Biomedical subjects
Publications and source records attributed to L E Levine.
Ultra-small-angle X-ray scattering data were obtained from deformed single-crystal aluminium samples. These data are consistent with recent theoretical predictions of scattering from dislocation walls, allowing quantitative microstructural parameters to be extracted.
Extensive simulations of a strain percolation model for a deforming metal have been performed to examine its strain behavior. We find that the total strain exhibits critical power-law behavior that is well explained by two-dimensional percolation theory. Near the critical point, most of the strained cells organize themselves around a state having the minimum or at least marginally stable strain regardless of the initial conditions. A strain much greater than the minimum stable strain generally decays to a lower value when transmitted to an unstrained cell. The universal behavior of the total strain in the system is a consequence of the self-organizing character of the strain in the critical cluster. Although the probability distributions for the total strain and cluster size appear to exhibit nonuniversal behavior, this may merely represent a transient response before crossover to a true asymptotic, universal behavior occurs. Other critical aspects of the model are also discussed.
A distinctive acral erythema developed in four patients with myelogenous leukemia, subsequent to blood transfusions and intensive chemotherapy with cytarabine. The clinical and histopathologic features of the eruption were suggestive of a drug-induced toxic eruption. To our knowledge, only one previous similar case has been reported in the literature. For patients in whom this self-limited condition develops, reassurance should serve as the mainstay of therapy.
Diabetics may have an increased susceptibility to cutaneous blister formation clinically manifest as the bullous eruption of diabetes. We evaluated the mechanical force necessary to induce suction blisters in fifteen insulin-dependent diabetics and twenty age-matched normal controls. The mean suction blister threshold for the diabetics was 31.9 minutes versus 68.0 minutes for the controls, a highly significant difference (p less than 0.01). Histologic appearance of suction blisters was similar in diabetic and normal skin, under both light and electron microscopic examination, with a noninflammatory subepidermal separation in the lamina lucida between the cell membrane and the basal lamina. These results demonstrate that insulin-dependent diabetics have a marked reduction in suction blister threshold as compared to age-matched controls.
The association of acanthosis nigricans with pituitary tumors and insulin-resistant diabetes suggests that a pituitary peptide may promote papillomatosis and acanthosis characteristic of acanthosis nigricans. Although such a peptide has not been isolated, it may derive by sequential cleavage from the 31,000-dalton precursor peptide to ACTH and beta-lipotropin (beta-LPH). In order to evaluate the role of pituitary peptides in the pathogenesis of acanthosis nigricans, we compared plasma levels of beta-endorphin (beta-EP) and ACTH in plasma of 8 fasting patients with obesity-associated benign acanthosis nigricans and 7 fasting normal controls utilizing sensitive radioimmunoassay procedures. Mean plasma beta-EP levels for the acanthosis nigricans and control subjects were not significantly different (90 pg/ml vs. 140 pg/ml), nor was any significant difference observed between plasma ACTH levels of the 2 groups (42.3 and 31.2 pg/ml, respectively.) Our data indicate that plasma levels of the pituitary-derived peptides ACTH and beta-EP are not increased in obesity-associated benign acanthosis nigricans, and suggest that its proposed hormonal mediator might originate independently from the large peptide precursor of ACTH, beta-LPH and their fragments.
Skin necrosis is a rare complication of heparin administration that is usually localized to injection sites. A 32-year-old insulin-dependent diabetic patient, receiving intravenous (IV) and low-dose heparin sodium therapy, had cutaneous necrosis in areas distant to the sites of injection. Prior to the onset of cutaneous lesions, thrombocytopenia develop]ed in the patient that may have been heparin induced. Heparin may induce the production of platelet aggregating immunoglobulins that predispose persons who are sensitive to the drug to thrombocytopenia, skin necrosis, and thrombotic events. Obesity, diabetes, and treatment with broad-spectrum antibiotics seem to increase the risk of such complications. Cutaneous necrosis secondary to heparin administration may serve as a warning of the potentially lethal complications of IV use. In patients in whom skin necrosis or thrombocytopenia develops, heparin therapy should be discontinued and anticoagulation with an oral agent should be considered.
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