genetics - What is the distinction between F' plasmid and R plasmid?

If I understand the nomenclature correctly, an R plasmid is just any plasmid containing an antibiotic (R)esistance gene (eg. Amp, Kan, Cm, etc.). It's a bit of an outdated name from when people didn't know how exactly the plasmids conferred such resistance.

An F-plasmid is any plasmid that contains the genes necessary for (F)ertility, eg:horizontal gene transfer via the tra operon.

The two do not have to appear together -- eg: Many F plamids will contain resistance genes (along with other random chunks from the genome), but resistance doesn't always have to be part of the payload. Likewise, it is common in labs to build pure resistance vectors that lack any horizontal transfer capability in order to select for particular clones.

coordinates in ICRF - Astronomy

The International Celestial Reference Frame (ICRF) is defined based on distant quasars and the origin is the barycentre of the Solar system. So, how can we measure the coordinates (alpha, delta) of an object, say, star in ICRF. In web, the coordinates are often reported as (alpha, delta) in ICRF analogous to (alpha, delta) in equatorial coordinate system. And what role does distant quasars playing here.
I know how the coordinates are defined in equatorial coordinate system.

hubble telescope - Is there a legend for these 88 HST images?

Is there a legend for these 88 Hubble Space Telescope images?

I have a 6000px x 4800 px version of this image (reduced & rotated to 480x600 here) that I use for an image slide show. I would like to add the description of each image into the slide show software.

On this system the file name is HubbleGallery.jpg but I suspect I coined that title (it was a long time ago it was downloaded). The original image is 5,150,779 bytes in size.

Searching on the smaller, rotated version of the image points to pages like Astronomy Printshop, but there is nothing closely related to NASA in the first pages of the search, and the pages listed did not have much detail (certainly no legend).

It might possible to search on the clipped, individual images, but I was hoping to avoid having to do that 88 times.

Can visible wavelength spectroscopy study an exoplanet's chemical composition directly?

I know spectroscopy of light in visible wavelengths is very effective for studying and determining the chemical composition of bodies within the solar system and bright objects outside of it. However, can this same method be used with exoplanets?

In looking about some related articles, I've learned that it is possible, if a planet passes between us and its star, to filter out the star's light leaving only what passes through the planet's atmosphere.
But what if there is no such occultation? Can we filter out the star's light in other wavelengths like UV or infrared and look at just the planet via its own emitted radiation (assuming the planet is large and hot as these are what we are most able to detect at this time)?

neuroscience - How and where, in the human brain, are memories stored?

Unfortunately, we are all still "confuzzled" by how memory works. We are far from a complete understanding of how memory is stored and recalled. Nonetheless, we do know a little, so read on.

Your understanding of basic neural function is almost correct. First, an individual neuron will signal through its single axon onto the dendrites of many downstream neurons, not the other way around. Second, I am not sure what you mean by "focusing them based on their permutations," but it is true that neural information can undergo many transformations as it propagates through a circuit. Third, if there is a behavioral outcome of the network activity like a muscle response or hormone release, those effects are mediated by nerves communicating with muscles and hormone-releasing cells. I'm not sure if that is what you meant by "focused response mechanism."

Finally, as you have discovered, the analogy of neural circuits to electrical circuits is relatively poor at any reasonably sophisticated level of analysis. My opinion is that biological systems are often poorly served by being framed as engineering problems. Others will disagree with that, but I think understanding a biological system on its own terms makes many things much clearer.

The key thing missing from the electrical circuit analogy turns out to be one of the keys to understanding information storage in neural circuits--the synapse, the site where one neuron communicates with another. The synapse transforms the electrical signal from the upstream neuron into a chemical signal. That chemical signal is then converted back into an electrical signal by the downstream neuron.

The strength of the synapse can be adjusted in a long-term way by changing the level of protein expression--this is called long-term potentiation (LTP) or long-term depression (LTD). LTP and LTD therefore can regulate the ease with which information can flow along a particular path. As a basic example (that should not be taken too seriously), imagine a set of neurons that represents "New York City" and another set of neurons that represents "My Friend John." If you then happen to be in New York City with your friend John, both of those groups of neurons will be active and synapses between these two networks will be strengthened because they are co-active (see Hebbian plasticity). In this way, the idea of NYC and the idea of John are now bound together.

Where are these neurons that represent NYC and John? We are still not totally clear on this, and the question is complicated because there are many different types of memory. For instance, your memory of how to ride a bike (procedural memory) is not treated the same as your memory of what you ate for breakfast (episodic memory). However, a best current answer is that the hippocampus and its associated regions are important for the initial encoding of memories and the neocortex is where longer term memories are stored. There is substantial communication between these two areas so that memories can be effectively adjusted over time.

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Update

In response to Jule's comment asking for some resources, I realize it is important to make the point that the Hebbian model I outlined hasn't been definitively shown. Like with all aspects of neuroscience, there is a lot of good work at the molecular and cellular level and good work at the behavioral level, but the causal link between the two is not so clear. Nonetheless, Hebb's idea is still the mainstream working model for how memory works. Some reading might include:

1) Neves, G., Cooke, S.F., Bliss, T.V.P., 2008. Synaptic plasticity, memory and the hippocampus: a neural network approach to causality. Nature Reviews Neuroscience 9, 65–75.
A review on hippocampal memory and its relation to LTP/LTD and Hebbian theory. Notes the general difficulty of proving the theory and some ways for experiments to move forward.

2) Lisman, J., Grace, A.A., Duzel, E., 2011. A neoHebbian framework for episodic memory; role of dopamine-dependent late LTP. Trends in Neurosciences 34, 536–547.
A review proposing an elaboration of the Hebbian model that includes neuromodulatory influence on plasticity and memory process.

3) Johansen, J.P., Cain, C.K., Ostroff, L.E., LeDoux, J.E., 2011. Molecular Mechanisms of Fear Learning and Memory. Cell 147, 509–524.. An excellent review on fear learning and memory with an extensive section on Hebbian theory.

4) Liu, X., Ramirez, S., Pang, P.T., Puryear, C.B., Govindarajan, A., Deisseroth, K., Tonegawa, S., 2012. Optogenetic stimulation of a hippocampal engram activates fear memory recall. Nature. A research article which is perhaps a realization of some of suggestions in the Neves et al review. They use light to reactivate a fear memory. This suggests that activation of the hippocampal network that was active during memory formation is sufficient to elicit the memory.

dna - Synthetic biology using existing cells

There is this guy, Martin Hanczyc, working on protocells to better understand how the beginning of life occurred. He makes synthetic protocells. They don't have any DNA in them but they are pretty cool and maybe the beginnings to making synthetic cells. Perhaps once science has figured out how cells began and their very minimal needs they can create completely synthetic cells.

http://www.ted.com/talks/martin_hanczyc_the_line_between_life_and_not_life.html

Also, just thinking, what would we consider completely synthetic cells? If we took synthetic protocells and they eventually evolved into a cell with DNA would that still be synthetic?

human biology - How do the brain and nerves create electrical pulses?

So, let us introduce some keywords.

The "electrical pulse" that "is sent from between brain and nerves" is called an Action Potential (AP). This is then propagated along a nerve fiber until the target organ.

Basically, a neuronal cell has a body and several long extended structures that "sprout" from the cell body. Dendrites receive signals from other cells and they convey signals towards the cell body by creating small electrical currents. The axon is a single "sprout" that is usually much thinner and longer than the dendrites and it conveys action potentials from the near the cell body to target cells and organs. Some axons can be as long as 80-90 cm (imagine!)! At the place where axon leaves the nerve cell body there is a small protrusion called the axon hillock.

The AP originates at a special part of the axon called the axon initial segment (AIS). The initial segment is the first part of the axon as it leaves the cell body and sits immediately after the axon hillock.

The electrical pulse is the short electrical discharge, that can be seen as a sudden movement of many charged particles from one place to another. In our cells we have ions of Na⁺ (sodium), K⁺ (potassium) and Cl^- (chloride) (and in some cases also Ca²⁺) that constitute these charged particles.

There are two types of driving forces for these particles: besides the potential gradient, e.g. the difference in the total charge in two different places there is also another force called concentration gradient, e.g. the difference in concentration at two different places. These force can point into opposite directions, and thus by exploiting one force (let's say concentration gradient) we can influence another one.

What we need here again is a so-called semi-permeable membrane, this is just a barrier for ions, but only for specific ones. We need this because our main ions -- Na⁺ and K⁺ -- are both positively charged. Therefore the cell membrane acts as a semi-permeable membrane, letting K⁺ into the cells and Ca²⁺ ions outwards but not the opposite. Therefore we have two concentration gradients: Na⁺ (outside is the peak) and K⁺ (inside is the peak).

In order to start the pulse we need to initiate a massive ionic drift from one place to another. This is done by the cell, and the first event here is the drastic change (increase) of the permeability for Na⁺ ions. Na⁺ ions massively enter the cell and their charges, moved into the cell, form the upstroke of the action potential.

The protective mechanism of the cell immediately start working against the Na⁺ invasion and open the reserve shunts -- the K⁺ channels. K⁺ leaves the cell, taking away some charge and this is revealed as the decay of the action potential. But potassium channels are generally slower, that is why the decay of the pulse is more steady, not as sharp as the upstroke.

You might be wondering now: what triggers the rapid change of membrane permeability then? There are several factors here that may contribute into this process.

1. Potential change of the membrane. Sodium and potassium channels are voltage-sensitive, meaning if you manage to change the resting potential of the membrane, formed due to concentration gradients and normally being about -90..-80 mV (millivolts) up to about -40 mV it will trigger the sodium channels. This is how the impulse propagates -- having originated at one place it just decreases the resting potential of the adjacent membrane area, sodium enters the cell there and the AP travels along the nerve. The AIS is the site of AP initiation because this part of the cell has a very high density of voltage-gated sodium channels.




2. Chemical agents, called neurotransmitters, can be detected by receptors on the cell membrane. Some of these receptors are ion channels themselves and open directly when neurotransmitter is bound. Other receptors act through intracellular signals to open ion channels. This is how the signal appears at the sites of nerve cell contacts -- neurotransmitters, like acetylcholine or adrenaline, just act here as triggers for membrane permeability.