Liver damage in bleomycin-induced pulmonary fibrosis in mice.

Pulmonary fibrosis is an emerging disease with a poor prognosis and high mortality rate that is even surpassing some types of cancer. This disease has been linked to the concomitant appearance of liver cirrhosis. Bleomycin-induced pulmonary fibrosis is a widely used mouse model that mimics the histopathological and biochemical features of human systemic sclerosis, an autoimmune disease that is associated with inflammation and expressed in several corporal systems as fibrosis or other alterations. To determine the effects on proliferation, redox and inflammation protein expression markers were analyzed by immunohistochemistry. Analyses showed a significant increase in protein oxidation levels by lipoperoxidation bio-products and in proliferation and inflammation processes. These phenomena were associated with the induction of the redox status in mice subjected to 100 U/kg bleomycin. These findings clearly show that the bleomycin model induces histopathological alterations in the liver and partially reproduces the complexity of systemic sclerosis. Our results using the bleomycin-induced pulmonary fibrosis model provide a protocol to investigate the mechanism underlying the molecular alteration found in the liver linked to systemic sclerosis.

Sox2 expression in breast tumours and activation in breast cancer stem cells.

The cancer stem cell (CSC) model does not imply that tumours are generated from transformed tissue stem cells. The target of transformation could be a tissue stem cell, a progenitor cell, or a differentiated cell that acquires self-renewal ability. The observation that induced pluripotency reprogramming and cancer are related has lead to the speculation that CSCs may arise through a reprogramming-like mechanism. Expression of pluripotency genes (Oct4, Nanog and Sox2) was tested in breast tumours by immunohistochemistry and it was found that Sox2 is expressed in early stage breast tumours. However, expression of Oct4 or Nanog was not found. Mammosphere formation in culture was used to reveal stem cell properties, where expression of Sox2, but not Oct4 or Nanog, was induced. Over-expression of Sox2 increased mammosphere formation, effect dependent on continuous Sox2 expression; furthermore, Sox2 knockdown prevented mammosphere formation and delayed tumour formation in xenograft tumour initiation models. Induction of Sox2 expression was achieved through activation of the distal enhancer of Sox2 promoter upon sphere formation, the same element that controls Sox2 transcription in pluripotent stem cells. These findings suggest that reactivation of Sox2 represents an early step in breast tumour initiation, explaining tumour heterogeneity by placing the tumour-initiating event in any cell along the axis of mammary differentiation.

Manejo anestésico de una masa tumoral abdominal gigante / No disponible

No disponible

Eclampsia y amaurosis total bilateral en una paciente condiagnóstico a posteriori de leucoencefalopatía posterior reversible / Eclampsia and total bilateral amaurosis in a woman subsequently diagnosed with reversible posterior leukoencephalopathy syndrome

La eclampsia es una de las complicaciones de la preeclampsiay se define ante la aparición de convulsionesgeneralizadas y/o coma en ausencia de cualquier otroproblema neurológico. En general, no suele existir déficitneurológico focal ni coma prolongado después deuna crisis. Por ello, su aparición nos debe hacer considerarotros cuadros clínicos que puedan requerir untratamiento especial.Presentamos el caso de una gestante con amaurosis bilateraltotal después de una convulsión generalizada tónicoclónica,que fue diagnosticada a posteriori de leucoencefalopatíaposterior reversible, entidad clínico-radiológicaque puede relacionarse con numerosas etiologías comoencefalopatía hipertensiva, eclampsia, insuficiencia renal otratamiento con inmunosupresores. Cursa con cefalea,alteración de la consciencia, trastornos visuales (inclusiveceguera) y convulsiones, generalmente coincidiendo conaumento rápido en las cifras de tensión arterial. La neuroimagenes esencial para su diagnóstico y el hallazgo típicoes el edema en los hemisferios cerebrales posteriores. Lahipótesis más aceptada para explicar su mecanismo fisiopatológicoes el fallo de la autorregulación cerebral condesarrollo de edema vasogénico. Su pronóstico es bueno ylas anomalías se suelen resolver completamente con el tratamientoadecuado, que no difiere del propio manejo de laeclampsia, con riguroso control de la tensión arterial (AU)

Eclampsia is a complication of preeclampsia and ischaracterized by the appearance of grand mal seizuresand/or coma, in the absence of any other neurologicalabnormalities. Neither focal neurological deficit norprolonged coma tends to develop following a crisis.Eclampsia should therefore lead us to consider otherclinical entities that may require special treatment.We report the case of a pregnant woman who presentedtotal bilateral loss of vision following a grand mal seizure.The patient was subsequently diagnosed with reversibleposterior leukoencephalopathy syndrome, which has clinicaland radiologic manifestations linked to several causes, suchas hypertensive encephalopathy, eclampsia, kidney failure,and immunosuppressant therapy. The syndrome involvesheadache, altered states of consciousness, changes in vision(including blindness), and seizures; these symptomsgenerally coincide with a rapid increase in blood pressure.Diagnosis requires neuroimaging, and the typical finding isedema in the posterior zones of the brain hemispheres.The most widely accepted hypothesis concerning thepathophysiologic mechanism underlying this syndromeis failure of cerebral autoregulation with developmentof vasogenic edema. The prognosis is good and thealterations usually resolve completely with appropriatetreatment, which is the same as for the management ofeclampsia, with strict monitoring of blood pressure (AU)

A dual and opposite effect of Calendula officinalis flower extract: chemoprotector and promoter in a rat hepatocarcinogenesis model.

Calendula officinalis extracts have protective and cytotoxic effects. We previously reported the dual activity of C. officinalis in primary rat hepatocyte cultures treated with N-nitrosodiethylamine. At nM concentrations it was anti-genotoxic while at microM concentrations it exhibited genotoxic effects. Here we tested the activity of Calendula officinalis in vivo in male Fischer 344 rats initiated with N-nitrosodiethylamine, promoted with 2-acetylaminofluorene, and 70 % partially hepatectomized. Liver gamma-glutamyltranspeptidase positively altered hepatocyte foci 25 days after initiation were our end point. The protective effect of C. officinalis started at 0.1 mg/kg concentration, increased at 0.5 mg/kg and reached its maximum at 2.5 mg/kg, when it decreased the area and number of altered foci by 55 % and 49 %, respectively, in comparison with rats treated only with carcinogen. At 5 mg/kg the number and area of altered hepatocyte foci were still lower, but almost reached the figures of carcinogen-treated rats. Ten and 20 mg/kg doses produced a notorious increment in the area and number of altered hepatic foci, and at 40 mg/kg of extract the increment was 40 % and 53 %, respectively. Additionally, when 2-acetylaminofluorene was substituted by a 40 mg/kg C. officinalis extract, a promoting effect was observed with increments of 175 % and 266 % in area and number of altered hepatocyte foci with respect to controls. When N-nitrosodiethylamine was substituted by 40 mg/kg of extract, the latter did not show initiator activity. In summary, we showed a protecting activity of C. officinalis at low doses, but doses above 10 mg/kg increased altered hepatocyte foci. This dual effect is an example of the phenomenon of hormesis. Furthermore, 40 mg/kg of dry weight extract administered instead of 2-acetylaminofluorene induced a clear promoting activity. These in vivo results are similar and consistent with those reported by us in primary rat liver cell cultures.

[Neonatal oliguria associated with hyperuricemia]. / Oliguria neonatal asociada a hiperuricemia.

Acute renal failure syndrome in the newborn has many etiologic factors. Hyperuricemia as unique etiology of this syndrome has been seldom cited in literature, although is a well know factor operating together with others. From nine newborns with oliguria, hyperuricemia vas a contributing factor in appearance of the syndrome in seven. In the other two cases hyperuricemia was the sole possible etiologic factor in development of oliguria which was classified as functional. Hyperuricemia alone may be the unique etiologic factor in functional oliguria of the newborn being further investigations needed to understand its precise mechanism.