Posts tagged science
Articles and news from the latest research reports.
Face off: Disney scientists reveal technique to ‘clone’ a human face onto an animatronic head
Disney has revealed its scientists have perfected how to recreate a human face on a robot head.
The team at Disney’s Zurich research lab say the breakthrough could lead to a new generation of digital animatronic characters far more lifelike than those currently seen in its theme parks.
'We propose a complete process for designing, simulating and fabricating synthetic skin for an animatronics character that mimics the face of a given subject and expressions', Disney said in a researcher paper.
HOW IT WORKS:
- The multi-step process begins with a three-dimensional scan to capture every detail of the actor’s face.
- Measurements that catalog minute details such as facial hairs are taken and entered into a virtual rendering of the actor’s face.
- Scientists then take the image from virtual to physical, using a carefully developed synthetic skin made of silicone placed on an animatronic head to complete the model.
- During their experiments, researchers let the completed head sit for seven days at room temperature before installing the complex robotics inside.
The human microbiome: Me, myself, us
Looking at human beings as ecosystems that contain many collaborating and competing species could change the practice of medicine.
A human being is an individual who has grown from a fertilised egg which contained genes from both father and mother. A growing band of biologists, however, think this definition incomplete. They see people not just as individuals, but also as ecosystems. In their view, the descendant of the fertilised egg is merely one component of the system. The others are trillions of bacteria, each equally an individual, which are found in a person’s gut, his mouth, his scalp, his skin and all of the crevices and orifices that subtend from his body’s surface.
A healthy adult human harbours some 100 trillion bacteria in his gut alone. That is ten times as many bacterial cells as he has cells descended from the sperm and egg of his parents. These bugs, moreover, are diverse. Egg and sperm provide about 23,000 different genes. The microbiome, as the body’s commensal bacteria are collectively known, is reckoned to have around 3m. Admittedly, many of those millions are variations on common themes, but equally many are not, and even the number of those that are adds something to the body’s genetic mix.
Scientists have cracked a molecular code that may open the way to destroying or correcting defective gene products, such as those that cause genetic disorders in humans.
The code determines the recognition of RNA molecules by a superfamily of RNA-binding proteins called pentatricopeptide repeat (PPR) proteins.
When a gene is switched on, it is copied into RNA. This RNA is then used to make proteins that are required by the organism for all of its vital functions. If a gene is defective, its RNA copy and the proteins made from this will also be defective. This forms the basis of many terrible genetic disorders in humans.
RNA-binding PPR proteins could revolutionise the way we treat disease. Their secret is their versatility - they can find and bind a specific RNA molecule, and have the capacity to correct it if it is defective, or destroy it if it is detrimental. They can also help ramp up production of proteins required for growth and development.
The new paper in PLOS Genetics describes for the first time how PPR proteins recognise their RNA targets via an easy-to-understand code. This mechanism mimics the simplicity and predictability of the pairing between DNA strands described by Watson and Crick 60 years ago, but at a protein/RNA interface.
A mysterious region deep in the human brain could be where we sort through the onslaught of stimuli from the outside world and focus on the information most important to our behavior and survival, Princeton University researchers have found.
The researchers report in the journal Science that an area of our brain called the pulvinar regulates communication between clusters of brain cells as our brain focuses on the people and objects that need our attention. Like a switchboard operator, the pulvinar makes sure that separate areas of the visual cortex — which processes visual information — are communicating about the same external information, explained lead author Yuri Saalmann, an associate research scholar in the Princeton Neuroscience Institute (PNI). Without guidance from the pulvinar, an important observation such as an oncoming bus as one is crossing the street could get lost in a jumble of other stimuli.
Saalmann said these findings on how the brain transmits information could lead to new ways of understanding and treating attention-related disorders, such as attention deficit hyperactivity disorder (ADHD) and schizophrenia.
A 2,684 year old human brain was recently discovered “exceptionally preserved” in a waterlogged U.K. pit, according to a new Journal of Archaeological Science study.
The organ is the oldest known intact human brain from Europe and Asia, according to the authors, who also believe it’s one of the best-preserved ancient brains in the world. The condition of the brain is remarkable for it’s age.
The skull, containing the brain remnants was found at Heslington, Yorkshire, in the United Kingdom.
The ancient body cause of death after so many years, indicates the damage to the neck vertebrae was consistent with a hanging.
The brain had the consistency of tofu, and had none of the distinctive smell so often associated with dead corpses.
(Source: americanlivewire.com)
When we touch something, how do sensations from our hands get translated into perceptions by our brains? Meet two scientists who are trying to answer that question with a curious tool: rat whiskers. Just like hands are to humans, whiskers are rats’ primary sensors of touch. Analyzing how whisker sensations get processed by rats’ brains is providing a powerful model that’s helping reveal the mysteries of our own sense of touch.
(Source: sciencebytes.org)
Common Parasite May Trigger Suicide Attempts
August 16th, 2012
A parasite thought to be harmless and found in many people may actually be causing subtle changes in the brain, leading to suicide attempts.
New research appearing in the August issue of The Journal of Clinical Psychiatry adds to the growing work linking an infection caused by the Toxoplasma gondii parasite to suicide attempts. Michigan State University’s Lena Brundin was one of the lead researchers on the team.
About 10-20 percent of people in the United States have Toxoplasma gondii, or T. gondii, in their bodies, but in most it was thought to lie dormant, said Brundin, an associate professor of experimental psychiatry in MSU’s College of Human Medicine. In fact, it appears the parasite can cause inflammation over time, which produces harmful metabolites that can damage brain cells.
“Previous research has found signs of inflammation in the brains of suicide victims and people battling depression, and there also are previous reports linking Toxoplasma gondii to suicide attempts,” she said. “In our study we found that if you are positive for the parasite, you are seven times more likely to attempt suicide.”
The work by Brundin and colleagues is the first to measure scores on a suicide assessment scale from people infected with the parasite, some of whom had attempted suicide.
The Toxoplasma gondii parasite has been linked to inflammation in the brain, damaging cells. Image adapted from MSU press release image.
The results found those infected with T. gondii scored significantly higher on the scale, indicative of a more severe disease and greater risk for future suicide attempts. However, Brundin stresses the majority of those infected with the parasite will not attempt suicide: “Some individuals may for some reason be more susceptible to develop symptoms,” she said.
“Suicide is major health problem,” said Brundin, noting the 36,909 deaths in 2009 in America, or one every 14 minutes. “It is estimated 90 percent of people who attempt suicide have a diagnosed psychiatric disorder. If we could identify those people infected with this parasite, it could help us predict who is at a higher risk.”
T. gondii is a parasite found in cells that reproduces in its primary host, any member of the cat family. It is transmitted to humans primarily through ingesting water and food contaminated with the eggs of the parasite, or, since the parasite can be present in other mammals as well, through consuming undercooked raw meat or food.
Brundin has been looking at the link between depression and inflammation in the brain for a decade, beginning with work she did on Parkinson’s disease. Typically, a class of antidepressants called selective serotonin re-uptake inhibitors, or SSRIs, have been the preferred treatment for depression. SSRIs are believed to increase the level of a neurotransmitter called serotonin but are effective in only about half of depressed patients.
Brundin’s research indicates a reduction in the brain’s serotonin might be a symptom rather than the root cause of depression. Inflammation, possibly from an infection or a parasite, likely causes changes in the brain’s chemistry, leading to depression and, in some cases, thoughts of suicide, she said.
“I think it’s very positive that we are finding biological changes in suicidal patients,” she said. “It means we can develop new treatments to prevent suicides, and patients can feel hope that maybe we can help them.
“It’s a great opportunity to develop new treatments tailored at specific biological mechanisms.”
Source: Neuroscience News
Evolutionary Increase in Size of the Human Brain Explained: Part of a Protein Linked to Rapid Change in Cognitive Ability
ScienceDaily (Aug. 16, 2012) — Researchers have found what they believe is the key to understanding why the human brain is larger and more complex than that of other animals.
The human brain, with its unequaled cognitive capacity, evolved rapidly and dramatically.
"We wanted to know why," says James Sikela, PhD, who headed the international research team that included researchers from the University of Colorado School of Medicine, Baylor College of Medicine and the National Institutes of Mental Health. "The size and cognitive capacity of the human brain sets us apart. But how did that happen?"
"This research indicates that what drove the evolutionary expansion of the human brain may well be a specific unit within a protein — called a protein domain — that is far more numerous in humans than other species."
The protein domain at issue is DUF1220. Humans have more than 270 copies of DUF1220 encoded in the genome, far more than other species. The closer a species is to humans, the more copies of DUF1220 show up. Chimpanzees have the next highest number, 125. Gorillas have 99, marmosets 30 and mice just one. “The one over-riding theme that we saw repeatedly was that the more copies of DUF1220 in the genome, the bigger the brain. And this held true whether we looked at different species or within the human population.”
Sikela, a professor at the CU medical school, and his team also linked DUF1220 to brain disorders. They associated lower numbers of DUF1220 with microcephaly, when the brain is too small; larger numbers of the protein domain were associated with macrocephaly, when the brain is too large.
The findings were reported today in the online edition of The American Journal of Human Genetics. The researchers drew their conclusions by comparing genome sequences from humans and other animals as well as by looking at the DNA of individuals with microcephaly and macrocephaly and of people from a non-disease population.
"The take home message was that brain size may be to a large degree a matter of protein domain dosage," Sikela says. "This discovery opens many new doors. It provides new tools to diagnose diseases related to brain size. And more broadly, it points to a new way to study the human brain and its dramatic increase in size and ability over what, in evolutionary terms, is a short amount of time."
Source: Science Daily
Discovery of Immune Cells That Protect Against Multiple Sclerosis Offers Hope for New Treatment
ScienceDaily (Aug. 16, 2012) — In multiple sclerosis, the immune system attacks nerves in the brain and spinal cord, causing movement problems, muscle weakness and loss of vision. Immune cells called dendritic cells, which were previously thought to contribute to the onset and development of multiple sclerosis, actually protect against the disease in a mouse model, according to a study published by Cell Press in the August issue of the journal Immunity. These new insights change our fundamental understanding of the origins of multiple sclerosis and could lead to the development of more effective treatments for the disease.
"By transfusing dendritic cells into the blood, it may be possible to reduce autoimmunity," says senior study author Ari Waisman of University Medical Center of Johannes Gutenberg University Mainz. "Beyond multiple sclerosis, I can easily imagine that this approach could be applied to other autoimmune diseases, such as inflammatory bowel disease and psoriasis."
In an animal model of multiple sclerosis known as experimental autoimmune encephalomyelitis (EAE), immune cells called T cells trigger the disease after being activated by other immune cells called antigen-presenting cells (APCs). Dendritic cells are APCs capable of activating T cells, but it was not known whether dendritic cells are the APCs that induce EAE.
In the new study, Waisman and his team used genetic methods to deplete dendritic cells in mice. Unexpectedly, these mice were still susceptible to EAE and developed worse autoimmune responses and disease clinical scores, suggesting that dendritic cells are not required to induce EAE and other APCs stimulate T cells to trigger the disease. The researchers also found that dendritic cells reduce the responsiveness of T cells and lower susceptibility to EAE by increasing the expression of PD-1 receptors on T cells.
"Removing dendritic cells tips the balance toward T cell-mediated autoimmunity," says study author Nir Yogev of University Medical Center of Johannes Gutenberg University Mainz. "Our findings suggest that dendritic cells keep immunity under check, so transferring dendritic cells to patients with multiple sclerosis could cure defects in T cells and serve as an effective intervention for the disease."
Source: Science Daily