肛瘘经括约肌间瘘管结扎后肛门功能恢复的相关影响因素分析

目的 探讨肛瘘经括约肌间瘘管结扎后肛门功能的恢复情况及其影响因素。方法 采取病例对照研究方法,选取海口市中医医院2019年1月—2022年8月收治的172例肛瘘患者作为研究对象。统计分析患者手术前后肛门功能恢复情况,根据患者术后3个月的肛门功能恢复情况将其分为良好组140例、不良组32例。比较两组患者的手术指标、术后并发症及基线资料,采用多因素一般Logistic回归分析影响手术后肛门功能恢复的相关因素。结果 良好组手术后创面愈合更早（P <0.05）,疼痛持续时间更短（P <0.05）,总体平均住院总时间短于不良组（P <0.05）。良好组与不良组术后1、2、3个月的Wexner量表评分比较,采用重复测量设计的方差分析,结果 ①不同时间点的Wexner量表评分有差异（P <0.05）;②两组的Wexner量表评分有差别（P <0.05）,良好组Wexner量表评分较不良组低,肛门功能恢复较好。③两组的Wexner量表评分变化趋势有差异（P <0.05）。良好组患者的病程、瘘管长度、Parks分型、术后切口感染率、二次手术率（再次实施清创手术）、治疗依从性（术后用药是否遵从医嘱）、术后机械性刺激率（术后各种外因刺激肛门）与不良组比较,差异均有统计学意义（P <0.05）。多因素一般Logistic回归分析结果显示,肛瘘患者病程［O^R =1.842（95% CI：1.105,3.073）］、瘘管长度［O^R =1.788（95% CI：1.137,2.812）］、术后切口感染［O^R =1.694（95% CI：1.081,2.653）］、再次手术［O^R =1.347（95% CI：1.018,1.783）］、治疗依从性［O^R =1.493（95% CI：1.058,2.108）］是肛瘘患者括约肌间瘘管结扎后肛门功能恢复不良的影响因素（P <0.05）。结论 肛瘘患者经括约肌间瘘管结扎后肛门功能大部分恢复良好,但是肛瘘患者病程较长、瘘管长度较长、出现术后切口感染、术后再次手术、治疗依从性差可能会增大患者术后肛门功能恢复不良的风险。     

血清鸢尾素、脂联素水平与颈动脉粥样硬化的关系

目的 探讨血清鸢尾素及脂联素（APN）水平与颈动脉粥样硬化的关系。方法 选取2020年1月—2022年1月海南省人民医院收治的124例H型高血压患者作为研究组,另选取同期来该院体检的健康者112例作为对照组。比较两组血清鸢尾素、APN水平,分析研究组颈动脉粥样硬化斑块形成的影响因素,采用受试者工作特征（ROC）曲线分析血清鸢尾素、APN水平预测颈动脉粥样硬化斑块形成的价值。结果 研究组血清鸢尾素、APN水平低于对照组（P <0.05）。斑块形成组与非斑块形成组性别、年龄、体重指数、吸烟史、饮酒史、收缩压、舒张压、血压控制良好、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、一氧化氮、尿酸、肌酐、内皮素水平比较,差异无统计学意义（P>0.05）。斑块形成组甘油三酯、同型半胱氨酸水平高于非斑块形成组（P <0.05）,鸢尾素、APN水平低于非斑块形成组（P <0.05）。多因素一般Logistic回归分析结果显示：同型半胱氨酸水平[■=4.415(95%CI:1.817,10.730)]、血清鸢尾素水平[■=4.027(95%CI:1.657,9.787)]、AP...     

含Arg-Gly-Asp肽与仿生PLGA-(ASP-PEG)材料结合的实验研究

设计合成含Arg-Gly-Asp[Arg(R)-精氨酸,Gly(G)-甘氨酸,Asp(D)-天冬氨酸]的非病毒基因载体的肽(K16-GRGDSPC) (K-赖氨酸,S-丝氨酸,P-脯氨酸,C-半胱氨酸),用其作材料聚(丙交酯-co-乙交酯)-(天冬氨酸-聚乙二醇)交替预聚物[PLGA-(ASP-PEG)]的表面修饰.合成K16-GRGDSPC, 将PLGA-(ASP-PEG)制成A、B、C三块薄片.薄片 A 、B与交联剂反应,反应后的薄片A再与肽反应,薄片 C作为对照.质谱仪(MS)、高效液相色谱分析仪(HPLC)检测肽的分子量及纯度;x线光电子能谱法(XPS)检测材料表面硫元素;分光光度仪检测残液未反应肽含量.HPLC检测肽的纯度为94.13%,MS检测肽分子量为2741.26.XPS检测改性薄片A中硫元素结合能为164 eV,碳、硫元素的含量比值(C/S)为99.746:0.1014;反应后薄片 B中硫元素结合能为162 eV与 164 eV,C/S为99.574:0.4255; 薄片 C中无硫元素.残液管OD值为0.069, 薄片A表面接枝肽密度为0.04 mg/mm2.提示通过交联剂可将所合成的肽K16-GRGDSPC结合到仿生材料PLGA-(ASP-PEG)表面.     

The essential role of stimulus temporal patterning in enabling perceptual learning

Little is known about how temporal stimulus factors influence perceptual learning. Here we demonstrate an essential role of stimulus temporal patterning in enabling perceptual learning by showing that 'unlearnable' contrast and motion-direction discrimination (resulting from random interleaving of stimuli) can be readily learned when stimuli are practiced in a fixed temporal pattern. This temporal patterning does not facilitate learning by reducing stimulus uncertainty; further, learning enabled by temporal patterning can later generalize to randomly presented stimuli.     

Nitric Oxide Modulates MCP-1 Expression in Endothelial Cells: Implications for the Pathogenesis of Pulmonary Granulomatous Vasculitis

Monocyte chemoattractant protein-1 (MCP-1) is a pivotal mediator of angiocentric granuloma formation in glucan-induced pulmonary granulomatous vasculitis. Based on the rationale that mononuclear phagocytes retrieved from granulomas are rich sources of nitric oxide (NO) and that the recruitment of mononuclear phagocytes into lesions abates as granuloma formation slows, we tested the hypothesis that MCP-1 gene expression is regulated by a NO-sensitive mechanism. Preexposure of endothelial cell (EC) monolayers to NO donor compounds markedly reduced cytokine-induced MCP-1 expression and cytosolic-to-nuclear translocation of nuclear factor-kappa B (NF-B), reversed fluctuations in endothelial reduced glutathione (GSH) pools but did not affect cGMP concentrations. The lungs of mice bearing targeted disruptions of the inducible nitric oxide synthase (iNOS) gene exhibited significantly higher concentrations of MCP-1 following glucan infusion than did those of wild-type mice. Cumulatively, these data suggest that NO suppresses MCP-1 expression by blunting the redox changes associated with cytokine-induced EC activation.     

Loss of LFA-1, but not Mac-1, protects MRL/MpJ-Fas(lpr) mice from autoimmune disease

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune complex-mediated tissue injury. Many different adhesion molecules are thought to participate in the development of SLE; however, few studies have directly examined the contributions of these proteins. Here we demonstrate that LFA-1 plays an essential role in the development of lupus in MRL/MpJ-Fas(lpr) mice. Mice deficient in LFA-1, but not Mac-1, showed significantly increased survival, decreased anti-DNA autoantibody formation, and reduced glomerulonephritis. The phenotype of the LFA-1-deficient mice was similar to that observed in beta(2) integrin-deficient (CD18-null) MRL/MpJ-Fas(lpr) mice, suggesting a lack of redundancy among the beta(2) integrin family members and other adhesion molecules. These studies identify LFA-1 as a key contributor in the pathogenesis of autoimmune disease in this model, and further suggest that therapeutic strategies targeting this adhesion molecule may be beneficial for the treatment of SLE.     

CVB3-VP1基因免疫诱导特异性抗病毒免疫应答及保护作用

目的 :构建表达柯萨奇病毒B3(CVB3)主要包膜蛋白VP1的基因疫苗 ,并研究该疫苗诱导CVB3特异性免疫应答及免疫保护的作用。方法 :抽提CVB3RNA ,以RT PCR扩增VP1基因 ,克隆于真核表达载体 pcDNA3中 ,构建质粒pcDNA3 VP1。将该质粒转染Hela细胞 ,观察其表达情况 ;以 5 0 μgpcDNA3 VP1质粒DNA肌注免疫BALB/c小鼠 3次 ,检测CVB3特异性体液和细胞免疫应答。间隔 4wk以 5×LD50 的CVB3攻击小鼠 ,观察攻击后小鼠的存活情况。结果 :构建了重组质粒 pcDNA3 VP1,并在体外获得有效表达。以该质粒肌肉免疫BALB/c小鼠 ,可诱生高水平的IgM和IgG ,VP1多肽特异性淋巴细胞增殖反应及CTL活性均显著高于 pcDNA3免疫的对照组。病毒攻击试验表明 ,pcDNA3 VP1免疫组33.3%小鼠可长期存活 ,其心肌组织未见明显的病理学改变 ;而对照小鼠平均仅存活 6 .7d ,心肌显示大量的局灶性坏死和炎性细胞浸润。结论 :pcDNA3 VP1免疫可诱生CVB3特异性体液及细胞免疫应答 ,保护免疫小鼠抵抗CVB3的致死性攻击     

16例应激性溃疡的临床诊治体会

目的 报告应激性溃疡的临床诊治体会。方法 全组16例,男12例,女4例。术前均无溃疡病史,血红蛋白检查均正常。术后早期应用糖皮质激素9例,出血前发生肺不张、严重呼吸道感染、呼吸功能不全6例,低血容量休克5例,急性重症出血坏死性胰腺炎4例,食管癌、贲门癌术后6例,严重烧伤(80％(?)Ⅱ°)1例。14例保守治疗,2例保守治疗无效而手术治疗。结果14例经治疗后(2例手术治疗)痊愈出院,2例死亡。结论 应激性溃疡大出血患者多病情危重,难以忍受二次手术,死亡率约为50％,因此应采取有效的保守治疗,对于保守治疗无效、大出血休克或胃肠穿孔者应及时手术治疗。     

The calpain system

The calpain system originally comprised three molecules: two Ca2+-dependent proteases, mu-calpain and m-calpain, and a third polypeptide, calpastatin, whose only known function is to inhibit the two calpains. Both mu- and m-calpain are heterodimers containing an identical 28-kDa subunit and an 80-kDa subunit that shares 55-65% sequence homology between the two proteases. The crystallographic structure of m-calpain reveals six "domains" in the 80-kDa subunit: 1). a 19-amino acid NH2-terminal sequence; 2). and 3). two domains that constitute the active site, IIa and IIb; 4). domain III; 5). an 18-amino acid extended sequence linking domain III to domain IV; and 6). domain IV, which resembles the penta EF-hand family of polypeptides. The single calpastatin gene can produce eight or more calpastatin polypeptides ranging from 17 to 85 kDa by use of different promoters and alternative splicing events. The physiological significance of these different calpastatins is unclear, although all bind to three different places on the calpain molecule; binding to at least two of the sites is Ca2+ dependent. Since 1989, cDNA cloning has identified 12 additional mRNAs in mammals that encode polypeptides homologous to domains IIa and IIb of the 80-kDa subunit of mu- and m-calpain, and calpain-like mRNAs have been identified in other organisms. The molecules encoded by these mRNAs have not been isolated, so little is known about their properties. How calpain activity is regulated in cells is still unclear, but the calpains ostensibly participate in a variety of cellular processes including remodeling of cytoskeletal/membrane attachments, different signal transduction pathways, and apoptosis. Deregulated calpain activity following loss of Ca2+ homeostasis results in tissue damage in response to events such as myocardial infarcts, stroke, and brain trauma.     

STAT3 couples with 14-3-3σ to regulate BCR signaling,B-cell differentiation,and IgE production

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