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.     

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。     

经皮穿刺椎体成形术治疗合并肺气肿的胸椎压缩性骨折

目的 探讨合并严重肺气肿的胸椎压缩性骨折进行经皮穿刺椎体成形术的技术特点和治疗效果。方法 7例(10个椎体)合并严重肺气肿并且透视椎体显示不清的胸椎骨质疏松椎体压缩骨折患，侧卧位在CT结合C型臂透视引导下进行经皮穿刺椎体成形术。术前、术后2d和随访时分别测定疼痛强度评分、止痛药使用和活动能力评分。随访2-8个月，平均5个月。结果 7例皆顺利完成手术，注射骨水泥的量平均2．2ml／椎体(1．0～4．0m1)，无临床并发症，手术时间2—3．5h／例。疼痛强度评分值术后2d比术前平均减低3．9，随访时进一步下降0．2—2．9，活动能力和止痛药使用术后均明显改善。结论 合并肺气肿的胸椎压缩性骨折患行经皮穿刺椎体成形术治疗前应进行骨折椎体透视检查，显示不清选择侧卧位在CT结合C型臂透视引导下穿刺注射可获得良好疗效。     

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.     

急性重型颅脑损伤ET和CGRP含量变化及其临床意义

目的　探讨急性重型颅脑损伤 (ASBI)患者血浆中内皮素 (ET)和降钙素基因相关肽 (CGRP)的含量变化及其临床意义。方法　用放免法测定 2 8例ASBI患者伤后 6～ 2 4h血浆中ET及CGRP含量。结果　ASBI患者ET含量明显增多 ,差别有显著性 (P <0 .0 5 ) ;CGRP也有一定的增多 ,但无显著性差异。结论　ET和CGRP共同参与ASBI病理生理反应过程 ,ET释放增加是加重脑继发性损害的重要因素     

Alpha-smooth muscle actin in pathological human disc nucleus pulposus cells in vivo and in vitro

That a contractile actin isoform has been found in cells of other cartilage tissues in healing and disease states prompted this investigation of the presence of alpha-smooth muscle actin (alpha-SMA) in pathological human intervertebral disc tissue. The presence of this isoform has been reported in human intervertebral disc specimens obtained at autopsy from subjects for whom there were no reported symptoms. An objective of this study was to evaluate the cell density and percentage of alpha-SMA-containing cells in pathological nucleus pulposus tissue obtained from lumbar disc surgery from 17 patients. Additionally, explants of nucleus pulposus material were cultured to determine how alpha-SMA expression changed with time in vitro. Seventy-six 5-mm diameter explants (approximately 2 mm thick) pooled from six lumbar surgeries were cultured for 1, 2, 4, or 6 weeks. Microtomed sections of paraffin-embedded specimens were stained with hematoxylin and eosin or a monoclonal antibody to alpha-SMA. Histologically, cells were categorized as to alpha-SMA phenotype (positive or negative), and the areal cell density was determined. The evaluation of the cultured nucleus pulposus explants also included documentation of the percentage of cells that were round or elongated and the percentage of the cells that were part of a group (group: >/= 2 cells). Every nucleus pulposus section exhibited the presence of alpha-SMA-containing cells, which accounted for approximately 24 percent of the cells in vivo. In vivo, the cell density was significantly higher in older individuals (p = 0.02). The average time for cell outgrowth from the explants was 8.6 days. Approximately 10-15 percent of the cells in the explants stained positive for alpha-SMA. The time in culture had no significant effect on any of the outcome measures except the percentage of alpha-SMA-containing cells that were round (p = 0.008), with values decreasing through 4 weeks and then slightly rising at 6 weeks. The role of alpha-SMA in intervertebral disc pathology warrants further investigation.