Category: Health

{African Americans may be less responsive to asthma treatment and more likely to die from the condition, in part, because they have a unique type of airway inflammation, according to a study led by researchers at the University of Illinois at Chicago College of Medicine.}

Airway inflammation is a key component of asthma, and innovations in treatment are becoming more personalized based on the specific type of airway inflammation in a patient, says Dr. Sharmilee Nyenhuis, assistant professor of medicine at UIC and corresponding author on the study.

“Emerging evidence suggests that differences in airway inflammation can affect a patient’s response to treatment, but whether the patterns of airway inflammation vary across race has, until now, been very unclear,” said Nyenhuis, of UIC’s division of pulmonary, critical care, sleep and allergy.

Black men and women are two to three times more likely than whites to be hospitalized or die from asthma. And while many factors contribute to the burden of asthma in African Americans — such as access to health care and environmental exposures — rates are disproportionate even when social and environmental elements are taken into account.

Nyenhuis and her colleagues performed a secondary analysis of more than 1,000 sputum samples obtained from AsthmaNet, a nationwide clinical research network created by the National Heart Lung and Blood Institute, and the Asthma Clinical Research Network. Samples of the coughed-up fluids were from past clinical trial participants over the age of 12 with mild or moderate persistent asthma and who had not smoked within the last year. The samples were tested for the presence of eosinophils — a type of white blood cell.

The study is one of the largest and most diverse trials conducted in the U.S. on race and asthma, with 26 percent of the patients self-identifying as African American. Researchers found that black patients were more likely to exhibit eosinophilic airway inflammation than whites, despite taking comparable doses of asthma medication, such as inhaled corticosteroids.

The results are published in the Journal of Allergy and Clinical Immunology.

“Our findings of higher numbers of African Americans with this type of airway inflammatory pattern suggests a mechanism that may account for more severe and difficult to control asthma in African Americans,” said Nyenhuis. “It follows that the persistence of eosinophilic airway inflammation in African Americans may be associated with asthma exacerbations and an impaired response to corticosteroids.”

The findings suggest that black patients with eosinophilic airway inflammation may not benefit from increasingly strong corticosteroid treatment — instead, other targeted therapies may need to be considered and researched as a treatment option for those black patients with difficult to control eosinophilic asthma.

{Doctors have found a way to manipulate wounds to heal as regenerated skin rather than scar tissue. The method involves transforming the most common type of cells found in wounds into fat cells — something that was previously thought to be impossible in humans. Researchers began this work at the Perelman School of Medicine at the University of Pennsylvania, which led to a large-scale, multi-year study in connection with the Plikus Laboratory for Developmental and Regenerative Biology at the University of California, Irvine. They published their findings online in the journal Science on Thursday, January 5th, 2017.
}

Fat cells called adipocytes are normally found in the skin, but they’re lost when wounds heal as scars. The most common cells found in healing wounds are myofibroblasts, which were thought to only form a scar. Scar tissue also does not have any hair follicles associated with it, which is another factor that gives it an abnormal appearance from the rest of the skin. Researchers used these characteristics as the basis for their work — changing the already present myofibroblasts into fat cells that do not cause scarring.

“Essentially, we can manipulate wound healing so that it leads to skin regeneration rather than scarring,” said George Cotsarelis, MD, the chair of the Department of Dermatology and the Milton Bixler Hartzell Professor of Dermatology at Penn, and the principal investigator of the project. “The secret is to regenerate hair follicles first. After that, the fat will regenerate in response to the signals from those follicles.”

The study showed hair and fat develop separately but not independently. Hair follicles form first, and the Cotsarelis lab previously discovered factors necessary for their formation. Now they’ve discovered additional factors actually produced by the regenerating hair follicle to convert the surrounding myofibroblasts to regenerate as fat instead of forming a scar. That fat will not form without the new hairs, but once it does, the new cells are indistinguishable from the pre-existing fat cells, giving the healed wound a natural look instead of leaving a scar. As they examined the question of what was sending the signal from the hair to the fat cells, researchers identified a factor called Bone Morphogenetic Protein (BMP). It instructs the myofibroblasts to become fat. This signaling was groundbreaking on its own, as it changed what was previously known about myofibroblasts.

“Typically, myofibroblasts were thought to be incapable of becoming a different type of cell,” Cotsarelis said. “But our work shows we have the ability to influence these cells, and that they can be efficiently and stably converted into adipocytes.” This was shown in both the mouse and in human keloid cells grown in culture.

“The findings show we have a window of opportunity after wounding to influence the tissue to regenerate rather than scar,” said the study’s lead author Maksim Plikus, PhD, an assistant professor of Developmental and Cell Biology at the University of California, Irvine. Plikus began this research as a postdoctoral fellow in the Cotsarelis Laboratory at Penn, and the two institutions have continued to collaborate.

These discoveries have the potential to be revolutionary in the field of dermatology. The first and most obvious use would be to develop a therapy that signals myofibroblasts to convert into adipocytes — helping wounds heal without scarring.

“It’s highly desirable from a clinical standpoint, but right now it’s an unmet need,” Cotsarelis said.

But the increase of fat cells in tissue can also be helpful for more than just wounds. Adipocyte loss is a common complication of other conditions, especially treatments for HIV, and right now there is no efficient strategy for treatment. The cells are also lost naturally because of the aging process, especially in the face, which leads to permanent, deep wrinkles, something anti-aging treatments can’t fix in a cosmetically satisfactory way.

“Our findings can potentially move us toward a new strategy to regenerate adipocytes in wrinkled skin, which could lead us to brand new anti-aging treatments,” Cotsarelis said.

The Cotsarelis Lab is now focusing on the mechanisms that promote skin regeneration, especially with respect to hair follicle regeneration.

The Plikus Laboratory is focusing on other aspects of cell reprogramming in skin wounds. Researchers there are examining the role of other signaling factory beyond BMP as well as conducting further studies using human cells and human scar tissue.

{Annual ACS report identifies significant disparities in cancer burden by gender, race.}

A steady decline over more than two decades has resulted in a 25% drop in the overall cancer death rate in the United States. The drop equates to 2.1 million fewer cancer deaths between 1991 and 2014.

The news comes from Cancer Statistics 2017, the American Cancer Society’s comprehensive annual report on cancer incidence, mortality, and survival. It is published in CA: A Cancer Journal for Clinicians and is accompanied by a consumer version of the publication, Cancer Facts and Figures 2017.

The report estimates that in 2017, there will be 1,688,780 new cancer cases and 600,920 cancer deaths in the United States. Over the past decade of available data, the overall cancer incidence rate was stable in women and declined by about 2% per year in men, while the cancer death rate declined by about 1.5% annually in both men and women.

The cancer death rate dropped from its peak of 215.1 (per 100,000 population) in 1991 to 161.2 (per 100,000 population) in 2014, the latest year for which data was available to analyze. The drop is the result of steady reductions in smoking and advances in early detection and treatment, and is driven by decreasing death rates for the four major cancer sites: lung (- 43% between 1990 and 2014 among males and -17% between 2002 and 2014 among females), breast (-38% from 1989 to 2014), prostate (-51% from 1993 to 2014), and colorectal (-51% from 1976 to 2014).

The report also finds significant gender disparities in incidence and mortality. For all sites combined, the cancer incidence rate is 20% higher in men than in women, while the cancer death rate is 40% higher in men.

The gender gap in cancer mortality largely reflects variation in the distribution of cancers that occur in men and women, much of which is due to differences in the prevalence of cancer risk factors. For example, liver cancer, a highly fatal cancer, is three times more common in men than in women, partly reflecting higher Hepatitis C virus infection, historical smoking prevalence, and excess alcohol consumption in men. The largest sex disparities are for cancers of the esophagus, larynx, and bladder, for which incidence and death rates are about 4-fold higher in men. Melanoma incidence rates are about 60% higher in men than in women, while melanoma death rates are more than double in men compared to women.

Racial disparities in cancer death rates continue to decline. The excess risk of cancer death in black men has dropped from 47% in 1990 to 21% in 2014. The black/white disparity declined similarly in women, from a peak of 20% in 1998 to 13% in 2014. Although the cancer death rate remained 15% higher in blacks than in whites in 2014, increasing access to care as a result of the Patient Protection and Affordable Care Act may expedite the narrowing racial gap. From 2010 to 2015, the proportion of blacks who were uninsured dropped in half, from 21% to 11%, as it did for Hispanics (31% to 16%). Gains in coverage for traditionally underserved Americans will facilitate the broader application of existing cancer control knowledge across every segment of the population.

“The continuing drops in the cancer death rate are a powerful sign of the potential we have to reduce cancer’s deadly toll,” said Otis W. Brawley, M.D., FACP, chief medical officer of the ACS. “Continuing that success will require more clinical and basic research to improve early detection and treatment, as well as creative new strategies to increase healthy behaviors nationwide. Finally, we need to consistently apply existing knowledge in cancer control across all segments of the population, particularly to disadvantaged groups.”

Cancer Statistics has been published by American Cancer Society researchers since 1967 to inform and guide clinicians, investigators, and others in public health in prioritizing efforts to reduce the burden of cancer. It is one of the most highly cited scientific journal articles every year.

{Vitamin D deficiency may increase the risk of chronic headache, according to a new study from the University of Eastern Finland. The findings were published in Scientific Reports.}

The Kuopio Ischaemic Heart Disease Risk Factor Study, KIHD, analysed the serum vitamin D levels and occurrence of headache in approximately 2,600 men aged between 42 and 60 years in 1984-1989. In 68% of these men, the serum vitamin D level was below 50 nmol/l, which is generally considered the threshold for vitamin D deficiency. Chronic headache occurring at least on a weekly basis was reported by 250 men, and men reporting chronic headache had lower serum vitamin D levels than others.

When the study population was divided into four groups based on their serum vitamin D levels, the group with the lowest levels had over a twofold risk of chronic headache in comparison to the group with the highest levels. Chronic headache was also more frequently reported by men who were examined outside the summer months of June through September. Thanks to UVB radiation from the sun, the average serum vitamin D levels are higher during the summer months.

The study adds to the accumulating body of evidence linking a low intake of vitamin D to an increased risk of chronic diseases. Low vitamin D levels have been associated with the risk of headache also by some earlier, mainly considerably smaller studies.

In Finland and in other countries far from the Equator, UVB radiation from the sun is a sufficient source of vitamin D during the summer months, but outside the summer season, people need to make sure that they get sufficient vitamin D from food or from vitamin D supplements.

No scientific evidence relating to the benefits and possible adverse effects of long-term use in higher doses yet exists. The Finnish Vitamin D Trial, FIND, currently ongoing at the University of Eastern Finland will shed light on the question, as the five-year trial analyses the effects of high daily doses of vitamin D on the risk factors and development of diseases. The trial participants are taking a vitamin D supplement of 40 or 80 micrograms per day. The trial also investigates the effects of vitamin D supplementation on various pain conditions.

{Michigan State University researchers have discovered that a chemical compound, and potential new drug, reduces the spread of melanoma cells by up to 90 percent.}

The human-made, small-molecule drug compound goes after a gene’s ability to produce RNA molecules and certain proteins in melanoma tumors. This gene activity, or transcription process, causes the disease to spread but the compound can shut it down. Up until now, few other compounds of this kind have been able to accomplish this.

“It’s been a challenge developing small-molecule drugs that can block this gene activity that works as a signaling mechanism known to be important in melanoma progression,” said Richard Neubig, a pharmacology professor and co-author of the study. “Our chemical compound is actually the same one that we’ve been working on to potentially treat the disease scleroderma, which now we’ve found works effectively on this type of cancer.”

Scleroderma is a rare and often fatal autoimmune disease that causes the hardening of skin tissue, as well as organs such as the lungs, heart and kidneys. The same mechanisms that produce fibrosis, or skin thickening, in scleroderma also contribute to the spread of cancer.

Small-molecule drugs make up over 90 percent of the drugs on the market today and Neubig’s co-author Kate Appleton, a postdoctoral student, said the findings are an early discovery that could be highly effective in battling the deadly skin cancer. It’s estimated about 10,000 people die each year from the disease.

Their findings are published in the January issue of Molecular Cancer Therapeutics.

“Melanoma is the most dangerous form of skin cancer with around 76,000 new cases a year in the United States,” Appleton said. “One reason the disease is so fatal is that it can spread throughout the body very quickly and attack distant organs such as the brain and lungs.”

Through their research, Neubig and Appleton, along with their collaborators, found that the compounds were able to stop proteins, known as Myocardin-related transcription factors, or MRTFs, from initiating the gene transcription process in melanoma cells. These triggering proteins are initially turned on by another protein called RhoC, or Ras homology C, which is found in a signaling pathway that can cause the disease to aggressively spread in the body.

The compound reduced the migration of melanoma cells by 85 to 90 percent. The team also discovered that the potential drug greatly reduced tumors specifically in the lungs of mice that had been injected with human melanoma cells.

“We used intact melanoma cells to screen for our chemical inhibitors,” Neubig said. “This allowed us to find compounds that could block anywhere along this RhoC pathway.”

Being able to block along this entire path allowed the researchers to find the MRTF signaling protein as a new target.

Appleton said figuring out which patients have this pathway turned on is an important next step in the development of their compound because it would help them determine which patients would benefit the most.

“The effect of our compounds on turning off this melanoma cell growth and progression is much stronger when the pathway is activated,” she said. “We could look for the activation of the MRTF proteins as a biomarker to determine risk, especially for those in early-stage melanoma.”

According to Neubig, if the disease is caught early, chance of death is only 2 percent. If caught late, that figure rises to 84 percent.

“The majority of people die from melanoma because of the disease spreading,” he said. “Our compounds can block cancer migration and potentially increase patient survival.”

{People who live close to high-traffic roadways face a higher risk of developing dementia than those who live further away, new research from Public Health Ontario (PHO) and the Institute for Clinical Evaluative Sciences (ICES) has found.}

Led by PHO and ICES scientists, the study found that people who lived within 50 metres of high-traffic roads had a seven per cent higher likelihood of developing dementia compared to those who lived more than 300 meters away from busy roads.

Published in The Lancet, the researchers examined records of more than 6.5 million Ontario residents aged 20-85 to investigate the correlation between living close to major roads and dementia, Parkinson’s disease and multiple sclerosis.

Scientists identified 243,611 cases of dementia, 31,577 cases of Parkinson’s disease, and 9,247 cases of multiple sclerosis in Ontario between 2001 and 2012. In addition, they mapped individuals’ proximity to major roadways using the postal code of their residence. The findings indicate that living close to major roads increased the risk of developing dementia, but not Parkinson’s disease or multiple sclerosis, two other major neurological disorders.

“Little is known in current research about how to reduce the risk of dementia. Our findings show the closer you live to roads with heavy day-to-day traffic, the greater the risk of developing dementia. With our widespread exposure to traffic and the greater tendency for people to live in cities these days, this has serious public health implications,” says Dr. Hong Chen, environmental and occupational health scientist at PHO and an adjunct scientist at ICES. Dr. Chen is lead author on the paper titled Living Near Major Roads and the Incidence of Dementia, Parkinson’s Disease, and Multiple Sclerosis: A Population-based Cohort Study.

“Our study is the first in Canada to suggest that pollutants from heavy, day-to-day traffic are linked to dementia. We know from previous research that air pollutants can get into the blood stream and lead to inflammation, which is linked with cardiovascular disease and possibly other conditions such as diabetes. This study suggests air pollutants that can get into the brain via the blood stream can lead to neurological problems,” says Dr. Ray Copes, chief of environmental and occupational health at PHO and an author on the paper.

As urban centres become more densely populated and more congested with vehicles on major roads, Dr. Copes suggests the findings of this paper could be used to help inform municipal land use decisions as well as building design to take into account air pollution factors and the impact on residents.

This research was conducted in collaboration with scientists from the University of Toronto, Carleton University, Dalhousie University, Oregon State University, and Health Canada. The study was funded by Health Canada.

{{Key findings:}}

Using data held at ICES, the researchers examined records of more than 6.5 million Ontario residents, aged 20-85, and mapped them according to residential postal codes five years before the study started.

Between 2001 and 2012, 243,611 cases of dementia, 31,577 cases of Parkinson’s disease, and 9,247 cases of multiple sclerosis were identified in Ontario.
People who lived within 50 metres of high-traffic roads had a seven per cent higher likelihood of dementia than those who lived more 300 meters away from busy roads.

The increase in the risk of developing dementia went down to four per cent if people lived 50-100 metres from major traffic, and to two per cent if they lived within 101-200 metres. At over 200 metres, there was no elevated risk of dementia.

There was no correlation between major traffic proximity and Parkinson’s disease or multiple sclerosis.

{Research challenges prevalent views that brain enlargement and dental reduction co-evolved.}

A new study from the George Washington University’s Center for the Advanced Study of Human Paleobiology (CASHP) found that whereas brain size evolved at different rates for different species, especially during the evolution of Homo, the genus that includes humans, chewing teeth tended to evolve at more similar rates. The finding suggests that our brains and teeth did not evolve in lock step and were likely influenced by different ecological and behavioral factors.

This research challenges the classically accepted view that reduction of tooth size in hominins is linked with having a larger brain. The reasoning is that larger brains allowed hominins to start making stone tools and that the use of these tools reduced the need to have such large chewing teeth. But recent studies by other authors found that hominins had larger brains before chewing teeth became smaller, and they made and used stone tools when brains were still quite small, which challenges this relationship.

The new study evaluates this issue by measuring and comparing the rates at which teeth and brains have evolved along the different branches of the human evolutionary tree.

“The findings of the study indicate that simple causal relationships between the evolution of brain size, tool use and tooth size are unlikely to hold true when considering the complex scenarios of hominin evolution and the extended time periods during which evolutionary change has occurred,” said Aida Gómez-Robles, lead author of the paper and a postdoctoral scientist at GW’s CASHP.

To conduct the research, Dr. Gómez-Robles and her colleagues analyzed eight different hominin species. The researchers identified fast-evolving species by comparing differences between groups with those obtained when simulating evolution at a constant rate across all lineages, and they found clear differences between tooth evolution and brain evolution. If the classical view proposing co-evolution between brains and teeth is correct, they expected to see a close correspondence between species evolving at a fast rate for both traits. The differences they observed indicate that diverse and unrelated factors influenced the evolution of teeth and brains.

“Once something becomes conventional wisdom, in no time at all it becomes dogma,” said Bernard Wood, university professor of human origins at GW and a co-author of the paper. “The co-evolution of brains and teeth was on a fast-track to dogma status, but we caught it in the nick of time.”

{Milk has a lot of health benefits, but many adults fail to drink enough milk, as they tend to believe that milk is meant for children.}

Check out some health benefits of milk that would make you want to drink more milk:

{{1. For your heart health }}

Milk is a good source of potassium, which is good for your heart health. An increase in potassium intake alongside a decrease in sodium intake can reduce the risk of cardiovascular disease.

{{2. Type 2 Diabetes }}

Studies have found that a good consumption of low fat dairy products can help reduce the risk of type 2 diabetes.

Type 2 diabetes have been a common problem in many adults in the world today, and a 2005 study found that there was a reduced risk of type 2 diabetes when there was an increase in the intake of low fat dairy.

{{3. Stronger bones }}

Milk consumption can also help your bone health. Milk contains a good amount of calcium, phosphorus and magnesium which are all essential to healthy and stronger bones.

{{4. Healthy teeth }}

The calcium and phosphorus present in milk are also good for the development and maintenance of strong, healthy teeth.

{{5. Healthier skin }}

Milk has a lot of properties that can aid for a healthy and glowing skin. Milk contains antioxidants which can fight off toxins, it contains lactic acid which can act as an exfoliant to help smoothen the skin, as well as amino acids that can help keep the skin moisturised.

{{6. Ease stress }}

A warm glass of milk can help you relax and ease stress after a long day at work. Research has found that milk has the properties to reduce symptoms of PMS.

{{7. Muscles }}

Milk is also a good form of fluid that can be used to hydrate yourself after working out. It contains protein which can help rebuild your muscles.

Have you been avoiding milk? You have been missing a lot of its health benefits.

{Experts suggest ways for hospitals to engineer social incentives among friends and family to improve health care.}

Leveraging existing relationships with friends and family may be a more effective way to improve patients’ health and encourage new healthy habits and behaviors than increasing interactions with physicians or other clinicians. In a new perspective published by the New England Journal of Medicine, Penn Medicine behavioral economists suggest a five-step ladder to effectively engineering social engagements that promote health and to test their acceptability and effectiveness.

“Spouses and friends are more likely to be around patients when they are making decisions that affect their health — like taking a walk versus watching TV, or what to order at a restaurant. Patients are also more likely to adopt healthy behaviors — like going to the gym — when they can go with a friend,” explains co-author David Asch, MD, MBA, a professor of Medicine at the Perelman School of Medicine at the University of Pennsylvania and director of the Penn Medicine Center for Health Care Innovation. “Though people are more heavily influenced by those around them every day than they are by doctors and nurses they interact with only occasionally, these cost-free interactions remain largely untapped when engineering social incentives for health. That’s a missed opportunity.”

Because of these lost opportunities, and the high costs when doctors and nurses keep tabs on their patients, the authors say it’s important to engineer social engagements that enlist the social support patients already have, and allow organizations to test their acceptability. “Concerns about privacy are often the reason doctors and hospitals avoid organizing social support,” Asch says. “But while privacy is very important to some patients under some circumstances, more often patients would love if their friends and family helped them manage their diabetes, and those friends and family want to help people get their health under control.”

The authors define a ladder with escalating rungs of social support ranging from no social engagement — such as when a patient is expected to take medication as part of a routine, without anyone seeing them do it or holding them accountable — to a design that relies on reputational or economic incentives, and incorporates teams or other designs that hold patients accountable for their health behaviors and habits.

“Although we don’t normally think of competition or collaboration among patients are part of managing chronic diseases like high blood pressure, heart failure, or diabetes, research shows that behavior is contagious, and programs that take advantage of these naturally occurring relationships can be very effective,” said co-author Roy Rosin, MBA, chief innovation officer at Penn Medicine. “Most health care interventions are designed for the individual patient, but there’s a growing body of research that shows how health care organizations can use social engagement strategy to enhance health for patients who want to be involved in group activities or team competitions aimed at improving health.”

For example, in the fourth rung, where social incentives are designed with reciprocal support, the authors point to a study in which some patients with diabetes were asked to talk on the phone weekly with peers — a technique known as reciprocal mentorship — and others received more typical nurse-led management. Results showed that those who worked directly with peers saw a more significant decline in glycated hemoglobin levels than those who worked with clinical staff.

“Sure, health care is serious business,” Asch says, “but who says it can’t be social?”