Displaying publications 1 - 20 of 1522 in total

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  1. Cheong IKS
    Family Practitioner, 1981;4:28-33.
    Matched MeSH terms: Nephrotic Syndrome
  2. Loke KH
    Family Practitioner, 1986;9:60-62.
    Matched MeSH terms: Neuroleptic Malignant Syndrome
  3. Kruszka P, Porras AR, Addissie YA, Moresco A, Medrano S, Mok GTK, et al.
    Am J Med Genet A, 2017 Sep;173(9):i.
    PMID: 28816424 DOI: 10.1002/ajmg.a.38408
    The cover image, by Paul Kruszka et al., is based on the Original Article Noonan Syndrome in Diverse Populations, DOI: 10.1002/ajmg.a.38362. Design Credit: Darryl Leja.
    Matched MeSH terms: Noonan Syndrome
  4. Wong CK, Ng CF, Tan HJ, Wan Yahya WNN
    BMJ Case Rep, 2021 Feb 26;14(2).
    PMID: 33637510 DOI: 10.1136/bcr-2020-241244
    Matched MeSH terms: Syndrome
  5. Yeo HP
    Family Practitioner, 1985;8(5):82-83.
    Matched MeSH terms: Behcet Syndrome*
  6. Islam MA, Alam F, Kamal MA, Gan SH, Sasongko TH, Wong KK
    PMID: 28824414 DOI: 10.3389/fnagi.2017.00250
    Growing evidences are supporting towards the involvement of antiphospholipid antibodies [aPLs e.g., lupus anticoagulant (LA), anticardiolipin (aCL) and anti-β2-glycoprotein I (anti-β2-GPI) antibodies] in various neurological manifestations including migraine, epilepsy and dementia in the presence or absence of autoimmune diseases such as antiphospholipid syndrome or systemic lupus erythematosus. The aim of this systematic review and meta-analysis was to assess the presence of aPLs in dementia patients without a diagnosis of any autoimmune disease. Electronic databases (e.g., PubMed, Web of Science, Scopus, ScienceDirect and Google Scholar) were searched without any year or language restrictions and based on the inclusion criteria, nine prospective case-control studies assessing only aCL were included involving 372 dementia patients and 337 healthy controls. No studies were found to assess the presence of both LA or anti-β2-GPI. The study-specific odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using random-effects model. We observed the prevalence of aCL in dementia was higher (32.80%) than that of controls (9.50%) e.g., 3.45 times higher risk of presenting with dementia than the controls, and significant presence of aCL antibodies was detected in dementia patients compared to controls (OR: 4.94, 95% CI: 2.66 - 9.16, p < 0.00001; I2 = 32%, p = 0.16). Publication bias was not observed from Egger's (p = 0.081) and Begg's tests (p = 0.180). Based on the study quality assessment using modified Newcastle-Ottawa Scale for case-control studies, seven of nine studies were of high methodological quality scoring ≥ 7 (median value). In summary, aCL antibodies were significantly present in dementia patients suggesting that aCL antibodies are generated due to the autoimmune-derived effects of dementia or there might be a potential causative role of this autoantibody in dementia pathogenesis.
    Matched MeSH terms: Antiphospholipid Syndrome*
  7. Cheong IKS
    Family Practitioner, 1983;6:37-40.
    Matched MeSH terms: Nephrotic Syndrome
  8. Ong S, Ng WH
    Med J Malaysia, 1979 Sep;34(1):86-8.
    PMID: 542159
    Matched MeSH terms: Marfan Syndrome/diagnosis*; Marfan Syndrome/therapy
  9. Raj JM, Kanagaratnam K, Mohammad NM, Abdul Rahman Z, Badmanaban B, Chong YS, et al.
    Med J Malaysia, 2013 Apr;68(2):171-2.
    PMID: 23629569 MyJurnal
    Matched MeSH terms: Brugada Syndrome*
  10. Yew KL
    Med J Malaysia, 2013 Apr;68(2):186.
    PMID: 23629576
    Matched MeSH terms: Mucocutaneous Lymph Node Syndrome*
  11. Shahrizaila N, Yuki N
    Expert Rev Neurother, 2011 Sep;11(9):1305-13.
    PMID: 21864076 DOI: 10.1586/ern.11.114
    Guillain-Barré syndrome (GBS) is typically classified into two major subtypes: acute inflammatory demyelinating neuropathy and acute motor axonal neuropathy. Its most recognizable variant is Fisher syndrome. The last two decades have seen considerable advances in our understanding of GBS. Of note, various autoantibodies against ganglioside antigens have been identified and found to have significant associations with the axonal forms of GBS and Fisher syndrome. In this article, we discuss the different clinical presentations in GBS and the role of antiganglioside antibodies in their underlying pathogenesis. We also discuss the impact that antiganglioside antibodies have had in the development of experimental models and treatment modalities in GBS.
    Matched MeSH terms: Miller Fisher Syndrome/immunology*; Miller Fisher Syndrome/physiopathology*; Miller Fisher Syndrome/therapy; Guillain-Barre Syndrome/immunology*; Guillain-Barre Syndrome/physiopathology*; Guillain-Barre Syndrome/therapy
  12. Lee YS
    Med J Malaysia, 1982 Mar;37(1):80-1.
    PMID: 7121354
    Matched MeSH terms: Budd-Chiari Syndrome/diagnosis*
  13. Cheo SW, Ahmad Akbar RZ, Abd Rahman F, Abdul Rashid WNF', Tan YA, Low QJ
    QJM, 2020 Nov 01;113(11):809-812.
    PMID: 32275748 DOI: 10.1093/qjmed/hcaa122
    Matched MeSH terms: Immune Reconstitution Inflammatory Syndrome*
  14. Leong AS
    J Singapore Paediatr Soc, 1976 Apr;18(1):38-42.
    PMID: 966741
    Matched MeSH terms: Reye Syndrome*
  15. Subramaniam M
    Med J Malaya, 1966 Sep;21(1):95-6.
    PMID: 4224886
    Matched MeSH terms: Tourette Syndrome*
  16. Hiew FL, Ramlan R, Viswanathan S, Puvanarajah S
    Clin Neurol Neurosurg, 2017 Jul;158:114-118.
    PMID: 28514704 DOI: 10.1016/j.clineuro.2017.05.006
    OBJECTIVES: This study aimed to evaluate the clinical and electrophysiological characteristics of various distinctive classical and localised Guillain-Barré syndrome (GBS) subtypes.

    PATIENTS AND METHODS: Clinical characteristics and electrophysiological data of sixty-one consecutive patients admitted between 2012 and 2015 were systematically analysed and reclassified according to the new GBS clinical classification. Neurophysiology was evaluated with Hadden et al.'s vs recently proposed Rajabally et al.'s criteria. Functional severity and clinical outcome of various GBS subtypes were ascertained.

    RESULTS: All patients initially identified as GBS or related disorders can be sub-classified into having classical GBS (41, 67%), classic Miller-Fisher Syndrome (MFS) (6, 10%), Pharyngeal-cervical-brachial (PCB) (3, 5%), paraparetic GBS (4, 7%), bifacial weakness with paresthesia (3, 5%), acute ophthalmoparesis (AO) (1, 2%) and overlap syndrome (3, 5%): one (2%) with GBS/Bickerstaff brainstem encephalitis overlap and 2 (3%) with GBS/MFS overlap. Greater proportion of axonal classical GBS (67% vs 55%, p=0.372) seen with Rajabally et al.'s criteria and a predominantly axonal form of paraparetic variant (75%) independent of electrodiagnostic criteria were more representative of Asian GBS cohort. Classical GBS patients had lowest admission and discharge Medical Research Council Sum Score (MRCSS), greater functional disability and longest length of in-patient stay. Twenty (20/21, 95%) patients who needed mechanical ventilation had classical GBS. Patients required repeated dose of intravenous immunoglobulin (5/6, 3%) or plasma exchange (4/4, 100%) more frequently had axonal form of classical GBS.

    CONCLUSION: Phenotype recognition based on new GBS clinical classification, supported by electrodiagnostic study permits more precise clinical subtypes determination and outcome prognostication.

    Matched MeSH terms: Miller Fisher Syndrome/classification; Miller Fisher Syndrome/diagnosis; Miller Fisher Syndrome/physiopathology; Guillain-Barre Syndrome/classification*; Guillain-Barre Syndrome/diagnosis*; Guillain-Barre Syndrome/physiopathology*
  17. Muhammad Shazwan S, Muhammad Aliff M, Asral Wirda AA, Hayati AR, Maizatul Azma M, Nur Syahrina AR, et al.
    Malays J Pathol, 2016 Dec;38(3):273-283.
    PMID: 28028298 MyJurnal
    INTRODUCTION: Antiphospholipid antibodies (aPL) are autoantibodies that attack phospholipid through anti-beta 2-glycoprotein 1. The actions of aPL are associated with events leading to thrombosis and morbidity in pregnancy. Antiphospholipid syndrome (APS) is diagnosed when a patient is persistently positive for aPL and also has recognised clinical manifestations such as recurrent pregnancy losses, arterial or venous thrombosis and in a catastrophic case, can result in death. Unfortunately, the pathogenesis of APS is still not well established. Recently, microRNA expressed in many types of diseased tissues were claimed to be involved in the pathological progression of diseases and has become a useful biomarker to indicate diseases, including APS.

    OBJECTIVE: This systematic review aims to search for research papers that are focussing on microRNA expression profiles in APS.

    METHOD: Three search engines (Ebcohost, ProQuest and Ovid) were used to identify papers related to expression of specific microRNA in antiphospholipid syndrome.

    RESULTS AND DISCUSSION: A total of 357 papers were found and screened, out of which only one study fulfilled the requirement. In this particular study blood samples from APS patients were tested. The microRNAs found to be related to APS were miR-19b and miR-20a. No data was found on specific microRNA being expressed in obstetric antiphospholipid syndrome. Analysis on the microRNA target genes revealed that most genes targeted by miR-19b and miR-20a involve in TGF-Beta Signalling and VEGF, hypoxia and angiogenesis pathways.

    CONCLUSION: In view of the limited data on the expressions of microRNA in APS we recommend further research into this field. Characterization of microRNA profile in blood as well as in placenta tissue of patients with APS could be useful in identifying microRNAs involved in obstetric APS.
    Matched MeSH terms: Antiphospholipid Syndrome/genetics*
  18. Arifin A, Thambiah SC, Abdullah H, Samsudin IN
    Clin Chem, 2021 06 01;67(6):823-826.
    PMID: 34059896 DOI: 10.1093/clinchem/hvab031
    Matched MeSH terms: DiGeorge Syndrome*
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