Abstract Objective: Only a few studies have investigated the development trends in spatial working memory and attention among a large sample of primary school students over a wide range of ages, while the efficiency of learning and memory processes is fundamental to academic performance, particularly for children, who are in a key developmental stage when their life opportunities can be altered. We aimed to explore how the spatial working memory and attention of primary school children are affected by grade, academic performance, and sex. Methods: In this cross-sectional observational study, students (144 boys, 139 girls, 6–13 years old) were recruited from Experimental Primary School Affiliated to Shanghai Jiao Tong University in Shanghai, China in 2018. The study protocol was reviewed and approved by the Bio-Ethics Board of the Bio-X Institutes, Shanghai Jiao Tong University. Based on a simple Spatial Working Memory and Attention Test on Paired Symbols test, we evaluate 283 participants’ working memory and attention ability. Results: Attention and working memory performance were enhanced as a positive function of grade in primary school children, and students who showed better academic achievement also performed better on the working memory task. However, attention and working memory performance were not affected by sex. Conclusion: Attention and working memory performance of primary school students develop with grade and corresponds to Better academic performance. Attention and working memory ability do not differ significantly between boys and girls.
{"title":"Effects of grade, academic performance, and sex on spatial working memory and attention in primary school children: a cross-sectional observational study","authors":"Nengpeng Zhan, Xuelian Fan, Fengtao Shen, Lulu Song, Chenhuan Zhou, Jiayi Xiao, Xun Wu, Leonardo Jiahao Li, Jiayao Xi, Sophia Li, Suhua Zeng, Can Li, Lihui Wang, Weidong Li","doi":"10.1097/JBR.0000000000000120","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000120","url":null,"abstract":"Abstract Objective: Only a few studies have investigated the development trends in spatial working memory and attention among a large sample of primary school students over a wide range of ages, while the efficiency of learning and memory processes is fundamental to academic performance, particularly for children, who are in a key developmental stage when their life opportunities can be altered. We aimed to explore how the spatial working memory and attention of primary school children are affected by grade, academic performance, and sex. Methods: In this cross-sectional observational study, students (144 boys, 139 girls, 6–13 years old) were recruited from Experimental Primary School Affiliated to Shanghai Jiao Tong University in Shanghai, China in 2018. The study protocol was reviewed and approved by the Bio-Ethics Board of the Bio-X Institutes, Shanghai Jiao Tong University. Based on a simple Spatial Working Memory and Attention Test on Paired Symbols test, we evaluate 283 participants’ working memory and attention ability. Results: Attention and working memory performance were enhanced as a positive function of grade in primary school children, and students who showed better academic achievement also performed better on the working memory task. However, attention and working memory performance were not affected by sex. Conclusion: Attention and working memory performance of primary school students develop with grade and corresponds to Better academic performance. Attention and working memory ability do not differ significantly between boys and girls.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"1 3","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120908307","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 : 2022-06-01DOI: 10.1097/JBR.0000000000000127
L. Parodi, C. Pujol
Abstract Hereditary spastic paraplegia type 56 (SPG56-HSP) is a rare autosomal recessive disorder caused by loss of function mutations in CYP2U1, leading to an early-onset limbs spasticity, often complicated by additional neurological or extra-neurological manifestations. Given its low prevalence, the molecular bases underlying SPG56-HSP are still poorly understood, and effective treatment options are still lacking. Recently, through the generation and characterization of the SPG56-HSP mouse model, we were able to take few important steps forward in expanding our knowledge of the molecular background underlying this complex disease. Leveraging the Cyp2u1-/- mouse model we were able to identify several new diagnostics biomarkers (vitamin B2, coenzyme Q, neopterin, and interferon-alpha), as well as to highlight the key role played by the folate pathway in SPG56-HSP pathogenesis, providing a potential treatment option. In this review, we discuss the major role played by the Cyp2u1-/- model in dissecting clinical and biological aspects of the disease, opening the way to a series of new research paths ranging from clinical trials, biomarker testing, and to the expansion of the underlying genetic and molecular, emphasizing how basic mouse model characterization could contribute to advance research in the context of rare disorders.
{"title":"Hereditary spastic paraplegia type 56: what a mouse can tell – a narrative review","authors":"L. Parodi, C. Pujol","doi":"10.1097/JBR.0000000000000127","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000127","url":null,"abstract":"Abstract Hereditary spastic paraplegia type 56 (SPG56-HSP) is a rare autosomal recessive disorder caused by loss of function mutations in CYP2U1, leading to an early-onset limbs spasticity, often complicated by additional neurological or extra-neurological manifestations. Given its low prevalence, the molecular bases underlying SPG56-HSP are still poorly understood, and effective treatment options are still lacking. Recently, through the generation and characterization of the SPG56-HSP mouse model, we were able to take few important steps forward in expanding our knowledge of the molecular background underlying this complex disease. Leveraging the Cyp2u1-/- mouse model we were able to identify several new diagnostics biomarkers (vitamin B2, coenzyme Q, neopterin, and interferon-alpha), as well as to highlight the key role played by the folate pathway in SPG56-HSP pathogenesis, providing a potential treatment option. In this review, we discuss the major role played by the Cyp2u1-/- model in dissecting clinical and biological aspects of the disease, opening the way to a series of new research paths ranging from clinical trials, biomarker testing, and to the expansion of the underlying genetic and molecular, emphasizing how basic mouse model characterization could contribute to advance research in the context of rare disorders.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"3 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"117170078","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 : 2021-12-09DOI: 10.1097/JBR.0000000000000118
M. Olaniyan, Tolu Olaniyan
Abstract Objective: Human immunodeficiency virus (HIV) p24 antigen and antibody and herpes simplex virus 2 IgM are seromarkers indicating infection with HIV and herpes simplex virus-2 (HSV-2), respectively, whereas tumor necrosis factor a is an inflammatory biomarker that can be triggered by infections. Female children of single parents are faced with many socio-economic challenges that make them vulnerable to sexual influences and prone to sexually transmitted infections. The goal of this work was to determine HIV p24 antigen/antibody, HSV-2 IgM and tumor necrosis factor-a plasma levels in adult female children living in single-parent households. Methods: In this case-control observational study, 100 adult female children living with a single parent (50 living with a single mother and 50 living with a single father; age: 18-22years) and 100 age-matched women living with both parents were recruited to serve as the test and control groups, respectively. All subjects were negative for acid-fast bacilli, plasmodium, hepatitis C virus, and hepatitis B virus. Human tumor necrosis factor a, HSV-2 IgM, antibody to hepatitis C virus, hepatitis B surface antigen and human immunodeficiency virus p24 antigen and antibody (HIV p24 Ag/Ab) levels were determined by ELISA, while the detection of acid-fast bacilli in sputum and Plasmodium in blood was carried out by optical microscopy. This work was carried out in the Owo/Ose Federal Constituency in Ondo State that shares boundaries with Edo State. The study protocol was approved by the Research and Ethical Committee of the Department of Medical Laboratory Science, Achievers University, Owo, Nigeria (AUO/MLS/2020/127) on August 27, 2020. Results: HIV p24Ag/Ab was detected in 0 adult female children living with a single mother, 1 (2%) adult female child living with a single father and 1 (1%) adult female child living with both parents. HSV-2 IgM was detected in 9 (18%) adult female children living with a single mother, 13 (26%) adult female children living with a single father, and 5 (10%) adult female children living with both parents. Conclusion: This work shows that adult female children of single parents are vulnerable to sexual influences, and thereby more prone to HSV-2 and possibly HIV, especially adult female children of single fathers.
{"title":"Human immunodeficiency virus p24 antigen and antibody, herpes simplex virus-2 IgM and tumor necrosis factor alpha plasma levels in adult female children living in single-parent households: a case-control observational study","authors":"M. Olaniyan, Tolu Olaniyan","doi":"10.1097/JBR.0000000000000118","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000118","url":null,"abstract":"Abstract Objective: Human immunodeficiency virus (HIV) p24 antigen and antibody and herpes simplex virus 2 IgM are seromarkers indicating infection with HIV and herpes simplex virus-2 (HSV-2), respectively, whereas tumor necrosis factor a is an inflammatory biomarker that can be triggered by infections. Female children of single parents are faced with many socio-economic challenges that make them vulnerable to sexual influences and prone to sexually transmitted infections. The goal of this work was to determine HIV p24 antigen/antibody, HSV-2 IgM and tumor necrosis factor-a plasma levels in adult female children living in single-parent households. Methods: In this case-control observational study, 100 adult female children living with a single parent (50 living with a single mother and 50 living with a single father; age: 18-22years) and 100 age-matched women living with both parents were recruited to serve as the test and control groups, respectively. All subjects were negative for acid-fast bacilli, plasmodium, hepatitis C virus, and hepatitis B virus. Human tumor necrosis factor a, HSV-2 IgM, antibody to hepatitis C virus, hepatitis B surface antigen and human immunodeficiency virus p24 antigen and antibody (HIV p24 Ag/Ab) levels were determined by ELISA, while the detection of acid-fast bacilli in sputum and Plasmodium in blood was carried out by optical microscopy. This work was carried out in the Owo/Ose Federal Constituency in Ondo State that shares boundaries with Edo State. The study protocol was approved by the Research and Ethical Committee of the Department of Medical Laboratory Science, Achievers University, Owo, Nigeria (AUO/MLS/2020/127) on August 27, 2020. Results: HIV p24Ag/Ab was detected in 0 adult female children living with a single mother, 1 (2%) adult female child living with a single father and 1 (1%) adult female child living with both parents. HSV-2 IgM was detected in 9 (18%) adult female children living with a single mother, 13 (26%) adult female children living with a single father, and 5 (10%) adult female children living with both parents. Conclusion: This work shows that adult female children of single parents are vulnerable to sexual influences, and thereby more prone to HSV-2 and possibly HIV, especially adult female children of single fathers.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"300 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123084928","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 : 2021-12-09DOI: 10.1097/JBR.0000000000000117
Ting Chu, Maosheng Yang
Abstract An increasing body of evidence supports the hypothesis that atherosclerosis is caused by multiple factors and mechanisms. A better understanding of the contribution of hypertriglyceridemia or oleic acid to the pathogenesis of atherosclerosis would significantly increase our ability to successfully treat these diseases. We propose that oleic acid promotes atherosclerosis via multiple pathophysiological mechanisms. Here we suggest that (1) atherosclerosis may develop through multiple pathophysiological mechanisms and that this may be a common feature of human diseases; (2) diseases may be the consequence of natural selection or the interaction of internal and external factors; (3) diseases should be recognized with “biological diversity,” and that this concept should be introduced into medical education, clinical treatment, drug research and development, and medical research. The work reported here will benefit a new generation of medical trainees and promote the development of the relevant medical fields.
{"title":"Oleic acid promotes atherosclerosis via multiple pathophysiological mechanisms: a narrative review","authors":"Ting Chu, Maosheng Yang","doi":"10.1097/JBR.0000000000000117","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000117","url":null,"abstract":"Abstract An increasing body of evidence supports the hypothesis that atherosclerosis is caused by multiple factors and mechanisms. A better understanding of the contribution of hypertriglyceridemia or oleic acid to the pathogenesis of atherosclerosis would significantly increase our ability to successfully treat these diseases. We propose that oleic acid promotes atherosclerosis via multiple pathophysiological mechanisms. Here we suggest that (1) atherosclerosis may develop through multiple pathophysiological mechanisms and that this may be a common feature of human diseases; (2) diseases may be the consequence of natural selection or the interaction of internal and external factors; (3) diseases should be recognized with “biological diversity,” and that this concept should be introduced into medical education, clinical treatment, drug research and development, and medical research. The work reported here will benefit a new generation of medical trainees and promote the development of the relevant medical fields.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124088304","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}
Abstract Objective: The coronavirus disease 2019 (COVID-19) epidemic resulting from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has still spread globally. The occurrence of the Delta variant, which is more infectious and spreads faster than earlier forms of the virus that causes COVID-19, makes infection prevention more challenging. Therefore, this study aimed to gain a comprehensive insight into the transmission routes of SARS-CoV-2 for curbing the propagation of SARS-CoV-2 in human populations. Methods: We studied a prospective cohort of 576 patients admitted consecutively to the First Affiliated Hospital of Guangzhou Medical University from January 21 to June 8, 2020. These patients were chosen based on their similar clinical phenotypes or imaging findings. There were 21 (3.6%) laboratory-confirmed COVID-19 patients (16 severe and 5 mild cases) and 555 non-COVID-19 patients. The antibody response and routes and duration of viral shedding were systematically evaluated in serial clinical specimens. Moreover, SARS-CoV-2 RNA was also detected in a mouth rinse, urine, and tear samples. This study was approved by the Medical Ethical Committee of The First Affiliated Hospital of Guangzhou Medical University (approval No. 2020-77). Results: SARS-CoV-2 mainly existed in sputum, nasal and throat swabs, and feces samples. Virus latency was longer in sputum and feces samples than in nasopharyngeal samples. IgG antibody response in respiratory samples was related to disease severity. Although droplets and aerosols are the major transmission routes for COVID-19, covert routes of transmission from asymptomatic patients, contaminated surfaces, and wastewater are also of interest. Conclusion: Our findings provide a solid foundation for developing prophylactic measures against SARS-CoV-2.
{"title":"A prospective cohort study of the presence of SARS-CoV-2 in clinical samples from multiple bodily sites: implications for transmission routes of COVID-19","authors":"Meixian Liu, Huimin Huang, Xiqing Bian, Zhi-Jia Zheng, Na Li, Baoqing Sun, Jian-Lin Wu","doi":"10.1097/JBR.0000000000000114","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000114","url":null,"abstract":"Abstract Objective: The coronavirus disease 2019 (COVID-19) epidemic resulting from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has still spread globally. The occurrence of the Delta variant, which is more infectious and spreads faster than earlier forms of the virus that causes COVID-19, makes infection prevention more challenging. Therefore, this study aimed to gain a comprehensive insight into the transmission routes of SARS-CoV-2 for curbing the propagation of SARS-CoV-2 in human populations. Methods: We studied a prospective cohort of 576 patients admitted consecutively to the First Affiliated Hospital of Guangzhou Medical University from January 21 to June 8, 2020. These patients were chosen based on their similar clinical phenotypes or imaging findings. There were 21 (3.6%) laboratory-confirmed COVID-19 patients (16 severe and 5 mild cases) and 555 non-COVID-19 patients. The antibody response and routes and duration of viral shedding were systematically evaluated in serial clinical specimens. Moreover, SARS-CoV-2 RNA was also detected in a mouth rinse, urine, and tear samples. This study was approved by the Medical Ethical Committee of The First Affiliated Hospital of Guangzhou Medical University (approval No. 2020-77). Results: SARS-CoV-2 mainly existed in sputum, nasal and throat swabs, and feces samples. Virus latency was longer in sputum and feces samples than in nasopharyngeal samples. IgG antibody response in respiratory samples was related to disease severity. Although droplets and aerosols are the major transmission routes for COVID-19, covert routes of transmission from asymptomatic patients, contaminated surfaces, and wastewater are also of interest. Conclusion: Our findings provide a solid foundation for developing prophylactic measures against SARS-CoV-2.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"43 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132949832","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 : 2021-09-30DOI: 10.1097/JBR.0000000000000113
Yingying Xu, Wenqing Hu, K. Xiao, Feng Wang, W. Guan, L. Zong
Abstract Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasm of the digestive system and are not sensitive to traditional chemotherapy. Therefore, historically, surgical resection was the only effective therapy. However, the emergence of tyrosine kinase inhibitors (TKIs) has revolutionized the treatment of GISTs, because they target c-Kit and PDGF receptor-a (PDGFRA), which are important in GIST development and progression. As research into c-Kit and PDGFRA continues, an increasing number of different TKIs are being used in the clinical setting. This review aims to discuss the current state of chemotherapy for the treatment of GISTs with different genotypes.
{"title":"The current state of chemotherapy for the treatment of gastrointestinal stromal tumors with different genotypes: a narrative review","authors":"Yingying Xu, Wenqing Hu, K. Xiao, Feng Wang, W. Guan, L. Zong","doi":"10.1097/JBR.0000000000000113","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000113","url":null,"abstract":"Abstract Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasm of the digestive system and are not sensitive to traditional chemotherapy. Therefore, historically, surgical resection was the only effective therapy. However, the emergence of tyrosine kinase inhibitors (TKIs) has revolutionized the treatment of GISTs, because they target c-Kit and PDGF receptor-a (PDGFRA), which are important in GIST development and progression. As research into c-Kit and PDGFRA continues, an increasing number of different TKIs are being used in the clinical setting. This review aims to discuss the current state of chemotherapy for the treatment of GISTs with different genotypes.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"49 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121713877","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 : 2021-09-30DOI: 10.1097/JBR.0000000000000112
Xiaolong Zhang, Hongyang Wang, Qiuju Wang
Abstract KCNQ4 gene mutation can lead to deafness non-syndromic autosomal dominant 2A, which is a type of autosomal dominant non-syndromic hearing loss. Deafness non-syndromic autosomal dominant 2A patients with KCNQ4 gene mutation usually present with symmetrical, delayed, progressive high-frequency-affected hearing loss, which eventually can involve all frequencies. In this article, we comprehensively reviewed the research on the role and function of KCNQ4 gene in genetic hearing loss. We discussed the pathological and physiological mechanisms of KCNQ4 gene and the related clinical phenotypes of KCNQ4 gene mutations. We also reviewed the latest developments in the treatment of KCNQ4 gene mutation-related genetic hearing loss, including selective potassium channel activation drugs and gene therapy.
{"title":"Progression of KCNQ4 related genetic hearing loss: a narrative review","authors":"Xiaolong Zhang, Hongyang Wang, Qiuju Wang","doi":"10.1097/JBR.0000000000000112","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000112","url":null,"abstract":"Abstract KCNQ4 gene mutation can lead to deafness non-syndromic autosomal dominant 2A, which is a type of autosomal dominant non-syndromic hearing loss. Deafness non-syndromic autosomal dominant 2A patients with KCNQ4 gene mutation usually present with symmetrical, delayed, progressive high-frequency-affected hearing loss, which eventually can involve all frequencies. In this article, we comprehensively reviewed the research on the role and function of KCNQ4 gene in genetic hearing loss. We discussed the pathological and physiological mechanisms of KCNQ4 gene and the related clinical phenotypes of KCNQ4 gene mutations. We also reviewed the latest developments in the treatment of KCNQ4 gene mutation-related genetic hearing loss, including selective potassium channel activation drugs and gene therapy.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"11 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131832313","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}
Abstract Objective: Early identification of acute kidney injury (AKI) is essential to improve the prognosis of patients with acute heart failure (AHF). We aimed to determine the utility of neutrophil/lymphocyte ratio (NLR), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), urea, and creatinine (Cr), as well as combinations of these, for the prediction of AKI in patients with AHF. Methods: A total of 153 patients with AHF under the care of Sun Yat-sen Memorial Hospital, Sun Yat-sen University from October 2009 to October 2019 were included in this retrospective observational study. Their NLR, NT-proBNP, urea, and Cr concentrations were measured on admission. AKI was defined using the Acute Kidney Injury Network criteria. Receiver operating characteristic (ROC) curves, the areas under the curves (AUCs), sensitivity, and specificity were employed to evaluate the ability of each biomarker and their combinations to identify AKI. This study was approved by the Ethics Committee of Sun Yat-sen Memorial Hospital, Sun Yat-sen University (approval No. SYSEC-KY-KS-2021-126) on June 22, 2021. Results: Forty-six (30.1%) participants developed AKI during hospitalization. The NLR and NT-proBNP of the participants with AKI were higher than those without (NLR: median 7.886 vs 4.717, P < 0.0001; NT-proBNP, median 6774 vs 2786pg/mL, P < 0.0001). ROC analyses demonstrated that high NLR and NT-proBNP were associated with higher incidences of AKI (NLR: cut-off 5.681, AUC 0.716, sensitivity 58.9%, specificity 80.4%; NT-proBNP: cut-off 5320pg/mL, AUC 0.700, sensitivity 72.9%, specificity 65.2%). Moreover, a combination of NLR, NT-proBNP, urea, and Cr yielded an AUC of 0.815, sensitivity 80.4%, and specificity of 74.8%. In addition, the AUCs for the prediction of AKI in the participants with New York Heart Association (NYHA) classes II, III, and IV were 0.936, 0.860, and 0.772, respectively, using this combination. Conclusion: A combination of NLR, NT-proBNP, urea, and Cr, measured at admission, may represent a promising tool for the prediction of AKI in patients with AHF. This method performs best for AKI risk assessment in patients with NYHA II, followed by those with NYHA III or IV.
摘要目的:早期识别急性肾损伤(AKI)对改善急性心力衰竭(AHF)患者预后至关重要。我们的目的是确定中性粒细胞/淋巴细胞比率(NLR)、脑钠肽n端原激素(NT-proBNP)、尿素和肌酐(Cr)的效用，以及这些指标的组合，用于预测AHF患者的AKI。方法:选取2009年10月至2019年10月中山大学附属中山纪念医院收治的AHF患者153例进行回顾性观察性研究。入院时测量NLR、NT-proBNP、尿素和Cr浓度。AKI的定义采用急性肾损伤网络标准。采用受试者工作特征(ROC)曲线、曲线下面积(auc)、敏感性和特异性来评估每种生物标志物及其组合识别AKI的能力。本研究经中山大学孙逸仙纪念医院伦理委员会批准(批准号:sysec - key - ks -2021-126)于2021年6月22日生效。结果:46名(30.1%)参与者在住院期间发生AKI。AKI患者的NLR和NT-proBNP均高于无AKI患者(NLR:中位数7.886 vs 4.717, P < 0.0001;NT-proBNP，中位数6774 vs 2786pg/mL, P < 0.0001)。ROC分析显示，高NLR和NT-proBNP与较高的AKI发生率相关(NLR: cut-off 5.681, AUC 0.716，敏感性58.9%，特异性80.4%;NT-proBNP:截止5320pg/mL, AUC 0.700，敏感性72.9%，特异性65.2%)。此外，NLR、NT-proBNP、尿素和Cr组合的AUC为0.815，敏感性为80.4%，特异性为74.8%。此外，使用该组合预测纽约心脏协会(NYHA) II、III和IV类受试者AKI的auc分别为0.936、0.860和0.772。结论:入院时测量NLR、NT-proBNP、尿素和Cr的组合可能是预测AHF患者AKI的一个有希望的工具。该方法对NYHA II型患者AKI风险评估效果最好，其次是NYHA III或IV型患者。
{"title":"Value of neutrophil/lymphocyte ratio, N-terminal pro-B-type natriuretic peptide, urea, and creatinine for the prediction of acute kidney injury in acute heart failure: a retrospective observational study","authors":"Lisi Huang, Jian He, Xianghua Lin, Ling Luo, Ri-hui Zhong, Xiaoying Xie, Xiao-Hui Peng, C. Duan","doi":"10.1097/JBR.0000000000000115","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000115","url":null,"abstract":"Abstract Objective: Early identification of acute kidney injury (AKI) is essential to improve the prognosis of patients with acute heart failure (AHF). We aimed to determine the utility of neutrophil/lymphocyte ratio (NLR), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), urea, and creatinine (Cr), as well as combinations of these, for the prediction of AKI in patients with AHF. Methods: A total of 153 patients with AHF under the care of Sun Yat-sen Memorial Hospital, Sun Yat-sen University from October 2009 to October 2019 were included in this retrospective observational study. Their NLR, NT-proBNP, urea, and Cr concentrations were measured on admission. AKI was defined using the Acute Kidney Injury Network criteria. Receiver operating characteristic (ROC) curves, the areas under the curves (AUCs), sensitivity, and specificity were employed to evaluate the ability of each biomarker and their combinations to identify AKI. This study was approved by the Ethics Committee of Sun Yat-sen Memorial Hospital, Sun Yat-sen University (approval No. SYSEC-KY-KS-2021-126) on June 22, 2021. Results: Forty-six (30.1%) participants developed AKI during hospitalization. The NLR and NT-proBNP of the participants with AKI were higher than those without (NLR: median 7.886 vs 4.717, P < 0.0001; NT-proBNP, median 6774 vs 2786pg/mL, P < 0.0001). ROC analyses demonstrated that high NLR and NT-proBNP were associated with higher incidences of AKI (NLR: cut-off 5.681, AUC 0.716, sensitivity 58.9%, specificity 80.4%; NT-proBNP: cut-off 5320pg/mL, AUC 0.700, sensitivity 72.9%, specificity 65.2%). Moreover, a combination of NLR, NT-proBNP, urea, and Cr yielded an AUC of 0.815, sensitivity 80.4%, and specificity of 74.8%. In addition, the AUCs for the prediction of AKI in the participants with New York Heart Association (NYHA) classes II, III, and IV were 0.936, 0.860, and 0.772, respectively, using this combination. Conclusion: A combination of NLR, NT-proBNP, urea, and Cr, measured at admission, may represent a promising tool for the prediction of AKI in patients with AHF. This method performs best for AKI risk assessment in patients with NYHA II, followed by those with NYHA III or IV.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"9 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130057488","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 : 2021-09-13DOI: 10.1097/JBR.0000000000000110
Lingge Yang, Yuan Wu, Liangkun You, Binbin Xie, Jun Lou, W. Han, Kai Wang
Abstract Objective: Most patients with advanced lung cancer have a poor prognosis. Recent studies have identified TRIM59 as a novel molecule that serves as a prognostic factor for the progression of non-small cell lung cancer. In the present study, we investigated the role of TRIM59 in predicting the prognosis of lung adenocarcinoma (LUAD) as well as the correlation between TRIM59 expression and immune infiltrates. Methods: We analyzed TRIM59 expression in normal and tumor tissues based on RNA-sequencing datasets from The Cancer Genome Atlas and Genotype-Tissue Expression databases. Forty-seven cases of LUAD tissues and their matching adjacent tissues were collected, and TRIM59 expression in tissue samples was demonstrated by immunohistochemistry. All tissue specimens were obtained under the approval of the Medical Ethics Committee of the Second Affiliated Hospital of Zhejiang University School of Medicine (approval No. IR2019001101; approved on April 3, 2019). The immune cell scores were calculated using the CIBERSORT database. The Tumor Immune Estimation Resource database was used to analyze the correlation between TRIM59 and immune cell activities. Results: TRIM59 was up-regulated in most cancer types. High TRIM59 expression predicted a worse prognosis in patients with LUAD (overall survival, P = 0.00096; disease-specific survival, P = 0.00056; disease-free interval, P = 0.0009; progression-free interval, P = 0.0012). Moreover, TRIM59 was highly expressed in patients with LUAD who had a poorer prognosis. TRIM59 also showed a significant correlation with the ESTIMATE score (P = 0.04) and stromal score (P = 0.005) in patients with LUAD. Notably, a significant correlation between TRIM59 and the tumor mutation burden was found in LUAD but in no other cancer types (P < 0.001). Further investigation showed that TRIM59 had a significant correlation with gene markers on neutrophils and dendritic cells. Conclusion: TRIM59 is a potential prognosticator in LUAD and may be correlated with immune cell identification, immune cell infiltration, and immunotherapy checkpoints in LUAD.
{"title":"Integrated bioinformatics analysis reveals correlations of high TRIM59 expression with worse prognosis and immune infiltrates in lung adenocarcinoma","authors":"Lingge Yang, Yuan Wu, Liangkun You, Binbin Xie, Jun Lou, W. Han, Kai Wang","doi":"10.1097/JBR.0000000000000110","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000110","url":null,"abstract":"Abstract Objective: Most patients with advanced lung cancer have a poor prognosis. Recent studies have identified TRIM59 as a novel molecule that serves as a prognostic factor for the progression of non-small cell lung cancer. In the present study, we investigated the role of TRIM59 in predicting the prognosis of lung adenocarcinoma (LUAD) as well as the correlation between TRIM59 expression and immune infiltrates. Methods: We analyzed TRIM59 expression in normal and tumor tissues based on RNA-sequencing datasets from The Cancer Genome Atlas and Genotype-Tissue Expression databases. Forty-seven cases of LUAD tissues and their matching adjacent tissues were collected, and TRIM59 expression in tissue samples was demonstrated by immunohistochemistry. All tissue specimens were obtained under the approval of the Medical Ethics Committee of the Second Affiliated Hospital of Zhejiang University School of Medicine (approval No. IR2019001101; approved on April 3, 2019). The immune cell scores were calculated using the CIBERSORT database. The Tumor Immune Estimation Resource database was used to analyze the correlation between TRIM59 and immune cell activities. Results: TRIM59 was up-regulated in most cancer types. High TRIM59 expression predicted a worse prognosis in patients with LUAD (overall survival, P = 0.00096; disease-specific survival, P = 0.00056; disease-free interval, P = 0.0009; progression-free interval, P = 0.0012). Moreover, TRIM59 was highly expressed in patients with LUAD who had a poorer prognosis. TRIM59 also showed a significant correlation with the ESTIMATE score (P = 0.04) and stromal score (P = 0.005) in patients with LUAD. Notably, a significant correlation between TRIM59 and the tumor mutation burden was found in LUAD but in no other cancer types (P < 0.001). Further investigation showed that TRIM59 had a significant correlation with gene markers on neutrophils and dendritic cells. Conclusion: TRIM59 is a potential prognosticator in LUAD and may be correlated with immune cell identification, immune cell infiltration, and immunotherapy checkpoints in LUAD.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"22 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129842558","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 : 2021-09-13DOI: 10.1097/JBR.0000000000000111
F. Dong, Xiao-wen Hu, Shasha Zhang, Fan He, Amber Naz, Lin He, Hongxin Zhu
Abstract Objective: Rubicon is an inhibitory interacting protein of the autophagy-related protein Uvrag. We previously showed that Rubicon deficiency promotes autophagic flux in vivo and that autophagy can degrade lipid droplets. This study aimed to investigate the effects of Rubicon deficiency on fasting-induced hepatic steatosis. Methods: Two-month-old wild-type (WT) and Rubicon-deficient mice were subjected to feeding or fasting for 24 hours to induce hepatic steatosis. The distribution of liver lipid droplets was revealed by oil red O staining. Hepatic and plasma triglyceride, nonesterified fatty acid (NEFA), and cholesterol levels were detected using commercially available kits. Real-time reverse transcriptasepolymerase chain reaction was performed to analyze the mRNA expression of genes related to lipid metabolism in the liver. Western blot was conducted to assess autophagy-related protein levels in the liver. The animal experiments were approved by the Institutional Animal Care and Use Committee at Shanghai Jiao Tong University, China. Results: We showed that under fasting conditions, Rubicon-deficient mice had more lipid droplets in the liver than WT controls. Consistent with these results, the hepatic triglyceride, NEFA, and cholesterol levels in fasted Rubicon-deficient mice were significantly higher than those of fasted WT controls. The levels of SREBP-1, a key regulator of lipid synthesis, were significantly lower in livers from fasted WT mice than those of fed WT mice. However, the decrease in SREBP-1 in fasted mice was attenuated by Rubicon deficiency. Western blot analysis demonstrated that the fasting-induced increase in autophagic flux was amplified by Rubicon deficiency. Finally, we showed that Rubicon deficiency in mice led to elevated plasma triglyceride and NEFA acid levels under fasting conditions. Conclusion: Rubicon deficiency exacerbates fasting-induced hepatic steatosis in mice.
{"title":"Rubicon deficiency exacerbates fasting-induced hepatic steatosis","authors":"F. Dong, Xiao-wen Hu, Shasha Zhang, Fan He, Amber Naz, Lin He, Hongxin Zhu","doi":"10.1097/JBR.0000000000000111","DOIUrl":"https://doi.org/10.1097/JBR.0000000000000111","url":null,"abstract":"Abstract Objective: Rubicon is an inhibitory interacting protein of the autophagy-related protein Uvrag. We previously showed that Rubicon deficiency promotes autophagic flux in vivo and that autophagy can degrade lipid droplets. This study aimed to investigate the effects of Rubicon deficiency on fasting-induced hepatic steatosis. Methods: Two-month-old wild-type (WT) and Rubicon-deficient mice were subjected to feeding or fasting for 24 hours to induce hepatic steatosis. The distribution of liver lipid droplets was revealed by oil red O staining. Hepatic and plasma triglyceride, nonesterified fatty acid (NEFA), and cholesterol levels were detected using commercially available kits. Real-time reverse transcriptasepolymerase chain reaction was performed to analyze the mRNA expression of genes related to lipid metabolism in the liver. Western blot was conducted to assess autophagy-related protein levels in the liver. The animal experiments were approved by the Institutional Animal Care and Use Committee at Shanghai Jiao Tong University, China. Results: We showed that under fasting conditions, Rubicon-deficient mice had more lipid droplets in the liver than WT controls. Consistent with these results, the hepatic triglyceride, NEFA, and cholesterol levels in fasted Rubicon-deficient mice were significantly higher than those of fasted WT controls. The levels of SREBP-1, a key regulator of lipid synthesis, were significantly lower in livers from fasted WT mice than those of fed WT mice. However, the decrease in SREBP-1 in fasted mice was attenuated by Rubicon deficiency. Western blot analysis demonstrated that the fasting-induced increase in autophagic flux was amplified by Rubicon deficiency. Finally, we showed that Rubicon deficiency in mice led to elevated plasma triglyceride and NEFA acid levels under fasting conditions. Conclusion: Rubicon deficiency exacerbates fasting-induced hepatic steatosis in mice.","PeriodicalId":150904,"journal":{"name":"Journal of Bio-X Research","volume":"47 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116504313","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：