心力衰竭患者血浆凋亡相关因子水平的变化及其临床意义

目的 :探讨作为凋亡抑制因子Fas (sFas)和凋亡诱导因子Fas配体 (sFasL)在心力衰竭患者血浆中的水平及其临床意义。方法 :采用酶联免疫吸附法测定 6 7例心力衰竭患者 (心力衰竭组 )和 2 0例健康人 (正常对照组 )血浆中的sFas、sFasL、肿瘤坏死因子α、白细胞介素 6水平。结果 :心力衰竭不同心功能状态患者血浆sFas、肿瘤坏死因子α水平均高于正常对照组 ,心功能Ⅲ级、Ⅳ级患者中sFas水平 ,心功能Ⅲ级患者白细胞介素 6水平亦高于正常对照组 (P <0 0 5～ 0 0 1) ,并随心功能下降而上升 ,与心功能状态呈负相关 ,其水平与原发病无关。sFas和肿瘤坏死因子α水平在心功能Ⅱ级和Ⅳ级患者间比较有显著差异 (P <0 0 5 )。结论 :心力衰竭患者血浆中的sFas和sFasL的水平显著升高 ,提示sFas和sFasL水平升高乃至整个Fas/FasL系统可能在心力衰竭的发病中起着重要作用     

急性脑出血患者外周血sFas和sFasL的变化及意义

目的探讨急性脑出血（ACH）患者可溶性Fas（sFas）和可溶性Fas配体（sFasL）的变化与出血量、部位、形态及ACH病情变化的关系。方法 ACH患者60例为病例组,同期无脑血管疾病体检者30例为对照组。采用ELISA法测定血清sFas和sFasL,并按出血灶大小、部位、形状进行分组,比较各组之间sFas和sFasL差异。结果 ACH组6 h血清sFas低于对照组（P〈0.01）,24 h、2 d、7 d血清sFas高于对照组（P〈0.01）,ACH组6 h、24 h、2 d、7 d血清sFasL高于对照组（P〈0.01）,血清sFas和sFasL峰值与出血灶的大小、部位、形态有关（P均〈0.01）。结论血浆sFas、sFasL的峰值高可能提示ACH患者的出血灶较大、形态不规则和预后较差。     

急性脑梗死患者血清sFas和sFasL水平的观察研究

目的 通过检测急性脑梗死(acute cerebral infarction,ACI)患者血清可溶性Fas(soluble Fas,sFas)和可溶性Fas配体(soluble Fasligand,sFasL)表达水平的变化,探讨sFas和sFasL与ACI病情变化的关系.方法 60例ACI患者(男性32例,女性28例)为研究组,30例健康体检者(男性12例,女性18例)为对照组.用酶联免疫吸附法检测两组血清sFas和sFasL水平,比较两组之间sFas和sFasL浓度的差异.结果 ACI组48 h、7 d和14 d时血清sFas水平分别为(6.27±1.48)ng/L、(4.99±1.15)ng/L和(3.74±0.58)ng/L,均显著高于对照组的(3.00±0.38)ng/L(F=7.29,P<0.01);ACI组48 h、7 d和14 d时血清sFasL水平分别为(4.40±1.32)ng/L、(3.19±0.94)ng/L和(1.91±0.45)ng/L,均显著高于对照组的(1.15±0.21)ng/L(F=8.60,P<0.01).大梗死组sFas和sFasL水平分别为(7.63±0.64)ng/L和(5.01±1.16)ng/L,显著高于小梗死组的(4.98±0.91)ng/L(t=12.12,P<0.01)和(3.58±0.87)ng/L(t=5.35,P<0.01).ACI患者血清sFas和sFasL水平呈正相关性(r=0.748,P=0.01).结论 血清sFas和sFasL水平高提示ACI患者梗死体积较大.     

外周血核因子-κB及sFas/sFasL活性与心力衰竭严重程度的相关性

目的:探讨充血性心力衰竭(CHF)患者外周血单个核细胞(PBMCs)核因子-κB(NF-κB) 和血浆sFas/sFasL活性变化的意义。方法: 采用ELISA法检测76例CHF患者和30例对照组PBMCs的核蛋白提取物NF-κB和血浆sFas/sFasL的活性,并与患者心功能及超声心动图参数相比较,分析其与心功能及心肌重构的关系。结果: CHF患者PBMCs中NF-κB及血浆sFas/sFasL活性高于对照组,二者与心脏收缩功能相关指标呈显著负相关,与心肌重构相关指标呈显著正相关,并且NF-κB的活化与sFas/sFasL水平呈正相关(P<0.05)。结论: CHF患者NF-κB及sFas/sFasL活性明显增高, 并与心功能恶化及心肌重构程度密切相关。     

缬沙坦治疗慢性心力衰竭对血清sFas与sFasL的影响

目的观察慢性心力衰竭(CHF)患者血清sFas和sFasL的变化以及缬沙坦对其影响。方法100例CHF患者随机分成两组:常规治疗组(48例),给予常规抗心力衰竭治疗;缬沙坦组(52例),在常规治疗的基础上加用缬沙坦80mg,每日一次,连服4周。采用双抗体夹心酶联免疫法(ELISA)检测CHF患者治疗前后及健康对照组(30例)血清中sFas和sFasL水平。采用彩色多普勒超声心动图测定CHF患者左室射血分数(LVEF)。结果CHF患者血清中sFas和sFasL水平显著高于健康对照组(P<0.01),且随着心功能的损害加重而升高,sFas水平在不同心功能状态各组间比较差异有统计学意义(P<0.05),血清sFas和sFasL水平与LVEF呈显著负相关。(γ=-0.65,-0.57;P<0.01),缬沙坦组与常规治疗组治疗后血清sFas和sFasL水平均显著下降(P<0.05),且缬沙坦组较常规治疗组治疗后血清sFas、sFasL水平下降似更明显,但无统计差异。结论CHF患者血清sFas和sFasL水平可反映CHF的严重程度,可作为评价CHF心功能的参考指标。     

慢性乙型肝炎患者血清sFas和sFasL的水平及临床意义

目的:探讨可溶性Fas(sFas)和可溶性FasL(sFasL)在慢性乙型肝炎患者血清中水平的高低及临床意义。方法:采用ELISA双抗体夹心法检测97例慢性乙型肝炎患者血清中sFas和sFasL的水平,并以30名健康献血员作为对照。结果:慢性重型肝炎、肝炎肝硬化、慢性活动性肝炎患者血清中sFas和sFasL的水平,与正常对照组之间存在显著差异(P<0.01),随着病情加重,sFas和sFasL的水平逐渐升高,以重型肝炎升高更为显著;但sFas/sFasL比值呈明显下降趋势。结论:慢性乙型肝炎患者血清中sFas、sFasL水平与病情严重程度密切相关,临床测定慢性乙型肝炎患者血清sFas和sFasL水平,时病情判断及预测转归有一定的参考价值。     

慢性乙型肝炎患者肝组织Fas的表达与血清sFas水平的关系

目的:探讨慢性乙型肝炎(慢乙肝)患者肝组织中Fas的表达与血清可溶性Fas(sFas)水平的关系。方法:应用免疫组化法和ELISA法检测60例慢性乙型肝炎患者肝组织Fas的表达和血清sFas的水平。结果:重度慢乙肝患者血清中sFas水平最高,中度次之,而轻度最低,3组均明显高于健康献血员;随着肝组织炎症程度的加重,肝组织Fas抗原的表达明显增强,血清中sFas水平也明显升高。结论:Fas可分泌或脱落至细胞外,成为sFas,抑制肝细胞Fas表达将有助于减轻肝细胞损伤的程度。     

哮喘患儿血清sFas、sFasL、Eotaxin的变化及其意义

目的探讨血清可溶性Fas受体(sFas)及其配体(sFasL)、嗜酸性粒细胞趋化因子(Eotaxin)在哮喘患儿中的变化及其临床意义。方法选取确诊哮喘急性发作期患儿90例(急性期组)、选取同期哮喘缓解期患儿90例(缓解期组)、健康儿童90例(对照组),采用ELISA法检测三组血清sFas、sFasL、Eotaxin水平并进行比较,并分析不同病情的急性发作期患儿血清sFas、sFasL、Eotaxin水平及与血清总IgE(sIgE)的相关性。结果急性发作期组患儿的血清sFas、sFasL、Eotaxin、sIgE水平显著的高于缓解期组和对照组(P 0. 05),缓解期组患儿的血清sFas、sFasL、Eotaxin、sIgE水平显著的高于对照组(P 0. 05);重度组、中度组急性发作期组患儿的血清sFas、sFasL、Eotaxin水平显著的高于轻度组患儿(P 0. 05),重度组患儿的血清sFas、sFasL、Eotaxin水平显著的高于中度组(P 0. 05);重度组患儿的s IgE显著的高于轻度组(P 0. 05);急性发作期哮喘患儿血清sFas、sFasL、Eotaxin水平与血清sIgE呈显著的正相关关系(P 0. 05)。结论哮喘患儿血清sFas、sFasL、Eotaxin水平显著的升高,并且与病情、发作情况有关。     

原发性胆汁肝硬化患者血清可溶性Fas、FasL水平变化及意义

采用双抗体夹心酶联免疫吸附法法检测20例原发性胆汁性肝硬化患者(PBC组)和24例正常体检者(对照组)血清可溶性Fas、FasL、(sFas、sFasL)水平.结果与对照组比较,PBC组血清sFas水平明显升高(P＜0.05),sFasL水平无明显差异(P＞0.05).提示检测血清sFas水平有助于PBC的诊断.     

初治肺结核患者外周血sFas、sFasL检测的临床意义

用酶联免疫吸附法测定初治肺结核患者治疗前后外周血可溶性凋亡相关因子(sFas)、可溶性凋亡相关因子配体(sFasL)水平变化并与正常对照组进行比较,结果治疗前肺结核组外周血sFas、sFasL水平明显高于正常对照组,肺结核组治疗后血浆sFas、sFasL水平明显降低.认为sFas、sFasL的异常改变参与了结核病的免疫机制,外周血sFas、sFasL水平变化可能作为肺结核患者病情判断、估计治疗效果及预后的指标.     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

CagA-Hp抗体IgG与胃炎的组织学分析

研究幽门螺杆菌(Hp)感染与胃炎的关系。方法对204例慢性胃炎患者胃粘膜进行观察分析,并测定其中137例Hp阳性患者血清CagA-Hp抗体IgG水平,与组织学对照。结果慢性萎缩性胃炎伴肠上皮化生患者血清CagA抗体IgG明显高于对照组(P＜0.01);其他类型胃炎患者血清CagA抗体IgG水平无明显增高(P＞0.05)。结论CagA-Hp可能是导致慢性萎缩性胃炎伴肠上皮化生的因素之一,对这类患者应密切随访观察。     

慢阻肺急性加重期患者预后的影响因素分析

目的探讨慢性阻塞性肺病急性加重期(AECOPD)患者预后的相关危险因素。方法回顾性调查、收集58例AECOPD患者可能影响其预后的相关因素,并对其分别进行单因素分析。并进行Logistic多元逐步回归进行多因素分析,筛选影响AECOPD患者预后的独立危险因素。结果单因素分析后将结果 P0.1的因素纳入多因素Logistic回归,分析发现是否合并呼吸衰竭、气促程度、白细胞计数、APACHEⅡ、应用抗氧化剂、慢阻肺治疗依从性为影响AECOPD患者预后不佳的独立因素(P0.05)。结论根据AECOPD患者预后的独立危险因素,及早判断,选择合适的后续治疗方案,对提高其生存率及生存质量具有重要意义。     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Results of treatment of fistula-in-ano

To evaluate the application of Parks' classification in the management of patients with fistula-in-ano, a study was undertaken to assess the outcome of surgery, especially with respect to the recurrence rate and alteration of continence. A retrospective analysis of 160 consecutive patients who were classified at the time of operation was conducted. The distribution of fistulas was as follows: intersphincteric, 41.9 percent, transsphincteric, 52.1 percent, suprasphincteric, 1.3 percent, extrasphincteric, 0. A horseshoe extension occurred in 8.8 percent of the fistulas and 3.8 percent did not exactly conform to the classification as they were either complex or combinations of more than one type of fistula. The sole immediate postoperative complication was bleeding, which occurred one week postoperatively and ceased spontaneously (0.7 percent). Alteration in continence occurred in 6 percent of patients with 2.6 percent experiencing temporary incontinence to flatus, 1.3 percent to liquid stool, and 0.7 percent to solid stool. Permanent loss of control for flatus occurred in one patient (0.7 percent) and for liquid stool in one patient (0.7 percent). No patients suffered loss of control for solid stool. Recurrence developed in 6.3 percent of patients, all between five and 25 months postoperatively. Classifcation was found to be a useful guide in the operative management of patients with fistula-in-ano. Read at the joint meeting of the American Society of Colon and Rectal Surgeons with the Section of Colo-Proctology, Royal Society of Medicine, and the Section of Colonic and Rectal Surgery, Royal Australasian College of Surgeons, New Orleans, Louisiana, May 6 to 11, 1984.