query: the cells in the testes that produce testosterone are called

pos: Leydig cell Leydig cell Leydig cells, also known as interstitial cells of Leydig, are found adjacent to the seminiferous tubules in the testicle. They produce testosterone in the presence of luteinizing hormone (LH). Leydig cells are polyhedral in shape, display a large prominent nucleus, an eosinophilic cytoplasm and numerous lipid-filled vesicles. The mammalian Leydig cell is a polyhedral epithelioid cell with a single eccentrically located ovoid nucleus. The nucleus contains one to three prominent nucleoli and large amounts of dark-staining peripheral heterochromatin. The acidophilic cytoplasm usually contains numerous membrane-bound lipid droplets and large amounts of smooth endoplasmic reticulum (SER). Besides the obvious

pos: Testosterone reticulum to yield a variety of C steroids. In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone. The largest amounts of testosterone (>95%) are produced by the testes in men, while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta. In the testes, testosterone is produced by the Leydig cells.

pos: Gonadotropin ovaries — are the primary target organs for LH and FSH. The gonadotropins affect multiple cell types and elicit multiple responses from the target organs. As a simplified generalization, LH stimulates the Leydig cells of the testes and the theca cells of the ovaries to produce testosterone (and indirectly estradiol), whereas FSH stimulates the spermatogenic tissue of the testes and the granulosa cells of ovarian follicles, as well as stimulating production of estrogen by the ovaries. Although gonadotropins are secreted in a pulsatile manner (as a result of pulsatile GnRH release), unlike the case of GnRH and GnRH agonists, constant/non-pulsatile

pos: Lipoid congenital adrenal hyperplasia hormone synthesis. The fetal testes make AMH, which prevents a uterus and inner vagina from forming, but since the Leydig cells fail to make testosterone during development even in response to hCG, the testes are usually remain in the abdomen or lodge in the inguinal canals (undescended testes) and are nonfunctional. Consequently, XY patients do not undergo puberty and remain infertile. In addition to the testes remaining inside, formation of the penis, also dependent on testosterone, is compromised. Hence, the external genitalia in most of infants resemble that of normal females (though the vagina is a short, blind pouch), or

pos: Pharmacology of bicalutamide if any, that development of lobuloalveolar structures (a form of epithelial tissue) contributes to breast size and/or shape. Spermatogenesis and male fertility are dependent on , , and high levels of testosterone within the testicles. does not seem to be involved in spermatogenesis outside of its role in inducing production of testosterone by the Leydig cells in the seminiferous tubules (which make up approximately 80% of the bulk of the testes), whereas this is not the case for , which is importantly involved. In accordance with the fact that the testes are the source of 95% of circulating testosterone in

pos: Franz Leydig ("Leydig cells"), a body enclosed in a smooth endoplasmic reticulum and holding lipid granules and crystals, which occur adjacent to the seminiferous tubules of the testes. The cells produce the male hormone testosterone. Leydig had described the interstitial cells in his detailed account of the male sex organs. The above description clearly indicates that Leydig recognized the specific morphology of those cells: only recently, have their endocrine nature and ultrastructure been fully understood. In addition to its historical importance, Leydig’s "Lehrbuch" is significant for his description of a large secretory cell, found in the epidermis of fishes and larvae amphibians.

pos: Puberty shaft of the penis will increase and the glans penis and corpora cavernosa will also start to enlarge to adult proportions. The testes have two primary functions: to produce hormones and to produce sperm. The Leydig cells produce testosterone, which in turn produces most of the male pubertal changes. Most of the increasing bulk of testicular tissue is spermatogenic tissue (primarily Sertoli and Leydig cells). By the end of puberty, adult men have heavier bones and nearly twice as much skeletal muscle. Some of the bone growth (e.g. shoulder width and jaw) is disproportionately greater, resulting in noticeably different male

pos: Diphallia "SRY" gene encodes testis-determining SRY factor (TDF) protein that promotes expression of several other genes such as SRY-box 9 ("SOX-9") gene and steroidogenic factor-1 ("SF1") gene, causing differentiation of the medulla of bipotential gonad into testis by week six. Sertoli cells of testes secrete anti-Mullerian hormone (AMH) causing Mullerian ducts to generate, and Leydig cells of testes secrete testosterone and its derivative dihydrotestosterone (DHT) which is converted from testosterone by 5α-reductase, causing the Wolffian ducts to convert into seminal vesicles, vas deferens and epididymis by week ten. Initial development of external genital is independent of androgens before indifferent gonads differentiate

pos: Anabolic steroid the two gonadotropins, follicle stimulating hormone (FSH) and luteinizing hormone (LH). In adult males, LH stimulates the Leydig cells in the testes to produce testosterone which is required to form new sperm through spermatogenesis. AAS consumption leads to dose-dependent suppression of gonadotropin release through suppression of GnRH from the hypothalamus (long-loop mechanism) or from direct negative feedback on the anterior pituitary to inhibit gonadotropin release (short-loop mechanism), leading to AAS-induced hypogonadism. The pharmacodynamics of AAS are unlike peptide hormones. Water-soluble peptide hormones cannot penetrate the fatty cell membrane and only indirectly affect the nucleus of target cells through their interaction

pos: Cryptorchidism only during this programming window. The testes begin as an immigration of primordial germ cells into testicular cords along the gonadal ridge in the abdomen of the early embryo. The interaction of several male genes organizes this developing gonad into a testis rather than an ovary by the second month of gestation. During the third to fifth months, the cells in the testes differentiate into testosterone-producing Leydig cells, and anti-Müllerian hormone-producing Sertoli cells. The germ cells in this environment become fetal spermatogonia. Male external genitalia develop during the third and fourth months of gestation and the fetus continues to grow,

pos: Ergogenic use of anabolic steroids himself. In 2002, a study replicating Brown-Séquard's method determined that the amount of testosterone obtained was too low to have any clinical effect. Testosterone, the most active anabolic-androgenic steroid produced by Leydig cells in the testes, was first isolated in 1935 and chemically synthesized later in the same year. Synthetic derivatives of testosterone quickly followed. By the end of the following decade, both testosterone and its derivatives were applied with varying degrees of success for a number of medical conditions. It was not until the 1950s, however, that athletes began to discover that anabolic steroids could increase their muscle mass.

pos: Vasectomy performed on bulls. A vasectomy is done to prevent fertility in males. It ensures that in most cases the person will be sterile after confirmation of success following surgery. The procedure is regarded as permanent because vasectomy reversal is costly and often does not restore the male's sperm count or sperm motility to prevasectomy levels. Men with vasectomies have a very small (nearly zero) chance of successfully impregnating a woman, but a vasectomy has no effect on rates of sexually transmitted infections. After vasectomy, the testes remain in the scrotum where Leydig cells continue to produce testosterone and other male

pos: Puberty the Leydig cells of the testes to make testosterone and blood levels begin to rise. For much of puberty, nighttime levels of testosterone are higher than daytime. Regularity of frequency and amplitude of gonadotropin pulses seems to be less necessary for progression of male than female puberty. However, a significant portion of testosterone in adolescent boys is converted to estradiol. Estradiol mediates the growth spurt, bone maturation, and epiphyseal closure in boys just as in girls. Estradiol also induces at least modest development of breast tissue (gynecomastia) in a large proportion of boys. Boys who develop mild gynecomastia or even

pos: Testicular immunology by activated rat testicular macrophages: these macrophages produce significantly less TNFα and IL-1β than activated rat peritoneal macrophages. Aside from responding to infectious stimuli, testicular macrophages are also involved in maintaining normal testis function. They have been shown to secrete 25-hydroxycholesterol, a sterol that can be converted to testosterone by Leydig cells. Their presence is necessary for the normal development and function of the Leydig cells, which are the testosterone-producing cells of the testis. B-lymphocytes take part in the adaptive immune response and produce antibodies. These cells are not normally found in the testis, even during inflammatory conditions. The lack

pos: Leydig cell testis by a population of 'fetal'-type Leydig cells from the 8th to the 20th week of gestation, which produce enough testosterone for masculinisation of a male fetus. Leydig cells release a class of hormones called androgens (19-carbon steroids). They secrete testosterone, androstenedione and dehydroepiandrosterone (DHEA), when stimulated by the pituitary hormone luteinizing hormone (LH). LH increases cholesterol desmolase activity (an enzyme associated with the conversion of cholesterol to pregnenolone), leading to testosterone synthesis and secretion by Leydig cells. Prolactin (PRL) increases the response of Leydig cells to LH by increasing the number of LH receptors expressed on Leydig cells. Leydig

pos: Leydig cell hypoplasia required, and, if necessary, an orchidopexy (relocation of the undescended testes to the scrotum) may be performed as well. Leydig cell hypoplasia Leydig cell hypoplasia (or aplasia) (LCH), also known as Leydig cell agenesis, is a rare autosomal recessive genetic and endocrine syndrome affecting an estimated 1 in 1,000,000 genetic males. It is characterized by an inability of the body to respond to luteinizing hormone (LH), a gonadotropin which is normally responsible for signaling Leydig cells of the testicles to produce testosterone and other androgen sex hormones. The condition manifests itself as pseudohermaphroditism (partially or fully underdeveloped genitalia), hypergonadotropic hypogonadism

pos: Leydig cell hypoplasia with Leydig cell hypoplasia type I display no response to the hCG stimulation test; there is no increase in serum levels of testosterone and dihydrotestosterone. Leydig cell hypoplasia type II can display either a pronounced rise of testosterone levels or no rise. In any case, the diagnosis is confirmed on biopsy of the testes, revealing either absent or hypoplastic Leydig cells. The inside of the testis will be grayish and mucous, displaying arrested spermatogenesis and the presence of Sertoli cells. The diagnosis can also be confirmed by looking for mutations in the gene for the LH receptor. A diagnosis of

pos: Human sexuality the duct system, the prostate and seminal vesicles, and the Cowper's gland. The testicles are the male gonads where sperm and male hormones are produced. Millions of sperm are produced daily in several hundred seminiferous tubules. Cells called the Leydig cells lie between the tubules; these produce hormones called androgens; these consist of testosterone and inhibin. The testicles are held by the spermatic cord, which is a tubelike structure containing blood vessels, nerves, the vas deferens, and a muscle that helps to raise and lower the testicles in response to temperature changes and sexual arousal, in which the testicles are

pos: Polyestradiol phosphate negative feedback on the hypothalamic–pituitary–gonadal axis. This blocks the secretion of luteinizing hormone, which in turn reduces testosterone production in the Leydig cells of the testes. Estradiol also decreases the free percentage of testosterone by increasing sex hormone-binding globulin (SHBG) levels. In addition, it exhibits direct cytotoxicity on prostate cancer cells. Estrogens have effects on liver protein synthesis, including on the synthesis of plasma proteins, coagulation factors, lipoproteins, and triglycerides. These effects can result in an increased risk of thromboembolic and cardiovascular complications, which in turn can result in increased mortality. Studies have found a markedly increased 5-year risk of

pos: Lipoid congenital adrenal hyperplasia also essential for sex steroid synthesis in the testis and ovary, the production of testosterone by Leydig cells in the testis and androgens (which leads to estrogen production by granulosa cells) and progesterone by ovarian theca cells and luteal cells, respectively, can also be impaired. Similar to the adrenal gland, cholesterol accumulation damages the Leydig cells of the testes. In the ovary, the damage begins after puberty, the time when the ovary starts making steroid with follicle development. The placenta also makes steroid to help maintain pregnancy. However, since StAR is not required for placental steroid production, pregnancy goes to

pos: Luteinizing hormone/choriogonadotropin receptor chorionic gonadotropins in case a pregnancy is developing. In turn, luteal function is prolonged and the endocrine milieu is supportive of the nascent pregnancy. In the male the LHCGR has been identified on the Leydig cells that are critical for testosterone production, and support spermatogenesis. Normal LHCGR functioning is critical for male fetal development, as the fetal Leydig cells produce testosterone to induce masculinization. LHCGR have been found in many types of extragonadal tissues, and the physiologic role of some has remained largely unexplored. Thus receptors have been found in the uterus, sperm, seminal vesicles, prostate, skin, breast, adrenals, thyroid,

pos: Persistent Müllerian duct syndrome differentiate into epididymides, vasa deferentia and seminal vesicles under the influence of testosterone, produced by the fetal Leydig cells The main form of treatment is laparotomy, a modern and minimally invasive type of surgery. Laparotomy properly positions the testes within the scrotum (orchidopexy) and remove Mullerian structures being the uterus and fallopian tubes. Occasionally they are unsalvageable if located high in the retroperitoneum. During this surgery, the uterus is usually removed and attempts made to dissect away Müllerian tissue from the vas deferens and epididymis to improve the chance of fertility. If the person has male gender identity himself and

pos: Hypogonadotropic hypogonadism develop secondary sexual characteristics, allow for the growth and closure of the epiphyseal plate, as well as improving sexual function. This therapy does not restore fertility as gonadotropins are required for spermatogenesis and folliculogenesis. If fertility is desired, pulsatile GnRH therapy or gonadotropin therapy is necessary. Gonadotropin therapy involves the use of human chorionic gonadotropin (hCG) and FSH. In the male, hCG stimulates Leydig cells to produce testosterone so that plasma and testicular levels increase. With the increased levels of testosterone, sexual activity, libido and overall wellbeing should improve. Administration of FSH is required to induce spermatogenesis by acting on

neg: Male reproductive system have the potential to become either testes or ovaries. Reproductive sex organs for both male and female are derived from the same embryonic tissues and are considered homologous tissues or organs. After the testes have differentiated, male sex hormones, called androgens, are secreted from interstitial cells (cells of Leydig). The major androgens secreted by these cells is testosterone and secretion begins 8 to 10 weeks after conception. Testosterone secretion reaches a peak at 12 to 14 weeks, and declines to very low levels by the end of the second trimester (about 21 weeks). Levels are the barely detectable 4–6 months

neg: Sex organ the middle, and the urethra behind the protuberance. If the fetus has testes, and if the testes produce testosterone, and if the cells of the genitals respond to the testosterone, the outer urogenital folds swell and fuse in the midline to produce the scrotum; the protuberance grows larger and straighter to form the penis; the inner urogenital swellings grow, wrap around the penis, and fuse in the midline to form the penile urethra. Each sex organ in one sex has a homologous counterpart in the other one. See a list of homologues of the human reproductive system. In a larger

neg: Testicular immunology the testes of rats. Also present in the testes of rats and humans are natural killer cells and Natural killer T cells have been found in rats and mice. Mast cells are regulators of immune responses, particularly those against parasites. They are also involved in the development of autoimmune diseases and allergies. Mast cells have been found in relatively low numbers in the testes of humans, rats, mice, dogs, cats, bulls, boars and deer. In the mammalian testis mast cells regulate testosterone production. There are two lines of evidence that restriction of mast cell activation in the testis could be

neg: Male reproductive system embryonic testes. Testosterone, however, is not the active agent within these organs. Once inside the target cells, testosterone is converted by means of an enzyme called 5α-reductase into the dihydrotestosterone (DHT). DHT mediates the androgen effect in these organs. At nine weeks, male differentiation of the gonads and the testes is well underway. Internal changes include the formation of the tubular seminar Chris tubules in the Rete testis from the primary sex cord. Developing on the outside surface of each testis is a Phibro muscular cord called the gubernaculum. This structure attaches to the inferior portion of the testis and

neg: Hypothalamic–pituitary–gonadal axis a negative feedback loop by inhibiting the production of GnRH in the hypothalamus. Inhibin acts to inhibit activin, which is a peripherally produced hormone that positively stimulates GnRH-producing cells. Follistatin, which is also produced in all body tissue, inhibits activin and gives the rest of the body more control over the axis. In males LH stimulates the interstitial cells located in the testes to produce testosterone, and FSH plays a role in spermatogenesis. Only small amounts of estrogen are secreted in males. Recent research has shown that a neurosteroid axis exists, which helps the cortex to regulate the hypothalamus’s production

neg: Bicalutamide ductal development, bicalutamide has been found to produce moderate lobuloalveolar development of the breasts. However, full lobuloalveolar maturation necessary for lactation and breastfeeding will not occur without progestogen treatment. Bicalutamide monotherapy seems to have minimal effect on testicular spermatogenesis, testicular ultrastructure, and certain aspects of male fertility. This seems to be because testosterone levels in the testes (where ~95% of testosterone in males is produced) are extremely high (up to 200-fold higher than circulating levels) and only a small fraction (less than 10%) of the normal levels of testosterone in the testes are actually necessary to maintain spermatogenesis. As a

neg: Intersex medical interventions to prevent virilization from rising testosterone. Testes in androgen insensitivity are a special case: if there is any degree of responsiveness to testosterone, they should be removed before puberty. On the other hand, if androgen insensitivity is complete, the testes may be left to produce estradiol (via testosterone) to induce breast development, but there is a slowly increasing risk of cancer in adult life. Streak gonads without a Y chromosome cell line need not be removed but will not function. Finally, the gonads in true hermaphroditism must be directly examined; atypical gonads with Y line or potential testicular function should

neg: Spermatogenesis takes place under the influence of testosterone, which removes the remaining unnecessary cytoplasm and organelles. The excess cytoplasm, known as "residual bodies", is phagocytosed by surrounding Sertoli cells in the testes. The resulting spermatozoa are now mature but lack motility, rendering them sterile. The mature spermatozoa are released from the protective Sertoli cells into the lumen of the seminiferous tubule in a process called "spermiation". The non-motile spermatozoa are transported to the epididymis in "testicular fluid" secreted by the Sertoli cells with the aid of peristaltic contraction. While in the epididymis the spermatozoa gain motility and become capable of fertilization.

neg: Male reproductive system of age postnatal. High levels of testosterone will not appear again until the time of puberty. Internal accessory sex organs to develop and most of these are derived from two systems of embryonic ducts. Male accessory organs are derived from mesonephric (wolfian) ducts. The developing tubules within the testes secretes a polypeptide Müllerian inhibition factor (MIF). MIF causes the regression of the paramesonephretic ducts 60 days after fertilization. Testosterone secretion by the interstitial cells of the testes then causes the growth and development of the mesonephric ducts into male secondary sex organs. The Müllerian ducts atrophy, but traces of their

neg: Spermatocyte leads to the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) produced by the anterior pituitary gland (Figure 4). The release of FSH into the testes will enhance spermatogenesis and lead to the development of sertoli cells, which act as nursing cells where spermatids will go to mature after Meiosis II. LH promotes leydig cell secretion of testosterone into the testes and blood, which induce spermatogenesis and aid the formation of secondary sex characteristics. From this point on, the secretion of FSH and LH (inducing production of testosterone) will stimulate spermatogenesis until the male dies. Increasing the hormones FSH

neg: Seminiferous tubule Seminiferous tubule Seminiferous tubules are located within the testes, and are the specific location of meiosis, and the subsequent creation of male gametes, namely spermatozoa. The epithelium of the tubule consists of a type of sustentacular cells known as Sertoli cells, which are tall, columnar type cells that line the tubule. In between the Sertoli cells are spermatogenic cells, which differentiate through meiosis to sperm cells. Sertoli cells function to nourish the developing sperm cells. They secrete testis-determining factor, a binding protein which increases the concentration of testosterone inside the seminiferous tubules. Embryologically, they also secrete the anti-Müllerian hormone (AMH)

neg: Spermatogenesis hormone (FSH) and testosterone. In contrast to FSH, LH appears to have little role in spermatogenesis outside of inducing gonadal testosterone production. FSH stimulates both the production of androgen binding protein (ABP) by Sertoli cells, and the formation of the blood-testis barrier. ABP is essential to concentrating testosterone in levels high enough to initiate and maintain spermatogenesis. Intratesticular testosterone levels are 20–100 or 50–200 times higher than the concentration found in blood, although there is variation over a 5- to 10-fold range amongst healthy men. FSH may initiate the sequestering of testosterone in the testes, but once developed only testosterone

neg: Anorchia despite lacking the necessary masculinizing hormones during prenatal, childhood, and adolescent development. Anorchic individuals who have a female identity may be administered estrogen alone in place of testosterone as no androgen blockers are necessary due to the lack of gonads. Other names for anorchia include Anorchia Anorchia (also called anorchidism or anorchism) is a disorder of sex development in which a person with XY karyotype, which usually corresponds to male sex, is born without testes. Within a few weeks of fertilization, the embryo develops rudimentary gonads (testes), which produce hormones responsible for the development of the reproductive system. If the

neg: AMHR2 (gene) different isoforms have been identified. [provided by RefSeq, Sep 2009]. AMHR2 (gene) Anti-Mullerian hormone receptor type 2 is a protein that in humans is encoded by the AMHR2 gene. This gene encodes the receptor for the anti-Mullerian hormone (AMH) which, in addition to testosterone, results in male sex differentiation. AMH and testosterone are produced in the testes by different cells and have different effects. Testosterone promotes the development of male genitalia while the binding of AMH to the encoded receptor prevents the development of the mullerian ducts into uterus and Fallopian tubes. Mutations in this gene are associated with persistent

neg: AMHR2 (gene) AMHR2 (gene) Anti-Mullerian hormone receptor type 2 is a protein that in humans is encoded by the AMHR2 gene. This gene encodes the receptor for the anti-Mullerian hormone (AMH) which, in addition to testosterone, results in male sex differentiation. AMH and testosterone are produced in the testes by different cells and have different effects. Testosterone promotes the development of male genitalia while the binding of AMH to the encoded receptor prevents the development of the mullerian ducts into uterus and Fallopian tubes. Mutations in this gene are associated with persistent Mullerian duct syndrome type II. Alternatively spliced transcript variants encoding

neg: Anti-mullerian hormone receptor type 2 Anti-mullerian hormone receptor type 2 Anti-Mullerian hormone receptor type 2 is a protein that in humans is encoded by the AMHR2 gene. This gene encodes the receptor for the anti-Mullerian hormone (AMH) which, in addition to testosterone, results in male sex differentiation. AMH and testosterone are produced in the testes by different cells and have different effects. Testosterone promotes the development of male genitalia while the binding of AMH to the encoded receptor prevents the development of the mullerian ducts into uterus and Fallopian tubes. Mutations in this gene are associated with persistent Mullerian duct syndrome type II. Alternatively spliced

neg: Endocrine gland uptake and metabolism by most body cells. Somatostatin is released by Delta cells and act as an Inhibitor of GH, Insulin and Glucagon. The ovaries of the female, located in the pelvic cavity, release two main hormones. Secretion of estrogens by the ovarian follicles begins at puberty under the influence of FSH. Estrogens stimulate maturation of the female reproductive system and development of the secondary sexual characteristics. Progesterone is released in response to high blood levels of LH. It works with estrogens in establishing the menstrual cycle. The testes of the male begin to produce testosterone at puberty in response

neg: Anti-mullerian hormone receptor type 2 transcript variants encoding different isoforms have been identified. [provided by RefSeq, Sep 2009]. Anti-mullerian hormone receptor type 2 Anti-Mullerian hormone receptor type 2 is a protein that in humans is encoded by the AMHR2 gene. This gene encodes the receptor for the anti-Mullerian hormone (AMH) which, in addition to testosterone, results in male sex differentiation. AMH and testosterone are produced in the testes by different cells and have different effects. Testosterone promotes the development of male genitalia while the binding of AMH to the encoded receptor prevents the development of the mullerian ducts into uterus and Fallopian tubes. Mutations in

neg: Ovarian follicle of granulosa cells and theca of follicle. Once a month, one of the ovaries releases a mature egg (ovum), known as an oocyte. The nucleus of such an oocyte is called a "germinal vesicle (see picture)." Cumulus oophorus is a cluster of cells (called cumulus cells) that surround the oocyte both in the ovarian follicle and after ovulation. It contains numerous granulosa cells. Granulosa cells or follicular cells are cells that surround the oocyte within the follicle; their numbers increase directly in response to heightened levels of circulating gonadotropins or decrease in response to testosterone. They also produce peptides involved

neg: Pharmacology of bicalutamide testosterone in the testes, in that it is likely that systemic bicalutamide therapy is unable to achieve concentrations of the drug within the testes that are able to considerably block androgen signaling in this part of the body. This is particularly so considering that bicalutamide increases circulating testosterone levels, and by extension gonadal testosterone production, by up to two-fold in males, and that only a small fraction of normal intratesticular testosterone levels, and by extension androgen action, appears to be necessary to maintain spermatogenesis. In contrast to bicalutamide and other pure antiandrogens or , antigonadotropic antiandrogens suppress gonadotropin secretion, which

neg: Complete androgen insensitivity syndrome the Y chromosome. They may be located intra-abdominally, at the internal inguinal ring, or may herniate into the labia majora, often leading to the discovery of the condition. Testes in affected women have been found to be atrophic upon gonadectomy. Testosterone produced by the testes cannot be directly used due to the mutant androgen receptor that characterizes CAIS; instead, it is aromatized into estrogen, which effectively feminizes the body and accounts for the normal female phenotype observed in CAIS. Immature sperm cells in the testes do not mature past an early stage, as sensitivity to androgens is required in order

neg: Spermatozoon necessary medium for sperm and egg to meet. Algae and lower plant sperm cells are often multi-flagellated (see image) and thus morphologically different from animal spermatozoa. Some algae and fungi produce non-motile sperm cells, called spermatia. In higher plants and some algae and fungi, fertilization involves the migration of the sperm nucleus through a fertilization tube (e.g. pollen tube in higher plants) to reach the egg cell. Spermatozoa are produced in the seminiferous tubules of the testes in a process called spermatogenesis. Round cells called spermatogonia divide and differentiate eventually to become spermatozoa. During copulation the cloaca or vagina gets

neg: Testicle Testicle The testicle or testis is the male reproductive gland in all animals, including humans. It is homologous to the female ovary. The functions of the testes are to produce both sperm and androgens, primarily testosterone. Testosterone release is controlled by the anterior pituitary luteinizing hormone; whereas sperm production is controlled both by the anterior pituitary follicle-stimulating hormone and gonadal testosterone. Males have two testicles of similar size contained within the scrotum, which is an extension of the abdominal wall. Scrotal asymmetry is not unusual: one testicle extends further down into the scrotum than the other due to differences in

neg: XY gonadal dysgenesis testosterone, the wolffian ducts fail to develop, so no internal male organs are formed. Also, the lack of testosterone means that no dihydrotestosterone is formed and consequently the external genitalia fail to virilize, resulting in normal female genitalia. Without AMH, the Müllerian ducts develop into normal internal female organs (uterus, fallopian tubes, cervix, vagina). A baby who is apparently a girl is born and is normal in most anatomic respects except that the child has nonfunctional streak gonads instead of ovaries or testes. As girls' ovaries normally produce no important body changes before puberty, a defect of the reproductive system

neg: Puberty into nearby cells called granulosa cells. Smaller increases of FSH induce an increase in the aromatase activity of these granulosa cells, which converts most of the testosterone to estradiol for secretion into the circulation. The remaining testosterone, together with adrenal androgens is responsible for the typical androgenic changes of female puberty: pubic hair, other androgenic hair as outlined above, body odor, acne. The bioactivity of testosterone is to a large degree limited by SHBG which in turn is mainly controlled by estradiol and prolactin levels (estradiol stimulates, prolactin decreases SHBG synthesis). Rising levels of estradiol produce the characteristic estrogenic body

neg: Sexual differentiation in humans also known as the SRY gene. In the presence of a functional SRY gene, the bipotential gonads develop into testes. Gonads are histologically distinguishable by 6–8 weeks of gestation. Subsequent development of one set and degeneration of the other depends on the presence or absence of two testicular hormones: testosterone and anti-müllerian hormone (AMH). Disruption of typical development may result in the development of both, or neither, duct system, which may produce morphologically intersex individuals. Males: The SRY gene when transcribed and processed produces SRY protein that binds to DNA and directs the development of the gonad into testes. Male

neg: Pharmacology of bicalutamide the body, local levels of testosterone inside of the testes are extremely high, ranging from 20- to 200-fold higher than circulating concentrations. Moreover, high levels of testosterone within the testes are required for spermatogenesis, although only a small fraction (5–10%) of normal levels appears to actually be necessary for spermatogenesis. Unlike with antigonadotropic antiandrogens like and analogues, it has been reported that bicalutamide monotherapy (at 50 mg/day) has very little effect on the ultrastructure of the testes and on sperm maturation in humans even after long-term therapy (>4 years). This may be explained by the extremely high local levels of

neg: Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency an undervirilized male with normal sensitivity to testosterone. If the infant boy is only mildly undervirilized, the hypospadias can be surgically repaired, testes brought into the scrotum, and testosterone supplied at puberty. Management decisions are more difficult for a moderately or severely undervirilized genetic male whose testes are in the abdomen and whose genitalia look at least as much female as male. Male sex can assigned and major reconstructive surgery done to close the midline of the perineum and move the testes into a constructed scrotum. Female sex can be assigned and the testes removed and vagina enlarged surgically. A

neg: Hypothalamic–pituitary–gonadal axis remain low through childhood. During puberty the HPG axis is activated by the secretions of estrogen from the ovaries or testosterone from the testes. This activation of estrogen and testosterone causes physiological and psychological changes. Once activated, the HPG axis continues to function in men for the rest of their life but becomes deregulated in women, leading to menopause. This deregulation is caused mainly by the lack of oocytes that normally produce estrogen to create the positive feedback loop. Over several years, the activity the HPG axis decreases and women are no longer fertile. Although males remain fertile until death,

neg: Testicle their contents during the breeding season, and then being reabsorbed by the body. Before the next breeding season, new sperm ampullae begin to form and ripen. The ampullae are otherwise essentially identical to the seminiferous tubules in higher vertebrates, including the same range of cell types. Testicle The testicle or testis is the male reproductive gland in all animals, including humans. It is homologous to the female ovary. The functions of the testes are to produce both sperm and androgens, primarily testosterone. Testosterone release is controlled by the anterior pituitary luteinizing hormone; whereas sperm production is controlled both by the

neg: Azoospermia testes to produce sperm. Examples include hypopituitarism (for various causes), hyperprolactinemia, and exogenous FSH suppression by testosterone. Chemotherapy may suppress spermatogenesis. Pretesticular azoospermia is seen in about 2% of azoospermia. Pretesticular azoospermia is a kind of non-obstructive azoospermia. In this situation the testes are abnormal, atrophic, or absent, and sperm production severely disturbed to absent. FSH levels tend to be elevated (hypergonadotropic) as the feedback loop is interrupted (lack of feedback inhibition on FSH). The condition is seen in 49–93% of men with azoospermia. Testicular failure includes absence of failure production as well as low production and maturation arrest during

neg: Spermatogenesis system. The initial stages occur within the testes and progress to the epididymis where the developing gametes mature and are stored until ejaculation. The seminiferous tubules of the testes are the starting point for the process, where spermatogonial stem cells adjacent to the inner tubule wall divide in a centripetal direction—beginning at the walls and proceeding into the innermost part, or "lumen"—to produce immature sperm. Maturation occurs in the epididymis. The location [Testes/Scrotum] is specifically important as the process of spermatogenesis requires a lower temperature to produce viable sperm, specifically 1°-8 °C lower than normal body temperature of 37 °C

neg: Human chorionic gonadotropin things. HCG is commonly used during and after steroid cycles to maintain and restore testicular size as well as normal testosterone production. High levels of AASs, that mimic the body's natural testosterone, trigger the hypothalamus to shut down its production of gonadotropin-releasing hormone (GnRH) from the hypothalamus. Without GnRH, the pituitary gland stops releasing luteinizing hormone (LH). LH normally travels from the pituitary via the blood stream to the testes, where it triggers the production and release of testosterone. Without LH, the testes shut down their production of testosterone. In males, HCG helps restore and maintain testosterone production in the

neg: Reproductive biology together in order to produce offspring. The female reproductive system includes the structures involved in ovulation, fertilization, development of an embryo, and birth. These structures include: Estrogen is one of the sexual reproductive hormones that aid in the sexual reproductive system of the female. The male reproductive system includes sex accessory glands, sex accessory ducts, testes, and external genitalia. Testosterone, although present in both males and females, is relatively more abundant in males. Testosterone serves as one of the sexual reproductive hormones in the male reproductive system. Animal reproduction occurs by two modes of action, including both sexual and asexual

neg: Pharmacodynamics of estradiol mid-cycle estradiol-induced surge in gonadotropin levels in women. This is how progestins prevent ovulation and primarily mediate their contraceptive effects in women. High concentrations of estrogens appear to have toxic effects in the testes and, with long-term (>3 years) therapy, can permanently reduce the capacity of the testes to produce testosterone. In addition to their antigonadotropic effects, estrogens at high concentrations can significantly decrease androgen production by the adrenal glands. A study found that treatment with a high dosage of 100 µg/day ethinylestradiol reduced circulating adrenal androgen levels by 27 to 48% in transgender women. Another study found similar effects

neg: Boar taint quality and to be safe for consumers to eat. The vaccine works by stimulating the pig's immune system to produce specific antibodies against gonadotropin-releasing hormone (GnRH). This temporarily inhibits testes function and thus stops the production and accumulation of boar taint–causing compounds. By stimulating production of antibodies specific to GnRH, the vaccine stops the chain of events that lead to the release of testosterone and other steroids from the testes, including androstenone, one of the two causes of boar taint. The other major taint-causing compound, skatole, is also eliminated because the lower steroid levels allow the liver to more efficiently

neg: Prostate cancer It is located in the pelvis, under the urinary bladder and in front of the rectum. The prostate surrounds part of the urethra, the tube that carries urine from the bladder during urination and semen during ejaculation. Because of its location, prostate diseases often affect urination, ejaculation, and rarely defecation. The prostate contains many small glands which make about 20% of the fluid constituting semen. In prostate cancer, the cells of these prostate glands mutate into cancer cells. The prostate glands require male hormones, known as androgens, to work properly. Androgens include testosterone, which is made in the testes; dehydroepiandrosterone,

neg: Organizational-Activational Hypothesis prenatally there is an organizing effect on sexual behavior, permanently altering normal female mating behavior as adults. Sexual behavior in rats is organized prenatally and activated with steroids hormones in adulthood. In males high levels of testosterone produced by testes and travel to the brain. Here, testosterone is aromatized to an estradiol and masculinizes and defeminizes the brain. Thus, estradiol is responsible for many male-typical behavior. In females, the ovaries produce large amounts of estrogen during gestation. Rats have alpha-fetoprotein that binds to the estrogen before it can reach the brain. The estrogen is eventually metabolized in the liver. This

neg: Congenital adrenal hyperplasia due to 21-hydroxylase deficiency testosterone in the blood can enlarge the phallus, partially or completely close the vaginal opening, enclose the urethral groove so that it opens at the base of the phallus, on the shaft or even at the tip like a boy. Testosterone can cause the labial skin to become as thin and rugated as a scrotum, but cannot produce palpable gonads (i.e., testes) in the folds. Thus, depending on the severity of hyperandrogenism, a female infant can be mildly affected, obviously ambiguous, or so severely virilized as to appear to be a male. Andrea Prader devised the following Prader scale as

neg: Puberty developing swellings under nipples during puberty are told the effects are temporary in some male teenagers due to high levels of estradiol. Another hormonal change in males takes place during the teenage years for most young men. At this point in a male's life the testosterone levels slowly rise, and most of the effects are mediated through the androgen receptors by way of conversion dihydrotestosterone in target organs (especially that of the bowels). As the amplitude of LH pulses increases, the theca cells of the ovaries begin to produce testosterone and smaller amounts of progesterone. Much of the testosterone moves

neg: Sex and gender distinction applied to sexually dimorphic traits that are hypothesized to be evolved consequences of sexual selection. Anisogamy, or the size differences of gametes (sex cells), is the defining feature of the two sexes. By definition, males have small, mobile gametes (sperm); females have large and generally immobile gametes (ova or eggs). In humans, typical male or female sexual differentiation includes the presence or absence of a Y chromosome, the type of gonads (ovary or testes), the balance of sex hormones (testosterone and estrogen), the internal reproductive anatomy (e.g. uterus or prostate gland), and the external genitalia (e.g. penis or vulva). People

neg: Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency intra-ovarian steroid production. The most difficult management decisions are posed by the more ambiguous genetic (XY) males. Most who are severely undervirilized, looking more female than male, are raised as females with surgical removal of the nonfunctional testes. If raised as males, a brief course of testosterone can be given in infancy to induce growth of the penis. Surgery may be able to repair the hypospadias. The testes should be salvaged by orchiopexy if possible. Testosterone must be replaced in order for puberty to occur and continued throughout adult life. Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency Congenital adrenal hyperplasia

neg: Anorchia if the testes are lost after 14 weeks, the baby will have partial male genitalia with the notable absence of gonads. Tests include observable lack of testes, low testosterone levels (typical female levels), elevated follicle stimulating hormone and luteinizing hormone levels, XY karyotype, ultrasound or magnetic resonance imaging showing absent gonadal tissue, low bone density, low anti-Müllerian hormone levels, and surgical exploration for evidence of male gonadal tissue. Treatment includes androgen (testosterone) supplementation to artificially initiate puberty, testicular prosthetic implantation, and psychological support. Gender Dysphoria may result in anorchic individuals who are assigned male at birth and raised as male

neg: Sexual differentiation in humans development can only occur when the fetal testis secretes key hormones at a critical period in early gestation. The testes begin to secrete three hormones that influence the male internal and external genitalia: they secrete anti-müllerian hormone (AMH), testosterone, and dihydrotestosterone (DHT). Anti-müllerian hormone causes the paramesonephric ducts to regress. Testosterone converts the mesonephric ducts into male accessory structures, including the epididymis, vas deferens, and seminal vesicle. Testosterone will also control the descending of the testes from the abdomen into the scrotum. Many other genes found on other autosomes, including"WT-1", "SOX9", "SF-1" also play a role in gonadal development. Females:

neg: Foekje Dillema on the Y is the testis determining factor, so Dillema may have had infertile testes or ovotestes palpable in her groin. These ovotestes produce more testosterone than ovaries. Higher testosterone levels were considered unfair towards the competition. Foekje Dillema Foekje Dillema (18 September 1926 – 5 December 2007) was a Dutch track and field athlete. Dillema was named "athlete of the match" in 1949 after winning the 100 metres and 200 metres race during a tournament in London. She was an important rival for another Dutch athlete Fanny Blankers-Koen, who won four gold medals during the 1948 Summer Olympics and

neg: Svadhishthana the front of the body (i.e. its kshetram) is barely below the belly button. It is connected with the sense of taste, (the tongue) and with reproduction (the genitals). It is often associated with the testes and ovaries. They produce the hormones testosterone or estrogen, which influence sexual behaviors. They are stored in areas where genetic information lies dormant, in the same way that samskaras lie dormant within Svadhishthana. Practices in kundalini yoga to control and balance the energy in Svadhisthana chakra include vajroli mudra (contraction of the genitals), ashvini mudra (contraction of the anus), and various asanas and pranayamas.

neg: Charles-Édouard Brown-Séquard this therapy could not have possibly worked because, unlike the thyroid gland, the testes do not store the hormones they produce and, therefore, obtaining a therapeutic dose of testosterone directly from animal glands "would require about one-quarter ton of bull's testes." The positive response by many men is now thought to have been a placebo effect, but apparently this was "sufficient to set the field of endocrinology off and running." In 1886 Brown-Séquard was elected to the Board of the Sugar Club. He also was a member of the Royal Society of London. Brown-Séquard was a keen observer and experimentalist.

neg: XXYY syndrome sex chromosomes in each of a male's cells (48,XXYY). Extra copies of genes on the X chromosome interfere with male sexual development, preventing the testes from functioning normally and reducing the levels of testosterone. Many genes are found only on the X or Y chromosome, but genes in areas known as the pseudoautosomal regions are present on both sex chromosomes. Extra copies of genes from the pseudoautosomal regions of the extra X and Y chromosome contribute to the signs and symptoms of 48,XXYY syndrome; however, the specific genes have not been identified. The condition 48,XXYY is not inherited; it usually

neg: Nilutamide and along with decreased hair growth, were the earliest sign of feminization. Nilutamide did not change the size of the prostate gland (which is the same as with high-dosage cyproterone acetate and ethinylestradiol treatment for as long as 18 months), but was found to alter its histology, including increased stromal tissue with a significant reduction in acini and atrophic epithelial cells, indicating glandular atrophy. In addition, readily apparent histological changes were observed in the testes, including a reduction in tubular and interstitial cells. Nilutamide was found to more than double luteinizing hormone (LH) and testosterone levels and to triple estradiol

neg: Hypothalamic–pituitary–gonadal axis the activity of the HPG axis decreases. As males age, the testes begin to produce less testosterone, leading to a condition known as post-pubertal hypogonadism. The cause of the decreased testosterone is unclear and a current topic of research. Post-pubertal hypogonadism results in progressive muscle mass decrease, increase in visceral fat mass, loss of libido, impotence, decreased attention, increased risk of fractures, and abnormal sperm production. Sex steroids also affect behavior, because sex steroids affect the brains structure and functioning. During development, hormones help determine how neurons synapse and migrate to result in sexual dimorphisms. These physical differences lead to

neg: Male infertility to a non-disjunction error during cell division. Resulting in males having smaller testes, reducing the amount of testosterone and sperm production. Males with this syndrome carry an extra pair of X chromosomes, meaning they have 47 pairs of chromosomes compared to the normal 46 pairs in each cell. This extra pair of chromosomes directly affects sexual development before birth and during puberty (links to learning disabilities and speech development have also been shown to be affected). There are varieties in Klinefelter Syndrome, where some cases may have the extra X chromosome in all cells, referred to as Mosaic Klinefelter Syndrome,

neg: Anisogamy more selective of males as well as making the timing of fertilization potentially more frequent if males are scarce. For males of all species, the sperm cells they produce are optimized for ensuring fertilization of the female egg. These sperm cells are created through spermatogenesis, a form of gametogenesis that focuses on developing the most possible gametes per sexual encounter. Spermatogenesis occurs in the testes, a male specific organ that is also produces hormones that trigger the development of secondary sex characteristics. Since the male's gametes are energetically cheap and abundant in every ejaculation, a male can greatly increase his

neg: INHBB safrole. INHBB Inhibin, beta B, also known as INHBB, is a protein which in humans is encoded by the "INHBB" gene. INHBB is a subunit of both activin and inhibin, two closely related glycoproteins with opposing biological effects. Inhibins are heterodimeric glycoproteins composed of an α subunit (INHA) and one of two homologous, but distinct, β subunits (βA or βB, this protein). mRNA for the two subunits has been demonstrated in the testes of adult rats. Inhibin can bind specifically to testicular interstitial cells throughout development and may be an important regulator of Leydig cell testosterone production or interstitial cell

neg: INHBB INHBB Inhibin, beta B, also known as INHBB, is a protein which in humans is encoded by the "INHBB" gene. INHBB is a subunit of both activin and inhibin, two closely related glycoproteins with opposing biological effects. Inhibins are heterodimeric glycoproteins composed of an α subunit (INHA) and one of two homologous, but distinct, β subunits (βA or βB, this protein). mRNA for the two subunits has been demonstrated in the testes of adult rats. Inhibin can bind specifically to testicular interstitial cells throughout development and may be an important regulator of Leydig cell testosterone production or interstitial cell function.

neg: Domestic sheep reproduction testing and performance recording schemes as a means of improving their flocks. In 2008, for the first time in history, researchers at Chiswick CSIRO research station, between Uralla and Armidale, New South Wales have used stem cells to develop surrogate rams and bulls. These males then produce the viable semen of another male. The approach in these sheep experiments involves irradiating a ram’s testes while placing stem cells from a second ram into the testes of the first, ram A. In the following weeks ram A produces semen the usual way, but is using the stem cells of ram B

neg: Androgen the zona reticularis, the innermost layer of the adrenal cortex. Adrenal androgens function as weak steroids (though some are precursors), and the subset includes dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), androstenedione (A4), and androstenediol (A5). Besides testosterone, other androgens include: Determined by consideration of all biological assay methods (circa 1970): Ovaries and adrenal gland produce much lower levels than the testes. Regarding the relative contributions of ovaries and adrenal gland to female androgen levels, in a study with six menstruating women the following observations have been made: During mammalian development, the gonads are at first capable of becoming either ovaries or

neg: Progestogen 17α-hydroxyprogesterone. These progestogens, along with another steroid, 17α-hydroxypregnenolone, are the precursors of all other endogenous steroids, including the androgens, estrogens, glucocorticoids, mineralocorticoids, and neurosteroids. Thus, many tissues producing steroids, including the adrenal glands, testes, and ovaries, produce progestogens. In some tissues, the enzymes required for the final product are not all located in a single cell. For example, in ovarian follicles, cholesterol is converted to androstenedione, an androgen, in the theca cells, which is then further converted into estrogen in the granulosa cells. Fetal adrenal glands also produce pregnenolone in some species, which is converted into progesterone and estrogens by

neg: Eucestoda organs, then proglottids with mature female reproductive organs, and then proglottids with fertilized eggs in the uterus, a condition commonly referred to as "gravid." An atrium on the lateral margin of each proglottid contains the openings to both the male and female genital ducts. Follicular testes produce sperm, which are carried by a system of ducts to the cirrus, an eversible copulatory organ that usually has a hypodermic system of spines and a holdfast system of hooks. The main specialized female reproductive organs are an ovary that produces eggs and a vitellarium that produces yolk cells. Yolk cells travel in

neg: Testicular immunology of B-lymphocytes in the testis is significant, since these are the antibody-producing cells of the immune system. Since anti-sperm antibodies can cause infertility, it is important that antibody-producing B-lymphocytes are kept separated from the testis. T-lymphocytes (T-cells) are white blood cells which take part in cell-mediated immunity. They are often found within tissues where they can be activated by antigen-presenting cells upon infection. They are present in rat and human testes, where they constitute approximately 10 to 20% of the immune cells present, as well as mouse and ram testes. Both cytotoxic T-cells and Helper T cells are found in

neg: Side effects of bicalutamide with increases or decreases in testosterone levels. It appears that testosterone levels within the normal physiological range are not importantly involved in sexual desire or function in women. Bicalutamide reduces the size of the prostate gland and seminal vesicles, though not of the testes. Significantly reduced penile length is also a recognized adverse effect of . Reversible hypospermia or aspermia (that is, reduced or absent semen/ejaculate production) may occur. However, bicalutamide does not appear to adversely affect spermatogenesis, and thus may not necessarily abolish the capacity/potential for fertility in men. Due to the induction of chronic overproduction of and testosterone,

neg: Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency an alternate route of testosterone synthesis from androstenediol in the testes. 3β-HSD deficiency results in large elevations of pregnenolone, 17α-hydroxypregnenolone, and DHEA. However, complexity arises from the presence of a second 3β-HSD isoform (HSD3B1) coded by a different gene, expressed in the liver and placenta, and unaffected in 3β-HSD-deficient CAH. The presence of this second enzyme has two clinical consequences. First, 3β-HSD II can convert enough of the excess 17α-hydroxypregnenolone to 17α-hydroxyprogesterone to produce 17α-hydroxyprogesterone levels suggestive of common 21-hydroxylase deficient CAH. Measurement of the other affected steroids distinguishes the two. Second, 3β-HSD I can convert enough DHEA to testosterone

neg: Testicle and large testes compared to body weight (0.3%). Human testicular size falls between these extremes (0.08%). Testis weight also varies in seasonal breeders like deer and horses. The change is related to changes in testosterone production. Human testicles are smaller than chimpanzee testicles but larger than gorilla testicles. Under a tough membranous shell called the tunica albuginea, the testis of amniotes, as well as some teleost fish, contains very fine coiled tubes called seminiferous tubules. Amphibians and most fish do not possess seminiferous tubules. Instead, the sperm are produced in spherical structures called "sperm ampullae". These are seasonal structures, releasing

neg: Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency 3β-HSD CAH comprised significant proportions of girls with premature pubic hair or older women with hirsutism have not been confirmed and it now appears that premature pubarche in childhood and hirsutism after adolescence are not common manifestations of 3β-HSD CAH. Undervirilization of genetic males with 3β-HSD CAH occurs because synthesis of testosterone is impaired in both adrenals and testes. Although DHEA is elevated, it is a weak androgen and too little testosterone is produced in the liver to offset the deficiency of testicular testosterone. The degree of undervirilization is more variable, from mild to severe. Management issues are those of

neg: Sexual dysfunction rare cause of erectile dysfunction. In individuals with testicular failure like in Klinefelter syndrome, or those who have had radiation therapy, chemotherapy or childhood exposure to mumps virus, the testes may fail and not produce testosterone. Other hormonal causes of erectile failure include brain tumors, hyperthyroidism, hypothyroidism or disorders of the adrenal gland. Structural abnormalities of the penis like Peyronie's disease can make sexual intercourse difficult. The disease is characterized by thick fibrous bands in the penis which leads to a deformed-looking penis. Drugs are also a cause of erectile dysfunction. Individuals who take drugs to lower blood pressure or

neg: Dexatrim use of ginseng (under 3 months) is unlikely to produce side effects and appears safe for most people. Side effects, often associated with longer term use, can include headaches, insomnia, and gastrointestinal problems. There are many conditions in which ginseng use has special precautions and warnings. These include pregnancy, diabetes, auto-immune diseases, and bleeding disorders. Dehydroepiandrosterone (DHEA) is a steroid hormone produced by the adrenal glands (and by the testes in men), which can be converted in the body to male and female sex hormones, including estrogen and testosterone. DHEA is used to treat a variety of conditions (without FDA

neg: Sex and female forms—spermatozoa and egg cells. These gametes combine to form embryos which develop into a new organism. The male gamete, a spermatozoon (produced in vertebrates within the testes), is a small cell containing a single long flagellum which propels it. Spermatozoa are extremely reduced cells, lacking many cellular components that would be necessary for embryonic development. They are specialized for motility, seeking out an egg cell and fusing with it in a process called fertilization. Female gametes are egg cells (produced in vertebrates within the ovaries), large immobile cells that contain the nutrients and cellular components necessary for a

neg: Male reproductive system turn determines whether the gonads of the embryo will be testes or ovaries; and the presence or absence of testes, finally, determines whether the sex accessory organs and external genitalia will be male or female. This sequence is understandable in light of the fact that both male and female embryos develop within the maternal environment - high in estrogen secreted by the mother’s ovaries and the placenta. If estrogen determined the gender, all embryos would become feminized. During puberty increased gonadotropin secretion stimulates a rise in sex steroids creation from the testes. The increased secretion of testosterone from the testes

neg: Androgen testes. In humans, starting at about week 4, the gonadal rudiments are present within the intermediate mesoderm adjacent to the developing kidneys. At about week 6, epithelial sex cords develop within the forming testes and incorporate the germ cells as they migrate into the gonads. In males, certain Y chromosome genes, particularly SRY, control development of the male phenotype, including conversion of the early bipotential gonad into testes. In males, the sex cords fully invade the developing gonads. The mesoderm-derived epithelial cells of the sex cords in developing testes become the Sertoli cells, which will function to support sperm cell

neg: Reproductive system particularly testosterone. The testes release a hormone that controls the development of sperm. This hormone is also responsible for the development of physical characteristics in men such as facial hair and a deep voice. The human female reproductive system is a series of organs primarily located inside of the body and around the pelvic region of a female that contribute towards the reproductive process. The human female reproductive system contains three main parts: the vulva, which leads to the vagina, the vaginal opening, to the uterus; the uterus, which holds the developing fetus; and the ovaries, which produce the female's

neg: Male infertility to hypogonadotropic hypogonadism. Although controversial, off-label clomiphene citrate, an antiestrogen, may also be effective by elevating gonadotropin levels. Though androgens are absolutely essential for spermatogenesis and therefore male fertility, exogenous testosterone therapy has been found to be ineffective in benefiting men with low sperm count. This is thought to be because very high local levels of testosterone in the testes (concentrations in the seminiferous tubules are 20- to 100-fold greater than circulating levels) are required to mediate spermatogenesis, and exogenous testosterone therapy (which is administered systemically) cannot achieve these required high local concentrations (at least not without extremely supraphysiological dosages).

neg: Gametogonium Retinoic acid is the major factor in meiosis, upregulating genes including ‘‘Stra8’‘, ‘‘Dmc1’‘ and ‘‘Sycp3’‘, which all have a role in meiosis. The male germ cells are protected from external signalling, like retinoic acid from the mesonephros, by the Leydig and Sertoli cells. Spermatogonium are the stem cell population that reside in the testes and undergo spermatogenesis to form sperm. They remain within the testes throughout adulthood. Oogonium are the stem cells for oocytes, and were previously thought to be depleted during development during the production of the primary oocytes. However, some of these stem cells have been found in

neg: Congenital adrenal hyperplasia due to 21-hydroxylase deficiency stimulation test may be needed in mild cases, but usually the random levels of 17OHP are high enough to confirm the diagnosis. The mainstay of treatment is suppression of adrenal testosterone production by a glucocorticoid such as hydrocortisone. Mineralocorticoid is only added in cases where the plasma renin activity is high. A third key aspect of management is suppression of central precocious puberty if it has begun. The usual clues to central puberty in boys are that the testes are pubertal in size, or that testosterone remains elevated even when the 17OHP has been reduced toward normal. In girls central

neg: Human reproductive ecology years of age and ending by 16-17, and girls starting around 10-11 and ending at 15-17. Activity in the hypothalamic–pituitary–gonadal axis (HPG axis) initiates puberty by secreting gonadotropin-releasing hormone (GnRH) from the hypothalamus into the anterior pituitary. The anterior pituitary releases the gonadotropins luteunizing hormone (LH) into the ovaries, which produce estrogen, and follicle-stimulating hormone (FSH) into the testes, which produce testosterone. The central event in puberty for females is menarche, the first menstrual bleeding. For males, it is the first ejaculation. The onset of menarche is easier to determine due to the evidence of menstrual bleeding, while the first

neg: Serge Voronoff the world, "The Lancet", suggested that the file on Voronoff's work be reopened and in particular that "the Medical Research Council should fund further studies on monkey glands." By 1994, there were calls for a qualified apology from the orthodox medical establishment for dismissing Voronoff's work. In particular, since modern medicine has established that the Sertoli cells of the testes constitute a barrier to the immune system, rendering the testes an immunologically privileged site for the transplantation of foreign tissue, the thin slices of monkey testicles Voronoff implanted into the patient's testicles may in theory have survived to produce some

neg: Muse cell in somatic cells, while the same genes were very high in ES and iPS cells. These gene expression pattern and level may explain why Muse cells are pluripotent but without tumorigenic activity. Unlike ES and iPS cells, transplanted Muse cells in testes of immunodeficient mice -a commonly used experiment to test the tumorigenicity of stem cells- have not been reported to form teratomas, even after six months. Thus, Muse cells are pluripotent but are non-tumorigenic. Similarly, epiblast stem cells cultured under certain conditions also do not form teratomas in testes, even though they show pluripotency in vitro. Thus, pluripotent stem

neg: Endocrinology or activated a constituent of the blood or that the testes removed an inhibitory factor from the blood. It was not proven that the testes released a substance that engenders male characteristics until it was shown that the extract of testes could replace their function in castrated animals. Pure, crystalline testosterone was isolated in 1935. The Graves' disease was named after Irish doctor Robert James Graves, who described a case of goiter with exophthalmos in 1835. The German Karl Adolph von Basedow also independently reported the same constellation of symptoms in 1840, while earlier reports of the disease were also

neg: Testosterone Testosterone Testosterone is the primary male sex hormone and an anabolic steroid. In male humans, testosterone plays a key role in the development of male reproductive tissues such as testes and prostate, as well as promoting secondary sexual characteristics such as increased muscle and bone mass, and the growth of body hair. In addition, testosterone is involved in health and well-being, and the prevention of osteoporosis. Insufficient levels of testosterone in men may lead to abnormalities including frailty and bone loss. Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen

neg: Castration Castration Castration (also known as gonadectomy) is any action, surgical, chemical, or otherwise, by which an individual loses use of the testicles. Surgical castration is bilateral orchiectomy (excision of both testes), and chemical castration uses pharmaceutical drugs to deactivate the testes. Castration causes sterilization (preventing the castrated person or animal from reproducing); it also greatly reduces the production of certain hormones, such as testosterone. Surgical castration in animals is often called neutering. The term "castration" is sometimes also used to refer to the removal of the ovaries in the female, otherwise known as an oophorectomy or, in animals, spaying. Estrogen