Displaying all 6 publications

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  1. Lakhan A, Abed Mohammed M, Kadry S, Hameed Abdulkareem K, Taha Al-Dhief F, Hsu CH
    PeerJ Comput Sci, 2021;7:e758.
    PMID: 34901423 DOI: 10.7717/peerj-cs.758
    The intelligent reflecting surface (IRS) is a ground-breaking technology that can boost the efficiency of wireless data transmission systems. Specifically, the wireless signal transmitting environment is reconfigured by adjusting a large number of small reflecting units simultaneously. Therefore, intelligent reflecting surface (IRS) has been suggested as a possible solution for improving several aspects of future wireless communication. However, individual nodes are empowered in IRS, but decisions and learning of data are still made by the centralized node in the IRS mechanism. Whereas, in previous works, the problem of energy-efficient and delayed awareness learning IRS-assisted communications has been largely overlooked. The federated learning aware Intelligent Reconfigurable Surface Task Scheduling schemes (FL-IRSTS) algorithm is proposed in this paper to achieve high-speed communication with energy and delay efficient offloading and scheduling. The training of models is divided into different nodes. Therefore, the trained model will decide the IRSTS configuration that best meets the goals in terms of communication rate. Multiple local models trained with the local healthcare fog-cloud network for each workload using federated learning (FL) to generate a global model. Then, each trained model shared its initial configuration with the global model for the next training round. Each application's healthcare data is handled and processed locally during the training process. Simulation results show that the proposed algorithm's achievable rate output can effectively approach centralized machine learning (ML) while meeting the study's energy and delay objectives.
  2. Hsu CH, Langdown J, Lynn R, Fisher C, Rose A, Proven M, et al.
    Hemoglobin, 2018 May;42(3):199-202.
    PMID: 30328734 DOI: 10.1080/03630269.2018.1513849
    We report a novel hemoglobin (Hb) variant with a β chain amino acid substitution at codon 78 (CTG>CCG) (HBB: c.236T>C), detected through prenatal screening via capillary electrophoresis (CE) in an otherwise healthy and asymptomatic 38-year-old female of Southeast Asian ancestry. The variant, named Hb Penang after the proband's Malaysian city of origin, underwent further characterization through high performance liquid chromatography (HPLC), reversed phase HPLC, Sanger sequencing, isopropanol stability testing and isoelectric focusing (IEF).
  3. Chien SY, Hsu CH, Lin CC, Chuang YC, Lo YS, Hsi YT, et al.
    Environ Toxicol, 2017 Aug;32(8):2085-2092.
    PMID: 28383207 DOI: 10.1002/tox.22423
    Nasopharyngeal carcinoma (NPC), a tumor arising from epithelial cells that cover the surface and line the nasopharynx, is a rare malignancy worldwide but is prevalent in certain geographical areas, such as Southern Asia (Taiwan, Hong Kong, Singapore, Malaysia, and Southern China) and North Africa. Despite advances in diagnostic techniques and improvements in treatment modalities, the prognosis of NPC remains poor. Therefore, an effective chemotherapy regimen that enhances tumor sensitivity to chemotherapeutics is urgently required. Nimbolide, derived from Azadirachta indica, has a wide range of beneficial effects, including anti-inflammatory and anticancer properties. The present study evaluated the antitumor activity of nimbolide in NPC cells and its underlying mechanisms. Our results revealed that the treatment of HONE-1 cells with nimbolide potently inhibited cell viability. Moreover, nimbolide led to cell cycle arrest, which subsequently activated caspase-3, -8, and -9 and poly (ADP-ribose) polymerase to induce cell apoptosis. Moreover, nimbolide induced Bik, Bax, and t-Bid expression in HONE-1 cells. The results indicated that nimbolide induces apoptosis through the modulation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) pathways. Nimbolide induces apoptosis in human NPC cells and is a potential chemopreventive agent against NPC proliferation. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 2085-2092, 2017.
  4. Kawarada O, Hozawa K, Zen K, Huang HL, Kim SH, Choi D, et al.
    Cardiovasc Interv Ther, 2020 Jan;35(1):52-61.
    PMID: 31292931 DOI: 10.1007/s12928-019-00602-z
    With technological improvements in the endovascular armamentarium, there have been tremendous advances in catheter-based femoropopliteal artery intervention during the last decade. However, standardization of the methodology for assessing outcomes has been underappreciated, and unvalidated peak systolic velocity ratios (PSVRs) of 2.0, 2.4, and 2.5 on duplex ultrasonography have been arbitrarily but routinely used for assessing restenosis. Quantitative vessel analysis (QVA) is a widely accepted method to identify restenosis in a broad spectrum of cardiovascular interventions, and PSVR needs to be validated by QVA. This multidisciplinary review is intended to disseminate the importance of QVA and a validated PSVR based on QVA for binary restenosis in contemporary femoropopliteal intervention.
  5. Chen LT, Martinelli E, Cheng AL, Pentheroudakis G, Qin S, Bhattacharyya GS, et al.
    Ann Oncol, 2020 03;31(3):334-351.
    PMID: 32067677 DOI: 10.1016/j.annonc.2019.12.001
    The most recent version of the European Society for Medical Oncology (ESMO) Clinical Practice Guidelines for the diagnosis, treatment and follow-up of hepatocellular carcinoma (HCC) was published in 2018, and covered the diagnosis, management, treatment and follow-up of early, intermediate and advanced disease. At the ESMO Asia Meeting in November 2018 it was decided by both the ESMO and the Taiwan Oncology Society (TOS) to convene a special guidelines meeting immediately after the Taiwan Joint Cancer Conference (TJCC) in May 2019 in Taipei. The aim was to adapt the ESMO 2018 guidelines to take into account both the ethnic and the geographic differences in practice associated with the treatment of HCC in Asian patients. These guidelines represent the consensus opinions reached by experts in the treatment of patients with intermediate and advanced/relapsed HCC representing the oncology societies of Taiwan (TOS), China (CSCO), India (ISMPO) Japan (JSMO), Korea (KSMO), Malaysia (MOS) and Singapore (SSO). The voting was based on scientific evidence, and was independent of the current treatment practices, the drug availability and reimbursement situations in the individual participating Asian countries.
  6. Braun DA, Rao J, Mollet G, Schapiro D, Daugeron MC, Tan W, et al.
    Nat Genet, 2017 Oct;49(10):1529-1538.
    PMID: 28805828 DOI: 10.1038/ng.3933
    Galloway-Mowat syndrome (GAMOS) is an autosomal-recessive disease characterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain anomalies. Here we identified recessive mutations in OSGEP, TP53RK, TPRKB, and LAGE3, genes encoding the four subunits of the KEOPS complex, in 37 individuals from 32 families with GAMOS. CRISPR-Cas9 knockout in zebrafish and mice recapitulated the human phenotype of primary microcephaly and resulted in early lethality. Knockdown of OSGEP, TP53RK, or TPRKB inhibited cell proliferation, which human mutations did not rescue. Furthermore, knockdown of these genes impaired protein translation, caused endoplasmic reticulum stress, activated DNA-damage-response signaling, and ultimately induced apoptosis. Knockdown of OSGEP or TP53RK induced defects in the actin cytoskeleton and decreased the migration rate of human podocytes, an established intermediate phenotype of SRNS. We thus identified four new monogenic causes of GAMOS, describe a link between KEOPS function and human disease, and delineate potential pathogenic mechanisms.
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