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Biomedical subjects

T Sudo

Publications and source records attributed to T Sudo.

At least 163 records · Page 9Linked to original sources

Effect of glucagon on bile acid metabolism after resection of liver cancer in patients with cirrhosis.

After hepatectomy patients with cirrhosis and liver cancer may develop progressive hepatic dysfunction and eventually hepatic failure. Insulin and glucagon are often used to treat certain kinds of hepatic dysfunction and hepatic insufficiency. We investigated the effect of glucagon on bile acid metabolism and pancreatic endocrine function. In 7 patients with severe cirrhosis and cancer of the liver, 1 mg of glucagon was injected intravenously pre- and post-operatively, and total bile acids, C-AMP, and bile acid fractions were determined. In the pre-operative glucagon tolerance test, the C-AMP level rose from a baseline of 14 +/- 0.8 PMol/ml to 362 +/- 94 PMol/ml 30 min after the injection of glucagon (p less than 0.01); and the level of total bile acids decreased from a baseline of 28 +/- 9 microMol/ml to 11 +/- 3 microMol/ml 60 min after the injection of glucagon. The post-operative C-AMP level increased from a baseline of 13 +/- 1 PMol/ml to 192 +/- 58 PMol/ml level of 30 min after the injection of glucagon (p less than 0.01), and the post-operative level of total bile acids decreased from a baseline of 64 +/- 20 microMol/ml to 26 +/- 7 microMol/ml 60 min after the injection of glucagon. There was a significant correlation between the 5-min increment ratio of C-AMP and the decrement ratio of total bile acids (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Acids and Salts↗

Assessment of antimicrobial penetration into the pancreatic juice in dogs.

The pancreatic ductal penetration of piperacillin, cefuzonam, fosfomycin and netilmicin, injected intravenously, was studied in four dogs with chronic pancreatic fistula. Serum and pancreatic juice were collected simultaneously, frozen, and later assayed for antibiotic concentration. Each antibiotic achieved its therapeutic serum level. The pancreatic ductal levels of piperacillin and cefuzonam were therapeutic, in contrast, the fosfomycin and netilmicin levels were subtherapeutic. These results are considered to be of interest in prevention and treatment of pancreatic infections.

Animals↗

[Clinical studies on hypercreatine phosphokinasemia in emergency diseases].

Unexplained serum creatine phosphokinase (CPK) elevation is not a rare clinical problem, especially in emergency diseases. We studied hypercreatine phosphokinasemia (hyper-CPK-emia) in 161 cases of emergency diseases. Correlations between CPK and various laboratory data, various conditions were investigated. The hyper-CPK-emia was found to obtain no correlations with GPT, GOT, LDH, creatinine and body temperature. For this reason, we could not discover the unknown factors of which contributed to elevate the serum CPK. The sources of the serum CPK in these diseases were concluded to be the skeletal muscle. This is based on the facts that CPK MM (muscle type) is specifically increased among the CPK isozymes. The elevation of serum CPK activity in emergency diseases was considered to result from muscle hypoxia due to severe stress and general circulatory failure.

Adolescent↗

Effect of intravenously administered fat emulsion on liver function in totally depancreatized dogs.

Total Pancreatectomy was performed under nembutal anesthesia in 16 adult mongrel dogs after a 24-hour fast, and the depancreatized dogs were given parenteral nutrition containing fat emulsion. Serum lipids, intravenous fat tolerance and post-heparin lipolytic activity were determined and liver biopsy was done to demonstrate the presence or absence of fatty liver. The animals were divided into three groups: group A (n = 6) received fat emulsion 1 g/kg/day; group B (n = 5), fat emulsion 2 g/kg/day; and group C (n = 5), no fat emulsion. Blood levels of cholesterol and phospholipid were increased in group B, while only a mild elevation of the blood triglyceride (TG) level was noted in group A. In group C, cholesterol and phospholipid levels were decreased, and hypoglycemia was liable to occur. The rate of disappearance of blood fat (K2) was decreased two weeks after surgery in group B, but there were no significant change in the other two groups. These findings suggest that if insulin is present, the administration of fat emulsion will not cause fatty liver.

Animals↗

Effect of tumour angiogenesis factor on proliferation of endothelial cell and tube formation.

The effect of a tumour angiogenesis factor on proliferation of various kinds of cells was examined in vitro. The factor (TAF) a polypeptide of 14000 molecular weight, was extracted and purified from the conditioned medium of ovarian clear cell carcinoma cell line (HUOCA-II). TAF at concentrations of 10 ng/ml and 100 ng/ml promoted proliferation of the endothelial cells and induced tube formation. However, it had no stimulatory effect on the proliferation of fibroblasts, endometrial columnar cells, squamous epithelial cells or cancer cells.

Angiogenesis Inducing Agents↗

Effects of diltiazem on the pharmacokinetics of nifedipine.

To evaluate the effect of diltiazem pretreatment (60 mg three times a day for 3 days) on pharmacokinetics and pharmacodynamic effect of nifedipine, six healthy subjects received 20 mg nifedipine orally on two occasions using a double-blind cross-over, placebo-controlled method. Diltiazem induced a marked increment of the area under the plasma concentration-time curve (AUC) for nifedipine by a mean of 140% and reduced the total body clearance (Cl) from 0.0043 +/- 0.0019 to 0.0017 +/- 0.0006 ml/min/kg (p less than 0.05, mean +/- SD). The biological half-life (t1/2) of nifedipine was prolonged from 2.46 +/- 0.65 to 3.21 +/- 0.92 h (p less than 0.05) without any changes in indocyanine green (ICG) clearance. Diltiazem did not produce significant changes of AUC, Cl, and t1/2 for the acid metabolite of nifedipine. Blood pressure (BP) after nifedipine administration with diltiazem pretreatment was more decreased than that without diltiazem. Both a decreased hepatic clearance and an increased bio-availability of nifedipine by diltiazem probably explain the significant changes in pharmacokinetics and hemodynamics of nifedipine. A clinically important drug interaction may occur with nifedipine when diltiazem is administered concurrently.

Adult↗

[Effect of glucagon on bile acid after hepatectomy in patients with hepatocellular carcinoma associated with cirrhosis].

Hepatic function frequently becomes worse, after hepatectomy in patients with hepatocellular carcinoma associated with cirrhosis. We usually use insulin and glucagon to treat patients with poor hepatic function, so we examined hepatic function in these patients in relation to bile acid metabolism. 1) Total serum bile acid levels were increased in patients with cirrhosis, and serum GCDCA, TCDCA values were especially high. After surgery, they rose even higher. 2) Glucagon was shown to stimulate C-AMP and decreased total serum bile acid, and especially serum GCDCA and TCDCA values.

Bile Acids and Salts↗

IL-7 promotes thymocyte proliferation and maintains immunocompetent thymocytes bearing alpha beta or gamma delta T-cell receptors in vitro: synergism with IL-2.

IL-7 induced the proliferation of normal thymocytes and the effect was synergistically potentiated by a small dose of IL-2, which by itself hardly affected thymocyte proliferation. No synergism was observed between IL-7 and any one of the other lymphokines including IL-1, IL-3, and IL-4. The thymocyte culture stimulated with IL-7 and IL-2 consisted of single positive (CD4+CD8- and CD4-CD8+) and double negative (CD4-CD8-) populations, and double positive (CD4+CD8+) cells were completely deleted. Both single positive and double negative thymocytes expressed CD3, but only the former exhibited V beta 8 and V beta 6 in an expected proportion (approximately 30% in BALB/c mice) and the latter none at all. Immunoprecipitation of the cultured thymocytes by anti-TCR gamma antibody, on the other hand, revealed the presence of a TCR gamma chain. Taken together, these results indicated that the thymocyte cultured with IL-7 and IL-2 consisted of mature T cells bearing alpha beta or gamma delta TCR. Experiments using preselected thymocyte subpopulations indicated that double negative cells responded to both IL-7 and IL-2 with positive synergism when combined, while thymocytes enriched for single positive cells preferentially responded to IL-7 with little response to IL-2 and no detectable synergism. Double positive thymocytes showed no proliferation in response to IL-7 and IL-2. In contrast to single positive thymocytes, splenic T cells hardly responded to IL-7, although significant proliferation was induced in the presence of a low dose of IL-2. Thymocytes cultured with IL-7 and IL-2 showed little nonspecific cytotoxic activity, but responded to Con A or alloantigen, whereas those stimulated with a high dose of IL-2 alone exhibited potent cytotoxic activity. These results indicated that IL-7 was involved in the generation of immunocompetent T cells in the thymus in concert with IL-2.

Animals↗

A stimulatory effect of recombinant murine interleukin-7 (IL-7) on B-cell colony formation and an inhibitory effect of IL-1 alpha.

Using a clonal culture system, we investigated the lymphohematopoietic effects of recombinant interleukin-7 (IL-7) obtained from conditioned media of transfected COS 1 cells. IL-7 alone acted on murine bone marrow cells and supported the formation of B-cell colonies. These colony cells were positive for B220, and some of them were also found to have either IgM or Thy-1. B220+, IgM- cells, but not B220- cells sorted from fresh bone marrow cells were able to form B cell colonies in the presence of IL-7. Thus, IL-7 supported the differentiation of B220+, IgM- cells to B220+, IgM+ cells. B220+, IgM+ cells did not proliferate in the presence of IL-7. IL-7 did not affect the myeloid colony formation supported by IL-3, IL-5, IL-6, granulocyte macrophage colony stimulating factor (GM-CSF), and G-CSF. On the other hand, lymphocyte colony formation was not affected by IL-2, IL-3, IL-4, IL-5, IL-6, GM-CSF, or G-CSF. Interestingly, IL-1 alpha inhibited IL-7-induced B cell colony formation in a dose-dependent manner, while the same concentration of IL-1 alpha enhanced the myeloid colony formation by IL-3. This reciprocal effect of IL-1 alpha may act on hematopoietic progenitor cells without accessory cells. These data show that IL-7 is a B cell growth factor and that IL-1 alpha may play an important role in differentiation of myeloid and lymphoid lineages.

Animals↗

Putative metal finger structure of the human immunodeficiency virus type 1 enhancer binding protein HIV-EP1.

The region containing two copies of the sequence GGGACTTTCC in the human immunodeficiency virus type 1 (HIV-1) long terminal repeat, that is an NF-kappa B binding site, functions as an enhancer element for HIV transcriptional regulation. By a Southwestern method we have isolated a cDNA encoding the HIV-1 enhancer binding protein (HIV-EP1) from a human B-cell lambda gt11 library. DNase I footprinting analysis using the HIV-EP1 protein expressed in Escherichia coli showed that HIV-EP1 specifically bound to the HIV-1 enhancer. HIV-EP1 protein contains a domain with two tandem "zinc finger" sequences initially described in the Xenopus transcription factor IIIA. This represents the first demonstration of the structural feature of the protein that binds to the HIV-1 enhancer.

Amino Acid Sequence↗

Interleukin 7 production and function in stromal cell-dependent B cell development.

The role of IL-7 in the stromal cell-dependent B cell development was investigated using two stromal cell clones, ST2 and PA6; the former supports B lymphopoiesis while the latter can not. We demonstrate here that: (a) the ability of the stromal cell clone to produce IL-7 correlates well with the stromal cell activity to support B lymphopoiesis; (b) IL-7 production by ST2 is inducible rather than constitutive; (c) the IL-7-dependent B cell itself is a potent inducer of IL-7 production by ST2; (d) addition of rIL-7 to the PA6 layer renders this in vitro environment B lymphopoietic; and (e) the differentiation from early B progenitor to pre-B cell requires both IL-7 and other stromal cell molecule(s) yet to be identified.

Animals↗

A case of concomitant association of duodenal carcinoma and jejunal carcinoma with cerebral metastasis.

A case of concomitant association of primary suprapapillary and jejunal carcinomas with cerebral metastasis is reported. A 42-year-old woman was admitted to our hospital complaining of melena. Preoperative endoscopy and abdominal angiography showed primary suprapapillary carcinoma, and brain CT showed a high density mass in the right parietal lobe causing involuntary movement of the left upper extremity. During surgery another tumor was revealed in the jejunum about 80 cm from the Treitz' ligament. These were removed surgically and examined histologically.

Adenocarcinoma↗

Macrophage factors which enhance the mixed leukocyte reaction initiated by dendritic cells.

Stimulator cells for the allogeneic MLR are dendritic cells but not macrophages (M phi). M phi, however, enhance the MLR initiated by relatively low doses of dendritic cells. The present report demonstrates that the enhancement of the MLR is mediated by two factors produced by M phi. One is IL-1, inasmuch as it has a Mr approximately 15 kDa, and both partially purified IL-1 and rIL-1 also enhance the MLR. The other has been identified as granulocyte-macrophage (GM)-CSF. It had a Mr approximately 25 kDa, and is reproduced by rGM-CSF. Moreover, the MLR-enhancing activity of both the 25-kDa molecule and rGM-CSF have been neutralized by anti-GM-CSF antiserum. Both IL-1 and GM-CSF have autonomous enhancing activity, but they collaborate with each other in enhancing the MLR. Both factors act on DC to augment their stimulatory activity for allogeneic T lymphocytes.

Adjuvants, Immunologic↗

[Effects of glucagon and insulin on poly(ADP-ribose) polymerase activity and blood ketone body ratio after partial hepatectomy in rats].

The effects of glucagon and insulin on liver nuclear poly(ADP-ribose) polymerase activity and blood ketone body ratio after rat partial (68%) hepatectomy were examined. Liver weight regeneration rate was enhanced by glucagon and insulin after 5th posthepatectomy day. The maximal value of poly(ADP-ribose) polymerase activity without glucagon and insulin was revealed as 368 +/- 64 pmole/mg/min on 5 days after the hepatectomy. In contrast, the enzyme activity with glucagon and insulin reached to the peak value as 253 +/- 42 pmole/mg/min on 2 days after the hepatectomy. The amounts of DNA per nuclear protein showed similar changes with the changes of poly (ADP-ribose) polymerase activity after the hepatectomy. Blood ketone body ratio showed almost similar changes in both groups, except transitional decrease in the group without glucagon and insulin on 5th postoperative day. It is suggested that, to promote remnant liver regeneration, the combined therapy of glucagon and insulin may act directly to nucleic acid metabolism through the changes of poly(ADP-ribose) polymerase activity and preserve energy charge level by the suppression of NAD consumption by massive poly(ADP-ribose) formation.

Animals↗

Leucine zipper structure of the protein CRE-BP1 binding to the cyclic AMP response element in brain.

By screening a lambda gt11 library with the multimerized sequence of the cAMP response element (CRE), we isolated human clones encoding the CRE binding protein, CRE-BP1, from a human brain cDNA library. CRE-BP1 expressed in Escherichia coli bound not only to the CRE element of the somatostatin and fibronectin genes, but also to the CRE element of the adenovirus E4 gene, suggesting that the protein was not distinguishable from the adenovirus transcription factor, ATF. The human CRE-BP1 clone encoded a 54.5 kd protein similar at its carboxy terminus to the leucine zipper motifs found in other enhancer binding proteins such as C/EBP and c-jun/AP-1. CRE-BP1 mRNA was expressed in all of the cells examined and was abundant in brain. The structure of CRE-BP1 and its recognition elements suggest that cellular response to extracellular stimuli is controlled by a family of transcription factors that bind to related cis-active elements and that contain several highly conserved domains.

Activating Transcription Factor 2↗