Bovine cysticercosis remains as one of the most important cause of carcasses and viscera condemnation in Brazilian slaughterhouses. However, the efficiency of post-mortem inspection for the diagnosis of this zoonotic disease is relatively low, and few available studies were performed through serological exams. This study evaluated the frequency of bovine cysticercosis in cattle herds located in different farms of the state of Rondônia, Brazil. Among the 987 animals slaughtered from 33 farms, 21 animals (Frequency 2.13%; 95C.I. 1.23-3.03) were considered as positive through indirect ELISA and confirmed by Immunoblot tests and the cysticercosis was detected in 12 farms (36.36% - C.I. 95% 19.95-52.78). The disease was detected in the municipalities Vale do Paraíso (12.50%), Theobroma (8.11%), Guaporé (7.27%), Rolim de Moura (5.71%), Presidente Médici (5.0%), Ouro Preto do Oeste (4.69%), Nova União (1.77%), Nova Brasilândia d'Oeste (1.14%) and Ministro Andreazza (1.01%). Therefore, prophylactic measures should be taken to improve beef production, control bovine cysticercosis and reduce costs to public health in this Brazilian state.Background Interdisciplinary research among health care professionals has gained importance over the last 20 years, but little is known about its impact on career development. Purpose This study examined professional development outcomes associated with interdisciplinary research. Methods An integrative review was conducted using Whittmore and Knafl's framework. PubMed, Embase, PsycInfo, Web of Science, and CINAHL were searched to identify studies. Findings Thirteen studies were included. The majority used bibliometric analyses, finding that moderate level of interdisciplinary collaboration was associated with a greater amount and higher quality of publications. Interdisciplinary publications allocated more credit (i.e., had more authors). Interdisciplinary research proposals had less funding success than single discipline proposals. Important cultural and personal aspects of interdisciplinary research (e.g., work and communication styles, research goals) have not been assessed to date. Discussion Rigorous qualitative studies are needed to characterize benefits and challenges of interdisciplinary research to scholars and to institutions.SET domain with lysine methyltransferase 7/9 (Set7/9), a histone lysine methyltransferase (HMT), recently suggested to exert a critical role among kidney disorders, whereas its role in diabetes associated IRI co-morbidity remains complete elusive. The present study aimed to understand the role of SET7/9 and histone methylation in regulation of inflammatory signaling under IRI in diabetes mellitus and non-diabetic rats. https://www.selleckchem.com/products/AV-951.html Our results demonstrated that IRI caused renal dysfunction via increased blood urea nitrogen (BUN) levels in ND and DM rats. The NF-κB mediated inflammatory cascade like increased p-NF-κB, reduced IκBα levels followed by enhanced leukocyte infiltration as shown by increased MCP-1 expressions. IRI results in increased histone H3 methylation at lysine 4 and 36 (H3K4Me2, H3K36Me2), and decreased histone H3 methylation at lysine 9. Additionally, IRI increased the protein and mRNA expression of H3K4Me2 specific histone methyltransferase-SET7/9 in DM and ND rats. The abovementioned results remain prominent in DM rats compared to ND rats followed by IRI. Further, treatment with a novel SET7/9 inhibitor; cyproheptadine, significantly improved renal functioning via reducing the BUN levels in ND and DM rats. Hence, this study demonstrated the role of SET7/9 in mediating active transcription via H3K4Me2, ultimately regulated the NFκB-mediated inflammatory cascade. Therefore, SET7/9 can be explored as novel target for drug development against IRI under DM and ND conditions.Licorice is a popular medicinal plant, and it has been used to treat various diseases, including liver diseases. Glycycoumarin (GCM) is a major coumarin compound isolated from licorice with favorable bioavailability property. Our previous studies have shown that GCM is capable of inhibiting lipoapoptosis in both cell culture and methionine-choline-defcient (MCD) diet-induced mouse model of non-alcoholic steatohepatitis (NASH) through mechanisms involving suppression of endoplasmic reticulum (ER) stress. Perilipin 5 (PLIN5), a newly identified lipid drop protein in the perilipin family, is highly expressed in oxidative tissues including the liver and is suggested to play an important role in protecting against hepatic lipotoxicity. Give the hepatoprotective role of PLIN5, we hypothesized that induction of PLIN5 might contribute to the hepatoprotective effect of GCM via mitigating ER stress and inflammatory responses. Results showed that PLIN5 and its downstream target Sirt1 were induced by GCM both in vitro and in vivo. Inhibition of either PLIN5 or Sirt1 led to significantly attenuated protective effect of GCM on palmitic acid (PA)-induced lipoapoptosis and inflammatory responses, supporting involvement of PLIN5-Sirt1 axis in the protective effect of GCM on hepatic lipotoxicity. The findings of the present study provide novel insight into the understanding of mechanisms underlying the hepatoprotective effect of GCM.Caenorhabditis elegans is a useful animal model to determine the underlying mechanism for the response to simulated microgravity. In this study, we employed C. elegans as an animal model to investigate the role of lipid metabolic sensors in regulating the response to simulated microgravity. Among the lipid metabolic sensors, simulated microgravity treatment could increase the expressions of sbp-1 and mdt-15. RNAi knockdown of sbp-1 or mdt-15 induced a susceptibility to toxicity of simulated microgravity, suggesting the alteration in SBP-1 and MDT-1 mediated a protective response to simulated microgravity. Tissue-specific activity analysis demonstrated that both MDT-15 and SBP-1 could act in the intestine to regulate the response to simulated microgravity. Genetic interaction analysis further indicated that intestinal MDT-15 acted upstream of SBP-1 to regulate the response to simulated microgravity. During the control of response to simulated microgravity, fatty acyl CoA desaturase FAT-6 was identified as the downstream target of intestinal SBP-1.