http://www.saber.ula.ve/handle/123456789/2337 Articulos, Pre-prints del Laboratorio de Microbiología y Salud Pública del Estado Mérida. ULA-ULE 2026-05-16T02:56:52Z http://www.saber.ula.ve/handle/123456789/16111 Correspondence Pérez, Saberio 2007-04-25T09:00:00Z http://www.saber.ula.ve/handle/123456789/16103 Uso de Aripiprazol en adolescente con esquizofrenia refractaria. Pérez Lo Presti, Alirio; Pérez Lo Presti, Annabelle; Pérez, Saberio; Dávila Federico, José Uso de Aripiprazol en adolescente con esquizofrenia refractaria. A propósito de un caso. Pérez Lo Presti, Alirio; Pérez Lo Presti, Annabelle; Pérez Lo Presti, Saberio y Dávila Federico, José Resumen El presente trabajo reporta el caso de un adolescente masculino con síntomas psicóticos recurrentes y hospitalizaciones desde los doce años de edad. Luego de múltiples tratamientos farmacológicos, respondió favorablemente al uso de aripiprazol a dosis de 22,5 mg., permaneciendo asintomático durante un año de seguimiento. Abstract This study reports a case of a male adolescent with psychotic recurrent symptoms who was repeatedly referred to the hospital since the age of twelve years old. After receiving multiple pharmacological treatments, he responded well to aripiprazol (22,5 mg. / day). During the following year he was free of any psychopathological symptom. 2007-03-28T09:00:00Z http://www.saber.ula.ve/handle/123456789/16105 A simple algorithm for the diagnosis of AIDS associated genitourinary tuberculosis. Pérez, Saberio; Bracho, Yoshira; Andrade, Martin; Bergel, Patrick; Waard, Jacobus 2007-03-28T09:00:00Z http://www.saber.ula.ve/handle/123456789/16109 Chlamydophila pneumoniae infection of human aortic endothelial cells induces the expression of fc y receptor II (FCyRII) Vielma, Silvana; Virella, Gabriel; Gorod, Adam J.; Lopes Virella, Maria F. Chlamydophila pneumoniae infection of human aortic endothelial cells induces the expression of fc y receptor II (FCyRII). (Vielma, Silvana; Virella, Gabriel; Gorod, Adam J.; Lopes Virella, Maria F.) Abstract Chronic endothelial infection is believed to be one of the factors able to cause endothelial cell damage and trigger the onset of human atherosclerosis. Chlamydophila pneumoniae infects endothelial cells and has received special attention because of both epidemiological and experimental evidence supporting its role as a risk factor for atherosclerosis. It is also possible that otherwise independent risk factors for atherosclerosis may have synergistic effects. Immune phenomena, such as the formation of circulating immune complexes (IC) containing modified LDL and corresponding antibodies, have been linked to the development of coronary artery disease. The antibodies involved in the immune response to modified lipoproteins are predominantly of the pro-inflammatory IgG1 and IgG3 subclasses. However, it is difficult to understand how circulating IC could cause endothelial damage and initiate the atherosclerotic process, unless they were formed in the subendothelial space or immobilized by endothelial cells. The last hypothesis would be possible if endothelial cells expressed Fcy receptors. Healthy endothelial cells do not express Fcy receptors, but endothelial cells infected by a variety of infectious agents do. Thus we decided to investigate whether infection of endothelial cells with C. pneumoniae is also able to cause the expression of Fcy receptors. The expression of Fcy receptors (CD64, 32, and 16) on human aortic endothelial cells infected with C. pneumoniae for 4, 24, 36, and 48 h was studied by flow cytometry. Twenty-four hours after infection 30-40% of the endothelial cells had detectable inclusion bodies, 8-9% of the total number of cells (approximately 25% of the infected cells) expressed FcyRII, and about 1.5-2% (5% of infected cells) expressed FcyRI and FcyRIII. Double-staining studies confirmed that the expression of FcyRII was limited to C. pneumoniae- infected endothelial cells. We conclude that C. pneumoniae infection induces primarily the expression of FcyRII by endothelial cells and this may be a significant link between two proposed pathogenic mechanisms involved in the pathogenesis of human atherosclerosis. Published on: Clinical Immunology Vol. 104, No. 3, September, pp. 265-273, 2002 doi:10.1006/clim.2002.5237 2006-02-24T09:00:00Z http://www.saber.ula.ve/handle/123456789/16107 Chlamydophila pneumoniae induces ICAM-1 expression in human aortic endothelial cells via protein kinase c-dependent activation of nuclear factor-kb. Vielma, Silvana; Lopes Virella, Maria F.; Krings, Gregor Chlamydophila pneumoniae induces ICAM-1 expression in human aortic endothelial cells via protein kinase c-dependent activation of nuclear factor-kb. (Vielma, Silvana; Krings, Gregor; Lopes Virella, Maria F.) Abstract Chlamydophila pneumoniae has an epidemiological link with atherosclerosis and acute cardiovascular events. One mechanism that may explain such a link is the increased expression of intracellular adhesion molecule-1 (ICAM-1) in C pneumoniae-infected endothelial cells. Upregulation of ICAM-1 by C pneumoniae is well recognized and has been extensively studied, but the signaling pathways involved are not yet defined. Because upregulation of ICAM-1 by cytokines and other stimuli has been shown to be mediated by either mitogen-activated protein kinase, protein kinase C (PKC), or nuclear factor-kB (NF-kB) pathways, we examined whether these pathways were involved in the ICAM-1 upregulation induced by C pneumoniae. Our data show a time-dependent phosphorylation of p44/p42 and SAPK/JNK pathways in C pneumoniae-infected cells. However, inhibition of the classic mitogen-activated protein kinase pathway using the PD98059 and U0126 inhibitors and inhibition of SAPK/JNK pathway did not suppress C pneumoniae-induced ICAM-1 expression. C pneumoniae also activates the NF-kB pathway at 30 minutes after infection. Treatment of human aortic endothelial cells (HAECs) with the NF-kB inhibitors BAY117085 and caffeic acid phenethyl ester led to a concentration-dependent inhibition of C pneumoniae-induced ICAM-1 upregulation. Finally, C pneumoniae-infected HAECs show membrane translocation of total PKC 30 minutes after cell infection. Calphostin C, a general PKC inhibitor, blocked both C pneumoniae-induced ICAM-1 expression and C pneumoniae-induced NF-kB translocation. In conclusion, we demonstrated that C pneumoniae-induced ICAM-1 expression in HAECs requires NF-kB and PKC activation and that NF-kB activation is PKC dependent. 2005-07-25T09:00:00Z