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Biomedical subjects

H Hamaguchi

Publications and source records attributed to H Hamaguchi.

At least 181 records · Page 10Linked to original sources
PubMed1993

[Hyperlipidemia, hypoalphalipoproteinemia and liver dysfunction in Japanese school-age children with obesity].

Three hundred and twenty nine obese children (206 boys, 123 girls) whose obesity index were above 40% were screened among 6,278 school-age children living in Ibaraki Prefecture. Six hundred and fifty-eight school-age children without obesity were used as controls. The mean levels of total cholesterol and triglyceride of obese boys were significantly higher than those of control boys. The mean levels of HDL-cholesterol of both boys and girls with obesity were significantly lower than those of controls. Hypercholesterolemia, hypertriglyceridemia and hypoalphalipoproteinemia in the boys with obesity were significantly more frequent than those in control boys. In the girls with obesity, hypoalphalipoproteinemia was significantly more frequent than that in control girls. Liver dysfunction (GPT > or = 40 IU/l) in obese children was significantly more frequent than in controls: Although none of controls had liver dysfunction, 24.8% of obese boys and 11.4% of obese girls had liver dysfunction. These findings indicated that atherogenic dyslipidemias and liver dysfunction were common in Japanese school-age children with obesity, especially in boys.

Adolescent↗
PubMed1992

Genetics of neurofibromatosis 1 in Japan: mutation rate and paternal age effect.

We have performed formal genetic studies on 26 patients (14 males, 12 females) with neurofibromatosis 1 (von Recklinghausen's disease, NF1) in Japan. Family studies of 74 members of 18 kindreds revealed that 50% of the cases were caused by a new mutation; the mutation rate was assumed to be 7.3-10.5 x 10(-5). A tendency of paternal age effect, which was not accounted for by the maternal age effect, was observed, but live-birth order had no significant effect. Genetic linkage of neurofibromatosis 1 to the NF1 gene or the genetic marker in the pericentric region of chromosome 17 was established in 3 informative families.

Age Factors↗
PubMed1992

Electrophysiological study on hydranencephaly.

An electrophysiological study was performed on 2 children with hydranencephaly diagnosed by CT and/or MRI. Case 1 was a 4-month-old boy who had no rostral tissues above the midbrain. Case 2 was a 5-year-old boy in whom CT showed retention of the thalamus. Short latency somatosensory evoked potentials (SSEP) in both cases exhibited the absence of cortical activity (N1 and P4) with the preservation of waves of brain stem origin. However, in case 1, wave component No was not observed, while No was seen in case 2. It was postulated, thus, that the No component of SSEP on median nerve stimulation in children, which corresponds to N16 in adults, may originate in the thalamus.

Child, Preschool↗
PubMed1992

Prolonged survival of rat hepatic allografts after total-body irradiation of the donors.

The effect of total-body irradiation of the donor on hepatic allograft survival was studied in the rat, with ACI(RT1a) as the donor and LEW(RT1(1)) as the recipient. LEW recipients of ACI liver transplants experienced severe acute rejection, with a mean survival of only 10.2 +/- 0.3 days. The doses of irradiation were 450, 750, and 1000 rads administered 24 hr prior to harvesting or subsequent transplantation. TBI with a dose of 750 rads significantly prolonged the survival of the hepatic allograft to 30.3 +/- 1.7 days, without concomitant immunosuppression. However, neither 450 rads nor 1000 rads of TBI resulted in successful suppression of graft rejection. TBI appeared to have a beneficial effect on hepatic allograft survival and to have no deleterious effect on isograft survival, suggesting a possible modulation of the immunogenicity of the donor organ. Although the cause of this beneficial effect is not clear, TBI with a dose of 750 rads 24 hr prior to organ harvest seems to be optimal to eliminate-antigen presenting cells in the donor organs.

Animals↗
PubMed1992

[Importance of lipoprotein(a) in patients with ischemic heart disease].

Elevated levels of lipoprotein(a) [Lp(a)] have been associated with an increased risk of ischemic heart disease (IHD), and higher levels of Lp(a) are associated with lesions of significantly greater severity. We have examined Lp(a), total cholesterol (TC) and high density lipoprotein-cholesterol (HDL-C) levels in patients with IHD including those with normal coronary arteries with vasospastic angina. The study population consisted of 206 patients (166 males and 40 females) who underwent diagnostic coronary angiography for known IHD. Twenty-eight patients had effort angina, 36 rest angina, 8 unstable angina and 134 old myocardial infarction. IHD patients were categorized as zero vessel disease (0VD), single vessel disease (SVD) and multi-vessel disease (MVD). To investigate the relationship between atherosclerosis and IHD, these patients were further divided into 3 groups based on angiographic findings. Eighteen patients had entirely normal coronary arteries (normal group), 24 discretely diseased coronary arteries (discrete group) and 80 diffusely diseased coronaries (diffuse group). The results were compared with those obtained from 50 healthy individuals. Lp(a) levels for IHD patients (12.4 mg/dl) were significantly higher than those of controls (7.1 mg/dl, p < 0.05). However, there were no statistical differences between 0VD (13.1 mg/dl) and MVD (12.8 mg/dl). Similarly, no statistical differences of Lp(a) values were found among the normal group (13.3 mg/dl), discrete group (12.0 mg/dl) and diffuse group (12.9 mg/dl). Mean levels of HDL-C in 0VD (51.3 +/- 13.5 mg/dl) were significantly higher than those of SVD (42.9 +/- 11.5 mg/dl, p < 0.05). However, no significant differences were observed between controls (59.5 +/- 15.3 mg/dl) and 0VD (51.3 +/- 13.5 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Apolipoprotein A-I deficiency due to a codon 84 nonsense mutation of the apolipoprotein A-I gene.

The molecular genetic defect of a female patient with apolipoprotein A-I (apoA-I) deficiency and premature atherosclerosis was examined. Her parents were first cousins. Her plasma density fraction from 1.063 to 1.21 g/ml contained no apoA-I on SDS/PAGE and no measurable high density lipoprotein cholesterol. Southern blot hybridization showed no gross abnormality to be present in the patient's apoA-I gene and homozygosity for a haplotype of restriction fragment length polymorphisms in the apoA-I gene region. Sequencing after amplification by PCR revealed a codon 84 nonsense mutation (CAG----TAG, Gln----stop) of exon 4 and a codon 67 missense mutation (GCC----ACC, Ala----Thr) of exon 3 in the patient's apoA-I gene. The data from dot-blot hybridization with allele-specific oligonucleotide probes indicated that she was homozygous for the apoA-I gene with regard to the two mutations. The codon 37 missense mutation was also detected in the apoA-I gene of 6 out of 60 controls, who all had normal levels of apoA-I and high density lipoprotein cholesterol, suggesting that the missense mutation is polymorphic and not associated with apoA-I deficiency. These findings indicate that homozygosity for the apoA-I gene with codon 84 nonsense mutation causes the deficiency of apoA-I and of high density lipoprotein cholesterol in the patient.

Adult↗
PubMed1991

A case of trisomy 21 with holoprosencephaly: the fifth case.

A case of trisomy 21 with holoprosencephaly, the fifth case in the literature, is described. The patient also had extracephalic malformations frequently associated with Down syndrome. The possibility of a causal relationship between trisomy 21 and holoprosencephaly is discussed.

Abnormalities, Multiple↗
PubMed1991

Chromosomal assignments of the human endothelin family genes: the endothelin-1 gene (EDN1) to 6p23-p24, the endothelin-2 gene (EDN2) to 1p34, and the endothelin-3 gene (EDN3) to 20q13.2-q13.3.

Chromosomal assignments of the genes for the human endothelin family, the endothelin-1 gene (EDN1), the endothelin-2 gene (EDN2), and the endothelin-3 gene (EDN3), were accomplished by in situ hybridization to human metaphase chromosomes using a 3H-labeled human preproendothelin cDNA probe for each endothelin. The chromosomal assignment of the EDN2 was also performed by Southern blot analysis of somatic cell hybrid DNAs. EDN1, EDN2, and EDN3 were mapped to 6p23-p24, 1p34, and 20q13.2-q13.3, respectively.

Chromosome Banding↗
PubMed1990

Fine structural localization of RNA in myeloma cells detected by the enzyme-gold method.

The ultrastructural localization of RNA in myeloma cells was studied by the RNase-gold method. Gold particles indicating the presence of RNA were observed in large numbers, particularly in the granular component of the nucleolus and periphery of the rough endoplasmic reticulum, but not in the Golgi area, mitochondria, intranuclear inclusion bodies, cytoplasmic inclusion bodies, dense bodies, or cisternae of the rough endoplasmic reticulum. In the nuclear chromatin and nucleolus, gold particles were more numerous as these structures were less mature. They were found in larger numbers also in the cytoplasm of immature cells. In plasma cells from patients with macroglobulinemia, gold particles were fewer than in myeloma cells of multiple myeloma, but there was no difference in their distribution pattern.

Adult↗
PubMed1990

Interaction of monocytes and T cells in the regulation of normal human megakaryocytopoiesis in vitro: role of IL-1 and IL-2.

Autologous or allogeneic peripheral blood T cells can stimulate the human megakaryocyte progenitor cell (CFU-Meg)-derived colony formation in a dose-dependent fashion in agar cultures of nonadherent (NA), T cell-depleted (NT) bone marrow (BM) cells. Low concentrations of monocytes and T cells can collaborate in the stimulation of CFU-Meg colony formation or in the production of megakaryocyte colony stimulating factor (Meg-CSF) by T cells in the presence of mitogens or IL-2. Monocytes alone can produce only negligible Meg-CSF under any conditions. When monocyte conditioned medium (CM) was added to T cell-stimulated NA, NT BM cell cultures, CFU-Meg colony growth was appreciably increased compared with that stimulated by T cells alone. Dose-dependent increase in CFU-Meg colony growth was noted when varying concentrations of IL-1 were added to T cell-stimulated NA, NT cell cultures, although IL-1 itself could support no CFU-Meg colony growth in the absence of T cells. These data suggest that a synergistic interaction between T cells and monocytes during the production of Meg-CSF by T cells could be partly mediated by IL-1. IL-2 was found to stimulate Meg-CSF production by T cells in the presence or absence of mitogens. IL-2-stimulated Meg-CSF production by T cells was augmented by the addition of monocytes. Although IL-2 itself had no stimulatory effect on CFU-Meg colony growth, dramatic augmentation in the CFU-Meg colony number was noted when IL-2 was added to T cell-stimulated NA, NT cell cultures. High concentrations of monocytes and prostaglandin E (PGE) inhibited the CFU-Meg colony formation. These results suggest that IL-1 and IL-2 may play a stimulatory role on the normal human in vitro megakaryocytopoiesis, and may be involved in the development of reactive thrombocytosis and bone marrow megakaryocytic hyperplasia in various inflammatory diseases.

Cell Communication↗
PubMed1990

Association of hypercholesterolemia and apolipoprotein E4 in school children.

To investigate the association of apolipoprotein (APO) E4 and hypercholesterolemia in children, we studied the APOE phenotypes of 51 school-age children with hypercholesterolemia and of 51 age, sex and obesity index-matched controls with normocholesterolemia by two-dimensional gel electrophoresis APOE4 was present in 21 of 51 hypercholesterolemic children (41.2%), and in nine of 51 control subjects (17.6%). The difference was significant (p less than 0.01). This finding indicates that APOE4 is associated with hypercholesterolemia in children.

Adolescent↗