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Studies the prewetting transition in the silica-water-2,5-dimethylpyridine system through adsorption isotherms. Universality of the wetting phenomena; Description of the physical properties.

Examines the phase change possibilities in the surface phase formed in a binary liquid system in contract with a solid on the basis of adsorption isotherms. Layering in surfaces as a phase surface change leading to condensed phase from a gaslike one; Packing effects in liquid mixtures.

The wetting behavior of the water–2,5 lutidine system has been studied around the lower consolute point (Tc=13.1 °C). We have measured contact angles and surface tensions by varying the concentration and temperature. In the diphasic region, a wetting transition has been observed at 46–47 °C on a silica wall by direct observation of the solid–liquid–liquid contact angle. The perfect wetting occurs close to Tc, the wetting phase is water rich. At the liquid–vapor interface, the analysis of the values of the surface tensions shows that, close to Tc, they obey critical laws and that a lutidine rich phase perfectly wets the vapor and the water rich phase. These behaviors have been analyzed on the basis of the contact angles of the monophasic on a silica wall on both sides of the coexistence curve, and the general variation of the surface tensions. A second wetting transition has been shown on a differently washed glass surface. Reference is made to the theoretical and experimental works following the early work of Cahn. [ABSTRACT FROM AUTHOR]

Experimental data of surface tensions along the critical isochore (1) and the two branches of the coexistence curve (2,3) for the water-2,5 lutidine system have been used in order to check signs and values of the universal amplitude ratios of the critical laws in the forms σα,j=σc+A(T-Tc)+Bj(T-Tc)μ, j=1,2,3, with imposed μ=1.26. A and the Bj’s being highly correlated, several statistical tests using the values of the ratios have been used. Experimental values are compatible with P+=B/Bi=-0.59 (B: isochore; Bi: interfacial tension in the two phases system), maybe with Q=B/B‘=-0.83 (B‘ one branch of the coexistence curve) and certainly with its sign. The other ratios cannot be verified at all by the experimental data. [ABSTRACT FROM AUTHOR]

Background: TNBC is an heterogeneous group of tumors for some of which the Epithelial Growth Factor Receptor pathway (EGFR) may play an important role. We evaluated the efficacy and toxicity of an anti-EGFR antibody (panitumumab) combined with a standard neoadjuvant chemotherapy in order to identify predictive biomarkers of efficacy and target biologically defined subpopulations for potential further development. Methods: Sixty patients with stage II-IIIA disease were prospectively included in this multicentre neoadjuvant study. Systemic therapy (ST) consisted of panitumumab (9 mg/kg q.3 weeks x8) combined with FEC 100 (500/100/500 mg/m² q.3 weeks x4) followed by 4 cycles of T (100 mg/m² q.3weeks x4). All patients underwent surgery at completion of ST. Paraffin-embedded and frozen samples were systematically collected before and after ST for biologic studies. Patients characteristics are as follows: mean age 50 [27-72]; median tumor size: 40 mm [20-120]; invasive ductal carcinoma: 96.7%; Scarff-Bloom-Richardson Grade III: 71.7%, grade II: 28.3%. Complete pathological response (pCR) rate was 52.3% [95% IC: 37.3-67.5] (Sataloff's classification) and 46.7% [95% IC: 31.6-61.4](Chevallier's classification). Conservative surgery was performed in 88% of cases. Skin toxicity was the main side-effect: Cutaneous toxicity grade IV: 5%, grade III: 30%, grade II: 20%. Neutropenia grade IV: 27%; febrile neutropenia: 5%. Infection: 0%. Hand- foot syndrome grade III: 3.3%. Ungueal toxicity grade III: 1.6%, grade II: 20%. Results: We performed a ROC curve to identify the best cut-off value for KI-67, EGFR, cytokeratin 5-6 and p53 in order to predict a pCR. Tumors with more than 40% of positive cells for KI-67 and tumors with a score for EGFR greater than 70 tend to be associated with pCR according to Chevallier's classification (p = 0.06). No predictive value was identified for Cytokeratin 5-6 and p53 (p = 0.61 and p = 0.27, respectively). Immunohistochemistry results show that two thirds of tumors have more than 40% of positive cells for KI-67 and that two thirds of tumors present a score for EGFR greater than 70. About half of the tumors express cytokeratin 5-6 and p53 (cut off: 1%). Chi-squared tests were performed to assess relations between cutaneous toxicities and pCR. The cutaneous toxicities were not predictive of pCR (p = 0.94) and no correlations were found with KI-67, EGFR, Cytokeratin 5-6 and p53. In terms of BRCA1 and BRCA2 status, 35 tumors were analysed so far: BRCA1: 6 mutations (17%); BRCA2 (30 patients): 1 mutation (3.3%). Conclusions: These results suggest the possibility to identify a subpopulation with high probability of pCR (KI-67 > 40%, EGFR score > 70). Further biological studies are ongoing and will be presented at the meeting, including EGFR polymorphisms, C-met, ALDH1, pCadherine and PTEN. This will help us further define subpopulations of TNBC patients, potential targets for antiEGFR development. [ABSTRACT FROM AUTHOR]