استكشف المجموعة الواسعة من العناوين المتاحة.

In 1952 the Korean War was exploding. The Marines were in dire need of reinforcements, and enlistments were falling off. Draftees were rounded up and there was a mighty push to transform these lazy civilians into disciplined troops. I was one of them. And among the steely drill instructors was Sgt. William G. Adamaitis, charged with training Platoon 304 at Parris Island. I was his prize goat. He was my master. To Sergeant Adamaitis I was Miss [Norman S. Morris] and when it came to dealing out punishment I was Sergeant Adamaitis's favorite object for the platoon to study. I turned to the Internet. Within minutes, the name William Adamaitis materialized on the screen, in Dayton, Ohio. I reached for the phone but hesitated before dialing. All the what-if's hung in the air. What if this was D.I. Adamaitis? What would we say to each another? What if he had no recollection of me? What if his estimation of me had never changed? And why, after all this time, did I still care what William Adamaitis thought of me? A woman answered. ''Yes, you have the right number. I'll see if he can pick up. '' I have a good ear for voices, but when Lt. Col. William G. Adamaitis said hello, the voice I heard was not easily recognizable. The voice I remembered was always shouting and raucous. This one was subdued, but when the colonel learned that he was talking to Miss Morris, an intensity crept in. Platoon 304 was the last platoon Sergeant Adamaitis ever trained, and Colonel Adamaitis could still see Miss Morris in his mind.

\"WHAT a great house,\" he said, perfect for Tony's little tryst. And right aside a wooded stream. Perfect.\" I was showing one of Tony

Randomized controlled trials have shown the importance of tight glucose control in type 1 diabetes (T1DM), but few recent studies have evaluated the risk of cardiovascular disease (CVD) and all-cause mortality among adults with T1DM. We evaluated these risks in adults with T1DM compared with the non-diabetic population in a nationwide study from Scotland and examined control of CVD risk factors in those with T1DM. The Scottish Care Information-Diabetes Collaboration database was used to identify all people registered with T1DM and aged ≥20 years in 2005-2007 and to provide risk factor data. Major CVD events and deaths were obtained from the national hospital admissions database and death register. The age-adjusted incidence rate ratio (IRR) for CVD and mortality in T1DM (n = 21,789) versus the non-diabetic population (3.96 million) was estimated using Poisson regression. The age-adjusted IRR for first CVD event associated with T1DM versus the non-diabetic population was higher in women (3.0: 95% CI 2.4-3.8, p<0.001) than men (2.3: 2.0-2.7, p<0.001) while the IRR for all-cause mortality associated with T1DM was comparable at 2.6 (2.2-3.0, p<0.001) in men and 2.7 (2.2-3.4, p<0.001) in women. Between 2005-2007, among individuals with T1DM, 34 of 123 deaths among 10,173 who were <40 years and 37 of 907 deaths among 12,739 who were ≥40 years had an underlying cause of death of coma or diabetic ketoacidosis. Among individuals 60-69 years, approximately three extra deaths per 100 per year occurred among men with T1DM (28.51/1,000 person years at risk), and two per 100 per year for women (17.99/1,000 person years at risk). 28% of those with T1DM were current smokers, 13% achieved target HbA(1c) of <7% and 37% had very poor (≥9%) glycaemic control. Among those aged ≥40, 37% had blood pressures above even conservative targets (≥140/90 mmHg) and 39% of those ≥40 years were not on a statin. Although many of these risk factors were comparable to those previously reported in other developed countries, CVD and mortality rates may not be generalizable to other countries. Limitations included lack of information on the specific insulin therapy used. Although the relative risks for CVD and total mortality associated with T1DM in this population have declined relative to earlier studies, T1DM continues to be associated with higher CVD and death rates than the non-diabetic population. Risk factor management should be improved to further reduce risk but better treatment approaches for achieving good glycaemic control are badly needed. Please see later in the article for the Editors' Summary.

Chronic obstructive pulmonary disease (COPD) results in airflow obstruction and a marked reduction in exercise capacity and health-related quality of life (HRQoL). Affecting over 1 in four Australians aged over 75 years, COPD remains one of the major causes of disability and death in the world. To date there have been over 80 randomised controlled trials examining the role of exercise training in a range of settings for individuals with COPD. This review will synthesise existing literature and provide health practitioners with broad evidence-based guidelines for exercise-training in this growing population. Position stand. Synthesis of randomised controlled trials of exercise training and of existing guidelines for exercise in COPD. Systematic reviews of alternative modes of exercise training will also be reviewed. There is convincing evidence that in adults with COPD, exercise-training improves exercise capacity, decreases symptoms such as dyspnoea and fatigue, and improves HRQoL. There is emerging evidence in this population that alternative modes of exercise training such as high intensity interval training (HIIT), aquatic based therapy, tai chi and neuromuscular electrical stimulation improve exercise outcomes when compared to no exercise. For individuals with COPD, an exercise program of aerobic and strength exercises delivered over at least an 8-week period, that engages lower and upper body skeletal muscles, will deliver significant health improvements. Programs should be individualised, take into consideration relevant co-morbid conditions and be delivered appropriately qualified health practitioners experienced in clinical exercise prescription.

ObjectiveThe objective of this study was to compare international trends in pre-eclampsia rates and in overall pregnancy hypertension rates (including gestational hypertension, pre-eclampsia and eclampsia).DesignPopulation data (from birth and/or hospital records) on all women giving birth were available from Australia (two states), Canada (Alberta), Denmark, Norway, Scotland, Sweden and the USA (Massachusetts) for a minimum of 6 years from 1997 to 2007. All countries used the 10th revision of the International Classification of Diseases, except Massachusetts which used the 9th revision. There were no major changes to the diagnostic criteria or methods of data collection in any country during the study period. Population characteristics as well as rates of pregnancy hypertension and pre-eclampsia were compared.ResultsAbsolute rates varied across the populations as follows: pregnancy hypertension (3.6% to 9.1%), pre-eclampsia (1.4% to 4.0%) and early-onset pre-eclampsia (0.3% to 0.7%). Pregnancy hypertension and/or pre-eclampsia rates declined over time in most populations. This was unexpected given that factors associated with pregnancy hypertension such as pre-pregnancy obesity and maternal age are generally increasing. However, there was also a downward shift in gestational age with fewer pregnancies reaching 40 weeks.ConclusionThe rate of pregnancy hypertension and pre-eclampsia decreased in northern Europe and Australia from 1997 to 2007, but increased in Massachusetts. The use of a different International Classification of Diseases coding version in Massachusetts may contribute to the difference in trend. Elective delivery prior to the due date is the most likely explanation for the decrease observed in Europe and Australia. Also, the use of interventions that reduce the risk of pregnancy hypertension and/or progression to pre-eclampsia (low-dose aspirin, calcium supplementation and early delivery for mild hypertension) may have contributed to the decline.

The physiological link between neuropathic pain and depression remains unknown despite a high comorbidity between these two disorders. A mouse model of spared nerve injury (SNI) was used to test the hypothesis that nerve injury precipitates depression through the induction of inflammation in the brain, and that prior exposure to stress exacerbates the behavioral and neuroinflammatory consequences of nerve injury. As compared with sham surgery, SNI induced mechanical allodynia, and significantly increased depressive-like behavior. Moreover, SNI animals displayed increased interleukin-1β (IL- 1β) gene expression within the frontal cortex and concurrent increases in the expression of glial fibrillary acidic protein (GFAP) within the periaqueductal grey (PAG). Additionally, exposure to chronic restraint stress for 2 weeks before SNI exacerbated mechanical allodynia and depressive-like behavior, and resulted in an increase in IL-1β gene expression in the frontal cortex and brain-derived neurotrophic factor (BDNF) gene expression in PAG. Treatment with metyrapone (MET), a corticosteroid synthesis inhibitor, before stress eliminated deleterious effects of chronic stress on SNI. Finally, this study showed that interference with IL- 1β signaling, through administration of IL-1 receptor antagonist (IL-1ra), ameliorated the effects of neuropathic pain on depressive-like behavior. Taken together, these data suggest that peripheral nerve injury leads to increased cytokine expression in the brain, which in turn, contributes to the development of depressive-like behavior. Furthermore, stress can facilitate the development of depressive-like behavior after nerve injury by promoting IL- 1β expression. Molecular Psychiatry (2010) 15, 404-414; doi: 10.1038/mp.2009.91; published online 22 September 2009 Keywords: spared nerve injury; depressive-like behavior; interleukin-1 b; stress; glucocorticoid; neuropathic pain

The Caribbean basin is home to some of the most complex interactions in recent history among previously diverged human populations. Here, we investigate the population genetic history of this region by characterizing patterns of genome-wide variation among 330 individuals from three of the Greater Antilles (Cuba, Puerto Rico, Hispaniola), two mainland (Honduras, Colombia), and three Native South American (Yukpa, Bari, and Warao) populations. We combine these data with a unique database of genomic variation in over 3,000 individuals from diverse European, African, and Native American populations. We use local ancestry inference and tract length distributions to test different demographic scenarios for the pre- and post-colonial history of the region. We develop a novel ancestry-specific PCA (ASPCA) method to reconstruct the sub-continental origin of Native American, European, and African haplotypes from admixed genomes. We find that the most likely source of the indigenous ancestry in Caribbean islanders is a Native South American component shared among inland Amazonian tribes, Central America, and the Yucatan peninsula, suggesting extensive gene flow across the Caribbean in pre-Columbian times. We find evidence of two pulses of African migration. The first pulse--which today is reflected by shorter, older ancestry tracts--consists of a genetic component more similar to coastal West African regions involved in early stages of the trans-Atlantic slave trade. The second pulse--reflected by longer, younger tracts--is more similar to present-day West-Central African populations, supporting historical records of later transatlantic deportation. Surprisingly, we also identify a Latino-specific European component that has significantly diverged from its parental Iberian source populations, presumably as a result of small European founder population size. We demonstrate that the ancestral components in admixed genomes can be traced back to distinct sub-continental source populations with far greater resolution than previously thought, even when limited pre-Columbian Caribbean haplotypes have survived.