Present and previous studies suggest that the Wnt/beta-catenin/Tcf-Lef pathway is activated in normal matrix cells of the HF to induce differentiation to the hair shaft. Additionally, the beta-catenin mutation in matrix cells of the HF stabilizes beta-catenin protein, which translocates into the nucleus, where it activates of gene transcription together with lymphoid enhancer factor-1 producing pilomatrixoma. These mutations occur without an underlying defect in DNA mismatch repair.

Summary E-cadherin (E-CD) is a calcium-dependent cell-cell adhesion molecule which is expressed in almost all epithelial tissues. E-CD expression is involved in epidermal morphogenesis and is reduced during tumour progression of mouse epidermal carcinogenesis. It has been suggested that E-CD could play a role as an invasion-suppressor molecule. In the present work we have studied the E-CD expression in 31 patients with basal cell carcinoma (BCC) using an immunohistochemical technique with a monoclonal antibody (HECD-1) specific for human E-CD. E-CD expression was preserved in all specimens of superficial and nodular BCC, and was reduced in 10 of 15 infiltrative BCCs. A heterogeneous distribution of cells with different immunostaining intensity was more frequently observed in specimens of infiltrative BCC. These results suggest that E-CD might be related to the growth pattern and the local aggressive behaviour of BCC, and support the idea that E-CD might play a role as an invasion-suppressor molecule in vivo.

Diabetes mellitus by itself, is a frequent and increasing public health problem. The prevalence in most Western countries varies between 2 to 5% and it is rapidly increasing in Asiatic countries due to changes in dietary habits during the last years. The association between diabetes mellitus and hypertension has been described in 60 to 65% of diabetics. In hypertension we find insulin resistance mainly in skeletal muscle involving the conversion of glucose to glycogen independently of blood flow. The degree of resistance is related to the severity of hypertension and varies between races. States of

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Our results suggest that exposure to cigarette smoke increases NO synthesis, such that NO may act in a compensatory way as an inhibitor of lipid peroxidation. Smoking also activates other antioxidative mechanisms such as involving vitamin C. These protective mechanisms appear to be enough in preventing accumulation of oxidative products such as MDA and avoiding oxidative damage.

Summary P-cadherin (P-CD) and E-cadherin (E-CD) are expressed by keratinocytes and play an important role in skin morphogenesis. P-CD expression is restricted to the basal layer of normal epidermis, whereas E-CD is expressed in all the living layers. We have previously reported a reduced expression of E-CD in most cases of infiltrative basal cell carcinoma (BCC). In the present work we have investigated by immunohistochemistry the expression of both P-CD and E-CD in a new series of 32 patients with BCC. Most cases of superficial multicentric BCC and some nodular tumours had preserved expression of both cadherins in all tumour cells. The majority of nodular BCCs had partially reduced expression of one or both cadherins with an ordered distribution of cells showing different cadherin staining throughout the tumour mass. A severe reduction of E-CD expression with a disordered distribution of cells with different immunostaining intensity was observed in most specimens of infiltrative BCC. In contrast, P-CD expression was preserved in all cases of infiltrative BCC. These results suggest that P-CD and E-CD play different roles in the growth pattern of BCC. In addition, both anomalous P-CD expression and reduced E-CD expression were frequently observed in the spinous layer of epidermis overlying tumours. This phenomenon was significantly associated with the presence of keratinocytic atypia, which suggests that disturbed cadherin expression could be a marker of premalignant changes and/or hyperproliferative activity in human epidermis.

Serum levels of malondialdehyde increase, and serum levels of nitric oxide diminish within 24 hours after the onset of thrombotic stroke onset. This suggests that serum malondialdehyde level could be used as potentially reliable and sensitive marker for reperfusion, whereas nitric oxide levels could acts as potential biochemical sensor for nonreflow phenomenon.

Hypertension is a very common condition and the most important risk factor for the occurrence of cardiovascular events. The hyperactivity of the renin-angiotensin-aldosterone system is considered a cardiovascular risk factor in subjects with essential hypertension. The intrinsic vascular abnormality in which the renin-angiotensin-aldosterone system is clearly the milieu for the development of the pathologic changes in blood vessel walls is one of the causes of the establishment of hypertension. Many drugs with different mechanisms of action have been used for the treatment of hypertension and its vascular complications. Nevertheless, the utilities of many drugs are limited by their adverse effects. Continuous research in the search for new pharmacological agents for the treatment of hypertension has led to the development of angiotensin II receptor type AT1 blockers. The most important functions mediated by AT1 receptors include: vasoconstriction, induction of the production and release of aldosterone, renal reabsorption of sodium, cardiac cellular growth, proliferation of vascular smooth muscle, increase of peripheral noradrenergic action and the central activity of the sympathetic nervous system, stimulation of vasopressin release, and inhibition of renin release from the kidney. The angiotensin II receptor type AT1 blockers inhibit the interaction of angiotensin II with its AT1 receptor. These agents lower blood pressure without producing cough as a side effect since, unlike the angiotensin-converting enzyme inhibitors they do not influence the levels of bradykinin or substance P. Hence, these drugs are suitable for the treatment of hypertensive patients who require therapy with a drug blocking the effect of angiotensin-converting enzyme but cannot use angiotensin-converting enzyme inhibitors due to cough as a side effect.