30例感染性心内膜炎的临床分析

目的:探讨感染性心内膜炎(IE)的病因,致病微生物的变迁及抗生素的选择。方法:对1995年5月～2003年8月间住院的30例IE患者的临床资料进行回顾性分析。结果:风湿性心脏瓣膜病为其主要的基础心脏病变。链球菌在致病微生物中依然居首位,但凝固酶阴性葡萄球菌(CNS)等其它菌种逐渐增多,且对青霉素耐药发生率高,为临床诊治造成困难。结论:对于IE患者应尽可能早期明确诊断,早期选用有效的抗生素。CNS在IE的致病微生物中的地位有待进一步提高。     

延续性护理在心脏瓣膜置换术患者中的应用效果分析

目的 探讨延续性护理在心脏瓣膜置换术患者中的应用效果.方法 选取2017年1月—2019年1月在四川省德阳市人民医院接受心脏瓣膜置换术治疗的80例瓣膜性心脏病患者作为研究对象,随机分为观察组和对照组各40例.出院后对照组不进行主动护理,观察组采用延续性护理,对两组患者干预前后服药依从性、生活质量及心功能进行比较分析.结果 出院时两组服药依从性、生活质量及心功能比较差异无统计学意义(P>0.05),出院后6个月观察组服药依从性、生活质量及心功能均优于对照组,差异有统计学意义(P<0.05).结论 延续性护理应用于心脏瓣膜置换术出院患者中可提高患者服药依从性,提升患者生活质量及心功能恢复,值得临床借鉴推广.     

血栓弹力图评价全髋置换术围手术期应用利伐沙班后的凝血功能改变

目的研究血液凝固性在全髋关节置换术前、后的改变以及术后服用利伐沙班对其影响。方法随机选择2011年在我科行全髋关节置换术的患者66例。所有患者术后第1天开始口服利伐沙班,并分别于术前、术后第1天、术后第4天行血栓弹力图（thromboelastography,TEG）检查。比较各阶段TEG重要指标的差异。结果全髋关节置换术后TEG各指标中凝血反应时间（r）、血细胞凝集块形成时间（k）、凝血时间（r＋k）值短于术前,血细胞凝集块形成速率（α）、最大振幅（ma）、凝血指数（CI）值高于术前,差异有统计学意义;术后服用利伐沙班后TEG各指标中r、r＋k时间长于服药前,差异有统计学意义;k、α、ma、CI无显著变化,差异无统计学意义。结论全髋关节置换术可明显增加患者的血液凝固性,而增加血栓风险;术后短期口服利伐沙班可降低血液凝固性。     

Nosocomial and community acquired uropathogenic isolates of Proteus mirabilis and antimicrobial susceptibility profiles at a university hospital in Sub–Saharan Africa

ObjectiveTo ascertain antimicrobial susceptibility profile of Proteus mirabilis (P. mirabilis) from clinical urine specimens at a university hospital in the spate of its recorded increasing resistance patterns.MethodsThe study was retrospective in nature. Data generated from urine cultures of patients at University of Calabar Teaching Hospital for a period of five years (2004–2009) were compiled. Relevant information obtained were age and gender of patients, organisms recovered and their antibiotic susceptibility patterns. P. mirabilis was identified using standard laboratory procedures.ResultsP. mirabilis showed the highest resistance against ampicillin, cloxacillin, amoxicillin, tetracycline, co-trimoxazole, erythromycin and chloramphenicol (100%–37.2%) while colistin, ofloxacin, ciprofloxacin, ceftriaxone, nalidixic acid and nitrofurantoin recorded the highest activity (59.1%–96.9%) with no drug recording 100% activity. The resistance of the nosocomial isolates of the organism were significantly higher than the community acquired isolates against that of the common antibiotics in use (P<0.05).ConclusionsExtreme caution should be exercised in antibiotic administration in hospital setting and the potential benefits adequately assessed while control of nosocomial infections be given a priority so as to limit the spread of resistant bacteria.     

TLIF术式在布氏杆菌性脊柱炎病人中的临床疗效及安全性分析

目的 对比分析单纯后路内固定+一期经腰椎间孔病椎间病灶清除(TLIF)与经典的前后联合手术在布氏杆菌性脊柱炎患者中的临床疗效及安全性。 方法 对我院2015年1月至2017年12月收治的93例布病性脊柱炎患者的临床资料进行分析。按手术方式分为观察组(45例)和对照组(48例)。对两组患者的基础数据、临床指标、术前术后各项指标水平以及术后并发症、植骨治愈情况。 结果 观察组与对照组基础数据比较,差异无统计学意义(P>0.05)。观察组患者的手术时间、住院天数、术中出血量及术后下床时间均明显低于对照组(P<0.01)。两组患者术后3个月的ODI、VAS、CRP、ESR及Cobb角均明显低于术前(P<0.05);术后3个月,观察组患者的ODI、VAS、CRP、ESR及Cobb角均明显低于对照组(P<0.05)。观察组术后并发症发生率(4.4%)明显低于对照组(25.0%)(Χ²=7.674,P<0.01)。 结论 TLIF治疗布氏杆菌性脊柱炎患者的临床疗效突出,安全性较好,更有利于患者术后身体的恢复。     

Impairment of brain redox homeostasis caused by the major metabolites accumulating in hyperornithinemia–hyperammonemia–homocitrullinuria syndrome in vivo

Ornithine, ammonia and homocitrulline are the major metabolites accumulating in hyperornithinemia-hyperammonemia-homocitrullinuria syndrome, a genetic disorder characterized by neurological regression whose pathogenesis is still not understood. The present work investigated the in vivo effects of intracerebroventricular administration of ornithine and homocitrulline in the presence or absence of hyperammonemia induced by intraperitoneal urease treatment on a large spectrum of oxidative stress parameters in cerebral cortex from young rats in order to better understand the role of these metabolites on brain damage. Ornithine increased thiobarbituric acid-reactive substances (TBA-RS) levels and carbonyl formation and decreased total antioxidant status (TAS) levels. We also observed that the combination of hyperammonemia with ornithine resulted in significant decreases of sulfhydryl levels, reduced glutathione (GSH) concentrations and the activities of catalase (CAT) and glutathione peroxidase (GPx), highlighting a synergistic effect of ornithine and ammonia. Furthermore, homocitrulline caused increases of TBA-RS values and carbonyl formation, as well as decreases of GSH concentrations and GPx activity. Hcit with hyperammonemia (urease treatment) decreased TAS and CAT activity. We also showed that urease treatment per se was able to enhance TBA-RS levels. Finally, nitric oxide production was not altered by Orn and Hcit alone or in combination with hyperammonemia. Our data indicate that the major metabolites accumulating in hyperornithinemia-hyperammonemia-homocitrullinuria syndrome provoke lipid and protein oxidative damage and a reduction of the antioxidant defenses in the brain. Therefore, it is presumed that oxidative stress may represent a relevant pathomechanism involved in the brain damage found in patients affected by this disease.     

Pristanic Acid Provokes Lipid,Protein, and DNA Oxidative Damage and Reduces the Antioxidant Defenses in Cerebellum of Young Rats

Zellweger syndrome (ZS) and some peroxisomal diseases are severe inherited disorders mainly characterized by neurological symptoms and cerebellum abnormalities, whose pathogenesis is poorly understood. Biochemically, these diseases are mainly characterized by accumulation of pristanic acid (Prist) and other fatty acids in the brain and other tissues. In this work, we evaluated the in vitro influence of Prist on redox homeostasis by measuring lipid, protein, and DNA damage, as well as the antioxidant defenses and the activities of aconitase and α-ketoglutarate dehydrogenase in cerebellum of 30-day-old rats. The effect of Prist on DNA damage was also evaluated in blood of these animals. Some parameters were also evaluated in cerebellum from neonatal rats and in cerebellum neuronal cultures. Prist significantly increased malondialdehyde (MDA) levels and carbonyl formation and reduced sulfhydryl content and glutathione (GSH) concentrations in cerebellum of young rats. It also caused DNA strand damage in cerebellum and induced a high micronuclei frequency in blood. On the other hand, this fatty acid significantly reduced α-ketoglutarate dehydrogenase and aconitase activities in rat cerebellum. We also verified that Prist-induced increase of MDA levels was totally prevented by melatonin and attenuated by α-tocopherol but not by the nitric oxide synthase inhibitor N^ω-nitro-l-arginine methyl ester, indicating the involvement of reactive oxygen species in this effect. Cerebellum from neonate rats also showed marked alterations of redox homeostasis, including an increase of MDA levels and a decrease of sulfhydryl content and GSH concentrations elicited by Prist. Finally, Prist provoked an increase of dichlorofluorescein (DCFH) oxidation in cerebellum-cultivated neurons. Our present data indicate that Prist compromises redox homeostasis in rat cerebellum and blood and inhibits critical enzymes of the citric acid cycle that are susceptible to free radical attack. The present findings may contribute to clarify the pathogenesis of the cerebellar alterations observed in patients affected by ZS and some peroxisomal disorders in which Prist is accumulated.