Earlier this month, 400 protestors destroyed a field trial of genetically modified Golden Rice in the Philippines. Aided by well-meaning but misguided organizations such as Greenpeace, such mobs are potentially destroying the opportunity to avoid 680,000 deaths each year.
It’s the left. That’s their goal.
Environmentalists who are skeptical about genetically modified crops should think again, judging from a study published last June. Researchers reported in the journal Nature that transgenic cotton bred to resist pests increases biodiversity by reducing the amount of insecticide sprayed on fields.
I apologise for having spent several years ripping up GM crops. I am also sorry that I helped to start the anti-GM movement back in the mid 1990s, and that I thereby assisted in demonising an important technological option which can be used to benefit the environment.
As an environmentalist, and someone who believes that everyone in this world has a right to a healthy and nutritious diet of their choosing, I could not have chosen a more counter-productive path. I now regret it completely.
The Indians knew what they were doing.
“These discoveries put a lot of what we see today medically in a broader context,” said Bustamante. “For example, this man, who died when he was about 45 years old, was likely very fit. He got lots of exercise and ate a true paleo diet. And yet he had begun to develop heart disease. This shows that the selective forces we’re familiar with today just weren’t in the picture then. These types of disease were probably common, but they didn’t kill people. People died instead of an arrow in the back or in hunting accidents. There is still so much more to learn.”
No, seriously!
Canadian scientists have discovered that
identical twins do not have identical genes, a common assumption by researchers for more than a century, and a development that could have implications into the study of medicine and human behaviour.
Associate law professor Nita A. Farahany describes her blog as “a daily digest of legal opinions featuring cognitive neuroscience and behavioral genetics”.
Sometimes, even judges suffer from the “CSI” effect. The district court judge in the case today may have missed a few important days of his genetics class in high school or in college. Perhaps they didn’t teach genetics in the late 1960′s?
This may make for good sarcasm, but it’s a stupid criticism. Much of what the average student learned about genetics in high school as recently as 20 years ago, (let alone the 60’s) has been modified or even overturned by recent discoveries in genetics – the field of epigenetics among them. Nita Farahany ought to know this. Unless of course, she doesn’t know this.
The Defendant in this case, convicted of possession of child pornography, was given an “unreasonable” sentence based on the judge’s invented genetic theory that the defendant’s incorrigible genes made him act the way he did, and that there was nothing he could do about it.
Am I the only one mystified by the legal and societal contradiction that while sexual attraction to persons of the same sex is “not a choice”, sexual attraction to pre-adolescents is?
Well, good luck with that. I predict that a “my genes made me do it” defense for pedophilia will eventually be legitimized by the courts – blog snark notwithstanding, and Judge Sharpe noted as “ahead of his time”. The societal ground work is already in place.
Via.
Genetic screening of newborns…
…. is creating unexpected upheaval for families whose infants test positive for risk factors but show no immediate signs of the diseases, a new UCLA study warns.
“Although newborn screening undoubtedly saves lives, some families are thrown on a journey of great uncertainty,” said UCLA sociology professor Stefan Timmermans, the study’s lead author. “Rather than providing clear-cut diagnoses, screening of an entire population has created ambiguity about whether infants truly have a disease — and even what the disease is.” […]
[T]he study paints a picture of families caught in limbo as they wait months for conclusive evidence that their children are out of the woods for conditions that have been associated with schizophrenia, mental retardation, heart and lung disease, coma and sudden death.
In many cases, the medical results never come; the children slowly age out of having risk factors for up to 29 metabolic, endocrine or hemoglobin conditions. But by that time, some families are so traumatized that they follow unwarranted and complicated regimens for years afterward, including waking their children up in the middle of the night, enforcing restrictive diets and limiting contact with other people. “Years after everything appears to be fine, parents are still very worried,” Timmermans said.
For three years, Timmermans and Buchbinder followed 75 California families whose newborns received screenings that sent up red flags for diseases characterized by an inability to digest food containing fat, proteins or sugars. Of the total, 40 of the infants became what the researchers describe as “patients-in-waiting” — children who have not developed symptoms but whose genetic tests raise flags.
“The parents don’t know whether their child is a false positive or they’re a true positive,” Timmermans said.
Why the hell would they do this to themselves, you ask?
The advent of new screening technologies in the late 1990s vastly increased the number of potential diseases that could be detected with a blood sample easily obtained by pricking the heel of a newborn. Genetic testing of newborns got another shot in the arm in 2005 when the American College of Medical Genetics called for mandatory screening of 29 conditions and 24 sub-conditions. By 2009, all 50 U.S. states and the District of Columbia screened for at least 21 of the 29 recommended conditions, and the full recommendations had been adopted by 44 states, including California.
…have a distinct set of physiological traits that help with the dangers of high altitude: decreased arterial oxygen content (low levels of oxygen in the blood), increased resting ventilation (rapid breathing while resting), lack of hypoxic pulmonary vasoconstriction (meaning blood vessels don’t constrict when oxygen content of the blood is low), lower incidence of reduced birth weight, and reduced hemoglobin concentration (hemoglobin is a protein in red blood cells that helps transport oxygen from lungs or gills to the body). Put together, this means that Tibetans have evolved to function with far less oxygen in their blood than other people – perfect for high altitudes with low oxygen.
A new study focuses on this final trait, the reduced hemoglobin concentration. Tibetans have 3.6 grams per deciliter less hemoglobin than other populations. When you go up to the insane altitudes that mountain climbers tend to go for, your body ramps up red blood cell production in order to compensate for the low levels of oxygen. This is why athletes train at high altitude — to get more red blood cells into their system, and transfer oxygen around more efficiently. However, a side effect of this increase is the that your blood increases in viscosity. When it gets really bad, your body is pushing around blood the density of motor oil, something it’s not designed to do. By naturally having much lower hemoglobin levels, people from Tibet (and assumedly Nepal, and other regions in the area) maintain proper blood fluidity.
I hasten to add – none of this undermines the overwhelming academic consensus that the forces of evolutionary selection apply to all living organisms except humans.
Mitochondria are found by the hundreds in every human cell. They convert glucose to energy, and possess their own tiny genomes, separate and distinct from the organismal genome found in each cell nucleus.
That, and it comes in really handy when law enforcement officials state that the odds that they got the wrong guy are “one in a quadrillionzillion!”
In the mid-1990s, law enforcement added mitochondrial DNA comparison to its forensic genetic toolkit. Because there are so many mitochondria in each cell, readable copies of their genomes can often be found even when the nuclear genome has been damaged. This is especially useful for old, highly degraded biological samples.
Mitochondrial DNA-matching is based on the assumption that it doesn’t vary much in an individual: Aside from a few inevitable mutations, mitochondrial DNA are generally supposed to be the same in, say, heart cells and hair cells. But when Papadopoulos’ team applied the latest in gene-sequencing technology to mitochondrial genomes from nine tissue types in two people, that’s not what they found.
Instead, each person seemed to have a mixture of mitochondrial genotypes. One DNA variant, for example, was found in about 7 percent of a person’s skeletal-muscle mitochondria, but 90 percent of their kidney mitochondria. That spread was typical.
“It’s more than was thought, and was present in almost every tissue we looked at,” said Papadopoulos. Further research into these variations is needed, but forensic specialists should be careful to compare the same types of tissue, he said.
And don’t get me started on the practice of basing “evolutionary clocks” on the stuff.
Upon learning of the paper, John Planz, associate director of the DNA Identity Laboratory at the University of North Texas Health Science Center, cautioned that further studies are needed.
I’ll bet he did.
Who won the Nobel Peace Prize in 1970? Who still teaches at Texas A&M at the age of 86?
An interview with Norman Borlaug (from April, 2000), who passed away Sept. 12.
h/t Doug Y.
The Scientist; (free registration may be required)
An illness that has been decimating US honeybees for more than three years probably isn’t caused by a single virus, but by multiple viruses that wear down the bees’ ability to produce proteins that can guard them against infection, according to a new study.
[…]
Berenbaum and colleagues at the US Department of Agriculture screened thousands of transcripts in the guts of bees from both healthy and CCD-stricken colonies from the east and west coasts of the US.
CCD bees had several unusual RNA fragments resulting from broken, malfunctioning ribosomes. Multiple infections with a family of viruses called the picorna-like viruses, which seem to especially afflict CCD bees, could cause the appearance of such RNA fragments as they overwhelmed ribosomes and limited the cells’ ability to manufacture functioning proteins. Bees that are not able to make proteins cannot mount effective responses to viral or bacterial infection or respond to dietary shortages, Berenbaum said.
Although the study didn’t uncover a single cause for CCD, said Dan Weaver, a Texas-based apiculturist who was not involved with the research, it “provides some hints and suggestive evidence that maybe there’s a general impairment of bees’ ability to cope with pathogens at a basic regulatory step.”
Berenbaum said that CCD may not be the result of one particular pathogen or environmental factor, but rather may occur when multiple viral infections overwhelm the bees’ translational machinery. Bees may be able to handle one or two viral infections simultaneously, but not three or four. “You can recover from a gunshot wound,” Berenbaum said, “unless someone is kicking you in the head at the same time.”
While apiculturists like Weaver would rather have a single pathogenic cause of CCD in hand, the disorder, which has caused widespread bee mortalities in the US since 2006, appears to be more complex than that. “It would be better if we had more definitive evidence of what exactly is going on,” Weaver said. “I think that would be everyone’s fervent hope. But so far that hasn’t materialized.”
Berenbaum’s study does, however, rule out some of the previously suggested theories for the cause of CCD. For example, the screen failed to turn up elevated expression of pesticide response genes in CCD bees. “The pattern we saw was inconsistent with pesticides as a cause,” said Berenbaum, adding that this will probably not stop some in the honeybee business from blaming pesticide manufacturers for the disorder. Interestingly, the screen also failed to find increased expression of immune response genes, suggesting that the bees were not able to mount effective responses to the pathogens attacking their colonies.
Also at the BBC.
“Genetics could have made Britain’s bankers take risks, scientists say”
Dr Joan Chiao, assistant professor of psychology at Northwestern University in Chicago, said: “As we sort out the devastating consequences of the financial crisis, it might be useful to note how our genetic heritage is influencing our economic behaviour.
“Think about how the excessive risks taken by just a few affected so many, from large institutions to average people.”
If the British banking system is anything like Wall Street’s Lucky Y Chromosome club, they may very well be onto something!
Wall Street, for all it’s glamour and glory was basically an elitist’s club where blue bloods and Ivy Leaguers who never really worked a day in their lives all of the sudden got six figure jobs because of their daddy (Chelsea Clinton is a perfect example, how does a 26 year old child get a hedge fund manager position?)
Do these people know how to allocate capital? Do they know what they best investments are? Of course not.
Which is why it should be no surprise the markets are off 45% and none of the “Bulge Bracket” elites remain in their previous form.
If anything, it is proof positive that the “best” and the “elite” are nothing more than spoiled brat nepotists who achieved their “elite” status through inheritance or no feat of their own and is why the system ultimately is crashing in that they have no inherent value or wealth production abilities.
“If sociologists ignore genes, will other academics — and the wider world — ignore sociology?“
Somebody stop these people.
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