Venezuela the next frontier for HIV/AIDS: what about female protection?

En diciembre de 1997, CONTRASIDA (Organización No-Gubernamental) tomó un paso histórico en la lucha contra el Sida en Venezuela al intoducir el condón femenino. Un grupo particularmente en riesgo para la infección con virus de inmunodeficiencia humana (HIV), y susceptible de infectar otros con el HIV es el grupo de las trabajadoras sexuales (FCSWS). Teniendo múltiples compañeros, quienes frecuentemente rehúsan usar un método de barrera, así las FCSWS están en gran riesgo para adquirir la infección. Además, como el HIV no puede detectarse dentro de los 3-6 meses de adquirir la infección, estas mismas FCSWS puede inconscientemente infectar sus clientes, quienes a su vez pueden infectar a sus esposas y/o compañeras (os). Esto últimmo es lo que se denomina "la teoría sexual de red": gente conectada por sus contactos sexuales, y por lo tanto forma la llamada "modelos de redes sexuales". CONTRASIDA elaboró un cuestionario e implementó un proyecto de información que alcanzó 1.000 mujeres, la mayoría FCSWS en Venezuela. Dentro del marco de la "teoría sexual de red" CONTRASIDA incluyó también clientes/compañeros de FCSWS en los cursillos sobre el condón femenino. Además, organizó cursillos especiales para ama de casas, estudiantes y profesionales femeninos que participaron en el proyecto, como un instrumento efectivo en la lucha contra el HIV y otras enfermedades de transmisión sexual

[Virtual intravascular endoscopy in the renal arteries: a new way of observing 3-D-MIR angiography data sets]. / Virtuelle intravasale Endoskopie in den Nierenarterien: Eine neuartige Betrachtungsform von 3-D-MRA-Datensätzen.

PURPOSE: To determine the potentials and limitations of a recently developed algorithm for virtual intravascular endoscopy (VIE) based on 3-dimensional (3-D) magnetic resonance (MR) data sets. METHOD: The data from 6 patients derived from gadolinium-enhanced MR angiography of the renal arteries were reviewed. All patients had unilateral or bilateral renal arterial pathologies (stenoses n = 2, aneurysms n = 4). Imaging was performed on a 1.5-T scanner using a 3-D gradient-echo MR sequence. The imaging parameters were as follows: TR/TE/flip angle 3.9/1.9/40 degrees, matrix 256 x 192, slice thickness 1.5 to 2 mm, FOV 32 cm, and 48 slices. Image acquisition time was 28 seconds under apnoeia conditions. A total of 60 ml 0.5 molar Gd-DTPA was injected during the scan. RESULTS: 3-D data sets could be obtained in all patients and postprocessed for VIE. The intraluminal vessel wall was depicted with high clarity in all cases. All pathologies that were not intraparenchymal could be easily seen. Limitations to the technique include the image quality of the original data set, use of the ideal threshold to minimise intraluminal artifacts, and a complicated prescription sequence. CONCLUSIONS: We have shown that VIE can be consistently performed in the renal arteries using MR data sets acquired with a contrast enhanced 3-D gradient-echo technique. It provides a hitherto unused approach to viewing 3-D vascular MR data sets.

Suppression of secondary cellular immunity to a tumor allograft by cyclophosphamide and 1,3-bis(2-chloroethyl)-1-nitrosourea.

C57BL/6 mice (H-2b) were immunized with lethally x-irradiated Moloney virus-induced lymphoma cells of BALB/c origin (H-2d) on Days 0 and 10 and received rug on Days 11 and 14. Their spleen cells were then tested for reactivity against Moloney virus-induced lymphoma of BALB/c origin by the 51Cr-release cytotoxicity assay. In non-drug-treated mice the secondary cytotoxic response was maximal on Days 14 to 15, declined rapidley, and recurred after Day 21. The cytotoxic effector cells were shown to be theta-bearing T-lymphocytes. Cyclophosphamide (CY), 180 mg/kg, given on Day 11, totally prevented the development of a cytotoxic response and when given on Day 14 abolished the response already established. CY, 48 mg/kg, as well as 1,3-bis(2-chloroethyl)-1-nitrosourea 33 mg/kg, were almost as suppressive. Immune mice given CY on Day 14 and reimmunized on Day 36 exhibited a normal tertiary response. Mice similarly immunized on Days 1 and 10 and given drugs on Day 14 were challenged on Day 15 with up to 3.5 x 10-8 viable Moloney virus-induced lymphoma cells of BALB/c origin. Despite H-2 incompatibility, all nonimmune control mice developed ascites and died, whereas all mice immunized but not given drug failed to develop ascites. By contrast, 17 of 34 immunized mice given CY, 180 mg/kg, and 7 of 34 given 1,3-bis(2-chloroethyl)-1-nitrosourea developed ascites. The ascites eventually regressed. THE RESULTS SHOW THAT CY and 1,3-bis(2-chloroethyl)-1-nitrosourea can suppress a secondary cellular immune response as measured by the T-cell-mediated 51Cr-release cytotoxicity assay in vitro and by viable tumor challenge in vivo.