Much of the risk of developing incontinence before middle age is determined by our genes. Genetic factors can explain half of people's susceptibility to urinary incontinence, a study of twins at the University of Gothenburg and Karolinska Institutet (Sweden) reveals.
Urinary incontinence is very common, especially among women, with around one in three affected at some point in life. Incontinence, overactive bladder and other lower urinary tract symptoms can be caused by factors such as old age, excess weight, pregnancy and childbirth, as well as stroke and other neurological disorders.
"Incontinence is caused by a combination of factors," says gynaecologist Anna Lena Wennberg, one of the researchers behind the study. "We already knew that there are hereditary factors, but now we've been able to show for the first time how important the genetic component is for various types of urinary tract disorder."
Conducted in collaboration with the Swedish Twin Registry at Karolinska Institutet in Stockholm, the study looked at just over 25,000 Swedish twins aged 20 to 46. Information about urinary incontinence, overactive bladder and other lower urinary tract symptoms were analysed using a statistical method which measures how much of the difference between people is due to genetic variation. By comparing the prevalence of these symptoms in identical twins, who have identical genes, and non-identical twins, who share half of their genetic material, the researchers were able to draw conclusions about the relative significance of genetic and environmental factors.
"With urinary incontinence, we saw that just over half of the variation (51%) can be explained by genetic factors," says Wennberg. "This doesn't mean that half of all people with urinary incontinence inherit it from their parents, but that around 50% of people's susceptibility to urinary incontinence can be explained by their genes."
Genes also turned out to be significant for nocturia - the need to get up in the night to urinate. In this case, around a third (34%) of the variation has a genetic explanation.
Wennberg does not believe that there is a single incontinence gene, rather that a number of different genes play a role. These genes combine with various environmental factors or cause disorders which, in turn, increase the risk of urinary incontinence.
"Urinary incontinence is a multifactorial condition, and while we now know that much of the variation between people is down to their genes, treatment will continue to focus on environmental factors which are easier to influence, such as smoking and excess weight."
Notes:
The study was published recently in the online version of the journal European Urology.
URINARY INCONTINENCE: There are several different forms of urinary incontinence. Stress incontinence is where the sphincter between the bladder and the urethra leaks under pressure from the abdomen when coughing, lifting or exercising. Urge incontinence is where the bladder contracts abnormally, resulting in an urge to urinate even when the bladder is not full. Overflow incontinence is where the bladder does not empty as it should, with the result that urine escapes when the bladder is full. Urinary incontinence can also be caused by various neurological disorders or as a side-effect of some medicines.
Source:
Anna-Lena Wennberg
University of Gothenburg
суббота, 31 марта 2012 г.
суббота, 24 марта 2012 г.
Gene Linked To Preterm Birth Among Hispanic Women
Researchers at Yale School of Medicine have found that the gene ENPP1 is linked to preterm birth and low birth weight among Hispanic women.
Errol Norwitz, M.D., associate professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale, presented preliminary results from this research at the Society for Maternal Fetal Medicine Annual Meeting on February 2 in Dallas, Texas.
One out of eight babies in the United States is born prematurely - delivery prior to 37 weeks gestation. These babies don't fare as well as their full-term counterparts, especially if they are born prior to 28 weeks gestation. In many cases, it is still unclear why preterm births occur, but Norwitz said that both the genetic make-up of the mother and the genetic make-up of the baby play a role.
Norwitz and his collaborators sought to understand the mechanisms responsible for the onset of labor at term and how these mechanisms are either overwhelmed or short-circuited, leading to preterm birth. Some women, especially African-American women, are genetically pre-disposed to preterm births, even after taking into account socioeconomic status, demographics, underlying medical conditions and multiple pregnancies. Norwitz said that multiple genes or a single particular genetic variant - single nucleotide polymorphism - may be involved.
In his study, Norwitz and colleagues tried to tease out some of the genetic factors that are important for preterm birth. They isolated DNA in blood samples from a largely Hispanic population of mothers with a history of preterm birth and compared them to the DNA of women who had only had full-term pregnancies. They then screened the DNA for 128 different genetic variations in 77 candidate genes. While these genetic variants have been known to cause clinical disorders, no one had ever investigated them in the context of preterm birth before.
Four polymorphisms were associated with premature birth, but - to the team's surprise - a variant of the ENPP1 gene was the one most closely linked. ENPP1 has been associated with insulin resistance, glucose intolerance and a risk of developing type-2 diabetes. In certain people, it is associated with hardening of the arteries and high blood pressure. In the context of prematurity, say the researchers, it is possible that the variant form of ENPP1 is associated with deranged energy metabolism.
"In our original study, 85 percent of the population was Hispanic," said Norwitz. "It appears that there are genetic variations unique to each ethnic population. We are now in the process of validating our findings in African-American, Caucasian and Native-American populations."
Other authors on the study included Victoria Snegovskikh, Charles Lockwood, Edward Kuczynski, Louis Muglia, Daniel Robert Tilden, Beth Ann Kozel, Edmund Funai, Mert Ozan Bahtiyar, Guoyang Luo, Stephen Thung and Thomas Morgan.
A discussion on this topic is available on Yale University iTunes U, "Health and Medicine" section.
Source: Karen N. Peart
Yale University
Errol Norwitz, M.D., associate professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale, presented preliminary results from this research at the Society for Maternal Fetal Medicine Annual Meeting on February 2 in Dallas, Texas.
One out of eight babies in the United States is born prematurely - delivery prior to 37 weeks gestation. These babies don't fare as well as their full-term counterparts, especially if they are born prior to 28 weeks gestation. In many cases, it is still unclear why preterm births occur, but Norwitz said that both the genetic make-up of the mother and the genetic make-up of the baby play a role.
Norwitz and his collaborators sought to understand the mechanisms responsible for the onset of labor at term and how these mechanisms are either overwhelmed or short-circuited, leading to preterm birth. Some women, especially African-American women, are genetically pre-disposed to preterm births, even after taking into account socioeconomic status, demographics, underlying medical conditions and multiple pregnancies. Norwitz said that multiple genes or a single particular genetic variant - single nucleotide polymorphism - may be involved.
In his study, Norwitz and colleagues tried to tease out some of the genetic factors that are important for preterm birth. They isolated DNA in blood samples from a largely Hispanic population of mothers with a history of preterm birth and compared them to the DNA of women who had only had full-term pregnancies. They then screened the DNA for 128 different genetic variations in 77 candidate genes. While these genetic variants have been known to cause clinical disorders, no one had ever investigated them in the context of preterm birth before.
Four polymorphisms were associated with premature birth, but - to the team's surprise - a variant of the ENPP1 gene was the one most closely linked. ENPP1 has been associated with insulin resistance, glucose intolerance and a risk of developing type-2 diabetes. In certain people, it is associated with hardening of the arteries and high blood pressure. In the context of prematurity, say the researchers, it is possible that the variant form of ENPP1 is associated with deranged energy metabolism.
"In our original study, 85 percent of the population was Hispanic," said Norwitz. "It appears that there are genetic variations unique to each ethnic population. We are now in the process of validating our findings in African-American, Caucasian and Native-American populations."
Other authors on the study included Victoria Snegovskikh, Charles Lockwood, Edward Kuczynski, Louis Muglia, Daniel Robert Tilden, Beth Ann Kozel, Edmund Funai, Mert Ozan Bahtiyar, Guoyang Luo, Stephen Thung and Thomas Morgan.
A discussion on this topic is available on Yale University iTunes U, "Health and Medicine" section.
Source: Karen N. Peart
Yale University
суббота, 17 марта 2012 г.
Amnesty International Affirms New Abortion Policy Despite Opposition From Catholic, Conservative Leaders
Amnesty International on Friday affirmed a policy that supports a woman's right to have an abortion under certain circumstances despite opposition from Roman Catholic and conservative leaders worldwide, BBC News reports (Pigott, BBC News, 8/18). The organization at the end of its biennial meeting in Mexico City said it would work to "support the decriminalization of abortion, to ensure women have access to health care when complications arise from abortion and to defend women's access to abortion ... when their health or human rights are in danger" (Reuters, 8/17). According to London's Times, the new policy is automatically binding for Amnesty's members in each member country, including where abortion is illegal (Caldwell/Syal, Times, 8/21).
According to the policy, safe abortions should be available to women in cases of rape or incest, or when the health or life of a pregnant woman is at risk. Amnesty Senior Policy and Campaigns Director Widney Brown has said the policy is part of the group's global campaign to stop violence against women. The policy does not acknowledge abortion as a "fundamental right" for women, and the organization supports the right of states to put "reasonable limitations" on abortion providers and to prosecute those who risk women's lives by performing unsafe abortions, according to Brown.
According to the policy, safe abortions should be available to women in cases of rape or incest, or when the health or life of a pregnant woman is at risk. Amnesty Senior Policy and Campaigns Director Widney Brown has said the policy is part of the group's global campaign to stop violence against women. The policy does not acknowledge abortion as a "fundamental right" for women, and the organization supports the right of states to put "reasonable limitations" on abortion providers and to prosecute those who risk women's lives by performing unsafe abortions, according to Brown.
Reaction
Critics have said that Amnesty has abandoned its principles by changing its previously neutral position on abortion (Kaiser Daily Women's Health Policy Report, 7/30). Cardinal Renato Martino, head of the Vatican's justice and peace department, in June called on Roman Catholics and Catholic organizations to withhold contributions to Amnesty because of the policy. Noeleen Hartigan, program director for Amnesty International Irish Section, said the affiliate recently decided to effectively opt out of the policy and will not participate in Amnesty's abortion-related campaigns (Kaiser Daily Women's Health Policy Report, 7/30).
Michael Evans, Roman Catholic bishop of East Anglia in England, has ended his membership with Amnesty after the group affirmed its support for the new policy, his office confirmed Tuesday, AFP/Yahoo! News reports (AFP/Yahoo! News, 8/21). Evans, who wrote a prayer for the Amnesty's "protect the human" campaign, in a statement on his Web site said, "Very regretfully, I will be ending my 31-year membership of Amnesty International" (Kelland, Reuters, 8/21). "Appalling violence must not be answered by violence against the most vulnerable and defenseless form of human life in a woman's womb," Evans said, adding, "There is no human right to access to abortion, and Amnesty should not involve itself even in such extreme cases."
Kate Gilmore, Amnesty's executive deputy secretary-general, said the group simply supports "women's human rights to be free of fear, threat and coercion as they manage all consequences of rape and other grave human rights violations" (Times, 8/21). Suzanne Trimmel, spokesperson for Amnesty International USA, said that a "handful" -- probably fewer than 200 -- of the chapter's 400,000 members have quit because of the policy change (Kaiser Daily Women's Health Policy Report, 7/30). According to BBC News, Amnesty's international council "overwhelmingly" supported the policy change (BBC News, 8/18).
"Reprinted with permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation . © 2005 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
суббота, 10 марта 2012 г.
GOP Chair Steele Calls Abortion An 'Individual Choice,' Says He Disagrees With Roe V. Wade
Republican National Committee Chair Michael Steele in an interview this week with GQ magazine said that abortion is an "individual choice" and that decisions regarding the procedure should be left to the states, the Washington Times reports. In the interview, which was posted on the magazine's Web site on Wednesday, Steele said his background as an adopted child showed him "the power of life … and the power of choice." Steele continued, "The choice issue cuts two ways. You can choose life or you can choose abortion. You know, my mother chose life. So, you know, I think the power of the argument of choice boils down to stating a case for one or the other." When asked whether he thinks women have the right to choose an abortion, Steele replied, "Yeah. Absolutely," adding, "I think that's an individual choice."
During the interview, Steele also said he disagrees with the Supreme Court's 1973 decision in Roe v. Wade. Steele said that "as a legal matter, Roe v. Wade was a wrongly decided matter." When asked how women would have the ability to choose abortion if Roe were overturned, Steele responded that "states should make that choice." He elaborated, "That's what the choice is. The individual choice rests in the states. Let them decide."
The Times reports that although Steele has always categorized himself as "pro-life" and received an endorsement from the antiabortion-rights group National Right to Life Committee when he ran for the Senate in 2006, he "often has been viewed with suspicion" by conservatives who oppose abortion rights. For example, Steele worked with Christine Todd Whitman, a Republican abortion-rights supporter, to form the Republican Leadership Council. During a 2006 interview on NBC's "Meet the Press," Steele said that he thought Roe should be followed as a settled law. Steele during the 2006 interview also would not say that he would support a constitutional amendment to ban abortion (Morton, Washington Times, 3/12).
Reprinted with kind permission from nationalpartnership. You can view the entire Daily Women's Health Policy Report, search the archives, or sign up for email delivery here. The Daily Women's Health Policy Report is a free service of the National Partnership for Women & Families, published by The Advisory Board Company.
© 2009 The Advisory Board Company. All rights reserved.
During the interview, Steele also said he disagrees with the Supreme Court's 1973 decision in Roe v. Wade. Steele said that "as a legal matter, Roe v. Wade was a wrongly decided matter." When asked how women would have the ability to choose abortion if Roe were overturned, Steele responded that "states should make that choice." He elaborated, "That's what the choice is. The individual choice rests in the states. Let them decide."
The Times reports that although Steele has always categorized himself as "pro-life" and received an endorsement from the antiabortion-rights group National Right to Life Committee when he ran for the Senate in 2006, he "often has been viewed with suspicion" by conservatives who oppose abortion rights. For example, Steele worked with Christine Todd Whitman, a Republican abortion-rights supporter, to form the Republican Leadership Council. During a 2006 interview on NBC's "Meet the Press," Steele said that he thought Roe should be followed as a settled law. Steele during the 2006 interview also would not say that he would support a constitutional amendment to ban abortion (Morton, Washington Times, 3/12).
Reprinted with kind permission from nationalpartnership. You can view the entire Daily Women's Health Policy Report, search the archives, or sign up for email delivery here. The Daily Women's Health Policy Report is a free service of the National Partnership for Women & Families, published by The Advisory Board Company.
© 2009 The Advisory Board Company. All rights reserved.
суббота, 3 марта 2012 г.
Study Examines The Mechanisms That Silence The Estrogen Receptor Gene Alpha During Breast Cancer
The mechanisms that silences the estrogen receptor gene alpha (ER-?±) in certain breast cancer cell lines may be closer to being unlocked, according to a study by researchers at Temple University's Sbarro Institute for Cancer Research and Molecular Medicine.
The researchers reported their findings, "Epigenetic Modulation of Estrogen Receptor-?± by pRb Family Proteins: A Novel Mechanism in Breast Cancer," in the Aug. 15 issue of the journal Cancer Research
In a previous study, the researchers found that in estrogen receptor-positive and estrogen receptor-negative mammary cell lines of women who have been affected with breast cancer, the tumor-suppressing gene pRb2/p130 binds to a specific region of the estrogen receptor gene alpha and forms molecular complexes recruiting and/or interacting with several proteins. They discovered that in estrogen receptor-negative cells which are able to silence the expression of the estrogen receptor pRb2/p130 forms a specific molecular complex recruiting a different sequence of proteins than in the estrogen receptor positive cells.
In the current study, lead by Antonio Giordano, M.D., Ph.D., director of the Sbarro Institute (shro), the researchers showed that the presence of specific pRb2/p130 multimolecular complexes bound to the estrogen receptor gene strongly correlates with the methylation (chemical modification) of the gene.
"Our hypothesis is that the sequence of epigenetic events for establishing and maintaining the silenced state of the estrogen receptor gene alpha during the breast cancer progression is mediated by pRb2/p130 in association with specific proteins that modified the DNA structure through specific mechanisms," said Giordano, who discovered the Rb2 gene while working at Temple's Fels Cancer Institute in the early 1990s.
"In other words, the presence of a specific pRb2/p130 multimolecular complex may dictate a local change of the DNA structure of the estrogen receptor alpha gene and influence its susceptibility to chemical modification (DNA methylation), as well as to different epigenetic alterations leading to estrogen receptor alpha silencing," added Marcella Macaluso, research assistant professor at the Sbarro Institute and the study's lead author.
Giordano says this study provides a basis for understanding how the complex pattern of estrogen receptor gene alpha methylation and transcriptional silencing is generated, as well as for understanding the relationship between this pattern and its function during breast cancer progression.
By understanding this mechanism of how pRb2/p130 recruits molecules, he says, researchers will be able to design therapies and drugs that are very precise in the target they recognize.
"One gene on its own doesn't mean anything," he explains. "It's the dialogue among the genes that are writing the sentences, and this finding really writes a very important sentence in the book that we are authoring on uncovering the understanding of how a normal cell functions and why some therapies work or some therapies don't work. It also clearly shows that cancer is not the event of one gene, but an army of genes and it looks like pRb2/p130 is one of the generals."
Giordano and Macaluso were joined in this study by research fellow Micaela Montanari and doctoral students Paul Bart Noto and Valter Gregorio from the Sbarro Institute, and Professor Christian Bronner from the Centre National de la Recherche Scientifique/Universit?© Louis Pasteur in France.
The study was coordinated by Giordano and carried out at Temple's Sbarro Institute and the Department of Human Pathology and Oncology at the University of Siena in Italy. It was funded by the National Institutes of Health, the U.S. Army Medical Research and Material Command and the Sbarro Health Research Organization.
Temple University
301 University Services Bldg.1601 North Broad St.
Philadelphia, PA 19122
United States
temple.edu
The researchers reported their findings, "Epigenetic Modulation of Estrogen Receptor-?± by pRb Family Proteins: A Novel Mechanism in Breast Cancer," in the Aug. 15 issue of the journal Cancer Research
In a previous study, the researchers found that in estrogen receptor-positive and estrogen receptor-negative mammary cell lines of women who have been affected with breast cancer, the tumor-suppressing gene pRb2/p130 binds to a specific region of the estrogen receptor gene alpha and forms molecular complexes recruiting and/or interacting with several proteins. They discovered that in estrogen receptor-negative cells which are able to silence the expression of the estrogen receptor pRb2/p130 forms a specific molecular complex recruiting a different sequence of proteins than in the estrogen receptor positive cells.
In the current study, lead by Antonio Giordano, M.D., Ph.D., director of the Sbarro Institute (shro), the researchers showed that the presence of specific pRb2/p130 multimolecular complexes bound to the estrogen receptor gene strongly correlates with the methylation (chemical modification) of the gene.
"Our hypothesis is that the sequence of epigenetic events for establishing and maintaining the silenced state of the estrogen receptor gene alpha during the breast cancer progression is mediated by pRb2/p130 in association with specific proteins that modified the DNA structure through specific mechanisms," said Giordano, who discovered the Rb2 gene while working at Temple's Fels Cancer Institute in the early 1990s.
"In other words, the presence of a specific pRb2/p130 multimolecular complex may dictate a local change of the DNA structure of the estrogen receptor alpha gene and influence its susceptibility to chemical modification (DNA methylation), as well as to different epigenetic alterations leading to estrogen receptor alpha silencing," added Marcella Macaluso, research assistant professor at the Sbarro Institute and the study's lead author.
Giordano says this study provides a basis for understanding how the complex pattern of estrogen receptor gene alpha methylation and transcriptional silencing is generated, as well as for understanding the relationship between this pattern and its function during breast cancer progression.
By understanding this mechanism of how pRb2/p130 recruits molecules, he says, researchers will be able to design therapies and drugs that are very precise in the target they recognize.
"One gene on its own doesn't mean anything," he explains. "It's the dialogue among the genes that are writing the sentences, and this finding really writes a very important sentence in the book that we are authoring on uncovering the understanding of how a normal cell functions and why some therapies work or some therapies don't work. It also clearly shows that cancer is not the event of one gene, but an army of genes and it looks like pRb2/p130 is one of the generals."
Giordano and Macaluso were joined in this study by research fellow Micaela Montanari and doctoral students Paul Bart Noto and Valter Gregorio from the Sbarro Institute, and Professor Christian Bronner from the Centre National de la Recherche Scientifique/Universit?© Louis Pasteur in France.
The study was coordinated by Giordano and carried out at Temple's Sbarro Institute and the Department of Human Pathology and Oncology at the University of Siena in Italy. It was funded by the National Institutes of Health, the U.S. Army Medical Research and Material Command and the Sbarro Health Research Organization.
Temple University
301 University Services Bldg.1601 North Broad St.
Philadelphia, PA 19122
United States
temple.edu
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