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Biomedical subjects

K Fukushima

Publications and source records attributed to K Fukushima.

At least 289 records · Page 16Linked to original sources
PubMed1995

Pregnancy outcome among long-term survivors with acute leukemia.

By means of a mail questionnaire, we evaluated the influence of treatment for acute leukemia on offspring of long-term survivors and determined whether the outcome of pregnancy in patients (or spouses) induced relapse of acute leukemia. In 322 replies from the 445 institutions where a questionnaire was sent, there were 1136 adult long-term survivors. We analyzed the 43 adults who had become pregnant or become a father after postremission therapy. The mean age at the leukemia onset was 26.4 and 21.6 years for males and females. Forty-six normal children (26 boys and 20 girls) were born of long-term survivors including 7 pairs of siblings and a pair of twin sisters. There were no malformed babies. There were five abortions. The average duration until delivery was 79 months after diagnosis, and 49 months after the final postremission therapy. Four of 38 parents of live offspring died (3 relapse, 1 other disease), and the other 34 parents of live offspring were in complete remission at the point of this survey. The adverse effect of treatment on the offspring of long-term survivors could not be clarified in this survey. Additional lifetime follow-up of long-term survivors with acute leukemia and their offspring may be necessary.

Acute Disease↗
PubMed1995

Carcinoma of the ampulla of Vater synchronously associated with early gastric cancer--a report of two cases.

We report two cases of carcinoma of the ampulla of Vater synchronously associated with early gastric cancers. The gastric lesions were diagnosed pre-operatively in one patient and at the time of examination of the resected specimen following pancreatoduodenectomy in the other. Specific problems in the diagnosis and management of these multiple primary carcinomas are discussed. Careful evaluation of the stomach prior to the surgical treatment for ampullary carcinoma is recommended.

Aged↗
PubMed1995

Carbohydrate structures of a normal counterpart of the carcinoembryonic antigen produced by colon epithelial cells of normal adults.

Normal faecal antigen-2 (NFA-2) and non-specific cross-reacting antigen-2 (NCA-2), cross-reacting with anticarcinoembryonic antigen (CEA) antibodies, were found in normal human faeces and meconium, respectively. Because NFA-2, NCA-2 and CEA are considered as the same gene products, NFA-2 and NCA-2 should be normal counterparts of CEA produced by colon epithelial cells of normal adults and fetuses, respectively. Comparison of sugar chain structures of these three antigens is indispensable in order to unravel the structural alteration induced by malignant transformation and development of colon epithelial cells. The sugar chain structures of CEA (Yamashita, K. et al., Cancer Res., 47, 3451-3459, 1987) and NCA-2 (Yamashita, K. et al., J. Biol. Chem., 264, 17873-17881, 1989) were previously reported. In this paper, the structures of the oligosaccharides released from four NFA-2 samples by hydrazinolysis were studied by means of lectin-affinity column chromatography, endo- and exo-glycosidase digestion, methylation analysis, hydrazinolysis-nitrous acid deamination and electrospray ionization mass spectrometry. NFA-2 contains 24-27 mol of N-linked sugar chains/molecule, which is similar to NCA-2 (27 mol) and CEA (24-27 mol). In contrast to CEA, which contains approximately 8% high-mannose-type sugar chains, all sugar chains of NFA-2 are mono- to tetra-antennary complex-type chains having four types of tri-mannosyl cores, with or without bisecting N-acetylglucosamine and fucose residues. The structures of their outer chain moieties comprise Gal beta 1-->3(HSO(3-)-->6)GlcNAc, Neu5Ac alpha 2-->3Gal beta 1-->3GlcNAc, Type 1, repeating chain, Type 2, Type 2H, Type 1H, Lex, Lea and Leb antigenic determinants. Approximately 50% of the outer chain moieties of the oligosaccharides of NFA-2 contain Type 1 chain, in contrast to those of CEAs produced by the liver metastases of colon tumours in which only a trace amount of Type 1 chain was detected.

Adult↗
PubMed1995

A gene for autosomal dominant nonsyndromic hereditary hearing impairment maps to 4p16.3.

Mapping genes for nonsyndromic hereditary hearing impairment may lead to identification of genes that are essential for the development and preservation of hearing. We studied a family with autosomal dominant, progressive, low frequency sensorineural hearing loss. Linkage analysis employing microsatellite polymorphic markers revealed a fully linked marker (D4S126) at 4p16.3, a gene-rich region containing IT15, the gene for Huntington's disease (HD). For D4S126, the logarithm-of-odds (lod) score was 3.64 at theta = 0, and the overall maximum lod score was 5.05 at theta = 0.05 for D4S412. Analysis of recombinant individuals maps the disease gene to a 1.7 million base pair (Mb) region between D4S412 and D4S432. Genes for two types of mutant mice with abnormal cochleovestibular function, tilted (tlt) and Bronx waltzer (bv), have been mapped to the syntenic region of human 4p16.3 on mouse chromosome 5. Further studies with the goals of cloning a gene for autosomal nonsyndromic hearing impairment and identifying the murine homologue may explain the role of this gene in the development and function of the cochlea.

Adolescent↗
PubMed1995

Localization of a gene for non-syndromic hearing loss (DFNA5) to chromosome 7p15.

Progressive hearing loss affects approximately 50% of the elderly by the age of 80, and is most likely caused by an interaction of genetic and environmental factors. Identification of the genes responsible for hereditary hearing loss is therefore important. Families with pure genetic degenerative hearing disorders may be helpful as the same genes may be also involved in age-related hearing loss in general. In this study we have performed a genome search in an extended Dutch family with autosomal dominant progressive hearing loss starting in the high frequencies. The gene causing hearing loss in this family was localized to the short arm of chromosome 7, in a 15 cM interval between markers D7S493 and D7S632.

Chromosome Mapping↗
PubMed1995

A human recessive neurosensory nonsyndromic hearing impairment locus is potential homologue of murine deafness (dn) locus.

A locus for recessive neurosensory nonsyndromic hearing impairment maps to chromosome 9q13-q21 in two regionally separate consanguineous families from India. Each family demonstrates a LOD score greater than 4.5 to this region. D9S15, tightly linked to the Friedreich's ataxia locus, a region that has been defined with over 1 Mb of YAC contig information and several expressed sequences, is one of the flanking markers. In mice, the deafness (dn) locus maps to mouse chromosome 19 and flanking loci are syntenic to human chromosome 9q11-q21. The dn mouse is a potential model for the hearing impairment found in both these families.

Chromosome Mapping↗
PubMed1995

Linkage of a gene for dominant non-syndromic deafness to chromosome 19.

Inherited hearing impairment can occur either in the presence of other clinical features (syndromic hearing loss, SHL) or in isolation (non-syndromic hearing loss, NSHL). The latter is more common and is highly heterogeneous. To date, six NSHL loci have been mapped. We report the identification of a seventh locus (DFNA4) on chromosome 19q13 and suggest DM kinase as a possible candidate gene.

Chromosome Mapping↗
PubMed1995

Consanguineous nuclear families used to identify a new locus for recessive non-syndromic hearing loss on 14q.

Hearing impairment is inherited most frequently as an autosomal recessive isolated clinical finding (non-syndromic hearing loss, NSHL). Extreme heterogeneity and phenotypic variability in the audiometric profile preclude pooling of affected families and severely hamper gene mapping by conventional linkage analysis. However, in instances of consanguinity, homozygosity mapping can be used to identify disease loci in small nuclear families. This report demonstrates the power of this technique by identifying a locus for recessive NSHL on 14q (DFNB4).

Chromosome Mapping↗
PubMed1995

Plasma N-methylhistamine concentration as an indicator of histamine release by intravenous d-tubocurarine in humans: preliminary study in five patients by radioimmunoassay kits.

Histamine disappears rapidly from plasma because of its short half-life. Because a metabolite of histamine, N-methylhistamine, is stable and has a longer half-life, determination of its plasma concentration can be useful in retrospective determination of histamine release. In this study, we measured plasma histamine and N-methylhistamine concentrations after d-tubocurarine (dTc) administration to evaluate the use of plasma N-methylhistamine measurement for confirming histamine release. After the induction of anesthesia, five patients received dTc, 0.8 mg/kg intravenously. A radioimmunoassay kit was used to determine plasma histamine and N-methylhistamine before and 1, 3, 5, and 10 min after administration of dTc. Histamine released by the injection of dTc reached a maximum level at 1 min, but decreased rapidly, whereas N-methylhistamine increased at 1 min and remained increased for at least 10 min. Good correlations were found between histamine concentration at 1 min and N-methylhistamine concentrations at 1, 3, 5, and 10 min, especially r = 0.999 (n = 5) at 10 min. N-Methylhistamine measurement with this kit can ascertain histamine release retrospectively in a semiquantitative manner.

Anesthesia↗
PubMed1995

An autosomal recessive nonsyndromic form of sensorineural hearing loss maps to 3p-DFNB6.

Autosomal recessive nonsyndromic hearing loss (ARNSHL) is the most common form of congenitally acquired inherited hearing impairment. Although numerous loci are believed to exist, only five have been identified. Using a pooled genomic DNA screening strategy, we have identified a sixth locus, DFNB6, on 3p in the interval bounded by D3S1619 and D3S1766.

Alleles↗
PubMed1995

Discharge characteristics of vestibular and saccade neurons in the rostral midbrain of alert cats.

1. The interstitial nucleus of Cajal (INC) is involved in generation of vertical eye movements. To further explore the neural substrates of INC involvement in eye movements, we examined the discharge characteristics of neurons in the rostral midbrain that discharge for vestibular stimulation and saccades in alert cats. We analyzed 75 vestibular and saccade neurons (VSNs) that showed characteristic discharge during pitch rotation. Of these, 50 exhibited gradually increasing activity during upward slow phases and burst of action potentials during downward fast phases induced by downward pitch. The remaining 25 cells showed the opposite response pattern: gradually increasing activity during downward slow phases and a burst during upward fast phases induced by upward pitch. We classified these cells as downward VSNs and upward VSNs, respectively. The effects of electrical stimulation of the contralateral vestibular nerve were tested for 13 downward VSNs and 2 upward VSNs; all of them were activated at short latencies. 2. All vertical VSNs also showed burst activity associated with spontaneous saccades. The preferred direction for the burst was always the same for saccades and vestibular fast phases. The onset of burst activity preceded the onset of fast eye movement by an average of 35 +/- 14 ms (mean +/- SD). During fast eye movement in other directions, many of these cells also showed an inconsistent burst and the burst often began after the onset of saccades. Half of the upward VSNs examined showed a pause in activity during downward fast eye movement. 3. Burst parameters in the preferred directions were correlated with saccade parameters in half of the vertical VSNs examined, although the correlation coefficients were typically 0.5-0.6. 4. All vertical VSNs had irregular resting activity. Half of the downward VSNs examined showed eye-position sensitivity toward the direction opposite to the preferred direction for the burst activity but only if the period of analysis was restricted to discharge shortly before and after saccades. 5. All downward VSNs examined during sinusoidal rotation in several vertical planes received strong excitatory input from the contralateral anterior canal. Three of four upward VSNs examined received contralateral posterior canal excitation; the exception received ipsilateral posterior canal excitation.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1995

Volatile fatty acids, metabolic by-products of periodontopathic bacteria, inhibit lymphocyte proliferation and cytokine production.

Short-chain fatty acids are a major by-product of anaerobic metabolism and can be detected in gingival fluid from periodontal pockets. Since most T cells are present subjacent to the pocket epithelium in conjunction with the plasma cells, it is important to know how these T cells are affected by short-chain fatty acids produced by subgingival plaque. The purpose of this study is to examine the effects of extracellular metabolites from periodontopathic bacteria on the proliferation and cytokine production of mouse splenic cells as a potential mechanism of imbalance among host-microbial interactions. A low-molecular-weight, heat-stable agent present in the two-day culture filtrate of Porphyromonas gingivalis, Prevotella loescheii, and Fusobacterium nucleatum significantly depressed Con A- and LPS- induced cell proliferation. To determine whether short-chain fatty acids present in the filtrate could account for the depression, we tested extracted volatile and non-volatile fatty acids for their effects on mitogenic activity. The volatile fatty acids extracted from immunosuppressive supernatants greatly inhibited T- and B- cell proliferation. Among these volatile fatty acids, butyric, propionic, valeric, and isovaleric acids impaired cell proliferation dose-dependently. From gas-liquid chromatographic analysis data, it is suggested that immuno-inhibitory activities in culture filtrates are mainly attributable to butyric and isovaleric acids in P. gingivalis, to propionic, butyric, and isovaleric acids in P. loescheii, and to butyric acid in F. nucleatum. Furthermore, these fatty acids significantly depressed interleukin 2 (IL-2), IL-4, IL-5, IL-6, and IL-10 production by Con A-stimulated splenic-T cells dose-dependently.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Transient elevation of granulocyte colony-stimulating factor levels in cerebrospinal fluid at the initial stage of aseptic meningitis in children.

At the early stage of aseptic meningitis, there is a transient increase in neutrophil counts in the cerebrospinal fluid. Some factors in the cerebrospinal fluid might induce migration of neutrophils into the cerebrospinal fluid. Granulocyte colony-stimulating factor (G-CSF) plays an important role, not only as a hemopoietic factor but also as a regulating factor for a biologic defense system by neutrophils in the foci of infection. To analyze the role of G-CSF on accumulating neutrophils in the cerebrospinal fluid, we have measured G-CSF levels in the cerebrospinal fluid of children with aseptic meningitis, paying particular attention to the phasal transition. Within the first 2 d from the onset, G-CSF levels in the cerebrospinal fluid were 223 +/- 97 ng/L, significantly higher than those of the patients without meningitis (p < 0.01). Beyond the second day after the onset, the G-CSF levels rapidly decreased to below the detectable level, even though the patients manifested meningeal signs and symptoms. There was a direct relationship between G-CSF levels and neutrophil counts in the cerebrospinal fluid (r = 0.763, p < 0.01). During the first 2 d after the onset, the G-CSF level in the cerebrospinal fluid in each case was remarkably higher than that in the serum. This finding suggests that the G-CSF in the cerebrospinal fluid was produced in the spinal cavity. From our results, the transient elevation of G-CSF levels might lead to the transient increase in neutrophil counts in the cerebrospinal fluid by recruiting them from the peripheral blood at the initial stage of aseptic meningitis.

Adolescent↗
PubMed1995

Purification and characterization of glutathione-independent denitration enzyme of organic nitrate esters in rabbit hepatic cytosol.

The enzyme responsible for glutathione (GSH)-independent denitration of organic nitrate esters was purified by gel chromatography, ion-exchange chromatography and affinity chromatography from rabbit hepatic cytosol. The enzyme showed a molecular mass of 175 kDa and consisted of three subunits of 59 kDa. The enzyme exerted its maximum activities at around pH 9, when isosorbide dinitrate (ISDN) was used as substrate. The enzyme possessed a low Km value (10(-6) M) for various organic nitrate esters. The present enzyme is likely to be involved in the denitration of organic nitrate esters in conjunction with known enzymes, GSH S-transferase (GST) and cytochrome P450.

Ammonium Sulfate↗
PubMed1995

Metabolism of a nitrate ester, dihydropyridine derivative in rabbit hepatic microsomes and cytosol.

1. The metabolism of a nitrate ester-substituted dihydropyridine derivative (NND) in vitro was characterized with rabbit hepatic microsomes and cytosol. 2. Denitration activity was located in both the microsomal and cytosolic fractions, whereas oxidation to the pyridine analogue was solely located in the microsomal fraction. 3. Oxidation to the pyridine analogue required NADPH and was inhibited by carbon monoxide, miconazole and SKF-525A, suggesting that oxidation was catalysed by P450. 4. Denitration activity in the microsomes required either NADPH or GSH. Together with these results, responses to various inhibitors indicate participation of both P450 and glutathione S-transferase (GST). 5. Denitration activity in cytosol was activated by glutathione (GSH), and by dithiothreitol (DTT) to a greater extent. GSH-dependent denitration was inhibited by S-hexyl GSH, an inhibitor of GST, but DTT-dependent denitration was not. Moreover, the formation patterns of the mono-denitrated metabolites, M1 and M2, were shown to be different in each incubation condition. 6. These results suggest that the denitration of NND in cytosol could be catalysed by a GSH-independent enzyme as well as the GSH-dependent enzyme, GST.

Animals↗