Serum asprosin levels of diabetic rats were found to be decreased compared to the control group. This is the first study in the literature that reports the presence of asprosin in liver, kidney, heart, stomach, testis and brain tissues in rats. The aim of the study is to determine the presence of ASP, a newly discovered adipokine, in various tissues and to examine tissue and serum level changes in STZ-induced diabetes.The main goal of this study was to assess the effect of different sterilization treatment for sterilization of decellularized kidney tissue. Rabbit kidneys were decellularized by the perfusion-based method using sodium dodecyl sulfate (SDS) and Triton X-100. Then, decellularized kidney slices were prepared and sterilized by an antibiotic cocktail, PAA (0.5 %, 1% and 1.5 %), 5KG γ-irradiation and 320-480 nm UV-irradiation. Histological evaluations, DNA quantification assay, MTT assay, scanning electron microscopy (SEM), mechanical test and bacterial and fungal culture tests were performed to determine the quality of decellularization and sterilization processes. The kidney slices were seeded by adipose-derived mesenchymal stem cells (ASCs) to assess the cell adhesion capability after treatment. The results of the current study indicated that PAA 0.5 % was the most efficient method to completely decontaminate rabbit decellularized kidney tissue while preserving the mechanical properties and main components of the matrix which are necessary for cell-matrix interaction and cell adhesion. The 5KG γ-irradiation was determined to be the most destructive sterilization method, with reduced the mechanical strengths as well as altered microstructure of the kidney matrix and no cell adhesion. In addition, UV-irradiation is not able to sterile the decellularized tissues. Therefore PAA 0.5 % sterilization method can be a powerful means for sterilization of biological scaffolds.The ovarian development of Callinectes ornatus and Arenaeus cribrarius was described using histochemistry and ultrastructure. Both species shows the same ovarian stages, which are the juvenile (JUV), adult rudimentary (RUD), developing (DEV), intermediary (INT), mature (MAT), and spent (OV) stages. The JUV and RUD stages showed similar characteristics, and previtellogenesis is characterized by meiotic prophase chromosomes. In the primary vitellogenesis, the oocyte cytoplasm shows many small and large cytoplasmic glycoprotein vesicles. These vesicles correspond to the dilated cisternae of the rough endoplasmic reticulum (RER), which produces the immature (endogenous) yolk. Secondary vitellogenesis (exogenous phase) begins at the DEV stage with the fusion of pinocytic vesicles and vesicles with immature yolks to form mature yolk granules. At the INT stage, the formation of the chorion begins, and the mature yolks increase in size and number, while the RER diminishes. In the MAT stage, the oocytes are completely formed, and the cytoplasm is filled with mature yolk, lipid droplets, and glycogen. There are no significant variations between the gonadosomatic and hepatosomatic indices, which allows us to infer that the transfer of reserves from the hepatopancreas is nearly constant during ovarian development, since we observed primiparous and multiparous females in the same sampled population.High-conductance, voltage- and calcium-activated potassium channels (BKCa) and store-operated calcium channels (SOCs) are belong to K+ channels superfamily and calcium channels superfamily respectively. Since BKCa potassium channels can be activated by calcium ions, we set out to examine whether SOCs are coupled with BKCa and to probe the relationship of BKCa and SOCs. First, we proved that BKCa immunoprecipitated with Orai1, and confocal microscopy showed that BKCa co-localized with Orai1. Next, we mapped that the exact binding sites locate in the 350aa-371aa fragment of the first regulatory domain associated with K+ conduction (RCK1) and the 720aa-814aa fragment in the second regulatory domain associated with K+ conduction (RCK2) via GST-pull-down assays. Then, we showed, by calcium imaging that BKCa overexpression enhanced endogenous and exogenous store-operated calcium entry (SOCE) and this enhancement could be blocked by Orai1 knockdown. Finally, we proved that SOCE could enhance the activity of BKCa by patch-clamp. From these results we conclude that BKCa can form a positive feedback loop with SOCs, as the Ca2+ influx from SOCs can active BKCa, which can hyperpolarize the plasma membrane. In turn, the hyperpolarized membrane will form a higher electric potential difference and give more force, allowing Ca2+ influx via SOCs.Wnt/β-Catenin signaling is required for the development and differentiation of cochlear hair cells. Total of 80 natural compounds derived from the FDA-approved Drug Library of Selleck were screened by T-cell factor Reporter Plasmid (TOP)-Flash assay to identify the activation of Wnt/β-Catenin signaling. The mouse cochlear hair cells (HEI-OC1) were treated with cisplatin with or without Guaiacin, and the relative expression of β-Catenin and TRIM33 were detected by qRT-PCR and Western blots. selleck inhibitor The viability of HEI-OC1 was assayed by MTT method, and mouse cochlear cultures were utilized to detect the Ex vivo survival of cochlear hair cells. Guaiacin was testified to have the most vigorous ability to promote Wnt/β-Catenin signaling among 80 compounds detected, and it can also improve the β-Catenin signaling in mouse cochlear hair cells with up-regulated β-Catenin protein expression, unchanged β-Catenin mRNA expression, and down-regulated TRIM33 expression. Guaiacin increased the viability of HEI-OC1 cells cultured with or without cisplatin, and such a protective effect was also testified in mouse cochlear cultures. Our data indicate that Guaiacin could increase Wnt/β-Catenin signaling by regulating TRIM33/β-Catenin axis, which contributes to the improved survival of cochlear hair cells.Coptisine is an alkaloid with many biological functions, but studies on its mechanism in myocardial ischemia-reperfusion (I/R) injury are less reported. Hypoxia-reoxygenation (H/R) -treated cardiomyocytes injury and I/R-induced myocardial tissues damage were created in rat models with or without the pre-treatment of coptisine. The proliferation and apoptosis of cardiomyocytes and changes of myocardial tissues were observed after the pre-treatment of coptisine. The pre-treatment of coptisine promoted cell proliferation and inhibited apoptosis of H/R-injured cardiomyocytes, and alleviated the myocardial tissue injury caused by I/R in rats. Moreover, coptisine promoted the expressions of anti-apoptotic proteins and inhibited the expressions of pro-apoptotic proteins in vivo and in vitro. The current study found that coptisine had protective effects on I/R-induced myocardial damage, which may provide a new insight into the treatment of I/R.