波尔山羊重复超排效果的研究

对 2 0只波尔山羊实施两次超排处理。其结果如下 :1.第 1次超排处理时 2 0只供体羊全部发情并进行采卵 ,超排有效率为 10 0 % ;平均排卵数为 2 0 .2 5枚 /只 ,平均采集胚胎数 19.2 5枚 /只 ,平均采集可用胚胎数为 17.3枚 /只 ;第 2次超排处理时有 3只羊推迟发情 ,超排有效率为 85 % ;平均排卵数 19.2 9枚 /只 ,平均采集胚胎数 18.5 3枚 /只 ,平均采集可用胚胎数 17.35枚 /只 ;2 .两次超排所获得的平均可用胚胎数差异不显著(p >0 .0 5 )。     

二硫代氨基甲酸吡咯烷诱导人肝癌细胞凋亡的铜离子依赖性机制

目的：测定二硫代氨基甲酸吡咯烷（PDTC）处理对人肝癌细胞Hep3B凋亡的诱导作用及Cu^2 对这种作用的影响。方法：运用细胞增殖力、膜损伤、DNA片断化、细胞周期DNA含量测定分析PDTC对人肝癌细胞株Hep3B细胞的增殖抑制及凋亡诱导作用及Cu^2 在其中发挥的作用。结果：PDTC处理后，细胞增殖能力显著下降。乳酸脱氢酶（LDH）分析显示细胞膜并没有被破坏，DNA凝胶电泳及细胞周期DNA含量测定发现明显的凋亡特征性DNA片断及亚G1峰，显示细胞增殖能力的降低源于细胞凋亡的发生。低浓度Cu^2 显著加强了PDTC的细胞增殖抑制及凋亡诱导作用，而Cu^2 络合剂Bathocuproine disulfonate(BCS)显著抑制PDTC的两种作用。结论：PDTC铜离子依赖性地抑制人肝癌细胞增殖并诱导细胞凋亡。     

中心静脉压联合全心舒张末容积指数指导感染性休克患者容量治疗的效果

目的 评价中心静脉压(CVP)联合全心舒张末容积指数(GEDVI)指导感染性休克患者容量治疗的效果.方法 感染性休克患者23例,性别不煨,年龄18～64岁,休克时间＜6h,急性生理和慢性健康状况评分13～31分,采用随机数字表法,将其随机分为2组:CVP指导容量治疗组(Ⅰ组,n=12)和CVP联合GEDVI指导容量治疗组(Ⅱ组,n=11).2组均静脉输注生理盐水和6％羟乙基淀粉200/0.5,晶体液和胶体液的比例为1∶(0.5 ～ 1.0),输注速率800～ 1600 ml/h,容量治疗过程中Ⅰ组维持CVP8～ 12mmHg;Ⅱ组维持CVP＞8 mm Hg和GEDVI 600 ～ 750 ml/m2.分别于容量治疗前及容量治疗开始后6h时采集动脉及中心静脉的血样,测定血乳酸浓度和中心静脉血氧饱和度(ScvO2),计算乳酸和ScvO2的变化率.结果 与Ⅰ组比较,Ⅱ组乳酸变化率升高(P＜0.05),ScvO2变化率差异无统计学意义(P＞0.05).结论 与CVP指导容量治疗比较,CVP联合GEDVI指导感染性休克患者容量治疗时可增加组织灌注,其效果较好.     

改良颈腮腺入路切除咽旁间隙高位良性肿瘤

目的 探讨改良颈腮腺入路在高位咽旁间隙良性肿瘤手术中的应用疗效。 方法 7例咽旁间隙良性肿瘤患者,术前影像学检查提示为高位、肿瘤巨大、哑铃型且边界欠清,采用改良颈腮腺入路术式,解剖辨认面神经总干及颞面干后,于外耳道软骨前方、腮腺的后缘以及颞面干的上方间隙向深部分离至肿瘤上极,剥离子分离并下压肿瘤与下方常规颈部自下而上肿瘤游离会师后,从颌下区取出肿瘤。腮腺浅叶不切除,面神经分支不做过多解剖。 结果 所有患者均一次性完整切除肿瘤;术后病理示多形性腺瘤6例,神经鞘瘤1例;术中出血均少于300 mL;1例患者出现术后同侧眼睑轻度闭合障碍,两周后完全正常;所有患者面容美学保存理想。 结论 对于高位咽旁间隙良性肿瘤采用改良颈腮腺入路术式,不仅可以安全完整地切除肿瘤,同时由于减少了面神经及腮腺浅叶的处置,术后相关神经并发症及腮腺区凹陷性改变的发生率下降。     

Durable efficacy of early postoperative radiation therapy for high-risk pT3N0 prostate cancer: the importance of radiation dose

Objectives. To determine the durable efficacy of early postoperative radiation therapy (RT) in patients with pT3N0 prostate cancer who were at an increased risk of biochemical failure. We also evaluated the long-term benefit derived from using higher RT doses.Methods. Seventy-nine patients with pathologic Stage T3N0 prostate cancer and high-risk postoperative features underwent RT within 6 months after surgery. No patient received prior hormonal therapy. Fifty-nine patients had positive surgical margin, 29 had pathologic seminal vesicle invasion, and 27 had persistently elevated postoperative prostate-specific antigen (PSA) levels. Freedom from biochemical relapse (bNED) was defined as an undetectable (less than 0.2 ng/mL) PSA level. Median follow-up time was 39 months, and the median radiation dose was 64.8 Gy. All patients were followed for at least 2 years to be considered biochemically controlled.Results. Patients receiving adjuvant RT for an undetectable pre-RT PSA level had a 3-year bNED rate of 90%, compared with 44% for those receiving salvage RT for a detectable level (P < 0.0001). In the group of adjuvant patients, RT doses more than 61.2 Gy resulted in a 3-year bNED rate of 90% compared with 64% for those receiving a lower dose (P = 0.015). The salvage patients irradiated with a dose of 64.8 Gy or greater had a 3-year bNED rate of 52% compared with 18% for those irradiated with lower doses (P = 0.048). Severe late RT-related complications were infrequent and did not correlate with dose.Conclusions. In patients with high-risk pT3N0 prostate cancer, an RT dose response may exist. Although some studies suggest limited durable efficacy for early postoperative RT, our data suggest that RT doses of 64.8 Gy or more appear superior to prevent future biochemical failures. A prospective randomized study evaluating a postoperative RT dose response is warranted.     

Cystic fibrosis and the phenotypic expression of autosomal dominant polycystic kidney disease

Recent experiments in cultured cyst epithelial cells from kidneys of patients with autosomal dominant polycystic kidney disease (ADPKD) have shown that the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) is present in the apical surface of these cells and mediates chloride (Cl-) and fluid secretion in vitro. To determine whether the presence of CF with the expression of mutated CFTR proteins modifies cyst formation in ADPKD, we studied a large family with both inherited diseases. ADPKD in this family is linked to PKD1. The family is composed of 26 members; 11 members with ADPKD, 4 members with CF, and 2 members with both diseases. Renal volumes measured by computerized tomography (CT), calculated creatinine clearances, and other clinical parameters in the family members with ADPKD and CF were compared with those in the family members with ADPKD alone, as well as to a large population of patients with ADPKD. The patients with CF and ADPKD, but not the CF heterozygote carriers with ADPKD, had less severe polycystic kidney and liver disease, as indicated by normal renal function; smaller renal volume, even when corrected for height and body surface area; and the absence of hypertension and liver cysts. These observations suggest that the coexistence of CF may reduce the severity of ADPKD.