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Biomedical subjects

M Villalba

Publications and source records attributed to M Villalba.

103 records · Page 6Linked to original sources
PubMed1985

Modulation by the ratio S-adenosylmethionine/S-adenosylhomocysteine of cyclic AMP-dependent phosphorylation of the 50 kDa protein of rat liver phospholipid methyltransferase.

The present results show that the catalytic subunit of cyclic AMP-dependent protein kinase phosphorylates the 50 kDa protein of rat liver phospholipid methyltransferase at one single site on a serine residue. Phosphorylation of this site is stimulated 2- to 3-fold by S-adenosylmethionine. S-adenosylmethionine-dependent protein phosphorylation is time- and dose-dependent and occurs at physiological concentrations. S-adenosylhomocysteine has no effect on protein phosphorylation but inhibits S-adenosylmethionine-dependent protein phosphorylation. S-Adenosylmethionine/S-adenosylhomocysteine ratios varying from 0 to 5 produce a dose-dependent stimulation of the phosphorylation of the 50 kDa protein. In conclusion, these results show, for the first time, that the ratio S-adenosylmethionine/S-adenosylhomocysteine can modulate phosphorylation of a specific protein.

Animals↗
PubMed1985

Phospholipid methyltransferase phosphorylation by intact hepatocytes: effect of glucagon.

We have obtained a rabbit antiserum that specifically immunoprecipitates the 50K and 25K proteins of rat liver phospholipid methyltransferase. Exposure of intact rat hepatocytes preincubated with [32P]phosphate to glucagon induces a time-dependent phosphorylation of the 50K protein of phospholipid methyltransferase. The incorporation of 32P into the 50K protein was only on phosphoserine. These data support the concept that the activation of rat liver phospholipid methyltransferase by glucagon is mediated by phosphorylation of the enzyme.

Animals↗
PubMed1984

Activation of partially purified rat liver lipid methyltransferase by phosphorylation.

Incubation of partially purified rat liver lipid methyltransferase with MgATP and the catalytic subunit of the cyclic AMP dependent protein kinase results in up to 4-fold activation of the methylation reaction. When (gamma-32p) MgATP is included in the assay mixture, the analysis of the phosphoprotein products by electrophoresis shows the incorporation of 32p into a single protein band of about 50K and pI 4.75. It is concluded that rat liver lipid methyltransferase can be converted from a low activity dephosphorylated form to a high activity phosphorylated form.

Adenosine Triphosphate↗
PubMed1984

Steroid effect on capillary permeability in gram-negative septic shock. Evaluation by vitreous fluorophotometry.

The purpose of this study was to use vitreous fluorophotometry to evaluate the effects of glucocorticoids on capillary permeability during gram-negative septic shock. Twelve preconditioned mongrel dogs were cannulated with arterial lines and Swan-Ganz catheters for complete hemodynamic monitoring. All 12 dogs were injected with fluorescein and live Escherichia coli intravenously. Six of the 12 dogs were administered methylprednisolone at set intervals after the initiation of the E coli infusion. Vitreous fluorophotometric recordings were taken hourly. Leakage of fluorescein into the extravascular space occurred in both groups, up to several hours after E coli infusion. However, in the steroid group, the capillary permeability decreased and stabilized following the initial increase in permeability. We conclude that steroids, when administered during the development of gram-negative septic shock, may modify capillary permeability changes.

Animals↗
PubMed1983

Fluorophotometric evaluation of capillary permeability in gram-negative shock.

We developed a new method by which capillary permeability changes secondary to gram-negative sepsis can be easily monitored. In a preliminary trial, ten dogs were injected intravenously with live Escherichia coli. Progressive extravasation of fluorescein from the retinal capillary bed was demonstrated by retinal angiography, thus indicating "capillary leak." In a subsequent trial, fluorophotometry facilitated direct quantitation of this leak. Three control and three septic dogs underwent continuous hemodynamic and physiologic monitoring. Hourly retinal fluorophotometric measurements were recorded. The control group demonstrated no capillary leak nor any change in hemodynamic and physiologic status. In the septic group, there was a dramatic increase in extravascular fluorescein concentration two to four hours after E coli infusion, correlating well with hemodynamic and physiologic parameters typical of gram-negative shock.

Animals↗
PubMed1979

The etiology of post-traumatic empyema and the role of decortication.

Decortication post-traumatic empyema (PTE) was performed in 27 patients from 1972 through 1977. All 27 patients had penetrating chest wounds and were refractory to antibiotics and tube thoracostomy. Factors associated with PTE included unrecognized diaphragmatic perforation, large hemothorax greater than 500 ml, pulmonary contusion, extrathoracic extension of hematoma within the chest wall, and incomplete expansion of the lung with initial tube thoracostomy. Prophylactic antibiotic usage did not prevent PTE nor lead to negative intrapleural cultures preoperatively. The timing of decortication varied with indication: two patients with infected pneumothorax had surgery within 1 week; 15 patients with infected pleural clot had surgery within 4 weeks; ten including nine who were readmitted to the hospital had surgery more than 4 weeks after injury. Prevention of PTE requires early recognition of hemo- or pneumothorax, early tube thoracostomy with complete evacuation of blood and expansion of lung, careful daily monitoring of subsequent fluid accumulation, and prompt evacuation when such fluid accumulates. Once PTE becomes well established and refractory to standard modalities, decortication with evacuation of the empyema cavity should be performed as soon as possible.

Adolescent↗
PubMedDate not supplied

Age-related changes in calcium homeostatic mechanisms in synaptosomes in relation with working memory deficiency.

Aging is associated with alterations in different systems that govern neuronal calcium homeostasis. This study was designed to determine whether any of these alterations may contribute to the decline in spatial working memory that is observed in old rats. Several parameters [initial (5 s) and steady state (15 min) 45Ca2+ uptake, FCCP-releaseable 45Ca2+, [Ca2+]i levels, depolarization-induced phosphoprotein (P97, PP65, P42) dephosphorylation and acetylcholine levels and release) involved in calcium homeostasis/signaling were determined in whole brain synaptosomes derived from adult (9-month-old) and old (24-month-old) rats that were evaluated for spatial memory performance in the eight-arm radial maze. The neurochemical analysis indicated that both the 9- and 24-month-old rats were impaired with respect to 3-month-old animals. When learners (animals reaching criterion; RC) were compared to memory impaired rats (MI), it was found that the FCCP-releaseable 45Ca2+ of synaptosomes, that reflects mitochondrial calcium, was lower in the MI than the RC rats and was correlated with the behavioral performance of the rats in their first testing sessions. The results suggest that the loss of calcium uptake capacity in synaptic mitochondria during aging may be associated with impaired working memory in old animals.

Acetylcholine↗
PubMedDate not supplied

Altered cell calcium regulation in synaptosomes and brain cells of the 30-month-old rat: prominent effects in hippocampus.

A deficient regulation of neuronal cytosolic calcium levels has been suggested to play a role in the pathogenesis of neurodegeneration. However, evidence for an alteration in cytosolic calcium regulation in old age is at present controversial. The present work was aimed at studying whether changes in synaptosomal calcium homeostasis in 30-month-old rats are uniform throughout the brain or affect specific brain regions. A second question addressed in this work is whether the effect of ageing on calcium homeostasis is restricted to the nerve terminal or a more general process affecting also cell bodies. To study these questions cytosolic calcium regulation was studied in parallel in synaptosomes and a preparation of acutely dissociated brain cells obtained from different regions of 3- and 30-month-old rats. 45Ca2+ accumulation and distribution in mitochondria (assessed as FCCP-releasable 45Ca2+) was also studied. Mean [Ca2+]i obtained at rest and after high K+ depolarization were unchanged in cerebral cortex synaptosomes but increased in hippocampal synaptosomes at 30 months. Resting [Ca2+]i also increased with age in hippocampal, but not cerebral cortex cells, whereas the increase in [Ca2+]i obtained by depolarization was larger in both brain regions. Calcium compartmentation in mitochondria from hippocampal neurons incubated under high K+ conditions was also decreased with ageing. An altered calcium regulation in cell bodies and synaptic terminals in the hippocampus may be involved in the development of functional impairments in the hippocampal formation.

Aging↗