An empty vector (pKAN3) was transformed as a negative control Th

An empty vector (pKAN3) was transformed as a negative control. The U791 mutation was chosen, because this mutation was shown to be the most detrimental to ribosome function compared with other possible mutations at this position without affecting the assembly of the 30S ribosomal subunit (Song et al., 2007). Selleckchem PD332991 To select for genomic library clones

containing genes that restored protein synthesis ability in U791 ribosomes when overproduced, transformants were plated on LB-agar medium containing 50 μg of chloramphenicol per milliliter of LB (Cm50); at this concentration, cells expressing pRNA122-U791 ribosomes could not grow. The survival ratio for the transformants was about 3 × 10−4, which was about 400 × higher than the background (7 × 10−6 when pKAN3 was transformed).

Plasmids were prepared separately from 50 of BIBF 1120 order the surviving geneomic clones and cotransformed with pRNA122-U791 into E. coli cells. The resulting transformants were tested for their degree of resistance to chloramphenicol in the presence and absence of the inducer IPTG. All clones derived from the genomic library were resistant to Cm100 (MIC=150) only in the presence of IPTG. These results indicated that the CAT mRNA translation in these cells was dependent on both pRNA122-A789 ribosomes and genomic clones. However, all clones showed a MIC of 50 regardless of the presence of an inducer when 10 of the clones derived from cells harboring an empty vector were subjected to the same procedure as described above.

These negative control clones may have survived initially because they managed to grow on selective media due to heavy plating of cells or chromosomal mutations. Restriction enzyme sites analyses were tuclazepam performed with plasmids purified from the 50 clones using the initial EcoRI cloning site. All the clones exhibited a common 6 kbp EcoRI fragment. The results of sequencing analysis of the chromosomal DNA in five clones that contained only the 6.0 kb EcoRI fragment showed that the fragment was located at ∼20 min of the E. coli chromosome. It contained the coding regions of aat, cydC, cydD, two unknown ORFs, and infA. We chose to test whether overexpression of infA was responsible for the partial restoration of the protein synthesis function of the pRNA122-U791 ribosome because this gene encodes a known translational factor, IF1. The coding region for the infA gene was subcloned into pKAN6B, a derivative of pKAN3, and expressed under the arabinose-inducible promoter (pKAN6-IF1). Plasmid pKAN6-IF1 was cotransformed with pRNA122-U791 into DH5α cells and the resulting transformants were tested for their degree of resistance to chloramphenicol in the presence and absence of the inducer IPTG.

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maritimum NCIMB2154T obtained at 24 and 48 h using the


maritimum NCIMB2154T obtained at 24 and 48 h using the

three E. coli JM109 lux-based biosensor strains carrying pSB536, pSB401 or pSB1075 to detect a wide range of AHLs differing in the length of their acyl chain. TLC analysis revealed the presence of short-chain AHLs using the E. coli JM109 pSB536 biosensor (Fig. 1). A search for AHL-type QS signals in extracts obtained from the culture media of another eight representative isolates of T. maritimum using the same technique revealed the presence of short-chain AHL activity in all of them, although differences were recorded in relation to their peak in activity (Table 1). LC-MS analysis confirmed the presence of N-butyryl-l-homoserine lactone (C4-HSL) in the culture media of T. maritimum NCIMB2154T grown in both FMM (Fig. 2) and MB (data not shown). This AHL was unequivocally identified by comparison Forskolin of its mass spectra with those of pure standards (Fig. 3). As this is the

first description of the production of AHLs by a pathogenic member of the CFB cluster, the analyses were carried out simultaneously in both laboratories using different chromatographic conditions. The results confirmed unequivocally the presence of the C4-HSL. So far, no physiological role other than as QS signals has been assigned to AHLs, except as a chelator, for tetramic acid (a derivative of 3-oxo-C12) or antibiotic activity for both 3-oxo-C12-HSL and tetramic acid (Kaufmann et al., 2005; Schertzer et al., 2009). In addition, a role as biosurfactant has been attributed to long-chain AHLs (Daniels et al., 2006). Therefore, even though the physiological features under the control of these molecules in T. maritimum remain to be investigated, the production of C4-HSL by T. maritimum strains extends the paradigm of AHL-mediated QS beyond the Proteobacteria. Fenbendazole As the physiological processes under the control of AHL-mediated QS have so far been described for a limited number of genera of the Alpha-, Beta- and Gammaproteobacteria, many

of them human or plant pathogens (Williams et al., 2007), the ecological significance of AHL-mediated QS has been questioned as a key switch controlling gene expression within bacterial populations in nature (Manefield & Turner, 2002). The fact that genera outside the Proteobacteria produce the same signal molecules, and that AHL-degrading activity has been found in Gram-positive, Gram-negative and Cyanobacteria (Dong & Zhang, 2005; Romero et al., 2008) and in mammalian cells (Chun et al., 2004), reinforces the ecological significance of AHL-mediated QS processes. The presence of AHL-mediated QS beyond the Proteobacteria is not surprising, as a phylogenetic study based on the LuxI/LuxR genes suggested that QS mechanisms were established very early in the evolution of bacteria, although horizontal transfer may have also played an important role in the distribution of QS genes, at least within this group (Lerat & Moran, 2004).

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Periods off cART with a duration of >90 days were omitted from th

Periods off cART with a duration of >90 days were omitted from the primary analysis. A new cART regimen was defined as a regimen created from an existing PD 332991 regimen by the addition of one or more new antiretrovirals, or by the replacement of one or more antiretrovirals in the existing regimen with one or more new antiretrovirals. NeurocART status was assigned

to those regimens with a CPE rank of 8 or more, with the CPE rank calculated using the 2010 rankings process [17]. CD4 cell counts and viral loads were taken as the latest measurement from up to 90 days prior to regimen commencement. HIV viral load measurements of ≤400 copies/mL were defined as undetectable because more sensitive assays were not uniformly available for all observations. Coinfection with hepatitis

B virus (HBV) or hepatitis C virus (HCV) was defined as the detection of HBV surface antigen or HCV antibody, respectively. A secondary composite endpoint of AIDS or mortality within 90 days of cessation of treatment was also investigated. Follow-up was calculated from the start date of each new cART regimen (or the date of cohort enrolment if later), until cessation of that cART regimen. Loss to follow-up was defined as no clinic visit in the 12 months prior to 31 March 2009 (cohort censoring date). Patients lost to follow-up were censored at their last clinic visit. We used an intention-to-continue treatment approach and ignored any changes to, or interruptions or termination of, treatment after baseline. For each new cART regimen we created a new set of baseline covariates and assessed Cabozantinib datasheet the risk of death on that cART regimen adjusted for those baseline covariates. Variables updated at change in cART regimen were neurocART status, Phosphoribosylglycinamide formyltransferase CD4 count (<50, 50–99, 100–199, 200–349 and ≥350 cells/μL, or missing), HIV viral load (≤400 or >400 HIV-1 RNA copies/mL,

or missing), prior AIDS-defining illness (ADI), cART regimen count (first, second, third, fourth or more), months of prior neurocART exposure (never, or 1–9, 10–18 or >18 months), and months of prior cART (not neurocART) exposure (never, or 1–18 or >18 months). Additional variables examined were age (<30, 30–39, 40–49 or ≥50 years), sex, mode of HIV exposure [men who have sex with men (MSM), heterosexual, injecting drug use (IDU), other or missing], HCV coinfection, HBV coinfection, and neurocART type prior to entry (naïve, cART and not neurocART, or neurocART). We also analysed the incidence of HAD. As there is some evidence that progressive multifocal leucoencephalopathy (PML) may respond better to neurocART than non-neurocART [20], PML data were also analysed. We did not have data on patients’ CD4 cell count nadirs. An administrative censoring date of 31 March 2009 was used. Univariate Cox proportional hazards models were developed for all variables.

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S8 The mutants orsAΔ and AN7903Δ lack production of violaceols

S8. The mutants orsAΔ and AN7903Δ lack production of violaceols. Fig. S9. Extracted ion chromatograms of metabolic extracts from the reference and ausAΔ strains. Fig. S10.1H NMR spectrum of 3,5-dimethylorsellinic acid in dimethyl sulfoxide-d6. Fig. S11.1H NMR spectrum of dehydroaustinol in CDCl3. Fig. S12.1H NMR spectrum of arugosin A open form in dimethyl sulfoxide-d6. Table S1. PCR primers for Gateway assembly. Table S2. Oligonucleotide primers for diagnostic PCR. Table S3. Additional oligonucleotides used in the study. Table S4. The constructed Aspergillus nidulans PS-341 chemical structure strains have been

deposited into the IBT Culture Collection. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials

supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“We are concerned regarding Chapter 11 of the draft British HIV Association (BHIVA) monitoring guidelines ‘Technical aspects of viral load testing’ [1]. This states that ‘based on available information, viral RNA in blood samples collected into EDTA tubes is stable for at least 2–3 days at room temperature, allowing transportation of the sample by post or collection over a weekend’. We believe that the references cited [2, 3] may not be applicable to current practice because they relate to the stability of HIV-1 RNA in whole blood in patients who, crucially, are not taking antiretroviral therapy (ART). There is

current concern regarding low-level viraemia in patients on ART LBH589 supplier Thiamet G [4] which is incompletely understood. We believe that time to processing of samples for HIV-1 RNA testing plays an important part in the genesis of low-level viraemia. At our HIV clinic in York we observed more patients on ART with detectable viral loads than expected and therefore conducted a service evaluation during March to May 2009. We took paired samples for HIV-1 RNA testing from 21 patients who had been stable on ART for 6 months. One sample had plasma separated in York Microbiology Department (York Teaching Hospital NHS Foundation Trust) prior to transportation to the virology lab in Leeds and the other was transported as whole blood in an ethylenediaminetetraacetic acid (EDTA) monovette tube. The mean time to local centrifugation was 4 hours and to processing at the virology lab was 28 hours. Samples were assayed using the Roche TaqMan v2.0 (COBAS® AmpliPrep/COBAS® TaqMan® HIV-1 Test, Roche Molecular Diagnostics, UK). We found that nine of 21 whole-blood samples (43%) had an HIV-1 viral load above 400 HIV-1 RNA copies/mL, i.e. at a level where resistance testing or therapeutic drug monitoring would be instigated and treatment augmentation/switch considered [5]. In contrast, no separated sample had a viral load > 400 copies/mL. Twelve of 21 whole-blood samples (57%) had an HIV-1 viral load > 200 copies/mL, i.e.

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The median CD4 lymphocyte count was 420 cells/μL and 74 patients

The median CD4 lymphocyte count was 420 cells/μL and 74 patients (24%) had CD4 counts of <200 cells/μL. The outcomes of treatment are shown in Table 1. Of the 310 patients,

156 [50.3%; 95% confidence interval (CI) 42.1–53.3%] experienced treatment failure under definition 1, 10 (3.2%; 95% CI 1.5–5.8%) experienced treatment failure under definition 2, and 16 (4.5%; 95% CI 2.5–7.4%) experienced treatment failure under definition 3 over the 108 months of follow-up. Figure 1 shows the Kaplan–Meier analysis of the proportion of individuals who would have been deemed Epigenetics inhibitor to have experienced treatment failure on the basis of the three different definitions. There was selleck chemicals llc a significant difference (P=0.01) in the probability of failure between definitions 1 and 2 and between definitions 1 and 3 (P=0.01), but not between definitions 2 and 3 (P=0.5). To determine whether any definition could show a significant reduction in treatment failure over time, we compared treatment failure during the first half of the study period (2000–mid-2004) with that during the second half (mid-2004–2008) for each of the three definitions separately (Fig. 2a–c). Treatment failure

was different between the two time periods only for definition 1 (P=0.5), and not for either definition 2 (P=0.5) or definition 3 (P=0.5). Table 2 shows the comparison of the three different definitions for assessing virological response with the characteristics of an ideal quality measure. We compared three definitions of HIV treatment failure in a single clinical service and compared them with the characteristics of ideal quality outcome measures. The striking observation was that the failure rate was very much higher for the definition using TLOVR than for the other definitions because ceasing treatment for any reason is defined as treatment

failure in the TLOVR definition. Because individuals most often ceased or changed treatment for reasons other than virological rebound, the TLOVR definition was the least useful Depsipeptide purchase representation of clinical prognosis. In contrast, the rate of failure in definitions 2 and 3 was too low to allow detection of meaningful changes over time, even in a large clinic service such as ours. No single definition stood out as superior for the other requirements of a quality outcome measure. This is the first study to assess different definitions of HIV treatment failure and to compare these with the requirements used to evaluate quality outcome measures in a single health service. On the basis of these findings, it may be that the best option is to set a benchmark level for either definition 2 or definition 3 and to monitor it to ensure that it remains high. This study has a number of limitations that should be considered when evaluating these data.

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In healthy individuals, small amounts of urinary albumin are filt

In healthy individuals, small amounts of urinary albumin are filtered by the glomerulus, and, while most albumin is reabsorbed by the tubules, if protein leak exceeds the capacity of tubular cells to absorb it, it is found in the urine [20]. In glomerular lesions (e.g. HIVAN and HIVICK), the structure and charge barrier to filtration are damaged, and albumin and other protein are filtered, resulting in a higher level of albuminuria [20]. In tubular disease (e.g. cART-related tubular toxicity), urinary proteins are derived from a failure to reabsorb filtered protein and other proteins that originate from damage to tubular cells [21],

and are not picked up by the assay for albumin, but will be picked up by a total protein assay (e.g. uPCR). Some tubular proteins learn more [e.g. neutrophil gelatinase-associated lipocalin (NGAL), N-acetyl-β-D-glucosaminidase (NAG), cystatin C and β2-microglobulin] may be quantified using specific assays, but these assays are expensive and not routinely available. We recently showed that a urine albumin/total protein ratio (uAPR), which is the ratio check details of urine albumin to total protein (uACR/uPCR), was highly sensitive and specific for tubulointerstitial disease in

the general population [22]. This was tested by examining the urine immunoelectrophoretic pattern and in some cases correlating this with histology. We hypothesized that, as in HIV infection one of the key decisions in patient management is to decide if the treatment is causing renal dysfunction (primarily through tubular dysfunction), the measurement of uAPR might be helpful in such assessments. Thus, we tested the hypothesis that uAPR may help to distinguish those patients with cART-associated toxicity from patients requiring further nephrological input, and possibly mafosfamide biopsy in patients in whom there is significant proteinuria. The study sample consisted of HIV-infected patients attending an urban HIV out-patient

clinic in Brighton, UK between 1 September 2007 and 31 August 2009. All uPCR results were retrospectively identified from clinic and laboratory databases. A subsample of patients with concurrent uACR and uPCR results was identified and the uAPR calculated. Patient demographics (sex, ethnicity, sexuality and age at time of uAPR sampling), HIV factors (nadir CD4 count, duration of HIV diagnosis and cART details) and relevant biochemical markers of renal function [estimated glomerular filtration (eGFR), random plasma phosphate and fractional excretion of phosphate] were assessed. The association between cART use and proteinuria was evaluated by ascertaining whether any TDF, boosted PI or simultaneous TDF and boosted PI were used before or at the time of uPCR and uACR sampling. Urine total protein was measured by turbidimetry and urine albumin by immunoturbimetric assay.

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91 (95% CI 083–100); P = 0040] The proportional hazards assum

91 (95% CI 0.83–1.00); P = 0.040]. The proportional hazards assumption was not violated. Overall, 495 patients were diagnosed with TB in the first year after ART initiation during 5728 person-years of follow-up. The overall incidence rate was 8.6/100 PYAR (95% CI 7.9–9.4 PYAR). The incidence

RG7204 rate fell from 8.2/100 PYAR (95% CI 7.0–9.5 PYAR) in 2005 to 6.5/100 PYAR (95% CI 5.3–8.1 PYAR) in 2007, and then rose in 2008 (9.5/100 PYAR (95% CI 7.6–11.9 PYAR)] and 2009 [15.6/100 PYAR (95% CI 12.4–19.7 PYAR)]; the log-rank test for equality of survivor functions was P = 0.003. The cumulative incidence of TB in the first year after ART initiation is depicted in Figure 3. The proportional hazards assumption of the multivariable Cox MK-2206 cost proportional hazards model was violated. We therefore stratified our analysis for the years 2005, 2006 and 2007 versus 2008 and 2009, based on the difference in TB incidence. The two models showed the same covariates to be significantly associated with the outcome with similar HR estimates, and visual inspection of the curves also showed a great similarity between the two periods. A multivariable

Cox proportional hazards model was therefore run on all data and showed lower baseline CD4 cell count and male sex at ART initiation to be significantly associated with TB incidence in the first year (Table 3). Patients initiating ART later were more likely to be diagnosed with TB in the first year of ART initiation

[HR per year of later ART initiation, 1.13 (95% CI 1.05–1.21); P = 0.001]. This is one of the first studies to relate decreasing mortality rates in ART initiators to changing patient characteristics and improved TB case finding Arachidonate 15-lipoxygenase after the rapid scale-up of ART in East Africa. In our large urban HIV-infected cohort, baseline CD4 cell counts increased significantly over time, which was associated with a decrease in mortality. A later year of ART initiation was independently associated with improved survival. Our findings show that major programmatic changes are possible in resource-limited settings and that these are associated with a measurable effect on all-cause mortality. There are some published data on changing CD4 cell counts over time since the roll-out of large-scale antiretroviral therapy in the developing world. The ART-LINC of IeDEA (ART in Lower Income Countries collaboration of the International Databases to Evaluate AIDS) cohort study, reporting on 17 ART programmes and 36 715 patients initiating ART in 12 countries in sub-Saharan Africa, South America and Asia, showed increasing median baseline CD4 counts between 2001 and 2006, with the lowest CD4 counts for the sub-Saharan African region (60 cells/μL in 2001 increasing to 122 cells/μL in 2006) [19]. In studies specifically looking at sub-Saharan Africa, most data originate from South Africa, where this trend has also been noted [20, 21].

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0 or above 60

When the refolding experiments were carri

0 or above 6.0.

When the refolding experiments were carried out under acidic conditions (pH range between 2.0 and 6.0), the recombinant Af-Tth showed 4THase activity. The maximum activity was obtained when the refolding was carried out at pH 4.0 (Table 1a). When nitric acid was used instead of sulfuric acid for pH adjustment and 0.4 M ammonium nitrate instead of 0.4 M ammonium sulfate was also used, the activity could be detected after refolding at pH 4.0. Therefore, it was the acidity and not the sulfate from acidification with sulfuric acid that conferred activity on 4THase. Because considerable refolding has been successfully performed in the presence of glycerol, the effects of glycerol find more concentrations were evaluated. Refolding to provide an active protein was performed in the presence of 0–50% glycerol, with the maximum 4THase activity observed with 30% (Table 1b). The effect of 14–60-h incubation periods was also evaluated, but longer dialysis and incubation periods did not have a significant effect on the refolding yield. The effects IDH inhibitor review of the initial protein concentration were also evaluated because

a high initial protein concentration has been reported to lead to aggregation and poor recovery of refolded protein (Singh & Panda, 2005). When inclusion bodies were solubilized in a 6 M guanidine hydrochloride solution containing 10 mM dithiothreitol at a concentration of 0.01 mg mL−1, 95% of the recombinant protein was recovered in the soluble fraction. However,

very low specific activity (2.8 U mg−1) was detected at that concentration. About 90% of the recombinant protein in the soluble fraction may not be successfully refolded Sorafenib price in spite of its being in soluble form. On the other hand, when inclusion bodies were solubilized in the buffer at concentrations of 0.05–0.5 mg mL−1, 25–45% of the recombinant protein was recovered in the soluble fraction. At a concentration of >1.0 mg mL−1, almost all proteins aggregated and the yield of the refolded protein was <10%. The highest yield of soluble 4THase, with a specific activity of 19.8 U mg−1, was obtained when the refolding was performed at the high initial protein concentration of 0.5 mg mL−1. The primary structure of Af-Tth showed a similarity to PQQ-dependent enzymes such as PQQ-dependent dehydrogenases. Recently, the 4THase (Ac-TetH) from Acidithiobacillus caldus, which is an acidophile and obtains energy for growth from the oxidation of reduced inorganic sulfur compounds, has been suggested to contain quinoid compounds as a cofactor (Rzhepishevska et al., 2007). Refolding experiments in the presence and absence of 70 μM PQQ revealed no significant effect on the activation of the enzyme activity. We further attempted to detect quinoid compounds in the refolded enzyme (the specific activity was 20 U mg−1) by NBT-glycinate staining.

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Countries rarely traveled in by the Bank staff, with person-days

Countries rarely traveled in by the Bank staff, with person-days lower than 147 (15 percentile) within 3 years, were

not included in the incidence calculation and were marked as “not enough travel data” to map. A follow-up survey was distributed to the 341 staff reporting at least one road crash over the past 3 years, asking for more detailed descriptions of crash circumstances. The questions addressed who was driving, use of seatbelts, speed of the car, other circumstances of the crash, response time of assistance, need for medical treatment, use of first aid kit, use of cardiopulmonary resuscitation (CPR), need for sick-leave, and nature of the injuries. A total of 3,760 people took the online survey (response rate = 25.6%). More than half of the respondents have at least four travel missions in a year and around 18% of the respondents Depsipeptide in vivo traveled at least or more than 10 times during a year. Table 1 shows the demographic and travel-related profiles of respondents. Of 3,109 survey respondents who reported that they made at least one mission in a typical year, we were able to match 3,004 with HR staff travel data. All analyses were conducted among the 3,004 matched travelers. A total of 4,100 near crashes were reported by WBG staff, which can be converted to 1 near crash per 15 missions.

There were 341 road crashes reported, or 1 in 175 missions. The most often stated contributing factors included driver’s decision errors, speeding, and road or weather conditions. MycoClean Mycoplasma Removal Kit Forty percent of crash victims reported that seatbelt was not in use at the time of crash. Seventy percent INCB018424 chemical structure of crashes took place in taxis. The distribution of high-risk countries, regardless of the indicator used to measure risk profile, reflected the pattern of typical travel destinations in the Bank, including mostly low- and middle-income countries. Responses to the question about perception of road safety were mapped to show overall picture of safety concerns of countries around

the world (indicator 3). The top 10 high-risk countries with respect to perception of risk were India, Kenya, South Africa, Egypt, Nigeria, Vietnam, Indonesia, Pakistan, Bangladesh, and Tanzania. The reported crashes and near crashes were highly associated. The correlation coefficient was 0.89, which is a strong positive association. Therefore we selected indicator 8 (incidence rate of total number of crashes and near crashes), as a main indicator of road safety risk by country. The list of high-risk countries for this indicator is presented in Table 2, the map in Figure 1. In response to the question “Do you have any suggestions to provide better road safety for Bank travelers?,” 1,068 suggestions and safety comments were collected and categorized in Table 3. Similar responses were compiled under the most common statement to avoid redundancies, and finally condensed to themes.

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In general, we considered a strong candidate to be associated wit

In general, we considered a strong candidate to be associated with GO terms such as cell proliferation, expressed in the adult mouse brain, and involved in known pathway(s) that regulated adult neurogenesis. Statistical analyses were performed with JMP v8.0 statistical software (SAS Institute, Cary, NC, USA). For

all analysis of BrdU+ cell counts and analysis on cell cycle, data were expressed as mean values ± SEM and were considered significant at P < 0.05. Two-tailed Student’s t-tests were used when comparing the two parental strains. The linear density of BrdU+ cells of different RI strains were compared by one-way analysis of variance (anova). Normality of data distribution was examined using Shapiro–Wilk’s W test. Both TSA HDAC ic50 age and sex were previously identified as regulatory factors influencing adult neurogenesis (Enwere et al., 2004; Tanapat et al., 1999), so we wanted to examine

whether the number of ICG-001 research buy proliferative cells traveling along the RMS was influenced by these two variables. An age effect on phenotype was examined by regression analysis and a gender effect was assessed by fitting one-way anova as a linear model. We also examined the effects of body weight using linear regression. As all three variables may serve as potential confounding covariates that influence our genetic linkage analysis, we adjusted the RMS linear density for age, body weight and sex. Residuals were obtained

from a multiple regression fitting new all three covariates for linear density (Rosen et al., 2009). The adjusted RMS linear density was then calculated from adding the residuals to the average RMS linear density by strain (Lu et al., 2008). Both the residuals and the adjusted linear density are normally distributed and are not significantly associated with any of the three regressors. The adjusted RMS linear density data are available at the GeneNetwork (Trait ID # 10167) and are positively correlated with the original trait data (r = 0.97; P < 0.0001). The adult RMS is composed largely of neuroblasts that give rise to different subtypes of interneurons in the OB (Lledo et al., 2008). In order to quantify strain differences in the actively dividing population of neuroblasts, we used BrdU, a thymidine analog which gets incorporated into DNA during the S-phase of the cell cycle and is commonly used in the detection of proliferating cells. After 1 h of BrdU exposure, the RMS of A/J mice had a significantly larger population of labeled S-phase (i.e. BrdU-immunoreactive) cells (81 ± 4.56 cells/mm, n = 6) than C57BL/6J mice (49 ± 4.85 cells/mm, n = 9) (P = 0.0006; Fig. 2). Differences in BrdU-labeled cells could be due to either A/J having more rapidly proliferating cells than C57BL/6J or because the proliferating cells in A/J have a relatively longer S-phase to overall cell cycle length compared with C57BL/6J.

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