Bin Chen
· Mammalian Brain DevelopmentVerifiedUniversity of California, Santa Cruz · Molecular, Cell, and Developmental Biology
Active 1993–2026
About
Dr. Bin Chen is a Principal Investigator and Professor of MCD Biology at the University of California Santa Cruz. He holds a B.S. and M.S. from Beijing University, a Ph.D. from SUNY Stony Brook, and completed postdoctoral training at Stanford University. Dr. Chen serves as the Editor-in-Chief of Developmental Neurobiology. His professional profile is presented as part of the Chen Lab at UC Santa Cruz, with noted lab periods from 2021-2022 and 2024-2025. The page lists Dr. Chen among other lab members but does not provide further details on his specific research focus or key contributions.
Research topics
- Biology
- Cell biology
- Cancer research
- Medicine
- Ophthalmology
- Chemistry
- Surgery
- Biochemistry
- Genetics
- Internal medicine
Selected publications
Frontiers in Public Health · 2026-04-08
articleOpen accessAs an integral component of the human diet, dairy products are rich in high-quality protein, lactoferrin, conjugated linoleic acid, calcium, vitamin D, and various other nutrients and bioactive compounds. They exert broad health benefits through core mechanisms involving multiple pathways and targets. This article systematically reviews the nutritional composition of dairy products, provides an in-depth analysis of their fundamental mechanisms-such as gut-immune axis regulation and antioxidant-anti-inflammatory synergy-and comprehensively summarizes their preventive value in metabolic-related diseases, bone health, degenerative diseases, and malignancies. The interplay and synergistic effects among multiple components and mechanisms are discussed, along with future research directions, to offer a scientific basis for the application of dairy products in public health and clinical nutrition.
Buildings · 2026-01-02
articleOpen accessCorrespondingA comfortable and livable living environment can be created through the design of patios in traditional southern rural Chinese dwellings. By connecting indoor and outdoor spaces, patios enable the comprehensive functions of ventilation and shading. To investigate the effects of patios on the building environment and energy conservation, the field parameters of the Wu Family Mansion in Cuijiao Village, Fujian Province, southern China, were measured in August 2016. The results indicate that patios located at the center of dwellings can effectively mitigate the impact of outdoor climate on the indoor environment. Furthermore, a reasonable depth-to-width ratio of the patio is conducive to natural ventilation and energy utilization. Through discussions and simulations using CFD and EcoTECT, it is determined that the reasonable depth-to-width ratio should not be less than 0.06, and a depth of 1.6 m is the most appropriate for patio design to achieve adequate ventilation and illumination. With the Adaptive Predicted Mean Vote (APMV) value ranging from 0 to 1.41, the indoor environment of this rural building falls within the adaptive comfort zone. Compared with air-conditioned rooms, the energy-saving rate achieved by natural ventilation is approximately 26.2%.
BMC Neurology · 2025-07-07 · 11 citations
reviewOpen accessOBJECTIVE: To investigate the imaging characteristics and management strategies of amyloid-related imaging abnormalities (ARIA) in Alzheimer's disease (AD) patients treated with lecanemab. METHODS: We report two clinical cases of ARIA following lecanemab treatment and analyze the imaging features, risk factors, and management strategies of ARIA based on the latest literature. RESULTS: The occurrence of ARIA is associated with risk factors such as advanced age, ApoE ε4 carrier status, cerebral amyloid angiopathy (CAA), and a history of cerebrovascular disease. CONCLUSION: During lecanemab treatment for AD, it is essential to fully understand the mechanisms, imaging characteristics, and management strategies of ARIA. Close monitoring of clinical symptoms and imaging changes is crucial for the timely detection and appropriate management of ARIA.
World Neurosurgery · 2025-12-12
articleOpen accessSenior authorBACKGROUND: This study aims to describe converging decompression technique (CDT) procedure in detail and assess its clinical efficacy in comparison with foraminoplasty percutaneous transforaminal endoscopic discectomy (PTED) for the management of very highly up-migrated lumbar disc herniation (VHUM-LDH). METHODS: A retrospective study was performed on 66 patients diagnosed with VHUM-LDH who underwent surgery between January 2020 and January 2024. Of these, 27 patients were treated with CDT (CDT group), and 39 with foraminoplasty PTED (PTED group). Clinical parameters, including Oswestry Disability Index, visual analog scale scores for back and leg pain, and modified MacNab criteria were analyzed. RESULTS: Both groups demonstrated significant postoperative improvements in leg and back pain visual analog scale scores and Oswestry Disability Index scores. No significant differences were observed between the groups at any follow-up time point (P>0.05). The PTED group required fewer fluoroscopic exposure times (10.82±2.47 vs. 18.74±3.66, P<0.05) compared to the CDT group. However, the CDT group had a shorter endoscopic procedure duration (46.96±4.17 vs. 59.77±8.31 min, P<0.05). There were no significant differences between the groups regarding complication rates or good-to-excellent outcomes as per the modified MacNab criteria (P>0.05). CONCLUSIONS: Both CDT and foraminoplasty PTED are safe and effective treatments for VHUM-LDH. However, CDT offers enhanced endoscopic efficiency and a reduced risk of postoperative nucleus pulposus remnants. Further prospective studies with larger cohorts and extended follow-up are required to fully assess the advantages and limitations of both techniques.
Competing Programs Shape Cortical Sensorimotor-Association Axis Development
bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-27 · 8 citations
preprintOpen accessThe neocortex is organized along a dominant sensorimotor-to-association (S-A) axis, anchored by modality-specific primary sensorimotor areas at one end and transmodal association areas that form distributed networks supporting abstract cognition at the other. The developmental mechanisms shaping this axis remain elusive. Here, we present converging multispecies evidence supporting the Multinodal Induction-Exclusion in Network Development (MIND) model, in which S-A patterning is governed by competing processes of induction and exclusion, driven by opposing transcriptomically-defined identity programs emerging from different nodes. Key molecular and connectional features of association cortices arise through pericentral programs, originating around fronto-temporal poles and partially regulated by retinoic acid. They progress inward toward central territories of the naïve neocortex along fronto-temporally polarized trajectories. Central programs are induced through interactions between topographically separated first-order sensorimotor thalamocortical inputs and the neocortex, promoting the formation of primary areas while excluding pericentral programs. Influenced by SATB2 and ZBTB18, these evolutionarily conserved programs compete for the same territory and create spatial compartmentalization of axon guidance, cell-cell adhesion, retinoic acid signaling, synaptogenesis, Wnt signaling, and autism risk genes. Notably, PLXNC1 and SEMA7A exhibit anti-correlated expression and repulsive functions in shaping cortico-cortical connectivity along the S-A axis. These processes of induction and exclusion establish an S-A equilibrium and topography in which primary sensorimotor areas emerge as focal islands within the broader ocean of distributed associative networks. The MIND model provides a unifying framework for understanding experimental, evolutionary, and clinical phenomena, revealing induction and exclusion as antagonistic complementary principles shaping the S-A axis and processing hierarchies.
Frontiers in Surgery · 2025-04-22 · 2 citations
articleOpen accessBackground: In the endoscopic endonasal approach skull base surgery repair and reconstruction of the base of the skull is a critical step. Free mucosal flaps are primarily used to repair low-flow cerebrospinal fluid (CSF) leaks, whereas they are not adequate in the face of high-flow CSF leaks. We propose a modified approach-termed the "Fishing method"-which utilizes free mucosal flaps in combination with absorbable sutures and an artificial dura to reverse-plug the defect, to repair high-flow CSF leaks with a clear point of origin. Objective: To investigate the application of the "Fishing method" to repair high-flow CSF leaks caused by large diaphragma sellae rupture and small dura leak that occur unexpectedly during endoscopic endonasal sellae area surgery. Methods: A retrospective analysis was conducted including 15 patients with unexpected intraoperative high-flow cerebrospinal fluid leaks. The "Fishing method" was applied to reconstruct and repair the skull base in these patients, and the results were evaluated. Results: In 10 cases of large diaphragma sellae rupture that occurred during pituitary adenomas resection, all 10 patients were successfully repaired in a single operation using the "Fishing method", with no cerebrospinal fluid nasal leakage (100%); in 5 cases of small dura ruptures that occurred during chordoma resection, 4 patients underwent successful repair in a single operation, with no cerebrospinal fluid nasal leakage occurring in 80% of cases, resulting in an overall success rate of 93.3%. Conclusion: The "Fishing method" is a reliable technique for skull base reconstruction and serves as an effective solution for high-flow CSF leaks caused by unexpected large diaphragma sellae rupture or a small dura leak occurring intraoperatively.
International Journal of Radiation Oncology*Biology*Physics · 2025-09-01
articleOrphanet Journal of Rare Diseases · 2025-02-08 · 1 citations
reviewOpen accessAbstract Background A correlation between various sites or types of mutations in mitochondrial DNA ND3 and the development of a specific mitochondrial disease or phenotype has yet to be fully established. Methods This study reports a rare case of adult-onset Leigh syndrome (LS) and Leber hereditary optic neuropathy and dystonia (LDYT) overlap syndrome caused by the m.10197G>A mutation in ND3 . A review of the literature was conducted to investigate the clinical spectrum, treatment and outcome resulting from the m.10197G>A mutation. Phenotypes associated with the m.10197G>A mutation were classified into three categories: LS/LS+ (LS-involved overlap syndrome), Leber hereditary optic neuropathy (LHON)/LHON+ (LHON-involved overlap syndrome) and other mitochondrial encephalopathies or presentations. Results A total of 84 participants (78 patients and 6 asymptomatic carriers) with the m.10197G>A mutation retrieved from 33 articles and the patient whose case we reported were included in the review and meta-analysis. Among all the participants, 55.3% (47/85) and 28.2% (24/85) presented with LS/LS+ and LHON/LHON+, respectively. The median age at onset for LS/LS+ was significantly younger than that for LHON/LHON+ [median, (Q1–Q3), 3.0 (0.58–9.5) vs. 13.5 (5.75–41.75), P = 0.001]. A negative linear correlation was observed between mutation load and age of onset in patients who presented with LS/LS+ (R 2 = 0.592, P < 0.001), with the age of onset ranging from infancy to adulthood. Patients with an older age at onset [OR (95% CI), 1.46 (1.12–1.91), P = 0.005] or higher mutation loads [OR (95% CI), 1.14 (1.03–1.26), P = 0.011] were more likely to present with LHON/LHON+ than with LS/LS+. A total of 17 patients were documented as having received a combination of mitochondrial cofactor treatments. Compared with patients with LHON/LHON+, patients with LS/LS+ exhibited an exceedingly high probability of a stable or worsen outcome (93.8% vs. 33.3%, P = 0.006). Conclusions LS/LS+ and LHON/LHON+ are the predominant presentations of the m.10197G>A mutation. An older age at onset and greater mutation load increases the probability of an LHON/LHON+ presentation. Patients presenting with LS/LS+ have an exceedingly high possibility of an unfavorable outcome. The identification of factors and outcomes associated with phenotypes in patients with the m.10197G>A mutation facilitates the provision of improved prognostic counseling for patients and their family members who are carriers of this mutation.
Multi‐Omics Analysis and Experimental Validation Identify RAD51 as a Key Biomarker in OSCC
IET Systems Biology · 2025-01-01
articleOpen accessCorrespondingOral squamous cell carcinoma (OSCC) is an aggressive malignancy associated with high morbidity and mortality. RAD51 recombinase (RAD51), a central DNA repair protein, plays a crucial role in homologous recombination and has been implicated in cancer progression through mechanisms such as genomic instability, chemoresistance and immune modulation. However, its specific function and regulatory mechanisms in OSCC remain incompletely elucidated. We conducted an integrated multiomics analysis including differential expression, single-cell transcriptomics, prognostic evaluation, functional enrichment and immune infiltration profiling. Experimental validation was performed using siRNA-mediated RAD51 knockdown in OSCC cell line HSC-3, followed by functional assays to assess proliferation, migration, invasion, reactive oxygen species (ROS) accumulation and chemosensitivity. RAD51 was significantly overexpressed across multiple cancers, including OSCC, and exhibited high diagnostic accuracy for OSCC (AUC = 0.956). Single-cell RNA sequencing revealed elevated RAD51 expression in malignant and proliferating T cells, associating it with aggressive phenotypic traits. High RAD51 expression predicted poor prognosis in OSCC and other cancers. Functional analyses indicated its involvement in the Fanconi anaemia pathway, DNA damage repair and cell cycle regulation. Immune infiltration analysis revealed significant negative correlations with multiple immune cell subtypes and tumour microenvironment scores. Experimentally, RAD51 knockdown suppressed malignant behaviours and enhanced ROS production and chemosensitivity in HSC-3 cells. RAD51 drives OSCC progression by enhancing malignant phenotypes, suppressing immune infiltration, promoting aberrant DNA repair, elevating oxidative stress and promoting therapy resistance. These findings support RAD51's potential as both a prognostic biomarker and a therapeutic target in OSCC.
Cell Death and Differentiation · 2025-07-13 · 7 citations
article
Recent grants
Lineage Progression of Cortical Neural Stem Cells
NIH · $4.7M · 2015–2026
NIH · $356k · 2018–2022
NIH · $554k · 2022–2026
NIH · $136k
Transcriptional regulation of neuronal identity and connectivity
NIH · $3.7M · 2011–2023
Frequent coauthors
- 50 shared
Junrong Cai
Southern Medical University
- 50 shared
Lifei Guo
Xijing Hospital
- 49 shared
Helen S. Zitkovsky
Lahey Medical Center
- 49 shared
Min Gao
Jilin University
- 26 shared
Lan Liu
Sun Yat-sen University
- 22 shared
Senhua Chen
Sun Yat-sen University
- 18 shared
Zaiqiang Zhang
Yichang Central People's Hospital
- 16 shared
Jingyun Jin
Shanghai University of Traditional Chinese Medicine
Labs
Chen LabPI
University of California Santa Cruz
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