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Biomedical subjects

H Aikawa

Publications and source records attributed to H Aikawa.

At least 109 records · Page 6Linked to original sources
PubMed1986

Lesions in the skin, intestine, and central nervous system induced by an antimetabolite of niacin.

Pellagra in the human is characterized by the clinical "three D's," namely, dermatitis, diarrhea, and dementia. Newborn mice that received a single intraperitoneal injection of 6-aminonicotinamide (6-AN) (50 mg/kg body weight), an antagonist of niacin, consistently developed lesions in the skin, intestinal tract, and central nervous system. Anterior horn cells in the spinal cord as well as motor neurons in the brain showed the ultrastructural features of neuronal chromatolysis, while glial and ependymal cells showed postinjection (PI) edematous changes on Day 5. In the skin, correlating with clinical delay of hair growth, the first discernible microscopic abnormality was vacuolar change in the hair follicles on PI Day 3. By PI Day 5, hyperkeratosis and irregular acanthosis were noted. Edematous swelling of the enteric glial cells was observed in the myenteric plexus of the descending colon on PI Day 5. Although the pathologic features of these 6-AN-treated mice may not be exactly identical to those of human pellagra, possible contributory mechanisms in the development of pellagra lesions may be elucidated by this experimental model.

6-Aminonicotinamide↗
PubMed1986

Strain difference in learning impairment in rats following lead administration during brain development.

High and stable avoidance with low variability (THA) rats and non-select Wistar rats were administered 2 mg/ml lead acetate solution (0.2-0.27 g/Kg/day as lead) up to seven weeks of age; via placenta from the 13th day of gestation and from maternal milk before weaning, and per os after weaning. Results were as follows. 1) Significant differences were not observed between the lead-exposed rats and the controls regarding the developmental landmarks in both the Wistar rats and THA rats. Body weight of the exposed rats, however, were significantly less than that of the controls of the two rat strains. 2) Low rate of avoidance, slow acquisition of learning and large individual variabilities were exhibited in both the controls and the exposed rats of the Wistar strain throughout the test sessions. No significant difference was indicated between the controls and the exposed rats of the Wistar strain. In the control THA rats, avoidance learning was acquired rapidly, and a high level and very small individual variabilities of avoidance were demonstrated during the latter sessions of the test. Meanwhile, in the exposed THA rats, slow learning acquisition and large individual variabilities were displayed. It is thought that the learning impairment appearing in the THA exposed rats was induced primarily by lead.

Animals↗
PubMed1986

[Saccular aneurysm arising from the basilar artery fenestration: a case report].

This patient, 29-year-old female, had an attack of subarachnoid hemorrhage. On admission a cerebral angiogram showed a saccular aneurysm arising from the proximal origin of the fenestrated basilar artery (Fig. 1). The aneurysm was clipped successfully with two steps under a right retromastoidal suboccipital craniectomy (Fig. 2). Association of the fenestrated basilar artery and saccular aneurysm is rare. To our knowledge, 9 cases have been found in the literature and only 4 cases were operated. The authors discussed the pathogenesis and treatment of such aneurysms.

Adult↗
PubMed1985

Enteric gliopathy in niacin-deficiency induced by CNS glio-toxin.

6-Aminonicotinamide (6-AN), an antagonist of niacin and a potent CNS glio-toxin, selectively caused degeneration of glial cells in the central nervous system (CNS) of rodents. Suckling mice treated with 6-AN developed diarrhea clinically and displayed vacuolated degenerating glial cells in the myenteric plexus as well as in the CNS. Myenteric neurons were well preserved. These findings provide further evidence for possible functional similarities between the glial cells in the central and enteric nervous systems.

6-Aminonicotinamide↗
PubMed1985

Atypical Alzheimer's disease with spastic paresis and ataxia.

An unusual case of Alzheimer's disease (AD) is reported. The patient was a 33-year-old Japanese housewife who had progressive dementia, severe spasticity, and mild ataxia for six years. Postmortem examination revealed severe changes of AD and degeneration of the corticospinal tracts, as well as neuritic plaques and plaquelike degeneration in the cerebellum. This appears to be the twelfth reported case of AD with spasticity and ataxia.

Adult↗
PubMed1985

Internodal microvillus-like Schwann cell fingers in myelinated fibres in mouse spinal roots.

Collections of microvillus-like Schwann cell fingers identical to those described previously in the nodal gap substance were commonly found along the internodes of large myelinated fibres in the spinal roots of adult mice. They were covered by Schwann cell basal lamina and focally protruded from the outer cytoplasmic Schwann cell compartment. Unlike nodal Schwann cell fingers, these internodal fingers had no contact with the axolemma, but were directed toward the endoneurium. These were not recognized in the distal peripheral nerves. The frequent occurrence of internodal Schwann cell fingers in the spinal root fibres suggests that these structures may be involved in some electrophysiological regulatory mechanism in this particular region of the nervous system.

Animals↗
PubMed1985

Aqueduct stenosis induced by a single injection of antivitamin.

Hydrocephalus with aqueduct stenosis was a consistent feature in mice which received a single intraperitoneal injection of 6-aminonicotinamide (6-AN) on day 5 postnatal. Chronological investigation revealed that 6-AN-treated mice had aqueductal obstruction with edematously swollen ependymal cells and spongy changes in the periaqueductal gray matter in the early stage (on days 5 and 7 postinjection). However, these cytoplasmic edema of the ependymal and glial cells totally subsided by day 30 postinjection, leaving an obliterated aqueduct with a few remnants of ependymal cells without reactive gliosis. This abnormality of aqueductal lesions in the chronic stage was similar to those of human congenital hydrocephalus. These findings raise the possibility that some form of human congenital hydrocephalus may result from ependymal cell degeneration due to exposure to certain noxious substances in the perinatal period.

6-Aminonicotinamide↗
PubMed1984

Quantitation of apolipoprotein A-I in pooled human serum by single radial immunodiffusion and sodium dodecyl sulfate-polyacrylamide gel electrophoresis.

Apolipoprotein A-I was released from human HDL particles by treatment with 8 M urea, and the free apolipoprotein exhibited identical antigenicity and the same low mobility as purified apolipoprotein A-I in electrophoresis. Treatment of serum with 8 M urea enabled enabled quantitation of apolipoprotein A-I by single radial immunodiffusion assay, as judged by comparison with sodium dodecyl sulfate-polyacrylamide gel electrophoresis.

Apolipoprotein A-I↗
PubMed1984

Low energy levels in thiamine-deficient encephalopathy.

Pyrithiamine-induced acute thiamine-deficient encephalopathy was produced in adult male Wistar rats. Twenty-four hours before the onset of neurological signs the brain showed no morphological abnormalities. Encephalopathic rats had symmetrical lesions of edematous necrosis localized in the thalamus, mammillary body, and pontine tegmentum. Biochemically, encephalopathic rats had brain thiamine levels less than 20% of controls. For the assay of the concentrations of adenosine triphosphate (ATP) and phosphocreatine, the brains were fixed using 5 KW microwave irradiation and were divided into four parts: cerebral cortex, diencephalon, lower brainstem, and cerebellum. In the lower brainstem of the encephalopathic rats ATP concentrations were 89.5% of normal controls. Phosphocreatine levels were lowered to 70% of controls in the diencephalon and to 75% in the lower brainstem. Total high energy phosphate levels were decreased to 89% of controls in the diencephalon and 91% in the lower brainstem before the onset of neurological signs and to 76% and 79%, respectively, after the onset. In the cerebral cortex and cerebellum high energy phosphates were not significantly reduced. Lower high energy phosphate levels and the distribution of edematous lesions were coincident in the brain. These findings suggest that a low energy state is closely related to the formation of edematous lesions in thiamine-deficient encephalopathy.

Animals↗
PubMed1984

6-Aminonicotinamide-induced hydrocephalus in suckling mice.

Following a single intraperitoneal injection of 6-aminonicotinamide (6-AN, 50 mg/kg of body weight) into newborn mice of the Institute of Cancer Research strain, hydrocephalus consistently developed nine days after injection, with rapid progression. All of these mice died before reaching adulthood. The most striking early histologic change in these mice was cytoplasmic vacuolation of ependymal cells, which was observed as early as 24 hours after injection. Vacuolation of subependymal astrocytes appeared during the next few days. After day seven, the aqueduct was obliterated by swollen vacuolated ependymal cells and subependymal astrocytes. The aqueduct remained obliterated even after the vacuolation of the ependymal cells subsided after day nine, when vacuolation of subependymal astrocytes was still pronounced. These morphological observations reveal that, in newborn mice, the ependymal cells are the most sensitive to the toxic action of 6-AN and suggest that the pathogenesis of 6-AN-induced hydrocephalus is likely to be due to the combination of ependymal cell damage and compression of the lumen by the edematous periaqueductal gray matter. This is a highly reproducible animal model of drug-induced hydrocephalus.

6-Aminonicotinamide↗
PubMed1984

Indomethacin suppresses prolactin release in men.

Indomethacin administered intrarectally at a dose of 100 mg elicited a statistically significant decrease of serum prolactin level in men. Serum LH level was depressed slightly but the decrease was not statistically significant. There was no effect on serum FSH concentration.

Adolescent↗
PubMed1983

Ultrastructural observation on the thalamic neuronal inclusions in young mice.

Neuronal intracytoplasmic inclusions were found in the ventrolateral and posterior nuclei of the thalamus of 3-month-old thiamine-deficient mice and quaking mice. An electron-microscopic study revealed that these inclusions were composed of condensation of parallel rectilinear 10-nm filaments with interconnecting cross-bridges as a hallmark of neurofilaments. They were morphologically indistinguishable from those described in aged mice. This observation indicates that neuronal inclusions in the thalamus, which have been constantly reported in aging mice, can be seen even in young mice in the presence of cellular metabolic disturbances.

Animals↗