5A,B). Additionally, inhibition of HO activity RG7204 resulted in increased hepatocyte cell death and apoptosis with SnPP treatment (Fig. 5C,D). Moreover, overexpression of HO-1 by adenoviral gene transfer in hepatocytes increases autophagy, compared to control adenoviral transfection; however, in

LPS-treated hepatocytes, there is no additional gain of function with this gene transfer (data not shown). This may be secondary to the finding that HO-1 levels are substantially increased in LPS-treated cells. To determine whether autophagic signaling contributes to protection against cell death, autophagy was suppressed in vivo by siRNA specific for VPS34. CLP-induced VPS34 was shown to be dependent on HO-1 (Fig. 4D). C57BL/6 mice were treated with scrambled or VPS34-specific siRNA by hydrodynamic tail vein injection 72 hours before cecal ligation and puncture. Adequate knockdown of VPS34 in the liver was determined by RT-PCR of liver homogenates and immunohistochemistry (Fig. 6A,B). The influence of autophagy was measured by TEM, looking for autophagosomes (Fig. 6C), and immunohistochemistry, in a search for LC3 (data not shown). CLP increased hepatic autophagic signaling in control

scrambled siRNA-treated mice; however, VPS34 siRNA-treated mice demonstrated minimal induction of autophagy (Fig. 6C). Moreover, inhibition of autophagy with VPS34 siRNA resulted Acalabrutinib in increased cell death and tissue injury, as measured by alanine aminotransferase (Fig. 6D,E). These findings were recapitulated in LPS-treated hepatocytes, which demonstrated decreased autophagy and increased cell death after treatment with VPS34 siRNA or the pharmacological inhibitor 3-MA. The mechanism by which HO-1 induces autophagy was next investigated. These studies focused on the MAPKs, which have been shown to modulate the induction of autophagic signaling. LPS-treated hepatocytes increased the phosphorylation of p38 MAPK (Fig. 7A), but

not p42/44 MAPK or JNK (data not shown). selleck screening library HO inhibition with SnPP decreased LPS-induced phosphorylation of p38 MAPK. Additionally, pharmacological inhibition of p38 MAPK with SB203580 (10 μM) prevented LPS-induced autophagic signaling, as demonstrated by LC3 punctae formation (Fig. 7B) and western blotting (Fig. 7C). Similar results were found in vivo. CLP increased HO-1 protein expression and phosphorylation of p38 MAPK. Inhibition of HO-1 with in vivo–specific siRNA decreased CLP-induced phosphorylation of p38 MAPK (Fig. 7D), Thus, knockdown of HO-1 or inhibition of HO activity decreases sepsis or LPS-induced p38 MAPK, VPS34, and LC3. The role of p38 MAPK in the induction of VPS34 and autophagy was next investigated. Mice were treated with SB203580 before CLP to inhibit the phosphorylation of p38 MAPK. SB203580 prevented CLP-induced VPS34 and LC3 (Fig. 8).

2003a, Dehn et al. 2006a). Conclusions on Hg biomagnification are mixed. Dehn et al. (2006b) found little Selleckchem PLX3397 evidence for Hg biomagnification, whereas data from Atwell et al. (1998) suggest a significant, positive log relationship between [Hg] and δ15N values in arctic food webs. Theory and empirical studies show

that [Pb] is lowest in top trophic level consumers (Michaels and Flegal 1990), because Pb is biodepleted relative to its biogeochemical analogue calcium. The combination of [Pb] and stable Pb isotopes (207Pb/206Pb) have been especially useful in documenting historical shifts in the source(s) and sometimes concentrations of Pb between preindustrial and modern times (Smith

et al. 1990, Outridge et al. 1997, Caurant et al. 2006). Most of the studies on organochemical contaminants evaluate exposure at the community or ecosystem level and present data from multiple trophic levels CT99021 research buy that often include one or more marine mammal species. Significant, positive correlations among PCB, DDT, and FOC concentrations and trophic level, as derived from δ15N values, are strong evidence for bioaccumulation of these compounds in marine food webs (Jarman et al. 1996, Fisk et al. 2001, Hobson et al. 2002, Tomy et al. 2004). Coupled contaminant and δ13C analysis also suggest differences in FOC contaminant loads among marine mammal species that occupy nearshore versus offshore habitats (Van de Vijver et al. 2003). The blending of contaminant and SIA also yields information on population structure and niche variation at the individual, population, or species level. At first, contaminant concentrations alone were used in this capacity (see review by Aguilar 1987). More recently, however, researchers have begun to integrate toxicological and isotopic proxies. In essence, geographic

variability in natural elements (i.e., food web isotope values) or anthropogenic compounds (i.e., contaminants) provides independent but complimentary chemical tracers that can have signatures unique to the region(s) in which an organism forages. This strategy has been applied to small FER cetacean populations in the southwestern Mediterranean Sea, the northeast Atlantic Ocean, and Black Sea (Das et al. 2000, 2004b; Borrell and Aguilar 2005; Borrell et al. 2006); ringed seal populations in the Canadian Arctic (Fisk et al. 2002a); minke whales in the North Atlantic (Born et al. 2003); and killer whale ecotypes in the North Pacific Ocean (Herman et al. 2005; Krahn et al. 2007, 2008). As with most ecological applications of stable isotope analysis, diet and habitat preferences are the primary pieces of information acquired through study of population structure and niche separation.

[84] A retrospective cohort study has demonstrated that antitubercular treatment together with antiretroviral therapy increases the risk for DILI by 8.5-fold as compared to antiretroviral therapy alone.[85] Indeed, there is growing concern for EFV-associated DILI,[86] and a series of recent studies have provided compelling evidence that EFV can induce mitochondrial toxicity in vitro.[65, 87] Therefore, and in view of our recent data that combined exposure of hepatocytes to both EFV and INH greatly potentiates hepatocellular injury (Lee and Boelsterli, unpublished, 2014), the

possibility of an increased risk www.selleckchem.com/products/apo866-fk866.html for DILI during combined EFV/INH treatment should be monitored in patients. It has become clear selleck chemicals llc that multiple pathways are involved in INH-induced hepatotoxicity, and one single mode of action is likely not sufficient

to explain DILI (Fig. 4). Underlying mechanisms include electrophile stress through the generation of reactive metabolites, a possible immune response via the formation of drug-modified proteins and cellular stress signals, disruption of endogenous metabolism, oxidative stress signaling through mitochondrial dysfunction, and disruption of energy homeostasis through mitochondrial functional impairment. However, these mechanisms are all driven by drug-specific factors and merely describe a toxicological hazard. Most data have been derived from cellular models or other nonclinical approaches, including attempts to generate animal models. In contrast, in patients, a number of determinants of susceptibility may positively or negatively modulate this hazard and, together with the actual exposure to INH, translate it into a real risk of developing DILI. Thus, the classical paradigm describing the mode of action and the mechanisms involved in INH hepatotoxicity have been drastically changing over the past years. For example, CYP2E1

and NAT2, previously thought to be key players, seem to have lost some of their mechanistic importance. Similarly, the role of human PXR, previously thought to play a major TCL role in regulating CYPs, has been shifted to other metabolic pathways (e.g. regulation of heme synthesis). Furthermore, novel reactive intermediates have been implicated in covalent adduct formation and hapten-mediated immune responses. A role of the adaptive immune system has been further corroborated by the striking correlation of certain HLA haplotypes with the occurrence of INH-induced DILI. Finally, mitochondrial stress caused by INH and/or metabolites has been emerging as a new paradigm. Importantly, exposure of normal healthy animals (or exposure of primary hepatocyte cultures isolated from normal healthy rodents) elicits only marginal effects on mitochondrial function. However, in the presence of underlying mitochondrial dysfunction that may be phenotypically inconspicuous, overt cell injury may ensue. Thus, the latent mitochondrial effects are likely amplified by other factors (e.g.

37 Furthermore, after prolonged and effective control of HBV replication in patients treated with potent antivirals, an add-on application of anti-HBs may facilitate HBsAg clearance in appropriately selected patients. The authors thank Eithan Galun, principal investigator of the clinical investigation,13 which provided data for mathematical modeling, and Dov Terkieltaub for technical assistance. Additional Supporting Information may be found in the online version of this article. “
“Gastric adenocarcinoma Selleckchem I BET 762 is the second leading cause of cancer death worldwide. It is more prevalent in males in Asia. Helicobacter pylori

infection plays a major role in the pathogenesis of gastric cancer. Endoscopy is the most valuable and commonly used

technique for diagnosis of gastric cancer. Surgery remains the curable therapy for resectable disease. Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) can be useful for treatment of early gastric cancer. “
“Non-alcoholic steatohepatitis (NASH) is the hepatic Epigenetics Compound Library manifestation of metabolic syndrome (MS). Monosodium glutamate (MSG)-treated ICR mice is a useful model of MS and NASH, but it shows the different patterns of steatosis from human NASH. Because inbred aged DIAR (ddY, Institute for Animal Reproduction) mice spontaneously show the similar pattern of steatosis as NASH, we analyzed their liver pathology after administering MSG. MSG-treated DIAR mice (DIAR-MSG) and untreated DIAR mice (DIAR-controls)

were sacrificed and assessed histopathologically at 29, 32, 40, 48, and 54 weeks of age. The NASH CYTH4 activity score, body mass index, blood glucose level, and oral glucose tolerance test were also assessed. The body mass index and blood glucose levels of DIAR-MSG were significantly higher than controls. The oral glucose tolerance test revealed a type 2 diabetes pattern in DIAR-MSG. The livers of DIAR-MSG mice showed macrovesicular steatosis, lobular inflammation with neutrophils, and ballooning degeneration after 29 weeks. At 54 weeks, mild fibrosis was observed in 5/6 DIAR-MSG and 2/5 DIAR-control mice. In imaging mass spectrometry analysis, cholesterol as well as triglyceride accumulated in the liver of DIAR-MSG mice. Atypical liver nodules were also observed after 32 weeks in DIAR-MSG, some with cellular and structural atypia mimicking human hepatocellular carcinoma. The NASH activity score of DIAR-MSG after 29 weeks was higher than that of control mice, suggesting the development of NASH. DIAR-MSG had NASH-like liver pathology and liver nodules typically associated with MS symptoms. DIAR-MSG provides a valuable animal model to analyze NASH pathogenesis and carcinogenesis.

037) and pathological grade (P = 0.021). p38 MAPK inhibitors clinical trials Moreover, the overall survival of patients with negative IGFBP7 expression was significantly (P = 0.003) poorer than that of IGFBP7-positive patients. Cox regression analyses showed that IGFBP7 expression was an independent

predictor of overall survival (P = 0.02). Conclusion: The expression of IGFBP7 is significantly reduced in gastric cancer, which is associated with higher T stage and differentiation grade. IGFBP7 may serve as a prognostic marker as well as a potential therapeutic target for gastric cancer. Key Word(s): 1. gastric neoplasm; 2. RT PCR; 3. Western blotting; 4. survival analysis; Presenting Author: WEIHAO SUN Additional Authors: XIAOLIN LI, HAO ZHANG, KUN SUN, KAI ZHANG Corresponding Author: WEIHAO SUN Affiliations: The First Affiliated Hospital of Nanjing Medical University Objective: The current study evaluated the antitumor effects of Harmine (HM) on human gastric cancer both in vitro and in vivo. Methods: Growth inhibitory activity was assayed by the Methyl thiazolyl MLN8237 clinical trial tetrazolium (MTT) assay, apoptotic staining and Flow cytometry analysis. The wound-healing and transwell invasion assays were performed to evaluate the effect of HM on inhibiting tumor invasion and metastasis. The protein expressions involved in regulating apoptosis

and invasion and metastasis were detected by western blot. Results: HM inhibited the proliferation of human gastric cancer cell lines BGC-823 and SGC-7901 in a dose- and time-dependent manner. In addition, HM effectively promoted the apoptosis of gastric cancer cells (Fig. 1) through dose-dependently inhibiting the expression of cyclooxygenase-2 (COX-2) (Fig. 2). Moreover, HM could induce apoptosis through a direct impact on many apoptosis-related proteins, such as Bcl-2 and Bax (Fig. 2). Most importantly, HM dramatically inhibited migration and invasion of gastric cancer by down-regulating the matrix metalloproteinase-2 (MMP-2) expression regulated by COX-2. In vivo, HM suppressed gastric xenograft tumor growth significantly. Fig. 1 Apoptosis

of BGC-823 and SGC-7901 cells detected by Flow cytometry. BGC-823 and SGC-7901 cells were treated with harmine at 0, 4, 8, and 16 μg/ml NADPH-cytochrome-c2 reductase for 24 hours. (A, B) Representative annexin V-FITC/PI stained BGC-823 (A) and SGC-7901 (B) cells. (C, D) The histograms on the right represent the rates of apoptotic cells in BGC-823 and SGC-7901 groups. All data represent the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01 vs. control (0 μg/ml). Fig. 2 Effects of harmine on the COX-2, Bcl-2 and Bax protein expressions in BGC-823 and SGC-7901 cells. BGC-823 and SGC-7901 cells were treated with harmine at 0, 4, 8, and 16 μg/ml for 24 hours. (A, B) Representative COX-2, Bcl-2 and Bax protein expressions in BGC-823 (A) and SGC-7901 (B) cells detected by western blot analysis.

Sequence analysis of HSD3B7 revealed that the proband and her 32-year-old cousin were homozygous for a frameshift mutation (c.45_46del AG, p.T15Tfsx27) in exon 1. The diagnosis of 3β-HSD deficiency was confirmed by documenting high levels of 3β-hydroxy-Δ5 bile acids in the serum of the proband and the 32-year-old first cousin using mass spectrometry. To our knowledge, the 32-year-old

relative in this family represents the oldest asymptomatic patient with this disorder. Conclusion: This study highlights the clinical utility of homozygosity mapping in diagnosing autosomal recessive metabolic disorders. This family illustrates the wide variation in expressivity that occurs in 3β-HSD deficiency and underscores the need to consider a bile acid synthetic defect as a possible cause of liver disease in adults. (HEPATOLOGY 2012) Bile acids are synthesized in the liver from cholesterol by

a complex series of enzymatic Midostaurin concentration reactions.1 The rate-limiting step in the pathway is the addition of a hydroxyl group to the carbon at the 7 position (C7) of the sterol ring, a reaction catalyzed by the enzyme cholesterol 7α-hydroxylase (CYP7A1). This is followed by isomerization of the Δ5 bond to the Δ4 position MS-275 clinical trial and oxidation of the 3β-hydroxyl group to a 3-oxo moiety. Both of these reactions are catalyzed by 3β-hydroxy-Δ5-C27 steroid oxidoreductase (3β-HSD), a 369 amino acid membrane-bound protein in the endoplasmic reticulum that is encoded by HSD3B7.2 Mutations in HSD3B7 cause 3β-HSD deficiency (#OMIM 607765),3 a rare autosomal recessive disorder that represents the most common inborn error of bile acid synthesis.2, 4 The disorder was originally described by Clayton et al.5 in 1987. The diagnosis was established by measuring bile acids in the urine using mass spectrometry in a consanguineous Saudi Arabian family in which several family members presented as neonates with giant cell hepatitis and bridging cirrhosis.5 Over 50 patients with this disorder from at least 40 unrelated

families have subsequently been reported.3, 6-16HSD3B7 was cloned by Schwarz et al. in 200017 and 21 different mutations have been described that cause 3β-HSD deficiency.3, 6, 7, 12, 13 3β-HSD deficiency usually presents in the neonatal period or in early childhood with cholestatic jaundice, Phosphatidylinositol diacylglycerol-lyase hepatosplenomegaly, steatorrhea, rickets, bleeding, and failure to thrive.2 The disease invariably progresses to cirrhosis. In a few cases of late-onset 3β-HSD deficiency, the disease presents in the second or third decades of life.3, 6, 18 Typical clinical features that distinguish 3β-HSD deficiency from other causes of early onset liver disease include the absence of pruritus, a normal serum level of gamma glutamyl transpeptidase (GGT), and normal or low levels of total serum primary bile acids when measured by routine methods, despite the presence of cholestasis.

The project was

also supported in part by grant UL 1RR025747 from the National Center of Research Resources, National Institutes of Health, USA. Betsy Sleath, Guadalupe Ayala, Dennis Williams and Gail Tudor designed the study. Delesha Carpenter, Ashley Beard and Christopher Gillette helped analyse the data and provided feedback on the draft manuscript. Betsy Sleath, Delesha Carpenter, Guadalupe Ayala and Gail Tudor drafted the manuscript. All Authors state that they had complete access to the study data that support the publication. GSK 3 inhibitor “
“An important goal of hospice care is to relieve pain and suffering of terminal cancer patients. Anticholinergic medications are effective in the symptom palliation among terminal cancer patients. However, use of these medications has been associated with increased click here risk of side effects, which might lead to premature mortality. Short lengths of stay in hospice care leave patients with a higher level of unmet needs. The study was conducted to examine the effect

of increasing anticholinergic load on the length of stay of cancer patients in hospice care in the USA. The National Home and Hospice Care Survey 2007 was Pregnenolone used as the data source. The Cox proportional hazards model was used to investigate the risk of death among users of moderate and high anticholinergic load compared with users of low anticholinergic load in presence of other prognostic factors. Cancer patients on a moderate anticholinergic

load had a 12.7% lower hazard of death (P = 0.0244), while those on a high anticholinergic load had a 15.6% lower hazard of death (P = 0.0071) as compared with those patients on a low anticholinergic load. Among other prognostic factors, non-elderly age group, male gender, white race, metropolitan hospice agency, non-profit hospice agency, severe activities of daily living dependency and cognitive impairment were significantly associated with a higher probability of death. These results provide no evidence for increasing anticholinergic load increasing mortality in cancer patients using hospice care. Thus, high anticholinergic load might have conferred a protective effect on the patients because of better symptom control.

Once encapsulated, the trapped bacteria subsequently die (Silva et al., 2002). Cytotoxic factors targeting immunocytes are good candidates for the mediators of immunosuppression (Clarke, 2008). Plu1961/Plu1962 caused death of CF-203 cells via necrosis. Further studies on the necrotic and apoptotic activities of Plu1961/Plu1962 against insect hemocytes will be necessary to elucidate its role in immunosuppression. Confocal

microscopy revealed that Plu1961/Plu1962 caused a notable decrease in cellular tubulin of CF-203 cells. Microtubule, one of the principal components of cytoskeleton, is critical to cell shape, cell movement, intracellular transport of organelles, and the separation of chromosomes during mitosis (Archuleta

et al., 2011). As a result, microtubule is a prime target for pathogens and their virulence factors. Mouse macrophages treated with Bacillus anthracis lethal toxin (LT) induced Selleckchem GSK3 inhibitor a notable decrease in the level of cellular tubulin and altered stability of the microtubule network (Chandra et al., 2005). Treatment of human colonocytes with Clostridium difficile toxin A resulted in tubulin deacetylation and subsequent microtubule depolymerization (Nam et al., 2010). Assembly of the two components Sorafenib mouse is essential for binary toxins to exhibit their cytotoxicity (Schleberger et al., 2006). However, the stage at which the assembly of the binary toxin components occurs is debatable. Previous study suggested that intoxication by binary toxins initially involved specific, receptor-mediated binding of ‘B’ component to a targeted cell as monomers that form homoheptamers on the cell surface. The ‘B’ heptamer–receptor complex then acts as a docking platform that subsequently translocates the enzymatic ‘A’ component into the cytosol. Once inside the cytosol, ‘A’ component can inhibit normal cell functions (Barth et al., 2004).

It was reported that at low toxin concentrations, complex formation might enhance the efficiency of the binary toxin (Kaiser et al., 2006). Our data demonstrated that buy Palbociclib when co-expressed in the same cytoplasm, Plu1961 and Plu1962 could interact with each other and form a complex. This could in part explain the observation that Plu1961 and Plu1962 mixed in vitro did not affect the growth of mammalian cells, but while co-expressed in the same cytoplasm, Plu1961/Plu1962 exhibited cytotoxic effect against B16, 4T1, and HeLa cells. In conclusion, we have identified XaxAB-like binary toxin from P. luminescens TT01, which exhibits highly injectable toxicity against insect larvae. Plu1961/Plu1962 mixture could cause rapid cell necrosis when applied to insect midgut CF-203 cells. However, co-expression in the same cytoplasm is essential for Plu1961/Plu1962 to exhibit cytotoxic activity against mammalian cells. The biological role of Plu1961/Plu1962 in the infection process needs further study.

The spectral width in the carbon dimension was 170 p.p.m. and 180 p.p.m., respectively. All spectra were processed and analyzed using Bruker’s topspin

(v3.0) software. Usually, zero-filling was applied to double the number of real points in each dimension. Chemical shifts were referenced to the HDO resonance at 4.7 p.p.m. Chemical shift assignments for 13C were determined indirectly from HSQC and HMBC spectra. Pseudomonas sp. strain Chol1 was subjected to random transposon mutagenesis MDV3100 solubility dmso by insertion of the transposon mini-Tn5 Km1 and screened for transposon mutants showing altered growth with cholate as described previously (Birkenmaier et al., 2007). One mutant, strain G12, was analyzed further. Strain G12 could not grow with cholate as the sole substrate, but it could grow with succinate in the presence of cholate. HPLC analysis of supernatants from these cultures revealed that strain G12 did not transform cholate at all. We then checked Anti-infection Compound Library whether strain G12 could grow with intermediates of cholate degradation. With supernatants containing DHADD (VIII), strain G12 could grow after a long lag phase. Notably, cells of strain G12 induced for growth with DHADD were also induced for cholate transformation during growth with succinate in

the presence of cholate. HPLC analysis revealed that cholate was transformed into several compounds with an absorption maximum at 244 nm, which is indicative of steroids with a 3-keto-1,4-diene structure of the A-ring (Philipp et al., 2006). In the next step, we identified the gene in strain G12, in which the mini-Tn5 Km1 had been inserted. The transposon Ergoloid was inserted into an

ORF of 1212 bp at bp 333. The predicted protein had 403 amino acids and showed high identity to nonspecific lipid transfer proteins from various bacteria. Among these were two bacteria, for which growth with cholate had been demonstrated, namely Pseudoalteromonas haloplanktis strain TAC125 (Birkenmaier et al., 2007) and Comamonas testosteroni strain KF-1 (Rösch et al., 2008). The nonspecific lipid transfer proteins from strains TAC125 and KF-1 showed 80% and 68% identity, respectively, to the gene product from strain Chol1 (Fig. 2). This gene was named skt (for steroid β-ketothiolase) for reasons that will be described below. To investigate the function of skt for cholate degradation further, we decided to construct a defined mutant of this gene by subjecting strain Chol1 to insertional mutagenesis with the suicide vector pKnockoutG. The resulting strain Chol1-KO[skt] could not grow with cholate; growth with cholate was restored when an intact copy of skt was provided in trans on the vector pBBR1MCS-5 (Fig. 3a). This complementation clearly showed that the phenotype of this mutant was caused by the inactivation of skt. Strain Chol1-KO[skt] could grow with succinate in the presence of cholate (Fig. 3b).

Another study demonstrated that the risk of S.

aureus infection among colonized HIV-infected SB525334 mouse patients with CD4 counts <100 cells/μL was as high as 10% for every 6-month interval over which they were colonized. Bloodstream infections and skin and soft issue infections (SSTIs) were the most common types of infection described in this study, and were largely community-acquired (CA). Furthermore, most infecting strains were identical to the colonizing S. aureus strain [2]. Historically, infections caused by methicillin-resistant Staphylococcus aureus (MRSA) impart a higher morbidity and mortality compared with infections caused by methicillin-susceptible S. aureus [5]. Among HIV-negative patients, established risk factors for MRSA colonization and infection include a history of hospitalization, a history of a surgical procedure, haemodialysis, the presence of an indwelling catheter, and residence in a long-term care facility [6]. Clinical AIDS has also been described as a risk for MRSA colonization, and this has been attributed to various behavioural factors and underlying medical conditions. Among HIV-infected patients, studies differ in their identification of risk factors for MRSA infection and have included a CD4 count <50 cells/μL, an HIV viral load

greater than 100 000 HIV-1 RNA copies/ml, HIV acquisition via men who have sex with men (MSM), use of beta-lactam antibiotics within 6 months, a history of syphilis, undergoing an invasive procedure within 12 months, prior incarceration, past or MAPK Inhibitor Library cell line current injecting drug use (IDU), and lack of trimethoprim-sulfamethoxazole prophylaxis for more than 4 months [7–10]. Additionally, the emerging epidemiology of USA-300 CA MRSA among HIV-infected patients has not been fully described with regard to the impact of the USA-300 CA-MRSA strain. The goal of our study was to describe the epidemiology of MRSA in our HIV-infected patient population, which predominantly consists of heterosexual

minorities, in order to identify risk factors for MRSA colonization or infection as well as those for USA-300 CA-MRSA colonization or infection. The Infectious Diseases (ID) out-patient clinic is affiliated with the Medical University of South Carolina (MUSC), a 650-bed academic medical centre located in Charleston, South Carolina, USA. We TCL performed a retrospective chart review of 900 HIV-infected patients who received care at our ID clinic from January 2002 until December 2007 to identify those who were colonized or infected with MRSA. Our study was approved by the MUSC institutional review board. To determine risk factors associated with MRSA colonization or infection, we performed an unmatched case–control study in which cases were defined as HIV-infected patients seen at least once in the ID clinic during the study period, who were colonized or infected with MRSA at any time after their HIV diagnosis.