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Biomedical subjects

S Yamaguchi

Publications and source records attributed to S Yamaguchi.

At least 469 records · Page 26Linked to original sources
PubMed1997

Gastric corpus IL-8 concentration and neutrophil infiltration in duodenal ulcer patients.

BACKGROUND: The purpose of the present study was to examine the association between interleukin-8 (IL-8) in the gastric body due to Helicobacter pylori infection and histological gastritis, as well as elucidating the effect of acid secretion inhibitors on H. pylori associated body gastritis in duodenal ulcer patients. METHODS: Twenty H. pylori-negative patients, 20 H. pylori-positive patients with chronic gastritis without peptic ulceration, and 20 H. pylori-positive duodenal ulcer patients (DU) were studied. Four biopsy samples were taken, each from the greater curvature of the antrum and body of the stomach. Biopsies were histologically investigated by ELISA to determine the density of H. pylori, the degree of neutrophil infiltration and the IL-8 concentration in the mucosa. RESULTS: In the gastric mucosa of H. pylori-negative subjects, no IL-8 and hardly any neutrophil infiltration were observed. In contrast, enhanced IL-8 production and increased neutrophil infiltration were present in those infected with H. pylori. In H. pylori-positive patients, a significant correlation was observed between the IL-8 concentration and the degree of neutrophil infiltration, but no correlation was found in the body mucosa of those with DU. Twelve of 20 DU patients demonstrated hardly any neutrophil infiltration, despite the increased mucosal IL-8 content in the body. The administration of omeprazole in DU patients markedly increased mucosal neutrophil infiltration even though it did not cause any significant change in the H. pylori density and IL-8 concentration in the body. Although the effect of omeprazole was transient, a significant increase in neutrophil infiltration continued in comparison with the status before omeprazole administration in those subsequently undergoing maintenance treatment with H2-blockers. CONCLUSION: In H. pylori-positive chronic gastritis, IL-8 concentration is enhanced in the mucosa of the body, and is associated with increased neutrophil infiltration. However, in DU patients, despite increases in body IL-8 concentration, neutrophil infiltration is reduced and the gastritis may be localized in the antrum.

Adult↗
PubMed1997

Glycosaminoglycans in crystal-surface binding substances and their role in calcium oxalate crystal growth.

OBJECTIVE: To clarify the role of glycosaminoglycans (GAGs) in crystal-surface binding substances (CSBS) on the growth of calcium oxalate crystals in urine. MATERIALS AND METHODS: Urine samples (24 h) were collected from healthy men (aged 25-42 years) and CSBS were obtained from the pooled urine samples. The CSBS were digested with heparitinase or proteinase and the inhibition of crystal growth assessed before and after enzyme digestion. Anion-exchange chromatography and high-performance liquid chromatography (HPLC) were used to determine the types of GAGs contained in the CSBS. RESULTS: The inhibitory activity of CSBS on crystal growth decreased with concentration when digested with heparitinase or proteinase. HPLC showed that CSBS contained a small amount of dermatan sulphate and abundant heparan sulphate, both of which inhibited crystal growth. CONCLUSION: Both heparan sulphate and dermatan sulphate may inhibit calcium oxalate crystallization, the former being the predominant GAG in CSBS.

Adult↗
PubMed1997

A WD repeat protein controls the cell cycle and differentiation by negatively regulating Cdc2/B-type cyclin complexes.

In the fission yeast Schizosaccharomyces pombe, p34(cdc2) plays a central role controlling the cell cycle. We recently isolated a new gene named srw1(+), capable of encoding a WD repeat protein, as a multicopy suppressor of hyperactivated p34(cdc2). Cells lacking srw1(+) are sterile and defective in cell cycle controls. When starved for nitrogen source, they fail to effectively arrest in G1 and die of accelerated mitotic catastrophe if regulation of p34(cdc2)/Cdc13 by inhibitory tyrosine phosphorylation is compromised by partial inactivation of Wee1 kinase. Fertility is restored to the disruptant by deletion of Cig2 B-type cyclin or slight inactivation of p34(cdc2). srw1(+) shares functional similarity with rum1(+), having abilities to induce endoreplication and restore fertility to rum1 disruptants. In the srw1 disruptant, Cdc13 fails to be degraded when cells are starved for nitrogen. We conclude that Srw1 controls differentiation and cell cycling at least by negatively regulating Cig2- and Cdc13-associated p34(cdc2) and that one of its roles is to down-regulate the level of the mitotic cyclin particularly in nitrogen-poor environments.

Amino Acid Sequence↗
PubMed1997

Genomic and mutational analysis of the mitochondrial trifunctional protein beta-subunit (HADHB) gene in patients with trifunctional protein deficiency.

Mitochondrial trifunctional protein (TP), an enzyme of beta-oxidation, is a multienzyme complex composed of four molecules of the alpha-subunit (HADHA) containing the enoyl-CoA hydratase and 3-hydroxyacyl-CoA dehydrogenase domains and four molecules of the beta-subunit (HADHB) containing the 3-ketoacyl-CoA thiolase domain. An inborn error of this enzyme complex can cause sudden infant death syndrome, acute hepatic encephalopathy or liver failure, skeletal myopathy, or hypertrophic cardiomyopathy. TP deficiency is classified into two different biochemical phenotypes: one represents the existence of both subunits and the lack of only the 3-hydroxyacyl-CoA dehydrogenase activity and the other represents the absence of both subunits and the lack of all three TP activities, although their clinical features are similar. We have identified two Japanese patients with this disorder. Three enzyme activities of TP were undetectable in fibroblasts from these two patients. We detected two mutations in the HADHB gene from two Japanese patients, an exonic single T insertion which created a new cryptic 5' splice site and a G1331A transition (R411 K). Patient 1 was a compound heterozygote, while patient 2 was a homozygote of a G1331A transition.

Animals↗
PubMed1997

Effects of midazolam on contractions in smooth muscle of the rabbit mesenteric artery.

We investigated the undetermined effects of midazolam on agonist-induced contraction in vascular smooth muscle strips from the rabbit mesenteric resistance artery. Midazolam, in concentrations more than 10 microM, attenuated norepinephrine ([NE] 0.3-10 microM)-induced contractions in Krebs solution. The attenuating effect was more potent on the tonic and oscillatory responses than on the rapid phasic response. When voltage-operated Ca2+ channels (VOC) were blocked by nifedipine, midazolam, in concentrations more than 1 microM, attenuated both phasic and tonic responses. In Ca(2+)-free solution, midazolam, in concentrations more than 1 microM, attenuated NE-induced contractions, but not caffeine-induced contractions. When NE and caffeine were applied successively, midazolam attenuated NE-induced contractions, but enhanced caffeine-induced contractions. Because the attenuating effect of midazolam on NE-induced contractions in high K+, Ca(2+)-free solution were not different from the effect in normal Ca(2+)-free solution, the attenuating effects of midazolam could not have been induced via membrane hyperpolarization. These results indicate that midazolam attenuated the agonist-induced contractions by inhibition of Ca2+ influx occurring not only through VOC, but also through agonist-mediated Ca2+ channels and by the inhibition of Ca2+ release from intracellular store sites.

Adrenergic alpha-Agonists↗
PubMed1997

Characterization of the extracellular domain in vascular endothelial growth factor receptor-1 (Flt-1 tyrosine kinase).

Flt-1 tyrosine kinase, vascular endothelial growth factor (VEGF) receptor-1, binds VEGF and a new VEGF-related ligand, placenta growth factor, but KDR/Flk-1 (VEGF receptor-2) binds only VEGF. To characterize the functional regions in the Flt-1 extracellular domain such as the ligand binding region and the dimer formation of the receptor, we constructed a series of mutants of the Flt-1 extracellular domain as soluble forms in a baculovirus system. We found that a region carrying the N-terminal 1st to 3rd immunoglobulin (Ig)-like domains of Flt-1 binds both ligands with high affinity. However, for dimer formation of soluble Flt-1, a region further downstream in the Flt-1 extracellular domain was required. Mutant Flt-1 receptors expressed in COS cells confirmed the requirement of the 4th to 7th Ig region for the activation of Flt-1 tyrosine kinase. Soluble Flt-1 carrying the N-terminal 1st to 3rd Ig region suppressed VEGF-dependent endothelial proliferation in vitro to the same level as the larger forms of soluble Flt-1, suggesting that the binding of one soluble Flt-1 molecule to one subunit of the VEGF homodimer may be sufficient to block the VEGF activity.

Animals↗
PubMed1997

Studies of bronchial asthma induced by chironomid midges (Diptera) around a hypereutrophic lake in Japan.

There have been few reports on hypersensitivity to chironomid midges in bronchial asthmatic patients around the area of hypereutrophic natural lakes, which have been notorious as an environmental hazard due to the massive occurrence of adult chironomids during several periods of the year. Our study investigated IgE antibodies to chironomid midges in bronchial asthmatic patients around the Lake Suwa area in comparison with those of the Matsumoto area (control area). A total of 123 adult patients with bronchial asthma were investigated by measurement of IgE antibodies with extracts of three chironomid midges (Chironomus yoshimatsui, C. plumosus, and Tokunagayusurika akamusi), mite, and silkworm. In addition, in the allergy testing, 12 common inhalant antigens were used. Of 123 adult patients with bronchial asthma, 65 (52.8%) produced positive allergy tests. Thirty-three (50.8%) were positive to mite, 28 (43.1%) to silkworm, 11 (16.9%) to C. yoshimatsui, eight (12.3%) to C. plumosus, and three (4.6%) to T. akamusi. We compared our results with the previous reports. The number of positive tests to silkworm in the Lake Suwa area was higher than in other areas. However, C. plumosus and T. akamusi showed a lower number of positive reactions. We considered the lower positive number of C. plumosus and T. akamusi tests in the Lake Suwa area to be related to the advanced age of patients in this area. The chironomids are an important cause of asthma, together with mite and silkworm, in the Lake Suwa area, but affect old asthmatic patients less than asthmatic children.

Administration, Inhalation↗
PubMed1997

Assembly of the switch complex onto the MS ring complex of Salmonella typhimurium does not require any other flagellar proteins.

The cytoplasmic portion of the bacterial flagellum is thought to consist of at least two structural components: a switch complex and an export apparatus. These components seem to assemble around the MS ring complex, which is the first flagellar basal body substructure and is located in the cytoplasmic membrane. In order to elucidate the process of assembly of cytoplasmic substructures, the membrane localization of each component of the switch complex (FliG, FliM, and FliN) in various nonflagellated mutants was examined by immunoblotting. It was found that all these switch proteins require the MS ring protein FliF to associate with the cell membrane. FliG does not require FliM and FliN for this association, but FliM and FliN associate cooperatively with the membrane only through FliG. Furthermore, all three switch proteins were detected in membranes isolated from fliE, fliH, fliI, fliJ, fliO, fliP, fliQ, fliR, flhA, flhB, and flgJ mutants, indicating that the switch complex assembles on the MS ring complex without any other flagellar proteins involved in the early stage of flagellar assembly. The relationship between the switch complex and the export apparatus is discussed.

Antibodies, Bacterial↗
PubMed1997

An extreme clockwise switch bias mutation in fliG of Salmonella typhimurium and its suppression by slow-motile mutations in motA and motB.

Pseudorevertants (second-site suppressor mutants) were isolated from a set of parental mutants of Salmonella with defects in the flagellar switch genes fliG and fliM. Most of the suppressing mutations lay in flagellar region IIIb of the chromosome. One fliG mutant, SJW2811, gave rise to a large number of suppressor mutations in the motility genes motA and motB, which are in flagellar region II. SJW2811, which has a three-amino-acid deletion (delta Pro-Ala-Ala) at positions 169 to 171 of FliG, had an extreme clockwise motor bias that produced inverse smooth swimming (i.e., swimming by means of clockwise rotation of a hydrodynamically induced right-handed helical bundle), and formed Mot(-)-like colonies on semisolid medium. Unlike previously reported inverse-swimming mutants, it did not show a chemotactic response to serine, and it remained inverse even in a delta che background; thus, its switch is locked in the clockwise state. The location of the mutation further underscores the conclusion from a previous study of spontaneous missense mutants (V. M. Irikura, M. Kihara, S. Yamaguchi, H. Sockett, and R. M. Macnab, J. Bacteriol. 175:802-810, 1993) that a relatively localized region in the central part of the FliG sequence is critically important for switching. All of the second-site mutations in motA and motB caused some impairment of motility, both in the pseudorevertants and in a wild-type fliG background. The mechanism of suppression of the fliG mutation by the mot mutations is complex, involving destabilization of the right-handed flagellar bundle as a result of reduced motor speed. The mutations in the MotA and MotB sequences were clustered to a considerable degree as follows: in transmembrane helices 3 and 4 of MotA and the sole transmembrane helix of MotB, at helix-membrane interfaces, in the cytoplasmic domains of MotA, and in the vicinity of the peptidoglycan binding region of the periplasmic domain of MotB. The potential importance of Lys28 and Asp33 of the MotB sequence for proton delivery to the site of torque generation is discussed.

Amino Acid Sequence↗
PubMed1997

Decreased cortical glucose metabolism correlates with hippocampal atrophy in Alzheimer's disease as shown by MRI and PET.

OBJECTIVE: To investigate the relation between atrophy of the hippocampus and parahippocampal gyrus (the % hippocampal area) and cerebral metabolic rate for glucose (CMRGlc) in Alzheimer's disease. METHODS: 13 patients with probable Alzheimer's disease by NINCDS-ADRDA criteria (six men; seven women, mean age 71 years, mini mental state 13.8 (SD 4.6)) and age matched controls were studied. T1 weighted MRI (0.5T) images were used for evaluation of the hippocampal area. With a digitiser system, a percentage of the hippocampal area to the brain (the % hippocampal area) was calculated. Eight patients received another T1 weighted MRI (1.5T) for further evaluation of the minimum thickness of the hippocampus. Regional CMRGlc (rCMRGlc) was measured using PET and the FDG technique. RESULTS: The hippocampal area in patients with Alzheimer's disease was significantly lower than that of controls (P < 0.01). All the cortical rCMRGlc values in patients with Alzheimer's disease were lower than those of controls (P < 0.01). A significant correlation (P < 0.05) was found between the % hippocampal area and rCMRGlc in the temporal lobe, temporoparieto-occipital (TPO) region, and frontal lobe in Alzheimer's disease. There was a significant correlation between minimal hippocampal thickness and ipsilateral TPO metabolism on both sides. CONCLUSION: The ipsilateral correlation between hippocampal atrophy and decreased TPO metabolism in Alzheimer's disease suggests a functional relation and the asymmetries show that Alzheimer's disease is an asymmetric disease in its early stages.

Aged↗
PubMed1997

Analysis of bronchoalveolar lavage fluid in patients with chronic hepatitis C before and after treatment with interferon alpha.

BACKGROUND: Previous studies have shown that patients with idiopathic pulmonary fibrosis (IPF) were more likely to be seropositive for hepatitis C virus (HCV) than normal controls, and that patients with chronic hepatitis C treated with interferon alpha (IFN-alpha) sometimes developed pulmonary fibrosis. The possibility that HCV infection and/or treatment with IFN-alpha are involved in the pathogenesis of pulmonary fibrosis or alveolitis was investigated. METHODS: A prospective non-randomised study was performed in 13 healthy controls and in patients with chronic hepatitis C before (n = 13) and after (n = 10) treatment with IFN-alpha. Bronchoalveolar lavage (BAL) fluid cell counts, ratios and T cell subsets, and the concentrations of interleukin (IL)-1 beta, tumour necrosis factor(TNF)-alpha, and hepatocyte growth factor (HGF) were measured. RESULTS: Lymphocyte counts in the BAL fluid were significantly increased in both groups of patients (median (range) values: before treatment, 36.8 (1.5-226.0); after treatment, 16.2 (4.5-97.6)) compared with the normal controls (3.3 (0.5-32.3)). In the pretreatment group the activated T cell (HLA-Dr positive) count was also increased (51 (40-74)) compared with that in the normal controls (27 (4-52)), but after treatment it was decreased (40 (0-76)) compared with the pretreatment count. Administration of IFN-alpha did not affect these parameters. IL-1 beta, TNF-alpha, and HGF were not detected. CONCLUSIONS: These findings suggest that HCV infection is associated with increased counts of lymphocytes and neutrophils in BAL fluid and that treatment with IFN-alpha appears to alter lymphocyte surface markers.

Adult↗
PubMed1997

Effects of Y-24180, a long-acting and potent antagonist to platelet-activating factor, on immediate asthmatic response in guinea pigs.

The effect of Y-24180, a potent antagonist to-platelet-activating factor (PAF), was evaluated on the antigen-induced immediate asthmatic response (IAR) in actively sensitized guinea pigs that were pretreated with an antihistaminic agent, pyrilamine. Then, the effect was compared with that of other antiasthmatic agents. In a dose-dependent manner, Y-24180 (0.01-1 mg/kg, p.o.) suppressed the IAR, and WEB 2086 (0.1-10 mg/kg, p.o.), another PAF antagonist, also suppressed IAR in the same fashion as Y-24180. In contrast, AA-2414 (1-100 mg/kg,p.o.), a thromboxane A2 (TXA2) antagonist, was effective only at the beginning of the IAR and ONO-1078 (1-100 mg/kg, p.o.), a peptide leukotriene (pLT) antagonist, was effective only in the latter period, OKY-046, a TXA2 synthetase inhibitor, showed no significant suppression of the IAR at doses up to 100 mg/kg. Thus, PAF antagonists were more effective than the other agents tested in the present model for IAR. In a subsequent test, Y-24180 (1 mg/kg, p.o.) was confirmed to enhance the suppressive effects of theophylline (10 and 30 mg/kg, p.o.), procaterol (0.1 and 1 microgram/kg, i.v.), OKY-046 (100 mg/kg, p.o.) and ONO-1078 (100 mg/kg, p.o.) on the IAR. A combination of three agents, namely Y-24180 with OKY-046 and ONO-1078, completely suppressed the IAR. The results demonstrate that Y-24180 not only suppresses the IAR, but also enhances the suppressive effect of other antiasthmatic agents. Therefore, Y-24180 would be a clinically promising drug for the treatment of bronchial asthma.

Animals↗
PubMed1997

Effect of Y-24180, a long-acting antagonist to platelet-activating factor (PAF), on PAF-induced reactions: a relationship between the partial structure of the compound and its duration of the action.

(+/-)-4-(2-Chlorophenyl)-2-[2-(4-isobutylphenyl)ethyl]-6,9-dime thy l-6H- thieno[3,2-f][1,2,4]triazolo[4,3-a][1,4]diazepine (Y-24180) is a platelet-activating factor (PAF) antagonist, being similar to WEB 2086. One of the structural differences between the two PAF antagonists is the presence of a methyl substituent in Y-24180 at the 6-position of its ring system. Orally administered Y-24180 and WEB 2086 both dose-dependently prevented PAF-induced airway hyperresponsiveness (ED50: 0.0010 and 0.019 mg/ kg, respectively) and bronchoconstriction (ED50: 0.0014 and 0.024 mg/kg, respectively) in guinea pigs. Against the bronchoconstriction, here, the inhibitory effect of Y-24180 was significantly more potent and longer acting than that of WEB 2086. On the other hand, Y-24180 (10 mg/kg, p.o.) showed insignificant effects on the bronchoconstriction induced by leukotriene D4, histamine, serotonin, acetylcholine, arachidonic acid, or bradykinin. In an in vitro test, Y-24180 and WEB 2086 inhibited the PAF-induced aggregation of the rabbit washed platelets in a concentration-dependent manner (IC50: 1.2 and 64 nmol/l, respectively). Compared with desmethyl-Y-24180 and WEB 2086, Y-24180 and methyl-WEB 2086, both of which have a methyl substituent on the 6-position of their thienodiazepine ring, exhibited a longer acting suppressive effect on PAF-induced bronchoconstriction and significantly more stable binding to the PAF receptor after the washing-out procedure of the test compounds from platelets. Therefore, the 6-methyl substituent should be responsible for the PAF receptor binding stability of Y-24180, namely, for its long-acting anti-PAF effects in vivo. These results indicate that Y-24180 possesses the specific and long-acting PAF antagonistic effects in the airway.

Acetylcholine↗
PubMed1997

Tissue angiotensinogen gene expression induced by lipopolysaccharide in hypertensive rats.

There is now convincing evidence that various tissues express their own tissue renin-angiotensin system, which may be regulated independently of the systemic renin-angiotensin system. However, little information is available on the regulation of the tissue renin-angiotensin system. We investigated the regulation of tissue angiotensinogen gene expression with respect to the development of hypertension. We measured basal and lipopolysaccharide-stimulated plasma angiotensinogen concentrations by radioimmunoassay and examined the expression of tissue angiotensinogen by Northern blot analysis in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) at 4 and 13 weeks of age. Basal plasma angiotensinogen concentration in SHR was comparable to that in WKY at 4 weeks of age and was significantly higher than that in WKY at 13 weeks of age. Lipopolysaccharide induced a significant increase in plasma angiotensinogen concentration in both WKY and SHR at 4 and 13 weeks of age. At 4 weeks of age, the basal levels of angiotensinogen mRNA in the liver, fat, adrenal, and aorta were higher in WKY than in SHR. At 13 weeks of age, the basal levels of angiotensinogen mRNA in the fat, adrenal, aorta, spleen, and kidney were higher in WKY than in SHR, while that in the liver did not differ significantly between the two strains. At 4 weeks of age, pretreatment with lipopolysaccharide increased the angiotensinogen mRNA levels in the liver, fat, adrenal, and aorta in both WKY and SHR. At 13 weeks of age, pretreatment with lipopolysaccharide increased the angiotensinogen mRNA levels in the liver, aorta, and adrenal; decreased those in the spleen; and had no effect in the kidney in both WKY and SHR. Interestingly, lipopolysaccharide increased the angiotensinogen mRNA level in fat only in SHR, with no effect in WKY, at 13 weeks of age. Lipopolysaccharide stimulated tumor necrosis factor-a mRNA expression in fat of WKY and SHR, and the increase in tumor necrosis factor-alpha mRNA level in SHR was significantly greater than that in WKY. Therefore, the increased tumor necrosis factor-alpha mRNA expression may be involved in the increased lipopolysaccharide-induced expression of angiotensinogen gene in fat of SHR at 13 weeks of age. These data suggest that the transcriptional and probably posttranscriptional regulation of angiotensinogen mRNA differs between SHR and WKY, that the regulation of angiotensinogen gene expression is tissue-specific, and that the altered expression of the angiotensinogen gene may be involved in the development of hypertension.

Angiotensinogen↗
PubMed1997

Subcortical silent brain infarction as a risk factor for clinical stroke.

BACKGROUND AND PURPOSE: No prospective studies have examined the rate of symptomatic ischemic or hemorrhagic stroke in patients with subcortical silent brain infarction (SSBI) who were otherwise neurologically normal at entry into the study. This report investigates SSBI, detected by MRI, as a clinical stroke risk factor. METHODS: MRI scans were performed in 933 neurologically normal adults (30 to 81 years; mean age, 57.5 +/- 9.2 years) without history of cerebrovascular diseases who received our health screening of the brain 1 to 7 years before investigation. We obtained information of their clinical stroke onset through sending out a questionnaire for subjects. We detected SSBI (focal T2 hyperintensities larger than 3 mm with correlative T1 hypointensity), FWT2HL (focal white matter T2 hypertensity lesions similar to SSBI but without correlative T2-hypointensity), and PVH (periventricular hyperintensity) by MRI. Age, sex, family history of stroke, history of hypertension, diabetes mellitus, lipids, hematocrit, blood pressure, fasting blood sugar, smoking, alcohol habits, ischemic changes on electrocardiogram, and sclerotic changes of retinal arteries were included in the analysis. RESULTS: Incidence of SSBI was 10.6% in all subjects. No cortical infarct was detected in this series. Multiple logistic regression analysis showed that hypertension (odds ratio [OR], 4.07; 95% CI, 2.57 to 6.45), diabetes (OR, 2.41; 95% CI, 1.20 to 4.85), alcohol habits > or = 58 g/day (OR, 2.58; 95% CI, 1.50 to 4.45), retinal artery sclerosis (OR, 2.14; 95% CI, 1.32 to 2.38), and age (OR, 1.77; 95% CI, 1.32 to 2.38) were significant and independent risk factors for SSBI. For FWT2HL, hypertension (OR, 4.49; 95% CI, 2.54 to 7.96) and age (OR, 2.08; 95% CI, 1.45 to 3.00) were also independent risk factors. Risk factors for PVH were age (OR, 3.46; 95% CI, 2.23 to 5.36), hypertension (OR, 3.06; 95% CI, 1.62 to 5.78), and retinal artery sclerosis (OR, 2.25; 95% CI, 1.02 to 4.96). We found 14 brain infarctions, 4 brain hemorrhages, and 1 subarachnoid hemorrhage during observation. Annual incidence of clinical stroke was higher in the subjects with SSBI than in those without focal lesions (10.1% versus 0.77%). ORs for clinical stroke onset were 10.48 for SSBI (95% CI, 3.63 to 30.21) and 4.81 for FWT2HL (95% CI, 1.13 to 20.58). The PVH did not relate to clinical stroke onset. CONCLUSIONS: The strong association of SSBI, FWT2HL, and PVH with hypertension suggests a common underlying mechanism (presumably small-vessel vasculopathy). The SSBI showed the most significant association for clinical subcortical stroke. The FWT2HL was also a risk factor for the stroke but was less significant than SSBI. The subjects with SSBI should be considered at high risk for clinical subcortical brain infarction or brain hemorrhage.

Adult↗
PubMed1997

Poststroke apathy and regional cerebral blood flow.

BACKGROUND AND PURPOSE: Although apathy has been reported as one of the neuropsychiatric symptoms following stroke, there have been no studies on regional cerebral blood flow (rCBF) in patients with apathy. In this study we estimated the severity of apathy using the Apathy Scale and examined its relationship to rCBF in 40 stroke patients (mean age, 71.4 years). METHODS: Neuropsychiatric batteries were performed including the Apathy Scale, verbal intelligence and frontal function tests, a depression scale, and an assessment of activities of daily living. The cortical rCBFs were measured by the 133Xe inhalation method. RESULTS: Twenty patients (50%) showed apathy. These patients showed significantly lower scores on verbal intelligence and frontal function tests and a significantly higher depression score than the nonapathetic group. On MRI images there was no relationship between the apathy score and specific regional distribution of lesions. The rCBFs of the bilateral hemisphere were significantly lower in the apathetic group than in the nonapathetic group. The apathetic group showed a significantly reduced rCBF in the right dorsolateral frontal and left fronto-temporal regions. Furthermore, the apathy score for all patients was significantly negatively correlated with rCBF in the same regions. CONCLUSIONS: These findings demonstrate that apathy is a frequent symptom among elderly stroke patients and may be accompanied by cognitive impairments, depressive state, and frontal dysfunction. The hypoactivity in the frontal lobe and anterior temporal regions may contribute to symptoms of apathy after stroke.

Activities of Daily Living↗
PubMed1997

Enzymes of ketone body utilization in human tissues: protein and messenger RNA levels of succinyl-coenzyme A (CoA):3-ketoacid CoA transferase and mitochondrial and cytosolic acetoacetyl-CoA thiolases.

We describe the distribution in human tissues of three enzymes of ketone body utilization: succinyl-CoA:3-ketoacid CoA transferase (SCOT), mitochondrial acetoacetyl-CoA thiolase (T2), and cytosolic acetoacetyl-CoA thiolase (CT). Hereditary deficiency of each of these enzymes has been associated with ketoacidosis. Physiologically the two mitochondrial enzymes have different roles: SCOT mediates energy production from ketone bodies (ketolysis), whereas T2 functions both in ketogenesis and ketolysis. In contrast, CT is implicated in cytosolic cholesterol synthesis. We investigated the tissue distribution of these enzymes in humans by quantitative immunoblots and by Northern blots. In most tissues, polypeptide and mRNA levels were proportional. CT and T2 proteins were detected in all tissues examined. CT levels were highest in liver, were 4-fold lower in adrenal glands, kidney, brain, and lung, and were lowest in skeletal and heart muscles. T2 was most abundant in liver but substantial amounts were present in kidney, heart, adrenal glands, and skeletal muscle. SCOT was detected in all tissues except liver: myocardium > brain, kidney and adrenal glands. The relative amounts of T2 and SCOT were similar in all tissues except for liver (T2 > > SCOT) and brain (SCOT > T2). The observed distribution of SCOT, T2, and CT is consistent with current views of their physiologic roles.

Acetyl-CoA C-Acetyltransferase↗