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What are the migratory patterns of Orcas in the Pacific Northwest? Do they pass by Vancouver in the Fall?
What are the migratory patterns of Orcas in the Pacific Northwest? Do the pass by Vancouver in the Fall?
I know you can never predict the sightings of a wild creature, but I was wondering what the migratory patterns of orca pods are in October in the Pacific Northwest, and what the possibilities are that they may be passing through Vancouver?
How large is the population of the migratory orca pods passing in the fall (if one can even know that)?
Thanks!

I think this question would be better on-topic on Travel.SE.

You can see orcas around Vancouver (and Vancouver island) between from March to October. So yes, you should still have good luck of seeing an orca in October. While you can sometimes see orcas directly from the city, this is quite rare. The easiest to go on one of the many whale watching trip. Many of them are based on the island (from Victoria for example).

There are three ecotypes of orcas which are all members of the same species but tend to display different behaviours, communicate differently and have different prey preference. The most common ecotype near Vancouver are the Resident Orcas, specifically the Southern Resident Orca population. This population is comprised of the J-pod, K-pod and L-pod. These populations feed mainly on salmon which as scarce in the Salish Sea during the winter. Therefore, resident orcas tend to disperse in search of food during winter months in the as far north as Alaska and as far south as Califorina.
As salmon travel to the ocean from inland rivers for food during the summer, the Southern Resident Orcas return to the Salish Sea to feed. By October, many salmon return to their natal stream to spawn and therefore, the abundance of prey for the Southern Resident Orcas depletes. During this time, orcas will begin to disperse North and Southward in search of more abundant prey but some will linger to feed on the salmon late for spawning.
If you're interested in more information about this population, check out Orcas of the Salish Sea

As hamilthj said, Resident orca movements depend on the availability of their preferred prey: Chinook salmon. Southern Residents spend more time in the Salish Sea and Juan de Fuca strait in the summer, with occasional (but rare) sightings near Tsawwassen and Vancouver, but their movements are a lot less predictable in the winter. I second hamilthj's note that Southern Residents have been sighted as far notrh as Alaska and as far south as California. Swiftsure Bank was recently included as part of Southern Resident's Critical Habitat, as passive acoustic monitoring revealed they visited the location year-round (although less frequently during the winter). There are still large knowledge gaps regarding the complete movement patterns of Resident killer whales during the winter.
Transient orca movements depend on a different type of prey: marine mammals (especially seals and porpoises). They seldom stay around any given location for long because once they've made a kill, the rest of animals they prey upon have been alerted to their presence and have fled. They rely on stealth to hunt.
If you would like to get live updates of orca sightings in the Salish Sea, you may subscribe to Orca Network (top right corner: mailing lists > Sign up for sightings reports). You can also follow Orca Behavior Institute, who frequently post sightings on social media. Finally, The Whale Tail lists several locations where killer whales might be seen from land (although quite unpredictably).


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How did researchers find out that it was only the maternal chromosome that underwent deletion in Angelman syndrome?
It is known that in Angelman syndrome, the chromosome 15 undergoes deletion in the maternal chromosome while in Prader-Willi it's in the paternal.
I understand it can be detected by FISH or other chromosomal staining methods (which would have been used those times), the chromosome number which underwent the deletion.
How could they figure out which chromosome (maternal or paternal)  had undergone the change. My question is, which technique allows the chromosome to be marked maternal or paternal? Which technique was originally used?

Don't have time to make a proper answer so just leaving a comment. As far as I know there is no way to specifically stain either the maternal or paternal chromosome. It was basically genome analysis of Angelman and Prader-Willi patients to find a correlation with both diseases and a deletion on chr15 (same in both). Genome analysis of parents showed that the inherited deletions showed that Prader-Willi patients always got the deletion from their fathers, and Anelman patients from their mothers. Source: https://www.ncbi.nlm.nih.gov/pubmed/2564739

This was further corroborated by the fact that the key player, the gene Ube3a, was an imprinted gene that had parent-of-origin specific (namely maternal) expression. Source: https://www.ncbi.nlm.nih.gov/pubmed/8988171 . It would be expected that a gene expressed this way would only cause disease disease when a deletion was inherited from the parent whose chromosome the gene will be expressed from. A parental deletion would be irrelevant to Angelman syndrome because Ube3a is silenced on the paternal chromosome in the relevant tissues regardless.

The kicker would be a mouse model where maternal Ube3a deletions always cause the phenotype in progeny, and paternal Ube3a deletions never do. This probably exists but I'm too lazy to look. Such breeding experiments would confirm causality as all variables except the maternal deletion would be controlled for, although I'm convinced enough by the genomic correlations with specific parents.

If that's enough of an answer please let me know.

Thanks! Just the first comment was enough for my answer. I wqs assuming this to've been pretty old sruff when genome analysis and all hadn't yet arrived. Thanks.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Why was it initially thought that Mendel's findings were contradictory to Darwin's natural selection?
When I read about the modern evolutionary synthesis, the text said that it showed both ideas to be compatible, once thought to be contradictory. Would it be because Mendel described an element of "randomness" in character transmission, as opposed to the mechanism of natural selection originally described by Darwin, or is it something else? I do not yet have a big knowledge on evolution, so pardon any mistakes.

Welcome to Biology.SE. Can you please link to the article you are referring and indicate where it says that " both ideas to be compatible, once thought to be contradictory"?

Thank you. Sorry, I guess article was a poor choice of words, I've changed it now. It was a college text I've read in portuguese, in case you understand: http://aprender.ead.unb.br/pluginfile.php/23405/mod_resource/content/2/A_Sintese_Moderna_Ridley.pdf

It's thought that Mendel's communications were anti-Darwinist, and some argue that his original paper was written specifically as a refutation of Darwin's descent with modification. Mendel believed species were created by God and not Darwinian evolution. Because of this, when he found a law defining constant probabilities of heredity, he saw it as more of an argument for the consitency of genetic information and thus species. To him this was in contrast to the ability of heritable traits to vary slightly in progeny, leading to selective advantages. Source I paraphrased: http://jhered.oxfordjournals.org/content/87/3/205.full.pdf

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Is there a biological basis for race (re: Nicholas Wade's article)
I just recently read this article by Nicholas Wade on Time Magazine's website about a biological basis for race.  It all sounded very racist, but of course my Western liberal attitudes about racism shouldn't cloud my stronger Western liberal convictions about Science giving every empirical claim a fair hearing.
So, that said, where can I learn more about the evidence supporting and contradicting this view?  I found on his Wikipedia page that a number of scientists have condemned his work, but I'd like to actually know the evidence and arguments underneath all this.
I suppose I should also ask more generally about the state of biological evidence for the reality of race.  I had heard in college that there is no biological basis for race, but I'm wondering if that is an out-dated view in light of recent work in genomics.  I read this stack exchange question but it had more to do with whether there is a consensus rather than on the arguments surrounding the issue.

The linked article doesn't appear to provide any empirical evidence about a biological basis for race. The biology is limited to two paragraphs at the start which are presented as FACT with no citations. The only (obliquely) cited arguments are Darwin, some (economic) historians, and a reference to book in the sociology field from 1975. He can't make scientific arguments without directly linking to the science. These are red flags for me but it's hard to rebut the biological evidence when he hasn't presented any.

Don't you think saying "Western liberal" instead of simply "liberal" is regionalist if not mildly racist?

@WYSIWYG My understanding is that liberal has different meanings in different places.  No attempt at racial division was intended.

Not sure why this was downvoted - it's an honest question about an admittedly touchy subject, but the OP asks it in an open manner and wants a clear, unbiased, scientific answer - exactly what we're here for.

Related: Like other animals, why humans don't have species & breeds?

Possible duplicate of Do humans have enough biological differences to be grouped into races or subspecies? and Like other animals, why humans don't have species & breeds?

I think it's best if you check out Wikipedia article on Race. Race is not a taxonomic term. In a nutshell, you can't define it in a useful way that has anything to do with the usual associations of the word, or gives it a practical value in science.
The problem with arguing about the existence of races in humans is that this is an argument about a word without an agreed definition, so there's never a true or false. This author is merely making some controversial extrapolations from quite obvious biology: Of course human genomes change over time, and it is also possible to an (impressive) extent to trace genetic lineages geographically. Of course there are subgroups that share a small set of characteristics not found in the rest of the human population. Some of these subgroupings are for example medically relevant.
Essentially, "race" ends up a loosely defined term that has something to do with subgrouping a species based on whatever criteria chosen. The reason why it's not a useful word to argue about in humans is because whatever subgrouping you might make, and for whatever purpose you are subgrouping, there are better, more meaningful (and quite importantly, less controversial) terms to describe those subgroups.

You will probably be interested in the American Association of Physical Anthropolologists' statement on Biological Aspects of Race. It's rather long and detailed, so I won't attempt to reproduce it here, and it's rather well written, so my summation wouldn't really do it justice.
In science, when we classify something, we need to have inclusion and exclusion criteria. You either carry a certain gene variant that has a deletion mutation that increases your risk of cancer, or you don't. To be a zebra, you need four legs and stripes. If you have stripes, but six legs, you're not a zebra. If you have four legs, but spots, you're not a zebra. So how then do you classify a race? Taking the three major old (and racist) classifications, people were either thought to be mongoloid, caucasoid, or negroid. How do you tell if someone is negroid? Well, their skin is dark brown! Caucasoids have white/pink skin. But where's the cutoff? How would you classify someone of Arab descent, with skin darker than a northern European, but lighter than a sub-Saharan African? How would you classify the offspring of a northern European and a sub-Saharan African?
People are a blend of phenotypes. While you can always define a group of people that look one way, and another group of people that look a different way, you'll always be able to find people somewhere in the middle. We are all the same species; every single fertile male on Earth can reproduce with any fertile female, regardless of social class, national or geographical origin, ethnicity, culture, skin color, or any other factor. This is not true of robins and cardinals, or elephants and zebras, or dogs and cats. (Yes, some species can form hybrids with other species, but that's a different topic.)
Within our species one can define certain groups based on physical characteristics, such as those of Han Chinese descent, that are grossly similar to one another, but far from identical. This group may share some common gene alleles, but there will still be (sometimes significant) variations from one person to another. One of the problems identifying that group as a race is that there is no strict biological definition of the term, with explicit inclusion and exclusion criteria, and the reason for that is it is almost impossible to identify these strict criteria that more than a handful of people would meet, due to the variation I mentioned earlier.
Now, of course there are groups of people with similar ancestry that share certain common gene variations that protect them from or predispose them to any number of diseases or conditions. There are also confounding cultural, socioeconomic, and environmental factors that make absolute connections between these gene variations and the associated diseases tough, as well (African-Americans and heart disease, native Americans and alcoholism, etc.). However, calling these different groups "races" is not helpful, and most of the time not even accurate (again, getting back to the lack of a clear definition of race).
Race is a social construct, based on a long and dark history of misguided attempts at classifying people. The concept likely has some utility to sociologists (I'm not one, so I don't know) so that people can voluntarily choose to identify with a group, and likely other reasons as well. However, because of the vagueness surrounding its meaning, and the incredible genetic diversity and identity between people, the concept really has no biological basis. I can just as easily study why people with certain genetic markers are predisposed to heart disease, for example, as I can study why many African-Americans get the disease, and I actually have a clearer criteria for subjects to include in the different arms of my study because I have a solid genetic definition, not just one based on skin color, which is completely irrelevant to the subject at hand.

Thank you for the link, I'll try to read it in as much detail as I can.  So I've actually been arguing this point with someone who was trying to argue that race is real.  I've made a lot of these same points, granted with not quite as much education or detail as you have.  I've also mentioned that even if we pretend races are well-defined and sample Fins and a certain group in Africa, we find that in-group variation is many times larger than between-group variation--I believe this falls within the statistical theory of ANOVA, yes?

Also, even if races existed we still have no evidence that valuative properties are heritable, like intelligence or morality--again, here, there is a measurement problem just like with the problem of race.  IQ has been found a poor measure for a few reasons, and of course morality is even less possible to measure.  Just wanted to say these out loud to someone who might know more than me in case I'm making any mistake.

@Addem I don't know about the statistics, so I can't judge that claim one way or the other. It all depends on what you're measuring. Regarding your argument with your friend, race is real depending on what your definition of reality is (seriously). If you're talking about police (mis)behavior, then yes, race is definitely very real. If you're talking about biological classification, then it is not - there's just not enough differences between people, and there are no good ways of defining inclusion and exclusion criteria, as I've written.

I'm not quite sure what you mean by "valuative properties". There is definitely a genetic component to intelligence, but the nature vs. nurture debate is very relevant in that area - you can take offspring of two very intelligent people and have them raised by uneducated, economically disadvantaged people in an overcrowded, under-funded school district, and they won't turn out anywhere near as well as if they were raised in a wealthy home with attentive, highly-educated parents with access to the best educational and enrichment resources.


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What word/expression is used to describe a band's share in the stained portion of the electrophoretic lane?
I was translating the following sentence from Russian, and realized I was not sure how to put it right:

The study shows that the electropherograms of the studied samples of DRUG NAME obtained in reducing conditions contain two clearly delineated bands with a mean total coverage of 99%, while the minor bands have a coverage of 1%.

The intended meaning is: of the whole stained area of the lane, the two principal bands cover 99%, while the minor bands only contribute an insignificant amount: 1%.
The original Russian word is содержание (content), but this is ambiguous, because we are really describing the contribution of the bands.
I'm not sure what word/expression to use. Is this "coverage" traditionally measured as the area, or as the length, of the band relative to the total area/length of the lane? How is it usually described?

You can compare band thickness but if a band is occupying more than 5% of the lane (of a usual SDS-PAGE gel) then it is not really a good band and you need to reduce the protein amount in the sample. Moreover, these kind of band quantifications (of specific proteins) are usually done after western blot.

@WYSIWYG  - the bands really occupy only a minor part of the actual lane, it's that the two principal bands contain 99% of the staining, I mean, of the dyed part of the lane.

@WYSIWYG - the word might be density, according to this document. They measure density of the bands, then look how much this or that band controbuted to this total density.

You might also try posting to Math SE. A representation of data is essentially a mathematical object, and mathematicians tend to be very precise with their words. If you just want non-expert suggestions, I might say "accounting for 99% of the stained area".


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How does bath application of KCl depolarize a neuron?
Increasing extracellular KCl is often a way to depolarize neurons in experiments.
My understanding is that increasing K+ extracellular concentration changes K+ reversal potential to more positive values and hence depolarises the neuron as the open leaky potassium channels will lead to influx of K+ into the neuron. Is this correct?
However, this explanation does not take into account Cl- ions.
How can this be explained in terms of Goldman equation?
Also, how does intracellular injection of KCl affect neuron membrane potential as compared to extracellular KCl application? In patch clamp experiments, often the pipette is loaded with KCl and injected into neurons that leads to depolarization. How can this be explained?

Cl does not play an important role in membrane depolarization and AP. Chloride channels are not very common in neurons (unlike K⁺, Na⁺ and Ca²⁺ channels) and therefore play a minor role. However there are reports of chloride channels that can regulate excitability of neurons

Yes. But how can you explain this in terms of changes in electrochemical driving force and derive from Nernst/Goldman equations?

Well. It essentially means membrane has a low permeability for chloride and therefore it (Cl0 does not diffuse much. Therefore its contribution in membrane potential (described by GHK equations) would be less.

Membrane potential (measured electrophysiologically, or calculated using the Goldman equation) depends on two things: concentrations and permeabilities. In the Goldman equation you see this directly: concentrations multiplied by permeability, in both the numerator and denominator.
If the membrane is not permeable to an ion (PIon=0), that ion will not affect the reversal potential. In a typical resting neuron, in the absence of any synaptic activity, Chloride conductance is near zero compared to ions like potassium.
I'm not as clear what you are asking about patch clamp experiments, I will try to just describe the process and hopefully that helps.
In a whole-cell patch clamp, the inside of the cell is continuous with the patch pipette solution, which usually contains high concentrations of potassium, like the normal intracellular environment. This is done on purpose, to try to record from cells in the most natural condition that can be replicated simply.
During the process of making a whole-cell recording, however, the experimenter has to first place a patch pipette down near the cell. While doing this, some solution is leaking out of the pipette and increasing extracellular potassium concentrations, which can depolarize surrounding cells. So, patch quickly my friends, you are making it uncomfortable for everybody before you make a good seal.
(the process would be similar for inside-in patches; for on-cell or inside-out patches, one would use different ionic concentrations in the pipette to mimic the extracellular space, or these would vary depending on the exact experiment performed)
edit: Just wanted to note that a statement in your question is mostly wrong; "the pipette is loaded with KCl and injected into neurons that leads to depolarization" - KCl inside a cell would not depolarize that cell, unless the concentration of K+ was lower than the typical K+ concentration of the cell, in which case you would probably have other issues and a dead cell from osmolarity problems.


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Is there such substances that body can only send to storage (as fat)?
I watched video with statement that there are such part of substance in potato chips which body can't use ("empty calories"), that they surely will be stored as fat.
It was here on 12:23:
https://www.youtube.com/watch?v=-jCd6vIF8Co
Is she talking nonsense ?

You might want to read this. If this helps you, I might post this as an answer.

An empty calorie is still a calorie.
"Empty calories" was coined to describe foods that only provide calories without significant amounts of other nutrients. The idea is that if you're eating a lot of empty calorie foods, you're eating less food with proper nutrition. The implication is that you will not be getting the vitamins, amino acids and other essential nutrients required to sustain you in a healthy manner.
If you can store it as fat, your body can use it. Where does the fat go when people lose weight? Those calories get "burned" when there aren't enough calories in your current diet to provide energy for your metabolic needs.


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(Non-expert-question) What exactly do chloroplasts do when they "convert light into chemical energy"?
Disclaimer: This question is kind of sprayed over biology, chemistry and physics.
Anyway, I had to learn more about photosynthesis recently, and although it is quite complex, I think I got it - except for one thing: Everywhere it is basically just said, that chloroplasts convert light energy into chemical energy. But seemingly no one is interested in how they do it. I couldn't find an explanation after some googling. Not even Wikipedia had something for me (at least nothing I was able to sort out of the technical jargon).
So my question now is: What exactly happens in this process? It'd be good if the answer wouldn't include to much jargon, because I'm not really experienced in the field. (Just the usual knowledge and a little more due to being interested in science in general).

The overall process is photosynthesis, the chloroplast is the structure that accomplishes this in most photosynthesizing organisms. You'll find a description in any Biology text. Here's a reference with diagrams to illustrate the role of the chloroplast: https://www2.estrellamountain.edu/faculty/farabee/BIOBK/BioBookPS.html

@bpedit Thanks, that is already a little more information. It states In the Light Dependent Processes (Light Reactions) light strikes chlorophyll a in such a way as to excite electrons to a higher energy state. In a series of reactions... But it doesn't mention what these reactions are. The electrons gain more energy, but that's only part of the answer.

Your question is broad. Please narrow it down to a specific issue.

@WYSIWYG You did notice that there is already an accepted answer which provides exactly the information I asked for, right? And I don't think that the question is too broad. "What exactly happens when the light is turned into chemical energy" is quite specific I think. What would you have needed to understand it better?

@Namnodorel just because there is an accepted answer it does not mean that the question itself is very good. Perhaps you got your answer but to a general reader the question and the answer should be coherent, understandable and useful. "What exactly happens when the light is turned into chemical energy": you can find an entire book chapter on this topic. You can go into great level of detail; people are still doing extensive research on mechanisms of photosynthesis. You should therefore clarify what exactly you are looking for. The question should be clear and explicit.

Moreover, the currently accepted answer is very basic (I am not saying it is bad). If you were actually seeking such an answer then you are expected to do some research yourself. This kind of basic information (in fact more details) can be found in Wikipedia or similar resources. Whenever you say "I searched so and so" you should clarify what you found there and why was it not satisfactory (or not understandable) so that people can focus their answers on the points that you actually need to understand.

@WYSIWYG Well, what I found was just "Chloroplasts turn light into chemical energy" which I mentioned in the question. I had no idea what happened to do that, so I couldn't ask for the exact reactions or what happens to the electrons, because I couldn't be sure if it would be important/fill my knowledge-gap. Maybe that would be irrelevant, and I'd get an unsatisfying answer? What I meant with the accepted answer is that it is exactly what I looked for, so how could I have made it more specific so you know that I mean exactly that?

Too too vast lots of things chloroplasts do.  Light capture is just one task which is done with help of Antenna-systems, LHC (light harvesting complex)s and reaction centres. But beside all main step of photosynthesis (all steps of light reaction and light-independent reaction), chloroplasts have role in various metabolic works like synthesis of some lipids, amino-acids, secondary metabolites etc, and take part in synthesis and storage of plant hormones (growth regulators). The've role sensing specific light-stimuli. Besides, they (and all plastids) have some own genetic machinery.

@AlwaysConfused Okay, I can see that. Better now?

I see you've given this a try, so here's a synopsis hopefully appropriate to both your current knowledge level and curiosity.
Light excites electrons in chlorophyll to a higher energy. Higher energy means less stable, those electrons want to return to a state of lower energy. The chloroplast is structured in such a way that the electrons, instead of just plopping back to the lower energy state in the chlorophyll to liberate the light they just absorbed, are handed off to another molecule. As the electrons get passed off to other molecules, they lose energy. All of this is taking place on a membrane within the chloroplast. The energy being "lost" by the electrons is harnesed to pump hydrogen ions across that "thylakoid" membrane in the cholorplast. The increased concentration of H+ within the thylakoid space is another form of energy that can do work. The work done is the creation of ATP.
We're not done with those electrons yet. They get passed off to yet more molecules, losing energy again in each hand-off. This energy is used to create additional energy-rich substances that will power the creation of energy-rich organic molecules in a process termed the Calvin Cycle. The Calvin Cycle, which creates the sugar G3P from inorganic CO2 from the atmosphere, also takes place within the chloroplast.
So, the chloroplast is a multi-talented factory for the conversion of CO2 into sugars. These sugars provide both energy and carbon, in a useable organic form, for other processes in the plant. Chloroplasts also contain DNA. This, and other evidence, suggests that chloroplasts, like mitochcondria, were once free living organisms that got co-opted by other organisms and now exist within cells in a mutualistic association (the Endosymbiont Theory).

Thanks a lot, finally a good explanation ^^ I'll probably need to think multiple times over this to fully understand it, but it is something to work with :)


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Spermatogenesis in humans - timing of phases and chromatin modifications
I'm interested in the timing of events during human spermatogenesis, ideally with some references I can build off of. Specifically, I am trying to pin down the number of days for:

Spermatogenesis, beginning to end (I have come across 65, 75, and 100).
Leptotene stage
Zygotene stage
Pachytene stage
Spermatozoa maturation and histone-protamine transition
Time in epididymis (I have come across 12 days)

Again, I want to know the timing of these events in humans, not mice or rats. Specifically, I am trying to pin down the major epigenetic reprogramming stages, with a focus on those occurring in mature males.

Spermatogenesis (Beginning to end):
64 +- 8 days (range 42 to 76)

There is considerable individual variation. This includes time in epididymis.
Amann 2008 argue for 74 days based on early study by Clermont 1972.
Also argue that biopsies are still needed on top of radiolabelling.
Substages:
Calculated from Amann 2008, Figure 1 using percent time in 16 day cycles.
Leptotene:
26.5 days (~70 days total - 26.5 days = ~ 43.5 days pre-ejaculation/conception)

Zygotene:
31.2 days (~70 days total - 31.2 days = ~ 38.8 days pre-ejaculation/conception)

Pachytene:
32 days (~70 days total - 32.0 days = ~ 38 days pre-ejaculation/conception)

Histone-Protamine transfer:
68.8 days (~70 days total - 68.8 = ~2 days pre-ejaculation).

The resolution of the data doesn’t really let us get at Epididymis vs. histone-protamine transfer, though.
Time in the Epidymis:
10-14 days.

References:

Misell LM, Holochwost D, Boban D, Santi N, Shefi S, Hellerstein MK,
  Turek PJ. 2006. A Stable Isotope-Mass Spectrometric Method for
  Measuring Human Spermatogenesis Kinetics In Vivo. The Journal of
  Urology 175:242–246.
Amann RP. 2008. The Cycle of the Seminiferous Epithelium in Humans: A
  Need to Revisit? Journal of Andrology 29:469–487.
Durairajanayagam D, Rengan AK, Sharma RK, Agarwal A. 2015. Sperm
  Biology from Production to Ejaculation. In: Schattman GL, Esteves SC,
  Agarwal A, editors. Unexplained Infertility. New York, NY: Springer
  New York. p. 29–42. Available from:
  http://link.springer.com/10.1007/978-1-4939-2140-9_5

Great effort, thanks for coming back to your question!


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What is this spider

What is this spider? Is it poisonous?

What is the location and climate? What is the approximative size?

The eyes (and other structure of the head) are key for spider identification. Can you take a picture of the dorsal side of the spider?

This is unambiguously a female Araneus, and judging from coloration pattern of the legs and ventrum — very likely the common cross spider Araneus diadematus: see ventral view photos, or some other very similar species. A better photo of the specimen from the dorsal side and some information on the location would be very helpful.
And no, these spiders are not poisonous.

Photo: Michael Gäbler, via Wikimedia Commons


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Time required to evolve advanced chromatophores in octopuses and squid?
Do we have any idea how long it took primitive Coleoida to evolve from non-color changing organisms to color changing organisms?  Granted, not all coleoidans can change color (vampire squids are good example), many of them do.
(Coleoida is the subclass below Cephalopoda that includes all squid, cuttlefish and octopuses.  Nautilus' are excluded.)

Here is a print screen from oneZoom.org.

Coleoida include decapods and octopods, both of which have chromatphores, so their MRCA (which lived 330 millions years ago) probably did as well. Coleoida is a sister group to the nautiloids. They branched +400 millions years ago. Together they form the group of cephalopods. As nautiloids do not have chromatophores, the evolution of chromatophores probably occurred in between these two nodes (between MRCA of cephalopods and MRCA of coleoida). In other words, it occurred at some point during a period of about +70 millions years.


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Is it possible to both extract DNA sequences from plasmids and fuse them using primers for Gibson assembly?
Maybe I'm overcomplicating this, but I'm having some issues with a construct.
So, I have three plasmids containing a total of eight DNA sequences that I need to fuse into one linear sequence. I plan to fuse the sequences using Gibson assembly. However, before I can fuse them, I need to amplify (PCR) them out of their plasmids.
I would like to use as few primers as possible, so my question is this; can I use the Gibson assembly primers to amplify them out of the plasmids and add the overlap sequences separately, then fuse them all together in a separate reaction without primers? Would the overlap sequences already added to each sequence separately be enough to act as primers for assembly? Even better (but I doubt it would work), could I amplify them out of their plasmids and fuse them in the same reaction?
If both these scenarios are unrealistic, I can still just order another round of primers to extract the sequences from their plasmids, but I would like to just use the primers I have if I can.

It's a little unclear what you mean by 'add the overlap sequences seperately' Normal gibson primers look like this:
5'Overlap sequence- Binding region-3'
You can use these to PCR our the fragments without any issue. I've added 5' extensions of 60bp without problems. Gibson assembly normally occurs without any primers as you purify the PCR fragments first. Your reaction will be very inefficient with 8 fragments, gibson really peters off at 6 put you can be lucky sometimes...

@mimat - I am mostly wondering if the plasmids will get in the way of my assembly at all. After a little discussion with some colleagues, I have determined that it will probably be fine as long as I add the overlap sequences first with their amplification primers, then fuse them in a different PCR reaction (in Gibson assembly, I have always just added my sequences and the overlap primers to the same PCR reaction). I forgot to mention in my original question that I will actually be splitting the fusion of all eight sequences into two or four different reactions. Thank you for clarifying.


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Drugs to make rats easier to trap
What drugs will make rats less cautious/sensible and/or more hungry so they'll go to my snap traps more?
What dosage and how do I deliver it to the rats?
Background info:
The rats trapped in my crawl space I imagine have limited food, if any.
The snap traps are well coated with peanut butter scent but the process is very slow -- one by one.
They have rat mites (blood-sucking parasitic barely-visible mites) and I want them out ASAP.
It's been several months because:

They reproduced down there.
One of the vents got broke open again so a second batch got in. I don't know how many. 25 rats have been trapped so far (2 today and I hear more).

I've checked the house so well. Sealed up with caulk and expanding foam every hole. Checked the roof. Sealed wire mesh on all the plumbing stacks and exhaust vents on the sides of the house.
There's really nothing else. I'm positive it was the broken foundation vent that let the new ones in. But now that everything is sealed securely and won't be broken open again, I think it's only a matter of removing the existing rats.
I don't want to poison them because then they'd die inaccessibly and their mites would swarm the house. They have to die in the traps that I check several times a day, so they can be removed before the mites spread.

If the rats become less cautious then I would suspect that it's more likely they will come in to your home and cause further problems. If you are laying traps I guess that is something you are trying to stop. You'd be better off seeking professional pest control advice

Coming from an island rat-eradication standpoint, I would second @Michael_A's point: if you're giving rats a drug with the intention of killing them, make the drug lethal.
If you want to kill using snap-traps for ethical reasons (deaths from anticoagulants are not, generally, pleasant), I would suggest habituating the rats to the traps by putting bait on an unarmed trap for several nights until the rats learn to ignore their trap-shyness, then repeating with an armed trap.

@bshane, yep, I think anticoagulants are cruel and wouldn't use them. I've updated the answer to reflect that. The producers of the rat trap that I linked in my answer have produced good literature for using traps and their traps appear to be highly targeted and effective.

@user193661, Something like the traps in my answer may work well, they use a formulated attractant and their literature may be worth a look. The suggestion from rg255 seems like a good one, a professional may be the fastest option.

I keep somewhat up-to-date with pest control measures. I haven't heard of chemicals being used to alter rat behaviour but using parasites that alter rat and mouse behaviour (Toxoplasma spp.) has been studied. The infection increases predation rates and also appears to increase the rate at which they are trapped. Toxoplasmosis also affects humans with cats being the main source of infection. I am uncomfortable about approaches that increase the prevalence of toxoplasmosis.
If you're going to the trouble of administering a drug to a pest why not make the drug lethal? The extra step seems unnecessary but I personally would opt for traps given that many poisons (particularly warfarin) seem cruel.
For traps good bait (uncooked bacon, lard, peanut butter, dog biscuits) makes rats;

less cautious/sensible and/or more hungry.

The right trap can make a big difference. This one can self-reload > 20 times and is instantaneous. The linked website contains advice for setting traps.


text:
Why is Hydra classified under Hydrozoa when it has neither a planula larva, nor a medusoid form?
If the general basis of classification of cnidarians is with respect to the body form - medusoid or polypoid, or in the incidence of metagenesis (as is common in hydrozoa), both, then, on what basis is Hydra placed in class Hydrozoa?

I'd say modern taxonomy doesn't (or at least tries not to?) classify things based on how they appear, but based on how related they are.

Probably relevant: Nawrocki et al. 2013. Phylogenetic placement of Hydra and relationships within Aplanulata (Cnidaria: Hydrozoa)


text:
Please identify this bug/insect
Ten of these bugs were found behind my bed. I live in Northern California.
The bug is 5mm in length.

It seems to me a kind of larva.

I think you are correct. After doing a web search, I believe it is carpet beetle larva. Here is a link: http://www.bugzapperpestcontrol.com/blog/wp-content/uploads/2016/05/Varied-Carpet-Beetle-Larva.jpg

Sure looks like the picture. If your room is carpeted and the carpet is edible, e.g. wool versus a total synthetic, that might offer some conformation.

Thank you all for your help.  I will mark it as a duplicate as per rg255's suggestion. My room is fortunately not carpeted, but I had some old rope behind my bed, and I think they were eating that.

Carpet beetle larvae  feed on basically any organic matter... Also, yes, this is definitely a carrpet beetle larvae


text:
Washing bacteria out with water
When I wash my running shoes by my hands,
I leave them near the window to dry them quickly.
Although they got sunlight in daytime and well dried after I came back from work, I could feel bad smell from them.
The smell was worse than when it was not washed for long time.
So I guess that the water increases the number of bad bacteria on shoes.
My conclusion is that water should be used to wash dirty things out only for a short time and
it should be dried as soon as possible.
Although our body is alive and can resist against bad bacteria on our skin which get nutrition from water, it seems that water should be used for a short time.
Am I right? Please advise on my thinking.
Thanks.

I think that "bad bacteria" isn't the right term to use here. Maybe mold is more accurate? What do you mean by "use water for a short time"? Do you mean dry out quickly?

It means washing with water for a short time, and we should dry out quickly as well, if water is helpful for 'the bad bacteria'. I had thought water was always helpful for removing smells in the past.


text:
Enzyme with long tube leading to active site?
Are there any enzymes that force one or more of their substrates to travel a relatively long distance through a small opening/tube through the enzyme and  to the active site? (not a transport protein)

First of all, as you mentioned, there are a lot of membrane / transport proteins with very nice, well defined tunnels. But you're looking for a soluble / cytosolic enzyme.
Some oxygen-dependent enzymes have quite long tunnels that oxygen is using. For example this one: http://www.jbc.org/content/283/36/24738.short or this one: http://europepmc.org/articles/PMC2698890
Then there are some enzyme with just deep active sites, I think the p450 BM3 is quite known for that, but any enzyme with a reasonable specificity (and especially those that have very reactive cofactors) will have a "tunnel".
You can also find long "tunnels" in enzymes that accept long substrates. I like this example of squalene synthase: http://science.sciencemag.org/content/277/5333/1811.full. The substrate first has to go deep into the enzyme to find the proton it needs to start a quite interesting reaction.
If you want to find new tunnels in your enzyme there are also tools available, such as CAVER: http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1002708 If you look at the papers citing this tool you might also find some cavities.

According to information on the CAVER website:
The access tunnel is sometimes described as a "keyhole" in which analogy the lock is the enzyme and the substrate is the key that goes through the keyhole to the active site. The tunnels are commonly found in all six enzyme groups: Oxidoreductases,Transferases, Hydrolases, Lyases, Isomerases, and Ligases. Source: https://youtu.be/M6bW8lcM9jk

http://europepmc.org/articles/PMC2698890/figure/F2/

Other tunnel finding softwares include: (Mole, MolAxis, Hollow, etc.). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341237/


text:
Black spider identification
Location is in Canada / Ottawa
I did a web search, but I can't figure out what species it is.

If it is still there could you take pictures showing its eyes?

plz mention some measurement; approximate at least

This is very likely an araneid (or Orb-weaver spider) in the family Araneidae.
Without further evidence/details, it's hard to narrow down to a species.
One possibility is Larinioides sclopetarius (the bridge spider or gray cross spider).

 Source: Ed Nieuwenhuys

 Source: Eurospiders.com

Description:

Prosoma grey to grey-brown. Opisthosoma grey to grey-brown, dorsally with pronounced, white margined pattern. [Source: University of Bern]

See University of Bern for detailed drawings of anatomical structures.

Size: females = 10-14 mm ; males = 8-9 mm.
Web: orb webs can have diameters of up to 70 cm.
Ecology: often lives on briges or near water; often found on steel structures.
Range: holoarctic including Ottawa, Canada

What it's NOT
Although visually similar, this is not
Nuctenea umbratica (walnut orb-weaver)

 Source

This species is confined to Europe, Asia and Africa.

The specimen is also unlikely Larinioides ixobolus, which generally has a black outline (vs white) on their backs And is constrained to Europe/Asia:

 Source

you posted a similar answer in a different question

Possibly incorrect, but it looks like some kind of orb weaver - from the shape of the abdomen and the posture, it's very similar to a lot of orb weavers and potentially is in the Araneus genus.
I don't think it's this species, but you can perhaps see the similarities;
http://www.spiders.us/species/araneus-diadematus/#more_pictures
It could also be an immature, hard to know :/


text:
How can I tell if a certain marker is useful to date a phylogeny?
If I have a phylogenetic tree for a genus, how can I tell if a certain protein would be a good phylogenetic marker to use if one wanted to use a molecular clock to date the age of some speciation event in that a genus? How can I look for it on a tree?

Speed of Sequence Divergence
You need to use a sequence which diverged only little among most closely related lineages in your tree and diverge quite a lot among most distantly related lineages. In other words, you need a sequence that diverge at a rate that is convenient for your needs.
If you investigate a young tree (a tree which MRCA of all lineages lived recently) you need a sequence that diverge quickly through time. If you investigate an "old tree" (a tree which MRCA of all lineages lived a long time ago) you need a sequence that diverge slowly through time.
Selection
Selection is affecting how fast two sequences diverge. But because selection is specific to the environment experienced by the individuals in each lineages, it can be more difficult to use sequences under selection as a molecular clock (exception of highly conserved selection which are under purifying selection used for very large trees). So we use neutral sequences.
Rate at which mutations fix
Let $u$ be the mutation rate for the sequence of interest and $N$ be the population size. The number of new mutations per year is equal to $2Nu$ (assuming a diploid population). Now, knowing that the sequence is not under selection, the probability of reaching a single mutation to fix (=to reach a frequency of 1 in the population) is $\frac{1}{2N}$ (see this post for a very introduction to why the probability of fixation is inversely proportional to $N$). As a consequence, the rate at which mutations fix is $2 N u \frac{1}{2N}=u$. In other words, the rate of mutation fixation is the mutation rate (for neutral sequences).
Rate at which mutations fix and sequences divergence
The term, sequence divergence is not clearly define. Typically, one would mean "average number of pairwise differences". Assuming that each new mutation that fixes occurred at a new locus (infinite allele model), then the number of pairwise differences between two lineages is the addition of the number of mutations that fixed in each lineage, that is $2u$. Always under the infinite allele model, the probability of the average number of pairwise differences to equal k is given by a Poisson distribution.
Wrapping up

how can I tell if a certain protein would be a good phylogenetic marker

The sequence

has to be neutral (it makes things easier)
has to have a mutation rate of the right order of magnitude (it improves accuracy of the estimate and therefore improves statistical power)


text:
histones in the Hershey / Chase experiment
When DNA is injected into the cell why aren't histones(protein) also injected and why wouldn't the radioactive sulfur therefore also be present in the infected cell

Bacteria do not have histones - the DNA is just naked in the cytoplasm. Therefore no protein was transferred.

@MattDMo The DNA injected onto the bacteria was T2 bacteriophage DNA.

It's true that eukaryotic chromosomes have histones associated with them. But the DNA in the Hershey-Chase experiment was viral, no histones.


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What is the significance of cysteine in a protein sequence?
What is the importance of cysteine-cysteine in amino acid sequence? What can I infer if I get a high percentage of C from a protein sequence?

What can I infer if I get a high percentage of C from a protein
  sequence?

A highly stable structure that is likely found in the extra-cellular space.

Cysteine can form a disulphide bond with another cysteine. Cysteine can be found as a lone cysteine, but is often paired with another cysteine in the tertiary structure to form these bonds.
Disulphide bonds play important roles in protein folding and stability (60 kcal/mol compared to around 1 and 5 kcal/mol for a hydrogen bond depeneding on the environment). Notably though, cysteine disulphide bonds are usually only used in extracellular secreted proteins, as they are unstable in the cytoplasm.
As an example, take the structure 2ksk. Look at how the structure is held together by cysteines that are distant in the sequence. If you see cysteines in a sequence, expect interesting folding!
The cartoon is going from blue to red, whilst cysteines are shown with sticks and the S-S bonds are in yellow.

Side note, they are annotated as SSBOND in the PDB.

Cysteine is one of the two sulfur containing amino acids, but far more important than the other (methionine) due to its reactive sulfydryl or thiol group (-S-H). The said sulfydryl group cannot be substituted or replaced by any other amino acid. Importance of these groups lie  on the fact that they involve in the formation of disulfide bonds, the most significant cross linkage in tertiary and quatenary structure of proteins. methionine being more hydrophobic than cysteine and sterically large, acts less reactively and does not participate in disulfide formation.
Cysteine can be easily oxidized (oxidative folding) to form cystine (two cysteine bound by disulfide linkage) via interchain and intra chain bonding. The bonding is covalent and adds stability to the overall protein structure as compared to H bonding (Energy disulfide bond - 60 kcal/mol, H bond - 1-5 kcal/mol depending on the environment). Therefore, energy required to break disulfide bonds are way too high than other covalent bonds. Therefore, higher the number of disulfide bonds a protein has, higher the stability of it.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Is the variance of a trait related to its rate of evolution?
Posed with a question that has me stuck:

Is increased variance of a phenotypic trait in a population associated with slower evolution of that trait?

I have to either 'disagree or agree' and argue my point. And I disagree. For this question, I think that if the variance of phenotypic trait has a genetic basis (additive genetic variance =/= 0) then increased additive genetic variance should speed up it's evolution. The greater the additive genetic variance, the greater the response to selection in the next generation. So increased additive genetic variance should increase the rate of evolution of that trait.
However, at the same time, if there is variation in a phenotypic trait but it does not have a genetic basis (narrow sense heritability is zero) and the basis for variation is due to an environmental, dominance, or interactive effect, then increased variation would have no effect in the rate of evolution. Or so I think. I'm not too sure how the rate of evolution would be affected in the case of a non-genetic basis of variation.

The question can be understood in different ways
Causality
I think the question is a bit unclear in using the term associated in terms of what is being causal. Is the interest to understand how do processes that affect speed of evolution also affect phenotypic variance or is the question `how does a change in phenotypic variance affect the speed of evolution.
What is meant by speed of evolution
Speed of evolution has no strict definition. Or rather it has two standard definitions and it can be measured in Haldanes or in Darwins (which are units).
Quite often by "speed of evolution" authors mean "response to selection over medium to long term" as for example in the wiki article for rate of evolution.
Below I am answering to two different questions.
How does processes that affect "speed of evolution" at neutral sequences also affect phenotypic variance
At neutral sequences, the rate at which mutations fixes is equal to the mutation rate (see this answer for explanation). And all else being equal (typically without changing the mutational effect), high mutation rate leads to high phenotypic variance.
How does a sudden change in the phenotypic variance affect the response to selection in regard to this trait?
I think you pretty much said it all. I will just rephrase what you just said with a few simple equations.
Breeder's equation and heritability
The response $R$ to selection $S$ is given by
$$R=S h_N^2$$
, where $h_N^2$ is the heritability in the narrow sense. This above equation is known as the breeder's equation and is a fundamental result from quantitative genetics. The heritability in the narrow sense is defined as
$$h_N^2 = \frac{V_A}{V_P}$$
, where $V_A$ is the additive genetic variance and $V_P$ is the phenotypic variance.
Partitioning phenotypic variance
So it feels like increasing $V_P$ would decrease $h_N^2$ and therefore the response to selection $R$, but that would be very naive as $V_P$ is not independent of $V_A$. It is quite standard to decompose the phenotypic variance into genetic ($V_G$) and environment variances ($V_E$) $\left(V_P = V_G + V_E\right)$. Of course in reality, we should take into account variance due to other factors such as epistasis or developmental noise for example and all of their covariances. The genetic variance can further be decomposed into additive genetic variance $V_A$ and dominance genetic variance $V_D$ $\left(V_G = V_A + V_D\right)$.
Interdependence between $V_P$ and $V_A$
$V_P$ is a function of $V_A$. So as currently stated, it is impossible to answer the question by a simple yes or no. The shortest correct answer would probably be "The response to selection will decrease if the increased variance is not (not mainly) related to increase in additive genetic variance".
To be perfectly accurate, let $\Delta_P$ be the increase phenotypic variance and $\Delta_A$ be the increased genetic additive variance such that $\Delta_P > \Delta_A$. All else being equal the increase in $V_P$ will cause faster response to selection if and only if $\frac{Va+\Delta_A}{V_P+\Delta_P} > \frac{Va}{V_P}$. Isolating the term of interest $\Delta_P$, we got
$$\Delta_P < \frac{\Delta_A V_P}{V_A} = \frac{\Delta_A}{h_N^2} $$
In other words, all else being equal, an increase of phenotypic variance of $\Delta_P$ above the original variance $V_P$ increases the response to selection if and only if this increase is lower than the increase in additive genetic variance $\Delta_A$ multiplied by the inverse of the original heritability (heritability before a change in phenotypic variance occured)."

I think the question is supposed to be
" How does a sudden change in the phenotypic variance affect the response to selection in regard to this trait? "

Perfect, this is on this part of the post that I spent most time! Do you feel like it answers your question?

Depends on how you phrase the question, ie, on how you write the breeder's equation.
The breeder's equation can be written in two ways:
$R=h^2 \cdot S$
or
$R=V_A \cdot \beta$
where $R$ is response to selection, $h^2$ is narrow sense heritability, $S$ is selection differential, $V_A$ is additive genetic variance, and $\beta$ is selection gradient.$^*$
Total phenotypic variance is pretty much a denominator which gets shunted between the right-hand quantities of the two versions, since $h^2=\frac{V_A}{V_P}$ and $\beta = \frac{S}{V_P}$. Rewriting the two versions, they become
$R=\frac{V_A}{V_P} \cdot S$
and
$R= V_A \cdot \frac{S}{V_P}$
So to answer your question: for a fixed selection gradient $\beta$, only the additive genetic variance $V_A$ matters. But for a fixed selection differential $S$, it is the ratio $\frac{V_A}{V_P}$ (narrow sense heritability) which matters.

$^*$The selection differential is the covariance between relative fitness and the trait value: $S=cov(w,z)$. The selection gradient is the regression coefficient between relative fitness and trait value: $\beta=\frac{cov(w,z)}{cov(z,z)}$. Note that the denominator $cov(z,z)$ is just the covariance of trait value with itself, ie, the variance of trait value: hence, $\beta = \frac{S}{V_P}$.
The selection differential is often described as the difference between the overall first generation's mean phenotype, and the selected parents' mean phenotype; this is true for viability selection, where parents either simply do or don't reproduce, with no other differences in fecundity.
For multivariate evolution of correlated traits, the selection gradient is actually the partial regression coefficient of relative fitness and trait value: partial because it isolates the 'direct effect' due to selection on the trait (as opposed to the residual 'indirect effect' due to selection on other, correlated traits). The multivariate breeder's equation is $\vec{R}=\mathbf{G}\cdot\vec{\beta}$, where: $\vec{R}$ is a vector of responses to selection (each element being the response of one trait); $\vec{\beta}$ is a vector of selection gradients on those traits; and $\mathbf{G}$ is the additive genetic variance-covariance matrix (each element being the additive genetic covariance of one trait with another; the elements on the diagonal give the additive genetic covariance of the traits with themselves, ie, their additive genetic variances).

Variance of a phenotype/genotype with respect to the rate of mutagenesis is an indicator of selection pressure. High variance would denote lower selection and vice versa. Note that this has to be normalized to the mutation rate; if you have high mutation rate then you would get high variance even in the presence of a moderate selection pressure.
With protein coding genes, the rate of selection is measured by comparing the number of non-synonymous mutation with the number of synonymous mutations (a gross indicator of general mutation rate). Se Ka/Ks ratio.
For more information you can have a look at this review by Gingerich (2009).


text:
Are there plants that produce (audible) sound?
Are there any plants that are at least able to produce some sort of sound? Actively, I mean - depleting energy reserves to produce an audible output, preferably with no experimental amplification. Ultra- or infrasound is also ok.
Edit: I guess a different way of asking this is, "Are there any plant parts whose function is to produce sound?"

I have heard anecdotally that you can hear the corn fields growing (at the peak time of growth). I am sure some of this is wind blowing but also the new growth rustling the drier outside leaves in thousands and thousands of plants.  Bamboo I have heard the same thing about.

There are several plants, which, as a way of seed spreading, "explode", which will make an audible sound. Plants that do this are for example: lupine.

These are good points, but the sound here is a byproduct - the plant "doesn't care" whether or not it is produced. I've edited to maybe make the question clearer.

Do you mean, 'intentionally' produce sound? Intentional would be only for communication, right?

@Polisetty well, not necessarily - perhaps as a warning, or attracting something, or to generate vibrations for some other reason. Communication would entail a) also a listening apparatus and, more importantly, b) some way of actually interpreting the sound - some sort of neural system.

@Zubo: I don't think a listening apparatus is necessary.  After all, plants communicate with pollinators & seed dispersers by using odors and visual cues.  I can't think of any fundamental reason they couldn't have evolved to use sound cues as well, though I don't know of an example.

It seems like Ritman and Milburn have done some work on acoustic emissions from plants. These two articles might be a starting point for you @Zubo : Acoustic Emissions from Plants: Ultrasonic and Audible Compared and Monitoring of Ultrasonic and Audible Emissions from Plants With or Without Vessels

arthropods can probably hear plants hydrating, through their leg vibration sense. Sound is air displacement born of fast mechanical movement/diaphragms. few plants have mechanical movement. Sound has little use in defense, even insects don't use it, arthropods mostly use it for advertising their presence and strength and energy. investing in an auditory structure isn't economically and ecologically documented for a plant.

not audible to us humans without some tweaking, but apparently plants do! https://www.cnet.com/news/listen-to-the-sound-of-plants-responding-to-the-world/

Plants make noise all the time as they transport water but that is believed to be an unintentional by-effect. As to the possibility of plants intentionally making noise,
my intuitive answer was no but I might well be wrong, there is actually increasing evidence that plants might produce vibrations for communication.
Two examples: Gagliano (2012) discovered that young maize roots subjected to a 220 Hz sound (check out the figure, not sure if I'm allowed to copy it here) grow towards the sound source and additionally emit periodic bursts of sound themselves for as of yet unclear reasons.  Gagliano, Renton, et al. (2012) demonstrated that chili plant seedlings grow faster in the presence of an adult fennel plant even though this adult plant was isolated in a such a way that it could not communicate via any known mechanism (chemical, light) with the seedlings, indicating influence through an unknown mechanism. The authors consider both magnetism and sound as possible unknown communication methods.
I don't think any of these sounds would be audible for humans though.
Acoustic emission analysis and experiments with physical model systems
reveal a peculiar nature of the xylem tension.
Laschimke, R., Burger, M., & Vallen, H. (2006).
Journal of plant physiology, 163(10), 996-1007.

Towards understanding plant bioacoustics
Gagliano, Monica et al.
Trends in Plant Science , Volume 17 , Issue 6 , 323 - 325

Out of Sight but Not out of Mind: Alternative Means of Communication in Plants.
Gagliano M, Renton M, Duvdevani N, Timmins M, Mancuso S (2012)
PLoS ONE 7(5): e37382. doi:10.1371/journal.pone.0037382

This is a more anecdotal answer, and it may not be what you are looking for, but I had a couple of water-hungry leafy plants in the past (Cannabis spec) that would look something like this -

Source: Sensi Seeds
...Note that mine were a lot bigger. After watering them and leaving them in the sun (enhances re-hydration by promoting water flow through evaporation of water through the leaves) you could literally see the leaves and stem erecting themselves again by the re-hydration process. If I remember correctly, some of those leaves would make audible sounds when they became dis-entangled from underlying leaves (popping sounds). They would look something like this after watering them.

source: AllBud
Note that these audible effects likely only happen in leafy, swift-growing (rapid metabolizing) plants like Cannabis.


text:
How do neuroblastoma cells divide? Is it via mitosis?
My name is Daniel and I'm 17 years old. I am currently designing a study to investigate compounds that potentially increase the replication of neural cells. I will be using neuroblastoma cells and creating different water based media to apply to these cells. I don't however understand how they divide. Is it via mitosis or do they replicate in a different way as they are essentially, cancer cells.

don't cancer cells divide by mitosis as well - it's just not as regulated as in a normally dividing cell

I thought it was mitosis but it was increased. I could calculate the mitotic index of control groups with no media applied to it and then calculate the mitotic index of the cells where the compunds have been added? How reliable would this be as evidence?

you're correct (as far as I know) - cancer cells divide similar to other cells... it's just much more rapid... what is your question that you're trying to ask with your experiment? A well-focused questions is of paramount importance prior to conducting a well-controlled study.

Pathologists do indeed calculate mitotic indices to determine how rapidly the cells are dividing compared to normal cells, but you need to establish what's normal first. That is your control group.

It isn't really an closed question that I'm trying to answer, it is investigating which substances can increase the rate of cell division. The substances have been decided by reading about speculation surrounding these substances as to whether they actually have the potential to do this. If you want to hear more about a method, I'd be happy to share my ideas. Hopefully if there are any flaws, you can help rectify them as I am only an A-level student at the minute.


text:
Identification of caterpillar in Texas
I found this caterpillar eating my parsley, around Austin, TX.
It looks very monarch-ish, but apparently monarchs don't eat parsley.  Plus it has knobs on its back.
But it also does not look like the Eastern Swallowtail since there is almost no hint of green in its color.
Hoping that this turns into some type of pretty butterfly I am letting it run amok on the parsley for the moment.

Any ideas?

It is the caterpillar of Papilio polyxenes.

The pupae may be green or brown, but not depending on surroundings or the background on which they have pupated. The color of the chrysalis is determined by a local genetic balance that ensures the majority of pupae will blend in.[10] A section of the green pupae will turn a much darker green at the very end of the pupae stage. This color change occurs a few hours to a full day before hatching.[10] Unusually, this butterfly's chrysalis is girdled with a loop, with its feet attached to the silk pad, which helps the butterfly to unfold its very large wings when crawling out.[11]

Here is a photo of black swallowtail caterpillars at different life stages:

Here is a link to a post, which describes all the stages your caterpillar will eventualy go through.


text:
Why pain caused by blunt objects vanish after some time and return at the event of touching?
Background
When any bone/muscle of body is hit badly by a blunt object, it hurts pretty bad of course for some time. But, after some time the pain goes off completely or to some extent.
Then, if we touch the wounded spot, the terrible pain returns.
Why?
If the pain goes off as the healing process of severed tissues, blood capillaries, then why does it return at the event of touching?
My reasoning: I think there is a sophisticated pain mechanism responsible for this phenomenon.Firstly, pain warns our nervous system to be cautious against any new injury. As time goes on, sensory adaptation diminishes the pain. But the event of touching is a new pressure for the blunt wound.So, the pain comes back again. But, I need well-referenced answer to support my view.
Papers: The most relevant paper I've found till now: 1 which is behind paywall

perhaps the first shock cause some invisible injury

Invisible? The pain is in the same place?

I meant injury in cells and tissues, that can't be seen from macroscopic vision. Pain is commonly a response to tissue-damage.

I meant if an injury is caused, it takes time to heal. So within this time if we touch the injured place, easily the injuries increase than healthy tissues. However that is just one guess. Also maybe it is due to some other cause such as maybe  at wounded place the cells tend to release pain signal molecules at milder threshold than healthy tissue. However the question is good.

Well, then if the pain is gone, the damaged tissue is repaired, no? Then where did the new damage come from?

Yes I meant damage remains for a certain period. And a cracky paper is more brittle than an intact new paper. Isn't? ((However comments are not for extended discussion, so I should wait for a valid, referenced answer))

I am not even sure why the pain goes in the first place if it's not completely healed. Maybe our brain has this weird pain mechanism which after sometime reduces pain and then triggers pain when touched to give a signal that something is wrong. Maybe it's evolution.

There might evolutionary significance so that we can protect the injured organ from further damage.

Let us continue this discussion in chat.

BASIC REASON WHY THE PAIN DISAPPEARS FOR SOMETIME:
There are gating mechanisms involving pain both in the spinal cord and in the brain.
Although the pain gating pathways in the brain are multifold complex,the spinal pathway can be simplified.
The latter may be understood in a simplified manner in 2 ways:

When there is a nociceptive stimulus,the epicritic receptors are stimulated.Sensory fibres from them synapse with internuncial neurons which inturn transmits impulses via the ascending tract to the periaquiductal grey. This region is capable of inhibiting pain impulse transmission to the spinal cord or thalamus by modulating impulses via the descending tracts.
This type is called supraspinal control
Another spinal reflex-type gate control operates in which stimulus like rubbing over the pained area ,application of warmth or cold causes inhibition of pain.
This is due to the impulses by large type (myelinated)A-fibres which arises from the  rubbed areas synapse with the internuncial neurons which are already synapsed with the epicritic sensory neurons of the dorsal root.The ends of such type of fibres release neurotransmitters that inhibits transmission of pain impulses through the internuncial neurons .
This is termed as segmental suppression

WHY DOES THE PAIN RETURN AGAIN:
This is because the pain receptors are the slowest to adapt.It's exactly as you said because it keeps the body apprised of tissue damaging stimulus.
So when there is the return of the noxious stimulus we can understand the tremendous summation effect which takes precedence over the gate control.
This occurs by a greater output of neurotransmitters from the synapse of the pain sensory fibres which outdoes the inhibitory effect of the neurotransmitters favouring gate control of pain.


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Are the human genes' promoters all known?
It seems to be a basic question, but I couldn't find a certain answer.
The human genome is known for more than a decade, and is available through several data providers as the NCBI etc. For the genes' promoters however there seems to be much less information. There are some characteristics known (like the TATA box, which appears in ~25% of human genes), some prediction methods (like CpG sites appearance), some rough estimations for the location (100-1000kbp long, in the adjacent 2kbp upstream from the TSS), but I couldn't find any data set with a closed list of human genes' promoters.
Is this really yet to exist?

Not 100%. People are still working on it using by studying nucleosome positioning and transcription factor binding sites and other factors. For many ncRNAs, even the TSS is not well annotated. Techniques like CAGE are quite recent. But you should clarify what you really mean by promoter: the minimal promoter (TATA-box etc) or all TFBS?

@WYSIWYG Thanks! I'm looking for the whole TFBS (as far as I understand). What I'm doing is comparing and trying to optimize CpG islands (CGIs) identifying algorithms (e.g. as Takai's, and recent CpG clustering algorithm). One major parameter for scoring is how well do results lay withing promoters. Sort of chicken and egg situation.
Do you happen to know if CpG methylation suppresses expression only when appears within the promoter area, or in it's surroundings as well (up/downstream)

Nope. The human genome is still quite unexplored, new genes are still being discovered and the annotation of non-protein-coding regions (that include promoters) is still far from being complete. For example, look at the Statistics comparison of the current and previous Human GENCODE Release, it clearly shows that the annotation of the human genome is still an ongoing process.


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Carbohydrate in egg white
I looked up online to find which type of carbohydrate is found in egg white, but the only information I found is the quantity of sugar. I would like to know the exact name of the carbohydrate found in the egg white in order to draw the sugar molecule.

It's all in a glycosylated protein (as noted in the answer), the composition of which is not homogeneous. But I found: "MALDI MS of the N-glycans released from α-ovomucin by PNGase F revealed that the most abundant glycan structure is a bisected type of composition GlcNAc(6)Man(3)." (http://www.uniprot.org/citations/21484392)

The one I found is Ovomucin,though it's not a pure carbohydrate.

Ovomucin is a highly glycosylated protein and approximately 33% of ovomucin is made up of carbohydrates.

Nutritional Values of Egg White Proteins paragraph of
http://ps.oxfordjournals.org/content/92/12/3292.full
So you can see it's mostly a protein.

Ovomucin is a trypsin inhibitor found in raw egg white.
Ovomucin is responsible for the gel properties of fresh egg white and is believed to be involved in egg white thinning. Ovomucin is composed of two subunits:

α-ovomucin - carbohydrate-poor with a molecular mass of 254kDa

β-ovomucin - carbohydrate-rich with a molecular mass of 400-610kDa

Souce: Wikipedia

I'll add more info as soon as I find some.

I did some research about the ovomucin but I didn't found it molecular stucture... Have you any idea about the ccomposition of the sugar?

No sorry about that.


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Does DNA helicase or topoisomerase actually "unwind" DNA?
I am reading through my textbook (Genetics, Brooker 4th edition) and the summary it gives seems imprecise for the functionality of helicase and topoisomerase.
The following is an exerpt:
At each replication fork, DNA helicase unwinds the DNA and topisomerase alleviates positive supercoiling.
Is it proper to say that helicase "unwinds" DNA? In other places in the book, it says the function of helicase is to separate the two strands of DNA, and topoisomerase "relieves the supercoiling" caused by the strand separation activity of helicase.
Pardon my ignorance, but it seems rather like helicase actually induces more winding, and topoisomerase (gyrase) actually unwinds DNA.
Is this just a case of poor wording, or does helicase actually somehow unwind (untwist) DNA? I am finding this particularly frustrating because virtually every resource I can find says that helicase unwinds DNA, but based on the mechanisms they offer, it definitely does not "unwind".

It would be pretty difficult to separate the strands without unwinding them. As you pull the strands apart, the adjacent regions will either have to rotate (unwind) to accomodate this or break.

Why wouldn't the replication complex just rotate (spiral) along the double helix?

The strands must be separated so the incoming nucleotides for the newly fabricating strand can be base-paired to the template strand. The other (antisense) strand must be moved out of the way for this to occur.

I mean, I get that they're separated but how do they "unwind"?

Got a short piece of three stranded rope handy? (I don't think they make two stranded rope.) Hold the rope firmly in each hand about 5 cm apart. Twist in the direction opposite the winding. The strands of the rope will separate in the region between your hands. The unwinding and the separation of the strands are, um, inseparable from one another. You can't separate the strands without unwinding.
The heilcase unwinding is merely straightening out the double helix in a very local area. This separates the strands such that one strand can serve as a template for transcription or replication.
But a consequence of the unwinding in the local region where the strands are being separated, is that other nearby regions get more tightly wound. This occurs because the DNA is far too long for the ends to spin around to accomodate this unwinding. These more tightly wound areas are what is refered to as supercoiling. The topoisomerase alleviates this stressful coiling. https://en.wikipedia.org/wiki/Topoisomerase
So, the answer is both helicase and topoisomerase result in the unwinding of DNA.


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What is a topological domain?
I found this definition on Wikipedia, but I didn't quit undestand it :

Topologically associating domains (TADs) are genomic regions ("chromosome neighborhoods") used to summarize the three-dimensional nuclear organization of mammalian genomes.

Can anyone explain it more, and give examples if it's possible ?

TADs were initially discovered by computing contact probabilities between regions of the genome using HiC (a chromosome conformation capture method, that try to provide an idea on how the genome is organized inside the nucleus by computing the probability of each contact to be located nearby another locus). People have found that instead of being random, some loci were in contact with some regions of the genome rather than the others, implying some form of functional significance.
In short: a TAD is a genomic region of increased contact probability. They are of functional relevance (for instance, Enhance-Promoter gene expression regulation occurs primarily within one TAD rather than between two (adjacent TADs).
You might be interested in the following papers:

A 3D Map of the Human Genome at Kilobase Resolution Reveals Principles of Chromatin Looping (might be behind paywall)
Topological Domains in Mammalian Genomes Identified by Analysis of Chromatin Interactions

Finally, the following picture (extracted from the latter publication) provides an example of two TADS:

The bottom panel shows the contact probability: two regions of the genome appear to be isolated whereas they are nearby. They show significant self-interaction. One interpretation for that (top panel) is to imagine that the genome exhibit some reproducible condensation, explaining the increased contacts.

Topological aspects of DNA structure arise primarily from the fact that the two DNA strands are repeatedly intertwined. Untangling these two strands, which occurs in all major genetic processes may prove rather difficult. In the simplest case of a linear DNA in solution, untangling is possible due to the free rotation of the ends of the DNA. However, for all natural DNAs, free end rotation is either restricted or forbidden altogether. Consequently, untangling the two DNA strands becomes topologically impossible (Figure 1 illustrates this for the imaginary case of a circular DNA molecule where the two strands are tangled only once).

A DNA segment constrained so that the free rotation of its ends is impossible is called a topological domain (Figure 2). A canonical example of a topological domain is circular DNA, which is typical of bacteria, mitochondria, chloroplasts, many viruses, etc. In this case, there are obviously no DNA ends at all, since both DNA strands are covalently closed. Although eukaryotic chromosomes are linear overall, they consist of large DNA loops firmly attached to the nuclear matrix. These loops represent topological domains, i.e. they are equivalent to circular DNA topologically. The ends of linear DNA can also be affixed to the membrane, as has been shown for some viruses, making this DNA topologically closed. Finally, a stretch of DNA situated between the two massive protein bodies can also be considered a topological domain.

Source : DNA Topology Fundamentals


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What is the Specific Nature of Observable Micro-evolution
I am wondering what the proven mechanisms of micro-evolution are. For instance, in the case of bacteria, when a strain evolves that is resistant to antibiotics
1) Is the genetic combination that enables the bacteria to resist the antibiotics present the entire time and only made prevalent by the environment through natural selection, or do mutations occur to the DNA that change the organism so that it can then survive?
2) With the antibiotics removed, is the evolved strain generally more resilient in a normal environment or weaker?

A good answer would require writing a whole introduction to evolutionary biology which is way too broad. You should have a look at a very introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

In short, (1) No, mutations do not occur strategically in order to adapt. They just occur, their effect on the phenotype is random but sometimes such random effect is beneficial and it then gets selected for. (2) A priori we would think there is a trade-off and evolving defense against an antibiotic would come at a cost which makes this antibiotic-resistent strain less competitive in an environment without antibiotic. However, this prediction might well fail in many cases where such trade-off do not exist or are negligible

I agree with remi.b that the question suggests some misconception about evolution. The question could be refined to asking about the relative importance/contribution, to the process of adaptation, made by standing and novel genetic variation which is an important topic in evolutionary biology.

Please note that, to biologists, there is no such thing as "microevolution" or "macroevolution" - there is just evolution.

@MattDMo - Remi. b notes in one of his answers that it was microbiologists themselves who invented the term macro/micro evolution (http://biology.stackexchange.com/questions/39711/have-there-been-any-macro-evolution-experiements?rq=1). If this terminology is unacceptable then what terms are used to draw distinctions between evolutionary behavior observed in a lab vs. that which is inferred from fossil records and theory? I would think that this is a useful distinction.

@Ian please read the rest of what Remi wrote in that answer. The term was never properly defined, it has been heavily criticized in the intervening 90 years, and today has been appropriated by creationists and proponents of intelligent design, two hypotheses which have no place in scientific discussion. As I implied in my previous comment, there is no distinction between evolution observed in a lab vs. that observed from fossils, etc. - why should there be? Is there something about a lab experiment on human timescales that makes it less scientific or something?

@MattDMo - Yeah, I read the whole thing. But as a layperson I find the terms helpful even if they have baggage. The difference is that the precise mechanisms and characteristics of evolution observed in the fossil record are currently unknowable, right? When evolution occurs in a lab or within a generation it can be analyzed and understood, which makes it quite a bit more interesting (at least to me).

@Ian evolution works the same way regardless of whether you're in a lab or the Badlands of the Dakotas digging up dinosaur bones. I strongly suggest reading Understanding Evolution from the University of California, Berkeley to learn more. It's not just that the terms have baggage, it's that they're meaningless. You insist on creating a dichotomy when there is none. The only difference is in the number of genes that are affected, and that's a continuum, not a discrete separation into "micro" and "macro".

@MattDMo - Well I actually do plan on reading that page cuz I'm interested, but right off the bat I notice that they too use the term microevolution (evolution on a small scale) :) (http://evolution.berkeley.edu/evolibrary/article/evo_36).

There are several mechanisms through which a bacteria can evolve antibiotic resistance.
One way is by acquiring an already-existing gene from another bacteria or virus by what is called horizontal gene transfer. In this case, there is no requirement for any mutation to occur although the new gene can be integrated into the host genome and so, in a sense, the genome itself is mutated since it now contains a new gene but the gene itself is not.
Another way of acquiring resistance is indeed by genetic mutations. One beautiful example of this is the resistance acquired toward some aminoglycoside antibiotics. This class of antibiotics interferes with the ribosome assembly by binding to a specific site of it. In some cases, a simple point mutation of the aminoglycoside-binding-site is enough to acquire resistance. Some strains of bacteria exhibit aminoglycoside resistance due to a transport defect (mutation of a channel for example) or membrane impermeabilization (mutation of a pump), acquired by other mutations. Others use specific enzymes to digest the antibiotic, different variants (mutants) of such enzymes broaden the spectrum of resistance.
There are many other different cases in which a simple mutation is enough to acquire resistance.
Here some references:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC182597/
http://www.uphs.upenn.edu/bugdrug/antibiotic_manual/aminoglycosideresistance.htm
http://www.antibioresistance.be/aminoglycosides.html
https://www.ncbi.nlm.nih.gov/pubmed/27690121
https://www.ncbi.nlm.nih.gov/pubmed/27651364
https://www.ncbi.nlm.nih.gov/pubmed/27699821
With the antibiotics removed, is the evolved strain generally more resilient in a normal environment or weaker? No, in general, there is no extra advantage in being resistant to an antibiotic if the antibiotic is not present.


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Is this insect some kind of pest?
I live near Paris, France. I would like to know if this small flying insect was some kind of pest or not. More specifically, I want to know if it might be a meal moth or a clothing moth. Here is the little fella :
It's approx 1.5 cm (0.6 in) long

This is Hypena obsitalis, aka the Bloxworth snout, a moth of the family Noctuidae.
Personally I hate the word pest, but this little beauty eats Parietaria und Urtica (Nettle) so I can't think of anyone seeing this as a pest species.


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Over winding vs under winding of a DNA

DNA supercoiling refers to the over- or under-winding of a DNA strand.

Source : DNA supercoil

When a relaxed DNA is subjected to bends, or openings of DNA, over winding or unwinding, its base pairs per turn changes, and the DNA is subjected to stress and strain.  In order to overcome such distortion, which has rendered the DNA unstable, the DNA twist around itself, like a circular rubber band undergoing twisting, such a twists on its own thread is called Super coiling; it is also referred to as tertiary structure.

Source : DNA Super Coiling
What they mean by over winding and under winding of a DNA ?

Imagine a covalently closed circular double-stranded DNA plasmid. In its "natural", or "relaxed" state you could spread it out, flat, on a suitable surface.
Now imagine cutting one of the strands of the DNA (i.e., cutting the sugar-phosphate backbone, the way that an endonuclease would, leaving a nick, the 5'-end of the nick has the phosphate, and the 3'-end of the nick has an -OH group), and rotating that nicked strand in a clockwise direction, several times, around the other, intact, DNA strand.  This does not involve breaking any of the basepairs, or unravelling the strands, you are just twisting it around.
Now imagine sealing that nick, by ligating the 5' phosphate to the 3' OH.  At this point the dsDNA helix is slightly "overwound", and will no long lie completely flat. It has begun to be supercoiled; these are positive supercoils.
If, alternatively, you had rotated the nicked DNA strand several turns in the counter-clockwise direction before re-sealing it then that molecule would also start to be supercoiled, but it would be "underwound" with negative supercoils (and it would also no longer lie flat on the surface).
There is an enzyme called DNA topoisomerase I that cuts, and re-seals, one of the two strands like this.  Another enzyme called DNA topoisomerase II cuts both strands before introducing supercoils.

There are two types of supercoiling:

Positive (right-handed/overwound) : the double helix is twisted to such an extent that it begins to ‘knot’.
Negative (left-handed/underwound) : this type of coil goes against the natural direction of the double helix structure.

Negative supercoiling is a highly regulated process, performed by specific enzymes such as topoisomerases. There exist two types: topoisomerase I and topoisomerase II. The former relaxes the supercoil whereas the latter increases the extent to which the DNA is supercoiled.
In E. coli, there are at least four different types of topoisomerases responsible for regulating DNA supercoiling.
Source : SUPERCOILING


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Are the human placenta chorionic villi and villous tree the synonyms?
Are the human placental chorionic villi and the villous tree the synonyms? Or, if not, can I say that these tissues would have practically the same gene expression profile in an RNA microarray experiment?


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Do non-migratory canada geese still exhibit migration behaviors?
I have noticed that many of the geese in my region (NE US) remain overwinter. I also see many of what I guess (but am not sure) may be the same geese flying in migration patterns. One thing that makes me think that non migrating geese do this, is that I observe group formations flying in all directions, not just southwards in the fall.
Does anyone know whether the resident geese still like to fly in migration patterns, or is it always the migrating geese that you see doing this?

The answer is yes, also sedentary geese do use migration patterns (V-formations). When they move from roosting place to feeding areas (or vice versa) geese always tend to fly in formations. I speak for personal experience of resident and wintering birds in Europe and America.
They do so because they save energy as explained here: http://jeb.biologists.org/content/128/1/445.short and here: http://www.nature.com/nature/journal/v413/n6857/full/413697a0.html
The second study also show how not all the positions in the formation are the same regarding energy expenditure. The one closer to the front of the V shape need to flap the wing more often.
Have fun


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Do they have scales?
Do Channa striatus and Channa punctatus have scales?
They are both snake headed species of the genus Channa. I'm trying to figure out the distinguishing characters.

Did you try to google the species names and the word "scale" and either look at pictures or one of the first links. Here is the search result I got with "scale Channa-striata" (the answer is in the second link).

I'm sorry. I shouldn't have created this post in the first place.

Channa striata
Environment/climate/range

Freshwater; brackish; benthopelagic; pH range: 7.0 - 8.0; dH range: ? - 20; potamodromous (Ref. 51243); depth range 1 - 10 m (Ref. 2686), usually 1 - 2 m (Ref. 4515).   Tropical; 23°C - 27°C (Ref. 1672), preferred ?; 35°N - 18°S

Length at first maturity / Size / Weight / Age

Maturity: Lm 18.0, range 23 - ? cm
  Max length : 100.0 cm SL male/unsexed; (Ref. 2686); common length : 61.0 cm TL male/unsexed; (Ref. 44091); max. published weight: 3.0 kg (Ref. 40637)

Short description

Dorsal spines (total): 0; Dorsal soft rays (total): 38-43; Anal spines: 0; Anal soft rays: 23 - 27. Body sub-cylindrical; head depressed; caudal fin rounded (Ref. 2847). The dorsal surface and sides is dark and mottled with a combination of black and ochre, and white on the belly; a large head reminiscent of a snake's head; deeply-gaping, fully toothed mouth; very large scales (Ref. 44091).

More information here

Channa punctata
Environment / Climate / Range

Freshwater; brackish; benthopelagic; potamodromous (Ref. 51243).   Tropical; 22°C - 28°C (Ref. 2059), preferred ?

Size / Weight / Age

Max length : 31.0 cm TL male/unsexed; (Ref. 4833); common length : 15.0 cm TL male/unsexed; (Ref. 6028)

Description

In Sri Lanka, the young have a chocolate-coloured body with three yellow stripes which are lighter ventrally. There is also a golden lateral stripe from the snout, through the eye to the middle of the caudal fin. At 13 mm, black body scales appear along with three dark bands on the caudal fin. Adult colouration arrives at a size of 70 mm upwards ( Deraniyagala 1929 ).

More information here and here


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Is excess of potassium as strenuous and harmful for kidneys as excess of sodium or worst?
I was wondering since channels of body's cell membranes deal with potassium and sodium ions differently and considering the fact that potassium lowers blood pressure and sodium raises it :

What is the most expensive in energy for kidneys between having to excrete an excess of potassium and an excess of sodium, for a healthy person and without considering blood pressure? Which process is the longest?
I know that insulin tends to make kidneys reabsorb sodium but does glucose help the kidneys to get rid of the excess potassium in any way?
On long term, what is the most harmful for the kidneys' circulatory system considering blood pressure and in the case of a kidney failure? For tubules and nephrons?


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Can human eys/the brain be trained to see with bidirectional monocular vision?
Most people have a dominant eye, and while it uses its non-dominant eye in tandem with the dominant eye most of the time, the brain, being an expert in eliminating redunant information, ignores the images received from the non-dominant eye.  However, with special training or practice most individuals can force the brain to temporarily switch to receiving images from their non-dominant eye, even to receive images from both at once, resulting in a blurred chamelion-like or image.
Some individuals however, have a non-dominant eye so weak, that not only does the brain ignore the images it sends, the eye it self no longer moves in tandem with the dominant eye.  This is known as strabismus or Lazy eye.
My question is, if the eyes are capable of not moving in tandem in those people, why can't we all train our eyes to move independently, and couldn't we also train our eyes to focus on two different images (on opposite sides) at once?

I edited your post to remove the alien reference. While I, and maybe others may think it's funny, many users of this forum will disapprove and possibly downvote your question. They do have a point in not wanting the forum bloated with humor. [This comment to be removed.]

@bpedit well couldn't you have least edited it, not simply remove it?  I wanted to know if people with strabismus could see like chameleons.

What are your sources on this information? Note that stereoscopic vision is lost entirely with only one dominant eye doing the work. I.e., ...couldn't we also train our eyes to focus on two different images (on opposite sides) at once? is the very basis of binocular vision. I quite frankly don't understand your question.


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Evolutionary explanation of the bicuspid on the left and tricuspid on the right
The left heart handles more pressure and logically it would make sens to have a valve with three leafs on the left (If I had got to choose, I'd have put three on both sides).
Other than being more susceptible to valvular disease (also because the pressure is higher on the left), the bicuspid having 2 leaves don't do any good (To my knowledge).
Since this is not the case, there might be some evolutionary constraints that might have caused this difference.
Any explanation according to valvular evolution along the phyla?

Logically it would be better to have less number of valves as pressure to be handled increases.

I agree more valves makes it structurally weaker.


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Why are valves preferentially affected in endocarditis?
The inside of the heart is covered by endothelium throughout. Why are valves predisposed to endocarditis? I know it can affect other structires like the septum, chordae etc. But why the valves? Especially bacterial endocarditis.
Wouldn't a place on the ceiling of the atria be quieter and have less turbulence?
Robbin's Pathology says that valves derive nutrition from the surrounding blood and there vessels but mostly on the proximal side. So it might not be due to nutrition.
Are there theories for this?


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Do action potentials cause the neuron to heat up as well as its environment?
I have read that we might be yawning to cool our brains down, so then a thought occurred to me. If we need to cool down our brain, then our brain but heat up for some reason. The only reason I could see would be the action potential causing some sort of temperature increase. My query is how exactly would a neuron heat up, if it does do so in the first place?

While it is possible that action potentials themselves result in waste heat, there are other processes within the neuron likely to contribute much more to energy lost as heat. The action potential itself uses energy that's been stored in chemical and electrical gradients that are the result of numerous sodium-potassium pumps which require the energy in ATP. There would be some loss of energy in the operation of these pumps.
But far more heat is likely generated by the mitochondria within the neurons. These are the structures that convert most of the energy in the breakdown products of carbohydrates and fats into the ATP the Na-K pumps require. Generous estimates put the efficiency of this production at roughly 50%. That means about half the energy from the food-stuffs used to create the ATP is lost as heat.

How much heat can a neuron waste? Is it enough to effect its function?

"Waste heat" simply means energy that escapes during a transfer of energy from one form to another. We call the roughly 50% of the energy in carbohydrates that can't be converted into ATP waste heat because it doesn't end up in the desired form of ATP. But that "waste heat" is what mammal's bodies uses to maintain a high body temperature enabling us to be more active than, say, reptiles in colder environments. The body has many mechanisms to dispel heat if it begins to get too hot, think sweating for example. Blood helps carry heat from the brain to where sweat can occur.