The questionnaire requested sociodemographic details, practice-related characteristics, and proposed three clinical situations with multiple choice questions (MCQ). To identify factors associated with a higher level of specific knowledge in travel medicine, results were studied by uni- and multivariate analyses. An overall score was calculated based on the MCQ answers and a motivation score was calculated based on parameters such as frequency and developments in pre-travel consulting at BAY 73-4506 ic50 the practice,

PCPs’ personal experience as travelers, and the formal agreement of PCPs to administer yellow fever vaccination. The response rate was 37.5%, with 150 questionnaires returned completed and suitable for analysis. After multivariate logistic regression, the three variables associated with a higher score were: proximity of a vaccination center (p = 0.001), motivation

score (p = 0.004), and absence of request for expert advice on malaria prophylaxis (p = 0.007). PCPs play an important role in travel medicine. This study showed that their high level of knowledge in travel medicine was mostly linked to their motivation to practice in this specialized discipline. Global international travel has increased considerably over the last few decades. The number of international travelers is roughly estimated at 900

million per year and should reach 1.6 billion per year in 2020.[1] Each Crenolanib price year, 50 million people travel from industrialized countries to tropical areas. International travel from France mirrors this pattern, with around five million inhabitants visiting tropical areas each year.[1] Traveling abroad can lead to exposure to various diseases and following the expansion of international travel, primary care physicians (PCPs) are often consulted to provide medical pre-travel advice.[2] Travel 3-oxoacyl-(acyl-carrier-protein) reductase medicine is an emerging discipline born from the rising demand of the population but is not thoroughly studied by physicians. As the role of PCPs as first-line contacts for travelers seeking pre-travel advice has become increasingly significant, several worldwide surveys have investigated the quality of travel medicine practice among PCPs since 1987: four in the UK,[3-6] three in New Zealand,[7-9] two in Germany,[10, 11] one in America,[12] one in Qatar,[13] one in Australia,[14] and one in Switzerland.[11] In France, Bouldouyre et al.[15] recently published a survey focusing on the quality of pre-travel advice given by specialized physicians working in a travel medicine and vaccine center, but no study has yet focused on the quality of pre-travel advice given by French PCPs.

The method of Pena and colleagues was applied

with minor modifications for use on floating sections (modifications listed in supporting Appendix S1). Sections were rinsed in Tris-buffered saline (TBS) and incubated with proteinase K for 5 min at 37°C, washed twice in TBS, then post-fixed for 5 min in 4% PFA. After washing once in 0.2% glycine/TBS Fulvestrant manufacturer and twice in TBS, sections were incubated in freshly prepared 1-methylimidazole solution, and then immersed in EDC fixative for 60 min at room temperature. Sections were washed again, followed by acetylation with triethanolamine and acetic anhydride, to inactivate endogenous alkaline phosphates and peroxidases. After 10 min of prehybridization, sections were incubated overnight in 4 pmol of LNA probe diluted in 200 μL hybridization buffer. A hybridization temperature of 20°C below selleck the Tm of the experimentally determined miRNA–LNA probe duplex was used. The LNA probes were synthesized and melting temperatures were experimentally determined in the Tuschl laboratory (Pena et al., 2009). After post-hybridization washes, the sections were treated with 3% hydrogen peroxide and washed, before being blocked and incubated with anti-DIG-AP for 1 h at room temperature (Roche). LNA probes were visualized with either the NBT/BCIP chromogen system or the Cy3 fluorescent system. The NBT/BCIP chromogen

system produces a purple reaction product in the presence of alkaline phosphatase (Roche). The TSA Plus Cy3 System (PerkinElmer Life Sciences) were used for observing dendritic staining and gives an orange-red fluorescent staining. Slides for fluorescent

staining were mounted with Prolong® Gold antifade reagent with DAPI (Invitrogen). At the end of electrophysiological recording rats were decapitated, and the dentate gyrus was rapidly dissected on ice and homogenized. Samples were boiled in sample buffer (Bio-Rad) and resolved on 10% or 8% SDS–PAGE minigels. Proteins were transferred to polyvinylidene difluoride membranes (Amersham Biosciences), which were then blocked, probed with antibodies and developed using chemiluminescence reagents (ECL, Amersham Biosciences). The blots were scanned using Gel DOC EQ (Bio-Rad), Amobarbital and band intensities were quantified using analytical software (Quantity one 1D analysis software; Bio-Rad). Proteins were normalized to α-tubulin. Significant differences between the treated and non-treated dentate gyrus were determined using Student’s t-test for dependent samples. The P-value for significance was 0.05. Antibodies used for Western blotting were as follows: anti-anti-methyl CpG-binding protein (MeCP2; 1 : 1000; Millipore Temecula, CA, USA), p250 GTPase-activating protein (p250GAP; 1 : 1000; gift of Takanobu Nakazawa, U. Tokyo, Japan), anti-Arc (C7) (1 : 500; Santa Cruz Biotechnology) and anti-α-tubulin (1 : 1000; Sigma).

The purpose of this study was to establish whether individual differences in the amount of visual attention

to mouth articulations between 6 and 9 months of age are associated with neural signatures of AV speech processing (the ERP AVMMR). Given that previous eye-tracking http://www.selleckchem.com/products/AZD6244.html data has shown the presence of developmental change in visual attention to speaking mouth between 6 and 9 months of age (Lewkowicz & Hansen-Tift, 2012; Tomalski et al., 2012), we expected to see a related change in brain responses to AV speech within the same age range. In particular, we asked whether the increased looking time to the mouth between 6 and 9 months of age indicates either: (i) an increased interest in AV mismatch or (ii) an enhanced use of visual speech cues in an attempt to integrate the auditory and visual information. We measured ERPs in response to congruent and incongruent

AV speech cues, and subsequently recorded face-scanning patterns using eye tracking while infants watched the same stimuli. We found a strong association between neural responses (the AVMMR) and the length of looking to the mouth in the same condition (VbaAga-combination). The amplitude of AVMMR (290–390 ms from sound onset) in Linsitinib order the ERP task was strongly negatively correlated with looking times to the mouth during the presentation of the VbaAga-combination stimulus in the subsequent eye-tracking task. The AVMMR is thought to reflect quick automatic brain detection of mismatch between cues from two modalities, similarly to the pre-attentive auditory-only mismatch response (Kushnerenko et al., 2008). Previously it has been shown that the auditory mismatch response in infants undergoes a prolonged maturational process Enzalutamide molecular weight with a large positivity gradually decreasing in amplitude from the age of 3 months

until approximately the end of the first year of life (Kushnerenko et al., 2002b; Kushnerenko, E., Van den Bergh, B.R.H., & Winkler, I., (under review); Morr et al., 2002). Moreover, while no group differences were found in auditory ERPs between 6 and 9 months of age, large inter-individual variability was reported (e.g., Kushnerenko et al., 2002a,b), suggesting that this maturational change occurs at different rates in individual infants and is rather loosely related to chronological age (Kushnerenko et al., 2002b). We suggest that the same principle may be applicable to maturation of AV speech processing. Indeed, in the present study the AVMMR amplitude was associated with a specific looking preference rather than with chronological age. The AVMMR was only observed in the NMP subgroup which, according to the recent study of Lewkowicz & Hansen-Tift (2012), could be considered less mature in AV processing.

History of HIV infection and hepatitis A, B or C was obtained from the interview and confirmed serologically and using medical charts. Serological proof of coinfection with HCV and HIV was obtained using the Procleix HIV-1/HCV nucleic acid testing kit (Gen-Probe, San Diego, CA, USA) [23]. Plasma MDA was tested as the marker of oxidative stress using the TBAR kit (ZeptoMetrix, Buffalo, NY, USA). In this test, thiobarbituric acid was reacted with MDA, and the concentration of MDA in plasma determined by fluorimetry at an excitation wavelength of 530 nm and emission of 550 nm. Plasma glutathione peroxidase activity was determined using the Total Glutathione Peroxidase assay kit (ZeptoMetrix).

Plasma levels of zinc and selenium were determined by flame atomic absorption spectrophotometry. Plasma vitamin A and vitamin E levels were determined by selleck chemicals high-performance liquid chromatography (HPLC). Weight and height were obtained in participants wearing light clothing and no shoes utilizing a standard scale calibrated prior to each measurement. Height was measured with the participant’s heels touching the base of the vertical board of the stadiometer. The moveable headboard was brought to the most superior point on the head with sufficient pressure to compress the hair. Body mass index (BMI) was calculated using the standard formula that divides weight in kilograms by the square of height in

metres (kg/m2). To estimate liver disease stage, we calculated the aminotransferase to platelet ratio index (APRI) and fibrosis index (FIB-4) indexes, Volasertib chemical structure which include routine tests to predict liver fibrosis in patients with HIV/HCV coinfection [24]. The objectives were (1) to determine whether there was a significant difference in the proportion and degree of liver damage between the HIV/HCV-coinfected and HIV-monoinfected groups and (2) to determine whether there was a relationship between the stage of

liver disease and oxidative stress and plasma antioxidants, regardless of the aetiology of liver damage and HCV status. The APRI was calculated according to the formula: [AST (× upper limit of normal range) × 100]/platelet count (109 cells/L). The upper limit of normal for the present study was 0.45. The FIB-4 formula uses age and the relatively inexpensive test of transaminases (AST and ALT) and platelet counts Prostatic acid phosphatase (PLT): [age (years) × AST (U/L)]/[PLT (109 cells/L) × ALT1/2 (U/L)]. At a cut-off of <1.45, the negative predictive value to exclude advanced fibrosis (stages 4–6 of the Ishak scale) was 90% with a sensitivity of 70%. A cut-off of >3.25 had a positive predictive value of 65% and a specificity of 97% to predict advanced disease [24]. Animal and human studies have associated obesity, type 2 diabetes and hypertriglyceridaemia with increased oxidative stress and nonalcoholic liver disease [25,26]. For this reason, only the values for participants without diabetes, whose BMI was <28 kg/m2, and who had plasma triglycerides <150 mg/dL were used in the final analysis.

History of HIV infection and hepatitis A, B or C was obtained from the interview and confirmed serologically and using medical charts. Serological proof of coinfection with HCV and HIV was obtained using the Procleix HIV-1/HCV nucleic acid testing kit (Gen-Probe, San Diego, CA, USA) [23]. Plasma MDA was tested as the marker of oxidative stress using the TBAR kit (ZeptoMetrix, Buffalo, NY, USA). In this test, thiobarbituric acid was reacted with MDA, and the concentration of MDA in plasma determined by fluorimetry at an excitation wavelength of 530 nm and emission of 550 nm. Plasma glutathione peroxidase activity was determined using the Total Glutathione Peroxidase assay kit (ZeptoMetrix).

Plasma levels of zinc and selenium were determined by flame atomic absorption spectrophotometry. Plasma vitamin A and vitamin E levels were determined by Ixazomib order high-performance liquid chromatography (HPLC). Weight and height were obtained in participants wearing light clothing and no shoes utilizing a standard scale calibrated prior to each measurement. Height was measured with the participant’s heels touching the base of the vertical board of the stadiometer. The moveable headboard was brought to the most superior point on the head with sufficient pressure to compress the hair. Body mass index (BMI) was calculated using the standard formula that divides weight in kilograms by the square of height in

metres (kg/m2). To estimate liver disease stage, we calculated the aminotransferase to platelet ratio index (APRI) and fibrosis index (FIB-4) indexes, learn more which include routine tests to predict liver fibrosis in patients with HIV/HCV coinfection [24]. The objectives were (1) to determine whether there was a significant difference in the proportion and degree of liver damage between the HIV/HCV-coinfected and HIV-monoinfected groups and (2) to determine whether there was a relationship between the stage of

liver disease and oxidative stress and plasma antioxidants, regardless of the aetiology of liver damage and HCV status. The APRI was calculated according to the formula: [AST (× upper limit of normal range) × 100]/platelet count (109 cells/L). The upper limit of normal for the present study was 0.45. The FIB-4 formula uses age and the relatively inexpensive test of transaminases (AST and ALT) and platelet counts Bumetanide (PLT): [age (years) × AST (U/L)]/[PLT (109 cells/L) × ALT1/2 (U/L)]. At a cut-off of <1.45, the negative predictive value to exclude advanced fibrosis (stages 4–6 of the Ishak scale) was 90% with a sensitivity of 70%. A cut-off of >3.25 had a positive predictive value of 65% and a specificity of 97% to predict advanced disease [24]. Animal and human studies have associated obesity, type 2 diabetes and hypertriglyceridaemia with increased oxidative stress and nonalcoholic liver disease [25,26]. For this reason, only the values for participants without diabetes, whose BMI was <28 kg/m2, and who had plasma triglycerides <150 mg/dL were used in the final analysis.

The majority of women (63%) were diagnosed with HIV infection through routine antenatal screening. A history of sexual abuse was reported by 45% of patients (18 of 40). Housing and financial problems were reported by over half of the group [58% (36 of 62) and 62% (34 of 55), respectively].

Over half of the patients were unemployed. Of 23 students, six were of compulsory schooling age at conception. An STI screen in the 12-month period pre-conception was documented in 92% of women (33 of 36) and there were no data for 46% (31 of 67). A history of STIs was reported by 43% of women (20 of 46), with no documentation in 31% (21 of check details 67). Condoms were used by 35% of women (14 of 40) and 65% (26 of 40) reported no contraception use, while contraception use was not documented in 40% (27 of 67). Contraception advice in the 12 months preceding pregnancy was documented in 60% of women (15 of 25) diagnosed with HIV infection before pregnancy. Discussion of contraception Selleck Obeticholic Acid post-delivery was only documented in less than half (45%) of the notes reviewed. Conception within 6 months after delivery occurred

in 10% (seven of 67) and a further 15% (10 of 67) conceived within 12 months; 47% (eight of 17) of these pregnancies occurred despite documented contraception advice, 88% (15 of 17) were unplanned and 12% (two of 17) were terminated (data not shown). The majority of pregnancies (82%; 41 of 50) were unplanned. Only four patients were taking HAART at conception. Of the 94% (63 of 67) who started ART during pregnancy, prevention of vertical transmission was the sole indication in Olopatadine 81% (51 of 63). ZDV monotherapy was prescribed in 22% of patients. Forty-eight per cent were on a PI-based regimen and 30% on an NNRTI-based combination. ART-associated side effects were

reported by 31% of women (20 of 63), the most frequent being nausea and vomiting (14 of 20). Two patients developed a rash. Treatment was interrupted in 15% of women (three of 20) who reported side effects (data not shown). One hundred per cent adherence was self-reported by 59% of women (34 of 58). An HIV VL <50 copies/mL at or closest to delivery was documented in 62% of women (39 of 63). Pregnancy-related complications such as gestational diabetes (n=1), pre-eclamptic toxaemia (n=2) and antepartum haemorrhage (n=1) were seen in 13% of patients (individual data not shown). Mode of delivery was normal vaginal delivery in 29%, elective Caesarean section in 56% and emergency Caesarean section in 15%. Of the 67 deliveries, 14 (21%) were preterm (<37 weeks) with more than half (eight of 14) occurring at ≤34 weeks. More than half of patients (64%; 36 of 56) received intrapartum intravenous ZDV. There were 66 (99%) live births, of which 82% (50 of 61) received ZDV monotherapy as prophylaxis. The one HIV-infected infant had a positive HIV DNA PCR test within 48 h of delivery, indicating in utero transmission.

, 2002; Gonzalez Barrios et al., 2006). Escherichia coli O157:H7 harbors QS-regulated virulence genes on a pathogenicity island termed the locus of enterocyte effacement (LEE) (Surette & Bassler, 1998) that is organized mainly into the five polycistronic operons LEE1–LEE5 (Kaper et al., 2004). The first gene in LEE1, LEE-encoded regulator (ler), produces the principal transcriptional activator of the LEE genes (Elliott et al., 2000) and its expression was reported to be positively regulated by both AI-3 and norepinephrine (Sperandio et al., 2003; Jelcic et al., 2008). In patients with E. coli O157:H7 infection,

antibiotic use is generally limited because bacterial cells lysed by antibiotic treatment release MS275 an excessive quantity of Shiga toxin, thereby aggravating the patient’s state and resulting in HUS (Wong et al., 2000). To avoid this risk, an antimicrobial treatment that involves attenuation of bacterial virulence by inhibiting QS has been proposed (Ren et al., 2004). Halogenated furanone compounds as QS inhibitors were isolated from marine macroalga, Delisea pulchra (Givskov et al., 1996). Many of the synthesized furanone

derivatives have also been identified as QS inhibitors both in vitro (Martinelli et al., 2004) and in vivo (Wu et al., 2004). However, most of the characterized QS inhibitors have not yet been qualified as chemotherapeutic agents because they are composed see more of halogens that exert toxic effects in humans. Thus, more efforts should be made to develop safer QS inhibitors from natural products. As a soluble fiber, broccoli (Brassica oleracea) contains a large amount of vitamin C and multiple mafosfamide nutrients with potent anticancer properties (Vasanthi et al., 2009). However, the effect of broccoli against infection by pathogenic bacteria has never been reported. In this study, we demonstrate the inhibitory effects of broccoli extract (BE) on bacterial QS using E. coli O157:H7 as a model organism. The in vivo effects of the BE against E. coli O157:H7 infection were also elucidated in a Caenorhabditis elegans killing

assay. Finally, we tested three different flavonoid compounds (quercetin, kaempferol and myricetin) reported to be present in BE (He et al., 2008; Schmidt et al., 2010) in order to gain better insight into the active inhibitory compound in BE. An E. coli O157:H7 strain ATCC 43894 producing Shiga toxins I and II, an avirulent E. coli OP50 strain and Chromobacterium violaceum CV026 were grown in Luria–Bertani broth (LB, 10 g tryptone, 5 g NaCl, 5 g yeast extract L−1) at 37 °C. Vibrio harveyi BB170, an AI-2 reporter strain, was grown at 30 °C with agitation (175 r.p.m.) in the AB medium (Fong et al., 2001). The AB medium consisted of 10 mM potassium phosphate (pH 7.0), 0.3 M NaCl, 0.05 M MgSO4, 0.2% Casamino acids (Difco), 2% glycerol, 1 mM l-arginine, 1 μg mL−1 of thiamine, and 0.01 μg mL−1 of riboflavin. Quercetin, kaempferol and myricetin were purchased from Sigma-Aldridge (St.

These data pointed to the disparate metabolic networks operative in these systems and to the possible accumulation of KG and its utilization in combating oxidative stress. Roscovitine manufacturer It has been shown that KG is involved in the detoxification

of ROS with the concomitant formation of succinate. Ketoacids are known to eliminate ROS in a nonenzymatic manner (Brookes et al., 2006; Fedotcheva et al., 2006). Hence, it is not unlikely that P. fluorescens reprogrammed its metabolism in an effort to generate KG during the challenge posed by H2O2. This ketoacid has been shown to contribute to a decrease in oxidative tension (Li et al., 2009). The increased presence of succinate and KG in stressed cells would point to such a possibility. As KG was an important metabolite during oxidative stress, its utilization and production were monitored. ICDH, KGDH, and GDH are the three main participants in modulating the concentration of KG. In this study, there was a sharp increase in ICDH-NADP with a concomitant decrease in KGDH in the cells challenged by H2O2. As histidine was the only source of nitrogen and a possible precursor of KG, the presence of GDH-NAD and GDH-NADP was investigated. Although GDH-NADP was barely discernable in the control cells, there was a marked increase

in the H2O2-stressed cells. While LDK378 there was a mild increase in GDH-NAD, ICDH-NAD was sharply decreased in the H2O2-challenged cells. This is not surprising as NADH, a pro-oxidant, is known to further exacerbate the oxidative burden of the cell (Finkel & Holbrook, 2000; Thomas et al., 2009). Hence, the H2O2-stressed P. fluorescens may

have downregulated its formation. However, the upregulation of the NADPH production will be beneficial as this moiety plays a pivotal role in maintaining the reductive force of the microorganism during oxidative stress. Furthermore, the enhancement of these to enzymatic reactions (ICDH-NADP and GDH-NADP) will lead to the production of KG (Mailloux et al., 2009a, b). The decrease of KGDH has the net effect of increasing the pool of KG, a key contributor to the elimination of H2O2 (Brookes et al., 2006; Fedotcheva et al., 2006). Furthermore, the KGDH-mediated reaction has been shown to generate ROS (Starkov et al., 2004). To ascertain that the direct interaction between histidine and H2O2 does not lead to KG production, the growth medium with added H2O2 was monitored for 48 h without P. fluorescens. No KG was discerned (data not included). Hence, its downregulation will quell the oxidative burden of the microorganism, and limit the synthesis of NADH, a pro-oxidant. Thus, the enhanced activities of ICDH-NADP and GDH-NADP, coupled with the decreased activity of ICDH-NAD and KGDH, help generate KG and NADPH, two key ingredients necessary for survival during oxidative stress. As glutamate was an important supplier of KG, it was important to evaluate the status of other enzymes involved in the utilization or the formation of this substrate.

These new recombinant forms may reflect the diversification of the HIV-1 epidemic in this country, as a result of both migration from neighbouring countries and recombination events within the local population. This increasing diversity could lead to the emergence of new resistance pathways that could affect first-line

therapy in the future. Several studies have suggested that non-B isolates show a different pattern of resistance mutations from subtype B [10,11]. Reports have shown that the mutation V106M confers resistance to NNRTIs in subtype C HIV [12], and is preferentially selected in vivo [13], and that the D30N mutation is not preferentially selected in HIV-1 click here subtype C in the development of resistance to nelfinavir [14]. We have previously shown that subtype K reverse transcriptase may preferentially select for the thymidine analogue mutation 2 (TAM-2) pathways in the presence of NRTIs [15]. Differences in the way in which resistance evolves among subtypes may mean that some second-line regimens will be less effective than previously thought. Moreover, treatment of patients with primary resistance will be compromised from the DNA/RNA Synthesis inhibitor outset, potentially leading to onward transmission of drug-resistant HIV. Use of compromised treatment regimens may not result in the expected prevention benefits; that is, decreased HIV transmission. The

World Health Organization (WHO) currently recommends first-line therapy with two NRTIs and one NNRTI, a combination with high efficacy, tolerability and simplicity and low cost, and showing high adherence to treatment [16]. First-line regimens in Mali are based on this recommendation. Antiretroviral drugs have been made available in Mali

since 1997, and have been free since 2004. The recommended first-line regimen is a fixed-dose combination of stavudine/lamivudine/nevirapine, currently prescribed free of charge for the majority of patients. The alternative first-line regimens are zidovudine/lamivudine/efavirenz and zidovudine/lamivudine/nevirapine. The recommended second-line regimen is abacavir/didanosine/indinavir, and the alternative drugs are tenofovir Histone demethylase and lopinavir [7] or indinavir/ritonavir. An increase in the prevalence of primary resistance could jeopardize these second-line options. The availability of antiretrovirals has brought great hope to HIV-infected individuals in resource-limited countries. The emergence and transmission of resistant virus could compromise the effectiveness of specific treatments in areas where therapeutic options are limited [17]. There were limited data on primary antiretroviral drug resistance before 2000 in these countries [18]. Preliminary data suggest that resistance may be emerging in countries currently scaling up access to antiretroviral therapy [19]. Data from Africa support this suggestion.

18 Hentrich M, Berger M, Hoffmann C et al. HIV-associated Hodgkin’s lymphoma (HIV-HL): results of a prospective multicenter trial. J Clin Oncol 2010; 28(Suppl 15): Abstract 8035. 19 Jacobson CA, Abramson JS. HIV-associated Hodgkin’s lymphoma: prognosis and therapy in the era of cART. Adv Hematol 2012; 2012: 507257. 20 Lister TA, Crowther D, Sutcliffe SB et al. Report of a committee convened to discuss the evaluation and staging of patients with Hodgkin’s disease: Cotswolds meeting. J Clin Oncol 1989; 7: 1630–1636. 21 Hasenclever Selleck E7080 D, Diehl V. A prognostic score for advanced Hodgkin’s disease. International Prognostic Factors Project on Advanced Hodgkin’s Disease. N Engl J Med 1998; 339: 1506–1514. 22 Spina M, Re A, Vaccher E

et al. High international prognostic score predicts a worse outcome for patients with Hodgkin’s disease and HIV infection: results of a signaling pathway prospective study with Stanford V regimen. Ann Oncol 2003; 14: 655–656. 23 Hentrich M, Maretta L, Chow KU et al. Highly active antiretroviral therapy (HAART) improves survival in HIV-associated Hodgkin’s disease: results of a multicenter study. Ann Oncol 2006; 17: 914–919. 24 Ribera JM, Navarro JT, Oriol A et al. Prognostic impact

of highly active antiretroviral therapy in HIV-related Hodgkin’s disease. AIDS 2002; 16: 1973–1976. 25 Errante D, Gabarre J, Ridolfo AL et al. Hodgkin’s disease in 35 patients with HIV infection: an experience with epirubicin, bleomycin, vinblastine and prednisone chemotherapy in combination with antiretroviral therapy and primary use of G-CSF. Ann Oncol

1999; 10: 189–195. 26 Bohlius J, Schmidlin K, Costagliola D et al. Incidence and risk factors of HIV-related non-Hodgkin’s lymphoma in the era of combination antiretroviral therapy: a European multicohort study. Antivir Ther 2009; 14: 1065–1074. 27 Clifford GM, Rickenbach M, Lise M et al. Hodgkin lymphoma in the Swiss HIV Cohort Study. Blood 2009; 113: 5737–5742. 28 Dauby N, De Wit S, Delforge M et al. Characteristics of non-AIDS-defining malignancies in the HAART era: a clinico-epidemiological study. J Int AIDS Soc 2011; 14: 16. 29 Franzetti M, Adorni F, Vergani B et al. Incidence trends and outcome of non-aids-defining malignancies (NADM) in a cohort of HIV-infected patients during the period 1985–2008. Infection 2011; 39: S30. 30 Lanoy E, Rosenberg Obeticholic Acid ic50 PS, Fily F et al. HIV-associated Hodgkin lymphoma during the first months on combination antiretroviral therapy. Blood 2011; 118: 44–49. 31 Lanoy E, Rosenberg PS, Fily F et al. Risk of HIV-associated Hodgkin lymphoma during the first months after initiation of combination antiretroviral therapy. Infect Agents Cancer 2010; 5(Suppl 1): A71. 32 Mwakigonja AR, Kaaya EE, Mgaya EM. Malignant lymphomas (ML) and HIV infection in Tanzania. J Exp Clin Cancer Res 2008; 27: 9. 33 Eichenauer DA, Engert A, Dreyling M. Hodgkin’s lymphoma: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol 2011; 22(Suppl 6): vi55–58.