CharonY

In the oldest organisms signaling occurs chemically, where diffusion is the time limiting step. Once distances became longer, different solutions were needed. Neurons are a rather early in the evolutionary tree and has remained mostly unchanged. (I am not sure why you think transmission speed would be significant? Unless you are misunderstanding my point of signal transmissions pre-neurons). My objection to trying to explain mechanisms based on evolutionary usefulness is that it creates an interesting narrative, which usually is not testable and typically is more a distraction. Ultimately they are also not terribly useful as the mechanism itself and their properties tell us much more.

It depends on what you calculate and it depends on what you want to talk about. Most mammals have the same functional genes. The reason is that we have the same basic physiology. However, while the genes are very similar to each other, they will have sequence differences. Alternative estimates are based on actual sequence similarities. Here again several possibilities for comparisons exist and each have their own relevance in specific contexts. One could look at sequence divergence in well conserved genes. Here you get a conservative estimate of divergence as many mutations in those genes would likely be selected against. This is what has been used mostly in the past as it was too costly to sequence whole genomes. You can also compare align all identified genes, instead of selected ones which will show more divergence. Or you can also try to look at non-coding regions, which will have a much higher mutation rate. It would also make a difference whether you look at the cDNA level or on the raw sequence (containing introns). Or you could look at divergence on the amino acid level. You could also include intergenic regions which are more variable (as they do not code for proteins). Or you could look at differences in the gene order and see if they are similar. Your link actually express similarities in various ways if you read them carefully. Each of these measures are relevant in different contexts and used for different models.

I would dismiss evolutionary speculations as they are unlikely to hold significant explanatory power and concentrate on the physiology of our sense instead. I had a lengthy reply but lost it and have not the time to retype everything. Just some short notes: The dynamic range of our sense is huge, eyes can resolve about 24 bit of contrast, but not the whole range at once. Instead our sense shift to the apparent level (e.g. adapt to bright/loud situations differently than to dim/silent ones). That allows us to see something in a dim room at candlelight as well as under sunlight, for example. There are several mechanisms that allow that, and typically dissect the signal via the use of different sensory neurons and different ways of how they encode the info as action potentials (which basically encode everything as frequencies). Example are for auditory neurons that some are not very sensitive (need strong stimulus to activate) but when they activate they fire at high frequency. Others have a low threshold, but fire slowly. Frequency processing at the afferent pathways and finally location in the brain are used to figure out how loud something is (to put it very simply). Speakers can get to 120 dB and louder but may start distortion (but I am not sure how that is really relevant, especially that loudness would be highly unconfortable). However for most music it does not make much sense to go much beyond 16bit (96 dB). 24 bit is more relevant for processing rather than playback. That coincides with the total dynamic range of our hearing which goes up to 120 dB. While this is a bit more than 16 bit, it really hurts and I would assume that there is no good reason to listen to something at that level.

The interpretation in OP seems correct. What they will have analyzed is the age of each case. There is no reason why the patients should have a perfect continuous age distribution.

Precisely as I stated, or is something unclear to you about that?

Ultimately the problem that was solved is how can I transmit information over long distances, without losing details. The solution was to use action potentials which basically allow a mostly loss-less transmission. The strength of a stimulus is encoded via frequency. The other thing is how to differentiate and sense minutiae of the stimulus itself (such as frequency of sound for example) here the encoding is often at or near the sensor levels. For example you have stereocilia in your ear and the interesting bit is that they some react stronger to a certain frequency. Hence if air pressures reaches them (transduce and transmitted via eardrum and associated bones) the frequency is decoded via the type and area of stereocilia reacts to them.

It seems to me you are conflating two very different systems, multicellular organisms and unicellular ones. The effects are vastly different. A clonal cell population can undergo high-risk events (read up on SOS-response) where they increase mutation rate for example. Even if a large amount of the cells die, they will still have a largely clonal pool in the next generation. This is not true for more complex organisms. And to reiterate, the mutation are fairly minor as they are on the regulatory side. They did not create new flagella, they just restarted the their regulation. Even in eukaryotes small mutations in central regulators are known to be able to result in massive phenotypic changes (the HOM genes being prime examples).

A long but very interesting read on Arab secularism in the 20th century.

Considering how media dealt with ebola the opposite seems to be the case (also it is SARS and AFAIK after the outbreak no further ones have been detected). No evidence whatsover. I read somewhere that some TV people speculated that it might, which again supports that the media likes to overplay these scenarios. I am not sure what the relevance of the comparison of HIV (AIDS is the syndrome) and the ebola virus. But that is also not how ebola acts. There is a similarity between these viruses as both destroy macrophages. Ebola is much more aggressive and infects other cell lines quite efficiently. I do not understand the sentence, but if your question is why they do not provide vaccination, the answer is that those are still under (rushed) development. The main target being the infected areas (Sierra Leone, Guinea and Liberia).

It is on the level of an encyclopedia, as such, it generally aggregates high level information. Virtually any proper scientific communication requires much more depth. If you think in terms of a term paper, then it can be a starting point to inform you on the general topic or assist with some definition. However if you find that your writing has no more depth (and you are, say in graduate school) you are likely not covering enough depth.

There is nothing that beats doing some actual lab or field work. The only thing you can really do is talk to lecturers and ask them whether e.g. there are some summer or other projects that you could do or things you could assist in.

Not at all, the buggers accumulate massive amounts of mutations under routine cultivation conditions. In fact selection for new resistant strains or other reverting auxotroph mutants is something we are often do as in low-level microbio courses. It is actually quite a bit of a problem for cases where you create mutations to investigate stress-related responses. Sometimes they are only sensitive for a few generation and then somehow regain a wildtype phenotype. In the olden days that was it, but nowadays sequencing has become so (relatively) cheap that you could look at where the mutations are. I envy the kids nowadays.

Actually it is not. But it is more of a technical kind, but there is one thing that I find not precisely expressed. What you need to know what cDNA is and how it is produced. Based on that It is weird that it states that the restriction enzyme does not cleave the cDNA when you digest the genomic DNA. Can you tell me why? Hint: it probably means that the restriction site is not found in the cDNA sequence. Revisit how the cDNA may differ from the actual genomic sequence. Based on that, what are potential causes of multiple bands to which the probe hybridize to? Why would labeling the different end make any difference? It should be noted that the interpretation may be different if you have a pro- or an eukaryote. I assume it is the latter, though. (Also, not to be mean, but ignore the stuff above it is incorrect and has no bearing on the question whatsoever). Also I am going to move it to the homework section.

It is far to early as your exposure will only be on a very basal level. At this point there will be very little similarity to the actual research one would be doing. It would be best to get more exposure before any kind of decision is made. Another important point is to consider if one actually want to take the PhD route (as at one point or another you will have also to think about what jobs you could get).

It is in some way far easier. What was mutated was not the flagellum itself but a central regulator. Loss of it stops the bacterium from initiating motility. However, there are homologs (related genes with similar sequences) that were able to have a similar role (i.e. initiate motility) once the right mutation(s) hit. In this case only two steps were needed. One, to increase the expresssion of the homolog and a second to allow it bind the regulatory sequence of the flagellar system. This goes into the larger (known) aspect that regulatory mechanisms are a the main source of rapid changes as few mutations can result in far reaching physiological changes. If the whole flagellar operon (i.e. the genes that actually synthesize the flagellum) was lost, it would have taken much longer.

Also, at least from the crop, I am not even sure how level the camera is, relative to the persons. So it is not even clear where the center of gravity precisely is (at least I cannot clearly see how her legs are positioned). That being said, it is incredible that we are page two already.

While we got into it, I would like to throw out that even before that Reza Shah introduced secularism into Iran in the 20s. At that time religious clothing, including hijabs were banned from public places. Also he was deposed by the British and the Soviets. Also in that light it is quite hypocritical to demand other countries to become secular democracies in a shorter time frame (but obviously only the right type of democracy that favors certain economies). In Iran there was always the balance act between the modern, urbanized centers and the more conservative, religious rural areas (hence my mentioning of socioeconomic issues).

That is appalling for any country leader, and much worse for the (then) leader of the UK. That also means that his aides did not clue him in, which in turn makes me wonder what their intelligence platform for dealing with Iran or other countries in general is. Do they reset their intelligence after each election? Geez.

That is an excellent point. With English being the de facto lingua franca the anglosphere does have an advantage to begin with.

I try not to think too much about that line of reasoning. I am pretty sure that it will result in brain cancer.

An interesting take on the whole Muslims and enlightenment thing: Guardian. The article provides a timeline of modernization events. An interesting comparison one could do, from the perspective of enlightenment as a constitutional viewpoint is to contrast the development of Muslim-majority countries with e.g. African Christian-majority countries. Especially Iran in early 20th and Ottoman empire in the late 19th century would be interesting comparisons to their contemporaries. Again, it would be very shortsighted to try to understand the current geopoltical situation without its broader historic context. Unfortunately, that is not a format that is very conducive to internet (or other) fora of non-specialists. I do think it is important not to discuss a caricature of one's belief and take it as reality.

IIRC the Tamron SP90 is a macro, isn't it? They are typically quite sharp and rather, well not nice in the wrong/right light. Best to take a pic across the street and crop to taste ;p I would agree to that. But personally I would consider that more as a lie from the photographer's side, as he/she actively creates the image (both during shoot as well as post) rather than a lie of the camera (it does faithfully what its optics determines). One could say that all photography is a lie and it is about taking a moment out of context. In the end it is semantics and what one would like to define as the reference of the truth.

It depends on how you define lying, I think. Of course there will be various levels of distortions and it will not represent the real thing, but that is true for all types of sensing, including our eyes. And if you think of it that way, then all detection methods have some levels of lying built in, and the photographer only selects the type of lie. What the photograph can do is create an image (potentially with further software manipulation to remove lens distortions, color balance and similar effects) that mimics the image that is most similar to the image you would see with your eyes. But is that closer to the truth or just closer to the lie your eyes tell you? Edit: Severely cross posted.

I see what you mean. Just have not heard it referred to as dodging and burning. For the rest I will just say that I disagree that device is capable of lying, it will just produce data based on a given input and leave it at that (and even then you typically have to at least activate the device).

What is sad is that the same energy could have been spent to learn something. Instead it is used to deny knowledge.