text:
Why do we go blind for a few seconds after switching off the light?
At night, when I switch off the lights, I always seem to go blind for a while. The room becomes pitch black and I am unable to see anything. After a while, however, my vision slowly recovers and I start to see things around me again. I always have to wait a while before my vision returns to that functional state.
I am interested in knowing the mechanism behind this phenomenon. What do we call it?

Short answer
The eyes need to adapt to the low lighting condition after you switch off the lights, a process called dark adaptation.
Background
The process behind the reduced visual function when going from bright ambient light to low-lighting conditions is caused by a process called dark adaptation. The visual system works on a huge intensity scale. The only way to do that is by adapting to ambient lighting intensity.
The sensitivity of our eye can be measured by determining the absolute intensity threshold, i.e., the minimum luminance of a stimulus to produce a visual sensation. This can be measured by placing a subject in a dark room, and increasing the luminance of the test spot until the subject reports its presence.
Dark adaptation refers to how the eye recovers its sensitivity in the dark following exposure to bright light. The sensitivity of the visual system increases approximately 35 times after dark adaptation.
Dark adaptation forms the basis of the Duplicity Theory which states that above a certain luminance level (about 0.03 cd/m2), the cone mechanism is involved in mediating vision, called photopic vision. Below this level, the rod mechanism comes into play providing scotopic (night) vision. The range where two mechanisms are working together is called the mesopic range, as there is not an abrupt transition between the two mechanism.
The dark adaptation curve shown below (Fig. 1) depicts this duplex nature of our visual system. The sensitivity of the rod pathway improves considerably after 5-10 minutes in the dark. Because after you switch off the light the rod system is still inactive, you are unable to perceive much. The reason why rods are inactive is because they are said to be photo bleached. Photo bleaching refers to the visual pigments in the rods and cones to become used up because of the high light intensities when the light was still on. The pigment needs to be regenerated and that takes time.

Fig. 1. Dark adaptation curves of rods and cones. Source: Webvision
Reference
- Kolb et al (eds). Webvision. The organization of the retina and the visual system (2012)

Also this is the reason pirates wore eyepatches (to be able to quick switch between sunlit deck and dark rooms inside ships), and why you should keep your eyes shut or stay in a dark room for several minutes before a telescope session.

@Mindwin There isn't any historical evidence for that theory, beyond the eyepatch wearing pirate being a common trope.

@MJeffryes I stand corrected.http://message.snopes.com/showthread.php?t=86177

Try this, 1- Turn off all the lights in your room for 5 minutes or until you start to make out objects in the room while being in the dark, Now your pupils have adjusted and are in night vision mode. 2- Cover one eye with your palm and turn on the lights. 3- Wait about a minute while keeping the eye closed and covered during the minute. 4- Turn off the lights again and you will be in pitch black darkness, open the covered eye now and "instant night vision"

@TheVoid an easier test, instead of sitting in the dark for 5min, would be to try this in the morning after waking up & before turning on the lights (if the room's dark)

Eyepatch: it works, as illustrated on mythbusters.  Officers whose duities moved between inside and outside woukd have had a competitive advantage if they figured that out.  Btw, I wonder if a red fikter, rather than opaque patch, would work ok.


text:
Do homing pigeons fly straight home or follow certain "highways"?

Homing pigeons (Columba livia) have been prized for their navigational abilities for thousands of years. They’ve served as messengers during war, as a means of long-distance communication, and as prized athletes in international races. (Source)

Do all homing pigeons just pick a direction, and fly "straight" home, or do they all follow certain "tunnels" or "roads" to get closer to their home area, before heading home? (similar to cars getting on a highway between two regions)
Does any information about that exist? I'd be interested to know if pigeons released in the same area (with different target locations in one common direction) tend to do follow the same paths, or if it's just a chaotic crisscross.

Some time ago I saw a TV programme (probably on BBC in the UK) that claimed they follow literal highways, i.e. they mostly navigate by flying above roads and remembering which intersection to turn off at. (But I've no idea how clearly established this is, given that my reference is a TV programme.)

I would guess visual cues alone would not be enough, as pigeons are rarely transported in an airplane while being able to look out the window. Most of the time they are transported on the ground to the place they have to return home from.

@Nathaniel - Homing pigeons do prefer to navigate along roads, railroads, and other long, straight landmarks, according to Mann et al., 2014 and Lipp et al., 2004

They have mental maps of landmarks, which they use as well as "compass" cues:

... experienced birds can accurately complete their memorized routes by using landmarks alone. Nevertheless, we also find that route following is often consistently offset in the expected compass direction, faithfully reproducing the shape of the track, but in parallel.

--Pigeons combine compass and landmark guidance in familiar route navigation
Landmarks are more important than compass cues in general, and pigeons develop their own landmark maps:

we show that homing pigeons (Columba livia) not only come to rely on highly stereotyped yet surprisingly inefficient routes within the local area but are attracted directly back to their individually preferred routes even when released from novel sites off-route. This precise route loyalty demonstrates a reliance on familiar landmarks throughout the flight, which was unexpected under current models of avian navigation.

--Familiar route loyalty implies visual pilotage in the homing pigeon
That means that different birds do use different routes:

Here, we demonstrate that birds develop highly stereotyped yet individually distinctive routes over the landscape, which remain substantially inefficient.

--Homing pigeons develop local route stereotypy
In fact the same bird might use different routes over time as it learns new landmarks:

a wide intraindividual variability was observed in repeated tosses at the same site; some pigeons remained faithful to the first route, whereas other birds tried successive new routes which, in most cases, were significantly shorter than previous ones. This result indicates that pigeons try, and are actually able, to improve their performance in subsequent releases from the same site.

--Pigeon homing: The influence of topographical features in successive releases at the same site

+1 Great answer. To add to this, homing pigeons are also able to sense magnetic fields (magnetoreception), such as that of earth, to assist them in orientation and navigation: https://en.wikipedia.org/wiki/Magnetoreception

Also solar cues, stars, smell, and (according to at least one group of researchers) gravitational anomalies; and they are able to determine when one of these is being messed with and deprecate the unreliable information.

They use the Earths magnetic field to navigate. <References
Mora C. V., Davison C. V., Wild J. M. & Walker M. M. Nature, 432. 508 - 511 (2004). | Article | PubMed | ISI | ChemPort |>

I study sharks and I have found that several things have electroreceptors like cockroaches, bees, platypus and even pigeons. On top of that. Mammals have what is known as magnetite crystals in the brain. A compass works because it is a weaker magnet than that of the earths magnetic field and aligns with the stronger field. I have a feeling that pigeons use a combination of all of this as well as memory of landmarks and such but I am unsure. I study sharks
https://en.m.wikipedia.org/wiki/Magnetoreception#In_homing_pigeons
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC49775/

source: Stack Exchange

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

sort: votes


text:
Can viruses be toxic?
Bacteria can produce toxins like endotoxins and exotoxins. In diseases like cholera or tetanus they can harm infected people due to these toxins.
Now, although viruses are much smaller and are dependent on the host cell for their production, are there DNA sequences in viruses which can produce similar toxins, or are viruses made of something that is toxic?
If not, can viruses be seen as causing an allergic reaction because like common allergies they don't harm directly, only our immune system generates the problems?

In general, DNA that encodes toxins can be incorporated in a viral genome and thus it can be expressed in the infected host inducing toxicity.
Here an example: http://www.sciencedirect.com/science/article/pii/S1438422104000542
Also, viruses can trigger allergic reactions (http://www.ncbi.nlm.nih.gov/pubmed/21980825) or promote them (http://erj.ersjournals.com/content/19/2/341).
Finally, there are some reports about viruses causing "with symptoms that mimic allergies" (https://www.youtube.com/watch?v=iDF07R1XHSk)

"The genes encoding Stx are encoded in the genome of heterogeneous lambdoid prophages (Stx-converting bacteriophages; Stx-phages)" You say in general but is Stx the only known viral toxin? If I understood the article well it comes originally from a bacteriophage but are there also viruses that could programme our own cells by producing toxins?

@Marijn Ofc. not, there are many toxic viruses, e.g. ebola has (at least one) toxin too. http://www.ncbi.nlm.nih.gov/pubmed/15596847

In addition to @alec_djinn's answer, viruses can also indirectly be toxic by causing lysis in cells that themselves have toxic components. The presence of bacterial endotoxins in poorly filtered solutions of early attempts at phage therapy is probably the canonical example of this.

In theory, there's no reason why a virus couldn't encode bacterial toxins. In practice, that doesn't happen much because viruses have no incentive to sabotage their host cells in that manner - there's largely no fitness advantage, all it would do is make the viral genome larger and shut down the host cell preventing further replication.
Even if a virus specifically wanted to shut down its host cells, it's more efficient to spawn large numbers of copies of itself and exhaust the host cell's resources.
in short:
virus produces toxins in host cell -> host cell dies -> no replication opportunity and virus gets trapped in the cell
virus produces large numbers of copies of itself -> host cell runs out of resources and dies -> numerous replications and avoid getting trapped

Yes viruses can import toxin encoding genes, at least in humans and in plants.
With Ebola a protein called Delta-Peptide is released in large amounts by the virus genome, and it attaches to cell walls and makes them more permeable.
it does this to the cell wall, and some researches have described it as ebola toxin.

http://jvi.asm.org/content/early/2017/05/18/JVI.00438-17
https://www.sciencedaily.com/releases/2015/01/150121103304.htm
Toxin from a maize virus:
http://www.sciencedirect.com/science/article/pii/0006291X87903792
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2171720/
Conversely, plants generally use alkaloids as toxins. Alkaloids are a large family of N containing organic molecules, for example those found in Datura, Angel of Death mushroom, Cyanide, etc. and I found no evidence that viruses make us produce alkaloids. Scientists research on the anti-viral abilities of some alkaloids.
Tonins in venoms are more often protein based... Tangentially to your question, here's a page on the diversity of venom toxins for background.
https://en.wikipedia.org/wiki/Venom#Diversity

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


text:
What prevent us from synthesizing a cell from "scratch"?
In this recent article "Design and synthesis of a minimal bacterial genome", they created a minimal cell with only 473 genes. However, they didn't synthesize all of the necessary components of the cell to get going. How much of those extra stuff can we currently synthesize, and what are the ones that we can't synthesize in the lab to create a working cell from scratch?

You mean ribosomes and other cellular organs by "necessary components"?

It is nearly impossible for even nature to create a cell from scratch (this might be debatable). Note that new cells in organisms are made from pre-existing cells via cellular division, and almost all necessary substances are provided to new cell from parent cell only.

Designing/engineering functional proteins from scratch is feasible but would take a ridiculous amount of work. Michael Hecht is one person I know of who has done this (example: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0015364). J Craig Venter wants to determine the minimal set of molecular machines required for life, regardless of their origin. This would begin to illuminate which protein functions are absolutely required for life. I believe we could design and engineer proteins de novo to perform all of those functions in theory, but in practice it would be unrealistic. I think the key point to glean from their synthetic cell is the set of functions, not specific genes, required for life. Those functions could be performed by evolved or synthetic molecules.
As a side note, while I believe that to be the overarching goal, they do note the surprising lack of functional characterization in the syn3.0 genome.


text:
What are cranial nerve nuclei?
I am having a really hard time trying to understand what cranial nerve nuclei are. I have been reading/watching videos and I keep hearing, "that is where the cranial nerves make connection with the brainstem." Also, I keep hearing that some cranial nerves may have multiple nuclei and some nuclei may have multiple nerve synapsing there; however, this information doesn't really help me understand what they are. Are they a processing center? If so, doesn't information get processed in the cortex?
So the main question is: What is a cranial nerve nucleus and what is it's function? What does it mean by "where nerves make connections"?
I am attaching the image which I've been studying. You may refer to that when answering this question.

Nerves (including cranial nerves) are constituted of neurons, and other supporting cells and structures (e.g. myelin sheath and extracellular protein matrix). Neurons are highly specialized cells that have a particular cellular anatomy:

As you can see, the cell body (or soma) contains the nucleus, and projects it's axon towards other structures in the body, sometimes more than a meter away! Cranial nerves (like other nerves) are a collection of the axons, not the cell bodies themselves. The cell bodies reside together, in the brainstem, forming what we call nuclei. So that's simply what they are.

That makes more sense now. I was overthinking a "nucleus". But the reason I was doing that was because of the picture I posted. How would interpret those colored columns and relate them back to this? I am thinking that those colored columns represent different types of nuclei? If so, how do you explain their size?

@JagmeetSingh The colored columns represent the nuclei themselves. The larger they are, the larger the number of cell bodies and the bigger the nerve they project. For example, the sensory part of the CN V (Trigeminal, in blue) innervates the skin of the whole face, whereas CN VI (Abducens, in yellow) innervates one single extra-ocular muscle (the lateral rectus). So you can imagine why the trigeminal sensory nucleus is much larger than the abducens nucleus.

A cranial nerve nucleus is not the nucleus of a nerve cell (neuron). As Wikipedia says, a cranial nerve nucleus is a collection of neurons in the brain stem.

@mgkrebbs That contradicts what Maljam said. Do you know where information (sensory or motor) goes after it synapses at the nuclei and via what medium? Am I even thinking in the right direction? If so, I am slowly starting to understand CN nuclei, even though the long colored columns still confuse me.

The neurons of a CNN connect cranial nerves to the brainstem.  Information flows both ways: sensory neurons within a CNN conduct info from the associated cranial nerve into the brainstem, and motor neurons in the same CNN conduct info in the reverse direction into the same cranial nerve.


text:
Does cancer cells come from same process as evolution?
Here is how I understand it:
DNA replication is not 100% perfect and error can happen, this error can be good(evolution) or bad(cancer properties).
But its not the only source of cancer cells - DNA can be damaged by environment, and in rare cases it can receive cancer properties.
Am I correct?

Welcome to Biology.SE. I think this is a duplicate but I could not find the other post for the moment.

Yes, you are about correct. A cancer is an evolutionary process. There are selection pressures both at the multicellular levels and at the cell level. Note that the dichotomy are associated terms this error can be good(evolution) or bad(cancer properties) suggests some misunderstanding about what evolution is about.

@Remi.b this is not a duplicate of that. I do seem to remember another dupe...


text:
the evolution of the human brain size
I was thinking, as I know, sometimes the process of producing DNA did not work well(correct me if I'm wrong), so it gives us some changes in the object we gonna have(for example: increasing or decreasing a part, enabling  or disabling  a part), could human brain grow more that it is now?

Short answer: yes.

This question basically asks if there is a possibility that human brain can evolve to be bigger or more complex. This is an open ended question and cannot be addressed based on facts.

I assume, you mean by "producing DNA" Neanderthals had larger brains than us. Basically, this is possible and generally, brain size correlates with body size. What you may ask here is: Can our brain size to body size ratio increase? Probably yes... I can't think of a reason, why not?
But please please be aware of that intelligence, does not have to correlate with brain size. e.g. elephants and humans. There may be some limits of the smallest possible brain size for certain mental tasks and skills. But wiring and plasticity is probably more important than the bulk size.

Referenced material would be useful. Right now it's just your opinion and I see no attempt to answer the question beyond a purely opinion based "yes"


text:
The alignment of fingers in our hand
I noticed that in my hand the index and middle finger are aligned in one direction and the next two fingers somewhat in the opposite direction. My question is, why are our fingers aligned in that way?
Moreover, is it of any evolutionary significance?
For clarity, I am posting a picture of my hand.

I think (and only think) its more about physics than biology. Fingers are thick at bottom and thin at top, so all fingers make an angle with others when joined together. Also, if you have a look at anatomy of hand, you might get your answer (like http://i1.wp.com/scghed.com/wp-content/uploads/2013/12/Hand-anatomy.gif or http://www.visualdictionaryonline.com/images/human-being/anatomy/skeleton/hand.jpg)

@another'Homosapien' Even if you separate all the fingers, they still seem to bend in one direction(try it). So, I don't think it has anything to do with the angle between the fingers. Also, the images too don't explain much about the orientation even as they show that the fingers ARE oriented.

Please elaborate what you mean by 'bend in one direction'. I don't think that I really did get you on this.

@another'Homosapien' What I mean is, when the fingers are separated i.e. kept at some distance from each other the apex of the index and middle finger seems to be slightly bent in the left direction as seen in the image.

Okay, this doesn't seem to have evolutionary advantage. I mean, just think of a work which a person with "index and middle finger slightly bent in the left direction" can do better than person without it, and which would provide substantial benefit to person with "index and middle finger slightly bent in the left direction" ;)

@another'Homosapien' Agreed, they don't have any evolutionary advantage, but then why are they bent at all?

Well, we would need a second/third opinion from another expert to confirm that they aren't evolutionarily beneficial. For why they are bent at all, it could be a matter of chance (http://i1.wp.com/scghed.com/wp-content/uploads/2013/12/Hand-anatomy.gif and http://www.visualdictionaryonline.com/images/human-being/anatomy/skeleton/hand.jpg again).

Notice that it takes a bit of muscular effort to hold your hand flat like that?  Let everything relax, so your fingers are slightly cupped, and if your hand's like mine, the fingers will now be aligned.

This is normal, and the effect is accentuated dramatically if you pretend to be holding an imaginary round object (somewhat smaller than a baseball, for instance.) The fingertips will all approximately point towards the very end of the thumb.

(See upper right image.) If the stone were smaller, the effect would be more visible.)
This orientation of the fingers makes the hand and fingers extremely versatile, being able to grasp and manipulate objects of a wide variety of shapes.
It also allows fine manipulation of thumb and fingers. Touching each fingertip to the tip of the thumb quickly shows the same effect - the fingertips approximately align with the thumb. If they didn't align this way, we would lose some of our very fine (as in requiring great precision, not as in quality) motor skills.
I'm not going to hypothesize on why the hand evolved the way it did; it's very efficient and that seems reason enough.

Is it always the case? Do all people have this kind of hand structure? Are there any studies that say so?

@WYSIWYG - This is, as I said, "normal". I'm sure it's in an anatomy textbook someplace. Does it sound wrong to you?

No. The theory sounds quite plausible but I haven't come across any text that actually pinpoints the morphology in this fine detail. I could find these two articles: 1 and 2, when I searched but I cannot find either of them specifying this. Can you please cite a reference as this does to seem quite obvious to me (and probably other readers)?

@WYSIWYG - I haven't had a good anatomy textbook since mine was stolen on one of my surgery rotations. I was taught this by surgeons (including orthopedists) who work with their hands for a living. They were probably wrong, because they didn't cite a source for me, either. So feel free to remove for lack of a source.

Observation: The bend in the fingers gives the straight hand a more compact appearance so that we can actually tightly close the gaps between the fingers.
Hypothesis: Without the bend small gaps would remain between the tip and the first joint of the fingers unless we press the fingers together with force. Not having this gap could protect the fingers from injury while walking or running through tight underbrush because the likelyhood of entangling the fingers in some vine or branch is lower. Also, being able to compact the hand may help us to easier scoop up water with our hands.
(yes my hand show the same slight bend in the fingers)

Could you elaborate on the part 'not having this gap.....likelihood of entangling the fingers in some vine or branch is lower' ?

well, its like the difference between running a comb and a ruler through your hair, which is more likely to get entangled?


text:
Is it possible to have different genes in different parts of our body?
I want to understand genetic mutation specially in the context of multicellular organisms like humans.
I studied biology only till high school and I can’t fully understand wikipedia pages on this subject.
I know that genetic material is in chromosomes inside the nucleus of a cell. When that cell multiplies, the chromosomes too generates a copy of themselves and both child cells get one set of the chromosomes.
I would like to know:

Does genetic mutation mean an error in chromosome generation at fission stage or will it occur later in the life of the cell?
Multicellular organisms begin their life from a single cell (zygote). Under normal circumstances, every cell that grows from this single cell should have the same genetic material. Can genetic mutation eventually result in us having different genetic material in cells of different parts of our body? For example, when only a part of our body gets exposed to radiation.
If answer to question 2 is yes, which genetic material will control the behaviour of the cells? Let’s say, for example, that the genetic material of cells in our stomach favour high growth rate of hair but the cells in the scalp themselves do not have that particular gene. What will be the result?

Welcome to Biology.SE! 1-Genetic mutation means error in base sequence, not chromosome generation. 2- No. No effect would be so powerful that it would alter your genetic material. That'd mean that you are half human and half elephant (or something worse). 3- the result would be no hair at all (stomach would burn the hair on its lining, and scalp wouldn't generate hair at all). If you're satisfied with this, then I can post it as an answer with some more details.

@another'Homosapien'  I don't agree, there are many ways DNA can be altered, and smaller genetic changes in single cells happen due to errors in all the time.  Of course this does not turn you into half-elephant, but it is certainly possible that the different cells in the body have differences in their genetic material.

@Roland I know, I just gave an introduction to these topics and said that I would give more details on this. However, iayork has already posted an answer which, I think, answers many parts of the question. :)

More information on protein variation among despite little to no genetic variation: More variation in proteins than genes. Why?

@Kanj, I think your question (3) is causing some confusion. What do you mean by "which genetic material will control the behaviour" ?  Each cell has its own copy of the genetic material (genome), and if the genome of one cell is changed by a mutation, various things can go awry in that particular cell, but it does not affect other cells in the body.  Perhaps you can clarify your stomach--scalp example?

@Roland- When asking question 3, I assumed that each cell has the entire genetic material not just the part that's relevant to it. I hope that's correct. What I want to know is that if cells in separate parts of the body develop conflicting genetic material due to mutation, genes of which part of the body would control the organism. The answer, I gather from this discussion, is that cell's growth and behaviour would depend on the genetic material it has; not on the genes present in other parts of the body. So high hair growth rate cells of the stomach can not affect hair on the scalp.

The general answer is that no, it's not possible to have different genes in different parts of the body.  There are two interesting classes of exceptions, but they are exceptions.
The first is that mutations can and do occur in cells during their growth.  Most of these are probably neutral - they occur in the vast wasteland of genetic junk in the chromosome, and nothing happens.  But some of them are harmful, and this is what puts cells on the pathway toward cancer.  Outright cancers, that we can detect, are the result of at least a half-dozen mutations occurring in the same cell lineage, that cumulatively allow the cells in that lineage to grow in uncontrolled manner, to avoid immune clearance, to encourage their own blood vessel growth, and so on.  (In fact, cancer cells generally have far more than a half-dozen mutations, because a route toward getting the mutations they need is to turn down DNA repair, allowing mutations to accumulate with minimal control.  For example, Genomic landscape of DNA repair genes in cancer, Genomic profiling of pediatric acute myeloid leukemia reveals a changing mutational landscape from disease diagnosis to relapse.)
The second set of exceptions is in the immune system.  Both B cells and T cells specifically modify their chromosomes during their development, making huge numbers (trillions) or new genes.  The catch is that these are all in the same region, the antibody or T cell receptor genes.  It's part of the mechanism by which the adaptive immune system "remembers" which pathogens it's interacted with in the past.  The wikipedia article on V(D)J recombination is a starting point.

Good, but your examples show (in contrast to the first sentence) that the general answer is yes, it is possible to have different genetic material in different cell types of the body.  "Different genes" sounds strange, but definitely different alleles of genes.

Genetic mutation usually refers to any errors made while copying DNA. This can certainly occur in the lead-up to cell division, when chromosomes are copied, although they can also occur when repairing DNA that has been damaged.
I'm reading your use of the term genetic material as referring to DNA. Genetic mutation can change the sequence of DAN, but it doesn't really change what genetic material we have in any given cell. I think that it's important to understand that all of the cell in our bodies contain the same genome, or set of genes. What differs from one cell type to another is which genes are active (or "expressed" as biologists say). Mutations can alter gene activity. Say, for instance, that the deletion of a single nucleotide causes a frameshift; this can lead to the loss of that gene product in the affected cell and its daughters.
Understanding that all genes are present, but only some genes are active/expressed should help clear up your third question.

For (2), how do you figure that a genetic mutation does not change the genetic material?

@Roland - DNA remains DNA despite any mutations. At least, that was the way that I interpreted the OP's question. It sounded like he was confused about really basic things like what genetic material is. I felt that a more complicated answer risked straying too far off-target and becoming a broader biology lesson. I'll edit the answer to make that a little clearer, though. :-)

I agree that (2) is unclear. Personally, I also I find the expression "genetic mutation" a bit ridiculous and I would only expect non-biologist to use this term instead of just "mutation".

By definition, the DNA sequence changes with mutations, which means that the "genetic material" has changed. I think the OP's question 2 is pretty clear: the question is whether somatic mutations occur. (And yes, they do.)


text:
A good software for agent based modelling?
Hello i'm gonna start my master degree in systems biology and i'm thinking of working with agent based modelling, but i really don´t know which platform can be the best to simulate interactions between cells, like chemotaxis communication or between molecules. Some of my advisors have recommended me Netlogo because his simplicity and good interface, but i don´t know if it is enough powerful to run simulations of many interactions between a lot of agents. I hear that MASON is also good but you need a little background in java programming. So, which one do you think it could be the most appropriate or which other platform can you recommend me that also can be good?

Can you please elaborate a little more on what you are trying to achieve / to simulate? Don't be afraid of needing "little background in Java" as you will learn quickly.

My boss is a big fan of Repast HPC, but since Repast is a C++ framework it might not be the right choice for you. It takes a loooong time to write a good C++ program (even for someone who already knows the language fairly well), although it will run very quickly once it's written. A one or even two year long Master's program will end up going by surprisingly quickly, so if I was in your shoes I'd choose to start with the simplest thing possible (ie Netlogo). Once you have a finished product, even if it's somewhat more simplistic than you'd like, it'll be much easier to work your way up from there.
Really though, consider the choice of modeling framework to be part of your research project! Only you can come up with the right choice for your project, though as a practical matter you should heavily favor any framework that at least one person in your department already has some experience using. Things will go wrong, you will have questions, and Stack Overflow won't be able to answer all of them.
Here's a list of the more interesting agent-based modeling frameworks that I found from a few minutes of googling:

Repast HPC

pros:

C++ based
The only performance focused one of the bunch

cons:

C++ based
For simple models, would be like building a supercomputer to use as a pocket calculator

Netlogo

pros:

Focused on being accessible to non-programmers
Scripting language seems pretty straightforward

cons:

In my experience frameworks that try to implement their own scripting language in an attempt to be accessible to non-programmers ultimately end up being much more complicated to use than frameworks based around an established language. But I'm not the target audience.

Mesa

This one is Python based, so it's the one I would personally try first since I find Python to be the best language for quickly writing scientific programs of reasonable complexity. That's my own personal bias, so your mileage may vary

MASON

The fact that Repast HPC does not imply that a user will need to modify the model by him/herself. It should not be a "con". Also, it does not take so much time to code in C++ in comparison to other languages as long as the project is important enough. Disclaimer: I know nothing about the softwares.


text:
Is $F_{ST}$ a probability and a correlation coefficient?
$F_{ST}$ is one of the most famous and most important statistics of all of evolutionary biology. Yet, many people misunderstand it or misuse the classical results from the literature on $F_{ST}$ (Whitlock and McCaughley,1999).
Fixation Index in infinite islands model
In a panmictic population, the probability of identity by descent $F(t)$ in generation $t$ is the probability of sampling the same allele twice plus the probability of not sampling the same allele multiplied by the probability of identity by descent in the previous generation
$$F(t) = \frac{1}{2N} + \left(1-\frac{1}{2N}\right) F(t-1)$$
, where $N$ is the population size. Here I am assuming diploid population and no mutation. In an infinite allele model, these probabilities must be weighted by the probability that none of the parent migrated in the previous generation.
$$F(t) = (1-m)^2\left(\frac{1}{2N} + \left(1-\frac{1}{2N}\right) F(t-1)\right)$$
, where $m$ is the migration rate between any two demes. Setting $F(t) = F(t-1) = \hat F = F_{ST}$, assuming that $m$ is low and solving for $F_{ST}$ yield to the classic result from Sewall Wright
$$F_{ST} = \frac{1}{1+4Nm}$$
Definitions of $F_{ST}$
$F_{ST}$ was defined by S. Wright as
$$F_{ST} = \frac{var(p)}{\bar p(1-\bar p)}$$
, where $var(p)$ is the variance of allele frequency among population and $\bar p$ is the overall average allele frequency.
From Nei (1973)

Wright showed that the variation in gene frequency among subpopulations may be analyzed by the fixation indices or F-statistics. He derived the formula
  $$1 - F_{IT}= (1 - F_{IS}) (l-F_{ST})$$
  where FIT and F1s are the correlations between two uniting gametes to produce the individuals relative to the total population and relative to the subpopulations, respectively, while $F_{ST}$ is the correlation between two gametes drawn at random from each subpopulation. $F_{IT}$ and $F_{IS}$ may become negative, but $F_{ST}$ is nonnegative.

Question
In the derivation of the fixation index in infinite island model, $F_{ST}$ is a probability of identity. In the quotation from Nei (1973) (and other sources), $F_{ST}$ is presented as a correlation coefficient. In Wright's and Nei's definition, I don't see the relation from the equations to either a probability or a correlation coefficient. Can you help to clarify this for me?
For example, I would expect that $E\left[\frac{var(p)}{\bar p (1-\bar p)}\right] ≈ \frac{1}{4Nm+1}$, where $E[X]$ is the expected value of the variable $X$. Can you demonstrate that this is true?


text:
what is meta-sympathetic nervous system?
I always knew about the sympathetic and para-sympathetic nervous systems, and today I was told about the meta-sympathetic nervous system, but I didn't understand well the man who told me about it and I didn't find enough or reliable information about this system, and if it's accepted in the scientific world or it's arguable.

The concept of a metasympathetic part of the autonomic nervous system (distinct from the sympathetic and parasympathetic parts) seems to be an idea discussed almost exclusively in the Russian scientific literature.(src)  Many, if not a majority, of the papers concerned with it seem to have one A. D. Nozdrachev as one of the authors.  He has been publishing on it at least since 1980 ("Structuro-functional organization of the vegetative (autonomic) nervous system"); most recently is from 2006 quoted in another answer ("The Metasympathetic System of the Brain").  The presentation in the latter paper seems almost incoherent to me, and apparently not due to translation.  This idea doesn't seem to have much traction, particularly outside of Russia.

As @mgkrebbs says, metasympathetic nervous system is still a matter of debate and is not fully accepted in the scientific world due to lack of research and evidence.
Metasympathetic nervous system, just like sympathetic and parasympathetic nervous system, is a part of Autonomic Nervous System.

On the basis of a number of structural and functional indices, application of pharmacological analysis as well as recording of neuronal activity, the autonomic nervous system is subdivided into the sympathetic, parasympathetic and metasympathetic parts. The metasympathetic system includes the complex of microganglia situated in the walls of visceral organs and having marked motility activity (the heart, ureters, intestine, stomach). According to the localization, separate areas of this system can be defined by its site (for example, the cardiometasympathetic area in the heart). The metasympathetic system attains the features of true autonomy. Its cells have no direct connection with the high centers: this connection is established through mono- and polysynaptic sensory and afferent units of sympathetic and parasympathetic nature.

Source

Full article here
How is it different from sympathetic & parasympathetic systems?
One major difference is in the location.
The Metasympathetic system

includes the complex of microganglia situated in the walls of visceral organs and having marked motility activity (the heart, ureters, intestine, stomach).

while Sympathetic system

consists of cells with bodies in the lateral grey column from T1 to L2/3. These cell bodies are "GVE" (general visceral efferent) neurons and are the preganglionic neurons. There are several locations upon which preganglionic neurons can synapse for their postganglionic neurons:

and Parasympathetic system

consists of cells with bodies in one of two locations: the brainstem (Cranial Nerves III, VII, IX, X) or the sacral spinal cord (S2, S3, S4). These are the preganglionic neurons, which synapse with postganglionic neurons in these locations:

For detailed location, see this image:

Did you understand what the difference between sympathetic to meta-sympathetic? I don't. In addition the heart doesn't have nerves... it has its own electrical conduction system which consist of myocardial pacemaker cells, they are not neurons.

@Assiduous this is not my theory. You wanted a reliable source for metasympathetic system and I gave you one. Also, you can never be so sure for something in biology on which research is going on. I also could never think of most of my body not being in my conscious control, but it is. I will add difference between sympathetic & metasympathetic.

don't  understand me wrong. I love your comment and I appreciate it, I just said that I didn't understand the differences:) The intonation in words is not always clear... In my case I meant to the politely intonation. Thank you and I'm very sorry if you felt inconvenience due to my first comment. :)

@Assiduous its okay, nothing about inconvenience. I was just a bit surprised as the way you asked the question in comment, it seemed to me that you think that I am expert in metasympathetic nervous system ;)

The concept of the meta-sympathetic system is founded by singles in Russian of the 80's. This theory wasn't accepted in the academic or scientific world. The most of the results in PubMed shows that they are from Russian, and a some of them are even from the same person (which published it on 80's and came back in 2006 with a new publishing of his theory, unsuccessfully.
The theory about meta-sympathetic system is not studied at the universities of the western countries such as US, Israel, UK, Australia, Canada etc. I talked with scientists from all these countries which told me these things. We can't even find any mention about this theory in the professional textbooks of biology or physiology such as Campbell biology and more.
Look at this conversion also:  https://en.wikipedia.org/wiki/Wikipedia:Reference_desk/Science#what_is_meta-sympathetic_system.3F

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


text:
Can you identify this phyllanthus tree?
I have this tiny tree in my garden in Cancun, Q.Roo Mexico.

(More photos available here.)
The little tree started to grow in a planter. I did not pay any attention to it until it grew to 10 cm. It does grow like any bigger tree, starting with one curving branch with regular leaves. I buy unsterilized soil from locals and always get something growing without planting.
It is a phyllanthus plant, but that is all we know so far.
By now I have 20 little ones and one big one, which is a year and a half old.
It certainly is not a phyllanthus Niuri which is an incredible medicinal plant, but with way less "tree attitude" than this one.
This lovely bonsai tree could be unknown to the world, hidden in the deep vegetation of the Yucatan peninsula, one of the world's regions with the highest tree variety.
Can you identify this tree for me?

Phyllanthus caroliniensis

Phyllanthus caroliniensis, the Carolina leaf-flower, is a flowering plant native to the Americas, from the southeastern United States1 all the way to Argentina.2 The flowers are small and located where the leaf meets the stem.2

Kingdom: Plantae
Subkingdom: Tracheobionta
Superdivision: Spermatophyta
Division: Magnoliophyta
Class: Magnoliopsida – Dicotyledons
Subclass: Rosidae
Order: Euphorbiales
Family: Euphorbiaceae – Spurge family
Genus: Phyllanthus L. – leafflower

Sources:

http://plants.usda.gov/core/profile?symbol=PHCA9
https://en.wikipedia.org/wiki/Phyllanthus_caroliniensis
http://www.easttennesseewildflowers.com/gallery/index.php/Summer-Roadsides-White/Seedleaf50001
http://sura.ots.ac.cr/florula4/find_sp3.php?key_species_code=LS001041&key_kingdom=&key_phylum=&key_class=&key_order=&key_family=&key_genus=&specie_name=caroliniensis

Hello Jordi Thanks or your reply. It's close in appearance, but the stems of the P carolinensis are thicker and green. And the leaves don't seem to be  translucent as the ones from my plant.   http://i.imgur.com/U7mU1DG.jpg

the tree is identified.
http://chalk.richmond.edu/flora-kaxil-kiuic/p/phyllanthus_liebmannianus.html
Saludos
Bernhard


text:
Are alleles equally sized?
If alleles occur at the same locus on a chromosome, does that mean they are of the same size? I was under the impression that they were, but I saw a gel electrophoresis testing different alleles of the same gene and saw them separate. I don’t understand how they could separate if they are of the same size, but if they aren’t, then how can they be housed in the exact same locus?

Are you sure it is just a normal gel electrophoresis? It could be some technique like RFLP which can differentiate alleles.

If they are not on the same locus, then you can find them using electrophoresis. Basically you are checking for copy number. However, alleles at same locus can be of different sizes (but I don't think the differences are that great, in most cases). There are a lot of possibilities but unless you provide details, it is hard to explain what exactly you observed in your experiment.

In general, alleles don't have to be the same size. Two major examples which come to mind are the Huntingtin gene and FMR1.
Huntingtin is the causative gene of Huntington's disease. In people with Huntington's, a sequence of three nucleotides is repeated. The number of repeats varies, from a low of 9 in unaffected individuals, to more than 60 in severely affected ones. So depending on how many repeats you have, each of your Huntingtin alleles may have a different nucleotide size.
FMR1 is the causitive agent of Fragile X syndrome. Like Huntingtons, the gene varies in the number of trinucleotide repeats, but for FMR1, affected individuals can have over 1000 repeasts, meaning an extra 3 kilobases of genetic material versus the alleles of an unaffected individual.
Other genetic disorders are also related to the difference in allele size. You can have a deletion of a region of DNA (or an insertion) which is normally silent (recessive). The normal-length allele compensates for the defective allele, but the differently-sized disease allele is still present in the population, and counts as an allele of the gene.
It's not just disease-prone alleles which exhibit length polymorphism. A number of other genes will show variation on both the DNA and on the protein level. If the insertion/deletion is a multiple of three nucleotides and occurs in a loop region of the protein or on an intrinsically disordered domain, the insertion has a reasonable chance of minimal structural effect on the expressed protein. For one (completely arbitrary) example, PER3 has two major length variants in the population, with a 54 base pair difference between the two. Different populations have vastly different prevalence for each, with a range of 20-90% for the shorter version.
One thing to keep in mind is that "locus" points are just a human convention to help us map DNA. To the cell, DNA is just a single long molecule. (Or multiple molecules, for different chromosomes.) There isn't any labels for absolute position in the cell, so inserting or deleting a chunk of DNA mainly affects just the local environment. There isn't any sort of long-range indexing that gets messed up by the insertion.

So what exactly happens when the repeats increase? Does this gene code for a specific enzyme? Do the increased repeats change the enzyme activity?

@curious_cat the exact function of huntingtin is not really known. In most of these poly-Q proteins, the repeat is not present in any functional (binding/catalytic) regions. This ideally should not affect their activity but there are other factors at play here. The exact mechanisms of poly-Q toxicity are still not clear: one thing that is known is that this causes a stress response.

@WYSIWYG What about in general? Say alleles that determine other phenotypic features, say eye color or sickle cell anemia or hemophilia etc. How do the difference in amino acid repeats / type lead to the feature difference. What is the mechanism. Is it a specific enzyme's activity alone or something else?

@curious_cat usually the differences in alleles (at least the coding region of mRNA) are mostly substitutions (which can lead to a change in the activity). Indels are dangerous as they can disrupt the reading frame. Amino acid repeats like in poly-Q diseases arise because of homopolymeric expansion of the CAG triplet. As I said, how poly-Q affects the activity of the affected protein is not fully known. Moreover, different polyQ diseases have diverse kinds of affected proteins ranging from androgen receptor to TATA-binding protein.

Are not all these examples of genetic aberration and not normal functional alleles? Can normal functional alleles have difference in sizes?

@OneFace The disease causing variants are the most obvious, as they're the most studied and have substantial length variation. But even in asymptomatic individuals there's a variation in length for Huntingtin and FMR1. Variations in other, non-disease-associated genes exist too, and I added an example I found from a quick literature search.

One possibility of what you were looking at was a nuclease digestion experiment. A subject's gene sequence could be amplified from their DNA using PCR, giving a band of a certain size when electrophoresed on a gel. The PCR'd product could then be digested with another nuclease that specifically cuts one allelic variant, but not another. For example, check out this rather unrefined image I made:

Lane 1 is the molecular weight ladder. Lane 2 shows the PCR product of our gene of interest, which has two possible alleles - one that can be cut with our nuclease, and one that can't. The rest of the lanes show the result of incubating the PCR product from different individuals with our nuclease. Lane 3 shows a homozygote for one allele, the one that cannot be cut. Lane 4 shows a heterozygote, where the uncut 900 bp band is also seen with the cut 400 and 500 bp fragments. Lane 5 shows a homozygote carrying the cuttable allele on both chromosomes - there is no intact 900 bp band.

This does provide an example of why alleles could run differently on a gel, but fails to answer the underlying question about allele size


text:
What's the difference between CREs and DHSs?
I would like to know what's the difference between cis-regulating elements and DNase I–hypersensitive sites, in order to produce a meaningful segregation of non coding elements affecting gene expression.

Have you read https://en.wikipedia.org/wiki/Cis-Regulatory_element and https://en.wikipedia.org/wiki/DNase_I_hypersensitive_site ?

Cis-regulatory elements are simply DNA regions upstream or downstream of a gene that can affect its expression (basically they have to be in the same chromosome).
DNAse-I hypersensitive sites (DHS) are regions of chromatin that get digested during the DNAse treatment because they are exposed i.e. not protected by a protein (complex). The protein complex can either be a nucleosome or a transcription factor. It should be noted that a DNA region can be DNAse insensitive also because of its conformation.
Usually the cis-regulatory elements exert their effects by serving as a binding site for a transcription factors (or chromatin remodellers). If the proteins bind at these sites then these regions would be protected from DNAse digestion thereby making them not-DHS. However, it is known that DNA elements can act in trans as well (see papers on 3C- chromosome conformation capture, and its variants). Moreover, whether a site is protected from DNAse or not does not tell anything about its function.


text:
How to safely conserve my current DNA methylation marks?
I read the Wikipedia article on DNA methylation
Let's say I want to extract and then stock my current DNA methylation marks somewhere so that I can use it safely 20 years in the future for a medical procedure that doesn't exist yet.
What method should I use?

Welcome to Biology.SE. Your DNA will be the same in 20 years from now.

@Remi.b Sorry for the misconception. I have reformulated the question.

To record the current methylation state of your DNA, you can use bisulfite sequencing. Basically, you take half of your DNA sample and treat with bisulfite, which deaminates cytosines (C->U) , so they read as T instead of C. Methylated cytosines are protected, so they still read as C. You run two sequencing reactions, one with bisulfite-treated and the other with untreated DNA, so you can tell where the true Cs are in the genome. See the below diagram:

Wikimedia commons
Note that if you're thinking of doing this from a longevity point of view, that there are hugely different methylation patterns in different cell types; I'm not sure which cell type you'd want to pick. Also, methylation is not the only covalent modification of DNA that exists, there's also hydroxymethylation, and I'd bet there are more that we haven't discovered yet. There certainly are in bacteria and phage (glucosyl-hydroxymethylcytosine, for one). The hard thing about saving things for the future is that we really don't understand the full picture of what's happening now epigenetically, and as such, we don't have assays to detect things we don't know about.

I believe the DNA is going to be as stable in native form as it should be after bisulfite treatment. You can use commercially available methods of storing DNA samples and safely assume it will be intact in 20 years time.


text:
Why were dinosaur skeletons so light compared to mammal skeletons?
I was watching a presentation by Dr. Jessica Theodor [1] who discusses (at 38:10), among other things, the skeletal structure of dinosaurs vs. mammals. "Dinosaurs have way lighter skeletons, which means that for the amount of material they can be bigger. If we start to look at sauropods, they have this really interesting set of structures, these big holes in their vertabrae...
it allows you to build a lighter, stronger skeleton. Mammals can't do that. It's not how we build our bones."
Why don't mammals do this? Are there fundamental trade-offs that make our (apparently) weaker, heavier bones better, or is it just chance that we haven't matched this development?
(Of course I'm open to the possibility that I misunderstood the talk, or that it was simplified to the point of inaccuracy on this point.)
[1] Jessica Theodor, Being Giant: Why are mammals not as big as dinosaurs? (2015)

If one wonder about why mammals in general are so much smaller than dinosaurs, I think the answer lies somewhere in that we simply have not gone down the competitional path of pure size. Just in the same way as we generally don't have evolved to use flight (except for bats) or live an aquatic life (except for whales and dolphins). One could say that we don't have bone structure suited for extreme growth and size just like we don't have bone structure suited for flight.

That is because, they have twenty one percent of body mass than minimum skeletal volume.
In Dr.Bill Sellers's journal "Biology Letters", it was said that they laser scanned Brachiosaur as they were estimating it to weigh about 80 tons. But, it actually weighed 23 tons which is relatively light.

@Alex: It's more like "why don't mammals have lighter skeletons, following dinosaur's plans".

@Alex: But also remember that what we know of dinosaurs (and extinct mammals) comes only from fossil remains that have been found.  Until relatively recently, big bones sticking out of the ground were a lot more likely to have been discovered than little tiny ones.  I suspect, though I don't know for sure, that larger bodies were more likely to have become fossils in the first place.

you link to a private video. It's not possible to check your source... found this video which is probably it: https://www.youtube.com/watch?v=whxn9Cc1_Ho

@Frieke It wasn't private when I posted it! I imagine your link is correct, I'll change it.

I have also heard the claim that dinosaur bones were lighter than mammal bones of equivalent  size, and at the moment I do not believe it.  I will not believe it until somebody explains it to me how that is possible.
If you have a structure that you want to add more weight to, to support that weight, you want to ADD structural elements, not subtract them.  If the structure could support itself before adding more weight, then adding structural elements will make it stronger (unless it's already at the absolute limit).  Otherwise, the structure does not stand at all.
If you google about the weight of bird bones, you can find recent research saying that bird bones are actually not lighter than mammal bones.  Their weight is just distributed differently (more densely on the outside of the bone, as opposed to more evenly spread throughout the bone as in mammals) to resist bending and twisting better at the cost of being weaker to impacts.  Birds arguably have a much stronger reason to lose weight than dinosaurs, but their bones are still just as heavy as ours.  Since birds are dinosaurs, I find it very unlikely that ancient terrestrial dinosaurs had magic bones lighter than both mammals and birds.
Also, I'm aware that the internal structure of our bones is very efficient.  As I understand it, the bone on the inside of a bone grows thicker where it is more stressed.  If you train a computer to calculate the ideal lattice structure to support the stresses of a given bone shape, the computer calculates pretty much the exact same lattice as what actually exists in our bones.  So, if the internal structure of our bones adapts to better handle the stresses we experience in life, and if the bones of vertebrates can evolve into any external shape whatever, I cannot imagine how dinosaur bones could be stronger than ours unless they were made of a different material.  I am not aware that this is the case.

Welcome to Biology.SE! Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. In particular, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. Thanks!

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


text:
Detection of bacteria to measure quality of water
I have been working on a science project were I have built a water filter.
To prove that it works I would need to test if there are bacteria in a sample which has been treated vs a sample that hasn't been treated.
I really just need to know if there are bacteria not how many. I looking to do this at home.

Put your filter on a nice and rich medium in a petri-dich and it will give you an idea of whether there are bacteria. Fitlering different amount of water will allow you to quantify. There are always potential bacteria you will not be able to grow on this specific medium and therefore it is pretty much impossible to really prove that something is completely sterile.

https://en.wikipedia.org/wiki/Bacteriological_water_analysis

There are many techniques. You should add some details to narrow down the question, which include- the available infrastructure, ease of experimentation, monetary budget, time required for analysis and other relevant information.

There are many ways to do this. User Grb's answer is good but his method requires access to equipment.
If this is a highschool level project, you could make two Nutrient Agar petri plates. Spread 1 milliliter of unfiltered water on one and 1 milliliter of filtered water on the other. Make sure this is done in a sterile environment (using a Bunsen burner for example). The presence of colonies on your filtered plate would indicate that there are still bacteria in the filtered water.
You can also count the number of colonies on both plates. If there are less colonies on the plate with filtered water, your filter works to a certain extent. If the counts are identical, your filter does not work. If you use colony counts, make sure you repeat the experiment multiple times to obtain statistically rigorous result.

IF you are looking at a much faster technique but don't mind spending a bit and have some research equipment access, there are ways by which bacterial contamination can be detected by measuring ATP (Adenosine tri-phosphate). See this research publication. There are commercial kits available which you can use: Here is one of them by Thermofisher.
Again, this is only if you have access to the research equipments and funds.


text:
How were (many) dinosaurs' brains so small?
Brain size (or its proxy, encephalization quotient) usually varies allometrically with mass -- larger creatures need larger brains to control their larger bodies, apparently.
Dinosaurs are popularly known as small-brained. While this certainly doesn't hold in general -- theropods and especially birds were particularly intelligent -- but sauropods and thyreophorans (ankylosaurs and stegosaurs) seem to have preposterously small brains. How were they able to control their large bodies with such small brains? Are there modern animals with similar proportional brain size, and if so does that give any clues as to how these dinosaurs functioned?

I would like to know why a small brain cannot control a big body, if that is the case. A small brain would be so much less metabolically expensive. You'd think that there would be a strong selection pressure to have the smallest brain that could do the job. So a lion should have the same size brain as a house cat, and so on.

I don't think there is a concrete answer, because we don't really know the minimum size of a vertebrate brain in relation to body size. Many vertebrates, including many fish, get along fine with tiny brains in large bodies.
For many decades, scientists speculated for this very reason of small brain size, that dinosaurs seemed to have an extra brain, or ganglion, at the hip. Especially sauropods and thyreophorans appear to have had a widening of the spinal cord cavity around the sacral area suggesting this possibility. This pelvic ganglion or "hip brain" was then presumed to be responsible for running the hind legs and tails. However, this idea has not gained any further evidence or traction in the scientific community and is generally dismissed.

I too had read this theory (bulged portions in spinal chord) in certain science magazine; which concluded dinosaurs were dependent on much more on quick reflex than thought-activities.

Interesting theory. Can you please add some references to your answer?

FWIW I've heard the plausible conjecture that the lower limit of brain mass is roughly the mass of the spinal cord (i.e., the brain + cord is at least roughly twice the cord).

A good modern point of comparison in modern animals is the koala. The giant pandas are likely headed in the same direction, too. It seems that the lack of a need to process complex sensory information to acquire food or avoid predators, the nutritional inefficiency of the diet, and the fact that the number of systems isn't increasing, just their size, is also relevant. Do we have coprolites from these dinos to see how well digested their food was?

Well, as I said, there is not really any scientific traction for the "pelvic ganglion" theory anymore, so there is not much documentation to find other than some speculative papers. Dinosaurs are now generally presumed to be simply small-brained vertebrates for the most part.


text:
What does it mean "specialized populations of neurons"?
I'm reading now the Campbell biology book (10th), and on page 1063 is written:

In all but the simplest animals, specialized populations of
  neurons handle each stage of information processing.

What does it mean "specialized populations of neurons"? I always knew that there is a population in biological hierarchy of creatures rather than the cells which assemble the creatures.

As in the occipital lobe handling vision processing, the prefrontal lobe intiating motor activities, etc...

I'm voting to close this question as off-topic because it is about English language usage, not biological terminology.

It's just a specialized group of neurons. You can call a group of cells a population of cells. They are specialized because those particular neurons carry out a specific function.


text:
Do Asian giant hornets (Vespa mandarinia) prey on other nests of Asian giant hornets?
Asian giant hornets are known to attack nests of other bees and wasps, but should they encounter another nest of their own, would they attack it?

Yes. According to this clip uploaded to YouTube on the Smithsonian channel, Asian giant hornets will attack and pillage other nests (of Asian Giant Hornets) if no other food source is readily available.


text:
How much time do the different mechanisms of gene regulation need to take effect?
I am thinking of the major regulatory mechanisms, like general transcription factors, activators, repressors, and RNA interference.
If non-active regulator genes using each of the different mechanisms were activated, what would be delay (on average) between each of those genes' activation and their downstream regulatory effect?

I don't have an answer for you, but people often imprecisely say that type of regulation takes place on the order of many minutes to hours, and that may be as precise as you can get given the variable kinetics of any given pathway. I will say this though: the kinetics of knockdown in RNAi could largely depend on the rate of degradation of the protein (which is HIGHLY variable). Even if you take away the mRNA, the protein is still there until it's degraded. If it's normally degraded fast, the kinetics of mRNA degradation will be limiting. If it's slow, then you have to wait for the protein.

Also, all genes in eukaryotes require general transcription factors, but basically all of them also require activators to act first to recruit the GTFs and histone modifying components (which allow GTFs and their friend RNA polymerase to access genes). So, they are really downstream of activators and  their recruitment is part of what contributes to the kinetics.

People often imprecisely say that type of regulation takes place on the order of many minutes to hours, and that may be as precise as you can get given the variable kinetics of any given pathway.
Also, all genes in eukaryotes require general transcription factors, but basically all of them also require activators to act first to recruit the GTFs and histone modifying components (which allow GTFs and their friend RNA polymerase to access genes). So, they are generally downstream of activators and their recruitment is part of what contributes to the kinetics in euakryotes.
For RNAi, the kinetics of knockdown in RNAi could largely depend on the rate of degradation of the protein (which is HIGHLY variable). Even if you take away the mRNA, the protein is still there until it's degraded. If it's normally degraded fast, the kinetics of mRNA degradation will be limiting. If it's slow, then you have to wait for the protein to be degraded by its natural mechanisms (https://en.wikipedia.org/wiki/Proteasome).
Sigma is saying RNAi effects can be seen in around 24 hours
http://www.sigmaaldrich.com/life-science/functional-genomics-and-rnai/sirna/learning-center/mission-sup-reg0/experimental-design0.html#s3
Thermo is implying something similar by saying RNAi effects can be seen for 5-7 days post-transfection (i.e. they imply that it can be seen after a day).
https://www.thermofisher.com/ca/en/home/references/ambion-tech-support/rnai-sirna/tech-notes/duration-of-sirna-induced-silencing.html


text:
How long can one leave sample in lysis buffer for DNA extraction?
I am trying to do some DNA extraction for my professor, and I make a lysis buffer with proteinase K. I did not have the time to continue the procedure so the hair and the buffer have been sitting together at room temperature for about 12 days. My professor stated it would be "fine" to continue on with my DNA isolation procedure, but I have my doubts.
Should I continue my DNA extraction( vortexing, boiling, centrifugation and collection of supernatant, storage at -20 degree Celsius) or would this be pointless at this time? My goal is to run PCR and then a gel.
EDIT:
Here is the composition of the lysis buffer:
In 20 ml of Lysis buffer:
final concentrations are $0.1 M$ TAE, $0.5M$ $\ce{NaCl}$, 0.2% SDS.
To $800 ul$ of Lysis buffer I added $5 ul$ of proteinase K at a concentration of $250 ug/ml$.
(Proteinase K was made via:  $ 0.0025 g$ up to $10 ml$ of TAE buffer( $1 M $))
This was in a $1.5 ml$ centrifuge tube that has been now sitting for 12 days.

Can you put in the composition of the lysis buffer here?

@Chris                    I put the composition of the buffer, thanks for reminding me.

What do you mean by 0.1M TAE? TAE normally stands for Tris-Acetate-EDTA, but you already have EDTA as a component.

@MarchHo              Yea your right, I was not thinking sorry let me fix that.

@rosiv
Hi Ro, I wanted to know if your PCR was succesfull. I am planning to Transport WORM samples in Lysis Buffer at ambient temperature from Asia to Germany, do you have any suggestions for me?? Thanks!

@Tegudet                 I have not done it yet, since im a slacker... I also dont plan on doing it any time soon. I am a novice at biology methods, so I wouldnt have any suggestions. Sorry and good luck.

It should be fine. Unless they have been contaminated with DNase, none of the components will damage or denature DNA. I've left purified plasmid DNA on the bench for weeks with no apparent degradation, so you should be okay (not that I recommend doing that on a regular basis). I would continue with the purification, according to your professor's recommendation, because you've already come this far. If worst comes to worst, you won't get anything, and you'll have to re-purify. However, the chances of your getting something are pretty high, so you may as well go with it.

Ironically I tried to continue my extraction and failed spectacularly, so I might have to redo the sample collection. This will help for the future though.

Your concentration of EDTA seems to be rather high. When performing lysis for DNA extraction, I usually use 1mM EDTA in the lysis buffer. Concentrations that are too high may result in inhibition of the PCR reaction later on, unless the DNA is first purified.
This could be a reason why your reaction failed.

I had less EDTA than that, the EDTA I mentioned previously was the final concentration of EDTA in my TAE, I removed it because I was not thinking clearly sorry. The final concentration of my EDTA in my TAE is 0.025 M i believe.  Also I have not ran my reaction yet, but many thanks for the advice.

@rosiv how then did you know your reaction failed? Boiling the mixture should result in precipitation of proteins, which should be removed by the spin. You will be left with the DNA solution which you can either use directly or use after desalting.


text:
Why do sperm have centrioles and do female eggs cells even have centrioles?
I was just wondering why it is that sperm have centrioles underneath the acrosome, but that also prompted a thought as to whether eggs have them too?

Oocytes do not have centrioles. During fertilization, the centrioles of the sperm become the centrioles of the zygote. Only one pair is needed, as there is only one cell (i.e. zygote) right after fertilization.

Please add a link, summary, and/or citation for a source to back up your claims.

During fertilization the centrosme inter the ooplasm with the sperm nucleus,  if the oocyte still keep its centrosme there will result 2 centrosme in zygote with 4 centriole. Each one will migrate to pole of cell and produce 4 poles not two and the 4 daughter cells of one division will have one centriole in this case through mitosis will shut off.

Please add some reliable references to this answer :) If you have any questions or concerns about answering questions, please see the Help Center https://biology.stackexchange.com/help


text:
How scientists can be confident that human embryo tail is really a tail?
From Wikipedia:

Human embryos have a tail that measures about one-sixth of the size of the embryo itself. As the embryo develops into a fetus, the tail is absorbed by the growing body.

How are we sure that it is a real tail and is not a superficial resemblance of something else?
I ask this because some creationist guy challenged me in this regard.

I just want to ask one thing: what else could it (tail-like thing) be, another hand or another leg?

It is an extension of the vertebrae. Isn't that a good reason?

@user40602 If you consider your question has been answered, you can check your favourite answer.

We can be sure it's a tail because it is an extension of the vertebrae, and we define "tail" as an extension of the vertebrae, among other things.

tail
tāl/
noun: tail; plural noun: tails

the hindmost part of an animal, especially when prolonged beyond the rest of the body, such as the flexible extension of the backbone in a vertebrate, the feathers at the hind end of a bird, or a terminal appendage in an insect.

Emphasis mine. Source: www.oxforddictionaries.com

Some mention of the identical embryology would make this better, the human tail is not just a tail because of its location. not all tails are the same.  the human tail is homologous with other vertebrate tails.

Well, what would you call it? Have a look at the images below (source):

If you would call what other species have tails, then the human one should also be called so. After all, they are extremely similar (the last image, k, is human):

a Echidna or spiny anteater (Tachyglossus aculeatus).
  Because of the extreme rarity of monotreme material we
  were only able to obtain this embryo, which is younger than the
  tailbud stage. b Brush-tailed possum (Trichosurus vulpecula). c
  Eastern Australian native “cat” (Dasyurus quoll). d Domestic cat*
  (Felis catus). e Domestic dog (Canis familiaris). f Domestic sheep
  (Ovis aries). g Scaly anteater (Manis javanica). h Rat (Rattus norvegicus).
  i Rabbit (Oryctolagus cuniculus). j Hedgehog (Erinaceus
  europaeus). k Human (Homo sapiens).

The above image was taken from M.K. RIchardson et. al.,Anat Embryol (1997) 196:91–106 (a PDF can be found here)

FUN FACT
Let's start with a fun fact!
In some rare cases, humans can get born with a tail. These tails can then be removed by surgical procedure. Such procedure are quite simple and are a relatively old procedure (see Speigelmann et al. 1985).
What is a tail?

The tail is the section at the rear end of an animal's body [..]. It is the part of the body that corresponds roughly to the sacrum and coccyx in mammals, reptiles, and birds

Source: Wikipedia
Sacrum and Coccyx are the last parts of the vertebral column. A tail is therefore, just an extension of the vertebral column.
How does it look like in humans?

Is it really a tail that we see?
Yes! Human embryo have been dissected and histologic analyses were performed. There are no doubt, it is a tail!
See Dao and Netski (1984), Belzberg et al. (1991) and Fallon and Simandi (2005) for further description and evidence.


text:
Brain capacity of Cro-magnon man vs Modern man
Cranial capacity of Cromagnon man was about 1650cc whereas average cranial capacity in modern human is 1450cc.
My question is, why during the course of evolution, a reduction in cranial capacity is seen ?

What you call brain capacity is actually called cranial capacity (see wiki). At the end of your question you seem to try to discretely assume that lower cranial capacity induces lower intelligence but it is not necessarily true. You might want to remove this assumption otherwise, the question might get closed as being primarily opinion based.

Stanyon et al. 1993 is probably a good reading on the subject.

Some of the possible explanations are summarized in Selection for smaller brains in Holocene human evolution. It's a blog post (but from a well-regarded anthropologist and heavily referenced), but I'll excerpt a few quotes here:

Less well known is that the terminal Pleistocene and Holocene (ca. 30,000 years ago to present) witnessed a substantial decline in endocranial volume ... This decrease of approximately 240 ml in 10,000 years is nearly 36 times the rate of increase during the previous 800,000 years.  ...

He considered one possible explanation, that the smaller brain size is due to smaller stature, and determined that it's not likely:

Here, I apply a quantitative genetic model to test the hypothesis that Holocene evolution of brain size may be explained by reductions in body size. ... The net change in endocranial volume, roughly 130 ml from the terminal Pleistocene to late Holocene skeletal sample would predict a reduction in stature of 13 cm, if the brain size had changed only because of correlated changes in stature. That degree of stature reduction is not biologically impossible although it would be extreme. ... The evidence suggests substantial reductions in brain size in some recent human populations, more than can be explained by correlated changes in body size.

He then lists six possible alternate explanations, which are not mutually exclusive:

Chance.
Plasticity.
Climate.
Nutrition.
Function.
Development.

He spends some time discussing each but concludes that at the present time the cause can't be definitely determined.
Here's his conclusion:

The available skeletal samples show a reduction in endocranial volume or vault dimensions ... This reduction cannot be explained as an allometric consequence of reductions of body mass or stature in these populations. The large population numbers in these Holocene populations, particularly in post-agricultural Europe and China, rule out genetic drift as an explanation for smaller endocranial volume. ... Therefore, smaller endocranial volume was correlated with higher fitness during the recent evolution of these populations. Several hypotheses may explain the reduction of brain size in Holocene populations, and further work will be necessary to uncover the developmental and functional consequences of smaller brains.


text:
What is this bird of prey with white belly?
This bird was around the house in northern Switzerland (alt: ~700 m) on January 17th 2016, and I am just wondering what kind of species it is.

The legs are yellow and the under (I do not have picture while flying, but saw it just before) is almost all white with just a black (or dark) stripe on the end of the tail.
For me it looks like a nordic species of Buteo buteo but can any specialist confirm it?

Common Buzzard, Buteo buteo
Belonging to the Accipitridae family, which consists of ~32 birds of prey in Europe, Buteo buteo is a fairly common bird of prey through much of Europe. Resident up to Northern limits of approximately Britain, Denmark, southern Sweden, Northern Germany, Poland, Belarus, and Ukraine, and through to the Southern limits of Europe. Also found in summer in Eastern Europe, Western Russia, Finland, and most of Sweden. Therefore, your location is within the typical range. Often seen in farmland, marshes, etc. which it uses as hunting grounds for small rodents, rabbits, birds, frogs, lizards etc. and seen perching on poles, posts, and other man made structures, just like in your picture.
Identifying features
The wingspan is between 1.1 and 1.4 metres, making it medium-large relative to many European birds of prey. It has a short neck and medium length of tail which is fan shaped when the bird is in flight, and the tail is about as long as the wings are wide (distance between front and back edge of wings). In these pictures you can see an adult first, and a juvenile. The juvenile has a much lighter colour, and has distinctive black markings on the leading edges of the wings, shaped like commas or speech-marks. Common Buzzards also have dark tips to the tails and wings, becoming much more prominent in the adult, and yellow legs and beak.

Images from RSPB. See also, Collins Bird Guide, ISBN: 978-0007267262.

See the image in Chris' answer for a picture of juvenile in a similar pose to the one you saw. This answer is here to provide more general and in-depth tips for identifying the Common Buzzard made in complement to Chris' answer.

I think your identification is correct - this is a juvenile Common buzzard (Buteo buteo), which have a lighter coat than the grown-up birds. See this image (from here), which also shows a juvenile bird:


text:
Anaerobic nutrient expenditure
Doing some research into different forms of exercise and energy systems and I realized something odd about the way we talk about energy.
When we eat, we take on macronutrients that are broken down into their smaller components, but on it's face the assertion is that:
Fat = 9 Calories/gram
Carbs = 4 Calories/gram
Protein = 4 Calories/gram

However, when you look at the Krebs cycle, one acetyl sugar molecule generates 32 ATP molecules. Contrast that against Anaerobic metabolism and the Cori cycle, 1 sugar molecule generates 2 molecules (at a cost of 6 ATP in the liver later).
There are all sorts of fitness calculators out there, most of the calculations are based on the Assessment of Physical Activity and Energy Expenditure: An Overview of Objective Measures book, most of which was put together through measuring oxygen in put versus carbon dioxide output (in conjunction with heat radiation.  The clear problem with associating that with weight training and other anaerobic activities is that the other activities don't immediately create CO2 and don't immediately require O2. Some attempts have been made to make estimates based on lactate production in the blood stream, but I'm not confident in those results.
My question is, when there is anaerobic activity taking place, are we actually "burning" more base ingredients than we are exercising aerobically?
In other words, even if I'm only burning 100 Calories lifting weights, would I actually be burning the equivalent of 1,600 Calories based on the glucose I would have converted to ATP aerobially?

The Urea cycle doesn't generate energy and it doesn't break down amino acids. It uses energy to convert ammonia and carbon dioxide to urea. The Cori cycle isn't a metabolic pathway generating energy as you imply. It's a system whereby lactate produced in muscle exercise is goes into the blood and is taken up by the liver, converted back to pyruvate and then to glucose which goes back into the bloodstream. There is no net generation of energy. The liver expends energy so that muscle can use it. You need to sort your question out.

@David Removed the bit about the Urea cycle. I used the Cori Cycle as a shorthand for anaerobic metabolism and the Cori cycle. As stated in the question, not only is there not a net generation of energy, there's a net loss in energy, the muscles create energy at 16 times lower rate than oxidation and the liver expends energy making more glucose, which is the driving factor in the question.


text:
Evolution of parasite into ideal parasite
An ideal parasite is a parasite which thrives within a host without harming it (according to my NCERT textbook).
Then, quite obviously, why hasn't that happened yet? I mean, natural selection can lead to such a species, which is beneficial to us and also, not at all detrimental to the parasite.

It has happened, many times; commensal and mutualistic species are common.  Mitochondria and chloroplasts, lichens, etc are examples.   But there is no specific reason, other than common misunderstandings of natural selection, to expect this to be inevitable.  You may want to explain your reasoning for that point (or put it as a separate question).

@iayork You are right. However, how are mitochondria and chloroplasts examples of ideal parasite? Also, which point are you asking me to explain?

Do you understand the current understanding of how mitochondria and chloroplasts arose? If so, please clarify why they don't fit your question.  If not, check wikipedia, linked above. The other point I suggest you explain separately  is your claim about evolution, which I believe indicates a misunderstanding of natural selection.

@iayork Yes, I didn't know about the current understanding on how chloroplast and mitochondria arose, so that's clear now. Also, edited the question!

Why are you asking why something didn't happen, then, when as you can see it has happened many times?  Is there more to your question?

@iayork I knew such species existed, but didn't think of them as an ideal parasite. Because, when you think of a parasite, lichen, mitochondria and chloroplasts are not the first things to come to your mind. You opened up my mind :D

@iayork I think you can make an answer by developing further your comment.

Related: Why do parasites sometimes kill their hosts?

There was a recent opinion article in science which hypothesizes that mitochondria and chloroplasts could have been parasites. In my opinion, the paper has a lot of incorrect presuppositions and also makes far-fetched assumptions. IMO, mitochondria and chloroplasts would have been preys and not parasites. Anyway, an ideal parasite is the one that survives anything. What your textbook says is one possible way by which it can do that. You should see the post that @Remi.b mentioned.

Post is related to Why do parasites sometimes kill their hosts? and I think duplicate of Why have parasites not evolved to be harmless?.


text:
In theory how fast could nerve signals travel if the nerve fibre was perfectly insulated?
My question is purely theoretical and my main aim is to find out the maximum speed that a nerve signal can travel within a nervous system and and whether this speed represents the physical limit of how fast a nerve signal can travel. This could also extend to designs not seen in nature and possible artificially designed nerves i.e. synthetic biology. Apologies for an awkward question!! Any input is welcome!!

There are multiple factors besides insulation that go into electrochemical impulse speed. For example, the thickness of the axon also contributes very much. These links may interest you: https://en.wikipedia.org/wiki/Nerve_conduction_velocity http://biology.stackexchange.com/questions/21790/how-long-does-a-signal-from-the-brain-take-to-reach-the-limbs

For some background on saltatory conduction: https://en.wikipedia.org/wiki/Saltatory_conduction
I feel that a "perfectly insulated" neuron couldn't actually allow the signal to travel. Insulation (which, in neurons, is basically layers of fat wrapped around axons so ions cannot pass) allows the electrical signal to move further along axons (less ionic leakage) and faster (due to decreased membrane capacitance-it takes less charge movement to generate the same potential difference across the membrane; see this question: How is membrane capacitance related to the increased speed of saltatory conduction?)
Also, you should check out wikipedia's page on cable theory of neurons:
https://en.wikipedia.org/wiki/Cable_theory
This is why myelination increases conduction speed, as you may or may not already know. The increased length of the ionic signal (due to the inhibited leakage) allows voltage-gated ion channels which are further away to be activated as a result of any given local membrane depolarization. This all happens faster due to the lower capacitance.
However, the only way the action potential can actually "travel" at all is due to the sequential activation of voltage-gated ion channels along the axon. This is the case in both myelinated and unmyelinated axons, it's just that the spacing is greater when myelinated. In the insulated, fat-wrapped regions of axonal membrane, there are no ion channels, voltage-gated or otherwise. If there were, the layers of fat would not allow ions to pass through anyway at this point. Thus, the "perfectly insulated" axon could never actually propagate a signal, because the signal still requires the chain reaction of voltage-gated ion channel activation and sodium influx at some point. Myelinated conduction is faster because the spacing is increased, but increasing the spacing to infinity would not allow the action potential to be passed on.
I suspect that there is a certain threshold in the extent of myelination where the spacing between nodes of Ranvier becomes to great to have effective propagation of action potentials. I wouldn't be surprised if evolution has resulted i a relatively optimal spacing of nodes. I suppose a better question might be: what is the speed of conduction between nodes?
I suppose it would be possible to send current through a perfectly insulated axon and potentially activate a voltage gated calcium channel at the terminal. However, This would be different than an action potential and would be effectively reducing the neuron to an electrical wire. Sometimes it's better to keep things simple.

I think that by "perfectly insulated," the OP probably meant "optimally insulated," as in "what is the physical limit of how fast an electrical signal can travel through an axon with the best possible insulation?" (@MICHAEL TAYLOR, correct me if I misinterpreted your question.)

OK should I delete this?

No. You have a lot of good information here, I just don't think it's what the OP is looking for. You could just edit it. But wait for the OP to clarify his question before you change anything, it could be exactly what he wanted.

Thanks for your answer Jory and your comments @CDB. Your answer is what I was looking for! Its really thorough and informative and actually clarifies my chain of thought in regards to nerve conduction and its properties and limitations.


text:
Why did this project encode information in DNA in binary and not in base 4?
I have read an article about Harvard scientists encoding 700Tb of data in DNA strands. But they encoded the information in base 2, so T and G both represent 1 and C and A both represent 0. But why binary? Why didn't they just use base 4?
EDIT: here the link

Simply because silicon-based computers fundamentally work with and store information in binary. So even if we wanted to think of the data in base-4, the computer would still have to convert to binary

In the research article on the effort, they give the following explanation for doubling up nucleotides, rather than have each nucleotide stand for two bits:

This allows us to encode messages many ways in order to avoid sequences that are difficult to read or write such as extreme GC

In practice, they chose which base of the pair it was randomly (so a 50% GC content), while disallowing homopolymer runs greater than three.
Their scheme also uses barcodes and addresses as the "table of contents"/"index"/"page numbers". (The data wasn't stored on a single long piece of DNA, but on a large number of shorter fragments.) By having a slightly flexible coding scheme, this allows them to potentially avoid inserting those annotation elements within the contents.
Furthermore, a slightly flexible coding scheme would allow them to avoid accidentally encoding a text with part of a select agent's genome. (That is, you wouldn't want to synthesize part of the smallpox genome when you're storing your novel. If you can change the nucleotides used, you can avoid that.)

Interesting. When I first read the question I wrongly assumed that they had just used two bases in the synthetic DNA, and I wondered if they had avoided C because of its spontaneous deamination to U. This might seem better for long term storage. Wonder why they didn't do that. Presumably something structural.


text:
How many paraphyletic groups can be formed from a phylogeny?
How many paraphyletic groups can theoretically be created from this phylogeny?

I found (2n)-2. Is this correct?
This is not homework nor exam, just a question about paraphyletic groups.

If we define a paraphyletic group as any group on a phylogeny that is not monophyletic, I count there to be 2^n - 2*n paraphyletic groups for a fully ladderized tree with n tips.
There are 2^n possible groups of n species. Of these groups, 2*n of them are monophyletic: n groups containing a single species, and n groups containing multiple species.

I cant find a good explanation for paraphyletic group, what are all possible para. Groups if n=3?

@Nemexia The term "paraphyletic" doesn't really have a hard definition, but the way I defined it, a tree with 3 tips will have 2^3 - 2*3 = 2 paraphyletic groups: {1,3} and {2,3}.

Why arent these paraphyltic? {1,2} with common ancestor( first and secound node)?

{1,2} is a monophyletic group because it contains all descendants of the MRCA of {1,2} (the ancestor of {1,2} only has 1 and 2 as descendants, so the {1,2} group is monophyletic.


text:
Cellular demand for antioxidants
Antioxidants such as ascorbate and glutathione serve to inactivate radicals and counteract spontaneous oxidation reactions, such as unwanted disulfide bonds in proteins. These systems are cycles, where a "spent" antioxidant (say, oxidized glutathione) is convert back to its reduced form by another reducing agent, usally NADPH.
My question is, how much NADPH (or reducing equivalents) does a cell devote to this antioxidant defense? What is the flux, in molar amounts per unit time, through these systems? Does it represent a large portion of the energy metabolism of cells?
I am guessing that the flux is quite large, but I have never seen any data on this. Most likely it varies a lot between cell types, but I would be happy to see any numbers. I think this is important for understanding antioxidant chemistry in cells, yet it is rarely discussed in the literature.

Most experiments to try to get at this type of question use stable isotope tracers to measure NADPH production from the various pathways that can make it, and then subtract away the amount that's predicted to be needed for growth/anabolism (based on the observed growth rate and biomass composition). I think this paper is by far the best example:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104482/.
Quote:

The overall demand for NADPH for biosynthesis is > 80% of total cytosolic NADPH production (Figure 4b), with a majority of this NADPH consumed by fatty acid synthesis. At least in transformed cells growing under aerobic conditions, most cytosolic NADPH is devoted to biosynthesis, not redox defense.

Note that these are fast growing cells without additional oxidative stress. Interestingly, what the authors find is that imposing additional oxidative stress doesn't actually change NADPH production that much, but it slows down growth as more NADPH is used for anti-oxidant defense (Extended figure 9).
For skin cells, the situation might be a bit different, at least in terms of the increase in NADPH production upon oxidative stress. You might look at this paper: http://www.cell.com/molecular-cell/fulltext/S1097-2765(15)00456-6

Yes, I am aware of Rabonowitz 's paper. It doesn't contain any direct data on antioxidant fluxes afaik --- the values you refer to are rather model-based predictions.  Zamboni's paper does not really address the question I believe ; it is about pentose phosphate fluxes. But perhaps this is the only data available.

So the major error in the model would come if there was a source or a sink of cytosolic NADPH that was not being considered. Probably you can judge for yourself how likely that is to be, but I for one am reasonably satisfied with the set of reactions taken into account. If anything, I would guess that an unidentified sink (with a net NADPH->NADH result, such as a lipid synthesis and degradation cycle) is more likely than an unidentified source, which would even further lower the estimate of NADPH used for antioxidant defense.

Also I can reemphasize that to me, the major caveat is really the cell type and environment being considered -- doing this type of exercise in a real in vivo context as opposed to a cell line would be really fascinating.


text:
Species identification - greenish blue ocean worm (nudibranch?) in Perhentian Islands, Malaysia
We found this on a beach at the Perhentian Islands, Malaysia in March, 2016 and cannot identify it.  It's some sort of worm-type creature with many legs and bluish back about 15cm long.  The legs undulated along the body as it swam.
back:

belly side:

It's hard to identify from the photos provided, but I think it is Chloeia flava (a species of polycaete worm, within the phylum Annelida), also known in English as the "Golden Fireworm".
The size is roughly similar to what you describe (they are typically about 7-10 cm long). The individual you observed looks like it lives in sandy bottom environments (not a typical environment for a nudibranch), and this worm does also. It is commonly found all across the warmer Indo-Pacific as well, and looks like the individual observed in your photo.
If it is not this species, I think it is another species of the same family, Amphinomidae.

Thanks! We're happy to have seen a nudibranch in real life.  We just learned about their existence a few months ago when a blue dragon washed up in Australia.  We're lucky we weren't stung by this one since we were swimming very close to it to study it.

Sorry my answer was edited. It is not a nudibranch or mollusk but a polycaete worm. If you want to find a nudibranch I recommend checking tidal pools or near coral. If you aren't a diver yet, the best way to observe them is to take up scuba diving.

:( So not a nudibranch but still very interesting.

Sorry for my mistaken edit. My mind was so set on a nudibranch that I didn't even spot the mistake even though I visited the wikipedia page for C. flava.

@fileunderwater No problem! Thank you for the edit. It was my first post and I learned how to format posts now.

@Sudachi Welcome to BioSE! Here is a useful overview of html/markdown formatting at SE.