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Objective: Enterotypes (ETs) are the clustering of gut microbial community structures, which could serve as indicators of growth performance and carcass traits. However, ETs have been sparsely investigated in waterfowl. The objective of this study was to identify the ileal ETs and explore the correlation of the ETs with growth performance and carcass traits in Muscovy ducks., Methods: A total of 200 Muscovy ducks were randomly selected from a population of 5,000 ducks at 70-day old, weighed and slaughtered. The growth performance and carcass traits, including body weight, dressed weight and evidenced weight, dressed percentage, percentage of apparent yield, breast muscle weight, leg muscle weight, percentage of leg muscle and percentage of breast muscle, were determined. The contents of ileum were collected for the isolation of DNA and 16S rRNA gene sequencing. The ETs were identified based on the 16S rRNA gene sequencing data and the correlation of the ETs with growth performance and carcass traits was performed by Spearman correlation analysis., Results: Three ETs (ET1, ET2, and ET3) were observed in the ileal microbiota of Muscovy ducks with significant differences in number of features and α-diversity among these ETs (p<0.05). Streptococcus, Candida Arthritis, and Bacteroidetes were the presentative genus in ET1 to ET3, respectively. Correlation analysis revealed that Lactococcus and Bradyrhizobium were significantly correlated with percentage of eviscerated yield and leg muscle weight (p<0.05) while ETs were found to have a close association with percentage of eviscerated yield, leg muscle weight, and percentage of leg muscle in Muscovy ducks. However, the growth performance of ducks with different ETs did not show significant difference (p>0.05). Lactococcus were found to be significantly correlated with leg muscle weight, dressed weight, and percentage of eviscerated yield., Conclusion: Our findings revealed a substantial variation in carcass traits associated with ETs in Muscovy ducks. It is implied that ETs might have the potential to serve as a valuable biomarker for assessing duck carcass traits. It would provide novel insights into the interaction of gut microbiota with growth performance and carcass traits of ducks.

Aberrant expression and activation of signal transducer and activator of transcription 3 (STAT3) is implicated in several malignancies, including glioblastoma, and is correlated with poor outcomes in patients with glioblastoma, rendering STAT3 a potential therapeutic target. However, few STAT3 inhibitors have been approved for clinical use. We recently developed an orally active small-molecule compound with anti-STAT3 activity, HJC0152. This study aimed to test the effect of this novel drug on glioblastoma cell lines, and provide possibility to improve clinic prognosis of patients with glioblastoma in the future. In the present study, we aimed to determine the effects of HJC0152 on the growth, proliferation, and chemosensitivity of glioblastoma cell lines and xenograft tumors. We found that HJC0152 inactivated STAT3 via inhibiting phosphorylation of the Tyr705 residue. In vitro , HJC0152 suppressed the proliferation and motility of glioblastoma cells, induced apoptosis, and enhanced the chemosensitivity of glioblastoma cells. Furthermore, HJC0152 inhibited the growth of glioblastoma xenograft tumors in vivo . This study provides a rationale for developing HJC0152 as a STAT3-targeting therapy for treating human glioblastoma in the future., Competing Interests: None.

Alpinia zerumbet is a miao folk medicinal plant widely used in the Guizhou Province of southwest China that contains several bioactive constituents and possesses protective effects against cardiovascular diseases. In the present study, we evaluated the protective effect of essential oils derived from Fructus Alpiniae zerumbet (EOFAZ) on oxidized lowdensity-lipoprotein- (ox-LDL-) induced apoptosis in human aortic endothelial cells (HAECs). Following exposure to ox-LDL, HAECs presented with classical characteristics of apoptosis. However, EOFAZ ameliorated these morphological alterations and also inhibited the decrease in cell viability. In addition, EOFAZ abrogated the number of TUNEL or Hoechst 33258 stained positive cells observed after ox-LDL challenge. Investigation into the mechanisms of this inhibition revealed that EOFAZ treatment resulted in a downregulation of Bax and Caspase-3 at both the protein and mRNA expression levels. Moreover, EOFAZ was found to upregulate Bcl-2 protein and mRNA levels and to attenuate ox-LDL-induced HAECs injury caused by apoptosis, revealing both its therapeutic potential for endothelial cell injury protection and its clinical application for atherosclerosis.

Objective: To study the protective effect of oxymatrine (OMT) on myocardial fibrosis induced by acute myocardial infarction in rats and its effect on TGF-beta-Smads signal pathway., Method: Arteria coronaria ligation-induced acute myocardial infarction model was established in rats. The survived rats were randomly allotted into the model group, 50, 25, 12.5 mg x kg(-1) OMT groups, the 50 mg x kg(-1) captopril group, and the Sham-operated group which was treated as the model group without the arteria coranaria ligation. After 8 weeks of ligation, myocardial fibrosis was detected by HE and Masson staining, and the RT-PCR method were used to detect the expression of mRNA of TGF-beta-Smads signal system., Result: The histopathological examination showed decrease in cardiocytes, deposition of extra-cellular matrix, and increase of collagen contents after 8 weeks of ligation. RT-PCR results showed that mRNA expressions of TGF-beta1, TbetaR1, Smad2, Smad3 and Smad4 significantly increased, but mRNA expression of Smad7 is remarkable lower than the sham-operated group. Treatment with OMT for 8 weeks could remarkably inhibit myocardial fibrosis, decrease mRNA expressions of TGF-beta1, TbetaR1, Smad2, Smad3, and Smad4, and increase mRNA expressions of Smad7., Conclusion: OMT has the inhibitory effect on the experimental myocardial fibrosis induced by AMI in rats. Its mechanism may be closely related to TGF-beta-Smads signal system.