Rationale Accurately identifying use of life support in hospital administrative data enhances the data's value for quality improvement and research in critical illness.Objectives To assess the accuracy of administrative hospital data for identifying invasive mechanical ventilation (IMV), acute renal replacement therapy (RRT), and intravenous vasoactive drugs in unselected adult intensive care unit (ICU) patients.Methods We employed the administrative dataset of the Discharge Abstract Database from the Province of Manitoba during 2007-2012, using nationally standardized diagnosis and procedure codes to identify the three types of life support. The criterion standard was the Winnipeg ICU Database, which contains daily clinical information about all admissions to all 11 adult ICUs within the Winnipeg Regional Health Authority. For all individuals aged 40 years or older at ICU admission, we calculated sensitivity, specificity, positive predictive value (PPV), and negative predictive value of the administrative daved at least one of the two other types assessed. Considering use of any one or more of the three forms of life support, the administrative data had a PPV of 97% (95% CI, 96-97%) and a negative predictive value of 69% (95% CI, 68-70%).Conclusions Administrative data accurately identify IMV but not use of vasoactive drugs or acute RRT.Impaired manganese (Mn) homeostasis can result in excess Mn accumulation in specific brain regions and neuropathology. Maintaining Mn homeostasis and detoxification is dependent on effective Mn elimination. Specific metal transporters control Mn homeostasis. Human carriers of mutations in the metal transporter ZIP14 and whole-body Zip14 KO (WB-KO) mice display similar phenotypes, including spontaneous systemic and brain Mn overload, and motor dysfunction. Initially, it was believed that Mn accumulation due to ZIP14 mutations caused by impaired hepatobiliary Mn elimination. However, liver-specific Zip14 KO mice (L-KO) did not show systemic Mn accumulation or motor deficits. ZIP14 is highly expressed in the small intestine and is localized to the basolateral surface of enterocytes. Thus we hypothesized that basolaterally-localized ZIP14 in enterocytes provides another route for elimination of Mn. Using wild type and intestine-specific ZIP14 KO (I-KO) mice, we have shown that ablation of intestinal Zip14 is sufficient to cause systemic and brain Mn accumulation. The lack of intestinal ZIP14-mediated Mn excretion was compensated for by the hepatobiliary system; however, it was not sufficient to maintain Mn homeostasis. When supplemented with extra dietary Mn, I-KO mice displayed some motor dysfunctions, brain Mn accumulation based on both MRI imaging and chemical analysis, thus demonstrating the importance of intestinal ZIP14 as a route of Mn excretion. A defect in intestinal Zip14 expresssion likely could contribute to the Parkinson-like Mn accumulation of manganism.The gastrointestinal system is arguably one of the most complicated developmental systems in a multicellular organism as it carries out at least four major functions - digestion of food, absorption of nutrients, excretion of hormones, and defense against pathogens1. Anatomically the fetal gut has a tubular structure with an outer layer of smooth muscle derived from lateral splanchnic mesoderm and an inner lining of epithelium derived from the definitive endoderm. During morphogenesis of the gut tube, the definitive endoderm transforms into a primitive gut tube with a foregut, midgut, and hindgut. During the course of further development, the midgut gives rise to the small and proximal large intestine and the hindgut gives rise to the distal large intestine and rectum2. The small intestine is subdivided into three parts duodenum, jejunum, and ileum, whereas the large intestine is subdivided in to the cecum, colon, and rectum3.Liver resection induces robust liver regrowth or regeneration to compensate for the lost tissue mass.  https://www.selleckchem.com/products/Novobiocin-sodium(Albamycin).html  In a clinical setting, pregnant women may need liver resection without terminating pregnancy in some cases. However, how pregnancy affects maternal liver regeneration remains elusive. We performed 70% partial hepatectomy (PH) in non-pregnant mice and gestation day 14 mice, and histologically and molecularly compared their liver regrowth during the next 4 days. We found that, compared with the non-pregnant state, pregnancy altered the molecular programs driving hepatocyte replication, indicated by enhanced activities of EGFR and STAT5A, reduced activities of cMet and p70S6K, decreased production of IL-6, TNFα, and HGF, suppressed cyclin D1 expression, increased cyclin A1 expression, and early activated cyclin A2 expression. As a result, pregnancy allowed the remnant hepatocytes to enter the cell cycle at least 12 hours earlier, increased hepatic fat accumulation, and enhanced hepatocyte mitosis. Consequently, pregnancy ameliorated maternal liver regeneration following PH. A report showed that maternal liver regrowth after PH is driven mainly by hepatocyte hypertrophy rather than hyperplasia during the second half of gestation in young adult mice. In contrast, we demonstrate that maternal liver relies mainly on hepatocyte hyperplasia instead of hypertrophy to restore the lost mass after PH. Conclusion Overall, we demonstrate that pregnancy facilitates maternal liver regeneration likely via triggering an early onset of hepatocyte replication, accumulating excessive liver fat, and promoting hepatocyte mitosis. The results from our current studies enable us to gain more insights into how maternal liver regeneration progresses during gestation.OBJECTIVE Postprandial dyslipidemia is a common feature of insulin resistant states and contributes to increased cardiovascular disease risk. Recently, bile acids have been recognized beyond their emulsification properties as important signaling molecules that promote energy expenditure, improve insulin sensitivity, and lower fasting lipemia. While bile acid receptors have become novel pharmaceutical targets, their effects on postprandial lipid metabolism remain unclear. Here we investigated the potential role of bile acids in regulation of postprandial chylomicron production and triglyceride excursion. Approach and Results Healthy C57BL/6 mice were given an intraduodenal infusion of taurocholic acid (TA) under fat-loaded conditions and circulating lipids were measured. Targeting of bile acid receptors was achieved with GW4064, a synthetic agonist to the farnesoid X receptor (FXR), and with deoxycholic acid (DCA), an activator of the Takeda G-protein-coupled receptor 5. TA, GW4064, and DCA treatments all lowered postprandial lipemia.