Buhlrooney8868

Over the last two decades, the development and production of innovative, customer-tailored food products with enhanced health benefits have seen major advances. However, the manufacture of edible materials with tuned physical and organoleptic properties requires a good knowledge of food microstructure and its relationship to the macroscopic properties of the final food product. Food products are complex materials, often consisting of multiple phases. Furthermore, each phase usually contains a variety of biological macromolecules, such as carbohydrates, proteins and lipids, as well as water droplets and gas bubbles. Micronutrients, such as vitamins and minerals, might also play an important role in determining and engineering food microstructure. Considering this complexity, highly advanced physio-chemical techniques are required for characterizing the microstructure of food systems prior to, during and after processing. Fast, in situ techniques are also essential for industrial applications. Due to the wide variety of instruments and methods, the scope of this paper is focused only on the latest advances of selected food characterization techniques, with emphasis on soft, multi-phasic food materials. Fecal coliform bacteria are a key indicator of human health risks; however, the spatiotemporal variability and key influencing factors of river fecal coliform have yet to be explored in a rural-suburban-urban watershed with multiple land uses. In this study, the fecal coliform concentrations in 21 river sections were monitored for 20 months, and 441 samples were analyzed. Multivariable regressions were used to evaluate the spatiotemporal dynamics of fecal coliform. The results showed that spatial differences were mainly dominated by urbanization level, and environmental factors could explain the temporal dynamics of fecal coliform in different urban patterns except in areas with high urbanization levels. Reducing suspended solids is a direct way to manage fecal coliform in the Beiyun River when the natural factors are difficulty to change, such as temperature and solar radiation. The export of fecal coliform from urban areas showed a quick and sensitive response to rainfall events and increased dozens of times in the short term. Landscape patterns, such as the fragmentation of impervious surfaces and the overall landscape, were identified as key factors influencing urban non-point source bacteria. The results obtained from this study will provide insight into the management of river fecal pollution. BACKGROUND Enterochromaffin-like (ECL) cells in the stomach express gastrin/CCK2 receptors and are known to expand under hypergastrinemia, but whether this results from expansion of existing ECL cells or increased production from progenitors has not been clarified. METHODS We utilized mice with fluorescent reporter expression in ECL cells (Hdc-GFP) as well as Cck2r-CreERT2 and Hdc-CreERT2 mice combined with R26-tdTomato mice, and studied their expression and cell fate in the gastric corpus by using models of hypergastrinemia (gastrin infusion, omeprazole treatment). RESULTS Hdc-GFP marked the majority of ECL cells, located in the lower third of the gastric glands. Hypergastrinemia led to expansion of ECL cells that was not restricted to the gland base, and promoted cellular proliferation (Ki67) in the gastric isthmus but not in basal ECL cells. Cck2r-CreERT2 mice marked most ECL cells, as well as scattered cell types located higher up in the glands, whose number was increased during hypergastrinemia. Cck2r-CreERT2+ isthmus progenitors, but not Hdc+ mature ECL cells, were the source of ECL cell hyperplasia during hypergastrinemia and could grow as 3D spheroids in vitro. Moreover, gastrin treatment in vitro promoted sphere formation from sorted Cck2r+Hdc- cells, and increased chromogranin A (CgA) and pERK expression in CCK2R-derived organoids. Gastrin activates ERK pathway in vivo and in vitro, and treatment with the MEK1 inhibitor U0126 blocked hypergastrinemia-mediated changes, including CCK2R-derived ECL cell hyperplasia in vivo as well as sphere formation and CgA expression in vitro. CONCLUSION We show here that hypergastrinemia induces ECL cell hyperplasia that is primarily derived from CCK2R+ progenitors in the corpus. Gastrin-dependent function of CCK2R+ progenitors is regulated by the ERK pathway. BACKGROUND & AIMS Bile acids are important metabolic signaling molecules. Bile acid receptor activation promotes body weight loss and improves glycemic control. The incretin hormone GLP-1 and thyroid hormone activation of T4 to T3 have been suggested as important contributors. Here, we identify the hepatic bile acid uptake transporter Na+ taurocholate co-transporting polypeptide (NTCP) as target to prolong postprandial bile acid signaling. selleck compound METHODS Organic anion transporting polypeptide (OATP)1a/1b KO mice with or without reconstitution with human OATP1B1 in the liver were treated with the NTCP inhibitor Myrcludex B for 3.5 weeks after the onset of obesity induced by high fat diet-feeding. Furthermore, radiolabeled T4 was injected to determine the role of NTCP and OATPs in thyroid hormone clearance from plasma. RESULTS Inhibition of NTCP by Myrcludex B in obese Oatp1a/1b KO mice inhibited hepatic clearance of bile acids from portal and systemic blood, stimulated GLP-1 secretion, reduced body weight, and decreased (hepatic) adiposity. NTCP inhibition did not affect hepatic T4 uptake nor lead to increased thyroid hormone activation. Myrcludex B treatment increased fecal energy output, explaining body weight reductions amongst unaltered food intake and energy expenditure. CONCLUSIONS Pharmacologically targeting hepatic bile acid uptake to increase bile acid signaling is a novel approach to treat obesity and induce GLP1- secretion. BACKGROUND & AIMS In Short Bowel Syndrome (SBS), inadequate intestinal adaptation is responsible for the majority of complications, including sepsis, liver failure and death. In this study, we sought to further delineate the adaptive response to identify potential therapeutic targets. METHODS We performed a 75% small bowel resection (SBR) or sham operation on C57Bl/6J wild-type, lipocalin-2 (LCN2) -/- and Interleukin-22 (IL-22) -/- mice. Exogenous IL-22 was administered to SBR WT mice. Cecal fecal matter from SBR WT and SBR LCN2 -/- mice were transplanted into germ-free mice. Intestinal permeability, inflammation, proliferation and microbiome were evaluated one week following surgery. CD4+IL-22+ laminal propria lymphocytes were sorted by flow cytometry. Naïve T cells were polarized to Th22 cells with or without LCN2. RESULTS 75% SBR in a mouse recreates the increased intestinal permeability, enterocyte proliferation and intestinal dysbiosis seen in SBS. LCN2 expression increases following 75% SBR, and this increase can be abrogated with broad-spectrum antibiotic treatment.