albicans strain (Asai et al., 1999). Several enzymes of the postsqualene ergosterol biosynthetic pathway require molecular oxygen, making ergosterol biosynthesis an oxygen-dependent process. When grown under aerobic conditions, S. cerevisiae is buy Erlotinib able to synthesize sterols, and is unable to acquire exogenous sterols, a phenomenon known as aerobic sterol exclusion (Andreasen & Stier, 1953). Under anaerobic conditions, the activity of the postsqualene sterol pathway is decreased, and as a consequence, sterol

scavenging becomes the major mechanism for obtaining sterols (Andreasen & Stier, 1953). While S. cerevisiae is only able to take up exogenous sterols during anaerobic growth, some filamentous fungi such as Aspergillus fumigatus are able to take up sterols under aerobic conditions (Xiong et al., 2005). The molecular mechanisms behind aerobic sterol exclusion have not been elucidated, but heme has been implicated in the process. Cells are able to sense oxygen availability through selleck chemical the levels

of heme, which is produced in an oxygen-dependent mechanism. Heme stimulates transcription through the Hap1 transcriptional activator, and both heme and Hap1 are involved in aerobic ergosterol biosynthesis. Hap1 is responsible for aerobic induction and anaerobic repression of ROX1 (Ushinsky & Keng, 1994), a well-known repressor of hypoxic genes, which is activated upon expression of Hap1 in a heme-dependent mechanism (Keng, 1992). Many genes involved in the later steps of ergosterol biosynthesis require molecular oxygen for catalysis, and as a result, these enzymes are downregulated as the supply of oxygen declines. Likewise, because heme production is dependent on the supply of oxygen, heme-mediated Rox1 repression of hypoxic genes declines as oxygen levels decrease, resulting in an increased expression of nearly all Buspirone HCl Rox1 repressed genes (Kwast et al., 1997). The upregulation of hypoxic genes and decreased activity of

ergosterol biosynthetic genes results in exogenous sterol uptake. Many genes involved in cholesterol biosynthesis have homologs in ergosterol biosynthesis, and while many of these have been identified within the P. carinii genome, P. carinii does not appear to encode all of the genes necessary to synthesize cholesterol through a de novo pathway (e.g. C-5 desaturase). Thus, it is unlikely that P. carinii is able to synthesize cholesterol, and most, if not all, of the cholesterol found within the membranes of P. carinii was scavenged from host cells by P. carinii. The ability of P. carinii to scavenge lipids was confirmed after incubation of P. carinii with the fluorescent fatty acid analog Bodipy-C12. Fluorescent microscopy and fluorimetry indicated that P. carinii readily scavenged Bodipy-C12 from the medium and incorporated the fatty acid uniformly in all morphological forms of P. carinii (Furlong et al., 1997). Uptake of Bodipy-C12 by P.

Furthermore, hyperinsulinaemia

(a characteristic of insulin resistance) is a major risk factor for coronary artery disease in non-HIV-infected individuals [34,35]. There are no generally accepted criteria for diagnosing insulin resistance in routine clinical practice. The so-called “gold-standard” of euglycaemic clamping is useful for intensive physiological studies of small numbers of subjects, but a simpler method such as use of the HOMA-IR index has proved to be robust and is more appropriate for epidemiological studies [36]. We found that HOMA-IR is a strong independent predictor of IGT or DM, which suggests that it may usefully indicate patients who should undergo an OGTT in order to investigate their glucose metabolism further. The association between low CD4 cell counts and IGT or DM is less clear and more difficult to explain. One hypothesis

is that patients with GDC-0449 ic50 low CD4 cell counts have higher concentrations of pro-inflammatory cytokines, which stimulate lipolysis and inhibit adipose tissue lipogenesis, thus exacerbating selleckchem increases in fatty acid concentrations (reviewed in Florescu and Kotler [37]). We were unable to verify this hypothesis because we did not assay cytokine levels in parallel with glycaemia but, as the independent association between CD4 cell counts and IGT or DM was not confirmed by our second multivariable model, further studies are necessary to determine whether this association is strong and consistent. Unlike others [6–8,21,38], we did not find that the classic risk factors for DM, including gender, age, lipid profile Vitamin B12 and family history, were associated with abnormal glucose tolerance. This may be explained by the fact that most of our patients had a normal BMI and waist circumference, a negative family history of DM, and a normal lipid profile, and were <50 years old, and/or by the fact that we used the combination of IGT and DM as the dependent variable rather than full-blown

DM alone. Patients coinfected with HCV are at higher risk of developing abnormal glucose metabolism, including DM [10,39–41], and Huang et al. found a higher prevalence of OGTT-detected pre-diabetes or DM in patients with chronic HCV infection and normal FPG levels than in uninfected controls [42]. We may therefore have overestimated the risk of IGT in our HIV-infected patients because of the high prevalence of HCV coinfection; we did not find a clear association between HBV coinfection and OGTT-detected IGT or DM, but this was probably because of the small number of patients with HBV infection, the small number of patients with IGT or DM, or both. Our study has one further limitation: as there is no accepted threshold for defining abnormal HOMA-IR values, we used the median value in our population and this may not apply to different settings; further studies are necessary to identify a shared and validated threshold of this insulin-resistance index.

Four weeks following 6-OHDA lesions, rats receiving dopamine grafts were anesthetized with a chloropent solution and secured in a stereotaxic apparatus.

Two injections of 1.5 μL of cell suspension were injected into the striatum at one site (A/P = 0 mm from bregma, M/L = 3.0 mm from bregma) this website at two depths (D/V 1 = 4.3 mm from skull, D/V 2 = 3.8 mm from skull; approximately 100 000 cells total per site) at a flow rate of 0.5 μL/min using a Hamilton 26-gage needle for a total of 200 000 cells implanted in each rat. Sham-grafted rats received equal volumes of the cell-free suspension media. For all grafts, the needle was left in place for 3 min following deposition of tissue or vehicle. To assess the effects of dendritic spine preservation in sham- and dopamine-grafted rats on dyskinesias, rats received injections of levodopa and the peripheral decarboxylase inhibitor benserazide (12.5 mg/kg levodopa; 12.5 mg/kg benserazide) in sterile injection saline 1 day a week every 2 weeks, beginning at 4 weeks post-grafting and continuing till the end of the study (20 weeks post-grafting). This subchronic paradigm of levodopa dosing was used to examine graft efficacy on levodopa-induced

dyskinesia expression while minimizing any effects of levodopa itself on MSN spines. While different from daily chronic levodopa paradigms often employed to induce selleck kinase inhibitor severe stable dyskinesias, in rats with severe dopamine depletion, such as those

used in this study, subchronic dosing results in levodopa-induced dyskinesia expression on first exposure (Lundblad et al., 2002). For selleck chemicals llc behavioral assessment of graft efficacy, levodopa-induced rotational analyses were performed once a week every 2 weeks from week 4 to week 20 post-grafting. Amphetamine was not used in these studies as it has been shown to induce alterations to MSN dendritic spines (Robinson & Kolb, 2004). Rats received intraperitoneal injections of levodopa (12.5 mg/kg levodopa; 12.5 mg/kg benserazide), and rotational behavior was quantified for 1 min precisely 30 min post-injection. A final rotational asymmetry score was calculated as (contralateral rotations/total rotations × 100). Data are expressed as mean ± SEM. For behavioral assessment of lesion success and graft efficacy, rats were evaluated for vibrissae-induced forelimb response by a researcher blinded to treatment group. Rats were held with their forepaw ipsilateral to the lesion and hindpaws restrained. Their whiskers contralateral to the lesion were then brushed lightly against a raised surface. The number of times the rat responded to whisker stimulation by placing their unrestrained forepaw (contralateral to the lesion and graft) to the flat surface was calculated as a measure of striatal function (Schallert, 2006). Data are expressed as the number of successful touches per 10 trials.

Four weeks following 6-OHDA lesions, rats receiving dopamine grafts were anesthetized with a chloropent solution and secured in a stereotaxic apparatus.

Two injections of 1.5 μL of cell suspension were injected into the striatum at one site (A/P = 0 mm from bregma, M/L = 3.0 mm from bregma) click here at two depths (D/V 1 = 4.3 mm from skull, D/V 2 = 3.8 mm from skull; approximately 100 000 cells total per site) at a flow rate of 0.5 μL/min using a Hamilton 26-gage needle for a total of 200 000 cells implanted in each rat. Sham-grafted rats received equal volumes of the cell-free suspension media. For all grafts, the needle was left in place for 3 min following deposition of tissue or vehicle. To assess the effects of dendritic spine preservation in sham- and dopamine-grafted rats on dyskinesias, rats received injections of levodopa and the peripheral decarboxylase inhibitor benserazide (12.5 mg/kg levodopa; 12.5 mg/kg benserazide) in sterile injection saline 1 day a week every 2 weeks, beginning at 4 weeks post-grafting and continuing till the end of the study (20 weeks post-grafting). This subchronic paradigm of levodopa dosing was used to examine graft efficacy on levodopa-induced

dyskinesia expression while minimizing any effects of levodopa itself on MSN spines. While different from daily chronic levodopa paradigms often employed to induce Pritelivir nmr severe stable dyskinesias, in rats with severe dopamine depletion, such as those

used in this study, subchronic dosing results in levodopa-induced dyskinesia expression on first exposure (Lundblad et al., 2002). For Mannose-binding protein-associated serine protease behavioral assessment of graft efficacy, levodopa-induced rotational analyses were performed once a week every 2 weeks from week 4 to week 20 post-grafting. Amphetamine was not used in these studies as it has been shown to induce alterations to MSN dendritic spines (Robinson & Kolb, 2004). Rats received intraperitoneal injections of levodopa (12.5 mg/kg levodopa; 12.5 mg/kg benserazide), and rotational behavior was quantified for 1 min precisely 30 min post-injection. A final rotational asymmetry score was calculated as (contralateral rotations/total rotations × 100). Data are expressed as mean ± SEM. For behavioral assessment of lesion success and graft efficacy, rats were evaluated for vibrissae-induced forelimb response by a researcher blinded to treatment group. Rats were held with their forepaw ipsilateral to the lesion and hindpaws restrained. Their whiskers contralateral to the lesion were then brushed lightly against a raised surface. The number of times the rat responded to whisker stimulation by placing their unrestrained forepaw (contralateral to the lesion and graft) to the flat surface was calculated as a measure of striatal function (Schallert, 2006). Data are expressed as the number of successful touches per 10 trials.

Four weeks following 6-OHDA lesions, rats receiving dopamine grafts were anesthetized with a chloropent solution and secured in a stereotaxic apparatus.

Two injections of 1.5 μL of cell suspension were injected into the striatum at one site (A/P = 0 mm from bregma, M/L = 3.0 mm from bregma) mTOR inhibitor at two depths (D/V 1 = 4.3 mm from skull, D/V 2 = 3.8 mm from skull; approximately 100 000 cells total per site) at a flow rate of 0.5 μL/min using a Hamilton 26-gage needle for a total of 200 000 cells implanted in each rat. Sham-grafted rats received equal volumes of the cell-free suspension media. For all grafts, the needle was left in place for 3 min following deposition of tissue or vehicle. To assess the effects of dendritic spine preservation in sham- and dopamine-grafted rats on dyskinesias, rats received injections of levodopa and the peripheral decarboxylase inhibitor benserazide (12.5 mg/kg levodopa; 12.5 mg/kg benserazide) in sterile injection saline 1 day a week every 2 weeks, beginning at 4 weeks post-grafting and continuing till the end of the study (20 weeks post-grafting). This subchronic paradigm of levodopa dosing was used to examine graft efficacy on levodopa-induced

dyskinesia expression while minimizing any effects of levodopa itself on MSN spines. While different from daily chronic levodopa paradigms often employed to induce selleck screening library severe stable dyskinesias, in rats with severe dopamine depletion, such as those

used in this study, subchronic dosing results in levodopa-induced dyskinesia expression on first exposure (Lundblad et al., 2002). For however behavioral assessment of graft efficacy, levodopa-induced rotational analyses were performed once a week every 2 weeks from week 4 to week 20 post-grafting. Amphetamine was not used in these studies as it has been shown to induce alterations to MSN dendritic spines (Robinson & Kolb, 2004). Rats received intraperitoneal injections of levodopa (12.5 mg/kg levodopa; 12.5 mg/kg benserazide), and rotational behavior was quantified for 1 min precisely 30 min post-injection. A final rotational asymmetry score was calculated as (contralateral rotations/total rotations × 100). Data are expressed as mean ± SEM. For behavioral assessment of lesion success and graft efficacy, rats were evaluated for vibrissae-induced forelimb response by a researcher blinded to treatment group. Rats were held with their forepaw ipsilateral to the lesion and hindpaws restrained. Their whiskers contralateral to the lesion were then brushed lightly against a raised surface. The number of times the rat responded to whisker stimulation by placing their unrestrained forepaw (contralateral to the lesion and graft) to the flat surface was calculated as a measure of striatal function (Schallert, 2006). Data are expressed as the number of successful touches per 10 trials.

, 2000; McGrath et al., 2007; Rasmussen et al., 2009; Toledo-Arana et al., 2009), and we now know that

the microbial transcriptome is much more complicated than previously thought, and includes long antisense RNAs and many more noncoding RNAs than identified previously (Rasmussen et al., 2009; Toledo-Arana et al., 2009). While microarrays have been instrumental in our understanding of transcription, we have started to reach limitations in their applicability Saracatinib (Bloom et al., 2009). Microarray technology (like other hybridization techniques) has a relatively limited dynamic range for the detection of transcript levels due to background, saturation and spot density and quality. Microarrays need to include sequences covering multiple strains, as mismatches can significantly affect hybridization efficiency and hence oligonucleotide probes designed for a single strain may not be optimal for other strains. This may lead to a high background due to nonspecific or cross-hybridization.

In addition, comparison of transcription levels between experiments is challenging and usually requires complex normalization methods (Hinton et al., 2004). Hybridization technologies such as microarrays measure a response in terms of a position on a spectrum, whereas cDNA sequencing scores in number of hits for each transcript, which Dipeptidyl peptidase is a census-based method. The census-based method

used in sequencing has major advantages in terms of quantitation and the dynamic range achievable, although it also raises complex statistical issues in MK-8669 cost data analysis (Jiang & Wong, 2009; Oshlack & Wakefield, 2009). Finally, microarray technology only measures the relative level of RNA, but does not allow distinction between de novo synthesized transcripts and modified transcripts, nor does it allow accurate determination of the promoter used in the case of de novo transcription. Many of these issues can be resolved by using high-throughput sequencing of cDNA libraries (Hoen et al., 2008), and jointly tiling microarrays and cDNA sequencing can be expected to lead to a rapid increase in data on full microbial transcriptomes, as outlined in this article. This review is not meant as an in-depth discussion of sequencing technologies, as there are several excellent recent reviews available (Hall, 2007; Shendure & Ji, 2008; MacLean et al., 2009). It is, however, important to discuss the consequences of the selection of a specific NextGen sequencing technology for the purpose of transcriptome determination. All three commercially available technologies (Roche 454, Illumina and ABI SOLiD) have their pros and cons, and in many cases, access or local facilities will influence the final choice of sequencing technology.

The biochemical aspects of ‘canal’ formation have been particularly well studied for S. occidentalis (Dmitriev et al., 1980), in which the appearance of canals was proposed to occur as the result of enzyme hydrolysis of basic polysaccharides at particular sites in the cell wall; these sites thereafter become hydrophobic and accumulate protein. The presence of reaction products produced by oxidative enzymes in the canals and by cytochrome P-450 at distinct sites in the cell walls indicates that the complexes of enzymes

participating in the primary oxidation of hydrocarbons most likely are localized in these structures (Van Beilen et al., 2006). In the other group of microorganisms studied here, namely the non-canal-forming yeasts and bacteria, oxidative enzymes revealed by cytochemical Ribociclib in vivo staining occurred primarily on the surface layer of the cell wall and within exocellular polymer structures, suggesting that the primary oxidation of oil hydrocarbons occurs in

both locations. It is highly improbable that the above-described exopolymers are emulsifiers (Van Hamme et al., 2003; Wentzel et al., 2007) that are released by microorganisms during growth on petroleum hydrocarbons. The exocellular polymer constructions, described in the present paper, are sufficiently strong; they remain strongly bound to the cells even during treatment with alcohol and acetone Proteasome assay that was used to prepare the samples for electron microscopic examinations. Probably, these exopolymers are similar to the earlier reported ‘flocs’ produced by Rhodococcus jostii RHA1 during growth on hydrocarbons (Perry et al., 2007). The flocs were shown to consist of a high-molecular-mass

polymer of a repeating tetrasaccharide unit composed of d-glucuronic acid, d-glucose, d-galactose, l-fucose and O-acetyl (1 : 1 : 1 : 1 : 1). In the present Non-specific serine/threonine protein kinase work, it was shown that the exocellular polymers yielded a positive cytochemical reaction for oxidative enzymes. It is known that depending on the physiological situation, exopolymers fulfill various functions in microbial associations. They can: (1) retain cells inside a local space, thus establishing a macrostability against outer physical factors, preventing wash-out; (2) maintain a macrostructure of the microbial community providing short diffusion distances for metabolite transfer; (3) bind nutrients; and (4) protect the association against adverse outer factors, for example such as toxic chemicals or predation by protozoa. The present study has added one more function: participation of exopolymers in the primary utilization of hydrophobic substrates by the formation of trophosomes.

A cross-sectional analysis was performed on 18 June 2011. Based on the last two values obtained in RT-PCR assays on that date, the patients were classified into three groups: strictly undetectable VL, i.e. the last two RT-PCR assays detecting no signal (group 1); detectable VL below the threshold, i.e. at least one RT-PCR assay detecting a signal < 20 copies/mL (group 2); and at least one RT-PCR assay measuring a VL of 20–50 copies/mL (group 3). Demographic data (age, sex and probable route of infection), therapeutic data (total duration

of cART, duration of current regimen, number of previous regimens, and duration of viral suppression < 50 copies/mL), and medical history (presence of an associated hepatitis infection, known duration of HIV infection, past AIDS-defining event, CD4 T-cell nadir, VL zenith (highest ever VL), and Panobinostat mouse last CD4 T-cell count) were collected and compared between groups. All categorical data are described by frequencies and compared using χ2 tests. Continuous data are described by means (standard deviation) and compared using analysis of variance (ANOVA). Two multivariate analyses were performed. One analysed the characteristics of patients with strictly undetectable viral load (group 1) compared with those of patients with detectable learn more VL below the threshold of 20 copies/mL (group 2). The second analysed the characteristics

of patients with a strictly undetectable viral load (group 1) compared with those of patients with a VL of 20–50 copies/mL (group 3). All characteristics

with a P-value < 0.20 were then included in two multivariate logistic regressions comparing group 2 with group 1 and group 3 with group 1. Tests < 0.05 were considered statistically significant. All analyses were performed using sas version 9 (SAS Institute, Cary, NC). Of note, VL values < 20 copies/mL with or without Non-specific serine/threonine protein kinase signal were reported to the clinic until the date of analysis as being below the threshold of 20 copies/mL, preventing any modification of the cART regimen. The study population included 1392 patients, with a mean age of 48 ± 10 years, of whom 69% were men. The mean time since HIV diagnosis was 14 ± 7 years and 20% had a past AIDS-defining event (stage C). The mean CD4 T-cell count nadir and VL zenith were, respectively, 225 ± 169 cells/μL and 4.6 ± 1.4 log10 copies/mL. The VL zenith was > 5 log10 copies/mL in 46% of the patients. The current mean CD4 T-cell count was 675 ± 333 cells/μL. The mean duration of viral suppression was 50 ± 36 months. The mean total duration of cART was 10 ± 5 years, with a mean number of previous anti-retroviral regimens of 5 ± 3. The current cART regimen was based on two nucleoside reverse transcriptase inhibitors (NRTIs) plus one bPI or one NNRTI or raltegravir in, respectively, 43, 45 and 12% of patients. The mean total duration of the current cART regimen was 35 ± 23 months.

At inclusion in the DHCS, baseline characteristics are recorded. Of special interest for the present study, HIV transmission group is recorded in the following categories: men who have sex with men (MSM), heterosexual (HSX), IDU and other/unknown. An individual is recorded as hepatitis C virus (HCV) positive if either an HCV antibody test or HCV RNA test is positive. Data are updated annually with information on antiretroviral treatment, development of opportunistic infections and other AIDS-defining

illnesses and laboratory values, including HIV RNA and CD4 cell count. Individuals living in Denmark aged 16 years or older with a diagnosis of HIV infection at the time of study entry (1 January 1995) or individuals who were diagnosed with HIV infection during the study period were eligible Cytoskeletal Signaling inhibitor as cases for the study, and we aimed to identify up to 19 HIV-uninfected population control individuals who were matched on sex and age to the corresponding case on the FK506 nmr day of the case’s HIV diagnosis. We identified an average of 18.9 population control individuals per HIV-infected individual. HIV-infected patients were identified from the DHCS. All other individuals were presumed to be

HIV-uninfected. Risk factor information was unavailable for control individuals. Medians and interquartile ranges were determined for age, time since first HIV infection diagnosis, time to SAB and CD4 cell count. For other variables, frequencies were computed. Intergroup baseline characteristics were compared using the χ2 test for dichotomous variables and the Kruskal–Wallis test for continuous variables. The person-years at risk were counted from 1 January 1995, the date of HIV diagnosis or the date of immigration (whichever came last) until emigration, death or 31 December 2007 (whichever came first). In the analysis of risk factors, individuals were censored after the first episode of SAB identified in the Danish Staphylococcal 3-oxoacyl-(acyl-carrier-protein) reductase Database. We computed IRs for three time periods, and stratified by HIV transmission group. To split person-years of observation (PYO) for calculation of IR, we used the Stratify macro created for sas [23].

Poisson regression analysis was used to estimate the overall incidence rate ratio (IRR) for SAB among HIV-infected individuals vs. HIV-uninfected individuals. Poisson regression analysis was also used in a substudy to identify risk factors for the first episode of SAB in HIV-infected individuals only and in HIV-infected individuals stratified by HIV transmission group. In the univariate model we included HIV infection (infected vs. uninfected), gender (male vs. female), age (<30, 30–39, 40–49, 50–59 and ≥60 years as a time-updated variable), calendar time period in intended clusters of 4 years (1995–1998, 1999–2002 and 2003–2007), race (Caucasian vs. non-Caucasian), HIV transmission group (MSM, HSX, IDU and other), latest CD4 count (<100, 100–349 and ≥350 cells/μL as a time-updated variable), ever initiated HAART (yes vs.

At inclusion in the DHCS, baseline characteristics are recorded. Of special interest for the present study, HIV transmission group is recorded in the following categories: men who have sex with men (MSM), heterosexual (HSX), IDU and other/unknown. An individual is recorded as hepatitis C virus (HCV) positive if either an HCV antibody test or HCV RNA test is positive. Data are updated annually with information on antiretroviral treatment, development of opportunistic infections and other AIDS-defining

illnesses and laboratory values, including HIV RNA and CD4 cell count. Individuals living in Denmark aged 16 years or older with a diagnosis of HIV infection at the time of study entry (1 January 1995) or individuals who were diagnosed with HIV infection during the study period were eligible LY2157299 supplier as cases for the study, and we aimed to identify up to 19 HIV-uninfected population control individuals who were matched on sex and age to the corresponding case on the www.selleckchem.com/pharmacological_MAPK.html day of the case’s HIV diagnosis. We identified an average of 18.9 population control individuals per HIV-infected individual. HIV-infected patients were identified from the DHCS. All other individuals were presumed to be

HIV-uninfected. Risk factor information was unavailable for control individuals. Medians and interquartile ranges were determined for age, time since first HIV infection diagnosis, time to SAB and CD4 cell count. For other variables, frequencies were computed. Intergroup baseline characteristics were compared using the χ2 test for dichotomous variables and the Kruskal–Wallis test for continuous variables. The person-years at risk were counted from 1 January 1995, the date of HIV diagnosis or the date of immigration (whichever came last) until emigration, death or 31 December 2007 (whichever came first). In the analysis of risk factors, individuals were censored after the first episode of SAB identified in the Danish Staphylococcal Nabilone Database. We computed IRs for three time periods, and stratified by HIV transmission group. To split person-years of observation (PYO) for calculation of IR, we used the Stratify macro created for sas [23].

Poisson regression analysis was used to estimate the overall incidence rate ratio (IRR) for SAB among HIV-infected individuals vs. HIV-uninfected individuals. Poisson regression analysis was also used in a substudy to identify risk factors for the first episode of SAB in HIV-infected individuals only and in HIV-infected individuals stratified by HIV transmission group. In the univariate model we included HIV infection (infected vs. uninfected), gender (male vs. female), age (<30, 30–39, 40–49, 50–59 and ≥60 years as a time-updated variable), calendar time period in intended clusters of 4 years (1995–1998, 1999–2002 and 2003–2007), race (Caucasian vs. non-Caucasian), HIV transmission group (MSM, HSX, IDU and other), latest CD4 count (<100, 100–349 and ≥350 cells/μL as a time-updated variable), ever initiated HAART (yes vs.