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Biomedical subjects

M Maeda

Publications and source records attributed to M Maeda.

At least 163 records · Page 9Linked to original sources
PubMed2001

[Reoperation for late postoperative right ventricular outflow tract obstruction].

Between February 1993 and July 2000, 18 patients with a mean age of 7.9 years underwent re-operation for critical stenosis of the right ventricular outflow tract. Their diagnoses of these patients included tetralogy of Fallot (n = 7), transposition of the great arteries (n = 6), truncus arteriosus communis (n = 3), and double outlet right ventricle with pulmonary stenosis (n = 2). The first operations were extracardiac conduit operations (n = 9), arterial switch operations (n = 6) and patch reconstruction of the right ventricular outflow tract (n = 3). At re-operation, the right ventricular outflow tract obstruction was released completely and reconstructed using a monocusp ventricular outflow patch (n = 14), valved pericardial roll (n = 2), or bovine pericardial patch sparing the native pulmonary valve annulus (n = 2). There were no early deaths, although one patient died of arrhythmia 2.6 years after re-operation. The pressure gradient across the right ventricular outflow tract, right ventricular systolic pressure, and right ventricle to systemic systolic pressure ratio were satisfactorily relieved (84.3 +/- 19.0 vs. 16.7 +/- 19.7 mmHg, 109.2 +/- 20.5 vs. 48.7 +/- 16.7 mmHg, 0.92 +/- 0.25 vs. 0.43 +/- 0.16; p < 0.001, p < 0.001, p < 0.001, respectively). The right ventricular end-diastolic volume index and right ventricular ejection fraction were also improved (166.3 +/- 85.2 vs. 105.6 +/- 28.8% of normal, 38.3 +/- 12.6 vs. 50.9 +/- 8.8%; p < 0.05, p < 0.005, respectively). Re-operation should be done before the development of marked right ventricular dysfunction, while it can still be performed at a low risk with satisfactory results.

Child↗
PubMed2001

[Surgical treatment of coronary artery-pulmonary artery fistula with coronary aneurysm].

We experienced 4 cases of coronary artery-pulmonary artery fistula with coronary aneurysm, three patients had symptoms of chest pain, and 1 patient had cardiac murmur. Coronary arteriography showed that three patients had fistulas from the left coronary artery to the pulmonary artery; and that 1 patient had a fistula from both the right and left coronary arteries to the pulmonary artery. Moreover, 1 patient had 90% diameter stenosis of segment 7. The maximum diameter of the coronary aneurysm ranged from 12 to 20 mm (average: 15.3 mm). One patient underwent closure of the opening of the fistula, 2 patients underwent multiple ligatures of fistulas, and 1 patient underwent multiple ligatures of fistulas with coronary artery bypass grafting. The postoperative course of every patient was uneventful. There have been 42 reports on this abnormality in Japan. We should treat the fistula as early as possible to prevent cardiac complications such as myocardial ischemia and rupture of coronary aneurysm.

Adult↗
PubMed2001

Identification of missense mutation (G365R) of the butyrylcholinesterase (BCHE) gene in a Japanese patient with familial cholinesterasemia.

A point mutation which caused a silent phenotype of human serum butyrylcholinesterase (BChE) was identified in the genomic DNA of a 57-year-old Japanese woman who visited our hospital because of pneumonia. The propositus exhibited an unusually low level of BChE activity, whereas her son and daughter had an intermediate level. Immunologically, there was an absence of BChE protein in the propositus's serum. DNA sequence analysis of the propositus demonstrated a point mutation at codon 365 (GGA-CGA), resulting in a Gly-Arg substitution. A family study showed her son and daughter to have the same mutation.

Butyrylcholinesterase↗
PubMed2001

[Propofol anesthesia combined with thoracic epidural anesthesia for thymectomy for myasthenia gravis--a report of eleven cases].

We report 11 cases of thymectomy for myasthenia gravis using propofol and thoracic epidural anesthesia. Considering the influence of nitrous oxide to environment and muscular relaxation of volatile anesthetics, we selected this anesthetic method. By proper sedation with propofol and sufficient analgesia with epidural anesthesia, the hemodynamics during operation was stable and the emergence was rapid. The patients were extubated early after operation except in one case in which oxygenation was not good because of sputum. We conclude that our anesthetic method is useful. Moreover, we applied Fuchu hospital scoring system for prediction of the need of postoperative mechanical ventilation in patients with myasthenia gravis to the present 11 cases. These predictions corresponded well with the results. Therefore Fuchu hospital scoring system is useful for managing these patients by our anesthetic method.

Adult↗
PubMed2000

Rescue of ischemic brain injury by adenoviral gene transfer of glial cell line-derived neurotrophic factor after transient global ischemia in gerbils.

Glial cell line-derived neurotrophic factor (GDNF), a member of the transforming growth factor (TGF)-beta superfamily, is one of the most potent neurotrophic factors and promotes survival of many populations of cells. We examined neuroprotective effect of an adenoviral vector encoding glial cell line-derived neurotrophic factor (AxCAhGDNF) on the transient global ischemia. Gerbils received administration of AxCAhGDNF or an adenoviral vector encoding bacterial beta-galactosidase gene (AxCALacZ) through the lateral ventricle. Two days later, occluding bilateral common carotid arteries for 5 min using aneurysm clips produced the transient global forebrain ischemia. Animals showed intense immunolabeling for GDNF in ependymal cells on 2, 4 and 7 days after the operation. The exogenous gene transducted by adenovirus in the same cells was detected by in situ hybridization. The treatment with AxCAhGDNF significantly prevented the loss of hippocampal CA1 pyramidal neurons 2 to 7 days after the operation, as compared to AxCALacZ treatment. Also terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) staining was markedly reduced in the case with AxCAhGDNF treatment at 7 days after the operation. These results indicated that the adenovirus-mediated gene transfer of GDNF might prevent the delayed neuronal death of stroke and other disorders of the cerebral vasculature.

Adenoviridae↗
PubMed2000

Inhibition of thrombin by sulfated polysaccharides isolated from green algae.

Eight different sulfated polysaccharides were isolated from Chlorophyta. All exhibited thrombin inhibition through a heparin cofactor II (HCII)-dependent pathway, and their effects on the inhibition of thrombin were more potent than those of heparin or dermatan sulfate. In particular, remarkably potent thrombin inhibition was found for the sulfated polysaccharides isolated from the Codiales. In the presence of these sulfated polysaccharides, both the recombinant HCII (rHCII) variants Lys(173)-->Leu and Arg(189)-->His, which are defective in interactions with heparin and dermatan sulfate, respectively, inhibited thrombin in a manner similar to native rHCII. This result indicates that the binding site of HCII for each of these eight sulfated polysaccharides is different from the heparin- or dermatan sulfate-binding site. All the sulfated polysaccharides but RS-2 significantly stimulated the inhibition of thrombin by an N-terminal deletion mutant of HCII (rHCII-Delta74). Furthermore, hirudin(54-65) decreased only 2-5-fold the rate of thrombin inhibition by HCII stimulated by the sulfated polysaccharides, while HD22, a single-stranded DNA aptamer that binds exosite II of thrombin, produced an approximately 10-fold reduction in this rate. These results suggest that, unlike heparin and dermatan sulfate, the sulfated polysaccharides isolated from Chlorophyta activate HCII primarily by an allosteric mechanism different from displacement and template mechanisms.

Antithrombins↗
PubMed2000

Essential role of NAT1/p97/DAP5 in embryonic differentiation and the retinoic acid pathway.

NAT1/p97/DAP5 is a newly identified protein that shares homology with the translation initiation factor eIF4G. Studies in vitro and in transfected cells indicated that NAT1 might suppress global translation, thereby repressing cellular proliferation. Here we studied the functions of NAT1 in vivo by disrupting its gene in mice. NAT1(-/-) embryos died during gastrulation, indicating a crucial role for NAT1 in embryogenesis. Undifferentiated NAT1(-/-) embryonic stem cells were normal in morphology, proliferation, global translation and gene expression profile. However, NAT1(-/-) cells exhibited an impaired ability to differentiate: they were resistant to differentiation induced by retinoic acid, and teratomas derived from them consisted of undifferentiated and poorly differentiated tissues. The expression of retinoic acid-responsive genes, such as the cell-cycle inhibitor p21(WAF1), was selectively impaired in NAT1(-/-) cells. Transcription from synthetic retinoic acid-responsive elements was also impaired. These data demonstrated that this translation initiation factor homolog controls specific gene expression pathways required for cellular differentiation.

Animals↗
PubMed2000

Identification of mammalian TOM22 as a subunit of the preprotein translocase of the mitochondrial outer membrane.

A mitochondrial outer membrane protein of approximately 22 kDa (1C9-2) was purified from Vero cells assessing immunoreactivity with a monoclonal antibody, and the cDNA was cloned based on the partial amino acid sequence of the trypsin-digested fragments. 1C9-2 had 19-20% sequence identity to fungal Tom22, a component of the preprotein translocase of the outer membrane (the TOM complex) with receptor and organizer functions. Despite such a low sequence identity, both shared a remarkable structural similarity in the hydrophobicity profile, membrane topology in the Ncyt-Cin orientation through a transmembrane domain in the middle of the molecule, and the abundant acidic amino acid residues in the N-terminal domain. The antibodies against 1C9-2 inhibited the import of a matrix-targeted preprotein into isolated mitochondria. Blue native polyacrylamide gel electrophoresis of digitonin-solubilized outer membranes revealed that 1C9-2 is firmly associated with TOM40 in the approximately 400-kDa complex, with a size and composition similar to those of the fungal TOM core complex. Furthermore, 1C9-2 complemented the defects of growth and mitochondrial protein import in Deltatom22 yeast cells. Taken together, these results demonstrate that 1C9-2 is a functional homologue of fungal Tom22 and functions as a component of the TOM complex.

Adenosine Triphosphatases↗
PubMed2000

The design of cyclic AMP--recognizing oligopeptides and evaluation of its capability for cyclic AMP recognition using an electrochemical system.

A novel 17-mer peptide ligand for cyclic AMP was designed using the amino acid sequences of essential subsites in various cyclic AMP-dependent protein kinase (protein kinase A) families. The Au disk electrode, which was modified with the designed 17-mer oligopeptide, responded to cyclic AMP but virtually did not respond to any other cyclic nucleotides using the ion channel sensor mechanism. On the other hand, a scrambled peptide, which had the same amino acid composition as and had an amino acid sequence different from the 17-mer oligopeptide, did not respond to any nucleotides. This indicates that the designed 17-mer peptide actually acted as a selective ligand for cyclic AMP. This ligand-designing strategy using peptide sequences in target-binding proteins may possibly be extended to the design of peptide ligands for other second messengers.

Cyclic AMP↗
PubMed2000

The K(+) affinity of gastric H(+),K(+)-ATPase is affected by both lipid composition and the beta-subunit.

It is generally assumed that negatively charged residues present in the alpha-subunit of gastric H(+),K(+)-ATPase are involved in K(+) binding and transport. Despite the fact that there is no difference between various species regarding these negatively charged residues, it was observed that the apparent K(+) affinity of the pig enzyme was much lower than that of the rat H(+),K(+)-ATPase. By determining the K(+)-stimulated dephosphorylation reaction of the phosphorylated intermediate K(0.5) values for K(+) of 0.12+/-0.01 and 1.73+/-0.03 mM were obtained (ratio 14.4) for the rat and the pig enzyme, respectively. To investigate the reason for the observed difference in K(+) sensitivity, both enzymes originating from the gastric mucosa were either reconstituted in a similar lipid environment or expressed in Sf9 cells. After reconstitution in K(+)-permeable phosphatidylcholine/cholesterol liposomes K(0.5) values for K(+) of 0.16+/-0.01 and 0.35+/-0.05 mM for the rat and pig enzyme respectively were measured (ratio 2.2). After expression in Sf9 cells the pig gastric H(+),K(+)-ATPase still showed a 4.1 times lower K(+) sensitivity than that of the rat enzyme. This means that the difference in K(+) sensitivity of the rat and pig gastric H(+), K(+)-ATPase is not only due to a different lipid composition but also to the structure of either the alpha- or beta-subunit. Expression of hybrid enzymes in Sf9 cells showed that the difference in K(+) sensitivity between the rat and pig gastric H(+),K(+)-ATPase is primarily due to differences in the beta-subunit.

Animals↗
PubMed2000

Developmental changes in the spatial expression of genes involved in myosin function in Dictyostelium.

We analyzed the spatial expression patterns of the genes involved in myosin function by in situ hybridization at the tipped aggregate and early culmination stages of Dictyostelium. Myosin heavy chain II mRNA was enriched in the anterior prestalk region of the tipped aggregates, whereas it disappeared from there and began to appear in both upper and lower cups of the early culminants. Similarly, mRNAs for essential light chain, regulatory light chain, myosin light chain kinase A, and myosin heavy chain kinase C were enriched in the prestalk region of the tipped aggregates. However, expression of these genes was distinctively regulated in the early culminants. These findings suggest the existence of mechanisms responsible for the expression of particular genes.

Animals↗
PubMed2000

Loss of fragile histidine triad gene expression is associated with progression of esophageal squamous cell carcinoma, but not with the patient's prognosis and smoking history.

BACKGROUND: Recently, fragile histidine triad (FHIT) gene abnormality has been thought to be associated with several malignancies and smoking history. The authors previously discovered that methylation of the 5' CpG island of the FHIT gene was closely associated with transcriptional inactivation in esophageal squamous cell carcinoma (SCC); however, the clinical impact of the FHIT gene in esophageal carcinoma is still unknown. METHODS: In this article, the authors evaluated the clinical impact of the FHIT gene in 149 esophageal squamous cell carcinoma (SCC) patients retrospectively using immunohistochemical analysis. They also examined the correlation between FHIT protein expression and smoking history. RESULTS: Among 149 curative resection (R0) cases of esophageal SCC, normal FHIT protein expression was noted in only 33 cases (22.1%), whereas reduced FHIT protein expression was noted in 67 cases and there was no FHIT expression in 50 cases. When a tumor invaded the muscle layer, FHIT protein expression was markedly reduced. The cases with reduction or loss of FHIT protein expression tended to have poor prognoses (P = 0.069). However, Cox multivariate analysis revealed that FHIT protein reduction had no relation to prognosis. FHIT protein expression had no relation to smoking history. CONCLUSIONS: FHIT protein expression was associated with progression of esophageal SCC, however, it may not be associated with the patient's prognosis and smoking history.

Aged↗
PubMed2000

Loss of a member of the aquaporin gene family, aqpA affects spore dormancy in Dictyostelium.

We isolated and characterized a gene from Dictyostelium discoideum, which encodes a protein of 279 amino acids (30.6kDa) containing six transmembrane domains with two highly conserved motifs of asparagine-proline-alanine (NPA) found in the aquaporin family of water-channel proteins, although the second motif of the protein has been modified into NPV (asparagine-proline-valine). The deduced amino acid sequence of the gene, which we have named aqpA, is 39% identical to D. discoideum WacA, 26% identical to human Aqp5, 26% identical to Oryza sativa PIP2a, 25% identical to yeast Aqy1 and 24% identical to E.coli AqpZ. Southern analyses indicated that aqpA is present as a single copy in the genome. Northern blot analysis showed that the developmentally regulated 1kb mRNA transcript first appears at the tight mound stage (12h), and is abundant in fingers (16h) and late culminants (20h). In-situ hybridization of slugs revealed that aqpA mRNA accumulated in cells of the prespore region but not in those of the prestalk region. Disruption of aqpA by homologous recombination did not significantly affect growth or developmental morphogenesis. Although mutant spores were viable, when assayed soon after encapsulation, they became permeable to propidium iodide and lost viability after a week on the top of a fruiting body. Thus, AqpA is essential to maintain spore dormancy perhaps through the regulation of water flow.

Amino Acid Sequence↗
PubMed2000

Noninsecticidal parasporal proteins of a Bacillus thuringiensis serovar shandongiensis isolate exhibit a preferential cytotoxicity against human leukemic T cells.

A Bacillus thuringiensis isolate, 89-T-34-22, belonging to the serovar shandongiensis (H22) produced noninsecticidal and nonhemolytic proteins crystallizing into irregular-shaped parasporal inclusions. The proteins showed in vitro cytotoxicity to human cells, including cancer cells, only when activated by protease treatment. The human leukemic T (MOLT-4) cells were > 100 times more susceptible than HeLa and normal T cells to the proteins of 89-T-34-22. The cytotoxicity was dose dependent and the median effective concentration for the MOLT-4 was 3.5 microg/ml. The cytopathy induced by the 89-T-34-22 proteins was characterized by remarkable condensation of the nucleus and cell-ballooning. Five major parasporal proteins of 89-T-34-22, with molecular masses in the range of 16-160 kDa, shared no similarity with the previously reported proteins in terms of the N-terminal sequence.

Amino Acid Sequence↗
PubMed2000

A clinicopathologic study of gastric mucosa-associated lymphoid tissue lymphoma.

BACKGROUND: It is still unclear which patients with gastric mucosa-associated lymphoid tissue (MALT) lymphoma will benefit from the eradication of Helicobacter pylori. METHODS: The authors studied a total of 34 patients. Twenty-three patients had primary gastric lymphoma and underwent gastric resection as initial treatment. Eleven patients with gastric MALT lymphoma who received antibiotics against H. pylori as initial treatment were also included. In all 34 patients, the presence of H. pylori, endoscopic findings, and pathologic features were evaluated. Immunohistochemical expression of Bcl-2, p53, and proliferating cell nuclear antigen (PCNA) was classified as follows: (-), no reactive cells; (+), scattered positive cells; (2+), nests of positive cells; (3+), diffuse positive cells. RESULTS: Patients with low grade MALT lymphoma (LG) tended to be positive for H. pylori (6 of 9), to localize within the submucosa (7 of 9), not to have lymph node involvement (7 of 8), and to have lower tumor stage compared with patients with high grade MALT components (HG). Bcl-2 protein was expressed with high frequency by LG (7 of 9). Strong expression of p 53 was more common in the HG tumors (4 of 14), and strong expression of PCNA showed a significant difference between LG (1 of 8) and HG patients (12 of 13). Investigation of the patients with long term follow-up (n = 4) revealed that LG remained superficial for a long time and showed gradual progression. Most of these tumors were Bcl-2+/p53-approximately+/-/ PCNA- approximately +. There were two patients whose superficial LG (sm/Bcl-2+/p53-/PCNA- approximately +) regressed after the disappearance of H. pylori. On the other hand, one patient developed ulcerated LG (sm/Bcl-2 /p53+/PCNA3+) after disappearance of H. pylori. The authors found complete regression of MALT lymphoma in 9 of 11 patients after H. pylori eradication. Initial tumors of these 9 patients were superficial/sm/n(-)/low grade/Bcl-2+approximately +/-/p53-approximately+ (n = 9), /PCNA-approximately+(n = 6), /PCNA 2+ (n = 3). Two local recurrence and one non-Hodgkin lymphoma in other sites were observed after initial therapy. CONCLUSIONS: Gastric MALT lymphoma with (H. pylori positive/superficial/sm/low grade/Bcl-2 +/p53- approximately +/PCNA- approximately +) pattern will disappear after a patient is cured of H. pylori infection.

Adult↗
PubMed2000

Transcriptional regulation of the ATP citrate-lyase gene by sterol regulatory element-binding proteins.

In an attempt to identify unknown target genes for SREBP-1, total RNA from a stable Chinese hamster ovary cell line (CHO-487) expressing a mature form of human SREBP-1a (amino acids 1-487) with a LacSwitch Inducible Mammalian Expression System was subjected to a polymerase chain reaction subtraction method. One of the fragments was found to have 90 and 86% homology with rat and human ATP citrate-lyase (ACL) cDNA, respectively. When Hep G2 cells are cultured under either sterol-loaded or -depleted conditions, expression of the gene is induced approximately 2-3-fold by sterol depletion. To investigate the direct effect of SREBP-1a on transcription, luciferase assays using the promoter of the human ACL gene were performed. These deletion studies indicated that a minimum 160-base pair segment contains the information required for the transcriptional regulation brought about by enforced expression of SREBP-1a. Luciferase assays using mutant reporter genes revealed that SREBP-dependent transcriptional regulation is mediated by two nearby motifs, the SREBP-binding site (a TCAGGCTAG sequence) and the NF-Y-binding site (a CCAAT box). It was confirmed by gel mobility shift assays that recombinant SREBP-1a binds to the sequence. Data from studies with transgenic mice and reporter assays show that the ACL gene promoter is activated by SREBP-1a more strongly than SREBP-2 in contrast to the HMG CoA synthase and LDL receptor gene promoters, which exhibit the same preference for the two factors. Therefore, SREBPs transcriptionally regulates ACL enzyme activity, which generates the cytosolic acetyl CoA required for both cholesterol and fatty acid synthesis.

ATP Citrate (pro-S)-Lyase↗