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Archive for the ‘Female Genetics’ Category

Genetic factors and hormones that determine gender

In the nucleus of every cell of his or her body, a human being has 46 chromosomes. 22 chromosome pairs (numbered from 1-22) belong to the autosomes and 1 pair to the sex chromosomes or gonosomes. They are denoted as X and Y. A female has two X-chromosomes and a male an X and a Y-chromosome. In a woman, one of the two X-chromosomes is inactivated in the form of heterochromatin (sex chromatin), the Barr body - diagnosis of the genetic gender is made on this basis. This inactivation already takes place in the blastocyst stage 3 - randomly - either on the paternal or maternal X chromosome. When a Y chromosome is present, the development takes place in the direction of manhood; if it is missing, a feminine development occurs.

It is not the number of gonosomes that is decisive for the gender, but rather the presence or absence of the Y-chromosome, as can be seen in the following table.

Phenotypicalgender

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An aneuploidy (anomaly in the number of chromosomes) of the gonosomes (sex chromosomes) is not rare, whereby Klinefelter's syndrome and Turner'ssyndromes occur the most frequently.Klinefelter's syndromeandTurner's syndrome

It is clear that the information encoded on the Y-chromosome is not enough to guide the formation of such a complicated organ as the testicles, but a localized gene on this chromosome, the SRY (sex determining region Y gene) operates very early in the development as a guide or "master gene". It has a testis-determining effect on the indifferent gonads. This small gene (a single exon), which is localized on the shorter arm of the Y chromosome (Yp), gets expressed in the precursors for the supporting cells (Sertoli). It controls a whole number of further genes on the autosomes as well as on the X chromosome. It is only through the concerted workings of this SRY-gene together with genes on other chromosomes that the development of the testicles is possible. (Diagram of the molecular factors involved in the development of the genital apparatus)

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Special case of a dissociation between the karyotype and phenotype.

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Genetic factors and hormones that determine gender

Female Genetic Contributions to Sperm Competition in …

Abstract

In many species, sperm can remain viable in the reproductive tract of a female well beyond the typical interval to remating. This creates an opportunity for sperm from different males to compete for oocyte fertilization inside the female's reproductive tract. In Drosophila melanogaster, sperm characteristics and seminal fluid content affect male success in sperm competition. On the other hand, although genome-wide association studies (GWAS) have demonstrated that female genotype plays a role in sperm competition outcome as well, the biochemical, sensory and physiological processes by which females detect and selectively use sperm from different males remain elusive. Here, we functionally tested 26 candidate genes implicated via a GWAS for their contribution to the female's role in sperm competition, measured as changes in the relative success of the first male to mate (P1). Of these 26 candidates, we identified eight genes that affect P1 when knocked down in females, and showed that five of them do so when knocked down in the female nervous system. In particular, Rim knockdown in sensory pickpocket (ppk)+ neurons lowered P1, confirming previously published results, and a novel candidate, caup, lowered P1 when knocked down in octopaminergic Tdc2+ neurons. These results demonstrate that specific neurons in the female's nervous system play a functional role in sperm competition and expand our understanding of the genetic, neuronal and mechanistic basis of female responses to multiple matings. We propose that these neurons in females are used to sense and integrate signals from courtship or ejaculates, to modulate sperm competition outcome accordingly.

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Are Calico Cats Always Female? – thesprucepets.com

Many people are surprised to hear that the vast majority of calico cats are female. Why is this? Can a calico cat to ever be male? Learn more about the genetics of coat color in felines.

A calico cat is not a breed of cat, it is a color pattern. To be called "calico," three colors must be present: black, white, and orange. Variations of these colors include gray, cream, and ginger. A true calico cat has large blocks of these three colors. Other names for calico cats include tortoiseshell or "torties," brindle, or tricolor cats.

Calico cats areusually female. And, this is due in large part togenetics.Coat color is a complex process that is the result of dominant and non-dominate genes interacting within the X chromosomes. Since coat color is a sex-linked trait, it is one of the cat's physical traits that vary based on gender.

Female animals have two X chromosomes (XX), while males have one X chromosome and one Y chromosome (XY). The genetic coding for having black or orange color in thecoat is found in the X chromosome. The color display is either orange or black.The coding for white is a completely separate gene.

In femalemammals, one of the X chromosomes is randomly deactivated,called X-inactivation,in each cell.For calico cats, the random mix of color genes that are activated or deactivated gives the blotchy orange and black color display.

Since females have two X chromosomes, they are able to have two different colors (orange or black, depending what X was deactivated) and white; creating the three-color calico mix.

Since males have only one X chromosome, they only have one black or orange gene and can only display orange or black (plus or minus white, controlled by another gene).

Calico cats are not always female. Male calico cats do exist and typically have a chromosomal aberration of two X chromosomes and one Y chromosome (XXY). Cats with this chromosomal configuration are usually sterile,which means that they are not able to breed. This syndrome is similar to a condition in humans called Klinefelter's syndrome, or XXY syndrome.

On October 1, 2001, the calico cat became the official cat of the state of Maryland in the United States.Calico cats are believed to bringgood luckin the folklore of many cultures.Japanese sailors often had a calicoship's catto protect against misfortune at sea.

Cat genetics is responsible for producing many different varieties of cats and coat types. Common types include the bicolor or tuxedo cat (mostly black with a white chest), striped or marbled tabby cats, and solid color cats.

White cats, true albino cats, are quite rare. Much more common is the appearance of white coat color that is caused by a lack ofmelanocytes, or pigmentation cells, in the skin.White cats with one or two blue eyes have a particularly high likelihood of being deaf.

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NIH launches largest-ever study of breast cancer genetics …

News Release

Wednesday, July 6, 2016

Findings could inform breast cancer disparities.

The largest study ever to investigate how genetic and biological factors contribute to breast cancer risk among black women launched today. This collaborative research project will identify genetic factors that may underlie breast cancer disparities. The effort is funded by the National Cancer Institute (NCI), part of the National Institutes of Health.

This effort is about making sure that all Americans no matter their background reap the same benefits from the promising advances of precision medicine.

Douglas R. Lowy, M.D., Acting Director, NCI

The Breast Cancer Genetic Study in African-Ancestry Populations initiative does not involve new patient enrollment but builds on years of research cooperation among investigators who are part of the African-American Breast Cancer Consortium, the African-American Breast Cancer Epidemiology and Risk (AMBER) Consortium, and the NCI Cohort Consortium. These investigators, who come from many different institutions, will share biospecimens, data, and resources from 18 previous studies, resulting in a study population of 20,000 black women with breast cancer.

This effort is about making sure that all Americans no matter their background reap the same benefits from the promising advances of precision medicine. The exciting new approaches to cancer prevention, diagnosis, and treatment ring hollow unless we can effectively narrow the gap of cancer disparities, and this new research initiative will help us do that, said Douglas R. Lowy, M.D., acting director of NCI. Im hopeful about where this new research can take us, not only in addressing the unique breast cancer profiles of African-American women, but also in learning more about the origin of cancer disparities.

Survival rates for women with breast cancer have been steadily improving over the past several decades. However, these improvements have not been shared equally; black women are more likely to die of their disease. Perhaps of most concern is that black women are more likely than white women to be diagnosed with aggressive subtypes of breast cancer. The rate of triple-negative breast cancer, an aggressive subtype, is twice as high in black women as compared to white women.

The exact reasons for these persistent disparities are unclear, although studies suggest that they are the result of a complex interplay of genetic, environmental, and societal factors, including access to health care. Large studies are needed to comprehensively examine these factors, and NCI is supporting several such efforts.

As part of the study, the genomes of 20,000 black women with breast cancer will be compared with those of 20,000 black women who do not have breast cancer. The genomes will also be compared to those of white women who have breast cancer. The project will investigate inherited genetic variations that are associated with breast cancer risk in black women compared to white women. In addition, researchers will examine gene expression in breast cancer tumor samples to investigate the genetic pathways that are involved in tumor development.

This $12 million grant in combination with previous investments should help advance our understanding of the social and biological causes that lead to disparities in cancer among underserved populations, said Robert Croyle, Ph.D., director of NCIs Division of Cancer Control and Population Sciences (DCCPS), which is administering the grant. A better understanding of the genetic contributions to differences in breast cancer diagnoses and outcomes among African-Americans may lead to better treatments and better approaches to cancer prevention.

A number of studies have suggested that genetic factors may influence breast cancer disparities, so were hopeful that this project can help to shed further light on this matter. said Damali Martin, Ph.D., program director for the DCCPS Genomic Epidemiology Branch. Dr. Martins office is working directly with the grant recipients as well as the consortia groups that have been researching black women and breast cancer.

The grant has been awarded to Wei Zheng, M.D., Ph.D., of Vanderbilt University, Nashville, Tennesee; Christopher Haiman, Sc.D., of the University of Southern California, Los Angeles; and Julie Palmer, Sc.D., of Boston University. Additionally, minority scientists from various institutions, including from one Historically Black College and University medical school, are playing an important role in this study, and they have been involved in previous research that this study builds upon. For example, the Southern Community Cohort Study, a contributing study for this grant, represents a 15-year partnership between Vanderbilt and historically black Meharry Medical College in Nashville, Tennessee. In addition, this grant will provide training opportunities for scientists from minority populations.

Support for ongoing research in this area represents NCIs continued commitment to fund a comprehensive portfolio of research aimed at reducing cancer risk, incidence, and mortality, as well as improving quality of life for cancer survivors across all demographic groups.

The National Cancer Institute leads the National Cancer Program and the NIHs efforts to dramatically reduce the prevalence of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI website at http://www.cancer.gov or call NCI's Cancer Information Service at 1-800-4-CANCER.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

ReferenceBreast Cancer Genetic Study in African-Ancestry Populations, Grant Number R01CA202981

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Serious question about female genetics? | Yahoo Answers

Don't think that either is superior however, each is superior at specific things, obviously.

But here is some fodder for thought. Interesting Genetic Fact:

The female population currently outweighs the male population by 1% or so making the ratio 51% to 49% roughly. However, the male population is predicted to catch up and perhaps surpass the female population only slightly with modern medicine. Why? Because the sex chromosomes, XX for woman and XY for men, carry different genes. The X chromosomes carry large amounts of DNA information while the Y chromosome which is shorter than the X chromosome, only carries a few bits of genetic information such as the gene for becoming male. Essentially, we all start out female! It is the presence of the testis gene, called SRY, that determines the male gender.

Because the X chromosome carries large amounts of genetic information while the Y does not, males are more likely to suffer from disease and abnormalities than women. In genetics, two genes come together to determine a trait. One or both can be dominant or recessive. Disease genes are recessive as are abnormalities but if a male receives a recessive gene for a disease or abnormality, he is likely to express that gene given the lack of extra DNA information from the Y chromosome. Therefore, more male die in infancy than females. Does this make females genetically superior? Modern medicine will help combat early deaths from a genetic standpoint, helping even out the population. Let's not forget that females also develop faster overall, emotionally, physically, and intellectually.

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Female genetic hair loss? | Yahoo Answers

In women, hair loss usually begins at menopause. Although hair loss in females normally occurs after the age of 50 or even later when it does not follow events like pregnancy, chronic illness, crash diets, and stress among others, there has been rare cases reported, in which hair loss affects women as young as 15 or 16. However, unlike with men, hair loss in women typically begins later and is generally not to the full-head state that is generally seen in men.

Balding is genetic and hereditary, and it's thereby logical to think that by looking at family members can be helpful in determining the fate of one's hairline. Sometime it is the case that grandson and maternal grandfather will end up with the similar hairlines, but it's not that foolproof, not the ultimate reference point it's treated as, so better not to consider it at all when wondering if the baldness gene is one you have inherited. Genetic hair loss affects both men and women equally.

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Male and female ability differences down to socialisation …

It is the mainstay of countless magazine and newspaper features. Differences between male and female abilities from map reading to multi-tasking and from parking to expressing emotion can be traced to variations in the hard-wiring of their brains at birth, it is claimed.

Men instinctively like the colour blue and are bad at coping with pain, we are told, while women cannot tell jokes but are innately superior at empathising with other people. Key evolutionary differences separate the intellects of men and women and it is all down to our ancient hunter-gatherer genes that program our brains.

The belief has become widespread, particularly in the wake of the publication of international bestsellers such as John Gray's Men Are from Mars, Women Are from Venus that stress the innate differences between the minds of men and women. But now a growing number of scientists are challenging the pseudo-science of "neurosexism", as they call it, and are raising concerns about its implications. These researchers argue that by telling parents that boys have poor chances of acquiring good verbal skills and girls have little prospect of developing mathematical prowess, serious and unjustified obstacles are being placed in the paths of children's education.

In fact, there are no major neurological differences between the sexes, says Cordelia Fine in her book Delusions of Gender, which will be published by Icon next month. There may be slight variations in the brains of women and men, added Fine, a researcher at Melbourne University, but the wiring is soft, not hard. "It is flexible, malleable and changeable," she said.

In short, our intellects are not prisoners of our genders or our genes and those who claim otherwise are merely coating old-fashioned stereotypes with a veneer of scientific credibility. It is a case backed by Lise Eliot, an associate professor based at the Chicago Medical School. "All the mounting evidence indicates these ideas about hard-wired differences between male and female brains are wrong," she told the Observer.

"Yes, there are basic behavioural differences between the sexes, but we should note that these differences increase with age because our children's intellectual biases are being exaggerated and intensified by our gendered culture. Children don't inherit intellectual differences. They learn them. They are a result of what we expect a boy or a girl to be."

Thus boys develop improved spatial skills not because of an innate superiority but because they are expected and are encouraged to be strong at sport, which requires expertise at catching and throwing. Similarly, it is anticipated that girls will be more emotional and talkative, and so their verbal skills are emphasised by teachers and parents.

The latter example, on the issue of verbal skills, is particularly revealing, neuroscientists argue. Girls do begin to speak earlier than boys, by about a month on average, a fact that is seized upon by supporters of the Men Are from Mars, Women Are from Venus school of intellectual differences.

However, this gap is really a tiny difference compared to the vast range of linguistic abilities that differentiate people, Robert Plomin, a professor at the Institute of Psychiatry in London, pointed out. His studies have found that a mere 3% of the variation in young children's verbal development is due to their gender.

"If you map the distribution of scores for verbal skills of boys and of girls you get two graphs that overlap so much you would need a very fine pencil indeed to show the difference between them. Yet people ignore this huge similarity between boys and girls and instead exaggerate wildly the tiny difference between them. It drives me wild," Plomin told the Observer.

This point is backed by Eliot. "Yes, boys and girls, men and women, are different," she states in a recent paper in New Scientist. "But most of those differences are far smaller than the Men Are from Mars, Women Are from Venus stereotypes suggest.

"Nor are the reasoning, speaking, computing, emphasising, navigating and other cognitive differences fixed in the genetic architecture of our brains.

"All such skills are learned and neuro-plasticity the modifications of neurons and their connections in response experience trumps hard-wiring every time."

The current popular stress on innate intellectual differences between the sexes is, in part, a response to psychologists' emphasis of the environment's importance in the development of skills and personality in the 1970s and early 1980s, said Eliot. This led to a reaction against nurture as the principal factor in the development of human characteristics and to an exaggeration of the influence of genes and inherited abilities. This view is also popular because it propagates the status quo, she added. "We are being told there is nothing we can do to improve our potential because it is innate. That is wrong. Boys can develop powerful linguistic skills and girls can acquire deep spatial skills."

In short, women can read maps despite claims that they lack the spatial skills for such efforts, while men can learn to empathise and need not be isolated like Mel Gibson's Nick Marshall, the emotionally retarded male lead of the film What Women Want and a classic stereotype of the unfeeling male that is perpetuated by the supporters of the hard-wired school of intellectual differences.

This point was also stressed by Fine. "Many of the studies that claim to highlight differences between the brains of males and females are spurious. They are based on tests carried out on only a small number of individuals and their results are often not repeated by other scientists. However, their results are published and are accepted by teachers and others as proof of basic differences between boys and girls.

"All sorts of ridiculous conclusions about very important issues are then made. Already sexism disguised in neuroscientific finery is changing the way children are taught."

So should we abandon our search for the "real" differences between the sexes and give up this "pernicious pinkification of little girls", as one scientist has put it?

Yes, we should, Eliot insisted. "There is almost nothing we do with our brains that is hard-wired. Every skill, attribute and personality trait is moulded by experience."

Cambridge University psychologist and autism expert Simon Baron-Cohen:

"The female brain is predominantly hard-wired for empathy. The male brain is predominantly hard-wired for understanding and building systems"

Writer and feminist Joan Smith:

"Very few women growing up in England in the late 18th century would have understood the principles of jurisprudence or navigation because they were denied access to them"

John Gray, author of Men are from Mars, Women are from Venus:

"A man's sense of self is defined through his ability to achieve results. A woman's sense of self is defined through her feelings and the quality of her relationships"

Sociologist Beth Hess:

"For two millennia, 'impartial experts' have given us such trenchant insights as the fact that women lack sufficient heat to boil the blood and purify the soul, that their heads are too small, their wombs too big, their hormones too debilitating, that they think with their hearts or the wrong side of the brain. The list is never-ending"

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Treating female pattern hair loss – Harvard Health

Noticeable hair loss in women can be deeply distressing. Here are some medical treatments that may help.

About one-third of women experience hair loss (alopecia) at some time in their lives; among postmenopausal women, as many as two-thirds suffer hair thinning or bald spots. Hair loss in women often has a greater impact than hair loss does on men w, because it's less socially acceptable for them. Alopecia can severely affect a woman's emotional well-being and quality of life.

The main type of hair loss in women is the same as it is men. It's called androgenetic alopecia, or female (or male) pattern hair loss. In men, hair loss usually begins above the temples, and the receding hairline eventually forms a characteristic "M" shape; hair at the top of the head also thins, often progressing to baldness. In women, androgenetic alopecia begins with gradual thinning at the part line, followed by increasing diffuse hair loss radiating from the top of the head. A woman's hairline rarely recedes, and women rarely become bald.

There are many potential causes of hair loss in women , including medical conditions, medications, and physical or emotional stress. If you notice unusual hair loss of any kind, it's important to see your primary care provider or a dermatologist, to determine the cause and appropriate treatment. You may also want to ask your clinician for a referral to a therapist or support group to address emotional difficulties. Hair loss in women can be frustrating, but recent years have seen an increase in resources for coping with the problem.

Clinicians use the Ludwig Classification to describe female pattern hair loss. Type I is minimal thinning that can be camouflaged with hair styling techniques. Type II is characterized by decreased volume and noticeable widening of the mid-line part. Type III describes diffuse thinning, with a see-through appearance on the top of the scalp.

Almost every woman eventually develops some degree of female pattern hair loss. It can start any time after the onset of puberty, but women tend to first notice it around menopause, when hair loss typically increases. The risk rises with age, and it's higher for women with a history of hair loss on either side of the family.

As the name suggests, androgenetic alopecia involves the action of the hormones called androgens, which are essential for normal male sexual development and have other important functions in both sexes, including sex drive and regulation of hair growth. The condition may be inherited and involve several different genes. It can also result from an underlying endocrine condition, such as overproduction of androgen or an androgen-secreting tumor on the ovary, pituitary, or adrenal gland. In either case, the alopecia is likely related to increased androgen activity. But unlike androgenetic alopecia in men, in women the precise role of androgens is harder to determine. On the chance that an androgen-secreting tumor is involved, it's important to measure androgen levels in women with clear female pattern hair loss.

In either sex, hair loss from androgenetic alopecia occurs because of a genetically determined shortening of anagen, a hair's growing phase, and a lengthening of the time between the shedding of a hair and the start of a new anagen phase. (See "Life cycle of a hair.") That means it takes longer for hair to start growing back after it is shed in the course of the normal growth cycle. The hair follicle itself also changes, shrinking and producing a shorter, thinner hair shaft a process called "follicular miniaturization." As a result, thicker, pigmented, longer-lived "terminal" hairs are replaced by shorter, thinner, non-pigmented hairs called "vellus."

Each hair develops from a follicle a narrow pocket in the skin and goes through three phases of growth. Anagen (A), the active growth phase, lasts two to seven years. Catagen (B), the transition phase, lasts about two weeks. During this phase, the hair shaft moves upward toward the skin's surface, and the dermal papilla (the structure that nourishes cells that give rise to hair) begins to separate from the follicle. Telogen (C), the resting phase, lasts around three months and culminates in the shedding of the hair shaft.

A clinician diagnoses female pattern hair loss by taking a medical history and examining the scalp. She or he will observe the pattern of hair loss, check for signs of inflammation or infection, and possibly order blood tests to investigate other possible causes of hair loss, including hyperthyroidism, hypothyroidism, and iron deficiency. Unless there are signs of excess androgen activity (such as menstrual irregularities, acne, and unwanted hair growth), a hormonal evaluation is usually unnecessary.

Medications are the most common treatment for hair loss in women. They include the following:

Minoxidil (Rogaine, generic versions). This drug was initially introduced as a treatment for high blood pressure, but people who took it noticed that they were growing hair in places where they had lost it. Research studies confirmed that minoxidil applied directly to the scalp could stimulate hair growth. As a result of the studies, the FDA originally approved over-the-counter 2% minoxidil to treat hair loss in women. Since then a 5% solution has also become available when a stronger solution is need for a woman's hair loss.

Clearly, minoxidil is not a miracle drug. While it can produce some new growth of fine hair in some not all women, it can't restore the full density of the lost hair. It's not a quick fix, either for hair loss in women . You won't see results until you use the drug for at least two months. The effect often peaks at around four months, but it could take longer, so plan on a trial of six to 12 months. If minoxidil works for you, you'll need to keep using it to maintain those results. If you stop, you'll start to lose hair again.

How to use minoxidil: Be sure that your hair and scalp are dry. Using the dropper or spray pump that's provided with the over-the-counter solution, apply it twice daily to every area where your hair is thinning. Gently massage it into the scalp with your fingers so it can reach the hair follicles. Then air-dry your hair, wash your hands thoroughly, and wash off any solution that has dripped onto your forehead or face. Don't shampoo for at least four hours afterwards.

Some women find that the minoxidil solution leaves a deposit that dries and irritates their scalp. This irritation, called contact dermatitis, is probably caused not by the minoxidil itself, but rather by the alcohol that is included to facilitate drying.

Side effects and concerns: Minoxidil is safe, but it can have unpleasant side effects even apart from the alcohol-related skin irritation. Sometimes the new hair differs in color and texture from surrounding hair. Another risk is hypertrichosis excessive hair growth in the wrong places, such as the cheeks or forehead. (This problem is more likely with the stronger 5% solution.)

Because the patent on Rogaine (the brand-name version of minoxidil) has expired, many generic products are available. They all contain the same amount of minoxidil, but some include additional ingredients, such as herbal extracts, which might trigger allergic reactions.

Anti-androgens. Androgens include testosterone and other "male" hormones, which can accelerate hair loss in women. Some women who don't respond to minoxidil may benefit from the addition of the anti-androgen drug spironolactone (Aldactone) for treatment of androgenic alopecia. This is especially true for women with polycystic ovary syndrome (PCOS) because they tend to make excess androgens. Doctors will usually prescribe spironolactone together with an oral contraceptive for women of reproductive age. (A woman taking one of these drugs should not become pregnant because they can cause genital abnormalities in a male fetus.) Possible side effects include weight gain, loss of libido, depression, and fatigue.

Iron supplements. Iron deficiency could be a cause of hair loss in some women . Your doctor may test your blood iron level, particularly if you're a vegetarian, have a history of anemia, or have heavy menstrual bleeding. If you do have iron deficiency, you will need to take a supplement and it may stop your hair loss. However, if your iron level is normal, taking extra iron will only cause side effects, such as stomach upset and constipation.

Hair transplantation, a procedure used in the United States since the 1950s to treat androgenic alopecia, involves removing a strip of scalp from the back of the head and using it to fill in a bald patch. Today, 90% of hair-transplant surgeons use a technique called follicular unit transplantation, which was introduced in the mid-1990s.

During this procedure, surgeons remove a narrow strip of scalp and divide it into hundreds of tiny grafts, each containing just a few hairs. Each graft is planted in a slit in the scalp created by a blade or needle in the area of missing hair. Hair grows naturally this way, in small clusters of one to four follicles, called follicular units. As a result, the graft looks better than the larger "plugs" associated with hair transplants of yesteryear.

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Treating female pattern hair loss - Harvard Health

Genetics May Explain Why Birth Control Doesn’t Always Work …

Some women release an enzyme that canbreak down the hormones from birth control, which may makethese contraceptive methods less effective in preventing pregnancy. (Credit: Image Point Fr/Shutterstock)

No form of birth control is 100 percent effective. Now, a new study provides an explanation for why a small number of women who use hormonalcontraceptive methods still become pregnant, even if they use them correctly.

A new study published in Obstetrics & Gynecologyexplains that somewomen have an uncommon genetic difference that makes hormonal contraception less effective for them.

In the paper, researchers at the University of Colorado School of Medicinesay that around5 percent of women carry a gene that makes their bodies produce an enzyme that breaks down the hormones in birth control faster than usual. The researchers think that the enzyme leaves women with hormone levels that may be too low to prevent pregnancy, particularly among users of low-dose contraceptives.

Hormonal contraceptive methods like the pill, implant or injection work by releasing synthetic versions of female hormones, usually estrogen and progestin, thatoverrides awomans monthly cycle andprevents ovulation. Receiving these hormones, ironically, tricks a womans body into thinking its pregnant, which stops the release of an egg each month. Thehormones also work to prevent pregnancy by thickening the mucus near the cervix, which preventssperm from reaching the egg.

To learn how a womans genetic makeup influences birth control hormones,the researchers examined 350 healthy women with a median age of 22.5 years old who had received a contraceptive implant. This long-lasting birth control device sits under the skin and delivers the hormones necessary toprevent ovulation.

The researchers found that around 5percent of women tested positive for agenetic variant, called CYP3A7*1C. And among these women, the researchers observed lower levels of birth control hormones in their system. Its thought thattheenzyme somehow interferes with the ovulation-suppressing effects of hormonal birth control.

Lead study author Aaron Lazorwitz said that the CYP3A7*1C gene normally shuts off during gestation, before a woman is ever born. But in some women that never happens and evidently impacts how they process steroid hormone-based drugs, like birth control.Better understanding genetic differences in medication effectiveness could be a game-changer in womens healthcare, Lazorwitz said.

The field of pharmacogenomics, looking at how genetics affects drugs, has been a hot topic in multiple areas of medicine [but] womens health research has unfortunately not focused much on this field to this point, he said. As we use the same types of hormonal medications for so many different treatments in womens health, the impact of genetics on these medications has huge potential to change how we take care of women.

According to the Centers for Disease Control and Prevention, 24 percent of women use a hormonal form of contraception like the pill or the implant. Lazorwitz said that many cases of birth control failure come down to user error such as missing a few pills. But, as this study shows, there arefactors outside of a womans controlthat can impact birth control effectiveness, and there are probably more to find, according to Lazorwitz.

We think that genetics is part of the equation, but there likely are other things we havent even considered yet, he said. This is just the first step in our work to try and figure out this complicated issue. Thankfully, we have extremely efficacious birth control methods like intrauterine devices and the [contraceptive] implant that we know work very well for the vast majority of women.

Lazorwitz said the findings likely apply to all forms of hormonal birth control such as the pill, implant or injection because the hormones used in these methods are similar and are processed similarly in the body. But future studies are needed to prove this.

The unintended pregnancy risk for women carrying this genetic variant cannot be quantified yet because its too early. Because the implant releases more than enough hormones needed to prevent pregnancy, Lazorwitz said the variant probably does not impact efficacy of the contraceptive implant. The researchers are more concerned that the genetic variant could affect the effectiveness of lower-dose hormonal methods, like the pill.

For now, Lazorwitz saidwomen should continue to work with their doctorsin finding the best birth control method for them.

We want to reassure women taking hormonal birth control that they dont need to go get genetic screening or anything like that at this time We hope that this kind of research will one day lead to enough information that we can develop some tools or screenings to help guide women on their individualized decision-making process in choosing a birth control method, he said.

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Lick Your Rats – Genetics

In our society, we think of anxious behavior as being a disadvantage. But that's because, for the most part, we live in a nutrient-rich, low-danger environment. In the rat equivalent to our world, the relaxed rat lives a comfortable life. It is likely to reach a high social standing, and it doesn't have to worry about where its next meal is coming from. An anxious rat, on the other hand, doesn't do so well. It is more likely to have a low social standing and suffer from diabetes and heart disease.

In another environment, however, the tables turn. The anxious, guarded behavior of the low-nurtured rat is an advantage in an environment where food is scarce and danger is high. The low nurtured rat is more likely to keep a low profile and respond quickly to stress. In the same environment, a relaxed rat might be a little too relaxed. It may be more likely to let down its guard and be eaten by a predator.

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Lick Your Rats - Genetics

Women’s Contributions to Early Genetics Studies Were …

As a postdoctoral researcher at the University of California, Berkeley, Emilia Huerta-Snchez noticed something strange in the fine print of an old population genetics study. In the acknowledgements, the studys author, a well-known geneticist, wrote, I wish to thank Mrs. Jennifer Smith for ably programming and executing all the computations.

Huerta-Snchez showed the odd credit line to fellow postdoc Rori Rohlfs. Smiths level of computing, she remarked, would normally warrant authorship today. In all likelihood, the two scientists mused privately, other womens contributions to the burgeoning field of population genetics had also been relegated to the footnotes.

Years later, after watching the 2016 movie Hidden Figures, which depicts the black female mathematicians behind NASAs human spaceflight program, Huerta-Snchez and Rohlfsnow with university appointments of their owndiscussed the idea again. This time, they wanted to test the hypothesis. How many programmers had been left in the footnotes of their field, they wondered, and how many of those less-acknowledged contributors were women?

Huerta-Snchez and Rohlfs assembled a team of student researchers to flip through the archival pages of 20 years worth of articles in the programming-heavy journal Theoretical Population Biology, documenting the authors and the names in the acknowledgements and categorizing them by gender. After the group reviewed 800-plus articles by over 1,000 authors (about 93 percent of whom were men), Huerta-Snchezs initial suspicion proved correct. Women whod contributed to influential studies tended to receive a hat-tip in the acknowledgements rather than full authorship.

In a recent study published in the journal Genetics, the San Francisco State University and Brown University researchers found that just under half of the 46 acknowledged programmers they identified in theoretical population genetics studies were women, in contrast to only about seven percent of credited authors. Ezequiel Lopez Barragan, one of the San Francisco State University students who worked on (and got authorship) for the new study, says he felt the skewed acknowledgement of women as programmers was just not fair, not equitable.

By identifying the biases in old research conventions, the team hopes to draws attention to who doesand does notreceive acknowledgement in scientific papers today.

Population genetics, which sprouted up in the first half of the 20th century after the rediscovery of Gregor Mendels foundational work in genetics, is a computation-heavy field that looks at genetic variation to better understand how natural selection and population makeup influence evolution. By the 1970s, one of the decades reviewed in the new study, computer-generated models had become accessible tools for scientists, and technological advances made it possible to gather detailed protein variation data. The field of population genetics took off, Rohlfs says.

Some of the data couldnt be analyzed by hand, which is where the acknowledged programmers came in, computing on the new machines to conduct numerical analysis. These programming roles were often carried out by women, but the researchers crunching the numbers didnt receive the same acknowledgment in published research that they might expect today.

The practice of downplaying womens scientific contributions isnt anything new, says historian Marsha Richmond, who studies womens early contributions to academic biology. Instead, she says, it follows a long trend that was probably first established in astronomy. The Harvard computers, for example, who calculated the positions and characteristics of thousands of stars at Harvard Observatory at the turn of the 20th centuryand made many important discoveries in astronomy along the waymirrored the mathematical roles that women played at NASA more than half a century later.

Historically, women tended to enter emerging fields like ecology or radiation science, and as employees, they were cheaper to hire than their male counterparts. But once the field develops, they get rather marginalized and the men take over, Richmond says. Although the 1960s and 70s heralded increased visibility for some female scientists, like ecologist Rachel Carson and geneticist Charlotte Auerbach, both genetics and the initially pink-collar field of programming followed the pattern of sidelining women contributors. The proportion of female acknowledged programmers in the new study, for instance, decreased between the 1970s and 1980s as the field became more male-dominated and lucrative.

Richmond calls Huerta-Snchez and Rohlfs paper exciting. It was the first shed learned of women involved in this era of evolutionary biology. The lack of female scientists and programmers in the historic record, Richmond says, is not just a problem of science and society but also of historians. Historians have tended to gravitate towards the males who are considered geniuses.

Both Richmond and the studys principal investigators emphasized that uncovering the presence of women in population genetics could inspire future scientists and guard against the negative impact of gender stereotypes in science. Such work reveals paths to success in a field thats still relatively male-dominated. The more we see women doing science, the more its normal, Rohlfs says, and we hope that will lead to change.

Margaret Wu is an early contributor to population genetics and one of the acknowledged programmers whose name cropped up repeatedly in the new study. As the Atlantics Ed Yong explains, her work help develop a statistical toolstill used todaythat approximates the level of genetic diversity in a population.

But when the team behind the study finally reached Wu, she initially thought theyd contacted the wrong person. Wu, after working as a research assistant at Monash University in Australia, has gone on to specialize in educational statistics, not population genetics. She earned a PhD almost 30 years after the highly-cited study that she contributed numerical work to, and she is now on the faculty of the University of Melbourne.

I was in no way frustrated about the authorship. I didnt even think I should be acknowledged that was the norm in those days, Wu writes in an email. But she also says shes observed and experienced gender discrimination throughout her career in academia. My conclusion was that men are often mates (to use an Australian term), she says, and they unite and are unwilling to contradict each other even though someone is not doing the right thing.

Upon reading about Margaret Wu in the Atlantic, Jess Wade, a physics postdoc at Imperial College London whos created around 510 Wikipedia pages for female scientists, made Wu a Wikipedia page. Wade says via Twitter that her first reaction to the study was anger. I made [the Wikipedia page] because Im sick of these people being written out of history.

Rohlfs also pointed to norms, not individuals, as being responsible for the lack of acknowledgement for women. Because authorship, which is totally crucial for career advancement, can be distributed subjectively, its subject to all the biases we have, she says. Today, for instance, the contributions of technicians might be overlooked, and technicians, Rohlfs says, are more often women and people of color.

Everybody just thought it was okay that these women didnt get authorship, she says. I think that leads us directly then to think about what are our authorship norms today, and who are we excluding because we just tacitly agree that its right to exclude those people.

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Women's Contributions to Early Genetics Studies Were ...

Women’s History in Science Is Hidden in the Footnotes …

Read: Hidden Figures and the appeal of math in an age of inequality

One name sprang readily to mind: Jennifer Smith. Huerta-Snchez remembered reading a classic, decades-old paper in which Smith was thanked in the acknowledgments for ably programming and executing all the computations. That seemed odd. Today, programming is recognized as crucial work, and if a scientist did all the programming for a study, she would expect to be listed as an author. It was weird to me that Smith was not an author on that paper, Huerta-Snchez says. [Rori and I] wanted to see if there were more women like her.

The duo recruited five undergraduate students, who looked at every issue of a single journalTheoretical Population Biologypublished between 1970 and 1990. They pored through hard copies of almost 900 papers, pulled out every name in the acknowledgments, worked out whether they did any programming, and deduced their genders where possible. Rochelle Reyes, one of the students, says that she was extremely motivated to do this work, having grown up on stories of under-recognized pioneers like Rosalind Franklin, who was pivotal in deciphering the structure of DNA, and Henrietta Lacks, whose cells revolutionized medical research. I was fortunate to grow up in a diverse environment with a passion for science as well as social justice, Reyes says.

She and her colleagues found that in the 1970s, women accounted for 59 percent of acknowledged programmers, but just 7 percent of actual authors. That decade was a pivotal time for the field of population genetics, when the foundations of much modern research were laid. Based on authorship at the time, it seems that this research was conducted by a relatively small number of independent individual scientists, nearly all of whom were men, the team writes. But that wasnt the case.

Its hard to know what sort of contributions people in the past have made behind the scenes, says Jessica Abbott, a geneticist at Lund University. But this study shows that its possible to get the right kind of data if you think creatively.

Margaret Wu, for example, was thanked in a 1975 paper for help with the numerical work, and in particular for computing table I. She helped to create a statistical tool that scientists like Huerta-Snchez still regularly use to estimate how much genetic diversity there should be in a population of a given size. That tool is called the Watterson estimator, after the 1975 papers one and only authorG. A. Watterson. The paper has since been cited 3,400 times.

Skeptics might argue that the programmers listed in these old papers were just doing menial work that wasnt actually worthy of authorship. Rohlfs says thats unlikely, especially in the cases of Wu, Jennifer Smith, and Barbara McCann, who were repeatedly name-checked in many papers. They were doing work that was good enough that they were being called back again and again, she says. The team even talked with William Hill, Smiths former supervisor at the University of Edinburgh, who described her work as both technical and creative. (He didnt, unfortunately, know where Smith ended up, and the team never managed to track her down.)

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Women's History in Science Is Hidden in the Footnotes ...

Grateful Casey Female Cannabis Seeds by Connoisseur Genetics

Here we have reversed the True Cannabliss cut of Head Seeds Casey Jones, now widely available on the Amsterdam coffee shop scene and we used it to pollinate itself. Casey Jones is a true elite strain in seed form and we are extremely grateful to Head Seeds for bringing it to the world. The spectrums of flavour we hope to represent with these S1s are a meaty/earthy funk with sweet fruity diesel undertones. We give all credit to grateful Head Seeds as all we did was remake his already outstanding work into fem seed Expect monster yields.

All our descriptions and images have come direct from the breeders who operate in a legal climate much different to that within the United Kingdom. Take note, you should NEVER try cultivating any cannabis plants within ANY jurisdiction where such cultivation is illegal. Our seeds are sold purely for souvenirs and should be treated as a curio or novelty item and should never be germinated. PLEASE DO NOT BREAK THE LAW!

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Grateful Casey Female Cannabis Seeds by Connoisseur Genetics

heredity | Definition & Facts | Britannica.com

Heredity was for a long time one of the most puzzling and mysterious phenomena of nature. This was so because the sex cells, which form the bridge across which heredity must pass between the generations, are usually invisible to the naked eye. Only after the invention of the microscope early in the 17th century and the subsequent discovery of the sex cells could the essentials of heredity be grasped. Before that time, ancient Greek philosopher and scientist Aristotle (4th century bc) speculated that the relative contributions of the female and the male parents were very unequal; the female was thought to supply what he called the matter and the male the motion. The Institutes of Manu, composed in India between 100 and 300 ad, consider the role of the female like that of the field and of the male like that of the seed; new bodies are formed by the united operation of the seed and the field. In reality both parents transmit the heredity pattern equally, and, on average, children resemble their mothers as much as they do their fathers. Nevertheless, the female and male sex cells may be very different in size and structure; the mass of an egg cell is sometimes millions of times greater than that of a spermatozoon.

The ancient Babylonians knew that pollen from a male date palm tree must be applied to the pistils of a female tree to produce fruit. German botanist Rudolph Jacob Camerarius showed in 1694 that the same is true in corn (maize). Swedish botanist and explorer Carolus Linnaeus in 1760 and German botanist Josef Gottlieb Klreuter, in a series of works published from 1761 to 1798, described crosses of varieties and species of plants. They found that these hybrids were, on the whole, intermediate between the parents, although in some characteristics they might be closer to one parent and in others closer to the other parent. Klreuter compared the offspring of reciprocal crossesi.e., of crosses of variety A functioning as a female to variety B as a male and the reverse, variety B as a female to A as a male. The hybrid progenies of these reciprocal crosses were usually alike, indicating that, contrary to the belief of Aristotle, the hereditary endowment of the progeny was derived equally from the female and the male parents. Many more experiments on plant hybrids were made in the 1800s. These investigations also revealed that hybrids were usually intermediate between the parents. They incidentally recorded most of the facts that later led Gregor Mendel (see below) to formulate his celebrated rules and to found the theory of the gene. Apparently, none of Mendels predecessors saw the significance of the data that were being accumulated. The general intermediacy of hybrids seemed to agree best with the belief that heredity was transmitted from parents to offspring by blood, and this belief was accepted by most 19th-century biologists, including English naturalist Charles Darwin.

The blood theory of heredity, if this notion can be dignified with such a name, is really a part of the folklore antedating scientific biology. It is implicit in such popular phrases as half blood, new blood, and blue blood. It does not mean that heredity is actually transmitted through the red liquid in blood vessels; the essential point is the belief that a parent transmits to each child all its characteristics and that the hereditary endowment of a child is an alloy, a blend of the endowments of its parents, grandparents, and more-remote ancestors. This idea appeals to those who pride themselves on having a noble or remarkable blood line. It strikes a snag, however, when one observes that a child has some characteristics that are not present in either parent but are present in some other relatives or were present in more-remote ancestors. Even more often, one sees that brothers and sisters, though showing a family resemblance in some traits, are clearly different in others. How could the same parents transmit different bloods to each of their children?

Mendel disproved the blood theory. He showed (1) that heredity is transmitted through factors (now called genes) that do not blend but segregate, (2) that parents transmit only one-half of the genes they have to each child, and they transmit different sets of genes to different children, and (3) that, although brothers and sisters receive their heredities from the same parents, they do not receive the same heredities (an exception is identical twins). Mendel thus showed that, even if the eminence of some ancestor were entirely the reflection of his genes, it is quite likely that some of his descendants, especially the more remote ones, would not inherit these good genes at all. In sexually reproducing organisms, humans included, every individual has a unique hereditary endowment.

Lamarckisma school of thought named for the 19th-century pioneer French biologist and evolutionist Jean-Baptiste de Monet, chevalier de Lamarckassumed that characters acquired during an individuals life are inherited by his progeny, or, to put it in modern terms, that the modifications wrought by the environment in the phenotype are reflected in similar changes in the genotype. If this were so, the results of physical exercise would make exercise much easier or even dispensable in a persons offspring. Not only Lamarck but also other 19th-century biologists, including Darwin, accepted the inheritance of acquired traits. It was questioned by German biologist August Weismann, whose famous experiments in the late 1890s on the amputation of tails in generations of mice showed that such modification resulted neither in disappearance nor even in shortening of the tails of the descendants. Weismann concluded that the hereditary endowment of the organism, which he called the germ plasm, is wholly separate and is protected against the influences emanating from the rest of the body, called the somatoplasm, or soma. The germ plasmsomatoplasm are related to the genotypephenotype concepts, but they are not identical and should not be confused with them.

The noninheritance of acquired traits does not mean that the genes cannot be changed by environmental influences; X-rays and other mutagens certainly do change them, and the genotype of a population can be altered by selection. It simply means that what is acquired by parents in their physique and intellect is not inherited by their children. Related to these misconceptions are the beliefs in prepotencyi.e., that some individuals impress their heredities on their progenies more effectively than othersand in prenatal influences or maternal impressionsi.e., that the events experienced by a pregnant female are reflected in the constitution of the child to be born. How ancient these beliefs are is suggested in the Book of Genesis, in which Laban produced spotted or striped progeny in sheep by showing the pregnant ewes striped hazel rods. Another such belief is telegony, which goes back to Aristotle; it alleged that the heredity of an individual is influenced not only by his father but also by males with whom the female may have mated and who have caused previous pregnancies. Even Darwin, as late as 1868, seriously discussed an alleged case of telegony: that of a mare mated to a zebra and subsequently to an Arabian stallion, by whom the mare produced a foal with faint stripes on his legs. The simple explanation for this result is that such stripes occur naturally in some breeds of horses.

All these beliefs, from inheritance of acquired traits to telegony, must now be classed as superstitions. They do not stand up under experimental investigation and are incompatible with what is known about the mechanisms of heredity and about the remarkable and predictable properties of genetic materials. Nevertheless, some people still cling to these beliefs. Some animal breeders take telegony seriously and do not regard as purebred the individuals whose parents are admittedly pure but whose mothers had mated with males of other breeds. Soviet biologist and agronomist Trofim Denisovich Lysenko was able for close to a quarter of a century, roughly between 1938 and 1963, to make his special brand of Lamarckism the official creed in the Soviet Union and to suppress most of the teaching and research in orthodox genetics. He and his partisans published hundreds of articles and books allegedly proving their contentions, which effectively deny the achievements of biology for at least the preceding century. The Lysenkoists were officially discredited in 1964.

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heredity | Definition & Facts | Britannica.com

Androgenetic alopecia – Genetics Home Reference – NIH

A variety of genetic and environmental factors likely play a role in causing androgenetic alopecia. Although researchers are studying risk factors that may contribute to this condition, most of these factors remain unknown. Researchers have determined that this form of hair loss is related to hormones called androgens, particularly an androgen called dihydrotestosterone. Androgens are important for normal male sexual development before birth and during puberty. Androgens also have other important functions in both males and females, such as regulating hair growth and sex drive.

Hair growth begins under the skin in structures called follicles. Each strand of hair normally grows for 2 to 6 years, goes into a resting phase for several months, and then falls out. The cycle starts over when the follicle begins growing a new hair. Increased levels of androgens in hair follicles can lead to a shorter cycle of hair growth and the growth of shorter and thinner strands of hair. Additionally, there is a delay in the growth of new hair to replace strands that are shed.

Although researchers suspect that several genes play a role in androgenetic alopecia, variations in only one gene, AR, have been confirmed in scientific studies. The AR gene provides instructions for making a protein called an androgen receptor. Androgen receptors allow the body to respond appropriately to dihydrotestosterone and other androgens. Studies suggest that variations in the AR gene lead to increased activity of androgen receptors in hair follicles. It remains unclear, however, how these genetic changes increase the risk of hair loss in men and women with androgenetic alopecia.

Researchers continue to investigate the connection between androgenetic alopecia and other medical conditions, such as coronary heart disease and prostate cancer in men and polycystic ovary syndrome in women. They believe that some of these disorders may be associated with elevated androgen levels, which may help explain why they tend to occur with androgen-related hair loss. Other hormonal, environmental, and genetic factors that have not been identified also may be involved.

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Androgenetic alopecia - Genetics Home Reference - NIH

Female genetics – Women and Alzheimer’s

Several genes are known to be associated with higher risk of Alzheimers disease (conversely, in some cases these genes have been found to protect against the disease). One of these genes is known as APOE.

APOE has three common forms:

APOE2, the least common gene, is believed to play a role in reducing the risk of Alzheimers diseaseAPOE4, more common than APOE2, is believed to increase the risk of Alzheimers diseaseAPOE3, the most common gene, has not been found to increase or decrease the risk of developing Alzheimers disease

Inheriting one of the APOE4 gene variants found in about 20% of the populationmay increase the chance of developing Alzheimers disease by a factor of four. Inheriting two of APOE4 variants (one from each parent) will increase the chance by a factor of 10. Additionally, a 2014 study found that women with the APOE4 gene were twice as likely to get Alzheimers disease than women who do not carry the gene; for men with the APOE4 gene the risk factor does not increase.

Known genetic factors such as this account for a small percentage of all Alzheimers disease cases, but current research supported by Cure Alzheimers Fund and others indicates that genetics have a far greater influence than was previously thought. Additional candidate genes are being discovered and studied to determine their possible role in the disease. The genes we do know about account for a large percentage of early-onset cases: The rare Presenilin 1 and Presenilin 2 genes, for example, virtually guarantee development of Early Onset Alzheimers disease.

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Female genetics - Women and Alzheimer's

Causes of Hair Loss in Women | Bernstein Medical

Common baldness in women, also called female pattern alopecia, is genetically inherited and can come from either the mothers or fathers side of the family. Female alopecia most commonly presents in a diffuse pattern, where hair loss occurs over the entire scalp. Less commonly, women exhibit a patterned distribution where most of the thinning occurs on the front and top of the scalp with relative sparing of the back and sides.

The type of hair loss, diffuse or patterned, has important implications for treatment. Women with diffuse hair loss are generally best treated medically, whereas women with patterned hair loss may be good candidates for hair transplant surgery. Interestingly, patterned hair loss is the most common type seen in men and accounts for why a greater proportion of men are candidates for surgery compared to women.

In women who are genetically predisposed to hair loss, both diffuse and patterned distributions are caused by the actions of two enzymes: aromatase (which is found predominantly in women) and 5-a reductase (which is found in both women and men). Diffuse hair loss is most often hereditary, but it can also be caused by underlying medical conditions, medications, and other factors; therefore, a thorough medical evaluation is an important part of the management.

In the next sections, we will take a closer look at both the mechanisms of genetically induced female hair loss as well as the medical conditions and drugs that can cause diffuse hair loss in women.

As with hair loss in men, female genetic hair loss largely stems from a complex stew of genes, hormones, and age. However, in women, there are even more players. In addition to 5-a reductase, testosterone, and dihydrotestosterone (DHT); which are also found in mens hair loss; also present in women are the enzyme aromatase and the female hormones estrone and estradiol. So lets break down the process that leads to common hair loss in women.

In both men and women, 5-a reductase reacts with testosterone to produce DHT, the hormone responsible for the miniaturization (shrinking) and the gradual disappearance of affected hair follicles. This explains why both men and women lose their hair. But one of the reasons why women seldom have the conspicuous bald areas that men do is because women naturally have only half the amount of 5-a reductase compared to men.

Adding to this complexity, in women, the enzyme aromatase is responsible for the formation of the female hormones, estrone, and estradiol, counteract the action of DHT. Women have higher levels of aromatase than men, especially at the frontal hairline. It is this presence of aromatase which may help explain why hair loss in women looks so different than in men, particularly with respect to the preservation of the frontal hairline. It may also explain why women have a poor response to the drug finasteride (Propecia), a medication widely used to treat hair loss in men that works by blocking the formation of DHT.

The following is a schematic chart of how the female hormones estrone and estradiol are produced and their relationship to DHT:

Womens hair seems to be particularly sensitive to underlying medical conditions. Since systemic medical conditions often cause a diffuse type of hair loss pattern that can be confused with genetic balding, it is important that women with undiagnosed alopecia be properly evaluated by a doctor specializing in hair loss (i.e., a dermatologist).

Below is a list of medical conditions that can lead to a diffuse pattern of hair loss:

A relatively large number of drugs can cause telogen effluvium, a condition where hair is shifted into a resting stage and then several months later shed. Fortunately, this shedding is reversible if the medication is stopped, but the reaction can be confused with genetic female hair loss if not properly diagnosed. Chemotherapy and radiotherapy can cause a diffuse type of hair loss called anagen effluvium that can be very extensive. This hair loss is also reversible when the therapy is over, but the hair does not always return to its pre-treatment thickness.

Causes of Telogen Effluvium

Causes of Anagen Effluvium

A host of dermatologic conditions can cause localized hair loss in women. The pattern that they produce is usually quite different from the diffuse pattern of female genetic hair loss and is easily differentiated from it by an experienced dermatologist. Occasionally, the diagnosis is difficult to make and tests, such as a scalp biopsy are necessary.

Localized hair loss in women may be sub-divided into scarring and non-scarring types.

Non-Scarring Alopecias

Alopecia Areata is a genetic, auto-immune disease that typifies the non-scarring type. It manifests with the sudden onset of discrete, round patches of hair loss associated with normal underlying skin. It usually responds quite well to local injections of corticosteroids.

Localized hair loss can be also be caused by constant pulling on scalp hair, either through braiding, tight clips or hair systems. Traction alopecia, the medical term for this condition, often causes reversible thinning but, if the tugging on the follicles persists for an extended period of time, the hair loss can be permanent. The most common presentation is thinning, or complete hair loss, at the frontal hairline and in the temples of women who wear their hair pulled tightly back. Early traction alopecia can reverse itself by simply wearing the hair loose. A hair transplant may be needed to restore the hair that is permanently lost from sustained traction.

Scarring Alopecias

Scarring hair loss can be caused by a variety of medical or dermatologic conditions such as Discoid Lupus, Lichen Planus, and infections. It can also be caused by thermal burns or local radiation therapy. Face-lift surgery may result in permanent localized hair loss that can be particularly bothersome if it occurs at the frontal hairline or around the temples. Fortunately, localized hair loss from injury or from medical problems are often amenable to hair transplantation.

Many of the factors that cause the rate of loss to speed up or slow down are unknown, but we do know that with age, a persons total hair volume will decrease. This is referred to as senile alopecia. Even when there is no predisposition to genetic balding, hair across the entire scalp will thin over time resulting in the appearance of less density. The age at which these effects finally manifest themselves varies from one individual to another and is mainly related to a persons genetic makeup.

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Causes of Hair Loss in Women | Bernstein Medical

Lasker Awards Given for Work in Genetics, Anesthesia and …

The coveted prize was awarded to a Scottish veterinarian, two scientists who championed an overlooked protein and a pioneering researcher who helped advance the careers of other women.

The Lasker Awards, which are among the nations most prestigious prizes in medicine, were awarded on Tuesday to a Scottish veterinarian who developed the drug propofol, two scientists who discovered the hidden influence of genetic packing material called histones and a researcher who in addition to doing groundbreaking work in RNA biology, paved the way for a new generation of female scientists.

The awards are given by the Albert and Mary Lasker Foundation and carry a prize of $250,000 for each of three categories. They are sometimes called the American Nobels because 87 of the Lasker recipients have gone on to win the Nobel Prize.

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He developed the drug propofol, now a widely used anesthetic that has transformed surgery.

Dr. Glen, the recipient of the Lasker-DeBakey Clinical Medical Research Award, is only the second veterinarian to win a Lasker in 73 years, according to the foundation.

A pharmaceutical career was an unlikely path for Dr. Glen, but the fact that he was interested in anesthesia was no surprise: for years, he had taught the subject to students at Glasgow Universitys veterinary school. I was anesthetizing dogs, cats, horses whatever animals came around, Dr. Glen said in an interview. Once he used anesthesia on a pelican to fix its beak.

When he arrived in the 1970s at ICI Pharmaceuticals, later acquired by AstraZeneca, Dr. Glen had turned his attention to humans and was on the hunt for a replacement for thiopentone, a widely used anesthetic that quickly put patients to sleep but often made them groggy afterward.

In lab tests on mice, he and his colleagues discovered that one of the companys existing compounds, propofol, seemed to work as well as thiopentone but wore off quickly, without the hangover effect of the earlier drug. Propofol was approved in 1986 in the United Kingdom and in the United States three years later.

The drug, known as the milk of amnesia because of its milky consistency, has since been used by hundreds of millions of patients and is credited with leading to the rapid expansion of outpatient surgery because patients recover so quickly.

In 2009, propofols reputation took a hit after Michael Jacksons personal physician, Dr. Conrad Murray, administered a lethal dose of the drug to the singer. Dr. Murray was convicted in 2011 on charges of involuntary manslaughter, and Dr. Glen said he followed the trial closely.

It was never intended to be used in that way, Dr. Glen said. But of the drugs broader success, he said, Im delighted that it has become so widely used.

She became a champion of women in her field and trained nearly 200 future scientists.

Dr. Steitz, the recipient of the Lasker-Koshland Award for Special Achievement in Medical Science, said winning the award is particularly significant because it signals how far she has come since her days as an undergraduate lab technician in the early 1960s.

When I started out being excited by science but seeing that there werent any women scientists I thought I had no prospects whatsoever, she said in an interview. The one thing that I really wanted was to have the respect of my peers for the scientific contributions I made, and for my participation in the scientific community.

More than four decades later, Dr. Steitz has her own lab at Yale University and her work has led to several breakthroughs in the understanding of RNA, a type of molecule that carries out many tasks in the cell, such as helping to read the information in our genes.

One of her biggest discoveries was particles made up of RNA molecules and proteins, known as small nuclear ribonucleoproteins, or snRNPs for short. Theyre scattered throughout cells and among other things, they help cut messenger RNA into pieces, some of which get pasted back together. This process, called splicing, is essential to the process of making proteins from genes. This discovery led to an entire new field of research in cell biology.

She was an author of a 2007 National Academy of Sciences report that recommended specific steps for maximizing the potential of women in academic science and engineering. Since then, she gives talks about how to encourage more women in science and is also being recognized for her work as a mentor. She has trained almost 200 students and postdoctoral fellows, according to the Lasker foundation.

Of the 360 papers that have come from her laboratory, 60 do not include her name, a gesture of generosity that reflects her belief that students and postdoctoral fellows who work completely independently should be allowed to publish on their own, according to the Lasker foundations citation.

In an interview, Dr. Steitz downplayed this detail. She said in her early days running her own lab, she frequently left her name off papers because she was following in the scientific tradition she had learned as a young researcher.

As for her role as an activist, I sort of feel a little embarrassed by that, because there are so many women that have done so much more, she said. What she has done, she said is to be a good citizen and try to help women and other underrepresented people to fulfill their potential.

They took a new look at a protein once considered the packing material of DNA.

From opposite ends of the country, Dr. Allis, whose lab is at The Rockefeller University in New York, and Dr. Grunstein, at the University of California, Los Angeles, pioneered work that elevated the importance of histones, proteins in the chromosomes that previously had gone overlooked. They are the recipients of the Albert Lasker Basic Medical Research Award.

DNA molecules are so long that, if they were stretched from end to end, one strand would reach six feet. Histones are the proteins that coil and cram these strands into a microscopic cell and they were long seen as little more than DNA spools, part of the basic machinery of the cell.

I went into the field thinking, everyones working on gene activity, I want to work on packing material, Dr. Grunstein said in a video produced by the Lasker foundation. I didnt want to go the direction everyone else was going in.

What Dr. Grunstein and Dr. Allis discovered is that, in fact, histones play a crucial role in turning genes on and off, which allows each cell to do its assigned task. The two worked separately, Dr. Grunstein focusing on genetics, and Dr. Allis on biochemical processes.

While their award is for basic science, the practical implications for their discoveries are profound. Mistakes in setting this up seem to be very clearly causing cancer, Dr. Allis said in the video.

Drug developers used the evolving understanding of histones to come up with new treatments, including to treat cancer, such as Zolinza, sold by Merck. More are in the pipeline.

Its spawned really a whole new area of potential therapies in humans, and thats pretty rewarding, Dr. Allis said.

More coverage of the Lasker Awards

Katie Thomas covers the business of health care, with a focus on the drug industry. She started at The Times in 2008 as a sports reporter. @katie_thomas

Go here to read the rest:
Lasker Awards Given for Work in Genetics, Anesthesia and ...

The 50 Most Important Women in Science – Discover Magazine

Melissa Franklin Professor of Physics, Harvard University "I build things, and then I fix them when I build them badly," says the experimental physicist, offering a deceptively modest description of her work. The objects she tinkers with are complex particle detectors, including the powerful proton-antiproton Collider Detector at Fermilab in Batavia, Illinois, which she used to spot the top quark in 1995.

Maria Zuber Professor of Geophysics and Planetary Science, MIT Using laser ranging, gravity measurements, and data from spacecraft, Zuber maps surface features and probes the interior of Mars, Venus, Jupiter's moons, and our own moon. Her goal is to "figure out the processes that acted on a particular body in the past in order to make its surface the way it is now."

Fame Passed Them By

History has not always been kind to women scientists. Many have passed long days and nights in the lab stirring noxious concoctions or gathering piles of data only to see the credit for their discoveries awarded to a male colleague. Sometimes the work was obscured by a famous mentor. Here is a selection of female scientists who deserve greater notice:

Lise Meitner (1878-1968) In 1938, after she escaped from the Nazis to Sweden, she carried out the key calculations that led to the discovery of nuclear fission. Her collaborator, Otto Hahn, who stayed behind in Germany, was the sole recipient of the Nobel Prize in chemistry in 1944. In 1997 Meitner was finally honored when element 109 was named meitnerium.

Emmy Noether (1882-1935) She devised a mathematical principle, called Noether's theorem, which became a foundation stone of quantum physics. Her calculations helped Einstein formulate his general theory of relativity. "It is really through her that I have become competent in the subject," he admitted.

Frieda Robscheit-Robbins (1893-1973) Together with George Whipple, she discovered that a diet rich in liver cured anemia in dogs, which in turn led directly to treatment for pernicious anemia in humans. Although she coauthored numerous papers with Whipple, it was he who was honored with the 1934 Nobel Prize in medicine.

Hilde Mangold (1898-1924) Under the guidance of Hans Spemann, she carried out the experiments that led to the discovery of the organizer effect, which directs the development of embryonic cells into tissues and organs. She died after being set afire by an alcohol stove on which she was heating food for her baby. Eleven years later, Spemann won the Nobel Prize.

Cecilia Payne-Gaposchkin (1900-1979) In her 1925 Ph.D. thesisdescribed by the noted astronomer Otto Struve in 1960 as "the most brilliant . . . ever written in astronomy"she proposed that all stars are made mostly of hydrogen and helium. Astronomers dismissed her observations until four years later, when they were confirmed by a man. She was the first woman to become a professor of science at Harvard.

Beatrice "Tilly" Shilling (1909-1990) A prize-winning motorcycle racer and aeronautical engineer, she designed a small metal ring that fit onto the fuel line of an aircraft engine to keep the flow of fuel constant. This enabled World War II British fighter pilots to dive without fear that their engines would cut out.

Chien-Shiung Wu (1912-1997) In 1957 she and her colleagues overthrew a principle previously considered immutable in physics: that nature does not distinguish between right and left. Chien-Shiung found that this rule does not hold true for interactions between subatomic particles involving the so-called weak force. The Nobel Prize was awarded to two male colleagues.

Rosalind Franklin (1920-1958) Her X-ray photographs of crystallized DNA, taken in the early 1950s, proved that the molecule was a helix. This data was used, without her knowledge, by James Watson and Francis Crick to elucidate the structure of DNA. By the time they were awarded the Nobel Prize in 1962, Franklin had died of ovarian cancer.

Jocelyn Bell Burnell (1943-) With the aid of a radio telescope she built herself, she became the first astronomer to detect pulsarsrapidly spinning, extremely dense neutron stars. But she was deemed too inexperienced to receive the Nobel Prize, which was given instead in 1974 to her thesis adviser, Anthony Hewisha man who later referred to her as "a jolly good girl [who] was just doing her job."

Josie Glausiusz

Originally posted here:
The 50 Most Important Women in Science - Discover Magazine

12 Female Hormones Facts – Understanding your Hormones Today

The key stages of female hormones and how hormonal imbalance affects your body.

Index:

You inhabit an amazing body that performs a myriad of functions every second of the day. This incredible feat is controlled by your brain and co-ordinated by your hormones. Millions of women are affected by hormonal changes throughout their lives but have little idea about how or why. Hormonal imbalances can lead to:

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Hormones are essentially chemical messengers secreted by endocrine glands in the body that are designed to adjust metabolic functions in cells. They do this by regulating the production of a specific protein or by activating enzymes.

There are two basic types of hormones, steroid and peptide. They travel to their target organs in the bloodstream and work in complicated harmony to maintain balance at all times. Steroid hormones are fat soluble compounds that can easily pass through cell membranes.

Some of these include:

Peptide hormones are water soluble compounds that are able to dissolve in the blood in order to be transported around the body. Some of these include:

Hormones are secreted by the endocrine system which is largely controlled by the pituitary gland - in the brain - under the direction of the hypothalamus.

Hormone balance (Homeostasis) is maintained by a key regulatory mechanism called negative feedback which either opposes the release of certain hormones or causes hormones to act antagonistically by opposing each others actions.

For example if blood sugar (glucose) levels are too high the brain sends a signal to release insulin which lowers blood glucose. If blood glucose levels drop too low the brain triggers the release of glucagon which raises blood sugar.

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Hormones co-ordinate many diverse areas including:

When the correct balance of hormones is maintained most daily challenges are met and the body thrives, but if levels are too high or low it can lead to health problems such as thyroid disease, polycystic ovaries, endometriosis, infertility, fibroids, depression and acne.

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Female hormones exist primarily to promote growth and reproduction and have a significant effect on a womans development throughout her life. The two main female hormones, oestrogen and progesterone are produced predominantly in the ovaries but also in the adrenal glands which sit just above the kidneys.

At puberty oestrogen is responsible for the development and maturation of the uterus, fallopian tubes, breasts and vagina. It also plays a key role in the growth spurt and deposition of fat around the buttocks, hips and thighs.

There are at least six different oestrogens, however only three are synthesised in significant amounts:

Beta-estradiol, Estrone & Estriol.

Progesterone is involved in regulating the menstrual cycle and is vital for supporting a healthy pregnancy. It is also particularly important for balancing and controlling oestrogen performance, opposing some of the powerful effects of excess oestrogen. For instance oestrogen triggers release of the stress hormone cortisol while progesterone counters it.

Oestrogen stimulates cell growth, while progesterone ensures growth is maintained at healthy levels. Low progesterone levels lead to uncontrolled oestrogen which results in hormonal imbalances. Low levels of progesterone may affect:

Women also produce a little testosterone (normally considered a male hormone) from their ovaries, which helps to promote muscle mass and bone growth. These levels naturally decline post menopause.

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Puberty:

During this stage the ovaries are stimulated by luteinising hormone (LH) and follicle-stimulating hormone (FSH) which are secreted by the pituitary gland under the influence of the hypothalamus.

These hormones bring about the physical changes associated with puberty. Menstruation usually occurs around the time that a womans growth spurt slows down. The whole process takes around 4 years.

Pregnancy:

This is a time when a womans hormones change dramatically:

Menopause:

The lead up to the menopause (the peri-menopause) starts around the age of 40 and ends on average at age 52. Whilst there are considerable hormonal changes that occur during puberty and the childbearing years - the menopause and post menopause seem to be the most problematic. This life stage can be extremely challenging for some women.

Oestrogen plays a vital role in protecting the heart, bones, bladder and vagina as well as maintaining the breasts. Lack of oestrogen and progesterone during the menopause can create hormonal imbalances which have significant consequences for health with an increased risk of osteoporosis and heart disease and can also result in a range of distressing symptoms.

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The ratio between oestrogen and progesterone is critical for the maintenance of homeostasis. Often the effects of high oestrogen are due to a combination of mildly high oestrogen levels together with a mild progesterone deficiency.

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An increase in the ratio of oestrogen to progesterone can lead to:

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Hormone function can be disrupted if too much of a hormone is produced or too little. This may be due to a number of factors including:

Malnutrition

Undereating, a poor diet, insufficient calories and nutrients, reliance on stimulants and junk food can lead to a nutrient deficiency which will ultimately affect hormone production. For example, Studies have found that B6 supplementation has positive effects on some PMS symptoms. It is likely that B6 helps to balance oestrogen and progesterone levels mid cycle. B6 is also a co-factor in the synthesis of serotonin.

Being underweight with insufficient fat reduces cholesterol which is needed to produce sex and stress hormones. During the menopause oestrogen is produced in the abdominal fat cells as ovarian function diminishes.

Poor liver function

Oestrogen has to be metabolised by the liver and excreted in bile. If the liver is not functioning efficiently oestrogen levels in the blood may remain relatively high.

Overloading the liver with alcohol, drugs, caffeine and chemicals in food may lead to poor liver function.

Certain Foods

Too much sugar, alcohol, chocolate, fried foods, trans fats and refined carbohydrates can affect liver function which could contribute to higher oestrogen levels.

Constipation

Before used oestrogen can be eliminated via the stool it has to be modified by intestinal bacteria and bound to fibre. This bulks out the stool and encourages normal bowel movements.

Good levels of healthy gut bacteria and plenty of dietary fibre are essential for this process otherwise the used oestrogen may be recirculated.

Chemicals in food

Certain chemicals such as pesticide residues found in non-organic dairy and meat products can mimic oestrogens in the body.

Oestrogens are also included in cattle feed to fatten them up.

Environmental factors and xenoestrogens

There are many petrochemical products that affect the balance of hormones in the body. These include:

Alkylphenol ethoxylates in detergents and emulsifiers; nonylphenol ethoxylates used as spermicides and plasticisers; bisphenols used in certain industrial and chemical processes and dental fillings, the birth control pill and HRT

Genetics

There may be a family history of early menopause or low thyroid function.

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12 Female Hormones Facts - Understanding your Hormones Today

Genetic Reasons: Female Hair Loss | Women’s ROGAINE

WHAT IS THE LIFE CYCLE OF HAIR

The average person is born with 100,000 hair follicles on their head, which are in a constant state of change. When a follicle is first activated, it grows thick hairs for several years. When the growth cycle is complete, the follicle undergoes a transitional phase before entering into a resting period where the hair is eventually shed, and the cycle begins again.

Hereditary hair loss starts with a progressive shortening of the hairs growth cycle and involves gradually shrinking hair follicles that eventually are no longer able to produce normal hair.

DIFFERENT TYPES OF HAIR LOSS

Hair thinning is surprisingly common. More than 1 out of every 4 women will experience it at one time or another. While certain lifestyle factors can absolutely have an impact on your hairs thickness, over 90% of all hair loss is due to genetic factors. So before you start blaming your diet or blow dryer, get to know the facts behind the science of genetic hair thinning.

NOT ALL HAIR LOSS IS CREATED EQUAL

In general, hair loss falls into one of 2 categories: hereditary and non-hereditary. Hereditary hair loss is known as androgenetic alopecia (AGA) and is a genetic condition that shortens the time that the hair spends actively growing. AGA eventually causes the hair follicles to slowly shrink. Women with hereditary hair loss experience a general thinning of the hair, with the most extensive hair loss occurring on the top of the head and along the part. The number of women with this type of hair loss increases with age, but it can start as early as your 20s. Womens ROGAINE Foam is only indicated to treat hereditary hair loss.

On the flipside, temporary hair loss, known as telogen effluvium, happens when stress, diet, a hormonal imbalance, or a traumatic event causes the hair follicles to remain in the resting state, causing increased hair shedding and a temporary thinning of hair across the whole scalp. While the amount of time someone stays in telogen effluvium varies, once the imbalance has been corrected, the hair will return to its previous thickness.

A third kind of hair loss is called alopecia areata, an autoimmune disorder that is recognized by well-defined patches of hair loss, which may happen rapidly and can lead to complete hair loss. If you have no history of hair loss in your family and are experiencing this kind of hair loss, consult your doctor.

If youre not certain about what kind of hair thinning youre experiencing, our quizcan help you start to sort things out.

WHOS TO BLAME? MOM OR DAD?

Its a commonly held myth that genetic hair loss is only inherited from one side of the family or the other. In reality, you can inherit the thinning hair gene from either your mother or father (or both). That being said, if a number of close relatives have thinning hair, your chances of experiencing it increase, but are by no means inevitable.

NOT JUST FOR MEN

Incorrectly thought of as only a male ailment, both men and women experience hair loss, but in varying patterns and severity. Men will tend to recede at the hair line and/or experience hair loss around the crown of the head, whereas a womans hair loss usually involves a more dispersed thinning on the top of the head, which may be especially noticeable as a widening part.

More here:
Genetic Reasons: Female Hair Loss | Women's ROGAINE

Common ancestors of all humans (using genetics)

In fact, by focusing only on common ancestry of DNA that gets inherited,all CA's found in genetic studies will be much older than the MRCA.

Our most recent female-female line ancestor is called "Mitochondrial Eve"since Mitochondrial DNA passes (almost) entirely through the female lineand so may be used to estimate a date for her.Contrary to a lot of confused discussion,e.g. [Ayala, 1995],Mitochondrial Eve's existence is not in doubt.We can work it out from our armchair.What is in dispute is the date,which has been estimated at 100,000 to 200,000 years ago.

Also contrary to much confused discussion by paleontologists,no date for Mitochondrial Eve implies any sort ofpopulation bottleneck at that time. Mitochondrial Eve would have co-existedwith huge numbers of male andfemale relations from whom we also descend.Indeed, [Ayala, 1995] points out thatour inheritance from Mitochondrial Evewould be only 1 part in 400,000 of our DNA.The rest we inherit from her contemporaries.But he still spends half the paper attacking the ideaof a small ancestral population - an idea that no one believes.

As a result of thinking about Y chromosome Adam, we can see that if we use surnames strictly in the male line forever into the future,then not only will all hereditary titles die out,but all surnames except one will die out too.

The world does not of course strictly follow that surname rule,but the West approximately does,and surnames do go extinct.Without a mechanism for generating entirely new surnames from scratch(not belonging to either parent)the diversity of surnames can only decline.Neil Frasernicely describes it as"a random walk - next to a cliff. The only force acting on the system is that once a name randomly stumbles to zero it is gone and can never recover."

Say for one gene, your father's two copies are AB,your mother's are CD.You could end up with AC, your sibling could end up with BD.For this gene only,there is no genetic evidence of your recent common ancestry.

If there are n events at which to choose betweenyour father's grandfather copy and grandmother copy,the probability of you inheriting from himnone of your grandfather's DNA (*)is:

(*) If you are your father's daughter.If his son, you must inherit the Y chromosome.We will ignore the special cases of themale-male and female-female lines.Admittedly these are hard to ignore with grandparents,since they are 2 of only 4 lines,but these 2 special lines can be ignored as we go back 10 generations or more.

[Chang, 1999, author's reply]discusses this extreme case.I'm not sure if n=23 here(the no. of chromosomes).Then the probability of all grandmother,none from grandfather, would be(1/2)23= 1 in 223= 1 in 8.4 million.

If we allow for crossover, the probability of all grandmother,none from grandfather, is:

If n=23,(1/4)23= 1 in 246= 1 in 70 trillion.

Q. Is n=23?

If n=23probability (3/4)23 = 1 in 747.

How does crossover affect this?If one great-grandparent is c,your father has 3/4 chance of getting either c,or c crossed with d.He then has 3/4 chance of passing this on,either as is or crossed over.So you have (3/4)2 = 0.56 chance of inheriting some c,or 1 - (3/4)2 = 0.44 chance of inheriting none.So we get chance of inheriting no DNAfrom a great-grandparent is:

If n=23probability (0.44)23= 1 in 181 million.

Q. Is n=23?

If n=23, the probability depends on t.This is equal to 1/2 for:1-(1/2)t-1 = 0.971/2t-1 = 0.032t-1 = 33.7t-1 = 5In other words, more than 6 generations back,the prob. of inheriting no DNA at all from one of yourancestors is more than 1/2.

But what about crossover?With crossover, the probability of inheriting none of the DNAof an ancestor at generation t is:

If n=23, the probability depends on t.This is equal to 1/2 for:(3/4)t-1 = 0.03t-1 = 12In other words, more than 13 generations back,the prob. of inheriting no DNA at all from one of yourancestors is more than 1/2.Note that at 13 generations back (c. 1500s - 1600s) you have8192 ancestors.

Q. Is n=23?

For small n, it is easier (more probable) to not inherit from an ancestor.With a single event (n=1), it could easily lose that event.With a large number of events, it is unlikely it losesthem all.For large n, it is harder to not inheritfrom an ancestor.As n goes to infinity, you must have inherited some DNAfrom the ancestor.

We can see that above, for any finite t,as n goes to infinity,the probability of not inheriting goes to zero.

For an MRCA 30 generations ago,you need 230 people = 1 billion peopleto be sure that their samples of1 part in 230 of the ancestor's DNAmust overlap.

As I say, I need to do more reading on this.I'm sure this has been discussed before.There is some discussion of this in[Wiuf and Hein, 1999].

So the "real" CAs (the CA1s) outnumber the CAs of a gene (the CA4s),but do they vastly outnumber them?As genome size tends to infinity(i.e. n goes to infinity)it becomes impossible for an actual ancestor (CA1) not to be at leasta partial genetic ancestor (CA2) as well.So the difference between CA1 and CA2 breaks down.

I used to say on this page:

but now we can see this is not so.(At least I put in "(I think)" in the correct place!)The difference between CA2 and CA3 does not break down.For any finite n, you are getting a larger inheritance from the ancestoralright,but it is still only 1 part in 2t,so for any 2 descendants it is quite possible that their samplesdo not overlap (for any reasonable size t).The probability of overlap depends on t, not on n.

For instance, [O'Connell, 1995] is confused about Mitochondrial Eve's relation to the fossil record- no date for Mitochondrial Eve, no matter how recent,could possibly contradict the fossil record studied by the paleontologists.This is based on the error of assuming that Mitochondrial Eve is important(see above).

One could even say that genealogy is the pursuit of statistical artefacts.

Link:
Common ancestors of all humans (using genetics)

The Genetics of Depression Are Different for Men and Women

A wiring diagram of a human brain.Illustration: NIH

There may not be a single depression gene, but theres no question that our genetic makeup is an important factor in whether or not we get depressed. And our sex, it turns out, can be a factor in how those genes are expressed. In men and women diagnosed with major depressive disorder, the same genes show the opposite changes. In other words, the molecular underpinnings of depression in men and women may be different.

Thats according to a new postmortem brain study published on Wednesday in the journal Biological Psychiatry. The study could in the future help lead to more effective treatments for depression, if it turns out that men and women need different types of treatment.

To arrive at that conclusion, researchers at the University of Pittsburgh and Torontos Centre for Addiction and Mental Health analyzed gene expression levels in the postmortem brain tissue of 50 people who had major depressive disorder, of which 26 were men and 24 were women. (The data on their subjects was collected from several existing published data sets.) They also looked at the postmortem brain tissue of 50 men and women not diagnosed with depression. Gene expression levels are an indication of how much of a particular protein an individual gene is producing.

In the women with depression, they found that genes affecting synapse function were more expressed, meaning genes that play a role in how electrical activity is transferred between cells were producing more protein. In men, those same genes had decreased expression. In other genes with altered expression, a particular change occurred in only men or only women. Of 706 gene variants in men with depression and 882 variants in women with depression, 52 of the genes showed opposite changes in expression between the men and women. Only 21 genes changed in the same way in both sexes.

In the study, researchers focused on three regions of the brain that regulate mood: the dorsolateral prefrontal cortex, subgenual anterior cingulate cortex, and basolateral amygdala. To bolster their findings, they also looked at a smaller dataset of men and women with major depressive disorder and found similar results. More research, including studies in living patients, will be necessary to further validate the results.

The study is significant for two reasons. For one, it is the first to suggest an opposing pathology for depression in men and women, which could eventually influence how depression is treated. Depression is complex disease that occurs in different regions of the brain, and increased understanding of the neurology and genetics of depression may lead to tailored depression treatments that are far more effective.

But the study also highlights the necessity of diversity in scientific study. Major depressive disorder affects women about twice as often as men. Women are also more likely to experience symptoms like weight gain along with depression, suggesting the biological mechanisms at work may be different. But many depression studies only look at men, and ones that look at both sexes do not necessarily differentiate between the two when reporting findings.

The science of genetics overwhelmingly suggests how similar we all really are. But it also underscores how much there is to gain from understanding and embracing how we are different.

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The Genetics of Depression Are Different for Men and Women

Is Infertility Genetic? | Female Infertility Genetic …

Many women are unable to conceive and deliver a healthy baby due to genetic factors. Sometimes this is due to an inherited chromosome abnormality. Other times it is because of a single-gene defect passed from parent to child.

In addition, if other women in your family have had problems conceiving due to premature menopause, endometriosis or other factors, you may be at increased risk of the same problems.

Chromosomally abnormal embryos have a low rate of implantation in the mothers uterus, often leading to miscarriages. If an abnormal embryo does implant, the pregnancy may still result in miscarriage or the birth of a baby with physical problems, developmental delay, or mental retardation.

There are several kinds of chromosome abnormalities:

Translocation is the most common of these. Although a parent who carries a translocation is frequently normal, his or her embryo may receive too much or too little genetic material, and a miscarriage often results.

Couples with specific chromosome defects may benefit from pre-implantation genetic diagnosis (PGD) in conjunction with in vitro fertilization (IVF).

Down syndrome is usually associated with advanced maternal age and is a common example of aneuploidy. Down syndrome is caused by having an extra number-21 chromosome (three instead of two). It is also referred to as trisomy 21.

More rare is the existence of an inherited genetic disease due to abnormal genes or mutations. Chromosome analysis of the parents blood identifies such an inherited genetic cause in less than 5 percent of couples.

Single-gene abnormalities are mutations caused by changes in the DNA sequence of a gene, which produce proteins that allow cells to work properly. Gene mutations alter the functioning of cells due to a lack of a protein.

Single-gene disorders usually indicate a family history of a specific genetic disease such as cystic fibrosis (CF) an incurable and fatal disease affecting the mucous glands of vital organs and Tay Sachs, also a fatal disorder, in which harmful quantities of a fatty substance build up in tissues and nerve cells in the brain.

Though generally rare, these diseases are usually devastating to a family. Fortunately, much progress has been made in detection through pre-implantation genetic diagnosis (PGD) in conjunction with in vitro fertilization (IVF).

Although a couple may otherwise have no fertility problems, IVF and PGD can work together to spare mother and father from heartache in cases where there is a known single-gene family history.

Learn more about genetic causes of infertility

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Is Infertility Genetic? | Female Infertility Genetic ...

Twin Genetics and Heredity – Understanding Genetics

-A curious adult

June 25, 2014

That is a very interesting question! And one that many people wonder about. In fact, we answered a very similar question many years ago.

Twin genetics depend on what kind of twins we are talking about. Having identical twins is not genetic. On the other hand, fraternal twins can run in families.

Genetics can definitely play a role in having fraternal twins. For example, a woman that has a sibling that is a fraternal twin is 2.5 times more likely to have twins than average!

However, for a given pregnancy, only the mothers genetics matter. Fraternal twins happen when two eggs are simultaneously fertilized instead of just one. A fathers genes cant make a woman release two eggs.

It sounds like fraternal twins do indeed run in your family! But, since your son is the father, his genes are on the wrong side of the family tree. So, your family history likely didnt play a role in his wifes twin pregnancy.

The answer would be different if you were asking about a daughter. Also, although your sons family history of twins cant increase his wifes chance of having twins, he can pass those genes down to your granddaughter. With your strong family history of fraternal twins, this just might increase the chances of your granddaughter having twins!

But, your daughter-in-law is not necessarily having twins because of her genetics. Other things like environment, nutrition, age, and weight have also been linked to having twins as well. And there is always simple chanceevery woman has a chance at having fraternal twins. It is just that some women have a higher or lower chance.

Huh? Help Me Understand the Genetics!

Wait a minute. One type of twins has a genetic basis and the other does not? And, only the moms genetics matter? How is that possible?

Dont worry. It makes a lot of sense once we break down the biology.

The important difference between identical and fraternal twins is the number of fertilized eggs involved. Identical twins come from a single fertilized egg. Fraternal twins come from two different ones.

Identical twins happen when a single embryo splits in two soon after fertilization. This is why identical twins have identical DNA. They came from the same fertilized egg.

Since embryo splitting is a random event that happens by chance, it doesnt run in families. Genes are not involved. The same is not true for fraternal twins.

Fraternal twins happen when two independent eggs are each fertilized by different sperm. This is why the DNA of fraternal twins is different. In fact, fhe DNA of fraternal twins is no more similar than the DNA any other sibling pair.

Usually, a woman only releases a single egg at a time. Fraternal twins can only happen if a mother releases two eggs in one cycle. This is called hyperovulation.

Unlike embryo splitting, ovulation is a normal biological process that is controlled by our genes. And, different women can have different versions of these ovulation genes.

Some women have versions (called alleles) of these genes that make them more likely to hyperovulate. This means there is a higher chance that two eggs could get fertilized at once, leading to fraternal twins.

The gene versions that increase the chance of hyperovulation can be passed down from parent to child. This is why fraternal twins run in families.

However, only women ovulate. So, the mothers genes control this and the fathers dont.

This is why having a background of twins in the family matters only if it is on the mothers side. And why your sons family genetics did not play a role in his twins.

We went over a lot of this stuff in our previous answer, but your question got me thinking. Our last answer on twins was done so long ago. Has recent research discovered anything new on this fascinating topic? They have indeed at least if you are a sheep!

Counting Sheep can Teach us about Twins

Scientists often turn to animals when they want to study a biological process. Some of the newest information we have about twin genetics comes from studying sheep.

Sheep were chosen because, like people, they typically give birth to a single lamb. However, they can sometimes have twins and triplets.

Different breeds of sheep naturally have higher or lower twin rates. These different breeds have different versions (called alleles) of some of their genes. Specific alleles can make certain breeds more likely to have twins.

We can compare the genes between these different breeds to try to find the genes controlling twinning. And, this is just what scientists did.

A thorough search for genes controlling twining in sheep identified several interesting ones. The breeds with higher twin rates had different alleles of these genes!

Three key sheep genes identified were named BMP15, GDF9, and BMPR1B. The specific gene names are not really important. Just know that all of these genes are involved in controlling ovulation. Which makes sense!

Remember, hyperovulation increases the chance of having fraternal twins. The sheep breeds with higher than average twin rates had versions of the genes that increase ovulation.

Sheep are a great tool to help us study twin genetics. The tricky part is connecting these findings to people.

It is harder to study humans. Scientists have tried to find links between the genes identified in sheep and human twin genetics. So far theyve found that some match up and some dont. This, in and of itself, is interesting!

Another gene called follicle-stimulating hormone, or FSH for short, has also been linked to twins in humans. Like the other three genes identified, this FSH is also involved in promoting ovulation, and mothers of fraternal twins often have high levels of it.

It seems that twin genetics is more complicated in humans than in sheep. More genes are likely involved. But, each new bit of information about the genes involved adds another puzzle piece to the complete genetic picture.

Maybe someday we will know all the genes that cause fraternal twins in people. But for now, you can just tell your son that his genetics likely didnt cause his twins. Scientists are still trying to figure out which, if any, genes on his wifes side could possibly be the culprits!

By Dr. Anja Scholze, Stanford University

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Twin Genetics and Heredity - Understanding Genetics

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