us understand how exactly calcium increases the risk of death, if non calcium-based treatments reduce the risk of death, and whether certain types of treatments may be more effective and beneficial than others," says Dr. Jamal.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our urology / nephrology section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Hospital, Women\'s College. "In patients with kidney disease, calcium linked to increased risk of heart disease and death." Medical News Today. MediLexicon, Intl., 24 Jul. 2013. Web.
24 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

posted by Will Smith on 24 Jul 2013 at 3:46 am

Once again someone publishes a report on the bad impacts of calcium on health without specifing what type of calcium supplements that they referring to. There is a big difference between how the body uses calcium carbonate from how it uses calcium citrate. This article would be of more value if the authors had specified which calcium compound(s), they used in the study.

| post followup | alert a moderator |

'In patients with kidney disease, calcium linked to increased risk of heart disease and death'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

New functions identified for autoimmune disease 'risk' gene

Main Category: Immune System / Vaccines
Also Included In: Genetics
Article Date: 24 Jul 2013 - 0:00 PDT Current ratings for:
New functions identified for autoimmune disease 'risk' gene

Researchers at the University of Minnesota have identified infection-fighting and inflammation-suppressing functions for a gene associated with human autoimmune disease.

The discovery, centered on a gene known as PTPN22, could set into motion new treatment approaches for autoimmune diseases like lupus, rheumatoid arthritis and type 1 diabetes. The key to these advances may lie with a better understanding of how a variant of PTPN22, known as a "risk variant," impacts autoimmune disease development and the behavior of myeloid cells that act as the body's "first responders."

The study appears in the journal Immunity.

In launching their latest research project, University of Minnesota Center for Immunology researchers set out to determine how PTPN22 could regulate immune system function in health and disease.

"Almost a decade ago, researchers at the University of Minnesota and other institutions discovered that people carrying a variant form of the PTPN22 gene bear an increased risk of becoming sick with certain autoimmune diseases. However, we have lacked a deep understanding how the variant creates that increased risk," said Erik J. Peterson, M.D., one of the study's lead authors and a University of Minnesota Medical School associate professor in the Division of Rheumatic and Autoimmune Diseases. "We wanted to understand the molecular basis for PTPN22 association with disease."

Much of the work carried out in the latest study took place in Peterson's laboratory, which utilizes genetic, biochemical, and primary human sample-based approaches to investigate how "risk" genes predispose to development of autoimmune disease.

According to the study's authors, previous research showed that PTPN22 works in immune cells, but few studies had specifically examined PTPN22's function in infection-fighting cells called myeloid cells.

"Myeloid cells are among the body's 'first responders' to a challenge with a virus or bacterium," said Yaya Wang, Ph.D., one of the study's co-first authors and a research associate in the Center for Immunology. "Upon recognizing the presence of an infection, myeloid cells produce chemicals that increase inflammation and help fight the invading microbe. We were intrigued by the idea that PTPN22 and its disease-associated variant might have a role in myeloid cell functions."

Researchers found that both mouse and human myeloid cells carrying the PTPN22 "risk" variant show decreased production of molecules called type 1 Interferons. Type 1 Interferons are needed to boost immune responses to viruses and other infections. In mice lacking the PTPN22 gene, reduced type 1 Interferon production correlates with an impaired ability to fight infections.

But the PTPN22 gene does more than simply fight infection, the study showed.

"Unexpectedly, we also found that PTPN22 suppresses inflammation," said Wang. "Furthermore, we showed that the PTPN22 risk variant is defective in suppressing inflammatory arthritis."

"We anticipate that our findings will open new lines of investigation into how PTPN22 and other autoimmune disease 'risk' genes could work in infection-fighting and anti-inflammatory processes. Ultimately, we hope that the research will accelerate the drive toward better treatments and cures for autoimmune disorders," said Peterson.

More research is underway to determine the impact of the PTPN22 variant in the function of myeloid blood cells, particularly in patients suffering from lupus. Researchers are also comparing immune responses to influenza A vaccines between carriers and non-carriers of the PTPN22 variant. The goal is to understand the role of the disease-associated variant in mounting a normal response to immunizations against viruses.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our immune system / vaccines section for the latest news on this subject.

This project was funded by grants from the National Institutes of Health (NIH), R01AR057781 (awarded to Peterson) and R01AI070544 (awarded to co-senior author Nunzio Bottini, M.D., Ph.D.), as well as from several other sources, including: the American College of Rheumatology Within Our Reach Campaign, the American Diabetes Association, the Alliance for Lupus Research, and the Lupus Foundation of Minnesota.

University of Minnesota Academic Health Center

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

University of Minnesota Academic Health Center. "New functions identified for autoimmune disease 'risk' gene." Medical News Today. MediLexicon, Intl., 24 Jul. 2013. Web.
24 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'New functions identified for autoimmune disease 'risk' gene'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

People who carry a particular gene allele APOE4 can be over 10 times more likely to develop late-onset Alzheimer's disease

Main Category: Alzheimer's / Dementia
Also Included In: Neurology / Neuroscience
Article Date: 24 Jul 2013 - 10:00 PDT Current ratings for:
People who carry a particular gene allele APOE4 can be over 10 times more likely to develop late-onset Alzheimer's disease

The molecular pathway linking a genetic variant to the common, non-familial form of Alzheimer's disease is revealed in Nature this week. The study boosts our knowledge of the pathology of this neurodegenerative disease, and hints at new directions for therapy.

People who carry a particular gene allele APOE4 can be over 10 times more likely to develop late-onset Alzheimer's disease (LOAD). Asa Abeliovich and colleagues now show that the pattern of gene expression in the brains of APOE4 carriers has similarities to the patterns of gene expression in LOAD patients, and suggest that this altered profile might be an early hallmark of the disease. They identify a handful of genes thought to regulate this unusual transcription profile, including novel and previously known regulators of the amyloid precursor protein (APP), a molecule that has long been implicated in Alzheimer's disease. Genetic variants found at two of the genes may even affect the age when LOAD may set in.

Finally, the team tested a possible therapy, the drug levetiracetam, which inhibits one of the genes identified, and is currently used clinically to treat seizures. The drug suppresses APP processing in cells cultured from APOE4 carriers, making it a molecule worthy of further study.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our alzheimer's / dementia section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Nature. "People who carry a particular gene allele APOE4 can be over 10 times more likely to develop late-onset Alzheimer's disease." Medical News Today. MediLexicon, Intl., 24 Jul. 2013. Web.
24 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'People who carry a particular gene allele APOE4 can be over 10 times more likely to develop late-onset Alzheimer's disease'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Preventing infection in hosts receiving transplanted fetal tissues for neurodegenerative disease damage repair

Main Category: Parkinson's Disease
Also Included In: Huntingtons Disease;  Stem Cell Research
Article Date: 24 Jul 2013 - 1:00 PDT Current ratings for:
Preventing infection in hosts receiving transplanted fetal tissues for neurodegenerative disease damage repair

The use of central nervous system fetal tissues derived from routine elective abortions to provide stem cells for transplantation procedures aimed at restoring damage done by neurodegenerative diseases is an established therapy. However, fetal tissue microbial contaminants have been known to cause brain infections in cell transplantation recipients. Now, a research team from Germany has developed a "washing" technique that decontaminates the fetal tissues from which stem cells are derived.

The study appears as an early e-publication for the journal Cell Transplantation, and is now freely available on-line.*

"Fetal neural tissue transplantation has become a potential treatment option for patients suffering from neurodegenerative diseases such as Parkinson's disease (PD) and Huntington's disease (HD)," explained study co-author Dr. Guido Nikkah of the Department of Neurosurgery, Erlangen University Clinic, Erlangen, Germany. "However, in Europe neural transplantation of fetal tissue must be performed in accordance with guidelines on "Good Manufacturing Processes," which means that aspects of microbiological safety have to be investigated in detail."

According to the researchers, aborted fetal human tissues carry the risk of bacterial contamination from the abortion process and this is the contributing factor to the subsequent risk of infection to cell recipients. The researchers noted that prior to their study it was not clear whether fetal tissue contamination, or subsequent surgical contamination during cell transplantation normally had the greatest impact as potential contributing factors to microbial infection in hosts.

Their study revealed a wide range of microbial contamination in fetal tissues that could cause infections. 47.7 % of the fetal tissues they sampled were positive for microbial infection. They also found that the risk of bacterial infection was higher than the risk of fungal infection.

To prevent microbial infection in cell transplantation hosts, the researchers developed and tested a microbial "washing" technique. In laboratory tests using rats as transplantation hosts, the technique has been shown to eliminate microbial contamination. Based on the technique's success in decontaminating fetal tissue cells transplanted into laboratory animals, the washing technique was subsequently used in clinical practice.

"To date, more than 350 PD and approximately 100 HD patients have received primary fetal grafts, and so far no contamination has been reported," said Dr. Nikkah.

The researchers noted that although the risk of infection is very low after their procedure, they still recommend antibiotic prophylaxis.

"Detection of a relevant microbial contamination within the narrow time-window prior to transplantation remains difficult," concluded the authors. "While contamination of the transportation fluid is not an exclusion criterion for tissue transplantation, detection of contamination after washing steps is critical."

"The potentially deleterious impact of microbial contamination on the use of cells or tissues for transplantation is an important health factor that cannot be ignored." said Dr. Shinn-Zong Lin, professor of Neurosurgery and superintendent at the China Medical University Hospital, Beigang, Taiwan. "Procedures to reduce the likelihood of contamin

ation such as that described within this paper are therefore of great importance." Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our parkinson's disease section for the latest news on this subject.

Citation: Piroth, T.; Pauly, M. C.; Schneider, C.; Wittmer, A.; Mollers, S.; Dobrossy, M.; Winkler, C.; Nikkhah, G. Transplantation of human fetal tissue for neurodegenerative diseases : Validation of a new protocol for microbiological analysis and bacterial decontamination. Cell Transplantation. Appeared or available online: April 29, 2013

The Coeditors-in-chief for CELL TRANSPLANTATION are at the Diabetes Research Institute, University of Miami Miller School of Medicine and Center for Neuropsychiatry, China Medical University Hospital, Beigang, Taiwan.

Cell Transplantation Center of Excellence for Aging and Brain Repair

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Cell Transplantation Center of Excellence for Agi. "Preventing infection in hosts receiving transplanted fetal tissues for neurodegenerative disease damage repair." Medical News Today. MediLexicon, Intl., 24 Jul. 2013. Web.
24 Jul. 2013. APA
Cell Transplantation Center of Excellence for Agi. (2013, July 24). "Preventing infection in hosts receiving transplanted fetal tissues for neurodegenerative disease damage repair." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/263803.php.

Please note: If no author information is provided, the source is cited instead.

'Preventing infection in hosts receiving transplanted fetal tissues for neurodegenerative disease damage repair'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Ticks confirmed to harbor Heartland virus, a recently discovered disease in the US

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Public Health
Article Date: 24 Jul 2013 - 1:00 PDT Current ratings for:
Ticks confirmed to harbor Heartland virus, a recently discovered disease in the US

Scientists have for the first time traced a novel virus that infected two men from northwestern Missouri in 2009 to populations of ticks in the region, providing confirmation that lone star ticks are carrying the recently discovered virus and humans in the area are likely at risk of infection. The findings were published online in the American Journal of Tropical Medicine and Hygiene.

Dubbed Heartland virus or HRTV, the infection causes fever, headaches, and low white blood cell and platelet counts. The two men infected in 2009, who live about 70 miles apart, were sufficiently ill to require hospitalization. They eventually recovered, and no other cases have been reported. Disease experts anticipate, however, that more people could become infected. The Missouri Department of Health and Senior Services is working with the US Centers for Disease Control and Prevention (CDC) to identify additional cases and determine the role of this novel virus as a human pathogen.

"Ten samples of ticks tested positive for the Heartland virus, nine of which were collected from the property of one of the patients and one that came from conservation lands nearby," said Harry M. Savage, PhD, a research entomologist at CDC in Fort Collins, Colorado and the lead author of the paper. "It's pretty strong evidence that the virus is persisting from season to season in tick populations and that these ticks play an important role in disease transmission."

There is no treatment available for HRTV. Unlike other tick-borne diseases like Lyme, ehrlichiosis and Rocky Mountain spotted fever, HRTV is a virus and thus does not respond to antibiotics.

Disease Hunting

HRTV was discovered when a doctor at the hospital treating the two infected men, who had reported being bitten by ticks, sent blood samples to a CDC laboratory in Atlanta for testing. All involved assumed the tests would reveal ehrlichiosis, the tick-borne disease that is most common in the area. Instead, the tests revealed a virus that had never been recognized. Subsequent analysis showed that HRTV belongs to a group of viruses known as phleboviruses, which can be carried by sandflies, mosquitoes or ticks. Savage said there is a separate team of researchers conducting tests with animals in the area in an effort to identify the "reservoir hosts" that are carrying the virus and passing it along to ticks.

Since the HRTV discovery, which was reported in August 2012 in the New England Journal of Medicine, scientists have been combing the area for the source of the infection. Savage and his team, which included investigators from Missouri Western State University, collected 56,428 ticks from April to August of 2012. They employed a variety of collection methods. Flannel pads used in infant bedding were mounted to bamboo poles to act as a sort of fly-paper for ticks. Plastic food containers were "baited" with dry ice, which emits carbon dioxide - a natural attractant for the ticks. Researchers even removed ticks from horses and dogs.

"Finding a virus in ticks requires the collection and testing of large numbers of ticks," Savage said. The virus infection rate in nymph stage ticks from one farm owned by a patient was about one in five hundred over the study period. Humans are likely to become infected when they are bitten by a tick carrying the virus. Savage said one of the HRTV patients recounted pulling dozens of ticks off his body each night before bed.

According to Savage, the ticks that carry the virus - known as lone star ticks for the single white spot found on females - are common in the area and in many other parts of the country as well. Currently, there are no reports of HRTV in any other tick populations aside from those isolated in northwestern Missouri. He said it's hard to predict where the virus might be located in the US and if the virus will spread.

HRTV appears to be related to another new disease recently discovered in China, a life-threatening virus called severe fever with thrombocytopenia (SFTSV). SFTSV also appears to be tick-borne, though there is evidence of person-to-person transmission as well.

"This research illustrates the ever-changing world we live in and why we must sustain our nation's investment in research into these types of diseases that the majority of Americans will never hear of," said David H. Walker, MD, president of the American Society of Tropical Medicine and Hygiene, whose research has included a focus on tick-borne diseases. "It is only by getting trained experts into the field and doing the necessary work of collecting and testing thousands of specimens, as these scientists did, that we can be one step ahead of what could become another serious health threat carried by ticks."

To prevent Heartland virus and other diseases spread by ticks, CDC recommends taking the following steps:

Wear repellent Check for ticks daily Shower soon after being outdoors Call your doctor if you get a fever or rashArticle adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject.

For more information on tick-borne diseases, visit http://www.cdc.gov/ticks

American Journal of Tropical Medicine and Hygiene

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

American Journal of Tropical Medicine and Hygiene. "Ticks confirmed to harbor Heartland virus, a recently discovered disease in the US." Medical News Today. MediLexicon, Intl., 24 Jul. 2013. Web.
24 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Ticks confirmed to harbor Heartland virus, a recently discovered disease in the US'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Researcher finds way to convert blood cells into autoimmune disease treatment

Main Category: Immune System / Vaccines
Also Included In: Blood / Hematology;  Arthritis / Rheumatology;  Crohn's / IBD
Article Date: 19 Jul 2013 - 2:00 PDT Current ratings for:
Researcher finds way to convert blood cells into autoimmune disease treatment

Cells from one's own blood could be converted into a treatment for autoimmune diseases, like rheumatoid arthritis and Crohn's disease, based on the discovery of a Purdue University researcher.

Chang Kim, a professor of comparative pathobiology, has created a way to direct the differentiation of T-cells, a white blood cell that is a key player in the body's immune system. The method uses naive T-cells, immature cells from which all T-cells develop, and induces them to become suppressive T-cells that block the development of painful inflammation associated with autoimmune diseases.

Naive T-cells can be gathered from a patient's blood, treated and then re-injected, said Kim, who also is a university faculty scholar and member of Purdue's Center for Cancer Research and Weldon School of Biomedical Engineering.

"These cells are being directed to become a type of cell that is already present in our bodies, where a fine balance between inflammatory T-cells and suppressive T-cells is maintained," he said. "We are just tipping the scales in favor of suppressive T-cells to reduce inflammation. Because of this there are none of the toxic side effects associated with many immune-suppressive drugs. In addition, cells from one's own body aren't rejected and remain in the body much longer. Instead of taking a pill every day, this could lead to a treatment administered, for example, every six months."

Autoimmune diseases occur when the immune system attacks one's own body instead of fending off infection from viruses, bacteria and other foreign cells. An overactive immune system sends T-cells to healthy tissue and organs where they cause inflammation and tissue destruction.

Suppressive T-cells migrate to areas of inflammation and suppress the T-cells there without significantly lowering the number of T-cells in other areas of the body where they are needed for proper immune function, Kim said.

"Treatment with suppressive T-cells has the potential to be a much more precise and targeted regulation of immune function than what currently exists," he said. "Treating autoimmune diseases without compromising a patient's immune system has been a big problem in the field. We need to catch the thief without taking down the house, and this has that potential."

Kim discovered that naïve T-cells cultured in the presence of the hormone progesterone can be induced to become suppressive T-cells. This discovery and his work have been detailed in papers in the Journal of Immunology and the European Journal of Immunology. The group also filed a patent based on this work. The national Institutes of Health and the Crohn's and Colitis Foundation of America funded the research.

Studies in mice showed that about 500,000 suppressive T-cells are needed to have an effect on inflammation, Kim said.

"More work needs to be done to determine the appropriate dosage of cells for a human patient, but the amount of blood many people regularly donate would likely yield multiple treatments," he said.

Kim next plans to study at the molecular level how progesterone causes the cells to differentiate into suppressive T-cells and to uncover the proteins and protein receptors involved. An understanding of the molecular regulation of these cells could lead to a way to control their differentiation and function without using progesterone, he said.

Article adapted by Medical News Today from original press release. Source:

Purdue University

Visit our immune system / vaccines section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

University, Purdue. "Researcher finds way to convert blood cells into autoimmune disease treatment." Medical News Today. MediLexicon, Intl., 19 Jul. 2013. Web.
20 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

posted by Su Su on 20 Jul 2013 at 6:54 am

How long will this take to get it helping those suffering and on Big Drugs with deadly side effects? I would like to share with Chang Kim what I have learned about RA.

| post followup | alert a moderator |

'Researcher finds way to convert blood cells into autoimmune disease treatment'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Synthetically optimized HIF-1 alpha DNA delivery using CELLECTRA provides significant therapeutic effects for peripheral arterial disease

Main Category: Vascular
Article Date: 19 Jul 2013 - 2:00 PDT Current ratings for:
Synthetically optimized HIF-1 alpha DNA delivery using CELLECTRA provides significant therapeutic effects for peripheral arterial disease

Inovio Pharmaceuticals, Inc. (NYSE MKT: INO) has announced that the use of its proprietary electroporation technology significantly enhanced the ability of a DNA therapy to stimulate blood vessel growth, which may be beneficial for the treatment of critical limb ischemia (CLI) and other forms of peripheral arterial disease (PAD). CLI's severe blockage of arteries of the lower extremities markedly reduces blood flow, resulting in notable medical impacts and death. In a mouse model, delivery of a synthetically optimized hypoxia-inducible factor-1 alpha (HIF-1a) gene using Inovio's CELLECTRA® electroporation delivery technology produced significant growth of new blood vessels and improved limb blood flow, limb function recovery, and survival from limb necrosis and amputation. The results were published in a paper entitled, "In vivo electroporation of constitutively expressed HIF-1a plasmid DNA improves neovascularization in a mouse model of limb ischemia," in the peer-reviewed Journal of Vascular Surgery.

Finding an effective therapy for PAD and CLI is imperative because the current standard of care relies primarily on palliative drugs and amputation. PAD affects 8 -12 million Americans and is associated with a 20 - 30% risk of cardiovascular death within five years. CLI is a more severe stage of PAD affecting over one million people in the US. Up to 20% of CLI patients will die within 12 months of diagnosis; the five-year mortality rate exceeds 70%. The disease is characterized by ischemic rest pain - severe pain in the legs and feet while a person is not moving - or non-healing sores on the feet or legs as well as gangrene. Major limb amputation occurs in up to 40 - 50% of CLI patients within 12 months of diagnosis.

Dr. J. Joseph Kim, Inovio's president and CEO, said: "We have tremendous momentum and clinical data in achieving best-in-class immune responses with our SynCon® DNA vaccines delivered using our CELLECTRA electroporation system. Others have attempted to treat PAD using angiogenic growth factor DNA therapies without success. This study shows that combining our synthetic gene optimization techniques with our proprietary delivery systems could lead to an effective therapy. While early, this new application in treating PAD and other major chronic diseases offers Inovio a promising therapeutic avenue and additional commercial opportunity."

In this study, the gene sequence for HIF-1a was synthetically optimized to enhance expression of the growth factor. This DNA therapy was then delivered using Inovio's CELLECTRA constant current electroporation device, which has been shown to enhance the delivery of DNA plasmids by a 1000 fold using a millisecond pulse. A total of 39 mice were divided into 3 groups: (1) one group receiving HIF-1a DNA delivered with electroporation (EP) (n=13); (2) one group receiving HIF-1a DNA without EP (n=14) and (3) one group receiving a control empty plasmid (pVAX) delivered with EP (n=12). The left femoral artery in each mouse was tied up surgically to simulate an arterial blockage. The right legs were not treated and served as internal controls. The mice were then observed and scored for their limb function. Blood flow in their legs was measured by laser Doppler perfusion imaging.

The results demonstrated that EP delivery of synthetically optimized HIF-1a plasmid DNA significantly improved blood flow in the left hind legs and reduced necrosis (premature cell death) in a mouse model of hind limb ischemia when compared to the results from the two control groups. The treatment also improved survival from severe limb damage and amputation, reduced tissue damage, and increased the number of new capillaries and formation of larger collateral vessels.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our vascular section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Pharmaceuticals, Inovio. "Synthetically optimized HIF-1 alpha DNA delivery using CELLECTRA provides significant therapeutic effects for peripheral arterial disease." Medical News Today. MediLexicon, Intl., 19 Jul. 2013. Web.
20 Jul. 2013. APA
Pharmaceuticals, I. (2013, July 19). "Synthetically optimized HIF-1 alpha DNA delivery using CELLECTRA provides significant therapeutic effects for peripheral arterial disease." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/263614.php.

Please note: If no author information is provided, the source is cited instead.

'Synthetically optimized HIF-1 alpha DNA delivery using CELLECTRA provides significant therapeutic effects for peripheral arterial disease'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Researchers Discover A Role For A Protein That Has Implications For Treatment Of Cancer And Heart Disease

Main Category: Cancer / Oncology
Also Included In: Heart Disease
Article Date: 14 Jul 2013 - 0:00 PDT Current ratings for:
Researchers Discover A Role For A Protein That Has Implications For Treatment Of Cancer And Heart Disease

St. Jude Children's Research Hospital scientists have discovered that a protein used by cancer cells to evade death also plays a vital role in heart health. This dual role complicates efforts to develop cancer drugs that target the protein, but may lead to new therapies for heart muscle damage. The research appeared in a recent edition of the scientific journal Genes & Development.

The protein, MCL1, is currently the focus of widespread cancer drug development efforts. MCL1 is best known as an inhibitor of death via the cell's suicide pathway in a process called apoptosis. The protein is elevated in a variety of cancers, and a number of MCL1 inhibitors are in the cancer drug development pipeline worldwide. The protein has also been linked to drug resistance in cancer patients. Until now, however, MCL1's role in heart muscle cells was unclear.

"Our study shows that MCL1 is required for normal cardiac function and that the protein may be critical in protecting the heart from apoptosis," said Joseph Opferman, Ph.D., an associate member of the St. Jude Department of Biochemistry and the paper's corresponding author. Unlike skin or blood cells, heart muscle cells cannot be replaced, so even a small loss through apoptosis can be devastating. In this study, knocking out MCL1 in mice led to death from cardiomyopathy within weeks.

"These findings suggest that cancer-related drug development efforts should focus on reducing MCL1 expression in target cells rather than eliminating the protein's function completely," Opferman said.

The results also have implications for treating heart muscle damage following heart attacks or other insults. While limiting MCL1 in cancer cells might aid in destroying them, providing higher levels of the protein in heart muscle cells might benefit a patient recovering from a heart attack or other heart damage. "These findings have broad implications for human health," Opferman said.

MCL1 belongs to a protein family involved in regulating apoptosis. The body uses apoptosis to rid itself of damaged, dangerous or unneeded cells. MCL1 prevents apoptosis by blocking the activity of other members of the same protein family that promote the process.

This research builds on previous work from Opferman's laboratory that identified a second form of MCL1. That form works inside rather than outside the mitochondria and helps to produce the chemical energy that fuels cells. Mitochondria are specialized structures inside cells that serve as their power plants.

The latest results suggest both forms of MCL1 are necessary for normal heart function, said the paper's first author Xi Wang, a University of Tennessee Health Science Center graduate student working in Opferman's laboratory.

When investigators knocked out the mouse version of the human MCL1 gene in the heart and skeletal muscle of both embryonic and adult mice, the animals rapidly developed lethal cardiomyopathy. Without MCL1, researchers found that muscle fiber in heart muscle cells was replaced by fibrous tissue, and the pumping ability of the animals' hearts diminished. Loss of MCL1 was also associated with a rise in apoptosis sufficient to cause fatal heart muscle weakness.

To better understand MCL1's role in normal heart function, researchers blocked apoptosis by deleting genes for the proteins Bak and Bax as well as MCL1. Bak and Bax promote apoptosis. Knocking out all three genes restored normal heart function in the mice. The animals lived longer, but mitochondria in the heart muscle did not look or function normally. These results suggest that normal heart function requires both forms of MCL1. "The question is whether, with time, you would see deleterious effects from the loss of MCL1 separate from apoptosis," Opferman said.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject.

The other authors are Madhavi Bathina, John Lynch, Brian Koss, Christopher Calabrese, Sharon Frase, John Schuetz and Jerold Rehg, all of St. Jude.

The research was funded in part by a grant (HL102175) from the National Institutes of Health (NIH), a grant (CA021765) from the National Cancer Institute (NCI) at the NIH, the National Cancer Society and ALSAC.

St. Jude Children's Research Hospital

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

St. Jude Children\'s Research Hospital. "Researchers Discover A Role For A Protein That Has Implications For Treatment Of Cancer And Heart Disease." Medical News Today. MediLexicon, Intl., 14 Jul. 2013. Web.
14 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Researchers Discover A Role For A Protein That Has Implications For Treatment Of Cancer And Heart Disease'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

The Obese Are At Increased Risk For Heart Disease When Exposed To Cigarette Smoke

Main Category: Smoking / Quit Smoking
Also Included In: Obesity / Weight Loss / Fitness;  Heart Disease;  Genetics
Article Date: 13 Jul 2013 - 0:00 PDT Current ratings for:
The Obese Are At Increased Risk For Heart Disease When Exposed To Cigarette Smoke

New insights into why obese cigarette smokers experience a high risk of heart disease suggest that cigarette smoke affects the activity of hundreds of key genes that both protect the heart and lungs and expose them to damage. The study, published in ACS' Chemical Research in Toxicology, suggests that the effects may be especially profound in obese nonsmokers who inhale "sidesteam smoke" from cigarettes smoldering nearby.

Diana J. Bigelow and colleagues point out that active smoking doubles the risk of heart disease, while second-hand smoke exposure increases this risk by about one-third. They set out to gain more information on why the risks are especially high among people with obesity, using specially fed laboratory mice that are stand-ins for humans in such experiments.

The report describes how mainstream smoke and to a greater extent, sidestream smoke, inhibit the activity of genes that protect the heart and lungs, and activate genes associated with an increased risk of heart disease. Those changes were more profound in obese mice than normal-weight mice. "The present study is the first, to our knowledge, that addresses the in vivo transcriptional response of the heart to cigarette smoke exposure in the setting of high fat diet and obesity, and thus takes a first step toward identifying the molecular basis of adaptive responses that may lead to an increased risk of heart disease in obese smokers," the report states.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our smoking / quit smoking section for the latest news on this subject.

The authors acknowledge funding from the Exposure Biology Program in the National Institute of Environmental Health Sciences, part of the National Institutes of Health.

American Chemical Society

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

American Chemical Society. "The Obese Are At Increased Risk For Heart Disease When Exposed To Cigarette Smoke." Medical News Today. MediLexicon, Intl., 13 Jul. 2013. Web.
14 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

posted by miki mario on 14 Jul 2013 at 2:29 pm

New insights into why obese cigarette smokers experience a high risk of heart disease suggest that cigarette smoke affects the activity of hundreds of key genes that both protect the heart and lungs and expose them to damage. The study, published in ACS’ Chemical Research in Toxicology, suggests that the effects may be especially profound in obese nonsmokers who inhale “sidesteam smoke” from cigarettes smoldering nearby.

| post followup | alert a moderator |

'The Obese Are At Increased Risk For Heart Disease When Exposed To Cigarette Smoke'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here