Blood Traits Research Articles

Potential Predictive Value of Platelet Distribution Width for Functional Outcome After Ischemic Stroke.

Complete blood cell count (CBC) is the most common and readily available laboratory test in clinical practice. The relationships of some CBC indices with ischemic stroke have been reported in observational studies; however, the causal direction is not specified. This study aimed to explore the causal relationships between CBC indices and the modified Rankin Scale (mRS) score at 3months after ischemic stroke. Genetic associations of 22 blood cell traits were obtained from the UK Biobank database (n = 350,475). The outcome data for ischemic stroke were obtained from the Genetic Ischemic Stroke Functional Outcome (GISCOME) network (n = 6021). We implemented two-sample Mendelian randomization (TSMR) and several complementary analyses to assess the causal association between blood traits and unfavorable outcome (3-month mRS > 2). The clinical cohort was validated based on the results of the MR analysis. TSMR result indicated causal association between genetically determined platelet distribution width (PDW) and adverse functional outcome after ischemic stroke (OR 1.48; 95% CI 1.13-1.95; p = 0.005). Complementary analyses showed negligible causal effect of genetic variants on stroke subtypes. In cohort study (n = 351), higher level of PDW was observed in the unfavorable outcome group. However, the multivariable logistic regression analysis failed to identify the improvement in predictive performance of stroke outcomes by adding PDW to the prediction model. Further correlation analysis revealed that PDW is positively correlated with serum glucose levels, and the level of PDW in the non-thrombolysed group was significantly higher than that in the thrombolysis group, indicating that PDW may be involved in stroke prognosis in an indirect way.

Genome-wide association study reveals the underlying regulatory mechanisms of red blood traits in Anadara granosa

BackgroundAnadara granosa, commonly known as the blood clam, exhibits the unusual characteristic of having red blood among invertebrates. There is significant individual variation in blood color intensity among blood clams; individuals with vibrant red blood are deemed healthier and exhibit stronger stress resistance. However, the molecular basis underlying these red blood traits (RBTs) remains poorly understood.ResultsIn this study, we performed genome-wide association studies (GWAS) in a population of 300 A. granosa individuals, focusing on RBTs as measured by hemoglobin concentration (HC), total hemocyte count (THC), and heme concentration (HEME). Our analysis identified 18 single nucleotide polymorphisms (SNPs) correlated with RBTs, subsequently selected 117 candidate genes within a 100 kb flanking region of these SNPs, potentially involved in the RBTs of A. granosa. Moreover, we discovered two haplotype blocks specifically associated with THC and HEME. Further analysis revealed eight genes (Septin7, Hox5, Cbfa2t3, Avpr1b, Hhex, Eif2ak3, Glrk, and Rpl35a) that significantly influence RBTs. Notably, a heterozygous A/T mutation in the 3’UTR of Cbfa2t3 was found to promote blood cell proliferation. These genes suggest that the hematopoietic function plays a significant role in the variability of RBTs in A. granosa.ConclusionsOur findings reveal a conservation of the regulatory mechanisms of RBTs between blood clams and vertebrates. The results not only provide a scientific basis for selective breeding in blood clams, but also offer deeper insights into the evolutionary mechanisms of RBTs in invertebrates.

Variance quantitative trait loci reveal gene-gene interactions which alter blood traits.

Gene-gene (GxG) interactions play an important role in human genetics, potentially explaining part of the "missing heritability" of polygenic traits and the variable expressivity of monogenic traits. Many GxG interactions have been identified in model organisms through experimental breeding studies, but they have been difficult to identify in human populations. To address this challenge, we applied two complementary variance QTL (vQTL)-based approaches to identify GxG interactions that contribute to human blood traits and blood-related disease risk. First, we used the previously validated genome-wide scale test for each trait in ∼450,000 people in the UK Biobank and identified 4 vQTLs. Genome-wide GxG interaction testing of these vQTLs enabled discovery of novel interactions between (1) CCL24 and CCL26 for eosinophil count and plasma CCL24 and CCL26 protein levels and (2) HLA-DQA1 and HLA-DQB1 for lymphocyte count and risk of celiac disease, both of which replicated in ∼140,000 NIH All of Us and ∼70,000 Vanderbilt BioVU participants. Second, we used a biologically informed approach to search for vQTL in disease-relevant genes. This approach identified (1) a known interaction for hemoglobin between two pathogenic variants in HFE which cause hereditary hemochromatosis and alters risk of cirrhosis and (2) a novel interaction between the JAK2 46/1 haplotype and a variant on chromosome 14 which modifies platelet count, JAK2 V617F clonal hematopoiesis, and risk of polycythemia vera. This work identifies novel disease-relevant GxG interactions and demonstrates the utility of vQTL-based approaches in identifying GxG interactions relevant to human health at scale.

Sequence variants influencing the regulation of serum IgG subclass levels

Immunoglobulin G (IgG) is the main isotype of antibody in human blood. IgG consists of four subclasses (IgG1 to IgG4), encoded by separate constant region genes within the Ig heavy chain locus (IGH). Here, we report a genome-wide association study on blood IgG subclass levels. Across 4334 adults and 4571 individuals under 18 years, we discover ten new and identify four known variants at five loci influencing IgG subclass levels. These variants also affect the risk of asthma, autoimmune diseases, and blood traits. Seven variants map to the IGH locus, three to the Fcγ receptor (FCGR) locus, and two to the human leukocyte antigen (HLA) region, affecting the levels of all IgG subclasses. The most significant associations are observed between the G1m (f), G2m(n) and G3m(b*) allotypes, and IgG1, IgG2 and IgG3, respectively. Additionally, we describe selective associations with IgG4 at 16p11.2 (ITGAX) and 17q21.1 (IKZF3, ZPBP2, GSDMB, ORMDL3). Interestingly, the latter coincides with a highly pleiotropic signal where the allele associated with lower IgG4 levels protects against childhood asthma but predisposes to inflammatory bowel disease. Our results provide insight into the regulation of antibody-mediated immunity that can potentially be useful in the development of antibody based therapeutics.

The Effect of Adding Azolla Plant Powder in Quail Diets on The Carcass Traits and Some Blood Traits

The Effect of Adding Azolla Plant Powder in Quail Diets on The Carcass Traits and Some Blood Traits

PRCP is a promising drug target for intracranial aneurysm rupture supported via multi-omics analysis

BackgroundCerebral aneurysms are life-threatening cerebrovascular disorders. Currently, there are no effective treatments for preventing disease progression. Mendelian randomisation (MR) is widely used to repurify licensed drugs and identify new therapeutic...

Tropomyosin 1 deficiency facilitates cell state transitions and enhances hemogenic endothelial cell specification during hematopoiesis

Tropomyosins coat actin filaments to impact actin-related signaling and cell morphogenesis. Genome-wide association studies have linked Tropomyosin 1 (TPM1) with human blood trait variation. TPM1 has been shown to regulate blood cell formation invitro, but it remains unclear how or when TPM1 affects hematopoiesis. Using gene-edited induced pluripotent stem cell (iPSC) model systems, we found that TPM1 knockout augmented developmental cell state transitions and key signaling pathways, including tumor necrosis factor alpha (TNF-α) signaling, to promote hemogenic endothelial (HE) cell specification and hematopoietic progenitor cell (HPC) production. Single-cell analyses revealed decreased TPM1 expression during human HE specification, suggesting that TPM1 regulated invivo hematopoiesis via similar mechanisms. Analyses of a TPM1 gene trap mouse model showed that TPM1 deficiency enhanced HE formation during embryogenesis, without increasing the number of hematopoietic stem cells. These findings illuminate novel effects of TPM1 on developmental hematopoiesis.

Impact of olive leaves supplementation in Awassi lambs ration on some productive and biochemical blood traits

Impact of olive leaves supplementation in Awassi lambs ration on some productive and biochemical blood traits

Causal relationship between blood traits and severe influenza A(H1N1)pdm09 infection in East Asian: A Mendelian randomization study.

Although a range of blood traits have been reported to be associated with influenza A(H1N1)pdm09 (H1N1pdm09) disease severity, their underlying causal relationships and biological mechanisms have remained unclear. This study aimed to investigate the causal relationship between blood traits and H1N1pdm09 using a two-sample Mendelian randomization analysis. Based on the data from our in-house genome-wide association study (GWAS) on H1N1pdm09 disease severity (Ncase [severe] = 70, Ncontrol [mild] = 95) and GWAS summaries of 44 blood traits from Biobank Japan (N = 12 303-143 658), we identified the potential causal effect of blood traits on severe H1N1pdm09. The inversevariance weightedmethodanalysis revealed significant causal effects of lower aspartate aminotransferase (AST, β = -3.212, p = 0.019), low-density-lipoprotein cholesterol (LDL-C, β = -1.372, p = 0.045), and basophil counts (Baso, β = -1.638, p = 0.047) on severe H1N1pdm09 disease. Additionally, polygenic risk score analysis further confirmed genetic overlap between these blood traits and severe H1N1pdm09 disease. This study provided evidence linking the lower level of AST, LDL-C, and lower count of Baso with severe H1N1pdm09 disease, potentially identifying new therapeutic targets for patients with severe influenza.

The broad impact of cell death genes on the human disease phenome

Cell death mediated by genetically defined signaling pathways influences the health and dynamics of all tissues, however the tissue specificity of cell death pathways and the relationships between these pathways and human disease are not well understood. We analyzed the expression profiles of an array of 44 cell death genes involved in apoptosis, necroptosis, and pyroptosis cell death pathways across 49 human tissues from GTEx, to elucidate the landscape of cell death gene expression across human tissues, and the relationship between tissue-specific genetically determined expression and the human phenome. We uncovered unique cell death gene expression profiles across tissue types, suggesting there are physiologically distinct cell death programs in different tissues. Using summary statistics-based transcriptome wide association studies (TWAS) on human traits in the UK Biobank (n ~ 500,000), we evaluated 513 traits encompassing ICD-10 defined diagnoses and laboratory-derived traits. Our analysis revealed hundreds of significant (FDR < 0.05) associations between genetically regulated cell death gene expression and an array of human phenotypes encompassing both clinical diagnoses and hematologic parameters, which were independently validated in another large-scale DNA biobank (BioVU) at Vanderbilt University Medical Center (n = 94,474) with matching phenotypes. Cell death genes were highly enriched for significant associations with blood traits versus non-cell-death genes, with apoptosis-associated genes enriched for leukocyte and platelet traits. Our findings are also concordant with independently published studies (e.g. associations between BCL2L11/BIM expression and platelet & lymphocyte counts). Overall, these results suggest that cell death genes play distinct roles in their contribution to human phenotypes, and that cell death genes influence a diverse array of human traits.

The The Effect of Adding Different Levels of Aqueous Extract of Cloves to the Drinking Water of Broiler Chickens (Ross 308) on Blood Biochemical Characteristics and Some Indicators of Oxidative Stress

This study was conducted in the poultry field of the Department of Animal Production College of Agriculture - University of Karbala for a period of 35 days, from 6/10/2022 to 9/11/2022, to demonstrate the effect of the aqueous extract of cloves added to the drinking water of broiler chickens on blood traits. Biochemistry and some indicators of oxidation, where 240 Ross308 broiler chicks were used, one day old, unsexed, and the average weight of the chicks was 40 gm, distributed randomly into 4 treatments and each treatment 3 replicates of 20 chicks "for each replicate, and the aqueous extract was added to the drinking water Since the first day, my agencies: T1: control treatment without addition, T2: adding 10 ml / liter of water, T3: adding 20 ml / liter of water, T4: adding 30 ml / liter of water, and the most important results that we obtained were summarized: A highly significant increase (p≤ 01) in the blood serum glucose concentration of the T4 treatment compared to the control treatment. As for the T3 treatment, it excelled at the level of (p≤ 0.01) in the concentration of total protein, albumin and globulin, as well as cholesterol, triglycerides and LDL, compared to the control treatment. The results showed a highly significant increase (p ≤ 0.01) in the ALT enzyme for the T3 treatment. As for the AST enzyme, its concentration increased in the T2 treatment, which was similar to the control treatment in the significance of this enzyme. In the same results, a highly significant (p ≤ 0.01) superiority was observed in the concentration of GPX enzyme for T4, T3 treatment over T2, T1 treatments. As for the CAT enzyme, its concentration increased at a significant level (p ≤ 0.01) in T3 treatment birds, but it was significantly similar to the control treatment. As for the T4 treatment, it increased significantly in the MDA rate compared to the control treatment

Searching for gene-gene interactions through variance quantitative trait loci of 29 continuous Taiwan Biobank phenotypes.

Introduction: After the era of genome-wide association studies (GWAS), thousands of genetic variants have been identified to exhibit main effects on human phenotypes. The next critical issue would be to explore the interplay between genes, the so-called "gene-gene interactions" (GxG) or epistasis. An exhaustive search for all single-nucleotide polymorphism (SNP) pairs is not recommended because this will induce a harsh penalty of multiple testing. Limiting the search of epistasis on SNPs reported by previous GWAS may miss essential interactions between SNPs without significant marginal effects. Moreover, most methods are computationally intensive and can be challenging to implement genome-wide. Methods: I here searched for GxG through variance quantitative trait loci (vQTLs) of 29 continuous Taiwan Biobank (TWB) phenotypes. A discovery cohort of 86,536 and a replication cohort of 25,460 TWB individuals were analyzed, respectively. Results: A total of 18 nearly independent vQTLs with linkage disequilibrium measure r 2 < 0.01 were identified and replicated from nine phenotypes. 15 significant GxG were found with p-values <1.1E-5 (in the discovery cohort) and false discovery rates <2% (in the replication cohort). Among these 15 GxG, 11 were detected for blood traits including red blood cells, hemoglobin, and hematocrit; 2 for total bilirubin; 1 for fasting glucose; and 1 for total cholesterol (TCHO). All GxG were observed for gene pairs on the same chromosome, except for the APOA5 (chromosome 11)-TOMM40 (chromosome 19) interaction for TCHO. Discussion: This study provided a computationally feasible way to search for GxG genome-wide and applied this approach to 29 phenotypes.

The impact of using slow-release urea instead of fast-release urea in feed on the milk production of Awassi sheep and some blood traits

The impact of using slow-release urea instead of fast-release urea in feed on the milk production of Awassi sheep and some blood traits

Genetic estimates studies of morphometric, physiological and blood traits of mixed breed of rabbits

This study was conducted to determine the genetic estimates and blood traits of mixed breed of rabbits at different stages of growth. Three hundred and sixty rabbits comprising crosses of New Zealand White and Chinchilla breeds were used. Morphometric traits such as body weight, shoulder to tail length, head to shoulder length, trunk length, height at withers, ear length, heart girth, forelimb length, hind limb length and nose to shoulder length were recorded weekly. Blood samples were taken at 32 and 48 weeks to assess haematological and serum biochemical indices while physiological parameters such as rectal temperature, pulse rate and respiratory rate were determined as well. The data collected were analyzed using SAS (2008) to determine the phenotypic correlations among blood and physiological traits of mixed breed of rabbits; to estimate realized heritability and repeatability of morphometric and physiological traits. Results obtained are low to high heritability (0.13 to 0.99) and repeatability (0.07 to 0.90) estimates of morphometric and physiological parameters from mixed breeds of rabbits at different ages were obtained in this study. The high heritability estimates could be as a result of additive gene effect that gave rise to high genetic variability. The implication of this is that individual selection will lead to high genetic gain, while the repeatability of these traits being high, suggests that the likelihood to repeat these records is high. Further studies should be conducted involving larger datasets, which would yield more precise estimates of heritability and repeatability Cette étude a été menée pour déterminer les estimations génétiques et les traits sanguins de races mixtes de lapins à différents stades de croissance. Trois cent soixante lapins issus de croisements de races néo-zélandaises blanches et chinchillas ont été utilisés. Les caractéristiques morphométriques telles que le poids corporel, la longueur de l'épaule à la queue, la longueur de la tête à l'épaule, la longueur du tronc, la hauteur au garrot, la longueur des oreilles, la circonférence du cœur, la longueur des membres antérieurs, la longueur des membres postérieurs et la longueur du nez à l'épaule ont été enregistrées chaque semaine. Des échantillons de sang ont été prélevés à 32 et 48 semaines pour évaluer les indices hématologiques et biochimiques sériques, tandis que les paramètres physiologiques tels que la température rectale, le pouls et la fréquence respiratoire ont également été déterminés. Les données collectées ont été analysées à l'aide de SAS (2008) pour déterminer les corrélations phénotypiques entre les traits sanguins et physiologiques des races mixtes de lapins ; pour estimer l'héritabilité et la répétabilité réalisées des traits morphométriques et physiologiques. Les résultats obtenus sont des estimations d'héritabilité faible à élevée (0,13 à 0,99) et de répétabilité (0,07 à 0,90) des paramètres morphométriques et physiologiques de races mixtes de lapins à différents âges ont été obtenues dans cette étude. Les estimations élevées de l'héritabilité pourraient résulter d'un effet génétique additif qui a donné lieu à une forte variabilité génétique. Cela implique que la sélection individuelle entraînera un gain génétique élevé, tandis que la répétabilité de ces caractères étant élevée, cela suggère que la probabilité de répéter ces enregistrements est élevée. D'autres études devraient être menées sur des ensembles de données plus vastes, ce qui permettrait d'obtenir des estimations plus précises de l'héritabilité et de la répétabilité.

Investigation on adaptations of broiler chickens to high dietary free amino acid levels in nitrogen utilisation and plasma amino acid concentrations

ABSTRACT 1. A reduction in crude protein (CP) in feed for broiler chickens necessitates elevated free amino acid (AA) levels to meet the requirement of each AA. This study investigated adaptations following a change to diets with increasing free AA concentrations and possible reasons for the limitation caused by the inclusion of more free AA. 2. Male Ross 308 broiler hatchlings received a starter diet (164 g CP/kg containing 80 g/kg soy protein isolate (SPI)) until d 7. From d 7–22, birds received a diet almost identical to the starter diet or two other diets, where 50% or 100% of digestible AA in SPI were substituted with a free AA mixture. Birds were allocated to metabolism units located in the same barn to determine performance (n = 7 units) and blood traits (n = 14 birds). Total excreta collection was performed on d 7–8, 8–9, 9–10, 11–12, 14–15 and 21–22. Blood samples were collected on d 7, 8, 9, 11, 14 and 21. 3. Average daily weight gain (ADG) and average daily feed intake (ADFI) was unaffected at 50% AA substitution but decreased at 100% AA substitution on d 7–22 (p ≤ 0.001). The 100% substitution led to a decline in ADG and ADFI consistently on all days (p ≤ 0.037) except on d 11–12. A 50% AA substitution resulted in lower ADFI on d 7–8 and 14–15 (p ≤ 0.032). Nitrogen utilisation efficiency (NUE) was on a level of ~ 0.74 and was only affected by treatment up to d 11–12 (p ≤ 0.008). Concentrations of 10, 9, 8, 10 and 4 plasma free AA were affected on d 8, 9, 11, 14 and 21, respectively (p ≤ 0.037). 4. Following a change to diets containing high levels of free AA, NUE and free AA concentrations in the circulation became more balanced within 3 to 7 d. The results suggested that peptide-bound and free AA did not cause different NUE, particularly 3 and 7 d after the diet change.

Biological basis of extensive pleiotropy between blood traits and cancer risk.

The immune system has a central role in preventing carcinogenesis. Alteration of systemic immune cell levels may increase cancer risk. However, the extent to which common genetic variation influences blood traits and cancer risk remains largely undetermined. Here, we identify pleiotropic variants and predict their underlying molecular and cellular alterations. Multivariate Cox regression was used to evaluate associations between blood traits and cancer diagnosis in cases in the UK Biobank. Shared genetic variants were identified from the summary statistics of the genome-wide association studies of 27 blood traits and 27 cancer types and subtypes, applying the conditional/conjunctional false-discovery rate approach. Analysis of genomic positions, expression quantitative trait loci, enhancers, regulatory marks, functionally defined gene sets, and bulk- and single-cell expression profiles predicted the biological impact of pleiotropic variants. Plasma small RNAs were sequenced to assess association with cancer diagnosis. The study identified 4093 common genetic variants, involving 1248 gene loci, that contributed to blood-cancer pleiotropism. Genomic hotspots of pleiotropism include chromosomal regions 5p15-TERT and 6p21-HLA. Genes whose products are involved in regulating telomere length are found to be enriched in pleiotropic variants. Pleiotropic gene candidates are frequently linked to transcriptional programs that regulate hematopoiesis and define progenitor cell states of immune system development. Perturbation of the myeloid lineage is indicated by pleiotropic associations with defined master regulators and cell alterations. Eosinophil count is inversely associated with cancer risk. A high frequency of pleiotropic associations is also centered on the regulation of small noncoding Y-RNAs. Predicted pleiotropic Y-RNAs show specific regulatory marks and are overabundant in the normal tissue and blood of cancer patients. Analysis of plasma small RNAs in women who developed breast cancer indicates there is an overabundance of Y-RNA preceding neoplasm diagnosis. This study reveals extensive pleiotropism between blood traits and cancer risk. Pleiotropism is linked to factors and processes involved in hematopoietic development and immune system function, including components of the major histocompatibility complexes, and regulators of telomere length and myeloid lineage. Deregulation of Y-RNAs is also associated with pleiotropism. Overexpression of these elements might indicate increased cancer risk.

The Born in Guangzhou Cohort Study enables generational genetic discoveries.

Genomic research that targets large-scale, prospective birth cohorts constitutes an essential strategy for understanding the influence of genetics and environment on human health1. Nonetheless, such studies remain scarce, particularly in Asia. Here we present the phase I genome study of the Born in Guangzhou Cohort Study2 (BIGCS), which encompasses the sequencing and analysis of 4,053 Chinese individuals, primarily composed of trios or mother-infant duos residing in South China. Our analysis reveals novel genetic variants, a high-quality reference panel, and fine-scale local genetic structure within BIGCS. Notably, we identify previously unreported East Asian-specific genetic associations with maternal total bile acid, gestational weight gain and infant cord blood traits. Additionally, we observe prevalent age-specific genetic effects on lipid levels in mothers and infants. In an exploratory intergenerational Mendelian randomization analysis, we estimate the maternal putatively causal and fetal genetic effects of seven adult phenotypes on seven fetal growth-related measurements. These findings illuminate the genetic links between maternal and early-life traits in an East Asian population and lay the groundwork for future research into the intricate interplay of genetics, intrauterine exposures and early-life experiences in shaping long-term health.

A Pregnancy and Childhood Epigenetics Consortium (PACE) meta-analysis highlights potential relationships between birth order and neonatal blood DNA methylation

Higher birth order is associated with altered risk of many disease states. Changes in placentation and exposures to in utero growth factors with successive pregnancies may impact later life disease risk via persistent DNA methylation alterations. We investigated birth order with Illumina DNA methylation array data in each of 16 birth cohorts (8164 newborns) with European, African, and Latino ancestries from the Pregnancy and Childhood Epigenetics Consortium. Meta-analyzed data demonstrated systematic DNA methylation variation in 341 CpGs (FDR adjusted P < 0.05) and 1107 regions. Forty CpGs were located within known quantitative trait loci for gene expression traits in blood, and trait enrichment analysis suggested a strong association with immune-related, transcriptional control, and blood pressure regulation phenotypes. Decreasing fertility rates worldwide with the concomitant increased proportion of first-born children highlights a potential reflection of birth order-related epigenomic states on changing disease incidence trends.

Multi-omics Mendelian randomization integrating GWAS, eQTL, and mQTL data identified genes associated with breast cancer.

Breast cancer (BC) remains a major disease posing a threat to women's health, but the underlying biological interpretation remains largely unknown. Here, we aimed to identify genes associated with breast cancer and analyze their pathophysiological mechanisms based on multi-omics Mendelian randomization (MR). Summary-data-based MR (SMR) was performed to estimate the causal effects of blood and breast mammary tissue expression quantitative trait loci (eQTLs) on BC. External validation analysis was used to validate the identified genes. Integration analyses BC GWAS summaries with eQTLs and DNA methylation QTLs (mQTLs) from the blood were conducted using SMR to prioritize putative blood genes and their regulatory elements associated with BC risk. Finally, two prior genes (ATG10 and RCCD1) from blood tissue reached significant levels in both BCAC (ATG10: ORBRCR = 0.91, PBRCR = 1.29 × 10-11; RCCD1: ORBRCR = 0.90, PBRCR = 3.72 × 10-15) and FinnGen cohorts (ATG10: ORFinnGen = 0.89, PFinnGen = 8.55 × 10-5; RCCD1: ORFinnGen = 0.89, PFinnGen = 2.38 × 10-8). Additionally, those two genes from breast tissues also replicated in both BCAC (ATG10: ORBRCR = 0.95, PBRCR = 1.02 × 10-9; RCCD1: ORBRCR = 0.87, PBRCR = 4.70 × 10-10) and FinnGen cohorts (ATG10: ORFinnGen = 0.93, PFinnGen = 2.38 × 10-4; RCCD1: ORFinnGen = 0.85, PFinnGen = 3.81 × 10-6). Sensitive analysis and external validation analysis validated those two identified genes. Multi-omics MR analysis showed that the SNP signals associated with ATG10 and RCCD1 were significant across the data from BC Genome-wide association study (GWAS), eQTL, and mQTL studies. In conclusion, we identified two priority genes that are potentially associated with BC. These findings improve our limited understanding of the mechanism of BC and shed light on the development of therapeutic agents for treating BC.

The effect of replacing slow-release urea (Menogen) instead of fast-release urea on the weight of ewes and Awassi lambs until weaning, milk production, and some biochemical blood traits

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