RESUMEN
Basal cell carcinoma (BCC) is the most common skin cancer, with an increasing incidence in Europe particularly in young individuals. Nodular basal cell carcinoma is the most common subtype and accounts for approximately 57.6-78.7% of all BCCs. We performed an observational, morphological study which involved 68 patients with the diagnosis of nodular BCC. The localization and diameter of the lesion, histological subtype of the lesion, dermoscopic patterns, Fitzpatrick skin type and sex of each patient were recorded. The most common dermoscopic pattern seen in nodular BCCs was irregular vascularity and, arborizing vessels (>0.2mm in diameter) being the most frequent irregular vascular pattern. The second most common dermoscopic feature in patients with nodular BCCs was translucency. The most common dermoscopic features of the 12 pigmented BCCs were: pigmented islands (blue-gray globules and blue-gray ovoid nests); the pigmented distribution pattern (with (maple leaf-like structures and spoke wheel-like areas); arborizing vessels and white streaks/white areas. The histopathological analysis of the 68 BCCs revealed that the nodular type was the most frequently identified for 71.7% of cases The differential diagnosis between basal cell carcinoma and other skin lesions and inflammatory skin diseases is very important, since serious morbidity may result from an undiagnosed tumor.
RESUMEN
Mitochondria-related oxidative stress is a pathomechanism causally linked to coronary heart disease (CHD) and diabetes mellitus (DM). Recently, mitochondrial monoamine oxidases (MAOs) have emerged as novel sources of oxidative stress in the cardiovascular system and experimental diabetes. The present study was purported to assess the mitochondrial impairment and the contribution of MAOs-related oxidative stress to the cardiovascular dysfunction in coronary patients with/without DM. Right atrial appendages were obtained from 75 patients randomized into 3 groups: (1) Control (CTRL), valvular patients without CHD; (2) CHD, patients with confirmed CHD; and (3) CHD-DM, patients with CHD and DM. Mitochondrial respiration was measured by high-resolution respirometry and MAOs expression was evaluated by RT-PCR and immunohistochemistry. Hydrogen peroxide (H2O2) emission was assessed by confocal microscopy and spectrophotometrically. The impairment of mitochondrial respiration was substrate-independent in CHD-DM group. MAOs expression was comparable among the groups, with the predominance of MAO-B isoform but no significant differences regarding oxidative stress were detected by either method. Incubation of atrial samples with MAOs inhibitors significantly reduced the H2O2 in all groups. In conclusion, abnormal mitochondrial respiration occurs in CHD and is more severe in DM and MAOs contribute to oxidative stress in human diseased hearts with/without DM.