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Contemp Top Lab Anim Sci. 1999 Sep;38(5):47-49.
Epidermotropic Lymphoma (Mycosis Fungoides) in an ICR Mouse.

Lohmiller JJ, Swing SP, Valli VE, Li X.

Department of Pathology and Committee on Comparative Medicine and Pathology, University of Chicago, Chicago, IL 60637.

A case of epidermotropic lymphoma with systemic spread into lymph nodes and visceral organs was observed in a 7- to 8-month-old, female ICR mouse. The mouse developed progressive and generalized alopecia and lymphadenopathy of several weeks' duration. The affected skin was markedly and diffusely thickened, with multiple serous to hemorrhagic crusts, ulcerated plaques, and raised nodules. Microscopically, random and/or perivascular infiltration of pleomorphic lymphoid cells was present in the skin, lymph nodes, thymus, spleen, lungs, and liver. On cytologic examination, the lymphoid cells were similar in all affected tissues, and had hyperchromatic and irregularly oval, cleaved, and occasionally convoluted nuclei, approximately 6 to 9 mm in diameter. On immunohistochemical examination, most infiltrating cells were labeled with anti-CD3 (panT cell) antibody. A smaller proportion of the cells (, 5%) were labeled with anti-CD79a (panB cell) antibody.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12086417&dopt=Abstract [PubMed - as supplied by publisher]

J Dermatol Sci. 2002 Aug;29(2):85-90.
Antioxidant enzymes and lipid peroxidation in the scalp of patients with alopecia areata.

Akar A, Arca E, Erbil H, Akay C, Sayal A, Gur AR.

Department of Dermatology, GATA School of Medicine, 06018, Ankara, Turkey. aakaata.edu.tr

Alopecia areata (AA) is an autoimmune inflammatory disease. However, little is known about the alterations in lipid peroxidation and antioxidant enzymes in the scalp of patients with AA. Therefore, the aim of this study was to investigate the status of oxidative stress in the scalp of patients with AA. We measured the levels of thiobarbituric acid reactive substances (TBARS) as lipid peroxidation status, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as antioxidant enzymes in the scalp of ten patients with AA and ten control subjects. The levels of TBARS in scalp of patients with AA (3654.1+/-621.2 nmol/g tissue) were significantly higher than those of controls (1210.2+/-188.8 nmol/g tissue) (P=0.002). The levels of SOD (134.8+/-23.8 U/g tissue) and GSH-Px (332.7+/-66.2 U/g tissue) in scalp of patients with AA were also significantly higher than those of controls (63.2+/-8.8 U/g tissue, 112.0+/-18.4 U/g tissue, respectively) (P=0.019, P=0.002, respectively). The mean levels of TBARS, SOD and GSH-Px in early phase of disease were increased 2-fold as compared with late phase of the disease. These results indicate that oxidative status is affected in AA. Lipid peroxidation and antioxidant enzymes may be involved in the pathogenesis of AA. Furthermore, we found high SOD and GSH-Px activities in the scalp of patient with AA. These high levels could not protect the patients against the reactive oxygen species, because lipid peroxidation could not be lowered in AA patients.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12088608&dopt=Abstract

Mol Endocrinol. 2002 Jul;16(7):1524-37.
Deletion of deoxyribonucleic acid binding domain of the vitamin D receptor abrogates genomic and nongenomic functions of vitamin D.

Erben RG, Soegiarto DW, Weber K, Zeitz U, Lieberherr M, Gniadecki R, Moller G, Adamski J, Balling R.

Institute of Animal Physiology, Ludwig Maximilians University, 80539 Munich, Germany. r.erberz.uni-muenchen.de

The vitamin D hormone 1,25-dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)], the biologically active form of vitamin D, is essential for an intact mineral metabolism. Using gene targeting, we sought to generate vitamin D receptor (VDR) null mutant mice carrying the reporter gene lacZ driven by the endogenous VDR promoter. Here we show that our gene-targeted mutant mice express a VDR with an intact hormone binding domain, but lacking the first zinc finger necessary for DNA binding. Expression of the lacZ reporter gene was widely distributed during embryogenesis and postnatally. Strong lacZ expression was found in bones, cartilage, intestine, kidney, skin, brain, heart, and parathyroid glands. Homozygous mice are a phenocopy of mice totally lacking the VDR protein and showed growth retardation, rickets, secondary hyperparathyroidism, and alopecia. Feeding of a diet high in calcium, phosphorus, and lactose normalized blood calcium and serum PTH levels, but revealed a profound renal calcium leak in normocalcemic homozygous mutants. When mice were treated with pharmacological doses of vitamin D metabolites, responses in skin, bone, intestine, parathyroid glands, and kidney were absent in homozygous mice, indicating that the mutant receptor is nonfunctioning and that vitamin D signaling pathways other than those mediated through the classical nuclear receptor are of minor physiological importance. Furthermore, rapid, nongenomic responses to 1,25-(OH)(2)D(3) in osteoblasts were abrogated in homozygous mice, supporting the conclusion that the classical VDR mediates the nongenomic actions of 1,25-(OH)(2)D(3).

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12089348&dopt=Abstract

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