Skip to content
View DrZoggg's full-sized avatar

Highlights

  • Pro

Block or report DrZoggg

Block user

Prevent this user from interacting with your repositories and sending you notifications. Learn more about blocking users.

You must be logged in to block users.

Content in all repositories owned by your account will be closed.
Maximum 250 characters. Please don’t include any personal information such as legal names or email addresses. Markdown is supported. This note will only be visible to you.
Report abuse

Contact GitHub support about this user’s behavior. Learn more about reporting abuse.

Report abuse
DrZoggg/README.md
Ge Zhang — AI for Science and Biomedical Knowledge Discovery

Integrating multimodal clinical data, multi-omics, computational inference, and mechanistic biology to decode complex chronic diseases.

Zhengzhou University  ·  Cardiovascular Medicine  ·  Computational Biomedicine

Academic Website  ·  Google Scholar  ·  ORCID  ·  ResearchGate


Scientific Focus

I study how disease heterogeneity emerges across clinical, molecular, cellular, and temporal scales, with particular emphasis on atherosclerosis, vascular smooth muscle cell plasticity, and circadian disruption.

Research Architecture

01 · CLINICAL INTELLIGENCE

AI for Science & Multimodal Clinical Intelligence

Interpretable models for population-scale risk stratification and discovery.
02 · VASCULAR SYSTEMS

Atherosclerosis & Vascular Systems Biology

Plaque vulnerability, vascular microenvironments, and smooth muscle cell plasticity.
03 · CROSS-SCALE OMICS

Multi-omics & Translational Discovery

Cross-scale integration to resolve heterogeneity and prioritize mechanistic drivers.
04 · TEMPORAL BIOLOGY

Circadian Disruption & Disease Biology

Circadian dysregulation linking molecular states, vascular dysfunction, and disease progression.

Selected Research

Research Domain Scientific Contribution
AIHFLevel Clinical AI · Heart failure Interpretable multicenter survival assessment and individualized risk stratification.
APVS Atherosclerosis · Plaque biology Biologically interpretable quantification of plaque vulnerability.
ClockProCRC Circadian systems biology · Cancer Cross-cohort inference of circadian misalignment and molecular clock states.
KIF13B Vascular biology · VSMC fate Mechanistic resolution of a VSMC state axis governing plaque stability.
LDL Atherosclerosis · State transitions Transition signals and high-resolution networks across lesion states.

Selected Publications

  1. AI hybrid survival assessment for advanced heart failure patients with renal dysfunction
    Nature Communications · 2024

  2. Vascular smooth muscle cell-derived KIF13B inhibits proinflammatory responses to protect against atherosclerosis
    Journal of Clinical Investigation · 2026

  3. System biology analysis reveals circadian rhythm disorder associated with development and progression in colorectal cancer
    npj Precision Oncology · 2026

  4. Atherosclerotic plaque vulnerability quantification system for clinical and biological interpretability
    iScience · 2023

Explore the complete, maintained record on the Academic Website or Google Scholar.

Research Ecosystem

Clinical phenotypes → cross-scale omics → computational inference → mechanistic discovery → translation.

Connect

For the full research record, publication-level resources, and current scientific program, visit drgezhang.com. Persistent identity: ORCID 0000-0002-3116-3246.

Decoding complexity into biomedical knowledge

Popular repositories Loading

  1. AIHFLevel AIHFLevel Public

    5

  2. APVS APVS Public

    An atherosclerotic plaque vulnerability quantification system

    R 1

  3. ALS ALS Public

    1

  4. ClockProCRC ClockProCRC Public

    R

  5. KIF13B-in-Atherosclerosis KIF13B-in-Atherosclerosis Public

    R

  6. LDL LDL Public

    R