清麴酱激酶的溶栓活性可减轻栓塞性脑梗死后脑损伤

Cheonggukjang is a soybean paste made by fermenting whole cooked soybean with Bacillus subtilis. Cheonggukjang contains a fibrinolytic enzyme that may have clinical applications in removing blood clots. In this study, we use the term “cheonggukjang kinase” (CGK) to refer to this fibrinolytic enzyme. We used fibrin clot lysis and platelet-rich clot lysis assays to clarify the mechanisms by which CGK exerts thrombolytic effects, and, specifically, whether it acts more like a plasminogen activator or like plasmin. Additionally, we examined the thrombolytic effects of CGK in a rat model of cerebral embolic stroke produced by middle cerebral artery occlusion (MCAO) with respect to infarct volume and behavioral performance. In both the fibrin clot lysis and platelet-rich clot lysis assays, the thrombolytic activity was highest in CGK that had been cultured for 40 h. Furthermore, T50%, the time needed to decompose half the clot, did not differ in the presence or absence of plasminogen, indicating that CGK is a plasmin-like protein, not a plasminogen activator. In the rat model of cerebral embolic stroke, clots were no longer visible in rats that received an intravenous infusion of CGK (1 U plasmin-like activity/100 μg CGK/kg) 1 h after MCAO. CGK-treated groups showed a significant dose-dependent reduction in infarct volume. Treatment with CGK also improved functional recovery, as assessed by neurological deficit scores. Reduction of infarct volume and improvement in functional recovery after CGK treatment (1 U plasmin-like activity/100 μg CGK/kg) was greater than after treatment with recombinant tissue plasminogen activator (r-tPA; 10 mg/kg). These data suggest that CGK is an effective agent for reducing infarct volume and improving functional recovery following ischemic brain injury. Moreover, CGK may be a more efficacious clot-dissolving agent than r-tPA. CGK has a number of potential clinical applications in the treatment of stroke.     

内热针松解术治疗腰椎间盘突出症的疗效与安全性

目的 对内热针松解术治疗腰椎间盘突出症的疗效与安全性进行评价。方法 研究对象为我院2019年1月～2020年1月期间收治的50例腰椎间盘突出症患者,按照数字表法将其随机分为实验组与对照组,每组各25例,实验组使用内热针松解术进行治疗,对照组使用常规理疗进行治疗。对比分析两组患者VAS评分、SF-36评分、不良反应发生情况。结果 两组患者治疗1个月后与治疗3个月后的VAS评分显著低于治疗前、SF-36的各维度评分显著高于治疗前（P＜0.05）,且实验组显著优于对照组（P＜0.05）;实验组不良反应总发生率显著低于对照组（P＜0.05）。结论 在腰椎间盘突出症治疗中使用内热针松解术,可有效减轻患者疼痛,提高患者生活质量,降低不良反应发生率,安全性良好,疗效显著。     

腹腔镜治疗小儿肠粘连分析(附27例报告)

目的探讨治疗小儿粘连性肠梗阻的新方法，即腹腔镜下治疗小儿术后粘连性肠梗阻的可行性和适应证。方法对1994-2004年10月因粘连性肠梗阻腹腔镜下肠粘连松解术的27例病人进行回顾性分析。结果该组病例均获满意的疗效，无术后并发症。均随访至今无复发。结论腹腔镜肠粘连松解术创口小、腹膜创面少、操作轻柔、腹腔干扰少，能较大限度地减少术后腹腔内再粘连，为粘连性肠梗阻的外科治疗提供了一种新方法。     

Overall haemostatic potential can be used for estimation of thrombin-activatable fibrinolysis inhibitor-dependent fibrinolysis in vivo and for possible follow-up of recombinant factor VIIa treatment in patients with inhibitors to factor VIII.

Thrombin generation induced by recombinant factor VIIa (rFVIIa) in patients with haemophilia and/or inhibitors to factor VIII/IX could enhance generation of thrombin-activatable fibrinolysis inhibitor (TAFI), a recently described link between coagulation and fibrinolysis. TAFI is unstable and it is not easy to measure its active form in vivo. Overall haemostatic potential (OHP) is a novel method for haemostasis estimation, based on determination of the fibrin aggregation curve in which tiny amounts of thrombin are used for activation of clotting. We measured OHP in six patients with inhibitors to factor VIII before injection of rFVIIa and 10 and 120 min thereafter. Overall fibrinolytic potential (OFP) and clot lysis time (CLT) analysed by this method could be used for indirect estimation of TAFI generation. We found no change in pro-TAFI and total TAFI antigen before and after treatment with rFVIIa. OHP was almost undetectable before treatment but increased into the range of normal pooled plasma 10 and 120 min after rFVIIa treatment, as did CLT. However, after addition of potato tuber carboxypeptidase inhibitor, a specific inhibitor of TAFI, the shortening of CLT was lower than that in NPP. OFP was increased in patient plasma both 10 and 120 min after treatment compared with NPP. There was a strong positive correlation between pro-TAFI concentration and shortening of CLT after PTCI addition and a negative correlation between pro-TAFI concentration and OFP 10 min after rFVIIa injection. Thus, rFVIIa normalizes OHP and CLT 10 min after injection. While this improvement slightly decreases, but still exists after 2 hours, it suggests efficacy in bleeding prevention using a protocol based on rFVIIa administration every 2 hours.     

血清HBV—DNA模板不同提取方法的比较和选择

目的比较直接煮沸法、碱裂解法、浓缩碱裂解法和碱裂解3倍量提取法四种提取法提取样本核酸的差异;选择简便、可靠的检测乙肝病毒DNA（HBV—DNA）提取方法。方法运用中山医科大学达安基因股份有限公司生产的HBV—DNA试剂盒中推荐的浓缩碱裂解法,与直接煮沸法、碱裂解法、碱裂解3倍量提取法,分别提取血清样本核酸模板,用美国MJ实时荧光定量PCR仪检测HBV—DNA,对结果进行对比分析。结果共89例乙肝表面抗原（HB—sAg）阳性患者血清,浓缩碱裂解法和碱裂解3倍量提取法检测,两者均有62例HBV—DNA阳性（〉1000拷贝／ml定性为阳性）阳性率69．6％,阳性拷贝／ml均值用对数形式表示分别为（6．652±1．301）和（6．601±1．282）,两者间结果无明显差异（P〉0．05）;直接煮沸法检测出47例阳性（均在上述62例中）阳性率52．8％;碱裂解法测出57例阳性（均在上述62例中）阳性率64．0％,阳性拷贝／ml均值与浓缩碱裂解法和碱裂解3倍量提取法相比较,阳性检出率较低,有非常显著性差异（P〈0．01）和显著性差异（P〈0．05）。结论碱裂解3倍量提取法操作简单,省时、省材料,重复性好,阳性检出率与浓缩碱裂解法一致,建议使用碱裂解3倍量提取法检测HBV—DNA。     

侵袭性NK细胞白血病发生肿瘤溶解综合征1例报告及文献复习

目的:提高对侵袭性NK细胞白血病和肿瘤溶解综合征(Tumour Lysis Syndrome,TLS)的认识。方法:报告1例侵袭性NK细胞白血病患者在治疗过程中发生TLS,介绍目前关于TLS的研究进展。结果:确诊侵袭性NK细胞白血病1例,予CHOP方案治疗。在治疗过程中患者出现高钾、高磷、高尿酸及尿素氮血症及肌酐升高等肿瘤溶解综合征的特点,经积极对症、支持治疗得以纠正。血象恢复后复查骨髓达完全缓解。结论:侵袭性NK细胞白血病是一种少见疾病,预后不良;而治疗中发生肿瘤溶解综合征,使结局进一步恶化.但若能早期预测、发现TLS,并予积极的治疗,能得到好的转归。     

双腔管冲洗引流并尿激酶溶解术治疗高血压脑出血

目的:探讨双腔管冲洗引流并尿激酶溶解术治疗高血压脑出血的方法及效果.方法:回顾性分析38例在CT定位钻孔抽吸部分血肿后行双腔管冲洗引流并尿激酶注入治疗的高血压脑出血病人的临床特点及疗效.结果: 血肿清除率高,病人恢复良好,死亡率低,并发症少.结论:双腔管冲洗引流并尿激酶溶解术是高血压脑出血的一种简单、有效的治疗方法.     

CPM在膝关节强直松解术后的应用

１４例膝关节强直患者于松解术后第２天至第１０天应用持续被动关节活动器（ＣＰＭ）和微波治疗，每日二次，每次１小时。１０例对照，只用微波治疗。结果显示：切口拆线时ＣＰＭ治疗组膝关节主动活动度（ＡＲＯＭ）为６７．４±９．６，显著大于对照组４８．３±１２．１（Ｐ＜０．０１），住院天数、患膝关节水肿消除时间均比对照组缩短，但无统计差异，ＣＰＭ治疗组无一例发生切口延期愈合，且疼痛感比对照组轻。     

Lysis of pathogenic and nonpathogenic Entamoeba histolytica by human complement: methodological analysis

The effect of nonimmune human serum on Entamoeba histolytica trophozoites was studied: (a) using whole serum in the presence of Ca and Mg ions allowing complement activation via both the alternative and classical pathways or in the presence of MgEGTA permitting alternative pathway activation only; (b) using different E. histolytica isolates; (c) varying serum and trophozoite concentrations and the time of incubation; and (d) using three different methods to quantify lysis, i.e., microscopic inspection, flow cytometry and 111In release. All three methods yielded similar results, with flow cytometry being most sensitive in identifying membrane damage and 111In release being most valid in determining cell death. Microscopic analysis was reliable only when a chamber was used to calculate the number of complement treated cells in relation to the initial cell count. E. histolytica isolates were classified into three groups according to their susceptibility to lysis by complement: (i) pathogenic isolates after long term cultivation in vitro were susceptible; (ii) pathogenic isolates after recent in vivo passage were less susceptible; and (iii) nonpathogenic isolates were nearly unaffected by exposure to the alternative pathway alone. The extent of lysis of the various isolates correlated with the degree of complement consumption in the serum samples, suggesting that unlysed isolates did not activate complement under the conditions employed. In general, lysis of susceptible trophozoites increased with the serum concentration and with the time of incubation. However, when the trophozoite concentration was 10(6)/ml or higher, lysis no longer reflected complement susceptibility because of exhaustion of the complement supply.     

Tissue factor-expressing monocytes inhibit fibrinolysis through a TAFI-mediated mechanism, and make clots resistant to heparins

Background

Thrombin is the main activator of the fibrinolysis inhibitor TAFI (thrombin activatable fibrinolysis inhibitor) and heightened clotting activation is believed to impair fibrinolysis through the increase of thrombin activatable fibrinolysis inhibitor activation. However, the enhancement of thrombin generation by soluble tissue factor was reported to have no effect on plasma fibrinolysis and it is not known whether the same is true for cell-associated tissue factor. The aim of this study was to evaluate the effect of tissue factor-expressing monocytes on plasma fibrinolysis in vitro.

Design and Methods

Tissue factor expression by human blood mononuclear cells (MNC) and monocytes was induced by LPS stimulation. Fibrinolysis was spectrophotometrically evaluated by measuring the lysis time of plasma clots containing LPS-stimulated or control cells and a low concentration of exogenous tissue plasminogen activator.

Results

LPS-stimulated MNC (LPS-MNC) prolonged fibrinolysis time as compared to unstimulated MNC (C-MNC) in contact-inhibited but not in normal citrated plasma. A significantly prolonged lysis time was observed using as few as 30 activated cells/μL. Fibrinolysis was also impaired when clots were generated on adherent LPS-stimulated monocytes. The antifibrinolytic effect of LPS-MNC or LPS-monocytes was abolished by an anti-tissue factor antibody, by an antibody preventing thrombin-mediated thrombin activatable fibrinolysis inhibitor activation, and by a TAFIa inhibitor (PTCI). Assays of thrombin and TAFIa in contact-inhibited plasma confirmed the greater generation of these enzymes in the presence of LPS-MNC. Finally, the profibrinolytic effect of unfractionated heparin and enoxaparin was markedly lower (~50%) in the presence of LPS-MNC than in the presence of a thromboplastin preparation displaying an identical tissue factor activity.

Conclusions

Our data indicate that LPS-stimulated monocytes inhibit fibrinolysis through a tissue factor-mediated enhancement of thrombin activatable fibrinolysis inhibitor activation and make clots resistant to the profibrinolytic activity of heparins, thus providing an additional mechanism whereby tissue factor-expressing monocytes/macrophages may favor fibrin accumulation and diminish the antithrombotic efficacy of heparins.