Tag Archives: university research

How Aerobic Exercise Suppresses Appetite

How aerobic exercise suppresses appetite

Those of you who run, bike, swim, or otherwise engage in aerobic exercise have probably noticed that in spite of burning scads of calories during your chosen activity, the last thing you feel when you’re finished is hungry.
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The researchers discovered that aerobic exercise produces increased peptide YY levels while lowering ghrelin, leading to decreased appetite. Weight training was associated with a decrease in ghrelin, but no change in peptide YY, meaning that there was a net suppression of appetite, but not to the same degree as observed with treadmill training. In both cases, changes in appetite lasted for about two hours.

I know I find this to be true for me.

Bird Brain

Bird-brains smarter than your average ape

In a recent study 20 individuals from the great ape species were unable to transfer their knowledge from the trap-table and trap-tube or vice versa, despite the fact that both these puzzles work in the same way. Strikingly the crows in The University of Auckland study were able to solve the trap-table problem after their experience with the trap-tube.

“The crows appeared to solve these complex problems by identifying causal regularities,” says Professor Russell Gray of the Department of Psychology. “The crows’ success with the trap-table suggests that the crows were transferring their causal understanding to this novel problem by analogical reasoning. However, the crows didn’t understand the difference between a hole with a bottom and one without. This suggests the level of cognition here is intermediate between human-like reasoning and associative learning.”

“It was very surprising to see the crows solve the trap-table,” says PhD student Alex Taylor. “The trap table puzzle was visually different from the trap-tube in its colour, shape and material. Transfer between these two distinct problems is not predicted by theories of associative learning and is something not even the great apes have so far been able to do.”

The Chip That Designs Itself

The chip that designs itself by Clive Davidson , 1998

Adrian Thompson, who works at the university’s Centre for Computational Neuroscience and Robotics, came up with the idea of self-designing circuits while thinking about building neural network chips. A graduate in microelectronics, he joined the centre four years ago to pursue a PhD in neural networks and robotics.
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To get the experiment started, he created an initial population of 50 random circuit designs coded as binary strings. The genetic algorithm, running on a standard PC, downloaded each design to the Field Programmable Gate Arrays (FPGA) and tested it with the two tones generated by the PC’s sound card. At first there was almost no evidence of any ability to discriminate between the two tones, so the genetic algorithm simply selected circuits which did not appear to behave entirely randomly. The fittest circuit in the first generation was one that output a steady five-volt signal no matter which tone it heard.

By generation 220 there was some sign of improvement. The fittest circuit could produce an output that mimicked the input – wave forms that corresponded to the 1KHz or 10KHz tones – but not a steady zero or five-volt output.

By generation 650, some evolved circuits gave a steady output to one tone but not the other. It took almost another 1,000 generations to find circuits that could give approximately the right output and another 1,000 to get accurate results. However, there were still some glitches in the results and it took until generation 4,100 for these to disappear. The genetic algorithm was allowed to run for a further 1,000 generations but there were no further changes.

See Adrian Thompson’s home page (Department of Informatics, University of Sussex) for more on evolutionary electronics. Such as Scrubbing away transients and Jiggling around the permanent: Long survival of FPGA systems through evolutionary self-repair:

Mission operation is never interrupted. The repair circuitry is sufficiently small that a pair could mutually repair each other. A minimal evolutionary algorithm is used during permanent fault self-repair. Reliability analysis of the studied case shows the system has a 0.99 probability of surviving 17 times the mean time to local permanent fault arrival. Such a system would be 0.99 probable to survive 100 years with one fault every 6 years.

Very cool.

Related: Evolutionary Design – Invention Machine – Evo-Devo

Harnessing Light to Drive Nanomachines

A team led by researchers has shown that the force of light indeed can be harnessed to drive machines – when the process is scaled to nano-proportions. Their work opens the door to a new class of semiconductor devices that are operated by the force of light. They envision a future where this process powers quantum information processing and sensing devices, as well as telecommunications that run at ultra-high speed and consume little power.

The energy of light has been harnessed and used in many ways. The “force” of light is different — it is a push or a pull action that causes something to move. “While the force of light is far too weak for us to feel in everyday life, we have found that it can be harnessed and used at the nanoscale,” said team leader Hong Tang, assistant professor at Yale. “Our work demonstrates the advantage of using nano-objects as ‘targets’ for the force of light – using devices that are a billion-billion times smaller than a space sail, and that match the size of today’s typical transistors.”

Full Press release

How Cells Age

A new study by Harvard Medical School researchers reveals that the biochemical mechanism that makes yeast grow old has a surprising parallel in mice, suggesting it may be a universal cause of aging in all organisms.
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In young organisms, SIRT1 effectively doubles as a gene-expression regulator and a DNA repairer. But when DNA damage accumulates—as it does with age—SIRT1 becomes too busy fixing broken DNA to keep the expression of hundreds of genes in check. This process is so similar to what happens in aging yeast that its discoverers believe it may represent a universal mechanism of aging.

Harvard researchers gain new insight into aging

Aging may be a case of neglect — an absentee landlord at the cellular level that allows gene activity to go awry, according to a study published today.

Scientists have long known that aging causes gene expression to change, and DNA damage to accumulate. But now, research led by Harvard Medical School scientists explains the connection between the two processes in mammals.

The paper, published in the journal Cell, found that a multi-tasking protein called SIRT1 that normally acts as guardian of the genome gets dragged away to DNA fix-it jobs. When the protein abandons its normal post to work as a genetic handyman, order unravels elsewhere in the cell. Genes that are normally under its careful watch begin to flip on.

“What this paper actually implies is that aspects of aging may be reversible,” said David Sinclair, a Harvard Medical School biologist who led the research. “It sounds crazy, but in principle it should be possible to restore the youthful set of genes, the patterns that are on and off.”

The study is just the latest to draw yet more attention to sirtuins, proteins involved in the aging process

Aging is fascinating. By and large people just accept it. We see it happen to those all around us, without exception. But what causes biological aging? It is an interesting area of research.

Rat Brain Cells, in a Dish, Flying a Plane

Adaptive Flight Control With Living Neuronal Networks on Microelectrode Arrays (open access paper) by Thomas B. DeMarse and Karl P. Dockendorf Department of Biomedical Engineering, University of Florida

investigating the ability of living neurons to act as a set of neuronal weights which were used to control the flight of a simulated aircraft. These weights were manipulated via high frequency stimulation inputs to produce a system in which a living neuronal network would “learn” to control an aircraft for straight and level flight.

A system was created in which a network of living rat cortical neurons were slowly adapted to control an aircraft’s flight trajectory. This was accomplished by using high frequency stimulation pulses delivered to two independent channels, one for pitch, and one for roll. This relatively simple system was able to control the pitch and roll of a simulated aircraft.

When Dr. Thomas DeMarse first puts the neurons in the dish, they look like little more than grains of sand sprinkled in water. However, individual neurons soon begin to extend microscopic lines toward each other, making connections that represent neural processes. “You see one extend a process, pull it back, extend it out — and it may do that a couple of times, just sampling who’s next to it, until over time the connectivity starts to establish itself,” he said. “(The brain is) getting its network to the point where it’s a live computation device.”

To control the simulated aircraft, the neurons first receive information from the computer about flight conditions: whether the plane is flying straight and level or is tilted to the left or to the right. The neurons then analyze the data and respond by sending signals to the plane’s controls. Those signals alter the flight path and new information is sent to the neurons, creating a feedback system.

“Initially when we hook up this brain to a flight simulator, it doesn’t know how to control the aircraft,” DeMarse said. “So you hook it up and the aircraft simply drifts randomly. And as the data come in, it slowly modifies the (neural) network so over time, the network gradually learns to fly the aircraft.”

Although the brain currently is able to control the pitch and roll of the simulated aircraft in weather conditions ranging from blue skies to stormy, hurricane-force winds, the underlying goal is a more fundamental understanding of how neurons interact as a network, DeMarse said.

Broken Window Theory Bolstered with Experiments

The broken window theory is that as the visible deterioration of an area (broken windows, graffiti, lettering…) takes place, crime will increase. And that this starts a cycle of decline for the area feeds upon itself (a negatively reinforcing loop in system thinking parlance). The theory was put forth in an article in The Atlantic in 1982 by George L. Kelling and James Q. Wilson.

Criminology Can the can, The Economist

Kees Keizer and his colleagues at the University of Groningen deliberately created such settings as a part of a series of experiments designed to discover if signs of vandalism, litter and low-level lawbreaking could change the way people behave.
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The most dramatic result, though, was the one that showed a doubling in the number of people who were prepared to steal in a condition of disorder. In this case an envelope with a â‚¬5 ($6) note inside (and the note clearly visible through the address window) was left sticking out of a post box. In a condition of order, 13% of those passing took the envelope (instead of leaving it or pushing it into the box). But if the post box was covered in graffiti, 27% did. Even if the post box had no graffiti on it, but the area around it was littered with paper, orange peel, cigarette butts and empty cans, 25% still took the envelope.

The researchers’ conclusion is that one example of disorder, like graffiti or littering, can indeed encourage another, like stealing. Dr Kelling was right. The message for policymakers and police officers is that clearing up graffiti or littering promptly could help fight the spread of crime.

Single-Celled Giant Provides New Early-Evolution Perspective

Discovery of Giant Roaming Deep Sea Protist Provides New Perspective on Animal Evolution
Biologist Mikhail “Misha” Matz and his colleagues recently discovered the grape-sized protists and their complex tracks on the ocean floor near the Bahamas. DNA analysis confirmed that the giant protist found by Matz and his colleagues in the Bahamas is Gromia sphaerica, a species previously known only from the Arabian Sea.

Matz says the protists probably move by sending leg-like extensions, called pseudopodia, out of their cells in all directions. The pseudopodia then grab onto mud in one direction and the organism rolls that way, leaving a track. Hr says the giant protists’ bubble-like body design is probably one of the planet’s oldest macroscopic body designs, which may have existed for 1.8 billion years.

“I personally think now that the whole Precambrian may have been exclusively the reign of protists,” says Matz. “Our observations open up this possible way of interpreting the Precambrian fossil record.”

He says the appearance of all the animal body plans during the Cambrian explosion might not just be an artifact of the fossil record. There are likely other mechanisms that explain the burst-like origin of diverse multicellular life forms.

Single-Celled Giant Upends Early Evolution

Slowly rolling across the ocean floor, a humble single-celled creature is poised to revolutionize our understanding of how complex life evolved on Earth.

A distant relative of microscopic amoebas, the grape-sized Gromia sphaerica was discovered once before, lying motionless at the bottom of the Arabian Sea. But when Mikhail Matz of the University of Texas at Austin and a group of researchers stumbled across a group of G. sphaerica off the coast of the Bahamas, the creatures were leaving trails behind them up to 50 centimeters (20 inches) long in the mud.

The trouble is, single-celled critters aren’t supposed to be able to leave trails. The oldest fossils of animal trails, called ‘trace fossils’, date to around 580 million years ago, and paleontologists always figured they must have been made by multicellular animals with complex, symmetrical bodies.

How Bleach Kills Bacteria

Developed more than 200 years ago and found in households around the world, chlorine bleach is among the most widely used disinfectants, yet scientists never have understood exactly how the familiar product kills bacteria. In fact, Hypochlorite, the active ingredient of household bleach, attacks essential bacterial proteins, ultimately killing the bugs.

“As so often happens in science, we did not set out to address this question,” said Jakob, an associate professor of molecular, cellular and developmental biology. “But when we stumbled on the answer midway through a different project, we were all very excited.”

Jakob and her team were studying a bacterial protein known as heat shock protein 33 (Hsp33), which is classified as a molecular chaperone. The main job of chaperones is to protect proteins from unfavorable interactions, a function that’s particularly important when cells are under conditions of stress, such as the high temperatures that result from fever.

“At high temperatures, proteins begin to lose their three-dimensional molecular structure and start to clump together and form large, insoluble aggregates, just like when you boil an egg,” said lead author Jeannette Winter, who was a postdoctoral fellow in Jakob’s lab. And like eggs, which once boiled never turn liquid again, aggregated proteins usually remain insoluble, and the stressed cells eventually die.

Jakob and her research team figured out that bleach and high temperatures have very similar effects on proteins. Just like heat, the hypochlorite in bleach causes proteins to lose their structure and form large aggregates.

These findings are not only important for understanding how bleach keeps our kitchen countertops sanitary, but they may lead to insights into how we fight off bacterial infections. Our own immune cells produce significant amounts of hypochlorite as a first line of defense to kill invading microorganisms. Unfortunately, hypochlorite damages not just bacterial cells, but ours as well. It is the uncontrolled production of hypochlorite acid that is thought to cause tissue damage at sites of chronic inflammation.

How did studying the protein Hsp33 lead to the bleach discovery? The researchers learned that hypochlorite, rather than damaging Hsp33 as it does most proteins, actually revs up the molecular chaperone. When bacteria encounter the disinfectant, Hsp33 jumps into action to protect bacterial proteins against bleach-induced aggregation.

“With Hsp33, bacteria have evolved a very clever system that directly senses the insult, responds to it and increases the bacteria’s resistance to bleach,” Jakob said.

Engineering A Golf Swing

Golf secret not all in the wrists

After decades of research, the world may be closer to the perfect golf swing. University of Surrey engineer Robin Sharp has found the key is not in using full power from the start, but by building up to it quickly.

Surprisingly, the wrists don’t play a critical role in the swing’s outcome, according to the new model. The analysis also shows that while bigger golfers might hit further, it’s not by much. Any golfer will tell you that the idea of swinging harder to hit farther is not as straightforward as it might seem; the new results indicate that how – and when – the power develops is the key to distance.
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Prof Sharp used a computer model first to fit to the swing styles of three professionals whose swings were measured with high-speed photography in 1968: Bernard Hunt, Geoffrey Hunt and Guy Wolstenholme.

The model showed that the club-head speed, and thus drive distance, of these professionals could have been improved by increasing the torque quickly to the maximum value and maintaining it throughout the rest of the swing. It’s a delicate balance, however, and Sunday duffers may find it hard to implement Prof Sharp’s prescription.

The application of science to sports is an interesting area. Previous posts: Science of the High Jump – Sports Engineering @ MIT – Physicist Swimming Revolution – Baseball Pitch Designed in the Lab