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Klim Dyachkov
Klim Dyachkov

Buy Follicle Stimulating Hormone

This test measures the level of follicle-stimulating hormone (FSH) in your blood. FSH is made by your pituitary gland, a small gland located underneath the brain. FSH plays an important role in sexual development and functioning.

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FSH works closely with another hormone called luteinizing hormone to control sexual functions. So a luteinizing hormone test is often done along with an FSH test. These tests are used in different ways, depending on whether you are a woman, man, or child.

In children, high FSH levels, along with high levels of luteinizing hormone, may mean puberty is about to start or has already started. If this is happening before age 9 in a girl or before age 10 in a boy (precocious puberty), it may be a sign of:

FSH levels are normally low in children. As puberty approaches (usually between ages 10 and 14), the hypothalamus produces gonadotropin-releasing hormone (GnRH), which triggers FSH and LH. This begins the changes toward sexual maturity and development.

In boys or children assigned male at birth (AMAB), FSH and LH work together to trigger their testes to begin producing testosterone. This is the hormone responsible for the physical changes of puberty (such as body hair growth and voice deepening) and the production of sperm.

In girls or children assigned female at birth (AFAB), FSH and LH trigger their ovaries to begin producing estrogen. This hormone is responsible for physical changes of puberty, such as breast development and menstruation.

Each month, between days six and 14 of the menstrual cycle, FSH causes follicles in one of the ovaries to begin to mature. However, during days 10 to 14, only one of the developing follicles forms a fully mature egg. At about day 14 in the menstrual cycle, a sudden surge in LH causes the mature follicle to rupture and release its egg (ovulation).

After ovulation, the ruptured follicle forms a corpus luteum (a temporary endocrine gland) that produces high levels of progesterone. Progesterone blocks the release of FSH and helps prepare the uterine lining for pregnancy.

In return, hormones that your testes or ovaries release control the amount of GnRH your hypothalamus makes, starting the cycle over again. However, different amounts of some hormones in this system affect the release of other hormones differently.

Again, any disruption or issue in this hormone release chain causes a lack of sex hormones. This prevents normal sexual development in children and normal function of the testicles or ovaries in adults.

Follicle stimulating hormone is a glycoprotein with molecular mass of 30 kDa. FSH is a heterodimeric hormone consisting of 92 amino acids alpha chain and 111 amino acids beta chain. Optimized DNA sequence encoding Human FSH mature chain was expressed in Chinese Hamster Ovary (CHO) cells.

In women, when FSH levels fall towards the end of the menstrual cycle. This is sensed by the hypothalamus, which produces more gonadotrophin-releasing hormone (GnRH), which in turn stimulates the pituitary gland to produce more follicle stimulating hormone (FSH) and luteinising hormone (LH), and release these into the bloodstream. The rise in follicle stimulating hormone stimulates the growth of the follicle in the ovary.

As the follicles in the ovary grow, they produce increasing amounts of oestradiol and inhibin. In turn, these hormones act on the hypothalamus and pituitary gland to reduce the release of gonadotrophin-releasing hormone and follicle stimulating hormone (negative feedback). This causes a fall in FSH, which prevents too many follicles developing each cycle. The largest follicle is less dependent on FSH for its growth and is able to continue growing even if FSH levels fall. However, smaller follicles can no longer survive as FSH levels fall due to negative feedback, enabling the emergence of a single dominant follicle.

In summary, during each menstrual cycle, there is a rise in follicle stimulating hormone secretion in the first half of the cycle (follicular phase) that stimulates follicular growth in the ovary. After ovulation the ruptured follicle forms a corpus luteum that produces high levels of progesterone (luteal phase). Towards the end of the cycle the corpus luteum breaks down, progesterone production decreases and the next menstrual cycle begins as follicle stimulating hormone levels start to rise again.

In men, the production of follicle stimulating hormone is regulated by circulating levels of inhibin. If spermatogenesis is impaired, this will lead to less inhibin being produced by the testes. The usual action of inhibin is to inhibit FSH release from the pituitary gland. Thus, impaired spermatogenesis leads to less inhibin and thus an increase in FSH release from the pituitary gland.

Testosterone levels within the testes are also needed for spermatogenesis. This testosterone production within the testes is stimulated by the action of luteinising hormone. This 'negative feedback' control of testosterone on LH secretion and spermatogenesis on inhibin secretion ensures that the production of spermatogenesis and sex steroids remains steady. Excess testosterone in the body (for example after taking extra testosterone-like drugs in order to stimulate muscle growth) can result in low levels of FSH and LH and thus impair spermatogenesis.

Most often, raised levels of follicle stimulating hormone are a sign of malfunction in the ovary or testis. If the gonads fail to create enough oestrogen, testosterone and/or inhibin, due to loss of negative feedback on the pituitary gland, the levels of both follicle stimulating hormone and luteinising hormone will rise. This condition is called hypergonadotrophic-hypogonadism, and is associated with primary ovarian insufficiency or testicular failure. This is seen in conditions such as Klinefelter's syndrome in men and Turner syndrome in women.

In women, follicle stimulating hormone levels also start to rise naturally in women in the lead up to menopause, reflecting a reduction in the function of the ovaries and decline of oestrogen and inhibin production.

There are very rare pituitary conditions that can raise the levels of follicle stimulating hormone in the bloodstream. This overwhelms the normal negative feedback loop and can (rarely) cause ovarian hyperstimulation syndrome in women. Symptoms of this include enlarging of the ovaries and a potentially dangerous accumulation of fluid in the abdomen (triggered by the rise in ovarian steroid output), which leads to pain in the pelvic area.

Sufficient follicle stimulating hormone action is also needed for full sperm production. In the case of complete absence of follicle stimulating hormone in men, lack of puberty and infertility due to lack of sperm (azoospermia) can occur. Partial follicle stimulating hormone deficiency in men can cause delayed puberty and limited sperm production (oligozoospermia), but fathering a child may still be possible. If the loss of follicle stimulating hormone occurs after puberty, there will be a similar loss of fertility.

A major gonadotropin secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Follicle-stimulating hormone stimulates GAMETOGENESIS and the supporting cells such as the ovarian GRANULOSA CELLS, the testicular SERTOLI CELLS, and LEYDIG CELLS. FSH consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is common in the three pituitary glycoprotein hormones (TSH, LH, and FSH), but the beta subunit is unique and confers its biological specificity.

Background: In adult humans, the follicle-stimulating hormone (FSH) receptor is expressed only in the granulosa cells of the ovary and the Sertoli cells of the testis. It is minimally expressed by the endothelial cells of gonadal blood vessels.

Purpose: To explore how follicle-stimulating hormone (FSH) may contribute to cardiovascular, metabolic, skeletal, and cognitive events in men treated for prostate cancer, with various forms of androgen deprivation therapy (ADT).

Porcine follicle-stimulating hormone (pFSH), comprising α and β subunits, is commonly used to induce superovulation in domestic animals in assisted reproduction technologies; however, the practical application of pFSH is inhibited by the limited efficiency of its production. Recombinant yeast-derived FSH offers a practical alternative; however, the heterologous expression efficiency remains disappointingly low. To improve FSH production in Pichia pastoris, a series of molecular strategies, together with fermentation optimization, were tested in the present study. By comparing clones of the Muts phenotype strain, it was observed that the yield of soluble pFSH increased by approximately 96% in clones of the Mut+ phenotype strain. The protein levels of soluble pFSHβ, which confers biological specificity, increased by approximately 143 and 22% after two kinds of codon optimization strategies, respectively. Moreover, compared with the production of soluble pFSHβ and SUMO-pFSHβ, the production of soluble protein HSA-pFSHβ was significantly improved. Furthermore, the optimum pH and methanol concentration for expressing soluble HSA-pFSH in strain H3-3 were determined as 5.0-6.0 and 1.5-2% in shake-flask, and the yield of soluble HSA-pFSH could reach 40.8 mg/l after purification. In vitro bioactivity assays showed that recombinant HSA-pFSH could efficiently stimulate cAMP synthesis in HEK293 cells expressing porcine FSHR. In conclusion, our results demonstrated that the application of phenotypic selection of aox1 mutants, combined with codon optimization, the choice of fusion partners, and fermentation optimization, considerably increased the yield of pFSH in supernatant of P. pastoris and thus provided a valuable reference for the large-scale recombinant expression of pFSH.

Intervention: Laparoscopic electrocautery of the ovaries followed by clomiphene citrate and recombinant follicle stimulating hormone if anovulation persisted, or induction of ovulation with recombinant follicle stimulating hormone. 041b061a72


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