Search PubMed⌕ Search

Biomedical subjects

N Terada

Publications and source records attributed to N Terada.

At least 73 records · Page 4Linked to original sources
PubMed2000

Expression of keratan sulfate at the arthroplasty surface after cup arthroplasty.

Fibrous tissue which regenerated on the acetabular arthroplasty surface was obtained from a 52-year-old woman who underwent total hip replacement after cup arthroplasty. The histological features of this newly formed fibrous tissue and expression of keratan sulfate, which is a characteristic matrix component of articular cartilage, were studied. Microscopic observation revealed that the arthroplasty surface consisted mainly of fibrous tissue which did not show metachromasia with toluidine blue staining, but there were many nodular structures communicating with the bone marrow. Immunostaining for keratan sulfate revealed clear positive staining around the cells of the nodular structures communicating with the bone marrow, while only weakly positive staining was observed in the superficial layer of the loose fibrous tissue. The present study revealed marked formation of articular cartilaginous tissue in areas having good communication with the bone marrow, which indicates that maintenance of this communication may be necessary to improve the outcome of cup arthroplasty.

Arthroplasty, Replacement, Hip↗
PubMed2000

Hyaluronan in synovial fluid of patients with loose total hip prosthesis. Comparison with hyaluronan in patients with hip osteoarthritis and idiopathic osteonecrosis of femoral head.

The concentration and molecular weight of hyaluronan (HA) in the synovial fluid of the hip joint were determined in 13 patients (aged 62.8 +/- 9.4 years) who had undergone prior total hip arthroplasty(THA), 23 patients (aged 65.0 +/- 8.2 years) with osteoarthritis of the hip joint (OA), and 13 patients (aged 40.2 +/- 2.7 years) with idiopathic osteonecrosis of the femoral head (ION). A sample of synovial fluid was obtained during revision THA because of loosening of the total hip prosthesis for the THA group, and during the first replacement surgery or osteotomy for the OA and ION groups. The concentration of HA in the synovial fluid was 0.64 +/- 0.42 mg/ml in the THA group, 1.07 +/- 0.28 mg/ml in the OA group, and 1.30 +/- 0.56 mg/ml in the ION group. The concentration of HA in the synovial fluid of the THA patients was significantly lower than that of the OA and ION patients (P = 0.0156 vs OA, P = 0.003 vs ION). The molecular weight of HA was 309 +/- 88.3 x 10(4) Da in the THA group, 377 +/- 201 x 10(4) Da in the OA group, and 240 +/- 148 x 10(4) Da in the ION group; these values do not differ significantly (P = 0.259 vs OA, P = 0.174 vs ION). Among the THA patients, there was no relation between the concentration of HA and the age of the patient, length of time since the first operation, or type of prosthesis fixation; there was also no relation between the molecular weight of HA and each of these factors. These results suggest that a pseudosynovial membrane is regenerated after THA, and that it produces HA of the same molecular weight as that in patients with OA and ION, although in smaller quantities.

Adult↗
PubMed2000

Gallbladder agenesis with no other biliary tract abnormality: report of a case and review of the literature.

We report a rare adult case of gallbladder agenesis with no other biliary tract abnormality. The patient was a 29-year-old man with pain in the right upper-quadrant of the abdomen, and vomiting. The gallbladder was not visualized by ultrasonography, computed tomography, or endoscopic retrograde cholangiography. The common bile duct was slightly dilated. No other abnormalities, including anomalous choledochopancreatic duct junction, were found. Based on these imaging findings and the patient's right hypochondrial pain, there was a high index of suspicion of chronic cholecystitis caused by incarcerated gallstones in the neck of the gallbladder. At operation, we carefully observed the gallbladder fossa, using laparoscopy, and found gallbladder to be absent. Although the operation involved only observation via a laparoscope, the patient has since remained well and asymptomatic. It is difficult to make a correct diagnosis of gallbladder agenesis preoperatively. We believe that, if the gallbladder is not visualized by imaging techniques, it may be better to perform laparoscopy for observation before performing laparotomy, in order to reduce surgical stress.

Adult↗
PubMed2000

Acute appendicitis caused by amebiasis.

We report a case of appendicitis caused by amebiasis in a 45-year-old Japanese man. He presented to our hospital with bloody stools in June 1998. Sigmoidoscopy disclosed erosion, and a biopsy of the erosion showed colitis caused by Entamoeba histolytica infection. Four months later, he was admitted to our hospital with a small elastic mass and severe pain in the lower quadrant of the abdomen, which was diagnosed as acute appendicitis. He underwent appendectomy. Histopathological examination revealed numerous E. histolytica trophozoites, and we diagnosed acute appendicitis caused by E. histolytica. The patient has been free of symptoms, colonoscopy has revealed no erosion, and biopsy has revealed no E. histolytica for 12 months after the operation.

Appendicitis↗
PubMed2000

Histological study of articular cartilage in experimental rat knee arthritis induced by intracapsular injection of cationic polyethyleneimine.

Degeneration of proteoglycans and abnormalities in their metabolism have been assumed to be critical at an early stage of osteoarthritis. To clarify a trigger mechanism of osteoarthritis, anionic sites of knee articular cartilage were blocked by intracapsular injection of cationic polyethyleneimine of 2000 or 70,000 molecular weight (MW) into rat knee joints. Experimental or normal rats were examined by gross observation, roentgenography, cytokine interleukin-1beta (IL-1beta) assay, and light or electron microscopy. In both groups with the polyethyleneimine injection, the rats showed temporarily limping and swelling of their knee joints. By light or electron microscopic studies, knee articular cartilage was found to be degenerated at an early stage, but IL-1beta was within normal levels. At 2, 4, or 6 months, the deformity of the knee joints was obvious by roentgenography. Degeneration and hypofunction of proteoglycans might be related to the ultrastructural changes of articular cartilage at an early stage, though the inflammatory cytokine was not involved. At later stages the pathophysiology of the knee joints advanced chronically to typical osteoarthritis, which was more radically induced by the large molecular polyethyleneimine (70,000 MW). The functional impairment of anionic sites is a key point for elucidating the mechanism of osteoarthritic development in this animal model.

Animals↗
PubMed2000

Chronic treatment with FK506 increases p70 S6 kinase activity associated with reduced nitric oxide synthase activity in rabbit hearts.

FK506, an immunosuppressant, modulates phosphorylation of nitric oxide (NO) synthase, and induces cardiac hypertrophy in clinical settings. Having recently reported that chronic treatment with an inhibitor of NO synthase induces cardiac hypertrophy associated with the activation of 70-kD S6 kinase (p70S6K), which plays an important role in cardiac hypertrophy by regulating protein synthesis, we investigated the effects of chronic administration of FK506 on NO synthase and p70S6K activities in hearts. Twenty rabbits were divided into four groups: untreated rabbits, those treated with low-dose FK506 (0.10 mg/kg), those treated with medium-dose FK506 (0.20 mg/kg), and those treated with high-dose FK506 (0.40 mg/kg). FK506 was administered intravenously twice a day. After 4 weeks of treatment with FK506, calcium-dependent NO synthase activity in myocardium in the high-dose FK506 group was lower (P < 0.05) than in the untreated group. p70S6K activity in myocardium in the high-dose group was higher (P < 0.05) than in the untreated group. There was a significant (P < 0.05) inverse correlation between NO synthase and p70S6K activities in myocardium. However, the endothelial-dependent vasodilation of aortic rings or plasma levels of NO metabolites during experimental protocols did not differ among the groups studied. These findings suggest that chronic treatment of FK506 activates p70S6K and reduces NO synthase activity in rabbit hearts. Reduced NO synthase and/or activated p70S6K activities in hearts might contribute to the cardiac hypertrophy observed in some patients receiving FK506.

Acetylcholine↗
PubMed2000

Inhibition of nitric oxide synthesis induces coronary vascular remodeling and cardiac hypertrophy associated with the activation of p70 S6 kinase in rats.

Chronic inhibition of nitric oxide (NO) synthesis is reported to induce the thickening of coronary artery walls and cardiac hypertrophy in vivo via angiotensin II receptors. Increased protein synthesis is the main feature of these structural changes. Activation of 70 kD S6 kinase (p70S6K) phosphorylates the 40S ribosomal protein S6 that regulates protein synthesis. We examined the role of p70S6K in the vascular and myocardial structural changes induced by the chronic inhibition of NO synthesis. The following 5 groups were studied: untreated Wister-Kyoto rats, those treated with an inhibitor of NO synthase, Nomega-nitro-L-arginine methyl ester (L-NAME), those treated with L-NAME and an angiotensin I converting enzyme inhibitor (imidapril), those treated with L-NAME and hydralazine, and those treated with L-NAME and an inhibitor of p70S6K (rapamycin). After 8 weeks, wall-to-lumen ratio in myocardium and cardiomyocyte cross-sectional areas were quantified. L-NAME increased systolic blood pressure, wall-to-lumen ratio, and cardiomyocyte cross-sectional area compared with control animals. Imidapril or rapamycin, but not hydralazine, markedly reduced these structural changes. L-NAME increased p70S6K activity in myocardium compared with control rats. Imidapril or rapamycin prevented the activation of p70S6K activity in myocardium induced by L-NAME. These results suggest that activation of p70S6K plays an important role in coronary vascular remodeling and cardiac hypertrophy induced by the chronic inhibition of nitric oxide synthesis in vivo.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Significant association of the tumor necrosis factor receptor 2 (TNFR2) gene with human narcolepsy.

We report on the association study of the tumor necrosis factor receptor 2 (TNFR2) gene with human narcolepsy. A single-nucleotide polymorphism in TNFR2, which is involved in an amino acid substitution [methionine(M)/arginine(R)] at position 196, was investigated in 149 Japanese narcoleptic patients and 204 healthy individuals as controls. Results reveal that the frequency of the TNFR2-196R allele significantly increased in the patients as compared with that in the controls (P=0.029), suggesting that TNFR2 is likely associated with the susceptibility to narcolepsy. In addition, the analyses of the relationship of TNFR2 and TNF-alpha with the susceptibility to narcolepsy indicate the possibility that an additive effect on the susceptibility to the disorder lies between TNFR2-196R and TNF-alpha(-857T) alleles.

Amino Acid Substitution↗
PubMed2000

Interleukin-13 and tumour necrosis factor-alpha synergistically induce eotaxin production in human nasal fibroblasts.

BACKGROUND: There is increasing evidence that eotaxin is a key mediator in the development of tissue eosinophilia. However, the mechanism involved in the production of eotaxin has yet to be clarified. Most recently, it has been shown that interleukin (IL) -4 induces eotaxin in dermal fibroblasts. A novel cytokine termed IL-13, which binds to the alpha-chain of the IL-4 receptor, shares many biological activities with IL-4. It is known that fibroblasts express the IL-4 receptor and produce collagen type I upon stimulation with IL-4. OBJECTIVE: We investigated whether IL-13, as well as IL-4, are able to induce eotaxin production in human nasal mucosal fibroblasts (HNMFs). Furthermore, we investigated the effect of costimulation of IL-13 and TNFalpha on eotaxin production. METHODS: HNMFs, isolated from inferior nasal mucosa samples, were stimulated by various kind of cytokines for 1-36 h at 37 degrees C in 5% CO2. The change in the expression of eotaxin mRNA was then evaluated by reverse transcriptase-polymerase chain reaction and the Southern blot analysis. The amount of eotaxin in the culture media was measured by ELISA. RESULTS: IL-13 as well as IL-4 dose-dependently induced eotaxin expression in HNMFs. Furthermore, IL-13 and TNFalpha synergistically induced eotaxin expression in HNMFs, while they hardly induced eotaxin expression in endothelial cells, epithelial cells or eosinophils. The synergy was observed when pre-incubation of HNMFs with IL-13 was followed by a stimulation with TNFalpha, or HNMFs were simultaneously stimulated with IL-13 and TNFalpha. CONCLUSION: These results strongly indicate that IL-13, as well as IL-4, may be important in eotaxin-mediated eosinophilic inflammation in nasal mucosa. In addition, in nasal mucosa, fibroblasts are the major cell source for eotaxin.

Adult↗
PubMed2000

Transepithelial migration of activated eosinophils induces a decrease of E-cadherin expression in cultured human nasal epithelial cells.

BACKGROUND: The damage of respiratory epithelium in allergic diseases has a close correlation with the extent of eosinophil infiltration. It seems to be a good possibility that eosinophil infiltration could induce the changes in the expression of the epithelial cell adhesion molecules, which play a key role in the maintenance of structural and functional rigidity of epithelium. OBJECTIVE: We observed the expression of E-cadherin in cultured human nasal epithelial cells (HNECs) to study whether could it be affected by transepithelial migration of inflammatory cells, especially eosinophils. METHODS: In vitro study of the transmigration assay was designed using various types of inflammatory cells and HNEC monolayers. Various assays of each experimental group were done under the stimulation of interleukin-5 (IL-5) and/or platelet activating factor (PAF). Subsequently immunohistochemistry for E-cadherin was performed in the HNECs. The intensity of immunofluorescence of E-cadherin was quantified using confocal laser scanning microscopy (CLSM) system and compared before and after the transmigration. RESULTS: The mean intensity of immunofluorescence for E-cadherin decreased significantly after the transmigration of any types of inflammatory cells. Above all, the migration of eosinophils treated with IL-5 and PAF had an eminent effect on the decrease, whereas the degranulation extracts derived from eosinophils activated by IL-5 and secretory IgA (sIgA) did not affect the intensity. CONCLUSION: This work suggests that transepithelial migration of inflammatory cells can directly induce the decrease in epithelial E-cadherin expression. Furthermore, the most prominent change was induced by transmigration of activated eosinophils, which might be caused by some mechanisms independent of the eosinophil contents. The decrease in E-cadherin expression may trigger the damage of epithelial barrier, which contributes to the pathogenesis of allergic diseases.

Adolescent↗
PubMed2000

Molecular analysis of zebrafish photolyase/cryptochrome family: two types of cryptochromes present in zebrafish.

BACKGROUND: Cryptochromes (CRY), members of the DNA photolyase/cryptochrome protein family, regulate the circadian clock in animals and plants. Two types of animal CRYs are known, mammalian CRY and Drosophila CRY. Both CRYs participate in the regulation of circadian rhythm, but they have different light dependencies for their reactions and have different effects on the negative feedback loop which generates a circadian oscillation of gene expression. Mammalian CRYs act as a potent inhibitor of transcriptional activator whose reactions do not depend on light, but Drosophila CRY functions as a light-dependent suppressor of transcriptional inhibitor. RESULTS: We cloned seven zebrafish genes that carry members of the DNA photolyase/cryptochrome protein family; one (6-4)photolyase and six cry genes. A sequence analysis and determination of their in vitro functions showed that these zebrafish cry genes constitute two groups. One has a high sequence similarity to mammalian cry genes and inhibits CLOCK:BMAL1 mediated transcription. The other, which has a higher sequence similarity to the Drosophila cry gene rather than the mammalian cry genes, does not carry transcription inhibitor activity. The expressions of these cry genes oscillate in a circadian manner, but their patterns differ. CONCLUSIONS: These findings suggest that functionally diverse cry genes are present in zebrafish and each gene has different role in the molecular clock.

ARNTL Transcription Factors↗
PubMed2000

Effects of transforming growth factor beta-1 and all-trans-retinoic acid on androgen-induced development of neonatal mouse bulbourethral glands in vitro.

Effects of transforming growth factor beta-1 (TGF-beta1) and all-trans-retinoic acid (All-trans-RA) on development of bulbourethral glands (BUGs) of neonatal mice were investigated in vitro. BUGs from 0-day-old male mice were cultured for 6 days in serum-free, chemically defined medium containing transferrin and bovine serum albumin, supplemented with 5alpha-dihydrotestosterone (DHT; 10-8 M) and insulin (10 microg/mL) alone or in combination. Prior to culture, BUGs from 0-day-old mice consisted of a simple epithelial rudiment encapsulated by mesenchyme. Epithelial growth and ductal branching occurred in BUGs cultured in medium containing DHT and insulin or DHT alone, but epithelial branching did not occur in BUGs cultured in the presence of insulin alone. Addition of TGF-beta1 at concentrations of > 5 ng/mL (0.2 x 10-9 M) to medium containing both insulin and DHT, inhibited the expected increase in overall size of BUGs, epithelial area and ductal branching in a dose-dependent manner. TGF-beta1 also decreased [3H]-thymidine labelling indices of both epithelium and mesenchyme. TGF-beta1 at 10 ng/mL elicited these inhibitory effects on BUGs cultured in medium containing DHT alone. Addition of All-trans-RA (10-8 to 10-6 M) to the medium containing DHT plus insulin, or DHT alone did not exert significant effects on either overall size of BUGs or epithelial growth and ductal branching. All-trans-RA at 10-6 M decreased the [3H]-thymidine labelling index of mesenchyme of BUGs cultured in medium with DHT plus insulin or DHT alone, but did not decrease the [3H]-thymidine labelling index of epithelium. The present results indicate that TGF-beta1 inhibits androgen-induced epithelial and mesenchymal growth as well as epithelial morphogenesis of BUGs from neonatal mice. Such an inhibitory effect of TGF-beta1 is not mimicked by All-trans-RA at physiological concentrations.

Animals↗
PubMed2000

Primary hepatic leiomyosarcoma in a patient with hepatitis C virus-related liver cirrhosis.

We describe an autopsy case of primary hepatic leiomyosarcoma in a 68-year-old man with hepatitis C virus-related liver cirrhosis. The patient, who had a history of acute hepatitis 20 years previously, died of a ruptured hepatic tumor. At autopsy, a well-circumscribed 14 x 16 x 15 cm tumor replaced the medial site of the right hepatic lobe with multiple intrahepatic and distant metastases. Histologically the tumor, which had extensive central necrosis, consisted predominantly of well or moderately differentiated spindle-shaped cells, which were positive for smooth muscle actin and vimentin on immunohistochemical staining. In addition, clusters of markedly atypical cells and myxoid change of the matrix were discretely found in the focal and small areas of the tumor. These findings indicated that many sections were necessary for the histologically accurate estimation of primary hepatic smooth muscle tumor. The histological examination of a non-tumorous lesion showed liver cirrhosis. Hepatitis C virus was detected in the cytoplasm of cirrhotic hepatocytes by immunohistochemistry and reverse transcriptase-polymerase chain reaction, but not in the tumor cells. This suggested that the virus was not directly involved in the development of primary hepatic leiomyosarcoma.

Actins↗
PubMed2000

Dynamic ultrastructure of mouse pulmonary alveoli revealed by an in vivo cryotechnique in combination with freeze-substitution.

A morphological approach to cell dynamics is usually difficult, since routine preparative techniques for electron microscopy always induce artifacts due to cessation of the blood supply into organs. An in vivo cryotechnique followed by the freeze-substitution method probably reduces such problems. It was applied for examining the pulmonary alveoli of BALB/c mice in vivo. The following ultrastructural features were revealed. (1) A surfactant layer provided a continuous covering to the alveolar epithelium. (2) Pleural epithelial cells, alveolar cells and endothelial cells contained many small vesicles and pits. In the alveolar epithelium, they were often localised near microtubules. (3) Typical lamellar structures in large alveolar epithelial cells were rarely detected. (4) Circulating erythrocytes with various shapes were observed in branching blood capillaries. (5) A close association between erythrocytes and the endothelium was seen at the peripheral alveolar septum. Such ultrastructural arrangements may be appropriate for the physiological functions of the pulmonary alveoli, such as exchanges of gases or materials in vivo.

Animals↗
PubMed2000

Inhibition by an angiogenesis inhibitor, TNP-470, of the growth of a human hepatoblastoma heterotransplanted into nude mice.

BACKGROUND/PURPOSE: The effect of TNP-470, an angiogenesis inhibitor, on the growth of a hepatoblastoma transplanted into nude mice was examined. METHODS: A hepatoblastoma obtained from a 3-year-old girl was serially transplanted into nude mice subcutaneously, and the transplant tumors of the seventh and eighth generations were used for experiments. Expression of various markers in the tumors was examined immunohistochemically. TNP-470 was injected subcutaneously every other day into tumor-bearing mice from 3 weeks after tumor transplantation. The proliferation of tumor cells and endothelial cells was estimated by means of the bromodeoxyuridine labeling index. RESULTS: The original hepatoblastoma showed the histology of the epithelial type, consisting of both the fetal and embryonal subtypes and was positively stained with anti-alpha-fetoprotein (AFP), anti-cytokeratin-19 and polyclonal anticarcinoembryonic antigen antibodies, and an antihuman hepatocyte antibody (hepatocyte paraffin 1). The transplant tumors consisted of solid nests of tumor cells with numerous vascular lakes of various sizes, and showed positive staining with all antibodies that reacted positively with the original hepatoblastoma. Injections of TNP-470 at the doses of 15 mg and 30 mg/kg body weight suppressed the tumor growth and the increase in the serum level of AFP dose dependently. Injections of TNP-470 also suppressed the proliferation of tumor cells and endothelial cells in the tumors. CONCLUSIONS: Hepatoblastomas maintained in nude mice retained the immunohistochemical characteristics of the original hepatoblastoma, and TNP-470 suppressed the growth of hepatoblastomas transplanted into nude mice. TNP-470 may be worth investigating further as to its usefulness as a therapy for hepatoblastomas.

Angiogenesis Inhibitors↗
PubMed2000

CD40 and adenosine A2 receptor agonist-cyclic adenosine monophosphate rescue B-cell antigen receptor-induced apoptosis through independent pathways and converge to prevent caspase activation.

BACKGROUND: Antigen receptor ligation induces apoptosis of B lymphocytes, but the molecular mechanisms underlying induction of apoptosis remain unclear, although the growing family of IL-1beta-converting enzyme cysteine proteases (caspases) are recognized to be major effectors of cellular death. OBJECTIVE: We sought to delineate and compare the rescue of B-cell apoptosis through CD40 ligand-CD40 interaction and cyclic adenosine monophosphate (cAMP)-dependent protein kinase A in human B cells. METHODS: By using tonsillar B cells and the B-lymphoblastoid cell line Ramos, rescue from B-cell apoptosis was compared, as were signaling pathways after activation of cells through CD40 and the adenosine A2 receptor. RESULTS: Both CD40 ligand-CD40 interaction and activation of intracellular cAMP rescue B cells from apoptosis after antigen receptor ligation. Although these pathways do not overlap, they converge by preventing the anti-IgM-induced activation of CPP32 (caspase 3), a member of the IL-1beta-converting enzyme protease family. CONCLUSION: These data indicate that the cAMP-protein kinase A-dependent and CD40-signaling pathways regulate B-cell survival and converge at a common point, the inhibition of antigen receptor-induced activation of caspases.

Antibodies↗