PubMed HealthSearch

Biomedical subjects

Yuanyuan Wang

Publications and source records attributed to Yuanyuan Wang.

7 recordsLinked to original sources

Beyond Photometric Consistency: Addressing Loss Insensitivity to Depth Noise in Endoscopic Estimation via Error Calibration.

Self-supervised monocular depth estimation in endoscopy is fundamentally constrained by the ill-posed nature of photometric supervision. In this work, we identify a critical yet overlooked cause of this ambiguity: the inherent insensitivity of photometric loss to depth noise. To overcome this intrinsic limitation, we propose Depth Error Calibration Learning (DECL), a two-stage framework that suppresses prediction variance and mitigates residual errors in self-supervised depth estimation. In Stage I (Variance Reduction), a cyclic depth generation strategy produces multiple depth hypotheses for the input image. The per-pixel empirical variance is quantified and integrated into a dedicated variance loss term, which penalizes inconsistent predictions and encourages the network to generate more stable and reliable depth estimates. In Stage II (Bias Calibration), an image-conditioned diffusion model refines the Stage-I depth prior and mitigates structured residuals through iterative denoising, thereby improving geometric accuracy and global consistency. Extensive experiments on three public endoscopic datasets demonstrate that DECL achieves consistent improvements over representative self-supervised monocular depth estimation methods under the evaluated protocols. Moreover, ablation studies on two representative backbones indicate that DECL is not restricted to a single network implementation, while broader validation on additional backbone families remains necessary. The source code is publicly available at https://github.com/DavidLuBit/EndoDenoising.

Journal Article

A regulatory network underlying idiopathic pulmonary fibrosis.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease in which genetic susceptibility interacts with epithelial, immune, and mesenchymal remodeling. Although the chromosome 11p15.5 locus contains established IPF susceptibility signals near MUC5B and TOLLIP, the broader regulatory architecture of this region remains incompletely resolved. METHODS: We integrated IPF genome-wide association study summary statistics with methylation, expression, and protein quantitative trait loci using summary-data-based Mendelian randomization (SMR). SMR-prioritized candidates were evaluated in independent transcriptomic and methylation cohorts and further contextualized using microRNA, transcription-factor, protein-interaction, machine-learning, single-cell, and spatial transcriptomic analyses. Fibrosis-associated expression patterns were assessed in a bleomycin-induced pulmonary fibrosis rat model. RESULTS: The analyses recovered the established MUC5B and TOLLIP signals and prioritized BRSK2 as a comparatively underexplored candidate supported by eQTL-based SMR and independent molecular evidence. The BRSK2 pQTL association did not pass the HEIDI test and was therefore not interpreted as convergent protein-level genetic evidence. Network analyses linked BRSK2 to cell-cycle, metabolic-stress, and senescence-related programs, while cross-cohort machine learning prioritized FOXA2, CDC25B, and NFE2 as informative network features. Single-cell and spatial analyses localized BRSK2 preferentially to fibroblast and myofibroblast compartments and to regions with greater histological fibrosis severity. In fibrotic rat lungs, BRSK2 expression increased, whereas FOXA2 and CDC25B decreased at the transcript and protein levels. CONCLUSIONS: These findings refine the molecular landscape of the chromosome 11p15.5 IPF susceptibility locus and prioritize BRSK2 as a candidate component of an IPF-associated profibrotic fibroblast state. Its causal contribution, direct regulatory relationships, and therapeutic tractability require targeted mechanistic validation.

Idiopathic Pulmonary Fibrosis

Online Social Anxiety in the Digital Age: Transitions, Predictors, and Mental Health Associations in Emerging Adulthood.

BACKGROUND: Online social anxiety (OSA), a multidimensional form of social evaluative anxiety in online social contexts, disproportionately affects emerging adults who constitute the largest active group of media users and face heightened psychological sensitivity due to growing pressures and immature sociocognitive regulation during the transition to adulthood. However, its heterogeneity, transitions, and longitudinal associations with mental health outcomes remain underexplored. METHODS: This study utilized data from two waves of a three-wave longitudinal survey, with 849 Chinese participants (Meanage = 21.6 years; 50.4 percent female) assessed at 4-month intervals. Individuals were classified using latent profile analysis and the stability and changes of profiles were assessed via latent transition analysis (LTA). Multinomial logistic regressions were conducted separately at baseline and follow-up to identify correlates of profile membership. Predictors of profile transitions were examined using manual three-step LTA models, and associations between latent transition patterns and follow-up mental health outcomes were examined using BCH-LTA distal outcome analyses controlling for the corresponding baseline symptom level. RESULTS: Four profiles of OSA were identified: low, privacy-sensitive, moderate-high, and high OSA. Extreme profiles (low/high OSA) showed high stability (80.4 percent and 79.1 percent), while privacy-sensitive OSA exhibited the lowest stability (55.1 percent). Profile memberships were influenced by social-cognitive biases and digital interaction, particularly fear of negative evaluation and online interpersonal trust, whereas profile transitions were mainly associated with anxiety. Transitions toward less severe OSA profiles were generally associated with better subsequent mental health, whereas transitions toward more severe profiles corresponded to poorer outcomes, particularly for offline social anxiety. CONCLUSION: OSA was heterogeneous in its manifestation, severity and transitions. Personalized and early interventions targeting profile-specific vulnerabilities are critical to prevent the worsening of OSA and mitigate its psychological burden.

Humans

Apolipoprotein E promotes papillary thyroid carcinoma progression by activating PINK1/Parkin-mediated mitophagy.

BACKGROUND: Increasing evidence supports a progression-related role of apolipoprotein E (APOE) in papillary thyroid carcinoma (PTC), yet a clear mechanistic explanation for this association is still lacking. Considering the pivotal role of mitochondrial homeostasis in tumorigenesis, the potential role of APOE in promoting PTC progression through mitophagy regulation was investigated. Additionally, the involvement of the PINK1/Parkin-associated pathway in this process was examined to provide insights into its contribution to tumor progression. METHODS: APOE in thyroid carcinoma was characterized in terms of its expression profile, diagnostic relevance, and potential biological functions, based on integrative evidence derived from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. APOE and mitophagy-related protein expression were further examined in PTC tissues by immunohistochemistry. Further evaluation of APOE in PTC cell lines focused on its association with proliferation, apoptosis, and mitophagy, with bidirectional functional perturbation serving as the basis for assessment. Pharmacological inhibitors were used to assess the involvement of mitophagy-related signaling in the observed APOE-dependent phenotypes. Additionally, the in vivo impact of APOE on PTC tumor growth and mitophagy was further investigated through a nude mouse xenograft model, providing insight into its potential role in tumor progression. RESULTS: A significant upregulation of APOE was observed in thyroid carcinoma tissues and PTC cell lines, supporting its potential relevance as a diagnostic biomarker. The modulation of APOE expression significantly influenced PTC cell proliferation and apoptosis, with overexpression promoting cell proliferation and inhibiting apoptosis, while knockdown led to the opposite effects. Mechanistically, APOE overexpression increased AMP-activated protein kinase (AMPK) phosphorylation and decreased mammalian target of rapamycin (mTOR) phosphorylation, accompanied by increased PINK1 and Parkin expression and mitophagy-related changes, including altered mitochondrial membrane potential, reduced overall reactive oxygen species levels, and increased autophagosome formation. Pharmacological inhibition of mitophagy attenuated the proliferative and antiapoptotic effects of APOE. CONCLUSIONS: These findings demonstrate that APOE promotes PTC progression in association with PINK1/Parkin-related mitophagy and modulation of the AMPK/mTOR axis. The APOE-associated mitophagy axis may provide a rationale for future preclinical investigation in PTC.

Apolipoprotein E (APOE)

Integrated pan-cancer profiling highlights OSR2 as a prognostic indicator and immune-associated biomarker.

BACKGROUND: Odd-skipped-related 2 (OSR2), encoded by the OSR2 gene, has been reported to function as a checkpoint associated with CD8⁺ T-cell exhaustion in the tumor microenvironment of solid malignancies, suggesting its potential as a therapeutic target to improve immunotherapeutic responses. Nevertheless, the molecular and clinical significance of OSR2 across diverse cancer types has not yet been systematically investigated, and its pan-cancer expression profile, prognostic implications, and associations with tumor immunity remain to be fully elucidated. METHODS: In this study, we integrated datasets from The Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx) portal, and the Human Protein Atlas to construct a systematic pan-cancer profile of OSR2. The prognostic value of OSR2 was comprehensively assessed using univariate Cox regression, survival analysis, and receiver operating characteristic (ROC) curve analysis. In addition, we performed an in-depth analysis of the relationships between OSR2 and multiple molecular and immunological features, including copy number variation (CNV), DNA methylation, tumor mutational burden (TMB), microsatellite instability (MSI), immune-related gene expression, immune cell infiltration, and drug sensitivity, with the aim of exploring its potential immunological associations with the tumor microenvironment. RESULTS: OSR2 expression was significantly upregulated or downregulated in the majority of tumor tissues relative to normal counterparts and exhibited distinct cancer-type-specific patterns across clinical stages. CNV alterations and aberrant DNA methylation were closely associated with abnormal OSR2 mRNA expression in multiple cancers. Prognostic analyses indicated that OSR2 expression was significantly associated with overall survival, disease-specific survival, disease-free interval, and progression-free interval across multiple cancer types, showing either risk-associated or protective associations in a tumor-context-dependent manner. Furthermore, OSR2 expression showed strong associations with immune cell infiltration, particularly T-cell subsets, and was significantly correlated with the expression of multiple immune checkpoint-related genes across diverse malignancies. OSR2 expression was also closely associated with TMB, MSI, and sensitivity to multiple anticancer agents. CONCLUSION: Taken together, these findings suggest that OSR2 is associated with prognosis and immune-related features across multiple cancer types. OSR2 may be linked to features of the tumor immune microenvironment through its relationships with immune cell infiltration, immune checkpoint gene expression, and genomic instability, and thus may serve as a candidate biomarker for further investigation in cancer immunotherapy.

CD8⁺ T-cell

Widespread Molecular Imprints in the Serum Proteome of COVID-19 Convalescents Uncovering Immune System Sequelae.

Post-COVID-19 sequelae have become an emerging global health issue, but the mechanisms for the sustained susceptibility of convalescents to the sequelae remain poorly understood. Here we report the use of a restricted open-search approach to explore the molecular imprints of SARS-CoV-2 infection left on the proteome of 412 COVID-19 patients and convalescences. A total of 827 non-standard amino acid variations, chemically modified residues as well as post-translational modifications, termed non-coded amino acids (ncAAs), are found spreading over 29,814 sites in patient's serum proteins. Markedly, widespread ncAAs are induced and sustainedly imprinted on the serum proteome predominately perturbing the immunoglobulin-mediated immune response, complement activation and coagulation regulation even 12 months after recovery. Sustained amino acid variations and chemical modifications are found in the complementary‑determining regions (CDRs) of the variable region of immunoglobulin contributing to the interactions between the emerging antibody and antigens; durable chemical amino acid modifications found in the hyper ncAA-modified regions of the constant region of immunoglobulin important for the interaction with the complement and regulatory receptors. In the complement system, inducible ncAAs are memorized in the components essential for the complement activation, amplification cascades and membrane attack processes. Thus, the workflow described in this study can be used to identify the molecular imprints of viral infection at the proteomic scale, particularly the specific antibodies and the immune targets left in COVID-19 patients and convalescents.

Humans

Marine air promotes structural compaction and coating growth of soot aerosols after long-range transport from East Asia.

Soot aerosol, a key global warming contributor, undergoes morphological and chemical transformations during atmospheric transport, particularly in humidified marine environments. This study investigates morphology, mixing state, and aging mechanisms of soot particles collected in the Bohai Sea and Yellow Sea. Transmission electron microscopy analyses reveal that coated soot particles dominate the marine atmosphere, accounting for over 98 % of soot-containing particles, with a mean mixing state index (χ) of 0.83. The fractal dimension (Df) of soot particles is 1.84 ± 0.05 in the Northern Yellow Sea, 1.90 ± 0.08 in the Bohai Sea, and 1.96 ± 0.07 in the Southern Yellow Sea, indicating structural compaction during long-range transport. Correspondingly, the average Dp/Dcore ratios (particle to core size ratio) are 5.3 in the Bohai Sea, 4.2 in the Northern Yellow Sea, and 3.9 in the Southern Yellow Sea. Notably, those ratios are higher in marine environments compared to those observed during continental regional transport from northern to southern China (3.54), suggesting enhanced coating growth in humid marine air. The results highlight the important role of marine atmospheres in accelerating soot aging, which in turn leads to significantly stronger light absorption compared to soot in continental air. Our results highlight the necessity of incorporating compact morphologies, uniform mixing states, and thick coatings into optical models for accurate radiative forcing simulations.

Aerosols