Pediatric cutaneous malignant fibrous histiocytoma.

Malignant fibrous histiocytoma (MFH) is an aggressive soft-tissue sarcoma that most commonly occurs in the skeletal muscle of the extremities or retroperitoneum of adults. Although the majority of MFH is located beneath the fascia, the tumor occasionally occurs in the subcutaneous tissue. MFH rarely occurs in children and the disease course, prognosis, and outcome in younger patients has not been well described. We report a case of cutaneous MFH presenting on the thigh of a 12-year-old boy.

Photoageing: the role of UVB, solar-simulated UVB, visible and psoralen UVA radiation.

We have studied the morphological and histological effects of chronic exposure of two strains of haired mice (albino Balb/c and pigmented C3H-) to various types of radiation. UVB (280-320 nm) radiation from unfiltered sunlamp bulbs for 20 and 30 weeks produced marked epidermal acanthosis and dyskeratosis which was reversible in mice exposed for 20 weeks followed by a 20-week rest. In the dermis the elastic fibres were altered and in the pigmented mice these changes had almost completely reversed 29 weeks after cessation of exposure. Cellulose acetate-filtered sunlamp bulbs (greater than 289 nm) produced similar but less marked changes. Chronic exposure to UVA (320-400 nm) radiation produced minimal alterations in the dermis while the epidermis was normal. Visible (greater than 400 nm) radiation in large doses produced no degenerative changes. Methoxsalen/UVA radiation produced epidermal acanthosis, dermal sclerosis, and alteration of elastic fibres, which was prominent in both strains at 40 weeks. These findings suggest that the UVB component of sunlight is largely responsible for photoageing of the skin. Furthermore, chronic exposure to methoxsalen/UVA therapy is likely to potentiate solar-induced photoageing.

An acquired form of epidermolysis bullosa without immunoreactants. Report of a case.

A patient with a 10-year history of an acquired, scarring bullous eruption localized to the anterior surfaces of the lower extremities is described. Clinical, histologic, and electron microscopic features of an acquired form of epidermolysis bullosa are shown to occur in the absence of immune deposits, a finding not previously documented.

Galactosamine-induced cell death in primary cultures of rat hepatocytes.

Primary cultures of rat hepatocytes were exposed to 0.5 mM D-galactosamine. After 36 hours, only 10-20% of the original cells were viable, as assessed by trypan blue exclusion. In the absence of galactosamine, there was no loss of viability over this same period. The addition of 3 mM uridine to the culture medium completely prevented the cell death produced by galactosamine. Glucosamine had no effect on the viability of the hepatocytes. The extent of galactosamine-induced cell death was dependent upon the concentration of Ca++ ions in the culture medium. With the only source of Ca++ that added with the fetal calf serum, galactosamine had only a very slight effect on viability. With higher Ca++ than with the fetal calf serum, galactosamine had only a very slight effect on viability. With higher Ca++ concentrations, from 0.9 to 3.6 mM, the viability ranged from 75% to 31% 18 hours after treatment with galactosamine. The addition of 1.4 microM chlorpromazine to culture medium containing 1.8 mM Ca++ decreased the extent of the galactosamine-induced cell death. This protective effect was progressively reduced by raising the Ca++ concentration to 3.6 and 5.4 mM. Chlorpromazine given to intact rats 2 hours after treatment with 400 mg/kg galactosamine prevented the appearance of liver cell necrosis. At the same time, chlorpromazine prevented the increases in liver cell Ca++ content. These results indicate that many of the features of the effect of galactosamine on intact rat liver cells can be reproduced in primary cultures of these same cells. The data also support the hypothesis that a disturbance in intracellular Ca++ homeostasis leading to accumulations of these ions is causally related to the cell death produced by galactosamine.

Prevention by chlorpromazine of ischemic liver cell death.

Ischemic liver tissue was produced by clamping the portal venous and hepatic arterial blood supply to the left lateral and median lobes of rat liver. If, after 2 to 3 hours of ischemia, reflow to the liver was established by removing the clamp, two-thirds or more of the liver cells were histologically dead 24 hours later. Pretreatment with chlorpromazine (20 mg/kg) 30 minutes before inducing ischemia for up to 3 hours virtually completely prevented this ischemic cell death. If the animals were kept alive for an additional 24 hours with no further treatment, the extent of liver cell necrosis at 48 hours was still markedly less than that seen in the untreated ischemic controls. Administration of chlorpromazine after induction of ischemia and immediately prior to the onset of reflow reduced but did not completely prevent ischemic cell death as determined at 24 hours. This protective action of chlorpromazine was confirmed by the ability of the treated animals to regenerate cellular ATP levels after 3 hours of ischemia. In addition, chlorpromazine was shown to significantly reduce the increases in total liver cell and mitochondrial calcium ion contents that accompany the return of blood flow to irreversibly injured liver cells. The protective effect of chlorpromazine could not be attributed to any effect either on the rate or extent to which the liver cells became ischemic or on the perfusion patterns following release of the obstruction, and it is concluded that the action of chlorpromazine must be on some component(s) of the reaction of the cells to the ischemia itself. The possible basis of this action is discussed.