经皮冠状动脉腔内成形术对急性心肌梗塞行早期血运重建

１２例急性心肌梗塞患者应用经皮冠状动脉腔内成形术进行早期血运重建，１１例梗塞相关血管再灌注血流为ＴＩＭＩ３级，残留狭窄１５．５±８．８％，１例并发血管内膜夹层形成行紧急冠状动脉旁路移植术，术后死亡。结果认为急性心肌梗塞早期直接进行经皮冠状动脉腔内成形术可实现稳定有效的血运重建，有利于减少心肌梗塞面积及心脏泵功能损害、降低再梗塞率和病死率。     

中效人胰岛素联合瑞格列奈治疗磺脲类降糖药继发性失效临床观察

目的观察中效人胰岛素与瑞格列奈联合应用治疗磺脲类降糖药继发性失效的疗效。方法将磺脲类降糖药继发性失效(SFS)36例病例随机分成两组,分别接受睡前小剂量中效人胰岛素加瑞格列奈(A组,20例)和单纯瑞格列奈(B组,16例)治疗,比较两组各生化指标。结果①治疗前空腹血糖(FPG)、餐后2小时血糖(2hPG)、C肽(C-P)、糖化血红蛋白(HbA1c)水平两组间无统计学差异;②治疗3个月后两组自身的FPG、2hPG、C-P、HbA1c水平均较治疗前明显改善,P值分别为0.01、0.05、0.05、0.01;③治疗3个月后FPG、2hPG、C-P、HbA1c水平A组均低于B组,P值分别<0.01、0.05、0.05、0.01。结论中效人胰岛素联合瑞格列奈和单用瑞格列奈治疗磺脲类降糖药继发性失效均有疗效,胰岛素和瑞格列奈联用优于单用瑞格列奈。     

Cloning of Human α-defensin-1 (HNP-1) Gene and Construction of Its Eukaryotic Expression Vector

1 Introduction Defensins are small cationic antimicrobial peptides that function in the host's innate immune system. The human defensin family includes three small peptides from the azurophil granules of polymorphonuclear cells named human neutrophil peptide (HNP)-1, HNP-2, HNP-3,which consist 5%-7% of the protein of human neutrophil. HNP-4 is approximately one hundred times less abundant. They demonstrate antibacterial, antifungal and antiviral properties in vitro. HNPs are important component of nonoxidative mechanism in macrophages, and can direct inactivate the enveloped viruses. Because only special cells express defensins. And it is hard to extract them naturally and the production is few. So researcher expect to obtain defensins highly through heterogenous expression by gene engineering technology. In order to express HNP-1, we cloned the cDNA of HNP-1 from human polymorphonuclear cells in peripheral blood, and constructed its eukaryotic expression vector, which provided a base for the further study on its mechanism of antimicrobial effect.     

Segmental intestinal muscular thinning: a possible cause of intestinal obstruction in the newborn

Intestinal obstruction proximal to a transition zone without an interposed physical barrier usually indicates Hirschsprung disease. The authors report one case of focal small bowel muscular thinning just distal to a transition zone that produced clinical and radiographic findings that simulated long-segment Hirschsprung disease in a 2-day-old infant.     

Preferential expression of insulin-like growth factor binding proteins-1, -3, and -5 during early diabetic renal hypertrophy in rats

The renal insulin-like growth factor-I (IGF-I) system has been implicated in the pathogenesis of renal hypertrophy, altered hemodynamics, and extracellular matrix expansion associated with early diabetes. The relative abundance of IGF binding proteins (IGFBPs) in the renal microenvironment may modulate IGF-I actions. However, the precise IGFBPs expressed in the glomerular and tubulointerstitial compartments during diabetic renal growth have not been characterized. In the present study, in situ hybridization studies were performed to examine the expression of IGFBP-1 to -6 messenger RNAs (mRNAs) 3, 7, and 14 days after streptozotocin (STZ) injection in rats. In control, nondiabetic kidneys, all six IGFBP mRNAs were differentially expressed with a predominance of IGFBP-5. The onset of renal hypertrophy in STZ-induced diabetes was associated with a rapid and site-specific induction of IGFBP-1, -3, and -5 mRNAs. In contrast, basal expression of IGFBP-2, -4, and -6 mRNAs was not altered in diabetic rats. IGFBP-5 mRNA expression increased in diabetic glomeruli, cortical, and inner medullary peritubular interstitial cells at days 3, 7, and 14. Although normal glomeruli failed to express IGFBP-3, it was induced concomitantly with IGFBP-5 in diabetic glomeruli and cortical peritubular interstitial cells. IGFBP-1 mRNA levels also increased in cortical tubular cells at each time point tested. Peak induction of IGFBP-3 and -5 was observed at day 3, whereas IGFBP-1 was delayed until day 7. IGFBP-1, -3, and -5 mRNA levels declined by day 14, but remained persistently elevated above control. By immunoperoxidase staining, similar alterations in the pattern of IGFBP-3 and -5 protein expression were observed at each time point. The preferential and site-specific increase in IGFBP-1, -3, and -5 suggest that these IGFBPs may regulate the local autocrine and/or paracrine actions of IGF-I and contribute to the pathogenesis of the early manifestations of diabetic nephropathy.     

移植于脊髓的断离肋间神经重发新支至原去神经肋间肌的实验观察

将15只大鼠左侧第11或12肋间神经从根部向外,自周围组织完全分离出20～35mm,并于此处剪断。再将其近端改向植入脊髓左侧半 L_(1～2) 之间的髓节内。在存活57～413天后解剖观察,发现自移植神经的干上发出1～3条新分支,分布于原去神经的肋间肌。经光、电镜观察证实是成活的再生神经纤维。于移植神经干注射 CB-HRP 后,发现这些神经纤维来源于原肋间神经髓节的前角和移植部髓节内的神经细胞。故认为外周神经缺损,不作神经对接或桥接,不经断离神经的远段,在一定条件下可以由近段发出再生纤维组成新支,分布于去神经的靶组织。     

香萱解郁方对血清剥夺诱导HT22细胞损伤模型的神经保护作用

探讨香萱解郁方含药血清对血清剥夺致小鼠海马神经元HT22细胞损伤模型的影响。方法 采用血清剥夺培养HT22细胞建立神经损伤体外模型,实验分为对照组、模型组和中药组［中药组A（含药血清15%浓度）、中药组B（含药血清20%浓度）］,各组血清剥夺12 h后,通过CCK8法检测各组细胞活力,确定15%浓度含药血清干预后细胞的存活率最高,设定为后续实验中药组的药物浓度。免疫荧光染色法检测神经元特异性微管蛋白（β-Tubulin Ⅲ）在各组中的表达,蛋白质免疫印迹法及qPCR法检测脑源性神经营养因子（BDNF）蛋白及其mRNA在各组中的表达。结果 在加药后培养12 h,中药组的细胞活力明显高于对照组与模型组（P＜0.001）。培养24 h,模型组细胞活力较对照组明显下降（P＜0.001）,中药组较模型组明显提高（P＜0.001）。培养36 h,模型组细胞活力较对照组显著下降（P＜0.001）,中药组较模型组明显提高（P＜0.001）。模型组BDNF蛋白含量及 BDNF mRNA表达量较对照组显著降低（P＜0.05,P＜0.001）,模型组少数神经元长出突起;中药组BDNF蛋白含量及BDNF mRNA表达量较模型组显著增加（P＜0.05）,中药组HT22细胞轴突突起长度和分支增加,β-Tubulin Ⅲ阳性表达明显增多。结论 香萱解郁方含药血清对血清剥夺诱导小鼠海马神经元HT22细胞损伤具有神经保护作用,可能与促进BDNF蛋白表达有关     

The nuclear pore complex protein Tpr is a common autoantigen in sera that demonstrate nuclear envelope staining by indirect immunofluorescence

We studied the autoantigen targets of 75 human sera that had antibodies to the nuclear envelope (NE) as identified by indirect immunofluorescence (IIF) on HEp‐2 cells. Several different IIF staining patterns could be identified when antibodies to different components of the nuclear membrane (NM) and nuclear pore complexes (NuPC) were identified: a smooth membrane pattern characteristic of antibodies to nuclear lamins, a punctate pattern typical of antibodies to the nuclear pore complex and more complex patterns that included antibodies to nuclear and cytoplasmic organelles. Western immunoblotting of isolated nuclear and NE proteins and immunoprecipitation of radiolabelled recombinant proteins prepared by using the full‐length cDNAs of the Translocated promoter region (Tpr), gp210 and p62 were used to identify specific autoantibody targets. Fifty‐two of the 75 (70%) sera bound to Tpr, 25 (33%) bound to lamins A, B or C, 15 (20%) reacted with gp210 and none reacted with p62. Sixteen (21%) did not react with any of the NE components tested in our assays. The clinical features of 37 patients with anti‐NE showed that there were 34 females and three males with an age range of 16–88 years (mean 59 years). The most frequent clinical diagnosis (9/37 = 24%) was autoimmune liver disease (ALD; two with primary biliary cirrhosis), followed by seven (19%) with systemic lupus erythematosus (SLE), four (11%) with a motor and/or sensory neuropathy, three (8%) with anti‐phospholipid syndrome (APS), two with systemic sclerosis (SSc), two with Sjögren's syndrome (SjS), and others with a variety of diagnoses. This report indicates that Tpr, a component of the NuPC, is a common target of human autoantibodies that react with the NE.