Wound healing after laser injury to skin--the effect of occlusion and vitamin E.

The skin of Yorkshire pigs was irradiated with various doses of argon and copper-vapor laser and evaluated for effects on healing time of pretreatment with topical or intramuscular vitamin E or the Op-Site wound dressing. Incident irradiance for both lasers was between 3.5 and 4.

Histologic changes in nude mouse skin and human skin xenografts following exposure to sulfhydryl reagents: arsenicals.

This report documents the histological changes in nude mouse skin and in human skin xenografts on nude mice following exposure to phenyldichloroarsine (PDA), a vesicant arsenical. Under light microscopy, we observed in PDA-treated human skin grafts: 1) degeneration of epidermal cell nuclei (apparent by 2 hr after exposure with increasing severity through 48 hr); 2) loss of epidermal cytoplasmic basophilia (apparent by 4 hr, maximal within 12 hr); 3) epidermal cytoplasmic vacuolization (vacuoles appeared within 4 hr and increased in size through 24 hr); 4) cleft formation within the basement membrane zone (apparent by 12 hr, increasing in severity through 24 hr); 5) inflammation evidenced by polymorphonuclear leukocyte (PMN) infiltration (apparent by 4 hr and increasing through 48 hr). The PMNs frequently formed a wall around the lesion, but did not infiltrate the treated area.

Electron microscopy of HeLa cells infected with adenoviruses.

HeLa cells were infected with adenoviruses (types 1-4) and sectioned for electron microscopy after intervals of 20 to 48 hours. Clusters of virus-like particles were found within the nuclei of infected cultures but not in those of uninfected controls. The particles were often arranged in rows as if in crystalline formation.

Globoid structures in the cytoplasm of rapidly growing HeLa cells.

During the course of electron microscopic study of rapidly growing uninfected HeLa cells, it was found that numerous globoid bodies occurred in the cytoplasm. Reasons are given for suspecting that these structures are mitochondria.