Análisis retrospectivo del decaimiento en Pinus sylvestris L. (Sierra de Gúdar, Teruel) mediante el análisis de la composición isotópica (13C/12C, 18O/16O) en anillos de crecimiento.

Al 2002 es van detectar els primers símptomes de decaïment en Pinus sylvestris, a la Serra de Gúdar (Teruel). Individus afectats i sans es trobaven barrejats. El contrast tèrmic de finals de 2001 es presumeix com a factor incitador del decaïment, degut a la manca d’enduriment i pèrdua de la conductivitat hidràulica. També es va detectar un factor de predisposició dels arbres en relació a una possible inanició del carboni sota un estrés hídric perllongat. Possiblement això va afectar prèviament als arbres decaiguts, donada la seva major sensibilitat davant de l’estrès hídric demostrada en el present estudi mitjançant els isòtops estables (δ13C, δ18O).

Avaluació de la dieta d'una mostra de pacients fumadors i no fumadors

Les principals causes de mortalitat en el món són les malalties cardiovasculars, les malalties respiratòries i el càncer. Entre els factors de risc que predisposen a l’individu a patir aquestes malalties s’hi situen el tabac i la dieta poc saludable així com també la inactivitat física com el consum nociu d’alcohol.

EndoG links Bnip3-induced mitochondrial damage and caspase-independent DNA fragmentation in ischemic cardiomyocytes

Mitochondrial dysfunction, caspase activation and caspase-dependent DNA fragmentation are involved in cell damage in many tissues. However, differentiated cardiomyocytes repress the expression of the canonical apoptotic pathway and their death during ischemia is caspase-independent. The atypical BH3-only protein Bnip3 is involved in the process leading to caspase-independent DNA fragmentation in cardiomyocytes. However, the pathway by which DNA degradation ensues following Bnip3 activation is not resolved. To identify the mechanism involved, we analyzed the interdependence of Bnip3, Nix and EndoG in mitochondrial damage and DNA fragmentation during experimental ischemia in neonatal rat ventricular cardiomyocytes. Our results show that the expression of EndoG and Bnip3 increases in the heart throughout development, while the caspase-dependent machinery is silenced. TUNEL-positive DNA damage, which depends on caspase activity in other cells, is caspase-independent in ischemic cardiomyocytes and ischemia-induced DNA high and low molecular weight fragmentation is blocked by repressing EndoG expression. Ischemia-induced EndoG translocation and DNA degradation are prevented by silencing the expression of Bnip3, but not Nix, or by overexpressing Bcl-xL. These data establish a link between Bnip3 and EndoG-dependent, TUNEL-positive, DNA fragmentation in ischemic cardiomyocytes in the absence of caspases, defining an alternative cell death pathway in postmitotic cells.

El síndrome metabólico en el paciente renal

Se defi ne como síndrome metabólico al conjunto de factores que se dan en un individuo que le llevan a presentar resistencias a la insulina con hiperinsulinismo compensador que se asocia a trastornos del metabolismo hidrocarbonado, hipertensión arterial, alteraciones lipídicas y obesidad. Esta demostrado que este síndrome aumenta la posibilidad de padecer una enfermedad cardiovascular o diabetes mellitus por lo que se considera un factor de riesgo cardiovascular y de mortalidad en la población general. En pacientes...

TGF-β dependent regulation of oxygen radicals during transdifferentiation of activated hepatic stellate cells to myofibroblastoid cells

Background: The activation of hepatic stellate cells (HSCs) plays a pivotal role during liver injury because the resulting myofibroblasts (MFBs) are mainly responsible for connective tissue re-assembly. MFBs represent therefore cellular targets for anti-fibrotic therapy. In this study, we employed activated HSCs, termed M1-4HSCs, whose transdifferentiation to myofibroblastoid cells (named M-HTs) depends on transforming growth factor (TGF)-β. We analyzed the oxidative stress induced by TGF-β and examined cellular defense mechanisms upon transdifferentiation of HSCs to M-HTs. Results: We found reactive oxygen species (ROS) significantly upregulated in M1-4HSCs within 72 hours of TGF-β administration. In contrast, M-HTs harbored lower intracellular ROS content than M1-4HSCs, despite of elevated NADPH oxidase activity. These observations indicated an upregulation of cellular defense mechanisms in order to protect cells from harmful consequences caused by oxidative stress. In line with this hypothesis, superoxide dismutase activation provided the resistance to augmented radical production in M-HTs, and glutathione rather than catalase was responsible for intracellular hydrogen peroxide removal. Finally, the TGF-β/NADPH oxidase mediated ROS production correlated with the upregulation of AP-1 as well as platelet-derived growth factor receptor subunits, which points to important contributions in establishing antioxidant defense. Conclusion: The data provide evidence that TGF-β induces NADPH oxidase activity which causes radical production upon the transdifferentiation of activated HSCs to M-HTs. Myofibroblastoid cells are equipped with high levels of superoxide dismutase activity as well as glutathione to counterbalance NADPH oxidase dependent oxidative stress and to avoid cellular damage.

Cáncer colorrectal hereditario

El cáncer colorrectal (CCR) es una de las neoplasias más frecuentes en nuestro medio. En la actualidad, constituye la segunda neoplasia tanto en varones como en mujeres, tras el cáncer de pulmón y de mama, respectivamente. Cuando se consideran ambos sexos conjuntamente, ocupa el primer lugar en incidencia y representa la segunda causa de muerte por cáncer. En los últimos años hemos asistido a un avance muy significativo en el conocimiento de los mecanismos que participan en el desarrollo y progresión del CCR. Este avance abarca desde la identificación de diversos factores genéticos o moleculares implicados en la fisiopatología de esta neoplasia, hasta la caracterización de múltiples aspectos epidemiológicos involucrados en su génesis. En concreto, la demostración del potencial premaligno del adenoma colorrectal y la identificación de los genes responsables de las formas hereditarias de CCR han dado pie a diversas estrategias preventivas que pueden contribuir significativamente a disminuir la incidencia y la morbimortalidad por CCR.

Bivalirudin for patients with acute coronary syndromes

Background: Current guidelines for patients with moderate- or high-risk acute coronary syndromes recommend an early invasive approach with concomitant antithrombotic therapy, including aspirin, clopidogrel, unfractionated or low-molecular-weight heparin, and glycoprotein IIb/IIIa inhibitors. We evaluated the role of thrombin-specific anticoagulation with bivalirudin in such patients. Methods: We assigned 13,819 patients with acute coronary syndromes to one of three antithrombotic regimens: unfractionated heparin or enoxaparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin plus a glycoprotein IIb/IIIa inhibitor, or bivalirudin alone. The primary end points were a composite ischemia end point (death, myocardial infarction, or unplanned revascularization for ischemia), major bleeding, and the net clinical outcome, defined as the combination of composite ischemia or major bleeding. Results: Bivalirudin plus a glycoprotein IIb/IIIa inhibitor, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with noninferior 30-day rates of the composite ischemia end point (7.7% and 7.3%, respectively), major bleeding (5.3% and 5.7%), and the net clinical outcome end point (11.8% and 11.7%). Bivalirudin alone, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with a noninferior rate of the composite ischemia end point (7.8% and 7.3%, respectively; P = 0.32; relative risk, 1.08; 95% confidence interval [CI], 0.93 to 1.24) and significantly reduced rates of major bleeding (3.0% vs. 5.7%; P<0.001; relative risk, 0.53; 95% CI, 0.43 to 0.65) and the net clinical outcome end point (10.1% vs. 11.7%; P = 0.02; relative risk, 0.86; 95% CI, 0.77 to 0.97). Conclusions: In patients with moderate- or high-risk acute coronary syndromes who were undergoing invasive treatment with glycoprotein IIb/IIIa inhibitors, bivalirudin was associated with rates of ischemia and bleeding that were similar to those with heparin. Bivalirudin alone was associated with similar rates of ischemia and significantly lower rates of bleeding. (ClinicalTrials.gov number, NCT00093158.)

Multislice CT for assessing in-stent dimensions after left main coronary artery stenting: a comparison with three dimensional intravascular ultrasound

Objective: To evaluate the agreement between multislice CT (MSCT) and intravascular ultrasound (IVUS) to assess the in-stent lumen diameters and lumen areas of left main coronary artery (LMCA) stents. Design: Prospective, observational single centre study. Setting: A single tertiary referral centre. Patients: Consecutive patients with LMCA stenting excluding patients with atrial fibrillation and chronic renal failure. Interventions: MSCT and IVUS imaging at 9-12 months follow-up were performed for all patients. Main outcome measures: Agreement between MSCT and IVUS minimum luminal area (MLA) and minimum luminal diameter (MLD). A receiver operating characteristic (ROC) curve was plotted to find the MSCT cut-off point to diagnose binary restenosis equivalent to 6 mm2 by IVUS. Results: 52 patients were analysed. Passing-Bablok regression analysis obtained a β coefficient of 0.786 (0.586 to 1.071) for MLA and 1.250 (0.936 to 1.667) for MLD, ruling out proportional bias. The α coefficient was −3.588 (−8.686 to −0.178) for MLA and −1.713 (−3.583 to −0.257) for MLD, indicating an underestimation trend of MSCT. The ROC curve identified an MLA ≤4.7 mm2 as the best threshold to assess in-stent restenosis by MSCT. Conclusions: Agreement between MSCT and IVUS to assess in-stent MLA and MLD for LMCA stenting is good. An MLA of 4.7 mm2 by MSCT is the best threshold to assess binary restenosis. MSCT imaging can be considered in selected patients to assess LMCA in-stent restenosis

Coexistence of protease sensitive and resistant prion protein in 129VV homozygous sporadic Creutzfeldt-Jakob disease: a case report

Introduction: The coexistence of different molecular types of classical protease-resistant prion protein in the same individual have been described, however, the simultaneous finding of these with the recently described protease-sensitive variant or variably protease-sensitive prionopathy has, to the best of our knowledge, not yet been reported. Case presentation: A 74-year-old Caucasian woman showed a sporadic Creutzfeldt-Jakob disease clinical phenotype with reactive depression, followed by cognitive impairment, akinetic-rigid Parkinsonism with pseudobulbar syndrome and gait impairment with motor apraxia, visuospatial disorientation, and evident frontal dysfunction features such as grasping, palmomental reflex and brisk perioral reflexes. She died at age 77. Neuropathological findings showed: spongiform change in the patient"s cerebral cortex, striatum, thalamus and molecular layer of the cerebellum with proteinase K-sensitive synaptic-like, dot-like or target-like prion protein deposition in the cortex, thalamus and striatum; proteinase K-resistant prion protein in the same regions; and elongated plaque-like proteinase K-resistant prion protein in the molecular layer of the cerebellum. Molecular analysis of prion protein after proteinase K digestion revealed decreased signal intensity in immunoblot, a ladder-like protein pattern, and a 71% reduction of PrPSc signal relative to non-digested material. Her cerebellum showed a 2A prion protein type largely resistant to proteinase K. Genotype of polymorphism at codon 129 was valine homozygous. Conclusion: Molecular typing of prion protein along with clinical and neuropathological data revealed, to the best of our knowledge, the first case of the coexistence of different protease-sensitive prion proteins in the same patient in a rare case that did not fulfill the current clinical diagnostic criteria for either probable or possible sporadic Creutzfeldt-Jakob disease. This highlights the importance of molecular analyses of several brain regions in order to correctly diagnose rare and atypical prionopathies

Dificultad en la comunicación del riesgo de padecer cáncer hereditario.

Diferentes estudios han demostrado que, en ocasiones, los pacientes tienen dificultades a la hora de entender lo que el médico quiere comunicarles. El presente artículo intenta reflexionar sobre cuáles son los determinantes que pueden influir en el proceso de comunicación del riesgo en pacientes que tienen antecedentes familiares de cáncer y acuden a las Unidades de Consejo Genético en busca de asesoramiento. Existen estudios que señalan que los pacientes con antecedentes familiares de cáncer se preocupan por padecer dicha enfermedad. Sólo algunos de ellos han explorado cómo los pacientes entienden y perciben el concepto de riesgo y los posibles sesgos asociados a él. Como primeras aproximaciones, creemos que es necesario utilizar un lenguaje sencillo, claro y fácil de entender por parte de los pacientes, huyendo del lenguaje epidemiológico o médico. Del mismo modo es importante diseñar programas de formación psicoeducativos y material de soporte adecuado, así como el correcto manejo del counselling como herramienta principal de trabajo por parte de los profesionales y fomentar futuras investigaciones en este área determinada.

Personalidad premórbida y factores de riesgo en la enfermedad de Alzheimer

El presente artículo hace un repaso de los principales estudios respecto a los factores de riesgo para la enfermedad de Alzheimer, priorizando los factores psicosociales y especialmente los que se refieren a la personalidad premórbida. Entre los factores psicosociales de riesgo, aparecen como los más destacados un bajo nivel educativo y una actividad-relación social restringida. Necesidad de protección, tutelaje y dependencia de otras personas, relación social e interpersonal restringida e introversión, son los elementos de riesgo más relevantes para la personalidad premórbida. Los factores que aparecen en los estudios mencionados tienen relación con la hipótesis de trabajo de la investigación que se desarrolla actualmente, acerca de los perfiles de riesgo en la personalidad premórbida. Esta hipótesis los sitúa en el campo de lo emocional y de la relación interpersonal: fragilidad de la identidad personal y sostenimiento del yo a través de una relación simbiótica con el otro.

Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like disease

Chronic obstructive pulmonary disease (COPD) is a lethal progressive lung disease culminating in permanent airway obstruction and alveolar enlargement. Previous studies suggest CTL involvement in COPD progression; however, their precise role remains unknown. Here, we investigated whether the CTL activation receptor NK cell group 2D (NKG2D) contributes to the development of COPD. Using primary murine lung epithelium isolated from mice chronically exposed to cigarette smoke and cultured epithelial cells exposed to cigarette smoke extract in vitro, we demonstrated induced expression of the NKG2D ligand retinoic acid early tran - script 1 (RAET1)as well as NKG2D-mediated cytotoxicity. Furthermore, a genetic model of inducible RAET1 expression on mouse pulmonary epithelial cells yielded a severe emphysematous phenotype characterized by epithelial apoptosis and increased CTL activation, which was reversed by blocking NKG2D activation. We also assessed whether NKG2D ligand expression corresponded with pulmonary disease in human patients by staining airway and peripheral lung tissues from never smokers, smokers with normal lung function, and current and former smokers with COPD. NKG2D ligand expression was independent of NKG2D receptor expression in COPD patients, demonstrating that ligand expression is the limiting factor in CTL activation. These results demonstrate that aberrant, persistent NKG2D ligand expression in the pulmonary epithelium contributes to the development of COPD pathologies.

Sobre tránsitos, identidades y crecimiento postraumático en cáncer hereditario

A lo largo de la historia de la psico-oncología los conceptos de personalidad e identidad de los pacientes oncológicos se han utilizado frecuentemente tanto para explicar la aparición de la enfermedad como los cambios personales inducidos por la misma. Ya sea históricamente vinculado a los orígenes y causas en forma de personalidad que predispone al enfermar, o como transformación identitaria una vez el sujeto ha superado la enfermedad, las formas de ser constituyen también punto de arranque y destino de una parte importante del trabajo psicoterapéutico. Tras analizar las teorías socio-cognitivas de Janoff-Bulman y de Tedeschi y Calhoun sobre el fenómeno denominado crecimiento postraumático los autores se interrogan sobre el posible impacto de los modelos identarios y de crecimiento personal aplicados al ámbito del cáncer hereditario y el consejo genético.

Relationship between oral cancer and implants: clinical cases and systematic literature review

The use of implants for oral rehabilitation of edentulous spaces has recently been on the increase, which has also led to an increase in complications such as peri-implant inflammation or peri-implantitis. Chronic inflammation is a risk factor for developing oral squamous cell carcinoma (OSCC). Objectives: To review the literature of cases that associate implant placement with the development of oral cancer. Study design: We present two clinical cases and a systematic review of literature published on the relationship between oral cancer and implants. Results: We found 13 articles published between the years 1996 and 2009, referencing 18 cases in which the osseointegrated implants are associated with oral squamous cell carcinoma. Of those, 6 articles were excluded because they did not meet the inclusion criteria. Of the 18 cases reported, only 7 cases did not present a previous history of oral cancer or cancer in other parts of the body. Conclusions: Based on the review of these cases, a clear cause-effect relationship cannot be established, although it can be deduced that there is a possibility that implant treatment may constitute an irritant and/or inflammatory cofactor which contributes to the formation and/or development of OSCC.

Diagonal ear lobe crease and atherosclerosis: a review of the medical literature and dental implications

In Spain a significant number of individuals die from atherosclerotic disease of the coronary and carotid arteries without having classic risk factors and prodromal symptoms. The diagonal ear lobe crease (DELC) has been characterized in the medical literature as a surrogate marker which can identify high risk patients having occult atherosclerosis. This topic however has not been examined in either the medical or dental literature emanating from Spain. The majority of clinical, angiography and postmortem reports support the premise that DELC is a valuable extravascular physical sign able to distinguish some patients at risk of succumbing to atherosclerosis of the coronary arteries. A minority of studies have however failed to support this hypothesis. More recently reports using B mode ultrasound have also linked DELC to atherosclerosis of the carotid artery and another report has related DELC to the presence of calcified carotid artery atheromas on panoramic radiographs. DELC is readily visible during head and neck cancer screening examinations. In conjunction with the patient"s medical history, vital signs, and panoramic radiograph, the DELC may assist in atherosclerotic risk assessment