Liang He

The paper identifies a mature dendritic cell subtype associated with improved immune response and prognosis in melanoma patients treated with anti-PD-1 checkpoint inhibitors.

The paper identifies DNA methylation markers associated with breast cancer risk in twin pairs, showing most are independent of genetic effects and linked to environmental factors.

The paper introduces a robust and fast two-sample test for equal Pearson correlations, demonstrating its accuracy and efficiency in detecting differential co-expression.

The paper identifies inter- and intra-chromosomal polymorphisms that modulate the risk of Alzheimer's disease associated with APOE ε2 and ε4 alleles through LD analysis and functional analysis.

The paper identifies allele-specific eQTLs for Alzheimer's disease variants in brain regions and cell types using bulk RNA-seq and single nuclei data.

NEBULA improves differential expression and co-expression analysis in large-scale multi-subject single-cell data by efficiently handling overdispersion with a negative binomial mixed model.

This study identifies exonic variants in ERN1, TACR3, and SPPL2C associated with Alzheimer's disease through exome-wide age-of-onset analysis, with functional insights into their regulatory roles.

The paper deconvolves 3,387 post-mortem brain samples using SPLITR to identify cell-type-specific eQTLs and genetic effects in mental disorders.

This paper introduces COXMEG, an efficient R package for GWAS of age-at-onset traits using Cox mixed-effects models, demonstrating improved computational efficiency and statistical power.

This paper introduces a causal inference method to estimate genetic variance and pleiotropy from GWAS summary data, showing improved power and accuracy in simulations and real-world applications.

The paper introduces HiDRA, a method for high-resolution functional analysis of regulatory regions, identifying 13,000 driver elements and linking them to disease-associated variants.

This paper introduces a Bayesian method to identify causal genes in Alzheimer’s disease by distinguishing mediation from pleiotropy using summary statistics, finding 206 causal genes.