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Biomedical subjects

I Virgolini

Publications and source records attributed to I Virgolini.

131 records · Page 8Linked to original sources
PubMed1988

Decrease of prostaglandin I2 binding sites in thyroid cancer.

The properties of specific prostaglandin I2 (prostacyclin, PGI2) binding sites in normal thyroid tissue have been characterised. Tissue samples obtained intraoperatively from patients with 'cold' solitary thyroid nodules (as preoperatively selected by thyroid gland scintigraphy, thyroid gland ultrasonography and Papanicolaou cytology following fine needle aspiration of the nodule area) have been used for thyroid membrane preparation. Employing [3H]iloprost, a chemically stable PGI2-analogue as a radioligand, saturation experiments for comparative binding studies have been attempted. Scatchard analysis of the binding data obtained for normal thyroid parenchyma distant to the nodule area revealed heterogeneity of the [3H]iloprost sites exhibiting a high-affinity binding capacity (Bmax) of 613.2 +/- 130.4 fmol mg-1 membrane protein and a low-affinity binding capacity of 5.1 +/- 1.6 pmol mg-1 membrane protein. The equilibrium dissociation constant (Kd) amounted to 18.9 +/- 8.9 nM and to 131.5 +/- 39.2 nM, respectively. Scatchard analysis of the binding data obtained for benign thyroid adenoma indicated significant lower binding capacities exhibiting a Bmax of 325.8 +/- 110.0 fmol mg-1 membrane protein (Kd: 31.0 +/- 7.5 nM) for the high-affinity sites and of 3.9 +/- 2.5 pmol mg-1 membrane protein (Kd: 364.9 +/- 183.6) for the low affinity sites. In cancer tissue a selective loss of the low affinity sites and a significant diminution of the high-affinity sites was observed: in well differentiated cancer the high-affinity sites showed a Bmax of 299.7 +/- 46.0 fmol mg-1 membrane protein (Kd: 38.9 +/- 7.3 nM), in anaplastic cancer, less differentiated papillar and follicular cancers of 180.6 +/- 25.1 fmol mg-1 membrane protein (Kd: 54.6 +/- 16.7 nM). Well differentiated papillar and follicular cancers did not differ from each other.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1988

Effects of exercise on parameters of blood coagulation, platelet function and the prostaglandin system.

Acute exercise causes a temporary short lasting activation of blood coagulation, platelet function and the prostaglandin system, the extent of these alterations being significantly less pronounced in well trained athletes than in untrained persons. The reversal is also much faster in athletes, thus providing an underestimated indicator of the individual training status. Changes in platelet function and some plasma parameters of coagulation exhibit a significant correlation to base excess, pH and lactate. Immediately after acute exercise there is, therefore, an increased risk for acute thrombosis if an additional risk such as doping and/or smoking and/or contraceptive pill use is present. This risk is again higher in untrained than in well exercised persons. Patients with clinically manifest atherosclerosis (predominantly with risk factors) performing only occasionally anaerobic exercise are more likely to be at special risk. The overall response of the coagulation system, platelet function and prostaglandin system is significantly impaired. In contrast, regular exercise causes decreased activity of platelets and the coagulation system resulting in an improvement in haemostatic balance. As well as the psychological factors beneficially influencing the subjective feeling, it seems rather likely that the above mentioned mechanisms may be one factor underlying the decreased death rate from cardiovascular disease in persons performing regular physical activity.

Blood Coagulation↗
PubMedDate not supplied

Serum levels of vasoactive intestinal peptide (VIP) in patients with adenocarcinomas of the gastrointestinal tract.

BACKGROUND: VIP acts as a neuroendocrine mediator under physiological conditions, with an important role in water and electrolyte secretion in the gut. Recent findings suggest that VIP also promotes growth and proliferation of normal as well as malignant cells. We have investigated the VIP-serum levels in patients with pancreatic cancer and colonic adenocarcinoma as compared to healthy controls. This was accompanied by immunohistochemical investigations and in vitro experiments to further define the role of the peptide in pancreatic and colorectal cancer. MATERIALS AND METHODS: Serum levels of VIP were evaluated under standardized conditions in a total of 135 patients; 45 patients had metastatic colorectal cancer, 45 suffered from metastatic pancreatic cancer, and 45 healthy volunteers served as controls. Human pancreatic and colorectal carcinoma cell lines were incubated over 5 days with VIP in increasing concentrations. RESULTS: In healthy controls, a median VIP-serum level of 42.44 +/- 2.540 pg/ml (range, 12.9-98.5 pg/ml) was found, while patients with pancreatic cancer had a median level of 40.58 +/- 3.013 pg/ml (range, 6.9-102.4 pg/ml). In patients with cancer originating in the colon, however, a median serum level of 116 +/- 10.14 pg/ml (range, 51.6-487 pg/ml) was found. While no difference between healthy controls and patients with pancreatic cancer could be detected (p = 0.6381), a significant difference between patients with colorectal cancer and healthy controls (p < 0.0001) and patients with pancreatic cancer (p < 0.0001) was demonstrated. The median VIP-concentrations found in the patients sera for pancreatic and colonic tumor patient groups, 40 pg/ml and 115 pg/ml respectively, had no significant effect on the proliferation of PANC-1 and HT29, inhibited ASPC-1, BxPC3, COLO201 and HCT-15 cells, and stimulated the growth of one pancreatic (CAPAN-1) and one colonic (COLO320DM) cell line under these conditions. CONCLUSIONS: As opposed to pancreatic cancer and healthy controls, patients in our series had elevated serum VIP-levels. Further studies are warranted to evaluate whether VIP can be used as a tumor marker in this disease.

Adenocarcinoma↗