Perfect magnets
Close-Up of the First Mechanical Gear Ever Found in Nature
The biological form of a mechanical gear was observed in nature for the first time in juvenile planthoppers (Genus: Issus), a common insect that can be found in gardens across Europe.
The insect has hind-leg joints with curved cog-like strips of opposing ‘teeth’ that intermesh, rotating like mechanical gears to synchronize the animal’s legs when it launches into a jump. The finding demonstrates that gear mechanisms previously thought to be solely man-made have an evolutionary precedent.
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ALL ROLLED UP
A newly identified mineral christened merelaniite tightly rolls up like a scroll as it crystallizes, forming shiny dark gray needles up to a few millimeters in length (Minerals 2016, DOI: 10.3390/min6040115). The overall formula of the mineral is Mo₄Pb₄VSbS₁₅. It crystallizes into a sheet composed primarily of alternating ultrathin layers of MoS₂ and PbS. “It’s like a natural nanocomposite,” says research team leader John A. Jaszczak of Michigan Technological University. Strain from the interacting layers likely causes the crystalline sheets to wrap around themselves as they grow. Jaszczak and coworkers named the mineral for the Merelani mining district in Tanzania, where the merelaniite samples originated. Collaborating research institutions included the U.K. Natural History Museum, U.S. National Museum of Natural History, and University of Florence.
Credit: Minerals (both)
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A UT Dallas scientist has found a new neurological mechanism that appears to contribute to a reduction in pain.
According to Dr. Ted Price, associate professor in the School of Behavioral and Brain Sciences, the discovery of neuroligin-2 as a cause exacerbating chronic pain is significant for the research community. Although the findings likely won’t immediately lead to new pain therapies, the findings offer a potential new therapeutic direction to investigate, he said.
Price’s research on the topic has recently been published online in Pain, the journal of the International Association for the Study of Pain.
The study focused on the body’s inhibitory networks — a series of biochemical reactions that decrease certain neurological activity, such as pain. Price said a great deal of previous research in this area has focused on the activity of the neurotransmitter GABA, a chemical released by nerve cells in the brain.
Normally, a GABA neurotransmitter acts to inhibit neuronal activity, such as pain. However, when pain becomes chronic there is strong evidence that a process called GABAergic plasticity can cause GABA to lose its inhibitory activity, sometimes making the pain even worse.
The source of these excitatory actions in neuronal circuits has been broadly attributed to chloride ions, but Price’s research has found another potential cause of GABAergic plasticity: synaptic adhesion molecules called neuroligin-2.
“From a basic science perspective, we’re really excited about it because it demonstrates that the types of GABAergic plasticity that can occur in the setting of chronic pain are more diverse than we’ve appreciated before,” he said.
Price, who heads the undergraduate research program in neuroscience in the school, focuses much of his research on understanding the neuroscience behind pain, particularly chronic pain. He said individuals with chronic pain typically don’t receive the pain-reduction benefits delivered by inhibitory systems. Instead, they often experience increased pain.
“When you hit your hand with a hammer, almost everybody has the same reflex reaction — that is, to rub your finger which, in turn, helps to reduce pain. The reason that works is because it increases GABAergic inhibition in the spinal cord,” Price said. “However, people who have chronic pain — if they do the same thing — find that rubbing it actually makes the pain worse. That’s because the GABAergic system loses its efficacy and, in fact, can become excitatory.”
Price said the research is another step in determining why the GABAergic system stops working correctly in some people and provides a second theory for what drives the system.
“Having two ideas and different models will allow us to determine what the therapeutic opportunities are — creating something that will change that back to normal. The lack of performance in the inhibitory system is very detrimental to those who are in chronic pain,” he said.
Price said the development of chronic pain is, in essence, one’s body “learning” something that is bad.
“It’s changing the way the body functions — it’s learning. That learning, in the case of chronic pain, is aberrant — it’s causing the situation to get worse. If we can figure out what that form of learning was, then we can potentially reverse it. Understanding that the GABAergic system changes during this form of learning potentially offers a new therapeutic avenue,” he said.