“Steven and David Elmore were born identical twins, but their first days in this world could not have been more different. David came home from the hospital after a week. Steven, born four minutes later, stayed behind in the ICU. For a month he hovered near death in an incubator, wracked with fever from what doctors called a dangerous viral infection. Even after Steven recovered, he lagged behind his twin. He lay awake but rarely cried. When his mother smiled at him, he stared back with blank eyes rather than mirroring her smiles as David did. And for several years after the boys began walking, it was Steven who often lost his balance, falling against tables or smashing his lip.

Those early differences might have faded into distant memory, but they gained new significance in light of the twins’ subsequent lives. By the time Steven entered grade school, it appeared that he had hit his stride. The twins seemed to have equalized into the genetic carbon copies that they were: They wore the same shoulder-length, sandy-blond hair. They were both B+ students. They played basketball with the same friends. Steven Elmore had seemingly overcome his rough start. But then, at the age of 17, he began hearing voices…”

Read the rest of this great article at Discover Magazine Online.

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Read the rest of the article by clicking here

http://bit.ly/c7oy0b

“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 Greece 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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Got ideas that could help produce the next drug,diagnostic test or process.Could you come up with the answer to a company’s research question?
Want to some earn money for solving these problems…then this is for you..

Become a solver:
http://www.nature.com/openinnovation?moreChallenges=true

http://www2.innocentive.com/

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“When hackers leaked thousands of e-mails from the Climatic Research Unit (CRU) at the University of East Anglia in Norwich, UK, last year, global-warming sceptics pored over the documents for signs that researchers had manipulated data. No such evidence emerged, but the e-mails did reveal another problem — one described by a CRU employee named “Harry”, who often wrote of his wrestling matches with wonky computer software….”

Excerpt  from Nature.com/news;Read more by clicking the following link:http://bit.ly/bpZBOD

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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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Single Protein crystal of Lysozyme;Image via Wikipedia

Washington, D.C. (September 14, 2010) — Because one of the main bottlenecks in determining the structure of protein molecules is producing good isolated single crystals, improved crystallization techniques would be useful in a wide range of genomics and pharmaceutical research.

Research reported in The Journal of Chemical Physics uses fluorescence correlation spectroscopy (FCS) to investigate the processes at the surface of a growing crystal. By focusing a laser on the crystal surface and measuring the resulting fluorescence, FCS can resolve dimensions as small as a single wavelength of the light.

FCS

Fluorescence correlation spectroscopy (FCS) is one of the many different modes of high-resolution spatial and temporal (relating to time) analysis of extremely low concentrated biomolecules.”In contrast to other fluorescence techniques, the parameter of primary interest is not the emission intensity itself, but rather spontaneous intensity fluctuations caused by the minute deviations of the small system from thermal equilibrium. In general, all physical parameters that give rise to fluctuations in the fluorescence signal are accessible by FCS. It is, for example, rather straightforward to determine local concentrations, mobility coefficients or characteristic rate constants of inter- or intramolecular reactions of fluorescently labeled biomolecules in nanomolar concentrations. FCS is a is a versatile technique that already has demonstrated its vast possibilities for many different problems.It is often used together with other confocal fluorescence readout techniques – one of the standard tools used for high-throughput screening, combining very short data acquisition times with straightforward analysis.[1]

“Another advantage of fluorescence is that it provides a high signal-to-noise ratio,” says author Shinpei Tanaka of Hiroshima University in Japan. “We are able to measure very dilute solutions at the crystal interface.”

Research Findings

The researchers found that when single tetragonal crystals of egg-white lysozyme formed, there was no concentration gradient between the solution and the crystal surface. However, in formation of clumps of needle-like branched crystals, called spherulites, the observed concentration at the surface was several times higher than that of the bulk solution. The authors attributed the difference to aggregates of loosely bound molecules near the interface.

Characterization of the dynamics near the crystal by FCS may provide direction for improving the crystallization process — currently as much an art as a science, based on trial and error — because the spherulites are not usable for structural characterizations.

“Although we knew something was different between the two crystal forms, the degree of concentration of the molecules in spherulites compared to that of the homogeneous state around tetragonal single crystals was surprising,” says Tanaka.

The analytical result could lead to improvements in isolation of good crystals of biomolecules. For example, the results suggest that local heating by a laser could be used to control local concentrations and avoid spherulite formation.

“Slow molecular dynamics close to crystal surfaces during crystallization of a protein lysozyme studied by fluorescence correlation spectroscopy” by Shinpei Tanaka appears in The Journal of Chemical Physics. http://link.aip.org/link/jcpsa6/v133/i9/p095103/s1

http://www.eurekalert.org/pub_releases/2010-09/aiop-hdy091310.php

References

[1] http://www.biophysics.org/Portals/1/PDFs/Education/schwille.pdf

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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

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)

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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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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