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Biomedical subjects

A Ueki

Publications and source records attributed to A Ueki.

At least 91 records · Page 5Linked to original sources
PubMed1996

[Changes in symptoms after the great Hanshin Earthquake in patients with dementia].

Factors related to changes in symptoms after the great Hanshin Earthquake in patients with dementia were studied. Interviews were conducted with family members of thirty patients given the diagnosis of dementia at the Center for Elderly Dementia of Hyogo College of Medicine between August 1993 and December 1994. The earthquake occurred on January 17, 1995, and the interviews were conducted three months later. Patients were classified into two groups: Group 1: those whose symptoms changed after the earthquake (n = 13); Group 2: those whose symptoms did not change after the earthquake (n = 17). Symptoms were exacerbated within 1 week after the earthquake. The percentage of patients with mild dementia was higher in Group 1 than in Group 2. Scores on the Mini-Mental State examination and on Hasegawa's dementia scale were lower in Group 2 than in Group 1. On a modified GBS-scale, patients in Group 2 scored higher than those in Group 1 in impaired intellectual function and in reduced motivation, and they scored lower than those in Group 1 in impaired emotional function. CT scans showed that cortical atrophy and ventricular enlargement were greater in Group 2 than in Group 1. These findings suggest that after the earthquake symptoms became more severe in patients with mild dementia at an early stage, who have anxiety, irritability, and emotional lability.

Aged↗
PubMed1996

[The analysis of peripheral blood lymphocytes of patients with silicosis and effects of silica in vitro].

It is well known that patients with silicosis are frequently associated with hyperglobulinemia, RA or PSS. It is also suggested that silica can drive and activated the immune system. In this study, we intended to measure the percentage of CD4+CD45RA+ cells in the peripheral blood of patients with silicosis and to investigate whether silica can actually activate human lymphocytes in vitro or not. Peripheral blood from 45 patients with silicosis was stained with OKT4 and 2H4 monoclonal antibodies, and measured by FACS analysis at 1st day and also checked similarly after 6 days-incubation without patients' sera. The intracellular Ca++ level was also checked after incubation with the normal human lymphocytes with silica by FACS analysis, using Fluo3-AM. CD4+CD45RA+ T cells decreased significantly in number. One to 5 minutes after the incubation with silica, intracellular Ca++ level increased markedly, which means the activation of lymphocytes in vitro. These results revealed that silica can activate human lymphocytes in vitro, but the role in vivo remains to be clarified.

Aged↗
PubMed1995

N-Methyl-beta-carboline-3-carboxamide (FG 7142): An anxiogenic agent in cigarette smoke condensate and its mechanism of formation.

beta-Carboline-3-carboxylic acid methylamide (FG 7142), an anxiogenic agent has been found in cigarette smoke condensate, but not in the cigarette itself. When a cigarette, except its filter portion, was immersed in 20 ml of potassium phosphate buffer, pH 7.4, then heated at 60 degrees C for 2 days with or without presence of methylamine, FG 7142 was detected only in the mixture containing methylamine. Furthermore, when the mixtures of beta-carboline derivatives and various amounts of methylamine hydrochloride were heated at 60 degrees C for 5 days, FG 7142 was formed only in the mixtures containing methylamine and 1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-caroxylic acid (MTCA) or 1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid (TCCA). FG 7142 was also produced in the mixture of glucose, l-tryptophan and methylamine when heated at 200 degrees C in a dry condition. These observations suggest that FG 7142 is formed through the smoking process and that methylamine in cigarette smoke may play an important role in the formation of FG 7142.

Journal Article↗
PubMed1995

Genetic association of the very low density lipoprotein (VLDL) receptor gene with sporadic Alzheimer's disease.

A specific isoform of apolipoprotein E has been associated with the accelerated rate of disease expression of sporadic Alzheimer's disease (AD) and late-onset familial AD (FAD). An earlier age at onset has also been demonstrated in familial AD patients with mutations in the amyloid precursor protein (APP) gene (APP717 and APP670/671)13 carrying the APOE epsilon-4 allele compared to those who do not, but not in familial AD patients with APP692 or 693 mutations, or in chromosome 14-linked familial AD patients. Hypothesizing that receptors for apoE-containing lipoproteins act as a potential risk factor for AD, we performed an association study using a polymorphic triplet (CGG) repeat in the gene for the VLDL receptor (VLDL-R), a receptor for apoE-containing lipoproteins. The frequency of the 5-repeat allele was significantly higher in all of the Japanese sporadic AD patients (P < 0.02) than in the Japanese controls. Moreover, the odds ratio was significantly increased in the AD patients homozygous for the 5-repeat allele (OR = 2.1, 95% CI = [1.1-4.2]). Multiple logistic regression analysis reveals that the relative risk conferred by the presence of two copies of the 5-repeat allele and at least one copy of the APOE epsilon-4 allele is 8.7 (95% CI = [2.9-25.8]). Our results suggest that the VLDL-R gene is a susceptibility gene for AD.

Alleles↗
PubMed1995

Screening for mutations at codon 717 of the amyloid precursor protein gene in Alzheimer's disease.

Three kinds of missense mutation at codon 717 of amyloid precursor protein (APP) gene (Val --> Ile; Val --> Gly; Val --> Phe) were screened in 114 patients with familial and sporadic Alzheimer's disease (AD), using a rapid testing method for each Val --> Gly and Val --> Phe mutation and Goate's method for Val --> Ile mutation based on the polymerase chain reaction. Mutations were not found in the subjects, confirming earlier suggestions that these three mutations at codon 717 of APP gene account for only a small proportion of cases of not only familial AD but also sporadic AD.

Aged↗
PubMed1995

[Epidemiological study of the prognosis and relevant factors of demented patients].

One hundred twenty patients diagnosed as having dementia at the Center for Elderly Dementia in Hyogo College of Medicine, were recruited for this study to investigate the factors related to the prognosis of dementia. Patients were classified into the following two groups: those staying at home (group 1); those who died at home (group 2). The proportion of various dementias was almost equal in each group: vascular dementia, 30%; senile dementia of Alzheimer's type, 40%; mixed dementia, 20%; Alzheimer's disease, 10%. The average duration of disease in the two groups were not significantly different. The average age of onset in group 2 was higher than that in group 1. The rate of those with severe dementia was higher in group 2 than group 1. Those in group 2 scored less on the Mini-Mental State examination than those in group 1. Symptoms of dementia were assessed by the modified GBS-scale. In group 2, patients scored higher in impaired intellectual and motor functions. The CT findings suggested cortical atrophy, ventricular enlargement and periventricular lucency more often in group 2 than in group 1. Laboratory findings revealed that decrease in red blood cell count, hemoglobin, hematocrit and serum protein were more apparent in group 2 than group 1. It was considered that impaired motor functions, cortical atrophy, white matter lesions, anemia and malnutrition enhanced the probability of death. The study has confirmed that the prognosis of dementia is not only related to intellectual impairment but also deteriorated physical conditions such as motor dysfunction, anemia and malnutrition.

Aged↗
PubMed1994

On the plasticity of the cerebellar renin-angiotensin system: localization of components and effects of mechanical perturbation.

This study focuses on the renin-angiotensin system (RAS) in the cerebellar cortex and changes within this system after mechanically induced cerebellar injury. Using radioactive and non-radioactive in situ hybridization and immunocytochemistry angiotensinogen mRNA, angiotensinogen, angiotensin II and, for the first time, N-terminal angiotensin fragment (1-7) immunoreactivities, respectively, were demonstrated in the rat cerebellum. Angiotensinogen mRNA and angiotensinogen immunoreactivity (IR) were both present in glial cell populations of all layers, especially in the Purkinje and granular cell layers and within the cerebellar nuclei. Angiotensin II IR was demonstrated in glial cell populations in all layers using a monoclonal angiotensin II antibody, while with a polyclonal angiotensin II antiserum (Denise) some Purkinje cell bodies were labelled. After lesioning the cerebellar cortex mechanically by an injection cannula a strong increase in angiotensinogen gene expression as well as in angiotensin II and angiotensin (1-7) immunoreactivities were observed in the glial cell populations. Furthermore, putative Bergmann glial processes, as indicated from the morphological appearance became strongly angiotensin II and angiotensinogen immunoreactive in the region close to the mechanically induced lesion. It could inter alia be demonstrated for the first time using confocal laser microscopy of ANG II IR and GFAP IR that ANG II in vivo in the intact cerebellar cortex is present in astroglial processes in the molecular layer and presumably secreted into the extracellular space in form of small spheric bodies and/or taken up by other cell types. In contrast, the N-terminal fragment angiotensin (1-7) IR was restricted to the glial cell populations and appeared only after the lesion event. Thus, it is suggested that the cerebellar RAS shows marked changes in response to mechanically induced lesions. The expression of angiotensinogen as well as the production of angiotensinogen IR and angiotensin II like IR is even after mechanical lesion restricted to astrocytes, i.e., cerebellar astrocytes and putative Bergmann glial cells, and in case of immunoreactivities it spreads to the radially oriented Bergmann glial processes in the molecular layer.

Angiotensin I↗
PubMed1994

No allelic association between Parkinson's disease and dopamine D2, D3, and D4 receptor gene polymorphisms.

Parkinson's disease is thought to be caused by a combination of unknown environmental, genetic, and degenerative factors. Evidence from necropsy brain samples and pharmacokinetics suggests involvement of dopamine receptors in the pathogenesis or pathophysiology of Parkinson's disease. Genetic association studies between Parkinson's disease and dopamine D2, D3 and D4 receptor gene polymorphisms were conducted. The polymorphism was examined in 71 patients with Parkinson's disease and 90 controls. There were no significant differences between two groups in allele frequencies at the D2, D3, and D4 dopamine receptor loci. Our findings do not support the hypothesis that susceptibility to Parkinson's disease is associated with the dopamine receptor polymorphisms examined.

Adult↗
PubMed1994

Association of apolipoprotein E4 with sporadic Alzheimer's disease is more pronounced in early onset type.

Apolipoprotein E genotypes in 88 unrelated Japanese patients with NINCDS-ADRDA sporadic Alzheimer's disease (AD) were examined and compared with those of 93 healthy controls. Frequency of epsilon 4 allele was increased in patients with AD (31%) compared with controls (10%), as was reported previously. Individuals homozygous or heterozygous for the allele epsilon 4 had a 5.9-fold increased risk of AD. This tendency was more pronounced in early onset sporadic (= non-familial) type than late onset type. The relative risk was also greater for early onset type (RR = 11.7; 95% CI, 4.9-28.3) than late onset type (RR = 4.3; 95% CI, 2.1-8.8). Moreover, patients with homozygote for the allele epsilon 4 had a 14.7-fold increased risk of early onset sporadic AD (P < 0.005, chi 2 = 9.0, df = 1, 95% CI, 2.5-85.1). Our findings indicated that association of apolipoprotein epsilon 4 with sporadic Alzheimer's disease is more pronounced in early onset type than in late onset type.

Age of Onset↗
PubMed1994

Impairment in the acquisition of passive and active avoidance learning tasks due to bilateral entorhinal cortex lesions.

The relationship between the entorhinal cortex and learning behavior was examined. The initial stage of Alzheimer's disease has been shown to be characterized by neuropathological alteration in the entorhinal cortex, with the appearance of the greatest number of neuronal tangles and severe neuronal loss in comparison with other brain regions involved. This entorhinal cortex, because of its anatomical relationship to the hippocampus, may play a crucial role in memory formation. In this study, rats with bilateral ibotenic acid-induced lesions of the entorhinal cortices were tested for acquisition of passive and active avoidance learning tasks. These animals displayed no sensorimotor disturbances as shown by evaluation of locomotor activity and shock sensitivity. However, they did show impair acquisition of passive and active avoidance responses. On the other hand, when the lesions were induced after training, there was no extinction of the acquired passive and active avoidance responses. The results demonstrate the importance of the entorhinal cortex in learning acquisition and indicate that rats with partial neuronal loss in the entorhinal cortex may be a useful model for studying the memory disturbance of Alzheimer's disease.

Animals↗
PubMed1994

Candida albicans aspartic proteinase cleaves and inactivates human epidermal cysteine proteinase inhibitor, cystatin A.

It is known that the cysteine proteinase inhibitor, cystatin, has a defence function against exogenous pathogens. Human epidermal cysteine proteinase inhibitor, cystatin A, which is a member of the cystatin family, is localized in the upper epidermal layer. In this study, the relationship between cystatin A and Candida aspartic proteinase (CAP), a putative Candida virulence factor, was studied. CAP activity was not affected by human epidermal cystatin A, while 90% of cystatin A activity was lost after incubation with CAP for 12 h at 37 degrees C. Human epidermal cystatin A was cleaved into small peptides by CAP, and the released peptides had no cystatin activity. These results suggest that CAP may induce an imbalance between cysteine proteinase and its inhibitor in cutaneous Candida infectious lesions through the degradation and inactivation of epidermal cystatin A.

Amino Acid Sequence↗
PubMed1994

Polyclonal human T-cell activation by silicate in vitro.

Silica (SiO2) or related substances such as silicone ([-R2Si-O-]n), which is used in plastic surgery, or asbestos (e.g. chrysotile; 3MgO.2SiO2.H2O) have 'adjuvant effects'. In a study of scleroderma patients in Germany more than 78% had experienced exposure to silicate dust. T-cell receptor (TcR) V beta gene analysis on CD4- CD8- double-negative alpha beta T cells from scleroderma patients, using polymerase chain reaction (PCR), showed that certain V beta genes, V beta 5, V beta 7 and V beta 17, were predominantly expressed in the cells. We found that certain V beta repertoires, V beta 5.3 and V beta 6.7, were predominantly expressed on fractionated T cells with a high Ca2+ level that had been stimulated by chrysotile in vitro. The intracellular Ca2+ level in human peripheral blood mononuclear cells (PBMC) increased after incubation with silica or chrysotile. Interleukin-2 (IL-2) release from PMBC also rose significantly with chrysotile stimulation, but no change was observed when major histocompatibility complex (MHC) class II DP/DR positive cells were depleted. Therefore, our results support the possibility that silicate acts as a superantigen.

Adult↗
PubMed1993

A high frequency of apolipoprotein E4 isoprotein in Japanese patients with late-onset nonfamilial Alzheimer's disease.

Phenotypes of apolipoprotein E (apo E) were determined by the iso-electric focusing method in 42 Japanese patients with nonfamilial late-onset Alzheimer's disease (AD) and 96 age-matched controls without hyperlipidemia and/or diabetes. There was a striking difference in the distribution of apo E phenotypes between patients with AD and controls (P < 0.0001). Such a difference was mostly attributable to different frequencies of phenotypes E4/3 and E3/3. The apo E4/3 phenotype was detected in 24 (57.1%) of 42 patients with AD, more than six times oftener than in nine (9.4%) of 96 controls. In contrast, apo E3/3, which is the most common apo E phenotype in various ethnic groups, was detected in only 15 (35.7%) patients with AD. These results indicate a strong association between apo E4 isoprotein and Japanese late-onset nonfamilial AD, and that apo E4 is a possible risk factor for the development of this type of AD.

Adult↗
PubMed1993

The vigilance-promoting drug modafinil counteracts the reduction of tyrosine hydroxylase immunoreactivity and of dopamine stores in nigrostriatal dopamine neurons in the male rat after a partial transection of the dopamine pathway.

We studied the ability of the vigilance-promoting drug modafinil to modulate the anterograde and retrograde changes in tyrosine hydroxylase (TH) immunoreactivity and in dopamine (DA) stores in the nigro-neostriatal DA neurons, following a partial hemitransection of this ascending DA system, using a combined morphometrical, biochemical and behavioural analysis. Modafinil was given daily i.p. in doses of 10-100 mg/kg, starting 15 min after the lesion, and the partially hemitransected rats were killed 2 weeks later. Changes in TH-immunoreactive nerve cell bodies and nerve terminals induced by the partial hemitransection were studied in the substantia nigra and neostriatum in combination with image analysis. The substantia nigra and neostriatum were also subjected to biochemical analysis of DA, 3,4-dihydroxyphenylacetic acid and homovanillic acid levels. Modafinil treatment dose-dependently (10-100 mg/kg) counteracted the hemitransection-induced disappearance of nigral TH-immunoreactive nerve cell body profiles and neostriatal TH-immunoreactive nerve terminal profiles. A 2-week treatment with 100 mg/kg of modafinil also counteracted the hemitransection-induced depletion of DA stores in the neostriatum and the ventral midbrain. Moreover, the repeated daily treatment with modafinil (100 mg/kg) protected against the hemitransection-induced disappearance of striatal 5-hydroxytryptamine, 5-hydroxyindoleacetic acid and noradrenaline levels. Striatal DA function was analysed by studying apomorphine-induced (1 mg/kg, s.c.) ipsilateral rotational behaviour 4 and 11 days after the operation. A marked dose-dependent reduction of ipsilateral rotational behaviour was demonstrated after the daily modafinil treatment in the partially hemitransected rats. In another model involving unilateral nigral microinjections of 6-hydroxydopamine, acute (one single dose) modafinil (100 mg/kg) did not affect the contralateral rotational behaviour induced by apomorphine (0.05 mg/kg s.c.), when given 30 min before the apomorphine. Taken together, morphological, neurochemical and behavioural evidence has been obtained that anterograde and retrograde changes induced in the DA stores and TH immunoreactivity of the nigro-neostriatal DA neurons by a partial hemistransection are counteracted by modafinil in a dose dependent way with 100 mg/kg producing a significant protective action against impairment of DA transmission. The results of this study open up the possibility that modafinil may protect against the anterograde and retrograde degeneration of nigrostriatal DA neurons seen after mechanically induced injury.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗