利多卡因对N-甲基-D-天冬氨酸抑制大鼠肾上腺嗜铬细胞瘤细胞增殖的影响

目的 观察利多卡因对 N-甲基-D-天冬氨酸(NMDA)抑制大鼠肾上腺嗜铬细胞瘤细胞(PC12细胞)增殖的影响。方法 将体外培养的 PC12细胞分为6组，分别采用正常不含药液的培养基(C组)；含400μmol·L(-1)NMDA 的培养基(N组)；NMDA 分别混合10μmol·L~(-1)(L_1组)、10~2μmol·L~(-1)(L_2组)、10~3μmol·L~(-1)(L_3组)以及10~4μmol·L~(-1)(L_4组)利多卡因的培养基培养5d，应用流式细胞仪测定细胞 DNA 相对含量，解析细胞周期，计算 S 期细胞荧光强度占受测细胞总荧光强度的百分数为 S期分数(SPF)和 S 期与 G_2期细胞荧光强度之和与 M 期细胞荧光强度的比值[(S G_2)/M]。结果 与C 组比较，N、L_1组 SPF 和(S G_2)/M 均降低(P<0.05)，L_4组 SPF 降低(P<0.05)，而 L_2及 L_3组 SPF和(S G_2)/M 差异无统计学意义(P>0.05)。与 N 组比较，L_2、L_3及 L_4组 SPF 和(S G_2)/M 升高(P<0.05)，L_1组 SPF 升高(P<0.05)，而(S G_2)/M 差异无统计学意义(P>0.05)。结论 NMDA 可以通过抑制 PC12细胞 DNA 合成而影响细胞的增殖活性，利多卡因能拮抗 NMDA 对 PC12细胞增殖的抑制作用。     

中国男性原发不育的遗传高风险因子:Y染色体DAZ基因拷贝缺失

目的 探讨Y染色体无精症因子C区(azoospermia factor C，AZFe)无精症缺失基因(deleted-in-azoospermia，DAZ)家族基因拷贝缺失与中国男性原发不育之间的关系。方法 运用多重PCR与PCR-RFLP检测技术，对210例已生育男性、216例原发无精症与189例严重少精症患者Y染色体AzFc区域DAZ基因家族的基因拷贝数进行分析。结果 在所有已生育男性中未检出DAZ基因拷贝的完全或部分缺失，而在原发无精症与严重少精症患者中DAZ基因拷贝完全缺失率分别为8．8％和12．2％，DAZ1／DAZ2共缺失率分别为8．3％和5．3％。结论 在中国男性原发无精症与严重少精症患者中存在较高频率的DAZ基因拷贝缺失现象，提示Y染色体AZFc区域DAZ基因家族基因拷贝的完全与部分缺失是中国男性原发不育的遗传高风险因子。     

重症肌无力胸腺切除术后呼吸道管理与并发症的防治

目的 探讨重症肌无力胸腺切除术后呼吸道管理与并发症的防治.方法 32例ICU收治的重症肌无力胸腺切除术后的患者,根据危象预测积分,分为普通组(积分＜12分,n=21)和高危组 (积分＞12分,n=11),对两组患者术后呼吸机支持时间、拔管前后肌力恢复情况、自主呼吸情况、动脉血气分析情况以及两组患者术后体温、胸片和痰培养结果进行统计分析.结果 高危组患者术后呼吸支持时间(18 ～ 30 h,平均26 h)大于普通组患者(4 ～ 28 h,平均14 h),两组有显著性差异(P＜0.01),同时术后发热、胸片渗出影以及阳性痰培养结果的发生率也高于普通组.结论 术后给予高危患者严密的监测和充分的呼吸支持,有助于降低重症肌无力危象的发生率和死亡率,同时应充分重视气道护理和感染的防治.     

低脉压与晚期慢性心衰患者利钠肽和死亡率升高独立相关

目的:脉压(PP)升高一贯用来预测有心血管疾病危险患者和轻度慢性心衰(CH F)患者的心血管疾病发生率和死亡率增高。相反,PP降低与急性失代偿性心衰患者死亡率升高相关。然而,尚不清楚PP对于晚期CH F患者的预测价值。方法和结果:采用Cox比例风险回归分析研究了1901例N YH A III或IV级CH F患者(平均年龄65岁,平均射血分数26%)的资料,经校正其他危险因素后,分析PP对死亡率的影响。检测了1个亚组患者的利钠肽水平。多元Cox回归分析表明,PP降低与死亡率增高相关(每增加10m m H g的H R为0.91,95%CI0.93～0.99),这一相关性独立于平均…     

超声诊断异位妊娠249例临床分析

目的为了提高对异位妊娠的诊断技术。方法选择在我院经手术病理证实的异位妊娠249例住院患者行2DB超和CDFI的声像图特征进行分析。结果2D超声声像图特征在249例异位妊娠中内膜增厚223例，厚度为4—8mm／2；宫内假环状孕囊28例，大小为4．12mm；宫外探及孕囊178例，大小为8-48mm；盆腔混合性包块28例，大小为40．80mm：伴有黄体囊肿的123例，存活宫外孕3例，可显示原始心管搏动；CDFI声像图特征为宫外孕急性破裂的患者显示肿块及周围组织的彩色血流信号增多，动脉频谱血流速度增快，RI降低。结论超声检查对妇产科急诊有显著性作用，可直接指导临床明确诊断，选定治疗方案。     

桡骨颈骨折经皮撬拨复位的远期疗效

用经皮撬拨复位治疗桡骨颈骨折56例,其中复位良好46例,较好6例和不良4例;经3年7个月平均随访,复位良好和较好的44例中,后期疗效良好32例,较好11例和一般1例。骨折解剖复位、撬拨复位的手术损伤轻和石膏固定时间较短是后期疗效满意的关键。成人桡骨颈骨折伴肘内侧副韧带严重损伤比儿童多见,但儿童桡骨颈骨折严重倾斜移位和完全移位比成人多见,后期疗效更满意。     

Relationship among dosages of aminophylline, plasma levels of theophylline and variation of pulmonary arterial pressure]

The relationship among the dosages of aminophylline, plasma levels of theophylline and variations of mean pulmonary arterial pressure (mPAP) in 72 patients with COPD was investigated. The results showed that after a different loading dosage of aminophylline (6 mg/kg, 5 mg/kg and 4 mg/kg) was administered by intravenous injection, mPAP in the 6 mg/kg group was decreased more significantly (P less than 0.01) than that in the 4 mg/kg group. In the 6 mg/kg group, the decreased mPAP period sustained for 120 min, which was longer than that in the other 2 groups. The plasma levels of theophylline in the 6 mg/kg group of patients 30 to 120 min after loading dose injected were 115.54-79.04 mumol/L, which were higher than that in the others. Within the 120 min period of observation after the drug was administered no patients in any of these groups showed severe untoward effects. According to the results of this experiment, we suggest that the 6 mg/kg as a loading dose should be advised for the treatment of pulmonary hypertension in COPD. The optimum time to give the maintenance dosage should be set within 2 h after the loading dose. It is necessary to monitor the plasma levels of theophylline while aminophylline is administered, so that optimal therapeutic effects could be achieved without side effects.     

单用达那唑治疗慢性再生障碍性贫血19例临床观察

单用达那唑（ＤＮＺ）治疗１９例慢性再生障碍性贫血（ＣＡＡ）病人。结果表明，基本治愈１例，缓解５例，明显进步７例，有效者共１３例，总有效率为６８．４％，初治者５／７例有效，有效率为７１．４％；复治者８／１２例有效，有效率为６６．７％。治疗后与治疗前比较，血红蛋白、白细胞、血小板和网织红细胞均明显升高（Ｐ＜０．００１）；骨髓红系、粒系及巨核细胞明显增高（Ｐ＜０．０５）；Ｔ辅助细胞（ＣＤ４）明显增加、Ｔ抑制细胞（ＣＤ８）明显降低，ＣＤ４／ＣＤ８比值明显升高（Ｐ＜０．０５）。并结合文献对ＤＮＺ的作用原理进行讨论。     

Hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case.

Hyperoxaluria is frequently seen in patients with inflammatory bowel disease, or after resection of the ileum. It is assumed to be responsible for the development of nephrolithiasis, nephrocalcinosis (oxalate nephrosis) and progressive renal impairment in these patients. Steatorrhea may aggravate the severity of hyperoxaluria. A 60-year-old male underwent massive resection of the jejunum and ileum 10 years prior to admission, due to strangulation of the small bowel, with occlusion of the superior mesenteric artery. He remained well except for steatorrhea which developed two-and-a-half years prior to admission, when microhematuria, proteinuria and oxaluria developed progressively. Since that time, the nephrolithiasis, nephrocalcinosis and renal failure have continued to worsen despite therapy with oxalate restriction and oxalate-binding agents. A renal biopsy, performed late in the clinical course, showed severe changes in the renal parenchyma. The decline in renal function proved irreversible. The unusual metabolic consequences of massive resection of the small intestine and their mechanisms are discussed.     

Adenosine''s role in the genesis of bradyarrhythmias induced by acute myocardial hypoxia.

A close or even causal relation between myocardial adenosine and bradyarrhythmias during acute myocardial hypoxia was testified in guinea pig, rabbit and dog mainly by using specific competitive antagonist and synchronous quantitative analysis of 3 variables: intensity of myocardial hypoxia, degree of endogenous adenosine increment and severity of bradyarrhythmias. Results disclosed: A) striking resemblance of the bradyarrhythmias with hypoxic origin to those caused by exogenous adenosine, B) same locality of A-V conduction block induced by both myocardial hypoxia and exogenous adenosine, C) precise parallelism among the above-listed 3 variables with very high correlativity (r = 0.99, P < 0.01), D) frequent accompaniment of reversal of hypoxic bradyarrhythmias through resupply of 21% O2 with normalization of preexisted increase in myocardial adenosine, E) satisfactory blockade of hypoxic bradyarrhythmias by adenosine's specific antagonist--aminophylline and their augmentation by adenosine's uptake inhibitor--dipyridamole, F) close similarity of the characteristic curve representing relation among the above 3 variables to that among intensity of myocardial hypoxia, degree of endogenous adenosine increment and amount of coronary blood flow in which adenosine's role as a mediator has been well documented and G) reproducible persistence of bradyarrhythmias during myocardial hypoxia irrespective of preliminary vagotomy and atropinization, denoting independence of the occurrence of such dysarrhythmias upon vagal drive, suggestive of a mechanism other than vagotonia. We advocated that hypoxia-induced bradyarrhythmias was caused by increment in endogenous adenosine.