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Biomedical subjects

D Cocchi

Publications and source records attributed to D Cocchi.

At least 181 records · Page 10Linked to original sources
PubMedDate not supplied

Effect of hypophysectomy and growth hormone replacement on hypothalamic GHRH.

Long-term (7 and 14 days) hypophysectomy resulted in a striking decrease in growth hormone releasing hormone-like immunoreactivity (GHRH-LI) in the median eminence (ME) of adult male rats, evaluated by both radioimmunoassay and immunohistochemistry. Treatment with human GH (125 micrograms/rat, twice daily IP for 14 days) prevented, though partially, depletion of GHRH-LI from the ME, as assessed by both methods. These results demonstrate that circulating GH levels regulate the function of GHRH-producing structures, via a feedback mechanism.

Animals↗
PubMedDate not supplied

Growth hormone regulation of growth hormone-releasing hormone gene expression.

Slot-blot hybridization technique was used to evaluate growth hormone-releasing hormone (GHRH) mRNA levels in the hypothalamus of long-term (14 days) hypophysectomized (HPX) rats treated or not with 125 micrograms hGH/rat, twice daily IP, since the first day postsurgery. In addition, mRNA levels were determined in the hypothalamus of short-term (4 days) GH-treated (250 micrograms hGH/rat, twice daily IP) intact rats. GHRH mRNA levels were increased in HPX rats, and GH treatment partially counteracted this rise. Short-term administration of GH decreased GHRH mRNA levels in intact rats. These results, evaluated together with previous findings showing decreased hypothalamic GHRH-like immunoreactivity in both HPX rats and intact rats given GH (6, 7, 9), indicate that GH exerts a negative feedback action on the synthesis and release of GHRH.

Animals↗
PubMedDate not supplied

Reduced growth hormone releasing factor (GHRF)-like immunoreactivity and GHRF gene expression in the hypothalamus of aged rats.

Growth hormone releasing factor-like immunoreactivity (GHRF-LI) and GHRF mRNA levels were evaluated in the hypothalamus of aged (24 months) and young (3 months) rats by semiquantitative immunocytochemistry and slot blot hybridization technique, respectively. Simultaneous detection of reduced GHRF-LI and GHRF mRNA levels in aged rats as compared to young counterparts demonstrates the existence in aged rats of an impaired function of GHRF-producing neurons.

Aging↗
PubMedDate not supplied

Testosterone and GHRH gene expression in adult and old rats.

The effect of castration and testosterone replacement on GHRH gene expression was evaluated in adult male rats. Castration for 21 days did not affect GHRH mRNA levels, and also ineffective in this context was acute or chronic administration of testosterone to castrated rats. Hypothalamic GHRH mRNA was significantly reduced in aged male rats, but restoration of plasma testosterone concentrations via implanted capsules did not modify the low levels of GHRH mRNA. All in all, these findings support the notion that in adult and aged male rats GHRH-producing structures are insensitive to androgens.

Aging↗
PubMedDate not supplied

Feedback effects of growth hormone on growth hormone-releasing hormone and somatostatin are not evident in aged rats.

In 8- and 20-month-old male rats, treated or not with growth hormone (GH) for 4 days, simultaneous evaluation of hypothalamic GH-releasing hormone (GHRH) and somatostatin (SS) gene expression, GH secretion from anterior pituitaries (APs) in vitro (basal and GHRH-stimulated) and plasma IGF-I levels was performed. Twenty-month-old rats showed decreased GHRH mRNA levels, decreased GH secretion from APs in vitro (not responsive to GHRH stimulation) and reduced plasma IGF-I levels as compared to younger counterparts. SS mRNA levels were only slightly reduced in the hypothalamus of aged rats. Short-term administration of biosynthetic human GH (125 microgram/rat, twice daily, IP) to 8-month-old rats abolished the in vitro GHRH-stimulated GH release from APs and altered GH regulatory neuropeptides gene expression, i.e., reducing GHRH mRNA levels and increasing SS mRNA levels. In 20-month-old rats, hGH administration increased plasma IGF-I levels but did not change significantly GHRH and SS gene expression. These data indicate that the feedback effects exerted by circulating GH on GHRH and SS neurons, while evident in adult rats, are not detectable in aged rats.

Aging↗
PubMedDate not supplied

Evaluation of tuberoinfundibular dopamine function by neuropharmacologic means in old male rats.

Baseline prolactin (PRL) levels and the PRL-lowering effect of nomifensine (Nom), an indirect dopamine (DA) agonist, were evaluated in young adult (3-5 months) and old (21 and 27 months) male rats. In addition, PRL responsiveness to acute or repeated administration of haloperidol (Hal), a DA receptor antagonist, was assessed in either young or old rats. Baseline PRL levels did not differ significantly between young and aged rats either when rats were killed by decapitation or underwent sampling from the retro-orbital venous plexus. Administration of Nom (10.0 mg/kg i.p.), a drug which inhibits PRL levels in normal rats and humans but lacks any action in conditions of impaired tuberoinfundibular DA (TIDA) function, affected PRL levels in aged rats not differently than in young rats. The PRL inhibition induced by the drug was greater in both groups when basal PRL levels were higher. Acute administration of Hal (0.5 mg/kg i.p.) increased significantly and to the same extent as PRL levels in aged and young rats. In aged rats treated chronically with Hal (0.5 mg/kg i.p., twice daily for 14 days) and sampled at the 8th day, 1 h after the first daily Hal injection, plasma PRL rose to levels about 3-fold as high as those after the first injection; in young rats, instead, the PRL-releasing effect of Hal was similar to that evoked by the first administration. 3 days after Hal withdrawal, baseline PRL levels were significantly higher in aged Hal-treated rats than in vehicle-injected or young Hal-treated rats and so were pituitary concentrations of PRL.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMedDate not supplied

Growth hormone response to GHRH during lifespan.

Recent evidence has shown that growth hormone-releasing hormone (GHRH) enables investigation of the pathophysiology of GH secretion in a variety of different states, but it cannot be used as a test for probing pituitary somatotrophic function, due to the extreme inter- and intra-subject variability in normal subjects. This task is better accomplished when compounds which deprive the pituitary of inhibitory (somatostatinergic) influences, e.g. pyridostigmine, arginine, etc., are given in combination with GHRH. Administration of GHRH in both animals and humans reveals a state of GH hyperresponsiveness in the immediate postnatal period, which is likely to be due to a reduced pituitary sensitivity to somatostatin. GH responses to GHRH are relatively constant throughout the different stages of pubertal development, though further studies are needed to confirm these findings, and decline after the third-fourth decade in men, after menopause in women. It is apparent that during aging the releasable pool of GH is preserved and that impaired GH secretion is due to defective hypothalamic GHRH function and a relative predominance of somatostatinergic function.

Aging↗
PubMedDate not supplied

Phagocytosis and killing of Candida albicans of polymorphonuclear cells in patients with organ transplant of periodontal disease.

BACKGROUND: The easiest defence system carried out by the organism, the inflammatory response, happens with the support of phagocyting cells: the polymorphonuclear leukocytes (PMNL) or neutrophils are the most important cell line acting as the first defence of the organism against bacterial agents. Previous studies have shown a correlation between a reduction of the immune function and development of periodontal disease. Furthermore, it is well known that transplant patients show a variety of oral lesions as a consequence of their therapy, in particular to immunosuppressive drugs. The aim of this study is to evaluate the phagocytosis and killing functions of PMNL in transplant patients and in patients with periodontal disease in comparison with a group of healthy subjects. METHODS: PMNL, were isolated by spontaneous sedimentation from heparinized blood and centrifugation of plasma on density medium. Phagocytosis rate was expressed as the percentage of Candida albicans phagocyted after 20' incubation and phagocyting PMNLs. Intracellular killing was expressed as the percentage of yeast cells killed. RESULTS: We did not find a significant decrease of phagocytosis in transplant patients and patients with periodontal disease while these two groups of patients showed a decrease of PMNL killing activity in respect to healthy controls, an effect which was unrelated to the severity of periodontal disease. CONCLUSIONS: These results suggest that a reduction of killing activity, either spontaneous or drug-induced, would contribute to the development of periodontal disease.

Adult↗