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Silk leaf

http://www.dezeen.com/2014/07/25/movie-silk-leaf-first-man-made-synthetic-biological-leaf-space-travel/

Livro de Rita Vilela

O monte Bromo (em indonésio: Gunung Bromo; em javanês: Gunung Brama é um estratovulcão ativo da ilha de Java, Indonésia,[1] situado na província de Java Oriental e regência de Probolinggo.

Faz parte do maciço de Tengger e o cume ergue-se a 2 239 metros de altitude. Apesar de não ser o vulcão mais alto do maciço, é o mais conhecido. A cratera tem cerca de 800 m de diâmetro e 200 m de profundidade. O maciço faz parte do Parque Nacional de Bromo-Tengger-Semeru e é uma das áreas de Java Oriental mais visitadas por turistas. O nome Bromo deriva da pronúncia javanesa de Brama, o deus criador do hinduísmo.O vulcão ergue-se no meio de uma planície chamada Mar de Areia (em javanês: Segara Wedi; em indonésio: Lautan Pasir), classificada como reserva natural desde 1919

     Bromo Volcano Crater

“The Stella Pinafore Toilette.”

Enquire Within, Ladies Home Journal

5th February 1916.

Interessante!!

Sensation of Taste Is Built into Brain

Roast turkey. Stuffing. Mashed potatoes and gravy. Pie. Thanksgiving conjures up all sorts of flavors. If you close your eyes you can almost taste them. In fact, one day you may be able to—without food.

Scientists from Columbia University have figured out how to turn tastes on and off in the brain using optogenetics—a technique that uses penetrating light and genetic manipulation to turn brain cells on and off. They reported their findings in an article published in Nature. By manipulating brain cells in mice this way, the scientists were able to evoke different tastes without the food chemicals actually being present on the mice’s tongues.

The experiments “truly reconceptualize what we consider the sensory experience,” said Charles Zuker, head of the Zuker lab at Columbia and co-author on the paper. The results further demonstrate “that the sense of taste is hardwired in our brains,” Zuker said, unlike our sense of smell, which is strongly linked to taste but almost entirely dependent on experience.

Typically when we eat, the raised bumps, or papillae, that cover our tongues, pick up chemicals in foods and transmit tastes to the brain. There are five main types of papillae corresponding to each of the five basic tastes—sweet, sour, salty, bitter and umami. Contrary to popular belief, these aren’t clustered in particular places on the tongue, with bitter in the back and sweet at the front, but are spaced about evenly on the tongue.

A taste map may in fact exist, but it appears to be in the brain rather than on the tongue. First the researchers singled out the mice’s sweet and bitter taste centers in the brain, which are separated by approximately two millimeters in the insula. They concentrated on only sweet and bitter because the two are the most distinct from each other and also the most salient for humans, mice and other animals due their evolutionary importance to survival. Sweet usually indicates the presence of nutrients, whereas bitter signals potential danger of poison.

Zuker and his team then optogenetically stimulated the areas with light and in a series of behavioral tests, were able to have the mice taste sweet or bitter with only plain water. When the researchers activated the sweet neurons, they observed behavior consistent what with happens when mice normally encounter sweet foods: their licking increased significantly, even when the animals’ thirst was satiated. When the scientists stimulated neurons associated with bitter flavors, the mice stopped licking, seemed to scrub at their tongues and even gagged, depending on the level of optogenetic stimulation.

The researchers then performed the tests on animals that had never tasted sweet or bitter in their lives and found the same results. In the last set of experiments the researchers applied to the tongue of the mice chemicals that tasted sweet and bitter and compared their reactions to what happened when they simply stimulated the corresponding neurons optogenetically. There was no difference in the way the animals responded, “proving taste is hardwired in the brain,” Zuker said.

This doesn’t mean that there is no such thing as an “acquired taste,” Zuker clarified. For example, hákarl, fermented shark meat and national dish of Iceland, once called “the single worst, most disgusting and terrible tasting thing,” by famously acerbic food critic Anthony Bourdain is relished by many on the Nordic island nation. Humans are more complicated than mice. Taste can also be shaped by experience and culture. But the basics of this sensation are present from the beginning.

“Every baby smiles to sweet and frowns for bitter,” Zuker explained. “Taste mostly retains that hardwired response unless there is something that supersedes it. There are some things we consume [that] are innately aversive. But we take the gain with the bad if they have a positively reinforcing result.” Coffee or alcohol, for instance, are distinctly bitter, but many people learn to enjoy them over time due to the feelings of stimulation and inebriation they bring, respectively.

Gary Beauchamp, president of the Monell Chemical Senses Center in Pennsylvania, calls the research “a very clear and elegant approach,” confirming the long-standing hypothesis that taste is indeed evolutionarily hardwired. But Beauchamp also notes that sweet and bitter compounds can influence each other in the mouth to affect taste before they reach the brain. “In the real world, where foods are mixtures of things, it’s much more complex than what this study would suggest. Nevertheless, this is excellent work showing that these pathways are innately organized,” he said.  

Zuker is aware that sweet and bitter are at the extremes of the taste spectrum and may not be representative of all tastes. But he expects similar results testing other tastes, which are also evolutionarily based. Salt, for example, signals electrolytes. “The next question is how activity in these cortical fields integrates with rest of brain,” to form experience and lasting taste memories – such as those we make at Thanksgiving.

Source: Scientific American

(Image caption: Motor neurons (green) form synapses (highlighted in magenta) on muscle fibers in a fruit fly. MIT neuroscientists have discovered a pathway that contributes to strengthening these synapses. Credit: Troy Littleton)

Neuroscientists reveal how the brain can enhance connections

When the brain forms memories or learns a new task, it encodes the new information by tuning connections between neurons. MIT neuroscientists have discovered a novel mechanism that contributes to the strengthening of these connections, also called synapses.

At each synapse, a presynaptic neuron sends chemical signals to one or more postsynaptic receiving cells. In most previous studies of how these connections evolve, scientists have focused on the role of the postsynaptic neurons. However, the MIT team has found that presynaptic neurons also influence connection strength.

“This mechanism that we’ve uncovered on the presynaptic side adds to a toolkit that we have for understanding how synapses can change,” says Troy Littleton, a professor in the departments of Biology and Brain and Cognitive Sciences at MIT, a member of MIT’s Picower Institute for Learning and Memory, and the senior author of the study, which appears in the Nov. 18 issue of Neuron.

Learning more about how synapses change their connections could help scientists better understand neurodevelopmental disorders such as autism, since many of the genetic alterations linked to autism are found in genes that code for synaptic proteins.

Richard Cho, a research scientist at the Picower Institute, is the paper’s lead author.

Rewiring the brain

One of the biggest questions in the field of neuroscience is how the brain rewires itself in response to changing behavioral conditions — an ability known as plasticity. This is particularly important during early development but continues throughout life as the brain learns and forms new memories.

Over the past 30 years, scientists have found that strong input to a postsynaptic cell causes it to traffic more receptors for neurotransmitters to its surface, amplifying the signal it receives from the presynaptic cell. This phenomenon, known as long-term potentiation (LTP), occurs following persistent, high-frequency stimulation of the synapse. Long-term depression (LTD), a weakening of the postsynaptic response caused by very low-frequency stimulation, can occur when these receptors are removed.

Scientists have focused less on the presynaptic neuron’s role in plasticity, in part because it is more difficult to study, Littleton says.

His lab has spent several years working out the mechanism for how presynaptic cells release neurotransmitter in response to spikes of electrical activity known as action potentials. When the presynaptic neuron registers an influx of calcium ions, carrying the electrical surge of the action potential, vesicles that store neurotransmitters fuse to the cell’s membrane and spill their contents outside the cell, where they bind to receptors on the postsynaptic neuron.

The presynaptic neuron also releases neurotransmitter in the absence of action potentials, in a process called spontaneous release. These “minis” have previously been thought to represent noise occurring in the brain. However, Littleton and Cho found that minis could be regulated to drive synaptic structural plasticity.

To investigate how synapses are strengthened, Littleton and Cho studied a type of synapse known as neuromuscular junctions, in fruit flies. The researchers stimulated the presynaptic neurons with a rapid series of action potentials over a short period of time. As expected, these cells released neurotransmitter synchronously with action potentials. However, to their surprise, the researchers found that mini events were greatly enhanced well after the electrical stimulation had ended.

“Every synapse in the brain is releasing these mini events, but people have largely ignored them because they only induce a very small amount of activity in the postsynaptic cell,” Littleton says. “When we gave a strong activity pulse to these neurons, these mini events, which are normally very low-frequency, suddenly ramped up and they stayed elevated for several minutes before going down.”

Synaptic growth

The enhancement of minis appears to provoke the postsynaptic neuron to release a signaling factor, still unidentified, that goes back to the presynaptic cell and activates an enzyme called PKA. This enzyme interacts with a vesicle protein called complexin, which normally acts as a brake, clamping vesicles to prevent release neurotransmitter until it’s needed. Stimulation by PKA modifies complexin so that it releases its grip on the neurotransmitter vesicles, producing mini events.

When these small packets of neurotransmitter are released at elevated rates, they help stimulate growth of new connections, known as boutons, between the presynaptic and postsynaptic neurons. This makes the postsynaptic neuron even more responsive to any future communication from the presynaptic neuron.

“Typically you have 70 or so of these boutons per cell, but if you stimulate the presynaptic cell you can grow new boutons very acutely. It will double the number of synapses that are formed,” Littleton says.

The researchers observed this process throughout the flies’ larval development, which lasts three to five days. However, Littleton and Cho demonstrated that acute changes in synaptic function could also lead to synaptic structural plasticity during development.

“Machinery in the presynaptic terminal can be modified in a very acute manner to drive certain forms of plasticity, which could be really important not only in development, but also in more mature states where synaptic changes can occur during behavioral processes like learning and memory,” Cho says.

The study is significant because it is among the first to reveal how presynaptic neurons contribute to plasticity, says Maria Bykhovskaia, a professor of neurology at Wayne State University School of Medicine who was not involved in the research.

“It was known that the growth of neural connections was determined by activity, but specifically what was going on was not very clear,” Bykhovskaia says. “They beautifully used Drosophila to determine the molecular pathway.”

Littleton’s lab is now trying to figure out more of the mechanistic details of how complexin controls vesicle release.

“Pauta do Congresso agora é vingança contra MP e Judiciário”, diz procurador - O Antagonista

Adorei!!

A sushi stitch!

Videographer takes you on a timelapse trip around the world covering locations they filmed in 2017 and earlier. Enjoy! Original caption:

The past year has been unreal. New Zealand, South Africa, the Atacama Desert, La Palma the beautiful Dolomites just to count a few of the incredible locations I’ve been lucky enough to visit. Together with the footage from my past travels to Patagonia, Chile, Norway and a volcanic eruption we are proud to show you the best Timestorm Films has to offer.