
Yinmin Morris Wang
· ProfessorVerifiedUniversity of California, Los Angeles · Materials Science and Engineering
Active 1991–2026
About
Yinmin Morris Wang is a Professor of Materials Science and Engineering at UCLA Samueli School of Engineering. His research interests bridge the synthesis of nanostructured materials, additive manufacturing, and understanding the mechanisms that control the mechanical behavior of advanced materials such as metals, alloys, carbon-based materials, 2D materials, and porous materials. His group employs in situ characterization techniques, including synchrotron x-ray diffraction, computed tomography, and transmission electron microscopy, to probe defect interactions with surfaces or interfaces. The focus of his research is on achieving high-performance structural materials through microstructure engineering, with occasional interest in their functional properties like electrical conductivity, corrosion resistance, catalytic activities, and electrochemical energy storage capacity. His experimental work is often coupled with computer modeling to deepen understanding of structure-property relationships. He has made notable contributions to the field, including research on metal 3D printing, defect-induced softening in nanocrystalline metals, and additively manufactured hierarchical stainless steels, among others. Dr. Wang earned his Ph.D. in Materials Science from Johns Hopkins University in 2003 and has received numerous awards, including being recognized as one of the top 2% most cited researchers in his field and being a Fellow of the American Physical Society.
Research topics
- Internal medicine
- Medicine
- Biology
- Pathology
- Genetics
- Cell biology
- Endocrinology
- Oncology
- Surgery
- Gastroenterology
- Immunology
- Cardiology
Selected publications
DA-GMGENet: A Domain Adaptation Framework for 3D CT-Based ECE Identification in Head and Neck Cancer
2026-04-08
article1st authorCorrespondingIdentification of lymph node Extracapsular Extension (ECE) is crucial for the diagnosis and clinical decision making of head and neck squamous cell carcinoma (HNSCC). Despite the advancements of automatic ECE identification, the effect of adversary during transferring the developed model to different environments may still cause instability in the performance metrics. The aim of this study is to develop a model which can perform under adversary and reduce the discrepancy between the source and target domain. Here, we introduce Domain Adaptation enhanced Gradient Mapping Guided Explainable Network (DA-GMGENet) which leverages an automatic ECE identification from unlabeled target dataset as well as ensures the transfer ability of the model by increasing the robustness under worst case domain shift. Evaluation on a public dataset gives the best AUC of 78.1% and sensitivity of 71.6% compared to some existing methods. Finally, we utilize the Kernel Density Estimate (KDE) plot to visualize the features between the source and target data which shows features of both domains can be aligned using the proposed method.
Energy · 2026-05-04
articleNon‐Invasive Brain Targeted Delivery of Cannabidiol for Alleviating Neuroinflammatory Disease
Advanced Materials · 2026-04-29
articleOpen access1st authorCorrespondingChronic neuroinflammation is a known etiopathogenic factor in neurodegenerative disease. While cannabidiol (CBD) has demonstrated anti-inflammatory effects, unfavorable pharmacokinetics and poor blood-brain barrier (BBB) permeability lead to low brain exposure. Here, we greatly improve the efficacy of CBD to treat neuroinflammation by incorporating CBD in a BBB-permeable glucose nanoparticle (GNPs) that by design also incorporates tissue-targeting moieties and uses reactive oxygen species responsive polymer to selectively target neuroinflammatory lesions. We achieved a high drug concentration over 20 times higher than naked cargo and demonstrate potent therapeutic effects in two mouse models of neuroinflammatory disease. Mechanistically, disease amelioration resulted from repolarizing microglia from the neurotoxic M1 to the neuroprotective M2 phenotype, leading to neuronal cell regeneration by enhanced secretion of brain derived neurotropic and anti-inflammatory factors. Our approach for brain targeted CBD delivery may provide a versatile platform for treating other CNS disorders characterized by neuroinflammation.
Epitranscriptomic control of VSMC plasticity: expanding the landscape beyond m6A
Cardiovascular Research · 2026-04-21
articleSenior authorTargeting Fcgr1 to repress FAPy-adenine-induced osteoporosis in osteosarcoma receiving chemotherapy
Biomedical Technology · 2025-11-19 · 1 citations
articleOpen accessChemotherapy-induced bone loss in patients with osteosarcoma (OS) has attracted increasing attention worldwide. Previous studies have revealed the interactions between OS cells and osteoclasts via secretion of various cytokines. However, the specific impacts of chemically injured OS cells on osteoclast functions remain unknown. Untargeted metabolomics is a high-throughput analytical technique used to screen potential biomarkers and identify unknown metabolites in various biological samples. In this study, cisplatin (CDDP)-injured OS cell supernatant promoted the osteoclast differentiation of bone marrow macrophages (BMMs). Untargeted metabolomic analysis revealed the metabolic profile of injured OS cells, and FAPy-adenine (FA), which was upregulated by approximately 2000-fold, was identified in the supernatant. FA promoted the osteoclast differentiation of BMMs in a dose-dependent manner. RNA sequencing revealed increased Fc gamma receptor 1 (Fcgr1) expression levels in FA-treated BMMs. Fcgr1 overexpression promoted the osteoclast differentiation of BMMs and Cathepsin K expression, whereas its knockdown inhibited the pro-osteoclast differentiation effect of FA. Furthermore, FA accelerated osteoporosis progression in ovariectomy model rats. Upregulation of Fcgr1 levels promoted bone loss, whereas its silencing inhibited the bone loss induced by FA in ovariectomy model rats. Collectively, these findings suggest that FA released from CDDP-injured OS cells contributes to osteoporosis progression by upregulating Fcgr1 levels, providing new insights into chemotherapy-induced bone loss in patients with OS.
Frontiers in Medicine · 2025-12-18
articleOpen accessBackground Timely administration of antivenom remains the cornerstone of treatment for hemotoxic snakebite envenoming, primarily aimed at neutralizing circulating toxins and halting the progression of venom-induced consumption coagulopathy (VICC), thus facilitating gradual recovery of the hemostatic system. However, immediate access to antivenom is not always possible, and variations in venom composition among snake species, along with individual patient differences, can result in significant morbidity (including persistent complications of coagulopathy) and mortality. Methods This retrospective study evaluated 116 cases of hemotoxic snakebite envenoming caused by Trimeresurus stejnegeri, T. mucrosquamatus , and Agkistrodon halys at three hospitals in Yunnan Province, China (The First People's Hospital of Yunnan Province 63 cases, The People's Hospital of Linxiang District 28 cases, and The First People's Hospital of Xuanwei City 25 cases). Among these, thirty-three patients consented to receive adjunctive therapy with fibrinogen (Fg) in addition to standard antivenom treatment ( Agkistrodon acutus antivenom or Agkistrodon halys antivenom), while the remaining 83 received antivenom alone. Coagulation parameters were measured at admission and discharge. Statistical analyses were performed using IBM SPSS Statistics and GraphPad Prism, employing the Mann-Whitney U test for non-normally distributed data and Student's t -test for normally distributed data. Results In the antivenom-only group, significant reductions were observed in prothrombin time (PT), international normalized ratio (INR), activated partial thromboplastin time (APTT), and D-dimer (DD2) levels (all P < 0.05), accompanied by increases in Fg and fibrin degradation products (FDP; P < 0.05). Patients receiving the combined regimen demonstrated decreases in PT, INR, thrombin time (TT), APTT, FDP, and DD2 (all P < 0.05), along with a significant rise in Fg levels ( P < 0.05). Those who received Fg presented with more severe coagulation deficits at baseline. Despite this, by the time of discharge, the median Fg level in the combination group [1.94 (1.52–2.20) g/L] was significantly higher than in the antivenom-only group [0.84 (0.68–1.17) g/L] ( P < 0.0001), and closer to the physiological range (2–4 g/L). Moreover, the hospital stay in the combination group (4.88 ± 1.47 days) was significantly shorter than in the antivenom-only group (7.07 ± 2.02 days; P < 0.0001). Conclusions These findings suggest that adjunctive Fg supplementation may improve the laboratory parameters of coagulopathy and reduce the length of hospital stay in hemotoxic snakebite envenoming. However, further clinical evaluations are needed to support the use of Fg as an adjuvant in the management of hemotoxic snakebite envenoming.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-15
articleOpen accessAbstract Previous single-cell and single-nucleus heart atlases, often limited by small sample sizes, lack the statistical power needed for phenotype association analysis, particularly for cardiovascular diseases and cardiac aging. To address this, we integrated data from 436 samples across 12 single-cell studies, harmonized the corresponding sample metadata, and constructed a comprehensive heart atlas comprising 355,762 cells and 1,436,719 nuclei. Consensus annotation identified 10 broad cell types and 54 fine-grained subsets. Associating gene expression patterns and cell type proportions with phenotypic data, we identified NRG1 -expressing endocardial cells linked to multiple cardiac diseases and found that interferon (IFN) response signatures mark aging in multiple heart cell types. Importantly, we also developed PopComm, a novel computational method for inferring ligand–receptor (LR) interactions from population-scale single-cell data and quantifying interaction strength for individual samples. Using PopComm, we revealed a close association between the IFN response state and altered cell–cell communication during cardiac aging.
Materials Chemistry and Physics · 2025-12-02
articleBMC Surgery · 2025-12-16
articleOpen accessThis study aimed to evaluate the effects of different tubeless anesthesia strategies on postoperative recovery in patients undergoing video-assisted thoracoscopic (VATS) wedge resection within an enhanced recovery after surgery (ERAS) protocol. In this prospective randomized controlled trial, 120 patients scheduled for elective VATS wedge resection were randomly assigned to one of three groups: double-lumen endotracheal tube intubation (DLETT), laryngeal mask airway combined with intercostal nerve block (LMA + INB), or laryngeal mask airway combined with paravertebral block (LMA + PVB). Primary outcomes included length of hospital stay, time to ambulation and oral intake, and visual analog scale (VAS) pain scores. Secondary outcomes included intraoperative hemodynamics, arterial blood gas analysis, serum inflammatory cytokines (IL-6, IL-1β, TNF-α), postoperative complications, and total hospitalization costs. Patients in the LMA + PVB group had significantly shorter hospital stays and earlier ambulation compared to the DLETT group (p < 0.001). VAS pain scores at rest and during coughing were consistently lower in the LMA + PVB group from 6 to 24 h postoperatively (p < 0.01). Heart rate, mean arterial pressure, and oxygenation parameters—including peripheral capillary oxygen saturation (SpO₂), partial pressure of arterial oxygen (PaO₂), and arterial oxygen saturation (SaO₂)—remained within physiological ranges in all groups throughout the perioperative period. IL-6 and IL-1β levels at 24 h were significantly lower in the LMA groups (p < 0.01). While DLETT provided better surgical field visibility, it was associated with higher rates of sore throat and hoarseness, as well as greater hospitalization costs. Tubeless anesthesia, particularly LMA + PVB, enhances postoperative recovery following VATS wedge resection by reducing pain, inflammation, and hospitalization duration. These findings suggest that LMA + PVB may be a feasible alternative to conventional intubation-based anesthesia in selected clinical settings. This study was registered at the Chinese Clinical Trial Registry (ChiCTR2300073484) on July 12, 2023.
NUAK1 Promotes Diabetic Kidney Disease by Accelerating Renal Tubular Senescence via the ROS/P53 Axis
Diabetes · 2025-11-20 · 2 citations
articleDiabetic kidney disease (DKD) progression involves intricate interactions among senescence, oxidative stress, inflammation, and fibrosis. This study systematically investigates the regulatory role and molecular mechanisms of NUAK1 in DKD pathogenesis. Bioinformatics analysis of Gene Expression Omnibus data sets identified NUAK1 as a differentially expressed gene, validated in human kidney proximal tubule epithelial (HK-2) cells, high-fat diet and streptozotocin-induced DKD mice, d-galactose-induced senescent mice, and human peripheral blood mononuclear cells. Functional studies demonstrated that NUAK1 inhibition via siRNA knockdown, pharmacological inhibitors, or kidney tubule-targeted adeno-associated virus serotype carrying shRNA against NUAK1 delivery attenuated reactive oxygen species-tumor protein 53 (ROS/P53) axis-mediated renal tubular senescence, oxidative stress, inflammation, and fibrosis in vitro and in vivo. Mechanistically, chromatin immunoprecipitation quantitative PCR revealed that transcription factor ETS1 directly binds to the NUAK1 promoter, driving its transcriptional activation in DKD. Furthermore, molecular docking and dynamics simulations identified Asiatic acid (AA) as a potent NUAK1 inhibitor, with a stable binding affinity. AA suppressed NUAK1 expression and downstream pathological processes, ameliorating renal injury in DKD models. These findings elucidate the role and regulatory mechanisms of NUAK1 in modulating ROS/P53 axis-driven tubular senescence and oxidative stress, providing a theoretical basis for structure optimization in drug development targeting NUAK1. ARTICLE HIGHLIGHTS: Mechanisms linking renal tubular senescence to diabetic kidney disease (DKD) progression remain poorly understood. Systematic elucidation of the regulatory role of NUAK1 in the pathogenesis of DKD and its regulatory mechanisms is provided. NUAK1 is upregulated in DKD, promoting senescence via reactive oxygen species-tumor protein 53 under transcriptional activation by E26 transformation-specific 1, while Asiatic acid (AA) directly binds NUAK1 to suppress these pathological processes. NUAK1 emerges as a therapeutic target for DKD, and AA provides a natural scaffold for NUAK1 inhibitor development, offering a strategy to combat diabetes-related renal decline.
Recent grants
NIH · $1.6M · 2014
NIH · $4.7M · 2017
NIH · $3.2M · 2013
Novel Regulatory Circuit in Cardiac Hypertrophy Via RNA Splicing
NIH · $1.5M · 2014–2018
Epigenomic Mechanisms of Heart Failure
NIH · $2.6M · 2015–2020
Frequent coauthors
- 196 shared
Shuxun Ren
- 95 shared
Christoph Rau
Diamond Light Source
- 84 shared
Thomas M. Vondriska
University of California, Los Angeles
- 76 shared
Kenneth R. Chien
Karolinska Institutet
- 74 shared
Weizhong Zhu
- 74 shared
Khalid Chakir
National Institute on Aging
- 74 shared
David A. Kass
Johns Hopkins University
- 69 shared
Shao-jie Fu
Nankai University
Education
- 1993
Ph.D., Cell Biology
Baylor College of Medicine
- 1988
BS, Biological Sciences
New York State Department of State
- 1986
Diploma
Fudan University
Awards & honors
- Top 2% of the most cited researchers throughout their career…
- Director’s S&T Award, Lawrence Livermore National Laboratory…
- Fellow of American Physical Society (2014)
- Selected top five reviewers of Scripta Materialia (2008)
- Nano 50 Innovator Award, Nanotech Brief (2008)
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