Contradictiontonature - Sapere Aude

Heart Regeneration

If a person suffers a heart attack and survives, chances are their heart muscle will never be quite the same. Indeed, the associated scarring often results in permanent damage that can lead to heart failure and eventual death. Scientists are therefore searching for possible ways to promote regeneration of damaged hearts, and it’s possible that newborn mice may hold the answer. For a few weeks after birth, these animals can almost entirely regenerate their heart tissue after an injury. And new research suggests a key process that may be critical for this regenerative ability: regrowth of nerves. Blocking nerve growth specifically in experimental animals completely prevented the regrowth of damaged heart tissue. In control animals, the nerves regrew into their normal branching patterns—like those pictured. Thus if researchers are to have any hope of regenerating adult hearts after injury, their best bet might be to boost accompanying nerve growth.

Written by Ruth Williams

Image from work by Ian A. White and colleagues

Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, USA

Image copyright held by the American Heart Association

Published in Circulation Research, December 2015

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Scientists show how drug binds with ‘hidden pocket’ on flu virus

A new study led by scientists at The Scripps Research Institute (TSRI) is the first to show exactly how the drug Arbidol stops influenza infections. The research reveals that Arbidol stops the virus from entering host cells by binding within a recessed pocket on the virus.

The researchers believe this new structural insight could guide the development of future broad-spectrum therapeutics that would be even more potent against influenza virus.

“This is a very interesting molecule, and now we know where it binds and precisely how it works,” said study senior author Ian Wilson, Hanson Professor of Structural Biology, chair of the Department of Integrative Structural and Computational Biology and member of the Skaggs Institute for Chemical Biology at TSRI.

The study was published in the journal Proceedings of the National Academy of Sciences.

Rameshwar U. Kadam, Ian A. Wilson. Structural basis of influenza virus fusion inhibition by the antiviral drug Arbidol. Proceedings of the National Academy of Sciences, 2016; 201617020 DOI: 10.1073/pnas.1617020114

This is a 3-dimensional illustration showing the different features of an influenza virus, including the surface proteins hemagglutinin (HA) and neuraminidase (NA)/CDC

The south side of Jupiter, observed by the Voyager 1 space probe on March 1, 1979.

The Hubble Space Telescope captured this picture of the wispy remains of a supernova explosion. The dust cloud in the upper center of the picture is the actual supernova remnant. The dense concentration of stars in the lower left is the outskirts of star cluster NGC 1850. Full resolution picture here. More info here. Credit: NASA, ESA, Y.-H. Chu (Academia Sinica, Taipei)

Dancing Flames - Aluminium’s reactivity 

aluminium’s protective oxide layer can make it difficult to see its true reactivity in the context of metals reacting with aqueous solutions. (Do not try to recreate experiment without the presence of a trained professional)

Procedure:

Dissolve copper(II) chloride in the hydrochloric acid and set the solution aside. Take a piece of aluminium foil approximately the width of the base of the conical flask and approximately 20 cm long. Roll it loosely just enough to be able to fit through the neck of the flask – use a splint or spatula to gently push it home so it lies on its side on the base of the flask. Have a source of ignition nearby with some splints. Pour the solution inside the flask and swirl the flask gently to get the reaction going. 

After a few seconds, the mixture will begin to react vigorously and produce hydrogen gas. Hold the lit splint by the opening of the flask and the gas will ignite. If you have timed it right, the flame will sink back into the flask and dance inside above the reaction with an eerie green color from the copper.

Reaction:

2Al(s) + 3CuCl2(aq) → 2AlCl3(aq) + 3Cu(s)

2Al(s) + 6HCl(aq) → 2AlCl3(aq) + 3H2(g)

The primary objective here is to show how reactive aluminium is. The aluminium oxide layer protects the metal beneath from further reaction with air, water or acid. But chloride ions can ligate aluminium ions at the metal–oxide interface and break down the protective layer, allowing the reaction to proceed. -rsc

Giffed by: rudescience  From: This video

Getting Enraged By Specific Noises Has A Genuine Neurological Basis. Does the sound of whistling enrage you? How about the noise of someone eating? It now seems likely that those people who get infuriated by certain sounds might not just be being fussy, but actually have brains hardwired to produce an excessive emotional response to particular noises.

Complement Pathways

Components of complement pathways of the immune system. 

Classical Pathway: binds to the pathogen surface

C1 binds to phosphocholine on bacteria, which activates C1r to cleave C1s.

Activated C1s cleaves C4 to C4a and C4b.

C4b binds to the microbial surface and also binds C2.

C2 is cleaved to C2a and C2b by C1s, forming the C4bC2a complex.

The C4bC2a complex cleaves C3 to C3a and C3b.

C3b binds to the surface and causes opsonization.

MB-Lectin Pathway: uses mannin-binding lectin to bind to mannose-containing carbohydrates on the pathogen surface

Mannin-binding lectin (MBL) binds to the pathogen surface and activates MASP-2.

MASP-2 cleaves C4 to C4a and C4b.

C4b binds to the microbial surface and also binds C2.

C2 is cleaved to C2a and C2b by MASP-2, forming the C4bC2a complex.

The C4bC2a complex cleaves C3 to C3a and C3b.

C3b binds to the surface and causes opsonization.

Alternative Pathway: binds to the pathogen surface with spontaneously activated complement, amplifies C3b

C3b deposited by the C3 convertase binds to factor B.

Factor B is cleaved by factor D into Ba and Bb, forming the C3bBb complex.

The C3bBb complex cleaves C3 into C3a and C3b.

C3 spontaneously hydrolyzes to C3(H2O).

C3(H2O) binds to factor B, and factor D cleaves factor B.

Upon factor B cleavage, the C3(H2O)Bb complex is formed.

The C3(H2O)Bb complex cleaves C3 into C3a and C3b.

Factor B binds to C3b on the surface and is cleaved to Bb.

WATCH: Incredible Fungi Timelapse from Planet Earth II [video]

My new favorite: Solvatofluorescence of Nile Red

Solvatochromism is the ability of a chemical substance to change color due to a change in solvent polarity, so it has different color in different solvents.

Also in some cases, the emission and excitation wavelength both shift depending on solvent polarity, so it fluoresces with different color depending on the solvent what it’s dissolved in. This effect is solvatofluorescence.

On the video the highly solvatochromic organic dye, Nile Red was added to different organic solvents and was diluted with another, different polarity organic solvent. As the polarity of the solution changed, the emitted color from the fluorescent dye also varied as seen on the gifs above and as seen on the video:

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(Image caption: The synapses of pyramid cells in the cerebral cortex form functional groups. Some of the related synapses are shown in green in the reconstruction. Credit: © MPI of Neurobiology / Scheuss)

Neurons form synapse clusters

The cerebral cortex resembles a vast switchboard. Countless lines carrying information about the environment, for example from the sensory organs, converge in the cerebral cortex. In order to direct the flow of data into meaningful pathways, the individual pyramidal cells of the cerebral cortex act like miniature switchboard operators. Each cell receives information from several thousand lines. If the signals make sense, the line is opened, and the information is relayed onward. Scientists at the Max Planck Institute of Neurobiology in Martinsried have now shown for the first time that contact points between specific neuron types are clustered in groups on the target neuron. It is probable that signals are coordinated with each other in this way to make them more “convincing”.

The cells of the cerebral cortex have a lot to do. They process various types of information depending on the area in which they are located. For example, signals from the retina arrive in the visual cortex, where, among other things, the motion of objects is detected. The pyramidal cells of the cerebral cortex receive information from other cells through thousands of contact points called synapses. Depending on where, how many and how often synapses are activated, the cell relays the signal onward – or not.

Information is passed on in the form of electrical signals. The neurobiologists were able to measure these signals at various contact points of the neuron. “The exciting thing is that the signals that a cell receives from, say, ten simultaneously active synapses can be greater than the sum of the signals from the ten individual synapses,” says Volker Scheuss, summarizing the basis of his recently published study. “However, until now it was unclear whether this phenomenon can be explained by a specific arrangement of synapses on pyramidal cells.”

By combining modern methods, the neurobiologists in Tobias Bonhoeffer’s Department have analysed the arrangement of synapses. They were able to selectively activate a specific type of pyramid cell in brain slices from mice using optogenetics. Thanks to simultaneous “calcium imaging”, they were then able to observe and record the activity of individual synapses under a two-photon microscope. In this way, they succeeded in showing for the first time how synapses are arranged with respect to each other.

The result of such synapse mapping analysed with a newly developed algorithm was clear: The synapses of pyramidal cells form clusters consisting of 4 to 14 synapses arranged within an area of less than 30 micrometres along the dendrite. “The existence of these clusters suggests that the synapses interact with each other to control the strength of the combined signal,” explains Onur Gökçe, author of the study. This is the first anatomical explanation for the disproportionate strength of clustered synapse signals in comparison to the individual signals – a finding known from activity measurements. The observation in layer 5 pyramidal cells was of particular interest, as the activity of these cells oscillates synchronously. “This rhythmic activity, which probably influences the processing of visual information, could synchronously activate synapse clusters, thus boosting the overall signal received,” says Scheuss.