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Biomedical subjects

N Murayama

Publications and source records attributed to N Murayama.

At least 163 records · Page 9Linked to original sources
PubMed1988

[Preoperative intra-arterial infusion chemotherapy in locally advanced primary breast cancer-tissue concentrations of 5-fluorouracil and adriamycin, and the histological evaluation].

The effect of preoperative intra-arterial infusion of mitomycin C, 5-fluorouracil (5-FU) and adriamycin (ADM) were studied in seven patients with locally advanced breast cancer, including five inflammatory carcinomas, and a patient with stromal sarcoma of the breast. Reducing rate of the primary tumor of more than 30% was observed in all cases, and remarkable degenerative changes of tumor cells were histologically noted in six out of eight surgical specimens. The tissue concentrations of 5-FU and ADM were also studied in five breast cancer patients. There was no correlation between the concentration of 5-FU or ADM and histological effect. In intra-arterial infusion, ADM seemed to have a high affinity to the regional lymphnode and breast tumor, compared to normal breast tissue and might also be applicable to the control of lymphnode metastasis. Three out of six cases which received radical mastectomy subsequently had recurrence except in the regional lymphnodes and the prognosis was unsatisfactory (5 year survival was 2/4). Other alternative or multi-disciplinary treatment seems to be necessary for improving the survival rate.

Adult↗
PubMed1988

[A comparative study of the effects of drug therapy and bladder training therapy].

Treatment of enuresis was studied in 168 patients. The patients were divided into two groups, the drug therapy group which consisted of 88 patients who were treated with drugs only, and the bladder training therapy group which consisted of 80 patients who were treated mainly with bladder training supplemented with drug therapy. In the drug therapy group imipramine was the first choice and was used at bed time. The dose of imipramine was initially 1 mg/kg and was gradually decreased if it worked well, and changed to other drugs if it did not work well. In the bladder training therapy group, bladder training was performed in all patients for 3 months, and 22 patients who cured further bladder training was continued, whereas the rest of the patients (58 patients) drug therapy was started in addition to bladder training. After 3 months, drug therapy was effective for 54 patients (61%) including 10 patients (11%) who were cured, and bladder training therapy plus drug therapy was effective for 55 patients (69%) including 22 patients (28%) who were cured. The number of cured patients in the bladder training therapy group was significantly larger than that of the drug therapy group (p less than 0.01). After 6 months, drug therapy was effective for 56 patients (64%) including 16 patients (18%) who were cured, and bladder training therapy plus drug therapy was effective for 66 patients (83%) including 30 patients (38%) who were cured. The number of effective and cured patients in the bladder training therapy group was significantly larger than that in the drug therapy group (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Suppression of levels of phenobarbital-inducible rat liver cytochrome P-450 by pituitary hormone.

The effect of pituitary factor on the constitutive and inducible levels of hepatic phenobarbital (PB)-inducible major cytochrome P-450, P-450b and P-450e, in male and female rat livers was studied by immunoblot analyses. Although only trace amounts (approximately 4 pmol/mg protein) of P-450b and P-450e were detected in untreated adult rats, hypophysectomy increased the contents of P-450b and P-450e 58- and 14-fold, respectively, in male rats and 118- and 30-fold, respectively, in female rats. The increases were also observed in treatment with dexamethasone, which suppressed the pituitary function. Treatment with PB increased more effectively the hepatic contents of P-450b and P-450e, but their contents were still 4-fold higher in the male than the female. Treatment of hypophysectomized female rats with PB increased the contents of P-450b and P-450e 4-fold higher than the contents in PB-treated nonhypophysectomized female rats. Consequently, the sex-related difference in their contents was reduced less than 1.4-fold in the hypophysectomized rats treated with PB. Similar results were also obtained from the quantitation of microsomal O-pentylresorufin O-depentylation and testosterone 16 beta-hydroxylation. Either intermittent injection or continuous infusion of human growth hormone, but not of ovine prolactin, into hypophysectomized male and female rats decreased the contents of both cytochromes. These results indicate that growth hormone acts as a repressive factor for the constitutive and inducible levels of P-450b and P-450e in a manner different from the regulation of P-450-male and P-450-female.

Aging↗
PubMed1987

Calcitonin inhibits Na+ gradient-dependent phosphate uptake across renal brush-border membranes.

This study was undertaken to determine whether calcitonin inhibits Na+-(Pi) cotransport across luminal brush-border membrane (BBM) of proximal tubules. Further, we determined the relative inhibitions of inorganic phosphate (Pi) transport in BBM vesicles (BBMV) derived from superficial cortical tissue (BBMV-SC) and juxtamedullary tissue (BBMV-JM). The effects of maximally phosphaturic doses of calcitonin were compared with those of parathyroid hormone (PTH). Experiments were performed in acutely thyroparathyroidectomized (TPTX) rats fed either normal (NPD, 0.7%) or low (LPD, 0.07%) Pi diets. After measurement of the fractional excretion of phosphate (FEPi) by clearance, the BBMV-SC and BBMV-JM were prepared from kidneys of the same animals and uptakes of 32Pi were determined. Both calcitonin and PTH inhibited BBMV transport of Pi to a greater degree in BBMV-JM than in BBMV-SC, in rats fed NPD or LPD. Kinetic analysis shows that administration of calcitonin resulted in marked decrease of apparent Vmax for Pi without any changes in apparent Km for Pi. However, in spite of a decreased capacity for Na+ gradient-dependent 32Pi uptake in BBMV-JM and much lesser in BBMV-SC in response to administration of calcitonin and PTH in Pi-deprived rats, these phosphaturic peptides did not increase FEPi. We conclude that calcitonin administration decreases the capacity for Na+-Pi cotransport across BBM in proximal tubules of the acutely TPTX rat.

Animals↗
PubMed1987

Further studies on the persistence of neonatal androgen imprinting on sex-specific cytochrome P-450, testosterone and drug oxidations.

Neonatal castration completely suppressed the expression of P-450-male and expressed P-450-female; and testosterone treatment in a neonatal period partially reversed the effect of castration, i.e., neonatal imprinting (Kamataki et al., 1984; Waxman et al., 1985). In the present communication, we investigate the reversibility and persistency of neonatal imprinting on the expression of P-450-male and P-450-female. To our surprise, testosterone treatment at adulthood (8 weeks old) caused full expression of P-450-male and restored the activities of 2 alpha- and 16 alpha-testosterone hydroxylases in neonatally castrated rats. The levels of ethylmorphine N-demethylation, propoxycoumarin O-depropylation and benzo(a)pyrene hydroxylation were increased to the levels of adult male rats by adult testosterone-treatment. Moreover, treatment with testosterone of neonatally castrated rats at the age of 19 weeks did not cause a complete recovery of P-450-male content and drug-metabolizing activities. Testosterone administration into neonatal female rats did not significantly alter the contents of sex-dependent cytochrome P-450 and drug and steroid metabolizing activities in adulthood. Additional testosterone treatment in adulthood only slightly affected these parameters. All these results indicate that neonatal androgen imprinting on sex-dependent cytochrome P-450 and drug and steroid metabolizing activities in rat liver microsomes is not a permanent programming process and is modified by the presence and absence of sex-steroid hormones.

Androgens↗
PubMed1987

Regulation of hepatic sulfotransferase catalyzing the activation of N-hydroxyarylamide and N-hydroxyarylamine by growth hormone.

The regulatory mechanism of hepatic sulfation of N-hydroxyarylamine and N-hydroxyarylamide by endocrine factors has been studied in rats. The cytosolic sulfations of N-hydroxy-2-acetylaminofluorene (N-hydroxy-AAF) and 2-hydroxyamino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (N-hydroxy-Glu-P-1), which were determined by the reductive formations of 2-acetylaminofluorene and Glu-P-1, were seven to nine times and three times higher, respectively, in male than female rats. Hypophysectomy of male rats decreased their activities to 23% and 41% of the levels of the untreated animals, respectively. Intermittent treatment of hypophysectomized male and female rats with human growth hormone (hGH) significantly increased their sulfating activities of both compounds. Infusion of hGH also enhanced the sulfating activity of N-hydroxy-AAF but not of N-hydroxy-Glu-P-1. The sulfating activity of N-hydroxy-AAF was also decreased by castration at neonate and was increased by the administration of testosterone propionate to gonadectomized male and female rats. Testosterone propionate and estradiol benzoate had no effect on hypophysectomized rats, but estradiol benzoate repressed the sulfating activities of N-hydroxy-AAF and N-hydroxy-Glu-P-1 in hGH-treated hypophysectomized male rats. These results indicate that sex steroids elicit their effects on the sulfations of N-hydroxyl-aryl compounds through modulating the action of growth hormone at hypothalamus-pituitary and hepatic levels in rat livers.

2-Acetylaminofluorene↗
PubMed1986

Atrial natriuretic peptide elevates cGMP contents in glomeruli and in distal tubules of rat kidney.

Effect of synthetic rat atrial natriuretic peptide (1-28) (ANP) on the cGMP content was studied using defined nephron segments of rat kidney. ANP elevates cGMP contents in glomeruli in a concentration and time-dependent manner. The increase of cGMP was observed in glomeruli, distal convoluted tubule (DCT) and cortical collecting tubule (CCT) (delta %; 279 +/- 35, 148 +/- 10 and 152 +/- 18, respectively), and no effect was observed in proximal convoluted (PCT) and straight tubule (PST). These results suggest that ANP may act directly on the tubular cells as well as glomeruli. In glomeruli, effects of ANP and carbamylcholine on cGMP contents were additive suggesting that these two agents may act on different receptors. Angiotensin II and norepinephrine failed to affect the ANP-induced cGMP production in the glomeruli.

Angiotensin II↗
PubMed1986

Selective depressant action of antidromic impulses on gustatory nerve signals.

The depressant action of antidromic volleys of impulses on gustatory nerve signals from the tongues of bullfrogs was studied. Electrical stimulation of the glossopharyngeal nerve at a rate of 100 Hz for 10 s and at supramaximal intensity slightly depressed the integrated glossopharyngeal nerve responses to quinine and to mechanical taps to the tongue. The same antidromic stimuli resulted in a 30-40% reduction in the responses to salt, acid, water, and warmed saline, but depressed greater than 80% of the afferent impulses firing spontaneously. The magnitude of responses to quinine and NaCl and the number of spontaneous discharges decreased gradually with an increase in either the frequency or the duration of antidromic stimuli. Similar results were obtained with intensities above the threshold for exciting gustatory and slowly adapting mechanosensitive fibers. The time required to recover from termination of the antidromic stimuli to two-thirds of the maximal amount of depression ranged between 6 and 7 min, with no significant differences among the depressions. The possible mechanisms involved in the antidromic depression of gustatory nerve signals are discussed.

Afferent Pathways↗
PubMed1986

The regulation by growth hormone of microsomal testosterone 6 beta-hydroxylase in male rat livers.

The relationship between growth hormone and testosterone (T) 6 beta-hydroxylase was investigated in normal and hypophysectomized (hypox) male rats. The administration of human growth hormone (hGH) by either intermittent injections or continuous infusion to normal and hypox rats decreased the activity of T 6 beta-hydroxylase in hepatic microsomes. Hypophysectomy did not reduce, but rather increased the 6 beta-hydroxylase activity, while the 16 alpha-hydroxylase activity decreased. These results, together with the data from a Western blot, indicate that growth hormone acts as a repressive factor for the expression of T 6 beta-hydroxylase in a manner different from the regulation of T 16 alpha-hydroxylase.

Animals↗
PubMed1986

Effect of growth hormone and ectopic transplantation of pituitary gland on sex-specific forms of cytochrome P-450 and testosterone and drug oxidations in rat liver.

The effects of growth hormone and ectopic transplantation of pituitary gland on the amounts of sex-specific cytochrome P-450, P-450-male and P-450-female, and the activities of testosterone and drug hydroxylases in male rat liver microsomes were studied. Hypophysectomy decreased the content of P-450-male, without changing the total cytochrome P-450 level. The continuous infusion of growth hormone into hypophysectomized rats and the transplantation of pituitary gland under the renal capsule caused a further decrease in P-450-male content and an expression of P-450-female. In contrast, the intermittent injection of growth hormone into hypophysectomized rats increased P-450-male content to the level seen in intact male rats. The activities of testosterone 2 alpha- and 16 alpha-, but not 6 beta-, 7 alpha-, or 15 alpha-hydroxylase, were changed in association with the level of P-450-male by these treatments. Anti-P-450-male immunoglobulin G inhibited testosterone 2 alpha- and 16 alpha-hydroxylations, but not 6 beta-, 7 alpha- or 15 alpha-hydroxylation. These results indicate that growth hormone regulates the expression of P-450-male responsible for testosterone 2 alpha- and 16 alpha-hydroxylations. The metabolism of 7-propoxycoumarin, benzo(a)pyrene and aminopyrine also changed with the content of P-450-male, although the correlation was less than that observed with testosterone 2 alpha- and 16 alpha-hydroxylation.

Animals↗
PubMed1986

Dynamics of nucleotides in distal nephron of mice with nephrogenic diabetes insipidus.

In mice with hereditary nephrogenic diabetes insipidus (NDI), the high activity of cAMP-phosphodiesterase (cAMP-PDIE) in medullary collecting tubules (MCT) prevents the increase in cAMP content in response to vasopressin [Arg8]vasopressin (AVP). Even when the cAMP response to AVP is partly corrected by cAMP-PDIE inhibitor 1-methyl-3-isobutylxanthine (MIX), under all tested conditions the cAMP levels in MCT of NDI mice remained much lower than in controls (B. A. Jackson, R. M. Edwards, H. Valtin, and T. P. Dousa, J. Clin. Invest. 66: 110-122, 1980). In the present study, we explored which factors may account for this defect. We determined contents of ATP, nicotinamide adenine dinucleotide (NAD), and the levels of cAMP in MCT and in medullary thick ascending limb of Henle's loop (MAL) microdissected from control and NDI mice. In the presence of 1 microM AVP and 0.05 mM MIX, the cAMP levels accumulated in MCT of NDI mice were four times lower compared with controls, but the levels of ATP and NAD were not different. ATP levels in MAL of NDI mice were slightly (delta -23%) lower than in MAL from controls, and in distal convoluted tubules (DCT) of NDI mice the ATP levels were also decreased (delta -49%). Although AVP alone had little effect on cAMP levels in mouse MAL in the presence of 0.1 mM forskolin, the AVP elicited a 20-fold increase of cAMP of both the control and NDI mice. Addition of 0.1 mM forskolin further increased the cAMP accumulation in MCT incubated with AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1986

[Undifferentiated carcinoma of the pancreas with a choriocarcinomatous feature producing human chorionic gonadotropin].

An undifferentiated carcinoma of the pancreas in a 50-year-old man was found to be associated with a very elevated level of serum hCG. Syncytiotrophoblastic tumor cells were seen sporadically in the cancer nest, and they showed diffuse positive staining for hCG by immunohistochemical techniques. Positive staining for hCG was also observed in a few mononucleated cancer cells. The results indicated ectopic production of hCG by pancreatic cancer with a choriocarcinomatous feature and tended to support the hypothesis of the retrodifferentiation theory holding that choriocarcinoma is derived from a pre-existing pancreas cancer through metaplastic proliferation.

Carcinoma↗
PubMed1985

Effect of antidromic stimulation of the glossopharyngeal nerve on afferent discharges occurring with and without sensory stimulation of the frog tongue.

Repetitive stimulation of the bullfrog glossopharyngeal nerve at a rate of 100 Hz for 10 s and at a supra-maximal intensity resulted in little depression of the glossopharyngeal nerve responses to application of quinine and mechanical taps to the tongue, in a 30-40% decrease in the responses to salt, acid, water and warmed saline and in a 80% decrease in the number of spontaneous discharges from the tongue. Such a selective depression existed throughout changes in the frequency and the duration of the antidromic stimuli. The phenomena were attributed to antidromic impulses in high-threshold glossopharyngeal nerve afferents.

Animals↗
PubMed1985

Defective enzyme causes lecithin-cholesterol acyltransferase deficiency in a Japanese kindred.

Lecithin-cholesterol acyltransferase mass levels and activity and apolipoproteins A-I, A-II, B and D were measured in a Japanese family who have a familial lecithin-cholesterol acyltransferase deficiency. This analysis was performed to gain insight into the molecular basis of the enzyme deficiency and to compare findings in this family with other families with familial lecithin-cholesterol acyltransferase deficiency. The mass of the enzyme in plasma was determined by a sensitive double antibody radioimmunoassay, and enzyme activity was measured by using a common synthetic substrate comprised of phosphatidylcholine, cholesterol and apolipoprotein A-I liposomes prepared by a cholate dialysis procedure. The lecithin-cholesterol acyltransferase-deficient subject had an enzyme mass level that was 35% of normal (2.04 micrograms/ml, as compared with an average normal level of 5.76 +/- 0.95 micrograms/ml in 19 Japanese subjects) and an enzyme activity of less than 0.1% of normal (0.07 nmol/h per ml, as compared with normal levels of 100 nmol/h per ml). This subject also had lower levels of apolipoproteins: apolipoprotein A-I was 53 mg/dl (42% of normal), apolipoprotein A-II was 10.6 mg/dl (31% of normal), apolipoprotein B was 68 mg/dl (68% of normal), and apolipoprotein D was 3.6 mg/dl (60% of normal). The three obligate heterozygotes had enzyme mass levels ranging from 65% to 100% of normal and enzyme activity levels ranging from 23% to 65% of normal (23.4, 56.8, and 64.7 nmol/h per ml, respectively). The proband's sister had an enzyme mass level of 6.55 micrograms/ml (114% of normal) and an enzyme activity of only 64.8 nmol/h per ml (65% of normal), suggesting that she was also a heterozygote for lecithin-cholesterol acyltransferase deficiency. The obligate heterozygotes and the sister had normal apolipoprotein levels. We conclude that the lecithin-cholesterol acyltransferase deficiency in this family is due to the production of a defective enzyme that is expressed in the homozygote as well as in the heterozygotes, and, further, that this family's mutation differs from that reported earlier for other Japanese lecithin-cholesterol acyltransferase-deficient families.

Female↗