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Biochemical markers of cellular stress/injury have been proposed to indicate outcome after head injury. The aim of the present study was to determine whether plasma von Willebrand factor (VWF) levels correlate with primary outcome and with clinical variables in severe traumatic brain injury (TBI). Forty-four male patients, victims of severe TBI, were analyzed. Clinical outcome variables of severe TBI comprised survival and neurological assessment using the Glasgow Outcome Scale (GOS) at intensive care unit (ICU) discharge. Computerized tomography (CT) scans were analyzed according to Marshall CT classification. Three consecutive venous blood samples were taken: first sample (11.4 +/- 5.2 h after trauma, mean +/- SD), and 24 h and 7 days later. The result of mean plasma VWF concentration was significantly higher in the TBI group (273 U/dL) than in the control group (107 U/dL; p < 0.001). Severe TBI was associated with a 50% mortality rate. Nonsurvivors presented significantly higher APACHE II scores than survivors (nonsurvivors mean, 18.8; survivors mean, 12.7; p < 0.001), and also presented higher scores in Marshall CT classification (nonsurvivors mean, 4.6; survivors mean, 2.7; p < 0.05). There was a significant positive correlation between plasma levels at second plasma sampling and scores in Marshall CT classification (p < 0.05). The sensitivity of plasma VWF concentration in predicting mortality according to the cut-off of 234 U/dL was 64%, with a specificity of 68%. Therefore, VWF increases following severe TBI may be a marker of unfavorable outcome.

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The synchronous occurrence of GISTs and other primary neoplasm is not an uncommon entity and usually they are discovery incidentally. Epithelial tumors of the gastrointestinal tract are the most associated with concomitant GISTs. Further studies are required to clarify the molecular and genetic mechanisms of carcinogenesis and progression associating GIST and synchronous tumors.

In the current study we present a Gompertzian model for cell growth as a function of cell phenotype using six human tumour cell lines (A-549, NCI-H596, NCI-H520, HT-29, SW-620 and U-251). Monolayer cells in exponential growth at various densities were quantified over a week by sulforhodamine B staining assay to produce cell-growth curves. A Gompertz equation was fitted to experimental data to obtain, for each cell line, three empirical growth parameters (initial cell density, cell-growth rate and carrying capacity - the maximal cell density). A cell-shape parameter named deformation coefficient D (a morphological relationship among spreading and confluent cells) was established and compared by regression analysis with the relative growth rate parameter K described by the Gompertz equation. We have found that coefficient D is directly proportional to the growth parameter K. The fit curve significantly matches the empirical data (P < 0.05), with a correlation coefficient of 0.9152. Therefore, a transformed Gompertzian growth function was obtained accordingly to D. The degree of correlation between the Gompertzian growth parameter and the coefficient D allows a new interpretation of the growth parameter K on the basis of morphological measurements of a set of tumour cell types, supporting the idea that cell-growth kinetics can be modulated by phenotypic organization of attached cells.