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Biomedical subjects

H Fujii

Publications and source records attributed to H Fujii.

At least 379 records · Page 21Linked to original sources
PubMed1998

Dentin bridge formation following direct pulp capping in dog's.

The effectiveness of two different calcium hydroxide pastes; "Calvital and "Dycal", for the direct pulp capping in dog's permanent teeth with incompletely formed roots were evaluated in this study. Forty-eight vital permanent premolar teeth with incompletely formed apices were obtained from 6 dog's (6 months of age). Exposure sites on contralateral pairs of teeth were capped with either "Calvital" or "Dycal". Then intravenous injections of tetracycline were administered to the dogs at various intervals. Animals were sacrificed at 56 days. The teeth were fixed, undecalcified ground sectioned, observed by microradiography, and evaluated by ultraviolet light. In cases treated with "Calvital", a fluorescent line resulting from tetracycline administration 7 days after experimental procedures was seen in the newly formed dentin bridge. In cases treated with "Dycal", a fluorescent line resulting from tetracycline administration 14 days after experimental procedures was seen in the newly formed dentin bridge. Continued physiological root formation was observed well in all teeth. This experiment may explain why some "Dycal" failures occur in the earlier postoperative periods; serves as a stimulus potential for a hardening reaction.

Animals↗
PubMed1998

[Familial cortisol resistance and mutations of the glucocorticoid receptor gene].

Patients with familial cortisol resistance have continuously elevated serum cortisol without any clinical manifestations of Cushing's syndrome due to hyposensitivity to cortisol in all tissues including the hypothalamus and the pituitary. Clinical symptoms of the disease are hypertension with hypokalemia and hyporeninemia, virilism in women and mild general fatigue. As the cause of the disease, a defect in glucocorticoid receptor affinity or binding capacity due to mutations in the glucocorticoid receptor gene has been reported. Another cause of the disease is the presence of heat labile glucocorticoid receptor. In 4 of 5 families with cortisol resistance reported so far, mutations of the glucocorticoid receptor gene have been demonstrated.

Fatigue↗
PubMed1998

[Operative results of composite aortic root replacement by a Svensson's method].

The results of reconstruction of the aortic root performed on 9 patients by Svensson's method were examined. Nine subjects comprised 6 men and 3 women aged 23-69 years. In the preoperative diagnosis, annulo-aortic ectasia (AAE) was found in 7 cases, acute Type A aortic dissection in 1 case and AAE accompanied by chronic dissection after AVR in 1 case. Every patient underwent reconstruction by direct implantation of the right coronary artery button and interposition grafting for the left coronary artery, using a composite valve graft made of SJM valve and collagen coating artificial graft. Although one patient was lost due to multiple cerebral infarction, no marked changes were observed in other 8 patients. Angiography at short-term after operation showed no problems in the composite valve graft, and revealed good coronary arterial flow. Now, 2-62 months after operation (41 months on average), no late death occurred. On angiography of 2 cases performed after a long-term period, patency of the interposition graft was excellent. The early and late results of aortic root reconstruction by Svensson's method appeared favorable.

Adult↗
PubMed1998

[t(3;5) (q21;q31) chromosomal abnormality in a patient with acute myelogenous leukemia with trilineage myelodysplasia].

A 60-year-old woman was admitted in June 1993, because of anemia and purpura and given a diagnosis of acute myelogenous leukemia with trilineage dysplasia. She entered partial remission (PR) after three courses of low-dose Ara-C and G-CSF, but never reached complete remission (CR) in spite of additional chemotherapy. In October 1994, the number of leukocytes, myeloblasts, and erythroblasts in the patient's peripheral blood increased, and her clinical condition deteriorated. The disease was resistant to other therapy. The patient had pneumonia and died of septic shock in December 1994. A chromosomal analysis performed on admission showed 46,XX,t(3;5) (q21;q31) [9/9]. As an additional chromosomal abnormality, deletion of the X chromosome was observed in January, 1994. Analysis of the p53 gene by the polymerase chain reaction-single strand conformation polymorphism method showed one base transposition, from TAT to TGT (Tyr to Cys), at codon 220 of exon 6. Karyotype evolution and p53 gene mutation were observed during the disease course and may have been related to progression of the disease.

Chromosomes, Human, Pair 3↗
PubMed1998

[Influence of left ventricular wall thickening on myocardial injury in aortic valve replacement].

We retrospectively examined the influence of left ventricular wall thickening on myocardial injury in aortic valve replacement. Thirty-five patients who underwent aortic valve replacement in our hospital between January 1995 and July 1997 were studied. We divided these patients into 3 groups: group N (left ventricular thickness (LVT) < or = 10 mm), group H (10 < LVT < or = 15 mm), and group S (LVT > 15 mm). All patients of group S had aortic stenosis. CK and CK-MB were significantly higher and the cardiac index was significantly lower in group S than in the other groups. Intra-aortic balloon pumping was required for 50% of patients in group S, and a total dose of catecholamine above 10 micrograms/kg/min was also required for 50% of patients in this group. In the other groups, these percentages were significantly lower. Myocardial protection and postoperative care were difficult for patients with severe left ventricular hypertrophy with LVT over 15 mm in this study. Left ventricular wall thickness was a more important factor in determining difficulty with intraoperative myocardial protection than was left ventricular mass.

Adolescent↗
PubMed1998

Comparison of loss heterozygosity in primary and recurrent ductal carcinoma in situ of the breast.

Ductal carcinoma in situ (DCIS) of the breast is often an indolent disease, although some cases are reported to recur many years after a limited surgical resection. It is not known whether these recurrences reflect a resurgence of residual disease or an independent development of a second tumor in susceptible individuals. Therefore, we conducted a longitudinal molecular study of four women with reappearance of DCIS 2 to 15 years after an initial conservative resection. Loss of heterozygosity (LOH) was characterized in both tumors in each case, using several polymerase chain reaction-amplified microsatellite markers on five chromosomal arms commonly affected in breast cancer. In three cases with ipsilateral recurrent disease, all of the allelic losses seen in the initial tumors were also seen in the recurrent lesions, suggesting a common genetic pathway for the development of both lesions and continuous proliferation of residual disease. The presence of at least one additional LOH in all of the three recurrent tumors, however, suggests that the recurrent tumors developed after genetic progression. In contrast, in one case of DCIS that was followed by the development of DCIS in the contralateral breast 7 years later (a case of bilateral DCIS), unrelated LOH patterns were present in the two lesions. These findings suggest that the reappearance of DCIS in the same breast is most commonly the result of a tumor derived from (but not identical to) the original lesion, with acquisition of additional genetic changes, even when the recurrent lesion manifested itself many years (15 years, in one case) after the initial presentation. Furthermore, genetic progression could be detected in tumors recurring in as little as 2 years after the initial resection.

Adult↗
PubMed1998

Aorto-atrial fistula associated with recurrent aortic dissection after ascending aorta replacement.

A 70-year-old woman with a bicuspid aortic valve had undergone ascending aorta replacement for acute DeBakey type I dissection. Computed tomography and aortography 2 months after the operation revealed a thrombosed false lumen in the ascending aorta proximal to the prosthetic graft. However, recurrence of dissection was found at the aortic root proximal to the graft 4 years after the initial operation. Significant aortic stenosis was also noted. Despite intensive medical treatment, she had refractory and progressive heart failure. At the second surgery, an aorto-right atrial fistula, which probably was responsible for the severe heart failure was revealed. Closure of the aorto-right atrial fistula, and aortic root replacement were performed using Piehler's method, with a composite graft. The etiology and management of this rare case are discussed.

Aged↗
PubMed1997

Nitric oxide inactivates NADPH oxidase in pig neutrophils by inhibiting its assembling process.

The effects of nitric oxide (NO) on superoxide (O-2) generation of the NADPH oxidase in pig neutrophils were studied. NO dose-dependently suppressed O-2 generation of both neutrophil NADPH oxidase and reconstituted NADPH oxidase. Effects of NO on NADPH-binding site and the redox centers including FAD and low spin heme in cytochrome b558 and the electron transfer rates from NADPH to heme via FAD were examined under anaerobic conditions. Both reaction rates and the Km value for NADPH were unchanged by NO. Visible and EPR spectra of cytochrome b558 showed that the structure of heme was unchanged by NO, indicating that NO does not affect the redox centers of the oxidase. In reconstituted NADPH oxidase system, NO did not inhibit O-2 generation of the oxidase when added after activation. The addition of NO to the membrane component or the cytosol component inhibited the activity by 24.0 +/- 5.3 or 37.4 +/- 7.1%, respectively. The addition of NO during the activation process or to the cytosol component simultaneously with myristate inhibited the activity by 74.0 +/- 5.2 or 70.0 +/- 8.3%, respectively, suggesting that cytosol protein(s) treated with myristate becomes susceptible to NO. Peroxynitrite did not interfere with O-2 generation.

Animals↗
PubMed1997

Stimulatory effects of EGF and TGF-alpha on invasive activity and 5'-deoxy-5-fluorouridine sensitivity in uterine cervical-carcinoma SKG-IIIb cells.

We investigated the effects of epidermal growth factor (EGF) and transforming growth factor (TGF)-alpha on migration, invasion and matrix metalloproteinase (MMP) expression of uterine cervical-carcinoma SKG-IIIb cells, and whether these growth factors affect pyrimidine-nucleoside-phosphorylase (PyNPase) activity and 5'-deoxy-5-fluorouridine (5'-dFUrd) sensitivity of tumor cells. Tumor-cell migration along a gradient of substratum-bound fibronectin and invasion into reconstituted basement membrane were stimulated by 0.1 to 100 ng/ml of EGF and TGF-alpha in a concentration-dependent manner. The zymography of tumor-conditioned medium showed that the treatment of tumor cells with EGF and TGF-alpha resulted in an increase of the 92-kDa type-IV collagenase (MMP-9), which was confirmed by immunoblot analysis. These growth factors also up-regulated the expression of PyNPase activity of tumor cells and consequently enhanced the anti-proliferative action of 5'-dFUrd, a cytostatic that is biotransformed to 5-fluorouracil (5-FUra) by PyNPase. However, EGF and TGF-alpha did not have significant effects on the 5-FUra sensitivity of tumor cells. These results suggest that EGF and TGF-alpha, tumor environmental factors, simultaneously up-regulate the potential of uterine cervical-carcinoma cells to invade extracellular matrices and their PyNPase activity, which are subsequently associated with the specific action of 5'-dFUrd selectively killing tumor cells of gynecological origin with high invasive and metastatic potential.

Basement Membrane↗
PubMed1997

Metabolic inactivation of retinoic acid by a novel P450 differentially expressed in developing mouse embryos.

Retinoic acid (RA) is a physiological agent that has a wide range of biological activity and appears to regulate developmental programs of vertebrates. However, little is known about the molecular basis of its metabolism. Here we have identified a novel cytochrome P450 (P450RA) that specifically metabolizes RA. In vitro, P450RA converts all-trans RA into 5,8-epoxy all-trans RA. P450RA metabolizes other biologically active RAs such as 9-cis RA and 13-cis RA, but fails to metabolize their precursors, retinol and retinal. Overexpression of P450RA in cell culture renders the cells hyposensitive to all-trans RA. These functional tests in vitro and in vivo indicate that P450RA inactivates RA. The P450RA gene is not expressed uniformly but in a stage- and region-specific fashion during mouse development. The major expression domains in developing embryos include the posterior neural plate and neural crest cells for cranial ganglia. The expression of P450RA, however, is not necessarily inducible by excess RA. These results suggest that P450RA regulates the intracellular level of RA and may be involved in setting up the uneven distribution of active RA in mammalian embryos.

Amino Acid Sequence↗
PubMed1997

Molecular analysis of eight biochemically unique glucose-6-phosphate dehydrogenase variants found in Japan.

We analyzed the molecular mutations of eight known Japanese glucose-6-phosphate dehydrogenase (G6PD) variants with unique biochemical properties. Three of them were caused by novel missense mutations: G6PD Musashino by 185 C-->T, G6PD Asahikawa by 695 G-->A, and G6PD Kamiube by 1387 C-->T. Predicted amino acid substitutions causing asymptomatic variants G6PD Musashino (62 Pro-->Phe) and G6PD Kamiube (463 Arg-->Cys) were located in regions near the amino or carboxyl end of the polypeptide chain, whereas an amino acid change 232 Cys-->Tyr causing a class 1 variant G6PD Asahikawa was located in the region where amino acid alterations in some class 1 variants were clustered. The other five variants had known missense mutations, namely, G6PD Fukushima, 1246 G-->A, G6PD Morioka, 1339 G-->A, and G6PD Iwate, G6PD Niigata and G6PD Yamaguchi, 1160 G-->A, which cause variants, G6PD Tokyo, G6PD Santiago de Cuba, and G6PD Beverly Hills, respectively.

Anemia, Hemolytic, Congenital Nonspherocytic↗
PubMed1997

Frame shift mutation, exon skipping, and a two-codon deletion caused by splice site mutations account for pyruvate kinase deficiency.

Three novel splice site mutations and two novel missense mutations were identified by molecular analysis of pyruvate kinase (PK) deficiency associated with hereditary nonspherocytic hemolytic anemia. A Nepalese PK variant, PK Kowloon, was found to have a homozygous transversion at the 5'-splice site of the seventh intervening sequence (IVS) of the L-type PK gene (Ivs7[+1]gt --> tt). Using a reverse transcription polymerase chain reaction (RT-PCR) assay, we showed that the R-type PK mRNA in the proband's reticulocytes included the seventh IVS between the seventh and eighth exon, introducing a stop codon 3 nucleotides downstream of the mutated site. Consequently, the translational product may lack 44% of the R-PK polypeptide. A transition at the last nucleotide of exon 9 (1269GCG --> GCA) was found in a Japanese PK variant, PK 'Kamata.' The mutation did not alter the amino acid sequence, but caused skipping of the ninth exonic sequence in the R-PK transcripts. As a result, the affected R-type PK lost 51 amino acid residues (373Met-423Ala del). A transversion at the splice acceptor site of the third IVS (Ivs 3[-2]ag --> tg) was identified in PK 'Aomori.' The mutation resulted in aberrant splicing at a cryptic splice site within exon 4, causing deletion of two codons in the aberrant R-PK transcript (95 Gly-96 Pro --> del). Both PK 'Kamata' and PK 'Aomori' had a missense mutation on the other allele, 1044AAG --> AAT (348Lys --> Asn) and 1075CGC --> TGC (359Arg --> Cys), respectively. Although both 348Lys and 359Arg were located in the sixth loop of A domain (beta/alpha)8 barrel, which has been shown to contain the substrate and cation binding sites, the degree of anemia was much more severe in PK 'Kamata' than PK 'Aomori,' possibly because the 51 amino acid deletion of PK 'Kamata' but the 2 amino-acid deletion of PK 'Aomori' may abolish PK catalytic activity.

Anemia, Hemolytic, Congenital Nonspherocytic↗
PubMed1997

Resonance Raman spectroscopic characterization of alpha-hydroxyheme and verdoheme complexes of heme oxygenase.

Heme oxygenase (HO) is the microsomal enzyme that catalyzes the oxidative degradation of protoheme (iron protoporphyrin IX) and the generation of carbon monoxide. The enzyme converts protoheme into biliverdin through two known heme derivatives, alpha-hydroxyheme and verdoheme. To gain insight into the degradation mechanisms of the two intermediates, the resonance Raman spectra were observed for alpha-hydroxyheme and verdoheme complexes of HO and compared with those of apomyoglobin (apo-Mb) complexes. The ferrous alpha-hydroxyheme complexed with both HO and apo-Mb shows a resonance Raman spectral pattern similar to that of the protoheme complexes. On the contrary, the ferric alpha-hydroxyheme and ferrous verdoheme complexes of HO and apo-Mb show atypical Raman patterns, which are interpreted as the result of the symmetry lowering of the porphyrin-conjugated pi-electron system. The comparison of the resonance Raman spectra of the verdoheme complexed with HO and apo-Mb with those of the five- and six-coordinate model complexes of verdoheme shows that the ferrous forms of the verdoheme-protein complexes are six-coordinate. The Fe-CO and Fe-CN stretching frequencies of ferrous verdoheme compounds are distinct from those of ferrous heme compounds. It is inferred that the positive charge of the verdoheme ring possesses some of the charge density on the iron atom, causing unique characteristics of the iron ligand stretching vibrations and altered ligand binding properties.

Heme↗
PubMed1997

Magnetic resonance imaging of skeletal muscles in the polymyositis.

Magnetic resonance imaging of skeletal muscles was performed in 11 patients with polymyositis. Two types of muscle lesions were revealed. The first, inflammation, showed increased signal intensity on T2-weighted images and iso-intensity on T1-weighted images. The second, fatty replacement, showed increased signal intensity on both images. The coronal sections could elucidate the extension of the lesion in each affected muscle. Inflammation was relatively diffuse, while homogeneous fatty replacement tended to begin at the lower myotendinous junctions.

Adipose Tissue↗
PubMed1997

Determination and characterization of nitric oxide generation in mice by in vivo L-Band EPR spectroscopy.

The authors have shown direct, real-time, in vivo measurement of nitric oxide (NO) in mice by using the water soluble metal chelator complex, N-methyl-D-glucamine dithiocarbamate (MGD), and Fe(II) as monitored by EPR at L-band. The three-line EPR spectrum from the product [(MGD)2-Fe(II)-NO] was observed noninvasively in lipopolysaccharide (LPS)-treated mice. The spectrum was markedly suppressed by the administration, before LPS injection, of phenyl N-tert-butyl nitrone (PBN), an inhibitor of the expression of induced nitric oxide synthase (iNOS). When 15N-arginine was administered to LPS-treated mice, a diagnostic EPR spectrum was observed, consisting of both three- and two-line EPR signals, due to (MGD)2-Fe(II)-14NO and (MGD)2-Fe(II)-15NO, respectively. The results strongly suggested that the NO detected in these experiments was synthesized by iNOS. In vivo EPR measurements of [(MGD)2-Fe(II)-NO] at several regions in the body (from the head to the tail) indicated that the NO was generated mostly in the upper abdomen near the liver. These observations were confirmed by ex vivo EPR measurements on isolated organs where higher NO levels were detected in vivo in the liver and kidney. The spectroscopic results, combined with the pharmacokinetic data, support the model that NO detected in LPS-treated mice was produced mainly in the liver, and that it did not reflect NO-adduct complex accumulated in the liver via the blood circulation.

Animals↗
PubMed1997

Carcinoma of the gallbladder and anomalous arrangement of the pancreaticobiliary ductal system: cell kinetic studies of gallbladder epithelial cells.

Anomalous arrangement of the pancreaticobiliary ductal system (AAPB), a congenital anomaly defined as a union of the pancreatic and biliary ducts located outside the duodenal wall, is a newly designated disease entity, and is frequently found in adult patients with gallbladder carcinoma (GBX). In the present study, the relationship of AAPB and GBX was investigated. We studied 27 patients with GBX and AAPB, 34 patients with AAPB and without GBX, and as a control group, 56 patients without AAPB (10 with GBX, 24 with cholecystolithiasis, and 22 with normal gallbladder). Tissue sections from cancerous and non-cancerous mucosa of the gallbladder of all of these patients were stained for proliferating cell nuclear antigen (PCNA), Ki-67 nuclear antigen, and bromodeoxyuridine (BrdU). The Ki-67 labeling index (Ki-67-LI), PCNA labeling index (PCNA-LI), and BrdU labeling index (BrdU-LI) of the noncancerous mucosa in the patients with AAPB and/or GBX were significantly higher than those in the patients without GBX and AAPB (P < 0.01). These indices of the noncancerous mucosa in the patients with AAPB and GBX were significantly higher than those in the patients with either AAPB or GBX (P < 0.05). Cell proliferation in the gallbladder epithelia was accelerated in patients with AAPB. Consequently, AAPB appears to be an important risk factor for the occurrence of GBX.

Adult↗