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Biomedical subjects

G Ruiz

Publications and source records attributed to G Ruiz.

At least 73 records · Page 4Linked to original sources

[Congenital malformations: a model predictive based on risk factors].

Several risk factors were studied in regard to congenital malformations. Malformed newborns (n = 1200) and controls (n = 1200) seen at the Universidad de Chile Hospital between 1969 and 1979 were examined. Their mothers were asked about possible risk factors. Parenteral age and birth order was significantly higher for malformed newborns than for controls. A family history of congenital malformations was more frequent in malformed newborns. Infertility, metrorrhagia and maternal diseases during pregnancy were more frequent in malformed newborns than in controls. A function that discriminates between controls mothers and mothers of malformed newborns was obtained by a logistic regression model. This function correctly predicted 65% of cases.

Congenital Abnormalities↗

Prostaglandin F2 alpha effects on intraocular pressure negatively correlate with FP-receptor stimulation.

According to the current working classification for prostanoid receptors, the prostaglandin F2 alpha-sensitive receptor (FP-receptor) may be identified by comparing the rank order of activity of prostaglandin F2 alpha (PGF2 alpha) and its analogues. In order to further understand the pharmacology of PGF2 alpha-induced ocular hypotension, the intraocular pressure response to PGF2 alpha and selected analogues was compared with their rank order of activity in typical FP-receptor preparations such as contraction of the cat iris sphincter and affinity for corporal luteal membrane binding sites. The rank order of potency for decreasing intraocular pressure was as follows: PGF2 alpha greater than PGF1 alpha greater than 16-phenoxytetranor PGF2 alpha greater than 17-phenyltrinor PGF2 alpha = fluprostenol (inactive). For cat iris sphincter contraction, the rank order of potency appears to be fluprostenol = 17-phenyltrinor PGF2 alpha greater than 16-phenoxytetranor PGF2 alpha = PGF2 alpha greater than PGF1 alpha. The rank order of potency for PGF2 alpha analogues in decreasing intraocular pressure appears to negatively correlate with the rank order for cat iris sphincter contraction and literature values for corporal luteal membrane binding. It is concluded that the ocular hypotensive effect of PGF2 alpha is not mediated by the FP-receptor.

Administration, Topical↗

The pattern of callosal connections in posterior neocortex of congenitally anophthalmic rats.

In an effort to assess the innate capacity of the central visual system to specify corticocortical connectivity in the absence of retinal afferents, we examined the tangential distribution of callosal cells and terminations in posterior neocortex of congenitally anophthalmic rats. Although our results indicate that the callosal pattern is clearly anomalous in these rats, all features of the normal visual callosal pattern are recognizable in mutant rats, indicating that central visual pathways can generate many aspects of normal interhemispheric connectivity in the absence of input from the periphery. On the other hand, the presence of anomalies in the pattern indicates that the eyes are necessary to fine-tune the distribution of callosal connections at some developmental stage. Moreover, the fact that abnormalities in the callosal pattern of mutant rats are the same as those previously described in rats enucleated at birth suggests that the eyes begin to exert their influence on callosal development after birth.

Agenesis of Corpus Callosum↗

Effect of phenytoin on cytoskeletal protein phosphorylation and neuronal structure in the rat sensory cortex.

Phenytoin (PH) is commonly used as an anticonvulsant drug, and it causes several collateral effects including morphological changes in brain cortex neurons and teratogenic lesions in infants of epileptic mothers. Several lines of evidence indicate that PH may exert its action through the modification of phosphorylation patterns of neuronal polypeptides. We have studied the effects of PH on the phosphorylation of cytoskeletal proteins, because this could be related to the structural modifications induced by PH administration. The dendritic pattern of deep layers of the somatosensory cortex is clearly modified by PH but not the cell number, indicating that the drug disturbs the architecture of the neurons examined. In fact, the pattern of phosphorylation in cytoskeletal extracts of brains of 30-day-old rats is changed by PH. In vitro labeling experiments show decrease in the [32P] level of a 43-kDa polypeptide, whereas 38- and 120-kDa polypeptides show increases in their [32P] contents. The 43-kDa polypeptide has been identified as actin by in vitro experiments using a novel approach to determine cytoskeletal polypeptide behavior. We conclude that PH affects the posttranslational phosphorylation of actin and other related cytoskeletal proteins and in this manner may alter the normal morphological layout of dendritic patterns in the somatosensory cortex.

Age Factors↗

[Hematologic values and altitudinal distribution of Chilean amphibians].

Blood values were measured on a series of Chilean species of frogs and toads from low and high altitudes, ranging from near sea level up to 4,500 m. Average values of red cell number, blood hemoglobin concentration and cell hemoglobin concentration were all higher in the high altitude group (6 species), while the average cell size was larger in the low altitude group (16 species). Hematocrits and cell hemoglobin content showed poor or no correlation with the altitudinal distribution of the examined species.

Altitude↗

[Heat transfer, convection and altitudinal gradient].

Measurements of heat loss from fur covered aluminium cylinders were made under barometric pressures ranging from 760 to 368 torr (sea level up to 5.8 km, simulated altitudes). Heat transfer diminished at high altitudes and a relative greater diminution was observed when forced convection was applied. The virtual increase in thermal insulation at high altitudes may be useful to compensate the expected larger difference between body and ambient temperatures.

Adaptation, Physiological↗

Short-term stimulation by adenosine of basal and insulin-induced glycogen synthesis in rat adipose tissue.

The effects of adenosine on glycogen metabolism have been studied in isolated fat-pads from epididymal adipose tissue. Adenosine caused a sustained short-term increase in the incorporation of [U-14C]glucose into glycogen, as well as a stimulation of both basal and insulin-induced [1-14C]glucose oxidation. Adenosine produced changes also in the activity of glycogen synthase and phosphorylase, these effects being apparent only when glucose was present in the incubation medium. The addition of adenosine prevented the depressed synthesis of glycogen observed in the presence of dibutyryl cyclic AMP. In the presence of adenosine deaminase, the stimulation by insulin of glycogen synthesis was markedly decreased. The results suggest that adenosine may have a regulatory role on glycogen synthesis by facilitating the glucose transport.

Adenosine↗

Pharmacological characterization of beta-adrenoceptor subtype involvement in the ocular hypotensive response to beta-adrenergic stimulation.

The decrease in intraocular pressure elicited by isoproterenol in ocular normotensive animals is widely recognized. The participation of the beta-adrenoceptor subtypes in mediating this ocular hypotensive response has, however, remained unclear, because previous studies have been limited to monitoring the activity of single, supramaximal doses of relatively selective beta 2-adrenoceptor agonists. The studies herein report a relatively extensive pharmacological characterization of beta 1- and beta 2-adrenoceptor involvement in ocular hypotension associated with beta-adrenergic stimulation in the pigmented rabbit. A beta 2-adrenoceptor mechanism was indicated by the following evidence: isoproterenol and relatively selective beta 2-adrenoceptor agonists produced ocular hypotension over a similar dose range (0.001-0.1%; beta 1-adrenoceptor agonists, at doses likely to confer beta 1-adrenoceptor specificity, did not cause a similar decrease in intraocular pressure; the ocular hypotensive response to isoproterenol was abolished by topical timolol and pindolol and the relatively selective beta 2-adrenoceptor antagonist ICI 118551, whereas the relatively selective beta 1-adrenoceptor antagonists metoprolol and betaxolol were topically inactive; intravenous injection of beta 1-adrenoceptor-specific doses of metoprolol and betaxolol had little effect on isoproterenol-induced ocular hypotension, whereas the response was antagonized by a beta 2-adrenoceptor-specific i.v. dose of ICI 118551. These pharmacological results are consistent with radioligand binding and beta-adrenoceptor-linked adenylate cyclase studies which indicate a predominantly beta 2-adrenoceptor population associated with the ocular ciliary processes. None of the beta-blockers themselves altered normal intraocular pressure in the pigmented rabbit.

Adrenergic beta-Agonists↗

Involvement of cyclic AMP-dependent protein kinase on the phosphorylase kinase inhibition by glucose-6-phosphate in adipose tissue extracts.

In order to achieve further clarification of the regulation of glycogenolysis in adipose tissue, we studied the effect of glucose-6-phosphate on phosphorylase activation in Sephadex G-25 filtrate of adipose tissue. The activity of phosphorylase kinase was decreased by 50% and by 75% in the presence of 0.5 mM and 2 mM of glucose-6-phosphate, respectively. This inhibition could be partially prevented by 0.5 mM AMP. Furthermore, we investigated the influence of glucose-6-phosphate on the effect of cyclic-AMP-dependent protein kinase on the activation of phosphorylase. The addition of cyclic-AMP and cyclic-AMP-dependent protein kinase caused a decrease in the inhibition of the phosphorylase activation by glucose-6-phosphate. Also, the glucose-6-phosphate at physiological concentration, decreased adipose tissue cyclic-AMP-dependent protein kinase activity.

Adenosine Monophosphate↗

Membrane-bound form of acetylcholinesterase activated during postnatal development of the rat somatosensory cortex.

We are interested in the expression of synapse-specific macromolecules and its correlation with the appearance of neuronal types and synaptogenesis during development of the mammalian brain. We report here studies showing that the appearance of acetylcholinesterase (AChE) at layer IV of the rat somatosensory cortex is correlated with the expression of a membrane-bound AChE. Both its electrophoretic mobility and its sedimentation coefficient remain unaltered during maturation; however, its kinetics parameters, the heat and fixative sensitivities and the substrate inhibition changed through development. Our results suggest that an adult form of membrane-bound AChE is expressed postnatally.

Acetylcholinesterase↗

Age-related responses of skeletal muscle after ectopic innervation, with particular reference to 16S acetylcholinesterase, in adult rats.

The formation of ectopic junctions between the foreign fibular nerve and the soleus muscle of young (35-day-old) and mature (200-day-old) adult rats was induced by severing the normal nerve 4 weeks after implanting the foreign nerve. The various molecular forms of acetylcholinesterase (AChE) were studied both at the implanted region and at the original denervated endplates. The velocity of contraction was also studied. In young rats the 16S form was first detected in the ectopic junctions around day 5 after reinnervation; this form rapidly increased during the following weeks, reaching a plateau by day 20. By contrast, in mature rats the appearance of the 16S AChE was dramatically delayed; in fact, it could not be observed before day 80 after reinnervation. (The 16S AChE form appeared at day 20 after reinnervation in the original denervated endplates of young rats; however, at the same time, no effect was observed in mature animals.) The original, slow muscle fibers of the soleus became faster upon reinnervation; this change occurred also much earlier in younger than in mature rats. Our results indicate a loss of plasticity in the skeletal muscle of mature rats. We suggest caution in the use of the ectopic innervation model to study development in mature adult rats.

Acetylcholinesterase↗

Effects of vasoactive drugs on the natriuresis of nephrotic rats.

Seven nephrotic rats with edema, massive proteinuria and reduced glomerular filtration rate and filtration fraction were compared with ten normal rats. The experiment consisted of three consecutive periods: C, control; Ach, in which acetylcholine (40-60 ng/min) was continuously infused directly into the left renal artery; and Ach-AN-NA, in which angiotensin II (AN, 0.025 ng/min) + noradrenaline (NA, 0.25 micrograms/min) was systemically infused to elevate blood pressure, without interrupting acetylcholine infusion. Mean arterial pressure (MAP) and renal function parameters were measured. In both groups, MAP remained unchanged from C to Ach (P greater than 0.05) and was increased (P less than 0.05) from Ach to Ach-AN-NA (136 +/- 3.3 to 148 +/- 2.9 mmHg in normal animals, and 132 +/- 5.8 to 148 +/- 4.9 mmHg in nephrotic animals). In the normal group, intrarenal acetylcholine infusion increased (P less than 0.05) natriuresis from 3.75 to 7.93 microEq min-1 kd-1 kg BW-1 and a further, but transitory, increment up to 10.20 microEq min-1 kd-1 kg BW-1 was observed (P less than 0.05) when MAP was elevated. These natriuretic changes occurred without alterations of glomerular filtration rate (P greater than 0.05). Therefore, as previously reported in the literature, normal rats were responsive to intrarenal infusion of acetylcholine (vasodilator) followed by increased blood pressure, a condition known as pressure natriuresis. However, no natriuretic response was observed in the nephrotic group either to intrarenal acetylcholine infusion or to blood pressure elevation. We assume that nephrotic rats are insensitive to pressure natriuresis.

Acetylcholine↗

Stimulating role of potassium ions and ouabain on glycogen synthesis in adipose tissue.

1. Exposure of fat-pads to increasing concentrations of K+ in the presence of insulin stimulates the incorporation of labelled glucose into glycogen. In the absence of hormone, only a slight incorporation of glucose into glycogen and slight glucose oxidation were detectable. 2. Ouabain alone, up to 100 microM, had no effect on synthesis of glycogen. Ouabain reinforced the effect of insulin on the conversion of glucose into glycogen in a Na+ medium and in a equimolar Na+-K+ medium, but not in a K+ medium. In addition, ouabain modified the optimal K+/Na+ ratio for glycogen synthesis. 3. The proportion of glycogen synthase in the active form was increased in a K+ medium, and a faster rate of conversion of synthase b into a was observed under these conditions. No difference was detected in the rate of inactivation of phosphorylase in a K+ or a Na+ medium. 4. Even though these results, taken together, are consistent with the proposed role of phosphorylase a in the regulation of synthase activation, the molecular mechanism of action of K+ in adipose tissue in increasing synthesis of glycogen cannot be explained simply by a faster inactivation of phosphorylase a. It is concluded that some undetermined effector(s) or signal could itself be a primary determinant for the greater activation of synthase observed in a K+ medium.

Adipose Tissue↗

Cyclic AMP-dependent protein kinase activity and lipolysis in adipose tissue. Effect of fasting, oligomycin and iodoacetamide.

The release of glycerol into the medium, the concentration of cAMP, and the cAMP-dependent protein-kinase activity were studied in adipocytes and in fat-pads obtained from epididymal adipose tissue of rats under different conditions of feeding. An increase in the tissue concentration of cAMP and in the protein-kinase activity was observed in vivo at 48 and 96 h of fasting. A diminished release of glycerol was found in adipocytes from rats fasted for 48 h, in the absence of glucose, and the maximum concentration of cAMP was inferior to that of fed rats. Oligomycin and iodoacetamide, in the presence of epinephrine and glucose, produce a diminution in the values of the parameters studied. No significant differences were observed, however, in the responses of tissue obtained from fed and fasting rats to these compounds. The present results confirm previous observations and show the dependence of the lipolytic process on carbohydrate metabolism.

Adipose Tissue↗