Toxicidad pulmonar por gemcitabina / No disponible

Describimos el caso clínico de un paciente que presentó una insuficiencia respiratoria aguda en muy probable relación a toxicidad por gemcitabina. El aumento de incidencia de enfermedades neoplásicas conlleva un mayor uso de este fármaco en el tratamiento de las mismas, y esto a su vez provoca una mayor incidencia de efectos secundarios. La toxicidad pulmonar es especialmente relevante por el posible desenlace fatal que puede conllevar. Detectado y tratado a tiempo, el pronóstico es favorable. Con la intención de aumentar la casuística en este campo de la neumología exponemos el siguiente caso (AU)

We present a case of pulmonary toxicity associated with gemcitabina that caused respiratory insufficiency. The rise in incidences of neoplasms has led to an increase in the use of this drug. This, in turn, has led to a greater probability of side effects. Lung toxicity is particularly relevant as it can be fatal, but with rapid diagnosis and treatment the prognosis can be positive. This description of pulmonary toxicity induced by gemcitabine should provide additional information to what is already known in this field

The fate of chondrocyte in osteoarthritic cartilage of transgenic mice expressing bovine GH.

OBJECTIVE: The aim of the present study was to demonstrate whether bGH transgenic mice develop OA. We therefore studied in this animal model the structural features of cartilage and the subchondral bone changes of the knee joints that may be associated with osteoarthritic lesion. METHOD: Degenerative changes in the knee joints of bGH transgenic female mice (N = 11) and control mice (N = 11) were histologically analyzed at the age of 7 months. Histochemical and stereological studies were conducted. Immunohistochemistry on cell cyclin activity (assessed by anti-PCNA labeling) and cell viability (assessed by bcl-2 expression), as well as ribosomal activity (AgNOR), TNF-alpha expression and apoptosis (TUNEL technique) were performed. In ten 7-month-old female mice (Tg+ N = 5; control N = 5) the knee articular cartilages were studied with electron microscopy techniques. RESULTS: Disruption of the articular surface (18.2%), cleft (63.7%), cloning (81.8%), hypocellularity of chondrocytes (18.2%), moderate (54.6%) to severe (45.4%) loss of safranin-O staining, and duplication and rupture of the tidemark (54.5%) were some of the main features observed in articular cartilage chondrocytes of bGH transgenic mice. Furthermore, cell cyclin activity and cell viability decreased, while TNF-alpha expression and TUNEL+ cells increased. These chondrocytes also showed an increase in the number of black dots per cell, as revealed by the AgNOR technique. CONCLUSION: Our results show that bGH transgenic mice develop a lesion of the articular cartilage consistent with that described in osteoarthritis.

Regulation of beta-adrenoceptor-mediated relaxation of the rat aorta is modulated by endogenous ovarian hormones.

The aim of this study was to assess the influence of the endogenous status of ovarian hormones on the relaxation induced by the beta-adrenoceptor agonists isoprenaline (isoproterenol) and dobutamine in thoracic aorta segments, precontracted with noradrenaline, from age-matched (13-week-old) virgin (oestrus) and ovariectomized (OVX) prepubertal female Wistar rats. Isoprenaline-induced relaxation was decreased in intact aortic segments from OVX rats compared with that in segments from oestrus rats. Relaxation was significantly reduced by endothelium removal, 1 micromol/l propranolol or 100 micromol/l N(G)-nitro-L-arginine methyl ester (L-NAME). The beta(1)-adrenoceptor agonist dobutamine induced less relaxation in intact arteries from oestrus rats than did isoprenaline, and dobutamine-induced relaxation was markedly less in intact segments from OVX compared with oestrus rats. This dobutamine-induced relaxation was abolished by endothelium removal, and reduced by 1 micromol/l propranolol, 100 micromol/l L-NAME or 1 micromol/l yohimbine. Cholera toxin (an activator of the stimulatory G-protein G(s)) caused relaxation in intact arteries from oestrus rats; this relaxation was decreased by both deprivation of ovarian hormones and endothelium removal. Forskolin (a direct activator of the catalytic subunit of adenylate cyclase) and sodium nitroprusside (a nitric oxide donor and cGMP-dependent vasodilator agonist) induced similar endothelium-independent relaxation in arteries from both oestrus and OVX rats. These results suggest that the relaxation elicited by endothelial beta-adrenoceptor activation in the rat thoracic aorta is impaired by deprivation of female ovarian hormones; this impairment is caused, at least in part, by decreases in both the endothelial release of NO and G(s) function.

[Selective autotransplant of the spleen. An experimental study]. / Autotrasplante selectivo de bazo. Estudio experimental.

A study was carried out on 40 dogs. Four groups of ten dogs each were established. A laparotomy group, a simple splenectomy group and two groups which underwent a selective autotransplant of the medium an deep layers of a centrifugated solution of splenic medulla respectively. Immunisation with BSA showed that humoral immune response with formation of anti-BSA antibodies is more intense in the control group which underwent laparotomy than in the splenectomised group. The response obtained in dogs subjected to autotransplant of deep layer is almost identical to that of the control group while that of the medium layer showed a slightly lower response. Cellular immune response is more accentuated in the group which underwent autotransplant from the deep layer, while those from the medium layer showed a higher response than that of the splenectomised group.