[A case of neoplastic angioendotheliosis with B cell lymphoma].
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Biomedical subjects
Publications and source records attributed to I Akiguchi.
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Using a high-resolution magnetic resonance imaging system, we studied 3 patients who had exhibited pontine ataxic hemiparesis. In each patient, the ischemic lesions responsible for the contralateral ataxia were located in the dorsomedial basis pontis. The isointensity bands in the ischemic area on T2-weighted images showed the spared transverse fibers originating from the contralateral pontine nuclei, and this may explain the cause of the unilateral ataxia.
Morphological changes in astrocytes have been studied in the primary motor cortex of persons dying with or without amyotrophic lateral sclerosis (ALS). Glial fibrillary acidic protein (GFAP) and S-100 protein were used as immunohistochemical markers for reactive astroglia. In 12 brains of individuals without neurological disease glial cells showing moderate immunoreactivity for both GFAP and S-100 protein were uniformly distributed in the primary motor cortex in the upper regions of layer I and layer II. In 8 of 11 ALS cases, intensely immunoreactive cells were additionally found to occur and were scattered irregularly, mostly in layers II and III, but occasionally in layers IV and V. Clusters of these intensely positive cells occurred in patches about 200-400 micron in diameter, each containing about 6 to greater than 20 such cells. GFAP-positive astrocytes were seen in some of the 36 brains from persons with neurological problems other than ALS but the pattern was different. The abnormal appearance of clusters of positive astrocytes of the primary motor cortex may be intimately associated with the ALS disease process.
Among 39 cases with acute-onset amnestic syndrome having unilateral localized infarct, 8 cases with anteromedial thalamic infarct ("thalamic" amnesia), and 18 cases with medial temporal lobe infarct including hippocampus in the posterior cerebral artery territory ("PCA" amnesia) were studied in terms of X-CT and MRI findings and neuropsychological examinations. Results were as follows: 7 out of 8 cases with thalamic amnesia (88%), and 15 of 19 cases with PCA amnesia (78%) showed left side lesions on CT scan. All groups showed a prolonged recent memory loss with little loss of immediate recall and remote memory, and disorientation and dyscalculia. In both types of amnesia, patients having a left sided lesion showed recent memory loss with new learning disabilities of verbal materials. Patients having a right sided lesion showed recent memory loss with new learning disabilities of both verbal and visuospatial materials. Judging from the X-CT and MRI findings, the lesions most probably causing amnesia in these cases seemed to be the anterior and dorsomedial nuclei of the thalamus in thalamic amnesia and hippocampus in PCA amnesia. Differential diagnosis in amnestic syndrome with localized infarct is also discussed.
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Using a new coupled peroxidation method modified by adding nickel ammonium sulfate, we demonstrated the localization of monoamine oxidase (MAO) in the rat peripheral nervous system. MAO was localized in the endothelial cells of endoneurial vessels, in Schwann cell cytoplasm encircling myelinated axons, and in some unmyelinated axons. The morphometric ratio of these MAO-containing axons to the total unmyelinated axons was 10-13%. These MAO-containing unmyelinated axons were assumed to coincide with postganglionic sympathetic noradrenergic ones passing in the sciatic nerve. Histochemical MAO staining may be utilized to identify the postganglionic sympathetic nerves in normal and pathological conditions at the electron microscopic level in particular.
Abnormal granular structures, which stained positively with periodic acid-Schiff (PAS-positive granular structures; PGS), were observed in the brain of senescence accelerated mouse (SAM). They were small, round to ovoid, homogeneous structures measuring up to 5 microns in diameter and usually grouped in clusters. PGS were localized in the hippocampus, piriform cortices, olfactory tubercle, nucleus of the trapezoid body, and cerebellar cortices. Quantitative analysis revealed that PGS remarkably increased in the hippocampus of SAM-P/8, a substrain of SAM, with advancing age, although a few PGS also appeared in the aged control mice, SAM-R/1 and DDD. Their histochemical nature, morphological features and distribution pattern were different from those of corpora amylacea and other similar bodies. A close anatomical relationship between PGS and glial fibrillary acidic protein-positive astrocytes was inferred from immunohistochemical studies. PGS is considered to be one of the morphological manifestations of senescence in mice brains, and are found to occur more numerously in the brains of learning or memory deficit mice, SAM-P/8.
We studied a family with autosomal dominant osteosclerosis associated with familial spinal canal stenosis. The propositus, a 44-year-old Japanese woman, had a 9-month history of occipitalgia and left tinnitus, and also had a 2-month history of pain and numbness of the right upper limb. Radiographic skeletal survey showed osteosclerotic changes in the neurocranium, diaphysis of the long bone, mandible, shoulder, clavicle, and ribs. Serum alkaline phosphatase was normal, and no periosteal excrescences were seen. The inheritance pattern was autosomal dominant. The propositus and her daughter, both with severe osteosclerosis, showed spinal canal stenosis, but her son, whose osteosclerosis was moderate, did not. This is the first report of autosomal dominant osteosclerosis associated with familial spinal canal stenosis.
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