Stability of delayed virus infection model with a general incidence rate and adaptive immune response

We present the dynamical behaviors of a virus infection model with general infection rate, immune responses and two intracellular delays which describe the interactions of the HIV virus, target cells, CTL cells and antibodies within host. Three factors are incorporated in this model: (1) the intrinsic growth rate of uninfected cells, (2) a nonlinear incidence rate function considering both virus-tocell infection and cell-to-cell transmission, and (3) a nonlinear productivity and removal function. By the method of Lyapunov functionals and LaSalle’s invariance principle, we show that the global dynamics of the model is determined by the reproductive numbers for viral infection R0, for antibody immune response R1, for CTL immune response R2, for CTL immune competition R3 and for antibody immune competition R4. The numerical simulations are given to illustrate our theoretical results

Cobalt phosphide nanorods as an efficient electrocatalyst for the hydrogen evolution reaction

Cobalt phosphide (Co2P) nanorods are found to exhibit efficient catalytic activity for the hydrogen evolution reaction (HER), with the overpotential required for the current density of 20mA/cm2 as small as 167mV in acidic solution and 171mV in basic solution. In addition, the Co2P nanorods can work stably in both acidic and basic solution during hydrogen production. This performance can be favorably compared to typical high efficient non-precious catalysts, and suggests the promising application potential of Co2P nanorods in the field of hydrogen production. The HER process follows a Volmer-Heyrovsky mechanism, and the rates of the discharge step and desorption step appear to be comparable during the HER process. The similarity of charged natures of Co and P in the Co2P nanorods to those of the hydride-acceptor and proton-acceptor in highly efficient Ni2P catalysts, [NiFe] hydrogenase, and its analogues implies that the HER catalytic activity of the Co2P nanorods might be correlated with the charged natures of Co and P

Comparative proteomic analysis reveals alterations in development and photosynthesis-related proteins in diploid and triploid rice

Six pairs of primers were designed for gene-specific transcript amplification. (DOC 25 kb

Dysregulated expression of androgen metabolism genes and genetic analysis in hypospadias

Abstract Background The aberrant expression of genes involved in androgen metabolism and genetic contribution are unclear in hypospadias. Methods We compared gene expression profiles by RNA sequencing from five non‐hypospadiac foreskins, five mild hypospadiac foreskins, and five severe hypospadiac foreskins. In addition, to identify rare coding variants with large effects on hypospadias risk, we carried out whole exome sequencing in three patients in a hypospadias family. Results The average expression of androgen receptor (AR) and CYP19A1 were significantly decreased in severe hypospadias (p < .01) and mild hypospadias (p < .05), whereas expression of several other androgen metabolism enzymes, including CYP3A4, HSD17B14, HSD3B7, HSD17B7, CYP11A1 were exclusively significantly expressed in severe hypospadias (p < .05). Compound rare damaging mutants of AR gene with HSD3B1 and SLC25A5 genes were identified in the different severe hypospadias. Conclusions In conclusion, our findings demonstrated that dysregulation of AR and CYP19A1 could play a crucial role in the development of hypospadias. Inconsistent AR expression may be caused by the feedback loop of ESR1 signaling or combined genetic effects with other risk genes. This findings complement the possible role of AR triggered mechanism in the development of hypospadias

Whole-exome sequencing study of hypospadias

Summary: Hypospadias results from the impaired urethral development, which is influenced by androgens, but its genetic etiology is still unknown. Through whole exome sequencing analysis, we identified NR5A1, SRD5A2, and AR as mutational hotspots in the etiology of severe hypospadias, as these genes are related to androgen signaling. Additionally, rare damaging variants in cilia-related outer dynein arm heavy chain (ODNAH) genes (DNAH5, DNAH8, DNAH9, DNAH11, and DNAH17) (p = 8.5 × 10−47) were significantly enriched in hypospadias cases. The Dnah8 KO mice exhibited significantly decreased testosterone levels, which had an impact on urethral development and disrupted steroid biosynthesis. Combined with trios data, transcriptomic, and phenotypical and proteomic characterization of a mouse model, our work links ciliary genes with hypospadias. Overall, a panel of ODNAH genes with rare damaging variants was identified in 24% of hypospadias patients, providing significant insights into the underlying pathogenesis of hypospadias as well as genetic counseling

Vagus Nerve Stimulation Alleviates Hepatic Ischemia and Reperfusion Injury by Regulating Glutathione Production and Transformation

Inflammation and oxidative stress are pivotal mechanisms for the pathogenesis of ischemia and reperfusion injury (IRI). Vagus nerve stimulation (VNS) may participate in maintaining oxidative homeostasis and response to external stimulus or injury. We investigated whether the in vivo VNS can protect the liver from IRI. In this study, hepatic IRI were induced by ligating the vessels supplying the left and middle lobes of the liver, which underwent 1 h occlusion followed with 24 h reperfusion. VNS was initiated 15 min after ischemia and continued 30 min. Hepatic function, histology, and apoptosis rates were evaluated after 24 h reperfusion. Compared with the IRI group, VNS significantly improved hepatic function. The protective effect was accompanied by a reduction in histological damage in the ischemic area, and the apoptosis rate of hepatocytes has considerable reduction. To find the underlying mechanism, proteomic analysis was performed and differential expression of glutathione synthetase (GSS) and glutathione S-transferase (GST) was observed. Subsequently, test results indicated that VNS upregulated the expression of mRNA and protein of GSS and GST. Meanwhile, VNS increased the plasma levels of glutathione and glutathione peroxidases. We found that VNS alleviated hepatic IRI by upregulating the antioxidant glutathione via the GSS/glutathione/GST signaling pathway