[Epidemiologic study of muscular dystrophy at school age in Gifu city].
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Adolescent↗
Biomedical subjects
M Nishimura
Publications and source records attributed to M Nishimura.
[Possible involvement of donor-derived B cells in development of post-transfusion graft-versus-host disease].
Post-transfusion graft-versus-host disease(PT-GVHD) is one of the most severe side effects of blood transfusion. To clarify the mechanism of development PT-GVHD, we characterized possible effector lymphocyte clones, presumably involved in the occurrence of PT-GVHD. By lymphocyte cloning from peripheral blood of a PT-GVHD patient, not only donor-derived cytotoxic T cell clones but also donor-derived B cell clones were established. The B cell clones produce cytotoxic IgG, directed against the patient's class II HLA. It was strongly suggested that donor-derived B cells, through production of cytotoxic IgG directed against the patient's HLA, were involved in the pathogenesis of the PT-GVHD in this case.
B-Lymphocytes↗
[Serum hepatocyte growth factor as a possible indicator of vascular lesions].
To investigate the possible involvement of hepatocyte growth factor (HGF) with vascular lesions, we studied the relationship between serum HGF concentrations and the grades of retinal arteriosclerosis, coronary atherosclerosis, and the proliferative changes in the retina of diabetic subjects. Individuals with more advanced grades of arteriosclerotic change showed higher serum HGF values (grade 0, 0.056 +/- 0.004ng/ml; grade 1, 0.132 +/- 0.026ng/ml; grade 2-3, 0.271 +/- 0.023ng/ml). The serum HGF concentration was increased (p < 0.05) in subjects with double- (0.323 +/- 0.037ng/ml) or triple-(0.345 +/- 0.027ng/ml) vessel coronary heart diseases, as compared to that in subjects with single-vessel coronary heart disease (0.191 +/- 0.027ng/ml). Serum HGF in diabetics without retinopathy was lower than that in nondiabetic subjects (0.041 +/- 0.003ng/ml vs 0.080 +/- 0.010ng/ml, p < 0.05), but did not differ from other diabetic subjects with background retinopathy (0.058 +/- 0.007ng/ml) or preproliferative retinopathy (0.048 +/- 0.010ng/ml). Serum HGF was increased in proliferative retinopathy without photocoagulation (0.138 +/- 0.035ng/ml, p < 0.01), but not with photocoagulation (0.040 +/- 0.008ng/ml). Increased serum HGF may be involved in the pathogenesis of arteriosclerosis/atherosclerosis or retinal neovascularization, and measurement of serum HGF may be a useful test to predict the presence of these vascular lesions.
Arteriosclerosis↗
[Secondary forms of diabetes].
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Diabetes Mellitus↗
Immunological functions of adult T cell leukemia cells of a patient complicated with synchronous double primary gynecologic cancer.
A patient with triple malignancies is reported, who presented cervical cancer, vulvar cancer and adult T cell leukemia (ATL). ATL was diagnosed as a smouldering type, because antibody to human T cell leukemia virus associated antigen (ATLA) was positive with a titer of 1:160. Although her malignant cells had an OKT 4+8-3+Tac+ phenotype, the cells did not display helper T cell functions. Namely they showed no response to Phytohemagglutinin (PHA) and Interleukin 2 (IL-2) and suppressed the PWM driven IgG synthesis of B cells obtained from healthy donor. They did not produce IL-2 by stimulation with PHA and phorbol myristate acetate (PMA). Furthermore, these ATL cells were producing IL-2 inhibitor like factors. As synchronous triple malignancies are extremely rare, two gynecologic cancers seem to ascribe to the suppressing state of the immunosurveillance mechanism by viral infection.
Aged↗
[Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure].
In patients with diabetic renal failure, attention must be paid to the prevention of atherosclerosis as well as the preservation of renal function. Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. A low-protein diet (LPD) is recommended for patients with advanced renal disease, but a large proportion of the total caloric intake is supplied from carbohydrates and fat in LPD. Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). Secondly, risk factors of atherosclerosis were measured before and two weeks after the introduction of LPD in patients with diabetic renal failure. LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis.
Diabetic Nephropathies↗
Host modifier genes affect mouse autoimmunity induced by the lpr gene.
A defect in apoptotic signal transmission through CD95 is an essential genetic mechanism for lymphoproliferation and autoimmunities in lpr or gld mice. However, disease manifestations are largely affected by the host genetic background. To identify and map such host genes modifying lpr gene effect, ie, the lpr modifier (Lprm) genes, 82 MRL/lpr x (MRL/lpr x C3H/lpr) F1 mice were subjected to immunopathological and genetical analyses. High-grade vasculitis and glomerulonephritis among backcross mice were observed in separate groups of mice. Microsatellite analysis revealed that there were two host genes affecting the occurrence of vasculitis, Lprm1 (chromosome 4) and Lprm2 (chromosome 3). A recessive MRL allele at Lprm1 enhanced vasculitis to occur in both sexes, whereas that of Lprm2 inhibited its development selectively in females. Genotype combinations of these two genes explained the severity of vasculitis in crosses of MRL/lpr and C3H/lpr mice and also the vasculitis-prone recombinant inbred strain McH5/lpr. A recessive MRL allele at Lprm3 (chromosome 14) suppressed glomerulonephritis. The weight of the spleen was increased by a recessive MRL allele at Lprm4 (chromosome 5) yielding a logarithm of odds score of 2.02 in a quantitative trait locus analysis. In contrast, the weight of axillary lymph nodes was increased by a recessive MRL allele at a locus on chromosome 2, but its presence was not supported by the quantitative trait locus analysis. The titer of anti-dsDNA autoantibody was controlled by the locus Lprm5 on chromosome 16, which had an logarithm of odds score of 3.41. Possible candidate genes for Lprm genes deduced from their map locations are discussed and compared with the autoimmunity genes reported thus far. In conclusion, autoimmune disease manifestations by the lpr mutation are affected by multiple host genes separately.
Animals↗
Augmentation rhinoplasty by subcutaneous midline forehead flap simultaneous with implant removal.
Implant exposure after augmentation rhinoplasty with alloplastic materials is usually associated with some degree of infection, and it is commonplace to remove the implant and wait for several months before re-augmentation. However, some patients cannot accept the resultant deformity after implant removal. We introduced the midline forehead flap for augmentation simultaneous to the removal and obtained favorable results, even when considering the donor site scar on the forehead. We report the surgical technique and two patients treated with this procedure. The advantages and disadvantages of this procedure are also discussed.
Aged↗
Two different hard palate closure techniques in two-stage palatoplasty: effects on velopharyngeal closure and articulation.
Two different hard palate closure techniques, in two-stage palatoplasty, was evaluated in 12 patients. The lip and soft palate were closed at 3 to 7 months of age. The patients were then divided into two groups of six and the hard palate closed at 17 to 23 months of age, either by a vomer flap (VF) with a skin graft (Osada's two-stage palatoplasty) in the VF group, or by the push-back (PB) procedure of the mucoperiosteal flap in the PB group. Velopharyngeal closure (VPC) during a gag reflex before and after hard palate closure, and the articulation of these patients after closure, were evaluated and compared between the two groups. Regarding VPC before hard palate closure, three "Poor" and three "Borderline" outcomes were noted in each group. We conclude that, by introducing the pharyngeal flap, the patients in the VF group obtained good articulation, actually comparable to that in the PB group.
Articulation Disorders↗
Changes in trough levels of whole blood cyclosporine and graft function of a kidney transplant recipient with onset of hypothyroidism after transplantation.
The immunosuppressive and toxic effects of cyclosporine (CsA) are affected by many factors. We present the first case of a kidney transplant patient who had an onset of hypothyroidism about two months after the transplantation. In this case, trough levels of whole blood CsA and total serum cholesterol levels increased at the same time. But the decrease in renal function was not as severe as expected from the very high trough levels of whole blood CsA. Elevation of the trough level of whole blood CsA may be due to a decrease in CsA clearance resulting from the decreased cytochrome P-450 activity in hypothyroidism. Furthermore, a decrease in thyroid hormone level and increase in plasma lipoprotein level might have affected the distribution of CsA, and this change might have influenced the toxic effect of CsA In conclusion, our case suggests that thyroid function and plasma lipoprotein level should be considered important factors that affect the pharmacokinetics and action of CsA.
Adult↗
Relation between dynamic midventricular obstruction and unexplained chest pain in patients with normal echocardiograms at rest.
The relation between dynamic mid-ventricular obstruction provoked by dobutamine infusion and chest pain was investigated in 16 patients with normal echocardiograms at rest who had histories of unexplained chest pain. Chest pain was induced in 63% of dynamic mid-ventricular obstruction and beta blockers suppressed either dynamic mid-ventricular obstruction or Chest pain.
Acebutolol↗
Block of Na+ channel by bepridil in isolated guinea-pig ventricular myocytes.
The effects of bepridil, a potent antiarrhythmic agent, on the Na+ current (INa) of single guinea-pig ventricular myocytes were studied using the whole-cell patch-clamp technique. Bepridil inhibited INa in a dose-dependent manner without causing any change in the I-V. relationship for INa. Bepridil suppressed INa with Kd values of 342 and 40 microM when cells were clamped to holding potentials of -140 and -90 mV, respectively. 10 microM bepridil shifted the steady-state inactivation curve for INa toward more negative potentials by 7.7 mV (n = 6). Bepridil also produced marked use-dependent block with a rapid onset. Recovery of INa from inactivation was retarded (time constant 290 ms) at a holding potential of -140 mV in the presence of 10 microM bepridil. When the onset of INa block was studied in experiments using a double-pulse protocol, bepridil blocked INa by 11.5% after a 4-ms pre-pulse, but significantly blocked it after pre-pulses longer than 16 ms. These results suggest that: (1) bepridil has a higher affinity for the inactivated state than the resting state of Na+ channel; (2) the drug also produces an open channel block; and (3) the drug shows a lidocaine-like fast kinetic block of Na+ current.
Animals↗
Structure and expression of two highly related genes encoding SCM-1/human lymphotactin.
SCM-1/lymphotactin is a chemokine-like molecule produced selectively, if not exclusively, by activated CD8+ T cells. Here we report that there are two highly homologous SCM-1 genes, which we designate as SCM-1alpha and SCM-1beta. Both genes have three exons and two introns. The 1st intron of SCM-1alpha contains a pseudogene of the ribosomal large subunit L7a. In SCM-1beta, a 1.5-kb region including about a quarter of the L7a pseudogene is deleted from the 1st intron. Otherwise, the two genes are highly homologous including the 5' and 3' flanking regions. Both genes were mapped to human chromosome 1q23. The two genes were similarly induced in peripheral blood mononuclear cells by mitogenic stimulation. Primer extension and RNase protection revealed several transcription initiation sites. The biological activities of SCM-1alpha and SCM-1beta, which have two amino acid differences at positions 7 and 8 in the mature proteins, remain to be compared.
Amino Acid Sequence↗
Formation of crossline as a fluorescent advanced glycation end product in vitro and in vivo.
Crossline is one of the major advanced glycation end products resulting the reaction mixture of free amino group(s) such as epsilon-one in lysine with D-glucose in vitro. To study crossline formation on proteins in vitro and in vivo, polyclonal antiserum to the crossline hapten was prepared. This antiserum reacted with bovine and human serum albumin that had been modified by prolonged incubation with glucose as well as with crossline itself. Antisera did not react with unmodified serum albumin or the other Maillard-related compounds. Crossline was formed in a time-dependent manner when a mixture of six different proteins was incubated with glucose at pH 7.2 or 9.0. Crossline levels could be measured in rat lens proteins and the levels increased with age. The crossline content of lens proteins in diabetic rats was more than two-fold higher than that of age-matched controls. Results of this study suggest that most proteins containing advanced glycation end products have crossline-like structures. Measurement of crossline-like structures in biological specimens may provide an index of aging and of the development of diabetic complications.
Animals↗
Post-infectious encephalitis with anti-galactocerebroside antibody subsequent to Mycoplasma pneumoniae infection.
Galactocerebroside (Gc) is a major component of myelin in both the peripheral and central nervous systems. Although it is regarded as an important glycolipid hapten of myelin in rabbit experimental allergic neuritis (EAN), its role in human demyelinating diseases is not known. We studied three post-infectious encephalitis (PIE) patients related to Mycoplasma pneumoniae infection. All three of three patients with encephalitis and M. pneumoniae infection were positive for Gc antibodies (100%), while 25% of 32 M. pneumoniae-infected patients without neurological disease were positive, and 3.8% of 52 healthy controls. This indicates anti-Gc antibody is induced by M. pneumoniae infection. One of the PIE patients, who had extraordinary high titer antibody to Gc, showed an extensive, diffuse white matter demyelination and poor recovery. Since circulating anti-Gc antibody induces central nervous system demyelination in animals with elevated antibody titers and disruption of the blood-brain barrier, anti-Gc antibody may have an important function in the increased demyelination in PIE patients after M. pneumoniae infection.
Antibodies↗
PCR-based restriction fragment length polymorphism (RFLP) analysis and serotyping of Campylobacter jejuni isolates from diarrheic patients in China and Japan.
A molecular typing approach for Campylobacter jejuni was applied with restriction fragment length polymorphism (RFLP) analysis of a 702-bp PCR-amplified portion of the flagellin-A (flaA) gene. We analyzed a total of 179 strains, including 69 independent clinical isolates from diarrheic patients in Japan, 85 isolates in China, and 25 heat-stable (HS) serotype strains by Penner and Hennessy (1980) J. Clin. Microbiol. 12, 732-737). Six AfaI, seven MboI, and five HaeIII RFLPs were found in the 702-bp flaA segment from the 179 strains. Using a combination of these three enzymes, 25 separate RFLP groups were recognized. While 59 of 154 (38.3%) strains obtained in Japan and China were nontypeable by the HS antigenic scheme, all but two of 154 (98.7%) could be typed by RFLP typing. All 11 isolates of HS-19 strains, which are frequently isolated from Guillain-Barré syndrome (GBS) patients, showed an identical RFLP pattern (Cj-1), and Cj-1 consisted only of HS-19 strains. This suggests that the HS-19:Cj-1 strain is distinct among C. jejuni strains. This molecular typing method provides a rapid and reliable typing scheme for epidemiological studies of C. jejuni, and may also be useful for the analysis of C. jejuni subtypes from GBS patients.
Bacteriological Techniques↗
Five candidate genes for hamster cardiomyopathy did not map to the cardiomyopathy locus by FISH analysis.
The Syrian cardiomyopathic hamster (BIO14.6), that develops both muscular dystrophy and progressive cardiomyopathy, is widely used as an animal model of autosomal recessive cardiomyopathy mimicking human hypertrophic cardiomyopathy, and five genes have been proposed as strong candidates for the cause of cardiomyopathy. We recently mapped the cardiomyopathy locus of the hamster to the centromeric region of chromosome 9qa2.1-b1 by construction of a genetic linkage map of the Syrian hamster. Thus, we analyzed the loci of the five candidate genes, alpha tropomyosin, cardiac troponin T, adhalin, calpain 3 and cardiac myosin binding protein-C, by the FISH method, and found that these genes were mapped on the distal portion of chromosome 12qa5 and 4pa2 and the proximal portion of chromosomes 9qb7, 1qc1.1 and 1qb3, respectively. These results provide strong evidence that the five candidate genes previously proposed are not related to the hamster cardiomyopathy.
Animals↗
Molecular cloning of a novel T cell-directed CC chemokine expressed in thymus by signal sequence trap using Epstein-Barr virus vector.
Precursors of most secreted and cell surface molecules carry signal sequences at their amino termini. Here we describe an efficient signal sequence trap method and isolation of a novel CC chemokine. An expression library was constructed by inserting 5' portion-enriched cDNAs from phytohemagglutinin-stimulated peripheral blood mononuclear cells into upstream of signal sequence-deleted CD4 cDNA in an Epstein-Barr virus shuttle vector. After electroporation into Raji cells, CD4 antigen-positive cells were enriched by repeated cell sorting and plasmids were recovered in Escherichia coli. Out of 100 plasmid clones examined, 42 clones directed expression of CD4 antigen on the cell surface. Among them were signal sequences of CD6, beta2-microglobulin, MGC-24, and T cell receptor epsilon-chain, and at least four novel potential signal sequences. A cDNA clone encoding a novel CC chemokine was isolated by using one of the trapped fragments. The gene designated as TARC from Thymus and Activation-Regulated Chemokine was expressed transiently in phytohemagglutinin-stimulated peripheral blood mononuclear cells and constitutively in thymus. Radiolabeled recombinant TARC specifically bound to T cell lines and peripheral T cells but not to monocytes or granulocytes. The binding of radiolabeled TARC to the high-affinity receptor (Kd, 2.1 nM) on Jurkat was displaced by TARC but not by interleukin-8, MIP-1alpha, RANTES, or MCP-1. TARC also bound to the promiscuous chemokine receptor on erythrocytes (Kd, 17 nM). TARC induced chemotaxis in T cell lines Hut78 and Hut102. Pretreatment of Hut78 with pertussis toxin abolished the TARC-induced cell migration. Collectively, T cells express a highly selective receptor for TARC that is coupled to pertussis toxin-sensitive G-protein. TARC may a factor playing important roles in T cell development in thymus as well as in trafficking and activation of mature T cells.
Amino Acid Sequence↗