Thickness effects of a carbon-supported platinum catalyst layer on the electrochemical reduction of oxygen in sulfuric acid solution

The influence of the thickness of a carbon-supported platinum catalyst layer on the oxygen reduction reaction (orr) has been studied in sulfuric acid solution by means of a thin-film rotating disk electrode. Pronounced changes in the Pt utilization, electrode activity and the orr kinetics have been observed upon varying the catalyst layer thickness. The thicker film electrode exhibits a higher Pt utilization efficiency and higher activity, and promotes the orr kinetics at potentials relevant to fuel cell operations. The participation of Pt surfaces not in contact with the electrolyte solution in electrochemical reactions via the spillover of adsorbed hydrogen and oxygen species, is proposed to be responsible for the changes. The thicker catalyst layer is likely to modify the Pt particle–particle distance by providing shared Pt sites between adjacent carbon supports, to improve the surface density of active catalyst particles per single carbon support by sharing adjacent catalyst sites, and to increase the ratio of the particle surfaces free of blocking anions to the catalyst|electrolyte interface surfaces. The carbon-supported platinum catalyst layer becomes active at 0.90 V vs RHE only when the catalyst layer is thicker than 1 μm. To provide reasonable activity, the minimum catalyst layer thickness should be around 2–4 μm. These results should be considered in the design of the cathode catalyst layer of polymer electrolyte membrane fuel cells.     

亚低温对大鼠脑损伤后脑组织炎性反应的影响

目的探讨颅脑外伤后早期应用亚低温治疗对脑组织炎性反应的影响。方法采用Feeney自由落体改良模型,设定对照组、颅脑外伤模型组及亚低温组,每组再根据伤后不同生存时间随分为3个亚组。取伤灶脑组织检测髓过氧化酶(MPO)活性,做细胞间黏附子-1(ICAM-1)免疫组化染色,光镜下计数ICAM-1阳性血管数。结果亚低温组各时间点伤灶区ICAM-1阳性血管数明显低于颅脑外伤模型相应时间点(P<0.01)。亚低温组各时间点MPO活性均明显低于颅脑外伤模型组相应时间点(P<0.01)。结论亚低温治疗能明显减少伤灶区白细胞浸润及ICAM-1的表达,有助于改善颅脑外伤后脑组织炎性反应引起的继发性脑损伤。     

The role of HLA‐DQβ1 alleles in susceptibility to rheumatoid arthritis

Aim: Rheumatoid arthritis (RA) is the most common chronic inflammatory erosive joint disease with the worldwide distribution of approximately 0.5–1.0%. Etiology of RA is not exactly known but immunologic and genetic factors play an important role in the pathogenesis of the disease. Genetic factors such as human leukocyte antigens (HLA) are responsible for many autoimmune diseases; therefore we decided to look for a correlation between RA and the presence of HLA‐DQβ1 alleles as possible genetic markers. Methods: Genomic DNA from the whole blood samples of 25 patients with RA and 86 normal individuals as control group were extracted by salting out method. The genomic DNA was amplified by polymerase chain reaction‐sequence specific primer (PCR‐SSP) technique. HLA‐typing was done by this method after optimizing the PCR reaction for each allele. In this procedure seven serological subclasses of HLA‐DQβ1 can be detected. Results: Comparing the results between the patients and controls show a significant increase in the frequency of HLA‐DQ8 (*0302, *0305) alleles in RA patients. The P‐values were 0.007 and the relative risk for these alleles was evaluated higher than 1. Conclusions: The results suggest that DQ8 is the dominant HLA‐DQβ1 allele that is associated with susceptibility to RA in north‐eastern Iran.     

颈动脉粥样硬化斑块中COX-2、mPGES-1表达及塞来昔布对其的影响作用

目的探讨兔颈动脉粥样硬化斑块中环氧化物酶-2（COX-2）、诱导型前列腺素合成酶-1（mPGES-1）的表达机制及塞来昔布对其表达的影响。方法采用32只雄性新西兰大白兔．其中正常对照组8只（A组），另24只将特制的硅橡胶圈置于兔右侧颈动脉。术后给予1％高胆固醇喂养14d，建立兔颈动脉粥样硬化性狭窄动物模型，将模型兔随机分为颈动脉狭窄无干预组（B组1、小剂量塞来昔布治疗组（15mg／kg，C组），大剂量塞来昔布治疗组（35mg／kg，D组），每组各8只。治疗4周后取双侧颈动脉并分为平等2段，分别行半定量逆转录聚合酶链反应（RT—PCR）及Western blot法测定颈动脉斑块干预后COX-2及mPGES-1的表达。结果与A组比较,B、C、D组颈动脉粥样硬化模型兔的斑块中COX-2及mPGES．1表达增高，差异具有显著性（P〈0．05）；与B组比较，C、D组颈动脉斑块的C0X-2及mPGES．1表达显著下调，差异有显著性（P〈0．051。结论在颈动脉粥样硬化斑块的病理过程中炎症反应可能起着主导作用。塞来昔布干预可抑制COX-2及mPGES—1的表达，减缓颈动脉粥样硬化的进展。     

氯胺酮对脂多糖诱导下人脐静脉内皮细胞活化的影响

目的 观察氯胺酮和N-甲基-D-天门冬氨酸(NMDA)受体非竞争性拮抗剂MK-801对脂多糖(LPS)刺激下人脐静脉内皮细胞(HUVECs)胞间粘附分子-1(ICAM-1)表达及核因子-kappa B(NF-kB)易位表达的影响。方法 采用Jaffe方法培养的HUVECs随机分为10组:对照组(C组,RPMI-1640),LPS组(L组,LPS1μg/ml),氯胺酮组(K组,依浓度不同分为KⅠ、KⅡ、KⅢ、KⅣ亚组,即氯胺酮12.5、25.0、100、300μmol/L LPS1μg/ml),MK-801组(M组,依浓度不同分为MⅠ、MⅡ、MⅢ、MⅣ亚组,即MK-801 1.25、2.50、10、30μmol/L LPS1μg/ml)。在37℃、5％CO_2中孵育18h后,用流式细胞仪检测ICAM-1的表达阳性率。NF-kB易位表达的测定分组处理同上,在LPS1μg/ml刺激2h后,用免疫组化(SP)方法测定内皮细胞中NF-kB p65亚基的表达。结果 KⅡ、KⅢ、KⅣ亚组可抑制LPS作用下HUVECs表面ICAM-1的表达和细胞内部NF-kB的易位表达(P<0.05),且两者的变化呈正相关(r=0.985,P<0.01)。M组各亚组对LPS作用后HUVECs表面ICAM-1的表达和NF-kB的易位表达无明显影响(P>0.05)。结论 氯胺酮对炎症反应中内皮细胞的活化具有抑制作用,但并非通过NMDA受体途径。     

Characterization of a highly polymorphic marker adjacent to the SLC4A1 gene and of kidney immunostaining in a family with distal renal tubular acidosis.

BACKGROUND: Mutations in the human SLC4A1 (AE1/band 3) gene are associated with hereditary spherocytic anaemia and with distal renal tubular acidosis (dRTA). The molecular diagnosis of AE1 mutations has been complicated by the absence of highly polymorphic genetic markers, and the pathogenic mechanisms of some dRTA-associated AE1 mutations remain unclear. Here, we characterized a polymorphic dinucleotide repeat close to the human AE1 gene and performed an immunocytochemical study of kidney tissue from a patient with inherited dRTA with a defined AE1 mutation. METHODS: One CA repeat region was identified in a phage P1-derived artificial chromosome (PAC) clone containing most of the human AE1 gene and the upstream flanking region. We determined its heterozygosity value in multiple populations by PCR analysis. Genotyping of one family with dominant dRTA identified the AE1 R589H mutation, and family member genotypes were compared with the CA repeat length. AE1 and vH(+)-ATPase polypeptides in kidney tissue from an AE1 R589H patient were examined by immunocytochemistry for the first time. RESULTS: This CA repeat, previously reported as D17S1183, is approximately 90 kb upstream of the AE1 gene and displayed considerable length polymorphism, with small racial differences, and a heterozygosity value of 0.56. The allele-specific length of this repeat confirmed co-segregation of the AE1 R589H mutation with the disease phenotype in a family with dominant dRTA. Immunostaining of the kidney cortex from one affected member with superimposed chronic pyelonephritis revealed vH(+)-ATPase-positive intercalated cells in which AE1 was undetectable, and proximal tubular epithelial cells with apparently enhanced apical vH(+)-ATPase staining. CONCLUSIONS: The highly polymorphic dinucleotide repeat adjacent to the human AE1 gene may be useful for future studies of disease association and haplotype analysis. Intercalated cells persist in the end-stage kidney of a patient with familial autosomal dominant dRTA associated with the AE1 R589H mutation. The absence of detectable AE1 polypeptide in those intercalated cells supports the genetic prediction that the AE1 R589H mutation indeed causes dominant dRTA.     

腹腔镜与开放手术治疗上尿路移行细胞癌的对比研究

目的　评价联合尿道电切镜、腹膜后镜行肾输尿管切除术的临床效果。　方法　肾盂输尿管癌患者 4 4例 ,采用联合尿道电切镜、腹腔后镜行肾输尿管切除术 15例 (A组 ) ,开放性肾输尿管切除术 2 9例 (B组 )。对两组的临床疗效、术后恢复、费用及并发症等进行对比研究。　结果　A组术中出血量 (75 .1± 2 9.5 )ml、术后 (2 4 .1± 12 .6 )h肠功能恢复、(2 4 .3± 10 .5 )h下床活动、应用止痛药(3.0± 0 .8)d、静脉应用抗生素 (7.2± 3.1)d、术后住院 (6 .3± 1.2 )d、(2 8.0± 7.8)d恢复正常工作 ,明显优于B组 ,差异有显著性意义 (P <0 .0 1或P <0 .0 5 )。B组手术时间、手术治疗费用、住院总费用优于A组 ,差异有显著性意义 (P均 <0 .0 1)。A组并发症明显少于B组。两组随访 14～ 36个月 ,均未见肿瘤复发。　结论　联合尿道电切镜、腹膜后镜肾输尿管切除术与开放手术相比 ,疗效相当 ,创伤小、痛苦少、术后恢复快、并发症少 ,费用较高。     

软骨细胞老化特征及机制的研究进展

软骨细胞的老化是一个极其复杂的过程，其特征包括：细胞不可逆的生长停滞于G1期；老化相关β-半乳糖苷酶的表达；端粒长度缩短；软骨细胞分化特征的改变。目前认为其机制为基因表达的程序性或减进性改变，包括肿瘤抑制基因p53和pRb等在细胞生长停滞中的作用；端粒结合蛋白和端粒酶对端粒长度的调节；细胞骨架蛋白的重组使软骨细胞形态的变化；基质降解酶类表达增加以及各种细胞因子的变化对软骨细胞代谢的影响。