Study confirms anatomic existence of the elusive G-spot
April 25, 2012
For centuries, women have been reporting engorgement of the upper, anterior part of the vagina during the stage of sexual excitement, despite the fact the structure of this phenomenon had not been anatomically determined.
A new study published in The Journal of Sexual Medicine documents that this elusive structure does exist anatomically.
Adam Ostrzenski, M.D., Ph.D., of the Institute of Gynecology in St. Petersburg, FL, conducted a stratum-by-stratum anterior vaginal wall dissection on an 83-year-old cadaver. The dissection established the presence of the G-spot, a well-delineated sac structure located on the dorsal (back) perineal membrane, 16.5 mm from the upper part of the urethral meatus, creating a 35 degree angle with the lateral (side) border of the urethra.
Having 3 distinct regions, the G-spot emerged with dimensions of length (L) of 8.1 mm x width (W) 3.6 mm to 1.5 mm x height (H) 0.4 mm. Upon removal of the entire structure with the adjacent margin tissues, the G-spot stretched from 8.1 to 33 mm.
“This study confirmed the anatomic existence of the G-spot, which may lead to a better understanding and improvement of female sexual function,” Ostrzenski concludes.
Irwin Goldstein, editor-in-chief of The Journal of Sexual Medicine believes that research in women’s sexual health issues is important. “This case study in a single cadaver adds to the growing body of literature regarding women’s sexual anatomy and physiology.”
Contact: Amy Molnar
healthnews@wiley.com
201-748-8844
Wiley-Blackwell
Excessive worrying may have co-evolved with intelligence
April 12, 2012
Worrying may have evolved along with intelligence as a beneficial trait, according to a recent study by scientists at SUNY Downstate Medical Center and other institutions. Jeremy Coplan, MD, professor of psychiatry at SUNY Downstate, and colleagues found that high intelligence and worry both correlate with brain activity measured by the depletion of the nutrient choline in theGlaxoSmithKline Pharmaceuticals, Sackler Institute of Columbia University, NIH/National Institute of Mental Health, National Alliance for Research on Schizophrenia and Depression, Psychiatric Institute subcortical white matter of the brain. According to the researchers, this suggests that intelligence may have co-evolved with worry in humans.
“While excessive worry is generally seen as a negative trait and high intelligence as a positive one, worry may cause our species to avoid dangerous situations, regardless of how remote a possibility they may be,” said Dr. Coplan. “In essence, worry may make people ‘take no chances,’ and such people may have higher survival rates. Thus, like intelligence, worry may confer a benefit upon the species.”
In this study of anxiety and intelligence, patients with generalized anxiety disorder (GAD) were compared with healthy volunteers to assess the relationship among intelligence quotient (IQ), worry, and subcortical white matter metabolism of choline. In a control group of normal volunteers, high IQ was associated with a lower degree of worry, but in those diagnosed with GAD, high IQ was associated with a greater degree of worry. The correlation between IQ and worry was significant in both the GAD group and the healthy control group. However, in the former, the correlation was positive and in the latter, the correlation was negative. Eighteen healthy volunteers (eight males and 10 females) and 26 patients with GAD (12 males and 14 females) served as subjects.
Previous studies have indicated that excessive worry tends to exist both in people with higher intelligence and lower intelligence, and less so in people of moderate intelligence. It has been hypothesized that people with lower intelligence suffer more anxiety because they achieve less success in life.
The results of their study, “The Relationship between Intelligence and Anxiety: An Association with Subcortical White Matter Metabolism,” was published in a recent edition of Frontiers in Evolutionary Neuroscience, and can be read at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3269637/pdf/fnevo-03-00008.pdf.
The study was selected and evaluated by a member of the Faculty of 1000 (F1000), placing it in their library of the top 2% of published articles in biology and medicine.
SUNY Downstate Medical Center, founded in 1860, was the first medical school in the United States to bring teaching out of the lecture hall and to the patient’s bedside. A center of innovation and excellence in research and clinical service delivery, SUNY Downstate Medical Center comprises a College of Medicine, Colleges of Nursing and Health Related Professions, a School of Graduate Studies, a School of Public Health, University Hospital of Brooklyn, and an Advanced Biotechnology Park and Biotechnology Incubator.
SUNY Downstate ranks eighth nationally in the number of alumni who are on the faculty of American medical schools. More physicians practicing in New York City have graduated from SUNY Downstate than from any other medical school.
Contact: Ron Najman
ron.najman@downstate.edu
718-270-2696
SUNY Downstate Medical Center
On the path to age-defying therapies
March 30, 2012
FINDINGS: The drug rapamycin has been shown to extend lifespan in lab animals, yet rapamycin has also been linked to impaired glucose tolerance and insulin sensitivity, two hallmarks of diabetes. By teasing apart rapamycin’s activity at the cellular level, researchers at Whitehead Institute and the University of Pennsylvania have determined that inhibiting only the protein cluster known as the mechanistic target of rapamycin complex 1 (mTORC1) prolongs life in mice without adversely affecting glucose tolerance or insulin sensitivity.
RELEVANCE: With this novel understanding of how rapamycin produces its anti-aging effects, researchers may be able to develop a drug that specifically targets mTORC1, thereby promoting longevity while preventing the adverse effects associated with rapamycin.
CAMBRIDGE, Mass. (March 29, 2012) – One of the secrets to a longer, healthier life is simply to eat less. When subjected to calorie restriction (CR), typically defined as a 20-40% reduction in caloric intake with corresponding maintenance of proper nutrition, animals in labs not only live longer, but also have improved insulin sensitivity and glucose tolerance, both of which decline during aging.
Yet, for all of its benefits, CR’s restricted diet is a stumbling block for most Americans. If only we had a drug that could do the same thing.
Well, we do, sort of. The drug rapamycin, which is used for immunosuppression in organ transplantations, mimics the longevity effects of CR and may tap into the same cellular pathway as CR. Unlike CR, however, rapamycin actually impairs glucose tolerance and insulin sensitivity, two hallmarks of diabetes. Clearly, rapamycin is doing something CR is not.
To understand better rapamycin’s benefits and risks, researchers from the lab of Whitehead Institute Member David Sabatini and Joseph Baur, assistant professor of Physiology, at the University of Pennsylvania’s Perelman School of Medicine, have discovered precisely how rapamycin is behaving at the cellular level. Their intriguing results are published this week in the journal Science.
“We know that despite its adverse effects, rapamycin still prolongs lifespan, so there’s a potential that we could make it better by just having lifespan affected and not induce the adverse effects,” says Sabatini, who is a professor of biology at MIT and a Howard Hughes Medical Institute (HHMI) investigator. “The data in this paper suggest that it’s possible.”
Rapamycin, which is also called sirolimus and marketed in the United States as Rapamune, is a known inhibitor of the mechanistic target of rapamycin complex 1 (mTORC1), a protein complex that regulates many cellular processes linked to growth and differentiation. mTORC1 is part of a cellular signaling pathway, called mTOR, which responds to nutrients and growth factors. Mechanistic target of rapamycin complex 2 (mTORC2) is also part of the mTOR pathway and regulates insulin signaling.
Rapamycin has generally been thought to target primarily mTORC1. But work by Dudley Lamming and Lan Ye, co-authors of the Science paper and postdoctoral fellows in the Sabatini and Baur labs respectively, indicates that in mice, rapamycin also inhibits mTORC2, thereby reducing insulin sensitivity.
To see if rapamycin’s positive effects on lifespan effects could be separated from its negative metabolic effects, Lamming and Ye bred mice whose mTORC1 activity was partially inhibited but whose mTORC2 activity remained largely intact. The females of this mouse population lived longer than control mice while maintaining normal insulin sensitivity.
“This shows that disrupting mTORC1 alone is capable of extending lifespan, if you can find a way do that,” says Lamming.
For Baur, the experiments’ results indicate that there is a possibility of identifying a better anti-aging drug than rapamycin.
“Our work highlights the potential utility of molecules that target mTORC1 specifically and suggests there is hope that by targeting this pathway, you could really get something that ameloriates age-related diseases without causing more problems than it solves,” says Baur. “If you’re taking an anti-aging drug as a preventive measure, you probably don’t want to pay the price of diabetes.”
This work was supported by the National Institutes of Health (NIH), the National Cancer Institute (NCI), the American Federation of Aging Research (AFAR), the Institute on Aging at the University of Pennsylvania, the Damon Runyon Cancer Research Foundation, the American Heart Association, and the Academy of Finland.
Written by Nicole Giese Rura
David Sabatini’s primary affiliation is with Whitehead Institute for Biomedical Research, where his laboratory is located and all his research is conducted. He is also a Howard Hughes Medical Institute investigator and a professor of biology at Massachusetts Institute of Technology.
Full Citation:
“Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity”
Science, published March 30, 2012
Dudley W. Lamming (1*), Lan Ye (2*), Pekka Katajisto (1), Marcus D. Goncalves (3), Maki Saitoh (1), Deanna M. Stevens (1), James G. Davis (2), Adam B. Salmon (4), Arlan Richardson (4), Rexford S. Ahima (3), David A. Guertin (1,5), David M. Sabatini (1), and Joseph A. Baur (2).
1. Whitehead Institute for Biomedical Research, Cambridge MA 02142; Department of Biology, MIT, Cambridge, MA 02139; Howard Hughes Medical Institute, MIT, Cambridge, MA 02139; Broad Institute of Harvard and MIT, Seven Cambridge Center, Cambridge, MA 02142; The David H. Koch Institute for Integrative Cancer Research at MIT, Cambridge, MA 02139
2,3. Institute for Diabetes, Obesity, and Metabolism and Departments of 2:Physiology and 3:Medicine, University of Pennsylvania School of Medicine, Philadelphia PA 19104
4. The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio TX.
5. Present Address: University of Massachusetts Medical School, Worcester, MA
* These authors contributed equally to this work
Contact: Nicole Giese Rura
rura@wi.mit.edu
617-258-6851
Whitehead Institute for Biomedical Research
Is there good research evidence for health systems interventions?
March 21, 2012
Research evidence is key to developing strong health systems, but the assessment of such evidence is not always straightforward. This week in PLoS Medicine, the last paper in a three-part series on health systems guidance addresses the question of how much confidence to place in different types of research evidence, which the authors argue is key to informing judgements regarding policy options to address health systems problems.
Simon Lewin from the Norwegian Knowledge Centre for the Health Services in Oslo, Norway and colleagues say that useful tools are available to assess evidence of the effectiveness of various health systems interventions, but that there remains a need to develop tools to assist judgements regarding evidence from systematic reviews on other key factors such as the acceptability of policy options to stakeholders, implementation feasibility, and equity.
In a related Perspective article that reflects on the entirety of the three-part health systems guidance series, David Peters and Sara Bennett from Johns Hopkins University in Baltimore, USA (uninvolved in the series) say that the series offers important contributions to improving the quality of evidence-informed decision-making in health systems. But they also caution against being too rigid when developing approaches to the development of guidelines and applying evidence to policy.
Peters and Bennett conclude that “Recognizing the diversity of stakeholders and complexity of health systems issues, it will be important to ensure that evidence-informed guidelines that emerge are tested with continued humility and skepticism, and that they do not become rigid models for inquiry dominated by a limited number of disciplines. They should not serve to blind us toward the need to address a wide variety of questions and incorporate the different types of evidence brought to bear by many fields of science. Further guidance is one important way to shape policy, but we must not fail to situate it in the broader context of sustained dialogue between researchers and policy makers.”
Article by Simon Lewin and colleagues
Funding: The development of the Handbook was supported by a grant to the WHO by the Rockefeller Foundation, which had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The paper represents the views of the authors and neither WHO nor the Rockefeller Foundation.
Competing Interests: The Swiss Tropical and Public Health Institute and the Norwegian Knowledge Centre for the Health Services received funds from the WHO for the contributions of DD, PS, LB, SL, and XBC to developing a Handbook to produce health systems guidance, and some of this work is reported in this article. DG is a member of the PLoS Medicine Editorial Board. EAA and GEV are members of the GRADE Working Group. All other authors declare no competing interests.
Citation: Lewin S, Bosch-Capblanch X, Oliver S, Akl EA, Vist GE, et al. (2012) Guidance for Evidence-Informed Policies about Health Systems: Assessing How Much Confidence to Place in the Research Evidence. PLoS Med 9(3): e1001187. doi:10.1371/journal.pmed.1001187
CONTACT:
Simon Lewin
Norwegian Knowledge Centre for the Health Services
Oslo
Norway
simon.lewin@nokc.no
Perspective by David Peters and Sara Bennett
Funding: No specific funding was provided for writing this article.
Competing Interests: SB in the past has been a co-author on papers with authors of the health systems guidance series: Lucy Gilson (2011), John Lavis (2009), Gunn Vist (2008), Andy Haines (2004), and Rifat Atun (unpublished policy brief in 2008). SB was employed under the same grant programme during the 1990s with Gilson. John Lavis and Lucy Gilson have served on the Scientific and Technical Advisory Committee of the Alliance for Health Policy and Systems Research, and John-Arne Rottingen is the Chair of the Alliance Board, on which SB also serves. Fadi El-Jardali and Lucy Gilson are on the Editorial Advisory Board of the journal Health Policy and Planning, for which SB is a co-editor. DHP has declared that no competing interests exist.
Citation: Peters DH, Bennett S (2012) Better Guidance Is Welcome, but without Blinders. PLoS Med 9(3): e1001188. doi:10.1371/journal.pmed.1001188
CONTACT:
David Peters
Johns Hopkins University Bloomberg School of Public Health
Baltimore
Maryland
United States of America
dpeters@jhsph.edu
First paper in PLoS Medicine series on health systems guidance, published March 6th:
Bosch-Capblanch X, Lavis JN, Lewin S, Atun R, Røttingen J-A, et al. (2012) Guidance for Evidence-Informed Policies about Health Systems: Rationale for and Challenges of Guidance Development. PLoS Med 9(3): e1001185. doi:10.1371/journal.pmed.1001185
Second paper in PLoS Medicine series on health systems guidance, published March 13th:
Lavis JN, Røttingen J-A, Bosch-Capblanch X, Atun R, El-Jardali F, et al. (2012) Guidance for Evidence-Informed Policies about Health Systems: Linking Guidance Development to Policy Development. PLoS Med 9(3): e1001186. doi:10.1371/journal.pmed.1001186
Contact: Clare Weaver
press@plos.org
44-122-344-2834
Public Library of Science
The mathematics of a heart beat could save lives
February 17, 2012
What we perceive as the beating of our heart is actually the co-ordinated action of more than a billion muscle cells. Most of the time, only the muscle cells from the larger heart chambers contract and relax. But when the heart needs to work harder it relies on back-up from the atrial muscle cells deep within the smaller chambers (atria) of the heart.
The health of these ‘high-performance’ atrial cells relies on specific concentrations of cellular calcium. Now, for the first time, scientists at The University of Nottingham have produced a mathematical model of calcium activity within the atrial heart cell which will significantly improve our chances of treating heart disease and stroke.
This break-through, which takes scientists into a world of cell activity currently beyond the scope of imaging technology, has just been published in the journal Proceedings of the National Academy of Sciences (PNAS),
Dr Rüdiger Thul, a lecturer in applied mathematics in the School of Mathematical Sciences, said: “This new model provides clinically relevant insights into the initiation and propagation of sub-cellular calcium signals. Thus, for the first time we can manipulate cellular properties throughout a whole atrial muscle cell in order to deduce which conditions give rise to abnormalities. This has the potential to point to new treatments for heart disease and irregular heart beat such as atrial fibrillation, which can lead to thrombosis and stroke.”
The importance of the atrial kick
A human heart will beat more than one billion times during our lifetime. The main function of the heart is to pump blood. To generate the necessary force to propel blood through all the blood vessels, the heart beats with every contraction of its cells.
Most of these muscle cells surround the larger chambers of the heart, the ventricles. Under resting conditions, the ventricles are mainly responsible for contracting the heart. When blood needs to be pumped more quickly – for instance during exercise – the smaller chambers of the heart contribute to the contraction. This is known as the atrial kick.
As we age or when something is wrong with our heart – such as atrial fibrillation – the atrial muscle cells start to deteriorate. As a result we lose the support of the atrial kick. Atrial fibrillation constitutes the most common form of cardiac arrhythmia – irregular heart beat.
The role of calcium in keeping our heart fit
Several experimental studies have revealed that to trigger contraction in atrial muscle cells the calcium concentration follows an elaborate choreography which shows different concentration values in different parts of the cell. This is in contrast to ventricular cells where the calcium concentration is almost entirely uniform throughout the cell.
In order to fully understand atrial calcium dynamics we need to be able to monitor the atrial cell in its entirety. Unfortunately this is currently beyond even the best state-of-the-art experimental technology. Moreover, experimental manipulations of cells usually interfere with more than one cellular control mechanism making it harder to tease apart the contributions of different pathways. Therefore, developing cutting edge models of atrial cellular behaviour is crucial to our understanding.
New mathematical model could save lives
Dr Thul said: “The strength of our model is that we can study the intracellular calcium concentration throughout the whole volume of the atrial muscle cell at the same time. This allows for a detailed exploration of the spatio-temporal calcium patterns associated with both healthy and pathological conditions.
“Moreover, we can selectively activate, deactivate, over or under express cellular properties and see how they shape the calcium patterns. Hence, we can deduce which conditions give rise to abnormalities and might lead to diseases such as atrial fibrillation. It is important to remember that whatever pharmaceutical treatment is administered, it acts at the single cell level. The response of an organ always results from the interaction of its cellular components. Looking ahead to treatments of atrial fibrillation and other cardiac pathologies, a fully three-dimensional model of an atrial cell offers an ideal testing ground for new drugs.”
Contact: Lindsay Brooke
lindsay.brooke@nottingham.ac.uk
44-011-595-15751
University of Nottingham
The onset of cognitive decline begins at 45
January 9, 2012
Increased life expectancy implies fundamental changes in the composition of populations, with a significant rise in the number of elderly people. These changes are likely to have a massive influence on the life of individuals and on society in general. Abundant evidence has clearly established an inverse association between age and cognitive performance, but the age at which cognitive decline begins is much debated. Recent studies concluded that there was little evidence of cognitive decline before the age of 60.
However, clinical studies demonstrate a correlation between the presence of amyloid plaques in the brain and the severity of cognitive decline. It would seem that these amyloid plaques are found in the brains of young adults.
Few assessments of the effect of age on cognitive decline use data that spans over several years. This was the specific objective of the study led by researchers from Inserm and the University College London.
As part of the Whitehall II cohort study, medical data was extracted for 5,198 men and 2,192 women, aged between 45 and 70 at the beginning of the study, monitored over a 10-year period. The cognitive functions of the participants were evaluated three times over this time. Individual tests were used to assess memory, vocabulary, reasoning and verbal fluency.
The results show that cognitive performance (apart from the vocabulary tests) declines with age and more rapidly so as the individual’s age increases. The decline is significant in each age group.
For example, during the period studied, reasoning scores decreased by 3.6 % for men aged between 45 and 49, and 9.6 % for those aged between 65 and 70. The corresponding figures for women stood at 3.6% and 7.4% respectively.
The authors underline that evidence pointing to cognitive decline before the age of 60 has significant consequences.
“Determining the age at which cognitive decline begins is important since behavioural or pharmacological interventions designed to change cognitive aging trajectories are likely to be more effective if they are applied from the onset of decline.” underlines Archana Singh-Manoux.
“As life expectancy continues to increase, understanding the correlation between cognitive decline and age is one of the challenges of the 21st Century” she adds.
This research is part of the Whitehall II cohort study and focused on more that 7,000 people over a ten-year period.
Sources
Timing of onset of cognitive decline: results from Whitehall II prospective cohort study
Archana Singh-Manoux research director 1 2 3, Mika Kivimaki professor of social epidemiology 2, M Maria Glymour assistant professor 4, Alexis Elbaz research director 5 6, Claudine Berr research director7 8, Klaus P Ebmeier professor of old age psychiatry9, Jane E Ferrie senior research fellow10, AlineDugravot statistician 1
1Institut National de la Santé et de la Recherche Médicale (INSERM), U1018, Centre for Research in Epidemiology and Population Health, Hôpital Paul Brousse, 94807 Villejuif Cedex, France;
2Department of Epidemiology and Public Health, University College London, London, UK;
3Centre de Gérontologie, Hôpital Ste Périne, AP-HP, France;
4Department of Society, Human Development, and Health, Harvard School of Public Health, Boston, MA, USA;
5Institut National de la Santé et de la Recherche Médicale (INSERM), U708, F-75013, Paris, France;
6UPMC Univ Paris 06, UMR_S 708, F-75005, Paris;
7Institut National de la Santé et de la Recherche Médicale (INSERM) U1061 Université Montpellier 1, Montpellier,France;
8CMRR Languedoc-Roussillon, CHU Montpellier;
9Oxford University Department of Psychiatry, Warneford Hospital, Oxford, UK;
10University of Bristol, Bristol, UK
BMJ janvier 2012
Contact chercheur
Archana Singh Manoux
Email : Archana.Singh-Manoux@inserm.fr
Contact: Inserm Press Office
presse@inserm.fr
INSERM (Institut national de la santé et de la recherche médicale)
Research shows progress toward a genital herpes vaccine
January 5, 2012
An investigational vaccine protected some women against infection from one of the two types of herpes simplex viruses that cause genital herpes, according to findings in the New England Journal of Medicine.
The vaccine was partially effective at preventing herpes simplex virus type 1 (HSV-1), but did not protect women from herpes simplex virus type 2 (HSV-2). There were less than half of the cases of genital herpes caused by HSV-1 – 58 percent fewer — in women who received the investigational vaccine compared to women who received the control vaccine.
“There is some very good news in our findings. We were partially successful against half of the equation – protecting women from genital disease caused by HSV-1,” said Robert Belshe, M.D., director of the Saint Louis University Center for Vaccine Development and lead author of the study.
“It’s a big step along the path to creating an effective vaccine that protects against genital disease caused by herpes infection. It points us in the direction to work toward making a vaccine that works on both herpes simplex viruses.”
Both HSV-1 and HSV-2 are members of the herpesvirus family. Typically, HSV-2 causes lesions and blisters in the genital area. HSV-1 generally causes sores in the mouth and lips, although it increasingly has been found to cause genital disease.
There currently is no cure or approved vaccine to prevent genital herpes infection, which affects about 25 percent of women in the United States and is one of the most common communicable diseases. Once inside the body, HSV remains there permanently. The virus can cause severe neurological disease and even death in infants born to women who are infected with HSV and the virus is a risk factor for sexual transmission of HIV.
The clinical trial of an investigational genital herpes vaccine was funded by the National Institute of Allergy and Infectious Diseases (NIAID), which is part of the National Institutes of Health, along with GlaxoSmithKline (GSK), and conducted at 50 sites in the U.S. and Canada.
The study enrolled 8,323 women between ages 18 and 30 who did not have HSV-1 or HSV-2 infection at the start of the study. They were randomly assigned to receive either three doses of the investigational HSV vaccine that was developed by GSK or a hepatitis A vaccine, which was the control.
Participants were followed for 20 months and evaluated carefully for occurrence of genital herpes disease. In addition, all study participants were given blood tests to determine if asymptomatic infection with HSV-1 or HSV-2 occurred during the trial. Researchers found that two or three doses of the investigational vaccine offered significant protection against genital herpes disease caused by HSV-1. However the vaccine did not protect women from genital disease caused by HSV-2.
“We were surprised by these findings,” said Belshe, who also is a professor of infectious diseases and immunology at Saint Louis University School of Medicine. “We didn’t expect the herpes vaccine to protect against one type of herpes simplex virus and not another. We also found it surprising that HSV-1 was a more common cause of genital disease than was HSV-2.”
HSV-1 infection has become an increasingly common cause of genital disease, likely because more couples are engaging in oral sex. HSV-1 and HSV-2 are spread by direct contact – mouth to mouth, mouth to genitals and genitals to genitals – even when the infected person shows no symptoms, Belshe added.
Researchers are conducting laboratory tests on serum obtained from study participants as they continue to study why the vaccine protected women from genital disease caused by HSV-1 and not HSV-2.
One hypothesis, Belshe said, is HSV-1 is more easily killed by antibodies than is HSV-2. This means that the vaccine antibodies might work better against HSV-1 and result in protection from HSV-1 but not HSV-2.
Earlier studies of the investigational herpes vaccines showed it protected against genital herpes disease in women who were not infected with HSV-1 or HSV-2, but whose sexual partners were known to have genital herpes. Researchers believe the reason for the different outcome in the most recent clinical trial could be related to the fact that different populations were studied. The women in the earlier studies may have been protected due to immunologic or behavioral factors not present in the later study.
“It’s always important to confirm scientific findings in repeated studies, which is why we investigated the vaccine in a large, placebo controlled trial,” Belshe said. “Our findings confirmed the validity of the scientific process. You’ve got to have good scientific evidence that something actually works.”
Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: cancer, infectious disease, liver disease, aging and brain disease and heart/lung disease.
Contact: Nancy Solomon
solomonn@slu.edu
314-977-8017
Saint Louis University
How work tells muscles to grow
January 3, 2012
We take it for granted, but the fact that our muscles grow when we work them makes them rather unique. Now, researchers have identified a key ingredient needed for that bulking up to take place. A factor produced in working muscle fibers apparently tells surrounding muscle stem cell “higher ups” that it’s time to multiply and join in, according to a study in the January Cell Metabolism, a Cell Press journal.
In other words, that so-called serum response factor (Srf) translates the mechanical signal of work into a chemical one.
“This signal from the muscle fiber controls stem cell behavior and participation in muscle growth,” says Athanassia Sotiropoulos of Inserm in France. “It is unexpected and quite interesting.” It might also lead to new ways to combat muscle atrophy.
Sotiropoulos’ team became interested in Srf’s role in muscle in part because their earlier studies in mice and humans showed that Srf concentrations decline with age. That led them to think Srf might be a culprit in the muscle atrophy so common in aging.
The new findings support that view, but Srf doesn’t work in the way the researchers had anticipated. Srf was known to control many other genes within muscle fibers. That Srf also influences the activities of the satellite stem cells came as a surprise.
Mice with muscle fibers lacking Srf are no longer able to grow when they are experimentally overloaded, the new research shows. That’s because satellite cells don’t get the message to proliferate and fuse with those pre-existing myofibers.
Srf works through a network of genes, including one known as Cox2. That raises the intriguing possibility that commonly used Cox2 inhibitors – think ibuprofen – might work against muscle growth or recovery, Sotiropoulos notes.
Treatments designed to tweak this network of factors might be used to wake muscle stem cells up and enhance muscle growth in circumstances such as aging or following long periods of bed rest, she says. Most likely, such therapies would be more successfully directed not at Srf itself, which has varied roles, but at its targets.
“It may be difficult to find a beneficial amount of Srf,” she says. “Its targets, interleukins and prostaglandins, may be easier to manipulate.”
Contact: Elisabeth (Lisa) Lyons
elyons@cell.com
617-386-2121
Cell Press
President Obama and leading GOP presidential candidate support health research
December 28, 2011
Research!America’s new national voter education initiative, Your Candidates-Your Health, features responses from President Obama and Republican Presidential candidate Newt Gingrich on important health research and prevention issues. Among the highlights: both Obama and Gingrich agree that research to improve health and prevent disease is part of the solution to rising health care costs, and boosting investment in medical research creates jobs that benefit a wide variety of industries. Their positions on embryonic stem cell research differ.
“For too long, patients and families have suffered from debilitating, incurable diseases and we know that stem cell research offers hope to millions of Americans across the country. I am committed to supporting responsible stem cell research now, and in the future,” said President Obama in his response to the questionnaire.
“I strongly support adult stem cell research,” said Gingrich. “I will oppose at every turn any process of destroying embryos.”
In the area of global competitiveness, Gingrich said, “Considering today’s American tax and regulatory systems, it is increasingly likely that the full implementation of the new [scientific] knowledge will first occur outside the United States and be imported by us. This will be tragic for Americans in lost health opportunities, lost jobs and prosperity, and unnecessarily higher healthcare costs.”
“To compete for the jobs and industries of our time, we have to make America the best place on earth to do business and out-innovate, out-educate, and out-build the rest of the world,” said Obama. “I have called for a level of research and development we haven’t seen since the height of the Space Race and sent budgets to Congress that helps us meet that goal.”
Obama and Gingrich also responded to questions about support for the National Institutes of Health, the Centers for Disease Control and Prevention, the Food and Drug Administration, science, technology, engineering and math education, and government investment in health research for military veterans. www.yourcandidatesyourhealth.org. All presidential candidates were invited to participate.
The responses from Obama and Gingrich largely reflect public sentiment on federal support for research. In new public opinion poll data, a vast majority of Americans (86%) believe investing in health research is important for job creation and economic recovery and (54%) say research is part of the solution to rising health care costs. Seventy-seven percent believe the U.S. is losing its global competitive edge in science and innovation. However, 60% say they are uninformed about their representatives’ positions on medical, health and scientific research.
“Unfortunately, many elected officials and candidates have failed to elevate these issues in their campaigns,” said Mary Woolley, president and CEO of Research!America. “The poll underscores Americans’ willingness to make research a high priority to address our economic and health challenges.”
In other polling data, most Americans say it’s important to increase funding for federal health research agencies — (86%) for the Centers for Disease Control and Prevention (CDC), (79%) for the Food and Drug Administration (FDA) and (75%) for the National Institutes of Health (NIH).
“Americans realize that massive spending cuts for federal agencies like the NIH would move our country in the wrong direction,” said Research!America’s chair, former Illinois Congressman John Porter. “A strong investment in research will yield more scientific discoveries, boost our global competitiveness and help lower health care costs. We need elected officials who will aggressively support and expand research and development.”
Additional findings from the public opinion poll include:
- 85% think research and innovation is important to their state economy.
- 48% say there is not enough government investment in health research for the benefit of military veterans and service members.
- 82% say it’s important to conduct medical or health research to eliminate health disparities.
- 73% believe the federal government should place more emphasis on increasing the number of young Americans who pursue careers in science, technology, engineering and mathematics.
- 61% favor expanding federal funding for research using embryonic stem cells.
About the Poll: Research!America commissioned JZ Analytics to conduct an online survey of 800 adults nationwide in October 2011. The sample is representative of the nation’s demographics, including geography, gender and ethnicity, with a theoretical error of ±3.0%. The full results can be found at http://www.researchamerica.org/uploads/December2011PollRelease.pdf
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Supersized market economy, supersized belly: Wealthier nations have more fast food and more obesity
December 23, 2011
New research from the University of Michigan suggests obesity can be seen as one of the unintended side effects of free market policies.
A study of 26 wealthy nations shows that countries with a higher density of fast food restaurants per capita had much higher obesity rates compared to countries with a lower density of fast food restaurants per capita.
“It’s not by chance that countries with the highest obesity rates and fast food restaurants are those in the forefront of market liberalization, such as the United States, the United Kingdom, Australia, New Zealand and Canada, versus countries like Japan and Norway, with more regulated and restrictive trade policies,” said Roberto De Vogli, associate professor in the U-M School of Public Health, and lead researcher of the study.
For example, in the United States, researchers reported 7.52 fast food restaurants per 100,000 people, and in Canada they reported 7.43 fast food restaurants per 100,000 people. The paper reported the obesity rates among US men and women were 31.3 percent and 33.2 percent, respectively. The obesity rates for Canadian men and women were 23.2 percent and 22.9 percent, respectively.
Compare that to Japan, with 0.13 fast food restaurants per 100,000 people, and Norway, with 0.19 restaurants per capita. Obesity rates for men and women in Japan were 2.9 percent and 3.3 percent, respectively. In Norway, obesity rates for men and women were 6.4 percent and 5.9 percent, respectively. The relationships remain consistent even when researchers controlled for variables such as income, income inequality, urban areas, motor vehicles and internet use per capita.
Obesity research largely overlooks the global market forces behind the epidemic, De Vogli said.
“In my opinion the public debate is too much focused on individual genetics and other individual factors, and overlooks the global forces in society that are shaping behaviors worldwide. If you look at trends overtime for obesity, it’s shocking,” De Vogli said.
“Since the 1980s, since the advent of trade liberalization policies that have indirectly promoted transnational food companies we see rates that have tripled or quadrupled. There is no biological, genetic, psychological or community level factor that can explain this. Only a global type of change can explain this.”
Researchers chose one fast food restaurant to use as a proxy measure for how many fast food restaurants were present per 100,000. The study is in no way an indictment of that restaurant, De Vogli said, but rather an indicator of fast food density in a particular area.
Fast food refers to food sold in restaurants or stores with preheated or precooked ingredients, and served to the customer in a packaged form. A typical fast food meal includes a hamburger, fries and a soft drink, the paper said. Fast food is usually high in fat and calories, and several studies have found associations between fast food intake and increased body mass index, weight gain and obesity. Obesity accounts for approximately 400,000 deaths each year in the United States alone. Fast food consumption is also related to insulin resistance and type II diabetes, another major worldwide public health threat.
The paper, “Globesization: ecological evidence on the relationship between fast food outlets and obesity among 26 advanced economies,” will be published in the December print issue of Critical Public Health. The study was funded by a grant from the Economic and Social Research Council.
For more on De Vogli: http://www.sph.umich.edu/iscr/faculty/profile.cfm?uniqname=rdevogli.
The University of Michigan School of Public Health has been promoting health and preventing disease since 1941, and is ranked among the top public health schools in the nation. Whether making new discoveries in the lab or researching and educating in the field, our faculty, students, and alumni are deployed around the globe to promote and protect our health. http://www.sph.umich.edu/
Contact: Laura Bailey
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