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Articles by H Wong
Total Records ( 3 ) for H Wong
  J Tong , H Wong , M Guttman , L. C Ang , L. S Forno , M Shimadzu , A. H Rajput , M. D Muenter , S. J Kish , O Hornykiewicz and Y. Furukawa
 

-Synuclein is a major component of Lewy bodies and glial cytoplasmic inclusions, pathological hallmarks of idiopathic Parkinson's disease and multiple system atrophy, and it is assumed to be aetiologically involved in these conditions. However, the quantitative status of brain -synuclein in different Parkinsonian disorders is still unresolved and it is uncertain whether -synuclein accumulation is restricted to regions of pathology. We compared membrane-associated, sodium dodecyl sulfate-soluble -synuclein, both the full-length 17 kDa and high molecular weight species, by western blotting in autopsied brain of patients with Parkinson's disease (brainstem-predominant Lewy body disease: n = 9), multiple system atrophy (n = 11), progressive supranuclear palsy (n = 16), and of normal controls (n = 13). Brain of a patient with familial Parkinsonism-dementia due to -synuclein locus triplication (as positive control) showed increased membrane-associated, sodium dodecyl sulfate-soluble -synuclein levels with abundant high molecular weight immunoreactivity. In multiple system atrophy, a massive increase in 17 kDa membrane-associated, sodium dodecyl sulfate-soluble -synuclein was observed in highly pathologically affected regions, including putamen (+1760%, range +625–2900%), substantia nigra [+1000% (+356–1850%)], and white matter of internal capsule [+2210% (+430–6830%)] together with numerous high molecular weight species. Levels of 17 kDa membrane-associated, sodium dodecyl sulfate-soluble -synuclein were only modestly increased in less affected areas (cerebellar cortex, +95%; caudate, +30%; with both also showing numerous high molecular weight species) and were generally normal in cerebral cortices. In both Parkinson's disease and progressive supranuclear palsy, membrane-associated, sodium dodecyl sulfate-soluble -synuclein levels were normal in putamen and frontal cortex whereas a trend was observed for variably increased 17 kDa membrane-associated, sodium dodecyl sulfate-soluble -synuclein concentrations [+184% (–60% to +618%)] with additional high molecular weight species in Parkinson's disease substantia nigra. No obvious correlation was observed between nigral membrane-associated, sodium dodecyl sulfate-soluble -synuclein accumulation and Lewy body density in Parkinson's disease. Two progressive supranuclear palsy cases had membrane-associated, sodium dodecyl sulfate-soluble -synuclein accumulation in substantia nigra similar to multiple system atrophy. Several Parkinson's disease patients had very modest high molecular weight membrane-associated, sodium dodecyl sulfate-soluble -synuclein accumulation in putamen. Levels of 17-kDa membrane-associated, sodium dodecyl sulfate-soluble -synuclein were generally positively correlated with those of high molecular weight membrane-associated, sodium dodecyl sulfate-soluble -synuclein and there was a trend for a positive correlation between striatal dopamine loss and 17-kDa membrane-associated, sodium dodecyl sulfate-soluble -synuclein concentrations in multiple system atrophy. Brain membrane-associated, sodium dodecyl sulfate-soluble -synuclein accumulations in Parkinson's disease and multiple system atrophy are regionally specific, suggesting that these sporadic -synucleinopathies, unlike familial Parkinsonism-dementia, are not associated with a simple global over-expression of the protein. Despite a similar extent of dopamine depletion, the magnitude of brain membrane-associated, sodium dodecyl sulfate-soluble -synuclein changes is disease specific, with multiple system atrophy clearly having the most severe accumulation. Literature discrepancies on -synuclein status in ‘Parkinson's disease’ might be explained by inclusion of cases not having classic brainstem-predominant Lewy body disease and by variable -synuclein accumulation within this diagnostic classification.

  H Wong , R. C Wu , G Tomlinson , M Caesar , H Abrams , M. W Carter and D. Morra
  Background

The objective of this study is to determine the effect of day of the week, holiday, team admission and rotation schedules, individual attending physicians and their length of coverage on daily team discharge rates.

Methods

We conducted a retrospective analysis of the General Internal Medicine (GIM) inpatient service at our institution for years 2005 and 2006, which included 5088 patients under GIM care.

Results

Weekend discharge rate was more than 50% lower compared with reference rates whereas Friday rates were 24% higher. Holiday Monday discharge rates were 65% lower than regular Mondays, with an increase in pre-holiday discharge rates. Teams that were on-call or that were on call the next day had 15% higher discharge rates compared with reference whereas teams that were post-call had 20% lower rates. Individual attending physicians and length of attending coverage contributed small variations in discharge rates. Resident scheduling was not a significant predictor of discharge rates.

Conclusions

Day of the week and holidays followed by team organization and scheduling are significant predictors of daily variation in discharge rates. Introducing greater holiday and weekend capacity as well as reorganizing internal processes such as admitting and attending schedules may potentially optimize discharge rates.

  J Guan , H. L Zhao , L Baum , Y Sui , L He , H Wong , F. M. M Lai , P. C. Y Tong and J. C. N. Chan
 

Background. Diabetic nephropathy represents a heterogeneous group of renal pathologies that may be associated with genetic susceptibility. There have been clinical reports on the risk association of diabetic nephropathy with an apolipoprotein E (ApoE) exon 4 polymorphism although its correlations with renal histopathological changes have not been explored.

Methods. A total of 213 adult autopsies with type 2 diabetes and 111 non-diabetic control cases were analysed. Genomic DNA samples were obtained from spleen tissues. The ApoE genotype was determined by PCR-LDR analysis. Histopathological examination of kidney sections was performed in a subset of 51 diabetic and 111 control cases. ApoE protein expression in diabetic carriers with similar clinical status was examined by immunohistochemical staining.

Results. In type 2 diabetes, 2 carriers (P = 0.04; odds ratio = 5.42; 95% CI: 1.10–26.8) and 3/4 (P = 0.04; odds ratio = 22.5; 95% CI: 1.11–454.90) genotype carriers were more likely to have glomerular hypertrophy than were 3/3 carriers. The 2 carriers showed an increase in glomerular ApoE protein expression. A correlation between ApoE genotype and nodular glomerulosclerosis was not found.

Conclusions. Our findings confirm the risk association of the ApoE polymorphism with diabetic nephropathy in clinical studies and is the first study demonstrating the correlations between ApoE genotypes, protein expression and structural changes in diabetic nephropathy.

 
 
 
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