慢性低氧时小鼠肺组织低氧诱导因子-1α的表达

目的：研究低氧时小鼠肺组织中低氧诱导因子-1α(HIF-k)表达的变化。方法：实验用雄性小鼠,低氧仓浓度分别为10％、7％、5％。用免疫荧光组织化学技术及共聚焦显微术,检测小鼠在低氧条件下肺组织中HIF-1α表达的变化。结果：正常组小鼠肺组织HIF-1α无表达,低氧组HIF-1α表达增加,且随低氧时间的延长及低氧强度的增加而增强。结论：低氧可诱导小鼠肺组织中HIF-1α的表达增强,(HIF-k)可能参与肺组织细胞凋亡的发生。     

Reliability testing of tendon disease using two different scanning methods in patients with rheumatoid arthritis

Objective. To assess the intra- and interobserver reliability of musculoskeletal ultrasonography (US) in detecting inflammatory and destructive tendon abnormalities in patients with RA using two different scanning methods. Methods. Thirteen observers examined nine patients with RA and one healthy individual in two rounds independently and blindly of each other. Each round consisted of two consecutive examinations, an anatomy-based examination and a free examination according to personal preferences. The following tendons were evaluated: wrist extensor compartments 2, 4 and 6, finger flexor tendons 3 and 4 at MCP level, tibialis posterior tendon and both peronei tendons. Overall, positive and negative agreements and κ-values for greyscale (GS) tenosynovitis, peritendinous power Doppler (PPD) signal, intratendinous power Doppler (IPD) signal and GS tendon damage were calculated. Results. Intraobserver κ-value ranges were 0.53-0.55 (P?相似文献   

乌审旗3000名妇女宫颈癌筛查结果分析

目的：了解乌审旗妇女宫颈癌及癌前病变的发病现状,探讨子宫颈液基细胞学（Thinprep paptest,TCT）结合阴道镜检查的诊断价值。方法：对3 000名乌审旗妇女进行TCT筛查,对TCT阳性（细胞学TBS分类为不典型鳞状细胞以上）的妇女进行阴道镜及镜下多点活组织检查（活检）,分析TCT阳性者的阴道镜检查及活检结果,比较TCT阳性者中不同年龄段患者的活检结果。结果：3 000名受检者中,TCT阳性537例（17.9%）,其中经活检证实为宫颈上皮内瘤变（cervical intraepthelial neoplasia,CIN）190例（6.3%）,宫颈浸润癌2例（0.07%）,537例TCT阳性者中,阴道镜检查正常264例（49.2%）,其中活检结果为CIN34例,阴道镜的假阴性率为12.9%,异常273例（50.8%）,其中活检结果为湿疣34例,CIN或浸润癌158例,阴道镜与活检的诊断符合率达70.3%（192/273）。TCT为轻度鳞状上皮内病变、高度鳞状上皮内病变、鳞状细胞癌的病例与活检的诊断符合率分别为50.4%,88.3%和2/2,假阳性率则分别为49.6%、11%和0。537例TCT阳性者中,2030岁组、3140岁组,4147岁组的CIN检出率分别为33.7%、44.5%2、6.7%（P〈0.05）。结论：乌审旗妇女CIN的发生率高,是宫颈癌的高发人群。TCT结合阴道镜检查是较好的宫颈癌筛查手段之一。     

慢性肾小球肾炎伴肾衰患者血清α1肾上腺素受体和抗血管紧张素Ⅱ受体1型自身抗体检测结果分析

目的 探讨抗血管紧张素Ⅱ受体1型（AT1-受体）、α1-肾上腺素受体（α1-受体）、自身抗体是否与慢性肾小球肾炎（CaN）发病有关。方法 以合成的AT1受体和α1受体多肽片段为抗原，应用酶联免疫吸附测定（ELISA）技术，检测66例CGN患者、58例高血压病患者及柏例正常人血清中抗AT1和α1受体自身抗体。结果 CGN肾功能不全组抗AT1和α1受体抗体阳性率分别为56．1％（37／66）和53．0%（36／66），高于高血压无肾损害组（分别为15．5％和12．1％）及正常对照组（分别为10％和12．5％），P〈0．01。结论 抗G蛋白偶联型受体自身抗体可能与慢性肾小球肾炎发病有关。     

Inactivation of factor XIa in human plasma assessed by measuring factor XIa-protease inhibitor complexes: major role for C1-inhibitor

From experiments with purified proteins, it has been concluded that factor XIa (FXIa) is inhibited in plasma mainly by alpha 1-antitrypsin (a1AT), followed by antithrombin III (ATIII), C1-inhibitor (C1Inh), and alpha 2-antiplasmin (a2AP). However, the validity of this concept has never been studied in plasma. We established the relative contribution of different inhibitors to the inactivation of FXIa in human plasma, using enzyme-linked immunosorbent assays (ELISAs) for the quantification of complexes of FXIa with a1AT, C1Inh, a2AP, and ATIII. We found that 47% of FXIa added to plasma formed complexes with C1Inh, 24.5% with a2AP, 23.5% with a1AT, and 5% with ATIII. The distribution of FXIa between these inhibitors in plasma was independent of whether FXIa was added to plasma, or was activated endogenously by kaolin, celite, or glass. However, in the presence of heparin (1 or 50 U/mL), C1Inh appeared to be the major inhibitor of FXIa, followed by ATIII. Furthermore, at lower temperatures, less FXIa-C1Inh and FXIa-a1AT complexes but more FXIa-a2AP complexes were formed. These data demonstrate that the contribution of the different inhibitors to inactivation of FXIa in plasma may vary, but C1Inh is the principal inhibitor under most conditions.     

In vitro and in vivo effects of prestorage filtration of apheresis platelets

BACKGROUND: The effect of prestorage filtration on the quality of apheresis platelet concentrates stored for transfusion is undetermined. STUDY DESIGN AND METHODS: Investigation of 11 plateletpheresis components used a concurrent paired-study design. On the day of collection, each component was equally divided into two suspensions; one half was filtered, and the other half was not. Each suspension was stored for 5 days. In vitro testing was performed on the day of collection (Day 0) for cell counts and on Day 5 for measurements of lactate, glucose, blood gases, pH, platelet ATP, hypotonic stress ratio, extent of shape change in response to ADP, tissue necrosis factor alpha, interleukin 8, interleukin 1 alpha, interleukin 1 beta, interleukin 6, and platelet surface glycoproteins by flow cytometry. At the end of the 5-day period, a sample was taken from each of the two suspensions, radiolabeled with either 51Cr or 111In, and transfused concurrently. Posttransfusion samples were drawn for measurements of recovery and platelet survival and for functional assessment of the ex vivo ability of the circulating radiolabeled platelets to aggregate in response to ADP. RESULTS: The apheresis component had a mean platelet yield of 3.2 +/? 0.4 × 10(11) and a white cell yield ranging from 1 × 10(5) to 1 × 10(8), with a median of 2 × 10(7). Filtration resulted in a platelet loss of approximately 10 percent and a variable 2 to 3 log10 reduction in white cell content. No significant differences between filtered and unfiltered suspensions in paired t tests that would likely have an impact on platelet quality were observed in the in vitro tests. The in vivo recovery and survival were highly similar and not statistically different in filtered and unfiltered paired suspensions: the mean difference was 1.2 +/? 4.0 percent for recovery and 7.0 +/? 15 hours for survival. The functional assessment by aggregation to ADP showed no difference between filtered and unfiltered suspensions. A small decrease in tumor necrosis factor alpha and interleukin 8 was evident in the filtered suspension as compared to levels in the unfiltered suspensions. CONCLUSION: Prestorage white cell reduction in apheresis components resulted in WBC reduction by several log10 with no evident adverse effect on platelet viability or function.     

Induction of IL-5 expression by IL-2 is resistant to the immunosuppressive agents cyclosporin A and rapamycin

T cell cytokine expression may be induced by the cytokine IL-2 or via the TCR complex. The comparative effects of cytokine- and TCR-mediated signalling on the induction of human IL-5 mRNA were examined. Cytokine mRNA expression was analysed by RT-PCR in fresh peripheral blood mononuclear cells (PBMC) from normal individuals and in populations of activated T lymphocytes, derived from phytohaemagglutinin (PHA)- stimulated PBMC. rIL-2 induced IL-5 expression in PBMC, the kinetics of which were similar to the effects of PHA. rIL-4 induced IL-5 mRNA expression in activated T lymphocytes. IL-5 expression induced by either IL-2 or PHA was completely abolished by the protein synthesis inhibitor cycloheximide. rIL-2-induced IL-5 expression was resistant to cyclosporin A (CsA), whereas IL-5 expression elicited by PHA was inhibited by CsA, at doses as low as 10 ng/ml. Rapamycin (RAP) had no effect on rIL-2-stimulated IL-5 expression, but suppressed IL-5 expression induced by PHA. The inhibitory effect of RAP on PHA-induced IL-5 expression was more apparent at 12 and 24 h after stimulation than at earlier times. The resistance of IL-2 receptor (IL-2R) signalling to CsA and RAP indicates that the IL-2R and the TCR are associated with different pathways regulating IL-5 expression.