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People who consume an egg a day could significantly reduce their risk of cardiovascular diseases compared with eating no eggs, suggests a study carried out in China, published in the journal Heart.

Cardiovascular disease (CVD) is the leading cause of death and disability worldwide, including China, mostly due to ischaemic heart disease and stroke (including both haemorrhagic and ischaemic stroke).

Unlike ischaemic heart disease, which is the leading cause of premature death in most Western countries, stroke is the most responsible cause in China, followed by heart disease.

Although ischaemic stroke accounted for the majority of strokes, the proportion of haemorrhagic stroke in China is still higher than that in high income countries.

Eggs are a prominent source of dietary cholesterol, but they also contain high-quality protein, many vitamins and bioactive components such as phospholipids and carotenoids.

Previous studies looking at associations between eating eggs and impact on health have been inconsistent, and most of them found insignificant associations between egg consumption and coronary heart disease or stroke.

Therefore, a team of researchers from China and the UK led by Professor Liming Li and Dr Canqing Yu from the School of Public Health, Peking University Health Science Center, set out to examine the associations between egg consumption and cardiovascular disease, ischaemic heart disease, major coronary events, haemorrhagic stroke and ischaemic stroke.

They used data from the China Kadoorie Biobank (CKB) study, an ongoing prospective study of around half a million (512,891) adults aged 30 to 79 from 10 different geographical areas in China.

The participants were recruited between 2004-2008 and were asked about the frequency of their egg consumption. They were followed up to determine their morbidity and mortality.

For the new study, the researchers focused on 416,213 participants who were free of prior cancer, cardiovascular disease (CVD) and diabetes.

From that group at a median follow-up of 8.9 years, a total of 83,977 cases of CVD and 9,985 CVD deaths were documented, as well as 5,103 major coronary events.

At the start of the study period, 13.1% of participants reported daily consumption (usual amount 0.76 egg/day) and 9.1% reported never or very rare consumption

(usual amount 0.29 egg/day) of eggs.

Analysis of the results showed that compared with people not consuming eggs, daily egg consumption was associated with a lower risk of CVD overall.

In particular, daily egg consumers (up to one egg/day) had a 26% lower risk of haemorrhagic stroke - the type of stroke with a higher prevalence rate in China than in high-income countries - a 28% lower risk of haemorrhagic stroke death and an 18% lower risk of CVD death.

In addition, there was a 12% reduction in risk of ischaemic heart disease observed for people consuming eggs daily (estimated amount 5.32 eggs/week), when compared with the 'never/rarely' consumption category (2.03 eggs/week).

This was an observational study, so no firm conclusions can be drawn about cause and effect, but the authors said their study had a large sample size and took into account established and potential risk factors for CVD.

The authors concluded: "The present study finds that there is an association between moderate level of egg consumption (up to 1 egg/day) and a lower cardiac event rate.

"Our findings contribute scientific evidence to the dietary guidelines with regard to egg consumption for the healthy Chinese adult."

ROCHESTER, Minn. -- In a recent study published in the Journal of Clinical Investigation, Mayo Clinic researchers identified that an FDA drug approved for myelodysplastic syndrome may be useful to treat triple-negative breast cancer, which is one of the most aggressive and lethal types of breast cancer.

In this study, Mayo investigators identified that the drug 5-aza-2'-deoxycytidine (decitabine) which is FDA approved for the treatment of certain hematological (blood) cancers, could significantly inhibit the growth of triple-negative breast cancers, and importantly this effect was also seen in tumors resistant to chemotherapy. This response was dependent on the presence of certain critical proteins called DNA methyl transferase proteins that are present in only a subset of triple negative breast cancers. This provides a way to identify which patients could benefit from this therapy.

"There is a great need to identify additional treatment options for triple-negative breast cancer, which is one of the most difficult to treat subtypes of breast cancer," says Mayo researcher Liewei Wang, M.D., Ph.D. "The study is a demonstration that we can take advantage of many existing FDA approved drugs to expand their usage by better understanding the mechanisms of how they work and applying them to other cancers."

This study was part of the ongoing work from the Breast Cancer Genome-Guided Therapy (BEAUTY) study, co-led by Matthew Goetz, M.D., a Mayo medical oncologist and Judy Boughey, M.D., a Mayo breast surgeon. The BEAUTY study generated patient derived xenografts (immortalizing breast tumor cells) from patients with breast cancer treated with chemotherapy.

"Patients whose tumor does not respond well to chemotherapy are known to be at significantly increased risk of recurrent breast cancer and death," says Dr. Boughey. "Therefore our focus is to identify new treatment options for these patients."

In the living xenografts from BEAUTY, Mayo investigators found that when DNA methyl transferase proteins were present, decitabine showed an effect in triple-negative breast cancer at a low therapeutic dose. The low doses would result in less toxicity and might allow the drug to be used for a longer time, all of which might help to achieve greater therapeutic efficacy.

According to Dr. Goetz, plans are underway to prospectively study the impact of decitabine in a prospective clinical trial, called BEAUTY2, which is focused on women with triple negative breast cancer that is resistant to chemotherapy.

A new study conducted by the Center for Injury Research and Policy and the Central Ohio Poison Center at Nationwide Children's Hospital found that there were more than 156,000 calls to US Poison Control Centers regarding exposures to attention-deficit hyperactivity disorder (ADHD) medications among children and adolescents 19 years of age and younger from January 2000 through December 2014, averaging 200 calls each week or 29 calls per day.

The study, published online today in the journal Pediatrics, found that while the number of calls about ADHD medication exposures among children and adolescents fluctuated throughout the years of the study there was on overall increase of 61% during the study period. The increase in calls coincided with an increase in ADHD diagnoses and medication prescriptions during the same time period nationally.

"Pediatric exposures to ADHD medications are an increasing problem in the US, affecting children of all ages," said Gary Smith, MD, DrPH, the senior author of the study and director of the Center for Injury Research and Policy at Nationwide Children's Hospital. "We need to do more to prevent these esposures."

The majority of calls were about children 12 years of age and younger (76%). Among children younger than 6 years old, most exposures were associated with the exploratory behavior seen in that age group, for example, accessing improperly stored medications. Exposures among children 6-12 years were most often associated with therapeutic errors, such as taking or being given too much medication, a dose too soon after the previous dose, or the wrong medicine. Among teenagers (13-19 years), about half of reported exposures were intentional abuse/misuse or suspected suicide attempt. As a result, the exposures in this age group were more likely to lead to serious outcomes than those among younger children.

"In young children, it is exploratory behavior and access to the medication bottle, while in school age children it is usually the busy family schedule and a double-dosing medication error," said Rick Spiller, co-author and director of the Central Ohio Poison Center at Nationwide Children's Hospital. "In adolescents it tends to be an intentional exposure. The strategies to prevent these events change as the child gets older, but the risks of a problem remain."

Overall, most (about 60%) of exposed individuals did not receive treatment in a health care facility, and about 25% were treated/evaluated and released. About 6% were admitted to a hospital for medical treatment and there were 3 deaths. While only about 28% of exposure calls had clinical effects reported, the most common clinical effects were agitation/irritability (11%), rapid heart rate (10%), drowsiness/lethargy (3%), high blood pressure (3%), and vomiting (2%). Methylphenidate and amphetamine medications each accounted for about 45% of exposures.

Data for this study were obtained from the National Poison Data System, which is maintained by the American Association of Poison Control Centers (AAPCC). The AAPCC receives data about calls to poison control centers that serve the US and its territories. Poison control centers receive phone calls through the Poison Help Line and document information about the product, route of exposure, individual exposed, exposure scenario, and other data.

Research published in the journal Clinical Science suggests that an immune signalling protein called interleukin (IL)-26 is increased among chronic smokers with lung disease and this involvement reveals disease mechanisms of interest for developing more effective therapy for these hard-to-treat patients.

Chronic tobacco smokers have a substantially increased rate of chronic obstructive pulmonary disease (COPD), chronic bronchitis and bacterial lung infections and these disorders respond poorly to currently available therapies. This is thought to be associated with the accumulation of a type of white blood cell, called neutrophils, in their airways.

Dr Karlhans Fru Che and Professor Anders Lindén at Karolinska Institutet, Stockholm, led a team of researchers from universities in Sweden and Finland to investigate why chronic smokers with lung disease have such high levels of neutrophils. They found that an immune signalling protein called IL-26 is present at high levels in the lungs of these patients. This IL-26 is thought to be a pro-inflammatory 'neutrophil mobilizer' and has previously been found at high concentrations in patients with autoimmune conditions such as Crohn's disease and rheumatoid arthritis, as well as chronic infections such as hepatitis C, all of which are also associated with excessive accumulation of neutrophils.

"Previous research shows that the immunological alterations in the airways of chronic smokers, with or without COPD and chronic bronchitis, include an excessive accumulation of neutrophils in parallel with an enhanced frequency of bacterial infections. Our findings show for the first time that IL-26 may be involved in the mobilization of neutrophils and in the response to bacterial colonization in chronic smokers with or without COPD" commented the lead author on the study, Dr Karlhans Fru Che from Karolinska Institutet, Sweden.

Dr Che and his colleagues looked at the effects of water-soluble tobacco smoke components on human lung cells and found that the exposure triggered the cells to start producing higher than normal amounts of IL-26. They also found increased amounts of other pro-inflammatory proteins in the tobacco-exposed cells such as NF-κB, which appeared to increase in response to increased IL-26 concentrations. Abnormal regulation of NF-κB has been linked to autoimmune disease, infections and cancer in other research.

While the researchers found that IL-26 levels were higher than normal in the chronic smokers, regardless of whether they had clinically stable COPD, they also found that those who did have chronic bronchitis or growth of bacteria had higher levels of IL-26 than those who did not. Moreover, the chronic smokers with exacerbations of COPD had higher levels of IL-26 than those with clinically stable COPD.

"In a previous study, we showed that IL-26 is released by a bacterial compound in healthy human airways and that it enhances the chemotactic response of neutrophils. By now showing that IL-26 is involved in the excessive mobilization of neutrophils in chronic smokers with or without COPD and chronic bronchitis, we strengthen the evidence that this cytokine bears potential as a target for monitoring of and therapeutic intervention in airway disorders characterized by neutrophilic inflammation. However, more studies are needed to improve the understanding of the more precise mechanisms of action of IL-26 before this cytokine can be targeted in clinical trials" explained Dr Che.

The researchers believe their work indicates that IL-26 is a promising target to monitor lung disease risk or burden in chronic smokers and that this knowledge could help develop more effective therapies for this difficult-to-treat group in the future. However, they acknowledge that further work is needed to confirm this.

"Our findings position IL-26 as a promising molecular target that may help improve our understanding of the pathogenic mechanisms behind pulmonary morbidities in chronic tobacco smokers. This knowledge may prove useful for developing new diagnostic tools and criteria as well as for monitoring of disease over time. In a longer perspective, this knowledge may even prove useful for developing new therapy against tobacco-related lung diseases such as COPD, chronic bronchitis and, perhaps, against repeated bacterial infections in the airways." commented Dr Che.

Professor Ilja Striz, Associate Editor of Clinical Science commented "The pathogenesis of chronic obstructive pulmonary disease (COPD) in chronic tobacco smokers is associated with an excessive accumulation of neutrophils in the airways. Results of this collaborative study of authors from Sweden and Finland show that interleukin-26 (IL-26), a neutrophil-mobilizing cytokine, is increased in the airways of chronic smokers with or without COPD. Upregulation of IL-26 in the airways in response to tobacco smoke represents a novel mechanism by which neutrophil recruitment to the lung is regulated and emerges as a new promising molecular target."

ATS 2018, San Diego, CA - A long-term study of the health of Canadian children has found that exposure to ozone (O3), a common air pollutant, at birth was associated with an 82 percent increased risk of developing asthma by age three. The study, which was a 10-year follow-up to the 2006 Toronto Child Health Evaluation Questionnaire (T-CHEQ), was presented at the 2018 American Thoracic Society International Conference.

"Our findings show that the hazard ratios for ozone measured at birth as a single pollutant showed statistically significant higher risks for development of asthma, allergic rhinitis and eczema," said lead author Teresa To, PhD, senior scientist, Child Health Evaluative Services at The Hospital for Sick Children (SickKids), Toronto, Ontario, Canada. "The results of our study are important because the study examines the effect of pollution on health outcomes in early childhood, and has the longest longitudinal follow-up of a cohort of school-aged children in Canada."

A hazard ratio is a statistical formula used to determine risk.

For this part of the T-CHEQ study, 1,881 children were followed from birth to 17 years of age, on average. Amongst these children, 31 percent developed asthma, 42 percent had allergic rhinitis and 76 percent had eczema. An 82 percent higher risk of developing asthma was associated with each 10 parts per billion, or ppb increase in exposure to ozone at birth. A similar risk was not observed in association with exposure to nitrogen dioxide or PM2.5, a type of pollutant.

The researcher team took annual average concentrations of pollutants from fixed monitoring stations across Ontario. They assigned these measurements based on study participants' postal codes at birth. Development of asthma, allergic rhinitis and eczema were determined based on any records of health services used for these conditions. The researchers adjusted for variables such as parental history of asthma and early home exposure to pollutants.

Some studies have shown that ozone depletes antioxidant activity and increases indications of inflammation in the respiratory tract fluid lining and affects lung growth.

"We examined O3 and NO2, as well as particulate matter PM2.5 and ultrafine particulates (UFP - not discussed in this abstract), because these are the key pollutants that have been suggested in the literature to exacerbate asthma, diabetes, hypertension and chronic obstructive pulmonary disease (COPD)," said Dr. To, who is also a professor in the Graduate School of Public Health at the University of Toronto. "It is well supported by research findings that short-term and long-term exposure to NO2 and particulate matter can increase asthma exacerbations, respiratory symptoms, hospitalizations and even mortality. Similarly, short-term exposure to O3 can decrease lung function and increase the risk of respiratory infections in children."

Children are at a higher risk because their lungs and other respiratory organs are smaller, and they spend more time in outdoor physical activities that make them breathe faster and more deeply. Poor air quality may have a larger impact on them.

"The quality of air in Ontario, Canada is relatively good on most days of the year, yet we observed an adverse effect on health outcomes in children who were exposed to air pollution at birth and in early life," said Dr. To. "This has significant implications for other countries that have higher levels of pollution. It is well established that short-term exposure to pollutants such as ozone can decrease lung function, exacerbate asthma and increase the risk of respiratory infections. There is now mounting evidence that long-term exposure can lead to disease progression, such as from asthma to COPD and could increase the risk of death."

The World Health Organization (WHO) 2016 report on air pollution and health indicated that 92 percent of the world's population lives in places where air quality levels exceeded WHO limits. According to WHO, one in eight deaths in the world is a result of air pollution exposure, making air pollution the single largest global environmental health risk.

"Air pollution isn't only one or a few countries' problems, but rather a global public health concern," Dr. To said. "While there are individual actions one can consider to reduce exposure to air pollutants, it also requires action by public authorities at the national, regional and international levels. Reducing air pollution could save millions of lives."

Participating in exercise 4-5 days per week is necessary to keep your heart young, according to new research published in The Journal of Physiology. These findings could be an important step to develop exercise strategies to slow down such ageing.

The optimal amount of exercise required to slow down ageing of the heart and blood vessels has long been a matter of vigorous debate. As people age, arteries - which transport blood in and out of the heart - are prone to stiffening, which increases the risk of heart disease. Whilst any form of exercise reduces the overall risk of death from heart problems, this new research shows different sizes of arteries are affected differently by varying amounts of exercise. 2-3 days a week of 30 minutes exercise may be sufficient to minimise stiffening of middle sized arteries, while exercising 4-5 days a week is required to keep the larger central arteries youthful.

The authors performed a cross-sectional examination of 102 people over 60 years old, with a consistently logged lifelong exercise history. Detailed measures of arterial stiffness were collected from all participants, who were then categorised in one of four groups depending on their lifelong exercise history: Sedentary: less than 2 exercise sessions/week; Casual Exercisers: 2-3 exercise sessions per week; Committed Exercisers: 4-5 exercise sessions/week and Masters Athletes: 6-7 exercise sessions per week. (NB: an exercise session was at least 30 minutes).

Upon analysing the results, the research team found that a lifelong history of casual exercise (2-3 times a week) resulted in more youthful middle sized arteries, which supply oxygenated blood to the head and neck. However, people who exercised 4-5 times per week also had more youthful large central arteries, which provide blood to the chest and abdomen, in addition to healthier middle sized ones.

The fact the larger arteries appear to require more frequent exercise to remain youthful will aid the development of long-term exercise programmes. They also enable the research team to now focus on whether or not ageing of the heart can be reversed by exercise training over a long period of time.

The research may have been limited by the fact that individuals were allocated to groups based on past exercise frequency, as opposed to other components of exercise programmes such as intensity, duration or mode, all of which could have large impacts on vascular adaptations. Furthermore, additional, unmeasured factors such as dietary intake and social background could influence arterial compliance indirectly through reduced adherence, or by non-exercise related means.

Benjamin Levine, one of the authors of the study, is excited to investigate this in the future:

"This work is really exciting because it enables us to develop exercise programmes to keep the heart youthful and even turn back time on older hearts and blood vessels. Previous work by our group has shown that waiting until 70 is too late to reverse a heart's ageing, as it is difficult to change cardiovascular structure even with a year of training. Our current work is focussing on two years of training in middle aged men and women, with and without risk factors for heart diseases, to see if we can reverse the ageing of a heart and blood vessels by using the right amount of exercise at the right time".

According to the University of Pittsburgh School of Medicine scientists who conducted the study, theirs is the first large-scale evaluation of the impact of in-hospital opioid prescribing on post-discharge opioid use.

"Most previous studies of opioid use in health care have focused on the outpatient setting," said lead study author Jason Kennedy, MS, research project manager in Pitt's Department of Critical Care Medicine. "But opioids are often introduced during hospitalization. That's something clinicians can control, so we looked at inpatient prescription of these drugs to identify targets that may reduce opioid use once patients are out of the hospital."

The researchers analyzed the medical records of 357,413 non-obstetrical adults hospitalized between 2010 and 2014 at 12 University of Pittsburgh Medical Center (UPMC) hospitals in southwestern Pennsylvania. The region is one of the areas of the country where opioid addiction is a major public health problem. The researchers focused on the 192,240 patients who had not received an opioid in the year prior to their hospitalization - otherwise known as "opioid naïve" patients.

Nearly half (48 percent) of these patients received an opioid while hospitalized. After discharge, those patients receiving hospital opioids were more than twice as likely to report outpatient opioid use within 90-days (8.4 percent vs. 4.1 percent).

The study also found that:

Those who took an opioid for more than three-quarters of their hospital stay were 32 percent more likely than those who took an opioid for less than one-fourth of their stay to be prescribed an opioid within 90 days of leaving the hospital.

Those who used an opioid within 12 hours of discharge were twice as likely as those who stopped taking an opioid more than 24 hours before discharge to be prescribed an opioid within 90 days of leaving the hospital.

33 percent received an opioid during the 24 hours prior to discharge from the hospital.

20 percent of those receiving opioids in the ICU received intravenous opioids on transfer to the medical ward.

The findings suggest some inpatient interventions that might reduce opioid use in outpatient settings, Mr. Kennedy said.

"Reducing use of opiates near the end of a hospital stay, especially in the 24 hours before discharge, may reduce outpatient prescription of opioids," he said. "And weaning ICU patients off of intravenous opioids, the most potent way of administering these pain killers, before transitioning them to the medical ward may also help reduce outpatient usage."

Further study, ideally with randomized, controlled trials, would be necessary to provide definitive guidance to doctors and other health care providers, he added.

Bottom Line: An early study suggests it may be feasible to use human aortic grafts preserved by freezing to rebuild windpipe and airway sections removed because of disease.

Why The Research Is Interesting: Airway replacement could potentially benefit many patients with lung cancer and be an option for patients with end-stage tracheobronchial disease.

Who and When: 20 patients with lung tumors or tracheal lesions, of which 13 patients had diseased airway sections removed and underwent airway transplantation (5 tracheal, 7 bronchial and 1 carinal, which is where the trachea divides into the bronchi of the lungs); study conducted from October 2009 through February 2017, with final patient follow-up in November 2017

What (Study Measures): Airway transplantation using a cryopreserved aortic graft and custom-made stent inserted into the graft to keep the airway from collapsing but was later removed (exposure); 90-day morality (primary outcome)

How (Study Design): This was a cohort study where people were followed over time.

Authors: Emmanuel Martinod, M.D., Ph.D., Assistance Publique-Hopitaux de Paris, Bobigny, France, and coauthors

Results:

Overall 90-day mortality among initial 20 patients was 5% because one patient who underwent carinal transplantation died

No deaths after 90 days among patients who underwent tracheal or bronchial reconstruction

10 of 13 patients who underwent transplantation alive after nearly four years

8 of 10 breathing normally through newly formed airways after stent removal

New generation of cartilage was observed in transplanted areas

Study Limitations: Limited number of patients in this feasibility study at a single center without a comparison group; larger studies needed to further assess effectiveness and safety

Study Conclusions: This study demonstrated the feasibility for complex tracheal and bronchial reconstruction.

PORTLAND, OR - Twenty five years after it opened for enrollment, the landmark Prostate Cancer Prevention Trial has delivered a final verdict. Finasteride, a common hormone-blocking drug, reduces mens' risk of getting prostate cancer without increasing their risk of dying from the disease. Initial study findings suggested there may be a link between use of the drug and a more lethal form of prostate cancer, but long-term follow-up shows that is not true.

Dr. Ian Thompson, Jr., principal investigator of SWOG's Prostate Cancer Prevention Trial, or PCPT, will deliver the findings May 19 at the Journal of Urology Lecture at the 2018 Annual American Urological Association Meeting in San Francisco. The meeting is the largest gathering of urologists in the world.

"What we can now say is that finasteride not only significantly reduces a man's risk of prostate cancer, it is safe to use based on very long-term follow-up in our study," said Thompson. "In PCPT, we found no increased risk of prostate cancer death in men who took finasteride compared with men who did not. These results are transformational. Prostate cancer is the most common cancer diagnosed in American men, and we have found an inexpensive, effective drug that can prevent it. I'm pleased to report that we've answered the questions and closed the book."

Thompson is chair of SWOG's genitourinary cancer committee, overseeing development of all urologic cancer studies for the federally-funded cancer clinical trials group, and serves as president of CHRISTUS Santa Rosa Hospital - Medical Center in San Antonio, Texas and as emeritus professor at the University of Texas Health Science Center. Thompson led SWOG's landmark PCPT. He and his team set out to determine whether finasteride, a drug used to treat symptoms of prostate enlargement as well as male pattern baldness, would prevent prostate cancer in men over the age of 55. At the time, scientists and doctors knew that prostate cancers were hormonally sensitive, and finasteride, the first 5-alpha-reductase inhibitor, which targets and blocks the action of androgens like testosterone, became available to test.

The PCPT randomized 18,882 men from 1993 to 1997 to finasteride or a placebo - making it one of the largest cancer prevention trials ever mounted. The trial intervention was stopped in 2003 when investigators found a significant, positive result: finasteride reduced prostate cancer risk by 25 percent. But the study also showed that finasteride produced a small increase in the number of high-grade prostate cancers - a negative finding that resulted in a "black box" warning posted by the U.S. Food and Drug Administration on prescription drug labels to flag potentially disabling or life-threatening side effects.

Subsequent SWOG analyses of PCPT data revealed unexpected benefits of finasteride. It improved detection of prostate cancer in screening tests and biopsies, and also improved detection of high-grade cancers. Additional analysis also revealed that men enrolled in the study lived about the same amount of time - regardless of whether they took finasteride or the placebo. Still, despite evidence of the benefits of finasteride, the label warning had an impact. Few men today take the generic drug to lower their cancer risk.

As most deaths from prostate cancer are caused by high-grade cancers, years of PCPT findings still left a critical question unanswered: Would the increased number of high-grade cancers detected in the PCPT years ago result in more prostate cancer deaths over time?

Thompson and his team went back to the study and matched participants to the National Death Index, a centralized database of death record information managed by the U.S. Centers for Disease Control and Prevention. This analysis allowed researchers to determine if a trial participant had died and to determine the cause of death. With almost 300,000 person-years of follow-up and a median follow-up of 18.4 years, they found 42 deaths due to prostate cancer on the finasteride arm and 56 on placebo. Thus, there was no statistically significant increased risk of prostate cancer death with finasteride.

"This discovery could benefit tens of thousands of men each year in the United States by identifying a drug that can safely and effectively prevent prostate cancer," Thompson said. "Treatment for the disease is costly and can have serious side effects, such as impotence and urinary incontinence. My hope is that the visionary decision of our National Cancer Institute colleagues to conduct this study, and the scientific evidence it produced these last 25 years, will provide a lasting benefit for patients."

East Hanover, NJ. May 18, 2018. Stroke researchers have confirmed that the presence of frontal cortical lesions moderated response to prism adaptation treatment after right-brain stroke. Their findings are detailed in "Frontal lesions predict response to prism adaptation treatment in spatial neglect: A randomised controlled study" (doi: 10.1080/09602011.2018.1448287), which was published online ahead of print on March 20, 2018 by Neuropsychological Rehabilitation. The authors are Kelly M. Goedert, PhD, of Seton Hall University, Peii Chen, PhD, of Kessler Foundation, Anne L. Foundas, MD, of Tulane University, and A.M. Barrett, MD, director of Stroke Rehabilitation Research at Kessler Foundation.

Spatial neglect is a common cause of functional disability after right hemisphere stroke. Prism adaptation treatment is a promising intervention to promote functional recovery from spatial neglect; however, some individuals fail to respond. The current study randomized individuals with spatial neglect to two groups, treatment and control. The treatment group received ten days of prism adaptation treatment; the control group received standard care.

The researchers confirmed their earlier findings that frontal lesions moderated response to prism treatment. In the treatment group, improvement in spatial neglect symptoms was seen only in individuals with frontal lesions. In the control group, the presence of frontal lesions did not modify response.

"Our research shows that patients with frontal cortical lesions may benefit from prism adaptation treatment for spatial neglect," affirmed Dr. Barrett. "Early identification of patients with hemiparesis and frontal lesions is critical to their optimal recovery," she emphasized, "and could reduce the substantial costs of stroke care and improve public health. Because spatial neglect goes undetected in as many as 80% of stroke survivors, this is a major challenge. Meeting that challenge requires educating stroke professionals about targeted prism treatment, and conducting further research on a larger scale in the stroke population."

HOUSTON - (May 18, 2018) - A study led by a neurologist from McGovern Medical School at The University of Texas Health Science Center at Houston (UTHealth) showed that a computed tomography (CT scan) could be sufficient for determining thrombectomy treatment in stroke.

The late-breaking results were presented by Amrou Sarraj, M.D., today at the European Stroke Organization Conference in Sweden.

Thrombectomy surgery can be performed to remove a large blood clot lodged in a blood vessel. It has been shown to be an effective treatment for improving clinical outcomes in stroke up to 24 hours from onset. Stroke is the leading cause of long-term disability and fourth leading cause of death globally. Imaging must be done to determine the location of the clot and whether the patient is a good candidate for thrombectomy. Physicians use non-contrast simple CT and/or advanced CT with an injected contrast dye (CT perfusion) to see the area.

"The results show that simple imaging, while not perfect, may be good enough. This basic technique is faster, which means patients could potentially be treated more quickly," said Sarraj, associate professor of neurology at McGovern Medical School at UTHealth. "The advanced imaging of CT perfusion isn't available everywhere, so this could open up the door to identify more people for potential treatment, especially in remote areas."

Sarraj was principal investigator of the study, Optimizing Patient Selection for Endovascular Treatment in Acute Ischemic Stroke (SELECT). The clinical trial enrolled 445 patients who received both simple and advanced imaging at nine academic health centers across the U.S. from January 2016 to February 2018. Senior author was Gregory Albers, M.D., of Stanford University.

The results showed that patients who were treated based on simple imaging had identical clinical outcomes to those treated based on advanced imaging. In addition, those patients who had a good imaging profile - a smaller area of dead brain tissue - had the same clinical outcomes regardless of which imaging was used.

"If those treated using simple imaging can do as well as those treated by CT perfusion, this is an extremely important breakthrough that warrants further exploration and testing because it could broaden the number of patients having and benefiting from thrombectomy," said Sarraj, who is also director of UTHealth's vascular neurology fellowship program and an attending physician at Memorial Hermann-Texas Medical Center.

However, the study also revealed that 42 percent of patients who were excluded from thrombectomy by one of the imaging profiles, but had a good profile on the other type of imaging, had positive clinical outcomes.

"Our results should not be interpreted that advanced perfusion images are not necessary or should not be acquired at all as they still identified a group of patients that may be treated with thrombectomy when CT alone was not enough. The numbers involved are significant because 17.6 percent of patients could have been excluded from having surgery if the CT or CT perfusion were relied on alone, so there's a real opportunity here to help more people if both forms of imaging are available," Sarraj said.

The study did not randomize patient selection by simple imaging versus advanced imaging.

"Although this was the first large cohort study with pre-specified imaging criteria, analyses and objectives to look at imaging type selection, there is room for further refinement to truly test our initial findings and see if they are more affirmative and conclusive," Sarraj said.

In "Does Armodafinil Improve Driving Task Performance and Weight Loss in Sleep Apnea? A Randomized Trial," Nathaniel Marshall, PhD, and his colleagues at the Woolcock Institute for Medical Research, University of Sydney, report on their study of armodafinil, which has been approved by the U.S. Food and Drug Administration to treat excessive daytime sleepiness due to OSA, narcolepsy and other conditions.

The researchers found that armodafinil did not improve the driving performance of those with OSA after six months of use, the study's primary outcome. Nor did those taking the drug report less daytime sleepiness than those receiving a placebo, as measured by the Epworth Sleepiness Scale and the Functional Outcomes of Sleep Questionnaire.

In the study, 113 participants (ages 18 to 70) were randomly assigned to either receive 150 mg of armodafinil daily or a placebo. Participants had moderate to severe OSA, were moderately obese and did not use continuous positive airway pressure (CPAP) or an oral appliance that advances their lower jaw. Both therapies treat OSA by preventing the pauses in breathing that occur in OSA when the back of the throat collapses.

All participants were also randomly assigned to one of two popular diets in Australia: the Australian Guide to Healthy Eating diet, which is similar to the American Dietary Guidelines "Choose My Plate," or a low-glycemic index, high-protein diet. Driving ability was assessed during a simulated 90-minute drive.

According to Dr. Marshall, a clinical trials epidemiologist, about half of patients seen in sleep clinics fall into the category of having sleep apnea and abdominal obesity but being unable to tolerate CPAP or an oral appliance. "My clinical colleagues and I call these patients the 'forgotten patients,'" he said. "We felt we needed to help our patients lose weight to address their metabolic risks over the longer term whilst addressing their sleepiness and neurocognitive dysfunction immediately with armodafinil."

He added that sporadic reports indicate that patients using armodafinil and its cousin modafinil to improve wakefulness experienced weight loss, so he and his coauthors wanted to test whether the drugs might increase the success of a deliberate weight loss program.

In the current study, armodafinil did, in fact, have a positive effect on body mass. Participants on the drug lost more body fat on either of the diets, which appeared to reduce weight equally well, than those who received the placebo. At six months, those in the armodafinil arm of the study lost an average of 6.4 pounds more body fat than those receiving the placebo. The researchers said that some of this additional weight loss may be due to the increased activity levels of those receiving the drug, as measured by an activity tracker. Importantly, the authors noted that armodafinil did not appear to increase blood pressure.

Armodafinil also appeared to improve driving ability after three months. The researchers speculate that those taking armodafinil learned their simulated driving tasks faster than those receiving the placebo because by six months there was no difference between the two groups. Even with the improvements that came with practice, the authors noted that, on average, driving ability among these participants with untreated OSA was two standard deviations worse than healthy people without OSA.

CORVALLIS, Ore. - Researchers at Oregon State University have developed a computer program that represents a key step toward better understanding the connections between mutant genetic material and disease.

Known as bpRNA, the software is a big-data annotation tool for secondary structures in ribonucleic acids.

"It's capable of parsing RNA structures, including complex pseudoknot-containing RNAs, so you end up with an objective, precise, easily-interpretable description of all loops, stems and pseudoknots," said corresponding author David Hendrix. "You also get the positions, sequence and flanking base pairs of each structural feature, which enables us to study RNA structure en masse at a large scale."

RNA works with DNA, the other nucleic acid - so named because they were first discovered in the cell nuclei of living things - to produce the proteins needed throughout the body. DNA contains a person's hereditary information, and RNA delivers the information's coded instructions to the protein-manufacturing sites within the cells. Many RNA molecules do not encode a protein, and these are known as noncoding RNAs.

"There are plenty of examples of disease-associated mutations in noncoding RNAs that probably affect their structure, and in order to statistically analyze why those mutations are linked to disease we have to automate the analysis of RNA structure," said Hendrix, assistant professor of biochemistry and biophysics in the College of Science. "RNA is one of the fundamental, essential molecules for life, and we need to understand RNAs' structure to understand how they function."

Secondary structures are the base-pairing interactions within a single nucleic acid polymer or between two polymers. DNA has mainly fully base-paired double helices, but RNA is single stranded and can form complicated interactions.

Hendrix says bpRNA, presented this month in a paper in Nucleic Acids Research, features the largest and most detailed database to date of secondary RNA structures.

"To be fair it's a meta-database, but our special sauce is the tool to annotate everything," said Hendrix, who is also an assistant professor in the OSU College of Engineering. "Before there was no way of saying where all the structural features were in an automated way. We provide a color-coded map of where everything is. These annotations will enable us to identify statistical trends that may shed light on RNA structure formation and may open the door for machine learning algorithms to predict secondary RNA structure in ways that haven't been possible."

Researchers have successfully tested the tool on more than 100,000 structures, "many of which are very complex, with lots of complex pseudoknots."

"Every day new RNAs are discovered and researchers are making huge progress in understanding their function," Hendrix said. "We're starting to appreciate that the genome is full of noncoding RNAs in addition to messenger RNAs, and they're important biological molecules with big effects on human health and disease."

PHILADELPHIA - An antibody used to treat the skin disease psoriasis and other chronic autoimmune diseases such as rheumatoid arthritis and inflammatory bowel disease has no effect on aortic inflammation - a key marker of future risk of major cardiovascular events - unlike other antibodies that target different aspects of the immune system. Researchers from the Perelman School of Medicine at the University of Pennsylvania, in collaboration with the National Heart, Lung, and Blood Institute (NHLBI), led a multi-center, randomized, double-blind, placebo-controlled study and found patients taking the drug adalimumab - marketed as Humira - saw no change in aortic inflammation, as assessed by nuclear imaging, when compared to the placebo group. However, the drug did improve other key markers of inflammation known to predict future cardiovascular events - which suggests the drug may have a cardiovascular benefit despite the lack of change in aortic vascular inflammation. The study was published today in the journal Circulation: Cardiovascular Imaging, and senior author Joel M. Gelfand, MD MSCE, a professor of Dermatology and Epidemiology at Penn, will present the findings today at the International Investigative Dermatology 2018 Annual Meeting in Orlando, Florida.

Psoriasis is a chronic inflammatory disease that causes skin cells to multiply faster than normal resulting in raised, red patches covered by silvery scales. It occurs most commonly on the scalp, knees, and elbows but can appear anywhere on the body including the face, genitals, nails, and other places. In moderate to severe cases, it carries an increased risk of heart attack, stroke, and premature death, a finding established by Gelfand in a 2006 landmark study. The National Psoriasis Foundation estimates psoriasis affects about 7.5 million Americans.

Adalimumab is an antibody that blocks tumor necrosis factor alpha (TNF-a), a protein that promotes inflammation in the body. It's approved by the U.S. Food and Drug Administration to treat psoriasis, psoriatic arthritis, rheumatoid arthritis, ulcerative colitis, and Crohn's Disease, among other conditions. TNF inhibitors are the most popular prescribed biologic medications for inflammatory diseases, and Penn researchers have previously found another biologic drug, ustekinumab (Stelara), led to a 19 percent reduction in aortic inflammation in psoriasis patients. The researchers wanted to know whether adalimumab provided a similar benefit.

Ninety-seven patients at eight different enrollment sites were randomly divided into three groups. One group received adalimumab, another received a placebo, and a third received Ultraviolet B phototherapy - another common treatment for psoriasis which works by suppressing inflammation locally in the skin as opposed to systemically, as is the case with adalimumab. Patients were evaluated at 12 weeks, and patients in the two active treatment groups saw significant improvement in their psoriasis relative to placebo. At the end of the initial 12 weeks, all patients received adalimumab - with those already on the drug getting 40 weeks and those taking it for the first time getting 52 weeks so all patients ended up with 52 weeks of treatment.

At both the 12-week and 52-week evaluation periods, patients in the adalimumab group saw no change compared to placebo or baseline, respectively, in aortic vascular inflammation. Patients receiving phototherapy saw a four percent reduction compared to baseline at 12 weeks but the difference was not statistically significant from placebo.

"These results are similar to prior clinical trials which showed adalimumab did not reduce aortic inflammation in patients with psoriasis. They are, however, in contrast to a previous study which showed an improvement in aortic vascular inflammation at 12 weeks in patients taking ustekinumab - a biologic that targets a different aspect of the immune system," Gelfand said.

Despite neutral imaging results, adalimumab did improve other key markers of inflammation in the blood including GlycA, CRP, TNF, and IL-6.

"Each of these increases future risk of heart attack and diabetes, so observing a reduction of these markers of systemic inflammation provides compelling evidence of beneficial effects of anti-TNF therapy in psoriasis," said the study's lead author Nehal N. Mehta, MD MSCE FAHA, chief of the Laboratory of Inflammation and Cardiometabolic Diseases at the NHLBI.

Understanding cholesterol effects of adalimumab by new techniques was another goal of Gelfand and Mehta's study.

"We know that HDL, the good cholesterol, is low in psoriasis, but here, we now show that despite reduction in systemic inflammation following adalimumab therapy, HDL particle size got smaller (not a good thing) and the HDL worked less effectively to remove cholesterol from the body," Mehta said.

Gelfand noted the impact on HDL may be balanced by the improvement seen in markers of systemic inflammation that are reduced as psoriasis improves. Gelfand also emphasized that this class of drug is commonly used, so understanding its potential cardiovascular effects is highly important. Future studies in this area are already underway at Penn and the NHLBI.

DENVER/May 17, 2018 - Morris Animal Foundation-funded researchers from the University of Sydney have found a previously undiscovered hepadnavirus in an immunocompromised cat, and subsequently in banked feline blood samples. The research team published their results today in the prestigious journal Viruses.

"This is a very exciting discovery," said Dr. Julia Beatty, Professor of Feline Medicine at the University of Sydney School of Veterinary Science. "The domestic cat hepadnavirus is in the same family as hepatitis B virus of people. Until now, we didn't know that companion animals could be get this type of infection. We obviously need to understand the impact of this infection on cat health."

Beatty noted that similar viruses can cause hepatitis and liver cancers in other species, but that there is no risk to humans or other pets from the newly discovered cat hepadnavirus.

"The importance of this finding cannot be overstated," said Dr. Kelly Diehl, Senior Scientific and Communications Adviser at Morris Animal Foundation. "Finding a new virus responsible for disease is the first step in developing a vaccine to prevent infection. It's especially exciting if the vaccine could prevent a future cancer from developing in immunocompromised or other vulnerable cats."

The team at the University of Sydney, led by Beatty, first identified the virus in a feline immunodeficiency virus positive cat that died of lymphoma, a common cancer of cats. Once the team identified the virus, they tested stored blood sample from adult pet cats. To the team's surprise, they found evidence of infection with the hepadnavirus in the banked samples. The new virus was identified in 10 percent of the FIV-infected cats and 3.2 percent of non-FIV infected cats.

"Apart from its relevance for feline health, this discovery helps us understand how hepatitis viruses, which can be deadly, are evolving in all species," said Beatty.