目的 探讨早期外周灌注指数(PI)、乳酸及降钙素原(PCT)对脓毒性休克患者预后的预测价值.方法选择ICU住院的脓毒性休克患者80例,根据患者住院第28天的生存情况分为生存组48例和死亡组32例.回顾性收集患者入住ICU当天(D0)和经过标准治疗1 d(D1)的PI、乳酸及PCT等资料,绘制D1时PI、乳酸及PCT单独及联合预测患者预后的受试者工作特征(ROC)曲线,计算曲线下面积(AUC)、敏感度、特异度及单独预测时的Cut-off值.结果D0时两组PI、乳酸及PCT水平比较差异均无统计学意义(P均>0.05).D1时死亡组PI低于生存组,乳酸及PCT水平均高于生存组(P均<0.05).D1时PI、乳酸及PCT单独预测患者预后的AUC分别为0.906(95％CI:0.8424～0.9688)、0.795(95％CI:0.6953～0.8946)、0.809(95％CI:0.6974～0.9205),敏感度分别为87.5％、72.9％、89.6％,特异度分别为81.2％、78.1％、71.9％,Cut-off值分别为0.27、4.30、3.73.PI、乳酸及PCT联合预测患者预后的AUC为0.932(95％CI:0.879～0.985),均高于三项指标单独预测的AUC.结论脓毒性休克患者经过标准治疗1 d后PI低于0.27、乳酸高于4.30 mmol/L、PCT高于3.73 ng/mL均提示预后不良,PI与乳酸、PCT三项指标联合检测可更好地预测患者预后.

目的:探究血清脑源性神经营养因子(BDNF)、白细胞介素-8(IL-8)、肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)水平对新生儿缺氧缺血性脑病(HIE)严重程度及预后的评估价值.方法:回顾性分析68例HIE患儿的临床资料,根据病情严重程度将纳入患儿分为轻度组(n=27例)、中度组(n=23例)、重度组(n=18例),另选取同期50例健康新生儿作为正常对照组,均检测血清BDNF、IL-8、TNF-α、SOD水平,Spearman相关性分析血清BDNF、IL-8、TNF-α、SOD水平与HIE严重程度的关系,受试者工作特征曲线(ROC)分析血清BDNF、IL-8、TNF-α、SOD值单一或联合对HIE患儿预后的预测价值.结果:HIE组血清BDNF、SOD水平低于正常对照组(P<0.05),血清IL-8、TNF-α水平高于正常对照组(P<0.05);随着HIE病情加重,患儿血清BDNF、SOD水平逐渐降低,血清IL-8、TNF-α水平逐渐上升,组间两两比较差异均有统计学意义(P<0.05);Spearman相关性分析显示HIE患儿血清BDNF、SOD水平与病情严重程度呈显著负相关关系(r=-0.621、-0.598,P<0.05),IL-8、TNF-α与病情严重程度呈显著正相关关系(r=0.562、0.663,P<0.05);ROC分析结果显示联合预测HIE患儿预后结局曲线下面积(AUC)0.955大于BDNF、IL-8、TNF-α、SOD值单一预测0.805、0.754、0.855、0.762(P<0.05).结论:血清BDNF、IL-8、TNF-α、SOD水平可用于评估HIE严重程度,可有效预测患儿预后.

目的 分析成人重症破伤风患者的临床诊治关键环节.方法 回顾性分析2013年1月至2019年6月西安交通大学第一附属医院外科ICU收治的6例成人重症破伤风患者的临床特点和治疗方法.结果 6例成人重症破伤风患者均有明确外伤史,但预防接种史不详.平均年龄(49.5±7.25)岁,潜伏期(4～12)d,其中Ablett分级 Ⅲ级2例(33.3％),Ⅳ级4例(66.7％).张口困难是早期和典型的临床症状.5例患者气管切开并行机械通气,平均机械通气时间(9.67±4.13)d,后均继发肺部感染;4例患者并发自律性不稳定;2例患者并发横纹肌溶解,其中1例行连续肾脏替代疗法(CRRT)治疗.经积极治疗后,2例Ⅳ级患者放弃治疗,自动出院后死亡,死亡原因为难以控制的抽搐、感染及多脏器功能不全;4例患者(2例 Ⅲ 级,2例 Ⅳ 级)治愈后出院.ICU平均住院时间(25.33±13.92)d,死亡率为33.3％.结论 以控制抽搐和自律性不稳定为重点,以积极的气道管理为核心,通过早期评估分级和重症监护,制定个体化精准镇静方案,结合并发症处理和接种免疫是治疗重症破伤风的有效措施.

目的 探讨不同种类肿瘤中miR-338-3p表达谱及其表达异常的表观遗传修饰调控机制.方法 生物信息学大数据库(TCGA Pan-Cancer)分析miR-338-3p在15种不同种类肿瘤组织中的表达谱;以胃癌为研究对象,分析数据库中45例正常胃组织和366例胃癌组织中miR-338-3p表达情况;CRCH37数据库预测miR-338-3p上游启动子区组蛋白修饰位点;利用染色质免疫共沉淀获取组蛋白结合的DNA,PCR扩增miR-338-3p启动子区片段,凝胶电泳验证PCR产物.结果 miR-338-3p在包括食道癌(ESCA)等不同种类肿瘤中表达异常,其中ESCA、头颈部鳞状细胞癌(HNSC)、肾嫌色细胞癌(KICH)、肾乳头状肾细胞癌(KIRP)、肺鳞癌(LUSC)和甲状腺癌(THCA)中表达显著下调(P＜0.05),而在结肠腺癌(COAD)、肾透明细胞癌(KIRC)和肝细胞肝癌(LIHC)表达显著上调(P＜0.05);366例胃癌组织中miR 338 3p表达普遍下调;染色质免疫共沉淀结合PCR证实组蛋白H3K9m2和H3K4m3是可能引起miR-338 3p下调的两个修饰位点.结论 miR-338 3p在胃癌中表达下调,组蛋白H3K9和H3K4甲基化修饰是潜在原因.

目的 新生儿化脓性脑膜炎预后一直是临床工作中关注点.本病具有发病率高,死亡率高,致残率高三大特点.近年来,其病死率呈逐年下降趋势,但是病残率下降并不明显,神经系统后遗症比较多见,此类患儿基本包含在新生儿病房非治愈出院的人数中,以出院结局为分组因素,将非治愈出院的患儿与治愈出院患儿进行对照分析,探讨可造成非治愈出院患儿的相关因素,为预测新生儿化脓性脑膜炎不良预后提供思路及理论依据.方法 本研究收集西安交通大学附属西安市儿童医院新生儿科2015年1月至2016年12月期间确诊为新生儿化脓性脑膜炎患儿的临床病历,按照诊断标准及研究信息要求,整理出相关资料,共计患儿168例.采用回顾性研究方法,收集患儿一般情况(患儿性别、出生体质量、日龄、发病时间等)、围生期相关因素(胎膜早破、宫内窘迫、羊水污染,母亲病史等)、临床症状和体征(反应、吃奶、惊厥、肌张力、原始反射等)、辅助检查(白细胞计数、血小板计数、脑脊液细胞数、脑脊液葡萄糖、脑脊液蛋白、血培养等)和治疗相关(抗生素使用、住院天数、呼吸机支持等)资料;根据患儿出院时转归情况将患儿分为治愈出院组和非治愈出院组,两组之间进行比较和统计分析.临床资料中计数资料以率(％)表示,计数资料组间比较采用 χ2检验(若理论频数小于1,则采用Fisher'精确概率法),计量资料采用t检验,不能满足t检验要求时采用非参数秩和检验,结果均以ɑ=0.05为检验水准,P<0.05为有统计学意义.结果 非治愈组患儿40例,出院原因依次为:病情严重,有严重并发症,预后不良可能性大14(35.0％)例;经治疗后脑脊液指标部分有好转,但未正常,有合并症,住院时间较长21(52.5％)例;合并疾病未治愈,好转出院4(10.0％);入院姓名有误,临床治疗好转,疗程不足,因改名字1(2.5％)例.在一般情况方面(日龄、胎龄、出生体质量及住院时间),孕期因素(母孕期感染、合并妊娠高血压及高龄产妇因素),围产期因素(胎膜早破、低出生体质量、羊水污染、宫内窘迫及剖宫产娩出),临床症状(吃奶差、发热、母乳喂养及惊厥病史),神经系统查体(反应异常、颈强直及反射异常),实验室检查(在PCT升高、Hs-CRP升高及白细胞计数异常),超声影像学(脑膜异常、脑室管膜炎、硬膜下积液及超声结果异常),两组患儿均无统计学差异.在临床表现方面(高颅压表现及肌张力增高),非治愈组患儿比率较治愈组明显升高,具有统计学差异;实验室检查,非治愈组患儿在Hs-CRP、脑脊液细胞数、葡萄糖及蛋白方面明显高于治愈组,两组数据具有统计学差异,非治愈组在血培养阳性率及PL T减少比率方面,较治愈组明显升高,具有统计学差异,非治愈组患儿在脑脊液细胞数升高、细胞数明显升高、葡萄糖降低及蛋白升高比率方面均高于治愈组患儿,两组数据具有统计学意义;影像学检查方面,超声检查提示脑室扩张患儿比率及核磁共振成像检查阳性率,非治愈组患儿阳性率明显高于治愈组,具有统计学意义.结论 本研究从治疗结局出发,分析未治愈患儿相关资料,在发现查体方面颅内压及肌张力增高表现与不良结局存在相关性,在辅助检查方面血小板计数减低及血培养阳性与不良结局存在相关性,在脑脊液检查方面细胞数及蛋白明显升高和葡萄糖降低与不良结局存在相关性,在影像学检查方面超声提示脑室扩张及M RI异常结果与不良结局存在相关性,以上均具有统计学意义.通过研究发现,对于以上特点患儿,在积极干预治疗的同时,预测其不良结局可能性大,需要与患儿家属积极沟通,改善治疗措施,避免医疗纠纷和不良结局.

Objective To investigate the expression of hsa-miR-106a in gastric cancer and explore its clinical significance. Methods Total RNA was extracted from 19 pairs of gastric cancer tissues and normal tissues. The expression levels of miR-106a were detected by quantitative reverse transcriptase polymerase chain reaction. The association between miRNA expression and clinicopathological features was investigated. Results The miR-106a was highly expressed in 14 cases of gastric cancer,and the level was significantly higher in gastric cancer tissues than that in normal tissues( P 0. 01). The miR-106a expression in gastric tumor was associated with the pathological grading and clinical stage( P 0. 05) Conclusion These results suggest that hsa-miR-106a might be involved in the progression and development of gastric cancer.

Objective To observe the expression of neuronal nitric oxide synthase(nNOS) in different encephalic regions and at different time points after focal cerebral ischemia in adult rats and explore the effect of Ligustrazine on nNOS expression.Methods SD male adult rats were randomly divided into five groups: sham operation,ischemic model,low dose(20mg/kg),medium dose(40mg/kg) and high dose(80mg/kg) Ligustrazine groups.According to the time after ischemia,each group was further divided into 5 sub-groups: 1,3,7,14,and 21d(3 rats in each sub-group).Middle cerebral artery occlusion(MCAO) model was established by placement of an intraluminal filament at the origin of MCA.Ligustrazine was administered intraperitoneally at a daily dose of 20,40 or 80mg/kg starting at 2h after MCAO,respectively,until 2h before sacrifice.Immunohistochemical staining was adopted to observe nNOS expression in subventricular zone(SVZ) of the lateral cerebral ventricle,corpus callosum(CC),striatum and cortex peri-infarction,CA1 area,and dentate gyrus(DG).Results Expression of nNOS at different time points was similar in sham operation group,with no significant difference(P0.05).In SVZ,nNOS expression in ischemic model group was reduced on days 1-14,but increased on day 21;after Ligustrazine administration,nNOS expression was obviously decreased on days 3-14 in all Ligustrazine dose groups,but began to increase on day 21.In CC,nNOS expression in ischemic model group was reduced on days 3-14,and began to increase on day 21;in the different-dose Ligustrazine groups,nNOS expression was significantly decreased on days 3-14,especially in medium-and high-dose groups,but increased on day 21.In striatum and cortex peri-infarction,nNOS expression in ischemic model group was obviously decreased on days 3 and 7,but enhanced on days 14 and 21;in various-dose Ligustrazine groups,nNOS expression was decreased on days 3-21,especially in medium-and high-dose groups,but increased slightly on day 21.In DG and CA1 areas,nNOS expression in ischemic model group was reduced on days 3 and 7,but began to increase on day 14;nNOS expression in all Ligustrazine groups were decreased during 3-21d.There were significant differences between ischemic model group and different-dose Ligustrazine groups at different time points(P0.05).Conclusion Ligustrazine has a significantly inhibitory effect on nNOS expression in different encephalic regions during 3-14d after focal cerebral ischemia,suggesting that Ligustrazine might play a brain-protecting role by inhibiting nNOS expression and reducing NO production.

微量元素是人体必不可少的无机营养素,虽然饮食中只需极少的量,但其缺乏或过量都会对人体健康和疾病造成影响.尤其在临床中人体微量元素的生理功能和缺乏状况更为重要.因此,理解无机元素和微量元素的正常作用,了解缺乏或过量所造成的影响以及了解微量元素的测量方法和限制对临床营养基础的学习非常重要.

Objective: To observe the neuroprotective effect of Ligustrazine after focal cerebral ischemia in rats. Methods: The model of the middle cerebral artery occlusion (MCAO) was established by placement of an intraluminal filament at the origin of left middle cerebral artery. Volume of cerebral infarction was measured by triphenyltetrazolium chloride (TTC) staining. Cerebral water content was detected with dry-wet weight method. Changes of neurons in peripheral infarction were observed by Golgi silver staining. Results: Ligustrazine obviously decreased the cerebral infarction volume and the brain water content, and this effect increased with the increase of Ligustrazine dose. The Golgi silver staining showed that peripheral neurons in the cortex infarction of model group were increased obviously 14 days after ischemia. Degenerative neurons displayed disruption, thickening, and rosary processes, and reduction of dendritic spines. Peripheral neurons in the cortex infarction of Ligustrazine group outnumbered those in the model group, and the neuronal degeneration was less. Conclusion: Ligustrazine can reduce the cerebral infarction volume and hydrocephalus, and protect neurons around ischemia area, confirming that Ligustrazine has the protective function on damage caused by cerebral ischemia.