{"title":"Stroke and Vascular Cognitive Impairment: The Role of Intestinal Microbiota Metabolite TMAO.","authors":"Ruxin Tu, Jian Xia","doi":"10.2174/1871527322666230203140805","DOIUrl":"10.2174/1871527322666230203140805","url":null,"abstract":"<p><p>The gut microbiome interacts with the brain bidirectionally through the microbiome-gutbrain axis, which plays a key role in regulating various nervous system pathophysiological processes. Trimethylamine N-oxide (TMAO) is produced by choline metabolism through intestinal microorganisms, which can cross the blood-brain barrier to act on the central nervous system. Previous studies have shown that elevated plasma TMAO concentrations increase the risk of major adverse cardiovascular events, but there are few studies on TMAO in cerebrovascular disease and vascular cognitive impairment. This review summarized a decade of research on the impact of TMAO on stroke and related cognitive impairment, with particular attention to the effects on vascular cognitive disorders. We demonstrated that TMAO has a marked impact on the occurrence, development, and prognosis of stroke by regulating cholesterol metabolism, foam cell formation, platelet hyperresponsiveness and thrombosis, and promoting inflammation and oxidative stress. TMAO can also influence the cognitive impairment caused by Alzheimer's disease and Parkinson's disease via inducing abnormal aggregation of key proteins, affecting inflammation and thrombosis. However, although clinical studies have confirmed the association between the microbiome-gut-brain axis and vascular cognitive impairment (cerebral small vessel disease and post-stroke cognitive impairment), the molecular mechanism of TMAO has not been clarified, and TMAO precursors seem to play the opposite role in the process of poststroke cognitive impairment. In addition, several studies have also reported the possible neuroprotective effects of TMAO. Existing therapies for these diseases targeted to regulate intestinal flora and its metabolites have shown good efficacy. TMAO is probably a new target for early prediction and treatment of stroke and vascular cognitive impairment.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"102-121"},"PeriodicalIF":3.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10653231","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":"Ablation of Shank1 Protects against 6-OHDA-induced Cytotoxicity via PRDX3-mediated Inhibition of ER Stress in SN4741 Cells.","authors":"Ye-Ping Xu, Jing Zhang, Xue Mei, Yan Wu, Wei Jiao, Yu-Hai Wang, Ai-Qin Zhang","doi":"10.2174/1871527322666230216124156","DOIUrl":"10.2174/1871527322666230216124156","url":null,"abstract":"<p><strong>Background: </strong>Postsynaptic density (PSD) is an electron-dense structure that contains various scaffolding and signaling proteins. Shank1 is a master regulator of the synaptic scaffold located at glutamatergic synapses, and has been proposed to be involved in multiple neurological disorders.</p><p><strong>Methods: </strong>In this study, we investigated the role of shank1 in an in vitro Parkinson's disease (PD) model mimicked by 6-OHDA treatment in neuronal SN4741 cells. The expression of related molecules was detected by western blot and immunostaining.</p><p><strong>Results: </strong>We found that 6-OHDA significantly increased the mRNA and protein levels of shank1 in SN4741 cells, but the subcellular distribution was not altered. Knockdown of shank1 via small interfering RNA (siRNA) protected against 6-OHDA treatment, as evidenced by reduced lactate dehydrogenase (LDH) release and decreased apoptosis. The results of RT-PCR and western blot showed that knockdown of shank1 markedly inhibited the activation of endoplasmic reticulum (ER) stress associated factors after 6-OHDA exposure. In addition, the downregulation of shank1 obviously increased the expression of PRDX3, which was accompanied by the preservation of mitochondrial function. Mechanically, downregulation of PRDX3 via siRNA partially prevented the shank1 knockdowninduced protection against 6-OHDA in SN4741 cells.</p><p><strong>Conclusion: </strong>In summary, the present study has provided the first evidence that the knockdown of shank1 protects against 6-OHDA-induced ER stress and mitochondrial dysfunction through activating the PRDX3 pathway.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"402-410"},"PeriodicalIF":3.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10736087","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}
Sarah Lei Qi Khor, Khuen Yen Ng, Rhun Yian Koh, Soi Moi Chye
{"title":"Blood-brain Barrier and Neurovascular Unit Dysfunction in Parkinson's Disease: From Clinical Insights to Pathogenic Mechanisms and Novel Therapeutic Approaches.","authors":"Sarah Lei Qi Khor, Khuen Yen Ng, Rhun Yian Koh, Soi Moi Chye","doi":"10.2174/1871527322666230330093829","DOIUrl":"10.2174/1871527322666230330093829","url":null,"abstract":"<p><p>The blood-brain barrier (BBB) plays a crucial role in the central nervous system by tightly regulating the influx and efflux of biological substances between the brain parenchyma and peripheral circulation. Its restrictive nature acts as an obstacle to protect the brain from potentially noxious substances such as blood-borne toxins, immune cells, and pathogens. Thus, the maintenance of its structural and functional integrity is vital in the preservation of neuronal function and cellular homeostasis in the brain microenvironment. However, the barrier's foundation can become compromised during neurological or pathological conditions, which can result in dysregulated ionic homeostasis, impaired transport of nutrients, and accumulation of neurotoxins that eventually lead to irreversible neuronal loss. Initially, the BBB is thought to remain intact during neurodegenerative diseases, but accumulating evidence as of late has suggested the possible association of BBB dysfunction with Parkinson's disease (PD) pathology. The neurodegeneration occurring in PD is believed to stem from a myriad of pathogenic mechanisms, including tight junction alterations, abnormal angiogenesis, and dysfunctional BBB transporter mechanism, which ultimately causes altered BBB permeability. In this review, the major elements of the neurovascular unit (NVU) comprising the BBB are discussed, along with their role in the maintenance of barrier integrity and PD pathogenesis. We also elaborated on how the neuroendocrine system can influence the regulation of BBB function and PD pathogenesis. Several novel therapeutic approaches targeting the NVU components are explored to provide a fresh outlook on treatment options for PD.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"315-330"},"PeriodicalIF":3.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9574667","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":"Brain-Derived Neurotrophic Factor - The Protective Agent Against Neurological Disorders.","authors":"Prathyusha Koyya, Ram Kumar Manthari, Santhi Latha Pandrangi","doi":"10.2174/1871527322666230607110617","DOIUrl":"10.2174/1871527322666230607110617","url":null,"abstract":"<p><p>The burden of neurological illnesses on global health is significant. Our perception of the molecular and biological mechanisms underlying intellectual processing and behavior has significantly advanced over the last few decades, laying the groundwork for potential therapies for various neurodegenerative diseases. A growing body of literature reveals that most neurodegenerative diseases could be due to the gradual failure of neurons in the brain's neocortex, hippocampus, and various subcortical areas. Research on various experimental models has uncovered several gene components to understand the pathogenesis of neurodegenerative disorders. One among them is the brain-derived neurotrophic factor (BDNF), which performs several vital functions, enhancing synaptic plasticity and assisting in the emergence of long-term thoughts. The pathophysiology of some neurodegenerative diseases, including Alzheimer's, Parkinson's, Schizophrenia, and Huntington's, has been linked to BDNF. According to numerous research, high levels of BDNF are connected to a lower risk of developing a neurodegenerative disease. As a result, we want to concentrate on BDNF in this article and outline its protective role against neurological disorders.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"353-366"},"PeriodicalIF":2.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11348470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9592406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marianna Mazza, Georgios D Kotzalidis, Giuseppe Marano, Domenico De Berardis, Giovanni Martinotti, Enrico Romagnoli, Giuseppe Biondi-Zoccai, Antonio Abbate, Gabriele Sani
{"title":"Lorcaserin: Worthy of Further Insights? Results from Recent Research.","authors":"Marianna Mazza, Georgios D Kotzalidis, Giuseppe Marano, Domenico De Berardis, Giovanni Martinotti, Enrico Romagnoli, Giuseppe Biondi-Zoccai, Antonio Abbate, Gabriele Sani","doi":"10.2174/1871527322666230330124137","DOIUrl":"10.2174/1871527322666230330124137","url":null,"abstract":"<p><p>Lorcaserin is a 3-benzazepine that binds 5-HT<sub>2C</sub> serotonin receptors in the hypothalamus, where it mediates lack of hunger and/or satiety, and in the ventral tegmental area, the site of origin of the mesolimbic and mesocortical dopaminergic projections, which mediate pleasure and reward. The drug has been first developed for the treatment of obesity, where it has shown efficacy, and subsequently trialed to counter substance use (mostly cocaine, cannabis, opioids, and nicotine) and craving, but showed inconsistent effects. Since 2020, the US Food and Drug Administration obtained that the drug was voluntarily withdrawn from the US market on the grounds that its long-term use was found to be associated with a greater incidence of some types of cancer. Provided it can show to be free from cancerogenic effects, ongoing research suggests that lorcaserin may have therapeutic potential for a variety of disorders and conditions beyond obesity. Since 5-HT<sub>2C</sub> receptors are involved in many diversified physiological functions (mood, feeding, reproductive behavior, neuronal processes related to impulsiveness, and modulating reward-related mechanisms) this drug has the potential to treat different central nervous system conditions, such as depression and schizophrenia.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"278-283"},"PeriodicalIF":3.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9618849","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}
Jayaraman Rajangam, Arun Prasath Lakshmanan, K Umamaheswara Rao, D Jayashree, Rajan Radhakrishnan, B Roshitha, Palanisamy Sivanandy, M Jyothi Sravani, K Hanna Pravalika
{"title":"Bell Palsy: Facts and Current Research Perspectives.","authors":"Jayaraman Rajangam, Arun Prasath Lakshmanan, K Umamaheswara Rao, D Jayashree, Rajan Radhakrishnan, B Roshitha, Palanisamy Sivanandy, M Jyothi Sravani, K Hanna Pravalika","doi":"10.2174/1871527322666230321120618","DOIUrl":"10.2174/1871527322666230321120618","url":null,"abstract":"<p><p>Bell palsy is a non-progressive neurological condition characterized by the acute onset of ipsilateral seventh cranial nerve paralysis. People who suffer from this type of facial paralysis develop a droop on one side of their face, or sometimes both. This condition is distinguished by a sudden onset of facial paralysis accompanied by clinical features such as mild fever, postauricular pain, dysgeusia, hyperacusis, facial changes, and drooling or dry eyes. Epidemiological evidence suggests that 15 to 23 people per 100,000 are affected each year, with a recurrence rate of 12%. It could be caused by ischaemic compression of the seventh cranial nerve, which could be caused by viral inflammation. Pregnant women, people with diabetes, and people with respiratory infections are more likely to have facial paralysis than the general population. Immune, viral, and ischemic pathways are all thought to play a role in the development of Bell paralysis, but the exact cause is unknown. However, there is evidence that Bell's hereditary proclivity to cause paralysis is a public health issue that has a greater impact on patients and their families. Delay or untreated Bell paralysis may contribute to an increased risk of facial impairment, as well as a negative impact on the patient's quality of life. For management, antiviral agents such as acyclovir and valacyclovir, and steroid treatment are recommended. Thus, early diagnosis accompanied by treatment of the uncertain etiology of the disorder is crucial. This paper reviews mechanistic approaches, and emerging medical perspectives on recent developments that encounter Bell palsy disorder.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"203-214"},"PeriodicalIF":3.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9169300","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":"Bumetanide, a Diuretic That Can Help Children with Autism Spectrum Disorder.","authors":"Esraa Shaker, Osama El Agami, Abeer Salamah","doi":"10.2174/1871527322666230404114911","DOIUrl":"10.2174/1871527322666230404114911","url":null,"abstract":"<p><strong>Background: </strong>Autism Spectrum Disorder (ASD) is a common child neurodevelopmental disorder, whose pathogenesis is not completely understood. Until now, there is no proven treatment for the core symptoms of ASD. However, some evidence indicates a crucial link between this disorder and GABAergic signals which are altered in ASD. Bumetanide is a diuretic that reduces chloride, shifts gamma-amino-butyric acid (GABA) from excitation to inhibition, and may play a significant role in the treatment of ASD.</p><p><strong>Objective: </strong>The objective of this study is to assess the safety and efficacy of bumetanide as a treatment for ASD.</p><p><strong>Methods: </strong>Eighty children, aged 3-12 years, with ASD diagnosed by Childhood Autism Rating Scale (CARS), ⩾ 30 were included in this double-blind, randomized, and controlled study. Group 1 received Bumetanide, Group 2 received a placebo for 6 months. Follow-up by CARS rating scale was performed before and after 1, 3, and 6 months of treatment.</p><p><strong>Results: </strong>The use of bumetanide in group 1 improved the core symptoms of ASD in a shorter time with minimal and tolerable adverse effects. There was a statistically significant decrease in CARS and most of its fifteen items in group 1 <i>versus</i> group 2 after 6 months of treatment (p-value <0.001).</p><p><strong>Conclusion: </strong>Bumetanide has an important role in the treatment of core symptoms of ASD.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"536-542"},"PeriodicalIF":2.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9252403","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":"The Use of Midazolam as an Antiseizure Medication in Neonatal Seizures: Single Center Experience and Literature Review.","authors":"Raffaele Falsaperla, Ausilia Desiree Collotta, Vincenzo Sortino, Simona Domenica Marino, Silvia Marino, Francesco Pisani, Martino Ruggieri","doi":"10.2174/1871527322666230608105206","DOIUrl":"10.2174/1871527322666230608105206","url":null,"abstract":"<p><strong>Background: </strong>Existing therapeutic alternatives for neonatal crises have expanded in recent decades, but no consensus has been reached on protocols based on neonatal seizures. In particular, little is known about the use of midazolam in newborns.</p><p><strong>Aim: </strong>The aim of our study is to evaluate the response to midazolam, the appearance of side effects, and their impact on therapeutic decisions.</p><p><strong>Methods: </strong>This is a STROBE-conformed retrospective observational study of 10 patients with neonatal seizures unresponsive to common antiseizure drugs, admitted to San Marco University Hospital's neonatal intensive care (Catania, Italy) from September 2015 to October 2022. In our database search, 36 newborns were treated with midazolam, but only ten children met the selection criteria for this study.</p><p><strong>Results: </strong>Response was assessed both clinically and electrographic. Only 4 patients at the end of the treatment showed a complete electroclinical response; they were full-term infants with a postnatal age greater than 7 days. Non-responders and partial responders are all premature (4/10) or full-term neonates who started therapy in the first days of life (< 7th day) (2/10).</p><p><strong>Conclusion: </strong>Neonatal seizures in preterm show a lower response rate to midazolam than seizures in full-term infants, with poorer prognosis. Liver and renal function and central nervous system development are incomplete in premature infants and the first days of life. In this study, we show that midazolam, a short-acting benzodiazepine, appears to be most effective in full-term infants and after 7 days of life.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"1285-1294"},"PeriodicalIF":3.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9598930","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}
Hammad Riaz, Mohammad Uzair, Muhammad Arshad, Ali Hamza, Nedal Bukhari, Faisal Azam, Shahid Bashir
{"title":"Navigated Transcranial Magnetic Stimulation (nTMS) based Preoperative Planning for Brain Tumor Treatment.","authors":"Hammad Riaz, Mohammad Uzair, Muhammad Arshad, Ali Hamza, Nedal Bukhari, Faisal Azam, Shahid Bashir","doi":"10.2174/1871527322666230619103429","DOIUrl":"10.2174/1871527322666230619103429","url":null,"abstract":"<p><p>Transcranial Magnetic Stimulation (TMS) is a non-invasive technique for analyzing the central and peripheral nervous system. TMS could be a powerful therapeutic technique for neurological disorders. TMS has also shown potential in treating various neurophysiological complications, such as depression, anxiety, and obsessive-compulsive disorders, without pain and analgesics. Despite advancements in diagnosis and treatment, there has been an increase in the prevalence of brain cancer globally. For surgical planning, mapping brain tumors has proven challenging, particularly those localized in expressive regions. Preoperative brain tumor mapping may lower the possibility of postoperative morbidity in surrounding areas. A navigated TMS (nTMS) uses magnetic resonance imaging (MRI) to enable precise mapping during navigated brain stimulation. The resulting magnetic impulses can be precisely applied to the target spot in the cortical region by employing nTMS. This review focuses on nTMS for preoperative planning for brain cancer. This study reviews several studies on TMS and its subtypes in treating cancer and surgical planning. nTMS gives wider and improved dimensions of preoperative planning of the motor-eloquent areas in brain tumor patients. nTMS also predicts postoperative neurological deficits, which might be helpful in counseling patients. nTMS have the potential for finding possible abnormalities in the motor cortex areas.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"883-893"},"PeriodicalIF":3.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9672972","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}
Carmen Rubio, Noel Gallardo, Vanessa Mena, Alonso Portilla, Moisés Rubio-Osornio
{"title":"The Participation of Ca<sup>2+</sup> Channels in Epilepsy: A Bibliometric Analysis of the Scientific Literature in Latin America.","authors":"Carmen Rubio, Noel Gallardo, Vanessa Mena, Alonso Portilla, Moisés Rubio-Osornio","doi":"10.2174/1871527322666230518115952","DOIUrl":"10.2174/1871527322666230518115952","url":null,"abstract":"<p><strong>Background: </strong>Bibliometric analysis allows us to quantify and evaluate scientific activity, and it has become increasingly important in all areas of scientific literature. Thanks to these analyses, we can infer where science should put greater efforts into elucidating the underlying mechanisms of diseases that have yet to be fully described or investigated.</p><p><strong>Objective: </strong>This paper delves into published articles related to the involvement of calcium (Ca<sup>2+</sup>) channels in epilepsy, which is a condition with a high prevalence in Latin America.</p><p><strong>Methods: </strong>We followed the scientific publication on SCOPUS and analyzed the impact of publications from Latin America in the field of epilepsy and the study of Ca<sup>2+</sup> channels. We identified the countries with the largest number of publications and found that 68% of them were experimental (animal models), while 32% were clinical. We also identified the main journals, growth over time, and citation numbers.</p><p><strong>Results: </strong>We found a total of 226 works produced by Latin American countries from 1976 to 2022. The countries that have contributed the most to the topic are Brazil, Mexico, and Argentina, with occasional collaborations between them to make contributions to the study of epilepsy and Ca<sup>2+</sup> channels. Additionally, we found that the journal with the most citations is Nature Genetics.</p><p><strong>Conclusion: </strong>The number of authors per article ranges from 1 to 242, and neuroscience journals are the preferred target for researchers, with a predilection for publishing original articles, although 26% of the publications are review articles.</p>","PeriodicalId":10456,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":"784-790"},"PeriodicalIF":3.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9737335","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}