Klara Gadó, Malaz Khodier, Andrea Virág, Gyula Domján, Gabriella Dörnyei
{"title":"Anemia of geriatric patients.","authors":"Klara Gadó, Malaz Khodier, Andrea Virág, Gyula Domján, Gabriella Dörnyei","doi":"10.1556/2060.2022.00218","DOIUrl":"https://doi.org/10.1556/2060.2022.00218","url":null,"abstract":"<p><p>Anemia is a common finding in the elderly. Approximately 10 percent of the elderly suffers from anemia. Anemia per se is an independent factor of mortality in older patients regardless its cause. Frailty is also frequent in geriatric patients. That means that there is a decreased reserve capacity to react to different stress factors including anemia. The frequent presence of heart failure and also impaired cerebrovascular circulation makes more difficult to tolerate anemia in older age. Anemia is a symptom, finding and treating the underlying cause is also important. Treatment always depends on clinical findings: the more severe the symptoms, the more important to treat them. Severity of anemia depends not only the underlying cause, degree of anemia, co-morbidities and frailty of the patients, but also the speed of its development. Sudden blood loss due to an accident is less well tolerated than the same degree of anemia due to B12 deficiency. Main causes of anemia in the elderly include nutritional deficiencies, chronic diseases, tumors, and certain hematological malignancies such as chronic lymphocytic leukemia, multiple myeloma, myelodysplastic syndrome.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":"109 2","pages":"119-134"},"PeriodicalIF":1.4,"publicationDate":"2022-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40549499","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}
Mohammad Mehdi Heidari, Seyed Ali Madani Manshadi, Ahmad Reza Eshghi, Fatemeh Talebi, Mehri Khatami, José Bragança, Mahtab Ordooei, Reyhane Chamani, Farzaneh Ghasemi
{"title":"Mutational and bioinformatics analysis of the NKX2.1 gene in a cohort of Iranian pediatric patients with congenital hypothyroidism (CH).","authors":"Mohammad Mehdi Heidari, Seyed Ali Madani Manshadi, Ahmad Reza Eshghi, Fatemeh Talebi, Mehri Khatami, José Bragança, Mahtab Ordooei, Reyhane Chamani, Farzaneh Ghasemi","doi":"10.1556/2060.2022.00224","DOIUrl":"https://doi.org/10.1556/2060.2022.00224","url":null,"abstract":"<p><p>Congenital hypothyroidism (CH) occurs with a relatively alarming prevalence in infants, and if not diagnosed and treated in time, it can have devastating consequences for the development of the nervous system. CH is associated with genetic changes in several genes that encode transcription factors responsible for thyroid development, including mutations in the NK2 homeobox 1 (NKX2.1) gene, which encodes the thyroid transcription factor-1 (TTF-1). Although CH is frequently observed in pediatric populations, there is still a limited understanding of the genetic factors and molecular mechanisms contributing to this disease. The sequence of the NKX2.1 gene was investigated in 75 pediatric patients with CH by polymerase chain reaction (PCR), single-stranded conformation polymorphism (SSCP), and direct DNA sequencing. Four missense heterozygous variations were identified in exon 3 of the NKX2.1 gene, including three novel missense variations, namely c.708A>G, p.Gln202Arg; c.713T>G, p.Tyr204Asp; c.833T>G, p.Tyr244Asp, and a previously reported variant rs781133468 (c.772C>G, p.His223Gln). Importantly, these variations occur in highly conserved residues of the TTF-1 DNA-binding domain and were predicted by bioinformatics analysis to alter the protein structure, with a probable alteration in the protein function. These results indicate that nucleotide changes in the NKX2.1 gene may contribute to CH pathogenesis.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":"109 2","pages":"261-277"},"PeriodicalIF":1.4,"publicationDate":"2022-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40549498","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}
Behrouz Rahmani, Elham Ghashghayi, Morteza Zendehdel, Ali Baghbanzadeh, Mina Khodadadi
{"title":"Molecular mechanisms highlighting the potential role of COVID-19 in the development of neurodegenerative diseases.","authors":"Behrouz Rahmani, Elham Ghashghayi, Morteza Zendehdel, Ali Baghbanzadeh, Mina Khodadadi","doi":"10.1556/2060.2022.00019","DOIUrl":"https://doi.org/10.1556/2060.2022.00019","url":null,"abstract":"<p><p>Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In addition to the pulmonary manifestations, COVID-19 patients may present a wide range of neurological disorders as extrapulmonary presentations. In this view, several studies have recently documented the worsening of neurological symptoms within COVID-19 morbidity in patients previously diagnosed with neurodegenerative diseases (NDs). Moreover, several cases have also been reported in which the patients presented parkinsonian features after initial COVID-19 symptoms. These data raise a major concern about the possibility of communication between SARS-CoV-2 infection and the initiation and/or worsening of NDs. In this review, we have collected compelling evidence suggesting SARS-CoV-2, as an environmental factor, may be capable of developing NDs. In this respect, the possible links between SARS-CoV-2 infection and molecular pathways related to most NDs and the pathophysiological mechanisms of the NDs such as Alzheimer's disease, vascular dementia, frontotemporal dementia, Parkinson's disease, and amyotrophic lateral sclerosis will be explained.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":"109 2","pages":"135-162"},"PeriodicalIF":1.4,"publicationDate":"2022-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40549501","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}
Klara Gadó, Aranka Katalin Kovács, Gyula Domján, Zoltán Zsolt Nagy, Gabriella Dörnyei Bednárik
{"title":"COVID-19 and the elderly.","authors":"Klara Gadó, Aranka Katalin Kovács, Gyula Domján, Zoltán Zsolt Nagy, Gabriella Dörnyei Bednárik","doi":"10.1556/2060.2022.00203","DOIUrl":"10.1556/2060.2022.00203","url":null,"abstract":"<p><p>COVID-19 has become a great burden of the world in respect of health care, social, and economical reason. Several million people died worldwide so far and more and more mutants are generated and spread. Older people with co-morbidities and frailty syndrome have a significantly higher risk to get the infection and also higher the risk of a more serious disease process. Mortality of COVID-19 is also higher in case of geriatric patients. In this review we attempted to summarize the factors of the higher susceptibility for more serious disease, what actions need to be taken for defending older patients and also special aspects of clinical presentation including ophthalmic symptoms.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2022-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41811967","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}
Georgina Gyarmati, Ildikó Toma, Audrey Izuhara, James L Burford, Urvi Nikhil Shroff, Stella Papadouri, Sachin Deepak, János Peti-Peterdi
{"title":"The role of TRPC6 calcium channels and P2 purinergic receptors in podocyte mechanical and metabolic sensing.","authors":"Georgina Gyarmati, Ildikó Toma, Audrey Izuhara, James L Burford, Urvi Nikhil Shroff, Stella Papadouri, Sachin Deepak, János Peti-Peterdi","doi":"10.1556/2060.2021.00205","DOIUrl":"10.1556/2060.2021.00205","url":null,"abstract":"<p><p>Podocyte calcium (Ca2+) signaling plays important roles in the (patho)physiology of the glomerular filtration barrier. Overactivation of podocyte transient receptor potential canonical (TRPC) channels including TRPC6 and purinergic signaling via P2 receptors that are known mechanosensors can increase podocyte intracellular Ca2+ levels ([Ca2+]i) and cause cell injury, proteinuria and glomerular disease including in diabetes. However, important mechanistic details of the trigger and activation of these pathways in vivo in the intact glomerular environment are lacking. Here we show direct visual evidence that podocytes can sense mechanical overload (increased glomerular capillary pressure) and metabolic alterations (increased plasma glucose) via TRPC6 and purinergic receptors including P2Y2. Multiphoton microscopy of podocyte [Ca2+]i was performed in vivo using wild-type and TRPC6 or P2Y2 knockout (KO) mice expressing the calcium reporter GCaMP3/5 only in podocytes and in vitro using freshly dissected microperfused glomeruli. Single-nephron intra-glomerular capillary pressure elevations induced by obstructing the efferent arteriole lumen with laser-induced microthrombus in vivo and by a micropipette in vitro triggered >2-fold increases in podocyte [Ca2+]i. These responses were blocked in TRPC6 and P2Y2 KO mice. Acute elevations of plasma glucose caused >4-fold increases in podocyte [Ca2+]i that were abolished by pharmacological inhibition of TRPC6 or P2 receptors using SAR7334 or suramin treatment, respectively. This study established the role of Ca2+ signaling via TRPC6 channels and P2 receptors in mechanical and metabolic sensing of podocytes in vivo, which are promising therapeutic targets in conditions with high intra-glomerular capillary pressure and plasma glucose, such as diabetic and hypertensive nephropathy.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2021-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9200898/pdf/nihms-1787714.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9641958","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":"The miR-1906 mimic attenuates bone loss in osteoporosis by down-regulating the TLR4/MyD88/NF-κB pathway.","authors":"H Xie, L Cao, L Ye, G Shan, W Song","doi":"10.1556/2060.2020.00042","DOIUrl":"https://doi.org/10.1556/2060.2020.00042","url":null,"abstract":"<p><p>In this study, the ability of microRNA-1906 (miR-1906) to attenuate bone loss in osteoporosis was evaluated by measuring the effects of a miR-1906 mimic and inhibitor on the cellular toxicity and cell viability of MC3T3-E1 cells. Bone marrow-derived macrophage (BMM) cells were isolated from female mice, and tartrate-resistant acid phosphatase signalling was performed in miR-1906 mimic-treated, receptor-activated nuclear factor kappa-B (NF-κB) ligand (RANKL)-induced osteoclasts. In-vivo, osteoporosis was induced by ovariectomy (OVX). Rats were treated with 500 nmol/kg of the miR-1906 mimic via intrathecal administration for 10 consecutive days following surgery. The effect of the miR-1906 mimic on bone mineral density (BMD) in OVX rats was observed in the whole body, lumbar vertebrae and femur. Levels of biochemical parameters and cytokines in the serum of miR-1906 mimic-treated OVX rats were analysed. The mRNA expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), p-38 and NF-κB in tibias of osteoporotic rats (induced by ovariectomy) was observed using quantitative reverse-transcription polymerase chain reaction. Treatment with the miR-1906 mimic reduced cellular toxicity and enhanced the cell viability of MC3T3-E1 cells. Furthermore, osteoclastogenesis in miR-1906 mimic-treated, RANKL-induced osteoclast cells was reduced, whereas the BMD in the miR-1906 mimic-treated group was higher than in the OVX group of rats. Treatment with the miR-1906 mimic also increased levels of biochemical parameters and cytokines in the serum of ovariectomised rats. Finally, mRNA expression levels of TLR4, MyD88, p-38 and NF-κB were lower in the tibias of miR-1906 mimic-treated rats than in those of OVX rats. In conclusion, the miR-1906 mimic reduces bone loss in rats with ovariectomy-induced osteoporosis by regulating the TLR4/MyD88/NF-κB pathway.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":"107 4","pages":"469-478"},"PeriodicalIF":1.4,"publicationDate":"2021-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39127527","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 \"GG\" genotype of rs26802 variant in the ghrelin gene is a potential protective factor against nonalcoholic fatty liver disease.","authors":"Gholamreza Rezamand, Touraj Mahmoudi, Seidamir Pasha Tabaeian, Hamid Farahani, Fatemeh Shahinmehr, Hossein Nobakht, Reza Dabiri, Asadollah Asadi, Fariborz Mansour-Ghanaei, Mohammad Reza Zali","doi":"10.1556/2060.2021.00183","DOIUrl":"https://doi.org/10.1556/2060.2021.00183","url":null,"abstract":"<p><strong>Background: </strong>Nonalcoholic fatty liver disease (NAFLD) is an emerging global chronic liver disease worldwide. Considering the powerful association between NAFLD, insulin resistance (IR) and obesity, as well as the key role of ghrelin in these metabolic disorders, we hypothesized that some single nucleotide polymorphisms (SNPs) of the ghrelin (GHRL) and ghrelin receptor (GHSR) genes might be associated with NAFLD.</p><p><strong>Methods: </strong>We conducted a case-control retrospective study of 150 cases with biopsy-proven NAFLD and 155 controls. The diagnosis of NAFLD was established before the start of the genotyping process. All the 305 subjects were genotyped for GHRL SNP rs26802 or -501T>G and GHSR SNP rs572169 or Arg159Arg using the PCR-RFLP method.</p><p><strong>Results: </strong>The GHRL rs26802 \"GG\" genotype compared with the \"TT\" genotype and \"TT+TG\" genotype appears to be a marker of decreased NAFLD susceptibility even after adjustment for confounding factors (P = 0.006; OR = 0.14, 95% CI = 0.03-0.56 and P = 0.003; OR = 0.16, 95% CI = 0.05-0.53, respectively). However, we observed no significant difference in genotype or allele frequencies between the cases and controls for GHSR SNP rs572169.</p><p><strong>Conclusions: </strong>These findings proposed, for the first time, that the GHRL rs26802 \"GG\" genotype has a protective effect against NAFLD. Nonetheless, this observation warrants further investigations in other populations.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":" ","pages":"342-352"},"PeriodicalIF":1.4,"publicationDate":"2021-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39422290","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}
Dániel Csala, Bence Márk Kovács, Péter Bali, Gábor Reha, Gergely Pánics
{"title":"The influence of external load variables on creatine kinase change during preseason training period.","authors":"Dániel Csala, Bence Márk Kovács, Péter Bali, Gábor Reha, Gergely Pánics","doi":"10.1556/2060.2021.30019","DOIUrl":"https://doi.org/10.1556/2060.2021.30019","url":null,"abstract":"<p><strong>Objective: </strong>The aim of the present study was to analyse the relationships between creatine kinase (CK) concentration, an indirect marker of muscle damage, and global positioning system (GPS)-derived metrics of a continuous two-week-long preseason training period in elite football.</p><p><strong>Design: </strong>Twenty-one elite male professional soccer players were assessed during a 14-day preseason preparatory period. CK concentrations were determined each morning, and a GPS system was used to quantify the external load. A generalized estimating equation (GEE) model was established to determine the extent to which the external load parameter explained post-training CK levels.</p><p><strong>Results: </strong>The GEE model found that higher numbers of decelerations (χ 2 = 7.83, P = 0.005) were most strongly associated with the post-training CK level. Decelerations and accelerations accounted for 62% and 11% of the post-training CK level, respectively, and considerable interindividual variability existed in the data.</p><p><strong>Conclusion: </strong>The use of GPS to predict muscle damage could be of use to coaches and practitioners in prescribing recovery practices. Based on GPS data, more individualized strategies could be devised and could potentially result in better subsequent performance.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":"108 3","pages":"371-382"},"PeriodicalIF":1.4,"publicationDate":"2021-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9473830","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":"Perturbation-based balance assessment: Examining reactive balance control in older adults with mild cognitive impairments.","authors":"Lakshmi N Kannan, Tanvi S Bhatt","doi":"10.1556/2060.2021.00181","DOIUrl":"https://doi.org/10.1556/2060.2021.00181","url":null,"abstract":"<p><strong>Background: </strong>Older adults with mild cognitive impairment (OAwMCI) present subtle balance and gait deficits along with subjective memory decline. Although these presentations might not affect activities of daily living (ADLs), they attribute to a two-folded increase in falls. While changes occurring in volitional balance control during ADLs have been extensively examined among OAwMCI, reactive balance control, required to recover from external perturbations, has received little attention. Therefore, this study examined reactive balance control in OAwMCI compared to their healthy counterparts.</p><p><strong>Methods: </strong>Fifteen older adults with mild cognitive impairment (OAwMCI), fifteen cognitively intact older adults (CIOA) (>55 years), and fifteen young adults (18-30 years) were exposed to stance perturbations at three different intensities. Behavioral outcomes postural COM state stability, step length, step initiation, and step execution were computed.</p><p><strong>Results: </strong>Postural COM state stability was the lowest in OAwMCI compared to CIOA and young adults, and it deteriorated at higher perturbation intensities (P < 0.001). Step length was the lowest among OAwMCI and was significantly different from young adults (P < 0.001) but not from CIOA. Unlike OAwMCI, CIOA and young adults increased their step length at higher perturbation intensities (P < 0.001). OAwMCI showed longer recovery step initiation times and shorter execution times compared to CIOA and young adults at higher perturbation intensities (P < 0.001).</p><p><strong>Conclusion: </strong>OAwMCI exhibit exacerbated reactive instability and are unable to modulate their responses as the threat to balance control altered. Thus, they are at a significantly higher risk of falls than their healthy counterparts.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":" ","pages":"353-370"},"PeriodicalIF":1.4,"publicationDate":"2021-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39422289","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":"Ferulic acid attenuates osteoporosis induced by glucocorticoid through regulating the GSK-3β/Lrp-5/ERK signalling pathways.","authors":"Wei Zhou, Bo Chen, Jingbo Shang, Renbo Li","doi":"10.1556/2060.2021.00180","DOIUrl":"https://doi.org/10.1556/2060.2021.00180","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate in-vivo and in-vitro effects of ferulic acid (FA) on glucocorticoid-induced osteoarthritis (GIO) to establish its possible underlying mechanisms.</p><p><strong>Methods: </strong>The effects of FA on cell proliferation, cell viability (MTT assay), ALP activity, and mineralization assay, and oxidative stress markers (ROS, SOD, GSH LDH and MDA levels) were investigated by MC3T3-E1 cell line. Wistar rats received standard saline (control group) or dexamethasone (GC, 2 mg-1 kg) or DEX+FA (50 and 100 mg-1 kg) orally for 8 weeks. Bone density, micro-architecture, bio-mechanics, bone turnover markers and histo-morphology were determined. The expression of OPG, RANKL, osteogenic markers, and other signalling proteins was assessed employing quantitative RT-PCR and Western blotting.</p><p><strong>Results: </strong>The findings indicated the elevation of ALP mRNA expressions, osteogenic markers (Runx-2, OSX, Col-I, and OSN), and the β-Catenin, Lrp-5 and GSK-3β protein expressions. FA showed the potential to increase MC3T3-E1 cell differentiation, proliferation, and mineralization. FA increased oxidative stress markers (SOD, MDA, and GSH) while decreasing ROS levels and lactate dehydrogenase release in GIO rats. The OPG/RANKL mRNA expression ratio was increased by FA, followed by improved GSK-3β and ERK phosphorylation with enhanced mRNA expressions of Lrp-5 and β-catenin.</p><p><strong>Conclusion: </strong>These findings showed that FA improved osteoblasts proliferation with oxidative stress suppression by controlling the Lrp-5/GSK-3β/ERK pathway in GIO, demonstrating the potential pathways involved in the mechanism of actions of FA in GIO therapy.</p>","PeriodicalId":20058,"journal":{"name":"Physiology international","volume":" ","pages":"317-341"},"PeriodicalIF":1.4,"publicationDate":"2021-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39422291","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}