Neuropeptides最新文献

{"title":"The regulatory effects of the apelin/APJ system on depression: A prospective therapeutic target","authors":"Yanjun Tian ,&nbsp;Ruihao Wang ,&nbsp;Lin Liu ,&nbsp;Wenhuan Zhang ,&nbsp;Haiqing Liu ,&nbsp;Liqing Jiang ,&nbsp;Yunlu Jiang","doi":"10.1016/j.npep.2023.102382","DOIUrl":"10.1016/j.npep.2023.102382","url":null,"abstract":"<div><p>Depression is a debilitating neuropsychological disorder characterized by high incidence, high recurrence, high suicide, and high disability rates, which poses serious threats to human health and imposes heavy psychological and economic burdens on family and society. The pathogenesis of depression is extremely complex, and its etiology is multifactorial. Mounting evidence suggests that apelin and apelin receptor APJ, which compose the apelin/APJ system, are related to the development of depression. However, the specific mechanism is still unclear, and research in this area in human is still insufficient. Acceleration of research into the regulatory effects and underlying mechanisms of the apelin/APJ system in depression may identify attractive therapeutic targets and contribute to the development of novel intervention strategies against this devastating psychological disorder. In this review, we mainly discuss the regulatory effects of apelin/APJ system on depression and its potential therapeutic applications.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"102 ","pages":"Article 102382"},"PeriodicalIF":2.9,"publicationDate":"2023-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10268679","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":"Mate calling alters expression of neuropeptide, cocaine- and amphetamine- regulated transcript (CART) in the brain of male frog Microhyla nilphamariensis","authors":"Shobha Bhargava ,&nbsp;Ketaki Shetye ,&nbsp;Swapnil Shewale ,&nbsp;Nitin Sawant ,&nbsp;Sneha Sagarkar ,&nbsp;Nishikant Subhedar","doi":"10.1016/j.npep.2023.102380","DOIUrl":"10.1016/j.npep.2023.102380","url":null,"abstract":"<div><p><span>Croaking is a unique component of reproductive behaviour<span> in amphibians which plays a key role in intraspecies communication and mate evaluation. While gonadal hormones are known to induce croaking, central regulation of sound production is less studied. Croaking is a dramatic, transient activity that sets apart an animal from non-croaking individuals. Herein, we aim at examining the profile of the neuropeptide cocaine- and amphetamine-regulated transcript (CART) in actively croaking and non-croaking frog </span></span><em>Microhyla nilphamariensis</em><span><span>. In anurans, this peptide is widely expressed in the areas inclusive of acoustical nuclei as well as areas relevant to reproduction. CART immunoreactivity<span><span> was far more in the preoptic area (POA), anteroventral </span>tegmentum (AV), ventral </span></span>hypothalamus<span><span><span> (vHy), pineal (P) and pituitary gland of croaking frog compared to non-croaking animals. On similar lines, tissue fragments collected from the mid region of the brain inclusive of POA, vHy, AV, pineal and pituitary gland of croaking frog showed upregulation of CART mRNA. However, CART immunoreactivity in the neuronal </span>perikarya of </span>raphe (Ra) was completely abolished during croaking activity. The data suggest that CART signaling in the brain may be an important player in mediating croaking behaviour in the frog.</span></span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"102 ","pages":"Article 102380"},"PeriodicalIF":2.9,"publicationDate":"2023-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10256589","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":"Reduced mastication during growth inhibits cognitive function by affecting trigeminal ganglia and modulating Wnt signaling pathway and ARHGAP33 molecular transmission","authors":"Eri Misawa-Omori,&nbsp;Hidemasa Okihara,&nbsp;Takuya Ogawa,&nbsp;Yasunori Abe,&nbsp;Chiho Kato,&nbsp;Hideyuki Ishidori,&nbsp;Akiyo Fujita,&nbsp;Satoshi Kokai,&nbsp;Takashi Ono","doi":"10.1016/j.npep.2023.102370","DOIUrl":"10.1016/j.npep.2023.102370","url":null,"abstract":"<div><p>Binding of brain-derived neurotrophic factor (BDNF) to its receptor tyrosine kinase B (TrkB) is essential for the development of the hippocampus, which regulates memory and learning. Decreased masticatory stimulation during growth reportedly increases BDNF expression while decreasing TrkB expression in the hippocampus. Increased BDNF expression is associated with Wnt family member 3A (Wnt3a) expression and decreased expression of Rho GTPase Activating Protein 33 (ARHGAP33), which regulates intracellular transport of TrkB. TrkB expression may be decreased at the cell surface and affects the hippocampus via BDNF/TrkB signaling. Mastication affects cerebral blood flow and the neural cascade that occurs through the trigeminal nerve and hippocampus. In the current study, we hypothesized that decreased masticatory stimulation reduces memory/learning in mice due to altered Wnt3a and ARHGAP33 expression, which are related to memory/learning functions in the hippocampus. To test this hypothesis, we fed mice a powdered diet until 14 weeks of age and analyzed the BDNF and TrkB mRNA expression in the right hippocampus using real-time polymerase chain reaction and Wnt3a and ARHGAP33 levels in the left hippocampus using western blotting. Furthermore, we used staining to assess BDNF and TrkB expression in the hippocampus and the number of nerve cells, the average size of each single cell and the area of intercellular spaces of the trigeminal ganglion (TG). We found that decreased masticatory stimulation affected the expression of BDNF, Wnt3a, ARHGAP33, and TrkB proteins in the hippocampus, as well as memory/learning. The experimental group showed significantly decreased numbers of neurons and increased the area of intercellular spaces in the TG. Our findings suggest that reduced masticatory stimulation during growth induces a decline in memory/learning by modulating molecular transmission mechanisms in the hippocampus and TG.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"102 ","pages":"Article 102370"},"PeriodicalIF":2.9,"publicationDate":"2023-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10085261","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":"An inclusive study of recent advancements in Alzheimer's disease: A comprehensive review","authors":"Sukanya Singh ,&nbsp;Mitali Mahajan ,&nbsp;Dhawal Kumar,&nbsp;Kunika Singh,&nbsp;Mehvish Chowdhary,&nbsp;Amit","doi":"10.1016/j.npep.2023.102369","DOIUrl":"10.1016/j.npep.2023.102369","url":null,"abstract":"<div><p>Alzheimer's disease<span><span><span><span> (AD) has remained elusive in revealing its pathophysiology and mechanism of development. In this review paper, we attempt to highlight several theories that abound about the exact pathway of AD development. The number of cases worldwide has prompted a constant flow of research to detect high-risk patients, slow the progression of the disease and discover improved methods of </span>treatment that may prove effective. We shall focus on the two main classes of </span>drugs that are currently in use; and emerging ones with novel mechanisms that are under development. As of late there has also been increased attention towards factors that were previously thought to be unrelated to AD, such as the gut </span>microbiome, lifestyle habits, and diet. Studies have now shown that all these factors make an impact on AD progression, thus bringing to our attention more areas that could hold the key to combating this disease. This paper covers all the aforementioned factors concisely. We also briefly explore the relationship between mental health and AD, both before and after the diagnosis of the disease.</span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"102 ","pages":"Article 102369"},"PeriodicalIF":2.9,"publicationDate":"2023-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10414878","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":"Naloxone could limit morphine hypersensitivity: Considering the molecular mechanisms","authors":"Mojgan Baratzadeh ,&nbsp;Samira Danialy ,&nbsp;Shima Abtin ,&nbsp;Homa Manaheji","doi":"10.1016/j.npep.2023.102345","DOIUrl":"10.1016/j.npep.2023.102345","url":null,"abstract":"<div><h3>Background</h3><p><span><span>Naloxone<span><span> has been used as an opioid antagonist to prevent multiple adverse side effects of opioid-like tolerance and </span>hyperalgesia. This study has investigated naloxone combined with morphine to limit pain </span></span>hypersensitivity. In addition, the expression of brain-derived neurotrophic factor (BDNF) and K</span>⁺ Cl⁻ cotransporter2 (KCC2) were also studied.</p></div><div><h3>Methods</h3><p><span><span>Forty-eight adult male Wistar rats (180–220 g) were divided into eight groups, with six rats in each group. Rats were divided into two tolerance and hyperalgesia groups; the sham group, the morphine group, the treatment group (naloxone along with morphine), and the sham group (naloxone along with saline) for eight consecutive days. Tail-flick test was performed on days 1, 5, and 8, and the plantar test on days 1 and 10. On days 8 and 10, the lumbar segments of the spinal cord were collected, and BDNF and KCC2 expression were analyzed using </span>western blotting and </span>immunohistochemistry, respectively.</p></div><div><h3>Results</h3><p>Results showed that tolerance and hyperalgesia developed following eight days of repeated morphine injection. BDNF expression significantly increased, but KCC2 was downregulated. Co-administration of naloxone and morphine decreased tolerance and hyperalgesia by decreasing BDNF and increasing KCC2 expression, respectively.</p></div><div><h3>Conclusion</h3><p>This study suggests that BDNF and KCC2 may be candidate molecules for decreased morphine tolerance and hyperalgesia.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102345"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9749388","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":"Changes in working memory induced by lipopolysaccharide administration in mice are associated with metabotropic glutamate receptors 5 and contrast with changes induced by cyclooxygenase-2: Involvement of postsynaptic density protein 95 and down syndrome cell adhesion molecule","authors":"Katarzyna Stachowicz ,&nbsp;Patrycja Pańczyszyn-Trzewik ,&nbsp;Magdalena Sowa-Kućma ,&nbsp;Paulina Misztak","doi":"10.1016/j.npep.2023.102347","DOIUrl":"10.1016/j.npep.2023.102347","url":null,"abstract":"<div><p><span>The strength and quality of the signal propagated by the glutamate<span><span> synapse (Glu) depend, among other things, on the structure of the postsynaptic part and the quality of adhesion between the interacting components of the synapse. Postsynaptic density protein 95 (PSD95), </span>mammalian target of rapamycin<span> (mTOR), and Down syndrome cell adhesion molecule<span><span> (DSCAM) are components of the proper functioning of an excitatory synapse. PSD95 is a member of the membrane-associated </span>guanylate kinases protein family, mainly located at the postsynaptic density of the excitatory synapse. PSD95, via direct interaction, regulates the clustering and functionality of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and </span></span></span></span><em>N</em><span><span><span>-methyl-D-aspartic acid (NMDA) receptors at a synapse. Here, the effects of treatment with an antagonist of mGluR5 (MTEP) and </span>NS398<span><span> (cyclooxygenase-2, COX-2 inhibitor) on PSD95, mTOR, and DSCAM in the hippocampus<span> (HC) of C57B1/6 J mice using Western blots in the context of learning were examined. Moreover, the sensitivity of selected proteins to </span></span>lipopolysaccharide (LPS) was monitored. </span></span>MTEP injected for seven days induced upregulation of PSD95 in HC of mice. The observed effect was regulated by a COX-2 inhibitor and concurrently by LPS. Accompanying alterations in DSCAM protein were found, suggesting changes in adhesion strength after modulation of glutamatergic (Glu) synapse via tested compounds.</span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102347"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10126371","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":"Intrathecal administration of botulinum toxin type a antagonizes neuropathic pain by countering increased vesicular nucleotide transporter expression in the spinal cord of chronic constriction injury of the sciatic nerve rats","authors":"Yongqiang Shi ,&nbsp;Chaoyang Gong ,&nbsp;Wei Nan ,&nbsp;Wenming Zhou ,&nbsp;Zeyuan Lei ,&nbsp;Kaisheng Zhou ,&nbsp;Linna Wang ,&nbsp;Guanghai Zhao ,&nbsp;Haihong Zhang","doi":"10.1016/j.npep.2023.102346","DOIUrl":"10.1016/j.npep.2023.102346","url":null,"abstract":"<div><p><span><span><span>Botulinum toxin type A (BoNT/A) induces direct </span>analgesic effects<span><span> in neuropathic pain by inhibiting the release of substance P, calcitonin gene-related peptide (CGRP) and </span>glutamate<span>. Vesicular nucleotide transporter<span> (VNUT) was responsible for the storage and release of ATP in vivo, and one of the mechanisms underlying neuropathic pain is VNUT-dependent release of extracellular ATP from dorsal horn neurons. However, the analgesic effect of BoNT/A by affecting the expression of VNUT remained largely unknown. Thus, in this study, we aimed to elucidate the antinociceptive potency and analgesic mechanism of BoNT/A in </span></span></span></span>chronic constriction injury<span> of the sciatic nerve (CCI) induced neuropathic pain. Our results showed that a single </span></span>intrathecal<span><span> injection of 0.1 U BoNT/A seven days after CCI surgery produced significant analgesic activity and decreased the expression of VNUT in the spinal cord of CCI rats. Similarly, BoNT/A inhibited the CCI-induced increase in ATP content in the rat spinal cord. Overexpression of VNUT in the spinal cord of CCI-induced rats markedly reversed the antinociceptive effect of BoNT/A. Furthermore, 33 U/mL BoNT/A dramatically reduced the expression of VNUT in pheochromocytoma (PC12) cells but overexpressing SNAP-25 increased VNUT expression in </span>PC12 cells. Our current study is the first to demonstrate that BoNT/A is involved in neuropathic pain by regulating the expression of VNUT in the spinal cord in rats.</span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102346"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9749394","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":"Metformin promotes Schwann cell remyelination, preserves neural tissue and improves functional recovery after spinal cord injury","authors":"Zucheng Huang ,&nbsp;Junyu Lin (1,) ,&nbsp;Hui Jiang ,&nbsp;Wanrong Lin ,&nbsp;Zhiping Huang ,&nbsp;Jiayu Chen ,&nbsp;Wende Xiao ,&nbsp;Qiong Lin ,&nbsp;Jun Wang ,&nbsp;Shifeng Wen ,&nbsp;Qingan Zhu ,&nbsp;Junhao Liu","doi":"10.1016/j.npep.2023.102348","DOIUrl":"10.1016/j.npep.2023.102348","url":null,"abstract":"<div><p><span><span>Patients with a spinal cord injury (SCI) usually suffer lifelong disability as a result. Considering this, SCI </span>treatment<span> and pathology study are urgently needed. Metformin, a widely used </span></span>hypoglycemic drug<span><span><span>, has been indicated for its important role in central nervous system diseases<span>. This study aimed to investigate the potential effect of metformin on remyelination after SCI. In the present study, we established a cervical contusion SCI model and metformin treatment was applied after SCI. Biomechanical parameters and behavioral assessment were used to evaluate the </span></span>severity of injury<span> and the improvement of functional recovery after SCI, respectively. The immunofluorescence and </span></span>western blot<span> were performed at the terminal time point. Our results showed that treating with metformin after SCI improved functional recovery by reducing the white matter loss and promoting Schwann cell<span><span> remyelination, and the Nrg1/ErbB signaling pathway may be involved in promoting remyelination mediated by </span>oligodendrocytes and Schwann cells. In addition, the area of spared tissues was significantly increased in the metformin group. However, metformin had no significant effects on the glial scar and inflammation after SCI. In summary, these findings indicated that the role of metformin in Schwann cell remyelination after SCI was probably related to the regulation of the Nrg1/ErbB pathway. It is, therefore, possible to suggest that metformin may be a potential therapy for SCI.</span></span></span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102348"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10108683","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":"Protective effect of Prolactin releasing peptide against 1,2-diacetylbenzene -induced neuroinflammation","authors":"Ngoc Minh Hong Hoang,&nbsp;Wonhee Jo,&nbsp;Min-Sun Kim","doi":"10.1016/j.npep.2023.102349","DOIUrl":"10.1016/j.npep.2023.102349","url":null,"abstract":"<div><p><span>Prolactin-releasing peptide (PrRP) has been investigated as a potential therapeutic for diabetes by the effect of food intake reduction, increasing leptin signaling, and insulin tolerance. Recent studies focused on its </span>synaptogenesis<span><span><span><span> and protective effects against neurodegeneration. Whereas 1,2-diacetylbenzene (DAB), a common metabolite of a neurotoxicant 1,2-diethyl benzene, causes memory impairment and </span>neurotoxicity<span> partly through the inflammatory process. Our present study assessed the effect of PrRP in microglia and its action in balancing the inflammation to protect against DAB. We observed that PrRP modulated </span></span>NADPH oxidase - regulated NLRP3 </span>inflammasome<span> and PRL signaling pathways differently between physical and toxic conditions in microglia.</span></span></p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102349"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10126418","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":"Arginine vasopressin effects on membrane potentials of preoptic area temperature-sensitive and -insensitive neurons in rat hypothalamic tissue slices","authors":"Yu Tang ,&nbsp;Siyuan Liu ,&nbsp;Lingzhi Xu ,&nbsp;Min Huang ,&nbsp;Ke Zhang","doi":"10.1016/j.npep.2023.102344","DOIUrl":"10.1016/j.npep.2023.102344","url":null,"abstract":"<div><p><span>Arginine vasopressin<span><span> (AVP) plays a hypothermic regulatory role in thermoregulation and is an important </span>endogenous mediator<span> in this mechanism. In the preoptic area (POA), AVP increases the spontaneous firing and thermosensitivity of warm-sensitive neurons and decreases those of cold-sensitive and temperature-insensitive neurons. Because POA neurons play a crucial role in precise thermoregulatory responses, these findings indicate that there is an association between the hypothermia and changes in the firing activity of AVP-induced POA neurons. However, the electrophysiological mechanisms by which AVP controls this firing activity remain unclear. Therefore, in the present study, using in vitro hypothalamic brain slices and whole-cell recordings, we elucidated the membrane potential responses of temperature-sensitive and –insensitive POA neurons to identify the applications of AVP or V</span></span></span>_1a<span> vasopressin receptor antagonists. By monitoring changes in the resting potential and membrane potential thermosensitivity of the neurons before and during experimental perfusion, we observed that AVP increased the changes in the resting potential of 50% of temperature-insensitive neurons but reduced them in others. These changes are because AVP enhances the membrane potential thermosensitivity of nearly 50% of the temperature-insensitive neurons. On the other hand, AVP changes both the resting potential and membrane potential thermosensitivity of temperature-sensitive neurons, with no differences between the warm- and cold-sensitive neurons. Before and during AVP or V</span>_1a vasopressin receptor antagonist perfusion, no correlation was observed between changes in the thermosensitivity and membrane potential of all neurons. Furthermore, no correlation was observed between the thermosensitivity and membrane potential thermosensitivity of the neurons during experimental perfusion. In the present study, we found that AVP induction did not result in any changes in resting potential, which is unique to temperature-sensitive neurons. The study results suggest that AVP-induced changes in the firing activity and firing rate thermosensitivity of POA neurons are not controlled by resting potentials.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"100 ","pages":"Article 102344"},"PeriodicalIF":2.9,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9750152","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}