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Biomedical subjects

M Y Chung

Publications and source records attributed to M Y Chung.

At least 37 records · Page 2Linked to original sources
PubMed1995

Survey of public awareness, understanding, and attitudes toward epilepsy in Taiwan.

A survey of public awareness and understanding of and attitudes toward epilepsy was made in Taipei City and Chin-San Village, Taiwan in 1992. In a population sample of 2,610 adults, 87% had read or heard about epilepsy, 70% knew someone who had epilepsy, 56% had seen someone having a seizure, 18% would object to having their children associated with persons with epilepsy, 72% would object to having their children marry a person with epilepsy, 31% believed that epileptic persons should not be employed in jobs as other persons are, 7% believed that epilepsy was a form of insanity, 34% did not know the cause of epilepsy, 13% did not know what an epileptic attack was like, and 18% did not know what to recommend if their friends or relatives had epilepsy. Youth, higher education, and upper levels of employment were correlated with answers that were more favorable concerning epilepsy in all survey questions except for the question regarding marriage, for which the reverse was noted. The attitudes toward epilepsy disclosed by this study were more favorable than those detected in a similar survey conducted in Henan Province, China. The comparison suggests that the exposure to Western culture and socioeconomic system in Taiwan might have helped reduce the discrimination against epilepsy.

Age Factors↗
PubMed1994

Role of Ca2+ in alloxan-induced pancreatic beta-cell damage.

Pretreatment of rats with verapamil, a Ca(2+)-antagonist, completely prevented alloxan-induced hyperglycemia. Verapamil also abolished the inhibition of insulin secretion by alloxan and H2O2 in isolated rat pancreatic islets. H2O2 generation from alloxan was not affected by verapamil, but alloxan- and H2O2-induced DNA strand breaks were completely prevented. Treatment of beta-cells with alloxan and H2O2 caused elevation of cytosolic free Ca2+, and this increase of Ca2+ was also abolished by verapamil. These results suggest that alloxan-derived oxygen radicals may disturb intracellular Ca2+ homeostasis by increasing Ca2+ influx, which results in secondary reactions ultimately leading to DNA strand breaks and cytotoxicity of beta-cells.

Animals↗
PubMed1994

Identification and characterization of the gene causing type 1 spinocerebellar ataxia.

Spinocerebellar ataxia type 1 (SCA1) is a neurodegenerative disorder caused by expansion of a CAG trinucleotide repeat. In this study, we describe the identification and characterization of the gene harbouring this repeat. The SCA1 transcript is 10,660 bases and is transcribed from both the wild type and SCA1 alleles. The CAG repeat, coding for a polyglutamine tract, lies within the coding region. The gene spans 450 kb of genomic DNA and is organized in nine exons. The first seven fall in the 5' untranslated region and the last two contain the coding region, and a 7,277 basepairs 3' untranslated region. The first four non-coding exons undergo alternative splicing in several tissues. These features suggest that the transcriptional and translational regulation of ataxin-1, the SCA1 encoded protein, may be complex.

Alternative Splicing↗
PubMed1994

Extracranial carotid atherosclerosis and vascular risk factors in different types of ischemic stroke in Taiwan.

BACKGROUND AND PURPOSE: The clinical patterns of stroke and the angiographic distribution of cerebral atherosclerosis in Chinese people are different from those in whites. Studies relating carotid atherosclerosis and vascular risk factors to various types of stroke in Chinese people are lacking. METHODS: Based on clinical information, we separated 367 stroke patients living in Taiwan into four subgroups: cortical infarction (CI), subcortical infarction (SCI), vertebrobasilar artery infarction (VBAI), and cardioembolic infarction (CEI). We assessed the extent and severity of extracranial carotid artery atherosclerosis in different types of ischemic stroke using duplex ultrasonography. Vascular risk factors and carotid atherosclerosis were then correlated with each subgroup of ischemic stroke. RESULTS: Our data revealed that 32% of the CI subgroup, 3% of the SCI subgroup, 7% of the VBAI subgroup, and 21% of the CEI subgroup possessed severe carotid stenosis (> or = 50% stenosis or occlusion). The extent of atherosclerosis of extracranial carotid arteries, measured by plaque score, was also more severe in the CI subgroup than in the other subgroups. Diabetes mellitus was more frequent in the CI subgroup. Cardiomegaly and left ventricular hypertrophy were more commonly seen in the CEI subgroup. The VBAI subgroup was younger than the other subgroups. There were no differences in hypertension, prior stroke, alcohol intake, or serum levels of glucose, uric acid, hematocrit, lipids, and lipoproteins among the subgroups. CONCLUSIONS: Of the Chinese patients living in Taiwan, the extent and severity of extracranial carotid artery atherosclerosis were more prominent in patients with CI than in patients with other types of ischemic stroke. In Chinese patients with CI, severe carotid stenosis is not uncommon; in Chinese patients with SCI, however, the frequency of carotid stenosis is quite low.

Age Factors↗
PubMed1994

Adult Fanconi syndrome with proximal muscle weakness and hypophosphatemic osteomalacia: report of a case.

A 42-year-old female presented with progressive proximal muscle weakness, generalized hyperreflexia, marked bone pain, severe lumbago and knee arthralgia. Electromyographic study showed short-duration (5-10 msec), variable amplitude (200-2500 microV) polyphasic potentials. A muscle biopsy specimen revealed non-specific type II fiber atrophy. After a comprehensive laboratory work-up, adult Fanconi syndrome was diagnosed. The patient's symptoms, including bone pain and proximal muscle weakness, were relieved after a six-week supplement of tricalcium phosphate, vitamin D3 and sodium bicarbonate. The hyperreflexia also became less brisk.

Adult↗
PubMed1994

Molecular and clinical correlations in spinocerebellar ataxia type I: evidence for familial effects on the age at onset.

The spinocerebellar ataxias are a group of debilitating neurodegenerative diseases for which a clinical classification system has proved unreliable. We have recently isolated the gene for spinocerebellar ataxia type 1 (SCA1) and have shown that the disease is caused by an expanded, unstable, CAG trinucleotide repeat within an expressed gene. Normal alleles have a size range of 19-36 repeats, while SCA1 alleles have 42-81 repeats. In this study, we examined the frequency and variability of the SCA1 repeat expansion in 87 kindreds with diverse ethnic backgrounds and dominantly inherited ataxia. All nine families for which linkage to the SCA1 region of 6p had previously been established showed repeat expansion, while 3 of the remaining 78 showed a similar abnormality. For 113 patients from the families with repeat expansion, inverse correlations between CAG repeat size and both age at onset and disease duration were observed. Repeat size accounted for 66% of the variation in age at onset in these patients. After correction for repeat size, interfamilial differences in age at onset remained significant, suggesting that additional genetic factors affect the expression of the SCA1 gene product.

Adolescent↗
PubMed1993

Mapping and cloning of the critical region for the spinocerebellar ataxia type 1 gene (SCA1) in a yeast artificial chromosome contig spanning 1.2 Mb.

The gene responsible for spinocerebellar ataxia type 1 (SCA1) has been localized to a 6.7-cM region between the centromeric marker D6S109 and the telomeric marker D6S89. We screened two yeast artificial chromosome (YAC) libraries using sequence-tagged sites at D6S89 and at newly identified markers in 6p22-p23. Fifty YAC clones were identified and 34 insert termini were isolated from some of these YACs for detailed overlap mapping and long-range restriction analysis. A large YAC contig estimated to span 2.5 Mb was developed and genetic analysis in five large SCA1 kindreds using highly informative dinucleotide repeat polymorphisms mapped to this contig allowed the identification of D6S274 as the closest centromeric flanking marker for SCA1. Long-range restriction analysis determined the size for the critical SCA1 region, as defined by the two flanking markers D6S274 and D6S89, to be 1.2 Mb. This region is spanned by a minimum set of four nonchimeric YAC clones. The development of a 2.5-Mb YAC contig in 6p22-p23 provides valuable reagents for characterization of this genomic region and for the cloning of the SCA1 gene.

Animals↗
PubMed1993

Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1.

Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant disorder characterized by neurodegeneration of the cerebellum, spinal cord and brainstem. A 1.2-Megabase stretch of DNA from the short arm of chromosome 6 containing the SCA1 locus was isolated in a yeast artificial chromosome contig and subcloned into cosmids. A highly polymorphic CAG repeat was identified in this region and was found to be unstable and expanded in individuals with SCA1. There is a direct correlation between the size of the (CAG)n repeat expansion and the age-of-onset of SCA1, with larger alleles occurring in juvenile cases. We also show that the repeat is present in a 10 kilobase mRNA transcript. SCA1 is therefore the fifth genetic disorder to display a mutational mechanism involving an unstable trinucleotide repeat.

Base Sequence↗
PubMed1993

Evidence for a mechanism predisposing to intergenerational CAG repeat instability in spinocerebellar ataxia type I.

Spinocerebellar ataxia type I (SCAI) is an autosomal dominant neurodegenerative disease caused by the expansion of a CAG trinucleotide repeat on chromosome 6p. Normal alleles range from 19-36 repeats while SCA1 alleles contain 43-81 repeats. We now show that in 63% of paternal transmissions, an increase in repeat number is observed, whereas 69% of maternal transmissions showed no change or a decrease in repeat number. Sequence analysis of the repeat from 126 chromosomes reveals an interrupted repeat configuration in 98% of the unexpanded alleles but a contiguous repeat (CAG)n configuration in 30 expanded alleles from seven SCA1 families. This indicates that the repeat instability in SCA1 is more complex than a simple variation in repeat number and that the loss of an interruption predisposes the SCA1 (CAG)n to expansion.

Base Sequence↗
PubMed1993

Regional differences in the levels of biogenic amines and their metabolites in rat brain after tricyclic antidepressant treatments.

Changes in the levels of biogenic amines in different brain regions and the cerebrospinal fluid in rats were measured after acute or chronic treatment with tricyclic antidepressants. After single or 3 weeks' treatment with imipramine or desipramine, blocks of tissues were obtained from seven regions of the brain (frontal cortex, corpus striatum, hippocampus, thalamus, hypothalamus, substantia nigra and cerebellum) immediately after collection of the cerebrospinal fluid (CSF) from the cisterna magna. The concentrations of biogenic amines and their metabolites (norepinephrine, epinephrine, dopamine, 5-hydroxytryptamine (5-HT), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA)) in brain tissues and the CSF were measured using the high performance liquid chromatography-electrochemical detection system (HPLC-ECD). Treatment with desipramine or imipramine caused major alterations in the concentrations of central norepinephrine or 5-HT and its metabolite, respectively. Brain regional responses were variable according to the kind of tricyclic antidepressants and the duration of treatment. It is noteworthy that chronic treatment with both desipramine and imipramine caused altered hippocampal concentrations of norepinephrine and/or 5-HT and its metabolites. Striatal DOPAC concentrations were also changed after acute or chronic treatment with both drugs. These results suggest that tricyclic antidepressants altered neurotransmission according to the brain region, and the hippocampal norepinephrine and 5-HT and/or the striatal dopamine may have a significant role for the expression of antidepressant action of tricyclic antidepressants.

Animals↗
PubMed1992

Determination of serum catalase activity on a centrifugal analyzer by an NADP/NADPH coupled enzyme reaction system.

We developed a simple, kinetic method for the determination of catalase activity in which i) the enzyme catalyzes the peroxidation of ethanol by hydrogen peroxide to acetaldehyde and water, and ii) the acetaldehyde so formed is rapidly oxidized to acetic acid and NADPH by the addition of an excess of NADP+ and aldehyde dehydrogenase. The rate of NADPH production was monitored at 340 nm in a COBAS centrifugal analyzer. The reaction was linear to 800 U/L or a delta A of 0.020/min. Using human serum pools containing 80 and 460 U/L of peroxidase activity, the within-run coefficients of variation (CV) were 1.9 and 1.3%, respectively. Between-run CV values were 5% for both pools. The reference range for sera from 72 males and 52 females was 23 to 158 U/L (mean + 2 SD) by log normal transformation. The activity in red cells was 600 U/g hemoglobin but did not change the reference range appreciably provided that serum without visible hemolysis was used. Preliminary observations on sera from nine patients with various pancreatic disorders showed a poor correlation between the activities of catalase (peroxidase) and amylase in serum. The reasons for this discrepancy are under investigation.

Aldehyde Dehydrogenase↗
PubMed1991

A clinical study of stress fractures in sports activities.

One hundred thirty-one patients with 169 stress fractures were treated between January 1984 and January 1990. The highest incidence was in teenage girls (25.5%), and the predominant sites were tibia (31.5%) and femur (12.5%). The mean interval between the start of hard training and the onset of symptoms was 2.7 months and the mean amount of increased activities was 93.7%. Volleyball (24.3%) and running (17.3%) had the majority of incidents, and 95 (72.5%) patients were professional athletes. Radionuclide bone scans were needed in 61 (46.6%) patients and 16 (12.2%) showed multiple lesions. Asymptomatic stress fractures were found in 12 (9.2%) patients, and only five showed recurrence at the other sites. Eleven (6.5%) cases were treated operatively, and involved the tarsal navicular (2.9%) and femur (2.4%).

Adolescent↗
PubMed1990

[Progressive supranuclear palsy: clinical report on 7 cases and review of literature].

Progressive supranuclear palsy is sufficiently rare and difficult to diagnose that it escaped clinical recognition until 1964, when Steele, Richardson, and Olszewski clarified it as a pathologic entity. From January 1981 to June 1989, 7 patients who fulfilled the Golbe's criteria of progressive supranuclear palsy were admitted to the neurological department of National Taiwan University Hospital. The mean age at onset was 60 years (range: 53-69 years), and the mean age at diagnosis was 63 years), and the mean age at diagnosis was 63 years (range: 55-71 years). The study failed to identify any specific risk factors associated with progressive supranuclear palsy. Unsteady gait, vertical gaze palsy, pseudobulbar palsy, parkinsonian features and dementia were noted in all cases. The brain computed tomography revealed mild cortical atrophy and ventricular dilatation in 5 patients. Additionally, electroencephalography revealed diffuse theta waves in 4 patients and temporal theta waves in 2 patients, but these findings were nonspecific. Nystagmograms were performed in 3 patients, and hypometric saccades were noted in all of these patients, and uninhibited neurogenic bladder was proven by cystometry in 2 of these patients. All patients were treated with levodopa, but none of the patients showed any beneficial effects. Two patients died of aspiration pneumonia; the average duration from onset to death was about 4 years.

Aged↗
PubMed1989

Vacor inhibits insulin release from islets in vitro.

It has been reported that Vacor, a rodenticide containing N-3-pyridylmethyl-N'-p-nitrophenyl urea, causes insulin-dependent diabetes mellitus. The pathomechanism of Vacor-induced diabetes mellitus has not been clarified yet. The effect of Vacor, therefore, was studied in terms of insulin release from isolated rat pancreatic islets. Vacor suppressed glucose-stimulated insulin release, but did not affect the insulin release induced by theophylline or 12-o-tetra-decanoylphorbol 13-acetate. It is suspected that the suppression of insulin release from pancreatic islets by Vacor may contribute to the pathogenesis of Vacor-induced diabetes mellitus and that this suppression might not be related to cAMP and C-kinase.

Animals↗
PubMed1989

Acute primidone intoxication: report of a case.

A case of acute primidone intoxication, due to overdose, was evaluated at National Taiwan University Hospital. Serial assessment of the clinical manifestations, electroencephalograms and serum levels of primidone and phenobarbital were made. From these data, we conclude that the toxic effects, such as depression of the central nervous system and dysequilibrium, are due mostly to primidone itself, rather than its metabolite, phenobarbital.

Adult↗