慢性肾功能衰竭患者外周血细胞CD146的表达及意义

目的 探讨CD146在慢性肾功能衰竭(CRF)患者外周血细胞中的表达及意义.方法 收集本院2007年8月至2009年7月门诊及住院CRF患者51例为CRF组,33例正常人为健康对照组,流式细胞术检测两组外周血细胞CD146的表达并比较两组之间的差异,分析CRF患者外周血细胞CD146表达与血尿素氮(BUN)、血肌酐(Scr)的相关性.结果 与对照组比较,CRF组单核细胞、中性粒细胞CD146+细胞百分率及CD45-CD146+细胞数量均显著升高[(4.09±3.48)%比(0.20±0.10)%;(4.71±3.94)%比(0.79±0.14)%;(16.43±10.48)个/μl比(2.16±0.81)个/μl,均P<0.001].CRF患者外周血CD45-CD146+细胞数量与BUN、Scr均呈正相关(r=0.480、0.595,均P<0.01).结论 外周血单核细胞及中性粒细胞CD146的表达及升高与CRF的发生有关,CD45-CD146+细胞数量增加与CRF的发生及严重程度有关.     

副溶血性弧菌污染情况调查

目的对广州市海珠区的海产品等食品及腹泻病人粪便标本共86份进行了副溶血性弧菌的检测,其中海产品51份,熟食5份,咸菜3份,腹泻病人粪便标本27份。方法按照《广东省卫生防疫病原微生物检验常规》和尿素酶试验进行检验。结果食品样品中分离到副溶血性弧菌5株,阳性率8.47%,按尤氏生化分型为I型2株,II、IV、V型各1株,病人粪便均未分离到此菌。结论尿素酶试验在致病学鉴定上具有重要意义。     

Influence of acotiamide on 13C-urea breath test for Helicobacter pylori diagnosis

The Helicobacter pylori infection and functional dyspepsia are often coexisted. The effect of acotiamide, a drug for functional dyspepsia, on the result of Helicobacter pylori diagnosis has yet to be studied. We evaluated the influence of acotiamide on the results of Helicobacter pylori diagnosis in the ¹³C-urea breath test. Twenty patients with Helicobacter pylori-positive functional dyspepsia were treated with 100 mg of acotiamide three times a day for two weeks. Changes in ¹³C-urea breath test were investigated before and after administration, and two weeks after administration as the follow-up period. The ¹³C-urea breath test and the medical questionnaire of modified frequency scale for the symptoms of gastroesophageal reflux disease were conducted at every period. Nineteen patients were included for analysis. No patients showed negative in ¹³C-urea breath test at Weeks 2 and 4. On the symptom scale, dyspepsia and total scores decreased from Week 0 to Week 2 and increased from Week 2 to Week 4, and the improvement rates of the dyspepsia score at Week 2 was 63%. In conclusion, we confirmed that acotiamide is unlikely to influence the result of ¹³C-urea breath test and it may improve the symptoms of functional dyspepsia during Helicobacter pylori eradication treatment.     

Cisplatin induced toxicity in rat tissues: The protective effect of Lisosan G

The protective effect of a powder of grain (Lisosan G) against cisplatin-induced toxicity in rats was studied. Male rats were fed with Lisosan G before injection of cisplatin and four days later they were killed and blood was collected along with hepatic, renal and testicular tissues. The results showed that cisplatin treatment increased plasma blood urea nitrogen, creatinine and hydrogen peroxide and decreased cytochrome P450 content in renal and hepatic tissues. It also reduced the plasmatic testosterone level and caused a depletion of testicular 17α-progesterone hydroxylase activity. In the group fed with Lisosan G and treated with cisplatin blood urea nitrogen and creatinine returned to the control level indicating a protective effect of Lisosan G. It was also observed that the ones fed with Lisosan G were able to attenuate the decrease in the P450-dependent activities and the activities of antioxidant enzymes as well. Lisosan G protected the testicular 17α-progesterone hydroxylase activity and increased the plasma testosterone level compared to animals treated only with cisplatin. Our results showed a protective effect of Lisosan G against the cisplatin induced toxicity. The protective effect of Lisosan G could be associated mainly with the attenuation of the oxidative stress and the preservation in antioxidant enzymes.     

Acute Presentation and Management of the Encephalopathic Child With an Undiagnosed Inborn Error of Metabolism

Background

Inborn errors of metabolism (IEM) commonly present in infancy and, less commonly, later in life.

Revisiting the contribution of negative charges on the chaperonin cage wall to the acceleration of protein folding

Chaperonin GroEL mediates the folding of protein encapsulated in a GroES-sealed cavity (cage). Recently, a critical role of negative charge clusters on the cage wall in folding acceleration was proposed based on experiments using GroEL single-ring (SR) mutants SR1 and SRKKK2 [Tang YC, et al. (2006) Cell 125:903–914; Chakraborty K, et al. (2010) Cell 142:112–122]. Here, we revisited these experiments and discovered several inconsistencies. (i) SR1 was assumed to bind to GroES stably and to mediate single-round folding in the cage. However, we show that SR1 repeats multiple turnovers of GroES release/binding coupled with ATP hydrolysis. (ii) Although the slow folding observed for a double-mutant of maltose binding protein (DMMBP) by SRKKK2 was attributed to mutations that neutralize negative charges on the cage wall, we found that the majority of DMMBP escape from SRKKK2 and undergo spontaneous folding in the bulk medium. (iii) An osmolyte, trimethylamine N-oxide, was reported to accelerate SRKKK2-mediated folding of DMMBP by mimicking the effect of cage-wall negative charges of WT GroEL and ordering the water structure to promote protein compaction. However, we demonstrate that in-cage folding by SRKKK2 is unaffected by trimethylamine N-oxide. (iv) Although it was reported that SRKKK2 lost the ability to assist the folding of ribulose-1,5-bisphosphate carboxylase/oxygenase, we found that SRKKK2 retains this ability. Our results argue against the role of the negative charges on the cage wall of GroEL in protein folding. Thus, in chaperonin studies, folding kinetics need to be determined from the fraction of the real in-cage folding.     

消化道出血与血清尿素氮的相关性分析

目的通过对消化道出血患者与健康人进行血清尿素氮（BUN）水平比较与观察，分析血清BUN与消化道出血的相关性。方法收集雅安市人民医院72例消化道出血患者作为试验组，并设健康对照组72例，每人清晨抽取空腹静脉血5mL，分离血清，用全自动生化分析仪以酶法测定血清BUN。结果消化道出血组血清BUN水平明显高于健康对照组，两组差异有统计学意义。结论血清“BUN水平与消化道出血的发生存在明显的相关性，测定血清BUN水平，有助于对消化道出血患者的诊断和疗效进行评估，血清BUN可作为消化道出血患者诊断和疗效的一项独立评估因素。     

Infrared spectral analysis of extractables from poly(etherurethane urea) (PEUU) elastomers

Poly(etherurethane urea) (PEUU) elastomers when employed as biomedical devices may be susceptible to extraction upon implantation. Four PEUU elastomers containing a single PEUU formulation, but varying in terms of their additives, were subjected to an in vitro extraction procedure. The additives in the PEUUs were Methacrol® 2138 F at 5 wt% and Santowhite® powder at 1 wt % levels. Only 1-2 wt % of the PEUUs was extractable with methanol. Fourier transform infrared spectroscopy (FT-IR) furnished qualitative and quantitative information on the extractables. The extractables consisted of a PEUU component that on the average was richer in soft segment than the bulk PEUU, and the two additives, Methacrol® 2138 F and Santowhite^® powder.     

IL-6 has no acute effect on the regulation of urea synthesis in vivo in rats

Abstract

Background. Clinical or experimentally induced, active inflammation up-regulates the in vivo capacity of urea synthesis (CUNS), which promotes nitrogen removal from the body and metabolic catabolism. We have shown that tumor necrosis factor α (TNF-α) up-regulates CUNS and increases interleukin 6 expression (IL-6) within hours of administration. The described effect of TNF-α on nitrogen homeostasis may, therefore, depend on IL-6. Methods. Three hours after the i.v. injection of 125 μg.kg^?1 of IL-6 or placebo, we evaluated the CUNS, hepatocyte urea cycle enzyme protein levels and the mRNA levels of the urea cycle enzyme genes in rats. The prevailing rat serum acute phase proteins and their liver mRNA levels were also measured. Results. IL-6 did not change CUNS or hepatocyte urea cycle enzyme protein levels, whereas urea cycle enzyme mRNA levels, except for ornithine transcarbamylase (OTC), decreased by approximately 20%. The liver mRNA levels of α2MG, haptoglobin and α1AGP all increased by 1.5- to 2-fold (p < 0.001). In serum, only the α2MG concentration slightly increased (p < 0.001), whereas the levels of the other circulating acute phase proteins remained unchanged. Conclusion. IL-6 is not the mediator of the in vivo CUNS up-regulation observed 3 h after TNF-α administration, but it may be involved in the down-regulation of urea cycle genes. IL-6 may also mediate TNF-α effects on acute phase protein gene expression. Thus, IL-6 did not contribute to the in vivo hepatic component of inflammation-associated catabolism.