Neuropeptides最新文献

{"title":"Neuropeptide FF prevented histamine- or chloroquine-induced acute itch behavior through non-NPFF receptors mechanism in male mice","authors":"Honghai Tang ,&nbsp;Ting Zhang ,&nbsp;Jiamin Feng ,&nbsp;Mengna Zhang ,&nbsp;Biao Xu ,&nbsp;Qinqin Zhang ,&nbsp;Ning Li ,&nbsp;Nan Zhang ,&nbsp;Quan Fang","doi":"10.1016/j.npep.2024.102481","DOIUrl":"10.1016/j.npep.2024.102481","url":null,"abstract":"<div><div>The neuropeptide FF (NPFF) system regulates various physiological and pharmacological functions, particularly pain modulation. However, the modulatory effect of NPFF system on itch remains unclear. To investigate the modulatory effect and functional mechanism induced by NPFF system on acute itch, we examined the effects of supraspinal administration of NPFF and related peptides on acute itch induced by intradermal (i.d.) injection of histamine or chloroquine in male mice. Our results indicated that intracerebroventricular (i.c.v.) administration of NPFF dose-dependently prevented histamine- or chloroquine-induced acute itch behaviors. In addition, the modulatory effect of NPFF was not affected by the selective NPFF receptor antagonist RF9. Furthermore, we investigated the effects of NPVF and dNPA, the selective agonists of NPFF₁ and NPFF₂ receptors respectively, on the acute itch. The results demonstrated that both NPFF agonists effectively prevented acute itch induced by histamine or chloroquine in a manner similar to NPFF, and their effects were also not modified by RF9. To further investigate the possible mechanism of the NPFF receptors agonists, the NPFF-derived analogues [Phg⁸]-NPFF and NPFF(1–7)-NH₂ that could not activate NPFF receptors in cAMP assays were subsequently tested in the acute itch model. Interestingly, [Phg⁸]-NPFF, but not NPFF(1–7)-NH₂, prevented acute itch behavior after i.c.v. administration. In conclusion, our findings reveal that NPFF and related peptides prevent histamine- and chloroquine-induced acute itch through a NPFF receptor-independent mechanism. And it was revealed that the C-terminal phenyl structure of NPFF may play a crucial role in these modulatory effects on acute itch.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102481"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142587200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid metabolism: Novel approaches for managing idiopathic epilepsy","authors":"Chao Wang,&nbsp;Jinxia Zhai,&nbsp;Xuemei Zhou,&nbsp;Yongjun Chen","doi":"10.1016/j.npep.2024.102475","DOIUrl":"10.1016/j.npep.2024.102475","url":null,"abstract":"<div><div>Epilepsy is a common neurological condition characterized by abnormal neuronal activity, often leading to cellular damage and death. There is evidence to suggest that lipid imbalances resulting in cellular death play a key role in the development of epilepsy, including changes in triglycerides, cholesterol, sphingolipids, phospholipids, lipid droplets, and bile acids (BAs). Disrupted lipid metabolism acts as a crucial pathological mechanism in epilepsy, potentially linked to processes such as cellular ferroptosis, lipophagy, and immune modulation of gut microbiota (thus influencing the gut-brain axis). Understanding these mechanisms could open up new avenues for epilepsy treatment. This study investigates the association between disturbances in lipid metabolism and the onset of epilepsy.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102475"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142375735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The protective effects of orexin B in neuropathic pain by suppressing inflammatory response","authors":"Zuqing Zhu ,&nbsp;Gang Chen ,&nbsp;Jiangtao He ,&nbsp;Yuanting Xu","doi":"10.1016/j.npep.2024.102458","DOIUrl":"10.1016/j.npep.2024.102458","url":null,"abstract":"<div><p>Chronic pain induced by pathological insults to the sensorimotor system is a typical form of neuropathic pain (NP), and the underlying mechanism is complex. Currently, there are no successful therapeutic interventions for NP. Orexin B is a neuropeptide with a wide range of biological functions. However, the pharmacological function of orexin B in chronic neuropathic pain has been less studied. Here, we aim to examine the neuroprotective effects of orexin B in chronic constriction injury (CCI)- induced NP. Firstly, we found that orexin type 2 receptor (OX2R) but not orexin type 1 receptor (OX1R) was reduced in the spinal cord (SC) of CCI-treated rats. Mechanical withdrawal threshold and thermal withdrawal latency assays display that administration of orexin B clearly ameliorated CCI-evoked neuropathic pain dose-dependently. Notably, orexin B treatment also effectively prevented microglia activation by reducing the levels of IBA1. Additionally, orexin B was also found to suppress the inflammatory response in the SC tissue by reducing the levels of IL-6, TNF-α, iNOS, and COX-2 as well as the production of NO and PGE₂ in CCI-treated rats. Furthermore, orexin B administration attenuated oxidative stress (OS) by increasing the activity of SOD and the levels of GSH. Mechanically, orexin B prevented activation of JNK/NF-κB signaling in the SC of CCI-treated rats. Based on these findings, we conclude that orexin B might have a promising role in ameliorating CCI-evoked neuropathic pain through the inhibition of microglial activation and inflammatory response.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102458"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142162195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphorylated NPY1R regulates phenotypic transition of vascular smooth muscle cells, inflammatory response and macrophage infiltration to promote intracranial aneurysm progression","authors":"Jian He ,&nbsp;Yonghong Duan ,&nbsp;Yuanding Jiang ,&nbsp;Jie Luo ,&nbsp;Tao Wang ,&nbsp;Richu Liang ,&nbsp;Ting Tang","doi":"10.1016/j.npep.2024.102465","DOIUrl":"10.1016/j.npep.2024.102465","url":null,"abstract":"<div><h3>Background</h3><div>Rupture of intracranial aneurysm (IA) could give rise to spontaneous subarachnoid hemorrhage, leading to a high disability rate and even death. NPY1R expression was upregulated in aneurysm tissues of IA patients. However, the role and underlying mechanism of NPY1R remains unknown.</div></div><div><h3>Methods</h3><div>The IA model of mice was established using inducing systemic hypertension and injecting elastase. The expression of genes and proteins was detected by RT-qPCR and western blot. The number of T cells, macrophages, and neutrophils in IA mice was detected using flow cytometry and IF assay. The levels of inflammatory factors were measured using ELISA. Patho-morphology and inflammatory cells in aneurysm tissues were evaluated by HE staining. The interaction between TK and NPY1R was validated using Co-IP.</div></div><div><h3>Results</h3><div>NPY1R expression was greatly elevated in aneurysm tissues in IA patients and mice, which were positively related to macrophage infiltration. Besides, exogenous overexpression of NPY1R resulted in the promotion of contractile phenotype to the synthetic phenotype of vascular smooth muscle cells (VSMCs), inflammatory response and M1 macrophage polarization. In terms of the underlying mechanism, NPY1R protein could be modified by TK-mediated phosphorylation and TKI could decrease IA formation and suppresse contractile phenotype to synthetic phenotype of VSMCs, inflammatory response and M1 macrophage polarization in IA mice. Furthermore, ablating mouse macrophages abolished NPY1R overexpression-mediated promotion of IA formation and rupture in mice.</div></div><div><h3>Conclusion</h3><div>Phosphorylated NPY1R contributed to IA progression through promoting contractile phenotype to synthetic phenotype of VSMCs, inflammatory response and M1 macrophage polarization in IA.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102465"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142358313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuritogenesis and protective effects activated by Angiotensin 1–7 in astrocytes-neuron interaction","authors":"Gabriel Alberto de Carvalho Barbosa ,&nbsp;Marina Prado Rubinho ,&nbsp;Milton Kennedy Aquino-Júnior ,&nbsp;Jéssica Rodrigues Pedro ,&nbsp;Lívia Fligioli Donato ,&nbsp;Leonardo Trisciuzzi ,&nbsp;Alessandra Oliveira Silva ,&nbsp;Silvia Graciela Ruginsk ,&nbsp;Carla Speroni Ceron ,&nbsp;Nathalia Peixoto ,&nbsp;Marcos Vinícios Salles Dias ,&nbsp;Marília Gabriella Alves Goulart Pereira","doi":"10.1016/j.npep.2024.102480","DOIUrl":"10.1016/j.npep.2024.102480","url":null,"abstract":"<div><div>The renin angiotensin system (RAS) has been studied for its effects on various neurological disorders. The identification of functional receptors for Ang-(1–7) and Ang II peptides in astrocytes highlights the physiological modulation and the important role of these cells in the central nervous system. The present study aims to understand the role of RAS peptides, particularly Ang-(1–7) and Ang II, in the secretion of trophic factors by astrocytes and their effects on hippocampal neurons. We used primary cultures of astrocytes and neurons from the hippocampus of either sex neonate of Wistar strain rats. In the present study, we demonstrated that the treatment of astrocytes with Ang-(1–7) acts on the modulation of these cells, inducing reactive astrogliosis, identified through the increase in the expression of GFAP. Furthermore, we obtained a conditioned medium from astrocytes treated with Ang-(1–7), which in addition to promoting the secretion of neurotrophic factors essential for neuronal-glial interactions that are fundamental for neuritogenesis and neuronal survival, showed a neuroprotective effect against glutamatergic excitotoxicity. In turn, Ang II does not exhibit the same effects on astrocyte modulation, exacerbating deleterious effects on brain RAS. Neuron-astrocyte interactions have been shown to be an integral part of the central effects mediated by RAS, and this study has significantly contributed to the understanding of the biochemical mechanisms involved in the functioning of this system.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102480"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142578926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physiologically relevant lactate accumulation from exercise or peripheral injection does not alter central or peripheral appetite signaling in mice","authors":"Seth F. McCarthy ,&nbsp;Michael S. Finch ,&nbsp;Rebecca E.K. MacPherson ,&nbsp;Tom J. Hazell","doi":"10.1016/j.npep.2024.102473","DOIUrl":"10.1016/j.npep.2024.102473","url":null,"abstract":"<div><div>Lactate has been implicated in exercise-induced appetite suppression though little work has explored the mechanisms underpinning its role. Recent work suggests lactate accumulation via exercise and intracerebroventricular injection can alter central appetite regulating pathways, though a supraphysiological dose of lactate was administered centrally and there was no assessment of peripheral appetite markers. Therefore, we examined how physiologically relevant lactate accumulation via exercise or intraperitoneal injection altered central and peripheral appetite signaling pathways and whether the lactate dehydrogenase inhibitor oxamate could blunt any exercise effect. Forty 10-week-old C57BL/6 J male mice (<em>n</em> = 10/group) were assigned to either: 1) sedentary (SED + SAL; saline); 2) exercise (EX+SAL; saline); 3) exercise with oxamate (EX+OX; 750 mg‧kg⁻¹ body mass); or 4) lactate (SED + LAC; 1.0 g‧kg⁻¹ body mass). Blood, stomach, and hypothalamus samples were collected ∼2 h post-exercise/injection. Though oxamate blunted exercise-induced lactate accumulation compared to the EX+SAL condition (<em>P</em> = 0.044, <em>d</em> = 0.73), there were no differences in circulating acylated ghrelin or stomach ghrelin O-acyltransferase content between groups (<em>P</em> &gt; 0.213, <span><math><msubsup><mi>η</mi><mi>p</mi><mn>2</mn></msubsup></math></span>&lt;0.125). There were also no differences in hypothalamic content for neuropeptide Y, proopiomelanocortin, agouti-related peptide, and alpha melanocyte-stimulating hormone (<em>P</em> &gt; 0.150, <span><math><msubsup><mi>η</mi><mi>p</mi><mn>2</mn></msubsup></math></span>&lt;0.170). Exercise did increase phosphorylated-total signal transducer and activator of transcription 3 (pSTAT3) compared to EX+OX (<em>p</em> = 0.065, <em>d</em> = 1.23) but there were no differences in other markers of lactate signaling: phosphorylated-total adenosine monophosphate activated protein kinase, and protein kinase b (<em>P</em> &gt; 0.121, <span><math><msubsup><mi>η</mi><mi>p</mi><mn>2</mn></msubsup></math></span>&lt;0.160). Our results suggest that lactate accumulation due to exercise or peripheral injection does not alter central or peripheral appetite signaling when measured 2 h post-exercise/injection, though pSTAT3 was blunted with oxamate.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102473"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adrenomedullin-mediated depressor response with visceral afferent-specific membrane depolarization in isolated nodose ganglion neurons from adult female rat","authors":"Yan Feng ,&nbsp;Ying Li ,&nbsp;Hua Liu","doi":"10.1016/j.npep.2024.102476","DOIUrl":"10.1016/j.npep.2024.102476","url":null,"abstract":"<div><div>Adrenomedullin (ADM) is an endogenous and vasoactive neuropeptide that possesses potent central/peripheral regulations on blood pressure (BP) and sex-related vasodilation under physiological conditions. However, the role of ADM on baroreflex afferent function is largely unknown. Here, BP was monitored in adult female rats while ADM was microinjected into the nodose ganglion (NG); Fluorescent intensity against ADM was analyzed in the tissue level and membrane responses elicited by ADM were tested in identified NG neurons isolated from adult female rats with gap-free protocol under current-clamp mode with or without ADM antagonist. The results showed that BP was reduced by ADM (30–300 nM) concentration-dependently; myelinated (HCN1-positive) neurons showed significantly higher fluorescent intensity against ADM antibody vs. unmyelinated (HCN1-negative) neurons. Interestingly, patch-clamp data indicated that membrane potential was not changed in 50 % (6/12) of identified A-types, only 4/12 was hyperpolarized by 30 nM ADM, while 100 nM ADM induced brief hyperpolarization followed by depolarization in 2/12 of recordings; Robustly, ADM depolarized 100 % tested myelinated Ah-type neurons with dramatic and concentration-dependent repetitive discharges; While, a majority (8/9) of unmyelinated C-types were depolarized and few with repetitive dischargers. By application of ADM (22–52), the depolarization elicited by ADM 100 nM was partially or completely abolished in Ah-types or C-types, respectively. These datasets demonstrated for the first time that baroreflex afferents especially female-distributed subpopulation of Ah-types would be a key player in ADM-mediated depressor response unveiling the dominate role of peripheral ADM in neurocontrol of hypotension via baroreflex afferent function and gender-dependent vasodilation promoted by female sex steroid.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102476"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropeptides or their receptors in pathogenesis of lung diseases and therapeutic potentials","authors":"Changgen Li ,&nbsp;Na Zang ,&nbsp;Enmei Liu","doi":"10.1016/j.npep.2024.102482","DOIUrl":"10.1016/j.npep.2024.102482","url":null,"abstract":"<div><div>There are complex interactions between the immune system and the nervous system in the lung. The nervous system perceives environmental stimuli and transmits these signals to immune cells via neurotransmitters, which is essential for effective immunity and environmental balance. Neuropeptides are important neurotransmitters in the lung, where they regulate immune responses through direct and indirect mechanisms, affecting the occurrence and development of lung diseases. In this review, we emphasize the role of neuropeptides in the pathogeneis of lung diseases and their potential therapeutic value for lung diseases.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102482"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Upregulation of Xbp1 in NPY/AgRP neurons reverses diet-induced obesity and ameliorates leptin and insulin resistance","authors":"Jason Ajwani,&nbsp;Eunsang Hwang,&nbsp;Bryan Portillo,&nbsp;Linh Lieu,&nbsp;Briana Wallace,&nbsp;Anita Kabahizi,&nbsp;Zhenyan He,&nbsp;Yanbin Dong,&nbsp;Kyle Grose,&nbsp;Kevin W. Williams","doi":"10.1016/j.npep.2024.102461","DOIUrl":"10.1016/j.npep.2024.102461","url":null,"abstract":"<div><p>The molecular mechanisms underlying neuronal leptin and insulin resistance in obesity and diabetes are not fully understood. In this study, we show that induction of the unfolded protein response transcription factor, spliced X-box binding protein 1 (Xbp1s), in Agouti-Related Peptide (AgRP) neurons alone, is sufficient to not only protect against but also significantly reverse diet-induced obesity (DIO) as well as improve leptin and insulin sensitivity, despite activation of endoplasmic reticulum stress. We also demonstrate that constitutive expression of Xbp1s in AgRP neurons contributes to improved insulin sensitivity and glucose tolerance. Together, our results identify critical molecular mechanisms linking ER stress in arcuate AgRP neurons to acute leptin and insulin resistance as well as liver glucose metabolism in DIO and diabetes.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102461"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142056176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropeptide Y Y2 receptors in acute and chronic pain and itch","authors":"Paramita Basu ,&nbsp;Bradley K. Taylor","doi":"10.1016/j.npep.2024.102478","DOIUrl":"10.1016/j.npep.2024.102478","url":null,"abstract":"<div><div>Pain and itch are regulated by a diverse array of neuropeptides and their receptors in superficial laminae of the spinal cord dorsal horn (DH). Neuropeptide Y (NPY) is normally expressed on DH neurons but not sensory neurons. By contrast, the Npy2r receptor (Y2) is expressed on the central and peripheral terminals of sensory neurons but not on DH neurons. Neurophysiological slice recordings indicate that Y2-selective agonists inhibits spinal neurotransmitter release from sensory neurons. However, behavioral pharmacology studies indicate that Y2 agonists exert minimal changes in nociception, even after injury. Additional discrepancies in the behavioral actions of the Y2-antagonist BIIE0246 – reports of either pronociception or antinociception – have now been resolved. In the normal state, spinally-directed (intrathecal) administration of BIIE0246 elicits ongoing nociception, hypersensitivity to sensory stimulation, and aversion. Conversely, in the setting of nerve injury and inflammation, intrathecal BIIE024 reduced not only mechanical and thermal hypersensitivity, but also a measure of the affective dimension of pain (conditioned place preference). When administered in chronic pain models of latent sensitization, BIIE0246 produced a profound reinstatement of pain-like behaviors. We propose that tissue or nerve injury induces a G protein switch in the action of NPY-Y2 signaling from antinociception in the naïve state to the inhibition of mechanical and heat hyperalgesia in the injured state, and then a switch back to antinociception to keep LS in a state of remission. This model clarifies the pharmacotherapeutic potential of Y2 research, pointing to the development of a new non-opioid pharmacotherapy for chronic pain using Y2 antagonists in patients who do not develop LS.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102478"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}