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Self-Powered Photoelectrochemical Aptasensor for Oxytetracycline Cathodic Recognition Using a Double Z-Scheme WO3/g-C3N4/MnO2 Photoanode.
FXR agonism also reduced intestinal triglyceride content and activity of microsomal triglyceride transfer protein, involved in chylomicron assembly. Importantly, TA effects (but not DCA) were largely lost in FXR knockout mice. These bile acid effects are reminiscent of the anti-diabetic hormone glucagon-like peptide-1 (GLP-1). While the GLP-1 receptor agonist exendin-4 retained its ability to acutely lower postprandial lipemia during bile acid sequestration and FXR deficiency, it did raise hepatic expression of the rate limiting enzyme for bile acid synthesis. CONCLUSIONS Bile acid signaling may be an important mechanism of controlling dietary lipid absorption and bile acid receptors may constitute novel targets for the treatment of postprandial dyslipidemia.To investigate the role of bile acids (BAs) in the pathogenesis of diet-induced nonalcoholic steatohepatitis (NASH), we fed a "Western-style diet" [high fructose, high fat (HFF)] enriched with fructose, cholesterol, and saturated fat for 10 wk to juvenile Iberian pigs. We also supplemented probiotics with in vitro BA deconjugating activity to evaluate their potential therapeutic effect in NASH. Liver lipid and function, cytokines, and hormones were analyzed using commercially available kits. Metabolites, BAs, and fatty acids were measured by liquid chromatography-mass spectrometry. Histology and gene and protein expression analyses were performed using standard protocols. HFF-fed pigs developed NASH, cholestasis, and impaired enterohepatic Farnesoid-X receptor (FXR)-fibroblast growth factor 19 (FGF19) signaling in the absence of obesity and insulin resistance. Choline depletion in HFF livers was associated with decreased lipoprotein and cholesterol in serum and an increase of choline-containing phospholipids atty liver disease (NAFLD) patients. However, therapeutic interventions with FXR agonists have produced contradictory results. In a swine model of pediatric nonalcoholic steatohepatitis (NASH), we show that the uncoupling of intestinal FXR-FGF19 signaling and a decrease in FGF19 levels are associated with a choline-deficient phenotype of NASH and increased choline excretion in the gut, with the subsequent dysbiosis, colonic hyperplasia, and accumulation of trimethylamine-N-oxide in the liver.PURPOSE No questionnaire is currently available to evaluate sexual function after male to female (MtF) gender affirming surgery. Such a limit leads to a suboptimal evaluation in post-operative sexual function in these patients. We aimed at developing and validating a new questionnaire, the operated Male to Female Sexual Function Index (oMtFSFI), for assessing sexual function in MtF patients after surgery. MATERIAL AND METHODS A panel of experts in gender dysphoria defined the main content areas to be assessed genital self-image, desire, arousal, lubrication, orgasm, satisfaction, and sexual pain. After a pre-test on 10 patients, in the main study oMtFSFI was applied to 65 operated MtF patients (oMtFp), recruited in 7 Italian centres, and 57 women. The participants provided self-ratings on on-line oMtFSFI, FSFI, BDI-PC, and SF-36 questionnaires. oMtFp completed oMtFSFI twice, four weeks apart. RESULTS Principal component analysis performed on self-ratings provided by oMtFp on the oMtFSFI items yielded a 3-domain structure Sexual Dissatisfaction, Sexual Pain and Genital self-image. The three domains were internally consistent and test-retest reliable. Convergent associations with FSFI scales emerged for Sexual Dissatisfaction and Sexual Pain, but not for Genital Self-image. MtF patients reported lower sexual function levels in comparison with cis-women. CONCLUSIONS The present preliminary results supported reliability and psychometric validity of the oMtFSFI in the assessment of key sexual function domains in transgender women, further revealing that Genital self-image represents an assessment area to be taken into account in MtF patients, in addition to domains which are salient for cis-women as well.Serum soluble Fas levels (sFas) is associated to erythropoietin (Epo) hyporesponsiveness in patients with chronic kidney disease (CKD). If sFas could predict the need for erythropoiesis-stimulating agents (ESA) usage and influence in erythropoiesis remains unclear. We evaluated the relation between sFas and ESA therapy in CKD patients with anemia and its effect on erythropoiesis in vitro. First, we performed a retrospective cohort study with 77 anemic patients with non-dialysis CKD. We performed in vitro studies to investigate whether sFas could interfere with the behavior of hematopoietic stem cells (HSC). HSC were isolated from umbilical cord blood and incubated with recombinant sFas protein in a dose-dependent manner. Serum sFas positively correlated with Epo levels (r=0.30, p=0.001) but negatively with Hgb (r=-0.55, p less then 0.001) and eGFR (r=-0.58, p less then 0.001) in CKD patients at baseline. Elevated sFas serum levels (4,316±897 vs 2,776±749; p less then 0.001) with lower eGFR (26.2±10.1 vs 33.5±14.3; p=0.01) and reduced Hgb concentration (11.1±0.9 vs 12.5±1.2; p less then 0.001) were identified in patients who required ESA therapy in comparison with non-ESA patients. After, we detected that sFas level was slight correlated with a necessity of ESA therapy in non-dialysis anemic CKD patients. In vitro assays demonstrated that erythroid progenitor cells frequency negatively correlated with sFas concentration (r=-0.72, p less then 0.001). There was decreased erythroid colony formation in vitro when CD34+ HSC cells were incubated with higher concentration of sFas protein (1.56±0.29, 4.33±0.53; p less then 0.001). EGFR inhibition Our findings suggest that sFas is a potential predictor for ESA therapy in patients with non-dialysis CKD and elevated sFas could affects erythropoiesis in vitro.Corticotropin-releasing factor (CRF) regulates diverse physiologic functions, including bladder control. We recently reported that Crfexpression is under genetic control of Aoah, the locus encoding acyloxyacyl hydrolase (AOAH), suggesting that AOAH may also modulate voiding. Here, we examined the role of AOAH in bladder function. AOAH-deficient mice exhibited enlarged bladders relative to wild type mice and had decreased voiding frequency and increased void volumes. AOAH-deficient mice had increased non-voiding contractions and increased peak voiding pressure in awake cystometry. AOAH-deficient mice also exhibited increased bladder permeability and higher neuronal firing rates of bladder afferents in response to stretch. In wild type mice, AOAH was expressed in bladder projecting neurons and co-localized in CRF-expressing neurons in Barrington's nucleus (BN), an important brain area for voiding behavior, and Crf was elevated in BN of AOAH-deficient mice. We previously identified aryl hydrocarbon receptor (AhR) and peroxisome proliferator-activated receptor gamma (PPARg) as transcriptional regulators of Crf, and conditional knockout of AhR or PPARgin Crf-expressing cells restored normal voiding in AOAH-deficient mice.
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