Methicillin-resistant staphylococcus aureus (MRSA) remains a prominent human pathogen.Traditionally, MRSA infections occurred exclusively in hospitals and were limited to immunocompromised patients or individuals with predisposing risk factors. However, recently there has been a worldwide epidemic caused by community-associated (CA)-MRSA strains, which can cause severe infections that can result in necrotizing fasciitis or even death in otherwise healthy children or adults outside of healthcare settings. People have made great progress to explain the reasons for enhanced virulence of CA-MRSA, here we review the recent progress made towards four virulence determinants, which are Panton-Valentine leukocidin (PVL), α-Hemolysin (Hla),α-type phenol-soluble modulin ( PSMα) and arginine catabolic mobile element (ACM E) .

ObjectiveTo investigate relationship between the degree of placenta praevia, vaginal bleeding and clinical outcomes. MethodsRecords of 89 patients with placenta praevia(mild praevia group 43; severe praevia group 46) were reviewed retrospectively, and outcomes were compared. ResultsThe gestational age at the first bleeding and diagnosis was significantly smaller in severe group than that in mild one (P<0.05). The incidence of antepartum haemorrhage, the times of bleeding and the episodes of heavy bleeding in two groups showed no significant differences(P>0.05). The gestational age at diagnosis and delivery and birthweight were significantly smaller in women with antepartum bleeding than in those without( P<0.01 ). The number of deliveries by emergency caesarean section in women with antepartum bleeding was significantly higher than that in those without (P<0.01). ConclusionThe clinical outcomes of placenta praevia are highly variable. There are no obvious clinical features that are typical in predicting the clinical outcomes. The number of bleeding episodes and the degree of praevia are not associated with outcomes, so they can't be the proof to determine the treatment plan ahead of time.

To explore the effects of angiotensin Ⅱ on plasminogen activator inhibitor 1 (PAI 1) gene expression in human glomerular mesangial cells.Glomerular mesangial cells (GMCs) were cultured from a healthy adult human kidney (unsuitable for renal transplantation) and then treated with angiotensin Ⅱ at concentration of 10 -9 ,10 -8 , 10 -7 and 10 -6 mol/L, respectively. The mRNA expressions of angiotensinⅡAT1 and AT2 receptor, and PAI I were examined with RT PCR and Northern blot analysis, respectively. Plasminogen activator activity in the supernatants of the GMCs was measured with fibrin plate method. After the GMCs were stimulated by angiotensin Ⅱ, the mRNA level of the AT1 receptor was markedly enhanced, but the AT2 receptor mRNA level was still undetectable as that in normal condition. When GMCs were treated with angiotensin Ⅱ for 48 hours, PAI 1 mRNA expression was increased in a dose dependent manner. The plasminogen activator activity was significantly reduced in the supernatants of the angiotensinⅡ treated GMCs. the results suggested that angiotensinⅡ promote PAI 1 gene expression of the GMCs possibly through its AT1 receptor.

To observe the high glucose concentration on proliferation and fibronectin (FN) synthesis of glomerular mesangial cells (GMC),a culture of human GMC was established and the cell proliferation was assessed using MTT method and cell counting, and the changes in FN was analyzed with RT PCR and ELISA. It was found that high glucose concentration inhibited GMC proliferation and increased FN synthesis in dose and time dependent manner.The results suggest that hyperglycemia may have important role in the development of diabetic nephropathy.

To investigate the changes of local RAS in kidney of aged rats and the regulative effect of AT1 RA, sixteen-month-old male Wistar rats were treated with the valsartan (25mg/kg) until sacrificed at the age of 24 months, and their results were compared with young and aged controls. Renin, angiotensinⅡ levels and the expressions of ATlaR mRNA, AT1bR mRNA and AT2R mRNA were measured. The results showed that plasma renin and angiotensin Ⅱ levels decreased with aging, whereas angiotensin Ⅱ in kidney cortex increased. Valsartan increased the angiotensin Ⅱ level of the aged kidney significantly . AT1aR mRNA and AT1bR mRNA were down-regulated in aged rats compared with the young group. The expression of AT2R mRNA was up-regulated with aging. Valsartan increased AT1aR mRNA, but did not modify AT1b R mRNA and AT2 R mRNA. This results indicated that angiotensin Ⅱ receptors were regulated differently with aging. Our conclusion is that in rat kidney valsartan increases renal angiotensinⅡlevel, blocks AT1R, but has no effect on gene expression of AT2R, which might enhance the protective effect by the stimulation of AT2R.

Objective To observe the effects of chronic angiotensin Ⅱ blockade on gene expression of extracellular matrix at different segments of nephron in aged rats. Methods Glomeruli and tubules of rat kidney were isolated by laser microdissection and pressure catapulting system. Gene expression level of transforming growth factor (TGF-? 1) and fibronectin (FN) were assessed. Fifteen -month-old male Wistar rats were treated with the valsartan (25mg/kg) until sacrificed at age 24 months, and their TGF-? 1 and FN expression levels were compared with that of young and aged controls. Results Compared with young rats, TGF-? 1 mRNA and FN mRNA expression were both up-regulated in isolated glomeruli and tubules in aged rats. Although Valsartan had no effect on the gene expression of TGF-? 1 in isolated glomeruli, it down regulated TGF-? 1 mRNA in tubules of aged rats. Valsartan also down regulated FN mRNA in both glomeruli and tubules of aged rats. Conclusion The results indicate that changes in TGF-? 1 and FN expression might be involved in the aging related changes of gomeruli and tubules. Activation of RAS at the different segments of nephron in aged rats might regulate the gene expression of ECM through diverse mechanisms.

Observing the effects of Arg-Gly-Asp-Ser(RGDS) peptides on the actin organization and apoptosis in human glomerular mesangial cells, in order to explore the interaction mechanism of extracellular matrix (ECM)-integrin receptor-cy-toskeleton. Methods The alterations of actin microfilaments in glomerular mesangial cells were observed under laser scanning confocal microscope. And DNA electrophoresis and flowcytometry were used for assessing apoptosis. Results After two hours of incubation with RGDS peptides, some of the attached glomerular mesangial cells began to round up, with a prominent marginaliza-tion of the actin microfilaments which were bundled in thick aggergates to one edge of the cell. Later these cells detached and floated in the culture medium.The above sequently-occuring changes showed a time-dependent pattern. After ten hours of incubation with RGDS peptide, most of the cells had detached, and features of apoptosis appeared in them, such as inter-nucleo-somal DNA fragmentation and decreased DNA content. Conclusion RGDS tetrapeptide can disrupt the organization of cytoplasmic actin mi-crofilament, inhibit the attachment of the cultured glomerular mesangial cells and cause apoptosis in them.

Objective To study the effects of classification-partition-distribution emergency nursing management for severe trauma patients. Method A total of 60 patients from June 2014 to May 2015 were set as control group receiving common nursing and other 62 patients from June 2015 to June 2016 as observation group treated with emergency hierarchical partition and triage nursing. Result The treatment success rate in the observation group were both significantly higher than that of the control group (P<0.05). Conclusion Classification-partition-distribution emergency nursing management for severe trauma patients can increase treatment success rate .

r governments and mescal institutions in their prevention and control.

Prion diseases are infectious and fatal neurodegenerative diseases. The pathogenic agent is an abnormal prion protein aggregate. Microglial activation in the centre nervous system is a characteristic feature of prion disease. In this study, we examined the effect of PrP 106-126 on PrP mRNA gene expression in Mouse microglia cells BV-2 by real-time quantitative PCR. PrP mRNA expression level was found to be significantly increased after 18 h exposure of BV-2 cells to PrP 106-126, with 3-fold increase after 18 h and 4.5-fold increase after 24 h and BV-2 cells proliferating occurred correspondingly. Our results provide the first in vitro evidence of the increase of PrP mRNA levels in microglial cells exposed to PrP 106-126, and indicate that microglial cells might play a critical role in prion pathogenesis.