Security Enhancement of E-Voting System

The term E-Voting1C1; is used in variety of different ways and it encompasses all voting techniques involving electronic voting equipments, voting over the internet, using electronic booths in polling stations and sometimes even counting of paper ballots. A voting system that can be proven correct has many concerns. The basic reasons for a government to use electronic systems are to increase election activities and to reduce the election expenses. Still there is some scope of work in electronic voting system in terms of checking the authenticity of voters and securing electronic voting machine from miscreants. Biometrics is automated tool for verifying the identity of a person based on a physiological or behavioral characteristic. It has the capability to reliably distinguish between an authorized person and an imposter. Since biometric characteristics are distinctive, can not be forgotten or lost and the person to be authenticated needs to be physically present at the point of identification, biometrics is inherently more reliable and more capable than traditional knowledgebased and token-based techniques. In this paper, we have proposed a model to enhance the security of electronic voting system by incorporating fast and accurate biometric technique to prevent an unauthorized person to vote

Cancer of the uterine cervix and human papillomavirus infection

Human papillomaviruses (HPVs) have emerged as the principal sexually transmitted causal agents in the development of cancer of the uterine cervix in women. They also cause a variety of benign lesions, warts, intraepithelial neoplasia and anogenital, oral and pharyngeal papillomas. Presently, more than 100 HPV genotypes have been identified in humans, and about one-third of them have been sequenced. Of these, while HPV types 16 and 18 are considered to be the high-risk types, HPV 6 and 11 are the low-risk types in the development of cervical cancer. Evidence for causal role of HPV in the development of cervical neoplasia comes from the etiological and epidemiological observations together with the experimental findings of the molecular pathways elicited by HPV-transforming genes. Further evidence in favour of papillomavirus as the carcinoma virus comes from the findings of presence of HPV infections in cancers of oral, esophageal, larynx and nonmelanoma skin cancers. The oncogenic potentials of the virus have been attributed to its E6 and E7 genes. The products of these two genes stimulate cell proliferation by activating the cell-cycle-specific proteins and interfere with the functions of cellular growth-regulatory proteins, p53 and Rb. Identification and characterization of several human pathogenic HPV types warrant prevention of viral infection through vaccination or therapeutic intervention which could eventually control infection and expression of human pathogenic papillomaviruses

Alternate cyclin D1 mRNA splicing modulates P27\u3csup\u3eKlP1\u3c/sup\u3e binding and cell migration

Cyclin D1 is an important cell cycle regulator but in cancer its overexpression also increases cellular migration mediated by p27KlP1 stabilization and RhoA inhibition. Recently, a common polymorphism at the exon 4-intron 4 boundary of the human cyclin D1 gene within a splice donor region was associated with an altered risk of developing cancer. Altered RNA splicing caused by this polymorphism gives rise to a variant cyclin D1 isoform termed cyclin D1b, which has the same N-terminus as the canonical cyclin D1a isoform but a distinct C-terminus. In this study we show that these different isoforms have unique properties with regard to the cellular migration function of cyclin D1. Whereas they displayed little difference in transcriptional co-repression assays on idealized reporter genes, microarray cDNA expression analysis revealed differential regulation of genes including those that influence cellular migration. Additionally, while cyclin D1a stabilized p27KIP1 and inhibited RhoA-induced ROCK kinase activity, promoting cellular migration, cyclin D1b failed to stabilize p27KIP1 or inhibit ROCK kinase activity and had no effect on migration. Our findings argue that alternate splicing is an important determinant of the function of cyclin D1 in cellular migration

P53 tumor suppressor gene mutations in hepatocellular carcinoma patients in India

Background: Specific mutations of the p53 tumor suppressor gene in hepatocellular carcinoma (HCC) have been reported from several parts of the world, but to the authors' knowledge to date the status of this gene has not been studied in HCC patients in India, where HCC is one of the major cancers and the frequency of chronic hepatitis B virus (HBV) as well as hepatitis C virus (HCV) infection and exposure to dietary aflatoxin B1 is very high. The most frequent mutation of the p53 gene in HCC is an AGGArg to AGTSer missense mutation at codon 249 of exon 7. Methods: Liver biopsy specimens from 21 HCC patients and 10 healthy controls were obtained through surgery or by needle biopsy technique. Phenol-chloroform-extracted DNA specimens were employed for the detection of HBV infection and p53 gene mutations. Nucleotide mutations of exons 4-9 of the p53 gene were analyzed by polymerase chain reaction (PCR), single strand confirmation polymorphism, and direct sequencing. Third-generation sandwich enzyme-linked immunosorbent assay (ELISA) was used for the serologic detection of HBV and HCV infection. Results: Analysis of exons 4-9 of the p53 gene revealed only 3 mutations (3 of 21 specimens, 14.28%; 95% confidence interval, -0.7-29.3), 2 mutations at codon 249 showing G→T transversions, and 1 mutation (4.7%) at codon 250 with a C→T transition. The base substitutions at the third base of codon 249 resulted in a missense mutation leading to a change in amino acid from arginine to serine whereas at codon 250 it caused a change from proline to serine. Dot blot hybridization and PCR for HBV DNA from HCCs revealed 58.8% (10 of 17 specimens) and 90.47% (19 of 21 specimens), positivity, respectively. ELISA for hepatitis B virus surface antigen in serum showed a positivity of 71.42% (15 of 21 specimens), but there was only 40% positivity (8 of 20 specimens) for hepatitis B virus envelope antigen whereas 6 of 17 patients (35.29%) showed the presence of antibodies against hepatitis B virus envelope protein. No patient was found to be positive for the HCV antibody. Conclusions: The very low frequency of p53 mutations and the extremely high frequency of HBV infection (> 90%) in HCC indicate that the mutations in the p53 gene frequently found in HCC reported from different endemic areas of the world may not play a direct role in the development of HCC in India. HBV infection and, possibly, exposure to the dietary aflatoxin B1 appear to play major roles in the molecular pathogenesis of HCC in India

Cav1 Suppresses Tumor Growth and Metastasis in a Murine Model of Cutaneous SCC through Modulation of MAPK/AP-1 Activation

Caveolin-1 (Cav1) is a scaffolding protein that serves to regulate the activity of several signaling molecules. Its loss has been implicated in the pathogenesis of several types of cancer, but its role in the development and progression of cutaneous squamous cell carcinoma (cSCC) remains largely unexplored. Herein, we use the keratinocyte cell line PAM212, a murine model of cSCC, to determine the function of Cav1 in skin tumor biology. We first show that Cav1 overexpression decreases cell and tumor growth, whereas Cav1 knockdown increases these attributes in PAM212 cells. In addition, Cav1 knockdown increases the invasive ability and incidence of spontaneous lymph node metastasis. Finally, we demonstrate that Cav1 knockdown increases extracellular signaling–related kinase 1/2 mitogen-activated protein kinase/activator protein-1 pathway activation. We attribute the growth and invasive advantage conferred by Cav1 knockdown to increased expression of activator protein-1 transcriptional targets, including cyclin D1 and keratin 18, which show inverse expression in PAM212 based on the expression level of Cav1. In summary, we demonstrate that loss of Cav1 affects several characteristics associated with aggressive human skin tumors and that this protein may be an important modulator of tumor growth and invasion in cSCC

Cyclin D1 integrates G9a-mediated histone methylation.

Lysine methylation of histones and non-histone substrates by the SET domain containing protein lysine methyltransferase (KMT) G9a/EHMT2 governs transcription contributing to apoptosis, aberrant cell growth, and pluripotency. The positioning of chromosomes within the nuclear three-dimensional space involves interactions between nuclear lamina (NL) and the lamina-associated domains (LAD). Contact of individual LADs with the NL are dependent upon H3K9me2 introduced by G9a. The mechanisms governing the recruitment of G9a to distinct subcellular sites, into chromatin or to LAD, is not known. The cyclin D1 gene product encodes the regulatory subunit of the holoenzyme that phosphorylates pRB and NRF1 thereby governing cell-cycle progression and mitochondrial metabolism. Herein, we show that cyclin D1 enhanced H3K9 dimethylation though direct association with G9a. Endogenous cyclin D1 was required for the recruitment of G9a to target genes in chromatin, for G9a-induced H3K9me2 of histones, and for NL-LAD interaction. The finding that cyclin D1 is required for recruitment of G9a to target genes in chromatin and for H3K9 dimethylation, identifies a novel mechanism coordinating protein methylation

Engineering crops for tolerance against abiotic stress through gene manipulation

Plant genetic engineering took birth in the mid-eighties when, for the first time, plants were successfully engineered for improved virus, herbicide and insect resistance. This sphere has been ever-increasing since then. Abiotic stresses (such as high salt levels, low water availability leading to drought, excess water leading to flooding, high and low temperature regimes, etc.) adversely affect crop plants. The genetic responses of plants to these stresses are complex involving simultaneous expression of a number of genes. Till the early-nineties it was inconceivable that there would be any success in attaining the goal of improving resistance of crop plants to abiotic stresses. Continuing efforts of the stress biologists have resulted in engineering of plants resistant to low temperature, high temperature and excess salinity. A satisfactory progress has also been achieved in the area of generating plants resistant to water stress and flooding. While what has been achieved is impressive, it is still a challenging task to pyramid useful genes for high-level resistance to such stresses. The limiting factor in extension of biotechnology to abiotic stresses is the lack of information on what are the 'useful genes'-genes which would lead to better stress tolerance. We have reviewed how these genes are being searched to enable further development of strategies for stress management in crop plants. This is important because the strategics for coping with the abiotic stresses (and also for several other applications in plant biotechnology) have also come through the research work of scientists working on as diverse organisms as bacteria and fish

Multi-environment genomic selection in rice elite breeding lines

Abstract Background: Assessing the performance of elite lines in target environments is essential for breeding programs to select the most relevant genotypes. One of the main complexities in this task resides in accounting for the genotype by environment interactions. Genomic prediction models that integrate information from multi-environment trials and environmental covariates can be efficient tools in this context. The objective of this study was to assess the predictive ability of different genomic prediction models to optimize the use of multi- environment information. We used 111 elite breeding lines representing the diversity of the International Rice Research Institute (IRRI) breeding program for irrigated ecosystems. The lines were evaluated for three traits (days to flowering, plant height, and grain yield) in 15 environments in Asia and Africa and genotyped with 882 SNP markers. We evaluated the efficiency of genomic prediction to predict untested environments using seven multi-environment models and three cross-validation scenarios. Results: The elite lines were found to belong to the indica group and more specifically the indica-1B subgroup which gathered improved material originating from the Green Revolution. Phenotypic correlations between environments were high for days to flowering and plant height (33% and 54% of pairwise correlation greater than 0.5 ) but low for grain yield (lower than 0.2 in most cases). Clustering analyses based on environmental covariates separated Asia’s and Africa's environments into different clusters or subclusters. The predictive abilities ranged from 0.06 to 0.79 for days to flowering, 0.25 to 0.88 for plant height, and -0.29 to 0.62 for grain yield. We found that models integrating genotype-by-environment interaction effects did not perform significantly better than models integrating only main effects (genotypes and environment or environmental covariates). The different cross-validation scenarios showed that, in most cases, the use of all available environments gave better results than a subset. Conclusion: Multi-environment genomic prediction models with main effects were sufficient for accurate phenotypic prediction of elite lines in targeted environments. The recommendation for the breeders is to use simple multi-environment models with all available information for routine application in breeding programs