Ben Mauk on the case of Ai Weiwei’s “million-dollar” broken vase: http://nyr.kr/1jFqhwR
“Stories of vandalism, destruction, forgery, and theft fascinate us because they are such tidy allegories of our relationship to art, a relationship that, at least since the time of the Armory Show, has consisted of a bizarre admixture of suspicion, discomfort, and occult reverence. Today, these attitudes are neatly characterized by the large fortunes that art sometimes commands.”
Photograph: Joe Raedle/Getty
"Everything is Art, Everything is Politics."
Researchers at the University of Bristol and University College London found that lactate – essentially lactic acid – causes cells in the brain to release more noradrenaline (norepinephrine in US English), a hormone and neurotransmitter which is fundamental for brain function. Without it people…
Ilham Tohti, economist and critic of the economic development model in Xinjiang, figured prominently in a chapter of Chinese Characters. He has been arrested on suspicion of “breaking the law” and advocating violent protest among Uighurs. Ananth Krishnan gives and update on the case on PRI’s The World.
The Bride in a Gown
Many finally found Jesus
Inside a Buddhist temple.
Some found the real Buddha
Serving quietly in a soup kitchen.
Others found themselves…
Sitting on a rubbish dump.
Gave up the search.
Gave up the search.
The rest are ruminating Rumi,
Washing up after the meditation
And falling in love with love
In all its ceremonial gowns.
Ken Holmes, January 2014
Increased inflammation following an infection impairs the brain’s ability to form spatial memories – according to new research. The impairment results from a decrease in glucose metabolism in the brain’s memory centre, disrupting the neural circuits involved in learning and memory.
Researchers from Massachusetts Eye and Ear, Harvard Medical School, Massachusetts Institute of Technology and Massachusetts General Hospital have demonstrated, for the first time, that aspirin intake correlates with halted growth of vestibular schwannomas (also known as acoustic neuromas), a…
Setting the stage for possible advances in pain treatment, researchers at The Johns Hopkins University and the University of Maryland report they have pinpointed two molecules involved in perpetuating chronic pain in mice. The molecules, they say, also appear to have a role in the phenomenon…
Image caption: MMP-9 controls onset of paralysis in ALS mice. Sections of muscle stained for nerve (green) and muscle (red); nerve-muscle contacts appear yellow. In the SOD1 mouse, muscles that move the eye (left) retain nerve contacts and are active. Fast leg muscles (center) in the same animal lose nerve contacts (red stain only) and become paralyzed. Fast muscles from which MMP-9 has been genetically removed (right) retain their nerve contacts, and therefore muscle function, for nearly 3 months longer. This suggests that inhibiting MMP-9 in human patients with ALS should be beneficial. Credit: The Henderson Lab/Columbia University Medical Center.
Columbia University Medical Center (CUMC) researchers have identified a gene, called matrix metalloproteinase-9 (MMP-9), that appears to play a major role in motor neuron degeneration in amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease. The findings, made in mice, explain why most but not all motor neurons are affected by the disease and identify a potential therapeutic target for this still-incurable neurodegenerative disease. The study was published today in the online edition of the journal Neuron.
“One of the most striking aspects of ALS is that some motor neurons—specifically, those that control eye movement and eliminative and sexual functions—remain relatively unimpaired in the disease,” said study leader Christopher E. Henderson, PhD, the Gurewitsch and Vidda Foundation Professor of Rehabilitation and Regenerative Medicine, professor of pathology & cell biology and neuroscience (in neurology), and co-director of Columbia’s Motor Neuron Center. “We thought that if we could find out why these neurons have a natural resistance to ALS, we might be able to exploit this property and develop new therapeutic options.”
To understand why only some motor neurons are vulnerable to ALS, the researchers used DNA microarray profiling to compare the activity of tens of thousands of genes in neurons that resist ALS (oculomotor neurons/eye movement and Onuf’s nuclei/continence) with neurons affected by ALS (lumbar 5 spinal neurons/leg movement). The neurons were taken from normal mice.
“We found a number of candidate ‘susceptibility’ genes—genes that were expressed only in vulnerable motor neurons. One of those genes, MMP-9, was strongly expressed into adulthood. That was significant, as ALS is an adult-onset disease,” said co-lead author Krista J. Spiller, a former graduate student in Dr. Henderson’s laboratory who is now a postdoctoral fellow at the University of Pennsylvania. The other co-lead author is Artem Kaplan, a former MD-PhD student in the lab who is now a neurology resident at NewYork-Presbyterian Hospital/Columbia University Medical Center.
In a follow-up experiment, the researchers confirmed that the product of MMP-9, MMP-9 protein, is present in ALS-vulnerable motor neurons, but not in ALS-resistant ones. Further, the researchers found that MMP-9 can be detected not just in lumbar 5 neurons, but also in other types of motor neurons affected by ALS. “It was a perfect correlation.” said Dr. Henderson. “In other words, having MMP-9 is an absolute predictor that a motor neuron will die if the disease strikes, at least in mice.”
Taking a closer look at the groups of vulnerable motor neurons, the researchers found differences in MMP-9 expression at the single-cell level. Fast-fatigable neurons (which are involved in movements like jumping and sprinting and are the first to die in ALS) were found to have the most MMP-9 protein, whereas slow neurons (which control posture and are only partially affected in ALS) had none. “So, MMP-9 is not only labeling the most vulnerable groups of motor neurons, it is labeling the most vulnerable subtypes within those groups, as well,” said Dr. Spiller.
In another experiment, the researchers tested whether MMP-9 has afunctional role in ALS by crossing MMP-9 knockout mice with SOD1 mutant mice (a standard mouse model of ALS). Progeny from this cross with no MMP-9 exhibited an 80-day delay in loss of fast-fatigable motor neuron function and a 25 percent longer lifespan, compared with littermates with two copies of the MMP-9 gene. “This effect on nerve-muscle synapses is the largest ever seen in a mouse model of ALS,” said Dr. Spiller.
The same effect on motor neuron function was seen when MMP-9 was inactivated in SOD1 mutant mice using chemical injections or virally mediated gene therapy.
“Even after treatment, these mice didn’t have a normal lifespan, so inactivating MMP-9 is not a cure,” said Dr. Henderson. “But it’s remarkable that lowering levels of a single gene could have such a strong effect on the disease. That’s encouraging for therapeutic purposes.”
The researchers are still investigating how MMP-9 affects motor neuron function. Their findings suggest that the protein plays a role in increasing stress on the endoplasmic reticulum, an organelle involved in transporting and processing materials within cells. “Our goal is to learn more about MMP-9 and related pathways and to identify a new set of therapeutic targets,” said Dr. Henderson.