北京和上海3～5岁儿童饮食行为干预效果的研究

目的为改善北京和上海3～5岁儿童的不健康饮食行为及其父母的营养相关知识和态度,采用多途径健康教育进行干预,并对干预效果进行评估。方法采用多阶段随机整群抽样的方法,从北京、上海各选取810名3～5岁儿童及其家长作为研究对象,根据《中国居民膳食指南》(2007)和《中国孕期、哺乳期妇女以及0-6岁儿童膳食指南》(2007)开展为期6个月的健康教育干预,采用问卷调查的方法分别在干预前后收集儿童饮食行为及其父母营养相关知识、态度等信息。结果干预后,北京和上海3～5岁儿童偏食、喝含糖饮料的人数比例分别从干预前的44.5%和70.4%降低到35.5%和31.7%,有固定进餐时间、地点、可独立进餐、吃饭定时定量、能专心吃饭的儿童比例分别由干预前的80.0%、87.3%、73.4%、32.1%和27.1%升高到91.7%、91.9%、83.7%、45.9%和41.2%;干预后,儿童父母营养知识的知晓率显著提高,对待儿童饮食行为的态度也有所改善。结论通过健康教育干预,改善了儿童的不健康饮食行为,丰富了儿童家长的营养知识,改善了其对儿童的饮食行为态度,为其正确指导儿童健康饮食提供了理论基础。     

经静脉途径移植骨髓间充质干细胞修复梗死心肌的可行性与安全性研究

目的探讨经静脉注射移植同种异体骨髓来源间充质干细胞(MSC)修复损伤心肌是否可行和安全,观察移植MSC在宿主的归巢与组织学分布。方法雄性Wistar大鼠30只,分为正常大鼠MSC移植组,急性心肌梗死MSC移植组,假手术组,每组10只。结扎冠状动脉左前降支,建立大鼠急性心肌梗死模型。体外分离纯化、扩增同种大鼠骨髓MSC,于建立心肌梗死模型24h给各组大鼠经静脉输注4’6’二乙酰基2苯基吲哚(DAPI)标记的MSC,4周后处死、摘取心脏等脏器,行组织病理切片和免疫组织化学染色。结果(1)在急性心肌梗死MSC移植组,梗死区及其周边部位可见到DAPI标记的MSC;(2)在梗死心肌周边区,移植的MSC胞浆心肌特异性蛋白肌钙蛋白I和转录因子4免疫组织化学染色阳性;(3)在各组大鼠其他脏器,移植的MSC主要分布在肺脏、脾脏和肝脏;(4)细胞移植大鼠心肌组织切片未见淋巴细胞增殖,各脏器没有肿瘤形成。结论经静脉移植的MSC可归巢至大鼠梗死心肌部位,并分化为心肌细胞表型,该方法治疗缺血性心脏病安全、可行。     

射频消蚀失败的快速心律失常电生理检查及手术治疗（附三例报告）

报告３例射频消蚀术失败的快速心律失常经外科手术获得治愈。３例病人分别合并致心律失常性右室发育不良、风湿性联合瓣膜病和感染性心内膜炎并主动脉瓣关闭不全的器质性心脏病。手术均经心内电生理检查和心外膜标测定位，术后经电生理检查证实手术成功。随访３～７个月无心动过速发作。本组经验提示，合并器质性心脏病的快速心律失常在电生理标测导引下行外科治疗可获得满意疗效     

C反应蛋白在下呼吸道感染中的诊断价值：系统性综述

目的 对于经放射学影像证实的肺炎，评价C反应蛋白的诊断准确性，及其在区分下呼吸道细菌感染和病毒感染方面的作用。 资料来源 Medline和Embase（1966年1月至2004年4月）等医学文献数据库，核实了参考文献。 研究的选择 研究纳入了将C反应蛋白与胸片或微生物学作为对照进行比较的文章。由两位作者独立评价研究方法。 结果 没有一项研究符合全部有效标准。有6项研究采用胸片浸润影作为对照检查，敏感性为10％～98％，特异性为44％～99％。在5项研究的亚组分析中，成人C反应蛋白和浸润影之间的关系显示曲线下面积为0．80（95％可信区间是0．75～0．85）。在12项研究中，进行了C反应蛋白和下呼吸道感染的细菌病原学的相关性研究，敏感性为8％～99％，特异性为27％～95％。由于这些数据在流行病学和统计学上存在异质性，因此不能计算出一个统一的结果。 结论 对于胸片浸润影与下呼吸道感染中的细菌病原体之间的关系，C反应蛋白检测既不能敏感地排除其相关性，也不能特异地确定其类型。这些诊断性研究的方法学质量普遍不高，所得证据不能持久和充分地支持广泛应用C反应蛋白作为一种快速检查来指导抗生素使用。     

冷盐水灌注导管消融持续性房性心动过速一例

本文报道普通射频温控导管消融未成功时，及时更换使用冷盐水灌注导管而消融成功，尤其是射频功率很低时，难以取得远期效果。本文价值在于提醒医师思维广泛，及时改变思路、方法，以取得成功。[编者按]     

妊娠晚期突发意外性胎死宫内原因分析

目的分析妊娠晚期突发意外性胎儿宫内死亡原因,为进一步改善国产期保健工作、减少医患矛盾提供依据.方法应用回顾性分析方法,对1998年以来在辽宁地区发生的突发意外性胎儿宫内死亡522例进行临床原因分析.分析指标包括:孕妇年龄、孕周、孕产次、是否进行系统孕期保健和产前检查、胎死宫内距最后一次产前检查时间、临床分析及生化、病毒、遗传检测和胎儿尸体解剖结果,进行综合判定胎儿死亡原因.结果单胎妊娠胎儿宫内死亡的发生率为0.54%,双胎妊娠胎儿宫内死亡的发生率为0.97%,两者比较P＜0.01;胎儿宫内猝死在进行系统孕期保健孕妇和未进行系统孕期保健孕妇均有发生,比例为46.55%对比53.45%;引起胎儿宫内猝死原因如下:脐带因素占48.28%、胎儿因素占20.50%、胎盘因素占12.45%、宫内感染因素占3.07%、妊娠合并症和并发症占7.47%、羊水异常占2.87%、不明原因占4.02%、双胎输血综合征为双胎妊娠特有并发症,占双胎死亡原因的14.89%.结论1.双胎患者发生妊娠中晚期突发意外性胎儿宫内死亡率高于单胎妊娠;2.系统围产期保健不能避免胎儿宫内猝死,胎儿宫内猝死常具有较大的不可预见性和无法避免性;3.引起胎儿宫内猝死的原因众多,但脐带因素、胎儿及胎盘因素是主要原因.     

Clinical and polysomnographic features of patients with multiple system atrophy in Southwest China

Purpose

The association between clinical features and polysomnographic variables of Chinese patients with multiple-system atrophy (MSA) remains largely unknown.

Methods

This study assessed 30 patients with MSA from Southwest China using the Unified Multiple-System Atrophy Rating Scale (UMSARS). Each patient also underwent video-polysomnography. Twenty age and gender matched healthy volunteers were performed video-polysomnography as control group.

Results

Of the 30 patients, 23 (76.7 %) were classified as having MSA-C and seven (23.3 %) were diagnosed with MSA-P. The mean age of the patients at disease onset was 53.2?±?8.5 years, and the mean duration of their disease was 3.6?±?2.8 years. Twenty-one patients complained of sleep disorders. The mean scores of UMSARS-I, UMSARS-II, and UMSARS-IV of patients with MSA-P were significantly higher than those of patients with MSA-C. Polysomnography revealed that 29 patients had sleep architecture alteration. A longer duration of stage N1 sleep, a shorter REM sleep, as well as decreased sleep efficiency and total sleep time (TST) were detected. Twenty-one patients had obstructive sleep apnea. Patients with MSA-C demonstrated longer sleep onset latencies compared with patients with MSA-P. TST was negatively correlated with MSA duration, whereas sleep latency was positively correlated with MSA duration. Moreover, TST, and mean SaO₂ were negatively correlated with motor disability.

Conclusions

Various sleep disorders are common in Chinese MSA patients. Sleep architecture and sleep-associated breathing disorders are predominant polysomnographic findings. Sleep quantity was reduced with disease progression.     

Peritonitis due to Burkholderia gladioli

We report a case of continuous ambulatory peritoneal dialysis (CAPD)–related peritonitis. Burkholderia gladioli, as a plant pathogen, were cultured from peritoneal effluent. Peritonitis healed after intraperitoneal cefazolin and gentamicin. This case indicated that CAPD effluent may be contaminated by B. gladioli, causing CAPD-related peritonitis. On the other hand, it can be successfully treated with intraperitoneal antimicrobials without removal of the Tenckhoff catheter.     

Interferon regulatory factor 8 functions as a tumor suppressor in renal cell carcinoma and its promoter methylation is associated with patient poor prognosis

Interferon regulatory factor 8 (IRF8), as a central element of IFN-γ-signaling, plays a critical role in tumor suppression. However, its expression and underlying molecular mechanism remain elusive in renal cell carcinoma (RCC). Here, we examined IRF8 expression and methylation in RCC cell lines and primary tumors, and further assessed its tumor suppressive functions. We found that IRF8 was widely expressed in human normal tissues including kidney, but frequently downregulated by promoter methylation in RCC cell lines. IRF8 methylation was detected in 25% of primary tumors, but not in adjacent non-malignant renal tissues, and associated with higher tumor nuclear grade of RCC. Ectopic expression of IRF8 inhibited colony formation and migration abilities of RCC cells, through inducing cell cycle G2/M arrest and apoptosis. IFN-γ could induce IRF8 expression in RCC cells, together with increased cleaved-PARP. We further found that IRF8 inhibited expression of oncogenes YAP1 and Survivin, as well as upregulated expression of tumor suppressor genes CASP1, p21 and PTEN. Collectively, our data demonstrate that IRF8 as a functional tumor suppressor is frequently methylated in RCC, and IRF8-mediated interferon signaling is involved in RCC pathogenesis.     

乳腺癌中E-cadherin和BCA-225蛋白表达与预后的相关性研究

目的探讨乳腺癌组织中E-cadherin和BCA-225蛋白表达及其与临床病理因素和预后的关系。方法应用SP免疫组化方法检测70例原发性乳腺癌组织和10例良性乳腺病变中E-cadherin和BCA-225蛋白的表达。结果乳腺癌组织中E-cadherin的高表达率显著低于良性乳腺疾病,其表达与肿瘤大小、临床TNM分期、组织学分级、淋巴结转移状态密切相关（P〈0.05）,而与雌孕激素受体状态及癌基因Her-2无关。BCA-225的高表达率显著高于良性乳腺疾病（P〈0.01）,其表达与组织学分级及癌基因Her-2密切相关（P〈0.05）,而与肿瘤大小、临床TNM分期、淋巴结转移、及雌孕激素受体状态无关。E-cadherin与BCA-225两者表达无相关性。Kaplan-Meier生存曲线分析显示E-cadherin高表达患者的生存状况较对应情况好,且差异有统计学意义（P〈0.05）。多因素Cox回归分析表明,E-cadherin蛋白为乳腺癌有效的独立的预后指标,其风险系数exp为-1.795954,（P〈0.05）。结论乳腺癌E-cadherin表达缺失或减少,与肿瘤的发生发展、增殖、侵袭转移及预后密切相关,可作为评价乳腺癌患者独立的预后指标。乳腺癌BCA-225表达上调与肿瘤的分化程度相关,但作为乳腺癌患者独立的预后评价指标还尚待进一步深入探讨。