Neuroscience Letters最新文献

{"title":"Acute restraint stress and epinephrine administration disrupt cognitive and emotional functions in male rats via modulation of proinflammatory cytokines, MCT-2, and neurogranin","authors":"Zehra Sezgin ,&nbsp;Hale Sayan Ozacmak ,&nbsp;Inci Turan","doi":"10.1016/j.neulet.2025.138382","DOIUrl":"10.1016/j.neulet.2025.138382","url":null,"abstract":"<div><div>Stress triggers neuroendocrine and physiological changes, often resulting in cognitive impairments and heightened anxiety. This study aims to investigate the effects of acute stress and epinephrine administration on learning, memory, and anxiety-like behavior, as well as their impact on proinflammatory cytokines, neurogranin expression, and brain energy metabolism.</div><div>In this study, three experimental groups were established, each comprising eight rats: control, acute stress, and acute stress combined with epinephrine. The acute stress model consisted of 60 min of restraint stress. Epinephrine was administered following the stress procedure. Memory performance was evaluated using the Morris water maze (MWM), while anxiety-like behavior was assessed through the open field test (OFT). Levels of proinflammatory cytokines, neurogranin, MCT2, glycogen, and corticosterone levels were measured.</div><div>In the probe test, the acute stress group exhibited significantly poorer performance compared to the control group. Epinephrine administration induced anxiogenic effects in stressed animals. Neurogranin and glycogen levels in the hippocampus and prefrontal cortex were significantly reduced in rats exposed to stress + epinephrine compared to controls. MCT2 expression was also significantly lower in the stress + epinephrine group. IL-1β level was elevated in the prefrontal cortex of the stress + epinephrine group compared to the control group, while, TNF-α levels were found to be elevated in the hippocampus.</div><div>Epinephrine administration in conjunction with acute stress has been shown to reduce hippocampal levels of neurogranin, MCT-2, and glycogen, while simultaneously increasing proinflammatory cytokine levels. These molecular alterations appear to contribute to both impaired hippocampal-dependent learning and heightened anxiety-like behavior.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138382"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blockade of acid-sensing ion channels 1a in the mice dorsal raphe nucleus inhibits panic-like responses: Role of 5-HT1A receptors in the dorsal periaqueductal gray","authors":"Alana Tercino Frias,&nbsp;Paloma Molina Hernandes,&nbsp;Helio Zangrossi Jr","doi":"10.1016/j.neulet.2025.138389","DOIUrl":"10.1016/j.neulet.2025.138389","url":null,"abstract":"<div><div>Panic attacks, characterized by intense fear accompanied by autonomic and respiratory changes, can be experimentally modeled in humans and rodents by exposure to high concentrations of CO₂. Acid-sensing ion channels (ASICs), particularly the ASIC1a subtype, are activated by decrease in pH and have been implicated in defensive responses triggered by hypercapnia. ASIC1a are found in key panic-associated areas such as the lateral wings of the dorsal raphe nucleus (lwDRN) and the dorsal periaqueductal gray (dPAG). Here, we first investigated whether ASIC1a channels in the lwDRN modulate the expression of panic-associated escape response in mice. C57BL/6 mice received intra-lwDRN injections of psalmotoxin-1 (Pstx-1; 12.5 or 25 ηg/50 ηL), a selective ASIC1a blocker, and were exposed to 20% CO₂. ASIC1a blockade significantly reduced escape behavior without affecting baseline locomotion, suggesting a panicolytic-like effect. This effect was site-specific and abolished by intra-dPAG administration of WAY100635 (0.74 ηmol/50 ηL), a 5-HT_1A receptor antagonist. Our study provides novel evidence that ASIC1a channels in the lwDRN contribute to CO₂-evoked escape responses and that this modulation depends on serotonergic signaling via 5-HT_1A receptors in the dPAG. These findings offer new insights into the neurobiology of panic attacks paving the way for the development of more precise treatments for PD.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138389"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145138070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repetitive transcranial magnetic stimulation alleviates radiation-induced brain injury in rats: involving the inhibition of ferroptosis","authors":"Xin-Xin Wei ,&nbsp;Hao-Jun Liu ,&nbsp;Zhou-Zan Liao ,&nbsp;Xiang-Xiang Li ,&nbsp;Liang-Liang Ma ,&nbsp;Wei Zou ,&nbsp;Gui-Juan Zhou ,&nbsp;Xiao-Qing Tang","doi":"10.1016/j.neulet.2025.138368","DOIUrl":"10.1016/j.neulet.2025.138368","url":null,"abstract":"<div><div>Radiation-induced brain injury (RIBI) is a prevalent complication following radiotherapy for head and neck tumors, and its effective therapeutic strategies are lacking. Ferroptosis, an iron-dependent cell death, has recently emerged as an important mechanism of radiation-induced cell death. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive neuro-interventional technique with antioxidant and neuroprotective properties. The present study aimed to explore whether rTMS attenuates RIBI by inhibiting ferroptosis. We demonstrated that rTMS alleviated neuronal injury and death in the hippocampus of RIBI rats. rTMS also improved the mitochondrial ultrastructure in the hippocampus of RIBI rats. Moreover, rTMS reduces the accumulation of iron, reactive oxygen species (ROS), and lipid peroxidation products in the hippocampus of RIBI rats. In addition, rTMS increased the expression of Glutathione peroxidase 4 (GPX4), Solute carrier family 7 member 11 (SLC7A11), and Ferritin heavy chain 1 (FTH1) and decreased the expression of Acyl-CoA synthetase long-chain family member 4 (ACSL4). These findings indicate that rTMS attenuates RIBI and the underlying mechanism involves the inhibition of ferroptosis. Our study highlights rTMS as a potentially effective therapeutic intervention for treating RIBI. The mechanistic insights shed light on the role of ferroptosis and expand our knowledge of its potential as a therapeutic target for diseases beyond RIBI.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138368"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145030286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COPII component Sec13 is required for peripheral myelination and Schwann cell maintenance","authors":"Debao Wu ,&nbsp;Zhenghao Li ,&nbsp;Xiaoyun Lu ,&nbsp;Li Li ,&nbsp;Wenxiu Dai ,&nbsp;Xuemin Wang ,&nbsp;Liang Zhang","doi":"10.1016/j.neulet.2025.138386","DOIUrl":"10.1016/j.neulet.2025.138386","url":null,"abstract":"<div><div>Peripheral nerve myelination critically relies on the timely and efficient delivery of myelin proteins and membranes. Although Coat Protein Complex II (COPII) is a canonical vesicular trafficking machinery, the cell-type-specific functions of its components in Schwann cell remain uncharacterized. Here, we show that Sec13, an essential component of COPII, is abundantly expressed in Schwann cells of the sciatic nerve. Furthermore, conditional knockout of Sec13 in Schwann cells (<em>Sec13</em>cKO) results in hindlimb weakness and lethality in mutant mice. Morphological analysis revealed that <em>Sec13</em>cKO nerves are thin and translucent, with immunostaining for myelin basic protein showing a progressive reduction in myelin coverage. Transmission electron microscopy demonstrated fewer myelinated axons, loosely wrapped or absent lamellae, and an increased <em>g</em>–ratio, indicating thinner, poorly compacted sheaths. At the cellular level, <em>Sec13</em> deletion caused a marked decrease in Sox10⁺ Schwann cell density from P7 onward, concomitant with reduced proliferation of Sox10⁺, Sox2⁺, and Oct6⁺ populations, and a significant increase of cell death at P14. Together, these findings suggest that Sec13 is indispensable for Schwann cell proliferation, survival, and execution of the myelination program.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138386"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D3 alleviates AD-like pathology in APP/PS1 mice by inhibiting pyroptosis and neuroinflammation via DJ-1/PARK7","authors":"Chunyu Zhou ,&nbsp;Yulin Wang ,&nbsp;Longfei Zuo ,&nbsp;Yufan Miao ,&nbsp;Wenjie Li ,&nbsp;Xing Li ,&nbsp;Yuan Xue ,&nbsp;Mengxin Li","doi":"10.1016/j.neulet.2025.138385","DOIUrl":"10.1016/j.neulet.2025.138385","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is the most common primary progressive neurodegenerative disorder, with inflammatory responses involved in its onset and progression. Vitamin D (VD) is known for its health benefits, including antioxidant effects. Recently, Deglycase protein 1 (DJ-1/<em>PARK7</em>) has been shown to potentially regulate in antioxidant activity and inflammation regulation. In this study, we investigated the therapeutic effects of VD₃ (30 IU/g/w) in <em>Dj-1</em> knockdown APPswe/PS1E9 (APP/PS1) mice. Pathological changes were assessed using the Morris water maze and Barnes maze, as well as immunofluorescence, thioflavin S staining, Nissl staining, TUNEL staining, Western blot, and RT-PCR. The results demonstrated that VD₃ significantly ameliorated cognitive deficits and attenuated AD-like pathology in APP/PS1 mice. Moreover, VD₃ upregulated DJ-1 expression and suppressed neuroinflammation and neuronal pyroptosis by modulating the NF-κB/NLRP3/caspase-1 and caspase-3/GSDME signaling pathways. Collectively, these findings suggest that DJ-1 mediate these protective effects, as its knockdown reversed VD₃-induced improvements in neuroinflammation and neuronal pyroptosis, implicating that DJ-1 is a crucial modulator in the effects of VD₃ on Alzheimer’s disease pathology.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138385"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mini-Review: Cathodal tDCS over the right prefrontal cortex and inhibitory control: Pinpointing an electrode montage to disrupt a domain-general system","authors":"Carlos J. Gómez-Ariza ,&nbsp;Javier Pacios","doi":"10.1016/j.neulet.2025.138388","DOIUrl":"10.1016/j.neulet.2025.138388","url":null,"abstract":"<div><div>While many tDCS studies have focused on enhancing inhibitory control, only a few have employed tDCS to disrupt the neural activity of specific brain regions and gain understanding of their contribution to inhibitory control. This mini-review describes and discusses the results of studies that specifically applied cathodal tDCS over the right dorsolateral prefrontal cortex. The majority of these studies employed variants of experimental procedures that assessed the ability to inhibit either inappropriate motor responses or competing memories during selective retrieval. In both domains, action stopping and memory downregulation, neuroimaging research has shown that successful inhibitory control engages common areas within the right lateral prefrontal cortex. Strikingly, although a significant proportion of the reviewed studies reported behavioral effects that can be interpreted as a consequence of hindering inhibitory control, they have not been previously considered or discussed altogether despite its theoretical and methodological implications. This consistent disruptive effect challenges the common belief that cathodal tDCS is ineffective in modulating performance when applied to prefrontal regions. Additionally, the results provide causal evidence that supports the proposed role of the right lateral prefrontal cortex in a domain-general inhibitory system, particularly in relation to stopping actions and downregulating competing memories.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138388"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-term effects of sertraline against depressive-like behaviors in a rat model of neonatal hypoxic encephalopathy","authors":"Marie-Michèle Serghani ,&nbsp;Sondos Kassem-Moussa ,&nbsp;Rawan Makki ,&nbsp;Abdallah Kurdi ,&nbsp;Marawan Elbaset ,&nbsp;Helene Hajjar ,&nbsp;Reem El Jammal ,&nbsp;Gabriel T. Flath-Everhard ,&nbsp;Ishaan Prasad ,&nbsp;Assaad Eid ,&nbsp;Aida Habib ,&nbsp;Eva Hamade ,&nbsp;Fletcher A. White ,&nbsp;Bassam Badran ,&nbsp;Makram Obeid","doi":"10.1016/j.neulet.2025.138392","DOIUrl":"10.1016/j.neulet.2025.138392","url":null,"abstract":"<div><div>Hypoxic encephalopathy of the newborn is associated with long-term neurodevelopmental behavioral deficits that lack a definitive “optimal” treatment approach. We previously demonstrated that periadolescent depressive-like behaviors occur in a rat model of early-life hypoxia. Here, we investigated the short-term effects of the selective serotonin reuptake inhibitor, sertraline, against later-life behavioral deficits. Rats were exposed to global hypoxia at postnatal day 10 (P10) and then received either sertraline or its vehicle (P24 to P30). Normoxic controls received sertraline or its vehicle. Depressive-like and anxiety-like behaviors were assessed using the forced swim test (FST) and open field test (OFT), respectively. The FST was conducted at P25-26 and the OFT at P27. Rats were sacrificed at P30 to assess hippocampal microRNA (miR) expression and to histologically evaluate hippocampal neuronal densities and synaptophysin (Syp) protein levels. Early-life hypoxic seizures resulted in increased immobility in the FST (p &lt; 0.05) and decreased exploration in the OFT (p &lt; 0.05). Hypoxia also resulted in chronic alterations in the expression of 25 miRs, 22 of which are known to modulate inflammatory responses and synaptic function. Sertraline treatment normalized hypoxia-induced increased immobility and reversed 17 out of 25 alterations in miR expression. However, sertraline potentiated hypoxia-induced exploratory deficits (p &lt; 0.05). The drug treatment also resulted in OFT deficits in controls (p &lt; 0.05) and 13 unique dysregulations in miR expression. Neuronal densities and Syp levels were comparable among all groups. We demonstrate that sertraline reverses hypoxia-induced depressive-like behaviors, possibly by targeting inflammation and synaptic remodeling. Sertraline-induced anxiety-like behaviors may reflect its known transient early side effects and warrant further research on long-term outcomes.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138392"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145176615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Laughing your… brain off. New insights on the adaptive meaning of humour","authors":"Maria Elide Vanutelli ,&nbsp;Mirella Manfredi","doi":"10.1016/j.neulet.2025.138411","DOIUrl":"10.1016/j.neulet.2025.138411","url":null,"abstract":"","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138411"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tanshinone IIA and hydroxy safflower yellow A reduce cerebral injury via TLR4/NF-κB pathway in rats","authors":"Bin Luo ,&nbsp;Yu Zheng ,&nbsp;Qi Miao ,&nbsp;Yimin Zhang ,&nbsp;Ye Lei ,&nbsp;Qingyun Xu ,&nbsp;Wenwu Li ,&nbsp;Jingao Yu ,&nbsp;Xiao Zhu ,&nbsp;Jianlin Yuan ,&nbsp;Huiyuan Zhu","doi":"10.1016/j.neulet.2025.138390","DOIUrl":"10.1016/j.neulet.2025.138390","url":null,"abstract":"<div><div>Cerebral ischemia–reperfusion injury (CIRI) is a cerebrovascular disorder with high rates of incidence, disability, and death. It has been identified that Salvia miltiorrhiza and safflower have a protective effect in CIRI. However, the mechanisms of which remain to be elucidated. In this study, we investigated the protective mechanisms of the components of Salvia miltiorrhiza and safflower in CIRI, based on the TLR4/NF-κB signaling pathway. Sprague Dawley (SD) rats were used to establish the rat middle cerebral artery occlusion/reperfusion (MACO/R) model by the suture method. Drugs were injected intraperitoneally at 0 and 2 h, followed by once-daily treatment for 3 days. Neurological function and the volume of brain infarction were evaluated, and the pathological changes in brain tissue were examined using HE staining. ELISA kits were used to detect the concentrations of TNF-α and IL-6, while RT-qPCR, Western blot, and immunofluorescence were employed to evaluate the mRNA and protein expression in brain tissue. Following a combination of tanshinone IIA and hydroxy safflower yellow A treatment, our findings indicated that cerebral infarct volume and neurological deficits were reduced. The findings of HE staining revealed an improvement in cerebral histopathological damage in rats with MCAO/R. The levels of TNF-α and IL-6 in serum, as well as the expression of TLR4 and NF-κB in rat brains, were significantly reduced (P &lt; 0.0001). Taken together, these results indicate that the combination of tanshinone ⅡA and hydroxyl safflower yellow A may exhibit a neuroprotective effect on cerebral I/R injury in rats by activating the TLR4/NF-κB signaling pathway.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138390"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145138080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotine exacerbates fear and depression-like behaviors by promoting microglial phagocytosis of synaptic protein in a mouse model of foot shock","authors":"Jiaquan Wang ,&nbsp;Xiao-kang Gong ,&nbsp;Jing Yu ,&nbsp;Liangwei Wu ,&nbsp;Yuheng Zhang ,&nbsp;Pan Li ,&nbsp;Min Qin ,&nbsp;Xiao-chuan Wang ,&nbsp;Xi-ji Shu ,&nbsp;Jian Bao","doi":"10.1016/j.neulet.2025.138394","DOIUrl":"10.1016/j.neulet.2025.138394","url":null,"abstract":"<div><div>Post-traumatic stress disorder (PTSD) is a severe psychiatric disorder characterized by a complex interplay of genetic and environmental influences. Substantial evidence has demonstrated an intricate nexus between nicotine, the principal psychoactive constituent of cigarette smoke, and PTSD neuropathology. Nevertheless, the intricate mechanism underlying the relationship between nicotine consumption and PTSD has not yet been fully understood. Following two weeks of intraperitoneal nicotine administration at two doses (5 mg/kg and 1 mg/kg), we initiated behavioral testing. Our findings reveal that nicotine supplementation exacerbates fear and depression-like behaviors while promoting microglial phagocytosis of synaptic proteins. Moreover, we observed synaptic protein loss and microglial activation in both the hippocampus and cortex in the 5 mg/kg group. CX3CR1-Cre driven Cre recombinase (Cre) is a widely used genetic tool for enabling gene manipulation in microglia. Here, we investigated a genetic ablation method of the CX3CR1 using a Cre-responsive adeno-associated virus (AAV) vector expressing diphtheria toxin subunit-A (DTA). Conversely, microglial ablation via rAAV-EF1a-DIO-DTA-WPRE hGH pA injection in the ventral hippocampus CA1 region of CX3CR1-Cre mice appears to mitigate the pathologies and behavioral abnormalities induced by nicotine. Our results underscore the role of nicotine in the progression of PTSD and demonstrate that microglial depletion mitigates nicotine-induced pathologies and behavioral disturbances. Consequently, our findings suggest that nicotine enhances microglial phagocytosis of synaptic proteins in PTSD, thereby exacerbating fear and depressive symptoms.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138394"},"PeriodicalIF":2.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}