新生儿病房铜绿假单胞菌感染状况及耐药性的5年监测

目的监测2005年至2009年间铜绿假单胞菌在新生儿病房的分离情况及其耐药趋势,为临床感染的预防和治疗提供实验室依据。方法回顾分析2005年至2009年间新生儿病房所有标本中铜绿假单胞菌的分离率,菌株在标本中的分布以及对常见的13种抗菌药物的耐药性。结果铜绿假单胞菌的分离率有逐年升高的趋势,从2005年的1.19%增至2009年的5.16%;其在呼吸道标本中的分离率最高(86.3%),在其他标本中的检出率都相对较低。铜绿假单胞菌的耐药株也有逐年增多的趋势,特别是对复方新诺明的耐药性已发展成为全部耐药。结论铜绿假单胞菌在新生儿病房的分离率在不断地增加,其对多种抗菌药物有较高的耐药性,加之新生儿免疫系统发育不完善,应引起临床医师的高度重视。     

Effects of the antioxidant drug tempol on renal oxygenation in mice with reduced renal mass

We tested the hypothesis that reactive oxygen species (ROS) contributed to renal hypoxia in C57BL/6 mice with ⅚ surgical reduction of renal mass (RRM). ROS can activate the mitochondrial uncoupling protein 2 (UCP-2) and increase O(2) usage. However, UCP-2 can be inactivated by glutathionylation. Mice were fed normal (NS)- or high-salt (HS) diets, and HS mice received the antioxidant drug tempol or vehicle for 3 mo. Since salt intake did not affect the tubular Na(+) transport per O(2) consumed (T(Na/)Q(O2)), further studies were confined to HS mice. RRM mice had increased excretion of 8-isoprostane F(2α) and H(2)O(2), renal expression of UCP-2 and renal O(2) extraction, and reduced T(Na/)Q(O2) (sham: 20 ± 2 vs. RRM: 10 ± 1 μmol/μmol; P < 0.05) and cortical Po(2) (sham: 43 ± 2, RRM: 29 ± 2 mmHg; P < 0.02). Tempol normalized all these parameters while further increasing compensatory renal growth and glomerular volume. RRM mice had preserved blood pressure, glomeruli, and patchy tubulointerstitial fibrosis. The patterns of protein expression in the renal cortex suggested that RRM kidneys had increased ROS from upregulated p22(phox), NOX-2, and -4 and that ROS-dependent increases in UCP-2 led to hypoxia that activated transforming growth factor-β whereas erythroid-related factor 2 (Nrf-2), glutathione peroxidase-1, and glutathione-S-transferase mu-1 were upregulated independently of ROS. We conclude that RRM activated distinct processes: a ROS-dependent activation of UCP-2 leading to inefficient renal O(2) usage and cortical hypoxia that was offset by Nrf-2-dependent glutathionylation. Thus hypoxia in RRM may be the outcome of NADPH oxidase-initiated ROS generation, leading to mitochondrial uncoupling counteracted by defense pathways coordinated by Nrf-2.     

GC-MS法分析甘肃和青海蕨麻中的脂肪酸成分

为了研究蕨麻的化学成分以更好地利用蕨蔴资源,采用索氏提取法提取了青海和甘肃两个地区产的蕨麻中的脂溶性成分,利用气相色谱-质谱联用(GC-MS)对蕨麻中的脂肪酸成分进行分析。结果表明,来自甘肃产地的蕨麻含有11种脂肪酸,青海地区产的蕨麻含有7种脂肪酸,二者的共同成分有7种;甘肃产蕨麻中硬脂酸含量最高,辛烷含量最低;青海产蕨麻中邻苯二酚含量最高,棕榈酸含量最低。表明不同产地的蕨麻所含脂肪酸种类和脂肪酸含量均存在差异。     

Mite allergen Der-p2 triggers human B lymphocyte activation and Toll-like receptor-4 induction

Background

Allergic disease can be characterized as manifestations of an exaggerated inflammatory response to environmental allergens triggers. Mite allergen Der-p2 is one of the major allergens of the house dust mite, which contributes to TLR4 expression and function in B cells in allergic patients. However, the precise mechanisms of Der-p2 on B cells remain obscure.

Methodology/Principal Findings

We investigated the effects of Der-p2 on proinflammatory cytokines responses and Toll-like receptor-4 (TLR4)-related signaling in human B cells activation. We demonstrated that Der-p2 activates pro-inflammatory cytokines, TLR4 and its co-receptor MD2. ERK inhibitor PD98059 significantly enhanced TLR4/MD2 expression in Der-p2-treated B cells. Der-p2 markedly activated mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) and decreased p38 phosphorylation in B cells. MKP-1-siRNA downregulated TLR4/MD2 expression in Der-p2-treated B cells. In addition, Der-p2 significantly up-regulated expression of co-stimulatory molecules and increased B cell proliferation. Neutralizing Der-p2 antibody could effectively abrogate the Der-p2-induced B cell proliferation. Der-p2 could also markedly induce NF-κB activation in B cells, which could be counteracted by dexamethasone.

Conclusions/Significance

These results strongly suggest that Der-p2 is capable of triggering B cell activation and MKP-1-activated p38/MAPK dephosphorylation-regulated TLR4 induction, which subsequently enhances host immune, defense responses and development of effective allergic disease therapeutics in B cells.