Computer-aided analysis of the affected genes also revealed the presence of inverted repeats highly similar

to the conserved Rex-binding site, -TTGTGAAW4TTCACAA-, in the promoter regions of most, but not all genes identified by microarray (Schau et al., 2004; Gyan et al., 2006; Pagels et al., 2010). Efforts to investigate whether Rex can bind to the promoter of the targeted genes and how NAD+/NADH balances affect Rex-regulated gene expression are ongoing It is apparent that Rex-deficiency did not have any significant effect on the morphology and growth rate of the deficient mutant when grown planktonically under the conditions studied (Fig. 1a). However, the deficient selleck chemicals llc mutant did show a decreased ability to develop biofilms on a surface, and it formed biofilms with an altered structure (Figs 2 and 3). These defects could be in part attributed to the altered expression of genes central to carbohydrate fermentation and energy metabolism (e.g. pflC and pdhAB), NAD+/NADH recycling (e.g. adhE, adhAB and frdC) and oxidative homeostasis (mleSP and gshR) (Table 2 and Table S1). One particularly interesting observation of the Rex-deficient mutant is that while it had a decreased ability to form biofilms, it also appeared to generate more glucans (Figs 2 and 3). Streptococcus mutans possesses at least three glucosyltransferases (GtfB, -C and -D) and one fructosyltransferase CAL 101 (Ftf).

The enzymes use sucrose as the primary substrate, assembling glucans and fructans from the glucose- and fructose-moiety of sucrose, respectively (Burne, 1998). At a significant level of P<0.01, gtfC was also identified by DNA microarray analysis to be Bay 11-7085 upregulated by 1.56-fold in TW239, but not gtfB, gtfD and ftf (data not shown). When analyzed by RealTime-PCR, the expression of gtfC was found to be increased by >13-fold in TW239 (Table 2), but again no significant differences were detected in the expression of either gtfB, gtfD or ftf. Similar observations were also made recently in S. mutans grown with aeration (Ahn et al., 2007). Consistent with the severely impaired ability to form biofilms,

S. mutans grown in the presence of oxygen showed major changes in the amount and localization of the Gtf enzymes. In particular, the cell surface-associated GtfC was found by Western blotting to be dramatically increased in cells grown aerobically, as compared with those prepared under anaerobic conditions. However, it remains to be investigated whether the localization of any of the Gtf enzymes were altered in S. mutans as a result of Rex-deficiency. Glucosyltransferase GtfB is known to produce α1,3-linked, water-insoluble glucans that play a central role in S. mutans adherence and accumulation on surfaces, whereas the glucan products of GtfC contain α1,3-linked, water-insoluble and a substantial amount of α1,6-linked water-soluble glucans (Bowen & Koo, 2011).

Reactivation of latent virus is common in those with advanced immunosuppression and frequently does not cause end-organ disease. Detection of CMV in urine, blood or BAL without evidence of end-organ involvement implies CMV infection but not disease. CMV isolation in BAL (by culture or PCR)

is common in individuals with HIV infection, who have low CD4 T-cell counts [120,121]. Typical symptoms are dry non-productive cough and exertional dyspnoea with fever; and this presentation is similar to many other pulmonary conditions [120,122]. Hypoxaemia is often marked [120]. The chest radiograph and CT scan most often show bilateral interstitial infiltrates or ground glass attenuation, but unilateral alveolar consolidation, bilateral nodular opacities, MK-2206 ic50 pleural effusions or rarely cavities or hilar adenopathy may occur [120,122,123]. There may be concomitant evidence of extra-pulmonary CMV [120] and a dilated eye examination should be performed to rule out CMV retinitis. The major diagnostic challenge is to differentiate CMV shedding in respiratory secretions from cases with CMV pneumonitis. Culture, positive PCR or antigen

assay for CMV from BAL or biopsy specimen do not distinguish CMV shedding from pneumonitis, and hence must be interpreted with caution [124,125]. A negative culture result, with its high negative predictive value, however, does reasonably exclude CMV pneumonia [126]. Diagnosis of CMV pneumonia requires a biopsy specimen to provide evidence of pulmonary check details involvement in association with a compatible clinical syndrome (category III recommendation). Evidence ADAM7 of intranuclear or intracytoplasmic viral inclusions, positive immunostaining for CMV antigens or detection of CMV by molecular techniques such as in situ hybridization on a pulmonary biopsy specimen establishes the diagnosis in the setting of a compatible clinical syndrome

[120]. CMV replication in the respiratory tract is most frequently only a marker of immunosuppression and not of pneumonia. The majority of individuals in whom microbiological tests on BAL, or biopsy, demonstrate CMV should not receive treatment for CMV (category III recommendation). This approach is supported by evidence that when treatment is withheld, in individuals with evidence of CMV on BAL or biopsy, clinical outcome is not adversely altered [127]. However, the benefits of treatment to the select subset of individuals who have evidence of a compatible clinical syndrome, positive microbiology and histology for CMV and no alternative diagnosis have been suggested by retrospective case series that show improved clinical outcomes with treatment [121]. The management of individuals with positive histology for CMV but identification of a second pulmonary pathogen is also controversial.

Long-term randomized trials are needed to address optimal treatment duration. We recommend that, for drug-sensitive TB not involving the CNS, regimens of 6 months should be given [41,50,51,55,56]. These should include at least 182 doses of isoniazid and rifampicin, and 56 doses of pyrazinamide (see ‘Definition of completion of TB therapy’).

[AII] See also ‘Intermittent therapy’ [AII] and ‘Use of rifabutin’ [BII]. In HIV-infected adults with pulmonary or pleural TB, corticosteroids do not improve survival or reduce TB recurrence [57,58] and are not generally recommended [59]. In the general population, NICE guidelines recommend steroids in cases of active meningeal or spinal cord TB [1]. At present there is insufficient SB431542 price evidence GKT137831 in vivo regarding their use in HIV-infected people. A randomized controlled trial in Vietnam showed no difference in mortality or a combined outcome of death and disability in HIV-infected people with a clinical diagnosis of TB meningitis, whether they were given dexamethasone or placebo with standard TB treatment [60]. However, there were few HIV-infected people in this study and the diagnosis of TB was confirmed microbiologically in fewer than 50% of cases. This study may therefore have missed a clinically important difference. Until more data are

available we recommend that HIV-infected adults with meningeal or spinal cord TB should be given corticosteroids. [BII] NICE guidelines recommend steroids for active pericardial

TB. There are limited data to support this in HIV coinfection. A small randomized controlled trial of HIV-infected adults with presumed tuberculous pericarditis treated with standard TB therapy found that prednisolone resulted in better outcomes than placebo [61]. Mortality was reduced with prednisolone compared with placebo, and improvement Racecadotril in raised venous pressure, hepatomegaly, ascites and physical activity occurred more rapidly. Interestingly there was no faster resolution of pericardial fluid on chest radiography or echocardiogram, and as only 38% had positive M. tuberculosis cultures, some of the subjects may not have had pericardial TB. These results should therefore be interpreted with caution. Until more data are available in HIV-positive patients, we recommend that adults with pericardial TB should be given corticosteroids. [AII] Other uses of steroids have included their use in preventing ureteric stenosis in renal TB or enlargement of, for example, a mediastinal lymph node causing collapse of a lung lobe and in management of TB-related IRIS (see ‘IRIS’). The optimal dose of adjunctive corticosteroids is not known. Rifampicin induces the liver metabolism of corticosteroids, thus increasing their plasma clearance [62].

The concentration of l-leucine could be a trigger for the Lrp-dependent regulation of genes that function during feast or famine (Calvo & Matthews, 1994). Because l-methionine is a key metabolite in the sulphur, methylation and trans-sulphuration pathways, the accumulation of its oxidized forms may significantly perturb cell metabolism. Thus, both l-leucine hydroxylation and l-methionine oxidation could be also involved in the metabolic regulatory network. The authors thank Ms N.Y. Rushkevich for help in gene cloning. “
“In

Colpoda cucullus, the morphogenetic transformation was preceded by an enhancement of the in vivo protein phosphorylation level. Immunofluorescence microscopy using antiphosphoserine antibody showed that these Selleck Forskolin phosphorylated proteins

were localized in the macronucleus and other cytoplasmic regions. Biotinylated Phos-tag/ECL assays of isolated macronuclei showed that a 33-kDa protein (p33) was localized within them. The p33 obtained from isolated macronuclei was tentatively identified as ribosomal P0 protein by LC-MS/MS analysis. In addition, among the encystment-specific phosphoproteins obtained by phosphate-affinity chromatography, the 29-, 31-, and Venetoclax molecular weight 33-kDa proteins (p29, p31, and p33) were tentatively identified as ribosomal P0 protein, whereas the 24-kDa phosphoprotein (p24) was tentatively identified as ribosomal S5 protein. The resting cyst formation (encystment) of protozoans is a kind of cryptobiosis that involves a drastic cellular morphogenesis. The molecular mechanism of cellular differentiation during en- and excystment has been studied especially extensively in parasitic protozoans. For example, encystment-specific key proteins such as cysteine peptidase (Ebert et al., 2008), serine protease (Moon et al., 2008), and enolase (Bouyer et al., 2009; Segovia-Gamboa et al., 2010, 2011) have recently been identified in Acanthamoeba or Entamoeba. In Giardia, proteins such as cyst wall proteins, cyst wall glycopolymer biosynthetic enzymes, transcription factors, and signaling proteins have been reported to play a

role in cellular differentiation during encystment (Lauwaet et al., 2007b; Carranza & Lujan, 2010; and references Ergoloid therein). In signal transduction pathways leading to en- or excystment, protein phosphorylation and dephosphorylation were shown to occur (Abel et al., 2001; Slavin et al., 2002; Ellis et al., 2003; Gibson et al., 2006; Bazán-Tejeda et al., 2007; Lauwaet et al., 2007a; Alvarado & Wasserman, 2010), and phosphorylated proteins such as 14-3-3 protein and 70-kDa heat shock protein have been shown to play a role (Alvarado & Wasserman, 2010). In free-living ciliates, on the other hand, the morphogenetic transformation that occurs during en- and excystment is poorly understood at the molecular level, although it is known that the encystment is gene-regulated (Grisvard et al.

AChE/AChR ratios were determined at the neuromuscular

junctions (NMJ). The decrease in AChR levels that occurred as the disease progressed resulted in a dramatic increase in this ratio, and a significant recovery towards normal ratios occurred after EN101 treatment. Lumacaftor clinical trial This improvement was primarily due to increased synaptic AChR content. Our findings emphasise the tight connection between AChR and AChE at the myasthenic NMJ, and the importance of the AChE/AChR ratio in maintaining the required cholinergic balance. “
“It was suggested that gap junctional intercellular communication (GJIC) and connexin (Cx) proteins play a crucial role in cell proliferation and differentiation. However, the mechanisms of cell coupling in regulating cell fate during embryonic development are poorly understood. To study the role of GJIC in proliferation and differentiation, we used a human neural progenitor cell line derived from the ventral mesencephalon. Fluorescence recovery after photobleaching (FRAP) showed that dye coupling was extensive in proliferating cells but diminished after the induction of differentiation, as indicated

by a 2.5-fold increase of the half-time of fluorescence recovery. Notably, recovery half-time decreased strongly (five-fold) in the later stage of differentiation. Western blot analysis revealed a similar time-dependent expression profile of Cx43, acting as the main gap junction-forming protein. Interestingly, large amounts of cytoplasmic Cx43 were retained mainly in the Golgi network HIF inhibitor during proliferation but decreased when differentiation was induced. Furthermore, down-regulation of Cx43 by small interfering RNA reduced functional cell coupling, which

in turn resulted in a 50% decrease of both the proliferation rate and neuronal differentiation. Our findings suggest a dual function of Cx43 and GJIC in the neural development of ReNcell VM197 human progenitor cells. GJIC accompanied by high Cx43 expression is necessary (1) to maintain cells in a proliferative state and (2) to complete neuronal differentiation, including the establishment of a neural network. However, uncoupling of cells is crucial in the early stage of differentiation during cell fate commitment. “
“Functional stereotactic GNA12 lesions in the central lateral nucleus of the medial thalamus have proved to be an effective treatment of neurogenic pain and other neurological disorders associated with thalamocortical dysrhythmia. The mechanisms underlying patient recovery after surgery are currently being explored using quantitative electroencephalography. Here we test the hypothesis that the particular role played by the non-specific medial thalamic nuclei in thalamocortical dysrhythmia is based on the divergent connectivity between these non-specific and reticular nuclei.

Travel destinations were sub-Saharan Africa (58%), Asia (21%), and South America (18%). Among the 608 patients (83%) traveling to malaria-endemic areas, malaria prophylaxis was in accordance with guidelines in 578/608 patients (95.1%, 95% CI: 93–96.5), and doxycycline was the regimen of choice (48%). Inappropriate malaria prophylaxis was given to eight patients, one of whom developed plasmodium falciparum malaria. All 413 patients (100%, 95% CI: 99–100) traveling

to yellow fever-endemic areas who needed vaccination were correctly vaccinated. However, three patients received yellow fever vaccination without indication. Also, 442 of 454 patients (97.4%, Alectinib in vitro 95% CI: 95.4–98.5) eligible to receive hepatitis A vaccination were immunized. Conclusion. Appropriate advice for malaria prophylaxis, yellow fever, and hepatitis A vaccinations was provided in a travel medicine and vaccine center where trained physicians used a computerized decision support system. Even in this setting, however, errors can occur and professional practices should be regularly assessed to improve health care. In 2007, more than 4 million French residents traveled to a tropical area.1 When they

returned, 15 to 64% were diagnosed with a disease related to their journey.2–4 It is therefore important that travelers receive appropriate advice before their trip to reduce this risk of travel-related diseases. In France, GSI-IX in vitro the vast majority of travelers’ health advice is provided by travel clinics approved by the ministry of health, most of them being located in hospitals with tropical medicine departments. Also, prescribing medications (malaria prophylaxis, vaccination5,6) is usually restricted to physicians and cannot be delegated to nurses. To improve their services to travelers, travel clinics should regularly AMP deaminase assess the quality of travel health information given by health care professionals working in their setting. To assess the appropriateness of advice given to travelers in our center, we performed a 3-month prospective

study to measure the adequacy of prescriptions written for malaria prophylaxis, hepatitis A, and yellow fever vaccinations to the national recommendations. This prospective study was conducted from May 5 to August 5, 2008 in the Travel Medicine and Vaccine Center of Saint-Louis Hospital in Paris, France. This 3-month period before summer holidays was targeted because it is a time during which a high number of travelers come to our center for travel advice. Only travelers older than 15 years can be seen in our center. Travel visits take place each Saturday without appointment and are provided by 14 different physicians (two or three per Saturday), all trained in tropical medicine. Travelers can also have a scheduled visit during the week with the senior physician in charge of the travel medicine center. All patients therefore see a physician when they come to our center.

Tg2576 mice or wild-type (WT) littermates were treated daily with MRK-560 (30 μmol/kg) or vehicle for 4 (acute) or 29 days (chronic). The subsequent MEMRI analysis revealed a distinct axonal transport dysfunction in the Tg2576 mice compared with its littermate controls. Interestingly, the impairment of axonal transport could be fully reversed by chronic administration of MRK-560, in line

with the significantly lowered levels of both soluble and insoluble forms of Aβ found in the brain and olfactory bulbs (OBs) following Osimertinib supplier treatment. However, no improvement of axonal transport was observed after acute treatment with MRK-560, where soluble but not insoluble forms of Aβ were reduced in the brain and OBs. LY294002 order The present results show that axonal transport is impaired in Tg2576 mice compared with WT controls, as measured by MEMRI. Chronic treatment in vivo with a gamma-secretase inhibitor, MRK-560, significantly reduces soluble and insoluble forms of Aβ, and fully reverses the axonal transport dysfunction. “
“The reaction times of saccadic eye movements have been studied extensively as a probe for cognitive behavior controlled by large-scale cortical and subcortical neural networks. Recent studies have shown that the reaction times of targeting saccades

toward peripheral visual stimuli are prolonged by fixational saccades, the largest miniature eye movements including microsaccades. We have shown previously that the frequency of fixational saccades is decreased by volitional action preparation controlled internally during the antisaccade paradigm (look away from a stimulus). Instead, here we examined whether fixational saccade modulation induced externally by sensory events could also account for targeting saccade facilitation by the same sensory events. When targeting saccades were facilitated by prior fixation stimulus disappearance Janus kinase (JAK) (gap effect), fixational

saccade occurrence was reduced, which could theoretically facilitate targeting saccades. However, such reduction was followed immediately by the rebound of fixational saccade occurrence in some subjects, which could eliminate potential benefits from the previous fixational saccade reduction. These results do not mean that fixational saccades were unrelated to the gap effect because they indeed altered that effect by delaying targeting saccade initiation on trials without the fixation gap more strongly than trials with it. Such changes might be attributed to the disruption of volitional saccade preparation because the frequency of fixational saccades observed in this study was associated with the ability of volitional control over antisaccade behavior.

g. disease-specific or health-related quality of life). In 14 of the 16 (88%) studies Linsitinib concentration reporting

prescribing outcomes, analyses were based on 90% or more of participants at baseline. In seven studies, the authors reported statistical analyses were adjusted for possible clustering effects. Of 20 studies with a comparison group, nine addressed the issue of possible contamination of the study groups (for example, physicians or pharmacists were only allocated sessions with intervention or control patients). Table 5 summarises the number of studies reporting at least one positive outcome and statistically significant improvement in favour of the CDSS on the majority (≥50%) of outcomes. All 21 studies reported at least one positive outcome (prescribing,

clinical or patient); two-thirds had statistically significant results in favour of CDSS on the majority of outcomes (Table 5). Studies addressing drug-safety issues were more likely to report statistically significant changes in the desired direction on the majority of outcomes than QUM studies (91 versus Etoposide molecular weight 40% studies with statistically significant changes on the majority of outcomes reported). This difference in proportions was statistically significant (P= 0.01) More studies showed CDSS benefits if systems were conducted in institutional rather than ambulatory care settings (88% of studies reporting statistically significant changes on the majority of outcomes versus 54%), were user-initiated compared to system-initiated (100 versus 88%), and involved CDSS alone rather than multi-faceted interventions (75 versus 62%). However, none of the differences in proportions for these comparisons was statistically significant.

Studies reporting prescribing outcomes, a surrogate measure, rather than clinical outcomes were more likely to show positive results (100 versus 0% of studies reporting these outcomes, P= 0.002). None of the five studies reporting patient outcomes demonstrated statistically significant changes on the majority of these outcomes. There were too few studies across the individual Amrubicin clinical domains to draw any conclusions about the impact of CDSS in specific clinical areas. All six studies reporting prescribing outcomes demonstrated at least one measure in favour of the CDSS and three reported significant improvements on the majority of prescribing outcomes. Of the latter, two[16,17] used the same methods and intervention to increase prescribing of secondary prevention medications in patients with coronary heart disease; the only difference was the setting (teaching hospital, community hospital). The third study[22] addressed switching calcium-channel blockers to other antihypertensive agents and dose changes for angiotensin-converting enzyme (ACE) inhibitors in the setting of a US Veterans Affairs clinic. None of the QUM studies reported significant improvements on the majority of clinical or patient outcomes assessed.

, 1997; Viprey et al., 1998; Kaneko et al. 2000; 2002; Göttfert et al., 2001; Krishnan et al., 2003; de Lyra Mdo et al., 2009; see http://www.kazusa.jp/rhizobase/). The genes encoding the core components of rhizobial T3SS are called rhc (Rhizobium conserved) and are located in a gene cluster known as tts (type three secretion) (Viprey et al., 1998). Mutational studies Selleck Gefitinib on the tts gene clusters provided the first evidence

that rhizobia deficient in T3SS are positively or negatively impaired in their ability to form nodules, depending on their hosts (Meinhardt et al., 1993; Bellato et al., 1997; Viprey et al., 1998; Marie et al., 2001; Krause et al., 2002; Deakin & Broughton, 2009). Most of the rhizobial T3S genes are expressed in response to plant flavonoids. Their promoter regions harbor a regulatory motif known as tts box (Viprey et al., 1998; Krause et al., 2002; Krishnan et al., 2003; Hubber et al., 2004; López-Baena et al., 2008; Zehner et al., 2008; Sánchez et al., 2009), a binding site for the transcriptional activator TtsI whose production is flavonoid dependent (Kobayashi et al., 2004; Marie et al., 2004; Wassem et al., 2008). In B. japonicum, the expression of the T3SS genes is induced by seed extract and genistein that is also an inducer of the nodulation genes (Krause et al., 2002; Süß et al., 2006; Wei

et al., 2010). Transcriptional profiling revealed that T3SS genes of B. japonicum NU7441 purchase are downregulated in bacteroids relative to free living conditions, suggesting SB-3CT that the secretion of proteins via the T3SS may play a role during the nodule initiation (Chang et al., 2007). Rhizobial proteins secreted by T3SSs are designated Nops (nodulation outer proteins) (Marie et al.,

2001). The specific roles of the various effector proteins in nodulation are not yet known, although a few of them have been shown to affect the nodulation in a host-dependent manner (Marie et al., 2003; Skorpil et al., 2005; Dai et al., 2008; Yang et al., 2009). Despite the importance of type III secretion in pathogenesis, there has been very little work on its function in symbiotic bacteria. Previous studies have shown that B. japonicum contains a functional T3S and > 30 putative T3S effector genes, many of which have homologs in plant and animal pathogenic bacteria (Göttfert et al., 2001; Kaneko et al., 2002; Krause et al., 2002; Süß et al., 2006; Yang et al., 2010). Proteomic analyses have shown that at least 14 effectors are secreted in culture (Süß et al., 2006; Zehner et al., 2008; Hempel et al., 2009). So far, the only secreted protein studied in B. japonicum is NopE1 (Wenzel et al., 2010; Schirrmeister et al., 2011), while a biochemical role of some other T3S secreted proteins can be inferred from the studies of their homologs in other rhizobia. NopT1 and NopT2, two putative T3S effectors of B. japonicum, share homology to members of the YopT/AvrPphB family.

We thank Professor L. Chieco Bianchi, Professor F. Zacchello, Dr E. Ruga, Dr A. M. Laverda, Dr R. D’Elia and Ms S. Oletto (Padua); Dr T. Schmitz, Dr R. Weigel and Dr S. Casteleyn (Berlin); Dr S. Burns, Dr N. Hallam, Dr P. L. Yap selleckchem and Dr J. Whitelaw (Edinburgh); Ms A. van der Plas and Ms E. M. Lepoole

(Amsterdam); Dr K. Westling, Ms A. B. Hjelm, A. Aronsohn and L. Rolfhamre (Sweden); Dr A. Ferrazin, Dr R. Rosso, Dr G. Mantero, Professor S. Trasino, Dr B. Bruzzone, Dr M. Setti and Dr J. Nicoletti (Genoa); Dr E. Mur (Barcelona); Dr G. Zucotti (Milan); Professor P. A. Tovo and Dr C. Gabiano (Turino); Dr T. Bruno (Naples), The Regional Health Office and RePuNaRC (Naples); M. Kaflik (Medical University of Warsaw, Poland). We would like to thank Dr C. Townsend for her helpful comments on drafts of this paper. Financial support The ECS is a co-ordination action of the European Commission (PENTA/ECS 018865). CT is supported by a Wellcome Trust Research Career Development Fellowship. The centre at Universita degli Studi di Padova is supported by Progetto di Ricerca sull

AIDS – Istituto Superiore di Sanità– 2006. Writing committee: K. Boer, K. England, M. H. Godfried and C. Thorne. Dr C. Thorne, Professor M. L. Newell, Ms S. Mahdavi and Dr K. England (ECS Co-ordinating Centre, UCL Institute of Child Health, London, UK); Dr C. Giaquinto, Dr O. Rampon, Dr A. Mazza and Professor A. De Rossi (Universita degli Studi di Padova, selleck compound Italy); Professor I. Grosch Wörner (Charite Virchow-Klinikum, Berlin, Germany); Dr J. Mok (Royal Hospital for Sick Children, Edinburgh, UK); Dr Ma I. de José, Dra B. Larrú Martínez, Dr J. Ma Peña, Dr J. Gonzalez Selleckchem Abiraterone Garcia, Dr J. R. Arribas Lopez and Dr M. C. Garcia Rodriguez (Hospital Infantil La Paz, Madrid, Spain); Professor F. Asensi-Botet,

Dr M. C. Otero and Dr D. Pérez-Tamarit (Hospital La Fe, Valencia, Spain); Dr H. J. Scherpbier, Ms M. Kreyenbroek, Dr M. H. Godfried, Dr F. J. B. Nellen and Dr K. Boer (Academisch Medisch Centrum, Amsterdam, The Netherlands); Dr L. Navér, Dr A. B. Bohlin, Dr S. Lindgren, Dr A. Kaldma and Dr E. Belfrage (Karolinska University Huspital, Huddinge and Solna, Sweden); Professor J. Levy, Dr P. Barlow, Dr Y. Manigart, Dr M. Hainaut and Dr T. Goetghebuer (Hospital St Pierre, Brussels, Belgium); Professor B. Brichard, Dr J. J. De Bruycker, Ms N. Thiry and Ms H. Waterloos (UCL Saint-Luc, Brussels, Belgium); Professor C. Viscoli (Infectious Diseases Clinic, University of Genoa, Genoa, Italy); Professor A. De Maria (Department of Internal Medicine, University of Genoa and S.S. Infettivologia, Istituto Nazionale per la Ricerca sul Cancro, IST, Genova, Italy); Professor G. Bentivoglio, Dr S. Ferrero and Dr C.