Response study of canola (Brassica napus L.) cultivars to multi-environments using genotype plus genotype environment interaction (GGE) biplot method in Iran

To study the interaction of genotype and environment in canola crop, a study was carried out in 2010. Ten genotypes (Modena, Okapi, Hyola 401, Licord, Opera, Zarfam, RGS 003, SLM046, Sarigol, and Hyola 308) of canola were studied under normal conditions of irrigation in four locations (Karaj, Birjand, Shiraz, and Kashmar) using randomized complete block design with three replications. Using GGE biplot method, grain yield was investigated for each cultivar. According to analysis of variance, there was a very significant difference among the regions. According to the yield average and genotype stability, Licord, Hyola 308, Modena and Zarfam were the best cultivars. The graphs obtained from GGE biplot software indicated that Hyola 401, Opera, and Sarigol were better than the rest of the genotypes based on stability and yield performance. At location Shiraz, none of the genotype had appropriate stability or yield. Four locations were divided into three mega-environments including Karaj, Kashmar (first mega-environment), Birjand (second mega-environment), and Shiraz (third mega-environment). Moreover, Karaj was recognized as the best region of the classification and ranking of genotypes. The study indicated that the highest and lowest genotypic reaction rates belonged to Licord and SLM 046 cultivars, respectively.Keywords: Canola, genotype environment interaction, grain yield, GGE biplot

Population genetic structure of the white sardine, Sardinella albella, in the Persian Gulf and Sea of Oman by analysis of mitochondrial control region

Several studies on the white sardine: Sardinella albella, have focused on the identification of stock composition and behavior. In this study population genetic structure and historical demography of S. albella along the cost of the Persian Gulf and Sea of Oman were investigated with a 500-bp segment of mt-DNA control region. In total 40 samples were collected from 3 locations: Jask in Sea of Oman, Qeshm in Strait of Hormuz and Lengeh in the Persian Gulf during 2012-2013. 33 haplotype were obtained none of which were presented in all sampling sites. Analysis of molecular variance (AMOVA) indicated low genetic differentiation among regions (F_ST=0.024, p<0.05). The average pair wise differences between regional population were small but significant (0.0158-0.165). Molecular variance explained by differences among three regions was significantly different from zero but the F_ST did not show clear phylogeographic isolation. This observation can support the conclusion that S. albella has a widespread dispersal potential

The in vivo effect of methyl tert-butyl ether on liver, gills and kidney tissues of Rutilus caspicus

This study was conducted to evaluate histopathological responses in liver, gills and kidney in Rutilus caspicus exposed to concentrations of 50, 100, 150 mg L^-1 of methyl tert-butyl ether, for 7, 14, and 21 days. The experiments were conducted in water temperature of 19±1 °C, dissolved oxygen of 7.6 ± 0.2 mg L^-1 and zero salinity. A total of 156 fish were studied in this experiment. In the first, second and third week of the experiment, three fish were taken randomly from each aquarium. To examine the tissues, the liver, gills and kidney were isolated and prepared for evaluation using standard histological techniques. Tissue damage in the liver includes: blood congestion, congestion of sinusoid, melano macrophage aggregation, hepatocyte hypertrophy, vacuolation, degeneration and cellular necrosis. Gill tissue damage includes: hyperplasia, degeneration lifting, telangiectasis, in secondary lamellae, blood congestion in primary and secondary lamellae, S formation of lamellae, and reduction in length of secondary lamella, lamellar fusion and cellular necrosis. Tissue damage in the kidney includes: tubular shrinkage, blood congestion, melano macrophage aggregation, glomerular shrinkage, cellular necrosis, tubular degeneration, reduction in interstsial cells and interstisial hematopoietic tissue degeneration. The amount of tissue damages in high concentrations of pollutants was high, while gill, liver and kidney in the control group were observed in the normal outline. The results of this study showed that methyl tert-butyl ether (MTBE) can cause damage in vital tissues of R. caspicus and even, eventually lead to death

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

BACKGROUND Despite 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. METHODS Linkage 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). RESULTS Positive genetic correlation was observed between MD and AD (rgMD−AD = + 0.47, P = 6.6 × 10−10). AC-quantity showed positive genetic correlation with both AD (rgAD−AC quantity = + 0.75, P = 1.8 × 10−14) and MD (rgMD−AC quantity = + 0.14, P = 2.9 × 10−7), while there was negative correlation of AC-frequency with MD (rgMD−AC frequency = −0.17, P = 1.5 × 10−10) 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 × 10−6). There was no evidence for reverse causation. CONCLUSION This 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

Diabetes mortality and trends before 25 years of age: an analysis of the Global Burden of Disease Study 2019

Background Diabetes, particularly type 1 diabetes, at younger ages can be a largely preventable cause of death with the correct health care and services. We aimed to evaluate diabetes mortality and trends at ages younger than 25 years globally using data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019. Methods We used estimates of GBD 2019 to calculate international diabetes mortality at ages younger than 25 years in 1990 and 2019. Data sources for causes of death were obtained from vital registration systems, verbal autopsies, and other surveillance systems for 1990–2019. We estimated death rates for each location using the GBD Cause of Death Ensemble model. We analysed the association of age-standardised death rates per 100 000 population with the Socio-demographic Index (SDI) and a measure of universal health coverage (UHC) and described the variability within SDI quintiles. We present estimates with their 95% uncertainty intervals. Findings In 2019, 16 300 (95% uncertainty interval 14 200 to 18 900) global deaths due to diabetes (type 1 and 2 combined) occurred in people younger than 25 years and 73·7% (68·3 to 77·4) were classified as due to type 1 diabetes. The age-standardised death rate was 0·50 (0·44 to 0·58) per 100 000 population, and 15 900 (97·5%) of these deaths occurred in low to high-middle SDI countries. The rate was 0·13 (0·12 to 0·14) per 100 000 population in the high SDI quintile, 0·60 (0·51 to 0·70) per 100 000 population in the low-middle SDI quintile, and 0·71 (0·60 to 0·86) per 100 000 population in the low SDI quintile. Within SDI quintiles, we observed large variability in rates across countries, in part explained by the extent of UHC (r2=0·62). From 1990 to 2019, age-standardised death rates decreased globally by 17·0% (−28·4 to −2·9) for all diabetes, and by 21·0% (–33·0 to −5·9) when considering only type 1 diabetes. However, the low SDI quintile had the lowest decline for both all diabetes (−13·6% [–28·4 to 3·4]) and for type 1 diabetes (−13·6% [–29·3 to 8·9]). Interpretation Decreasing diabetes mortality at ages younger than 25 years remains an important challenge, especially in low and low-middle SDI countries. Inadequate diagnosis and treatment of diabetes is likely to be major contributor to these early deaths, highlighting the urgent need to provide better access to insulin and basic diabetes education and care. This mortality metric, derived from readily available and frequently updated GBD data, can help to monitor preventable diabetes-related deaths over time globally, aligned with the UN's Sustainable Development Targets, and serve as an indicator of the adequacy of basic diabetes care for type 1 and type 2 diabetes across nations.publishedVersio

RNA sequencing of identical twins discordant for autism reveals blood-based signatures implicating immune and transcriptional dysregulation

Background: A gap exists in our mechanistic understanding of how genetic and environmental risk factors converge at the molecular level to result in the emergence of autism symptoms. We compared blood-based gene expression signatures in identical twins concordant and discordant for autism spectrum condition (ASC) to differentiate genetic and environmentally driven transcription differences, and establish convergent evidence for biological mechanisms involved in ASC. Methods: Genome-wide gene expression data were generated using RNA-seq on whole blood samples taken from 16 pairs of monozygotic (MZ) twins and seven twin pair members (39 individuals in total), who had been assessed for ASC and autism traits at age 12. Differential expression (DE) analyses were performed between (a) affected and unaffected subjects (N = 36) and (b) within discordant ASC MZ twin pairs (total N = 11) to identify environmental-driven DE. Gene set enrichment and pathway testing was performed on DE gene lists. Finally, an integrative analysis using DNA methylation data aimed to identify genes with consistent evidence for altered regulation in cis. Results: In the discordant twin analysis, three genes showed evidence for DE at FDR < 10%: IGHG4, EVI2A and SNORD15B. In the case-control analysis, four DE genes were identified at FDR<10% including IGHG4, PRR13P5, DEPDC1B, and ZNF501. We find enrichment for DE of genes curated in the SFARI human gene database. Pathways showing evidence of enrichment included those related to immune cell signalling and immune response, transcriptional control and cell cycle/proliferation. Integrative methylomic and transcriptomic analysis identified a number of genes showing suggestive evidence for cis dysregulation. Limitations: Identical twins stably discordant for ASC are rare, and as such the sample size was limited and constrained to the use of peripheral blood tissue for transcriptomic and methylomic profiling. Given these primary limitations, we focused on transcript-level analysis. Conclusions: Using a cohort of ASC discordant and concordant MZ twins, we add to the growing body of transcriptomic-based evidence for an immune-based component in the molecular aetiology of ASC. Whilst the sample size was limited, the study demonstrates the utility of the discordant MZ twin design combined with multi-omics integration for maximising the potential to identify disease-associated molecular signals

Integrated analysis of environmental and genetic influences on cord blood DNA methylation in new-borns

Epigenetic processes, including DNA methylation (DNAm), are among the mechanisms allowing integration of genetic and environmental factors to shape cellular function. While many studies have investigated either environmental or genetic contributions to DNAm, few have assessed their integrated effects. Here we examine the relative contributions of prenatal environmental factors and genotype on DNA methylation in neonatal blood at variably methylated regions (VMRs) in 4 independent cohorts (overall n = 2365). We use Akaike’s information criterion to test which factors best explain variability of methylation in the cohort-specific VMRs: several prenatal environmental factors (E), genotypes in cis (G), or their additive (G + E) or interaction (GxE) effects. Genetic and environmental factors in combination best explain DNAm at the majority of VMRs. The CpGs best explained by either G, G + E or GxE are functionally distinct. The enrichment of genetic variants from GxE models in GWAS for complex disorders supports their importance for disease ris