Role of lateral neck dissection in cancers of the larynx and hypopharynx with No neck

Radical neck dissection is a standard procedure carried out for the teatment of palpable nodes in the neck but if carried out electively in cases where there are no palpable nodes in the neck it is considered to be an overtreatment with its associated morbity. Lateral neck dissection was carried out on twenty patients who had T31 T4 lesion of the larynx and hypophar-vnx with NO neck. The dissection entails removal of Level II. III and IV nodes. Occult metastasis 80% and 85% respectively. The mean follow up was 13 monts. It appears from our study that elective lateral neck dissection is a promising and safe procedure and may be useful as an important prognostic tool in sampling the lymph nodes and predicting recurrences in the neck.     

黄芪、水蛭、地龙不同配伍治疗缺血性中风实验研究

提出气虚血瘀络阻为缺血性中风的基本病机,而益气活血通络则为基本治法。通过黄芪水蛭地龙、黄芪水蛭、黄芪地龙、水蛭地龙四个配伍组比较,以观察其对急性脑缺血大鼠血浆一氧化氮(NO)、丙二醛(MDA)、血小板聚集性及大鼠在体血栓形成时间的影响。结果表明,黄芪水蛭地龙配伍组在以上诸方面的作用明显优于其他组。     

哮喘急性发病与IL-5、sIL-2R及NO关系的研究

目的;探讨白介素－５（ＩＬ－５）、可溶性白介素－２受体（ｓＩＬ－２Ｒ）、一氧化氮（ＮＯ）及嗜酸粒细胞（ＥＯＳ）计数在哮喘急性发病中的意义。方法：对急性发作期哮喘患者及正常对照者血清ＩＬ－５,ｓＩＬ－２Ｒ和ＮＯ水平及ＥＯＳ计数进行了研究。使用ＩＬＩＳＡ法检测血清ＩＬ－５、ｓＩＬ－２Ｒ水平,硝酸还原酶法检测ＮＯ,伊红粉法计数ＥＯＳ。结果：哮喘急性发作组血清ＩＬ－５,ｓＩＬ－２Ｒ,ＮＯ及ＥＯＳ水平均明显     

The induction of nitric oxide-mediated relaxation of human isolated pulmonary arteries by PACAP

1. The effects of pituitary adenylate cyclase-activating peptide (PACAP) and vasoactive intestinal peptide (VIP) were analysed in human isolated circular segments of pulmonary arteries. Guinea-pig pulmonary arteries were used for comparison. The responses obtained were analysed in relation to the vascular endothelium and the nitric oxide (NO) synthase inhibitor N^G-monomethyl L-arginine (L-NMMA).
2. PACAP and VIP induced concentration-dependent relaxations of precontracted pulmonary arteries. The maximal dilator response (I_max,%) and the potency (pEC₅₀ value) were the same for both peptides, and there were no differences in the effects obtained on human and guinea-pig segments. PACAP and VIP were both more potent that acetylcholine (ACh).
3. Removal of the vascular endothelium abolished the PACAP induced dilator response in pulmonary arteries from both species. The VIP induced dilatation was unaffected, whereas the response to ACh was abolished. L-NMMA given before PACAP inhibited the dilatation. Furthermore, L-NMMA also reversed the dilatation already induced by PACAP and excess concentrations of L-arginine restored the dilator response of the L-NMMA treated arteries.
4. PACAP is a potent dilator of human pulmonary arteries. Although the dilator effect seems to be similar in amplitude to the one induced by VIP, the present results suggest differences in the underlying mechanisms of action (endothelium-dependency) between the two peptides.

     

Involvement of nitric oxide in the inhibition of angiogenesis by interleukin-2

Interleukin-2 (IL-2), an immunoregulatory cytokine possessing antitumour activity, is an inducer of nitric oxide (NO) synthesis in mice and man. In this study, the possibility that IL-2 possesses antiangiogenic properties that account for its antitumour effects in vivo was examined. IL-2 caused a dose-dependent inhibition of angiogenesis in the chick embryo chorioallantoic membrane (CAM). This inhibition was completely reversed by the NO synthase inhibitor N^G-nitro-L-arginine methylester (L-NAME). Furthermore, IL-2 was capable of stimulating NO synthase activity in the CAM in vitro and this effect was suppressed by L-NAME. Addition of IL-2 to human umbilical vein endothelial cells (HUVECs) in culture, had no effect on their growth characteristics. These results suggest that IL-2 may be an important antiangiogenic molecule causing its effect via nitric oxide synthesis. The antiangiogenic activity of IL-2 may be, at least in part, responsible for its antitumour properties.     

Nitric oxide synthase activity is inducible in rat,but not rabbit alveolar macrophages,with a concomitant reduction in arginase activity

Alveolar macrophages were obtained by broncho-alveolar lavage of isolated rat and rabbit lungs and cultured (2.5 × 10⁶ cells/dish) for 18 h in the absence or presence of bacterial lipopolysaccharides (LPS) alone or in combination with cytokines. Thereafter, accumulation of ³H-citrulline (NO synthase activity) and ³H-ornithine (arginase activity) were determined.During incubation of rat alveolar macrophages with ³H-arginine clear amounts of ³H-citrulline and ³H-ornithine (3.8 and 4.6% of the added ³H-arginine, respectively) were formed and most of these metabolites appeared in the incubation medium (ratios extra-/intracellular of 17 and 70 for ³H-citrulline and ³H-ornithine, respectively). When rat alveolar macrophages had been cultured with LPS the formation of ³H-citrulline was increased about 30-fold and this was accompanied by a reduction in ³H-ornithine formation of about 60%. The effects of LPS were largely attenuated by dexamethasone (10 mol/1). Inhibition of NO synthase by N^G-monomethyl-l,-arginine (l-NMMA, 100 mol/1) in LPS treated alveolar macrophages reduced the formation ³H-citrulline by more than 90% and restored the ³H-ornithine formation. After culturing in the presence of LPS the ratios extra/intracellular of ³H-citrulline and ³H-ornithine were markedly enhanced and this effect was not dexamethasone sensitive. During incubation of rabbit alveolar macrophages a marked formation of ³H-ornithine (about 5.3% of the added ³H-arginine), but no significant formation of ³H-citrulline could be detected. Pretreatment with LPS tended to enhance the formation of ³H-ornithine (by 50%) without effects on ³H-citrulline. Rabbit-interferon and/or tumor necrosis factor- present together with LPS during the culture period did not result in a significant ³H-citrulline formation. Under all conditions tested, culture media of rabbit alveolar macrophages did not contain significant amounts of nitrite (less than 0.5 nmol) whereas in culture media of untreated rat alveolar macrophages 22 nmol nitrite (per 18 h) were detected, and LPS induced a 3-fold nitrite accumulation, an effect prevented by dexamethasone.In conclusion, in rabbit alveolar macrophages NO synthase activity was not detectable and could also not be induced by LPS and different cytokines, whereas in rat alveolar macrophages NO synthase was readily inducible. Alveolar macrophages of both species showed marked arginase activity. After induction of marked NO synthase activity, ornithine formation was largely reduced possibly by concomitant inhibition of arginase and/or withdrawn of arginine from arginase.     

冷损伤血管NO合成酶活力的变化及其生物学意义

目的 观察不同程度冷损伤血管ＮＯ合成酶（ＮＯＳ）活力的变化,并研究超氧化物歧化酶（ＳＯＤ）和ＶｉｔＣ对这各变化影响。方法分离Ｗｉｓｔａｒ大鼠主动脉,并在ＰＢＳ培育培养１小时,然后使其暴露于－２０℃环境。以全自动生化分析仪测定血管培养液中乳酸脱氢酶（ＬＤＨ）活力,以Ｇｒｉｅｓｓ化学法观测血管ＮＯＳ活力,以肾上腺肾自氧化法血管ＳＯＤ活力。结果 当血管暴露于－２０℃环境１、２、４分钟后,血管２液中ＬＤＨ     

高压氧对急性一氧化碳中毒患者血浆NO及ET-1影响的研究

为研究高压氧对缺氧病人血浆内一氧化氮（NO）和内皮素（EF－1）的影响,对28例急性一氧化碳重度中毒病人,经高压氧治疗前后即刻进行静脉血浆NO和ET－1含量的测定,结果显示：高压氧治疗后病人血浆NO水平较治疗前显著增高（P＜0．01）,ET-1含量较治疗前显著降低（P＜0．01）,病人病情明显好转。提示：高压氧可显著提高急性一氧化碳中毒病人血缸浆中NO水平,降低ET－1含量,两值经相关性分析,r＝－0．435,P＜0．01,呈高度负相关。     

示波极谱法测定血清和组织中的亚硝酸盐

用示波极谱法测定血清和组织匀浆中的亚硝酸盐。取０．１０ｍｌ血清或组织匀浆,样液中的ＮＯ－２在稀盐酸介质中,与磺胺和盐酸萘乙二胺反应生成偶氮化合物,在氨碱性介质中,该偶氮化合物可产生灵敏的极谱波,波高与ＮＯ－２含量在一定范围内成正比关系。本法检出限为０．５６μｇ／Ｌ（相应血清浓度和组织含量分别为０．６１μｍｏｌ／Ｌ和０．２２μｇ／ｇ）,相对标准差为６．１％～７．８％。加标回收率为９２．０％～１０８．０％（平均１００．６％）。本法具有灵敏度高,操作简便和样品不需除蛋白即可直接测定等优点。     

红细胞血型糖蛋白A位点正常变异及肿瘤放疗的影响

目的了解血型糖蛋白Ａ（ＧＰＡ）背景突变水平,观察照射近期的变化规律。方法在正常人和肿瘤放疗病人中进行ＧＰＡ突变分析,结合单克隆抗体标记和流式细胞技术,检测ＭＮ杂合子个体中罕见的变异细胞ＮＯ和ＮＮ,确定变异率。结果对２８个正常成人的初步测定,ＮＯ／ＮＮ变异率（Ｖａｒｉａｎｔｆｒｅｑｕｅｎｃｙ,Ｖｆ）（８．３±４．１３）／（５．５０±３．７７）×１０－６;ＮＮ变异率与年龄相关性接近显著意义（Ｐ＝０．０５７）,男女之间、吸烟与不吸烟者均无显著差异。随访肿瘤病人,６例治疗前ＧＰＡ变异率ＮＯ（１２．９±６．６０）×１０－６,ＮＮ（７．７±５．０１）×１０－６,与同年龄者无显著差异。连续盆腔照射１月Ｖｆ已有升高,照射２个月的病人ＮＮＶｆ（１７．５±８．９５）×１０－６,显著高于未照病人（Ｐ＝０．０４６８）。结论正常人ＧＰＡ变异率基本与文献相符,年龄等因素可影响背景水平;病人照射后Ｖｆ变化不一,表明个体对辐射敏感性不同,照射近期主要是ＮＮ的变化,是较晚造血周期细胞突变的表现。