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.”
Tool use is rare in wild animals, but of widespread interest because of its relationship to animal cognition, social learning and culture. Despite such attention, quantifying the costs and benefits of tool use has been difficult, largely because if tool use occurs, all population members typically exhibit the behavior. In Shark Bay, Australia, only a subset of the bottlenose dolphin population uses marine sponges as tools, providing an opportunity to assess both proximate and ultimate costs and benefits and document patterns of transmission.
We compared sponge-carrying (sponger) females to non-sponge-carrying (non-sponger) females and show that spongers were more solitary, spent more time in deep water channel habitats, dived for longer durations, and devoted more time to foraging than non-spongers; and, even with these potential proximate costs, calving success of sponger females was not significantly different from non-spongers. We also show a clear female-bias in the ontogeny of sponging. With a solitary lifestyle, specialization, and high foraging demands, spongers used tools more than any non-human animal. We suggest that the ecological, social, and developmental mechanisms involved likely (1) help explain the high intrapopulation variation in female behaviour, (2) indicate tradeoffs (e.g., time allocation) between ecological and social factors and, (3) constrain the spread of this innovation to primarily vertical transmission.
The dolphins use the sponge to push along the ocean floor and disturb fish, that are hidden. Once the fish start swimming away the dolphin abandons the sponge and catches and eats the fish. Then the dolphin goes back and gets the sponge and continues.
Since the first antibiotics reached the pharmacy in the 1940s, researchers discovered that they target various pieces of machinery in bacterial cells, disrupting the bacteria’s ability to build new proteins, DNA, or cell wall. But these effects alone do not cause death, and a complete explanation of what actually kills bacteria after they are exposed to antibiotics has eluded scientists.
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The group found that all bactericidal antibiotics, regardless of their initial targets inside bacteria, caused E. coli to produce unstable chemicals called hydroxyl radicals. These compounds react with proteins, DNA, and lipids inside cells, causing widespread damage and rapid death for the bacteria.
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With the results of these two experiments, the researchers were able to identify three major processes implicated in gentamicin-induced cell death: protein transport, a stress response triggered by abnormal proteins in the cell membrane, and a metabolic stress response.
An analysis of the germs unleashed from a single commuter’s sneeze showed that within minutes they are being passed on via escalator handrails or seats on trains and underground carriages. At the busiest stations, one sneeze not smothered by a tissue or handkerchief will provide enough germs to infect another 150 commuters.
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A single sneeze expels 100,000 droplets of germs into the air at 90mph. Individual droplets get transferred to handles, rails and other areas frequently held or touched. Up to 10 per cent of all commuters will come into contact with an area infected by that one sneeze, Dr Henderson calculated.
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Researchers asked 1,300 workers about their health and found 99 per cent of commuters suffered at least one cold last winter. In contrast, just 58 per cent of those who work from home and 88 per cent of those who walk to work regularly caught a cold last winter.
It is amazing (or maybe not but I find it amazing) how well cold viruses have evolved to have us sneeze and send out personal virus jet packs to spread them all over and let them infect others. It is sad how impolite some people are as they go around potentially infecting hundreds of other people. Partially their ignorance of basic science may also be to blame for their behavior. It is too bad others have to suffer due to their bad manners and ignorance.
The retina, which is located in the back of the eye, has an outer layer of cells that detect light and translate it into electrical signals. It also has inner layers, which process the signals and send them to the brain.
In degenerative disorders like macular degeneration and retinitis pigmentosa, outer-layer cells, called photoreceptors, break down in the early stages of disease, leading to loss of vision. Extensive research has focused on replacing these cells, in an effort to restore sight. In people with advanced disease or blindness, however, the inner cell layers may also break down or become disorganized and need to be rebuilt, says Rose.
“The outer retina is like the CPU, and the inner retina is like the motherboard,” he says. “If I attach a new CPU to a dead motherboard, it won’t do any good, no matter how great a CPU it is.”
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In lower vertebrates like fish and chickens, retinal cells are known to generate new neurons in response to damage, often restoring sight. While mammals do not have the same self-healing capacity, some previous research has suggested that under particular circumstances, mammals’ retinas might be able to generate new neurons.
Authors of a new study hope to begin a debate challenging the conventional wisdom about early detection of breast cancer. In an article in today’s Archives of Internal Medicine, they ask: Do breast tumors ever go away on their own?
Researchers of this controversial article note that one type of cancer found through screening — a rare childhood tumor, called neuroblastoma — sometimes disappears. In the new article, researchers try to learn if the same phenomenon occurs with invasive breast cancers found with mammograms
Conclusions: Because the cumulative incidence among controls never reached that of the screened group, it appears that some breast cancers detected by repeated mammographic screening would not persist to be detectable by a single mammogram at the end of 6 years. This raises the possibility that the natural course of some screen-detected invasive breast cancers is to spontaneously regress.
As with so much medical research the results are not completely clear. Studies need to be followed by more studies, which often lead to more studies. As long as progress is being made this is a perfectly reasonable course of scientific inquiry. And even if progress is not being made this can be perfectly reasonable – finding answers can be hard.
Webcast from 23andme on human evolution. Continued: What are genes?, What are SNPs? (Single Nucleotide Polymorphisms), Where do your genes come from? and What is phenotype?. These webcasts provide an easy to understand overview. Sergey Brin, Google co-founder and husband of 23andme co-founder Anne Wojcicki. People have 23 pairs of chromosomes.
For a variation to be considered a SNP, it must occur in at least 1% of the population. SNPs, which make up about 90% of all human genetic variation, occur every 100 to 300 bases along the 3-billion-base human genome.
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SNPs do not cause disease, but they can help determine the likelihood that someone will develop a particular illness. One of the genes associated with Alzheimer’s disease, apolipoprotein E or ApoE, is a good example of how SNPs affect disease development. ApoE contains two SNPs that result in three possible alleles for this gene: E2, E3, and E4. Each allele differs by one DNA base, and the protein product of each gene differs by one amino acid.
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.
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.
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.
Vanishing Arctic sea ice brought on by climate change is causing the crucially important microscopic marine plants called phytoplankton to bloom explosively and die away as never before, a phenomenon that is likely to create havoc among migratory creatures that rely on the ocean for food, Stanford scientists have found.
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Phytoplankton throughout the world’s oceans is the crucial nutrient at the base of the food web on which all marine life depends; when it’s plentiful, life thrives and when it’s gone, marine life is impossible.
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“It’s a complex system,” Arrigo said in an interview, “but as the changes in ice cover throw the timing of phytoplankton abundance off, then the birds and animals whose brains have long been programmed to migrate north at specific times of the year will have missed the boat if there’s no nourishment for them when they get there.”
Every spring and summer, phytoplankton in the Arctic blooms richly in explosive pulses, nourished by nitrogen and phosphorous in the seawater, and when those chemicals are consumed, the blooms end, Arrigo said.
Photograph of dolphin with a sponge it uses to hunt, courtesy of Ewa Krzyszczyk, PLoS,