Base pairing and replicative processing of the formamidopyrimidine-dG DNA lesion.

The 2,6-diamino-4-hydroxy-5-formamidopyrimidine of 2'-deoxyguanosine (FaPydG) is one of the major DNA lesions found after oxidative stress in cells. To clarify the base pairing and coding potential of this major DNA lesion with the aim to estimate its mutagenic effect, we prepared oligonucleotides containing a cyclopentane based analogue of the DNA lesion (cFaPydG). In addition, oligonucleotides containing the cyclopentane analogue of 2'-deoxyguanosine (cdG), and oligonucleotides containing 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) were synthesized.

Topical vitamin B12--a new therapeutic approach in atopic dermatitis-evaluation of efficacy and tolerability in a randomized placebo-controlled multicentre clinical trial.

Background: Vitamin B(12) is an effective scavenger of nitric oxide (NO). As the experimental application of a NO synthase inhibitor, N omega-nitro-L-arginine, led to a clear decrease in pruritus and erythema in atopic dermatitis, it would be reasonable to assume a comparable effect of vitamin B(12).

Objectives: The efficacy and tolerability of a new vitamin B(12) cream as a possible alternative to current therapies was examined.

Mechanisms of apoptosis: UVA1-induced immediate and UVB-induced delayed apoptosis in human T cells in vitro.

Objective: The decreased number of lymphocytes combined with the induction of apoptosis and necrosis seems to be the key mechanism of many phototherapeutic agents. The purpose of our study was to determine the regulating pathway, time course and dose dependence of UVA1- vs. UVB-induced cell death in human T lymphocytes.

Mononuclear cells in atopic dermatitis in vivo: immunomodulation of the cutaneous infiltrate by medium-dose UVA1 phototherapy.

Introduction: Recently, medium-dose UVA1 phototherapy (50 J/cm2) has achieved great therapeutic success within the treatment of severe atopic dermatitis (AD). Histologically, AD is recognised by a pathological perivascular dermal infiltrate including T lymphocytes, eosinophils and Langerhans cells. The purpose of our study was to investigate the extent to which UVA1 irradiation is able to modulate the mononuclear dermal inflammatory infiltrate using different monoclonal antibodies.