4d resonant inelastic x-ray scattering in gadolinium.
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Journal Article↗
Biomedical subjects
M Nakazawa
Publications and source records attributed to M Nakazawa.
Growth of the neopulmonary valve annulus after arterial switch operation in transposition of the great arteries.
BACKGROUND: It is known that supravalvular pulmonary artery stenosis can occur in patients with d-transposition of the great arteries (TGA) after arterial switch operation (ASO). However, little is known about the growth of the neopulmonary valve annulus after the ASO. This study investigated the growth potential of the neopulmonary (old aortic) valve annulus. METHODS AND RESULTS: Annular diameters of the old aortic and neopulmonary valve were measured from cineangiograms in patients who underwent cardiac catheterizations both before and > 1 year after the ASO. Of 71 patients, 13 (18%) had either a small annulus (< 70% of the expected normal value) or no significant growth of the neopulmonary annulus after the ASO, and 4 (6%) had a pressure gradient of > 30 mm Hg across the valve. The small annulus or no growth of the neopulmonary valve was more frequent in patients with a history of pulmonary artery banding. After the ASO, the valve diameter in patients with a ventricular septal defect was 80 +/- 15% of normal (n = 24), and the value was significantly less than in patients with an intact ventricular septum (91 +/- 11%, n = 47). In all patients with an intact ventricular septum who underwent the one-stage ASO, the valve diameters before and after the ASO were within normal limits, and a significant increase in the pulmonary valve annulus was observed. CONCLUSIONS: These data indicate that not only supravalvular pulmonary stenosis but also pulmonary valvular stenosis due to a small annulus can occur in TGA, especially in patients with a history of pulmonary artery banding and in patients with ventricular septal defect.
Humans↗
Resonant X-Ray Fluorescence Spectroscopy of Correlated Systems: A Probe of Charge-Transfer Excitations.
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Journal Article↗
Binding properties of SA4503, a novel and selective sigma 1 receptor agonist.
The binding profiles of SA4503 (1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine dihydrochloride), a novel sigma receptor ligand, to sigma 1 and sigma 2 receptor subtypes in guinea pig and rat brain membranes were evaluated. SA4503 showed a high affinity for the sigma 1 receptor subtype labeled by (+)-[3H]pentazocine (IC50 = 17.4 +/- 1.9 nM), while it had about 100-fold less affinity for the sigma 2 receptor subtype labeled by [3H]1,3-di(2-tolyl)guanidine ([3H]DTG) in the presence of 200 nM (+)-pentazocine. SA4503 showed little affinity for 36 other receptors, ion channels and second messenger systems. The inhibition curves of SA4503 for (+)-[3H]pentazocine binding were shifted to the right in the presence of guanosine 5'-o-(3-thiotriphosphate) (GTP gamma S), as similar to those of (+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine ((+)-3-PPP) and (+)-pentazocine, sigma 1 receptor agonists. SA4503 significantly increased the KD value, but did not affect the Bmax value for specific (+)-[3H]pentazocine binding. These results indicated that SA4503 is a potent and selective agonist for the sigma 1 receptor subtype in the brain. In addition, SA4503 inhibited specific (+)-[3H]pentazocine binding in a competitive manner.
Animals↗
Autosomal dominant cone-rod dystrophy associated with mutations in codon 244 (Asn244His) and codon 184 (Tyr184Ser) of the peripherin/RDS gene.
OBJECTIVE: To characterize clinical findings associated with mutations in codon 244 (Asn244His) and codon 184 (Tyr184Ser) of the peripherin/RDS gene. DESIGN: Case reports with clinical features and results of fluorescein angiography, electroretinography, kinetic visual field testing, and DNA analysis. SETTING: University medical center. PATIENTS: Four affected members of two Japanese families with autosomal dominant cone-rod dystrophy associated with transversion mutations in codon 244 (Asn244His) and codon (Tyr184Ser) of the peripherin/RDS gene. RESULTS: Characteristic features included the initial symptoms of decreased visual acuity, macular degeneration, central or paracentral scotoma, cone-mediated electroretinographic responses that were more impaired than rod-mediated responses, and pigmentary degeneration in the midperipheral retina in the late stage. These phenotypic features corresponded to cone-rod dystrophy type 2a by the classification of Szlyk and associates. CONCLUSIONS: The Asn244His and Tyr184Ser mutations in the peripherin/RDS gene cause con-rod dystrophy type 2a. These findings imply that a mutation in codon 244 or codon 184 of the peripherin/RDS gene affects the functions and/or structural stability of cones and rods.
Adult↗
Variable expressivity in a Japanese family with autosomal dominant retinitis pigmentosa closely linked to chromosome 19q.
OBJECTIVE: To describe the clinical features of a Japanese family with autosomal dominant retinitis pigmentosa, the locus of which has been mapped on chromosome 19q. DESIGN: Ophthalmologic testing, including visual acuity, slit-lamp biomicroscopy, and fundus examinations, for all family members examined. Selected members underwent kinetic visual field testing, electroretinography, and fluorescein angiography. PATIENTS: Eleven symptomatic members, two asymptomatic obligate carriers, and nine nonaffected members in four generations of a single family with autosomal dominant retinitis pigmentosa. RESULTS: Asymptomatic carriers showed mildly affected fundus and fluorescein angiographic images. Visual field testing disclosed restricted central and midperipheral fields. Electroretinograms disclosed reduced amplitudes of rod-isolated responses in both of these family members, indicating functional abnormalities. CONCLUSION: Marked variability in expressivity of the retinitis pigmentosa phenotype was found in a family with autosomal dominant retinitis pigmentosa linked to chromosome 19q.
Aged↗
Melanin-laden macrophages in cerebrospinal fluid in Vogt-Koyanagi-Harada syndrome.
OBJECTIVE: To identify basophilic granules in the cytoplasm of macrophages in cerebrospinal fluid (CSF) smears from patients with Vogt-Koyanagi-Harada (VKH) syndrome as melanin pigment. DESIGN: Morphological and immunocytochemical studies were performed on CSF smears obtained from 7 patients with VKH syndrome. Specimens were stained with May-Grünwald and evaluated by a silver impregnation method (Fontana-Masson staining). For immunocyto-chemical study, the smear was reacted with mouse anti-human melanoma cell (HMB-45) monoclonal antibody. RESULTS: Basophilic granules were detected in the cytoplasm of macrophages in CSF cell smears obtained from 6 of 7 patients with VKH syndrome in the early stages (within 25 days). Using the silver impregnation method, these basophilic granules were strongly stained black. Moreover, they were identified as melanin by positive immunocytochemical staining. The total number of cells containing cytoplasmic granules ranged from 3 to 8 per 10,000 total cells in CSF. In contrast, no cells containing cytoplasmic granules were found in control CSF cell smears from patients with viral, bacterial, or noninflammatory diseases. CONCLUSION: The identification of melanin-laden macrophages in the CSF of patients with VKH syndrome suggests that these cells are responsible for pleocytosis in the immunopathologic process of VKH syndrome.
Adult↗
Influence of genetic and maternal diabetes in the pathogenesis of visceroatrial heterotaxy in mice.
The NOD mouse is known as a spontaneous model of insulin-dependent diabetes mellitus. Fetuses in this strain present anomalies of the viscera, and the incidence increases in fetuses from dams with clinically manifested diabetes. To examine the role of maternal diabetes and the genetical influence in inducing heterotaxy, NOD dams were mated with males of the ICR strain (the original strain of the NOD) and with C57BL/6J sires (not genetically related to the NOD). The frequency of visceroatrial heterotaxy in fetuses from diabetic dams varied with the fetal genotype, being 65% (33/51) in NODxNOD (dam X sire, respectively), 24% (12/50) in NODxICR, and 7% (4/57) in NODxC57BL/6J. The cases with heterotaxy showed a tendency toward right isomerism of the viscera and had severe cardiac defects, such as endocardial cushion defect and double-outlet right ventricle or transposition of the great arteries. The fetal body weight from diabetic dams in each mating was lower than that from non-diabetic dams (P < 0.05), suggesting that maternal diabetes, rather than abnormal situs, is the main determinant for decreased fetal growth. These findings demonstrate that the liability to heterotaxy induced by maternal diabetes is influenced by the fetal genotype.
Abnormalities, Multiple↗
Hypoplasia of cushion ridges in the proximal outflow tract elicits formation of a right ventricle-to-aortic route in retinoic acid-induced complete transposition of the great arteries in the mouse: scanning electron microscopic observations of corrosion cast models.
BACKGROUND: The major morphologic change associated with retinoic acid (RA)-induced complete transposition of the great arteries (TGA), a congenital malformation of the heart, was investigated in a mouse model in which TGA was found in 80% of surviving fetuses. METHODS: Corrosion casts of embryonic hearts with or without prior exposure to retinoic acid were observed under a scanning electron microscope. RESULTS: In control hearts, indentations caused by expanded parietal and septal ridges in the outflow tract established right ventricle-to-left ventral pulmonic and left ventricle-to-right dorsal aortic routes before the aorticopulmonary septum completion. In RA-treated hearts, indentations of proximal regions of the parietal and septal ridges were small in the proximal outflow tract, whereas those in the distal regions developed well. These morphological features in the RA-treated hearts elicited right ventricle-to-right ventral aortic and left ventricle-to-left dorsal pulmonic routes in the TGA morphology. CONCLUSIONS: Hypoplasticity of the proximal regions of parietal and septal ridges in the outflow tract is one of the primary morphological abnormalities of the RA-induced TGA.
Animals↗
A congenitally "poor" pulmonary artery is a major reason for exclusion from Fontan operation.
We reviewed the clinical records of 185 patients who were possible candidates for Fontan operation. We did this to clarify whether all patients with suitable anomalies ultimately underwent a Fontan operation. Of the 152 patients with decreased pulmonary blood flow, 38 (26%) did not fulfill the criteria for Fontan operation, and 17 of the 33 patients (52%) with increased pulmonary blood flow (P < 0.01) were excluded as candidates. Of 48 non-candidate survivors, 19 had high pulmonary artery (PA) pressure or resistance and small PA (which we term "poor PA"), 17 had pulmonary hypertension, 6 had a markedly distorted PA, and 6 had severe ventricular dysfunction. A significant proportion of possible candidates with a suitable anomaly ultimately did not undergo a Fontan operation, because of "poor PA", a congenital condition that precluded Fontan operation.
Adolescent↗
Pathological study of Japanese quail embryo with acid alpha-glucosidase deficiency during early development.
A pathological study was performed on the tissues of 11 Japanese quail embryos with type II glycogen storage disease (GSD II) between incubation day (ID) 3 and ID 15. Accumulation of glycogen in vacuoles derived from lysosomes was first seen in cardiac muscle at ID 3, in liver at ID 5, in wing muscle at ID 7, and in pectoral muscle at ID 10. The number and size of the glycogen vacuoles gradually increased during development, especially in cardiac muscle. Cytoplasmic glycogen particles, showing the same density as membrane-enclosed glycogen particles, were first seen as masses in cardiac muscle at ID 3, in liver at ID 5, in pectoral muscle at ID 10, and in wing muscle at ID 15. The area of cytoplasm occupied by the glycogen particles increased during development. Myofibrillar degeneration was not seen, although myofibrils appeared in disarray in the early stages, as in normal embryos. This is the first study of the development of embryonic tissues of Japanese quails with GSD II. GSD II in the Japanese quail appears to be clinically analogous to the human late (juvenile)-onset disease, although the disorder starts at very early stages in quail embryos. Therefore, Japanese quails with GSD II can provide a model for elucidating the pathogenetic process of human GSD II.
Animals↗
Immunopharmacological activities of the nontoxic monophosphoryl lipid A of Porphyromonas gingivalis.
The low endotoxic lipid A derived from Porphyromonas gingivalis 381, 1-phospho beta(1-6)-linked glucosamine disaccharide with 3-hydroxy-15-methylhexadecanoyl and 3-hexadecanoyloxy-15-methylhexadecanoyl groups at the 2- and 2'-positions, respectively, induced mitogenic responses in LPS low responder C3H/HeJ as well as LPS responder C3H/HeN mouse splenocytes. The mitogenic activities of P. gingivalis lipid A in splenocytes of LPS responder mice were comparable to that of the synthetic Escherichia coli-type lipid A (compound 506). The addition of polymyxin B resulted in the inhibition of mitogenic activity. P. gingivalis lipid A also stimulated strongly nonspecific host resistance against Pseudomonas aeruginosa infection in BALB/c mice, and specific immune response in guinea pigs against infection with P. gingivalis. Furthermore, P. gingivalis lipid A demonstrated antitumour activity against MH134 hepatoma in C3H/HeN mice. These life-preserving with tumour regression properties were comparable to those of monophosphoryl lipid A derived from Salmonella minnesota Re 595. Thus, P. gingivalis lipid A appears to have beneficial properties as an immunopharmacological agent.
Adjuvants, Immunologic↗
Dual infection with attaching and effacing Escherichia coli and enterotoxigenic Escherichia coli in post-weaning pigs.
Post-weaning diarrhoea in pigs occurred on two farms in Hokkaido, Japan, in 1994. Four piglets aged 35 or 45 days were examined after death. At necropsy, ecchymotic haemorrhages were seen on the mucosal surface of the caecum and colon. Histopathologically, numerous Gram-negative bacilli adhered to the brush border of the small intestines, but the brush border itself was intact. Typical attaching and effacing (AE) lesions were seen in the caecum and colon. Immunohistochemically, the bacilli which adhered to the brush border gave positive results with antisera against serogroup O149 of Escherichia coli; the bacilli which caused the AE lesions, however, belonged to serogroup O45. It was concluded that the disease resulted from dual infection with attaching and effacing E. coli (AEEC) and enterotoxigenic E. coli (ETEC).
Animals↗
Cross-reactive idiotypes on rabbit anti-SEA antibodies stimulate anti-idiotype spleen and lymph node cell responses of mice infected with Schistosoma mansoni.
Antibodies to Schistosoma mansoni soluble egg antigens (SEA) generated in outbred rabbits from two different sources were used to study cross-reactive idiotype/anti-idiotype (Id/anti-Id) interactions in S. mansoni-infected mice in two different locations. Immunoaffinity purified rabbit polyclonal anti-SEA antibody preparations (RabId) were predominantly Ig by SDS-PAGE and demonstrated anti-SEA activity by ELISA and Western blot. RabId prepared from three separate rabbits and used at 40 micrograms/ml in vitro stimulated lymphocyte proliferative responses of spleen cells from mice with eight week infections (Mean +/- SEM [E-C]) of 3869 +/- 764, 18594 +/- 3046 and 8962 +/- 1734 cpm. Spleen cells from uninfected mice exposed to the same RabId preparations in vitro had respective [E-C] values of 206 +/- 144, 494 +/- 154 and 363 +/- 180. Lymph node cells from mice infected for 8 weeks demonstrated [E-C] of 123 +/- 400, 5073 +/- 828 and 2361 +/- 656 upon exposure to these 3 RabId preparations. Lymph node cells from uninfected mice had [E-C] of 220 +/- 76, 194 +/- 82 and 143 +/- 72 when exposed to these RabId. Maximum in vitro proliferative response to Ig from unimmunized rabbits was 761 +/- 400 by spleen cells from mice with eight week infections. These data indicate the presence of cross-reactive Id on rabbit anti-SEA antibodies from different rabbits that can stimulate in vitro lymphoproliferative responses of spleen or lymph node cells from S. mansoni-infected mice.
Animals↗
Requirement of CD80 and CD86 molecules for antigen presentation by eosinophils.
The authors analysed the antigen-presenting ability of eosinophils purified from peritoneal exudate cells of interleukin-5 (IL-5) transgenic mice. The granulocyte-macrophage colony-stimulating factor (GM-CSF)-treated eosinophils induced proliferative responses of primed lymph node T cells and thymus T cells to staphylococcal enterotoxin B (SEB), while untreated eosinophils induced little or no response. GM-CSF-treated eosinophils also induced proliferation of ovalbumin (OVA)-primed lymph node T cells to OVA. Although untreated eosinophils expressed no MHC class II molecule on the surface the eosinophils could be induced to express major histocompatibility complex (MHC) class II molecules when treated with GM-CSF. In the present study, anti-I-Ak monoclonal antibodies (MoAbs) strongly inhibited proliferation of thymus T cells and proliferation of OVA-primed lymph node T cells in response to OVA, but weakly inhibited proliferation of primed T cells in response to SEB. Furthermore, CD80 (B7-1) and CD86 (B7-2) were expressed on the surfaces of untreated eosinophils. The expression of those two molecules on the eosinophils was increased by incubation with GM-CSF. Moreover, anti-CD80 or anti-CD86 MoAbs blocked proliferative responses of primed lymph node T cells and thymus T cells to SEB, and also blocked responses of primed lymph node T cells to OVA. Thus, CD80 and CD86 play an important role in stimulation of T cells by eosinophils.
Animals↗
Iron nutrition and anaemia in a malaria-endemic environment: haematological investigation of the Gidra-speaking population in lowland Papua New Guinea.
Blood examination was conducted for the four Gidra-speaking village groups in Papua New Guinea, who were characterized by high Fe intake and high malaria prevalence with marked inter-village differences. The northern riverine villagers, whose Fe intake was higher than the other three village groups, did not suffer from Fe-deficiency anaemia in their malaria-endemic environment; nor did the inland villagers, with their second highest Fe intake and their malaria-free environment, suffer from Fe-deficiency anaemia. However, several individuals of the southern riverine village suffered from anaemia in a malaria-endemic environment, although their Fe intake was almost the same as the inland villagers'. A considerable proportion of the coastal villagers were anaemic, reflecting the lowest Fe intake and the highest malaria prevalence. An inter-village comparison of the relationships between haemoglobin levels and transferrin saturation revealed that the southern riverine villagers needed smaller amounts of circulating Fe for erythropoiesis than the northern riverine and inland villagers, reflecting the long-term human-environment conditions such as the density of malaria vectors and the people's dietary habits. Fe supplementation was not judged effective against hypoferraemia and/or anaemia in such a population. As the incidence of malaria had no significant long-lasting effect on Fe stores or circulating Fe concentration, but did have an effect on anaemia, the hypothesis that malaria causes a transfer of Fe from the blood to parenchymal tissues as a defence against infectious diseases was not supported.
Anemia, Iron-Deficiency↗
Autosomal dominant cone-rod dystrophy associated with a Val200Glu mutation of the peripherin/RDS gene.
OBJECTIVE: Mutations of the peripherin/RDS gene have been reported in several kinds of retinal dystrophy, and they show a variety of manifestations. The authors identified a novel Val200Glu mutation of the peripherin/RDS gene in a Japanese family with autosomal dominant cone-rod dystrophy (CRD). This report describes a genotype-phenotype correlation of the Val200Glu mutation. PATIENTS AND METHODS: Fifteen members of one Japanese family with autosomal dominant CRD were screened for mutations in the peripherin/RDS and ROM 1 genes. Clinical features were identified by visual acuity, visual field testing, fundus examination, and electroretinography. RESULTS: A Val200Glu mutation was found in all of the affected family members examined and was segregated with the disease. No patient had a mutation in the ROM 1 gene. Phenotypic characteristics of each affected member in this family showed intrafamilial similarity. Characteristic features included cone function more severely impaired than rod function and degenerative change in the macular region associated with peripheral retinal degeneration. CONCLUSION: The mutation at codon 200 of the peripherin/RDS gene causes both cone and rod degeneration. The Val200Glu mutation results in a type of autosomal dominant CRD.
Adult↗
A new adherent form of an attaching and effacing Escherichia coli (eaeA+, bfp-) to the intestinal epithelial cells of chicks.
The adherent site of "attaching and effacing Escherichia coli" (AEEC; O103: H-, SK-1 strain) on the intestinal epithelial cells of chicks infected naturally and experimentally was ultrastructurally investigated. The eaeA gene was detected by polymerase chain reaction in the SK-1 strain of E. coli isolated from the intestinal content of a chick infected naturally, however, the bundle-forming pilus (bfp) gene could not be detected. The SK-1 strain (bfp-) of AEEC could attach to the intestinal epithelial cell and induce attaching-effacing lesions in the intestine of chicks. Transmission electron microscopy revealed numerous pilus-like microfilaments in the space between colibacilli and the membranes of the intestinal epithelial cells. The present study suggests that SK-1 strain (eaeA+, bfp-) may attach closely to the intestinal epithelial cells by a novel adhesion different from bfp.
Animals↗