On average, someone has a stroke every 40 seconds. The gaps for patients diagnosed with a stroke are the availability

of physicians who specialize in stroke care and access to evidence-based stroke care. Telemedicine has assisted in bridging this gap to provide effective stroke treatment. The purpose of this article is to describe how the implementation Selleckchem SKI606 of a hub and spoke model using telemedicine has assisted in increasing patient access to neurology expertise and receiving evidence-based treatment of recombinant tissue plasminogen activator, thereby improving patient outcomes. Cindy Murray, Elizabeth Ortiz, and Cay Kubin The purpose of this article is to present an option for a model of care that allows small rural hospitals to be able to provide specialty physicians for critical care patient needs in lieu of on-site critical care physician coverage. A real-time, 2-way audio and video remote presence robot is used to bring a specialist to the bedside to interact with patients. This article discusses improvements in quality and finance outcomes as well as care team and patient satisfaction associated with this model. Discussion also includes expansion of the care model to the emergency department for acute stroke care. Kristine K. Powell and Rita J. Fowler This article describes the Baylor Health Care System (BHCS) approach to decreasing sepsis-related mortality within a large complex adaptive health care Selleck LY2109761 system. BHCS implemented

sepsis care improvement initiatives based on the Surviving Sepsis Campaign early goal directed therapy guidelines. By adhering to rigorous process improvement and evidence-based practice principles, BHCS has demonstrated improvements in sepsis care processes and a significant reduction in sepsis mortality. Amy Veenstra and Emylene Untalan Surgical patients with known or unknown obstructive sleep apnea are at increased risk for postoperative complications. By implementing evidence-based practices and a validated screening tool, the postoperative surgical patients at the authors’ hospital have Methamphetamine a decreased risk of postoperative complications, specifically oversedation.

This article discusses the pathophysiology, prevalence, risk factors, care of the postsurgical patient, and use of the validated STOP-Bang questionnaire with obstructive sleep apnea as the focus. Ryan Beseda, Susan Smith, and Amy Veenstra Providing evidence-based care to patients with return of spontaneous circulation after a cardiac arrest is a recent complex innovation. Once resuscitated patients must be assessed for appropriateness for therapeutic hypothermia, be cooled in a timely manner, maintained while hypothermic, rewarmed within a specified time frame, and then assessed for whether hypothermia was successful for the patient through neuroprognostication. Nurses caring for therapeutic hypothermia patients must be knowledgeable and prepared to provide care to the patient and family.

, 2007). Activation of FAK, which is demonstrated by an increase

in phosphorylation and its subsequent association to actin, was seen in endothelial cells treated with L. obliqua venom. Both processes follow a coincident time-dependent pattern at the first minutes, indicating a causal relationship of FAK phosphorylation with the assembly of actin stress fibers observed in vitro, and the rapid alterations AZD6244 nmr in endothelial response in vivo. Vascular injury is associated with increased expression of adhesion molecules, growth factors, cytokines and inducible enzymes by endothelial cells. Those enzymes not only contribute to the onset of the reaction through the synthesis of pro-inflammatory molecules, but also to the resolution of inflammatory response (Sprague and selleck inhibitor Khalil, 2009). The

sequential appearance of inducible enzymes in endothelial cells is a very characteristic of an inflammatory response and their induction is transcriptionally controlled by NF-κB activation (Chen et al., 1998). Accordingly, we have shown that L. obliqua venom directly induces NF-kB activation in endothelial cells that is followed by increasing expression of COX-2, iNOS and HO-1. These results are consistent with other studies that showed the release of PGI2 and NO by HUVEC stimulated with the venom fraction, Lopap ( Fritzen et al., 2005) and the up-regulation of COX-2 gene in fibroblasts ( Pinto et al., 2008). The induction of HO-1 by L. obliqua venom was higher at the latter time points of analysis (18 h). This enzyme catabolizes heme to generate billiverdin, bilirubin and carbon monoxide, and numerous studies have reported a role for HO-1 as a defense mechanism against oxidative insults. Additionally, it was also observed that endothelial cells are activated by L. obliqua venom to produce and secrete MMP-2/9, the two most important www.selleck.co.jp/products/Abiraterone.html MMPs expressed in endothelial cells ( Egeblad and Werb, 2002). Increased expression of tissues matrix metalloproteinases (MMPs) has been observed in almost every inflammatory condition. However, matrix degradation is neither the shared nor predominant function of

these enzymes. MMPs should not be viewed solely as proteinases of matrix catalysis, but rather as extracellular processing enzymes involved in regulating cell–cell and cell–matrix signaling events, quite typically, gain-of-function processing of latent proteins ( Page-McCaw et al., 2007) The increase in MMP-2/9 expression induced by L. obliqua venom in endothelial cells surely support the vascular inflammatory response trigger by envenomation. Taken together the data demonstrate that L. obliqua venom, at low and non-hemorragic doses, exerts a direct pro-inflammatory effect on endothelial cells, promoting cytoskeleton reorganization, increasing focal adhesion and the expression of crucial molecules to the onset of a vascular inflammatory response.

The weakly nonlinear approach is inconsistent but effective to reduce computational cost because nonlinear radiation and diffraction forces are missing. The nonlinear Froude–Krylov pressure is calculated by Taylor expanding of the incident wave potential about the calm water level as follows: equation(15) z<0ϕI=gAωekzsin(k(x+Ut)cosβ+kysinβ−ωt)0

nonlinear Froude–Krylov pressure works with an extension of restoring pressure, which is negative above the calm water level. The nonlinear pressure is integrated over the instantaneously wetted surface. The linear part of the dynamic pressure is obtained by dropping the terms related with the incident wave selleck chemicals llc potential from Eq. (14) as equation(17) pLD=−ρ(∂∂t−U¯⋅∇)(Φ+ϕd)+∇Φ⋅∇(12Φ+ϕd)The linear part is integrated over the mean body surface. For calculation of slamming forces, the ship is discretized into 2-D sections along the longitudinal axis, which covers the whole ship from stern to bow. The sections are perpendicular to the free surface of the calm water in Fig. 2. Longitudinal

mesh for each section is used to integrate slamming loads. Symmetric slamming forces acting on the sections are considered by either wedge approximation or GWM. Only water entry problem is considered. Asymmetric slamming forces for torsion and horizontal bending are not considered. NLG919 in vitro Wedge approximation is based on momentum conservation, which is expressed O-methylated flavonoid as equation(18) F=ddtMaḣ=Mah¨+∂Ma∂tḣThe relative displacement and velocity are calculated as follows: equation(19) ḣ=−∂u→∂t⋅(0,0,1)+∂ζI∂t

equation(20) h=−u→⋅(0,0,1)+ζI+DWedge approximation follows von Karman׳s solution with simplified wedge shapes. Once the surrounding flow is assumed as a potential flow, the infinite frequency added mass of the wedge is calculated as equation(21) Ma=π2ρb2(t)(1−γ2π) In case of GWM, the body geometry enters water with a vertical velocity shown in Fig. 3. Slamming pressure is limited to the water entry problem without flow separation. The space-fixed coordinate system is used, the origin of which is located at the intersection of the vertical axis of symmetry and the free surface of the calm water. The set of the initial value problem is expressed as follows (Zhao and Faltinsen, 1993, Korobkin, 2010 and Khabakhpasheva et al., 2014): equation(22) 2∇φ=0∇2φ=0 equation(23) φ=0(y=H(t)) equation(24) S(x,t)=φy(x,H(t),t)(|x|>c(t)) equation(25) φy=f′(x)φx−ḣ(t)(y=f(x)−h(t),|x|

Epigallocatechin gallate (EGCG, 95% purity) and gallic acid (GA, ≥ 98%) were purchased from Sigma–Aldrich Handels GmbH (Vienna, Austria), and copper sulphate anhydrous (CuSO4) was bought from Merck (VWR International GmbH, Vienna, Austria). Solutions of different concentration ratios of Cu:GA (1:0, 1:0.5, 1:1, 1:2, 1:10 for X-band measurements and 1:5 for S-band measurements) and Cu:EGCG (1:0, 1:0.5, 1:1, 1:2, 1:5 for X-band measurements and 1:5 for S-band measurements) were prepared Selleckchem SKI 606 with pH values ranging between

1 and 13 with a constant Cu(II) concentration of 2 mM. EPR spectra were recorded at room temperature and low temperature (77 K or 160 K) at both X- and S-band frequencies in solutions containing 5% glycerol, which was added to aid glass formation for the frozen solution studies. EPR spectra were acquired as first derivatives of the microwave click here absorption with either a Bruker EMX CW spectrometer, operating at X-band frequencies (9 GHz) or a Bruker 200D SRC operating at S-band frequencies (3 GHz). For X-band measurements, a high sensitivity cavity was used and microwaves were generated by a Gunn diode;

the microwave frequency was recorded continuously with an in-line frequency counter. Low temperature spectra were recorded using a quartz “finger dewar” containing liquid nitrogen inserted into the microwave cavity. S-band EPR spectra were obtained using a S-band bridge (v = 2–4 GHz) SB-1111 Jagmar (Poland), and low temperatures were controlled with a Bruker ER 4111VT variable

temperature unit. The Cu(II) EPR spectra were acquired using 20 mW microwave power (MP) for room temperature and 2 mW MP for low temperature measurements, 100 kHz modulation frequency (MF) and 1 mT modulation amplitude (MA). g-values were determined by reference to the signal of DPPH (g = 2.0036), which was used as an external standard. Rutecarpine Signal intensities of the fluid solution spectra were determined by double integration (DI) using the Bruker WINEPR software. For determination of the Cu(II) intensity, the DI of the whole Cu(II) spectrum was carried out, followed by subtraction of the DI of the intensity of the free radical signal in the measurements at very high pH. Easyspin [20] was used for spectral simulation and analysis. Parameters were determined for the frozen solution spectra using the fitting function “pepper”, and these were then used as the basis for simulation of the fluid solution spectra. The Easyspin software assumes the natural abundance ratio of 63Cu and 65Cu isotopes, but returns hyperfine splittings for the 63Cu isotope only; thus the tabulated results apply only to this nucleus (note: the Cu hyperfine parameters for many spectra reported in the literature give a weighted mean from the two isotopes).

Evidence for this theory originates from studies which have shown that DA agonists that enhance dopaminergic activity strengthen positive affect (Beatty, 1995). Furthermore, there is ample evidence that DA selectively modulates cognitive control processes (Braver et al., 1999 and Reynolds et al., 2006). Interestingly, the antisaccade task has been shown to be modulated by dopamine levels in the brain. For instance, patients with schizophrenia have higher error rates and longer latencies than controls on antisaccade tasks (Fukushima et al., 1990 and Sereno and

Holzman, 1995), similarly to advanced Parkinson patients (Kitagawa, Fukushima, & Tashiro, 1994). Because these disorders have been linked to an imbalance in dopaminergic states in the brain, these abnormalities in the PARP cancer antisaccade task may be due to disturbances in dopaminergic neurotransmission. Although we did not measure dopamine levels directly in the current experiment1, we speculate that the observed modulations of positive affect on the antisaccade task might therefore be due to changes in dopaminergic levels in the brain. Higher levels of dopamine result in the enhanced ability to overcome dominant responses. Such fluctuations in DA levels might be expected to modulate activity particularly in those oculomotor circuits that are densely innervated by dopaminergic

projections. Results further showed that the effect of induced positive affect on oculomotor inhibition was restricted to the eye movements with short latencies (80–130 ms). It click here is known that these erroneous ‘express’ saccades reflect a different

and distinct phenomenon than erroneous saccades with a longer latency (>130 ms) (Klein and Fischer, 2005 and Klein et al., 2010). Therefore, it seems that the induced positive affect exclusively improves the oculomotor inhibition of reflex-like prosaccades. This finding might seem inconsistent with Vasopressin Receptor the idea that induced positive affect increases cognitive control, because it has been suggested that only errors with a regular latency are correlated with (‘higher’) cognitive measures, like executive function and working memory (Klein et al., 2010). Although speculative, it is interesting to consider the possible neural mechanisms underlying the effect of induced positive affect on the oculomotor inhibition of reflex-like prosaccades. When a saccade is required in the direction opposite to the visual hemifield in which a stimulus onset occurs, several distinct but interrelated oculomotor processes come into play: (1) active fixation of the oculomotor system, (2) intentional saccade initiation, and (3) selective suppression of saccades until the program of the appropriate eye movement has been fully developed.

Expression of AR was significantly associated with increasing age > 50 years (P = .040), low or intermediate grade (I and II) tumors (P = .001), expression of ER (P = .002), PR (P = .001), and therapeutic modalities

including endocrine (P = .004) and chemotherapy (P = .015). There were no significant differences observed between AR expression and tumor size, lymph node involvement, HER2 status, tumor type, radiation therapy, and expression of pAkt and pPTEN ( Table 2). Survival analysis Selleckchem Dolutegravir was performed on 82 patients who had been followed for five or more years. A total of 16 deaths were reported during this period. The mean OS time was 9.2 ± 0.41 years, and lost to follow-up was 17% (n = 14) only. Women with AR-expressing or positive tumors had significantly higher OS (mean OS = 10.2 ± 0.465 years) than women whose tumors did not express AR (mean OS = 5.8 ± 0.348 years) (P = .042; Figure 2A). Lymph node involvement showed a significant (P = .043) association

with lower OS. Patients with large tumor size (P = .069) and positive pAkt status (P = .243) tended to also have decreased OS ( Table 3). To compare the potential prognostic value of AR and ER coexpression on survival, patients were Proteases inhibitor categorized into the following four groups: 1) AR+/ER+ (n = 19), 2) AR+/ER− (n = 16), 3) AR−/ER+ (n = 10), and 4) AR−/ER− (n = 37). Although survival analyses showed no significant OS difference among the four groups Resveratrol (P = .214), women with AR+/ER+ tumors showed a trend for a better OS (mean OS = 5.0 ± 0.257 years) compared to the AR−/ER+ (mean OS = 4.4 ± 0.573 years)

subgroup. We also found a survival advantage of AR expression in the AR+/ER− group with only 12.5% deaths (2 of 16), compared to 27% (10 of 37) deaths in patients with AR−/ER− tumors (P = .214; Figure 2B). The association of AR expression with OS in the subgroup of patients receiving endocrine therapy was investigated (n = 26). In this subgroup, patients with AR-positive tumor showed significantly better OS compared to patients whose tumors did not express AR (P = .020; Figure 2C). To compare the potential prognostic impact of AR and pPTEN coexpression on survival, patients were categorized into the following four groups: 1) AR+/pPTEN+ (n = 14), 2) AR+/pPTEN− (n = 20), 3) AR−/pPTEN+ (n = 22), and 4) AR−/pPTEN− (n = 16). Although survival analyses showed that there was no significant OS difference among the four groups (P = .289), women with AR+/pPTEN+ tumors had better survival with only 7.1% deaths (1 of 14), compared to 32% deaths (5 of 16) in the AR−/pPTEN− group of patients with BCa. We also found a survival benefit of AR expression in the AR+/pPTEN− group with only 10% deaths (2 of 20), compared to 22.7% deaths in the group of patients with AR−/pPTEN + tumors (5 of 22) (P = .289; Figure 2D).

After washing, 100 μL of o-phenylenediamine (0.33 mg/mL in citrate buffer, pH 5.2, in the presence of 0.04% hydrogen peroxide) was added to the wells. The reaction was stopped after 20 min by the addition of 20 μL of a 1:20 sulfuric acid solution. Absorbance values were determined at 490 nm using an ELISA plate reader (BIO-RAD, 680 models). Duplicate readings were taken for all samples and the means were calculated. For the immunoblotting, an SDS-PAGE gel using H. lunatus venom was run according to the method of Laemmli (1970) using 12.5% gels and transferred onto Dabrafenib nitrocellulose membrane (

Towbin et al., 1979). The membrane was blocked with PBS-Tween 0.3% for 1 h. After washing three times for 5 min with PBS-Tween 0.05%, the membrane was incubated with anti-H. lunatus rabbit serum (1:1500) for 1 h and 30 min. The membrane was washed (PBS-Tween 0.05%) more three times and immunoreactive proteins were detected using anti-rabbit IgG conjugated to peroxidase (1:8000) for 1 h at room temperature. After washing three times for 5 min with PBS-Tween 0.05%, blots were developed using DAB/chloronaphthol according to manufacturer’s instructions. The lethality of the H. lunatus soluble venom to mammals was examined using mice. After intracranial

(i.c.) and intraperitoneal injection (i.p.) toxic and lethal effects were observed. The LD50 value was determined as 0.1 mg/kg and 21.55 mg/kg (respectively). Injected mice displayed typical symptoms of intoxication such as excitability, agitation, salivation, eye secretions, sweating, convulsions and paralysis of legs. The symptoms lasted for 30–120 min before death. The observed CP-690550 solubility dmso symptoms closely resemble those produced by the venom of Buthidae scorpions of the genera Centruroides or Tityus ( Possani et al.,

1977). The venoms from some species of Brazilian scorpions were analyzed regarding their lethality in mice by Nishikawa and co-workers, in 1994 via intraperitoneal injection, the same used by us. In this study, the venoms were grouped O-methylated flavonoid as highly toxic Tityus stigmurus (LD50 = 0.773 mg/kg), Tityus bahiensis (LD50 = 1.062 mg/kg) and T. serrulatus (LD50 = 1.160 mg/kg); moderately toxic Tityus cambridgei (LD50 = 12.136 mg/kg) and practically non-toxic Rhopalurus agamemnon (LD50 = 36.363 mg/kg) and Brotheas amazonicus (LD50 = 90.909 mg/kg). In view of the results observed in our experiments and compared to the previous data, H. lunatus venom can be classified as moderately toxic. The value found for LD50 of the venom of H. lunatus (i.p. route) was more than three times lower than that found by Zavaleta et al. (1981). This divergence can be explained by the fact that in our experiments the venom collected was immediately diluted in ultrapure water (milli Q), pooled and stored at −20 °C until use and never lyophilized. The proteolytic activity (caseinase) of H. lunatus venom was detected, for the first time, by the dimethylcasein method ( Lin et al.

Also known by its gene name WFDC2 (whey acidic protein four-disulfide core domain protein 2), HE4 was initially identified as an mRNA transcript specific to the distal epididymal

tissue [15]. Through microarray gene-expression profiling, it was discovered http://www.selleckchem.com/products/AZD2281(Olaparib).html that HE4 was moderately expressed in lung adenocarcinomas, breast carcinomas, transitional cell endometrial carcinomas and pancreatic carcinomas, but consistently highly expressed in ovarian carcinomas [16], [17], [18] and [19]. Furthermore, Drapkin et al. showed that HE4 is relatively specific to the serous subtype of epithelial ovarian carcinomas (EOCs), as expression was observed in approximately 93% of serous carcinomas but it was also present in a smaller proportion of endometrioid, mucinous, and clear cell carcinomas [20]. Taken together, there was strong evidence that this secreted glycoprotein was a putative serum marker for ovarian cancer. In a pilot study measuring serum levels of HE4 in ovarian cancer patients, Hellstrom et al. concluded that HE4 may be comparable to CA125 as a monitoring serum tumour marker as both displayed a sensitivity

of 80% and a specificity of 95% when used to classify blinded late stage cases and healthy controls [21]. HE4 was approved by the FDA in 2009 as a serum marker for monitoring recurrence Tenofovir of ovarian cancer. A final approach to OvCa diagnosis that is becoming increasingly prevalent Amino acid is the use of multimarker panels derived from high-throughput discovery efforts. The

rationale is that the use of multiple markers may provide a more accurate representation of whether or not disease is present especially when the disease (such as OvCa) is heterogeneous across different individuals. In a study by Yurkovetsky et al., it was determined that from a list of 96 potential OvCa serum biomarkers, a panel of CA125, HE4, carcinoembryonic antigen, and vascular cell adhesion molecule 1 displayed a sensitivity of 86% for early-stage OvCa and 93% for late-stage OvCa at a set specificity of 98% when used to diagnose OvCa patients from healthy controls [22]. The authors were able to further validate this model on an independent blinded validation cohort while additionally showing that the panel was specific to OvCa as it displayed sensitivities of 33% for benign pelvic disease, 6% for breast cancer, 0% for colorectal cancer, and 36% for lung cancer. Furthermore, two other multimarker-based algorithms have recently gained FDA-approval for the discrimination of benign versus malignant pelvic masses – the Risk of Ovarian Malignancy Algorithm (ROMA) and the OVA1™ test. The ROMA incorporates serum levels of CA125 and HE4, which was identified through microarray studies, while the OVA1™ test incorporates serum levels of CA125 and four other markers identified through MS (beta-2 microglobulin, transferrin, transthyretin, apolipoprotein A1).

Guldin and Grüsser (1998) identified the parieto-insular vestibular cortex (PIVC) as the core region of the vestibular

cortical network. The PIVC is strongly interconnected with other cortical areas receiving vestibular and multimodal projections, such as the somatosensory cortex and the ventral intraparietal area (Guldin and Grüsser, 1998). The human homologue of the monkey PIVC has been identified in a distributed pattern of activations in the posterior and anterior insula, the superior temporal gyrus and the inferior parietal lobule (Angelaki and Cullen, 2008; Bense et al., 2001; Bottini et al., 1994, PD0332991 chemical structure 1995; Fasold et al., 2002). Moreover, human neuroimaging studies have also revealed other cortical vestibular projections in the primary and secondary somatosensory cortex (Fasold et al., 2002; Bottini et al., 1994; Emri AUY-922 manufacturer et al., 2003), primary motor cortex and premotor cortex (Bense et al., 2001; Fasold et al., 2002). Traditionally, this convergence was thought to combine vestibular information with that from other sensory modalities, to generate optimal descriptions of the animal’s relation to its external environment (Bremmer et al., 2001). Clinical evidence suggests a functional link between vestibular and somatosensory systems. In particular, left cold caloric vestibular stimulation (CVS) produces

dramatic transitory perceptual changes in tactile perception. A temporary remission of tactile hemianaesthesia MRIP in right (Vallar et al., 1990, 1993) and left brain-damaged patients (Bottini et al., 2005) has been observed immediately after left cold CVS. However, such data cannot distinguish between direct vestibular effects on tactile sensation, and indirect effects based on the hypothesised shift in spatial attention towards the left side induced by left cold CVS (Vallar et al., 1990, 1993). Evidence in right brain-damaged patients also suggests abnormal vestibular control of eye movements. Thus, Doricchi et al. (2002) found reduced leftward slow-phase

nystagmus and Ventre-Dominey et al. (2003) found a rightward vestibulo-ocular reflex (VOR) bias in right brain-damaged patients affected by neglect. Both these results suggest some cortical involvement in vestibular control of gaze. On this basis, one might predict that left cold CVS could facilitate right-hemisphere neural circuits for gaze control disrupted by right brain damage, rather then simply reallocating spatial attention towards the neglected left space (Doricchi et al., 2002; Ventre-Dominey et al., 2003). However, Figliozzi et al. (2005) showed that vestibular inputs could produce spatiotopic shifts of attention, even under central fixation in VOR suppression conditions. Therefore, vestibular stimulation may independently affect both oculomotor and attentional processes. Moreover, vestibular stimulation interacts with other somatosensory submodalities.

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 DZNeP concentration 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 » 5-FU 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 C59 research buy 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.