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Objetivo: Evaluar la efectividad de dos formas diferentes de prescribir la analgesia postoperatoria en pacientes sometidos a cirugía del hallux valgus con alta en el día. Material y método: A través de un cuestionario telefónico se evaluó la efectividad, grado de cumplimiento y complicaciones de dos protocolos de analgesia en pacientes ambulatorios intervenidos de hallux valgus. Los dos protocolos sólo se diferenciaron en la forma de prescripción de los mismos. Se recogieron datos de 48 pacientes distribuidos al azar en dos grupos mediante una hoja diseñada para este propósito. Resultados: La intensidad del dolor postoperatorio fue menor, tanto en las primeras 24 horas, como después, cuando se dio al paciente un protocolo de analgesia detallado minuciosamente, mejorando también el grado de cumplimiento. Las complicaciones (náuseas, vómitos, mareos) fueron más frecuentes en el grupo que no recibió una prescripción detallada. Un 34,5% de los pacientes padeció dolor bastante intenso en algún momento, pese a la analgesia. El dolor fue más intenso en las primeras 24 horas, cuando se asoció corrección de otros procesos y en los pacientes más jóvenes. Conclusiones: Comunicar al paciente de una forma muy detallada (por escrito) la pauta analgésica adecuada hace que su postoperatorio sea menos doloroso y reduce la incidencia de complicaciones, así como facilita su cumplimiento (AU)

Objective: To evaluate the effectiveness of two different ways to prescribe the postoperative analgesia subjected patients to surgery intervention of hallux valgus with discharge from hospital in the same day. Material and method: Through a telephone questionnaire we evaluated the effectiveness, fulfilment and complications of two analgesia protocols in ambulatory patients under hallux valgus surgery. Both analgesia protocols were only different in the prescription form. We analyzed the feed back from 48 patient random distributed in two groups. Each group was assigned to different a analgesia protocol prescription. Results: The intensity of the postoperative pain was smaller at the first 24 hours but also after that, when the prescription of analgesia protocol was given to the patient meticulously detailed. It also improved the protocol fulfilment by the patient. The complications (sickness, vomits, dizziness) were also more frequent in the group that did not receive a detailed prescription. A 34.5% of the patients suffered quite intense pain sometime, even when they have already taken the analgesia. The pain was more intense in the first 24 hours, when correction of other processes was associated and in the youngest patients. Conclusions: To communicate to the patient the analgesia protocol in a very and meticulous way (even by written) achieves a less distressful and painful postoperative process. It even reduces the postoperative complications and increases the correct analgesia protocol achievement (AU)

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The translocated and normal bcl-2 alleles in the DHL-4 cell line with the t(14;18) translocation were separated by pulsed field electrophoresis. An in vivo footprint over a potential WT1 binding site in the bcl-2 5'-flanking sequence was identified on the normal silent allele. Electrophoretic mobility shift assays with the bcl-2 WT1 site demonstrated a single specific complex. UV cross-linking and Western analysis revealed that this gel shift complex contained WT1 protein. Deletion or mutation of the WT1 site resulted in an increase in activity of the bcl-2 promoter in DHL-4 cells. Cotransfection with a 3:1 ratio of a WT1 expression vector to the bcl-2 promoter construct led to a 3.0-fold repression of the bcl-2 promoter. Cotransfection with a WT1 expression vector and the bcl-2 promoter with the mutated WT1 site resulted in only 1.2-fold repression. We conclude that the WT1 site functions as a negative regulatory site for the normal silent bcl-2 allele in t(14;18) lymphomas. The WT1 site is not occupied on the translocated bcl-2 allele.

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Engagement of surface immunoglobulin on mature B cells leads to rescue from apoptosis and to proliferation. Levels of bcl-2 mRNA and protein increase with cross-linking of surface immunoglobulin. We have located the major positive regulatory region for control of bcl-2 expression in B cells in the 5'-flanking region. The positive region can be divided into an upstream and a downstream regulatory region. The downstream regulatory region contains a cyclic AMP-responsive element (CRE). We show by antibody supershift experiments and UV cross-linking followed by denaturing polyacrylamide gel electrophoresis that both CREB and ATF family members bind to this region in vitro. Mutations of the CRE site that result in loss of CREB binding also lead to loss of functional activity of the bcl-2 promoter in transient-transfection assays. The presence of an active CRE site in the bcl-2 promoter implies that the regulation of bcl-2 expression is linked to a signal transduction pathway in B cells. Treatment of the mature B-cell line BAL-17 with either anti-immunoglobulin M or phorbol 12-myristate 13-acetate leads to an increase in bcl-2 expression that is mediated by the CRE site. Treatment of the more immature B-cell line, Ramos, with phorbol esters rescues the cells from calcium-dependent apoptosis. bcl-2 expression is increased following phorbol ester treatment, and the increased expression is dependent on the CRE site. These stimuli result in phosphorylation of CREB at serine 133. The phosphorylation of CREB that results in activation is mediated by protein kinase C rather than by protein kinase A. Although the CRE site is necessary, optimal induction of bcl-2 expression requires participation of the upstream regulatory element, suggesting that phosphorylation of CREB alters its interaction with the upstream regulatory element. The CRE site in the bcl-2 promoter appears to play a major role in the induction of bcl-2 expression during the activation of mature B cells and during the rescue of immature B cells from apoptosis. It is possible that the CRE site is responsible for induction of bcl-2 expression in other cell types, particularly those in which protein kinase C is involved.

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The translocated and normal bcl-2 alleles in the DHL-4 cell line with the t(14;18) translocation were separated by pulsed field electrophoresis. An in vivo footprint over a cAMP response element (CRE) in the bcl-2 5'-flanking sequence was identified on the translocated allele. Electrophoretic mobility shift assays with the bcl-2 CRE demonstrated complexes with mobilities identical to those with a consensus CRE. UV cross-linking experiments revealed that proteins with molecular masses of 34, 43, and 67 kDa bound to the bcl-2 CRE site. Electrophoretic mobility shift assay with an antibody specific to the phosphorylated cAMP response-binding protein (CREB) demonstrated that phosphorylated CREB was present in DHL-4 cells. Treatment with phorbol 12-myristate 13-acetate (PMA) led to an increase in both the amount of phosphorylated CREB and the bcl-2 promoter activity. The response to PMA was dependent on an intact CRE site. The activity of the bcl-2 promoter was increased 20-fold in a construct with the immunoglobulin heavy chain enhancers, and mutation of the CRE site abolished most of the induction. The addition of PMA increased the activity of the bcl-2-immunoglobulin enhancer construct by 3.5-fold. Access to the CRE site is blocked in the silent normal bcl-2 allele, while CREB proteins bind to the site on the translocated allele. We conclude that the CRE site functions as a positive regulatory site for the translocated bcl-2 allele in t(14;18) lymphomas.

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