Stability of Z strings in strong magnetic fields.
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Biomedical subjects
Publications and source records attributed to J Garriga.
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The retinoblastoma-related protein p130 is a putative negative regulator of cell proliferation in mammalian cells. In this study, p130 is shown to exist in multiple phosphorylated forms in human cells. In glioblastoma T98G cells synchronized by serum deprivation, specific phosphorylated forms of p130 are found at different times after serum re-stimulation. Two phosphorylated forms of p130 only found in serum-arrested T98G cells and in early G1 phase associate with the adenovirus oncoprotein E1A in vitro. One of these two forms corresponds to the in vivo E1A-associated p130 in 293 cells, which express endogenous E1A protein. Moreover, p130 undergoes an abrupt shift to a unique phosphorylated form in mid G1 which is the only p130 form found during the remaining phases of the cell cycle. This phosphorylated form possesses an associated histone H1 kinase activity that is most active in late S phase and G2/M. The cell cycle-dependent expression pattern of cyclins in T98G cells is compatible with cyclin D1/CDK complexes driving the shift to this phosphorylated p130 form in mid G1. These results suggest that the putative growth inhibitory function of p130 is regulated by phosphorylation of this protein. They also suggest that differential phosphorylation of p130 during the cell cycle plays distinct roles in the regulation of p130 function.
We have previously demonstrated that maize (Zea mays) 2,3-bisphosphoglycerate-independent phosphoglycerate mutase (PGAM-i) is not related to 2,3-bisphosphoglycerate-dependent phosphoglycerate mutase. With the aid of specific anti-maize PGAM-i antibodies, we demonstrate here the presence of a closely related PGAM-i in other plants. We also describe the isolation and sequencing of a cDNA-encoding almond (Prunus amygdalus) PGAM-i that further demonstrates this relationship among plant PGAM-i. A search of the major databases for related sequences allowed us to identify some novel PGAM-i from different sources: plants (Arabidopsis thaliana, Oryza sativa and Antithamniom sp.), monera (Escherichia coli, Bacillus subtilis and Bacillus megaterium) and animals (Caenorhabditis elegans). All of these amino acid sequences share a high degree of homology with plant PGAM-i. These observations suggest that the PGAM-i from several biological kingdoms constitute a family of protein different from other proteins with related enzymatic function and arose from a common ancestral gene that has diverged throughout its evolution.
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Ethanol and anaesthetics increase glycogen levels in the brain. However, no data have been reported about the effect of ethanol on glycogen and glucose metabolism in specific brain regions. We have studied the concentrations of glycogen, glucose, glucose 6-P, glucose 1,6-P2 and fructose 2,6-P2 and the activities of glycogen synthase, glycogen phosphorylase and glycogen phosphorylase kinase in seven brain regions of starved rats following treatment with a single dose or several doses of ethanol. Our results show that: (1) the effect of ethanol on glucose metabolism depends on whether it is given in one single dose or in a series of doses; (2) glycogen concentration increases after a single dose of ethanol but not after long exposure; (3) glucose, glucose 6-P in some areas, and the bisphosphorylated sugar, fructose 2,6-P2 significantly increase after prolonged exposure to ethanol; and (4) the enzymatic activities of glycogen metabolism are not modified after a long exposure to ethanol. In summary, these data show that ethanol may modify the use of glycogen, glucose and derivatives in brain. Moreover, the changes produced depend on the pattern of ethanol intake and the brain area considered.
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We have studied the changes in concentration of glycogen, glucose and the bisphosphorylated sugars, glucose 1,6-P2 and fructose 2,6-P2, in several rat brain regions during 72 h of starvation. The animals were killed by focused microwave irradiation. The activities of glycogen metabolizing enzymes in the different areas were measured. A large decrease in glycogen and glucose concentration was observed in all areas. The concentrations of bisphosphorylated sugars changed, suggesting that an increase in glycolysis could take place at the beginning of starvation, with blood glucose as a major energy source. Differences in metabolite concentration before starvation disappeared after 72 h. The activities of glycogen synthase, glycogen phosphorylase and glycogen phosphorylase kinase were similar in all areas, and they did not change during starvation.
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Usually, nutritional status of patients with neoplasia is poor. This is an important factor when the radical resection of the tumor implies aggressive surgery, and it has a clear influence on postoperative morbidity and mortality. From 1979 to 1988, 33 cephalic duodenopancreatectomies for carcinoma of the ampullary region have been carried out in the Servicio de Cirugía Digestiva, hospital "Santa Cruz y San Pablo". For retrospective evaluation of postoperative parenteral nutrition patients have been divided in two groups: group A, with routine parenteral nutrition and group B, with parenteral nutrition only if required. In group A, 75% of patients did not present postoperative morbidity, compared to 38% of patients in group B. There were 7 deaths: all of them in group B. The time of hospitalization was lower in group A. Differences in the three parameters under consideration was statistically significant. We conclude that, in order to improve morbidity and mortality as well as to reduce the hospitalization time, postoperative parenteral nutrition is necessary in patients submitted to cephalic duodenopancreatectomy for neoplasia.
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The authors report experience with three patients with leiomyomas of the rectum between the years 1979 and 1987. Since Malassez's first description in 1872, approximately 200 cases have been reported. The diagnosis of these rare tumors is difficult. The authors present the ultrasonic characteristics of rectal leiomyoma by means of endorectal ultrasound, a method which, although not definitive, does delimit and orient the diagnosis in regard to the rectal mass and the follow-up of these tumors. A histologic diagnosis constitutes a dilemma between benign and malignant forms. The authors believe that treatment should always be surgical, realizing local extirpation when the histologic study reveals no signs of malignancy; even though it is mandatory to perform regular follow-up checkups (mainly with endorectal ultrasound) and radical treatment in regard to malignant lesions and local relapse of the anterior forms.