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Biomedical subjects

A Catania

Publications and source records attributed to A Catania.

At least 73 records · Page 4Linked to original sources
PubMed1997

Vascular anastomoses among abdominal organs in laboratory animals.

Vascular anastomoses among abdominal organs were studied in 289 laboratory mammals. Arterial anastomoses joining the wall or the parenchyma of the abdominal organs were studied in 108 animals and were found among the stomach, the spleen and the pancreas. In the cat, such anastomoses occur in 86.7% of cases, in the guinea pig in 73.3%, in the hedgehog in 61.1%, in the rabbit in 3.3%. The highest mean value was found in the cat: 3.1 anastomoses. Venous anastomoses were studied in 181 animals and were found among the stomach, the spleen and the pancreas, too. With the exception of the guinea pig (found in 89.1% of cases), these anastomoses were found almost in all cases of other five examined species. They mostly occur between the stomach and the spleen, and between the spleen and the pancreas with some differences in the guinea pig and the cat. The highest mean value was found in the rat: 6.1 anastomoses. For the present, it is not possible to state any significant differences among orders and species examined. As these vascular anastomoses occur also in man, we believe that they should be preserved during surgical procedures.

Animals↗
PubMed1997

[Parathyroidectomy: our school experience].

The Authors evaluated the results obtained in 145 patients operated on for hyperparathyroidism: 109 patients had primary hyperparathyroidism and 36 patients had secondary hyperparathyroidism. Preoperative localization by ultrasonography was assured in all cases, while only few patients were preoperatively evaluated by arteriography and selected venous sampling of the parathyroid hormone concentration. After surgical resection for primary hyperparathyroidism, transient postoperative hypoparathyroidism occurred in 30 patients (27.5%), recurrent disease occurred in 3 patients (2.7%), while 1 patient experienced persistent hypoparathyroidism (1%). In 3 patients (3%), resection of a solitary adenoma and biopsy of all parathyroid glands resulted in a permanent hypoparathyroidism which required long-term administration of vitamin D and oral calcium. Neither recurrent nor persistent hyperparathyroidism occurred in patients surgically treated for secondary hyperparathyroidism, and no postoperative hypoparathyroidism was registered. The Authors emphasize the importance of an adequate surgical strategy and accurate initial cervical exploration of the parathyroid glands as a necessary step for the correct treatment of this challenging disease.

Humans↗
PubMed1997

[Surgery of differentiated cancer of the thyroid].

A retrospective study on patients with differentiated thyroid carcinoma operated on at the 3rd Department of General Surgery of the University "La Sapienza" of Rome from 1970 to 1996 was performed. In 709 patients total thyroidectomy was performed as the minimal procedure acceptable, while 19 patients had subtotal thyroidectomy out of necessity. A functional ipsilateral or bilateral lymphnectomy of the neck was performed in 256 cases. This wider operation is indicated in the presence of metastatic lymph nodes and on principle in patients older than forty-five years in which at least another risk factor is present. Long term follow-up (12 years) was assured in 302 patients and the survival rate was 92% independently from the histotype (papillary or follicular). The survival rate of a group of 120 patients (80 with papillary and 40 with follicular carcinoma) was analyzed in relation to the risk factors. This group analysis demonstrated a very low mortality rate in patients with low risk index and an increased rate in patients with a high risk index.

Carcinoma↗
PubMed1997

Leukocyte flow properties, polymorphonuclear membrane fluidity and cytosolic Ca2+ content in subjects with vascular atherosclerotic disease.

In a group of subjects with monovascular atherosclerotic disease (MVAD) and in a group of subjects with polyvascular atherosclerotic disease (PVAD) we evaluated white blood cell (WBC) filtration (unfractionated, mononuclear -MN-, polymorphonuclear -PMN- cells), using the St. George Filtrometer and considering respectively the initial relative flow rate (IRFR) and the clogging rate (CR), the polymorphonuclear leukocyte membrane fluidity, employing the fluorescent probe 1.4-(trimethylamino)-phenyl-4-phenylhexatriene (TMA-DPH) and calculating the fluorescence polarization degree, and the polymorphonuclear leukocyte cytosolic Ca2+ content, adopting the fluorescent probe Fura 2-AM. Only the filtration parameters (IRFR, CR) of unfractionated WBCs discriminate normals from MVAD and PVAD subjects, and also monovascular and polyvascular VAD subjects between them. The filtration parameters of mononuclear and polymorphonuclear leukocytes do not distinguish normals from MVAD and PVAD subjects. PMN membrane fluidity does not differentiate normals from MVAD and PVAD subjects, while PMN cytosolic Ca2+ content discriminates normals from MVAD and PVAD subjects, but does not distinguish the two groups of VAD subjects. In conclusion, in subjects with vascular atherosclerotic disease we noted an alteration of the unfractionated leukocyte flow properties, more evident in PVAD subjects, and an increase of the PMN cytosolic Ca2+ content.

Aged↗
PubMed1996

alpha-MSH production, receptors, and influence on neopterin in a human monocyte/macrophage cell line.

alpha-Melanocyte-stimulating hormone (alpha-MSH), a tridecapeptide derived from pro-opiomelanocortin, has potent antiinflammatory activity in laboratory animals. alpha-MSH inhibits nitric oxide production by murine macrophages, an influence believed to reflect activation of an autocrine circuit in these cells, one that is based on production and release of alpha-MSH and subsequent stimulation of melanocortin receptors. We found that THP-1 cells, human monocytic cells, produced alpha-MSH; this production was increased by interleukin-6, tumor necrosis factor a, or concanavalin A. These cells also expressed the gene for the human alpha-MSH receptor MC1. Unlike murine macrophages, THP-1 cells produced little nitrite in response to interferon-gamma (IFN-gamma) and lipopolysaccharide, and a-MSH inhibited this production only slightly. However, production of neopterin, a presumed primate homologue of nitric oxide in lower animals, was increased in THP-1 cells stimulated with INF-gamma plus TNF-alpha and alpha-MSH significantly inhibited this production. The evidence indicates that an autocrine regulatory circuit based on alpha-MSH occurs in human monocyte/macrophages much as in murine macrophages. alpha-MSH-induced modulation of specific inflammatory mediators/cytotoxic agents appears to differ depending on the importance of the mediators in the myelomonocytic cells of different species.

Amino Acid Sequence↗
PubMed1996

The neuropeptide alpha-MSH has specific receptors on neutrophils and reduces chemotaxis in vitro.

The proopiomelanocortin-derived peptide alpha-melanocyte stimulating hormone (alpha-MSH) has potent anti-inflammatory effects in all animal models of inflammation against which it has been tested. Understanding of the mechanism by which this occurs is incomplete, although there is recent evidence for alpha-MSH receptors in murine and human macrophages and for modulation of production of proinflammatory cytokines and related mediators by alpha-MSH. Because of the prominence of neutrophils in early stages of inflammatory reactions where alpha-MSH is effective, we examined human neutrophils for evidence of mRNA for alpha-MSH receptors and for inhibition of neutrophil chemotaxis. There was accumulation of mRNA for melanocortin receptor 1 (MC1) in RT/PCR product from neutrophils stimulated with interferon and LPS. In subsequent studies alpha-MSH inhibited migration of neutrophils from most normal volunteers when the cells were placed in FMLP or IL-8 gradients. The inhibition by alpha-MSH could be traced to alterations in cAMP in neutrophils. The presence of alpha-MSH receptor message in neutrophils is consistent with the established anti-inflammatory effects of the peptide. Direct inhibition of neutrophil chemotaxis likely contributes to the anti-inflammatory activity of alpha-MSH.

Analysis of Variance↗
PubMed1996

Leukocyte flow properties, polymorphonuclear membrane fluidity, and cytosolic Ca2+ content in subjects with vascular atherosclerotic disease with and without noninsulin-dependent diabetes mellitus.

The aim of this research was the evaluation of white blood cell (WBC) filtration, reflecting WBC flow properties, polymorphonuclear cell membrane fluidity, and cytosolic Ca2+ content in subjects with vascular atherosclerotic disease (VAD) and in VAD subjects with noninsulin-dependent diabetes mellitus (NIDDM), in good hemodynamic balance. The authors examined WBC filtration (unfractionated, mononuclear [MN], polymorphonuclear [PMN] cells), using the St. George Filtrometer and considering, respectively, the initial relative flow rate (IRFR) and the clogging rate (CR); the PMN membrane fluidity, employing the fluorescent probe TMA-DPH and calculating the fluorescence polarization degree; and the PMN cytosolic Ca2+ content, adopting the fluorescent probe Fura 2-AM and considering the ratio between the Fura 2-Ca2+ complex and the unchelated Fura 2 fluorescence intensity. The obtained data showed that only the filtration parameters (IRFR, CR) of unfractionated WBCs discriminated normal subjects from VAD groups, whereas the filtration parameters of MN and PMN cells did not demonstrate any distinction. PMN membrane fluidity did not distinguish normal subjects from VAD groups, whereas PMN cytosolic Ca2+ content was significantly increased in VAD groups in comparison with normal subjects. No relationship was evident between WBC filtration and plasma metabolic parameters; the correlations obtained between PMN filtration and other PMN parameters need further investigation.

Aged↗
PubMed1995

Evidence of autocrine modulation of macrophage nitric oxide synthase by alpha-melanocyte-stimulating hormone.

alpha-Melanocyte-stimulating hormone (alpha-MSH) is a potent inhibitory agent in all major forms of inflammation. To identify a potential mechanism of antiinflammatory action of alpha-MSH, we tested its effects on production of nitric oxide (NO), believed to be a mediator common to all forms of inflammation. We measured NO and alpha-MSH production in RAW 264.7 cultured murine macrophages stimulated with bacterial lipopolysaccharide and interferon gamma. alpha-MSH inhibited production of NO, as estimated from nitrite production and nitration of endogenous macrophage proteins. This occurred through inhibition of production of NO synthase II protein; steady-state NO synthase II mRNA abundance was also reduced. alpha-MSH increased cAMP accumulation in RAW cells, characteristic of alpha-MSH receptors in other cell types. RAW cells also expressed mRNA for the primary alpha-MSH receptor (melanocortin 1). mRNA for proopiomelanocortin, the precursor molecular of alpha-MSH, was expressed in RAW cells, and tumor necrosis factor alpha increased production and release of alpha-MSH. These results suggest that the proinflammatory cytokine tumor necrosis factor alpha can induce macrophages to increase production of alpha-MSH, which then becomes available to act upon melanocortin receptors on the same cells. Such stimulation of melanocortin receptors could modulate inflammation by inhibiting the production of NO. The results suggest that alpha-MSH is an autocrine factor in macrophages which modulates inflammation by counteracting the effects of proinflammatory cytokines.

Amino Acid Oxidoreductases↗
PubMed1995

Endogenous cytokine antagonists during myocardial ischemia and thrombolytic therapy.

We tested the idea that cytokine antagonists are released during acute myocardial ischemia to counteract proinflammatory effects of cytokines. We investigated changes in plasma concentrations of the anticytokine molecules alpha-melanocyte-stimulating hormone (alpha-MSH), interleukin-1 receptor antagonist (IL-1ra), and soluble tumor necrosis factor receptor (sTNFr) in patients with acute myocardial infarction (AMI) or unstable angina (UA). Blood samples were collected at presentation in the coronary care unit, at 3-hour intervals for 24 hours, and daily for 4 days thereafter. There were no significant differences in the concentrations of cytokine antagonists in patients with AMI or UA. However, whereas concentrations of alpha-MSH were increased in early samples of patients with AMI or UA who were treated with a thrombolytic agent, they were consistently low in untreated patients. IL-1ra concentrations likewise were greater 3 and 6 hours after treatment in patients who underwent thrombolysis, whereas there was no significant difference in plasma sTNFr between the two groups. We suggest that during myocardial ischemia and thrombolysis anticytokine molecules released from the injured myocardium become available to reduce inflammation caused by cytokines and other mediators of inflammation.

Adult↗
PubMed1995

Platelet membrane fluidity and platelet membrane lipid pattern in essential hypertension.

In a group of subjects with essential hypertension platelets were studied in resting conditions: platelet membrane fluidity was measured with the fluorescent probe 1.4-(trimethylamino)-phenyl-4-phenylhexatriene (TMA-DPH), platelet membrane cholesterol/phospholipid ratio was evaluated separating the membrane lipids with column chromatography, and platelet membrane individual phospholipids were determined using two-dimensional thin-layer chromatography. From the obtained results, it is evident that platelet membrane fluidity does not differentiate normals from hypertensives; platelet membrane cholesterol/phospholipid ratio is increased in hypertensives, while of the platelet membrane individual phospholipids, only the phosphatidylcholine is increased. In normals and hypertensives, no relation is evident between platelet membrane fluidity, platelet membrane lipid pattern, and systolic and diastolic blood pressure values.

Adult↗
PubMed1995

Cytosolic Ca2+ content and membrane fluidity of platelets and polymorphonuclear leucocytes in diabetes mellitus.

Considering the role played by platelets and leucocytes in diabetic disease and keeping in mind the strong correlation between functional and metabolic aspects that characterizes this clinical condition, we evaluated, in two groups of diabetics, respectively the platelet and polymorphonuclear (PMN) cytosolic Ca2+ content (employing the fluorescent probe Fura 2-AM) and membrane fluidity (using the fluorescent probe TMA-DPH and considering the fluorescence polarization degree, inversely related to the membrane fluidity). From the obtained results, it is evident that the platelet cytosolic Ca2+ content does not distinguish normals from diabetics of type 1 and 2; the platelet membrane fluidity instead does not discriminate normals from diabetics, but differentiates diabetics of type 1 and 2 (type 1 = 0.284 +/- 0.015; type 2 = 0.314 +/- 0.018; p < 0.001). PMN cytosolic Ca2+ content and membrane fluidity do not discriminate normals from diabetics. In the two groups of diabetics none of the platelet and PMN parameters (cytosolic Ca2+ content and membrane fluidity) are related to the glycometabolic pattern.

Adolescent↗
PubMed1995

Membrane fluidity, membrane lipid pattern, and cytosolic Ca2+ content in platelets from a group of type II diabetic patients with macrovascular complications.

OBJECTIVE: To evaluate platelet membrane fluidity and some platelet metabolic parameters in type II diabetic patients with macrovascular complications. RESEARCH DESIGN AND METHODS: In a group of 21 type II diabetic patients with macrovascular complications, we evaluated platelet membrane fluidity [marking intact resting platelets with the fluorescent probe 1,4-(trimethylamino)-phenyl-4-phenylhexatriene (TMA-DPH)], platelet membrane lipid pattern (cholesterol:phospholipid [C:PL] ratio and individual phospholipids), and platelet cytosolic Ca2+ content (marking intact resting platelets with the fluorescent probe Fura 2AM). RESULTS: Platelet membrane fluidity is decreased in type II diabetic patients with macrovascular complications compared with normal subjects (P < 0.001). Platelet membrane C:PL ratio and cytosolic Ca2+ content do not discriminate normal subjects from diabetic patients, and for individual phospholipids, only phosphatidylethanolamine is decreased in diabetic patients compared with control subjects (P = 0.051). In normal subjects, the polarization degree of TMA-DPH is related to phosphatidylserine (P < 0.05) and phosphatidylcholine (P < 0.05), and in diabetic patients the polarization degree of TMA-DPH is related to C:PL ratio (P < 0.05) and sphyngomyelin (P < 0.05). CONCLUSIONS: In type II diabetic patients with macrovascular complications, we observed an abnormality of platelet membrane fluidity, which may contribute to platelet functional alteration present in this clinical condition.

Aged↗
PubMed1994

The neuropeptide alpha-melanocyte-stimulating hormone inhibits experimental arthritis in rats.

alpha-Melanocyte-stimulating hormone (alpha-MSH) modulates inflammatory processes in models of acute inflammation and in models of sepsis/septic shock/adult respiratory-distress syndrome (ARDS). Because this neuropeptide inhibits actions of cytokines and other mediators of imflammation that are also believed to underlie aspects of chronic inflammation, tests were performed to compare the effects of repeated administration of the peptide with those of prednisolone and saline on the development of adjuvant arthritis in rats. alpha-MSH (50 micrograms), injected i.p. twice daily, markedly inhibited the clinical and histological signs of experimental arthritis and moderated the weight loss observed in control animals. Prednisolone (100 mg/kg), given twice per day, prevented development of arthritis but caused marked and progressive weight loss. The results confirm the potent anti-inflammatory influence of alpha-MSH, in this case in a model of chronic inflammation that has immune components.

Animals↗
PubMed1994

Plasma concentration of cytokine antagonists in patients with HIV infection.

There is increasing evidence that cytokines contribute to the immunopathogenesis of human immunodeficiency virus (HIV) infection. It may be, therefore, that compensatory rises in circulating cytokine antagonists also occur in HIV infection and that such changes mark disease progression. To test this idea, plasma concentrations of the cytokine antagonists alpha-melanocyte-stimulating hormone (alpha-MSH), interleukin-1 receptor antagonist (IL-1ra), and soluble tumor necrosis factor receptor (sTNFr) were measured in patients of different Centers for Disease Control (CDC) categories of HIV infection and in seronegative controls. Plasma levels of all these cytokine antagonists were higher in HIV-infected patients. IL-1ra and sTNFr concentrations were correlated with indicators of disease activity: positively with plasma neopterin and negatively with CD4+ T lymphocyte counts. alpha-MSH and sTNF r were greater in CDC groups III and IV, whereas IL-1ra was elevated only in the latter group. Because cytokines activate the hypothalamic-pituitary-adrenal axis and adrenal steroids inhibit cytokine production, we measured circulating adrenocorticotropic hormone (ACTH) and cortisol in HIV-infected patients and investigated relations among these hormones, cytokine antagonists, and markers of disease progression. It appears that these physiological modulators of cytokine activity are not closely linked to sTNFr, IL-1ra and alpha-MSH: there were no significant correlations between plasma concentrations of ACTH or cortisol and those of cytokine antagonists, nor were there correlations between hormones and markers of disease progression such as neopterin or CD4+ T cell counts. It is notable that severe adrenal insufficiency was extremely rare (3%) in HIV-infected patients; it was confined to the AIDS group and was consistently secondary to ACTH deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1994

Central neurogenic antiinflammatory action of alpha-MSH: modulation of peripheral inflammation induced by cytokines and other mediators of inflammation.

The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) has potent antipyretic and antiinflammatory properties. When administered systemically, the naturally occurring molecule and its COOH-terminal tripeptide sequence inhibit inflammation induced by peripherally applied irritants and intradermal injections of mediators of inflammation such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF alpha). We recently found that alpha-MSH can act solely within the brain to inhibit inflammation caused by a general irritant applied to the skin. This activity appears to be shared with salicylate drugs and the combined observations suggest the existence of descending neurogenic antiinflammatory signals capable of modulating inflammation in peripheral tissues. To improve our knowledge of the scope of this action of the peptide, alpha-MSH was injected into the cerebral ventricles (i.c.v.) of mice that had received intradermal injections in the ear of mediators of inflammation: IL-1 beta, IL-8, leukotriene B4, and platelet-activating factor. The centrally administered peptide inhibited the actions of all of these proinflammatory agents as determined from comparisons with measures of ear edema over time in control animals; this indicates that the central peptide can alter inflammation induced in the periphery by major mediators of inflammation. In tests confined to IL-1 beta, central administration of alpha-MSH(11-13) was also effective. These findings support the concept of a descending neurogenic antiinflammatory influence promoted by an action of alpha-MSH within the brain, an inhibitory influence that is not restricted to modulation of just one or a limited set of the mediators of inflammation.

Animals↗
PubMed1994

Antiinflammatory influences of alpha-MSH molecules: central neurogenic and peripheral actions.

alpha-Melanocyte-stimulating hormone (alpha-MSH1-13) and its COOH-terminal tripeptide alpha-MSH11-13 (Lys Pro Val) inhibit inflammation when administered systemically. Recent evidence indicates that alpha-MSH1-13 can likewise inhibit inflammation in the skin solely via an action within the brain. Because of the potential importance of this discovery to understanding the control of inflammation and because alpha-MSH molecules might be useful for treatment of inflammation, experiments were performed to learn more about the mechanisms of action of these peptides. In tests on inflammation induced in the mouse ear by intradermal injections of recombinant human interleukin-1 beta, alpha-MSH1-1-13 administered intracerebroventricularly effectively reduced inflammation. This effect of centrally administered alpha-MSH1-13 was inhibited by systemic injection of the nonspecific beta-adrenergic receptor blocker propranolol and by administration of a specific beta 2-adrenergic receptor antagonist; the effect was not altered by blockade of cholinergic, alpha-adrenergic, or beta 1-adrenergic receptors. In mice with inflammation induced in a hind paw and with the spinal cord transected, the antiinflammatory effect of centrally administered alpha-MSH1-13 was prevented, indicating that intact descending neuronal pathways are required for the antiinflammatory influence of the central peptide. Systemic injection of alpha-MSH1-13 in animals with spinal cord transection had a smaller and later antiinflammatory effect, which suggests that the molecule also has an action, albeit lesser, in the periphery. However, alpha-MSH11-13 injected intraperitoneally had marked antiinflammatory activity in animals with spinal cord transection.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗