Pub Date : 2013-01-01DOI: 10.4172/2157-7536.S3-001
R. Paulin, S. Bonnet
Vascular remodeling is characterized by a narrowing of the lumen of the vessels, resulting in decreased blood flow, increased pressure and heart failure. This process is found in diseases like atherosclerosis, restenosis after angioplasty, transplants coronary disease, systemic and pulmonary hypertensive vascular disease, and is stimulated by elevated levels of cholesterol, inflammation, oxidative stress, excess of vasodilating molecules and growth factors. Efficient treatments able to fix or prevent the progression of this process are still missing. The hormone dehydroepiandrosterone (DHEA), which levels decrease with aging while cardiovascular risks increase, was hypothesized to have a role in the pathophysiology of vascular diseases. Despite the fact that numerous properties such as fat-reducing, anti-oxidant, vasodilating, anti-inflammatory and anti-proliferative have emerged from two decade of studies, DHEA remain clinically underused in the treatment of vascular remodeling diseases. The lack of understanding of the exact mechanism of action and some controversial epidemiological studies are not foreign to the fact that DHEA is shunned. Nonetheless, we believe that DHEA cannot be ignored since promising results were obtained pre-clinically and clinically in the treatment of vascular remodeling diseases. We are probably close to understand the function of this molecule, especially by its action as a peroxisome proliferator, and it will be a shame to deprive patient of a way to improve their quality of life, or worst a way to extend their survival.
{"title":"Dehydroepiandrosterone, Over-studied but Under-used in the Treatment of Vascular Remodeling Diseases","authors":"R. Paulin, S. Bonnet","doi":"10.4172/2157-7536.S3-001","DOIUrl":"https://doi.org/10.4172/2157-7536.S3-001","url":null,"abstract":"Vascular remodeling is characterized by a narrowing of the lumen of the vessels, resulting in decreased blood flow, increased pressure and heart failure. This process is found in diseases like atherosclerosis, restenosis after angioplasty, transplants coronary disease, systemic and pulmonary hypertensive vascular disease, and is stimulated by elevated levels of cholesterol, inflammation, oxidative stress, excess of vasodilating molecules and growth factors. Efficient treatments able to fix or prevent the progression of this process are still missing. The hormone dehydroepiandrosterone (DHEA), which levels decrease with aging while cardiovascular risks increase, was hypothesized to have a role in the pathophysiology of vascular diseases. Despite the fact that numerous properties such as fat-reducing, anti-oxidant, vasodilating, anti-inflammatory and anti-proliferative have emerged from two decade of studies, DHEA remain clinically underused in the treatment of vascular remodeling diseases. The lack of understanding of the exact mechanism of action and some controversial epidemiological studies are not foreign to the fact that DHEA is shunned. Nonetheless, we believe that DHEA cannot be ignored since promising results were obtained pre-clinically and clinically in the treatment of vascular remodeling diseases. We are probably close to understand the function of this molecule, especially by its action as a peroxisome proliferator, and it will be a shame to deprive patient of a way to improve their quality of life, or worst a way to extend their survival.","PeriodicalId":17132,"journal":{"name":"Journal of steroids & hormonal science","volume":"56 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91404059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.4172/2157-7536.S2-006
G. E. Jensen, N. Nikolov, Karin Dreisig, A. Vinggaard, J. Russel, Niemelä
For the development of QSAR models for Androgen Receptor (AR) antagonism, a training set based on reporter gene data from Chinese hamster ovary (CHO) cells was constructed. The training set is composed of data from the literature as well as new data for 51 cardiovascular drugs screened for AR antagonism in our laboratory. The data set represents a wide range of chemical structures and various functions. Twelve percent of the screened drugs were AR antagonisms; three out of six statins showed AR antagonism, two showed cytotoxicity and one was negative. The newly identified AR antagonisms are: Lovastatin, Simvastatin, Mevastatin, Amiodaron, Docosahexaenoic acid and Dilazep. A total of 874 (231 positive, 643 negative) chemicals constitute the training set for the model. The Case Ultra expert system was used to construct the QSAR model. The model was cross-validated (leave-groups-out) with a concordance of 78.4%, a specificity of 86.1% and a sensitivity of 57.9%. The model was run on a set of 51,240 EINECS chemicals, and 74% were within the domain of the model. Approximately 9.2% of the chemicals in domain of the model were predicted active for AR antagonism. Case Ultra identified common alerts among different chemicals. By comparing biophores (alerts in positive chemicals) and biophobes (alerts in negative chemicals), it appears that chlorine (Cl) and bromine (Br) enhance AR antagonistic effect whereas nitrogen (N) seems to decrease the effect. A specific study of benzophenones and benzophenone derivatives indicate that a radical with a “high” number of atoms in 4-position and/or other positions generally decrease the anti-androgenic effect.
{"title":"QSAR Model for Androgen Receptor Antagonism - Data from CHO Cell Reporter Gene Assays","authors":"G. E. Jensen, N. Nikolov, Karin Dreisig, A. Vinggaard, J. Russel, Niemelä","doi":"10.4172/2157-7536.S2-006","DOIUrl":"https://doi.org/10.4172/2157-7536.S2-006","url":null,"abstract":"For the development of QSAR models for Androgen Receptor (AR) antagonism, a training set based on reporter gene data from Chinese hamster ovary (CHO) cells was constructed. The training set is composed of data from the literature as well as new data for 51 cardiovascular drugs screened for AR antagonism in our laboratory. The data set represents a wide range of chemical structures and various functions. Twelve percent of the screened drugs were AR antagonisms; three out of six statins showed AR antagonism, two showed cytotoxicity and one was negative. The newly identified AR antagonisms are: Lovastatin, Simvastatin, Mevastatin, Amiodaron, Docosahexaenoic acid and Dilazep. A total of 874 (231 positive, 643 negative) chemicals constitute the training set for the model. The Case Ultra expert system was used to construct the QSAR model. The model was cross-validated (leave-groups-out) with a concordance of 78.4%, a specificity of 86.1% and a sensitivity of 57.9%. The model was run on a set of 51,240 EINECS chemicals, and 74% were within the domain of the model. Approximately 9.2% of the chemicals in domain of the model were predicted active for AR antagonism. Case Ultra identified common alerts among different chemicals. By comparing biophores (alerts in positive chemicals) and biophobes (alerts in negative chemicals), it appears that chlorine (Cl) and bromine (Br) enhance AR antagonistic effect whereas nitrogen (N) seems to decrease the effect. A specific study of benzophenones and benzophenone derivatives indicate that a radical with a “high” number of atoms in 4-position and/or other positions generally decrease the anti-androgenic effect.","PeriodicalId":17132,"journal":{"name":"Journal of steroids & hormonal science","volume":"290 1","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78523512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.4172/2157-7536.1000141
A. L. Cerda-Molina, L. Hernández-López, Javier I. Borráz-León, C. O‐Rodríguez, R. Chavira-Ramírez
Previous research has shown that axillar and vaginal odors from ovulating women are recognized by men, but no research has been done exploring whether body odors signal other physical attributes of women such as waist-to-hip ratio (WHR) or endocrine status. Our goal was to investigate whether testosterone increased in men after smelling axillary odors of women with different WHR and with low or high levels of steroid hormones. We measured men’s testosterone before and after 30 min of being exposed to fresh axillar odors collected from young women or a neutral odor as control situation. Men had to rate the attractiveness and intensity of the scent. We compared the response of men according to women’s WHR and salivary testosterone, estradiol and progesterone. Although the main literature commonly reports that men judge a WHR around 0.7 to be more visually attractive, our results showed that men rated samples of high WHR (0.75-0.84) and high estradiol women as more attractive. In addition, men’s testosterone increased after smelling the odors of high WHR, high estradiol and high testosterone women. High WHR women exhibited the highest testosterone and estradiol levels compared to the other WHR categories (0.66-0.74). We concluded that scents are cues that not only signal fertility but also physical attributes related to reproductive health.
{"title":"MenâÂÂs Exposure to WomenâÂÂs Odors: The Effect of WomenâÂÂs Waist to Hip Ratioand Steroid Hormones","authors":"A. L. Cerda-Molina, L. Hernández-López, Javier I. Borráz-León, C. O‐Rodríguez, R. Chavira-Ramírez","doi":"10.4172/2157-7536.1000141","DOIUrl":"https://doi.org/10.4172/2157-7536.1000141","url":null,"abstract":"Previous research has shown that axillar and vaginal odors from ovulating women are recognized by men, but no research has been done exploring whether body odors signal other physical attributes of women such as waist-to-hip ratio (WHR) or endocrine status. Our goal was to investigate whether testosterone increased in men after smelling axillary odors of women with different WHR and with low or high levels of steroid hormones. We measured men’s testosterone before and after 30 min of being exposed to fresh axillar odors collected from young women or a neutral odor as control situation. Men had to rate the attractiveness and intensity of the scent. We compared the response of men according to women’s WHR and salivary testosterone, estradiol and progesterone. Although the main literature commonly reports that men judge a WHR around 0.7 to be more visually attractive, our results showed that men rated samples of high WHR (0.75-0.84) and high estradiol women as more attractive. In addition, men’s testosterone increased after smelling the odors of high WHR, high estradiol and high testosterone women. High WHR women exhibited the highest testosterone and estradiol levels compared to the other WHR categories (0.66-0.74). We concluded that scents are cues that not only signal fertility but also physical attributes related to reproductive health.","PeriodicalId":17132,"journal":{"name":"Journal of steroids & hormonal science","volume":"117 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79486409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.4172/2157-7536.1000131
R. Bánhegyi, I. Lacz, F. Fülöp, E. Mellár, B. Pikó
Nowadays we cannot find a cancer, in which the targeted therapy based on targeted diagnostics (immunohistochemistry, FISH, etc.) would not stand in the centre of the investigations. Breast cancer is not an exception either. Although the optimally performed surgery and the adequately planned radiotherapy are still important elements in the treatment of breast cancer and the achievement of effective local tumor control but their role has essentially changed in the last few years. In the treatment of patient who has been suffering from breast cancer for years either with or without his/her knowledge, the surgery should not be performed as soon as possible but when the patient “benefits” the most from this procedure. If distant metastases are present the removal of the tumor from the breast which means only the tip of the iceberg is absolutely unnecessary or it is required only in special cases. Systemic tumor control can be reached only by medicinal treatment. Regarding these treatments the importance of endocrine therapies (antiestrogens, aromatase inhibitors, LH-RH analogues etc.) traditional and modern chemotherapies (antracyclines, taxanes, platinum and pyrimidine derivatives, eribulin etc.) and the targeted biological therapies (trastuzumab, lapatinib, bevacizumab, olaparib etc.) can be emphasized. The targets of these biological therapies are either extracellular or intracellular molecular targets, such as estrogen receptor (tamoxifen, anastrazole, letrozole, exemestane, fulvestrant etc.) HER2 (trastuzumab, lapatinib, etc.), VEGF (bevacizumab, etc.) PARP (olaparib). It is well-known that due to frequent hormone sensitivity of breast cancer drugs influencing the hormonal effect are very effective. From these the importance of fulvestrant is discussed in our article. Based on literature data fulvestrant proved to be efficient both in locally advanced and metastatic breast cancers even if it was administered not as first (or second) line therapy.
{"title":"The Role of Fulvestrant in the Treatment of Metastatic Breast Cancer: A Case Report","authors":"R. Bánhegyi, I. Lacz, F. Fülöp, E. Mellár, B. Pikó","doi":"10.4172/2157-7536.1000131","DOIUrl":"https://doi.org/10.4172/2157-7536.1000131","url":null,"abstract":"Nowadays we cannot find a cancer, in which the targeted therapy based on targeted diagnostics (immunohistochemistry, FISH, etc.) would not stand in the centre of the investigations. Breast cancer is not an exception either. Although the optimally performed surgery and the adequately planned radiotherapy are still important elements in the treatment of breast cancer and the achievement of effective local tumor control but their role has essentially changed in the last few years. In the treatment of patient who has been suffering from breast cancer for years either with or without his/her knowledge, the surgery should not be performed as soon as possible but when the patient “benefits” the most from this procedure. If distant metastases are present the removal of the tumor from the breast which means only the tip of the iceberg is absolutely unnecessary or it is required only in special cases. Systemic tumor control can be reached only by medicinal treatment. Regarding these treatments the importance of endocrine therapies (antiestrogens, aromatase inhibitors, LH-RH analogues etc.) traditional and modern chemotherapies (antracyclines, taxanes, platinum and pyrimidine derivatives, eribulin etc.) and the targeted biological therapies (trastuzumab, lapatinib, bevacizumab, olaparib etc.) can be emphasized. The targets of these biological therapies are either extracellular or intracellular molecular targets, such as estrogen receptor (tamoxifen, anastrazole, letrozole, exemestane, fulvestrant etc.) HER2 (trastuzumab, lapatinib, etc.), VEGF (bevacizumab, etc.) PARP (olaparib). It is well-known that due to frequent hormone sensitivity of breast cancer drugs influencing the hormonal effect are very effective. From these the importance of fulvestrant is discussed in our article. Based on literature data fulvestrant proved to be efficient both in locally advanced and metastatic breast cancers even if it was administered not as first (or second) line therapy.","PeriodicalId":17132,"journal":{"name":"Journal of steroids & hormonal science","volume":"5 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74254679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.4172/2157-7536.1000135
I. Sakuma, J. Saito, Y. Matsuzawa, M. Omura, S. Matsui, K. Nishimoto, K. Mukai, T. Nishikawa
A 52-year old woman was admitted to our hospital for evaluation of left adrenal incidenataloma. Endocrinological examination showed Cushing’s syndrome (CS) complicated with masked primary aldosteronism (PA). On the other hand, multiple sampling from the central veins and one or two tributaries of the adrenal veins before and after ACTH-stimulation (multiple AVS) clearly revealed bilateral hyperaldosteronism with excess cortisol secretion from the left adrenal. Thus, we diagnosed this case as CS due to left adrenal tumor with bilateral hyperaldosteronism, and left adrenalectomy was done. Immunohistochemical analysis of the removed left adrenal showed cortisol-producing adenoma and multiple aldosterone-producing cell clusters (APCCs) expressing CYP11B2 within the attached adrenal. Bilateral PA is mostly diagnosed as idiopathic hyperaldosteronism (IHA). IHA has not been examined enough pathologically. We first describe here a possible involvement of APCCs inducing hyperaldosteronism in a case of bilateral PA with a cortisol-producing-adenoma.
{"title":"Multiple Sampling from the Central Veins with their Tributaries can Detect Bilateral Hyperaldosteronism with a Cortisol-Producing Adenoma in a Hypertensive Patient","authors":"I. Sakuma, J. Saito, Y. Matsuzawa, M. Omura, S. Matsui, K. Nishimoto, K. Mukai, T. Nishikawa","doi":"10.4172/2157-7536.1000135","DOIUrl":"https://doi.org/10.4172/2157-7536.1000135","url":null,"abstract":"A 52-year old woman was admitted to our hospital for evaluation of left adrenal incidenataloma. Endocrinological examination showed Cushing’s syndrome (CS) complicated with masked primary aldosteronism (PA). On the other hand, multiple sampling from the central veins and one or two tributaries of the adrenal veins before and after ACTH-stimulation (multiple AVS) clearly revealed bilateral hyperaldosteronism with excess cortisol secretion from the left adrenal. Thus, we diagnosed this case as CS due to left adrenal tumor with bilateral hyperaldosteronism, and left adrenalectomy was done. Immunohistochemical analysis of the removed left adrenal showed cortisol-producing adenoma and multiple aldosterone-producing cell clusters (APCCs) expressing CYP11B2 within the attached adrenal. Bilateral PA is mostly diagnosed as idiopathic hyperaldosteronism (IHA). IHA has not been examined enough pathologically. We first describe here a possible involvement of APCCs inducing hyperaldosteronism in a case of bilateral PA with a cortisol-producing-adenoma.","PeriodicalId":17132,"journal":{"name":"Journal of steroids & hormonal science","volume":"IM-31 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84744958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.4172/2157-7536.1000142
Emmanuela Quental Callou de Sá, Francisco Carleial Feijio de Sa, A. Neto, Juliana Viana Pinheiro
In this century cardiovascular disease (CVD) is the most common isolated cause of death in developed countries. Many studies have suggested that men with low testosterone levels present higher incidence of components of metabolic syndrome and are at a greater risk of developing CVD. Testosterone can affect the development of atherosclerosis in the coronary arteries. While this androgen seems to have a cardioprotective effect by benefiting endothelial function, inducing vasodilation, and reducing fat mass, insulin resistance and chronic inflammation, it also appears to increase endothelin, thromboxane A2 and reactive oxygen species and renal smooth muscle cells. The relation between testosterone and coronary disease in men has been the focus of study of many authors. Most studies point to a neutral and/or protective effect of endogenous testosterone in male cardiovascular health. Unfortunately, many intervention studies have not been able to confirm this effect with testosterone therapy. More studies are needed to elucidate the pathogenic mechanisms of testosterone in cardiovascular health and to evaluate androgen receptor polymorphisms and their physiological responses to testosterone.
{"title":"Testosterone and Cardiovascular Disease in Men","authors":"Emmanuela Quental Callou de Sá, Francisco Carleial Feijio de Sa, A. Neto, Juliana Viana Pinheiro","doi":"10.4172/2157-7536.1000142","DOIUrl":"https://doi.org/10.4172/2157-7536.1000142","url":null,"abstract":"In this century cardiovascular disease (CVD) is the most common isolated cause of death in developed countries. Many studies have suggested that men with low testosterone levels present higher incidence of components of metabolic syndrome and are at a greater risk of developing CVD. Testosterone can affect the development of atherosclerosis in the coronary arteries. While this androgen seems to have a cardioprotective effect by benefiting endothelial function, inducing vasodilation, and reducing fat mass, insulin resistance and chronic inflammation, it also appears to increase endothelin, thromboxane A2 and reactive oxygen species and renal smooth muscle cells. The relation between testosterone and coronary disease in men has been the focus of study of many authors. Most studies point to a neutral and/or protective effect of endogenous testosterone in male cardiovascular health. Unfortunately, many intervention studies have not been able to confirm this effect with testosterone therapy. More studies are needed to elucidate the pathogenic mechanisms of testosterone in cardiovascular health and to evaluate androgen receptor polymorphisms and their physiological responses to testosterone.","PeriodicalId":17132,"journal":{"name":"Journal of steroids & hormonal science","volume":"1978 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90271794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.4172/2157-7536.1000E113
Juan Ding
Dry eye disease (DED) is a very prevalent eye disorder, affecting 40 million people in the United States alone. The primary cause of DED is meibomian gland dysfunction (MGD) [1], which by itself is a disease entity. The meibomian gland is a large sebaceous gland located in the tarsal plate of the eye lids. It functions to synthesize and secrete lipids onto the ocular surface. These lipids make up the outer-most layer in the tear film and reduce tear evaporation. When the quantity or quality of the lipids is compromised such as occurs in MGD, tears evaporate more quickly, leading to increased DED, ocular surface discomfort, impaired vision and decreased quality of life.
{"title":"Hormones and Dry Eye Disease","authors":"Juan Ding","doi":"10.4172/2157-7536.1000E113","DOIUrl":"https://doi.org/10.4172/2157-7536.1000E113","url":null,"abstract":"Dry eye disease (DED) is a very prevalent eye disorder, affecting 40 million people in the United States alone. The primary cause of DED is meibomian gland dysfunction (MGD) [1], which by itself is a disease entity. The meibomian gland is a large sebaceous gland located in the tarsal plate of the eye lids. It functions to synthesize and secrete lipids onto the ocular surface. These lipids make up the outer-most layer in the tear film and reduce tear evaporation. When the quantity or quality of the lipids is compromised such as occurs in MGD, tears evaporate more quickly, leading to increased DED, ocular surface discomfort, impaired vision and decreased quality of life.","PeriodicalId":17132,"journal":{"name":"Journal of steroids & hormonal science","volume":"37 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75693931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.4172/2157-7536.S12-E001
Kevin A Zwetsloot Andrew R Shanely, E. Merritt, J. McBride
Skeletal muscle is the most abundant tissue in the adult human body, comprising more than 40% of total body mass in normal, healthy individuals [1], and is required for movement and locomotion. Muscle mass (volume) is an important determinant of muscle function, such that physiological cross-sectional area is correlated to peak isometric force [2,3]. The maintenance of skeletal muscle mass exists as a delicate balance between the rates of muscle protein synthesis and muscle protein degradation. Rates of muscle protein synthesis and degradation are finely tuned according to activity level, nutrient availability, and health status. For example, rates of muscle protein synthesis are positively influenced by exercise and nutrition, and negatively regulated by inactivity (e.g. disuse), aging (i.e. sarcopenia), and muscle wastingrelated diseases (e.g. cancer) [4]. The PI3K/Akt signaling pathway controls both catabolic and anabolic mechanisms in skeletal muscle. Activating this pathway through exercise and nutritional interventions has a positive effect on skeletal muscle. Phytoecdysteroids (PEs) are natural steroid analogs synthesized by many plant species that possess biological, pharmacological, and medicinal properties with no known side effects in mammals [5], and are believed toelicitanabolic effects on skeletal muscle, in a non-androgenic manner,via activation of the PI3K/Akt signaling pathway.
{"title":"Phytoecdysteroids: A Novel, Non-Androgenic Alternative for Muscle Health and Performance","authors":"Kevin A Zwetsloot Andrew R Shanely, E. Merritt, J. McBride","doi":"10.4172/2157-7536.S12-E001","DOIUrl":"https://doi.org/10.4172/2157-7536.S12-E001","url":null,"abstract":"Skeletal muscle is the most abundant tissue in the adult human body, comprising more than 40% of total body mass in normal, healthy individuals [1], and is required for movement and locomotion. Muscle mass (volume) is an important determinant of muscle function, such that physiological cross-sectional area is correlated to peak isometric force [2,3]. The maintenance of skeletal muscle mass exists as a delicate balance between the rates of muscle protein synthesis and muscle protein degradation. Rates of muscle protein synthesis and degradation are finely tuned according to activity level, nutrient availability, and health status. For example, rates of muscle protein synthesis are positively influenced by exercise and nutrition, and negatively regulated by inactivity (e.g. disuse), aging (i.e. sarcopenia), and muscle wastingrelated diseases (e.g. cancer) [4]. The PI3K/Akt signaling pathway controls both catabolic and anabolic mechanisms in skeletal muscle. Activating this pathway through exercise and nutritional interventions has a positive effect on skeletal muscle. Phytoecdysteroids (PEs) are natural steroid analogs synthesized by many plant species that possess biological, pharmacological, and medicinal properties with no known side effects in mammals [5], and are believed toelicitanabolic effects on skeletal muscle, in a non-androgenic manner,via activation of the PI3K/Akt signaling pathway.","PeriodicalId":17132,"journal":{"name":"Journal of steroids & hormonal science","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83103518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.4172/2157-7536.1000130
A. Goessaert, Johan, É. Walle, A. Kapila, K. Everaert
Nocturnal polyuria (NP) is an important cause of nocturia and it is related to an imbalance in water and/or sodium homeostasis. Antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) are believed to play an important role in this excessive urine production overnight, however, many other hormones are involved. ADH and ANP are both directly and indirectly influenced by the renin-angiotensin-aldosterone system (RAAS), prostaglandins antagonize both ADH and RAAS and sex hormones have a predominantly antidiuretic effect by stimulating ADH and RAAS, meaning that any disturbance can lead to an imbalance in diuresis. Since nocturia is a condition affecting sleep, melatonin secretion can also be affected, leading to a decrease in the antidiuretic effect and to an increase of nocturnal urine production. Depending on the underlying condition affecting any of these hormones, a more specific therapeutic approach might lead to a restoration of the normal diuresis cycle and to a good night’s sleep. The characteristics of each of these hormones, the pathophysiology in NP and the therapeutic implications are set out in this review.
{"title":"Hormones and Nocturia: Guidelines for Medical Treatment?","authors":"A. Goessaert, Johan, É. Walle, A. Kapila, K. Everaert","doi":"10.4172/2157-7536.1000130","DOIUrl":"https://doi.org/10.4172/2157-7536.1000130","url":null,"abstract":"Nocturnal polyuria (NP) is an important cause of nocturia and it is related to an imbalance in water and/or sodium homeostasis. Antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) are believed to play an important role in this excessive urine production overnight, however, many other hormones are involved. ADH and ANP are both directly and indirectly influenced by the renin-angiotensin-aldosterone system (RAAS), prostaglandins antagonize both ADH and RAAS and sex hormones have a predominantly antidiuretic effect by stimulating ADH and RAAS, meaning that any disturbance can lead to an imbalance in diuresis. Since nocturia is a condition affecting sleep, melatonin secretion can also be affected, leading to a decrease in the antidiuretic effect and to an increase of nocturnal urine production. Depending on the underlying condition affecting any of these hormones, a more specific therapeutic approach might lead to a restoration of the normal diuresis cycle and to a good night’s sleep. The characteristics of each of these hormones, the pathophysiology in NP and the therapeutic implications are set out in this review.","PeriodicalId":17132,"journal":{"name":"Journal of steroids & hormonal science","volume":"30 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76413242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.4172/2157-7536.1000128
M. Burek, A. Haghikia, R. Gold, N. Roewer, A. Chan, Carola Y Frster
Objective: Multiple sclerosis (MS) is a neurodegenerative disorder of the central nervous system (CNS). Damage of the blood-brain barrier integrity is a key pathogenic event leading to the migration of lymphocytes into the CNS and subsequent demyelination. This process is tightly regulated by chemokines and cytokines which are target of therapeutic strategies in MS, such as anti-inflammatory glucocorticosteroid treatment. Here, we examine the effects of dexamethasone-treatment and MS patient sera on the expression of cytokines and chemokines in brain microvascular cell line, cEND in vitro. Methods: We conducted 96-well Mouse Cytokines and Receptors qPCR arrays to quantitatively compare the cytokine and chemokine expression profiles after treatment with dexamethasone. For selected cytokines, we studied the effects of pre-treatment with MS patient sera from active phase of disease (exacerbation) or in relapse (remission) in combination with dexamethasone. Results: After dexamethasone treatment, colony stimulating factor 3 (Csf3) and interleukin 17F (IL17f) were significantly up-regulated, whereas the chemokine (C-C motif) ligand 12 (CCL12/MCP-5), chemokine (C-X-C motif) receptor 3 (CXCR3) and kit oncogene (Kit) were significantly down-regulated. These results were confirmed in qRT-PCR using gene-specific primers. For Csf3 and CCL12 we analyzed the dexamethasone-mediated changes in protein levels secreted into the cell culture medium. Dexamethasone treatment increased the release of Csf3 into the culture medium and decreased the release of CCL12 by cEND. Additionally, we examined the effects of MS-patient sera on dexamethasone-induced cytokine secretion. Pretreatment with MS-patient serum from exacerbation phase augmented dexamethasone effects on Csf3 and CCL12 release in cEND cells. The expression of Csf3- and CCL12-receptors was demonstrated on protein and mRNA level in cEND cells. Conclusion: We identified Csf3 (G-Csf) and CCL12 as cytokines differentially regulated by dexamethasone on mRNA and protein level. This effect was even more pronounced after pretreatment with MS patient serum, especially from patients with acute relapses.
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