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Biomedical subjects

M Eguchi

Publications and source records attributed to M Eguchi.

At least 19 recordsLinked to original sources
PubMed2004

Vitamin D deficiency rickets due to soybean milk.

We describe vitamin D deficiency rickets in an infant nursed with soybean milk (not specifically designed for infants) instead of cow's milk-based infant formula. Symptoms included irritability and carpopedal spasm when crying. The infant's condition improved with nutrition by vitamin-enriched cow's milk-based infant formula, oral administration 1 alpha-hydroxy vitamin D3 and exposure to sunlight. Content analysis of the milk showed very low calcium, phosphate, magnesium and vitamin D levels compared to cow's milk-based infant milk formulas. This case highlights the unsuitability of soybean milk as the sole provider of infant nutrition and demonstrates the false perception that soybean milk is a healthy food for infants. It is necessary to be cautious about not only health claims for soybean milk, but also today's health and natural food booms. Social enlightenment and correction of such misperceptions are necessary.

Humans↗
PubMed2003

Molecular typing of Mannheimia (Pasteurella) haemolytica serotype A1 isolates from cattle in Japan.

Pulsed field gel electrophoresis (PFGE) and random amplified polymorphic DNA (RAPD) methods were applied for molecular typing of 130 Mannheimia (Pasteurella) haemolytica serotype A1 isolates obtained from 13 prefectures in Japan. These isolates were divided into 15 ApaI PFGE profiles that formed six distinct clusters (clusters A-F). Fifty-three (40.7%) isolates were classified in cluster B, and 20.0, 13.8, 12.3, 6.9 and 6.1% of isolates were in clusters E, A, F, D and C, respectively. The isolates of cluster B were differentiated into seven subtypes (B1-B7) and subtype B5 contained 63% (34/53) of isolates. RAPD revealed four banding patterns (types I-IV), and among 130 isolates 60.7% (79/130) of isolates were RAPD type I. All of the RAPD type I isolates were grouped into clusters A-C by PFGE. There was no relationship between molecular typing and geographic origin of these isolates. These results indicate that isolates of M. haemolytica A1 strain with various molecular profiles have already spread in Japan and may have caused sporadic infections.

Animals↗
PubMed2002

Quantitative assessment of right ventricular structural abnormalities by right ventricular polar mapping of single photon emission computed tomogram.

The identification of right ventricular (RV) abnormalities is clinically important in the evaluation of arrhythmogenic substrates in right ventricular-originated ventricular tachycardia (RVT). The purpose of this study was to determine the diagnostic benefit of quantitative analysis in RV single photon emission computed tomography (SPECT) imaging with (99m)Tc-tetrofosmin/sestamibi in patients with RVT. Thirty patients with RVT (15 with idiopathic RVT and 15 with arrhythmogenic right ventricular cardiomyopathy (ARVC)) were compared with 27 control subjects (including 11 with right bundle branch block) with regard to the semiquantitative RV uptake score in each of six segments and the quantitative RV extent score in polar coordinate map displays by SPECT imaging. The RV total score and RV extent score were compared with the RV global function. Perfusion abnormalities were more frequently detected (P = 0.0001) in the ARVC group (59/90, 65.6%) than in the idiopathic RVT group (4/90, 4.4%) or controls (1/162, 0.6%). The RV extent score in the ARVC group (53.0 +/- 24.8) was significantly higher than that in the idiopathic RVT group (8.4 +/- 10.1) or controls (1.2 +/- 4.9). The RV extent score correlated well with the regional RV perfusion score (P < 0.0001) and with the RV ejection fraction (P < 0.0001). Non-invasive RV perfusion mapping using a (99m)Tc-labelled tracer is useful for the quantitative evaluation of RV substrates in patients with ARVC.

Adolescent↗
PubMed2002

Male siblings with dyserythropoiesis, microcephaly and intrauterine growth retardation.

Male siblings with intrauterine growth retardation, hydrops, mild liver dysfunction, chronic diarrhoea, failure to thrive and microcephaly are reported. In both patients, the intrauterine growth retardation was detected in the second trimester of pregnancy. Relatively severe early onset neonatal jaundice, microcytosis, anisocytosis and abnormal iron metabolism were also seen. Bone marrow examination in the second sibling showed marked ringed sideroblasts and multilobulated erythroblasts in late developmental stages. The brain was very small with enlarged cerebrospinal fluid space, a reduced number of gyri and a thin cortex. The clinical and laboratory findings in these patients appear to be unique.

Anemia, Dyserythropoietic, Congenital↗
PubMed2001

Superior outcome of infant acute myeloid leukemia with intensive chemotherapy: results of the Japan Infant Leukemia Study Group.

This study analyzed data on 35 infants with acute myeloid leukemia (AML) who were treated with intensive chemotherapy between 1995 and 1998 in Japan. The incidence of boys, younger age (< 6 months old), and hyperleukocytosis at onset was high in patients with the M4/M5 subtype (n = 23) in the French-American-British classification, compared with the non-M4/M5 subtype (n = 12). Thirteen (56%) and 16 (70%) patients with the M4/M5 subtype also showed 11q23 translocations and MLL gene rearrangements, respectively, whereas only one patient with the non-M4/M5 subtype had this rearrangement. All 35 patients were treated with the ANLL91 protocol consisting of etoposide, high-dose cytarabine, and anthracyclines. Overall survival and the event-free survival (EFS) rates at 3 years of all patients were 76% (95% confidence interval [CI], 61.3%-90.7%) and 72% (95% CI, 56.4%-87.9%), respectively. EFS showed no significant difference between 2 subgroups divided by age, gender, presence of the MLL gene rearrangements, and white blood cell count at onset; EFS in patients with the M4/M5 subtype tended to be better than those with the non-M4/M5 subtype. Although all 6 patients who underwent allogeneic stem cell transplantation (SCT) have been in complete remission, no benefit of SCT was confirmed. These findings suggest that the intensive chemotherapy with the ANLL91 protocol might have been responsible for the observed good outcome of infant AML, even without SCT. The presence of the MLL gene rearrangements or the age at onset had no impact on the outcome of infant AML.

Aclarubicin↗
PubMed2001

Evidence for the presence of murine primitive megakaryocytopoiesis in the early yolk sac.

During mouse embryogenesis, primitive erythropoiesis occurs in blood islands of the yolk sac (YS) on the seventh day of gestation. This study demonstrated for the first time the presence of unique primitive megakaryocytic (Mk) progenitors in the early YS, which disappeared by 13.5 days postcoitum (dpc). When 7.5 dpc YS cells were incubated in the presence of stem cell factor (SCF), interleukin (IL)-3, IL-6, erythropoietin (EPO), thrombopoietin (TPO), and granulocyte colony-stimulating factor in methylcellulose clonal culture, not only erythroid bursts but also megakaryocyte colonies were observed. The megakaryocytes in the colonies matured to proplatelet stages and produced platelets as early as day 3 of culture, much earlier than those from adult bone marrow, although their ploidy class was lower. These megakaryocytes were stained with acetylcholine esterase, and expressed platelet glycoprotein (GP)Ib beta, GPIIIa, and platelet factor 4 by reverse transcription-polymerase chain reaction analysis. The analysis of hemoglobin types in erythrocytes obtained from hematopoietic multilineage colonies containing the megakaryocytes indicated that the Mk progenitors originated from primitive hematopoiesis. The primitive Mk progenitors formed colonies in the absence of any cytokines in fetal bovine serum (FBS)-containing culture, and SCF, IL-3, EPO, and TPO significantly enhanced the Mk colony formation. In FBS-free culture, however, no colony formation was induced without these cytokines. Because megakaryocytes were detected in 8.5-dpc YS, these unique primitive Mk progenitors may rapidly mature and give rise to platelets to prevent hemorrhage in the simultaneously developing blood vessels until definitive hematopoiesis begins to produce platelets. (Blood. 2001;97:2016-2022)

Animals↗
PubMed2001

Breakage and fusion of the TEL (ETV6) gene in immature B lymphocytes induced by apoptogenic signals.

TEL-AML1 fusion resulting from the t(12;21)(p13;q22) is one of the most common genetic abnormalities in childhood acute lymphoblastic leukemia. Recent findings that site-specific cleavage of the MLL gene can be induced by chemotherapeutic agents such as topoisomerase-II inhibitors suggest that apoptogenic agents can cause chromosomal translocations in hematopoietic cells. This study demonstrates a possible relationship between exposure to apoptogenic stimuli, TEL breaks, and the formation of TEL-AML1 fusion in immature B lymphocytes. Short-term culture of immature B cell lines in the presence of apoptogenic stimuli such as serum starvation, etoposide, or salicylic acid induced double-strand breaks (DSBs) in intron 5 of the TEL gene and intron 1 of the AML1 gene. TEL-AML1 fusion transcripts were also identified by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis in cell lines treated by serum starvation or aminophylline. DSBs within the TEL gene were also associated with fusion to other unknown genes, presumably as a result of chromosomal translocation. We also examined 67 cord blood and 147 normal peripheral blood samples for the existence of in-frame TEL-AML1 fusion transcripts. One cord blood sample (1.5%) and 13 normal peripheral blood samples (8.8%) were positive as detected by nested RT-PCR. These data suggest that breakage and fusion of TEL and AML1 may be relatively common events and that sublethal apoptotic signals could play a role in initiating leukemogenesis via the promotion of DNA damage.

Aminophylline↗
PubMed2001

Restricted chromosome breakpoint sites on 11q22-q23.1 and 11q25 in various hematological malignancies without MLL/ALL-1 gene rearrangement.

We analyzed 32 patients with various hematological malignancies including acute myelocytic leukemia and non-Hodgkin lymphoma with a breakpoint at 11q22-q25 of chromosome 11, but who did not have rearrangements of the MLL/ALL-1 gene. The breakpoint in each patient was identified by fluorescence in situ hybridization using 21 cosmid probes and 2 YAC probes. Breakpoints for each "rearrangement" involving translocations such as t(1;11), t(2;11), inv(11), t(11;15), and t(10;11) found in 5 of the 11 patients had breakpoints in a small region from Ccl11-430 to Ccl11-526 at 11q22-q23.1. Furthermore, breakpoints for chromosome deletions at 11q21-q23 in 10 patients were located in the same region as that of translocations. A commonly deleted region among 8 patients was identified from Ccl11-526 to Ccl11-555 at 11q23.1. Fluorescence in situ hybridization analysis revealed that breakpoints for additive chromosome [add(11)] aberrations, which had additional material of unknown origin at 11q23 to 11q25 in 11 patients, were not located at 11q23 but rather at the more telomeric site of Ccl11-503 to VIJ(2)2072 at 11q25. These results indicated that the patients had several restricted breakpoint sites, which means that these chromosomal regions have recurrent oncogenes and tumor suppressor genes for pathogenesis for leukemia and lymphoma.

Acute Disease↗
PubMed2001

GPHN, a novel partner gene fused to MLL in a leukemia with t(11;14)(q23;q24).

We report a novel MLL-associated chromosome translocation t(11;14)(q23;q24) in a child who showed signs of acute undifferentiated leukemia 3 years after intensive chemotherapy that included the topoisomerase-II inhibitor VP 16. Screening of a cDNA library of the patient's leukemic cells showed a novel fusion transcript between MLL and the Gephyrin (GPHN) gene on 14q24. The resulting MLL-GPHN fusion gene encodes MLL AT hook motifs and a DNA methyltransferase homology domain fused to the C-terminal half of Gephyrin, including a presumed tubulin binding site and a domain homologous to the Escherichia coli molybdenum cofactor biosynthesis protein MoeA. Genomic breakpoint analysis showed potential in vitro topoisomerase-II DNA-binding sites spanning the breakpoints in both MLL and GPHN but no flanking sequences that might mediate homologous recombination. This suggests that MLL-GPHN may have been generated by VP 16/topoisomerase-II-induced DNA double-strand breaks, followed by error-prone DNA repair via non-homologous end joining. Gephyrin was originally identified as a submembraneous scaffold protein that anchors and immobilizes postsynaptic membrane neurotransmitter receptors to underlying cytoskeletal elements. It also is reported to bind to phosphatidylinositol 3,4,5-triphosphate binding proteins involved in actin dynamics and downstream signaling and interacts with ATM-related family member RAFT1. Gephyrin domains in the chimeric protein therefore could contribute novel signal sequences or might modify MLL activity by oligomerization or intracellular redistribution.

Amino Acid Sequence↗
PubMed2001

Electron microscopic and cytochemical studies of peroxidase-negative acute nonlymphoblastic leukemia.

Cytochemical and ultrastructural studies of 42 patients with acute nonlymphoblastic leukemia (ANLL) lacking myeloperoxidase as detected by light microscopy were performed. These ANLL patients were classified into minimally differentiated acute myeloid leukemia (AML-M0) (26 cases), mixed-lineage leukemia (9 cases), and acute undifferentiated leukemia (AUL) (7 cases). Ultrastructural morphology revealed blasts from AML-M0 as very immature myeloid cells, blasts from mixed-lineage leukemia as having partially lymphoid cell features, and blasts from AUL as undifferentiated blasts with myeloid nature to some extent. Ultrastructurally, myeloperoxidase activity was positive in 81% of AML-M0 patients and less positive in the mixed-lineage leukemia and AUL patients. The DNA in the nuclei of the AML-M0 blasts was dispersed, as was observed in the immature myeloid cells. Some of the blasts from the mixed-lineage leukemia patients showed condensation of DNA, resembling blasts from acute lymphoblastic leukemia (ALL). The distribution of periodate-reactive glycoconjugates revealed that glycogen particles were absent or, if present, very scanty in AML-M0. Most of the blasts from the AUL patients lacked glycogen particles, and the blasts from those with mixed-lineage leukemia contained clustered glycogen particles, as was observed in the blasts from all patients. These findings disclosed that three subtypes of immature ANLL showed different cytochemical and ultrastructural features in accordance with their immunophenotypical classification.

Adolescent↗
PubMed2001

A field evaluation of in situ biodegradation of trichloroethylene through methane injection.

A field study of biodegradation of trichloroethylene (TCE) through methane injection was conducted at the yard of a home in Japan. Methane was selected as the safest substrate for injection into groundwater. Methane, oxygen, nitrate, and phosphate were introduced into groundwater contaminated with 220 microg/L of TCE. After a week of biostimulation, methane concentrations gradually decreased below the detection limit. Methane oxidizing bacterial numbers increased from 10 to 10(4) cells/mL with methane consumptions. During methane injection. 10-20% of TCE removal was observed. The biotransformation yield was 3-13 mgTCE/gCH4 in this field test. After methane injections were stopped, TCE removal was not observed. These results indicated that bioremediation using methane was useful as a safe technology for a TCE-contaminated area near homes.

Biodegradation, Environmental↗
PubMed2001

Oligoclonal expansion of alphabeta T lymphocytes in Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis with abnormal karyotypes.

We observed a fatal case of Epstein-Barr virus (EBV)-associated hemophagocytic lymphohistiocytosis (HLH) with an abnormal karyotype. Increased levels of alphabeta T cells of the patient were investigated using an inverse polymerase chain reaction (PCR) of the T-cell receptor variable region gene, followed by Jbeta-PCR and single-strand conformation polymorphism (SSCP) to confirm the clonality of specific alphabeta-T cell subsets. A high frequency (>15%) was recognized in Vbeta9 at onset, but not in any Vbeta and Valpha families 2 weeks after chemotherapy. High levels (>20%) of some Jbeta genes were detected in all Vbeta families investigated, and the predominant bias of the Jbeta2 gene relative to the Jbeta1 gene (86.1% versus 13.9% at onset, and 77.4% versus 23.5% after chemotherapy) was recognized in pan-alphabeta T cells. When each Vbeta-Jbeta fragment was compared among the samples at onset and after chemotherapy by SSCP analysis, several distinct bands were observed that indicate a clonal evolution. Thus, the findings suggest that some of the alphabeta T cell clones could be associated with abnormal karyotypes in EBV-HLH. The present findings provide molecular evidence of the presence of oligoclonal T cells in pan-alphabeta-T cells and clonal evolution during a short clinical course in EBV-HLH with abnormal karyotypes.

Child↗
PubMed2001

Enhanced accessibility of peptide substrate toward membrane-bound metalloexopeptidase by supramolecular structure of polyrotaxane.

A L-phenylalanlylglycylglycine- (H-L-PheGlyGly-) terminated polyrotaxane in which many alpha-cyclodextrins (alpha-CDs) are threaded onto poly(ethylene oxide) (PEO) was synthesized to evaluate the effect of alpha-CD threading on the degradation of the terminal H-L-PheGlyGly by a membrane-bound metalloexopeptidase (aminopeptidase M). The threading of alpha-CDs and introducing H-L-PheGlyGly to the terminals were confirmed by gel permeation chromatography and (1)H NMR spectroscopies. In vitro degradation and kinetic studies revealed that the supramolecular structure of the polyrotaxane enhanced the accessibility toward aminopeptidase M despite the higher molecular weight of the polyrotaxane (M(n): approximately 16,000). This finding provides a new design of biodegradable polymers for biomedical applications with controlled degradation profile.

Cell Membrane↗