Construction of retroviral vectors to induce a strong expression of human interferon-β gene in human hepatoma cells

ClassIinterferonisapotent1mmunemodu-latingfactorinvivo,andplaysanimportantrolelnactivatinganti-tumorcytotoxicTlymphocytesandnonuspecificeffectorcellssuchasNKcellsLlJ.ln-terferonandmanyothercytokinegeneswereintro-ducedintotumorcells,tumorinterstitialcellsandtumorinfiltratinglymphocytes['-']inordertosustainaneffectiveanti-tumorconcentrationofcy-tokinelocatedattumorsites.Itwasshownthatsomecytokinegenemodifiedtumorcellslosttheirtumorigenicityandinhibitedthegrowthofparentaltumorinanimalmodels.Pra…     

Study of the role of vitamin B12 and folinic acid supplementation in preventing hematologic toxicity of zidovudine

Abstract: A prospective, randomized study was conducted to evaluate the role of vitamin B₁₂ and folinic acid supplementation in preventing zidovudine (ZDV)-induced bone marrow suppression. Seventy-five human immunodeficiency virus (HIV)-infected patients with CD4 + cell counts < 500/mm³ were randomized to receive either ZDV (500 mg daily) alone (group I, n = 38) or in combination with folinic acid (15 mg daily) and intramascular vitamin B₁₂ (1000 μg monthly) (group II, n = 37). Finally, 15 patients were excluded from the study (noncompliance 14, death 1); thus, 60 patients (31 in group I and 29 in group II) were eligible for analysis. No significant differences between groups were found at enrollment. During the study, vitamin B₁₂ and folate levels were significantly higher in group II patients; however, no differences in hemoglobin, hematocrit, mean corpuscular volume, and white-cell, neutrophil and platelet counts were observed between groups at 3, 6, 9 and 12 months. Severe hematologic toxicity (neutrophil count < 1000/mm³ and/or hemoglobin < 8 g/dl) occurred in 4 patients assigned to group I and 7 assigned to group II. There was no correlation between vitamin B₁₂ or folate levels and development of myelosuppression. Vitamin B₁₂ and folinic acid supplementation of ZDV therapy does not seem useful in preventing or reducing ZDV-induced myelotoxicity in the overall treated population, although a beneficial effect in certain subgroups of patients cannot be excluded.     

特发性甲状旁腺功能低下（附13例分析）

本文观察分析了13例特发性甲状旁腺功能低下患者、查PTH6例。患者血清中除有本病低血钙、高血磷的固有特征外，其它微量元素也有改变，如血清镁值减低。这与文献[1]的报道相符。碱性磷酸酶2例明显升高。磷廓清率S例降低。肾小管磷重吸收率5例升高。放免甲功：抗甲状腺微粒体2例升高。T细胞亚群1例低于正常值。本病有家族性，与遗传有关。     

育龄妇女月经周期中心血管功能的变化

本研究采用先进的三维超声成像技术及多普勒技术对正常育龄妇女月经周期中心血管功能进行研究。结果：月经周期中ＨＲ、ＢＰ无变化；血清Ｅ２是周期性变化，排卵前达高峰。ＳＶ、ＣＯ、ＥＦ在排卵前期升高达峰值，显著高于月经期和黄体期；ＳＶＲ排卵前期最低，而Ｖｅｄ、Ｖｅｓ无变化。Ｖｍａｘ、Ａ、Ｅ在内源性Ｅ２高峰时明显加快，而Ｅ／Ａ比值无明显变化。结果提示：月经周期中随内源性Ｅ２的周期性变化，心脏功能也发生周期性变化。Ｅ２高峰时，心输出量、心搏量和射血分数达最高。外周阻力最低，心脏内血流速度加快。     

白血病患者血清铜、锌的变化

本文报道57例白血病血清铜,锌含量的测定结果。白血病治疗前血清铜升高,铜/锌值增大;治疗后,病情缓解者下降,未缓解者则更高。血清锌在治疗前后无何差异。急性淋巴细胞性白血病骨髓中白血病细胞百分数与血清铜浓度呈正相关。检测血清铜,锌对白血病疗效的预测及判断预后有一定意义。     

实验性骨折愈合中骨吸收活动的超微结构观察

将50只家兔造成实验性桡骨骨折,分批取骨痂标本,用光镜和电子显微镜观察表明,在骨折愈合过程中,破骨细胞是骨吸收的主要执行者,巨噬细胞能吞噬死骨,但不能吸收骨质。     

黑蔓不同部位微量元素的测定

为了了解吉林省长白县山区所产卫矛科雷公藤属植物黑蔓的药理作用,扩大它的药用部位和应用范围,我们从无机元素与中药药效有密切关系的角度出发,实验测出黑蔓含有Ba、Si、Cu、Fe、Zn、Sn、Co、Mn、Mg、Ca、Se等无机元素,本文重点对其中人体必需的微量元素Cu、Fe、Zn、Se作了定量分析。     

Skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) by inhibiting activation of the IGF-I signaling pathways.

We showed that unloading markedly diminished the effects of IGF-I to activate its signaling pathways, and the disintegrin echistatin showed a similar block in osteoprogenitor cells. Furthermore, unloading decreased alphaVbeta3 integrin expression. These results show that skeletal unloading induces resistance to IGF-I by inhibiting activation of the IGF-I signaling pathways at least in part through downregulation of integrin signaling. INTRODUCTION: We have previously reported that skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) with respect to bone formation. However, the underlying mechanism remains unclear. The aim of this study was to clarify how skeletal unloading induces resistance to the effects of IGF-I administration in vivo and in vitro with respect to bone formation. MATERIALS AND METHODS: We first determined the response of bone to IGF-I administration in vivo during skeletal unloading. We then evaluated the response of osteoprogenitor cells isolated from unloaded bones to IGF-I treatment in vitro with respect to activation of the IGF-I signaling pathways. Finally we examined the potential role of integrins in mediating the responsiveness of osteoprogenitor cells to IGF-I. RESULTS: IGF-I administration in vivo significantly increased proliferation of osteoblasts. Unloading markedly decreased proliferation and blocked the ability of IGF-I to increase proliferation. On a cellular level, IGF-I treatment in vitro stimulated the activation of its receptor, Ras, ERK1/2 (p44/42 MAPK), and Akt in cultured osteoprogenitor cells from normally loaded bones, but these effects were markedly diminished in cells from unloaded bones. These results were not caused by altered phosphatase activity or changes in receptor binding to IGF-I. Inhibition of the Ras/MAPK pathway was more impacted by unloading than that of Akt. The disintegrin echistatin (an antagonist of the alphaVbeta3 integrin) blocked the ability of IGF-I to stimulate its receptor phosphorylation and osteoblast proliferation, similar to that seen in cells from unloaded bone. Furthermore, unloading significantly decreased the mRNA levels both of alphaV and beta3 integrin subunits in osteoprogenitor cells. CONCLUSION: These results indicate that skeletal unloading induces resistance to IGF-I by inhibiting the activation of IGF-I signaling pathways, at least in part, through downregulation of integrin signaling, resulting in decreased proliferation of osteoblasts and their precursors.