text:
Why "broad" instead of "large" cross-immunoreactivity?
From the articles I read, expressions like "broad cross-immunoreactivity" pops up a lot. So, I was wondering, why "broad" is used here instead of large? Is there a specific reason?

I'm voting to close this because it's about English usage.

@canadianer Stone correctly identified a scientific buzzword by its somewhat awkward placement. This is not about general English usage.

@tel It's a stretch to say that the sentence is referring to broadly neutralizing antibodies, especially without more context. Sometimes broad just means broad.

I vote to re-open, because it fits perfectly under the tag "terminology", which is: "How terms are used or the meaning of words as used in scientific literature".

In this context, "broad" is a buzzword, a piece of scientific jargon. It's a callback to Broadly Neutralizing Antibodies[1], bNAbs. The basic idea with bNAbs is that they target parts of viral proteins that tend not to mutate or change very much between individual strains of some particular virus.
Edit:
To clarify, I am not suggesting that an antibody with "broad cross-immunoreactivity" is the same thing as a bNAb. Immunoreactivity and neutralization are not the same thing (although there is some overlap).

1: Zwick, M. B., Labrijn, A. F., Wang, M., Spenlehauer, C., Saphire, E. O., Binley, J. M., et al. (2001). Broadly Neutralizing Antibodies Targeted to the Membrane-Proximal External Region of Human Immunodeficiency Virus Type 1 Glycoprotein gp41. Journal of Virology, 75(22), 10892–10905. http://doi.org/10.1128/JVI.75.22.10892-10905.2001

Broad means wide as in a wide range. Normally, antibodies have one epitope they recognize, i.e., one specific target; they are said to have a narrow range of targets.
Some antibodies, however, recognize multiple targets, i.e. the number of targets they recognize is larger and their target range is widened. They are said to have a broad cross-immunoreactivity.
A 'large' cross-immunoreactivity, however, is ambiguous, as 'large' can also imply 'large reactivity', and then 'large' becomes synonymous to 'strong'. Wide is unambiguous as it always implies a large range.


text:
What is self-immunoreactivity?
I read something like "some tested variants show self-immunoreactivity". So, what exacly is self-immunoreactivity? Is it something like antibodies induced by a specific variant showing immunoreactivity to this specific variant?

Where did you read this? It would be good to know this to be able to explain the context.

The basic concept of the immune system is that it has to discriminate between self and foreign and that is only allowed to launch an immune reaction against something foreign. This is called immune tolerance which basically makes sure that all immune cells which are directed against the own organism are destroyed.
If these antibodies survive, they can attack the own body (and are hence called self immunoreactive) and cause damage. Self-immunoreativity is a reaction of the body against itself. Problems with the immune tolerance are called autoimmune diseases, examples would be  systemic lupus erythematosus, rheumatoid arthritis or type 1 diabetes.

source: Stack Exchange

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

sort: votes


text:
Do I have to use sucrose to induce a lac promoter?
I'd like to optimize the expression of a Fab fragment in Escherichia coli.
For induction of the lac promoter on the pAK400 vector I use IPTG and sucrose. Do I optimize the expression in case I would just add IPTG?

You can induce the lac operon by two things: Lactose (or more precisely Allolactose a metabolite of it) and lactose analogons which are not metabolized by the bacteria.
Lactose induces the expression and is metabolized while IPTG is not a target of the $\beta$-Galactosidase and will give you a strong and permanent induction. Sucrose will not have any effect on the promoter.

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


text:
What is the trigger of pollen tube formation when the pollen is on the stigma?
What is the mechanism of pollen tube formation when the pollen is close to the stigma ?
Is it because of chemotaxis? In other words, is the growth triggered by some chemical substance that is released by the stigma?
We have learnt that on a stigma of a flower, you can sometimes find pollen of other plant species. Would these pollen grains also form tubes in response to a possible signal from the stigma of a different species?
EDIT :

So in this experiment we put pollen grains in 2 bottles which contained all chemical substance required for the formation of pollen tube.
In bottle 2 we observe that all pollen tubes are oriented to the stigma! If it really is some kind of chemotaxis then what is the chemical substance that causes this?

Germination of the pollen tube begins when the pollen grain becomes hydrated on the tip of the stigma. The pollen grain absorbs water and also exchanges signals with the stigma. Microchannels form between the pollen grain and the tip of the stigma papillae and water is transferred from the stigma to the pollen grain (Taylor 1997). cAMP, which is produced by the protein PSiP, and cytosolic free calcium can be used as signals to orient the pollen tube to grow in the proper direction (Moutinho et al 2001).
Pollen tubes can also germinate in vitro even without contacting a stigma. If you place a pollen grain in germination medium, which contains calcium and boron, among other things, the tube will germinate but it will not grow to its full length.
Often when pollen of a different species lands on the stigma, the pollen will germinate but the pollen tube growth will stop before it reaches the ovary (Ascher and Peloquin 1968). Mating barriers are very complicated, however, and there are many different mechanisms for species recognition and arrest of pollen tube growth. In some cases, the tube is halted in the style while in other cases the tube grows, but slowly and inefficiently (Swanson et al. 2004). Species recognition in some species (for example, tobacco) is related to self-incompatibility and the S-locus. Species recognition can also be unilateral: that is, the pollen of species A can fertilize the ovule of species B, but the pollen of species B cannot fertilize the ovule of species A.
I would recommend that Swanson paper if you want to read more.

Thank you so much ! So the chimiotaxis is just for animals ?! Or calcium is a chimiotaxis ?

@user233658 According to wikipedia, chemotaxis is the movement of an organism in response to chemical stimulus. So yes, this is an example of chemotaxis

But here my teacher told me that the experience ( see edit ) is even not true !

@user233658 Among other things cAMP and cytosolic tree calcium act as the chemicals involved in the chemotaxis


text:
What effects would be caused by exposure to common life forms with opposite enantiomer biology?
Pretend a human had their body "reflected": heart on the wrong side, etc.; but also at the biochemical level: proteins, sugars, cells, DNA, everything.
What would the effects be of that human's exposure to other Earth life?
I assume that quick death from malnutrition would be inevitable, but would there be more immediate life-threatening consequences?
Would anyone who comes into contact with the mirrored person be at risk?
Would reflected bacteria pose an immediate threat to the ecosystem?

The title and the text of the question are pretty different. The answer to the title is that all biological proteins are enantiopure.

I'm going to rephrase it.

dont mix left/right-hand symmetry with anti-matter substances. those would annihilate "normal" matter

I'm not referring to antimatter.  Even if it were a "perfect" reflection it wouldn't be antimatter; only the spins of particles would flip.  (At first I thought the weak force would couple with the wrong-orientation elements, but since it would be an emanation of the same field, there would be no change there either.)

Can the question be reduced to: Can a hypothetical human life form based on D-amino acids survive in our present world? This would, to my opinion, be a rigorous question. Note that the question now is too broad. Also note that folks with partly mirrored organs exist. Until edit I vote to close as too 'broad'.

@AliceD  My question is more specific than your proposal, though.  I don't only mean a human based on D-aminos, I mean a human whose structure exactly matches the reverse: amino acids and proteins, but also simple chemicals like glucose (they would taste the sweetness, but it would provide no energy because it cannot be metabolized).  This is relevant for the "would the bacteria that came with them destroy everything or die" scenario.  I'll try to rephrase the question later today, though.

Please rephrase. It sounds interesting, but as of now it is unclear what you are after. Also, if everything is mirrored, how would you know that glucose will not be metabolized? The issue with hypothetical "what if" questions is that they cannot be answered, only speculated upon. Speculative questions are pretty much always closed. Research on D-amino acids exists afaik and that's why I brought it up as suggestion. Good luck!


text:
Can a lack of sleep degrade balance?
For years, I've noticed that the day after a night of poor sleep (4 hours or less), my balance noticeably degrades. For instance, while walking 20 feet to the coffee maker, I might stumble into the fridge. Is this a shared experience among humans, and is there a physiological explanation for it?
I have noticed that other functions of my body degrade as well (e.g., my ability to focus), but I am particularly interested in the change in my ability to balance.

Welcome to Biology S.E.! If you need additional assistance, please visit The Help Center. I will warn you, this question may be voted to close as being a personal health question. I will try to support this question to keep it from being closed because this isn't something that just you suffer from.

@L.B. It is not a health question, just an observation.

@AliceD Yep. I was concerned some people may view it as a health question.

Short answer
Sleep negatively impacts attention, which in turn impairs balance control in cognitively challenging situations.
Background
Schlesinger et al. (1998) argue that under normal conditions, postural control appears to be automatic, and to require little or no attention in young, healthy adults during quiet standing with full sensory input. However, postural control appears to require increased attention when sensory integration or motor coordination are required. Examples of such challenging conditions where increased attention is required are situations during reduced or conflicting sensory input conditions, or when one is subjected to balance perturbations. The regulation of attention, in turn, is dependent on sleep, because sleep deprivation causes deficits in attention. Hence, although sleep deprivation per se has little or no effect on standing postural control, it can impair postural balance when one has to perform a cognitive challenging task.
Reference
- Schlesinger et al., NeuroReport (1998); 9(1): 49-52


text:
Why sister chromatids and daughter cells but not brother chromatids and son cells?
In biology, why do we have terminologies in terms of female relatoinships such as daughter cells and sister chromatids and not in terms of male relationships. When did this custom started and is there a reason for it ?

During the days when philosophers used to debate, they tended to regard  reproduction as a feminine trait. So naturally organisms/cells capable of producing offspring are also given a feminine trait. The parent cell is often called the mother cell, and the daughter cells are so named because they eventually become mother cell themselves.
I presume there exists a similar argument for sister chromatids, in that they are identical. When they separate, they are usually termed as undivided chromosomes.

Can you back up this answer with a citation?

@MarchHo Tough to provide a scientific recommendation for this as this is common knowledge. I can link to other places on the web where they say the same thing though..https://answers.yahoo.com/question/index?qid=20070810035548AACEcrl

Abit like why we call ship and storm she. There has yet to be a storm or hurricane called Bob..

@JayCkat But there are plenty of hurricanes with male names!

hmm looks like my reference on meteorology is a bit old. Looks like the practice of naming hurricanes solely after women came to an end in 1978 when men's and women's names were included in the Eastern North Pacific storm lists. In 1979, male and female names were included in lists for the Atlantic and Gulf of Mexico. I feel old.

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


text:
How is it determined in a zygote state of foetus, that which side is mouth and which side is for anus?
After the fertilization when the zygote  is in the growing state to a foetus, the main canal is introduced first, from mouth to anus. But my question is when the canal is created first how does it determine which side is for mouth and which side is for anus?

This question reminded me of the fact that humans are assholes

From my understanding, the location of the initial fold (blastopore) during gastrulation always becomes the anus (in deuterostomes, e.g. humans). I don't know how the polarity of the primitive streak is formed though.

You have enough rep now to  upvote mate.

The gut tube is formed from endoderm that migrates through the primitive streak. Before this, however, the anterior-posterior axis of the embryo is defined by the formation of the streak at the beginning of gastrulation. In mice, which are phylotypic with humans at this stage, the streak forms posteriorly and then extends to the anterior. I'm not sure if you'll be able to find much research on humans, but mice and chicks are quite well studied. That said, I don't know the molecular and cellular mechanisms which define where the primitive streak forms. I don't even know if it is known. How much detail are you looking for? If I find the time, I can try and elaborate on this further. In the mean time, this review looks promising:
http://m.dev.biologists.org/content/136/5/701.long

Thank you so much for the answer. Actually as much research paper and books I studied so far didn't get any particular answer for my question. I will will statisfied if I get to know the determination of position of anterior and posterior axis in which basis. I mean if an anterior and posterior axis is chosen for the purpose then can the place where anterior is present could be for posterior position?  I heard from my teacher that it's determined by a particular protein condrin. Though couldnt understand the answer properly.

And the link is good and sorry couldn't vote up the answer as dont have enough reputation, just joined today.

apparently polarity is already present in the gametes. I tried to formulate an answer but gave up because of the complexity.

@AliceD Is that true of amniotes? Maternal effect is quite contentious in this class.

This wiki-section should be relevant to your answer: Wikipedia: Gastrulation - Formation of the primitive streak, and it contains references to a couple of signalling pathways and protein involved.


text:
When and How do pacemaker cells develop during the cell aggregation process of Dictyostelium discoideum?
I was reading a paper by Tang & Othmer about oscillations and waves in Dictyostelium discoideum. Under certain condition like starvation period in the life cycle of a Dictyostelium discoideum community, they evolve itself into a multicellular organism in a process of cellular aggregation. I have read about Pacemaker cells among these individuals which transmits periodic cAMP and attracts other cells towards them.
So I was wondering: When and How do these Pacemaker cells develop from a "normal" cell into a pacemaker cell excreting cAMP?
References, links or answers would be very helpful for me.

What exactly do you mean: 1) How are they are evolving (into the next coming million years?); 2) How did they evolve (in the last couple of million years?) or 3) How they come into being in a micro environment like an erlenmeyer flask with cAMP floating around (wax and waning effect in a few hours time)?

AliceD : By evolving, I mean how do some cells "become" Pacemakers.

Thanks. I have linked that same article again you linked before, as it is the same literature you are referring to am I right?

@AliceD : Done. I have attached the paper.

We were working on it simultaneously: all good :) Thanks! +1

Yes, this happened twice now.


text:
THYROGLOBULIN (19S) comes to a heavier position than ferritin (51S). Why?
Sedimentation values of thyroglobulin and ferritin containing iron are 19S
[1] and 51S [2], respectively. But, by density gradient centrifuge, it seems thyroglobulin (19S) migrates faster than ferritin (51S). Could anyone explain this?
Figure 3 in this article shows a migration pattern of GE High molecular weight marker containing ferritin and thyroglobulin. Thyroglobulin comes almost at the bottom but ferritin, in the middle, which I did not expect.
PS
I asked GE and confirmed ferritin in the marker contains Fe ions.

Ferritin and iron-containing ferritin are different and the latter
would of course be heavier; it will therefore sediment faster.
Figure 3 of the third article uses thyroglobulin and ferritin as molecular weight markers. For your information thyroglobulin is 650kDa whereas ferritin is 440kDa. Also note that apoferritin i.e. ferritin that is not bound with iron has a sedimentation rate of 18S (from the same article that measures the sedimentation rate of iron bound ferritin - ref#2).

There seems to be some confusion regarding the sedimentation rate of ferritin. From this article:

One molecule of ferritin can bind up to 4500 Fe2+ ions.
  When fully loaded with iron, the ferritin can increase in mass up to
  ca 900 kDa; it then has a sedimentation coefficient of 24S (Chasteen &
  Harrison 1999).

55S for ferritin seems dubious.

I confirmed that ferritin they used contains iron. I directly asked GE because the marker is their product. (I accidentally sent wrong message before.)

@243 There is some confusion with the sedimentation rate measurement of ferritin. See the edit.


text:
Term for trait that is advantageous to a population only as long as it is rare
I remember reading about a concept—in evolutionary biology or natural selection, I think—whereby a particular trait is advantageous to the population or species but only so long as that trait is only exhibited by a minority of the population. That is, the population is more likely to survive if the trait's existence and expression is maintained, but only if that expression is limited to a small percentage of the population. If the trait becomes too common, the selection advantage of having it will decrease, and the fact that most of the population has it may even negatively impact the survivability of that population.
I can't recall where I encountered it. It may have been in the context of reading about ADD, Aspberger's/Autism, neurotypicality, introversion, or mania/OCD. I want to revisit the topic and learn some more about it, but Google is failing me.
Can anyone tell me the name of or term for the concept I'm thinking of?

If I recall correctly, in humans, there is a recessive genetic trait which gives resistance to malaria in the heterozygous state (Tt) but causes  malformed red blood cells in the homozygous recessive state (tt).  Surely, this qualifies as an example, because if the gene is uncommon, the homozygous recessive becomes rare?

@nickalh I don't think that counts as an example. I think the term "heterozygote advantage" more accurately describes the behavior of the sickle-cell condition.

Frequency-dependent selection is the term you are looking for, I believe. Positive frequency-dependent selection encompasses traits that become more advantageous as they become more common. Negative frequency-dependent selection encompasses traits that become more advantageous as they become rarer.

That was it. Looks like I stumbled across the term it via http://en.wikipedia.org/wiki/Highly_sensitive_person. Thanks!


text:
Is there a name for the evolutionary loss of vestigial structures?
Consider a biological structure which no longer benefits an organism, such as the eyes of an organism whose population now lives in total darkness.  I can think of three reasons why such a structure might disappear:
0) Random changes to the structure over time wouldn't be corrected by selection favoring the functional version of the structure, leading to a wider variation where most versions of the structure no longer effectively function.
1) The resources the structure demands could be better spent on structures which are actually being used; e.g. human eyes require a lot of blood that could be used elsewhere.
2) Perhaps the existence of a very complex structure leads to biological problems which would no longer be an issue if the structure were not present; e.g. human breasts plus breast hormones frequently leads to cancer.
Are these three examples reasonable means by which a feature would disappear?  Are there any other possible reasons?
Is there a general name for the phenomenon of evolutionary removal of vestigial features due to those features no longer being useful to a population?

Natural selection?

I'm referring specifically to the loss of unused structures, because I've heard some biology students claim "it doesn't happen" which is overly broad.  It would be useful if there were a name for when "it actually does happen".

Your examples are fine, but in general you should try to avoid "just-so" stories when considering evolutionary events. The truth is always a combination of the kinds of reasons you listed. The most you can say for sure are post-hoc phenomenological observations, ie "The fitness of the population which lost its tails increased relative to the fitness of the population which retained them".

I didn't mean to imply that those reasons were in any way mutually exclusive.

This phenomenon can be (and has been) described as regressive evolution (the loss of a phenotypic trait). There are several reasons why this occurs:

Neutral mutations which become fixed through genetic drift.
Positive selection of regressive mutations that are beneficial.
Pleiotropic antagonism: positive selection for one trait may have the consequence of disrupting another trait which isn't strongly selected for.

The eye degeneration example you chose is a good one because it is well studied in cavefish (which evolved from sighted surface fish and have degenerate eyes). Normal eye development is under the control of the Pax6 transcription factor. Expression of another transcription factor, Shh, reduces Pax6 expression. Shh expression along the embryonic midline is responsible for splitting the eye field bilaterally. Overexpression of Shh in surface fish leads to eye degeneration and, indeed, it was found that cavefish have an expanded Shh expression pattern.
Cavefish have also undergone a behavioural shift to bottom feeding and have become less aggressive to focus more on finding food. As it happens, the expanded Shh expression also causes a widening of the jaw and amplification of taste buds, both of which aid in scooping and sampling the river bottom. Furthermore, increased Shh expression during brain development influences a decrease in aggressiveness and a shift to foraging behaviour.
This is an example of pleiotropic antagonism: positive selection for jaw enhancements and behavioural changes via expanded Shh expression, which increase fitness in cave environments, can explain why the eye degenerated.

Thank you so much for your detailed answer.  By describing the terminology and addressing the subject around it, I think you've helped me understand the underlying concept itself much better.

@TrixieWolf You're welcome

So-called "vestigial" features are defined in a post-hoc fashion as features which do not have a positive correlation with a population's fitness under its current living conditions. There are no special names for the evolutionary processes that lead to their loss, since they are exactly the same evolutionary processes that act upon any feature that has a neutral/negative effect on fitness.


text:
Relationship between toxicity of drugs and negative effects on brain
Are psychoactive drugs with lower lethal doses more neurotoxic (more damaging to the brain)? For example, tetrahydrocannabinol (one of the active components of cannabis) has a much higher lethal dose than benzoylmethylecgonine (cocaine), so could we deduce that cocaine is more damaging to the brain?
Moreover, is a mathematical relationship between neurotoxicity and lethal doses known?

I think this is the wrong way of looking at the question. Neurotoxins are more lethal (have a lower LD50) because less of it is required to kill the organism due to their specific action.

@March Ho I figured it wasn't that simple. My chemistry/biology knowledge is very limited

Short answer
The causes of death after heroin, cocain or cannabis overdose are mainly due to cardiac and respiratory arrest, and not to neurotoxic effects.
Background
The cause of death after a lethal overdose of your mentioned drugs are the following :

Cocaine (lethal dose: 30 mg - 5 g via mucus membrane (EMCDDA)): Cocaine-related deaths are often a result of cardiac arrest followed by an arrest of breathing (NIH). Cardiac effects are mediated via increased sympathetic output and a local anesthetic effect (Schwartz et al., 2010);
THC: (lethal dose: ~1000mg/kg i.v. in primates (Drug library)): No known cases of human fatalities. Toxicity appears as achypnea (rapid breathing), tachycardia (fast heart rate), ataxia, hyperexcitability, and seizures (Fitzgerald et al., 2013), but death seems mostly associated with respiratory arrest and cardiac failure (Drug library);
Heroin: (lethal dose 200 - 2000 mg i.v.(EMCDDA)): overdose often due to respiratory arrest (Anoro et al. 2004) caused by mu-opiate receptor activation in the brainstem (Karch, 2006).

Hence, heroin, THC and cocain are lethal mainly due to peripheral causes (i.e., cardiac and respiratory arrest). Although these effects are mediated, at least partly, through central mechanisms (i.e., occurring in the central nervous system and specifically the brain), the drugs themselves do not cause death because of neurotoxicity.
And a closing comment, with credits to @MarchHo - In general, neurotoxins do not cause death due to neural toxicity per se. Most notably even botulotoxin, being one of the most potent neurotoxins known, causes death due to respiratory failure (CDC).
References
- Anorro et al., Rev Esp Salud Publica (2004); 78(5): 601-8
- Fitzgerald et al., Top Companion Anim Med (2013); 28(1):8-12
- Karch, Drug Abuse Handbook (2006)
- Schwartz et al., Circulation (2010); 122:2558-69

I think that this answer is only partially correct, since almost all (I can't think of one which does not) neurotoxins cause death indirectly via paralysis of nerves or muscles.

@MarchHo - the question is on drugs of abuse.

What I mean is that in general, neurotoxic drugs cannot cause death solely by their neurotoxicity.

@MarchHo - I checked it quickly and you are absolutely right. I'll add a sentence.

Hm, I would say that botulotoxin does indeed cause death because of neurotoxicity; it is simply a peripheral neurotoxin, and since the vagus nerve is paralyzed, death ensues. But if it were not neurotoxic, respiratory arrest would not occur. Things are a bit muddled here. There are lots of neurotoxins; I'd still say their mechanism of action and the cause of death is due to neurotoxicity. I might have to consult a toxicology text. :-/

I would agree with @anongoodnurse. If it is interrupting the normal function of peripheral nerves, then it is a neurotoxic event, usual interfering with ligand receptor binding. That being said, it depends on whether or not you consider pacemaking cardiomyocytes equivalent to neurons, so that disruption of their electrical rhythm would be a neurological event.

@anongoodnurse Ah! I read the title again... It is asking for effects on the brain. Christiaan's answer is placing it in that perspective.


text:
What is the protein sequence taken as input in the Path-A prediction system
Considering the Path-A based metabolic pathway prediction (http://nar.oxfordjournals.org/content/34/suppl_2/W714.short). It uses machine learning for pathway prediction. Suppose that the input was a protein sequence of a query organism. I do not understand what these protein sequences are? Are these the enzymes for the reactions?

The basic algorithm has two inputs: a set of protein sequences from the query organism and a set of model pathways, one for each target pathway.

Not necessarily, they can be enzymes, but they include a lot more (the whole proteome).

It takes a FASTA format file containing a set of query protein sequences from a single organism (a partial or complete proteome) and identifies those sequences that are likely to participate in any of its supported metabolic pathways
Path-A predicts the pathways supported by arbitrary sets of proteins, using validated prediction techniques based on sequence alignment and machine learning.

The whole proteome as in the whole genetic sequence available?

@Rishika No, the proteome.

so basically a proteome is the list of all the available proteins in an organism??


text:
Brain regeneration - book recommendation
Searching for an up-to-date book on regenerative brain medicine with a focus on stem cell therapy.
Also interesting in genetic engineering of neuronal stem cells for this purpose.
Alternatively, a comprehensive review article is welcomed too.

I modified the wording - feel free to roll back.

Are you interested in neural regeneration in strictly the CNS, or in the PNS as well?

Neural regeneration is addressed broadly in this chapter from a book published in 2013 (though I would say for a topic such as this, you're probably going to want to read primary literature or recent, less comprehensive reviews in addition to any book chapters published in the few years):
Neural Regeneration by Melissa M. Steward, Akshayalakshmi Sridhar, Jason S. Meyer, published in New Perspectives in Regeneration.
The chapter includes two sections on stem cell therapy and one section on reprogramming of somatic cells to neural lineages.

Regeneration... What a lovely word since 2010
You could start with This text published on 2010 which shows how P21 and it's controller(P53 gene) could regulate regeneration of mammalians' body parts and within them is neurons too.

Regeneration of a hole on ear of MRL mouse or p21 knockout one
This event was accidentally observed ten years before the text get published.
They just couldn't find the ear tagged mice, because there was no hole on their ear anymore.
And you could continue with this text which explains:
p53-Independent Cyclin G Expression in a Group of Mature Neurons and Its Enhanced Expression during Nerve Regeneration
Google Scholar is full of texts, experiments and their results which you need to gadder your information about pathways just by studying and comparing them.
But the most interesting one of them for me was p21 knocked out mice.
As physics helps computation world(Quantum Computers) to do biophysical calculations faster and faster, watching how these proteins and genes play with each other in a 3D simulated human cell like software, will not be a dream anymore.
hope it helps

You've included figures from PNAS, which could get Biology SE in trouble over copyright issues, especially since I do not believe the article in question is Open Access.

PNAS's image is removed and users could have access to it and their related full text through links provided for them while they are open for public if you search on google scholar.


text:
classical conditioning paradigm for hippocampal learning
I wanted to know what a suitable classical conditioning experiment would be to analyze learning and memory capabilities in rodent models with respect to hippocampal long-term potentiation.
For example, I want to subject the animal to conditioning and test the behavioral readout at a certain time point after conditioning. Many , like fear conditioning experiments, are mostly attributed to amygdala processes.
I wish to know some classical conditioning task where I can understand primarily hippocampal processes.
Also is there a way to monitor hippocampal CA1-CA3 firing pattern after the training period or during the training ?
That is, I want to check if LTP will sustain after the training period or is there is any increased sustenance of LTP post training.
But if I am to do this electrophysiological experiment in hippocampal brain slices, how will I incorporate the conditioned and unconditioned aspect to this ?

First of all, your first sentence assumes something which may not be true and is still controversial in the literature. Learning and memory are thought to be related to the phenomenon of LTP but it appears you are taking this as a given.
There is a huge swath of literature on hippocampal-dependent behavioural tests like the Morris-water maze etc so I assume you are already aware of these. If you wish to monitor the HPC firing pattern:
1) during training --- you can set-up an in-vivo electrophysiology platform coupled to a virtual navigation interface and record from cells while the animals are performing a spatial navigation task.
2) after training- you can take slices from the animals as is classically done and try to induce LTP and see if your spatial learning task has influenced the amount of LTP you can get. The condidtioned and unconditioned animals will simply be the two groups which you can compare to see if the behavioural readout(spatial memory task) corresponds to changes in what is though as the cellular basis for memory(LTP)

Whitlock, J.R., Heynen, A.J., Shuler, M.G., and Bear, M.F. (2006). Learning Induces Long-Term Potentiation in the Hippocampus. Science 313, 1093–1097.
Goh, J.J., and Manahan-Vaughan, D. (2013). Synaptic depression in the CA1 region of freely behaving mice is highly dependent on afferent stimulation parameters. Front Integr Neurosci 7.
Heynen, A.J., and Bear, M.F. (2001). Long-Term Potentiation of Thalamocortical Transmission in the Adult Visual Cortex In Vivo. J. Neurosci. 21, 9801–9813.


text:
Why can action potentials not be initiated at dendrites?
Why are action potentials not initiated at dendrites, although dendrites are the first to receive input from the presynaptic cell?
In fact, excitatory postsynaptic potentials (EPSPs) at the dendrites are smaller than in the cell body and axon.
Considering the fact that dendrites have enough voltage gated ion channels, why is it that cation influx through these channels is not able to depolarize the dendrite above threshold and generate an action potential?

What makes you think there are enough voltage gated sodium channels?

@DevonRyan There aren't enough voltage gated sodium channels at  soma and dendrites as there are at the nodes along the axon. But there are VGCCs.So can't action potentials be initiated at dendrites and soma with the help of VGCCs ?What are the channels required for AP?Also how is it that action potentials are initiated at axon hillock,although the input is at dendrites?Why can't enough depolarization happen at dendrites and soma?As a corollary,if enough depolarization cannot occur at dendrites and soma,how then is it propagated to the axon, which is further down anatomically , in the neuron ?

They can't? https://en.wikipedia.org/wiki/Dendritic_spike

The exact site of action potential generation is debated, as is the underlying physiological mechanism (Colbert & Johnsten, 1996). It is generally agreed upon that the initiation site is beyond the soma, at the axon hillock, or even further in the initial segment of the axon.
The reason for the distal axonal initiation site of action potentials is, according to the classical view, that the density of Na+ channels is not high enough in the soma, while the density in the axon initial segment is substantially higher and sufficient. However, it has also been proposed that the threshold of action potential generation is lower at the initial segment (Kole et al., 2008).
Regarding your questions in the comments:

So can't action potentials be initiated at dendrites and soma with the help of VGCCs?
Answer: No. Channel density is too low;
What are the channels required for AP?
Answer: Basically Na+ and K+ channels;
How is it that action potentials are initiated at axon hillock, although the input is at dendrites? Why can't enough depolarization happen at dendrites and soma?
Answer: Either due to a low density of Na+ channels, and/or a higher action potential threshold (e.g., due to the presence of K+ channels in the soma counteraction depolarization);
As a corollary,if enough depolarization cannot occur at dendrites and soma,how then is it propagated to the axon, which is further down anatomically , in the neuron?
Answer: If the EPSP reaches a region with sufficient Na+ channels, depolarization becomes sufficient to activate a critical amount of Na+ channels that causes a sufficient increase in the membrane potential to sustain a full-blown action potential. Along the way, leaky K+ channels decrease the depolarization so a critical amount of channels is necessary, otherwise the EPSP dies out.
What about backpropagating APs from axon hillock to dendrites ? How is that possible?
Answer: the soma and dendritic region are believed to represent too big an electrical load to ensure action potential propagation in both the orthodromic and the antidromic direction. This impedance mismatch can be overcome for an action potential propagating from the axon back into the somato-dendritic region when the initial segment and axon hillock provide additional current. This can be achieved with a high density of sodium channels in that region (Lüscher & Larkum, 1998).

References
- Colbert & Johnsten, J Neurosci (1996), 16(21): 6676–86
- Kole et al., Nature Neurosci (2008); 11: 178-86
- Lüscher & Larkum, J Neurophysiol (1998); 80(2): 715-29


text:
Is the blastocyst a coeloblastula?
A coeloblastula is that type of blastula which has a fluid-filled cavity. Since the blastocyst of mammals has a fluid-filled cavity too, can it be called a coeloblastula? My book however mentions the two as different, and it gives the frog as an example of animals having the coeloblastula and mammals as an example of having the blastocyst.

What book are your using? Can you post a quote?

This is a bit tricky.
The blastocoel in e.g. amphibians separates ectoderm from endoderm and prevents cells of the blastocoel roof from inductive influence of vegetal cells. If you cut out the marginal zone and squish the roof onto vegetal cells, you will end up with mesoderm only:

Blastocoel is not homologous to blastocystic cavity. One could consider a tiny space between epiblast and hypoblast during gastrulation as a homologue of blastocoel, this however does not appear in mice. Blastocystic cavity forms at 32-cell stage thanks to Na+/K+ pumps as well as aquaporins. The inner cell mass is a mixture of cells expressing Gata6 and Nanog, which will form hypoblast and epiblast respectively.
But worry not, many people still call that cavity a blastocoel, in fact, I've seen it happen on Wikipedia. Anyway, I'd still recommend using separate terms for coeloblastula and blastocyst due to the non-homologous nature of blastocystic cavity and the blastocoel.

My sources:

https://kjcscientific.wordpress.com/project-excalibur/
Gilbert's Developmental Biology
Ćwiczenia z Biologii Rozwoju Zwierząt [Marek Maleszewski et al., University of Warsaw, Polish language publication]


text:
Does "mind" has any physical reality in biology? Or is it just an assumptive concept?
Biologically,  Brain controls our thinking,  ideas,  decisions everything along with controlling each body parts. My question is,  is there anything real as "mind "?  If it's controlled by brain then how does brain controls the mind?

This might be a better question for the Psychology SE.  Neuropsychology studies the relationship between the brain and the mind, to an extent.  Neurology can touch on this, however, because self-report of experiences (as unreliable as it may be) is often the easiest way to get information about the mind.  A patient describing depersonalization isn't describing anything that you can measure easily without talking to the person, for one.  I'll try to answer below.

@TrixieWolf - Psychology SE does not exist as separate entity anymore. Please refer users to Cognitive Sciences instead.

@AliceD  Thanks.  I apologise for not checking first (I belong there more than here anyway).

@TrixieWolf - Please don't apologize :) I have been pointed out to it myself by others :) Still going through your answer - it looks good, but have to dig it through before upvoting :)

The mind is an abstraction which arises from physical and chemical processes within the brain.  For a crude analogy, think of the brain as an incredibly complex, self-modifying, multithreaded program.  The mind would then be the abstraction arising from the behavior of the program as it runs.  Consciousness would be the abstraction arising from the behavior of one particular thread in the program: a thread which has access to a limited buffer of its own (that thread's) behavior, and control over limited input and output from the body.  All of the other (unconscious) threads may affect the conscious thread, but the conscious thread has very limited access to information about the behavior of the other threads.
Since the conscious part of the mind has access to information about its own behavior, there is actually some recursive looping going on when it comes to thinking and feeling.  The feeling that this goes in circles somehow (which you seem to be expressing) is a common intuition, and it's almost certainly a correct one.  But the manner in which this occurs is not well-understood, and it's definitely not well-understood within biology at the macro level because the brain is unbelievably complex and plastic.  We really don't have a clue how to begin modeling the brain's processes.  This is one reason artificial intelligence is still extremely crude today (despite what Elon Musk and Bill Gates may try to say).
If you want to read a scientifically-inspired theory of from whence consciousness comes, and of how it arises from the brain, I would recommend the book Godel, Escher, Bach by Douglas Hofstadter.  Douglas does a good job of combining computational theory with biology, music, and art to illustrate a theory of consciousness the reader can grasp even if you don't have a strong background in any of those subjects.

+1 - You should definitely check out Cognitive Sciences too! But there's definitely overlap, so don't just run away - expaND :)

The Emperor's New Mind by Roger Penrose is another book on the subject that's worthwhile.


text:
Current along an axon
When an action potential is induced on a neuron, the local transmembrane potential jumps from $E_{\mbox{rest}}$, the resting potential of the neuron, to $E_{\mbox{eq}}$, the equilibrium potential of an ion or group of ions in the vicinty. Current thus travels in and out of a part of the neuron's cell membrane as ions are exchanged during an action potential. This effect repeats itself as the neighboring regions of the membrane are depolarized, causing the action potential to propagate along the neuron's axon.
Take $\Delta Q$ to be the total charge exchanged locally during an action potential, $C$ to be the membrane capacitance, and $\Delta t$ to be the duration of the action potential. While we can approximate the local average current through an neuron's membrane by taking $$I = \frac{\Delta Q}{\Delta t} = C\frac{\Delta V}{\Delta t} = C\frac{E_{\mbox{eq}} - E_{\mbox{rest}}}{\Delta t}$$ Is there a way to approximate current traveling along the axon of the neuron? Is there even such a thing?

I might be wrong here, but do you mean to obtain the current in units of amperes or similar? I presume that's going to be difficult as the capacitance (or inversely resistance) will vary from cell to cell due to different densities and will never be accurate enough for  generalization. Thats why perhaps people measure the voltage rather than current?

@RoverEye, yes, current in amperes. Please feel free to make assumptions about average capacitance or inverse resistance. I'm just looking for a very rough way to model this. Thanks!

Well, the thing is you really cant model a neuron, as there are quite a few types of varying sizes and lengths... there is a ppt online which I found, which my be helpful to you? http://www.columbia.edu/cu/biology/courses/w3004/Lecture5.pdf

Can you clarify what you mean by "current along the axon" by describing a possible measurement that would detect the phenomenon?  There isn't really a current travelling down the axon.  The charges that rush in and out aren't being carried down the axon.  They're part of the mechanical system that makes the wave move, but the speed of the wave is not fundamentally related to the amount of charge apart from how the whole thing works; you could do a similar thing with a pressure wave, etc.

As far as I was able to find there exists two models of the action potential by using RC circuits. Do note that there is no flow of electrons per se across a tube, but rather a migration of potential. See this.
The Hodgkins Huxley model :

The Hodgkin–Huxley model, or conductance-based model, is a mathematical model that describes how action potentials in neurons are initiated and propagated. It is a set of nonlinear differential equations that approximates the electrical characteristics of excitable cells such as neurons and cardiac myocytes, and hence it is a continuous time model

http://en.wikipedia.org/wiki/Hodgkin%E2%80%93Huxley_model
The Fitzhugh-Nagumo model:

The FitzHugh–Nagumo model is a simplified version of the Hodgkin–Huxley model which models in a detailed manner activation and deactivation dynamics of a spiking neuron. In the original papers of FitzHugh, this model was called Bonhoeffer–van der Pol oscillator...

http://en.wikipedia.org/wiki/FitzHugh%E2%80%93Nagumo_model
http://en.wikipedia.org/wiki/Quantitative_models_of_the_action_potential
Hodgkin, Allan L., and Andrew F. Huxley. "Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo." The Journal of physiology 116.4 (1952): 449-472.
Now, I have not dealt with differential equations in quite a while, and hence may not be the best source for explaining the model itself, but I'll try and update the post with what (if anything) I understand.

It would be very helpful if you could explain the terms in the H-H equation in a more physiological context. I am from a non-math background and find it difficult to understand the equation in a bioological perspective

Although it is not a flow of electrons like in an electronic circuit, it is nonetheless current flow which drives action potential propagation. It could be seen as a positive current flow (outward Na+), followed by a negative one (inward K+) going from dendrite to synapse.
In fact, a neuron can be modeled by a a basic electronic circuit with resistors (representing ion channels), capacitors (representing the membrane capacitance) and batteries (representing the various ion charge/concentration gradients that power the action potential), see Fig. 1.

Fig. 1. Model of a neuron. Source: Yale university

Could you please explain the direction of current flow I(Na) and I(K ) in the figure above ?

Of course - Because it is an electronic-circuit model, both Na and K currents flow from + to -, like electrons from a battery.

Usually in a circuit, current flow is from the positive to negative terminal of battery, right ? But here, you have depicted current flow from negative (small bar) to positive (large bar) end ? I may be wrong since I am from a non-phy/math background .

In reality, electrons go from - to +. Often it is still drawn from + to - because it was decided early on (say, in the 1600's) that current goes from + to 1 (electrons and their charge were unknown). Hence, the convention is persistent and + to - is often still in use. I don't like it :)

to - I meant to say, not + to 1 :)


text:
How sterile is sterile when working with nucleic acids to prevent contamination?
I am reading up on preparatory work on working with nucleic acids and a lot of the instructions speak on excessive procedures on cleaning environments with high %ethanol and making sure the equipment is nuclease free, and autoclaved.
Are these sterilization steps really necessary when doing research /running gels? Buying all of this equipment seems very excessive, and given that just one nuclease could compromise my results why bother?

If in doubt, add controls.

Short answer: Yes
Long answer: Depends what you are working with.
DNA: If you are working with DNA, its pretty stable and you can usually get away with a 70% ethanol wash/autoclave (mainly to prevent contamination and obtain consistent results). EDIT: Read Chris's answer also below
RNA: If you are working with RNA well.. whatever you did for DNA doesnt apply anymore. You have to take it to the next level.  You will need to replace everything, you'll need nuclease free water, tubes, reagents and whatnots. Throw out ethanol and bring in RNAZap, DEPC water or something like that.

An RNase free environment is essential when working with RNA samples. There are two main reasons for RNA degradation during RNA analysis.
First, RNA by its very structure is inherently weaker than DNA. RNA is made up of ribose units, which have a highly reactive hydroxyl group on C2 that takes part in RNA-mediated enzymatic events. This makes RNA more chemically labile than DNA. RNA is also more prone to heat degradation than DNA.
Secondly, enzymes that degrade RNA, ribonucleases (RNases) are so ubiquitous and hardy; removing them often proves to be nearly impossible. For example, autoclaving a solution containing bacteria will destroy the bacterial cells but not the RNases released from the cells. Furthermore, even trace amounts of RNases are able to degrade RNA. Note that RNAses are present everywhere (skin, reagents, normal plastic etc).
Therefore, it is essential to avoid inadvertently introducing RNases into the RNA sample during or after the isolation procedure.

Remember that following microbiological aseptical techniques is usually good practice (and a requirement) when working in a molecular biology lab.
There are excellent guides available online for working with RNA:
I took the above paragraph from here:
http://www.bioline.com/us/rna-hints-and-tips
Life tech has a few more tips for you: https://www.lifetechnologies.com/uk/en/home/references/ambion-tech-support/nuclease-enzymes/general-articles/working-with-rna.html
Here is a good pdf to have in your labbook as a reference sheet:http://genomics.no/oslo/uploads/PDFs/workingwithrna.pdf
If this scares you , that's good because when working with RNA there are a million things that can go wrong the first few times you try it. You have to be very careful, and adapting a cavalier attitude such as not bothering is going to come back and haunt you at night...

I tend to disagree. What use will 70% ethanol have on most contaminations? Mostly none, and I even doubt that it will inhibit bacteria (as people only spray it on or do a short wipe).

@Chris What I meant was for surface cleansing. We tend to spray the ethanol and wait a few minutes and then wipe it out ? I was always told that ethanol denatured proteins ?

I keep the surface of my bench clean, so I don't need any extra cleaning before I start working. And yes, ethanol can denaturate proteins, but I wouldn't rely on this. Besides that: Your reaction will take place inside plastic tubes which are clean.

@Chris true that, but I always assume the worst. I was trained in cell biology before mol biology, and yeah... suffice to say I my just have a 70% ethanol spray somewhere in my pocket :)

I do a lot of cell culture, too. And many people spray everything (even the outside of single-packaged plastic pipettes, which will never get into contact with everything.

@Chris Alcohol is a solvent and a solution ;)

First of all, sterility is not necessary. It takes much more effort to reach this than just to wipe down everything with ethanol. What you need is a clean and controlled work environment (but this is something you need anyway to get reproducible results) and good and clean equipment. You will need more precautions for RNA work as RNA is more sensitive and RNAses are ubiquituous, but the general rules are the same. Some remarks from me about it:

There is no need to wipe down everything in your environment before working. Will you DNA touch the desk or the outside of you pipette? Simply wear gloves, use fresh plasticware, do not touch the plasticware with your bare finger and you will be fine.
There is no general need to autoclave everything what you use (unless you explicitly need it sterile). Do not touch the stuff with your bare fingers. Autoclaves can also be a souce for contamination when they are badly maintained or used to also autoclave trash. Plasticware is generally nuclease free, thanks to the production process (melted plastic is not a good place to live on).
If you work with RNA try to set up a separated working space to avoid contaminations by your normal work. If you use glassware, wash it with DEPC treated water and autoclave it to get it RNAse free. Use gloves! Also use a different set of chemicals for this work to avoid cross-contamination. Filter-tips can be a good idea here. Besides being careful, RNA work is no magic but solid handcraft.
If you do PCR try to set up a different work place seperated from your normal work. PCR is very sensitive to contaminations sitting in you pipettes from your normal work. I have seen a number of cases of false positive amplifications from normal work.

Re #1: Many people work with DNA without wearing gloves (including touching the plastic ware), and it rarely causes problems if your tips and the insides of your tubes are clean. Re #4: In many cases (cloning or synthetic biology), it is extremely unlikely that the contaminant would have the right primer annealing sequences to compete with your intended reaction. See for instance Colony PCR, a very "dirty" PCR full of "contaminants".

@Superbest True. But I have also seen people working with sequences (which they cloned) and then used the same set of pipettes to search for the same sequence. It took a while for them to find out that they managed to contaminate their pipettes through inproper pipetting. But otherwise I agree.


text:
How exactly is glyceraldehyde 3-Phosphate reverted to ribulose 1,5-bisphosphate for the continuation of the calvin cycle?
Around 6 molecules of G3P is produced at the end of the Calvin Cycle (light independent reactions of photosynthesis), and 5 of which are reverted back to RuBp.
The general equation that I read is 5 G3P -----> 3 RuBp using 3 ATP.
It however doesn't seem to add up (regarding balancing of the atoms) as 5 phosphates would be converted to 6.
I would appreciate a link to any resource explaining this process in detail.
Thank you and have a nice day ^^

The detailed mechanism is available on http://en.wikipedia.org/wiki/Light-independent_reactions#Steps

You need to account for free phosphates (Pi) that derive from ATP and are released in phosphatase reactions. The regeneration of 3 ribulose-1,5-2P has the overall reaction
5 glyceraldehyde-3P + 3 ATP $\rightarrow$ 3 ribulose-1,5-2P + 3 ADP + 2 Pi
So in total eight phosphates (here counting ATP as 1) are redistributed, 6 of which end up in ribulose-1,5-2P, and two are released as free phosphates. (These Pi are then recaptured during ATP synthesis in the light-dependent reactions.)
The above is a summary reaction of course; the complete scheme involves 10 enzymatic reactions that rearrange carbons in various ways to form 5-carbon sugars from 3-carbon ones (which takes a bit of juggling of atoms). Release of free Pi occurs in the fructose biphosphatase and seduheptulose biphosphatase steps.
A detailed account can be found in any major biochemistry textbook, like Stryer's Biochemistry. Online resources like MetaCyc can also be helpful.


text:
What would be required to evolve an animal (non-human) brain to obtain human-level cognition?
Could any animal subject to the right conditions evolve human-level intelligence? Suppose that an artificial intelligence (AI) decided to artificially evolve a population of octopus (don't ask why, its for science) by restricting them to calculated environmental pressures, and over millions of years, the AI manages to produce a relative of the octopus that has a similar level of cognition to humans. Is this possible? If it is possible, what are some steps (in general) that might be required to evolve a complex animal brain (to human-level cognition or beyond)?

I think this question is far too broad and answers will probably be opinion-based/speculative, and have therefore voted to close.

@fileunderwater - I disagree. There are many factors identified that have resulted in the development of the human brain. Particularly the cerebral (neo) cortex is associated with higher cognitive skills; the subcortical structures have been very stable during evolution. No need to close this one. The formulation may be a bit awkward (OP is a computer scientist I guess, explaining the question pitch) but i see no reason for closure.

@AliceD Just because something is answerable in some kind of shape and form(at) doesn't mean it is a good fit for the site. This is spanning from neurobiology to evolution, natural selection and evolutionary constrains, is very speculative, and is asking if this scenario is "possible" (by definition "opinion-based"). I just think it is problematic to keep these kinds of questions open, if we aim to treat all questions in a consistent way. However, users of the site will decide if this should be kept open.

@fileunderwater, you might be right, I agree it is a bit of hazy question... It's just interesting stuff. Perhaps i am biased. Perhaps not. I could make a bash at re-writing this question into something more rigid, but somehow I don't like the idea of that...

Answering the question what is needed for a human brain to evolve starting from a cephalopod brain is hard. However, I can expand on what is thought to have been the driving forces behind the evolution of the humanoid brain (Hawks, 2013):
The species of the famous Lucy fossil, Australopithecus afarensis (~3-4 mln yrs ago), had skulls with internal volumes of between 400 and 550 milliliters, which is comparable to chimpanzees and gorillas. Australopithecine brains started to show subtle changes in structure and shape as compared with apes. however. For instance, the neocortex was expanding, which is an indication that the evolutionary pressure on higher functions of the brain was important.
Homo habilis, the first of our genus Homo, who appeared 1.9 million years ago, saw a modest hop in brain size, including an expansion of a language-connected part of the frontal lobe called Broca's area. The first fossil skulls of Homo erectus, 1.8 million years ago, had brains averaging a bit larger than 600 ml. This shows that language development is a likely factor that has driven evolution of the human brain.
By 500,000 years ago, the humanoid brain reached a volume of about 1,000 ml. Early Homo sapiens had brains within the range of people today, averaging 1,200 ml or more. It is thought that cultural and linguistic complexity, dietary needs and technological prowess took a significant leap forward at this stage, and that our brains grew to accommodate the changes. The shape changes we see accentuate the regions related to depth of planning, communication, problem solving and other more advanced cognitive functions.
Interestingly, in the past 10,000 years of human existence the brain actually shrank. Limited nutrition in agricultural populations may have been an important driver of this trend. Industrial societies in the past 100 years, however, have seen brain size rebound as nutrition increased and disease declined (Hawks, 2013).
Indeed, one of the driving components behind the expansion of the human brain is increased availability of fatty fish to sustain the large amounts of fat needed in a brain - survival of the fattest (Cunnane, 2006).
Although the past does not predict future evolution, a greater integration with technology may lead to further expansion of the human brain (Hawks, 2013).
References
- Cunnane, Med Sci (Paris) (2006); 22(6-7):659-63
- Hawks, Sci Am (2013)

but "what are some steps (in general) that might be required to evolve a complex animal brain"?

The bolded-out points in my answer are some essential human skills on which evolutionary pressure may have had its effects driving evolution (as to the question title: requirements). I have, admittedly, not directly attempted to answer the question what steps are needed. I find steps needed a vague term, and open for various interpretations (spanning molecular level to anatomical levels). Instead, I have focused on the what was important for early humanoids and how did that affect the brain. This is less opinion based from my point of view.


text:
How do bumblebees and hornets avoid the negative effects of inbreeding?
I just learned that all hornets and bumblebees except for the queen die at the end of the year and the queen starts a new nest in spring.
But that means the next generation of queens have only brothers to breed with.
Should this lead to severe inbreeding, which over a couple of years would cause serious problems for survival?

As far as I know, the drones leave their nests before the end of the season and try to mate with the young queens that arise at the end of the summer. This way there is mixing of genes and also they avoid inbreeding.

@Chris this should be an answer I think.

I can do that, but I have to at least look up where I read this.

Queens do not generally breed with their brothers, but with males from other nests. In the life cycle of bees (and other social Hymenoptera), new queens are born late in the season along with haploid male drones. These all leave the nest and disperse in the landscape to find mates to reproduce with. After mating, all males die and the queens overwinter to start new colonies next spring. The situation is therefore not all that different compared to other annual, semelparous (single reproductive event) species, since you have population mixing before mating and reproduction.
Here are a couple of mechanisms that bees avoid inbreeding:

Population mixing before reproduction (see above).
Inbreeding avoidance
That queens prefer not to mate with close relatives has been shown in several species, see e.g. Foster (1992) and Whitehorn et al (2009).
Polyandry
Each queen generally mates with several males (regulary more than 10 in honey bees, see Palmer & Oldroyd, 2000) and stores their sperm to fertilize eggs during the next year, which means that workers and the queens of next year will have different fathers (increasing genetic variability).

References:

Foster. 1992. Nestmate Recognition as an Inbreeding Avoidance Mechanism in Bumble Bees (Hymenoptera: Apidae). Journal of the Kansas Entomological Society 65(3)
Whitehorn et al. 2009. Kin recognition and inbreeding reluctance in bumblebees. Apidologie, 40(6)
Palmer & Oldroyd. 2000. Evolution of multiple mating in the genus Apis. Apidologie 31(2)


text:
External sensory stimuli that awaken a person from sleep
An external sound or touch can awaken someone.
Can a light? It would have to be very strong, but part of the reason might be that it would have to penetrate the eyelids.
And can a smell or taste?
When we are awake, the impact of sensory stimuli and of changes in them depend on which sense is stimulated.
My question concerns the kind and strength of impact the stimulation of each sense has when we are asleep, in relation to what is needed to wake us up.
Note
Thanks to @Mithoron for linking to another question, asked on this website by @Taladris. That question is certainly quite similar to this one and its answer contains some relevant material, even if the answer is not of high quality because of course our senses are "dimmed" when we are asleep and of course it is not true that "that we respond to our own names in a similar fashion in sleep and in wakefulness". The present question asks specifically about awakening because of sensory input. I believe I am sometimes awakened by smells, although it is hard for me to tell whether or not I am right. Part of my question asks for views or facts concerning whether people can be woken by smells at all. This is different from asking whether we can smell when we are asleep.

possible duplicate of What senses are active while sleeping?

This is not a duplicate in my opinion, as anongoodnurse's answer on the linked question doesn't address vision.

Can someone please remove the box saying "This question may already have an answer here". I have now edited to explain why this question is different.


text:
Why are abiogenesis and evolution considered unrelated?
When a discussion about evolution comes across abiogenesis - the typical reaction is that they are unrelated (see the headline at http://www.factsnotfantasy.com/abiogenesis.php).
It seems to be that both are stochastic processes in which less ordered structures become ordered.  It seems that, in general, abiogenesis is the process of forming of life (whatever that is) whereas evolution is the process in which life would develop into more complex forms.  In other words, it seems that it's really just two phases of the same type of process and I'm wondering why they are considered as such isolated fields.

I wouldn't go so far as to say that they are entirely unrelated -- our understanding of selective processes can certainly inform our study of the origin of life -- but I would say that they are quite different projects.
One important reason is that evolutionary biologists can use phylogenetic information to reconstruct much of the history of life. For example, genetic sequencing techniques allowed us to definitively work out the evolutionary relationships among humans, chimps, and gorillas. But this approach can only allow us to back as far as the last universal common ancestor (LUCA). LUCA was presumably a DNA-based (uni-)cellular lifeform, given that these characteristcs are shared across the entire tree of life. So we have no phylogenetic information that we can leverage to reconstruct what happened to get us from a soup of organic molecules to LUCA.
Another reason is that evolutionary biology focuses on what happens to a population in which we have variation, heritability, and selection. Early in the origin of life, a structured system of heredity would not yet have arisen and so we would not see natural selection occurring in the form that we usually study it -- though there could be interesting selective dynamics in such a system.

So is the answer is that they use different tools to study the development so the sciences are different?  Eg.  Maybe astrophysics vs pool-table-physics.  Ultimately its the same physics but the types of problems they are solving are different and require different tools and specialized knowledge?  Is that the idea/direction?

Yes, that's right. And not only do we use different tools, the people doing the work are often in different departments. In addition to biologists, chemists, geologists, and atmospheric scientists play an important role in the study of life's origins.


text:
What are the "minimum requirements" for a single cell?
I saw a description of the "minimum requirements" for a cell at http://creation.com/origin-of-life in the section called "What are the minimum requirements for a cell to live?" and I'm wondering if this is scientifically accurate - and if not - what are the real requirements?
[note/warning - the link above is to a creationist site - I'm only quoting this source because I'm trying find the science involved and I didn't find other sources talking about all the necessary pieces. I'm not trying to promote creationism with this question so please don't attack the source or me for bringing it.  If you can find a non-creationist source which outlines these requirements, I'll be happy to update the question and remove this source.)
In summary it lists the requirements as follows:

cell membrane
way of storing information (DNA)
way of reading 2. to make components needed

RNA polymerase
gyrases to untwist DNA
ribosomes to make proteins
(a few others I omitted b/c I don't know if they're really important)

means of creating fuel (ATP synthase)
a means of copying the information for reproduction

The context of the question is similar to Can scientists create totally synthetic life? and a question I wrote What is the most complex biological organism (or precursors) that we have been able to synthesize from raw materials?.
I'm trying to understand what would be involved in making a cell from scratch. Somehow I found this source but I don't know if it's accurate.

An even more minimalistic approach would use a single molecule to do the enzymatic job while storing evolvable informations. In this case RNA alone has been proposed as substitute for proteins and DNA in a very minimal cell. In theory also DNA alone could do the same. However the minimal tasks needed to be done: maintain the self (to be compartimentalized), to grow (to have a flux of molecule not in equilibrium), to divide, to maintain the information stably enough to be useful for the next generation and at the same time prone too mutability to evolve.

So to make cells from scratch you would need: amphiphilic molecules to form a membrane, a decent mix of simple molecules (sugars, nucleic acids, peptides) that serve as reactant and building blocks for more complex things, some simple catalyzer (metals, minerals, pepetides, aptamers, etc..) to run the reactions, enough energy to maintain lots of reactions running and keep them far from the equilibrium. Of course, lots of time...

@alec_djinn - could add you comments as an answer so I could upvote them?

The website is called creation.com; how ironical :P

I don't think this question makes much sense. Just because many cells living today satisfy that list of "requirements", that doesn't mean it's the only way to arrive at self-reproducing entities. If you define life as self-reproduction, then any molecule that catalyses its own synthesis is "alive". Beyond self-replication, the requirements gets pretty arbitrary. If you for some reason list a lipid membrane as "required", then yes you need some lipids. Otherwise not.

I specifically didn't mention the minimum requirements of "life" to avoid these discussions.  I think the concept of a cell is pretty universal and fundamental aspect of all life today. The fact that some people can choose a definition of less sophisticated structures that have characteristics of life is irrelevant for this question.  If you want to make a "cell" (which I think is pretty well defined) - what's involved?

looks like from the discussion below that there are some differences in the definition of a "cell" - but it seems there is more consensus than disagreement.

"so please don't attack the source" Too late. What you will never find at any creationist website are the "minimal requirements for an intelligence/consciousness", because all such known, scientifically demonstrated minds require... you guessed it, brains, cells, DNA and other parts that ID claims require intelligence, which require cells, etc. ID is a circular fallacy and/or relies totally on faith in minds without parts humans need to be intelligent. Furthermore, ID goes backwards from science; simple to complex, and is thus doomed to fail to answer any life or universe-origins questions.

So, to make cells from scratch you would need: amphiphilic molecules to form a membrane, a decent mix of simple molecules (sugars, nucleic acids, peptides) that serve as reactant and building blocks for more complex things, some simple catalyzer (metals, minerals, pepetides, aptamers, etc..) to run the reactions, enough energy to maintain lots of reactions running and keep them far from the equilibrium. Of course, lots of time...
An even more minimalistic approach would use a single molecule to do the enzymatic job while storing evolvable informations. In this case RNA alone has been proposed as substitute for proteins and DNA in a very minimal cell. In theory also DNA alone could do the same. However the minimal tasks needed to be done: maintain the self (to be compartimentalized), to grow (to have a flux of molecule not in equilibrium), to divide, to maintain the information stably enough to be useful for the next generation and at the same time prone too mutability to evolve.
One more point. Life itself doesn't strictly require to be compartmentalized.
You can think of a network of chemical reactions that have the ability to grow, to replicate its components etc but without a cell membrane. However I think that a cell-like form of life is somewhat more likely to happen.

Why a down vote? The answer is pertinent and correct...

I downvoted because it is basically a list of what is needed in a typical cell, not a minimal cell. Hence it doesn't really address the question. Apologies for not commenting earlier. Happy to upvote after edits. Please ping me.

Well, maybe it was not clear enough but as catalysts I have listed metals, mineral and peptides instead enzymes and a have specified that a mix of simple molecules will be needed, this is what would make a cell 'minimal'.Indeed the difference between a minimal cell and a proper cell is the complexity of its building blocks. So, the minimal cell requires the same basic components of a normal cell, but you may expect to have a simpler version of them (less complex, less diverse, less optimized).

Thanks :) good edit and +1 for the RNA enzymatic activity

Cell is the structural and functional unit of life, made up of a small mass of protoplasm delimited by a semi permeable membrane and capable of self reproduction without any living medium. This is a proper definition of cell and the minimal requirements would be all these mentioned here.
You can also see cell theory by M.J. Schleiden and Theodor Schwann.
But most importantly not only genetic information and membrane are required, most required part will be Cell should be capable of self reproduction without any living medium
Like for example RBC is not called cell cause they can't reproduce themselves. But nerve cell is called cell cause though they are not divisible but in embryonic condition the cell division occurred. Also in case of virus, as they can't reproduce without a host,they can't be called cell.
Red blood corpuscles aren't cells have a good proof in this article (check blood trivia part)
red blood corpuscle

Nucleus in case of eukaryotic. But there should be genetic information in prokaryotic cell.

You do realize that the 'C' in 'RBC' stands for 'cell'?

Good to start with a working definition of a cell though, since it is relatively meaningless to answer this question without one. Are your italicized definition a quote or your own?

@fileunderwater actually no. It stands for corpuscle. Not cell. It's very big misconception and sometimes given in book too which is wrong.

@fileunderwater Originally it was called Red Blood Corpuscles.

And I Italicised the definition given in any good book of cell biology. Obviously isn't my own.

@WYSIWYG Well, in that case there seems to be some disagreements, since the American Society of Hematology at least seems to label them Red Blood Cells.

If it does then I am afraid there might be some different logic used there. As you will understand,  RBC is not cell because it can't self reproduce and greatly depend on bone marrow. Where as cell can definitely reproduce itself.

@Demietra95 Well, that's fine. It's just a good idea to add references when you quote something. "Any good book" could be just about everything, and might not be helpful when answers to the question might actually hinge on the specific definition used.

It's probably because they are derived from erythroblast (~immature RBCs), which do have a nucleus. However, the most useful point is probably that definitions of cells aren't black & white. Lots of cells are dependent on other structures to survive (not just RBCs and bone marrow), and the passage "...capable of self reproduction without any living medium" isn't without problems.

For my study I used a book by Sailesh Guha. If it was capable of self reproduction without a living medium then viruses would have been considered as cells. But they doesn't come under cells.

*they don't come under cells  (viruses) .

@fileunderwater Not disagreeing. I just said that originally they were called corpuscles but "red blood cells" is a standard term.

@Demietra95 Incapable of self-reproduction without a living medium goes for many parasites as well, especially obligate intracellular parasites (e.g. some bacteria, fungi and protozoa), but these are arguably still cells.

@fileunderwater I agree with you that there are various intracellular parasites who are incapable of self reproduction and comes under prokaryotes. But they are part of arguments too. In term of evolution they can be defined as the misg link between  molecules

*In term of evolution they are the link between living molecules and and developed cell. But like viruses they are the part of argument whether they are cell or not. Completely It can't be denied neither accepted

I will also recommend you the virology course offered by Columbia University in mooc  where it's seen how they are defined as the neither a complete living cell neither non livings.

@Demietra95 I don't fully understand your last comments. Are you saying that many unicellular (especially intracellular parasites) and maybe some multicellular parasites shouldn't be labelled cells? If so, that would be quite controversial and far outside the mainstream. Also, many intracellular parasites are eukaryotes, not prokaryotes. We should probably move this to chat though.

@fileunderwater according to the proposed cell theory it should  reproduce.  If it doesn't but it has all other living characteristics it doesn't come under a living cell. They stay in a middle portion where neither they can be called living cells neither non living beings. As when they get host, they do reproduce but without it they can't stay alive, they are as good as non living particles. Though I do agree it has many controversies related with it. Even generally in any wiki article or same ranked articles do propose other theories but till now it isn't completely excepted. :)

Here I found a good reference of my words www.redbloodcellbooks.com/rbc7.html check blood trivia part.

Though this may be an old post, there are some things that aren't quite right. First off you are mistaking Terminal Differentiation as not being a cell. Many cells in multicellular organisms are terminally differentiated and will never reproduce themselves. A part of a Red Blood Cells terminal differentiation is to lose most all of its organelles and its genome. Also you make mention of Cell theory, but no where is cell theory does it say that a cell has to be able to replicated itself, only that it arose from a preexisting cell that was living. RBCs fit that definition just fine.


text:
Which wavelength to use to determine algae using a colorimeter?
I am doing a Biology project involving the measurements of the density of algae (Nannochloropsis) using absorbance colorimetry. What wavelength should I set my colorimeter to?
The issue is that there are two types of chlorophyll, each with a different absorbance optimum, there is spectral scatter to consider, as well as UV absorption when going to low wavelengths. What to do?

From Biotek I learned the following:

Spectral scans of algae cultures demonstrate significant absorbance below 400 nm as well as two distinct absorbance peaks at 440 nm and 675 nm (Figure 1). Cell number determination is most consistent when light scatter is used rather than absorbance by cellular constituents. In order to avoid influence from absorbing material 600 nm [is best] to monitor growth.

Figure 1. Absorbance spectral curve of Microcystis aeruginosa suspension cultures.Source: Biotek


text:
How the pattern of fertilization path is determined before the cell division to form the blastocyst? Is it individually specific?
After sperm meets ovum,the inactive nucleus starts following a particular path inside the zygote rather chase a path.This path is biologically known as fertilization path (as mentioned in an article of a local magazine named "science reporter"). But my question is how the pattern of the path is determined?  I came to know from the article that for every individual this particular path is very specific. Is it true?  If so then what does that specific path determine and why is it specific for every individual?

Can anybody please make me understand it?

This is a tad unclear.. are you asking about molecular pathways that underlie embryogenesis starting at fertilization? Even so, this is very broad and there are many players involved. You may need to clarify exactly which aspects need explaining.

Is the article one of these: http://nopr.niscair.res.in/handle/123456789/30751 ?  It seems like "Science Reporter" is behind a pay wall, but I was looking at least for the article.

No..I don't think they post online articles. But I checked. The article isn't from here.

First of all, the more commonly used term is "copulation path," and I don't ether is used as a formal biological term, but rather in models for the public.  The term that is used in literature is "pronuclear fusion" for the process as a whole, and I don't know of a more technical term for the path itself.  Your inability to find information may have been linked to terms used.
Anyway, the copulation path doesn't have as much variability as the penetration path, which is what determines the copulation path.  The copulation path tends to be a relatively straight line between the two pronucleoli, dictated by and pushed along the cytoskeleton (Lian et al, 2014).  It is worth noting that it is often not the shortest straight line (think of the number of lines between a smaller sphere and a larger one), but still a relatively straight line.  People tend to care about this, because what ever the copulation path, it sets the axis of division, which can effect in vitro fertilization techniques, particularly in plants.
Getting at what I think you are trying to ask, the penetration path is variable because it is an oscillatory phenomenon.  You actually have to move back in the fertilization process to the sperm impact angle (Hedrih et al, 2015 is the coolest model I've seen of this) to see how this can change.
To understand oscillatory phenomenon in general, you need to understand that a lot of the processes in biology are driven by the chaotic (used in the formal since) vibrating or shaking of molecules and fluid microcurrents.  This means that we can not know (regardless of how sensitive we measure) the conditions specific enough to create the specific path.  These things are not tied to genes or to the person in general (perhaps exuding of mutations/disorders that effect the morphology of sperm or egg).  Rather it is specific to any single fertilization reaction simple because of chance/chaos.

Thanks a lot. You really understood my problem well and I am sattisfied with your answer.

@Demietra95 It's still not a wonderfully worded question.  The "because I read..." section is both poor grammar and doesn't say where you read it.  You should always include references/links to the source materials you've been looking at that lead into a question.

I am really sorry for my mistakes :( Actually I read it in a local science magazine and there it was referred as fertilization path.

@Demietra95  That's fine, you can go back and edit the question to include a reference to the magazine article.  It doesn't matter if it's not in English.

Thank you so much. Just edited it. Though the magazine is an English science of magazine, it's local,  it's mostly popular in our country but probably not outside.


text:
Why does the inhibition of translation initiation cause the accumulation of 80S ribosomal monosomes?
As I have read in (1), inhibition of translation initiation will increase the number of 80S ribosomes while decreasing the fraction of polysomes due to the polysome-runoff. The net effect is to decrease the polysome/monosome (P/M) ratio and we observe it for example by inducing ER stress by tunicamycin in (2).
I understand the reduction in polysomes - since we don't interefere with elongation, polysomes work as normal, fallling of eventually, but new monosomes cannot proceed to polysomal stage due to inhibited initation.
However, why do the 80S ribosomes accumulate? I have always thought that 80S ribosome is always bound to mRNA, otherwise it dissociates as separate 40S and 60S subunits. Does this effect therefore mean that the accumulated 80S fraction is mRNA-free and therefore "vacant 80S ribosomes", as decribed in (1), can exist?
Thanks a lot!

https://books.google.co.uk/books?id=6sEq1xLu_hcC&pg=PA130&lpg=PA130&dq=polysome+translation+initiation&source=bl&ots=Un6JjImBJX&sig=ln9mn0KoJDJaVOGK8LbrEmMz9XE&hl=cs&sa=X&ei=x2JiVci8N4jX7Ab02YLgBQ&ved=0CGQQ6AEwCw#v=onepage&q=polysome%20translation%20initiation&f=false
http://jcs.biologists.org/content/115/11/2443/F4.large.jpg

It will depend on the drug you are using. There is a pathway that forms the translational initiation complex that starts with binding the mRNA's cap, the small subunit scans to find the AUG, then the large subunit binds, and so on. The 80 S peaks on the density gradients are not vacant, they are poised on mRNAs waiting to initiate (if you removed the inhibitor).


text:
Is Batesian mimicry more important for females?
Myrmarachne plataleoides  is a jumping spider that mimics the Kerengga or weaver ant (Oecophylla smaragdina) in both morphology and behaviour. However, the two sexes appear different:

Myrmarachne plataleoides (Female)

Myrmarachne plataleoides (Male)
Some links suggest that in dimorphic arthropods the females more exactly mimic the model. Is this true? If so, why would this sex difference exist?
Reference
Phyologenetics of mimicry

I slightly edited your question. However, the reference link is empty. I like this question a lot. +1

@AliceD:Sorry I just put insects there, LOL.....thank you for ur answer and edition. You did well

All good! Thanks for the interesting question.

In sexually dimorphic ant-mimicking spiders, it depends on the specific species which sex resembles the ant most (Cushing, 2012).
In many cases of sexually dimorphic spider myrmecomorphs, the male is more mimetic than the female, such as in Corinnidae species and the genus Castianeira, Oonopidae and Antoonops.
Such sexual dimorphism may be adaptive if the sexes are exposed to different predation pressures. The spider's mimicry of noxious ant species yields protective benefit from predators who would avoid the ants. However, the mimicry often results in being more conspicuous in their color markings than related spider species that are more camouflaged. Hence, conspicuousness can be considered a cost of Batesian mimicry. A palatable species may be evolutionary maximizing its level of protection for the smallest cost (in terms of conspicuousness). Sexual dimorphism, in which the more active sex (which, in spiders, is typically the males) evolves mimetic resemblance to noxious ants, whereas the other sex remains relatively more concealed and camouflaged behaviorally and morphologically.
Reference
Cushing, psyche (2012); 151989: 1-24

Great reference - wonderful review of a very interesting association!

"whereas the other sex remains relatively more concealed and camouflaged behaviorally and morphologically." this points towards the female, but the female is the more closest resemblance. Then how could it be called as concealed and camouflaged. Do you mean the resemblance itself is camouflage ?

@Jay, The author says that it is often the males that mimic the ants more closely, see the bolded-out text

The male (Myrmarachne plataleoides) pictured have a pair of fangs, which make it differ from the female counter part. So here the female is the closest mimic and without these fangs the males would be too. I think these fangs are for display.

agreed, totally. it depends on the species.

the article you referred seems awesome.

One more think. male spiders(most males) needs some extra decorations and attachments in order to attract females and catch a fight for sex. The males are considered to be more mimetic but they do have an overhead of putting up these male display, in this case they may vary from the model. Isnt ?

@Jay  - I am not an enthomologist, but from what I understand your theory is correct and mimicry and sexual dimporphism is species dependent. I however don't know if spider males fight, for one thing.


text:
Evolution and Phenotypes.
This may be better suited for the English language SE, but When discussing evolutionary changes in species is it proper to refer to their phenotypes?
In this context:

"Imagine if a cow did not have to cart around however many gallons of
  culture nor expend personal time and effort into chewing its cud. It
  could lose all that anatomy and energy expenditure from its phenotype."

it could just be me, but it sounds strange using it in that context.

Yes, absolutely. That's what a phenotype is (definition from the biology online dictionary):

noun, plural: phenotypes
(1) The physical appearance or biochemical characteristic of an
  organism as a result of the interaction of its genotype and the
  environment.
(2) The expression of a particular trait, for example, skin color,
  height, behavior, etc., according to the individual’s genetic makeup
  and environment.

I don't see anything strange in the sentence you quoted. It is phenotypes that are selected for. Genotype differences that don't affect phenotype will have no selective advantage (or disadvantage) and cannot be acted upon by evolutionary forces. What else would you use when discussing evolutionary changes? That's what the word phenotype is for.


text:
Is missing Q wave characteristic for Wolff-Parkinson-White Syndrome?
No my study books says about that no Q waves in WPW syndrome.
They are about wide QRS complex often however.
I heard today that the characteristic property of WPW is often a missing Q wave, like here

This is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles.
However, some books are about delta waves which is characteristic in the above picture.
However, it is many times very difficult to see.
These missing Q waves are however much easier when PRS complexes.
How much false positives do you get if you categorize all missing Q waves and PRS complexes as WPW syndrome?
How characteristic is the missing Q wave for WPW syndrome?

In Wolff-Parkinson-White syndrome, the normal Q wave is usually masked by the preexcitation action potential which produces the delta wave. Despite this, missing Q wave is not a diagnosis criteria of the syndrome, and up to 70 percent of the patients show a negative delta wave which causes differential diagnosis problems because it is confused with Q, according to Emergency Electrocardiography.

When the delta wave is negative, this simulates a Q-wave. This is known as a pseudo-infarction pattern, and is seen in up to 70% of patients with WPW.

And this negative delta wave also helps in determining action potential origin, according to Medscape.

A general rule is that Q waves (negative delta waves) point away from the earliest site of ventricular activation, which is typically the insertion point of the bypass tract.

No, you can't categorize PRS complexes as WPW syndrome. In fact there is no PRS complex. A classic ECG of WPW will show a shortened PR segment and a widened QRS (or RS or RSr' or however it looks) complex.


text:
Can sugar be absorbed orally within seconds?
Whenever I feel a little light headed or tired, it helps to eat something sweet.
Specifically, simply chewing or sucking on a sweet seems to aleviate the symptoms within a matter of seconds and then the sugar seems to kick in. So I was wondering whether it is just a psychological effect, or whether sugars are absorbed in our mouth and reach the brain (or wherever the sugars exert their effects?) within seconds. Or is perhaps the taste of sugar sufficient to signal the body that it can safely release some extra energy as resupply is imminent?

Welcome to Biology.SE! You can make the experience yourself. Put a piece of bread in your mouth for several minutes. Don't chew (would be cheating) and see how the bread starts to degrade.

@RoryM - is this a duplicate? I think OP is basically asking whether the sugar can kick in within seconds. Although this is addressed in the linked question, it is not answered there as such. I vote to re-open after edits in this question.

@user3461075 - could you verify that it is a few seconds?

@AliceD Thank you. You did point out the essential question of this matter. The effect really occurs within seconds.

@AliceD Speed is answered in the first answer as far as I can tell?

@RoryM - I searched for a reference to 'time taken' several times in the linked question - it's not there afaik

Yes we do. The first part of digestion starts in mouth. Digestion begins in the mouth, where chemical and mechanical digestion occurs. Saliva  produced by the salivary glands (located under the tongue and near the lower jaw), is released into the mouth. Saliva begins to break down the food, moistening it and making it easier to swallow. A digestive enzyme (amylase) in the saliva begins to break down the carbohydrates (starches and sugars).


text:
Where does the term "cos site" come from?
The word cosmid is derived from cos sites of lambda phages.
Why are cos sites called cos sites? What does this "cos" refer to?

"Cos" is the abbreviation of "cohesive end site". This is a speciality of the lambda phage which has to be linearized to fit into the phages head, but circularizes in the host cell. To achieve this, it has the cohesive (or sticky) sites at each end.
See here and also the publication by Allan Campbell on "Bacteriophages".

The 12 bp overlapping sticky ends at the termini of pure lambda DNA are generated during DNA packaging. Another term for this complementary base-pairing is "cohesive" and so cos is an abbreviation of that term. I believe it was italicized because it could also be mapped genetically. Scott Emmons is credited with coining this term (and using it first) when he was a grad student at Stanford.

Cos is for "cohesive," as in these sites rather easily recircularize the linear phage DNA through complementary base-pairing (they're sticky ends, generally G-C rich). See Wikipedia.

The term cos comes from its originator Dr. Scott Emmons.  He coined it by using "co" from the word cohesive and "s" from the word site (cohesive ends site).  He was going to use ces (for cohesive ends site), but decided the term ces was suggestive of sanitary waste.

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