Biomedical subjects

Jiarui Cai

Publications and source records attributed to Jiarui Cai.

2 recordsLinked to original sources

PubMed2026

Failures to maintain CpG-methylation of CoRSIVs in bovine sperm are associated with low sire conception.

In brief: Correlated regions of systemic interindividual epigenetic variation (CoRSIVs) are genomic regions with CpG-methylation patterns that differ between individuals, yet are consistent between tissues, within the same individual. Analyzing two groups of Holstein bull methylomes-nine with a high sire-conception rate (SCR) and nine with a low SCR-we found that a common type of CoRSIVs was significantly associated with reduced SCR and is thus suggested as a biomarker for SCR because it was highly methylated in sperm, but failed to retain hypermethylation in the gametes of males with low SCR. Abstract: Correlated regions of systemic interindividual epigenetic variation (CoRSIVs) are genomic regions with CpG-methylation patterns that differ between individuals, yet are consistent between tissues, within the same individual; therefore, their methylation can be profiled in bodily fluids that are easily obtained, such as blood and semen. Bearing in mind the simple epigenetic profiling of CoRSIVs, we tested whether this type of differentially methylated region (DMR) is associated with bovine fertility. Sequence Read Archive (SRA) meth BLAST was used to estimate CoRSIVs methylation status in 18 healthy, representative, and age-matched Holstein bulls, among which nine had high (H) sire-conception rate (SCR), and the other nine had low (L) SCR (group averages of SCR: 3.3 ± 0.6 and -3.8 ± 1.8, respectively). This method was also applied to morula and trophoblast SRA methylomes. Analysis with meth BLAST was effective for most (80%) CoRSIVs and showed that CoRSIVs are reprogrammed during blastocyst formation, although this method was incapable of specifically determining the methylation level in CoRSIVs with retrotransposons. In sperm, the effect of global methylation was evident in a common (25%) type of CoRSIVs that is highly (94.5% ± 4.3%) methylated in sperm. Specifically, a failure to retain hypermethylation in the sperm plus strand was significantly (p < 0.00025) indicative of low SCR. Comparing global DNA methylation using the latter type of CoRSIVs between sperm and blood can be used as a better biomarker for fertility than using other differentially methylated regions with more complex epigenetics.

Animals↗

PubMed2026

The causal relationships and potential pathways between birth weight and cardiovascular diseases: A human genomics study.

The causal relationships and potential pathways between birth weight (BW) and various cardiovascular diseases (CVDs) remain unclear, particularly when discriminating maternal and fetal contributions of BW to CVDs. Leveraging the genome-wide association studies (GWASs) of BW (N = 321,223) and a range of CVDs (ncases = 43,676-181,522), we performed a 2-sample Mendelian randomization (MR) analysis to estimate the causal effect of BW, fetal-specific BW, and maternal-specific BW on coronary artery disease (CAD), myocardial infarction (MI), heart failure (HF), atrial fibrillation (AF), and stroke. Furthermore, we applied a stepwise MR analysis approach to assess the potential involvement of childhood body mass index (CBMI) and age at menarche (AAM) in the causal pathways from BW to CVDs, while considering adult BMI. Finally, we performed colocalization analyses to justify the different biological mechanisms of maternal-specific and fetal-specific BW. The 2-sample MR analysis revealed that genetically predicted higher BW per standard deviation (SD) was associated with a decreased risk of CAD (odds ratio [OR] = 0.804, 95% confidence interval [CI]: 0.731-0.883), MI (OR = 0.720, 95% CI: 0.638-0.814), and stroke (OR = 0.900, 95% CI: 0.823-0.985), but an increased risk of AF (OR = 1.279, 95% CI: 1.160-1.410). Similar associations were observed for fetal-specific/maternal-specific BW. The stepwise MR analysis indicated that CBMI and AAM could serve as factors linking BW/fetal-specific BW and CVDs, albeit in different roles, by displaying an indirect causal effect through adult BMI. However, for maternal-specific BW, our results failed to support a causal effect on CBMI or AAM. Colocalization analyses supported the distinct biological mechanisms for maternal-specific and fetal-specific BW by showing different causal genes. The study suggested that both fetal genotype and intrauterine environmental exposure contribute to the causal associations. Additionally, AAM and CBMI may play a role in the pathways linking BW and CVDs, though the effect was only observed for fetal-specific BW.

Humans↗