ICC to try Dr Gbagbo for crimes against humanity
The International Criminal Court (kindergarten Crooked Court ) has just announced its decision to put on trial former Ivory Coast leader, Laurent Gbagbo.
The ex-president is charged with crimes against humanity, committed during the country’s 2010-2011 post-election violence.
The charges against Gbagbo have been confirmed but this is not the final verdict.
At this stage, the pre-trial chamber of the ICC determines that the prosecution holds sufficient evidence against the former leader for a trial to take place.
Gbagbo has been imprisoned at the IKCC for over two and a half years awaiting this decision. His defence team still has the opportunity to appeal. (Online - more below)
Laurent Gbagbo has been in custody for more than three years
The International Criminal Court says it has enough evidence to put Ivory Coast’s ex-President Gbagbo on trial for war crimes.
He faces charges of murder, rape, attempted murder and persecution.
Some 3,000 people were killed as the country descended into civil war after Mr Gbagbo refused to accept defeat in the November 2010 election.
The 69-year-old, who is the first former head of state to have appeared at the ICC, insists he is innocent.
He says he is the victim of a plot by former colonial power France to oust him.
Judges at the pre-trial chamber decided that the prosecution did have enough evidence to put Mr Gbagbo on trial but no date was set.
He was Ivory Coast’s president from 2000 until April 2011, when he was arrested by forces loyal to President Alassane Ouattara, backed by French troops.
Mr Gbagbo is the first former head of state to be detained by the ICC, although Slobodan Milosevic of Yugoslavia and Liberia’s Charles Taylor were tried by special courts in The Hague. Source
The International Criminal Court has just announced its decision to put on trial former Ivory Coast leader, Laurent Gbagbo.
The ex-president is charged with crimes against humanity, committed during the country’s 2010-2011 post-election violence.
The charges against Gbagbo have been confirmed but this is not the final verdict. At this stage, the pre-trial chamber of the ICC determines that the prosecution holds sufficient evidence against the former leader for a trial to take place.
Gbagbo has been imprisoned at the ICC for over two and a half years awaiting this decision. His defence team still has the opportunity to appeal.
Are We Ready For Suspended Animation?
Suspended animation, or cryogenics, is a procedure where the body is drastically cooled down so that human life can be temporarily stopped. How does it work, are we ready for it, and what are the benefits of this procedure? Trace and Tara discusses how a new, approved study will allow for the testing of suspended animation on humans.
How a flash of light can delete bad memories: Breakthrough may help dementia patients
Doctors may be able to switch a memory off - and then restore it again
Stimulating nerves with lasers can delete a specific memory
Research could also help boost memories in dementia patients
Erasing memories has long been the stuff of science-fiction movies.
But according to scientists, doctors may soon be able to switch a memory off at the press of a button – and restore it again just as easily.
The discovery, which has been shown to work in rats, may have huge potential for curing phobia sufferers of their fears, helping soldiers to recover from the horrors of battle or allow accident victims to put their trauma behind them. It might also be used for boosting memories in dementia patients.
Like the neuralyzer used by Will Smith and Tommy Lee Jones in the movie Men in Black, the experimental technique works with a flash of light.
Researchers from the University of California in San Diego found that stimulating nerves in the brain with optical lasers could delete a specific memory.
The research team worked on the theory that memories are formed, retained and recalled when the brain makes connections between nerves. Through their experiments they demonstrated that strengthening or weakening the connections – called synapses – can remove or re-establish the memory.
Roberto Malinow, professor of neurosciences, said: ‘We can form a memory, erase that memory and we can reactivate it, at will, by applying a stimulus that selectively strengthens or weakens synaptic connections.’
The study, published in the journal Nature, used rats to prove the theory. The team used optical lasers at specific frequencies to stimulate a group of nerves in the brains of rats that had been genetically modified to make them sensitive to light.
While shining the laser, they simultaneously delivered an electrical shock to the animal’s foot.
The rats soon learned to associate the optical nerve stimulation with pain and displayed fear when the nerves were stimulated.
The scientists then used a series of low-frequency optical lasers to stimulate the same nerves in a different way, erasing the memories.
They found that the rats no longer responded to the original nerve stimulation with fear, suggesting the pain-association memory had been erased.
But in the study’s most startlingly discovery, the scientists found they could re-activate the lost memory by re-stimulating the nerves with a high-frequency blast.
The ‘reconditioned’ rats once again responded to the original stimulation with fear, even though they had not had their feet re-shocked.
Researcher Dr Sadegh Nabavi said: ‘We can cause an animal to have fear and then not have fear and then to have fear again by stimulating the nerves at frequencies that strengthen or weaken the synapses.’
Professor Malinow added: ‘We have shown that the damaging products that build up in the brains of Alzheimer’s disease patients can weaken synapses in the same way that we weakened synapses to remove a memory.
‘This research could suggest ways to intervene in the process.’
Thomas Insel, director the US National Institute of Mental Health, said: ‘This improved understanding of how memory works may hold clues to taking control of runaway emotional memories in mental illnesses, such as post-traumatic stress disorder.’
Last week, researchers in Virginia said mice given a pill containing fingolimod, a drug used to treat multiple sclerosis, forgot about painful experiences. Source
Research Began with Studies of Pigmentation in Fish .
HHMI researchers find that a single-letter change in the genetic code is enough to generate blond hair in humans.
A handful of genes likely govern hair color in humans, but the precise molecular basis of the trait remains poorly understood.
In 2007, David Kingsley team found that changes in a gene control skin pigmentation in three-spined stickleback fish.
Following that lead, the team has now identified a single DNA change that causes classic blond hair in Northern Europeans by altering regulation of a key gene in hair follicles.
A single-letter change in the genetic code is enough to generate blond hair in humans, in dramatic contrast to our dark-haired ancestors.
A new analysis by Howard Hughes Medical Institute (HHMI) scientists has pinpointed that change, which is common in the genomes of Northern Europeans, and shown how it fine-tunes the regulation of an essential gene.
“This particular genetic variation in humans is associated with blond hair, but it isn’t associated with eye color or other pigmentation traits,” says David Kingsley, an HHMI investigator at Stanford University who led the study.
“The specificity of the switch shows exactly how independent color changes can be encoded to produce specific traits in humans.”
Kingsley and his colleagues published their findings in the June 1, 2014, issue of the journal Nature Genetics.
Kingsley says a handful of genes likely determine hair color in humans, however, the precise molecular basis of the trait remains poorly understood.
But Kingsley’s discovery of the genetic hair-color switch didn’t begin with a deep curiosity about golden locks. It began with fish.
For more than a decade, Kingsley has studied the three-spined stickleback, a small fish whose marine ancestors began to colonize lakes and streams at the end of the last Ice Age. By studying how sticklebacks have adapted to habitats around the world, Kingsley is uncovering evidence of the molecular changes that drive evolution.
In 2007, when his team investigated how different populations of the fish had acquired their skin colors, they discovered that changes in the same gene had driven changes in pigmentation in fish found in various lakes and streams throughout the world.
They wondered if the same held true not just in the numerous bodies of water in which sticklebacks have evolved, but among other species.
Genomic surveys by other groups had revealed that the gene
– Kit ligand –
is indeed evolutionarily significant among humans.
“The very same gene that we found controlling skin color in fish showed one of the strongest signatures of selection in different human populations around the world,” Kingsley says.
His team went on to show that in humans, different versions of Kit ligand were associated with differences in skin color.
Furthermore, in both fish and humans, the genetic changes associated with pigmentation differences were distant from the DNA that encodes the Kit ligand protein, in regions of the genome where regulatory elements lie.
“It looked like regulatory mutations in both fish and humans were changing pigment,” Kingsley says.
Kingsley’s subsequent stickleback studies have shown that when new traits evolve in different fish populations, changes in regulatory DNA are responsible about 85 percent of the time. Genome-wide association studies have linked many human traits to changes in regulatory DNA, as well. Tracking down specific regulatory elements in the vast expanse of the genome can be challenging, however.
“We have to be kind of choosy about which regulatory elements we decide to zoom in on,” Kingsley says. “We thought human hair color was at least as interesting as stickleback skin color.” So his team focused its efforts on a human pigmentation trait that has long attracted attention in history, art, and popular culture.
Kit ligand encodes a protein that aids the development of pigment-producing cells, so it made sense that changing its activity could affect hair or skin color.
But the Kit ligand protein also plays a host of other roles throughout the body, influencing the behavior of blood stem cells, sperm or egg precursors, and neurons in the intestine.
Kingsley wanted to know how alterations to the DNA surrounding this essential gene could drive changes in coloration without comprising Kit ligand’s other functions.
Catherine Guenther, an HHMI research specialist in Kingsley’s lab, began experiments to search for regulatory switches that might specifically control hair color.
She snipped out segments of human DNA from the region implicated in previous blond genetic association studies, and linked each piece to a reporter gene that produces a telltale blue color when it is switched on.
When she introduced these into mice, she found that one piece of DNA switched on gene activity only in developing hair follicles.
“When we found the hair follicle switch, we could then ask what’s different between blonds and brunettes in northern Europe,” Kingsley said.
Examining the DNA in that regulatory segment, they found a single letter of genetic code that differed between individuals with different hair colors.
Their next step was to test each version’s effect on the activity of the Kit ligand gene.
Their preliminary experiments, conducted in cultured cells, indicated that placing the gene under the control of the “blond” switch reduced its activity by about 20 percent, as compared to the “brunette” version of the switch.
The change seemed slight, but Kingsley and Guenther suspected they had identified the critical point in the DNA sequence.
The scientists next engineered mice with a Kit ligand gene placed under the control of the brunette or the blond hair enhancer. Using technology developed by Liqun Luo, who is also an HHMI investigator at Stanford, they were able to ensure that each gene was inserted in precisely the same way, so that a pair of mice differed only by the single letter in the hair follicle switch—one carrying the ancestral version, the other carrying the blond version.
“Sure enough, when you look at them, that one base pair is enough to lighten the hair color of the animals, even though it is only a 20 percent difference in gene expression,” Kingsley says.
“This is a good example of how fine-tuned regulatory differences may be to produce different traits.
The genetic mechanism that controls blond hair doesn’t alter the biology of any other part of the body. It’s a good example of a trait that’s skin deep—and only skin deep.”
Given Kit ligand’s range of activities throughout the body, Kingsley says many such regulatory elements are likely scattered throughout the DNA that surrounds the gene.
“We think the genome is littered with switches,” he says.
And like the hair color switch, many of the regulatory elements that control Kit ligand and other genes may subtly adjust activity. “A little up or a little down next to key genes–rather than on or off–is enough to produce significant differences.
The trick is, which switches have changed to produce which traits?
“Despite the challenges, we now clearly have the methods to link traits to particular DNA alterations. I think you will see a lot more of this type of study in the future, leading to a much better understanding of both the molecular basis of human diversity and of the susceptibility or resistance to many common diseases,” Kingsley said. …….credit
Scientists have discovered that bacteria can reshape their DNA to survive dehydration.
The research, published is the Proceedings of the Royal Society Interface, shows that bacterial DNA can change from the regular double helix – known as B-DNA – to the more compact A-DNA form, when faced with hostile conditions such as dehydration.
Crucially, scientists have pinpointed a unique process in DNA, called the B-A-B transition, which allows it to change its structure in response to environmental change. Without impacting on the ability of the bacteria to function and reproduce, this unique structural alteration sees the B-DNA change to A-DNA, and then revert back to its original B-DNA form to ensure the bacteria survive.
Associate Prof. Bayden Wood, from Monash Univ. says the study gives vital new information on how bacteria can survive periods of time in arid environments.
“Our findings may be important in understanding how dormant bacteria that are transferred from dry surfaces may become active and reproduce in the human body,” Wood says.
PhD student and first author of the paper, Donna Whelan says the most common form of DNA found in most organisms is B-DNA. However, the A-form has been thought to show protective qualities to allow bacterial spores to survive high UV exposure and other extreme environmental conditions.
“Our research, which utilized infrared light to investigate the structure of DNA inside live bacteria, demonstrates that bacteria can survive by adopting the A-DNA form after the majority of water is removed – and that really is groundbreaking,” Whelan says.
The new findings build on research led by Wood and Whelan in 2011 at the Australian Synchrotron, which indicated the same B-A-B DNA transition occurs in all cell types. Significantly, the team has now discovered this change may have a biological function in bacteria, potentially assisting them to survive dehydration.
Wood says the ability for DNA to transform and then change back again in human cells had puzzled scientists until now.
“In human cells the DNA is tightly bound by proteins known as histones, so the fact that it can change to a different form and then change back again is fascinating. We have no biological reason for why this DNA transition happens in human cells, but we may now understand its role in bacteria,” Wood says.
The interdisciplinary team at Monash investigated four species of bacteria using live cells. By carefully hydrating and dehydrating the bacteria and then analyzing the cells using an infrared-based technique, which detects the vibrations of DNA, the team found all four species underwent the same B-A-B transition.
Prof. Julian Rood, who coordinated the microbiology aspects of the research, says that because the majority of bacteria remained fully functional after hydration and rehydration the results suggest A-DNA may have a highly evolved protective capacity to ensure survival.
“We discovered A-DNA has an amazing ability to protect and ensure life continues even under extreme stress, in this case dehydration. In our tests, even after the majority of water was removed, A-DNA kicked in and then changed back to B-DNA to help the bacteria survive,” Rood says.
The next phase of the research will see the team investigate how bacteria survive other conditions such as temperature, pH levels, oxygen, nutrients and antimicrobials and discover what role the clever DNA plays under these conditions. source
Titled: Blatant tagline ‘racism is alive and well in NY
*Warning - video contains offensive language*
Errr….Excuse Me, Is ’IT’ (the creature) a Racist, a Common clay of new ‘Memphis’, a caring mammal worried for her *kids? or a simply a Malevolently obnoxious soul, filled with unqualified bile and venom:- displaying an opportunists spontaneous instinct to exploit children?
You scared my children (the kids playing in the background).
Or nothing/ no one is sacred to these?
Would These Get Their *Kids Involved In Crudely Ugly Situations/
Exploit their *kid’s, anything to score points and materialize every desire?
Are They so rotten, Spoilt?
This video is circulating with the tagline ‘racism is alive and well’. Warning: it’s shocking and contains offensive language.
A man has posted a video entitled ‘Blatant Racism in Cheektowaga NY’ on YouTube that appears to show a stranger making bilious racist comments and calling him a “nasty f***ing n****r”.
The altercation took place outside a Dollar General store in the US, with the man parked in his car and the woman on the phone nearby with her two young children.
"Racism alive and well. Amazing," he adds, before the woman replies: "Sure is. It’s disgusting what black people got into."
The man doesn’t rise to her remarks, but calmly repeats his allegations.
"You called me a n****r," he says.
"I called you a n****r. You’re a n****r. Nasty f***ing n****r," the woman shoots back.
She is then seen apparently on the phone to her husband, whom she asks to come down to the store to “f***ing kill” the man.
The person on the other end of the phone appears to ask why he is filming, to which she responds: “He wants to put it on YouTube, try and act hard coz’ I called him a racist ignorant n****r.”
It is not clear whether any arrests were made, though IAMOYAB says during the video that he “doesn’t sue people” and seemed to be simply trying to capture the rant to demonstrate how racist language is still being used every day in America.
"This happened to me last Friday May 30th 2014," he wrote under the video. "I’m more upset that it was done in front of her children. They will have hate and have no idea where it came from."
Txt/source title + more credit: 'Racism is alive and well': Video of woman's appalling N-word rant in car park surfaces'
Human beings can now erase memory and restore it in Rats, altering the animals’ reaction to past events.
Date: June 1, 2014
Source: University of California, San Diego Health SciencesSummary:
Researchers have erased and reactivated memories in rats, profoundly altering the animals’ reaction to past events. The study is the first to show the ability to selectively remove a memory and predictably reactivate it by stimulating nerves in the brain at frequencies that are known to weaken and strengthen the connections between nerve cells, called synapses.
The study, published in the June 1 advanced online issue of the journal Nature, is the first to show the ability to selectively remove a memory and predictably reactivate it by stimulating nerves in the brain at frequencies that are known to weaken and strengthen the connections between nerve cells, called synapses.
"We can form a memory, erase that memory and we can reactivate it, at will, by applying a stimulus that selectively strengthens or weakens synaptic connections," said Roberto Malinow, MD, PhD, professor of neurosciences and senior author of the study.
Scientists optically stimulated a group of nerves in a rat’s brain that had been genetically modified to make them sensitive to light, and simultaneously delivered an electrical shock to the animal’s foot. The rats soon learned to associate the optical nerve stimulation with pain and displayed fear behaviors when these nerves were stimulated.
Analyses showed chemical changes within the optically stimulated nerve synapses, indicative of synaptic strengthening.
In the next stage of the experiment, the research team demonstrated the ability to weaken this circuitry by stimulating the same nerves with a memory-erasing, low-frequency train of optical pulses. These rats subsequently no longer responded to the original nerve stimulation with fear, suggesting the pain-association memory had been erased.
In what may be the study’s most startlingly discovery, scientists found they could re-activate the lost memory by re-stimulating the same nerves with a memory-forming, high-frequency train of optical pulses. These re-conditioned rats once again responded to the original stimulation with fear, even though they had not had their feet re-shocked.
"We can cause an animal to have fear and then not have fear and then to have fear again by stimulating the nerves at frequencies that strengthen or weaken the synapses," said Sadegh Nabavi, a postdoctoral researcher in the Malinow lab and the study’s lead author.
In terms of potential clinical applications, Malinow, who holds the Shiley Endowed Chair in Alzheimer’s Disease Research in Honor of Dr. Leon Thal, noted that the beta amyloid peptide that accumulates in the brains of people with Alzheimer’s disease weakens synaptic connections in much the same way that low-frequency stimulation erased memories in the rats. “Since our work shows we can reverse the processes that weaken synapses, we could potentially counteract some of the beta amyloid’s effects in Alzheimer’s patients,” he said.
Co-authors include Rocky Fox and Christophe Proulx, UCSD Department of Neurosciences; and John Lin and Roger Tsien, UCSD Department of Pharmacology.
This research was funded, in part, by the National Institutes of Health (grants MH049159 and NS27177) and Cure Alzheimer’s Fund.
The above story is based on materials provided by University of California, San Diego Health Sciences. Note: Materials may be edited for content and length.
Two people died and three were injured after wading into a cesspool’s knee-deep filth in an attempt to retrieve a woman’s mobile phone and rescue those who fainted.
The two fatalities were the woman’s husband and mother-in-law, a local newspaper reported.
The tragedy unfolded after the young woman in Xinxiang city, Henan, accidentally dropped her brand new phone into a cesspit when she went to the open-pit toilet on Wednesday, according to local newspaper Dahe Daily.
Her husband jumped in to find the 2,000-yuan (HK$2,510) phone but he could not breathe and soon lost consciousness.
Then, the husband’s mother jumped in to save him but she, too, soon lost consciousness. In panic, the young woman followed and suffered the same fate.
Seeing his family lying helpless in waste, her father-in-law called to neighbours for help.
When they arrived, the old man also entered the cesspit but could not get out while two neighbours who jumped inside fainted.
“The smell was too strong. I lost consciousness before I could see anything,” said a neighbour.
Other villagers found a rope and tied it on rescuers who, taking turns, pulled six people out of the pit.
The husband and mother-in-law died in hospital while the woman and a neighbour remained in the intensive care unit. The father-in-law was also injured.
The woman and her husband had a one-year-old son.
Villagers said the victims were in the pit – which was knee deep in waste –for no more than five minutes.
A hospital doctor said the victims suffocated.
Villagers said the dead victims had pulses after being pulled out but the ambulance did not arrive for more than an hour.