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Biomedical subjects

H Nagara

Publications and source records attributed to H Nagara.

At least 19 recordsLinked to original sources
PubMed1995

[Epidural anesthesia for the repair of the femoral neck fracture in elderly patients].

For the repair of the femoral neck fracture in the elderly patients, an epidural catheter was inserted immediately after injury and epidural anesthesia was employed to allow radical operation as early as possible. The subjects were 45 patients with a mean age of 81.4 years. Surgical procedures were osteosynthesis and replacement of the femoral cap. The preoperative management of pain included insertion of an epidural catheter at the L2-L4 interspace immediately after injury for injection of 0.25% bupivacaine. The catheter was inserted 1.5 days on average after injury, and surgery was undertaken 1.4 days on average after the insertion. The intraoperative management included epidural anesthesia by injection of 1.5% mepivacaine. The mean duration of anesthesia was 150 min, and the total amount of mepivacaine used during the operation averaged 284 mg. For postoperative management, the epidural catheter was retained for 5 days on average to achieve adequate pain relief. The incidence of postoperative complications was relatively low, and the post operative course was also favorable.

Aged↗
PubMed1993

The zitter rat: membranous abnormality in the Schwann cells of myelinated nerve fibers.

Ultrastructural alterations of the Schwann cells were chronologically examined in zitter and in control rats. The membranous abnormalities closely involving the nuclear membranes of the Schwann cells and mesaxons were constantly observed in the zitter rats. These structures consisted of scroll- or whirl-like unit membrane accumulations directly extending to the nuclear envelope. Occasionally, similar membranous structure were observed in association with the endoplasmic reticulum, lysosome or mitochondria in the cytoplasm of the Schwann cells. In the control rats, whirl-like membranous structures in the nuclear membranes of the Schwann cells were observed only intermittently at 1, 5 and at 7 days of age in the developing process. In conclusion, we postulate that the zitter rat, which is an established animal model for hypomyelination of the central nervous system (CNS), has some inherited abnormality related to the membrane biosynthesis and its regulation in Schwann cells as well as in oligodendrocytes.

Aging↗
PubMed1992

Early myelination in zitter rat: morphological, immunocytochemical and morphometric studies.

Early myelination in zitter rat was investigated by light and electron microscopic observations, by immunostaining for myelin basic protein (MBP), proteolipid protein (PLP) and myelin-associated glycoprotein (MAG), and by morphometric analysis from the 1st to the 28th day of age. Although the commencement of myelination in zitter rats was not delayed in comparison with control rats, the density or the number of myelinated fibers in zitter rats was significantly below that in controls, both in the ventral column of the cervical spinal cord and in the optic nerve. In contrast, the density or the number of aberrant myelin sheaths was increased in zitter rats, and this difference became more marked with increasing age. The persistent presence of abnormal membranous structures associated with the oligodendroglial nuclear membrane and the increased number of aberrant myelin sheaths were characteristic to the zitter mutation, although these alterations were also observed transiently in control rats. Quantitative analysis supported the proposition that hypomyelination in zitter rats is primarily pathological and becomes more prominent with advancing age. However, the fundamental structure of the myelin lamellae appeared to be normal and the immunoreactivities for MBP, PLP and MAG were slightly delayed and weakend in comparison with age-matched controls. Thus, in zitter rat there is the functional abnormality of the oligodendrocytes to integrate the processes of membrane biosynthesis and to expel excessive production of membranous structures associated with the membranous organellae such as nuclear membrane, and it is postulated that this functional abnormality is characteristic to only the zitter mutation.

Aging↗
PubMed1991

Adrenoleukodystrophy: a correlation between saturated very long-chain fatty acids in mononuclear cells and phenotype.

Saturated very long-chain fatty acids in erythrocyte membranes, blood plasma, and mononuclear cells were studied in 4 patients with childhood-adolescent adrenoleukodystrophy and 4 patients with adult adrenoleukodystrophy and 19 normal control subjects by using high-performance liquid chromatography. Ratios of C26:0 to C22:0 in mononuclear cells, erythrocyte membranes, and blood plasma in patients with childhood-adolescent and adult adrenoleukodystrophy were significantly higher than in normal control subjects. Furthermore, ratios of C26:0 to C22:0 in mononuclear cells were significantly higher in patients with childhood-adolescent adrenoleukodystrophy than in patients with adult adrenoleukodystrophy, whereas there was no significant difference in the ratios in erythrocyte membranes and blood plasma between the two groups of patients with adrenoleukodystrophy. These results suggest that there is a correlation between phenotype and ratio of C26:0 to C22:0 within mononuclear cells in patients with adrenoleukodystrophy.

Adolescent↗
PubMed1991

An ultrastructural study of oligodendrocytes in zitter rat: a new animal model for hypomyelination in the CNS.

The ultrastructural alterations in oligodendrocytes in the zitter rat--a newly established animal model of CNS hypomyelination--were studied in animals between 3 and 37 weeks of age. Throughout the observation period, the most characteristic alteration was the presence of abnormal structures associated with nuclear membranes and resembling split myelin lamellae. The structures consisted of stacks of membranes continuous with the inner and outer membranes of the nuclear envelope or with plasma membranes. This abnormality was prominent at 3 weeks of age, when initial myelination was probably still occurring. It was decreased transiently at 12 weeks of age and then again increased slightly with advancing age. However, the mean incidence of this abnormality was approximately 5% of the oligodendrocyte nuclei in randomly examined electron micrographs. As the small membranous abnormalities were observed in a few serial sections, the actual incidence is believed to be several times higher than 5%. Such membranous abnormalities were also detected in some mitochondria, in some cisternae of rough endoplasmic reticulum, and in some lysosomes, all at lower incidence rates. Some aberrant or elongated myelin sheath formations, an increased number of radial components and intracytoplasmic inclusions in oligodendrocytes were also observed. These findings suggest that functional abnormalities in membrane biosynthesis including the myelin sheaths and the nuclear membranes in oligodendrocytes are closely related to the hypomyelination in the CNS and may be related to the genetic abnormality in the zitter rat.

Aging↗
PubMed1991

CNS pathology in the neurological mutant rats zitter, tremor and zitter-tremor double mutant (spontaneously epileptic rat, SER). Exaggeration of clinical and neuropathological phenotypes in SER.

The pathological alterations in the central nervous system (CNS) were examined in three kinds of mutant rat; the zitter (zi/zi; Zi), the tremor rat (tm/tm; Tm) and the spontaneously epileptic rat (SER) which is a double mutant carrying both zitter and tremor genes. Two major alterations demonstrated in these mutants were hypomyelination and vacuolation or spongy degeneration. Hypomyelination was observed predominantly in SER and to a lesser extent in Zi, and was accompanied by a redundant or aberrant myelin sheath formation in addition to a decreased number of myelinated fibres. This appeared to be related to the occurrence of tremor. There was no abnormality in the structure of the myelin lamellae and oligodendrocytes or any destruction of myelin sheaths by phagocytic cells. The number of radial components in CNS myelin was increased almost equally in Zi, Tm and SER. Vacuolation was prominent in SER and Tm, especially in the brainstem and thalamus. Zi also developed mild vacuolation with advancing age. Vacuolation seemed to be related to the epileptic phenomena in SER and Tm. Vacuoles consisted mainly of swollen astrocytic processes and enlargement of the extracellular space, as well as occasional enlargement of periaxonal spaces. Thus both pathological findings--the hypomyelination derived from the zitter mutation with tremor, and the vacuolation from the tremor mutation with epileptic symptoms--were mutually exaggerated in SER. It is postulated that the two different genetic loci with zi and tm mutations interact and synergistically reinforce each other both clinically and pathologically in SER.

Aging↗
PubMed1991

Clustering of three cases of Creutzfeldt-Jakob disease near Fukuoka City, Japan.

During a 4-month period we encountered three patients with Creutzfeldt-Jakob disease (CJD). All lived in a limited area near Fukuoka City in Japan. Such a significantly close spatial and temporal clustering of cases suggests exposure to a common CJD infectious agent. Except for dental-related treatments, there were no evident causative agents common to these three patients.

Aged↗
PubMed1989

The twitcher mouse: attenuated processes of Schwann cells in unmyelinated fibers.

Morphological alterations occurring in Schwann cells of unmyelinated fibers (unmyelinated Schwann cells) were investigated in the sciatic nerve of the twicher mouse, a murine model of human globoid cell leukodystrophy. After postnatal day 10, the number of Schwann cell-axon units gradually increased and the number of unmyelinated axons per unit progressively decreased in the twitcher mouse. However, the total number of unmyelinated axons showed no significant differences between twitcher and normal mice. Thus, these alterations of unmyelinated Schwann cells in the twitcher mouse suggest that attenuated branching of cellular processes develops at an early stage and progresses together with progression of demyelination in this mutant.

Animals↗
PubMed1989

The twitcher mouse: accumulation of galactosylsphingosine and pathology of the central nervous system.

In the twitcher mouse, a murine model of globoid cell leukodystrophy (GLD), pathological changes of various parts of the central nervous system correlated well with the concentration of galactosylsphingosine (psychosine). The development of GLD lesions was more obvious in tracts with a more rapid progression of myelination. It was suggested that accumulation of galactosylsphingosine subsequent to myelin maturation caused suicidal death of myelin forming cells.

Aging↗
PubMed1989

A comparison of erythrocytes, lymphocytes and blood plasma as samples in fatty acid analysis for the diagnosis of adrenoleukodystrophy.

We studied the very-long-chain fatty acids of blood plasma, erythrocyte membranes and lymphocytes in 4 adrenoleukodystrophy patients, 5 adrenoleukodystrophy obligate carriers, 12 normal controls and 81 patients with various neurological disorders by high-performance liquid chromatography and compared the reliabilities in the diagnosis of adrenoleukodystrophy of these 3 components of peripheral blood. Of 81 patients with various neurological disorders, 2 myotonic dystrophy and 2 spinocerebellar degeneration patients showed increased ratios of C26:0 to C22:0 in erythrocyte membranes, but not in blood plasma and lymphocytes. None of the 12 normal controls showed increased ratios of C26:0 to C22:0 in erythrocyte membranes, blood plasma and lymphocytes. These results suggest that fatty acid analysis for the diagnosis of adrenoleukodystrophy is more reliable when blood plasma and lymphocytes are used than when erythrocyte membranes are used.

Adolescent↗
PubMed1988

The twitcher mouse: accumulation of galactosylsphingosine and pathology of the sciatic nerve.

Morphological and biochemical changes were investigated in the early developmental stages of sciatic nerve of the twitcher mouse, a murine model of human globoid cell leukodystrophy. The concentration of galactosylsphingosine (psychosine) and the chronological changes of the twitcher mouse peripheral nerve pathology correlated well. Galactosylsphingosine had already accumulated at birth and dramatically increased with age. Characteristic inclusions were observed in Schwann cells and macrophages of the twitcher mouse on the 5th postnatal day. Endoneurial edema developed after 10 postnatal days and the hypomyelination was pronounced at 15-20 postnatal days. These findings suggest that galactosylsphingosine is cytotoxic for myelin-forming cells and is closely related to pathogenetic events in the twitcher mouse.

Aging↗
PubMed1987

Effects of intracarotid hyperosmolar mannitol in triethyl tin (TET)-induced rat brain edema--preservation of blood-brain barrier (BBB) in TET edema.

The effect of intracarotid hyperosmolar mannitol on the blood-brain barrier (BBB) in triethyl tin (TET)-induced rat brain edema was examined by using intravenous Evans blue (EB, MW 68,000) and Adriamycin (ADM, MW 580) as tracers. Three ml of 1.4 M mannitol solution were administered through the right carotid artery during 45 s for BBB opening. The barrier was opened for 60-120 minutes and then re-established. The reversibility was preserved in TET-treated rats and controls. In fact, the intravenous injection of EB stained both TET-treated and non-treated cerebral hemispheres with mannitol-induced transient BBB disruption, but not without BBB disruption. BBB was resistant to both high and low molecular weight substances in TET-induced edema. The importance of this hyperosmotic studies provides the evidence for normal BBB function in TET-induced brain edema.

Animals↗
PubMed1987

Neurotoxicity of adriamycin passed through the transiently disrupted blood-brain barrier by mannitol in the rat brain.

Neurotoxicity of adriamycin (ADM) was investigated following the transient disruption of the blood-brain barrier (BBB) in rats. The BBB disruption by the hyperosmotic agent (1.4 M mannitol) was confirmed by the leakage of ADM and Evans blue administered intravenously. Neuropathological changes due to the toxicity of ADM were found as early as day 4. The neurons in the cerebral cortex and nucleus caudatus-putamen showed focal clearing of the nuclear chromatin, increased dense bodies in the cytoplasm and dilatation of the cisternae of the rough endoplasmic reticulum (r-ER) and Golgi apparatus. By day 7, nucleolar segregation and irregular membranous structures appeared in the nuclei with the progression of cytoplasmic changes. By day 10, the cytoplasm of many neurons was vacuolated. Electron-microscopically, the cisternae of the r-ER and Golgi apparatus were prominently dilated in these neurons. Neuronal microtubules were increased in number, in particular in the perinuclear region. Numerous whorl-like membranous structures and separation of nuclear membrane were also observed. Some astrocytic processes surrounding the blood vessels revealed loss of organelles and a few pericytes showed an increased number of lysosomes on days 7 and 10. This experiment clearly demonstrates that ADM has strong neurotoxic effects in the central nervous system when the BBB is disrupted, and provides the warning for the possibilities of neurotoxic side effects when ADM is administered, in combination with a hyperosmotic agent, for the treatment of human malignant tumors, including brain tumors.

Animals↗
PubMed1987

Cerebellar efferent fibers around the dentate nucleus. Pathological anatomy in olivo-ponto-cerebellar and dentato-pallido-luysian atrophy.

In patients with olivo-ponto-cerebellar atrophy (OPCA), the deep cerebellar white matter showed evidence of severe degeneration and gliosis. However, the circumferential white matter enclosing the dentate nucleus was less involved. In addition, the Holzer stain verified the presence of mild gliosis inside the wrinkled band of the dentate gray matter. In contrast, dentato-rubro-pallido-luysian atrophy (DRPLA) affected the mantle layer covering the dentate nucleus. The fibers encircling the dentate nucleus, which degenerate in DRPLA and are spared in OPCA, are anatomically noticeable to be dentatofugal pathways. Moreover, the afferent fibers from the cerebellar cortex and other systems may reach the dentate nucleus partly from the medial aspect via the hilus, as was noted in cases of OPCA.

Cerebellar Ataxia↗
PubMed1987

Formalin fixed brains are useful for magnetic resonance imaging (MRI) study.

We carried out magnetic resonance imaging (MRI) studies on human brains which had been fixed in formalin solution for over 2 years and had been proven neuropathologically to be cases of multiple sclerosis (MS), progressive multifocal leukoencephalopathy (PML), and Balo's concentric sclerosis (Balo). Using spin echo (SE) and inversion recovery (IR) pulse sequences to detect demyelinated lesions in a living person with MS, the demyelinated lesions of the fixed brains in cases of MS, PML and Balo definitely re-appeared, although T1 and T2 in the gray and white matter were reduced following fixation. High signal areas on the SE images corresponded not only to the characteristic distribution of demyelinated lesions in the white matter but also to sparse myelin, gliosis and mild perivascular cuffing in the white matter around the demyelinated foci in cases of the fixed MS, PML and Balo brains. On the IR images, only MS plaques were evident. This MRI study of fixed brains proved useful to elucidate clinicopathological correlations.

Adolescent↗
PubMed1987

Effects of methylcobalamin on vitamin B1- and B-deficient encephalopathy in rats.

Vitamin B1- and B-deficient encephalopathy was produced in adult Wistar rats and the effect of methylcobalamin was studied. These experiments were performed in vitamin B1- or B-deficient rats with or without the administration of guanidine, a magnesium antagonist. These encephalopathic rats showed symmetrical lesions in the pontine tegmentum. No pathological changes in the brainstem were seen in guanidine-administered rats. This suggests that guanidine itself doesn't produce these brainstem lesions. Moderate to severe pathological changes occurred in vitamin B-deficient rats with guanidine administration, whereas these pathological changes were milder in vitamin B1-deficient rats with guanidine administration and in vitamin B1- and B-deficient rats with the combination of the guanidine and methylcobalamin administrations. These facts suggest that vitamin B12, methylcobalamin, plays an important preventive role in the development of the pontine lesions in this experiment.

Animals↗