Stress et prévention de la récurrence de la maladie coronarienne

Les facteurs habituellement associés à l'augmentation du risque de maladie coronarienne (MC), tels le régime alimentaire, l'hyperlipidémie, la cigarette, l'inactivité physique et l'hérédité sont maitenant bien connus. Toutefois, Keys et al ainsi que d'autres auteurs ont montré que ces facteurs jouent un rôle dans seulement la moitié ou moins des cas de maladie coronarienne et qu'il y a assez d'exceptions pour indiquer la présence d'autres facteurs étiologiques. L'apparition de cette malade est aussi reliée à des caractéristiques psychologiques et sociales aussi bien qu'à des événements stressants de la vie. Enfin, d'autre études ont suggéré que les survivants d'épisodes coronariens ont une vie plus stressante, parfois aggravée par l'interaction d'autres facteurs intervenant avant, durant, et après l'infarctus ; par exemple, la durée de la maladie, la période de convalescence, l'attitude des amis, les conditions familiales et de travail. La nature de la réaction du patient et de sa famille au stress et aux conflits apparaît alors essentielle pour déterminer s'il y aura ou non rechute de la maladie ou nécessité d'une réhospitalisation. De plus, en s'appuyant sur les précédentes données, il devrait être possible de prédire, par la surveillance du niveau de stress, à quel moment une personne atteinte de cette maladie aura un nouvel épisode coronarien. Mieux encore, il devrait être possible d'aider les patients à résoudre les problèmes qui engendrent ce stress et dans certains cas, prévenir ainsi les rechutes.A good deal of recent research suggests that a period of mounting life stress is a precursor of many physical illnesses, including episodes of coronary heart disease (CHD). It should be possible then, by monitoring levels of stress to predict when a high risk individual is likely to suffer a further illness episode, and in some cases to prevent the episode by alleviating stress producing problems.Based on this concept, we have telephone-monitored (at monthly intervals) 37 CHD patients discharged from the coronary unit of the Montreal General Hospital. Stress was measured using a 20-item, self-report scale (Goldberg), and charted for each patient over a seven month period. When a patient's stress rose above a critical level he received a home visit by the project nurse, who investigated his problems and attempted to alleviate them. Interventions varied from simple reassurance to referral for psychiatric treatment or legal aid.Monitoring stress in this way revealed a picture remarkably like the theoretical model. None of the 15 consistently low-scoring patients required rehospitalization. Eleven patients had low scores at the time of discharge, but their scores rose above the critical level in subsequent months. Nine of them responded in a gratifying way- to the home visit and subsequent intervention by the nurse, and none required rehospitalization. The one patient of this type who did require hospitalization had not received a home visit because no nurse was available at the time. Four of the nine patients with consistently high scores required eight rehospitalization s for CHD episodes. These patients seemed to be chronically stressed, and often required continuous support from the nurse.Our study suggests that life stress may be more important than the traditional physical risk factors (obesity, smoking, hypertension, family history of CHD, lack of exercise) in the etiology of recurrent CHD when patients receive adequate medical care.Some of our findings suggest that the nurse's interventions do reduce rehospitalizations, but a large scale controlled study is called for.We conclude that this technique is worth further evaluation, both as a research method and as a practical device for the prevention of rehospitalization of CHD patients and of other types of episodic illnesses

Gene expression changes induced by the tumorigenic pyrrolizidine alkaloid riddelliine in liver of Big Blue rats

<p>Abstract</p> <p>Background</p> <p>Pyrrolizidine alkaloids (PAs) are probably the most common plant constituents that poison livestock, wildlife, and humans worldwide. Riddelliine is isolated from plants grown in the western United States and is a prototype of genotoxic PAs. Riddelliine was used to investigate the genotoxic effects of PAs via analysis of gene expression in the target tissue of rats in this study. Previously we observed that the mutant frequency in the liver of rats gavaged with riddelliine was 3-fold higher than that in the control group. Molecular analysis of the mutants indicated that there was a statistically significant difference between the mutational spectra from riddelliine-treated and control rats.</p> <p>Results</p> <p>Riddelliine-induced gene expression profiles in livers of Big Blue transgenic rats were determined. The female rats were gavaged with riddelliine at a dose of 1 mg/kg body weight 5 days a week for 12 weeks. Rat whole genome microarray was used to perform genome-wide gene expression studies. When a cutoff value of a two-fold change and a <it>P</it>-value less than 0.01 were used as gene selection criteria, 919 genes were identified as differentially expressed in riddelliine-treated rats compared to the control animals. By analysis with the Ingenuity Pathway Analysis Network, we found that these significantly changed genes were mainly involved in cancer, cell death, tissue development, cellular movement, tissue morphology, cell-to-cell signaling and interaction, and cellular growth and proliferation. We further analyzed the genes involved in metabolism, injury of endothelial cells, liver abnormalities, and cancer development in detail.</p> <p>Conclusion</p> <p>The alterations in gene expression were directly related to the pathological outcomes reported previously. These results provided further insight into the mechanisms involved in toxicity and carcinogenesis after exposure to riddelliine, and permitted us to investigate the interaction of gene products inside the signaling networks.</p

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

Meeting abstrac

Análise e classificação dos fatores humanos nos acidentes industriais Analysis and classification of the human factors in industrial accidents

O presente texto apresenta a evolução do conhecimento do fenômeno "acidente", mostrando a mudança do conceito do acidente como obra do destino para um componente do processo produtivo de qualquer segmento - industrial, aeronáutico, serviços, transporte dentre outros. O método de análise e classificação dos fatores humanos nos acidentes é apresentado e discutido quanto à viabilidade de implementação. Finalmente, conclui-se que a forma atual e moderna para prevenção de acidentes está baseada na identificação antecipada das falhas latentes da organização e do sistema, e que a ferramenta apresentada contribui para a gestão proativa e conseqüentemente para a diminuição do impacto dos acidentes do trabalho no processo produtivo.<br>The present text presents the evolution of the knowledge of the phenomenon "accident", showing the change of the concept of the accident as workmanship of the destination for one component of the productive process of any segment - industrial, aeronautical, services, transports amongst others. The method of analysis and classification of the human factors in the accidents is presented and argued how much to the implementation viability. Finally one concludes that the current and modern form for prevention of accidents is based on the anticipated identification of the latent failures of the organization and the system, and that the presented tool contributes consequently for the pro-active management and in the reduction of the impact of the employment-related accidents in the productive process

Interferon-dependent IL-10 production by Tregs limits tumor Th17 inflammation

The capacity of IL-10 and Tregs in the inflammatory tumor microenvironment to impair anticancer Th1 immunity makes them attractive targets for cancer immunotherapy. IL-10 and Tregs also suppress Th17 activity, which is associated with poor prognosis in several cancers. However, previous studies have overlooked their potential contribution to the regulation of pathogenic cancer-associated inflammation. In this study, we investigated the origin and function of IL-10–producing cells in the tumor microenvironment using transplantable tumor models in mice. The majority of tumor-associated IL-10 was produced by an activated Treg population. IL-10 production by Tregs was required to restrain Th17-type inflammation. Accumulation of activated IL-10(+) Tregs in the tumor required type I IFN signaling but not inflammatory signaling pathways that depend on TLR adapter protein MyD88 or IL-12 family cytokines. IL-10 production limited Th17 cell numbers in both spleen and tumor. However, type I IFN was required to limit Th17 cells specifically in the tumor microenvironment, reflecting selective control of tumor-associated Tregs by type I IFN. Thus, the interplay of type I IFN, Tregs, and IL-10 is required to negatively regulate Th17 inflammation in the tumor microenvironment. Therapeutic interference of this network could therefore have the undesirable consequence of promoting Th17 inflammation and cancer growth