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Biomedical subjects

F Suzuki

Publications and source records attributed to F Suzuki.

At least 379 records · Page 21Linked to original sources
PubMed1989

Trisomy of chromosome 9q: specific chromosome change associated with tumorigenicity during the process of X-ray-induced neoplastic transformation in golden hamster embryo cells.

We have reported that trisomy of chromosome 7 is commonly observed in anchorage-independent clones isolated from X-irradiated golden hamster embryo cells. All 10 clones derived from different irradiated populations showed tumorigenicity when 1 x 10(7) cells were injected s.c. into nude mice (BALB/c, nu/nu). From karyotypic analysis, we found that 8 of 10 cells showed trisomy of chromosome 9. One cell line had a translocation between chromosomes 9q and 19q and trisomy of chromosome 7. The other cell line contained trisomy of chromosome 9 and a translocation between chromosomes 7q and 8q. Using Southern blot analysis, we observed no amplification of v-myc, v-Ha-ras, v-Ki-ras or N-ras-related oncogenes. Furthermore, we could not detect either an increase in expression of v-myc- and v-Ha-ras-related genes or the activation of any oncogene, by the NIH 3T3 transfection assay. Our results suggest that trisomy of chromosome 7 is insufficient for the expression of tumorigenicity and that increased dosage of chromosome 9q may play an important role in the malignant progression of X-ray-induced neoplastic transformation.

Animals↗
PubMed1989

Proteinic prorenin-releasing-stimulator (PRS) in the rat submandibular gland.

The release of prorenin as well as renin from rat renal slices was confirmed by a rat prorenin-prosegment ELISA system and an assay system for determining the renin activity. A significant increase of the prorenin release was found by adding rat submandibular gland extract to the slice medium, indicating the existence of a prorenin-releasing stimulator (PRS) in the extract. The pI and molecular mass of PRS were 8.5-8.7 and 28-30 kDa, respectively. The PRS was completely inactivated by boiling or a proteinase treatment.

Animals↗
PubMed1989

Demonstration of receptors for parathyroid hormone on cultured rabbit costal chondrocytes.

Parathyroid hormone (PTH) receptors on cultured rabbit costal chondrocytes were demonstrated using HPLC-purified, radioiodinated [Nle8,-Nle18, Tyr34] bovine PTH-(1-34)amide. PTH binding was found to be specific for PTH agonists and antagonists and dependent on the time and temperature of incubation. Both growth cartilage (GC) cells and resting cartilage (RC) cells were shown to have a single class of saturable, high affinity PTH binding sites with a dissociation constant of 0.6-0.7 nM. However, the numbers of receptors per cell were approximately 49,000 on GC cells and 19,000 on RC cells. After crosslinking the receptors on these cells with the radioligand, one, major 125I-labeled band of 76 kDa was separated by SDS-PAGE.

Animals↗
PubMed1989

Establishment of a clonal human chondrosarcoma cell line with cartilage phenotypes.

A clonal cell line with cartilage phenotypes and tumorigenicity during more than 3 years in culture was established from a human chondrosarcoma. In sparse cultures, the clonal line, named HCS-2/8, consisted of slightly elongated polygonal cells, which proliferated with a doubling time of 3.5 days. The cells became polygonal to spherical as they became confluent. After reaching confluence, the cells continued to proliferate slowly and formed nodules, which showed metachromasia when stained with toluidine blue. The nodules were three-dimensional in structure; cells were multilayered in the surface regions, overlying a thick layer of extracellular matrix, which showed metachromasia. Electron microscopically, the cells resembling chondrocytes in vivo were surrounded by an extracellular matrix consisting of thin collagen-like fibrils with numerous fine granules, presumably of proteoglycans. The cells actively synthesized proteoglycans as determined by [35S]sulfate incorporation. The hydrodynamic size of major proteoglycan monomers synthesized by the cells was that of so-called cartilage-specific proteoglycans, as determined by glycerol gradient centrifugation. Immunostaining identified type II collagen but not type I collagen. Fluorography and immunoblotting of collagens separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis also demonstrated the synthesis of type II collagen but not type I collagen. Inoculation of HCS-2/8 cells into athymic mice resulted in the formation of chondrosarcomas that resembled the original tumor. Because of having these characters, HCS-2/8 cells should be useful not only in studies on the differentiated phenotypes of human chondrocytes but also in basic studies on the diagnosis, treatment, and etiology of human chondrosarcomas.

Aged↗
PubMed1989

Oxygen radicals in influenza-induced pathogenesis and treatment with pyran polymer-conjugated SOD.

The pathogenicity of influenza virus infection in the mice involves, at least in part, overreaction of the immune responses of the host rather than a direct effect of virus multiplication. Xanthine oxidase, which is responsible for the generation of oxygen free radicals, was elevated in serum and lung tissue of mice infected with influenza virus. To test the theory that oxygen-free radicals are involved in pathogenesis, free radicals were removed by injecting superoxide dismutase (SOD), a specific superoxide radical scavenger, which was conjugated with a pyran copolymer. The conjugate protected mice against a potentially lethal influenza virus infection if administered 5 to 8 days after infection. These findings indicate that oxygen radicals are important in the pathogenesis of influenza virus infection, and that a polymer-conjugated SOD has therapeutic potential for this virus infection and other diseases associated with free radicals.

Animals↗
PubMed1989

Multistep nature of X-ray-induced neoplastic transformation in golden hamster embryo cells: expression of transformed phenotypes and stepwise changes in karyotypes.

We have examined the expression of transformed phenotypes and genetic changes associated with the expression of each transformed phenotype after X-ray irradiation. Unirradiated cells grown at a constant growth rate until 8 passages (population doubling number, 15) exhibited little morphological change and ceased to divide thereafter. X-irradiated cells escaped from senescence and showed morphological alteration and anchorage independence after a population doubling number of 20. The acquisition of tumorigenicity in nude mice was observed much later (35 population doublings after irradiation). From cytogenetic analysis, all anchorage-independent clones were consistently found to have trisomy of chromosome 7. Furthermore, cells derived from tumors contained three copies of chromosome 9q in addition to the trisomy of chromosome 7. We have not detected any augmented expression of v-Ha-ras- and v-myc-related oncogenes with RNA dot-blot analysis and could not find activation of any type of oncogenes by NIH3T3 transfection experiments. Our studies demonstrated that X-ray-induced neoplastic transformation is a multistep phenomenon and that the numerical change of specific chromosomes may play an important role in the expression of each transformed phenotype. The results suggest that different endogenous oncogenes, other than the ras gene family and myc oncogene, could be responsible for the progressive nature of neoplastic transformation.

Animals↗
PubMed1989

Regulation of colony formation of differentiated chondrocytes in soft agar by transforming growth factor-beta.

Fibroblast growth factor (FGF) induces colony formation by chondrocytes in soft agar (Y. Kato et al., J. Cell. Physiol., 1987), and the present study revealed that transforming growth factor-beta(TGF-beta) does not induce the same effect. TGF-beta did, however, increase the efficiency of colony formation by chondrocytes 3- to 4-fold in the presence of a maximal dose of FGF. Furthermore, TGF-beta decreased the concentrations of FGF needed for the induction of cell growth in soft agar by 40- to 100-fold. These results suggest that TGF-beta is involved in the control of cartilage growth possibly by increasing the responsiveness of chondrocytes to FGF.

Animals↗
PubMed1989

Stimulation of cartilage-matrix proteoglycan synthesis by morphologically transformed chondrocytes grown in the presence of fibroblast growth factor and transforming growth factor-beta.

The effects of transforming growth factor-beta (TGF-beta) on the synthesis of cartilage-matrix proteoglycan by cultured rabbit chondrocytes were examined. Rabbit chondrocytes were seeded at low density and exposed to a 1:1 mixture of Dulbecco's modified Eagle's medium and Ham's F-12 medium supplemented with 0.5% fetal bovine serum, 1% bovine serum albumin, 50 micrograms/ml ascorbic acid, and 2 x 10(-7) M hydrocortisone (Medium A). Various combinations of TGF-beta, insulin-like growth factor-I (IGF-I), and fibroblast growth factor (FGF) were also added to Medium A, and the chondrocytes were grown to confluency. Chondrocytes grown with TGF-beta or FGF alone became flat or fibroblastic, those grown with FGF and TGF-beta became very elongated and formed distinct foci, and those grown with FGF and IGF-I showed the spherical configuration characteristic of overtly differentiated chondrocytes. Nevertheless, the incorporation of 3H with glucosamine into the large, chondroitin sulfate proteoglycan synthesized by cultures with FGF and TGF-beta was similar to that in cells grown with FGF and IGF-I and five times that in cells cultured with FGF alone. The increases in incorporation of 3H reflected real increases in proteoglycan synthesis, because chemical analyses showed an increase in the accumulation of macromolecules containing uronic acid in cultures with FGF and TGF-beta or with FGF and IGF-I. However, FGF in combination with either TGF-beta or IGF-I had little effect on the incorporation of 3H into small proteoglycans or hyaluronic acid. These results indicate that chondrocytes morphologically transformed with TGF-beta and FGF fully express the differentiated proteoglycan phenotype rather than the transformed glycosaminoglycan phenotype.

Animals↗
PubMed1989

Changes in the distribution of intramembranous particles and filipin-reactive membrane sterols during in vitro capacitation of golden hamster spermatozoa.

Membrane alterations accompanying in vitro capacitation of hamster spermatozoa were examined using the freeze-fracture technique with or without use of filipin, a sterol-binding probe. In the spermatozoa prior to or at 10 min after start of incubation in capacitating medium, large (about 11 nm) and small (8-9 nm) intramembranous particles (IMPs) were present in the periacrosomal region of the sperm plasma membrane (PAPM). Filipin sterol complexes (FSCs) were densely (about 500/micron 2) distributed in the PAPM prior to incubation. The density of FSCs in the PAPM was reduced by 70-80% of the original density by 2 hr of incubation. At the same time, small patches of IMP-free areas appeared in the plasma membrane above the equatorial and middle segments of the acrosome. By the end of 3 hr of incubation, the majority of small IMPs had disappeared from the PAPM. Remaining large and small IMPs tended to aggregate in the PAPM. During incubation in capacitation medium, "cords," or linear arrangements of closely packed IMPs, appeared near the posterior ring of the sperm head. These observations strongly suggest that the acrosome reaction of the hamster spermatozoa is preceded by the removal (deletion) of filipin-reactive sterols (FRSs) and the disappearance of small IMPs from the lipid bilayer of PAPM.

Acrosome↗
PubMed1989

Stimulation of non-specific resistance to tumors in the mouse using a poly(maleic-acid-styrene)-conjugated neocarzinostatin.

The development of non-specific resistance to tumors following stimulation with poly(maleic-acid-styrene)-conjugated neocarzinostatin (SMANCS), a polymer-conjugated derivative of neocarzinostatin, was investigated in mice. The growth of syngeneic solid tumors (Meth-A fibrosarcoma and RL male 1 leukemia) inoculated into BALB/c mice was suppressed after one treatment with SMANCS at doses ranging from 0.14 mg/kg to 3.4 mg/kg i.v. 24 h before tumor implantation. Since previously observations concerning SMANCS have shown that it disappeared within 1.5 h after i.v. administration in mice and that it was inactivated quickly in plasma, SMANCS evidently inhibited tumor growth by mediating non-specific resistance. In addition, the non-specific resistance to tumors stimulated by SMANCS could be passively transferred to untreated mice by serum which was shown to contain interferon (IFN) from 12 h to 20 h after SMANCS administration. However, the resistance was not produced by serum prepared from mice at 8 h or 32 h after administration presumably because of the observation that the interferon activity was only demonstrated from 12 h to 28 h after SMANCS stimulation. When the serum specimens were treated with anti-IFN-gamma antiserum, the antitumor activity of the sera was abrogated. However, no significant change was detected in the antitumor activity of the specimens following treatment with anti-IFN-alpha/beta antiserum. Treatment of mice with SMANCS and anti-IFN-gamma antiserum together resulted in the elimination of the non-specific resistance to tumors. The IFN induced in the sera of mice by SMANCS was shown to be 57% IFN-gamma and 41% IFN-alpha/beta. Half of the interferon produced in SMANCS-stimulated mice could be eliminated by treatment with anti-IFN-gamma, and treatment of SMANCS-stimulated mice with both anti-IFN-gamma and anti-IFN-alpha/beta antisera resulted in a total absence of detectable interferon. These findings suggest that while the administration of SMANCS induces both IFN-gamma and IFN-alpha/beta production, in this case, it is only the former which mediates the non-specific resistance to tumors.

Animals↗
PubMed1989

Establishment from mouse growth cartilage of clonal cell lines with responsiveness to parathyroid hormone, alkaline phosphatase activity, and ability to produce an endothelial cell growth inhibitor.

Three clonal cell lines with differences in responsiveness to parathyroid hormone (PTH), alkaline phosphatase activity, and ability to produce an endothelial cell growth inhibitor(s) during more than 3 years, more than 58 passages, in culture were established from growth cartilage (GC) of mouse ribs. In sparse cultures the three clonal cell lines, MGC/T1.4, MGC/T1.17, and MGC/T1.18, all showed fibroblast-like morphology. However, as they became confluent, MGC/T1.4 cells became polygonal and then multilayered. MGC/T1.18 cells also became polygonal, but showed contact inhibition. MGC/T1.17 cells remained fibroblastic in confluent cultures and formed nodules when cultured for more than 7 days after they became confluent. These nodules calcified in the presence of beta-glycerophosphate. Glycosaminoglycan (GAG) synthesis in the parent uncloned line, MGC/T1 cells, at early passages was about 50-75% of that of primary cultures of mouse GC cells. The GAG syntheses in the three clonal lines were much lower than that of primary cultures of GC cells. Moreover, the sizes of proteoglycan monomers synthesized by these cells were not the same as that of cartilage-specific proteoglycan. The three clonal lines mainly synthesized type I collagen. PTH increased the intracellular cyclic AMP level in MGC/T1, MGC/T1.4, T1.17, and T1.18 cells: their maximal levels, observed after 2 minutes, were, respectively, about 160, 150, 70, and 200 times that of controls. The activity of alkaline phosphatase in MGC/T1.17 cells was higher than that in primary cultures of mouse GC cells, whereas those in MGC/T1 and T1.4 cells were comparable with that of GC cells, and that in MGC/T1.18 was lower. The three clonal lines, and especially MGC/T1.4, secreted a heat-stable, nondializable growth inhibitor(s) of endothelial cells into the culture medium. Because of their different properties, these cell lines should be useful for studies on endochondral ossification, the actions of PTH on skeletal cells, and anti-angiogenesis factors.

Alkaline Phosphatase↗
PubMed1989

Intracranial glossopharyngeal neurinomas. Report of two cases with special emphasis on computed tomography and magnetic resonance imaging findings.

Two patients with intracranial glossopharyngeal neurinoma are described. In both patients, neurologic signs and findings of conventional radiologic and computed tomography examinations suggested a diagnosis of acoustic neurinoma. Magnetic resonance imaging, however, definitely indicated that the mass had actually arisen from the lower cranial nerves. This was confirmed at operation. The superb sensitivity and specificity of magnetic resonance imaging in the diagnosis of posterior fossa extraaxial mass are emphasized.

Cranial Nerve Neoplasms↗
PubMed1989

Adenoma and stone formation of the biliary tract in puppies that had choledochopancreatic anastomosis.

A canine model of anomalous choledochopancreatic ductal junction (APCDJ) was produced by choledochopancreatic end to side ductal anastomosis performed in 77 mongrel puppies weighing between 1.5 and 5 kg. Histopathological studies of the biliary tract showed that as the post-operative period became lengthened metaplasia and hyperplasia increased. In nine dogs that lived for over 5 years after the operation, papillomatous adenoma occurred in four (44%), and biliary stones in seven (78%). The histological changes seen in the biliary epithelium of our experimental canine model suggest that bile duct carcinoma may be due to the persistent return of pancreatic juice into the bile duct in patients with APCDJ.

Anastomosis, Surgical↗
PubMed1989

Electrophysiological demonstration of anterograde concealed conduction in accessory atrioventricular pathways capable only of retrograde conduction.

Anterograde concealed conduction into the concealed accessory atrioventricular (AV) pathway has been postulated to be one of the factors preventing the reciprocating process via the accessory pathway in patients with the concealed Wolff-Parkinson-White(WPW) syndrome but its presence has not been documented. To demonstrate the occurrence of anterograde concealment, 12 patients with the concealed WPW syndrome were selected for study. A pacing protocol was designed in which the retrograde conduction of the ventricular extrastimulus over the accessory pathway was assessed during ventricular pacing alone (conventional method) and during the AV simultaneous pacing (simultaneous method); the results were then compared. When the high right atrium was simultaneously paced, the effective refractory period of the concealed accessory pathway shortened as compared with the conventional method in five of 12 patients (from 341.7 +/- 110.8 to 312.5 +/- 108.2 msec, n = 12), whereas, it decreased in all patients studied when the coronary sinus near the accessory pathway was simultaneously paced (from 375.7 +/- 135.0 to 287.1 +/- 116.1 msec, n = 7). These results demonstrate that the AV simultaneous pacing frequently shortens the refractoriness of the concealed accessory AV pathway and such facilitation seems to be well explained by the probable anterograde concealment in it and peeling back of the refractory barrier.

Atrioventricular Node↗
PubMed1989

Antiviral activity of carboxyethylgermanium sesquioxide (Ge-132) in mice infected with influenza virus.

The protective effect of carboxyethylgermanium sesquioxide (Ge-132) in mice infected with a mouse-adapted strain of influenza virus (H2N2) was investigated. When mice were exposed to a 10 LD50 dose of influenza virus via aerosol and were treated orally with 20 or 100 mg/kg of Ge-132 daily for 6 consecutive days, a significant protective effect was demonstrated. The antiviral effect of Ge-132 was indicated by an increase of survivors, a prolongation of mean survival days, an inhibition of the development of lung consolidation, and a decrease of virus titer in lung tissues, as compared to infected control mice treated with phosphate-buffered saline. Natural killer (NK) cell activity in the spleens and lungs of the infected mice was also significantly augmented after the oral administration of Ge-132. In addition, NK cells stimulated with Ge-132 in vivo showed killing activity against NK-insensitive Meth-A cells infected with influenza virus. Because no virucidal or virustatic activities of Ge-132 on the virus were found in vitro, this protective effect in mice against influenza virus infection may be displayed through immunomodulating activities of this compound such as the augmentation of NK cell activity.

Animals↗