{"title":"EEG-ERP Correlates of Cognitive Dysfunction in Polycystic Ovarian Syndrome.","authors":"Neethu Showkath, Meenakshi Sinha, Jayshri R Ghate, Sarita Agrawal, Sucharita Mandal, Ramanjan Sinha","doi":"10.1177/09727531221115318","DOIUrl":"https://doi.org/10.1177/09727531221115318","url":null,"abstract":"<p><strong>Background: </strong>Polycystic ovarian syndrome (PCOS) has been shown to affect the psychological and cognitive status of a woman. However, amidst various conflicting reports in this regard, very few studies attempted to assess these aspects objectively using electroencephalography (EEG) and event-related potential (ERP).</p><p><strong>Purpose: </strong>To assess changes in neurocognitive and psychological parameters of PCOS women without any other comorbidities.</p><p><strong>Methods: </strong>PCOS women aged 18 years to 35 years, diagnosed from obstetrics and gynecology OPD who are otherwise free of any other comorbidities, were assessed for psychological status (anxiety and depression using the State-Trait Anxiety Inventory and Beck Depression Inventory, respectively). Thereafter, a cognitive assessment was done subjectively by the Montreal Cognitive Assessment (MoCA) questionnaire and objectively by using EEG [absolute and relative power of alpha, beta, and theta waves along with theta/beta ratios (TBR) and theta/alpha ratio (TAR)] and P300 amplitude and latency of ERP during a visual oddball paradigm task in control (<i>n</i> = 30) and PCOS (<i>n</i> = 37) subjects.</p><p><strong>Results: </strong>PCOS women showed significantly higher anxiety and depression scores along with low MoCA scores. Significantly reduced absolute alpha, increased frontal beta, and markedly increased theta (relative) power with increased TAR in the PCOS group were seen. Also, a significant reduction in P300 amplitude with prolonged latency during the visual oddball paradigm task was evident in them.</p><p><strong>Conclusion: </strong>Reduced alpha and higher theta activity with increased TAR are indicative of poor neural processing ability. Reduced P300 amplitude with more latency also suggests a cognitive decline, which is corroborated by reduced MoCA scores. Our study objectively indicates the presence of subclinical cognitive impairment in PCOS patients even without any comorbidities.</p>","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 4","pages":"225-232"},"PeriodicalIF":1.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b3/df/10.1177_09727531221115318.PMC10101155.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9686351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Switching to Tenecteplase from Alteplase for Ischemic Stroke: Is it the Time for Universal Adoption?","authors":"Sanjeev Kharel, Riwaj Bhagat","doi":"10.1177/09727531221125589","DOIUrl":"https://doi.org/10.1177/09727531221125589","url":null,"abstract":"Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons AttributionNonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-Commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https:// us.sagepub.com/en-us/nam/open-access-at-sage). Commentary","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 4","pages":"201-202"},"PeriodicalIF":1.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/08/bf/10.1177_09727531221125589.PMC10101158.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9686353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Anesthetic Challenges in a Patient of Morquio Syndrome Associated with Acromegaly.","authors":"Nidhi Singh, Rashi Sarna, Manjul Tripathi, Rajeev Chauhan, Sanjay Kumar","doi":"10.1177/09727531221137403","DOIUrl":"https://doi.org/10.1177/09727531221137403","url":null,"abstract":"<p><p>Morquio syndrome is one of the rare storage disorders associated with excessive deposition of keratin sulfate and chondroitin-6-sulfate in bones, cartilages, heart valves, and cornea. Although most individuals with this syndrome appear normal at birth; skeletal abnormalities often develop within the first year of life. Restricted breathing, joint stiffness, and cardiac abnormalities are also common. The multisystem involvement in these patients poses unique anesthestic challenges and there is a paucity of literature regarding the anesthetic management of patients with this condition. We report a successful management of a rare case of 34 years old male with Morquio syndrome who presented an association of acromegaly and was planned for surgical resection of the tumor under general anesthesia. Such rare disorders primarily require thorough knowledge about the disease, its presentation and management strategies for a better outcome. Keeping in mind the multisystem involvement a proper teamwork and coordination of various specialities becomes an utmost importance.</p>","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 4","pages":"245-248"},"PeriodicalIF":1.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b0/dd/10.1177_09727531221137403.PMC10101157.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9686352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mai A Zahra, Eman S Kamha, Hanan K Abdelaziz, Howaida A Nounou, Hany M El Deeb
{"title":"Aberrant Expression of Serum MicroRNA-153 and -199a in Generalized Epilepsy and its Correlation with Drug Resistance.","authors":"Mai A Zahra, Eman S Kamha, Hanan K Abdelaziz, Howaida A Nounou, Hany M El Deeb","doi":"10.1177/09727531221077667","DOIUrl":"https://doi.org/10.1177/09727531221077667","url":null,"abstract":"<p><strong>Background: </strong>Epilepsy is one of the common neurological disorders affecting approximately 50 million people worldwide. Despite the recent introduction of new antiepileptic drugs, about one-third of patients with epilepsy have seizures refractory to pharmacotherapy. Early recognition of patients with drug-resistant epilepsy may help direct these patients to appropriate nonpharmacological treatment.</p><p><strong>Purpose: </strong>The possible use of serum microRNAs (miRNAs) as noninvasive biomarkers has been explored in various brain diseases, including epilepsy. In this study, we are aiming at analyzing the expression levels of circulating miRNA-153 and miRNA-199a in patients with generalized epilepsy and their correlation with drug resistance.</p><p><strong>Methods: </strong>Our study comprised 40 patients with generalized epilepsy and 20 healthy controls. 22 patients were drug-resistant and 18 patients were drug-responsive. The expression levels of miRNA-153 and -199a in serum were analyzed using quantitative real-time polymerase chain reaction. Data analysis was done by IBM SPSS Statistics 20.0.</p><p><strong>Results: </strong>The expression of miRNA-153 and -199a in serum was significantly downregulated in patients with generalized epilepsy compared with that of the healthy control (<i>P</i> < .001). Combined expression level of serum miRNA-153 and -199a had a sensitivity of 85% and a specificity of 90% in the diagnosis of generalized epilepsy. Furthermore, the expression levels of miRNA-153 and -199a were significantly decreased in drug-resistant patients compared to the drug-responsive group, and the combination of both markers gave the best results in differentiating between the two groups.</p><p><strong>Conclusion: </strong>We suggest that serum miRNAs-153 and -199a expression levels could be potential noninvasive biomarkers supporting the diagnosis of generalized epilepsy. Moreover, they could be used for the early detection of refractory generalized epilepsy.</p>","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 4","pages":"203-208"},"PeriodicalIF":1.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/07/cf/10.1177_09727531221077667.PMC10101161.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9686348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tracking the Progression and Influence of Beta-Amyloid Plaques Using Percolation Centrality and Collective Influence Algorithm: A Study Using PET Images.","authors":"Gautam Kumar Baboo, Raghav Prasad, Pranav Mahajan, Veeky Baths","doi":"10.1177/09727531221117633","DOIUrl":"https://doi.org/10.1177/09727531221117633","url":null,"abstract":"<p><strong>Background: </strong>The study of brain networks, particularly the spread of disease, is made easier thanks to the network theory. The aberrant accumulation of beta-amyloid plaques and tau protein tangles in Alzheimer's disease causes disruption in brain networks. The evaluation scores, such as the mini-mental state examination (MMSE) and neuropsychiatric inventory questionnaire, which provide a clinical diagnosis, are affected by this build-up.</p><p><strong>Purpose: </strong>The percolation of beta-amyloid/tau tangles and their impact on cognitive tests are still unspecified.</p><p><strong>Methods: </strong>Percolation centrality could be used to investigate beta-amyloid migration as a characteristic of positron emission tomography (PET)-image-based networks. The PET-image-based network was built utilizing a public database containing 551 scans published by the Alzheimer's Disease Neuroimaging Initiative. Each image in the Julich atlas has 121 zones of interest, which are network nodes. Furthermore, the influential nodes for each scan are computed using the collective influence algorithm.</p><p><strong>Results: </strong>For five nodal metrics, analysis of variance (ANOVA; <i>P</i> < .05) reveals the region of interest (ROI) in gray matter (GM) Broca's area for Pittsburgh compound B (PiB) tracer type. The GM hippocampus area is significant for three nodal metrics in the case of florbetapir (AV45). Pairwise variance analysis of the clinical groups reveals five to twelve statistically significant ROIs for AV45 and PiB, respectively, that can distinguish between pairs of clinical situations. Based on multivariate linear regression, the MMSE is a trustworthy evaluation tool.</p><p><strong>Conclusion: </strong>Percolation values suggest that around 50 of the memory, visual-spatial skills, and language ROIs are critical to the percolation of beta-amyloids within the brain network when compared to the other extensively used nodal metrics. The anatomical areas rank higher with the advancement of the disease, according to the collective influence algorithm.</p>","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 4","pages":"209-224"},"PeriodicalIF":1.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fa/17/10.1177_09727531221117633.PMC10101156.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9686350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neurocognitive Changes in Sickle Cell Disease: A Comprehensive Review.","authors":"Tarun Sahu, Babita Pande, Meenakshi Sinha, Ramanjan Sinha, Henu Kumar Verma","doi":"10.1177/09727531221108871","DOIUrl":"https://doi.org/10.1177/09727531221108871","url":null,"abstract":"<p><strong>Background: </strong>Sickle cell disease (SCD) is a type of hemoglobinopathy characterized by abnormal hemoglobin molecules, which includes numerous acute and chronic complications. Ischemic stroke, silent cerebral infarction, headache, and neurocognitive impairment are the most common neurological complications associated with SCD.</p><p><strong>Summary: </strong>Acute anemia because of SCD can cause cognitive impairments because of cerebral hypoxia. Cognitive abnormalities in SCD manifest in various aspects such as working memory, verbal learning, executive functions, and attention. These neurocognitive impairments have been associated with poor functional results, such as transitioning from juvenile to adult care, adherence to medications, and unemployment.</p><p><strong>Key message: </strong>In this review, we focus on neurocognitive aspects of SCD patients based on different imaging techniques, psychological batteries, associated neuromarkers, and interventions for managing of cognitive deficiencies..</p>","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 4","pages":"255-268"},"PeriodicalIF":1.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/48/32/10.1177_09727531221108871.PMC10101159.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9686354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Current Status of Transcranial Magnetic Stimulation in Mental and Behavioral Health Treatment.","authors":"Krishan Kumar, M L Charan, Akshay Anand","doi":"10.1177/09727531231159515","DOIUrl":"https://doi.org/10.1177/09727531231159515","url":null,"abstract":"Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons AttributionNonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-Commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https:// us.sagepub.com/en-us/nam/open-access-at-sage). Editorial","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 4","pages":"197-198"},"PeriodicalIF":1.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/43/b9/10.1177_09727531231159515.PMC10101160.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9686355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effectiveness of Neurofeedback Therapy Adjunct to Cognitive Behavioral Therapy in Agoraphobia: A Case Study.","authors":"Titiksha Paul, Aakriti Varshney, Anand Pratap Singh","doi":"10.1177/09727531221145768","DOIUrl":"https://doi.org/10.1177/09727531221145768","url":null,"abstract":"<p><p>Agoraphobia has been defined as marked fear or anxiety being in enclosed or open places, using public transportation, and being in a crowd or outside of home alone. Such individuals make active attempts to avoid those places which cause intense distress. The neuronal areas that play a significant role in agoraphobia are uncinate fasciculus, which connects the prefrontal lobe and amygdala and various alterations in anterior cingulate cortex, insula, amygdala, and lateral prefrontal cortex. Neurofeedback is a type of biofeedback which teaches self-control of brain functions by measuring brain waves with the help of electroencephalography (EEG) and providing a feedback signal. With the help of alpha and beta training protocol, neurofeedback therapy will help in enhancing the connectivity between prefrontal cortex and amygdala. The present study aims to explore the therapeutic effectiveness of neurofeedback therapy as an adjunct treatment with cognitive behavioral therapy (CBT) in patients with agoraphobia disorder. A single case study method was adopted. The patient having the symptoms of agoraphobia disorder diagnosed as per ICD-10 criteria was taken in the study. After going through detailed case history and mental status examination, the patient was assessed on psychological measures on baseline and other follow-up visits. A total of 18 therapeutic sessions of neurofeedback therapy (alpha and beta protocol) along with CBT were conducted. Intermittent assessments on Draw A Person Test (DAPT), EEG parameters, Visual Analogue Scale (VAS), and Panic and Agoraphobia Scale (PAS) were conducted to compare the pre- and post-assessment findings. The results indicated significant improvement in the symptoms of the patient after intervention. The pre- and post-assessment findings and the neurofeedback therapy along with CBT were observed to be effective in treating the symptoms of agoraphobia. Neurofeedback therapy and CBT were proven to be effective in removing the symptoms of agoraphobia disorder within the patient.</p>","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 4","pages":"249-254"},"PeriodicalIF":1.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/15/5a/10.1177_09727531221145768.PMC10101153.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9316103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Altered Intestinal Permeability Biomarkers in Schizophrenia: A Possible Link with Subclinical Inflammation.","authors":"Kuppan Gokulakrishnan, Joyappa Nikhil, Sreeraj Vs, Bharath Holla, Chinnasamy Thirumoorthy, Narasimhan Sandhya, Sonika Nichenametla, Harsh Pathak, Venkataram Shivakumar, Monojit Debnath, Ganesan Venkatasubramanian, Shivarama Varambally","doi":"10.1177/09727531221108849","DOIUrl":"10.1177/09727531221108849","url":null,"abstract":"<p><strong>Background and purpose: </strong>Emerging studies have shown that gut-derived endotoxins might play a role in intestinal and systemic inflammation. Although the significance of intestinal permeability in modulating the pathogenesis of Schizophrenia (SCZ) is recognized, not much data on the specific role of intestinal permeability biomarkers, viz., zonulin, lipopolysaccharide-binding protein (LBP), and intestinal alkaline phosphatase (IAP) in SCZ is available. Therefore, we measured the plasma levels of zonulin, LBP, and IAP and its correlation with neutrophil-to-lymphocyte ratio (NLR); a marker of systemic inflammation in patients with SCZ.</p><p><strong>Methods: </strong>We recruited 60 individuals, patients with SCZ (<i>n</i> = 40) and healthy controls (<i>n</i> = 20), from a large tertiary neuropsychiatry center. Plasma levels of zonulin, IAP, and LBP were quantified by enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>Plasma levels of both LBP and zonulin were significantly increased (<i>P</i> <0.05), whereas the IAP levels (<i>P</i> <0.05) were significantly decreased in patients with SCZ compared to healthy controls. Pearson correlation analysis revealed that zonulin and LBP had a significant positive correlation with NLR, and IAP negatively correlated with NLR. Individuals with SCZ had higher independent odds of zonulin [odds ratio (OR): 10.32, 95% CI: 1.85-57.12], LBP [OR: 1.039, 95% CI: 1.02-1.07], and IAP [OR: 0.643, 95% CI: 0.471-0.879], even after adjusting for potential confounders.</p><p><strong>Conclusion: </strong>Our study demonstrates an association of zonulin, LBP, and IAP in Asian Indian SCZ patients and correlates with NLR. Our results indicate that low-grade inflammation induced by metabolic endotoxemia might be implicated in the pathoetiology of SCZ.</p>","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 2-3","pages":"151-158"},"PeriodicalIF":1.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/56/0d/10.1177_09727531221108849.PMC9676334.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10729445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cytomorphological Analysis and Interpretation of Nitric Oxide-Mediated Neurotoxicity in Sleep-Deprived Mice Model.","authors":"Reena Chittora, Ayushi Jain, Sunil Dutt Shukla, Maheep Bhatnagar","doi":"10.1177/09727531211059925","DOIUrl":"https://doi.org/10.1177/09727531211059925","url":null,"abstract":"<p><strong>Background: </strong>Sleep deprivation (SD) is a biological stress condition for the brain, and the pathogenesis of SD is closely related to elevated oxidative stress, mitochondrial dysfunction, a major cause of neurodegeneration. This oxidative stress-mediated cell death is attributed to rise in calcium ion influx which further excites or alters the neurotransmitters level by activating neuronal nitric oxide (NO) synthase (nNOS) release of NO in mouse SD model. This study indicates that the nitrergic neurons are possible therapeutic targets for the amelioration of SD-induced cognitive dysfunction and behavioral alterations.</p><p><strong>Purpose: </strong>SD is considered as a risk factor for various neurodegenerative diseases. SD leads to biochemical, behavioral, and neurochemical alterations in animals. This study was designed to explore the possible involvement of a nitrergic neuron system in six days SD-induced morphological and neurodegenerative changes in mice.</p><p><strong>Methods: </strong>Using nNOS immunohistochemistry, we have investigated the effects of SD on nNOS positive neurons. Immunohistochemical study for the distribution of nNOS positive neuronal cell bodies was carried out in the hippocampus, prefrontal cortex (PFC), and amygdaloid nuclei of mice brain.</p><p><strong>Results: </strong>Sleep-deprived animals showed a significantly increased number of nNOS positive neurons and altered neuronal cytomorphology as compared with the control group.</p><p><strong>Conclusion: </strong>These results indicate that total SD may induce morphological changes in nNOS positive neurons in the brain, thus increasing NO synthesis, which is implicated in SD-induced neuronal cell death.</p>","PeriodicalId":7921,"journal":{"name":"Annals of Neurosciences","volume":"29 1","pages":"7-15"},"PeriodicalIF":1.5,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f1/58/10.1177_09727531211059925.PMC9305911.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40631556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}