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Biomedical subjects

T Yanagihara

Publications and source records attributed to T Yanagihara.

At least 253 records · Page 14Linked to original sources

Elevation of carcinoembryonic antigen in cerebrospinal fluid among patients with meningeal carcinomatosis.

The concentration of carcinoembryonic antigen (CEA) in cerebrospinal fluid (CSF) was determined by using an enzyme immunoassay for 204 patients with various nonneoplastic neurologic disorders, 8 patients with systemic infectious diseases, 19 patients with systemic neoplastic diseases without involvement of the nervous system, and 35 patients with neoplastic neurologic disorders. The highest CEA level in CSF among patients without neoplastic neurologic disorders was 0.6 ng/ml. Of 35 patients with neoplastic neurologic disorders, 10 had CEA levels in CSF that exceeded 0.6 ng/ml, the highest level being 70.5 ng/ml. All 10 patients had carcinomas. Among 14 patients with neoplastic meningitis, 5 of 8 patients with meningeal carcinomatosis had elevated CEA concentrations. Although the efficacy of the assay for CEA in CSF must be compared with that of other laboratory tests such as cytologic examination and the assay for beta-glucuronidase--and any potentially false-positive results should be ruled out by determination of the serum CEA level--the CEA concentration in CSF can be used as an adjunctive diagnostic procedure for detection of meningeal carcinomatosis.

Carcinoembryonic Antigen↗

[CT findings of ongoing intracerebral hematoma].

Three cases of ongoing intracerebral hematoma are reported. In all cases, a very small hematoma on the initial CT taken within 2 hours after onset increased in size to such an extent that surgical intervention was necessary. A round radiolucent zone in high density clots was seen on the initial CT of all cases. The attenuation values of each pixels in hematoma formed V-figure in profile display, vfrying from minimum density (40-60) in the center of radiolucent zone to the maximum density (80-90) in peripheral clots. Experimental data have established that the density of blood in circulation and, therefore, one immediately after extravasation is directly related to the patient's hemoglobin and hematocrit levels. Hemoconcentration following clot formation and serum absorption in the brain tissue results in further increase of hematoma density. The radiolucent zone in a intracerebral hematoma suggests extravasated fresh blood. Therefore, we conclud that this is an evidence of active bleeding which calls for immediate surgery.

Acute Disease↗

Repetitive involuntary movement associated with episodic cerebral ischemia.

Clinical characteristics of 12 patients with carotid occlusive disease who experienced episodes of repetitive involuntary movement were analyzed and correlated with laboratory findings. The majority of patients had rhythmic involuntary movements of one or both extremities on one side, which were characteristically precipitated by standing, walking, or hyperextension of the neck and were promptly alleviated by assuming a sitting or supine position. Six patients had a history of a prior transient ischemic attack or stroke. Electroencephalograms contained no epileptiform activity at rest or during sleep in any patient or during the involuntary movements in 2 patients. Cerebral angiography revealed either occlusion or high-grade stenosis of the internal or common carotid artery on the side opposite the involuntary movement in all patients. We conclude that the repetitive involuntary movements result from transient hemodynamic ischemic episodes rather than partial (focal) epilepsy.

Aged↗

A decade of progress for the adhesive fixed partial denture.

The history of the development of adhesive fixed partial dentures was reviewed and present clinical problems discussed. Longitudinal studies are not available because adhesive prostheses with 4-META adhesive resin were introduced only a few years ago. However, scientific advances will make placement of resin-bonded metal prostheses a more stable, standard technique in fixed prosthodontics.

Adhesives↗

Assay for beta-glucuronidase in cerebrospinal fluid: usefulness for the detection of neoplastic meningitis.

The specificity and sensitivity of the assay for beta-glucuronidase in cerebrospinal fluid were evaluated to determine the usefulness of this test for the detection of neoplastic meningitis. The enzyme activity was first measured in cerebrospinal fluid from 131 patients with various disorders and was then prospectively measured in cerebrospinal fluid from 30 patients with cytologic results that were positive for or suggestive of malignant disease. Within the first group, elevated levels of beta-glucuronidase were found only among patients with neoplastic processes in the central nervous system, including neoplastic meningitis. Among 26 patients with neoplastic processes in the central nervous system, including neoplastic meningitis. Among 26 patients with positive cytologic results, 13 had elevated beta-glucuronidase activities. Elevated values were more frequent among patients with adenocarcinoma (75%) and myelogenous leukemia (60%). The patients with these two disorders also had the highest enzyme activities. The correlation of th beta-glucuronidase level with other cerebrospinal fluid values, including total protein, glucose content, and cell count, was not significant. The findings of this study indicate that measurement of beta-glucuronidase in cerebrospinal fluid can be used as an adjunctive diagnostic test for neoplastic meningitis. The results should be interpreted with caution, however, because of the possibility that the elevated enzyme levels may be due to acute or subacute bacterial or fungal meningitis.

Cerebrospinal Fluid↗

Cerebral ischemia in rabbit: a new experimental model with immunohistochemical investigation.

Regional cerebral ischemia was produced in the rabbit by unilateral transorbital occlusion of the middle cerebral artery (procedure I); the middle cerebral and azygos anterior cerebral or anterior communicating artery (procedure II); or the middle cerebral, azygos anterior cerebral or anterior communicating, and internal carotid artery (procedure III). Evolution of ischemic lesions was examined with the immunohistochemical reaction for tubulin. With procedure I, ischemic lesions did not become constantly visible for 6 h in the basal ganglia and for 8 h in the frontoparietal region of the cerebral cortex. With procedure II, it was shortened to 3 h in the basal ganglia and to 6 h in the cerebral cortex. With procedure III, the ischemic lesions were observed in 1 h both in the basal ganglia and in the cerebral cortex as loss of the reaction for tubulin in the neuropil, nerve cell bodies, and dendrites. The evidence of neuronal damage became apparent in the same areas later by staining with hematoxylin-eosin. The experimental model presented here may be suitable for investigation of the mechanism that shifts reversible ischemia to cerebral infarction and for evaluation of the effectiveness of pharmacological intervention.

Animals↗

Immunohistochemical investigation of cerebral ischemia in gerbils.

Experimental cerebral ischemia was produced in gerbils by occlusion of the right common carotid artery in the neck. The evolution of the ischemic lesions was followed from five minutes to six hours by using the immunohistochemical techniques for tubulin and creatine kinase BB-isoenzyme. The earliest lesion was found in the subiculum-CA1 and CA2 regions of the hippocampus in five minutes. There was loss of staining in the apical dendrites and perikarya of the pyramidal cells. The earliest lesion in the cerebral cortex, visible in ten minutes, was a laminar loss of staining for tubulin. Evolution of the ischemic lesions in the thalamus and caudoputamen was delayed. However, in two hours widespread ischemic lesions were seen there. Evolution of the ischemic lesions was slightly slower with the reaction for creatine kinase BB-isoenzyme as compared to the reaction for tubulin, but was far more sensitive than hematoxylin-eosin staining. The distribution of ischemic lesions detected by the immunohistochemical method compared to ischemic areas detected by an India ink perfusion study suggested that both the extent of regional ischemia and regional difference in tissue vulnerability were contributing factors for the emergence of early ischemic lesions. The mechanism for prompt disappearance of the immunohistochemical reaction for tubulin is not clear, but the present investigation demonstrates the usefulness of the immunohistochemical technique for detecting early ischemic lesions and provides a possible biochemical mechanism for cellular damage after ischemic insults.

Animals↗

Emergency embolectomy for acute occlusion of the middle cerebral artery.

Twenty cases treated with emergency embolectomy for acute occlusion of the middle cerebral artery were reviewed. There were 10 males and 10 females, with an average age of 55 years. The left middle cerebral artery was involved in 17 patients and the right in three. Flow was restored in 16 patients (75%). The embolus originated in the heart in seven, the carotid artery in seven, the aorta in three, an aneurysm in one, and an indeterminate source in two. It was technically most difficult to achieve patency with atheromatous emboli from the aorta. Two patients (10%) had an excellent result with no neurological deficit, five (25%) were left with a minimal deficit but were employable, seven (35%) had a fair result but were still independent and employable, four (20%) did poorly, and two (10%) died. Patients with an associated ipsilateral carotid artery occlusion did poorly. Collateral flow, as judged from preoperative angiograms, was the best predictor of outcome.

Acute Disease↗

Immunohistochemical investigation of cerebral ischemia during recirculation.

Immunohistochemical methods for the determination of tubulin, creatine kinase BB-isoenzyme, and astroprotein-glial fibrillary acidic protein were used to investigate recovery of the ischemic lesion after temporary occlusion of a common carotid artery in the gerbil and the evolution of the postischemic lesion following reperfusion. One group of gerbils was followed from 15 minutes to one month after an ischemic period of 30 minutes, and another group was examined after 7 days following an ischemic period of 5 to 30 minutes. It was found that the postischemic lesion, visualized as loss of the immunohistochemical reaction for tubulin and creatine kinase BB-isoenzyme, evolved within 60 minutes after reperfusion in the hippocampus and cerebral cortex and within 3 hours in the caudoputamen and thalamus. Resolution of the preexisting ischemic lesion was possible only after an ischemic period of less than 10 minutes in the cerebral cortex and caudoputamen and less than 15 minutes in the thalamus. In the CA1-CA2 region of the hippocampus, the ischemic lesion already existed after an ischemic period of 5 minutes and was mostly irreversible. The immunohistochemical method of testing for different cellular and subcellular components was very useful for investigation of cerebral ischemia and may also be advantageous for investigation of other pathophysiological conditions of the nervous system.

Animals↗

Nuclear binding sites for triiodothyronine in the gerbil brain following ischemia and recirculation.

The effect of cerebral ischemia and subsequent recirculation on the nuclear thyroid hormone receptors was investigated. Ischemia was produced by occlusion of the right common carotid artery in the Mongolian gerbil. The thyroid hormone receptors were measured in vitro by a [125I]triiodothyrorine (T3) binding assay with isolated nuclei and Scatchard analysis. A rapid increase of the total number of binding sites for T3 appeared within 30 min of ischemia and reached over 40% by 3 h. During the same 3-h period, the relative binding affinity was reduced by 25%. Upon recirculation after 30 min or 3 h of ischemia, a rapid reversal of measured T3 binding sites occurred, which progressed to 20-30% below the control value by the recirculation period of 3 h. If the ischemic period was only 30 min, the nuclear T3 binding capacity recovered toward the control level and the affinity constant returned normal after recirculation for 24 h. When the ischemic period was extended to 3 h, there was progressive loss of receptor sites, and no tendency for recovery of the affinity constant was observed. These results demonstrated a prompt alteration of a specific nuclear regulatory component in cerebral ischemia, which may indicate the importance of such changes within the nuclear regulatory mechanism for reversibility of cerebral function following ischemic insult.

Animals↗

Serum creatine kinase B concentrations in acute cerebrovascular diseases.

Serum creatine kinase B (CKB) concentrations were measured every 12 hours for five days in 38 patients during acute cerebrovascular diseases and in nine controls. Mean CKB concentration was 6.2 +/- 0.8 ng/mL. The fluctuation of the CKB concentration following ischemic stroke was as notable as the elevation immediately after the ischemic event. The two abnormalities were observed in 13 of 17 patients with acute cerebral infarction, and the extent of abnormalities roughly correlated with the volume of tissue damage. The profiles were normal for patients with transient vascular events. Patients with subarachnoid hemorrhage demonstrated wide fluctuation along with high CKB concentration. Although transient elevation of the CKB concentration in some patients with subarachnoid hemorrhage was observed after angiography or clinical worsening, the fluctuation in patients with ischemic stroke was not associated with worsening of neurologic conditions or recurrence of ischemic events.

Cerebrovascular Disorders↗

Cyclic AMP-dependent phosphorylation of erythrocyte variant pyruvate kinase.

Cyclic AMP-dependent phosphorylation of a variant erythrocyte pyruvate kinase (PK; EC 2.7.1.40) was studied. This variant PK shows a faster electrophoretic mobility than the normal enzyme. The decreased enzyme activity observed in this variant is associated with a quantitative decrease of enzyme protein. Other parameters are within normal ranges. The partially purified variant PK is phosphorylated with a subsequent increase of k0.5s (phosphoenolpyruvate) similar to the normal control, suggesting that the structural abnormality of the variant enzyme has no influence on the phosphorylation-deactivation mechanism. On the other hand, the variant PK in the erythrocyte was less extensively phosphorylated than PK in normal erythrocytes. This may be the result of abnormal metabolism in the patient's red cells, including increased 2,3-diphosphoglycerate and decreased adenosine triphosphate levels.

Adolescent↗