, 2009). We also found evidence of genetic exchange between Xanthomonas and Betaproteobacteria. A contig from Xcm 4381 (Fig. 2c) most

closely resembled the genome of Acidovorax species JS42 (95% sequence identity over 7935 nucleotides) and, slightly more distantly (94% identity over 3327 nucleotides), resembled the genome of X. campestris pathovar vesicatoria 85-10. This region encodes a predicted learn more TrbK-like protein. TrbK is usually plasmid associated (Haase et al., 1996), but the corresponding genomic regions in Acidovorax species JS42 and in X. campestris pathovar vesicatoria 85-10 appear to be chromosomally located. It is unclear whether the 23-kb Xcm 4381 contig (Fig. 2c) represents a plasmid or is part of the chromosome. Plant-pathogenic Xanthomonas pathovars require a T3SS to secrete and translocate effector proteins (Alfano & Collmer, 2004; Yang et al., 2005; Grant et al., 2006; Gurlebeck et al., 2006;

White et al., 2006, 2009; Kay & Bonas, 2009; Buttner & Bonas, 2010) in order to cause disease. These effectors have evolved to manipulate host cellular processes to the benefit of the pathogen; however, many plants have evolved resistance whereby they can recognize specific effectors, triggering the hypersensitive response. Therefore, in the context of a resistant plant, these effectors show an ‘avirulence’ activity, thus limiting the pathogen’s host range (Alfano & Collmer, 2004; Yang et al., 2005; Grant et al., 2006; Gurlebeck et al., 2006; White et al., 2006, 2009; IMP dehydrogenase Kay & Bonas, 2009; Buttner & BTK inhibitor supplier Bonas, 2010). A single Xanthomonas genome

typically encodes 20–30 T3SS effectors. The repertoire of effectors varies between species and strains within species and is believed to be a key determinant in the host range of a given pathogen. The draft genomes of both Xcm 4381 and Xvv 702 encoded a complete T3SS apparatus. To identify homologues of known T3SS effectors, we used blast searches against catalogues of proteins from the Pseudomonas syringae Hop Identification and Nomenclature Home Page (http://www.pseudomonas-syringae.org/), The Xanthomonas Resource (http://www.xanthomonas.org/t3e.html) and papers by White et al. (2009) and Gurlebeck et al. (2006). In common with all previously sequenced Xanthomonas genomes, both draft genomes encode homologues of the candidate T3SS effectors AvrBs2, AvrGf1, XopF, XopK, XopL, XopN, XopP, XopQ, XopR, XopX and XopZ. Both strains also encode homologues of XopA, XopB, XopG, XopH, XopI, XopY, XopAA, XopAD, XopAE and XopAK, which are conserved in a subset of the previously sequenced Xanthomonas genomes (http://www.xanthomonas.org/t3e.html). Both Xcm 4381 and Xvv 702 also encode proteins sharing 71% amino acid sequence identity with P. syringae effector HopW1; these have no significant sequence similarity to any known Xanthomonas protein (Fig. 3). Both draft genomes contained genes encoding homologues of the P.

These observations,

combined with the above-mentioned demonstrations of human resistin storage in neutrophil granules and resistin release in response to microbial stimuli, indicate that neutrophil granules were the source of the resistin released in our study. This conclusion is supported by the simultaneous release of resistin and granule-associated elastase (Fig. 4a and b). We have little information on how degranulation of neutrophils is stimulated by leukotoxin. Johansson et al. (2000) reported that leukotoxin induced degranulation of PMNs and that the polyclonal antibodies against LFA-1 subunits had no effect on degranulation. Moreover, signals involved in triggering degranulation by neutrophils stimulated by leukotoxin are poorly understood. Integrins, which are heterodimeric transmembrane adhesion receptors localized at cell–matrix selleck inhibitor contact sites, link extracellular matrix components to the actin cytoskeleton and interact with multiple structural and signaling molecules. LFA-1, a member of the β2-integin family, including CD11a and CD18, is a leukotoxin receptor located on the GSK-3 phosphorylation surface of neutrophils (Lally et al., 1997). The significant decrease in leukotoxin-induced resistin release from

neutrophils pretreated with TS1/18 in the present study provides evidence for the involvement of CD18 in resistin release (Fig. 5a), as a recent study reported that CD18 is essential for the biological effect induced by leukotoxin (Dileepan et al., 2007). Our results differ from those reported by Johansson et al. (2000), and we cannot completely explain the discrepancy. It is possible the polyclonal antibodies used by Johansson et al. (2000) were less effective than the monoclonal antibodies that we used in the inhibition study. Furthermore, the inhibition

of leukotoxin-induced resistin release from neutrophils incubated with PP1 indicates that an Src family tyrosine kinase participates in resistin release (Fig. 5a). Src family tyrosine kinases have been reported to be important mediators acting downstream of integrins to affect adhesion-dependent degranulation of neutrophils (Mocsai et al., 1999). Although PP1 inhibited adhesion-dependent degranulation, it had no effect on adhesion-independent Alanine-glyoxylate transaminase degranulation induced by phorbol 12-myristate 13-acetate. The results obtained from experiments with TS1/18 and PP1 suggest that leukotoxin binds to LFA-1 on the surface of neutrophils and then activates an Src family tyrosine kinase, leading to the release of resistin from neutrophils by degranulation, as well as adhesion-dependent degranulation. Release of resistin and elastase still occurred, but a lower level, when stimulated by the mutant strain (Fig. 4). Moreover, pretreatment with TS1/18 or PP1 inhibited release of resistin and elastase from neutrophils stimulated by the mutant strain (Fig. 5a and b). Another molecule of A. actinomycetemcomitans might interact with CD18.

29%) and all clones in microcosm MY11 belonged to alphaproteobacterial magnetotactic cocci, no identical OTU was found between them. The most related OTUs from MY8 and MY11 were this website OTU 29 and OTU 51 with 98.89% similarity. Other OTUs from MY8 showed ≤97% similar to that from MY11 (Fig. 3). The communities of MTB within each microcosm did vary from February to April (Fig. 2b). For microcosm MY8, although ‘M. bavaricum’-like OTU 1 was

most dominant in MY8a (84.21%), it dramatically decreased in March and April, and only left 16.67% and 18.52% in the libraries MY8b and MY8c, respectively. OTU 8 comprised 5.26% of MY8a; however, it significantly increased to 79.17% and 77.78% in MY8b and MY8c, respectively, and became the most dominant group. OTUs 2, 29 and 50, on the other hand, were time specific. For microcosm MY11, OTU 14 was the dominant group in MY11a (52.94%),

but it was not observed in MY11b and MY11c (Fig. 2b). In contrast, OTU 51, not detected in MY11a, became the most dominant OTU in MY11b (82.60%) and MY11c (80.95%). OTU 17 was relatively evenly distributed over time (4.35–14.29%). OTU 15 was detected only in MY11a (5.88%) and MY11b (4.35%), while OTU 53 was only found in MY11b (4.35%) and MY11c (4.76%). Other OTUs were time specific, for example OTUs 13 and 21 were solely observed in MY11a and OTU 52 was specifically detected in MY11b. The MTB communities in six clone libraries were compared using unweighted unifrac analysis. Tanespimycin molecular weight The PCoA plot showed that MTB clustered by microcosms rather than collection time (Fig. 4a). Samples from microcosm MY11 clustered together to the left along PC1, which accounted for 66.7% of the variation, while samples from

microcosm MY8 grouped to the right. This result was supported by Jackknife environment clusters MG-132 purchase with high Jackknife values (Fig. 4b). Pearson’s correlation analysis between the unweighted PC1 factors and the physical–chemical variables demonstrated that the former significantly correlated with the concentrations of NO3− (Table 2, P<0.05). Because few efforts have been made to explore the distribution and ecology of MTB, so far, knowledge on spatiotemporal variations of MTB communities is scarce. In the present study, a combination of a molecular approach, unifrac analysis of phylogenetic data and Pearson’s correlation analysis of two freshwater sediment microcosms provides an insight into the dynamics of MTB communities in nature. 16S rRNA gene analysis shows that the majority clones of both microcosms MY8 and MY11 belong to magnetotactic cocci within Alphaproteobacteria (64.29% of clones from MY8 and all clones from MY11), which is normally the dominant type of MTB found in most freshwater and marine environments (Amann et al., 2006; Lin & Pan, 2009; Pan et al., 2009a). The presence of ‘M. bavaricum’-like MTB, confirmed by our previous observation in Lake Miyun (Lin et al., 2009), is only detected in microcosm MY8 (Fig. 3).

3E–E6) suggests that these cells first migrate caudally in the

lateral subpallium before turning, and migrating in the lateral-to-medial direction within the EA. In sum, our analysis revealed that scgn+ cells cytoarchitecturally resembling migrating neurons formed a continuous stream along the palliosubpallial boundary before reaching their final destinations in the OB or EA (Fig. 4). Next, we analyzed the distribution of scgn+ neurons BKM120 molecular weight in neonatal mouse brain. We observed that the migration of scgn+ cells concluded by birth and scgn+ neurons inhabited, in an anterior-to-posterior direction, the spatially interrelated nuclei of the BST, interstitial nucleus of the posterior limb of the anterior commissure (IPAC), ventral pallidum (VP), dorsal substantia innominata (SI), and the central and medial amygdaloid nuclei (CA and MA; Fig. 5A–A7). Morphometric analysis revealed that scgn identifies divergent neuron

subpopulations with different somatic diameters in the VP and EA (Fig. 5B). By using genetically tagged reporter mice we demonstrated that scgn+ neurons either adopted a GABA phenotype along the longitudinal axis of the EA (Fig. 5D and D1), similar to scgn+/GABA+ neurons in AZD5363 datasheet the embryonic OB (Fig. 5C and C1), or co-express ChAT when found in small-diameter cholinergic neurons of the dorsal SI (Fig. 5E and E1). Collectively, our data suggest that by E18 scgn+ neurons can acquire a distribution pattern resembling that in the adult brain, and differentiate into neurochemically distinct subtypes of EA

neurons. Systematic analysis along the longitudinal axis of the fetal primate brain revealed the first contingent of scgn+ neurons in the granular and glomerular layers of the OB (Fig. 6A). However, unlike in the adult primate brain (Mulder et al., 2009b), neuroblasts migrating in the prenatal rostral migratory stream (Pencea & Luskin, 2003) did not harbour scgn expression (Fig. 6A). Pallial areas were devoid of discernible new scgn immunoreactivity. In the basal forebrain, scgn+ neurons were seen in the horizontal diagonal band, nucleus accumbens, medial septum, VP, GP and SI (Fig. 6A1–A7). In contrast to scgn distribution in the neonatal rodent brain, scgn+ cells were only infrequently found in either the CA or MA. In the hypothalamus, substantial scgn+ neuron populations occupied the paraventricular and periverticular nuclei and the supraoptic nucleus (Fig. 6A5–A7). A morphological dichotomy of scgn+ neurons was evident in the basal telencephalon (Fig. 6B): small-to-medium-sized scgn+ neurons populated the horizontal diagonal band, SI and CA. In contrast, large-diameter scgn+ neurons were found in the IPAC and GP.

95, P = 0.11 and P = 0.57 respectively): overall, the basic model explained the data best. Misclassification

bias, due to bacterial sepsis causing severe disease manifestations in children with co-incidental parasitaemia, was assessed by PCR to detect NTS or S. pneumoniae bacteraemia in 160 (54.1%) study subjects with suitable samples (85 of 169 (50.3%) UM and 75 of 127 (59.1%) SM cases); none (95% CI 0–2.3%) were positive. Additionally no study subjects received intravenous antibiotics, making significant misclassification unlikely. selleck inhibitor Sensitivity analysis revealed that the model was highly robust to a realistic range of variation in parameters ( Table 4). The power to detect a 7-fold difference in median sequestered biomass between subjects with UM and SM, UM and SNP, and UM and LA, was 87%,

76%, and 72% respectively. Improved understanding of the pathophysiology of SM may allow a rational approach to improving supportive care, and provide explanations for why so many interventions to date have proved ineffective or even harmful.9 and 10 Unraveling the pathophysiology of SM is difficult because studies in humans can only describe associations, and cannot prove causality, whilst the relevance of animal models of SM in humans is contentious.35 Microcirculatory impairment is often thought to be central to the pathogenesis of both CM and LA,11, 18 and 19 but it is not conclusively established whether extensive pRBC sequestration DAPT price is the primary cause of microcirculatory impairment,36 or a consequence of inflammatory endothelial activation and dysfunction which then facilitates pRBC sludging and adherence.11, 17 and 37 Furthermore, it is uncertain whether different mechanisms underlie different SM syndromes. The assumption

www.selleck.co.jp/products/azd9291.html that a single mechanism, pRBC sequestration, causes all SM, led the authors of a recent study to conclude that a “U-shaped” relationship between plasma PfHRP2 and mortality was due to many children with low PfHRP2 concentrations dying from non-malarial causes.30 Another explanation for this interesting observation is that SM arises from heterogeneous mechanisms, some related to high parasite burden, and some occurring at lower total parasite burden. The present study was undertaken to assess the role of one of the most fundamental processes in P. falciparum malaria, the sequestration of pRBCs, in causing severe disease. If SM is caused by extensive sequestration of pRBCs within the microvasculature, then the sequestered biomass would be expected to be higher in SM than in UM. We found that all indices of parasite biomass (parasitaemia, parasite density, PfHRP2 concentration, circulating parasite biomass, and total parasite biomass) except the sequestered biomass were higher in SM compared with UM, suggesting that extensive pRBC sequestration does not uniformly underlie SM.

As SRL has a long-half-life, C0 obtained 5–7 days after

the start of treatment or dosage change should be used Selleck CP 868596 to determine dose adjustments while 4 days at the most is needed for EVR owing to its shorter half-life. After the initial dose titration, weekly SRL C0 measurements during the first month, then every 2 weeks, have been recommended [55]. There are several assays available to measure blood mTOR inhibitor levels, with High-Pressure Liquid Chromatography coupled with Mass Spectrometry (HPLC/MS) being the most accurate and specific method. Immunoassay is also a reliable and more convenient alternative. It is important to know which assay is being used, as immunoassays may lead to overestimation of EVR and SRL concentrations as a result of cross-reactivity with metabolites [56]. Differences in immunosuppressive dosages and regimens among the studies make it difficult to determine the optimum dosing strategy for TAC with mTOR inhibitors. Therapeutic target ranges for TAC when

used in combination with EVR or SRL are not as yet established. It should be Venetoclax nmr remembered, however, that higher doses of mTOR inhibitors are required when administered with TAC than with CsA [44]. In general, there is little interaction between TAC and mTOR inhibitors, whereas interactions between CsA and mTOR inhibitors are more pronounced and result in higher blood levels of mTOR inhibitors [40] and [44]. Consequently, higher starting doses of EVR are needed when combined with low-dose TAC than with CsA to

prevent increased risk of rejection. In addition, careful concentration monitoring of both EVR and SRL is advisable when patients are switched between CNIs [34]. Thymidylate synthase The EVR/CsA interaction is one of the reasons twice-daily dosing is recommended for EVR. Clinical data on the use of EVR or SRL in TAC minimization strategies in renal transplantation are limited. Available evidence suggests that treatment with EVR allows early and substantial TAC minimization when used with basiliximab induction and corticosteroids. The lack of clear differentiation in TAC exposure between standard- and reduced-dose TAC groups in the US09 and ASSET studies highlights ongoing reluctance to reduce CNI exposure even in the presence of EVR. SRL has also been used successfully as part of a TAC-minimization strategy, resulting in similar efficacy and less nephrotoxicity when compared with SRL/standard TAC. However, comparative studies support the use of other regimens (e.g., SRL/MMF, MMF/TAC) over SRL/TAC in this population. The findings with SRL, however, reflect single-center experiences. AEs are common in all transplant patients receiving immunosuppressive therapy. Several safety concerns may arise from using an mTOR inhibitor and TAC minimization therapy.

The study conforms to the APS Guiding Principles for the Care and Use of Animals in Research. A total of 20 ESDs were performed (10 with each technique). The dissection time was shorter with HK-CB (4.9±3.2 vs. 13.8 ±10.8 min; p=0.002), even if the time to apply the CB device was included (9.0±6.5 vs. 13.8±10.8 min; p=0.008). The dissection speed was faster with HK-CB (0.8±0.4 vs. 0.4±0.3 cm2/min; p=0.014), No differences were observed in the remaining variables. There was one perforation in each group. The CB traction method shortens the duration of the dissection phase of gastric ESD in a live porcine model. This method may facilitate the introduction of ESD

especially in the beginning of the learning curve. check details “
“After non-curative endoscopic submucosal dissection (ESD) for differentiated-type early gastric cancer (EGC), if a positive lateral margin (LM) or piecemeal resection is the only non-curative factor, non-surgical management (close observation or immediate additional endoscopic treatment) can be performed instead of gastrectomy due to the negligible risk

of metastasis. However, the most appropriate management is unknown because of Selleck Copanlisib limited research. To examine the long-term outcomes and risk factors for residual/recurrent cancer in non-curative ESD cases of differentiated-type EGC with a positive LM or piecemeal resection. Among 3,782 EGC lesions (3,316 Nintedanib (BIBF 1120) patients) treated with ESD at our institution between 1997 and 2010, 85 non-curative differentiated-type EGC lesions (83 patients) were included in this study which met both of the following criteria: i) non-curative factor limited to a positive LM or piecemeal resection, and ii) follow-up period > 1 year. These patients underwent gastrectomy, immediate additional endoscopic treatment, or close observation after ESD. Close observation was performed only when no residual tumor was found endoscopically just after

ESD, and involved endoscopic follow-up every 3 to 6 months with computed tomography as needed for the first 3 years, followed by annual follow-ups. We retrospectively evaluated the occurrence of residual/locally recurrent cancer, metastasis, metachronous gastric cancer and death. To identify risk factors for residual/recurrent cancer among various clinicopathological features (see Table 1), univariate and multivariate logistic regression analyses were performed. The clinical course is summarized in Figure 1. The median follow-up period was 50 months (range 13-163). A total of 16 of the 85 lesions (18.8%) had residual/locally recurrent cancer; no metastasis occurred. The median period for local recurrence after ESD was 13 months (range 4-89). All residual/locally recurrent lesions were mucosal differentiated-type adenocarcinoma. There were 12 cases of metachronous gastric cancer. The 5-year disease-specific and overall survival rates were 100% and 92.1%, respectively.

For detection and/or quantification of cell death, forward/sideward light scattering analysis and AnnexinV/propidium iodide-staining were used as described (Bernhard et al., 2003). AnnexinV/PI− staining allows the discrimination of intact viable cells (AnnexinV− negative and PI− negative), early apoptotic (AnnexinV− positive and

PI− negative) and necrotic cells (AnnexinV− positive and PI− positive). The number of viable cells was determined using the XTT assay (Biomol GmbH, Hamburg, Germany). HUVECs were seeded into gelatine coated 96-well plates. After 24 h the medium was replaced by fresh medium and the cells were treated with various Cd concentrations ATM/ATR inhibitor review for the indicated times. For further details see manufacturers’ instructions. The amount of BTK inhibitor lactate dehydrogenase (LDH) released from cells was quantified using the LDH cytotoxicity kit II (Biovision) according to the manufacturer’s instructions. For the detection and quantification of nuclear DNA content, HUVECs were seeded into gelatine coated 6-well plates and allowed to adhere over night. After replacing the medium with fresh medium, the cells were incubated with various Cd concentrations for the indicated times. After enzymatic detachment, the cells were permeabilized with saponin (1 mg/ml), stained with propidium iodide (50 μg/ml) and analysed and quantified

by flowcytometry using a Cytomics FC 500 (Beckmann Coulter, Brea, CA, USA). To analyse the subcellular localization of DNAse II, HUVECs were treated with Cd for the indicated times. After treatment, the cells were washed with PBS and fixed with 4% PFA for

3 min at room temperature. Fixed cells were washed with PBS and permeabilized with 0.3% Triton X-100 for 30 min. Following an additional washing step with PBS, non-specific binding sites were blocked with 1% bovine serum albumin (BSA) in PBS for 30 min at room temperature followed by staining with primary antibody against DNAse II (mouse polyclonal antibody, Abnova GmbH, Heidelberg, Germany; 10 μg/ml) for 1 h at room temperature. After 3 washing steps with PBS, the cells were incubated with secondary antibody (Alexa Fluor 488, Bay 11-7085 goat anti-mouse, Invitrogen, Carlsbad, CA, USA) for 1 h in the dark and at room temperature. Thereafter, the monolayer was washed 3 times with PBS and nuclear staining was performed using propidium iodide (1 μg/ml) for 8 min at room temperature in the dark. After 3 final washing steps, cells were mounted in ProLong Gold (Invitrogen, Carlsbad, CA, USA) and analysed using a LSM 510 Meta attached to an Axioplan 2 imaging MOT using ZEN software (Zeiss, Oberkochen, Germany). To analyse cytosolic nuclease activity of Cd treated HUVECs, nuclear DNA was extracted from endothelial cells using a DNA purification kit (Promega GmbH, USA). Nuclear DNA (2 μg) was then incubated with cytosolic extracts of Cd-treated HUVECs and controls (30 μg) for 3 h at 37 °C. DNA fragmentation was analysed by agarose gel electrophoresis (0.5%).

This condition is known as pericardial constriction, or constrictive pericarditis. Several imaging modalities are used to evaluate the pericardium, including MR, computed tomography, and echocardiography, which can all play a complementary role aiding diagnosis. This article focuses on MR imaging and its role in the detection and evaluation of pericardial constriction.

MR imaging has many advantages compared with other modalities including precise delineation of the pericardial thickness, evaluation of ventricular function, detection of wall motion abnormalities, and provision of information about common (and potentially buy CYC202 harmful) sequelae of pericardial constriction. Kimberly Kallianos, Gustavo L. Moraes, and Karen G. Ordovas The role of cardiac magnetic resonance (MR) imaging as a prognostic tool in patients with ischemic heart disease is well established. However, an increasing body of data now demonstrates that cardiac MR imaging can provide prognostic information in a variety of nonischemic and diffuse myocardial diseases including myocarditis, dilated and hypertrophic cardiomyopathies, sarcoidosis, amyloidosis, and arrhythmogenic selleck products right ventricular cardiomyopathy. Cardiac MR imaging can also supply incremental information above established prognostic indicators, providing an additional tool for

use in the prediction of disease progression, response to treatment, and risk stratification. David M. Naeger and Spencer C. Behr PET and magnetic resonance (MR) imaging have each become essential tools in the workup and management of cardiac patients. Combined PET/MR systems have recently been developed, allowing for single-session imaging using both modalities. Sitaxentan This new technology holds great promise for cardiac applications given the different, yet complementary, information each modality provides. Research in

this area is still nascent, although early studies have been promising. Ashenafi M. Tamene, Carolina Masri, and Suma H. Konety Patients with cancer are subject to short-term and long-term adverse cardiovascular outcomes from cancer therapies. It is important to identify patients at risk for cardiotoxicity so that appropriate therapy can be instituted early. Cardiovascular magnetic resonance (MR) imaging is emerging as a promising imaging modality with unique applications beyond standard left-ventricular systolic function assessment. It can provide comprehensive evaluation of most cardiac structures in one setting. This article provides an overview of cardiac MR imaging in cardio-oncology. Masaki Ishida and Hajime Sakuma Magnetic resonance (MR) imaging of the coronary arteries has been challenging, owing to the small size of the vessels and the complex motion caused by cardiac contraction and respiration.

Ces lignes datent de 15 ans. Aujourd’hui, on peut répondre que les méthodes invasives sont de moins en moins agressives, tandis que l’ARM comme le PET-scan n’ont qu’une spécificité relative avec un certain nombre de faux-positifs et de faux-négatifs. L’apparition toute récente, il y a quelques mois de la méthode de la compression pour l’IRM avec un temps d’acquisition des images très court, de l’ordre de 15 minutes au lieu de 45 minutes avec une meilleure qualité, rend compte de la nécessité de suivre

de très près les techniques d’avenir. C’est ce que faisait Jean en assistant tous les ans à Chicago à la réunion de l’ARNA (Société de radiologie Protein Tyrosine Kinase inhibitor nord-américaine) et en rapportant ensuite devant l’Académie

de médecine les dernières nouveautés qui peuvent être des bouleversements. Mais il faut des moyens techniques pour « faire connaître le savoir » find more et le Collège français de pathologie vasculaire est fondé le 21 avril 1966 avec comme Président, le Doyen Fontaine et comme Secrétaire général, Claude Olivier. Jean en fait partie rapidement, entre au Conseil d’administration en 1968, est le Président du congrès en 1976, le Secrétaire général de 1977 à 1990 et le Président de 1990 à 2002, mais ce Collège était « SDF ». En 1998, le siège du Collège français de

pathologie Urocanase vasculaire est établi 18, rue de l’Université dans le 7e arrondissement de Paris, dans des locaux que Claude Olivier avait repérés lors d’une de ses promenades dans le quartier et qui devait faire l’objet d’une prochaine vente aux enchères. Jean s’est rendu à cette vente à la chandelle et l’avait acquis, mais sa qualification de local commercial a été contestée : il aurait été occupé « bourgeoisement » quelque vingt ans plus tôt. Heureusement, grâce à votre serviteur et à la chance, nous avons pu le conserver. C’est ainsi qu’est née cette « Maison de l’angiologie » que beaucoup de sociétés nous envient. Enfin, en 1999, le siège du congrès dans des lieux historiques mais mal commodes pour une réunion qui devenait d’année en année plus importante a été transféré à la Maison de la Chimie. Il convient de rappeler dans ce bref historique le rôle essentiel de notre secrétaire, Françoise Staub, qui a accompagné le Collège pendant ces pérégrinations, ainsi que celui du cabinet Fournier qui assure tout ce côté financier que nous serions incapables de maîtriser. Cette date de 1999 est la dernière que j’ai retrouvée dans la liste des livres et des monographies qu’il adressait après leur publication à la bibliothèque de l’Académie de Médecine.