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New Data Analysis Tool Developed

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A  recently published paper in Science reports a new data analysis tool that is able to search complex data sets for relationships and trends that are invisible in other types of statistical analysis.
Take, for example, bacterial species that colonize the gut of humans and other mammals: There are trillions of bacteria; even narrowing down the data set to just seven thousand yields over 22 million potential relationships between assorted pairs of bacteria. How can microbiologists keep themselves from drowning in such a huge sea of data, and know in advance what kinds of patterns to look for? Challenges like this are faced not only by microbiologists: Large, complex data sets with thousands of variables are increasingly common in fields such as genomics, physics, political science, economics and more, and there is thus an increasing need for data-analysis tools to make sense of them.
The tool,developed by Yakir Reshef,David Reshef and Hilary Finucanet,under the guidance of advisers Michael Mitzenmacher of the Harvard University School of Engineering and Applied Sciences and Pardis Sabeti of the Broad Institute – is called the maximal information coefficient, or MIC for short. It is based on the idea that if two variables are related to each other, there should be a way to draw a grid on a scatterplot of the two variables in a way that captures the relationship between them. The algorithm that calculates the MIC searches through many such grids and uses the one best able to quantify how strong the relationship is. Researchers can calculate the MIC on each pair of variables in their data set, rank the pairs by their scores (the higher the score, the more related the pair) and then examine the top-scoring pairs – that is, the pairs that affect each other the most.
To test how well the algorithm works, Yakir, David and Hilary applied the MIC to data sets in a variety of fields – global health, gene expression, human gut microbiota and even major-league baseball – and compared the MIC results to those of current methods.
How did they fare? With regard to the microbiota data, the MIC was able to narrow down 22 million variable pairs to just a few hundred interesting relationships, many of which had not been observed before. For instance, it identified examples of “non-coexistent” species in which if one bacterium is abundant, the other is not, and vice versa. Some of the non-coexistent relationships identified were familiar – known to be caused by differences in host diet – while others were novel. This finding raises the possibility of the existence of additional factors that, like diet, affect the make-up of the human microbiome.

In another example, the team examined a data set from the World Health Organization covering 200 countries and containing 357 variables per country. One of the identified relationships was between female obesity and household income in the Pacific Islands, in which obesity increases with income, in contrast with other countries. It turned out that obesity, rather than being an anomaly, is considered a sign of status in the Pacific Islands. Most methods would treat this separate trend as “noise,” but the MIC is able to identify relationships, such as this one, that include more than one trend.
MIC is part of a suite of statistical tools called MINE for Maximal Information-based Nonparametric Exploration.One of the greatest strengths of this newly discovered tool within MINE is its ability to detect and analyze a broad spectrum of patterns and characterize them according to a number of different parameters a researcher might be interested in. Other statistical tools work well for searching for a specific pattern in a large data set, but cannot score and compare different kinds of possible relationships. Researchers can also use MINE to generate new ideas and connections.
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Ecological Model Mystery Solution Proposed

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In 1972 physicist Robert May of Oxford University developed a ground-breaking mathematical model that represented the relationship between ecosystem stability and diversity.It proved that sufficiently large or complex ecological networks have a probability of persisting that is close to zero,directly contradicting previous expectations.According to May’s model, ecosystems that harbor large numbers of interacting species would necessarily be extremely unstable–so unstable that even slight perturbations, such as variable weather and environmental conditions, would be enough to trigger massive extinctions within them. Therein lies a paradox: According to May’s modeling, the persistence in nature of the complex ecosystems such as coral reefs and junglethat contain many species co-existing and interacting  should be exceedingly improbable.

But now, Stefano Allesina and Si Tang, both of the University of Chicago, have solved that vexing modeling mystery, and have thereby laid the groundwork for improvements in the modeling of complex ecosystems to environmental change.The researchers’ work,  funded by the National Science Foundation (NSF), is published in this week’s issue of Nature. (link)

Remarkably, Allesina says that he and Tang cracked the biodiversity mystery without supercomputers or other high-tech instruments that are so frequently at the core of current biological discoveries: “We did the necessary calculations with just a pen and paper after finding a 1988 article on quantum physics that gave us the key to crack the problem.”

In their Nature paper, Allesina and Tang explain why May’s results do not accurately describe ecosystems in which predator-prey relationships are prevalent. Allesina explains: “May’s model assumes that any two species in a large ecological network interact with one another at random, and without any consideration of the specific type of interaction between them, whether it is a predator-prey relationship, a mutualistic relationship or a competitive relationship.”But in their recent research, Allesina and Tang modeled ecosystems in which species consume each other in addition to interacting with one another as competitors or mutualists. Their results explain why large numbers of species thrive instead of necessarily going extinct as predicted by May’s model. This advance provides the foundation for the development of increasingly sophisticated analyses of ecosystem responses to environmental change.

Allesina believes that it is predator/prey relationships (not competitor or mutualistic relationships) that provide the necessary stability for almost infinite numbers of species to exist in ecosystems. They do so by keeping the size of species populations in check at supportable levels. Allesina explains, “When prey are high, predators increase and reduce the number of prey by predation. When predators are low, prey decrease and thus reduce the number of predators by starvation. These predator/prey relationships thereby promote stability in ecosystems and enable them to maintain large numbers of species.”

Allesina says that May’s model mixed various types of species interactions but could not represent these relationships accurately because of technical modeling constraints that he and Tang overcame.

Allesina says that he and Tang intend to further improve their ecosystem model by embedding into it well-known interactions that exist between particular species. He also says that the insights gleaned through this study may be used to improve models of other types of networks that are unrelated to ecology, such as various types of gene regulatory networks and chemical reactions.

Adapted from:eurekaalert

Nature Paper:Stability Criteria for Complex ecosystems

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R-loops break walls of gene silencing

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From :http://www.news.ucdavis.edu/search/news_detail.lasso?id=10165

Researchers at the University of California, Davis, have figured out how the human body keeps essential genes switched “on” and silences the vast stretches of genetic repeats and “junk” DNA.

Frédéric Chédin, associate professor in the Department of Molecular and Cellular Biology, describes the research in a paper published today (March 1) in the journal Molecular Cell. The work could lead to treatments for lupus and other autoimmune diseases, by reversing the gene-silencing process known as cytosine methylation.

“R-loops” are the key, say graduate student Paul Ginno, Chédin and colleagues. The loops emerge in the RNA transcription process in DNA sections that are rich in cytosine and guanine, the C and G in the four-letter DNA code. These C and G stretches serve as “on” switches, or promoters, for about 60 percent of human genes.

Scientists have known since the 1980s that these so-called CG island promoters are not subject to methylation. But, Chédin said, the mechanism has been a long-standing mystery.

The UC Davis researchers built a catalog of almost 8,000 CG islands in the human genome, studied their DNA sequences and found the CG sequences to be skewed toward having one strand of the double helix rich in guanine, and the complementary strand rich in cytosine.

Then, in RNA transcription, the G-rich RNA remains stably bound to a C-rich DNA strand, forcing the G-rich DNA strand into a loop — which then prevents methylation.

DNA methylation is considered part of the new field of epigenetics, which studies inheritable genetic changes that are not directly coded in the DNA sequence. However, the new work shows that, at least at CG islands, the epigenetic state is determined by the DNA sequence.

Scientists know that reduced methylation of DNA plays a key role in triggering autoimmunity in lupus, Chédin said. However, the molecular events behind this DNA under-methylation have been unclear.

“Our work establishes that excessive R-loop formation may drive under-methylation and autoimmunity,” Chédin said.

Co-authors: Paul Lott, graduate student; Holly Christensen, undergraduate; and Ian Korf, associate professor in the Department of Molecular and Cellular Biology and the Genome Center.

The National Institutes of Health and the Foundation for Prader-Willi Research supported the project.

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Scientists suggest that cancer is purely man-made

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“Cancer is a modern, man-made disease caused by environmental factors such as pollution and diet, a study by University of Manchester scientists has strongly suggested.

The study of remains and literature from ancient Egypt and and earlier periods – carried out at Manchester’s KNH Centre for Biomedical Egyptology and published in Nature Reviews Cancer – includes the first histological diagnosis of cancer in an Egyptian mummy.

Excerpt from article at physorg.com.

View the paper in NatureReviews by clicking here.

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Colorado researcher discovers mechanism for changing adult cells into stem-like cells

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A scheme of the generation of induced pluripot...

A scheme of the generation of induced pluripotent stem (iPS) cells. 1. Isolate and culture host cells. e.g. mouse embryonic fibroblasts and adult human dermal fibroblasts. 2. Introduce the ES specific genes (iPS factors) into the cells by using retrovirus vector. Red cells indicate the cells expressing the exogenous genes. 3. Harvest and culture the cells according to the method for ES cell culture using feeder cells (gray). 4. A subset of the cells generates ES-like colonies, that is, iPS cells;Image via Wikipedia

 

In 2006, Dr. Shimya Yaminaka of Kyoto University in Japan set the stem cell and regenerative medicine research world on fire when he successfully transformed differentiated mouse skin cells into cells that looked and behave like embryonic stem cells. Embryonic stem cells, the subject of much controversy when used in research, have the ability to differentiate into any type of tissue.

Yaminaka’s creation of induced pluripotent stem cells [iPSCs] meant that in the future, research to improve human disease might be able to use iPSCs in lieu of embryonic stem cells. Since then, researchers around the world have been able to replicate his process. However, no one has been able to unlock the mechanism that allows cells to be regressed from differentiated to undifferentiated cells—until now.

University of Colorado Cancer Center researcher Chuan-Yuan Li, PhD, and his group have discovered that so-called “grim-reaper” caspase genes are the gatekeepers that can open the door to allow differentiated adult cells to regress to undifferentiated iPSCs.

Caspases, or cysteine-aspartic proteases/cysteine-dependent aspartate-directed proteases are part of a group of enzymes known as cysteine proteases. Caspases play essential roles in apoptosis (programmed cell death-can occur in a sinle cell surrounded by viable cells), necrosis (premature cell death caused by factors outside a tissue such as trauma or infection-occurs in many cells simultaneously), and inflammation.They exist within the cell as inactive pro-forms or zymogens. These zymogens can be cleaved to form active enzymes following the induction of apoptosis. Failure of apoptosis is one of the main known contributiors to tumour development and autoimmune diseases; this, coupled with the unwanted apoptosis that occurs with ischemia or Alzheimer’s disease, has stimulated interest in caspases as potential therapeutic targets since they were discovered in the mid-1990s.[1,2]

“By doing experiments in which we added caspase inhibitor genes to the Yaminaka protocol, we discovered that when caspases are turned off, you cannot make IPSCs,” says Li, professor of radiation oncology at the University of Colorado School of Medicine. “We were able to shut down the process almost completely.”

The discovery is the cover article in the Oct. 8, 2010 issue of Cell Stem Cell.

“For practical reasons, the discovery is important because even though the transformation to iPSCs is a straightforward process on surface, it is not very efficient, and this information can help increase efficiency,” Li says. “It can also help with the problem of cells that don’t complete the transformation process acting like cancer cells. And from a purely scientific perspective, it is fascinating to understand why the magic happens.”

Li’s group had been working on the roles of caspases in wound healing when Yaminaka published his initial iPSC work in mice. That got Li thinking about potential roles of caspases in iPSC generation.

“I thought maybe caspases could also induce iPS cells instead of the four transcriptional factors that Yamanaka used,” he says. “If that was true, it would be very exciting.”

For six months, his group tried different experiments using various caspase genes to coax human skin cells into iPS cells, but they had no success. Although caspases were not sufficient to make iPS cells, Li kept going with the idea that caspases were somehow involved.

They made their discovery when they introduced the caspase inhibitors into skin cells, which almost completely shut down the induction of iPS cells.

Caspases, Li says, appear to loosen up the built-in controls that make a cell differentiated or undifferentiated, just like a clutch allows a driver to switch gears while driving. Undifferentiated stem-like cells and differentiated cells from one person have the exact same genes. The difference between them is which genes are turned on or off.

In other words, he says, caspases could be the key to a kind of cellular reincarnation—taking a cell that, during human development, became a skin cell back to its original state to become any kind of cell.

“About twenty years ago, a scientist who was among the first to clone the caspase 3 gene named the gene Yama, the Hindu Lord of Death who was responsible for both killing a being and setting him on his way into his reincarnated life,” Li said. “It is now becoming clear that caspases don’t just kill, but they can change the cell’s fate. They could be a mediator of epigenetic changes in multi-cellular organisms.”

###

Members of Li’s research group who were integral to the studies include Fang Li, the paper’s lead author, Zhimin He, Jingping Shen, Qian Huang, Wenrong Li, Xinjian Liu, Yujun He and Frank Wolf.

Sources:

  1. http://www.eurekalert.org/pub_releases/2010-10/uocd-uoc100610.php
  2. Fang Li, Zhimin He, Jingping Shen, Qian Huang, Wenrong Li, Xinjian Liu, Yujun He, Frank Wolf, Chuan-Yuan Li. Apoptotic Caspases Regulate Induction of iPSCs from Human Fibroblasts. Cell Stem Cell, Volume 7, Issue 4, 508-520, 8 October 2010 DOI: 10.1016/j.stem.2010.09.003

References

  1. http://www.sgul.ac.uk/depts/immunology/~dash/apoptosis/caspases.html
  2. http://www.bioscience.org/news/scientis/caspase.htm
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Researchers ask for new focus on ‘sudden death’ heart disorder

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An abrupt, fatal heart attack in a young athlete on the playing field is a tragedy destined to repeat itself over and over until more is understood about hypertrophic cardiomyopathy (HCM), a genetic disorder that is the most common cause of sudden death in young people but which affects people of all ages. So says a task force of cardiologists and cardiac biologists, headed by Thomas L. Force, M.D., James C. Wilson Professor of Medicine at Thomas Jefferson University, in the September 14th online edition of the journal Circulation.

Their special report is the culmination of a 1.5-year effort to sum up the relatively little that is known, and much that remains a mystery, about HCM, and to list what future research priorities should be – all with a goal of developing novel treatments. All 21 researcher-physicians, from institutions around the country, participated in an HCM working group convened by the National Heart, Lung, and Blood Institute. HCM is believed to affect 1 in 500 people, yet without a detailed family and genetic history, many people may not know they are at risk for sudden death, says Dr. Force, who, as a nationally-known cardiology investigator, had led a number of symposiums and study groups to focus on causes and novel therapies for patients with sickened hearts.

“Unbelievably to me, this problem is still not understood or even known to exist by many people, and it remains a very challenging disease to treat,” he says. “The medical management of HCM has changed very little over the past decades.”

HCM

HCM is a thickening of a portion of the myocardium (heart muscle) without any obvious cause.A cardiomyopathy is a primary disease that affects the muscle of the heart. With hypertrophic cardiomyopathy (HCM), the sarcomeres (contractile elements) in the heart replicate causing heart muscle cells to increase in size which causes the heart muscle to thicken. In addition, the normal alignment of muscle cells is disrupted, a phenomenon known as myocardial disarray. HCM also causes disruptions of the electrical functions of the heart.[1]

Genetics  of HCM

HCM is most commonly due to a mutation  in one of of 9 sarcomeric genes that results in a mutated protein in the sarcomere, the primary component of the myocyte (the muscle cell of the heart).[1,3]The sarcomere is a network of proteins that make up the molecular motor of the heart and coordinate the contraction and relaxation of the heart muscle.Around two-thirds of all cases of hypertrophic cardiomyopathy are due to mutations in one of three genes, which code for proteins called the beta -myosin heavy chain, the cardiac troponin T, and myosin binding protein-C.[2]

Hypertrophic cardiomyopathy is an autosomal dominant condition. The term autosomal means that the genes which can cause the disease are located on autosomes, and not on sex chromosomes (in humans there are 22 pairs of autosomes and also the X and Y sex chromosomes ).As a result, this condition can affect females and males in equal numbers and the term dominants means that only one copy of the gene needs to be inherited for the disease to develop.[2]

There are also other genes, including genes that are important in maintaining the heart’s energy supply from stored sugar (glycogen),that can cause a condition that mimics HCM, causing a similar-appearing thickening of the heart muscle.[3]

Inheritance of HCM

A person that carries a mutation has a 50% chance of passing the mutation on to his/her children, regardless of whether he/she has an obvious diagnosis.HCM can also arise in people who have no known family history of it. There may be a few reasons for this to happen. The mutation may have arisen spontaneously in that individual during early embryologic development, rather than being inherited from an affected parent. This is referred to as a sporadic or spontaneous mutation and is typically contained in all, or most, of the cells in the body. Therefore,a person with a sporadic mutation has the same 50/50 chance of passing the mutation on to his/her children as a person with an established and recognized family history of HCM. [3]

Task Force Findings

Diagram of the Heart-Blue components indicate de-oxygenated blood pathways and red components indicate oxygenated blood pathways

“The reason it can be deadly is because people with the disease are often unaware that they have it and physical exertion – such as sports – can bring on the sudden, fatal series of events that causes the heart to go into arrest,” Dr. Force says.

HCM patients can also be significantly disabled by heart failure, and atrial and ventricular tachyarrhythmas. A few medical therapies such as implanting a cardiac defibrillator exist for selected, high-risk patients, but most medical therapies have largely focused on alleviating symptoms of the disease, not on altering its natural history, he says.

Because so little is known about HCM, some have lobbied for mass screening of young athletes, but most physicians feel it is impractical and would lead to a lot of false positives. “A cardiac exam in a general practitioner’s office is not very precise, and more detailed examinations such as routine ECGs would likely be prohibitively expensive and might still miss a significant number of children or could needlessly alarm parents and children,” he says. “Some children with HCM have only a minor amount of hypertrophy in their hearts but they are still prone to sudden death, and people can experience sudden death before any symptoms of heart trouble occur. Again family history becomes very important in identifying potentials at risk”

Given these issues, the recommendations of the task force are important in identifying mechanisms and, ultimately, developing novel therapies, Dr. Force says.

Among them are to:

  • Define all genetic causes: HCM is caused by hundreds of different mutations in genes that encode components of the sarcomere, the contractile apparatus of cardiac muscle. But knowledge of the full spectrum of genes and mutations in HCM is needed to explain how the disease develops and, thus, how it can be treated. For example, Dr. Force says some mutations lead to heart failure, while others lead to sudden death with little evidence of heart damage.
  • Study the natural history of the disease: Establish a multi-center prospective observational cohort study of HCM that represents a range of mutations. This will provide insights into the diagnosis and progression of HCM that will refine clinical practice.
  • Support clinical trials: When potential therapeutic strategies are identified in pre-clinical studies and early clinical trials, a randomized, placebo-controlled multi-center clinical trial should test the therapies. A major goal in treatment of HCM is to limit the life-threatening consequences of arrhythmia, the researchers say.
  • Prevent mutant gene expression: Pharmacologic therapies may only alleviate symptoms, so in order to impact patient survival, strategies are needed that significantly reduce or eliminate expression of HCM mutant genes, the task force says.

Sources

http://www.eurekalert.org/pub_releases/2010-09/tju-rna091410.php

http://circ.ahajournals.org/cgi/content/extract/122/11/1130

References

[1] Hypertrophic Cardiomyopathy wiki

[2] http://www.brighthub.com/science/genetics/articles/77009.aspx#ixzz0zY3P4f4B

[3] http://www.brighamandwomens.org/cvcenter/genetics/documents/GeneticsBasics-long.pdf (pdf)

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Watercress may ‘turn off’ breast cancer signal

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Watercress Beds - Headbourne Worthy;Image by neilalderney123 via Flickr

New scientific research from the University of Southampton has revealed that a plant compound in watercress may have the ability to suppress breast cancer cell development by ‘turning off’ a signal in the body and thereby starving the growing tumour of essential blood and oxygen.

The research, unveiled at a press conference today (14 September 2010), shows that the watercress compound is able to interfere with the function of a protein which plays a critical role in cancer development.

As tumours develop they rapidly outgrow their existing blood supply so they send out signals which make surrounding normal tissues grow new blood vessels,a process called angiogenesis, into the tumour which feed them oxygen and nutrients. Angiogenesis is the physiological process involving the growth of new blood vessels from pre-existing vessels.It is a normal and vital process in growth and development, as well as in wound healing. However, it is also a fundamental step in the transition of tumors from a dormant state to a malignant one.

The research, led by Professor Graham Packham of the University of Southampton, shows that the plant compound (called phenylethyl isothiocyanate) found in watercress can block this process, by interfering with and ‘turning off’  the function of a protein called Hypoxia Inducible Factor (HIF).HIF is a transcription factor that responds to decreases in  oxygen levels or hypoxia,in the cellular environment.”

“Dietary intake of isothiocyanates (ITC) has been associated with reduced cancer risk. The dietary phenethyl ITC (PEITC) has previously been shown to decrease the phosphorylation of the translation regulator 4E binding protein 1 (4E-BP1). Decreased 4E-BP1 phosphorylation has been linked to the inhibition of cancer cell survival and decreased activity of the transcription factor hypoxia-inducible factor (HIF), a key positive regulator of angiogenesis, and may therefore contribute to potential anti-cancer effects of PEITC.”[1] The current study examined the the in vitro and in vivo effects of watercress, which is a rich source of PEITC.

Professor Packham, a molecular oncologist at the University of Southampton, comments: “The research takes an important step towards understanding the potential health benefits of this crop since it shows that eating watercress may interfere with a pathway that has already been tightly linked to cancer development.”

“Knowing the risk factors for cancer is a key goal and studies on diet are an important part of this. However, relatively little work is being performed in the UK on the links between the foods we eat and cancer development.”

Working with Barbara Parry, Senior Research Dietician at the Winchester and Andover Breast Unit, Professor Packham performed a pilot study in which a small group of healthy participants who had previously been treated for breast cancer, underwent a period of fasting before eating 80g of watercress (a cereal bowl full) and then providing a series of blood samples over the next 24 hours.

The research team was able to detect significant levels of the plant compound PEITC in the blood of the participants following the watercress meal, and most importantly, could show that the function of the protein HIF was also measurably affected in the blood cells of the women.

The researchers stated that “dietary intake of watercress may be sufficient to modulate this potential anti-cancer pathway”.However “further investigations with larger numbers of participants are required to confirm these findings”.[1]

The two studies, which have been published in the British Journal of Nutrition and Biochemical Pharmacology, provide new insight into the potential anti-cancer effects of watercress, although more work still needs to be done to determine the direct impact watercress has on decreasing cancer risk.[1,2,3]The findings build on studies that have shown people who vegetables rich in isothiocyanates, such as broccoli and cabbage, are at lower risk of developing cancer [4]

Watercress Alliance member Dr Steve Rothwell says: “We are very excited by the outcome of Professor Packham’s work, which builds on the body of research which supports the idea that watercress may have an important role to play in limiting cancer development.”

A summary of the research has been accepted for inclusion in the Breast Cancer Research Conference which is taking place in Nottingham from 15 to 17 September.

Sources:

[1] Syed Alwi SS, Cavell BE, Telang U, Morris ME, Parry BM, Packham G.(2010)In vivo modulation of 4E binding protein 1 (4E-BP1) phosphorylation by watercress: a pilot study.Br J Nutr. 2010 Jun 15:1-9. [Epub ahead of print]

[2]Inhibition of hypoxia inducible factor by phenethyl isothiocyanate (2009)Biochemical Pharmacology
Volume 78, Issue 3, 1 August 2009, Pages 261-272

[3] Press release:http://www.soton.ac.uk/mediacentre/news/2010/sep/10_94.shtml

[4]Compounds in broccoli, cauliflower, and watercress block lung cancer progression

Further Reading:

Five reasons you should eat watercress

Dietary Chemopreventive Phytochemicals: Too Little or Too Much?

Watercress wiki

Watercress Recipes

http://www.watercress.co.uk/recipes/

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Fraudulent Scientific Paper?-Theres a Site for that…

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Embryonic Stem Cells. (A) shows hESCs. (B) sho...

Human embryonic stem cells A: Cell colonies that are not yet differentiated. B: Nerve cell.Image via Wikipedia

A new website,aptly named Scientific Red Cards,has been set up  to take  inventory of scientific publications for which research misconduct has been assessed.The database is based on user contributions,with the focus being on fraudulent articles and not scientists.

According to a note in Nature, one in three scientists confesses to having misbehaved in the past three years.Few will forget the case of Woo Suk Hwang,a South Korean stem cell researcher, who in 2006 was found to have falsely claimed to have cloned eleven patient- specific embryos in a scientific paper .The storm that followed  set back the field of therapeutic cloning and eroded public trust in science.However, in a twist if fate, it was later found that Hwang and his team had managed to produce stem cells-just not through cloning-but instead through a process called parthenogenesis.Scientists have long hoped to use parthenogenesis to produce stem cells.

‘In parthenogenesis, an unfertilized egg is stimulated to start dividing as if it had been joined by sperm. It develops for a while under the control of its own DNA. Some species, such as sharks, can reproduce that way. ‘However human eggs can’t develop long enough to make a baby.

In cloning,an egg’s DNA is removed and replaced with genetic material from a person. It is then stimulated, as in parthenogenesis, but it develops under the control of the donor’s DNA rather than its own DNA.

In the discredited 2004 paper, Hwang and his co-authors addressed the possibility of parthenogenesis. They wrote that they couldn’t completely rule it out, but they presented evidence to support their claim of cloning.So what happened? Were they fooled or did they deliberately lie?The answer is that we don’t know and may never know…

References

http://www.scientificredcards.org/content/about

http://www.nature.com/news/specials/hwang/index.html

http://www.msnbc.msn.com/id/20090129/

Further Reading

http://www.msnbc.msn.com/id/10589085/

http://en.wikipedia.org/wiki/Hwang_Woo-Suk#

http://www.the-scientist.com/blog/display/55879/

http://sciyo.com/

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Irish Researchers Fighting Fungal Infections With Bacteria

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Pseudomonas aeruginosa

Pseudomonas aeruginosa;Image by denn via Flickr

A bacterial pathogen can communicate with yeast to block the development of drug-resistant yeast infections according to Irish scientists writing in the May issue of Microbiology. The research could be a step towards new strategies to prevent hospital-acquired infections associated with medical implants.

Read more at: http://www.scientificblogging.com/subtle_science/blog/irish_researchers_fighting_fungal_infections_bacteria_0

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Flower Could Revolutionise Leukemia Treatment

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From the Daily Mail

Baby's Breath

“Scientists unveiled a major medical breakthrough that could revolutionise the treatment of leukaemia patients and save thousands of lives.

Experts have discovered that an extract from the white flower commonly known as Baby’s Breath can boost the efficiency of anti-cancer drugs by a staggering million times.

They found that molecules called saponins, extracted from the Gypsophila Paniculata plant, appear to break down the membrane of cancer cells.”



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