Prevalence of coagulase-positive staphylococci in the skin of dogs; antibacterial resistance and plasmid profile of the isolates

This study was designed to understand the prevalence of coagulase-positive staphylococci in the skin of dogs and the role of dogs as reservoirs of pathogenic and antimicrobial-resistant staphylococci. Swab samples were taken from the surface of the skin at muzzle sites of 100 clinically normal dogs. Antibiotic susceptibility of coagulase-positive staphylococci isolates was assessed by antibiotic disc diffusion method using filter paper discs and plasmid DNAs were extracted from the isolates. Staphylococci were isolated from 79 of the 100 dogs sampled and of these 51 were coagulase positive. All coagulase-positive staphylococci isolates were resistant to penicillin G, amoxicillin, cefazolin, streptomycin, erythromycin, ampicillin, tetracycline, gentamicin, trimethoprim-sulfamethoxazole, and enrofloxacine at 100%, 100%, 72%, 48%, 44%, 44%, 12%, 4%, 8%, and 4% respectively. Characterization of plasmid DNAs by agarose gel electrophoresis showed that 22 out of the 51 coagulase-positive staphylococci isolates harbored a single plasmid. The results of the present study indicate that pathogenic and resistant staphylococci are located in the skin of the dogs and may transfer to human and other hosts. It is important to establish reliable antibiotic sensitivity data regarding these bacteria to select suitable antibacterial treatment.     

妊娠高血压综合征患者胎盘绒毛组织内皮素1和内皮型一氧化氮合成酶的基因表达及其脐动脉血流变化

目的　研究妊娠高血压综合征 (简称妊高征 )患者胎盘绒毛组织内皮素 1(endothelin- 1,ET- 1)及内皮型一氧化氮合成酶 (endothelial nitric oxide synthase,e NOS)的基因表达 ,探讨 ET- 1及一氧化氮在妊高征患者胎儿胎盘循环中对脐动脉血流变化的作用。　方法　对妊高征患者及正常妊娠孕妇的胎盘绒毛组织 ,用地高辛标记的 ET- 1及 e NOS互补脱氧核糖核酸 (com plem entary deoxyri-bonucleotide,c DNA)探针进行点印迹杂交 ,利用 L eica QWIN图象处理系统测量每个杂交点的平均光密度值。在分娩前一日用彩色超声多普勒仪测定其脐动脉血流 S/ D值。　结果　妊高征患者胎盘绒毛组织 ET- 1基因表达明显增多 ,其平均光密度值妊高征组为 0 .43± 0 .0 3,正常组为 0 .2 3± 0 .44两组间差别显著 P<0 .0 5。而妊高征组胎盘绒毛组织 e NOS基因的表达明显低于正常对照组 ,其平均光密度值妊高征组为 0 .19± 0 .2 2 ,正常组为 0 .38± 0 .0 2 ,两组间差别显著 P<0 .0 5。妊高征组脐动脉S/ D值明显高于正常对照组 ,分别为 5 .92± 2 .13和 2 .11± 0 .2 2 ,两组间差别显著 P<0 .0 5。　结论　妊高征患者胎盘绒毛组织 ET- 1的表达明显增加 ,而内 e NOS的表达明显减少 ,脐动脉血流阻力亦明显增加。妊高征患者脐动脉血流     

抗衰Ⅰ号方的药效学研究

抗衰Ⅰ号方能延长果蝇平均寿命和最高平均寿命 ,也能延长小鼠的游泳时间和常压耐缺氧时间 ,提示该方具有延长寿命和抗疲劳作用。     

Reference group choice and antibiotic resistance outcomes

Two types of cohort studies examining patients infected with methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci (VRE) were contrasted, using different reference groups. Cases were compared to uninfected patients and patients infected with the corresponding, susceptible organism. VRE and MRSA were associated with adverse outcomes. The effect was greater when uninfected control patients were used.     

Health and economic outcomes of vancomycin-resistant enterococci

BACKGROUND: The health and economic impact of vancomycin-resistant enterococci has not been quantified. METHODS: A retrospective matched cohort study was conducted comparing the outcomes of patients with vancomycin-resistant enterococci (cases) with those of control subjects matched for length of hospital stay until inclusion in the cohort, hospital location, and calendar date. The propensity to be a vancomycin-resistant enterococci case was modeled based on patient characteristics, and included in multivariable models to adjust for confounding. Analyses included the following: (1) conditional logistic regression for mortality, surgery, intensive care unit admission, and discharge to long-term care; (2) linear regression for the logarithm of cost; and (3) accelerated failure time model for length of stay. RESULTS: A total of 233 cases were compared with 647 controls. Groups were similar in age (mean, 62 years), sex (female, 47%), and length of stay before inclusion in the cohort (mean, 8.1 days), but differed in primary diagnosis and comorbidities, past infection or colonization with methicillin sodium-resistant Staphylococcus aureus or Clostridium difficile, and treatment with cephalosporins or metronidazole. These variables were included in the propensity score, which had good to excellent prediction. Outcomes for cases vs controls and adjusted risks (relative risks [RRs]) were as follows: (1) case fatality rate, 17% vs 6% (RR, 2.13; P =.04); (2) length of stay after inclusion in the cohort, 15.1 vs 8.5 days (RR, 1.73; P<.001); (3) hospital costs, $52 449 vs $31 915 (RR, 1.40; P<.001); (4) surgery after inclusion in the cohort, 18% vs 10% (RR, 2.74; P =.001); (5) intensive care unit admission after inclusion in the cohort, 25% vs 14% (RR, 3.47; P<.001); and (6) transfer to an institution, 51% vs 35% (RR, 2.01; P =.001). CONCLUSION: Compared with a matched hospital population, a population with vancomycin-resistant enterococci was associated with severe adverse outcomes: increased mortality, morbidity, and costs.     

Renoprotective effects of chronic candesartan treatment in uninephrectomized rat

The authors recently observed an age-dependent reduction in the diuretic and natriuretic responses to plasma volume expansion in uninephrectomized control and glucose-intolerant rats. To determine the involvement of angiotensin II AT receptors in this phenomenon, the authors tested the hypothesis that chronic candesartan treatment preserves renal excretory function in the uninephrectomized rat. Control and glucose-intolerant rats underwent right nephrectomy at 4 weeks of age. Two weeks later, the animals in each group were further subdivided and maintained on tap water containing either candesartan cilexetil (10 mg. kg(-1). day(-1) ) or vehicle. Renal excretory responses to acute extracellular fluid volume expansion (5% of body weight over 30 min) were determined in the 9-month-old conscious animal. Candesartan treatment markedly reduced the mean arterial pressure of controls and glucose-intolerant rats. Nonetheless, the baseline rates of fluid and electrolyte excretion, as well as the saline volume-induced diuretic, natriuretic, and kaliuretic responses, were greater in the candesartan-treated rats than in their vehicle-treated counterparts. The augmented baseline rates of fluid and sodium excretion in candesartan-treated rats were caused by a reduction in tubular reabsorption activity and an increase in glomerular filtration rate. However, the candesartan-mediated enhancement in saline volume-induced diuresis and natriuresis was caused by a reduction in tubular reabsorption activity. In addition to improving renal function, candesartan treatment reduced proteinuria in both groups. In conclusion, chronic blockade of the angiotensin II receptors exerts hypotensive and renoprotective effects in the aging uninephrectomized rat.     

DNA damage and expression of checkpoint genes p21(WAF1/CIP1) and 14-3-3 sigma in taurine-deficient cardiomyocytes

OBJECTIVE: Taurine depletion is associated with development of cardiomyopathy. Further, oxidative stress is advanced as a critical factor mediating the effect of taurine deficiency on target organs. However, the molecular mechanism(s) linking taurine deficiency with the development of cardiomyopathy remains elusive. Since transition between apoptotic degeneration and cell proliferation in stress conditions is regulated at cell cycle checkpoints, we determined the expression of two such genes, namely p21(WAF1/CIP1) and 14-3-3 sigma as well as p53 that are responsible for oxidative stress and DNA damage. We also carried out quantitative determination of DNA damage. METHODS: Cardiomyocytes from beta-alanine-induced taurine-depleted (TD) rats were used for this investigation. Single- and double-stranded DNA damage was quantified using comet assay analysis. Western blot and two-dimensional polyacrylamide gel electrophoresis with immunoblotting analysis were applied for protein analysis. RESULTS: Comet assay analysis indicated that the extent of double-stranded DNA damage was greater in TD than in control cardiomyocytes. Whereas only traces of both p53 and p21(WAF1/CIP1) and no detectable expression of 14-3-3 sigma were found in cardiomyocytes of control animals, the TD cardiomyocytes expressed all three genes. CONCLUSIONS: DNA damage and the consequent up-regulation of checkpoint proteins observed in TD cardiomyocytes indicate the involvement of cell cycle control mechanisms in the effect of taurine deficiency on cardiomyocytes. Single- and double-stranded DNA damage and the consequent arrest of cell proliferation in both G(1) and G(2) phases of the cell cycle induced by checkpoint proteins may trigger the cardiomyopathy that is associated with taurine deficiency.     

Taurine modulates arginine vasopressin-mediated regulation of renal function

Taurine has been implicated in the regulation of arginine vasopressin (AVP) secretion, and we have previously shown altered renal excretory function in the taurine-depleted rat. To further elucidate the role of taurine in AVP-mediated renal responses, the effects of an antagonist for renal AVP receptors were examined in four groups of conscious rats: control, taurine-supplemented, taurine-depleted, and taurine-repleted. Control and taurine-supplemented rats displayed similar and significant AVP receptor antagonist-induced elevations in fluid excretion, sodium excretion, and free water clearance but a marked reduction in urine osmolality. These effects are consistent with inhibition of endogenous AVP activity. By contrast, in the taurine-depleted rats, the magnitude and the time course of drug-induced renal excretory responses lagged behind those of the control and taurine-supplemented groups. Further, baseline urine osmolality was significantly higher in the taurine-depleted compared with the control or taurine-supplemented groups. However, after administration of the antagonist, taurine-depleted rats manifested a delayed but more marked reduction in urine osmolality, thereby eliminating the baseline differential that existed between the taurine-depleted rats and control or taurine-supplemented groups. Consistent with these observations, plasma AVP was significantly increased in the taurine-depleted compared with the control rats. Interestingly, taurine repletion shifted all responses closer to the control group. Analysis of the data suggests that the effect of the antagonist on renal excretory function is related primarily to altered tubular reabsorption activity. These observations suggest that taurine modulates renal function, and, thereby, body fluid homeostasis, through an AVP-dependent mechanism.