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N Seriu

Publications and source records attributed to N Seriu.

13 recordsLinked to original sources
PubMed1997

Inheritance and strain distribution of a persistent hyaloid vascular system in mice.

The mode of inheritance of a persistent hyaloid vascular system was investigated in an inbred strain of Senescence-Accelerated Mouse P9 (SAMP9) by conducting crosses between SAMP9 and SAMR1, a strain which shows normal regression of the hyaloid vascular system. We also examined the distribution of this abnormality in 12 inbred SAM strains and in eight commonly used inbred strains of mice. Ophthalmoscopic examination of the eyes of 5-week-old mice, which have transparent lenses, revealed the persistence of a hyaloid vascular system in only one female F1 hybrid out of 66 offspring. The observed segregation ratio of affected to unaffected mice was 25:52 in males and 37:44 in females, following the reciprocal backcross progeny between SAMP9 mice and F1 hybrids. The results of the strain distribution study indicated that 8-97% of the mice among six strains of SAM exhibited the persistence of a hyaloid vascular system, whereas the other inbred strains did not exhibit this abnormality. These observations suggest that at least two major genes may contribute to the persistence of a hyaloid vascular system, and suggest that the SAM strains comprise a group of related inbred strains.

Animals↗
PubMed1995

Age-related decrease of nerve growth factor-like immunoreactivity in the basal forebrain of senescence-accelerated mice.

The senescence-accelerated mouse P10 (SAMP10) is a murine model of accelerated senescence characterized by the deterioration of learning and memory with advancing age. In the present study, we examined the distribution of nerve growth factor (NGF) immunohistochemically in SAMP10 mice and its control strain, SAMR1. In both strains, NGF-like immunoreactivity (NGF-IR) was observed in neurons throughout the entire forebrain and in glial cells in a particular location. In aged SAMP10 mice, each layer of the cerebral cortex retained its NGF-IR, although the thickness of the cortical mantle was markedly decreased in comparison with younger animals. There was an age-related decline in NGF-IR in the substantia innominata of SAMP10 mice at the age of 10 months, when compared to 2-month-old SAMP10. These results indicate age-related decrease of NGF in the basal forebrain in SAMP10 mice.

Age Factors↗
PubMed1995

Monoamine oxidase-B-positive granular structures in the hippocampus of aged senescence-accelerated mouse (SAMP8).

We examined the histochemical localization of monoamine oxidase in the hippocampus of young and old senescence-accelerated mouse (SAM). We found a monoamine oxidase-B-positive granular structure (MGS) in the hippocampus of old SAMP8, an accelerated senescence-prone line of SAM. The MGS was a round-shaped granular structure of 0.5 to 5 microns diameter and usually formed a cluster, the largest diameter of which ranged from 50 to 150 microns. No MGS were found in the hippocampus of young SAMP8 or of young SAMR1, an accelerated senescence resistant line of SAM, and only few, if any, were seen in old SAMR1. A monoamine oxidase-positive astrocyte was usually observed in the central area of each cluster of MGS. Furthermore, the MGS was in close anatomical relationship with monoamine oxidase-positive astrocytic processes. The enzyme inhibition experiments showed that monoamine oxidase activities localized in the MGS and astrocytes were both predominantly of type B. These findings suggest MGS occurs at least partly in monoamine oxidase-B-positive astrocytes. Furthermore, the MGS was similar to a periodic acid-Schiff-positive granular structure, a polyglucosan body previously documented in the brains of old SAMP8 and some other aged mice strains including C57BL/6 and nude mice, in terms of their size, morphological appearances and topographical distribution in the hippocampus. Thus, the present results suggest that monoamine oxidase type B is a proteinaceous component of the periodic acid-Schiff-positive granular structure in aged mice brains, and might provide some clues for clarifying the mechanisms of age-related occurrence of periodic acid-Schiff-positive granular structures in mice brains.

Aging↗
PubMed1992

MRI and SPECT findings in amyotrophic lateral sclerosis. Demonstration of upper motor neurone involvement by clinical neuroimaging.

MRI was performed in 21 patients and single photon emission computed tomography (SPECT) with N-isopropyl-p-123I iodoamphetamine in 16 patients, to visualize upper motor neurone lesions in amyotrophic lateral sclerosis. T2-weighted MRI revealed high signal along the course of the pyramidal tract in the internal capsule and cerebral peduncle in 4 of 21 patients. SPECT images were normal in 4 patients, but uptake was reduced in the cerebral cortex that includes the motor area in 11.

Adult↗
PubMed1992

SPECT findings in Parkinson's disease associated with dementia.

Dementia in Parkinson's disease is thought to be attributable not only to subcortical lesions but also to cortical alterations, especially frontal lobe dysfunction. To evaluate cortical function, the regional cerebral blood flow (rCBF) was estimated of 13 demented and 13 non-demented age matched patients with Parkinson's disease compared with that of 10 age matched controls using I-123 iodoamphetamine single photon emission tomography (IMP-SPECT). The rCBF of the nondemented Parkinson's patients showed no significant differences from that of the control subjects. In the demented patients, the bilateral frontal and parietal and left temporal regional blood flow was significantly less than in the controls. Four demented patients showed isolated frontal hypoperfusion, 8 showed fronto-parietal hypoperfusion, and 1 showed isolated parietal hypoperfusion. Frontal hypoperfusion was therefore present in 12 of the 13 demented patients, and this finding agrees with the frontal lobe dysfunction hypothesis. Parietal rCBF had a significant positive correlation with cortical functions such as calculation and language ability in the MMSE scores. The parietal and temporal reduction in rCBF probably reflects the presence of Alzheimer pathology, cortical Lewy body disease, or both.

Aged↗
PubMed1992

[Autonomic dysfunction of central nervous system disorders].

Central nervous system disorders, such as cerebrovascular or spinal cord lesions often cause dysfunctions of the autonomic nervous system. In most cases of acute cerebrovascular accidents, blood pressure is transiently elevated. Some patients, especially with pontine or thalamic hemorrhage, suffer from extremely high fever. In patients with large lesions in the cerebral hemisphere or lesions in the brainstem, cardiopulmonary state may be affected. In spite of absence of acute myocardial infarction, electrocardiogram may show ST-T changes resembling acute myocardial infarction. Cheyne-Stokes respiration or sleep apnea can occur. Lesions in the medulla oblongata cause dysfunctions of automatic respiration. Patients with large cerebrovascular lesions in the unilateral hemisphere often show transient hyperhidrosis on the contralateral side. Prognosis of patients with these autonomic failures is poor. In patients with spinal shock, blood pressure and heart rate are reduced. In chronic stage, autonomic hyperreflexia, such as attacks of episodic hypertension can occur. Lesions in the high cervical cord often bring nonsymptomatic perforating gastric ulcer.

Autonomic Nervous System Diseases↗
PubMed1991

Cerebellar ataxia with glutamic aciduria.

We report a case of cystinuria and glutamic aciduria, presenting with progressive cerebellar manifestations. She had cerebellar type dysarthria and limb ataxia. Head MRI revealed cerebellar atrophy. Urinary amino acid analysis showed excessive excretion of glutamate and the dibasic amino acids (cystine, arginine, lysine, and ornithine). Cystine and glutamic acid are thought to be transported in a common membrane transport system. Reduction of glutamic acid and cystine in the cerebrospinal fluid was revealed. A relationship between cystinuria and cerebellar manifestation was discussed.

Adult↗
PubMed1990

MRI demonstration of cortical laminar necrosis and delayed white matter injury in anoxic encephalopathy.

We performed serial radiological examinations on a patient with anoxic encephalopathy. In the early term after the anoxic insult, T1-weighted MRI revealed high signal intensity areas distributed laminarly in the cerebral cortex and diffusely in the putamen, which were thought to reflect the cortical necrosis and necrosis in the putamen. Single photon emission computed tomography using I-123 isopropylamphetamine showed persistent hypoperfusion in the arterial watershed zones. T2-weighted MRI performed several months after the anoxic episode revealed diffuse high-intensity lesions in the arterial water-shed zones. These delayed-onset white matter lesions continued to extend over several months.

Adult↗
PubMed1990

Magnetic resonance imaging of medial medullary infarction.

Medial medullary infarction is characterized by ipsilateral hypoglossal nerve palsy, contralateral hemiparesis sparing the face, and contralateral disturbance of deep sensation. Although it is possible to make a clinical diagnosis in typical patients, diagnosis is difficult if hypoglossal nerve palsy is absent. We describe a patient with medial medullary infarction without hypoglossal nerve palsy. The patient suffered from left hemiplegia and homolateral disturbance of deep sensation. Magnetic resonance imaging revealed the site of the lesion to be in the medial portion of the upper medulla oblongata. The result of somatosensory evoked potential testing was compatible with disturbance of the medullary medial lemniscus. In a review of the literature, we examined the relation between clinical features and lesion location in 16 patients with medial medullary infarction and compared these to the present patient. Motor paresis was present in every patient, while disturbance of deep sensation was recorded in nine of 13 patients and hypoglossal nerve palsy in six of 14 patients. In atypical patients with medial medullary infarction (such as the present patient), magnetic resonance imaging is necessary to detect the lesion and to make a clinical diagnosis.

Aged↗
PubMed1990

[Medial medullary infarction demonstrated by MRI].

A 67-year-old woman with medial medullary infarction is reported, including clinical manifestations, MRI and angiographical findings, and results of evoked potentials. She suffered from contralateral hemiplegia and disturbance of deep sensation. Motor paresis of the tongue was absent. Magnetic resonance imaging revealed a lesion in the medial portion of the medulla oblongata. The 17 cases previously reported with medial medullary infarction are reviewed. Only 3 cases had triad of medial medullary infarction, contralateral hemiparesis, deep sensory disturbance, and ipsilateral hypoglossal paresis. Therefore, lesion detection is necessary to diagnose medial medullary infarction. Most infarctions limited to the upper third of the medulla were caused by occlusions of vertebral arteries or their branches and prognosis was good. In contrast, infarctions in the lower two thirds were caused by occlusions of anterior spinal arteries and their branches and the prognosis was poor. Thus localization of the lesion using MRI plays an important role to predict the prognosis.

Aged↗
PubMedDate not supplied

Neuropathological studies on strains of senescence-accelerated mice (SAM) with age-related deficits in learning and memory.

In a series of inbred Senescence-Accelerated mice (SAM) strains, accelerated-senescence prone SAMP substrains show early onset and rapid advancement of senescence. SAMP8 and SAMP10, in particular, exhibit a significant age-related deterioration in memory and learning for passive and active avoidance tasks with, respectively, a low and high incidence of systemic senile amyloidosis. In the brains of both SAMP8 and SAMP10 strains, we have found numerous morphological alterations. Here we review the changes seen in both neuronal or glial components in SAMP8/P10 brains. They may serve as markers of the neuronal degeneration leading to the deficits in learning and memory.

Aging↗