Predicting Death is Difficult, Making it Difficult To Save Money on End of Life Care

MedicalResearch.com Interview with:

Amy Finkelstein PhD John & Jennie S. MacDonald Professor of Economics MIT Department of Economics National Bureau of Economic Research Cambridge MA 02139 

Dr. Finkelstein

Amy Finkelstein PhD
John & Jennie S. MacDonald Professor of Economics
MIT Department of Economics
National Bureau of Economic Research
Cambridge MA 02139 

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Although only 5% of Medicare beneficiaries die in a given year, they account for almost 25% of Medciare spending.

This fact about high end of life spending has been constantly used to refer to inefficiency of the US healthcare system. A natural observation is that the fact is retrospective, and it motivated us to explore a prospective analog, which would take as an input the probability of someone dying in a given year rather than her realized outcome. We therefore used machine learning techniques to predict death, and somewhat to our surprise we found that at least using standardized and detailed claims-level data, predicting death is difficult, and there are only a tiny fraction of Medicare beneficiaries for whom we can predict death (within a year) with near certainty.

Those who end up dying are obviously sicker, and our study finds that up to half of the higher spending on those who die could be attributed to the fact that those who die are sicker and sick individuals are associated with higher spending.   Continue reading

Secret Relationship of Regulatory T cells, Tregs, on Basophils

MedicalResearch.com Interview with:
“Basophil” by GreenFlames09 is licensed under CC BY 2.0Jagadeesh BAYRY, DVM, PhD, HDR

Scientist CRCN/Associate Professor-INSERM
Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 1138
Centre de Recherche des Cordeliers
PARIS , FRANCE

 

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Basophils are rare granulocytes that are important for the protection against helminth parasites. In addition, basophils mediate T helper 2 responses, support B cell differentiation, and thus establish a vital link between innate and adaptive immunity. Although rare in number, basophils are implicated in various pathological conditions due to the fact that they undergo rapid activation in response to a wide range of stimuli they receive. These stimuli induce the release of diverse immune mediators including cytokines and mediators of hypersensitivity reactions histamine and leukotriene. Basophils are well known for their pathogenic role in allergic diseases. Recent data also advocate basophils in the pathogenesis of autoimmune and other inflammatory diseases. Therefore, considering the impact of dysregulated functions of basophils on the immune response in various diseases, we deliberated that it is essential to understand the regulatory mechanisms by which basophils are kept in check.

Among immunoregulatory cells, CD4+CD25+FoxP3+ regulatory T cells (Tregs) have been widely studied for their role in immune tolerance and in the maintenance of immune homeostasis. Tregs modulate autoimmune and inflammatory responses by exerting direct suppressive effects on various immune cells including dendritic cells, T cells, macrophages, monocytes, B cells, neutrophils, natural killer cells, and mast cells. In view of emerging reports on the role of basophils in various pathological conditions, we investigated if Tregs are able to control the activation and functions of basophils.

In contrast to the central dogma on Tregs as immunosuppressors, we discovered that human basophils are refractory to Treg-mediated suppression. On the contrary, we found that Tregs stimulate resting basophils to induce the expression of activation markers CD69, CD203c, and CD13, and release cytokines IL-4, IL-8, and IL-13. Treg-induced activation of basophils involves IL-3 and STAT5 but was not contact-dependent. These results provide evidence of direct positive effects that human Tregs have on basophil activation and reveal a previously unrecognized feature of this cell subset well known for immunosuppressive functions.  Continue reading

First Potential Treatment For Brain Damage From Cosmic Radiation

MedicalResearch.com Interview with:
“Space Shuttle Model” by terren in Virginia is licensed under CC BY 2.0Susanna Rosi, PhD
Director of Neurocognitive Research
Brain and Spinal Injury Center
Professor in the departments of Physical Therapy and Rehabilitation Science and of Neurological Surgery
UCSF

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: NASA and private space companies like SpaceX plan to send humans to the red planet within the next 15 years — but among the major challenges facing future crewed space missions is how to protect astronauts from the dangerous cosmic radiation of deep space.

In this study we identified the first potential treatment for the brain damage caused by exposure to cosmic rays — a treatment can be given after exposure and that prevents memory impairment in mice exposed to simulated space radiation.

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End of Honeymoon Period Means Whooping Cough Can Resurge

MedicalResearch.com Interview with:

This Gram-stained photomicrograph depicts numbers of Bordetella pertussis bacteria, which is the etiologic pathogen for pertussis, also known as whooping cough.

This Gram-stained photomicrograph depicts numbers of Bordetella pertussis bacteria, which is the etiologic pathogen for pertussis, also known as whooping cough.
CDC image

Matthieu Domenech de Cellès PhD
Department of Ecology and Evolutionary Biology
University of Michigan, Ann Arbor, MI, USA.
Biostatistics, Biomathematics, Pharmacoepidemiology, and Infectious Diseases Unit
Institut Pasteur, Inserm,
University of Versailles St-Quentin-en-Yvelines,
Versailles, France.

MedicalResearch.com: What is the background for this study? What are the main findings?

 

Response: Our main motivation was to elucidate an apparent paradox: Why has the US experienced a resurgence of pertussis (whooping cough) since the mid-1970s, despite persistently high vaccine coverage? A variety of hypotheses have been proposed to explain this resurgence, but most attention has focused on the potential shortcomings of the new generation of pertussis vaccines (called acellular pertussis vaccines). However, there remains considerable uncertainty about the degree and the mechanisms of protection conferred by pertussis vaccines.

Via a collaboration with the local department of public health, we used detailed surveillance data in the state of Massachusetts to test a number of hypotheses about pertussis vaccines. We found that, although pertussis vaccines are imperfect (in the sense that they do not provide lifelong, 100% protection to 100% of children vaccinated), they are still highly efficacious. Specifically, we estimated that vaccine protection wanes over time, but slowly, with about 85% of children still protected 10 years after vaccination. Despite this high vaccine efficacy, we showed that the resurgence of pertussis was, in fact, to be expected. What happens is that the introduction of routine vaccination leads to an overall reduction in transmission, not only in vaccinated children but also in the population at large. Accordingly, those who escaped vaccination as children (as a consequence of incomplete vaccine coverage or imperfect vaccine protection) increasingly age having also avoided natural infection. As a result, the number of individuals susceptible to contract pertussis gradually increases. Because such people are the “fuel” of epidemics, this sets the stage for pertussis’ resurgence, with increasing incidence among older individuals.

This overall effect is called the “end-of-honeymoon” and means that resurgence is therefore a predictable consequence of incomplete vaccination with efficacious, but imperfect, vaccines. Importantly, these results show that recent trends do not necessarily reflect recent changes in the epidemiology of pertussis. Rather, they may be interpreted as a legacy of past immunization practices, with long-to-manifest effects. This is a significant shift of perspective about pertussis epidemiology.  Continue reading

Obesity Fuels Resistance To Anti-VEGF Therapy in Breast Cancer Patients

MedicalResearch.com Interview with:

Dr. Fukumura

Dr. Fukumura

Dai Fukumura, M.D., Ph.D
Associate Professor, Radiation Oncology
Harvard Medical School
Deputy Director, Edwin L. Steele Laboratory,
Radiation Oncology, Massachusetts General Hospital
Boston, MA 

 

 

Joao Incio

Dr. Incio

Dr. Joao Incio PhD
Post-Doc, Edwin L. Steele Laboratory

 

 

 

 

 

Dr. Rakesh K. Jain PhD

Dr. Jain

Dr. Rakesh K. Jain PhD
Andrew Werk Cook Professor of Tumor Biology and director of the Edwin L. Steele Laboratories for Tumor Biology
Rradiation oncology department
Massachusetts General Hospital and Harvard Medical School.

 

MedicalResearch.com: What is the background for this study?  

Response: Based on promising data from preclinical studies and subsequent increase in progression-free survival in patients, anti-vascular endothelial growth factor (VEGF) therapy received accelerated approval for metastatic breast cancer. However, this approval was withdrawn in the United States based on the lack of overall survival benefit in several subsequent phase III studies in metastatic and adjuvant settings. Potential mechanisms of resistance to anti-VEGF therapy include the upregulation of alternative angiogenic and pro-inflammatory factors. Production of some of these factors has been shown to increase in obesity specifically in hypoxic adipose tissues including the breast. Given that up to 70% of breast cancer (BC) patients in the United States are overweight or obese, we addressed one simple but important question in this study: Is obesity contributing to anti-VEGF treatment resistance in breast cancer?

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Dietary Fiber Promotes Beneficial Bacteria, Improving Glucose Control in Diabetes

MedicalResearch.com Interview with:

Liping Zhao PhD, Professor Department of Biochemistry and Microbiology School of Environmental and Biological Sciences Rutgers University-New Brunswick NJ

Dr. Zhao

Liping Zhao PhD, Professor
Department of Biochemistry and Microbiology
School of Environmental and Biological Sciences
Rutgers University-New Brunswick NJ

MedicalResearch.com: What is the background for this study?

Response: Microbes in the human gut (collectively known as the gut microbiota) provide many functions that are important for human health. A notable example is that some gut bacteria are able to ferment non-digestible carbohydrates in our diet, e.g. dietary fibers, to produce short-chain fatty acids (SCFAs). These SCFAs nourish our gut epithelial cells, reduce inflammation, and play a role in appetite control. Deficiency of SCFAs has been associated with many diseases including type 2 diabetes. Many gut bacteria have the genes (and therefore the capacity) to produce SCFAs from carbohydrate fermentation. However, we know little about how these bacteria, as individual strains and as a group, actually respond to an increased supply of carbohydrates. This is key to improve clinical efficacy of dietary fiber interventions to improve human health. Continue reading

Babies Can Understand When The Effort Might Be Worth The Reward

MedicalResearch.com Interview with:

Shari Liu Dept Psychology Harvard University Cambridge, MA 02138 

Shari Liu -image by Kris Brewer.

Shari Liu
Dept Psychology
Harvard University
Cambridge, MA 02138 

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Every day, we look out into the social world and see more than pixels changing across our retinas, or bodies moving in space. We see people brimming with desires, governed by their beliefs about the world and concerned about the costs of their actions and the potential rewards those actions may bring. Reasoning about these mental variables, while observing only people’s overt behaviors, is at the heart of commonsense psychology. Continue reading

Small Cell Lung Cancers Form Chemotherapy-Resistant Circulating Tumor Spheres

MedicalResearch.com Interview with:

Prof. Gerhard Hamilton Department of Obstetrics and Gynecology Medical University of Vienna 

Prof. Hamilton

Prof. Gerhard Hamilton
Department of Obstetrics and Gynecology
Medical University of Vienna

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Small cell lung cancer (SCLC) is a highly aggressive tumor (15 % of all lung cancers) mainly of patients with high tobacco consumption which shows an extremely poor survival (< 5% 2-year survival rate). Unfortunately the
low survival rates of advanced SCLC cases has not improved significantly during the last decades, with platinum drugs/etoposide and topotecan employed for first- and second-line chemotherapy, respectively. All kinds of new chemotherapeutics, targeted drugs and immunotherapies either failed or resulted in prolongation of survival of several months at best. SCLC responds well to first-line therapy but relapses within a short time as chemoradioresistant tumor. The failure of hundreds of registered studies seem to be linked to the lack of knowledge of the mechanism of resistance of SCLCs and proper ways to reverse the refractoriness.

Small cell lung cancer is distinguished by excessive numbers of circulating tumor cells (CTCs) in advanced stages. CTCs contain the founder of metastasis and seem to constitute a highly chemoresistant cell population. Thus, we ware able to establish a panel of permanent CTC lines in vitro for the first time (8 SCLC lines so far from blood samples). Although CTCs were considered to be chemoresistant we detected that they are chemosensitive in vitro in form of single cell suspensions. However, all CTC lines developed spontaneously into large multicellular aggregates, termed tumorospheres, which grow up to 1-2 mm in size and exhibit high chemoradioresistance due to limited drug perfusion as well as content of quiescent and hypoxic cells. Resistance to irradiation seems to be caused by lack of oxygen, such limiting the generation of oxygen radicals. High resistance mediated by the occurrence of tumorospheres easily explains the failure of a large number of drugs – if one is not able to achieve a sufficient concentration of a drug in cancer cells and the cells are quiescent, the respective compounds will not be able to destroy the target cells, regardless of their chemical nature.

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Methylene Blue Has Potential As Anti-Aging Agent in Skin Care Products

MedicalResearch.com Interview with:

Kan Cao PhD Associate professor of cell biology and molecular genetics University of Maryland

Dr. Kan Cao

Kan Cao PhD
Associate professor of cell biology and molecular genetics
University of Maryland

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: In 2015, our group demonstrated a surprising positive effect of methylene blue in treating fibroblast cells from progeria patients, a severe premature aging disease. Interestingly, we also noticed a beneficial effect of methylene blue in protecting normal skin cells.

In this study, we followed the initial observation, compared methylene blue with other popular antioxidants, and conducted further analysis of the effects of methylene blue in 3d reconstructed skin.

The take home message is that we believe methylene blue has a great anti-aging potential. As it is also super safe, we suggest it a potent ingredient for skin care products.

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Drug For Diabetic Neuropathy May Also Target an Aggressive Form of Breast Cancer

MedicalResearch.com Interview with:
Chenfang Dong
Department of Pathology and Pathophysiology
Zhejiang Key Laboratory for Disease Proteomics
Zhejiang University School of Medicine
Hangzhou China 

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Basal-like breast cancer (BLBC), which generally falls into the triple-negative breast cancer subtype, is associated with an aggressive clinical history, early recurrence, distant metastasis and shorter survival. The treatment of BLBC is an unmet medical need due to the absence of effective targeted therapies and poor response to standard chemotherapy. Therefore, elucidating the determinants of aggressiveness and identifying the relevant targets in BLBC are urgently needed. In this study, we report that aldo-keto reductase 1 member B1 (AKR1B1) overexpression occurs specifically in BLBC and predicts poor prognosis in breast cancer patients.

Our data reveal that AKR1B1 as a key modulator of tumor aggressiveness provides tumorigenic and metastatic advantage in basal-like breast cancer through a positive regulatory feedback loop that activates the EMT program and enhances CSC-like properties. Interestingly, epalrestat, the only AKR1B1 inhibitor that has been approved in Japan for the targeted treatment of diabetic complications, significantly inhibited cancer cell migration and invasion in vitro, suppressed tumorigenicity and metastasis of BLBC cells in mice models, displaying potent efficacy against BLBC.

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Intestinal E. coli Linked to Arthritis in Inflammatory Bowel Disease

MedicalResearch.com Interview with:

Randy Longman, M.D. / Ph.D. Assistant Professor of Medicine Jill Roberts Center and Institute for Research in Inflammatory Bowel Disease Weill Cornell Medicine Division of Gastroenterology and Hepatology Joan and Sanford I. Weill Department of Medicine Department of Microbiology and Immunology New York, NY 10021

Dr. Randy Longman

Randy Longman, M.D. / Ph.D.
Assistant Professor of Medicine
Jill Roberts Center and Institute for Research in Inflammatory Bowel Disease
Weill Cornell Medicine
Division of Gastroenterology and Hepatology
Joan and Sanford I. Weill Department of Medicine
Department of Microbiology and Immunology
New York, NY 10021 

MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Inflammatory bowel disease is not limited to intestinal inflammation.  Up to 1/3 of patients with active disease suffer from extra-intestinal manifestations.

The most common extra-intestinal manifestations in IBD is joint inflammation or spondyloarthritis.  Peripheral joint spondyloarthritis  carries a prevalence of 20% in Crohn’s Disease and 10% in Ulcerative Colitis, predominantly affecting joints of the lower limbs.  It has long been suggested that gut bacteria can drive this systemic joint inflammation, but microbial targets have not been characterized.

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Reduced Stem Cells Link Congenital Heart Disease To Impaired Brain Growth

MedicalResearch.com Interview with:

Childrens National Research Team

Children’s National Research Team

Paul D. Morton, Ph.D.
Research PostDoc and lead study author of “Abnormal Neurogenesis and Cortical Growth in Congenital Heart Disease.”
Children’s National Health System Washington, DC

Nobuyuki Ishibashi, M.D.
Director of the Cardiac Surgery Research Laboratory at Children’s National Health System and co-senior study author.

Vittorio Gallo, Ph.D.
Director of the Center for Neuroscience Research at Children’s National Health System and co-senior study author.

 

 

Richard A. Jonas, M.D.
Chief of the Division of Cardiac Surgery at Children’s National Health System and co-senior study author.

MedicalResearch.com: What is the background for this study?

Response: Congenital heart disease (CHD) is the leading birth defect in the United States and often results in an array of long-term neurological deficits including motor, cognitive and behavioral abnormalities. It has become increasingly clear that children with CHD often have underdeveloped brains. In many cases of complex CHD, blood flow to the brain is both reduced and less oxygenated, which has been associated with developmental abnormalities and delay. The cellular mechanisms underlying the impact of CHD on brain development remain largely unknown. We developed a preclinical chronic hypoxia model to define these mechanisms.

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Syrosingopine Plus Metformin Have Potential Anti-Cancer Effects

MedicalResearch.com Interview with:
Dr. Don Gary Benjamin
Biozentrum, University of Basel
Basel, Switzerland.

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: We initiated the study to find a co-drug that would increase the anti-cancer effect of the commonly prescribed anti-diabetic drug metformin. Metformin is a very well tolerated medication, however the dosage required to show anti-cancer activity is higher than that usually prescribed, hence the aim of the study. We found that metformin in combination with a second drug, syrosingopine (an anti-hypertensive), potently kills cancer cells in a variety of pre-clinical models. Quite nicely, both these drugs combine to kill the cells at a concentration where they have no impact on cell growth when applied singly.

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Familial Hypercholesterolemia Diagnosed Through EHR and Genetics Data

MedicalResearch.com Interview with:

Michael F. Murray MD Geisinger Health System Danville, PA 17822

Dr. Michael Murray

Michael F. Murray MD
Geisinger Health System
Danville, PA 17822

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: The DiscovEHR cohort was formed as a result of a research collaboration between Geisinger Health System and Regeneron Pharmaceuticals. There are over 50,000 patient participants in the cohort who have volunteered to have their de-identified genomic sequence data linked to their de-identified EHR data for research purposes. We report in this paper findings around the identification of 229 individuals (1:256) with pathogenic or likely pathogenic variants in one of the three genes (LDLR, APOB, PCSK9) associated with Familial Hypercholesterolemia (FH). The study found that these individuals are unlikely to carry a diagnosis of FH and are at risk for early coronary artery disease.

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Gum Disease Linked to Autoimmunity in Rheumatoid Arthritis

MedicalResearch.com Interview with:

Maximilian F. Konig, MD Department of Medicine Massachusetts General Hospital Harvard Medical School

Dr. Maximilian F. Konig

Maximilian F. Konig, MD
Division of Rheumatology,
Johns Hopkins University School of Medicine
Current affiliation:
Department of Medicine
Massachusetts General Hospital
Harvard Medical School

MedicalResearch.com: What is the background for this study?

Response:The idea that rheumatoid arthritis (RA), an autoimmune disease that leads to chronic joint inflammation and destruction, may be initiated by a bacterial infection is not novel, but has been posited for more than a century. Based on the clinical observation that patients with RA frequently have severe periodontal disease (gum disease), gum inflammation has long been thought to contribute to disease development in RA. However, limited understanding of the mechanisms that fuel and sustain the autoimmune attack in RA made it difficult to pinpoint a specific bacterial trigger.

In recent years, our understanding of the abnormal immune response that attacks the joints in patients with RA has grown exponentially, and we now know that disease-specific autoantibodies (ACPAs) target modified self-proteins (this modification is known as citrullination). It is this abnormal immune response against citrullinated proteins that appears to drive the joint (and sometimes lung) inflammation seen in rheumatoid arthritis. Recent studies from our laboratory at The Johns Hopkins University (led by principle investigator Felipe Andrade, MD, PhD) suggested that an immune cell called the neutrophil, which normally protects us from infection at sites like the oral cavity or anywhere else in the body, also appears to be the source of the proteins attacked in RA. We were therefore interested to understand what drives the association of gum disease, an inflammation commonly triggered by bacteria, with RA.

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Diabetes Drug May Slow Progression of Parkinson’s Disease

MedicalResearch.com Interview with:

Patrik Brundin, M.D., Ph.D. Director, Center for Neurodegenerative Science Van Andel Research Institute

Dr. Patrik Brundin

Patrik Brundin, M.D., Ph.D.
Director, Center for Neurodegenerative Science
Van Andel Research Institute

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: The investigational drug at the heart of our study, MSDC-0160, has been in development to treat type 2 diabetes by improving cellular metabolism.

In Parkinson’s, reductions in cellular metabolism slow down vital housekeeping processes that clear out toxic proteins that otherwise accumulate with age. If these proteins aren’t removed, they clump together, leading to the damage and cell death that causes Parkinson’s hallmark symptoms, such as rigidity and tremor. MSDC-0160 helps keep these housekeeping processes working, ultimately protecting the brain.

We demonstrated that MSDC-0160 has strong, reproducible, positive effects across multiple models of Parkinson’s disease—it rescued dopamine-producing cells, improved behavioral deficits in mouse models and reversed inflammation. Overall, we believe it is a strong candidate for repurposing as a potential treatment that actually may slow the disease’s progression, rather than only mitigating symptoms.

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Protein Found To Enhance Ability To Kill MRSA

MedicalResearch.com Interview with:

Warren Leonard, M.D. NIH Distinguished Investigator Laboratory of Molecular Immunology NHLBI, NIH

Dr. Warren Leonard

Warren Leonard, M.D.
NIH Distinguished Investigator
Laboratory of Molecular Immunology
NHLBI, NIH

MedicalResearch.com: What is the background for this study?

Response: TSLP is a cytokine that has been well studied in the context of T cell helper type 2 (TH2) responses and the promotion of atopic diseases. TSLP is naturally expressed at barrier surfaces, such as the skin; however, its role in skin infections was not previously explored.

In our study, we investigated whether TSLP plays a role in host defense to Staphylococcus aureus skin infections, using the most common strain of methicillin-resistant S. aureus (MRSA) present in the United States.

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First Childhood Exposure Determines How Sick You Get From Flu As Adult

MedicalResearch.com Interview with:
Katelyn M. Gostic and
Monique Ambrose

Department of Ecology and Evolutionary Biology
University of California
Los Angeles

MedicalResearch.com: What is the background for this study? What are the main findings?

Monique Ambrose: Influenza pandemics pose a serious, recurrent threat to human public health. One of the most probable sources of future pandemic influenza viruses is the pool of influenza A virus (IAV) subtypes that currently circulate in non-human animals. It has traditionally been thought that the human population is immunologically naïve and unprotected against these unfamiliar subtypes. However, our work suggests that an individual ‘imprints’ to the influenza A virus (IAV) encountered in early childhood in such a way that they retain protection against severe disease if they later encounter a novel IAV subtype that belongs to the same genetic group as their first exposure.

Our research looked at human cases of H5N1 and H7N9, two avian IAV subtypes of global concern, to investigate what factors most strongly predicted risk of severe disease. The most striking explanatory factor was childhood IAV imprinting: our results suggest that individuals who had childhood imprinting on an IAV in the same genetic group as the avian IAV they encountered later in life experienced 75% protection against severe disease and 80% protection against death.

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Histone Switch Allows Some Cancer Cells To Become Immortal

MedicalResearch.com Interview with:

Paola Scaffidi, PhD Group Leader Cancer Epigenetics Laboratory The Francis Crick Institute London

Dr. Paola Scaffidi

Paola Scaffidi, PhD
Group Leader
Cancer Epigenetics Laboratory
The Francis Crick Institute
London

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Every cancer is different, but even within the same tumor cells are highly diverse, and only some of them are truly immortal and drive tumor growth. This is quite surprising if we think that cancer arises from one cell that keeps replicating itself. So why are some cancer cells more dangerous than others? And why do some cells “get tired” along the way and, at some point, stop dividing?

In our study we describe one cellular mechanism that provides some answers to these questions. We have found that to be able to divide indefinitely, cancer cells have to strongly reduce the levels of a nuclear protein called histone H1.0. This is needed to allow activation of many genes important for cancer cell proliferation, which otherwise would be somehow “hidden” within the cell nucleus. Importantly, though, while tumors grow, some cells raise back the levels of H1.0, which hides these genes again and makes the cells stop proliferating. So the end result is that within the same tumor we have a mix of cells, some which keep these important genes on, while others switch them off and, as a consequence, lose their ability to divide, and differentiate into a more mature state.

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Ingestible Sensor Demonstrates Positive Effects of Cinnamon

MedicalResearch.com Interview with:

Distinguished Professor Kourosh Kalantar-zadeh RMIT's School of Engineering Australia

Prof. Kourosh Kalantar-Zadeh

Distinguished Professor Kourosh Kalantar-Zadeh
RMIT’s School of Engineering
Australia

MedicalResearch.com: What is the background for this study? What are the main findings?

1- The development of “swallow-able gas sensor capsules”. This was the final test on animals and focused on the measurement of a food supplement (cinnamon) to show the extraordinary capability of this noninvasive tool that will revolutionise the future of Gastroenterology and Food Sciences

2- That cinnamon can improve the health of the stomach, and hence our overall health, by adjusting the acidity and enzymatic secretion in the stomach. So the good effect of cinnamon is not just a grandparent old advice – It is real.

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