Only in Holland can one stand in a windmill next to several policemen dressed as monsters & clowns, and watch a one-legged prostitute in a wooden clog feed her 11-month-old John-baby a de-crusted cocaine sandwich, free of all legal repercussion and woe. Seriously - we actually saw that once.
Well, we didn't see it so much as we drew a picture of it in a grade-school art class. Our teacher changed after that, as did our curriculum. Nonetheless, Holland is a different country. Not only does the Hollish language sound silly & trite, but the whole country likes really strange entertainment too.
In America to entice viewers, television gives out civilised prizes like millions of dollars, love, & several greasy humpings from Flavor Flav. In Holland that's all old hat. That's why their game show prizes are things like - the ability to not die, the power to keep living, & not having to be killed by your poor medical condition because you handled yourself well in the physical challenge.
Basically, there's three contestants with failing kidneys & a terminally ill prize-holder. You can figure it out from there.
Dutch television is such a powerful medium that Eddie Murphy used it to tell the world Mel B might be a skank-ho. The genre also has crazy reality TV - the most recent of which gives the prize of continuing life to the winner. As a brilliant entertainment blog put it like a paragraph ago:
"Basically, there's three contestants with failing kidneys & a terminally ill prize-holder. You can figure it out from there."
Oh - you read that right. Three people (contestants) have failing kidneys, and may just die on a transplant list. A terminally ill show participant will have the power to give life after she dies. As BBC News put it:
"The 37-year-old donor, identified only as Lisa, will make her choice based on the contestants' history, profile and conversation with their family and friends."
The show is called De Grote Donor Show which in Netherlandish for The Big Donor Show. The 'O' in the word 'Show' is shaped like a kidney. De Grote Donor Show is made by the same people who created Big Brother, and premieres on Friday. The whole country's not on the edge of their seat waiting for Friday night. Tons of them hate the idea. One such hater said:
"The set up of the programme bears no relationship to the way decisions are made about transplants in the real world. Living donors can choose altruistically to give one of their kidneys - usually to a family member. If organs become available after someone dies, health professionals with access to detailed information about those waiting for a transplant make objective decisions about who should receive those particular kidneys."
We think the kidneys should just be awarded to the best singer.
That would truly be best for global DNA.
Read More:'Big Brother' Kidney Show Condemned - Sky News
http://www.hecklerspray.com/barbaric-holland-gives-human-kidneys-as-tv-prizes/20068507.php
Wednesday, May 30, 2007
Kidney Notes PKD Blog
Angiotech Initiates European Trial Examining The Vascular Wrap(TM) Paclitaxel-eluting Mesh For Dialysis Patients With End-Stage Renal Disease
NY-Presbyterian Hospital/Columbia University Medical Center Doctors Presented At 2007 AUA Meeting
Report On Transurethral Detection And Resection Of Bladder Carcinomas Under White Or 5-ALA Induced Fluroescence Light
How Are We Training The Postgraduate Urologist In Minimally Invasive Surgery?
Challenges For Urologists In Living Kidney Donation
NY-Presbyterian Hospital/Columbia University Medical Center Doctors Presented At 2007 AUA Meeting
Report On Transurethral Detection And Resection Of Bladder Carcinomas Under White Or 5-ALA Induced Fluroescence Light
How Are We Training The Postgraduate Urologist In Minimally Invasive Surgery?
Challenges For Urologists In Living Kidney Donation
Tuesday, May 29, 2007
Kidney Notes from PKD Blog
Three kidney donations make for one close Westport family
WESTPORT - It's all in the family and this family is very close. Within less than two years, three women in Westport -- including two sisters and a daughter -- will have donated their kidneys to save other family members with polycystic kidney disease.
The two sisters are Christine Earle and Melissa Boudria. Mrs. Earle donated a kidney to her cousin, David McGinn, about a year ago.
On Tuesday, May 8, Mrs. Earle's stepdaughter, Kristin Wilkinson, successfully gave one of her kidneys to David's sister, Charlotte Toddings. In July, Ms. Boudria is scheduled to give a kidney to Charlotte's son, Kevin, who also has Down syndrome.
The family ties may sound complicated but as Ms. Boudria said, "We have an extended family all sorts of ways and we're all extremely close."
Read the rest
http://www.eastbayri.com/story/288999310057821.php
The two sisters are Christine Earle and Melissa Boudria. Mrs. Earle donated a kidney to her cousin, David McGinn, about a year ago.
On Tuesday, May 8, Mrs. Earle's stepdaughter, Kristin Wilkinson, successfully gave one of her kidneys to David's sister, Charlotte Toddings. In July, Ms. Boudria is scheduled to give a kidney to Charlotte's son, Kevin, who also has Down syndrome.
The family ties may sound complicated but as Ms. Boudria said, "We have an extended family all sorts of ways and we're all extremely close."
Read the rest
http://www.eastbayri.com/story/288999310057821.php
Tolvaptan for chronic heart failure: No antiremodeling benefit observed
May 29, 2007
Steve Stiles
Washington, DC - A year of treatment with the vasopressin-receptor antagonist tolvaptan (Otsuka America Pharmaceuticals) had no apparent effect on LV end-diastolic volume (LVEDV) in patients with chronic systolic heart failure who were already on evidence-based medical therapy in a small but randomized and placebo-controlled study [1].
However, there was a nonsignificant but "hypothesis-generating" signal of possible long-term benefit in a composite end point that was not prospectively defined—mortality or HF hospitalization—that appears consistent with earlier tolvaptan findings, write the authors, led by Dr James E Udelson (Tufts University School of Medicine, Boston, MA), in their report published online May 18, 2007 in the Journal of the American College of Cardiology.
Tolvaptan is an investigational agent in the US that is also under development for the treatment of hyponatremia and polycystic kidney disease and that has been studied in patients with acute decompensated heart failure (ADHF).
A placebo-controlled international tolvaptan trial that randomized more than 4000 patients with ADHF, called Efficacy of Vasopressin Antagonism in Heart Failure Trial (EVEREST), was published earlier this year [2,3]. As covered by heartwire at the time, those who received the drug in addition to standard IV therapy and who were discharged on it long term showed in-hospital improvements in a composite of patient-assessed clinical status and body weight but no significant clinical advantages out to a year. Its investigators then concluded that tolvaptan could potentially play a role in managing volume overload and alleviating symptoms in patients with ADHF.
In the current study, 240 patients with chronic, NYHA functional class 2-3 heart failure with an LVEF <30%, who were overwhelmingly on diuretics, beta blockers, and either an ACE inhibitor or angiotensin-receptor blocker, were randomized to receive either oral tolvaptan at 30 mg/day or a placebo. Baseline and follow-up quantitative radionuclide ventriculographic studies were available for 91 and 89 patients in the two respective groups.
No significant differences were observed over one year in ventriculographic measures of reverse remodeling, including the primary end point of change in LVEDV and the secondary end points of change in LVEF and in LV end-systolic volume. Nor were there differences throughout the follow-up in vital signs, measures of renal function, levels of the HF prognostic marker brain-type natriuretic peptide, or in self-assessed symptom status or quality of life.
Side effects such as urinary frequency, thirst, and dry mouth were more common in the tolvaptan group, but patients in both groups dropped out of the study due to side effects to the same extent.
In an accompanying editorial, Dr Gian Paolo Rossi (University Hospital, Padova, Italy) writes that the negative study had been designed for tracking any ventricular structural changes but also proposes that a much larger study using higher tolvaptan dosages in a similar population might conceivably show that the drug can improve LV end-diastolic volumes [4].
"All investigators and their institutions received support for this trial from Otsuka America Pharmaceuticals," according to the report, which also states that Udelson and coauthor Dr Marvin A Konstam (Tufts University) are consultants to Otsuka America and that coauthors Drs Christopher Zimmer and Cesare Orlandi are employees of the company.
http://www.theheart.org/article/793479.do
Steve Stiles
Washington, DC - A year of treatment with the vasopressin-receptor antagonist tolvaptan (Otsuka America Pharmaceuticals) had no apparent effect on LV end-diastolic volume (LVEDV) in patients with chronic systolic heart failure who were already on evidence-based medical therapy in a small but randomized and placebo-controlled study [1].
However, there was a nonsignificant but "hypothesis-generating" signal of possible long-term benefit in a composite end point that was not prospectively defined—mortality or HF hospitalization—that appears consistent with earlier tolvaptan findings, write the authors, led by Dr James E Udelson (Tufts University School of Medicine, Boston, MA), in their report published online May 18, 2007 in the Journal of the American College of Cardiology.
Tolvaptan is an investigational agent in the US that is also under development for the treatment of hyponatremia and polycystic kidney disease and that has been studied in patients with acute decompensated heart failure (ADHF).
A placebo-controlled international tolvaptan trial that randomized more than 4000 patients with ADHF, called Efficacy of Vasopressin Antagonism in Heart Failure Trial (EVEREST), was published earlier this year [2,3]. As covered by heartwire at the time, those who received the drug in addition to standard IV therapy and who were discharged on it long term showed in-hospital improvements in a composite of patient-assessed clinical status and body weight but no significant clinical advantages out to a year. Its investigators then concluded that tolvaptan could potentially play a role in managing volume overload and alleviating symptoms in patients with ADHF.
In the current study, 240 patients with chronic, NYHA functional class 2-3 heart failure with an LVEF <30%, who were overwhelmingly on diuretics, beta blockers, and either an ACE inhibitor or angiotensin-receptor blocker, were randomized to receive either oral tolvaptan at 30 mg/day or a placebo. Baseline and follow-up quantitative radionuclide ventriculographic studies were available for 91 and 89 patients in the two respective groups.
No significant differences were observed over one year in ventriculographic measures of reverse remodeling, including the primary end point of change in LVEDV and the secondary end points of change in LVEF and in LV end-systolic volume. Nor were there differences throughout the follow-up in vital signs, measures of renal function, levels of the HF prognostic marker brain-type natriuretic peptide, or in self-assessed symptom status or quality of life.
Side effects such as urinary frequency, thirst, and dry mouth were more common in the tolvaptan group, but patients in both groups dropped out of the study due to side effects to the same extent.
In an accompanying editorial, Dr Gian Paolo Rossi (University Hospital, Padova, Italy) writes that the negative study had been designed for tracking any ventricular structural changes but also proposes that a much larger study using higher tolvaptan dosages in a similar population might conceivably show that the drug can improve LV end-diastolic volumes [4].
"All investigators and their institutions received support for this trial from Otsuka America Pharmaceuticals," according to the report, which also states that Udelson and coauthor Dr Marvin A Konstam (Tufts University) are consultants to Otsuka America and that coauthors Drs Christopher Zimmer and Cesare Orlandi are employees of the company.
http://www.theheart.org/article/793479.do
Thursday, May 24, 2007
Kidney Notes PKD blog
Transforming Kidney Transplant Policy
American Association Of Kidney Patients Asks Congressional Leaders To Co-Sponsor Bill
Oxford Transplant Campaign - Seeking A Cure For Kidney And Pancreas Failure, UK
Green Tea May Protect The Bladder From Becoming Inflamed
Five Days Of LEVAQUIN(R) As Effective As 10 Days Of Ciprofloxacin In Complicated Urinary Tract Infections And Acute Pyelonephritis
Quality Versus Quantity: Transforming Kidney Transplant Policy - Alternative Process Proposed By Medical Expert Addresses Challenges
Collaborative Educational Initiative To Focus On Early Treatment Of Chronic Kidney Disease
ACE Inhibitors Help Preserve Kidney Function In IgA Nephropathy
American Association Of Kidney Patients Asks Congressional Leaders To Co-Sponsor Bill
Oxford Transplant Campaign - Seeking A Cure For Kidney And Pancreas Failure, UK
Green Tea May Protect The Bladder From Becoming Inflamed
Five Days Of LEVAQUIN(R) As Effective As 10 Days Of Ciprofloxacin In Complicated Urinary Tract Infections And Acute Pyelonephritis
Quality Versus Quantity: Transforming Kidney Transplant Policy - Alternative Process Proposed By Medical Expert Addresses Challenges
Collaborative Educational Initiative To Focus On Early Treatment Of Chronic Kidney Disease
ACE Inhibitors Help Preserve Kidney Function In IgA Nephropathy
Passing on knowledge about an inherited illness
5/21/2007 7:35:04 AM
By Jeff Hansel
The Post-Bulletin
Amy Berends of St. Charles doesn't want any more family secrets.
She has come to terms with the knowledge that her grandfather didn't share, before he died, what he knew about his own health. He had polycystic kidney disease, an inherited illness that can have devastating effects for the entire family.
"I remember being so angry. Like, why didn't he just tell us? Why didn't he share that with us," said Berends, who is a registered pediatric nurse.
Polycystic kidney disease causes clusters of cysts to develop in the kidneys, according to MayoClinic.com. Cysts can also form in other organs, and kidney failure can occur.
Families with PKD face many fears, said Mary Welder of Rochester, whose husband Scott's family has been affected. Some people worry if they get diagnosed that they'll lose health insurance, or won't be able to get any. Other's worry employers won't hire them, or they'll lose their jobs. Some fear being treated differently by friends or family, and some simply don't want to face the possibility they might be ill.
But diagnosis and information sharing is important for families, Scott Welder said.
"When somebody has it, there's a strong chance that a portion of the kids can have it too," he said.
There is no cure. "It's kind of one of those things where it's a ticking time bomb," he said.
Berends, who does not have PKD, said her aunt called and described some medical problems.
"I told her, well, that sounds like PKD. But it's inherited," Berends said.
Her aunt thought Berends' grandfather had gotten a letter saying he didn't have the condition. The opposite was true, "but he never told his wife. He didn't tell anybody," Berends said. Many family discussions, sometimes heated ones, ensued as Berends tried to get everyone tested.
"Everybody's a little gun shy. Nobody wants to do it," she said.
A person could live her whole life with PKD and never die from it, Berends said. But it's unpredictable.
"It's a hard thing to have in the family," she said. In her family, she said, "one thing that it did, I think, is pull us closer."
Scott Welder said he has been required to get tested for PKD when he gets life insurance, because his family history of the disease is known.
According to the PKD Foundation, the U.S. House passed a bill to ban discrimination by employers and insurers based on genetics .
http://www.postbulletin.com/newsmanager/templates/localnews_story.asp?z=10&a=294868
By Jeff Hansel
The Post-Bulletin
Amy Berends of St. Charles doesn't want any more family secrets.
She has come to terms with the knowledge that her grandfather didn't share, before he died, what he knew about his own health. He had polycystic kidney disease, an inherited illness that can have devastating effects for the entire family.
"I remember being so angry. Like, why didn't he just tell us? Why didn't he share that with us," said Berends, who is a registered pediatric nurse.
Polycystic kidney disease causes clusters of cysts to develop in the kidneys, according to MayoClinic.com. Cysts can also form in other organs, and kidney failure can occur.
Families with PKD face many fears, said Mary Welder of Rochester, whose husband Scott's family has been affected. Some people worry if they get diagnosed that they'll lose health insurance, or won't be able to get any. Other's worry employers won't hire them, or they'll lose their jobs. Some fear being treated differently by friends or family, and some simply don't want to face the possibility they might be ill.
But diagnosis and information sharing is important for families, Scott Welder said.
"When somebody has it, there's a strong chance that a portion of the kids can have it too," he said.
There is no cure. "It's kind of one of those things where it's a ticking time bomb," he said.
Berends, who does not have PKD, said her aunt called and described some medical problems.
"I told her, well, that sounds like PKD. But it's inherited," Berends said.
Her aunt thought Berends' grandfather had gotten a letter saying he didn't have the condition. The opposite was true, "but he never told his wife. He didn't tell anybody," Berends said. Many family discussions, sometimes heated ones, ensued as Berends tried to get everyone tested.
"Everybody's a little gun shy. Nobody wants to do it," she said.
A person could live her whole life with PKD and never die from it, Berends said. But it's unpredictable.
"It's a hard thing to have in the family," she said. In her family, she said, "one thing that it did, I think, is pull us closer."
Scott Welder said he has been required to get tested for PKD when he gets life insurance, because his family history of the disease is known.
According to the PKD Foundation, the U.S. House passed a bill to ban discrimination by employers and insurers based on genetics .
http://www.postbulletin.com/newsmanager/templates/localnews_story.asp?z=10&a=294868
Tuesday, May 22, 2007
PKD Blog Kidney Notes
Monday, May 07, 2007
New Agent Found To Fight Genetic Disorders - Zorro-Locked Nucleic Acid
\A study to appear in the June 2007 issue of The FASEB Journal describes a new agent, called "Zorro-LNA," which has the potential to stop genetic disorders in their tracks. In the study, researchers from the Karolinska Institute in Stockholm, Sweden, describe how they developed Zorro-LNA to bind with both strands of a gene's DNA simultaneously, effectively disabling that gene. This development has clinical implications for virtually every human condition caused by or worsened by dominant defective genes. Examples include: Huntington's disease, familial high cholesterol, polycystic kidney disease, some instances of glaucoma and colorectal cancer, and neurofibromatosis, among others. "Zorro-LNA is a new substance that targets DNA and turns off genes," said co-author Edvard Smith of the Karolinska Institute in Sweden. "It has the potential of becoming a new drug for the treatment of human genetic disease." The findings described in this article significantly raise the possibility that new therapies could arise where defective DNA is deactivated more completely and more thoroughly than ever before. For instance, Zorro-LNA could be used in combination with "RNA interference" (RNAi). Like Zorro-LNA, RNAi has the ability to deactivate genes, but does so by degrading the gene's RNA. In addition, Zorro-LNA could be used to deactivate certain genes in stem cells, which could eventually lead to the development of new cells, tissues, or organs. The discovery of RNAi was recognized by a Nobel Prize award in 2006 to two American scientists. "This is a major development in the treatment not only of genetic diseases, but also of acquired diseases when microbes or toxins cause genes to go awry" said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "One might say these researchers have found a gene-hunter's Holy Grail for which scientists have been hunting for many years. Zorro-LNA should give us a new, safe way of blocking the effects of errors in our genetic repertoire."
### The FASEB Journal is published by the Federation of American Societies for Experimental Biology (FASEB) and is consistently ranked among the top three biology journals worldwide by the Institute for Scientific Information. FASEB comprises 21 nonprofit societies with more than 80,000 members, making it the largest coalition of biomedical research associations in the United States. FASEB advances biological science through collaborative advocacy for research policies that promote scientific progress and education and lead to improvements in human health. Contact: Cody Mooneyhan Federation of American Societies for Experimental Biology
### The FASEB Journal is published by the Federation of American Societies for Experimental Biology (FASEB) and is consistently ranked among the top three biology journals worldwide by the Institute for Scientific Information. FASEB comprises 21 nonprofit societies with more than 80,000 members, making it the largest coalition of biomedical research associations in the United States. FASEB advances biological science through collaborative advocacy for research policies that promote scientific progress and education and lead to improvements in human health. Contact: Cody Mooneyhan Federation of American Societies for Experimental Biology
Tuesday, May 01, 2007
Kidney Notes
Advagraf® Now Approved Across Europe As A Once-daily Immunosuppressant In Organ Transplantation
In-Depth Research Provides Insight Into Trends, Efficacy And Outcomes Of Cerebral Aneurysm Treatment And The Ongoing Debate: Clip Versus Coil
Intact Specimen Extraction In Laparoscopic Nephrectomy Procedures: Pfannenstiel Versus Expanded Port Site Incisions.
Efficacy Of α-Blockers For The Treatment Of Ureteral Stones
In-Depth Research Provides Insight Into Trends, Efficacy And Outcomes Of Cerebral Aneurysm Treatment And The Ongoing Debate: Clip Versus Coil
Intact Specimen Extraction In Laparoscopic Nephrectomy Procedures: Pfannenstiel Versus Expanded Port Site Incisions.
Efficacy Of α-Blockers For The Treatment Of Ureteral Stones
Traditional Chinese medicine may help prevent polycystic kidney disease
From our ANI CorrespondentWashington, Apr 30: A new study has found that a centuries old Chinese traditional medicine, Triptolide has the potential to stop cyst formation in polycystic kidney disease Triptolide is derived from a Chinese medicinal herb named Lei Gong Teng, which has been used in traditional medicine to treat cancer, inflammation, and auto-immune diseases and, more recently, also has been tested in Phase I clinical trials as an anti-tumour agent.The research holds out hope for what would be the first treatment for the disease other than kidney transplant or frequent dialysis.The study was conducted by a team of researchers led by researcher Dr. Craig Crews at Yale University.During normal kidney development, cells lining the kidney tubules continue growing and dividing until they receive a signal that the tubule is fully formed. The switch that turns on that signal consists of the growth regulatory proteins PKD1 and PKD2, located on hair-like cilia in the lining of the developing tubules. When urine begins flowing through the tubules, the flow bends the cilia that set off the signal that no more growth is needed. In people who have a mutation in one of these growth regulatory proteins, however, the message to stop growing never gets delivered, even when urine is flowing and the cilia are bending. So, never sensing a signal to stop, the cells lining the fully-formed kidney tubules keep right on subdividing and growing. The result of this hyperproliferative, unregulated growth: uncontrolled growth of cells lining the tubules and the formation of large cysts in the kidneys.
Read More
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Prize Winners Announced At ISN's World Congress Of Nephrology
The 2007 Lillian Jean Kaplan International Prize Winners announced at the ISN's World Congress of Nephrology - a celebration of the Foundation's 25 years of "Help and Hope" Vicente Torres and Jing Zhou recognized for advancing critical insight into Polycystic Kidney Disease (PKD) through research of excellence. The International Society of Nephrology (ISN) has announced Vicente Torres, Professor of Medicine and Chair of the Division of Nephrology and Hypertension (Mayo Clinic - USA) and Jing Zhou, Associate Professor of Medicine and Director of the Harvard Center of Polycystic Kidney Disease Research (Harvard University Medical School - USA), as the 2007 winners of the Lillian Jean Kaplan International Prize. Honoring Vicente Torres' seminal contribution at both the clinical and experimental levels of PKD research, his years of dedication to the field have recently culminated in describing the efficacy of vasopressin receptor antagonists in mouse models of PKD. His outstanding efforts serving on the Scientific Advisory Board of the Polycystic Kidney Research Foundation (PKRF) have also been instrumental to advancing the field. Upon receiving the prize Torres expressed his gratitude and sense of optimism toward the future, "It is a great honor to receive this prize. I would like to thank Mr. Thomas Kaplan and the Lillian Jean Kaplan Foundation for this award and the generous support of PKD research as well as both the ISN and the PKD Foundation for sponsoring this event… we are closer than ever today to finding a solution to this disease." Jing Zhou's work, described by Kaplan as 'momentous' has contributed to important breakthroughs within the field such as the first pkd1 knockout mice revealing the roles of the PKD 1 protein, polycystin-1 in embryonic development, as well as the finding that polycystin-2 homologue, polycystin-L, was a calcium-permeable non-selective cation channel. Describing the critical links between calcium, cilia and the cell cycle, Jing Zhou and her group have undoubtedly and fundamentally helped to alter PKD research and attract essential interest from researchers from other related specialties. Commenting on the future directions toward combating the disease Kaplan expressed the ongoing dedication of the Foundation and his positive outlook for research over the coming years, "We are committed to finding ways to spur interest and investment in finding a solution to this disease… I think it is entirely reasonable that in forthcoming years we will see breakthroughs in research and treatment."### 1. Created in 2002, the Lillian Jean Kaplan International Prize for the Advancement in the Understanding of PKD was established through the generosity of Mr. Thomas Kaplan of New York in honor of his mother Lillian Jean Kaplan who died of polycystic kidney disease. The prize was created to recognize those who have increased the understanding and treatment of PKD and to stimulate interest in advancing research that will lead to new treatments and a cure for the disease. 2. The International Society of Nephrology is a not-for-profit society whose mission is the global advancement of nephrology. The Society promotes research and education to prevent and treat kidney disease throughout the world. Further information is available at: http://www.isn-online.org/. Contact: Amanda Wren International Society of Nephrology
Senate gets genetics 'civil rights' bill
Measure would make denying rights based on predisposition to disease illegal.
By DIANE STAFFORD
The Kansas City Star
It is once again the U.S. Senate’s turn to consider what one bill sponsor calls “landmark civil rights legislation.”
But to pass the Genetic Information Nondiscrimination Act — something the Senate has done twice before — an unnamed senator must be persuaded to release a confidential “hold” placed on the bill, which prevents it from going to the floor.
Supporters view the act as civil rights legislation because it would make it illegal for a health insurer to deny coverage or to charge higher premiums to a healthy person on the basis of a genetic predisposition to a disease.
The act also would bar employers from using genetic information in hiring, promotion or firing decisions.
Lobbying efforts turned to the Senate after the U.S. House on Wednesday passed, 420-3, its version of the act.
That passage came 12 years after it was first introduced in the House.
The Senate had in 2003 and 2005 passed previous versions of the bill unanimously. But it failed to become law because the House did not act.
The White House has issued a statement in support of the legislation, which also would prohibit insurers, employers and labor organizations from demanding genetic testing of individuals or their family members
Organizations such as the PKD Foundation, which advocates for people with polycystic kidney disease, urged the Senate to move forward.
“Regrettably, genetic discrimination in America is alive and well, jeopardizing the insurability and employability for all who inherit disease-causing genes through no fault of their own,” said PKD Foundation President Dan Larson. “While we are thrilled with the U.S. House vote, we now urge the U.S. Senate to move forward and pass this legislation.”
Advances in genetic testing make it possible for people to find out whether they are predisposed to certain diseases. That information, if known, can be used by insurers, who do not want to insure high-risk people, or by employers, who fear high costs, absences or turnover of employees who are genetically disposed to certain diseases or health problems.
Debra Ness, president of the National Partnership for Women and Families, also urged prompt Senate action. Many people who fear discrimination in insurance or employment avoid genetic testing that could help them receive preventive treatments, Ness said.
Source
By DIANE STAFFORD
The Kansas City Star
It is once again the U.S. Senate’s turn to consider what one bill sponsor calls “landmark civil rights legislation.”
But to pass the Genetic Information Nondiscrimination Act — something the Senate has done twice before — an unnamed senator must be persuaded to release a confidential “hold” placed on the bill, which prevents it from going to the floor.
Supporters view the act as civil rights legislation because it would make it illegal for a health insurer to deny coverage or to charge higher premiums to a healthy person on the basis of a genetic predisposition to a disease.
The act also would bar employers from using genetic information in hiring, promotion or firing decisions.
Lobbying efforts turned to the Senate after the U.S. House on Wednesday passed, 420-3, its version of the act.
That passage came 12 years after it was first introduced in the House.
The Senate had in 2003 and 2005 passed previous versions of the bill unanimously. But it failed to become law because the House did not act.
The White House has issued a statement in support of the legislation, which also would prohibit insurers, employers and labor organizations from demanding genetic testing of individuals or their family members
Organizations such as the PKD Foundation, which advocates for people with polycystic kidney disease, urged the Senate to move forward.
“Regrettably, genetic discrimination in America is alive and well, jeopardizing the insurability and employability for all who inherit disease-causing genes through no fault of their own,” said PKD Foundation President Dan Larson. “While we are thrilled with the U.S. House vote, we now urge the U.S. Senate to move forward and pass this legislation.”
Advances in genetic testing make it possible for people to find out whether they are predisposed to certain diseases. That information, if known, can be used by insurers, who do not want to insure high-risk people, or by employers, who fear high costs, absences or turnover of employees who are genetically disposed to certain diseases or health problems.
Debra Ness, president of the National Partnership for Women and Families, also urged prompt Senate action. Many people who fear discrimination in insurance or employment avoid genetic testing that could help them receive preventive treatments, Ness said.
Source
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