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Biomedical subjects

J Tateishi

Publications and source records attributed to J Tateishi.

At least 145 records · Page 8Linked to original sources
PubMed1989

Host genetic control of incubation periods of Creutzfeldt-Jakob disease in mice.

Host genetic control of the incubation period of Creutzfeldt-Jakob disease (CJD) was studied using various inbred strains of mice, including B10 congenic strains. Various incubation periods were found in mice injected either intracerebrally or intraperitoneally with the Fukuoka 1 strain of the CJD agent; NZW/Sea and A/JJms had the shortest, and B10.AKM/Ola and C57BL/6J the longest, incubation periods. Length of the CJD incubation period did not correlate with the genetic markers tested, i.e. the murine major histocompatibility (H-2) complex (which has previously been reported to be linked to a gene influencing CJD incubation period in mice), coat colour or sex genes. In NZW/Sea x C57BL/6J F1 hybrid mice the CJD incubation periods were similar to that of the parent with the longest incubation period. Incubation periods of the backcross progeny from F1 and NZW/Sea were intermediate between those of the parental mice and had a unimodal distribution pattern. A similar observation was made on the progeny of the A/JJms x C57BL/6J mating. On the other hand, the length of incubation period for the NZW/Sea x B10.AKM/Ola F1 hybrid fell between those for the two parents and the NZW/Sea x A/JJms F1 hybrid had a significantly longer incubation period than those of the two parents. These results suggest that polygenes probably control the length of the CJD incubation period in mice.

Alleles↗
PubMed1989

Subcellular distribution of the transmissible agent in Creutzfeldt-Jakob disease mouse brain.

To determine the intracellular localization of the Creutzfeldt-Jakob disease (CJD) agent in mouse brain, cerebrum tissue of the mouse brain affected with the Fukuoka-1 strain was separated into six subcellular fractions (microsome, nerve ending, myelin, mitochondria, nucleus, and soluble fractions) by differential sucrose density gradient, and then the CJD infectivity of these fractions was examined. Serially diluted samples of each subfraction were inoculated intracerebrally into groups of BALB/c mice, and the infectivity was determined as to end point titration value, incubation period, and number of affected mice. On the basis of the protein content, the highest CJD infectivity was observed in the microsomal fraction. The nerve ending (synaptic plasma membrane) and myelin fractions were also infective. The mitochondria and nucleus fractions showed the lower infectivity. The infectivity of the soluble fraction was the lowest among the six subcellular fractions. From the findings obtained in this study two possibilities as to the intracellular localization of CJD agent were suggested: 1) the transmissible agent of CJD is closely associated with surface membranes of neuronal and/or glial cells, including their processes; 2) the CJD agent is diffusely present intracellularly, including in the surface membranes, but for manifestation of infectivity the agent needs membrane components as prerequisite factors.

Animals↗
PubMed1989

Baroreceptor reflex to neck suction and its modification by diltiazem in man.

The carotid sinus baroreceptor reflex was studied in 15 healthy young men by a variable pressure neck suction chamber. Neck suction produced a reduction in blood pressure and an increase in RR interval, which were augmented by an increase of stimuli. Both responses occurred promptly and were attenuated with time. The reproducibility of the response was examined in 6 subjects. There were no differences in either hypotensive or bradycardiac responses between 2 runs separated by 1 hour, indicating good short-term reproducibility. In a long-term reproducibility study involving 2 runs separated by 2 weeks, hypotensive responses showed similar changes, whereas bradycardiac responses showed a wide variation. Based on this good reproducibility of responses, the effects of diltiazem on baroreflex function were studied in 9 men. Following the administration of diltiazem (20 mg, P.O.), the hypotensive responses to neck suction stimuli were significantly augmented compared to preadministration responses. On the other hand, diltiazem did not have a significant influence on heart rate responses. Thus, the present study shows that the neck chamber method is a feasible approach to studying the influence of given interventions on baroreflex function and demonstrates an enhancement of baroreflex-mediated hypotension by diltiazem.

Adult↗
PubMed1989

Beta-protein amyloid is widely distributed in the central nervous system of patients with Alzheimer's disease.

To clarify the distribution, morphology, and density of amyloid deposits in patients with Alzheimer's disease (AD), tissue sections from various areas of the central nervous system of 14 patients with AD and from 20 nondemented aged controls were investigated immunohistochemically using anti-beta protein antiserum. beta-protein amyloid deposits were present not only in the cores of the senile plaques and in the vascular wall (amyloid angiopathy), but also in various sized plaque-shaped fibrillary, perivascular, subpial, and subependymal deposits. Amyloid deposits were found mainly in the cerebral cortex in nondemented controls, while in AD they were distributed widely in the regions that were not affected in nondemented controls. The positivity of amyloid deposits in AD was 100% in the cerebral cortex, hippocampus, amygdala, thalamus, caudate nucleus, claustrum, hypothalamus, nucleus basalis of Meynert, and cerebellar cortex. Putamen and brain-stem nuclei were affected frequently, and the spinal cord, dentate nucleus, and globus pallidus were sometimes (less than 50%) affected. This result provides an evidence that Alzheimer's disease is a beta-protein amyloidosis of the central nervous system. An assessment of the distribution of amyloid deposits should prove to be useful for the histopathologic diagnosis of AD.

Aged↗
PubMed1989

Positive transmission of Creutzfeldt-Jakob disease verified by murine kuru plaques.

Kuru plaque is a pathognomonic feature in the brain of patients with Creutzfeldt-Jakob disease (CJD) and in the brain of CJD-infected mice. Kuru plaques from CJD-infected mice were immunolabeled with rabbit anti-murine prion protein (PrP) absorbed with human PrP, but not so with mouse anti-human PrP. Therefore, the murine kuru plaque is composed of the host (mouse) PrP and can be distinguished antigenically from human PrP. Immunostaining using the anti-murine PrP and formic acid enhancement on tissue sections revealed not only birefringent kuru plaques but also nonbirefringent diffuse and small PrP accumulations. This immunohistochemical detection of kuru plaques provides more positive evidence than heretofore employed histochemical approaches. There were kuru plaques in brains of the first passage mice inoculated with tissues from 30 (91%) of 33 patients with CJD, the 3 negative patients belonging to a type of Gerstmann-Sträussler syndrome. Tissues from 6 other demented patients did not produce kuru plaques. In the evaluation of spongiform changes, mice inoculated with tissues from 23 (70%) of 33 patients were considered cases of successful transmission. In some mice, kuru plaques were present in the absence of spongiform changes. Further inoculations from 9 mice with kuru plaques but no spongiform changes were successful in almost all mice. Therefore, mice with murine kuru plaques in the absence of spongiform changes are also infectious. Thus, the presence of murine-specific kuru plaques can serve as another hallmark of a successful transmission.

Adult↗
PubMed1989

Increased tau accumulation in senile plaques as a hallmark in Alzheimer's disease.

To identify the tau component in senile or kuru plaques, the authors examined brain sections from 12 patients with Alzheimer's disease (AD), 6 with Creutzfeldt-Jakob disease (CJD), and 20 nondemented aged controls using anti-beta protein, anti-buman prion protein, and affinity-purified tau-specific antibody. The tau component was identified both in senile and kuru plaques. In AD, tau-positive senile plaques were found in all cerebral cortices of almost all cases, and the tau-positivity of plaques in cerebral cortices was 5.1 to 27.5%. In CJD, tau-positive senile and kuru plaques were restricted to the hippocampus, and the tau-positivity was 4.3 and 1.2%, respectively. In nondemented aged controls, tau-positive senile plaques also were restricted mostly to the hippocampus, and the tau-positivity was 1.3%. Significant differences in the tau-positivity of senile plaques were found between AD and CJD and nondemented aged controls, and no significant differences were found between CJD and nondemented aged controls. These observations are important because increased tau accumulation in senile plaques can be a hallmark of AD.

Adult↗
PubMed1989

[Precordial ST segment depression in acute inferior myocardial infarction: the importance of posterolateral wall infarction].

To determine whether precordial ST segment depression during acute inferior myocardial infarction indicates posterolateral wall ischemia, anatomical predominance of coronary circulation was examined by coronary angiography and evaluated in 43 patients who experienced first acute inferior myocardial infarction. Among patients who underwent intracoronary thrombolysis within six hours from the onset of symptoms, the infarct-related artery was the right coronary artery (RCA) in 35. In addition, their early 12-lead electrocardiographic features were compared with those in eight patients having the infarct-related left circumflex coronary artery (group Cx). Thirty-five patients with RCA obstruction were categorized in four groups: Four patients with left predominant type (group L), 10 with balanced type (group B), five with right super-predominant type (group SR), and 16 with right intermediate type (group RI). Seventeen of the 21 patients in groups SR and RI demonstrated precordial ST segment depression, whereas it was present in only six of the 14 patients in groups L and B (p less than 0.05). Of the 29 patients in groups SR, Cx and RI, total ST segment depression in leads V1 through V4 (sigma ST) was greater in the 14 patients in groups L and B (p less than 0.05) than in other groups. Furthermore, in these 29, all patients in groups SR and Cx had greater sigma ST than did the patients in group RI (p less than 0.05). There was no significant difference in sigma ST between groups SR and Cx. Precordial ST segment depression did not correlate with concomitant disease of the left anterior descending artery and was not a mirror image of ST segment elevation in inferior leads. On thallium-201 scintigraphy, additional perfusion defects of the posterolateral wall were present in all eight patients in group Cx and in ten of the 21 patients in groups SR and RI. Thus, precordial ST segment depression during acute inferior myocardial infarction seemed to be affected by the pattern of coronary circulation. It was concluded that this ST depression represents more extensive involvement of the posterolateral wall in patients with right predominant coronary circulation as well as in those with left circumflex artery obstruction.

Adult↗
PubMed1989

[Ischemic heart disease evaluated by exercise stress thallium-201 myocardial scintigraphy: a comparison of SPECT and bull's eye display].

T1-201 stress myocardial scintigraphy was performed in 35 cases of ischemic heart disease (angina pectoris and myocardial infarction) to assess the accuracy of SPECT and bull's eye display in the quantitative diagnosis of coronary artery lesions. We evaluated the sites of ischemic heart disease using the following methods: 1. SPECT (visual): visual evaluation by myocardial SPECT images. 2. SPECT +bull's eye (visual): visual evaluation by stress, delayed and washout images of bull's eye display. 3. bull's eye (quantitative): quantitative evaluation by the washout rate and % uptake. The diagnostic accuracy of method 2 was higher than that of method 1 in all coronary arterial vessels; LAD (74% vs 80%), LCX (60% vs 63%) and RCA (57% vs 60%). The diagnostic accuracy of method 3 was approximately equal to that of method 2. The diagnostic accuracy of method 2 was higher than of method 1 in patients with three-vessel disease (43% vs 67%), while there was no such difference in patients with both single and two-vessel disease. Moreover, the diagnostic accuracy of method 3 was approximately equal to that of method 2 in patients with three-vessel disease. In some cases the redistribution was recognized only by using washout images or by calculating the washout rate as a quantitative evaluation. In conclusion, the bull's eye display improved the diagnostic accuracy of T1-201 scintigraphy, but the quantitative analysis did not further improve the accuracy. However, there were some possibilities of evaluating the redistribution in some cases by using quantitative analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

The range of renal blood flow for renal autoregulatory adjustments in resistance.

The study was designed to determine the range of renal blood flow over which autoregulation occurred. Pressure-flow relationships were obtained in the left kidney over a wide range of perfusion blood flow. Renal vascular resistance showed sigmoidal changes with changing renal blood flow over the range of 0.3 to 6.3 ml/min.g kidney wet weight. This curve shows two definite points of inflection at renal blood flows of 2.3 and 3.7 ml/min.g. Once renal blood flow rises above the normal range, renal vascular resistance changes hyperbolically with decreases in renal blood flow. We conclude that (1) the range of blood flow for autoregulatory adjustments in resistance is between 2.3 and 3.7 ml/min.g, and (2) the autoregulatory mechanism can be easily impaired by increasing renal blood flow far above the upper limit of the range.

Animals↗
PubMed1988

Gerstmann-Sträussler-Scheinker disease: immunohistological and experimental studies.

The older brother of the patient from whom the Fukuoka-1 strain was isolated was found to have numerous kuru plaques, the main finding common to both siblings. Other clinicopathological features including spongiform change were absent in the older brother. Immunostaining using anti-kuru plaque core protein and anti-beta-protein peptide revealed many kuru plaques and a few senile plaques in the older brother. Experimental transmission of the disease to laboratory animals was successful, using tissues from both siblings, through inoculation of fresh brain homogenates, purified prion protein, and formalin-fixed brain homogenates. Prion protein fractions from the patient's brain shortened the incubation periods and formalin-fixed mouse brains did not lengthen the periods. The disease in the two brothers can be classified as Gerstmann-Sträussler-Scheinker disease, a familial variant of Creutzfeldt-Jakob disease. Gerstmann-Sträussler-Scheinker disease manifests a variety of clinicopathological features. Immunohistological verification of kuru plaques has major diagnostic value in assessing dementia.

Aged↗
PubMed1988

Immunohistochemical verification of senile and kuru plaques in Creutzfeldt-Jakob disease and the allied disease.

We investigated paraffin-embedded brain sections from 41 patients with Creutzfeldt-Jakob disease (CJD) and from 9 with Gerstmann-Sträussler syndrome (GSS) using anti-human prion protein (PrP) antisera (anti-GSS kuru plaque cores and anti-PrP synthetic peptide) and anti-beta protein antiserum. The anti-human PrP antiserum reacted with the plaques in CJD and GSS, with or without degenerative neurites (neuritic components). In addition, the anti-beta protein antiserum immunolabeled kuru plaque-like compact plaques in some cases of CJD. Therefore, previous morphological classifications of the plaques may not always be valid. Senile plaques labeled with anti-beta protein antiserum were evident in 65% of the CJD brains and 50% of GSS brains from patients in their 60s, and in 73% of brains from CJD patients in their 70s, but not in brains from patients under 60 years of age. The incidence of the senile plaques was compatible with the normal aging process and was apparently not accelerated by the disease process of CJD or GSS. These immunostaining approaches using anti-human PrP and anti-beta protein antisera allow classification of plaque types and increase the reliability of the pathological diagnosis in persons with dementia.

Adult↗
PubMed1988

Brain stem gliomas: a clinicopathological analysis of 23 histologically proven cases.

The clinical and anatomic pathological findings in 23 patients with histologically proven brain stem glioma were reviewed. Eleven patients had malignant tumors (astrocytoma, grade III, and glioblastoma multiforme) and the remaining had low grade ones. The primary site of the tumor was the pons in 15 of 21 patients examined, followed by the medulla oblongata and midbrain. Continuous cephalad and caudad involvement of pontine tumors was evident in 14 patients, and was more extensive in the high grade gliomas. At autopsy, the tumor spread via the CSF was observed in all patients with high grade but not low grade tumors. Open surgical posterior fossa exploration was performed on 12 patients. Volume reduction, by partial removal of the tumor and/or by cyst evacuation, was performed on seven, with good results. Nineteen patients were given radiation therapy, with temporary improvement of the clinical conditions. While none of the patients with malignant tumors survived more than 15 months after diagnosis, those with low grade tumors had a five-year actuarial survival rate of 50.0%, and three survived more than ten years after the diagnosis. Our data indicate that brain stem gliomas are not a homogeneous group of tumors as far as the clinical and pathological features are concerned. This heterogeneity shows the need to design specific treatments for these tumors.

Adolescent↗
PubMed1988

Focal intracerebral accumulation of a novel type of amyloid protein. An early stage of cerebral amyloidoma?

The brain of a 60-year-old patient with bronchial carcinoma presented a focal amyloid deposit in the white matter associated with myelin and axonal destruction. An additional lesion was found in the basal ganglia. This silent focal intracerebral accumulation of amyloid substance may be a prestadium of a "cerebral amyloidoma". The histochemical and immunohistochemical analysis of the accumulated amyloid indicated that it may belong to a novel type of amyloid.

Amyloid↗
PubMed1988

Incidence and characterization of age related amyloid deposits in the human anterior pituitary gland.

To identify amyloid deposits in the anterior pituitary gland, we have immunohistochemical, histochemical and alkaline Congo red staining. The anti-human P component reacted positively with these amyloid deposits, while antisera against prealbumin, AA type amyloid fibril protein and various anterior pituitary hormones were negative. A combination of Congo red and anti-human P component staining was most sensitive and reliable for detection of amyloid in the anterior pituitary glands of 300 randomly autopsied patients. Amyloid deposits increased in parallel with the age of the patients, however, they appeared earlier and more frequently than heretofore reported. Deposition of amyloid was seen initially in the 3rd decade and the positivity rate of amyloid deposits was 73% in the 5th decade. The histochemical characteristics of these pituitary amyloid deposits differed from those of cerebral and systemic deposits, particularly those found in the amyloid of senile systemic amyloidosis.

Adolescent↗
PubMed1988

Aging and cerebral amyloid: early detection of amyloid in the human brain using biochemical extraction and immunostain.

To search for relationships between aging and cerebral amyloid, the brains of 66 clinically nondemented individuals were investigated, using the following three approaches for verification of the amyloid: Congo red staining as a histochemical method; immunostaining using anti-beta protein antiserum as an immunohistochemical identification; and biochemical extraction of amyloid from nonfixed brain tissues. That the incidence of cerebral amyloid increased with aging was determined using all three approaches. Immunostaining using anti-beta protein antiserum was more sensitive than Congo red staining. The biochemical extraction was most sensitive for detection of amyloid, and revealed that amyloid was extracted initially from more than half (67%) of the brains of 9 persons in their 50s and from almost all (97%) brains of 35 persons over 60 years of age. Amyloid was extracted even from brains in which amyloid deposits were not detected by histochemical or immunohistochemical methods. This result shows early appearance of the age-related cerebral amyloid.

Aging↗
PubMed1988

Capillary permeability and boron distribution in ethylnitrosourea-induced rat glioma.

The vasculature and capillary permeability of gliomas induced by ethylnitrosourea in Sprague-Dawley rats were studied with horseradish peroxidase and Evans blue dye. The distribution of the boron-10 compound, Na2(10)B12H11SH, which is now in clinical use for boron neutron capture therapy (BNCT) for brain tumors, was investigated quantitatively using neutron-induced alpha-autoradiography. The vasculature and the degree of capillary permeability varied widely, depending mainly on the size of the glioma, and were often heterogeneous even in the same tumor. The distribution of boron-10 also varied, correlating to capillary permeability. The boron-10 concentration and the tumor:blood concentration ratio in large and medium-sized gliomas were adequate for successful BNCT. This study suggests that the vasculature and capillary permeability of the target brain tumor exert an important influence on the therapeutic efficacy of BNCT.

Animals↗