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Week Ending FRIDAY June 19, 2009---------------------------News Archive / Return to News Alerts

Size DOES Matter for Some Crustaceans
Oldest evidence for reproduction with giant sperm uncovered at the European Synchrotron Radiation Facility

The mystery of giant sperm present in some living animal groups today has taken on a new dimension. In one group of micro-crustaceans new evidence shows the feature is at least 100 million years old.

Renate Matzke-Karasz, from Ludwig-Maximilians-Universität Munich (Germany), has led an international team of scientists, studying specimens from the London Natural History Museum's collections. Their research has revealed fossilised evidence for reproduction using giant sperm in a group of small aquatic crustaceans, called ostracods, dating back to 100 million years ago.

Matzke-Karasz said, 'In these microfossils, we detected organs that are required for transferring giant spermatozoa. Since modern ostracods still produce giant sperm and manoeuvre them with the same organs as 100 million years ago, it's safe to say this distinctive feature evolved only once in this group. It seems to be an evolutionarily successful reproduction strategy, even though it comes at an exceedingly high price for both genders, as a lot of energy is invested in producing and carrying such enormous sperm.'

The international team analysed Harbinia micropapillosa specimens from the Cretaceous Period that had remains of the soft body intact. These fossils had been collected, investigated and then donated to the Natural History Museum in 2000 by Robin Smith. Now at the Lake Biwa Museum, Japan, Smith is a member of the research team.

Eight years later, the same specimens were analysed using synchrotron X-ray holotomography at the European Synchrotron Radiation Facility (ESRF) in Grenoble, through collaboration with Paul Tafforeau, a palaeontologist at the ESRF. This method is currently the most powerful and sensitive way to investigate in three dimensions and at a microscopic scale, the internal anatomy of exceptional fossils without damaging them.

The X-ray examination of the fossilised ostracods revealed direct parallels with the complex reproductive apparatus of modern relatives of these Cretaceous fossils. The team also came across something of a surprise: two of the female specimens had inflated cavities that only occur in modern ostracods that have recently mated, meaning fossil evidence for an insemination had been uncovered.

A human sperm would have to be over 17 meters long in order to measure up against one group of modern ostracods, whose sperm are up to ten times as big as the animals themselves. Roughly 34,000 of the 50 micron-long human sperm would have to line up to match the body length of a man (of 1,70m).

The next stage of the research from the international team is to understand why and how reproduction with giant sperm has persisted for so long.


Pluripotent Vs Embryonic Stem Cells in Medical Therapies
Article by Elie Dolgin for The Scientist.com, Edited by The Visible Embryo

The excitement surrounding federal funding for human embryonic stem cell (ESC) research in the US could be overshadowing another promising therapeutic source of stem cells: those derived through parthenogenesis

Parthenogenetic embryonic stem cells (pESCs) are made with unfertilized eggs which can never form living embryos. They also have broader immunological potential than any other type of stem cell because some pESCs harbor a duplicated haploid genome, so these cells might pose less risk of tissue rejection.

But techniques such as induced pluripotent stem cells (iPSCs) could make this approach obsolete, and the final draft of the stem cell guidelines, due out by July 7, might put an end to all parthenote stem cells.

The published literature on pESCs is "rather scanty," noted John Gearhart, director of the University of Pennsylvania's Institute for Regenerative Medicine. The hundreds of well-characterized ESC lines created from fertilized embryos and the promise of iPSCs make parthenote-derived stem cells "less significant." What's more, the utility of pESCs is hampered by potential safety concerns associated with possible imprinting errors, a shortage of eggs, and the lack of federal funding.

In 2007, two Chinese research groups and a third team in the US and Russia independently reported the first fully characterized human pESCs. All three groups created embryos by activating unfertilized eggs with chemicals and not fertilized with sperm.

The findings marked "the beginning of a new era in [human embryonic stem] cell research," Linzhao Cheng, a stem cell biologist at Johns Hopkins University School of Medicine, wrote in a 2008. The stem cell field was abuzz with the potential for making customized stem cells. Both cloned and parthenogenetic ESCs share a common limitation - they require unfertilized eggs - where thousands of eggs are needed for nuclear cloning, which has never been shown to work, while only a handful of eggs are needed to make a viable pESC line.Parthenotes are much more efficient and require very little expertise," said Mitalipov.

Late in 2008 Cellular reprogramming in the form of embryonic-like iPSCs, promised the ability to create perfectly matched stem cells for any donor. The newer iPSCs make it "harder now to justify" pursuing pESCs for therapeutic applications, said Jose Cibelli, a stem cell researcher at Michigan State University in East Lansing.

However, Cibelli stressed "We should produce more [pESC] cell lines for some of the basic scientific questions." Tiziana Brevini, an embryologist at the University of Milan, Italy, feels parthenotes can be used to study the effects of asymmetric imprinting, genetic homozygosity, and drug toxicity on early embryonic development, but "I would be extremely cautious to suggest their use in therapy," she said.

But t
he publicly-traded southern California-based biotech company, International Stem Cell Corporation (ISCO), feels otherwise. The company has been arguing that only pESCs broad immune matching potential provide a perfect immunological match for the patient from which they are derived, as well as for use in different patients.

"Parthenogenetic stem cells really provide the only viable method for creating a true stem cell bank from which any patient who needs a cell based transplant can get cells that match his immune system," said ISCO chairman and CEO Kenneth Aldrich. The company has one cell line that matches more than 300 million people, Aldrich said. A strategically selected portfolio of 100 cell lines would be sufficient to cover the vast majority of the world's population, he noted, but trying to do the same with ESCs or iPSCs would require at least 10 times more cell lines.

UPenn's Gearhart remains skeptical. "We need a heck of a lot more work to really establish that [pESCs] are the same thing [as ESCs]," he said.

ISCO, which claims to have filed the first patents for deriving human pESCs in 2006, is currently testing pESC-derived retinal cells and liver cells in animal models. "Every indication we have is that they definitely are [safe]," said Aldrich. Mitalipov noted that many experiments show that pESCs can differentiate into any cell type in the body, just like ESCs. "There is no deficiency found, at least in vitro," he said. "These cells are actually functional."

ISCO plans to supply its cells to researchers investigating potential cell therapies. But under the 1995 Dickey-Wicker amendment, taxpayer-backed grants cannot be used to create any embryos - even parthenogenetic ones. What's more, even existing pESC lines would not be eligible for federal funding under the National Institutes of Health's proposed guidelines. "It will be a tragedy for the country" if the NIH doesn't amend its draft guidelines, Aldrich said. "It would force us to do a lot of things overseas that we'd rather be doing domestically."

Ronald M. Green, a bioethicist at Dartmouth College in New Hampshire, said that banning funding for pESCs is based on "uninformed apprehensions" that parthenotes might form viable embryos. "Ethically, it's unobjectionable in a deep sense" to fund pESCs, he said. "Sex cells are routinely destroyed and [creating parthenotes from unfertilized eggs] raises no ethical problems."

The jury's still out on whether pESCs will ultimately be used for transplantation or if the cells will remain confined to the culture dish. Either way, most researchers agree that the cells' full potential -- whatever it is - will only be realized with sufficient government-backed funding for basic research.


Overweight/Obese As Early Adult = Risk of Pancreatic Cancer
Young adults who are overweight or obese have an increased risk of pancreatic cancer, and being obese at an older age is associated with a lower overall survival rate for patients with pancreatic cancer, according to a study in the June 24 issue of JAMA, Journal of the American Medical Association

Pancreatic cancer is the fourth leading cause of cancer-related death for both men and women in the United States. As the prevalence of overweight and obesity have rapidly increased during the last 2 decades, accumulating evidence has emerged that excess body weight is a risk factor for pancreatic cancer.

“However, to our knowledge, no study has explicitly reported the association between excess body weight across an individual’s life span and the risk of pancreatic cancer or identified at which ages the key predisposing weight change usually occurs,” the authors write.

The researchers found that individuals who were overweight (a BMI of 25-29.9) from the ages of 14 to 39 years or obese (a BMI of 30 or greater) from the ages of 20 to 49 years had an associated increased risk of pancreatic cancer, independent of diabetes status.

The association between average BMI (per 5-unit increase) and risk of pancreatic cancer was stronger in men than in women. The association was statistically significant for each age group from 14 to 69 years in men but only from ages 14 to 39 years in women.

The estimated association of average BMI (per 5-unit increase) with cancer risk also was slightly stronger in ever smokers than in never smokers. It was estimated that 10.3 percent of never smokers and 21.3 percent of people who had ever smoked had pancreatic cancer attributable to being overweight or obese at an early age prior to cancer diagnosis (i.e., from the ages of 14-59 years).

Individuals who were overweight or obese from the ages of 20 to 49 years had an earlier onset of pancreatic cancer by 2 to 6 years (median [midpoint] age of onset was 64 years for patients with normal weight, 61 years for overweight patients, and 59 years for obese patients).

Compared with those with normal body weight and after adjusting for all clinical factors, individuals who were overweight or obese from the ages of 30 to 79 years or in the year prior to recruitment had reduced overall survival of pancreatic cancer regardless of disease stage and tumor resection status.

“While our observations require confirmation, they provide support for a role of excess body weight in the development and progression of pancreatic cancer,” the authors conclude.
(JAMA. 2009;301[24]:2553-2562. Available at www.jamamedia.org)


Targets for MicroRNA Gene Regulation Revealed
A new method promises to cut through the stubborn problem of determining the precise targets of microRNAs – the tiny but powerful bits of nucleic acid that tweak gene expression to influence many aspects of health and human disease, from early development and aging to cancer, heart disease, and diabetes

Researchers using the new technique, called HITS-CLIP, showed that in a single experiment they could map the binding points of scores of different microRNAs throughout a genome in living mouse or human tissue. The research by Howard Hughes Medical Institute investigator Robert Darnell and his colleagues Sung Wook Chi, Julie Zang, and Aldo Mele at The Rockefeller University was reported June 17, 2009, in an advanced online publication of the journal Nature.

Darnell believes that in speeding the mapping of microRNAs to their targets, the technique can alleviate a bottleneck in this burgeoning area of RNA research. His team has already used the approach identify the targets and binding sites of nearly 90 percent of the microRNAs that regulate gene expression in the mouse brain. “To a first approximation, we can map every site they bind to on every RNA transcript,” he says. Information gleaned from HITS-CLIP mapping could be helpful in learning how microRNAs influence the progression of diseases, and in identifying targets for new drug therapies, Darnell says.

RNA, a nucleic acid, is still best known for its role as a messenger, relaying instructions from the DNA of genes to parts of the cell that make proteins. MicroRNAs are short stretches of 20 to 22 nucleotides that do not encode instructions for making a protein. They regulate gene expression by blocking the production of specific proteins. These snippets of RNA do their work in the cell’s cytoplasm, where they intercept messenger RNA that carries a gene’s blueprint to the ribosome factories where proteins are made. MicroRNAs dock onto a binding site on messenger RNA. The interaction shortens the lifetime of the messenger RNA or blocks or weakens its instructions, thus reducing the output of protein.

Human genes are subject to the control of more than 500 different microRNAs – collectively thought to regulate more than half of our genes. And hundreds of microRNAs have been identified in other species, as well. To understand their full impact, researchers would like to have a comprehensive catalog of which genes are targeted by each microRNA, as well as where on each messenger RNA molecule that interaction occurs. Until now, however, there has been no efficient way of determining that information.

“To know what a particular microRNA is doing in a cell you need to know what messenger RNA it is binding to, and exactly where it binds,” says Darnell. But “the field hit a roadblock in finding out what any given microRNA does.”

That’s because microRNAs latch on to their target transcript with as few as six consecutive nucleotides. That six-nucleotide sequence might occur many times within a single messenger RNA, and finding the actual minuscule “footprint” is a technical challenge. The problem, Darnell explains, is that the messenger RNA “is like a long coastline with a lot of ports, and it’s been very difficult to know where the microRNA docks.” Biochemical and computer prediction methods are imperfect, he says, and so the tedious hunt for binding sites could only be done experimentally, one RNA at a time.

To get a clearer view of where microRNAs interact with messenger RNAs, Darnell and his colleagues used a technique to study protein-RNA interactions in living, intact cells. HITS-CLIP, which stands for high-throughput sequencing – cross linking immunoprecipitation, was first developed by the Darnell lab in 2008, and is an improvement on their development of CLIP in 2003. CLIP relies on an old laboratory trick that essentially “freezes protein-RNA complexes inside the living cell,” Darnell says.

To freeze these complexes, the researchers shine ultraviolet light onto the cells they are studying, which causes all the proteins and RNAs that are very close to each other become cross-linked – they form an unbreakable bond. Applying HITS-CLIP to a protein called Argonaute turned out to be an effective way of revealing microRNA-messenger RNA interactions. Argonaute assists the regulatory activity of microRNAs by latching onto a microRNA and guiding it, like a tugboat, to its dock on the messenger RNA. Ultraviolet crosslinking locks Argonaute into a complex with both the microRNAs and its messenger RNA target.

The cells can be broken open with a strong detergent that washes away everything but tightly bound RNAs and proteins. “Then we get rid of the proteins,” says Darnell, “and we’re left with just the microRNA and a tag of the Argonaute protein bound to the messenger RNA.” Sequencing those bits of genetic material reveals where Argonaute was bound to both the microRNA and the messenger RNA.

When those data sets are crunched with bioinformatic algorithms, what falls out is the tiny “footprint” on the messenger RNA where the microRNA attaches. “With high-throughput sequencing, we can instantly see all the microRNA binding sites on all the messenger RNAs,” Darnell says.

His lab is interested in human brain disorders, and they have been using HITS-CLIP to study how genes are regulated in brain tissue. They first applied HITS-CLIP to the set of microRNAs in the mouse brain and identified binding sites for about 90 percent of those microRNAs with better accuracy and specificity than computer predictions.

Darnell is excited about the prospect of using his method to glean a new understanding of how microRNAs tweak genes in defined pathways to shape development and other vital processes. He also plans to compare the role of microRNAs in healthy and diseased brains, and expects other researchers will carry out similar experiments to catalog microRNA interactions in other tissues and under different conditions.

“We hope to de-convolute an extremely complicated problem into something that begins to make sense,” he says. “It’s really beautiful.”


THURSDAY June 18, 2009---------------------------News Archive / Return to News Alerts

Tamiflu and Relenza Relatively Safe for Use in Pregnancy
With the H1N1 flu outbreak now elevated to pandemic level, a new article in CMAJ (Canadian Medical Association Journal) reports that oseltamivir (Tamiflu) and zanamivir (Relenza) are relatively safe drugs for use in pregnant and breast-feeding women

Pregnant women, especially those in the third trimester, are at high risk of serious complications from the H1N1 A influenza virus.

The study was conducted by researchers from the Motherisk Program at The Hospital for Sick Children (SickKids) in Toronto and the Japan Drug Information Institute in Pregnancy in Tokyo, Japan.

For treatment or prevention during the current pandemic, "oseltamivir appears to be the drug of choice because there are more data on its safety in pregnancy," writes Dr. Shinya Ito, Head of the Division of Clinical Pharmacology and Toxicology at SickKids. Zanamivir can be used, although there is less data available about its safety in pregnant women. Neither drug appears to affect the growth and development of the fetus, although ongoing data collection is important.

The groups at high risk of flu-related complications from the novel H1N1 influenza are the same as those for seasonal flu - pregnant women, children under 5 years, the elderly and others such as those with chronic lung conditions.

Only small amounts of oseltamivir and zanamivir are excreted into human milk. If an infant is breastfed by the mother on these drugs and needs treatment, the recommended dose of oseltamivir or zanamivir should be given to the infant.


Humans More Related to Orangutans than Chimps?
Researchers propose new grouping for humans, orangutans and common ancestors and lay out a scenario of the migration and evolution of 'dental hominoids' in the Journal of Biogeography

New evidence underscores the theory of human origin that suggests humans most likely share a common ancestor with orangutans, according to research from the University of Pittsburgh and the Buffalo Museum of Science. Reporting in the June 18 edition of the Journal of Biogeography, the researchers reject as "problematic" the popular suggestion, based on DNA analysis, that humans are most closely related to chimpanzees, which they maintain is not supported by fossil evidence.

Jeffrey H. Schwartz, professor of anthropology in Pitt's School of Arts and Sciences and president of the World Academy of Art and Science, and John Grehan, director of science at the Buffalo Museum, conducted a detailed analysis of the physical features of living and fossil apes that suggested humans, orangutans, and early apes belong to a group separate from chimpanzees and gorillas. They then constructed a scenario for how the human-orangutan common ancestor migrated between Southeast Asia—where modern orangutans are from—and other parts of the world and evolved into now-extinct apes and early humans. The study provides further evidence of the human-orangutan connection that Schwartz first proposed in his book The Red Ape: Orangutans and Human Origins, Revised and Updated (Westview Press, 2005).

Schwartz and Grehan scrutinized the hundreds of physical characteristics often cited as evidence of evolutionary relationships among humans and other great apes—chimps, gorillas, and orangutans—and selected 63 that could be verified as unique within this group (i.e., they do not appear in other primates). Of these features, the analysis found that humans shared 28 unique physical characteristics with orangutans, compared to only two features with chimpanzees, seven with gorillas, and seven with all three apes (chimpanzees, gorillas, and orangutans). Gorillas and chimpanzees shared 11 unique characteristics.

Schwartz and Grehan then examined 56 features uniquely shared among modern humans, fossil hominids—ancestral humans such as Australopithecus—and fossil apes. They found that orangutans shared eight features with early humans and Australopithecus and seven with Australopithecus alone. The occurrence of orangutan features in Australopithecus contradicts the expectation generated by DNA analysis that ancestral humans should have chimpanzee similarities, Schwartz and Grehan write. Chimpanzees and gorillas were found to share only those features found in all great apes.

Schwartz and Grehan pooled humans, orangutans, and the fossil apes into a new group called "dental hominoids," named for their similarly thick-enameled teeth. They labeled chimpanzees and gorillas as African apes and wrote in Biogeography that although they are a sister group of dental hominoids, "the African apes are not only less closely related to humans than are orangutans, but also less closely related to humans than are many" fossil apes.

The researchers acknowledge, however, that early human and ape fossils are largely found in Africa, whereas modern orangutans are found in Southeast Asia. To account for the separation, they propose that the last common human-orangutan ancestor migrated between Africa, Europe, and Asia at some point that ended at least 12 million to 13 million years ago. Plant fossils suggest that forests once extended from southern Europe, through Central Asia, and into China prior to the formation of the Himalayas, Schwartz and Grehan write, proposing that the ancestral dental hominoid lived and roamed throughout this vast area; as the Earth's surface and local ecosystems changed, descendant dental hominoids became geographically isolated from one another.

Schwartz and Grehan compare this theory of ancestral distribution with one designed to accommodate a presumed human-chimpanzee relationship. They write that in the absence of African ape fossils more than 500,000 years old, a series of "complicated and convoluted" scenarios were invented to suggest that African apes had descended from earlier apes that migrated from Africa to Europe. According to these scenarios, European apes then diverged into apes that moved on to Asia and into apes that returned to Africa to later become humans and modern apes. Schwartz and Grehan challenge these theories as incompatible with the morphological and biogeographic evidence.

Paleoanthropologist Peter Andrews, a past head of Human Origins at the London Natural History Museum and coauthor of The Complete World of Human Evolution (Thames & Hudson, 2005), said that Schwartz and Grehan provide good evidence to support their theory. Andrews had no part in the research, but is familiar with it.

"They have good morphological evidence in support of their interpretation, so that it must be taken seriously, and if it reopens the debate between molecular biologists and morphologists, so much the better," Andrews said. "They are going against accepted interpretations of human and ape relationships, and there's no doubt their conclusions will be challenged. But I hope it will be done in a constructive way, for science progresses by asking questions and testing results."

Schwartz and Grehan contend in the Journal of Biogeography that the clear physical similarities between humans and orangutans have long been overshadowed by molecular analyses that link humans to chimpanzees, but that those molecular comparisons are often flawed: There is no theory holding that molecular similarity necessarily implies an evolutionary relationship; molecular studies often exclude orangutans and focus on a limited selection of primates without an adequate "outgroup" for comparison; and molecular data that contradict the idea that genetic similarity denotes relation are often dismissed.

"They criticize molecular data where criticism is due," said Malte Ebach, a researcher at Arizona State University's International Institute for Species Exploration who also was not involved in the project but is familiar with it.

"Palaeoanthropology is based solely on morphology, and there is no scientific justification to favor DNA over morphological data. Yet the human-chimp relationship, generated by molecular data, has been accepted without any scrutiny. Grehan and Schwartz are not just suggesting an orangutan–human relationship—they're reaffirming an established scientific practice of questioning data."

A Link Between Gene and Pregnancy Weight Gain?
Even before last week’s release of revised pregnancy weight-gain guidelines, a researcher at the University of Rochester School of Nursing was studying why certain women gain more pounds than others and searching for ways to help them maintain healthy weights.

Susan Groth, Ph.D., R.N., W.H.N.P.-B.C., assistant professor at the School of Nursing, is looking at the relationship between women’s physical activity levels during pregnancy and the amount of weight gained. She wants to find out if these levels are impacted by the presence of a particular gene.

“The hope is that if this study proves there is indeed a link, then we can tell women how much physical activity they need to do to counter the genetic component and keep their weight gain at a healthy point leading to better outcomes for them and for their babies,” said Groth.

Excessive weight gain during pregnancy can have adverse effects including higher risk for cesarean section, gestational diabetes, high blood pressure for the mother, and large-for-gestational-age babies. Babies born to mothers who have excessive weight gain are also more likely to suffer obesity down the road. These health problems along with the rise in obesity in America led the Institute of Medicine (IOM) to issue new guidelines. Of particular note is the IOM’s recommendation that women who are obese at the start of their pregnancies limit their gain to 11 to 20 pounds.

“The new IOM guidelines are important in providing guidance in advising all women on the appropriate weight gain that leads to the best maternal and fetal outcomes, balancing benefit for both,” said Groth. “For my research, the addition of guidelines for obese women provides a structure that we did not have for them until these came out.”

Groth’s study focuses specifically on the weight gain of African American women, a demographic shown to have the highest prevalence of obesity. Based on data from the 2003-2004 National Health and Nutritional Examination Survey, 62 percent of all women were overweight or obese, but 82 percent of all African-American women were overweight or obese. The gene that Groth is studying is carried by 70 percent of African-American women.

“A maternal consequence of excess gestational weight gain is an increase in postpartum weight retention which can contribute to long term obesity,” said Groth. “This is of particular concern for African-American women because they are at high risk for long-term weight retention following pregnancy and also have a tendency to gain additional weight in the 3 to 12 months following pregnancy.”

Groth’s study, which began enrolling participants in October 2008, follows women through pregnancy up until six months after delivery measuring weight changes, diet and activity levels, as well as energy expenditure while lying in bed. “In the end, we’d like to be able to help women come out of pregnancy the healthiest they can be and with babies born at their optimum potential,” said Groth.

Pregnancy Weight Gain Chart


WEDNESDAY June 17, 2009---------------------------News Archive / Return to News Alerts

Smoking Pot Can Change DNA
A new study published by University of Leicester researchers has found "convincing evidence" that cannabis smoke damages DNA in ways that could potentially increase the risk of cancer development in humans.

Using a newly developed highly sensitive liquid chromatography-tandem mass spectrometry method, the University of Leicester scientists found clear indication that cannabis smoke damages DNA, under laboratory conditions.

They have now published the findings in the journal Chemical Research in Toxicology (1) .

The research was carried out by Rajinder Singh, Jatinderpal Sandhu, Balvinder Kaur, Tina Juren, William P. Steward, Dan Segerback and Peter B. Farmer from the Cancer Biomarkers and Prevention Group, Department of Cancer Studies and Molecular Medicine and Karolinska Institute, Sweden.

Raj Singh said: “Parts of the plant Cannabis sativa, also known as marijuana, ganja, and various street names, are commonly smoked as a recreational drug, although its use for such purposes is illegal in many countries.

“There have been many studies on the toxicity of tobacco smoke. It is known that tobacco smoke contains 4000 chemicals of which 60 are classed as carcinogens. Cannabis in contrast has not been so well studied. It is less combustible than tobacco and is often mixed with tobacco in use. Cannabis smoke contains 400 compounds including 60 cannabinoids. However, because of its lower combustibility it contains 50% more carcinogenic polycyclic aromatic hydrocarbons including naphthalene, benzanthracene, and benzopyrene, than tobacco smoke.”

Writing in the journal Chemical Research in Toxicology, the scientists describe the development of a mass spectrometry method that provides a clear indication that cannabis smoke damages DNA, under laboratory conditions.

The authors added: “It is well known that toxic substances in tobacco smoke can damage DNA and increase the risk of lung and other cancers. Scientists were unsure though whether cannabis smoke would have the same effect. Our research has focused on the toxicity of acetaldehyde, which is present in both tobacco and cannabis.”

The researchers add that the ability of cannabis smoke to damage DNA has significant human health implications especially as users tend to inhale more deeply than cigarette smokers, which increases respiratory burden. "The smoking of 3-4 cannabis cigarettes a day is associated with the same degree of damage to bronchial mucus membranes as 20 or more tobacco cigarettes a day," the team adds.

"These results provide evidence for the DNA damaging potential of cannabis smoke," the researchers conclude, "implying that the consumption of cannabis cigarettes may be detrimental to human health with the possibility to initiate cancer development."

The study was funded by the European Union Network of Excellence ECNIS, the Medical Research Council and Cancer Research UK.


Cells Are Like Robust Computer Systems
Gene regulatory networks in cell nuclei are similar to cloud computing networks, such as Google or Yahoo!, researchers report today in the online journal Molecular Systems Biology

The similarity is that each system keeps working despite the failure of individual components, whether they are master genes or computer processors.

This finding by an international team led by Carnegie Mellon University computational biologist Ziv Bar-Joseph helps explain not only the robustness of cells, but also some seemingly incongruent experimental results that have puzzled biologists.

"Similarities in the sequences of certain master genes allow them to back up each other to a degree we hadn't appreciated," said Bar-Joseph, an assistant professor of computer science and machine learning and a member of Carnegie Mellon's Ray and Stephanie Lane Center for Computational Biology.

Between 5 and 10 percent of the genes in all living species are master genes that produce proteins called transcription factors that turn all other genes on or off. Many diseases are associated with mutations in one or several of these transcription factors. However, as the new study shows, if one of these genes is lost, other "parallel" master genes with similar sequences, called paralogs, often can replace it by turning on the same set of genes.

That would explain the curious results of some experiments in organisms ranging from yeast to humans, in which researchers have recently identified the genes controlled by several master genes. Researchers have been surprised to find that when they remove one master gene at a time, almost none of the genes controlled by that master gene are de-activated.

In the current work, the Carnegie Mellon researchers and their colleagues in Israel and Spain identified the most probable backup for each master gene. They found that removing the master genes that had very similar backups had almost no noticeable effect, but when they removed master genes with less similar backups, the effect was significant. Additional experiments showed that when both the master gene and its immediate backup were removed, the effects became very noticeable, even for those genes with a similar backup gene. In one example, when the gene Pdr1 was removed, researchers found almost no decrease in activation among the genes it controls; when Pdr1 and its paralog were removed, however, 19 percent of the genes Pdr1 controls failed to activate.

"It's extremely rare in nature that a cell would lose both a master gene and its backup, so for the most part cells are very robust machines," said Anthony Gitter, a graduate student in Carnegie Mellon's Computer Science Department and lead author of the article. "We now have reason to think of cells as robust computational devices, employing redundancy in the same way that enables large computing systems, such as Amazon, to keep operating despite the fact that servers routinely fail.


Reducing Stress May Reduce Bladder Infections
A marker in the blood of both cats and humans that was identified in a recent study might signal both species’ susceptibility for a painful bladder disorder called interstitial cystitis, a condition that is often difficult to diagnose

Follow-up studies of the chemicals that appeared in blood samples suggest that the way tryptophan, an essential amino acid, is processed in cats and humans with interstitial cystitis ultimately could affect the way signals are transmitted in the brain. The results, while preliminary, suggest that the disease is not just a malfunction of the bladder, but might instead have origins in the central nervous system.

Symptoms of interstitial cystitis, known as IC, include recurring discomfort or pain in the bladder and pelvis, and often both an urgent and frequent need to urinate. A diagnosis typically follows tests to rule out other diseases, such as infections or cancer. No diagnostic test currently exists for IC, and the cause is unknown. Treatments range from oral medications to exercise for humans, and maintaining a safe environment for cats.

“What we know now is that this testing method is very sensitive and specific for the disorder in both humans and domestic cats. So far it hasn’t missed one diagnosis,” said Tony Buffington, senior author of the study and professor of veterinary clinical sciences at Ohio State University. The research is published in the current issue of the journal Analyst.

Buffington and colleagues collected samples from cats with feline interstitial cystitis, healthy cats and cats with other diseases, as well as samples from humans with the painful bladder syndrome, healthy humans and humans with other urological illnesses.

He and colleagues used infrared microspectroscopy to tell the difference between blood samples indicating the presence or lack of disease based on the samples’ molecular profiles. Infrared spectroscopy identifies the biochemical content of a blood sample based on where peaks of molecules appear in the infrared spectrum. Samples from humans and cats with interstitial cystitis demonstrated nearly identical molecular peaks.

“It’s a powerful enough technique that we might even be able to identify subtle differences in patients with multiple diseases that exist in addition to, but that are unrelated to, the interstitial cystitis,” he said. “We can put these cats into recovery, but I don’t think we cure them. It’s a chronic condition. It’s like lactose intolerance – you won’t get that gene back, but you can learn to avoid milk,” he said.

The researchers then determined the chemical structures within those molecular profiles, which showed that blood from cats with the syndrome contained at least 20 percent more tryptophan and kynurenine than did samples from healthy cats. Kynurenine is a brain compound produced when tryptophan breaks down in the body. An elevated level of kynurenine suggests that tryptophan is being diverted from its conversion into a chemical responsible for sending signals in the brain.

This testing method differentiated between diseases in humans as well, classifying the samples as coming from either healthy subjects, IC patients, or patients with another urological disorder, Buffington said.

In addition to improving the potential to diagnose interstitial cystitis, understanding chemical processes related to this chronic disease could offer new directions for the pursuit of treatments and even prevention strategies, he said. “It’s all speculative, but it may be that there is some kind of primary central nervous system disorder that results in problems in the bladder in some people, and in the gut or other organs in others,” Buffington said. “It is possible that this is a biomarker for the underlying vulnerability or susceptibility.”

Buffington has led studies that show that in cats, feline interstitial cystitis can be managed through a series of changes to the affected animals’ environment that reduce stressors and promote stability and predictability. “We can put these cats into recovery, but I don’t think we cure them. It’s a chronic condition. It’s like lactose intolerance – you won’t get that gene back, but you can learn to avoid milk,” he said.

So far, humans with the disorder have the option of bladder distention, dietary changes, exercise, oral drugs, electrical nerve stimulation or surgery. But all treatments target only symptoms because the underlying cause of the disease is unknown.

Buffington plans to test human samples from patients diagnosed with irritable bowel syndrome and fibromyalgia to see if the same biomarker is associated with these chronic pain disorders as well. These disorders, like IC, are categorized as what are known as medically unexplained or functional syndromes, and Buffington has explored the possibility that a common link exists among these types of diseases. He published a review paper in the April issue of the journal Psychotherapy and Psychosomatics in which he suggested that traumatic events experienced by pregnant females might transmit to fetuses a genetic change associated with the stress response.

Buffington suggests that such a genetic change would mean offspring born to these mothers might then have a genetic predisposition to be more vulnerable to certain stressors, and that in some individuals that vulnerability could lead to development of a chronic pain disorder in response to stress.

“When products of the stress response cross the placenta, they can change gene expression in offspring,” Buffington said. “My guess is that there are patterns or groups of genes that are changed. And these groups could have something to do with the magnitude and quality of the stress response. I think it’s another useful way to look at how these things develop.”


Autism Drug Ineffective, Causes Significant Side Effects
A drug commonly given to autistic children to reduce repetitive behaviors is ineffective compared to placebo and, in some children, may actually increase repetitive behaviors, the largest study of autistic children to date has found

“What we found, much to our surprise, is that there was no significant difference in positive response between kids treated with citalopram and kids who received the placebo. And the kids treated with citalopram tended to have more side effects,” said Linmarie Sikich, M.D., a co-author of the study and associate professor of psychiatry in the University of North Carolina at Chapel Hill School of Medicine.

“I cannot emphasize this enough: This was not at all what we expected to see,” Sikich said.

Results of the study, a randomized controlled clinical trial of the drug citalopram, are published in the June 29, 2009 issue of Archives of General Psychiatry. It was funded by the National Institutes of Health and took place at six academic medical centers across the country. Principal investigator and lead author of the study is Bryan H. King, M.D., who began the study at Dartmouth and continued to oversee it there after he moved to the University of Washington, where he is currently director of psychiatry and behavioral medicine at Seattle Children’s Hospital.

Citalopram, which is sold under the brand name Celexa, is one of a class of antidepressant drugs called selective serotonin reuptake inhibitors, or SSRIs. SSRIs are the most frequently used medications for children with autism. They are also used to treat depression, anxiety and obsessive compulsive disorder in both adults and children. Prior to this study there was very little scientific evidence to support the use of SSRIs in autistic children, but some preliminary studies showed promising results for citalopram, Sikich said.

Hypothesizing that citalopram would improve the overall functioning of autistic children and adolescents by reducing repetitive behavior, Sikich and colleagues recruited 149 children ages 5 to 17 to take part in the 12-week trial. Seventy-three received daily doses of liquid citalopram while 76 received daily doses of liquid placebo. Researchers measured the children’s’ response to treatment using the Clinical Global Impression-Improvement scale (CGI-I). They also recorded measures of repetitive behavior and side effects.

At the end of the trial, some children in both groups showed a positive response. However, there was no significant difference between the groups: the positive response in the citalopram group was 32.9 percent versus 34.2 percent in the placebo group. In addition, children in the citalopram group were significantly more likely to experience adverse side effects such as increased energy level, impulsiveness, decreased concentration, hyperactivity, increased repetitive movements and behaviors, diarrhea, insomnia, and dry itchy skin.

The researchers concluded that citalopram “is not an effective treatment” for autistic children with repetitive behaviors. In addition, they wrote, this trial shows that the use of SSRIs in autistic children “is not without risk” and “at present there is insufficient research evidence to merit a clear recommendation regarding the use of SSRIs as a class” for the treatment of repetitive behavior in children with autism spectrum disorders.

“The obvious short term message is, this treatment didn’t work. And that surprised us a great deal,” Sikich says. “But the really important take-home message is that we have to do large, scientifically-sound comparative studies like this to really know whether a specific treatment works and is safe. Simply relying on doctors’ and families’ impressions often leads us to use medications that really don’t work and may do more harm than good” says Sikich.

Safe and effective medication and behavioral treatments are desperately needed to help children with autism realize their potentials and keep from harming themselves or others, Sikich says.

“Well-done studies, using methods like the ones in this study, have shown that another drug, risperidone, is useful in reducing irritability and aggression in children with autism,” she says. “Thus, this study shouldn’t be interpreted as saying all medications don’t help people with autism and are harmful. Instead it says that citalopram doesn’t help most children with autism and is harmful to some children. Clearly we need more research to develop and test other interventions for this important problem.”

People with autism are severely impaired by the disorder and experience major problems with highly repetitive behaviors, often including self-injurious behaviors, communicating and interacting appropriately with others. Frequently the repetitive behaviors keep children with autism from learning in school or participating in age appropriate activities. When it is time to stop the repetitive behavior and begin a new, functional activity, many children with autism become distraught and aggressive. These repetitive behaviors also contribute to the difficulties that make it hard for most people with autism to live independently or work as adults, Sikich says.


TUESDAY June 16, 2009---------------------------News Archive / Return to News Alerts

Newborn Weight Affected by Environmental Contaminants
Recent epidemiological studies have revealed an increase in the frequency of genital malformations in male newborns (e.g., un-descended testes) and a decrease in male fertility

The role played by the growing presence in our environment of contaminants that reduce male hormone action could explain this phenomenon.

It is known that the birth weight of males is higher than that of females due to the action of male hormones on the male fetus.If the exposure of pregnant women to environmental contaminants that diminish the action of male hormones has increased over the years, one would expect to see a decrease in the sex difference in birth weight.

This is exactly what a new study published in the July 2009 issue of Epidemiology shows. Investigators analyzed the Public Health Agency of Canada's database on the birth weights of more than five million children born in Canada between 1981 and 2003.

Using statistical methods that control for changes over time of mother's age and parity, the investigators effectively show a sustained decrease in birth weight differences between boys and girls, which supports the hypothesis of growing endocrine disruption related to environmental contaminants. Contaminants found in plastic materials represent plausible candidates, since they are known to diminish the action of male hormones.

“Our study underlines the importance of probing the impact of environmental contaminants on the health of mothers and fetuses and on the reproductive potential of future generations,” says lead researcher Dr. Guy Van Vliet, a pediatric endocrinologist and investigator at the Sainte-Justine University Hospital Research Center and a professor at the Department of Pediatrics of the Université de Montréal.


How Parents Pass on Traits to Children
One of the mechanisms governing how our physical features and behavioural traits have evolved over centuries has been discovered by researchers at the University of Leeds in the United Kindgom

Darwin proposed that traits are passed from a parent to their offspring, with natural selection favouring those that give the greatest advantage for survival, but he did not have a scientific explanation for this process.

In research published this week, the University of Leeds team reports that a protein known as REST plays a central role in switching specific genes on and off, thereby determining how specific traits develop in offspring.

Their study shows that REST controls the process by which proteins are made, following the instructions encoded in genes. It also reveals that while REST regulates a core set of genes in all vertebrates, it has also evolved to work with a greater number of genes specific to mammals, in particular in the brain – potentially playing a leading role in the evolution of our intelligence.

Says lead researcher Dr Ian Wood of the University’s Faculty of Biological Sciences: “This is the first study of the human genome to look at REST in such detail and compare the specific genes it regulates in different species. We’ve found that it works by binding to specific genetic sequences and repressing or enhancing the expression of genes associated with these sequences.

“Scientists have believed for many years that differences in the way genes are expressed into functional proteins is what differentiates one species from another and drives evolutionary change – but no-one has been able to prove it until now.”

The Leeds team, in collaboration with scientists in Singapore, examined the repertoire of genes that REST regulates, in particular those which are expressed in the central nervous system. The team compared 16 whole genome sequences in fish, primates and humans to see where and how REST binds to them. Until now, the nature and extent of such variation has been unknown but the present study now completes some significant gaps in this knowledge.

Dr Wood says: “We were curious to look at REST and see what its functions are because it’s present in all vertebrates and it is also thought it may have a role to play in certain brain functions, such as levels of intelligence. It was a massive undertaking just to collate all the data required and put it into the right order before we could start any kind of analysis. Our research has not only completed some significant gaps in this knowledge, but has also explained some of the detail behind the process of natural selection, which Darwin correctly identified, but couldn’t explain.”


From the Glass to the Brain in Six Minutes

Just one drink goes quickly go to your head

Researchers in Heidelberg, Germany tested this well-known adage and found only six minutes after consuming an amount of alcohol equivalent to three glasses of beer or two glasses of wine, a blood alcohol level of 0.05 to 0.06 percent, changes had already taken place in the brain cells.

The scientists in Heidelberg used magnetic resonance spectroscopy (MRS) to prove their results. Previously the only available data came from animal trials. The results of the study were published in the Journal of Cerebral Blood Flow and Metabolism.

Apparantly, the brain reacts very quickly to alcohol. “Our study provides evidence for alternative energy utilization upon alcohol ingestion, i.e. the brain uses an alcohol breakdown product instead of glucose for energy demands,” explains Dr. Armin Biller of the working group for cerebral metabolism at the Department of Neuroradiology at Heidelberg University Hospital (Medical Director: Prof. Dr. Martin Bendszus).

Harmful effects set in quickly. During the experiment, the concentration of substances such as creatine (energy metabolism), which are attributed with protecting cells, decreases as the concentration of alcohol increases. Choline, a component of cell membranes, was also reduced. “That probably indicates that alcohol triggers changes in the composition of cell membranes," says Dr. Armin Biller.

Is all consumption of alcohol harmful for the brain?

“Our follow-ups on the next day showed that the shifts in brain metabolites after moderate consumption of alcohol by healthy persons are completely reversible,” says Dr. Armin Biller. “However, we assume that the brain’s ability to recover from the effect of alcohol decreases or is eliminated as the consumption of alcohol increases. The acute effects demonstrated in our study could possibly form the basis for the permanent brain damage that is known to occur in alcoholics. This should be clarified in future studies.”

Eight male and seven female subjects participated in the alcohol experiment. While lying in the MRI scanner, they drank the specified amount of alcohol through a long straw. The goal was to reach a blood alcohol content of 0.05 to 0.06 percent – a level that impairs ability to drive, but does not induce severe intoxication.

In the MRI scanner, the nuclei of atoms in brain tissue were stimulated by a high-frequency impulse and the signal transmitted during the return to the initial condition was received. The properties of this signal were analyzed, allowing conclusions to be made as to the contents of various products being metabolised in the tissue examined.

Interestingly, the study found no differences between the results of male and female individuals – the brains of female and male subjects reacted to alcohol consumption the same way.


Sperm’s Genes Packed with ON - OFF Instructions
New research shows that a father’s sperm passes along a previously unrecognized set of instructions that helps guide the early development of his children

The instructions likely tell the developing embryo when specific genes should be turned on or off.

Scientists have found that in sperm, most paternal genes important for embryonic development are flagged with special proteins bearing chemical tags. These proteins and their tags, called modified histones, influence when developmental genes and other key processes are turned on, shut off, or put on hold at critical stages in an embryo’s growth. The findings were reported in an advance online publication on June 14, 2009, in the journal Nature.

During fertilization, sperm and egg combine to form a zygote, a single cell that later divides to become many cells, and many cell types. Each cell type must emerge at the right time, and in the right place, for a healthy embryo to develop. The new research by Howard Hughes Medical Institute investigator Bradley R. Cairns addresses how an organism’s genetic material is packaged to execute that carefully choreographed process.

The findings show that sperm genes are packaged along with chemical “guideposts” that help determine which genes should be turned on or off at specific stages of development, says Cairns, who collaborated with Douglas Carrell and other colleagues at the University of Utah. Those developmental guideposts are epigenetic—meaning they regulate gene access and utilization without changing the DNA sequence of a gene.

Epigenetics influences gene expression in several ways: One is through methylation—the addition of a methyl group to a DNA molecule to deactivate a gene. Demethylation—subtraction of a methyl group—activates the gene. Genes can also be silenced or activated by modifying histone proteins that serve as spools on which DNA strands are wrapped.

Previous work in Cairns’ lab, in zebrafish and yeast, had shown that histones can package certain genes so they remain flexible during development. His group showed that genes in the ‘off’ position can also be poised to turn on later. “It’s gene packaging,” he says “that determines the potential for a gene’s activity.”

However, about 96 percent of the histone proteins in the genome are eliminated as sperm mature. The race to fertilize an egg goes to the swift—and having a small head, with DNA packaged even more tightly, is advantageous. So the histones in mature sperm are largely exchanged for another protein, protamine, which further compacts the DNA.

Many scientists have reasoned this protein swap might limit how much information is transmitted from sperm to egg during fertilization. But Cairns says the new work suggests that isn’t true. Using sperm from fertile human donors, the researchers separated out the chromatin, which contains the genetic material and proteins that make up chromosomes, into histone-bound and protamine-bound fractions. Their analyses of both fractions revealed that histones, although comparatively small in number, were still maintained at hundreds of genes important for embryo development.

“Those genes are the important decision makers in the embryo,” Cairns says. “You need to make sure those genes from the father turn on for normal development … and they have to turn on at the right time.”

The sperm apparently marks the genes that turn on early in embryo development with specific types of modified histones, Cairns says. A different type of modification is placed on genes that turn on later—a sort of “do not open till Christmas” label. This tagging ensures that genes are activated only when the embryo is ready for them—such as to achieve differentiation into cell types that constitute different body tissues.

Cairns explains that under this scheme, some genes that are activated early in development, for example, are marked with a ”green light” indicating they should be turned on. Others have both a green light and a red light, and require the removal of the red light to turn on later in development.

To transmit its information and guide development, this labeling must remain intact upon fertilization, when the protamine releases from the paternal DNA and the remainder of the sperm genome is repackaged with the egg’s histones.

This packaging parallels the way in which developmental genes are packed up in embryonic stem cells, Cairns says, with genes poised to act by the mix of green- and red-light markings. Such packaging could explain transgenerational inheritance, the proposition that traits can be passed to offspring by biochemical means other than DNA sequence. As for how a mother’s genes receive their instructions for development, “eggs remain a mystery,” he says. “This is an issue we are now addressing in zebrafish, from which thousands of eggs are easily obtained.”

Cairns says he is awestruck by nature’s solution to the problem of how to keep all genes from being transcribed at once—which would be disastrous—or of packaging them so tightly that the DNA can’t be accessed. “What has evolved is this very sophisticated and beautiful system of tailoring gene packaging and modifying gene packaging to allow for regulated access to the genes.”.

MONDAY June 15, 2009---------------------------News Archive / Return to News Alerts

Good News and Bad for Dad this Father's Day
Study explores dad's role in shaping a healthy baby

It was long believed that conception does not involve a meeting of equals. The egg is a relatively large, impressive biological factory compared with the tiny sperm, which delivers to the egg one copy of the father's genes. However, a new study from Huntsman Cancer Institute (HCI) at the University of Utah reveals that the father's sperm delivers much more complex genetic material than previously thought.

The findings could lead to a diagnostic test to help couples deal with infertility.

Researchers discovered particular genes packaged in a special way within the sperm, and that may promote the development of the fetus.

"Our findings show that the father plays an active role in packaging his genome to help ensure a healthy baby," says study co-leader Brad Cairns, Ph.D., investigator with HCI and the Howard Hughes Medical Institute, and professor of oncological sciences at the University of Utah. "However, they also raise the possibility that a man's aging, health and lifestyle may alter this packaging and negatively affect fertility and embryo development."

During fetal development, certain genes make decisions about organ and tissue development. The new research shows that in sperm, these genes are wrapped in special packaging materials called 'modified histones.' These modified histones appear to be key factors in ensuring genes are activated or repressed at the right level, place and time, which helps the fertilized egg develop properly.

Chromosomes are long strands of DNA containing thousands of genes, and their packaging helps determine which genes turn on and off. Understanding how these genes are activated or repressed leads to a better understanding of how disorders like birth defects and cancer develop.

"Genes have on-and-off switches, and understanding them allows us to target them, leading to possible treatments, cures or prevention strategies," says Cairns. "That's the good news."

The study is set for publication June 14 – a week before Father's Day – in the online edition of the journal Nature. The research involved collaboration between Cairns' lab at HCI and the University of Utah's in vitro fertilization (IVF) and andrology lab led by Doug Carrell – along with their joint graduate student, Sue Hammoud.

An implication of this study is that factors such as genetic mutations, age or lifestyle may affect sperm chromosome packaging, leading to infertility. "We are hopeful that this work will soon lead to a clinical diagnostic test that will help couples with infertility problems make better informed decisions regarding their prospects for a healthy child. We will also be testing if aspects of a man's lifestyle – such as age, diet or health – affect proper packaging and fertility," says Cairns. Other future work includes how decision-making genes are packaged in eggs, which remains a major mystery.


‘Designer Molecules’ Being Developed to Fight Disease
Researchers in the Department of Cardiovascular Sciences at the University of Leicester are developing a new way to make protein based drugs with potential applications in stroke, vascular inflammation, blood vessel formation, regenerative medicine and tissue engineering

The research carried out by doctoral student Shikha Sharma in Dr Nick Brindle’s group in Department of Cardiovascular Sciences aims to allow researchers to rapidly make ‘designer proteins’ that can bind to disease causing molecules in the body.

Shikha Sharma said “There are millions of different proteins that are involved in carrying out numerous functions in the human body. Over time each protein has evolved to optimise its function. Disease could result if any of these fail to perform efficiently.”

“By generating designer proteins in test tubes, we can produce molecules that have specific actions to control processes in the body. These proteins can be used to make drugs as a treatment for heart disease and cancer.”

She said: “While most drugs in current use are synthetic, these designer molecules are developed from natural proteins and are likely to have fewer side effects. Proteins perform a well defined but complex set of function in the body and protein therapeutic drugs can perform better when compared to some synthetic small molecule drugs that may have unwanted interactions within the body.”

“Current methods to generate protein therapeutic are cumbersome and time consuming. At the University of Leicester, we have developed a novel method to revolutionise the way in which we produce these designer protein drugs.

In principle this method mimics natural evolution to make new proteins but over a shorter timescale. Instead of taking millions of years, we can create new proteins in just a few weeks.”



Insurance Coverage and Care of Newborns with Birth Defects
In an unexpected result for the uninsured, a team of Yale School of Medicine and Yale-New Haven Children’s Hospital physicians has found that babies from uninsured families, who are born with congenital defects, are far more likely than those whose families have insurance to be transferred out of the large community hospitals where they are born and into children’s hospitals for corrective surgery

Paradoxically, these uninsured babies may receive better care at the children’s hospitals, which are fully staffed with pediatric specialists, say the researchers.

The team’s data were presented at the 40th annual meeting of the American Pediatric Surgical Association in Puerto Rico on May 30.

The Yale team studied around 6,000 infants with major congenital defects of the abdomen and esophagus, born in community hospitals between 1997 and 2006. During that period they saw a steady increase in the trend of uninsured pediatric patients being transferred, while insured patients were treated locally. By 2006, the uninsured babies were three times as likely as the insured to be sent to children’s hospitals.

Treatment of newborns with complex congenital anomalies requiring urgent surgical care is among the most costly challenges for the health care system. The mean hospitalization cost per patient is more than $155,000, with care for some infants rising above $1 million.

Because of this, “care of newborns with major anomalies can produce either a huge financial gain or loss to a hospital depending upon the patient’s insurance status,” according to corresponding author R. Lawrence Moss, M.D., the Robert Pritzker Professor and Chief of Pediatric Surgery, Yale School of Medicine, and Surgeon-in-Chief of Yale-New Haven Children’s Hospital. “The current reimbursement structure in the U.S. provides the incentive,” he adds.

Can You Locate Your Heart In Your Body?
Many patients and general public do not know the location of key body organs, even those in which their medical problem is located, which could have important consequences for doctor-patient communication

The level of anatomical knowledge in a sample of 722 participants was assessed on a multiple-choice questionnaire, with approximately 100 patients in each of 6 different diagnostic groups and 133 from the general population.

Comparisons of anatomical knowledge between present and earlier results, and across the clinical and general public groups were evaluated and adjusted for age and education.

Older studies had shown that patients often did not understand the terms used by doctors and many did not even have a rudimentary understanding of anatomy.

The present study was designed to investigate the levels of anatomical knowledge of different patient groups as well as the general public in order to see whether an improvement has been made over time and if patients with a specific organ pathology (e.g. liver disease) have a better understanding of the location of that organ.

But many patients and the general public still do not know the location of key body organs, even those with which they have an affiliated medical problem.

This lack of information could have important consequences for doctor-patient communication.

These results indicate that healthcare professionals still need to take care in providing organ specific information to their patients and should not assume that patients know the location of any organ including the one in which their major medical problem is harbored.

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