Adipose Tissue Inflammation Is Directly Linked to Obesity-Induced Insulin Resistance, while Gut Dysbiosis and Mitochondrial Dysfunction Are Not Required

Obesity is associated with adipose tissue hypertrophy, systemic inflammation, mitochondrial dysfunction, and intestinal dysbiosis. Rodent models of high-fat diet (HFD)-feeding or genetic deletion of multifunctional proteins involved in immunity and metabolism are often used to probe the etiology of obesity; however, these models make it difficult to divorce the effects of obesity, diet composition, or immunity on endocrine regulation of blood glucose. We, therefore, investigated the importance of adipose inflammation, mitochondrial dysfunction, and gut dysbiosis for obesity-induced insulin resistance using a spontaneously obese mouse model. We examined metabolic changes in skeletal muscle, adipose tissue, liver, the intestinal microbiome, and whole-body glucose control in spontaneously hyperphagic C57Bl/6J mice compared to lean littermates. A separate subset of lean and obese mice was subject to 8 weeks of obesogenic HFD feeding, or to pair feeding of a standard rodent diet. Hyperphagia, obesity, adipose inflammation, and insulin resistance were present in obese mice despite consuming a standard rodent diet, and these effects were blunted with caloric restriction. However, hyperphagic obese mice had normal mitochondrial respiratory function in all tissues tested and no discernable intestinal dysbiosis relative to lean littermates. In contrast, feeding mice an obesogenic HFD altered the composition of the gut microbiome, impaired skeletal muscle mitochondrial bioenergetics, and promoted poor glucose control. These data show that adipose inflammation and redox stress occurred in all models of obesity, but gut dysbiosis and mitochondrial respiratory dysfunction are not always required for obesity-induced insulin resistance. Rather, changes in the intestinal microbiome and mitochondrial bioenergetics may reflect physiological consequences of HFD feeding

Security price responses to unexpected earnings: a nonparametric investigation

Confidence bands, Earnings response coefficient, Measurement error, Spline, Wild bootstrap,

Long-term Outcomes After Deep Vein Thrombosis: Postphlebitic Syndrome and Quality of Life

In this review, we critically assess the literature on the incidence of postphlebitic syndrome, risk factors for its occurrence, available therapeutic options, and its effects on quality of life. As well, we describe available tools to measure postphlebitic syndrome. Recent prospective studies indicate that postphlebitic syndrome, a chronic, potentially disabling condition characterized by leg swelling, pain, venous ectasia, and skin induration, is established by 1 year after deep vein thrombosis (DVT) in 17% to 50% of patients. The only prospectively identified risk factor for its occurrence is recurrent ipsilateral DVT. In the sole randomized study available, daily use of elastic compression stockings after proximal DVT reduced the incidence of postphlebitic syndrome by 50%. Treatment options for established postphlebitic syndrome are limited, but include compression stockings and intermittent compressive therapy with an extremity pump for severe cases. To date, quality of life after DVT has received little attention in the literature. The recent development of the VEINES-QOL questionnaire, a validated venous-disease-specific measure of quality of life, should encourage researchers to include quality of life as a routine outcome measure after DVT. There is no criterion standard for the diagnosis of postphlebitic syndrome, but a validated clinical scoring system does exist. More research on postphlebitic syndrome is needed to enable us to provide DVT patients with comprehensive, evidence-based information regarding their long-term prognosis, to help quantify the prevalence and health care burden of postphlebitic syndrome, and by identifying predictors of poor outcome, to develop new preventive strategies in patients at risk of developing this condition

Telephone Medicine for Internists

The role of the telephone in medical practice is important, but often problematic. Mistakes in telephone diagnosis and triage can have severe consequences. An effective office system can reduce liability risks, and in some cases telephone contact can substitute for office visits. Internists feel unprepared to provide telephone care. Therefore, residency education needs to focus on documentation, consultant availability, and performance feedback. Research should focus on improving outcomes, reimbursement issues, and technologic advances. This article describes internists' telephone interactions with ambulatory patients, preparation for telephone medicine, and aspects of office telephone systems and makes comparisons with other primary care fields