For expression studies

of the trh-like genes in A veroni

For expression studies

of the trh-like genes in A. veronii isolates, total RNA was isolated from cells grown at the mid-log phase (OD600 nm=0.6) and the early stationary phase (OD600 nm=1) using TRIzol® LS reagent as per the manufacturer’s instructions (Invitrogen). Reverse transcription (RT)-PCR was performed using trh5 and trh6 primers for the detection of trh mRNA. Vibrio parahaemolyticus strain AQ4037 (trh+, tdh−) was used as a positive control. To show that the RNA preparation contains mRNA suitable for RT-PCR, normal metabolic gene gyrB was targeted using gyrB3F and gyrB14R primers to amplify a fragment of approximately 1100 bp (Yanez et al., 2003). All the three A. veronii isolates were TSA HDAC concentration positive for gyrB PCR, suggesting that the RNA preparation contains mRNA suitable for RT-PCR.

Further, to confirm the native expression, Trh-like hemolysin Western blotting was performed using Trh polyclonal antibodies developed in our laboratory. This antibody was developed by immunizing rabbits with a purified recombinant Trh protein of V. parahaemolyticus (Raghunath, 2008) by an intramuscular injection at 10-day intervals for 4 weeks consecutively. Animals were bled a week after the last dose by a cardiac puncture and antibody titers were determined ABT 199 using plate ELISA as described by Engvall & Perlman (1971). Aeromonas veronii isolates grown in LB broth at 37 °C overnight with shaking were harvested by centrifugation at 10 000 g for 10 min. Fifteen percent sodium dodecyl sulfate polyacrylamide gel electrophoresis was performed on the lysed pellet as well as the supernatant (Laemmli, 1970). Western blotting was performed as per the procedure of Towbin et al. (1979). Trh-producing V. parahaemolyticus (AQ4037) was used as a positive control. In this study, a total of

44 isolates of Aeromonas spp. were screened for the presence of the trh gene. Among the Aeromonas spp. tested, only three clinical isolates of A. veronii (NT3818, NT3871 and VTE599) tested positive for PAK5 the presence of this gene, and the results of duplex PCR (Fig. 2) confirm that the negative reaction in other strains was not due to the inhibition of PCR. All other Aeromonas spp. including the remaining seven clinical isolates of A. veronii did not harbor this gene. A positive reaction with colony hybridization using a digoxigenin-labelled probe further confirmed the presence of the trh homolog in the three A. veronii isolates. To rule out the possibility of misidentification of these isolates, PCR targeting the toxR gene of V. parahaemolyticus was performed (Kim et al., 1999). All the three isolates were negative for this PCR, thus confirming that they are not atypical strains of V. parahaemolyticus. A gyrB sequence analysis of the three A. veronii isolates showed that they were highly similar to each other and had about 98% identity to the A. veronii biovar veronii gyrB sequences available in GenBank. In a recent study, Gonzalez-Escalona et al.

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The absence of live extracellular bacteria was ensured after subc

The absence of live extracellular bacteria was ensured after subculture on agar plates. At each time point, cells were lysed by 0.1% Triton X-100, and viable intracellular bacteria were counted by plating

serial dilutions of lysates on blood agar plates. Peripheral blood mononuclear cells (106 mL−1) were stimulated with live bacterial cells for 45 min at a ratio of 1 : 10, as in preliminary experiments, this ratio was proved to be the most efficient in cytokine production. Afterwards, extracellular bacteria were lysed by lysostaphin Talazoparib mw (Sigma), and medium was replaced by CM supplemented with antibiotics. Cells were incubated for selected time points. Each experiment was carried out with mononuclear cells isolated from a single donor and performed in triplicate. Results are based on at least three experiments from different

donors. LPS (10 ng mL−1) was used as a positive control, and PBMCs without stimulants, bacteria or LPS were used to assess spontaneous levels of cytokine secretion (negative control). Supernatants were collected, and the levels of TNFα, IL-1β, IL-6, IL-8, GM-CSF and IL-12p40 were measured by Human Cytokine Multiplex Immunoassay kit manufactured by Linco Research Inc. using Luminex® xMAP™ technology, whereas the levels of IL-12p70, IFN-γ and IL-13 were measured by High Sensitivity Human Cytokine Multiplex Immunoassay selleck products kit. A five-parameter regression formula was used to calculate

the cytokine concentrations in samples from standard curves. MDMs (2 × 105 mL−1) were stimulated with bacteria at a ratio 1 : 10 for 45 min, extracellular bacteria were lysed by lysostaphin and medium was replaced by CM supplemented with antibiotics. Cells were incubated for additional 12, 24 and 48 h. Supernatants were collected, and the levels of TNFa, IL-1b, IL-6, IL-12p40 and IL-12p70 were assessed. Statistical analysis was performed using spss 17 statistical package (SPSS Inc.). Differences in PIA concentration between biofilm, planktonic and control cells and extracts were assessed by anova test followed by pairwise comparisons. Differential adhesion of biofilm and planktonic cells check details on human MDMs was evaluated using paired t-test. anova test was applied to assess differences in cytokine induction between reference and clinical strains for both parameters (planktonic and biofilm phase). No difference was found (anova P > 0.05); therefore, data analysis was performed after comparing results from all strains. Differences in cytokine concentrations between planktonic and biofilm phase were evaluated using paired t-test. Two-way anova was used to evaluate differences in intracellular survival between biofilm and planktonic phase cells. Statistical significance was set at α = 0.05.

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The contrast maps for group and regression analyses were threshol

The contrast maps for group and regression analyses were thresholded at P < 0.001 without correction for multiple comparisons, and the extent threshold for significant clusters was set to 40 voxels. We were aware that the application of an uncorrected threshold would

certainly limit the impact of possible results as it increases the probability of false positive findings. To justify the selection of an uncorrected threshold in our analyses, we provide the following issues. Taking into account the results of previous PD0332991 purchase findings in DTI studies in ADHD (Ashtari et al., 2005; Makris et al., 2008), we only expected discrete microstructural abnormalities in ADHD that may not be detectable adopting a corrected threshold with

a much higher risk of false negative findings. In this context, it is noteworthy that the only published voxel-based DTI study in ADHD – like a large number of imaging studies in the neuropsychiatric field – also used an uncorrected (P < 0.001) LY2835219 order threshold (Ashtari et al., 2005). T1-weighted templates were then overlaid with the statistically significant SPM clusters using MRIcro software for graphical presentation in neurological convention. The MRI atlas of human WM (Mori et al., 2005) was used for the identification of subcortical WM structures. The MNI coordinates and t-statistic of the peak voxel, the cluster size and the corresponding anatomical structures were determined (Mori et al., 2005). The mean FA and MD values of the peak voxel resulting from the voxel-based group analysis as well as from the voxel-based regression analyses were correlated with the measures for attentional performance (ADHD score), impulsivity (number of commission errors) and total ADHD symptomatology (BADDS score). Significance was set to P < 0.05 (uncorrected) for these regression analyses. Gender, age and IQ did not differ between groups (Table 1). Among patients, 16 (43%) were regular smokers, compared with 6 (18%) regular smokers in the control group. As expected,

MRIP we found significant group differences in ADHD semi-quantitative measures WURS and BADDS (Table 1). The ADHD score (TOVA) was significantly lower in patients with ADHD (−4.4 ± 5.7) than in controls (1.7 ± 2.0). RT was significantly longer and RT variability was significantly higher in patients with ADHD (Table 1). Patients’ performance was significantly poorer in the TMT-A, in the TMT-B, in the AVLT and in the WMS-R (Table 1). In the remaining neuropsychological tests (MWT, WCST), performance in the patient group was also poorer, but the differences did not achieve statistical significance (Table 1). As the tests examined different categories of neuropsychological performance and executive function, we did not use a Bonferroni correction for multiple comparisons.

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After both F2r and F2c injections, labeled neurons in the striatu

After both F2r and F2c injections, labeled neurons in the striatum were widely observed in the striatal cell bridge region and neighboring areas, as well as in the ventral striatum. The present results revealed that the origins of multisynaptic projections to F2c and F2r in the BG are segregated in the output stations of the BG, whereas intermingling rather than segregation is evident with respect to their input station. “
“Postnatal day (P)20 rats are sensitive to CA1 injury following a single injection of kainic acid (KA) but are resistant to this injury when animals have a CYC202 order history of two neonatal seizures.

We hypothesized that the two earlier seizures led to neuroprotection by a preconditioning mechanism. Therefore, morphology, [Ca2+]i

and NMDA subunit proteins of the hippocampus were examined after KA was administered once (1 × KA, on P6, P9, P13 or P20), twice (2 × KA, on P6 and P9) or three times (3 × KA, on P6, P9, P13 or P20). After 1 × KA on P20, the Golgi method revealed marked decreases in spine densities and aborization of CA1 and CA3 apical dendrites. After 3 × KA, morphological alterations were attenuated in CA1 neurons and were similar to pruning observed after 1 × KA on P6 or 2 × KA. After 1 × KA at P13, baseline [Ca2+]i was elevated within pyramidal and dentate granule cells. N-methyl-d-aspartate (NMDA) responses were simultaneously enhanced. After 3 × KA, Ca2+ elevations were attenuated. Immunohistochemistry revealed selective depletion of the NR2A/B subunit modulator in the same (-)-p-Bromotetramisole Oxalate areas. NR1 subunit expression was downregulated in the subiculum and increased in the CA3, causing a significant shift in the NR1:NR2A/B ratio throughout the hippocampus. After 1 × KA or 3 × KA at P20, reduced expression

was only observed in areas of cell injury. Results indicate that different changes in morphology and excitatory responses occur depending upon when seizures begin. Partial pruning and persistent shift in the NR1:NR2A/B ratio among excitatory synapses of the hippocampus early in life may produce epileptic tolerance and protect against subsequent insults. “
“Phasic firing of dopamine (DA) neurons in the ventral tegmental area (VTA) and substantia nigra (SN) is likely to be crucial for reward processing that guides learning. One of the key structures implicated in the regulation of this DA burst firing is the pedunculopontine tegmental nucleus (PPTg), which projects to both the VTA and SN. Different literatures suggest that the PPTg serves as a sensory-gating area for DA cells or it regulates voluntary movement. This study recorded PPTg single-unit activity as rats perform a spatial navigation task to examine the potential for both reward and movement contributions.

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For each time point, there were a pair of libraries that consiste

For each time point, there were a pair of libraries that consisted of the cycloheximide-untreated (Day-U; control) and the cycloheximide-treated samples

(Day-T; treated). Comparative sequence analysis was conducted by blast (Altschul et al., 1997) against the GenBank database (Benson et al., 2010) to obtain the taxonomic identity of all the clones. The sequences were converted to fasta format, imported SRT1720 in vivo into the software platform mothur (Schloss et al., 2009) and aligned against the eukaryotic SILVA database (Pruesse et al., 2007). Distance matrices were generated using phylip ( and pairwise comparisons of all the sequences were carried out between the control Cabozantinib purchase and the treatment within each time point to establish operational taxonomic units (OTUs) for each library (OTUs

established at≥97% similarity) at 95% confidence using mothur. The coverage of each library was calculated by dividing the number of OTUs by the nonparametric richness estimator Chao1 (Chao, 1984). libshuff (Singleton et al., 2001) was used to statistically compare the two libraries (control and treatment) for each time point. Previous studies have demonstrated that foodborne pathogens exhibit long-term survival in compost and soil and undergo a gradual die-off (Kudva et al., 1998; Jiang et al., 2002; Islam et al., 2004a, b). The decline in cell numbers has been attributed to temperature, moisture, pH, nutrient competition, antimicrobials as well as indigenous microbial communities, but we are unaware of any study that has correlated specific members of compost microbiota with a reduction of E. coli O157:H7. Our primary objective was to initiate

studies that would ultimately relate pathogen survival with the composition of the compost microbial communities. In the initial Org 27569 experiments, the reduction of E. coli O157:H7 was studied in autoclaved and unautoclaved compost incubated at 25 °C. This temperature was chosen as the cycloheximide used in this study was found to be stable under these conditions, while the effectiveness of this antimicrobial decreased at higher temperatures (data not shown). The abundance of E. coli O157:H7 in autoclaved compost remained essentially constant throughout the test period (Fig. 1). In marked contrast, within 16 days of incubation at 25 °C in unautoclaved compost, E. coli O157:H7 underwent a c. 4 log10 reduction. The means of linear regression slopes between the autoclaved and the unautoclaved samples were significantly different (P=0.005). This strongly suggested that background microbial communities significantly reduced E. coli O157:H7 in compost at 25 °C. Compost naturally contains high levels of bacteria, fungi and protists (Beffa et al., 1996). The experiment comparing the survival of E. coli O157:H7 in sterile and nonsterile compost (Fig. 1) suggested that the autochthonous microbial communities have an antagonistic effect on E. coli O157:H7.

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Additionally, although P malariae accounts for less than 2% of im

Additionally, although P malariae accounts for less than 2% of imported malaria cases in the United States,17 careful follow-up of such

patients after initial treatment may be necessary to ensure that chronic infection is not established. The authors would like to acknowledge financial support from US Navy, selleck products Department of Defense. R. H., J. J. F., A. I. S., and J. D. M. are military service members and employees of the US Government. This work was prepared as part of their official duties. Title 17 U.S.C. 105 provides that “Copyright protection under this title is not available for any work of the United States Government.” Title 17 U.S.C. 101 defines learn more a US Government work as a work prepared by a military service member or employee of the US Government as part of that person’s official duties. The assertions herein are the views of the authors and do not reflect official policy of the US Department of the Navy or the US Department of Defense. The authors state that they have no conflicts of interest to declare. “
“Chloroquine-resistant Plasmodium vivax (CRPV) infection is emerging as a clinically significant

problem. Detailed travel history is crucial to the management of imported malarial cases. We report a 58-year-old business traveler who returned from Indonesia and experienced relapse due to CRPV. The epidemiology and diagnostic challenges of CRPV for travel medicine clinicians are reviewed. Malaria is a clinically important cause of febrile illness in local populations as well as in travelers in areas with endemic transmission. Among ill travelers seen at GeoSentinel sites who had returned from all destinations and had fever, malaria accounted for 21% of specific causes identified.1 Although Plasmodium falciparum remains the major clinical concern due to severity

of illness and widespread drug resistance, there is growing awareness of the serious morbidity and emerging drug resistance associated with Plasmodium vivax infection.2 Chloroquine-resistant P. vivax (CRPV) was not reported until 1989,3 from and it remains relatively uncommon except in Papua New Guinea and Indonesia. Unless a detailed travel exposure history is obtained, the risk of CRPV may not be recognized among travelers, especially those who are present in countries that are non-endemic for malaria.4,5 We report here a Singaporean permanent resident who acquired CRPV malaria while traveling on business in Indonesia. A 58-year-old Indonesian man developed fever while traveling in Jakarta, Indonesia, during April 17 to 29, 2008. He had resided in Singapore for 10 years and was otherwise healthy. He reported hospitalization in Jakarta with the diagnoses of P.

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Therefore, S aureus has two independent factors responsible for

Therefore, S. aureus has two independent factors responsible for susceptibility to bacitracin. In conclusion, we found that a TCS, designated BceRS, senses bacitracin and also positively regulates the expression of two ABC transporters that function in bacitracin efflux. This work was supported by a grant-in-aid for scientific research from Health and Labor Sciences Research Grants from the Ministry of Health and Welfare of Japan. “
“Coxiella burnetii is a Gram-negative

pleomorphic bacterium and the causative agent of Q fever. During infection, the pathogen survives and replicates within a phagosome-like parasitophorous vacuole while influencing cellular functions throughout the host cell, indicating a capacity for effector protein secretion. Analysis of the C. burnetii (RSA 493 strain) genome sequence indicates that C. burnetii contains genes with homology to the Legionella LDE225 pneumophila Dot/Icm type IVB secretion system (T4BSS). T4BSSs have only been described in L. pneumophila and C. burnetii, marking it a unique virulence determinate. Characterization of bacterial virulence determinants ranging from autotransporter proteins to diverse secretion systems R428 cell line suggests that polar localization may be a virulence mechanism hallmark. To characterize T4BSS subcellular localization in C. burnetii, we analyzed C.

burnetii-infected Vero cells by indirect immunofluorescent antibody (IFA) and immunoelectron microscopy (IEM). Using antibodies against the C. burnetii T4BSS homologs IcmT, IcmV, and DotH, IFA show that these proteins are localized to the poles of the bacterium. IEM supports this finding, showing that antibodies against C. burnetii IcmT and DotH preferentially

localize to the bacterial cell pole(s). Together, these data demonstrate that the C. burnetii T4BSS localizes to the pole(s) of the bacterium during infection of host cells. The zoonotic disease Q fever is caused by Coxiella burnetii, an obligate intracellular bacterial pathogen (Maurin & Raoult, 1999) that has only recently been propagated in a cell-free medium (Omsland et al., 2009). Coxiella burnetii undergoes a biphasic life cycle initiated by the metabolically inactive, environmentally Bcl-w stable small cell variant (SCV) form of the bacteria. The SCV then goes on to develop into the replicative large cell variant (LCV) form. This may occur by 8 h of host cell infection (McCaul, 1991; Coleman et al., 2004). During the infectious cycle, C. burnetii lives within a parasitophorous vacuole (PV) that has the attributes of a mature phagolysosome (Akporiaye et al., 1983; Heinzen et al., 1996; Ghigo et al., 2002; Gutierrez et al., 2005; Sauer et al., 2005; Howe & Heinzen, 2006; Romano et al., 2007). Recent studies indicate that C. burnetii protein synthesis is required for the pathogen to influence host cell processes such as apoptosis (Voth & Heinzen, 2009) and vesicular trafficking (Howe et al., 2003a, b) from within the PV.

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2 (secondary infection)[12] The

2 (secondary infection).[12] The Roscovitine in vivo study protocol was approved by the institutional review board of the National Institute of Infectious Diseases, Japan.

Detection of DENV RNA by RT-PCR was performed as reported previously (Tables 1 and 3).[15, 16] Viral RNA was extracted using High Pure Viral RNA extraction kit (Roche Diagnostics, Mannheim, Germany) and DENV serotypes were determined by serotype-specific RT-PCR.[15, 16] Dengue-virus specific IgM antibody in serum samples was determined using IgM capture ELISA (Dengue Fever Virus IgM Capture ELISA, Focus Diagnostics, CA, USA) according to the manufacturer’s instructions. Dengue indirect IgG ELISA (Panbio, Queensland, Australia) was used for the detection of anti-DENV IgG antibody according to the manufacturer’s instructions.[15] Detection of the NS1 antigen was performed using Platelia Dengue NS1 Antigen (Biorad Laboratories, Marnes-la-Coquette, France) and Pan-E Dengue Early ELISA (Panbio) according to manufacturers’ instructions. The former kit was mainly used in the study. For the Platelia Dengue NS1 Antigen ELISA kit, 50 μL of serum sample, 50 μL of sample diluent (Diluent R7, phosphate buffer, Tween 20, and fetal calf serum supplemented with 0.15% ProClinTM 300) and 100 μL of diluted conjugate (anti-NS1 monoclonal antibody-coated

to horseradish peroxidase supplemented with 0.15% ProClinTM 300) were added to each anti-NS1 monoclonal antibody coated well. The assay plate was incubated at 37°C for 90 minutes. Positive controls and negative controls with calibrator sera were included in each assay. After six washings, 160 μL of tetramethylbenidine (TMB) substrate was added to each of the wells and the plate was further incubated at room temperature for 30 minutes in the dark. Reaction to was terminated with 100 μL of stop solution (1 N H2SO4). Optical density (OD) readings were obtained with a spectrophotometer at wavelengths of 450 nm/620 nm.

The index of each sample was calculated with the following formula: OD of samples/OD of calibrators. As the Biorad NS1 ELISA kit showed high sensitivity using 50 μL of patient serum samples, the serum sample volume was reduced and the assay was tested for detection rates. Serum samples were first diluted to 1:10 or 1:100 using diluent (Diluent R7, Platelia Dengue NS1 Ag, Biorad). The assay was then performed according to manufacturer’s instructions (Platelia Dengue NS1 Ag, Biorad). Results were interpreted in accordance with manufacturer’s recommendations. Sample ratios were determined by dividing the sample OD with the cut-off OD. Sample ratios of <0.5, 0.5–1.0, and >1.0 were classified as negative, equivocal, and positive, respectively. Equivocals were regarded as negative for analysis.

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To investigate surfactant production by R leguminosarum swarm ce

To investigate surfactant production by R. leguminosarum swarm cells, a drop-collapsing test was conducted following the method described by Jain et al. (1991). Briefly, swarm cells were grown in the swarm medium and then a suspension of cells from the edge of a swarming population was prepared isocitrate dehydrogenase inhibitor 7 days and 3 weeks after inoculation. A 10 μL cell suspension (OD600 nmc. 2.0) was spotted on the surface of the hydrophobic lid of a plastic Petri dish. The cell suspension drop was observed for

spreading, which would indicate the presence of surfactants. Distilled water and 0.2% sodium dodecyl sulfate were used as negative and positive controls, respectively. Transmission electron microscopy was Talazoparib order performed by slightly modifying the procedure used by Miller et al. (2007). The R. leguminosarum strains were grown on solid (1.3% agar) TY plates (for vegetative cells) and on swarm plates (for swarmer

cells). A suspension of the bacteria from the plate cultures was prepared using sterile double-distilled water. For the swarm plates, cultures were taken from the tip of the swarm front and from the center of the plate. A formvar carbon-coated grid was placed on top of a cell suspension drop for 3 min and excess liquid was removed. To determine the arrangement of the swarmer cells, the grid was placed directly on top of the swarm plate, at the tip of the swarm front. Staining was performed using 1% uranyl acetate for 30 s. Samples were observed using a Hitachi-7650 transmission electron microscope and images were taken using an AMT Image Capture Engine. The expression of flagellar genes in R. leguminosarum VF39SM swarmer cells was compared with the expression in R. leguminosarum vegetative cells. We used pre-existing gusA fusions to flagellin (flaA) and flagellar PD184352 (CI-1040) regulatory genes (visN, and rem) (Tambalo et al., 2010). Vegetative cells were grown on a solid swarm medium (1.3% Bacto agar) for 8 days at room temperature and in swarm broth medium for 48 h. Swarmer cells were grown in swarm

plates for 2 weeks at 22 °C. Broth cultures were directly used for a β-glucuronidase (gusA) assay, whereas for plate cultures, cells were taken from the edge of a swarming population and vegetative cell population and were suspended in swarm broth. The gusA activity of the fusions was measured as described by Jefferson et al. (1986) and modified by Yost et al. (2004). All data given are the means of triplicate experiments. The antibiotic resistance patterns of vegetative and swarmer cells of R. leguminosarum were determined by growing the cells in swarm medium using 1.3% (solid plate) and 0.7% (swarm plate) Bacto agar. Antibiotic solutions were added onto sterile paper discs and then dried for 20 min. The antibiotics used were cephalexin (50 μg), nalidixic acid (50 μg), rifampicin (20 μg), and chloramphenicol (30 μg).

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However, with a fat increase of 040 kg

per year after tN

However, with a fat increase of 0.40 kg

per year after tNRTI cessation, lipoatrophy may take over 5 years to resolve for many patients without additional intervention, at least for those with severe lipoatrophy [8]. Innovative antiretroviral MK2206 regimens using either new drugs (e.g. raltegravir or etravirine) or new treatment strategies (e.g. NRTI-sparing regimens) may warrant further evaluation in patients with severe lipoatrophy. The study was funded in part by educational grants from Abbott Laboratories and the Balnaves Foundation. The SHCS is financed in the framework of the Swiss HIV Cohort Study, supported by the Swiss National Science Foundation. Andrew Carr is a recipient of selleck inhibitor a Practitioner Fellowship from the Australian National Health and Medical Research Council. The authors also wish to acknowledge John Ray, for measurement and validation of the uridine plasma concentrations; Nicole Easy, who performed the CT scans in Sydney; Sophie Zawadynski and Nick Pocock for DEXA scan validation; Matthew Law for statistical advice; and Danièle Scherrer and Linda Hotong for pharmacy assistance. Author contributions: Study concept and design: A. Calmy and A. Carr. Analysis

and interpretation of data: A. Calmy, A. Carr, C. Delhumeau, H. Wand, M. Bloch, B. Hirschel and R. Finlayson. Data extraction: H. Wand and C. Delhumeau. Drafting of the manuscript:

A. Calmy. Critical revision of the manuscript for important intellectual RG7420 chemical structure content: all authors. Statistical analysis: H. Wand and C. Delhumeau. Generation of allocation sequence and assignment of patients to their randomization groups: H. Wand (the randomization form had to be faxed to H. Wand, at the National Center for HIV Epidemiology and Research, and receipt of the randomization was provided within one working day). Study supervision: A. Carr. Financial disclosures A. Calmy, H. Wand, C. Delhumeau, R. Finlayson, M. Rafferty and R. Norris have no conflict of interest. B. Hirschel has received travel grants and speakers’ honoraria from Abbott, Bristol-Myers Squibb, Gilead, GlaxoSmithKline, Merck Sharp & Dohme-Chibret and Roche. He also has participated in advisory boards for Merck, Tibotec and Pfizer. D. A. Cooper has received research funding from Boehringer-Ingelheim, Bristol-Myers Squibb, Gilead Sciences, Janssen-Cilag, Merck and Pfizer; consultancy fees and lecture and travel sponsorships from Abbott, Boehringer-Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Janssen-Cilag, Merck and Pfizer; and has served on advisory boards for Abbott, Boehringer-Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Janssen-Cilag, Merck and Pfizer. A.

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