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Biomedical subjects

A Cariani

Publications and source records attributed to A Cariani.

At least 19 recordsLinked to original sources
PubMed2006

Human T-cell lymphotropic virus type I (HTLV-I) confirmed by PCR-Southern blot and sequencing analysis in a woman with tropical spastic paraparesis.

Human T-cell lymphotropic virus type I (HTLV-I) is a human retrovirus and the aetiological agent of a progressive neurological disease called tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM), as confirmed by evidence accumulated in HTLV-I seroprevalence studies. TSP/HAM is rarely diagnosed in Italy, given the low prevalence of HTLV-I in the population. TSP/HAM begins insidiously in the fourth decade, mainly with spastic paraparesis of the lower extremities and positive Babinski reflex, as well as interfering with bowel and bladder functions. In this study we report the clinical, virological and haemato chemical data of a 54-year-old woman, born in the Ivory Cost, with symptoms suggestive of TSP. The presence of HTLV-I infection was demonstrated by the detection of antibodies in serum and in cerebrospinal fluid by immunoenzymatic assay and Western blot analysis. In addition, viral isolation was carried out in peripheral blood cells, and the presence of HTLV-I proviral DNA was confirmed by polymerase chain reaction/Southern blot and sequencing analysis. According to our results, HTLV-I testing might be useful when TSP/HAM is suspected.

Blotting, Southern↗
PubMed2001

Inhibition of neutrophil responses by cyclosporin A. An insight into molecular mechanisms.

OBJECTIVE: Cyclosporin A (CsA) is an effective agent in rheumatoid arthritis (RA), slowing joint damage progression. Its therapeutic effect on T lymphocytes has been studied extensively, but there is little information available about neutrophils, the cells responsible for a substantial proportion of inflammation. A study was performed to investigate the in vitro effects of CsA on neutrophil functions triggered by several agonists and determine whether the drug could counteract the binding of formyl-methionyl-leucyl-phenylalanine (fMLP) to its receptor and/or modulate changes in the intracellular Ca(2+) concentration ([Ca(2+)]i). METHODS: CsA was added to neutrophils 5-50 min before the incubation steps for neutrophil function assays (chemotaxis, superoxide anion production, lysozyme release), calcium measurements and receptor binding experiments. RESULTS: CsA appeared to be particularly effective in lowering chemotaxis, superoxide anion production and lysozyme release induced by different agonists. However, it did not significantly affect either basal or agonist-stimulated neutrophil [Ca(2+)]i and the interaction between fMLP and its receptor. CONCLUSIONS: Because of its in vitro inhibition of neutrophil functions, CsA appears to have considerable potential as an anti-inflammatory drug. Moreover, as it is also a potent immunosuppressive agent, it may reduce the progression of joint damage in RA. More work remains to be done to clarify the molecular mechanism of CsA action on neutrophils.

Binding, Competitive↗
PubMed1997

Two for-Met-Leu-Phe-OMe analogues trigger selective neutrophil responses. A differential effect on cytosolic free Ca2+.

For-Thp-Leu-Ain-OMe and for-Met-delta(z)Leu-Phe-OMe are two conformationally restricted fMLP-OMe analogues able to discriminate between different biological responses of human neutrophils. In this paper, we demonstrate that the former peptide, which evokes only chemotaxis, does not alter human neutrophil Ca2+ levels. In contrast, for-Met-delta(z)Leu-Phe-OMe, which induces superoxide anion release and degranulation but not chemotaxis, significantly increases the cation concentration. The chelation of Ca2+ in both extracellular and intracellular media abolishes O2- production triggered by for-Met-delta(z)Leu-Phe-OMe, while the same procedure does not affect neutrophil chemotaxis towards for-Thp-Leu-Ain-OMe. We therefore suggest that chemotaxis, unlike superoxide anion release, is independent of Ca2+ enhancement in human neutrophils.

Calcium↗
PubMed1975

[Physiological basis of homeostasis of the extracellular fluid volume].

Renal, glomerular and tubular, factors responsible for the volume control of extracellular liquid were examined. The part played by angiotensin II in mediating the compensation of this liquid losses was studied in patients with spontaneous polyuria due to diencephalo-posthypophyseal diabetes insipidus or psychogenic polydipsia and healthy subjects with induced hypotonic polyuria. It was noted that: 1) acute expansion elicited a natriuretic response and increased distal sodium load, due to an increase in filtrate and relative inhibition of proximal reabsorption, or proximal inhibition if the filtrate was unchanged. The efficiency of distal sodium transport was often unchanged. 2) Return to sodium balance parity during prolonged expansion of volume, was accomplished by varying renal means, in accordance with the experimental model employed. Distal reabsorption was essentially depressed during prolonged saline load (secondary hypoaldosteronism). When protracted mineralcorticoid treatment was used, however, distal reabsorption was high, even in the escape stage, and its saturation required marked augmentation of the sodium load reaching the distal tubules. 3) Depletion of volume caused by protracted natriuretic treatment in spontaneous polyuria reduced both diuresis and sodium excretion. This resistance to the natriuretic effect of the drug followed intrarenal compensation that reduced the distal sodium load and encouraged reabsorption in some distal sites (secondary hyperaldosteronism). 4) Infusion of angiotensin II in sub- or pauci-pressor doses causes an isosmotic sodium saving, since it reduced the glomerular filtrate and increases the fraction of filtrate reabsorbed by the proximal tubules; the tubular effect is likely secondary to increased vascular, especially postglomerular resistance. In the healthy subject, angiotensin II leads to antidiuresis referable, on account of its intensity and longer time cycle, to ADH release angiotensin-dependent.

Angiotensin II↗