Students who reported suffering from mouth dryness were about 4.5 times more likely to develop DE compared with

those who did not (OR = 4.5; 95% CI, 2.75–7.21). The odds of having DE in those with occasional bouts of vomiting were about 3.4 times compared with selleck chemicals those who did not experience vomiting (OR = 3.4; 95% CI, 2.25–5.05). Moreover, dietary habits had also a significant association with DE, keeping the drinks in mouth for a long time increased the risk of DE by 2.7 times compared with those who swallowed the drinks immediately (OR = 2.7; 95% CI, 2.17–3.25). Students who brushed their teeth after drinking soft beverages were 2.2 times more likely to have DE than those who did not brush after having a soft drink (OR = 2.2; 95% CI, 1.34–3.77). Additionally, rinsing the mouth after having a soft drink significantly decreased the probability of having DE (OR = 0.7; 95% CI, 0.57–0.95). The results revealed that lemon juice had harmful effect on teeth; students who drank lemon juice at bedtime were 23 times more likely to Selleckchem MI-503 have DE (OR = 23; 95% CI, 2.16–252.06). The odds were almost 18 when lemon was consumed more than twice daily, 8 and 4

when it was consumed only once daily or 2–4 times per week (OR = 18; 95% CI, 8.35–40.84; OR = 7.8; 95% CI, 4.84–12.62; and OR = 4; 95% CI, 2.77–5.72, respectively). On the other hand, the odds were 7.8 times when student had carbonated drinks at bedtime (OR = 7.8; 95% CI, 3.94–15.42). Sour candies were significantly tuclazepam associated with DE. Students who consumed sour candies more than twice daily were almost 24 times more prone to have DE than those who did not eat them at all (OR = 24; 95% CI, 12.39–48.33), students who consumed sour candies once daily were about 18 times more likely to have DE than those who did not (OR = 18; 95% CI, 7.99–40.14), for student who consumed sour candies 2–4 time per week, the odds were eight times (OR = 8; 95% CI, 5.46–12.26). Those who consumed it at least once weekly were

about one and a half times more likely to have DE than those who did not eat sour candies at all (OR = 1.5; 95% CI, 1.14–1.91). Logistic regression defined sports beverages as a causative indicator of DE. The odds of having DE increased by the increase in the frequency of beverages consumption; students who drank sports beverages more than two times daily were almost 29 times more prone to have DE than those who did not drink it at all (OR = 29; 95% CI, 9.38–91.23), students who had this drink once daily were about 14 times more likely to have DE than those who did not (OR = 14; 95% CI, 2.95–65.12) and for those who drank sports beverages 2–4 time per week, the odds were nearly 12 times than those who did not (OR = 12; 95% CI, 5.90–25.81).

Students using cortisol inhalers as treatment of asthma were about five times more likely to have DE than those who did not (OR = 4.8; 95% CI, 2.26–10.17). Students who reported suffering from mouth dryness were about 4.5 times more likely to develop DE compared with

those who did not (OR = 4.5; 95% CI, 2.75–7.21). The odds of having DE in those with occasional bouts of vomiting were about 3.4 times compared with Selleckchem Obeticholic Acid those who did not experience vomiting (OR = 3.4; 95% CI, 2.25–5.05). Moreover, dietary habits had also a significant association with DE, keeping the drinks in mouth for a long time increased the risk of DE by 2.7 times compared with those who swallowed the drinks immediately (OR = 2.7; 95% CI, 2.17–3.25). Students who brushed their teeth after drinking soft beverages were 2.2 times more likely to have DE than those who did not brush after having a soft drink (OR = 2.2; 95% CI, 1.34–3.77). Additionally, rinsing the mouth after having a soft drink significantly decreased the probability of having DE (OR = 0.7; 95% CI, 0.57–0.95). The results revealed that lemon juice had harmful effect on teeth; students who drank lemon juice at bedtime were 23 times more likely to SCH727965 order have DE (OR = 23; 95% CI, 2.16–252.06). The odds were almost 18 when lemon was consumed more than twice daily, 8 and 4

when it was consumed only once daily or 2–4 times per week (OR = 18; 95% CI, 8.35–40.84; OR = 7.8; 95% CI, 4.84–12.62; and OR = 4; 95% CI, 2.77–5.72, respectively). On the other hand, the odds were 7.8 times when student had carbonated drinks at bedtime (OR = 7.8; 95% CI, 3.94–15.42). Sour candies were significantly clonidine associated with DE. Students who consumed sour candies more than twice daily were almost 24 times more prone to have DE than those who did not eat them at all (OR = 24; 95% CI, 12.39–48.33), students who consumed sour candies once daily were about 18 times more likely to have DE than those who did not (OR = 18; 95% CI, 7.99–40.14), for student who consumed sour candies 2–4 time per week, the odds were eight times (OR = 8; 95% CI, 5.46–12.26). Those who consumed it at least once weekly were

about one and a half times more likely to have DE than those who did not eat sour candies at all (OR = 1.5; 95% CI, 1.14–1.91). Logistic regression defined sports beverages as a causative indicator of DE. The odds of having DE increased by the increase in the frequency of beverages consumption; students who drank sports beverages more than two times daily were almost 29 times more prone to have DE than those who did not drink it at all (OR = 29; 95% CI, 9.38–91.23), students who had this drink once daily were about 14 times more likely to have DE than those who did not (OR = 14; 95% CI, 2.95–65.12) and for those who drank sports beverages 2–4 time per week, the odds were nearly 12 times than those who did not (OR = 12; 95% CI, 5.90–25.81).

Various CDSS have been evaluated in different medical fields and have often demonstrated useful guidance for practitioners.4 So far, two CDSS have been designed for specific e-assistance in diagnosing infectious diseases, and in particular travel-related conditions: the Global Infectious Diseases and Epidemiology Network (GIDEON) (http://www.gideononline.com)5–7 and Fever Travel (http://www.fevertravel.ch) developed by Selleck C646 the

University of Lausanne, Switzerland.8 Each support system has a different design and focus. GIDEON is an expert system based on a probabilistic (Bayesian) approach and relies on an impressive global epidemiological database as an aid to diagnose infectious diseases worldwide. It focuses rather on infectious diseases specialists, gives a probability ranking of possible diagnoses with extensive documentation of diseases, but needs payment. Fever Travel has an algorithmic design based on both evidence and expert opinion, with the purpose of providing guidance in the management of travel-related conditions in nonendemic settings, mainly for clinicians not familiar with tropical diseases. It suggests BGB324 further work-up, reference to travel specialist or hospitalization, and even presumptive treatments. Fever Travel is freely downloadable. KABISA is a computer-based tutorial for tropical medicine, which has been used since 1992

for teaching at the Institute of Tropical Medicine, Antwerp, Belgium, as well as in many teaching centers overseas.9 Kabisa is Swahili for “hand in the fire, I’m absolutely certain,” referring to a clinician experiencing a straightforward pattern recognition. In 2008 the logical engine of this software

was used for the development of an interactive expert system, cAMP KABISA TRAVEL (version IV). This system relies on a database currently containing >300 diseases and >500 findings, which are classified in five main categories (epidemiological characteristics, symptoms, clinical signs, laboratory data, results of imaging). Prevalence of diseases and frequency of related findings were entered according to evidence-based data obtained from a large prospective study in our center which explored the etiology of fever after a tropical stay as well as to the global epidemiological results published by the GeoSentinel group.1,3,10 When the user enters a present (or absent) finding, the software calculates the disease probabilities and provides a ranking of hypotheses. It relies on an adapted Bayesian approach. Following Bayes’ theorem, pretest odds are multiplied by successive likelihood ratios, but the latter are recalculated at every step as the false positive rate depends on the spectrum of diseases still active at that moment of consultation (“dynamic specificity”).

Typhimurium; Prigent-Combaret et al., 2001) and for the P-pili of UPEC (Jones et al.,

1997). Bundle-forming pili are pivotal for EPEC to form microcolonies and to attach to host cells (Tobe & Sasakawa, 2001). The Cpx-TCS is induced by overexpression of the BFP subunit BfpA and by mature BFP (Nevesinjac & Raivio, 2005). This finding strongly indicates that intermediates other than unprocessed BfpA are also sensed by the Cpx-TCS (Nevesinjac & Raivio, 2005). The Cpx system controls curli fimbriae expression, which are involved in forming surface amyloidal fibres important for biofilm formation and host cell adhesion (Dorel et al., 1999; Jubelin et al., 2005; Barnhart & Chapman, 2006), and curli overexpression Gefitinib cell line selleck compound induces the Cpx response (Prigent-Combaret et al., 2001). P-pili are crucial for kidney colonization by UPEC strains and belong to the group of chaperone-usher pili (CU pili; reviewed in Waksman & Hultgren, 2009). Essential for the formation of CU pili is a periplasmic chaperone that guides the single subunits after release from the SecYEG

translocase across the periplasmic space to the usher in the outer membrane. Deletion of the chaperone PapD results in misfolded P-pilus subunits that become toxic for the cell and induces the Cpx response (Jones et al., 1997). Overexpression of CpxP suppresses the lethal phenotype by causing the misfolded pilus subunits to be degraded by DegP (Isaac et al., 2005). Because the induction

of the Cpx-TCS by PapG does not depend on the DegP protease (Hung et al., 2001) but rather on Bacterial neuraminidase CpxP, it was suggested that PapG induces the release of CpxP from CpxA resulting in the activation of the Cpx-TCS (Fig. 3d; Isaac et al., 2005). An elongated hydrophobic cleft on the convex surface of the CpxP dimer might act as a sensory part for pilus subunits (Zhou et al., 2011). However, it remains mysterious which region of pilus subunits is recognized by CpxP. Only two pilus subunits are known to activate the Cpx-TCS: the PapG adhesin and the fibrillum subunit PapE (Jones et al., 1997). It has been suggested that the N-terminal extension of PapE, which is essential for the assembly of pilus subunits, is crucial for recognition of PapE by CpxP (Lee et al., 2004; Isaac et al., 2005). However, PapG is missing an N-terminal extension that is present in the other subunits which are not recognized by the Cpx-TCS (Lee et al., 2004). Very recently, a crucial role of the Cpx system in inter-kingdom signalling between host and bacteria has been discovered (Karavolos et al., 2011). In S. Typhi, exposure to host stress neuroendocrine hormones leads to increased haemolytic activity through the secretion of haemolysin HlyE-containing membrane vesicles (Karavolos et al., 2011).

As a result of this, the gel can be injected in larger amounts click here and into deeper skin layers [13], an advantage given that HIV facial lipoatrophy typically involves larger atrophic surface areas than seen in the general population. The use of a more viscous type of hyaluronic acid for the treatment of HIV-associated lipoatrophy has only been described previously in two studies, both with

a follow-up period of 12 months [14,15]. The aim of our study was to evaluate the efficacy, safety and durability of a large particle hyaluronic acid in the correction of facial lipoatrophy in HIV-infected patients over a 3-year period. Twelve-month treatment results from this study have been reported earlier [14]. In the present study, we report longer-term efficacy, safety and durability data. Details of participants’ eligibility and baseline characteristics have been previously reported in the 52-week follow-up study report [14]. In short, HIV-infected patients older than 18 years of age with severe nasogenian atrophy (readily noticeable to a casual observer) that had not previously been treated with injectable

fillers were considered eligible for inclusion. The study protocol was evaluated by the Regional Committee for Medical Research Ethics and approved by the Norwegian Data Inspectorate. This study has been conducted in full accordance with the World Medical Association Declaration of Helsinki. Patients received injections of hyaluronic acid (Restylane Birinapant clinical trial SubQ) in each cheek in the nasogenian area at baseline, 12 and 24 months. The intended level of injection was deep subcutaneous. A touch-up treatment was offered 4 weeks after each treatment. Patients attended a post-treatment consultation approximately 6 weeks after each treatment. All injections were performed by the same plastic surgeon at the out-patient clinic of the Department of Plastic Surgery. The skin area was pen-marked with the patient in an upright position before the patient lay down

for treatment. Under local anaesthesia, a sharp 18-gauge cannula was used to perforate the skin laterally, just below Decitabine research buy the cheek bone. A blunt-tipped cannula with a side-exit (1.2 × 70 mm; 18 gauge) was then inserted downwards and subcutaneously on each side, to make a tunnel. The tunnel was then filled with hyaluronic acid gel while the cannula was being retracted. Filling with hyaluronic acid was carried out using a fanning injection technique (12–20 tunnelations). At the end of each treatment, the cheeks were gently massaged in order to shape the filler material to achieve optimal contour. The local anaesthetic technique was changed in the second year of the study from a subcutaneous local anaesthetic to an infraorbital nerve block via the buccal mucosa, the aim being to reduce swelling and therefore provide better visibility of the area to be treated.

For transformations with the plasmids obtained by plasmid rescue, 20 times smaller volumes were used. Each plasmid was digested with the restriction enzyme that had been used for the plasmid rescue (XhoI or ClaI). After 24–48 h at 37 °C, plates containing putative transformed colonies were overlayed with 4 mg L−1 ITR in RPMI, 1% agar. After 48 h, a differentiable new ring of growth was observable. The colonies that had a bigger or smaller ring than the majority were checked for their susceptibility to ITR by inoculating spores onto RPMI plates containing 2% glucose and 2% agar and containing either 0.50, 0.25 or 0.12 mg L−1 ITR. Mutants with

ITR susceptibilities clearly different from the parental isolate were subsequently tested for their MICs to four azoles (Table 1; Denning Buparlisib in vivo et al., 1997b). The MICs were read visually and were defined as the lowest drug concentration

with no visible growth. Fungal DNA was isolated using the DNeasy Plant Mini Kit (Qiagen, Crawley, UK). The presence of the integrated pPyrG plasmid was confirmed by PCR using primers Cf and Gr directed against the AmpR gene (Supporting information, Table S1). Genomic DNA (3 μg) was digested to completion with XhoI, ClaI or NcoI, as appropriate, separated in 0.8% agarose, transferred onto a positively charged nylon membrane (Roche Diagnostics, Lewes, UK) and hybridised overnight at 42 °C in DIG Easy Hyb (Roche) with a DIG-labelled probe consisting of the pUC19 DNA or the HindIII fragment of the pPyrG plasmid. Washing was carried out at 65 °C RXDX-106 datasheet in 0.5× SSC, 0.1% SDS with stringent washing using 0.1× SSC, 0.1% SDS. Plasmid rescue was carried out by digesting genomic DNA with XhoI or ClaI, separating the DNA in 0.8% agarose and purifying DNA of ± 1–2 kb of the estimated size according to the Southern hybridisations. DNA was ligated overnight at 16 °C with T4 DNA ligase and electroporated into Escherichia coli DH5α (Invitrogen, Paisley, UK) or

SCS110 (Stratagene, Amsterdam, the Netherlands). The sequence flanking the pPyrG insertion site was determined using primers FOR and REV, which hybridised 68 bp upstream and 88 bp downstream of the A. nidulans Isotretinoin pyrG XhoI site, respectively. Regions including ~1 kb upstream and 1 kb downstream of AFUA_5G07550, AFUA_2G11840, AFUA_2G11020, AFUA_4G10880 and AFUA_6G12570 were amplified by PCR using primers 5G07550F and 5G07550R, 2G11840F and 2G11840R, 2G11020F and 2G11020 R, 4G10880F and 4G10880R, and 6G12570F and R. Fifty microlitres PCR contained 25 μL 2× Phusion mastermix, 40 pM primers and 200 ng Af293 DNA according to the manufacturer’s instructions (New England Biolabs) and were subjected to 35 cycles at 96 °C for 15 s, 58 °C for 5 min and 72 °C for 80 s followed by an extension step at 72 °C for 5 min. Products were assessed by gel electrophoresis, gel purified using a Qiaex kit (Qiagen) and then cloned into pGEM-T (Promega).

However, the widespread use of vancomycin to treat MRSA infections has resulted in the increased frequency of isolation of vancomycin intermediate-level-resistant S. aureus (VISA) strains, from both clinical

and community sources (Walsh & Howe, 2002). These data underscore the need for a better understanding of the molecular underpinnings of how resistance may arise to www.selleckchem.com/products/sotrastaurin-aeb071.html existing, and in particular, investigational antimicrobials (Mangili et al., 2005). The generation of an S. aureus strain with reduced susceptibility to ramoplanin provides a model system to gain greater insight into the mechanisms of ramoplanin action and the evolution of resistance mechanisms in Gram-positive bacteria. Staphylococcus aureus strain NCTC 8325-4 (also known as NRS135; Novick, 1967) was obtained from the repository maintained by the Network on Antimicrobial Resistance in S. aureus (http://www.narsa.net). To generate ramoplanin-resistant S. aureus, a step pressure method was used. Isolated colonies of S. aureus NCTC 8325-4 were inoculated into 5-mL aliquots of cation-adjusted Muller–Hinton broth II supplemented with 0.02% Fraction V bovine serum albumin (CAMHB2+BSA) containing ramoplanin at concentrations of 0.1–10 μg mL−1. The cultures were incubated at 37 °C with aeration for 48 h. At 48 h, growth was observed in the culture containing 0.1 μg mL−1 ramoplanin. This culture was used to inoculate

5 mL CAMHB2+BSA containing ramoplanin at concentrations of 0.1–5 μg mL−1 at a cell density of ∼106 CFU mL−1. These cultures JAK cancer were incubated for 24–72 h at 37 °C with aeration. The culture with growth in the highest concentration of ramoplanin was used to inoculate another series at a cell density of ∼106 CFU mL−1. Passage of the culture was continued in this manner through the 16th series. In the 16th series, growth was observed in a culture containing 5 μg mL−1 ramoplanin. A sample from this culture was plated on tryptic soy agar (TSA) with no antibiotic and incubated at 37 °C overnight. An isolated colony was selected and streaked onto TSA and grown overnight at 37 °C twice, and then an isolated colony was selected and named RRSA16.

Oligonucleotide primers 16s_fw_sa (5′-CGTGCCTAATACATGCAAGTC-3′) and 16S_univ_rv (5′-ACGGGCGGTGTGTACAAG-3′) were used to amplify those a portion of the genes encoding the 16s rRNA from genomic DNA prepared from each NCTC 8325-4 and RRSA16. The nucleotide sequences obtained from reactions performed with primers 16s_fw_sa and 16S_univ_rv on the amplified sequences from NCTC 8325-4 and RRSA16 were identical to each other and the published sequence of NCTC 8325-4. An overnight culture of RRSA16 was subcultured into CAMHB2+BSA containing no antibiotics at a cell density of ∼104 CFU mL−1 and incubated overnight at 37 °C with shaking. The overnight growth was used to inoculate a fresh CAMHB2+BSA culture containing no antibiotic at a cell density of ∼104 CFU mL−1 and incubated overnight at 37 °C with shaking.

02). In the HIV-positive group, prior or current AIDS-defining events were reported for 30% of patients, 9% and 30% had CD4 counts of <200 and 200–500 cells/μL, respectively,

and 95% had HIV-1 RNA <50 copies/mL. Pneumonia (9%vs. 25%, respectively, in the HIV-positive and HIV-negative groups; P=0.01) and respiratory failure (9%vs. 21%, respectively; P=0.04) were less common in the HIV-positive group. Oseltamivir RG7204 in vitro (95%vs. 71% in the HIV-positive and HIV-negative groups, respectively; P=0.003) was administered more often in HIV-positive patients. Three patients (all HIV-negative) died. In the HIV-positive group, CD4 cell count and plasma HIV-1 RNA did Abiraterone not differ before and 4–6 weeks after influenza A H1N1 diagnosis (P>0.05). HIV infection did not increase the severity of influenza A H1N1 infection, and influenza A H1N1 infection did not have a major effect on HIV infection.

Influenza is a common cause of acute respiratory illness in HIV-infected adults [1,2]. Before the widespread use of effective combination therapy, small case series and anecdotal reports suggested that low CD4 cell counts or concomitant respiratory or cardiovascular comorbidities were associated with a higher risk for complications [3–8]. It is unclear to what extent effective antiretroviral therapy may have affected the risk for severe or complicated influenza, but HIV-infected patients are still considered to be Carnitine palmitoyltransferase II at a higher risk [9] and for that reason they are preferentially targeted for influenza vaccination [10–12]. Human infections with a novel A H1N1 influenza virus were first identified in April 2009 [13,14] and they were increasingly reported throughout the world in the following weeks [15]. The rapid spread of the infection and the extensive reporting of associated deaths occupied the attention of the media and contributed to increased awareness

in the general population [16,17]. Data from the beginning of the epidemics suggested that many influenza A H1N1 infections were not necessarily severe [18] and that HIV-infected patients were not overrepresented among those hospitalized or severely ill [14,19–21]. Nevertheless, health authorities considered that HIV-infected patients were at a higher risk for influenza A H1N1 complications, as they were for seasonal influenza, and this assumption remains unchanged [22–24]. With open access to combination antiretroviral therapy, many HIV-infected adults show sustained suppression of HIV replication in plasma, resulting in immunological and clinical benefits [25]. In Spain, health care for chronic conditions such as HIV infection and also for acute conditions and emergencies is provided free of charge by the public health care system [26].

However, 8.8% of cases required a visit to a doctor, and 3.2% needed hospitalization. Longer duration of stay and drinking beverages with

ice-cubes were associated with higher risk of diarrhea. Conclusions. About one third of the foreign backpackers in Southeast Asia had experienced diarrhea during their trip. Their current practices related to the risk of travelers’ diarrhea were inadequate and should be improved. Travelers’ diarrhea is a very common disease reported among travelers visiting developing countries. Although most travelers’ diarrhea is mild and self-limited,1,2 it can lead to long-term consequences, such as irritable bowel syndrome (IBS) and reactive arthritis, in some patients.3,4 Moreover, evidence has shown that an attack of diarrhea during a trip could force a significant BVD-523 clinical trial number of travelers to delay or change some of their itineraries.5,6 Southeast Asia is one of the most popular tropical destinations.

In 2009, approximately 62.1 million tourists visited Southeast Asia, an increase from 61.7 million visits in 2008.7 Among these visitors, backpackers were an important and unique group. They tended to stay longer and travel in more rural areas, and might be at higher risk of diarrhea while traveling. Several studies have estimated the incidence of travelers’ diarrhea in Southeast Asia to be in the range 5% to 17%8–10 among general travelers, to over 50% among Peace Corps’ volunteers11; data on backpackers are Palbociclib research buy very limited. The only study of backpackers in Southeast Asia comprised only Japanese backpackers.12 Therefore, these data may not be extrapolated to backpackers from western countries, that is, from Europe and North America, who comprise the majority of backpackers in Southeast Asia. Therefore, this study aimed to determine the incidence and impact of travelers’ diarrhea among foreign backpackers in Southeast Asia. The secondary objective was to assess their attitudes and practices toward the risk of travelers’ diarrhea. This was a cross-sectional, questionnaire-based

survey. Data were collected from foreign backpackers in the Khao San Road area, Bcl-w which is a famous backpacker center in Bangkok, Thailand. It is one of Bangkok’s liveliest areas, and plays host to backpackers from all around the world, with many guesthouses, budget hotels, travel agents, and other tourists facilities.13 The questionnaire was designed, then tested before actual data collection. The final version consisted of 20 questions in three parts: general information about the backpackers and their trip, perceptions and practices related to the risk of travelers’ diarrhea, and details of any diarrheal attack and its impact. In this study, passing three or more loose stools in a 24-h period was defined as travelers’ diarrhea. Sample size was calculated using the estimated risk of diarrhea in Southeast Asia and the number of backpackers in Khao San area (data from Tourism Authority of Thailand14).

Reduced treatment intensity in patients with early-stage Hodgkin’s lymphoma. N Engl J Med 2010; 363: 640–652. 35 Radford J, Barrington S, Counsell N et al. Involved field radiotherapy versus no further treatment in patients with clinical stages IA and IIA Hodgkin lymphoma and a ‘negative’ PET scan after 3 cycles ABVD. Results of the UK NCRI RAPID Trial. 54th

ASH Annual Meeting and Exposition. Atlanta, GA, December 2012 [Abstract 547]. 36 Hentrich M, Berger M, Wyen C et al. Stage-adapted treatment of HIV-associated Hodgkin lymphoma: results of a prospective multicenter study. J Clin Oncol 2012; 30: 4117–4123. GSK3235025 manufacturer 37 Eich HT, Diehl V, Gorgen H et al. Intensified chemotherapy and dose-reduced involved-field radiotherapy in patients with early unfavorable Hodgkin’s lymphoma: final analysis of the German Hodgkin Study Group HD11 trial. J Clin Oncol 2010; 28: 4199–4206. 38 Hoskin PJ, Lowry L, Horwich A et al. Randomized comparison of the Stanford DZNeP cell line V regimen and ABVD in the treatment of advanced Hodgkin’s lymphoma: United Kingdom National Cancer Research Institute Lymphoma Group Study ISRCTN 64141244. J Clin Oncol 2009; 27: 5390–5396. 39 Viviani S, Zinzani PL, Rambaldi A et al. ABVD versus BEACOPP for Hodgkin’s lymphoma when high-dose salvage is planned. N Engl J Med 2011; 365: 203–212. 40 Carde PP, Karrasch M, Fortpied C et al. ABVD (8 cycles) versus BEACOPP (4 escalated cycles => 4 baseline) in stage III-IV high-risk Hodgkin lymphoma (HL): First results of

EORTC 20012 Sclareol Intergroup randomized phase III clinical trial. ASCO Annual Meeting. Chicago, IL, June 2012 [Abstract 8002]. 41 Bauer K, Skoetz N, Monsef I et al. Comparison of chemotherapy including escalated BEACOPP versus chemotherapy including ABVD for patients with early unfavourable or advanced stage Hodgkin lymphoma. Cochrane Database Syst Rev 2011; 8: CD007941. 42 Xicoy B, Ribera J-M, Miralles P et al. Results of treatment

with doxorubicin, bleomycin, vinblastine and dacarbazine and highly active antiretroviral therapy in advanced stage, human immunodeficiency virus-related Hodgkin’s lymphoma. Haematologica 2007; 92: 191–198. 43 Spina M, Gabarre J, Rossi G et al. Stanford V regimen and concomitant HAART in 59 patients with Hodgkin disease and HIV infection. Blood 2002; 100: 1984–1988. 44 Hartmann P, Rehwald U, Salzberger B et al. BEACOPP therapeutic regimen for patients with Hodgkin’s disease and HIV infection. Ann Oncol 2003; 14: 1562–1569. 45 Shah BK, Subramaniam S, Peace D, Garcia C. HIV-associated primary bone marrow Hodgkin’s lymphoma: a distinct entity? J Clin Oncol 2010; 28: e459–460. 46 Tsimberidou AM, Sarris AH, Medeiros LJ et al. Hodgkin’s disease in patients infected with human immunodeficiency virus: frequency, presentation and clinical outcome. Leuk Lymphoma 2001; 41: 535–544. 47 Hessol NA, Pipkin S, Schwarcz S et al. The impact of highly active antiretroviral therapy on non-AIDS-defining cancers among adults with AIDS. Am J Epidemiol 2007; 165: 1143–1153.