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Liquid-liquid extraction (LLE) and cloud point extraction (CPE) of vanadium(V) ternary complexes with 4-(2-pyridylazo)resorcinol (PAR) and 2,3,5-triphenyl-2H-tetrazolum chloride (TTC) were investigated. The optimal conditions for vanadium extraction and spectrophotometric determination were identified. The composition (V : PAR : TTC) of the extracted species was 1 : 2 : 3 (optimal conditions; LLE), 2 : 2 : 2 (low reagents concentrations; LLE), 1 : 1 : 1 (short heating time; CPE), and 1 : 1 : 1 + 1 : 1 : 0 (optimal extraction conditions; CPE). LLE, performed in the presence of 1,2-diaminocyclohexane-N,N,N',N'-tetraacetic acid and NH4F as masking agents, afforded the sensitive, selective, precise, and inexpensive spectrophotometric determination of vanadium. The absorption maximum, molar absorptivity, limit of detection, and linear working range were 559 nm, 1.95 × 10 5 dm 3 mol −1 cm −1 , 0.7 ng cm −3 , and 2.2-510 ng cm −3 , respectively. The procedure thus developed was applied to the analysis of drinking waters and steels. The relative standard deviations for V(V) determination were below 9.4 % (4-6 × 10 −7 mass %; water samples) and 2.12 % (1-3 mass %; steel samples).

Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide. Although CRC has been comprehensively characterized at the molecular level, the tumor heterogeneity hinders the identification of reliable diagnostic, prognostic and predictive biomarkers. Molecular stratification of CRC is based on prevalent gene mutations and transcription profiles but its significance for clinical practice remains obscure. Indeed, activating mutations in the genes KRAS, NRAS and BRAF are the only predictive biomarkers for anti-EGFR antibody therapy routinely tested the clinic for advanced stages of CRC. Gene expression signatures are important for clarifying the molecular mechanisms of CRC development and progression, but only two such tests for predicting recurrence risk are commercially available. The aim of our study was to propose a diagnostic approach based on mutation and gene expression analysis that can be routinely applied in the clinic for defining the most appropriate treatment strategy for each patient. We used qPCR to determine the presence of KRAS mutations and measure the transcription levels of a panel of 26 genes in 24 CRC patients. Statistical analyses were applied to check for associations between clinico-pathological and molecular parameters. Our results reveal novel data concerning CRC carcinogenesis: almost universal downregulation of EGFR; differential role of the pro-inflammatory cytokines TNF-α and IL-6; overexpression of the vitamin B12 transporter transcobalamin 1; tumor-suppressor function of SETD2, CA7 and GUCA2B. The practical application of these findings has yet to be clarified.