QR Based Smart Shopping

The current system implemented in supermarkets is an inefficient use of supermarket?s time and resources. As technology is evolving continuously, it becomes necessary for the supermarkets to adapt to the changing technological needs and enhance the customer?s shopping experience, by maximizing the utilization of available resources. The purpose of the project is to identify and incorporate consumer motivations and attitudes towards new concept of QR based shopping in India. The proposed system is planned, designed and built to be implemented in supermarkets and small retail stores like Reliance Fresh, Big Bazaar. The system focuses on hassle free customer shopping and reducing the burden which customers have to face while physically carrying the trolleys and bags during shopping. The project also aims at synergizing the marketing initiatives in the super market industry

A record-linkage study of the development of hepatocellular carcinoma in persons with hepatitis C infection in Scotland

We investigated trends in first time hospital admissions and deaths attributable to hepatocellular carcinoma (HCC) in a large population based cohort of 22 073 individuals diagnosed with hepatitis C viral (HCV) infection through laboratory testing in Scotland in 1991 2006. We identified new cases of HCC through record linkage to the national inpatient hospital discharge database and deaths registry. A total of 172 persons diagnosed with HCV were admitted to hospital or died with first time mention of HCC. Hepatocellular carcinoma incidence increased between 1996 and 2006 (average annual change of 6.1, 95% confidence interval (CI):0.9 11.6%, P¼0.021). The adjusted relative risk of HCC was greater for males (hazard ratio¼2.7, 95% CI: 1.7 4.2), for those aged 60 years or older (hazard ratio ¼2.7, 95% CI: 1.9 4.1) compared with 50 59 years, and for those with a previous alcohol related hospital admission (hazard ratio¼2.5, 95% CI: 1.7 3.7). The risk of individuals diagnosed with HCV developing HCC was greatlyincreased compared with the general Scottish population (standardised incidence ratio¼127, 95% CI: 102 156). Owing to the advancing age of the Scottish HCV diagnosed population, the annual number of HCC cases is projected to increase, with a consequent increasing burden on the public healthcare system

Association of the rs738409 polymorphism in PNPLA3 with liver damage and the development of nonalcoholic fatty liver disease

<p>Abstract</p> <p>Background</p> <p>In a genome-wide association scan, the single-nucleotide polymorphism (SNP) rs738409 in the patatin-like phospholipase 3 gene (<it>PNPLA3</it>) was strongly associated with increased liver fat content. We investigated whether this SNP is associated with the occurrence and progression of nonalcoholic fatty liver disease (NAFLD) in the Japanese population.</p> <p>Methods</p> <p>SNP rs738409 was genotyped by the Taqman assay in 253 patients with NAFLD (189 with nonalcoholic steatohepatitis [NASH] and 64 with simple steatosis) and 578 control subjects. All patients with NAFLD underwent liver biopsy. Control subjects had no metabolic disorders. For a case-control study, the <it>χ</it>²-test (additive model) was performed. Odds ratios (ORs) were adjusted for age, gender, and body mass index (BMI) by using multiple logistic regression analysis with genotypes (additive model), age, gender, and BMI as the independent variables. Multiple linear regression analysis was performed to test the independent effect of risk allele on clinical parameters while considering the effects of other variables (age, gender, and BMI), which were assumed to be independent of the effect of the SNP.</p> <p>Results</p> <p>The risk allele (G-allele) frequency of rs738409 was 0.44 in the control subjects and 0.60 in patients with NAFLD; this shows a strong association with NAFLD (additive model, <it>P </it>= 9.4 × 10^-10). The OR (95% confidence interval) adjusted for age, gender, and BMI was 1.73 (1.25-2.38). Multiple linear regression analysis indicated that the G-allele of rs738409 was significantly associated with increases in aspartate transaminase (AST) (<it>P </it>= 0.00013), alanine transaminase (ALT) (<it>P </it>= 9.1 × 10^-6), and ferritin levels (<it>P </it>= 0.014), and the fibrosis stage (<it>P </it>= 0.011) in the patients with NAFLD, even after adjustment for age, gender, and BMI. The steatosis grade was not associated with rs738409.</p> <p>Conclusions</p> <p>We found that in the Japanese population, individuals harboring the G-allele of rs738409 were susceptible to NAFLD, and that rs738409 was associated with plasma levels of ALT, AST, and ferritin, and the histological fibrosis stage. Our study suggests that <it>PNPLA3 </it>may be involved in the progression of fibrosis in NAFLD.</p

Association between PPARGC1A polymorphisms and the occurrence of nonalcoholic fatty liver disease (NAFLD)

<p>Abstract</p> <p>Background</p> <p>Genetic factors as well as environmental factors are important in the development of NAFLD and in this study we investigated associations between polymorphisms of peroxisome proliferators-activated receptor γ coactivator 1α polymorphism (<it>PPARGC1A</it>) and NAFLD.</p> <p>Aims</p> <p>We recruited 115 patients with biopsy-proven NAFLD, 65 with NASH and 50 with simple steatosis, and 441 healthy control subjects and investigated 15 SNPs of <it>PPARGC1A</it>.</p> <p>Results</p> <p>SNP rs2290602 had the lowest <it>p </it>value in the dominant mode (<it>p </it>= 0.00095), and the odds ratio for NAFLD (95% CI) was 2.73 (1.48 – 5.06). rs2290602 was significantly associated with NAFLD even when the most conservative Bonferroni's correction was applied (<it>p </it>= 0.0143). The frequency of the T allele of rs2290602 was significantly higher in the NASH patients than in the control subjects (<it>p </it>= 0.00093, allele frequency mode), and its frequency in the NASH patients tended to be higher than in the simple steatosis patients (<it>p </it>= 0.09). The results of the real-time RT-PCR study showed that intrahepatic mRNA expression of <it>PPARGC1A </it>was lower in the TT group than in the GG or GT group at SNP rs2290602 (p = 0.0454).</p> <p>Conclusion</p> <p>This is the first study to demonstrate a significant association between genetic variations in <it>PPARGC1A </it>and NAFLD. This finding suggested that <it>PPARGC1A </it>polymorphism and lower expression of <it>PPARGC1A </it>mRNA in the liver are an important genetic contribution to etiology of NAFLD.</p

Corticotropin Releasing Factor-Induced CREB Activation in Striatal Neurons Occurs via a Novel Gβγ Signaling Pathway

The peptide corticotropin-releasing factor (CRF) was initially identified as a critical component of the stress response. CRF exerts its cellular effects by binding to one of two cognate G-protein coupled receptors (GPCRs), CRF receptor 1 (CRFR1) or 2 (CRFR2). While these GPCRs were originally characterized as being coupled to Gαs, leading to downstream activation of adenylyl cyclase (AC) and subsequent increases in cAMP, it has since become clear that CRFRs couple to and activate numerous other downstream signaling cascades. In addition, CRF signaling influences the activity of many diverse brain regions, affecting a variety of behaviors. One of these regions is the striatum, including the nucleus accumbens (NAc). CRF exerts profound effects on striatal-dependent behaviors such as drug addiction, pair-bonding, and natural reward. Recent data indicate that at least some of these behaviors regulated by CRF are mediated through CRF activation of the transcription factor CREB. Thus, we aimed to elucidate the signaling pathway by which CRF activates CREB in striatal neurons. Here we describe a novel neuronal signaling pathway whereby CRF leads to a rapid Gβγ- and MEK-dependent increase in CREB phosphorylation. These data are the first descriptions of CRF leading to activation of a Gβγ-dependent signaling pathway in neurons, as well as the first description of Gβγ activation leading to downstream CREB phosphorylation in any cellular system. Additionally, these data provide additional insight into the mechanisms by which CRF can regulate neuronal function