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Biomedical subjects

N Aoki

Publications and source records attributed to N Aoki.

At least 19 recordsLinked to original sources
PubMed1992

Detection of JC virus in the brains of aged patients without progressive multifocal leukoencephalopathy by the polymerase chain reaction and Southern hybridization analysis.

Ninety-one brain tissue sections taken at autopsy from 33 elderly patients (63-100 years old) without progressive multifocal leukoencephalopathy were examined for the presence of JC virus DNA by the polymerase chain reaction and Southern hybridization analysis after DNA extraction. JC virus DNA was detected in 15 sections from 10 patients. These results suggest that JC virus is frequently present in the brains of aged patients.

Aged↗
PubMed1992

Cardiac metastasis of lung cancer. A study of metastatic pathways and clinical manifestations.

BACKGROUND: Although lung cancer frequently spreads to the heart, details of cardiac metastases of lung cancer have not been fully discussed. The authors attempted to elucidate the relationship between the mechanisms of cardiac metastasis and a variety of clinical manifestations caused by cardiac metastasis. METHODS: Clinical and autopsy records were reviewed in 74 autopsied cases of lung cancer. In cases with cardiac metastasis, the metastatic pathways to the heart were determined by the macroscopic examinations, and the relationship between the metastatic pathways and the clinical manifestations were studied. RESULTS: Metastases to the pericardium or heart were seen in 23 cases (31%). A lymphatic metastatic pathway was detected in 18 cases (hilar lymphatic routing in 12 cases, and mediastinal lymphatic routing in 6 cases), and a hematogenous metastatic pathway was detected in 5 cases. Malignant pericardial effusion was documented in 15 of 23 cases. The metastatic pathway in 14 of 15 cases was lymphatic (hilar lymphatic routing in 10 cases, and mediastinal lymphatic routing in 4 cases). Patients showing lymphatic metastasis had higher incidence of malignant pericardial effusion than those with hematogenous metastasis (P less than 0.05). Of 23 cases of cardiac metastasis, myocardial infarction was found in 1 case, resulting from the compression of the coronary arteries by the tumor. Concurrent supraventricular arrhythmias were recorded in eight cases with cardiac metastasis. Patients with cardiac metastasis had higher incidence of arrhythmia than those without cardiac metastasis (P less than 0.05). In cases of cardiac metastasis, patients with arrhythmia were older (P less than 0.01) than those without arrhythmia. CONCLUSIONS: The authors concluded that the hilar lymphatic pathway is essential for early development of malignant pericardial effusion in lung cancer and that aging and cardiac metastasis may be responsible for arrhythmia in patients with lung cancer.

Age Factors↗
PubMed1992

Protein C deficiency Hong Kong 1 and 2: hereditary protein C deficiency caused by two mutant alleles, a 5-nucleotide deletion and a missense mutation.

We characterized a mutant protein C gene from an individual with no detectable protein C antigen in blood plasma. Southern blot hybridization analysis with human protein C cDNA demonstrated neither gross deletion nor rearrangement of the gene. Sequencing all the exons and exon-intron boundaries of the gene except the 3' noncoding region showed two mutant alleles. The one, derived from the mother, represents a deletion of 5 nucleotides (nt) (CCCGC) in the end of exon VI (mutation I), predicted to result in the generation of a new stop codon due to a reading frameshift and the premature termination of translation. The other, derived from the father, represents a point mutation (G to A) in exon IX (mutation II), resulting in an amino acid substitution, Gly-376(GGC) to Asp(GAC), in the catalytic domain of the protein. Allele-specific oligonucleotide probe hybridization confirmed the presence of the two mutations. Mutation I would result in a truncated polypeptide of 169 amino acid residues that lacks the heavy chain. Mutation II gives rise to an alteration of a highly conserved amino acid, Gly-376. These data indicate that this patient is a compound heterozygote of the two mutant alleles, each one inherited from each parent. Transient expression assays using COS-7 cells transfected with mutated protein C expression vectors suggested that each of the two mutations leads to the protein C deficiency by causing an impairment of secretion of the respective mutant proteins.

Amino Acid Sequence↗
PubMed1992

Molecular basis for Glanzmann's thrombasthenia (GT) in a compound heterozygote with glycoprotein IIb gene: a proposal for the classification of GT based on the biosynthetic pathway of glycoprotein IIb-IIIa complex.

The genetic basis for Glanzmann's thrombasthenia (GT) was elucidated on a compound heterozygote with glycoprotein (GP)IIb gene: an opal mutation at the end of exon 17 (CGA----TGA) results in only a trace amount of GPIIb mRNA, and a splicing mutation at the acceptor site of exon 26 (CAG----GAG) causes an in-frame, exon skipping process from exon 25 to 27. This aberrant transcript encodes a single-chain polypeptide characterized by a 42-amino acid deletion, which includes the proteolytic cleavage site(s) and a unique, proline-rich region at the location corresponding to the carboxyl-terminal of the normal GPIIb alpha-chain. These characteristics are shared by a previously reported defective GPIIb molecule, which is neither assembled with GPIIIa nor transported to the cellular surface. Despite its normal transcription level, expression of the present defective GPIIb molecule was significantly decreased (approximately 6% of the control level). Because the precursor GPIIb molecule is assembled with GPIIIa in the endoplasmic reticulum (ER) and its processing, as well as stability, is dependent on the GPIIIa subunit, the defective GPIIb molecule may be rapidly degraded by the intrinsic quality control system of the ER due to its inability to form a stable heterodimer complex as a consequence of its misfolded structure. Although we did not confirm that the GPIIIa genes of this individual were normal, GPIIIa may be secondarily decreased (approximately 11% of control), because a large part of it could not be complexed, making it vulnerable to proteolysis. To elucidate the molecular basis for GT, we propose here a classification of GT based on the biosynthetic pathway of the GPIIb-IIIa complex.

Base Sequence↗
PubMed1992

Chlorination of cellulose with N-chlorosuccinimide-triphenylphosphine under homogeneous conditions in lithium chloride-N,N-dimethylacetamide.

Microcrystalline cellulose was chlorinated with N-chlorosuccinimide-triphenylphosphine under homogeneous conditions in LiCl-N,N-dimethylacetamide. At the early stage of the reaction only replacement of the 6-hydroxyl groups with chlorine was observed, and 3-hydroxyl groups were replaced at a lower rate with Walden inversion. The effects of reaction conditions on the extent of chlorination were studied in detail. More than two equivalents of chlorination reagents per glucose residue were necessary to attain a high degree of substitution (ds) by chlorine, and the maximum ds attained was 1.86. Chlorinated disaccharides were found in the hydrolyzates of chlorodeoxycelluloses hydrolyzed under mild conditions, and their structures were studied by mass spectrometry.

Acetamides↗
PubMed1992

Frequent rearrangements of retinoic acid receptor alpha gene and myl gene, and rare mutations of RAS and FMS genes in acute promyelocytic leukemia.

To investigate leukemogenesis of acute promyelocytic leukemia (APL), we studied the involvements of retinoic acid receptor alpha (RAR alpha) and myl genes, and also the frequency of N-RAS, K-RAS, H-RAS, and FMS point mutations in sixteen patients with APL. By Southern blot analysis, the rearrangements of RAR alpha gene were detected in 13 patients (81.2%), and myl gene in 14 (87.5%). Either RAR alpha or myl gene rearrangements were found in all patients including one with normal karyotype. Breakpoints of both genes were clustered. By direct sequencing, no point mutations were found at codons 12, 13, and 61 of N-, K-, and H-RAS genes, and at codons 301 and 969 of FMS gene. These data indicate that myl-RAR alpha translocation occurs frequently in APL, whereas RAS and FMS mutations are rare in APL. It may be suggested that leukemogenesis of APL is different from other subtypes of acute myelogenous leukemia, and multistep leukemogenesis may not be a prevalent feature in APL.

Adolescent↗
PubMed1992

Percutaneous fenestration of dissecting intima with a transseptal needle. A new therapeutic technique for visceral ischemia complicating acute aortic dissection.

Noncardiac visceral ischemia is a major complication with acute aortic dissection and is caused by obstruction of the major visceral arteries by dissecting intima. Two patients with this condition underwent emergency percutaneous fenestration of dissecting intima, and the blood flow to the lower extremity and kidney was restored. A transseptal needle and peripheral angioplasty balloon catheter were used for fenestration. There were no associated complications in either patient. One patient was treated medically and another had ascending aortic replacement surgery the day after percutaneous fenestration. Clinical follow-up of 10 and 5 months, respectively, revealed good clinical outcomes. Percutaneous fenestration should be considered the treatment of choice for visceral ischemia due to acute aortic dissection.

Aortic Dissection↗
PubMed1992

A new therapeutic method for chronic subdural hematoma in adults: replacement of the hematoma with oxygen via percutaneous subdural tapping.

Seeking radical removal of chronic subdural hematoma using a simple and less invasive procedure, the author has devised a new method--replacement of the hematoma with oxygen via percutaneous subdural tapping. In this study, 40 patients were treated with this procedure. All patients made a full recovery after the treatment, without complications related to replacement of the hematoma with oxygen. Follow-up investigation showed recurrence of the lesion in two patients (5%). Because of its simplicity, reduced invasiveness, and short hospitalization, the procedure presented here is acceptable as an optimal therapeutic modality for chronic subdural hematoma in adults. Theoretical considerations supporting the safety of this procedure are discussed.

Adult↗
PubMed1992

Enzymic method for the spectrophotometric determination of choline in liquor.

A sensitive spectrophotometric method for the determination of choline in liquor is described. The method involves the conversion of choline into formaldehyde by sequential enzymic reactions (choline oxidase and catalase), followed by the formation of a chromophore with 4-aminopent-3-en-2-one. The calibration graph was linear in the range 0.4-15 micrograms cm-3 of choline. The relative standard deviation at 5 micrograms cm-3 of choline was 1.3%. There was no interference from most of the common ingredients of liquor. More than 95% of choline added at two levels was recovered from real samples. The method is simple, and the detection limit was 2 micrograms g-1 when 5 g of sample were assayed.

Alcohol Oxidoreductases↗
PubMed1992

Infantile acute encephalopathy with combined symmetrical hypodensities in the thalami and the putamen on computed tomography.

An eight-month-old boy with clinical features of acute encephalopathy with symmetrical low-density areas in the thalami and the putamen on computed tomography is presented. These particular computed tomography features suggest potential aetiology common to acute encephalopathy with low-density areas in the thalami and infantile bilateral striatal necrosis with an acute onset. The therapeutic consideration of these conditions is also discussed.

Acute Disease↗
PubMed1992

Muscimol suppresses rCGU increase in the substantia nigra after destruction of the caudate nucleus.

Injection of ibotenic acid into the caudate nucleus caused an increase in the uptake of 2-deoxyglucose (2DG) in the ipsilateral substantia nigra pars reticulata (SNr). Increased 2DG uptake was completely suppressed by chronic infusion of muscimol, the gamma-aminobutyric acid (GABA) agonist. While delayed shorter infusion of muscimol from the 3rd to the 7th day, when 2DG accumulation was the most prominent, partially prevented this increase. These data suggest that GABA-mediated transneuronal processes play an important role in the delayed elevation in 2DG uptake in SNR but hyperexcitation due to disinhibition by the loss of GABAergic inputs may play only a partial role in this increase.

Animals↗