[A randomized trial of chemotherapy of advanced prostatic cancer with ifosfamide alone versus ifosfamide, 5-fluorouracil and cisplatin (preliminary report)].
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Aged↗
Biomedical subjects
H Oshima
Publications and source records attributed to H Oshima.
[Abnormal calcium metabolism in myotonic dystrophy (II): Increased level of nephrogenous cyclic AMP and serum immunoreactive parathyroid hormone].
Myotonic dystrophy (MyD) is a multisystemic disorder characterized by muscle atrophy, myotonia and cataract. Although a number of reports have been accumulated showing the presence of bone changes in MyD patients, there are few published papers in which calcium metabolism was precisely examined. In the previous paper, we reported that intestinal calcium absorption was increased in MyD patients due to the elevation of plasma 1,25(OH)2D level. The present study was designed to elucidate the mechanism of increased level of serum 1,25(OH)2D concentration in MyD patients. Calcium tolerance tests were performed in 13 patients with MyD, 13 patients with other neuromuscular disorders (non-MyD) and 12 healthy control subjects according to the method of Broadus et al. Immunoreactive PTH (iPTH) levels and cyclic AMP (cAMP) levels were measured using commercially available RIA kits. The basal plasma calcium levels in MyD were slightly higher than those in the other two groups, but the difference was not statistically significant. The plasma 1,25(OH)2D levels, calcemic responses and calciuric responses in MyD were significantly higher than those in the other two groups. Serum iPTH levels in MyD (0.462 +/- 0.320 ng/ml, Mean +/- SD) were significantly higher than those in the other two groups (normal subjects 0.175 +/- 0.092, non-MyD 0.200 +/- 0.111; p less than 0.02). Nephrogenous cyclic AMP (NcAMP) levels in MyD (2.094 +/- 3.244 nmol/100 ml GF) were also higher than those in normal subjects (0.907 +/- 0.212, p less than 0.05) and in non-MyD (0.929 +/- 0.335, p less than 0.05). There was a significant correlation between serum iPTH levels and NcAMP levels, and therefore it might be possible to accept that these two measurements reflect the level of parathyroid function.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Antibody to tumor necrosis factor (TNF) reduces endotoxin fever.
Antibody to tumor necrosis factor (TNF), injected intravenously, reduced endotoxin fever in the rabbit. The fever-reducing effect was apparent in the latter half of the febrile response.
Animals↗
Changing expression of ABH blood group and cryptic T-antigens of noninvasive and superficially invasive papillary transitional cell carcinoma of the bladder from initial occurrence to malignant progression.
Thirteen patients who developed malignant progression after frequent recurrence of noninvasive or superficially invasive (Ta or T1) papillary transitional cell carcinoma of the bladder were studied for expression of ABH-antigens in tumor tissues throughout their clinical courses and cryptic Thomsen-Friedenreich antigen (T-Ag) expression in the tumor tissues was examined simultaneously in nine of them. Five patients who experienced recurrent bladder tumors for more than 5 years without any malignant progression were served as control. ABH-antigens in initial tumors were negative in only two of 13 patients developing malignant progression and in two of five controls. Cryptic T-Ag was positive in all patients examined. Recurrent tumors revealed eliminated or decreased expression of ABH-antigens and cryptic T-Ag before malignant progression in, respectively, ten of 11 and six of nine patients with antigen-positive initial tumors. In contrast, recurrent tumor of controls with antigen-positive initial tumors showed neither elimination nor decrease in expression of antigens throughout their clinical courses.
ABO Blood-Group System↗
Actinomycosis of urachal remnants.
We report a case of urachal actinomycosis. The patient presented with complaints of micturition pain and a lower abdominal mass. Computerized tomography and an echogram showed the mass extending from the dome of the bladder to just beneath the rectus muscle. Exploration revealed a hard mass in the urachal cord, which was near the dome of the bladder and extended to the umbilicus. The mass and urachal cord were resected, and histopathological examination revealed actinomycosis of the urachal remnants.
Actinomycosis↗
Endogenous tumor necrosis factor induction with Bordetella pertussis vaccine as a triggering agent and its therapeutic effect on MM46 carcinoma-bearing mice.
Induction of endogenous tumor necrosis factor (TNF) by administration of Bordetella pertussis vaccine (BPV) as a triggering agent and its therapeutic effect against MM46 carcinoma were investigated in C3H/He mice. Test triggering agents were injected intravenously into mice after intravenous injection of 4-fold dilution of macrophage activating factor (MAF) or 10(4) units of murine interferon-gamma (Mu-IFN-gamma). Then sera were obtained from the mice, and their TNF activities were assayed on L-929 cells by the method of Ruff and Gifford. The triggering activity of BPV was the highest among those of conventional triggers, such as lipopolysaccharide (LPS) of Escherichia coli, and OK-432. The levels of serum TNF activity triggered by BPV (4 X 10(9) cells), LPS of E. coli (3 micrograms) and OK-432 (3 KE) were 5350, 85 and 102 units/ml, respectively. Growth of MM46, a spontaneous mammary carcinoma cell line of C3H/He was observed for 35 days after tumor inoculation and was suppressed significantly by intravenous injection of MAF and BPV (4 X 10(9) cells). On local injection of BPV (2 X 10(9) cells) into murine tumors, complete regression was observed in 67% of the mice tested with or without MAF priming on day 25 after tumor inoculation, and intratumoral TNF activity was observed even in the case of the single injection of BPV.
Animals↗
Effects of inhibin from primate Sertoli cells on follicle-stimulating hormone and luteinizing hormone release by perifused rat pituitary cells.
We used a pituitary cell perifusion system to investigate the time course and selectivity of the inhibin effect on pulsatile GnRH-stimulated LH and FSH release. Dispersed pituitary cells from 7- to 8-week-old male rats were perifused on a Cytodex bead matrix and stimulated with 10 nM GnRH for 2 min every hour for 8-11 h. The addition of a preparation of inhibin partially purified from primate Sertoli cells reduced pulsatile FSH release within 2 h. After removal of inhibin from the perifusion medium, the effect was reversed within 3 h. GnRH-stimulated LH release was also influenced by inhibin, although the decline in LH was less than that in FSH (80 +/- 3% vs. 68 +/- 4% of control; P less than 0.025). Smaller doses of inhibin suppressed GnRH-induced FSH secretion, but had no effect on LH release. Further, prolonged incubation of pituitary cells with inhibin at the higher dose reduced its FSH inhibitory effect and eliminated the effect on LH. These results indicate that inhibin can reduce both LH and FSH secretion in vitro, although the specificity and magnitude of the effect are a function of both the dose and duration of inhibin treatment. Further, the actions of inhibin and GnRH on the pituitary may be interrelated.
Animals↗
Effects of gonadal steroids on gonadotropin secretion in males: studies with perifused rat pituitary cells.
The feedback effects of testosterone (T) and estradiol (E2) on FSH and LH secretion were compared in dispersed pituitary cells from adult male rats perifused with pulses of GnRH. Cells were stimulated with 10 nM GnRH for 2 min every 1 h. T (10 nM) pretreatment for 24 h reduced the amplitude of FSH and LH pulses to 77 +/- 4% (mean +/- SE) and 47 +/- 3% of control values, respectively (P less than 0.01), whereas 6-h T treatment was without effect. By contrast, interpulse secretion of FSH was increased after 24 h T to 184 +/- 7% of the control value (P less than 0.01), but interpulse LH release was unchanged (104 +/- 5%). E2 (0.075 nM) treatment of pituitary cells reduced GnRH-stimulated FSH and LH release within 2 h to 75 +/- 2% and 73 +/- 3% of control values, respectively (P less than 0.01). E2 pretreatment for 24 h stimulated (P less than 0.025) GnRH-induced FSH (136 +/- 10%) and LH (145 +/- 8%) release and also increased (P less than 0.01) interpulse FSH (127 +/- 5%) and LH (145 +/- 8%) secretion. These data indicate that the suppression of FSH and LH secretion by T in males is due in part to a direct effect on the pituitary. The findings that T suppresses GnRH-stimulated FSH less than LH, and that T stimulates interpulse FSH, but not LH, provide evidence for differential regulation of FSH and LH secretion by T. The dissimilar actions of T on GnRH-stimulated pulses and interpulse gonadotropin secretion suggest that interpulse secretion is unrelated to stimulation by GnRH, although its physiological significance is unknown. Since E2, in physiological levels for males, increased pituitary FSH and LH secretion, the suppression of gonadotropin secretion by E2 in vivo in males may result from an effect on the hypothalamic pulse generator; however, additional studies are needed before extending these conclusions to higher mammals and men.
Animals↗
Hyperparathyroidism in patients with myotonic dystrophy.
This study was designed to determine the possible presence of abnormal calcium metabolism in patients with myotonic dystrophy (MyD). Twenty-five patients with MyD, 13 patients with other neuromuscular disorders (non-MyD), and 12 normal subjects were studied. The mean plasma 1,25-dihydroxyvitamin D level in the MyD patients [83.2 +/- 23.1 (+/- SD) pmol/L] was significantly higher than those in the other two groups [normal subjects, 49.7 +/- 15.4 (P less than 0.01); non-MyD patients, 51.6 +/- 27.4 (P less than 0.01)]. On the contrary, the mean plasma 24,25-dihydroxyvitamin D levels were similar in the MyD patients and the normal subjects. The increments in serum calcium levels and urinary calcium excretion after oral calcium loading in the MyD patients were significantly greater than those in the normal subjects, suggesting that intestinal calcium absorption was augmented in the MyD patients. The mean nephrogenous cAMP excretion in the MyD patients (1.71 +/- 1.08 nmol/100 mL glomerular filtrate) also was higher than those in the other two groups (0.93 +/- 0.34 in the non-MyD patients; 0.91 +/- 0.21 in normal subjects). These results suggest that parathyroid function may be increased in MyD patients.
Adult↗
Unlinked regulation of the sensitivity of primary glucocorticoid-inducible responses in mouse mammary tumor virus infected Fu5-5 rat hepatoma cells.
The enzyme tyrosine aminotransferase (TAT) is induced by unusually low concentrations of glucocorticoids in Fu5-5 cells. We have isolated clones of Fu5-5 cells infected with mouse mammary tumor virus (MMTV) in order to simultaneously compare the glucocorticoid regulation of the host cell gene, TAT, with that of another primary inducible gene, MMTV. In the two clones that were examined in detail, MMTV RNA induction occurred at 4- to 11-fold higher concentrations of dexamethasone than those needed for induction of TAT mRNA. Furthermore, the amount of agonist activity displayed by the irreversible antiglucocorticoid dexamethasone 21-mesylate was greater for the induction of TAT mRNA than for MMTV RNA. These results extend our previous observations of unequal sensitivity of induction of TAT enzyme activity in two hepatoma cell lines and show that differential glucocorticoid regulation of gene induction within the same cell can occur at a pretranslational step. The present data also indicate that the unusual properties of TAT gene induction are not shared by all primary, glucocorticoid-inducible responses of the same cell and imply that additional factors mediating differential regulation of glucocorticoid-responsive genes are involved.
Animals↗
[Reevaluation of glucocorticoid therapy on polymyositis: dose-response relationship between glucocorticoid and long-term therapeutic effect].
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Adult↗
Characteristics of M-GTFI, a new inhibitor of Streptococcus mutans glucosyltransferase.
M-GTFI, originally screened as an inhibitor of Streptococcus mutans glucosyltransferase, strongly inhibited alpha-glucosidase, in a non-competitive manner especially when the synthetic substrate p-nitrophenyl-alpha-D-glucopyranoside was used. It also inhibited beta-glucosidase, beta-amylase and, to a lesser extent, beta-glucuronidase. The inhibitor was stable in neutral and alkaline pH ranges and dependency of the inhibition on pH and temperature was not observed. Some proteinases and polysaccharides-hydrolyzing enzymes as well as human saliva did not inactivate the inhibitor. There was a correlation between the release of sulfate anions from the inhibitor molecule on incubation with HCl (0.2 N) at 100 degrees C and loss of inhibitory properties of the molecule. It is suggested that the presence of sulfate ester linkages in the inhibitor molecule play an important role in the inhibition process.
Enzyme Inhibitors↗
[A study of prevention of ejaculatory disturbance after retroperitoneal lymph node dissection in testicular tumor].
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Adolescent↗
[Urodynamic evaluation of patients undergoing radical prostatectomy. A preliminary report].
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Aged↗
[Statistical analysis of clinicopathological profiles affecting prognosis of patients with bladder carcinoma by therapeutic modality].
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Adult↗
[Relations of clinicopathological findings to expression of ABH blood group and Thomsen-Friedenrich antigens in initially superficial papillary transitional cell carcinomas of the bladder developing subsequent malignant progression].
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ABO Blood-Group System↗
TNF induces endogenous TNF in vivo: the basis of EET therapy as a combination of rTNF together with endogenous TNF.
Enough amounts of tumor necrosis factor (TNF) in mice serum for the therapy were observed by treatment with 100 units of recombinant human TNF-alpha (rHuTNF-alpha) followed by administration of OK-432 (a streptococcal preparation). Optimal time interval between rTNF and OK-432 to produce endogenous TNF was 3 h, and priming activity of rTNF persisted for at least 10 h. The same effect was observed using novel human recombinant TNF-SAM2 (rHuTNF-SAM2) developed by our group. Production of endogenous TNF using rTNF-alpha or rTNF-SAM2 as a priming reagent was almost equal among various mice strains. Induced TNF in mice serum was completely neutralized by anti-MuTNF antiserum, but not by anti-HuTNF monoclonal antibody. rMuTNF could also induce the priming state; however, the dose-response kinetics of the priming effect to produce endogenous TNF was different between rHuTNFs and rMuTNF-alpha, suggesting species specificity among rTNFs used. The therapeutic effect against Meth A and MH134 tumors in mice treated by rHuTNFs in combination with OK-432 was superior to that by single administration of either OK-432 or rHuTNFs or by successive administrations of OK-432. Especially, the antitumor effect against MH134 hepatoma was superior to that of any other treatment using known biological response modifiers so far experienced. These results suggest that such combination antitumor therapy as rTNF together with OK-432 should be applicable to cancer patients.
Animals↗
[Urinary bladder tumor manifesting multiple bone metastases similar to prostatic carcinoma--a case report].
A 72-year-old patient was found to have a non-papillary bladder tumor extending from the vesical floor to the retrotrigone and manifested multiple bone metastases without evidence of any hematogenic metastases in other organs. The pattern of the above metastases were very similar to that of a prostatic carcinoma and suggests that the so-called specific pattern of bone metastases observed in prostatic carcinomas might be caused by the location of the original tumor and not by features of the prostatic carcinoma cells themselves.
Adenocarcinoma↗