Search PubMed⌕ Search

Biomedical subjects

F Suzuki

Publications and source records attributed to F Suzuki.

At least 397 records · Page 22Linked to original sources
PubMed1989

[A case of hepatocellular carcinoma (HCC) with lung metastasis which responded to chemotherapy with a single use of 1-hexylcarbamoyl-5-fluorouracil (HCFU)].

To our knowledge, there has been only one report pertaining to the efficacy of HCFU for treatment of metastatic lung lesion of HCC, so we reported a case of HCC with lung metastasis which responded to chemotherapy with a single use of HCFU. A 64-year-old male was diagnosed as having HCC with lung metastasis by biochemical examination, abdominal CT, hepatic arteriogram and chest X-P. He had been treated previously with gamma-interferon and mitoxantrone, which were assessed as NC and PD, respectively. Two months after last chemotherapy, HCFU was administrated at a dose of 400 mg/body everyday for 8 months. After 4 weeks metastatic lung lesions showed remarkable regression (47% decrease) and disappeared completely 9 weeks later. The size of primary liver tumor gradually decreased during therapy and revealed marked improvement (85.7% decrease) after about 2 months of this therapy. During these periods serum levels of alpha-fetoprotein dropped from 430 ng/ml to less than 10 ng/ml. He is presently still alive and the duration of the PR attained to 35 weeks. As side effects, hypoproteinemia, anorexia and hot sensation were observed.

Antineoplastic Agents↗
PubMed1989

[Craniopharyngioma with malignant transformation--a report of two cases].

Two cases of a craniopharyngioma with malignant transformation are reported. Case 1 involved a 3-year-old male who had received a partial resection and radiotherapy for a suprasellar tumor. Histologically, a biopsy specimen showed craniopharyngioma. Eight years later, the child died of an intracerebral and nasopharyngeal invasion of the recurrent tumor. Case 2 involved a 9-year-old male who initially had been diagnosed as having a craniopharyngioma in the suprasellar region. Five years after the first operation, he died from growth of the tumor in spite of radiotherapy and a partial resection. The pathological examinations of these two cases showed an apparent transition of the craniopharyngioma into a squamous cell carcinoma.

Ameloblastoma↗
PubMed1989

[Gastric remnant cancer--physical and laboratory examination and results of treatment].

A clinical evaluation of re-operation after primary gastric resection for stomach carcinoma as "Second Look Operation" was performed with reference to a surgical treatment for gastric remnant cancer. Ninety-one cases among gastrectomized patients with gastric cancer from 1973 to 1987 underwent re-operation. Gastric remnant cancer in 25 cases (27%), was the second indication for the operation next to ileus. It consisted of 17 cases of recurrent cancer and 8 cases of metachronous cancer. The mean interval between the primary and secondary laparotomy in the former (32 months) was significantly shorter than in the latter (117 months). Resectability of gastric remnant cancer was 100% (8/8) in metachronous cancer and 27% (9/33) in recurrent cancer. A long-term follow-up system for over 10 years with modern physical and laboratory examinations for gastrectomized patients has been a substitute for "Second Look Operation" for find cancer in the gastric remnant.

Biomarkers, Tumor↗
PubMed1988

Induction of S100 protein in 3T3-L1 cells during differentiation to adipocytes and its liberating by lipolytic hormones.

When confluent cultures of cloned mouse 3T3-L1 cells were differentiated to adipocytes by three days of treatment with a combination of 0.5 microM dexamethasone and 0.5 mM 1-methyl-3-isobutylxanthine, the S100 protein content in the cells increased markedly, as determined by a sensitive immunoassay system. The S100 protein induced in the cell was the alpha alpha form (S100ao), which is the predominant form of S100 protein in mouse adipose tissue. The S100ao concentration in preadipocytes was about 1-3 ng/mg protein, while the concentration in differentiated adipocytes was 60-200 ng/mg protein. The immunoblotting test of the crude extract of adipocytes confirmed that the immunoreactive substance in the cells was the alpha subunit of S100 protein. The treatment with 1-methyl-3-isobutylxanthine or dexamethasone alone neither elicited the S100 protein induction nor triacylglycerols accumulation in the cells. The accumulation of triacyglycerols in the cells was always preceded by the induction of S100ao protein under conditions where the differentiation to adipocytes was elicited. The induction of S100ao protein and accumulation of triacylglycerols in the cells treated with dexamethasone and 1-methyl-3-isobutylxanthine were inhibited by the addition of antimicrotubular drugs, colchicine and vinblastine, but not by cytochalasin B, an antimicrofilament drug. S100ao protein in 3T3-L1 adipocytes was released by incubation with a lipolytic hormone, adrenocorticotropic hormone or catecholamines, in a cyclic-AMP-dependent manner as observed with rat epididymal fat pads [Biochim. Biophys. Acta (1986) 889, 84-90]. These results also suggest that S100 protein may participate in the function of adipocytes.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Effect of transforming growth factor beta on cell proliferation and glycosaminoglycan synthesis by rabbit growth-plate chondrocytes in culture.

The effects of the transforming growth factor beta (TGF-beta) on the growth and glycosaminoglycan synthesis of rabbit growth plate-chondrocytes in culture were studied. In serum-free medium, TGF-beta caused dose-dependent inhibition of DNA synthesis by chondrocytes, measured as [3H]thymidine incorporation (ED50 = 0.1-0.3 ng/ml). The inhibitory effect was maximal at a dose of 1 ng/ml, and extended for a duration of 16-42 h. In contrast, TGF-beta potentiated the synthesis of DNA stimulated by fetal calf serum (FCS). Addition of TGF-beta (1 ng/ml) to cultures containing 10% FCS increased [3H]thymidine incorporation to 1.6-times that in cultures with 10% FCS alone. Consistent with this finding, TGF-beta potentiated DNA synthesis stimulated by the purified growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF) and fibroblast growth factor (FGF). The maximal stimulation of DNA synthesis by FGF (0.4 ng/ml) was further potentiated dose dependently by TGF-beta (ED50 = 0.1 ng/ml, maximum at 1 ng/ml). When the cultures were treated with the optimal concentrations of TGF-beta (1 ng/ml) and FGF (0.4 ng/ml), [3H]thymidine incorporation was 3-times higher than that of cultures treated with FGF alone. This TGF-beta-induced potentiation of DNA synthesis was associated with replication of chondrocytes, as shown by a marked increase in the amount of DNA during treatment of sparse cultures of the cells with the growth factors for 5 days. In contrast, TGF-beta caused dose-dependent stimulation of glycosaminoglycan synthesis in confluent cultures of growth-plate chondrocytes (ED50 = 0.3 ng/ml, maximum at 1 ng/ml). This stimulatory effect of TGF-beta was greater than that of insulin-like growth factor I (IGF-I) or PDGF. Furthermore, TGF-beta stimulated glycosaminoglycan synthesis additively with IGF-I or PDGF. Recently, it has been suggested that bone and articular cartilage are rich sources of TGF-beta, whereas epiphyseal growth cartilage is not. Thus, the present data indicate that TGF-beta may be important in bone formation by modulating growth and phenotypic expression of chondrocytes in the growth plate, possibly via a paracrine mechanism.

Animals↗
PubMed1988

Angiotensinogen gene expression in extrahepatic rat tissues: application of a solution hybridization assay.

Angiotensin II has numerous biological effects in a hitherto unsuspected variety of tissues. The generation of angiotensin in tissue requires the local presence of its high molecular weight precursor angiotensinogen and is best tested by investigating angiotensinogen gene expression. A quantitative solution hybridization assay for rapid and sensitive measurement of angiotensinogen mRNA was therefore established to study the extrahepatic expression of the angiotensinogen gene. We used a 714 bases BamHI angiotensinogen cDNA fragment cloned into vector pSPT18 and developed a sensitive and rapid assay with a detection limit of 0.5 pg RNA. Quantification of angiotensinogen mRNA from male Sprague-Dawley rats resulted in the following tissue levels (n = 10 for all tissues, except pituitary where n = 5), was expressed as fg mRNA per microgram total RNA, in descending order: liver (9950), hypothalamus (6050), midbrain (4450), brainstem (3950), total brain (2325), aorta (625), kidney (338), adrenal gland (170), and heart atrium (140). The high sensitivity of the assay in addition also allowed for the first time measurement of angiotensinogen mRNA in the low gene expression tissues pituitary (70), heart ventricle (30), and testis (30). This assay will allow detailed studies on the regulation of tissue angiotensinogen and the pathophysiological role of the tissue renin angiotensin systems.

Adrenal Glands↗
PubMed1988

Hydrocortisone stimulation of proliferation and glycosaminoglycan synthesis in rabbit craniofacial chondrocytes in vitro.

Hydrocortisone stimulated glycosaminoglycan (GAG) synthesis, a cartilage phenotype, in chondrocytes from mandibular condylar cartilage (MCC), nasal septal cartilage (NSC) and sphenooccipital synchondrosis (SOS). These stimulations were dose- and time-dependent, being maximal 27 h after addition of 10(-7) M hydrocortisone. The maximal induced increase of GAG synthesis was about 100%, 50% and 20% that of non-stimulated MCC, SOS and NSC chondrocytes, respectively. When stained with toluidine blue, all three types of cortisone-treated chondrocytes showed stronger metachromasia than non-treated controls. DNA synthesis was also increased by hydrocortisone, reaching a maximum 20 h after the addition; stimulation was also dose-dependent and maximal at a concentration of 10(-6) M. The maximal increase in DNA synthesis was 200% in NSC chondrocytes, 90% in SOS chondrocytes, and slight in MCC chondrocytes. However, there was no stimulation of DNA synthesis in serum-free medium, in contrast to that of GAG synthesis. These observations suggest that hydrocortisone regulates craniofacial growth by controlling the differentiation of these chondrocytes directly and their proliferation indirectly, and that the difference in their responses to hydrocortisone may reflect different responses in vivo.

Animals↗
PubMed1988

Suppressor Lyt 2+ T-cells demonstrated in mice late after thermal injury.

Biological properties of suppressor cells mediating second suppressive state (S-SupS) of IFN-gamma responsiveness in mice following thermal injury were investigated by their ability to inhibit [3H]thymidine incorporation by allogeneic cell-stimulated mononuclear cells (MNC) prepared from spleens of unburned normal mice (N-mice). Kinetic studies indicated that the suppressor cells appeared at approximately 15 days post-burn and persisted until 40 days after thermal injury. This cell population from the spleens of thermally injured mice (TI-mice) was inactivated by anti-Thy 1.2 monoclonal antibody (mAb) plus complement (C). Treatment with antimouse immunoglobulin and anti-Lyt 1.2 mAb followed by C failed to abrogate the activity. However, it could be eliminated by treatment with anti-Lyt 2.2 mAb and C. In addition, when Thy 1+ or Lyt 2+ T cells were depleted from spleen cells containing suppressor cell activities by treatment with mAbs and C, the suppressor activity for IFN-gamma production by N-mice splenic MNC stimulated with concanavalin A was also eliminated. However, no alteration in the suppression of IFN production was observed when this splenic cell population from TI-mice was treated with anti-Lyt 1.2 mAb and anti-mouse Ig followed by C. Since it has been reported [1] that the suppressor cell in spleens of TI-mice could neither be removed by plastic adherence nor by carbonyl-iron treatment, this secondarily-generated suppressor cell was concluded to be a T cell possessing the Lyt 1-2+ phenotype. The present report describes the demonstration, following a generation of suppressor macrophages [2], of suppressor Lyt 2+ T cells spleen of mice late after thermal injury.

Animals↗
PubMed1988

Changes in the distribution of intramembranous particles and filipin-sterol complexes during epididymal maturation of golden hamster spermatozoa.

Golden hamster spermatozoa in various segments of the excurrent duct system were studied by freeze-fracture with and without filipin treatment. Two types of regular IMP (intramembranous particle) patterns temporarily appear on the plasma membrane covering the sperm head. One is a hexagonal arrangement seen in the acrosomal region, and the other is a linear arrangement near the posterior ring. Both patterns are seen in the spermatozoa from the corpus epididymidis. The FSC (filipin-sterol complex) density in the plasma membrane covering the acrosome increases from about 400 to 500 FSC/microns2 during epididymal passage. In this region, the majority of the membrane sterols appears to reside on the outer leaflet of the lipid bilayer. When the spermatozoa reach the cauda epididymidis, FSCs in the outer acrosomal membrane virtually disappear from the apical segment, while they increase in the middle segment (250 FSC/microns2). These observations are discussed in relation to epididymal maturation.

Animals↗
PubMed1988

Terminal differentiation and calcification in rabbit chondrocyte cultures grown in centrifuge tubes: regulation by transforming growth factor beta and serum factors.

Rabbit chondrocyte cultures on plastic dishes are capable of depositing a cartilaginous matrix, although the matrix does not calcify unless high levels of phosphate are added to the medium. In the present study, we cultivated a pelleted mass of rabbit growth-plate chondrocytes in the presence of Eagle's minimum essential medium supplemented with 10% fetal bovine serum and 50 micrograms of ascorbic acid per ml in a plastic centrifuge tube. These cells proliferated for several generations and then reorganized into a cartilage-like tissue that calcified without additional phosphate. The deposition of minerals was observed only after synthesis of a short-chain collagen and alkaline phosphatase. Serum factors were required for the increases in alkaline phosphatase and calcium contents. 5-Bromo-2'-deoxyuridine abolished the increases in uronic acid, alkaline phosphatase, and calcium contents. Transforming growth factor beta, at very low concentrations, suppressed the expression of the mineralization-related phenotype by chondrocytes. These results suggest that cartilage-matrix calcification can be controlled by growth factor(s) and that chondrocytes induce the mineralization of extracellular matrix when terminal differentiation is permitted in the absence of an artificial substrate.

Alkaline Phosphatase↗
PubMed1988

Induction of angiotensinogen mRNA in hepatocytes by angiotensin II and glucocorticoids.

In isolated rat hepatocytes, exposed to angiotensin II and glucocorticoids, angiotensinogen mRNA increased within 30-60 min, and angiotensinogen secretion with a time lag of about 2 hours. After 4 hours, angiotensinogen mRNA, estimated by liquid hybridization with radiolabeled cRNA, was 5.9 +/- 0.4 in control, and 10.8 +/- 0.8, 11.7 +/- 0.4, 16.1 +/- 0.8 and 21.7 +/- 0.2 pg/micrograms of total RNA in cells exposed to angiotensin II (9 nM and 90 nM), hydrocortisone (100 microM) and dexamethasone (10 microM) respectively. The corresponding secretion rates of angiotensinogen were 72 +/- 7, 124 +/- 4, 132 +/- 12, 220 +/- 19 and 217 +/- 18 fmol angiotensinogen/mg wet weight/hour. Thus, angiotensin II stimulates angiotensinogen synthesis and secretion by acting at a pretranslational site.

Angiotensin II↗
PubMed1988

Tissue renin-angiotensin systems aspects of molecular biology and pharmacology.

Advances in molecular biology over the last few years have made it possible to extend studies concerned with the role of renin in blood pressure regulation and fluid balance to the genetic level. Epidemiological data from cross-sectional population studies as well as experimental findings in spontaneously hypertensive rats suggest a greater disposition towards hypertension in males than in females. Testosterone (T) is known to raise blood pressure in female and castrated male SH-rats, while concomitantly increasing tissue renin activities. The availability of recombinant DNA technology and of a 32P labeled mouse submandibular gland renin cRNA as a hybridization probe enabled us to quantitatively assess whether this increase is paralleled by enhanced renin gene expression. In groups of female NMRI mice injected with DHT, we were able to show, that cardiac renin activity was significantly increased after 2 hours (1.6 fold) and 21 days (1.9 fold) of dihydrotestosterone (DHT) treatment compared to controls. DHT had no effect on renin mRNA concentration in the uterus, whereas in the ovary it resulted in a 50% decrease. We conclude that enhanced renin-activity and mRNA levels in peripheral organs and in the central nervous system are due to direct or indirect effects (cis, transacting) of T on renin gene expression. Thus, T may participate in the development of hypertension by stimulating the activity of tissue renin-angiotensin systems.

Animals↗
PubMed1988

Quantification of renin mRNA in various mouse tissues by a novel solution hybridization assay.

A new solution hybridization assay was established for the measurement of renin mRNA. The assay makes use of a radioactively labelled renin complementary RNA as hybridization probe and allows rapid and sensitive detection of renin mRNA in amounts as low as 0.5 pg. With this assay it was possible to quantify renin mRNA in tissues with low-gene expression such as brain and heart as well as in testis, kidney and the submandibular gland (SMG) of mice. The concentrations in these organs were 0.03, 0.07, 1, 5.2 and 164 pg renin mRNA/micrograms RNA, respectively. These results are in agreement with Northern blotting experiments. The general applicability and ease of the solution hybridization assay described here should greatly improve the rapidity of mRNA measurements in future functional studies.

Animals↗
PubMed1988

Angiotensin II controls angiotensinogen secretion at a pretranslational level.

It has been proposed that feedback by angiotensin II, the effector peptide of the renin-angiotensin system stimulates hepatic angiotensinogen synthesis, since long-term infusion of this octapeptide in vivo induced an increase in plasma angiotensinogen concentrations. In the present study, the effects of angiotensin II (9 and 90 nmol/l) on angiotensinogen messenger (m)RNA concentrations and on angiotensinogen secretion of freshly isolated rat hepatocytes were compared with those of glucocorticoids (hydrocortisone, 10(-4) mol/l, and dexamethasone, 10(-5) mol/l). Angiotensin II and the glucocorticoids elevated angiotensinogen mRNA concentrations two- to threefold. Angiotensinogen secretion rates were correspondingly increased with a time lag of about 2 h. Differences in the time-course of changes in mRNA following onset or decay of the hormonal effect suggest that angiotensin II and glucocorticoids express their effects by different intracellular mechanisms. This view is supported by the observation that angiotensin II but not dexamethasone has a stabilizing effect on angiotensinogen mRNA, when further synthesis was blocked by actinomycin D.

Angiotensin II↗