Ryan Phillip Sixtus, Clint Gray, Heather Barnes, Emily Sarah Jane Paterson, Mary Judith Berry, Rebecca Maree Dyson
{"title":"Cardiovascular responses to heat and cold exposure are altered by preterm birth in guinea pigs.","authors":"Ryan Phillip Sixtus, Clint Gray, Heather Barnes, Emily Sarah Jane Paterson, Mary Judith Berry, Rebecca Maree Dyson","doi":"10.14814/phy2.70098","DOIUrl":"10.14814/phy2.70098","url":null,"abstract":"<p><p>Adversity early in life can modify the trajectory for disease risk extending decades beyond the event. Preterm birth produces persistent cardiovascular alterations that may appear maladaptive in adulthood. We have previously hypothesized that those born preterm may exhibit cardiovascular vulnerability in the climate change context. Further, this vulnerability may be present as early as childhood. We aimed to identify the early signs of cardiovascular dysfunction at childhood-equivalent age using our animal model of preterm birth. Using a whole-body thermal stress test, guinea pigs aged 35-d and 38-d (equivalent to 8-10-year-old children) and born at term or preterm gestations were exposed to progressive hyper- (T<sub>C</sub> = 41.5°C) and hypo-thermia (T<sub>C</sub> = 34°C; normothermia T<sub>C</sub> = 39°C). Comprehensive cardiovascular monitoring included ECG, blood pressure, microvascular perfusion, blood gas, and catecholamine profile, as well as skin and core body temperature. Preterm-born animals exhibited attenuated vascular responses to hyperthermic stress, and a significant elevation in systolic blood pressure in response to hypothermic stress. Such responses are similar to those observed in elderly populations and indicate the presence of cardiovascular dysfunction. This is the first study to demonstrate the impact of preterm birth on the cardiovascular response to both heat and cold stress. Further, this dysfunction has been observed at an earlier age than that achievable using traditional stress testing techniques. The present findings warrant further investigation.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11494451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472406","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}
Mona Esbjörnsson, Håkan C Rundqvist, Barbara Norman, Ted Österlund, Eric Rullman, Jens Bülow, Eva Jansson
{"title":"Decreased mitochondrial-related gene expression in adipose tissue after acute sprint exercise in humans: A pilot study.","authors":"Mona Esbjörnsson, Håkan C Rundqvist, Barbara Norman, Ted Österlund, Eric Rullman, Jens Bülow, Eva Jansson","doi":"10.14814/phy2.70088","DOIUrl":"10.14814/phy2.70088","url":null,"abstract":"<p><p>The aim was to examine the acute effects of sprint exercise (SIT) on global gene expression in subcutaneous adipose tissue (AT) in healthy subjects, to enhance understanding of how SIT influences body weight regulation. The hypothesis was that SIT upregulates genes involved in mitochondrial function and fat metabolism. A total of 15 subjects performed three 30-s all-out sprints (SIT). Samples were collected from AT, skeletal muscle (SM) and blood (brachial artery and a subcutaneous AT vein) up to 15 min after the last sprint. Results showed that markers of oxidative stress, such as the purines hypoxanthine, xanthine and uric acid, increased markedly by SIT in both the artery and the AT vein. Purines also increased in AT and SM tissue. Differential gene expression analysis indicated a decrease in signaling for mitochondrial-related pathways, including oxidative phosphorylation, electron transport, ATP synthesis, and heat production by uncoupling proteins, as well as mitochondrial fatty acid beta oxidation. This downregulation of genes related to oxidative metabolism suggests an early-stage inhibition of the mitochondria, potentially as a protective mechanism against SIT-induced oxidative stress.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11492148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472408","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":"A new approach to modeling transdermal ethanol kinetics.","authors":"Joseph C Anderson","doi":"10.14814/phy2.70070","DOIUrl":"10.14814/phy2.70070","url":null,"abstract":"<p><p>Measurement of ethanol above the skin surface (supradermal) is used to monitor blood alcohol concentrations (BAC) in both legal and consumer settings. Previously, the relationship between supradermal alcohol concentration (SAC) and BAC was described using partial and ordinary differential equations (PDE model: J. Appl. Physiol. 100: 649-55, 2006). Using a range of BAC profiles by varying absorption times and peak concentrations, the PDE model accurately predicted experimental measures of SAC. Recently, other mathematical models have relied on the PDE model. This paper proposes a new approach to modeling transdermal ethanol kinetics using a mass transfer coefficient and only ordinary differential equations (ODE model). Using a range of BAC profiles, the ODE model performed very similarly to the PDE model. The ODE model had slightly slower washout rates and slightly slower times to peak SAC and to zero SAC. Similar to the PDE model, a sensitivity analysis on the ODE model showed changes in solubility and diffusivity within the stratum corneum, stratum corneum thickness, and the volume of gas above the skin affected model performance. This new model will streamline integration into larger physiologic models, reduce computation time, and decrease the time to transform skin alcohol measurements to blood alcohol concentrations.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11446835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142366224","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}
L M Harrison-Bernard, L Raij, R X Tian, E A Jaimes
{"title":"Genetically conditioned interaction among microRNA-155, alpha-klotho, and intra-renal RAS in male rats: Link to CKD progression.","authors":"L M Harrison-Bernard, L Raij, R X Tian, E A Jaimes","doi":"10.14814/phy2.16172","DOIUrl":"https://doi.org/10.14814/phy2.16172","url":null,"abstract":"<p><p>Incident chronic kidney disease (CKD) varies in populations with hypertension of similar severity. Proteinuria promotes CKD progression in part due to activation of plasminogen to plasmin in the podocytes, resulting in oxidative stress-mediated injury. Additional mechanisms include deficiency of renal alpha-klotho, that inhibits Wnt/beta-catenin, an up regulator of intra-renal renin angiotensin system (RAS) genes. Alpha-klotho deficiency therefore results in upregulation of the intra-renal RAS via Wnt/beta-catenin. In hypertensive, Dahl salt sensitive (DS) and spontaneously hypertensive rats (SHR), we investigated renal and vascular injury, miR-155, AT1R, alpha-klotho, and TNF-α. Hypertensive high salt DS (DS-HS), but not SHR developed proteinuria, plasminuria, and glomerulosclerosis. Compared to DS low salt (DS-LS), in hypertensive DS-HS alpha-klotho decreased 5-fold in serum and 2.6-fold in kidney, whereas serum mir-155 decreased 3.3-fold and AT1R increased 52% in kidney and 77% in aorta. AT1R, alpha-klotho, and miR-155 remained unchanged in prehypertensive and hypertensive SHR. TNF-α increased by 3-fold in serum and urine of DS-HS rats. These studies unveiled in salt sensitive DS-HS, but not in SHR, a genetically conditioned dysfunction of the intermolecular network integrated by alpha-klotho, RAS, miR-155, and TNF-α that is at the helm of their end-organ susceptibility while plasminuria may participate as a second hit.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11458328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142392464","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":"Olfactory cilia, regulation and control of olfaction.","authors":"Hiroko Takeuchi","doi":"10.14814/phy2.70057","DOIUrl":"10.14814/phy2.70057","url":null,"abstract":"<p><p>The sense of smell is still considered a fuzzy sensation. Softly wafting aromas can stimulate the appetite and trigger memories; however, there are many unexplored aspects of its underlying mechanisms, and not all of these have been elucidated. Although the final sense of smell takes place in the brain, it is greatly affected during the preliminary stage, when odorants are converted into electrical signals. After signal conversion through ion channels in olfactory cilia, action potentials are generated through other types of ion channels located in the cell body. Spike trains through axons transmit this information as digital signals to the brain, however, before odorants are converted into digital electric signals, such as an action potential, modification of the transduction signal has already occurred. This review focuses on the early stages of olfactory signaling. Modification of signal transduction mechanisms and their effect on the human sense of smell through three characteristics (signal amplification, olfactory adaptation, and olfactory masking) produced by olfactory cilia, which is the site of signal transduction are being addressed in this review.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11446836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142366226","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}
Anderson Velasque Catarina, Gisele Branchini, Rafael Andrade Caceres, Renata Streck Fernandes, Bruna Pasqualotto Costa, Kleiton Lima De Godoy Machado, Tiago Becker, Luis Fernando Ferreira, Katya Rigatto, Jarbas Rodrigues de Oliveira, Fernanda Bordignon Nunes
{"title":"Fructose-1,6-bisphosphate reverses hypotensive effect caused by L-kynurenine in Wistar male rats.","authors":"Anderson Velasque Catarina, Gisele Branchini, Rafael Andrade Caceres, Renata Streck Fernandes, Bruna Pasqualotto Costa, Kleiton Lima De Godoy Machado, Tiago Becker, Luis Fernando Ferreira, Katya Rigatto, Jarbas Rodrigues de Oliveira, Fernanda Bordignon Nunes","doi":"10.14814/phy2.70033","DOIUrl":"https://doi.org/10.14814/phy2.70033","url":null,"abstract":"<p><p>Hypotension is one of the main characteristics of the systemic inflammation, basically caused by endothelial dysfunction. Studies have shown that the amino acid L-kynurenine (KYN) causes vasodilation in mammals, leading to hypotensive shock. In hypotensive shock, when activated by the KYN, the voltage-gated potassium channel encoded by the family KCNQ (Kv7) gene can cause vasodilation. Fructose-1,6-bisphosphate (FBP) it is being considered in studies an anti-inflammatory, antioxidant, immunomodulator, and a modulator of some ion channels (Ca2+, Na+, and K+). We analyzed the effects of KYN and FBP on mean blood pressure (MBP), systolic and diastolic (DBP) blood pressure, and heart rate variability (HRV) in Wistar rats. Results demonstrated that the administration of KYN significant decreased MBP, DBP, and increased HRV. Importantly, the FBP treatment reversed the KYN effects on MBP, DBP, and HRV. Molecular Docking Simulations suggested that KYN and FBP present a very close estimated free energy of binding and the same position into structure of KCNQ4. Our results did demonstrate that FBP blunted the decrease in BP, provoked by KYN. Results raise new hypotheses for future and studies in the treatment of hypotension resulting from inflammation.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11471349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472401","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}
Alexandra Vassilieva, Markus Harboe Olsen, Jane Skjøth-Rasmussen, Kirsten Møller, Martin Kryspin Sørensen
{"title":"Arterial to jugular-bulb lactate difference in patients undergoing elective brain tumor craniotomy.","authors":"Alexandra Vassilieva, Markus Harboe Olsen, Jane Skjøth-Rasmussen, Kirsten Møller, Martin Kryspin Sørensen","doi":"10.14814/phy2.70084","DOIUrl":"https://doi.org/10.14814/phy2.70084","url":null,"abstract":"<p><p>Hyperlactatemia is common during tumor craniotomy, but the underlying pathophysiology is unclear. This study measured simultaneous arterial and jugular-bulb lactate concentrations in patients undergoing brain tumor craniotomy to investigate the hypothesis that hyperlactatemia was associated with a net cerebrovascular lactate input. In 20 patients, arterial and jugular-bulb blood was collected hourly from the start of surgery to 6 h postoperatively for measurement of lactate, glucose, and oxygen concentration. For each marker, data were analyzed using a linear mixed-effects model with jugular-bulb concentration as dependent variable, arterial concentration as fixed effect, and patient as random effect. Furthermore, we generated regression lines between arterial and jugular-bulb concentrations. The slope of the regression line between arterial and jugular-bulb lactate was 0.95 (95% CI 0.93-0.97, R<sup>2</sup> = 0.98), indicating that increasing arterial lactate levels were associated with an increasingly positive net cerebrovascular balance (net input). The line crossed the identity line at 2.86 (95% CI 0.57-5.16) mmol/L, indicating that lower levels of lactate were associated with a negative net cerebrovascular balance (net output). This suggests a switch from net lactate output during normolactatemia towards net input during hyperlactatemia. Hyperlactatemia in tumor-craniotomy patients probably does not originate from the brain.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11483513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472404","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":"Agreement between equation-derived body fat estimator and bioelectrical impedance analysis for body fat measurement in middle-aged southern Indians.","authors":"Chiranjeevi Kumar Endukuru, Girwar Singh Gaur, Dhanalakshmi Yerrabelli, Jayaprakash Sahoo, Balasubramaniyan Vairappan","doi":"10.14814/phy2.70095","DOIUrl":"10.14814/phy2.70095","url":null,"abstract":"<p><p>Excess body fat (BF) contributes to metabolic syndrome (MetS). The Clínica Universidad de Navarra-Body Adiposity Estimator (CUN-BAE) is an equation-derived body fat estimator proposed to assess BF. However, its efficiency compared to the standard method is unknown. We aimed to compare the efficacy of CUN-BAE with the standard method in estimating BF in southern Indians. We included 351 subjects, with 166 MetS patients and 185 non-MetS subjects. BF was obtained from the standard bioelectrical impedance analysis (BIA) method and measured by CUN-BAE in the same subjects. We compared the efficacy of CUN-BAE in estimating BF with that of BIA via Bland-Altman plots, intraclass correlation coefficients, concordance correlation coefficients and the kappa index. The mean body fat percentage (BF%) values measured by BIA and CUN-BAE in all the subjects were 28.91 ± 8.94 and 29.22 ± 8.63, respectively. We observed significant absolute agreement between CUN-BAE and BIA for BF%. BIA and CUN-BAE showed good reproducibility for BF%. CUN-BAE had accuracy comparable to BIA for detecting MetS using BF%. Our findings indicate that CUN-BAE provides precise BF estimates similar to the BIA method, making it suitable for routine clinical practice when access to BF measurement devices is limited.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11492144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472403","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}
Siluleko A Mkhize, Ashmeetha Manilall, Lebogang Mokotedi, Sule Gunter, Frederic S Michel
{"title":"Involvement of pentraxin-3 in the development of hypertension but not left ventricular hypertrophy in male spontaneously hypertensive rats.","authors":"Siluleko A Mkhize, Ashmeetha Manilall, Lebogang Mokotedi, Sule Gunter, Frederic S Michel","doi":"10.14814/phy2.70086","DOIUrl":"10.14814/phy2.70086","url":null,"abstract":"<p><p>Hypertension drives the development of concentric left ventricular hypertrophy (LVH). However, the relative contribution of pentraxin-3 (PTX-3), a novel marker for inflammatory cardiovascular disease, in the hypertrophic response to pressure overload has not been adequately elucidated. We investigated the role of PTX-3 in the development of LVH in spontaneously hypertensive rats (SHR), untreated and treated with either captopril (an ACE inhibitor) or hydralazine (a non-specific vasodilator). Three-month-old SHR received either 20 mg/kg/day hydralazine (SHR + H, n = 6), 40 mg/kg/day captopril (SHR + C, n = 6), or plain gelatine cubes (untreated SHR, n = 7) orally for 4 months. Wistar Kyoto rats (WKY, n = 7) were used as the normotensive controls. Blood pressure (BP) was measured using the tail-cuff method. Cardiac geometry and function were determined using M-mode echocardiography. Circulating concentrations of inflammatory markers were measured in plasma by ELISA. LV fibrosis and cardiomyocyte width were assessed by histology. Relative mRNA expression of PTX-3 was determined in the LV by RT-PCR. Untreated SHR exhibited greater systolic BP and relative wall thickness (RWT) compared to WKY. Captopril and hydralazine normalized BP but only captopril reversed RWT in SHR. Circulating PTX-3 and VCAM-1 levels were elevated in untreated SHR and reduced with captopril and hydralazine. Circulating PTX-3 was positively associated with systolic BP but lacked independent relations with indices of LVH. LV relative mRNA expression of PTX-3 was similar between the groups. PTX-3 may not be involved in the development of LVH in SHR, but plausibly reflects the localized inflammatory milieu associated with hypertension.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11483509/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472412","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}
Kentaro Noda, Neha Atale, Amer Al-Zahrani, Masashi Furukawa, Mark E Snyder, Xi Ren, Pablo G Sanchez
{"title":"Heparanase-induced endothelial glycocalyx degradation exacerbates lung ischemia/reperfusion injury in male mice.","authors":"Kentaro Noda, Neha Atale, Amer Al-Zahrani, Masashi Furukawa, Mark E Snyder, Xi Ren, Pablo G Sanchez","doi":"10.14814/phy2.70113","DOIUrl":"https://doi.org/10.14814/phy2.70113","url":null,"abstract":"<p><p>The endothelial glycocalyx (eGC) is a carbohydrate-rich layer on the vascular endothelium, and its damage can lead to endothelial and organ dysfunction. Heparanase (HPSE) degrades the eGC in response to cellular stress, but its role in organ dysfunction remains unclear. This study investigates HPSE's role in lung ischemia-reperfusion (I/R) injury. A left lung hilar occlusion model was used in B6 wildtype (WT) and HPSE genetic knockout (<sup>-/-</sup>) mice to induce I/R injury in vivo. The left lungs were ischemic for 1 h followed by reperfusion for 4 h prior to investigations of lung function and eGC status. Data were compared between uninjured lungs and I/R-injured lungs in WT and HPSE<sup>-/-</sup> mice. WT lungs showed significant functional impairment after I/R injury, whereas HPSE<sup>-/-</sup> lungs did not. Inhibition or knockout of HPSE prevented eGC damage, inflammation, and cellular migration after I/R injury by reducing matrix metalloproteinase activities. HPSE<sup>-/-</sup> mice exhibited compensatory regulation of related gene expressions. HPSE facilitates eGC degradation leading to inflammation and impaired lung function after I/R injury. HPSE may be a therapeutic target to attenuate graft damage in lung transplantation.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505878","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}