Sentences with phrase «of estrogen activity»

However, we did see different patterns of estrogen activity change according to participants» body mass index (BMI).

Not exact matches

One of the concerns is that phytoestrogens, especially isoflavones, may have estrogen - like activity.

Researchers in England have found that in trace amounts, they activate estrogen receptors in cells, which in turn alters the activity of certain genes.

These smooth and sweet cuties pack some serious phytoestrogens, which mimic the activity of estrogen in the body.

Using in vitro, or test tube, experiments, the researchers applied these chemicals to human cancer cells to measure changes of estrogen receptor - and androgen receptor - target genes and transcriptional activity.

«We found bazedoxifene binds to the estrogen receptor and interferes with its activity, but the surprising thing we then found was that it also degrades the receptor; it gets rid of it,» said senior author Donald McDonnell, PhD, chair of Duke's Department of Pharmacology and Cancer Biology.

Gorelick, the lead author, Halpern and Alice Hung of Carnegie, along with Luke Iwanowicz and Vicki Blazer of the Fish Health Branch of the U.S. Geological Survey, used genetically modified zebrafish that show estrogen receptor activity on a cell's DNA.

Elevated exposure to estrogen over a long period is linked with higher breast cancer rates in adulthood and earlier onset of risky sexual activity.

Injection of estrogens (17β - estradiol or diethylstilbestrol) into immature chicks results in a marked (30 - to 50-fold) increase in the ornithine decarboxylase activity of oviductal homogenates within a 4 - hour period.

An elevation of decarboxylase activity was obtained in vitro when oviducts from immature chicks were incubated in the presence of estrogen.

Then, they added estrogen to see if gene activity changed, honing in on TLR8, an X chromosome - linked gene whose expression has already been implicated in the development of lupus.

The researchers experimentally manipulated estrogen levels over several months in healthy women with both versions of the gene while monitoring their brain activity as they performed a working memory task.

Enlarged male breasts, or gynecomastia, result from an imbalance between the activity of estrogens, which stimulate breast growth, and estrogen - inhibiting androgens.

Gwendolyn Thomas, assistant professor of exercise science, is the co-author of a groundbreaking article in the Obesity Journal (The Obesity Society, 2017) about the effects of exercise and physical activity on postmenopausal breast cancer survivors taking AIs — hormone - therapy drugs that stop the production of estrogen.

«We found that if we exposed mice to one of two common endocrine disruptors - bisphenol A (BPA) or ethinyl estradiol (EE), which is the estrogen present in birth control pills, during development, it caused later disruptions in voluntary physical activity once the mice became adults,» said Cheryl Rosenfeld, associate professor of biomedical sciences in the College of Veterinary Medicine and a researcher in the Bond Life Sciences Center at MU.

BPA is believed to exert its biological effects largely through loose occupancy of the estrogen receptor, and there are reports of both estrogen agonist [7] and androgen antagonist [8] activity.

«Our data further suggest that, despite the historical bias toward the effects of estrogen on the estrogen receptor, it's the progesterone receptor that dominantly controls estrogen receptor activity when both receptors are present and activated.»

Women's Health Initiative researchers found a relationship between obesity, physical activity and triple - negative breast cancer, a subtype of breast cancer characterized by a lack of estrogen, progesterone and HER2 expression.

Its chemical structure is similar to that of bisphenol A (BPA), and like BPA, is can mimic the activity of estrogen, a female sex hormone.

Estrogen and androgen receptor activities of hydraulic fracturing chemicals and surface and ground water in a drilling - dense region.

Recent estimates suggest that as many as 1.9 million children younger than 18 years have a sport - or recreation - related concussion each year in the United States.1 This injury is biomechanically induced, with symptoms resulting from neuronal dysfunction due to functional and neurometabolic alterations rather than gross structural abnormalities.2 Compared with boys involved in similar activities, girls experience higher rates of sport - related concussion,3 - 7 report more severe symptoms,8 - 11 demonstrate worse cognitive impairment,8 - 10, 12 and take longer to recover.11 The neural mechanisms behind these postconcussion sex differences are poorly understood but have been attributed to differences in neuroanatomy and physiology, 13 cerebral blood flow, 14 and the female sex hormones estrogen and progesterone.15 - 17

The activity of mPOA neurotensin neurons was more intense in female mice that had high estrogen levels or a mixture of estrogen and progesterone, which shoots up before they become fertile.

Susan Amara, USA - «Regulation of transporter function and trafficking by amphetamines, Structure - function relationships in excitatory amino acid transporters (EAATs), Modulation of dopamine transporters (DAT) by GPCRs, Genetics and functional analyses of human trace amine receptors» Tom I. Bonner, USA (Past Core Member)- Genomics, G protein coupled receptors Michel Bouvier, Canada - Molecular Pharmacology of G protein - Coupled Receptors; Molecular mechanisms controlling the selectivity and efficacy of GPCR signalling Thomas Burris, USA - Nuclear Receptor Pharmacology and Drug Discovery William A. Catterall, USA (Past Core Member)- The Molecular Basis of Electrical Excitability Steven Charlton, UK - Molecular Pharmacology and Drug Discovery Moses Chao, USA - Mechanisms of Neurotophin Receptor Signaling Mark Coles, UK - Cellular differentiation, human embryonic stem cells, stromal cells, haematopoietic stem cells, organogenesis, lymphoid microenvironments, develomental immunology Steven L. Colletti, USA Graham L Collingridge, UK Philippe Delerive, France - Metabolic Research (diabetes, obesity, non-alcoholic fatty liver, cardio - vascular diseases, nuclear hormone receptor, GPCRs, kinases) Sir Colin T. Dollery, UK (Founder and Past Core Member) Richard M. Eglen, UK Stephen M. Foord, UK David Gloriam, Denmark - GPCRs, databases, computational drug design, orphan recetpors Gillian Gray, UK Debbie Hay, New Zealand - G protein - coupled receptors, peptide receptors, CGRP, Amylin, Adrenomedullin, Migraine, Diabetes / obesity Allyn C. Howlett, USA Franz Hofmann, Germany - Voltage dependent calcium channels and the positive inotropic effect of beta adrenergic stimulation; cardiovascular function of cGMP protein kinase Yu Huang, Hong Kong - Endothelial and Metabolic Dysfunction, and Novel Biomarkers in Diabetes, Hypertension, Dyslipidemia and Estrogen Deficiency, Endothelium - derived Contracting Factors in the Regulation of Vascular Tone, Adipose Tissue Regulation of Vascular Function in Obesity, Diabetes and Hypertension, Pharmacological Characterization of New Anti-diabetic and Anti-hypertensive Drugs, Hypotensive and antioxidant Actions of Biologically Active Components of Traditional Chinese Herbs and Natural Plants including Polypehnols and Ginsenosides Adriaan P. IJzerman, The Netherlands - G protein - coupled receptors; allosteric modulation; binding kinetics Michael F Jarvis, USA - Purines and Purinergic Receptors and Voltage-gated ion channel (sodium and calcium) pharmacology Pain mechanisms Research Reproducibility Bong - Kiun Kaang, Korea - G protein - coupled receptors; Glutamate receptors; Neuropsychiatric disorders Eamonn Kelly, Prof, UK - Molecular Pharmacology of G protein - coupled receptors, in particular opioid receptors, regulation of GPCRs by kinasis and arrestins Terry Kenakin, USA - Drug receptor pharmacodynamics, receptor theory Janos Kiss, Hungary - Neurodegenerative disorders, Alzheimer's disease Stefan Knapp, Germany - Rational design of highly selective inhibitors (so call chemical probes) targeting protein kinases as well as protein interaction inhibitors of the bromodomain family Andrew Knight, UK Chris Langmead, Australia - Drug discovery, GPCRs, neuroscience and analytical pharmacology Vincent Laudet, France (Past Core Member)- Evolution of the Nuclear Receptor / Ligand couple Margaret R. MacLean, UK - Serotonin, endothelin, estrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function of GABA - A receptors; mode of action of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation of expression and function of the ATP - binding cassette (ABC) tranEstrogen Deficiency, Endothelium - derived Contracting Factors in the Regulation of Vascular Tone, Adipose Tissue Regulation of Vascular Function in Obesity, Diabetes and Hypertension, Pharmacological Characterization of New Anti-diabetic and Anti-hypertensive Drugs, Hypotensive and antioxidant Actions of Biologically Active Components of Traditional Chinese Herbs and Natural Plants including Polypehnols and Ginsenosides Adriaan P. IJzerman, The Netherlands - G protein - coupled receptors; allosteric modulation; binding kinetics Michael F Jarvis, USA - Purines and Purinergic Receptors and Voltage-gated ion channel (sodium and calcium) pharmacology Pain mechanisms Research Reproducibility Bong - Kiun Kaang, Korea - G protein - coupled receptors; Glutamate receptors; Neuropsychiatric disorders Eamonn Kelly, Prof, UK - Molecular Pharmacology of G protein - coupled receptors, in particular opioid receptors, regulation of GPCRs by kinasis and arrestins Terry Kenakin, USA - Drug receptor pharmacodynamics, receptor theory Janos Kiss, Hungary - Neurodegenerative disorders, Alzheimer's disease Stefan Knapp, Germany - Rational design of highly selective inhibitors (so call chemical probes) targeting protein kinases as well as protein interaction inhibitors of the bromodomain family Andrew Knight, UK Chris Langmead, Australia - Drug discovery, GPCRs, neuroscience and analytical pharmacology Vincent Laudet, France (Past Core Member)- Evolution of the Nuclear Receptor / Ligand couple Margaret R. MacLean, UK - Serotonin, endothelin, estrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function of GABA - A receptors; mode of action of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation of expression and function of the ATP - binding cassette (ABC) tranestrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function of GABA - A receptors; mode of action of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation of expression and function of the ATP - binding cassette (ABC) transporters

New research from Emory University School of Medicine and Harvard Medical School provides insight into how estrogen changes gene activity in the brain to achieve its protective effects.

On the other hand, some scientific evidence hints that higher levels of estrogen lead to an increased activity of the alpha - adrenergic receptors in the lower part of the body, which slow fat release and are the reason why many women have a pear shape fat distribution.

Soy may also mimic the activity of the hormone estrogen in your body and can interfere with hormonal and overall thyroid function.

Even low exposures of BPA, for example, a common chemical in plastics, can increase our risk of breast cancer because it has estrogen - mimicking biological activity.

This is partly due to reduction in the production of hormones such as testosterone, human growth hormone and estrogen and also because of lack of weight - bearing activity.

The biological activity of estrogen and testosterone, the sex hormones of the body, which are believed to play a part in type 2 diabetes development are regulated by a protein known as SHBG (sex hormone - binding globulin).

«A high level of circulating insulin could interfere with sex hormone activity and boost estrogen levels, both of which might increase the number of menstrual cycles and deplete egg supply faster, thus causing an earlier menopause.»

Consuming alcohol in big quantities has been correlated to boosting the activity of aromatization which is the process in which testosterone is converted into estrogen.

In addition, not only are some of them estrogen mimickers, but others will suppress your enzymatic activity necessary to produce androgen hormones, while other will block the receptor sites on the cell.

Estrogen reduces endothelial progenitor cell senescence through augmentation of telomerase activity.

They can mimic the action of estrogen produced in cells and can alter hormonal activity in women and men.

Some research has focused on parabens, which are preservatives used in some deodorants and antiperspirants that have been shown to mimic the activity of estrogen in the body's cells.

These estrogen mimickers not only affect the balance of estrogen to progesterone in our body but also affect estrogen metabolism and alter hormone activity.

BCPs can for that reason 1) raise estrogen levels — which either corrects an estrogen deficiency or helps balance the activity of runaway testosterone — and they can also 2) restore proper balance between estrogen and progesterone, which is important for keeping progesterone levels within their proper parameters.

If despite carefully increasing doses of bio-identical estrogens, your patient is still experiencing hot flushes and other menopausal symptoms suggestive of insufficient estrogen (e.g., night sweats, insomnia, memory and concentration difficulties, anxiety), she may be hyperexcreting estrogen due to upregulated Phase I (the cytochrome P450 family of enzymes) activity.

The blood activities after formation of the healthy 2 - hydroxy estrogens were compared to those of 4 - hydroxy estrogen.

The reasoning goes as follows: estrogen is a sex hormone that is essential to female bone health because it promotes the activity of osteoblasts, which are cells that produce bone.

EstroQuench ™ is used by healthcare professionals to reduce estrogens levels by inhibiting aromatase activity, which will decrease the conversion of androgens (testosterone and androstenedione) to estrogens (estradiol and estrone).

BHRT supports healthy sexual activity in women by restoring depleted levels of testosterone and estrogen, thereby restoring sexual interest to previous levels.

Balanced digestive flora also reduces the activity of an enzyme called beta - glucaronidase, which is linked to estrogen - related cancers.

In vivo, breast cancer growth is regulated by estrogens and peptide growth factors, such as epidermal growth factor (EGF), the receptor of which has intrinsic PTK activity.

This aromatase activity is the enzymatic conversion of androsterone and testosterone into estradiol, more commonly known as E2 or estrogen.

Around the time of ovulation, estrogen causes changes in the vaginal mucus, making it more tolerant of male penetration during sexual activity and more hospitable to sperm.

When we have high levels of estrogen, it generally means that we have lower levels of testosterone and higher levels of what is called aromatase activity.

First, we adjusted for age (in y), cigarette smoking (yes or no), physical activity (continuous), current estrogen use (yes or no), menopausal status (yes or no), socioeconomic status (categorical), family history of diabetes and stroke (yes or no), and systolic and diastolic blood pressures (continuous).

C - Reactive Protein levels fluctuate from day to day, and levels increase with aging, high blood pressure, alcohol use, smoking, low levels of physical activity, chronic fatigue, coffee consumption, having elevated triglycerides, insulin resistance and diabetes, taking estrogen, eating a high protein diet, and suffering sleep disturbances, and depression.

Low thyroid activity can also be a result of other things, such as chronic stress or excess estrogen.