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Anhedonia is one of the core symptoms of major depressive disorder (MDD), which is often inadequately treated by traditional antidepressants. The modern framework of anhedonia extends the definition from impaired consummatory pleasure or interest in rewards to a broad spectrum of deficits that impact functions such as reward anticipation, approach motivation, effort expenditure, reward valuation, expectation, and reward-cue association learning. Substantial preclinical and clinical research has explored the neural basis of reward deficits in the context of depression, and has implicated mesocorticolimbic reward circuitry comprising the nucleus accumbens, ventral pallidum, ventral tegmental area, amygdala, hippocampus, anterior cingulate, insula, orbitofrontal cortex, and other prefrontal cortex regions. Dopamine modulates several reward facets including anticipation, motivation, effort, and learning. As well, serotonin, norepinephrine, opioids, glutamate, Gamma aminobutyric acid (GABA), and acetylcholine are also involved in anhedonia, and medications targeting these systems may also potentially normalize reward processing in depression. Unfortunately, whereas reward anticipation and reward outcome are extensively explored by both preclinical and clinical studies, translational gaps remain in reward motivation, effort, valuation, and learning, where clinical neuroimaging studies are in the early stages. This review aims to synthesize the neurobiological mechanisms underlying anhedonia in MDD uncovered by preclinical and clinical research. The translational difficulties in studying the neural basis of reward are also discussed.

Spinal cord injury (SCI) leads to severe motor and sensory dysfunctions. Neural stem cells (NSCs) transplantation therapy plays a positive role in functional recovery after SCI, but the effectiveness of this therapy is limited by inadequate differentiation ability of transplanted NSCs. Mammalian achaete-scute homologue-1 (Mash-1) has been reported to improve differentiation of NSCs. Thus, this study modified NSCs with Mash-1 to repair SCI.

NSCs isolated from rat embryo hippocampus were cultured and identified in vitro and further transfected with the lentiviral vectors (Lv-Mash-1). After establishing a SCI rat model, the rats were transplanted with Mash-1 modified NSCs, the histopathological changes of rat spinal cord were detected by hematoxylin-eosin (HE) staining, and the locomotor activity of rats was evaluated with the Basso, Beattie and Bresnahan (BBB) scale. The NSCs cultured in vitro or extracted from SCI rat spinal cord were identified by immunofluorescence (IF). Mash-1, β3-Tubulin, and NeuN expressions in those cells were determined by Western blotting and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR).

NSCs isolated from rat embryo hippocampus were Nestin- and NeuN-positive. NSC transplantation modified by Mash-1 increased BBB score of SCI rats and promoted recovery in lesion site of SCI rats. Mash-1 overexpression also promoted β3-Tubulin and NeuN expressions in NSCs cultured in vitro or extracted from spinal cord of SCI rats.

Mash-1 overexpression promoted NSC differentiation into neurons, and further improved locomotor functional recovery of SCI rats.

Mash-1 overexpression promoted NSC differentiation into neurons, and further improved locomotor functional recovery of SCI rats.Sertoli cells are “nurturing cells” in the seminiferous tubules of the testis which have essential roles in the development, proliferation and differentiation of germ cells. These cells also divide the seminiferous epithelium into a basal and an adluminal compartment and establish the blood-testis barrier (BTB). BTB shields haploid germ cells from recognition by the innate immune system. Moreover, after translocation of germ cells into the adluminal compartment their nutritional source is separated from the circulatory system being only supplied by the Sertoli cells. The integrity of BTB is influenced by several organic/ organometallic, hormonal and inflammatory substances. Moreover, several environmental contaminants such as BPA have hazardous effects on the integrity of BTB. In the current review, we summarize the results of studies that assessed the impact of these agents on the integrity of BTB. These studies have implications in understanding the molecular mechanism of male infertility and also in the male contraception.Candida spp. have attracted considerable attention as they cause serious human diseases in immunocompromised individuals. The genomes of the pathogenic Candida spp. have been sequenced, but systemic characterizations of their kinomes are yet to be reported. As in various eukaryotes, the protein kinases play crucial regulatory roles in pathogenicity of Candida. Increased frequency of antifungal resistance in Candida spp. requires significant attention to explore novel therapeutic molecules for their control. The present in-silico study involves novel bioinformatics strategies to identify the kinase proteins and their potential drug targets with the purpose to combat fungal infections. LXS-196 in vitro The study reports 103, 107 and 106 kinase proteins from 3 Candida spp., C. albicans, C. parapsilosis and C. tropicalis, respectively. Moreover, 79 common kinase proteins were identified, of which 54 proteins play essential roles in Candida spp. and 42 proteins were human non-homologues. Among the essential and human non-homologous protein kinases, 9 were found to be common essential human non-homologues, of which 6 are uniquely present in Candida. These 6 protein kinases namely, Hsl1, Npr1, Ptk2, Kin2, Ksp1 and orf19.3854 (CAALFM_CR06040WA) are involved in various molecular and cellular processes regulating virulence or pathogenicity. Further, these 6 kinases are prioritized as potential drug targets and explored for discovering new lead compounds against candidiasis. The drug repurposing approach for these 6 kinases show 13 approved drugs and investigational compounds that might play substantial inhibitory roles during combating candidiasis.Fat tail is one of the most important domesticated characteristics in sheep; however its molecular mechanism is poorly understood. Here we took small-tailed F2 hybrid of wild Argali sheep and typical fat-tailed Bashby sheep as research object. First, histological analysis revealed that the mean diameter and area in tail and subcutaneous fat cells, and surface density in tail fat in Bashby sheep were significantly larger than that in F2 sheep, and surface density of fat in subcutaneous fat in Bashby sheep was significantly lower than that in F2 sheep. Second, 873 differentially expressed genes (DEGs) of tail fat between Bashby and F2 sheep were identified by RNA-seq. Third, the tissue expression profile and relative expression difference between Bashby and F2 sheep of 7 of 873 DEGs were analyzed by RT-PCR. SCD, ESR1, EMR1, PHYH, STAT3 and GPAM genes were highly expressed in fat, muscle and liver, and ALDH1A1 were highly expressed in small intestine. In addition, the expressions of SCD, PHYH and CPAM genes in tail fat of F2 sheep were lower than that of Bashby sheep, while the expression patterns of ESR1 and EMR1 were reversed.