Bakshaffer8958

There has been rapid growth in the use of transcriptomic analyses to study the interplay between gene expression and behavior. Experience can modify gene expression in the brain, leading to changes in internal state and behavioral displays, while gene expression variation between species is thought to specify many innate behavior differences. However, providing a causal association between a gene and a given behavior remains challenging as it is difficult to determine when and where a gene contributes to the function of a behaviorally-relevant neuronal population. Moreover, given that there are fewer genetic tools available for non-traditional model organisms, transcriptomic approaches have been largely limited to profiling of bulk tissue, which can obscure the contributions of subcortical brain regions implicated in multiple behaviors. Here, we discuss how emerging single cell technologies combined with methods offering additional spatial and connectivity information can give us insight about the genetic profile of specific cells involved in the neural circuit of target social behaviors. We also emphasize how these techniques are broadly adaptable to non-traditional model organisms. We propose that, ultimately, a combination of these approaches applied throughout development will be key to discerning how genes shape the formation of social behavior circuits.Individuals often respond to social disturbances by increasing prosociality, which can strengthen social bonds, buffer against stress, and promote overall group cohesion. Given their importance in mediating stress responses, glucocorticoids have received considerable attention as potential proximate regulators of prosocial behaviour during disturbances. However, previous investigations have largely focused on mammals and our understanding of the potential prosocial effects of glucocorticoids across vertebrates more broadly is still lacking. Here, we assessed whether experimentally elevated glucocorticoid levels (simulating endogenous cortisol responses mounted following disturbances) promote prosocial behaviours in wild groups of the cichlid fish, Neolamprologus pulcher. Using SCUBA in Lake Tanganyika, we observed how subordinate group members adjusted affiliation, helping, and submission (all forms of prosocial behaviour) following underwater injections of either cortisol or saline. Cortisol treatment reduced affiliative behaviours-but only in females-suggesting that glucocorticoids may reduce overall prosociality. Fish with elevated glucocorticoid levels did not increase performance of submission or helping behaviours. click here Taken together, our results do not support a role for glucocorticoids in promoting prosocial behaviour in this species and emphasize the complexity of the proximate mechanisms that underlie prosociality.Sialylation is the addition of sialic acids to the terminus of various glycoconjugates, and it is involved in many essential biological processes, such as cell adhesion, signal transduction, immune regulation, etc. The levels of sialylation in a cell are tightly regulated by two groups of enzymes, sialyltransferases (STs, responsible for sialylation) and sialidases (responsible for desialylation). link2 Many studies have reported that the occurrence, development, and survival rates of tumors are significantly associated with STs' abnormal changes. In recent years, the morbidity and mortality rates of gynecological malignant tumors have been continuously rising, which has caused great harm to women's reproduction and health. Abnormal changes of STs in gynecological malignant tumor cell membranes cause the changes of expression of sialic acids, promoting cell migration and, eventually, leading to tumor metastasis. In this review, we outlined the biological characteristics of STs and summarized the expression profiles of 20 STs in different tumors via transcriptome data from Gene Expression Profiling Interactive Analysis (GEPIA) database. Moreover, STs' functions in four common gynecological tumors (ovarian cancer, cervical cancer, endometrial cancer, and gestational trophoblast tumor) were reviewed.

COVID-19 outbreak has created a public health catastrophe all over the world. link3 Here, we have aimed to conduct a systematic review and meta-analysis on remdesivir use for COVID-19.

We searched Pubmed, Scopus, Embase, and preprint sites and identified ten studies for qualitative and four studies for quantitative analysis using PRISMA guidelines. The quantitative synthesis was performed using fixed and random effect models in RevMan 5.4. Heterogeneity was assessed using the I-squared (I

) test.

Comparing 10-day remdesivir group with placebo or standard of care (SOC) group, remdesivir reduced 14days mortality (OR 0.61, CI 0.41-0.91), need for mechanical ventilation (OR 0.73, CI 0.54-0.97), and severe adverse effects (OR 0.69, 95% CI 0.54 to 0.88). Clinical improvement on day 28 (OR 1.59, CI 1.06-2.39), day 14 clinical recovery (OR 1.48, CI 1.19-1.84), and day 14 discharge rate (OR 1.41, CI 1.15-1.73) were better among remdesivir group. Earlier clinical improvement (MD -2.51, CI -4.16 to -0.85); and clinical recovery (MD -4.69, CI -5.11 to -4.28) were seen among the remdesivir group. Longer course (10days) of remdesivir showed a higher discharge rate at day 14 (OR 2.11, CI 1.50-2.97), but there were significantly higher rates of serious adverse effects, and drug discontinuation than the 5-day course.

Remdesivir showed a better 14days mortality profile, clinical recovery, and discharge rate. Overall clinical improvement and clinical recovery were earlier among the remdesivir group. 10-day remdesivir showed more adverse outcome than 5-day course with no significant benefits.

Remdesivir showed a better 14 days mortality profile, clinical recovery, and discharge rate. Overall clinical improvement and clinical recovery were earlier among the remdesivir group. 10-day remdesivir showed more adverse outcome than 5-day course with no significant benefits.

Cisplatin is an anticancer agent marred by nephrotoxicity. Limiting this adverse effect may allow the use of higher doses to improve its efficacy. The Wnt/β-catenin signaling pathway plays a critical role in nephrogenesis and repair of renal diseases. BIO, a small molecule agonist of this pathway, exerted a protective effect in adriamycin nephropathy and promoted nephrogenesis. The aim of this study, therefore, was to investigate whether Wnt/β-catenin agonist BIO could protect against cisplatin-induced nephrotoxicity in vivo and in vitro, as well as its possible mechanism.

Male mice and human renal proximal tubular cells (HK-2) were subjected to cisplatin to study reno-protective effect of BIO. Renal function, cell viability, tubular apoptosis, production of reactive oxygen species (ROS) and proliferative level were analyzed respectively. Additionally, xenograft model was induced to investigate if BIO would impair the antitumor effect of cisplatin.

Cisplatin increased serum creatinine levels and promoted histological renal injury as well as oxidative stress levels. Besides, renal apoptotic level and the expression of pro-apoptotic proteins, Bax/bcl-2 and cleaved-caspase3 included, in the kidney were increased. All these features were decreased by BIO, which also activated Wnt/β-catenin pathway in cisplatin-induced nephrotoxicity. Similarly, accompanied by the motivation of Wnt/β-catenin pathway, BIO exerted a positively protective effect on HK-2 challenged cisplatin. Last, the chemotherapeutic effects of cisplatin in xenograft mice of ovary tumor models and in lung cancer cells weren't compromised by BIO.

Wnt/β-catenin agonist BIO has the potential to prevent cisplatin nephrotoxicity without compromising its anti-proliferation efficacy.

Wnt/β-catenin agonist BIO has the potential to prevent cisplatin nephrotoxicity without compromising its anti-proliferation efficacy.

Abnormal expression of long non-coding RNAs (lncRNAs) occurs in several diseases including renal fibrosis. Notably, growth arrest-specific 5 (Gas5) is a lncRNA, which functions as an essential modulator of cell proliferation and growth. However, the role and expression of lncRNA Gas5 associated with renal fibrosis remains controversial. Herein, we investigate the effect of lncRNA Gas5 deficiency in renal fibrosis induced by the operation of unilateral ureteric obstruction (UUO) in mice.

Sera and urine of mice were used to detect markers of renal function. Further, Masson and immunohistochemical staining, western blotting as well as qRT-PCR were performed to observe the distribution and expression of fibrosis marker in the kidney tissue of the mice.

Unlike the wild type mice, the obstructed kidney in Gas5

mice showed more severe renal fibrosis and collagen deposition. In the UUO-Gas5

group, the serum levels of uric acid, serum creatinine, and the urine levels of albumin-to-creatinine ratio were higher. Moreover, the expression of mRNA and protein of α-smooth muscle actin (α-SMA), vimentin, collagen IV, fibronectin, and matrix metalloproteinase 9 (MMP9) were higher, whereas that of phosphatase and tensin homolog (PTEN) were lower with the difference being statistically significant (p<0.05).

lncRNA Gas5 was up-regulated in renal fibrosis tissues, and its deficiency exacerbated renal fibrosis in the UUO mice model.

lncRNA Gas5 was up-regulated in renal fibrosis tissues, and its deficiency exacerbated renal fibrosis in the UUO mice model.Glucagon-like peptide-1 (GLP-1) receptor agonists are a class of antidiabetic drugs that improve the glycaemia via several molecular pathways. Recent evidence suggest that they also have additional effects modulating pathophysiologic pathways included in cognitive disorders. Since some forms of cognitive dysfunction such as Alzheimer's disease are more common among diabetic patients than in the normal population, antidiabetic drugs that have neuroprotective effects affording protection for cognitive disorders would be of benefit. Therefore, we reviewed the pharmacologic effects of GLP-1 analogues and found that they may have the additional benefit of improving cognitive performance via at least eight molecular mechanisms.

It has been widely reported that autophagy and inositol-requiring enzyme-1α (IRE1α)-c-Jun N-terminal kinase (JNK) pathway was involved in cell survival under endoplasmic reticulum (ER) stress, but their specific roles in hepatic steatosis remain unclear. This study aimed to determine the interaction between autophagy and IRE1α-JNK pathway on cell survival in response to ER stress during the initial phase of hepatic steatosis.

Hepatic steatosis was induced in HepG2 cells by supplementing oleic acid (OA). Lipid accumulation was evaluated by BODIPY493/503 staining. ER stress and IRE1α-JNK signaling were investigated by western blot. Autophagy was monitored by western blot, GFP-LC3 plasmid and immunofluorescence staining, while apoptosis was determined by western blotting, Annexin-V-FITC/PI staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining.

Aggravated lipid accumulation was found under increased ER stress during the initial phase of hepatic steatosis. Meanwhile, an increase of autophagy and no alteration of apoptosis were observed under increased ER stress.