VEGF和Ki－67在膀胱移行细胞癌中的表达和临床意义

目的探讨膀胱移行细胞癌（BTCC）组织中血管内皮生长因子（VEGF）和Ki-67的表达和临床意义。研究二者与肿瘤血管形成和肿瘤细胞增殖的关系。方法采用免疫组织化学SP法检测68例BTCC组织中VEGF和Ki-67的表达,分析VEGF和Ki-67表达与肿瘤病理分级、复发、转移及预后的关系。结果BTCC组织中VEGF阳性率为73．53％,Ki-67阳性率为70．59％。在不同病理分级BTCC组织中VEGF和Ki-67的表达有明显差异,病理分级高的明显高于分级低的（P〈0．05）;浸润性肿瘤明显高于表浅性肿瘤（P〈0．05）;复发组均明显高于无复发组（P〈0．05）;Ki-67和VEGF协同强阳性表达率差异有统计学意义（P〈0．01）。结论VEGF和Ki-67的阳性表达尤其是联合阳性表达对判断膀胱癌复发、评估预后具有重要意义。     

Sry基因监测腺病毒介导肝细胞生长因子修饰的骨髓间充质干细胞移植在大鼠烫伤创面愈合中的作用

目的 制备地高辛标记的Sry探针,监测局部异体移植携带人肝细胞生长因子基因的重组腺病毒(Ad-HGF)修饰的骨髓间充质干细胞(BMSCs)在烫伤创面愈合中的作用.方法 用雄性大鼠肝组织通过聚合酶链反应法克隆Sry基因,并将其构建至T Easy Vector上,用地高辛标记法制备Sry基因原位杂交探针.密度梯度离心法体外分离培养雄性Wistar大鼠BMSCs,并转染Ad-HGF.复制16只背部深Ⅱ度烫伤雌性大鼠模型,于造模成功后,将Ad-HGF修饰的BMSCs一次性多点注射于创面真皮下.21 d后,处死大鼠,取愈合创面新生组织和正常组织制作石蜡切片,原位杂交法检测组织切片中Sry基因的表达.结果 ①从8只雄性大鼠中成功克隆出Sry基因;②制备出地高辛标记的Sry探针;③16只雌性大鼠深Ⅱ度烧伤模型复制成功,用Ad-HGF修饰的BMSCs治疗后,原位杂交法证实全部雌鼠创面新生组织中有Sry表达,而正常组织中未检测到.结论 外源移植的BMSCs参与了大鼠烫伤创面的修复,Sry基因可作为细胞追踪标记,为细胞治疗追踪技术及利用BMSCs治疗创伤的研究提供依据.     

Non-syndromic bilateral enlarged vestibular aqueducts in two siblings

Enlarged vestibular aqueduct is one of the most frequent inner ear malformations with early manifested sensorineural hearing loss. It is often associated with Pendred syndrome. The non-syndromic familial enlarged vestibular aqueduct entity is less described with only a few cases reported in the literature. It is thought to be a varying presentation on the phenotypic spectrum of genetic mutation in the same locus of chromosome 7q31. The familial inheritance has been suspected to be autosomal recessive. In this case report, we present a patient who presented to the clinic with hearing loss after blunt head trauma with a soccer ball. Suspected enlarged vestibular aqueduct was confirmed to be bilateral on CT scan of the temporal bones. Additional inquiry into the family history revealed that her sister also had bilateral sensorineural hearing loss at an early age. Unpredictably, bilateral enlarged vestibular aqueducts were confirmed in the sister with similar imaging modality. The clinical presentation, diagnosis, and treatment strategies are reviewed along with the current literature.     

Role of penehyclidine in acute organophosphorus pesticide poisoning

BACKGROUND:Penehyclidine is a newly developed anticholinergic agent.We aimed to investigate the role of penehyclidine in acute organophosphorus pesticide poisoning(OP)patients.METHODS:We searched the Pubmed,Cochrane library,EMBASE,Chinese National Knowledge Infrastructure(CNKI),Chinese Biomedical literature(CBM)and Wanfang databases.Randomized controlled trials(RCTs)recruiting acute OP patients were identifi ed for meta-analysis.Main outcomes included cure rate,mortality rate,time to atropinization,time to 60%normal acetylcholinesterase(AchE)level,rate of intermediate syndrome(IMS)and rate of adverse drug reactions(ADR).RESULTS:Sixteen RCTs involving 1,334 patients were identifi ed.Compared with the atropineor penehyclidine-alone groups,atropine combined with penehyclidine significantly increased the cure rate(penehyclidine+atropine vs.atropine,0.97 vs.0.86,RR 1.13,95%CI[1.07–1.19];penehyclidine+atropine vs.penehyclidine,0.93 vs.0.80,RR 1.08,95%CI[1.01–1.15])and reduced the mortality rate(penehyclidine+atropine vs.atropine,0.015 vs.0.11,RR 0.17,95%CI[0.06–0.49];penehyclidine+atropine vs.penehyclidine,0.13 vs.0.08,RR 0.23,95%CI[0.04–1.28]).Atropine combined with penehyclidine in OP patients also helped reduce the time to atropinization and AchE recovery,the rate of IMS and the rate of ADR.Compared with a single dose of atropine,a single dose of penehyclidine also signifi cantly elevated the cure rate,reduced times to atropinization,AchE recovery,and rate of IMS.CONCLUSION:Atropine combined with penehyclidine benefi ts OP patients by enhancing the cure rate,mortality rate,time to atropinization,AchE recovery,IMS rate,total ADR and duration of hospitalization.Penehyclidine combined with atropine is likely a better initial therapy for OP patients than atropine alone.     

Polymethylmethacrylate augmentation of the pedicle screw: the cement distribution in the vertebral body

Many studies have proven that the polymethylmethacrylate (PMMA) augmentation of the pedicle screw can significantly increase stiffness and strength of spinal fixation. Some major complications have also been reported. However, there are no reports discussing cement distribution and its morphology in the osteoporotic vertebral body, which is critical in the analysis of the biomechanical strength of the pedicle screw and the risk of cement leakage after pedicle screw augmentation. In this study, we used computed tomography (CT) to evaluate the cement distribution in the osteoporotic vertebral body after PMMA augmentation of a pedicle screw and to analyze the factors leading to cement leakage. Two groups of patients were studied. Group A consisted 25 osteoporotic patients (mean age of 73 years) with spinal instrumentation who had a total of 145 pedicle screws and cement augmentation with biopsy needles. Group B consisted of 23 osteoporotic patients (mean age of 74.6 years) with spinal instrumentation who had a total of 125 cannulated pedicle screws with cement augmentation. All patients had CT evaluation of the cement distribution in the vertebral body after the surgery. The cement distribution in the vertebrae was divided into four zones in the axial CT view: anterior one-third, middle third, and posterior third of vertebral body, and the pedicle. The morphology of the cement distribution around the pedicle screw was defined as scattered type or concentrate type. The leakage pattern was divided to anterior–lateral, posterior–lateral, and canal leakage. The correlations among bone mineral density (BMD), the cement leakage rate, and cement distribution morphology were also analyzed. The results showed that most augmented pedicle screws had cement extension into three of the four zones of the vertebral body (66.3%), followed by two zones (20%), all four zones (11.5%), and only one zone (2.2%). Overall, 123 screws (84.8%) in Group A and 108 screws (86.4%) in Group B had cement concentrate type distribution. The cement leakage rate in Group A is 18.3% and 13.6% in Group B. Patients with a BMD <0.6 g/cm² had significantly higher rates of cement leakage and tended toward a scattered cement distribution. There was only one patient who had a symptomatic leakage (sciatica) in Group B. We concluded that the cement distribution after pedicle screw augmentation with biopsy needle or cannulated screw technique was mostly localized in three zones of the vertebral body, and patients with lower BMD had a higher risk of cement leakage and scattered cement distribution.     

上调肝脏HO-1抑制肥大细胞脱颗粒减轻大鼠肝脏缺血再灌注损伤

目的 探索HO-1对肝脏缺血再灌注损伤中肥大细胞脱颗粒的影响。方法 将20只SD大鼠随机分成4组：假手术组（Sham组）,缺血再灌注损伤组（I/RI组）,HO-1诱导剂钴原卟啉组(CoPP组,术前24h给予CoPP,5 mg/kg)及HO-1抑制剂锌原卟啉组(ZnPP组,术前24h给予ZnPP,20 mg/kg)。建立大鼠缺血再灌注损伤模型,各组于再灌注后2h收集标本。RT-PCR检测肝脏组织HO-1 mRNA表达,Western blot检测肝脏组织HO-1蛋白表达;测定血清中ALT、AST水平;肝脏组织甲苯胺蓝染色检测肥大细胞脱颗粒数量,HE染色评价肝脏组织损伤情况。结果 与Sham组相比,I/RI组、CoPP组、ZnPP组大鼠组织HO-1 RNA和蛋白表达增加,血清ALT、AST水平升高,肥大细胞脱颗粒数量增多,肝脏细胞损伤加重。CoPP组与I/RI组相比,HO-1 mRNA和蛋白表达增加,血清ALT、AST水平减低,肥大细胞脱颗粒数量减少,肝细胞损伤减轻。ZnPP组与I/RI组相比,HO-1 mRNA和蛋白表达减少,血清ALT、AST水平升高,肥大细胞脱颗粒数量增多、肝细胞损伤严重。组间比较差异具有统计学意义(P＜0.05)。结论 HO-1过表达能减轻肝脏I/RI,其机制可能与抑制肝脏组织中肥大细胞脱颗粒有关。     

Fatty liver-induced changes in stereotypic behavior in rats and effects of glucagon-like peptide-1 analog on stereotypy

Although understanding the relation between psychotic behavior and immune abnormalities has been the focus of research for many years, it remains to be elucidated whether the changes in cytokine levels are part of etiology or a result of the stress associated with the disorder. In accordance with previous studies on changes in cytokine levels due to metabolic changes and psychosis, we hypothesized that fatty liver may potentiate apomorphine-induced stereotypy in a rodent model and that a synthetic glucagon-like peptide-1 analog exenatide would ameliorate this effect. In this study, 18 male Sprague Dawley albino mature rats were used. We induced hepatosteatosis in these rats by feeding them with 30% fructose dissolved in drinking water for 8 weeks. The animals were divided into three groups, namely, the normal group, the intracerebroventricular (ICV) exenatide group, and the ICV NaCl group. Apomorphine-induced stereotypic behavior test was performed in all groups and the liver was removed for histopathological examination after all the rats were euthanized. In the nonalcoholic fatty liver (NAFL) group, stereotypy scores were significantly increased compared with the control group rats (p < 0.00001). A significant decrease in stereotypy scores were observed in the ICV exenatide group with NAFL when compared with the ICV saline group with NAFL (p < 0.005). In addition, brain malondialdehyde and tumor necrosis factor-α levels decreased in the ICV exenatide group. The results of this study showed that fatty liver enhances the effect of apomorphine on stereotypy, which was reversed by exenatide possibly by antioxidant and anti-inflammatory effects.     

The presence of the -866A/55Val/Ins haplotype in the uncoupling protein 2 (UCP2) gene is associated with decreased UCP2 gene expression in human retina

Uncoupling protein 2 (UCP2) is a mitochondrial transporter present in the inner membrane of mitochondria, and it uncouples substrate oxidation from ATP synthesis, thereby dissipating the membrane potential energy and consequently decreasing ATP production by mitochondrial respiratory chain. As a consequence of the uncoupling, UCP2 decreases the reactive oxygen species (ROS) formation by mitochondria. ROS overproduction is related to diabetic retinopathy (DR), a chronic complication of diabetes mellitus (DM). Recently, our group reported that the -866A/55Val/Ins haplotype (-866G/A, Ala55Val and Ins/Del polymorphisms) of the UCP2 gene was associated with increased risk for DR in patients with DM. The purpose of this study was to analyze the effect of this haplotype on UCP2 gene expression in human retina. In addition, MnSOD2 gene expression was also investigated according to different UCP2 haplotypes. This cross-sectional study included 188 cadaveric cornea donors. In a subset of 91 retinal samples differentiated according to the presence of the mutated UCP2 haplotype and risk alleles of the -866G/A and Ins/Del polymorphisms, UCP2 and MnSOD2 gene expressions were measured by semi-quantitative RT-qPCR. Mutated UCP2 haplotype carriers (homozygous?+?heterozygous) had a lower UCP2 gene expression than reference haplotype carriers (8.4?±?7.6 vs. 18.8?±?23.7 arbitrary units; P?=?0.046). Accordingly, UCP2 gene expression was decreased in -866A carriers when compared with G/G carriers (P?=?0.010). UCP2 gene expression did not differ between Ins allele carriers and Del/Del carriers (P?=?0.556). Interestingly, subjects carrying the heterozygous UCP2 haplotype showed increased MnSOD2 gene expression (P?=?0.025). This is the first report suggesting that the presence of the -866A/55Val/Ins haplotype is associated with decreased UCP2 gene expression in human retina. Possibly, MnSOD2 expression might influence the UCP2 effect in the protection against oxidative stress.