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Biomedical subjects

A Conforti

Publications and source records attributed to A Conforti.

14 recordsLinked to original sources

Desferrioxamine potentiated SOD antiinflammatory activity in rat adjuvant arthritis: role of iron and bacterial toxins.

In this paper we studied the modulating inflammatory activity of iron in the adjuvant arthritis, taking indomethacin as a standard antiinflammatory drug and a superoxide dismutase derivative (MPEG-SOD) as a scavenger of free radicals. Moreover, we evaluated the changes in potential intestinal pathogens requiring iron for growth, in order to study the role of bacteria in the altered gastrointestinal functions observed during arthritis. We observed a 50% arthritis inhibition on the 14th day with MPEG-SOD plus desferrioxamine, a significant decrease in serum iron in arthritic rats compared to controls, and a significant Cl. perfringens increase on the 28th day in the presence of MPEG-SOD. Our data demonstrate that hypoferremia, in arthritis, is a protective mechanism overall in the early phase and could protect the intestinal tract by inhibiting the development of potential pathogens.

Animals

The pigmentary system of planaria. I. Morphology.

The pigmentary system of the planaria, Dugesia gonocephala s.l. (Platyhelminthes, Turbellaria, Tricladida), has been studied by light and electron microscopy. The system consists of granules contained in chromatophore-like cells embedded in the parenchyma. The cell processes penetrate between the muscle layers and extend to the sub-epidermal basal lamina. The nature of the pigment and the comparative anatomical significance of the chromatophore structure is discussed.

Animals

The pigmentary system of planaria. II. Physiology and functional morphology.

The pigmentary system of the planaria, Dugesia gonocephala s.l. (Platyhelminthes, Turbellaria, Tricladida), consists of granules contained in chromatophore cells distributed in the parenchyma tissue. The administration of MSH release-inhibiting Factor (M.I.F.) leads to an easily observable general decolouration of the animal due to the migration of the pigment granules towards the deeper-lying cell nucleus. In planarians bisected transversely through the pharyngeal region, the decolouration occurs only in the cephalic segment, and the caudal segment remains dark. When, however, the decapitated caudal segment regenerates a head region, a decolouration response occurs when exposed to M.I.F. The significance of these results is discussed, and an hypothesis on the hormonal regulation of the pigmentary system is proposed.

Animals

Concerning the role of endogenous copper in the acute inflammatory process.

The development of two models of acute inflammation (carrageenan-induced foot oedema and pleurisy) was studied in rats after 1 month of a 0.2 p.p.m. copper-deficient diet and after 5 months of a 0.6-0.8 p.p.m. copper-deficient diet. A 'pro-inflammatory' effect of copper deficiency was observed with the 0.2 p.p.m. diet, whilst no effect was evident following the 0.6-0.8 p.p.m. copper deficient diet. These results are briefly commented upon.

Acute Disease

Ultrastructural nuclear changes in human lymphocytes following arabinosylcytosine treatment in vitro.

Human lymphocytes were separated by centrifugation and grown for 48--72 h in TC 199 medium. Synchronous cells, obtained by the addition of colchicine, were treated with arabinosylcytosine (Ara-C), an antimitotic substance which is known to produce nuclear changes in vivo and in vitro. In this case, alterations in the nuclear envelope closely resembling the malignancy associated changes described in human leukaemic cells were observed. The results allow us to suggest that such alterations may be due to a cellular derangement involving the renewal of the nuclear envelope in th G1 phase of the mitotic cycle.

Cell Nucleus

Subcellular reactions to injury. I. Ultrastructural and biochemical investigations on the hepatic cellular damage produced by haemorrhagic shock in dogs.

The ultrastructural changes produced by haemorrhagic shock in hepatocytes have been studied in dogs. The associated biochemical and biophysical system alterations allow us to propose a unitary pathogenetic mechanism of the cellular injury based on oxygen deprivation and its effect on the function and structure of the cellular compartments.

Animals

Serum calcitonin and blood mineral interrelationships in normal children aged six to twelve years.

Simultaneous measurements of serum immunoreactive thyrocalcitonin (iTCT), immunoreactive parathyroid hormone (iPTH), calcium, inorganic phosphate, magnesium, and alkaline phosphatase were made in 37 normal children whose ages ranged from 6-12 years. Between the ages of 6 and 12 there is a statistically significant rise in serum iTCT levels (r = 0.4638; P less than 0.01), and a fall in serum iPTH levels (r = 0.4976; P less than 0.01). There is a highly significant inverse correlation between serum iTCT and iPTH levels (r = 0.5248; P less than 0.005). Serum iTCT levels were inversely correlated with phosphate levels (r = 0.4989; P less than 0.01), the latter being age dependent and falling significantly between the ages of 6 and 12 (r = 0.4802; P less than 0.001). There was no significant relationship between serum calcium levels and iTCT, iPTH, or age. Serum magnesium levels were not correlated with calcium, iTCT, or iPTH levels.

Adult

[Copper and nervous system. An experimental study (author's transl)].

Sodium azide is known to produce alterations in mammalian copper proteins, thus rendering them unable to bind exogenous metal, which remains in the "labile pool" condition. Continuous administration of sodium azide at LD50 for 30 days causes copper accumulation in several tissues and even in the nervous system, with characteristic changes in neurones and glial cells, very much resembling the alterations observed in Wilson's disease. Dietary copper administration, on the contrary, though raising the level of tissue-bound metal, does not produce cellular damage. These findings allow us to suppose that sodium azide may alterate the coppper chelating proteins in the tissues, especially in the nervous system, thus causing the storage of cell-toxic "labile pool" metal. The pathogenesis of Wilson's disease and the problem of "pathoclisis" in the nervous system are debated.

Animals

Ultrastructural changes in human leukemic cell nuclei.

The ultrastructural changes of human leukemic cell nuclei have been investigated. Particular attention is paid to the alteration of the nuclear envelope and its constituents, i.e., the pores and the Zonula Nucleum Limitans which appear constantly involved in these pathologic processes. An alteration of the relationship between the components of the nuclear envelope and the chromatin itself may be responsible for the appearance of the most nuclear changes.

Cell Nucleus

Ultrastructural hypoxic changes in Ammon's horn and Purkinje cells.

Guinea pigs were exposed for varying periods to different degrees of hypoxia by respiration of controlled mixtures of O2-N2 and the CNS subjected to both light and electron microscopic examination after aldehyde fixation by perfusion. The subacute anoxia experiments revealed an alteration in the rough endoplasmic reticulum of the Purkinje cells consisting of the formation of 'paired cisternae'. In the chronic anoxia experiments, small ultrastructural alterations of the same cells were found in association with the appearance of monoparticulate glycogen. The authors debate the significance of these ultrastructural alterations in relation to the damage found in other organs.

Animals