Vitamin D plays role in healthy Testes function. This signaling occurs through genomic and non-genomic signaling pathways. Testosterone production is influenced, sperm motility and spermatogenesis is influenced.
study finds restoration of HPA in men with low T. This was performed via clomid therapy at 25 to 50 mg daily for 4 months. Increase in pulsatile LH, increase in serum Testosterone levels, and increase in sexual function was found. Clomid restores HPA function that is suppressed from estrogen inhibition. In this case, clomid is function as an estrogen antagonist.
I really don't understand the purpose of this study. Why give "healthy" men with normal lipids atorvastatin??? The study found a reduction in TC and LDL, but also a reduction in sperm number, decreased sperm vitality, increased sperm morphology, decreased prostatic acid pho sphatases, epididymal neutral alpha-glucosidase and L-carnitine levels resulted.
Bioidentical progesterone used in IVF. This is not new, the SQ administration is. So, physicians cry against BHRT, yet bioidentical progesterone has been used for years in the treatment of infertility.
The body of the white pimples is a common feature of boys entering puberty. Understanding their nature will help you no longer worry.
White pimples on the penis and pores, squeezing out with a white core. Do these acne affect fertility? This top concern in many young people will be answered right after.
steroid hormones typically interact with their cognate receptor in the cytoplasm for AR, glucocorticoid receptor (GR) and PR, but may also bind receptor in the nucleus as appears to often be the case for ERα and ERβ
This ligand binding results in a conformational change in the cytoplasmic NRs that leads to the dissociation of HSPs, translocation of the ligand-bound receptor to the nucleus
In the nucleus, the ligand-bound receptor dimerizes and then binds to DNA at specific HREs to regulate gene transcription
some steroid hormone-induced nuclear events can occur in minutes
the genomic effects of steroid hormones take longer, with changes in gene expression occurring on the timescale of hours
Classical steroid hormone signaling occurs when hormone binds nuclear receptors (NR) in the cytoplasm, setting off a chain of genomic events that results in, among other changes, dimerization and translocation to the nucleus where the ligand-bound receptor forms a complex with coregulators to modulate gene transcription through direct interactions with a hormone response element (HRE)
NRs have been found at the plasma membrane of cells, where they can propagate signal transduction often through kinase pathways
Membrane-localized ER, PR and AR have been reported to modulate the activity of MAPK/ERK, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), nitric oxide (NO), PKC, calcium flux and increase inositol triphosphate (IP3) levels to promote cell processes including autophagy, proliferation, apoptosis, survival, differentiation, and vasodilation
ERα36, a 36kDa truncated form of ERα that lacks the transcriptional activation domains of the full-length protein. Membrane-localized ERα36 can activate pathways including protein kinase C (PKC) and/or mitogen activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) to promote the progression of various cancers
G protein-coupled receptor 30 (GPR30), also referred to as G protein-coupled estrogen receptor (GPER), is a membrane-localized receptor that has been observed to respond to estrogen to activate rapid signaling
hormone-responsive G protein coupled receptor is Zip9, which androgens can activate
GPRC6A is another G protein-coupled membrane receptor that is responsive to androgen
androgen-mediated non-genomic signaling through this GPCR can modulate male fertility, hormone secretion and prostate cancer progression
non-NR proteins located at the cell surface can bind to steroid hormones and respond by eliciting rapid signaling events
Estrogens have been shown to induce rapid (i.e. seconds) calcium flux via membrane-localized ER (mER)
ER-calcium dynamics lead to activation of kinase pathways such as MAPK/ERK which can result in cellular effects like migration and proliferation
17β-estradiol (E2) has been reported to promote angiogenesis through the activation of GPER
Membrane NRs may also mediate rapid signaling through crosstalk with growth factor receptors (GFR)
A similar crosstalk occurs between the receptor tyrosine kinase insulin-related growth factor-1 receptor (IGF-IR) and ERα. Not only does IGF-IR activate ERα, but inhibition of IGF-IR downregulates estrogen-mediated ERα activity, suggesting that IGF-IR is essential for maximal ERα signaling
This is a bombshell that shatters the current right brain approach to ER. It completely shatters the concept of eat sugar, whatever you want, with cancer treatment in ER+ or hormonally responsive cancer!
Further, ER activates IGF-IR pathways including MAPK
GPER is involved in the transactivation of the EGFR independent of classical ER
tight interconnection between genomic and non-genomic effects of NRs.
non-genomic pathways can also lead to genomic effects
androgen-bound AR associates with the kinase Src at the plasma membrane, activating Src which then leads to a signaling cascade through MAPK/ERK
However, Src can also increase the expression of AR target genes by the ligand-independent transactivation of AR
extranuclear steroid hormone actions can potentially reprogram nuclear NR events
estrogen modulated the expression of several genes including endothelial nitric oxide synthase (eNOS) via rapid signaling pathways
epigenetic changes can then mediate genomic events in uterine tissue and breast cancer cells
The embryo is the combined form of a matured egg and sperm. It is generally known as the most critical stage of IVF treatment. Despite that, successful embryo implantation only decides the achievement of pregnancy, and when it fails, it obstructs the entire IVF process. It extensively occurs when a couple fails to develop a healthy embryo using their eggs and sperm because of poor health conditions.
The most generic question that interrupts every couple's mind is when the IVF process should be done. Is it done when one fails to conceive, or is it done when one suffers from secondary infertility.