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Increased levels of the gliofibrillar S100b protein can be detected during carotid endarterectomy (CEA). Whether the S100b protein increase is marker of brain ischemic sufferance and predictor of cognitive decline is controversial. Twenty-eight patients underwent clinical assessment and cranial computed tomography (CT) 24-48 hours before and 3 months after CEA. S100b serum levels were evaluated before surgery, at cross-clamping, 10 minutes later, at declamping, and 24-48 hours and 10-12 weeks after CEA. Increased S100b levels were detected in 11 patients (39%); eight (73%) of these patients had symptomatic carotid artery disease. Increased S100b level correlated with history of TIA or stroke ( p=0.005), low mini-mental state examination score ( p=0.02), and ischemic infarctions at preoperative CT ( p=0.03). Slight and transient increased S100b levels were detected in 39% of patients during CEA. The protein levels increased despite the absence of clinical events during surgery. Our findings suggest a failure of compensatory hemodynamic or metabolic mechanisms in peri-ischemic tissue, whose longterm effects on cognition remain to be investigated.

Sarcoidosis is a chronic systemic disease, characterized by an imbalance of immunity processes and the presence of granuloma. Endothelin-1, a new vasoactive and bronchoconstrictive peptide, is a powerful mitogen for smooth muscle cells and fibroblasts and plays a role in the inflammation state. We postulate that endothelin-1 has a role in sarcoidosis.We studied the behaviour of circulating levels of endothelin-1 in 20 patients with sarcoidosis and its correlation with some biochemical parameters of activity disease, such as erythrocyte sedimentation rate (ESR) and serum angiotensin-converting enzyme (SACE). We measured serum levels of ESR, SACE, calcium and plasma endothelin-1 levels in all patients at the beginning of the study and one again in 9 patients with clinical-biochemical remission of disease after steroid treatment.In patients with sarcoidosis, circulating levels of endothelin-1, SACE and ESR were significantly higher (p0.001) than those of healthy subjects. Moreover, in patients with pulmonary involvement, there was a significant statistical difference (p0.001) between endothelin-1 levels and radiological stage compared to normal subjects. In the 9 patients with remission of disease, both endothelin-1 levels and parameters of activity disease normalized.Our results seem to suggest that the increase of plasma endothelin-1 levels in active sarcoidosis can represent an expression of the endothelial dysfunction and reflect the picture of cellular activation.

PSA has been measured out with highly sensitive method both in liquid of mammary cysts and in cytosol of neoplastic cells. Our data point out that dysplastic, metaplastic and anaplastic breast epithelial cells produce PSA. Such production is, probably, related to expression of hormonal receptors.

Ca 125 was assayed in serum and in breast cyst fluid of 78 patients with GCD. Levels of the marker in cyst fluid are generally30 U/ml. More significative results were found in relation to cysts relapse. In apocrine cysts relapse levels were higher than 270 U/ml, in serum cysts not relapsed levels were between 31-270 U/ml. Ca 125 could have a significative role in cell differentiation and its control.

The present study was carried out on 152 patients divided into three groups: A) 73 underwent radical surgery for breast carcinoma without signs of metastases; B) 31 patients with radiologic and scintigraphic evidence of bone metastases originating from malignant mammary neoplasia (14 with only one and 17 with two or more localizations); C) 48 affected by simple mammary cysts. No patients had a previous history of primary or secondary bone pathologies or renal, hepatic or endocrine ones. Besides this, no patient took drugs influencing the metabolic turnover of the bony tissue in the three months preceding the study. After surgery all patients underwent standard clinical and laboratory follow-up, the latter including, every 3 months, the evaluation of serum CA 15.3, CA 27.29 MCA, and ostase. The ostase cut-off, obtained by the statistical elaboration of the serum values of the 48 patients with benign mammary cysts and the 73 disease free patients, was 17 microg./L. The mean concentration in the three groups and two subgroups was: 13.76 microg./L (patients without metastases), 31.84 (patients with metastases), 18.4 (limited bony metastases), 40.04 (diffused bony metastases) and 5.36 (mammary cists). The diagnostic sensitivity of ostase proved superior to that of CA 15.3 (84% vs 75%) except when considering the subgroup with limited metastases (71.4% vs 72.7%), while the specificity was similar (around 78%). CA 27.29 and MCA were not useful as markers of metastasis. In a longitudinal-perspective study it was possible periodically to test these markers in 13 patients, at first, disease free and then with signs of bone progression evidence by skeletal scintigraphy. In 11 of these patients ostase and CA 15.3 showed increased values, an average 136 and 131 days respectively, before instrumental evidence of progression. None of the 13 patients, at the time of bone progression diagnosis, showed clinical, laboratory or instrumental signs of disease in other organs. The precocity of the serum increase of ostase could have a triple role: 1) accomplishment of a closer follow-up in patients at "high risk" of bone disease; 2) aid in the interpretation "in a neoplastic sense" of an "uncertain image of hypercaptation"; 3) accomplishment of a supporting or specific oncology treatment at an earlier stage which may be of some advantage as regards quality of life.

Ca 15-3 was assayed in serum and in breast cysts fluid of 78 non neoplastic patients presenting Gross Cysts (GCD). In apocrine cysts and in the mixed type (serous and apocrine, class III) relapse was indicated by high serum and intracystic levels of the marker. Ca 15-3, therefore, may discriminate in a group of cysts a higher cellular resistance as well as an increased cell proliferation. Results suggest an important role of the marker in the follow up of patients with GCD and for the early detection of cyst relapse.