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Background Endometrial cancer (EC) is one of the most common gynaecological tumours in the worldwide. Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes cell proliferation, migration and invasion in EC cells. However, the molecular mechanisms of NEAT1 in EC have not been fully clarified. We conducted this study to reveal the function of NEAT1 in EC tissues and cell lines. Materials and methods Cancer and adjacent tissues were collected from EC patients. HEC-1A and Ishikawa cells were cultured in vitro. NEAT1 expression was downregulated by transfecting small hairpin RNA (shRNA) and miR-144-3p was overexpressed by transfecting miR-144-3p mimics. Cell proliferation was detected by MTT assay and colony formation assay. Cell migration and invasion abilities were assessed by transwell assay. A dual-luciferase reporter assay was used to verify the relationship among NEAT1, EZH2, and miR-144-3p. The expression level of EZH2 was measured by Western blot and qPCR. Results NEAT1 was highly expressed in EC tissues and cells. Knockdown of NEAT1 inhibited the proliferation, migration and invasion of EC cells. Additionally, NEAT1 acted as a ceRNA of miR-144-3p, leading to EZH2 upregulation. Overexpression of miR-144-3p suppressed the proliferation and invasion of EC cells. Conclusions NEAT1 promotes EC cells proliferation and invasion by regulating the miR-144-3p/EZH2 axis.

The transmission and dissemination of antibiotic resistance genes (ARGs) have increasingly drawn global attention. However, our knowledge of the antibiotic resistance gene pool in wild primates' gut microbiomes and its influencing factors remains limited. In this study, we focus on a social group of Tibetan macaques (Macaca thibetana) in Huangshan, utilizing behavioral and metagenomic data to investigate the effects of host sex, age, and social network on the ARG profiles of the gut microbiome. Our results demonstrate a high diversity of ARGs in the gut microbiota of Tibetan macaques, with multidrug, glycopeptide, and peptide resistance genes being the most prevalent. Although host age, sex, and social networks did not significantly affect the overall diversity of ARGs, these factors were significantly correlated with the relative abundance of several highly abundant ARG types, including gryB, rpoB, macB, novA, efrA, patB, Staphylococcus aureus mupA conferring mupirocin resistance, RanA, and cdeA. Further analysis revealed extensive interactions between gut bacteria and ARGs, with age emerging as a potentially key factor in this covariation process. These findings provide new insights into the formation and transmission mechanisms of antibiotic resistance in the gut microbiome of wildlife, particularly in social primates. Based on metagenomic and behavioral data from wild Tibetan macaques, this study reveals a unique gut resistome profile dominated by multidrug resistance genes. While individual factors like age, sex, and social centrality did not affect overall ARG diversity, they significantly influenced the abundance of specific, high‐prevalence ARGs. Furthermore, age emerged as a key driver of the co‐variation network between core gut bacteria and ARGs, providing new ecological insights into antibiotic resistance dynamics in wild social primates.

ObjectiveTo investigate the impact of Qing’e Pill (青娥丸, QEP) on the cancellous bone microstructure and its effect on the level of β-catenin in a mouse model of postmenopausal osteoporosis.MethodsNinety-six 8-week-old specific pathogen free C57BL/6 mice were randomly divided into 4 groups (24/group): sham, ovariectomised osteoporosis model, oestradiol-treated, and QEP-treated groups. Three months after surgery, the third lumbar vertebra and left femur of the animals were dissected and scanned using micro-computed tomography (micro-CT) to acquire three-dimensional (3D) parameters of their cancellous bone microstructure. The impact of ovariectomy, the effect of oestradiol and QEP intervention on cancellous bone microstructure, and the expression of β-catenin were evaluated.ResultsThe oestradioland the QEP-treated groups exhibited a significant increase in the bone volume fraction, trabecular number, trabecular thickneßs, bone surface to bone volume ratio (BS/BV), and β-catenin expression compared with those of the model group (P <0.05). In contrast, the structure model index, trabecular separation, and BS/BV were significantly decreased compared with those of the ovariectomised osteoporosis model group (P <0.05). No differences were observed in the above parameters between animals of the QEP- and oestradiol-treated groups.ConclusionsThe increased β-catenin expression may be the mechanism underlying QEP’s improvement of the cancellous bone microstructure in ovariectomised mice. Our findings provide a scientific rationale for using QEP as a dietary supplement to prevent bone loss in postmenopausal women.

The laying quail is a worldwide breed which exhibits high economic value. In our current study, the vasoactive intestinal peptide receptor-1 ( VIPR-1 ) was selected as the candidate gene for identifying traits of egg production. A single nucleotide polymorphism (SNP) detection was performed in 443 individual quails, including 196 quails from the H line, 202 quails from the L line, and 45 wild quails. The SNPs were genotyped using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Two mutations (G373T, A313G) were detected in all the tested quail populations. The associated analysis showed that the SNP genotypes of the VIPR-1 gene were significantly linked with the egg weight of G373T and A313G in 398 quails. The quails with the genotype GG always exhibited the largest egg weight for the two mutations in the H and L lines. Linkage disequilibrium (LD) analysis indicated that G373T and A313G loci showed the weakest LD. Seven main diplotypes from the four main reconstructed haplotypes were observed, indicating a significant association of diplotypes with egg weight. Quails with the h1h2 (GGGT) diplotype always exhibited the smallest egg weight and largest egg number at 20 weeks of age. The overall results suggest that the alterations in quails may be linked with potential major loci or genes affecting reproductive traits.

Neonatal pneumonia (NP) is a frequently occurring illness during the neonatal phase. The study investigated the molecular process and the role of microRNA (miR)-29a-3p in NP. Peripheral blood was collected from NP patients and healthy newborns. Human lung fibroblasts cell line (WI-38) were treated with lipopolysaccharide (LPS)) to establish a cellular model for NP. Then, miR-29a-3p and Krüppel-like Factor 4 (KLF4) levels were detected by RT-qPCR or Western blot. The relationship between miR-29a-3p and KLF4 was confirmed by dual luciferase reporter gene assay. Cell survival was assessed using the CCK-8 assay, whereas the levels of interleukin-6, tumor necrosis factor-α, and IL-1β were quantified using ELISA. Additionally, apoptosis was evaluated through flow cytometry. Meanwhile, Bax and Bcl-2 were detected by RT-qPCR. Neonatal rats were administered LPS intraperitoneally (3 mg/kg) to induce NP, and pathological injury and inflammatory reaction were analyzed. MiR-29a-3p was elevated but KLF4 was silenced in NP patient’s serum, LPS-treated WI-38 cell line, and LPS-treated newborn rats. Silence of miR-29a-3p or elevation of KLF4 constrained cell proliferation with inflammation of LPS-treated WI-38 cell line. MiR-29a-3p immediately targeted KLF4. Additionally, silence of miR-29a-3p alleviated LPS-stimulated lung injury and inflammation in neonatal rats. The protective action of silenced miR-29a-3p in LPS-treated WI-38 cell line and newborn rats was turned around by silencing KLF4. This study demonstrates originally that miR-29a-3p boosts inflammatory damage in NP via targeting KLF4, offering a basis for clinically diagnosing and treating NP.

Objective. To demonstrate the role of Wnt/β-catenin canonical pathway in postmenopausal osteoporosis by evaluating serum β-catenin levels in patients with postmenopausal osteoporosis and analyzing their possible relationship with serum OPG, RANKL, the ratio of RANKL/OPG, sclerostin, and bone turnover markers. Methods. 480 patients with postmenopausal osteoporosis and 170 healthy postmenopausal women were enrolled in the study. Serum β-catenin, OPG, RANKL, and sclerostin levels were measured by enzyme-linked immunosorbent assay. Bone status was assessed by measuring bone mineral density and bone turnover markers. Estradiol levels were also detected. Results. Serum β-catenin levels were lower in postmenopausal osteoporotic women compared to nonosteoporotic postmenopausal women (26.26±14.81 versus 39.33±5.47 pg/mL, P<0.001). Serum β-catenin was positively correlated with osteoprotegerin (r=0.232, P<0.001) and negatively correlated with the ratio of RANKL/OPG, body mass index, and sclerostin (r=-0.128, P=0.005; r=-0.117, P=0.010; r=-0.400, P<0.001, resp.) in patients with postmenopausal osteoporosis. Conclusion. The results indicate that lower serum β-catenin and concomitantly higher ratio of RANKL/OPG may be involved in the pathogenesis of postmenopausal osteoporosis. Functional communication between RANKL/RANK/OPG system and Wnt pathways plays an important role in postmenopausal osteoporosis.

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder characterized by recurrent abdominal pain or discomfort associated with abnormal bowel habits. Diarrhea-predominant IBS (IBS-D) is a major subtype of IBS, the predominant manifestations of which are abdominal pain and diarrhea. The pathogenesis of IBS-D remained unknown until recently. The effects of psychosocial stress, central hypervigilance, neuroendocrine abnormality, disturbed gastrointestinal motility, mucosal immune activation, intestinal barrier dysfunction, visceral hypersensitivity (VH), altered gut flora, and genetic susceptibility may be involved in its development. Recently, increased attention has been placed on the neural-immune-endocrine network mechanism in IBS-D, especially the role of various neuroendocrine mediators. As a member of the neurotrophin family, nerve growth factor (NGF) has diverse biological effects, and participates in the pathogenesis of many diseases. Basic studies have demonstrated that NGF is associated with inflammatory- and stress-related VH, as well as stress-related intestinal barrier dysfunction. The aim of this study is to summarize recent literature and discuss the role of NGF in the pathophysiology of IBS-D, especially in VH and intestinal barrier dysfunction, as well as its potential as a therapeutic target in IBS-D.

ObjectivesTo observe the regulation of Chinese herbal medicine, Modifified Qing’e Pill (加味青娥丸, MQEP), on the expression of adiponectin, bone morphogenetic protein 2 (BMP2), osteoprotegerin (OPG) and other potentially relevant risk factors in patients with nontraumatic osteonecrosis of the femoral head (ONFH).MethodsA total of 96 patients with nontraumatic ONFH were unequal randomly divided into treatment group (60 cases) and control group (36 cases). The treatment group were treated with MQEP while the control group were treated with simulated pills. Both groups were given caltrate D. Six months were taken as a treatment course. Patients were followed up every 2 months. The levels of plasma adiponectin, BMP2, OPG, von Willebrand factor (vWF), von Willebrand factor cleaving protease (vWF-cp), plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator (tPA), C-reactive protein (CRP), blood rheology, bone mineral density (BMD) of the femoral head and Harris Hip Score were measured before and after treatment.ResultsAfter 6 months of treatment, compared with the control group, patients in the treatment group had signifificantly higher adiponectin and BMP2 levels (P<0.01 and P=0.013, respectively), lower vWF, PAI-1 and CRP levels (P=0.019, P<0.01 and P<0.01, respectively), and lower blood rheology parameters. BMD of the femoral neck, triangle area and Harris Hip Score in the treatment group were signifificantly higher than those in the control group. Moreover, plasma adiponectin showed a positive association with BMP2 (r=0.231, P=0.003) and a negative association with PAI-1 (r=–0.159, P<0.05).ConclusionMQEP may play a protective role against nontraumatic ONFH by increasing the expression of adiponectin, regulating bone metabolism and improving the hypercoagulation state, which may provide an experimental base for its clinical effects.

Autophagy has been suggested to participate in the pathology of hypoxic-ischemic brain damage（HIBD）.However,its regulatory role in HIBD remains unclear and was thus examined here using a rat model.To induce HIBD,the left common carotid artery was ligated in neonatal rats,and the rats were subjected to hypoxia for 2 hours.Some of these rats were intraperitoneally pretreated with the autophagy inhibitor 3-methyladenine（10 m M in 10 μL） or the autophagy stimulator rapamycin（1 g/kg） 1 hour before artery ligation.Our findings demonstrated that hypoxia-ischemia-induced hippocampal injury in neonatal rats was accompanied by increased expression levels of the autophagy-related proteins light chain 3 and Beclin-1 as well as of the AMPA receptor subunit GluR 1,but by reduced expression of GluR 2.Pretreatment with the autophagy inhibitor 3-methyladenine blocked hypoxia-ischemia-induced hippocampal injury,whereas pretreatment with the autophagy stimulator rapamycin significantly augmented hippocampal injury.Additionally,3-methyladenine pretreatment blocked the hypoxia-ischemia-induced upregulation of Glu R1 and downregulation of GluR2 in the hippocampus.By contrast,rapamycin further elevated hippocampal Glu R1 levels and exacerbated decreased GluR2 expression levels in neonates with HIBD.Our results indicate that autophagy inhibition favors the prevention of HIBD in neonatal rats,at least in part,through normalizing Glu R1 and GluR2 expression.

Background： No data on the incidence ofpleural effusion （PE） in Chinese patients with pulmonary embolism are available to date. The aim of the current study was to investigate the frequency of PE in a Chinese population of patients with pulmonary embolism. Methods： This was a retrospective observational single-center study. All data of computed tomography pulmonary angiography （CTPA） performed over 6-year period on adult patients with clinically suspected pulmonary embolism were analyzed. Results： From January 2008 until December 2013, PE was identified in 423 of 3141 patients （13.5%） with clinically suspected pulmonary embolism who underwent CTPA, The incidence of PE in patients with pulmonary embolism （19.9%） was significantly higher than in those without embolism （9.4%） （P 〈 0.001 ）. Majority of PEs in pulmonary embolism patients were small to moderate and were unilateral. The locations of emboli and the numbers of arteries involved, CT pulmonary obstruction index, and parenchymal abnormalities at CT were not associated with the development of PE, Conclusions： PEs are present in about one fifth of a Chinese population of patients with pulmonary embolism, which are usually small, unilateral, and unsuitable for diagnostic thoracentesis.