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Abstract:In many traditional Chinese medicine (TCM) hospitals, most patients are elderly with chronic diseases. Nosocomial bloodstream infections (nBSIs) are an important cause of morbidity and mortality. A retrospective surveillance study was performed to examine the epidemiology and microbiology of nBSIs in a TCM hospital from 2009 to 2011. A total of 482 patients with nBSIs were included in the study period. The incidence rate was 5.7/1000 admissions. Escherichia coli (25.5%) was the most common Gram-negative and coagulase-negative staphylococcus (CoNS) (14.1%) was the most common Gram-positive organism isolated. One-third of the E. coli and Klebsiella pneumoniae isolated from the nBSIs were the third-generation cephalosporin-resistant. Half of the Acinetobacter species isolates were resistant to imipenem. Of all the CoNS isolates, 90.7% were resistant to methicillin. Carbapenems and glycopeptide were the most frequently used for nBSI therapy. Only about one-third of patients (157/482) received appropriate empirical therapy. Septic shock, hemodialysis, Pitt bacteremia score >4, urinary tract infection, and appropriate empirical therapy were most strongly associated with 28-d mortality. The incidence of nBSIs was low in the TCM hospital but the proportion of nBSIs due to antibiotic-resistant organisms was high. A high Pitt bacteremia score was one of the most important risk factors for mortality in nBSIs. Therefore, the implementation of appropriate empirical therapy is crucial to improve the clinical outcome of nBSIs.

Abstract. DNA-damaging agents have been reported to be associated with cardiovascular complications, however, the underlying mechanisms remain to be clarified. In the present study, the possible vascular effects of cisplatin was assessed by measuring its effects on the contractile function of thoracic aortic rings dissected from Sprague-Dawley (SD) rats. Contraction of the aortic ring was induced by 60 mM KCl or 10 -6 M phenylephrine (PE) in an ex vivo perfusion system. Cisplatin (200 µM) counteracted KCl-and PE-induced contraction by 57.6 and 91.8%, respectively, in endothelium-intact aortic rings. Similar results were obtained in endothelium-denuded aortas. Electromicroscopy analysis revealed severe damage to blood vessel walls in vivo by cisplatin. In addition, cisplatin significantly inhibited adenosine triphosphate (ATP)-induced intracellular Ca 2+ concentration ([Ca 2+ ] i ) increases in human umbilical vein endothelial cells (HUVECs). These results suggested that the DNA-damaging agent cisplatin can affect the contractile function of thoracic aortas. In addition, in accordance with its DNA-damaging properties, the cardiovascular toxicity of cisplatin may be the result of its direct cytotoxicity. IntroductionDNA-damaging agents, or genotoxic agents, are those chemicals that can produce alterations in the genetic material of the host. Such agents can be further subdivided into direct-and indirect-acting agents. Direct-acting agents are intrinsically reactive and do not require metabolic activation by cellular enzymes to interact with DNA. By contrast, indirect-acting agents require metabolic activation by cellular enzymes to form the DNA-reactive metabolite. DNA-damaging agents exist widely in our natural and social environment, with examples including some of the chemotherapeutic agents and environmental pollutants (1).Cisplatin, a direct-acting agent, is one of the most widely used chemotherapeutic agents in the treatment of a wide variety of malignancies (2). Although its biochemical mechanism of action has yet to be elucidated, cisplastin is believed to exert cytotoxic effects through the interaction and formation of adducts with DNA, which then leads to apoptosis and necrosis (3,4). Despite its clinical efficacy in treating malignancies, cisplatin-based chemotherapy regimens have been reported to be associated with vascular toxicity and serious vascular complications (e.g., myocardial infarction and stroke) (5-7). Such vascular toxicity has been manifested by increased von Willebrand factor plasma levels as well as an enhanced intima-media thickness of the carotid artery (8). In addition, cisplatin has the potential to induce ototoxicity and toxicity towards renal, peripheral sensory and autonomic nervous systems, potentially attributed to cisplatin-caused microvascular damage (9-11). Ca 2+ plays an important role in the regulation of vascular tone, which is generally relatively constant. Initiation of contraction in vascular smooth muscle is due to an increase in the free cytosolic Ca 2+ concentr...

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