CRRT对重症急性胰腺炎患者脂联素TNF-α和CRP的影响

目的探讨重症急性胰腺炎（SAP）患者脂联素、TNF-α和CRP水平的变化特点及连续性肾脏替代疗法（CRRT）对其影响。方法按照平行对照设计原理,将所有66例患者分为对照组和CRRT组。对两组患者的相关临床资料及脂联素、TNF-α和CRP水平进行比较。结果与CRRT组患者比较,对照组患者第1天TNF-α和CRP水平均明显升高（均P〈0．05）,脂联素水平明显降低（P〈0．05）;与CRRT组患者比较,对照组患者第2、3天TNF-α和CRP水平均明显升高（均P〈0．01）,脂联素水平明显降低（均P〈0．01）;治疗前两组患者脂联素、TNF-α和CRP水平,差异无统计学意义（均P〉0．05）;在年龄、性别、APACHEII评分等方面两组差异无统计学意义（均P〉0．05）。结论CRRT能通过降低TNF-α和CRP水平及升高脂联素水平,对SAP患者起到较好的治疗作用。     

The adaptor protein SAP regulates type II NKT‐cell development,cytokine production,and cytotoxicity against lymphoma

CD1d‐restricted NKT cells represent a unique lineage of immunoregulatory T cells that are divided into two groups, type I and type II, based on their TCR usage. Because there are no specific tools to identify type II NKT cells, little is known about their developmental requirements and functional regulation. In our previous study, we showed that signaling lymphocytic activation molecule associated protein (SAP) is essential for the development of type II NKT cells. Here, using a type II NKT‐cell TCR transgenic mouse model, we demonstrated that CD1d‐expressing hematopoietic cells, but not thymic epithelial cells, meditate efficient selection of type II NKT cells. Furthermore, we showed that SAP regulates type II NKT‐cell development by controlling early growth response 2 protein and promyelocytic leukemia zinc finger expression. SAP‐deficient 24αβ transgenic T cells (24αβ T cells) exhibited an immature phenotype with reduced Th2 cytokine‐producing capacity and diminished cytotoxicity to CD1d‐expressing lymphoma cells. The impaired IL‐4 production by SAP‐deficient 24αβ T cells was associated with reduced IFN regulatory factor 4 and GATA‐3 induction following TCR stimulation. Collectively, these data suggest that SAP is critical for regulating type II NKT cell responses. Aberrant responses of these T cells may contribute to the immune dysregulation observed in X‐linked lymphoproliferative disease caused by mutations in SAP.     

腹腔镜手术治疗急性重症胰腺炎腹内高压疗效分析

目的本文拟对SAP患者经膀胱间接监测IAH和早期应用腹腔镜技术治疗SAP和[AH重要性进行探讨。方法对我院12年来收治的201例SAP患者,进行了常规IAP测定,IAP〉25mmHg60例。按单双号将患者分为两组,A组30例进行腹腔镜下灌洗、引流、清除坏死组织手术,B组30例给予禁食、胃肠减压、抗感染、生长抑素等综合治疗待腹腔脓肿形成后再进行剖腹手术。结果两组病死率分别为16．7％、23．3％,并发AODS率为10．O％、20．0％。A组腹内高压持续时间和住院时间较B组明显缩短（P〈0．05）,腹腔感染发生率明显降低（P〈0．05）,血性感染发生率和死亡率也有所减少fP〈0．05）。结论SAP诊断成立IAP升高〉25mmHg以上,应尽早在腹腔镜下经腹膜外径路进行腹腔灌洗、引流、清除坏死组织。     

大黄对合并呼吸衰竭重症胰腺炎的治疗作用及对IL-6、CRP的影响

目的：观察大黄对合并呼吸衰竭重症胰腺炎（SAP）患者的治疗作用及对IL-6、CRP的影响。方法：将56例入住ICU伴呼吸衰竭的SAP患者分为大黄治疗组和对照组,观察2组患者氧合指数变化、机械通气天数、胃肠功能障碍持续时间、体温恢复时间及CRP、IL-6的变化。结果：2组患者第1、3天的血清CRP、IL-6水平相比无统计学差异（P〉0.05）;第5天血清CRP、IL-6水平大黄治疗组低于对照组（P〈0.05）,第7天,2组比较有统计学差异（P〈0.01）。第1、3、5、7天PaO2/FiO2大黄治疗组高于对照组,2组相比有统计学差异（P〈0.05）。大黄治疗组胃肠功能恢复所需时间与对照组比较,有统计学差异（P〈0.01）;体温恢复时间大黄组与对照组相比,有统计学差异（P〈0.05）;机械通气时间大黄治疗组与对照组比较有统计学差异（P〈0.01）。结论：大黄可有效改善胃肠功能障碍并减弱炎症反应,抑制炎症因子释放,并能加速肺损伤的恢复,减少机械通气时间。     

大承气汤和活血清胰汤对重型急性胰腺炎肺损伤治疗的实验研究

目的:研究重型急性胰腺炎(SAP)急性肺损伤的发生机制以及中西医结合治疗的机理.方法:应用大鼠重型急性胰腺炎模型,对比观察大承气汤(DT)、活血清胰汤(HQ)和善得定(SS)三种治疗方法对SAP模型大鼠肺泡巨噬细胞计数、活性以及巨噬细胞分泌的肿瘤细胞坏死因子(TNF)、白细胞介素-1(IL-1)和白细胞介素-6(IL-6)的影响.结果:SAP模型组肺泡巨噬细胞计数及活性、IL-1、IL-6和TNF明显高于对照组(P＜0.01),各治疗组肺泡巨噬细胞计数及活性、IL-1、IL-6和TNF明显低于SAP模型组(P＜0.05).结论:在SAP急性肺损伤中巨噬细胞聚集于肺泡并分泌大量细胞因子,大承气汤、活血清胰汤和善得定可以抑制肺泡巨噬细胞活化和分泌细胞因子,从而对SAP急性肺损伤起到保护作用.     

大黄素对大鼠重症胰腺炎TNFα、IL-6及胰腺腺泡细胞凋亡的影响

目的 :探讨大黄素治疗重症急性胰腺炎 (SAP)的作用机理。 方法 :用胰胆管内逆行注射去氧胆酸钠法制作大鼠SAP模型 ,随机分为对照组、SAP组、大黄素治疗组 ,动态测定术后 0h、6h、12h各组血清TNFα及IL - 6浓度 ,并取胰组织作病理学检查 ,同时应用TUNEL技术分析大鼠胰腺腺泡细胞凋亡的变化。 结果 :发现大黄素给药后 6h及 12h时血清TNFα、IL - 6水平明显降低 ,腹水量减少 ,胰组织病变程度改善 ;术后 6hSAP组胰腺腺泡细胞凋亡指数为 (3 92± 0 94 ) ,大黄素治疗组为(2 6 5 0± 6 72 ) ,两组比较 ,P <0 0 5。 结论 :大黄素可明显抑制大鼠胰酶及TNFα、IL - 6的释放 ,并且诱导已受损的不可恢复的腺泡细胞凋亡 ,从而改善大鼠重症胰腺炎的病情发展。     

冠心病患者血清hs-CRP和血浆脂联素检测的临床意义

目的：探讨了冠心病患者血清hs-CRP和血浆脂联素水平的变化及意义。方法：应用免疫比浊法和ELISA对68例冠心病患者进行测定，其中稳定型心绞痛31例，不稳定型心绞痛30例，急性心肌梗死7例，进行了血清hs-CRP和血浆脂联素水平测定，并与35名正常健康人作比较。结果：冠心病患者在治疗前血清hs-CRP水平非常显著地高于正常人组（P〈0．01），而血清脂联素水平则显著地低于正常人组（P〈0．01），急性心肌梗死组和不稳定型心绞痛组又高于稳定型心绞痛组（P〈0．01）。经治疗后一个月血清hs-CRP与正常人比较无显著性差异（P〉0．05）而脂联素水平与正常人比较仍有显著性差异（P〈0．05）。结论：检测冠心病患者血清hs-CRP和血浆脂联素水平对冠心病的发生、发展以及疗效和预后均有重要的临床价值。     

Evaluation and management of the cardiac amyloidosis

Cardiac amyloidosis describes clinically significant involvement of the heart by amyloid deposition, which may or may not be associated with involvement of other organs. The purpose of this review is to summarize the current state of evidence for the effective evaluation and management of cardiac amyloidosis. Acquired systemic amyloidosis occurs in more than 10 per million person-years in the U.S. population. Although no single noninvasive test or abnormality is pathognomonic of cardiac amyloid, case-control studies indicate that echocardiographic evidence of left ventricular wall thickening, biatrial enlargement, and increased echogenicity in conjunction with reduced electrocardiographic voltages is strongly suggestive of cardiac amyloidosis. Furthermore, newer echocardiographic techniques such as strain and strain rate imaging can demonstrate impairment in longitudinal function before ejection fraction becomes abnormal. Recent observational studies also suggest that cardiovascular magnetic resonance imaging yields characteristic findings in amyloidosis, offering promise for the early detection of cardiac involvement, and the presence of detectable cardiac troponin and elevated B-type natriuretic peptide in serum of affected patients portends an adverse prognosis. Management strategies for cardiac amyloid are largely based on nonrandomized single-center studies. One of the few published randomized studies shows the superiority of oral prednisolone and melphalan compared with colchicine in systemic AL amyloidosis. Intermediate-dose infusional chemotherapy regimes (such as vincristine, adriamycin, and dexamethasone) and high-dose chemotherapy with peripheral stem cell rescue have been used widely, but treatment-related mortality remains substantial with chemotherapy. Recent studies also indicate promising strategies to stabilize the native structures of amyloidogenic proteins; inhibit fibril formation; and disrupt established deposits using antibodies, synthetic peptides, and small-molecule drugs.     

基于因子分析的稳定型心绞痛证候要素研究

目的 探讨稳定型心绞痛证候要素,为该病的辨证论治提供依据.方法 设计前瞻性观察方案,选取经冠脉造影证实的251例冠心病心绞痛患者,观察其中医症状特点,通过因子分析提取证候要素并对其分布情况进行分析.结果 因子分析结果得出6个公因子(证候要素),其分布情况为血瘀占37.8%,气虚占33.1%,痰浊占16.7%,阴虚占12.4%.结论 稳定型心绞痛主要证候要素是血瘀、气虚;次要证候要素为痰浊、阴虚;病位在心,主要涉及肾、脾两脏.     

白术多糖通过调控TLR4/NF⁃κB信号通路对重症急性胰腺炎大鼠肠黏膜免疫屏障的影响

目的探讨白术多糖对重症急性胰腺炎(SAP)大鼠肠黏膜免疫屏障的保护作用及其机制研究。方法采用逆行胆胰管注射5%牛磺胆酸钠溶液法建立SAP模型,术后立即给予相应药物处理。于术后48 h,检测血清中淀粉酶、TNF?α(肿瘤坏死因子?α)、白介素IL?6和IL?1β水平;HE染色观察胰腺和小肠组织病理学变化;流式细胞术检测小肠黏膜中CD4⁺T细胞和CD8⁺T细胞亚群比例;放射免疫法检测小肠黏膜中sIgA(分泌性免疫球蛋白A)水平;Western blot检测小肠组织中TLR4/NF?κB通路相关蛋白表达。结果与假手术组比较,SAP模型组大鼠胰腺和小肠组织损伤严重,血清淀粉酶活性及TNF?α、IL?6和IL?1β水平增加,小肠黏膜CD4+T细胞亚群比例及CD4⁺/CD8⁺比值和sIgA水平降低,而CD8+T细胞亚群比例上升,同时小肠组织中MyD88(髓样分化因子)和TLR4蛋白及NF?κB p65蛋白磷酸化水平增加(均P<0.05)。与SAP模型组比较,白术多糖高剂量组和乌司他丁组大鼠胰腺和小肠组织损伤有所改善,血清淀粉酶活性和TNF?α、IL?6、IL?1β水平降低,小肠黏膜中CD4⁺T细胞亚群比例及CD4⁺/CD8⁺比值和sIgA水平增加,CD8⁺T细胞亚群比例降低,而小肠组织中MyD88、TLR4蛋白及NF?κB p65磷酸化水平降低(均P<0.05)。结论白术多糖可改善重症急性胰腺炎大鼠肠黏膜免疫屏障损伤,其机制可能与抑制TLR4/NF?κB信号通路活化有关。