Archive for May, 2014

By Traci Pedersen Associate News Editor Reviewed by John M. Grohol, Psy.D. on May 25, 2014

Neurons generated from the skin cells of schizophrenia patients behave strangely in the early developmental stages, offering clues that might lead to earlier detection and treatment, according to scientists from the Salk Institute.

The study, published in the journal Molecular Psychiatry, supports the theory that the neurological dysfunction that eventually leads to schizophrenia may begin in the brains of fetuses.

This study aims to investigate the earliest detectable changes in the brain that lead to schizophrenia, said Fred H. Gage, Ph.D., professor of genetics at Salk. We were surprised at how early in the developmental process that defects in neural function could be detected.

Up until now, scientists could only study the disease by examining the brains of cadavers; but age, stress, medication, or drug abuse had often changed or damaged these brains, making it harder to figure out the where it all began.

The Salk scientists were able to go around this obstacle by using stem cell technologies. They took skin cells from patients, coaxed the cells back to an earlier stem cell form and then prompted them to grow into very early-stage neurons called neural progenitor cells (NPCs). These NPCs are similar to cells found in the brain of a fetus.

The researchers tested the cells in two ways: In one test, they looked at how far the cells moved and interacted with particular surfaces; in the other test, they looked at cell stress by imaging mitochondria, tiny organelles that generate energy for the cells.

On both tests, the NPCs from schizophrenia patients differed in significant ways from those taken from people without the disease.

In particular, cells taken from people with schizophrenia showed unusual activity in two major classes of proteins: those involved in adhesion and connectivity, and those involved in oxidative stress. Schizophrenia neural cells seemed to have aberrant migration (which may result in the poor connectivity seen later in the brain) and greater levels of oxidative stress.

These results support the current theory that eventsduring pregnancy can contribute to schizophrenia, even though symptoms typically dont begin until early adulthood. For example, previous research suggests that pregnant mothers who experience infection, malnutrition, or extreme stress are at greater risk of having children with schizophrenia.

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Skin Cell Research Suggests Schizophrenia Begins in Womb

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Stem cell therapy | biopen Copy
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Stem cell therapy | biopen Copy - Video

PUBLIC RELEASE DATE:

25-May-2014

Contact: Scott LaFee slafee@ucsd.edu 619-543-6163 University of California - San Diego

Researchers at the University of California, San Diego School of Medicine have identified a mutated gene common to adenosquamous carcinoma (ASC) tumors the first known unique molecular signature for this rare, but particularly virulent, form of pancreatic cancer.

The findings are published in the May 25 advance online issue of Nature Medicine.

Pancreatic cancer is the fourth leading cause of cancer-related death in the United States, with roughly 45,220 new cases diagnosed and more than 38,400 deaths annually. Both numbers are rising. ASC cases are infrequent, but typically have a worse prognosis than more common types of pancreatic cancer.

"There has been little progress in understanding pancreatic ASC since these aggressive tumors were first described more than a century ago," said co-senior author Miles F. Wilkinson, PhD, professor in the Department of Reproductive Medicine and a member of the UC San Diego Institute for Genomic Medicine. "One problem has been identifying mutations unique to this class of tumors."

In their paper, Wilkinson, co-senior author Yanjun Lu, PhD, of Tongji University in China, and colleagues report that ASC pancreatic tumors have somatic or non-heritable mutations in the UPF1 gene, which is involved in a highly conserved RNA degradation pathway called nonsense-mediated RNA decay or NMD. It is the first known example of genetic alterations in an NMD gene in human tumors.

NMD has two major roles. First, it is a quality control mechanism used by cells to eliminate faulty messenger RNA (mRNA) molecules that help transcribe genetic information into the construction of proteins essential to life. Second, it degrades a specific group of normal mRNAs, including those encoding proteins promoting cell growth, cell migration and cell survival. Loss of NMD in these tumors may "release the brakes on these molecules, and thereby driving tumor growth and spread," said Wilkinson.

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Gene mutation found for aggressive form of pancreatic cancer

Crowd marches against genetic engineering of food
Crowd marches against genetic engineering of food.

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How Genetic Engineering Can Cure Drug Addiction? Michael Crichton on Treatment (2006)
Genetic engineering, also called genetic modification, is the direct manipulation of an organism #39;s genome using biotechnology. New DNA may be inserted in the...

By: Remember This

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How Genetic Engineering Can Cure Drug Addiction? Michael Crichton on Treatment (2006) - Video

Object Oriented Programming
In object oriented programming, "Objects" usually refer to bundles of information. For example, you can describe a Car as having #39;number_of_wheels = 4 #39; and #39;license_plate = 4BIUO11 #39;, and this...

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Object Oriented Programming - Video

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26-May-2014

Contact: Philippa Walker 44-117-928-8086 University of Bristol

An international team of scientists has made a major step forward in our understanding of how enzymes 'edit' genes, paving the way for correcting genetic diseases in patients.

Researchers at the Universities of Bristol, Mnster and the Lithuanian Institute of Biotechnology have observed the process by which a class of enzymes called CRISPR pronounced 'crisper' bind and alter the structure of DNA.

The results, published in the Proceedings of the National Academy of Sciences (PNAS) today, provide a vital piece of the puzzle if these genome editing tools are ultimately going to be used to correct genetic diseases in humans.

CRISPR enzymes were first discovered in bacteria in the 1980s as an immune defence used by bacteria against invading viruses. Scientists have more recently shown that one type of CRISPR enzyme Cas9 can be used to edit the human genome - the complete set of genetic information for humans.

These enzymes have been tailored to accurately target a single combination of letters within the three billion base pairs of the DNA molecule. This is the equivalent of correcting a single misspelt word in a 23-volume encyclopaedia.

To find this needle in a haystack, CRISPR enzymes use a molecule of RNA - a nucleic acid similar in structure to DNA. The targeting process requires the CRISPR enzymes to pull apart the DNA strands and insert the RNA to form a sequence-specific structure called an 'R-loop'.

The global team tested the R-loop model using specially modified microscopes in which single DNA molecules are stretched in a magnetic field. By altering the twisting force on the DNA, the researchers could directly monitor R-loop formation events by individual CRISPR enzymes.

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Breakthrough shows how DNA is 'edited' to correct genetic diseases

A level. O.10. Chi squared test and genetics (Ms Cooper)

By: Ms Cooper #39;s Cambridge A level Biology

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A level. O.10. Chi squared test and genetics (Ms Cooper) - Video

Joel Dudley : Assistant Professor of Genetics Genomics

By: Stanford Medicine

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Joel Dudley : Assistant Professor of Genetics & Genomics - Video

Minecraft: ADVANCED GENETICS MOD! Attack Of The B-Team Minecraft Mod Survival (40)
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The Sims 3: Perfect Genetics Challenge - Ep. 3

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The Sims 3: Perfect Genetics Challenge - Ep. 3 - Video

Combine some microbiologists with some mechanical engineers and you never know what might happen.

A recent collaboration of those two fields of scientists at Brigham Young University produced a machine so small it takes a microscope to see it.

It's not just for fun, however. It could pave the way for research into diseases including Alzheimer's, cancer and diabetes.

For decades scientists have conducted gene research by transferring genetic material into a new cell by a process called microinjection. It was just considered an unfortunate by-product of the process to have 40 percent of the cells die.

Enter BYU and a different process called nanoinjection, which occurs by transferring material including DNA into cells.

"Because DNA is naturally negatively charged, it is attracted to the outside of the lance using positive voltage," said Brian Jensen, a BYU professor of mechanical engineering, in a release. "Once we insert the lance into a cell, we simply reverse the polarity of the electrical force and the lance releases the DNA."

The lance being used is 10 times smaller than what was used previously. In the past, researchers used a hollow needle to pump a DNA-filled liquid into an egg cell nucleus, but the extra fluid caused many of the cells to swell and die.

With the new method, the team found that nearly 80 percent of the cells proceeded to the next stage of development, a significant increase from the previous 60 percent success rate.

No extra fluid is used and the cells undergo less stress and have a higher survival rate.

"It is really great engineering stuff," said Sandra Burnett, associate professor of microbiology at BYU.

Continued here:
Smaller is better: BYU creates new gene therapy technology

by Jason Whitely / WFAA.com

WFAA.com

Posted on May 24, 2014 at 10:38 AM

Updated yesterday at 10:38 AM

DALLAS Hispanics, African Americans and Asians have a more difficult time of getting a bone marrow transplant because the national database of potential donors doesnt include many minorities.

But, an effort is underway over the Memorial Day weekend to increase the number of minority donors.

Jose Barrera is among the thousands suffering from a blood cancer specifically Chronic Myeloid Leukemia but he never showed a symptom of it.

"Your body flushes out the white blood cells in your body," Barrera explained. "But with me, the dead ones were just staying in my blood stream and they were overcrowding and that's when you develop cancerous cells."

Barrera, 22, works weekends at Sherlock's Baker Street Pub on Park Lane and studies accounting at the University of North Texas.

Doctors discovered his CML during a routine eye exam at Wal-Mart last September. Fortunately, he said, its the most curable.

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Critical need for Hispanic, minority bone marrow donors

Towards the democratization of cell therapy

By: Roberto Hernan

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Towards the democratization of cell therapy - Video

Genetic Engineering...allowed to what extent?
To what extent the Genetic Engineering is allowed? #39; #39; #39; #39;

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Genetic Engineering...allowed to what extent? - Video

Scotch Moses: Genetic Engineering
For more from Scotch Moses, subscribe to their channel: http://www.youtube.com/subscription_center?add_user=scotchmosesofficial A pregnant couple decides just how much to mess with mother...

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AOTBT #21- Advanced Genetics Mod!
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The Sims 3 Perfect Genetics Challenge (Part 4) Baby Tucker!
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The world has great expectations that stem cell research one day will revolutionize medicine. But in order to exploit the potential of stem cells, we need to understand how their development is regulated. Now researchers from University of Southern Denmark offer new insight.

Stem cells are cells that are able to develop into different specialized cell types with specific functions in the body. In adult humans these cells play an important role in tissue regeneration. The potential to act as repair cells can be exploited for disease control of e.g. Parkinson's or diabetes, which are diseases caused by the death of specialized cells. By manipulating the stem cells, they can be directed to develop into various specialized cell types. This however, requires knowledge of the processes that regulate their development.

Now Danish researchers from University of Southern Denmark report a new discovery that provides valuable insight into basic mechanisms of stem cell differentiation. The discovery could lead to new ways of making stem cells develop into exactly the type of cells that a physician may need for treating a disease.

"We have discovered that proteins called transcription factors work together in a new and complex way to reprogram the DNA strand when a stem cell develops into a specific cell type. Until now we thought that only a few transcription factors were responsible for this reprogramming, but that is not the case," explain postdoc Rasmus Siersbaek, Professor Susanne Mandrup and ph.d. Atefeh Rabiee from Department of Biochemistry and Molecular Biology at the University of Southern Denmark.

"An incredibly complex and previously unknown interplay between transcription factors takes place at specific locations in the cell's DNA, which we call 'hotspots'. This interplay at 'hotspots' appears to be of great importance for the development of stem cells. In the future it will therefore be very important to explore these 'hotspots' and the interplay between transcription factors in these regions in order to better understand the mechanisms that control the development of stem cells," explains Rasmus Siersbaek.

"When we understand these mechanisms, we have much better tools to make a stem cell develop in the direction we wish," he says.

Siersbaek, Mandrup and their colleagues made the discovery while studying how stem cells develop into fat cells. The Mandrup research group is interested in this differentiation process, because fundamental understanding of this will allow researchers to manipulate fat cell formation.

"We know that there are two types of fat cells; brown and white. The white fat cells store fat, while brown fat cells actually increase combustion of fat. Brown fat cells are found in especially infants, but adults also have varying amounts of these cells.

"If we manage to find ways to make stem cells develop into brown rather than white fat cells, it may be possible to reduce the development of obesity. Our findings open new possibilities to do this by focusing on the specific sites on the DNA where proteins work together," the researchers explain.

Details of the study

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Stem cell development: Experts offer insight into basic mechanisms of stem cell differentiation

Arthritic knee 10 weeks after stem cell therapy by Dr Harry Adelson
Frank describes his results for his stem cell therapy injection by Dr Harry Adelson for his arthritic knee http://www.docereclinics.com.

By: Harry Adelson, N.D.

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4 Michael Jewett, MD Research Priorities, Survivorship, Genetics, Quality and Personalized Medicine
2014 Patient Conference.

By: KidneyCancerCanada

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4 Michael Jewett, MD Research Priorities, Survivorship, Genetics, Quality and Personalized Medicine - Video

Spinal cord research helps paralysed hand to move again
For the first time, scientists in Newcastle University #39;s Institute of Neuroscience have been able to restore the ability to grasp with a paralysed hand using...

By: Newcastle University

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Spinal cord research helps paralysed hand to move again - Video

Achondroplasia Gene Research
#39;Achondroplasia, a medical disorder of bone growth that is the most common form of short-limb dwarfism. The research project carried by USM researcher, Lee L...

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Achondroplasia Gene Research - Video

May 23, 2014

Image Caption: Microscopic image of human cells (stained purple), showing the primary cilium (green). A new study shows how FTO, a gene commonly associated with obesity, contributes to weight gain. Changes in this gene indirectly affect the function of the cilium -- a hair-like appendage found on brain and other cells. Irregularities in the cilium, in turn, can affect receptors for leptin, which suppresses appetite. Credit: Lab of Rudolph L. Leibel, M.D.

Columbia University Medical Center

Researchers have discovered how a gene commonly linked to obesityFTOcontributes to weight gain. The study shows that variations in FTO indirectly affect the function of the primary cilium, a little-understood hair-like appendage on brain and other cells. Specific abnormalities of cilium molecules, in turn, increase body weight, in some instances, by affecting the function of receptors for leptin, a hormone that suppresses appetite. The findings, made in mice, suggest that it might be possible to modify obesity through interventions that alter the function of the cilium, according to scientists at Columbia University Medical Center (CUMC).

If our findings are confirmed, they could explain how common genetic variants in the gene FTO affect human body weight and lead to obesity, said study leader Rudolph L. Leibel, MD, the Christopher J. Murphy Memorial Professor of Diabetes Research, professor of pediatrics and medicine, and co-director of the Naomi Berrie Diabetes Center at CUMC. The better we can understand the molecular machinery of obesity, the better we will be able to manipulate these mechanisms and help people lose weight.

The study was published on May 6 in the online edition of Cell Metabolism.

Since 2007, researchers have known that common variants in the fat mass and obesity-associated protein gene, also known as FTO, are strongly associated with increased body weight in adults. But it was not understood how alterations in FTO might contribute to obesity. Studies have shown that knocking out FTO in mice doesnt necessarily lead to obesity, and not all humans with FTO variants are obese, said Dr. Leibel. Something else is going on at this location that we were missing.

In experiments with mice, the CUMC team observed that as FTO expression increased or decreased, so did the expression of a nearby gene, RPGRIP1L. RPGRIP1L is known to play a role in regulating the primary cilium. Aberrations in the cilium have been implicated in rare forms of obesity, said Dr. Leibel. But it wasnt clear how this structure might be involved in garden-variety obesity.

Dr. Leibel and his colleague, George Stratigopoulos, PhD, associate research scientist, hypothesized that common FTO variations in noncoding regions of the gene do not change its primary function, which is to produce an enzyme that modifies DNA and RNA. Instead, they suspected that FTO variations indirectly affect the expression of RPGRIP1L. When Dr. Stratigopoulos analyzed the sequence of FTOs intronits noncoding, or nonprotein-producing, portionwe found that it serves as a binding site for a protein called CUX1, said Dr. Leibel. CUX1 is a transcription factor that modifies the expression of RPGRIP1L.

Next, Dr. Stratigopoulos set out to determine whether RPGRIP1L plays a role in obesity. He created mice lacking one of their two RPGRIP1L genes, in effect, reducing but not eliminating the genes function. (Mice that lack both copies of the gene have several serious defects that would obscure the effects on food intake.) Mice with one copy of RPGRIP1L had a higher food intake, gained significantly more weight, and had a higher percentage of body fat than controls.

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How Does Common Obesity Gene Contribute To Weight Gain?