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Biomedical subjects

A Catania

Publications and source records attributed to A Catania.

At least 19 recordsLinked to original sources
PubMed1992

Alpha-MSH peptides inhibit acute inflammation induced in mice by rIL-1 beta, rIL-6, rTNF-alpha and endogenous pyrogen but not that caused by LTB4, PAF and rIL-8.

The neuropeptide alpha-melanocyte stimulating hormone [alpha-MSH(1-13)] occurs in the pituitary, brain, skin and other tissues and receptors for this molecule are likewise widespread. In previous research, this tridecapeptide, which shares its amino acid sequence with ACTH(1-13), was shown to have both potent antipyretic activity and a role in the endogenous control of the febrile response. alpha-MSH(1-13) and its COOH-terminal tripeptide were subsequently found to inhibit inflammation induced by general stimuli such as topical application of an irritant. The aim in the present experiments was to determine if these peptides can inhibit acute inflammatory responses induced in mice by injection of individual cytokines, endogenous pyrogen (EP), a natural cytokine mixture, and other mediators of inflammation. Inflammation induced in the mouse ear by rIL-1 beta, rIL-6 or rTNF-alpha was inhibited by alpha-MSH and a D-valine-substituted analog of alpha-MSH(11-13) whereas substantial doses of alpha-MSH(1-13) did not alter inflammation induced by LTB4, PAF and IL-8. Both peptides inhibited edema caused in the mouse paw by local injection of EP. The results indicate that alpha-MSH molecules antagonize the actions of certain cytokine mediators of inflammation, consistent with previous observations of anti-cytokine activity of these peptides. Failure to inhibit edema caused by LTB4, PAF and IL-8 suggests that, in inflammation induced by general stimuli, such as EP, the peptides act prior to the release of these mediators of the inflammatory response. Because of the anticytokine/anti-inflammatory actions of the alpha-MSH molecules they may be useful in understanding the cytokine network and for treatment of inflammatory diseases.

Animals↗
PubMed1992

Inhibitory effect of somatostatin on abnormal GH response to TRH in primary hypothyroidism.

Thyrotropin releasing hormone (TRH) does not promote GH secretion in normal subjects but it stimulates GH in a proportion of hypothyroid patients. In this study the response of GH to thyrotropin releasing hormone (TRH) was evaluated in 21 patients with primary hypothyroidism of different origin: 12 with autoimmune thyroiditis, 3 idiopathic, 3 congenital, 3 iatrogenic. 11 of these patients had never been treated, the others were tested after a drug-free period of at least two weeks. Basal plasma concentration of GH was normal in all patients; after TRH administration, a significant increase in plasma GH was observed in 4 patients. In these responsive patients, somatostatin infusion inhibited the abnormal GH response to TRH. It is suggested that the abnormal GH response to TRH in primary hypothyroidism might be caused by a relative deficiency of somatostatinergic control, which is corrected by exogenous somatostatin administration.

Adult↗
PubMed1992

Scintigraphic study of extra-adrenal ganglioneuroma in a patient with overlap between multiple endocrine neoplasia types 1 and 2.

A 27-year-old woman was diagnosed with a pituitary prolactinoma. Seven years later, when she was 34, an abdominal mass was incidentally discovered and ascribed to the right adrenal gland on the basis of evidence from ultrasonography, computed tomography, and arteriography. Adrenal scintigraphy with Se-75 selenomethylcholesterol imaged both adrenal glands, but the right gland was distorted, suggesting external compression. I-131 MIBG was not taken up by the mass. At surgery, an extra-adrenal ganglioneuroma was found and excised. This case represents an overlap between multiple endocrine neoplasia types 1 and 2. The failure of the ganglioneuroma to concentrate MIBG was likely caused by secretory inactivity of a biologically mature tumor.

3-Iodobenzylguanidine↗
PubMed1991

Inhibition of acute inflammation in the periphery by central action of salicylates.

Understanding of the antiinflammatory actions of nonsteroidal drugs is incomplete, but these actions are believed to occur in the periphery, without any contribution from the central nervous system. Recent research on the antipyretic antiinflammatory neuropeptide alpha-melanocyte-stimulating hormone indicates that it can act centrally to inhibit peripheral inflammation; this raises the possibility that other agents, such as nonsteroidal antiinflammatory drugs, may have similar activity. In the present research both lysine acetylsalicylate and sodium salicylate inhibited edema, induced in the mouse ear by topical application of picryl chloride, when injected into the lateral cerebral ventricle. This inhibitory activity on a measure of acute inflammation was not due to escape of the drugs into the periphery, because systemic injection of doses that were effective centrally did not affect inflammation. In contrast, central administration of a dose of indomethacin that was antiinflammatory when given intraperitoneally did not inhibit peripheral inflammation. Thus indomethacin apparently lacks the central antiinflammatory action of the salicylates. This observation, plus our inability to demonstrate either an antiinflammatory effect of intracerebroventricular dexamethasone, a prostaglandin inhibitor, or a pro-inflammatory influence of prostaglandin E2, suggests that prostaglandins are not important to central modulation of inflammation. The results indicate that, in addition to having central influences on fever and pain, salicylates can act within the brain to inhibit acute inflammation in the periphery.

Animals↗
PubMed1991

Clinical experience with the adrenal scanning agents iodine 131-19-iodocholesterol and selenium 75-6-selenomethylcholesterol.

Adrenocortical scintigraphy with iodine 131-19-iodocholesterol or selenium 75-6-selenomethylcholesterol was performed in 94 patients with proven or suspected adrenal disease. According to the final diagnosis, 36 patients suffered from primary aldosteronism, 33 from Cushing's syndrome, 8 from low renin hypertension, 6 from nonfunctioning adrenal tumour, 4 from simple obesity, 3 from adrenal metastases, 1 from congenital adrenal hyperplasia, 1 from virilizing adrenal adenoma, 1 from extraadrenal phaeochromocytoma, 1 from ganglioneuroma. Surgical confirmation of the diagnosis was obtained in most cases. With a few exceptions, the scintigraphy results were consistent with the final diagnosis. The two tracers were equally effective adrenal scanning agents. Tracer concentration was measured in a number of surgical specimens, mostly from patients given selenocholesterol. This measurement in surgical samples has not been reported in previous studies with this agent. The results provided a direct validation of uptake measurements in vivo. The data, collected over a 17-year period, demonstrate that despite the advent of new imaging techniques, adrenal scintigraphy that gives both functional and morphologic information still has an important role in the diagnosis of adrenal disease.

19-Iodocholesterol↗
PubMed1991

Dexamethasone facilitates release of the neuropeptide alpha-MSH.

alpha-Melanocyte stimulating hormone (alpha-MSH) has important host defense properties, in part similar to those of corticosteroids. Previous research suggests that secretion of alpha-MSH and of ACTH are controlled separately. The relationship between release of alpha-MSH and the activity of the hypothalamic-pituitary-adrenal axis in the rabbit was examined by monitoring changes in circulating alpha-MSH, ACTH, and corticosterone in response to endotoxin and corticotropin-releasing hormone (CRH), both with and without dexamethasone pretreatment. Endotoxin (1 microgram/kg IV) did not cause alpha-MSH release, but it did increase plasma concentrations of ACTH and corticosterone. Similarly, CRH (1 and 10 micrograms/kg IV) did not affect plasma alpha-MSH, whereas it stimulated ACTH and corticosterone release. Dexamethasone pretreatment abolished the responses of ACTH and corticosterone to either stimulus and did not modify circulating alpha-MSH after CRH. In contrast, dexamethasone pretreatment did result in a significant increase in plasma alpha-MSH after a dose of endotoxin that was ineffective alone. These data indicate that corticosteroids can facilitate the release of alpha-MSH, a powerful anti-inflammatory hormone. Since corticosteroids are released with certain challenges, this facilitatory activity may be important to the host response.

Adrenocorticotropic Hormone↗
PubMed1991

Effect of chronic clonidine administration on GH secretion in adult human subjects.

It is well known that the acute administration of clonidine, an alpha 2-adrenergic agonist commonly used as an antihypertensive drug, stimulates GH secretion, likely via hypothalamic growth hormone releasing hormone (GHRH) release. Conversely, evidences of a hyperactivity of GHRH-GH-somatomedin C (SMC) axis during chronical administration of clonidine are controversial. In this study, GH and SMC levels have been evaluated in 16 hypertensive patients chronically treated with clonidine. The subjects were randomized to receive either TRH or saline with the aim of evaluating the non specific GH response to TRH as compared to spontaneous fluctuations during a control test. In basal conditions, GH and SMC concentrations in clonidine treated patients were similar to those observed in an age and sex matched group of normal untreated subjects. An abnormal increase in plasma GH occurred in 5 out of the 10 patients who received TRH, while plasma GH did not show significant variations during testing in the subjects who received saline. It is suggested that chronical administration of clonidine does not induce an hyperactivity of GHRH-GH-SMC axis as estimated by plasma GH and SMC concentrations, but may induce a disorder in hypothalamic control of GH secretion, possibly implicated in the abnormal GH responsivity to TRH.

Aged↗
PubMed1991

ACTH and cortisol secretion in patients with Alzheimer's disease.

The "glucocorticoid cascade hypothesis" for pathological ageing of the brain is supported by strong experimental data, but the clinical correlates are far less clear. The basal ACTH and cortisol secretion have been studied before and after the dexamethasone suppression test in patients in the early stages of clinically probable Alzheimer's disease and in controls, and the results were all normal. These findings do not support the hypothesis that the pathological brain ageing of Alzheimer's type is caused by hyperactivity of the pituitary-adrenal axis.

Adrenocorticotropic Hormone↗
PubMed1991

Red cell membrane dynamic properties and erythrocyte metabolic parameters in essential hypertension: preliminary report.

In a group of 12 subjects with essential hypertension (EH), we evaluated the erythrocyte membrane fluidity and red cell membrane transverse fluidity gradient. We also evaluated the total red cell Ca content, the red cell cytosolic free calcium, the red cell membrane cholesterol/phospholipid ratio and the red cell membrane individual phospholipids. From the data obtained, it is evident that the erythrocyte membrane fluidity and red cell membrane transverse fluidity gradient discriminate normals from hypertensives. None of the red cell metabolic parameters is able, however, to differentiate normals from hypertensive subjects. Our data underline the abnormality of the red cell membrane dynamic properties in hypertension; this abnormality is not, however, related to the red cell metabolic parameters considered.

Adult↗
PubMed1991

Rheological determinants and red cell lipidic pattern in essential obesity, in obese subjects with non-insulin-dependent diabetes mellitus (NIDDM) and in obese subjects with impaired glucose tolerance (IGT).

In a group of subjects with essential obesity, in a group of obese subjects with non-insulin dependent diabetes mellitus (NIDDM), and in a group of obese subjects with impaired glucose tolerance (IGT), we evaluated whole-blood filtration, mean erythrocyte aggregation, erythrocyte membrane fluidity and red cell lipid pattern. From these data, it is evident that the macro- and microrheological determinants are able to discriminate normals from each group of obese subjects. Regarding the red cell lipids, few are the variations between each group of obese subjects and normal controls.

Adult↗
PubMed1991

[The criteria for choosing the surgical approach to cervicomediastinal goiters].

The retrospective analysis of a series of 350 cases of intrathoracic goiters, out of a total of 5,000 thyroid operations derived from the joined case records of the 3rd General Surgery Institute (Director: Prof. G. Di Matteo) and the 8th Chair of Surgical Pathology (Director: Prof. F.P. Campana), has induced the authors to reconsider the surgical approach to this pathology on the basis of anatomo-surgical factors.

Goiter, Substernal↗
PubMed1990

CRH and lysine-vasopressin stimulation tests in the diagnosis of hypoadrenalism secondary to hypothalamic or pituitary disorders.

Ten patients with secondary hypoadrenalism have been tested with corticotropin releasing hormone (CRH) and lysine-vasopressin (LVP). One patient had isolated ACTH deficiency; 9 had deficiency of other pituitary hormones attributable to a primary pituitary disease in 3 and to an hypothalamic disorder in 6. After CRH administration, a definite increase in plasma ACTH was observed in all 6 patients with hypothalamic disorder. No response was elicited in the 3 patients with pituitary disease and in the patient with isolated ACTH deficiency. In the responsive patients. ACTH showed a delayed and prolonged pattern of response. Lysine-vasopressin administration produced an increase in plasma ACTH in 4 of the 6 hypothalamic patients and no response in those with pituitary disease and in the patient with isolated ACTH deficiency. These findings suggest that CRH represents a reliable test in differentiating hypothalamic from pituitary adrenal failure; LVP appeared a less sensitive diagnostic test.

Adolescent↗