Oligoasthenoteratozoospermia (OAT) is a common cause of infertility among males, and the majority of cases of idiopathic OAT are thought to be attributed to genetic defects. In this study, the role of the CEP78 protein in spermatogenesis was initially investigated using Cep78 knockout (Cep78-/-) mice. Notably, the male Cep78-/- mice exhibited the OAT phenotype and sterility. To elucidate the mechanisms underlying the functions of the Cep78 gene in spermatogenesis, the histomorphology of germ cells was investigated during different stages of mitosis, meiosis, and spermiogenesis. Apoptotic assays and RNA-sequencing analyses were additionally performed using the testicular tissue samples of control and Cep78-/- mice. The findings strongly suggested that defects in the Cep78 gene can lead to male infertility with OAT and that the CEP78 protein is essential for acrosomal biogenesis, sperm head shaping, and formation of flagella during spermiogenesis. The findings are expected to expand the spectrum of genetic defects in OAT and enhance the accuracy of genetic screening and clinical diagnosis.

Th17 cells represent important immune cells. Ursolic acid (UA) can regulate immune cell activities. This study was aimed to explore the effects of UA on Th17 cell differentiation and Schwann cell(SCs)-mediated migration and the potential mechanism. Naïve CD4 + T cells were isolated from rat peripheral blood, induced for Th17 cell differentiation, and treated with UA. The proportion of Th17 cells was detected by flow cytometry assay. SCs were co-cultured with Th17 cells. Th17 cell migration was detected by Transwell assay. The molecule expression was determined by Western blot and qRT-PCR. UA inhibited the Th17 cell differentiation and suppressed the STAT3/RORγt pathway. STAT3 overexpression up-regulated p-STAT3 and RORγt expression and promoted Th17 cell differentiation under the UA treatment. In LPS- and IFN-γ-stimulated-SCs, UA suppressed the expression of chemokines CXCL9/10, but had no significant effect of CCL20 expression. The expression CXCL9/10 receptor CXCR3 was higher in Th17 cells than that in Treg cells, while the expression CCL20 receptor CCR6 was lower in Th17 cells than that in Treg cells. UA, anti-CXCR3, and anti-CCR6 treatment inhibited SCs-mediated Th17 cell migration, and anti-CXCR3 exerted stronger inhibitory effect than Anti-CCR6. UA inhibited Th17 cell differentiation through STAT3/RORγt pathway and suppressed Th17 cell migration through down-regulating CXCL9/10 expression in SCs.

New Findings What is the central question of this study? What is the mechanism of miR-211 in an Alzheimer's disease cell model? What is the main finding and its importance? miR-211 was upregulated in an Alzheimer's disease cell model. It targeted neurogenin 2, reduced the activation of the phosphoinositide 3-kinase-Akt signalling pathway, inhibited the proliferation of the Alzheimer's disease cell model and promoted apoptosis. MicroRNAs (miRs) are aberrantly expressed in Alzheimer's disease (AD) patients. This study was intended to investigate the effect of miR-211 on an AD cell model and the involvement of neurogenin 2 (Ngn2). The appropriate dose and time for the effect of A beta(1-42) on PC12 cells were determined to establish an AD cell model. An effect of miR-211 expression on cell viability, proliferation and apoptosis was detected after cell transfection. Online prediction and a dual luciferase reporter gene assay were utilized to confirm the binding sequence of miR-211 and Ngn2. qRT-PCR and western blot analysis were applied to measure Ngn2 expression. A gain and loss of function assay of miR-211 and Ngn2 was performed, and activation of the phosphoinositide 3-kinase (PI3K)-Akt signaling pathway was detected. The AD cell model was induced by A beta(1-42) treatment. miR-211 expression was significantly enhanced after miR-211 transfection, leading to suppressed proliferation and promotion of apoptosis in A beta(1-42)-treated PC12 cells. In addition, miR-211 could downregulate Ngn2 mRNA and protein expression, while overexpression of Ngn2 could reverse the effects of miR-211 on A beta(1-42)-treated PC12 cells and significantly enhance the phosphorylated Akt and PI3K protein levels. miR-211 could inhibit growth of PC12 cells by suppressing Ngn2 expression and inactivating the PI3K-Akt signalling pathway.

Long noncoding RNAs (lncRNAs) play crucial roles in the regulation of human thyroid cancer (TC), including papillary thyroid carcinoma (PTC); PTC is the most common pathological subtype of TC. To date, the expression, function, and mechanism of the lncRNA CASC15 in PTC remain unclear. The present study results showed that CASC15 was overexpressed in PTC tissues compared with normal tissues and acted as a potent oncogene to promote the proliferation and tumorigenesis of PTC cells both in vitro and in vivo. Mechanistic studies demonstrated that CASC15 could serve as an endogenous miRNA sponge to absorb and downregulate miR-7151-5p, thereby preventing the inhibition of WNT7A during PTC progression. Furthermore, the study demonstrated that CASC15 activated the WNT/β‑catenin signaling pathway by upregulating WNT7A in PTC. Taken together, our findings identified CASC15 as a potential diagnostic marker or therapeutic target for PTC progression. DATA AVAILABILITY: Please contact the corresponding author for a data request.

Abstract Background: Atherosclerosis (AS) is a chronic inflammatory disease that contributes to multiple cardiovascular diseases (CVDs), and foam cell formation plays important roles in the progression of AS. There is an urgent need to identify new molecular targets for treating AS, and thereby improve the quality of life and reduce the financial burden of individuals with CVD. Methods: An in vitro model of AS was generated by treating THP-1 cells and human aortic vascular smooth muscle cells (HA-VSMCs) with oxidized low-density lipoproteins (ox-LDLs). HA-VSMC proliferation and foam cell formation were detected by the MTT assay and Oil Red O staining. C–X–C motif chemokine 12 (CXCL12) expression was suppressed by siRNA. An AS rat model was established by feeding rats a high-fat diet and vitamin D2 for 3 weeks. Histopathology examinations were conducted by Hematoxylin and Eosin (H&E) staining and the levels ionized calcium-binding adapter molecule 1 (IBA1) and α smooth muscle actin (α-SMA) expression were determined by ELISA assays and immunohistochemistry. Results: An in vitro model of AS was established with THP-1 cells. CXCL12 expression in the model THP-1 cells was significantly increased when compared with its expression in control cells. Suppression of CXCL12 expression reduced the progression of AS in the cell model. Moreover, CXCL12 promoted AS in the in vivo rat model. Conclusion: Our results suggest that CXCL12 plays an important role in promoting the progression of AS. Furthermore, inhibition of CXCL12 might suppress the development of AS by inhibiting HA-VSMC proliferation and their transformation to foam cells.

Background: Intrauterine adhesions (IUAs) are one of the most common reproductive system diseases in women worldwide. Emerging evidence has demonstrated that the upregulation or downregulation of genes plays an important role in IUAs. The aim of this study was to evaluate the role of NUS1 in IUAs in a rat model. Material/Methods: The expression of miR-466 in intrauterine adhesions tissues was detected by using RT-qPCR assay. RT-qPCR, IHC, and Western blot were used to investigate mRNA and proteins expression, respectively, of NUS1. MTT and colony-formation assays were used to evaluate cell growth. Transwell assays were used to detect cell migration and invasion. To investigate miR-466 and NUS1 functions in vivo, we established a rat model. The level of epithelial-to-mesenchymal transition (EMT)-related markers was analyzed by Western blot assay. Results: NUS1 was upregulated in IUAs tissues, and the high expression level of NUS1 was positively correlated with the severity of IUAs. NUS1 promoted cell proliferation in vitro. NUS1 overexpression on cell migration and invasion promoted the EMT process in vitro and in vivo. NUS1 acted as a target of miR-466 and played the stimulative role by regulating AKT/NF kappa B pathway. Conclusions: Our data suggest that miR-466 and NUS1 regulate proliferation and the EMT process through the AKT/NF kappa B pathway in IUAs in a rat model.

Riluzole, an anti-glutamate drug and sodium channel blocker with neuroprotective roles, which has been approved by US Food and Drug Administration (FDA) for amyotrophic lateral sclerosis. The purpose of this study was to explore whether Riluzole provides neuroprotection in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Intraperitoneal injection of Riluzole (6 mg/kg) significantly improved neurological deficit at 24, 48 and 72 h. Riluzole alleviated the blood brain barrier (BBB) permeability of cortex and brain edema, also reduced the glutamate concentration of cerebrospinal fluid, increased the GLT-1 expression of cortex, increased GSH content and attenuated MDA content and neuronal apoptosis of cortex at 72 h after SAH. These results suggested that Riluzole treatment may ameliorate early brain injury in experimental SAH model.

目的:观察复方公英散对大鼠正常子宫内膜及宫腔粘连内膜组织IL-8及TNF-a表达的影响.方法:刮宫法建立非动情期SD大鼠宫腔粘连模型,PCR法检测大鼠纤维化组织及空白对照组正常子宫内膜组织IL-8和TNF-a的mRNA表达,分析统计学差异;造模7天后,连续给药28天,比较观察治疗组与模型组纤维化内膜组织中IL-8 mRNA,TNF-amRNA的表达差异.结果:IL-8 mRNA和TNF-a mRNA在大鼠纤维化内膜组织高表达,与正常子宫内膜组织比较有统计学差异(P＜0.05);治疗组内膜组织IL-8mRNA表达下降,与模型组差异有统计学意义(P＜0.05);治疗组TNF-a mRNA表达有下降趋势,与模型组比较差异有统计学意义(P＜0.05).结论:IL-8、TNF-a在大鼠纤维化内膜组织中的表达高于正常子宫内膜组织,复方公英散可明显降低内膜组织中IL-8、TNF-a表达,对子宫内膜纤维化有一定治疗作用.

目的 探讨急性前循环脑梗死患者脑梗死体积与血清神经元特异性烯醇化酶水平的相关性.方法 收集2017年4月1日～9月30日我院收治的50～70岁的40例急性前循环脑梗死患者作为脑梗死组,另从我院查体中心随机抽取50例年龄、性别相匹配的健康志愿者做对照组,分别检测两组的血清初始NSE水平,并据颅脑磁共振DWI像计算脑梗死组患者的梗死体积.结果 脑梗死组血清初始NSE水平为(25.78±2.57)mmol/L,高于对照组的(7.96±0.23)mmol/L,统计学意义显著(P<0.001);颅脑磁共振的DWI相计算出的脑梗死体积与脑梗死组血清初始NSE水平呈高度相关(R=0.736,P<0.001).结论 神经元损伤的定量生化标志物NSE,其水平高低可反映脑卒中后神经功能及脑组织损伤的严重程度,或许可作为急性脑梗死患者病情监测和预后评估的一项重要指标.

目的:探讨半胱胺对局灶性脑缺血大鼠氧化应激及神经元凋亡水平的影响.方法:将60只清洁级Wistar雄性大鼠随机分为3组:假手术组(Sham)、局灶性脑缺血模型(MCAO)组和MCAO+半胱胺(半胱胺)组,每组20只.半胱胺组大鼠给予腹腔注射半胱胺20 mg/kg/d,1次/d×7 d,假手术组和MCAO组大鼠给予腹腔注射等量生理盐水,观察各组丙二醛(MDA)、还原型谷胱甘肽(GSH)及caspase?3的表达水平,同时Tunel法检测神经元凋亡水平.结果:半胱胺治疗可显著降低MCAO大鼠的ROS、MDA和caspase?3的表达,显著增加GSH活力,同时抑制神经元凋亡.结论:半胱胺可减轻局灶性脑缺血氧化应激和神经元凋亡水平,从而发挥神经保护作用.

Objective To ascertain the molecular mechanism by which Helicobacter pylori CagA upregulates CIP2A.Methods After AGS and GES-1 cells were separately cultured to exponential phase,AGS or GES-1 cells were separately transfected with either the recombinant plasmid WT-cagA or the control vector plasmid pcDNA3.1.The cells were then treated with a signal inhibitor of B-Raf or JNK2 and transfected with the plasmid recombinant WT-cagA.The expression of CIP2A was detected with Western blotting,and the cell clonogenic potential was determined using a cell cloning assay.Cell migration was detected with a cell migration assay.Results AGS and GES-1 cells transfected with the plasmid WT-cagA had a higher level of CIP2A expression than that in the control.After treatment with a signal inhibitor of B-Raf or JNK2 and subsequent transfection with the plasmid WT-cagA,the level of CIP2A expression in the cells was decreased.The cell clonogenic potential and cell migration decreased below the cell clonogenic potential and cell migration noted in cells transfected with the plasmid WT-cagA alone.Conclusion H.pylori CagA upregulates the expression of the oncogene CIP2A through B-Raf and JNK2,affecting the cell clonogenic potential and cell migration.

目的：观察艾灸至阴穴与膝胸卧位法矫正胎位不正的疗效。方法：观察组120例给予艾灸至阴穴治疗，对照组116例行膝胸卧位治疗。结果：总有效率观察组94.2%、对照组52.6%，两组比较差异有统计学意义（P＜0.01）。结论：艾灸至阴穴矫正胎位不正有效率明显高于膝胸卧位法。

Objective To prepare Helicobacter pylori Omp18 protein and polyclonal antibodies against that protein Methods The Omp18 gene was amplified using PCR and cloned into the vector pMD-18T.It was then was cloned into the prokaryotic expression plasmid vector pTriEx(TM)-4.The vector was transformed into Escherichia coli JM109DE.Omp18 protein was produced and purified,and then rabbits were repeatedly administered the protein to produce polyclonal antibodies.Results The Omp18 gene was successfully cloned into the prokaryotic expression vector pTriEx(TM)-4 and the vector was successfully transformed into E.coli JM109DE.Omp18 protein was successfully produced,and purified Omp18 protein was administered to rabbits to yield polyclonal antibodies.Conclusion Omp18 protein was successfully expressed in prokaryotic cells,and polyclonal antibodies were successfully prepared in rabbits.This research will benefit study of the function and regulation of Omp18 and it will lay a foundation for detection of H.pylori and preparation of vaccines.

Objective To prepare Helicobacter pylori Omp18 protein and polyclonal antibodies against that protein Methods The Omp18 gene was amplified using PCR and cloned into the vector pMD-18T.It was then was cloned into the prokaryotic expression plasmid vector pTriEx(TM)-4.The vector was transformed into Escherichia coli JM109DE.Omp18 protein was produced and purified,and then rabbits were repeatedly administered the protein to produce polyclonal antibodies.Results The Omp18 gene was successfully cloned into the prokaryotic expression vector pTriEx(TM)-4 and the vector was successfully transformed into E.coli JM109DE.Omp18 protein was successfully produced,and purified Omp18 protein was administered to rabbits to yield polyclonal antibodies.Conclusion Omp18 protein was successfully expressed in prokaryotic cells,and polyclonal antibodies were successfully prepared in rabbits.This research will benefit study of the function and regulation of Omp18 and it will lay a foundation for detection of H.pylori and preparation of vaccines.

Objective To determine if gastric epithelial cells produce IFN-γ and the mechanism of its production.Methods AGS gastric epithelial cells were infected with H.pylori and the production of IFN-γ was detected using RT-PCR and ELISA.AGS gastric epithelial cells were transfected with CagA plasmid and tested for IFN-γ using ELISA.MEK / ERK,Src,P38,and NF-kB inhibitors were then added to the cells transfected with CagA plasmid and they were tested for IFN-γ using ELISA.Results When AGS gastric epithelial cells were infected with H.pylori,the cells produced IFN-γ.When the cells were transfected with CagA plasmid,the cells also produced IFN-γ.When MeK/ErK,P38 and NF-kB inhibitors were added to the cells transfected with CagA plasmid,the production of IFN-γ was inhibited.Conclusion H.pylori AGS gastric epithelial cells to produce IFN-γ.As the main virulence factor for H.pylori,CagA induces cells to produce IFN-γ,and that production depends on signal pathways involving MeK / ErK,P38,and NF-kB.