目的探讨血清细胞因子信号转导负调控因子-3(suppressor of cytokine signaling 3,SOCS-3)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-16(interleukin-16,IL-16)及T辅助细胞1/T辅助细胞2(Th1/Th2)与妊娠期高血压...目的探讨血清细胞因子信号转导负调控因子-3(suppressor of cytokine signaling 3,SOCS-3)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-16(interleukin-16,IL-16)及T辅助细胞1/T辅助细胞2(Th1/Th2)与妊娠期高血压疾病(HDCP)的关系。方法选取2014年1月-2016年6月本院妇产科收治的妊娠期高血压疾病患者182例,其中妊娠期高血压组51例,轻度子痫前期组69例,重度子痫前期组62例。另选择同期分娩健康孕妇65例作为对照组。采用ELISA法检测各组孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2水平,分析重度子痫前期患者不良妊娠结局与各指标的关系。采用Spearman相关分析各组HDCP患者血清SOCS-3水平与TNF-α、IL-16及Th1/Th2的相关性。结果与对照组比较,轻度子痫前期组和重度子痫前期组血清SOCS-3水平均明显降低(0.59±0.12 vs 0.14±0.03和0.08±0.01;P均<0.05)。各组TNF-α、IL-16及Th1/Th2水平均高于对照组,且重度子痫前期组较轻度子痫前期组升高更明显[TNF-α(ng/L):12.58±2.37 vs 34.75±6.42和61.53±9.26;IL-16(ng/L):108.47±35.24 vs 187.63±81.47和284.62±113.58;Th1/Th2:9.27±2.38 vs20.15±4.82和26.48±6.13;P均<0.05]。重度子痫前期患者中,SOCS-3低表达组胎儿宫内窘迫综合征、胎儿生长受限及新生儿窒息的发生率均显著高于高表达组(P均<0.05),TNF-α、IL-16、Th1/Th2高表达组早产及胎儿生长受限的发生率均显著高于低表达组(P均<0.05)。相关分析显示,妊娠期高血压患者血清SOCS-3水平与TNF-α、IL-16、Th1/Th2均呈负相关(r=-0.528,r=-0.506,r=-0.126;P均<0.05)。结论监测孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2对妊娠期高血压疾病尤其是重度子痫前期的早发现、早诊断、早治疗具有一定的临床指导意义。展开更多
Anoctamin 1(ANO1) or TMEM16 A gene encodes a member of Ca^(2+) activated Cl^(-) channels(CaCCs) that are critical for physiological functions,such as epithelial secretion,smooth muscle contraction and sensory signal t...Anoctamin 1(ANO1) or TMEM16 A gene encodes a member of Ca^(2+) activated Cl^(-) channels(CaCCs) that are critical for physiological functions,such as epithelial secretion,smooth muscle contraction and sensory signal transduction.The attraction and interest in ANO1/TMEM16 A arise from a decade long investigations that abnormal expression or dysfunction of ANO1 is involved in many pathological phenotypes and diseases,including asthma,neuropathic pain,hypertension and cancer.However,the lack of specific modulators of ANO1 has impeded the efforts to validate ANO1 as a therapeutic target.This review focuses on the recent progress made in understanding of the pathophysiological functions of CaCC ANO1 and the current modulators used as pharmacological tools,hopefully illustrating a broad spectrum of ANO1 channelopathy and a path forward for this target validation.展开更多
文摘目的探讨血清细胞因子信号转导负调控因子-3(suppressor of cytokine signaling 3,SOCS-3)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-16(interleukin-16,IL-16)及T辅助细胞1/T辅助细胞2(Th1/Th2)与妊娠期高血压疾病(HDCP)的关系。方法选取2014年1月-2016年6月本院妇产科收治的妊娠期高血压疾病患者182例,其中妊娠期高血压组51例,轻度子痫前期组69例,重度子痫前期组62例。另选择同期分娩健康孕妇65例作为对照组。采用ELISA法检测各组孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2水平,分析重度子痫前期患者不良妊娠结局与各指标的关系。采用Spearman相关分析各组HDCP患者血清SOCS-3水平与TNF-α、IL-16及Th1/Th2的相关性。结果与对照组比较,轻度子痫前期组和重度子痫前期组血清SOCS-3水平均明显降低(0.59±0.12 vs 0.14±0.03和0.08±0.01;P均<0.05)。各组TNF-α、IL-16及Th1/Th2水平均高于对照组,且重度子痫前期组较轻度子痫前期组升高更明显[TNF-α(ng/L):12.58±2.37 vs 34.75±6.42和61.53±9.26;IL-16(ng/L):108.47±35.24 vs 187.63±81.47和284.62±113.58;Th1/Th2:9.27±2.38 vs20.15±4.82和26.48±6.13;P均<0.05]。重度子痫前期患者中,SOCS-3低表达组胎儿宫内窘迫综合征、胎儿生长受限及新生儿窒息的发生率均显著高于高表达组(P均<0.05),TNF-α、IL-16、Th1/Th2高表达组早产及胎儿生长受限的发生率均显著高于低表达组(P均<0.05)。相关分析显示,妊娠期高血压患者血清SOCS-3水平与TNF-α、IL-16、Th1/Th2均呈负相关(r=-0.528,r=-0.506,r=-0.126;P均<0.05)。结论监测孕妇血清SOCS-3、TNF-α、IL-16及Th1/Th2对妊娠期高血压疾病尤其是重度子痫前期的早发现、早诊断、早治疗具有一定的临床指导意义。
基金supported by grants from the National Natural Science foundation of China (81573410)the Ministry of Science and Technology of China (2018ZX09711001-004-006)+2 种基金Shandong Provincial Medicine and Health Technology Development Plan (2019WS145, China)Medical Research Guidance Plan of Qingdao Municipal Health Committee (2019-WJZD091, China)Qingdao Excellent Young Medical Talent Training Project。
文摘Anoctamin 1(ANO1) or TMEM16 A gene encodes a member of Ca^(2+) activated Cl^(-) channels(CaCCs) that are critical for physiological functions,such as epithelial secretion,smooth muscle contraction and sensory signal transduction.The attraction and interest in ANO1/TMEM16 A arise from a decade long investigations that abnormal expression or dysfunction of ANO1 is involved in many pathological phenotypes and diseases,including asthma,neuropathic pain,hypertension and cancer.However,the lack of specific modulators of ANO1 has impeded the efforts to validate ANO1 as a therapeutic target.This review focuses on the recent progress made in understanding of the pathophysiological functions of CaCC ANO1 and the current modulators used as pharmacological tools,hopefully illustrating a broad spectrum of ANO1 channelopathy and a path forward for this target validation.