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  1. Kaku Y
    Uirusu, 2004 Dec;54(2):237-42.
    PMID: 15745162
    Nipah virus (NiV), emerged in Peninsular Malaysia, caused an outbreak of severe febrile encephalitis in humans and respiratory diseases in pigs between 1998 and 1999. By May of 1999, the death of 105 humans and the culling of about 1.1 million pigs were reported. Fruitbats of Pteropid species were identified as the natural reservoir hosts. The epidemiological studies suggested that NiV was introduced into pig farms by fruitbats, and was than transmitted to humans (mainly pig farmers) and other animals such as dogs, cats and horses. In 2004, NiV reappeared in Bangladesh with greater lethality. In contrast to the Malaysia case, epidemiologic characteristics of this outbreak suggested the possibility of fruitbats-to-person, or person-to-person transmission. In this article, the epidemiological comparison between two outbreaks in Malaysia and Bangladesh, and the new-trends of virological studies of NiV will be discussed.
    Matched MeSH terms: Disease Outbreaks; Disease Vectors
  2. Bhidayasiri R, Hattori N, Jeon B, Chen RS, Lee MK, Bajwa JA, et al.
    Expert Rev Neurother, 2015;15(11):1285-97.
    PMID: 26390066 DOI: 10.1586/14737175.2015.1088783
    Most Parkinson's disease patients will receive levodopa therapy, and of these, the majority will develop some levodopa-induced complications. For many patients, the first complication to develop is the decline in the duration of therapeutic benefit of each levodopa dose, a phenomenon commonly termed 'wearing-off'. There is already extensive literature documenting the epidemiology and management of wearing-off in Parkinson's disease patients of western descent. However, data derived from these studies might not always apply to patients of Asian descent due to genetic variations, differences in co-morbidities or non-availability of certain drugs. This review summarizes the current literature regarding the epidemiology of wearing-off in Asian (including Arab) patients and discusses the management issues in the context of drug availability in Asia.
    Matched MeSH terms: Parkinson Disease/drug therapy*
  3. Sellappans R, Lai PS, Ng CJ
    BMJ Open, 2015 Aug 27;5(8):e007817.
    PMID: 26316648 DOI: 10.1136/bmjopen-2015-007817
    OBJECTIVE: The aim of this study was to identify the challenges faced by primary care physicians (PCPs) when prescribing medications for patients with chronic diseases in a teaching hospital in Malaysia.
    DESIGN/SETTING: 3 focus group discussions were conducted between July and August 2012 in a teaching primary care clinic in Malaysia. A topic guide was used to facilitate the discussions which were audio-recorded, transcribed verbatim and analysed using a thematic approach.
    PARTICIPANTS: PCPs affiliated to the primary care clinic were purposively sampled to include a range of clinical experience. Sample size was determined by thematic saturation of the data.
    RESULTS: 14 family medicine trainees and 5 service medical officers participated in this study. PCPs faced difficulties in prescribing for patients with chronic diseases due to a lack of communication among different healthcare providers. Medication changes made by hospital specialists, for example, were often not communicated to the PCPs leading to drug duplications and interactions. The use of paper-based medical records and electronic prescribing created a dual record system for patients' medications and became a problem when the 2 records did not tally. Patients sometimes visited different doctors and pharmacies for their medications and this resulted in the lack of continuity of care. PCPs also faced difficulties in addressing patients' concerns, and dealing with patients' medication requests and adherence issues. Some PCPs lacked time and knowledge to advise patients about their medications and faced difficulties in managing side effects caused by the patients' complex medication regimen.
    CONCLUSIONS: PCPs faced prescribing challenges related to patients, their own practice and the local health system when prescribing for patients with chronic diseases. These challenges must be addressed in order to improve chronic disease management in primary care and, more importantly, patient safety.
    Study site: Primary care clinic, University Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
    Matched MeSH terms: Chronic Disease/drug therapy*
  4. Castaño-Rodríguez N, Kaakoush NO, Lee WS, Mitchell HM
    Gut, 2017 02;66(2):235-249.
    PMID: 26508508 DOI: 10.1136/gutjnl-2015-310545
    OBJECTIVE: To conduct a comprehensive global systematic review and meta-analysis on the association between Helicobacter pylori infection and IBD. As bacterial antigen cross-reactivity has been postulated to be involved in this association, published data on enterohepatic Helicobacter spp (EHS) and Campylobacter spp and IBD was also analysed.

    DESIGN: Electronic databases were searched up to July 2015 for all case-control studies on H. pylori infection/EHS/Campylobacter spp and IBD. Pooled ORs (P-OR) and 95% CIs were obtained using the random effects model. Heterogeneity, sensitivity and stratified analyses were performed.

    RESULTS: Analyses comprising patients with Crohn's disease (CD), UC and IBD unclassified (IBDU), showed a consistent negative association between gastric H. pylori infection and IBD (P-OR: 0.43, p value <1e-10). This association appears to be stronger in patients with CD (P-OR: 0.38, p value <1e-10) and IBDU (P-OR: 0.43, p value=0.008) than UC (P-OR: 0.53, p value <1e-10). Stratification by age, ethnicity and medications showed significant results. In contrast to gastric H. pylori, non H. pylori-EHS (P-OR: 2.62, p value=0.001) and Campylobacter spp, in particular C. concisus (P-OR: 3.76, p value=0.006) and C. showae (P-OR: 2.39, p value=0.027), increase IBD risk.

    CONCLUSIONS: H. pylori infection is negatively associated with IBD regardless of ethnicity, age, H. pylori detection methods and previous use of aminosalicylates and corticosteroids. Antibiotics influenced the magnitude of this association. Closely related bacteria including EHS and Campylobacter spp increase the risk of IBD. These results infer that H. pylori might exert an immunomodulatory effect in IBD.

    Matched MeSH terms: Crohn Disease/epidemiology*
  5. Haerian BS, Baum L, Kwan P, Cherny SS, Shin JG, Kim SE, et al.
    Mol Neurobiol, 2016 10;53(8):5457-67.
    PMID: 26452361 DOI: 10.1007/s12035-015-9457-y
    Gamma-aminobutyric acid receptor (GABA-A) is the most common receptor of fast synaptic inhibition in the human brain. Gamma protein encoded by the GABRG2 gene is one of the subunits of the GABA-A receptor, which plays an essential role in the function of this receptor. Several studies have identified various febrile seizure (FS) and epilepsy risk variants of GABRG2 gene in different populations, but some others did not support these results. The aim of this case-control study is to investigate whether GABRG2 polymorphisms contribute to susceptibility for FS and epilepsy in pooled data of three cohorts, from Malaysia (composed of Malay, Chinese, and Indian), Hong Kong, and Korea. Furthermore, the pooled dataset of these cohorts with previous reports were meta-analyzed for determining the risk effect size of the rs211037 polymorphism on FS and symptomatic epilepsy (SE). The rs211037, rs210987, rs440218, rs2422106, rs211014, and rs401750 polymorphisms were genotyped in the 6442 subjects (1729 epilepsy and 4713 controls). Results of the case-control study showed associations between rs211037 and the risk of SE in the pooled data from all cohorts (T vs. C, p = 3 × 10(-5), and TT vs. CC, p = 2 × 10(-5)) and the risk of partial seizure in the combined data of Malaysia and Hong Kong (both T vs. C and TT vs. CC, p = 2 × 10(-6)). The rs211037-rs210987 and rs2422106-rs211014-rs401750 haplotypes were also associated with susceptibility to SE in Chinese. Meta-analysis of all Asians identified association between rs211037 and FS and SE (T vs. C, p = 4 × 10(-4), and p = 4 × 10(-3), respectively). In conclusion, rs211037 alone may be a risk factor for FS, partial seizure, and SE, and in linkage disequilibrium with rs210987 can contribute to FS and SE in Asians, particularly in Chinese.
    Matched MeSH terms: Genetic Predisposition to Disease*
  6. Amankwah EK, Lin HY, Tyrer JP, Lawrenson K, Dennis J, Chornokur G, et al.
    Genet Epidemiol, 2015 Dec;39(8):689-97.
    PMID: 26399219 DOI: 10.1002/gepi.21921
    Epithelial-mesenchymal transition (EMT) is a process whereby epithelial cells assume mesenchymal characteristics to facilitate cancer metastasis. However, EMT also contributes to the initiation and development of primary tumors. Prior studies that explored the hypothesis that EMT gene variants contribute to epithelial ovarian carcinoma (EOC) risk have been based on small sample sizes and none have sought replication in an independent population. We screened 15,816 single-nucleotide polymorphisms (SNPs) in 296 genes in a discovery phase using data from a genome-wide association study of EOC among women of European ancestry (1,947 cases and 2,009 controls) and identified 793 variants in 278 EMT-related genes that were nominally (P < 0.05) associated with invasive EOC. These SNPs were then genotyped in a larger study of 14,525 invasive-cancer patients and 23,447 controls. A P-value <0.05 and a false discovery rate (FDR) <0.2 were considered statistically significant. In the larger dataset, GPC6/GPC5 rs17702471 was associated with the endometrioid subtype among Caucasians (odds ratio (OR) = 1.16, 95% CI = 1.07-1.25, P = 0.0003, FDR = 0.19), whereas F8 rs7053448 (OR = 1.69, 95% CI = 1.27-2.24, P = 0.0003, FDR = 0.12), F8 rs7058826 (OR = 1.69, 95% CI = 1.27-2.24, P = 0.0003, FDR = 0.12), and CAPN13 rs1983383 (OR = 0.79, 95% CI = 0.69-0.90, P = 0.0005, FDR = 0.12) were associated with combined invasive EOC among Asians. In silico functional analyses revealed that GPC6/GPC5 rs17702471 coincided with DNA regulatory elements. These results suggest that EMT gene variants do not appear to play a significant role in the susceptibility to EOC.
    Matched MeSH terms: Genetic Predisposition to Disease*
  7. Ng KT, Oong XY, Pang YK, Hanafi NS, Kamarulzaman A, Tee KK
    Emerg Microbes Infect, 2015 Aug;4(8):e47.
    PMID: 26421270 DOI: 10.1038/emi.2015.47
    Matched MeSH terms: Disease Outbreaks*
  8. Furuya-Kanamori L, Liang S, Milinovich G, Soares Magalhaes RJ, Clements AC, Hu W, et al.
    BMC Infect Dis, 2016;16:84.
    PMID: 26936191 DOI: 10.1186/s12879-016-1417-2
    BACKGROUND: Chikungunya and dengue infections are spatio-temporally related. The current review aims to determine the geographic limits of chikungunya, dengue and the principal mosquito vectors for both viruses and to synthesise current epidemiological understanding of their co-distribution.
    METHODS: Three biomedical databases (PubMed, Scopus and Web of Science) were searched from their inception until May 2015 for studies that reported concurrent detection of chikungunya and dengue viruses in the same patient. Additionally, data from WHO, CDC and Healthmap alerts were extracted to create up-to-date global distribution maps for both dengue and chikungunya.
    RESULTS: Evidence for chikungunya-dengue co-infection has been found in Angola, Gabon, India, Madagascar, Malaysia, Myanmar, Nigeria, Saint Martin, Singapore, Sri Lanka, Tanzania, Thailand and Yemen; these constitute only 13 out of the 98 countries/territories where both chikungunya and dengue epidemic/endemic transmission have been reported.
    CONCLUSIONS: Understanding the true extent of chikungunya-dengue co-infection is hampered by current diagnosis largely based on their similar symptoms. Heightened awareness of chikungunya among the public and public health practitioners in the advent of the ongoing outbreak in the Americas can be expected to improve diagnostic rigour. Maps generated from the newly compiled lists of the geographic distribution of both pathogens and vectors represent the current geographical limits of chikungunya and dengue, as well as the countries/territories at risk of future incursion by both viruses. These describe regions of co-endemicity in which lab-based diagnosis of suspected cases is of higher priority.
    Erratum: Furuya-Kanamori L, Liang S, Milinovich G, Magalhaes RJ, Clements AC, Hu W, Brasil P, Frentiu FD, Dunning R, Yakob L. Erratum to: Co-distribution and co-infection of chikungunya and dengue viruses. BMC Infect Dis. 2016 Apr 29;16:188. doi: 10.1186/s12879-016-1519-x. PubMed PMID: 27129475; PubMed Central PMCID: PMC4851825.
    Matched MeSH terms: Disease Outbreaks
  9. Sun C, Molineros JE, Looger LL, Zhou XJ, Kim K, Okada Y, et al.
    Nat Genet, 2016 Mar;48(3):323-30.
    PMID: 26808113 DOI: 10.1038/ng.3496
    Systemic lupus erythematosus (SLE) has a strong but incompletely understood genetic architecture. We conducted an association study with replication in 4,478 SLE cases and 12,656 controls from six East Asian cohorts to identify new SLE susceptibility loci and better localize known loci. We identified ten new loci and confirmed 20 known loci with genome-wide significance. Among the new loci, the most significant locus was GTF2IRD1-GTF2I at 7q11.23 (rs73366469, Pmeta = 3.75 × 10(-117), odds ratio (OR) = 2.38), followed by DEF6, IL12B, TCF7, TERT, CD226, PCNXL3, RASGRP1, SYNGR1 and SIGLEC6. We identified the most likely functional variants at each locus by analyzing epigenetic marks and gene expression data. Ten candidate variants are known to alter gene expression in cis or in trans. Enrichment analysis highlights the importance of these loci in B cell and T cell biology. The new loci, together with previously known loci, increase the explained heritability of SLE to 24%. The new loci share functional and ontological characteristics with previously reported loci and are possible drug targets for SLE therapeutics.
    Matched MeSH terms: Genetic Predisposition to Disease*
  10. Tan YH, Sidik SM, Syed Husain SN, Lye MS, Chong PP
    Asian Pac J Cancer Prev, 2016;17(1):57-64.
    PMID: 26838255
    BACKGROUND: Tobacco smoking is considered a risk factor for cervical cancer development due to the presence of tobacco based carcinogenic metabolites in cervical cells of female smokers. In this study, we investigated the role of the T3801C (MspI) polymorphism of CYP1A1, a gene encoding an enzyme necessary for the initiation of tobacco based carcinogen metabolism, on cervical cancer risk. The T to C substitution may alter CYP1A1 activities, potentially elevating cervical cancer risk. Since results of gene-disease association studies vary according to the study population, the multi-ethnic population of Malaysia provides an excellent representative cohort for identifying and comparing the cervical cancer risk among the 3 major ethnics in Southeast Asia in relation to CYP1A1 MspI polymorphism.

    MATERIALS AND METHODS: A total of 195 Thin Prep Pap smear samples from HPV negative and cancer free females were randomly selected as controls while 106 formalin fixed paraffin embedded samples from females with invasive cervical cancer were randomly selected for the cases group. The polymorphisms were identified using restriction fragment length polymorphism (RFLP) PCR.

    RESULTS: We found no significant associations between CYP1A1 MspI polymorphism and cervical cancer in the general Malaysian female population. However, upon ethnic stratification, the variant C/C genotype was significantly associated with a 4.66-fold increase in cervical cancer risk in Malay females (95% CI= 1.21-17.9; p=0.03). No significant association was observed in the Chinese and Indian females. Additionally, there were no significant associations in the dominant model and allele frequency model analysis in both the general and ethnically stratified female population of Malaysia.

    CONCLUSIONS: Our findings suggest that the C/C genotype of CYP1A1 MspI polymorphism is associated with the development of cervical carcinoma in the Malay females of Malaysia.

    Matched MeSH terms: Genetic Predisposition to Disease/genetics
  11. Tan KK, Sy AK, Tandoc AO, Khoo JJ, Sulaiman S, Chang LY, et al.
    Sci Rep, 2015 Jul 23;5:12279.
    PMID: 26201250 DOI: 10.1038/srep12279
    Outbreaks involving the Asian genotype Chikungunya virus (CHIKV) caused over one million infections in the Americas recently. The outbreak was preceded by a major nationwide outbreak in the Philippines. We examined the phylogenetic and phylogeographic relationships of representative CHIKV isolates obtained from the 2012 Philippines outbreak with other CHIKV isolates collected globally. Asian CHIKV isolated from the Philippines, China, Micronesia and Caribbean regions were found closely related, herein denoted as Cosmopolitan Asian CHIKV (CACV). Three adaptive amino acid substitutions in nsP3 (D483N), E1 (P397L) and E3 (Q19R) were identified among CACV. Acquisition of the nsP3-483N mutation in Compostela Valley followed by E1-397L/E3-19R in Laguna preceded the nationwide spread in the Philippines. The China isolates possessed two of the amino acid substitutions, nsP3-D483N and E1-P397L whereas the Micronesian and Caribbean CHIKV inherited all the three amino acid substitutions. The unique amino acid substitutions observed among the isolates suggest multiple independent virus dissemination events. The possible biological importance of the specific genetic signatures associated with the rapid global of the virus is not known and warrant future in-depth study and epidemiological follow-up. Molecular evidence, however, supports the Philippines outbreak as the possible origin of the CACV.
    Matched MeSH terms: Disease Outbreaks/statistics & numerical data
  12. Razali SM, Abidin ZZ, Othman Z, Yassin MA
    Asian J Psychiatr, 2015 Aug;16:26-31.
    PMID: 26182843 DOI: 10.1016/j.ajp.2015.06.011
    The aim of the study is to screen and evaluate the efficacy of the screening tools in detecting subjects with sub-threshold psychosis among asymptomatic individuals at genetic risk, as compared with persons in the general public.
    Matched MeSH terms: Disease Progression*
  13. Eshkoor SA, Hamid TA, Mun CY, Ng CK
    Clin Interv Aging, 2015;10:687-93.
    PMID: 25914527 DOI: 10.2147/CIA.S73922
    Mild cognitive impairment (MCI) is a common condition in the elderly. It is characterized by deterioration of memory, attention, and cognitive function that is beyond what is expected based on age and educational level. MCI does not interfere significantly with individuals' daily activities. It can act as a transitional level of evolving dementia with a range of conversion of 10%-15% per year. Thus, it is crucial to protect older people against MCI and developing dementia. The preventive interventions and appropriate treatments should improve cognitive performance, and retard or prevent progressive deficits. The avoidance of toxins, reduction of stress, prevention of somatic diseases, implementation of mental and physical exercises, as well as the use of dietary compounds like antioxidants and supplements can be protective against MCI. The modification of risk factors such as stopping smoking, as well as the treatment of deficiency in vitamins and hormones by correcting behaviors and lifestyle, can prevent cognitive decline in the elderly. The progressive increase in the growth rate of the elderly population can enhance the rate of MCI all over the world. There is no exact cure for MCI and dementia; therefore, further studies are needed in the future to determine causes of MCI and risk factors of progression from MCI to dementia. This will help to find better ways for prevention and treatment of cognitive impairment worldwide.
    Matched MeSH terms: Disease Progression; Genetic Predisposition to Disease
  14. Chua KH, Lian LH, Sim XJ, Cheah TE, Lau TP
    Int J Mol Sci, 2015;16(5):9794-803.
    PMID: 25938972 DOI: 10.3390/ijms16059794
    The programmed cell death 1 (PDCD1) gene encodes for the PD-1 (programmed death 1) molecule, which negatively regulates self-reactive T- and B-cells in the maintenance of peripheral tolerance. A previous report had shown the development of lupus-like phenotypes in PD-1-deficient C57BL/6 mice, was suggestive to the role of PDCD1 in predisposing to systemic lupus erythematosus (SLE). Hence, we aimed to investigate the association between PDCD1 and SLE susceptibility in the Malaysian population. A TaqMan-based real-time PCR was employed to screen for PD1.1, PD1.3, PD1.5 and PD1.6 in both SLE and healthy control groups of 200 samples each. The observed frequency for PD1.5C/C genotype was significantly higher in Indian SLE patients and Malay controls (p < 0.01). On the other hand, the PD1.5C/T genotype might predispose the Malays to SLE, but confer a protective effect among the Indians (p < 0.01). The PD1.1, PD1.3 and PD1.6 were, however, not correlated to genetic predisposition of SLE in our Malaysian population. In conclusion, PD1.5 variant was significantly associated to SLE susceptibility in our Malaysian cohort. Our failure in replicating the association between other investigated PDCD1 variants and risk of getting SLE might due to ethnic and geographic variations in the distribution of these genetic variants.
    Matched MeSH terms: Genetic Predisposition to Disease*
  15. Sha'ari HM, Haerian BS, Baum L, Tan HJ, Rafia MH, Kwan P, et al.
    Mol Neurobiol, 2016 07;53(5):2869-2877.
    PMID: 25876511 DOI: 10.1007/s12035-015-9150-1
    Epilepsy is a common neurological disease characterized by recurrent unprovoked seizures. Evidence suggested that abnormal activity of brain-derived neurotrophic factor (BDNF) contributes to the pathogenesis of epilepsy. Some previous studies identified association between genetic variants of BDNF and risk of epilepsy. In this study, this association has been examined in the Hong Kong and Malaysian epilepsy cohorts. Genomic DNA of 6047 subjects (1640 patients with epilepsy and 4407 healthy individuals) was genotyped for rs6265, rs11030104, rs7103411, and rs7127507 polymorphisms by using Sequenom MassArray and Illumina HumanHap 610-Quad or 550-Duo BeadChip arrays techniques. Results showed significant association between rs6265 T, rs7103411 C, and rs7127507 T and cryptgenic epilepsy risk (p = 0.00003, p = 0.0002, and p = 0.002, respectively) or between rs6265 and rs7103411 and symptomatic epilepsy risk in Malaysian Indians (TT vs. CC, p = 0.004 and T vs. C, p = 0.0002, respectively) as well as between rs6265 T and risk of cryptogenic epilepsy in Malaysian Chinese (p = 0.005). The Trs6265-Crs7103411-Trs7127507 was significantly associated with cryptogenic epilepsy in Malaysian Indians (p = 0.00005). In conclusion, our results suggest that BDNF polymorphisms might contribute to the risk of epilepsy in Malaysian Indians and Chinese.
    Matched MeSH terms: Genetic Predisposition to Disease*
  16. Wong LP, Shakir SM, Atefi N, AbuBakar S
    PLoS One, 2015;10(4):e0122890.
    PMID: 25836366 DOI: 10.1371/journal.pone.0122890
    Efforts to stamp dengue in many dengue endemic countries has met little success. There is a need to re-examine and understand how the public at large view the dengue prevention efforts. This study aimed to examine the demographic factors, theoretical constructs of the Health Belief Model and knowledge about dengue and how these influence the practice of dengue prevention.
    Matched MeSH terms: Disease Transmission, Infectious/prevention & control*
  17. Mackenzie JS, Field HE, Guyatt KJ
    J Appl Microbiol, 2003;94 Suppl:59S-69S.
    PMID: 12675937
    Since 1994, a number of novel viruses have been described from bats in Australia and Malaysia, particularly from fruit bats belonging to the genus Pteropus (flying foxes), and it is probable that related viruses will be found in other countries across the geographical range of other members of the genus. These viruses include Hendra and Nipah viruses, members of a new genus, Henipaviruses, within the family Paramyxoviridae; Menangle and Tioman viruses, new members of the Rubulavirus genus within the Paramyxoviridae; and Australian bat lyssavirus (ABLV), a member of the Lyssavirus genus in the family Rhabdoviridae. All but Tioman virus are known to be associated with human and/or livestock diseases. The isolation, disease associations and biological properties of the viruses are described, and are used as the basis for developing management strategies for disease prevention or control. These strategies are directed largely at disease minimization through good farm management practices, reducing the potential for exposure to flying foxes, and better disease recognition and diagnosis, and for ABLV specifically, the use of rabies vaccine for pre- and post-exposure prophylaxis. Finally, an intriguing and long-term strategy is that of wildlife immunization through plant-derived vaccination.
    Matched MeSH terms: Communicable Disease Control; Disease Vectors
  18. Elsadig RE, Reimann K, Yip CH, Lai LC
    Anticancer Res, 2001 Jul-Aug;21(4A):2693-6.
    PMID: 11724341
    Oestrone sulphate is a major source of active oestrogens in the breast. It is converted to oestrone by oestrone sulphatase. Breast cyst fluid (BCF) is a rich source of sex hormones and growth factors. BCF obtained from British women has been shown to inhibit oestrone sulphatase activity in the MCF-7 oestrogen-receptor-positive breast cancer cell line. The aim of the present study was to assess whether BCF obtained from Malaysian women inhibited oestrone sulphatase activity in the MCF-7 and MDA-MB-231 breast cancer cell lines. The cell lines were grown in supplemented Dulbecco's Modified Eagle Medium for 3 days, following which a 3-day incubation with sterilised BCF was carried out. At the end of the treatment period the cell monolayers were assayed for oestrone sulphatase activity and the number of cell nuclei counted on a Coulter Counter. BCF was also fractionated on a Bio-Sil SEC 125-5 column by HPLC and the effects of the fractions collected on oestrone sulphatase activity in the MDA-MB-231 cell line were assessed. All 18 samples of BCF tested inhibited cell growth in the MDA-MB-231 cell line while 8 out of 10 samples inhibited MCF-7 cell growth; 15 out of 18 BCF samples inhibited oestrone sulphatase activity in the MDA-MB-231 cell line whereas 5 out of 10 samples stimulated oestrone sulphatase activity in the MCF-7 cell line. HPLC fractions corresponding to molecular weights of > 158 kDa and 28 kDa were found to inhibit oestrone sulphatase activity in the MDA-MB-231 cell line. Further work is required to fully characterise these substances as they may have roles to play in the prevention of breast cancer.
    Matched MeSH terms: Fibrocystic Breast Disease/metabolism*
  19. Chong HT, Kunjapan SR, Thayaparan T, Tong J, Petharunam V, Jusoh MR, et al.
    Can J Neurol Sci, 2002 Feb;29(1):83-7.
    PMID: 11858542
    BACKGROUND: An outbreak of viral encephalitis occurred among pig industry workers in Malaysia in September 1998 to April 1999. The encephalitis was attributed to a new paramyxovirus, Nipah virus. This is a description of the clinical features of 103 patients treated in the Seremban Hospital with characterization of the prognostic factors.

    METHODS: Clinical case records and laboratory investigations were reviewed. The case definition was: patients from the outbreak area, direct contact or in close proximity with pigs, clinical or CSF features of encephalitis.

    RESULTS: The mean age was 38 years, 89% were male, 58% were ethnic Chinese, 78% were pig farm owners or hired workers. The mean incubation period was 10 days. The patients typically presented with nonspecific systemic symptoms of fever, headache, myalgia and sore throat. Seizures and focal neurological signs were seen in 16% and 5% respectively. In the more severe cases, this was followed by drowsiness and deteriorating consciousness requiring ventilation in 61%. Autonomic disturbances and myoclonic jerks were common features. The mortality was high at 41%. Systolic hypertension, tachycardia and high fever were associated with poor outcome. On the other hand, 40% recovered fully. As for the other 19%, the residual neurological signs were mostly mild.

    CONCLUSION: Nipah virus caused an encephalitis illness with short incubation period and high mortality. The prognosis for the survivors was good.

    Matched MeSH terms: Disease Outbreaks*
  20. Stone SC, McNutt E
    Ann Emerg Med, 2001 Jul;38(1):83-4.
    PMID: 11423818
    Matched MeSH terms: Disease Outbreaks/statistics & numerical data*
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