催老小鼠重要脏器氧化水平和抗氧化能力的变化

目的　研究D 半乳糖催老小鼠心、肝、脑、肺、肾等重要脏器氧化水平和抗氧化能力的改变 ,并对其进行比较。　 方法 　 2 0只 2月龄雄性小鼠随机分为催老组和正常对照组 ;催老组每日皮下注射D 半乳糖 10 0mg·kg-1,正常对照组每日皮下注射等量生理盐水 ,持续 42d。以丙二醛 (MDA)含量反映氧化水平 ,超氧化物歧化酶(SOD)活性反映抗氧化能力。　 结果 　与正常对照组相比 ,D 半乳糖催老组小鼠心、肝、脑、肺、肾等重要脏器MDA含量明显增加 (P <0 0 1) ;肝、脑、肺和肾的SOD活性显著降低 (P <0 0 5 ) ,而心脏SOD活性无明显变化。　 结论　D 半乳糖催老小鼠心、肝、脑、肺、肾等重要器官氧化水平增加 ;肝、脑、肺、肾等器官抗氧化水平下降 ;各器官在改变程度上存在一定差异     

来曲唑联合地塞米松对多囊卵巢综合征患者血清Galectin-3及HSP70的影响

目的 探讨来曲唑联合地塞米松对多囊卵巢综合征(PCOS)患者血清半乳糖凝集素-3(Galectin-3)及热休克蛋白(HSP70)表达的影响。方法 选择2019年6月—2021年6月在我院治疗的PCOS患者220例为研究对象,按随机数表法分为对照组(n=110)和观察组(n=110),对照组常规给予来曲唑治疗。观察组在对照组的基础上加用地塞米松联合治疗。观察并比较两组患者的激素水平,促排卵情况,血清抗苗勒管激素(AMH)、Galectin-3、HSP70及单核细胞趋化蛋白-1(MCP-1)水平及不良反应发生率。结果 治疗后两组患者的性激素水平均改善,且观察组变化幅度高于对照组(P<0.05)。观察组患者雌二醇(E₂)用量低于对照组,成熟卵泡数量和最大卵泡直径均高于对照组(均P<0.05)。两组患者的早期流产率差异无统计学意义(P>0.05);观察组患者的妊娠率高于对照组(P<0.05)。治疗前两组患者AMH、Galectin-3、HSP70、MCP-1水平差异无统计学意义(P>0.05),治疗后两组患者的AMH、Galectin-3、...     

芪苈强心胶囊配合保元汤加减治疗慢性心力衰竭临床研究

目的:观察芪苈强心胶囊配合保元汤加减用于慢性心力衰竭的治疗效果。方法:选取收治的慢性心力衰竭患者104例作为研究对象,运用随机数字表法将其分为观察组(52例)和对照组(52例),两组患者均接受常规治疗,对照组采用保元汤治疗,观察组同时应用芪苈强心胶囊联合保元汤治疗。观察患者治疗前及治疗后6个月的6 min步行试验的步行距离(6MWD)及纽约心脏病学会心功能分级(NYHA)、血清学指标N末端B型利尿钠肽原(NT-proBNP)、半乳糖凝集素3(Galectin-3)及白介素6(IL-6)、超敏C反应蛋白(hs-CRP)、肿瘤坏死因子α(TNF-α)、心脏指数(CI)、左室射血分数(LVEF)、左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)、左室重量指数(LVMI)和室壁运动指数(WMI)、左室间隔厚度(IVST)变化情况。结果:治疗前后,两组患者比较心功能指标、Galectin-3、炎性因子指标、心室重构指标差异有统计学意义(P<0.05); 观察组与对照组患者相比,6 min步行距离、CI、LVEF、升高更为显著(P<0.05); 观察组患者NYHA分级、NT-proBNP、Galectin-3、IL-6、hs-CRP、TNF-α、LVEDD、LVESD、LVMI、WMI、IVST降低更为显著(P<0.05)。结论:芪苈强心胶囊辅助保元汤加减能够有效改善慢性心力衰竭患者心脏功能,有利于患者体内炎性因子及Galectin-3水平降低,抑制心室重构进展,患者心脏舒缩功能改善效果更佳。     

Galactose metabolites in blood from neonates with and without hypergalactosaemia detected by mass screening

Concentrations of galactose (Gal) in plasma and galactose metabolites in red blood cells (RBC) were determined in 18 normal neonates and 249 others with hypergalactosaemia according to the Paigen method. Normal neonatal values for plasma Gal, RBC galactose-1-phosphate (Gal-1-P), RBC uridine diphosphate glucose (UDP-Glc), and RBC uridine diphosphate galactose (UDP-Gal) were 0.96 ± 0.71 mg/dl, 1.69 ± 1.45 mg/dl of packed RBC, 1.00 ± 0.45 mg/dl of packed RBC, and 1.44 ± 0.45 mg/dl of packed RBC, respectively. The UDP-Gal concentration was higher and the UDP-Glc concentration lower than previously reported in normal children. Of the 249 cases with excessive Gal in whole blood, 23 showed high Gal concentrations in plasma; among these, four portacaval shunts and one case of congenital biliary atresia were diagnosed. In subjects homozygous or heterozygous for UDP-Gal-4 epimerase deficiency, concentrations of UDP-Gal and Gal-1-P were elevated only in RBC, corresponding to restriction of the metabolic abnormality to these cells. Most cases of hypergalactosaemia detected by the Paigen method have large excesses of Gal-1-P in RBC. Although a specific diagnosis based solely on blood Gal metabolites is difficult, individual concentrations reflect underlying conditions to some extent. Conclusion In neonates, uridine diphosphate galactose concentrations were higher and uridine diphosphate glucose concentrations were lower than previously reported paediatric values. Patients with high plasma galactose concentrations should be investigated by hepatic imaging. Received: 21 March 2000 / Accepted: 18 May 2000     

半乳糖氧化酶试验检测大肠癌

用半乳糖氧化酶-雪夫液方法检测35例结直肠癌及癌前病变组织切片中的β-D-GalGalNAc,94.28n/o阳性。制成试纸检测924例肛检粘液涂片。3.14％阳性。12例结直肠癌及5例癌前病变(腺瘤3,异型增生2)呈阳性,敏感性为91.14％(17/18),阳性预检值58.62％(17/29)。有结直肠症状组阳性率显著高于无症状组(P相似文献   

Peripheral nerve structure and function in long-term galactosemic dogs: morphometric and electron microscopic analyses

Experimental galactosemia for activating the polyol pathway is used extensively to explore the pathogenesis of diabetic complications. However, despite the presence of severe neuropathy in galactosemic rats, changes in the peripheral nerve have not been well established in galactosemic dogs. We therefore conducted biochemical, electrophysiological, and morphometric studies on peripheral nervous systems (PNS) in dogs given a 30% galactose diet for 44 months. Age- and sex-matched dogs given a 30% cellulose diet were used as control. Chronic galactosemia resulted in accumulation of galactitol and decrease in myo-inositol in the sciatic nerve. Electrophysiological and teased fiber analyses demonstrated no significant abnormalities in the ulnar and peroneal nerves in galactosemic dogs. Morphometric analyses revealed a tendency of myelinated fiber atrophy (24% reduction of average fiber size) associated with 20% decrease (P < 0.05 vs control) in mean myelinated fiber occupancy rate in the peroneal nerve in galactosemic dogs. In the anterior mesenteric ganglion, there was a slight but significant increase (8%) in mean neuronal cell size in galactosemic dogs (P < 0.05 vs control). Electron microscopy revealed that galactosemia did not produce dystrophic and degenerative changes in the autonomic ganglion in dogs. We conclude that structural and functional changes in the PNS of galactosemic dogs are mild and different from those of the rat model. These findings suggest that the severity of peripheral neuropathy induced by chronic galactosemia may be species dependent. Received: 10 July 1998 / Revised: 10 October 1998 / Accepted: 21 October 1998     

Metabolism of galactose in the brain and liver of rats and its conversion into glutamate and other amino acids

Time- and dose-dependent measurements of metabolites of galactose (with glucose as control) in various organs of rats are discussed. Not only the liver but especially the brain and to a lesser extent the muscles also have the capacity to take up and metabolize galactose. Primarily, the concentrations of UDP-galactose, a pivotal compound in the metabolism of galactose, and UDP-glucose are measured. An important feature lies in the demonstration that galactose and glucose are metabolized to amino acids and that the only increases observed in the brain appear in the concentrations of glutamate, glutamine, GABA measured after acute galactose loads. In addition the increase in the amino acid concentrations after galactose has been administered persists for longer periods of time than after glucose administration. This conversion of hexoses, especially galactose, to amino acids requires the consumption of ammonia equivalents in the brain; this finding might stimulate the use of galactose as a new means of removal of this neurotoxic compound from the brain in patients suffering from hepatic encephalopathy or Alzheimer’s disease.     

拟阿尔茨海默病大鼠模型中肠源性内毒素血症水平的研究

目的： 探索在D-半乳糖和三氯化铝(AlCl3)联合使用制备拟阿尔茨海默病(AD)动物模型是否伴有肠源性内毒素血症(IETM)。方法：选用Wistar大鼠,腹腔注射D-半乳糖和AlCl3,连续90 d,制备拟AD大鼠模型。给药结束后,通过Morris水迷宫观察模型大鼠学习记忆能力,鲎试剂法测定体内内毒素(LPS)水平,放射免疫法检测体内肿瘤坏死因子(TNF-α)、白细胞介素-1 (IL-1)水平,半定量RT-PCR技术检测大鼠海马β淀粉样前体蛋白(APP)、早老素1(PS1)、β位点APP内切酶(BACE)的mRNA表达。结果：拟AD模型大鼠血浆中LPS水平升高,海马APP mRNA、PS1 mRNA与BACE mRNA表达均明显升高(P<0.01)。结论：在D-半乳糖和AlCl3联合使用制备拟AD大鼠模型中有IETM的发生,并可能在AD发病中发挥重要作用。     

Noggin蛋白对D 半乳糖致衰老小鼠学习记忆及海马齿状回神经发生的影响

目的观察侧脑室注射Noggin蛋白后对D 半乳糖致衰老模型小鼠学习记忆行为能力与海马齿状回神经发生的影响。方法采用皮下注射D 半乳糖构建衰老小鼠模型后,连续7?d侧脑室注射Noggin蛋白,对照组同时注射等量生理盐水,造模42?d后对各组小鼠进行Y迷宫学习记忆能力测试,用BrdU标记海马齿状回增殖细胞。 结果Y迷宫检测结果表明,模型组小鼠学习记忆能力较正常对照组明显降低（P<0.05）,而模型治疗组小鼠学习记忆能力较模型对照组明显改善（P<0.05）;模型组与模型对照组小鼠海马齿状回BrdU阳性细胞数较正常对照组减少（P<0.05）,而模型治疗组BrdU阳性细胞数较模型组、模型对照组显著增多（P<0.05）。结论侧脑室给予Noggin蛋白可改善衰老模型小鼠的空间学习及记忆能力,可能与Noggin能保护海马神经元并促使齿状回神经干细胞增殖有关。        

New insights in the pathogenesis of immunoglobulin A vasculitis (Henoch-Schönlein purpura)

Immunoglobulin A vasculitis (IgAV), also referred to as Henoch-Schönlein purpura, is the most common form of childhood vasculitis. The pathogenesis of IgAV is still largely unknown. The disease is characterized by IgA1-immune deposits, complement factors and neutrophil infiltration, which is accompanied with vascular inflammation. Incidence of IgAV is twice as high during fall and winter, suggesting an environmental trigger associated to climate. Symptoms can resolve without intervention, but some patients develop glomerulonephritis with features similar to IgA nephropathy that include hematuria, proteinuria and IgA deposition in the glomerulus. Ultimately, this can lead to end-stage renal disease. In IgA nephropathy immune complexes containing galactose-deficient (Gd-)IgA1 are found and thought to play a role in pathogenesis. Although Gd-IgA1 complexes are also present in patients with IgAV with nephritis, their role in IgAV is disputed. Alternatively, it has been proposed that in IgAV IgA1 antibodies are generated against endothelial cells. We anticipate that such IgA complexes can activate neutrophils via the IgA Fc receptor FcαRI (CD89), thereby inducing neutrophil migration and activation, which ultimately causes tissue damage in IgAV. In this Review, we discuss the putative role of IgA, IgA receptors, neutrophils and other factors such as infections, genetics and the complement system in the pathogenesis of IgA vasculitis.