This study focused on the role of Saikosaponin A (SSA), a triterpenoid saponin derived from Bupleurum root, in regulating lipid metabolism and obesity. Sprague-Dawley rats were fed a high-fat diet, and 3T3-L1 preadipocytes were transformed into mature adipocytes. SSA was administered to both rats and mature adipocytes at different concentrations. Dual-luciferase reporter assays and RNA immunoprecipitation were conducted to explore the interaction between MOB1B and miR-26b-5p. The protein expression levels of key browning markers, including peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), cytochrome c (CytoC), and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), were quantified via Western blotting. Oil Red O staining was utilized to evaluate the effect of SSA on lipid deposition, while hematoxylin and eosin staining was employed to assess lipid droplet accumulation in epididymal white adipose tissue (eWAT). Immunohistochemistry was used to determine MOB1B in eWAT. As detected, SSA promoted the browning of eWAT and 3T3-L1 adipocytes by modulating the miR-26b-5p/MOB1B axis. The browning effect was demonstrated by a decrease in lipid droplet buildup and an increase in thermogenic and adipogenic markers such as PPARγ, C/EBPα, CytoC, and PGC1α. This study not only clarifies the novel mechanism of SSA induced eWAT browning through miR-26b-5p/MOB1B axis, but also provides experimental basis for the development of obesity therapeutic strategies based on natural components.

Obstructive sleep apnea (OSA) is a common sleep disorder characterized by the weakening or even termination of respiratory airflow during sleep. Patients with OSA have different degrees of damage to organs such as the brain, heart, liver, spleen, and intestines, with obvious metabolic disorders and inflammatory reactions. This study was designed to investigate the mechanism of G protein-coupled receptor 1 (GPR1) in chronic intermittent hypoxia (CIH)-induced neuroinflammation in a mouse model of obstructive sleep apnea (OSA). CIH activated ferroptosis in BV-2 cells and mouse hippocampal neurons. GPR1 level was decreased in CIH mouse model and BV-2 cell model. Upregulating GPR1 alleviated cognitive dysfunction, neuroinflammatory injury, and ferroptosis in CIH mice. Upregulating GPR1 attenuated BV-2 cell activation, inflammatory response, and ferroptosis. TAFA1 bound to GPR1 and regulated ferroptosis in CIH. Reducing TAFA1 mitigated the improvement of GPR1 upregulation on CIH mice or BV-2 cells. GPR1 effectively controls ferroptosis and attenuates the resulting neuroinflammation and injury in the context of OSA by regulating TAFA1.

IntroductionAsthma and bronchiolitis in children are considered common clinical problems associated with gut microbiota. However, the exact relationship between gut microbiota and the above-mentioned diseases remains unclear. Here, we discussed recent advances in understanding the potential mechanism underlying immune regulation of gut microbiota on asthma and bronchiolitis in children as well as the role of the gut-lung axis. MethodsWe retrieved and assessed all relevant original articles related to gut microbiota, airway inflammation-induced wheezing in children, and gut-lung axis studies from databases that have been published so far, including PubMed/MEDLINE, Scopus, Google Scholar, China National Knowledge Infrastructure (CNKI) and the Wanfang Database. ResultsThe infant period is critical for the development of gut microbiota, which can be influenced by gestational age, delivery mode, antibiotic exposure and feeding mode. The gut microbiota in children with asthma and bronchiolitis is significantly distinct from those in healthy subjects. Gut microbiota dysbiosis is implicated in asthma and bronchiolitis in children. The presence of intestinal disturbances in lung diseases highlights the importance of the gut-lung axis. ConclusionGut microbiota dysbiosis potentially increases the risk of asthma and bronchiolitis in children. Moreover, a deeper understanding of the gut-lung axis with regard to the gut microbiota of children with respiratory diseases could contribute to clinical practice for pulmonary diseases.

为满足健康中国战略下社会对卫生检验与检疫专业人才的需求,温州医科大学依据学科建设优势及专业办学经验,开展基于与医学检验技术专业融合的复合型人才培养模式探索,笔者从培养目标、课程体系、师资队伍和教学资源建设等方面介绍了思路、实施方法及在人才培养方面取得的初步成效,为新医科背景下的卫生检验与检疫专业高等教育改革提供经验.

笔者从推进课程思政建设的视角,阐述了医学检验技术专业课程体系中存在的问题,从专业育人角度对优化课程设置、挖掘思政教学内容、改善教学方法、拓宽教育渠道进行了深入分析,探讨了在课程思政原则的指导下,构建覆盖面广,层次性强,专业特色突出的课程体系的可行路径.

To investigate whether butyric acid could alleviate chronic intermittent hypoxia (CIH)-induced lipid formation in human preadipocytes-subcutaneous (HPA-s) through accumulation of human antigen R (HuR) and inactivation of AMP-activated protein kinase (AMPK) pathway, HPA-s were obtained and divided into three groups: Control group: cells were cultured under normal conditions; CIH group: cells were cultured in a three-gas incubator (10% O2); Butyric acid group: 10 mmol/l butyric acid added into cell culture medium. HuR-siRNA was futher transfected into CIH group for verification the function of HuR. Oil Red O was implemented for observation of lipid droplets within cells. Cell Counting Kit-8 (CCK8) assay was used for detecting cell viability. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-nick end labeling (TUNEL) assay as well as flow cytometry analysis was employed for determining cell apoptosis. Western blotting was used for measurement of protein expression levels. RT-qPCR analysis was used for detecting mRNA expression. CIH treatment increased adipocytes proliferation, while butyric acid inhibited cell proliferation and promoted cell apoptosis. The treatment of butyric acid in CIH group down-regulated expression of inflammatory factors and increased cell apoptotic rate. Butyric acid treatment increased HuR expression in both cytoplasm and nucleus and decreased the level of p-AMPK and p-ACC, while transfection of AMPK activator or HuR-siRNA would down-regulate HuR expression. Moreover, butyric acid alleviated CIH-induced cell proliferation, lipid formation and inflammatory status and promoted cell apoptosis through regulating related genes including p21, PPARγ, C/EBPa, IL-1β, IL-6, TLR4, caspase-8 and caspase-3. In conclusion, butyric acid could alleviate CIH-induced inflammation, cell proliferation and lipid formation through accumulation of HuR and inactivation of AMPK pathway.

目的 探究帕拉米韦对流感病毒感染小鼠免疫功能及炎症反应的调节作用.方法 将48只BALB/c小鼠随机分为对照组、感染组、低、高剂量治疗组,每组12只,病毒感染组、低、高剂量治疗组小鼠用H1N1病毒株(PR8)滴鼻途径攻毒,4 h后治疗组小鼠通过肌肉注射帕拉米韦4、20 mg/kg ? d,连续注射5 d,对照组和病毒感染组给予等量生理盐水;在攻毒后3d时,每组随机取2只小鼠处死,观察肺组织病理变化及其病毒载量;攻毒后5d时,每组随机取6只小鼠处死,取脾制成单细胞后,利用流式细胞仪检测T淋巴细胞亚群水平,取肺组织制成组织匀浆,利用酶联免疫吸附法(ELISA)检测白细胞介素-2(Interleukin-2,IL-2)、IL-6、肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)、干扰素-y(interferon-γ,IFN-γ)水平,每日观察小鼠状态,持续观察14 d,根据观察结果分析小鼠的存活率及平均生存时间.结果 攻毒14 d后,感染组小鼠全部死亡,死亡率明显高于低、高剂量治疗组(P＜0.05),低剂量治疗组的死亡率高于高剂量治疗组(P＜0.05);攻毒后3d时,低、高剂量治疗组小鼠的肺指数及肺组织病毒载量低于感染组(P＜0.05),高剂量治疗组上述指标变化更显著(P＜0.05);感染组小鼠肺组织的病理损伤及炎症浸润严重,低、高剂量治疗组小鼠的病理损伤及炎症浸润有不同程度减轻,且高剂量治疗组改善更明显;攻毒后5d时,低、高剂量治疗组小鼠的CD4+、CD4+/CD8+、IL-6、TNF-α水平低于感染组,IL-2、IFN-γ水平高于感染组(P＜0.05),且高剂量治疗组的IL-6、TNF-α水平低于低剂量治疗组,IL-2、IFN-γ水平高于低剂量治疗组(P＜0.05).结论 帕拉米韦通过抑制肺组织中流感病毒的释放和增殖,缓解过度免疫反应引起的炎症损伤,进而提高小鼠存活率.

为适应新形势下对人才的需求,温州医科大学医学检验技术专业结合早期办学经验,对实验教学体系做了一系列优化:改进专业课实验教学方法与手段,增加研究性、设计性、综合性实验比例;积极开展虚拟仿真实验建设,弥补传统实验由于条件限制所造成的不足;重视形态检验教学,形成实验教学特色;通过检验技能比赛,提高学生动手能力和职业素质;在实习教学过程中,临床实习和毕业论文两手一起抓;推动科研反哺教学,培养学生创新思维和科研能力;以培养既能充分掌握检验技术和实践技能,又同时具有创新、创业精神和能力的人才为目标,满足"新医科"背景下对医学检验技术专业教育教学改革的要求.

目的:观察间歇性低氧(IH)对人膀胱逼尿肌细胞凋亡和钙离子通道的影响,并初步探讨中药益智仁(AOF)的调节机制.方法:建立人膀胱逼尿肌细胞IH模型,IH模式为5％O260 min-20％O230 min,6个循环.体外培养人膀胱逼尿肌细胞,随机分为6组,每组设8孔,分别为P2X3受体拮抗剂+IH组(A组)、M3受体拮抗剂+IH组(B组)、β3受体拮抗剂+IH组(C组)、AOF+IH组(D组)、生理盐水+IH对照组(NC组)和空气模拟对照(AC)组.干预结束后普通光镜下细胞板计数比较各组细胞密度,免疫荧光法观察细胞形态改变,流式细胞术检测细胞凋亡,膜片钳法测定细胞钙离子表达变化.结果:(1)与AC组细胞比较,NC组细胞密度增高、反应活跃,部分细胞出现突起、变圆,细胞边界模糊;A组和D组细胞密度较NC组有显著减低(P<0.05);(2)免疫荧光检测细胞α-肌动蛋白(α-SMA)表达情况:与AC组比较;NC组的平均吸光度(MA)显著增高(F=3.25,P<0.05);A组、D组细胞分别与NC组比较均有不同程度显著降低(P<0.05).(3)与AC组细胞比较,NC组细胞凋亡率显著减低(P<0.05);A组与D组的细胞凋亡率分别与NC比较有显著增高(P<0.05);(4)与AC组细胞比较,NC组细胞钙离子通道表达显著减低(P<0.05);与NC组细胞比较,AOF组(100 mg/L)和AOF组(50 mg/L)钙离子通道表达显著增高(P均<0.05).结论:IH可通过P2X3膀胱神经受体调节逼尿肌细胞增殖和凋亡,中、高剂量AOF可改变钙离子通道并对IH诱导的细胞损害起保护作用.

本文基于"生物学"的课程特点,围绕创新育人和课程思政育人的教育理念,构思教学方法和教学环节,摸索课程改革,深入落实全员育人、全程育人和全方位育人.

本文基于"海洋生物学"课程的特点,构思教学方法和教学环节,摸索课程思政.将十九大报告中强调的生态文明建设融入课堂,深入落实全员育人、全程育人和全方位育人.

虚拟仿真技术具有真实性、互动性、多样性等特点.医学检验技术虚拟仿真平台是将医学检验技术与虚拟仿真高效、有机地进行结合,为专业理论教学与实践教学带来便利.本项目基于学校现有的教学资源与附属医院的仪器设备设计出一个集检验科、大型仪器、实验项目、诊断流程为一体的医学检验虚拟仿真平台,为培养医学检验技术专门人才提供信息平台.

自实行转专业制度以来,申请进入临床医学专业学习的学生人数逐年递增,通过跟踪评价某高校2008-2010年转入临床医学专业的学生医学主干课程成绩,了解学生在转专业后的学习效果,分析了可能存在的学业问题,为学校制定更全面合理的转专业考核筛选方式及更科学的管理、培养政策提供了参考.

Baicalin, an important flavonoid in Scutellaria baicalensis Georgi extracts, exerts a variety of pharmacological effects. In this study, we explored the effects of baicalin on chronic hypoxia-induced pulmonary arterial hypertension (PAH) and investigated the mechanism underlying these effects. Moreover, we examined whether the inflammatory response was mediated by the A2A receptor (A2AR) and stromal cell-derived factor-1 (SDF-1)/C-X-C chemokine receptor type 4 (CXCR4)-induced phosphatidyl inositol-3-kinase (PI3K) signaling in vivo.

通过回顾中国当代儿科医学教育的历程,结合国内儿科医学教育改革现状及面临的问题,从培养目标、课程设置、教学方法、临床技能和综合素质等方面进行分析,并提出一些可供参考的儿科医学教育模式和培养方式.

本文分析了现阶段住院医师规范化培训与临床医学专业学位研究生教育实施并轨的必要性,以及构建并轨创新模式的现状和面临的主要问题,结合温州医科大学住院医师规范化培训与临床医学硕士研究生教育并轨的培养模式进行讨论,提出在现阶段具体实施过程中的合理性建议.

近年来国内医学院校陆续开展了课程整合改革方面的研究与探索,积累了宝贵经验.从课程整合模式、教学方法、师资建设、教学管理、教学资源、实践能力与临床思维培养、考核方式、效果评价等八个方面对课程整合的现状进行归纳和对比分析,并对改革过程中所出现的若干问题的解决方案提出建议.

Objective To investigate the role of the adenosine A2A receptor(A2AR) and chronic hypoxia in the development of Pulmonary arterial hypertension(PAH) by determining the changes of pulmonary arterial pressure and vascular remodeling in adenosine A2AR knockout mice.Methods The genotypes of the mice(KO A2AR-/-or WT A2AR+/+) were respectively exposure to normoxia and hypoxic conditions(an atmosphere containing 9%-11% O2).Millar Mikro-Tip pressure catheter was used to monitor right ventricular systolic pressures(RVSP).An elevated ratio of the right ventricular weight over left ventricle plus ventricular septum(Fulton index) was observed.Pulmonary vascular remodeling was assessed by HE and with the Elastica-van Gomori method,ultrastructural features were evaluated by electron microscopy.Expression of α-SMA and PCNA in pulmonary resistance vessels were determined by immunohistochemistry.Results Compared to the WT mice,KO mice displayed that increased RVSP and Fulton index,increased wall area and thickness as well as enhanced smooth muscle actin immunoreactivity in pulmonary resistance vessels,increased PCNA positive cells,increased smooth muscle cells hypertrophy and collagen in the adventitia of pulmonary arterioles wall as revealed by electronic microscope.Furthermore,after exposure to hypoxia,parameters in hemodynamic and vascular remodeling were increased markedly in response to hypoxia.Conclusion adenosine A2AR represents an important physiological regulatory mechanism to control the development of PAH and pulmonary vascular remodeling.Increasing severity was demonstrated in A2AR-/-mice exposed to hypoxia.

通过对香港及英国皇家儿童及幼儿健康学院的教育模式的考察研究,结合国内儿科医生的培训现状,从教学方法、课程设置、专业的准入资格和考核方式、毕业后继续教育和专业持续发展等方面进行比较分析,并提出一些可供借鉴的儿科医学教育模式和培养方式.

我国是一个多灾国家,灾害发生频繁[1],面对全球化带来的挑战,培养适应全球化发展的医学救援人才,是目前救援医学专业教育中面临的重要任务[2].灾害医学发展40年来,受到世界各国医学界的高度重视,美国、日本及欧洲的一些国家不同程度地开展了灾害医学教育和训练活动,在大学专门开设有关灾害医学的课程来培养、训练学生的救灾技术[3] .相对而言,我国灾害医学教育还没有受到足够重视,灾害医学教育体系尚未建立,当前的医学本科教育架构中也很少涉及灾害医学相关内容.为了培养医学生多元化角色功能和综合素质,满足灾害救援工作对医学教育的实际需要,温州医学院对全校学生开设了灾害医学选修课,并在教学内容设置、方法选择、考核评价方面积累了经验.