Transactions of the American Clinical and Climatological Association
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Trans. Am. Clin. Climatol. Assoc. · Jan 2010
ReviewThe 2009 influenza A (H1N1) pandemic: what have we learned in the past 6 months.
The present review describes how the first influenza pandemic of the XXI century occurred, the characteristics of the virus that produced it, its epidemiology, clinical and pathological presentation, and the treatment and prevention methods that have been instituted. The lessons that have been learned in the first 6 months of the pandemic include: 1) predictions were not fulfilled (it was not an avian virus but a swine virus that caused the pandemic, it started in the American continent not in Asia), 2) international cooperation was critical, 3) mass media played a key role communicating to the public and health care professionals about this evolving, and 4) preparedness plans were very important to confront the pandemic.
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Trans. Am. Clin. Climatol. Assoc. · Jan 2009
Global climate change and health: developing a research agenda for the NIH.
Global climate change is receiving worldwide attention because of its anticipated impacts on the Earth's physical and biological systems. Through its effects on natural and human environments, climate change will likely impact economic viability and human health and well-being. The impact of climate change on human health is likely to be complex and significant, including effects on cancers, cardiovascular and respiratory disease, food-, water-, and vector-borne diseases, heat-related illness, mental and social well-being, nutrition, trauma, and vulnerable demographic sectors. ⋯ At the NIH, we have recently established an agency-wide planning group to assess the research questions in health and medicine that climate change presents, to link this agenda to parallel activities across other agencies of the U. S. Government (USG), and to advance a NIH research agenda in this area.
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Trans. Am. Clin. Climatol. Assoc. · Jan 2009
ReviewMedical and genetic differences in the adverse impact of sleep loss on performance: ethical considerations for the medical profession.
The Institute of Medicine recently concluded that-on average-medical residents make more serious medical errors and have more motor vehicle crashes when they are deprived of sleep. In the interest of public safety, society has required limitations on work hours in many other safety sensitive occupations, including transportation and nuclear power generation. Those who argue in favor of traditional extended duration resident work hours often suggest that there are inter- individual differences in response to acute sleep loss or chronic sleep deprivation, implying that physicians may be more resistant than the average person to the detrimental effects of sleep deprivation on performance, although there is no evidence that physicians are particularly resistant to such effects. ⋯ Given the magnitude of inter-individual differences in the effect of sleep loss on cognitive performance, and the sizeable proportion of the population affected by sleep disorders, hospitals face a number of ethical dilemmas. How should the work hours of physicians be limited to protect patient safety optimally? For example, some have argued that, in contrast to other professions, work schedules that repeatedly induce acute and chronic sleep loss are uniquely essential to the training of physicians. If evidence were to prove this premise to be correct, how should such training be ethically accomplished in the quartile of physicians and surgeons who are most vulnerable to the effects of sleep loss on performance without unacceptably compromising patient safety? Moreover, once it is possible to identify reliably those most vulnerable to the adverse effects of sleep loss on performance, will academic medical centers have an obligation to evaluate the proficiency of both residents and staff physicians under conditions of acute and chronic sleep deprivation? Should work-hour policy limits be modified to ensure that they are not hazardous for the patients of the most vulnerable quartile of physicians, or should the limits be personalized to enable the most resistant quartile to work longer hours? Given that the prevalence of sleep disorders has increased in our society overall, and increases markedly with age, how should fitness for extended duration work hours be monitored over a physician's career? In the spirit of the dictum to do no harm, advances in understanding the medical and genetic basis of inter-individual differences in the performance vulnerability to sleep loss should be incorporated into the development of work-hour policy limits for both physicians and surgeons.
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Climate change science points to an increase in sea surface temperature, increases in the severity of extreme weather events, declining air quality, and destabilizing natural systems due to increases in greenhouse gas emissions. The direct and indirect health results of such a global imbalance include excessive heat-related illnesses, vector- and waterborne diseases, increased exposure to environmental toxins, exacerbation of cardiovascular and respiratory diseases due to declining air quality, and mental health stress among others. ⋯ As a result, strategies to address climate change must include health as a strategic component on a regional level. The co-benefits of improving health while addressing climate change will improve public health infrastructure today, while mitigating the negative consequences of a changing climate for future generations.
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Trans. Am. Clin. Climatol. Assoc. · Jan 2009
ReviewThe inherited autoinflammatory syndrome: a decade of discovery.
The hereditary autoinflammatory diseases arise from mutations of genes regulating the innate immune system. These rare disorders are well characterized, both clinically and in terms of their molecular pathogenesis. The recurrent attacks of febrile polyserositis of Familial Mediterranean Fever (FMF) are due to defective pyrin, a protein that down-regulates inflammation. ⋯ TRAPS (TNF Receptor Associated Periodic Syndrome), formerly known as Familial Hibernian Fever, is caused by a defective membrane receptor for TNF. Three other hereditary disorders which overlap in their clinical expression - Familial Cold Autoinflammatory Syndrome, the Muckle Wells syndrome, and Neonatal Onset Multisystem Inflamatory Disease (NOMID) - are a consequence of gain-of-function mutations of the gene encoding cryopyrin, the scaffolding protein of the inflammasome. The PAPA syndrome (Pyogenic Arthritis, Pyoderma gangrenosum, Acne) results from mutations of a gene that increases the binding of its product (PSPSTPIP1) to pyrin, thereby blunting the inhibitory effect of pyrin on inflammasome activation.