特布他林对海水淹溺型肺水肿兔肺组织炎症反应的抑制作用

目的探讨特布他林对海水淹溺型肺水肿兔肺组织炎症反应的影响。方法36只机械通气的麻醉新西兰兔随机分成正常组（N组）、对照组（C组）和特布他林治疗组（T组）。C组和T组经颈动脉注入4ml／kg的配方海水，20min后C组经颈动脉注入2ml生理盐水，而T、组则注入0．15mg／kg特布他林，N组除未注入配方海水外，其余处理同C组。观察肺泡灌洗液（BALF）中TNF-α计量和中性粒细胞计数，取部分右下肺常规病理学检查，并分别用RT-PCR和ELISA检测肺组织中TNF-α、IL-1β和IL-8的mRNA表达及蛋白含量。结果病理学观察显示C组的肺组织内有大量的炎性细胞浸润，肺泡隔断裂、肺泡破裂、相互融合、肺泡大量萎陷，肺泡内有出血及透明膜形成。T组的上述改变轻于C组。T组肺组织内TNF-α、IL-1β和IL-8的mRNA表达及蛋白含量均显著低于C组（P〈0．05），BALF中TNF-α和中性粒细胞计数减少。结论特布他林可以抑制海水淹溺型肺水肿兔肺组织的TNF-α、IL-1β和IL-8，从而减轻肺组织炎症反应。     

重性抑郁障碍患者躯体症状与脑源性神经营养因子和炎性因子的相关性研究

背景 大量证据表明抑郁障碍患者的躯体症状的风险比正常人高,但躯体易感性的机制尚不明确。部分研究认为前者脑源性神经营养因子前体(ProBDNF)、炎性因子水平比正常人高,而这是否与伴随的躯体症状有关还没有明确的结论。目的 探讨重性抑郁障碍(MDD)患者躯体症状与脑源性神经营养因子(BDNF)、炎性因子的特征及其相关性。方法 选取2019年2月至2020年12月山西医科大学第一医院精神卫生科门诊或住院部MDD患者59例与同期社区招募的健康志愿者32例作为研究对象。根据躯体化症状自评量表(SSS)将MDD患者分为伴躯体症状抑郁障碍(SD)组37例(SSS总分>36分)和不伴躯体症状抑郁障碍(NSD)组22例(SSS总分≤36分),32例健康志愿者为健康对照组(HC组)。收集临床资料,包括性别、年龄、受教育年限、17项汉密尔顿抑郁量表(HAMD-17)评分、SSS评分、BDNF、ProBDNF与炎性因子[C反应蛋白(CRP)、白介素4(IL-4)、白介素6(IL-6)、白介素10(IL-10)、白介素18(IL-18)、白介素23a(IL-23a)、高迁移率族蛋白B1(HMGB1)、肿瘤...     

血清炎性因子在骨折延迟愈合患者富血小板血浆治疗中的变化

探讨血清炎性因子在骨折延迟愈合患者富血小板血浆治疗中的变化。方法 选取2020年4月—2021年4月我院收治的98例骨折患者,均予以富血小板血浆联合钢板内固定手术治疗,根据术后6个月内是否发生骨折延迟愈合分为延迟愈合组（37例）和正常愈合组（61例）。分别于骨折后1、4、8、12周采集患者血清样本,采用酶联免疫吸附法检测血清人可溶性细胞间粘附分子-1（sICAM-1）、人可溶性血管细胞粘附分子-1（sVCAM-1）、肿瘤坏死因子-α（TNF-α）等炎症因子水平,并绘制ROC曲线,评估其对骨折延迟愈合的预测价值。采用酶联免疫双抗体夹心法检测血清骨钙素（BGP）、Ⅰ型胶原氨基端肽原（PINP）、碱性磷酸酶（ALP）、胰岛素样生长因子-1（IGF-1）等骨生化代谢指标水平,并采用Pearson分析骨生化代谢指标与炎症因子的关系。结果 骨折1周时,两组患者血清sICAM-1、sVCAM-1、TNF-α等炎症因子水平比较差异无统计学意义（P＞0.05）;骨折4、8、12周时,延迟愈合组患者血清sICAM-1、sVCAM-1、TNF-α等炎症因子水平均高于正常愈合组（P＜0.05）,且随着时间推移,两组患者血清sICAM-1、sVCAM-1、TNF-α水平先升高后降低,但延迟愈合组炎症因子水平波动较正常愈合组更明显（P＜0.05）。骨折1周时,两组患者血清BGP、PINP、ALP、IGF-1等骨生化代谢指标水平比较差异无统计学意义（P＞0.05）,且两组各时间点血清ALP水平比较差异无统计学意义（P＞0.05）; 骨折4、8、12周时延迟愈合组患者血清BGP水平逐渐升高并高于正常愈合组,血清IGF-1水平逐渐升高但低于正常愈合组,骨折8、12周时延迟愈合组患者血清PINP水平低于正常愈合组（P＜0.05）。Pearson相关性分析结果显示,血清sICAM-1、sVCAM-1、TNF-α等炎症因子水平与血清BGP呈正相关（r=0.523,P＜0.001）,与血清IGF-1呈负相关（r=-0.467,P＜0.001）。ROC曲线分析结果显示,骨折8周时,血清炎症因子水平诊断骨折延迟愈合的曲线下面积高于0.7,提示其具有较好诊断价值,且联合检测对骨折延迟愈合诊断的灵敏度更高（P＜0.05）。结论 延迟愈合骨折患者血清sICAM-1、sVCAM-1、TNF-α等炎症因子指标水平随骨折时间增加呈现先升高后降低变化,炎症因子指标水平波动明显,且术后8周时血清炎症因子对预测骨折延迟愈合具有一定参考意义     

Takayasu arteritis: Follow-up studies for 20 years

We reviewed retrospectively 126 (5 male, 121 female) patients suffering from Takayasu arteritis who had been treated in our clinics from 1971 to 1990. The patients' ages ranged from 19 to 80yrs old (1990) with a mean age of 48.7 ± 11.8 years. HLA typing analysis in 98 patients revealed that 45 patients (47%) were confirmed as carrying the Bw52 antigen, a high result that is statistically significant as compared with that in healthy Japanese. Arteriograms (performed in 75 patients) revealed that 28 patients (37%) were affected in the aorta and its main branches by this disease (type IV by Nasu's classification) and 23 patients (31%) were affected only in the main branches (type I). The C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) improved significantly from 2.55 ± 0.28(+) and 57.0 ± 5.69 mm/hr to 0.53 ± 0.12(+) and 31.2 ± 3.45 mm/hr, respectively after treatment including steroid and antiplatelet therapy (P < 0.01).=" patients=" with=" bw52=" exhibited=" more=" severe=" inflammatory=" conditions=" than=" those=" without=" bw52.=" lung=" scintillations=" performed=" in=" 81=" patients=" showed=" pulmonary=" arterial=" lesions=" in=" 50=" patients=" (62%).=" echocardiograms=" revealed=" aortic=" regurgitation=" (ar)=" in=" 44=" patients=" (35%),=" with=" a=" significant=" difference=" noted=" between=" the=" bw52=" positive=" group=" and=" the=" bw52=" negative=" group=" [29/40=" (73%)=" versus=" 11/47=" (23%),=">P < 0.001].=" patients=" with=" bw52=" were=" prescribed=" higher=" doses=" of=" steroids=">P < 0.05)=" for=" longer=" periods=">P < 0.01)=" than=" those=" without=" bw52.=" of=" 11=" patients=" who=" died=" during=" our=" study=" period,=" 7=" died=" of=" cardiac=" complications,=" all=" of=" whom=" were=" suffering=" from=" ar.=" hla=" analysis=" performed=" in=" 6=" of=" these=" 7=" patients=" revealed=" that=" all=" carried=" the=" bw52=" antigen.=" in=" conclusion,=" the=" retrospective=" survey=" revealed=" that=" patients=" carrying=" the=" bw52=" antigen=" showed=" more=" severe=" inflammatory=" conditions=" and=" progressed=" more=" rapidly=" to=" complications=" and=" the=" fatal=" morbid=" condition,=" as=" compared=" with=" those=" without=" bw52.=" this=" suggests=" the=" important=" role=" of=" gene=" disequilibrium=" with=" this=" hla=">     

Regulation of cytokine synthesis in cardiac surgery: Role of extracorporeal circuit and humoral mediators <Emphasis Type="Italic">in vivo</Emphasis> and <Emphasis Type="Italic">in vitro</Emphasis>

Objective and design: Cardiopulmonary bypass (CPB) impairs monocyte and neutrophil proliferation, cytokine synthesis, and antigen presentation. This study compares in vivo data with results from an extracorporeal circulation (ECC) model, distinguishing direct effects on cytokine synthesis from regulatory mechanisms. Patients and methods: Whole blood from 18 patients prior to, during and after CPB was stimulated with lipopolysaccharide (LPS). Tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8 levels were measured. Additionally, blood from 4 volunteers was circulated in an ECC model. Cytokine levels were measured before and during mock ECC. Results: LPS-induced cytokine synthesis was reduced after CPB (TNF-α: 11 %; IL-6: 29 %; IL-8: 48 % of preoperative values, all p < 0.001). In mock ECC, cytokine production (except IL-8) was suppressed: TNF-α production was lowest 60 min after starting ECC, IL-6 synthesis was lowest at 90 min (33 % and 15 % vs. pre-ECC levels; both p < 0.001). Patient sera contained cytokine-inhibitory activity after CPB, an activity not found in mock ECC. Conclusions: (1) In patients, CPB induces early transient LPS hyporesponsiveness; (2) blood contact with foreign surfaces induces LPS hyporesponsiveness; (3) serum cytokineinhibitory activities are released after CPB, but not in mock ECC. Impaired leukocyte function may explain increased susceptibility to infections after CPB. Received 16 September 2006; accepted without revision by K. Visvanathan 18 October 2006     

炎症性肠病动物模型的研究概况

The etiology and pathogenesis of inflammatory bowel disease are up to now still not clear and definite. Establishing the ideal animal model to study its cause and pathogenesis of this disease is very important. The ideal animal model should have the same manifestation with human inflammatory bowel disease on clinical and pathologic feature etc. In this article, the method, the pathologic character isfics and concerning pathogenesis, of a few common useful experiment animal models are discussed.     

Morphological,immunohistochemical and molecular features of inflammatory bowel disease associated colorectal carcinoma and associated mucosal lesions – Single institution experience

Background

Patients with inflammatory bowel disease (IBD) – ulcerative colitis (UC) and Crohn’s disease (CD) have an elevated risk of developing colorectal carcinoma (CRC). Major risk factor in IBD patients is the continuous chronic inflammation leading to development of dysplasia and carcinoma. Nevertheless, other types of non-conventional but suspicious mucosal changes serrated change/dysplasia, NOS and villous hypermucinous change, have also been reported in IBD patients. Preneoplastic potential of these lesions is still not well elucidated.

Diagnostic value of anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies for inflammatory bowel disease: high prevalence in patients with celiac disease

Both celiac disease and inflammatory bowel disease (IBD) are characterized by chronic diarrhea and the presence of distinct (auto)antibodies. In the present study we wanted to determine the prevalence of serological markers for inflammatory bowel disease, i.e., perinuclear antineutrophil cytoplasmic antibodies (pANCA) and/or anti-Saccharomyces cerevisiae antibodies (ASCA), in 37 patients with biopsy-confirmed celiac disease (Marsh IIIb/c). The majority of the patients was positive for IgA (auto)antibodies typically associated with celiac disease, i.e., antiendomysium antibodies (EMA) (86.5%), antigliadin antibodies (AGA) (73%), and antirecombinant human tissue transglutaminase antibodies (rh-tTGA) (86.5%). Four patients with selective IgA deficiency could be identified by analyzing EMA, AGA, and rh-tTGA for the IgG isotype. The prevalence of pANCA and ASCA, markers that are used for IBD, was unexpectedly high in our cohort of patients with celiac disease: 8 patients were positive for pANCA (IgG) and 16 patients were positive for ASCA (IgG and/or IgA). These results indicate that the presence of pANCA or ASCA in the serum of patients with chronic diarrhea does not exclude celiac disease. A prospective study is required to determine whether pANCA and/or ASCA identify patients at risk for developing secondary autoimmune disease.