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T Mine

Publications and source records attributed to T Mine.

At least 19 recordsLinked to original sources
PubMed1992

Pertussis toxin blocks activin A-induced production of inositol phosphates in rat hepatocytes.

The present study was conducted to examine an involvement of G protein in the action of activin A in rat parenchymal liver cells. Activin A induced a dose-dependent increase in inositol phosphates in cells prelabelled with [3H]inositol. The effect of activin A was completely blocked by pretreatment of the cells with pertussis toxin. In contrast, pertussis toxin had little effect on angiotensin II-induced production of inositol phosphates. Both activin A and angiotensin II inhibited glucagon-mediated production of cAMP. Pretreatment of the cells with pertussis toxin blocked the inhibition induced by both activin A and angiotensin II. In permeabilized cells, activin A augmented production of inositol phosphates. Activin-mediated production of inositol trisphosphate was enhanced by GTP-gamma S and was attenuated by GDP-beta S. These results suggest that a pertussis toxin-sensitive G protein(s) may be involved in the action of activin A in hepatocytes.

Activins↗
PubMed1992

Isoflavonoids, genistein, psi-tectorigenin, and orobol, increase cytoplasmic free calcium in isolated rat hepatocytes.

Isoflavonoid compounds, genistein, psi-tectorigenin and orobol have been implicated as inhibitors of tyrosine-specific protein kinase and phosphatidylinositol turnover. These compounds have been frequently used as a pharmacological tool to assess signal transduction pathways in various cell systems. In the course of analyzing signaling pathways in rat hepatocytes, we obtained an unexpected finding that these compounds transiently increase cytoplasmic free calcium. Since the Ca2+ mobilizing effect was observed in 1 microM calcium containing buffer, the source of the Ca2+ may be intracellular stores. Thus, when interpreting data obtained using these compounds, caution is needed.

Aequorin↗
PubMed1992

Continuous local intraarterial infusion after prolonged arterial stasis in the fingers and toes.

Seven patients with trauma to eight digits and one toe went untreated for arterial stasis, with subsequent development of posttraumatic changes in skin coloration. In two patients involving two digits, a daily dose of 2,000 ml containing 240,000 U urokinase, 80 micrograms prostaglandin E1, and 10,000 U heparin in lactated Ringer's solution was administered by intravenous infusion for 10 consecutive days; one of the two digits became necrotic. In all subsequent patients, a daily dose of 80 ml containing 240,000 U urokinase, 40 micrograms prostaglandin E1, 10,000 U (maximum) heparin, and low-molecular-weight dextran was administered by continuous local intraarterial infusion for 10 consecutive days. These seven extremities survived, even in the case of two digits and one toe with over 50 hr of arterial stasis. We believe that revascularization of extremities following prolonged periods of arterial stasis may be possible by means of continuous local intraarterial infusion of antithrombotic agents.

Aged↗
PubMed1992

Congenital absence of the portal vein.

Absence of the terminal portion of the portal vein and its intrahepatic branches was demonstrated in a 22-year-old woman with focal nodular hyperplasia (FNH) of the liver. Various imaging studies and angiography showed that the portal vein entered into the inferior vena cava just above the renal veins. The clinical and radiological features of this patient and nine previously reported cases of this entity are herein reviewed.

Adult↗
PubMed1991

Comparison of effects of HGF and EGF on cellular calcium in rat hepatocytes.

We compared the effects of HGF and EGF on cytoplasmic free calcium concentration, [Ca2+]c, and inositol trisphosphate production in rat hepatocytes. HGF induced a prompt and transient elevation of [Ca2+]c. EGF also induced an immediate increase in [Ca2+]c, the magnitude of which was greater than that by HGF. In contrast, in the presence of 1 microM extracellular calcium EGF increased [Ca2+]c to a lesser extent than HGF. When cells were pretreated with EGF, the effect of HGF on [Ca2+]c was greatly enhanced. However, such enhancement was not observed in medium containing 1 microM extracellular calcium. In hepatocytes prelabeled with [3H]-inositol, both HGF and EGF increased [3H]inositol trisphosphate. HGF and EGF acted synergistically to stimulate production of inositol trisphosphate. These results indicate that both HGF and EGF increase [Ca2+]c by a mechanism involving phosphoinositide turnover and that the actions of HGF and EGF on hepatocyte calcium metabolism are not totally identical.

Animals↗
PubMed1991

Histological changes of the gallbladder and liver after extracorporeal shock wave lithotripsy for gallbladder.

The histological changes of the gallbladder and liver following extracorporeal shock wave lithotripsy (ESWL) were investigated in a canine model. After performing ESWL on human cholesterol stones placed in the gallbladder of 8 dogs, the gallbladder and livers were removed for pathological study. The mucosa of the gallbladder showed erosion and ulceration in three of the eight dogs. Edema and bleeding were found in the stroma of the gallbladder beds. Hemorrhagic necrosis and vacuolar degeneration occurred in liver parenchyma adjacent to the gallbladder bed, but the portal area was fairly well preserved. It can be said that ESWL caused damage to both the liver and the gallbladder, but its effects on the liver may be only slight because of the preservation of the portal area.

Animals↗
PubMed1991

An investigation of venous pressure and oxygen tension in human extremities: an experimental study of survival in pedicled venous flaps.

The pedicled venous flap is used at various sites, such as the finger, forearm, and leg. The authors previously reported that the reasons for the viability of such flaps, based on the digital dorsal vein and used for repairing digital skin defects in the earlier study, were high venous pressure or oxygen tension, as well as the possible effects of plasmatic imbibition and outflow through the draining vein. To investigate the importance of venous pressure and oxygen tension in the survival of these flaps at other sites in the body, measurements were made comparing these parameters in the digital vein, cephalic vein, and greater saphenous vein, which are all used clinically as draining veins in pedicled venous flaps. Although measurements in other sites were consistently lower than in the digital dorsal vein, since these other venous flaps are nevertheless viable in the clinical situation, their viability may not be due only to relatively high venous pressure and oxygen tension. The authors intend to carry out further comparative studies on plasmatic imbibition in the flap and outflow through the draining vein.

Adolescent↗
PubMed1991

Mechanism of glycogenolytic action of histamine in rat hepatocytes.

The mechanism by which histamine induces glycogenolysis was investigated in rat hepatocytes. Histamine induced stimulation of glucose output in hepatocytes in a dose-dependent manner. The maximal effect of the glycogenolytic action of histamine, which was approximately 60% of the maximal glucagon action, was obtained at 10(-6) M. These effects were inhibited by H1 receptor antagonists triprolidine hydrochloride and tripelennamine but not by a H2 receptor antagonist cimetidine. Histamine also increased the activity of phosphorylase a. When 10(-6) M histamine and 5 x 10(-9) M glucagon were added simultaneously, the actions of these two agents were additive. In contrast, there was no additivity when 10(-6) M histamine and 10(-8) M angiotensin II were added. Histamine did not increase adenosine 3',5'-cyclic monophosphate at any doses tested but induced a rapid increase in the cytoplasmic free calcium concentration ([Ca2+]c). Histamine increased [Ca2+]c even in the presence of 1 microM extracellular calcium, an observation suggesting that histamine caused calcium release from an intracellular calcium pool(s). When [3H]inositol-labeled hepatocytes were incubated with histamine, radioactivity in the D-myo-inositol trisphosphate fraction was rapidly increased. These results indicate that histamine acts on rat hepatocytes mainly via H1 receptors and stimulates glycogenolysis by activating the calcium messenger system.

Angiotensin II↗
PubMed1990

Difference in sensitivity to glucagon action in three different rat liver systems.

We compared sensitivity to glucagon in three different rat liver systems. In perfused liver, half-maximal response of glycogenolysis was obtained by 5 x 10(-11) mol/L glucagon. In contrast, half-maximal response was obtained by 10(-9) mol/L glucagon in batch incubation of isolated hepatocytes. In perifusion system using the same isolated hepatocytes, 9 x 10(-11) mol/L glucagon induced half-maximal response. In both perfused liver and perifusion system, dose response relationships for glucagon-induced cyclic adenosine monophosphate (cAMP) output were identical. In batch incubation of isolated hepatocytes, again much higher concentration of glucagon was needed to increase cAMP output. Inhibitors of glucagon degradation did not increase the sensitivity of hepatocytes in batch incubation system. When the liver was perfused in recirculation system, glycogenolytic response to glucagon was significantly less than when it was perfused in flow-through system. Also, when extract of lipophilic substances in conditioned medium of batch incubation system was included in perfusate, the glycogenolytic response to glucagon was diminished in perfused liver system. In contrast to the action of glucagon, sensitivities of hepatocytes to calcium mobilizing hormones, phenylephrine, and angiotensin II, in three systems were nearly identical. These results suggest that the diminished sensitivity of hepatocytes to glucagon observed in batch incubation system is due, at least in part, to a substance (or substances) released from hepatocytes.

Angiotensin II↗
PubMed1990

Interpeduncular high-density spot in severe shearing injury.

Thirty cases of severe shearing injury were analyzed utilizing serial computed tomography scans and clinical observations. Fatalities occurred in the majority of patients whose Glasgow Coma Scale scores at admission were 6 or less. The presence of perimesencephalic subarachnoid hemorrhage, hemorrhage in the corpus callosum, acute brain swelling, and intraventricular hemorrhage on computed tomography scans resulted in high mortality rates. In 13 patients, interpeduncular high-density spots were observed on computed tomography scans, which were performed in the acute stage of injury. Eight of these patients died, and those surviving had poorer neurological outcomes than corresponding patients with identical Glasgow Coma Scale scores on admission. In the management of severe shearing injury patients, more attention should be given to the presence of interpeduncular high-density spots as well as other important diagnostic computed tomography findings regarding diffuse brain injury.

Adolescent↗
PubMed1990

Mechanism of prostaglandin E2-induced glucose production in rat hepatocytes.

Effects of prostaglandin E2 (PGE2) on glycogenolysis were examined in rat hepatocytes. In a batch incubation system using isolated hepatocytes, PGE2 increased glucose output dose-dependently. The glycogenolytic effect of PGE2 was detected at a concentration of 10(-11) M, and 10(-8) M PGE2 elicited the maximum glucose output, which was equal to that by glucagon. PGE2 did not increase cAMP at any dose tested (10(-11)-10(-4) M). Instead, PGE2 increased the cytoplasmic free calcium concentration ([Ca2+]c). When the effect of PGE2 on [Ca2+]c was studied in aequorin-loaded cells, the effect of PGE2 on [Ca2+]c was detected at 10(-12) M, and the magnitude of the response increased in a dose-dependent manner. PGE2 increased [Ca2+]c even in the presence of 1 microM extracellular calcium, suggesting that PGE2 mobilizes calcium from an intracellular pool. In line with these observations, PGE2 increased the production of inositol trisphosphate. Compared with the action of PGE2, 16,16-dimethyl-PGE2, a PGE2 analog, was less potent in stimulating glycogenolysis. These results indicate that PGE2 stimulates glycogenolysis by activating the calcium messenger system.

16,16-Dimethylprostaglandin E2↗
PubMed1989

Calcium rather than cyclic AMP is an intracellular messenger of parathyroid hormone action on glycogen metabolism in isolated rat hepatocytes.

The synthetic 1-34 fragment of human parathyroid hormone (1-34hPTH) stimulated glucose production in isolated rat hepatocytes. The effect of 1-34hPTH was dose-dependent and 10(10) M-1-34 hPTH elicited the maximum glucose output, which was approx. 80% of that by glucagon. Although 1-34hPTH induced a small increase in cyclic AMP production at concentrations higher than 10(-9) M, 10(-10) M-1-34hPTH induced the maximum glucose output without significant elevation of cyclic AMP. This is in contrast to the action of forskolin, which increased glucose output to the same extent as 10(-10) M-1-34hPTH by causing a 2-fold elevation of cyclic AMP. In addition to increasing cyclic AMP, 1-34hPTH caused an increase in cytoplasmic free calcium concentration ([Ca2+]c). When the effect of 1-34hPTH on [Ca2+]c was studied in aequorin-loaded cells, low concentrations of 1-34hPTH increased [Ca2+]c: the 1-34hPTH effect on [Ca2+]c was detected at as low as 10(-12) M and increased in a dose-dependent manner. 1-34hPTH increased [Ca2+]c even in the presence of 1 microM extracellular calcium, suggesting that PTH mobilizes calcium from an intracellular pool. In line with these observations, 1-34hPTH increased the production of inositol trisphosphate. These results suggest that: (1) PTH activates both cyclic AMP and calcium messenger systems and (2) PTH stimulates glycogenolysis mainly via the calcium messenger system.

Animals↗
PubMed1989

Stimulation of glucose production by activin-A in isolated rat hepatocytes.

The effect of activin-A on glycogenolysis was studied in isolated rat hepatocytes. Activin-A stimulated glucose output in hepatocytes in a dose-dependent manner. The maximal effect of the glycogenolytic action of activin-A, which was about 50% of the glucagon action, was obtained at 10(-9) M. When 10(-9) M activin-A and 5 x 10(-9) M glucagon were added simultaneously, the actions of these two agents were additive. In contrast, there was no additivity when 10(-9) M activin-A and 10(-8) M angiotensin-II were added. Activin-A did not increase cAMP at any doses tested, but induced a rapid increase in cytoplasmic free calcium concentration. Activin-A increased the cytoplasmic free calcium concentration even in the presence of 1 microM extracellular calcium, suggesting that activin-A caused calcium release from an intracellular calcium pool(s). The internal calcium pool affected by activin-A appeared to be the same as that affected by either angiotensin-II or vasopressin. When [3H] inositol-labeled hepatocytes were incubated with activin-A, radioactivity in the inositol trisphosphate fraction was rapidly increased. These results indicate that activin-A acts on rat hepatocytes and stimulates glycogenolysis by activating the calcium messenger system.

Activins↗
PubMed1989

[Basic analysis of extracorporeal shock wave lithotripsy of gallstones].

Influence of extracorporeal shock wave lithotripsy (ESWL) on human gallstones placed in dog gallbladders was investigated. After irradiation of shock wave more than 600 times, maximal diameter of residual stones of 10 mm before irradiation was destroyed to 2 mm or less. Levels of serum transaminase (GOT.GPT) were elevated, in parallel with times of shock waves. These results suggested that 600 times of shock waves were enough to destroy one cholesterol stone, diameter of which was about 1 cm. Data of elevation of serum transaminase showed that more than 600 times of shock waves were possible to induce the damage of liver.

Alanine Transaminase↗
PubMed1989

[A case of pseudotumor cerebri associated with colon cancer].

A case of pseudotumor cerebri associated with iron deficiency anemia due to colon cancer is reported in a 37-year-old woman. Her initial symptoms were vomiting and severe headache. On physical examination, no lymph nodes and abdominal mass were palpable but marked anemia was noted in her skin and conjunctiva . Neurological examination revealed papilledema in her both eyes and stiff neck. There was no abnormal findings on CT scan on admission. Spinal puncture revealed CSF pressure as high as 620 mmH2O with normal cells, protein, sugar and chloride levels. Hematological examination revealed iron deficiency anemia and thrombocytosis. Angiography at third day revealed no sinus occlusion, but retention of contrast media was seen on the cortical vein of parietal lobe and right transverse sinus. Brain scintigram at sixth day revealed mild accumulation in left parietal lobe, so small venous infarction was suggested. There were two circumscribed stenotic lesions of right ascending colon in the barium enema, and right hemicolectomy was achieved. The pathological diagnosis was adenocarcinoma. The symptoms of pseudotumor cerebri was completely disappeared soon after the surgery together with resolution of anemia. She lives with no deficits now 1 year 3 months after surgery. In conclusion much attention is necessary to a patient of pseudotumor cerebri with iron deficiency anemia for the presence of cancer, because not only this central nervous system lesion is reversible and curable but also the cancer itself may be curable by surgery.

Adenocarcinoma↗