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In the News

BCM-95 Curcumin Disrupts Cancer Cell Communication

EXCEMED Launches new go-to Clinical Resource in Thyroid Disease

New Non-Invasive Technology Diagnoses Fatty Liver Disease

Study Suggests the Human Body Cannot be Trained to Maintain a Higher Metabolism

Journal of Autoimmunity Publishes Research Supporting Safety of Oats in the Celiac Diet

New Research Finds that Special Interest Lobbying Does Influence NIH Research Funding

Study Says Blood Test for Brain Insulin Resistance Accurately Predicts Alzheimer’s Disease Risk




Released: 11/12/14


BCM-95 Curcumin Disrupts Cancer Cell Communication

A recently published cellular study on colorectal cancer showed that high-absorption BCM-95 Curcumin is able to reduce the spread of cancer cells and potentially increase the effectiveness of chemotherapy in the treatment of advanced colon cancer. [Buhrmann C, Kraehe P, Lueders C, Shayan P, Goel A, et al. (2014) Curcumin Suppresses Crosstalk between Colon Cancer Stem Cells and Stromal Fibroblasts in the Tumor Microenvironment: Potential Role of EMT. PLoS ONE 9(9): e107514. doi: 10.1371/journal.pone.0107514]

Signaling (cellular communication) between cancer cells and normal cells is a key factor in how cancer progresses. This "signaling" increases the survival, proliferation, and malignant behavior of tumor cells and their ability to resist chemotherapy drugs. In this new study, researchers investigated the role of signaling between colon cancer cells and normal cells and how chemotherapy drugs and BCM-95 Curcumin affect that communication. Additionally, researchers examined the impact of the treatments on markers of cancer stem cells. Cancer stem cells are responsible for developing resistance to chemotherapy and the recurrence of cancer after treatment.

The study used a 3D tumor culture, which more closely replicates how tumors act in the body than other conventional in vitro cell culture models. The culture was treated with either 5?Fluorouracil (5-FU), which is a common chemotherapeutic agent used for colorectal cancer, BCM-95 Curcumin, or a combination of 5-FU and BCM-95 Curcumin.

One startling finding of this study was that treatment with 5-FU actually promoted the growth of cancer stem cells, which may account for the high incidence of recurrence in colon cancer. "Colorectal cancer is especially devastating because of its high recurrence rate," said Ajay Goel, PhD, Director of Epigenetics and Cancer Prevention, Baylor Research Institute, Baylor University Medical Center, Dallas, TX, one of the study's authors. "Cancer stem cells exist in very small numbers in a tumor and can hide from chemotherapy. They're very small in number, but they survive and cause cancer to reoccur, sometimes years later. I believe cancer stem cells are the main reason why we can't stop cancer.

"But our recent studies on curcumin continue to reveal its unique potential as a therapeutic strategy in the fight against cancer," continued Dr. Goel. "In this study, treatment with curcumin impeded cancer growth and proliferation by inhibiting signaling proteins and blocking tumor cell promotion. The beauty of curcumin is its ability to balance gene expression and positively influence anticancer pathways."

The best results for inhibiting cancer growth occurred when the curcumin was used as a pretreatment before chemotherapy. The addition of curcumin reduced the amount of 5?FU needed to inhibit cancer cell growth substantially and sensitized the cancer stem cells to chemotherapy treatment. "I'm particularly excited about curcumin's potential as a prophylactic to chemotherapy," said Dr. Goel. "We have great hope that using curcumin will extend survival and improve the quality of life of cancer patients."

It is important to note that the form of curcumin used in the study, BCM-95 Curcumin, has unique specifications, including high absorption and inclusion of turmeric essential oil, which is not found in standard curcumin. Therefore, results may not apply to other forms of curcumin.

SOURCE BCM-95 Curcumin

 

Released: 11/12/14


EXCEMED Launches new go-to Clinical Resource in Thyroid Disease

General practitioners, specialist endocrinologists and internists have a brand new reference point to support their daily clinical treatment and management of patients with thyroid dysfunction.

Manage Thyroid Online (managethyroidonline.org ), an initiative of EXCEMED, is a definitive resource to help healthcare professionals recognize the implications of diagnosing and treating different thyroid disorders such as hypothyroidism, hyperthyroidism, autoimmune disease, and nodular disease (including thyroid carcinoma).

"EXCEMED is proud to present this new tool to the healthcare community with particular acknowledgement to the truly global nature of what we are offering - the Scientific Committee for this project draws top experts in thyroid disorder from Europe, the Middle East, Asia and Latin America," says Roberta Cenci, Head of Educational Strategy for EXCEMED.

These top experts are Prof. Ali S. Alzahrani, King Faisal Specialist Hospital & Research Center Riyadh, Saudi Arabia; Prof. Gabriela Brenta, Cesar Milstein Hospital, Buenos Aires, Argentina; Prof. George J. Kahaly, Johannes Gutenberg University Medical Center, Mainz, Germany; and Prof. Nemencio A. Nicodemus Jr, UP-Philippine General Hospital, Manila, Philippines.

"The most current, international and evidence-based standards in thyroid practice are being employed on this website," says Prof. Kahaly. "As the site evolves, we will deliver up-to-date content on a variety of conditions including hypothyroidism, hyperthyroidism, goiter and nodular diseases, cardiovascular implications of thyroid dysfunction and special topics such as differentiated thyroid cancers, pregnancy - and age-related thyroid issues."

Healthcare practitioners will be able to select from practical and in-depth approaches to thyroid disease in formats such as expert editorials, slide presentations, video lectures and key conference summaries and CME-accredited e-learning courses.

SOURCE EXCEMED

 

Released: 11/11/14


New Non-Invasive Technology Diagnoses Fatty Liver Disease

ASX listed Resonance Health (ASX:RHT) officially launched an innovative new diagnostic imaging solution for liver patients worldwide at the American Association for the Study of Liver Diseases annual conference in Boston this week.

HepaFat-Scan technology was developed in collaboration with the University of Western Australia, and uses magnetic resonance imaging (MRI) scanners in a non-invasive manner, to measure the concentration of fat in the human liver.

This is the first and only technology of its kind to obtain regulatory clearances in the USA - FDA, Europe - CE Mark, and Australia - TGA and has also just won the coveted Western Australian Innovation of the Year award at the 2014 WA Innovator of the Year Awards.

Chief Scientist Professor Tim St Pierre said HepaFat-Scan addresses the growing prevalence of fatty liver disease in Australia and many other countries, as well as an unmet need for non-invasive diagnostic tools to diagnose and monitor liver disease.

"It reports volumetric fraction of fat in the liver, a measure that can be directly compared to a volumetric biopsy fat fraction measurement, providing patients and doctors with a more accurate diagnostic tool as part of a structured intervention protocol or clinical research trial."

Compared with the traditional gold standard for clinical assessment of liver fat - histopathological assessment, HepaFat-Scan is a much more objective and non-invasive MRI based method with greater reproducibility and significantly reduced sampling error.

Hence, clinicians and patients can greatly benefit from an accurate HepaFat-Scan measurement of liver fat to monitor and manage efficacy of treatment, and to provide prognoses for fatty liver disease and associated multiple hepatic and systemic disorders and many other related diseases.

All image analysis and reporting services are provided from Resonance Health's ISO 13485 certified Perth based facility and are utilised by hospitals in over 20 countries, and in international clinical trials.

The Innovator of the Year Program is an annual event run by the Western Australian Department of Commerce that fosters a culture of innovation in Western Australia and acknowledges the achievements of WA's leading innovation enterprises.

SOURCE Resonance Health

 

Released: 11/07/14


Study Suggests the Human Body Cannot be Trained to Maintain a Higher Metabolism

 New research suggests that high- and normal- protein diets are tied to higher metabolism and 45 percent more storage of lean tissue, or muscle mass, versus fat when compared to low-protein diets. Further, it shows that this increase in metabolism tied to a high-protein diet is not sustainable when changing to a normal-protein diet, suggesting that the human body cannot be trained to maintain a higher metabolism. Research results were unveiled today during an oral presentation by author Elizabeth Frost, PhD Candidate, Pennington Biomedical Research Center, at 8:00am ET at The Obesity Society Annual Meeting at ObesityWeek 2014 in Boston, Mass.

"Rather than conducting a weight-loss study, our focus was to explore whether high- or low- protein diets might lead to less weight gain when consuming excess calories due to the ability of the body to burn extra energy with a high-protein diet," said Frost. "What we found was that study participants all gained similar amounts of weight regardless of diet composition; however, there was a vast difference in how the body stored the excess calories. Those who consumed normal- and high- protein diets stored 45 percent of the excess calories as lean tissue, or muscle mass, while those who on the low-protein diet stored 95 percent of the excess calories as fat."

Researchers concluded that one mechanism for weight-loss success with high-protein diets, like the Atkins Diet or the Ideal Protein Diet, could be due to an increase in our body's natural process of metabolizing food for energy following meals.

TOS recognized Frost for her research by naming her as a finalist for the Ethan Sims Young Investigator Award, an annual award given to five young researchers to cover travel expenses associated with TOS's annual meeting. All five winners presented their research during a session today in competition for the final award – a $1,000 cash prize.

TOS says the study results reinforce the importance of energy deficit for weight loss, showing that weight loss regardless of diet composition is not possible without consuming fewer calories per day than those burned.

"High-protein diets for weight-loss or to build muscle mass can certainly be effective, but the diet composition must be maintained for dieters to continue to see and sustain results," said Steven R. Smith, TOS President. "Further, it's important to balance how many calories you eat and how many you burn on a daily basis. This concept, also known as energy balance, is vital for weight control. I congratulate Elizabeth Frost for her study, which further reinforces that it is not possible to achieve weight loss on a high-protein diet, or any diet, without burning more calories than calories consumed - also known as energy deficit."

The study was a randomized controlled overfeeding trial of 16 healthy individuals with varied amounts of protein (low 5 percent, normal 15 percent, high 25 percent) for eight weeks while living in a metabolic ward. Diet-induced thermogenesis (DIT), which is one of three components for the metabolic rate, was measured over four hours by indirect calorimetry following meals. Results showed that prolonged exposure to high-protein diets does not alter DIT, and suggests that it is under acute regulation and not involved in adaptive thermogenesis, or a sustained increase in metabolism.

 

Released: 11/07/14


Journal of Autoimmunity Publishes Research Supporting Safety of Oats in the Celiac Diet

ImmusanT, a company focused on restoring tolerance to gluten and overcoming the need for gluten-free diet in patients with celiac disease, today announced that an article published online in the Journal of Autoimmunity details new research describing the immune response in celiac disease when oats are ingested. According to researchers, the vast majority of patients with celiac disease can ingest oats without stimulating an immune response, providing further evidence suggesting exclusion of oats from the diet of patients is generally not necessary. The international team who led the study included ImmusanT’s collaborators at the Walter and Eliza Hall Institute (WEHI) of Medical Research in Australia: Melinda Hardy, PhD, and head celiac disease research Jason Tye-Din, PhD ImmusanT’s chief scientific officer, Bob Anderson, MD, PhD, is the senior author of the manuscript published today.

“This study demonstrates that proteins from barley and oats share the ability to activate a distinct subpopulation of gluten-responsive T cells in celiac disease”

“This study demonstrates that proteins from barley and oats share the ability to activate a distinct subpopulation of gluten-responsive T cells in celiac disease,” commented Dr. Anderson. “However, barley is much more efficient in stimulating the same subset of T cells. This is a noteworthy observation because clinicians have generally assumed in the past that gluten from each of the cereals toxic to celiac patients activates the same pool of gluten-reactive T cells in patients. Our study highlights that eating oats can have immune-activating effects similar to barley, and that future treatments for celiac disease will need to address gluten proteins that may not be present in wheat alone. ImmusanT is proud to contribute to the ongoing efforts to fully characterize the immunologic understanding of celiac disease.”

Wheat, rye, and barley are well known to contain gluten and cause gastrointestinal (GI) symptoms commonly associated with celiac disease. Oats do not contain gluten but instead are comprised of avenins, which are proteins that are considered to be non-toxic and tolerated by most celiac disease patients (source: The University of Chicago Celiac Disease Center). Despite this common knowledge, “the appropriateness of oats in the gluten-free diet has been pondered for over 20 years,” according to the Celiac Support Association (CSA).

“ImmusanT is committed to providing therapeutic and diagnostic solutions to people living with celiac disease. Through these published findings, we have provided the first in vivo evidence that although ingestion of oats activates avenin-specific T cells in celiac disease patients, the T cell response is rarely sufficient to reactivate celiac disease in the manner that is seen after patients consume wheat, rye or barley,” said Leslie Williams, president and chief executive officer of ImmusanT.

Although ingestion of oats alone rarely causes intestinal damage, one in 12 patients with celiac disease in the study showed elevated frequencies of T cells circulating in blood that respond to avenins. The research shows that while gluten-reactive T cells that respond to oats are commonly found in patients with celiac disease, these T cells are activated at higher rates by eating food that contains barley, as opposed to oats.

“This study shows that the peptides included in Nexvax2 that target wheat, rye and barley gluten-reactive T cells also address T cells responding to avenins, and cover the majority of the immune response in celiac disease,” continued Williams.

Nexvax2 is a therapeutic vaccine designed to restore immune tolerance to gluten and allow patients to resume an unrestricted diet. ImmusanT is also developing a toolbox of biomarkers including a proprietary, functional T cell test for use both as a standalone diagnostic for celiac disease and as a monitoring tool for Nexvax2.

Visit the Journal of Autoimmunity website to access the entire article. 

 

Released: 11/07/14


New Research Finds that Special Interest Lobbying Does Influence NIH Research Funding

In a new study, NYU Stern Professor Deepak Hegde and Bhaven Sampat of Columbia University investigate whether lobbying by special interest groups affects funding for research by the National Institutes of Health (NIH), a publicly funded federal agency and the world’s largest funder of medical research – nearly $30 billion each year. They found that lobbying does have an effect on NIH research grants, and showed the subtle mechanism of how lobbyists’ influence plays out.

“The NIH is known for funding research projects based on their scientific merit, but recent critics have alleged that disease advocates influence NIH funding decisions and distort funding toward research on diseases favored by special interest groups”

The authors analyzed lobbying and NIH funding for 955 rare and often fatal diseases – including Parkinson’s Disease, Cystic Fibrosis, Multiple Sclerosis, Sickle Cell Disease, Huntington’s Disease, Hodgkin’s Disease, Cerebral Palsy and Spina Bifida – between 1998 and 2008.

Key findings include:

·         Lobbying by disease advocates mobilizes political support in the form of Congressional “soft earmarks” for specific diseases. Soft earmarks refer to language in the reports that accompany Congressional appropriations bills urging the NIH to support research on particular diseases or research fields.

·         Lobbying is particularly effective in mobilizing political support when accompanied by scientific advances related to diseases and/or an increase in the number of related mortalities.

·         The NIH appears to respond to Congressional earmarks through special grant mechanisms (i.e., “Requests for Applications” and “Program Announcements”), which solicit research proposals in particular areas of research, rather than through grants for unsolicited investigator-initiated research.

·         The overall effect of lobbying and earmarks on NIH funding appears to be in the range of 3-15 percent of the agency’s new spending on rare diseases, which amounts to less than one-third of all NIH grants each year.

“The NIH is known for funding research projects based on their scientific merit, but recent critics have alleged that disease advocates influence NIH funding decisions and distort funding toward research on diseases favored by special interest groups,” says Professor Hegde. “Our research shows that the mechanisms for influence are complex, but that lobbying may have a useful, informational role and does impact federal funding for biomedical research. That said, the channels of political influence are subtle, affect only a small portion of funding and may not have a distortive effect on public science.”

The article, “Can Private Money Buy Public Science? Disease Group Lobbying and Federal Funding for Biomedical Research,” is forthcoming in Management Science

 

Released: 11/01/14


Study Says Blood Test for Brain Insulin Resistance Accurately Predicts Alzheimer’s Disease Risk

Brain insulin resistance is an abnormality in Alzheimer’s disease that contributes to neural cell damage and can be detected by a new blood test, according to a multi-site study that was published October 23 in the online issue of The FASEB Journal, The Journal of the Federation of American Societies for Experimental Biology. The highly statistically significant findings were made possible by a novel technique the researchers developed for measuring brain insulin resistance in living patients.

“This study shows that insulin resistance is a major central nervous system metabolic abnormality in AD that contributes to neural cell damage”

The technique involves using neuron-derived exosomes in the blood to measure insulin resistance in the brain as an indication of early-onset Alzheimer’s disease (AD). This new blood test can accurately reflect development of AD up to 10 years prior to clinical onset, the study said.

Prior to this study, it had not been possible to determine the prevalence of brain insulin resistance in living patients with AD. Nor had it been possible to determine how much time normally passes between the onset of brain insulin resistance and the appearance of clinically evident signs of AD.

In healthy individuals, the central nervous system (CNS) and other bodily tissues respond to insulin with enhanced uptake of glucose, an energy source for cells. The term “insulin resistance” describes a diverse range of reduced responses to insulin in the brain and peripheral tissues. Insulin resistance causes diminished glucose uptake in similar regions of the brain in both AD and type 2 diabetes.

Brain insulin resistance is caused by low insulin receptor signaling. This deficiency is attributable to its association with abnormal amounts of two different forms of insulin receptor substrate (IRS). The extent of these abnormalities appears to increase in patients as they progress along the AD spectrum, from mild cognitive impairment (MCI) to probable AD and with further worsening of AD.

The innovative approach used in this study allowed the researchers to extract and measure phosphorylated forms of IRS from isolated neural exosomes. Exosomes are tiny membrane-encased vesicles that are excreted from cells and are present in biological fluids such as blood, cerebrospinal fluid, etc. The ability to quantify the phosphorylated forms of IRS makes it possible to evaluate insulin resistance in the central nervous system using a blood-based assay with living patients.

The lead author of the study is Dimitrios Kapogiannis, MD, Clinical Investigator for the National Institutes of Health, in Bethesda, Md. and the Intramural Research Program, National Institute on Aging, in Baltimore, Md.

The study found that for patients with AD and type 2 diabetes, the mean levels of the two extracted phosphorylated forms of IRS and their ratio (known as the insulin resistance index) were significantly different than the values for the healthy control group. In addition, the researchers reported that the mean level of the brain insulin resistance index for AD was significantly higher than for either type 2 diabetes or frontotemporal dementia (FTD). 100 percent of the patients with AD in the study were correctly classified with the researcher’s technique, as were 97.5 percent of patients with type 2 diabetes. Thus, AD patients can be distinguished from the control subjects by the level of brain insulin resistance as measured by the novel blood test.

“This study shows that insulin resistance is a major central nervous system metabolic abnormality in AD that contributes to neural cell damage,” said Dr. Ed Goetzl, the senior author on the study and the originator of the exosome isolation technique. “As insulin resistance is a known condition in type 2 diabetes mellitus and is treatable with several classes of existing drugs, these treatments may be useful as part of a multi-agent program for AD.”

The exosome-based technology used in the study will be further developed by NanoSomiX, a sponsor of the study, to produce a commercially available blood-based assay for researchers in academia and pharmaceutical companies. The assay will provide valuable information to those that are developing drugs for AD by using a routine and cost effective approach for early identification of subjects for inclusion in clinical trials.

"This new assay measuring brain insulin resistance further strengthens our portfolio of blood-based biomarker assays for AD using neuron-derived exosomes," said John Osth, President and CEO of NanoSomiX. “We believe our assays will prove instrumental in identifying early-stage AD patients for entry in clinical trials and thereby help to enrich the study population. We invite pharmaceutical companies and university researchers to contact us about collaborating or partnering to generate additional data."

NanoSomiX will also be introducing an exosome-based blood test for p-tau, a biomarker for AD that is currently detected only in cerebrospinal fluid and with PET scans, in November.

Study sites for the just-published research included:

* Laboratory of Neurosciences, National Institute on Aging (Baltimore, Md.)

* The Department of Neurology, University of California-San Francisco (San Francisco, Calif.)

* Sanders-Brown Center on Aging, University of Kentucky (Lexington, Ky.)

* The Department of Neurology, Mayo Clinic (Rochester, Minn.)

* The Jewish Home of San Francisco (San Francisco, CA) 

 

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