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Kazuhiro Ishii

Publications and source records attributed to Kazuhiro Ishii.

10 recordsLinked to original sources
PubMed2005

Beta-site APP cleaving enzyme 1 (BACE1) is increased in remaining neurons in Alzheimer's disease brains.

Alzheimer's disease (AD) is characterized by the extensive deposition of amyloid beta protein (Abeta) in the brain cortex. Abeta is produced from beta-amyloid precursor protein (APP) by beta-secretase and gamma-secretase. beta-Secretase has been identified as beta-site APP cleaving enzyme1 (BACE1). We produced rabbit polyclonal antibodies against the amino and the carboxyl terminals of BACE1. Using these antibodies, BACE1 was characterized in temporal lobe cortices by Western blotting and immunohistochemistry. Immunohistochemical studies employing anti-GFAP and anti-MAP2 antibodies as well as anti-BACE1 antibodies showed that BACE1 was expressed exclusively in neurons but not in glial cells. Brain samples were directly extracted by 0.5% SDS and analyzed by Western blotting and densitometer. Although the mean level of BACE1/mg protein in AD brains was not increased, the ratio of BACE1 to MAP2 or to NSE was significantly increased compared with that in control brains. Taken together, these findings suggest that those neurons that survive in AD brains might generate more BACE1 than normal neurons in control brains, indicating that increased BACE1 activity could be one of the causes of AD. This could justify the development of anti-BACE1 drugs for AD treatment.

Alzheimer Disease↗
PubMed2005

Bladder and bowel dysfunction in chronic inflammatory demyelinating polyradiculoneuropathy.

We present a patient with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) who developed severe bladder and bowel dysfunction (BBD) as evidenced by constipation, voiding difficulty, and urinary urgency. These symptoms appeared 10 years after onset of CIDP. Cystometry showed disturbance of bladder sensation and detrusor areflexia. Magnetic resonance imaging (MRI) showed greatly enlarged nerve roots filling the lumbosacral spinal canal; this appeared to be the likely cause of BBD. A 3-day course of intravenous methylprednisolone (1 g/day), followed by 30 mg/day of oral prednisolone, ameliorated the sensory disturbance and muscle weakness, but not BBD.

Journal Article↗
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

Long-term results of the two-stage palatoplasty/Hotz' plate approach for complete bilateral cleft lip, alveolus and palate patients.

PURPOSE: To investigate the effects of the two-stage palatoplasty combined with the Hotz' plate on craniofacial development in patients with bilateral complete clefts. MATERIAL AND METHODS: Lateral and frontal cephalograms of two-stage palatoplasty/Hotz' plate group (n=10), one-stage palatoplasty group (n=11), and a non-cleft group (n=11), were evaluated at 6, 8, 10 and 12 years of age. The unpaired Student's t-test and Scheffe's F test (p<0.05) were applied. RESULTS: At 6 years the posterior upper facial height (PUFH) and PUFH/PFH ratio were greater in the two-stage group. At 10 years the PUFH, maxillary depth, convexity and ANB angle were greater in the same group. At 12 years, maxillary depth and ANB angle were also greater in this group. In the one-stage group, the L1/Mp. angle, PUFH and PUFH/PFH ratio were smaller when compared with the non-cleft group, whereas the palatal plane/SN angle was greater. In both cleft groups, the I.I. angle and tongue-PTM' distance were greater, and the U1/SN angle was smaller when compared with non-clefts. The UC-UC' and the ratios UC/MAX and UC/LC of both cleft groups were also smaller when compared with non-clefts. The ratio UM/MAX of the one-stage group was smaller when compared with the non-cleft group. CONCLUSION: The two-stage palatoplasty in combination with application of the Hotz' plate had good effects on the maxillary growth up to the age of 12 years.

Alveolar Process↗
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

Overexpression of basic fibroblast growth factor and Bcl-xL with adenoviral vectors protects primarily cultured neurons against glutamate insult.

OBJECTIVE: Excitatory amino acid (EAA) toxicity seems to be an important mechanism of neuronal cell death after cerebral infarction. We examined the inhibitory effects of neuronal cell death caused by EAA in vitro by means of adenoviral gene transfer of neurotrophic basic fibroblast growth factor (bFGF) and antiapoptotic Bcl-xL. METHODS: Recombinant adenoviral vectors expressing human bFGF gene with secretory signals of interleukin-2 and human Bcl-xL gene were constructed. Primarily cultured rat neuronal cells were treated with glutamate to cause EAA, and the neuroprotective effects of gene transfer by these adenoviral vectors were investigated at several time points of infection. RESULTS: Each adenoviral infection to primarily cultured neuronal cells exhibited neuroprotective effects against EAA caused by glutamate. Both gene transfer of bFGF with secretory signal and Bcl-xL transfer to neuronal cells exhibited the synergistic neuroprotective effects against EAA. These effects were most prominent with gene transfer 4 hours before glutamate insult; gene transfer performed simultaneously with and up to 4 hours after the insult exhibited definite neuroprotective effects. CONCLUSION: These experiments revealed marked neuroprotective effects of adenoviral gene transfer of bFGF and Bcl-xL into neuronal cells in vitro. The findings may lead to new approaches for treating occlusive cerebrovascular disease.

Adenoviridae↗