text:
What does "each pathway define an independent genotype" mean?
In a section of this paper.

However, if the question of independency is posed in the
  form: “Does each pathway shown define an independent
  genotype?,” then each of these three pathways is indeed
  independent. This is the way that MPS defines the independence
  of pathways.

What does “Does each pathway shown define an independent
genotype?,” mean?

Pathways cannot define a genotype. They are product of the genotype and they define the phenotype.

This is somewhat outside my field, but basically it seems they're defining the independence of the three hypothetical metabolic pathways in two different ways:

Mathematically the pathways are not independent since P₃ is a combination of P₁ and P₂.
Biologically the pathways are independent since each requires a different combination of enzymes and therefore genes (the genotype). This is the method used in MPS.

Does that answer your question?

I don't know, the answer you gave seems satisfiable so i would go with it...


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What is the difference between a graded potential and an action potential?
I was under the impression the only signals neurons send using changes in membrane potential are action potentials. But my biology professor showed us diagrams of graded potentials and action potentials and to me they looked very similar.
What is the difference between a graded potential and an action potential?

Short answer
An action potential is a binary all-or-nothing event, while a graded potential is an analog signal.
Background
Action potentials, once initiated, are basically all-or-nothing events. Amplitudes may admittedly be variable, but basically it is the spike rate that is relevant to the neural code (Gerstner et al., 1997).
In contrast, graded potentials code information mainly by amplitude. A notable example of the significance of graded potentials is the function of the inner hair cells in the cochlea (the inner ear). The mechanoreceptors on the hair cells open when deflected in one direction, while they close in the other. This is important, as that property depolarizes the cell on one phase of an input sinusoid, while it hyperpolarizes the cell in the subsequent phase. Also, stronger (louder) input increases the response, while softer stimulu generate less response (Fig. 1). In the auditory nerve this graded potential is translated into spike rates (Fig. 2). Basically the hair-cell and auditory nerve system is an analogue-to-digital converter.

Fig. 1. Cochlear microphonic: a graded potential that increases amplitude with increasing loudness. Source: Juaristi & Martínez-Conde, 2014

Fig. 2. In the auditory nerve amplitude is coded as action potential (spike) rates, low frequencies as burst-repetition rate. Source: NY University
References
- Gerstner et al., PNAS (1997); 94(24): 12740–1
- Juaristi & Martínez-Conde, Acta Otorrinolaringol Española (2014); 65(04)

This is a really nice answer. I have never understood this concept this well. It goes beyond a surface description and actually identifies the specific mathematical/code property that makes the two distinct. Really cool.

@StanShunpike - thanks for your nice feedback. I had to ponder on this one for a few days before answering :) I'm glad the answer was helpful. Thanks for accepting too. Late answers often don't get a lot of upvotes  :)

Graded potentials are initiated by a stimulus that vary in magnitude depending on the strength of the stimulus. (The stronger the stimulus the more gated channels open causing larger depolarisation). Graded potentials occur in dendrites, cell bodies and sensory receptors. Graded potentials dissipate with distance from stimulus.

On the other hand, action potentials occur when graded potentials reach the axon hillock at a certain level of depolarisation (around -55mV). This opens the activation gate letting sodium flood into the membrane. This is an "all or nothing" event, once the threshold triggers the membrane depolarises quickly to around +30mV.
I could just save you time and show you this table:

What was the source of the table? I'd like to reference this for future study.

source: Stack Exchange

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RNAi in nematode resistant plants
Background : Certain plants have been genetically engineered to have sense-antisense gene of a parasitic nematode. The dsRNA produced by the plant then inactivates the mRNA produced in the nematode, who, then isn't able to synthesize the corresponding protein and dies as a result.
Question : How is the dsRNA from the plant transfered to the nematode's cell ? By transformation ?

Apparently it is transferred by simply feeding. C.elegans feeding on E.coli producing dsRNA can produce the siRNA. C.elegans seems to have a lot of RNA transporters such as SID1.

Yes, in vitro you can simply soak the worms in a solution that contains the dsRNA (i.e. in a large-scale microtiter dish for HTP screening)--this is not the same as ingestion because the worms won't eat if there are not small particles  in the liquid.  For the bacteria the E. coli express the RNA hairpin in response to an inducer (IPTG) and then after ingestion the cell contents are released after the cells pass through the pharyngeal grinder, and the RNA is taken up by the gut cells, and then transferred to other cells by the transporters.

@wysiwyg thanks. Pls see my comments on Ilan's answer.

The question is little bit unclear: is in vitro or in vivo introduction in question?
In vivo:

As the nematode feeds on the plant during its parasitic phase, it
  consequently assures the introduction of dsRNA and/or siRNA molecules
  into the nematode’s digestive system.

in vitro introduction etc  ->
The status of RNAi-based transgenic research in plant nematology

Why does it feed on it ? Even if it does, won't the RNAases in its digestive system break down the RNA ?

@biogirl They feed on the plants for nutrition. RNAses should break down the RNA but I couldn't find much information about exoribonucleases in nematode digestive system. Apparently the RNA transporters are far more active. Perhaps an evolutionary adaptation.

@biogirl it is a part of a parasitic evolution. The mechanism of dsRNA introduction includes enzymatic interactions: dsRNA is introduced into the nematode digestive system by feeding on dsRNA-expressing E.coli. The dsRNA spreads to neighborhood (the SID-2 and SID-1 proteins actions), followed by cleavage of dsRNA by the RNaseIII, Dicer, in the cytoplasm. Attachment of siRNAs to the RNA-induced silencing complex (RISC) separates the strands of siRNAs and incorporates the siRNAs into the active RISC. These siRNAs target mRNA molecule and the RISC cleaves them and a gene is silenced.

@wysiwyg Thanks ! How are active RNA transporters evolutionarily advantageous ?

@biogirl That I cannot comment about. It could have been advantageous for some reason. There is too much to speculate here

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text:
What happens when we re-start a PCR reaction?
Recently when my PCR reaction was running there was power fluctuation and the entire lab was blacked out for a few minutes and unfortunately PCR that I was running got switched off. So, would it be okay to restart the PCR? What would happen if the same PCR program was run again?

How many cycles had elapsed? For how long was the power down?

about 12 cyces..

then you can run it for another 18 cycles. How long was the power down? Did the power come back immediately?

The power came back in half an hour

But what happens if the number of cycles is increased too much? how would that affect the reaction?

Theoretically, you can amplify your target sequences. Just run the number of cycles you planed in total. But no one tells the results. Loss of temp control may increase opportunities of none specific annealing and amplification. If it is qPCR, it could be very tricky... or I really don't know. If you just want to get PCR fragments, you could/might get bands. Then, just it is your decision. Remember you can not complain after you clone the PCR fragments into plasmids and the sequences turn out to be wrong.

The polymerase used in PCR is extremely stable at room temperature. I would expect you to be able to continue your PCR reaction from the cycle it was stopped at without too much trouble. However, it is important to not over cycle your product. This will produce non-specific products. If a clean result is imperative, take a 1-5ul sample from your original reaction to use as a template in a new reaction.

In this case you can run your PCR for another 18 cycles (if your total number of cycles was 30). However, do the initial denaturation for 1-2min. You may run the same program again (full 30 cycles) but you'll just end up wasting time because after a point all the dNTPs and primers would be exhausted and further cycles will have no effect on the concentration of the amplicon.


text:
Phosphorylation capacity of an enzyme
Let's think ProteinA can phosphorylate proteinB, proteinC and proteinD.
Condition1: All proteins are expressed and proteinA phosphorylates proteinB, proteinC and proteinD.
Condition2: Only proteinA and proteinB are expressed for that reason protein A phosphorylates only proteinB.
Which is more realistic?
1) In condition1; proteinB, proteinC and proteinD will be 3 times less phosphorylated in comparison to proteinB in condition2.
2) The proteins of both conditions will be phosphorylated same.
Cheers
Cankut

Is this a homework question?

No it is not, why?

it is a simplified version of my question which I could not find a clear answer.

I really do not understand why the people just vote for this question instead of giving a simple answer. if a person do not have any answer about a question then how he/she can vote for the question. First give an answer then be able to vote the question...

@Cankutçubuk please take the [tour] and read through the [help] to understand how this and all Stack Exchange sites work. Voting is nothing personal, it merely reflects the quality of the question or answer being voted on. In this case, the question is not in line with our homework policy, which is slightly mis-named, as it not only applies to homework but to all trivial and/or un-researched questions, especially those (like this one) that look very much like homework or exam problems. (...)

(...) If you wish to post questions such as these, please put in what research you have done to solve the question yourself, what you think the answer is or is not, and how you came to that conclusion. If you're stuck at some part, state exactly where you're stuck, and what you've come up with so far.

@MattDMo Just an additional information about my question; I am working on signal transduction and I had some difficulties to integrate phosphoproteomics and other omics data for that reason I needed some biological updated knowledge.

Don't be discouraged. At least in vitro, if there is ample chemical substrates (e.g. ATP) and protein A (i.e. kinase) remains active, the kinase will just keep phosphorylating its protein substrates (B alone or a mixture of B, C, D) until the substrates are depleted.
Thus, all substrates will be phosphorylated eventually. The contrived Condition 1 may occur only if you only supply enough ATP for A to phosphorylate one mol equivalent of its protein substrate AND A has exactly the same catalytic efficiency toward B, C, and D that are present in equal amount. Of course, any or all of B/C/D may have more than one phosphorylation sites, each of which has its own phosphorylation rate.

@SKY thank you very much for your precious answer.


text:
Could felines live without meat?
Algae are a source of taurine and mushrooms are a source of vitamin D3. Both also contain high protein. So, it seems possible to feed a cat or other felines without any meat. Are there any concerns to have them live with this kind of diet?

This seems to have already been answered on pets stack exchange

@RoryM Already read and they always mention the same things I have search all these times, VitaminD3 and Taurine, which I present here that it could possible because there are these things contain both. And while mushroom is not meat It is very meatlike with taste of glutamic so cat love them too

Related: Is there benefit to feeding my cats food that incorporates fruits and vegetables?

@Zaralynda sorry but not so related. Because fungi and algae aren't fruit and veggie in terms of nutrition. They are composed of animal part more than plant. High protein than sugar. And no one mention about them

No, fungi are not "animal more than plant". They are a third group, independently evolved and different from either. The fact that they share a flavor component with meat that plants generally don't (umami) does noit say anything at all about their nutritional content, and the latter is what matters. (I haven't tried offering my cats mushrooms. They might appreciate the umami flavor. Then again, one of them loves fish but is apparently allergic to it, so they don't always know what is and isn't good for them.

@keshlam I have already read about nutrition fact of mushroom so I selectively use the sentence "composed of animal part more than plant. High protein than sugar" (except some species contain high sugar). And I never said that fungi is animal


text:
What is the biological limit on hearing resolution?
I sometimes wonder how many different individual musical scales could be perceived by human ears. I define a musical scale as a collection of notes that relate to some fundamental frequency by specific ratios. For instance

do $2^{0}f$
re $2^{\frac{1}{6}}f$
mi $2^{\frac{1}{3}}f$
fa $2^{\frac{5}{12}}f$
sol $2^{\frac{7}{12}}f$
la $2^{\frac{9}{12}}f$
ti $2^{\frac{11}{12}}f$
do $2^{1}f$

I once did an experiment where I took various sine waves at different frequencies and multiplied them by the appropriate ratios. I found for the ones I tried that I did indeed heard the major scale. But a mathematician will look at the positive real numbers $\Bbb{R}^+$ and say there are an infinite, uncountable number of possible frequencies. However, Biologically I cannot imagine the human ear is capable of distinguishing between an infinite number of frequencies.
What is the biological limit on hearing resolution? Is there a way to estimate how many different major scales one can hear? In other words, how many different frequencies can be heard?

Short answer
The main limitation to frequency discrimination is loudness.
Background
The cochlea is tonotopically organized - it basically acts as a Fourier transformer, where different frequencies are analyzed on a place map  (Fig. 1). Frequency tuning of cochlear hair cells is mainly limited by sound intensity. The louder a pure-tone sound stimulus gets, the larger the area on the basilar membrane that is activated and hence the wider the range of cochlear hair cells that is activated, and hence the worse the frequency resolution becomes (Fig. 2).

Fig. 1. Cochlear tonotopy. Source: Cochlear Implant Help

Auditory nerve fiber tuning. The louder the stimulus, the worse the tuning to frequency. Source: - Fettiplace & Hackney, 2006
As to the quantitative aspect of this question, namely what the frequency difference limen is, and an indication how many frequency bands can be distinguished I refer you to below linked question. Both depend highly on the method used to determine the just-noticeable-difference, and as said also on the sound intensity applied. Moreover, it is dependent on the frequency under consideration. The higher the frequency, the larger the frequency band becomes expressed in Hz. This is an example of Weber-Fechner's law (Hecht, 1924). The cochlea is organized in octaves, meaning that higher frequencies have less cochlear space devoted to them and hence less hair cells to code a particular frequency range.
Further Readings
- What's the frequency resolution of the human ear?
Reference
- Hecht, J General Physiol (1924): 235-67
- Fettiplace & Hackney, Nature Rev Neurosci (2006); 7: 19-29

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text:
Interpretation of qPCR results for low expression genes
I am attempting to validate existence of a transcript using 40 cycle qPCR. I designed primers for a unique feature of this transcript, and also designed primers for a sequence in the transcript that is common to several transcripts of this gene, and finally I used GAPDH as a control. I already knew beforehand that this transcript has very low expression.
For the unique region, my ct values for primer 1 were between 31-34.8, and my ct values for primer2 and primer 3 were all consistently 35, and primers 4-6 gave no result at all.
For the region that is common to several transcripts of this gene, the ct values were between 30-34 for one primer, and consistently 35 for another primer.
For GAPDH, ct values were around 22.
Can I use these results to indicate that my transcript exists (or even may exist?) in the samples I tested? Is the fact that the ct values for the region unique to the transcript I am targeting and the region in common between several transcripts are quite close indicative of anything? On the graph from the qPCR, there are distinct rises respectively around 33 and 35 for the unique region amplicon.
EDIT: I was doing a bit more research, and it appeared that this study: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4296690/
also had results that came up "late cp call last five cycles has higher uncertainty" and considered these results positive if they could be replicated in a duplicate - if I were to show this as well, can I use this data in a paper?

What have you done to validate the conditions of your reverse-transcription and real-time PCR with respect to these transcripts? Can you get more input mRNA (say, enough so that $C_t$ values for GAPDH are well under 20)? Is the final PCR product for your transcript-specific primers at least the correct size based on your predicted transcript? Note that $C_t$ values differing by 4 units represent 16-fold differences in transcript abundance.

@EdM Well the mRNA was converted to cDNA quite a long time ago, and I simply ran a qpcr on the cDNA- the transcript I am trying to validate is a novel predicted one, so I guess I have not done anything to validate the conditions of the reaction specific to this transcript. The concentration of cDNA I used was 100 nanograms / microliter, so I guess I could try to increase the cDNA amount. How would I know if my product is the correct size from a qPCR? I am planning on establishing a concentration curve next Monday for the primer that seemed to work the best.

@pMarkov you validate PCR product size by running regular old-fashioned PCR with your primer pair of interest, and run the reaction out on a gel with a ladder for reference.

@MattDMo, ah silly me, thank you, I'll be sure to do that as soon as possible.

If you can't replicate the biological experiment, all the re-analysis of old cDNA isn't going to be good enough. Reproduce the conditions that led to the hypothesized production of the novel transcript, at a scale that allows better control of PCR conditions.

No prob. Sometimes we get too caught up in all the technology in the lab and forget about the simple stuff...

@EdM- could you elaborate a bit on the scale that would give me greater control on the PCR conditions? What types of parameters could I look into altering? The cDNA I am using is derived from the same phenotype that produced this "novel" transcript- I'm trying to validate existence of the transcript (/if primers work) in this abundant cDNA before I proceed to the more precious cDNA from samples I originally detected the transcript in. I was wondering if the results above were indicative enough to proceed testing, or what I could do/parameters to change to get stronger results before I move on

Transcripts from the same gene, and the gene itself, are notorious for low expression- I truly appreciate the advice/help!

To validate the existence of transcripts could be done by sequencing of PCR products amplified if you can deny contamination and amplification from genomic DNA.

When you have one copy of your target cDNA in a PCR tube, theoretically  Ct would be 34 around in an ideal condition: the PCR efficiency is 100%. You might want to check the efficiency of these primer sets.

@243- I'm guessing I would have to clean the qPCR product before I submit it for sequencing?- Usually we design a completely new set of primers from a different software for sequencing. I have not checked primer efficiency- good idea, another test to run next week. Can anyone speak to what (if any) conclusions may be drawn from the results above?

@pMarkov as MattDMo said, do a conventional PCR. Also do a 3'/5' RACE to confirm the actual size.


text:
Why don't our cells merge when their phospholipid membranes touch each other?
Membranes of our cells consist of lipid bilayer (with some other components mixed in).  Why wouldn't those lipid bilayers glue to each other and make the cells merge? If you suppose that it's due to additional components in the membrane that prevent them from gluing together, consider the case of liposomes, which don't contain additional components, but seemingly don't glue as well.
I'm primarily interested in quantitative physical chemistry aspect of the matter.

the membranes are not pure phospholipid double-layers, they contain proteins as well, those proteins have a plethora of functions, one being to prevent two membranes to stick together and merge. (Others being: gluing the membranes together at a distance, transporting chemicals through the membrane, being receptors for chemical signals, ...). But there is of course also an energy barrier due to the orientation of the molecules (with the polar ends sticking out in the water).

Phospholipid bilayers found in cells are usually negatively charged. The phosphate groups repel each other by like charges and prevent two membranes from coming too close to each other. Membranes are also full of proteins and often coated with carbohydrates, which serve to keep membranes from interacting too strongly. See this diagram of a membrane bilayer:

Even this diagram is probably cleaned up.
From a more physical chemistry perspective, the energy barrier for flipping a lipid in a bilayer is pretty high, since the polar head group doesn't like passing through the hydrophobic layer. Bringing two membranes together would require overcoming the charge-charge repulsion and flipping around the inner two layers of lipids, so you go from 4 layers to 2.
Interestingly, there are mechanisms for fusing membranes, such as using cationic lipids. These would turn charge repulsion into charge attraction. The lipid ion pairs tend to have shapes that don't support bilayer formation, and tend to prefer micelle or inverted micelle shapes. These have been utilized to break down vesicle membranes and allow large molecules to pass through, like DNA or proteins, and are used in genetic modification of cells.

Also, SNARE proteins facilitate membrane fusion.

well it's based on the tissue type for example take loose connective tissue which lies under epithelium they don't merge because of the profound matrix separating them while in the epithelium in cuboidal and columnar epithelium at side corner and upper portion of their membranes the two neighboring cells fused completely preventing any flow of material whatever may be the size it's called tight junction and is due to the physical change in lipid layer of both cell causing this adherence.
or if by merging you mean that the cells should remove their barriers (side membranes) to make their self one cell it is also depending on tissue like macro phages becoming giant cells by merging and forming one cell.

Yes, I mean why don't they make giant cells by merging?

well it's due to the enzymes synthesized by macrophages which other cells doesn't show this charesteristics and this fusion doesn't happens itself unless there is a stimulator like bacillus anthracis (causer of tuberculosis) when it enters the body the macrophages can swallow them but can't lyse them so they have to merge... so in that case the alterer of this phenomena is the bacteria mentioned by indirect stimulation of those gene which synthesis those enzymes which take part in fusion of macrophages...so the bottom line is not every cell can synthesis those fusion making enzymes.

I think lipid membranes in mutual contact do in some cases merge, search liposomes. However, this does not always happen, because the membranes have some degree of cohesiveness and quasi-rigidity. This is said to be due to hydrophobic effect - in aqueous environment, the lipid molecules are repelled from water molecules as the latter attract each other much more strongly than lipid molecules do (water molecules are polar + they experience hydrogen bonding).


text:
Which plant is this?
I'm curious what plant this is! I found it at 37°52'23.2"N 122°16'55.3"W (north of Oakland, California, USA).

Strongly seems a member of umbelliferae (apiaceae)

except yellow colour I didn't look it like mustard. Mustard family shows clear-cut racemose inflorescence but this one is umbel cymose

i have at my back yard ,i do not now the name .we have it in Eritrea we call it Chilan smell's good .we use it for holiday decoration.

That's East Indian Fennel. It's a member of the celery family. Every part is edible, including the root and the seeds. It's packed with vitamins, calcium and is used to stop restless leg syndrome, among other ailments. The feathers (leafs) can be used to wrap meat and fish before baking or eaten fresh on a green salad. Once par boiled they lose their licorice taste and can be eaten like steamed spinach. The Italians brought it over in the early 1800s and it flourished. It grows along the freeways of California and other states. I pick large batches of it for my juice extractor and other things. Look up the many medicinal uses of fennel. The flowers look similar to dill.

Welcome to Biology.SE! It isn't clear that this adds anything to the existing answer that actually addresses the question. Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. In particular, you are more likely to get a positive response to an answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. Thank you!

How can you tell the  difference between East Indian Fennel and wild fennel (Foeniculum vulgare)? Is there a difference?

i like it -----

Fennel is native to Europe, so I'm not sure why you would claim this is "East Indian Fennel". If you have any evidence that this is not Foeniculum vulgare please [edit] your post to include that information.

It looks a lot like Queen Anne's Lace, but yellow and with more slender leaves. I believe it's Sweet Fennel (Foeniculum vulgare). It's in the Apiaceae family, which has a lot of edibles: carrots, parsley, fennel, anise, caraway, celery, chervil, cicely, cilantro, cumin, dill, parsnips and more. Black swallowtail butterflies lay their eggs on this, so often you can find a really fine caterpillar on them; bees like the flowers as well.
Apiaceae has 3,700 species spread across 434 genera; it is the 16th-largest family of flowering plants. It has a few poisonous plants, like water hemlock (white flower) and poison hemlock (also white). Wild parsnip has a very similar yellow flower but it's sap is wildly irritating in the medical sense (it will cause pain and blisters); its leaves are very different.

If you crush some of the slender leaves between your fingers, it should smell like fennel (a common spice, e.g. in Italian sausage), or if you aren't familiar with that, a bit licorice-like.

Sweet fennel (left, up to 6 feet tall)        Wild Parsnip (right, 3-5 feet tall)

It does taste like licorice!

@naiad don't be so overconfident because many plants of umbelliferae looks very similar (so difficult to identify), as well there are highly toxic members.  Yes the plants of umbelliferae contains a lot of volatile oils, so have good smell and flavor. Many member from this family used as spices and condiments ('hot-spices').

@AlwaysConfused if I used this procedure, would I be safe? waiting an hour between each step of (1) lick (2) chew small piece, spit out (3) eat small piece (4) eat large piece. and, like, not continuing if it tastes unpleasant

@naiad I don't know.

For your kind information, poison-hemlock, that was given to Socrates, belong to this-family. https://en.wikipedia.org/wiki/Conium_maculatum

Since nothing has been happened I think you need-not to worry, but taste is usually (exceptions are there) not considered as a part of identification protocol. So may be this information possibly will not help in identification since most-other allied members too have pungent taste and strong aroma.

Also, the things described as 'toxic', may be strong or mild. Since nothing serious is happened I think you need not to worry but stay careful next time.

Briefly asking google about poison-hemlock, it seems like http://www.toxinz.com/Demo/6/UExIMDIyLzEwNGg%3D#secrefID0EJJAI I'd actually be fine if I ate a leaf of it (even if I didn't go to a hospital), I just might get painfully sick for several hours.

Poison hemlock has white flowers, is "leafier" (it's more commonly confused with parsley than with fennel), and doesn't smell or taste like licorice.  I would absolutely bet my life on your picture being of fennel based on the flowers alone.  :)  Another differentiator is that you're more likely to find fennel growing in drier areas (it's pretty common on hillsides and roadsides in the Bay Area) whereas hemlock likes moister conditions (usually near a creek or at least a depression in the terrain -- it grows all over Glen Canyon Park for example).


text:
How does spermaceti make a whale float?
In the biochemistry book I'm reading (Box 10-1, Lehninger Principles of Biochemistry), an example is given in whales of how spermaceti (a wax located in the whale head), when at sea level is a liquid, and allows the whale to float due to its buoyancy.
As the whale dives deeper, the wax turns into a solid (due to the colder temperatures), and hence this more dense wax is less buoyant and prevents the whale from floating back up due to the greater density of the seawater at these depths.
My limited understanding is that density effects buoyancy in so far as that the weight of the object displaces an equivalent weight of water. If the quantity of the water displaced is small enough that the surface area of the object isn't completely submerged, it can float.
Now with the whale example, considering the wax is fully enclosed by the head, how would this change in local density effect the buoyancy of the whale as a whole? The weight of the wax still remains the same (in so far as the example used in the book), the only thing that changes is its density inside the whale.
So with a constant weight, and only a variable local density enclosed by an object (the head) and limited to these conditions only (as this is all the example in the book uses), how is this possible?

It's volume, not weight that matters. I assume the solid wax takes up less space, and is therefore less buoyant.

So even if the volume of the head remains the same, this still holds? Ie: the local change in volume of the wax effects the overall buoyancy?

This page and its associated references seem to have your answer. It seems there are a number of hypotheses on the function of spermaceti, with buoyancy control being least likely.

@user4779 Your right that, with mass constant, the volume of water displaced by the head would have to change to affect buoyancy. Either the hand would have to shrink or water you have to be taken inside the organ.

@canadianer That makes sense, a change in volume of the head. Can I conclude the example in the book is misleading? I quote exactly: " When the temperature of the oil is lowered several degrees during
a deep dive, it congeals or crystallizes and becomes
denser. Thus the buoyancy of the whale changes to
match the density of seawater." Without any further specification of any other mechanisms involved, or any reference to volume.

@user4779 here's a different example. Say I have an airtight plastic bag filled with warm liquid wax. I toss it in cold water and it floats, because it's less dense than the water it's displacing. However, if I leave it there and the wax solidifies, it will become more dense (same weight, smaller volume) and may become either neutrally bouyant or it will sink, depending on the exact density change. This is what the example in your book was trying to get at, but apparently facts got in the way...

@MattDMo, interesting, that would explain it. Would this be due to a decrease in the surface area of the plastic bag, or is this irrelevant? For example if there was a large ship. Would putting all the cargo into one central spot versus spreading the cargo out, affect the buoyancy, where the surface area wouldn't change?

@user4779 The plastic bag is irrelevant, it's just there as a container for the liquid wax. Assume it is infinitely thin and infinitely flexible, with zero effect on the overall process. Buoyancy in water is directly related to the weight of the water that is displaced by an object - if the object weighs less than the weight of the water it displaces, it will float. Remember Archimedes - he was getting into his bath, and his body displaced the water, causing it to overflow the tub. That's what made him run down the street naked yelling "Eureka!" (Greek for "I have found it!"). Supposedly.

If you haven't already, try reading through this. It may help.

The important thing is that yes, the volume of the whale would have to decrease. This is quite normal for animals, every time you urinate, your body decreases its volume, it doesn't replace the urine with an equal volume of air. The surface area is not important in itself.

@MattDMo could you please share, how is this concept be applied to body functions? Clinical wise I found hydrotherapy.

@bonCodigo could you please clarify? What body functions are you talking about?

What version of Lehninger do you have? I just skimmed through section 10 (Lipids) of the 6th edition and found no mention of spermaceti.

This is for the 5th edition, page 347, part 10.1.

The buoyancy theory of the function of the spermaceti organ has essentially no empirical support. On the contrary, there is overwhelming support for the idea that the spermaceti organ, together with the associated structures named the "monkey's muzzle" and the "junk" (named so by whalers) are sound producing and focusing structures. The sound production theory was originally proposed by Norris and Harvey (1972) and has gained substantial support from experimental studies within the last decades. See for example Møhl et al (2003). In brief, the sounds are produced by air being pressed through the monkey's muzzle in the front of the nose, just below the blowhole. The sound is transmitted through the spermaceti oil in spermaceti organ, reflected by a parabolic mirror created by small air-pockets on the front of the skull and transmitted forward again through spermaceti-filled 'acoustic lenses' (known as the 'junk') below the spermaceti organ and into the water as an extremely directional and powerful sound beam. Next time you happen to see a sperm whale skull in a museum, take a look at the skull and once you see it, it is very difficult to see what else could explain the strange shape of the forehead.
The buoyancy model for the spermaceti organ on the other hand has some severe shortcomings. The theory is that the whale sucks in cold water through the blowhole when it wants to dive, hereby cooling and solidifying the spermaceti. The density increases by this cooling, making the whale sink. When the whale wants to surface, it heats the spermaceti by means of warm blood, whereby it expands and the whale rises. However, this would require a massive blood supply to the nose, inconsistent with anatomy, and the experimental data gathered by data recorders on diving sperm whales have shown no indication of water being inhaled upon diving. On the contrary, observations are entirely consistent with the airways being airfilled during the dive and involved in the sound production (Wahlberg et al. 2005). See also the paper by Cranfort et al (1996) where a plausible evolutionary explanation to the origin of the spermaceti organ is proposed.

Cranford, T. W., Amundin, M. and Norris, K. S. 1996. Functional morphology and homology in the odontocete nasal complex: implications for sound generation. Journal of Morphology 228:223-285.
Norris, K. S. and Harvey, G. W. 1972. A theory for the function of the spermaceti organ of the sperm whale (Physeter catodon L.). Pages 397-417  Animal orientation and navigation. NASA, Washington DC.
Møhl, B., Wahlberg, M., Madsen, P. T., Heerfordt, A. and Lund, A. 2003. The monopulsed nature of sperm whale clicks. Journal of the Acoustical Society of America 114:1143-1154.
Wahlberg, M., Frantzis, A., Alexiadou, P., Madsen, P. T. and Møhl, B. 2005. Click production during breathing in a sperm whale (Physeter macrocephalus) (L). Journal of the Acoustical Society of America 118:3404-3407.

Welcome to Biology.SE. Thank you for taking the tour and putting in the effort to craft what looks to be an excellent answer. I hope we see more from you in the future!

Buoyancy is controlled by "Archimedes' principle", as described in Britannica:

... any body completely or partially submerged in a fluid (gas or liquid) at rest is acted upon by an upward, or buoyant, force, the magnitude of which is equal to the weight of the fluid displaced by the body.

Here the weight is a force, not a mass, so the force that pushes an object is related to the density and volume of the object itself. In this context, considering the spermaceti, it's the temperature of the oil that matters, because it's going to change its density, thus the buoyancy force. However, the example you are referring to is a hypothesis on the spermaceti function developed by Clarke (1978). In summarizing, he stated that sperm whales are almost neutral at the surface, so they need to control their buoyancy in order to dive. So, it's possible they change the vascularization on the head (but also the blubber!) to change the density and descend or ascend.
Still, this remains a hypothesis that has not been confirmed nor rejected. Miller et al. (2004)  found data that don't support the theory proposed by Clarke, as the change in temperature and so density in the spermaceti should not be relevant for buoyancy during dives and sperm whales are not neutral at the surface; moreover, they actively swim while searching for food at the bottom, so they contrast the buoyancy force. A more studied and developed theory for the function of the spermaceti system (with the nasal apparatus) is that sound production and the change in density has a relevant role found for sound transmission.
Full references:

Clarke, M. R. (1978). Buoyancy control as a function of the spermaceti organ in the sperm whale. Journal of the Marine Biological Association of the United Kingdom, 58(1), 27-71;
Miller, P. J., Johnson, M. P., Tyack, P. L., & Terray, E. A. (2004). Swimming gaits, passive drag and buoyancy of diving sperm whales Physeter macrocephalus. Journal of Experimental Biology, 207(11), 1953-1967.

Hey all! It is good practice to provide full academic citations, as links can die.

Good suggestion! Thank you:)

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


text:
Why can't plasma proteins migrate from capillaries?
Why can't plasma proteins shift from capillaries to connective tissue but WBCs can be very rich in connective tissue even though obviously the WBCs had to go through capillaries.  Another example: in alveolar sacs neutrophils are there in the lumen  despite the presence of epithelia of alveolar sacs,  and it can only reach there via capillaries. So, how can they get into lumen despite the epithelia lining? Histology textbooks say that no plasma proteins can enter or leave capillaries, but WBCs (which are much larger than proteins) can move to connective tissue via capillaries?

I believe the white blood cells that invade inflamed areas do so via the lymphatic part of the circulatory system.

WBCs typically invade inflamed tissue through post-capillary venules.

See Leukocyte extravasation.

Cells of the endothelium are joined by tight cell junctions which are impermeable or selectively permeable. Generally, proteins can only migrate through the endothelium via active transcytosis.
Leukocytes (specifically neutrophils, lymphocytes and monocytes) express various adhesion molecules and cytokine receptors which allow them to interact with endothelial cells and facilitate their movement (diapedesis) either between (paracellular) or through (transcellular) the cells. The process of leukocytes leaving the endothelial lumen is known as extravasation.

Carman CV. 2009. Mechanisms for transcellular diapedesis: probing and pathfinding by `invadosome-like protrusions'. J Cell Sci 122:3025-3035.
(C,D) The process of diapedesis, whether during intravasation or extravasation, can occur by two distinct pathways: paracellular or transcellular. (C) Paracellular diapedesis. Leukocytes and endothelial cells coordinately disassemble endothelial cell-cell junctions and open up a gap between two or more endothelial cells (Muller, 2003). (D) Transcellular diapedesis. Leukocytes migrate directly through individual endothelial cells via a transient transcellular pore that leaves endothelial cell-cell junctions intact. Note that the two individual endothelial cells in C and D are distinguished by different shades of pink.

Generally, for plasma proteins to enter the tissue space, they must be able to passively diffuse out of the vessel into the tissue. This requires sufficiently large gaps between the endothelial cells of the vessel wall (and if passing into the lumen, space between the epithelial cells forming the barrier of entry into the lumen.
However, under the proper circumstances, white blood cells can actively invade the tissue across the endothelial barrier, migrate through the tissue, and may even cross over into the tissue lumen. This is a active, highly coordinated process  allowing the white blood cell to bind the endothelium and push its way through a gap and allowing it to bind extracellular matrix proteins to migrate through the tissue to its destination.

Sounds very good, and plausible. There are answers opposed. Why don't you add some reference.

Let me add that during the process of inflammation (e.g., the skin has been infected), there will be foreign materials introduced into the body which are picked up by resident macrophages and dendritic cells, which are basically waiting for this stuff to happen. Once they engulf a foreign particle, they will become activated and start releasing inflammatory molecules which attract other white blood cells to come into the said interstitial tissue (you called it CT). They come in because the capillaries in those areas become permeable to the white blood cells due to WBC-endothelial cell interactions, like adhesins and also the capillary cells (endothelial cells) may separate slightly from each other, forming little gaps, that allow proteins, more fluids to come out with the WBCs. So that's why you get swelling if you injure yourself, like if you broke your bone.. or if you got a pimple and it filled with pus (that's all the WBCs and proteins and plasma coming out of the blood vessels into the interstitium).
The reason why we want WCBs to come out during these times is because they clean up debris (macrophages), kill bacteria (neutrophils, macrophages, T-cells, etc), and the proteins may come out like antibodies, anti-bacterial proteins like complement, etc.
tldr; WBCs extravasate through capillaries in certain situations where they are needed (i.e. inflammation). The process of leukocyte (WBC) extravasation has been described by the other answers so I won't go into detail about it.

welcome to Bio. Please add sources or references. Unreferenced answers don't allow users t background read on the topics discussed.

I'd be interested in reference on "the capillaries in those areas become permeable" which might be different from and opposed to "extravasation". Third, there seems to be uptake and release of protein - LDL, VLDL - via endothelial cells' receptors.  - Is there reference on local lymphocytes (Langerhans) already situated on lumen side, as "somebody's go to do the job" of signalling for permeability (in the first place)?


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Why is it so hard to find the amount of biotin in food?
According to the WHO publications biotin is a thing we need. Although its non toxic, so you can't get too much.
However, excluding a few (small) lists that deal exclusively with biotin content there doesn't generally seem to be any information on how much of it given foods contain. For instance this page gives a very impressive summary of a kiwi, but there is no mention of biotin.
If this is something we need, why is it not normally listed?

Hello, and welcome to Biology Stack exchange. Unfortunately this seems to be a primarily opinion based question and won't result in good quality answers.

Biotin is also called vitamin H or vitamin B7. You might try searching for those.

I'm voting to close this question as off-topic

Apparently, it's really hard to measure biotin levels in food accurately.
From "Determination of the biotin content of select foods using accurate
and sensitive HPLC/avidin binding" (2004, emphasis added):

Total biotin content of 87 foods was determined using acid
  hydrolysis and the HPLC/avidin-binding assay. These values are consistent with published values
  in that meat, fish, poultry, egg, dairy, and some vegetables are relatively rich sources of biotin.
  However, these biotin values disagreed substantially with published values for many foods. Assay
  values varied between 247 times greater than published values for a given food to as much as 36%
  less than the published biotin value. Among 51 foods assayed for which published values were
  available, only seven agreed within analytical variability (720%). We conclude that published values
  for biotin content of foods are likely to be inaccurate.


text:
Do potassium channel blockers affect the resting membrane potential?
I am reading about scorpion venoms and toxins for my bio class and they appear to have a variety of potassium channel blockers. My professor asked "What effect would this have on a neuron?" and naturally two things came to mind

Potassium channels are necessary for repolarization
Potassium channels participate in controlling the concentration gradient of the cell.

I have found evidence in articles supporting the first claim, but I don't know much about the second.
Do potassium channel blockers affect the resting membrane potential?  Would they significantly alter the concentration gradient?

If you can access this paper, that would give a great idea how K+ channel blocking affect action potential.

Potassium channels participate in controlling the concentration gradient of the cell.

I would rephrase this to "Sodium/potassium pumps establish the concentration gradients of sodium and potassium across the cell membrane." Potassium channels do not.

I have found evidence in articles supporting the first claim, but I
  don't know much about the second.

Right; because the channels don't set up concentration gradients.

Do potassium channel blockers affect the resting membrane potential?

If they block the resting state "leak" potassium channels, you bet. The resting membrane potential is largely set by the electrical conductance through those channels. Blocking them would greatly depolarize the cell compared to typical resting membrane potential values. But there are many different potassium channels. You may be thinking of blocking the delayed rectifier potassium channel, which shouldn't do much at all to change the resting membrane potential.

Would they significantly alter the concentration gradient?

Probably not, since though the cell would be losing less potassium through this conductance, what matters more to the concentration gradient of potassium are the sodium/potassium pumps.

Short answer
Scorpion venom mostly affects neuronal firing activity by inhibiting recovery.
Background
There are some 100 subtypes of K+ channels and some 120 different scorpion toxins known. Of this host of toxins, the majority were tested on
Shaker-related channels (subfamily KV1.x). Some peptides were shown to act on the Ca2+-activated K+ channels (KCa1.1, KCa3.1, KCa2.x. The family of so-called g-KTx toxins is specific for the ether-a-go-go family of K+ channels (KV11.x) (Rodriguez de la Vega & Possani, 2004).
The Shaker subfamily and the ether-a-go-go family are all voltage-gated channels and hence closely involved in action potential generation (Coleman et al., 1999; Shepard et al., 2007)]; the Ca2+-activated K+ channels are activated when Ca2+ enters the cell, which is an event typically associated with action potentials too.
Hence, based on this information I conclude that scorpion venom mainly blocks the repolarization phase of neurons, meaning the maximum firing rate will be drastically reduced because recovery is blocked. Neurons can fire, but they will not be able to recover from continuous firing.
Scorpion venom is not strongly associated with potassium leak channels (KCNK family). Although other families may also affect the resting membrane potential, it is the KNCK family that is mostly associated with generating the cell resting membrane potential (Cohen et al., 2009). hence, scorpion venom will not affect the resting membrane potential too much.
References
- Coleman et al., J Neurochem (1999); 73: 849–58
- Rodriguez de la Vega & Possani, Toxicon (2004); 43: 865–875
- Shepard et al., Schizophrenia Bulletin; 33(6): 1263–9
- Cohen et al., Eur Biophys J (2009); 39(1): 61-73


text:
If a blocker prevents repolarization, will the neuron be stuck in a depolarized state forever?
Potassium channels help to repolarize the cell after depolarization. But if the potassium channels are blocked, potassium ions cannot flow out of the cell to increase the membrane potential. Thus, one would expect that, at least for some period of time, the cell would be "stuck" in a depolarized state.
How long can this state last? Can a neuron go on indefinitely in a depolarized state if potassium ion channels are blocked? Will it find some other way to depolarize the cell? Will the cell die?

The voltage-gated potassium channels are there only to swiftly repolarize the membrane potential. Ultimately it is the Na,K-ATPase that has to pump the various ions back where they belong (Na out, K in), also when potassium channels are active. So when the potassium channels are blocked, the Na,K-ATPase will restore the membrane potential, albeit in the order of seconds instead of milliseconds.

That was my intuition, but I couldn't find anyone who would confirm that the pumps have enough power to actually do that sufficiently to  return the membrane potential to its resting voltage. excellent!


text:
Does ATP hydrolysis reaction have a high or low activation energy?
I was recently studying about ATP and how it functions as an energy carrier to all biological processes; however, I came across a confusing and paradoxical statement from two sources:
(at 7:36)
and
(the free response question in the bottom of the page)
Basically, in the video, it says that ATP hydrolysis has a high activation energy which is why all of the ATP isn't randomly used by the cell processes.
And in the free response question, the answer is that ATP hydrolysis has a low activation energy and low free energy making it a spontaneous reaction.
A follow up question is: How then does the ATP of the cell used in a selective way to certain processes only?
Thanks for your help.

High and low are not very descriptive since they are relative. ATP hydrolysis may have a high activation energy compared to some reactions and low when compared to others.  The important point is that the activation energy is sufficiently high enough such that ATP is not rapidly hydrolysed under physiological conditions before it can do useful work. In other words ATP hydrolysis is kinetically unfavourable but thermodynamically favourable. The reaction rate is increased by enzymes (by lowering the activation energy), which couple ATP hydrolysis to other processes to do useful work.
Also, a note on reaction spontaneity: it has nothing to do with activation energy but rather depends on the change in free energy; ATP hydrolysis is spontaneous because it is exergonic.

If we take a look at the Sodium-Potasium pump (action potential), it looks like the ATP activation energy is low for that process. Otherwise it can't support the speed of the signal propogation, can it? Perhaps it's a very integrated complex chain reaction where a receptor actives within the cell, that literally tells, "for this particular work, the ATP activation energy should be pretty low" and so on. I am curious to know how it exactly applies in this scenario.

@bonCodigo I'm not really sure what you're getting at. Enzymes lower the activation energy of reactions.

So the video explanation is more accurate. Yes? And I am also confused in something (I am not sure if it was addressed in the answer or not though ) :How do cells control how ATP is used? Because on a wiki page I read that if ATP and ADP are placed in a water container at equillibrium then all the ATP will be converted to ADP.

@mariam Enzymes control how ATP is used.

The video response is more accurate. In particular, saying that the activation barrier is high enough for the reaction not to occur spontaneously in water means that the activation energy is much higher than the thermal energy, $k_B T$, where $k_B$ is Boltzmann's constant and $T$ is the temperature.
You ask, "How do cells control how ATP is used?". As mentioned in the other answer, this energy barrier is lowered by enzymes, in particular ATPases. These are 'machines', such as for example molecular motors or ion pumps, which have a binding pocket for an ATP. When the ATP comes inside this pocket, the activation barrier is lowered and hydrolysis can happen. And, crucially, these 'machines' then use the released energy to perform some useful task. If hydrolysis happened by itself in water, the released energy would be 'lost' in the form of heat.


text:
Neuroscience book recommendations
I'm looking for a textbook in neuroscience for a rigorous introduction to the topic as an autodidact. I have no prior exposure to the field.
In particular, I'm interested in the chemical mechanisms of enzyme modulation, ideally something similar to Lehninger's Principles of Biochemistry where specific Protein Databank ID's are given, so I can load an enzyme in PyMOL and view where the inhibitors/activators bind, in conjunction with an explanation of the actual pathways involved from a molecular level.
I've read Wade: Organic Chemistry, and a good part of Clayden's Organic Chemistry, before self-studying biochemistry for 6 months, to give a little background of my knowledge.
I'm leaning towards Kandel's Principles of Neuroscience after reading some other suggestions here, but this seems like a gigantic text, and I'm unsure how detailed the biochemistry side of things is (which is my main interest)? Could anyone share some thoughts regarding that, or recommend an alternative smaller text with a specific focus on biochemistry?
I'm also concerned that a large amount of data and publications in the field of neuroscience fail replication (something as high as 60% I believe), so the book would need to contain only factual, widely accepted information and not cutting-edge speculative studies that haven't been replicated and widely accepted. Also, as little pharmaceutical-industry influenced as possible.
Ultimately, my interest lies in understanding how different medications and drugs cause different mental states, their exact pathways and mechanisms, and how they form tolerance. I'd like to one day conduct research in how to minimize said tolerance, eg: reverse receptor desensitization. Which book should I begin with to head towards this goal?
Thanks!

My friend recommended this book Neuroscience by Purves, et al. :)

I realize this was a year and a half ago, but since this question was brought back up: as a (college-taught) neuroscience and biology student, I'm concerned about some of the opinions you mention. Where did you learn that neuroscience data was failing replication? The discussion of how scientific research and theory becomes treated as "factual" can be left for another time, but I'll leave it at this: in a field as new as neuroscience, most studies are, in fact, cutting-edge, and eliminating those will absolutely be detrimental to your understanding of the subject.

I don't have enough rep yet to comment on your question, but I have read the whole of Kandel's Principles of Neural Science in 2nd year of med school (last year) and I thoroughly enjoyed all of it!
I would recommend Part II: Cell and Molecular Biology of the Neuron to you, as this is where most detailed discussion about the molecolular structure of membrane proteins etc. is happening. And that's only about 110 pages. It probably doesn't go as far as what you are looking for, but I found it a very good introduction to the field of ion channels and how they work. The rest of the book is very interesting if you are keen to get a thorough overview of the whole field of neural science, but you won't find too much detail on the biochemical level there. Part III: Synaptic Transmission with about 150 pages is also a very good read.
For a specific focus on biochemistry you'll have to look for another book, but quite likely you'll find good candidates in the Selected Readings at the end of each chapter, here is one example of those lists from chapter 7:


text:
How do other primates treat their fingernails?
Do all primates have to trim their fingernails in some way, or do some primates' fingernails wear off through natural use?
Also, is constant nail growth common to all primates?

Both. Many primates bite their nails. Some do not. It's not species specific.
Chimpanzees, for example, usually bite their nails; some prefer to leave them alone. They do grow continuously, and nails not kept trimmed probably break off (looking at the thickness of those nails, I get the impression that this might be rather painful if they break too short.)
The caption for the picture below (taken from a chimpanzee sanctuary) states

Annie likes to pick Missy’s nose. Missy tolerates it but doesn’t seem to enjoy it. I don’t blame her – Annie doesn’t bite her nails down like the other chimps do.

They bite their toenails as well.

The follow-up question then is how do hunter-gatherer societies treat their nails? I'm just curious if continuously growing nails is one of those vestiges of evolution that lost its purpose. It would make more sense if nails grew to a certain length and then stopped (like body hair does). Continuous growth suggests to me that they're like sharks' teeth, they have to be continuously replaced due to wear.

But none of these require grooming (to the point of necessary discomfort when not treated). You don't really have to do anything about your skin or hair, to the point where if you don't trim them they would cause you significant discomfort on day-to-day activity. Also, body hair certainly doesn't continue to go in length, otherwise most people would look like Chubaka.

What's the evolutionary reason for this?

Why some human beings bite their nails? Because, they are primates - it is inherited way to treat our nails, called onychophagia. While normal in some primates (and this is the way they treat their nails), it is considered abnormal in human.

Abnormal or just gross?


text:
What's the feedback regulation of Thyroid diseases and body temperature?
While going through the feedback regulation, the control of blood glucose level by insulin and glucagon is quite discussed in multiple materials including the textbook. I also understand the basic fever and cold feedback regulation with regards to hypothalumus given in the below picture.

But I am not able to find either a digram or a material that explains the relationship between hypothalamus, pituitary gland and thyroid gland in controling temperature1, specially for those who are suffering from thyroid diseases. e.g. some people with thyroid issues feel too cold or too hot (fingers, hands, legs, skin is quickly cold or hot depending on the external change). Their body seem to fail in maintaining the set point of temperature.
What's the endocrine and feedback regulation behind this1 scenario? What's the hormone pathway? Also in terms of energy, heat and metabolism.


text:
What is the advantage of being tired after having a sex?
When we have a sex with partner, we feel so tired that we don't have any power to do anything. Then it would be disadvantage to the animals, of course humans too, for they are exposed to danger. For example, the predator's atack. But you know, we cannot help having a sex. Then what is the advantage of being tired after having a sex?

Why do you think there should be an advantage to everything that exists? And not everyone feels exhausted after sex.

The reason why we feel relaxed / sleepy after having sex is probably the release of endorphins, i.e. morphine-like chemicals. This is part of what makes the experience pleasurable. In a sense, we are rewarded with endorphins for having sex. Probably, a reason why we evolved this way is we would not mate as much if there was no reward for the behavior, hence the trait favors reproduction. We must sleep anyway. It is more advantageous to do so after having sex (or having eaten for that mater) than to sleep at other times, which would possibly make one miss an opportunity to mate or feed.


text:
Name/Examples of Traits whose benefit is non-obvious and/or which evolve despite apparent mal-adaptivness?
I'm a graduate student in cognitive science doing work on people's explanations and learning, particularly having to do with natural selection.
Often, students misunderstand natural selection as a "goal-directed" process, one in which organisms are directed to adapt towards beneficial traits. This kind of thinking can be tempting, since most evolved traits are beneficial in obvious and straightforward ways.
However, I'm very curious about traits whose benefits are NOT at all obvious, and can only be understood under careful consideration of the evolutionary process.
An prototypical example would be the evolution of altruism, or of homosexuality. But I'm looking for more examples like these, and preferably ones that are more specific/concrete (e.g., the existence of a specific trait/behavior, rather than someone general like altruism).
Any help would be appreciated.

Sounds like something to do with Saltationism and "hopeful monsters". https://en.wikipedia.org/wiki/Saltation_(biology)

Altruism is absolutely beneficial.

@MattDMo the user is looking for examples where the benefit is not obvious, given that an individual might sacrifice itself under altruism I'd say it's a good example. Also ageing http://biology.stackexchange.com/questions/17077/why-does-evolution-not-make-our-life-longer/17091#17091

I got some excellent answers on my cross-post here: https://www.reddit.com/r/biology/comments/3durzm/help_biologists_trying_to_brainstorm_traits_that/


text:
Is numbness the absence of one or all touch sensations?
I am studying the effects of tetrodotoxin and its symptoms when consumed. Numbness is one of the first sensations reported.
But I googled numbness and I couldn't find information about whether this means all touch sensations (e.g. thermal, mechano, etc) have to be absent for numbness or just one specific kind.
My Question:
Can someone

Define numbness
Explain whether numbness is the absence of one or more than one or all touch sensations.

1. This may be of your interest.

I think this is borderline off-topic, since the definition of numbness is basically a semantic issue. However, I assume that numbness can have a technical meaning in the medical field, and that this is what you're after(?).

Yeah, it came up in a homework assignment in my bio class. I just wasn't sure what it meant and brought it here.

The definition of numbness has been answered by yourself, and I will focus on the second part of the question.
In terms of the underlying physiological mechanism behind numbness I think it's good to narrow the question down and focus on local anesthetics, which numb a local area of the body for minor surgical procedures. Cocaine and related compounds have been shown to block not only pain, but also warmth, cold and touch perception, as well as blocking motor function. Cocain and related compounds are basically voltage-gated Na+ channel blockers, but also block K+ channels to some extent. Their affinity to various different channels differs, explaining the differential effects. E.g., pain is blocked more effectively than motor functions (Scholz, 2002).
We all know the feeling of numbness when our limbs are asleep due to restriction of blood flow. Likely all neural activity is blocked here too, as the cutting off of oxygen affects all neurons.
Given the broad range of effects of local anesthetics and restriction of blood flow, I would tentatively conclude that numbness can be interpreted as a reduction of sensitivity of all the senses.
Reference
- Scholz, Br J Anaesth (2002); 89; 52-61

This is much more what I had in mind. To be honest, I thought this was what numbness was before getting into the use of the term.

An Initial clarification of what "loss of sensation" means:

The history in the patient with “numbness” is extremely important. First of all, as with most neurologic complaints, you must determine what the patient means by “numbness.” Some patients are describing loss of sensitivity (anesthesia or hypesthesia) or distorted sensations (paresthesia), which is often described as tingling. Actual loss of sensitivity is more likely to represent true damage to sensory pathways in the nervous system, while paresthesia has a much broader differential. Dysesthesia, that is the perception of an unpleasant (often burning) sensation or allodynia (the perception of innocuous stimuli as being painful) may result from damage to the nervous system or, more commonly, be the manifestation of an underlying painful condition.

Some properties of numbness

The pattern of numbness may help define its origin. Numbness confined to a specific nerve or nerve root distribution (see the maps of dermatomes and peripheral nerve sensory innervation) lead to consideration of peripheral nerve or nerve root damage. Loss of sensation on one side of the body is more likely to result from central nervous system damage and if the sensory loss also involves the same side of the face, you can be sure that the cause is located above the level of the pons.
When there is a clear sensory level (a line on the body, below which sensations are lost), a spinal cord lesion must be suspected. Loss of sensation over the upper limbs or upper part of the trunk bilaterally, with preservation over the lower limbs and buttocks, suggests an expanding intraspinal mass. This so-called “sacral sparing” is seen with intraspinal tumors or syrinxes. Numbness over one side of the face, while being a relatively common presentation of psychiatric disease, can also be caused by damage to the lateral part of the brain stem, or upper spinal cord (spinal tract of the trigeminal). Lateral brain stem damage can also produce a picture of sensory decrease on one side of the head and on the opposite side of the body.

But the article concludes

In summary, the evaluation of numbness can be quite frustrating due to its subjective nature.

So it is in essence a term that can have specific meanings uncertain contexts, but one must be careful to clarify exactly how the term is being used since there isn't one single meaning.
This is all from this link here
https://www.dartmouth.edu/~dons/part_2/chapter_13.html

Does this answer (both of your) your question(s)?

Do you have anything to add? The sum of this seems to be it is subjective. If that is correct, then yes I am satisfied.

I wrote this mainly so that, in case the link breaks, the info is available.

I can add something to question two, which seems unanswered. Let me know if you are interested.

Yes, that will be great. I am going to accept your other answers too by the way. I just have had to mull them over a bit. Thanks for your efforts :)


text:
why do marine organisms orient with their bellies facing downwards?
why do marine organisms orient with their bellies facing downwards (like most creatures) given that they have relatively fewer constraints on their orientations than land or air organisms?

Maybe due to Counter-shading, a type of camouflage.  https://en.wikipedia.org/wiki/Countershading                                                             "A completely different function of animal (and military vehicle) coloration is to camouflage the top and bottom surfaces differently, to match their backgrounds below and above respectively. This was noted, for example, by Frank Evers Beddard in 1892:"

Also, keep in mind that the "belly" can be defined as the part that's pointing downwards in a horizontally-oriented creature such as a fish.

I'll address fish here. It's hard to tell which way is up with many sea-dwelling invertebrates, e.g. sea cucumbers. Sea urchins often are oriented "sideways" if you count their mouths as "down".
All animals normally orient themselves in the most advantageous manner dependent on their situation. Probably the most important determiners are field of vision and the inner ears, which work much like those of humans (who walk upright even if blind.) Unlike land vertebrates, the ear of fish is thought to have evolved as a vestibular organ for balance and orientation in space rather than as an auditory organ. Fish (and other sea creatures) also have other sensory apparatus which orient them, such as lateral lines.
Pipe fish swim in a horizontal manner like other fish, but rest vertically, swaying with the sea grass around it. Flatfish start "normal" but as the eye shifts position to the other side of the head, it will assume a bottom dwelling "sideways" position, with a contorted mouth and a fin squashed against the sand.

“Flatfish are the most asymmetrically-shaped vertebrate to ever live on earth,” says Alexander Schreiber, a flatfish expert at St. Lawrence University. “It sounds likes a really dramatic thing to say, but as far as vertebrates go, it’s true.”

Apparently flatfish brains start to receive stronger signals from one inner ear than the other.

Two organs — the eyes and inner ears — work together to keep typical fish in an upright swimming posture... If the eyes are not receiving the same amount of light on each retina... retinal neurons trigger the brain to tilt the entire animal and set it straight. ...As a fish’s vertical orientation in water changes, the brain combines information from the eyes and ears to figure out which way is up. ...[f]latfish larvae that are deliberately blinded adopt a sideways swimming posture.

When snorkeling, it is not at all uncommon to see any of a number of fish flip to their sides side to get a good look at you (floating above) with one eye, as opposed to maneuvering itself to face you. I imaging they assess the threat; since I wasn't a threat, they would just reorient themselves normally and go about their business.
Whatever aids survival within the parameters they are confined to (were born with) in that niche will be what you see.
The Improbable—but True—Evolutionary Tale of Flatfishes
The Vestibular System and Sense of Equilibrium in Fish


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Are there calcium channel blocking neurotoxins?
I am learning about calcium ion channel blockers (CCBs) and am confused whether there are neurotoxins that are CCBs.

If they exist, what is an example of a CCB neurotoxin?
What animals use CCB neurotoxins as a weapon / defense tool?

This seems like it would be easy to Google. Have you tried?

I did. Several times. I found plenty on sodium. Potassium was easy too. But not CCBs. If you find it, paste the link in bio chat and I can delete this.

Just to clarify, they can be toxic, but it's not clear to me if they are a neurotoxin used by animals in the same way that, for example, tetrodotoxin is.

First hit: http://www.nature.com/nature/journal/v372/n6503/abs/372272a0.html

But they are cone snails. Is that OK?

Yes, my professor mentioned those, although I do not think that she necessarily specified that cone snails contained calcium blockers. Thanks! I can find a bunch of info now

That was so helpful! Thanks again. In future, should I post this sort of "I cant find blah blah" in chat?

You can do that, sure. That's probably a pretty good place to do that. :)


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Why are our muscles limited to 7 Hertz?
I have heard from a (usually very knowledgeable) friend before, that a human can only tap his fingers 7 times per second.
I generalized this to "our muscles are limited to 7 hertz"
When my wife heard this she was like "no way, I'm faster" and we recorded a video of her blinking as fast as she could (her eyes hurt afterwards) and over 5 seconds she averaged exactly 7 blinks per second.
I can't find any articles on the subject, but I did find this video of a drummer doing 1208 beats in 60 sec, setting him up at 20.13hz, meaning 10hz each hand. However if you look at his hand, his muscles are not even really tapping, they are just in a vibration (like a spasm), while holding the drumsticks, which than do all the tapping...
Ussain Bolt sprinted 100m in 9.6 seconds, with 41 steps, that's a little over 4 steps per second.
Both these are very impressive. The drummer sticks out for coordinating his 10 taps per second on each hand, alternating with the other hand, while the motion is certainly faster then our eyes can see.
So what's up with the 7 Hz speed limit? Is it a thing, or did the drummer disprove it? Could the 100m world record be beaten by another 25% when we can find a tall guy capable of doing 7 or even 10 steps per second?

Could you imagine the activity where we need higher frequency for tapping?  Touch screen games? Do we need higher frequency?

I just tabbed a key on my keyboard and got to 182 characters in 20 seconds, so there's that. Anyways, it can either be neurologically limited (i.e. how fast you can switch between the motor unit recruitment for the muscles which antagonize each other for the given moment), as well as muscularly (how fast the muscle can actually contract and relax). This last thing varies widely across muscles, depending on the type of muscle fibers (i.e. which myosin heavy chain form they contain).

This is an interesting question. Is it limited by the speed, feedback mechanisms of nerve transmission, or the compliance-inertial limitations of the muscles? It turns out that the resonance of the human body is different depending on the parts of the body, however all the frequencies are near 7 Hz.

I have timed my personal max clicks/sec on a mouse and consistently get 10+- 1 click per second.

Our muscles are not limited to 7 hertz.
You provide two examples yourself. I can provide a third: world's fastest clapper: 804 claps in 1 minute (video here), which is an average of 13.4 claps/sec -- though, you can see his pace changes so at times he's doing more than that.
What about a non world-record holding example? I can provide one of those as well: I can tap my finger 12x per second (or after 10 attempts, an average of 10.4x (SD=1.02) per second).
@Docscience's answer should help provide some background to better understand the science behind muscle limitations in oscillatory movement.

According to the book, Principles of Animal Locomotion by R. McNeil Alexander, oscillatory movements in animals are limited by an organism's nature in general to minimize metabolic energy costs. The energy capacity, inertial, compliant, and dissipative forces involved in the muscles, tendons, skeleton, and non-actuating load all enter into this cost equation.
Strictly speaking these structures are very difficult to model with any degree of fidelity, and so are often approximated by simple mechanical lumped parameter systems of masses, springs and dashpots. From these simple systems, differential equations can be written, and the frequency that minimizes cost turns out to be the natural frequency - since at the natural frequency the system has the greatest ability to trap, store and re-use energy for the movement.
Size and compliance are therefore the two parameters that matter most. Highest oscillatory speeds are able to occur in the smallest, stiffest muscles, assuming dissipative forces are small and input energy is available.

The human hand-brain reaction time is normally 100ms minimum - 300ms average, which aligns with the frequency that you talk about. There are different types of muscle movement though, and trembling type movements are very fast.
Most trembling in medicine is at 4-8 Hz from Parkinson's disease etc., but orthostatic tremor is characterized by a fast (>12 Hz) rate, which includes teeth chattering and trembling from cold.
Interestingly, your example of a finger movement isn't actually a direct muscular contraction — the muscle of the fingers sit in the forearm, and travel through a ligament and 4 joints, making the contraction indirect.
The jaw can voluntarily chatter at about 4-10 Hz, but it can tremble at well above 12 Hz.
Other muscular actions such as clapping are caused by two sets of independent and opposed strong muscles, flexing independently, which can be synchronized to act very fast at the same speed and up to almost twice the 7 Hz limit you mentioned.


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How to Extract RNA and perform RT-qPCR from very few cells ( ~5,000)?
I am currently conducting an experiment which involves FACS-sorting a specific population of cells using an antibody of interest.
In order to validate the type of cells I have collected using this marker, I want to perform qPCR on their extracted RNA, using certain known cell-type marker primers.
My problem is that in each sorting session, I am only able to collect anywhere from 5,000 - 10,000 cells. Do you know if it is possible to perform RT-qPCR on such a small sample size?
I have collected the cells in 1mL of Trizol.
Would I maybe have to amplify the cDNA after reverse transcription in a general manner ( using random primers)?
Thanks for your help.

Wouldn't hurt to try. With the right primers and enough PCR cycles you should be able to amplify just about anything, maybe not perfectly though.

I think this should be possible, although you will not get very much cDNA, so you probably have only one shot. Besides this: Why are you using so much Trizol, I typically used 1ml for one well of a six well plate, which has ways more cells. When you precipitate, make sure your are using some co-precipitation agent as glycogen, so you won't lose sample. And you will probably not see the RNA pellet with so few cells.

Thanks Chris. How much Trizol would you recommend? I'm using 1mL because I sort into 1.5 Epp tubes and try to prevent the cells from sticking to the walls of the tube when they exit the sorter. Would amplifying all the cDNA after RT make sense? (Non-specific, just random primer amplification?)

Aren't you going to amplify the cDNA in your qPCR anyway? A pre-amplification would probably cause trouble with your data.

I wouldn't pre-amplify the DNA, as this can bring a lot of problems with biasing the ratios between the RNAs. Even if your cells stick to the wall of the tube, if you vortex the tube, the cells will be lysed. See how much Trizol is recommend for which cell number, if I remember correctly, there is a part in the manual. Besides not needing so much Trizol, you will also save money and produce less harmful waste.

1ml trizol is quite a lot. I use that much for ~1 million cells (a well of a 12-well plate- for HeLa. You generally need half of that). You can also try one of the RNA extraction kits. Add DNAse-I to remove any traces of DNA. Don't do a random primer amplification. Take a look here

You can consider use of single-cell RT-qPCR kits such as this one if you have the budget for them. (Note: I have not personally used this kit, just putting out an idea)

The Ambion® Single Cell-to-CT™ Kit contains a complete validated
  workflow for gene expression analysis for samples containing 1–10
  cells. Each kit contains reagents for sample preparation, reverse
  transcription, pre-amplification, and qPCR that have been optimized
  together in a simple workflow that can be completed in only 5 steps
  (see figure).

With good technique, you can reliably perform RT-PCR or RT-qPCR on a sample size of about 100 cells. Some of the comments are correct that you will need to compensate for the reduction of the initial cell input with additional PCR cycles. However, each magnitude in reduction of cells corresponds to about 3 extra PCR cycles (2^3 = 8 ~= 10), so your overall qPCR cycle number will not change significantly.
Since you are dealing with a small amount of cells, and isolating by TRIzol, the pellet could be difficult to see. I would suggest you use something like Glycogen (Glycoblue from Ambion) to co-precipitate the pellet into something more visible. You would add this prior to the Isopropanol to precipitate your nucleic acids.
Your use of extra TRIzol is not a problem unless you're lab is short of money. It will dilute your concentration of nucleic acid, which will make precipitation harder, but using glycogen will compensate for this. Using an amount less than the manual directed ratios can be problematic as it could result in incomplete lysis and denaturation of your cellular components.
As user137 recommends, Pre-amplification of the products is not a good idea as it will likely distort your final results. I'm not sure what gene expressions you're looking at, but it is always a good idea to include multiple housekeeping genes as baselines to calculate your relative expression numbers, provided you have enough RNA isolate to use as input.


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Flower identification: Moscow, Russia
I found this plant near the MSU, Moscow, Russia. Could someone help me to identify it?

Look into species in the Caprifoliaceae family, for instance species in the Knautia genus. The flowers and leafs in your pics look very similar to these.

It looks very similar to Cephalaria gigantea.


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Can a same gene stretch from one chromosome to another separate chromosome?
Can a gene continue on from one chromosome to another separate chromosome? For example, can part of an eye colour gene be on one chromosome and the rest of it be on the next chromosome?

Usually not (as described in the other answer, non-contiguous pieces of DNA are not considered as a part of a single gene). However there are some cases of trans-splicing in which the spliceosome can splice together RNAs arising from different genomic locations. But these are rare and do not have a direct effect on distinct phenotypes such as eye colour, to be classified as genes. Not much progress has happened in this aspect of transcriptomics, actually.

In the small free-living soil nematode, C. elegans, and in many other members of this phylum as well, ~ 85% of nuclear transcripts are trans-spliced to a 22 nt splice-leader sequence (usually just upstream of the AUG translational initiation codon). The splice leader 1 (SL1) is next to the 5S RNA gene: both of themes are repeated about 100 times on the right of the gene cluster on chromosome V.

@mdperry thanks for that information. In fact it has been most well studied in nematodes. There are some trans-splicing databases afaik.

No, a gene is confined to a single chromosome. A gene is characterized by a start sequence in the DNA (among many other things), which indicates that the nucleotides are to be read and transcribed to RNA. This stretch of DNA in the gene is contiguous, although some parts may be skipped in transcription. Because different chromosomes are physically distinct, the cellular machinery would require two start sequences, which really means there are just two separate genes. Instead of finding one eye color gene on multiple chromosomes, you instead find multiple eye color genes on multiple chromosomes.

Gene is usually defined as piece of DNA that produces certain product, be it RNA or polypeptide molecule. In both cases RNA is produced as intermediate or final product. Nature of RNA production from DNA (aka transcription) is such that it requires double-stranded DNA as substrate, that is a continuous polymer of nucleotides.
So, only parts of chromosomes (which are really long linear polymers) can be used as substrate or template for RNA production.
However, regulatory elements, which are extremely important, can be anywhere, as long as they are able to function. Since those elements are just special sequences of DNA that interact with transcription factors and other elements of DNA->RNA machinery, they can be on different chromosome than gene of interest.


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Wolbachia - cytoplasmic incompatibility
I read that cytoplasmic incompatibility in Wolbachia occurs when wolbachia-infected male insects mate with wolbachia-free female insects and produce non-viable offspring. By contrast, wolbachia-infected female hosts produce successful offspring irrespective of the infection status of their mate.
I was wondering - what are the long-term effects of this on the size/structure of a insect population? How will this be different from a non-infected population?


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Is each generation getting older?
So we know that our sperm and egg cells get set aside relatively early so that they aren't going through unnecessary cell divisions and causing DNA damage or telomere shortening, but since each new generation starts from one cell each generation has germ cells that have divided more than the previous generation's germ cells.
So, does this have an effect on age?
Is a second generation baby technically older than a first generation baby due to these extra cell divisions, or is telomerase and DNA repair able to keep each generation at the same relative life span?

In germ cells telomerase enzyme is active and elongates telomeres, so youngsters are not born older than their parents due to telomeres.
Still, they do receive mutations, accumulated by their parents' germ-line cells, i.e. eggs and sperm. Most of the mutations occur upon division of the cell. Egg cells don't undergo many divisions - they are created in the course of embryonic development of a woman and then are spent one-by-one. At the same time, precursors of sperm cells divide constantly, thus accumulating mutations at a constant rate.
Got no time to look for a hyperlink, but I read that no matter what is the age of the mother, she gives 15 new single-nucleotide mutations on average to her offspring. Father gives about 10 mutations for each year of his life after reaching puberty, historically 70 on average. Out of those mutations most are neutral or silent (due to genetic code degeneracy), but on average ~1/70 leads to a change in aminoacid sequence of some protein, usually harmful.
So, although babies don't get older, but alas, they get uglier as generations pass :( Natural selection is what saves us from deterioration, so that the weakest are sentenced to childlessness.
EDIT:
Added a couple of hyperlinks as requested: decay of cognitive indicators of children with parent's age:
http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1000040
Another link: drosophila simulation of middle-class neighborhood (MCN) population, where each family has exactly 2 children, son and daughter, and no natural selection pressure is applied: such population rapidly deteriorates with fitness in wilderness decreasing by 2% per generation:
http://www.ncbi.nlm.nih.gov/pubmed/9371795

Can you reference "they get uglier as generations pass"?

@MarchHo added a couple of links to papers about the rate of deterioration of population without natural selection and about negative effect of father's age on child's IQ. I mean that in absence of natural selection, we accumulate the spontaneous mutations in our genetic material and over generations get weaker and weaker.


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Textbook for quantitative biochemistry with thermodynamics, as an alternative to Voet, Voet & Pratt (Fundamentals of Biochemistry)?
I'm looking for a great textbook on biochemistry that covers core topics: relevant aspects of thermodynamics, reaction kinetics, metabolism (e.g. krebs cycle, respiration, etc.). Ideally it would also be quantitative in its approach and use mathematical models where relevant.
The classic textbook is Voet & Voet & Pratt (Fundamentals of Biochemistry) and I think that's a horribly written textbook. It uses concepts before actually defining them (and when it does define them the definitions are obtuse and have no conceptual motivation). Is there an alternative to this? Any recommendations?

Stryer?? As far as I remember it had the most thermodynamics of all other books. Example section. You should add more details on what exactly you are looking for. What level of thermodynamics you want etc. See the tag wiki for [tag:book-recommendation]

I've always liked Lehninger Principles of Biochemistry. Seems like it would be a good book for you.

I would also vote for Stryer. But none of the biochem books do the technical stuff (kinetics, thermodynamics) properly I think. For this, get a copy of Atkins' Physical Chemistry.


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Which step in endocytosis requires ATP?
Everybody seems to agree that endocytosis is an energy-using process, and as such requires ATP hydrolysis. However, which particular step requires it? More precisely, which 'molecular machine' involved in endocytosis requires ATP? I cannot seem to find a good answer in the literature.

Endocytosis can happen through several processes, such as clathrin coated pits or caveolae. Do you have one or the other in mind?

Sorry, yes, I was mainly thinking about clathrin-mediated endocytosis. We can focus on that one.

Endocytosis (specifically you asked about clathrin-mediated endocytosis) is indeed an energy consuming process. the coating of the vesicle may be "spontaneous", but the pinching off of the vesicle, the uncoating of the clathrin, and the transportaion of the vasicle inside the cell all require ATP/GTP hydrolysis.
Dynamin - dynamin forms a spiral around the neck of the vesicle, and uses GTP hydrolysis which in order tighten the coil around the vesicle neck causes it to break and results in the pinching off of the vesicle from the parent membrane.
The uncoating of the clathrin is also ATP/GTP consuming. proteins such as hsp70 chaperon and auxilin is thought to be involved in the ATP hydrolysis. the uncoating process starts after the pinching off of the vesicle.
the tranportation of the vesicle will also cost energy, proteins such as the Myosin family are considered to transport endocytic vesicles into the cell, and use ATP hydrolysis.
Dynamin - Wiki
Myosin  - Wiki
Uncoating process - Molecular Biology Of The Cell ed.6 p.701

Thank you for your answer. I asked this a while ago... Eventually I got a similar answer to yours on Reddit. It seems clear that energy is required for pinch-off and later processes, but perhaps the previous steps can occur spontaneously.