滋肾宁神胶囊对 D-半乳糖所致亚急性衰老模型大鼠的影响

[目的]观察滋肾宁神胶囊对D-半乳糖所致亚急性衰老模型大鼠的影响.[方法]选用SD大鼠随机分成空白对照组,模型组,七宝美髯丸组(剂量为2 g·kg-1·d-1),滋肾宁神丸组(剂量为3.33 g·kg-1·d-1),滋肾宁神胶囊高、中、低剂量组(剂量分别为9.96、4.98、2.49 g·kg-1·d-1);除空白对照...     

取代苄基/萘甲基异喹啉类及有关季铵衍生物的合成与生物活性

以具心血管活性的异喹啉类生物碱为先导物,结合某些钾通道阻滞剂的结构特征,设计合成了28个3,4-二氢(I_1～4)和1,2,3,4-四氢苄基/萘甲基异喹啉化合物(II_1～18)及有关季铵衍生物(I_5,6和II_19～22)。药理试验表明:除化合物I₄有一定升压作用外,大多化合物有不同程度的降压和减慢心率活性,其中化合物II1的降压活性最强。分析定量构效关系发现:化合物母核氮原子电荷愈大(即其绝对值愈小),降压作用愈强;反之,减慢心率作用愈强。异喹啉母核氮原子电荷可能为影响作用于血管或心脏组织的重要因素之一。     

是否存在超微小梁？一骨小梁微破裂及微骨痂的扫描电镜观察

目的应用扫描电镜观察骨小梁微破裂形态及微骨痂的微观结构，探讨微骨痂的超微结构特征。方法取63周龄雌性SD大鼠第6腰椎椎体，沿冠状面切开，蒸馏水冲洗净骨髓腔后乙醇梯度脱水，表面喷金后应用扫描电镜观察，在600倍下观察骨小梁微破裂以及微骨痂的形态，在2000倍和10000倍下观察微骨痂的细微及超微结构。结果观察到微破裂长度约80μm，在骨微破裂一端靠近小梁边缘处，可见有微骨痂形成，微骨痂为一种疏松多孔的海绵状结构，其超微结构呈珊瑚礁形貌，由直径约0．2～0．5μm大小网状排列的骨小梁类似结构构成。结论在微骨痂修复微破裂过程中可能存在一种“超微小梁”结构，这种结构对于受损骨小梁承受应力以及修复均有利。     

中医药干预治疗难治性肾病综合征研究进展

难治性肾病综合征（RNS），是指原发性肾病综合征经过强的松标准治疗无效者或经强的松的标准疗程治疗能缓解，但经常复发（1年内复发3次或半年内发作超过2次以上）者，约占原发性肾病综合征的39．9％-53．8％，目前西医常采用激素和细胞毒药物治疗，虽近期取得一定的疗效，但易复发并存在诸多副作用。鉴于此，临床医学研究者对中医药干预治疗难治性肾病综合症的研究越来越多，并积累大量的经验，本文就近5年来其有关文献综述如下。     

Carrier detection and presymptomatic identification of Wilson disease in Chinese by non-isotopic linkage analysis with four short tandem repeat polymorphisms

Ｗｉｌｓｏｎｄｉｓｅａｓｅ（ＷＤ）ｉｓａｎａｕｔｏｓｏｍａｌｒｅｃｅｓｓｉｖｅｄｉｓｏｒｄｅｒｏｆｃｏｐｐｅｒｍｅｔａｂｏｌｉｓｍｗｉｔｈａｗｏｒｌｄｗｉｄｅｆｒｅｑｕｅｎｃｙｏｆｂｅｔｗｅｅｎ１／５０００ａｎｄ１／３００００ｉｎｌｉｖｅｂｉｒｔｈｓ...     

胃疡安胶囊治疗消化性溃疡疗效观察

目的：观察胃疡安胶囊治疗消化性溃疡近期及远期疗效。方法：用胃疡安胶囊治疗消化性溃疡80例（胃溃疡29例,十二指肠球部溃疡51例）,与用雷尼替丁治疗的40例（胃溃疡12例,十二指肠球部溃疡28例）作对照,治疗30天评定近期疗效,随访1年观察远期疗效。结果：近期临床疗效及盲镜检查结果,治疗组均优于对照组（P＜0.05,P＜0．005）。随访观察近期治愈患者停药1年后溃疡复发情况,治疗组胃溃疡复发率为8．7％,十二搭肠球部溃疡复发率为9．3％;对照组胃溃疡复发率为60％,十二指肠球部溃疡复发率为58．8％,对照组复发率明显高于治疗组,治疗组远期疗效优于对照组（P＜0．01,P＜0．005）。结论：胃疡安胶囊为治疗消化性溃疡的有效药物,可降低消化性溃疡治疗后的复发率。     

Molecular analysis of 51 unrelated pedigrees with late-onset multiple acyl-CoA dehydrogenation deficiency (MADD) in southern China confirmed the most common <Emphasis Type="BoldItalic">ETFDH</Emphasis> mutation and high carrier frequency of c.250G>A

Multiple acyl-CoA dehydrogenation deficiency (MADD) is an autosomal recessive disease affecting amino acid, fatty acid, and choline metabolisms and is a common genetic defect responsible for lipid storage myopathy. Most forms of MADD are caused by a deficiency of electron transfer flavoprotein (ETF) or ETF dehydrogenase (ETFDH). However, its molecular feature has not been found uniformly in previous reports of Chinese patients. A large cohort of 56 late-onset MADD patients from 51 unrelated pedigrees in southern China was recruited to investigate a clear correlation between clinical phenotype and molecular genetic basis. All exons of ETFA, ETFB, and ETFDH, including the intron–exon boundaries, and 5′ and 3′ untranslated regions were directly sequenced. ETFDH deficiencies affected 94.1% (48/51) of the pedigrees. ETFDH-c.250G>A is the most common mutation, representing a high allelic frequency of 83.3% (80/96). Carrier frequency of c.250G>A is estimated to be 1.35% (7/520) in the normal population. A significant reduced expression of ETFDH was identified in the muscle of ETFDH-deficient patients. ETFDH deficiency is a major cause of riboflavin-responsive MADD in southern China, and c.250G>A is an important mutation that could be employed as a fast and reliable screening method.     

Molecular analyses of GCH-1, TH and parkin genes in Chinese dopa-responsive dystonia families

The symptomatic treatment of dopa-responsive dystonia (DRD) emphasizes the importance of molecular analyses of the GCH-1, TH and parkin genes. However, these analyses have not been extensively studied in Chinese DRD patients. Ten DRD families from the Han ethnic group including 14 patients and 28 clinically unaffected relatives were screened for GCH-1, TH and parkin mutations by direct sequencing, semiquantitative polymerase chain reaction (PCR), polymerase chain reaction-restriction fragment length polymorphism analysis and allele-specific PCR. Variations were verified in 200 unrelated control subjects. We have identified six novel mutations and three known mutations. The novel mutations are Leu91Val, Pro95Leu, Val204Gly and 628delC in GCH-1 gene; Gly216Ser in TH gene; and Cys253Phe in parkin gene. After molecular analyses of seven families with identified GCH-1 mutations, nine asymptomatic cases were found among 23 relatives, which confirmed the low penetrance of DRD. Unlike previous publications, male patients with GCH-1 mutations have early onset ages, while some female patients have very late onset ages in this medium-size series. Our data show that it is difficult to establish an evident genotype-phenotype correlation for DRD. However, it is necessary to know the genetic defects of DRD patients in clinics, which will help elucidate the mode of inheritance, facilitate causal therapy with levodopa and evaluate the prognosis.