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Question about flux and changes in net flux of molecules across a membrane
I've been reading a book called Principles of Human Physiology by Stanfield 5th edition, and was reading a chapter on membrane transport when I came across a figure question which will be posted below.
It says "As time passes, does the one-way flux from side 2 to side 1 increase, decrease, or stay the same?"
I have unfortunately been unable to comprehend why and how the answer is "Increase". I would suppose it stays the same, correct? There is no possible way that a flux would occur, unless by individual molecules (regularly) passing through each side on a equal basis.
It was a topic on Simple diffusion.
P.S. This book, as i've noticed hasnt been quite explaining some things in a clear-cut way to understand as a beginner, and also it has had some mistake within it.

Does it help to emphasize that the question is asking about flux from side 2 to side 1? It's not asking about flux from side 1 to side 2 or net flux.

Keep in mind that diffusion is just the random movement of particles. Over time, the solute will randomly distribute throughout the entire available volume. Under initial conditions, there is no solute in side 2 and so it cannot move to side 1 (thus flux from side 2 to side 1 is 0). At equilibrium, the net flux is 0 but there is still flux from side 1 to 2 and from side 2 to 1 (which is equal and opposite) due to the random motion of the solute. So, flux from side 2 to 1 goes from 0 at initial conditions to some non-zero value at equilibrium (ie it increases).

@canadianer You can post that as an answer. However this is a physical chemistry question and off-topic.

Diffusion is just the random movement of particles. Over time, the solute will randomly distribute throughout the entire available volume. Under initial conditions, there is no solute in side 2 and so it cannot move to side 1 (thus flux from side 2 to side 1 is 0). At equilibrium, the net flux is 0 but there is still flux from side 1 to 2 and from side 2 to 1 (which is equal and opposite) due to the random motion of the solute. So, flux from side 2 to 1 goes from 0 at initial conditions to some non-zero value at equilibrium (ie it increases).

This is also what is refered to as steady-state. Or dynamical equilibrium. Overall, the net flux is zero, but still there's constantly flux from side 2 to side 1, even more so when more solutes are in side 2.


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life based on different elements
It is commonly proposed to look for life based on silicon, based on it's relative abundance and similarity to carbon. However, carbon and silicon are not completely interchangeable. The bond strength between carbon or silicon and itself is different, thus, some molecules with high chain length can not be replicated with silicone. Similarely, molecules such as proteins, for which all carbon atoms are replaced with silicon, would not retain their form and thus not their function.
Is life based on silicone still possible, just under a different environment?
This would affect how we should look for aliens. Also, if silicon based life is unlikely, is there some other element that could lead to life?

A couple references might give you pointers to work of interest: 1) https://science.sciencemag.org/content/332/6034/1163; 2) Rampelotto, P. Henrique (2010). The Search for life on other planets : Sulfur-based, silicon-based, ammonia-based. The Journal of Cosmology, 5, 818-827.

Welcome to SE Biology. The Tour makes it plain that this is is a question and answer site, not a discussion forum. As the Help states  "You should only ask practical, answerable questions based on actual problems that you face". The only responses to the present question are speculation and discussion, which is why I have voted to close it as off-topic. (Oh, and you might check the difference between silicon and silicone.)

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Identify this bug (which looks like a cross between a beetle and a bed bug)
I am located in a large Eastern European city. During this summer, a new kind of bug has started appearing in my house (or more specifically, coming into my house from the garden). It's about 1.5-2 cm long, doesn't appear to have any wings, and a relatively strong exoskeleton (makes an audible crack when the bug is squished). Its favorite activities seem to be either sitting in the middle of the floor, waiting for someone to step on it, or sitting on the ceiling and then falling onto somebody's head. Whenever I see one of them, it's almost completely stationary, regardless of the time of day.
Here are pictures of it (sadly, they're very grainy due to my phone's camera's low quality).

looks kind of like a stink bug but the color is off and the image is so grainy that I cant quite make out its geometry.  Definitely some kind of beetle though. Did it stink when you stepped on it ?

I don't recall smelling anything. Most images of stink bugs I found on the internet had a different color on the end of their abdomens, and this is not the case here.

right, but again I can barely see the bug because the image resolution is so grainy.

It looks like your camera's smudged.. have you tried wiping it off?

That is a weevil. Coleoptera, Curculionidae. Weevils have distinctive snouts, and elbowed antennae. They can be crop pests, and eat seeds, but do not spread diseases to humans. I suspect these have just found their way into your home by mistake. https://bugguide.net/node/view/1126677

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Is this a bedbug or a book lice or what?
So basically i found this thing in my home. It's super small so I had to zoom it for you. Whiteish/yellowish colour. We had bedbug problem back in our dorms and I'm worried I somehow managed to transfer them home but I don't know if it's a bedbug nymph or a book lice or what kind of insect, so I'd really appreciate someone's opinion on this.
Edit: It's really small, like. really small. my mother wouldn't even see it and thought me crazy. Just zoom made it look bigger. I'd say 1.5mm maximum at the very best. Moves kinda quickly and I thought it jumped two times when i was trying to capturing but maybe it was just me doing it to it. Living in Europe, Slovakia specifically.

Only except its extra long antannae this bug seems to be Cimex sp.

Welcome to Biology.SE. How small is it? Where do you live? (You can edit those info directly in your post with the 'edit' button).

Heya. I edited it so maybe that could add some input. I know how an adult bedbug looks like but this one baffles me cause of it's size, that's why I even thought it could be nymph stage

This is not a bed bug, but some sort of book louse (order Psocoptera). Bed bugs have a more compact body shape, even in the early stages:
 (from http://www.bedbuginspectiongroup.com/facts/)
Compare this with a book louse, and I think it is much closer to your specimen:

(from https://commons.wikimedia.org/wiki/File%3ABook_louse_01.JPG)
Also, here is a page comparing them: http://bedbugger.com/2008/03/04/book-lice/
Hope you stay bed bug free!

Thanks a lot man! I shall calm myself down now. I'm moving tomorrow and I don't wanna infest everything where I go, my personality does the job good enough, who needs bed bugs with that. Thanks once again

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Can a gene-expression or epigenetic 'user-history' be found in the body?
(EDITED - a lot of what I am saying is implicit and simplified. I'm not looking to recreate the numerous textbooks and scientific papers on how DNA works).
As far as I can understand it, an organisms basic building blocks (proteins) are made up of DNA, Genes, and Chromosomes. The most basic form of this is DNA, made up of molecules in double helix strands. DNA carries all the instructions for the body in a simple 'database' or 'blueprint' form. Genes are chunks, or sequences, of the DNA telling the body 'what to do'(1) by reading the 'DNA database' in a myriad of unique coding sequences. Genes naturally(2) switch on and off throughout an organisms lifespan allowing amongst other things for an organism to grow from young to old. DNA is essentially(3) stored in Chromosomes.
External and environmental factors can influence the expression of genes, and the information stored in the DNA (4) - the study of which is Epigenetics. These Epigenetic factors can change over time, switching genes on and off. (5)
Does the body store a history of these expressions? Do the chromosomes (or some other part) of an older organism store a 'user-history' of which genes where previously activated when the organism was younger? eg, can you tell which genes where active when a person was 12, from the cells of an 80 year old?
Apologies, I do not have a background in Biology. (6)

EDIT NOTES
(1) what to do, how to do it, when to do it. not necessarily all life supporting instructions but also the minute-to-minute, day-to-day processes etc.
(2) naturally. there is no black and white in nature, only shades of grey.
(3) essentially. not exactly and not in all cases but mostly.
(4) As in, factors influence the expression of genes (which in turn are made up of DNA information). I am not suggesting that external factors can influence the 'DNA database' itself but rather just how they are 'read', sequenced and expressed as genes.
(5) again, naturally. no sharp on/offs but variations of concentrations.
(6) I may not have used the correct terminology.

Please avoid editing your post so drastically after an answer has been posted. Also, you do not have to hide your misunderstanding via loads of tiny inaccurate notes that only acknowledge that you realize you might be inaccurate. What you do not understand is of interest as it is what help people to understand what you are after and what is unclear to you. Finally, all these tiny notes look very messy and I would recommend keeping the old version.

@Remi.b I agree major changes may affect previous answers - I wanted to clarify the poor phrasing so future answers could focus on the question more. That's why I purposely left most of the original content intact (I pretty much only expanded the sentence about the DNA building blocks into 3 or4 sentences). I tried to leave my edits to the messy notes :) so that viewers wouldn't have to go view the previous version of the question. Unfortunately I couldn't figure out how to get subscripts for the edit notes to make it less messy. do you think listing the notes all at the end would be better?

Main question

Does the body store a history of these expressions? Do the chromosomes
  (or some other part) of an older organism store a 'user-history' of
  which genes where previously activated when the organism was younger?

Cells can sometimes have a "memory" of the gene expression state which allows the cell to perpetuate its gene expression programme. This is facilitated by epigenetic mechanisms. Cells can also maintain a short term memory via feedbacks and switches (Casadesús and D'Ari, 2002). Immune cells store the memory of previous exposures to a certain pathogen (in this case each clonal population stores one piece of history which is unlike one cell storing the entire history). However, I don't think there is an explicit "user history" kind of mechanism. Most responses are dynamic (and memoryless); there are only a very few situations (such as immune response) that really need a history log. Usually the cellular memory is just one level deep. Storing deeper than that would cost the cell a lot.

Other corrections not directly related to the question

As far as I can understand it, an organisms basic building blocks
  (proteins) are made up of DNA, Genes, and Chromosomes.

This statement is extreme oversimplification. As a matter of fact, water is the most abundant molecule in the bodies of most (if not all) organisms. RNAs and proteins are essential molecules required for cellular functions. Lipids are also important as they constitute the cell membrane. Moreover, proteins are not made up of "DNA, genes and chromosomes". Your subsequent explanation of how the genes work is correct but this statement is quite wrong.

The most basic form of this is DNA, made up of molecules in double
  helix strands.

Misleading again. It is not correct to call DNA as "most basic form". In what way? This statement is also opinion-based.

DNA is essentially(3) stored in Chromosomes.

Chromosome is an assembly consisting of the DNA and some proteins. In a way, DNA is contained in the chromosomes. As also pointed out by Remi, your statement can have misleading interpretations.

External and environmental factors can influence the expression of
  genes, and the information stored in the DNA (4) - the study of which
  is Epigenetics. These Epigenetic factors can change over time,
  switching genes on and off.

This process is simply called "gene regulation" or "regulation of gene expression". Epigenetic mechanisms (such as DNA methylation and histone modifications) are one of the mechanisms of gene regulation but they are not the only one. You can simply google "gene regulation" and you'll get plenty of resources on this topic.

Thanks for the answer. Using my popular science biology background. Could the junk dna (whose purpose is not fully understood) potentially store some sort of extra information?

@EveryBitHelps It potentially can (and would no more be junk) but storing such an extensive amount of information would require a lot of "space".

First Paragraph - let's debunk what was poorly phrased
Many sentences you wrote are quite misleading. You should have a look at an introduction to molecular genetic to have a better understanding such as what you can find on Khan Academy. In short:

the double helix DNA strands are the building blocks of an organism

This sentence is very opinion based. as a matter of proof, one could for example replace the term double helix DNA by "cells" (or other terms) and many would still be satisfied with the sentence.

Genes are chunks of DNA telling the body what to do.

A gene is a part of DNA which contains regions coding for proteins. There are many sequences which are not coding for any proteins that are essential for the individual survival (such as regulatory sequences or sequence coding for rRNA for examples).

Genes naturally switch on and off.

The regulation of gene expression is actually much more continuous than just on/off. Also, regulation of protein concentration can occur at different levels and not only by regulating gene expression.

DNA is essentially stored in Chromosomes.

This sounds like chromosomes are boxes in which one can find DNA. In reality, DNA is a type of molecule which can be found under different forms. In humans (and other eukaryotes) most of the DNA (but not all) is present in the form of chromosomes.
Second Paragraph - What is epigenetics?

External and environmental factors can influence the expression of genes,

This is correct

and the information stored in the DNA

This is wrong. Environmental factors do not affect the sequence of base pairs of the DNA. It only regulate its expression. Such regulation of expression can last for a long time and even be transmitted to the offspring. The term epigenetics is loosely defined. In short epigenetics refers to the set of mechanisms that affect gene expression at short and long term. The classic mechanism of interet in epigenetics in the methylation of histone tails (quickly speaking, histones are proteic structures around which DNA is wrapped).
Your question

Does the body store a history of these expressions? Do the chromosomes (or some other part) of an older organism store a 'user-history' of which genes where previously activated when the organism was younger? eg, can you tell which genes where active when a person was 12, from the cells of an 80 year old?

As explained above, some of the molecular mechanisms yielding to changes in gene expression can have long term consequences on gene expression (which can even be inherited). But there is not data bank (or other centralized or not source of information) that specifically record the expression of each gene at any one time in the history of the cell life.

Thanks for the answer in the last paragraph & half. I was trying not to get bogged down in the details of the basics (whole textbooks are devoted to) so that I could get to the question. I also appreciate I may not have used the correct terminology and a lot of what I was meaning was implied. But how can the first line you quoted about the DNA helix be referred to as 'cells'. eg "the cells are the basic building blocks of an organism"...no problem in itself. but now a follow up sentence "an organisms cells are found in cells"?? I'll fix the sentence idea to be clearer but not to cells.

I was only referring to the part of the sentence I quoted. My point was that calling "DNA strands" the building blocks of an organism makes little sense (or at best is very opinion based) and as a matter of proof, I wanted to show you that other concepts (like 'cells') could equally be called building blocks of an organism.

In between your post edit and your comment you seem to both much the clarification I tried to do on your sentences. You might be well aware of some of the things I tried to clarify and this is ok. The most important is to know whether your question was answered and if not, why. (In any case, I would recommend you waiting for answer or peer-review from other users before accepting an answer).

Ah! the cell comment makes sense then :) I was wondering about that! yeah, sorry. I must have missed your edit. I try accept answers once there is more than one answer as I find the ticked answer prevents users from attempting an answer.

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Formation of ammonia from air and moisture
On extended bicycle trips I sometimes slept under a plastic sheet, which helped with mosquitoes on hot nights. But there was a noticeable build-up of ammonia which made this almost impossible for more than an hour or so at a time.
Air is mostly nitrogen $(N_2)$ and there is always water (containing hydrogen) on a humid day. But I wonder about the mechanism for the formation of ammonia under these circumstances? There are (according to Wiki) trace amounts of methane and $H_2$ in the air. But methane and hydrogen (g) are I think pretty stable.
I wonder if the presence of exhaled air (containing $CO_2)$ could be a factor?
Thanks for any ideas.

If you're absolutely sure it's Ammonia ($NH_3$) you're smelling, it's probably from you.
Ammonia will not spontaneously form at any significant rate from the air. Molecular Nitrogen ($N_2$) is extremely stable.
What can happen is that during marathon-type activities, muscles turn from carbohydrates (which are later converted into glucose and enter into the Krebs Cycle) as an energy source to proteins themselves.
One of the waste products of protein catabolism is Ammonia, which is excreted in your sweat if the body can't convert it into Urea ($CH_4N_2O$) quickly enough:

Ammonia forms with the oxidation of amino groups (-NH2), which are removed from the proteins when they convert into carbohydrates. It is a very toxic substance and only one nitrogen atom is removed with it. A lot of water is needed for the ammonia excretion.

Yes, no mistake about the ammonia. This makes perfect sense. Long distance cycling with little to eat, intense humidity and heat. Thanks.


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Why is the quality range of fastq format so broad?
Referring to fastq format, it is clear that in fastq format, there are 94 quality value for a sequenced Nucleic Acid of a DNA sequence read and they are:
!"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHIJKLMNOPQRSTUVWXYZ[\]^_`abcdefghijklmnopqrstuvwxyz{|}~

So, I have two questions:

Why is the quality value range so broad (94 levels)?
In a particular case of analyzing data, we saw, the frequency of I is so high, which is not a good quality. So, why would we accept such a poor quality in research?

Initially, there were several quality encodings that used to follow different ranges of ASCII characters to denote the quality of read. The range that you mention is a union of all those encoding formats. Nowadays, the most common encoding is Phred+33 (used by Illumina, Sanger, Ion Torrent and other popular sequencers) which uses these characters:
!"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHI

Character I denotes a phred score of 40. Aligners, when they read fasta files, by default assign a score of 40 (I) to all positions. This might be one why reason you are seeing a lot of I.
Anyways, if your fastq follows the phred+33 format then 40 (I) is a pretty good score which denotes a good quality read. Or you could be aligning fasta files. It would be a bad score if your encoding is phred+64 which I guess, is not the case.
ADDITION
The file that you linked is a fastq file. This sequencing experiment has been done on 454 GS FLX Titanium machine. 454 machines use a different way of calculating quality scores compared to the traditional basecalling phred scores. From the manual:

6.6 Phred-equivalent Base Quality Scores
Quality scores for individual called bases are determined by a method developed in
  collaboration with the Broad Institute (Genome Research,18(5): 763-70,
  2008), whereby the methodology described by Ewing and Green (Genome
  Research, 8: 186-194, 1998) for the creation of quality scores as part
  of the Phred basecalling algorithm is applied to generating quality
  scores for 454 Sequencing reads. The quality scores computed for each
  called base are written to the CWF and SFF files (and optionally to a file paralleling the basecall FASTA file). Briefly, the method
  compares the properties of each base’s flowgram signals against
  properties that have been found to correlate with accurate and/or
  error-prone signal information, using training sets of read data. A
  multivariate analysis of those properties determines the sets of
  property values that best describe “bins” of basecalls, then assigns
  the training set accuracy rates of the basecalls in each bin as a
  quality score using the following scale:
$$Q = -10\ \text{log}_{10}(\text{error rate})$$

Usually, you'll have two files for 454 experiments — one that holds the sequence and the other that holds the quality at each position. These files can be combined to generate a fastq. This file is encoded in the phred+33 (also called Sanger/Illumina 1.9) format which I mentioned above. Phred+33, I guess, is also the standard encoding format adopted by NCBI/ENA/DDBJ and all new sequencing runs are encoded in this format. If you do not know the encoding you can run fastqc on your fastq file and it reports the type of encoding.
In your case, I would denote a score of 40 (ASCII value - 33) which means an error rate of 10-4 i.e. the read is of good quality.
The below graph is obtained by a fastqc run on your file. The bars denote quality statistics at each position. Note that the mean quality drops towards the end of the read.

A fasta file does not indicate quality but when you map them to your target, the aligner (I know of Bowtie based ones) assigns a default score of 40 at each position, during the alignment (and in the output).

I am sure that they are fastq files. This is an example file. However, now, my question is: how could I be a pretty good score? On the other hand, does fasta also give the quality value in this way? I did not find them here. Thanks for trying to help me.

FASTA format does not have this scores. I believe FASTQ is just an extension of FASTA to include the scores (and possibly other information). But I have no evidence this is actually the case.

@WYSIWYG Do aligners actually assign a default score of 40? (I really do not know!). Any reference I could take a look at regarding this? Thanks.

@ddiez Bowtie does it; that I am sure of. You can check the manual or try a dummy run. I think STAR also does it but I am not sure. The aligners also, by default assume a phred+33 encoding.

As mentioned by @WYSIWYG in his answer the quality scores in FASTQ file format are encoded in ASCII characters, and there has been several ways to encode this information. The wikipedia FASTQ page that you link in your question describes some (not sure if all) the different alternatives.
Now, why do we have this wide range of characters for the quality scores comes down to the question of what these characters really mean. What we really care is about the probability that a particular base has been assigned incorrectly. This is the base call error probability (p). We can define a quality score based on the error probability as:
q = -10 x log10(p)

So, if your base call is truly wrong (probability of error p = 1) then q = 0. If your base call is certainly correct (p = 0) then q -> Inf as p -> 0. Imagine your probability of error is p = 0.0001 (that is, most likely the base is correctly assigned). Then q = -10 * log10(0.0001) = 40. Therefore, a score of q = 40 means a probability of error in that base call of 1/10000. Quality scores are considered, as far as I know, between 0 and 40.
Now, another issue is how to include this information for each base in the FASTQ file. It would take too much storage space to include the score as a real value number (i.e. with decimals). A possibility instead is to round it- after all there is no much difference between a score of say 39.7 and 40- we care more about the order of magnitude. But then we will have to still store two digit integer numbers per base. What we can do is map the rounded score to the corresponding ASCII character + some offset. That is, as you can see in the FASTQ page the ASCII value for character I is 73. If you are using phred-33 encoding this actually means that character I = 73 corresponds to quality score q = 73 - 33 = 40, which means p = 0.0001. Voila. Character ! = 33 represents score 33 - 33 = 0 (p = 1). In a phred-64 representation a score q = 40 is encoded with character h = 104. Then q = 104 - 64 = 40.
Of course this is just a rough approximation about how the actual phred score is mapped. Phred is actually the name of a program that was developed to maps the quality scores to ASCII characters. The method in more detail is explained in the original publication (which I admit had only went through):
Ewing B, Green P. Base-calling of automated sequencer traces using phred. II. Error probabilities. Genome Res. 1998 Mar;8(3):186-94.


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How can I make sure my UV-purificator kills bacteria?
I'm going to show a UV-purificator for water on science fair. How can I easily check if purificator kills most of the bacteria? I need a quick and possibly easy method.

How did you use to test for whether your UV-purificator works? Did you just assume it works?

Well... I will also check if it works using this method. It's a student project so we can just follow the descriptions on the internet and hope that it will kill bacteria. And even if it won't work with 100% efficacy, we just want to show killing effect of UV.

There are not many quick inexpensive methods that can show the number of dead/viable cells. Staining+microscopy is a quick method but I am not sure if you can obtain a microscope and the stain (whether the school will fund you for that). Moreover counting bacterial cells directly would require some patience and expertise. Colony based methods (plating) are convenient but would take time.

Not having the equipment needed to actually count bacteria, you can use things you know bacteria does to find out how much they were affected.
My approach would be thus:

Select a model bacteria. There are a few candidates, but probably the most readily available is lactobacilli, which can be found in yogurt and (loosely translating terms of art) is a Gram-stainable fermentor-sometimes-breather.
Infect the water with a known quantity of bacteria and a food source (lactobacilli eat lactose - ie from milk) and equally divide it into a control and experimental group...
You'll need to find an alternative way to estimate the bacterial content in the volume of water used compared to a control colony. Since lactobacilli produce lactic acid, you could use the pH value of the water (either with an indicator or a meter) to detect bacterial metabolism, compare that to the control's pH value.
Record the UV exposure time from the experimental group, and isolate the control group from any potential UV light source, such as the sun.

Even if you find that, for example, your particular strain of lactobacilli is not sensitive to your UV light source, that's a perfectly scientific result! How did you obtain it? The source likely knows what kind of bacteria it is. Perhaps the UV light merely interferes with bacterial metabolism, and doesn't kill it. Unanswered questions are wonderful, you may have provided a place for further research to take place. You could then use the two groups to infect a food source (ie milk) and compare post-exposure growth, depending on how much time is available.

I think the main point that is left unaddressed is regarding the technique that can be used to quantify viable cells in the sample after treatment. Your answer as of now focusses only on how to set up the experiment properly.

OP is looking to "check if purificator kills most of the bacteria" - viable cell count is probably overkill for that. I suggest a simple comparative approach. Dead bacteria don't behave like live bacteria, so one only need compare the chemical content of the water containing "possibly dead" and "known live." Say there's no difference - it wouldn't make sense to do a cell count at all. You would expect the known live bacteria to do more than a dead one, thereby changing the chemistry of the water.

OP asked whether most bacteria are killed. So you count the live ones remaining to determine that. That's how it is usually done. The dead ones can also possibly cause harm because of endotoxins. Even in that case an explanation of an existing methodology to quantify the "chemical content" is, IMO, essential.


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Neuronal Architecture of the Brain
To what extent do brains (e.g. of humans) contain recurrent  connections?
I am studying artificial neuronal networks and frequently encountered the statement, that recurrent neural networks are closer to biological neuronal networks than for example feed forward networks. But I didn't find information on the question if feed forward or recurrent architectures dominate the brain architecture.

The recurrent patterns of connections in a network are known as network motifs.
You can check this paper out. They have identified common network motifs in different types of real networks including neural networks (of C.elegans though).
Apart from feed forward loops, bi-fan is also a common network motif in neural networks.
Perhaps the connectome project has data for human brain which you can analyze for identifying network motifs. You would have to request for the data, though.

Ok, let's talk about mammalian neocortex rather than about the entire central nervous system.
The vast majority of synapses within the cortex are formed between neurons within the same cortical area (Binzegger et al 2004). Although most of these synapses will not be self-connections (from a single neuron back to itself), they are recurrent in the sense that there is a high degree of interconnectivity within a cortical area. In visual cortex, connections within the superficial layers of cortex (layer 2/3 <-> layer 2/3) make up around 70% of all excitatory synapses in visual cortex!
In contrast, the "feed-forward" pathway into visual cortex makes up less than 1% of the excitatory synapses in visual cortex (Costa & Martin 2011).
If you change your scope to look only at inter-cortical-regional projections, then there is comparatively less recurrence (i.e. strong bi-directional connections between two cortical areas), although it still exists. Connections between cortical areas seem to be correlated with physical distance across the cortex (Vezoli et al. 2004). Connections between adjacent areas (V1 and V2, for example) are strong in both directions, and appear to project to similar cortical laminae in both directions. In contrast, projections over longer distances are comparatively weaker, and target different cortical laminae in either direction.


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Effect of myelination on inteligence in cephalopods
Cephalopods are known for their unique intelligence compared to other invertebrates.
The number of neurons of cephalopods is of the order $5*10^8$, similar to dogs. Humans have about $10^{11}$ neurons.
However, a major difference between cephalopods and humans and most vertebrates is the lack of myelination of their axons. Instead, to quickly transmit signals, cephalopod axons are much larger, reaching sizes of up to 1mm.
If we could edit the genome of an octopus, so that its axons are coated in myelin similar to a humans axon, whilst retaining their size, would this change the intelligence or behaviour of the octopus because of the increased processing speed?
Edit:
This is a repost of my original questions, to better conform with the guidelines of this forum. I am new to both this site and biology. Thank you very much for reading.


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What advantage does the pseudostratified epithelial structure type provide over squamous, cuboidal, and columnar?
I'm currently and have had difficulty receiving an answer about the role the pseudostratified columnar structure provides.
I understand that that the following have their respective advantages:

Cuboidal: Very tight cell junction
Columnar: Increased Surface Area relative to volume
Squamous: Allows easy passage for materials across

In the tissue we observed from a trachea, the ciliated pseudostratified columnar was responsible for the movement of material across its surface, however it seemed that the cilia provided that, not the structure.
Why not have ciliated columnar tissue? What does pseudostratified bring to the table?

Incidentally, your description of the advantage of columnar should probably be further explained. Columnar cells actually increase VOLUME of the cell relative to (apical) surface area. This is why secretory epithelial structures are usually columnar. And cuboidal cells do not necessarily have tighter cell junctions than other epithelial cells. That's a function of the actual junctions, not the shape of the cell. As far as the best barriers, those are actually stratified squamous epithelial tissues.

Why not have ciliated columnar tissue?

The respiratory epithelium in the trachea is columnar. The three classifications you bring up in your question: cuboidal, columnar, and squamous, describe the shape of individual cells. The trachea, as you saw in your trachea sample, has columnar epithelial cells (when healthy). The cells are longer along the axis perpendicular to the basement membrane than they are along the axis parallel to it.
You can also classify epithelium according to the number of cell layers between the basement membrane and the free surface of the epithelium. The two possible classifications here are simple (one cell layer) and stratified (more than one cell layer).
The classification pseudostratified means it looks like it's stratified, but it is actually simple. As with any other histological classification, this classification describes structure rather than function. The epithelium in the trachea is simple columnar because all the cells touch the basement membrane, but without knowing that (just by looking at a cross section) it would appear to be stratified because the nuclei of all the different cells do not line up. That is why it is called pseudostratified. The difficulty in distinguishing pseudostratified and stratified from an ordinary cross section of a trachea may be difficult to appreciate without an image. It is not obvious that there is only one cell layer above the basement membrane here, but there is:

As with other simple columnar epithelial tissues, the trachea is specialized for both secretion and barrier formation.
You could speculate on the possible strengths and weaknesses of the pseudostratified structure, but it just happens to be the case that a certain cell population that has nuclei that are closer to the basement membrane (here labeled BC), and a certain cell population has nuclei that are further from the basement membrane (here labeled CC). Those cells with the lower lying nuclei are sometimes called basal cells, and are not terminally differentiated. They provide a reserve for cell replacement in response to normal loss of cells and/or pathophysiological processes like infection and inflammation.
Now, other simple cuboidal epithelial structures, e.g., in the intestine, do not have a pseudostratified structure. If you look at a healthy section of large intestine, the nuclei of the epithelium clearly line up, and it's not hard to see that the structure is a simple epithelium. For those unfamiliar, the epithelium here is only the outer layer. The seemingly disorganized mass of cells deep to the epithelial basement membrane are connective tissue (labeled CT). Look for a thin pink line in each of these slides to help orient yourself to the epithelial tissue. That's the basement membrane.

This simple cuboidal epithelium is also renewed in response to normal loss of cells and pathophysiological processes like infection and inflammation, but doesn't have a pseudostratified structure. This means, clearly, you don't need a pseudostratified structure in order to renew an epithelial surface. So I would caution you not to expect structure and function to be so neatly tied together in histology. It's a descriptive science. You can learn and understand what these structures do, but it's not necessarily a good idea to try to shoehorn the structures into logical rules. The usual answer to "why" in histology, is "because that's what it looks like".
You can read the details in Ross Histology, Chs. 5 (for general classifications and the general concept of pseudostratified epithelium), 19 (for respiratory epithelium and the details on pseudostratified epithelium), and 17 (if you want to compare the respiratory structures to the epithelial structures in the GI tract). Images are from Ross Ch. 5.

I am not sure , but I think I read somewhere that the cells having their nuclei towards the base function as stem cells , i.e they function in replacing the tall cells ( cells with apical nuclei)

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What does this biomass measurement mean and how to translate it to volume
This is probably a softball question but because of the nature of the term, it's difficult to Google.  I am not a biologist, I am a web developer.  :-)
What does this measurement mean (it is a measurement of biomass production): 50 g m-2 d-1
I believe it means 50 grams per square meter per day - but not sure why there are '-' signs in there.
And perhaps more complicated, it is possible to translate this measurement to volume (either cubic meters or ideally cubic feet)?

Look for negative exponents to learn about the minus signs in the unit.

Could you please make clear, what you want to achieve? Turn "50 grams per square meter per day" to "XY cubic feet" or to "XY cubic feet per square meter per day"?

Thank you, @Marzipanherz.  Appreciate the Wikipedia link.  I was hoping to gather something like this: "50 grams per square meter per day" to "X grams per cubic foot" but based on Bryan's answer below, I see now this isn't a reasonable expectation.

50 g m-2 d-1 translates to "50 grams per square meter per day": the negative signs are negative exponents (check a math textbook). This is equivalent to writing
((50 g)/m2)/day
You cannot transform this into volume, doing so would lose the meaning: if you are talking about biomass growth of 50 grams per square meter per day, you are saying that there is 50 grams of new biological material produced within a square meter of land (say, a patch of grassland or forest). Talking about it in terms of volume doesn't make sense because the "height" coordinate doesn't produce additional biomass, since the source of energy is the sun.

Thank you, Bryan -- exactly what I was looking for.  This makes perfect sense now.


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Is there an ideal evolutionary body?
I am a science fiction fan, and when I watch movies with aliens, I get annoyed at the fact that they're all humanoid. I think, "What are the chances that it will look that similar to humans?" But I wondered recently "What if there is an ideal shape for an organism in a specific environment?" An example is that all mammals have 4 limbs, and all fish have gills and fins (except for some, but I will get to that). What if that is because that is the perfect form for an organism in that kind of environment? Along with that, some fish have evolved to do certain, unique things, whether to camouflage, attack, or develop a symbiotic relationship (am I correct on that?), which brings up the question, how much does the mindset and disposition of an organism affect its end body shape, and how much more random does it make the process of evolution? What I mean to say is, say biologists were able to create organisms and watch them evolve quickly. If you took two single celled organisms that had no similarities, and put them in the exact same environment, would they evolve to look similar? Or would they develop their own, unique ways of surviving in their environment?

This is a subject of deep interest to me since i am writing sci-fi. Trying to imagine alien life is extremely difficult if you want to make it plausible. I believe that every trait, belonging to an organism of today, had some benefit that aided survival at least once in its evolution. Then, the only reason for change would be if the trait was a detriment for survival. Thus, we have eyes that work better underwater. Rather than being the perfect creature for a certain environment today, I think that a modern lifeform would be more of a collage of traits that have been helpful over the eons.

All mammals have 4 limbs, and all fish have gills and fins (except for some, but I will get to that). What if that is because that is the perfect form for an organism in that kind of environment?

Different mammals species live in very different environments. We all have four limbs (except exceptions), not because it is adaptive to all of us for a specific environment but because there a strong phylogenetic signal. You should have a look at Why don't mammals have more than 4 limbs?.
All fishes have gills and fins (except exceptions). This is definitely because they inhabit a common environment. Gills allows fishes to get oxygen from water. Fins is a general structure that allows swimming. You will note that marine mammals also have fins (we often talk about convergent evolution) Btw, the post Do fish break a water molecule to absorb oxygen? might be of interest to you

how much does the mindset and disposition of an organism affect its end body shape, and how much more random does it make the process of evolution?

I don't really understand what you mean by "mindset" and "disposition".
Nothing is random except in the consideration of unknowns. One can make sense of a probability only by consideration of a priories. While tossing a coin is often considered as the random event by excellence, a toss of a coin is everything but random if you were to know the exact forces that apply to the coin. So asking is something is random without stating what are the a prioris you consider knowing and not knowing makes no sense (although it may make some sense in quantum physics).

say biologists were able to create organisms and watch them evolve quickly. If you took two single celled organisms that had no similarities, and put them in the exact same environment, would they evolve to look similar?

We are actually able to witness evolution in a matter of weeks in lab with organisms with short generation time such as yeast or E. coli.
The repeatability of evolution is a vast subject. The issue with such question is that it depends a lot. It depends typically on what evolution you are expecting to see and the size of the population. For example a simple change in allele frequency at a selected locus in a large population is typically very much repeatable. But if you think about larger time scale then, most think it is wise to consider that evolution would take a totally different path. There is a famous quote that says:
"If the tape of evolution were replayed a million times, a species like ours would not necessarily evolve" Stephen Jay Gould
You should have a look at Is evolution a predictive theory?.

Evolution doesn't plan. It's just a selection over the changes that already happened. This is important when you consider any complex adaptation.
But first, let's see a simple adaptation - the "return" of mammals to the sea, as seen with the whales. The split between the proto-whales and their land-based cousins was exactly what led to the new species - some of the population was having benefits from hunting or hiding in the sea, and it meant they were having more food than average, or their offspring survived with a higher chance or such; and among this population, being adapted to life in water was a significant evolutionary pressure. The ones that were better adapted had more food etc., so they were more likely to reproduce, and their offspring more likely to survive, and over time, they got to be bigger and bigger proportion of the whole population. Rather inevitably, they got to look quite a bit like fish - since that indeed is a shape that is exceedingly well suited to life in the sea. This is the mechanism beneath convergent evolution - two different organisms changing to be very similar due to a very similar environment.
But make no mistake - this is not a complex adaptation. All of the changes that happened during the evolution of today's whales required no pre-requisites - a change in bone length here, a more prominent diving reflex there... They didn't get gills. They didn't get an air sac. They're still mammals through-and-through.
A complex adaptation is much more rare, and quickly becomes rather fixed. First, you need an adaptation A, which must be useful on its own (remember, evolution doesn't plan ahead). Then, once the population is almost entirely made of organisms that already have A, it's possible for another beneficial adaptation, B (which depends on A), to exist and build up in the population. As time goes on, and the organisms keep changing, you might get an "updated" version of A, A', which leads to B', and a new adaptation, C, depends on A' and B'... evolution has no tool to make big changes (unless you count humans :P).
Complex adaptations are much less likely to be produced in convergent evolution (since the conditions that favoured A in the first place might not be present in another similar environment, so B will never have a chance of being useful). They also tend to be more fixed - there's a lot less place for tweaking. Consider the eye - while it has been "evolved" independently multiple times, the end results are very different. For example, our eyes have nerves in front of the sensor cells, while octopii have them the other way around. And our approach is worse, of course - it means we have the blind spot where the nerves have to go through the sensory cells, and it decreases the sensitivity of the sensory cells, since there's nerves above them. But it's extremely unlikely that this would ever be fixed naturally - the difference in the evolution happened very early, back when the complex adaptation wasn't there yet. There's no single step that could fix it now (as far as I know), and it isn't advantageous enough to have a chance of propagating in a population even if it did happen through mutation.
This is the second big point. While evolution itself isn't random (it's very statistical), mutation certainly is. Now consider any complex adaptation. You want C, because it gives you an advantage. But C needs B', which needs A', which needs B, which needs A... and each step must have been an advantage of it's own. But what if A is as advantageous as xA, but they are mutually exclusive? And if it so happens that B cannot work with xA? You'll have two populations, one of which is "stuck" on xA, while another is happily Cing. Or, as happened with us and the octopii, xA doesn't work with B, but it does work with xB, which leads to something suspiciously similar to C, yet different.
However, does this really apply to a whole alien biosphere that developed on a planet that is similar to Earth? That's quite impossible to tell. All life on Earth we know of is made of RNA, for example. This doesn't necessarily mean that RNA is the best ever - it may just mean that once RNA appeared, nothing else could survive, or there were complex adaptations that quickly got grafted on top of RNA. DNA is just an "update" on top of RNA - we use it for "main data storage", but it's usually transcribed to RNA before it gets used to build proteins, and signal, and all the other roles RNA has in the body. Every organism on Earth that we know of has a common ancestor - but that doesn't mean that the common ancestor is inevitable, or the best. It may just mean that once life existed, it consumed every other bit of proto-life it found. There's a good chance that new life from scratch simply cannot appear in an environment that's already settled by another form of life.
However, I would hazard a guess that the way aliens most often look in fiction is way too human. There's plenty of things that are 100% "accidental" in the whole ancestry of a modern human. Opposable thumbs sound useful for any tool-making creatures that use a muscle+bone combo; the fact that we have five fingers isn't. The way our heads are shaped is heavily built around the way many individual adaptations shaped our complex adaptations, and is unlikely to be similar elsewhere. A common trope in sci-fi is to have alien species which are humanoid reptiles, or humanoid avians, for example; but why would a humanoid reptile-like female have breasts? Or five fingers? Or hair? Bi-lateral symmetry is almost omni-present in mammals, and it sounds kind of right (it makes many things simpler, it yields well to manipulation and observation in a 3D environment...), but is it really something that would be universal in intelligent aliens?
That said, obviously the aliens in sci-fi (especially movies and TV shows) are designed in such a way to a) make it easier for humans to play aliens, b) make it easier for humans to relate to the aliens, both on-screen and in theatre, c) avoid making silly mistakes in the design of such aliens. Some shows try to handwave this or even outright justify it (the humanoid cats in Red Dwarf had a huge bonus from being as close to human as possible, since they were living on a ship that was designed for humans), with various levels of success (right, Star Trek, seeding life five billion years in the past is totally going to produce similar alien species five billion years later).

@AlwaysConfused Well, I'm not a native english speaker, so I have no idea what you consider complex here. Except for the trait dependencies, which simply are complex - that's the whole point. And I'm not sure what you mean by "mathematical steps". Apart from not providing multiple examples, I'm not sure what would make sense to remove - the question skirts a border between World Building and Biology.


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how did we breed after the fusion ? and why can't we bread with chimps?
after the chromosome fusion happened to one of our ancestors, how did he breed ? if he was allowed to breed because the chromosomal differences were still not very big back then, why can donkey and horse breed then ? ain't we supposed to be able to breed with chimps as well ?

There are plenty of people today with balanced Robertsonian translocations, they breed mostly fine, though Down's is more common than in the rest of the population, because meiosis is more likely to be messed up. If due to drift, people with those translocations became more common, eventually they could breed with each other, and make offspring with 22 pairs of chromosomes.  In theory, this drift could take over the whole human population.

Fusion of chromosome is not an absolute barrier. The two unfused chromosomes can pair up with the fused chromosome.
So long as all the genes are the same... offspring can be had.
However... a fused chromosome means that chromosome cross overs between the fused chromosome and its unfused chromosomes during meiosis will lead to unequal crossover of the chromosome, leading to massive lost or gain of genes... such germ cells if fertilized is usually lethal
Also if the fused chromosome is reassorted unequally with its unfused chromosomes during gamete formation.. will also lead to unbalanced genes for any fertilised embriyo... so again it is lethal.
So while there will be offspring... there will be few.
In effect... the fused chromosome creates a barrier.. not an absolute barrier... but one that makes free flow difficult.
So back to your question... the first individual with the fused chromosome could have reproduced by with a lower fitness with any member of the tribe. There will be children but it would be few. Those children with the fused chromosome can again reproduce with any member of the tribe but will have few children. However if two individuals with fused chromosome mate (sibling-sibling / parent-sibling) the pair will be fully fertile.
An interesting example
http://genetics.thetech.org/original_news/news124
Man with 44 chromosome instead of 46... Man has two chromosome composed of chr14-15 fusion. Produce of parents who are first cousin who both also have the Chr14-15 fusion.
Perhaps one day in the far future... this Man will be source of people with 44 chromosome.
Other example are families with balance translocation of chr21. They have a high incidence of down syndrome in the family.
As for Horse (2n=64) and Donkeys (2n=62).. not only is there chromosome fusion, but enough time has passed that changes in genes has occurred... ie specialization. As a result the reproductive cycles of jennies are affected.  Also Johns, are gelded as a matter of course. So no fertility to speak off. That being said, there have been instance of Jennies becoming pregnant and giving birth.. usually to a pure donkey (if sire is donkey) or pure horse (if the sire is horse)... an indication of some kind selective segregation of donkey and horse chromosomes... Perhaps donkey and horse centromeres do not play well together.

so you mean that we can't breed with chimps whilst donkeys can breed with horses because our speciation happened much earlier ? and not because of the number of chromosomes nor the differences of the genetic information ?


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Why didn't people taking up the Ice Bucket Challenge die?
I recently came across Vagal Inhibition. That article says,

(5) Sudden immersion of body in cold water.

can cause vagal inhibition and ultimately death.
Recalling the Ice Bucket Challenge. Going by what the above article says, shouldn't many of the participants have had a vagal inhibition ?

For one thing the ice bucket challenge is not immersion, you also might want to look at the mammalian dive reflex.

Theoretically, any treatment can cause death. Drinking water can be lethal and oxygen is highly toxic and a strong oxidizer.
To quantify toxicity we usually use Median Lethal Dose (LD50) metric. That is a dose at which half (50%) of test group is going to die.
To answer "Why didn't people taking up the Ice Bucket Challenge die?":
Dose that people used was not high enough to cause any significant increase in mortality. Maybe some people did die, but it was just masked by other news (to some degree)


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What is the process of degradation of proteins into amino acids inside living cells?
Just like beta oxidation does our cells have a distinct mechanism for degradation of proteins? There are processes for degradation of amino acids but where does these amino acids come from, is it all from dietary proteins? Are they not obtained from the proteins(enzymes) that are being continuously made inside the cells?

Proteolysis (the breakdown of proteins into amino acids by the action of enzymes)

There are two major pathways through which proteins are degraded in your generic cell: In a lysosome or in a proteasome.
The Lysosome
It's considered an organelle. It has a lipid bilayer that encloses a potent cocktail of acid hydrolases working at a low pH. The pH is maintained by a Cl-/H+ antiporter(Ref). Acid hydrolases that are being processed in the golgi are targeted to the lysosome through mannose-6-phosphate residues which are recognized by the trans golgi M6P receptors, packaged into clathrin vesicles, and targeted to acidic late endosomes which fuse, forming the lysososome (Ref).
So through endocytosis or phagocytosis, vesicles full of extracellular proteins are uptaken and may fuse with a lysosome. The hydrolases thus digest whatever they can. In a cell stress response cells may also digest their own contents with the aid of lysosomes in a process called autophagy. We can take a look here at some established lysosomal enzymes current to 2009, and if you spot a protease you can generally take a look at it's specific mechanism to see how it works. So I'll pick one out of the bunch (a lysosome has many different hydrolases remember), Dipeptidyl-peptidase I aka Cathepsin C. The mechanism of proteolysis is that of a cysteine protease which follows a bit of a generic mechanism like so:

... and so forth, you can look at a given given protease, and roughly determine how it cleaves peptides.
The proteasome
This one is a a much more directed form of protein degradation. Proteins must be tagged on lysine residues by molecules of ubiquitin, at least 4, referring to the term polyubiquitination. These are added sequentially by proteins denoted E1, E2 and E3 (see proteasome wiki). Proteins that get degraded in this manner are often damaged or come from within the cell, unlike the lysosome where the proteins probably came from outside the cell.
The catalytic domain of the proteasome is a threonine protease which follows the generic mechanism of the catalytic triad, one of the most well-studied protease mechanisms. We can view this generally through the mechanism of a serine protease, like so:

If you read through the whole thing, two notes: (1) the generic term for protein degradation is proteolysis, and (2) The mechanism depends on the protein performing the proteolysis, namely a protease.

Good answer. I would add that lysosomes also can degrade the cells own proteins (not only extracellular proteins obtained from endocytosis) during autophagy. https://en.wikipedia.org/wiki/Autophagy

@Roland Duly noted, added a tidbit on autophagy! Thank you.

@CMosychuk What are the main sources of these proteins that are being proteolysed?

@SanjuktaGhosh So there's a number of places it can possibly come from, and it depends on some conditions. Largely: When you eat, digestive proteolysis breaks whole protein into small peptides that are capable of passing into the bloodstream. Thus the bloodstream becomes the main source. Otherwise cells are capable of scavenging from extracellular fluid/matrix, or nearby cells that die or undergo apoptosis (specialized cells called phagocytes normally take care of dead cells, though).

In addition to proteasome and lysosome, soluble (non-organelle) proteases may become important, depending on circumstances.


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Colonial Cells Demonstrating Cell Specialization
Are there any living examples of cellular colonies demonstrating very primitive cellular specialization?  If so, what do we know about how they assimilate?  How independent are the individual cells and what do we know about their behavior (for example, do they, perhaps, migrate to different colonies in certain proximities)?

Probably not what you are looking for but the protozoan slime mold Dictyostelium discoideum lives as free amoebae which can coalesce into a multicellular migratory slug that eventually forms a fruiting body in which some cells form the stalk while others form spores.
Slug formation is by chemotactic signalling with cyclic AMP as the signal. I seem to remember that there is a predatory species of slime mold which uses cAMP to attract D. discoideum as prey, but I can't bring the name to mind and have failed to find it online.


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Surface area : Volume Ratio
I just have a quick question. I am currently studying for a test and I am confused as to what my book is saying. On the first page when learning about the gas exchange of insects it states that the insects have a large surface area : Volume ratio and this increases the rate of diffusion allowing the insects to get the oxygen they need at a fast enough rate to allow them to survive. Then on the next page when talking about the prevention of water loss it states that insects have a small surface area : Volume ratio to prevent water loss as it minimises the area at which the water can be lost. I am confused as the book states that an insect has both high and low surface area to volume ratios and because of this I'm not sure which is correct to write for the exam.
Thank you

Hello and welcome to Bio.SE! Can you provide the exact reference?

Hello, thank you for your welcome :) I have added pictures of the textbook where it talks about both things and contradicts itself. Inside the rectangle is where it states that small organisms have a large surface area to volume ratio and underneath the rectangle is where it states that the insect has a small surface area to volume ratio. Which statement is correct or am I interpreting it wrong?


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Blood Vessels (Artery Vs Arterioles)
I just have a quick question regarding what my textbook says. I have tried searching online but I have failed to find an answer. Basically, my textbook states that arterioles are smaller in diameter compared to arteries but have a larger lumen. Isn't the diameter measured across the lumen? So how can the artery have a smaller lumen but be larger in diameter?
Thank you

Do you have the exact quote in context from the textbook? You are right, that makes no sense at all and is false, the lumen of arteries is larger than the lumen of arterioles. It's possible they are referring to the ratio of the lumen to the overall diameter, but even in that case I'd be uncertain of the statement and my intuition is that it is still false.

I have added a photo showing what the textbook states. Thank you for your reply :)

The photo shows that the book states that arterioles have a larger muscle layer and lumen. Is this correct?

The key word you are missing is "relatively": I'm not clear what they mean "relatively" to based on where you cut off the passage, but they probably mean relative to the entire diameter of the vessel; the statement is probably not true for area but you would have to choose a particular artery and arteriole to compare, and both categories have a lot of variation in size within and between organisms.
Arterioles do have a "relatively" thicker muscle layer than the great arteries because they are the place where most of the contraction takes place that regulates the resistance of different vascular beds. Because of that, though, their lumen size varies quite a bit depending on the state of the muscle. When the smooth muscle in the vessel wall is relaxed, arterioles are much larger than when contracted. Even if the book is correct that according to whatever measure of "relative" they are using, arterioles have a wider lumen, I have a hard time believing this would be true over the entire range of contraction.

I will attach entire passage

Thank you for your answer. I understand the muscle layer part but I still don't know what I should write if an exam question was to come up. Should I write that the arterioles have a smaller or larger lumen?

Arterioles have a smaller lumen than arteries. The "ioles" at the end implies they are "little arteries." If I were you I would focus on the differences in function in your studying.


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Flying insects on olive tree
They may be responsible for why the leaves are drying out.
Location is in West Europe.
Their size may be 0.5 cm to 1 cm

Please update with your location, approximate size of the insect, and a better image (i.e., a close-up image) to receive a proper ID. Currently, I don't think anybody can provide an accurate sub-family identification. You can use the edit button below your post to update your question directly. Thanks.

done @theforestecologist

Maybe some sort of olive fruit fly

They look like three different kinds of insect. I have no identification for any of them.

All of the insects in the uppermost photo are parasitoid Hymenoptera; the smallest (and uppermost) may be from superfamily Chalcidoidea; the other two appear to be members of superfamily Proctotrupoidea (and may represent different families from that group: the elbowed antenna of the second reminds me of the family Diapriidae; the straight antenna of the third recalls Proctotrupidae).


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Why is Carbon Dioxide a Greenhouse Gas whereas Ammonia is not?
Why are some gases Greenhouse gases while some are not?
I did search this on the net but didn't get any clearcut/credible answers.
What exactly is the property that is common among Ozone, Water Vapour, CFC and Methane?

There is "no" ammonia in earth atmosphere ; maybe a concern on some other planet.

I'm voting to close this question as off-topic because it belongs on the earth science stack

@John - I would suggest Physics as the most appropriate for the precise physical mechanisms involved in the Greenhouse Effect, ie the ways molecules absorb and emit EMR and why different molecules respond differently. Other factors, like relative quantities and processes that cycle particular elements and compounds through the atmosphere would be in the realm of Earth Science. Chemistry... even though it has some relevance I'm not sure it would be the best.

@KenFabian climatics, weather, and climate change are all solidly within earth science. earth science =/= geology.  also the earth science stack already has questions and answers about this.

This is better suited for the Chemistry site, but there are two reasons.  1) The gas allows visible light to pass, but blocks infrared.  (Which has to do with the nature of the bonds between atoms &c.) 2) It exists in the atmosphere in sufficient quantity to have an effect, which ammonia doesn't: https://www.livescience.com/57305-ammonia-detected-in-atmosphere.html  It's quite reactive, so ammonia that's released from e.g. fertilizers or urine doesn't stay around long.

less good for chemistry, but a good fit for earth science stack, which covers climatology.

@John: I meant better for Chemistry to answer the question of whether ammonia (or any gas) does block infrared wavelengths, and if so, why it does.  To be an effective GHG, it has to block outgoing IR while letting visible wavelengths in, and IF it does, there has to be enough in the atmosphere to have a significant effect.


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Crossing over : Holliday model

In this figure out of the two heteroduplexes formed one is considered to be non-recombinant product(left) and the other recombinant product(right). My question is despite the exchange of middle DNA segment why is the right heteroduplex considered a non-recombinant product or patch. I've been reading two books:

Molecular Biology: Principles of Genome Function
By Nancy Lynn Craig, Rachel Green, Orna Cohen-Fix, Carol Greider, Gisela Storz, Cynthia
Molecular Biology
By Burton E. Tropp

both had the same illustration and descrpition.

Answer in brief

Heteroduplex called patch does not have double-stranded recombinant regions, there is a new fragment in a single strand only. It means that the two strands are not complementary at that regions and as soon as DNA repair systems detects it, the mistake will be corrected. In case of heteroduplex called splice, there are double-stranded changes, which do not go against the complementarity principle and thus, they will not be removed or corrected in any way.

Diagrammatic Explanation
After horizontal and vertical resolution patch and splice are formed respectively.

A better version of this diagram with complimentary base pairing is shown below $-$

In patch the heteroduplexes formed have only a single stranded middle recombinant region which is not complimentary to the other strand when this is detected by the DNA repair system and corrected the duplexes formed are same as the original duplexes (before crossing over) so the products of horizontal resolution is called non-recombinant products.
In splice the heteroduplexes formed have double stranded recombinant segments with middle non complementary region which when detected and fixed by the cell's DNA repair system two duplexes are formed having recombinant DNA segments, so they are together called recombinant products. The recombination in splice is well represented by the reversal of terminal genes.


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Recommendation of Ecology books
What are some of the standard books to study :

Biological Interactions: Symbiosis, Mutualism...etc
Concept of Limiting factors
Niche concept
Resource partitioning
Concepts of community change
Theories of climax
Models of Succession

P.S. I am looking for a book for beginners for studying ecology at UG level.

You must know by now that this question is going to be closed as too broad and/or primarily opinion based.

Nobody else ever did vote to close. Tyto Alba (second reincarnation of another name) is unfortunately long gone. So I've voted to close.

A classic standard textbook that I've used a lot myself (earlier editions) is Begon, Harper & Townsend. This book is very broad and comprehensive, but I know that some students dislike it's back-and-forth discussion style (fewer definite answers). I see this as a strength though.
Another good choice, that is much shorter, is Gotelli's A Primer of Ecology. This one has a slight theoretical leaning (many standard mathematical models), but can work well in a  introductory course. I don't have the book in front of me, but, looking at your list of topics, I suspect that A Primer... might be weak in some of them (e.g. climax, succession).

How good will Fundamentals of ecology be? I found an old copy of the book in my college library, it dates back to 1996.

@SanjuktaGhosh I've only browsed it, so I cannot really say. It's a classic that has gone through numerous editions though. Most well-known textbook has a good coverage though, and you cannot go too wrong for an overview of the major topics. The biggest differences are in writing/presentation style and emphasis. As I mentioned, A Primer.. has a slight theoretical bias (for an overview text) while e.g. Evolutionary Ecology (Pianka) emphasise, well, evolutionary aspects.

 Ecology Textbooks:
Molles, M.C. 2010. Ecology: Concepts and Applications. Fifth edition. McGraw-Hill. New York, NY. p. 572.

I'd say this is the "standard" undergraduate textbook. Those planning on continuing to graduate work should best know this book cover to cover by the end of their 1st year of graduate work.

Tons of pictures, lot's of definitions (with glossary), tons of references, and easy to read (as far as textbooks go).

Begon, M., C.R. Townsend & J.L. Harper. 2006. Ecology: From Individuals to Ecosystems. Fourth edition. Blackwell Publishing Ltd. Malden, MA. 738 pp.

As @fileunderwater said, this is the standard text for ecology. I'd say anyone moving through graduate work should know the concepts in this book front-to-back by the time they finish their graduate degree.

Strengths: Numerous relevant publications; good discussion; most in-depth/comprehensive of those I've read.

That being said, it's not the greatest place to start. There are no colorful pictures, there are no bolded definitions (and no glossary), and the discussion assumes you already have a grasp of simple concepts.

J Gurevitch, S.M. Scheiner & G.A. Fox. 2006. The Ecology of Plants. 2nd ed. Sinauer Associates, Inc Sunderland MA. 574 pp.

This is a great textbook to learn about the ecology of plants (well illustrated, lot's of definitions, fairly easy to read but still fairly comprehensive).

This book would best be read having already taken an intro ecology class.

Smith, R.L. and T.M. Smith. 2001. Ecology & Field Biology. 6th Edition. Benjamin Cummings, USA. 843 pp.

This book is very dated, which results in a number of more recent studies not being mentioned. However, if the goal is to develop a simple understanding of ecological principles, this book could be found very cheap online.

Bush, Mark B. 2003. Ecology of a Changing Planet. 3rd edition. Prentice-Hall, Inc, New Jersey. 477 pp.

This book is likewise very dated, which results in a number of more recent studies not being mentioned. However, again, if the goal is to develop a simple understanding of ecological principles, this book could be found very cheap online.

I would also say that the chapter introductions (as well as copied papers) in Foundations of Ecology (Real & Brown 1991) are great for catching you up on both the history of the field of ecology and the most important classic papers/researchers in the field.
 Books on Communities & Succession:
These are a bit more dated, but here are some of the classic books on these topics.

Bazzaz, F. A. 1996. Plants in Changing Environments: Linking
Physiological, Population, and Community ecology. Cambridge:
Cambridge University Press, 320 pp.

Bormann, F. Herbert, and Gene E. Likens. 1979. Pattern and Process in
a Forested Ecosystem: Disturbance, Development, and the Steady State
Based On the Hubbard Brook Ecosystem Study. Springer-Verlag, New
York. 253 pp.

Glenn-Lewin, David C., R K. Peet, and Thomas T. Veblen, eds. 1992.
Plant Succession: Theory and Prediction. Chapman & Hall, London. 352
pp.

West, D C., Daniel B. Botkin, and Herman H. Shugart, eds. 1981.
Forest Succession: Concepts and Application. Springer-Verlag, New
York. 517pp.

Whittaker, Robert H. 1975. Communities and Ecosystems. 2d ed.
Macmillan, New York. 385 pp.

Let me provide a second answer that summarizes the responses given by a number of ecologists from all over the world. These ecologists gave the below responses to a similar question asked on ECOLOG on Jan 30, 2018. This will hopefully broaden the search for others coming across this post in the future...

Note: The ECOLOG question specifically asked:

I’m looking for recommendations/suggestions of a general ecology book, preferably with at least some plant examples to supplement lectures and field in a brief introductory ecology class for adults who are interested in and often quite knowledgeable about (native) plants

The responses (in ABC order):

Cain, Michael L., William D. Bowman, and Sally D. Hacker. 2013. Ecology. 3rd Ed. (4th Ed. due May, 2018, authors same but start with Bowman). Oxford University Press.

It was fairly easy to consume and had lots of material to draw from...though I believe it was more geared towards theoretical ecology rather than naturalism.

Drury, William H. ed. John G.T. Anderson. 1998. Chance and change: ecology for conservationists. University of California Press, Berkeley.

Bill Drury, who wrote against models like "Classical succession", and after he died his family asked me to edit his manuscript for an "alternative" Ecology text book. It is by no means perfect, but it seems to have held up pretty well & provokes good discussion among students.

Ennos, Roland. 2016. Trees: a complete guide to their biology and structure. Comstock Publishing Associates.

It doesn't cover quite the subject matter you're looking for, but I quite enjoyed "Trees: A Complete Guide to Their Biology and Structure" by Roland Ennos. It's fairly small, but technical, almost like a chapter or two from a broader introductory textbook. It gave me a basic overview of the natural history of, well, trees.

Gurevitch, Jessica, Samuel M. Scheiner, and Gordon A. Fox.  2006.The Ecology of Plants, 2nd Ed. Oxford University Press/Sinauer Associates.

Book intro says it is basic ecology with plant focus. How about The Ecology of Plants?

Gotelli, Nicholas J. 2008. Primer of Ecology 4th Ed. Oxford University Press/ Sinauer Associates.

good and succinct, but might not be right for your audience. [technical with focus on models]

Karban, Richard, Mikaela Huntzinger & Ian S. Pearse. 2014. How to do ecology: a concise handbook 2nd Ed. Princeton University Press.

I also really like “How to do Ecology” by Karban and Hartzinger about the process of developing and conducting ecological research, but again, might not be right for this situation. [looks very useful for planning research projects]

Keddy, Paul A. 2017. Plant Ecology, origins, processes, consequences. 2nd Ed. Cambridge University Press. New York.

Covers basics but book intro suggests reviewing basic ecology text.

Marchetti, Michael P. & Peter B. Moyle. 2010. Protecting Life on Earth: an introduction to the science of conservation. University of California Press, Berkeley.

A short non-majors ecology/conservation biology text.  I think we did a solid job at explaining general ecology to nonscience people.  you might check it out, although it is not plant centered but there are plant examples.

Molles, Manuel C., Jr. 2014. Ecology: Concepts and applications 7th Ed. McGraw-Hill Higher Education.

Manuel Molles book is good. I like the idea that he focuses on students understanding the language of science (figs and table-with helpful annotations-still use some of those in my senior level cons bio class)

Relyea, Rick and Robert E. Ricklefs. 2017. The Economy of Nature 8th Ed. W.H. Freeman Publishers.

Completely redid all of the figures and photos, with lots of plant examples. I am pleased to report that the response from instructors and students has been very positive. [the chapter on line has a terrific discussion of soils, and plants and soil relations]

Stokols, Danel. 2017. Social ecology in the digital age: solving complex problems in a globalized world. Academic Press/Elsevier.

Know you’re interested in identifying a general ecology text, but in case you’re interested in a supplemental text on social and human ecology, this 2018 title might be a relevant resource for you and your students:  Social Ecology in the Digital Age - Solving Complex Problems in a Globalized World.

Apparently a good blog: fredsingerecology.com

Weekly blog that discusses recent papers in Ecology (~75%) and Conservation Biology (~25%).  Each post has background, hypotheses, data and a discussion of why this question is important or of interest. It's designed to be used for instruction at a high school/college level, and should work fine for interested adults, regardless of background. Emphasis on interactions, reflecting author's preferences, but has fair number of posts that focus on plants.


text:
Type I and Type II Topoisomerases
Type I topoisomerase changes the linking number by ±1 by changing the number of twist present in a DNA, breaking only one strand.
Type II topoisomerase changes the linking number by ±2 by changing the configuration of the writhe,breaking both the strands.
Am I right?

Sannukta. You should know better than to give a question a meaningless title like this. It shouldn't be hard to think of something involving topoisomerases and linking number.

The speculations are right.
Topoisomerase I changes the linking number by changing the number of twists and Topoisomerase II changes the linking the number by changing the writhe of DNA.
Confirmed by a college professor.


text:
What are these (eggs?) ? ( Location - India )

The picture can be zoomed in on clicking
Description:
There are 24 of them, each ovoid, 1mm long and attached to the switch's frame by suction cups connected by tubes. They are secured to the base and couldn't be brushed off with a stick. Found them in East of India.
UPDATE
The ovoid heads have reduced in number (17) and have turned brownish (10.04.2017). The number of ovoid heads are 11 now and two of them have a black spot at the proximal end (could be the eye spots of developing embryos) (13.04.2017). The bunch has 4 of them now (24.04.2017).
Research & Question:
Assuming those are eggs (resemble those of Green lacewing and with the changes observed it is evident), what group of arthropods have such stalked eggs other than Green lacewing?

Appears to be very similar to the specimens in this SE Post

Yeah, they do look like eggs (of Green lacewing). In fact they have turned brownish and the number of ovoid structures have decreased which makes me think that they are eggs of some arthropod. @theforestecologist

The group of insects called Neuropterans have several species that lay eggs on stalks. This group includes lacewings, owlflies and antlions, however stalked eggs are not a defining trait of the group. In addition to the Green lacewing, the Blue-eyed lacewing from Australia lays stalked eggs while owlflies do not. Mantidflies also have stalked eggs which are members of the Neuroptera order, but the stalks are relatively short compared to lacewings.
This thread provides some interesting discussion.
P.S. While not an arthropod, at least one Genus of Molluscs (Nucella), lay stalked eggs too.
These are certainly eggs from this order (Neuroptera). Incubation time for these type of eggs can be anywhere from 2-7 days so you may already be having hatching if there are less eggs than what was initially there.

You may also like to include the Berothidae, beaded lacewings with those having stalked eggs.


text:
What is meant by clones of B-cells?
I was reading Cellular and Molecular Immunology
By Abul K. Abbas, Andrew H. H. Lichtman, Shiv Pillai and stumbled upon the following excerpt $-$

In every individual there are millions of different clones of B-cells,each producing antibody molecules with the same antigen binding site and different in this site from the antibodies produced by other clones.

What are these clones of B-cells, one producing monoclonal antibodies and the other polyclonal antibodies?

When you read further you'll get it. Basically, when the antibody expressed on a B-cell recognizes an antigen, then the B-cell divides and expands its population to produce more antibodies (through plasma cells). This process is called clonal expansion.

This is correct, but a very short summary of a very complex (and cool) process. To expand a bit: After T-cell dependant B-cell activation through an antigen to the B-cell receptor, the B-cell divides into a few very short-lived plasma cells and centroblasts. The latter undergo somatic hypermutation and rapid cell expansion to result in many different B-cells which produce similar, but different antibodies). With the help of follicular T-cells, only centroblast with the antibody with the highest affinity to the antigene survives and this one undergoes clonal expansion.

@Narusan you are right. I kept the answer very simple because the OP was a beginner in this topic. Also, the reference is the same book (mentioned in the question).

Cytokines which are produced by effector T4-helper lymphocytes helps activated B-lymphocytes to proliferate and produce clones.
So, even if limited  B-lymphocytes may have an antibody molecule able to bind particular epitope, still many cells are produced with the this specificity. This is clonal expansion (https://i.sstatic.net/3OlfJ.jpg)
Link for this answer
https://bio.libretexts.org/Bookshelves/Microbiology/Book%3A_Microbiology_(Kaiser)/Unit_6%3A_Adaptive_Immunity/13%3A_Humoral_Immunity/13.1%3A_Antibodies_(Immunoglobulins)/13.1E%3A_Clonal_Selection_and_Clonal_Expansion

Welcome to Biology.SE! Your answer sounds reasonable, however, it is likely to receive a more favorable response if you include supporting references (primary literature is best, but a textbook available online would seem sufficient for this question). At a minimum, please edit your answer to include the source for the figure. ——— You may also benefit from taking the [tour] and then consulting the help pages for additional advice on [Answer] effectively on this site. Thanks!

Hi Twinkle. If I may offer some advice; please familiarize yourself with formatting. Secondly, and more importantly, please do not answer questions from 4 years ago that are adequately answered. You have been filling the front page with old material that is well suited for the archive!

Ok will follow your advice

@SPr — You may be correct in suggesting the contributor improves his formatting, although you give no indication of where he is deficient. However I do not accept that the age of the question is relevant if the contributor has something new. I do not regard a three sentence answer as "adequate", and this answer covers a different aspect from WYSIWYG. I would say the problem with this answer is that it does not explain things clearly enough. Of course this is such a basic question covered in text books that perhaps the question should be whether to answer at all.

B cells are a type of cells that produce antibodies. Each B cell produces a different type of antibody. For example, consider the following B cells: C1, C2, and C3, which produce antibodies A1, A2, and A3, respectively. We are dealing with 3 B cell clones, given that they produce 3 different types of antibodies.
Let's say that the B cell C1 happens to produce antibodies (A1) that are specific against the lipopolysaccharide (LPS) of a certain bacteria. When this bacteria enters the body, C1 will detect its presence and become activated. Two things happen when a B cell becomes activated: (1) differentiation, and (2) proliferation. Therefore, from the B cell clone C1 many more B cells will be produced through cell division, and all of these cells will produce antibodies A1 with the same affinity towards LPS. This would be a monoclonal antibody response, given that only antibodies from one B cell clone are produced.
If B cell C2 also produces antibodies (A2) with affinity for LPS, then upon bacterial infection C2 would become activated, proliferate, and differentiate. Given that antibodies (A1 and A2) from two different B cell clones (C1 and C2) are produced, this is a polyclonal antibody response.
Hope this helps!


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

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

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

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

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


text:
Are alpha-ketoglutarate and glutamate involved in all transamination reactions?
Is it true that for all biochemical transamination reactions, that alpha-ketoglutarate and glutamate serve as the amino group acceptor and donor, respectively?
If this is true, then is it safe to assume that alpha-ketoglutarate is necessary for every transamination reaction?

The major transaminases such as the aspartate transaminase and alanine transaminase involve the glutamate α-ketoglutarate interconversion. Even the GABA aminotransferase employs glutamate/α-ketoglutarate. It seems that all transaminases use glutamate/α-ketoglutarate; in fact most of them do.
These are a few that don't:

Beta-alanine--pyruvate transaminase.
Tryptophan--phenylpyruvate transaminase.
Pyridoxamine--pyruvate transaminase.
Aminolevulinate aminotransferase.
Serine--pyruvate transaminase.
Aspartate--prephenate aminotransferase.

And a few more (see here). Most of these are present in plants.


text:
What is two-start or zigzag model of 30 nm chromatin fibre?
I read some webpages describing the two-start model but could not get it. I'll be obliged if someone helped me understand the topic.
The websites I have been through are:
1.http://www.nature.com/nrm/journal/v13/n7/fig_tab/nrm3382_F4.html
2.http://www.mechanobio.info/topics/synthesis/go-0006323
3.http://www.fastbleep.com/biology-notes/41/118/1272

What do you mean by two-start model? Maybe it would be easier to answer, if you explain your question a bit better.

@Chris Two start model or Zigzag model is a model which explains the structure of 30nm chromatin fibre other than the solenoid model.

From the MB Info Wiki you linked:

In the one-start solenoid model, bent linker DNA sequentially connects each nucleosome cores, creating a structure where nucleosomes follow each other along the same helical path [4, 7]. Alternatively, in the two-start zigzag model, straight linker DNA connects two opposing nucleosome cores, creating the opposing rows of nucleosomes that form so called “two-start��? helix.

This means that in the one-start model each nucleosome is connected to the one adjacent to it, and this is a continuous cycle. Meaning that it is more like a phone chord.
The Zig-Zag model instead proposes that each nucleosome is connected to the nucleosome approximately opposite to it (parallel), and is a pattern that is continuous through out the chromatin fiber. This is more complicated to understand but imagine it being more like lacing on a shoe.It goes from a hole on one side to a hole on the other side parallel to it but not in the same plane as itself.
To move to the third nucleosome (and pack as tightly as possible) instead of it being directly below the 1st one it is slightly off to the side and not exactly parallel to the 2nd nucleosome.
However the 4rth nucleosome will be exactly parallel to the 3rd, and thus the same amount of degrees off-center from the 2nd nucleosome as the 3rd nucleosome is to the 1st, maintaining the pattern.
This forms a more 3-D tubular strucuture than an actual shoelace on a shoe would (which is more flat like a plane but serves for visual cue).
A 2D step-by-step representation of this would be like the image below:

Here is a model of final figure I made to help explain this:

In the MBI figure each "Green" nucleosome is connected to an opposite slighty lower "Purple" nucleosome and that purple one is connected to yet another green one that is slightly off center to the first green nucleosome:

In Theory (Not sure if correct):
This may mean that when this fiber "unwraps" it would act less like a spring coming undone(where the whole structure would start to unravel due to how it's linked) and instead each sequential nucleosome being pulled away from the fiber after the one its connected to has moved and experiences full tension.
For the ZigZag model imagine you take a piece of paper and fold it many times as if it were an accordion. Then hold the paper folded up in one hand. Take your opposite hand and pull the paper from one end slowly unfolding it. You'll notice that each fold comes out sequentially while the rest of the structure stays intact until the fold before it flattens out so the tension can pull it. At least that is what would happen in my mind. I could be totally off base.


text:
Book recommendation: Modern Synthetic theory
I'm a zoology minor. I wish to study modern synthetic theory (evolution) is there a good book available online for reading?
The book should cover a basic idea about what the elements of modern synthetic theory are and briefly what are the conclusions of the theory.
Feel free to suggest edits.

Please add details outlined in the tag-wiki for book-recommendation..

@WYSIWYG Is it okay ? I don't have much to write.

There is no modern book of evolutionary biology that is not about the modern synthesis. So what you are looking for is just an introductory book to evolutionary biology.
I think the 2 most common introductory textbook to evolutionary biology are:

"Evolution: Making Sense of Life" by Carl Zimmer
"Evolution" by Futuyma

Note by the way that one can find recommendation on population genetics (subfield of evolution) here.


text:
How do normal cell division chance into a tumor forming cell division?
Or its better to say what happens at molecular level that tumors are formed?
I tried normal google search and google books but couldn't find any appropriate explanation.
I am trying to understand why p53 or Rb genes are called tumor suppressor genes.I'm acquainted with the pathway through which p53 protein cause checkpoint arrest if the DNA is damaged and the pathway through which pRb protein cause G1 arrest.

In a word: mutation.
If you step back and think about it, multicellular organisms are really, really complex systems. Different cells have to do different kinds of things and interact with each other, they form organized tissues and organs and so on. That much is obvious.
For all of this to work in concert, cells have to grow and divide (to replace dying cells) in a nice orderly fashion/at a nice orderly pace. Since that's a complicated process, lots of the genes in any given cell play a role in managing how long that cell lives/how fast it divides (i.e., cell cycle regulation).
So now, if DNA in a given cell gets mutated, there's a chance that mutation will hit one or more of these genes that are involved in cell cycle regulation. And you can imagine there are two extremes of what might happen: On one extreme, the mutation could mess up the cell cycle in such a way that it's broken (the cell can't grow/divide, things get screwed up, and it dies off); on the other extreme, the mutation could instead destabilize the cell cycle in such a way that it's "kicked into overdrive."
In the first example, we wouldn't observe the effect; the mutated cell would just die off, no big deal. But in the second example, with the cell cycle in overdrive, that cell would barrel ahead, growing fast and dividing faster than the cells around it. And since each of its child cells would have the same DNA and thus have the same "kicked into overdrive" mutation, they'd divide too quickly as well, and so would their children…and eventually you'd have a crazy mass of out-of-control cells. That's a tumor.
p53 is a tumor suppressor because it effectively "sounds the alarm" when it notices DNA damage (mutation)—meaning, when it finds DNA damage, it initiates several processes to try and control/fix/stop it. This is important because if that DNA damage is like the second example above, it could lead to a cancer that harms or kills the whole organism.
If the p53 gene itself is mutated, then the cell has lost one of its major defenses against damaged DNA, and thus there's a much greater chance that a cancer-causing mutation in some other gene could go unchecked. That's why damaged p53 is found in lots of cancers: because the cell lost a big defense mechanism against cancer, and then cancer happened.