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Biomedical subjects

F Suzuki

Publications and source records attributed to F Suzuki.

At least 433 records · Page 24Linked to original sources
PubMed1987

Effects of various tumor promoters on expression of cartilage phenotypes in rabbit costal chondrocytes in culture.

12-O-Tetradecanoylphorbol-13-acetate (TPA), a skin tumor-promoting phorbol ester, and teleocidin and aplysiatoxin, which are potent tumor promoters in mouse skin but are chemically unrelated to phorbol esters, induced change of cultured rabbit costal chondrocytes from a polygonal to a fibroblastic shape and inhibited glycosaminoglycan (GAG) synthesis and metachromatic matrix formation in these cells. The potencies of teleocidin and aplysiatoxin to inhibit GAG synthesis were almost the same as that of TPA. On the other hand, Tween 60 and cantharidin, weak mouse skin tumor promoters, phenobarbital, a liver tumor promoter, and saccharin, a bladder tumor promoter, had no effect on the morphology or GAG synthesis of cultured chondrocytes. Like TPA, teleocidin and aplysiatoxin increased DNA and RNA syntheses of chondrocytes. Parathyroid hormone (PTH) and dibutyryl cyclic AMP reversed the morphological and histochemical changes caused by a 4-day treatment with teleocidin or aplysiatoxin as well as with TPA, reversal being apparent after 2 days. PTH increased intracellular cyclic AMP after 2 min in chondrocytes pretreated with teleocidin or aplysiatoxin as well as with TPA. PTH also increased ornithine decarboxylase [ODC; EC 4.1.1.17] activity in these chondrocytes after 4 h. These results show that retention of responsiveness to PTH is a typical characteristic of chondrocytes dedifferentiated by treatment with TPA-type tumor promoters such as TPA, teleocidin and aplysiatoxin. The results also suggest that ODC induction mediated by elevation of cyclic AMP plays an important role in re-differentiation of teleocidin- and aplysiatoxin-treated chondrocytes.

Animals↗
PubMed1987

Efficient cleavage by alpha-thrombin of a recombinant fused protein which contains insulin-like growth factor I.

The gene for insulin-like growth factor I (IGF-I) was constructed from chemically synthesized deoxyoligonucleotides and expressed in Escherichia coli, under the control of a trp promoter, as a set of fusion proteins which were connected with a portion of human growth hormone through the recognition sequence for a sequence-specific protease, either blood coagulation factor Xa or alpha-thrombin. Upon induction with 3-indoleacrylic acid, fusion proteins accumulated with a yield of 10-30% of the total protein. A fusion protein connected through a tetradecapeptide (Asp-Asp-Pro-Pro-Thr-Val-Glu-Leu-Gln-Gly-Leu-Val-Pro-Arg) was efficiently and correctly cleaved by alpha-thrombin, and the purified IGF-I possessed somatomedin-like activity, as determined by the enhancement of sulfation of glycosaminoglycans in cultured costal chondrocytes from rabbits.

Biological Assay↗
PubMed1987

Suppressor cells generated in mice late after thermal injury.

A second suppressive state (S-SupS) in interferon (IFN) response was demonstrated when mice with third-degree burns of approximately 30% of the body surface area (TI-mice) were stimulated in vivo by Staphylococcal enterotoxin A, a gamma IFN inducer. The first suppressive state in IFN production, appearing 3 to 7 days after thermal injury, was mediated by the generation of splenic suppressor macrophages. The S-SupS was demonstrated approximately 3 weeks post thermal injury. It persisted for almost 3 weeks and gradually disappeared by 7 weeks. Spleen cells from mice during the S-SupS produced less IFN in vitro than normal mouse splenic mononuclear cells (MNC) when stimulated with concanavalin A (Con A). Splenic MNC of mice during the S-SupS inhibited IFN production when they were co-cultured with normal mouse splenic MNC in the presence of Con A. Since this suppressor cell activity could not be removed from TI-mice splenic MNC by carbonyl iron treatment, or by a technique of adherence to a plastic surface, it is suggested that two different cell populations which are capable of suppressing the IFN response of TI-mice exist at different time periods following burn injury.

Animals↗
PubMed1987

Clinicopathologic and experimental studies on cases of abnormal pancreatico-choledocho-ductal junction.

An abnormal pancreatico-choledocho-ductal junction, in which free communication between the pancreatic duct and the common bile duct was present, was observed in 17 out of 120 cases (14.2%) of biliary tract carcinoma and in all of four cases of congenital biliary dilatation, but in noe of about 200 control patients without biliary tract disease. Outstanding findings in the pancreas, such as degeneration of the ductal epithelium and interlobular fibrosis, were found in 6 of 21 cases of abnormal junction. In an experimental study using 63 puppies given choledocho-pancreatic end-to-side ductal anastomosis, dilatation of the bile duct of varying degree occurred and mucosal hyperplasia of the biliary tract was observed in 12 of 25 anastomosed dogs for a duration of more than one month. Cell kinetics in biliary tract mucosa observed by the use of monoclonal antibody against bromodeoxyuridine (BrdU) was obviously elevated in dogs subject to long-term follow-up. As for pancreatic lesions, the incidence and histologic findings were similar to those of human studies, as follows: chronic pancreatitis in only a few animals, mild periductal parenchymatous change in 15 puppies and no significant change in 44 puppies. Therefore, an abnormal pancreatico-choledocho-ductal junction may be one of the significant factors producing biliary dilatation, biliary tract carcinoma and pancreatitis.

Animals↗
PubMed1987

S-100 protein in clonal astroglioma cells is released by adrenocorticotropic hormone and corticotropin-like intermediate-lobe peptide.

S-100 protein in clonal GA-1 and C6 rat glioma cell lines was released in serum-free medium supplemented with adrenocorticotropic hormone (ACTH). The induction of S-100 protein release by ACTH was dose-dependent, showing a half-maximal release at about 5 microM, and the S-100 protein concentration in the medium increased sharply within 3 min, but slightly during further incubation. The S-100 protein release was apparently accompanied by a decrease in the membrane-bound form of S-100 protein in the cell. The S-100 protein release was induced not by the ACTH1-24 fragment, which exhibits the known effects of ACTH, but by the ACTH18-39 fragment, which is designated as corticotropin-like intermediate-lobe peptide (CLIP). These results indicate that the C-terminal half of ACTH is responsible for the S-100 protein release. The enhancement of S-100 protein release by ACTH was also observed in normal rat glioblasts. The release induced by ACTH was apparently specific to S-100 protein, because little release of the cytoplasmic enzymes, creatine kinase, and enolase was observed under the same conditions. High concentrations (5 mM) of dibutyryl cyclic AMP or dibutyryl cyclic GMP were also found to induce S-100 protein release; however, catecholamines (epinephrine, norepinephrine, isoproterenol, and dopamine), acetylcholine, and glutamic acid did not enhance the release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

The effect of parathyroid hormone (1-34) on cyclic AMP level, ornithine decarboxylase activity, and glycosaminoglycan synthesis of chondrocytes from mandibular condylar cartilage, nasal septal cartilage, and spheno-occipital synchondrosis in culture.

Previously, we reported methods for isolating chondrocytes from the craniofacial complex and their culture in vitro. The response of these chondrocyte cultures to bovine parathyroid hormone (1-34) (PTH) has now been investigated. PTH stimulated glycosaminoglycan (GAG) synthesis, a characteristic of the cartilage phenotype in cultured chondrocytes isolated from mandibular condylar cartilage (MCC), nasal septal cartilage (NSC), and spheno-occipital synchondrosis (SOS). These stimulations of GAG synthesis by PTH were dose-dependent. PTH also increased accumulation of cyclic AMP (cAMP) and the activity of ornithine decarboxylase (ODC), a rate-limiting enzyme in polyamine biosynthesis. However, PTH did not stimulate DNA synthesis. The increases in the cAMP level, ODC activity, and GAG synthesis after addition of PTH (10(-7) mol/L) were greatest in MCC-chondrocytes and least in NSC-chondrocytes. The difference in the responses to PTH of these three types of chondrocytes may reflect differences of the characteristics of these cells in vivo.

Animals↗
PubMed1987

A factor in conditioned medium of rabbit costal chondrocytes inhibits the proliferation of cultured endothelial cells and angiogenesis induced by B16 melanoma: its relation with cartilage-derived anti-tumor factor (CATF).

Serum-free medium conditioned by exposure to rabbit costal chondrocytes in culture inhibited the proliferation and DNA synthesis of bovine pulmonary endothelial cells in culture. The factor in conditioned medium did not inhibit DNA synthesis in B16 melanoma cells, L1210 cells or 3T3 fibroblasts in culture, but it inhibited angiogenesis in the chorioallantoic membrane of chick embryos induced by B16 melanoma and growth of the tumor transplanted onto the membrane. These findings strongly suggest that rabbit costal chondrocytes produce an anti-angiogenesis factor that is similar to cartilage-derived anti-tumor factor (CATF).

Angiogenesis Inhibitors↗
PubMed1987

Chondrocytes dedifferentiated by serial monolayer culture form cartilage nodules in nude mice.

Chondrocytes isolated from rabbit costal growth cartilage grew rapidly and expressed the differentiated phenotypes of chondrocytes in primary monolayer cultures. They had a typical polygonal shape, synthesized glycosaminoglycan (GAG) actively and responded to parathyroid hormone (PTH). However, during successive passages they lost the abilities to proliferate and express differentiated phenotypes. They changed from polygonal to fibroblast-like morphology during the third to fourth passage. Their GAG synthesis rapidly decreased in the 4th passage to 10% of that during primary culture. The increase in GAG synthesis and intracellular cyclic AMP induced by PTH also became smaller and were lost in the 4th passage. From these findings, cells in the 4th passage appeared to be dedifferentiated. However, subcutaneous transplantation of cells at the 5th passage into nude mice resulted in the formation of cartilaginous nodules. Moreover, cells isolated from these nodules and cultured in vitro had a typical polygonal shape and synthesized GAG actively and PTH increased their metachromatic matrix and intracellular cyclic AMP level. These findings suggest that chondrocytes that appear to be dedifferentiated after serial passages still have the potential to differentiate.

Animals↗
PubMed1987

[Tumor growth inhibitory effects of SMANCS, a poly (styrene-maleic acid) conjugated derivative of neocarzinostatin, on various tissue culture cells].

Growth inhibitory effects of neocarzinostatin (NCS), and its conjugated derivative with poly (styrene-maleic acid), SMANCS, were examined on various tissue culture cells consisting of 13 lymphatic and 7 non-lymphatic cells (15 cell lines, 5 primary culture cells; 14 in suspension culture cells, 6 in monolayer cells). Both agents showed almost similar concentrations for the growth inhibition against 5 non-lymphatic cell lines (an average minimum growth inhibitory concentration of NCS, 0.076 microgram/ml, and SMANCS, 0.094 microgram/ml, a ratio of 1 : 1.24 (W/W), or 1.0 : 0.9 (mol/mol]. However, SMANCS showed a much less growth inhibitory effects against lymphatic 10 cell lines than NCS. Namely, an average 50% growth inhibitory concentration of NCS was 0.019 microgram/ml whereas that of SMANCS was 0.091 microgram/ml (a ratio of 1 : 4.79). From the consideration of each molecular weight, this ratio is 1 : 3.6. Similar results were obtained in experiments in which 2 primary non-lymphatic cells and 3 primary lymphatic cells were used. Although the largest drawback with NCS was known to be leukopenia, present results indicated the less toxicity of SMANCS than NCS on lymphatic cells and may provide a positive aspect of the new derivative, such as less incidence of leukopenia.

Animals↗
PubMed1987

[New operative technic for resecting cardiac cancers with dissection of the lower mediastinal lymph nodes through transabdominal phrenotomy using an improved hook suspender and an autosuture surgical stapling instrument].

To obtain a sufficient operative field at the operation for cardiac cancer, especially with esophageal infiltration, thoracotomy or sternotomy has been added to laparotomy. These procedures are not easy and cause great stress in patients. Through our new technique, left sided thoracotomy and sternotomy can be eliminated in favor of transabdominal phrenotomy, which is able to be performed much easier to obtain a good operative field. In order to perform the phrenotomy, the diaphragm has to be stretched using our modified hook suspender, by which the costal arch is lifted strongly upward and cranially. With these procedures, about a 5cm long esophagus is able to be resected with lymph node dissection in the lower mediastinum without difficulty. No marked influence of the hook suspender as well as the phrenotomy has been recognized on respiratory and circulatory systems. The anastomosis between the esophagus and jejunum or residual stomach seems to be very difficult, because the site of the anastomosis is located quite deep in the mediastinum. This problem, however, can be completely resolved by means of a surgical stapling autosuture instrument.

Cardia↗