1 Now, with approval for pharmacists to prescribe controlled drugs GPCR Compound Library solubility dmso for substance misuse, pharmacist involvement in substance misuse services (SMS) can expand.2 A pilot service in which two community pharmacist supplementary prescribers worked with local SMS teams to provide client follow-up and prescriptions from the community pharmacy through a clinical management plan was conducted from April 2012 to March 2013. The objective of this research was to evaluate questionnaire feedback obtained from this pilot service

to determine client and SMS team satisfaction. Self-administered structured satisfaction surveys were conducted to gather feedback from clients and members of the local SMS INCB024360 datasheet teams at sites involved in the pilot service. Ordinal responses were quantified on a scale of 1 to 5, with one (1) correlating to strongly disagree and five (5) correlating to strongly agree. Means, standard deviations and frequency of response were calculated for each question; and the median and inter-quartile ranges (IQR) were determined from the mean individual survey scores. Other client variables collected included gender and duration of pilot participation. Ethics approval was not required because this was an evaluation of a service. Survey results were gathered from 20 clients of the pilot service, as well as 9 SMS team members. The client group was majority male (n = 18), and the majority of clients had seen a pharmacist

prescriber participating in the pilot service for 4 months or more (n = 16). Myosin The highest frequency of a strongly agree rating in the client group were given to happiness with the service (80%), and the median client satisfaction score was 4.76 (IQR of 4.43 to 5). Feedback was obtained from two SMS teams, including nurses, doctors and administrators. Sixty-seven percent (67%) of the time, SMS team members strongly agreed with the statement that pharmacist prescribers in substance misuse

were beneficial. The median scores of the two SMS teams were 5 (n = 5) and 2.38 (n = 4), and the overall median survey score across teams was 4.75 (IQR of 2.63 to 5). Community pharmacist prescribers specialising in SMS provide an alternative model of service for clients and SMS teams. The results of this research suggest that clients find it helpful to see a pharmacist prescriber for substance misuse prescriptions, and like having the service provided by the pharmacist in a familiar community pharmacy environment. The results also suggest that SMS teams find that pharmacist prescribers complement the multidisciplinary approach. The scores of the two SMS teams differed significantly, and this variance was likely due to communication issues and caseload expectations. Overall, moderate to high levels of satisfaction were reported among client and SMS team survey groups, but due to the small sample size, no firm conclusions could be drawn.

These two genomic regions are shown in Fig. 1 as white boxes. Both genomic fragments were successfully amplified from all 26 cultivars, and sequencing analysis confirmed that all 26 strains harbored dnaD, imp, and idpA. These two region sequences have been deposited in the GenBank database: AB636356-407.

Analysis of the deduced amino acid sequences using sosui ver 1.11 (Hirokawa et al., 1998) yielded the predictions that Imp contains a transmembrane region in its N-terminal region and a hydrophilic domain, and that IdpA contains both N- and C-terminal transmembrane regions, as well as a central hydrophilic domain (Fig. 1b). These features are identical to those of other previously analyzed Imp and IdpA proteins (Kakizawa INK 128 mw et al., 2006a, 2009). Analysis of the Imp and IdpA sequences using the SignalP program with the hidden Markov model yielded the relatively high-probability predictions (0.885 and 0.824, respectively)

that the two proteins have signal sequences. The signal sequence cleavage sites were predicted to lie between amino acid residues 48 and 49 for Imp, and between residues 35 and 36 for IdpA. Analysis of the Imp and IdpA sequences using the Psort program suggested with low probability (0.300) that Imp may be secreted from the bacterial cell and with high probability that IdpA is an integral membrane protein. BEZ235 clinical trial There were no silent substitutions in the PoiBI imp genes. Of the 26 PoiBI Imp amino acid sequences obtained from the 26 PoiBI-infected cultivars, those from ‘Annette Hegg Maxi’, ‘Annette Hegg Pink’, ‘Annette Hegg Supreme’, ‘Arctic’, ‘Jingle Bells’, ‘Premium Red’, and ‘Winter Rose White’ were 100% identical, and those from ‘Prestige Bright Red’, ‘Primero Jingle Bells’, and ‘Vision of Grandeur’ were identical. Therefore, in comparing the encoded Imp amino acid sequences, we used those from ‘Winter Rose White’ and ‘Primero Jingle Bells’, respectively, to represent these two groups

of identical sequences. The resulting multiple alignment of these sequences and that of WX Imp is shown in Fig. 2a. Although variations in the PoiBI Imp sequences were noted at several positions, the sequence identity was overall very high. The lowest sequence identity score (97.2%) was obtained for the comparison of ‘Enduring Pink’ vs. ‘Jester Jingle Bells’, ‘Jester Marble’, and ‘Peterstar Vitamin B12 Marble’. A phylogenetic tree of the PoiBI Imp amino acid sequences is shown in Fig. 2b. In contrast to the diversity of imp genes, there was no difference in the sequences of the 16S rRNA gene, idpA, or dnaD genes from the 26 poinsettia cultivars. The amino acid sequences deduced from PoiBI and WX imp, idpA, and dnaD are shown in Fig. S1. Among the PoiBI and WX Imp amino acid sequences, identity scores ranged from 92.6% to 93.8%, with a mean identity of 93.3%. The PoiBI and WX amino acid sequences of DnaD and IdpA had identity scores of 98.0% and 64.

8 μm, and no minicells were observed. These data indicate that overexpression of MinEEc is not able to elongate B. subtilis cells or to produce a minicell phenotype. Deletion of B. subtilis min genes causes minicell formation and slight cell elongation (Levin et al., 1992, 1998). The possibility that proteins of the E.

coli Min system can restore the defects caused by a lack of their homologues in B. subtilis was investigated. The experiments were carried out without xylose induction and using two different xylose concentrations (0.05% and 0.3% w/v). The control experiments selleck kinase inhibitor with the parental strains IB1141 (ΔminCBs) and IB1056 (ΔminDBs) were performed without and in the presence of 0.05% xylose. In comparison with the wild-type cells (MO1099), with average cell lengths 2.3 μm, the ΔminCBs (IB1141) cells were elongated, with average cell lengths 3.3 μm without xylose (Fig. 2a) and 3.1 μm with 0.05% xylose (not shown). The minicells represented approximately 10% of

the cell population. In the ΔminCBs strain producing MinCEc (IB1159) even without xylose addition, the cells became more elongated than the parental strain, with an average cell length of 4.4 μm (Fig. 2b). When xylose was added, the average cell lengths increased to 4.8 μm ABC294640 (Fig. 2c). In both these conditions more than 50% of the cells were longer than 4 μm (Table 2). The number of minicells was not changed significantly and represented 9–12% of the cell population. These data imply that the overexpression of MinCEc

can causes inhibition of the cell division in B. subtilis, although it does not complement the deficiency of MinCBs under these conditions. According to previously published data, the minDBs disruption causes a typical minicell phenotype, with DNA-less minicells and short filaments being formed (Levin et al., 1992; Edwards & Errington, 1997; Marston et al., 1998). It was determined Carnitine dehydrogenase here that the average cell length of the filaments was 3.9 μm and that more than 50% of the ΔminDBs cells (IB1056) were longer than 4 μm (Table 2; Fig. 2d). In comparison with ΔminCBs strain, the number of minicells was slightly higher (11–15%). Afterwards, we compared the lengths of the ΔminDBs (IB1056) cells with the lengths of GFP-MinDEc expressed in the ΔminDBs background (IB1104). If GFP-MinDEc was able to complement MinDBs, the cells would become shorter and formation of minicells would be confined. Indeed, without addition of xylose (Fig. 2e) and at a low concentration of xylose (0.05% w/v; Fig. 2f), GFP-MinDEc was able to improve the phenotype of ΔminDBs cells. The average cell length dropped to 3.4 μm and the percentage of cells longer than 4 μm decreased to 28% (without xylose) (Fig. 2e) and 31% (in the presence of 0.05% xylose) (Fig. 2f). However, the minicell formation was not prevented completely, although it decreased to 8–10%. The use of 0.3% xylose increased the average cell length to 4.

8 μm, and no minicells were observed. These data indicate that overexpression of MinEEc is not able to elongate B. subtilis cells or to produce a minicell phenotype. Deletion of B. subtilis min genes causes minicell formation and slight cell elongation (Levin et al., 1992, 1998). The possibility that proteins of the E.

coli Min system can restore the defects caused by a lack of their homologues in B. subtilis was investigated. The experiments were carried out without xylose induction and using two different xylose concentrations (0.05% and 0.3% w/v). The control experiments selleck with the parental strains IB1141 (ΔminCBs) and IB1056 (ΔminDBs) were performed without and in the presence of 0.05% xylose. In comparison with the wild-type cells (MO1099), with average cell lengths 2.3 μm, the ΔminCBs (IB1141) cells were elongated, with average cell lengths 3.3 μm without xylose (Fig. 2a) and 3.1 μm with 0.05% xylose (not shown). The minicells represented approximately 10% of

the cell population. In the ΔminCBs strain producing MinCEc (IB1159) even without xylose addition, the cells became more elongated than the parental strain, with an average cell length of 4.4 μm (Fig. 2b). When xylose was added, the average cell lengths increased to 4.8 μm FK228 chemical structure (Fig. 2c). In both these conditions more than 50% of the cells were longer than 4 μm (Table 2). The number of minicells was not changed significantly and represented 9–12% of the cell population. These data imply that the overexpression of MinCEc

can causes inhibition of the cell division in B. subtilis, although it does not complement the deficiency of MinCBs under these conditions. According to previously published data, the minDBs disruption causes a typical minicell phenotype, with DNA-less minicells and short filaments being formed (Levin et al., 1992; Edwards & Errington, 1997; Marston et al., 1998). It was determined check details here that the average cell length of the filaments was 3.9 μm and that more than 50% of the ΔminDBs cells (IB1056) were longer than 4 μm (Table 2; Fig. 2d). In comparison with ΔminCBs strain, the number of minicells was slightly higher (11–15%). Afterwards, we compared the lengths of the ΔminDBs (IB1056) cells with the lengths of GFP-MinDEc expressed in the ΔminDBs background (IB1104). If GFP-MinDEc was able to complement MinDBs, the cells would become shorter and formation of minicells would be confined. Indeed, without addition of xylose (Fig. 2e) and at a low concentration of xylose (0.05% w/v; Fig. 2f), GFP-MinDEc was able to improve the phenotype of ΔminDBs cells. The average cell length dropped to 3.4 μm and the percentage of cells longer than 4 μm decreased to 28% (without xylose) (Fig. 2e) and 31% (in the presence of 0.05% xylose) (Fig. 2f). However, the minicell formation was not prevented completely, although it decreased to 8–10%. The use of 0.3% xylose increased the average cell length to 4.

, 2008) (see below). Influencing mutant SOD1 synthesis in muscle cells did not affect motor neuron degeneration in the mutant SOD1 mouse (Miller et al., 2006; Towne et al., 2008). However, overexpression of insulin-like growth factor isoforms exclusively in muscle did slow down progression (Dobrowolny et al., 2005). Therefore, the exact role of muscle in ALS remains an interesting topic of research. The removal of mutant

SOD1, the primary buy Ibrutinib cause of motor neuron toxicity, is an obvious therapeutic strategy. This has been achieved by the viral delivery of RNAi against SOD1 (Ralph et al., 2005; Raoul et al., 2005), by intracerebroventricular administration of antisense oligonucleotides (Smith et al., 2006) and by crossbreeding mutant

SOD1 mice with mice that express an shRNA against mutant SOD1 (Xia et al., 2006). Hence, gene silencing holds great promise as a therapy for ALS (and in fact for many neurodegenerative diseases; Maxwell, 2009). The first clinical studies investigating the feasibility of these approaches in humans are under way. As toxicity from aberrant secretion of mutant SOD1 is likely to play a role, targeting this pool of mutant SOD1 may be of interest. The burden of extracellular SOD1 could be reduced using an active or a passive immunization strategy, and this led to a slower disease progression ABT888 in mutant SOD1 mice (Urushitani et al., 2007). The mutant SOD1 mouse (and rat) has been used extensively

to study compounds or approaches with possible therapeutic value (Turner & Talbot, 2008). The validity of this model has been questioned CYTH4 because some of the compounds with a positive effect in the mouse were negative in human studies. There may be other explanations. The effects observed in the mouse were often small, and may be easily missed in a clinically and genetically heterogenous human ALS population. Furthermore, the differences in pharmacokinetics between mice and humans were often largely neglected. In addition, the ‘positive’ results obtained in mice often came from (inadequately powered) studies in which administration of the compound began before disease onset, while in humans therapeutic trials are done in patients who have had ALS for at least one, sometimes even several, years. The question is whether the mutant SOD1 mouse is a good model in which to study sporadic ALS. Obviously it is not ideal: sporadic ALS is definitely etiologically different from monogenic mutant SOD1-related familial ALS. Recent studies on transactivation response DNA-binding protein with molecular weight 43 kDa (TDP-43) suggest that there may also be a pathogenic difference, which will be discussed below. The role of TDP-43 was first suspected when it was identified as one of the major constituents of the intraneuronal inclusions characteristically observed in ALS and in frontotemporal lobar degeneration (FTLD)–ubiquitin (FTLD-U; Neumann et al., 2006).

It is hoped that these mutations will not affect the probability of treatment success on second-line regimens as they are based on a PI coupled with two novel NRTIs to which the patient has not been previously exposed [1]. A number

of studies have provided data consistent with this expectation [8–10]. However, the development of thymidine analogue mutations (TAMs) or other major NRTI mutations has the potential to render these second-line regimens ineffective because of the widespread cross-resistance with other NRTIs [11]. Recent studies have suggested that failing NNRTI-based regimens have a greater susceptibility to the development of NRTI resistance mutations than do boosted PI-based regimens [12,13]. In industrialized countries, RGFP966 molecular weight the increased frequency of these mutations is likely to be of little clinical consequence as regimens can be tailored to the individual resistance mutation profiles. However, whether these mutations would reduce effectiveness of the commonly available second-line regimens in RLSs is unknown. The aim of this study was to examine how the development of

specific drug resistance mutations among individuals on highly active antiretroviral therapy (HAART) could affect the likelihood of treatment success on the second-line regimens that are available in RLSs. The rationale for performing this study in British Columbia (BC), as compared with resource-limited settings, is that PIs are not widely available outside of industrialized countries MK-1775 research buy L-gulonolactone oxidase and almost never used as first-line therapy [14,15]. This means that such a comparison would be difficult to conduct in these settings. Our primary explanatory variable was the third drug class (boosted PI or NNRTI) included in the participant’s initial ART regimen. The HAART Observational Medical Evaluation and Research (HOMER) study is a prospective observational cohort of all antiretroviral-naïve patients aged 18 years and

older initiating HAART in BC, Canada. It has been described in more detail elsewhere [16,17]. The BC Centre for Excellence in HIV/AIDS (BC CfE) through the Drug Treatment Program distributes antiretroviral drugs free of charge based on specific guidelines generated by the centre’s therapeutic guidelines committee [18]. The guidelines are largely compatible with those of the International AIDS Society–USA panel [19]. Physicians enrolling HIV-infected individuals complete drug request forms, which compile information on the applicant’s address, past HIV-specific drug history, CD4 cell counts, plasma HIV-1 RNA, drugs requested and enrolling physician data. At the time of the first drug refill, participants are asked to provide informed consent for accessing additional medical information, including electronic records. The consent is optional and participants’ refusal to sign it does not limit access to free ART.

, 2007). In recent years, interest in the exploitation of valuable EPS has been increasing for various applications in the food and pharmaceutical industries (Wingender et al., 1999; Kumar et al., 2007), and for heavy metal removal (Zamil et al., 2008) and wastewater treatment (Aguilera et al.,

2008), etc. EPS was also considered an abundant source of structurally diverse polysaccharides, some of which may possess unique properties for special applications. In a previous study, we reported that Pseudomonas fluorescens BM07 secreted Carfilzomib order large amounts of exobiopolymer when grown on fructose at 10 °C (Lee et al., 2004b; Zamil et al., 2008) and played an important role in the bioremediation selleck chemical of heavy metals, especially in the cold season (Zamil et al., 2008). The main components of the cold-induced exobiopolymer in BM07 are water-insoluble hydrophobic polypeptide(s)

(up to 85%) and saccharides (8%). Carbohydrate analyses revealed glucose, glucosamine and galactosamine as major components of the sugar units in the exobiopolymer (Zamil et al., 2008). The isolated exobiopolymer exhibited an endothermic transition with an enthalpy of 84 J g−1 at 192 °C as well as a sharp X-ray diffraction pattern, suggesting a probable uniquely structured organization around cells (Zamil et al., 2008). In this study we report on the generation and characterization of P. fluorescens BM07 transposon mutants which were disrupted in exobiopolymer formation but increased its polyhydroxyalkanoates accumulation compared with the wild type. The bacterial strains, plasmids and oligonucleotides used in this study are listed in Table 1. Escherichia coli strains and all its recombinants harboring different plasmids were cultivated at 37 °C in Luria–Bertani (LB) medium. Pseudomonas fluorescens BM07 (Lee et al., 2001) and its mutants were grown at 30 °C in LB as inoculative medium and grown in shake flasks (2-L flasks)

containing 500 mL of M1 medium (Lee et al., 2001) with shaking at 150 r.p.m. Antibiotics were added to growth media in the following Fludarabine research buy concentrations: ampicillin, 100 μg mL−1; kanamycin, 20 μg mL−1; chloramphenicol, 34 μg mL−1. Standard DNA manipulation techniques (Sambrook & Russell, 2001) were used. Plasmid DNA was prepared using the Miniprep extraction kit (DNA-spin, Korea). Restriction enzymes and T4 DNA ligase were purchased from New England Biolabs (Hitchin, UK). PCR using Taq DNA polymerase (Invitrogen, Auckland, New Zealand) were performed according to the manufacturer’s protocol. Oligonucleotide primers were purchased from Genotech (Korea). DNA was sequenced using the BigDye terminator sequencing kit (Applied Biosystems, Warrington, UK) on an automated DNA Sequencer, model 310 (Perkin Elmer, Warrington, UK). Transposon mutants were generated by conjugating P. fluorescens BM07 with E. coli S17-1 (Simon et al.

We argue that this implicit measure was accessible to visuo-vestibular modulation of the sense of self, possibly mediated by shared neural processes in the insula involved in vestibular and interoceptive signalling, thermoregulation and multisensory integration. “
“The developing brain is not a small adult brain. Voltage- and transmitter-gated currents, like network-driven patterns, follow a developmental sequence. Studies initially performed in cortical structures and subsequently in subcortical structures have unravelled a developmental sequence of events in which intrinsic voltage-gated

calcium currents are followed by nonsynaptic calcium plateaux and synapse-driven giant depolarising potentials, orchestrated by VX-809 depolarizing actions of GABA and long-lasting NMDA receptor-mediated currents. The function of these early patterns is to enable heterogeneous neurons Akt inhibitor to fire and wire together rather than to code specific modalities. However, at some stage, behaviourally relevant activities must replace these immature patterns, implying the presence of programmed stop signals. Here, we show that the developing striatum follows a developmental sequence in which immature patterns are silenced precisely when the pup starts locomotion. This is

mediated by a loss of the long-lasting NMDA-NR2C/D receptor-mediated current and the expression of a voltage-gated K+ current. the At the same time, the descending inputs to the spinal cord become fully functional, accompanying a GABA/glycine polarity shift and ending the expression of developmental patterns. Therefore, although the timetable of development differs in different brain structures,

the g sequence is quite similar, relying first on nonsynaptic events and then on synaptic oscillations that entrain large neuronal populations. In keeping with the ‘neuroarcheology’ theory, genetic mutations or environmental insults that perturb these developmental sequences constitute early signatures of developmental disorders. Birth dating developmental disorders thus provides important indicators of the event that triggers the pathological cascade leading ultimately to disease. “
“In the published manuscript of Garcia-Lazaro et al. (2007) there were some mistakes in Figure 6 and the text due to a programming mistake the data analysis routine which attributed data points (firing rates) to the wrong stimulus parameters. In the article, it was stated that neural response gain appeared to be increasing with increased stimulus variance, whereas in reality it decreased. Corrections have been marked in bold in the text below. Last paragraph of the introduction Response level functions tended to become systematically steeper if the mean of the stimulus distribution was held approximately constant but stimulus variance was decreased.

The initial interim find more pharmacokinetic analysis

occurred after the first 12 patients had received ATV/r 300/100 mg during the third trimester with pre-specified criteria for a dose increase to 400/100 mg for all subsequent mothers entering the third trimester. The pre-specified criteria included requirements for Cmin or AUCτ values. If more than two of 12 patients had an ATV Cmin<150 ng/mL but 10 of 12 patients had an ATV Cmin≥50 ng/mL, then ATV/r would be increased to 400/100 mg qd. The AUCτ criterion stated that, if the geometric mean of ATV AUCτ for these 12 patients was <30 000 ng h/mL but ≥15 000 ngh/mL, then ATV/r would be increased to 400/100 mg qd. The dose increase occurred if either criterion was met, and, if a dose escalation was required, all patients at ≥week 28 were given the higher dose. Prophylaxis for prevention of mother-to-child transmission of HIV infection with ARVs (zidovudine and lamivudine) and Pneumocystis jiroveci pneumonia prophylaxis were recommended for all infants. Blood samples were collected after ≥2 weeks of adherent dosing. Adherence was assessed by pill count and was defined as taking all doses and the number of pills prescribed for each medication prescribed. ATV was sampled over

one dosing interval (24 h post-dose) from the mother in the second trimester, the third Lapatinib trimester and postpartum (median 43 days; range 24–71 days). A single blood collection from the mother and the umbilical from cord was performed at delivery. Samples were assayed by liquid chromatography

and tandem mass spectrometry. For ATV and RTV, the standard curves were fitted by a 1/X2-weighted quadratic equation over the concentration ranges of 10.0–10 000 and 5.0–5000 ng/mL, respectively. Values for precision for the analytical quality control (QC) samples were a coefficient of variation (CV) no greater than 7.9% and 9.4% for ATV and RTV, respectively, with deviations from the nominal concentrations of no more than ± 9.4% for ATV and ± 7.6% for RTV. The historical reference data for the current study were pooled from nonpregnant HIV-infected women and men receiving ATV/r 300/100 mg with a nucleoside reverse transcriptase inhibitor (NRTI) backbone (that did not include tenofovir) in two previous clinical studies that had concluded nearest the start of this study [19,20]. These pooled pharmacokinetic data are also similar to the data in the product label for ATV/r 300/100 mg qd and thus were considered representative data for infected patients. Pharmacokinetic parameters (Cmax, Cmin and AUCτ) were derived by noncompartmental methods.

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JJ. Association of cancer with AIDS-related immunosuppression in adults. JAMA 2001; 285: 1736–1745. 5 Dal Maso L, Franceschi S, Polesel J et al. Risk of cancer in persons with AIDS in Italy, 1985–1998. Br J Cancer 2003; 89: 94–100. 6 Herida M, Mary-Krause M, Kaphan R et al. Incidence of non-AIDS-defining selleck chemicals cancers before and during the highly active antiretroviral therapy era in a cohort of human immunodeficiency virus-infected patients. J Clin Oncol 2003; 21: 3447–3453. 7 International Collaboration on HIV and Cancer. Highly active antiretroviral

therapy and incidence of cancer in human immunodeficiency virus-infected adults. J Natl Cancer Inst 2000; 92: 1823–1830. 8 Bedimo R, Chen RY, Accortt NA et al. Trends in AIDS-defining and non-AIDS-defining malignancies among HIV-infected patients: 1989–2002. Clin Infect Dis 2004; 39: 1380–1384. 9 Tirelli U, Errante D, Dolcetti R et al. Hodgkin’s disease and HIV infection: clinicopathologic and virologic features of 114 patients from the Italian cooperative group on AIDS and tumors. J Clin Oncol 1995; 13: 1758–1767. 10 Re A, Casari S, Cattaneo C et al. Hodgkin disease developing in patients infected by human immunodeficiency virus results in clinical features and a prognosis similar to those in patients with human immunodeficiency virus-related non-Hodgkin lymphoma. Cancer 2001; 92: 2739–2745. 11 Glaser Epigenetics inhibitor SL, Clarke CA, Gulley ML et al. Population-based patterns of human immunodeficiency virus-related Hodgkin lymphoma in the Greater San Francisco Bay Area, 1988–1998. Cancer 2003; 98: 300–309. 12 Hoffmann C, Chow

KU, Wolf E et al. Strong impact of highly active antiretroviral therapy on survival in patients with human immunodeficiency virus-associated Hodgkin’s disease. Br J Haematol 2004; 125: 455–462. 13 Errante D, Zagonel V, Vaccher E et al. Hodgkin’s disease in patients with HIV infection and in the general population: comparison of clinicopathological features and survival. Ann Oncol 1994; 5(Suppl 2): 37–40. 14 Rapezzi D, Ugolini D, Ferraris AM et al. Histological subtypes of Hodgkin’s disease in the Ureohydrolase setting of HIV infection. Ann Hematol 2001; 80: 340–344. 15 Rubio R. Hodgkin’s disease associated with HIV: a clinical study of 46 cases. Cancer 1994; 73: 2400–2407. 16 Gerard L, Galicier L, Boulanger E et al. Improved survival in HIV-related Hodgkin’s lymphoma since the introduction of highly active antiretroviral therapy. AIDS 2003; 17: 81–87. 17 Montoto S, Shaw K, Okosun J et al. HIV status does not influence outcome in patients with classical Hodgkin lymphoma treated with chemotherapy using doxorubicin, bleomycin, vinblastine, and dacarbazine in the highly active antiretroviral therapy era.