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Biomedical subjects

C Soria

Publications and source records attributed to C Soria.

At least 127 records · Page 7Linked to original sources
PubMed1991

Detection of undegraded fibrin and tumor necrosis factor-alpha in venous leg ulcers.

The pathogenesis of venous leg ulcers is based on the leakage of fibrinogen leading to pericapillary fibrin cuff and plugging of capillaries by white blood cells. Eight patients with venous leg ulcers have been studied with a panel of antibodies reactive for fibrinogen, fibrin, fibrin degradation products, and various cell-associated markers for polymorphonuclear cells, monocytes, and B and T lymphocytes. Our results showed that pericapillary fibrin cuff was mainly composed of undegraded fibrin and that, in the granulation tissue, tumor necrosis factor-alpha and elastase activities were detectable in monocytes and polymorphonuclear cells, respectively. Only few activated lymphocytes were present. On the basis of these results, it is assumed that inflammation generated by activated white blood cells that accumulate under unrelieved pressure is the key event. Tumor necrosis factor-alpha synthesized by activated monocytes may therefore induce the formation of pericapillary fibrin cuffs. Pericapillary fibrin cuffs and toxic metabolites released by polymorphonuclear cells may explain the absence of wound repair.

Aged↗
PubMed1991

[3H]-flunitrazepam binding after morphine treatment and under abstinence syndrome.

Chronic morphine treatment produced increases in [3H]-flunitrazepam binding in some hippocampal areas of the rat brain. The differences in binding were statistically significant in some cases. Both morphine-dependent and morphine-deprived (abstinence syndrome) animals showed an identical response in binding, which confirms a real, although small, increase in benzodiazepine binding sites in the hippocampus after morphine treatment, that is not affected by a naloxone-induced abstinence syndrome under the conditions studied. These findings support the hypothesis of a morphine-induced up-regulation of benzodiazepine binding sites in the hippocampus. A possible different response in benzodiazepine binding sites 1 and 2 could explain the different findings reported in the literature. Our data suggest that the detected increase in benzodiazepine binding would be mainly due to type 2 binding sites, since the hippocampus has a higher density of this type of benzodiazepine binding sites.

Animals↗
PubMed1991

Treatment of pyoderma gangrenosum with cyclosporin A.

Two patients with recalcitrant pyoderma gangrenosum were treated with oral cyclosporin A (5 mg/kg body-weight/day). Healing of the lesions was achieved in Patient 1 within 1 month of starting treatment, but new areas of ulceration appeared when the dose was reduced to 3 mg/kg body-weight/day. The ulcers showed marked improvement by 3 weeks after the start of treatment in Patient 2 and remained inactive at a maintenance dosage of 100 mg/day, but there was no change in the associated seronegative arthritis. A steroid-sparing effect of CyA was evident in both patients. It is suggested that a lower dose of cyclosporin A than doses used previously in the treatment of pyoderma gangrenosum may be equally effective.

Adult↗
PubMed1991

End-stage renal disease in a patient with amyloidosis secondary to acne conglobata.

The clinical profile of a patient with a 15 years' evolution of acne conglobata developing systemic amyloidosis with severe renal involvement is described, and the possible influence of suppurative skin foci surgical excision on the rapid progression to terminal renal failure is discussed. This etiological cause of secondary amyloidosis has rarely been reported as a cause of end-stage renal disease.

Acne Vulgaris↗
PubMed1991

Dysfibrinogenemia and thrombosis.

A thrombotic tendency (venous or arterial) has been reported in some cases of dysfibrinogenemia. We report here the mechanism by which these thrombosis may occur. It may be related either to a defective clot lysis due to a poor reactivity toward fibrinolytic enzymes or to a defective thrombin binding capacity of the abnormal clot. Acquired fibrin clot structure anomalies may also be responsible for a defective thrombolysis.

Fibrin↗
PubMed1991

The role of fibroblasts in organization and degradation of a fibrin clot.

Older clots become less sensitive to fibrin degradation than newly formed ones. A possible role for fibroblasts in this defective thrombus lysis was studied. A system has been developed in which different clones of fibroblasts were incorporated into a floating whole blood clot. The effect of the incorporated fibroblasts on clot lysis has been analyzed in relation to their basic characteristics: clot retraction, production of plasminogen activators (PAs) and their inhibitors (PAIs), and secretion of collagen. In neoplastic fibroblast-enriched clots, secretion of PA was associated with spontaneous lysis of a whole blood clot. Normal fibroblasts, secreting levels of PA and PAI similar to those of the cancer cells, did not induce spontaneous lysis of the clot. Moreover, these cells protected whole blood clot from thrombolysis by added PA. Our data show that the resistance to fibrin clot degradation induced by normal fibroblasts was mainly mediated by collagen secretion and deposition rather than PAI secretion or retraction of the clot. We suggest a key role for normal fibroblasts in the acquisition of resistance to proteolytic fibrin degradation of whole blood clots through the secretion of collagen.

Collagen↗
PubMed1990

Degradation of fibrinogen by tissue plasminogen activator. Consequences for fibrin polymerization.

In patients treated with tissue plasminogen activator (t-PA), there was a marked increase in concentration of fibrinopeptide A (fpA). The purpose of this study was to analyse the activation of coagulation in plasma treated in vitro by pharmacological doses of t-PA. From our results, it appears that fpA release due to direct interaction of fibrinogen with t-PA, in the absence of plasminogen, is very low and not observed with pharmacological doses of t-PA. In contrast in the presence of plasminogen, the release of fpA is much higher and induces fibrin formation concomitantly to fibrinogen degradation.

Biopolymers↗
PubMed1990

Vegetating iododerma with underlying systemic diseases: report of three cases.

Three patients with vegetating iododerma as a result of potassium iodide therapy are presented. The first patient had polyarteritis nodosa, the second had monoclonal gammopathy of undertermined significance, and the third had multiple myeloma. Vegetating iododerma probably represents an idiosyncratic response to iodides; patients with polyarteritis nodosa and paraproteinemias may be predisposed.

Aged↗
PubMed1990

Neutrophilic eccrine hidradenitis in two neutropenic patients.

Neutrophilic eccrine hidradenitis is an uncommon, self-limited dermatosis with a variable clinical presentation. It seems to be due to chemotherapeutic drugs in most cases. Necrosis of the eccrine gland associated with a neutrophilic infiltrate is the histologic hallmark of this disease. We report two additional cases in neutropenic patients with acute myelogenous leukemia in which there was a striking lack of neutrophil infiltration. A new term, drug-associated eccrine hidradenitis, is suggested.

Adolescent↗
PubMed1990

Evolutionary stability of fibrinogen epitopes implicated in fibrin polymerization and in fibrinolysis.

In this work, fibrinogen evolution was analysed by testing the reactivity of fibrinogen from different species with monoclonal antibodies against human fibrinogen fragment D. One epitope concerning the fibrin polymerization site 'a' and two epitopes responsible for tPA binding to fibrin were conserved in all mammalian fibrogens tested but not in crab coagulogen or pleurodella fibrinogen. In these two species, some epitopes which are not implicated in fibrinogen function were conserved. Therefore, we can conclude that polymerizing site 'a' and tPA binding sites have not been modified for at least 80 million years.

Animals↗
PubMed1990

Fibrin degradation products generation and fibrinopeptide A release in normal plasma incubated with thrombolytic agents: proposed mechanisms.

Clinical data have shown that the evaluation of fibrin degradation products (FbDP) does not reflect the efficiency of thrombolytic therapy in vivo. In this study, we found that the addition of plasminogen activators to normal plasma resulted in generation of FbDP and release of fibrinopeptide A (FpA) as shown by ELISA and HPLC. This FpA release was concomitant with fibrinogen degradation, and was not inhibited by thrombin inhibition or by prothrombin depletion in plasma. Thus, the increase in FpA did not result from coagulation activation and may result from the plasmin-induced release of FpA from fibrinogen degradation product E1. The generation of cross-linked FbDP after tPA addition occurred in normal plasma as well as in factor-XIII-deficient plasma and quickly reached a plateau. It was not inhibited by hirudin. Therefore FbDP in these plasmas probably derived from the plasmin degradation of cellular transglutaminase cross-linked fibrin/fibrinogen derivatives present in plasma.

Aprotinin↗