wildcat2030

wildcat2030:

Thousand-strong robot swarm throws shapes, slowly
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Engineers in the US have built a swarm of 1,000 little robots that can shuffle into specific formations on command.
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 Each of the identical robots is given a picture of the required shape, and then they work together to make it happen. It takes up to 12 hours, but then this is the biggest throng of robots ever built and studied in this way. Inspired by biological examples, like cells forming organs or ants building bridges, the work could help develop self-assembling tools and structures. “Each robot is identical and we give them all the exact same program,” explained Dr Michael Rubenstein, the first author of the study, which is published in Science. “The only thing they have to go on, to make decisions, is what their neighbours are doing.” (via BBC News - Thousand-strong robot swarm throws shapes, slowly)

wildcat2030

wildcat2030:

DARPA announces Phase 1 of its XS-1 spaceplane program
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It takes a lot more money and preparation to launch a rocket than to have a plane take off. That’s why DARPA (the Defense Advanced Research Projects Agency) first initiated its Experimental Spaceplane (XS-1) program. The idea is that once built, the XS-1 could take off and land like a regular aircraft, but could also deliver satellite payloads into low-Earth orbit while airborne. Today, the agency announced its plans for Phase 1 of the program, which includes awarding contracts for designs of the autonomous spaceplane. As outlined in a previous article, plans call for the unmanned XS-1 to be able to make 10 flights within 10 days, reaching a speed of Mach 10 at least once, and launching payloads weighing between 3,000 and 5,000 pounds (1,361 to 2,268 kg) at under US$5 million a pop. A second-stage rocket carrying each payload will fire once it’s launched from the spaceplane at suborbital altitude, carrying the satellite to its final orbit. The XS-1 will proceed back to the ground, where it will land and immediately be prepared for its next launch. In today’s announcement, DARPA stated that it will be funding three companies to independently develop designs for an XS-1 demonstration vehicle. These include The Boeing Company (working with Blue Origin), Masten Space Systems (working with XCOR Aerospace), and Northrop Grumman Corporation (working with Virgin Galactic). The designs will be assessed based on criteria such as feasibility, performance, developmental and operational costs, and the potential for use in military, civil and commercial applications. (via DARPA announces Phase 1 of its XS-1 spaceplane program)

r2--d2
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cyborgorgy

cyborgorgy:

ExoHand – human-machine interaction

New scope for interaction 
between humans and machines 
The ExoHand from Festo is an exoskeleton that can be worn like a glove.

The fingers can be actively moved and their strength amplified; the operator’s hand movements are registered and transmitted to the robotic hand in real time. The objectives are to enhance the strength and endurance of the human hand, to extend humans’ scope of action and to secure them an independent lifestyle even at an advanced age. 

From assembly to medical therapy
The ExoHand could provide assistance in the form of force amplification in connection with monotonous and strenuous activities in industrial assembly, for example, or in remote manipulation in hazardous environments: with force feedback, the human operator feels what the robot grasps and can thus grip and manipulate objects from a safe distance without having to touch them.

Due to the yielding capacity of its pneumatic components, the ExoHand also offers potential in the field of service robotics. In the rehabilitation of stroke patients, it could already be used today as an active manual orthosis.

A strong hand with sensitive fingers
The exoskeleton supports the human hand from the outside and reproduces the physiological degrees of freedom – the scope of movement resulting from the geometry of the joints.

Eight double-acting pneumatic actuators move the fingers so that they can be opened and closed. For this purpose, non-linear control algorithms are implemented on a CoDeSys-compliant controller, which thus allows precise orientation of the individual finger joints. The forces, angles and positions of the fingers are tracked by sensors.

wildcat2030
neurosciencestuff:

The Secret Lives (and Deaths) of Neurons
As the human body fine-tunes its neurological wiring, nerve cells often must fix a faulty connection by amputating an axon — the “business end” of the neuron that sends electrical impulses to tissues or other neurons. It is a dance with death, however, because the molecular poison the neuron deploys to sever an axon could, if uncontained, kill the entire cell.
Researchers from the University of North Carolina School of Medicine have uncovered some surprising insights about the process of axon amputation, or “pruning,” in a study published May 21 in the journal Nature Communications. Axon pruning has mystified scientists curious to know how a neuron can unleash a self-destruct mechanism within its axon, but keep it from spreading to the rest of the cell. The researchers’ findings could offer clues about the processes underlying some neurological disorders.
“Aberrant axon pruning is thought to underlie some of the causes for neurodevelopmental disorders, such as schizophrenia and autism,” said Mohanish Deshmukh, PhD, professor of cell biology and physiology at UNC and the study’s senior author. “This study sheds light on some of the mechanisms by which neurons are able to regulate axon pruning.”
Axon pruning is part of normal development and plays a key role in learning and memory. Another important process, apoptosis — the purposeful death of an entire cell — is also crucial because it allows the body to cull broken or incorrectly placed neurons. But both processes have been linked with disease when improperly regulated.
The research team placed mouse neurons in special devices called microfluidic chambers that allowed the researchers to independently manipulate the environments surrounding the axon and cell body to induce axon pruning or apoptosis.
They found that although the nerve cell uses the same poison — a group of molecules known as Caspases — whether it intends to kill the whole cell or just the axon, it deploys the Caspases in a different way depending on the context.
“People had assumed that the mechanism was the same regardless of whether the context was axon pruning or apoptosis, but we found that it’s actually quite distinct,” said Deshmukh. “The neuron essentially uses the same components for both cases, but tweaks them in a very elegant way so the neuron knows whether it needs to undergo apoptosis or axon pruning.”
In apoptosis, the neuron deploys the deadly Caspases using an activator known as Apaf-1. In the case of axon pruning, Apaf-1 was simply not involved, despite the presence of Caspases. “This is really going to take the field by surprise,” said Deshmukh. “There’s very little precedent of Caspases being activated without Apaf-1. We just didn’t know they could be activated through a different mechanism.”
In addition, the team discovered that neurons employ other molecules as safety brakes to keep the “kill” signal contained to the axon alone. “Having this brake keeps that signal from spreading to the rest of the body,” said Deshmukh. “Remarkably, just removing one brake makes the neurons more vulnerable.”
Deshmukh said the findings offer a glimpse into how nerve cells reconfigure themselves during development and beyond. Enhancing our understanding of these basic processes could help illuminate what has gone wrong in the case of some neurological disorders.

neurosciencestuff:

The Secret Lives (and Deaths) of Neurons

As the human body fine-tunes its neurological wiring, nerve cells often must fix a faulty connection by amputating an axon — the “business end” of the neuron that sends electrical impulses to tissues or other neurons. It is a dance with death, however, because the molecular poison the neuron deploys to sever an axon could, if uncontained, kill the entire cell.

Researchers from the University of North Carolina School of Medicine have uncovered some surprising insights about the process of axon amputation, or “pruning,” in a study published May 21 in the journal Nature Communications. Axon pruning has mystified scientists curious to know how a neuron can unleash a self-destruct mechanism within its axon, but keep it from spreading to the rest of the cell. The researchers’ findings could offer clues about the processes underlying some neurological disorders.

“Aberrant axon pruning is thought to underlie some of the causes for neurodevelopmental disorders, such as schizophrenia and autism,” said Mohanish Deshmukh, PhD, professor of cell biology and physiology at UNC and the study’s senior author. “This study sheds light on some of the mechanisms by which neurons are able to regulate axon pruning.”

Axon pruning is part of normal development and plays a key role in learning and memory. Another important process, apoptosis — the purposeful death of an entire cell — is also crucial because it allows the body to cull broken or incorrectly placed neurons. But both processes have been linked with disease when improperly regulated.

The research team placed mouse neurons in special devices called microfluidic chambers that allowed the researchers to independently manipulate the environments surrounding the axon and cell body to induce axon pruning or apoptosis.

They found that although the nerve cell uses the same poison — a group of molecules known as Caspases — whether it intends to kill the whole cell or just the axon, it deploys the Caspases in a different way depending on the context.

“People had assumed that the mechanism was the same regardless of whether the context was axon pruning or apoptosis, but we found that it’s actually quite distinct,” said Deshmukh. “The neuron essentially uses the same components for both cases, but tweaks them in a very elegant way so the neuron knows whether it needs to undergo apoptosis or axon pruning.”

In apoptosis, the neuron deploys the deadly Caspases using an activator known as Apaf-1. In the case of axon pruning, Apaf-1 was simply not involved, despite the presence of Caspases. “This is really going to take the field by surprise,” said Deshmukh. “There’s very little precedent of Caspases being activated without Apaf-1. We just didn’t know they could be activated through a different mechanism.”

In addition, the team discovered that neurons employ other molecules as safety brakes to keep the “kill” signal contained to the axon alone. “Having this brake keeps that signal from spreading to the rest of the body,” said Deshmukh. “Remarkably, just removing one brake makes the neurons more vulnerable.”

Deshmukh said the findings offer a glimpse into how nerve cells reconfigure themselves during development and beyond. Enhancing our understanding of these basic processes could help illuminate what has gone wrong in the case of some neurological disorders.