As noted in the Selleck Vorinostat Introduction, the direct evidence available excludes neither possibility because it is clear that Ygf Z dimerizes readily, at least ex vivo (Teplyakov et al., 2004), and that at least some Ygf Z exists with a free thiol inside plant cells (Hägglund et al., 2008). It will not be possible to show definitively whether Ygf Z works as a disulphide-bonded dimer or as a thiol monomer (or both) until the action of Ygf Z can be reconstituted in vitro. However, the balance of present evidence favours the thiol monomer, as summarized

in the following. Firstly, there is reason to suspect that Ygf Z dimer formation is unphysiological. Thus, the three-dimensional structure of the dimer suggests that the intermolecular C228-C228′ disulphide bridge might not be functionally relevant because the dimer interface formed by multiple nonspecific van der Waals interactions is not extensive and contains none of the conserved dodecapeptide motif residues except C228 (Teplyakov et al., 2004). Moreover, in our pilot tests, recombinant Ygf Z isolated from E. coli was 65% monomeric even when no reductants were added (not shown). Secondly, E. coli Ygf Z has been shown to have a

redox-active cysteine, www.selleckchem.com/products/byl719.html i.e. a free thiol group, in vivo (Takanishi et al., 2007). Besides C228, Ygf Z has one other cysteine residue, C63, and it was not shown which is the redox-active one (Takanishi et al., 2007). However, the crystal structure places C63 at the C-terminal end of a β-strand in domain B, which makes the sulfhydryl solvent inaccessible, and C228 in an exposed surface loop between two α-helices (α9 and α10) of the Ygf Z monomer (Teplyakov et al., 2004), suggesting that the latter is the redox-active residue. Finally, Ygf Z belongs to the same protein family as sarcosine oxidase, dimethylglycine oxidase and the T-protein of the glycine-cleavage complex. All of these proteins

use tetrahydrofolate to accept a one-carbon (formaldehyde) unit (Teplyakov et al., 2004; Scrutton & Leys, 2005), and the one structurally closest to Ygf Z – the T-protein – acts on a thiol adduct of the one-carbon unit, borne by the H-protein of the complex (Douce et al., 2001). Formaldehyde is a ubiquitous metabolite that spontaneously forms harmful adducts with reactive protein side chains (Metz et al., Ceramide glucosyltransferase 2004), and it has been proposed that Ygf Z removes such inhibitory adducts from Fe/S enzymes by transferring the formaldehyde moiety to tetrahydrofolate (Waller et al., 2010). In such an enzyme repair mechanism, a cysteine thiol could logically play a go-between role, analogous to that of the active thiol in the glycine-cleavage complex, by binding formaldehyde after its removal from an Fe/S enzyme and before its transfer to tetrahydrofolate. A repair role for Ygf Z is not incompatible with the proposal that Ygf Z facilitates the breakdown of plumbagin (Lin et al.

The previous therapy regimens included ABV in 52, liposomal daunorubicin in 49, and liposomal doxorubicin in 40 patients. Moreover, only 77% were receiving concomitant HAART (all protease inhibitor based) and 33% started this treatment at the same time as the taxane chemotherapy. The paclitaxel protocol BIBW2992 supplier used was 100 mg/m2 fortnightly. The overall response rate was 56% with no significant difference in response rate when comparing patients on or not on HAART. Less surprising was the finding that patients on HAART had a significantly improved survival. The main side effect reported in these studies was neutropenia that generally

resolved prior to the next chemotherapy cycle [101]. A second study enrolled 17 patients with anthracycline refractory AIDS-KS, defined as KS that had progressed during or within 6 months of completing liposomal anthracycline chemotherapy. All patients were Ku 0059436 receiving a stable HAART regimen to avoid confounding of results. The treatment schedule was again 100 mg/m2 fortnightly. The objective response rate to paclitaxel was 71% (95% CI: 60–81), with 8 of 17 partial responses and 4 of 17 complete responses. There were no significant changes in CD4, CD8, CD16/56 (natural killer cells) and CD19

(B cells) lymphocyte subset cell counts during and for up to 1 year following chemotherapy. Similarly, plasma HIV-1 viral loads did not change significantly during or after treatment suggesting that the combined use of paclitaxel and HAART reduces the risk of chemotherapy-related immunological decline and opportunistic infections [102]. In contrast, previous trials without concomitant HAART were worrying in this respect; Gill [100] reported 51 AIDS-defining opportunistic infections in the 56 patients treated with paclitaxel (10.5/100 patient months on paclitaxel), only 36% of whom received HAART, and Welles [99] reported 27 opportunistic infections (8.4/100 person months on paclitaxel) among

her cohort of 28, none of whom received HAART. Thus the concomitant use of HAART Tyrosine-protein kinase BLK and paclitaxel appears to be safe and not detrimental to immune function despite initial concerns over pharmacological interactions [104–106]. These findings suggest that standard opportunistic infection prophylaxis guidelines may be followed when treating patients with taxane chemotherapy for KS. The higher rates of toxicity and the need for a 3-hour infusion make paclitaxel a less attractive first-line option than PLD [103]. The clinical experience in KS with docetaxel, another taxane, is much more limited though two small studies suggest that this agent can produce meaningful responses when used weekly [107], and in anthracycline pretreated individuals [108]. However, severe toxicities, including one death, have been reported in patients prescribed docetaxel with ritonavir-boosted protease inhibitors [109,110].

Furthermore, the quality and robustness of study designs were not assessed in this review as the main focus was to extract data regarding study methods and the inclusion or exclusion of performance feedback. Future studies, therefore, may wish to include assessment of study design quality. Eleven studies used the simulated-patient method in a purely covert manner, as a tool for assessing practice behaviour of pharmacists and their staff, although a further 10 did not provide immediate feedback, hence also using the study mainly for performance assessment. find more This finding is in accordance with a recent systematic review by Mesquita et al., whereby the results showed that

the focus of simulated-patient methods was primarily on assessment, rather than as an educational focus for enhancing practice skills of pharmacists and their staff.[19] This also highlights that although simulated patients have been used in pharmacy practice, little published

information and regard has focused on the role of performance feedback and training in pharmacy education, in shaping the behaviour of pharmacists and their staff.[19,45] The literature has revealed that this method may be a valuable tool to shape practice behaviour and, in the few studies that monitored acceptance of this as an educational tool, participants rated the experience positively. Therefore, because of its face validity, reliability and acceptance, it could be more widely used as a tool to assess current HSP inhibitor training needs in community pharmacy, identify potential barriers to change, and to compare different practice change strategies.[12,15,20] Of course to be used for educational purposes, i.e. to improve performance through immediate feedback, the simulated-patient visits need to be conducted with prior consent from participants to involve the Hawthorne effect, whereby performance improves with the

knowledge of impending assessment.[1,11] The Hawthorne effect is desirable, as it enables pharmacists and their staff to maintain a high level of performance, which then becomes routine practice. Therefore, simulated patients used in a consented, educational and Pregnenolone reflective framework, as part of continuing professional development, aims to improve future performance.[36] Written notes or checklists, documented as soon as possible after simulated-patient visits, were the most common method of data collection. This was also found by a systematic review by Watson et al.[23] In fact, the use of self-completed questionnaires are the most common method of data collection in pharmacy practice research in general.[28] However, problems can arise as a result of time separation between observation and data recording, with regards to the fallibility of recall and memory.

ostreatus. To develop a system for in vivo analysis of poxa1b promoter and its metal regulation, the gene-encoding GFP was adopted as reporter gene putting its expression under the control of 1400-bp-long poxa1b promoter region. GFP of the jellyfish Aequorea victorea emits fluorescence as a result of its intrinsic chromophore structure, not requiring any substrate or cofactor (Chalfie et al., 1994), and it represents a versatile reporter gene (Cubitt et al., 1995). The vector pEGFPea1b for in vivo analysis of P. ostreatus laccase promoters was constructed using the gene coding for

enhanced GFP (EGFP). A P. ostreatus poxa1b promoter region of 1336 bp was used as cis-regulatory element to drive expression of EGFP. An intron/exon fragment containing an intron/exon sequence of the poxc MG-132 clinical trial gene was included between the poxa1b promoter and the egfp gene, considering previous results showing that efficient GFP expression in Agaricus bisporus and Coprinus cinereus (Burns et al., 2005) and Phanerochaete chrysosporium (Ma et al., 2001) requires introns. A homologous selection marker, the mutant gene cassette CbxR, encoding a modified iron–sulfur protein Ip subunit of succinate dehydrogenase with an aminoacid substitution (His239 to Leu) and conferring

resistance to systemic fungicide carboxin (Honda et al., 2000), was adopted. Cotransformation with pTM1 vector conferring carboxin resistance and pEGFPea1b vector containing egfp gene under the control of poxa1b promoter region was carried out, by adopting check details an adapted version of transformation protocol reported by Salame et al. (2010). Moreover, an unique vector containing both the mutant gene cassette CbxR and the reporter cassette poxa1b promoter-egfp Celecoxib gene was constructed and adopted for transformation. Transformants were firstly screened for carboxin resistance. The carboxin-resistant colonies were subjected to at least four rounds

of selection by transferring on fresh selection medium. Around 50 carboxin-resistant transformants were obtained per μg of pTM1 DNA per 107 viable protoplasts in a transformation with pTM1 and pEGFPea1b, and five carboxin-resistant transformants were obtained per μg of pEGFPCBX DNA per 107 viable protoplasts in a transformation with this vector. Hence, cotransformation with vectors containing gene cassette CbxR and the reporter cassette poxa1b promoter-egfp gene allowed a 10-fold higher transformation efficiency than transformation with an unique vector containing both cassettes. This could be ascribed to the larger size of the latter construct. The carboxin-resistant transformants were further analyzed for checking the presence of egfp and fluorescence emission. Carboxin-resistant transformants were analyzed by PCR to verify the presence of the transforming DNA.

We therefore hypothesized that these molecules might play non-redundant roles. To test this hypothesis we generated mice lacking both genes (Trp53 −/−;p27 Kip1−/−) selleck inhibitor and analysed

the consequences on aSVZ cells and adult neuroblasts. Proliferation and self-renewal of cultured aSVZ cells were increased in the double mutants compared with control, but the mice did not develop spontaneous brain tumors. In contrast, the number of adult-born neuroblasts in the double mutants was similar to wild-type animals and suggested a complementation of the p27 Kip1−/− phenotype due to loss of Trp53. Cellular differences detected in the aSVZ correlated with cellular changes in the olfactory bulb and behavioral data on novel odor recognition. The exploration time for new odors was reduced in p27 Kip1−/− mice, increased in Trp53 −/−mice and normalized in the double Trp53−/−;p27 Kip1−/− mutants. At the molecular level, Trp53 −/−aSVZ cells were characterized by higher levels of NeuroD and Math3 and by the ability to generate neurons more readily. In contrast, p27 Kip1−/− cells generated fewer neurons, due to enhanced proteasomal degradation of pro-neural transcription factors. Together, these results see more suggest that p27 Kip1 and p53 function non-redundantly to modulate proliferation and self-renewal of aSVZ cells and

antagonistically in regulating adult neurogenesis. “
“Expression of connexin26 (Cx26), Cx30 and Cx43 in astrocytes and expression of Cx29, Cx32 and Cx47 in oligodendrocytes of adult rodent brain has been well documented, as has the interdependence of connexin expression patterns of macroglial cells in Cx32- and Cx47-knockout mice. To investigate this interdependence further, we

examined immunofluorescence labelling of glial connexins in transgenic Cx30 null mice. Ablation of astrocytic Cx30, confirmed by the absence of immunolabelling for this connexin in all brain regions, resulted in the loss of its coupling partner Cx32 on the oligodendrocyte side of astrocyte–oligodendrocyte (A/O) gap junctions, but had no effect G protein-coupled receptor kinase on the localization of astrocytic Cx43 and oligodendrocytic Cx47 at these junctions or on the distribution of Cx32 along myelinated fibres. Surprisingly, gene deletion of Cx30 led to the near total elimination of immunofluorescence labelling for Cx26 in all leptomeningeal tissues covering brain surfaces as well as in astrocytes of brain parenchyma. Moreover northern blot analysis revealed downregulation of Cx26 mRNA in Cx30-knockout brains. Our results support earlier observations on the interdependency of Cx30/Cx32 targeting to A/O gap junctions and further suggest that Cx26 mRNA expression is affected by Cx30 gene expression. In addition, Cx30 protein may be required for co-stabilization of gap junctions or for co-trafficking in cells. “
“The extracellular dopamine level is regulated not only by synaptic inputs to dopamine neurons but also by local mechanisms surrounding dopaminergic terminals.

We therefore hypothesized that these molecules might play non-redundant roles. To test this hypothesis we generated mice lacking both genes (Trp53 −/−;p27 Kip1−/−) learn more and analysed

the consequences on aSVZ cells and adult neuroblasts. Proliferation and self-renewal of cultured aSVZ cells were increased in the double mutants compared with control, but the mice did not develop spontaneous brain tumors. In contrast, the number of adult-born neuroblasts in the double mutants was similar to wild-type animals and suggested a complementation of the p27 Kip1−/− phenotype due to loss of Trp53. Cellular differences detected in the aSVZ correlated with cellular changes in the olfactory bulb and behavioral data on novel odor recognition. The exploration time for new odors was reduced in p27 Kip1−/− mice, increased in Trp53 −/−mice and normalized in the double Trp53−/−;p27 Kip1−/− mutants. At the molecular level, Trp53 −/−aSVZ cells were characterized by higher levels of NeuroD and Math3 and by the ability to generate neurons more readily. In contrast, p27 Kip1−/− cells generated fewer neurons, due to enhanced proteasomal degradation of pro-neural transcription factors. Together, these results MAPK Inhibitor Library suggest that p27 Kip1 and p53 function non-redundantly to modulate proliferation and self-renewal of aSVZ cells and

antagonistically in regulating adult neurogenesis. “
“Expression of connexin26 (Cx26), Cx30 and Cx43 in astrocytes and expression of Cx29, Cx32 and Cx47 in oligodendrocytes of adult rodent brain has been well documented, as has the interdependence of connexin expression patterns of macroglial cells in Cx32- and Cx47-knockout mice. To investigate this interdependence further, we

examined immunofluorescence labelling of glial connexins in transgenic Cx30 null mice. Ablation of astrocytic Cx30, confirmed by the absence of immunolabelling for this connexin in all brain regions, resulted in the loss of its coupling partner Cx32 on the oligodendrocyte side of astrocyte–oligodendrocyte (A/O) gap junctions, but had no effect Thalidomide on the localization of astrocytic Cx43 and oligodendrocytic Cx47 at these junctions or on the distribution of Cx32 along myelinated fibres. Surprisingly, gene deletion of Cx30 led to the near total elimination of immunofluorescence labelling for Cx26 in all leptomeningeal tissues covering brain surfaces as well as in astrocytes of brain parenchyma. Moreover northern blot analysis revealed downregulation of Cx26 mRNA in Cx30-knockout brains. Our results support earlier observations on the interdependency of Cx30/Cx32 targeting to A/O gap junctions and further suggest that Cx26 mRNA expression is affected by Cx30 gene expression. In addition, Cx30 protein may be required for co-stabilization of gap junctions or for co-trafficking in cells. “
“The extracellular dopamine level is regulated not only by synaptic inputs to dopamine neurons but also by local mechanisms surrounding dopaminergic terminals.

We therefore hypothesized that these molecules might play non-redundant roles. To test this hypothesis we generated mice lacking both genes (Trp53 −/−;p27 Kip1−/−) Selleckchem Obeticholic Acid and analysed

the consequences on aSVZ cells and adult neuroblasts. Proliferation and self-renewal of cultured aSVZ cells were increased in the double mutants compared with control, but the mice did not develop spontaneous brain tumors. In contrast, the number of adult-born neuroblasts in the double mutants was similar to wild-type animals and suggested a complementation of the p27 Kip1−/− phenotype due to loss of Trp53. Cellular differences detected in the aSVZ correlated with cellular changes in the olfactory bulb and behavioral data on novel odor recognition. The exploration time for new odors was reduced in p27 Kip1−/− mice, increased in Trp53 −/−mice and normalized in the double Trp53−/−;p27 Kip1−/− mutants. At the molecular level, Trp53 −/−aSVZ cells were characterized by higher levels of NeuroD and Math3 and by the ability to generate neurons more readily. In contrast, p27 Kip1−/− cells generated fewer neurons, due to enhanced proteasomal degradation of pro-neural transcription factors. Together, these results learn more suggest that p27 Kip1 and p53 function non-redundantly to modulate proliferation and self-renewal of aSVZ cells and

antagonistically in regulating adult neurogenesis. “
“Expression of connexin26 (Cx26), Cx30 and Cx43 in astrocytes and expression of Cx29, Cx32 and Cx47 in oligodendrocytes of adult rodent brain has been well documented, as has the interdependence of connexin expression patterns of macroglial cells in Cx32- and Cx47-knockout mice. To investigate this interdependence further, we

examined immunofluorescence labelling of glial connexins in transgenic Cx30 null mice. Ablation of astrocytic Cx30, confirmed by the absence of immunolabelling for this connexin in all brain regions, resulted in the loss of its coupling partner Cx32 on the oligodendrocyte side of astrocyte–oligodendrocyte (A/O) gap junctions, but had no effect Afatinib ic50 on the localization of astrocytic Cx43 and oligodendrocytic Cx47 at these junctions or on the distribution of Cx32 along myelinated fibres. Surprisingly, gene deletion of Cx30 led to the near total elimination of immunofluorescence labelling for Cx26 in all leptomeningeal tissues covering brain surfaces as well as in astrocytes of brain parenchyma. Moreover northern blot analysis revealed downregulation of Cx26 mRNA in Cx30-knockout brains. Our results support earlier observations on the interdependency of Cx30/Cx32 targeting to A/O gap junctions and further suggest that Cx26 mRNA expression is affected by Cx30 gene expression. In addition, Cx30 protein may be required for co-stabilization of gap junctions or for co-trafficking in cells. “
“The extracellular dopamine level is regulated not only by synaptic inputs to dopamine neurons but also by local mechanisms surrounding dopaminergic terminals.

Possible stimulation PLX3397 of an immune response by probiotic bacteria may explain potential therapeutic and prophylactic applications of such cultures in the treatment for infections and carcinogenesis. Because the improved intestinal microbial communities with probiotics primarily involve the stimulation of intestinal fermentation, the stimulation of short-chain fatty acid (SCFA) production is one of the essential

factors for the beneficial effects exerted by probiotics. A significant increase in indigenous lactobacilli in the large intestine as a result of probiotic Lactobacillus has been reported (Tsukahara & Ushida, 2001). Although increases in lactobacilli stimulate lactate click here production, lactate does not accumulate in the large intestine,

except in those patients with short bowel syndrome and dyspeptic diarrhea (Tsukahara & Ushida, 2001). Rather, lactate is normally metabolized to acetate, propionate, or butyrate by lactate-utilizing bacteria (Bourriaud et al., 2005; Belenguer et al., 2006). Lactate-utilizing bacteria from the human flora have been previously identified as belonging to the Clostridia cluster XIVa, based on their 16S rRNA gene sequences (Duncan et al., 2004). The increase in fecal SCFA by probiotic Lactobacillus would be due to this mechanism (Tsukahara et al., 2006). In fact, the oral administration of the lactate-utilizing and butyrate-producing bacterium, Megasphaera elsdenii, Cytidine deaminase with Lactobacillus plantarum has been shown to increase the butyrate production in the large intestine (Tsukuhara et al., 2002). Thus, the administration of probiotics with other lactate-utilizing bacteria, butyrate-producing bacteria, in particular, could be a more effective way to achieve maximum

health benefits. Coronary heart diseases and cardiovascular diseases (CVD), major causes of most death in adults, are conditions in which the main coronary arteries supplying the heart are no longer able to supply sufficient blood and oxygen to the heart muscle (myocardium). Although low-fat diets offer an effective means of reducing blood cholesterol concentrations, these appear to be less effective, largely due to poor compliance, attributed to low palatability and acceptability of these diets by the consumers. Therefore, attempts have been made to identify other dietary components that can reduce blood cholesterol levels. Individuals with CVD and those with a higher risk of developing the condition are treated in a number of ways to help lower their LDL cholesterol and triacylglycerol (TAG) concentrations while elevating their high-density lipoprotein cholesterol. The role of fermented milk products as hypocholesterolemic agents in human nutrition is still equivocal, as the studies performed have been of varying quality, and statistically analysis with incomplete documentation being the major limitation of most studies.

, 2001; Groom et al., 2001). While HMX has not been linked to phytotoxicity in plants such as lettuce and barley (Robidoux et al., 2003), HMX caused reproductive problems in earthworms (Robidoux et al., 2001) and decreased hatching success by 50% in lizard eggs that were incubated in an environment near maximum environmental Selleckchem AG14699 concentrations (McMurry et al., 2012). Inhaling contaminated dust particles and swallowing contaminated ground water are possible routes of exposure for military personnel and residents living near places that manufacture or use HMX. Information on the adverse health effects of HMX is limited,

but studies in rats, mice, and rabbits indicate that HMX is harmful to the liver and central nervous system if it is swallowed or has

contact with the skin (Sunahara et al., 2009; Agency for Toxic Substances and Disease Registry, 2010). Selleckchem ERK inhibitor HMX in soil and ground water is noticeably recalcitrant to degradation with half-lives of up to 2300 and 8000 days, respectively (Jenkins et al., 2003; Agency for Toxic Substances and Disease Registry, 2010). Because HMX remains in the soil and ground water for long periods of time, we can conclude that microorganisms in these environments cannot remediate the compound to any large extent under natural conditions. Some studies have shown biodegradation of HMX in sewage sludge (Hawari et al., 2000; Boopathy, 2001) and cold marine sediments (Zhao et al., 2004), which are typically oxygen-poor environments. Conclusions from studies with soil-dwelling bacteria and fungi under aerobic conditions indicate that, in many instances, selection and addition of an appropriate substrate to Molecular motor enhance the growth and biodegradation of contaminants in soil by indigenous microorganisms is a superior strategy to the introduction of nonindigenous microorganisms (Axtell et al., 2000; Monteil-Rivera

et al., 2003; Crocker et al., 2006). Phytoremediation of HMX has also been examined. Aquatic plants (Bhadra et al., 2001), and several indigenous and agricultural species demonstrated no transformation of the parent compound, but only translocation into the aerial tissues (Groom et al., 2001). We have been developing a technology called Phytoruminal bioremediation, in which cool-season grasses (accustomed to high levels of nitrogen) can be seeded over explosives-containing soil to accumulate energetic compounds into the shoots (Duringer et al., 2010) for grazing by sheep, where ruminal microorganisms then complete degradation of the explosives (Fleischmann et al., 2004; Smith et al., 2008; De Lorme & Craig, 2009; Eaton et al., 2011; Perumbakkam & Craig, 2012; Eaton et al., 2013). This technique combines aspects of both in situ and ex situ bioremediation technologies by leaving the contaminated soil in situ, but utilizing grasses and grazing sheep to remove the compounds to the ex situ rumen, which is a cheap and controlled anaerobic environment.

Mûr, Dr A. Payà, Dr M. A. López-Vilchez and Dr R. Carreras (Hospital del Mar, Universidad EPZ015666 manufacturer Autonoma, Barcelona, Spain); Dr N. H. Valerius and Dr V. Rosenfeldt (Hvidovre Hospital, Hvidovre, Denmark); Dr O. Coll, Dr A. Suy and Dr J. M. Perez (Hospital Clínic, Barcelona, Spain); Dr C. Fortuny and Dr J. Boguña (Hospital Sant Joan de Deu, Barcelona, Spain); Dr V. Savasi, Dr S. Fiore and Dr M. Crivelli (Ospedale L. Sacco, Milan, Italy); Dr A. Viganò, Dr V. Giacomet, Dr C. Cerini, Dr C. Raimondi and Professor G. Zuccotti (Department of Pediatrics, L. Sacco Hospital, University of Milan, Milan, Italy); Dr S. Alberico, Dr M. Tropea and Dr C. Businelli (IRCCS

Burlo Garofolo, Trieste, Italy); Dr G. P. Taylor and Dr E. G. H. Lyall (St Mary’s Hospital, London, UK); Ms Z. Penn (Chelsea and Westminster Hospital, London, UK); Drssa W. Buffolano and Dr R. Tiseo (Pediatric Dept, Federico II University,

Naples, Italy), Professor P. Martinelli, Drssa M. Sansone, Dr G. Maruotti and Dr A. http://www.selleckchem.com/products/GDC-0941.html Agangi (Obstetric Dept, Federico II University, Naples, Italy); Dr C. Tibaldi, Dr S. Marini, Dr G. Masuelli and Professor C. Benedetto (University di Torino, Torino, Italy); Dr T. Niemieç (National Research Institute of Mother & Child, Warsaw, Poland); Professor M. Marczynska, Dr S. Dobosz, Dr J. Popielska and Dr A. Oldakowska (Medical University of Warsaw, Infectious Diseases Hospital, Warsaw, Poland); Dr R. Malyuta, Dr I. Semenenko and Ms T. Pilipenko (ECS Ukraine co-ordinating centre). “
“The aim of the study was to describe the relationship between preterm delivery (PTD; < 37 weeks of gestation)

and antiretroviral Buspirone HCl therapy in a single-centre cohort of pregnant women with HIV infection. A retrospective analysis of data for 331 women who received care in a dedicated HIV antenatal clinic between 1996 and 2010 was carried out. Data on first CD4 cell count and viral load (HIV-1 RNA copies/mL) recorded in pregnancy, class and timing of antiretroviral therapy, gestational age at delivery, and risk factors for and causes of PTD were available from a clinical database. Overall, 13.0% of deliveries were preterm, of which 53% were severe preterm (< 34 weeks of gestation). The lowest rate of PTD was observed in women treated with zidovudine monotherapy (6.2%). Higher rates of PTD were observed in women starting combination antiretroviral therapy (cART) in pregnancy compared with women conceiving while on cART [odds ratio (OR) 2.52; 95% confidence interval (CI) 1.22–5.20; P = 0.011]. Of the women who were eligible for zidovudine monotherapy on the basis of CD4 counts and HIV viral load but who were treated with short-term cART to prevent HIV mother-to-child transmission, 28.6% delivered preterm. Women on short-term cART remained at the highest risk of PTD compared with zidovudine monotherapy in multivariate analysis (OR 5.00; 95% CI 1.49–16.79; P = 0.015). The causes of PTD are multiple and poorly understood.