Craig Hitchens Therapies - Health Online

Being able to sequence a human genome for $1,000 or less (which is the price most insurance companies are willing to pay) could open a new era in personal medicine, making it possible to precisely diagnose the cause of many diseases and tailor drugs and treatment procedures to the genetic make-up of an individual.

Professor Aleksei Aksimentiev at the University of Illinois at Urbana Champaignhas demonstrated a strategy for sequencing DNA by driving the DNA molecule back and forth through a nanopore capacitor in a semiconductor chip. As DNA passes through the nanopore, the DNA molecule’s electric field induces sequence-specific electrostatic potentials that can be detected at the top and bottom layers of the capacitor membrane.

“Despite the tremendous interest in using nanopores for sequencing DNA, it was unclear how, exactly, nanopores could be used to read the DNA sequence,”said Professor Aksimentiev. “We now describe one such method.”

“Through molecular dynamics simulations, we demonstrate that back-and-forth motion of a DNA molecule in a nanopore capacitor 1 nanometer in diameter produces an electrostatic fingerprint that can be used to read the genetic sequence,”said Aksimentiev, who also is a researcher at the Beckman Institute.

In the researchers’ simulations, performed at the university’s National Center for Supercomputing Applications, the nanopore capacitor consists of two conducting layers of doped silicon, separated by an insulating layer of silicon dioxide.

“A semiconductor device capable of reading the electrostatic potentials and decoding the genetic sequence is within the grasp of current technology”,Aksimentiev said.  “Nanometer pores in electronic membranes have been manufactured, and the voltage signals resulting from DNA movement through such pores have been recorded.”

The next big challenge, Aksimentiev said, is to minimize noise in the system, and reduce the speed of DNA molecules moving through the pore.

For further information, click on the following link:

http://www.news.uiuc.edu/news/07/1212dna.html

Elaine Warburton

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              DNA profiling

There has been a recent case in Northern Ireland whereby an Omagh bombing suspect was cleared of all murder charges as the integrity of the forensic test which made up the bulk of the prosecution case was called into question. 

The test in question is Low Copy Number DNA profiling or LCN DNA profiling.   LCN testing allows genetic profiles of offenders to be created from very small tissue samples that have only been detectable with new techniques available since 1999. These can be as tiny as a millionth the size of a grain of salt which can amount to as little as a few cells of skin or sweat left in a fingerprint.

The Forensic Science Service (FSS) in the UK say they have used LCN DNA about 21,000 times and generated profiles from items such as matchsticks, weapon handles and grabbed clothing, some dating back to unsolved crimes.  To do this, the minute samples, maybe comprising 1-2 strands of DNA, are magnified almost fifty times by PCR techniques and this is where critics say errors can creep in - if the DNA is damaged in any way, the replicated DNA will also include the damaged areas and therefore, may not truly reflect the original DNA.  The worst case scenario is that it reflects an innocent person’s DNA.

Traditional or so-called “gold standard” DNA profiles are created using larger samples of genetic material and are not under scrutiny.

As a result Police Forces in the UK and Northern Ireland have suspended use of this test.  In addition, other Police Forces around the world are reviewing cases where LCN DNA profiling resulted in the successful prosecution of suspects.  Included in this are several high profile international cases including the murder of Swedish Foreign Minister Anna Lindh by Mijailo Mijailovic and in Australia, the murder of a backpacker Peter Falconio by Bradley Murdoch.

Elaine Warburton

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Brain cells 

I just love this following article which tells us that there could be enough computing ability in just one brain cell to allow human and animals to feel! There is one question that springs to mind, though … if we have so many billion neurons each with the capability of storing vast amounts of information … why am I increasingly unable to retain the simplest of facts?  Think I need to upgrade my brain model!

The brain has 100 billion neurons but scientists had thought they needed to join forces in larger networks to produce thoughts and sensations. The complexity of the human brain and how it stores countless thoughts, sensations and memories are still not fully understood.

However, a research team from the Humboldt University in Germany and the Erasmus Medical Center in the Netherlands, stimulated single neurons in rats and found this was enough to trigger a behavioral response when their whiskers were touched.

A second research project from the US suggests the computational ability of each brain cell could be even more complex, with different synapses - the many junctions between neurons and other nerve cells - able to act independently from those found elsewhere on the same cell.

This could mean that, within a single neuron, different synapses could be storing or processing completely different bits of information.

Elaine Warburton

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Further to my article on Fragile X Syndrome the BBC health website has posted this article:

“Genetic engineering has been used to alleviate symptoms Fragile X in mice, which is a leading cause of inherited learning difficulties and autism. There is currently no treatment for Fragile X syndrome, also linked to epilepsy and abnormal body growth, but the new work raises hopes of progress.

A Massachusetts team were able to trigger big improvements in the mice by tweaking just one gene, FMRP. The researchers, from the Picower Institute for Learning and Memory at Massachusetts Institute of Technology, examined mice which lack the FMRP gene, and show many of the symptoms associated with fragile X.

They also created mice that not only lacked FMRP, but also had a 50% reduction in mGluR5. This second group of mice showed fewer symptoms of fragile X, fewer signs of abnormalities in the brain, and fewer signs of abnormal body growth. For example, loss of the FMRP gene produces overgrowth of connections between nerve cells called dendritic spines.   However, when coupled with a 50% reduction in mGluR5, spine density was completely normal. The ‘double mutant’ mice also showed substantial reduction in epileptic seizures.

Lead researcher Dr Mark Bear said: “These findings have major therapeutic implications for fragile X syndrome and autism.”

Fragile X syndrome is known to be caused by loss of the gene for “fragile X mental retardation protein” (FMRP), which is believed to act as a brake on protein synthesis in specific areas of brain circuitry. The authors’ idea was that loss of the “brake” would allow another protein that stimulates this process, called metabotropic glutamate receptor 5 (mGluR5), to function unchecked.

For further information on this research visit: www.cellpress.com

Elaine Warburton

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Researchers at the Albert Einstein College of Medicine of Yeshiva University, in New York, claim they have found the genes responsible for storing fat in cells.  They have identified the FIT1 and FIT2 (Fat-Inducing Transcripts 1 and 2) genes that package fat in the form of lipid droplets.  Storing fat in lipid droplets is important for enabling cells to use fat as an energy source ….  but having high amounts of these droplets leads to obesity.

Obesity is a major cause of Type 2 diabetes, which is becoming a world epidemic. The discovery of genes that influence the development of obesity could help allow scientists and physicians to understand why some people gain weight more than others.

The study’s findings could open up a wealth of new avenues to understand and treat obesity and obesity-related conditions such as Type 2 diabetes.

Elaine Warburton

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