scholarly journals Correction to: Hormonal modulation of ESR1 mutant metastasis

Oncogene ◽  
2021 ◽  
Author(s):  
Guowei Gu ◽  
Lin Tian ◽  
Sarah K. Herzog ◽  
Yassine Rechoum ◽  
Luca Gelsomino ◽  
...  
Keyword(s):  
Hormonal Modulation

Hormonal modulation of ishikawa cells during three-dimensional growth in vitro☆

1998 ◽  
Vol 5 (4) ◽  
pp. 217-223 ◽  
Author(s):  
D PINELLI ◽  
J DRAKE ◽  
M WILLIAMS ◽  
D CAVANAGH ◽  
J BECKER
Keyword(s):  
Three Dimensional ◽  
Ishikawa Cells ◽  
Hormonal Modulation ◽  
Dimensional Growth

scholarly journals Hormonal modulation of ESR1 mutant metastasis

Oncogene ◽  
2020 ◽  
Author(s):  
Guowei Gu ◽  
Lin Tian ◽  
Sarah K. Herzog ◽  
Yassine Rechoum ◽  
Luca Gelsomino ◽  
...  
Keyword(s):  
Hormonal Modulation

Role of physical forces in compensatory growth of the lung

1989 ◽  
Vol 257 (4) ◽  
pp. L179-L189 ◽  
Author(s):  
D. E. Rannels
Keyword(s):  
Cell Shape ◽  
Compensatory Growth ◽  
Normal Lung ◽  
Physical Factors ◽  
Physical Force ◽  
Isolated Cells ◽  
Paracrine Factors ◽  
Extracellular Matrix Components ◽  
Hormonal Modulation ◽  
Physical Forces

In many species, partial resection of the lung leads to rapid compensatory growth of the remaining tissue to restore normal lung mass and function. The response to partial pneumonectomy is closely controlled; both its rate and nature are subject to hormonal modulation. Physical factors, particularly distortion of the lung by altered inflation, are likely involved in regulation of the response, although the details of the regulatory mechanisms are not understood. In a number of tissues including the lung, application of external physical force leads to both acute and long-term changes in metabolism. In some cases these include cell growth and division, along with increased production of extracellular matrix components. Similar responses have been described after application of stress to isolated cells in culture. Independent lines of investigation have defined dramatic influences of cell shape on growth, differentiation, and metabolism, but stress-strain relationships at the cellular or subcellular levels are poorly defined. The mechanisms by which changes in cell shape are transduced to intracellular signals likely depend on receptor-mediated interactions with the cytoskeleton, but strain-associated transduction pathways may involve stretch-sensitive ion channels, G protein-dependent reactions, the action of locally produced autocrine or paracrine factors, or a combination of these factors. These observations suggest a general model of the response to pneumonectomy that may be used to formulate specific hypotheses as a basis for future investigations. This approach will provide insight into the mechanisms by which physical forces influence growth and metabolism in the lung and other tissues.

Hormonal modulation of extinction responses induced by sexual steroid hormones in rats

Life Sciences ◽  
1994 ◽  
Vol 54 (21) ◽  
pp. PL363-PL367 ◽  
Author(s):  
Selva Rivas-Arancibia ◽  
Francisca Vazquez-Pereyra
Keyword(s):  
Steroid Hormones ◽  
Sexual Steroid ◽  
Hormonal Modulation

scholarly journals Hormonal Modulation of Amino Acid Neurotransmitter Metabolism in the Arcuate Nucleus of the Adult Female Rat: A Novel Action of Estradiol

Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3237-3244 ◽  
Author(s):  
Tamara Blutstein ◽  
Peter J. Baab ◽  
H. Ronald Zielke ◽  
Jessica A. Mong
Keyword(s):  
Amino Acid ◽  
Adult Female ◽  
Arcuate Nucleus ◽  
Female Rat ◽  
Hormonal Modulation ◽  
Neurotransmitter Metabolism

Hormonal modulation of hepatic plasma membrane lactate transport in cultured rat hepatocytes

1990 ◽  
Vol 10 (6) ◽  
pp. 573-577 ◽  
Author(s):  
H. K. Metcalfe ◽  
R. D. Cohen ◽  
J. P. Monson
Keyword(s):  
Plasma Membrane ◽  
Primary Cultures ◽  
Rat Hepatocytes ◽  
Isolated Hepatocytes ◽  
Similar Magnitude ◽  
Potential Mechanism ◽  
Lactate Transport ◽  
Hormonal Modulation ◽  
Cultured Rat Hepatocytes

Hormonal modulation of hepatic plasma membrane lactate transport was studied in primary cultures of isolated hepatocytes from fed rats to examine the mechanism for the known enhancement of lactate transport in starvation and diabetes. Total cellular lactate entry was increased by 14% in the presence of dexamethasone; this was accounted for by an approximately 40% increase in the carrier-mediated component of entry with no effect on diffusion. A trend of similar magnitude was evident with glucagon. The effects of dexamethasone and glucagon on lactate transport constitute an additional potential mechanism for enhancement of gluconeogenesis by these hormones.

scholarly journals Cytotoxic Activity of Antineoplastic Agents on Fertility: A Systematic Review

2020 ◽  
Vol 42 (11) ◽  
pp. 759-768
Author(s):  
Gabriel Acácio de Moura ◽  
Paula Bruno Monteiro
Keyword(s):  
Antineoplastic Agents ◽  
Site Effect ◽  
Cytotoxic Action ◽  
Long Term Effects ◽  
Treatment Type ◽  
Number Of Patients ◽  
Serum Hormone ◽  
Hormonal Modulation ◽  
Selection Of

Abstract Objective To analyze the long-term effects of antineoplastic treatments on patient fertility. Selection of Studies The studies were selected through the New PubMed, Scielo and Lilacs databases along with references used for the creation of the present work. For the selection of studies, articles published between the periods from January 1, 2015 to April 6, 2020 in the English, Portuguese and Spanish languages were used. As inclusion criteria: cohort studies and studies conducted in vitro. As exclusion criteria: review articles, reported cases, studies that do not address thematic reproduction, studies that do not address the cancer theme, articles that used animals, articles that address the preservation of fertility and articles in duplicate in the bases. Data Collection The collected data included: age of the patient at the beginning of treatment, type of neoplasm, type of antineoplastic treatment, chemotherapy used, radiotherapy dosage, radiotherapy site, effect of antineoplastic agents on fertility and number of patients in the study. Data Synthesis Thirty studies were evaluated, antineoplastic chemotherapy agents and radiotherapy modulate serum hormone levels, reduces germ cell quantities and correlated with an increase in sterility rates. The effects mentioned occur in patients in the prepubertal and postpubertal age. Conclusion Antineoplastic treatments have cytotoxic effects on the germ cells leading to hormonal modulation, and pubertal status does not interfere with the cytotoxic action of therapies.

Pregnancy enhances G protein activation and nitric oxide release from uterine arteries

2001 ◽  
Vol 280 (5) ◽  
pp. H2069-H2075 ◽  
Author(s):  
L. P. Thompson ◽  
C. P. Weiner
Keyword(s):  
Nitric Oxide ◽  
Cholera Toxin ◽  
G Protein ◽  
Pertussis Toxin ◽  
Nitric Oxide Synthase Inhibitor ◽  
Protein Activation ◽  
Nitric Oxide Release ◽  
G Protein Activation ◽  
Hormonal Modulation ◽  
Synthase Inhibitor

We hypothesized that pregnancy modulates receptor-mediated responses of the uterine artery (UA) by altering G protein activation or coupling. Relaxation and contraction to NaF (0.5–11.5 mM), acetylcholine (10−9–10−5 M), and bradykinin (10−12–3 × 10−5 M) were measured in isolated UA of pregnant and nonpregnant guinea pigs. Responses were measured in the presence and absence of either cholera toxin (2 μg/ml) or pertussis toxin (Gαs and Gαiinhibitors, respectively). NaF relaxation was endothelium dependent and nitro-l-arginine sensitive (a nitric oxide synthase inhibitor). Relaxation to NaF, acetylcholine, and bradykinin were potentiated by pregnancy. Cholera but not pertussis toxin increased relaxation to acetylcholine and bradykinin in UA from nonpregnant animals, had no effect in UA from pregnant animals, and abolished the pregnancy-induced differences in acetylcholine relaxation. Cholera toxin potentiated the bradykinin-induced contraction of UA of both pregnant and nonpregnant animals, whereas pertussis toxin inhibited contraction of UA from pregnant animals only. Therefore, pregnancy may enhance agonist-stimulated endothelium-dependent relaxation and bradykinin-induced contraction of UA by inhibiting GTPase activity or enhancing Gαs but not Gαi activation in pregnant animals. Thus the diverse effects of pregnancy on UA responsiveness may result from hormonal modulation of G proteins coupled to their specific receptors.

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