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目的:评价抗角蛋白抗体、抗核周因子和抗环瓜氨酸肽抗体联合检测在幼年类风湿关节炎诊断及病情评估中的意义。方法:①观察对象及分组:选择2003-01/2005-12首都医科大学附属北京儿童医院风湿免疫病房住院治疗的76例幼年类风湿关节炎患儿及54例非幼年类风湿关节炎患儿,正常对照30例(家属均知情同意)。②检测上述人员血清抗角蛋白抗体、抗核周因子抗体和抗环瓜氨酸肽抗体水平;观察两组患儿出现临床症状、体征例数及实验室检测数据。③对幼年类风湿关节炎诊断的敏感性、特异性,阳性似然比、阴性似然比进行评价,并对幼年类风湿关节炎患儿中3种抗体联合检测阳性组阴性组的临床症状、体征及实验室检查方面的指标进行比较,资料作统计学分析。结果:两组患儿130例,正常儿童30例,全部进入结果分析。①两组患儿临床症状、体征例数及实验室检测值差异没有显著性意义。②抗角蛋白抗体、抗核周因子抗体和抗环瓜氨酸肽抗体联合检测对幼年类风湿关节炎组早期诊断缺乏有效性。③抗角蛋白抗体( )/抗核周因子抗体( )/抗环瓜氨酸肽抗体( )病例与抗角蛋白抗体(-)/抗核周因子抗体(-)/抗环瓜氨酸肽抗体(-)病例相比,关节强直病例明显增多,差异有显著性(较正χ2=3.902,P=0.048),抗链球菌溶血素“O”和C-反应蛋白均显著增高,差异有显著性(χ2=2.616,3.557,P=0.025,0.001)。结论:抗角蛋白抗体、抗核周因子抗体、抗环瓜氨酸肽抗体联合检测对幼年类风湿关节炎缺乏早期诊断意义及特异性,联合检测对判断疾病的活动性、病理损害程度和预后有临床意义。  相似文献   
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目的:利用核因子κBp65特异性小干涉核糖核酸抑制肿瘤坏死因子α诱导的关节滑膜细胞中一氧化氮合酶2和环氧合酶2的表达,探讨基因治疗类风湿性关节炎的新方法。方法:实验于2005-03/2006-03在北京大学医学部中心实验室(国家级)完成。①实验材料:清洁级健康近交系SD大鼠10只;一氧化氮合酶2,环氧合酶2,3-磷酸甘油醛脱氢酶引物(由北京奥科生物公司合成);肿瘤坏死因子α(Sigma公司);核因子κBp65特异性小干涉核糖核酸和转染条件由北京大学运动医学研究所陈连旭博士提供。②实验干预:切取大鼠髋关节和膝关节的滑膜体外培养滑膜细胞。利用脂质体siPORTTMLipid将核因子κBp65特异性小干涉核糖核酸转染滑膜细胞,再加入肿瘤坏死因子α刺激。阴性对照为任意编码的小干涉核糖核酸,阳性对照为针对3-磷酸甘油醛脱氢酶的小干涉核糖核酸。③实验评估:提取滑膜细胞中的核蛋白,利用电泳迁移率试验检测核因子κB的活性;提取滑膜细胞的核糖核酸和总蛋白,利用反转录聚合酶链反应和蛋白质免疫印记法从信使核糖核酸和蛋白质两水平检测一氧化氮合酶2和环氧合酶2的表达。结果:①肿瘤坏死因子α和核因子κBp65特异性小干涉核糖核酸对核因子κB转录活性的影响:与正常滑膜细胞相比,肿瘤坏死因子α可以显著提高核因子κB的结合能力,而事先转染小干涉核糖核酸48h,再用肿瘤坏死因子α刺激,核因子κB的结合能力又显著降低。②核因子κBp65特异性小干涉核糖核酸对核因子κB下游因子的影响:在培养的滑膜细胞中,肿瘤坏死因子α可以显著增加一氧化氮合酶2和环氧合酶2的表达;在转染小干涉核糖核酸抑制核因子κBp65的表达后再用肿瘤坏死因子α刺激,一氧化氮合酶2和环氧合酶2的表达被抑制。结论:①核因子κBp65特异性小干涉核糖核酸可降低肿瘤坏死因子α诱导的滑膜细胞中核因子κB的转录活性,抑制其下游因子一氧化氮合酶2和环氧合酶2的表达。②核因子κBp65特异性小干涉核糖核酸可用于基因治疗类风湿性关节炎的试验研究。  相似文献   
25.
目的:为了解心理应激对免疫功能的影响,对影响免疫功能的多种心理应激动物模型进行比较分析,以寻找合理可行的慢性情绪应激动物模型.方法:实验于2004-09/10在江西师范大学体育学院运动生理实验室完成,动物实验方法符合动物伦理学要求.①实验材料及分组:选用雄性SD大鼠32只,按随机数字表法分为4组(n=8),即对照组、空瓶组、束缚组及灯光加电击组.②实验方法:对照组大鼠正常饲养,其余各组建立相应的心理应激刺激模型.各组大鼠在正式实验之前适应性生活1周,不同强度情绪刺激为期2周.③实验评估:实验期间观察各组大鼠体质量变化.情绪应激后24 h应用放免法测定白细胞介素2、白细胞介素6含量,应用脲酶-Berthelot比色法测定血尿素氮含量.结果:32只大鼠全部进入结果分析.①实验期间各组大鼠体质量呈上升趋势,实验结束时,空瓶组大鼠体质量低于对照组(P<0.05).②各组大鼠的白细胞介素2、白细胞介素6含量差异无显著性意义(P>0.05).与对照组比较,空瓶组、束缚组白细胞介素2含量有下降趋势,白细胞介素6含量有上升趋势.③空瓶组大鼠血尿素氮含量显著高于对照组(P<0.01),其他各组差异无显著性意义(P>0.05).结论:体质量和血尿素氮是心理应激较为敏感的指标.空瓶、束缚及灯光加电击3种心理应激模型比较,空瓶刺激效果较好.  相似文献   
26.

Introduction

Rectal polypectomy causes thinning (or even perforation) of the rectal wall in addition to thermic injury at the polypectomy site.

Case report

We present a rare case of spontaneous rectal perforation after uncomplicated nerve sparing endoscopic extraperitoneal radical prostatectomy in a patient with a previous history of rectal polypectomy at the perforation site. The patient could be treated conservatively. There was complete healing of the fistula without any effect on functional results. This Conservative therapy for such rectal perforations is indicated if the patient''s general condition remains stable without any signs of infection.

Conclusions

Polypectomy is an important risk factor for rectal perforation during nsEERPE. Adequate time interval should be given to allow healing and avoid adding further thermal wall damage which may obscure healing leading to complications like fistula. Conservative therapy for small missed rectal perforations constitutes an attractive, feasible and non invasive treatment entity. Following this principle we have not faced this complication in following similar cases.  相似文献   
27.
The contribution of HLA DRB-DQB to type 1 diabetes (T1D) in Bahrainis, Lebanese, and Tunisians was investigated. DRB1*030101-DQB1*0201 was a locus that conferred susceptibility in three populations, while DRB1*040101-DQB1*0302 was a locus that conferred susceptibility only in Tunisians and Bahrainis. The DRB1*100101-DQB1*050101 (Bahrainis) and DRB1*150101-DQB1*060101 (Lebanese) loci were largely protective. The contribution of HLA to T1D must be evaluated with regard to ethnic background.  相似文献   
28.
Human leukocyte antigen (HLA) class II genes contribute to the genetic susceptibility to type 1 diabetes (T1D), and susceptible alleles and haplotypes were implicated in the pathogenesis of T1D. This study investigated the heterogeneity in HLA class II haplotype distribution among Tunisian patients with T1D. This was a retrospective case control study done in Monastir in central Tunisia. The subjects comprised 88 T1D patients and 112 healthy controls. HLA-DRB1 and -DQB1 genotyping was done by PCR-sequence-specific priming. Significant DRB1 and DQB1 allelic differences were seen between T1D patients and controls; these differences comprised DRB1*030101 and DQB1*0302, which were higher in T1D patients than in control subjects, and DRB1*070101, DRB1*110101, DQB1*030101, and DQB1*060101, which were lower in T1D patients than in control subjects. In addition, the frequencies of DRB1*030101-DQB1*0201 and DRB1*040101-DQB1*0302 were higher in T1D patients than in control subjects, and the frequencies of DRB1*070101-DQB1*0201 and DRB1*110101-DQB1*030101 haplotypes were lower in T1D patients than in control subjects. Multiple logistic regression analysis revealed the positive association of DRB1*030101-DQB1*0201 and DRB1*040101-DQB1*0302 and the negative association of only DRB1*070101-DQB1*0201 haplotypes with T1D. Furthermore, a significantly increased prevalence of DRB1*030101-DQB1*0201 homozygotes was seen for T1D subjects than for control subjects. Our results confirm the association of specific HLA-DR and -DQ alleles and haplotypes with T1D in Tunisians. The identification of similar and unique haplotypes in Tunisians compared to other Caucasians highlights the need for evaluating the contribution of HLA class II to the genetic susceptibility to T1D with regard to haplotype usage and also to ethnic origin and racial background.Type 1 (insulin-dependent) diabetes (T1D) is the most prevalent form of diabetes in children and young adults (12, 17) and results from autoimmune CD4+ and CD8+ T-cell-directed destruction of insulin-producing pancreatic ß islet cells, leading to irreversible hyperglycemia and related complications (4, 22). In addition to environmental factors, there is a strong genetic component to T1D pathogenesis, of which the human leukocyte antigen (HLA) locus, in particular the class II region (DR and DQ), account for 40 to 50% of T1D familial clustering (13, 30). This was evidenced by the enrichment of DR3, DR4, DQ2, and DQ8, and the lower prevalence of DR15 or DQ6.2 alleles among T1D patients, thereby assigning a susceptible or protective role for these alleles in T1D pathogenesis, respectively (3, 16, 21).The fact that not all carriers of a specific high-risk DR or DQ variant develop the disease and the strong linkage disequilibrium between select DRB1 and DQB1 alleles (28) indicate that the pathogenesis of T1D results from the complex interaction between several genes within the class II region, in which specific DRB1-DQB1 haplotypes contribute to disease susceptibility. Accordingly, the enrichment or decreased prevalence of select DRB1-DQB1 haplotypes in T1D patients imparts disease susceptibility or protection, respectively (3, 18, 24). This susceptibility or protection effect disappears when a different DRB1 or DQB1 allele replaces the specific allele in the haplotype (29). The contribution of specific HLA haplotypes toward T1D susceptibility depends on the ethnic/racial background (26), which was highlighted by the positive association of DRB1*030101-DQB1*0201 and DRB1*040101-DQB1*0302 haplotypes with T1D among Caucasians (3, 16) compared to DRB1*0405-DQB1*0401 and DRB1*0901-DQB1*0303 haplotypes and T1D in Japanese (18), while DRB1*1501-DQB1*0602 appeared to be protective of T1D in all populations (3, 16, 18). This indicates that association of a specific class II allele and DRB1-DQB1 haplotype with T1D must be evaluated in the context of the specific ethnic/racial background (26).We previously reported an association between HLA DRB1 and DQB1 alleles and haplotypes in Tunisian T1D patients (n = 50) and control subjects (n = 50) and identified two susceptible haplotypes (DRB1*030101-DQB1*0201 and DRB1*040101-DQB1*0302), but no protective haplotypes (27). Using haplotype estimation and regression analysis, here, we extend our investigation of HLA class II and T1D risk on a large sample size by confirming the association of these haplotypes and identified an additional T1D-protective haplotype.  相似文献   
29.
Aims. This article aims to review the literature published to date on the types, current use, the biomechanical effects and adverse effects of maternity support belts for low back pain during pregnancy, to identify future research directions. Background. Lumbar/pelvic support belts are frequently recommended for the prevention and treatment of low back pain during pregnancy. Design. Systematic review. Methods. MEDLINE, CINAHL, the Cochrane Library and patents databases were electronically searched. Results. Maternity support belts belong to one of the four main types of maternity support garments, which are widely commercially‐available. Current research showed limited evidence in support of the commercial maternity products regarding the effectiveness in the prevention and/or treatment of low back pain during pregnancy, other than that from the manufacturers. However, potential stabilisation effect of maternity support belt was demonstrated in some studies. Adverse effects reported include increased pain, fetal heart rate changes, skin irritation and discomfort. Conclusions. There is insufficient scientific evidence to conclude that wearing maternity support belts reduces pregnancy‐related low back pain and/or pelvic girdle pain. Future research directions in the area of biomechanics and physiology are recommended. Relevance to clinical practice. This review provides comprehensive understanding of the effectiveness of maternity support belts for the relief of low back pain during pregnancy which will facilitate healthcare professionals in providing evidence‐based advice to their patients.  相似文献   
30.
A 71-year-old woman presenting with severe low back pain was found to have a large oval area of increased sacral uptake on Tc-99m MDP scan, with corresponding T1-hypointense and T2-hyperintense areas on magnetic resonance (MR) images, highly suggestive of malignancy. Open biopsies showed only callus formation. The patient responded clinically to conservative measures, with twice-repeated follow-up Tc-99m MDP and MR scans documenting resolution of transient bone marrow oedema. We suggest that this form of marrow oedema represents a variant pattern of sacral insufficiency fractures.  相似文献   
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