1000 resultados para 338.9861
Resumo:
Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia.
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OBJECTIVE: To assess whether thalamic strokes presenting with a central Horner's syndrome (HS) show specific clinicoanatomic patterns. METHODS: From the Lausanne Stroke Registry (period 1993 to spring 2002), the authors selected all patients with thalamic stroke presenting with ipsilateral HS. Patients with complete infarction of the posterior cerebral artery territory, with involvement of middle cerebral artery territory or bilateral lesions, were excluded. Lesions on brain MRI were correlated with standard neuroanatomic templates. RESULTS: Nine patients with thalamic infarction presenting with central HS were found; all showed contralateral ataxic hemiparesis (AH). Lesions involved the anterior or paramedian thalamus and extended to the hypothalamic or rostral paramedian mesencephalic area in all but one subject. Associated clinical signs included dysphasia (two patients), somnolence (six), vertical gaze paresis (two), asterixis (two), and hemihypesthesia (three). CONCLUSION: The alternate clinical pattern of central HS with contralateral AH is a stroke syndrome of the diencephalic-mesencephalic junction, resulting from the involvement of the common arterial supply to the paramedian/anterior thalamus, the posterior hypothalamus and the rostral paramedian midbrain.
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Numérisation partielle de reliure
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As a consequence of growing global migration, physicians in French speaking Switzerland often face communicational difficulties with allophone patients. This paper first discusses advantages and shortcomings of various ways of dealing with this kind of situations. The indication of using professional interpreters will be addressed, as well as some specific therapeutic, linguistic and relational features of triadic consultations involving a physician, a patient and an interpreter. Finally, useful practical information and advices are provided to clinicians in order to help them optimize their consultations with allophone patients.
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Coats plus is a highly pleiotropic disorder particularly affecting the eye, brain, bone and gastrointestinal tract. Here, we show that Coats plus results from mutations in CTC1, encoding conserved telomere maintenance component 1, a member of the mammalian homolog of the yeast heterotrimeric CST telomeric capping complex. Consistent with the observation of shortened telomeres in an Arabidopsis CTC1 mutant and the phenotypic overlap of Coats plus with the telomeric maintenance disorders comprising dyskeratosis congenita, we observed shortened telomeres in three individuals with Coats plus and an increase in spontaneous γH2AX-positive cells in cell lines derived from two affected individuals. CTC1 is also a subunit of the α-accessory factor (AAF) complex, stimulating the activity of DNA polymerase-α primase, the only enzyme known to initiate DNA replication in eukaryotic cells. Thus, CTC1 may have a function in DNA metabolism that is necessary for but not specific to telomeric integrity.
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OBJECTIVES: To show the effectiveness of a brief group alcohol intervention. Aims of the intervention were to reduce the frequency of heavy drinking occasions, maximum number of drinks on an occasion and overall weekly consumption. METHODS: A cluster quasi-randomized control trial (intervention n = 338; control n = 330) among 16- to 18-year-old secondary school students in the Swiss Canton of Zürich. Groups homogeneous for heavy drinking occasions (5+/4+ drinks for men/women) consisted of those having medium risk (3-4) or high risk (5+) occasions in the past 30 days. Groups of 8-10 individuals received two 45-min sessions based on motivational interviewing techniques. RESULTS: Borderline significant beneficial effects (p < 0.10) on heavy drinking occasions and alcohol volume were found 6 months later for the medium-risk group only, but not for the high-risk group. None of the effects remained significant after Bonferroni corrections. CONCLUSIONS: Group intervention was ineffective for all at-risk users. The heaviest drinkers may need more intensive treatment. Alternative explanations were iatrogenic effects among the heaviest drinkers, assessment reactivity, or reduction of social desirability bias at follow-up through peer feedback.
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Myasthenia gravis (MG) can be difficult to treat despite an available therapeutic armamentarium. Our aim was to analyze the factors leading to unsatisfactory outcome (UO). To this end we used the Myasthenia Gravis Foundation of America classification system. Forty one patients with autoimmune MG were followed prospectively from January 2003 to December 2007. Outcomes were assessed throughout follow-up and at a final visit. 'Unchanged', 'worse', 'exacerbation' and 'died of MG' post-intervention status were considered UOs. During follow-up, UO rates reached 54% and were related to undertreatment (41%), poor treatment compliance (23%), infections (23%), and adverse drug effects (13%). The UO rate at final study assessment was 20%. UO during follow-up was significantly (P = 0.004) predictive of UOs at final assessment. When care was provided by neuromuscular (NM) specialists, patients had significantly better follow-up scores (P = 0.01). At final assessment UO rates were 7% and significantly better in patients treated by NM specialists, compared to other physicians where UO rates reached 27%. UO was a frequent finding occurring in more than half our patients during follow-up. Nearly two-thirds of the UOs could have been prevented by appropriate therapeutic adjustments and improved compliance. The differential UO rates at follow-up, their dependency on the degree to which the management was specialized and their correlation with final outcomes suggest that specialized MG care improves outcomes.
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Comprend : [Portrait en frontispice : portrait de l'auteur, Goethe.] Goethe. [Cote : m Yh 26/Microfilm R 132779] ; [Vignette à la Page de Titre : Marguerite et Faust.] [Cote : m Yh 26/Microfilm R 132779] ; [Vignette p.103. Partie I. : Faust rencontre Méphistophélès. Au loin, Marguerite.] [Cote : m Yh 26/Microfilm R 132779] ; [Pl. en reg. p.120. Partie I. :] Faust et Méphistophélès. Salut au savant dicteur! Vous m'avez rudement fait suer. [Cote : m Yh 26/Microfilm R 132779] ; [Pl. en reg. p.138. Partie I. :] Méphistophélès et Siebel. Sorcellerie! tombez sur lui, le drôle est condamné. [Cote : m Yh 26/Microfilm R 132779] ; [Pl. en reg. p.152. Partie I. :] Marguerite. Ah regardez-là! admirez-là! [Cote : m Yh 26/Microfilm R 132779] ; [Pl. en reg. p.159. Partie I. :] Faust et Marguerite. Qu'est cela? un bouquet! Non, un simple jeu. [Cote : m Yh 26/Microfilm R 132779] ; [Pl. en reg. p.167. Partie I. :] Lieschen. Oui-dà! Sybille me l'a dit aujourd'hui, elle a finie, elle aussi, par se laisser séduire. [Cote : m Yh 26/Microfilm R 132779] ; [Pl. en reg. p.170. Partie I. :] Faust. Voici mon lourdeau apprivoisé! Maintenat, au large! et tâchons de nous éclipser lestement; car j'entends déjà crier au meutre. [Cote : m Yh 26/Microfilm R 132779] ; [Pl. en reg. p.192. Partie I. :] Marguerite et Faust. Henri, tu me fais horreur! [Cote : m Yh 26/Microfilm R 132779] ; [Pl. en reg. p.225. Partie II. :] Faust. O prodige! elle grandit entre mes mains, elle s'enflamme, des éclairs en jaillissent! [Cote : m Yh 26/Microfilm R 132779] ; [Pl. en reg. p.338. Partie II. :] Les anges et Marguerite. Alors la pécgeresse se répand en actions de gra^ces aux pieds de la mère de Dieu. [Cote : m Yh 26/Microfilm R 132779]