The Kaohsiung journal of medical sciences最新文献_第8页

Development of a diagnostic support system for the fibrosis of nonalcoholic fatty liver disease using artificial intelligence and deep learning. 利用人工智能和深度学习开发非酒精性脂肪肝纤维化诊断支持系统。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-05-31 DOI: 10.1002/kjm2.12850

Noppamate Preechathammawong, Mongkon Charoenpitakchai, Nutthawat Wongsason, Julalak Karuehardsuwan, Thaninee Prasoppokakorn, Panyavee Pitisuttithum, Anapat Sanpavat, Karn Yongsiriwit, Thannob Aribarg, Parkpoom Chaisiriprasert, Sombat Treeprasertsuk, Sakkarin Chirapongsathorn

{"title":"Development of a diagnostic support system for the fibrosis of nonalcoholic fatty liver disease using artificial intelligence and deep learning.","authors":"Noppamate Preechathammawong, Mongkon Charoenpitakchai, Nutthawat Wongsason, Julalak Karuehardsuwan, Thaninee Prasoppokakorn, Panyavee Pitisuttithum, Anapat Sanpavat, Karn Yongsiriwit, Thannob Aribarg, Parkpoom Chaisiriprasert, Sombat Treeprasertsuk, Sakkarin Chirapongsathorn","doi":"10.1002/kjm2.12850","DOIUrl":"10.1002/kjm2.12850","url":null,"abstract":"Liver fibrosis is a pathological condition characterized by the abnormal proliferation of liver tissue, subsequently able to progress to cirrhosis or possibly hepatocellular carcinoma. The development of artificial intelligence and deep learning have begun to play a significant role in fibrosis detection. This study aimed to develop SMART AI-PATHO, a fully automated assessment method combining quantification of histopathological architectural features, to analyze steatosis and fibrosis in nonalcoholic fatty liver disease (NAFLD) core biopsies and employ Metavir fibrosis staging as standard references and fat assessment grading measurement for comparison with the pathologist interpretations. There were 146 participants enrolled in our study. The correlation of Metavir scoring system interpretation between pathologists and SMART AI-PATHO was significantly correlated (Agreement = 68%, Kappa = 0.59, p-value <0.001), which subgroup analysis of significant fibrosis (Metavir score F2-F4) and nonsignificant fibrosis (Metavir score F0-F1) demonstrated substantial correlated results (agreement = 80%, kappa = 0.61, p-value <0.001), corresponding with the correlation of advanced fibrosis (Metavir score F3-F4) and nonadvanced fibrosis groups (Metavir score F0-F2), (agreement = 89%, kappa = 0.74, p-value <0.001). SMART AI-PATHO, the first pivotal artificially intelligent diagnostic tool for the color-based NAFLD hepatic tissue staging in Thailand, demonstrated satisfactory performance as a pathologist to provide liver fibrosis scoring and steatosis grading. In the future, developing AI algorithms and reliable testing on a larger scale may increase accuracy and contribute to telemedicine consultations for general pathologists in clinical practice.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"757-765"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141181786","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}

引用次数: 0

Identification of southern Taiwan genetic variants in thyroid dyshormonogenesis through whole-exome sequencing. 通过全外显子组测序鉴定台湾南部甲状腺发育异常的基因变异。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-06-25 DOI: 10.1002/kjm2.12871

Ching-Chao Tsai, Yu-Ming Chang, Yen-Yin Chou, Shou-Yen Chen, Yu-Wen Pan, Meng-Che Tsai

{"title":"Identification of southern Taiwan genetic variants in thyroid dyshormonogenesis through whole-exome sequencing.","authors":"Ching-Chao Tsai, Yu-Ming Chang, Yen-Yin Chou, Shou-Yen Chen, Yu-Wen Pan, Meng-Che Tsai","doi":"10.1002/kjm2.12871","DOIUrl":"10.1002/kjm2.12871","url":null,"abstract":"Thyroid dyshormonogenesis (TDH) is responsible for 15%-25% of congenital hypothyroidism (CH) cases. Pathogenetic variants of this common inherited endocrine disorders vary geographically. Unraveling the genetic underpinnings of TDH is essential for genetic counseling and precise therapeutic strategies. This study aims to identify genetic variants associated with TDH in Southern Taiwan using whole exome sequencing (WES). We included CH patients diagnosed through newborn screening at a tertiary medical center from 2011 to 2022. Permanent TDH was determined based on imaging evidence of bilateral thyroid structure and the requirement for continuous medication beyond 3 years of age. Genomic DNA extracted from blood was used for exome library construction, and pathogenic variants were detected using an in-house algorithm. Of the 876 CH patients reviewed, 121 were classified as permanent, with 47 (40%) confirmed as TDH. WES was conducted for 45 patients, and causative variants were identified in 32 patients (71.1%), including DUOX2 (15 cases), TG (8 cases), TSHR (7 cases), TPO (5 cases), and DUOXA2 (1 case). Recurrent variants included DUOX2 c.3329G>A, TSHR c.1349G>A, TG c.1348delT, and TPO c.2268dupT. We identified four novel variants based on genotype, including TSHR c.1135C>T, TSHR c.1349G>C, TG c.2461delA, and TG c.2459T>A. This study underscores the efficacy of WES in providing definitive molecular diagnoses for TDH. Molecular diagnoses are instrumental in genetic counseling, formulating treatment, and developing management strategies. Future research integrating larger population cohorts is vital to further elucidate the genetic landscape of TDH.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"744-756"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141461528","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}

引用次数: 0

Coexisting cardiac disease and cervical spinal tuberculosis: Diagnostic challenges and treatment insights. 心脏疾病与颈椎结核并存：诊断挑战与治疗启示。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-05-20 DOI: 10.1002/kjm2.12842

Shu-Han Hsu, Yoon Bin Chong, Kun-Bow Tsai, Joon-Khim Loh

引用次数: 0

Rare cutaneous manifestation of zosteriform cutaneous metastases of lung cancer: Two cases and literature review. 肺癌带状皮肤转移的罕见皮肤表现：两例病例和文献综述。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-06-06 DOI: 10.1002/kjm2.12849

Ping-Yi Tsai, Yang Lo

引用次数: 0

Glutamate concentrations related to depression and mania symptoms in patients with Graves' disease: A 1H-magnetic resonance spectroscopy study. 与巴塞杜氏病患者抑郁和躁狂症状有关的谷氨酸浓度：1H-磁共振光谱研究。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-05-31 DOI: 10.1002/kjm2.12854

Shih-Hsien Lin, Po See Chen, Shih-Ming Huang, Yen Kuang Yang

引用次数: 0

Gut microbiota-derived metabolite trimethylamine N-oxide aggravates cognitive dysfunction induced by femoral fracture operation in mice. 肠道微生物群衍生代谢物三甲胺 N-氧化物会加重股骨骨折手术导致的小鼠认知功能障碍。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-07-04 DOI: 10.1002/kjm2.12873

Ying Xiong, Ya-Nan Pu, Li-Ya Li, Yang Su, Jia-Yuan Niu, Zhao-Yang Xiao

{"title":"Gut microbiota-derived metabolite trimethylamine N-oxide aggravates cognitive dysfunction induced by femoral fracture operation in mice.","authors":"Ying Xiong, Ya-Nan Pu, Li-Ya Li, Yang Su, Jia-Yuan Niu, Zhao-Yang Xiao","doi":"10.1002/kjm2.12873","DOIUrl":"10.1002/kjm2.12873","url":null,"abstract":"An increasing number of elderly individuals are experiencing postoperative cognitive dysfunction (POCD) problems after undergoing hip replacement surgery, with gut microbiota metabolites playing a role in its pathogenesis. Among these, the specific effects of trimethylamine N-oxide (TMAO) on POCD are still unclear. This study aimed to explore the role of TMAO on cognitive dysfunction and underlying mechanisms in mice. The POCD model was created through femoral fracture surgery in elderly mice, followed by cognitive function assessments using the Morris Water Maze and Novel Object Recognition tests. The gut microbiota depletion and fecal microbiota transplantation were performed to examine the relationship between TMAO levels and cognitive outcomes. The effects of TMAO treatment on cognitive dysfunction, microglial activation, and inflammatory cytokine levels in the brain were also evaluated, with additional assessment of the role of microglial ablation in reducing TMAO-induced cognitive impairment. Elevated TMAO levels were found to be associated with cognitive decline in mice following femoral fracture surgery, with gut microbiota depletion mitigating both TMAO elevation and cognitive dysfunction. In contrast, fecal microbiota transplantation from postoperative mice resulted in accelerated cognitive dysfunction and TMAO accumulation in germ-free mice. Furthermore, TMAO treatment worsened cognitive deficits, neuroinflammation, and promoted microglial activation, which were reversed through the ablation of microglia. TMAO exacerbates cognitive dysfunction and neuroinflammation in POCD mice, with microglial activation playing a crucial role in this process. Our findings may provide new therapeutic strategies for managing TMAO-related POCD and improving the quality of life for elderly patients.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"732-743"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141500092","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}

引用次数: 0

Ultrasound-guided posterior lateral branches steroid injections of the sacral foramina for chronic new-onset sacroiliac joint pain management after spinal fusion surgery: A prospective study of single-center in Vietnam. 超声引导下骶骨孔后外侧分支类固醇注射治疗脊柱融合术后慢性新发骶髂关节疼痛：越南单中心前瞻性研究。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-05-31 DOI: 10.1002/kjm2.12867

Tuan Anh Pham, Anh Minh Nguyen, Phuc Long Nguyen, Viet-Thang Le

引用次数: 0

METTL3 aggravates cell damage induced by Streptococcus pneumoniae via the NEAT1/CTCF/MUC19 axis. METTL3 通过 NEAT1/CTCF/MUC19 轴加剧肺炎链球菌诱导的细胞损伤。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-05-16 DOI: 10.1002/kjm2.12843

Dong-Bo Ma, Hui Zhang, Xi-Ling Wang, Qiu-Ge Wu

{"title":"METTL3 aggravates cell damage induced by Streptococcus pneumoniae via the NEAT1/CTCF/MUC19 axis.","authors":"Dong-Bo Ma, Hui Zhang, Xi-Ling Wang, Qiu-Ge Wu","doi":"10.1002/kjm2.12843","DOIUrl":"10.1002/kjm2.12843","url":null,"abstract":"Disruption of the alveolar barrier can trigger acute lung injury. This study elucidated the association of methyltransferase-like 3 (METTL3) with Streptococcus pneumoniae (SP)-induced apoptosis and inflammatory injury of alveolar epithelial cells (AECs). AECs were cultured and then infected with SP. Furthermore, the expression of METTL3, interleukin (IL)-10, IL-6, tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1), mucin 19 (MUC19), N6-methyladenosine (m6A), and NEAT1 after m6A modification were detected by qRT-PCR, Western blot, and enzyme-linked immunosorbent, m6A quantification, and methylated RNA immunoprecipitation-qPCR analyses, respectively. Moreover, the subcellular localization of NEAT1 was analyzed by nuclear/cytosol fractionation assay, and the binding between NEAT1 and CCCTC-binding factor (CTCF) was also analyzed. The results of this investigation revealed that SP-induced apoptosis and inflammatory injury in AECs and upregulated METTL3 expression. In addition, the downregulation of METTL3 alleviated apoptosis and inflammatory injury in AECs. METTL3-mediated m6A modification increased NEAT1 and promoted its binding with CTCF to facilitate MUC19 transcription. NEAT1 or MUC19 overexpression disrupted their protective role of silencing METTL3 in AECs, thereby increasing apoptosis and inflammatory injury. In conclusion, this is the first study to suggest that METTL3 aggravates SP-induced cell damage via the NEAT1/CTCF/MUC19 axis.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"722-731"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961256","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}

引用次数: 0

Advances in blood biomarkers for Alzheimer disease (AD): A review. 阿尔茨海默病（AD）血液生物标志物的研究进展：综述。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-06-18 DOI: 10.1002/kjm2.12870

Araya Dimtsu Assfaw, Suzanne E Schindler, John C Morris

{"title":"Advances in blood biomarkers for Alzheimer disease (AD): A review.","authors":"Araya Dimtsu Assfaw, Suzanne E Schindler, John C Morris","doi":"10.1002/kjm2.12870","DOIUrl":"10.1002/kjm2.12870","url":null,"abstract":"Alzheimer disease (AD) and Alzheimer Disease and Related Dementias (AD/ADRD) are growing public health challenges globally affecting millions of older adults, necessitating concerted efforts to advance our understanding and management of these conditions. AD is a progressive neurodegenerative disorder characterized pathologically by amyloid plaques and tau neurofibrillary tangles that are the primary cause of dementia in older individuals. Early and accurate diagnosis of AD dementia is crucial for effective intervention and treatment but has proven challenging to accomplish. Although testing for AD brain pathology with cerebrospinal fluid (CSF) or positron emission tomography (PET) has been available for over 2 decades, most patients never underwent this testing because of inaccessibility, high out-of-pocket costs, perceived risks, and the lack of AD-specific treatments. However, in recent years, rapid progress has been made in developing blood biomarkers for AD/ADRD. Consequently, blood biomarkers have emerged as promising tools for non-invasive and cost-effective diagnosis, prognosis, and monitoring of AD progression. This review presents the evolving landscape of blood biomarkers in AD/ADRD and explores their potential applications in clinical practice for early detection, prognosis, and therapeutic interventions. It covers recent advances in blood biomarkers, including amyloid beta (Aβ) peptides, tau protein, neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP). It also discusses their diagnostic and prognostic utility while addressing associated challenges and limitations. Future research directions in this rapidly evolving field are also proposed.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"692-698"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141422373","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}

引用次数: 0

HMGB1 inhibition blocks ferroptosis and oxidative stress to ameliorate sepsis-induced acute lung injury by activating the Nrf2 pathway. 抑制 HMGB1 可阻断铁变态反应和氧化应激，从而通过激活 Nrf2 通路改善败血症诱发的急性肺损伤。

The Kaohsiung journal of medical sciences Pub Date : 2024-08-01 Epub Date: 2024-06-05 DOI: 10.1002/kjm2.12851

Ya-Jie Jia, Sha Xiong, Ming Yao, Yu Wei, Yan He

{"title":"HMGB1 inhibition blocks ferroptosis and oxidative stress to ameliorate sepsis-induced acute lung injury by activating the Nrf2 pathway.","authors":"Ya-Jie Jia, Sha Xiong, Ming Yao, Yu Wei, Yan He","doi":"10.1002/kjm2.12851","DOIUrl":"10.1002/kjm2.12851","url":null,"abstract":"The proinflammatory properties of high-mobility group box protein 1 (HMGB1) in sepsis have been extensively studied. This study aimed to investigate the impact of HMGB1 on ferroptosis and its molecular mechanism in sepsis-induced acute lung injury (ALI). A septic mouse model was established using the cecal ligation and puncture method. Blocking HMGB1 resulted in improved survival rates, reduced lung injury, decreased levels of ferroptosis markers (reactive oxygen species, malondialdehyde, and Fe2+), and enhanced antioxidant enzyme activities (superoxide dismutase and catalase) in septic mice. In addition, knockdown of HMGB1 reduced cellular permeability, ferroptosis markers, and raised antioxidant enzyme levels in lipopolysaccharide (LPS)-stimulated MLE-12 cells. Silencing of HMGB1 led to elevations in the expressions of ferroptosis core-regulators in LPS-treated MLE-12 cells, such as solute carrier family 7 member 11 (SLC7A11), solute carrier family 3 member A2 (SLC3A2), and glutathione peroxidase 4. Furthermore, blocking HMGB1 did not alter ferroptosis, oxidative stress-related changes, and permeability in LPS-treated MLE-12 cells that were pretreated with ferrostatin-1 (a ferroptosis inhibitor). HMGB1 inhibition also led to elevated expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream targets, heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase 1 (NQO1) in LPS-treated MLE-12 cells and lung tissues from septic mice. The Nrf2-specific inhibitor ML385 reversed the effects of HMGB1 silencing on ferroptosis and cell permeability in LPS-treated MLE-12 cells. Our findings indicated that the inhibition of HMGB1 restrains ferroptosis and oxidative stress, thereby alleviating sepsis-induced ALI through the activation of Nrf2 signaling.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"710-721"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141261865","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}

引用次数: 0