Spermidine/Spermine N-Acetyltransferase, a New Biochemical Marker for Epithelial Proliferation in Rat Bladder

We examined the activity of spermidine/spermine N ¹-acetyltransferase (SAT), a rate-limiting enzyme of the biodegradation of polyamines, in N -butyl- N -(4–hydroxybutyI)nitrosamine-induced transitional cell carcinoma (TCC) and melamine-induced papillomatosis of rat bladder, and compared the activity to that of ornithine decarboxylase (ODC). Both activities were higher in both lesions than in control rats. The difference between SAT and ODC activities in cancerous tissue and papillomatosis was not significant. Cells stained for proliferating cell nuclear antigen (PCNA) were abundant in papillomatosis. TCC had areas with much PCNA. The results indicated that an elevation of SAT activity occurs in both reversible and irreversible proliferation of bladder epithelium and could be important in bladder carcinogenesis.     

Testicular amplificaion and impaired transmission of human butyrylcholinesterase cDNA in transgenic mice

Gene amplification occurs frequently in tumour tissues yet is,in general, non-inheritable. To study the molecular mechanismsconferring this restraint, we created transgenic mice carryinga human butyrylcholinesterase (BCHE) coding sequence, previouslyfound to be amplified in a father and son. Blot hybridizationof tail DNA samples revealed somatic transgene amplificationswith variable restriction patterns and intensities, suggestingthe occurrence of independent amplification events, in 31% (11/35)of mice from the FII generation but in only 3.5% (2/58) of theFII and FIV generations. In contrast, >10-fold amplificationsof the BCHE transgene and the endogenous acetylcholinesteraseand c-raf genes appeared in both testis and epididymis DNA from>80% of FIII mice. Drastic, selective reductions in testisBCHEmRNA but not in actin mRNA were detected by the PCR amplificationof testis cDNA from the transgenic mice, and apparently resultedin the limited transmission of amplified genes. The testicularamplification of the BCHE transgene may potentially representa general phenomenon with clinical implications in human infertility.     

卵巢恶性肿瘤的雌孕激素受体研究

用葡聚糖－活性碳吸附法（ＤＣＣ法）对８７例卵巢恶性肿瘤的雌激素受体（ＥＲ）及孕激素受体（ＰＲ）进行了测定。ＥＲ、ＰＲ的阳性率分别为５０．６％和５８．６％。在不同组织类型中，宫内膜样癌的ＥＲ与ＰＲ高于其它癌。ＰＲ与临床分期呈负相关。多因素分析显示ＥＲ、ＰＲ均阳性者预后好。ＥＲ与ＰＲ的测定有助于了解病人预后，对卵巢癌的内分泌治疗有一定指导作用。     

同种肾组织移植治疗慢性肾功能衰竭性贫血的实验研究

以Ｗｉｓｔａｒ雄性大鼠为受体，建立慢性肾功能衰竭动物模型，将鼠婴肾组织声多点植入受体双侧后肢皮下和筋膜下。结果表明，３０天后移植物的体积由１ｍｍ＾３增至４ｍｍ＾３大小，表面血管网丰富；光镜下见肾小球、肾小管结构正常。促红细胞生成素（ＥＰＯ）着色颗粒主要分布在肾小球区，移植组着色程度明显增高。血红蛋白和４促红细胞生成素随移植的时间延长而逐渐升高，实验结果提示，此方法有可能为治疗慢性肾功能衰竭性贫血提     

黄芪口服液治疗病毒性心肌炎50例

50例(男31,女19;年龄37±9a)症状未恢复且有免疫失控的病毒性心肌炎患者经黄芪口服液(健心饮)15g;bid;治疗3-6mo后,α-干扰素效价明显升高。在46例中测得天然杀伤细胞活性亦明显增高。11例进行核素心血管造影,治疗后左室功能明显改善。另12例予维生素C,辅酶A,脱氧核糖核酸等一般治疗者则无上述效应。提示黄芪口服液有调节患者免疫失控及改善心功能的作用。     

甲状腺功能亢进症患儿合并糖代谢紊乱10例临床分析

目的：探讨儿童甲亢患者糖代谢紊乱的特点。方法：用SUPER GLUCOCARD^TM血糖仪和放射免疫方法检测29例甲亢患儿餐前、餐后60min、120min血糖和餐前、餐后60min胰岛素、C肽、胰高糖素、皮质醇及T3、T4、TSH、TGA、TMA（其中10例糖耐量减低为甲亢1组，另19例糖耐量正常为甲亢2组），并与20例健康儿童进行比较。结果：（1）34．5％甲亢患儿出现糖代谢紊乱，病程大于1年和小于1年糖代谢紊乱发生率为50％，9％（P＜0．05）。（2）甲亢1组餐后60min胰岛素、胰岛素／血糖、胰岛素／胰高糖素显著升高（P＜0．05）。结论：甲亢儿童存在糖代谢紊乱现象，表现为葡萄糖耐量减低和胰岛素拮抗，其发生与病程有关，病程较长，发生率较高。糖代谢紊乱可能与自身免疫、胰岛β细胞功能受损及胰岛素拮抗有关。     

冠心病中医辨证与载脂蛋白关系的初步研究

对９６例各种类型冠心病患者进行中医辨证分型，检测其血清载脂蛋白ＡⅠ及Ｂ１００（ａｐｏＡⅠ及ａｐｏＢ１００），并设立对照组。结果显示各证型冠心病患者的ａｐｏＡⅠ，ａｐｏＢ１００及ａｐｏＢ１／ａｐｏＡⅠ均有不同程度的改变。在标实证中以痰浊型改变最为明显，其ａｐｏＡⅠ显著降低，ａｐｏＢ１００及ａｐｏＢ１００／ａｐｏＡⅠ显著升高。在本虚证型中以肾虚型改变最为明显、其ａｐｏＡⅠ显著降低。ａｐｏＢ１００／ａｐｏＡⅠ显著升高。这种各证型间的差异无疑对冠心病的中医辨证客观化有一定意义，值得进一步验证和探讨。     

Treatment of established osteoporosis with 1α (OH) vitamin D3 and low dose intermittent elcatonin (eel calcitonin derivative)

In addition to estrogen widely used all over the world for the prevention of postmenopausal osteoporosis, calcitonin and vitamin D derivatives are commonly employed to treat established osteoporosis at higher age in Japan. In order to critically assess the usefulness of vitamin D derivatives and calcitonin alone or in combination on the advancement of vertebral deformity at higher age, 32 osteoporotic patients with vertebral deformity with the mean age of 79 were randomly divided into 4 groups with indistinguishable age and severity of the vertebral deformity. Group 1 served as the control without specific medications for osteoporosis. Group 2 was treated with 10 units elcatonin (eel calcitonin derivative) injected intramuscularly twice a week. Group 3 was given 0.75 to 1.5μg/day 1α (OH) vitamin D₃ orally. Group 4 was given a combination of treatments used in Groups 2 and 3. In the lateral X-ray film of the spine taken prior to the test and every 6 months thereafter, the shape of the vertebral body T₈ through L₄ was monitored by measuring the anterior, central and posterior heights. Decrease of the vertebral height ratio; anterior or middle height/posterior or adjacent intact posterior height, by more than 20% of the original value or from above to below 0.80 both appeared to be inhibited during administration of 1α (OH) vitamin D₃. Such effect seems to be augmented by simultaneous administration of elcatonin. Actual decrease of vertebral height ratio values and the per cent fall from the original value significantly less in Groups 3 and 4 than in Group 1. Development of vertebral deformity assessed by the changes of the vertebral height thus appears to decrease during treatment with 1α (OH) vitamin D₃ especially together with calcitonin in established osteoporosis.     

Large French-Canadian family with Lewy body parkinsonism: exclusion of known loci.

The identification of rare, large families with Parkinson's disease (PD) has provided important clues that have contributed to our understanding of this complex disorder. We have identified a large French-Canadian kindred that spans five generations consisting of more than 90 individuals. A total of 65 individuals now have been examined, had venous blood drawn, and DNA extracted. Two-point and multipoint linkage analysis was performed to assess linkage to known PD genes or loci. Within the third and fourth generations of this family there are 10 living, plus 3 deceased members with well-documented levodopa responsive parkinsonism. Autopsy results on 1 member demonstrated the loss of pigmented neurons in the substantia nigra and the presence of alpha-synuclein positive Lewy bodies. Four of the PD patients have prominent postural and kinetic tremors that preceded their parkinsonism by up to 10 years. Two other individuals within the family have prominent isolated postural and kinetic tremors without parkinsonism. The alpha-synuclein(4q21.3-23), Parkin(6q25.2-27), PARK3 (2p13), PARK4, and ubiquitin carboxy terminal hydrolase-L1 (4p14-16.3) and PARK6 and PARK7 (1p35-36) loci were excluded in this kindred using closely linked markers. The clinical and pathological features of this family are consistent with the diagnosis of PD. This family further demonstrates the known genetic heterogeneity in PD and is large enough that a genome-wide screen has been undertaken in an effort to identify a novel PD gene.