[Mechanisms for flow-induced responses of vascular endothelial cells].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Masuda.
Explore the source record for details and available documents.
PURPOSE: We evaluated the prognostic significance of the Ki-67 labeling index in 70 patients with primary urothelial tumors of the renal pelvis and ureter. MATERIALS AND METHODS: Immunohistochemical staining for Ki-67 in archival tumor materials was done by the streptavidin-biotin method. RESULTS: Univariate survival analysis showed that the prognosis of patients with a high Ki-67 labeling index of 21.7 or more was significantly worse than that of patients with an intermediate labeling index of 13.3 to less than 21.7 (p < 0.01) or a low labeling index of less than 13.3 (p < 0.001). Multivariate survival analysis showed that staining for Ki-67 labeling index was significantly correlated with prognosis (p < 0.01). CONCLUSIONS: Analysis of Ki-67 labeling index provides useful prognostic information about patients with primary urothelial tumors of the renal pelvis and ureter.
A sixty-year-old woman visited our hospital with a complaint of left flank pain. Laboratory data showed a high level of serum CA19-9. Computerized tomography and ultrasonography revealed left hydronephrosis and hydroureter. No tumors were found in the liver, pancreas, gallbladder, gastrointestinal tract or genitourinary tract. The serum SPan-1 antigen level was elevated to 250 U/ml, and the serum CA19-9 level was also elevated to 580 U/ml. Since urological malignancy was not excluded from these findings, left nephroureterectomy was performed. Pathological findings revealed chronic inflammation, and malignant cells were not found in the resected specimens. Although high levels of SPan-1 antigen and CA19-9 have been reported in benign diseases, both are usually less than 100 U/ml. In this case, serum SPan-1 antigen and CA19-9 levels were extremely high (more than 1,000 U/ml). Since the serum SPan-1 antigen and CA19-9 levels were gradually reduced to normal levels within 4 months after the operation, a possible explanation for the high levels of the two tumor markers is hydronephrosis in the left kidney. We report this interesting hydronephrosis associated with high levels of serum SPan-1 antigen and CA19-9.
We report a case of superficial bladder cancer in a young female, with grade-up tumor after frequent recurrences. A 29-year-old woman complained of gross hematuria on April 25, 1991. Cystoscopic examination revealed a papillary pedunculated tumor and transurethral resection of bladder tumor (TUR-BT) was performed. Pathological examination showed transitional cell carcinoma (TCC) pT1 grade 1. In spite of prophylactic therapy, such as intravesical instillation of anticancer drugs and radiochemohyperthermia, she suffered frequent recurrences. At the 6th recurrence, the tumor deteriorated to grade 3 on September 2, 1992. Total cystectomy was done on February 15, 1993 because of uncontrollable bleeding from bladder cancer. Convalescence was uneventful, and no evidence of recurrence was present 2.8 years postoperatively.
Effect of the induction of cytochrome P4501A1 with 3-methylcholanthrene (3-MC) treatment on kinetics of bunitrolol (BTL) 4-hydroxylase activity of rat liver microsomes was investigated. The relationship between the rate and BTL concentration showed monophasic kinetics (KM = 0.74 +/- 0.13 microM) when microsomes from untreated rats were used, whereas microsomes from 3-MC-treated rats showed biphasic kinetics (KM1 = 0.76 +/- 0.13, KM2 = 646 +/- 16 microM). Anti-cytochrome P450 (P450) BTL (P4502D subfamily) antiserum inhibited the reaction > 90% when low concentrations (approximately 10 microM) of BTL were used in both microsomes. However, at high BTL concentrations (approximately 2,000 microM), the inhibition was only up to a half of control in microsomes from 3-MC-treated rats, whereas in microsomes from untreated rats, the rates were suppressed > 90%. Kinetics observed in microsomes from 3-MC-treated rats changed to nearly monophasic, with a KM value corresponding to KM2. Anti-P4501A1 IgG, on the other hand, hardly inhibited the reaction conducted by liver microsomes from 3-MC-treated rats when substrate concentrations were low, whereas at higher concentrations, it inhibited up to 50%, resulting in a monophasic kinetics with a KM value corresponding to KM1. These results clearly indicate that the biphasicity of kinetics in BTL metabolism in liver microsomes from 3-MC-treated rats is caused by the involvement of two P450 species: P450 BTL and P4501A1 in the reaction. This is the first direct evidence to the theoretical hypothesis that the biphasic kinetics of the enzyme reaction is caused by the involvement of at least two enzymes with different kinetic parameters.
A 48-year-old male patient underwent transurethral resection (TUR) for solitary bladder tumor in January 1985. Pathological finding of the specimen was non-invasive transitional cell carcinoma (TCC) G2 > G1. Following the operation, prophylactic intravesical instillation of antitumor agents, intrapelvic irradiation, and hyperthermia were done for the recurrences. In June 1987, left renal pelvic tumor revealed, and nephroureterectomy was performed. Histological examination of renal pelvic tumor showed TCC G1. Five months later, multiple bladder tumors and right renal pelvic tumor were detected. A total cystectomy, partial nephrectomy and nephrostomy were performed in February and March 1988. Pathology of the bladder and right kidney were TCC G3. One month after these operations, tumors recurred in the rest of the right kidney. Complete remission was achieved after systemic chemotherapy with methotrexate, vinblastine, doxorubicin and cisplatin (M-VAC). In January 1992, right renal pelvic tumor recurred again. After two cycles of M-VAC therapy, the rest of the right kidney was extirpated. Postoperative hemodialysis has been uneventful. He has lived without tumor recurrence for three years after the introduction of hemodialysis.
OBJECTIVE: To examine the role of central mechanisms on the production and release of an ouabain-like factor, the effects of intracerebroventricular injections of 6-hydroxydopamine on the tissue content and on the plasma level of the ouabain-like factor were determined in rats. METHODS: The vehicle (0.1% ascorbic acid in 0.9% saline) and 6- hydroxydopamine (250 micrograms/rat) were injected into the left lateral ventricle in ether-anaesthetized Wistar rats. Hypothalamus, pituitary, adrenal and venous blood was sampled 24h and 7 days later. The procedure was repeated using another rat group 7 days later. Characteristics of immunoreactive ouabain-like factor were determined by a combination of high-performance liquid chromatography and a highly sensitive enzyme-linked immunosorbent assay for ouabain. The level of the ouabain-like factor in these tissues and in plasma extracts measured by the enzyme-linked immunosorbent assay was compared between the two groups receiving 6-hydroxydopamine and the vehicle. RESULTS: Twenty-four hours after the intracerebroventricular injections of 6-hydroxydopamine, the ouabain-like factor level in the pituitary, hypothalamus and plasma had decreased significantly, whereas the ouabain-like factor level in the adrenal had not changed. The content of noradrenaline in the hypothalamus was also decreased markedly 7 days later and the content of ouabain-like factor in the pituitary remained low. On liquid chromatography the elution pattern of the ouabain-like factor in plasma and in tissue extracts coincided with that of authentic ouabain. CONCLUSIONS: Intracerebroventricular treatments with 6-hydroxydopamine elicited decreases in ouabain-like factor contents in the pituitary, the hypothalamus and the plasma. These results suggest that the production and release of ouabain-like factor are closely associated with the brain, particularly the hypothalamus-pituitary axis, and that noradrenergic or dopaminergic neurons, or both, play a key role in this mechanism.
Abnormalities in erythrocyte nucleotide metabolism are associated with hereditary nonspherocytic hemolytic anemia. Deficiency of adenylate kinase and pyrimidine 5'-nucleotidase and hyperactivity of adenosine deaminase shorten the red cell lifespan. Deficiency of adenylate kinase has been reported in four different families. Although in one family, total absence of this enzymatic activity was documented in one hematologically normal sibling, there is doubt about the capacity of this single enzyme deficiency to produce hemolysis. A deficiency of pyrimidine 5'-nucleotidase is a cause of hemolytic anemia characterized by red cells with basophilic stippling. This enzyme has been reported to catalyze the hydrolytic dephosphorylation of pyrimidine 5'-ribose monophosphate. Red cells of patients contain an increased concentration of pyrimidine nucleotides and reduced form of glutathione. In hyperactivity, the adenosine deaminase activity in erythrocytes may be increased to 100 times the normal level. The high adenosine deaminase activity of erythrocytes depletes adenine nucleotides, inhibiting its metabolism.
The assay for activated coagulation factors has recently been considered to be a useful tool for detecting hypercoagulable state. Measurement of activated factor XI and alpha 1 antitrypsin complex developed by us is the only one measure for detecting contact phase hypercoagulation. The ACTIVATED FACTOR XII kit (Shield Diagnostics) has recently been commercially available, and the reference range was reported in the instruction manual. However, because the recovery rate of purified factor XIIa (XIIa) in normal pooled plasma by this assay kit was strikingly decreased, the effects of inhibitors in plasma, such as low molecular weight serine proteinase inhibitor (diisopropyl fluoro-phosphate, DFP), the specific inhibitor for XIIa (corn trypsin inhibitor, CTI), the main inhibitor for XIIa (C1 inhibitor, C1I) were examined. These three inhibitors and XIIa were incubated for 18 hours, then the XIIa levels of these complexes and the recovery rate in the normal pooled plasma were assayed by this assay kit. The recovery ratios in the normal pooled plasma were; DFP-XIIa 82%, CTI-XIIa 63%, and C1I-XIIa 0%, XIIa without inhibitor 7%. These results suggest that this XIIa kit does not reflect the levels of complexed form of XIIa and inhibitors in plasma samples.
Between January, 1977 and December, 1994, 90 patients with grade 3 (G3) superficial bladder cancer were treated at Yokohama City University Hospital, Yokohama Municipal Hospital and Kanagawa Cancer Center. These patients were clinically observed. The prognostic factors of the patients with G3 superficial bladder tumors were age and growth pattern of tumors. Patients older than 67 showed significantly poor survival compared with younger patients (p < 0.01). Patients with non-papillary sessile tumors showed significantly poor survival compared with the other groups (p < 0.05). The five-year survival rate of the patients with G3 superficial tumors who were treated by total cystectomy was 75%, whereas all the patients who were treated by bladder preservation therapy died within 4 years, the difference being significant (p < 0.05). Eleven patients with G3 superficial bladder tumors died of cancer, and most of these patients had multiple and non-papillary sessile tumors. These findings suggest that the patients with G3 superficial tumors, which are non-papillary sessile tumors, should be treated by radical cystectomy.
An 81-year-old woman was admitted to our hospital with left flank pain. Excretory urography revealed left hydronephrosis. Abdominal computed tomography (CT) revealed a large heterogenous tumor in the upper pole and marked hydronephrosis and hydroureter in the lower portion of the left kidney. Left total nephroureterectomy was performed under the diagnosis of renal pelvic and ureter tumor. The pathological diagnosis was of renal cell carcinoma (spindle type, grade 3) in the kidney and transitional cell carcinoma (grade 2) in the ureter. Postoperative chemotherapy was not given. Convalescence was uneventful and fifteen months after the operation she is alive with no recurrence or metastasis.
Japanese Society of Cryopreserved Thoracic Tissue Implantation was recently set up. Cryopreserved allograft valves are about to pervade in Japan. To clarify the interest, demands and supply of cryopreserved allograft valve in the area of Kyushu and Yamaguchi, we performed questionnaire investigation regarding this issue. Collection rate of this questionnaire was 87.5% (35/40 hospitals). Ninety-seven percent of the hospitals answered that they were interested in cryopreserved allograft. Ninety-four percent of the hospitals answered that they did not ethically hesitate to use cryopreserved allograft. Ninety-one percent of the hospitals hoped to perform cardiac surgery using allograft aortic valve if allograft is available. With respect to securing donors of allograft, two-third of the hospitals did not decide whether they could be involved in obtaining donors of allograft. As the number of the cadaver kidney donors is about 20 per year in the area of Kyushu and Yamaguchi, shortage of donors of allograft valve is anticipated.
Here we report a case of acute myelogenous leukemia (M2, FAB classification) presenting with cytogenetic abnormalities of ins(21;8), +del(8) without t(8;21). A 8;21 chromosome translocation is frequently found in acute myelogenous leukemia, especially in the M2 subtype. The translocation results in a fusion transcript between AML1 and MTG8 (ETO), assigned on chromosomes 21 and 8, respectively. Among patients with a t(8;21) abnormality, solid leukemic tumor deposits outside the marrow or good response to chemotherapy are observed frequently. Decrease in neutrophil alkaline phosphatase score and positive rate, and eosinophilia in bone marrow or the blast cells with Auer rods expressing CD19, CD56 antigens occur at a relatively high rate. Although our case lacked these clinical, cytological and cytochemical features, expression of chimeric AML1-MTG8 mRNA was detected. AML1-MTG8 fusion transcript may play a critical role in leukemogenesis of AML M2. Studies on this case may help to reveal the oncogenic function of the AML1-MTG8 fusion gene in AML M2.
A 54-year-old woman with leukocytosis, was referred to our clinic in February 1982. Based on findings of pancytosis, high NAP score, high serum vitamin B12, increase in total red cell volume and splenomegaly, she was diagnosed as having polycythemia vera (PV). Since then, she has been treated with pipobroman, hydroxycarbamide and phlebotomy. Leukocytosis with increase in blastic cells and thrombocytopenia was noted in August 1995, and she was admitted to our hospital. Since the blastic cells were CD10(+)19(+)20(+), she was diagnosed as having acute lymphoblastic leukemia and treated with vincristine and prednisolone, resulting in remission. This case suggests that PV is a disease of multipotent stem cells including those with a lymphoid lineage.
The clinical efficacy and the safety of concomitant therapy with fluconazole and recombinant human granulocyte colony stimulating factor (rhG-CSF) was compared with fluconazole monotherapy in neutropenic patients with hematological disorders. The clinical efficacy rate was 73.5% (25/34) in the combination therapy and 48.1% (37/77) in monotherapy. The difference between the two is statistically significant. Side effects were not observed in the combination group, but laboratory abnormalities were found in 6 patients with an incident rate of 11%. The combination therapy with fluconazole and rhG-CSF may be selected as empiric therapy for systemic fungal infection associated with hematological disorders, since this combination therapy showed high efficacy and low incident of side effects. Some patients, however, did not show increased neutrophil counts in spite of rhG-CSF administration.
Explore the source record for details and available documents.
Somatostatin is known to be a potent inhibitor of pancreatic exocrine secretion, but the mechanism of its effect is not fully understood. The mechanism of the inhibition by centrally administered somatostatin was examined in conscious rats. Rats were prepared with cannulae draining bile and pancreatic juice separately, and with a duodenal cannula, an extrajugular vein cannula and a cerebroventricular cannula. Somatostatin was injected into the left lateral ventricle, and the inhibitory mechanism was examined using vagotomized rats and various drugs that affect sympathetic neurons. Intracerebroventricular administration of somatostatin significantly inhibited pancreatic exocrine secretion stimulated by bile-pancreatic juice diversion. The inhibitory effect was not abolished by vagotomy, pretreatment with propranolol, but was abolished by pretreatment with hexamethonium or phentolamine. The plasma level of somatostatin after its intracerebroventricular administration increased 3-fold, but its intravenous infusion at a rate giving a similar plasma somatostatin level to that produced by its intracerebroventricular injection, had no significant effect on pancreatic secretion. These results suggest that somatostatin inhibits pancreatic exocrine secretion centrally via sympathetic efferent nerves and that alpha-adrenergic receptors have an important role in its inhibitory action.
Cholecystokinin (CCK) is an abundant neurotransmitter peptide in the brain. CCK release from synaptosomes obtained from the cerebral cortex, the level of CCK mRNA and the tissue concentration of CCK were examined in young and old rats. CCK release stimulated by KCl was attenuated in old rats but that stimulated by calcium ionophore was comparable in animals at both ages. The CCK mRNA level in the cerebral cortex was decreased significantly in old rats despite the significant increase in CCK content. These results suggested that aging impaired CCK release, resulting in tissue accumulation and a decrease in the synthesis of CCK (the level of CCK mRNA).