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J Pineda

Publications and source records attributed to J Pineda.

At least 55 records · Page 3Linked to original sources

Oral dexamethasone administration: new pharmacological test for the assessment of growth hormone secretion.

Acute intravenous (i.v.) dexamethasone administration has been described recently as a new test for the diagnosis of growth hormone (GH) deficiency. In the present study, a new protocol of dexamethasone administration was evaluated. Twelve normal adults and 18 normal prepubertal children were studied. The dexamethasone i.v. test was performed in six adults at a dose of 4 mg and 12 children at a dose of 2 mg/m2. Blood samples were collected 15 min before, at time zero and every 15 or 30 min during 5 h, resulting in a total of 16 samples. In the remaining six adults and six children, 8 and 4 mg, respectively, of dexamethasone were administered orally at the subject's home, and blood sampling started 90 min later when they arrived at the hospital. Plasma GH was measured by radioimmunoassay. The dexamethasone-induced GH response (mean +/- SEM, micrograms/l) to the i.v. or oral protocol did not differ in either the adults (i.v. 8.2 +/- 2.1; oral 8.0 +/- 1.6) or the children (i.v. 14.9 +/- 1.3; oral 13.6 +/- 1.8). It is concluded that the simpler protocol of acute oral dexamethasone administration hereby presented can be a safe and suitable test of GH secretion.

Administration, Oral↗

Acute and chronic effects of reserpine on biochemical and functional parameters of central and peripheral alpha 2-adrenoceptors.

The specific binding of the agonist, [3H]UK 14304, and of the antagonist, [3H]RX 821002, to rat brain membranes, as well as clonidine-induced mydriasis, clonidine-induced inhibition and idazoxan-induced stimulation of brain 3,4-dihydroxyphenylalanine (DOPA) synthesis, and clonidine and UK 14304-induced inhibition of twitch responses in the vas deferens were used to evaluate the affinity and sensitivity of central and peripheral alpha 2-adrenoceptors after various treatments with reserpine. Treatment with reserpine (0.25 mg/kg s.c., every 48 h) for 4, 11 and 18 days induced consistent and significant increases in the affinity (KD values) of [3H]UK 14304 for the cortical alpha 2-adrenoceptor with no change in receptor density. Chronic treatment with reserpine also resulted in a greater affinity of (-)-adrenaline for the high-affinity state of the alpha 2-adrenoceptor when the catecholamine competed with the binding of [3H]RX 821002 to cortical membranes. In line with these radioligand binding data, various functional responses mediated by central and peripheral alpha 2-adrenoceptors were found to be potentiated after repeated treatment with reserpine. Thus, the inhibitory alpha 2-autoreceptor that modulates the synthesis of brain noradrenaline and the central postsynaptic inhibitory alpha 2-adrenoceptor that induces mydriasis displayed greater responses in vivo after chronic treatment with reserpine. Short-term and chronic treatments with reserpine also increased the sensitivity of peripheral presynaptic alpha 2-adrenoceptors in the vas deferens.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

Acute and chronic effects of cholinesterase inhibitors and pilocarpine on the density and sensitivity of central and peripheral alpha 2-adrenoceptors.

The specific binding of the agonists [3H]clonidine and [3H]UK 14304 (bromoxidine) and of the antagonist [3H]RX 821002 (2-metoxy idazoxan) to rat brain membranes, as well as clonidine-induced mydriasis, clonidine-induced inhibition of brain (3,4-dihydroxyphenylalaninme) DOPA synthesis and clonidine-induced inhibition of twitch responses in the vas deferens, was used to evaluate the density and sensitivity of central and peripheral alpha 2-adrenoceptors after prolonged activation of the cholinergic system. Acute (12 h), short-term (4 days) or chronic (7-18 days) treatment with the cholinesterase inhibitors neostigmine (0.1 mg/kg), physostigmine (0.1 mg/kg) and diisopropylfluorophosphate (2 mg/kg) and with the muscarinic receptor agonist pilocarpine (10 mg/kg) did not alter the density of brain alpha 2-adrenoceptors. In contrast, various functional responses mediated by central and peripheral alpha 2-adrenoceptors were potentiated after the repeated treatments. Thus, the inhibitory alpha 2-autoreceptor that modulates the synthesis of brain noradrenaline and the central postsynaptic inhibitory alpha 2-adrenoceptor that induces mydriasis displayed greater responses in vivo after chronic treatment with neostigmine or pilocarpine. These treatments also increased the sensitivity of peripheral presynaptic alpha 2-adrenoceptors in the vas deferens. The results indicate that prolonged activation of central and peripheral cholinergic pathways results in up-regulation of alpha 2-adrenoceptor function without apparent increases in receptor density.

Adrenergic alpha-Agonists↗

Stimulatory effects of clonidine, cirazoline and rilmenidine on locus coeruleus noradrenergic neurones: possible involvement of imidazoline-preferring receptors.

Clonidine and related drugs not only interact with alpha 2-adrenoceptors but also recognise non-adrenoceptor sites in the brain. The involvement of these imidazoline-preferring receptors in the regulation of the activity of locus coeruleus noradrenergic neurones (NA-LC) was investigated after inactivation of alpha 2-adrenoceptors with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ). In EEDQ-pretreated rats (6 mg/kg, i.p., 6 h), the characteristic inhibitory effect of low doses of clonidine on these neurones was abolished and a paradoxical, dose-dependent increase in firing rate was observed at higher doses (640-5120 micrograms/kg, i.v.) (ED50 = 702 micrograms/kg, Emax = 83%, n = 14). Guanfacine (0.3-20 mg/kg) did not modify neuronal activity but antagonised the stimulatory effect of clonidine. Cirazoline (80-640 micrograms/kg) and rilmenidine (0.3-10 mg/kg) also stimulated neuronal activity (ED50 = 192 micrograms/kg, Emax = 102%, n = 5; ED50 = 1563 micrograms/kg, Emax = 70%, n = 1-5, respectively) by an alpha 2-adrenoceptor-independent mechanism. The results suggest that these drugs can modulate the activity of locus coeruleus noradrenergic neurones through the activation of I1-imidazoline-preferring receptors.

Adrenergic alpha-Agonists↗

Corticoid-induced growth hormone (GH) secretion in GH-deficient and normal children.

Acute administration of corticoids is a potent stimulus of GH secretion in man. To ascertain their mechanism and point of action as well as the suitability of this novel test in the diagnosis of GH-deficient states, normal controls and GH-deficient children were studied. They were selected based on auxological criteria and the GH response to provocative stimuli. The GH-deficient children presented a blunted GH (mean +/- SEM; microgram/L) discharge after insulin-induced hypoglycemia (2.9 +/- 0.4), propranolol-exercise (7.4 +/- 1.5), and clonidine (6.5 +/- 0.8) compared with values in the normal children (7.2 +/- 2.2, 15.8 +/- 2.4, and 15.6 +/- 1.8, respectively). As expected, GH-releasing hormone (GHRH)-induced GH discharge in GH-deficient children (33.2 +/- 4.9) was similar to that in the control children (35.1 +/- 6.0). Administration of 2 mg/m2 body surface dexamethasone, iv, to normal children induced, 3 h later, a mean GH peak of 14.1 +/- 1.2 micrograms/L. This was significantly higher that the corticoid-induced GH peak in GH-deficient children (6.7 +/- 1.1 micrograms/L). The corticoid-induced areas under the secretory curve were 1130 +/- 55 and 616 +/- 54 for the control and GH-deficient children, respectively. GH release in children after dexamethasone administration followed the pattern previously described for adults, i.e. there were no modifications of basal GH levels in the first 2 h, the GH peak appeared around the third hour, and the GH levels remained increased until the fourth hour after dexamethasone administration. Individually considered, practically all control children, but only 2 of 12 GH-deficient children, presented a dexamethasone-induced GH peak over the 10 micrograms/L level. In both normal and GH-deficient patients, corticoids appeared just as potent a stimulus as propranolol-exercise and clonidine, and more potent than hypoglycemia. This new stimulus showed a pattern similar to that of the hypothalamic stimuli, but clearly different with respect to the pituitary one (GHRH), suggesting that corticoids activate GH secretion by acting at hypothalamic level. In conclusion, acute administration of corticoids could be a suitable test in the diagnostic armamentaria of GH-deficient states.

Adolescent↗

[Other indications for growth hormone treatment: chronic kidney failure and Turner's syndrome].

Recently, it has been demonstrated that treatment with growth hormone (GH) can accelerate height velocity in children with chronic renal insufficiency (CRI), after kidney transplantation and in Turner syndrome. The pathogenesis of growth retardation in CRI is complex. Possibly the most important factor involved is the presence of peripheral resistance to insulin-like growth factors. The administration of GH in high doses may restore catch-up growth, both in children with CRI and in kidney post-transplant patients. After 12 months of treatment height velocity increased from 4.3 to 6.6 cm/year in 4 children with CRI, and from 2.5 to 7.4 cm/year in 3 patients with kidney transplant. GH therapy alone, but even more in combination with oxandrolone increases the growth rate in Turner syndrome and may increase the final height, but the long-term results of this treatment are awaited. No undesirable collateral effects have been reported.

Body Height↗

Action of trypsin on glycinin. Mixed-type proteolysis and its kinetics; molecular mass of glycinin-T.

The formation of a relatively stable high-molecular-mass product on trypsin hydrolysis of glycinin (glycinin-T) is interpreted to be a result of 'zipper' proteolysis. Evidence of parallel one-by-one degradation of glycinin occurring after the formation of glycinin-T is presented. At a relatively low concentration of the substrate, the one-by-one proteolysis proceeds as a first-order reaction. A method of determination of the changes in the molecular mass of a protein during the mixed-type proteolysis and some other parameters of this process is developed on the basis of the analysis of the proteolysis kinetics. The value of the molecular mass of glycinin-T calculated by means of this method makes up 70% of the initial molecular mass and coincides with the result of direct determination by gradient gel electrophoresis.

Chromatography, Gel↗

Estradiol 17 beta-dehydrogenase: full enzymatic activity in the absence of zinc.

The precise catalytic mechanism of the steroid interconverting enzyme, human placental estradiol 17 beta-dehydrogenase (EC 1.1.1.62, estradiol-17 beta:NAD+ 17-oxidoreductase), is not known. Two general models for the catalytic mechanism of dehydrogenases have been defined. One model requires Zn2+ metal for the catalytic event, as has been shown for horse liver alcohol dehydrogenase (EC 1.1.1.1, alcohol:NAD+ oxidoreductase). Another model has been demonstrated for the 2-hydroxy acid dehydrogenases in which histidine residues are necessary for enzyme activity, without participation of a metal ion. In order to define which mechanism might be operative for the placental enzyme, it became important to determine whether Zn2+, or another metal ion, is associated with the macromolecule. Several homogeneous enzyme preparations, having protein concentrations from 5-80 microM, were extensively dialyzed in a buffer containing EDTA. Atomic absorption analysis of each sample demonstrated that no Zn2+ was present, although the enzymatic activity was maintained. In addition, there was no significant detection of Mg2+ or Mn2+ above background levels. When the isolated enzyme was dialyzed against buffer containing added 0.01-20 microM ZnCl2, no increase in specific activity of the enzyme was seen. The data indicate that the presence of zinc is not required for the catalytic event. These results, together with our previous affinity-labeling studies, which demonstrate a histidine residue in the catalytic region of the active site, allow us to propose that the catalytic mechanism of the human placental estradiol 17 beta-dehydrogenase is similar to that of the 2-hydroxy acid dehydrogenases.

Amino Acid Sequence↗

Transcervical salpingoplasty: current techniques and results.

In the last five years angio-interventional techniques have been applied to the recanalization of proximally occluded fallopian tubes in infertile women. The reported technical success of 90% and subsequent pregnancies in up to 54% of patients has led to considerable interest in this technique. This article will discuss current methodologies and review the reported results of this procedure.

Catheterization↗

Tumor necrosis factor alpha is elevated in the peritoneal fluid from women with ruptured ectopic pregnancies.

The purpose of this study was to determine whether exposure of the peritoneum to fetal tissue is associated with elevated tumor necrosis factor alpha (TNF alpha) levels in the peritoneal cavity. We measured TNF alpha levels in the peritoneal fluids and serum from women with ruptured ectopic, unruptured ectopic and intrauterine pregnancies, as well as nonpregnant women undergoing tubal ligation. The results showed that patients with ruptured ectopic pregnancies were more likely to have TNF alpha levels in the peritoneal fluid greater than 40 units/ml (68%), compared with women with unruptured ectopic or intrauterine pregnancies (21%) (p less than 0.05, Fisher exact test). No elevation of peritoneal fluid TNF alpha levels was found in nonpregnant patients. Because TNF alpha is primarily a product of activated macrophages, it is likely that elevated TNF alpha levels in the peritoneal fluid of women with ruptured ectopic pregnancies reflects activation of peritoneal macrophages.

Adolescent↗

Serum CA-125 levels in women with ectopic and intrauterine pregnancies.

In women with ectopic pregnancies the extrauterine compartments are exposed to fetal tissue. Since such tissue is known to express CA-125, we measured serum levels of CA-125 in patients with ectopic pregnancies and compared them to those in patients with intrauterine pregnancies. A total of 44 pregnant women were included in the study; all were in the first trimester. Twenty-seven of them had ectopic pregnancies, and 17 had intrauterine ones. Our results show that women with ectopic pregnancies, ruptured or unruptured, were more likely to have elevated levels of serum CA-125 than were women who had intrauterine pregnancies.

Adult↗

Laser vaporization of endometriosis in an infertile population: the role of complicating infertility factors.

One hundred twenty-two infertility patients with endometriosis were evaluated and treated using laparoscopy and laser vaporization to provide immediate elimination of all intraperitoneal disease. Ninety-five couples (77.8%) had one or more infertility factors (other than endometriosis) contributing to their infertility. Cervical factors, male factors, and luteal defects were associated with significantly decreased pregnancy rates, despite the use of laser vaporization. The number of contributing factors seemed to be unrelated to the likelihood of success in achieving pregnancy. The authors emphasize the need for total evaluation of other infertility factors in these patients. Such factors should be corrected prior to the use of laser laparoscopy, if possible, and dealt with on a continuing basis following use of this technique.

Endometriosis↗

Tumor necrosis factor in peritoneal fluid of women undergoing laparoscopic surgery.

The level of tumor necrosis factor (TNF) in peritoneal fluid (PF-TNF) of 74 women undergoing laparoscopy was determined. The difference between the mean concentration of PF-TNF of women with normal pelvic anatomy and women with moderate or severe endometriosis was significant (P less than 0.01). The proportion of PF-TNF-positive women with PID and those with moderate or severe endometriosis was also significantly higher when compared to women with normal pelvic anatomy (P less than 0.05; P less than 0.02). The proportion of PF-TNF positive women among nulligravid and nulliparous women was significantly higher than that of women with two or more pregnancies (P less than 0.01) and two or more deliveries (P less than 0.005). These results indicate that the presence of PF-TNF is associated with primary infertility and endometriosis.

Adolescent↗

Serum levels of CA-125 in patients with endometriosis: a preliminary report.

Seven out of 8 patients with endometriosis demonstrated levels of CA-125 antigen above 35 U/ml. None of 15 patients with other benign gynecologic diagnoses demonstrated elevated levels. This antigen has been proposed as a tumor marker for epithelial carcinoma and other gynecologic neoplasms. However, it cannot be used to differentiate clinically between cancer and endometriosis.

Adolescent↗

Patterns of Schistosoma haematobium egg distribution in the human lower urinary tract. I. Noncancerous lower urinary tracts.

Schistosoma haematobium egg burdens (eggs/g of tissue) of 17 anatomic segments of lower urinary tracts from 32 unselected Egyptian autopsies have been determined by tissue digestion and replicate counts of aliquots of the digestate. There were three anatomic patterns of egg distribution in these lower urinary tracts: apical, basal and diffuse. Regression of egg burdens of each of the anatomic segments as the dependent variable against egg burdens of the entire lower urinary burden yielded a good fit for 15 of 17 of these segments. Statistical analyses revealed that many of these equations for discrete anatomic segments can be combined, generally giving one equation for anatomic regions which are in continuity, indicating that the female worm lives and oviposits in specified venous plexes. These equations also suggest that there are differences in the rates, duration and onset of egg accumulation which may be responsible for schistosomal obstructive uropathy as a cause of death in fairly young individuals.

Adolescent↗