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Biomedical subjects

M Sakata

Publications and source records attributed to M Sakata.

At least 127 records · Page 7Linked to original sources
PubMed1995

Somatoform pain disorder in a case of Klinefelter's syndrome with multiply operated lower back.

We report a case of Klinefelter's syndrome with multiply operated low back (MOB). Psychological and/or psychosocial problems related to MOB have been of recent interest in the field of orthopedic surgery. Based on psychiatric interviews, this case was diagnosed as a somatoform pain disorder of the DSM-III-R somatoform disorders. In addition to psychological problems, the pain was partly explicable by severe osteoporosis, which was prematurely caused by endocrinological disturbances associated with Klinefelter's syndrome. Patients with this syndrome are more likely to develop severe osteoporosis. In the presenile period of Klinefelter's syndrome with severe osteoporosis, liaison psychiatrists may pay attention to somatoform disorders (e.g. somatoform pain disorder and conversion disorder) linked with the MO.

Bone Density↗
PubMed1995

Effects of sulfhydryl compounds on the accumulation, removal and cytotoxicity of inorganic mercury by primary cultures of rat renal cortical epithelial cells.

The effects of sulfhydryl compounds on the accumulation, removal and cytotoxicity of inorganic mercury (Hg) were investigated in primary cultures of rat renal cortical epithelial cells. The compounds investigated were 2,3-dimercaptosuccinic acid, 2,3-dimercapto-1-propanol, D-penicillamine, glutathione (GSH) and L-cysteine. In the accumulation experiment, the cells were co-incubated with Hg and the above compounds for 30 min. (short-term) or 18 hr (long-term). In the removal experiment, cells incubated with Hg were further incubated with the above compounds for 30 min. In both experiments, the alleviative effect of the compounds on the cytotoxicity was estimated by the uptake of neutral red or by cell growth. 2,3-Dimercaptosuccinic acid had the highest antidotal effects except for Hg removal. 2,3-Dimercapto-1-propanol exerted the least antidotal effects in the short-term, as well as in the long-term experiments, 2,3-dimercapto-1-propanol increased the Hg accumulation and the cytotoxicity despite its removal of most of the Hg. Although D-penicillamine, L-cysteine and GSH did not increase the Hg removal in the long-term experiment other antidotal effects were seen.

Animals↗
PubMed1995

Cyclic adenosine-3',5'-monophosphate stimulates mouse placental lactogen-I (mPL-I) secretion but inhibits mPL-II secretion at midpregnancy.

To determine whether cAMP regulates mouse placental lactogen-I (mPL-I) and mPL-II secretion at midpregnancy in vitro, mouse placental tissue from day 9 of pregnancy was dispersed with collagenase, cells were fractionated on a Percoll gradient, and the purified trophoblast cells were plated in a serum-free medium. The cells were then incubated with various agents that increased the intracellular cAMP level for 5 days. 8-Bromo-cAMP stimulated mPL-I secretion, but inhibited mPL-II secretion in a time- and dose-dependent manner without changing the amount of newly synthesized trichloroacetic acid-precipitable proteins. Cholera toxin and forskolin, which increase intracellular cAMP accumulation, also regulated mPL-I and mPL-II secretion in the same manner. 8-Bromo-cAMP increased the intracellular mPL-I concentration, decreased the intracellular mPL-II concentration, and increased the immunoprecipitable newly synthesized mPL-I concentration in both the medium and cells. 8-Bromo-cAMP increased the expression of mPL-I messenger RNA and decreased the expression of mPL-II messenger RNA. The sequential reverse hemolytic plaque assay and double immunocytochemistry indicated that 8-bromo-cAMP regulates the subpopulation of giant cells containing and releasing mPL. These findings suggest that an increase in intracellular cAMP stimulates mPL-I secretion, but inhibits mPL-II secretion by changing the subpopulation of giant cells containing and releasing mPL.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1995

Cyclic adenosine 3',5'-monophosphate stimulation of placental proliferin and proliferin-related protein secretion.

To identify factors that regulate proliferin (PLF) and PLF-related protein (PRP) secretion by the mouse placenta, placental cells from day 9 of pregnancy were cultured for up to 5 days, and PLF and PRP release into the medium was assessed by RIA. Transforming growth factor-alpha, interleukin-1 alpha, and interleukin-6 did not regulate either PLF or PRP secretion. However, treatment of primary placental cell cultures with 8-bromo-cAMP, cholera toxin, or forskolin resulted in 2- to 3-fold increases in the percentages of PLF- and PRP-producing cells in the population and corresponding increases in both PLF and PRP messenger RNA and secreted protein. The increase in the number of PLF-producing cells was accompanied by an increase in the number of cells expressing both PLF and mouse placental lactogen-I. These data suggest that cAMP levels can regulate trophoblast giant cell differentiation and, consequently, the amount of PLF and PRP secretion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1995

Estrogen induces epidermal growth factor (EGF) receptor and its ligands in human fallopian tube: involvement of EGF but not transforming growth factor-alpha in estrogen-induced tubal cell growth in vitro.

We studied the estrogen-dependent expression of epidermal growth factor (EGF), transforming growth factor (TGF) alpha, and EGF receptor gene transcripts in human fallopian tubes in vivo and in vitro. Competitive polymerase chain reaction (PCR) was performed on the fallopian tube RNA samples from the postmenopausal women with or without estrogen replacement. Amounts of EGF, TGF alpha, and EGF receptors gene transcripts in the estrogen-treated group (n = 3) were significantly (P < 0.01) more than those in the untreated group (n = 3). Competitive PCR also showed that EGF, TGF alpha, and EGF receptor gene transcripts level in tubal cells were increased by estrogen in vitro: messenger RNA levels of these factors were significantly (P < 0.01, n = 3) increased in cells incubated with 10(-8) M estrogen compared with those in cells without estrogen treatment. We studied whether EGF and/or TGF alpha is involved in the estrogen-induced tubal cell growth in vitro. Estrogen enhanced the [3H]-thymidine incorporation into the cell in dose- and time-dependent manners in culture: estrogen treatment for more than 12 h significantly (P < 0.05) enhanced the [3H]-thymidine incorporation into the cell at 10(-8) M. The estrogen-induced cell growth was observed in association with the increase in EGF, TGF alpha, and EGF receptor messenger RNA levels by estrogen. If the EGF and/or TGF alpha is involved in the cell growth, then the estrogen-induced cell growth should be suppressed by blocking the action of EGF and/or TGF alpha. Therefore, we examined the effects of neutralizing monoclonal antibodies against EGF, TGF alpha, and EGF receptors. Anti-EGF antibody significantly reduced the estrogen-induced increase in [3H]-thymidine incorporation, whereas anti-TGF alpha antibody failed to show the effect. Anti-EGF receptor antibody showed a significant suppressive effect on the estrogen-induced increase in [3H]-thymidine incorporation. Moreover, the growth inhibitory effect by 1 microgram/ml anti-EGF was restored by 10(-8) M EGF but not by TGF alpha even at 10(-6) M. All these data suggest that estrogen induces EGF and TGF alpha/EGF receptors in the human fallopian tube and that EGF but not TGF alpha may be involved in the estrogen-induced human tubal cell growth in vitro.

Antibodies, Monoclonal↗
PubMed1995

Soluble interleukin-6 (IL-6) receptor in the sera of pregnant women forms a complex with IL-6 and augments human chorionic gonadotropin production by normal human trophoblasts through binding to the IL-6 signal transducer.

To study the role of soluble interleukin-6 receptor (sIL-6R) during pregnancy, sIL-6R levels in the sera of pregnant women in the first, second, and third trimesters were determined and found to remain unchanged during pregnancy, but were significantly higher than those in nonpregnant women in the follicular, ovulatory, and luteal phases of the menstrual cycle (P < 0.001). IL-6 levels, however, in the sera of pregnant women at all trimesters showed no difference from those in nonpregnant women at any stage of the menstrual cycle. Recombinant sIL-6R (rsIL-6R) augmented hCG production by rIL-6-stimulated trophoblasts dose dependently, but failed to enhance hCG production by unstimulated trophoblasts. rIL-6- and rsIL-6R-induced hCG production was significantly blocked by anti-IL-6R antibody, PM1; antisignal transducing glycoprotein 130 (gp130) antibody, GPX7; or a tyrosine kinase inhibitor, genistein. Thus, sIL-6R in serum from pregnant women forms a complex with placental and decidual IL-6 in a manner similar to trophoblast membrane-bound IL-6R. These two discrete types of IL-6R and IL-6 complex might act cooperatively by binding to gp130 and subsequently evoking tyrosine kinase activity in the trophoblasts to produce hCG in vivo.

Abortion, Legal↗
PubMed1995

Na(+)- and energy-dependent transport of cadmium into LLC-PK1 cells.

Effects of sodium ions (Na+) and metabolic inhibitors on cadmium (Cd) uptake were investigated in LLC-PK1 cells derived from pig kidney under the nontoxic conditions of Cd. The inoculated cells became confluent on day 7 after the logarithmic growth phase. The initial uptake of Cd (1-60 microM) by the confluent cells (day 7) was assayed. The relationship between the Cd uptake at 37 degrees C and Cd concentration was nonlinear, but the relationship at 4 degrees C was linear. Subtraction of the Cd uptake at 4 degrees C from that at 37 degrees C showed a saturable uptake against the Cd concentration. By the Eadie-Hofstee analysis of saturable uptake, Km and Vmax were 24.6 microM and 164 pmol Cd/mg protein/min, respectively. The uptake of Cd by the cells was significantly decreased by ouabain and the metabolic inhibitors, and by the replacement of Na+ with potassium or choline ion in the incubation medium. These results suggest that Cd is incorporated into the confluent LLC-PK1 cells not only by simple diffusion but also by the carrier-mediated transport involved in Na(+)- and energy-dependent process(es).

2,4-Dinitrophenol↗
PubMed1995

Increase in human placental glucose transporter-1 during pregnancy.

Glucose transporter-1 (GLUT1) has been found in high abundance in human placentas. The purpose of this study was to analyze the changes in the level of GLUT1 during pregnancy. We have analyzed the gestational changes in human placental GLUT1 by [3H]cytochalasin B binding assay, immunoblot analysis and Northern blot analysis. Levels of [3H]cytochalasin B binding to placental membrane in pregnancy at 7-10, 18-20 and 38-40 weeks were 4.2 +/- 0.47, 5.2 +/- 0.46 and 7.2 +/- 0.40 (mean +/- SEM, N = 4) mumol/kg protein, respectively. Amounts of 49-kD and 60-kD proteins detected in immunoblot analysis increased during pregnancy in parallel with [3H]cytochalasin B binding to placental membrane. The GLUT1 mRNA levels also increased during pregnancy. Immunohistochemical examination showed that GLUT1 was localized in the plasma membranes of trophoblast cells. These findings showed that the GLUT1 level increased during pregnancy in human placentas and suggest that GLUT1 may play an important role in fetal development.

Blotting, Northern↗
PubMed1995

Involvement of epidermal growth factor in inducing adiposity of age female mice.

Aged mice exhibit an increase in their body weight (BW), which is associated with fat deposit increase. Epidermal growth factor (EGF) concentration in the submandibular gland also increases with aging. We examined the effects of elevated EGF on the adiposity of aged female mice. Studies were started in two groups of animals consisting of sham-operated (n = 10) and sialoadenectomized (n = 10, Sx; surgical removal of the submandibular glands) mice at 8 weeks of age. Body weight gain and food intake were measured throughout 78 weeks of age in these two groups. Body weight was significantly less in the Sx group throughout 78 weeks, while food intake was not changed by Sx after 12 weeks of age. To examine further if EGF plays a role in the induction of adiposity in aged female mice, sham-operated animals were given 100 microliters anti-EGF rabbit antiserum (anti-EGF group, n = 5) or normal rabbit serum (control group, n = 5) every 3 days, and Sx animals were given 5 micrograms/day EGF (Sx+EGF group, n = 5) or saline (Sx group, n = 5) from 78 weeks of age for 3 weeks. At 81 weeks of age, all animals of these four groups were killed, and carcass fat deposition and fat cell sizes were measured. Although the relative weights (weight ratio to BW) of the liver and kidney were not changed by Sx and anti-EGF treatment, the relative weights of mesenteric and subcutaneous fat tissues and adipocyte weights were significantly decreased in Sx and anti-EGF groups compared with the control group. Moreover, both acyl-CoA synthetase (ACS) and lipoprotein lipase (LPL) mRNA levels were significantly decreased by Sx or anti-EGF administration in mesenteric and subcutaneous fat tissues. On the other hand, EGF administration to Sx animals had no effect on BW, fat tissues and adipocyte weights, and ACS and LPL mRNA levels. The results, however, were consistent with the fact that adipose tissue EGF receptors were down regulated in Sx mice. These findings suggest that EGF may play a role in the induction of adiposity in aged female mice.

Adipose Tissue↗
PubMed1995

Activin inhibits but inhibin activates mouse placental lactogen-II secretion.

The regulation of mouse placental lactogen (mPL)-I and mPL-II secretion by activin and inhibin and the expression of activin and inhibin subunit mRNAs in the mouse decidua were examined. Activin-A at a concentration of 10 nM/l significantly inhibited mPL-II secretion by placental cells from days 9 and 12 of pregnancy. However, activin-A did not affect mPL-I secretion by cells from days 7 and 9 of pregnancy nor mPL-II secretion by cells from day 7 of pregnancy. By contrast, 10 nM/l inhibin activated mPL-II secretion by cells from day 12 of pregnancy. These effects of activin and inhibin on mPL-II secretion were dose-dependent. Follistatin, which binds to activin and blocks its bioactivity, completely eliminated the inhibitory effect of activin on mPL-II secretion. Incubation of placental cells from day 12 of pregnancy with activin-A resulted in a significant reduction of the mPL-II mRNA level assessed by Northern blot analysis. Northern blot analysis using poly(A)+RNA extracted from the decidua indicated that mouse decidua, as well as the placenta, express all activin and inhibin subunits and that their gene expressions increased during gestation. The expression of these mRNAs in the decidua was much higher than those in the placenta. These findings suggest that activin and inhibin regulate mPL-II secretion and suggest the presence of an autocrine or paracrine regulation of mPL-II secretion in mouse placenta by activin and inhibin after mid-pregnancy in vivo.

Activins↗
PubMed1995

Inhibition of mouse placental lactogen-II release from placental cells by interleukin-1 after mid-pregnancy.

The effects of interleukin (IL)-1 and granulocyte-macrophage colony stimulating factor (GM-CSF), which are present in the mouse placenta, on the secretion of mouse placental lactogen (mPL)-1 and mPL-II by placental cells were tested in vitro. IL-1 alpha and IL-1 beta, 2.5 nmol/l each, significantly inhibited mPL-II secretion by cells from days 9 and 12 of pregnancy, but did not affect mPL-II secretion by cells from day 7 of pregnancy or mPL-I secretion by cells from days 7, 9 or 12 of pregnancy. GM-CSF had no effect on mPL-I and mPL-II secretion by cells from days 7, 9 or 12 of pregnancy. The inhibitory effects of IL-1 alpha and IL-1 beta on mPL-II secretion were completely eliminated by the addition of antibodies to IL-1 alpha and IL-1 beta respectively. Western blot analysis for mPL-II indicated that IL-1 alpha significantly reduced the intensity of the mPL-II band. Steady-state levels of mPL-II mRNA, assessed by Northern blot analysis, were reduced by incubation of placental cells from day 12 of pregnancy with 2.5 nmol/l IL-1 alpha for 5 days. Co-incubation of 0.25 pmol/l IL-1 alpha, 25 pmol/l IL-6, and 25 pmol/l tumor necrosis factor-alpha, each of which did not significantly inhibit mPL-II secretion by itself, together inhibited mPL-II secretion. These results suggest that IL-1, but not GM-CSF, is a potent inhibitor of mPL-II secretion after mid-pregnancy, and that the combined action of cytokines can inhibit mPL-II secretion.

Animals↗
PubMed1995

Menstrual cycle specific expression of epidermal growth factor receptors in human fallopian tube epithelium.

We studied the expression of epidermal growth factor (EGF) receptor protein and messenger RNA (mRNA) in human fallopian tubes at three stages of the menstrual cycle: early follicular (n = 3), late follicular (n = 3) and luteal (n = 3). Immunohistochemical studies in the ampullary portion of the tubes showed that specific staining was localized to the epithelium and the vascular endothelium. Staining of the epithelium was intense at the late follicular and luteal stages, while it was weak at the early follicular stage. 125I-EGF binding study in the tubal plasma membranes revealed a class of high-affinity EGF receptors. Although dissociation constants were similar between the stages, numbers of binding sites at the late follicular and luteal stages were significantly (P < 0.01) greater than those at the early follicular stage. Western blotting showed that tubal plasma membranes contain M(r) 170,000 EGF receptor protein. The amounts were significantly (P < 0.01, n = 3) greater at the late follicular and luteal stages than those at the early follicular stage. Reverse transcription and polymerase chain reaction (RT-PCR) revealed that EGF receptor mRNA was expressed in all the 9 RNA samples (n = 3 for each stage) from the tubal ampullary portion. The amounts were significantly (P < 0.01, n = 3) greater at the late follicular and luteal stages than those at the early follicular stage (by a competitive PCR). Increase in the amounts of EGF receptor protein and mRNA occurred in association with an increase in serum oestradiol but not progesterone levels. Next we examined whether EGF receptor and its ligands (EGF and transforming growth factor alpha) are directly induced by oestrogen. We found that specific staining for EGF receptor and its ligands in the tubal epithelium was detected (by immunohistochemistry) in postmenopausal women with oestrogen replacement (n = 3), but not in subjects without oestrogen replacement (n = 3). These results suggested that EGF receptors in the human tubal epithelium are expressed in relation to specific stages of the menstrual cycle and that the expression may be induced by oestrogen.

Base Sequence↗
PubMed1995

Possible correlation between ormaplatin biotransformations and neurotoxicity.

Clinical development of ormaplatin has been delayed because of neurotoxicity that was not predictable on the basis of patient characteristics, total cumulative dose, or plasma pharmacokinetics. We report a detailed comparison of the plasma biotransformations of ormaplatin in two patients at the 123 mg/m2-dose administered as a 1-h infusion every 4 weeks. One of these patients developed neurotoxicity after 2 cycles (total cumulative dose = 246 mg/kg), while the other patient showed no symptoms of neurotoxicity through 2 cycles. The maximum plasma concentration and area under the curve for ultrafilterable platinum were greater for the patient that did not develop neurotoxicity. However, both maximum plasma concentration and area under the curve were greater for dichloro(d,l-trans)1,2-diaminocyclohexanedichloroplatinum(II), the major active biotransformation product of ormaplatin, in the patient that developed neurotoxicity. In addition, analysis of plasma biotransformation products suggested that the initial plasma concentrations of ormaplatin were also greater in the patient that developed neurotoxicity. These data suggest that analysis of individual plasma biotransformation products may be useful in predicting toxicity of platinum anticancer agents and should be included in future phase I studies.

Adult↗
PubMed1995

Endothelin-1 is not involved in serotonin-induced coronary spasm in a swine model.

OBJECTIVES: The role of endothelin-1 (ET-1) in the pathogenesis of coronary artery spasm is not well understood. We aimed to determine if ET-1 is involved in serotonin-induced coronary spasm in the swine model. METHODS: In 10 miniature pigs, a segment of the left anterior descending coronary artery was denuded and irradiated with X-ray. Three months after endothelial denudation, coronary vasomotion was assessed in vivo by quantitative arteriography. RESULTS: Intracoronary serotonin at 10 micrograms/kg provoked coronary spasm (augmented narrowing of the luminal diameter) at the denuded site (diameter reduction 93 +/- 4%) but not at the non-denuded control site (19 +/- 4%, P < 0.01) associated with ST segment elevation in the region perfused by the denuded artery. Intracoronary administration of ET-1 at 25 ng/kg caused mild vasoconstriction of the denuded (26 +/- 4) and non-denuded site (16 +/- 3%, n.s.), but provoked ST segment elevation in the regions perfused by both the denuded and non-denuded arteries. The treatment with an endothelin antagonist (BQ123 0.1 mg/kg) significantly attenuated coronary vasoconstriction and ST segment elevation evoked with ET-1, but did not alter serotonin-induced vasoconstriction either at the denuded or control site. CONCLUSIONS: The results of this study suggest that endogenous ET-1 may not be involved in the pathogenesis of serotonin-induced coronary spasm in our swine model.

Animals↗
PubMed1995

[A case of mitral valvuloplasty with concomitant CABG in an aged patient].

A 79-year-old man was referred to our hospital complaining of the manifestation of mild heart failure. Echo cardiography and LV gram showed sever mitral regurgitation by the prolapse of posterior leaflet. CAG revealed coronary artery disease affected two vessels (LAD and RCA) without symptoms. Quadrangular resection of posterior leaflet (McGoon's method) without annuloplasty and concomitant single CABG to the LAD using a saphenous vein were performed. Postoperative course was satisfactory and the manifestation of heart failure was diminished. Mitral valvuloplasty with concomitant CABG may be a safe and effective procedure in the treatment of aged patients.

Aged↗
PubMed1995

[Assessment of formulas of predicted creatinine clearance from serum creatinine].

Much effects have offered to make formulas of predicted creatinine clearance (Ccr) from serum creatinine, sex, age, body weight and height. In this study, we examined 13 kinds of predicted formulas of Ccr that have been previously published. And instead of an actual body weight, we have attempted to use 4 kinds of ideal body weight (two of them reported in Japan, the others in United States) or a lean body weight. A total of 13 subjects were studied (2 healthy males and 11 males with chronic renal disease) to determine Ccr with urine collection for one hour and simultaneous measurement of inulin clearance (Cin). A highly statistical correlation between determined Ccr and predicted Ccr was observed. From predicted formula with one hour urine collection, standard error of estimation (SEE) was smallest. According to determined Cin, the subjects examined was divided into two groups (group A; Cin > or = 50 ml/min, group B; Cin < 50 ml/min). In most formulas, B group had higher correlation than A group, and each regression line got nearer to the identical line (Y = X) and SEE became smaller. The subjects examined were divided into two groups by body mass index (BMI). One is an obese and the other is a nonobese. In an obese group, SEE became smaller when an ideal body weight or a lean body weight were used in formulas instead of actual body weight. We could conclude that the clearance time and ideal or lean body weight of the patients are most important factors to assess predicted Ccr.

Adult↗
PubMed1994

Tumor necrosis factor-alpha (TNF-alpha) inhibits expression of mouse placental lactogen-II through TNF-alpha type-I but not type-II receptor.

The aim of this study was to determine whether TNF-alpha inhibits mPL-II secretion through TNF-RI or TNF-RII, and to investigate the gestational profile of TNF-RI and TNF-RII gene expression. The mouse trophoblast cells from day 12 pregnancy were cultured with or without agonistic polyclonal antibodies directed against the individual TNF-alpha receptors, and mPL-II secretion in the medium was assessed by RIA. Anti-TNF-RI antibody significantly inhibited the mPL-II secretion in a dose- and time-dependent manner, but anti-TNF-RII antibody did not. Moreover, the TNF-RII antibody did not influence the inhibitory effect of the TNF-RI antibody on mPL-II secretion. TNF-RI antibody inhibited the mPL-II gene expression by Northern blot analysis. Amount of the gene expression of TNF-RI in the second half of pregnancy was higher than those in the first half of pregnancy both in vitro and in vivo, although the gene expression of TNF-RII was not detectable by Northern blot analysis using poly(A)+RNA. These results suggest that TNF-RI is a main receptor for TNF-alpha in mouse placenta and that TNF-alpha may have an important role in regulating mPL-II secretion after midpregnancy.

Animals↗