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Biomedical subjects

K Hayasaka

Publications and source records attributed to K Hayasaka.

At least 145 records · Page 8Linked to original sources
PubMed1994

[Treatment and prognostic factors of stage I and II non-Hodgkin's lymphoma].

In order to assess prognostic factors and therapeutic methods, 104 patients (aged 6 to 89; mean age 57.4; male 68, female 36; stage: I 45, II 59) with clinical stages I and II non-Hodgkin's lymphoma treated at our department between 1977 and 1991 were reviewed. Factors, such as sex, age, clinical stage, primary site, presence of general symptoms, pathology, tumor size, LDH and therapeutic methods (radiotherapy alone; initial radiotherapy plus chemotherapy; initial chemotherapy plus radiotherapy) were calculated by univariated analysis to determine important factors influencing the survival. The survival of patients with symptoms and large tumors (more than 70 mm) was shorter than that of those without symptoms and with small tumors (5 years survival: symptom B 17.9%, A 68.2%, p < 0.001; tumor more than 70 mm 44.0%, less than 70 mm 67.1%, p < 0.05). Regarding therapeutic methods, radiotherapy alone achieved a 5-year survival rate of 37.1%; initial radiotherapy plus chemotherapy had 64.6% and initial chemotherapy plus radiotherapy 78.5%, but a significant difference was noticed only between radiotherapy alone and initial chemotherapy plus radiotherapy (p < 0.001). These results suggest that important factors influencing the survival are presence of general symptoms, tumor size and therapeutic methods.

Adolescent↗
PubMed1993

Mutation of the myelin P0 gene in Charcot-Marie-tooth neuropathy type 1.

We had previously reported that the myelin P0 gene was responsible for Charcot-Marie-Tooth neuropathy type 1B (CMT1B). In this study we found a different mutation of the P0 gene in a family of Charcot-Marie-Tooth neuropathy type 1 without a DNA duplication in chromosome 17p11.2. The mutation, a histidine substitution for arginine at amino acid position 98, is located in the extracellular domain of P0 like as the mutations in the three pedigrees with CMT1B. The extracellular domain forms an immunoglobulin domain responsible for the function of P0 as an adhesion molecule. Alterations in the tertiary structure of the extracellular domain of P0 would modify the function of P0, resulting in an impairment of peripheral myelin compaction.

Adult↗
PubMed1993

Isolation and sequence determination of cDNA encoding human T-protein of the glycine cleavage system.

We present the full-length cDNA sequence of human T-protein of the glycine cleavage system. Overlapping cDNA clones were isolated by screening human liver cDNA libraries with bovine T-protein cDNA. The 1209 base pair open reading frame encodes 403 amino acid precursor protein, and the deduced amino acid sequence of the mature peptide shows 90 and 68% homology to that of bovine and chicken counterpart, respectively. RNA blot analysis of human liver transcripts and Southern blot analysis of human genomic DNA confirm that human T-protein is encoded by a single gene.

Adult↗
PubMed1993

Structure and chromosomal localization of the gene encoding the human myelin protein zero (MPZ).

We describe the cloning, characterization, and chromosomal mapping of the human myelin protein zero (MPZ) gene. The gene is about 7 kb long and consists of six exons corresponding to the functional domains. All exon-intron junction sequences conform to the GT/AG rule. The 5'-flanking region of the gene has a TA-rich element (TATA-like box), two CAAT boxes, and a single defined transcription initiation site detected by the primer extension method. The gene for human MPZ was assigned to chromosome 1q22-q23 by spot blot hybridization of flow-sorted human chromosomes and fluorescence in situ hybridization. The localization of the MPZ gene coincides with the locus for Charcot-Marie-Tooth disease type 1B, determined by linkage analysis.

Base Sequence↗
PubMed1993

The gamma-globin genes and their flanking sequences in primates: findings with nucleotide sequences of capuchin monkey and tarsier.

By sequencing extensive regions of the beta-globin gene cluster from capuchin monkey (New World monkey) and tarsier (prosimian) we confirmed that capuchin monkey and tarsier have two and one gamma-globin gene(s), respectively. These findings indicate that the ancestral anthropoid gamma-globin gene duplicated after anthropoids diverged from tarsier, but before they diverged into platyrrhines (New World monkeys) and catarrhines (Old World monkeys, apes, and human). The capuchin monkey gamma 1-globin gene promoter region accumulated many nucleotide substitutions, including a T to C substitution in the proximal CCAAT element. This adverse mutation, along with the previous finding that the gamma 1 locus in spider monkey is a pseudogene, suggests that in platyrrhines the gamma 2-globin gene may be the primary fetal beta-like globin gene. The aligned gamma gene sequences contain several conserved sequence elements (phylogenetic footprint) of 6 bp or longer in the 5' flanking region, but none in the 3' flanking region. Gene conversions frequently occurred in the 5' flanking and transcribed regions of the duplicated genes of anthropoids but rarely in the 3' flanking sequences. However, an absence of conversions within the capuchin and spider monkeys promoter regions suggests that in platyrrhines selection acted against conversions as they could decrease (or inactivate) gamma 2 expression.

Amino Acid Sequence↗
PubMed1993

Structure and localization of the gene encoding human peripheral myelin protein 2 (PMP2).

Peripheral myelin protein 2 (PMP2) is a small, basic, and cytoplasmic lipid binding protein of peripheral myelin. In this paper, we describe the cloning, characterization, and chromosomal mapping of the human PMP2 gene. The gene is about 8 kb long and consists of four exons. All exon-intron junction sequences conform to the GT/AG rule. The 5'-flanking region of the gene has a TA-rich element (TATA-like box) and a single defined transcription initiation site detected by the primer extension method. The gene for human PMP2 was assigned to chromosome 8q21.3-q22.1 by spot hybridization of flow-sorted human chromosomes and fluorescence in situ hybridization.

Base Sequence↗
PubMed1993

Tissue distribution of mutant mitochondrial DNA in mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS).

We analysed the distribution of mutant mitochondrial DNA (mtDNA) with A-to-G substitution mutation of tRNA(Leu)(UUR) in various autopsied tissues from a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). There was no significant difference in the proportion (76-86%) of mutant mtDNA in many tissues, except in the lung and spleen. Unequal partitioning of mtDNA in somatic cells appears less prominent than that in germ cells.

Adult↗
PubMed1993

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) decrease in diastolic left ventricular function assessed by echocardiography.

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) are known to be associated with cardiomyopathy. Systolic and diastolic left ventricular functions were assessed by M-mode and Doppler echocardiography in four patients with MELAS and in 14 normal controls. The interventricular septal thickness and left ventricular posterior wall thickness were greater (11.0 +/- 1.6 mm vs. 5.8 +/- 0.7 mm and 11.0 +/- 2.2 mm vs. 5.9 +/- 0.8 mm) in patients with MELAS than in a control group. Parameters of systolic left ventricular functions (ejection fraction, shortening fraction, systolic time intervals, and mean Vcf) and left ventricular dimensions were not significantly different between the two groups. To assess the diastolic function, blood flow velocity across the mitral valve was measured by Doppler echocardiography and various indexes were obtained. In patients with MELAS, the impairment of diastolic left ventricular filling was demonstrated by decrease in the following indexes: peak flow velocity in the early passive filling period (E) (0.76 +/- 0.10 m/s vs. 0.94 +/- 0.09 m/s), integrated velocity for total E (10.2 +/- 1.3 vs. 13.0 +/- 0.9), the ratio of E and late atrial filling integrated velocities (1.72 +/- 0.06 vs. 2.49 +/- 0.29).

Adolescent↗
PubMed1993

Atypical nonketotic hyperglycinemia confirmed by assay of the glycine cleavage system in lymphoblasts.

A 13-year-old girl with early-onset, mild, slowly progressive mental retardation caused by nonketotic hyperglycinemia is described. The plasma and cerebrospinal fluid glycine concentrations were elevated, but the cerebrospinal fluid/plasma glycine ratio was only mildly elevated. The diagnosis was confirmed by demonstration of a defect in the activity of the glycine cleavage system in cultured lymphoblasts.

Adolescent↗
PubMed1993

Charcot-Marie-Tooth neuropathy type 1B is associated with mutations of the myelin P0 gene.

P0, a major structural protein of peripheral myelin, is a homophilic adhesion molecule and maps to chromosome 1q22-q23, in the region of the locus for Charcot-Marie-Tooth neuropathy type 1B (CMT1B). We have investigated P0 as a candidate gene in two pedigrees with CMT1B and found point mutations which are completely linked with the disease (Z = 5.5, theta = 0). The mutations, glutamate substitution for lysine 96 or aspartate 90, are located in the extracellular domain, which plays a significant role in myelin membrane adhesion. Individuals with CMT1B are heterozygous for the normal allele and the mutant allele. Our results indicate that P0 is a gene responsible for CMT1B.

Alleles↗
PubMed1993

De novo mutation of the myelin P0 gene in Dejerine-Sottas disease (hereditary motor and sensory neuropathy type III).

We have investigated the myelin P0 gene on chromosome 1 as a candidate gene in two sporadic cases with Dejerine-Sottas disease or hereditary motor and sensory neuropathy (HMSN) type III. We found different mutations, a cysteine substitution for serine 63 in the extracellular domain and an arginine substitution for glycine 167 in the transmembrane domain. The patients were genetically heterozygous for the normal allele and the mutant allele, which was absent in their parents and in one hundred unrelated, healthy controls. The results strongly suggest that a de novo dominant mutation of the P0 gene is responsible for at least some sporadic cases of Dejerine-Sottas disease.

Adolescent↗
PubMed1993

Mutation of the myelin P0 gene in Charcot-Marie-Tooth neuropathy type 1B.

We have previously reported that the mutations of the myelin P0 gene were completely linked with Charcot-Marie-Tooth neuropathy type 1B (CMT1B) in two families. In this study we found a different mutation in another family with CMT1B. The mutation, a methionine substitution for isoleucine at amino acid position 30, is located in the extracellular domain, which constitutes an immunoglobulin domain responsible for the function of P0 as an adhesion molecule. The results confirmed that P0 is a gene responsible for CMT1B.

Adult↗
PubMed1993

The effect of serum on low density lipoprotein metabolism of human monocyte-derived macrophages.

Macrophages oxidatively modify low density lipoprotein (LDL). These cells then recognize and take up oxidized LDL (OxLDL) via the scavenger receptor. In the present study, we examined the effect of lipoprotein depleted serum (LPDS) on the oxidative modification of LDL and its uptake and degradation by human monocyte-derived macrophages. LPDS inhibited LDL oxidation in a concentration-dependent manner and the complete inhibition was observed in the concentration from 2.5 to 10.0%. In the presence of 5% of LPDS, cell-associated 125I-LDL was reduced by 70%, compared with that in the absence of LPDS. In contrast, 125I-LDL degradation increased in the presence of LPDS. The ratio of degradation products to cell-associated radioactivity in the presence of LPDS was five-fold greater than that in the absence of LPDS. In the presence of LPDS, unlabeled LDL competed for about 50% of cellular uptake and degradation of 125I-LDL. In the absence of LPDS, however, unlabeled LDL competed for only 20% of uptake and only 30% of degradation of 125I-LDL. Unlabeled OxLDL competed for about 80% of uptake and degradation in the absence of LPDS. These results suggest that LPDS inhibited the production of OxLDL which was taken up by macrophages via the pathway for the OxLDL.

Blood Physiological Phenomena↗
PubMed1993

New mutation of the myelin P0 gene in a pedigree of Charcot-Marie-Tooth neuropathy 1.

P0, the major structural protein of peripheral myelin, is a homophilic adhesion molecule with a single immunoglobulin (Ig) domain, which contains a single N-linked glycosylation site and two cysteines. We have previously reported four different mutations of the myelin P0 gene in four families of Charcot-Marie-Tooth neuropathy type 1 (CMT1). In this study we found a new mutation of the myelin P0 gene in a small family of CMT1. The affected persons had an A - to - G substitution of nucleotide 245 of the myelin P0 gene in one allele, leading to a cysteine substitution for tyrosine82 in the extracellular Ig-domain. An additional cysteine in the extracellular domain may form a disulfide bond and cause an inappropriate change in the tertiary structure of the functional Ig-domain of P0.

Adolescent↗
PubMed1993

[Changes in the blood flow in celiac artery and superior mesenteric artery after stellate ganglion block].

We evaluated the effect of stellate ganglion block (SGB) on the blood flow of celiac artery (CA) and superior mesenteric artery (SMA) by using the ultrasonic pulse Doppler technique. The subjects were 15 healthy volunteers (14 males, one female; average 26 years old; 22-38). Right C7-SGB was performed using 5 ml of 1% mepivacaine at the 7th cervical process. Blood pressure, heart rate, mean blood flow velocity and diameter in CA and SMA, were measured after 5 minute rest, before and after SGB. To measure the flow velocity and the diameter of vessels, ultrasonic diagnostic equipment SSA-270A or SSA-260A (Thoshiba CO, Ltd.) with convex electric-phased 3.75 MHz, probe was used. Doppler shiftgrams of the CA and SMA were recorded. Then, we calculated their flow volume and sectional area of vessels. In CA mean blood flow velocity tended to decrease (P < 0.05) and both flow volume and sectional area of vessels tended to increase (P < 0.001). In SMA, mean flow velocity tended to decrease (P < 0.05) and sectional area increased (P < 0.001). But flow volume did not show significant change. Our results indicate that right C7-SGB leads to an increase in the blood flow of CA.

Adult↗
PubMed1992

Isolation and sequence determination of cDNA encoding PMP-22 (PAS-II/SR13/Gas-3) of human peripheral myelin.

A full length cDNA of PMP-22 (PAS-II/SR13/Gas-3) of peripheral myelin has been isolated from a cDNA library of human fetus spinal cord. The clone is 1823 base pairs (bp) in length and contains a 480 bp open reading frame encoding a polypeptide of 160 residues. The deduced amino acid sequence is highly homologous to PMP-22 from bovine (PAS-II), rat (SR13) and mouse (Gas-3).

Amino Acid Sequence↗
PubMed1992

T lymphocytes increase the synthesis of esterified cholesterol in human monocyte-derived macrophages by activation of the scavenger pathway.

Immunohistochemical analyses have shown the presence of T lymphocytes (T-cells) in atherosclerotic places in addition to macrophages and smooth muscle cells. To elucidate the role of T-cells in the formation of atherosclerotic lesions, we studied whether T-cells can stimulate the scavenger pathway and promote esterified cholesterol (EC) synthesis by [14C]oleate incorporation in macrophages. Macrophages and T-cells were co-cultured in two ways. In one culture, macrophages were in direct contact with T-cells (direct contact form). In the other, macrophages and T-cells were separated by Transwell membrane, but shared the same culture medium via the membrane (indirect contact form). Based on the incorporation of [14C]oleate into EC, macrophages strikingly increased EC synthesis in both forms of co-culture. This increase was proportional to the number of T-cells present and was inhibited by cyclosporin A. When macrophages were co-cultured indirectly in contact with T-cells in the presence of AcLDL for 24 h, and the T-cells were subsequently removed, EC synthesis in macrophages increased. However, this increase was not observed in macrophages that were rinsed twice with PBS. When macrophages, previously incubated with AcLDL for 24 h, were co-cultured indirectly in contact with T-cells for 24 h, the medium were prepared as activated T-cell-conditioned medium (aTCM). EC synthesis in macrophages cultured with aTCM increased. The ability of aTCM to increase EC synthesis disappeared upon repeated freezing/thawing, boiling and trypsin treatment. T-cells (indirect contact form) and aTCM similarly increased AcLDL-binding and -degradation in macrophages. These results indicated that T-cells secreted an active substance(s), protein in nature, which could activate the scavenger pathway and increase EC synthesis in macrophages. These observations suggest that T-cells can promote the uptake of modified lipoproteins by macrophages to induce foam cell-formation.

Arteriosclerosis↗