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Biomedical subjects

M Shoji

Publications and source records attributed to M Shoji.

At least 325 records · Page 18Linked to original sources
PubMed1986

Immunocytochemical evidence for phorbol ester-induced protein kinase C translocation in HL60 cells.

The ability of tumor promoting 12-O-tetradecanoylphorbol-13-acetate (TPA) to redistribute protein kinase C in human promyelocytic leukemic HL60 cells was investigated. It was found that TPA caused a rapid translocation (within 10 min) of protein kinase C from the cytosolic (soluble) fraction to the particulate (membrane) fraction, as determined indirectly by assaying for the enzyme activity or by immunoblotting of the enzyme protein in the isolated subcellular fractions. Immunocytochemical localization of the enzyme demonstrated directly that the TPA caused an enzyme translocation t the plasma membrane. These findings suggest that translocation to the plasma membrane of the enzyme may represent initial events related to the TPA effect on terminal differentiation of HL60 cells to monocytes/macrophages.

Cell Compartmentation↗
PubMed1986

Phospholipid/calcium-dependent protein kinase (protein kinase C) system: a major site of bioregulation.

The substrate specificity determinants of protein kinase C are probed using synthetic peptides encompassing the major phosphorylation site serine 115 in bovine MBP. The results indicate that basic residues arginine 107 and 113 N-terminal to the phosphorylation site are essential for the substrate activity of the peptides. Substitutions of these basic residues by alanine cause a marked decrease in their substrate activity and the resulting peptide analogs become specific and rather potent inhibitors of protein kinase C. Leukemic cells are particularly abundant in protein kinase C and its substrate proteins, and the enzyme system has been shown to play a key role in cell growth. The agents that stimulate protein kinase C include tumor promoting phorbol esters (such as TPA) and mezerein, and the putative second messenger diacylglycerol. Many antineoplastic agents, on the other hand, inhibit the enzyme which include adriamycin, tamoxifen, alkyl-lysophospholipid, selenium, retinal and lipoidal amine CP-46, 665-1. Immunocytochemical studies of protein kinase C in leukemic cells indicate that it is localized in the plasma membrane, cytoplasm, nucleus and Golgi apparatus, and the subcellular distribution of the enzyme might be related to the phases of the cell cycle. TPA induces translocation of the enzyme to plasma membrane, suggesting an additional mode of action for the tumor promotor.

Animals↗
PubMed1986

Effects of human atrial natriuretic peptide on renal function and vasopressin release.

To assess the effects of atrial natriuretic peptide (ANP) on the renal function, cardiovascular system, renin-angiotensin-aldosterone system, and vasopressin release, synthetic human ANP (alpha-hANP) was administered at a dose of 0.08 microgram X kg-1 X min-1 iv for 40 min into anesthetized dogs (n = 6). In the control study (n = 6), saline alone was infused. alpha-hANP brought about a significant increase in renal plasma flow, urinary Na and K output, urine flow, and osmolar clearance and a significant decrease in urinary osmolality, free water clearance, and filtration fraction (FF), with no changes in glomerular filtration rate. Plasma Na concentrations and osmolality did not change significantly, but plasma K concentrations fell progressively. Mean arterial blood pressure decreased without any changes in heart rate. Plasma renin activity (PRA), plasma aldosterone concentrations (PAC), and plasma vasopressin concentrations did not rise, but rather PRA and PAC tended to fall during alpha-hANP infusion. In the control study, there were no changes in these parameters except a progressive fall in FF and plasma K concentrations. These results indicate that the alpha-hANP-induced increase in renal blood flow plays an important role in producing natriuresis, but vasopressin may not be involved in the process of diuresis.

Aldosterone↗
PubMed1986

Role of intracerebral angiotensin receptors in the regulation of vasopressin release and the cardiovascular system.

In order to investigate the physiological role of the brain renin-angiotensin system in the regulation of vasopressin (ADH) release, angiotensin II (Ang II, 10 ng/kg/min) or 1-Sar-8-Ile-Ang II (50 ng/kg/min), an Ang II antagonist, was administered intracerebroventricularly to dogs (n = 42) anesthetized with urethane and chloralose after morphine sedation. The effects of the intravenous infusion of either 0.15 M or 2.5 M NaCl (0.1 ml/kg/min, 75 min) were also studied. In control dogs, artificial cerebrospinal fluid (ACSF) was administered at a rate of 10 microliter/min for 105 min. ACSF given intracerebroventricularly plus 0.15 M NaCl given intravenously did not affect ADH release, but 2.5 M NaCl given intravenously raised the plasma ADH level in parallel with the rise in plasma osmolality. Heart rate and blood pressure did not change significantly in ACSF along with 0.15 M NaCl, but heart rate increased significantly in ACSF along with 2.5 M NaCl. Ang II along with 0.15 M NaCl significantly raised plasma ADH and decreased heart rate without any changes in blood pressure. Ang II along with 2.5 M NaCl brought about a significant rise in plasma ADH level, arterial blood pressure, heart rate, and plasma osmolality. But simultaneous application of Ang II and 2.5 M NaCl did not result in a larger rise in plasma ADH than that expected from the effects of the two stimulations given separately. Namely, Ang II did not potentiate ADH release elicited by osmotic stimulation. Ang II antagonist given intracerebroventricularly neither affected ADH release and the cardiovascular system in 0.15 M NaCl nor inhibited ADH release in response to osmotic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1986

Effects of acute water load, hypertonic saline infusion, and furosemide administration on atrial natriuretic peptide and vasopressin release in humans.

A new specific RIA for alpha-human atrial natriuretic hormone (alpha hANP) was used to determine whether changes in plasma volume elicited by acute water loading, hypertonic saline infusion, and furosemide administration caused changes in ANP release and resultant changes in renal and cardiovascular function in normal subjects. In addition, changes in plasma arginine vasopressin (AVP), PRA, and aldosterone concentrations were studied simultaneously. Mean plasma alpha hANP and AVP levels were 51.3 +/- 16.0 (+/- SE) and 3.1 +/- 0.6 pg/ml, respectively, in the basal state. Plasma alpha hANP rose to 77.8 +/- 27.6 in response to a 4.5% increase in plasma volume induced by water loading, increased further to 134.1 +/- 28.9 in response to a 23% volume increase induced by hypertonic saline, and fell to 70.2 +/- 15.8 pg/ml in response to a decrease in plasma volume after furosemide treatment (P less than 0.01-0.05). On the other hand, plasma AVP fell to 1.8 +/- 0.1 pg/ml after the water load, rose to 4.1 +/- 0.6 after hypertonic saline, and rose further to 5.8 +/- 0.8 pg/ml after furosemide (P less than 0.01-0.05). Water and hypertonic saline loading decreased PRA, but plasma aldosterone concentrations did not change; subsequent furosemide administration increased both (P less than 0.01-0.05). Arterial pressure and heart rate did not change significantly. Increases in urinary Na excretion and osmolar clearances were associated with a rise in plasma alpha hANP after water loading and hypertonic saline infusion (P less than 0.01-0.05), but changes in urine flow were mainly associated with alterations in AVP release. associated with alterations in AVP release.

Adult↗
PubMed1986

[Hormonal changes during incremental exercise in athletic women].

Recently, the number of women who participate in strenuous sports has increased rapidly. The evidence indicating a causal relationship between athletic activity and increased incidence of menstrual dysfunction has led to increased interest. Five basketball players who are among the top players in Japan were subjected to an investigation of the endocrinological responses effected by incremental exercise using a cycle ergometer. Serum levels of FSH and LH decreased significantly in the follicular phase, but there was no change in the luteal phase. Estradiol was seen to increase significantly in the luteal phase but no change occurred in the follicular phase. Progesterone did not show a significant change during exercise. Although TSH did not show any significant change, prolactin showed a significant increase in both phases. These results suggest that strenuous daily training leads to a frequent increase of prolactin in athletic women and this frequent increase of prolactin may be one of the major factors in causing menstrual dysfunction.

Adult↗
PubMed1986

[Transfer of cefmenoxime to lung tissue and thoracic muscle in thoracic surgery].

Twenty patients who were performed pulmonary resection for the disease of the lung were administered 2 g of cefmenoxime (CMX) intravenously during the operation. The CMX levels in serum, lung tissue and thoracic muscle were measured by agar-well technique. The CMX levels in lung tissue and thoracic muscle were higher than the MIC80 of CMX for Klebsiella pneumoniae, Haemophilus influenzae and Streptococcus pneumoniae which were commonly as isolated causative organisms from the patients with pulmonary infection. These results indicate that CMX will be useful agent for the prevention and treatment of pulmonary infection.

Adolescent↗
PubMed1986

Effects of selenium compounds on phospholipid/Ca2+-dependent protein kinase (protein kinase C) system from human leukemic cells.

Selenium compounds (selenium dioxide, selenious acid, and selenic acid) were found to inhibit phospholipid/Ca2+-dependent protein kinase (protein kinase C) and the phorbol ester-stimulated phosphorylation of endogenous substrate proteins from HL60 cells. Kinetic analysis indicated that selenium dioxide (SeO2) inhibited the enzyme noncompetitively with respect to phosphatidylserine (apparent Ki, 60 microM) and Ca2+ (apparent Ki, 68 microM). The inhibitory effect of SeO2 on protein kinase C was additive to that of another inhibitor of the enzyme (alkyl-lysophospholipid) when present together. SeO2 was also equally inhibitory to myosin light chain kinase, a calmodulin/Ca2+-dependent class of protein kinase. It, however, affected only very slightly cyclic adenosine 3':5'-monophosphate-dependent protein kinase. It is suggested that inhibition of Ca2+-dependent reactions might be related to the anticarcinogenic property of selenium.

Animals↗
PubMed1986

[Effect of menstrual cycle on cardiorespiratory system during incremental exercise].

According to the results of questionnaires to college athletes, they believe the follicular phase is better than luteal phase for competitive sports. However, it is not clear whether there is significant difference in athletic performance between the two phases of the menstrual cycle. The effects of the menstrual cycle on the cardiorespiratory system were investigated in exercising women who are top players of basketball in Japan. They performed incremental exercise on a cycle ergometer. During the exercise, the ECG and heart rate (HR) were monitored. The expired air was sampled continuously and expiratory gas volume/minute (VE), oxygen uptake (VO2), carbon dioxide output (VCO2), gas exchange ratio(R) and respiratory rate (Resp. E.) were measured. Blood samples were collected to measure the blood lactic acid concentration during the exercise. HR in the luteal phase is higher than in the follicular phase at rest and throughout the exercise. VE, R and Resp. R. at rest and during exercise indicated a tendency to a higher level in the follicular phase. The blood lactic acid concentration during exercise in the follicular phase indicated a tendency to increase more rapidly than in luteal phase. However, no statistical differences in the cardiorespiratory system were detected when the follicular and luteal phase were compared. These results did not indicate conclusively in which phase it is better for athletic women to take part in competitive sports.

Adult↗
PubMed1985

Inhibition of phospholipid/Ca2+-dependent protein kinase and phosphorylation of leukemic cell proteins by CP-46,665-1, a novel antineoplastic lipoidal amine.

CP-46,665-1, an antineoplastic lipoidal amine, was found to inhibit phospholipid/Ca2+-dependent protein kinase (PL/Ca-PK, or protein kinase C), with an IC50 (concentration causing a 50% inhibition) of 10 microM. Its inhibition of the enzyme was reversed by phosphatidylserine, but not by Ca2+. The agent also inhibited the enzyme activity which was further augmented by 12-0-tetradecanoylphorbol-13-acetate (TPA), mezerein or diolein. Phosphorylation of endogenous proteins from HL-60 cells by the enzyme, with or without being further augmented by TPA, was inhibited by CP-46,665-1 as well as by alkyllysophospholipid (an antineoplastic agent). CP-46,665-1, while without effect on cyclic AMP-dependent protein kinase, also inhibited myosin light chain kinase (a calmodulin/Ca2+-dependent protein kinase). The present findings suggest that inhibition of the Ca2+-effector enzymes may be related in part to the antimetastatic activity of the lipoidal amine.

Animals↗
PubMed1985

The presence of methionine-enkephalin in plasma and urine in normal human subjects and various patients.

The present study was performed to investigate whether or not there were enkephalins in plasma and urine in normal subjects and in patients with various diseases. Two kinds of antisera were developed to detect M-enk and L-enk. One has specific affinity with the C-terminus of methionine-enkephalin sulfoxide (M-O-enk), the oxidized form of M-enk, and the other with the N-terminus of L-enk. M-enk-like substance (MELS) was present in blood and urine in normal subjects, but not L-enk-like substance (LELS). Plasma MELS and its urinary output averaged 38 +/- 14 pg/ml (N = 19) and 605 +/- 235 ng/day (N = 15, M. +/- S.D.), respectively. There was a significant increase in plasma MELS and its urinary output in patients with pheochromocytoma. Plasma MELS did not show any significant increase or decrease in Cushing's disease. Addison's disease, panhypopituitarism or chronic glomerulonephritis. The urinary output of MELS was significantly increased in patients with essential hypertension, renovascular hypertension and primary aldosteronism, but was decreased in central diabetes insipidus.

Addison Disease↗
PubMed1985

Resistance of 1-deamino-[8-D-arginine]-vasopressin to in vitro degradation as compared with arginine vasopressin.

In order to elucidate the mechanism(s) responsible for the prolonged antidiuretic activity of 1-deamino-[8-D-arginine]-vasopressin (dDAVP), antidiuretic activities of dDAVP and arginine vasopressin (AVP) were determined in the rat following either oral administration or incubation with AVP-degrading enzymes and reagents. Oral administration of dDAVP to conscious water-loaded rats resulted in significant antidiuresis while AVP resulted in slight and transient antidiuresis. In the ethanol anesthetized water-loaded rats, antidiuretic activities of 136pg of AVP and 50pg of dDAVP, which were found to be equipotent, were compared after incubation with digestive enzymes (pepsin, trypsin, alpha-chymotrypsin), late pregnancy plasma, or sodium thioglycollate. The antidiuretic activity of AVP was completely destroyed by 30-min incubation with trypsin, alpha-chymotrypsin, or late pregnancy plasma and almost all AVP was inactivated by 0.2 M sodium thioglycollate. On the other hand, the antidiuretic activity of dDAVP was not destroyed by trypsin or pregnancy plasma but was partly destroyed by alpha-chymotrypsin and sodium thioglycollate. Neither the antidiuretic activity of AVP nor that of dDAVP was affected by pepsin. Thus, the antidiuresis observed after oral administration of dDAVP might be brought about by the resistance to digestive enzymes. Furthermore, the resistance of dDAVP to digestive enzymes, late pregnancy plasma and sodium thioglycollate might be responsible for the prolonged antidiuretic action of dDAVP in vivo.

Animals↗
PubMed1985

Effect of haemodialysis on plasma ADH levels, plasma renin activity and plasma aldosterone levels in patients with end-stage renal disease.

Changes in plasma ADH levels and plasma aldosterone levels (PA) were studied in patients with end-stage renal disease (N = 40). The patients were divided into two groups according to their plasma renin activity (PRA) into a low renin (LR, n = 9) and a high renin group (HR, n = 31). The metabolic clearance rate (MCR) of plasma ADH was also investigated in 4 patients and 5 normal volunteers. Additionally, it was examined whether plasma ADH, aldosterone and renin were permeable through the dialysis membrane. Pre- and post-dialysis plasma ADH levels in LR were similar to those in the HR group. However, pre- and post-dialysis PA in the HR group were significantly greater than those in the LR group. Post-dialysis PRA was significantly increased in HR compared to pre-dialysis, but not in LR. Pre- and post-dialysis plasma osmolality was increased in both groups, but effective plasma osmolality (EPosm) was within the normal range. There was a significant correlation between EPosm and plasma ADH level both before and after haemodialysis, but the majority of the abnormally high values of ADH compared to the normal values was found within the normal range of EPosm. The patients exhibited high blood pressure and a rise in body weight, and haemodialysis caused a significant fall in body weight and blood pressure in both groups. MCR of ADH was significantly lower in the patients than that in normal subjects. Plasma ADH proved to be permeable through the dialysis membrane in all cases, but aldosterone in only a few cases. Renin was not permeable.

Adolescent↗