Displaying publications 561 - 580 of 5421 in total

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  1. Srinivasan V, Pandi-Perumal SR, Maestroni GJ, Esquifino AI, Hardeland R, Cardinali DP
    Neurotox Res, 2005;7(4):293-318.
    PMID: 16179266
    The pineal product melatonin has remarkable antioxidant properties. It scavenges hydroxyl, carbonate and various organic radicals, peroxynitrite and other reactive nitrogen species. Melatonyl radicals formed by scavenging combine with and, thereby, detoxify superoxide anions in processes terminating the radical reaction chains. Melatonin also enhances the antioxidant potential of the cell by stimulating the synthesis of antioxidant enzymes like superoxide dismutase, glutathione peroxidase and glutathione reductase, and by augmenting glutathione levels. The decline in melatonin production in aged individuals has been suggested as one of the primary contributing factors for the development of age-associated neurodegenerative diseases, e.g., Alzheimer's disease. Melatonin has been shown to be effective in arresting neurodegenerative phenomena seen in experimental models of Alzheimer's disease, Parkinsonism and ischemic stroke. Melatonin preserves mitochondrial homeostasis, reduces free radical generation, e.g., by enhancing mitochondrial glutathione levels, and safeguards proton potential and ATP synthesis by stimulating complex I and IV activities. Therapeutic trials with melatonin have been effective in slowing the progression of Alzheimer's disease but not of Parkinson's disease. Melatonin's efficacy in combating free radical damage in the brain suggests that it may be a valuable therapeutic agent in the treatment of cerebral edema after traumatic brain injury.
    Matched MeSH terms: Alzheimer Disease/metabolism; Alzheimer Disease/pathology; Huntington Disease/metabolism; Huntington Disease/pathology; Parkinson Disease/metabolism; Parkinson Disease/pathology
  2. Stock I
    Med Monatsschr Pharm, 2014 Jan;37(1):4-10; quiz 11-2.
    PMID: 24490433
    Hand, foot and mouth disease (HFMD) is a highly contagious, world-wide distributed viral illness that affects predominantly children. It is caused by several enteroviruses, such as coxsackieviruses A6, A10, A16 and enterovirus 71. In most cases, HFMD follows a benign and self-limiting course. After an incubation period of 3 to 10 days, fever and sore throat, the first symptoms of the disease, appear. A few days later, maculopapular or vesicular eruptions form on the palms and soles as well as in the oral cavity. Since the year 2000, several large HFMD outbreaks have been reported in many Asian regions such as China, Malaysia and Vietnam. In some of these outbreaks, high incidences of severe progressive HFMD forms with some fatalities were observed. Such diseases have been caused primarily by enterovirus 71 strains and were characterized frequently by sudden onset of fever, encephalitis/meningitis and severe respiratory symptoms such as pulmonary edema. Further severe neurological and cardiac complications have also been observed during these outbreaks. Recently, some HFMD outbreaks caused by the coxsackievirus A6 have been reported in several parts of the world. These illnesses also affected adults and were characterized by more severe symptoms of "classical" HFMD. In addition, outbreaks of coxsackievirus-A6-associated HFMD in many countries were associated with onychomadesis, with the loss of nails occurring up to two months after initial symptoms. Treatment of "classical" HFMD is usually symptomatic, a generally recommended antiviral therapy does not exist. In severe HFMD cases, suitable treatment also encompasses mechanical ventilation, as well as the additional application of antiviral agents such as ribavirin. In the last years, several novel agents with good in vitro and in vivo activity against enteroviruses have been developed. A vaccine against HFMD is not yet available.
    Matched MeSH terms: Disease Outbreaks; Hand, Foot and Mouth Disease/diagnosis; Hand, Foot and Mouth Disease/drug therapy*; Hand, Foot and Mouth Disease/epidemiology; Hand, Foot and Mouth Disease/virology
  3. Chua KH, Lian LH, Kee BP, Thum CM, Lee WS, Hilmi I, et al.
    J Dig Dis, 2011 Dec;12(6):459-66.
    PMID: 22118696 DOI: 10.1111/j.1751-2980.2011.00533.x
    The aim of this study was to investigate the association of DLG5 and SLC22A5 gene polymorphisms with the onset of Crohn's disease (CD) in a Malaysian cohort.
    Matched MeSH terms: Crohn Disease/ethnology*; Crohn Disease/genetics*; Genetic Predisposition to Disease/ethnology; Genetic Predisposition to Disease/genetics
  4. Goh KJ, Tian S, Shahrizaila N, Ng CW, Tan CT
    Amyotroph Lateral Scler, 2011 Mar;12(2):124-9.
    PMID: 21039118 DOI: 10.3109/17482968.2010.527986
    Our objective was to determine the survival and prognostic factors of motor neuron disease (MND) in a multi-ethnic cohort of Malaysian patients. All patients seen at a university medical centre between January 2000 and December 2009 had their case records reviewed for demographic, clinical and follow-up data. Mortality data, if unavailable from records, were obtained by telephone interview of relatives or from the national mortality registry. Of the 73 patients, 64.4% were Chinese, 19.2% Malays and 16.4% Indians. Male: female ratio was 1.43: 1. Mean age at onset was 51.5 + 11.3 years. Onset was spinal in 75.3% and bulbar in 24.7% of the patients; 94.5% were ALS and 5.5% were progressive muscular atrophy (PMA). Overall median survival was 44.9 + 5.8 months. Ethnic Indians had shorter interval from symptom onset to diagnosis and shorter median survival compared to non-Indians. On Cox proportional hazards analysis, poor prognostic factors were bulbar onset, shorter interval from symptom onset to diagnosis and worse functional score at presentation. In conclusion, age of onset and median survival duration are similar to previous reports in Asians. Clinical features and prognostic factors are similar to other populations. In our cohort, ethnic Indians had more rapid disease course accounting for their shorter survival.
    Matched MeSH terms: Motor Neuron Disease/diagnosis*; Motor Neuron Disease/ethnology*; Motor Neuron Disease/mortality*; Motor Neuron Disease/epidemiology; Disease Progression
  5. Berhanu A, Ideris A, Omar AR, Bejo MH
    Virol J, 2010;7:183.
    PMID: 20691110 DOI: 10.1186/1743-422X-7-183
    Newcastle disease (ND), caused by Newcastle disease virus (NDV), is a highly contagious disease of birds and has been one of the major causes of economic losses in the poultry industry. Despite routine vaccination programs, sporadic cases have occasionally occurred in the country and remain a constant threat to commercial poultry. Hence, the present study was aimed to characterize NDV isolates obtained from clinical cases in various locations of Malaysia between 2004 and 2007 based on sequence and phylogenetic analysis of partial F gene and C-terminus extension length of HN gene.
    Matched MeSH terms: Newcastle Disease/virology*; Newcastle disease virus/classification; Newcastle disease virus/genetics*; Newcastle disease virus/isolation & purification*
  6. Zain SM, Mohamed Z, Pirmohamed M, Tan HL, Alshawsh MA, Mahadeva S, et al.
    Sci Rep, 2015 Aug 21;5:13306.
    PMID: 26293807 DOI: 10.1038/srep13306
    A recent genome-wide copy number (CNV) scan identified a 13q12.11 duplication in the exportin-4 (XPO4) gene to be associated with non-alcoholic steatohepatitis (NASH). We sought to confirm the finding in a larger cohort and to assess the serum XPO4 pattern in a broad spectrum of non-alcoholic fatty liver disease (NAFLD) cases. We analysed 249 NAFLD patients and 232 matched controls using TaqMan assay and serum XPO4 was measured. Copy number distribution was as follows: copy number neutral (NAFLD: 53.8%, controls: 68.6%), copy number losses (NAFLD: 13.3%, controls: 12.9%), copy number gains (NAFLD: 32.9%, controls: 18.5%). CNV gain was significantly associated with a greater risk of NAFLD (adjusted OR 2.22, 95% CI 1.42-3.46, P = 0.0004) and NASH (adjusted OR 2.33, 95% CI 1.47-3.68, P = 0.0003). Interestingly, subjects carrying extra copy number showed significantly higher serum ALT and triglyceride (P 
    Matched MeSH terms: Genetic Predisposition to Disease*; Non-alcoholic Fatty Liver Disease/blood; Non-alcoholic Fatty Liver Disease/genetics*; Non-alcoholic Fatty Liver Disease/pathology*
  7. Ahmed RH, Huri HZ, Al-Hamodi Z, Salem SD, Al-Absi B, Muniandy S
    PLoS One, 2016;11(4):e0154369.
    PMID: 27111895 DOI: 10.1371/journal.pone.0154369
    BACKGROUND: Genetic polymorphisms of the Dipeptidyl Peptidase 4 (DPP4) gene may play a role in the etiology of type 2 diabetes mellitus (T2DM). This study aimed to investigate the possible association of single nucleotide polymorphisms (SNPs) of the DPP4 gene in Malaysian subjects with T2DM and evaluated whether they had an effect on the serum levels of soluble dipeptidyl peptidase 4 (sDPP-IV).

    METHOD: Ten DPP4 SNPs were genotyped by TaqMan genotyping assays in 314 subjects with T2DM and 235 controls. Of these, 71 metabolic syndrome (MetS) subjects were excluded from subsequent analysis. The odds ratios (ORs) and their 95% confidence interval (CIs) were calculated using multiple logistic regression for the association between the SNPs of DPP4 and T2DM. In addition, the serum levels of sDPP-IV were investigated to evaluate the association of the SNPs of DPP4 with the sDPP-IV levels.

    RESULTS: Dominant, recessive, and additive genetic models were employed to test the association of DPP4 polymorphisms with T2DM, after adjusting for age, race, gender and BMI. The rs12617656 was associated with T2DM in Malaysian subjects in the recessive genetic model (OR = 1.98, p = 0.006), dominant model (OR = 1.95, p = 0.008), and additive model (OR = 1.63, p = 0.001). This association was more pronounced among Malaysian Indians, recessive (OR = 3.21, p = 0.019), dominant OR = 3.72, p = 0.003) and additive model (OR = 2.29, p = 0.0009). The additive genetic model showed that DPP4 rs4664443 and rs7633162 polymorphisms were associated with T2DM (OR = 1.53, p = 0.039), and (OR = 1.42, p = 0.020), respectively. In addition, the rs4664443 G>A polymorphism was associated with increased sDPP-IV levels (p = 0.042) in T2DM subjects.

    CONCLUSIONS: DPP4 polymorphisms were associated with T2DM in Malaysian subjects, and linked to variations in sDPP-IV levels. In addition, these associations were more pronounced among Malaysian Indian subjects.

    Matched MeSH terms: Graves Disease/genetics; Graves Disease/epidemiology; Hashimoto Disease/genetics; Hashimoto Disease/epidemiology
  8. Chan LG, Parashar UD, Lye MS, Ong FG, Zaki SR, Alexander JP, et al.
    Clin Infect Dis, 2000 Sep;31(3):678-83.
    PMID: 11017815
    From April through June 1997, 29 previously healthy children aged <6 years (median, 1.5 years) in Sarawak, Malaysia, died of rapidly progressive cardiorespiratory failure during an outbreak of hand, foot, and mouth disease caused primarily by enterovirus 71 (EV71). The case children were hospitalized after a short illness (median duration, 2 days) that usually included fever (in 100% of case children), oral ulcers (66%), and extremity rashes (62%). The illness rapidly progressed to include seizures (28%), flaccid limb weakness (17%), or cardiopulmonary symptoms (of 24 children, 17 had chest radiographs showing pulmonary edema, and 24 had echocardiograms showing left ventricular dysfunction), resulting in cardiopulmonary arrest soon after hospitalization (median time, 9 h). Cardiac tissue from 10 patients showed normal myocardium, but central nervous system tissue from 5 patients showed inflammatory changes. Brain-stem specimens from 2 patients were available, and both specimens showed extensive neuronal degeneration, inflammation, and necrosis, suggesting that a central nervous system infection was responsible for the disease, with the cardiopulmonary dysfunction being neurogenic in origin. EV71 and possibly an adenovirus, other enteroviruses, or unknown cofactors are likely responsible for this rapidly fatal disease.
    Matched MeSH terms: Disease Outbreaks; Hand, Foot and Mouth Disease/complications; Hand, Foot and Mouth Disease/mortality*; Hand, Foot and Mouth Disease/epidemiology; Disease Progression
  9. Ozawa Y, Ong BL, An SH
    Rev. - Off. Int. Epizoot., 2001 Aug;20(2):605-13.
    PMID: 11548530
    Traceback systems in most countries of Asia are not well developed, as indicated by responses to a questionnaire by veterinary officials in thirteen countries. Marking of animals for traceback is practised only in a limited number of countries in specific areas or zones and for specific purposes only. In Malaysia, traceback has been undertaken by marking farm code tattoos on pigs. This enables the identification of the farm of origin of pigs found to be infected by Nipah virus in sero-surveillance programmes. The origin of the foot and mouth disease (FMD) virus that surfaced in the Republic of Korea in March 2000 was investigated through several epidemiological studies of suspected sources of contamination such as imported hay, yellow sand, milk collection trucks and feed delivery trucks. None of these studies gave results that indicated the origin of the FMD virus. The origin of the FMD virus that was recorded in Japan in March 2000 was also investigated in epidemiological studies; in this case, imported wheat straw was incriminated as the most likely source of infection. Comparative studies of the pathogenicities of FMD (type O) viruses isolated in Taipei China, the Republic of Korea and Japan, suggest that these viruses might have originated as vaccine strains used in a third country.
    Matched MeSH terms: Disease Outbreaks/veterinary*; Foot-and-Mouth Disease/epidemiology*; Foot-and-Mouth Disease/transmission; Foot-and-Mouth Disease/virology
  10. Chia YC, Ching SM, Lim HM
    J Hypertens, 2017 05;35 Suppl 1:S50-S56.
    PMID: 28350621 DOI: 10.1097/HJH.0000000000001333
    OBJECTIVES: The current study aims to determine the relationship of long-term visit-to-visit variability of SBP to cardiovascular disease (CVD) in a multiethnic primary care setting.
    METHOD: This is a retrospective study of a cohort of 807 hypertensive patients over a period of 10 years. Three-monthly clinic blood pressure readings were used to derive blood pressure variability (BPV), and CVD events were captured from patient records.
    RESULTS: Mean age at baseline was 57.2 ± 9.8 years with 63.3% being women. The BPV and mean SBP over 10 years were 14.7 ± 3.5 and 142 ± 8 mmHg, respectively. Prevalence of cardiovascular event was 13%. In multivariate logistic regression analysis, BPV was the predictor of CVD events, whereas the mean SBP was not independently associated with cardiovascular events in this population. Those with lower SBP and lower BPV had fewer cardiovascular events than those with the same low mean SBP but higher BPV (10.5 versus 12.8%). Similarly those with higher mean SBP but lower BPV also had fewer cardiovascular events than those with the same high mean and higher BPV (11.6 versus 16.7%). Other variables like being men, diabetes and Indian compared with Chinese are more likely to be associated with cardiovascular events.
    CONCLUSION: BPV is associated with an increase in CVD events even in those who have achieved lower mean SBP. Thus, we should prioritize not only control of SBP levels but also BPV to reduce CVD events further.
    Matched MeSH terms: Coronary Disease/ethnology; Coronary Disease/epidemiology*; Peripheral Arterial Disease/ethnology; Peripheral Arterial Disease/epidemiology*
  11. Gimeno IM, Cortes AL, Faiz N, Villalobos T, Badillo H, Barbosa T
    Avian Dis, 2016 09;60(3):662-8.
    PMID: 27610727 DOI: 10.1637/11415-040116-Reg.1
    Herpesvirus of turkeys (HVT) has been successfully used as a Marek's disease (MD) vaccine for more than 40 yr. Either alone (broiler chickens) or in combination with vaccines of other serotypes (broilers, broiler breeders, and layers), HVT is used worldwide. In recent years, several vector vaccines based on HVT (rHVT) have been developed. At present, there are both conventional HVT and rHVTs in the market, and it is unknown if all of them confer the same level of protection against MD. The objective of this study was to further characterize the protection conferred by two conventional HVTs (HVT-A and HVT-B) and three recombinant HVTs (rHVT-B, rHVT-C, and rHVT-D) against MD in broiler chickens. In a first study we evaluated the efficacy of two conventional HVTs (HVT-A and HVT-B) administered at different doses (475, 1500, and 4000 PFU) at day of age on the ability to protect against an early challenge with very virulent plus strain 645. In a second experiment we evaluated the protection ability of several HVTs (both conventional and recombinant) when administered in ovo at a dose of 1500 PFU using the same challenge model. Our results show that each HVT product is unique, regardless of being conventional or recombinant, in their ability to protect against MD and might require different PFUs to achieve its maximum efficacy. In Experiment 1, HVT-A at 4000 PFU conferred higher protection (protection index [PI] = 63) than any of the other vaccine protocols (PI ranging from 36 to 47). In Experiment 2, significant differences were found among vaccine protocols with PI varying from 66 (HVT-A) to 15 (rHVT-D). Our results show that each HVT is unique and age at vaccination and vaccine dose greatly affected vaccine efficacy. Furthermore, they highlight the need of following manufacturer's recommendations.
    Matched MeSH terms: Marek Disease/prevention & control*; Marek Disease/virology; Marek Disease Vaccines/administration & dosage; Marek Disease Vaccines/pharmacology*
  12. Sivanandy P, Zi Xien F, Woon Kit L, Tze Wei Y, Hui En K, Chia Lynn L
    J Infect Public Health, 2018 09 10;12(2):153-158.
    PMID: 30213468 DOI: 10.1016/j.jiph.2018.08.005
    The H7N9 subtype of avian influenza is an enzootic and airborne virus which caused an influenza outbreak in China. Infected individuals mostly worked with poultry, suggesting H7N9 virus-infected poultry as the primary source of human infection. Significantly increased levels of proinflammatory mediators (chemokines, cytokines) during virus infection could hamper the immune system and aggravate the infection. Severe cases are marked by fulminant pneumonia, acute respiratory distress syndrome (ARDS) and encephalopathy. Left untreated, the condition may rapidly progress to multi-organ failure and death. Reverse transcription polymerase chain reaction (rRT-PCR) is the gold standard diagnostic test for H7N9 avian influenza. Use of neurominidase inhibitor antivirals remain the main treatment. New antivirals are developed to counteract neurominidase inhibitor resistance H7N9 viral strains. Corticosteroid use in viral pneumonia may provoke mortality and longer viral shedding time. Subjects at high risk of contracting avian influenza H7N9 infection are recommended to receive annual seasonal influenza vaccination.
    Matched MeSH terms: Disease Outbreaks*; Disease Transmission, Infectious/prevention & control; Disease Management*
  13. Ng CF, Tiau PW, Tan HJ, Norlinah MI
    J R Coll Physicians Edinb, 2019 Mar;49(1):37-39.
    PMID: 30838990 DOI: 10.4997/JRCPE.2019.108
    Levodopa is the most effective medical treatment for Parkinson's disease (PD) to date. As dopamine is known to increase cardiac inotropism and vasomotor tone, peripheral dopamine decarboxylase inhibitor is coadministered to suppress the peripheral conversion of levodopa to dopamine. Levodopa poses potential cardiovascular risks, thus its use in patients with existing coronary artery disease needs to be carefully monitored. We report a case of an elderly male with newly diagnosed PD who developed non-ST-elevation myocardial infarction following levodopa (Madopar) initiation.
    Matched MeSH terms: Coronary Artery Disease/complications*; Coronary Artery Disease/diagnosis; Parkinson Disease/complications; Parkinson Disease/drug therapy*
  14. Eslam M, Alkhouri N, Vajro P, Baumann U, Weiss R, Socha P, et al.
    Lancet Gastroenterol Hepatol, 2021 Oct;6(10):864-873.
    PMID: 34364544 DOI: 10.1016/S2468-1253(21)00183-7
    The term non-alcoholic fatty liver disease (NAFLD), and its definition, have limitations for both adults and children. The definition is most problematic for children, for whom alcohol consumption is usually not a concern. This problematic definition has prompted a consensus to rename and redefine adult NAFLD associated with metabolic dysregulation to metabolic (dysfunction)-associated fatty liver disease (MAFLD). Similarities, distinctions, and differences exist in the causes, natural history, and prognosis of fatty liver diseases in children compared with adults. In this Viewpoint we, an international panel, propose an overarching framework for paediatric fatty liver diseases and an age-appropriate MAFLD definition based on sex and age percentiles. The framework recognises the possibility of other coexisting systemic fatty liver diseases in children. The new MAFLD diagnostic criteria provide paediatricians with a conceptual scaffold for disease diagnosis, risk stratification, and improved clinical and multidisciplinary care, and they align with a definition that is valid across the lifespan.
    Matched MeSH terms: Disease Progression; Non-alcoholic Fatty Liver Disease/diagnosis*; Non-alcoholic Fatty Liver Disease/etiology*; Non-alcoholic Fatty Liver Disease/epidemiology; Non-alcoholic Fatty Liver Disease/pathology
  15. Jha NK, Sharma A, Jha SK, Ojha S, Chellappan DK, Gupta G, et al.
    Open Biol, 2020 Dec;10(12):200286.
    PMID: 33352062 DOI: 10.1098/rsob.200286
    Excessive exposure to toxic substances or chemicals in the environment and various pathogens, including viruses and bacteria, is associated with the onset of numerous brain abnormalities. Among them, pathogens, specifically viruses, elicit persistent inflammation that plays a major role in Alzheimer's disease (AD) as well as dementia. AD is the most common brain disorder that affects thought, speech, memory and ability to execute daily routines. It is also manifested by progressive synaptic impairment and neurodegeneration, which eventually leads to dementia following the accumulation of Aβ and hyperphosphorylated Tau. Numerous factors contribute to the pathogenesis of AD, including neuroinflammation associated with pathogens, and specifically viruses. The human immunodeficiency virus (HIV) is often linked with HIV-associated neurocognitive disorders (HAND) following permeation through the blood-brain barrier (BBB) and induction of persistent neuroinflammation. Further, HIV infections also exhibited the ability to modulate numerous AD-associated factors such as BBB regulators, members of stress-related pathways as well as the amyloid and Tau pathways that lead to the formation of amyloid plaques or neurofibrillary tangles accumulation. Studies regarding the role of HIV in HAND and AD are still in infancy, and potential link or mechanism between both is not yet established. Thus, in the present article, we attempt to discuss various molecular mechanisms that contribute to the basic understanding of the role of HIV-associated neuroinflammation in AD and HAND. Further, using numerous growth factors and drugs, we also present possible therapeutic strategies to curb the neuroinflammatory changes and its associated sequels.
    Matched MeSH terms: Alzheimer Disease/diagnosis; Alzheimer Disease/etiology; Disease Susceptibility*; Disease Management
  16. Firouzamandi M, Moeini H, Hosseini SD, Bejo MH, Omar AR, Mehrbod P, et al.
    Int J Nanomedicine, 2016;11:259-67.
    PMID: 26834470 DOI: 10.2147/IJN.S92225
    Plasmid DNA (pDNA)-based vaccines have emerged as effective subunit vaccines against viral and bacterial pathogens. In this study, a DNA vaccine, namely plasmid internal ribosome entry site-HN/F, was applied in ovo against Newcastle disease (ND). Vaccination was carried out using the DNA vaccine alone or as a mixture of the pDNA and dextran-spermine (D-SPM), a nanoparticle used for pDNA delivery. The results showed that in ovo vaccination with 40 μg pDNA/egg alone induced high levels of antibody titer (P<0.05) in specific pathogen-free (SPF) chickens at 3 and 4 weeks postvaccination compared to 2 weeks postvaccination. Hemagglutination inhibition (HI) titer was not significantly different between groups injected with 40 μg pDNA + 64 μg D-SPM and 40 μg pDNA at 4 weeks postvaccination (P>0.05). Higher antibody titer was observed in the group immunized with 40 μg pDNA/egg at 4 weeks postvaccination. The findings also showed that vaccination with 40 μg pDNA/egg alone was able to confer protection against Newcastle disease virus strain NDIBS002 in two out of seven SPF chickens. Although the chickens produced antibody titers 3 weeks after in ovo vaccination, it was not sufficient to provide complete protection to the chickens from lethal viral challenge. In addition, vaccination with pDNA/D-SPM complex did not induce high antibody titer when compared with naked pDNA. Therefore, it was concluded that DNA vaccination with plasmid internal ribosome entry site-HN/F can be suitable for in ovo application against ND, whereas D-SPM is not recommended for in ovo gene delivery.
    Matched MeSH terms: Newcastle Disease/genetics; Newcastle Disease/immunology; Newcastle Disease/prevention & control*; Newcastle disease virus/immunology
  17. Tan SW, Ideris A, Omar AR, Yusoff K, Hair-Bejo M
    J Virol Methods, 2009 Sep;160(1-2):149-56.
    PMID: 19447142 DOI: 10.1016/j.jviromet.2009.05.006
    SYBR Green I real-time PCR was developed for detection and differentiation of Newcastle disease virus (NDV). Primers based on the nucleocapsid (NP) gene were designed to detect specific sequence of velogenic strains and lentogenic/vaccine strains, respectively. The assay was developed and tested with NDV strains which were characterized previously. The velogenic strains were detected only by using velogenic-specific primers with a threshold cycle (C(t)) 18.19+/-3.63 and a melting temperature (T(m)) 86.0+/-0.28 degrees C. All the lentogenic/vaccine strains, in contrast, were detected only when lentogenic-specific primers were used, with the C(t) value 14.70+/-2.32 and T(m) 87.4+/-0.21 degrees C. The assay had a dynamic detection range which spans over a 5log(10) concentration range, 10(9)-10(5) copies of DNA plasmid/reaction. The velogenic and lentogenic amplifications showed high PCR efficiency of 100% and 104%, respectively. The velogenic and lentogenic amplifications were highly reproducible with assay variability 0.45+/-0.31% and 1.30+/-0.65%, respectively. The SYBR Green I real-time PCR assay detected successfully the virus from tissue samples and oral swabs collected from the velogenic and lentogenic NDV experimental infection, respectively. In addition, the assay detected and differentiated accurately NDV pathotypes from suspected field samples where the results were in good agreement with both virus isolation and analysis of the fusion (F) cleavage site sequence. The assay offers an attractive alternative method for the diagnosis of NDV.
    Matched MeSH terms: Newcastle Disease/diagnosis*; Newcastle Disease/virology; Newcastle disease virus/classification*; Newcastle disease virus/isolation & purification*
  18. Ramli N, Nair SR, Ramli NM, Lim SY
    Clin Radiol, 2015 May;70(5):555-64.
    PMID: 25752581 DOI: 10.1016/j.crad.2015.01.005
    The purpose of this review is to illustrate the differentiating features of multiple-system atrophy from Parkinson's disease at MRI. The various MRI sequences helpful in the differentiation will be discussed, including newer methods, such as diffusion tensor imaging, MR spectroscopy, and nuclear imaging.
    Matched MeSH terms: Parkinson Disease/diagnosis*
  19. Choi Y, Chang Y, Ryu S, Cho J, Rampal S, Zhang Y, et al.
    Heart, 2015 May;101(9):686-91.
    PMID: 25732752 DOI: 10.1136/heartjnl-2014-306663
    To investigate the association between regular coffee consumption and the prevalence of coronary artery calcium (CAC) in a large sample of young and middle-aged asymptomatic men and women.
    Matched MeSH terms: Coronary Artery Disease/epidemiology*
  20. Ashkani S, Rafii MY, Shabanimofrad M, Ghasemzadeh A, Ravanfar SA, Latif MA
    Crit Rev Biotechnol, 2016;36(2):353-67.
    PMID: 25394538 DOI: 10.3109/07388551.2014.961403
    Rice blast disease, which is caused by the fungal pathogen Magnaporthe oryzae, is a recurring problem in all rice-growing regions of the world. The use of resistance (R) genes in rice improvement breeding programmes has been considered to be one of the best options for crop protection and blast management. Alternatively, quantitative resistance conferred by quantitative trait loci (QTLs) is also a valuable resource for the improvement of rice disease resistance. In the past, intensive efforts have been made to identify major R-genes as well as QTLs for blast disease using molecular techniques. A review of bibliographic references shows over 100 blast resistance genes and a larger number of QTLs (∼500) that were mapped to the rice genome. Of the blast resistance genes, identified in different genotypes of rice, ∼22 have been cloned and characterized at the molecular level. In this review, we have summarized the reported rice blast resistance genes and QTLs for utilization in future molecular breeding programmes to introgress high-degree resistance or to pyramid R-genes in commercial cultivars that are susceptible to M. oryzae. The goal of this review is to provide an overview of the significant studies in order to update our understanding of the molecular progress on rice and M. oryzae. This information will assist rice breeders to improve the resistance to rice blast using marker-assisted selection which continues to be a priority for rice-breeding programmes.
    Matched MeSH terms: Disease Resistance/genetics*
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