Search PubMed⌕ Search

Biomedical subjects

Akira Tamaoka

Publications and source records attributed to Akira Tamaoka.

12 recordsLinked to original sources
PubMed2004

Diphenylarsinic acid poisoning from chemical weapons in Kamisu, Japan.

We noted a new clinical syndrome with prominent cerebellar symptoms in apartment building residents in Kamisu, Japan. The well that provided drinking water contained diphenylarsinic acid, a degradation product of diphenylcyanoarsine or diphenylchloroarsine, which were developed for use as chemical weapons, inducing severe vomiting and sneezing. Characteristics of diphenylarsinic acid poisoning include brainstem-cerebellar and cerebral symptoms. Mental retardation associated with brain atrophy in magnetic resonance images was evident in some infants. We must be vigilant to prevent or minimize the effects of further diphenylarsinic acid poisoning in Japan or elsewhere.

Adult↗
PubMed2003

Pravastatin at 10 mg/day does not decrease plasma levels of either amyloid-beta (Abeta) 40 or Abeta 42 in humans.

It has been assumed that statins work as a preventative drug for Alzheimer's disease (AD). Although some epidemiological observations raise doubts to the effectiveness of statins for AD, many in vitro and clinical studies insist on the effectiveness of statins decreasing amyloid-beta (Abeta) levels in medium or blood. To explore the effect of pravastatin on Abeta production, we followed the longitudinal plasma levels of both Abeta 40 and Abeta 42 during the allocation of pravastatin in 46 patients with hyperlipidemia. We found no correlation between plasma cholesterol levels or the decreasing values of total cholesterol and those of Abeta 40 or Abeta 42. Patients having Apolipoprotein E4 (ApoE4) had higher low-density lipoprotein levels and lower Abeta 40 levels in plasma, suggesting ApoE4 seems to influence plasma Abeta levels via cholesterol metabolism.

Adult↗
PubMed2003

[Down syndrome].

Explore the source record for details and available documents.

Adult↗
PubMed2002

Chrysamine G and its derivative reduce amyloid beta-induced neurotoxicity in mice.

The neurotoxicity of amyloid beta (Abeta) is widely believed to play a seminal role in neurodegeneration in Alzheimer's disease. We examined the effect of Chrysamine G (CG) on such neurotoxicity using the specific measurement of surviving neurons. CG was found to reduce the neurodegeneration induced by both the active short fragment of Abeta(25-35) and full-sized Abeta(1-40). In this study, we synthesized a new chemical compound from a monovalent structure of CG (hCG), with a lower affinity for Abeta, and compared its activity with that of CG. Both CG and hCG were found to be equally efficacious in reducing Abeta-induced neuronal death at a concentration of 0.1-1 microM, indicating that the mechanism of action for CG was not due to its chelating activity, but rather due to its anti-oxidant activity.

Amyloid beta-Peptides↗
PubMed2002

[A case of sensory perineuritis with Bowen disease].

A 60-year-old man was admitted because of subacutely progressive sensory disturbance characterized by fluctuating dysesthesia and light pain on the skin of his hands and feet. He exhibited mononeuritis multiplex, and a plaque with sloughing was observed on the left side of his back. Sural nerve biopsy revealed marked thickening of the perineurium with vascularization, and no necrotizing vasculitis. The pathological features of the nerve biopsy were compatible with sensory perineuritis. A biopsy from his skin lesion revealed Bowen's disease. There have been several reported cases of sensory perineuritis accompanied by malignant tumors. In these cases, immune dysfunctions were considered a common underlying cause in both diseases. This is the first reported case of sensory perineuritis associated with Bowen's disease.

Bowen's Disease↗
PubMed2001

Three-dimensional and fractal analyses of assemblies of amyloid beta protein subtypes [Abeta40 and Abeta42(43)] in canine senile plaques.

The three-dimensional (3D) distribution of amyloid beta protein (Abeta) subtypes [Abeta40 and Abeta42(43)] in canine senile plaques (SP) was observed using a confocal laser scanning microscope. In diffuse plaques (DP), Abeta42(43) alone was deposited as an uneven nebula-like assembly of fine granules. The border of the Abeta42(43) assembly was unclear and diffusely merged to the surrounding area. Mature plaques (MP), on the other hand, showed two patterns of Abeta deposition. In some MP, only Abeta40 was deposited as a defined assembly of very short fibrillary structures. Other MP consisted of both Abeta40 and Abeta42(43), and the deposition patterns of the two Abeta species were the same as those in single-positive plaques; fine granular with unclear margin for Abeta42(43), and short fibrillary structures for Abeta40. Additionally, we calculated the fractal dimensions (FD) of both Abeta40 and Abeta42(43) assemblies, and examined the serial change of FD in each SP. The FD of Abeta42(43)-positive DP ranged from 1.05 to 1.27, and those of Abeta40-positive MP ranged from 1.13 to 1.54 in single-positive plaques. In one double-positive MP, FD ranged from 1.02 to 1.36 for Abeta42(43) and from 1.01 to 1.51 for Abeta40. These results showed that the FD of canine Abeta40 assemblies was higher than that of Abeta42(43) assemblies, and the spatial changes of FD values for Abeta40 and Abeta42(43) in double-positive plaques were quite different. These morphological analyses clearly showed that canine DP and MP have completely different 3D structures, suggesting that their processes of formation are different.

Alzheimer Disease↗