No abstract

Excess molar volumes Vf, for the binary mixtures of A-methylformamide, AvV-dimethylformamide, 2-pyrrolidinone, A-methyl-2-pyrrolidinone, and A/^-dimethylacetamide with water have been measured using a continuous-dilution dilatometer at 303.15 and 308.15 K as a function of composition. In all mixtures, the excess molar volumes are negative over the entire composition range. The results were used to estimate the apparent molar volumes of the components. The values of these two properties have been discussed in terms of intermolecular interactions between the mixing components of the binary mixture.

Mitochondrial DNA alterations in recent years have been suggested as modifier events, providing a possible proliferative advantage to the tumor cells. In order to provide further insight into the process of tumorigenesis, a study of whole mitochondria genome was conducted in 134 tissue samples obtained from 2 unrelated cancers (tumor and adjacent normal tissues from 36 breast cancer and 31 esophageal squamous cell carcinoma (ESCC) patients) with known p53 somatic mutation background. Fifteen of 36 (41.66%) breast and 12 of 31 (38.71%) ESCC tumors were found to contain at least 1 mtDNA somatic mutation, which correlated significantly with the concomitant presence of somatic mutation in DNA binding domain of the p53 gene (Breast cancer, p 5 0.006; ESCC, p 5 0.002). Interestingly, mutations in the non Dloop region of the mtDNA contributed significantly (Breast cancer, p 5 0.004; ESCC, p 5 0.032) in comparison to the hotspot-DLoop-region. The concomitant presence of mutations in p53 and mtDNA were also predominant in breast cancer tumors with poor prognosis, that is, with the advanced stage, grade and the ER/PR negativity. Also, the observation made was apparently well explained in 10398A bearing N haplogroup genetic background with increased presence of novel and pathogenic germline mutation in mtDNA. Our study suggests that the concomitant presence of somatic alteration in mtDNA and the DNA binding domain of the p53 gene facilitates cell survival and tumorigenesis, requiring specialized therapeutic intervention because of a possible resistance to conventional chemotherapy. ' 2008 Wiley-Liss, Inc.Key words: mtDNA; breast cancer; esophageal cancer; somatic mutation; germline mutation; haplogroup The study of extranuclear mitochondrial genome has recently attained immense importance in cancer research to dissect out the molecular pathology of tumorigenesis. 1-3 A spate of reports detailing somatic alteration of mtDNA, including mutations, copy number variations or abnormal gene expression, confirm the involvement of mitochondria in tumorigenesis. [1][2][3][4][5][6][7] These observations find support in functional validation of some of the somatic mutations in critical mitochondria encoded genes for their putative role in tumorigenesis. 5,8 Many have claimed that somatic mtDNA mutation could be used as a biomarker in early diagnosis of cancer and its progression; whereas some suggest otherwise. 7,[9][10][11] The role of mitochondria in energy metabolism, generation of reactive oxygen species, aging and the initiation of apoptosis, permits the organelle to act as 1 of the key switches in shifting the cell from death to abnormal growth and contribute to the neoplastic process. [12][13][14][15] In evolutionary context, it has been proposed that numerous germline variations encountered in mtDNA which enabled early humans to energetically adapt to their ancestral milieu, act as modifiers of cancer risk 16 and could play a possible oncogenic role in conjunction with the mtDNA somatic mutations. With this background, the as...

The viscosity in binary liquid mixtures of water with ethylene glycol dimethyl ether (1,2-dimethoxyethane), CH3OCH2CH2OCH3, diethylene glycol dimethyl ether (bis(2-methoxyethyl) ether), CH3OCH2CH2OCH2CH2OCH3, triethylene glycol dimethyl ether (1,2-bis(2-methoxyethoxy)ethane), CH3OCH2(CH2OCH2)2CH2OCH3, and tetraethylene glycol dimethyl ether (2,5,8,11,14-pentaoxapentadecane), CH3OCH2(CH2OCH2)3CH2OCH3, have been determined at 298.15 K over the whole range of mixture compositions. The viscosity data have been analyzed by using the viscosity equations of McAllister and Heric. The values of the quantity Δη, which refer to the deviations of the experimental values of the dynamic viscosities of the mixtures from the mole fraction mixture law values, have been found to be positive for all the mixtures. The deviations in viscosity data Δη have been fitted to the Redlich−Kister polynomial relation to estimate the binary coefficients. Also, the values of the parameter d 12 have been calculated from the equation ln η = x 1 ln η1 + x 2 ln η2 + x 1 x 2 d 12, where η1 and η2 refer to the dynamic viscosities of the two pure liquids 1 and 2 whose mole fractions in the mixture are x 1 and x 2, respectively. The values of d 12 indicate the existence of a specific interaction between dissimilar molecules.

Type 2 diabetes (T2D) is a syndrome of multiple metabolic disorders and is genetically heterogeneous. India comprises one of the largest global populations with highest number of reported type 2 diabetes cases. However, limited information about T2D associated loci is available for Indian populations. It is, therefore, pertinent to evaluate the previously associated candidates as well as identify novel genetic variations in Indian populations to understand the extent of genetic heterogeneity. We chose to do a cost effective high-throughput mass-array genotyping and studied the candidate gene variations associated with T2D in literature. In this case-control candidate genes association study, 91 SNPs from 55 candidate genes have been analyzed in three geographically independent population groups from India. We report the genetic variants in five candidate genes: TCF7L2, HHEX, ENPP1, IDE and FTO, are significantly associated (after Bonferroni correction, p<5.5E−04) with T2D susceptibility in combined population. Interestingly, SNP rs7903146 of the TCF7L2 gene passed the genome wide significance threshold (combined P value = 2.05E−08) in the studied populations. We also observed the association of rs7903146 with blood glucose (fasting and postprandial) levels, supporting the role of TCF7L2 gene in blood glucose homeostasis. Further, we noted that the moderate risk provided by the independently associated loci in combined population with Odds Ratio (OR)<1.38 increased to OR = 2.44, (95%CI = 1.67–3.59) when the risk providing genotypes of TCF7L2, HHEX, ENPP1 and FTO genes were combined, suggesting the importance of gene-gene interactions evaluation in complex disorders like T2D.