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Past News Items - Jan 2016


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In the News

ACAM Addresses the Water Crisis in Flint

How Do Protective Immune Cells Protect Themselves?

Researchers Find a Small Protein That Plays a Big Role in the Heart

Factors in the Blood During Dieting May Have Anti-Diabetes Properties

Taking Vitamin D May Benefit People with MS

Two Alzheimer’s risk genes linked to brain atrophy, promise future blood markers




Released: 01/27/16


ACAM Addresses the Water Crisis in Flint

Flint, Michigan recently declared a State of Emergency in the wake of lead contamination in their drinking water from switching water sources. As a result, we are faced with the age-old discussion regarding the health implications of lead accumulation. We know that protecting all people from lead exposure is extremely important to lifelong health. Children, however, are particularly vulnerable to the harmful effects of lead because they absorb it much more readily than adults. The current controversy over treatment revolves around three questions:

1.      Who should be considered at higher risk for harm and offered treatment?

2.      What treatments should be offered to individuals with elevated lead levels?

3.      At what blood lead level burden is it appropriate to start therapy?

Unfortunately, this tragedy goes far beyond Flint. People worldwide continue to be exposed to potentially harmful levels of many toxic metals that can profoundly affect their health. They face potentially serious, complicated, and enduring health issues. Perhaps the major question, especially in children, is the level of lead in the blood to cause concern.

The CDC states, “Experts now use a reference level of 5 micrograms per deciliter to identify children with blood lead levels that are much higher than most children’s levels. This new level is based on the U.S. population of children ages 1–5 years who are in the highest 2.5% of children when tested for lead in their blood. In the past, blood lead level tests below 10 micrograms per deciliter of lead in blood may, or may not, have been reported to parents. The new lower value means that more children will likely be identified as having lead exposure allowing parents, doctors, public health officials, and communities to take action earlier to reduce the child’s future exposure to lead.”

The CDC also states, “What has not changed is the recommendation for when medical treatment is advised for children with high blood lead exposure levels. The new recommendation does not change the guidance that the therapy used to eliminate lead from the body be considered only when a child has been tested with a blood lead test result greater than or equal to 45 mcg/dL.”

However, medical science has determined that even very low blood lead levels in children can affect IQ, ability to pay attention and future academic achievement. It is now clear that IQ loss in lead-exposed children can occur at levels below 5.0 mcg/dL.

The American College for Advancement in Medicine (ACAM), an educational organization and a leading authority in the field of heavy metal toxicity and treatment believes, as the CDC does, that “No safe blood lead level in children has been identified.” The effects of lead exposure on child cognitive development and behavior may be permanent if no intervention occurs. Experts from ACAM believe that certain interventions may be useful in lessening the symptoms and long-term neurocognitive damage that lead causes in children.

ACAM experts also contend that the myriad, harmful effects that lead can cause in other organ systems in people of any age should also be lessened. The original guidelines for intervention in lead poisoning were based on early FDA drug approval studies from the minimal research conducted in pediatric patients with blood lead levels above 45 mcg/dL. ACAM believes that appropriate medical intervention may be beneficial to those suffering from lead levels even at the current CDC cutoff of 5 mcg/dl, the level that places the child in the upper 2.5% of tested individuals.

Due to the lack of current, cohesive, long-term studies in children with elevated blood levels below 45 mcg/dL, the decision of when to initiate chelation therapy is a personal choice between a patient and their physician. To better elucidate what is the best treatment strategy for lead poisoning, ACAM is calling for the immediate initiation of a collaborative long-term research project. The project, conducted through appropriate channels, could provide immediate medical attention and intervention to all children and adults in Flint who have high blood lead levels (>5 mcg/dl). This research project should also investigate assessing those common genetic and metabolic defects that could render individuals even more susceptible to the harmful effects of lead.

We can take a more proactive approach to prevent permanent damage and disability, not only in the population of Flint, but to everyone exposed to the potential devastation caused by lead.

About ACAM
The American College for Advancement in Medicine (ACAM) is a not-for-profit organization dedicated to educating physicians and other healthcare professionals on the safe and effective application of integrative medicine. ACAM's healthcare model focuses on prevention of illness and strives for total wellness.

Released: 01/25/16


How Do Protective Immune Cells Protect Themselves?

Researchers at St. Jude Children's Research Hospital have discovered the mechanism by which immune cells called regulatory T cells keep themselves intact and functional during their demanding task of holding the immune system in check. Such T cells are key to preventing the immune system from attacking the body in autoimmune disease.

The researchers said their findings suggest that drugs influencing this protective mechanism could be used to alert the immune system to fight cancers.

Led by corresponding author Hongbo Chi, PhD, a member of the St. Jude Department of Immunology, the research appeared on the Nature Immunology website today as an advance publication.

The researchers discovered that once regulatory T cells are activated to begin their work, they are protected by a kind of cellular "cleanup" process called autophagy. This natural destructive biological mechanism targets and degrades molecules that are no longer needed, essentially ridding the cell of molecular garbage. Until these studies, no one knew how regulatory T cells maintained themselves when activated.

"Regulatory T cells are very specialized cells that require activation to perform their function in curtailing undesirable immune responses," Chi said. "But this activation is a double-edged sword, in that this very activation can destabilize them. They need to modulate this activation, or they will lose their stability and many of them will die. That could damage immune function."

In their experiments, the researchers performed imaging studies in activated regulatory T cells that demonstrated autophagy was, indeed, functional in the cells. Next, in mouse studies, the scientists deleted key genes, called Atg7 or Atg5, whose function was necessary for autophagy in regulatory T cells. The scientists found that the mice showed key characteristics of regulatory T cell malfunction, including inflammatory and autoimmune disorders. The mice also more readily cleared tumors from their bodies, due to activated immune systems.

Chi said that eliminating autophagy also affected the fate of such regulatory T cells. "Once those T cells lack autophagy activity, they tend to undergo excessive cell death," he said. "But even for the remaining surviving cells, they tend to be overly activated and lose their identity, because they start to behave like non-regulatory T cells. That is why loss of autophagy in regulatory T cells produces a two-fold effect on both survival and stability."

Detailed analysis also revealed how the elimination of autophagy affected the basic energy-producing metabolic pathways of the T cells, compromising their function.

Chi said the new understanding of autophagy's role in regulatory T cells could enable a two-fold approach to immune therapy for cancers. The authors noted: "From this perspective, by strengthening tumor-associated immune responses, targeting [regulatory T cell] autophagy could act in synergy with strategies that block autophagy in tumor cells for added benefits in cancer therapy."

In the current studies, the researchers used a transplanted colon cancer cell line. In further studies, they plan to explore the role of autophagy in immune reactions toward other tumor cell types, to determine whether such therapies might be effective in a broad range of cancers.

The researchers will also aim at better understanding the detailed biochemical mechanisms regulating how autophagy connects to the cell's metabolic pathways.

St. Jude Children's Research Hospital
St. Jude Children's Research Hospital is leading the way the world understands, treats and defeats childhood cancer and other life-threatening diseases. It is the only National Cancer Institute-designated Comprehensive Cancer Center devoted solely to children. Treatments developed at St. Jude have helped push the overall childhood cancer survival rate from 20 percent to 80 percent since the hospital opened more than 50 years ago. St. Jude freely shares the breakthroughs it makes, and every child saved at St. Jude means doctors and scientists worldwide can use that knowledge to save thousands more children. Families never receive a bill from St. Jude for treatment, travel, housing and food—because all a family should worry about is helping their child live. To learn more, visit stjude.org.

Released: 01/19/16


Researchers Find a Small Protein That Plays a Big Role in the Heart

Researchers at UT Southwestern Medical Center have identified a previously unrecognized small protein in cells of the human heart that plays a key role in heart muscle contraction. The protein is made from an RNA that was previously believed to be a blank or non-coding RNA, suggesting there may be many other small “non-coding” segments that play important biological roles.

Significantly, the findings published recently in Science offer a potential new target for developing therapeutics to boost the strength of cardiac muscle contractions in patients with heart failure, a chronic condition in which the heart pumps too weakly to supply adequate oxygen to the body.

The new protein, which the researchers have named dwarf open reading frame (DWORF), comprises just 34 amino acids, making it the third smallest protein known to be encoded in the mouse genome. By comparison, an average-sized protein is 10 times larger, including about 350 amino acids. DWORF is also encoded in the human genome.

The DWORF protein stimulates a calcium-ion pump that controls muscle contraction. As DWORF increases, the heart pumps with more force.

“There’s a brake in the heart that controls pumping, and DWORF shuts off the brake, which has the effect of making heart muscle pump more vigorously,” said senior author Dr. Eric Olson, Chairman of the Molecular Biology, and Director of the Hamon Center for Regenerative Science and Medicine at UT Southwestern.

The researchers also found DWORF in some skeletal muscle, namely slow-twitch skeletal muscle fibers, the type of muscle fiber that allows a person to run marathons.

DWORF was found among a class of RNA transcripts that had been dismissed by scientists as non-coding RNA, sometimes colloquially called “junk” RNA. Emerging evidence, however, such as the discovery of DWORF, indicates that many small proteins with bioactive properties are hidden among these regions of the genome that are thought to be non-coding and, due to their small size, have evaded detection by scientists.

“Although small and non-enzymatic themselves, peptides like DWORF have the ability to regulate the function of much larger molecular complexes, analogous to the way that a tiny rudder determines the direction of a much larger ship,” said Dr. Catherine Makarewich, a postdoctoral fellow in Dr. Olson’s lab and a co-lead author of the study.

“Elucidating the full catalog of small proteins like DWORF could provide significant new insight into how the molecular machinery of the cell is regulated,” added Benjamin Nelson, a student in UT Southwestern’s Medical Scientist Training Program and co-lead author of the study.

“We dipped into the RNA ‘junk’ pile and came up with a hidden treasure,” said Dr. Rhonda Bassel-Duby, Professor of Molecular Biology and a study author.

This work was supported by grants from the National Institutes of Health, Foundation Leducq Networks of Excellence, the Cancer Prevention and Research Institute of Texas, the National Institute of Arthritis and Musculoskeletal Diseases, a Ruth L. Kirschstein National Research Service Award, and the Robert A. Welch Foundation.

About UT Southwestern Medical Center

 

UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty has included six who have been awarded Nobel Prizes since 1985. The faculty of almost 2,800 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in about 80 specialties to more than 92,000 hospitalized patients and oversee approximately 2.2 million outpatient visits a year.

Released: 01/09/16


Factors in the Blood During Dieting May Have Anti-Diabetes Properties

Factors in the blood from calorie-restricted rats can modify energy-producing mitochondria within the insulin-producing cells that regulate blood sugar levels, new research shows. This has a positive impact on glucose-stimulated insulin secretion and protects cells from fatty acid and glucose toxicity.

The findings suggest that insulin-producing cells’ mitochondria may be altered by signals independent of the body’s fuel levels and may represent a useful therapeutic target in type 2 diabetes. Additionally, identifying these blood factors may open even more targetable interventions against the disease.

“Our findings support the concept that the impact of diet on insulin secreting cells is mediated by signals traveling through the blood rather than the nutrients and metabolites themselves. These signals may be generated elsewhere in other organs such as fat tissue, liver, brain or even the immune cells,” said Dr. Orian Shirihai, co-author of The FEBS Journal study. “Our findings also suggest that at least in part the beneficial effect of reducing caloric intake is mediated by the appearance of a protective signal rather than the elimination of a harmful one. This study describes an experimental system through which such signals can be identified and characterized with the hope that in the future it can potentially be mimicked using a small compound.”

Story Source:

The above post is reprinted from materials provided by Wiley. Note: Materials may be edited for content and length.

Links: Materials:  http://www.wiley.com/WileyCDA/PressRelease/pressReleaseId-122762.html

 

Wiley  http://www.wiley.com/WileyCDA/Brand/id-35.html

Released: 01/04/16


Taking Vitamin D May Benefit People with MS

Taking a high dose of vitamin D3 is safe for people with multiple sclerosis (MS) and may correct the body’s hyperactive immune response, according to a study published in the December 30, 2015, online issue of Neurology®, the medical journal of the American Academy of Neurology.

Low levels of vitamin D in the blood are tied to an increased risk of developing MS. People who have MS and low levels of vitamin D are more likely to have greater disability and more disease activity.

For the study, 40 people with relapsing-remitting MS received either 10,400 IU or 800 IU of vitamin D3 supplements per day for six months. The current recommended daily allowance of vitamin D3 is 600 IU. Blood tests at the start of the study and again at three and six months measured the amount of vitamin D in the blood and the response in the immune system’s T cells, which play a key role in MS.

Side effects from the vitamin supplements were minor and were not different between the people taking the high dose and the people taking the low dose. One person in each group had a relapse of disease activity.

The people taking the high dose had a reduction in the percentage of T cells related to MS activity. When the increase in vitamin D in the blood was greater than 18 nanograms per milliliter (ng/ml), every 5 ng/ml increase in vitamin D led to a 1 percent decrease in the percentage of interleukin 17 T cells in the blood. The people taking the low dose did not have any changes in their T cells.

While researchers are still determining the optimal level of vitamin D in the blood for people with MS, the people in the study taking the high dose of vitamin D reached a level that has been proposed as a target for people with MS. Vitamin D levels above 30 ng/ml are considered sufficient for the general population, but researchers noted that for people with MS, it may be that levels above 50 ng/ml are necessary to reduce disease activity. The group taking the low dose did not reach this target.

“These results are exciting, as vitamin D has the potential to be an inexpensive, safe and convenient treatment for people with MS,” said study author Peter A. Calabresi, MD, of Johns Hopkins University School of Medicine in Baltimore, MD, and a Fellow of the American Academy of Neurology. “More research is needed to confirm these findings with larger groups of people and to help us understand the mechanisms for these effects, but the results are promising.”

The study was supported by the Kenneth and Claudia Silverman Family Foundation, Montel Williams Foundation and National Multiple Sclerosis Society. To learn more about multiple sclerosis, please visit www.aan.com/patients.

 

Neurology®http://www.neurology.org/content/early/2015/12/30/WNL.0000000000002316.short?rss=1

American Academy of Neurology:   https://www.aan.com/

www.aan.com/patients.:  www.aan.com/patients.

Released: 01/04/16


Two Alzheimer’s risk genes linked to brain atrophy, promise future blood markers

Two genetic variants previously linked to Alzheimer's disease have been more specifically tied to brain atrophy that is characteristic of the disease.

A newly reported study, led by Liana Apostolova, M.D., Barbara and Peer Baekgaard Professor of Alzheimer's Disease Research at the Indiana University School of Medicine, also found that the proteins produced by the genes and circulating in the blood were associated with the brain atrophy and could be used in Alzheimer's-related tests in the future.

The study is believed to be the first to directly link common variants of the genes -- ABCA7 and MA4A6A -- to atrophy in cortical and hippocampal regions of the brain, which are associated with memory and other key functions. It's also believed to be the first to link the atrophy to protein levels in the blood produced by the genes.

"We also found that the levels of the protein products of these genes, circulating in the peripheral blood, were associated with the cortical and hippocampal atrophy. This finding suggests that those results of gene expression could become useful biomarker blood tests for Alzheimer's disease," Dr. Apostolova said.

The study was published in the advance online edition of the journal Neurobiology of Aging.

Alzheimer's disease is a progressive illness that is the leading cause of dementia and the sixth leading cause of death in the United States, according to the Alzheimer's Association. There is no cure for the disease and currently available treatments can slow, but cannot stop, the deterioration.

Although scientists have been linking a growing number of gene variants to the risk of developing Alzheimer's disease, most of the associations have not identified the specific mechanisms that would increase the risk of developing the disease.

For the new study, the researchers identified the top nine genetic variants that have been associated with Alzheimer's disease risk, not including the APOe4 gene that has long been linked to increased risk for several characteristics of Alzheimer's disease.

Using magnetic resonance imaging tools to measure brain size and genetic analysis, the researchers looked for associations between the genetic variants and atrophy in the cortical and hippocampal regions of the brain, which are established physical biomarkers of Alzheimer's disease. The studies were conducted in 50 participants with no cognitive difficulties and 90 who had been diagnosed with mild cognitive impairment, a condition that is associated with increased risk of developing Alzheimer's disease. All of the participants were 50 years or older.

Just two of the genetic variants -- known as ABCA7 and MA4A6A -- appeared to be associated with the changes in brain structure.

Funding from the following sources supported the research: National Institutes of Health grants R01 AG040770, K02 AG048240, P50 AG16570 and P30 AG010133; and the Easton Consortium for Alzheimer’s Drug Discovery and Biomarker Development.

 

In addition to Dr. Apostolova, researchers contributing to the study were Leslie M. Ramirez of the Drexel University College of Medicine, Giovanni Coppola, Naira Goukasian, Sona Hurtz, Eric Klein, Shai Porat, Renee Sears, and Benjamin Wang of UCLA, Kristy S. Hwang of the Oakland University William Beaumont School of Medicine, Jennifer A. Eastman of the Northwestern University Feinberg School of Medicine and Nouchee Vang of the University of Minnesota.

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