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Biomedical subjects

G Capone

Publications and source records attributed to G Capone.

At least 19 recordsLinked to original sources
PubMed2006

Perinatal glucocorticoid treatment disrupts the hypothalamo-lactotroph axis in adult female, but not male, rats.

This study aimed to test the hypothesis that the tuberoinfundibular dopaminergic neurons of the arcuate nucleus and/or the lactotroph cells of the anterior pituitary gland are key targets for the programming effects of perinatal glucocorticoids (GCs). Dexamethasone was administered noninvasively to fetal or neonatal rats via the mothers' drinking water (1 mug/ml) on embryonic d 16-19 or neonatal d 1-7, and control animals received normal drinking water. At 68 d of age, the numbers of tyrosine hydroxylase-positive (TH+) cells in the arcuate nucleus and morphometric parameters of pituitary lactotrophs were analyzed. In control animals, striking sex differences in TH+ cell numbers, lactotroph cell size, and pituitary prolactin content were observed. Both pre- and neonatal GC treatment regimens were without effect in adult male rats, but in females, the overriding effect was to abolish the sex differences by reducing arcuate TH+ cell numbers (pre- and neonatal treatments) and reducing lactotroph cell size and pituitary prolactin content (prenatal treatment only) without changing lactotroph cell numbers. Changes in circulating prolactin levels represented a net effect of hypothalamic and pituitary alterations that exhibited independent critical windows of susceptibility to perinatal GC treatments. The dopaminergic neurons of the hypothalamic periventricular nucleus and the pituitary somatotroph populations were not significantly affected by either treatment regimen in either sex. These data show that the adult female hypothalamo-lactotroph axis is profoundly affected by perinatal exposure to GCs, which disrupts the tonic inhibitory tuberoinfundibular dopaminergic pathway and changes lactotroph morphology and prolactin levels in the pituitary and circulation. These findings provide new evidence for a long-term disruption in prolactin-dependent homeostasis in females, but not males, after inappropriate GC exposure in perinatal life.

Animals↗
PubMed2006

Early postnatal chronic inflammation produces long-term changes in pain behavior and N-methyl-D-aspartate receptor subtype gene expression in the central nervous system of adult mice.

The objective of this study was to test whether postnatal chronic inflammation resulted in altered reactivity to pain later in life when reexposed to the same inflammatory agent and whether this alteration correlated with brain-region-specific patterns of N-methyl-D-aspartate (NMDA) receptor subtype gene expression. Neonatal mouse pups received a single injection of complete Freund's adjuvant (CFA) or saline into the left hind paw on postnatal day 1 or 14. At 12 weeks of age, both neonatal CFA- and saline-treated animals received a unilateral injection of CFA in the left hind paw. Adult behavioral responsiveness of the left paw to a radiant heat source was determined in mice treated neonatally with saline or CFA before and after receiving CFA as adults. Twenty-four hours later, brains were dissected and NMDA receptor subunit gene expression was determined in four different brain areas by using an RNase protection assay. The results indicated that NMDA receptor subtype gene expression in adult mice exposed to persistent neonatal peripheral inflammation was brain region specific and that NMDA gene expression and pain reactivity differed according to the day of neonatal CFA exposure. Similarly, adult behavioral responsiveness to a noxious radiant heat source differed according to the age of neonatal exposure to CFA. The data suggest a possible molecular basis for the hypothesis that chronic persistent inflammation experienced early during development may permanently alter the future behavior and the sensitivity to pain later in life, especially in response to subsequent or recurrent inflammatory events.

Age Factors↗
PubMed1998

Regulation of the preprosomatostatin gene by cyclic-AMP in cerebrocortical neurons.

The gene coding for preprosomatostatin (ppSom), the molecular precursor of somatostatin (Som), is regulated at the level of transcription by calcium ions and cyclic-AMP [F. Baldino, S. Fitzpatrick-McElligott, T. O'Kane, I. Gozes, Hormonal regulation of somatostatin, Synapse 2 (1988) 317-325; M.R. Montminy, M.J. Low, L. Tapia-Arancibia, Cyclic AMP regulates somatostatin mRNA accumulation in primary diencephalic cultures and in transfected fibroblast cells, J. Neurosci. 6 (1986) 1171-1176.], or by agents which increase intracellular levels of cAMP directly, such as forskolin [M.R. Montminy, M.J. Low, L. Tapia-Arancibia, Cyclic AMP regulates somatostatin mRNA accumulation in primary diencephalic cultures and in transfected fibroblast cells, J. Neurosci. 6 (1986) 1171-1176.]. Transcriptional induction of the ppSom gene as examined in PC12 cells, transfected fibroblasts and primary diencephalic cultures, requires the highly conserved cAMP response element (CRE), which confers gene responsiveness to cAMP [M. Comb, N. Mermod, S.E. Hyman, Proteins bound at adjacent DNA elements act synergistically to regulate human proenkephalin cAMP inducible transcription, EMBO J. 7 (1988) 3793-3805; T. Tsukada, J.S. Fink, G. Mandel, Identification of a region in the human vasoactive intestinal polypeptide gene responsible for regulation by cyclic AMP, J. Biol. Chem. 262 (1987) 8743-8747.]. The ppSom gene is subject to stringent regulation during cerebrocortical development in vivo; however, little information is available regarding ppSom gene regulation by neurotransmitters or second-messengers in cortical neurons. We used primary cerebrocortical cell cultures from fetal mice to examine the dose-response and time-course of ppSom gene expression in response to the cyclic-AMP analogs, dibutyrl-cAMP (dbcAMP), and 8-bromo-cAMP (8-BrcAMP). We report a dose-response for both analogs in the range of 0.1-10 mM. Dose-response studies using agents which directly stimulate intracellular cAMP synthesis (forskolin) or inhibit its breakdown (3-isobutyl 1-methyl xanthine) were also performed. We observed an apparent synergistic effect on ppSom expression when used in combination. An increase in ppSom mRNA levels was observed by 4 h, with a maximal response at 12-24 h. No change in ppSom mRNA levels was observed in response to phorbol myristate acetate (PMA). Our findings confirm the specificity of ppSom gene regulation by cAMP and Ca2+ ions, and demonstrate the utility of using primary cerebrocortical cultures for the study of somatostatin gene expression by neurotransmitters and second-messengers as a model of human neurologic disorders.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1987

[Study of several proteins of the acute phase of surgical intervention].

The aim of this study is to evaluate the behaviour of some proteins of acute phase (C reactive protein, alpha 1 acid glycoprotein, fibrinogen) in patients undergoing surgical operation. C reactive protein seems to be the most responsive to surgical trauma; alpha 1 acid glycoprotein reveals complications post-operation.

Acute-Phase Proteins↗
PubMed1987

[The serum fructosamine test in the control plan of glucose homeostasis].

A new method to measure serum glycosylated proteins as index of diabetic control is evaluated. Precision, recovery and interference tests have been evaluated. A good correlation of fructosamine values with glycosylated haemoglobin and glucose in normal and diabetic patients was found. The analytical performance and its simple application to automated instruments make this test suitable for monitoring diabetes mellitus and for assessing intermediate-term control of blood glucose.

Blood Proteins↗
PubMed1985

Frequency of intracoronary filling defects by angiography in angina pectoris at rest.

Recent studies have shown that pain at rest in patients with unstable angina pectoris is often caused by transient reduction in regional myocardial perfusion. Coronary spasm has been implicated as a mechanism of this phenomenon. Recent reports have documented the occurrence of intracoronary thrombus in patients with unstable angina. Previous surveys have estimated a 6 to 12% frequency of intracoronary thrombus in this syndrome, but have not examined whether this incidence is related to how recent the angina at rest was. Angiograms of 119 patients with unstable angina who had rest pain within 14 days of angiography and 35 patients with stable angina were surveyed. Patients with unstable angina were subgrouped according to how recent angina at rest was at the time of angiography. Group I consisted of 44 patients in whom rest pain occurred within 24 hours before angiography. The 75 patients in group II had angina at rest between 1 and 14 days before angiography. Patients in group II had stable angina. The angiographic criterion for intracoronary thrombus was an intraluminal filling defect, surrounded by contrast medium on 3 sides, located just distal to or within a coronary stenosis, as assessed by each of 2 independent observers blinded to the nature of the anginal syndrome and its temporal proximity. Intracoronary thrombi were found in 44 of 119 patients with unstable angina (37%) and 0 of 35 patients with stable angina (p less than 0.00002). Intracoronary thrombi were found in 23 of 44 patients (52%) in group I and 21 of 75 (28%) in group II (p less than 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

[Effect of administration of alpha-amanitine on Mn2+ - dependent poly-A-polymerase in rat liver nuclei].

Mn2+-dependent poly(A) polymerase activity tested in isolated rat liver nuclei is unchanged both in the absence and presence of exogenous poly(A) 30 min. after administration of a dose of alpha-amanitin that inhibits DNA-dependent RNA polymerase B. Longer times of treatment cause poly(A) polymerase to drop to 50% in the absence of poly(A) and to increase almost twice in its presence.

Amanitins↗