sepsis/비만증

The purpose of this study was to better understand the role obesity plays in the inflammatory response during sepsis, specifically regarding the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway in the liver. We hypothesized that inhibiting STAT3 would lead to an

BACKGROUND It is well established that obesity-related hormones can have modulatory effects associated with the immune response. Ghrelin, a hormone mainly derived from endocrine cells of the gastric mucosa, regulates appetite, energy expenditure and body weight counteracting leptin, a hormone mainly

Sepsis and septic shock continue to contribute to our workload and stimulate our research activities although many fundamental questions remain. Studies reported on here focus on inotrope use and a novel way of predicting inotrope response. Continuing this theme more fundamental work is reported

Severe sepsis and septic shock are the biggest cause of mortality in critically ill patients. Obesity today is one of the world's greatest health challenges. Little is known about the extent of involvement of the white adipose tissue (WAT) in sepsis and how it is being modified by obesity. We sought

OBJECTIVE Obesity is associated with increased morbidity and mortality in critically ill patients. It is unclear whether this increase is due to exaggerated inflammatory response alone or due to lack of response to therapeutic agents used. The objective of this study was to determine whether

Animal, epidemiological and limited human studies have reported that obesity increases susceptibility to both bacterial and viral infections. Obesity has now reached worldwide epidemic proportions with a recent study estimating that there are currently 2.1 billion obese adults in the world. The

Sepsis is the leading cause of death in non-coronary intensive care units worldwide, with a very high cost of care. There is a growing body of evidence suggesting that the increase in morbidity associated with severe obesity in critically ill patients results in increased resource utilization adding

Obesity increases morbidity and mortality in acute illnesses such as sepsis and septic shock. We showed previously that the early/hyper-inflammatory phase of sepsis is exaggerated in obese mice with sepsis; sirtuin 2 (SIRT2) modulates sepsis inflammation in obesity. Evidence suggests that obesity

Sepsis is a major cause of hospital admissions and mortality. Nevertheless, there are significant gaps in our knowledge of the epidemiology of sepsis in obese people, who now represent more than one-third of the population in the United States. The objective of this study was to measure the

Septic shock is a frequent life-threatening condition and a leading cause of mortality in intensive care units (ICUs). Previous investigations have reported a potentially protective effect of obesity in septic shock patients. However, prior results have been inconsistent, focused on short-term

The glyco-isoforms of intact apolipoprotein C3 (ApoC3) were used to probe glycomic changes associated with obesity and recovery following bariatric surgery, liver diseases such as chronic hepatitis C (CHC) and alcoholic liver cirrhosis, as well as severe, multiorgan diseases such as sepsis and graft

OBJECTIVE To study the protective effect of lipoxin A4 (LXA4) against sepsis induced by lipopolysaccharide (LPS) in rats with obesity and its effect on the expression of Toll-like receptor 4 (TLR4) and TNF receptor-associated factor 6 (TRAF6) in the liver. METHODS A total of 60 male Sprague-Dawley

Sepsis, a global health issue, is the most common cause of mortality in the intensive care unit. The aim of this study was to develop a new model of sepsis that investigates the impact of prolonged western diet (WD) induced obesity on the response to early sepsis. Male C57BL/6 mice were fed either a