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C Pons

Publications and source records attributed to C Pons.

42 records · Page 3Linked to original sources

[A morbidity information system based on school absenteeism].

We present a pilot experience about the introduction of a information system designed for the knowledge of infant morbidity (4-15 years) in a 13 school week period in a representative sample of 60 schools of the Valencian Community. We studied school absences that lasted three days or longer. Reports of teachers and parents were the source of information (100% response rate). Medical certification was also requested to the pediatricians and general practitioners of the area of the schools (12.74% response rate). To test the validity of this information system, absences caused by hepatitis were compared with the registry of Notifiable Diseases System (NDS) for the same period. We recorded 3,968 absences, with a cumulative incidence of 100.68 per 1,000 (C.I., alpha = .05, +/- 4.97) for females, and 119.4 (C.I., alpha = .05, +/- 18.36) for males. These differences were statistically significant. There was a concordance of 80.25% of the hepatitis cases between the registry of absenteeism and that of the NDS (chi 2 goodness of fit test = 3.16, p = .754). Although absences shorter than 3 days were not taken into account, the information system provided relevant and valid estimates of morbidity. Moreover, collaboration of teachers was considered very positive, which led us to use this health information system in five health areas of the Valencian Community.

Absenteeism↗

Burden of myocardial damage in cardiac allograft rejection: scintigraphic evidence of myocardial injury and histologic evidence of myocyte necrosis and apoptosis.

BACKGROUND: Because myocardial damage determines morbidity and outcomes in heart transplant rejection, assessment of total burden of myocardial damage is highly desirable. In addition to myocyte necrosis, programmed cell death, or apoptosis, has recently been shown to contribute to cardiac allograft rejection. In the present study, we noninvasively determined myocardial damage by antimyosin scintigraphy and compared it with necrotic and apoptotic myocardial damage in endomyocardial biopsy (EMB) specimens. METHODS AND RESULTS: Forty scintigraphic and histologic studies were simultaneously performed. Of these, 19 patients had no EMB evidence of allograft rejection (group I, International Society of Heart and Lung Transplantation [ISHLT] grade 0/4), 12 had mild rejection (group II, ISHLT grades 1A and 1B), and 9 had evidence of moderate allograft rejection (group III, ISHLT grades 2, 3A, and 3B). None of the biopsies demonstrated severe allograft rejection (ISHLT grade 4/4). The severity of global myocyte damage in 40 patients was assessed by antimyosin scintigraphy. Endomyocardial biopsies were performed in these patients within 48 hours of imaging study; biopsy specimens were characterized for presence of myocyte necrosis and apoptosis. Evidence of myocyte necrosis was observed in 9 (23%) of 40 EMB specimens. Nineteen EMB specimens of group I had no inflammation and no myocyte necrosis, 12 of group II specimens showed interstitial mononuclear cell infiltration (only) but no myocyte necrosis, and all 9 of group III specimens had evidence of cellular infiltration and myocyte damage. Myocyte necrosis was assessed by hematoxylin-eosin and trichrome staining of EMB specimens. On the other hand, apoptosis of myocytes, as assessed by TUNEL staining of DNA fragments, was seen in 22 (55%) of the 40 biopsy specimens: 47%, 58%, and 67% in groups I, II and III, respectively. Abnormal antimyosin scan findings, indicating presence of myocardial damage, were observed in 9 of the 19 patients in group I and in all patients in groups II and III. Although positive antimyosin scan results in group III patients are concordant with the presence of histologic myocardial necrosis, myocardial uptake of antimyosin antibodies in groups I and II (no apparent myocyte damage at light microscopic examination) could reflect either sampling error of the biopsy or ongoing apoptotic myocyte damage. CONCLUSIONS: Apoptosis of myocytes is frequently observed during cardiac allograft rejection. The presence of apoptotic myocytes in the absence of histologic rejection activity in patients with antimyosin uptake suggests that apoptosis could be an additional mechanism of transplant-associated myocardial damage.

Adult↗

Effects of Ginkgo biloba extract (EGb 761) on arteriolar spasm in a rat cremaster muscle preparation.

The effects of an extract of Ginkgo biloba (EGb 761) on arteriolar spasm were confirmed using a preparation of rat cremaster muscle. When vasospasm was induced by rat serum, arteriolar constriction reached 25-30% of the initial diameter after 10 min. Intravenous injection of EGb 761 (30 mg/kg) 5 min after inducing spasm inhibited about 80% of this serum-induced vasoconstriction. As previous studies have shown that EGb 761 has an antiaggregatory effect on platelets, thrombin, serotonin (platelet-derived compounds that are present in the serum) and a thromboxane analogue (U46619) were also used to induce vasospasm. Administration of EGb 761 (30 mg/kg) 5 min after exposure of the preparation to serotonin (10(-3) M) or 10 min after exposure to thrombin (20 units) did not affect vasospasm induced by these agents. In contrast, treatment with this same dose of EGb 761 5 min after exposure of the preparation to U46619 (10(-4) M) abolished the arteriolar constriction induced by this agent in 15 min. The thromboxane/prostaglandin H2 receptor antagonist SQ29548 antagonized serum-induced vasospasm, indicating an involvement of thromboxane. Other experiments indicated that the effects of EGb 761 of counteracting vasospasm may be mediated in part by ginkgolide B, a triterpene constituent of the extract that is an antagonist of platelet-activating factor and in part by an 'NO-like' action of its proanthocyanidin constituents. Taken together, these results have revealed that EGb 761 treatment can antagonize the vasoconstrictor effect of thromboxane on arterioles. As thromboxane is implicated in many cardiovascular disorders, this property of EGb 761 may explain some of its beneficial clinical effects in such pathologies.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Effect of Ginkgo biloba extract (EGb 761) on the vasospastic response of mouse cutaneous arterioles to platelet activation.

The effect of intravenously administered Ginkbo biloba extract (EGb 761) on the vasospastic response to platelet activation has been assessed using a cutaneous flap preparation in anaesthetized mice. Arterioles of the axillary artery were observed by intravital microscopy, and platelets were activated by topical application of ADP under two steady state conditions: normothermia (37 degrees C) and hypothermia (24 degrees C). Responses of the cutaneous arterioles to stimulation by topical application of a thromboxane agonist (U46619) were also compared in animals treated intravenously with EGb 761 or with a thromboxane synthesis inhibitor (U63557). ADP induced a 34% constriction of the arterioles in control animals. However, no arteriolar constriction occurred in response to ADP in platelet-depleted animals (collagen-induced thrombocytopenia) or in animals treated with EGb 761 (60 mg/kg, i.v.). Exposure of the arterioles to hypothermia (24 degrees C) for 10 min induced constriction of 7-12% in all experimental groups of animals. Under these hypothermic conditions, either EGb 761 or thrombocytopenia abolished ADP-induced arteriolar constriction which was substituted by arteriolar dilation, indicating that EGb 761 can inhibit the vasospasm that is produced by platelet activation. As topically applied U46619 (10(-5) M) induced arterioles constriction (about 22%) that was abolished by intravenous treatment with EGb 761, the extract appears to act directly rather than as a thromboxane synthase inhibitor. Collectively, these findings indicate that platelet factors can play a significant role in cutaneous vasospasm, and that EGb 761, via an action on the thromboxane pathway, could be useful in treating Raynaud's phenomenon and other vascular disorders which involve increased thromboxane production.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗