Crystallization behaviour of TiO2−ZrO2TiO_{2}-ZrO_{2} composite nanoparticles

To investigate tumor vascularity by dual source volume perfusion computed tomography (VPCT) in advanced lung adenocarcinoma with positive EGFR-mutant and determine whether any of the VPCT parameters would predict the tumor response to gefitinib.Twelve patients (5 males and 7 females, Median age: 53 years, range: 36 - 69 years) with advanced lung adenocarcinoma received VPCT scan. All patients with positive EGFR-mutant were confirmed by pathological biopsy. After a 6-week therapy of gefitinib, VPCT was repeated and the short-term effect evaluated by the RECIST criteria. The VPCT parameters (blood volume, blood flow and permeability surface) of 12 patients were compared with their differentiation grade and short-term effect.Short-term effects were poor in those cases in whom BF increased after a 6-week of targeted therapy (P = 0.030). BF and PS at pre-therapy were negatively correlated with differentiation grade (r = -0.603, -0.694, P = 0.038, 0.012). There was a negative correlation between the rate of BF decline and differentiation grade (r = -0.686, P = 0.029); a negative correlation existed between the trend of BF and RECIST criteria (r = -0.707, P = 0.010). But there was no significant correlation with differentiation grade (P = 0.059). If the BF decline was considered effective, the dual source VPCT could predict the effect of RECIST criteria. The sensitivity, specificity, accuracy, positive predictive value and negative predictive value of VPCT was 100%, 66.7%, 83.3%, 75% and 100% respectively.Dual source VPCT of advanced lung adenocarcinoma can assess effectively tumor vascularity and perfusion changes after the therapy of gefitinib. It is important in evaluating the response of targeted therapy in lung cancer

Genome-wide gene-environment analyses of major depressive disorder and reported lifetime traumatic experiences in UK Biobank

Depression is more frequent among individuals exposed to traumatic events.Both trauma exposure and depression are heritable. However, the relationship between these traits, including the role of genetic risk factors, is complex and poorly understood. When modelling trauma exposure as an environmental influence on depression, both gene-environment correlations and gene-environment interactions have been observed. The UK Biobank concurrently assessed Major Depressive Disorder (MDD) and self-reported lifetime exposure to traumatic events in 126,522 genotyped individuals of European ancestry. We contrasted genetic influences on MDD between individuals reporting and not reporting trauma exposure (final sample size range: 24,094-92,957). The SNP-based heritability of MDD was greater in participants reporting trauma exposure (24%) than in individuals not reporting trauma exposure taking into account the strong, positive genetic correlation observed between MDD and reported trauma exposure. The genetic correlation between MDD 15 and waist circumference was only significant in individuals reporting trauma exposure (rg = 0.24, p = 1.8x10-7 versus rg = -0.05, p = 0.39 in individuals not reporting trauma exposure, difference p = 2.3x10-4). Our results suggest that the genetic contribution to MDD is greater when additional risk factors are present, and that a complex relationship exists between reported trauma exposure, body composition, and MDD

Evidence of causal effect of major depression on alcohol dependence: findings from the psychiatric genomics consortium

BackgroundDespite established clinical associations among major depression (MD), alcohol dependence (AD), and alcohol consumption (AC), the nature of the causal relationship between them is not completely understood. We leveraged genome-wide data from the Psychiatric Genomics Consortium (PGC) and UK Biobank to test for the presence of shared genetic mechanisms and causal relationships among MD, AD, and AC.MethodsLinkage disequilibrium score regression and Mendelian randomization (MR) were performed using genome-wide data from the PGC (MD: 135 458 cases and 344 901 controls; AD: 10 206 cases and 28 480 controls) and UK Biobank (AC-frequency: 438 308 individuals; AC-quantity: 307 098 individuals).ResultsPositive genetic correlation was observed between MD and AD (rg = + 0.47, P = 6.6 × 10 ). AC-quantity showed positive genetic correlation with both AD (rg = + 0.75, P = 1.8 × 10 ) and MD (rg = + 0.14, P = 2.9 × 10 ), while there was negative correlation of AC-frequency with MD (rg = -0.17, P = 1.5 × 10 ) and a non-significant result with AD. MR analyses confirmed the presence of pleiotropy among these four traits. However, the MD-AD results reflect a mediated-pleiotropy mechanism (i.e. causal relationship) with an effect of MD on AD (beta = 0.28, P = 1.29 × 10 ). There was no evidence for reverse causation.ConclusionThis study supports a causal role for genetic liability of MD on AD based on genetic datasets including thousands of individuals. Understanding mechanisms underlying MD-AD comorbidity addresses important public health concerns and has the potential to facilitate prevention and intervention efforts