PubMed Health⌕ Search

Biomedical subjects

L M Rodrigues

Publications and source records attributed to L M Rodrigues.

51 records · Page 3Linked to original sources
PubMed1986

Activation of hepatic glycogen phosphorylase b in vivo by sodium sulphate in normal (Wistar) and phosphorylase b kinase-deficient (gsd/gsd) rats.

Sulphate ions have been known for some years to enhance the activity of hepatic glycogen phosphorylase b in vitro. Here we report that intravenous injections of 4.92 mmol of Na2SO4/kg body wt. to rats induced marked hepatic glycogenolysis in vivo, accompanied by polyuria, glycosuria and a mild hyperglycaemia. These effects were observed both in normal (Wistar) rats and in gsd/gsd rats that lacked hepatic phosphorylase kinase. In both rat strains the activity of glycogen phosphorylase in liver extracts was enhanced by pretreatment of the animals with Na2SO4, but in phosphorylase kinase-deficient livers the enhancement was solely in phosphorylase b activity, whereas both the a and b forms of the enzyme were activated in normal livers. Hepatic glycogenolysis was also induced by perfusing rat livers, both normal and gsd/gsd, with 25 mM-Na2SO4. Under these conditions both the rat strains showed only enhanced activities of glycogen phosphorylase b. This suggested that the increased activity of phosphorylase a in the extracts of normal livers after Na2SO4 administration in vivo was due to a hormonally mediated conversion of the b form into the a form. The activation of glycogen phosphorylase b was stable to dilution and appeared to be due to a long-lasting structural change in the enzyme or very tight binding of an activator.

Animals↗
PubMed1986

Outbreak of penicillinase-producing Neisseria gonorrhoeae with an African connection.

Previous outbreaks of penicillinase-producing gonococcal infection in the United States have generally been attributed to importation of Southeast Asian strains. During July 1982 through July 1983, 110 cases of gonorrhea caused by penicillinase-producing strains were reported in metropolitan Atlanta, Georgia. Among the 53 infected women, 14 (26%) had pelvic inflammatory disease (PID). Compared to other infected women, those with PID experienced a greater delay from the time of last sexual exposure (19.1 vs 8.1 days) to receipt of appropriate antibiotic therapy (P less than .01). At least 22 prostitutes were involved in the outbreak. Sixteen (76%) of 21 isolates tested were serogroup 1A; 15 required arginine and proline for growth; and 17 (81%) possessed a 3.2 megadalton plasmid. Our data suggest that this outbreak was associated with both African and Southeast Asian strains.

Adult↗
PubMed1980

Control mechanisms in the acceleration of hepatic glycogen degradation during hypoxia.

Hepatic glycogen metabolism in aerobic and hypoxic conditions has been assessed with respect to glycogenolysis, phosphorylase alpha activity and nucleotide content. Insulin did not inhibit glycogen breakdown nor stimulate lipogenesis in the aerobic perfused liver. Partial ischaemia induced glycogen breakdown, release of glucose and changes in nucleotide content in the perfused liver. Phosphorylase alpha content increased within 2 min in response to total ischaemia, in vivo and in the perfused liver. This change was paralleled by an increase in hepatic AMP. Glycogen synthase alpha activity decreased, as did the hepatic content of both cyclic AMP and cyclic GMP.

Adenine Nucleotides↗
PubMed1979

The influence of vasopressin and related peptides on glycogen phosphorylase activity and phosphatidylinositol metabolism in hepatocytes.

The relative abilities of seven vasopressin-like peptides to activate hepatic glycogen phosphorylase and stimulate phosphate incorporation into phosphatidylinositol were compared. Although the individual peptides differed in their potencies, the concentrations required to stimulate phosphatidylinositol metabolism were always greater (about 10 times) than those needed to activate phosphorylase. The molecular specificity of the hepatic vasopressin receptor and the role of vasopressin-stimulated phosphatidylinositol turnover are discussed.

Animals↗
PubMed1978

Stimulation by vasopressin, angiotensin and oxytocin of gluconeogenesis in hepatocyte suspensions.

1. In hepatocytes from starved rats, vasopressin, angiotensin (angiotensin II) and oxytocin stimulated gluconeogenesis from lactate by 25--50%; minimal effective concentrations were about 0.02pM, 1 nM and 0.2 nM respectively. 2. Vasopressin and angiotensin also stimulated gluconeogenesis from alanine, pyruvate, serine and glycerol. EGTA decreased gluconeogenesis from these substrates. 3. Hormonal stimulation of gluconeogenesis from lactate was abolished in the absence of extracellular Ca2+. 4. Insulin did not prevent stimulation of gluconeogenesis by vasopressin or angiotensin. 5. The potency of the stimulatory effects of vasopressin and angiotensin on hepatic gluconeogenesis suggests they are operative in vivo. Also, the data suggest that Ca2+ plays a role in the stimulation by these hormones.

Angiotensin II↗
PubMed1978

Rapid stimulation by vasopressin, oxytocin and angiotensin II of glycogen degradation in hepatocyte suspensions.

1. The hormonal control of glycogen breakdown was studied in hepatocytes isolated from livers of fed rats. 2. Glucose release was stimulated by [8-arginine]vasopressin (10pm-10nm), oxytocin (1nm-1mum), and angiotensin II (1nm-0.1mum). These responses are all at least as sensitive to hormone as is glucose output in the perfused rat liver. 3. The effect of these three hormones on glucose release was critically dependent on extracellular Ca(2+), unlike that of glucagon. Half-maximal restoration of the vasopressin response occurred if 0.3mm-Ca(2+) was added back to the incubation medium. 4. Glycogen breakdown was more than sufficient to account for the glucose released into the medium, in the absence or presence of hormones. Lactate release by hepatocytes was not affected by vasopressin, but was inhibited by glucagon. 5. If Ca(2+) was omitted from the extracellular medium, vasopressin stimulated glycogenolysis, but not glucose release. 6. The phosphorylase a content of hepatocytes was increased by vasopressin, oxytocin and angiotensin II; minimum effective concentrations were 0.1pm, 0.1nm and 10pm respectively. This response was also dependent on Ca(2+). 7. These results demonstrate that hepatocytes can respond to low concentrations of vasopressin and angiotensin II, i.e. these effects are likely to be relevant in the intact animal. The role of extracellular Ca(2+) in the effects of these hormones on hepatic glycogenolysis and glucose release is discussed.

Angiotensin II↗
PubMed1976

Glycogen phosphorylase, glucose output and vasoconstriction in the perfused rat liver. Concentration-dependence of actions of adrenaline, vasopressin and angiotensin II.

1. Glycogen phosphorylase (a form, in rapidly freeze-clamped samples) and glucose release were measured in the perfused liver, in response to a range of concentrations of adrenaline, [8-arginine]vasopressin (anti-diuretic hormone) and angiotensin II. 2. All three hormones increased phosphorylase a activity by about 10 mumol/min per g of fresh liver, which was more than sufficient to explain concomitant glucose release (1-2mumol/min per g). 3. Minimally effective concentrations which activated phosphorylase were: adrenaline, 10nM (2ng/ml); vasopressin, 40pM (40pg/ml, 15 muunits/ml); angiotensin II, 60pM (60pg/ml). 4. Glycogen synthase activity was inhibited by adrenaline and vasopressin but not significantly by angiotensin II. 5. Vasoconstriction observed with adrenaline and angiotensin II (but not vasopressin) might explain part of the activation of phosphorylase, since equivalent vasoconstriction (in separate perfusions) activated phosphorylase, did not stimulate glucose output or inhibit synthase. 6. The potency of these effects suggests that all three hormones can stimulate hepatic glycogen degradation in vivo (by direct hepatic action). It is proposed that hormones, and ischaemia, stimulate glycogen degradation to provide glucose phosphates for disposal within the liver cell, as well as for release as free gluose.

Angiotensin II↗
PubMedDate not supplied

An assessment of 31P MRS as a method of measuring pH in rat tumours.

The contribution of extracellular components to the measurement of pHMRS of a variety of rat tumours (nitrosomethyl urea induced mammary tumours, GH3 prolactinomas, Hepatoma 9618a, UA hepatomas and Walker sarcomas) has been assessed. Acid extractable P(i) was between 2.6 and 12.5 mumol/G wet wt depending on tumour type, and of this 53 +/- 4.8% (mean +/- SEM) was MRS-visible. The P(i) content of tumour exudate was 2-3 mM, of interstitial fluid (sampled from a micropore chamber incorporated within a tumour) 1.7 mM, and of blood plasma 1.95 mM. The mean extracellular volumes of the tumours, measured by distribution of 3H2O and [14C]inulin, were 49-55% depending on tumour type and were at least twice that found in normal liver. Calculations suggested that for most tumours with an extracellular volume not exceeding 55%, at least 65% of the P(i)(MRS) signal was derived from intracellular P(i), and thus that pH(MRS) is a measure of pHi. For each tumour type, pHMRS was measured both in 'pulse-acquire' mode at 1.9 T which may include signals from surrounding tissue, and in localized mode at 4.7 T where the signal came uniquely from tumour tissue. The steady state pHMRS was either neutral or on the alkaline side of neutrality (pH range 7.04-7.37). Raised lactate content and decreased buffering capacity (compared to normal tissues) accompanied these neutral to alkaline pH values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

An assessment of artefacts in localized and non-localized 31P MRS studies of phosphate metabolites and pH in rat tumours.

UA hepatomas, GH3 prolactinomas and N-methyl-N-nitrosourea-induced mammary tumours, which were subcutaneously grown in rats, have been studied by 31P MRS using non-localized pulse-acquire, image selected in vivo spectroscopy (ISIS) and one-dimensional chemical shift imaging (1-D CSI) techniques. Comparisons have been made with measurements from acid extracts of these tumour types and surrounding tissues (i.e., muscle and skin). Since muscle containing high concentrations of phosphocreatine (PCr) is often found adjacent to the tumour, we have compared the ratio of the PCr to gamma-NTP peaks in the spectra with the same ratio calculated from the acid extract data, and have used deviations between the two sets of data to assess the discrimination of the MRS localization technique to signals from the tissue surrounding the tumour. Extract data showed an average NTP content of 1.25 mumol/g wet wt for all three tumour types. PCr (at 0.42 mumol/g wet wt), was significant only in the GH3 prolactinoma whereas it was negligible in the other tumour types (< 0.1 mumol/g wet wt). There was good agreement between the ISIS PCr/gamma-NTP ratio and the extract data for all tumours. However, the 1-D CSI data showed an unexpectedly large contamination of the tumour spectrum with PCr signals from the skin which was shown by subsequent phantom experiments to be due to the curved geometry of tumour and skin rather than Fourier bleed. In pH measurements by MRS it was found that biological variability was greater than the effects of artefacts (due to either the chemical shift artefact in the ISIS technique or partial volume effects) in the localization technique. An average pH of 7.2 was observed for all tumours. By initially comparing data from different localization schemes with that from chemical extracts potential sources of error have been highlighted and show that phantom studies alone are not sufficient to fully assess the accuracy of localized MRS data.

Animals↗
PubMedDate not supplied

Pattern recognition of 31P magnetic resonance spectroscopy tumour spectra obtained in vivo.

Pattern recognition has been applied to the analysis of in vivo 31P NMR spectra. Using four different classes of tumour and three types of normal tissue, cluster analysis and artificial neural networks were successful in separating and classifying the majority of samples analysed. Although the phosphomonoester and P(i) regions appeared to be the most important spectral features, data representing the entire 31P spectrum were required for best separation of the tumour and tissue classes.

Animals↗
PubMedDate not supplied

Lipid metabolite peaks in pattern recognition analysis of tumour in vivo MR spectra.

The ability to classify spectra of tumours according to their stage and type will be essential if magnetic resonance spectroscopy (MRS) is to be used as an aid in the diagnosis of cancer. MRS data are normally classified on the basis of selected peak measurements but these may be difficult to extract automatically. We present two alternative methods of feature extraction which we used to discriminate between spectra from tumours and normal tissues. Discrimination could be achieved either using features from the whole spectrum, or from a selected region containing the peaks from the phospholipid precursors in the phosphomonoester region.

Animals↗