Posts Tagged: children

The Irish Times – Tuesday, February 21, 2012

DICK AHLSTROM

AUTISM: RESEARCHERS AROUND the world continue to struggle with the complexity of autism. They now believe that genetic factors and brain changes triggered by man-made chemicals in the environment are equally to blame for the development of autism in young children.

Efforts to track the causes of autism were discussed yesterday in a session at the American Association for the Advancement of Science’s annual meeting in Vancouver.

“Autism is a very complicated disorder,” said Prof Scott Selleck of Pennsylvania State University. “We have come to know it has many, many genetic contributors.”

A number of genetic alterations have emerged as important in autistic disorders but persistent chemicals in the environment including flame retardants and polychlorinated biphenyls were also important, he said. “The balance of genetic and environmental contributors is about equal. It is 50/50.”

The panel, which included Prof Janine LaSalle and Prof Isaac Pessah, both of the University of California Davis, was completely dismissive of the now discredited theory that autism in its various forms was caused by “refrigerator parents” or “refrigerator moms”, parents who interacted only minimally with their children.

The phraseology arose in the 1950s. “The idea was that autism was caused because parents were distant. That idea has done a lot of damage,” Prof Selleck said and he ruled it out as nonsense.

He described his own research, cataloguing the number of “copy number variations” in the genomes of those with autism. These were either copied additions to the genome or deletions left out of the genome.

Prof LaSalle described her work on how exposure to persistent chemicals such as flame retardants could cause long-lived changes in how collections of genes were expressed, for example the genes associated with building neurological networks. This was referred to as “epigenetics”, she said, and the complex system involved could be perturbed by low-level environmental chemicals.

She exposed mouse models to the flame retardant PBE-47 and polychlorinated biphenyl MECP-2 at minute levels that matched human exposures.

It affected both sociability of these mice and also their learning behaviour.

There were now upwards of 80,000 non-natural chemicals in the environment produced by industrial processes and other sources, said Prof Pessah. Few had been tested for their neurotoxicity despite human exposures to these substances.

Originally posted here:
Genetics and man-made chemicals equally to blame, say researchers

By Daily Mail Reporter

Last updated at 3:15 PM on 17th February 2012

Created 5:25 PM on 6th February 2012

Bio-hazard: Scientists found three out of 234 people were virtually insensitive to the anthrax toxin. They said this could have implications for other pathogens like HIV

Some people have a natural genetic resistance to anthrax, according to scientists.

Research into anthrax found susceptibility to the deadly disease caused by the bacterium Bacillus anthracis varied from person to person – revealing that susceptibility to the toxin is a heritable genetic trait.

Among 234 people studied by researchers at the Stanford University School of Medicine in the United States, the cells of three people were virtually insensitive to the toxin, while the cells of some people were hundreds of times more sensitive than those of others.

The findings may have important implications for national security, as people known to be more resistant to anthrax exposure could be effective first-line responders in times of crises.

The research also highlights the fact that many lethal pathogens – including HIV, malaria, leprosy and hepatitis – rely on interactions with host genes to infect and replicate within human cells.

Inherited differences in the level of expression of these genes can lead to large variations in the relative susceptibility of different individuals to the pathogen.

Inherited differences in the level of expression of these genes can lead to large variations in the relative susceptibility of different individuals to the pathogen.

The senior author of the report, funded by the Defence Threat Reduction Agency of the U.S. Department of Defence, is Professor of genetics Stanley Cohen.

'Every pathogen has its own virulence strategy,' said Stanford professor of microbiology and immunology David Relman, who was not involved in the research.

'We already knew that infection by the same organisms in different people can have different outcomes.

'But until now it’s been very difficult to determine whether this variability was due to genetic or environmental factors.

'This is one of the few studies that has successfully identified a host-genetics-based molecular cause of this variability.'

In the new study, Prof Cohen and his colleagues found that variation in the level of expression of a gene that produces a cell-surface protein called CMG2 affects the success of the anthrax toxin in gaining entry into human cells.

The research suggests that analogous effects may occur in people exposed to anthrax bacteria.

Anthrax disease is caused by infection with the anthrax bacteria. Spores of the bacteria exist naturally in the environment.

When inhaled by humans or animals, the spores are transported by immune cells to lymph nodes, where the bacteria begin to multiply and are secreted into the bloodstream.

Once in the bloodstream, the bacteria begin to produce the anthrax toxin that infiltrates and kills host cells.

Many lethal pathogens – including HIV (pictured) malaria, leprosy and hepatitis – rely on interactions with host genes to infect and replicate within human cells

Untreated, anthrax infection can cause widespread tissue damage, bleeding and death.

The researchers studied immune cells called lymphocytes collected from 234 people of varying ethnic and geographic backgrounds: 84 Nigerians, 63 Americans whose ancestors came from northern and western Europe, 44 Japanese and 43 Han Chinese.

They found that, of the 234 samples, lymphocytes from three individuals of European ancestry were thousands of times more resistant to killing by an engineered hybrid toxin brought into the cells by protective antigen.

The extent of variation in sensitivity was surprising to the scientists.

Even excluding the virtually resistant cells, they sometimes had to apply as much as 250 times more toxin to kill a similar number of cells in one sample as in another.

In addition, they observed that cells isolated from parents and their children responded similarly, indicating that toxin sensitivity is an inherited trait.

Prof Relman said: 'This research offers an important proof of principle.

'They’ve showed that genetically-determined variations in the level of expression of a human protein can influence the susceptibility of host cells to anthrax toxin.

'The findings also provide a possible means for predicting who is likely to become seriously ill after exposure, which could be extremely useful when faced with a large number of exposed people, such as was the case during the 2001 anthrax attacks.

'Finally, they could lead to the development of novel treatment strategies, perhaps by blocking the interaction between the toxin and the receptor, or by down-regulating its expression.'

The authors note in the study that the research has implications beyond anthrax exposure.

Prof Cohen added: 'Our findings, which reveal the previously unsuspected magnitude of genetically determined differences in toxin sensitivity among cells from different individuals, suggest a broadly applicable approach for investigating pathogen susceptibility in diverse human populations.'

The research was published online in the Proceedings of the National Academy of Sciences.

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Genetic make-up determines whether we die from anthrax exposure

Moskovskiye Novosti

Church Calls for Ban on Stem Cell Research

The Russian Orthodox Church has called for recognizing fetuses as human life and for banning medical research that involves biological material procured from abortion procedures.

The church has sent a series of amendments to the cell technology bill, which iscurrently in the works, to Healthcare Minister Tatyana Golikova in the hope that “the ministry will heed its opinion.” “We, in turn, are ready for dialogue and discussion on each proposal,” said Bishop Panteleimon, head of the the Synodal Department for Church Charity and Social Ministry.

Incidentally, the clerics cite “enlightened” European policies on this issue. In October 2011, the European Court of Justice outlawed the patenting of stem cell research that destroys a human embryo as immoral. Russia’s Healthcare Ministry supported that decision and said the cell technology bill they were working on embraced similar ethical principles. Deputy Minister Veronika Skvortsova said the new bill would ban the use of a human fetus, embryo or gamete in preparing cell lines.

According to Father Panteleimon, this means that the government is ready to agree that a fertilized ovum constitutes a person. Therefore, it would only remain to legalize this statement. That would make it possible to refer to an embryo as a “child,” which in turn would make the 1959 Children’s Rights declaration applicable to the embryo, thus guaranteeing the “child” legal protection “before and after birth.”

One proposal would include church officials on the ministry’s expert council on biomedical ethics. The church has had a similar council since 1998.

“The ministry’s bill cites advanced cell technology that is not widely used in Russia,” a church official said. “At the same time, there are simpler technologies which also use fetal cells as biological material, and these are quite widespread.”

The letter sent to Minister Golikova mentions valid patents for using fetal cells in anti-aging treatments, mesotherapy and fetal tissue implants.

The bill, drafted by the Ministry of Healthcare, is currently in the public discussion stage, and could be submitted to the lower house this spring. Given current legislative trends, the church may well expect that its proposals will be heeded. However, Russian scientists involved in stem cell research fear that the bill would entirely halt research in this area.

According to Sergei Kiselyov from the Human Stem Cells Institute, very few cell technologies are actually used in medicine. The bill would drastically limit the current research and could affect projects that are already underway. This would lead to Russia’s lagging even further behind Western biotechnology, he said.

Kommersant

Russia Joins OECD Convention Against Bribery

The Russian Foreign Ministry notified the Organization for Economic Cooperation and Development (OECD) on Friday that Russia has joined the OECD Convention on Combating Bribery of Foreign Public Officials in International Business Transactions. Experts believe that joining the convention will stimulate the fight against corruption. Russia will be the 39th state party to the convention as of April 17.

The State Duma ratified the convention on January 13, 2012, and President Dmitry Medvedev signed it into law on February 1. Medvedev said at a judiciary meeting, “Accession will harmonize our legal system with international standards in the fight against corruption.”

“We have not joined this convention to please anybody,” First Deputy Foreign Minister Andrei Denisov clarified. “Joining is important in terms of our internal anti-corruption policy.”

Denisov added that ratifying the convention, a three-year process, is a condition for OECD accession. Russia, he said, will seek to join the organization in 2013, but the country will have to ratify 160 other conventions and instruments in 22 categories, including the introduction of international standards for economic statistics. Joining the anti-bribery convention requires Russia to pay annual dues of about 100,000 euros per year to the OECD Working Group on Bribery in International Business.

The convention was signed in 1997 and entered into force in February 1999. Most European countries are members, as are some Latin American countries and the United States. The main obligation for the states parties is to track and prosecute their citizens for bribery or attempted bribery of foreign officials and to track foreign officials on their territories who take bribes. The convention recommends not only criminalizing these acts, but also blacklisting the companies found guilty of bribing foreign public officials from tenders for government contracts. The convention discourages the practice of allowing income tax deductions for bribes to officials of foreign states: some companies in developing countries having been implicated in this practice. The convention aims to prevent parties from adding to corruption not only within their borders, but also beyond. However, fewer than 20% of participating countries actively apply the convention's provisions, according to a 2011 Transparency International report.

Even before ratifying the convention, Russia adopted a series of measures to fulfill it. In April 2011, Dmitry Medvedev's anti-corruption package introduced amendments to the Criminal Code, including multiple penalties for giving and receiving bribes, as well as mediation. Foreign officials as well as companies that give bribes to foreign officials or officials of international public organizations will be held liable.

Vladimir Yuzhakov, director of the Department for Administrative Reform at the Center for Strategic Studies, said that the practice of applying the convention will provide additional incentives to fight corruption in the country in general. Yuzhakov expects that the convention will require further steps in developing anti-corruption legislation – in particular, the introduction of more stringent procedures for investigating cases of bribery of foreign public officials.

RIA Novosti is not responsible for the content of outside sources.

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Russian Press – Behind the Headlines, February 20

Public release date: 17-Feb-2012
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Contact: Erin Tornatore
erin.tornatore@childrens.harvard.edu
617-919-3110
Children's Hospital Boston

Boston, Mass. ? Some 90 percent of people are exposed to the Epstein Barr virus (EBV) at some point in their life. Even though it is quickly cleared from the body, the virus can linger silently for years in small numbers of infected B cells. According to researchers at Children's Hospital Boston and the Immune Disease Institute (IDI), the immune system subdues the virus by watching for a single viral protein called LMP1, knowledge that has already helped suggest two new treatments for the EBV-fueled cancers seen in some immunosuppressed patients.

The study team, led by Klaus Rajewksy, MD, and Baochun Zhang, MD, PhD, of the Program in Cellular and Molecular Medicine at Children Hospital Boston and the IDI, reported their results online this week in the journal Cell.

While the immune system's T cells rapidly clear most EBV-infected B cells, about one in a million infected cells escapes destruction. Within these cells, the virus enters a latent phase, kept in check by the watchful eye of so-called memory T cells. This uneasy relationship usually holds steady the rest of a person's life, unless something ? such as infection with HIV or use of anti-rejection drugs following a transplant ? suppresses the immune system and breaks the surveillance. The virus can then reawaken and drive the development of B cell cancers like AIDS-associated B cell lymphoma and post-transplant lymphoproliferative disorder.

To better understand how the immune system maintains its watch and how the virus turns cells cancerous, Rajewsky and his team had generated a model mimicking latent EBV infection by engineering mice whose B cells contained an inducible version of viral LMP1. Researchers have long known that EBV needs LMP1 to turn B cells cancerous, but modeling this relationship in vivo had proven challenging.

“We had previously attempted to develop an animal model of LMP1 transformation of B cells,” said Rajewsky, who recently moved to the Max Delbr?ck Center for Molecular Medicine in Germany, “but we had never been able to get the mice in our models to actually produce any mature B cells. The immune response against the LMP1-producing B cells was so robust that the cells were eliminated very early on.”

Their breakthrough came when Zhang and colleagues reengineered the model to lack T cells. “The mice were initially fine, but succumbed within two to three months to aggressive B cell lymphomas,” Rajewsky said. “The profile mimicked very closely what we see in immunosuppressed lymphoma patients.” In additional experiments with Rajewsky's original model, the team eliminated the mice's T cells before activating the viral protein in B cells, sparking a similar but even more rapid fatal disease.

The team also made several observations with possible clinical application. First, they noted that in the mouse model the LMP1 producing B cells were being attacked by a specific kind of T cell called a CD4+ T cell. “Transplant patients who develop B cell lymphomas because they are immunosuppressed by their anti-rejection drugs are often treated with T cells that carry the CD8 marker,” Rajewsky noted. “These results would argue for also considering CD4+ T cells for treatment.”

Second, they found that tumors in the LMP1 producing mice often displayed targets recognized by another kind of immune cell called a natural killer (NK) cell. Seeing an opportunity, Rajewsky worked with cancer immunologist Glenn Dranoff, MD and colleagues at Dana-Farber Cancer Institute, to test a potential therapeutic agent that uses a portion of the NK cell activating receptor called NKG2D, fused to the stimulatory Fc portion of an antibody, a combination capable of activating and directing immune attack against tumor cells. In a transplantation model of LMP1-fueled lymphomas, the NKG2D-Fc fusion proved quite capable of reducing tumor growth and prolonging survival of the recipients.

“These preclinical results suggest administration of the NKG2D-Fc fusion protein, perhaps combined with treatment with CD4+ T cells, could benefit some patients with EBV-driven lymphomas,” Rajewsky said. “What we can say with certainty, though, is that LMP1 is the immune system's primary surveillance trigger following EBV infection and clearance, knowledge that we think will open doors to additional treatment options.”

###

This study was supported by the National Cancer Institute, the National Institute of Allergy and Infectious Diseases, the Leukemia and Lymphoma Society, the Japan Society for the Promotion of Science, and the Astellas Foundation for Research on Metabolic Disorders.

Children's Hospital Boston is home to the world's largest research enterprise based at a pediatric medical center, where its discoveries have benefited both children and adults since 1869. More than 1,100 scientists, including nine members of the National Academy of Sciences, 11 members of the Institute of Medicine and nine members of the Howard Hughes Medical Institute comprise Children's research community. Founded as a 20-bed hospital for children, Children's Hospital Boston today is a 395 bed comprehensive center for pediatric and adolescent health care grounded in the values of excellence in patient care and sensitivity to the complex needs and diversity of children and families. Children's also is the primary pediatric teaching affiliate of Harvard Medical School. For more information about research and clinical innovation at Children's, visit: http://vectorblog.org.

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A single protein helps the body keep watch over the Epstein-Barr virus

THURSDAY, Feb. 16 (HealthDay News) — Women with rheumatoid arthritis or systemic lupus erythematosus often have fewer children than they'd hoped for, according to a new study.

These autoimmune diseases, which typically develop during women's reproductive years, cause fertility problems and miscarriage, researchers said.

Lupus causes the body's immune system to attack healthy tissues and organs. Rheumatoid arthritis leads to painful joint inflammation.

For the study, researchers asked 578 women with rheumatoid arthritis and 114 women with lupus about their reproductive health, and divided them into three groups according to how their condition affected their desire and ability to have children.

Group A included women who had fewer children than planned. Group B was comprised of women who had number of children they had planned for, and women in Group C were no longer interested in having children due to their concerns about how their illness would affect their children.

More than 60 percent of the women surveyed fell into Group C and no longer wanted to have children, according to the study appearing Feb. 16 in Arthritis Care & Research.

“Our study highlights important reproductive health concerns for women with [rheumatoid arthritis and lupus],” study author Dr. Megan Clowse said in a journal news release.

Of the remaining women, 55 percent with rheumatoid arthritis and 64 percent of those of those with lupus had fewer children than originally planned.

Among these women, those with rheumatoid arthritis had an infertility rate of 42 percent, or 1.5 times higher than those in group B. Both groups had similar rates of miscarriage.

Women with lupus who had fewer children than planned had the same number of pregnancies as those in Group B, but their miscarriage rate was three times higher.

The authors concluded that informing women with lupus and rheumatoid arthritis about their medical options during pregnancy and how to control their disease will help them achieve their family planning goals.

“Further study of the underlying causes of infertility and pregnancy loss in women with [rheumatoid arthritis and lupus] is needed to help fulfill their desire for children,” Clowse said.

More information

The U.S. Department of Health and Human Services provides more information on women and autoimmune diseases.

Original post:
Lupus, Rheumatoid Arthritis Linked to Fertility Woes, Miscarriage

Public release date: 16-Feb-2012
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Contact: Dawn Peters
healthnews@wiley.com
781-388-8408
Wiley-Blackwell

New research shows that more than half of women with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) have fewer children than desired. While patient choice has some influence on the smaller family size, findings published today in Arthritis Care & Research, a journal of the American College of Rheumatology (ACR), suggest that higher rates of infertility and miscarriage may also impact the number of offspring born to women with these chronic conditions.

According to the ACR up to 322,000 U.S. adults have systemic lupus?a disease in which the body's immune system becomes overactive and attacks healthy cells, tissues, or organs. Roughly 1.3 million adult Americans suffer from RA, a chronic autoimmune disease that causes painful joint inflammation. Medical evidence reports that both RA and SLE are more common in women, and onset often occurs during reproductive years which can lead to challenges in family-building.

To further understand the role of infertility, pregnancy loss and family size choice in women with RA and SLE, Megan Clowse, M.D., Kaleb Michaud, Ph.D. and colleagues from institutes across the U.S. surveyed 1,017 female participants in the National Data Bank for Rheumatic Diseases. Respondents to the reproductive-health questionnaire included 578 women with RA and 114 with SLE, who based upon their responses, were then categorized as: those interested in having children at symptom onset who had either fewer children than planned (group A) or the same number as planned (group B), and those no longer interested in having children at diagnosis (group C).

Study findings reveal that over 60% of respondents were in group C. Researchers found that 55% of women with RA and 64% with SLE had fewer children than originally planned. Women with RA who were in group A had an infertility rate 1.5 times higher than those in group B, but both groups had similar rates of miscarriage. Women with SLE in group A had a similar number of pregnancies as those in group B, but a 3-fold higher miscarriage rate.

Overall the infertility rate among participants with RA was 42% in women who had fewer children than desired. In women diagnosed with RA during childbearing years the infertility rate was higher than in those diagnosed after childbearing was complete. For participants with SLE no significant increase in infertility was noted. However, among women with lupus having fewer children than desired was associated with pregnancy loss. The authors suggest that patient education to enhance awareness of safe medical options during pregnancy and effective control of these autoimmune diseases will assist women with achieving their childbearing goals.

“Our study highlights important reproductive-health concerns for women with RA and lupus,” said Dr. Clowse. Study findings reported that concerns about inability to care for their children, adverse effects from medications taken during pregnancy, and genetic transmission of their disease to offspring lead to fewer pregnancies in women with RA and SLE. “Further study of the underlying causes of infertility and pregnancy loss in women with RA and SLE is needed to help fulfill their desire for children,” concludes Dr. Clowse.

###

This study is published in Arthritis Care & Research. Media wishing to receive a PDF of this article may contact healthnews@wiley.com

Full citation: “The Effects of Infertility, Pregnancy Loss, and Patient Concerns on Family Size of Women with Rheumatoid Arthritis and Systemic Lupus Erythematosus.” Megan E. B. Clowse, Eliza Chakravarty, Karen H. Costenbader, Christina Chambers, Kaleb Michaud. Arthritis Care & Research; Published Online: February 16, 2012 (DOI: 10.1002/acr.21593).

About the Journal: Arthritis Care & Research is an official journal of the American College of Rheumatology (ACR), and the Association of Rheumatology Health Professionals (ARHP), a division of the College. Arthritis Care & Research is a peer-reviewed research publication that publishes both original research and review articles that promote excellence in the clinical practice of rheumatology. Relevant to the care of individuals with arthritis and related disorders, major topics are evidence-based practice studies, clinical problems, practice guidelines, health care economics, health care policy, educational, social, and public health issues, and future trends in rheumatology practice. The journal is published by Wiley-Blackwell on behalf of the American College of Rheumatology (ACR). For more information, please visit http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)2151-4658.

About Wiley-Blackwell:

Wiley-Blackwell is the international scientific, technical, medical, and scholarly publishing business of John Wiley & Sons, with strengths in every major academic and professional field and partnerships with many of the world's leading societies. Wiley-Blackwell publishes nearly 1,500 peer-reviewed journals and 1,500+ new books annually in print and online, as well as databases, major reference works and laboratory protocols. For more information, please visit http://www.wileyblackwell.com or our new online platform, Wiley Online Library (http://www.wileyonlinelibrary.com), one of the world's most extensive multidisciplinary collections of online resources, covering life, health, social and physical sciences, and humanities.

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Women with rheumatoid arthritis and lupus give birth to fewer children

BLACKSBURG, VA —

While doctors say she is not at risk, Jody Woodward knows all about polycistic kidney disease.

“As a little girl I used to go to with my grandmother to Charlottesville to be on dialysis and I used to watch the machines,” said Woodward.

The home health nurse wanted to donate a kidney to her cousin — when that didn't work out… she contacted the Medical Center at UVA in August, and by December, the procedure to give Doug Farmer, of Bluefield, West Virginia, a kidney, was all set.

“I didn't feel like I was giving him life, only God gives life. But I felt like I was giving him quality of life.”

Policy at UVA's hospital says the donor and recipient are not permitted to meet for one year…and in that case, the recipient must contact the donor. But both Farmer and Woodward had the meeting of a lifetime before the surgery ever began.

“Next thing you know, him and his family are all in the doorway, and we're all hugging and crying. It was a great moment. It ranks up there with the birth of my children.”

A t-shirt that reads thank you to uva's transplant team…reminds woodward of the bond that can be made between Hokies and Wahoos.

“I have seen what in stage renal failure does to families. If you can make a difference in one person's life that's what we need to do.”

Her efforts are just one page in what she hopes will be a new chapter in fighting this disease.

Read more from the original source:
Blacksburg nurse gives kidney to stranger as Christmas gift

BLACKSBURG, VA —

While doctors say she is not at risk, Jody Woodward knows all about polycistic kidney disease.

“As a little girl I used to go to with my grandmother to Charlottesville to be on dialysis and I used to watch the machines,” said Woodward.

The home health nurse wanted to donate a kidney to her cousin — when that didn't work out… she contacted the Medical Center at UVA in August, and by December, the procedure to give Doug Farmer, of Bluefield, West Virginia, a kidney, was all set.

“I didn't feel like I was giving him life, only God gives life. But I felt like I was giving him quality of life.”

Policy at UVA's hospital says the donor and recipient are not permitted to meet for one year…and in that case, the recipient must contact the donor. But both Farmer and Woodward had the meeting of a lifetime before the surgery ever began.

“Next thing you know, him and his family are all in the doorway, and we're all hugging and crying. It was a great moment. It ranks up there with the birth of my children.”

A t-shirt that reads thank you to uva's transplant team…reminds woodward of the bond that can be made between Hokies and Wahoos.

“I have seen what in stage renal failure does to families. If you can make a difference in one person's life that's what we need to do.”

Her efforts are just one page in what she hopes will be a new chapter in fighting this disease.

See more here:
Blacksburg gives kidney as Christmas gift

By Andre Picard, The Globe and Mail THE CANADIAN PRESS

TORONTO — Children with juvenile arthritis are four times more likely to develop cancer as other kids, a new study shows.
But the research, published in the medical journal Arthritis & Rheumatism, suggests that the powerful drugs used to treat the debilitating illness are not to blame. Rather it is the disease itself, which can wreak havoc with the immune system, that seems to hike cancer risk.

“This paper is good news. It provides reassurance that these drugs — which really improve the quality of life of these kids — are safe,” Dr. Ronald Laxer, a staff rheumatologist at the Hospital for Sick Children in Toronto, said in an interview. He was not involved in the research.
Children with juvenile idiopathic arthritis are often treated with tumour necrosis factor inhibitors. In 2009, after more than a decade on the market, the U.S. Food and Drug Administration placed a “black box” warning on the drugs, stating that they were associated with a higher risk of cancer.
This caused widespread consternation because, Laxer said: “These biologics have been dramatically helpful.”
He said the increased risk of cancer in children with JIA is concerning but must also be kept in perspective.
Childhood cancer is rare — about 14 cases per 100,000 — so a four-fold increase still means juvenile arthritis sufferers have a low risk, about 64 per 100,000.
Children with juvenile arthritis experience symptoms similar to adults with rheumatoid arthritis including joint pain, swelling, tenderness and stiffness. The inflammation can be so damaging that they require joint replacements.
JIA affects about 10,000 Canadian children, according to the Canadian Arthritis Network.
The new study was conducted by a team led by Dr. Timothy Beukelman of the University of Alabama at Birmingham.
They used U.S. Medicaid records from 2000 to 2005 to identify 7,812 children with JIA, and compared their health outcomes with those of children with two other chronic conditions, asthma and attention-deficit hyperactivity disorder.
The rate of cancer was 4.4 times higher among the children with juvenile arthritis.
However, the research showed that cancer rates were more or less the same in JIA patients treated with TNF inhibitors, another commonly used drug called methotrexate and those who received little treatment.
“While children with JIA have a higher incidence of cancer compared to peers without JIA, the greater frequency of malignancy does not appear to be necessarily associated with treatment,” Beukelman said.
About 19 per cent of juvenile arthritis sufferers were treated with TNF inhibitors, principally one drug etanercept. Another 44 per cent were treated with methotrexate, and five per cent with other immune modulating drugs. One-third of the children received no prescription drug treatments, though most take over-the-counter painkillers.
In a commentary also published in Arthritis & Rheumatism, Kenan Onel, a pediatric cancer researcher at the University of Chicago, said the findings of the study “are at once concerning and reassuring for physicians, parents and patients.”
He said that while there has been much concern about the cancer risk posed by drug treatments, “we have perhaps markedly understated the more significant risk of the disease itself.”
Juvenile idiopathic arthritis is one of the most common chronic illnesses in children. In about half of cases, children go into remission, meaning their symptoms disappear. But the disease can do a lot of damage, which can limit the activities of JIA sufferers in childhood and through to adulthood.
Laxer said one of the most significant problems is that it tends to take a long time for children to be diagnosed, with their complaints often dismissed as growing pains.
“It’s important for people to know that kids can get arthritis too, not just little old ladies,” he said.

Visit link:
Study looks at cancer risk for kids with juvenile arthritis: drugs not to blame

In Remaking Eden (Harper Perennial, 1998), geneticist Lee Silver envisioned a future in which humanity has split into two species: “Naturals,” the poor slobs who muddle along with the genes that nature gave them, and the “GenRich,” who can afford to boost their physical and mental talents via genetic engineering. Silver warns that over time, “the genetic distance between the Naturals and the GenRich has become greater and greater, and now there is little movement up from the Natural to GenRich class.”

We don’t have to wait until science catches up to science fiction for this unjust dystopia to be realized. It’s happening now, in the United States, as a result of policies that favor the rich at the expense of un-rich. Scholars are confirming with empirical studies what Occupy Wall Street protesters have been saying: our system is unfairly rigged in favor of the haves, who keep pulling away from have-nots.

Education can help the poor climb their way to a higher socioeconomic status. But according to Sabrina Tavernise of The New York Times, several studies have shown that “the achievement gap between rich and poor children is widening, a development that threatens to dilute education’s leveling effects.”

Race plays less of a role than it once did in this widening chasm. A study published last year by sociologist Sean Reardon found that the difference between standardized test scores of blacks and whites has narrowed since 1960, while the difference between low-income and wealthy students has surged 40 percent. “We have moved from a society in the 1950s and 1960s,” Reardon told The Times, “in which race was more consequential than family income, to one today in which family income appears to be more determinative of educational success than race.”

The simplest explanation for the divide is that the rich can afford to send their children to better schools, hire private tutors for them and give them other advantages. In 1972, affluent parents spent five times as much on their children, on average, as low-income parents; by 2007, that difference had almost doubled, to nine to one. “The pattern of privileged families today is intensive cultivation,” sociologist Frank Furstenberg told The Times.

The federal tax code is also stacked against the poor. The code caps taxes on long-term capital gains and dividends at 15 percent, which is why Mitt Romney is taxed at a lower rate than a grade-school teacher. Far from being progressive, with percentages rising with income, the tax code is regressive in this key area. Those who work for a living pay more in taxes, percentage-wise, than those who live off investments.

Political scientist Andrew Hacker documents the depths of our inequality in “We’re More Unequal Than You Think,” in The New York Review of Books this month. He estimates that since 1985 “the lower 60 percent of households have lost $4 trillion, most of which has ascended to the top 5 percent.” U.S. economic policies, Hacker says, now serve as a “giant vacuum cleaner” sucking money from low-income people and showering it upon the rich.

Economists quantify the inequality of a society on a scale called the Gini index. If everyone has the same income, the Gini index is zero; if one person makes all the moola, the Gini index is one. The U.S. Gini index has risen from .359 in 1972 to .440 in 2010, an increase of more than 20 percent, Hacker reports. In contrast, the Gini index of socialist Sweden is .230.

Hacker notes that “in a not-so-distant past, families of modest means made enough to put something aside for their children’s college fees. That cushion is gone, which is why millions of undergraduates are now forced to take much larger loans. Adding interest and penalties, many will face decades paying off six-figure debts.” (I’m facing this financial challenge myself; my son is entering college next fall and my daughter a year later.)

The U.S. exemplifies the Matthew effect, a sociological term that alludes to a passage in the Gospel of Matthew: “For to all those who have, more will be given, and they will have an abundance; but from those who have nothing, even what they have will be taken away.”

Our current presidential race features several Christian candidates—Rick Santorum, Newt Gingrich and Romney—who seem to view the Matthew effect as the Eleventh Commandment. These men trumpet their religiosity and rectitude, and yet they advocate economic policies that benefit the rich and hurt the poor, violating the most basic rules of moral decency. Naturals must join together with rich people with a conscience to create a more economically just society.

Image courtesy Wikimedia Commons, www.flickr.com/tracy_olson.

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Education Isn't Helping Americans Overcome Deepening Inequality

You might not know this from listening to the American Diabetes Association or Paula Deen, the new face of the disease, but the first line of defense against type 2 diabetes is weight loss.

So many comments came in to my post on Paula Deen's diabetes announcement, “Weighing in on Paula Deen,” that I thought it was worth revisiting a related column. The question came from a reader:

I have been diagnosed with type 2 diabetes and am very confused about insulin resistance, and what carbohydrates I can and cannot eat. So much of what I read is contradictory.

The first line of defense against type 2 diabetes is weight loss, but you would never know it from listening to Paula Deen, the celebrity Southern cook who recently announced that she has this disease, or even to the American Diabetes Association.

Having diabetes is no joke. It is a leading cause of blindness, kidney failure, leg and foot amputations, and premature death.

The disease comes in two forms — type 1 and type 2 — but type 2 accounts for 95 percent of cases. In both, levels of blood sugar are too high as a result of problems with insulin, a hormone that enables the body to use blood sugar for energy. But the reasons differ.

Type 1 is an autoimmune disease. It causes the pancreas to stop making insulin or not make enough. Type 1 is not yet preventable and requires insulin treatment. In type 2, insulin may be available, but body tissues resist its use.

Being overweight is the key factor in type 2. Most people can prevent it by not gaining weight. And most people with the type 2 disease can eliminate symptoms by losing some weight. Genetics is certainly a factor — many overweight people never develop the disease — but 85 percent or more of people diagnosed with type 2 diabetes are overweight or obese.

In genetically predisposed people, being overweight causes insulin resistance. Metabolism does not handle excess calories very well, and this means calories from any source, not just carbohydrates.

FAST FOOD, SOFT DRINKS

Children and adults who habitually consume fast food as well as soft drinks tend to take in more calories and weigh more and are more likely to develop symptoms than people who eat healthier diets and are more active.

This makes healthy eating and physical activity the most important approaches. The vast majority of overweight people at risk of type 2 diabetes can prevent symptoms by losing a few percent of their body weight and doing a couple of hours a week of moderate — not necessarily vigorous — physical activity. The same works for treatment. Some people will still need medications, but the drugs work better with diet and physical activity.

As the Centers for Disease Control and Prevention puts it: “[A]ll diabetes-care programs should make healthy weight a priority.”

Dietary advice for type 2 diabetes is the same as advice for everyone else: Eat a wide variety of relatively unprocessed foods, especially vegetables, fruits, and whole grains, and don't consume too much junk food or too many sugary beverages.

Scientists may argue endlessly about the relative importance of calories, sugars, and refined carbohydrates in the diets of people with type 2 diabetes, but everyone agrees that eating less of all three would help resolve symptoms.

Why isn't weight loss better recognized as a treatment strategy? Paula Deen's announcement said nothing about losing weight.

The ADA does talk about weight loss on its website, but you must search hard through several complicated screens before you find, “Losing just a few pounds through exercise and eating well can help with your diabetes control and can reduce your risk for other health problems.”

PHARMACEUTICALS

I can't help wondering if the lack of prominence given to weight loss might have something to do with the influence of pharmaceutical companies.

A few years ago, I gave a talk on the importance of weight loss in control of type 2 diabetes at an ADA annual meeting. Although many conference talks dealt with drug treatment, mine was the only one on diet — except for a session on sugars sponsored by Coca-Cola.

The exhibit hall was packed with drug company representatives dispensing free pens, writing pads, books, lab coats and stethoscopes — all with corporate logos.

The influence of drug companies on diabetes advice is worth attention. Deen represents a drug that costs hundreds of dollars a month. Drug companies give the ADA millions every year.

Eating less and being active make no money for anyone (unless people can be induced to join commercial weight-loss programs).

Losing weight is a losing battle for many people. It's hard to lose weight in today's “eat more” food marketing environment.

TEACHABLE MOMENT

But a diagnosis of type 2 diabetes should be a teachable moment. Shouldn't the ADA more strongly urge people with the disease to eat less, eat better, and move more, and help everyone find ways to cope with “eat more” messages?

The health and economic costs of type 2 diabetes, and its preventability, are reason enough to demand changes in the food environment. The ADA should be working hard to make it easier for everyone to eat more healthfully, be more active, and avoid the need for a lifetime of diabetes medications.

Image: upthebannerShutterstock.

This post also appears on Food Politics, an Atlantic partner site.

Read more here:
How to Fight Type 2 Diabetes

Children with juvenile idiopathic arthritis (JIA), the most common form of childhood arthritis, may be at higher risk of developing cancer than children who do not have the condition, according to a new study published in the journal Arthritis & Rheumatism.

Researchers identified 7,812 children with JIA and compared them with thousands of children not affected by JIA and found that the arthritic children developed about four times as many new growths considered likely to be cancerous as children who did not have arthritis. They followed the children for about 18 months.

Also Read

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Juvenile Idiopathic Arthritis May Raise Kids' Cancer Risk

Public release date: 13-Feb-2012
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Contact: Dawn Peters
healthnews@wiley.com
781-388-8408
Wiley-Blackwell

New research reports that incident malignancy among children with juvenile idiopathic arthritis (JIA) is four times higher than in those without the disease. Findings now available in Arthritis & Rheumatism, a journal published by Wiley-Blackwell on behalf of the American College of Rheumatology (ACR), suggest JIA treatment, such as tumor necrosis factor (TNF) inhibitors, does not necessarily explain the development of cancer in this pediatric population.

Children with JIA experience symptoms similar to adults with arthritis including joint pain, swelling, tenderness and stiffness. JIA is a general term used to describe the various chronic arthritis diseases in children and affects roughly 294,000 under the age of 17 in the U.S. according to a 2008 report from the National Arthritis Data Workgroup.

One of the drug types used to treat childhood and adult arthritis, along with a number of other rheumatic conditions, is TNF inhibitors. Studies have reported that more than 600,000 people worldwide have received anti-TNF therapy since their introduction 15 years ago. However, possible cancer risk has been associated with treatment, prompting the U.S. Food and Drug Administration (FDA) to place “black box” warnings of the potential malignancy risk on TNF inhibitors labels.

In the present study Dr. Timothy Beukelman from the University of Alabama at Birmingham and colleagues conducted one of the largest investigations into the rates of incident malignancy among JIA pediatric patients relative to their treatment. Using data from the U.S. Medicaid records from 2000 through 2005, researchers identified 7,812 children with JIA and two comparator groups without JIA; one group with asthma (652,234 children) and the second with attention-deficit hyperactivity disorder (ADHD; 321,821 children).

The team categorized patients' treatment with methotrexate and TNF inhibitors as “ever” or “never” used, though many children with JIA did not receive either of these treatments during the study. The research team did not have access to detailed medical records, and therefore categorized the identified incident malignancies as “possible,” “probable,” or “highly probable.”

Children diagnosed with JIA had a total follow-up time of 12,614 person-years with 1,484 children in this group contributing 2,922 person-years of anti-TNF exposure. The team determined that among all children with JIA compared to those without JIA, the incidence rate was 4.4 times higher for probable and highly probable malignancies. Pediatric JIA patients treated with methotrexate without TNF inhibitors had a similarly increased incidence of cancer, which was 3.9 times higher than children without JIA. No probable or highly probable malignancies were identified in patients following any use of anti-TNF during the study period.

In a related editorial published today in Arthritis & Rheumatism, Dr. Karen B. Onel and Dr. Kenan Onel from the University of Chicago state that the Beukelman et al. study indicates that children with JIA may be at increased cancer risk from the disease, but suggests that anti-TNF therapy may not be associated with a further increased cancer risk. Dr. Kenan Onel cautions, “Larger studies in different populations and with longer follow up are required to confirm Dr. Beukelman's findings.”

The editorial authors point out that most patients in this study were treated with etanercept, a soluble TNF receptor blocker, and the investigation of other anti-TNF agents working by different mechanisms may yield different results. Nonetheless, Dr. Onel argues, “By focusing on the possible cancer risk associated with the use of TNF inhibitors, the underlying cancer risk associated with JIA may have been understated, and it is important to make patients, families, and physicians aware of the possible late consequences of this disease.”

Dr. Beukelman concludes, “While our findings show children with JIA have a higher incidence of cancer compared to peers without JIA, the greater frequency of malignancy does not appear to be necessarily associated with treatment, including use of TNF inhibitors. This highlights the critical importance of appropriate comparator groups when evaluating the safety of new medications. Further confirmation of our findings with large-scale and long-term investigation of the association between cancer and JIA, and its treatment is needed.”

###

This research was supported by grants from the Agency for Healthcare Research and Quality (AHRQ), the Food and Drug Administration (FDA) U.S. Department of Health and Human Services (DHHS), and the National Institutes of Health (NIH).

This study is published in Arthritis & Rheumatism. Media wishing to receive a PDF of this article may contact healthnews@wiley.com

Full citations: “Rates of Malignancy Associated with Juvenile Idiopathic Arthritis and Its Treatment.” Timothy Beukelman, Kevin Haynes, Jeffrey R Curtis, Fenglong Xie, Lang Chen, Christina J. Bemrich-Stolz, Elizabeth Delzell, Kenneth G Saag, Daniel H Solomon, James D Lewis on behalf of the Safety Assessment of Biological thERapeutics (SABER) Collaboration. Arthritis & Rheumatism; Published Online: February 13, 2012 (DOI: 10.1002/art.34348).

URL Upon publication: http://doi.wiley.com/10.1002/art.34348.

Editorial: “TNF inhibitors and Cancer in JIA: Disentangling the Web.” Karen B Onel and Kenan Onel. Arthritis & Rheumatism; Published Online: February 13, 2012 (DOI: 10.1002/art.34349).

URL Upon publication: http://doi.wiley.com/10.1002/art.34349.

Author Contacts: To arrange an interview with Dr. Beukelman, please contact Bob Shepard with the University of Alabama at Birmingham at bshep@uab.edu . Media wishing to speak with Dr. Karen B. Onel or Dr. Kenan Onel may contact John Easton with the University of Chicago Medical Center at John.Easton@uchospitals.edu .

About the Journal:

Arthritis & Rheumatism is an official journal of the American College of Rheumatology (ACR) and the Association of Rheumatology Health Professionals (ARHP), a division of the College, and covers all aspects of inflammatory disease. The American College of Rheumatology (www.rheumatology.org) is the professional organization who share a dedication to healing, preventing disability, and curing the more than 100 types of arthritis and related disabling and sometimes fatal disorders of the joints, muscles, and bones. Members include practicing physicians, research scientists, nurses, physical and occupational therapists, psychologists, and social workers. The journal is published by Wiley-Blackwell on behalf of the ACR. For more information, please visit http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1529-0131.

About Wiley-Blackwell:

Wiley-Blackwell is the international scientific, technical, medical, and scholarly publishing business of John Wiley & Sons, with strengths in every major academic and professional field and partnerships with many of the world's leading societies. Wiley-Blackwell publishes nearly 1,500 peer-reviewed journals and 1,500+ new books annually in print and online, as well as databases, major reference works and laboratory protocols. For more information, please visit www.wileyblackwell.com or our new online platform, Wiley Online Library (wileyonlinelibrary.com), one of the world's most extensive multidisciplinary collections of online resources, covering life, health, social and physical sciences, and humanities.

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

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Cancer rate 4 times higher in children with juvenile arthritis

Children with juvenile idiopathic arthritis (JIA), the most common form of childhood arthritis, may be at higher risk of developing cancer than children who do not have the condition, according to a new study published in the journal Arthritis & Rheumatism.

Researchers identified 7,812 children with JIA and compared them with thousands of children not affected by JIA and found that the arthritic children developed about four times as many new growths considered likely to be cancerous as children who did not have arthritis. They followed the children for about 18 months.

“Based on the data, it appears that being diagnosed with JIA increases the likelihood of developing malignancies,” said Dr. Timothy Beukelman, the study's lead author and an associate professor of pediatrics at the University of Alabama at Birmingham.

But despite the statistically higher risk, Dr. Sampath Prahalad, associate professor of pediatrics and human genetics at the Emory University School of Medicine, said cancer in children with JIA is rare.

“The risk is very low, and it's more common for children with JIA to not get cancer,” he said. The study included only 7,812 children with JIA, and nationwide, there are about 300,000. Prahalad was not involved with the research.

Beukelman said there are a number of possible explanations for the finding, but so far, no one knows why JIA may predispose children to cancer. He stressed, however, that there was no association between cancer risk and any treatments for the condition, including the use of drugs known as tumor necrosis factor (TNF) inhibitors.

TNF inhibitors, including the brand-name drugs Enbrel and Humira, are considered by doctors to be revolutionizing treatments that can sometimes stop rheumatoid arthritis in its tracks.

But there have been a number of case reports linking the use of TNF inhibitors to an increased cancer risk in children, prompting the Food and Drug Administration (FDA) to add a black box warning to these drugs in 2009. A black box warning is the strongest warning used by the FDA and indicates a drug has potentially life-threatening effects.

“The initial concern about TNF inhibitors may have been overstated, since some of the risk likely comes from the disease itself,” Beukelman said.

Beukelman explained that when the FDA made its decision to include black box warnings on TNF inhibitors, the only data available compared children with JIA who took these drugs with healthy children.

“When we're evaluating the safety of these drugs, it's important to make comparisons to other children with the disease who didn't get the drugs and not comparisons to children in the general population,” he said.

Does Disease Itself Predispose to Cancer?

Previous studies have found a link between elevated cancer risk and certain inflammatory conditions in adults.

“There are studies that show that in adults with rheumatoid arthritis, the more severe the disease, the higher the disease activity, so the more likely the patient is to develop malignancy,” Beukelman said.

It could be, he explained, that because diseases like JIA attack the body's own immune system, the body isn't able to mount defenses against invading cancer cells.

Another possibility is that the persistent inflammation characteristic of JIA could lead to cancers, particularly in the blood cells, he said.

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Does Arthritis Raise Kids' Cancer Risk?

TORONTO – Researchers have been given the go-ahead to test stem cells from cord blood with the ultimate goal of reversing hearing loss in infants and toddlers whose inner ears have been damaged.

U.S. regulators have approved the Phase I study, which has a primary objective of determining the safety of the experimental stem cell therapy.

The therapy involves transfusing a baby's own stem cells from umbilical cord blood, banked by parents after their child's birth. Ten children aged six weeks to 18 months old with sensorineural hearing loss will be recruited for the study by doctors at Children's Memorial Hermann Hospital in Houston.

“We're looking more at the ones that suffer an injury around birth or shortly after birth,” said Dr. Samer Fakhri, a specialist in head and neck surgery and principal investigator of the study.

Fakhri, a Montreal native who received his medical training at McGill University, said such injuries to the inner ear can be caused by viral infections and even some medications.

Sensorineural hearing impairment occurs when structures in the inner ear or the nerve pathways between the inner ear and the brain are damaged. The critical structure in the inner ear is the snail-shell-shaped cochlea, which contains “hair cells” that gather electrical signals, which are transferred to the brain and perceived as sound.

A child with this kind of hearing loss can suffer significant impairment, Fakhri said from Houston. “You may hear parts of sounds. You may not hear the sounds at all, or you may hear very faint sounds.

“If they lose hearing at four weeks or five weeks due to a viral infection” — meningitis is a common cause — “we know that there is a tremendous impact,” he said.

“There's a lot of research that has been done in child development that has determined that there's really a critical window for children to develop speech, language and social development, and it's probably in the first 18 months.”

The idea for the trial was triggered by a 2008 study by European scientists, who infused human cord blood into laboratory mice with induced sensorineural hearing loss. An examination of the treated animals about two months later showed “inner ear organization and structure were basically restored,” said Fakhri.

“That was the study that was a proof of concept … That was such a dramatic result.”

Fakhri said the exact role of the stem cells in the repair of damaged tissue in the mice isn't known, but there are a couple of theories.

Stem cells can give rise to many different types of cells in the body, so it may be they effect the repair by regenerating lost hair cells. But a more recent theory suggests that stem cells may go to the site of injury and set off the body's innate repair mechanisms.

“In that sense, they play more of a supporting role,” he said.

While regenerating tissues is the great hope of stem cells — and they do appear to hold a lot of promise — the idea that they could restore damaged hearing in humans is still speculative, doctors say.

“This study is really very, very preliminary,” said Dr. Robert Harrison, a professor of head and neck surgery at the University of Toronto.

“That's the safety issue,” he said, stressing that the FDA-approved study must first ensure the stem cells do no harm to patients. Figuring out if they actually work to repair the organ of hearing would have to be proven in subsequent trials.

“We're a long way from looking at the possible therapeutic value of this in terms of restoring some sort of hearing,” said Harrison, a senior scientist at the Hospital for Sick Children and a director of the Hearing Foundation of Canada.

“It's a very theoretical concept, and in my opinion it's not going to happen soon.”

Current treatment of sensorineural hearing loss in young children is pretty well restricted to hearing aids or cochlear implants, surgically implanted electronic devices, Fakhri said. Both are used to amplify any residual hearing.

The rest is here:
Study looks at whether stem cells in cord blood might repair hearing loss in kids

Health care is dying for innovation and IVDiagnostics has no shortage of game–changing ideas to transform medicine and save lives.

“My wife has survived for 22 years with three bouts of cancer, and she is my personal inspiration,” says Valparaiso resident and IVDiagnostics CEO Frank Szczepanski.

“If you believe in the current paradigm of using an imaging test to determine if you have a solid tumor, in our opinion, that's too late. Wouldn't you rather find the cancer when it's microscopic?”

IVDiagnostics was formed to develop, test and market more effective diagnostic tools for rare circulating tumor cells (CTC), which find their way to a distant organ to start new cancer growth. CTCs are considered among the major causes for mortality among cancer patients, Szczepanski says.

With this company's technology, doctors will be able to perform a real–time diagnosis of a patient's CTCs without drawing blood.

The company's cofounders are Frank's brother, Tom, of East Chicago, and Wei He, who is a doctor of analytical chemistry and the team's lead scientist. “Our No. 1 goal is to save lives,” Frank Szczepanski says.

What's inside

IVDiagnostics is Szczepanski's ninth start–up company. Several years ago, he met Wei He who suggested a tactic of “in vivo,” or monitoring blood inside the body. Cells of two to 10 microns can be detected.

About 25 percent of the body's blood can be optically scanned in 30 minutes. The absence of needles is a benefit cancer patients are enthusiastic about, Szczepanski said.

The test, referred to as a liquid biopsy, also is more accurate and sensitive than surgical biopsies. “Once this gets to market there won't be a single doctor who won't want this for a patient,” Szczepanski said.

Repeated needle sticks common in intravenous disease treatment causes problems such as hardening of the arteries, bruising and even missed chemotherapy if clinicians can't draw blood on any given day.

The test also doesn't require administering toxic substances into the body such as radioactive materials used in some forms of images. “They have to light you up so they can diagnose and those isotopes stay in the body,” he said.

Innovation in medicine

The company also is developing a molecular test for pancreatic cancer, one of the hardest for early detection, which identifies mutations in DNA or deficiencies in certain proteins.

That test could be available in one year and also could be used as a susceptibility test. “Steve Jobs' family should have this test because they are undoubted carrying the mutation,” he says. “It's just a matter of who has it. It's scary because mutations can skip generations. If it skips you, good for you, but your children may end up getting it.”

Szczepanski says in the future both testing devices will handheld and wireless. “You can imagine the possibilities,” he says.

Patients could take the device with them so they could be monitored at home and wouldn't have to wait for routine consultations or follow–up visits.

IVDiagnostics' general target is metastatic cancer such as breast, lung, prostate, melanoma and ovarian. The company is doing live tissue sample testing now and with proper funding the entire portfolio of tests could be available within three years.

Slow burn sustainability

It takes awhile for many young firms to generate cash and survival depends on having an adequate supply of cash on hand to meet expenses.

The company was originally self–funded and in a three–year period received more than $1.5 million in seed capital from two rounds of friends and family funding. It also received $400,000 in federal funding from the National Institutes of Health and the National Cancer Institute.

IVDiagnostics was recently named The Revolutionary Technology Company of the Year by the Indiana Small Business Development Center. “The time it takes to do the research and development before a product can be marketed is hugely important,” says Bill Gregory, of the Northwest Indiana SBDC.

“You have to be able to raise all sorts of additional revenue and capital and find skilled people. They've had to do a lot to get where they've gotten. It takes passion, experience, innovation and patience to do work in biomedicine.”

In Indiana, fund investments steadily fell from $14.6 million in 2007–08 to just $6.6 million in 2009–10. “That is the legacy of this recession – not one or two missed companies, but a changed capital market,” said David Johnson, president and CEO of BioCrossroads, a statewide life sciences organization.

Private venture capital invested in life sciences within Indiana, from 2002–10 was $277 million.

Some of the partners are not taking a salary, but Szczepanski said the company is good at managing its burn rate.

Burn rate refers to the rate at which a company uses up its supply of cash over time and tells investors whether a company is self-sustaining. Companies with high cash burn rates can turn an investment into ashes.

Many other biotechnology firms have a burn rate of about $2 million per year, he said. IVDiagnostics' rate is 25 percent of that or roughly $500,000 annually.

“We have many people on our team that are sacrificing and taking equity instead of cash,” said Szczepanski. “But we can do that for only so long.”

Looking for angels

The next major round of financing hopes to secure $3 million to $5 million from angel group or venture capitalists to cover the cost of clinical trials and additional research and development.

IVDiagnostics is poised for exponential growth because of the known demand for its testing. A single community hospital has anywhere from 500 to 1,000 new cancer patients yearly and each patient could need monitoring up to five times annually.

Within five years, the company could generate $100 million in revenues. The anticipated cost to patients for the test would be $400 to $800 compared to $5,000 to $8,000 for a CAT scan.

Monitoring patients five times a year with IVDiagnostics technology compared to twice a year for an imaging test would result in annual savings of $12,000 to $15,000 per patient annually.

Worldwide, $300 billion is spent on cancer diagnosis and the United States market alone spends $124 billion. “If we can save half that amount because of better molecular medicine, the savings to the health care industry are huge,” Szczepanski says.

Restructuring Indiana's economy

Szczepanski is a leading entrepreneur who has been involved in nine startups in the last 20 years. He looks to the future and considers himself a successful technologist.

“Unless you have the vision, inspiration and perseverance to do something new, you're not an entrepreneur,” he said. “Everyone in our company shares a commonality that this is a noble cause.”

Indiana's position as a life science leader is clear and has long been thought of as the one of the state's bright economic spots.

It has weathered the recession well but tighter capital markets threaten to starve the risky process of medical innovation. That challenge is predicted to be permanently harder although the industry is still producing jobs.

The Indiana Business Research Center reported life science industry employment grew 2.9 percent between 2001 and 2007 compared to 0.2 percent for total employment and a loss of 1.9 percent for manufacturing.

According to BioCrossroads, total employment in life sciences in Indiana has held steady at around 50,000 jobs since 2007. In 2010, there were 854 establishments generating $4.3 billion in wages. The average Indiana life sciences wage was $86,537 which is more than twice the state's average wage.

The value of Indiana's life science exports totaled $9.0 billion in 2010, up from $5.0 billion in 2006.

Szczepanski sees the life sciences as the changing face of Indiana's economy – from a steelmaker in a hard hat and farmer on a tractor to a scientist in a white lab coat with a microscope.

The most important factors for success is an experienced and educated workforce. The Hoosier state is a major generator of life science graduates, so it has labor pool and an industry that can fight the brain drain of college graduates.

Szczepanski's vision for Northwest Indiana is for the university and medical communities to collaborate and form a center for advanced cancer research to accelerate molecular medicine.

“We're looking at a new form of manufacturing,” he says. “The footprint for Northwest Indiana can change its focus on steelmaking and agriculture to nano particle production and biomedical equipment which brings a higher level of jobs. It can be a motivator in our state for a different economic force to switch from raw materials processing to biotech.”

Excerpt from:
Local biotech company hopes save lives by focusing on microscopic cancer cells

Here is a eulogy for a pioneering scientist that says more about the lifelong effects of a dynamic teacher on his students than any “value-added” formula ever could.

The eulogy was delivered by Jeffrey Ravetch, head of the Leonard Wagner Laboratory of Molecular Genetics and Immunology at Rockefeller University in New York, at a memorial service last week for his former teacher and mentor, Norton Zinder, a ground-breaking geneticist and microbiologist. Zinder, who was my brother-in-law’s father, died this month at age 83.

In an era in which it is popular to make the assessment of teachers more “scientific” by using mathematical equations to determine a teacher’s worth, Ravetch’s tribute shows just how much of an art the process of teaching and mentoring really is. It’s a human exercise, not a numbers game.

Norton Zinder’s life story was classically inspirational. He was born in New York to parents who had immigrated from Eastern Europe. His father valued nothing more than education but could not afford to finish his own. He worked as a children’s dress salesman to feed his family, swearing that he would ensure his children were fully educated. He did.

Obviously brilliant as a child, Norton graduated from the Bronx High School of Science at age 15, and studied day and night to graduate from Columbia University at age 18. Then he joined Joshua Lederberg ’s famous laboratory at the University of Wisconsin as a graduate student. There he led the charge in the discovery of bacterial transduction, a process through which viruses transfer genes from one bacterium to another, one of the principal achievements for which Lederberg was awarded a Nobel Prize.

After earning his PhD, Zinder moved to Rockefeller University, where he continued to play a pivotal role in biological science and genetics over five decades. His research continued to break new ground, and he emerged — along with James Watson, the co-discoverer of DNA who became a close friend of Zinder’s — as a highly influential voice on science policy. His leadership of a committee that examined the work of the National Cancer Institute in the 1970s led to a major reorganization of the institute’s research structure.

Meanwhile, Zinder, who could be equally charming and cantankerous, managed to find time to talk to public school teachers about science, and he corresponded with an eighth grader about the youngster’s science project.

Ravetch, in his eulogy below, refers also to Zinder’s role as a founding member, along with Watson, of the Human Genome Project, a project to identify and map all of the approximately 20,000 genes on chromosomes in human cells. He also refers to Marilyn Zinder, Norton’s wife of many years who died in 2004.

Jeffrey Ravetch’s eulogy for Norton Zinder:

Norton was a larger-than-life figure in the scientific careers of his many s tudents during his 50 years at The Rockefeller University, advising, cajoling and reminding us of the impossibly high standards to which we were being held. He expected greatness; he demanded independence, creativity and critical thinking. And, above all, he wanted to see or hear something that was new and exciting. The challenge we all faced was how to say or do something interesting enough to get Norton's attention.

Patience wasn't one of his virtues. It was a common sight to see one of us following Norton down the hall, desperately trying to get him to turn around and listen to what we were saying. It was a place of energy, excitement and competition among peers. In other words, Norton's lab was a training ground for the real world of science we each aspired to conquer.

I was fortunate to have been a student of Norton's in the early ‘70's, a period of great ferment in genetic research. It was a transition period in the field, as we moved from the rigor and elegance of bacterial genetics, the field Norton pioneered and dominated, to the power and simplicity of molecular biology and recombinant DNA.

Norton was somewhat ambivalent about it all in the beginning. I convinced him to let me go up to Boston to learn the then-new technique of DNA sequencing from its inventors and to bring it back to Rockefeller, where DNA sequencing had yet to be introduced. I was eager to apply it to the freezer full of genetic mysteries that Norton had discovered during his career.

Within a few months, I had sequenced many of the phages that Norton had constructed, which provided the basis for that remarkable system of host restriction/modification, soon to be an essential component of recombinant DNA technology. Norton looked at my data and was, to my surprise, irritated.

“Trivial biochemistry,” he muttered, and walked away in a huff. What I had unwittingly done was to reduce the elegance of genetics to the triviality of a DNA sequence, a crime in Norton's pure genetic world.

However, it was a testament to Norton's commitment to science that, despite this early reaction to DNA sequencing, he was to become the champion of the Human Genome Project and the complete sequencing of our DNA. Or, as Norton once said to me: “The people who started all this are going to finish it.”

He was one of a kind, a singular, dominant intellect in the genetic revolution.

As my own career developed, I've come to understand and appreciate the enormous influence he’s had on my science. His standards weren't just high, they were nearly unattainable. When it came time to draft my thesis, Norton took me into his office and showed me the thesis he had written as a graduate student working with Josh Lederberg. It was simply a 17-page list of the strains he had constructed that led to his discovery of transduction, one of the three pillars of genetic exchange. I didn't need to be told that anything that I came up with would pale in comparison.

The lesson was clear: it wasn't good enough to be the best in your field. You had to create new fields and, in so doing, change the way everyone else understood the world.

Norton was brilliant, intuitive and often impossibly inscrutable, and for all those reasons he was a towering figure in my life and my career. He was also generous and gracious to those who worked with him, treating us as colleagues and even as members of an extended family. Being a ‘Zinderkinder,’ as he called his students, was more than being a student; it was a life-long bond with Norton and Marilyn.
I'm afraid I took that bond a bit too literally, when, a few years after I had returned to New York to start my own lab, I found myself living down the hall from Norton and Marilyn. One evening, realizing that I  needed to return to the lab to complete an experiment, I availed myself of that family bond with Norton. I left my son, then a few months old, in his care, promising to return in “just a bit.” A few hours later, I returned to find Norton, pacing up and back with a crying infant in his arms. “He cried from the minute you left. None of my children ever did that.” And while we spent the next 30 years talking about science, Rockefeller and life, we never spoke of that evening again.

And when my career eventually led me back to Rockefeller, where I took my place alongside Norton as a colleague at the university, I had the distinct sense that I was closer to understanding who Norton was and what made him inseparable from the institution where he had spent his entire career. While my research interests may have moved into immunology and away from bacterial genetics, I still enjoyed walking into Norton's office to show him some data in the hope that maybe he'd be impressed and find what I was doing interesting.

For, in the end, impressing Norton was what it was all about for many of us who trained in his lab. When I saw him this [past] summer at Cold Spring Harbor, on the occasion of his being celebrated for his contributions to the creation of modern molecular biology, I had the sense that maybe, after all, he approved. And while I will miss him as a mentor and friend, I'm comforted by the knowledge that his accomplishments, his students and his intellect are enduring and will continue to exemplify the very best in science.

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Eulogy for a brilliant mentor and teacher

In 1937, Joe Luecke called up a girl from high school to ask her if she wanted to come watch him play basketball. She said she couldn’t because her mother was making her go to church.

“My older sister said, ‘Hey, I know a girl who was next to my locker, Violet Anderson, and she’s pretty nice. Why don’t you give her a call?’” Joe said. “I asked, ‘How do you know her?’ and she said, ‘Everybody knows Violet Anderson.’”

Violet agreed to the date and went down to Kankakee to see Joe play. Seventy-five years later, the two are still together.

As the couple entered their 70th wedding anniversary party on Feb. 7 at the Carmelite Carefree Village in Darien, they were undoubtedly the talk of the room. At age 93, their happiness shone through, and they mirrored the roles of a President and First Lady in how they dressed and carried themselves.

Growing up in the Chicagoland area, Joe and Violet dated for five years before getting married because during the Great Depression, no one could afford to.

Joe worked 72 hours a week for 21 cents an hour. Six months later, Montgomery Ward opened, hiring him at 50 cents an hour.

“I thought, man, I’m going to own the country,” he said.

In 1942, the two got married, and because money was so tight, they had to basically go on a double date with another couple for their honeymoon so they could save money on gas.

Heading south, Joe and Violet realized they couldn’t get a hotel because an Elks National Convention in town had all the rooms booked, but Joe’s sister slipped the keys to her place in his pocket without him knowing.

“She already knew it was going to be all booked down there but didn’t tell him,” said their son, Brad Luecke of Downers Grove. “She made him go from hotel to hotel to hotel to try and find a spot to go to, and you know, it’s your honeymoon. … Eventually they stayed at his sister’s place.”

The honeymoon ended with them in Hot Springs, Ark.

Years into their marriage, Joe opened his own pattern shop and Violet did all the bookkeeping for it, but the two retired early and moved to Florida in 1972.

Over the course of 70 years of marriage, there are millions of little things forgotten, but it’s the priceless moments that stand out for the couple, like their children being born, countless traveling (including 14 trips to Australia) and racking up an enormous bar tab.

While at a country club in Florida, Joe hit a hole-in-one. To celebrate, normally the club picks up the bar tab with its insurance.

“We ran around in the housing development and knocked on the doors of all our friends to come down and have a drink,” Violet said. “Everyone showed up and had a drink, but the insurance didn’t cover it. We had to pay the whole bill.”

To some, Valentine’s Day, this Tuesday, has lost its luster over the years. The fact that half of all marriages end in divorce isn’t helping the holiday’s cause, either.

But for the 50-plus people watching Joe and Violet Luecke toast to their milestone — telling stories of their love the way giddy schoolkids would — the romantic feelings surrounding the week might be different.

Everyone wants to know the secret to a lasting marriage. For Joe, it’s a basic formula.

“The first thing you have to do is find a girl,” he said. “Second, she has to be pretty. Third she has to be smart and fourth, she has to be very agreeable.”

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Darien couple celebrates longevity, romance after 75 years

Public release date: 9-Feb-2012
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Contact: Lisa Lyons
elyons@cell.com
617-386-2121
Cell Press

A recent large and comprehensive analysis of 50,000 genetic variants across 2,000 genes linked to cardiovascular and metabolic function has identified four genes associated with type 2 diabetes (T2D) and six independent disease-associated variants at previously known loci. The findings, which provide valuable insight into the genetic risk for T2D across multiple ethnicities, add to the growing list of genetic variants that affect the risk of developing T2D and could pave the way for identification of valuable drug targets. The research will be published by Cell Press on February 9th in The American Journal of Human Genetics, the official journal of the American Society of Human Genetics.

Multiple environmental and genetic factors are linked with T2D, which is the most common form of diabetes. “Together, known T2D genetic variants explain only about 10% of the genetic variance, indicating that additional genetic factors are likely to contribute to disease risk,” explains senior co-author Dr. Brendan J. Keating, from The Children's Hospital of Philadelphia. “Further, previous studies have been based almost exclusively on individuals of European ancestry, and genetic contributors to T2D are less well understood in non-European populations. An important first step towards understanding genetic risk across populations is to establish whether known T2D-associated genes span ethnicities or are population specific.”

Dr. Keating, senior co-author Dr. Richa Saxena, from Massachusetts General Hospital and Harvard Medical School, and a large international cohort of colleagues undertook an ambitious genetic screening study to gain a better understanding of genetic variants associated with T2D. Their analysis, the largest T2D genomics study conducted to date, included 39 multiethnic T2D association studies representing more than 17,000 cases of T2D and 70,000 controls and was designed to assess the impact of genetic variants across multiple ethnicities.

“As a result of our large-scale genetic analysis, we uncovered previously unknown European and multiethnic genetic variants and confirmed that, together, known genetic risk factors influence T2D risk in multiethnic populations, including African-Americans, Hispanics, and Asians,” concludes Dr. Saxena. “Several additional signals were of borderline significance. Overall, our results demonstrate that this type of large multiethnic genome-wide screening study should lead to identification of additional T2D genetic variants relevant to multiple ethnic groups. Further, identification of additional genes associated with T2D may guide strategies for developing new therapeutics.”

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About The American Journal of Human Genetics

The American Journal of Human Genetics (AJHG) is ASHG?s official scientific journal, published by Cell Press. AJHG is the most highly regarded peer-reviewed journal dedicated to studies in human genetics, earning a current impact factor (2011) of 11.680. AJHG provides cutting-edge research and review articles related to genetics and genomics and the application of genetic principles in health, disease, medicine, population studies, evolution, andsocietal impacts. For more information about AJHG, visit: http://www.ajhg.org.

ABOUT THE AMERICAN SOCIETY OF HUMAN GENETICS

Founded in 1948, the American Society of Human Genetics (ASHG) is the leading professional membership organization for human genetics specialists worldwide. The nearly 8,000 members of ASHG include researchers, academicians, clinicians, laboratory practice professionals, genetic counselors, nurses, and others with a special interest in the field of human genetics. The Society?s mission is to serve research scientists, health professionals and the public by providingforums to: (1) share research results through the ASHG Annual Meeting and in The American Journal of Human Genetics (AJHG); (2) advance genetic research by advocating for research support; (3) educate current and future genetics professionals, health care providers, advocates, policymakers, educators, students, and the public about all aspects of human genetics; and (4) promote genetic services and support responsible social and scientific policies. For more information about ASHG, visit: http://www.ashg.org.

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

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Genetic risks for type 2 diabetes span multiple ethnicities

Gene therapy for congenital blindness has taken another step forward, as researchers further improved vision in three adult patients previously treated in one eye. After receiving the same treatment in their other eye, the patients became better able to see in dim light, and two were able to navigate obstacles in low-light situations. No adverse effects occurred.

Neither the first treatment nor the readministered treatment triggered an immune reaction that cancelled the benefits of the inserted genes, as has occurred in human trials of gene therapy for other diseases. The current research targeted Leber congenital amaurosis (LCA), a retinal disease that progresses to total blindness by adulthood.

Scientists from The Children's Hospital of Philadelphia and from the Perelman School of Medicine at the University of Pennsylvania led the study, published today in Science Translational Medicine.

“Patients have told us how their lives have changed since receiving gene therapy,” said study co-leader Jean Bennett, M.D., Ph.D., F.M. Kirby professor of Ophthalmology at Penn. “They are able to walk around at night, go shopping for groceries and recognize people's faces—all things they couldn't do before. At the same time, we were able to objectively measure improvements in light sensitivity, side vision and other visual functions.”

Other objective results came from brain signals seen in neuroimaging. When a dimly flickering checkerboard pattern flashed in front of a patient's recently treated eye, an area in the brain responsible for vision lit up during functional magnetic resonance imaging (fMRI).”This finding is telling us that the brain is responding to the eye's sensitivity to dim light,” said radiology researcher Manzar Ashtari, Ph.D., of The Children's Hospital of Philadelphia, the study's co-leader.

LCA is a group of hereditary retinal diseases in which a gene mutation impairs production of an enzyme essential to light receptors in the retina. The study team injected patients with a vector, a genetically engineered adeno-associated virus, which carried a normal version of a gene called RPE65 that is mutated in one form of LCA.

The researchers in the current study previously carried out a clinical trial of this gene therapy in 12 patients with LCA, four of them children aged 11 and younger when they were treated. Exercising caution, the researchers treated only one eye—the one with worse vision. This trial, reported in October of 2009, achieved sustained and notable results, with six subjects improving enough to no longer be classified as legally blind.

The Center for Cellular and Molecular Therapeutics (CCMT) at The Children's Hospital of Philadelphia sponsored both the initial clinical trial and the current study, and manufactured the vector used to carry the corrective gene. Katherine A. High, M.D., a co-author of both studies, is the director of the CCMT, and a pioneering gene therapy researcher.

The research team's experiments in animals had showed that readministering treatment in a second eye was safe and effective. While these results were encouraging, the researchers were concerned that readministering the vector in the untreated eye of the patients might stimulate an inflammatory response that could reduce the initial benefits in the untreated eye.

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Readministration of gene therapy improves vision in three patients with LCA