Maceration during

alcoholic fermentation was achieved by punching down fermentation caps three times per day. The residual glucose–fructose concentration was monitored on a daily basis with a balling meter. When residual glucose–fructose levels were approximately 10 g L−1 (sixth day), the wines were hydraulically pressed (2 bar) from grape skins. The pressed wine (4.4 L) including lees was dispensed into 4.5-L glass jars equipped with fermentation airlocks and fermentation was allowed to proceed to dryness (residual sugar ≤1.95 g L−1). Racking entailed that wines from each fermentation were carefully siphoned-off (avoiding lees sediment carryover), sulphited to 40 g mL−1 (free sulphur) and bottled (5 × 750-mL dark green glass bottles). Putative wild-type and transgenic yeast populations from completed wine fermentations were established by plating out www.selleckchem.com/products/pci-32765.html 100 μL of a dilution series onto YEPD plates containing 25 mg L−1 kanamycin sulphate (Roche, Germany) and 30 mg L−1 chloramphenicol (Sigma-Aldrich, MO). After incubation at 30 °C for 2–3 days, colonies representing VX-809 clinical trial putative transgenic yeast strains were randomly selected from plates (25 colonies per replicate sample) and assessed

for their resistance to SM, flocculation ability (HSP30p-FLO5 transformants) or lack of invasiveness (HSP30p-FLO11 transformants). Genomic DNA isolated from 25 colonies per replicate sample, putative wild-type BM45 and VIN13 isolates were S. cerevisiae strain-typed using PCR with primers that are specific for δ sequences (Ness et al., 1993). Isolated genomic DNA from S. cerevisiae BM45, EC1118, NT50, VIN13 and WE372 industrial wine yeast wild-type strains served as controls. The lees component (5 mL aliquots) from individual MycoClean Mycoplasma Removal Kit batch fermentations was washed three times with an equal volume of sterile 0.9% saline and stored at −20 °C for flocculation and sedimentation analysis. The lees was recovered by centrifugation and resuspended in 50 mL 100 mM EDTA by vigorous vortexing. Thereafter, the faster

settling amorphous solid debris was allowed to sediment for 20–30 min and the fraction containing only suspended yeast cells was recovered from just below the meniscus. Microscopic evaluation of cellular fractions determined whether extractions were to be repeated. Filter-sterilized Merlot must [24.4% sugar (glucose and fructose), 6 g L−1 titratable acidity and pH 5.2] was sulphited to 40 mg L−1 was prepared as described above. Yeast precultures in YEPD were prepared and processed as described previously (Govender et al., 2008). The flocculation potentials of wild-type and transgenic yeast strains were assessed in small-scale aerobic shake-flask experiments at 27 °C using 100 mL aliquots of filter-sterilized Merlot must. Small-scale batch alcoholic fermentation of 100 mL aliquots of filter-sterilized Merlot must were performed by the inoculation of preacclimatized yeast cell populations at a density of 2 × 106 cells mL−1.

[41] This was compared to screening of walk-in participants. The remaining study involved only targeted screening of at-risk participants; patients with high risk of osteoporosis were identified from a health centre

and referred to the pharmacy by their physician.[63] Eleven studies[23, 32, 34, 38, 50-53, 60, 70, 71] involved the use of questionnaires or risk assessment forms alone to determine participants’ risk of the disease in focus. In a further 22 studies, the screening intervention primarily used medical equipment to make physiological measurements. For example, spirometry was used to screen for respiratory disease,[26] and bone mineral density (BMD) measurements for osteoporosis.[22, 31, 42, 45, 59, 61-65, 67] The remaining 17 studies used both medical equipment and questionnaires. this website In four of these, all participants were screened using both questionnaires and medical equipment[33, 39, 47, Ensartinib 49] while in 13, questionnaires were used to gauge participants’ risk of the target disease, followed by further tests using medical equipment for those participants considered to be at high risk.[24, 25, 27, 28, 35, 36, 40, 42, 58, 63, 64, 66, 68] Crockett et al. 2008[27] and Krass et al. 2007[68] compared groups of participants that were screened with questionnaires only, to those screened with both questionnaires and medical equipment. Thirty (60%) of the included studies involved a form of staff training and/or education about

screening tools and the target disease. This included training in the use of equipment, e.g. spirometry or BMD measurement, use of screening questionnaires, e.g. the Men’s Health Risk Assessment Tool (MHRAT) to assess men’s health,[53] or general training about the disease in question or patient counselling. Twenty-eight studies (56%) reported the provision of education and/or counselling to participants as part of the intervention.

This generally included a Palmatine written or verbal overview of the disease being screened for and information about disease risk factors, disease prevention and management. The duration of follow-up for the 21 studies reporting this ranged from 24–48 hours in a chronic obstructive pulmonary disease (COPD) screening study[25] to 12 months in another study about sleep disorders.[50] In nine of those, follow-up was an integral part of the intervention, e.g. to reiterate advice and reinforce education or confirm diagnosis. In the other 12 studies, follow-up was used to assess the effects of the intervention (i.e. to collect outcome data). This involved collecting data about those referred for further investigation, evaluating participants’ adherence to pharmacist interventions, or determining self-initiated or provider-initiated changes. A summary of the outcomes reported in each study is given in Table S2. Forty-seven studies (94%) reported the proportions of participants who screened positively either for disease risk factors or the disease itself.

Quantitative invasion assay values were calculated as follows: We used an in vitro assay according to Trombert et al. (2010), modified from the method described by McCormick et al. (1993). Briefly, the colon carcinoma HT-29 cell line was grown to confluence (18–21 days) on 3.0-μm Lapatinib molecular weight pore-size filters (or transwells, Millicell®, Millipore) with glucose-free RPMI (Gibco). Each transwell was inoculated individually to the

apical surface with 400 μL of approximately 1 × 107 CFU mL−1 of bacterial cultures and immediately incubated for 60 min at 37 °C. After extensive washing with sterile PBS, the extracellular bacteria were killed by treatment of monolayers with gentamicin (50 μg mL−1). Immediately after gentamicin treatment, the medium from basal compartment

of the epithelial cell monolayer was collected and plated for CFU to assess the number of bacteria that passed through the cell monolayer. The polarization of cells was confirmed by transepithelial electrical Antiinfection Compound Library purchase resistance and transmission electron microscopy (data not shown). All results are expressed as means±SD of an individual experiment performed in triplicate. P-values were calculated according to Student’s t-test, and P<0.05 or P<0.01 values were considered statistically significant. To assess whether the sopD2 locus is a pseudogene in the serovar Typhi, we compared the available sequences of S. Typhi CT18 and S. Typhi Ty2 (McClelland et al., 2001; Parkhill et al., 2001; Deng et al., 2003). We observed that the sequence of sopD2 in S. Typhi contains a frameshift at codon 48 resulting in

a premature stop codon that disrupts the expected ORF. Accordingly, the online databases report sopD2 as a pseudogene (Fig. 1). To confirm the presence of this frameshift in our S. Typhi clinical strain collection, PCR assays were carried out using SopD21 and SopD22 primer pairs. The primers yield an 1800-bp amplicon in both S. Typhi and S. Typhimurium and were used to test the clinical strains obtained from Chilean typhoid patients (STH collection, Hospital Dr Lucio Córdova, Chile). The PCR products were sequenced and in silico comparison was performed with the reference strains (S. Typhi CT18, S. Typhimurium LT2 and Salmonella enterica serovar Paratyphi A ATCC 9150) using Fossariinae the bioinformatic available program (clustalw; http://www.ebi.ac.uk/Tools/msa/clustalw2/). Our results indicated that the deletion described in S. Typhi CT18 is conserved among S. Typhi clinical strains (Fig. 2). Therefore, the sopD2 frameshift mutation seems to be a feature in the genome of serovar Typhi. Recently, we reported that S. Typhi harboring the sseJ gene from S. Typhimurium significantly disrupted HT-29 monolayer compared with the wild-type strain (Trombert et al., 2010). In the same way, we infected polarized HT-29 monolayers with the S. Typhi wild-type and S. Typhi sopD2STM strains.

Meanwhile, the luminance pathway responds to a sum of weighted L, M and, under certain conditions (Ripamonti et al., 2009), S differential cone excitations (L + M + S). In a classical differential fear conditioning design where the orientation of grating stimuli predicted the occurrence of an aversive loud noise, we used either isoluminant (chromatic) or grayscale (luminance) pattern reversal at stable temporal rates to give steady-state visual evoked potentials (ssVEPs) in the visual cortex. Only the luminance pathway, potentially via preferential access to deep brain structures involved in fear conditioning, was

expected to mediate robust CS+ specific sensory enhancement. Twenty-six (16 female) students from University of Florida undergraduate psychology courses participated for course credit. The mean age was 19.5 ± 1.1 years (SD). All participants reported BMS-354825 nmr normal or corrected-to-normal vision and a negative personal and family history of seizure disorder. All procedures were in accordance with the Declaration of Helsinki, Carfilzomib mw and the study was approved by the Institutional Review Board of the University of Florida. All participants provided written informed consent. A differential-delay classical conditioning design was used, in which the orientation of a phase-reversing

Gabor patch signaled the presence (CS+) or absence (CS–) of an unconditioned stimulus (US) in the form of a 92-dB sound pressure level white noise, presented through speaker boxes placed

next to the participant. During the acquisition Tolmetin phase, the US was presented during the final interval of CS+ presentation and set to co-terminate with CS+ during the conditioning trials using a 100% reinforcement ratio (see Fig. 1). Both CSs were sinusoidal gratings multiplied with a Gaussian envelope (Gabor patch) and were oriented either at 15 or 345 °C relative to the vertical meridian. The assignment of Gabor patch orientations to conditions (i.e., CS+ signaling threat and CS– signaling safe) was counterbalanced across participants. Stimuli were designed to preferentially engage either the luminance-based or the chromatic-based channels of the human visual system. The low-spatial-frequency luminance stimulus consisted of a pair of anti-phasic Gabor patches with seven cycles, covering 8 °C of visual angle (20.7 cm on the screen surface and viewed from 1.5 m distance). They were designed to have 6.8% Michelson contrast and a low spatial frequency of 0.875 cycles per degree (cpd). The lightest point of the Gabor patch was 47 cd/m2 and the darkest point was 41 cd/m2. The high-spatial-frequency chromatic stimuli were two isoluminant (see below) gray-and-green and red-and-green Gabor patches with 29 cycles, covering 8 °C of visual angle (3.625 cpd). Both stimuli were shown on a gray background with a luminance of 44 cd/m2.

JAJ is a Health Scholar with the AHFMR and holds a Canada Research Chair in Diabetes Health Outcomes. The funding sources had no role in the design and conduct of the study the collection, analysis, interpretation of the data or in the decision to submit the manuscript for publication. We

thank Neil Drummond for the insights provided on this topic in face-to-face and e-mail discussion. PMB and MJR conceived the idea for this article together. DLL provided methodological advice and, along with PMB and MJR, screened abstracts and published articles. PMB took the lead role in writing the manuscript, while MJR, DLL and AZD1208 research buy JAJ provided comments and suggestions on several previous drafts. All authors read and approved the final manuscript. “
“The aims of the study were to assess job satisfaction and organisational commitment among pharmacists working in the public sector and its influence on their likelihood to stay within the public workforce. A cross-sectional survey was conducted among all fully registered pharmacists (FRPs) in the northern states of

Malaysia in 2009 (n = 467). The questionnaire consisted of three sections to capture the demographic characteristics of the respondents, assess job satisfaction and organisational commitment of the respondents and their likelihood Erismodegib ic50 of staying in public service. A total of 247 FRPs (response rate 52.9%) in the northern region of Malaysia participated in this survey. Majority of the respondents were women (n = 205, 83.0%), of Chinese ethnicity (n = 155, 62.8%), graduates from public universities (n = 173, 70.0%), single (n = 172, 69.6%), with old a median age of 27 years (interquartile range (IQR) 2.0) and had worked with the Ministry of Health for a median of 2.75 years (IQR 1.63). The mean job

satisfaction and organisational commitment score were 58.09 (standard deviation (SD) 11.83) and 53.46 (SD 6.65) respectively out of a maximum possible score of 90. Majority of the respondents claimed that they were likely to stay in public service (n = 176, 71.3%). Their likelihood of staying in public service was affected by respondents’ gender, ethnicity, job satisfaction and organisational commitment. The findings from this study provide stakeholders with evidence on factors and issues affecting pharmacists’ job satisfaction and commitment in the public workforce as well as the likely turnover rate with an early cohort of pharmacists affected by the compulsory service. “
“Despite the introduction of new oral anticoagulants, vitamin K antagonists remain the mainstay of the prevention and treatment of thromboembolism.

We then tested whether the addition of the H2O2 scavenger, 10 mM pyruvate (Mongkolsuk et al., 1998), the lipid peroxide inhibitor, 1 mM α-tocopherol (Aoshima et al., 1999), or the hydroxyl radical scavenger, Romidepsin purchase 1 M glycerol (Vattanaviboon & Mongkolsuk, 1998), could diminish the Cu killing effect in the ahpC mutant. Pyruvate, α-tocopherol, or glycerol was supplemented in the cultures before

treatment with 1 mM CuSO4. Supplementation with pyruvate, α-tocopherol, or glycerol rescued the ahpC mutant from death by Cu treatments (Fig. 3). The presence of pyruvate increased the survival percentage of the ahpC mutant by more than 10-fold compared with Cu killing without pyruvate. Likewise, the prior addition of α-tocopherol and glycerol led to a five and sevenfold increase in the survival of the ahpC mutant, respectively, after the Cu treatment relative to the control experiments. The protective effect of the scavengers in the ahpC mutant was consistent with the idea that the mutant accumulates ROS. Additionally, the data indicate that a principal Cu toxicity mechanism towards Xcc

www.selleckchem.com/products/AZD6244.html involves oxidative stress. In addition, investigations in Cu efflux machinery mutants, in which the intracellular Cu level is elevated, also showed enhancement of bacterial sensitivity to ROS (Sitthisak et al., 2007; Nawapan et al., 2009). This evidence supports the link between Cu exposure and oxidative stress. In conclusion, the in vivo data presented here suggest that the toxic effect of Cu ions in the presence of organic hydroperoxides, either endogenously generated or from an exogenous source, which could arise from lipid peroxidation, while increased the production of hydroxyl radicals, is associated with Cu ion-enhanced H2O2 toxicity. The research was supported by grants from the National Centre for Genetic Engineering and Biotechnology (BTB-01-PG-14-5112), the Chulabhorn Research Institute, and Mahidol University. S.N. was supported by the Chulabhorn Graduate Institute. The authors thank Dr James M. Dubbs

for critically reading the manuscript. “
“In previous work, only one culture (strain TA12) from a pristine site was reported to utilize the xenobiotic compound p-toluenesulfonate (TSA) as a sole source of carbon and energy for aerobic growth. ‘Strain TA12’ has now been recognized L-NAME HCl as a community of three bacteria: Achromobacter xylosoxidans TA12-A, Ensifer adhaerens TA12-B and Pseudomonas nitroreducens TA12-C. Achromobacter xylosoxidans TA12-A and E. adhaerens TA12-B were identified as the TSA degraders. These two organisms contain several tsa genes from the Tntsa cluster described previously in Comamonas testosteroni T-2 and use the tsa pathway. Apparently, due to vitamin auxotrophy, the growth of the pure cultures with TSA was markedly slower than the growth of the community with TSA. The third bacterium (P.

All four proteins possess three methionines that may be responsible for copper/silver binding and export. Interestingly, the three essential methionines present in CusA

(Franke et al., 2003) are located in a periplasmic cleft shown to be important for substrate binding and function in AcrB (Takatsuka & Nikaido, 2007). clustalw alignments showed that GesB belongs to the class of RND proteins containing MexQ (Pseudomonas aeruginosa, 69% identity), MexF (P. aeruginosa, Daporinad cost 62% identity), BpeF (Burkholderia mallei, 59% identity), SdeB (Serratia marcescens, 55% identity), and LmxF (L. pneumophila, 41% identity). Both MexQ and MexF export macrolides, biocides, fluoroquinolones, tetracycline, and chloramphenicol (Mima et al., 2007). SdeB is known to pump fluoroquinolones (Begic & Worobec, 2008). Chloramphenicol and trimethoprim are substrates of BpeF (Kumar et al., 2006). Further analysis of GesB showed that it may possess methionine residues capable of coordinating with metals. Like MexB of P. aeruginosa (Guan et al., 1999), GesB (42% identity) has two periplasmic loops that interact with substrates. Within loop 2 of learn more GesB (residues 567–881) resides three Met residues, M636, M639, and M864, and a potential metal ligand H826. Both H826 and M864 are conserved in proteins with high sequence identity to GesB, MexQ, and MexF, while M636 and M639 are conserved

only in proteins with high sequence identity to GesB and MexQ. GesB, MexQ, and MexF have >62% sequence identity to each other, which is higher than the CusA homologues stated above. As gold lies within Teicoplanin the same transition metal group as copper and silver (Group IB), it is expected that efflux will occur through interaction with metal-coordinating residues such as methionine and histidine, although the exact pathway is yet to be determined. In Salmonella, gesABC is adjacent to an operon encoding a Cu(I)-translocating P-type ATPase and a CueR-like regulator. Similarly, a GesB homolog (RPD_2310) in Rhodopseudomonas palustris is encoded

adjacent to a GesA homolog (RPD_2311) and a CueR-regulated Cu(I)-translocating P-type ATPase and a putative Cu(I) chaperone (RPD_2307, RPD_2308, and RPD_2309). In contrast, GesB-like proteins are encoded adjacent to genes encoding putative Cd(II), Zn(II), and Pb(II)-translocating P-type ATPases in P. aeruginosa LESB58 (CadA is PLES_26261; GesB is PLES_26281), Diaphorobacter sp. TPSY (CadA is Dtpsy_1151; GesB is Dtpsy_1153), and Shewanella sp. W3-18-1 (CadA is Sputw3181_1126; GesB is Sputw3181_1130). These examples show that the GesABC system is possibly not the only RND-type complex related to the broader MexQ family involved in the efflux of metals. However, at this time, the substrate range of these related transporters is not known and awaits further studies. The extended substrate spectrum of two metal-exporting RND systems was determined.

aureus 8325-4 cells. To observe whether there was any impact of LytM deletion on S. aureus autolysis, the lytM mutation was transferred to the S. aureus strain 8325-4 and the lyt− transposon mutant of strain 8325-4. There was no appreciable difference in the autolysis of the lytM mutant cells of strain 8325-4 relative to wild-type 8325-4 (Fig. 4). Additionally, no autolysis was observed in the case of the lyt− and lyt−:lytM double mutant during the course of the experiment (5 h) when autolysis was Doxorubicin nmr measured periodically (Fig. 4). The turbidity of the lyt− and lyt−:lytM cell suspension remained unchanged even after 24 h (data not shown). In zymographic investigations, several lytic-activity bands were

seen in samples selleck kinase inhibitor from the wild-type S. aureus strain 8325-4 (Fig. 5, lane 1). The pattern of autolytic bands was almost identical in samples from the lytM mutant of S. aureus strain 8325-4 (Fig. 5, lane 3). In these experiments,

the S. aureus lyt−:lytM double mutant was expected to be autolysin free based on the previous report that suggested the LytM protein to be responsible for the residual autolytic activity in the lyt−S. aureus (Ramadurai & Jayaswal, 1997). Surprisingly, in the zymographic investigations, the pronounced 36 kDa lytic activity band in lyt−S. aureus (Fig. 5, lane 2), postulated to be due to LytM, was present in the lyt−:lytM double mutant (Fig. 5, lane 4). This observation suggests that LytM is not responsible for the residual activity of the lyt− strain of S. aureus. To address the presence of the 36 kDa lytic activity band in the lyt−:lytM double mutant, the lytM gene was cloned in vector pRSETA and overexpressed in

E. coli. The protein band that appeared to be induced after the addition of IPTG was a 36 kDa protein (Fig. 6a, arrow comparing lanes 2 and 3). The size expected for the Nintedanib (BIBF 1120) full-length His-tagged LytM was 40 kDa. The protein that was repeatedly purified following metal chromatography was also 40 kDa in size (Fig. 6a, lane 1). It has been reported that the LytM signal peptide undergoes cleavage even in E. coli cells (Ramadurai & Jayaswal, 1997; Odintsov et al., 2004). This leads to the loss of the signal peptide and the approximately 4 kDa His-tag present on the N-terminus of the recombinant His-tagged LytM. It is speculated that the majority of the overexpressed LytM undergoes cleavage of the signal peptide and only a small fraction of LytM remains intact with the His-tag, which could be purified. In zymographic experiments, Ramadurai & Jayaswal (1997) reported three autolysin bands of 36, 22 and 19 kDa in extracts of E. coli cells that overproduced LytM and proposed that the lower lytic-activity bands were LytM-degraded products. However, in our zymographic experiments, no autolytic band was visualized even after prolonged incubation of the zymographic gel in the lane corresponding to purified His-tagged LytM (Fig. 6b, lane 4).

Testing rates improved over the study period from less than one in every 300 patients to, on introduction of POCT, just under half of attendees having an HIV test. The prevalence of hitherto undiagnosed HIV infection in our clinic is almost 1% (with an additional 0.8% of patients declining POCT because of known HIV-positive status). This could be a model for other acute medical settings where HIV prevalence is similar. The high rates of uptake of testing, and the reasons given for declining a test, indicate that offering HIV POCT in such settings is acceptable to patients (and staff). We recognize that our mechanism for measuring acceptability was limited by being contemporaneous, but over this period

we received only one adverse AZD1208 purchase selleck kinase inhibitor comment in our anonymous feedback questionnaire from an already HIV-positive man concerned about counselling for new reactives; he was reassured once our process of referral was explained. In addition, other studies in similar settings show that offers of HIV tests are acceptable in community and hospital clinics [14]. Although the higher uptake with POCT than with laboratory testing did not translate into a statistically greater rate

of new diagnoses, our data support previous evidence that POCT, specifically, overcomes additional barriers to testing, by demonstrating a significant increase in acceptance rate compared with a laboratory-based protocol, presumably as a consequence of the perceived reduction in the delay

in receiving a result [8, 9]. Furthermore, rapid HIV POCTs offer an economical advantage in HIV screening programmes [17]. Targeted testing strategies based on dissemination of guidelines and protocols have limited benefit [3, 18]; universal testing strategies, which can be relatively easily provided by a range of healthcare staff, are more effective [19-22]. Reasons for this include the destigmatization of testing, as well as less reliance on busy clinicians (from a range of specialties) to prioritize HIV testing where clinical diagnosis and management are focussed on alternative, more pressing, matters. Tacrolimus (FK506) This is particularly important if the increased international focus on testing is to identify patients with less advanced (and therefore often asymptomatic) disease. Although the numbers were limited, we have demonstrated that POCT screening may identify patients with higher CD4 cell counts, without clinically significant HIV disease. One would certainly expect more patients diagnosed with preserved immune status using a universal testing strategy than a targeted testing strategy based partly on indicator diseases, which are associated with varying degrees of immunosuppression [9]. A universal offer of an HIV test in this setting gives patients who may not attend conventional settings for HIV testing the opportunity to be tested.

Testing rates improved over the study period from less than one in every 300 patients to, on introduction of POCT, just under half of attendees having an HIV test. The prevalence of hitherto undiagnosed HIV infection in our clinic is almost 1% (with an additional 0.8% of patients declining POCT because of known HIV-positive status). This could be a model for other acute medical settings where HIV prevalence is similar. The high rates of uptake of testing, and the reasons given for declining a test, indicate that offering HIV POCT in such settings is acceptable to patients (and staff). We recognize that our mechanism for measuring acceptability was limited by being contemporaneous, but over this period

we received only one adverse Talazoparib clinical trial Z-IETD-FMK order comment in our anonymous feedback questionnaire from an already HIV-positive man concerned about counselling for new reactives; he was reassured once our process of referral was explained. In addition, other studies in similar settings show that offers of HIV tests are acceptable in community and hospital clinics [14]. Although the higher uptake with POCT than with laboratory testing did not translate into a statistically greater rate

of new diagnoses, our data support previous evidence that POCT, specifically, overcomes additional barriers to testing, by demonstrating a significant increase in acceptance rate compared with a laboratory-based protocol, presumably as a consequence of the perceived reduction in the delay

in receiving a result [8, 9]. Furthermore, rapid HIV POCTs offer an economical advantage in HIV screening programmes [17]. Targeted testing strategies based on dissemination of guidelines and protocols have limited benefit [3, 18]; universal testing strategies, which can be relatively easily provided by a range of healthcare staff, are more effective [19-22]. Reasons for this include the destigmatization of testing, as well as less reliance on busy clinicians (from a range of specialties) to prioritize HIV testing where clinical diagnosis and management are focussed on alternative, more pressing, matters. Selleckchem Venetoclax This is particularly important if the increased international focus on testing is to identify patients with less advanced (and therefore often asymptomatic) disease. Although the numbers were limited, we have demonstrated that POCT screening may identify patients with higher CD4 cell counts, without clinically significant HIV disease. One would certainly expect more patients diagnosed with preserved immune status using a universal testing strategy than a targeted testing strategy based partly on indicator diseases, which are associated with varying degrees of immunosuppression [9]. A universal offer of an HIV test in this setting gives patients who may not attend conventional settings for HIV testing the opportunity to be tested.