[A decrease in height in women with non-insulin-dependent diabetes mellitus (NIDDM)].
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Adult↗
Biomedical subjects
M Pavón
Publications and source records attributed to M Pavón.
Identification by two-dimensional gel electrophoresis of vaccinia virus and cellular phosphoproteins modified after inducible expression of the dsRNA-activated protein kinase.
The interferon (IFN)-induced double-stranded (ds) RNA-activated protein kinase (PKR) is a serine/threonine kinase that plays an important role in the biology of IFN, exerting antiviral and anticellular actions. These effects have been correlated with phosphorylation of the eukaryotic initiation factor eIF-2alpha and the NF-kappaB inhibitor IkappaB, although it has not been demonstrated that IkappaB is a direct target of PKR in vivo. In view of the various biological effects of PKR, it is likely that other cellular substrates are involved in PKR action. To identify novel substrates of PKR, we have carried out a systematic study of the phosphorylated proteins from cultured cells following PKR activation using high-resolution two-dimensional gel electrophoresis (2D-PAGE). We have used metabolic labeling with [32P]orthophosphate of HeLa cells infected with vaccinia virus (VV) recombinants expressing wild type (wt) or the catalytically inactive mutant form (K296R) of PKR under regulation of the Escherichia coli lacI operator/repressor system. Upon induction of PKR in the presence of isopropyl-beta-D-thiogalactoside (IPTG), the 68-kDA wt enzyme and eIF-2alpha are phosphorylated. These events lead to changes in the phosphorylation state of viral and cellular proteins. A distinct set of VV-induced phosphoproteins remained phophorylated, while the labeling of other viral proteins decreased markedly, probably as a result of a PKR-dependent translational block. Five proteins of unknown origin (68, 26, 20, 19, 15-16 kDA) appeared to be newly phosphorylated after PKR activation. Expression of the catalytically inactive K296R mutant form of PKR did not induce changes in the phosphorylation of VV proteins. Thus, by 2D-PAGE, we identified cellular and VV-induced phosphoproteins modified after PKR activation. Some or all of the phosphoproteins appearing or increasing in amount after PKR activation might not be direct targets of PKR, but rather indirect consequences of PKR activation.
Blotting, Western↗
The intraischemic and early reperfusion changes of protein synthesis in the rat brain. eIF-2 alpha kinase activity and role of initiation factors eIF-2 alpha and eIF-4E.
Rats were subjected to the standard four-vessel occlusion model of transient cerebral ischemia (vertebral and carotid arteries). The effects of normothermic ischemia (37 degrees C) followed or not by 30-minute reperfusion, as well as 30-minute postdecapitative ischemia, on translational rates were examined. Protein synthesis rate, as measured in a cell-free system, was significantly inhibited in ischemic rats, and the extent of inhibition strongly depended on duration and temperature, and less on the model of ischemia used. The ability of reinitiation in vitro (by using aurintricarboxylic acid) decreased after ischemia, suggesting a failure in the synthetic machinery at the initiation level. Eukaryotic initiation factor 2 (eIF-2) presented almost basal activity and levels after 30-minute normothermic ischemia, and the amount of phosphorylated eIF-2 alpha in these samples, as well as in sham-control samples, was undetectable. The decrease in the levels of phosphorylated initiation factor 4E (eIF-4E) after 30-minute ischemia (from 32% to 16%) could explain, at least partially, the impairment of initiation during transient cerebral ischemia. After reperfusion, eIF-4E phosphorylation was almost completely restored to basal levels (29%), whereas the level of phosphorylated eIF-2 alpha was higher (13%) than in controls and ischemic samples (both less than 2%). eIF-2 alpha kinase activity in vitro as measured by phosphorylation of endogenous eIF-2 in the presence of ATP/Mg2+, was higher in ischemic samples (8%) than in controls (4%). It seems probable that the failure of the kinase in phosphorylating eIF-2 in vivo during ischemia is due to the depletion of ATP stores. The levels of the double-stranded activated eIF-2 alpha kinase were slightly higher in ischemic animals than in controls. Our results suggest that the modulation of eIF-4E phosphorylation could be implicated in the regulation of translation during ischemia. On the contrary, phosphorylation of eIF-2 alpha, by an eIF-2 alpha kinase already activated during ischemia, represents a plausible mechanism for explaining the inhibition of translation during reperfusion.
Animals↗
[Age is the independent prognostic factor in acute myocardial infarct. The clinical course of infarct in the elderly patient].
We analyze the influence of age in the evolution of patients with acute myocardial infarction admitted to our Coronary Care Unit throughout two years (1990 and 1991). All 542 patients admitted during this period were classified in three groups: 299 less than 65 year old (group A), 170 between 65 and 74 year old (group B), and 73 with 75 year old or more (group C). Aged patients had a worse clinical condition, with significantly more previous heart failure, diabetes or hypertension, and the Killip's class was worse in group C than in group B, and worse in this than in group A (p = 0.00000). The mortality rate was 6.7% in group A, 12.9% in group B, and 31.5% group C (p = 0.00000). After a multivariate analysis, only three factors were significantly associated to prognosis: previous stroke, Killip's class, and group of age. Fibrinolytic therapy and coronary arteriography were less frequent with old people (p = 0.00000 and p = 0.00000 respectively). We conclude that age is an independent factor of prognosis during myocardial infarction. Old people have a worse clinical condition and the treatment is less aggressive than in young people.
Age Factors↗
[The prognosis for elderly patients admitted to a coronary unit for myocardial infarct: the changes over a decade].
INTRODUCTION AND AIM: New therapies have been added that improve prognosis of patients with myocardial infarction. Our purpose was to know if elderly patients reach benefit from these therapeutic changes. METHODS: We have analyzed the clinical data of 227 patients older than 70 who were admitted in our coronary care unit: 78 admitted in 1980-81 and 14 admitted in 1990-91. RESULTS: Although differences were not significant, in 1990-91 there were more women (36% versus 28%), less smoking (24% versus 33%), more patients with previous infarction (19% versus 12%), more hypertension (53% versus 43%), less anterior infarcts (38% versus 45%) more non Q infarcts (11% versus 1%), and less bundle branch block (21% versus 31%). In 1990-91, pacemakers were used less often (13% versus 27%, p = 0.03), thrombolytic therapy was given to 16 patients (10.7%), and the mortality rate was a little inferior (22% versus 30%, not significant). Female sex, not being a smoker, Killip class and bundle branch block were significantly related to mortality. After a multivariate analysis in which these factors we included, the date of admission resulted an independent predictor of mortality, with an odds ratio of 1990-91 to 1980-81 of 0.43 (p = 0.039). CONCLUSIONS: The management of patients older than 70 with myocardial infarction has improved, with a significantly lesser risk of dead after multivariate analysis, despite that thrombolysis has been scarcely applied.
Aged↗
Syncope induced by propranolol in hypertrophic cardiomyopathy.
A patient with chest pain was found to have obstructive hypertrophic cardiomyopathy. After the first oral dose of propranolol, syncope developed together with atrioventricular block. An electrophysiologic study revealed an intermittent advanced (His-Purkinje) block within the atrioventricular conduction system. Caution is recommended when treatment is initiated in patients with hypertrophic cardiomyopathy in whom there is any suspicion of abnormalities in the atrioventricular conduction tissues.
Cardiomyopathy, Hypertrophic↗