腹腔镜下子宫峡部环扎术

子宫峡部环扎术是治疗宫颈机能不全最主要的方法。对于反复经阴道环扎失败或宫颈解剖异常不能经阴道环扎的患者，可选择经腹腔镜子宫峡部环扎。腹腔镜子宫峡部环扎术可在非孕期或早孕期进行。孕中晚期发生胎儿异常需终止妊娠时可经剖腹或腹腔镜拆除缝线经后阴道分娩。足月妊娠则需要剖宫产终止妊娠。腹腔镜下子宫峡部环扎术是治疗宫颈机能不全的有效方法之一，但其是否能作为治疗宫颈机能不全的标准术式尚待多中心临床随机对照研究结果证实。     

黄芩苷对胃癌SGC-7901细胞TLR8、HIF-1α、PDGFβ和pten表达的影响

目的:探讨不同浓度的黄芩苷对胃癌SGC-7901细胞增殖的抑制作用,以及对pten和survivin基因的影响。方法:以不同浓度(10、20、40、80、160、320μmol/L)的黄芩苷处理胃癌SGC-7901细胞后,采用MTT法测定细胞活力;80、120、160μmol/L的黄芩苷处理胃癌SGC-7901细胞后,采用RT-q PCR法检测Toll样受体8(TLR8)、低氧诱导因子(HIF-1α)、血小板衍生生长因子β(PDGF-β)和第10号染色体上磷酸酶和张力白同源缺失性基因(pten)的表达,Western-blot法分别检测胃癌细胞TLR8、HIF-1α、PDGF-β和pten蛋白的表达。结果:不同浓度的黄芩苷均能抑制细胞增殖,RT-q PCR法检测显示TLR8、HIF-1α、PDGF-β基因表达下调,pten基因表达上调。结论:不同浓度的黄芩苷可抑制胃癌细胞增殖,并能上调pten和下调TLR8、HIF-1α、PDGF-βm RNA及蛋白的表达。     

桑白皮黄酮提取物对2型糖尿病大鼠非酒精性脂肪肝血管生成相关基因的影响

目的:初步探索桑白皮黄酮提取物对2型糖尿病大鼠非酒精性脂肪肝的治疗作用及机制研究。方法:将24只雄性大鼠随机分为3组,分别为正常组、模型组、桑白皮黄酮组(1.0 g·kg~(-1))。采用腹腔注射小剂量链脲佐菌素(streptozocin,STZ)结合高脂饲料喂养的方法,建立2型糖尿病伴非酒精性脂肪肝的模型,灌胃治疗16周时,观察比较桑白皮黄酮提取物对各组大鼠血清中空腹血糖(FBG),总胆固醇(TC),甘油三酯(TG),低密度脂蛋白胆固醇(LDL-C),糖耐量(OGTT)变化,油红O染色和苏木素-伊红(HE)染色观察肝脏病理改变,实时荧光定量聚合酶链式反应(Real-time PCR)检测肝脏血管内皮生长因子(vascular endothelial growth factor,VEGF),血小板衍生因子(platelet derived growth factor,PDGF)mRNA的表达。结果:灌胃干预16周后,与正常组比较,模型组大鼠FBG,TC,TG,LDL-C,含量均显著高于正常组(P0.05),应用桑白皮黄酮治疗后,上述生化指标较模型组均有显著下降(P0.05)。糖耐量试验显示模型组胰岛素敏感性下降,应用桑白皮黄酮治疗后胰岛素敏感性较模型组有显著改善。油红O染色结果显示模型组肝细胞胞浆内可见大量红染的脂肪滴,而桑白皮黄酮组肝细胞胞浆内未见红染的脂肪滴。HE染色结果显示模型组肝小叶中肝细胞发生明显的小泡样脂肪变性,部分肝细胞中脂滴融合成大的脂肪空泡,小叶中可见点状坏死,周围有炎性细胞浸润,而桑白皮黄酮组肝细胞结构正常。模型组肝脏中VEGF,PDGF mRNA表达量较正常组有显著升高,应用桑白皮黄酮治疗后,肝脏中VEGF,PDGF mRNA表达量明显降低(P0.05)。结论:桑白皮黄酮提取物对实验性2型糖尿病大鼠非酒精性脂肪性肝有一定的防治作用,其作用机制可能与抑制肝脏中VEGF,PDGF mRNA的表达有关。     

Metabolic syndrome: pathogenesis, medical care and dental implications

BACKGROUND: The dental literature contains little information about metabolic syndrome (MetS) and its dental implications. TYPES OF STUDIES REVIEWED: The authors conducted a MEDLINE search for the period 2000 through 2005, using the term "metabolic syndrome" to define its pathophysiology, medical treatment and dental implications. RESULTS: MetS is the co-occurrence of abdominal obesity, hyper-triglyceridemia, reduced high-density lipoprotein cholesterol levels, hypertension and impaired fasting glucose, which results from consumption of a high-calorie diet and decreased levels of physical activity superimposed on the appropriate genetic setting. Components of MetS synergistically promote the development of atherosclerosis, resulting in myocardial infarction and stroke. CLINICAL IMPLICATIONS: Deteriorating oral health status is associated with worsening of the atherogenic profile. Tooth loss often results in chewing difficulties because of inadequate occlusive surfaces and may lead to alterations in food selection and dietary quality. This, in turn, adversely affects body composition and nutritional status, both of which are related to vascular health. Dentists should develop treatment plans that preserve and restore the dentition, thus ensuring maximum masticatory efficiency and affording patients the optimum opportunity to consume food that will not foster atherogenesis.     

PDGF Receptor Signaling in Osteoblast Lineage Cells Controls Bone Resorption Through Upregulation of Csf1 Expression

The physiological functions of platelet-derived growth factor receptors (PDGFRs) α and β in osteoblast biology and bone metabolism remain to be established. Here, we show that PDGFRA and PDGFRB genes are expressed by osteoblast-lineage canopy and reversal cells in close proximity to PDGFB-expressing osteoclasts within human trabecular bone remodeling units. We also report that, although removal of only one of the two PDGFRs in Osterix-positive cells does not affect bone phenotype, suppression of both PDGFRs in those osteoblast lineage cells increases trabecular bone volume in male mice as well as in female gonad-intact and ovariectomized mice. Furthermore, osteoblast lineage-specific suppression of PDGFRs reduces Csf1 expression, bone marrow level of macrophage colony-stimulating factor (M-CSF), number of osteoclasts, and, therefore, bone resorption, but does not change bone formation. Finally, abrogation of PDGFR signaling in osteoblasts blocks PDGF-induced ERK1/2-mediated Csf1 expression and M-CSF secretion in osteoblast cultures and calcitriol-mediated osteoclastogenesis in co-cultures. In conclusion, our results indicate that PDGFR signaling in osteoblast lineage cells controls bone resorption through ERK1/2-mediated Csf1 expression. © 2020 American Society for Bone and Mineral Research (ASBMR).     

Efficient differentiation of vascular endothelial cells from dermal-derived mesenchymal stem cells induced by endothelial cell lines conditioned medium

Objective

To directionally-differentiate dermis-derived mesenchymal stem cells (DMSCs) into vascular endothelial cells (VECs) in vitro, providing an experimental basis for studies on the pathogenesis and treatment of vascular diseases.

PDGF家族在肾纤维化中的研究进展

血小板生长因子家族(Platelet-derived factors PDGFs)是重要的促有丝分裂剂,包括PDGF-A、PDGF-B、PDGF-C、PDGF-D四个配体及PDGFR-α、PDGF-β两种酪氨激酶受体链,通常情况下都是配体与其特异性受体结合调控多种病理生理活动,包括细胞增殖、迁移以及细胞生存及细胞外基质沉积等。研究表明,PDGF家族在多器官纤维化、动脉粥样硬化、伤口愈合及癌症等多种病理过程中起着重要作用。就PDGF家族在肾纤维化过程中的作用进行综述。     

不安运动阶段对早产儿运动发育结局的预测价值

目的比较全身运动质量评估(General movements assessment,GMs)不安运动阶段和Gesell发育量表(Gesell Developmental Test Scales,GDS)对早产儿运动发育结局的预测效度,及对两种评估方法和发育结局的一致性检测。方法对2011年6月-2013年6月共226例在本院儿童保健科随访的早产儿,在纠正5个月内采用GMs和GDS进行评估,在纠正12个月时临床诊断是否为脑瘫,并使用Peabody运动发育量表(Peabody Development Motor Scale 2,PDMS-2)确定其运动发育结局。对比分析两种评估方法的预测效度(包括敏感度、特异度、阳性预测值和阴性预测值),及与发育结局的相关性。结果 226例早产儿发育结局中运动发育正常176例,运动发育迟缓22例,脑瘫28例。不安运动阶段评估结果为正常者168例,异常为58例;GDS评估结果为正常者140例,异常为86例。不安运动及GDS预测脑瘫敏感度92.9%、71.4%,特异度83.8%、66.7%,阳性预测值44.8%、23.3%,阴性预测值98.8%、94.3%。不安运动及GDS预测运动发育结局敏感度88.0%、68.0%,特异度92.0%、70.4%,阳性预测值75.9%、39.5%,阴性预测值96.4%、88.6%。GDS和PDMS-2的一致性检验Kappa值0.306,P0.05,GMs和PDMS-2评估的一致性检验Kappa值0.757,P0.05,提示GMs、GDS对运动发育预测与发育结局均具有良好的一致性,GMs中不安运动阶段的预测与发育结局的一致性更高。结论 GMs的不安运动阶段能够超早期预测脑瘫等不良运动发育结局,在预测预后方面要优于GDS,能更早期的做出预测。     

Natural killer cells ameliorate liver fibrosis by killing activated stellate cells in NKG2D-dependent and tumor necrosis factor-related apoptosis-inducing ligand-dependent manners

BACKGROUND & AIMS: Viral hepatitis infection, which is a major cause of liver fibrosis, is associated with activation of innate immunity. However, the role of innate immunity in liver fibrosis remains obscure. METHODS: Liver fibrosis was induced either by feeding mice with the 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet or by injecting them with carbon tetrachloride. The Toll-like receptor 3 ligand, polyinosinic-polycytidylic acid, was used to activate innate immunity cells and mediators, including natural killer cells and interferon gamma. RESULTS: In the mouse model of DDC-induced liver fibrosis, natural killer cell activation by polyinosinic-polycytidylic acid induced cell death to activated hepatic stellate cells and attenuated the severity of liver fibrosis. Polyinosinic-polycytidylic acid treatment also ameliorated liver fibrosis induced by carbon tetrachloride. The observed protective effect of polyinosinic-polycytidylic acid on liver fibrosis was diminished through either depletion of natural killer cells or by disruption of the interferon gamma gene. Expression of retinoic acid early inducible 1, the NKG2D ligand, was undetectable on quiescent hepatic stellate cells, whereas high levels were found on activated hepatic stellate cells, which correlated with the resistance and susceptibility of quiescent hepatic stellate cells and activated hepatic stellate cells to natural killer cell lysis, respectively. Moreover, treatment with polyinosinic-polycytidylic acid or interferon gamma enhanced the cytotoxicity of natural killer cells against activated hepatic stellate cells and increased the expression of NKG2D and tumor necrosis factor-related apoptosis-inducing ligand on liver natural killer cells. Blocking NKG2D or tumor necrosis factor-related apoptosis-inducing ligand with neutralizing antibodies markedly diminished the cytotoxicity of polyinosinic-polycytidylic acid-activated natural killer cells against activated hepatic stellate cells. CONCLUSIONS: Our findings suggest that natural killer cells kill activated hepatic stellate cells via retinoic acid early inducible 1/NKG2D-dependent and tumor necrosis factor-related apoptosis-inducing ligand-dependent mechanisms, thereby ameliorating liver fibrosis.