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F D Malkinson

Publications and source records attributed to F D Malkinson.

11 recordsLinked to original sources

Subcutaneous or topical administration of 16,16 dimethyl prostaglandin E2 protects from radiation-induced alopecia in mice.

Alopecia, a common sequel of radiation treatment of brain tumors, increases patient stress to the extent that refusal of treatment may occur. The expectation that loss of hair will be prevented, or that regrowth will occur, is extremely important to patients. To investigate prostaglandin-induced radiation protection against alopecia, the hair of B6D2F1 male mice was plucked from the right thigh and surrounding area to induce anagen. Fourteen days later, mice were injected subcutaneously in the neck with 10 micrograms 16,16 dm PGE2 in 0.2 ml of vehicle, or with the vehicle alone. In another group of previously plucked mice, 16,16 dm PGE2 in the same concentration, or the vehicle was applied topically. One hour later, graded single doses from 6.5 to 12.5 Gy 137Cs gamma irradiation were given to groups of six animals. On day 21 post-plucking, all animals were killed and a portion of the irradiated site was excised. The average hair counts per field in irradiated animals were 85 +/- 4 (6.5 Gy), 25 +/- 5 (8.5 Gy), and 5.5 +/- 0.7 (10 Gy). Animals receiving the prostaglandin systemically had values of 60 +/- 10 (6.5 Gy), 54 +/- 3 (8.5 Gy), 66 +/- 6 (10 Gy), and 30.1 +/- 8 (12.5 Gy). Topical application of the prostaglandin resulted in protection that yielded 52 +/- 3 (8.5 Gy), 34 +/- 4 (10 Gy), and 3.2 +/- 0.9 (12.5 Gy) hairs per field. Both systemic and topical application of 16,16 dm PGE2 protected from some degree of radiation-induced alopecia, which supports the conclusion that prostaglandins may be useful in the protection of hair follicles in patients treated with radiation for brain tumors.

16,16-Dimethylprostaglandin E2

Topical or systemic 16, 16 dm prostaglandin E2 or WR-2721 (WR-1065) protects mice from alopecia after fractionated irradiation.

Our previous studies in mice demonstrated that systemic or topical 16,16 dm PGE2 protected against single dose radiation-induced hair loss. We have now investigated prostaglandin, or WR-2721, protection against murine alopecia produced by varying doses and schedules of fractionated radiation. On days one to eight after hair was plucked from the thighs of B6D2F1 mice, groups of 6 animals each were given daily exposures of 4.0 or 4.5 Gy for 5 days; 2.5, 3.5, 4.5 or 5.5 Gy for 10 days; or 2 Gy for 15 days. One hour before irradiation each mouse received 10 microgram 16,16 dm PGE2, either by subcutaneous injection into the neck or topical application, 8 mg WR-2721 by injection, or 0.3 mg WR-1065 by topical application. Three weeks later counts of regrowing hairs were recorded from excised skin samples. For the radioprotectors used, hair regrowth was increased 25-100% in the various radiation groups in comparison to irradiated-only control sites. In some studies with the radioprotector given systemically, WR-2721 afforded slightly greater radioprotection than 16,16 dm PGE2. The two compounds were essentially equally radioprotective in the topical application studies. Since both systemic and topical applications of the agents tested enhanced hair regrowth following radiation, we conclude that clinical use of these compounds may provide some protection of hair follicles, and perhaps other tissues, lying within a radiation therapy field.

16,16-Dimethylprostaglandin E2

Effects of neutron radiation on mouse hair matrix cell populations.

We have investigated the effects of a single low dose of 42 rads neutron radiation on hair matrix cell kinetics. Anagen hair skin sites in 3-mo-old Carworth Farms no. 1 female mice were exposed to a fast neutron beam yielding a modal energy of 3.6 MeV. In contrast to low LET (linear energy transfer) radiation at a 2 1/2 fold higher dose, neutrons induced a markedly prolonged depression (greater than 60%) in the mitotic index for more than 18 hr postradiation. In addition, from 10--18 hr after neutron irradiation sharp elevations (greater than 80%) in the labeling indices apparently reflected significant impairment in cell maturation rates and/or slowed exit rates from the proliferative compartments. Postradiation reductions of up to 20% in the size of proliferating matrix cell populations were found. At the cellular level, this study confirms previous findings of a disproportionately high relative biological effectiveness for neutron radiation following low dose level exposure.

Animals

Dapsone-induced peripheral neuropathy.

Peripheral neuropathy is a rare complication of dapsone therapy. This neuropathy appears primarily to be of the motor type, and recovery occurs on discontinuation of the drug therapy. The patient in this report developed a marked motor deficit as well as a selective marked loss of vibration sense shortly after the initiation of a relatively low dose of dapsone. Recovery was rapid on cessation of the therapy. This patient was found to be a slow acetylator of isoniazid, and therefore is probably a slow acetylator of dapsone. The possible mechanisms of the neurotoxicity of dapsone and the role of altered metabolism are discussed.

Acne Vulgaris

Herpesvirus hominis hepatitis and disseminated intravascular coagulation. Occurrence in an adult with pemphigus vulgaris.

Herpesvirus hominis (HVH) hepatitis, a rarely recognized manifestation of HVH infection in adults, occurred in a 36-year-old woman who had received prednisone therapy for pemphigus vulgaris continuously for seven years. After an acute terminal illness that was characterized by fulminant hepatic failure and disseminated intravascular coagulation (DIC), postmortem examination disclosed massive hepatic necrosis. Herpesvirus hominis (type 1) was isolated from the liver. The association of disseminated HVH infection with impaired immunologic defenses, as well as the occurrence of DIC in association with acute hepatic failure, are discussed. Greater awareness of the clinical manifestations of HVH hepatitis should lead to early diagnosis, although sucessful modes of therapy await development.

Adolescent

Staphylococcal scalded skin syndrome in an adult and a child.

Two patients had staphylococcal scalded skin syndrome (SSSS) with typical clinical and histopathologic findings. In both cases, the disease was reproduced by injections of staphylococci into mice. The adult patient, who had no other physical or laboratory abnormalities, showed intact humoral and cellular immunity; her uneventful clinical course was clearly different from the eight previously reported cases in adults. To our knowledge, the child represents the first case report of SSSS as a result of infection by a non-group 2 Staphylococcus.

Adult