(1) Single postganglionic neurones to hairy skin and hairless skin of the hindleg were investigated on spinal cord heating and spinal cord cooling in chloralose anesthetized cats.
(2) Lymphocyte blastogenesis in hairless descendants of Mexican hairless dogs was examined using the following mitogens: phytohemagglutinin (PHA-M), Concanavalin A (Con A), lipopolysaccharide (LPS) and pokeweed mitogen (PWM).
(3) In the second series of studies, GTN was administered topically to freshly excised, intact hairless mouse skin in conventional in vitro diffusion cells.
(4) Experimental data are presented for: (a) the flux of diflorasone diacetate through hairless mouse skin, (b) the percutaneous penetration profile of propylene glycol, (c) the effects of vehicle concentrations of polyoxypropylene 15 stearyl ether and propylene glycol on the percutaneous flux of diflorasone diacetate, (d) skin--vehicle partition coefficients of diflorasone diacetate, (e) the solubility profile of diflorasone diacetate as a function of solvent concentration, and (f) the alteration of the skin's resistance to the penetration of diflorasone diacetate due to propylene glycol.
(5) In this study, oral therapy with vitamin A or a synthetic analogue, etretinate, was tested for ability to protect hairless mice (Skh-hr1) from the development of skin tumours following exposure to broad-band light (280-700 nm) for 25 weeks.
(6) During the early part of the experiments, when the sink condition was maintained, FAH was the most effective for hairless mouse skin, whereas Azone showed the highest effect in the rat skin.
(7) Hairless mice were irradiated three times a week for 10 weeks with sunlamps (UVA and UVB) and the skin was examined using immunochemical and biochemical techniques.
(8) From the results of mating experiments, an autosomal dominant semi-lethal gene was considered to be responsible for the hairlessness accompanied by defective teeth in the dog.
(9) Albino hairless mice (Skh:HR-1) exposed chronically to suberythemal doses of ultraviolet (UV) radiation display visible and histological alterations in the skin.
(10) An abnormal hairless mouse epidermis was produced by three different methods: ultraviolet light irradiation, topical vitamin A acid and topical acetic acid.
(11) The carcinogenic effect of 3 commercially available ultraviolet A (UVA) tanning sources was studied in lightly pigmented hairless mice.
(12) ISDN permeation through excised hairless rat skin from the different devices was measured in vitro.
(13) If it is to be denuded and buried, however, great care must be taken to select a donor area that is as hairless as possible.
(14) There are two mechanisms for flux enhancement relative to passive flux on "fresh" hairless mouse skin: (1) the effect of the voltage in increasing mass transfer over the passive diffusion level, the effect of electroosmotic flow dominating this contribution in the systems studied in this report; and (2) the effect of prior current flow in increasing the "intrinsic permeability" of the skin.
(15) A comparison of the enhancing effect of 3% 1 on permeation of 2 through rat, hairless mouse, and human cadaver skin was made.
(16) Treatment of herpes simplex virus (HSV)-infected hairless mice with a 2% phosphonoacetic acid (PAA) ointment prevented the appearance of virus-induced skin lesions and subsequent central nervous system (CNS) involvement.
(17) Hairless albino mice were painted with 8-methoxypsoralen (8-MOP) and exposed to solar simulated radiation (SSR) for 0, 3 or 6 weeks and subsequently treated with the promoter 12-O-tetradecanoylphorbol-13-acetate (TPA).
(18) Dopa phosphates have been shown to increase pigment production in the epidermis of hairless mice.
(19) Chronic irradiation (three times a week) with ultraviolet B light of the skin of hairless mouse Uscd (Hr) strains resulted in the induction of skin tumors after 25 to 41 weeks.
(20) Several physiological parameters were measured in hairless mice maintained on a diet supplemented with antioxidants.