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Biomedical subjects

M C Wu

Publications and source records attributed to M C Wu.

At least 145 records · Page 8Linked to original sources
PubMed1986

Spironolactone therapy for hyperandrogenic anovulatory women--clinical and endocrinological study.

Seventeen patients with irregular menstrual periods and androgenic symptoms such as excessive hair growth, acne, and oily skin were treated with spironolactone. The basal levels of serum testosterone (T), dihydrotestosterone (DHT), estradiol (E2), and luteinizing hormone (LH) were significantly higher in the patients than in the controls. After a 4-week treatment with spironolactone, serum T and DHT showed significant decreases. Before treatment, the serum sex hormone binding globulin (SHBG) levels were significantly lower in the patients than in the controls. After initiation of the spironolactone treatment, the SHBG levels tended to increase but not significantly. Spironolactone treatment resulted in the improvement or disappearance of acne in 4 of 5 patients who suffered from this ailment. Improvement of hirsutism was obtained in 2 of 10 patients. Although 4 oligomenorrheic patients and 6 amenorrheic patients showed anovulatory bleeding but did not ovulate, 2 patients in the amenorrheic group ovulated. Two patients complained of tiredness and weakness, and 2 others of polyuria and polydipsia. Both groups showed only temporary symptoms, so treatment was not interrupted. Spironolactone has beneficial effects on ovarian function and few side effects, so it may prove to be an effective anti-androgen, especially for hyperandrogenic anovulatory patients.

Adult↗
PubMed1985

Uptake and metabolism of glutamine in cultured kidney cells.

The metabolism of glutamine was investigated in cultured rat kidney cells. Glutamine utilization and product formation were followed as a function of time at either 10 microM or 1 mM initial glutamine concentration. At 1 mM glutamine, glutamate and gamma-glutamylglutamate were the major products formed at the end of a 5-min incubation period; glutamate accounted for 46% while gamma-glutamylglutamate accounted for 33% of the glutamine utilized. With time, glutamate continued to accumulate while gamma-glutamyl peptide formation leveled off. The role of gamma-glutamyl transpeptidase was assessed by using hippurate, a physiological activator of gamma-glutamyl transpeptidase and acivicin, L-(alpha S,5S)-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid, an inhibitor of gamma-glutamyl transpeptidase. Hippurate, 4 mM, increased the utilization of glutamine and the formation of glutamate, gamma-glutamyl peptides and ammonia. Exposure of cells to acivicin resulted in 98% inhibition of gamma-glutamyl transpeptidase without effecting phosphate-dependent glutaminase activity. Acivicin inhibition resulted in a decreased utilization of glutamine and product formation as compared to control; 5-oxoproline appearance fell 70%. The fractional distribution of glutamine carbon and nitrogen into its metabolic products in control, hippurate and acivicin-treated cells showed no change at the end of 60 min. The data provide evidence that gamma-glutamyl transpeptidase utilizes glutamine and forms gamma-glutamyl peptides in cultured kidney cells.

Animals↗
PubMed1985

Cyclic therapy resulted in pregnancy in premature ovarian failure.

A successful pregnancy in a patient with premature ovarian failure is described. Increased serum gonadotropin titers, decreased serum estrogen levels, and lack of ovarian follicles on histologic examination confirmed the state of ovarian failure. The patient conceived after several courses of cyclical treatment with estrogen-progestin. A possible relationship between the estrogen treatment and subsequent pregnancy is discussed.

Adult↗
PubMed1985

Binding capacity of sex-hormone-binding globulin and free testosterone determination in evaluation of hirsute women.

To investigate the relation between free testosterone (T) and binding capacity of sex-hormone-binding globulin (SHBG-BC) and a degree of hirsutism, 34 women were classified into 3 groups according to the criteria of Ferriman and Gallway on the degree of the hirsutism; 11 patients with a total score of 1 to 3 (group 1), 8 patients with a total score of 4 to 10 (group 2), and 15 patients with a total score of 11 or more (group 3). Total plasma T, SHBG-BC, and free plasma T were measured in each group, and they were compared with those of controls. In groups 1 and 2, mean levels of total T were slightly higher than in controls but the differences were not significant. Total T levels were extremely elevated in group 3. Mean level of SHBG-BC in group 1 was slightly lower than in controls but was not statistically significant. SHBG-BC was drastically reduced in groups 2 and 3. The percent free T levels and free T concentrations were significantly higher than those of controls in groups 2 and 3, but not in group 1. The results suggested that decreased SHBG-BC and increased free T might be the cause of hirsutism in women with normal total T levels.

Amenorrhea↗
PubMed1985

[Changes in % free testosterone and sex-hormone binding globulin during danazol administration].

To clarify the androgen balance on the administration of danazol a study was conducted on the levels of % free testosterone (% free T) and sex-hormone-binding globulin (SHBG) during the therapy and the binding properties of danazol to SHBG and androgen receptor. It was found that danazol displaced testosterone (T) from SHBG and R1881 from androgen receptor, in vitro. During treatment with danazol, levels of % free T were increased about three fold, but in contrast the SHBG concentration were significantly decreased. Similar changes in % free T were observed by computer simulation. These data suggest that the androgenic effects of danazol were the results of increased free T levels by the T-displacing ability of danazol from SHBG. The concentration of SHBG might be reduced as a consequence of increased levels of free T. On the other hand, danazol binding to androgen receptor might partially inhibit the action of excess amounts of free T, because the androgenization during therapy was too weak to compare the levels of free T.

Computers↗
PubMed1985

Effect of estrogen, testosterone, and phenobarbital on uterine weight and liver microsomal enzymes in prepuberal mice.

Prepuberal female mice were treated with estradiol benzoate (EB), testosterone (T), or phenobarbital (PB), or were untreated. At 8 days after treatment treated mice had lower uterine weights than did untreated mice. Mice treated with EB and PB also had higher levels of hepatic cytochrome P450 at this time. The uteri of mice treated with EB, T, or PB were capable of responding to exogenous EB 8 days following the treatment with an increase in weight. In a second experiment mice were treated with a range of doses of EB, T, or PB,. At the lower doses there was an inverse association of uterine weight and cytochrome P450 levels. At higher doses there was no apparent association. These data indicate that uterine weight may be influenced in part by prior treatment that also affects the level of liver enzymes.

Animals↗
PubMed1984

Glutamine promotes colony formation in bone marrow and HL-60 cells; accelerates myeloid differentiation in induced HL-60 cells.

Several studies indicate that glutamine is a critical requirement for growth of cultured cells. The present studies describe the effect of deprivation of glucose or glutamine on mouse bone marrow cell or HL-60 cell colony formation in soft agar. The mouse bone marrow cells were induced to undergo granulocyte/macrophage type differentiation by colony-stimulating factor. Glutamine, but not glucose, was found to be an indispensable metabolite for the cloning of HL-60 cells or differentiated mouse bone marrow cells. In addition, the effect of glucose or glutamine on the rate of differentiation of dimethylsulfoxide (DMSO)-induced HL-60 cells in liquid culture was studied. Glutamine was found to be superior to glucose in its ability to support the proliferation and myeloid differentiation of HL-60 cells. When an optimal concentration of DMSO was used, the rate of differentiation of induced HL-60 cells was found to be a function of the concentration of glutamine. In addition to these studies glutamine utilization and product formation was studied in induced and uninduced HL-60 cells after 60 min incubation with 1 mM initial glutamine concentration. The fractional distribution of the glutamine carbon into its metabolic products remained unchanged in induced versus uninduced HL-60 cells. However, the rate of utilization of glutamine and product formation by terminally differentiated HL-60 cells was less than the rate of utilization of glutamine by undifferentiated HL-60 cells. The data do not explain the role of glutamine in the complex process of differentiation but establish the critical requirements for glutamine, but not glucose, in myelopoiesis.

Animals↗
PubMed1984

Granulocyte-macrophage colony-stimulating factor from cultured normal rat kidney cell line.

Serum-free medium conditioned by the normal rat kidney (NRK) cell line contains colony-stimulating factors (CSF) that stimulate the in vitro formation of granulocyte and macrophage colonies from rat, mouse, and human marrow. There are two types of CSF: NRK-CSF I stimulates rat and mouse marrow, while NRK-CSF II stimulates the human marrow. The NRK-CSF I has been partially purified to a specific activity of 5 X 10(7) units/mg by employing methods such as preparative isoelectrofocusing, gel filtration chromatography, and preparative gel electrophoresis. It has an isoelectric point of 5.1 and an apparent molecular weight of 35,000 daltons as estimated by gel filtration. It is stable at 50 degrees C for 30 min and relatively resistant to papain, but highly sensitive to trypsin, chymotrypsin, and subtilisin. The secretion of CSF by NRK cells is inhibited by actinomycin D (0.5 micrograms/ml) and cycloheximide (0.5 micrograms/ml), but not by cytosine arabinoside (5 micrograms/ml). Although the CSF activity is inactivated by periodate oxidation (5 mM), thus suggesting its glycoprotein nature, treatment of the CSF with neuraminidase and other glycosidases has no effect on its activity. Anti-NRK-CSF I antibody inhibits the rat/mouse-active CSF from all rat sources, but has no effect on the human-active CSF. Comparative studies with CSF from media conditioned by the transformed cell line (442) and from rat lung and spleen have shown that CSF I from different rat sources share similar isoelectric points, molecular weights, and immunological properties.

Animals↗
PubMed1984

Human myeloid leukemic cell (HL-60) autostimulator: relationship to colony-stimulating factor.

The human promyelocyte leukemic cell line HL-60 secretes a glycoprotein factor which stimulates HL-60 and myeloid cell growth and colony formation in vitro. Functional and biochemical studies indicate this autostimulatory activity (ASA) is distinct from colony-stimulating factor (CSF) activities reported previously. Human CSF I, CSF II, and HL-60 ASA stimulated HL-60 growth and colony formation. The ASA also demonstrated CSF activity for both granulocyte and macrophage colonies when assayed on normal mouse and human bone marrow cells. The ASA glycoprotein was partially purified 1200-fold to an apparent molecular weight of 25,000 on G-75 filtration and a pl of 4.9 after neuraminidase treatment. Serological cross-reactivity between human CSF I and HL-60 ASA was detectable by immune precipitation and neutralization of biological activity with rabbit anti-CSF I antibodies. The cross-reactive anti-CSF I antibodies also inhibited spontaneous HL-60 colony formation in vitro in the absence of exogenous CSF, ASA, or anti-HL-60 antibody activity. These results indicate that HL-60 ASA is an endogenous growth factor similar to CSF that may be required for HL-60 growth in vitro.

Animals↗
PubMed1984

Further evidence supporting an in vivo role for colony-stimulating factor.

Nude mice injected subcutaneously with CSF-producing human pancreatic carcinoma (MIA PaCa-2) cells developed tumors accompanied by a rise in serum CSF activity, granulocytosis, and expanded marrow granulocyte pools, the extent of all of which correlated with tumor size. The tumor origin of the CSF was demonstrated by neutralization with the specific antibody. Resection of the tumor resulted in restoration of normal granulocyte levels. These observations lend further support to an in vivo role for CSF in the regulation of granulopoiesis.

Animals↗
PubMed1982

Induced release and metabolism of arachidonic acid from myeloid cells by purified colony-stimulating factor.

The in vitro incubation of cells from turpentine-induced rat myeloid hyperplastic marrow and peritoneal monocyte/macrophage with 14C-arachidonic acid resulted in the incorporation of the radiolabel into the particulate phospholipids. Challenge of the radiolabeled cells with a highly purified type I CSF (CSF I) from human pancreatic carcinoma cells in continuous culture resulted in the hydrolysis and release of the 14C-arachidonic acid from the cellular phospholipids. The simultaneous challenge of the prelabeled cells with CSF-I and its specific antibody (anti-CSF-I antibody) inhibited the CSF-I induced hydrolysis of 14C-arachidonic acid from the cells. These results confer a specificity on the CSF-I induced release of arachidonic acid from the cellular phospholipids. Our data also demonstrated that the 14C-arachidonic acid released from the cellular phospholipids was further transformed into products of the cyclooxygenation and lipoxygenation pathways by cellular enzyme systems in both populations of cells. Interestingly, our data also indicate that the challenge of the granulocytic hyperplastic marrow cells and the monocyte/macrophage cells with purified CSF-I resulted in a higher generation of lipoxygenase products in the predominantly granulocytic cell population than in the population rich in monocyte/macrophage cells. The biological significance of this observation remains to be further explored. Thus, the CSF-I induced release of cellular arachidonic acid explains, at least in part, the presence of prostaglandins and other metabolites of arachidonic acid that are found in the media of hemopoietic cells incubated with a variety of CSF preparations.

Arachidonic Acid↗
PubMed1982

Sensitivity of cultured pancreatic carcinoma cells to Acinetobacter glutaminase-asparaginase.

Cultured human pancreatic carcinoma cells (MIA PaCa-2) have been shown previously to be very sensitive to E. coli L-asparaginase (EC II). The present studies have demonstrated that another enzyme, Acinetobacter glutaminase-asparaginase (AGA) is much more effective in inhibiting cell growth. At the concentration of 0.0025 U/ml of AGA activity the enzyme totally inhibited cell growth, whereas the EC II with the same concentration did not show any effect. The inhibition of cell growth correlated well with inhibition of protein and glycoprotein synthesis. The addition of L-glutamine at the concentration of 1 mM completely reversed the inhibition of protein synthesis. Similarly, the addition of L-glutamine at the concentration of 3 mM daily on 3 successive days after adding AGA resulted in significant reversal of growth inhibition. The results of this study indicate that the action of AGA on MIA PaCa-2 is, to a great extent, exerted through its L-glutaminase activity.

Acinetobacter↗
PubMed1982

Purification of human granulocyte-macrophage progenitor cells (CFU-C) using indirect immunofluorescence and cell sorting.

We have attempted to purify human bone marrow granulocyte-macrophage progenitor cells utilizing purified stimulating factor, indirect immunofluorescence and cell sorting. These cells can be labelled by sequential incubation with colony-stimulating factor (CSF), rabbit anti-CSF antibody and fluorescently labelled goat anti-rabbit gamma globulin. Flow photometry demonstrated that binding of CSF to marrow cells varied with CSF concentration and duration of incubation. Marrow cells were pre-concentrated by incubation with carbonyl iron followed by Percoll gradient centrifugation and then labelled by this indirect immunofluorescence method. Sorting of these cells yielded up to 95-fold purification of colony-forming cells and fractions containing in excess of 10% colony- and cluster-forming cells.

Bone Marrow Cells↗
PubMed1981

Immunological and functional differences between human type I and II colony-stimulating factors.

Two distinct types of colony-stimulating factor (CSF) have recently been described in human tissues and cultured cell lines. Antisera to purified type I and II CSF were prepared in rabbits. Anti-CSF I antibody inhibits CSF I, but has no effect on CSF II. It cross-inhibits CSF I from several other human sources, but does not inhibit CSF from mouse lung or mouse L cells. Anti-CSF II antibody inhibits the activity of CSF II, but has no effect on CSF I. A radioimmunoassay for CSF I has been established. Competitive binding assay further demonstrated the immunological differences between CSF I and II. When CSF II is used to stimulate human marrow cells fractionated by sedimentation velocity, two populations of CFU-C are separated, one sedimenting at 8 mm/h and forming colonies by day 7, and a second sedimenting at 6.8 mm/h and forming colonies by day 13. In contrast, CSF I does nt stimulate colony growth by day 7 but does do so by day 13 in cells sedimenting between 7.2-8.5 mm/h. These results indicate that CSF I and II are distinct in their biochemical, immunological, and functional properties.

Antigen-Antibody Complex↗