Amal Darwish, Nesrine S. El Sayed, A. Salama, M. Saad
AIM There is a well-founded relation between bullying and depression, which may eventually lead to suicidal behavior. Repurposing of antidiabetic drugs for the treatment of depression started to glow, which open new horizons to introduce the antidiabetic medications as new treatment picks in depression. Dulaglutide has been approved as remedy of type 2 diabetes mellitus (T2DM). Consequently, our scope of work is to investigate the ability of dulaglutide to indulgence depression via deeply reconnoitering the Glucagon-like peptide-1 receptor and cAMP/PKA Signaling Pathway. MATERIALS AND METHODS Eighty mice were divided into two groups; one with and the other without the induction of chronic social defeat stress (CSDS). Each group was subdivided into two subsets; the first one was treated with saline for 42 days, while the other was treated with saline for 20 days, then with dulaglutide (0.6 mg/kg/week) for four weeks. KEY FINDINGS CSDS group showed a lessening in the social interaction ratio and sucrose consumption. They spent less exploration time in the open arms, and more time in the closed arms in elevated plus maze test as compared to controls. Furthermore, the CSDS group had a higher expression of NOD- like receptor protein-3 which explained the elevation in inflammatory biomarkers (IL-1β, IL-18, IL-6 and TNF-α) along with diminution in GLP-1R, cAMP/PKA levels. Treatment with dulaglutide markedly reversed the above-mentioned parameters via bolstering the GLP-1R/cAMP/PKA pathway. SIGNIFICANCE NLRP3 inflammasome activation expedites depression. Dulaglutide activates the GLP-1R/cAMP/PKA pathway, hence offering a novel therapeutic intervention to hinder depression.
{"title":"Dulaglutide impedes depressive-like behavior persuaded by chronic social defeat stress model in male C57BL/6 mice: Implications on GLP-1R and cAMP/PKA signaling pathway in the hippocampus.","authors":"Amal Darwish, Nesrine S. El Sayed, A. Salama, M. Saad","doi":"10.2139/ssrn.4327439","DOIUrl":"https://doi.org/10.2139/ssrn.4327439","url":null,"abstract":"AIM\u0000There is a well-founded relation between bullying and depression, which may eventually lead to suicidal behavior. Repurposing of antidiabetic drugs for the treatment of depression started to glow, which open new horizons to introduce the antidiabetic medications as new treatment picks in depression. Dulaglutide has been approved as remedy of type 2 diabetes mellitus (T2DM). Consequently, our scope of work is to investigate the ability of dulaglutide to indulgence depression via deeply reconnoitering the Glucagon-like peptide-1 receptor and cAMP/PKA Signaling Pathway.\u0000\u0000\u0000MATERIALS AND METHODS\u0000Eighty mice were divided into two groups; one with and the other without the induction of chronic social defeat stress (CSDS). Each group was subdivided into two subsets; the first one was treated with saline for 42 days, while the other was treated with saline for 20 days, then with dulaglutide (0.6 mg/kg/week) for four weeks.\u0000\u0000\u0000KEY FINDINGS\u0000CSDS group showed a lessening in the social interaction ratio and sucrose consumption. They spent less exploration time in the open arms, and more time in the closed arms in elevated plus maze test as compared to controls. Furthermore, the CSDS group had a higher expression of NOD- like receptor protein-3 which explained the elevation in inflammatory biomarkers (IL-1β, IL-18, IL-6 and TNF-α) along with diminution in GLP-1R, cAMP/PKA levels. Treatment with dulaglutide markedly reversed the above-mentioned parameters via bolstering the GLP-1R/cAMP/PKA pathway.\u0000\u0000\u0000SIGNIFICANCE\u0000NLRP3 inflammasome activation expedites depression. Dulaglutide activates the GLP-1R/cAMP/PKA pathway, hence offering a novel therapeutic intervention to hinder depression.","PeriodicalId":11962,"journal":{"name":"EUREKA: Life Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90451000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-01DOI: 10.12968/s0261-2097(23)60463-0
Cobots have lowered the barriers to automation, but must still be operated safely – something that presents a range of different challenges.
协作机器人降低了自动化的门槛，但仍然必须安全操作，这带来了一系列不同的挑战。
{"title":"Cobots: Designing in Safety","authors":"","doi":"10.12968/s0261-2097(23)60463-0","DOIUrl":"https://doi.org/10.12968/s0261-2097(23)60463-0","url":null,"abstract":"Cobots have lowered the barriers to automation, but must still be operated safely – something that presents a range of different challenges.","PeriodicalId":11962,"journal":{"name":"EUREKA: Life Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88783458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-01DOI: 10.12968/s0261-2097(23)60468-x
{"title":"ABB Unveils New Cobot","authors":"","doi":"10.12968/s0261-2097(23)60468-x","DOIUrl":"https://doi.org/10.12968/s0261-2097(23)60468-x","url":null,"abstract":"","PeriodicalId":11962,"journal":{"name":"EUREKA: Life Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78800178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-01DOI: 10.12968/s0261-2097(23)60458-7
A novel, non-invasive diabetes screening device has met primary endpoints in two clinical investigations
一种新型的非侵入性糖尿病筛查设备在两项临床研究中达到了主要终点
{"title":"Firm Nails Diabetes Screening","authors":"","doi":"10.12968/s0261-2097(23)60458-7","DOIUrl":"https://doi.org/10.12968/s0261-2097(23)60458-7","url":null,"abstract":"A novel, non-invasive diabetes screening device has met primary endpoints in two clinical investigations","PeriodicalId":11962,"journal":{"name":"EUREKA: Life Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78355620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yujin Jin, Warisraporn Tangchang, Oh Seong Kwon, Ji-Yun Lee, K. Heo, H. Son
AIMS Overproduction of pro-inflammatory cytokines and its-mediated immune cell infiltration play a crucial role in asthma progression. In this study, we investigated the role of ginsenoside Rh1 (Rh1) in ovalbumin (OVA)/lipopolysaccharide (LPS)-induced allergic asthma both in vitro and in vivo. MATERIALS AND MAIN METHODS The phorbol ester (PMA) and LPS were used to induce inflammation in lung airway cells and macrophage activation, respectively. Western blotting, quantitative reverse transcription-PCR, and immunofluorescence (IF) assays were performed to elucidate the underlying molecular mechanisms. To evaluating the effects of Rh1 in vivo, OVA and LPS were used to establish allergic asthma models. KEY FINDINGS Rh1 significantly suppressed PMA-induced lung inflammation and macrophage activation by suppressing pro-inflammatory cytokines (TNF-α, IL-1β, MCP-1), ICMA-1, and matrix metallopeptidase 9 (MMP9) in A549 cells. Rh1 abolished the PMA-induced inflammation by suppressing MAPK, Akt, and NF-κB p65. Pretreatment with Rh1 blocked PMA-mediated translocation of NF-κB, a key marker of pro-inflammatory cytokine release, into the nucleus. Similar to PMA-induced lung inflammation, Rh1 suppressed LPS-induced macrophage activation by suppressing NF-κB p65 activation and inducible nitric oxide synthase protein and mRNA expression. Consistent with in vitro data, LPS injection enhanced the number of immune cells induced by OVA in bronchoalveolar lavage fluid, whereas 20 mg/kg Rh1 significantly decreased OVA/LPS-mediated immune cell induction. In addition, Rh1 inhibited eosinophil, macrophage, and neutrophil maturation through by IL-4 and OVA-specific IgE production. SIGNIFICANCE Rh1 protects against OVA/LPS-induced allergic asthma by suppressing immune cell infiltration by blocking the activation of MAPK, Akt, and NF-κB signaling pathways.
{"title":"Ginsenoside Rh1 ameliorates the asthma and allergic inflammation via inhibiting Akt, MAPK, and NF-κB signaling pathways in vitro and in vivo.","authors":"Yujin Jin, Warisraporn Tangchang, Oh Seong Kwon, Ji-Yun Lee, K. Heo, H. Son","doi":"10.2139/ssrn.4333539","DOIUrl":"https://doi.org/10.2139/ssrn.4333539","url":null,"abstract":"AIMS\u0000Overproduction of pro-inflammatory cytokines and its-mediated immune cell infiltration play a crucial role in asthma progression. In this study, we investigated the role of ginsenoside Rh1 (Rh1) in ovalbumin (OVA)/lipopolysaccharide (LPS)-induced allergic asthma both in vitro and in vivo.\u0000\u0000\u0000MATERIALS AND MAIN METHODS\u0000The phorbol ester (PMA) and LPS were used to induce inflammation in lung airway cells and macrophage activation, respectively. Western blotting, quantitative reverse transcription-PCR, and immunofluorescence (IF) assays were performed to elucidate the underlying molecular mechanisms. To evaluating the effects of Rh1 in vivo, OVA and LPS were used to establish allergic asthma models.\u0000\u0000\u0000KEY FINDINGS\u0000Rh1 significantly suppressed PMA-induced lung inflammation and macrophage activation by suppressing pro-inflammatory cytokines (TNF-α, IL-1β, MCP-1), ICMA-1, and matrix metallopeptidase 9 (MMP9) in A549 cells. Rh1 abolished the PMA-induced inflammation by suppressing MAPK, Akt, and NF-κB p65. Pretreatment with Rh1 blocked PMA-mediated translocation of NF-κB, a key marker of pro-inflammatory cytokine release, into the nucleus. Similar to PMA-induced lung inflammation, Rh1 suppressed LPS-induced macrophage activation by suppressing NF-κB p65 activation and inducible nitric oxide synthase protein and mRNA expression. Consistent with in vitro data, LPS injection enhanced the number of immune cells induced by OVA in bronchoalveolar lavage fluid, whereas 20 mg/kg Rh1 significantly decreased OVA/LPS-mediated immune cell induction. In addition, Rh1 inhibited eosinophil, macrophage, and neutrophil maturation through by IL-4 and OVA-specific IgE production.\u0000\u0000\u0000SIGNIFICANCE\u0000Rh1 protects against OVA/LPS-induced allergic asthma by suppressing immune cell infiltration by blocking the activation of MAPK, Akt, and NF-κB signaling pathways.","PeriodicalId":11962,"journal":{"name":"EUREKA: Life Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72913743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-01DOI: 10.12968/s0261-2097(23)60454-x
{"title":"Coffee Time Challenge","authors":"","doi":"10.12968/s0261-2097(23)60454-x","DOIUrl":"https://doi.org/10.12968/s0261-2097(23)60454-x","url":null,"abstract":"","PeriodicalId":11962,"journal":{"name":"EUREKA: Life Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135469437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zheyu Hu, Yixian Liu, Jin Tang, Renru Luo, Jiajia Qin, Zexun Mo, Jianjiang Xie, Xuan Jiang, Shuquan Wei, Chuwen Lin
AIMS Lung squamous cell carcinoma (LUSC) causes over 400,000 deaths annually, yet it lacks targeted therapy. A major antagonist of Hedgehog pathway, HHIP (Hedgehog Interacting Protein) plays an important role in LUSC; however, the regulatory mechanism remains unclear. Long non-coding RNA HHIP-AS1 plays suppressive or promotive roles in different cancers, but its role in LUSC remains unknown. This manuscript is to investigate regulatory mechanism of HHIP and the role of HHIP-AS1 in LUSC. MAIN METHODS Precision-cut lung slices (PCLS) from human LUSC samples are cultured to mimic LUSC growth. Overexpression and knockdown in multiple LUSC cell lines and PCLS are achieved by lentivirus infection. Transcriptome profile and lung cancer activity are evaluated by RNA-sequencing, immunostaining and CCK8 assay etc. KEY FINDINGS: HHIP is regulated independently of Hh pathway in LUSC. Additionally, downregulation of HHIP-AS1 is associated with poor prognosis. Consistently, HHIP-AS1 inhibits LUSC growth by suppressing cell proliferation and migration. Transcriptome profiling of HHIP-AS1 knockdown (KD) cells uncovered HHIP downregulation. Interestingly, a comparison between the transcriptomes of HHIP-AS1 KD or HHIP KD cells manifested high similarity. Subsequently it's confirmed that HHIP-AS1 regulates HHIP in LUSC cells. Notably, HHIP-AS1 regulation on LUSC growth is achieved through stabilizing HHIP mRNA rather than regulating MIR-153-3P/PCDHGA9 or MIR-425-5P/DNYC1I2. Finally, it's confirmed in PCLS from human LUSC samples that HHIP-AS1 suppresses LUSC via regulating HHIP mRNA. SIGNIFICANCE This study uncovers HHIP-AS1 as a novel tumor suppressor in LUSC and provides new insights into the molecular regulation of LUSC, which will help developing new therapeutic strategies.
{"title":"LncRNA HHIP-AS1 suppresses lung squamous cell carcinoma by stabilizing HHIP mRNA.","authors":"Zheyu Hu, Yixian Liu, Jin Tang, Renru Luo, Jiajia Qin, Zexun Mo, Jianjiang Xie, Xuan Jiang, Shuquan Wei, Chuwen Lin","doi":"10.2139/ssrn.4333540","DOIUrl":"https://doi.org/10.2139/ssrn.4333540","url":null,"abstract":"AIMS\u0000Lung squamous cell carcinoma (LUSC) causes over 400,000 deaths annually, yet it lacks targeted therapy. A major antagonist of Hedgehog pathway, HHIP (Hedgehog Interacting Protein) plays an important role in LUSC; however, the regulatory mechanism remains unclear. Long non-coding RNA HHIP-AS1 plays suppressive or promotive roles in different cancers, but its role in LUSC remains unknown. This manuscript is to investigate regulatory mechanism of HHIP and the role of HHIP-AS1 in LUSC.\u0000\u0000\u0000MAIN METHODS\u0000Precision-cut lung slices (PCLS) from human LUSC samples are cultured to mimic LUSC growth. Overexpression and knockdown in multiple LUSC cell lines and PCLS are achieved by lentivirus infection. Transcriptome profile and lung cancer activity are evaluated by RNA-sequencing, immunostaining and CCK8 assay etc. KEY FINDINGS: HHIP is regulated independently of Hh pathway in LUSC. Additionally, downregulation of HHIP-AS1 is associated with poor prognosis. Consistently, HHIP-AS1 inhibits LUSC growth by suppressing cell proliferation and migration. Transcriptome profiling of HHIP-AS1 knockdown (KD) cells uncovered HHIP downregulation. Interestingly, a comparison between the transcriptomes of HHIP-AS1 KD or HHIP KD cells manifested high similarity. Subsequently it's confirmed that HHIP-AS1 regulates HHIP in LUSC cells. Notably, HHIP-AS1 regulation on LUSC growth is achieved through stabilizing HHIP mRNA rather than regulating MIR-153-3P/PCDHGA9 or MIR-425-5P/DNYC1I2. Finally, it's confirmed in PCLS from human LUSC samples that HHIP-AS1 suppresses LUSC via regulating HHIP mRNA.\u0000\u0000\u0000SIGNIFICANCE\u0000This study uncovers HHIP-AS1 as a novel tumor suppressor in LUSC and provides new insights into the molecular regulation of LUSC, which will help developing new therapeutic strategies.","PeriodicalId":11962,"journal":{"name":"EUREKA: Life Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85209538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gabriel A. Grilo, Sirin N. Cakir, P. Shaver, R. Iyer, K. Whitehead, J. McClung, A. Vahdati, L. E. de Castro Brás
AIMS A peptide mimetic of a collagen-derived matricryptin (p1159) was shown to reduce left ventricular (LV) dilation and fibrosis after 7 days delivery in a mouse model of myocardial infarction (MI). This suggested p1159 long-term treatment post-MI could have beneficial effects and reduce/prevent adverse LV remodeling. This study aimed to test the potential of p1159 to reduce adverse cardiac remodeling in a chronic MI model and to elucidate p1159 mode-of-action. MATERIALS AND METHODS Using a permanent occlusion MI rodent model, animals received p1159 or vehicle solution up to 28 days. We assessed peptide treatment effects on scar composition and structure and on systolic function. To assess peptide effects on scar vascularization, a cohort of mice were injected with Griffonia simplicifolia isolectin-B4. To investigate p1159 mode-of-action, LV fibroblasts from naïve animals were treated with increasing doses of p1159. KEY FINDINGS Matricryptin p1159 significantly improved systolic function post-MI (2-fold greater EF compared to controls) by reducing left ventricular dilation and inducing the formation of a compliant and organized infarct scar, which promoted LV contractility and preserved the structural integrity of the heart. Specifically, infarcted scars from p1159-treated animals displayed collagen fibers aligned parallel to the epicardium, to resist circumferential stretching, with reduced levels of cross-linking, and improved tissue perfusion. In addition, we found that p1159 increases cardiac fibroblast migration by activating RhoA pathways via the membrane receptor integrin α4. SIGNIFICANCE Our data indicate p1159 treatment reduced adverse LV remodeling post-MI by modulating the deposition, arrangement, and perfusion of the fibrotic scar.
{"title":"Collagen matricryptin promotes cardiac function by mediating scar formation.","authors":"Gabriel A. Grilo, Sirin N. Cakir, P. Shaver, R. Iyer, K. Whitehead, J. McClung, A. Vahdati, L. E. de Castro Brás","doi":"10.2139/ssrn.4327441","DOIUrl":"https://doi.org/10.2139/ssrn.4327441","url":null,"abstract":"AIMS\u0000A peptide mimetic of a collagen-derived matricryptin (p1159) was shown to reduce left ventricular (LV) dilation and fibrosis after 7 days delivery in a mouse model of myocardial infarction (MI). This suggested p1159 long-term treatment post-MI could have beneficial effects and reduce/prevent adverse LV remodeling. This study aimed to test the potential of p1159 to reduce adverse cardiac remodeling in a chronic MI model and to elucidate p1159 mode-of-action.\u0000\u0000\u0000MATERIALS AND METHODS\u0000Using a permanent occlusion MI rodent model, animals received p1159 or vehicle solution up to 28 days. We assessed peptide treatment effects on scar composition and structure and on systolic function. To assess peptide effects on scar vascularization, a cohort of mice were injected with Griffonia simplicifolia isolectin-B4. To investigate p1159 mode-of-action, LV fibroblasts from naïve animals were treated with increasing doses of p1159.\u0000\u0000\u0000KEY FINDINGS\u0000Matricryptin p1159 significantly improved systolic function post-MI (2-fold greater EF compared to controls) by reducing left ventricular dilation and inducing the formation of a compliant and organized infarct scar, which promoted LV contractility and preserved the structural integrity of the heart. Specifically, infarcted scars from p1159-treated animals displayed collagen fibers aligned parallel to the epicardium, to resist circumferential stretching, with reduced levels of cross-linking, and improved tissue perfusion. In addition, we found that p1159 increases cardiac fibroblast migration by activating RhoA pathways via the membrane receptor integrin α4.\u0000\u0000\u0000SIGNIFICANCE\u0000Our data indicate p1159 treatment reduced adverse LV remodeling post-MI by modulating the deposition, arrangement, and perfusion of the fibrotic scar.","PeriodicalId":11962,"journal":{"name":"EUREKA: Life Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84868319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-01DOI: 10.12968/s0261-2097(23)60456-3
Advances in sensor and other technologies could help to revolutionise the market for robotic lawn mowers, with one recent innovation leading the way.
传感器和其他技术的进步可能有助于彻底改变机器人割草机的市场，最近的一项创新引领了这一潮流。
{"title":"A Cut Above","authors":"","doi":"10.12968/s0261-2097(23)60456-3","DOIUrl":"https://doi.org/10.12968/s0261-2097(23)60456-3","url":null,"abstract":"Advances in sensor and other technologies could help to revolutionise the market for robotic lawn mowers, with one recent innovation leading the way.","PeriodicalId":11962,"journal":{"name":"EUREKA: Life Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74065534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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