Presence of androgen receptors in the hen hypothalamus and pituitary

1989 ◽  
Vol 120 (2) ◽  
pp. 217-224 ◽  
Author(s):  
Mitsuo Kawashima ◽  
Michiharu Kamiyoshi ◽  
Katuhide Tanaka
Keyword(s):  
Marked Decrease ◽  
Soluble Fraction ◽  
Direct Action ◽  
Insoluble Fraction ◽  
Ovulatory Cycle ◽  
Buffer Solution ◽  
Hypotonic Buffer ◽  
Androgen Binding ◽  
Binding Component

Abstract. Soluble and insoluble fractions in a hypotonic buffer solution of hypothalamic-preoptic and median eminence areas, and of the anterior pituitary of the hen were found to contain a specific androgen binding component having the properties of a receptor. Administration of testosterone in vivo caused a marked decrease in specific [3H]R1881 (a synthetic androgen) bindings in the soluble fraction with a concomitant increase in the bindings in the insoluble fraction, whereas the sum of the bindings did not change. A similar relationship between the bindings of the two fractions was also observed during an ovulatory cycle. The results may provide an evidence for a direct action of androgens on the hen hypothalamus and pituitary.

scholarly journals Glucosamine metabolism in regenerating rat liver

1976 ◽  
Vol 158 (3) ◽  
pp. 589-592 ◽  
Author(s):  
N Akamatsu ◽  
H Nakajima ◽  
S Miyata
Keyword(s):  
Partial Hepatectomy ◽  
Rat Liver ◽  
De Novo ◽  
Specific Activity ◽  
Soluble Fraction ◽  
Amino Sugar ◽  
Insoluble Fraction ◽  
Regenerating Liver ◽  
Glycoprotein Synthesis

1. Glycoprotein synthesis was investigated with [1-14C]glucosamine in vivo. [14C]Glucosamine was administered intravenously 24h after hepatectomy to rats. 2. Incorporation into the acid-soluble fraction was maximum at 15 min after injection both in sham-operated and hepatectomized rats. 3. Enhancement of incorporation into UDP-N-acetylhexosamine in regenerating liver was observed. However, its specific activity was lower, because of a greater enhancement of synthesis de novo of the amino sugar. 4. In the liver acid-insoluble fraction, maximum incorporation of [14C]glucosamine was at 30 min in sham-operated rats and 2 h in hepatectomized rats respectively. 5. In sham-operated rats, incorporation into the plasma acid-insoluble fraction followed that of the liver acid-insoluble fraction, but hepatectomy resulted in a rapid enchancement of incorporation into plasma. 6. It is concluded that synthesis of liver glycoproteins is stimulated after partial hepatectomy and that glycoproteins synthesized are released rapidly into the plasma.

scholarly journals FRACTIONATION OF GELATIN

1929 ◽  
Vol 12 (3) ◽  
pp. 379-390 ◽  
Author(s):  
M. Kunitz ◽  
John H. Northrop
Keyword(s):  
Dilute Hydrochloric Acid ◽  
Soluble Fraction ◽  
Insoluble Fraction ◽  
Partial Hydrolysis ◽  
Free Solution ◽  
Buffer Solution ◽  
Solution Ph ◽  
Insoluble Material ◽  
The One ◽  
Hydrolysis Of

1. It is possible to fractionate gelatin by means of reprecipitation at 23°C. of a salt-free solution of pH 4.7 into two fractions, one of which is soluble in water at any temperature, and a second one which does not dissolve in water even when heated to 80°C. 2. The proportion of the soluble fraction in gelatin is much greater than of the insoluble one. 3. The insoluble fraction of gelatin does not swell when mixed with water, but it does swell in the presence of acid and alkali which finally dissolve it. 4. Blocks of concentrated gel made by dissolving various mixtures of the soluble and insoluble fractions of gelatin in dilute NaOH swell differently when placed in large volumes of dilute buffer solution pH 4.7 at 5°C. The gel consisting of the insoluble material shows only a trace of swelling, while those containing a mixture of soluble and insoluble swell considerably. The swelling increases rapidly as the proportion of the soluble fraction increases. 5. A 5 per cent gel made up by dissolving the insoluble fraction of gelatin in dilute NaOH loses about 70 per cent of its weight when placed in dilute buffer pH 4.7 at 5°C. A similar gel made up of ordinary gelatin loses only about 20 per cent of its weight under the same conditions. 6. It was not found possible to resynthesize isoelectric gelatin from its components. 7. An insoluble substance similar in many respects to the one obtained by reprecipitation of gelatin is produce on partial hydrolysis of gelatin in dilute hydrochloric acid at 90°C.

scholarly journals Paroxysmal Nocturnal Hemoglobinuria

Blood ◽  
1953 ◽  
Vol 8 (5) ◽  
pp. 444-458 ◽  
Author(s):  
WILLIAM H. CROSBY
Keyword(s):  
Hemolytic Activity ◽  
Soluble Fraction ◽  
Insoluble Fraction ◽  
Water Soluble ◽  
Red Cells ◽  
Distilled Water ◽  
Heat Stable ◽  
Heat Labile

Abstract This report demonstrates the role and to some extent the interrelations of various factors that are active in the PNH hemolytic system. 1. Activity of four plasma factors, probably protein in nature, has been demonstrated. Two of these factors are hemolytic against PNH red cells, but not against normal red cells. The other two inhibit PNH hemolysis. (a). The heat labile hemolytic factor is water soluble and is therefore present in the soluble fraction of serum that has been dialyzed against distilled water. It is almost completely destroyed by heating at 53 C. for 10 minutes. It is slowly inactivated by incubation at 37 C. with 100 units per ml. of thrombin. It is rapidly destroyed by concentrations of thrombin in excess of 200 units per ml. It is inactive unless the heat stable hemolytic factor is also present. (b). The heat stable hemolytic factor is insoluble in water and is therefore precipitated from serum by dialysis against distilled water. It is quite resistant to 100 units per ml. of thrombin and to incubation at 53 C. It is inactive unless the heat labile hemolytic factor is also present. (c). The heat labile inhibitor is insoluble in water and is therefore found in the insoluble fraction of serum dialyzed against distilled water. It is inactivated by heating at 53 C. for 10 minutes but not by incubation with 100 units per ml. of thrombin. (d). The heat stable inhibitor is found in the water-soluble fraction of dialyzed serum. It withstands dialysis poorly, but it is not affected by 30 minutes incubation at 53 C. Incubation at 37 C. with 100 units per ml. of thrombin for 10 minutes destroys its inhibitory activity. Apparently the inhibitors are not interdependent. 2. Calcium in small amounts is probably essential to the PNH hemolytic system. The concentration of calcium that is optimum for hemolysis lies in the neighborhood of 2.5 mM. The optimum is a little less than the amount normally present in the plasma. Calcium in excess inhibits hemolysis in vitro, and no hemolysis occurs when the concentration exceeds 25 mM. per liter. 3. Magnesium is also essential to the PNH hemolytic system. As magnesium is added to the system in vitro hemolytic activity increases until the concentration exceeds 10 mM. per liter. Amounts greater than that have some dampening effect. Magnesium appears to antagonize the heat stable inhibitor of the PNH hemolytic system. 4. Thrombin is involved in this system insofar as the heat stable inhibitor and the heat labile hemolytic factor may be destroyed by thrombic activity. The inhibitor is rapidly destroyed, the hemolytic factor slowly. Therefore, the sum of the reaction to small amounts of thrombin in the PNH hemolytic system is to increase hemolytic activity. 5. Dilute heparin and protamine increase the activity of the PNH hemolytic system in vitro, probably by blocking the two inhibitors. Heparin appears to work against the heat stable inhibitor, protamine against the heat labile inhibitor. 6. The intensity of PNH hemolytic activity whether in vitro or in vivo is probably related to a balance that exists between the inhibitors and the hemolytic factors. Hemolytic crises may occur when the hemolytic factors are increased or when their antagonists are depressed.

INVESTIGATIONS ON AN ANDROGEN-BINDING COMPONENT FROM COHN'S PLASMA FRACTION IV—4

1975 ◽  
Vol 80 (1_Suppla) ◽  
pp. S122
Author(s):  
W. Miscke ◽  
D. Graesslin ◽  
J. Tamm
Keyword(s):  
Plasma Fraction ◽  
Androgen Binding ◽  
Binding Component

THE BINDING OF [1,2-3H]TESTOSTERONE WITHIN NUCLEI OF THE RAT PROSTATE

1969 ◽  
Vol 44 (3) ◽  
pp. 323-333 ◽  
Author(s):  
W. I. P. MAINWARING
Keyword(s):  
Molecular Weight ◽  
Equilibrium Dialysis ◽  
Prostate Gland ◽  
Ventral Prostate ◽  
Rat Tissues ◽  
Receptor Complex ◽  
Rat Prostate ◽  
Binding Component

SUMMARY The specificity of the binding of [1,2-3H]testosterone to nuclei of various rat tissues in vivo has been studied. A significant amount of radioactivity was retained in the nuclei of androgen-dependent tissues only, particularly the ventral prostate gland. The bound radioactivity was only partially recovered as [1,2-3H]testosterone; the remainder was identified as [3H]5α-dihydrotestosterone. Efforts were made to characterize the binding component, or 'receptor', in prostatic nuclei. On digestion of nuclei labelled in vivo with [1,2-3H]testosterone, with enzymes of narrow substrate specificity, only trypsin released tritium, suggesting that the receptor is a protein. On the basis of subfractionation studies of labelled nuclei, the receptor is an acidic protein. The androgen—receptor complex could be effectively extracted from the prostatic nuclei in 1 m-NaCl and from the results of fractionations on a calibrated agarose column, the complex has a molecular weight 100,000–120,000. The specificity of the binding of steroids to such 1 m-NaCl extracts in vitro was investigated by the equilibrium dialysis procedure. Under these conditions, the specificity of the binding of [1,2-3H]testosterone demonstrated in vivo could not be simulated. The receptor is probably part of the chromatin complex but its precise intranuclear localization cannot be determined by biochemical procedures alone.

FGF-4 maintains polarizing activity of posterior limb bud cells in vivo and in vitro

Development ◽  
1993 ◽  
Vol 119 (1) ◽  
pp. 199-206 ◽  
Author(s):  
A. Vogel ◽  
C. Tickle
Keyword(s):  
Posterior Margin ◽  
Anterior Margin ◽  
Marked Decrease ◽  
Mesenchymal Cells ◽  
Apical Ectodermal Ridge ◽  
Limb Bud ◽  
Posterior Limb ◽  
Vertebrate Limb

The polarizing region is a major signalling tissue involved in patterning the tissues of the vertebrate limb. The polarizing region is located at the posterior margin of the limb bud and can be recognized by its ability to induce additional digits when grafted to the anterior margin of a chick limb bud. The signal from the polarizing region operates at the tip of the bud in the progress zone, a zone of undifferentiated mesenchymal cells, maintained by interactions with the apical ectodermal ridge. A number of observations have pointed to a link between the apical ectodermal ridge and signalling by the polarizing region. To test this possibility, we removed the posterior apical ectodermal ridge of chick wing buds and assayed posterior mesenchyme for polarizing activity. When the apical ectodermal ridge is removed, there is a marked decrease in polarizing activity of posterior cells. The posterior apical ectodermal ridge is known to express FGF-4 and we show that the decrease in polarizing activity of posterior cells of wing buds that normally follows ridge removal can be prevented by implanting a FGF-4-soaked bead. Furthermore, we show that both ectoderm and FGF-4 maintain polarizing activity of limb bud cells in culture.

Duodenal acid-induced gastric relaxation is mediated by multiple pathways

1999 ◽  
Vol 276 (6) ◽  
pp. G1501-G1506 ◽  
Author(s):  
Yuan-Xu Lu ◽  
Chung Owyang
Keyword(s):  
Gastric Motility ◽  
No Reduction ◽  
Direct Action ◽  
Intragastric Pressure ◽  
Afferent Pathways ◽  
Serotonin Antagonist ◽  
Intraduodenal Infusion ◽  
Rate Dependent ◽  
Vagal Afferent

In this study, we used an in vivo anesthetized rat model to investigate the mechanisms responsible for duodenal acid-induced inhibition of gastric motility. Intraduodenal infusion of HCl produced a rate-dependent decrease in intragastric pressure. Infusion of HCl at 2 ml/h produced a physiological plasma secretin level and elicited a decrease in intragastric pressure of 3.0 ± 0.2 cmH20. Infusion of rabbit secretin antiserum reduced the acid-induced inhibition of gastric motility by 85 ± 5%, suggesting mediation mainly by endogenous secretin. Administration of the cholecystokinin (CCK)-A antagonist MK-329 caused only a modest 10 ± 3% reduction in gastric relaxation, whereas the serotonin antagonist ICS-205930 had no effect. In contrast, immunoneutralization with the secretin antibody caused only a 15% reduction in the relaxation evoked by a higher rate of HCl infusion (3 ml/h), whereas MK-329 and ICS-205930 caused a 20 ± 4% reduction and no reduction, respectively. Bilateral truncal vagotomy or perivagal application of capsaicin completely abolished gastric relaxation in response to low rates (1–2 ml/h) of 0.1 N HCl infusion but only partially affected gastric relaxation in response to a higher infusion rate (3 ml/h). These observations indicate that multiple pathways mediate the duodenal acid-induced inhibition of gastric motility. At low rates of HCl infusion, gastric relaxation is mediated primarily by endogenous secretin, which acts through vagal afferent pathways. At higher rates of HCl infusion, gastric relaxation is mediated by endogenous secretin, CCK, and possibly by the direct action of HCl on vagal afferent pathways or yet unidentified neuropathways.

Diabetes increases stiffness of live cardiomyocytes measured by atomic force microscopy nanoindentation

2014 ◽  
Vol 307 (10) ◽  
pp. C910-C919 ◽  
Author(s):  
Juan C. Benech ◽  
Nicolás Benech ◽  
Ana I. Zambrana ◽  
Inés Rauschert ◽  
Verónica Bervejillo ◽  
...  
Keyword(s):  
Atomic Force Microscopy ◽  
Physiological Condition ◽  
Diabetic Mice ◽  
Cell Nuclei ◽  
Buffer Solution ◽  
Isolated Cardiomyocytes ◽  
Force Microscopy ◽  
Atomic Force ◽  
Myocardial Fibers

Stiffness of live cardiomyocytes isolated from control and diabetic mice was measured using the atomic force microscopy nanoindentation method. Type 1 diabetes was induced in mice by streptozotocin administration. Histological images of myocardium from mice that were diabetic for 3 mo showed disorderly lineup of myocardial cells, irregularly sized cell nuclei, and fragmented and disordered myocardial fibers with interstitial collagen accumulation. Phalloidin-stained cardiomyocytes isolated from diabetic mice showed altered (i.e., more irregular and diffuse) actin filament organization compared with cardiomyocytes from control mice. Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a) pump expression was reduced in homogenates obtained from the left ventricle of diabetic animals compared with age-matched controls. The apparent elastic modulus (AEM) for live control or diabetic isolated cardiomyocytes was measured using the atomic force microscopy nanoindentation method in Tyrode buffer solution containing 1.8 mM Ca2+ and 5.4 mM KCl (physiological condition), 100 nM Ca2+ and 5.4 mM KCl (low extracellular Ca2+ condition), or 1.8 mM Ca2+ and 140 mM KCl (contraction condition). In the physiological condition, the mean AEM was 112% higher for live diabetic than control isolated cardiomyocytes (91 ± 14 vs. 43 ± 7 kPa). The AEM was also significantly higher in diabetic than control cardiomyocytes in the low extracellular Ca2+ and contraction conditions. These findings suggest that the material properties of live cardiomyocytes were affected by diabetes, resulting in stiffer cells, which very likely contribute to high diastolic LV stiffness, which has been observed in vivo in some diabetes mellitus patients.

scholarly journals TNP-470 Suppresses the Tumorigenicity of HT1080 Fibrosarcoma Tumor Through the Inhibition of VEGF Secretion From the Tumor Cells

Sarcoma ◽  
2001 ◽  
Vol 5 (4) ◽  
pp. 197-202 ◽  
Author(s):  
Mitsunori Kaya ◽  
Takuro Wada ◽  
Satoshi Nagoya ◽  
Satoshi Kawaguchi ◽  
Toshihiko Yamashita ◽  
...  
Keyword(s):  
Conditioned Medium ◽  
Direct Action ◽  
Angiogenesis Inhibitor ◽  
Angiogenesis Inhibitors ◽  
Fibrosarcoma Cells ◽  
Ht1080 Cells ◽  
Human Fibrosarcoma Cells ◽  
And Migration

Angiogenesis inhibitors are a novel class of promising therapeutic agents for treating cancer. TNP-470, a systemic analogue of fumagillin, is an angiogenesis inhibitor capable of suppressing the tumorigenicity in several animal models even though the mechanisms of action have not been completely clarified. In the current study, we investigated the effects of TNP-470 on human fibrosarcoma cellsin vivoandin vitro. The administration of TNP-470 could suppress the tumorigenicity of HT1080 fibrosarcoma tumor. The conditioned medium from HT1080 fibrosarcoma cells treated with TNP-470 inhibited the proliferation and migration of human endothelial cell line, HUVEC and ECV304. The concentration of VEGF in the conditioned medium from HT1080 cells treated with TNP-470 was lower than that of the cells without TNP-470 treatment, indicating that TNP-470 downregulates the secretion of VEGF from HT1080 cells. These findings strongly suggest that the direct action of TNP-470 on sarcoma cells inhibits angiogenesis through the downregulation of VEGF secretion and this angiogenesis suppression resulted in the inhibition of tumorigenicity of HT1080 fibrosarcoma tumo.

Mechanism of phosphaturia elicited by administration of phosphonoformate in vivo

1988 ◽  
Vol 255 (5) ◽  
pp. F984-F994 ◽  
Author(s):  
M. VanScoy ◽  
M. Loghman-Adham ◽  
M. Onsgard ◽  
M. Szczepanska-Konkel ◽  
S. Homma ◽  
...  
Keyword(s):  
Direct Action ◽  
Fractional Excretion ◽  
Proximal Tubules ◽  
Camp Phosphodiesterase ◽  
Luminal Side ◽  
Metabolic Transformation ◽  
Rat Renal Cortical Slices ◽  
Fractional Excretion Of Phosphate

We examined whether phosphonoformate (PFA) can cause phosphaturia through its direct action on brush-border membrane (BBM) in vivo. Infusion of PFA or of parathyroid hormone (PTH) to thyroparathyroidectomized rats caused a marked increase in fractional excretion of phosphate without changes in excretion of Na+ or of GFR. The PFA-induced phosphaturia was not accompanied by an increase in urinary adenosine-3',5'-cyclic monophosphate (cAMP); moreover, PFA added in vitro did not influence the PTH-sensitive adenylate cyclase and cAMP-phosphodiesterase in proximal convoluted tubules. In BBM vesicles (BBMV) from rats with PFA-elicited phosphaturia, neither the rate of Na+-Pi symport nor Na+-dependent binding of [14C]PFA on BBMV was changed, whereas in BBMV from PTH-infused rats the Vmax of Na+-Pi symport decreased. PFA is almost completely ultrafiltrable; no metabolic transformation of PFA was detected after [14C]PFA exposure to rat renal cortical slices, homogenate, or to blood. We conclude that PFA causes phosphaturia by direct inhibition of Na+-Pi symport across BBM in proximal tubules, acting from the luminal side. Thus PFA (foscarnet) has a unique direct mechanism of phosphaturic effect, via its action on Pi reabsorption in proximal tubules in vivo.

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