Displaying publications 541 - 560 of 5421 in total

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  1. Cheah CK, Ramanujam S, Mohd Noor N, Gandhi C, D Souza BA, Gun SC
    Lupus, 2016 Feb;25(2):214-6.
    PMID: 26377236 DOI: 10.1177/0961203315606441
    Pseudo-pseudo Meigs' syndrome (PPMS) has been reported to be a rare presentation of patients with systemic lupus erythematosus (SLE). However, such a presentation is not common in other forms of connective tissue disease. We presented a case of gross ascites, pleural effusion, and marked elevation of CA-125 level (PPMS-like features) that led to a diagnosis of MCTD. The patient responded to systemic steroid therapy.
    Matched MeSH terms: Mixed Connective Tissue Disease*; Mixed Connective Tissue Disease/diagnosis*; Mixed Connective Tissue Disease/drug therapy; Mixed Connective Tissue Disease/pathology; Raynaud Disease/pathology*
  2. Jänisch T, Junghanss T
    Med. Klin. (Munich), 2000 Jul 15;95(7):392-9.
    PMID: 10943100
    Viruses have become more mobile alongside with increasing human mobility and speed of travel. At the same time we get access to information on viral outbreaks and epidemics from large parts of the world faster than ever before. Two recent epidemics will be presented to explore the value and the consequences of communicating epidemiological information through the Internet. The epidemiology, clinical features, diagnostic procedures and prophylaxis of imported viral infections are presented. Risk factors for the emergence and resurgence of viral diseases are being discussed.
    Matched MeSH terms: Communicable Disease Control/methods*; Disease Outbreaks/prevention & control*; Disease Outbreaks/statistics & numerical data; Disease Reservoirs; Disease Vectors
  3. Yuan F, Hung RJ, Walsh N, Zhang H, Platz EA, Wheeler W, et al.
    Cancer Res, 2020 Sep 15;80(18):4004-4013.
    PMID: 32641412 DOI: 10.1158/0008-5472.CAN-20-0447
    Registry-based epidemiologic studies suggest associations between chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma (PDAC). As genetic susceptibility contributes to a large proportion of chronic inflammatory intestinal diseases, we hypothesize that the genomic regions surrounding established genome-wide associated variants for these chronic inflammatory diseases are associated with PDAC. We examined the association between PDAC and genomic regions (±500 kb) surrounding established common susceptibility variants for ulcerative colitis, Crohn's disease, inflammatory bowel disease, celiac disease, chronic pancreatitis, and primary sclerosing cholangitis. We analyzed summary statistics from genome-wide association studies data for 8,384 cases and 11,955 controls of European descent from two large consortium studies using the summary data-based adaptive rank truncated product method to examine the overall association of combined genomic regions for each inflammatory disease group. Combined genomic susceptibility regions for ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis were associated with PDAC at P values < 0.05 (0.0040, 0.0057, 0.011, and 3.4 × 10-6, respectively). After excluding the 20 PDAC susceptibility regions (±500 kb) previously identified by GWAS, the genomic regions for ulcerative colitis, Crohn disease, and inflammatory bowel disease remained associated with PDAC (P = 0.0029, 0.0057, and 0.0098, respectively). Genomic regions for celiac disease (P = 0.22) and primary sclerosing cholangitis (P = 0.078) were not associated with PDAC. Our results support the hypothesis that genomic regions surrounding variants associated with inflammatory intestinal diseases, particularly, ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis are associated with PDAC. SIGNIFICANCE: The joint effects of common variants in genomic regions containing susceptibility loci for inflammatory bowel disease and chronic pancreatitis are associated with PDAC and may provide insights to understanding pancreatic cancer etiology.
    Matched MeSH terms: Celiac Disease/genetics; Chronic Disease; Crohn Disease/genetics; Genetic Predisposition to Disease*
  4. Parsi S, Pandamooz S, Heidari S, Naji M, Morfini G, Ahmadiani A, et al.
    Neuroscience, 2015 Jan 22;284:99-106.
    PMID: 25270904 DOI: 10.1016/j.neuroscience.2014.09.045
    Alzheimer's disease (AD) is characterized by progressive and irreversible cognitive and memory impairment. The discovery of familial forms of AD (fAD) in association with specific gene mutations facilitated the generation of numerous rodent models. These models in turn proved valuable for the study of molecular mechanisms underlying AD pathogenesis, and facilitated translational research and preclinical drug development. This study aimed to introduce a new rat model of AD simulating some aspects of the sporadic cases of disease.
    Matched MeSH terms: Alzheimer Disease/genetics*; Alzheimer Disease/physiopathology*; Disease Models, Animal*
  5. Botross NP, Riad AA, Viswanathan S, Nordin RB, Lock HN
    Scott Med J, 2014 May;59(2):e1-6.
    PMID: 24671628 DOI: 10.1177/0036933014529868
    Gaucher's disease is a lysosomal storage disorder caused by the deficiency of glucocerebrosidase. Gaucher's disease has three clinical types: non-neuronopathic (Type 1), Acute Neuropathic (Type 2) and chronic neuronopathic (Type 3). The chronic neuronopathic (Type 3) is characterised by a variety of disease variants with onset in childhood with hepatomegaly, skeletal lesions and later slow horizontal saccades, treatment-resistant generalised tonic-clonic and myoclonic seizures, dementia, progressive spasticity, cognitive deterioration, ataxia and death in the second or third decade of life.
    Matched MeSH terms: Gaucher Disease/diagnosis*; Gaucher Disease/enzymology; Gaucher Disease/physiopathology; Disease Progression
  6. Lin JY, Shih SR
    J Biomed Sci, 2014;21:18.
    PMID: 24602216 DOI: 10.1186/1423-0127-21-18
    Enterovirus 71 (EV71) is a member of Picornaviridae that causes mild and self-limiting hand, foot, and mouth disease (HFMD). However, EV71 infections can progress to polio-like paralysis, neurogenic pulmonary edema, and fatal encephalitis in infants and young children. Large EV71 outbreaks have been reported in Taiwan, China, Japan, Malaysia, Singapore, and Australia. This virus is considered a critical emerging public health threat. EV71 is an important crucial neurotropic enterovirus for which there is currently no effective antiviral drug or vaccine. The mechanism by which EV71 causes severe central nervous system complications remains unclear. The interaction between the virus and the host is vital for viral replication, virulence, and pathogenicity. SCARB2 or PSGL-1 receptor binding is the first step in the development of viral infections, and viral factors (e.g., 5' UTR, VP1, 3C, 3D, 3' UTR), host factors and environments (e.g., ITAFs, type I IFN) are also involved in viral infections. The tissue tropism and pathogenesis of viruses are determined by a combination of several factors. This review article provides a summary of host and virus factors affecting cell and tissue tropism and the pathogenesis of enteroviruses.
    Matched MeSH terms: Disease Outbreaks; Hand, Foot and Mouth Disease/genetics; Hand, Foot and Mouth Disease/epidemiology*; Hand, Foot and Mouth Disease/virology
  7. Lee CY, Hairi NN, Wan Ahmad WA, Ismail O, Liew HB, Zambahari R, et al.
    PLoS One, 2013;8(8):e72382.
    PMID: 24015238 DOI: 10.1371/journal.pone.0072382
    To assess whether gender differences exist in the clinical presentation, angiographic severity, management and outcomes in patients with coronary artery disease (CAD).
    Matched MeSH terms: Coronary Artery Disease/mortality; Coronary Artery Disease/epidemiology*; Coronary Artery Disease/pathology; Coronary Artery Disease/therapy
  8. Srinivasan V, Pandi-Perumal SR, Cardinali DP, Poeggeler B, Hardeland R
    Behav Brain Funct, 2006 May 04;2:15.
    PMID: 16674804
    Increased oxidative stress and mitochondrial dysfunction have been identified as common pathophysiological phenomena associated with neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). As the age-related decline in the production of melatonin may contribute to increased levels of oxidative stress in the elderly, the role of this neuroprotective agent is attracting increasing attention. Melatonin has multiple actions as a regulator of antioxidant and prooxidant enzymes, radical scavenger and antagonist of mitochondrial radical formation. The ability of melatonin and its kynuramine metabolites to interact directly with the electron transport chain by increasing the electron flow and reducing electron leakage are unique features by which melatonin is able to increase the survival of neurons under enhanced oxidative stress. Moreover, antifibrillogenic actions have been demonstrated in vitro, also in the presence of profibrillogenic apoE4 or apoE3, and in vivo, in a transgenic mouse model. Amyloid-beta toxicity is antagonized by melatonin and one of its kynuramine metabolites. Cytoskeletal disorganization and protein hyperphosphorylation, as induced in several cell-line models, have been attenuated by melatonin, effects comprising stress kinase downregulation and extending to neurotrophin expression. Various experimental models of AD, PD and HD indicate the usefulness of melatonin in antagonizing disease progression and/or mitigating some of the symptoms. Melatonin secretion has been found to be altered in AD and PD. Attempts to compensate for age- and disease-dependent melatonin deficiency have shown that administration of this compound can improve sleep efficiency in AD and PD and, to some extent, cognitive function in AD patients. Exogenous melatonin has also been reported to alleviate behavioral symptoms such as sundowning. Taken together, these findings suggest that melatonin, its analogues and kynuric metabolites may have potential value in prevention and treatment of AD and other neurodegenerative disorders.
    Matched MeSH terms: Alzheimer Disease; Huntington Disease; Parkinson Disease; Disease Progression; Carbamoyl-Phosphate Synthase I Deficiency Disease
  9. Yap TW, Chan WK, Leow AH, Azmi AN, Loke MF, Vadivelu J, et al.
    PLoS One, 2015;10(3):e0121908.
    PMID: 25799401 DOI: 10.1371/journal.pone.0121908
    BACKGROUND: Celiac disease (CD) is an immune-mediated disorder induced by the ingestion of gluten in genetically susceptible persons. The prevalence of CD in Malaysia is unknown. We aim to determine the seroprevalence of CD antibodies and also investigate the correlation between H. pylori infection and CD in the young and healthy multiracial Malaysian population.

    METHODS: Healthy young adult volunteers between the ages of 18-30 years were consecutively recruited from June 2012 to May 2014 at the University of Malaya Medical Centre (UMMC), Kuala Lumpur. Serum samples from all the participants were tested for anti-gliadin antibody immunoglobulin A/immunoglobulin G (IgA/IgG) and anti-tissue transglutaminase antibody (tTG) IgA/IgG. Samples positive for both anti-gliadin and anti-tTG were further validated for anti-human endomysial IgA antibodies (EmA). Serological diagnosis of CD was made when anti-gliadin, anti-tTG and anti-EmA were positive.

    RESULTS: 562 qualified participants with mean age 24 ± 2.4 years old were recruited into our study. CD was found in 7 participants where most of them were asymptomatic and unaware of their CD status. The median of anti-gliadin and anti-tTG IgA/IgG value was 38.2 U/ml (interquartile range, 28.3-60.4 U/ml) and 49.2 U/ml (interquartile range, 41.1-65.9 U/ml), respectively. Seroprevalence of CD antibodies was 1.9% (6 out of 324) in female while only 0.4% (1 out of 238) in male. Seroprevalence among Malay was 0.8% (2 of 236), Chinese was 1.7% (3 of 177) and Indian was 1.3% (2 of 149). Overall, seroprevalence of CD antibodies in healthy asymptomatic adults in the Malaysian population was 1.25% (95% CI, 0.78%-1.72%). No significant relationship was discovered between CD and H. pylori infection.

    CONCLUSIONS: The seroprevalence of CD antibodies in healthy young adults in the Malaysian population was 1.25% (1 in 100). CD is underdiagnosed and it could be a much greater problem in Malaysia than previously thought.

    Matched MeSH terms: Celiac Disease/blood; Celiac Disease/immunology; Celiac Disease/microbiology*; Celiac Disease/epidemiology*
  10. Cardosa MJ, Krishnan S, Tio PH, Perera D, Wong SC
    Lancet, 1999 Sep 18;354(9183):987-91.
    PMID: 10501361
    In mid-1997, several children died in Sarawak, Malaysia, during an epidemic of enterovirus-71 (EV71) hand, foot, and mouth disease. The children who died had a febrile illness that rapidly progressed to cardiopulmonary failure and the cause was not satisfactorily resolved. We describe the isolation and identification of a subgenus B adenovirus from the children who died.
    Matched MeSH terms: Disease Outbreaks/statistics & numerical data*; Hand, Foot and Mouth Disease/epidemiology*; Hand, Foot and Mouth Disease/virology*
  11. Abubakar S, Chee HY, Shafee N, Chua KB, Lam SK
    Scand. J. Infect. Dis., 1999;31(4):331-5.
    PMID: 10528868
    Enterovirus 5'UTR sequences were detected by RT-PCR in 22 out of 47 suspected hand, foot and mouth disease (HFMD) patients during an outbreak of the disease with incidences of fatal brainstem encephalomyelitis in Malaysia in 1997. Genetic and phylogenetic analyses of the isolates 5'UTR sequences suggest the presence of predominantly enteroviruses with high sequence similarities to Echovirus 1 and Coxsackievirus A9 in the Malaysian peninsula. No fatal cases, however, were associated with these isolates. The remaining isolates, including all (4/4) isolates of the fatal cases from the Malaysian peninsula and Sarawak shared very high sequence identity with enterovirus 71MS (EV71). These findings suggest that several enteroviruses were circulating in Malaysia during the outbreak period, with only EV71 causing fatal infections.
    Matched MeSH terms: Disease Outbreaks*; Hand, Foot and Mouth Disease/epidemiology*; Hand, Foot and Mouth Disease/virology*
  12. Hughes K, Yeo PP, Lun KC, Sothy SP, Thai AC, Wang KW, et al.
    Ann Acad Med Singap, 1989 May;18(3):245-9.
    PMID: 2774470
    Mortality from ischaemic heart disease in Singapore is now reaching comparability with the West. For the early 1980s, rates for Indians and Malays were higher than in U.S.A. and England and Wales and while those for Chinese were lower they were considerably higher than in Japan. In keeping with this the levels of the major risk factors in Singapore are now comparable to the West. Cigarette smoking in males is virtually the same as in Britain, while the proportion of hypertensives on medication is higher than in the West. The main cause for concern is the current high levels of serum cholesterol in Singapore and strenuous health education efforts are needed to bring about dietary changes.
    Matched MeSH terms: Coronary Disease/blood; Coronary Disease/ethnology; Coronary Disease/etiology; Coronary Disease/mortality*
  13. Shimizu H, Utama A, Yoshii K, Yoshida H, Yoneyama T, Sinniah M, et al.
    Jpn J Infect Dis, 1999 Feb;52(1):12-5.
    PMID: 10808253
    Enterovirus 71 (EV71), one of the major causative agents for hand, foot and mouth disease (HFMD), is sometimes associated with severe central nervous system diseases. In 1997, in Malaysia and Japan, and in 1998 in Taiwan, there were HFMD epidemics involving sudden deaths among young children, and EV71 was isolated from the HFMD patients, including the fatal cases. The nucleotide sequences of each EV71 isolate were determined and compared by phylogenetical analysis. EV71 strains from previously reported epidemics belonged to genotype A-1, while those from recent epidemics could be divided into two genotypes, A-2 and B. In Malaysia, genotype A-2 was more prevalent, while in Japan and Taiwan, B genotype was more prevalent. Two isolates from fatal cases in Malaysia and one isolate from a fatal case in Japan were genotype A-2. However, all isolates from three fatal cases in Taiwan belonged to genotype B. The severity of the HFMD did not link directly to certain genotypes of EV71.
    Matched MeSH terms: Disease Outbreaks*; Hand, Foot and Mouth Disease/epidemiology*; Hand, Foot and Mouth Disease/virology*
  14. Hilmi I, Tan YM, Goh KL
    World J Gastroenterol, 2006 Mar 07;12(9):1435-8.
    PMID: 16552816
    AIM: To determine the demography and clinical presentation of CD and secondly to determine any differences in the prevalence between the different ethnic groups in a multiracial Asian population.

    METHODS: Patients with CD who were seen in 2001-2003 in the University of Malaya Medical Centre (UMMC) were enrolled in this study. Prevalence of disease was calculated for the group as a whole and by race with hospital admissions per ethnic group as the denominator.

    RESULTS: Thirty-four patients were diagnosed to have CD. Basic demographic data of patients; male:female 17:17; mean age 29.1 years (+/-13.5 years); ethnic group: Malays 5 (14.7%), Chinese 12 (35.3%) and Indians 17 (50%).Twenty-six (76.5%) were diagnosed under the age of 40 and 8 (23.5%) were diagnosed over the age of 40. Location of the disease was as follows:ileocolonic 13 (38.2%), terminal ileum only 9 (26.5%), colon only 8 (23.5%), and upper gastrointestinal 4 (11.8%). Sixteen (47.1%) had penetrating disease, 9 (26.5%) had stricturing disease and 9 (26.5%) had non-penetrating and non-stricturing disease. The hospital admission prevalence of CD was 26.0 overall, Indians 52.6, Chinese 6.9, and Malays 9.3 per 10(5) admissions per ethnic group. The difference between Indians and Malays: [OR 5.67 (1.97, 17.53) P<0.001] was statistically significant but not between the Indians and the Chinese [OR 1.95 (0.89, 4.35) P=0.700]. The difference between the Chinese and the Malays was also not statistically significant. [OR 2.90 (0.95, 9.42) P=0.063].

    CONCLUSION: The clinical presentation of CD is similar to the Western experience. Although the overall prevalence is low,there appears to be a clear racial predominance among the Indians.

    Matched MeSH terms: Crohn Disease/ethnology*; Crohn Disease/epidemiology; Crohn Disease/pathology*; Crohn Disease/surgery
  15. Yanagisawa D, Ibrahim NF, Taguchi H, Morikawa S, Tomiyama T, Tooyama I
    Molecules, 2021 Mar 04;26(5).
    PMID: 33806326 DOI: 10.3390/molecules26051362
    Recent evidence suggests that the formation of soluble amyloid β (Aβ) aggregates with high toxicity, such as oligomers and protofibrils, is a key event that causes Alzheimer's disease (AD). However, understanding the pathophysiological role of such soluble Aβ aggregates in the brain in vivo could be difficult due to the lack of a clinically available method to detect, visualize, and quantify soluble Aβ aggregates in the brain. We had synthesized a novel fluorinated curcumin derivative with a fixed keto form, named as Shiga-Y51, which exhibited high selectivity to Aβ oligomers in vitro. In this study, we investigated the in vivo detection of Aβ oligomers by fluorine-19 (19F) magnetic resonance imaging (MRI) using Shiga-Y51 in an APP/PS1 double transgenic mouse model of AD. Significantly high levels of 19F signals were detected in the upper forebrain region of APP/PS1 mice compared with wild-type mice. Moreover, the highest levels of Aβ oligomers were detected in the upper forebrain region of APP/PS1 mice in enzyme-linked immunosorbent assay. These findings suggested that 19F-MRI using Shiga-Y51 detected Aβ oligomers in the in vivo brain. Therefore, 19F-MRI using Shiga-Y51 with a 7 T MR scanner could be a powerful tool for imaging Aβ oligomers in the brain.
    Matched MeSH terms: Alzheimer Disease/metabolism; Alzheimer Disease/pathology*; Disease Models, Animal*
  16. Poppema S
    J Pathol, 2021 01;253(1):1-10.
    PMID: 33044742 DOI: 10.1002/path.5567
    Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) was suggested as an entity separate from other types of Hodgkin lymphoma 40 years ago and recognized in the WHO classification in 2001. Based on its relatively benign course with late distant relapses, relation with lymph node hyperplasia with progressively transformed germinal centers, presence of clonal immunoglobulin gene rearrangements with somatic hypermutations and ongoing mutations, and relation with a number of inherited defects affecting the immune system, it has been suspected that NLPHL might be antigen-driven. Recent evidence has shown that cases of IgD-positive NLPHL are associated with infection by Moraxella catarrhalis, a common bacterium in the upper respiratory tract and in lymph nodes. This review summarizes the evidence for NLPHL as a B-cell lymphoma involving follicular T-lymphocytes normally found in germinal centers, its molecular features and relation to inherited immune defects, and its relation and differential diagnosis from similar entities. Finally, it discusses the evidence that in many cases a watch and wait policy might be a viable initial management strategy. © 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Matched MeSH terms: Hodgkin Disease/genetics; Hodgkin Disease/immunology*; Hodgkin Disease/microbiology; Hodgkin Disease/therapy
  17. Gopalai AA, Ahmad-Annuar A, Li HH, Zhao Y, Lim SY, Tan AH, et al.
    PMID: 27174169 DOI: 10.1002/ajmg.b.32454
    PARK16 was identified as a risk factor for Parkinson's disease in a Japanese cohort; however, subsequent studies in the other populations including the Chinese, European, Caucasian, and Chilean have shown a protective role instead. To investigate this locus in our Malaysian cohort, 1,144 individuals were screened for five SNPs in the PARK16 locus and logistic regression analysis showed that the A allele of the rs947211 SNP reduced the risk of developing PD via a recessive model (Odds ratio 0.57, P-value 0.0003). Pooled analysis with other Asian studies showed that A allele of the rs947211 SNP decreased the risk of developing PD via a recessive model (Odds ratio 0.71, P-value 0.0001). In addition, when meta-analysis was performed with other Asian population, three SNPs (rs823128, rs823156, and rs11240572) reduced risk of developing PD via a dominant model. © 2016 Wiley Periodicals, Inc.
    Matched MeSH terms: Parkinson Disease/genetics*; Parkinson Disease/metabolism; Parkinson Disease/physiopathology; Genetic Predisposition to Disease
  18. Hussein EA, Hair-Bejo M, Omar AR, Arshad SS, Hani H, Balakrishnan KN, et al.
    Microb Pathog, 2019 Apr;129:213-223.
    PMID: 30771470 DOI: 10.1016/j.micpath.2019.02.017
    Limited deep studies are available in the field of early stages of pathogenesis of Newcastle disease virus (NDV) infection and tissue tropism of NDV. In this study, 24 specific pathogen free (SPF) chickens of white leghorn breed were infected with Newcastle disease (ND) by intranasal administration of 10⁵ 50% EID50/0.1 mL of velogenic NDV (vNDV). A second group of 15 chickens were kept as a control group. Chickens were monitored every day to record clinical signs. Infected chickens were euthanized by cervical dislocation at successive times, namely at hours (hrs) 2, 4, 6, 12, days 1, 2, 4, and 6 post-inoculation (pi). Whereas, control group chickens were euthanized on days 0, 1, 2, 4, and 6 pi. Tissues of brain, trachea, lung, caecal tonsil, liver, kidney, spleen, heart, proventriculus, intestine, and thymus were collected, fixed in 10% buffered formalin, embedded in paraffin, and sectioned. HS staining, immunoperoxidase staining (IPS) and in situ PCR were applied. It was concluded that at hr 2 pi, virus seemed to be inclined to trachea and respiratory tract. Meanwhile, it attacked caecal tonsils, intestine and bursa of Fabricus. While primary viraemia was ongoing, virus created footing in kidney and thymus. At hr 4 pi, proventriculus, liver, and spleen were attacked. However, at hr 6 pi, brain and heart were involved. Secondary viraemia probably started as early as hr 12 pi since all collected tissues were positive. Tissue tropism was determined in trachea, caecal tonsil, liver, bursa of Fabricius, intestine, proventriculus, lung, spleen, thymus, kidney, heart, and brain.
    Matched MeSH terms: Newcastle Disease/pathology*; Newcastle Disease/virology*; Newcastle disease virus/physiology*
  19. Gopalai AA, Lim JL, Li HH, Zhao Y, Lim TT, Eow GB, et al.
    Mol Genet Genomic Med, 2019 Nov;7(11):e604.
    PMID: 31487119 DOI: 10.1002/mgg3.604
    BACKGROUND: The LRRK2 gene is associated with Parkinson's disease (PD) as a number of mutations within the gene have been shown to be susceptibility factors. Studies on various global populations have determined that mutations such as G2019S, G2385R, and R1628P in LRRK2 increase the risk of developing PD while the N551K-R1398H haplotype is associated with conferring protection against developing PD. Here we report a study looking at the N551K and R1398H variants for the first time in the Malaysian population.

    METHODS: Cases (523) which conformed to the United Kingdom PD Brain Bank Criteria for PD were recruited through trained neurologists and age- and ethnically matched controls (491) were individuals free of any neurological disorder. The N551K and R1398H mutations were genotyped using the Taqman SNP genotyping assay.

    RESULTS: A significant protective association for N551K was found in those of Malay ancestry, with a protective trend seen for R1398H. A meta-analysis of Chinese individuals in this cohort with other published cohorts of Chinese ancestry indicated a significant protective role for N551K and R1398H.

    CONCLUSION: This study reports that the N551K-R1398H haplotype is also relevant to the Malaysian population, with a significant protective effect found in those of Malay and Chinese ancestries.

    Matched MeSH terms: Parkinson Disease/genetics*; Parkinson Disease/epidemiology; Genetic Predisposition to Disease*
  20. Mustapha M, Mat Taib CN
    Bosn J Basic Med Sci, 2021 Aug 01;21(4):422-433.
    PMID: 33357211 DOI: 10.17305/bjbms.2020.5181
    Among the popular animal models of Parkinson's disease (PD) commonly used in research are those that employ neurotoxins, especially 1-methyl- 4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP). This neurotoxin exerts it neurotoxicity by causing a barrage of insults, such as oxidative stress, mitochondrial apoptosis, inflammation, excitotoxicity, and formation of inclusion bodies acting singly and in concert, ultimately leading to dopaminergic neuronal damage in the substantia nigra pars compacta and striatum. The selective neurotoxicity induced by MPTP in the nigrostriatal dopaminergic neurons of the mouse brain has led to new perspectives on PD. For decades, the MPTP-induced mouse model of PD has been the gold standard in PD research even though it does not fully recapitulate PD symptomatology, but it does have the advantages of simplicity, practicability, affordability, and fewer ethical considerations and greater clinical correlation than those of other toxin models of PD. The model has rejuvenated PD research and opened new frontiers in the quest for more novel therapeutic and adjuvant agents for PD. Hence, this review summarizes the role of MPTP in producing Parkinson-like symptoms in mice and the experimental role of the MPTP-induced mouse model. We discussed recent developments of more promising PD therapeutics to enrich our existing knowledge about this neurotoxin using this model.
    Matched MeSH terms: Disease Models, Animal*; Parkinson Disease/drug therapy*; Parkinson Disease/etiology*
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