广州地区小儿乙肝无症状携带者及其父母的HBV DNA基因型研究

目的扩增HBV DNA S基因,建立 HBV DNA的分型方法,研究家庭中小儿乙肝无症状携带者与其父母的基因型.方法利用PCR-RFLP基因分型方法,扩增HBV DNA S基因,以限制性内切酶AvaⅡ,MboⅠ酶切分型;结果 12个家庭共27例乙肝无症状携带者血清,其中两个家庭儿童与父母的基因型相同,均为B型;9个家庭儿童与母亲的基因型相同(7个B型,2个C型),父亲HBV DNA阴性;1个家庭儿童与母亲为B型,父亲为C型,结论本文利用的分型方法经济实用,分型率高,广州地区的基因型以B型,HBV DNA的传播具有家庭聚集性特点及母婴传播的特点.     

PCR-SSCP法检测结核分枝杆菌耐药性

目的：探讨耐多药结核分枝杆菌耐药基因突变与耐药性的关系以及聚合酶链反应-单链构象多态性分析(poly merase chain reaction-single strand cinfomlation polymorphism，PCR-SSCP)方法的临床应用价值。方法：用PCR-SSCP方法检测58株结核分枝杆菌临床分离株katG，rpoB，rpsL基因突变并与常规药敏试验检测结果进行对比。结果：经常规药敏试验检测，58株结核分枝杆菌临床分离株中共有41株耐药，其中，耐异烟肼(INH)为35株，高耐药株27株；耐利福平(RFP)为31株，高耐药株24株；耐链霉素(SM)有31株，高耐药株26株。同时耐3种药物的有21株(51．2％)，耐2种药物的14株(34．1％)，单耐药株6株(14．6％)．PCR-SSCP方法对58株临床分离株katG，rpoB，rpsL基因突变的检测率为40％(23／58)，45％(26／58)，38％(22／58)，其中检出3个基因同时突变的有13株(32％)，2种基因突变的12株(29％)，1种基因突变的有10株(23．8％)．常规药敏试验与PCR-SSCP法检出结核分枝杆菌同时耐3种药物的符合率为61．9％(13／21)，检出耐2种药物的符合率为85．70k，(12／14)，检出耐1种药物的符合率为50％(3／6)．高耐药株中突变率为80．5％(62／77)，低耐药株中突变率为60％(12／20)．结论：PCR-SS-CP方法对耐2种以上药物的结核杆菌检出率较高，且耐药基因突变率随着耐药浓度增高而增高。将PCR-SSCP法与药敏试验联合应用可互相弥补，已成为临床指导用药的好方法。     

桡骨远端骨折治疗失败的分析

桡骨远端骨折为全身中最常见的骨折,约占整个骨折患者的1/6,多见于老年患者。收治了桡骨远端骨折骨不连及畸形愈合的患者28例,分析原因如下。1临床资料1998-2004年,共治疗桡骨远端骨折治疗失败病例28例,其中桡骨远端粉碎骨折7例,骨不连21例。桡骨远端粉碎骨折组中,男4例,女3例;年龄21~65岁,平均41.3岁。其中石膏固定导致骨折再移位4例,外固定支架固定导致骨折再移位2例,克氏针内固定导致再移位1例。骨不连组中,男14例,女7例;年龄34~70岁,平均55.7岁。其中采用普通钢板固定7例,三棱针固定7例,克氏针加钢丝固定2例,单纯克氏针固定2例,外固定架…     

B超引导下脐静脉穿刺术临床应用

目的分析B超引导下脐静脉穿刺术的临床应用价值。方法对1200例临床怀疑异常的孕妇进行B超引导下脐静脉穿刺术,检测、分析所抽取的脐静脉血。结果成功率99.7%,发现异常胎儿349例。结论B超引导下脐静脉穿刺术成功率高,应用广泛,是一项安全的产前诊断方法。     

丘脑底核电刺激治疗帕金森病术后程控问题分析

目的 总结丘脑底核电刺激治疗帕金森病术后程控经验，提高术后程控水平，改善疗效。方法 对32例丘脑底核电刺激术后的帕金森病患者进行程控，其中单侧植入者6例，双侧26例；年龄40～73岁，在不同刺激器植入中心接受手术，程控时间术后3周至4年之间。程控前均停药10h以上，程控参数调整主要为刺激电极触点、电压、频率、脉宽四项，程控过程中密切观察病员肌张力和震颤等症状改变以及副反应发生情况，作好详细记录，并分别评估患者程控前后药物“关期”和“开期”症状改善情况，部分行UPDRS评分。结果 31例（97％）患者术后症状得到不同程度改善。刺激电极触点选择中，共29例患者采用单极模式，3例因出现持续、无法耐受的副反应采用双极模式。除1位患者使用循环模式外，其他患者均使用持续刺激模式。刺激电压2．0-4．0V，主要集中于2．8～3-3V，是主要的程控调整参数，电压的高低与病人UPDRS运动评分不具有相关性（P〉0．05）。刺激脉宽60～120μs，刺激频率130～185Hz。药物“关”期，患者UPDRS运动评分，在刺激器打开时，平均18．7分；刺激器关闭时平均47．9分。在刺激器打开情况下，药物“开”期患者症状仍然有进一步缓解．主要表现为步态、全身协调动作方面。合并异动患者6例中，3例适当降低刺激电量，1例提高电压后，异动缓解。结论 丘脑底核电刺激术是有效的帕金森病症状控制手段。准确植入刺激电极是术后获得良好症状控制的前提条件，而术后程控是脑深部刺激器置入术后的关键环节．精确的参数调整能够满意控制病人症状。     

重度充血性心力衰竭患者心率和每搏输出量的凌晨分离现象研究

目的 研究重度充血性心力衰竭患者血流动力学的昼夜节律改变.方法 选择2005年12月至2006年6月在南京中医药大学无锡附属医院心内科住院的重度充血性心力衰竭患者120例为心衰组,同期门诊体检的无心血管疾病者20名为对照组,采用生物阻抗法每小时1次动态监测心率(HR)和每搏输出量(SV).结果 心衰组与对照组HR、SV均存在昼夜节律,但分布规律存在差异,心衰组HR明显快于对照组(P＜0.5),而SV明显低于对照组(P＜0.05);对照组HR与SV呈正相关(P＜0.01),而心衰组HR与SV总体上也呈正相关(P＜0.01),但在凌晨100～400之间,两组HR与SV分布曲线明显不同,心衰组HR与SV分布曲线出现分离现象,HR下降而SV上升,呈负相关(P＜0.01),而同时段的对照组HR与SV则仍呈正相关(P＜0.01).结论 重度充血性心力衰竭患者HR和SV分布的昼夜节律受损,在凌晨100～400之间,HR与SV分布趋势存在分离现象.     

微囊化猪视网膜色素上皮细胞移植治疗帕金森病的实验研究(英文)

目的研究微囊化后的猪视网膜色素上皮细胞(retinal pigment epithelial,RPE)对帕金森病大鼠模型的移植疗效。方法原代培养RPE 并传代,高效液相色谱法测定培养液上清中多巴胺(dopamine, DA)和高香草酸(homovanillic acid, HVA)的含量,ELISA法检测脑源性神经营养因子(brain-derived neurotrophic factor, BDNF)和胶质细胞源性神经营养因子(glial-derived neurotrophic factor, GDNF)的含量。用高压静电成囊装置制备海藻酸钠-多聚赖氨酸-海藻酸钠微囊化细胞。6-羟基多巴胺(6-hydroxydopamine, 6-OHDA)毁损内侧前脑束 (medial fore-brain bundle,MFB)建立 SD 大鼠帕金森病模型。立体定向移植 RPE+ 微囊,检验旋转实验、免疫组化和脑内生化的变化。结果 RPE 培养上清液中DA、HVA、BDNF、GDNF 的含量稳定,微囊化后细胞长期存活,活性没有明显变化。6-OHDA毁损MFB建立大鼠帕金森病模型的成模率为83%。移植微囊化的RPE后有效率为33%。结论猪 RPE 体外培养生长旺盛,持续分泌 DA、BDNF 和 GNDF,微囊化不影响其分泌功能。RPE 移植对帕金森病大鼠有一定的治疗作用。     

颈外静脉穿刺置管在大量输液中的应用

目的探讨静脉药物配置室内不同操作距离对空气微粒污染的影响程度。方法在配置室内模拟配液加药，分别在距离操作者不同位置，用空气粒子计数器对空气微粒数进行检测，以了解空气微粒的污染情况。结果操作距离不同位置5个点的空气微粒污染程度比较，差异有显著性意义（均P〈0.01）。配置室内操作时空气微粒污染程度与操作距离有关，近操作者较远离操作者污染明显；此外，空气微粒污染程度还与洁净室的空间位置有关，回风口微粒污染明显，而送风口污染最轻。结论在万级洁净室内进行配液操作时，操作者周围空气中微粒污染仍严重，必须使用层流台或生物安全柜，以保证配液的质量和增强职业防护。     

阿托伐他汀改善对比剂对肾功能的短期影响

Objective To study the effects of atorvastatin on contrast induced renal function change and plasma hsCRP in patients undergoing coronary angiography. Methods 120 patients who underwent coronary angiography were randomized to receive atorvastatin (20 mg/qn, n = 60) or no atorvastatin (n =60) treatment 2 to 3 days before coronary angiography. Urinary α1-MG, TRF and mALB were checked for evidence of tubular or glomendar damage at start, 1 day and 2 days after the administration of a radiocontrast agent. Serum creatinine, BUN, cystatin C and hsCRP levels were also assessed at the same time. Ccr and GFR were calculated according to Cockcroft-Ganh and GFR(ml/min) = 74. 835/Cys C1.333formulas basing on serum creatinine or cystatin C concentration. Results (1) In control group, comparison with the value before coronary angiography,urinary α1-MG, TRF and mALB or serum cystatin C and hsCRP significantly increased at day 1 after angiography (P ＜ 0.01). In comparison to the levels at day 1 after angiography, urinary α1-MG, TRF, mALB, serum cystatin C significantly decreased at day 2 after angiography(P ＜ 0.01), but α1-MG, cystatin C still exceeded the values before coronary angiography, TRF and mALB levels at day 2 after angiography had no significant change compared to baseline(P ＞0.05), hsCRP LeveL at day 2 after angiography had no significant change compared to that at day 1 after angiography (P ＞ 0.05) too. (2) In comparison with the value before coronary angiography in atorvastatin-treated group, the levels of urinary α1-MG, TRF and mALB or serum cystatin C at day 1 and day 2 after angiography had no significant change compared to baseline(P ＞0.05). Serum hsCRP significantly increased at day 1 after angiography compared to baseline(P ＜ 0.01), but it had no significant change compared to day 2 after angiography (P ＞ 0.05). (3)To compare to the atorvastatin-treated group, the values of urinary α1-MG, TRF and mALB or Cys C and hsCRP significantly increased at day 1 after angiography in control group (P ＜ 0.01), the values of urinary α1 -MG, cystatin C and hsCRP still significantly increased at day 2 (P ＜ 0.01) too, but those of TRF and mALB had no significantly change at day 1 or day 2 after angiography between the two groups (P ＞ 0.05). There was no significant change in BUN, Cr, Ccr levels before and after angiography between the two groups. Conclusions Low dose contrast induces light renal function damage. Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days could significantly reduce procedural inflammatory reaction, attenuate urinary protein and the effect of degrading GFR in coronary angiography patients.     

Effect of AVP on brain edema following traumatic brain injury

Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤8) and moderate traumatic brain injury group ( MTBI, GCS >8). Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group) and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan. Results: plasma AVP levels (ng/L) were (mean±SD): control, 3. 06±1. 49; MTBI, 38. 12±7. 25; and STBI, 66. 61±17. 10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0. 01). And the AVP level was correlated with the severity (STBI r =0.919, P < 0.01; MTBI r = 0.724, P < 0.01) and the duration of brain edema (STBI r = 0. 790, P < 0. 01; MTBI r = 0. 712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.