[Treatment of malignant gastric tumors in the surgery "a" department of the Point G teaching hospital: 84 cases]. / Prise en charge des tumeurs malignes gastriques dans le service de chirurgie «a¼ du CHU du Point G a propos de 84 cas.

OBJECTIVE: To evaluate the short-term results of the treatment of malignant gastric tumors. PATIENTS AND METHODS: A 3-year retrospective study from january 2007 to december 2010 was conducted in the Surgery "A" department of the Point G Teaching Hospital. The clinical records of 84 patients with gastric cancers were collected. Included in this study were patients who underwent surgery for malignant gastric tumors confirmed by histology. Patients who did not undergo surgery and those who presented tumors of the cardia were not included in this study. RESULTS: The treatment consisted of a subtotal gastrectomy with ganglionic curettage taking out the first and the second relays in 33 patients (39.28%), total gastrostomy in 3 patients (3.57%), and the remaining 48 patients (57.14%) underwent gastro-entero anastomosis. Morbidity was 10.7%, represented by 7 cases of parietal suppuration and 2 cases of evisceration. Mortality rate was 11.11%, due to poor general condition of the patients. The global 1-year survival rate was 36.9%. The one and two-year survival rates after subtotal gastrostomy were 93.9% and 75.75%, respectively. No survival case was noticed one year after total gastrectomy and gastric enteric anastomosis. CONCLUSION: Partial gastrectomy with ganglionic curettage when possible associated with an early diagnosis could allow a sharp improvement of the gastric tumors' survival rate.

BUT: évaluer les résultats à court terme de la prise en charge des tumeurs malignes gastriques. PATIENTS ET MÉTHODES: Il s'agissait d'une étude rétrospective sur une période de 3 ans (janvier 2007 à décembre 2010) dans le service de chirurgie «A ¼ du CHU du Point G. Les dossiers cliniques de 84 malades atteints de cancers gastriques ont été colligés. Ont été inclus dans l'étude les malades opérés pour tumeurs malignes gastriques confirmées à l'histologie. Les malades non opérés et ceux présentant de tumeurs du cardia n'ont pas été inclus dans l'étude. RÉSULTATS: Une gastrectomie subtotale était réalisée chez 33 patients (39,28%) avec curage ganglionnaire emportant le premier et le deuxième relais, 3 gastrectomies totale (3,57%) et le reste du traitement a consisté en une gastro-entero-anastomose chez 48 malades (57,14 %). La morbidité était de 10,7 % représentée par 7 cas de suppuration pariétale, et 2 cas d'éviscération. Le taux de mortalité a été de 11,11% liée au mauvais état général des malades. Le taux de survie global à 1 an était de 36,90%. Le taux de survie à 1 an après gastrectomie subtotale était de 93,9%, et 75,75 % à 2 ans. Aucun cas de survie n'était enregistré à 1 an après gastrectomie totale et gastro-entero-anastomose. CONCLUSION: La gastrectomie partielle avec curage ganglionnaire chaque fois que sa réalisation est possible associée à un diagnostic précoce pourrait permettre une nette amélioration du taux de survie des tumeurs gastriques.

Inhibition of transforming growth factor-beta signaling accelerates atherosclerosis and induces an unstable plaque phenotype in mice.

Atherosclerosis is a disease of the arterial wall that seems to be tightly modulated by the local inflammatory balance. Whereas a large body of evidence supports a role for proinflammatory mediators in disease progression, the understanding of the role of the antiinflammatory component in the modulation of plaque progression is only at its beginning. TGF-beta1, -beta2, and -beta3 are cytokines/growth factors with broad activities on cells and tissues in the cardiovascular system and have been proposed to play a role in the pathogenesis of atherosclerosis. However, no study has examined the direct role of TGF-beta in the development and composition of advanced atherosclerotic lesions. In the present study, we show that inhibition of TGF-beta signaling using a neutralizing anti-TGF-beta1, -beta2, and -beta3 antibody accelerates the development of atherosclerotic lesions in apoE-deficient mice. Moreover, inhibition of TGF-beta signaling favors the development of lesions with increased inflammatory component and decreased collagen content. These results identify a major protective role for TGF-beta in atherosclerosis.

Fc-receptor-mediated intracellular delivery of Cu/Zn-superoxide dismutase (SOD1) protects against redox-induced apoptosis through a nitric oxide dependent mechanism.

BACKGROUND: Using specific antibodies against bovine Cu/Zn-superoxide dismutase (EC 1.15.1.1, SOD1) we demonstrated that anti-SOD antibodies (IgG1) are able to promote the intracellular translocation of the antioxidant enzyme. The transduction signalling mediated by IgG1 immune complexes are known to promote a concomitant production of superoxide and nitric oxide leading to the production of peroxynitrites and cell death by apoptosis. The Fc-mediated intracellular delivery of SOD1 thus limited the endogenous production of superoxide. It was thus of interest to confirm that in the absence of superoxide anion, the production of nitric oxide protected cells against apoptosis. Study in greater detail clearly stated that under superoxide anion-free conditions, nitric oxide promoted the cell antioxidant armature and thus protected cells against redox-induced apoptosis. MATERIALS AND METHODS: The murine macrophage cell-lines J774 A1 were preactivated or not with interferon-gamma and were then stimulated by IgG1 immune complexes (IC), free SOD1 or SOD1 IC and superoxide anion, nitric oxide, peroxynitrite, and tumor necrosis factor-alpha (TNF-alpha) production was evaluated. The redox consequences of these activation processes were also evaluated on mitochondrial respiration and apoptosis as well as on the controlled expression of the cellular antioxidant armature. RESULTS: We demonstrated that SOD1 IC induced a Fcgamma receptor (FcgammaR)-dependent intracellular delivery of the antioxidant enzyme in IFN-gamma activated murine macrophages (the J774 AI cell line). The concomitant stimulation of the FcyR and the translocation of the SOD1 in the cytoplasm of IFN-gamma-activated macrophages not only reduced the production of superoxide anion but also induced the expression of the inducible form of nitric oxide synthase (iNOS) and the related NO production. This inducing effect in the absence of superoxide anion production reduced mitochondrial damages and cell death by apoptosis and promoted the intracellular antioxidant armature. CONCLUSIONS: To define the pharmacologic mechanism of action of bovine SOD1, we attempted to identify the second messengers that are induced by SOD1 IC. In this work, we propose that Fc-mediated intracellular delivery of the SOD1 that reduced the production of superoxide anion and of peroxynitrite, promoted a NO-induced protective effect in inducing the antioxidant armature of the cells. Taken together, these data suggested that specific immune responses against antigenic SOD1 could promote the pharmacological properties of the antioxidant enzyme likely via a NO-dependent mechanism.