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  1. Mariana A, Ho TM, Sofian-Azirun M, Wong AL
    PMID: 11414418
    Allergy to house dust mites (HDM) is an important cause of asthma and rhinitis in Malaysia. This study was carried out to evaluate the dust mite fauna in the Klang Valley. Dust samples were collected from 20 houses from March 1994 to February 1995. Thirty-three dust samples from mattresses were examined monthly for the occurrence of HDM. A total of 22 species in 9 families of HDM was identified. The most common and densely populated species was Blomia tropicalis with an average density of 8,934 mites/g of dust. Dermatophagoides pteronyssinus was the next in abundance, followed by Malayoglyphus intermedius. All houses surveyed were found to be infested with HDM and every house had at least 6 species of HDM. B. tropicalis and D. pteronyssinus were found in all mattresses. HDM in the Klang Valley were found to be highly prevalent and present in high densities. In this study, counts of D. pteronyssinus was found to exceed the proposed exposure threshold of 500 mites/g dust, for triggering acute asthma. Although counts of B. tropicalis exceeded D. pteronyssinus, no conclusion could be made because there is currently no exposure threshold for triggering acute asthma, for this species. Monthly distribution of B. tropicalis and D. pteronyssinus showed 2 peaks and 4 peaks, respectively. The major peak for D. pteronysinus was in January 1995 whereas for B. tropicalis, the major peak was more variable and occurred between November 1994 to January 1995. Both the species showed minor peak in April 1994.
  2. Thuya WL, Cao Y, Ho PC, Wong AL, Wang L, Zhou J, et al.
    PMID: 39893129 DOI: 10.1016/j.cytogfr.2025.01.003
    The IL-6/JAK/STAT3 signaling pathway is a key regulator of tumor progression, immune evasion, and therapy resistance in various cancers. Frequently dysregulated in malignancies, this pathway drives cancer cell growth, survival, angiogenesis, and metastasis by altering the tumor microenvironment (TME). IL-6 activates JAK kinases and STAT3 through its receptor complex, leading to the transcription of oncogenic genes and fostering an immunosuppressive TME. This environment recruits tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and regulatory T cells (Tregs), collectively supporting immune evasion and tumor growth. IL-6/JAK/STAT3 axis also contributes to metabolic reprogramming, such as enhanced glycolysis and glutathione metabolism, helping cancer cells adapt to environmental stresses. Therapeutic targeting of this pathway has gained significant interest. Strategies include monoclonal antibodies against IL-6 or its receptor (e.g., Tocilizumab, Siltuximab), JAK inhibitors (e.g., Ruxolitinib), and STAT3-specific inhibitors (e.g., Napabucasin), which have exhibited promise in preclinical and initial clinical studies. These inhibitors can suppress tumor growth, reverse immune suppression, and enhance the efficacy of immunotherapies like immune checkpoint inhibitors. Combination therapies that integrate IL-6 pathway inhibitors with conventional treatments are particularly promising, addressing resistance mechanisms and improving patient outcomes. Advances in biomarker-driven patient selection, RNA-based therapies, and isoform-specific inhibitors pave the way for more precise interventions. This review delves into the diverse roles of IL-6/JAK/STAT3 signaling in cancer progression, therapeutic strategies targeting this pathway, and the potential for integrating these approaches into personalized medicine to enhance treatment outcomes.
  3. Syn NL, Wong AL, Lee SC, Teoh HL, Yip JWL, Seet RC, et al.
    BMC Med, 2018 07 10;16(1):104.
    PMID: 29986700 DOI: 10.1186/s12916-018-1093-8
    BACKGROUND: Genotype-guided warfarin dosing has been shown in some randomized trials to improve anticoagulation outcomes in individuals of European ancestry, yet its utility in Asian patients remains unresolved.

    METHODS: An open-label, non-inferiority, 1:1 randomized trial was conducted at three academic hospitals in South East Asia, involving 322 ethnically diverse patients newly indicated for warfarin (NCT00700895). Clinical follow-up was 90 days. The primary efficacy measure was the number of dose titrations within the first 2 weeks of therapy, with a mean non-inferiority margin of 0.5 over the first 14 days of therapy.

    RESULTS: Among 322 randomized patients, 269 were evaluable for the primary endpoint. Compared with traditional dosing, the genotype-guided group required fewer dose titrations during the first 2 weeks (1.77 vs. 2.93, difference -1.16, 90% CI -1.48 to -0.84, P 

  4. Thuya WL, Peyper JM, Myen TT, Anuar ND, Anwar A, Gudimella R, et al.
    Mil Med Res, 2024 Nov 18;11(1):72.
    PMID: 39558443 DOI: 10.1186/s40779-024-00575-y
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