The role of sex steroid in two avian song behaviours differing in ontogenetic process

1994 ◽  
Vol 50 (10) ◽  
pp. 972-974 ◽  
Author(s):  
M. Ikeda ◽  
H. -A. Takeuchi ◽  
K. Aoki
Keyword(s):  
Sex Steroid ◽  
Avian Song ◽  
Ontogenetic Process

scholarly journals Role of sex steroid receptors in pathobiology of hepatocellular carcinoma

2008 ◽  
Vol 14 (39) ◽  
pp. 5945 ◽  
Author(s):  
Mamta Kalra ◽  
Jary Mayes ◽  
Senait Assefa ◽  
Anil K Kaul ◽  
Rashmi Kaul
Keyword(s):  
Hepatocellular Carcinoma ◽  
Steroid Receptors ◽  
Sex Steroid ◽  
Sex Steroid Receptors

scholarly journals Sexual dimorphism in immune function: The role of sex steroid hormones

2018 ◽  
Vol 51 ◽  
pp. 02007
Author(s):  
Anna Mihailova ◽  
Indrikis Krams
Keyword(s):  
Immune System ◽  
Sexual Dimorphism ◽  
Infectious Diseases ◽  
Immune Function ◽  
Steroid Hormones ◽  
Adaptive Immunity ◽  
Gonadal Hormones ◽  
Sex Steroid ◽  
Innate And Adaptive Immunity

There is evidence of the relation of sex steroid hormones and sexual dimorphism in immune system response to infectious diseases. The aim of this review was to identify the role of sex hormones in immune function and sexual dimorphism of immune reactions. Gonadal hormones together with the immune system play an important role in process of immune responses to the disease [1]. Estrogens, progesterone and testosterone have different impacts on immune cells and different gonadal hormones are of high importance for responses of innate and adaptive immunity [1, 2]. Estrogens mainly enhance immune function while testosterone has a suppressive role. Higher progesterone during pregnancy leads to autoimmune disease remission and an elevated susceptibility toward certain infectious diseases [2, 3, 4]. The intensity and prevalence of viral infections are typically higher in males, whereas disease outcome could be worse for females [5]. Sexual dimorphism of immune function is based on different concentrations of sex hormones in males and females and on a specific mediating role of these hormones in immune function and response along with differences in innate and adaptive immunity.

Management of Puberty in Constitutional Delay of Growth and Puberty

2001 ◽  
Vol 14 (s2) ◽  
Author(s):  
F. De Luca ◽  
J. Argente ◽  
L. Cavallo ◽  
E. Crowne ◽  
H.A. Delemarre-Van de Waal ◽  
...  
Keyword(s):  
Social Relationships ◽  
School Performance ◽  
Low Dose ◽  
Well Being ◽  
Growth Potential ◽  
Sex Steroid ◽  
Optimal Timing ◽  
Short Course ◽  
Constitutional Delay

AbstractConstitutional delay of growth and puberty (CDGP) is the most common presenting form of short stature, but no single test can infallibly discriminate CDGP and isolated hypogonado- trophic hypogonadism. Management of puberty in CDGP aims to optimise not only growth - maintaining body proportions and improving peak bone mass without impairing growth potential - but also well-being; for example, the distress boys often suffer because of their lack of growth and pubertal progression can affect their school performance and social relationships. Typical sex steroid treatments to induce puberty in boys with CDGP include testosterone (T) enanthate, T undecanoate, mixed T esters, T transdermal patches, and oxandrolone p.o. Compared with other regimens, short-course low-dose depot T i.m. is an effective, practical, safe, well tolerated, and inexpensive regimen. Some unresolved problems in management include optimal timing and dose of sex steroid treatment, the role of GH in CDGP, and the management of CDGP in girls.

scholarly journals The role of sex steroid hormones, cytokines and the endocannabinoid system in female fertility

2011 ◽  
Vol 17 (3) ◽  
pp. 347-361 ◽  
Author(s):  
T. Karasu ◽  
T. H. Marczylo ◽  
M. Maccarrone ◽  
J. C. Konje
Keyword(s):  
Steroid Hormones ◽  
Endocannabinoid System ◽  
Sex Steroid Hormones ◽  
Female Fertility ◽  
Sex Steroid

Primary Osteoporosis in Men: Role of Sex Steroid Deficiency

2000 ◽  
Vol 75 (1) ◽  
pp. S46-S50 ◽  
Author(s):  
B. Lawrence Riggs ◽  
Sundeep Khosla ◽  
L. Joseph Melton
Keyword(s):  
Sex Steroid ◽  
Primary Osteoporosis ◽  
Osteoporosis In Men

scholarly journals Absent Progesterone Signaling in Kisspeptin Neurons Disrupts the LH Surge and Impairs Fertility in Female Mice

Endocrinology ◽  
2015 ◽  
Vol 156 (9) ◽  
pp. 3091-3097 ◽  
Author(s):  
Shannon B. Z. Stephens ◽  
Kristen P. Tolson ◽  
Melvin L. Rouse ◽  
Matthew C. Poling ◽  
Minako K. Hashimoto-Partyka ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Progesterone Receptors ◽  
Sex Steroid ◽  
Corpora Lutea ◽  
Neuronal Activation ◽  
Estrogen Regulation ◽  
Lh Surge ◽  
Normal Fertility ◽  
Periventricular Nucleus

Kisspeptin, encoded by Kiss1, stimulates GnRH neurons to govern reproduction. In rodents, estrogen-sensitive kisspeptin neurons in the anterior ventral periventricular nucleus and neighboring periventricular nucleus are thought to mediate sex steroid-induced positive feedback induction of the preovulatory LH surge. These kisspeptin neurons coexpress estrogen and progesterone receptors and display enhanced neuronal activation during the LH surge. However, although estrogen regulation of kisspeptin neurons has been well studied, the role of progesterone signaling in regulating kisspeptin neurons is unknown. Here we tested whether progesterone action specifically in kisspeptin cells is essential for proper LH surge and fertility. We used Cre-lox technology to generate transgenic mice lacking progesterone receptors exclusively in kisspeptin cells (termed KissPRKOs). Male KissPRKOs displayed normal fertility and gonadotropin levels. In stark contrast, female KissPRKOs displayed earlier puberty onset and significant impairments in fertility, evidenced by fewer births and substantially reduced litter size. KissPRKOs also had fewer ovarian corpora lutea, suggesting impaired ovulation. To ascertain whether this reflects a defect in the ability to generate sex steroid-induced LH surges, females were exposed to an estradiol-positive feedback paradigm. Unlike control females, which displayed robust LH surges, KissPRKO females did not generate notable LH surges and expressed significantly blunted cfos induction in anterior ventral periventricular nucleus kisspeptin neurons, indicating that progesterone receptor signaling in kisspeptin neurons is required for normal kisspeptin neuronal activation and LH surges during positive feedback. Our novel findings demonstrate that progesterone signaling specifically in kisspeptin cells is essential for the positive feedback induction of normal LH surges, ovulation, and normal fertility in females.

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