Acute leriche syndrome due to paradoxical embolism.

Paradoxical embolism, describing the passage of venous or right-sided cardiac thrombus into the arterial or systemic circulation through patent foramen ovale, is an uncommon cause of acute arterial occlusion. Here, we report acute Leriche syndrome in a young woman attributable to paradoxical embolism. Ischaemia, patent foramen ovale, and venous thrombosis were the triad of evidence for paradoxical embolism.     

帕司烟肼介入凝胶体外抗结核活性及安全性研究

目的 观察帕司烟肼凝胶体外抗结核作用和支气管介入的安全性。方法 手工法、仪器法分别测定帕司烟肼及其凝胶的最小抑菌浓度和最小杀菌浓度及家兔经支气管介入的安全性试验。结果 帕司烟肼凝胶对H37Rv标准株、牛型结核分枝杆菌、草分枝杆菌MIC值分别为0．1、0，1、0．4mg／L，MBC值分别为0，2、0．2和1．6mg／L；帕司烟肼凝胶与帕司烟肼单体MIC、MBC值无显著差异；动物实验表明该药应用安全。结论 帕司烟肼凝胶具有与帕司烟肼单体相同的抗结核菌药效，卡波姆基质不影响帕司烟肼的抗菌活性；以卡波姆为基质的帕司烟肼凝胶应用安全。     

4年间我院儿科临床大肠埃希菌耐药性变迁分析

目的：监测我院4年间儿科临床分离的大肠埃希菌的耐药情况，了解其耐药性发生和发展的规律，以指导儿科临床合理选用抗大肠埃希菌药物。方法：2001年1月-2004年12月从儿科临床标本分离的84株大肠埃希菌按照分离时间分为2001-2002年组（2001年1月-2002年12月）48株和2003-2004年组（2003年1月-2004年12月）36株，分别比较两组产超广谱B内酰胺酶（ESBLs）和对22种抗菌药物敏感性试验结果。结果：ESBLs检测结果：2001-2002年组产ESBLs株检测率为37．5％（15／40），2003-2004年组产酶株捡出率为46．9％（15／32），经x^2检验，P〉0．05，无显著性差异。药物敏感性实验结果：2003-2004年组比2001-2002年组耐药率明显升高，22种抗生素中除外亚胺培南未发现耐药菌外，其他抗生素耐药率均有不同程度增高，增幅为（16．7％-88．9％），经x^2检验，均有极显著性差异（P〈0．01），其中耐药率上升最快的5种抗生索分别为头孢曲松、头孢唑啉、头孢嚷肟、头孢拉定、头孢呋辛。耐药率上升较慢的5种抗生素分别为阿米卡星、头孢西丁、头孢哌酮／舒巴坦、头孢他定和四环素。结论：儿科临床大肠埃希菌耐药性发展迅速，以对头孢类抗生素耐药性上升最为显著，且呈多重耐药趋势。治疗上不宜选用头孢类抗生索和复方磺胺甲嗯唑，应选用头孢西丁、加酶抑制剂复合抗生素以及亚胺培南。     

2例Cornelia de Lange综合征病例报告并NIPBL基因突变研究

目的：对2例生长发育迟缓伴有特殊面容及肢体发育异常的患儿进行基因检测,实现罕见病的精准诊断,为遗传咨询提供指导。方法：应用单基因检测及全外显子组高通量测序技术对临床疑似CdLS患儿进行致病基因突变筛查,并行一代测序验证以及患儿父母的验证。结果：本研究中的2例患儿均检测到国内外尚未报道的NIPBL基因突变,c.2252 dupA、p.Asn751Lysfs以及NM-015384.4：c.6179dupA,父母均无携带,为新生变异。结论：对于发育迟缓伴特殊面容及肢体异常的患儿要考虑到Cornelia de Lang综合征可能,采用基因检测手段实现精准诊断,为患者及家属遗传咨询提供依据。     

Celastrol protects kidney against ischemia–reperfusion-induced injury in rats

Background

Ischemia–reperfusion (IR) causes various damages in renal tissues, which is exacerbated by hypoxia-induced excessive inflammation and deteriorates the prognosis of patients after kidney surgery. Celastrol is a potent inflammation inhibitor that has little toxicity. In this report, we investigated whether celastrol protects against IR-induced renal injury in rats.

Materials and methods

Renal IR injury was induced by occlusion of the bilateral renal pedicles for 45 min followed by reperfusion for 6 h. Celastrol or vehicle solution was intraperitoneally injected 30 min before renal ischemia, respectively. Renal histology, function, and pro-inflammatory cytokines and mediators were assessed. The effect of celastrol on nuclear translocation of nuclear factor kappa B (NF-κB) was also measured.

Results

Celastrol significantly suppressed elevation of the renal function markers and the lipid peroxidation level, alleviated renal tubular damage, and decreased the levels of tumor necrosis factor-α, interleukin-1β, and monocyte chemotactic protein-1 (MCP-1) messenger RNA in kidney caused by IR. Moreover, celastrol prevented IR-induced expression of pro-inflammatory mediators, which was associated with suppression of nuclear translocation of NF-κB subunit p65.

Conclusions

Celastrol ameliorated the acute kidney injury caused by IR, which was associated with inhibiting local NF-κB activation and inflammation. Our findings suggest that celastrol could be useful for preventing IR-induced renal injury.     

人股骨头坏死微观结构及成骨、破骨细胞活性的区域性分布特征

 目的 比较人股骨头坏死标本不同区域的骨微观结构及成、破骨细胞活性。方法 收集2011年3月至2013年5月行全髋关节置换的非创伤性股骨头坏死患者术后的股骨头标本10例（Ficat Ⅳ期）,男6例,女4例;年龄40～57岁,平均47.7岁。Micro-CT扫描后,根据影像学识别骨质密度不同,将每个标本分为软骨下骨区、坏死区、硬化区、健康区,通过病理学检测、纳米压痕、实时荧光定量PCR、免疫组化染色等方法对不同区域的骨微观结构、微观力学性能及成骨、破骨细胞活性进行比较。结果 Micro-CT结果显示,股骨头坏死标本软骨下骨区及坏死区的骨小梁连续性破坏;硬化区的骨小梁数目增多,间隙变窄;正常区域骨小梁结构完整,厚度分布均匀。软骨下骨区、坏死区、硬化区和健康区骨小梁的弹性模量分别为（13.808±4.22） GPa、（13.999±3.816） GPa、（17.266±3.533） GPa和（11.927±1.743） GPa;硬度分别为（0.425±0.173） GPa、（0.331±0.173） GPa、（0.661±0.208） GPa和（0.423±0.088） GPa。抗酒石酸酸性磷酸酶（Trap）染色结果显示,软骨下骨区和坏死区可见Trap染色阳性细胞,硬化区及健康区未见Trap染色阳性细胞。免疫组化染色结果显示,骨形成相关因子Runx2和BMP2在硬化区及健康区表达高于其他区域;骨吸收相关因子RANK和RANKL在软骨下骨区及坏死区表达高于其他区域。结论 股骨头坏死塌陷过程中,骨微观结构发生明显改变,而坏死区骨小梁微观力学强度较健康区无显著降低。股骨头坏死标本中软骨下骨区及坏死区破骨细胞活性增强,硬化区成骨细胞活性增强。     

肿瘤转移抑制蛋白1和E-钙黏蛋白在结直肠癌中的表达及相关性分析

目的探讨结直肠癌中肿瘤转移抑制蛋白1（MTSS1）和E-钙黏蛋白（E-cadherin）表达的差异性及其临床意义。 方法回顾性分析2004年10月至2017年10月中山大学附属第五医院223例结直肠癌病例资料,采用免疫组织化学技术检测MTSS1和E-cadherin在结直肠癌组织中的蛋白表达情况,比较其表达差异性与其临床病理特征的相关性。 结果MTSS1、E-cadherin蛋白在癌组织的阳性表达率明显低于正常肠组织和癌旁组织（P<0.001）,其蛋白表达与肿瘤分化程度、局部浸润深度、侵犯脉管、临床分期、淋巴结转移和肝转移方面显著相关（均P<0.05）。癌组织中MTSS1和E-cadherin的蛋白表达呈正相关关系（r=0.417,P<0.001）。MTSS1、E-cadherin单阴性组比阳性组预后差（χ2=8.764、4.771,P=0.003、0.029）,MTSS1和E-cadherin双阴性表达的患者预后更差（χ2=13.940,P=0.005）。 结论MTSS1和E-cadherin在结直肠癌中的表达呈正相关,且在低分化程度、深浸润、晚期、局部或肝转移病例中均为低表达,在结直肠癌侵袭转移中可能起协同作用,联合检测对预测肝转移和判断预后有一定临床价值。     

基于NLRP3/Caspase-1通路探讨薏苡仁多糖对溃疡性结肠炎体外炎症模型的干预作用及机制

目的：从炎症理论角度出发,探讨薏苡仁多糖（Coixan）对溃疡性结肠炎（ulcerative colitis,UC）体外炎症模型的干预作用及其机制。方法：体外培养NCM460细胞,采用不同剂量（0、2.5、5、10、20和40μg/mL）脂多糖（lipopolysaccharide,LPS）诱导NCM460细胞,筛选出最佳诱导剂量（20μg/mL）;用不同浓度（0、5、10、20、40和80μg/mL）的Coixan诱导NCM460,筛选出最佳促增殖浓度（10、20、40μg/mL）。实验随机设为空白组、模型组（LPS诱导）、LPS+Coixan低、中、高剂量（10、20、40μmol/L）组,LPS+柳氮磺吡啶（sulfasalazine,SASP）(200μg/mL)组,除空白组外用LPS(20μg/mL)刺激48 h建立UC体外细胞炎症模型后,分别以薏苡仁多糖及SASP进行48 h干预治疗后,ELISA法检测细胞上清液中炎症因子白细胞介素-1β(interleukin-1β,IL-1β)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)水平;免疫荧光...     

Pyruvate Effects on Red Blood Cells During In Vitro Cardiopulmonary Bypass With Dogs’ Blood

To investigate the effects of pyruvate (Pyr) on adenosine triphosphate (ATP), endothelial nitric oxide synthase (eNOS), and nitric oxide (NO) in red blood cells (RBCs) during the cardiopulmonary bypass procedure (CPB), blood, 500 mL, was collected from each of 10 healthy dogs (weight 12–18 kg). The blood was divided into two parts (250 mL each) and randomly assigned into the control group (Group C, n = 10) or the Pyr group (Group P, n = 10). The blood was commingled with an equal volume of 0.9% NaCl and pyruvated isotonic solution (Pyr 50 mM) in the extracorporeal circuit in the two groups, respectively. The CPB procedure was fixed at 120 min, and the transferring flow was 4 L/min. Contents of ATP in RBCs, eNOS activities, and NO productions in plasma were measured before CPB and during CPB at 30, 60, 90, and 120 min in both groups. The ATP level, eNOS activity, and NO production were not different prior to CPB between the two groups. A decline of ATP levels was shown in both groups but remained significantly higher in Group P than in Group C at the same time points during in vitro CPB (P < 0.01). Values of eNOS and NO were significantly increased in Group C but markedly reduced in Group P during CPB, compared with pre‐CPB (P < 0.01). The CPB procedure significantly damaged dogs’ RBCs in the ATP level, eNOS activity, and NO production, in vitro, but Pyr effectively protected RBCs in these functions during CPB. Pyr would be clinically protective for RBCs during CPB.