5 μg mL−1 tetracycline; all clones turned out to be tetracycline sensitive. For further proof, 20 clones were subjected to

colony PCR with the primers repA1 and repA2 designed to amplify the pSC101 replicon region, and no PCR product was obtained (data not shown), thus indicating that pSC101-BAD-gbaA was not left in the engineered strain. The correct genotype of the engineered strain (shown in Fig. 1) was verified by three PCR reactions. Primers KI1 and KI2 were designed to flank the endpoints of the targeted region; primers KG, KB, KE and KA were specific INK 128 cost to aacC1, bet, exo and recA, respectively. Colony PCR with ExTaq (Takara, Japan) of four strains all showed the expected 1.0 kb profile. The amplicons were subsequently cloned into pGEM-T easy (Promega) and sequenced. Sequence analysis indicated proper insertion of the functional elements and no mutations were incorporated. One strain was finally named as LS-GR. LS-GR has been deposited into the China General Microbiological Culture Collection Center under the accession number of CGMCC 3192. The recombineering function of LS-GR was characterized by pACYC184 and pECBAC1 (Frijters et al., 1997) modifications. pACYC184 is a p15A replicon origin, medium copy number vector; the homology arms flanked the p15A replicon, and the antibiotic resistance marker amplified from

pACYC184 was successfully used to clone foreign DNA fragments (Zhang buy Ku-0059436 et al., 2000). pECBAC1 is one of the most commonly used single copy number BAC vectors. With a cloned size up to 300 kb, the BAC vector is now the first choice for eukaryotic genomic library preparation. BACs are also the main targets in λ Red recombineering research (Sarov et al., 2006; Tessarollo et al., 2009). Similar recombineering steps were performed for pACYC184 and pECBAC1 modifications as described in Materials and methods. Primer

pairs AEN1–AEN2 and CEN1–CEN2 were used to amplify the homologous arm flanked neo targeting the tetracycline resistance gene of pACYC184 and the chloramphenicol resistance gene of pECBAC1, respectively. The primers were designed to contain at their 5′ extremity 50 nt homology to the flanking regions of the target Doxacurium chloride gene and at their 3′ extremity 21 nt homology to the neo gene. After LS-GR-mediated recombineering, both the tetracycline resistance gene of pACYC184 and the chloramphenicol resistance gene were replaced by neo. The same pACYC184 and pECBAC1 modifications with pKD46 and pSC101-BAD-gbaA as recombineering sources were simultaneously carried out to evaluate the recombination efficiency of LS-GR. As shown in Table 2, for pACYC184 modification, LS-GR showed about twofold recombination efficiency as pKD46 and 1.5-fold recombination efficiency as pSC101-BAD-gbaA; for pECBAC1 modification, three systems showed similar results.

Methods  Four focus groups were conducted with 32 South Australian pharmacists: two groups included community pharmacists and pharmacy owners;

one included hospital pharmacists and another, consultant pharmacists. Key findings  Four themes emerged: (1) poor awareness of health care reform agenda; (2) strong adherence to the supply model; (3) lack of appreciation of alternative models; and (4) communication barriers. Conclusions  Participants’ low awareness of Australia’s health care reforms and their expressed beliefs and attitudes to their current role in the health system suggest that they are not well prepared for the potential future roles expected of health professionals in the health care reform agenda. “
“Objective  To make a case for why UK pharmacy find more must adapt to the increasing demands of professionalism in practice. Methods  A review based on evidence

from the literature and personal opinion. Key findings  Pharmacists, just as with other occupational groups, have over the years been developing and fine-tuning ways through which they can attain full professional status and therefore command the same level of recognition and respect as the main traditional professions, notably medicine and law. Many commentators, however, believe that this ambition is far from being realised. Their argument is that the path to professional status is not that easily available to all occupations. Although there is a professionalisation process that the traditional professions go learn more through, it has been argued that services provided by pharmacy, beyond dispensing, can also promote its level of professionalism; for example, extensive counseling, medication therapy management, health screening, compounding or provision of durable medical equipment. Conclusions  As UK pharmacy and the wider UK National Health Service undergo changes and reconfiguration it is hoped that the creation of the GSK-3 inhibitor new professional body for pharmacy (the Royal Pharmaceutical Society) will help pharmacy in the UK develop the ideals

of professionalism. The old regulator (the Royal Pharmaceutical Society of Great Britain) in July 2009 published two documents, the Code of conduct for pharmacy students and Fitness-to-practise procedures in schools of pharmacy,[1] to help instil professionalism among future pharmacists. The code of conduct sets out the expectations of students studying pharmacy in the UK and is based on seven principles, which are to make the care of patients your first concern, to exercise your professional judgement in the interests of patients and the public, to show respect for others, to encourage patients to participate in decisions about their care, to develop your professional knowledge and competence, to be honest and trustworthy and to take responsibility for your working practices.

e. peripheral

blood mononuclear cells, cerebrospinal fluid, lymph node tissue) [7,8]. As stated, one step toward improving our understanding of ARV pharmacokinetics is to measure FU in plasma as FU is free to traverse biological membranes, penetrate target tissue and exert pharmacological effect [9]. Other factors also contribute to how well a drug reaches its site of action, including the degree to which a drug is influenced by transport proteins (e.g. P-glycoprotein) present on cellular membranes [9]. Changes in PB will be most clinically relevant for highly bound drugs, since small changes in binding of highly bound drugs can have substantial effects on FU [10]. For highly bound ARV drugs such as the PIs, clinical situations likely to impact FU include pregnancy, infancy, renal or liver disease or concomitant therapies that displace drugs from PB sites [11–13]. This is one of the first studies addressing the effect 3-MA order of pregnancy on PB of any ARV drug despite long-term knowledge that pregnancy causes substantial reductions in plasma protein concentrations.

Albumin concentrations fall from 3.5 to a range of 2.5 to 3.0 mg/dL during the first half of pregnancy and steroid and placental SB431542 in vivo hormones displace drugs from binding sites leading to an overall decrease in the binding capacity of albumin and an increase in FU [14]. For example, the FU of phenytoin, a drug that binds to albumin, increases during pregnancy [14]. Data describing changes in AAG with pregnancy are less definitive. Two studies report an overall decrease in AAG concentration over the course of pregnancy while others report no change [11,12]. PB during pregnancy also may be affected by increased concentrations of endogenous ligands (i.e. free fatty acids), that may compete for drug binding sites of albumin and AAG. LPV has been reported to bind to both albumin and AAG, as does the PI nelfinavir [15,16]. AAG and albumin concentrations in our subjects were significantly altered during pregnancy compared to PP (P<0.0001). This is expected due to the change in weight and fluid volume consistent with pregnancy. The Resminostat weight gain in

our subjects of up to 10–15 kg during the course of pregnancy is also expected, although mean total weight for our subjects is higher than weights expected for pregnant women in some international settings where women on average are of smaller stature. Weight gain alone is not expected to impact FU. Albumin concentrations did not appear significantly to influence FU, but AAG concentrations had a significant effect, in that each 100 mg/L increase in AAG was associated with a decrease in LPV FU of 0.07 and 0.05% for third trimester and PP evaluations, respectively (P<0.0001 during both time periods, with adjustment for total LPV, at the PP evaluation). In contrast, LPV dose and time of PP evaluations did not have a significant effect on FU.

, 2010). For instance, while the deletion of Pil1 leads to

clustering of the remaining eisosome components, aberrant plasma membrane invaginations and the reduction of the endocytic rate in yeast (Walther et al., 2006), the deletion of Pil1 homologue in A. oryzea, and A. nidulans had no effect on endocytosis (Higuchi et al., 2009; Vangelatos et al., 2010). In view of the important role of Nce102 in eisosome assembly in yeast and the possible involvement in nonclassical export of selleck chemicals llc some virulence factors to the cell surface (Nombela et al., 2006), we carried out a gene knock out study to understand the role of Nce102 homologue in the growth and pathogenesis of A. fumigatus. We first identified the gene in fungal genome data base, cloned it, and generated a deletion mutant. The intracellular localization of AfuNce102 was also examined using EGFP-tagged AfuNce102. AfuNce102 deletion mutant showed a clear delay in conidiophore formation at 37 °C and severely affected sporulation at 25 °C. Asexual sporulation is a complex process that requires highly coordinated activity of upstream and central developmental pathways. For instance, FluG pathway contains several upstream developmental activators that can activate an overlapping regulatory pathway containing key

conidiation regulators like brlA and wetA (Etxebeste et al., 2010). In examination of brlA expression levels as the central regulator of conidiation, we did not detect any difference between the parental strain and the AfuNce102 deletion mutant indicating that AfuNce102

may not APO866 influence brlA expression in A. fumigatus. AfuNce102 does not seem to be related to an extracellular sporulation activating factor (s), which is thought to be a product of fluG gene (D’Souza et al., 2001). This was concluded as the conidiation defect of AfuNce102 deletant was not suppressed when the mutant was grown in the vicinity of the wild type. In addition to the main regulatory pathways, several reports have introduced other key players in sporulation process. For example, Soid-Raggi et al. (2006) have identified a transmembrane flavoprotein, Tmpa, which is necessary for conidiophore formation in A. nidulans, and Li et al. (2007) demonstrated the role of normal sphingolipid metabolism in asexual sporulation. Although the deletion of eisosomal Loperamide proteins, Pil A, PilB, or SurG, in A. nidulans has not changed the growth phenotype, sporulation, or spore survival (Vangelatos et al., 2010), the deletion of Nce102 homologue in A. fumigatus caused abnormal sporulation. The most severe defect in conidiation was observed at 25 °C. This may indicate an additional function for AfuNCE102 in fungal development. It has been proposed that Nce102 can modulate plasma membrane organization through sphingolipid signaling in yeast. The overexpression of Nce102 in yeast can block the inhibitory effect of a sphingolipid synthesis blocker, myriocin, on eisosomes (Frohlich et al., 2009).

A-factor switches on the transcription of adpA, which encodes the

transcriptional activator AdpA, by binding to ArpA, the A-factor receptor protein that binds the adpA promoter, and by releasing DNA-bound ArpA Antidiabetic Compound Library chemical structure (Ohnishi et al., 1999). AdpA activates a number of genes required for morphological development and secondary metabolite formation (the so-called AdpA regulon) (Ohnishi et al., 2005). Key differences exist in the signaling events that initiate morphogenesis in S. coelicolor A3(2) and S. griseus (Chater & Horinouchi, 2003). For example, ramS, which encodes the SapB (lantibiotic-like peptide surfactin) precursor (Kodani et al., 2004), is induced by the bld signaling cascade in S. coelicolor A3(2) (Nguyen et al., 2002), while amfS, which corresponds to ramS (Ueda et al., 2002), is regulated by AdpA (i.e. A-factor) via amfR in S. griseus (Yamazaki check details et al., 2003). In spite of these differences, probable orthologs of all S. coelicolor A3(2) bld genes except the bldK cluster have been identified in the S. griseus genome (Table 1). Because S. griseus contains at least six putative oligopeptide transporters, we previously assumed that the apparent lack of a BldK transporter might be compensated (Ohnishi et al., 2008). Recently, we compared the extracellular proteomes of the WT and ΔadpA strains of S. griseus to identify AdpA-dependent (i.e. A-factor-inducible)

secreted proteins (Akanuma et al., 2009). These included SGR2418, a putative oligopeptide ABC transporter

solute-binding protein in S. griseus. SGR2418 and other components of the ABC transporter are encoded by a putative operon (Fig. 1a). We noticed that this operon was located on the S. griseus chromosome at a position corresponding to the bldK locus in S. coelicolor A3(2), although the order of genes in this operon was different from that in the S. coelicolor A3(2) else bldK operon (Fig. 1a). This observation, combined with its apparent A-factor dependence, prompted us to analyze the function of SGR2418. Because an SGR2418-deficient mutant exhibited a bald phenotype (as described below), we denoted the SGR2414, SGR2415, SGR2416, SGR2417, and SGR2418 genes as bldKE, bldKD, bldKA, bldKC, and bldKB, respectively, after the bldK genes in S. coelicolor A3(2). In S. coelicolor A3(2), bldKA and bldKC encode permeases, and bldKD and bldKE ATPases. Together with the solute-binding protein BldKB, they comprise the BldK ABC transporter (Nodwell et al., 1996). Hereafter, to discriminate between corresponding genes (and their products) in S. griseus and S. coelicolor A3(2), we have suffixed their names with -g or -c. Streptomyces griseus IFO13350 (=NBRC102592) was obtained from the Institute of Fermentation [(IFO), Osaka, Japan]. The S. griseusΔadpA and ΔafsA mutants have been described previously (Ohnishi et al., 1999; Kato et al., 2007).

05% (w/v) Tween 80. The number of spores was counted under a light microscope at × 400 magnification. A working solution of 107 spores mL−1 was generated and stored at 4 °C. Spore concentrations between 102 and 107 mL−1 were obtained by 10-fold serial dilutions. DNA was extracted and used to generate a spore standard curve by qPCR. An internal control was included in the assay by adding 8 × 106 CFU of the yeast Y. lipolytica to 2 mL of washing solution selleck chemicals of grape as described before (Tessonniere et al., 2009). The yeast was added to the sample before DNA extraction to ensure that controls for DNA preparation

and PCR amplification were available. To prepare the cell standard curve, Yarowia lipolitica was grown on YPD (yeast extract 0.5% w/v, peptone 1% w/v, dextrose 2% wv) at 28 °C at 140 r.p.m. After 48 h of incubation, a working solution of 1010 CFU mL−1 was generated and cell suspension concentrations ranging from 101 to 108 mL−1 were obtained by 10-fold serial dilutions. DNA was extracted and used to generate a cell standard curve by qPCR. DNA extraction from B. cinerea spores, Y. lipolitica cells and washing suspension was performed using a fungal DNA kit (EZNA®, Omega-Biotek). In detail, 2 mL of spore or cell solutions or 2 mL of the washing solution were centrifuged at 10 000 g for 20 min. The pellet was incubated with 600 μL Buffer FG1 and 5 μL RNase (20 mg mL−1)

for 1 min. 2-mercaptoethanol (10 μL) was added and the mix was incubated at 65 °C for at least 5 min. Then 140 μL Buffer FG2 was added and the mix was incubated on ice for 5 min. After a centrifugation at 10 000 g for 10 min, the supernatant was Dabrafenib research buy transferred and 1/2 volume of Buffer FG3 and 1 volume of absolute ethanol were added. The following steps implies DNA cleanup through Terminal deoxynucleotidyl transferase Hi-bond®spin column. In the final step, DNA was eluted in 100 μL of deionized water.

Specific B. cinerea primers targeting the ribosomal region between 28S and 18S genes (intergenic spacer) reported by Suarez et al. (2005) were used: Bc3F (5′-GCTGTAATTTCAATGTGCAGAATCC-3′) and Bc3R (5′-GGAGCAACAATTAATCGCATTTC-3′). Yarrowia lipolytica-specific primers YALF (5′-ACGCATCTGATCCCTACCAAGG-3′) and YALR (5′-CATCCTGTCGCTCTTCCAGGTT-3′), were selected from the LIP4 gene (AJ549517) and were used to amplify a 106-bp fragment (Tessonniere et al., 2009). All primers were purchased from Invitrogen (Cergy, France). The DNA sample (5 μL) was mixed in a final volume of 25 μL with 10 ×B. cinerea or Y. lipolytica primer mixture containing 0.56 μM of either, 2 × IQ™SYBR Green supermix (Bio-Rad, Marnes-la-coquette, France) or water. Reactions were performed in a Biorad iQ5 real-time PCR iCycler apparatus. We used a program of: 3 min at 95 °C, followed by 40 cycles of 15 s at 95 °C and 30 s at 62 °C. A melting curve was established by decreasing the temperature from 90 °C by 0.5 °C every 10 s. All reactions were performed in triplicate.

4 μM h−1), suggesting that N22-7 cells grown in the presence of MnO2 were deficient in the MnO2 reduction. When either oxygen, fumarate, nitrate, or dimethyl sulfoxide was used as an electron acceptor, N22-7 grew as fast as WT (data not shown). Besides, in MFCs, N22-7 generated a same level of current as WT, indicating that N22-7 retains the EET ability as that in WT (Fig. 2). These results suggest that Tn insertion in N22-7 find more resulted in a defect in a function specifically necessary for MnO2 reduction. Inverse-PCR and sequence analyses revealed that mini-Tn10 was inserted into SO3030, which is located in a gene cluster encoding a putative hydroxamate-type siderophore

biosynthesis system (SO3030 to SO3034). A deduced amino acid sequence of SO3030 showed the closest homology to a dihydroxamate siderophore (putrebactin) biosynthesis protein PubA (83% identity) in Shewanella sp. MR-4 (Kadi et al., 2008). Siderophores are high-affinity iron-chelating compounds secreted by organisms and are known to play important roles in iron acquisition (Wandersman & Delepelaire, 2004). In S. oneidensis MR-1, it has been reported that http://www.selleckchem.com/products/PD-0332991.html siderophores

are not involved in Fe(III) solubilization during anaerobic Fe(III)-oxide respiration (Fennessey et al., 2010). However, roles of siderophores in anaerobic respiration of other metals, including MnO2, have not yet been investigated. To confirm that the disruption of SO3030 was responsible for the decreased MnO2-reduction rate of strain N22-7, an in-frame deletion mutant of SO3030 (ΔSO3030) and a plasmid-complemented strain ΔSO3030(pBBR-3030) were constructed, and their abilities to reduce MnO2 were compared with that of WT. We found that initial reduction rates of ΔSO3030 (123 ± 11 μM h−1) and ΔSO3030(pBBR-3030) (218 ± 3 μM h−1) were 53% and 95%, respectively, of that of WT, demonstrating Methocarbamol that the disruption of the SO3030 gene caused the decreased MnO2-reduction rate of strain N22-7. In contrast, an iron-oxide reduction by ΔSO3030 was as fast as that by WT (data not shown); a similar result has also been reported for an SO3031 knockout

mutant (Fennessey et al., 2010). To confirm that SO3030 is involved in the production of siderophore (putrebactin; Kadi et al., 2008), culture supernatants of WT and ΔSO3030 were subjected to the LC-MS analyses. It was found that a peak at m/z 373.1, which corresponds to the protonated ion of putrebactin (Kadi et al., 2008), was detected in WT (Fig. 3a), but not from the ΔSO3030 extract (Fig. 3b). It was also detected in a culture supernatant of ΔSO3030(pBBR-3030) (data not shown). These results suggest that MR-1 most likely produces putrebactin, a siderophore produced by Shewanella putrefaciens strain 200 (Ledyard & Butler, 1997) and Shewanella sp. MR-4 (Kadi et al., 2008), and SO3030 is essential for its biosynthesis. We next investigated whether or not the siderophore deficiency affected intracellular iron contents.

Conflicts

of interest: The authors declare that they do not have any conflicts of interest. Authors’ contributions: All authors participated in the critical discussion of the results, and read and approved the final draft of the manuscript before submission. J. B.-F. prepared the data set and carried out the majority of data analysis and the writing of the manuscript. C. K. was responsible for database management, quality control, cleaning of data and data analysis. A. K. was responsible for data acquisition, quality control and co-ordination of the study. D. M.-K. was responsible for study co-ordination and data analyses in the early years of the study after implementation and contributed to the analysis. B. G.-B. supported the management and co-ordination of the study and contributed to improving data quality and coverage. O. H. was responsible Screening Library supplier for study design and the implementation of the project and supported the overall approach of the analyses and the writing of the manuscript. “
“Many HIV-infected patients with chronic hepatitis C virus (HCV) infection do not receive treatment for HCV infection, often because of contraindications or poor adherence

to anti-HIV therapy. The aim of this study was to identify factors influencing guideline-based HCV treatment initiation in a large cohort of HIV/HCV-coinfected patients. Between Dabrafenib 2005 and 2011, 194 (40.5%) of 479 coinfected patients not previously treated for HCV infection started this treatment based on current recommendations, i.e. a Metavir score > F1 for liver fibrosis; HCV genotype 2 or 3 infection; or HCV genotype 1 or 4 infection and low HCV viral load (< 800 000 IU/mL), whatever the fibrosis score. Clinical and biological data were compared between patients who started HCV therapy during follow-up and those who did not. In multivariate

analyses, good adherence to treatment for HIV infection, as judged by the patient’s physician, was associated with HCV treatment initiation [odds ratio (OR) 2.37; 95% confidence interval (CI) 1.17–4.81; P = 0.017], whereas patients with children (OR 0.53; 95% CI 0.30–0.91; P = 0.022) and those with cardiovascular disease or respiratory distress (OR 0.10; 95% CI 0.01–0.78; P = 0.03) were Liothyronine Sodium less likely to be treated. Adherence to treatment for HIV infection, as judged by the patient’s physician, appears to have a major influence on the decision to begin treatment for HCV infection in coinfected patients. This calls for specific therapeutic education and adherence support in order to ensure timely anti-HCV therapy in this population. “
“HIV-associated neurocognitive disorder (HAND) is an independent predictor of early mortality and is associated with many difficulties in activities of daily living. We sought to determine the prevalence of and risk factors for HAND in HIV-infected Koreans.

Adult inpatients receiving intravenous vancomycin during the study period were identified by a list that was generated this website by the microbiology department daily. Paediatric patients, patients receiving haemodialysis and patients admitted to wards that do not follow monitoring guidelines were excluded from this evaluation as they are not obliged to follow current guidance. Patients’ medical charts were reviewed, and data related to vancomycin prescribing was collected using a pre-designed data collection

form that was designed based on the research questions and the aims of the study, and incorporated guidance from relevant literature and expert opinions. The key information collected was patient demographics, the nature of infection and vancomycin dosing and monitoring information. Descriptive statistics were used to summarise monitoring episodes and whether vancomycin Ion Channel Ligand Library price was prescribed and monitored in accordance with local guidance. This evaluation was conducted under the Trust’s research guidance and ethical approval was not required for auditing current existing services. Of the 104 patients who received intravenous vancomycin over the study period, 82 met the inclusion criteria. The mean age of included patients was 60.6±18.5 years,

and 54 (65.9%) were male. The source of infection was unknown in 31 (37.8%) patients and main infection sources included blood Interleukin-3 receptor (18.3%), skin (15.9%) and lung (14.6%). The monitoring timing, monitoring results, dose adjustment and post dose adjustment monitoring are listed in the following table. Patients with pre-dose monitoring (N = 76) Pre-dose monitoring episodes (N = 265) Episodes of maintenance does change (N = 69) Correct timing (n = 45; 59.2%) Not in target range (n = 164; 61.9%) Correct dose adjustment (n = 54; 78.3%) Reached target therapeutic range (n = 12; 15.8%) Change made to dose (n = 86; 32.5%) Correct dose adjustment and post hoc monitoring (n = 26; 37.7%) Patients whose pre-dose monitoring time is correct may not always lead to an optimal blood level. One quarter of monitoring episodes with a suboptimal

pre-dose level did not result in a dose adjustment. This would result in patients receiving sub-therapeutic vancomycin levels for longer periods of time, and may lead to decreased bactericidal activity and hence poorer outcomes for patients. This short-term study only included a small cohort and relied on the records on drug charts for retrieving information about time of dosing and vancomycin monitoring. Future studies need to explore the reasons for non-adherence to clinical guidelines and evaluate the associated clinical outcomes. 1. Schilling A, Neuner E, Rehm SJ. Vancomycin: A 50-something-year-old antibiotic we still don’t understand. Cleveland Clinic Journal of Medicine. 2011;78(7):465–471. R. Haider, J. Mutch, A. Homer, H.

Table 1 presents the Bcl2 inhibitor patient profiles of the cohort. The mean age of HIV-positive men at the time of sample production was 37.9 years (range 24–67 years). The majority of men were unable or unwilling to pinpoint the timing/mode of transmission (46.4%) but where they were, a sexual cause predominated in

37.3% of patients. 11.2% were infected haematologically, the majority of whom were haemophiliacs and the reminder of whom received transfusions for other reasons. 3.4% were infected via injecting drug use and infected needle use, 1.3% via needlestick injuries, and one patient suggested possible trauma and exposure at the time of an assault to have caused transmission. The mean time between HIV diagnosis and the production of a sample for insemination was

7.8 years, with times ranging from almost immediately following diagnosis to 25 years. 72.0% of the cycles were performed for men on HAART (mean duration of use 4.9 years; TSA HDAC mouse range 0.5–19 years). A mean CD4 count of 489 cells/μL (range 92–1207 cells/μL) was found at insemination and 63.3% of cycles were performed with undetectable VL (ranging from 57 to 180 000 copies/mL when detectable). Table 2 shows the overall seminal profiles of the raw samples (mean volume, concentration, total count, progressive motility and per cent abnormal forms of 2.3 mL, 51.3 million/mL, 128.2 million, 41.6 and 74.2%, respectively) and post-wash samples (mean volume, concentration, progressive motility and total motile count inseminated of 0.49 mL, 12.9 million/mL, 79.3%

and 5.7 million, respectively). Total motile count inseminated is the product of volume × concentration × proportion of sperm with progressive motility. Tables 3 and 4 show the associations between continuous markers of HIV disease (using Spearman’s rank correlation) and categorical markers, respectively, and semen parameters. Spearman’s rank tests demonstrated a significant positive correlation between CD4 cell count and sperm count from (r=0.13, P=0.02) and progressive motility (type ‘a’+‘b’, r=0.11, P=0.05) and a significant negative correlation between CD4 cell count and abnormal sperm morphology (r=−0.14, P=0.01). Analysis of post-preparation samples demonstrated a significant positive correlation of CD4 cell count with post-preparation concentration (r=0.16, P=0.005) and TMCI (r=0.15, P=0.009). These results are supported by a significantly reduced ejaculate volume (3.0 vs. 2.6 mL; P=0.03), total sperm count (173.8 vs. 138.1 million; P=0.004), post-preparation concentration (15.0 vs. 12.1 million; P=0.004) and post-preparation TMCI (7.0 vs. 5.9 million; P=0.007), a reduced progressive motility of borderline significance (46.8 vs. 44.0%; P=0.08) and a significantly increased percentage of abnormal sperm (77.2 vs. 75.0%; P=0.03) in samples from men with CD4 counts less than compared to those above the median (450 cells/μL).