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Biomedical subjects

Y Kajiyama

Publications and source records attributed to Y Kajiyama.

53 records · Page 3Linked to original sources
PubMed1996

Relief of jaundice by 5-fluorouracil and folinic acid in patients with recurrent gastric cancer.

The aim of this study was to evaluate the effect of 5-fluorouracil (5-FU) and folinic acid on liver function and bile production in patients with recurrent gastric cancer and jaundice. Thirteen patients were studied for liver function and hyperbilirubinaemia, and six patients were studied for bile production retrospectively, who were treated with 5-FU [700 mg m(-2)] and folinic acid [20 mg m(-2)] for 4 days. Serum total bilirubin, aspartate aminotransferase (AST), gamma-glutamyl transferase (gamma-GT) and alkaline phosphatase (ALP) concentrations all improved with treatment (P<0.0001), and bile production increased significantly (P<0.0001) following treatment. 5-FU and folinic acid can significantly improve jaundice and liver function, and promote bile production. It is possible that 5-FU and folinic acid may become a new method for the relief of jaundice in patients with gastrointestinal tract malignancies.

Adult↗
PubMed1994

Switching from alpha 1- to beta-subtypes in adrenergic response during primary culture of adult-rat hepatocytes as affected by the cell-to-cell interaction through plasma membranes.

The alpha 1-adrenergic response was predominant over the beta-adrenergic one in adult rat hepatocytes, when the responses were measured as the agonist-induced generations of Ins(1,4,5)P3 and cyclic AMP, respectively. During primary culture of the adult rat hepatocytes, the beta-adrenergic response developed rapidly, whereas the alpha 1-response decreased gradually. Such receptor-subtype switching did not occur unless the cells were cultured under conditions favourable for cell growth, i.e. at low cell density (10(4) cells/cm2). The switching was prevented progressively as the cell culture density was increased up to 20-fold or the low-density culture was achieved by addition of increasing amounts of liver plasma membranes. The gradual decrease in alpha 1-response was accounted for by a concurrent decrease in the receptor site density, whereas rapid development of the beta-response definitely preceded the increase in beta-ligand binding sites during the culture. This rapid development of the beta-response reflected enhanced coupling of the receptor to G-protein during the early stage of culture, as evidenced by the progressively developed ability of GTP to lower the affinity of beta-agonist binding to membranes prepared from these short-time-cultured hepatocytes.

Adrenergic beta-Antagonists↗
PubMed1994

Radical lymph node dissection for cancer of the thoracic esophagus.

OBJECTIVE: The authors documented the localization and frequency of lymphatic spread in squamous cell carcinoma of the thoracic esophagus and evaluated the influence of radical systematic lymph node dissection on patient survival. SUMMARY BACKGROUND DATA: From accumulated surgical experience, it was suggested that some of the patients with lymph nodal involvement from cancer could be cured by its clearance. However, it is only recently that cancer of the esophagus has been evaluated in terms of analyzing lymphatic spread and results of lymphadenectomy. METHODS: Among 1298 patients admitted to the Toranomon Hospital between 1973 and 1993, 913 (70.3%) had resections, including curative and palliative procedures. For this study, 717 patients with TNM RO (resection with no residual tumor at operation in TNM classification) were analyzed. Survival was compared between groups of patients with less extensive thoracoabdominal (two-field) dissections and extensive collothoracoabdominal (three-field) dissections. RESULTS: Comparative study revealed that 5-year survival rate for TNM RO patients after free-field dissection (55.0%) was significantly better (log rank test, p = 0.0013) than the rate after two-field dissection (38.3%). The results were particularly significant in subgroups with stage III and IV (because of nodal factor). Overall 5-year survival rate after all resections was 42.4%. CONCLUSIONS: The role of radical lymph node dissection in cancer of the thoracic esophagus evaluated. Long-term survival was compared between two groups with two- and three-field dissection. It was concluded that survival rate was significantly better in patients with extensive three-field dissection.

Carcinoma, Squamous Cell↗
PubMed1994

Esophagectomy without thoracotomy with vagal preservation.

The techniques of vagal preservation for use in esophagectomy without thoracotomy are presented. The purpose of vagal preservation is to avoid the debilitating postvagotomy syndrome. The technique of preservation varies depending on the mode of esophagectomy, the primary disease and the organ selected to be used for esophageal reconstruction. The postoperative quality of life is improved by the preservation of vagal function.

Esophagectomy↗
PubMed1993

[Clinical effect and characteristics of low dose leucovorin and high dose 5-FU therapy in patients with recurrent gastric cancer--a new method of biochemical modulation].

The biochemical modulation of 5-fluorouracil (5-FU) and leucovorin (LV) has resulted in a remarkable increase of the response rate in patients with colorectal cancer. Recently, in the treatment of gastric cancer this biochemical modulation has been introduced into clinical practice and has also achieved good antitumor activity. A review of the literature indicates that 5-FU/LV therapy for gastric cancer is effective only when LV is administered at high doses (200 mg-500 mg/m2), and the efficacy of low dose LV (20 mg/m2) administration with the combination of high dose 5-FU is still unknown. Thirty-five patients with measurable recurrent gastric cancer received low dose LV and high dose 5-FU for 4 days. The schedule was as follows: iv injection of low dose leucovorin (20 mg/m2) and from one hour later 2-hour infusion of high dose 5-FU (700 mg/m2). This new treatment for recurrent gastric cancer achieved a response rate of 40.0%, and 80.0% of the patients with pronounced palliative effects measured as recurrence-related symptoms. It is very rare for 7 out of 8 patients (87.5%) to be relieved of obstructive jaundice, and we now prefer this therapy to percutaneous transhepatic biliary drainage in patients with jaundice. The toxicity of this biochemical modulation is leukopenia, stomatitis and diarrhea, and the number of patients with toxicity over grade 3 was 5 (14.3%). There was no treatment-related death.

Adult↗
PubMed1991

Transoral esophagectomy.

A technique for transoral esophagectomy is presented herein. The major advantages of this operative technique are: less tissue dissected, minimal chance of contamination of the surgical field and preservation of the vagus nerve when the occasion requires it. The operation can be done with small incisions, insignificant blood loss and, with more simplicity and safety than in other similar procedures.

Esophagectomy↗
PubMed1990

Possible involvement of different GTP-binding proteins in noradrenaline- and thrombin-stimulated release of arachidonic acid in rabbit platelets.

Noradrenaline (NA) stimulated the release of arachidonic acid (AA) from the [3H]AA-labelled rabbit platelets via alpha 2-adrenergic receptors, since the effect of NA was inhibited by yohimbine. The stimulatory effect of NA in digitonin-permeabilized platelets was completely dependent on the simultaneous presence of GTP and Ca2+. The NA- and thrombin-stimulated releases of AA were markedly decreased by the prior ADP-ribosylation of the permeabilized platelets with pertussis toxin. Antiserum directed against the pig brain Go (a GTP-binding protein of unknown function), recognizing both alpha 39 and beta 35,36 subunits, but not alpha 41, of pig brain, reacted with 41 kDa and 40 kDa bands, with not one of 39 kDa, in rabbit platelet membranes. Anti-Go antiserum inhibited guanosine 5'-[gamma-thio]triphosphate-, A1F4(-)-, NA- and thrombin-stimulated AA releases in the membranes. Although the effect of thrombin was inhibited by low concentrations of anti-Go antiserum, high concentrations of the antiserum was needed for inhibition of the NA effect. Antiserum directed against the pig brain G1 (inhibitory G-protein), recognizing both alpha 41 and beta 35,36 subunits, but not alpha 39, of pig brain, reacted with the 41 kDa band in platelets. Anti-G1 antiserum inhibited only the effect of NA. Reconstitution of the platelet membranes ADP-ribosylated by pertussis toxin with Go, not Gi, purified from pig brain restored the thrombin-stimulated release of AA. In contrast, reconstitution of those membranes with Gi, not Go, restored the NA-stimulated release of AA. These results indicate that different GTP-binding proteins, Gi- and Go-like proteins, may be involved in the mechanism of signal transduction from alpha 2-adrenergic receptors and thrombin receptors to phospholipase A2 in rabbit platelets.

Aluminum↗
PubMed1990

Histamine-stimulated and GTP-binding proteins-mediated phospholipase A2 activation in rabbit platelets.

Histamine is known to be a mediator of inflammation. In order to understand the role of histamine in platelets, we have examined the effects of histamine on arachidonic acid (AA) release, cAMP accumulation, inositol trisphosphate production, and serotonin secretion. Incubation of rabbit (and human) platelets with histamine resulted in rapid increase of [3H]AA release from the platelets prelabeled with [3H]AA. The effect of histamine was blocked by the addition of H1 receptor antagonist mepyramine. Histamine did not substantially affect the cAMP content and inositol trisphosphate production. Histamine-stimulated AA release was not observed in digitonin-permeabilized platelets, whereas histamine acted synergistically with GTP or GTP analog, guanosine 5'-(3-O-thio)triphosphate. Histamine-stimulated, and GTP analog-dependent AA release was inhibited by guanosine 5'-(2-O-thio) diphosphate. The effects of three receptor stimulants, thrombin, norepinephrine, and histamine were both diminished by 1 microgram/ml of pertussis toxin treatment and by the antiserum against GTP-binding proteins (G proteins) treatment. However, the antiserum against beta gamma subunits of G proteins inhibited the histamine effect, not thrombin effect. 4 beta-Phorbol 12-myristate 13-acetate (PMA) treatment enhanced histamine-stimulated AA release and serotonin secretion but inhibited thrombin-stimulated reactions. The effect of PMA was dose dependent and was due to enhance the coupling of histamine receptors and G proteins. The results show the existence of H1 histamine receptors which couple phospholipase A2 activation via pertussis toxin-sensitive G proteins. Histamine actions differ in sensitivities to anti-beta gamma antiserum treatment and PMA treatment from thrombin actions.

Animals↗
PubMed1990

Modes of inhibitory action of 4 beta-phorbol 12-myristate 13-acetate in thrombin-stimulated arachidonic acid release in intact and permeabilized platelets.

The tumor-promoting phorbol ester 4 beta-phorbol 12-myristate 13-acetate (PMA) inhibited thrombin-stimulated arachidonic acid (AA) release in rabbit and human platelets. PMA was effective over the same concentration range that activates protein kinase C in intact rabbit platelets: IC50 vs thrombin = 0.5 nM, greater than 90% inhibition at 10 nM. Suppression of thrombin-stimulated AA release was evident within 5 min of pretreatment with 1 nM PMA. A non-tumor-promoting phorbol ester, 4-O-methyl PMA, showed a very weak ability to inhibit AA release. Thrombin-stimulated serotonin secretion was progressively inhibited by PMA pretreatment in platelets, while PMA was a stimulus for secretion at higher concentrations. 1-(5-Isoquinolinylsulfonyl)-2-methyl-piperazine (H-7), a selective inhibitor of protein kinase C, blocked PMA-induced inhibition of AA release. Furthermore, H-7 enhanced the effect of thrombin on AA release. PMA pretreatment reduced the inhibitory effect of thrombin on forskolin-stimulated cAMP accumulation, but had no effect on nonstimulated cAMP metabolism in the presence of thrombin. PMA did not inhibit AA release caused by A23187 or melittin. In digitonin-permeabilized platelets, thrombin plus guanosine 5'-(3-O-thio)triphosphate (GTP gamma S)-stimulated AA release, but not GTP gamma S- and AIF4(-)-stimulated AA release, was abolished by PMA pretreatment. These results suggest that activation of protein kinase C may exert negative feedback on the receptor-mediated activation of phospholipase A2. A possible uncoupling of thrombin receptor to GTP-binding protein leading to activation of phospholipase A2 by PMA pretreatment is discussed.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

Pertussis toxin-sensitive GTP-binding proteins may regulate phospholipase A2 in response to thrombin in rabbit platelets.

Incubation of rabbit platelets with thrombin resulted in rapid accumulations of inositol trisphosphate (IP3) in [3H]inositol-labeled platelets, increases of [3H]arachidonic acid [( 3H]AA) release, and [3H]serotonin secretion from the platelets prelabeled with these labeled compounds. The experiments using phospholipase A2 or C inhibitor suggested that not only phospholipase C but also phospholipase A2 activity plays an important role in serotonin secretion. We then studied the regulatory mechanisms of phospholipase A2 activity. Guanosine 5'-(3-O-thio)triphosphate (GTP gamma S), guanyl-5'-(beta,gamma-iminio)triphosphate), or AlF4- caused a significant liberation of AA in digitonin-permeabilized platelets but not in intact platelets. Thrombin-stimulated AA release was not observed in permeabilized platelets, whereas thrombin acted synergistically with GTP or GTP analogs to stimulate AA release. GTP analog-stimulated AA release was inhibited by guanosine 5'-(2-O-thio)diphosphate) and was also inhibited by decreased Mg2+ concentrations. Thrombin-induced, GTP-dependent AA release, but not IP3 formation, was diminished by 100 ng/ml of pertussis toxin, associated with ADP-ribosylation of membrane 41-kDa protein(s). Thrombin-stimulated AA release from intact platelets and GTP gamma S-stimulated release from permeabilized platelets were both markedly dependent on Ca2+. However, Ca2+ addition could not enhance AA release without GTP gamma S even when Ca2+ was increased up to 10(-4) M in permeabilized platelets. The results show that thrombin-stimulated AA release from rabbit platelets is mainly mediated by phospholipase A2 activity, not by phospholipase C activity, and that Ca2+ is an important factor to the activation of phospholipase A2 but is not the sole factor to the regulation. GTP-binding protein(s) is involved in receptor-mediated activation of phospholipase A2.

Animals↗
PubMed1984

Thyrotoxic myopathy associated with subacute thyroiditis.

We report a case of subacute thyroiditis complicated by thyrotoxic myopathy. Previously thyrotoxic myopathy has been described as being associated with Graves' disease. The patient in this study was a 35-year-old man who developed proximal dominant muscular weakness and atrophy during the course of subacute thyroiditis. His myopathic symptoms regressed as his serum thyroxine and triiodothyronine levels returned to normal, however it took a relatively long period of time for them to do so. This suggests that marked myopathy may develop even in cases of subacute thyroiditis if the thyrotoxic state persists for a long period of time.

Adult↗
PubMedDate not supplied

A trial to improve the analysis of boron in biological materials.

For the spectrophotometric determination of boron in biological materials, two decomposition methods were used. One is the alkali fusion method, and the other is the acid decomposition method using a uniseal decomposition vessel. A long-range calibration curve for the former method was obtained by using an ultrapure sulfuric acid. The alkali fusion method was applied to samples into which paraboronophenylalanine (BPA) or its hydrochloric salt (BPA.HCl) had been injected. By the acid decomposition method using a uniseal vessel, 50 mg dried liver was digested by a mixed solution of 1 ml conc. sulfuric acid and 6 ml 30% hydrogen peroxide. A problem exists, however, in that the hydrogen peroxide remaining in the decomposition solution must be eliminated without loss of boron.

Alkalies↗
PubMedDate not supplied

A new choleretic effect of folinic acid.

BACKGROUND/AIMS: In the chemotherapy of recurrent gastric cancer with 5-fluorouracil and folinic acid, an interesting phenomenon, the reduction of jaundice and improvement of liver function, was observed. The aim of this study was to investigate the mechanism of this phenomenon, and to confirm a choleretic effect of folinic acid. METHODOLOGY: The bile duct of anesthetized rats was catheterized, and bile was collected. Bile volume and total bile acid production following intraperitoneal administration of folinic acid were determined and compared to those of control rats. RESULTS: Both bile volume and total bile acid production increased following intraabdominal administration of folinic acid. CONCLUSIONS: Folinic acid has a newly described pharmacologic effect of stimulating bile acid-dependent choleresis. It is possible that folinic acid may become a new drug for the treatment of jaundice or for the improvement of overall liver function.

Animals↗