About

Lu Chen is an assistant professor of philosophy at the University of Southern California. Her research focuses on mathematical metaphysics and philosophy of physics. She previously worked as an assistant professor in Istanbul from 2020 to 2023. Lu Chen received her Ph.D. degree in philosophy from the University of Massachusetts, Amherst. She is based in Los Angeles, where she is affiliated with USC's Mudd Hall of Philosophy and Stonier Hall. Her academic work involves exploring foundational issues in metaphysics and the philosophy of physics, contributing to ongoing discussions in these fields.

Research topics

• Neuroscience
• Internal medicine
• Computer Science
• Biology
• Medicine
• Endocrinology
• Environmental economics
• Economics
• Engineering
• Paleontology
• Automotive engineering
• Business
• Psychology
• Environmental science
• Physics
• Intensive care medicine
• Radiology
• Emergency medicine

Selected publications

• Combined single-cell transcriptome and immune repertoire analysis reveals hepatic and renal immune injury by heat stroke

  JCI Insight · 2026-03-23

  articleOpen access

  Heat stroke (HS) is the most severe heat-related emergency, and its pathophysiology remains largely unknown, especially for exertional HS (EHS), which affects younger populations, athletes, and manual workers. Herein, we performed single-cell-transcriptomics, T cell receptor sequencing, and flow cytometry of PBMCs from 9 healthy control participants, 9 patients with heat exhaustion, and 9 patients with EHS to explore complex immunological responses associated with HS pathobiology. We showcased that granzyme-positive T cells and CD56dim NK cells with high cytotoxicity features and IL-1B+NLRP3+ monocytes with high inflammation and pyroptosis scores were enriched in HS, while the CD161+ T cells with innate immune-like, low cytotoxicity, and clonal expansion features were reduced in HS. Importantly, elevated granzyme-positive T and NK cells might interact with monocytes to induce pyroptosis of hepatic and renal cells and target organ injuries, and blocking the NLRP3 inflammasome pathway prior to the induction could alleviate organ injury in HS. This study offers deeper insights into the pathogenesis of HS, supporting the development of optimal treatment strategies.

  PublisherOA PDFDOI

• High Efficiency (∼18%) Organic Solar Cells with 500 nm‐Thick Toluene Cast Active Layer by Aggregation Manipulation and Additive Engineering

  Advanced Materials · 2025-09-29 · 5 citations

  article1st authorCorresponding

  Thick-film organic solar cells (OSCs) are crucial for mass-production: however, the efficiency of such cells is limited by the lack of morphological control afforded by methods that rely on high-vapor-pressure solvents. Herein, a systematic solvent and additive engineering strategy is reported for improving the performance of thick-film (>300 nm) OSCs through aggregation modulation via solidification acceleration and electronic property enhancement. Two oligomers derived from the polymer donors PM6 and D18-Fu are employed as solid additives to prepare the active layer. Characterizations reveal that the D18-Fu-derived oligomer exhibits stronger interactions with both the benzodifuran donor (D18-Fu) and the acceptor (L8-BO-X), resulting in suppressed electron-phonon coupling, more balanced donor-acceptor fibrillation, and enhanced face-on molecular orientation. Devices treated with the D18-Fu-derived oligomer achieve a greater improvement in power conversion efficiency (PCE). Both additives enhance thickness- tolerance of the device owing to their structural compatibility with the D18-Fu-derived oligomer,- yielding superior performance. Notably, devices processed from toluene, a nonhalogenated solvent, demonstrate high PCEs with excellent thickness tolerance; the thick-film device (500 nm active layer) exhibits an independently certified PCE of ∼18%, a record for thick-film OSCs, with no significant loss in performance compared to its thin-film (100 nm) counterparts (>19%).

  PublisherDOI

• Anlotinib in combination with penpulimab and chemotherapy as first-line treatment for extensive-stage small cell lung cancer: A single-arm, prospective clinical study.

  Journal of Clinical Oncology · 2025-05-28

  article1st authorCorresponding

  e20136 Background: In recent years, the combination of immunotherapy and chemotherapy has emerged as a standard first-line treatment for extensive-stage small cell lung cancer (ES-SCLC). However, these regimens generally offer a median progression-free survival (mPFS) of around 6 months and a median overall survival (mOS) of approximately 15 months, which does not provide a significant advantage over chemotherapy alone. Our previous study on the first-line treatment of ES-SCLC using anlotinib plus EP/EC regimen demonstrated a 9-months PFS and a 19-months OS. Unlike other PD-1 monoclonal antibodies based on the IgG4 subtype, Penpulimab is a novel PD-1 monoclonal antibody based on the IgG1 subtype, which prevents aggregation and avoids immune escape associated with IgG4 monoclonal antibodies. Therefore, we conducted a single-center study evaluating anlotinib combined with Penpulimab and the EP/EC regimen as a first-line treatment for ES-SCLC. Methods: ES - SCLC patients aged 18 to 80 years, not received any treatment, no significant cardiac, hepatic, or renal dysfunction. This regimen comprised Anlotinib Hydrochloride (10mg,QD, from day 1 to 14 of each 21-day cycle), Penpulimab (200md, on day 1 of each 21-day cycle), Etoposide (100 mg/m² on days 1-3 of each 21-day cycle), and either CBP (AUC=4-5 on day 1 every 3 weeks) or DDP (70-75 mg/m² on day 1 every 3 weeks). The combination therapy was administered for 4 to 6 cycles. Following this, maintenance therapy with Anlotinib Hydrochloride (10mg ,qd, from day 1 to 14 of each 21-day ) and Penpulimab (200 mg on day 1 of each 21-day) was continued until disease progression or the occurrence of an intolerable adverse reaction. If Anlotinib was not tolerated, its dose could be reduced to 8 mg. The primary endpoints of observation included objective response rate (ORR), PFS, OS, and adverse reactions (ADR). Results: Between March 6, 2021, and March 31, 2024, a total of 25 patients with ES-SCLC were enrolled in this study and completed the treatment regimen. The mean age of the patients was 65.0 ± 8.5 years (range: 45-80 years), with 18 males (72%) and 7 females (28%). The median PFS was 11.0 months (95% CI: 9.38-12.62), and the median OS was 23.0 months (95% CI: 15.66-30.34). The ORR was 90%, and the DCR was 100%. Grade 3 or higher adverse reactions included neutropenia in 15 patients (60%), thrombocytopenia in 10 patients (40%), nausea and vomiting in 7 patients (28%), anemia in 3 patients (12%), fatigue in 8 patients (32%), hypertension and elevated transaminase levels in 5 patients each (20%), and hoarseness in 1 patients (4%). Conclusions: The combination of Anlotinib with Penpulimab and EP/EC regimens, has demonstrated superior PFS, OS, ORR, and DCR in initial ES-SCLC treatments, with manageable adverse events. A randomized, controlled phase III clinical study will be conducted to further validate these promising results. Clinical trial information: ChiCTR2200065238 .

  PublisherDOI

• TIM3 attenuates morphine antinociceptive tolerance and microglial neuroinflammation by suppressing the TRAF6/NF-κB pathway in male mice

  Neuropharmacology · 2025-08-19 · 1 citations

  articleSenior authorCorresponding
  PublisherDOI

• Structural characterization and anti-tumor mechanisms of an arabinan polysaccharide isolated from Rhodiola rosea

  International Journal of Biological Macromolecules · 2025-06-11 · 8 citations

  article1st authorCorresponding
  PublisherDOI

• Resolving Ternary Morphology for High-Performance Thickness-Insensitive Organic Solar Cells

  ACS Applied Materials & Interfaces · 2025-11-28 · 1 citations

  articleOpen access

  High-performance organic solar cells (OSCs) suffer from low active layer thickness tolerance, which is incompatible with large-scale printing technology originally envisioned for low-cost module manufacturing. Herein, by incorporating a large amount of small-molecule donor BTR-Cl into the prototypical PM6/Y6 blend film, we fabricated efficient ternary devices with a photoconversion efficiency of 17.7% at an active layer thickness of 300 nm, among the best-performing thick-film devices reported so far. To elucidate its morphological origin, we deuterated both Y6 and BTR-Cl to resolve their morphology in ternary blend films separately via grazing-incidence small-angle neutron scattering (GISANS). We observed enhanced short-range aggregation of both Y6 and BTR-Cl within the intermixed domains of the ternary blend film induced by the accelerated molecular assembly process. Those aggregates act as effective bridges between crystalline domains to improve connectivity in both donor and acceptor phases, resulting in enhanced carrier mobility, suppressed space charge accumulation, and consequently significantly improved thickness tolerance in ternary devices. Our work demonstrates the effectiveness of combined targeted deuteration and GISANS to resolve the complicated structures within multicomponent OSC active layers and highlights the critical role of amorphous nanomorphology in carrier transport connectivity and, consequently, the thickness tolerance of high-performance OSCs.

  PublisherDOI

• Sophoridine inhibits proliferation and migration by targeting PIM1 in breast cancer

  Pharmaceutical Biology · 2025-07-24

  articleOpen access1st author

  CONTEXT: Aiton (Fabaceae), has strong anti-tumor activity in a variety of malignancies. Nevertheless, the effects and underlying mechanism of sophoridine on breast cancer are not fully understood. OBJECTIVE: To identify the key targets and potential pharmacological mechanisms of sophoridine against breast cancer. MATERIALS AND METHODS: MCF-10A, MCF-7 and MDA-MB-231 cells were treated with sophoridine for 24 or 48 h. MTT, colony formation assay, flow cytometry, wound healing, and Transwell assay were employed to illustrate the anti-tumor effects of sophoridine on breast cancer. Network pharmacology and molecular docking were used to determine the targets for sophoridine in breast cancer, and confirmed by molecular dynamics simulation and CETSA-western blot assay. Additionally, the functional rescue and signaling pathway regulated by sophoridine was analyzed. RESULTS: value of sophoridine for 48 h in MCF-10A, MCF-7 and MDA-MB-231 was 363 μM, 87.96 μM and 81.07 μM, respectively. PIM1 was the key target for sophoridine in breast cancer. Furthermore, PIM1 overexpression significantly reversed the suppressive impacts of sophoridine on growth and migration in breast cancer cells. Mechanistically, sophoridine inhibited the phosphorylation of ASK1 and activated JNK/p38 MAPK signaling pathway by downregulating PIM1 expression, and thus exhibited anti-tumor effects. DISCUSSION AND CONCLUSION: Taken together, sophoridine relies on targeting PIM1 to inhibit cell proliferation and migration in breast cancer, which might be related to the activation of ASK1/MAPK axis, suggesting the therapeutic potential of sophoridine for breast cancer.

  PublisherDOI

• Cloning of the Na+-K+-2Cl−(NKCC) transporter in Macrobrachium rosenbergii and its role in osmoregulation

  Comparative Biochemistry and Physiology Part B Biochemistry and Molecular Biology · 2025-07-03 · 1 citations

  article
  PublisherDOI

• Gut microbiota and metabolic signatures of anxiety in ulcerative colitis: a cross-sectional study

  Therapeutic Advances in Gastroenterology · 2025-11-01

  articleOpen access

  Background: Patients with ulcerative colitis (UC) usually experience anxiety symptoms that seriously affect their quality of life, treatment, and prognosis. Dysbiosis of the gut microbiota plays an important role in UC and mental illness. However, little is known about the role of the gut microbiota in UC patients with anxiety. Objectives: To identify the gut-microbiome and fecal metabolome profiles uniquely associated with comorbid anxiety in UC patients and to explore potential biomarkers for diagnosis. Design: A cross-sectional, two-group comparative study. Methods: To study the underlying association between them, we recruited 126 UC patients in this study, including 78 with anxiety and 48 without anxiety. A total of 102 fecal samples were collected for metagenomic sequencing and metabolome sequencing. Microbial diversity, differential gut microbiota, functional pathways, and metabolites were analyzed. Multivariable logistic regression was used to identify independent risk factors associated with anxiety in UC patients, while Spearman correlation was employed to explore microbe-metabolite interactions and the performance of potential biomarkers. Results: We found that disease severity, steroid usage, and abdominal pain may promote the occurrence of anxiety. Compared to UC patients without anxiety, UC patients with anxiety had low fecal microbial community diversity, with an increase in the species Haemophilus sp. HMSC71H05 and Corynebacterium durum , and a decrease in the species Roseburia intestinalis ( RI ), Bifidobacterium longum ( BL ), and Enterococcus hirae . The metabolic pathways driven by the gut microbiota were disrupted. Moreover, the levels of most metabolites (such as L-kynurenine) were increased in the feces, while the levels of a few metabolites decreased, including indole-2-carboxylic acid, N-demethylmirtazapine, and tauroursodeoxycholic acid. Conclusion: Our research further revealed that these gut microbiota and metabolites are highly correlated. This study provides a new perspective for understanding the occurrence and development of anxiety in UC patients, suggesting that RI and BL may serve as potential candidate biomarkers to diagnose UC patients with anxiety.

  PublisherDOI

• FIRST (F18 Flurpiridaz In Real-world Stress Testing) - Laboratory Logistics and Feasibility

  Journal of Nuclear Cardiology · 2025-08-01

  article1st authorCorresponding
  PublisherDOI

Recent grants

• NIH Grant R01NS077906

  NIH · $2.5M · 2015

• Project 3

  NIH · $16.2M · 2020–2025

• NIH Grant F32MH065112

  NIH · $60k

• Developmental Pathophysiology of Synapses in a Mouse Model of Fragile X Syndrome

  NIH · $3.3M · 2014–2020

• NIH Grant P50MH086403

  NIH · $28.3M · 2021

Frequent coauthors

• Kristin R. Knight

  74 shared

• Jonathan R. Wolpaw

  Neurotech (United States)

  72 shared

• Xiang Yang Chen

  Albany Stratton VA Medical Center Albany

  56 shared

• Lillian Sung

  Hospital for Sick Children

  51 shared

• Eleanor Hendershot

  McMaster Children's Hospital

  51 shared

• Dale F. Kraemer

  Quality Research

  49 shared

• Biljana Gillmeister

  Children's Hospital of Philadelphia

  49 shared

• Mary Bancroft

  Children's Oncology Group

  49 shared

Education

• Ph.D., Philosophy

  Umass, Amherst