依那普利联合灯盏花素对糖尿病大鼠肾脏保护作用及机制

目的探讨依那普利联合灯盏花素对大鼠糖尿病肾脏保护作用及机制。方法大鼠随机分5组：对照组、糖尿病组、依那普利给药组、灯盏花素给药组及依那普利与灯盏花素联合给药组。8周后观察肾组织病理形态学变化，检测尿白蛋白排泄率（AER）、肾组织尿丙二醛（MDA）含量及肾组织蛋白激酶（PKC）活性；应用Western杂交检测肾组织PKC蛋白表达，免疫组化方法检测肾组织转化生长因子（TGF）β1蛋白表达。结果各给药组均可抑制糖尿病大鼠AER增加及肾组织病理结构损害，联合组优于单独给药组；对肾组织及尿MDA含量增加的抑制作用联合组也优于单给药组；各给药组均可抑制肾组织PKC活性与表达，以联合组最明显；糖尿病大鼠肾小球与肾小管-间质TGFβ1蛋白表达明显高于对照组，各给药组肾组织TGFβ1蛋白表达明显低于模型组，其中以联合组最明显。结论依那普利与灯盏花素联合给药对糖尿病肾脏保护作用优于任一单给药组，其机制部分与其对肾组织氧化应激增加、PKC激活及TGFβ1表达有协同抑制作用有关。     

Enzyme immunoassay of complement-binding rheumatoid factors

Summary We describe an enzyme immunoassay for the determination of complement-binding rheumatoid factors. Polystyrene tubes are coated with heat aggregated human IgG. The rheumatoid factors (RFs) of patients heat inactivated sera are allowed to bind to aggregated IgG and thereafter saturated with fresh human complement. The amount of C 3 complement bound is measured by indirect enzyme immunoassay. The levels of complement binding RFs were measured in 30 patients with seropositive rheumatoid arthritis (RA), in 19 patients with systemic lupus erythematosus (SLE), and in 30 healthy control subjects. Compared to the controls high levels of complement-binding RFs were found both in RA and in SLE (P<0.0005). The mean level of the complement binding RFs was higher (P<0.05) in active than in inactive SLE. Even though the 19 S IgM RF bound complement, in RA no correlation was found between the level of complement binding RFs and Waaler-Rose titre, but the level of complement binding RF correlated with the levels of nonagglutinating IgM RF (r=0.56, P<0.01) and IgG RF (r=0.70, P<0.001) that were obtained by enzyme immunoassay.     

同型半胱氨酸与2型糖尿病合并早期肾病的关系

目的　探讨同型半胱氨酸 (Homocysteine,Hcy)与 2型糖尿病病人合并早期糖尿病肾病的关系。方法　应用高效液相色谱分析法测定 6 7例 2型糖尿病病人和 4 7例正常人的血浆 Hcy水平 ,并同步检测可溶性血栓调节蛋白(s TM)、叶酸和维生素 B1 2 。结果　 2型糖尿病病人血浆 Hcy水平明显高于对照人群 (15 .2 7± 6 .0 4 μmol/L vs12 .10± 1.86 μmol/L;P<0 .0 1) ,而合并早期糖尿病肾病的血浆 Hcy水平又高于无糖尿病肾病患者 (17.86± 8.0 4 μmol/L vs13.83± 4 .0 0 μmol/L;P<0 .0 1) ;存在高 Hcy血症的糖尿病病人 ,其早期糖尿病肾病发生率明显高于无高 Hcy血症患者(5 2 .0 % vs2 6 .2 % ;P<0 .0 5 ) ,且前者存在着较高水平的 s TM(P<0 .0 5 )。结论　高 Hcy血症与 2型糖尿病早期肾病的发病有关 ,其机制可能是通过血管内皮损伤所致     

糖尿病肾病患者血同型半胱氨酸测定的意义

目的 探讨2型糖尿病并早期糖尿病肾病患者血清同型半胱氨酸的变化及临床意义.方法 应用酶联免疫吸附试验,分别测定56例2型糖尿病患者及51例早期糖尿病肾病患者和53例正常对照组的血浆HCY水平,并同步测定叶酸(FA)和维生素B12(VitB12)含量.结果 早期糖尿病肾病患者血清HCY水平明显高于普通2型糖尿病患者(P＜0.01),且高于正常对照组(P＜0.01).结论 高HCY血症与2型糖尿病早期肾病的发病有关,其测定有助于监测及判断糖尿病肾病的发生及发展.     

小剂量利妥昔单抗治疗系统性红斑狼疮或干燥综合征合并血小板减少症：长期随访研究

目的 评价小剂量利妥昔单抗治疗系统性红斑狼疮或干燥综合征合并重症难治性血小板减少症的长期有效性和安全性.方法 前瞻性纳入系统性红斑狼疮和干燥综合征合并重症血小板减少症病例,给予利妥昔单抗100mg,1次/周,共4次.原有糖皮质激素逐渐减量,并停用免疫抑制剂.首次利妥昔单抗治疗后第2、4、12、24、52、76、104、128和156周随访,以血小板计数为疗效评价指标,分别定义为有效（complete response,CR）（血小板计数〉100×109/L）,部分有效（partial response,PR）（50×109/L≤血小板计数≤100×109/L）和无效（no response,NR）（血小板计数〈50×109/L）.定期监测外周血B细胞、血清补体C3、C4和IgG水平等.结果 共纳入13例病例,包括11例系统性红斑狼疮和2例干燥综合征,均为女性患者,年龄为23~76岁,血小板减少症中位病程及中位随访时间分别为2年和25个月.首次应用利妥昔单抗第12周,有5例（38%）和2例（15%）病例分别达到CR和PR.第24周有6例（46%）和3例（23%）病例分别达到CR和PR.52周、104周和156周的总体反应率分别为6例（46%）、6例（46%）和4例（31%）.外周血B细胞均达到清除水平,血清补体C3、C4和IgG水平稳定.轻度输液反应2例,发生肺栓塞和活动性结核1例,并发股骨头无菌性坏死2例,1例在第25月因肺部真菌感染死亡.结论 小剂量利妥昔单抗治疗系统性红斑狼疮或干燥综合征合并血小板减少症的疗效较好,起效较快,长期疗效稳定,安全性较好,但需谨慎除外感染.     

彩色多普勒超声对糖尿病肾病患者颈动脉病变的检测价值

目的探讨彩色多普勒超声对糖尿病肾病患者颈动脉结构及血流动力学改变的检测价值。方法应用彩色多普勒超声检测158例糖尿病肾病患者(糖尿病肾病组)及123例糖尿病患者(对照组)颈动脉内、中膜厚度(intima-media thickness,IMT)、斑块发生率、血流收缩期峰值流速、舒张末期血流速度、阻力指数(resistanceindex,RI)。比较糖尿病肾病组与对照组以及糖尿病肾病组早中期亚组、中晚期非透析亚组及透析亚组间上述指标的差异。结果糖尿病肾病组颈动脉IMT、斑块发生率明显高于对照组,差异有统计学意义[0.69(0.62～0.78)mm vs.0.56(0.51～0.69)mm,P<0.05;81.0%vs.47.2%,χ2=35.4,P<0.05];糖尿病肾病组中早中期亚组、中晚期非透析亚组及透析亚组3组间随着疾病的发展,颈动脉IMT、斑块发生率也逐渐增加;且透析亚组颈总动脉内径与早中期亚组对比明显增厚,差异有统计学意义[7.36(6.79～7.80)mm vs.7.01(6.36～7.31)mm,P<0.05]。糖尿病肾病组颈动脉舒张末期血流速度减小、RI增大,与对照组相比,差异有统计学意义(P<0.05)。结论糖尿病肾病患者普遍存在颈动脉结构及血流动力学改变,应用彩色多普勒超声检测颈动脉粥样硬化的发生与发展对预测糖尿病肾病患者发生心、脑血管事件具有重要意义。     

An unusual case of intestinal pseudo-obstruction presenting in an adolescent with juvenile-onset systemic lupus erythematosus: A diagnostic challenge

Introduction

Systemic lupus erythematosus (SLE) is an autoimmune disease with multiple systemic manifestations. The disease itself typically causes only 2–30% of SLE-associated gastrointestinal conditions.

C‐peptide and diabetic kidney disease

Kidney disease is a serious development in diabetes mellitus and poses an increasing clinical problem. Despite increasing incidence and prevalence of diabetic kidney disease, there have been no new therapies for this condition in the last 20 years. Mounting evidence supports a biological role for C‐peptide, and findings from multiple studies now suggest that C‐peptide may beneficially affect the disturbed metabolic and pathophysiological pathways leading to the development of diabetic nephropathy. Studies of C‐peptide in animal models and in humans with type 1 diabetes all suggest a renoprotective effect for this peptide. In diabetic rodents, C‐peptide reduces glomerular hyperfiltration and albuminuria. Cohort studies of diabetic patients with combined islet and kidney transplants suggest that maintained C‐peptide secretion is protective of renal graft function. Further, in short‐term studies of patients with type 1 diabetes, administration of C‐peptide is also associated with a lowered hyperfiltration rate and reduced microalbuminuria. Thus, the available information suggests that type 1 diabetes should be regarded as a dual hormone deficiency disease and that clinical trials of C‐peptide in diabetic nephropathy are both justified and urgently required.     

Emerging roles of basophils in allergic inflammation

Basophils have long been neglected in immunological studies because they were regarded as only minor relatives of mast cells. However, recent advances in analytical tools for basophils have clarified the non-redundant roles of basophils in allergic inflammation. Basophils play crucial roles in both IgE-dependent and -independent allergic inflammation, through their migration to the site of inflammation and secretion of various mediators, including cytokines, chemokines, and proteases. Basophils are known to produce large amounts of IL-4 in response to various stimuli. Basophil-derived IL-4 has recently been shown to play versatile roles in allergic inflammation by acting on various cell types, including macrophages, innate lymphoid cells, fibroblasts, and endothelial cells. Basophil-derived serine proteases are also crucial for the aggravation of allergic inflammation. Moreover, recent reports suggest the roles of basophils in modulating adaptive immune responses, particularly in the induction of Th2 differentiation and enhancement of humoral memory responses. In this review, we will discuss recent advances in understanding the roles of basophils in allergic inflammation.