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  1. Liam CK, Wong KT, Lim YC
    Med J Malaysia, 1997 Mar;52(1):84-6.
    PMID: 10968059
    A 24-year-old man who was initially thought to have nocardiosis of his mediastinal lymph node which progressed to involve his right lung, had to undergo a right pneumonectomy when he failed to respond to treatment with sulphadiazine. Histology of the right lung specimen and a subsequent axillary lymph node biopsy revealed that he actually had lymphocyte-depleted Hodgkin's disease.
    Matched MeSH terms: Pneumonia/etiology*
  2. Wang CY, Yap BH, Delilkan AE
    Chest, 1993 Jun;103(6):1897-9.
    PMID: 8404124
    We present the case of a 24-year-old woman with acute septicemic melioidosis resulting from inhaled infective dust during a blast injury. With appropriate antibiotic treatment and supportive therapy in the ICU, the patient made an uneventful recovery.
    Matched MeSH terms: Pneumonia/etiology*
  3. Lee JK
    Med J Malaysia, 1993 Mar;48(1):93-4.
    PMID: 8341180
    Matched MeSH terms: Pneumonia/etiology*
  4. Jaafar MH, Mahadeva S, Morgan K, Tan MP
    J Nutr Health Aging, 2015 Feb;19(2):190-7.
    PMID: 25651445 DOI: 10.1007/s12603-014-0527-z
    OBJECTIVE: The objective of this systematic review was to evaluate existing studies on the effectiveness of percutaneous endoscopic gastrostomy (PEG) feeding compared to nasogastric (NG) feeding for patients with non-stroke related dysphagia.

    METHODS: We searched Ovid MEDLINE, EMBASE, the Cochrane Library, Web of Science and PubMed databases through to December 2013 using the terms "percutaneous endoscopic gastrostomy", "gastrostomy", "PEG", "nasogastric", "nasogastric tube", "nasogastric feeding" and "intubation". We included randomized controlled trials (RCTs) and non-RCTs which compared PEG with NG feeding in individuals with non-stroke dysphagia.

    RESULTS: 9 studies involving 847 participants were included in the final analysis, including two randomized trials. Pooled analysis indicated no significant difference in the risk of pneumonia [relative risk (RR) = 1.18, 95% confidence interval (CI) = 0.87-1.60] and overall complications [relative risk (RR) = 0.80, 95% confidence interval (CI) = 0.63-1.02] between PEG and NG feeding. A meta-analysis was not possible for mortality and nutritional outcomes, but three studies suggested improved mortality outcomes with PEG feeding while two out of three studies reported PEG feeding to be better from a nutritional perspective.

    CONCLUSIONS: Firm conclusions could not be derived on whether PEG feeding is beneficial over NG feeding in older persons with non-stroke dysphagia, as previously published literature were unclear or had a high risk of bias. A well-designed and adequately powered RCT, which includes carer strain and quality of life as outcome measures is therefore urgently needed.

    Matched MeSH terms: Pneumonia/etiology
  5. Khor CG, Kan SL, Tan BE
    Int J Rheum Dis, 2018 Jun;21(6):1322-1325.
    PMID: 24495523 DOI: 10.1111/1756-185X.12302
    We report a 29-year-old Malay man who had pulmonary manifestations as an initial presentation for systemic lupus erythematosus. He had prolonged hospitalization and was treated with intensive care therapy with immunosuppressants.
    Matched MeSH terms: Pneumonia/etiology*
  6. 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.
    Matched MeSH terms: Pneumonia/etiology*
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