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Summary The objective of this research was to compare the composition of bacterial microbiota associated with the ruminal content (RC), ruminal epithelium (RE) and faeces of Holstein dairy cows. The RC, RE and faecal samples were collected from six Holstein dairy cows when the animals were slaughtered. Community compositions of bacterial 16S rRNA genes from RC, RE and faeces were determined using a MiSeq sequencing platform with bacterial‐targeting universal primers 338F and 806R. UniFrac analysis revealed that the bacterial communities of RC, RE and faeces were clearly separated from each other. Statistically significant dissimilarities were observed between RC and faeces (P = 0.002), between RC and RE (P = 0.003), and between RE and faeces (P = 0.001). A assignment of sequences to taxa showed that the abundance of the predominant phyla Bacteroidetes was lower in RE than in RC, while a significant higher (P < 0.01) abundance of Proteobacteria was present in RE than in RC. When compared with the RC, the abundance of Firmicutes and Verrucomicrobia was higher in faeces, and RC contained a greater abundance of Bacteroidetes and Tenericutes. A higher proportions of Butyrivibrio and Campylobacter dominated RE as compared to RC. The faecal microbiota was less diverse than RC and dominated by genera Turicibacter and Clostridium. In general, these findings clearly demonstrated the striking compositional differences among RC, RE and faeces, indicating that bacterial communities are specific and adapted to the harbouring environment.

Central nervous system tumors are classified as diseases of special clinical significance with high disability and high mortality. In addition to cerebrovascular diseases and craniocerebral injuries, tumors are the most common diseases of the central nervous system. Hydrogen sulfide, the third endogenous gas signaling molecule discovered in humans besides nitric oxide and carbon monoxide, plays an important role in the pathophysiology of human diseases. It is reported that hydrogen sulfide not only exerts a wide range of biological effects, but also develops a certain relationship with tumor development and neovascularization. A variety of studies have shown that hydrogen sulfide acts as a vasodilator and angiogenetic factor to facilitate growth, proliferation, migration and invasion of cancer cells. In this review, the pathological mechanisms and the effect of hydrogen sulfide on the central nervous system tumors are introduced.

Hydrogen sulfide (H2S) is recognized to be a novel mediator after carbon monoxide and nitric oxide in the organism. It can be produced in various mammalian tissues and exert many physiological effects in many systems including the cardiovascular system. A great amount of recent studies have demonstrated that endogenous H2S and exogenous H2S-releasing compounds (such as NaHS, Na2S, and GYY4137) provide protection in many cardiovascular diseases, such as ischemia/reperfusion injury, heart failure, cardiac hypertrophy, and atherosclerosis. In recent years, many mechanisms have been proposed and verified the protective role exhibited by H2S against myocardial ischemia/reperfusion injury, and this review is to demonstrate the protective role of exogenous and endogenous H2S on myocardial ischemia/reperfusion injury.

In this study, we aimed to evaluate the effect of Nobiletin (NOB) on the placenta of Sprague–Dawley (SD) rats that had undergone reduced uterine perfusion pressure (RUPP) surgery and to evaluate the safety of NOB intervention during pregnancy. The results showed that NOB alleviated placental hypoxia, attenuated placental cell apoptosis, and inhibited placental damage in RUPP rats. No side effect of NOB intervention during pregnancy was observed. BeWo cell lines with P53 knockdown were then constructed using lentiviral transfection, and the P53 signaling pathway was found to be essential for NOB to reduce hypoxia-induced apoptosis of the BeWo cell lines. In summary, NOB attenuated hypoxia-induced placental damage by regulating the P53 signaling pathway, and those findings may contribute some insights into the role of NOB in placental development and the prevention of placental-related diseases.

Nasopharyngeal carcinoma (NPC) is a common head and neck malignant with a high incidence in Southern China. Genetic aberrations play a vital role in the pathogenesis, progression and prognosis of NPC. In the present study, we elucidated the underlying mechanism of FAS-AS1 and its genetic variation rs6586163 in NPC. We demonstrated that FAS-AS1 rs6586163 variant genotype carriers were associated with lower risk of NPC (CC vs. AA, OR = 0.645, P  = 0.006) and better overall survival (AC + CC vs. AA, HR = 0.667, P  = 0.030). Mechanically, rs6586163 increased the transcriptional activity of FAS-AS1 and contributed to ectopic overexpression of FAS-AS1 in NPC. rs6586163 also exhibited an eQTL trait and the genes affected by rs6586163 were enriched in apoptosis related signaling pathway. FAS-AS1 was downregulated in NPC tissues and over-expression of FAS-AS1 was associated with early clinical stage and better short-term treatment efficacy for NPC patients. Overexpression of FAS-AS1 inhibited NPC cell viability and promoted cell apoptosis. GSEA analysis of RNA-seq data suggested FAS-AS1 participate in mitochondria regulation and mRNA alternative splicing. Transmission electron microscopic examination verified that the mitochondria was swelled, the mitochondrial cristae was fragmented or disappeared, and their structures were destroyed in FAS-AS1 overexpressed cells. Furthermore, we identified HSP90AA1, CS, BCL2L1, SOD2 and PPARGC1A as the top 5 hub genes of FAS-AS1 regulated genes involved in mitochondria function. We also proved FAS-AS1 could affect Fas splicing isoform sFas/mFas expression ratio, and apoptotic protein expression, thus leading to increased apoptosis. Our study provided the first evidence that FAS-AS1 and its genetic polymorphism rs6586163 triggered apoptosis in NPC, which might have a potential as new biomarkers for NPC susceptibility and prognosis.

Aim： To investigate the effects of caffeic acid on early and delayed injuries after focal cerebral ischemia in rats, and the possible relation to 5-1ipoxygenase inhibition. Methods： Transient focal cerebral ischemia was induced by middle cerebral artery occlusion in Sprague-Dawley rats. Caffeic acid （10 and 50 mg/kg） was ip injected for 5 d after ischemia. The brain injuries were observed, and the levels of cysteinyl leukotrienes and leukotriene B4 in the brain tissue were measured. Results： Caffeic acid （50 mg/kg） ameliorated neurological dysfunction and neuron loss, and decreased infarct volume 24 h after ischemia; it attenuated brain atrophy, infarct volume, and particularly astrocyte proliferation 14 d after ischemia. In addition, it reduced the production of leukotrienes （5-1ipoxygenase metabolites） in the ischemic hemispheres 3 h and 7 d after ischemia. Conclusion： Caffeic acid has protective effect on both early and delayed injuries after focal cerebral ischemia in rats; and this effect may partly relate to 5-1ipoxygenase inhibition.

Renal ischemia reperfusion injury (IRI) is one of the pivotal event of acute kidney injury (AKI), and they are unavoidable in the process of kidney transplantation, which eventually leads to the loss of renal allograft. Ferroptosis is a newly identified programmed cell death. Recent studies have suggested that ferroptosis may participate in the pathophysiological process of renal IRI. Therefore, we aimed to determine biomarkers associated with ferroptosis during renal IRI and their impact on renal allografts. We conducted a comprehensive bioinformatics analysis and established an IRI-AKI animal model to illustrate the critical role of ferroptosis-related hub genes (FRHGs) in IRI-AKI and their potential impact on kidney transplantation. In this study, we identified 60 ferroptosis-related genes (FRGs) in renal IRI based on the GSE148420 dataset and FerrDb database. And then we performed functional annotation analysis using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. Protein-protein interaction (PPI) network was constructed by online tool String. EZH2, CDKN1A, PPARA, EGR1, ATF3, and CD44 were identited as six ferroptosis-related hubgenes (FRHGs) using four methods, including MMC, Degree, DMNC, and EPC. FRHGs expression level were verified by the validation sets GSE58438 and GSE126805. Protein expression level of FRHGs verified by Proteomics and Western blot. Cibersort was utilized to analyze immune cell infiltration during renal IRI as well as the correlation between FRHGs and immune cells. The GSE21374 dataset was used for renal allografts survival analysis. Finally, We induced the IRI-AKI animal model and illustrated the importance of FRGHs CD44 in ferroptosis and the accumulation of macrophages. We identified 6 FRHGs. We found that FRHGs not only exhibited significant correlation with immune cells but also directly influenced the survival of transplanted kidneys in the human population. Among six FRHGs, only CD44 was overexpressed at both the gene and protein levels. Anti-CD44 exerts a protective effect by inhibiting ferroptosis and the accumulation of M1 macrophages during renal IRI. This study provided new insights into the pathogenesis of renal IRI and provided new evidence for its treatment.

Aim： To evaluate the effects of aldosterone with or without high sodium intake on blood pressure, myocardial structure and left ven- tricular function in rats, and to investigate the mechanisms underlying the effects. Methods： Eight-week-old male Sprague-Dawley rats were randomly divided into 3 groups： （1） control （CON） group fed a normal sodium diet, （2） aldosterone （ALD） group receiving aldosterone infusion and a normal sodium diet, and （3） high sodium plus aldosterone （HS- ALD） group receiving 1% NaCI diet in conjunction with aldosterone infusion. Aldosterone was administered through continuously sub- cutaneous infusion with osmotic minipump at the rate of 0.75 pg/h for 8 weeks. The myocardium structure was observed using transt- horacic echocardiography and transmission electron microscopy. The collagen deposition in left ventricle was evaluated with Masson＇s trichrome staining. The expression of IL-18, p22phox, and p47phox proteins was examined using Western blot analysis. Results： The systolic blood pressure in the ALD and HS-ALD groups was significantly higher than that in the CON group after 2-week treatment. But the blood pressure showed no significant difference between the HS-ALD and ALD groups. The left ventricular hyper- trophy, myocardial collagen deposition and oxidative stress were predominantly found in the HS-ALD and ALD group. Furthermore, the breakdown of myocardial structure and oxidative stress were more apparent in the HS-ALD group as compared with tho~e in the ALD group. Conclusion： Long-term infusion of aldosterone results in hypertension and profibrotic cardiovascular responsesin rats fed a normal sodium diet, which were mediated by oxidative stress. High-sodium intake could aggravate myocardial injuries induced by aldosterone.

Assessing axillary lymph node (ALN) tumor burden (low burden: < 3 positive ALNs; high burden: ≥ 3 positive ALNs) preoperatively is essential for guiding treatment strategies. This study aimed to develop a radiomics-based nomogram by integrating clinical data, serologic markers, ultrasound imaging features, and ultrasound-derived radiomics features to predict axillary lymph node metastatic burden in breast cancer. A study was conducted on 234 breast cancer patients. Univariate and multivariate logistic regression analyses were used to identify independent risk factors from ultrasound imaging and clinical pathology, constructing a clinical model. Radiomics features were extracted from ultrasound images, and the best features were selected using the Least Absolute Shrinkage and Selection Operator (LASSO) algorithm to construct the Radiomics score. The Radiomics nomogram model was built by combining the Radiomics score and independent risk factors from the clinical model. The performance of the clinical model, radiomics model, and combined model in predicting axillary lymph node tumor burden was evaluated. Model performance was assessed by discrimination, calibration curves, and decision curves. Results showed that US-reported ALN status and CA153 were independent risk factors for high ALN tumor burden. The radiomics nomogram demonstrated good calibration and discrimination, with an area under the ROC curve of 0.815 (95% CI, 0.755-0.876) for the training set and 0.808 (95% CI, 0.678-0.938) for the testing set. Furthermore, compared to the clinical model and radiomics model, The differences in AUC between the nomogram model and the clinical model, as well as between the nomogram model and the radiomics model, were not statistically significant (nomogram model vs. clinical model: P = 0.2078; nomogram model vs. radiomics model: P = 0.4161). But the nomogram model provided greater net benefit for all patients in the probability threshold range of 0.05-0.70. This study highlights the potential of an ultrasound-based radiomics nomogram as a robust and non-invasive predictive tool for evaluating ALN tumor burden, offering valuable guidance for personalized treatment planning in breast cancer.

Background： Mutations of transthyretin （TTR） cause the most common type of autosomal-dominant hereditary systemic amyloidosis, which occurs worldwide. To date, more and more mutations in the TTR gene have been reported. Some variations in the clinical presentation are often observed in patients with the same mutation or the patients in the same family. The purpose of this study was to find out the clinicopathologic and genetic features of Chinese patients with hereditary TTR amyloidosis. Methods： Clinical and necessary examination materials were collected from nine patients of eight families with hereditary TTR amyloidosis at Peking University First Hospital from January 2007 to November 2014. Sural nerve biopsies were taken for eight patients and skin biopsies were taken in the calf/upper arm for two patients, for light and electron microscopy examination. The TTR genes from the nine patients were analyzed. Results： The onset age varied from 23 to 68 years. The main manifestations were paresthesia, proximal and/or distal weakness, autonomic dysfunction, cardiomyopathy, vitreous opacity, hearing loss, and glossohypertrophia. Nerve biopsy demonstrated severe loss ofmyelinated fibers in seven cases and amyloid deposits in three. One patient had skin amyloid deposits which were revealed from electron microscopic examination. Genetic analysis showed six kinds of mutations of TTR gene, including Val30Met, Phe33Leu, Ala36Pro, Val30Ala, Phe33Val, and Glu42Gly in exon 2. Conclusions： Since the pathological examinations ofsural nerve were negative for amyloid deposition in most patients, the screening for TTR mutations should be performed in all the adult patients, who are clinically suspected with hereditary TTR amyloidosis.