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  1. Attitudes, barriers and facilitators to the conduct of research in government hospitals: a cross-sectional study among specialists in government hospitals, northern states of Malaysia
    Teh LC, Prema M, Choy MP, Letchuman GR
    Med J Malaysia, 2017 02;72(1):26-31.
    PMID: 28255136 MyJurnal
    INTRODUCTION: Specialists constitute a major 'driving force' and catalyst for growth of research in their speciality. A clearer understanding is required as to what motivates their participation in research as well as the barriers they faced. This research aims to study the attitudes, barriers and facilitators faced by specialists and to identify strategies to promote and sustain research activities in their hospitals.

    METHODOLOGY: A cross-sectional survey using selfadministered questionnaires was conducted among all specialists working in government specialist hospitals in the northern states of Malaysia.

    RESULTS: Out of 733 questionnaires distributed, 467 were returned giving a response rate of 63.7%. Ninety-nine percent of the respondents believed that research benefits patients while 93.3% think research helps in their professional development. However, 34.8% think that under their present working conditions, it is unlikely they will participate in research. The major barriers identified were lack of funds for research (81%); lack access to expertise, software or statistical analysis (78.4%); interference with daily work schedule (75.1%) and inconsistent manpower in their department (74.2%). There are three barriers with statistically significant difference between hospitals with CRC compared to hospitals without CRC; lack of funds, mentors and access to expertise, software or statistical analysis. The demographic factors, attitudes and barriers contributing to involvement in research also investigated. The main facilitators for the conduct of research are potential to benefit patients and potential for professional development.

    CONCLUSION: Taking note of the findings, the Ministry of Health can implement appropriate strategies to improve specialist participation in research.

  2. Fulltext Toll-like receptor 2 and 4 have opposing roles in the pathogenesis of cigarette smoke-induced chronic obstructive pulmonary disease
    Haw TJ, Starkey MR, Pavlidis S, Fricker M, Arthurs AL, Nair PM, et al.
    Am. J. Physiol. Lung Cell Mol. Physiol., 2018 02 01;314(2):L298-L317.
    PMID: 29025711 DOI: 10.1152/ajplung.00154.2017
    Chronic obstructive pulmonary disease (COPD) is the third leading cause of morbidity and death and imposes major socioeconomic burdens globally. It is a progressive and disabling condition that severely impairs breathing and lung function. There is a lack of effective treatments for COPD, which is a direct consequence of the poor understanding of the underlying mechanisms involved in driving the pathogenesis of the disease. Toll-like receptor (TLR)2 and TLR4 are implicated in chronic respiratory diseases, including COPD, asthma and pulmonary fibrosis. However, their roles in the pathogenesis of COPD are controversial and conflicting evidence exists. In the current study, we investigated the role of TLR2 and TLR4 using a model of cigarette smoke (CS)-induced experimental COPD that recapitulates the hallmark features of human disease. TLR2, TLR4, and associated coreceptor mRNA expression was increased in the airways in both experimental and human COPD. Compared with wild-type (WT) mice, CS-induced pulmonary inflammation was unaltered in TLR2-deficient ( Tlr2-/-) and TLR4-deficient ( Tlr4-/-) mice. CS-induced airway fibrosis, characterized by increased collagen deposition around small airways, was not altered in Tlr2-/- mice but was attenuated in Tlr4-/- mice compared with CS-exposed WT controls. However, Tlr2-/- mice had increased CS-induced emphysema-like alveolar enlargement, apoptosis, and impaired lung function, while these features were reduced in Tlr4-/- mice compared with CS-exposed WT controls. Taken together, these data highlight the complex roles of TLRs in the pathogenesis of COPD and suggest that activation of TLR2 and/or inhibition of TLR4 may be novel therapeutic strategies for the treatment of COPD.
  3. Fulltext TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase
    Liu G, Haw TJ, Starkey MR, Philp AM, Pavlidis S, Nalkurthi C, et al.
    Nat Commun, 2023 Nov 14;14(1):7349.
    PMID: 37963864 DOI: 10.1038/s41467-023-42913-z
    Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly, TLR7 mRNA is increased in pre-existing datasets from patients with COPD, while TLR7+ mast cells are increased in COPD lungs and associated with severity of COPD. Our results thus support roles for TLR7 in mediating emphysema and COPD through mast cell activity, and may implicate TLR7 as a potential therapeutic target.
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