Journal of the Renin-Angiotensin-Aldosterone System最新文献

{"title":"Fibrinogen-to-Albumin Ratio Predicts Postcontrast Acute Kidney Injury in Patients with Non-ST Elevation Acute Coronary Syndrome after Implantation of Drug-Eluting Stents.","authors":"Yong Qiao,&nbsp;Mingkang Li,&nbsp;Linqing Li,&nbsp;Chengchun Tang","doi":"10.1155/2022/9833509","DOIUrl":"https://doi.org/10.1155/2022/9833509","url":null,"abstract":"<p><strong>Background: </strong>Postcontrast acute kidney injury (PC-AKI) is an adverse reaction to iodinated contrast agents. In this study, we investigated the use of fibrinogen-to-albumin ratio (FAR) as a novel inflammatory marker to track the development and progression of PC-AKI in patients with non-ST elevation acute coronary syndrome (NSTE-ACS) after the implantation of drug-eluting stents (DESs).</p><p><strong>Methods: </strong>A total of 872 patients with NSTE-ACS were enrolled in this study. PC-AKI was identified when serum creatinine (SCr) levels increased >26.5 mol/L (0.3 mg/dL) or was 1.5 times the baseline level within 48-72 h of exposure to an iodinated contrast agent. The effects of different variables on PC-AKI were evaluated using univariate regression analysis. Multivariate logistic regression analysis was used to determine the independent predictors of PC-AKI. The predictive value of FAR was assessed by estimating the area under the receiver operating characteristic (ROC) curve.</p><p><strong>Results: </strong>In total, 114 (13.1%) patients developed PC-AKI. The patients with PC-AKI had lower albumin levels (40.5 ± 3.4 vs. 39.0 ± 3.5, <i>P</i> < 0.001), higher fibrinogen levels (3.7 ± 0.6 vs. 4.1 ± 0.5, <i>P</i> < 0.001), and higher FAR levels (9.2 ± 1.7 vs. 10.5 ± 1.7, <i>P</i> < 0.001) than those with non-PC-AKI. There were no significant differences in the preoperative SCr levels between the two groups. After adjusting for confounding factors, FAR was found to be an independent predictor of PC-AKI (OR = 1.478, 95% CI = 1.298-1.684, <i>P</i> < 0.001). ROC analysis revealed that for PC-AKI prediction, the area under the curve for FAR was 0.702. The optimum cut-off value of FAR was 10.0, with a sensitivity of 64.9% and a specificity of 69.8%. Moreover, FAR had a higher predictive value for PC-AKI than the Mehran score (0.702 vs. 0.645).</p><p><strong>Conclusion: </strong>Our study showed that elevated preoperative FAR was closely associated with the development of PC-AKI in patients with NSTE-ACS after implantation of DESs. Therefore, it may be worth monitoring FAR as a guide for using preventive measures to avoid the development of PC-AKI.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"2022 ","pages":"9833509"},"PeriodicalIF":2.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9711978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10803490","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}

{"title":"Angiotensin-Converting Enzyme (ACE) Insertion/Deletion (I/D) Polymorphism as a Conjoint Regulator of Coagulation, Fibrinolytic, and RAAS Pathway in Infertility and Associated Pregnancy Complications.","authors":"Sunil Thakur,&nbsp;Vaishnavi Sharma,&nbsp;Dipneet Kaur,&nbsp;Pulakes Purkait","doi":"10.1155/2022/1695769","DOIUrl":"https://doi.org/10.1155/2022/1695769","url":null,"abstract":"<p><p>Despite the increase in assisted reproductive technologies, the high rates of infertility and pregnancy complications are a major concern to infertility specialists worldwide. Infertility may be attributed to pregnancy complications like thrombophilia, preeclampsia and fibrin-induced recurrent pregnancy loss (RPL). Renin-angiotensin-aldosterone system (RAAS) directly or indirectly causes preeclampsia and thrombophilia through the fibrinolytic pathway that ultimately leads to RPL or infertility. The underlying mechanisms of this interaction are still unclear. The present comprehensive review is intended to demonstrate the role and interaction of RAAS and fibrinolytic pathways in pregnancy complications. How this interaction can induce pregnancy complications, and ultimately infertility, is also discussed in the light of current evidence. This study also presents common markers that link RAAS and fibrinolytic processes in developing thrombophilia, preeclampsia and RPL. The common link in these pathways is ACE gene I/D polymorphism. Apart from ACE, PAI-1, VIIa, XIIa, AT1R, AT1AA, and TF are common molecules that can delineate the underlying causes of pregnancy complications and infertility.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"2022 ","pages":"1695769"},"PeriodicalIF":2.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9726265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10473780","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}

{"title":"Type XXVIII Collagen Regulates Renal Interstitial Fibrosis and Epithelial-Mesenchymal Transition by SREBP1-Mediated HKDC1 Expression.","authors":"Linlin Li,&nbsp;Qi Zou,&nbsp;Binbin Li,&nbsp;Lushi Huang,&nbsp;Lixin Wei","doi":"10.1155/2022/9582559","DOIUrl":"https://doi.org/10.1155/2022/9582559","url":null,"abstract":"<p><strong>Background: </strong>A novel collagen called type XXVIII collagen (COL28) is involved in cancer and lung fibrosis. Preliminary data showed that renal tubular epithelial cells could proliferate, migrate, and undergo an epithelial-mesenchymal transition (EMT) when COL28 was overexpressed; however, it is still unknown how this occurs and what the underlying mechanism is.</p><p><strong>Methods: </strong>We analyzed the differential expression of genes (DEGs) in the stable COL28 overexpression HK-2 cell lines by RNA-sequencing analysis, before which Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genomes (KEGG) analyses were performed. Genes related to COL28 promoting HK-2 cell proliferation and EMT were screened and verified. By using western blot and immunofluorescence, the effects of COL28 on the expression of <i>α</i>-SMA, E-cadherin, Snail, HKDC1, and SREBP1 were detected. The effect of COL28 overexpression on renal fibrosis in unilateral ureteral obstruction (UUO) mice was detected by H&E and Masson staining. HKDC1 interference agent was synthesized and transfected into the HK-2 cell line stably overexpressing COL28. In HK-2 cells, the effects of HKDC1 interference on the expression of <i>α</i>-SMA, E-cadherin, and Snail were detected.</p><p><strong>Results: </strong>We screened and verified that HKDC1 was related to COL28 and promoted HK-2 cell proliferation and EMT. WB showed that in HK-2 cells, COL28 overexpression increased <i>α</i>-SMA, Snail, HKDC1, and SREBP1 expressions and decreased E-cadherin expression. Overexpression of COL28 aggravated renal interstitial fibrosis in UUO mice; upregulated <i>α</i>-SMA, Snail, HKDC1, and SREBP1 expressions; and decreased the E-cadherin protein expression in UUO mice. Interference of HKDC1 expression promoted the E-cadherin protein expression while inhibiting <i>α</i>-SMA, Snail, HKDC1, and SREBP1 protein expressions.</p><p><strong>Conclusion: </strong>Overexpression of COL28 can aggravate renal interstitial fibrosis by encouraging renal tubular epithelial cells to undergo EMT, and interference with HKDC1 expression can alleviate fibrosis by reversing EMT induced by COL28 overexpression.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"2022 ","pages":"9582559"},"PeriodicalIF":2.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9719427/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10374407","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}

{"title":"Diagnosis of Hypoaldosteronism in Infancy","authors":"E. Vlachopapadopoulou, Myrto Bonataki","doi":"10.5772/intechopen.97448","DOIUrl":"https://doi.org/10.5772/intechopen.97448","url":null,"abstract":"Hypoaldosteronism is associated with either insufficient aldosterone production or lack of responsiveness to aldosterone and can be isolated or in the context of primary adrenal failure. Τhe severity of clinical manifestations is inversely correlated to age, with the neonatal period being the most vulnerable time for a patient to present with mineralocorticoid insufficiency. Salt-wasting forms of congenital adrenal hyperplasia (CAH), adrenal hypoplasia congenita (AHC), aldosterone synthase deficiency (ASD) and pseudohypoaldosteronism (PHA) are all causes of hypoaldosteronism in infancy. Affected infants present with salt wasting, failure to thrive and potentially fatal hyperkalemia and shock. Α blood sample for the essential hormonal investigations should be collected before any steroid treatment is given, in order to confirm aldosterone insufficiency and to determine the underlying cause. Renal ultrasonography and urine culture are also useful for exclusion of secondary causes of aldosterone resistance. Initial management requires treatment of electrolyte imbalances and restoration of intravascular fluid volume. In case of a salt-wasting crisis, affected infants are usually treated initially with both hydrocortisone and fludrocortisone, pending the results of investigations. Interpretation of the hormonal profile will guide further therapy and molecular analysis of candidate genes.","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"71 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2021-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90695642","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 Role of Renin: Angiotensin: Aldosterone System in the Pathogenesis and Pathophysiology of COVID-19","authors":"Ozlem G. Sahin","doi":"10.5772/intechopen.96478","DOIUrl":"https://doi.org/10.5772/intechopen.96478","url":null,"abstract":"The novel coronavirus also known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) whose origin is still having uncertainties related to the existence of an intermediate host, has created the currently ongoing pandemic of coronavirus disease 2019. (COVID-19) The binding assays of SARS-CoV-2 spike protein receptor binding domain disclosed enhanced affinity with human angiotensin II-converting enzyme receptor (hACE2) comparing to the bat ACE2 receptors. ACE2, is an essential component of the regulatory mechanism of the renin-angiotensin-aldosterone system, (RAAS) and this pathway is considered to interact with the pathophysiology of COVID-19. In this chapter, we will discuss the key role of RAAS in the pathogenesis of SARS-CoV-2.","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"8 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2021-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90170757","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":"Renin Angiotensin Aldosterone System Functions in Renovascular Hypertension","authors":"J. A. Gomez","doi":"10.5772/intechopen.97491","DOIUrl":"https://doi.org/10.5772/intechopen.97491","url":null,"abstract":"The renin angiotensin aldosterone system (RAAS) plays a key function in renovascular hypertension induced by renal artery stenosis (RAS). RAS causes a decrease in renal perfusion in the stenosed kidney which in turn stimulates renin the rate limiting enzyme in RAAS. This stimulation triggers a series of events starting with renin release leading to Ang II production, decrease in sodium excretion, increase sympathetic tone; all contributing to the development of renovascular hypertension. In RAS increase of superoxide reduce nitric oxide in the afferent arteriole increasing vasoconstriction and a marked decrease in glomerular filtration rate. In renovascular hypertension prostaglandins mediate renin release in the stenosed kidney. Targeting different RAAS components is part of the therapy for renovascular hypertension, with other options including renal nerves denervation and revascularization. Different clinical studies had explored revascularization, RAAS blocking and renal nerves denervation as a therapy. We will discuss organ, cellular and molecular components of this disease.","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"71 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2021-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90675305","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":"Diabetes and Renin-Angiotensin-Aldosterone System: Pathophysiology and Genetics","authors":"A. Nabi, A. Ebihara","doi":"10.5772/INTECHOPEN.97518","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.97518","url":null,"abstract":"Diabetes mellitus (DM) is a metabolic disorder and characterized by hyperglycemia. Being a concern of both the developed and developing world, diabetes is a global health burden and is a major cause of mortality world-wide. The most common is the type 2 diabetes mellitus (T2DM), which is mainly caused by resistance to insulin. Long-term complications of diabetes cause microvascular related problems (eg. nephropathy, neuropathy and retinopathy) along with macrovascular complications (eg. cardiovascular diseases, ischemic heart disease, peripheral vascular disease). Renin-angiotensin-aldosterone system (RAAS) regulates homeostasis of body fluid that in turn, maintains blood pressure. Thus, RAAS plays pivotal role in the pathogenesis of long-term DM complications like cardiovascular diseases and chronic kidney diseases. T2DM is a polygenic disease, and the roles of RAAS components in insulin signaling pathway and insulin resistance have been well documented. Hyperglycemia has been found to be associated with the increased plasma renin activity, arterial pressure and renal vascular resistance. Several studies have reported involvement of single variants within particular genes in initiation and development of T2D using different approaches. This chapter aims to investigate and discuss potential genetic polymorphisms underlying T2D identified through candidate gene studies, genetic linkage studies, genome wide association studies.","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"71 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2021-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83156136","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 Role of the Renin-Angiotensin-Aldosterone System in Cardiovascular Disease: Pathogenetic Insights and Clinical Implications","authors":"V. Capric, H. Chandrakumar, J. Celenza-Salvatore, A. Makaryus","doi":"10.5772/INTECHOPEN.96415","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.96415","url":null,"abstract":"Increased attention has been placed on the activation of the renin-angiotensin-aldosterone system (RAAS) and pathogenetic mechanisms in cardiovascular disease. Multiple studies have presented data to suggest that cardiac and arterial stiffness leading to adverse remodeling of both the heart and vasculature leads to the various pathological changes seen in coronary artery disease, heart failure (with preserved and reduced ejection fractions), hypertension and renal disease. Over-activation of the RAAS is felt to contribute to these structural and endocrinological changes through its control of the Na+/K+ balance, fluid volume, and hemodynamic stability. Subsequently, along these lines, multiple large investigations have shown that RAAS blockade contributes to prevention of both cardiovascular and renal disease. We aim to highlight the known role of the activated RAAS and provide an updated description of the mechanisms by which activation of RAAS promotes and leads to the pathogenesis of cardiovascular disease.","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"117 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2021-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79343428","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":"Comparison of biomarkers of endothelial dysfunction and microvascular endothelial function in patients with primary aldosteronism and essential hypertension.","authors":"Miaomiao Sang,&nbsp;Yu Fu,&nbsp;Chenmin Wei,&nbsp;Jing Yang,&nbsp;Xueting Qiu,&nbsp;Jingqing Ma,&nbsp;Chao Qin,&nbsp;Feiyan Wu,&nbsp;Xueling Zhou,&nbsp;Tao Yang,&nbsp;Min Sun","doi":"10.1177/1470320321999491","DOIUrl":"https://doi.org/10.1177/1470320321999491","url":null,"abstract":"<p><strong>Introduction: </strong>Studies have shown that primary aldosteronism (PA) has a higher risk of cardiovascular events than essential hypertension (EH). Endothelial dysfunction is an independent predictor of cardiovascular events. Whether PA and EH differ in the endothelial dysfunction is uncertain. Our study was designed to investigate the levels of biomarkers of endothelial dysfunction (Asymmetric dimethylarginine, ADMA; E-selectin, and Plasminogen activator inhibitor-1, PAI-1) and assess the microvascular endothelial function in patients with PA and EH, respectively.</p><p><strong>Methods: </strong>The biomarkers of endothelial dysfunction were measured by enzyme-linked immunosorbent assay (ELISA). Microvascular endothelial function was evaluated by Pulse amplitude tonometry (PAT).</p><p><strong>Results: </strong>Thirty-one subjects with EH and 36 subjects with PA including 22 with aldosterone-producing adenoma (APA) and 14 with idiopathic hyperaldosteronism (IHA) were enrolled in our study. The ADMA levels among the three groups were different (APA 47.83 (27.50, 87.74) ng/ml vs EH 25.08 (22.44, 39.79) ng/ml vs IHA 26.00 (22.23, 33.75) ng/ml; <i>p</i> = 0.04), however, when the APA group was compared with EH and IHA group, there was no statistical significance (47.83 (27.50, 87.74) ng/ml vs 25.08 (22.44, 39.79) ng/ml for EH, <i>p</i> = 0.11; 47.83 (27.50, 87.74) ng/ml vs IHA 26.00 (33.75) ng/ml, <i>p</i> = 0.07). The results of ADMA levels are presented as Median (p25, p75). Whereas, levels of PAI-1 and E-selectin, microvascular endothelial function were not significantly different between PA and EH subjects.</p><p><strong>Conclusions: </strong>Our study shows no significant differences between PA and EH in terms of biomarkers of endothelial dysfunction and microvascular endothelial function. The microvascular endothelial function of PA and EH patients is comparable.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"22 1","pages":"1470320321999491"},"PeriodicalIF":2.9,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320321999491","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25442918","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}

{"title":"Normotensive presentation in primary aldosteronism: A report of two cases.","authors":"Minyue Jia,&nbsp;Hanxiao Yu,&nbsp;Zhenjie Liu,&nbsp;Minzhi He,&nbsp;Shan Zhong,&nbsp;Xiaohong Xu,&nbsp;Xiaoxiao Song","doi":"10.1177/14703203211003780","DOIUrl":"https://doi.org/10.1177/14703203211003780","url":null,"abstract":"<p><p>Normotensive patients with primary aldosteronism (PA) are relatively rare. Herein, we report two patients with normotensive PA and present a literature review to improve an understanding of the disease. Patient 1, a 56-year-old man, presented with recurrent hypokalemia that lasted for more than 2 years. Patient 2 was a 33-year-old man who presented with sexual dysfunction and was diagnosed with a prolactinoma combined with adrenal insufficiency and hypogonadism. Neither of these patients had hypertension that was detectable on repeated manual measurements. In both patients, a typical biological profile of PA was demonstrated that included hypokalemia with kaliuresis, elevated plasma aldosterone concentration (PAC), suppressed plasma renin concentration, and a high aldosterone-to-renin ratio. Both patients did not have sufficiently suppressed PAC on the saline infusion test, confirming the diagnosis of PA. Computed tomography of the adrenal gland and adrenal venous sampling suggested an aldosteronoma, which was confirmed by lateralized hypersecretion of aldosterone. After removal of the benign adenoma, the biochemical abnormalities were corrected. As hypertension is not necessarily a sign of PA, we propose that all patients with hypokalemia should be screened for PA in order to prevent cardiovascular complications while balancing economics and effectiveness.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"22 1","pages":"14703203211003780"},"PeriodicalIF":2.9,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/14703203211003780","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25513177","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}