Gas chromatographic detection of gasoline in the blood: a case report.
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Acetone↗
Biomedical subjects
S Fujiwara
Publications and source records attributed to S Fujiwara.
Site of protein synthesis in cells infected with pseudorabies virus.
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Autoradiography↗
The role of myometrial acetylcholine in spontaneous and oxytocin induced contractions of the myometrium.
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Acetylcholine↗
The nucleoids of rat liver cell microbodies. Fine structure and enzymes.
The nucleoids of microbodies of rat liver cells were isolated in a highly homogeneous and pure state, by treating the microbody-rich fraction, prepared from 10% polyvinylpyrrolidone-0.25 M sucrose homogenate, with Triton X-100. Three treatments with 0.1% detergent were enough to render the nucleoids free from contamination with mitochondria, microsomes, lysosomes, and intact microbodies. Electron microscopically, the nucleoids were found to consist of parallel bundles of highly dense hollow tubules, the outer and inner diameters of which are approximately 150 and 50 A, respectively. Ten tubules are arranged around a longitudinal space 190 x 200 A in width. The nucleoids thus show a honeycomb appearance in the cross-plane and a parallel-packed structure in the longitudinal plane. Biochemically, the nucleoids were found to bear only urate oxidase among probably microbody-enzymes, and they might be the only cytoplasmic particles of rat liver cells in which the enzyme locates. Urate oxidase activity, on a unit protein basis, of the nucleoid preparation is approximately 380 times as high as that of the whole homogenate, and is almost comparable with that of a commercial type I enzyme preparation. No enzymes of mitochondrial, microsomal, and lysosomal origins were detected in the nucleoids. The fine structure of the nucleoids is described in detail, and a probable schematic diagram is presented.
Animals↗
[Experimental studies on an acetylcholine-like substance in the uterine muscle].
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Acetylcholine↗
Myocardial energy metabolism in the hypertrophied hearts of spontaneously hypertensive rats.
Age-related changes in the myocardial energy metabolism were studied in spontaneously hypertensive (SHR) rats of 5-15 weeks of age. Systolic blood pressure increased rapidly during 5 to 10 weeks of age (developing phase) and attained a plateau level at 10 to 15 weeks (sustained phase). Even during the developing phase, the heart was hypertrophic, as assessed by an increase in the ratio of the ventricular weight to body weight. However, myocardial contents of glycolytic intermediates and high energy phosphate compounds and thus, the myocardial energy state (phosphorylation potential) in SHR rats did not differ from those in age-matched normotensive Wistar-Kyoto (WKY) rats. The lactate/pyruvate ratio was significantly lower in SHR rats. On the other hand, during the sustained phase, cardiac hypertrophy progressed only gradually, and myocardial contents of creatine phosphate and ATP were lower, while the lactate content was higher than in WKY rats. The lactate/pyruvate ratio was elevated, while phosphorylation potential was lowered. These findings suggest that the energy state is normal during the developing phase of hypertension despite the presence of cardiac hypertrophy and the increased pressure load, whereas the energy state is at a lower level during the sustained phase of hypertension.
Adenosine Triphosphate↗
Impact-induced intracranial pressure caused by an accelerated motion of the head or by skull deformation; an experimental study using physical models of the head and neck, and ones of the skull.
An impact incurred by the movable head may bring about a change in intracranial pressure and this change may play an important part in the occurrence of the cerebral contusion. We have carried out the following experiments to determine whether the intracranial pressure change was attributed to an accelerated motion of the head or to a skull deformation. In the blow experiment in which the head was accelerated, a positive peak in the intracranial pressure was recorded immediately after impact at the impact site and a negative one at a site opposite the impact. In the one in which the skull could be deformed, the intracranial pressure curves at both sites contained harmonics. The modal analysis revealed an inbending in the frontal and occipital regions of the skull and an outbending in the parietal and temporal regions immediately after impact, followed by a reverse deformation. Regarding the intracranial pressure change, positive pressures were recorded in the frontal and occipital regions immediately after impact, followed by a negative one. This study demonstrated that the positive and negative peaks were caused by the accelerated motion of the head, and that the curve of the intracranial pressure changes contained harmonics which were caused by the deformation of the skull.
Acceleration↗
Differences in the intracranial pressure caused by a 'blow' and/or a 'fall'--an experimental study using physical models of the head and neck.
In cases of a severe head injury caused by a fall, coup contusions are either absent or very minor, in contrast to presence of extensive contre-coup damage. In cases of a severe blow to head, however, the reverse occurs, with contre-coup lesions a rarity and coup damage extensive. To investigate this further, head injuries caused by a 'blow' or a 'fall' have been studied, using physical human models of the head and neck, both filled with distilled, degassed water and fixed onto a dummy torso. An impact of a constant magnitude was applied to the midoccipital region in 'blow' and 'fall' experiments, and the acceleration of the head and changes in the intracranial pressure were measured, with the resulting data analyzed by a computer. In both experiments, the peak amplitude of the acceleration pulse were almost the same. Similarly, the intracranial pressure curve at the impact site consisted of a positive pulse that hardly differed, nor did the peak amplitude of that pulse vary significantly. In the 'blow' experiment, however, the intracranial pressure curve at the site opposite the impact consisted of a negative pulse, whereas in the 'fall' experiment, the intracranial pressure recorded at the same area was negative but of a longer duration, with an absolute value that was slightly greater. Our results indicate that an impact to the head triggers a different response in the intracranial space, dependent on whether that impact force was caused by a 'blow' or a 'fall'.
Acceleration↗
Immunologic detection of protein antigens after phenol-chloroform denaturation.
The study of gene expression in cells and tissues often begins with phenol-chloroform extraction of the biologic material of interest for the isolation of intact mRNA. In most cases, the proteins denatured by phenol-chloroform are discarded. However, we found that the proteins recovered from phenol-chloroform extractions maintain their antigenicity. Therefore a method was developed for recovering the proteins from phenol-chloroform-denatured extracts that could be saved in lyophilized form until immunologic analysis. In this way, the RNA and the protein analysis can utilize exactly the same sample, and the biologic material can be saved. This is important because often these materials are available only in limited quantities. The method has been used to examine the sea urchin ets-related antigen and sea urchin ets-2 mRNA.
Animals↗
Polymorphism of aldehyde dehydrogenase and ethanol elimination.
The influence of polymorphism of aldehyde dehydrogenase (ALDH) on ethanol elimination was investigated. Japanese healthy male volunteers were divided into two groups, i.e., a normal ALDH group of 52 subjects with the low Km isozyme of ALDH, and a deficient group of 48 subjects without it. The subjects of the normal group were given 0.4, 0.8, 1.2, 1.6 or 2.0 g/kg of ethanol, while those in the deficient group ingested 0.4, 0.8 or 1.2 g/kg of ethanol. Widmark's factors (beta 60, Co and r) and ethanol elimination rate (ER) were compared between the two groups. In the deficient group, beta 60 and ER were not clearly elevated with the increase of ethanol dose, while those in the normal ALDH group increased depending on the blood ethanol level. Blood acetaldehyde level was elevated with the increase of the ethanol dose in the deficient group, but not in the normal group. In the experiment of the repeated ingestion of ethanol in the deficient group, the second peak of blood acetaldehyde level was lower than that of the first one.
Acetaldehyde↗
Asymptomatic cerebral infarction in Kawasaki disease.
Meningitis, facial palsy, subdural effusion, and cerebral infarction have been reported to be some of the nervous system complications of Kawasaki disease which usually are clinically obvious. A 22-month-old boy with Kawasaki disease, who developed asymptomatic cerebral infarction, is reported. Hyperpyrexia persisted for 57 days; echocardiography and magnetic resonance imaging revealed the presence of aneurysms in the coronary, axillary, and internal iliac arteries. This study indicates that patients with Kawasaki disease may have silent cerebral infarction.
Caudate Nucleus↗
MR angiography of intracranial aneurysms: a comparison of 0.5 T and 1.5 T.
The objective of this paper is to compare the diagnostic efficacy of 3 DFT time-of-flight MR angiography (MRA) at middle-field-strength and high-field-strength in diagnosis of intracranial aneurysms. Thirty-one patients, including 26 patients with angiographically confirmed intracranial aneurysms (n = 28), underwent MRA at 0.5 and 1.5 T. Images were interpreted by six trained observers who were blinded to diagnosis. Twelve projections of MRA of the circle of Willis, by maximum-intensity projection algorithm, were reviewed using continuous confidence-judgement scales. It was found that MRA at 1.5 T was more sensitive than that at 0.5 T in detection of aneurysms. The sensitivity of six observers ranged between 50 and 64% (mean 56%) at 0.5 T, and between 61 and 86 86% (mean 75%) at 1.5 T. In the smaller aneurysms less than 5 mm, the differences between the units became greater. The sensitivity for small aneurysms ranged from 23 to 54% (mean 32%) at 0.5 T, and from 31 to 69% (mean 58%) at 1.5 T. Our conclusion was that high field strength confers higher accuracy in the detection of intracranial aneurysms with MRA with current-generation MR imagers.
Algorithms↗
Prediction of functional recovery in acute myocardial infarction: comparison between sestamibi reverse redistribution and sestamibi/BMIPP mismatch.
BACKGROUND: It has been known that Tc 99m sestamibi/iodine 123 betamethyliodophenylpentadecanoic (123I-BMIPP) (sestamibi/BMIPP) mismatch is an indicator of viable myocardium in acute myocardial infarction (AMI). We have reported that reverse redistribution of sestamibi in AMI indicates the patency of infarct-related artery and a preserved left ventricular function in the chronic stage. In this study we investigated the relationship between reverse redistribution of sestamibi and sestamibi/BMIPP mismatch in patients with AMI. METHODS: Twenty-three patients with AMI who received direct percutaneous transluminal coronary angioplasty underwent both BMIPP and sestamibi SPECT within 2 weeks after onset. Sestamibi images were obtained 1 hour (early) and 3 hours (delayed) after injection of sestamibi. BMIPP imaging was carried out 30 minutes after injection. The left ventricle was divided into 17 segments, and regional myocardial uptakes of the tracers in each segment were scored from 0 (normal) to 3 (no activity). A reverse redistribution pattern was defined as an increase of > or =1 in the regional score at the delayed images. More reduced BMIPP uptake than sestamibi uptake in each segment was determined as sestamibi/BMIPP mismatch. Contrast left ventriculography was performed soon after revascularization and repeated 1 month later. RESULTS: Of 15 patients with sestamibi reverse redistribution, sestamibi/BMIPP mismatch was observed in 14 patients (93%), whereas mismatch was seen in only one of seven patients (14%) without reverse redistribution (p < 0.01). In patients with sestamibi reverse redistribution, regional scores of BMIPP agreed with those of early and delayed images of sestamibi in 51 segments (46%) and in 92 segments (83%), respectively. In the chronic stage, both regional wall motion and left ventricular ejection fraction improved in patients with sestamibi reverse redistribution (wall motion score: 6.7 +/- 2.4 vs 2.7 +/- 2.1, p < 0.01; ejection fraction: 56% +/- 7% vs 64% +/- 8%, p < 0.01), but not in those without reverse redistribution. CONCLUSION: Both reverse redistribution of sestamibi and sestamibi/BMIPP mismatch reflect the recovery of left ventricular function and thus imply myocardial viability in AMI. Because the presence of reverse redistribution of sestamibi agreed with that of sestamibi/BMIPP mismatch, additional BMIPP images can be replaced by the delayed images after a single injection of sestamibi.
Aged↗
Effect of 2-phenylaminoadenosine (CV-1808) on ischemic ST-segment elevation in anesthetized dogs.
The effect of 2-phenylaminoadenosine (CV-1808) against myocardial ischemia was studied in anesthetized dogs. During intravenous infusion of CV-1808 (0.25 and 0.5 microgram/kg/min for 10 min) the ST-segment elevation in the epicardial ECG induced by a 5-min occlusion of a coronary arterial branch was occasionally enhanced in association with cardiac acceleration. In a dose of 0.5 microgram/kg/min, the agent inhibited the ST elevation 30 and 60 min after administration. The same dose did not change myocardial blood flow in the ischemic area despite significant systemic hypotension. In hearts with continuous coronary occlusion, CV-1808 (0.3 and 1.0 microgram/kg, i.v. bolus) increased the retrograde blood flow from the ischemic area immediately after administration, suggesting a collateral vasodilating action. Nifedipine (0.5 and 2.5 microgram/kg/min, i.v. for 10 min) and nitroglycerin (0.5 and 5.0 microgram/kg/min, i.v. for 10 min) had no influence on the ischemic ST-segment elevation, while a significant inhibition was seen with propranolol (0.5 mg/kg, i.v.). A moderate hypotension was induced by CV-1808, nifedipine, and nitroglycerin, while a significant reduction in cardiac function was seen after dosing with propranolol.
Adenosine↗
Dementia as a predictor of functional disability: a four-year follow-up study.
BACKGROUND: Prospective studies have shown that cognitive impairment is a strong and consistent risk factor of physical disability. However, cognitive impairment has been based on the result of a single screening tool. OBJECTIVE: To investigate the role of cognition in the subsequent incidence and decline of functional disability in basic activities of daily living (ADL) and instrumental activities of daily living (IADL) after a full assessment of dementia. METHODS: A group of 1,358 Japanese atomic bomb survivors aged 61 years or older who lived in the community or in institutions in Hiroshima City were followed for 4 years. During the baseline survey (1993-1995), subjects were administered a screening test for cognitive impairment. Those suspected of dementia underwent a series of cognitive tests (Hasegawa's dementia scale, Clinical Dementia Rating) and a neurological examination. The diagnosis of dementia was made according to DSM-III-R criteria. Study subjects were questioned about their reported ADL and their IADL. During the follow-up period, deaths were recorded and a follow-up survey (1997-1999) used to assess ADL and IADL performance. RESULTS: Dementia, even after adjustment for age, sex and history of stroke, was a strong predictor of functional disability, as indicated by ADL (odds ratio, OR = 14.0; confidence interval, CI = 5.4-36.3), IADL (OR = 10.1, CI = 2.2-46.4), and also by assessment of decline in ADL (OR = 9.8, CI = 4.2-22.8) or IADL status (OR = 3.9, CI = 1.8-8.3). CONCLUSION: Dementia is an important determinant of functional status. Deterioration in ADL is more significant than deterioration in IADL, suggesting that factors other than cognition, such as motivation or perceptual, sensory and motor abilities, may be important in IADL performance. This study confirms previous findings on risk factors that affect functional ability and extends our knowledge by examining several criteria of function that are important in the daily lives of elderly people.
Activities of Daily Living↗
Hemolysate-induced contraction in smooth muscle cells of the guinea pig basilar artery.
The hemolysate (10(-5)-10(-2) times dilution; original hemoglobin concentration was 0.83 +/- 0.10 X 10(-3)M) evoked the contraction in a dose dependent manner, and this contraction was composed of low and high sensitive responses as estimated from the Eadie-Hofstee's plot. Indomethacin (10(-7)-10(-5)M) inhibited the latter component in the hemolysate-induced contraction. The membrane potential of smooth muscle cells was -50 mV and the cell was electrically quiescent. The hemolysate (greater than 10(-2) times dilution) depolarized the membrane and increased the ionic conductance of membrane. In rare occasions, the spike potential was triggered on the hemolysate-induced depolarization. The hemolysate (10(-5)-3 X 10(-3) times dilution) produced the contraction with no change in the membrane property. Carbocyclic thromboxane A2 ( cTXA2 ; 2.8 X 10(-10)M) produced the contraction without depolarization of the membrane, yet the TXA2 synthesis inhibitor, OKY-1581 (10(-5)M), had no effect on the hemolysate-induced contraction. PGE1, PGE2 and PGF2 alpha (2.8 X 10(-6)M) produced the contraction with no change in the membrane property. The contraction evoked by 2.8 X 10(-6)M PGF2 alpha corresponded well with that evoked by 3 X 10(-3) times dilution of the hemolysate. Removal of the endothelium by mechanical rubbing modified the hemolysate-induced contraction. Under the assumption that OKY-1581 is a selective inhibitor for TXA2 synthesis, the major part of the contraction (the indomethacin sensitive component) of the basilar artery is postulated to be due to synthesis of the primary PG rather than TXA2 by the hemolysate, yet the hemolysate itself, has to some extent a direct action in evoking the small contraction.
Animals↗
Topographical distribution of barrier function in cervico-cephalic arteries of dog. Major cerebral arteries possess definite barrier function?
Topographic distribution of barrier function in normal canine cervico-cephalic arteries was studied using horseradish peroxidase (HRP) and Evans blue as tracers. The carotid sinus of the internal carotid artery (ICA) was conspicuously permeable to HRP when compared to other areas of major cervical arteries. The cavernous portion of the ICA also showed prominent permeation of HRP, especially through the outer surface, which is covered with venous endothelial cells. On the luminal side of the cavernous portion of the ICA, barrier deficiency was noted at angulated segments such as the carotid siphon. Intracranial segments of both ICA and vertebral arteries demonstrated incomplete barrier function of the first 1 to 4 mm from the origin of the intradural segments. These areas were considered to be transitional sites in barrier function between extra- and intracranial arteries. Focal, but definite, barrier disruption was also noted at the distal ends of the ICA and other arterial branching sites of major intracranial arteries. While opening of the interendothelial junctions was considered to be one of the mechanisms causing increased permeability in the cavernous ICA, the mechanisms for the permeation of HRP into the major cerebral arteries could not be confirmed ultrastructurally.
Animals↗
Presynaptic inhibitory action of adenosine on neuromuscular transmission in the canine cavernous carotid artery.
We investigated the effect of adenosine on neurogenic contraction of the canine cavernous carotid artery, using an isometric tension recording device and transmural nerve stimulation. Adenosine, in concentrations under 10(-5)M, had no relaxing effect on the contractions produced by high [K]o solution or 10(-5)M norepinephrine. Transmural nerve stimulation (stimulus: 1 msec duration, 100V intensity) evoked a frequency-dependent contraction, which was abolished by 3 X 10(-7)M tetrodotoxin. Adenosine in concentrations of 10(-6)M and 10(-5)M, inhibited the neurogenic contraction at each frequency, more so in the low frequency range. This inhibitory effect of adenosine was significantly antagonized by 10(-5)M theophylline. Pretreatment with 2 X 10(-8)M dipyridamole had no effect on neurogenic contractions, but augmented the inhibitory effect of adenosine. 10(-5)M theophylline did not augment the neurogenic contractions. The findings that both dipyridamole and theophylline failed to affect the neurogenic contractions in the absence of adenosine suggests that the presynaptic autoinhibition mechanism of adenosine may not be involved in neuromuscular transmission in this tissue. These results suggest that there is a presynaptic adenosine receptor in the nerve terminal which inhibits the release of neurotransmitter in canine cavernous carotid artery. It is also probable that the vasodilating effect of adenosine in the cavernous carotid artery is mainly due to its inhibitory effect on neurotransmission rather than to a direct relaxing effect on smooth muscle.
Adenosine↗