The Nature of the Inhibitory Effect of Normal Human Gastric Jiuice on Heidenhain Pouch Dogs

1958 ◽  
Vol 34 (2) ◽  
pp. 181-187 ◽  
Author(s):  
William O. Smith ◽  
Robert Hoke ◽  
Jerome Landy ◽  
Ranwel Caputto ◽  
Stewart Wolf
Keyword(s):  
Inhibitory Effect ◽  
Heidenhain Pouch ◽  
Normal Human

Inhibition of the Activities of α2-Plasmin inhibitor (PI) and CI inhibitor (CI-Inh) by the Synthetic Fibrinolytic Agent, 3-Hydroxypropyl Flufenamide (Flu-HPA)

1979 ◽  
Author(s):  
L Miles ◽  
J Burnier ◽  
M Verlander ◽  
M Goodman ◽  
A Kleiss ◽  
...  
Keyword(s):  
Plasminogen Activators ◽  
Inhibitory Effect ◽  
Mechanisms Of Action ◽  
Flufenamic Acid ◽  
Clot Lysis ◽  
Factor Xiia ◽  
Dependent Inhibition ◽  
Normal Human ◽  
Plasmin Inhibitor

Flu-HPA is one of a series of flufenamic acid derivations that enhances plasminogen-dependent clot lysis in vitro. Studies of possible mechanisms of action of Flu-HPA were undertaken. The influence of Flu-HPA on the inhibition of purified plasmin by purified PI was studied. PI activity was assessed by its inhibition of the clevage of the tripeptide S-2251 (H-D-Val-Leu-Lys-pNA) by plasmin. Flu-HPA was dissolved in DMF or in methonol and preincubated with PI before addition of plasmin. At Flu-HPA concentrations greater than 1mM and up to 60mM, the inhibitory activity of PI was totally lost. The inhibitory effect of normal human plasma on plasmin was also completely abolished at concentrations of Flu-HPA between 2.5 and 40mM. The effect of Flu-HPA on the inhibition of purified plasma kallikrein by purified CI-Inh was also studied. CI-Inh activity was measured by its inhibition of cleavage of the tripeptide Bz-Pro-Phe-Arg-pNA by kallikrein. When Flu-HPA, dissolved in DMF or in methonol, was preincubated with CI-Inh, a concentration dependent inhibition of CI-Inh activity was observed. CI-Inh activity was abolished by concentrations of Flu-HPA greater than 1mM. Flu-HPA also inhibited the activity of CI-Inh on purified Factor XIIa. These observations suggest that this flufenamic acid derivative may enhance fibrinolysis not only by inhibiting PI activity but also by decreasing the inactivation of plasminogen activators by CI-Inh.

ADRENERGIC CONTROL MECHANISM FOR ACTH SECRETION IN MAN

1973 ◽  
Vol 74 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Yoshikatsu Nakai ◽  
Hiroo Imura ◽  
Teruya Yoshimi ◽  
Shigeru Matsukura
Keyword(s):  
Intravenous Infusion ◽  
Human Subjects ◽  
Blocking Agent ◽  
Inhibitory Effect ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Glucose Levels ◽  
Alpha Receptors ◽  
Normal Human ◽  
Adrenergic Blocking

ABSTRACT In order to determine if an adrenergic mechanism is involved in the secretion of corticotrophin (ACTH), the effect of adrenergic-blocking or -stimulating agent on plasma ACTH, cortisol and glucose levels was studied in normal human subjects. The intravenous infusion of methoxamine, an alpha adrenergic-stimulating agent, caused a rise in plasma ACTH and cortisol. This increase in plasma ACTH and cortisol was significantly inhibited by the simultaneous administration of phentolamine, an alpha adrenergic-blocking agent, in combination with methoxamine. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused no significant change in plasma ACTH and cortisol, although it enhanced the plasma ACTH response to insulin-induced hypoglycaemia. On the other hand, alpha adrenergicblockade by intravenous infusion of phentolamine significantly suppressed the plasma ACTH response to insulin-induced hypoglycaemia. These studies suggest a stimulatory effect of alpha receptors and a possible inhibitory effect of beta receptors on ACTH secretion in man.

INHIBITION BY HUMAN SERUM OF THE ADIPOKINETIC EFFECT OF A HUMAN PITUITARY LIPID-MOBILIZING FACTOR

1972 ◽  
Vol 71 (3) ◽  
pp. 443-453 ◽  
Author(s):  
Olav Trygstad ◽  
Irene Foss
Keyword(s):  
Human Serum ◽  
Gel Filtration ◽  
Deae Cellulose ◽  
Inhibitory Effect ◽  
Disc Electrophoresis ◽  
Inhibitory Protein ◽  
Human Pituitary ◽  
Albumin Fraction ◽  
Pituitary Glands ◽  
Normal Human

ABSTRACT A lipid-mobilizing factor (LMF) with an adipotrophic effect in human and animal fat tissue has been prepared from human pituitary glands. The addition of normal human serum to LMF reduced its lipolytic effect, and it was completely abolished by serum from a group of obese patients, whereas the lipolysis was not influenced by serum from patients with generalized lipodystrophy. By DEAE-cellulose chromatography of human serum the inhibitory effect on LMF was found to be present in a protein fraction less acidic than the main serum albumin fraction. The inhibitory fraction was deprived of some contaminants by Sephadex gel filtration. Disc electrophoresis demonstrated the presence of three components in the inhibitory protein (IP), and they were identified as albumin, transferin, and haemopexin by immuno-electrophoresis. Precipitation of these proteins by their rabbit antisera demonstrated that the inhibitory effect was present in the albumin fraction. Insulin like activity was not observed in IP. A protein binding of LMF by IP could not be demonstrated. Incubation at 37°C for one hour of a mixture of LMF and IP eliminated the electrophoretic picture of LMF. It is concluded that the inhibitory effect of human serum may be due to proteolysis of LMF.

scholarly journals 1337: Inhibitory Effect of Tamsulosin on Normal Human Prostate Epithelial and Stromal Cells

2004 ◽  
Vol 171 (4S) ◽  
pp. 352-352 ◽  
Author(s):  
Tetsuya Takao ◽  
Akira Tsujimura ◽  
Kazutoshi Fujita ◽  
Yasuhiro Matsuoka ◽  
Tohru Takahashi ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Inhibitory Effect ◽  
Human Prostate ◽  
Normal Human

scholarly journals Interferon-Lambda 1 Inhibits Staphylococcus aureus Colonization in Human Primary Keratinocytes

2021 ◽  
Vol 12 ◽  
Author(s):  
Xia Wu ◽  
Yan Zhao ◽  
Ying Gu ◽  
Kun Li ◽  
Xiaojie Wang ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mrna Expression ◽  
Human Keratinocytes ◽  
Skin Lesions ◽  
Inhibitory Effect ◽  
Oxidase Inhibitor ◽  
Primary Keratinocytes ◽  
Intracellular Ros ◽  
Normal Human ◽  
Human Primary Keratinocytes

Atopic dermatitis (AD) is a common inflammatory skin disease. Staphylococcus aureus (S. aureus) colonization in skin lesions occurs in approximately 70% of AD patients. It has been found that IFN-λ1 can inhibit the colonization of S. aureus in normal human nasal mucosa. IFN-λ1 can increase IL-28RA in infected human keratinocytes. In this study, we found that IFN-λ1 can increase mRNA expression of FLG and antimicrobial peptides (AMPs) and inhibit TSLP mRNA expression in infected human keratinocytes. IFN-λ1 can increase intracellular ROS level, decrease STAT1 phosphorylation, and inhibit the colonization of S. aureus in human primary keratinocytes. These effects were attenuated by knocking-down IL-28R and NADPH oxidase inhibitor, suggesting that this function was mediated by JAK-STAT1 signaling pathway. These results suggest that IFN-λ1 might have an inhibitory effect on S. aureus colonization in AD lesions. Our findings might have potential value in the treatment for AD.

The Histidine Requirement of a Normal and a Leukaemia Cell-Line from Man: Comparative Effects on Cell Growth, Metabolism and Composition

1974 ◽  
Vol 15 (2) ◽  
pp. 407-417
Author(s):  
J. B. GRIFFITHS
Keyword(s):  
Cell Growth ◽  
Protein Composition ◽  
Inhibitory Effect ◽  
Leukaemia Cell ◽  
Leukaemia Cell Line ◽  
Marked Inhibitory Effect ◽  
Normal Human ◽  
Therapeutic Enzymes ◽  
Therapy Studies ◽  
Human Leukaemia

The object was to determine whether the depletion of histidine would have a more marked inhibitory effect on human leukaemia cells than on normal human cells, thus indicating a wider use for enzymes in cancer therapy. Studies of the effect of histidine concentration on cell growth, death, metabolism, protein composition, histidine uptake and utilization by cells were carried out. The medium and intracellular concentrations of histidine required for optimum cell growth and metabolism were much lower than for any other amino acid that has been studied. Also, there was very little evidence of cell death occurring in the absence of histidine. The results showed that cells in culture have a very low histidine requirement and that although the leukaemia cells were slightly more dependent upon histidine than normal cells the effect of histidine depletion is not critical enough to show much promise as a method of controlling leukaemia by therapeutic enzymes.

Bronchoprotective and bronchodilatory effects of deep inspiration in rabbits subjected to bronchial challenge

2001 ◽  
Vol 91 (6) ◽  
pp. 2511-2516 ◽  
Author(s):  
S. J. Gunst ◽  
X. Shen ◽  
R. Ramchandani ◽  
R. S. Tepper
Keyword(s):  
Human Subjects ◽  
Inhibitory Effect ◽  
Airway Responsiveness ◽  
Deep Inspiration ◽  
Contractile Apparatus ◽  
Airway Reactivity ◽  
Airway Response ◽  
Normal Human ◽  
Airway Responses

The effect of deep inspiration (DI) on airway responsiveness differs in asthmatic and normal human subjects. The mechanism for the effects of DI on airway responsiveness in vivo has not been identified. To elucidate potential mechanisms, we compared the effects of DI imposed before or during induced bronchoconstriction on the airway response to methacholine (MCh) in rabbits. The changes in airway resistance in response to intravenous MCh were continuously monitored. DI depressed the maximum response to MCh when imposed before or during the MCh challenge; however, the inhibitory effect of DI was greater when imposed during bronchoconstriction. Because immature rabbits have greater airway reactivity than mature rabbits, we compared the effects of DI on their airway responses. No differences were observed. Our results suggest that the mechanisms by which DI inhibits airway responsiveness do not depend on prior activation of airway smooth muscle (ASM). These results are consistent with the possibility that reorganization of the contractile apparatus caused by stretch of ASM during DI contributes to depression of the airway response.

Retinoic Acid Prevents Phosphorylation of pRB in Normal Human B Lymphocytes: Regulation of Cyclin E, Cyclin A, and p21Cip1

Blood ◽  
1999 ◽  
Vol 94 (4) ◽  
pp. 1348-1358 ◽  
Author(s):  
Soheil Naderi ◽  
Heidi Kiil Blomhoff
Keyword(s):  
Retinoic Acid ◽  
B Lymphocytes ◽  
Retinoic Acid Receptor ◽  
Cyclin E ◽  
Cyclin A ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Growth Inhibitory Effect ◽  
Growth Inhibitory ◽  
Normal Human

The mechanisms underlying the growth-inhibitory effect of retinoids on normal human B lymphocytes are not well understood. We addressed this issue by examining the effect of retinoic acid on the cell cycle machinery involved in G1/S transition. When retinoic acid was administered to B cells stimulated into mid to late G1 by anti-IgM antibodies (anti-μ) and Staphylococcus aureus crude cell suspension (SAC), the phosphorylation of pRB required for S-phase entry was prevented in a time- and dose-dependent manner. Thus, 2-hour treatment with retinoic acid at the optimal concentration of 1 μmol/L prevented phosphorylation of pRB, and effects were noted at concentrations as low as 10 nmol/L. Based on our results, we suggest that the rapid effect of retinoic acid on pRB phosphorylation is due primarily to the reduced expression of cyclin E and cyclin A in late G1. This could lead to the diminished cyclin E– and cyclin A–associated kinase activities noted as early as 2 hours after addition of retinoic acid. Furthermore, our results imply that the transient induction of p21Cip1 could also be involved. Thus, retinoic acid induced a rapid, but transient increased binding of p21Cip1 to CDK2. The retinoic acid receptor (RAR) agonist TTNPB mimicked the key events affected by retinoic acid, such as pRB phosphorylation, cyclin E expression, and expression of p21Cip1, whereas the RAR-selective antagonist Ro 41-5253 counteracted the effects of retinoic acid. This implies that retinoic acid mediates its growth-inhibitory effect on B lymphocytes via the nuclear receptors.

Sign in / Sign up

Export Citation Format

Share Document