Li Lu

Purpose: Medical students frequently undervalue basic medical courses prior to clinical training, resulting in learning difficulties. Current pedagogical approaches fail to integrate basic medical sciences with essential health communication skills. Consequently, strategies are needed to help students promptly recognize the value of basic courses while developing core communication competencies. Methods: This qualitative study explored the integration of health communication activities into basic medical courses for 42 undergraduate medical students (Years 1– 3). Students engaged in structured communication tasks and composed reflections on the relationship between basic science and health communication. Additionally, semi-structured interviews with 15 community members were conducted to assess their perceptions of students’ communication. Applied thematic analysis was employed to analyze the reflective essays. Results: The analysis identified 18 codes grouped into six themes: clinical health communication thinking, perception of scientific research, responsibility for health communication, communication of knowledge and skills, hands-on interaction, and knowledge system construction. Participants in the community interviews reported that students communicated clearly and professionally, with some indicating intentions to adjust health behaviors based on the information received. Conclusion: In this exploratory qualitative study, the integration of health communication into basic medical courses was associated with enhanced students’ appreciation of foundational knowledge and improved self-perceived communication skills. These findings suggest a potential approach to curriculum reform. However, further quantitative research is required to assess broader educational and public health outcomes.

Parkinson's disease (PD) is the second most common neurodegenerative disease, in which ferroptosis may be the crucial event leading to dopaminergic neuron death. Accumulated ferrous ions (Fe ²⁺ ) and increased intracellular viscosity promote of ferroptosis. Precisely monitoring Fe ²⁺ /Viscosity, especially in ferroptosis, is crucial for PD theranostic. However, a feasible strategy is lacking. In this study, series of Fe ²⁺ /Viscosity cascade‐activated near‐infrared fluorescence probes (NP1–5) are synthesized. Through optical characterization and theoretical calculations, NP3 is selected as the optimal probe to monitor Fe ^{2 +} /Viscosity via redox reactions and twisted intramolecular charge transfer processes. To verify this concept in the context of ferroptosis intervention in PD, an innovative nanoplatform is constructed based on NP3 and quercetin, modified with rabies virus glycoprotein‐29 and defined as PQR nanoparticles (PQR NPs). In vitro and in vivo experiments demonstrate that PQR NPs not only alleviate ferroptosis‐induced loss of dopaminergic neurons by reducing oxidative stress and neuroinflammation, mitigating α‐synuclein aggregation, and restoring mitochondrial function, but also could monitor the elevated Fe ^{2 +} /Viscosity in ferroptosis of PD models. Present study developed a facile tool for monitoring Fe ²⁺ /Viscosity in ferroptosis. The findings have strong application potential in theranostics of PD and other ferroptosis related diseases.

Background: Chromatin accessibility landscape is the basis of cell-specific gene expression and reflects the regulatory logic underlying cellular identity and function. However, a systematic multi-organ chromatin accessibility atlas in the rat (Rattus norvegicus), an important biomedical model organism, has been lacking. Results: We generated a multi-organ single-nucleus chromatin accessibility landscape of Rattus norvegicus using snATAC-seq. For this single-cell atlas, we constructed 25 libraries via snATAC-seq from 9 organs in the adult rat, with a total of over 110,000 cells. Cell classification integrating gene activity scores with known marker genes identified 77 cell types, which were strongly correlated with those in published mouse single-cell transcriptome atlases. We further investigated the enrichment of cell-type- and organ-specific transcription factors, shared and organ-specific features of endothelial and stromal cells, as well as cross-organ macrophage regulatory states, and the conservation and specificity of gene regulatory programs across species. Conclusion: This single-nucleus chromatin accessibility landscape provides a valuable foundation for dissecting tissue-specific regulatory mechanisms in the rat and facilitates cross-organ and cross-species cell type annotation and functional inference, supporting broader applications of rat model in systems biology and biomedical research.

Age‐related memory decline is a hallmark of brain aging and a primary risk factor for neurodegenerative disorders. Microglia play a crucial role in preserving memory function by maintaining brain homeostasis through phagocytosis, yet the specific mechanisms governing this protective function remain elusive. In the present study, we identified a population of Secreted Phosphoprotein 1 (Spp1)‐positive microglia in both aged mouse and human brains. To investigate the role of microglial Spp1 in aging, we generated microglia‐specific Spp1 knockout (Spp1‐cKO) mice. We demonstrate that Spp1 deficiency selectively precipitates memory deficits in aged mice, without affecting memory function in young mice, indicating an age‐dependent reliance on Spp1 signaling. Microglial phagocytic capacity positively correlates with Spp1 levels and is diminished by Spp1 deficiency. Mechanistically, Spp1 deficiency leads to the downregulation of the AKT/mitochondrial complex I pathway, thereby compromising microglial oxidative phosphorylation and function. Notably, microglia‐specific overexpression of Spp1 partially ameliorates the age‐related phenotypes induced by Spp1 deficiency. In conclusion, this study is the first to reveal the crucial role of microglial Spp1 in brain aging and to uncover its underlying mechanism, providing novel insights into age‐related memory decline.

Aims This study aims to elucidate how the hyperactivated enteric glial cells (EGCs) trigger Parkinson's Disease (PD) pathogenesis and if exogenous gut-brain regulatory hormone oxytocin could alleviate the phenotypes of PD. Methods Prodromal and clinical PD mice model were established via intragastric administration of rotenone (ROT). Intestinal and motor function of the mice were assessed. The expression of glial fibrillary acidic protein (GFAP), oxytocin receptor (OXTR) and tyrosine hydroxylase (TH) in the colon and midbrain were detected by immunofluorescence staining. The levels of α-synuclein (α-syn), oxytocin (OXT), and inflammatory factors in serum and colon were measured by ELISA, western blotting and qPCR. Exogenous OXT and EGCs inhibitor fluorocitrate (FC) were administered, and the rescue effect on PD mice was assessed by neurobehavioral assays. Results ROT administration induced constipation and motor PD symptoms in mice successively. The expression of GFAP and α-syn in the colon of PD mice were increased, while the OXT and OXTR levels were downregulate. Exogenous OXT or FC administration inhibited EGCs hyperactivation, reduced inflammatory factors levels and α-syn accumulation, and ultimately alleviated prodromal and clinical PD phenotypes. Conclusions EGCs hyperactivation plays a crucial role in PD pathogenesis, and exogenous OXT or FC could ameliorate the prodromal and clinical PD phenotypes.

Background: DSI Studio is an advanced imaging software specifically designed for the analysis of diffusion magnetic resonance imaging (dMRI). Its key features, which include fiber reconstruction, fiber tracking, and 3D visualization, have established its significant role in neuroscience research. Objective: A solid understanding of spatial relationships is crucial for students studying anatomy. However, there has been limited research in Chinese medical education regarding the integration of 3D imaging technology into anatomical instruction. To address this gap, we conducted an innovative study utilizing DSI Studio to enhance neuroanatomy education. Methods: An innovative study was conducted utilizing DSI Studio for fiber reconstruction and 3D visualization in neuroanatomy workshops. A total of 38 students participated in hands-on sessions, with 13 completing pre-training surveys and 19 completing post-training surveys. The students’ understanding of neuroanatomy prior to training, as well as their performance and experiences during the neuroanatomy learning process, were systematically recorded. Additionally, the effectiveness of DSI Studio software in enhancing neuroanatomy learning was assessed in conjunction with the reconstruction capabilities of the software. Results: The application of DSI Studio significantly improved students’ visualization of neural structures, surpassing traditional teaching limitations. It enhanced their understanding of three-dimensional brain anatomy, boosted enthusiasm, and improved learning efficiency. The workshops supported the students’ progression through the knowledge acquisition phases—understanding, mastery, and application. Conclusion: DSI Studio demonstrates potential as an educational tool in neuroanatomy, offering a supportive and flexible learning environment conducive to achieving learning objectives. Our findings preliminarily support the adoption of DSI Studio’s fiber reconstruction technology in undergraduate medical education.