GMO corn turns stomachs to mush

GMO

GMO

 

If you have stomach problems or gastrointestinal problems, a new study led by Dr. Judy Carman may help explain why: pigs fed a diet of genetically engineered soy and corn showed a 267% increase in severe stomach inflammation compared to those fed non-GMO diets. In males, the difference was even more pronounced: a 400% increase. (For the record, most autistic children are males, and nearly all of them have severe intestinal inflammation.)

The study was conducted on 168 young pigs on an authentic farm environment and was carried out over a 23-week period by eight researchers across Australia and the USA. The lead researcher, Dr. Judy Carman, is from the Institute of Health and Environmental Research in Kensington Park, Australia. The study has now been published in the Journal of Organic Systems, a peer-reviewed science journal.

The study is the first to show what appears to be a direct connection between the ingestion of GMO animal feed and measurable damage to the stomachs of those animals. Tests also showed abnormally high uterine weights of animals fed the GMO diets, raising further questions about the possibility of GMOs causing reproductive organ damage.

Proponents of corporate-dominated GMO plant science quickly attacked the study, announcing that in their own minds, there is no such thing as any evidence linking GMOs to biological harm in any animals whatsoever. And they are determined to continue to believe that, even if it means selectively ignoring the increasingly profound and undeniable tidal wave of scientific studies that repeatedly show GMOs to be linked with severe organ damage, cancer tumors and premature death.

“Adverse effects… toxic effects… clear evidence”

The study was jointly announced by GM Watch and Sustainable Pulse.

Lead author of the study Dr. Judy Carman stated, “We found these adverse effects when we fed the animals a mixture of crops containing three GM genes and the GM proteins that these genes produce. Yet no food regulator anywhere in the world requires a safety assessment for the possible toxic effects of mixtures. Our results provide clear evidence that regulators need to safety assess GM crops containing mixtures of GM genes, regardless of whether those genes occur in the one GM plant or in a mixture of GM plants eaten in the same meal, even if regulators have already assessed GM plants containing single GM genes in the mixture.”

The following photo shows one of the pig intestines fed a non-GMO diet vs. a pig intestine fed a GMO diet. As you can see from the photo, the pig fed the GMO diet suffered severe inflammation of the stomach:

Yet more evidence that GMOs damage mammals

The study adds to the weight of scientific evidence from others studies which show that rats fed a diet of GMOs grow horrifying cancer tumors and suffer premature death.

A scientific study published last year concluded that eating genetically modified corn (GM corn) and consuming trace levels of Monsanto’s Roundup herbicide was linked with rats developing shockingly large tumors, widespread organ damage, and premature death.

That study was also criticized by corporate GMO trolls who argued that scientists should not show pictures of rats with large cancer tumors caused by GMOs because the pictures scare consumers into being afraid of GMOs.

Here are some of the pictures they don’t want you to see, taken right from the public announcement of the study:

That study also found that rats fed GM corn suffered severe kidney damage as well as shockingly high rates of premature death.
Source:  naturalnews.com

Y Chromosome Retains Key Genes for Fertility

Study Dispels Theories of Y Chromosome’s Demise:

Stripped-Down Chromosome Retains Key Genes for Fertility

Stripped-Down Chromosome Retains Key Genes for Fertility

 

“Y chromosome has lost 90 percent of genes that once shared with the X chromosome, and some scientists have speculated that the Y chromosome will disappear in less than 5 million years ,” said evolutionary biologist Melissa A. Wilson Sayres a Miller Postdoctoral Fellow in the Department of Integrative Biology , University of California, Berkeley, and lead author of the new analysis .

Some mammals have lost their Y chromosome, although they still have men and women and reproduce normally . Researchers reported some shuffling genes in mice to create Y- less males could produce normal offspring , leading some analysts to wonder if the chromosome is superfluous.

“Our study shows that genes that have remained , and those who migrated from X to Y , that are important , and human and will stay for a long time,” he said.

Wilson Sayres and coauthor Rasmus Nielsen, in PLoS Genetics that patterns of variation in the Y chromosome among the 16 men are consistent with the selection naturally acts to maintain gene content there, many of which have been shown to play a role in male fertility. Insignificant size of the Y chromosome – which contains 27 unique genes in front of thousands of people in the other chromosomes – is a sign that is lean and stripped to essentials.

“The results are quite impressive. They show that because there is a lot of natural selection working on the Y chromosome , which has to be much more depending on the chromosome of people previously thought,” Nielsen said.

Variations in the Y chromosomes are used to track human populations moved around the world, and according to Nielsen , the new research will help improve estimates of the evolutionary history of humans.

” Melissa has shown that this strong negative selection – natural selection to eliminate deleterious genes – tends to make us think the dates are older than they are , which gives very different estimates of the history of our ancestors,” Nielsen said.  And it has degraded over the past 200 million

Before about 200 million years ago when mammals were relatively new to the Earth, the first versions of the sex chromosomes, X and Y, were like other pairs of chromosomes in each generation , they swapped a pair of genes for the children were a mix of genes from their parents. Fertilized eggs obtained two proto -X became females and eggs with a proto -X and proto -Y became men.

But for some reason , said Wilson Sayres , the gene that triggers the cascade of events that result in male characteristics became fixed on the Y chromosome and attracted other gene specific , such as those that control the development of the testes men , sperm and semen. Many of them proved to be harmful to women , so that the X and Y stopped exchanging genes and the two chromosomes began to evolve separately.

“Now the X and Y do not exchange DNA over most of its length , which means that Y can not be efficiently fix errors , so degraded over time,” he said. “In XX females , the X still has a partner to exchange with and correct mistakes , so we think the X has also degraded . ”

Wilson Sayres was fascinated by the strange story of the sex chromosomes , and in particular , the lack of genetic variation worldwide in the Y chromosome compared to the range observed in the DNA in the non-sex chromosomes. This variation , although used to trace human history, was poorly characterized in whole chromosome Y. .

” Y chromosomes are more similar to each other than we expect ,” said Wilson Sayres . “There has been some debate about whether this is because there are fewer men who contribute to the next generation , or whether natural selection acts to eliminate variation . ”

Did genes contribute fewer males the Y chromosome ?

UC Berkeley researchers showed that if fewer males were the only cause of low variability , mean that less than 1 in 4 men throughout history had happened in his chromosome each generation. Variations in other human chromosomes , including the X chromosome, making it an unlikely scenario . Instead, showed low variation will be explained by intense natural selection , ie , a strong evolutionary pressure to weed out the bad mutations that eventually cut the chromosome to its essential elements.

” We show that a model of purifying selection acting on the Y chromosome to eliminate harmful mutations , in combination with a moderate reduction in the number of men who are going into their chromosomes and may explain low Y diversity , ” said Wilson Sayres .

The researchers also found that 27 genes on the Y chromosome – 17 humans retained after 200 million years , and 10 genes more recently acquired but little known – are likely to be affected by natural selection . Most new gene, called ampliconic genes are present in multiple copies in the chromosome and the loss of one or more copies has been related to male infertility.

“These ampliconic regions that we have not really understood until now are obviously very important and probably should be researched and studied for fertility ,” he said .

Wilson Sayres was able to accurately measure the variable Y for first comparing the variation in the chromosome of a person with the variation in other 22 pairs of the person (called autosomes ) , the X chromosome and the mitochondrial DNA. She used data from the entire genome of 16 men whose DNA was sequenced by the company based in Mountain View , Complete Genomics Inc. , which is the most accurate of the Y chromosome sequences. The company was recently acquired by BGI , the Genome Institute of Bejing .

Comparative studies of populations of the variation in the Y chromosome are in their infancy , said, noting that more than 36 mammalian genomes sequenced to date, the full Y chromosomes are only available for three. Most human genomes sequenced + 1000 no longer have sufficiently accurate coverage And to make this type of comparison among individuals, but advances in technology to better characterize facilitate future DNA analysis of the Y chromosome , said.

Phobias memories passed down from ancestors

Phobias may be memories passed down in genes from ancestors:

Phobias may be memories passed down in genes from ancestors

Phobias may be memories passed down in genes from ancestors

 

Memories can be passed down to later generations through genetic switches that allow offspring to inherit the experience of their ancestors, according to new research that may explain how phobias can develop.

Scientists have long assumed that memories and learned experiences built up during a lifetime must be passed on by teaching later generations or through personal experience.

However, new research has shown that it is possible for some information to be inherited biologically through chemical changes that occur in DNA.

Researchers at the Emory University School of Medicine, in Atlanta, found that mice can pass on learned information about traumatic or stressful experiences – in this case a fear of the smell of cherry blossom – to subsequent generations.

The results may help to explain why people suffer from seemingly irrational phobias – it may be based on the inherited experiences of their ancestors.

So a fear of spiders may in fact be an inherited defence mechanism laid down in a families genes by an ancestors’ frightening encounter with an arachnid.

Dr Brian Dias, from the department of psychiatry at Emory University, said: “We have begun to explore an underappreciated influence on adult behaviour – ancestral experience before conception.

“From a translational perspective, our results allow us to appreciate how the experiences of a parent, before even conceiving offspring, markedly influence both structure and function in the nervous system of subsequent generations.

“Such a phenomenon may contribute to the etiology and potential intergenerational transmission of risk for neuropsychiatric disorders such as phobias, anxiety and post-traumatic stress disorder.”

In the study, which is published in the journal of Nature Neuroscience, the researchers trained mice to fear the smell of cherry blossom using electric shocks before allowing them to breed.

The offspring produced showed fearful responses to the odour of cherry blossom compared to a neutral odour, despite never having encountered them before.

The following generation also showed the same behaviour. This effect continued even if the mice had been fathered through artificial insemination.

The researchers found the brains of the trained mice and their offspring showed structural changes in areas used to detect the odour.

The DNA of the animals also carried chemical changes, known as epigenetic methylation, on the gene responsible for detecting the odour.

This suggests that experiences are somehow transferred from the brain into the genome, allowing them to be passed on to later generations.

The researchers now hope to carry out further work to understand how the information comes to be stored on the DNA in the first place.

They also want to explore whether similar effects can be seen in the genes of humans.

Professor Marcus Pembrey, a paediatric geneticist at University College London, said the work provided “compelling evidence” for the biological transmission of memory.

He added: “It addresses constitutional fearfulness that is highly relevant to phobias, anxiety and post-traumatic stress disorders, plus the controversial subject of transmission of the ‘memory’ of ancestral experience down the generations.

“It is high time public health researchers took human transgenerational responses seriously.

“I suspect we will not understand the rise in neuropsychiatric disorders or obesity, diabetes and metabolic disruptions generally without taking a multigenerational approach.”

Professor Wolf Reik, head of epigenetics at the Babraham Institute in Cambridge, said, however, further work was needed before such results could be applied to humans.

He said: “These types of results are encouraging as they suggest that transgenerational inheritance exists and is mediated by epigenetics, but more careful mechanistic study of animal models is needed before extrapolating such findings to humans.”

It comes as another study in mice has shown that their ability to remember can be effected by the presence of immune system factors in their mother’s milk

Dr Miklos Toth, from Cornell University in New York, found that chemokines carried in a mother’s milk caused changes in the brains of their offspring, affecting their memory in later life.

Genes from roses and celery create superflower

Scientists splice genes from roses and celery to create superflower:

 

Scientists splice genes from roses and celery to create superflower

Scientists splice genes from roses and celery to create superflower

 
 
The idea of offering celery as a Valentine’s Day gift to your loved one instead of chocolate might send the wrong message, but scientists working to improve the rose genome could make the low-calorie stem a popular Feb. 14 present after all. 
 
It turns out that one particular gene from celery — the one that controls the enzyme mannitol dehydrogenase — greatly improves the life and quality of rose petals when that gene is spliced into the rose genome. So in an effort to help you get more value from your Valentine’s Day gifts, North Carolina State horticultural scientists Dr. John Dole and Dr. John Williamson are leading an effort to insert that gene into roses to create a new superflower less prone to wilt and more resistant to disease, according to PhysOrg.com. 
 
“This gene is naturally found in many plants, but it’s uncertain whether the rose already has it,” said Williamson. “If it does, it doesn’t produce enough enzyme to help the plant fight against petal blight.”
 
Petal blight, or botrytis, is a common post-harvest disease in roses that produces wilty, mushy petals. It’s caused by invading fungal pathogens that break down the flower’s defenses by producing a sugar alcohol called mannitol. Plants that produce enough mannitol dehydrogenase enzyme, like celery, can better break down this sugar alcohol and thus maintain their form for longer.
 
Roses that contain the celery gene don’t smell any different than normal roses, according to the N.C. State researchers. The only noticeable difference between normal roses and these superflowers should be their vase life.
 
The research is part of a larger effort by Dole and Williamson to build a better rose. Besides implanting the celery gene, the researchers are also examining the types of sugars best suited for mixture with water to keep the plants thriving after they’ve been harvested. They are even studying how variance in water quality across the country affects the life expectancy of cut roses.
 
The ultimate goal, according to Dole, is to get roses to survive for up to three to four weeks after they’ve been harvested. If they succeed, before long your loved one may be able to cherish her Valentine’s Day gift well into spring.

Type 2 diabetes genes and metabolic markers

Type 2 diabetes: New associations identified between genes and metabolic markers:

diabetes-graphic

 

 

 

 

In two comprehensive studies, scientists from Helmholtz Zentrum Muenchen, Ludwig-Maximilians-Universitaet Muenchen and Technische Universitaet Muenchen discovered new associations of two major Type 2 diabetes risk genotypes and altered plasma concentrations of metabolic products. The “Virtual Institute Diabetes” joint research cooperation is thereby making an important contribution towards explaining the genetic and molecular basis of diabetes, The results have been published in the journals PLOS ONE and Metabolomics.

For these investigations, participants of the population-based cohort study KORA* carrying high-risk diabetes gene variants without having a diagnosed diabetes, as well as participants without an increased diabetes risk were recruited.

All study participants were subjected to a metabolic load. The nutritients, particularly sugars and fats, were administered either orally or intravenously. The scientists subsequently determined the concentrations of 163 metabolic products in blood samples from the participants. The teams headed by Prof. Dr. Thomas Illig (HMGU) and Dr. Harald Grallert (HMGU), Prof. Dr. Jochen Seißler (LMU), and Prof. Dr. Hans Hauner (TUM) and Dr. Helmut Laumen (TUM) were the first to supply a comprehensive characterisation of the metabolic performance in regard to the respective genotype.

It was observed that the concentrations of the recorded substances represent a particular metabolomic response pattern depending on the genotype. It was possible to verify specific metabolic effects, particularly for the TCF7L2 genotype, which is associated with an increased risk of type 2 diabetes. “We are aware of certain high-risk gene variants for type 2 diabetes. However, the causative mechanisms on the path to this disease are still largely unknown. With our results, we are helping to close the gap between disease-associated genes on the one hand and the development of diabetes on the other. A typically changed metabolic performance can supply early indications of diabetes”, explain Simone Wahl from HMGU and Cornelia Then from LMU, first authors of the two publications.

The scientists are currently investigating metabolic responses in additional genotypes. The objective is to advance the fundamental research on the widespread disease diabetes and to contribute the acquired knowledge to the clinical cooperation groups that have developed from the VID in order to promote the knowledge transfer between the laboratory and clinical care of patients suffering from diabetes.

Hidden Genetic Code

A hidden genetic code for better designer genes:

 

A hidden genetic code for better designer genes

A hidden genetic code for better designer genes

 

Scientists routinely seek to reprogram bacteria to produce proteins for drugs, biofuels and more, but they have struggled to get those bugs to follow orders. But a hidden feature of the genetic code, it turns out, could get bugs with the program. The feature controls how much of the desired protein bacteria produce, a team from the Wyss Institute for Biologically Inspired Engineering at Harvard University reported in the September 26 online issue of Science.

The findings could be a boon for biotechnologists, and they could help synthetic biologists reprogram bacteria to make new drugs and biological devices.

By combining high-speed “next-generation” DNA sequencing and DNA synthesis technologies, Sri Kosuri, Ph.D., a Wyss Institute staff scientist, George Church, Ph.D., a core faculty member at the Wyss Institute and professor of genetics at Harvard Medical School, and Daniel Goodman, a Wyss Institute graduate research fellow, found that using more rare words, or codons, near the start of a gene removes roadblocks to protein production.

“Now that we understand how rare codons control gene expression, we can better predict how to synthesize genes that make enzymes, drugs, or whatever you want to make in a cell,” Kosuri said.

To produce a protein, a cell must first make working copies of the gene encoding it. These copies, called messenger RNA (mRNA), consist of a specific string of words, or codons. Each codon represents one of the 20 different amino acids that cells use to assemble proteins. But since the cell uses 61 codons to represent 20 amino acids, many codons have synonyms that represent the same amino acid.

In bacteria, as in books, some words are used more often than others, and molecular biologists have noticed over the last few years that rare codons appear more frequently near the start of a gene. What’s more, genes whose opening sequences have more rare codons produce more protein than genes whose opening sequences do not.

No one knew for sure why rare codons had these effects, but many biologists suspected that they function as a highway on-ramp for ribosomes, the molecular machines that build proteins. According to this idea, called the codon ramp hypothesis, ribosomes wait on the on-ramp, then accelerate slowly along the mRNA highway, allowing the cell to make proteins with all deliberate speed. But without the on-ramp, the ribosomes gun it down the mRNA highway, then collide like bumper cars, causing traffic accidents that slow protein production. Other biologists suspected rare codons acted via different mechanisms. These include mRNA folding, which could create roadblocks for ribosomes that block the highway and slow protein production.

To see which ideas were correct, the three researchers used a high-speed, multiplexed method that they’d reported in August in The Proceedings of the National Academy of Sciences.

First, they tested how well rare codons activated genes by mass-producing 14,000 snippets of DNA with either common or rare codons; splicing them near the start of a gene that makes cells glow green, and inserting each of those hybrid genes into different bacteria. Then they grew those bugs, sorted them into bins based on how intensely they glowed, and sequenced the snippets to look for rare codons.

They found that genes that opened with rare codons consistently made more protein, and a single codon change could spur cells to make 60 times more protein.

“That’s a big deal for the cell, especially if you want to pump out a lot of the protein you’re making,” Goodman said.

The results were also consistent with the codon-ramp hypothesis, which predicts that rare codons themselves, rather than folded mRNA, slow protein production. But the researchers also found that the more mRNA folded, the less of the corresponding protein it produced — a result that undermined the hypothesis.

To put the hypothesis to a definitive test, the Wyss team made and tested more than 14,000 mRNAs – including some with rare codons that didn’t fold well, and others that folded well but had no rare codons. By quickly measuring protein production from each mRNA and analyzing the results statistically, they could separate the two effects.

The results showed clearly that RNA folding, not rare codons, controlled protein production, and that scientists can increase protein production by altering folding, Goodman said.

The new method could help resolve other thorny debates in molecular biology. “The combination of high-throughput synthesis and next-gen sequencing allows us to answer big, complicated questions that were previously impossible to tease apart,” Church said.

“These findings on codon use could help scientists engineer bacteria more precisely than ever before, which is tremendous in itself, and they provide a way to greatly increase the efficiency of microbial manufacturing, which could have huge commercial value as well,” said Wyss Institute Founding Director Don Ingber, M.D., Ph.D. “They also underscore the incredible value of the new automated technologies that have emerged from the Synthetic Biology Platform that George leads, which enable us to synthesize and analyze genes more rapidly than ever before.”

New light on how Genes turn off and on

New insights into how genes turn on and off:

New insights into how genes turn on and off

New insights into how genes turn on and off

 

Researchers at UC Davis and the University of British Columbia have shed new light on methylation, a critical process that helps control how genes are expressed. Working with placentas, the team discovered that 37 percent of the placental genome has regions of lower methylation, called partially methylated domains (PMDs), in which gene expression is turned off. This differs from most human tissues, in which 70 percent of the genome is highly methylated.

While PMDs have been identified in cell lines, this is the first time they have been found in regular human tissue. In addition to enhancing our understanding of epigenetics, this work could influence cancer research and help illuminate how environmental toxins affect fetal development. .

Since it was unraveled more than ten years ago, the human genome has been the focus of both popular interest and intense scientific focus. But the genome doesn’t act alone; there are many factors that influence whether genes are turned on or off. One of these is an epigenetic process called methylation, in which a group of carbon and hydrogen atoms (a methyl group) attaches to DNA, adjusting how genes are expressed.

“I like to think of epigenetics as a layer on top of your genetic code,” said senior author Janine LaSalle, professor of medical microbiology and immunology. “It’s not the DNA sequence but it layers on top of that — and methylation is the first layer. Those layers provide a lot of information to the cells on where and when to turn on the genes.”

How and when genes are activated (or inactivated) can have a profound impact on human development, cancer and the biological legacy of environmental toxins. Prior to this research, PMDs had only been found in cultured cell lines, which led some scientists to wonder if they existed outside the test tube. This study confirms they exist in placental tissue, a critically important window into fetal development.

“The placenta is the interface between mother and fetus,” said LaSalle, who is a researcher affiliated with the UC Davis MIND Institute. “It’s a time capsule from when a lot of important methylation events occurred.”

In addition, placental tissue was interesting to study because it has a number of invasive characteristics often associated with cancer. In fact, a number of cancers, such as breast and colon, have widespread PMDs. LaSalle notes that anti-cancer epigenetic therapies that adjust methylation could be refined based on this improved understanding of PMDs.

This work could also enhance our ability to detect genetic defects. Methylation, and other epigenetic data, provides information that cannot be found in the genome alone. For example, the vast majority of cells in the body contain identical genetic code. However, the added information provided by methylation allows scientists to determine where specific DNA came from.

“Methylation patterns are like fingerprints, showing which tissue that DNA is derived from,” LaSalle said. “You can’t get that information from just the DNA sequence. As a result, methylation studies could be a very rich source for biomarkers.”

In the study, PMDs encompassed 37 percent of the placental genome, including 3,815 genes, around 17 percent of all genes. When found in low-methylation regions, these genes were less likely to be transcribed into proteins. Researchers also found that PMDs also contain more highly methylated CpG islands (genomic areas with large numbers of cytosine-guanine pairs), which are often associated with gene transcriptional silencing of promoters.

Because the placental PMDs contained many genes associated with neuronal development, and specifically autism, LaSalle notes that future research could investigate how epigenetics impacts autism genes at birth.

“We are looking for biomarkers that predict neurodevelopmental outcomes,” LaSalle said. “Now we have a series of snap shots from a critical period where we think environmental factors are playing a role in the developing brain.”