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Biomedical subjects

J Schmutz

Publications and source records attributed to J Schmutz.

27 records · Page 2Linked to original sources

Clinicopathologic effects of cancer chemotherapeutic agents on human buccal mucosa.

Specimens of buccal mucosa obtained at autopsy from 216 patients were examined for histopathologic alterations. Atrophic oral epithelium was found in thirty cases. A retrospective study of the hospital records revealed that thirteen of these latter patients had been on a cancer chemotherapeutic regimen prior to death. There was a significantly higher incidence of atrophy in the chemotherapy group (p less than 0.001) than in control patients. These findings, as well as the expected inherent susceptibility of rapidly replicating oral epithelial cells to metabolic inhibitors, suggest a causal relationship between oral atrophy and the administration of cancer chemotherapeutic agents. This atrophy may therefore represent a preliminary stage of mucosal alteration that ultimately progresses to the clinical sequelae of stomatitis and oral ulcerations frequently encountered during cancer chemotherapy. Some alternative mechanisms are also discussed.

Adult↗

Neuroleptic piperazinyl-dibenzo-azepines. Chemistry and structure-activity relationships.

The chemistry and the molecular and physicochemical properties of the 11-piperazinyl derivatives of dibenz[b,f][1,4]-oxazepines and -thiazepines and of dibenzo[b,e][1,4]diazepines as well as those of the 6-piperazinyl-morphanthridines are reviewed. The physicochemical parameters sigma, pK, eta, RM and surface pressure are considered in relation to each other and in relation to two pharmacological effects, namely apomorphine antagonism and cataleptic activities. The influence of substituents, bridging moiety and basic side chain on structure-activity are discussed. Finally, the dibenzodiazepine derivative clozapine, which differs markedly from the classical neuroleptics in its biochemical, pharmacological and clinical properties and represents a new type of antipsychotic agent, is discussed.

Animals↗

[Activated protein C resistance and cardiolipin antibodies in leg ulcers].

BACKGROUND: We conducted a prospective study to determine the prevalence of activated protein C resistance and anticardiolipin antibodies in leg ulcers, whatever venous, arterial or arteriovenous. PATIENTS AND METHODS: One hundred fifteen patients hospitalized for leg ulcers, without antiphospholipid syndrome were included. The vascular abnormalities were studied by clinical examination, Doppler, duplex Doppler and, when required, arteriography. Activated protein C resistance was isolated by a "classic" test (normalized APTT ratio in PCa presence or absence) and by a "second generation test" (by preliminary dilution with deficient factor V plasma). All patients with abnormal results on the second test were screened for the factor V Leiden (by PCR amplication with use of restriction enzymes). Anticardiolipin antibodies were investigated with an ELISA method with Harris standards as reference, in which the positive threshold was established at 20 units. RESULTS: Among these 115 patients, 50 venous (43.5 p. 100), 23 arterial (20 p. 100), 42 arteriovenous (36.5 p. 100) leg ulcers were identified. Activated protein C resistance was isolated in 12 cases (10.4 p. 100) (heterozygous carriers): 7 venous ulcers, 3 arteriovenous, 2 arterial. Anticardiolipin antibodies were measured at significant level in 49 cases (42.6 p. 100): 21 venous ulcers, 18 arteriovenous, 10 arterial. DISCUSSION: In this study, there was no statistical difference between the activated protein C resistance prevalence in leg ulcers when compared with Lorraine population (p=0.27). Factor V Leiden or anticardiolipin antibodies abnormalities were isolated in 56 cases (48.7 p. 100) without statistical difference between the 3 types of ulcers. Finally, the pathophysiology of venous, arterial and arteriovenous leg ulcers remains complex, suggesting several coagulation perturbations.

Activated Protein C Resistance↗

Should we or shouldn't we treat condensing osteitis with root canal therapy?

The intent of this article is to review with the dental clinician the literature concerning a lesion labeled condensing osteitis. A radiographic and histologic picture is presented along with etiology and diagnosis. A conclusion is drawn from the available literature to treat these lesions with endodontic therapy.

Humans↗