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Androgenic alopecia – Wikipedia, the free encyclopedia

Androgenic alopecia (also known as androgenetic alopecia, alopecia androgenetica, or male pattern baldness) is hair loss that occurs due to an underlying susceptibility of hair follicles to androgenic miniaturization. It is the most common cause of hair loss and will affect up to 70% of men and 40% of women at some point in their lifetimes. Men typically present with hairline recession at the temples and vertex balding, while women normally thin diffusely over the top of their scalps.[1][2][3] Both genetic and environmental factors play a role, and many etiologies remain unknown.

Classic androgenic hair loss in males begins above the temples and vertex, or calvaria, of the scalp. As it progresses, a rim of hair at the sides and rear of the head remains. This has been referred to as a 'Hippocratic wreath', and rarely progresses to complete baldness.[4] The Hamilton-Norwood scale has been developed to grade androgenic alopecia in males.

Female androgenic alopecia is known colloquially as "female pattern baldness", although its characteristics can also occur in males. It more often causes diffuse thinning without hairline recession; and, like its male counterpart, rarely leads to total hair loss.[5] The Ludwig scale grades severity of androgenic alopecia in females.

Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice;[6]chimpanzees (Pan troglodytes); bald uakaris (Cacajao rubicundus); and stump-tailed macaques (Macaca speciosa and M. arctoides). Of these, macaques have demonstrated the greatest incidence and most prominent degrees of hair loss.[7][8]

Research indicates that the initial programming of pilosebaceous units begins in utero.[9] The physiology is primarily androgenic, with dihydrotestosterone (DHT) the major contributor at the dermal papillae. Below-normal values of sex hormone-binding globulin , follicle-stimulating hormone , testosterone, and epitestosterone are present in men with premature androgenic alopecia compared to normal controls.[10] Although follicles were previously thought permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitors from which the follicles arose.[11]

Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor at the dermal papillae, which is affected by DHT.[12]Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age,[13] androgens stimulate hair growth on the face, but suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.[14]

These observations have led to study at the level of the mesenchymal dermal papillae.[15][16]Types 1 and 2 5 reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles.[17] They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth.[14] Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but stimulate TGF 1, TGF 2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization.[14] Hair follicles in anaphase express four different caspases. Tumor necrosis factor inhibits elongation of hair follicles in vitro with abnormal morphology and cell death in the bulb matrix.[18]

Studies of serum levels of IGF-1 show it to be increased with vertex balding.[19][20] Earlier work looking at in vitro administration of IGF had no effect on hair follicles when insulin was present, but when absent, caused follicle growth. The effects on hair of IGF-I were found to be greater than IGF-II.[21] Later work also showed IGF-1 signalling controls the hair growth cycle and differentiation of hair shafts,[12] possibly having an anti-apoptotic effect during the catagen phase.[22]In situ hybridization in adult human skin has shown morphogenic and mitogenic actions of IGF-1.[23] Mutations of the gene encoding IGF-1 result in shortened and morphologically bizarre hair growth and alopecia.[24] IGF-1 is modulated by IGF binding protein, which is produced in the dermal papilla.[25]

DHT inhibits IGF-1 at the dermal papillae.[26] Extracellular histones inhibit hair shaft elongation and promote regression of hair follicles by decreasing IGF and alkaline phosphatase in transgenic mice.[27] Silencing P-cadherin, a hair follicle protein at adherens junctions, decreases IGF-1, and increases TGF beta 2, although neutralizing TGF decreased catagenesis caused by loss of cadherin, suggesting additional molecular targets for therapy. P-cadherin mutants have short, sparse hair.[28]

At the occipital scalp, androgens enhance inducible nitric oxide synthase (iNOS), which catalyzes production of nitric oxide from L-arginine.[14] The induction of iNOS usually occurs in an oxidative environment, where the high levels of nitric oxide produced interact with superoxide, leading to peroxynitrite formation and cell toxicity. iNOS has been suggested to play a role in host immunity by participating in antimicrobial and antitumor activities as part of the oxidative burst[29] of macrophages.[30] The gene coding for nitric oxide synthase is on human chromosome 17.[31]

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Androgenic alopecia - Wikipedia, the free encyclopedia

Difference Between Male and Female BirdsGenetics and …

Sex-Linked Traits in Bird Genetics

Understanding the ZZ/ZW sex chromosome system is important for people who breed birds, whether the interest is in chicken genetics, parrot genetics, or some other type of bird. The way sex-linked traits are inherited is opposite to the way they are inherited by humans and other mammals.

For example, in cockatiels, budgerigars (parakeets), lovebirds, and other small parrots, the lutino color mutation is a sex-linked recessive trait. Lutino birds lack the dark pigment melanin, which is responsible for black, gray, and blue coloration in birds. As a result, lutino birds appear to have significant yellow coloration, which would ordinarily be covered up by melanin.

The lutino gene is located on the Z chromosome. Since lutino females have only one Z chromosome, they will pass this chromosome down to all their sons (remember male birds are ZZ), but not to their daughters (female birds are ZW and get the Z chromosome from their fathers).

A male bird will be lutino only if his father has the gene and his mother has the mutation as well. With a non-lutino mother, a male that inherits lutino from his father will be a heterozygous carrier, but will not have a lutino phenotype. A lutino-colored male must be homozygous, since the trait is recessive. In this situation all his daughters will be lutino-colored and all his sons will be carriers.

For a non-lutino carrier male (heterozygous), each daughter has a 50% chance of being lutino, and each son has a 50% chance of being a carrier.

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Difference Between Male and Female BirdsGenetics and ...

Male Infertility | Genetic Abnormalities or Male …

The development of in vitro fertilitzation (IVF) has allowed many couples to have the families they might otherwise have been unable to create independently. At the same time, this technology has allowed researchers to study the genetic make-up of the earliest stages of embryos. These advances are providing insights into the link between genetics and infertility and how defects (mutations) in specific genes may result in male or female infertility.It is possible that many cases of unexplained infertility will one day be found to have a clear genetic basis.

What has been learned in the last two decades of assisted reproduction is that some cases of severe male factor infertility are clearly related to gene deletions, mutations or chromosomal abnormalities.

Some men with very severe male factor infertility will be found, upon testing their blood chromosomes (known as a karyotype) to have an extra X chromosome. That is, instead of having a 46 XY karyotype, they have a 47 XXY karyotype. This condition is known as Klinefelter Syndrome and can result in failure to achieve puberty or even when puberty is achieved, these men often have male infertility. Some men with Klinefelter Syndrome can father pregnancies through the use of in vitro fertilitzation (IVF) with Intra-Cytoplasmic Sperm injection (ICSI).So far, we are not seeing an increased risk of Klinefelter Syndrome or other chromosome abnormalities in the offspring achieved in these cases.

Also discovered in recent years is that some men with very severe low sperm counts will be found to have deletions in a certain part of their Y chromosome, known as the DAZ gene. Their karyotype is normal (46 XY) but close inspection of the Y chromosome shows there are sections of the chromosome that are missing. A portion of these men will have no recoverable sperm in the ejaculate or on testicular surgery and donor sperm is the only option. With other deletions in the DAZ gene, there is a small amount of sperm present and conception with IVF-ICSI is possible. In these cases, the male offspring which will always inherit their fathers Y chromosome, will also have this deletion, and will themselves be infertile.

A single gene mutation in the gene for Cystic Fibrosis (CF) is associated with absence of the part of the tube (the vas deferens) that leads from the testicle to the urethra in the penis. These men are usually carriers for the CF gene mutation and do not themselves have the disease of Cystic Fibrosis. Sperm can be recovered from the testicles in these men to be used for IVF with ICSI but it is imperative that their wife (or egg provider) be fully tested for CF mutations as well, otherwise there is significant risk of having a child with Cystic Fibrosis.

For men with sperm counts routinely in the less than 5 million total motile sperm range, testing for genetic conditions is warranted so that these men or couples can be made aware of the genetic issues and how these issues might affect their offspring.

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Male Infertility | Genetic Abnormalities or Male ...

Male infertility – Wikipedia, the free encyclopedia

Male infertility refers to a male's inability to cause pregnancy in a fertile female. In humans it accounts for 40-50% of infertility.[1][2][3] It affects approximately 7% of all men.[4] Male infertility is commonly due to deficiencies in the semen, and semen quality is used as a surrogate measure of male fecundity.[5]

Factors relating to male infertility include:[6]

Pre-testicular factors refer to conditions that impede adequate support of the testes and include situations of poor hormonal support and poor general health including:

Male smokers also have approximately 30% higher odds of infertility.[9][not in citation given] There is increasing evidence that the harmful products of tobacco smoking kill sperm cells.[10][11] Therefore, some governments require manufacturers to put warnings on packets. Smoking tobacco increases intake of cadmium, because the tobacco plant absorbs the metal. Cadmium, being chemically similar to zinc, may replace zinc in the DNA polymerase, which plays a critical role in sperm production. Zinc replaced by cadmium in DNA polymerase can be particularly damaging to the testes.[12]

Common inherited variants in genes that encode enzymes employed in DNA mismatch repair are associated with increased risk of sperm DNA damage and male infertility.[13] As men age there is a consistent decline in semen quality, and this decline appears to be due to DNA damage.[14] (Silva et al., 2012). These findings suggest that DNA damage is an important factor in male infertility.

Testicular factors refer to conditions where the testes produce semen of low quantity and/or poor quality despite adequate hormonal support and include:

Radiation therapy to a testis decreases its function, but infertility can efficiently be avoided by avoiding radiation to both testes.[20]

Post-testicular factors decrease male fertility due to conditions that affect the male genital system after testicular sperm production and include defects of the genital tract as well as problems in ejaculation:

The diagnosis of infertility begins with a medical history and physical exam by a physician or nurse practitioner. Typically two separate semen analyses will be required. The provider may order blood tests to look for hormone imbalances, medical conditions, or genetic issues.

The history should include prior testicular or penile insults (torsion, cryptorchidism, trauma), infections (mumps orchitis, epididymitis), environmental factors, excessive heat, radiation, medications, and drug use (anabolic steroids, alcohol, smoking).

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Male infertility - Wikipedia, the free encyclopedia

Size Genetics – Male Enhancement Reviews

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HitXP Science of Genetics behind the Hindu Gotra System …

This article is merely an attempt to find the scientific reasoning behind the origins of the ancient Gotra System and in no way endorses its imposition in the modern Hindu society to decide marriages or other things. In all probabilities, the modern Gotra system is no more relevant, and the best method to verify the genetic feasibility of a marriage, if at all required, would be to avoid cousin marriages (which have been proved to increase the risk of genetic disorders in the off springs) or to do a genetic test of the bride and grooms DNA for any possible genetic disorders in their off springs.

The Gotra is a system which associates a person with his most ancient or root ancestor in an unbroken male lineage. For instance if a person says that he belongs to the Bharadwaja Gotra then it means that he traces back his male ancestry to the ancient Rishi (Saint or Seer) Bharadwaja. So Gotra refers to the Root Person in a persons male lineage.

The Gotra system is practiced amongst most Hindus. See here for a List of Hindu Gotras practiced by different sections of the Hindu Society

Brahmins identify their male lineage by considering themselves to be the descendants of the 8 great Rishis ie Saptarshis (The Seven Sacred Saints) + Bharadwaja Rishi. So the list of root Brahmin Gotras is as follows

These 8 Rishis are called Gotrakarin meaning roots of Gotras. All other Brahmin Gotras evolved from one of the above Gotras. What this means is that the descendants of these Rishis over time started their own Gotras. The total number of established Gotras today is 49. However each of them finally trace back to one of the root Gotrakarin Rishi.

The word Gotra is formed from the two Sanskrit words Gau (meaning Cow) and Trahi (meaning Shed). Note that the English word Cow is a derived word of the Sanskrit word Gau with the same meaning Gau.

So Gotra means Cowshed, where in the context is that Gotra is like the Cowshed protecting a particular male lineage. Cows are extremely important sacred animals to Hindus and there were a large number of best breeds of Cows that ancient Hindus reared and worshipped, and hence the name Gotra referring to the system of maintaining individual male lineages seems more appropriate.

This Gotra system helps one identify his male lineage and is passed down automatically from Father to Son. But the Gotra system does not get automatically passed down from Father to Daughter. Suppose a person with Gotra Angirasa has a Son. Now suppose the Son gets married to a girl whose father belongs to Gotra Kashyapa. The Gotra of the girl automatically is said to become Angirasa after her marriage even though her father belonged to Gotra Kashyapa.

So the rule of the Gotra system is that the Gotra of men remains the same, while the Gotra of the woman becomes the Gotra of their husband after marriage. Now suppose a person has only daughters and no sons. In that case his Gotra will end with him in that lineage because his daughters will belong to the Gotras of their husbands after their marriage!

This was probably the reason why in the ancient vedic or hindu societies it was preferred to have atleast one Son along with any number of daughters, so that the Gotra of the father could continue.

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HitXP Science of Genetics behind the Hindu Gotra System ...

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