电视纵隔镜手术128例

目的探讨电视纵隔镜检查术（video-mediastinoscopy，VM）在肺癌术前分期、纵隔肿物诊断和恶性胸腔积液诊治中的价值。方法采用全麻单腔螺纹气管插管，48例行颈部纵隔镜术，33例行胸骨旁纵隔镜检查术，47例行经肋间纵隔镜术。结果125例经电视纵隔镜术后确诊：肺腺癌38例，肺转移性低分化鳞癌33例，结核9例，淋巴结炎症8例，肺小细胞癌7例，胸腺鳞状细胞癌6例，非霍奇金淋巴瘤5例，纵隔神经母细胞瘤4例，胸腺瘤4例，胸膜间皮瘤3例，霍奇金淋巴瘤2例，后纵隔神经鞘瘤2例，结节病1例，胸腺增生1例，类癌1例，中纵隔原始神经外胚叶肿瘤1例。1例电视纵隔镜检查纵隔淋巴结为反应性增生，行左下肺叶切除，病理为鳞癌。2例术前纤维支气管镜病理确诊左下肺鳞癌，电视纵隔镜检查右气管旁淋巴结转移。术中发生气胸1例、出血1例、喉返神经麻痹和切口感染各2例。结论电视纵隔镜术不但是肺癌术前病理分期、纵隔疾病的重要检查方法，而且也是诊治恶性胸腔积液的简便方法。     

慢性HBV感染患者精子中HBVDNA存在研究的初步报告

用Southern Blot方法,我们研究了13份慢性HBV感染患者(8份慢迁旰,5份慢活肝)和2份对照精液标本中HBV DNA存在状况。提取物一半用限制酶HindⅢ消化,各行琼脂电泳,转移到纤维膜上,然后用~(32)P—HBV—DNA探针分子杂交。在4份精子內检出HBV DNA,3份为游离形式,1份为整合形式。结果表明HBV DNA可以存在精于内,游离状态HBV DNA提示有传染性、整合序列HBV DNA的存在提示有通过生殖细胞遗传的可能。     

膀胱横纹肌肉瘤的病理组织学研究

本文对我院6例原诊断为膀胱葡萄簇状肉瘤的病例进行了临床随访并做了病理组织学研究。全部患者在术后2～12个月内死亡。6例瘤组织的病理学图象基本相同,但有些区域则呈恶性淋巴瘤样或粘液肉瘤样或平滑肌肉瘤样形态。它们虽貌似有多种组织成分,但经特柒证明却只含有胚胎性横纹肌肉瘤成分,而无其它良恶性问叶性瘤组织成分。因此,在病理学命名上,应将它诊断为膀胱横纹肌肉瘤,建议不再使用“葡萄簇状肉瘤”的名称。此外,作者并收集国内文献中报告过的膀胱横纹肌肉瘤(葡萄簇状肉瘤)共69例,结合本文报告6例,详细讨论了它的发病率、命名和组织发生学等临床和病理方面的问题。-     

片剂含量均匀度计量检验新方案的研究

本文通过大量测试工作,查明10批国产小剂量片剂的含量分布,在此基础上提出了计量检验新方案。采用计算机模拟随机抽样的方法,通过计算绘制了USP XX,BP,JP和新方案在正态分布和10批实际分布下的OC曲线。结果表明,当用于测定生产规模的片剂批时,与国外片剂含量均匀度计数检验方案中统计特性最优的USP XX方案相比,新方案NEW能在化验工作量相近的前提下,作出更准确的判断;新方案SMA能在不降低判断准确性的前提下,减少化验工作虽约三分之一。新方案还可减免分析方法误差对判定结果的影响。     

浙江省在鼠中检测到埃立克体及无形体DNA片段并测序分析

目的:了解鼠中自然感染埃立克体及无形体的状况。方法:用巢式PCR扩增鼠中埃立克体属及嗜粒细胞无形体属16S rDNA的5′末端片段,对阳性产物克隆后测序。结果:在浙江省金华市金东区捕到鼠128只。在黄毛鼠中检到阳性4份,阳性率为3.125%,并对其进行克隆后测序。与Genbank上比对分析,三份与牛埃立克体相同基因区最为接近,属无形体科,无形体属。一份与反刍动物埃立克体相同基因区最为接近,属无形体科,埃立克体属。均为国内首次报道。结论:初步认为浙江省存在埃立克体及无形体病原。黄毛鼠可能为埃立克体及无形体宿主,尚需进一步调查。     

医院内携带的葡萄球菌对8种抗生素的敏感度

测定216株葡萄球菌(126株金葡菌,90株凝固酶阴性葡萄球菌)对8种临床常用抗生素药敏。结果为:医院内携带的金葡菌对青霉素G、红霉素、林可霉素耐药率分别为76.42%、61.36%、27.26%,对头孢噻啶、利福霉素敏感性较好。医院内表葡菌对青霉素G、红霉素、林可霉素耐药率分别达65.29%、58.82%、50%。故治疗医院内金葡菌、表葡菌感染时要选用有效药物。医院内携带的金葡菌产酶率81.40%,CNS产酶率71.11%,绝大多数产酶株对青霉素G耐药,头孢噻啶对产酶株有良好的抗菌活性。     

含L-4-氧代赖氨酸和N3-(4-甲氧基富马酰)-L-2,3-二氨基丙酸寡肽类似物的合成及其抗白念珠菌活性

运用“违法传递”概念，根据白念珠菌对寡肽的传送特点，设计并合成了８个含Ｌ４氧代赖氨酸（以下称Ｉ６７７）和Ｎ３（４甲氧基富马酰）Ｌ２，３二氨基丙酸（以下称ＦＭＤＰ）的寡肽类似物，均系新化合物。体外抗白念珠菌试验表明：Ｉ６７７ＦＭＤＰ肽（Ｉ６７７ＦＭＤＰ，Ｉ６７７ＡＡＦＭＤＰ，其中ＡＡ＝Ｎｖａ，Ｖａｌ，Ｌｅｕ，Ｐｈｅ，Ｐｒｏ，Ｄ，ＬｐＣｌＰｈｅ，ＤＰｇｌｙ）是Ｉ６７７单体摩尔活性的４０～７７０倍，是ＦＭＤＰ的６０～１１３０倍，其摩尔最低抑菌浓度为６５６×１０－９～３５×１０－１０ｍｏｌ·ｄｉｓｋ－１。羧肽酶Ａ存在时化合物Ｉ６７７ＦＭＤＰ体外抗菌试验表明，含ＦＭＤＰ的化合物Ｉ６７７ＦＭＤＰ能抵抗羧肽酶Ａ的酶解。     

实验性免疫反应性中耳炎对内耳的影响

作者应用免疫荧光技术,对实验性免疫反应性中耳炎模型进行了研究。结果显示:实验动物早期出现前庭功能紊乱;免疫荧光分布于中耳粘膜和前庭囊壁上皮下、耳蜗血管纹和基底膜近蜗轴处;免疫荧光强度测定蜗底多、蜗顶少。     

Investigation of the anti-complement agents, FUT-175 and K76COOH, in discordant xenotransplantation

Abstract: We examined whether hyperacute rejection (HAR) of a discordant xenograft in a nonhuman primate model could be inhibited by the anticomplement agents, FUT-175 (FUT) and K76COOH (K76). The inhibitory effect of FUT and K76 on baboon sera was studied in vitro by i) complement-mediated hemolysis of sheep erythrocytes (by measuring serum CH50) and ii) cytotoxicity to cultured pig kidney (PK15) cells. The in vivo administration of FUT (at 0.2–25 mg/kg/h i.v. continuously) and K76 (50 mg/kg i.v. bolus) allowed evaluation of the serum levels of these drugs. Both FUT and K76 inhibited serum CH50 in a concentration-dependent manner. An enhanced effect was obtained by combining K76 with FUT therapy. High concentrations of FUT (>10^-4 M) and K76 (>10³ μxg/ml) were necessary to suppress serum CH50 to <5% of the normal level. However, PK15 cytotoxicity remained at >50% in the presence of i) 10^-4 M of FUT, ii) 10³ μg/ml of K76, and iii) 10^-6 M of FUT + 10³ μg/ml of K76. Pig heart transplantation (HTX) was performed in two baboons receiving FUT (1 mg/kg/h i.v. continuously) and K76 (at 200 mg/kg ×1 or 400 mg/kg + 200 mg/kg × 2 i.v, respectively). Cytotoxicity of the serum to PK15 cells at the time of HTX showed 39% and 1% cell death, respectively, in these two baboons, and the CH50 level was 1% (of control level) and 0%, respectively. Graft survival was 4.5 hours and 10 hours (with death of the baboon), respectively (compared with a mean of 29 minutes in control experiments). Both excised grafts showed typical features of hyperacute rejection. Immunopathological studies revealed deposition of C1q, C3d, C6, properdin, and Factor B, demonstrating that complement activation was not fully inhibited by FUT and K76. We conclude that i) FUT and K76 are indeed potent complement inhibitors, ii) the dosages of FUT and K76 necessary to suppress complement-mediated injury cannot be extrapolated from previously reported data obtained from serum CH50 levels, and iii) higher (possibly toxic) dosages will be required to inhibit complement activation completely. It seems unlikely that HAR will be prevented by these drugs alone, although they may be beneficial when combined with other forms of therapy.