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What is the function of dendritic cell in immunity?
I'm interested in how dendritic cells present antigens to  helper T-cells? I'm also interested in the molecular actions between a dendritic cell and a helper T-cell during the activation of the helper T-cell?  What function does the homing receptor on a T-cell have?

what is your question?

In the inflammatory response, dendritic cells mainly function as antigen-presenting cells, but the homing phenomenon happens under normal (non-inflammatory) conditions. Note that this is different from immune cell recruitment to the site of inflammation. You should specify under which context you'd like to know DC function.

@poka.nandor I must say the probability is high you are a good in-between lines reader :)... That edit...

@cagliari2005 - Thanks :) This seemed the most logical intention (at least for me) of the question based on title and the short description provided.

Dendritic cells are so called professional antigen-presenting cells (APCs) as pointed out by Sleepes in comment section. They express both MHC-I and MHC-II receptors on their cell surface on which they present small peptides. These small peptides come from digested proteins of their own (MHC-I) or antigens that were phagocited or taken up by receptor mediated endocytosis (MHC-II). They also express costimulatory molecules necessary for the activation of T-cells (eg. CD80/CD86).

source: http://journals.cambridge.org/fulltext_content/ERM/ERM2_09/S1462399400002143sup004.htm
As you can see in image above, activation of a T-cell requires two distinct signals: the recognition of an antigen and a co-stimulatory signal.

source: http://www.mhhe.com/biosci/ap/dynamichuman2/content/gifs/0158.gif
After activation T-cells undergo rapid division and diversification.
Details of T-cell activation by dendritic cells can be found in this article for example:
Immunol Cell Biol. 1997 Jun;75(3):223-30.
The role of dendritic cells in T cell activation.
Ni K1, O'Neill HC.


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What is the most reliable tumour suppressing gene for NSCLC?
I was looking at some tumour suppressing genes that can be helpful in diagnosing lung cancer (particularly NSCLC - Non-small-cell lung carcinoma) at an early stage. I came across a few such as p53, etc. However, as a beginner (and someone who has never pursued higher studies in biology), I do not have much knowledge as to which is the most reliable and the most extensively documented tumour suppressing gene for NSCLC.

Welcome to Biology SE! I took the liberty to edit your question to resolve the abbreviation. You can revert my edit any time if you wish.

The first resource I would look at would be the TCGA publication on NSCLC which can be found at this location. The first figure shows the most frequently mutated genes. TP53 rises to the top as most frequently mutated gene in the cohort studied, however, one also sees on the list KEAP1, NF1, ARID1A, SMARCA4, RB1, and CDKN2 as commonly altered tumor suppressors TSGs. You will want to take into account copy number data and mutation data in the frequency count in cohort also. Another issue to check in the data set is stage of the tumors in TCGA. You mentioned 'early stage' in your query, but if all the samples in TCGA are recurrent then it may not be appropriate for your question. The cBioPortal resource allows you to look and manipulate the data and I encourage you to look at that resource. It is very well done and shouldn't have too much of a learning curve. You will be able to put in TSGs and get back the freq of mutations. They may also have information on stage so might be possible to filter for only those samples. There are also a couple of text-mining resources that you can ask queries through pubmed to get back gene lists or to link gene lists. One tool is Glad4U (search this name in google) which allows you to type a query such as: "tumor suppressor AND early stage NSCLC" and it will return a ranked list of genes. Ranking is based on co-citation. However, one must check the returned list to make sure the genes returned are TSGs. A listing of putative TSGs can be found here. The second resource is CoCiter v2.0. On the Gene-Term search you can rank the lists of TSGs against search terms and it will return a ranking of the TSGs most associated with your search term. Hope this helps.

Thanks a lot. I was looking for such an answer for a long time. I'll go through all the sources that you have listed

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Ethanol production by fermentation?
As bacteria are involved in the production of ethanol through fermentation and ethanol is also used as antiseptic that kills bacteria, so how and why bacteria are involved in the synthesis of such alcohol which is lethal for itself(bacteria)?

Yeast can produce up to 16-17 v/v% ethanol without dying according to this article. Yeast is a primary industrial ethanol producer, it produces ethanol even under aerobic conditions, in contrast to bacteria that usually ferment sugar to ethanol under anaerobic conditions. Bacteria can also withstand up to several percent v/v concentration ethanol in their media. Check this paper for details. They produce ethanol because it is a natural byproduct of their cellular metabolism. Under anaerobic conditions sugar as the primary energy source cannot be oxidized and utilized as well as in aerobic conditions.

Alcoholic fermentation converts one mole of sucrose into two moles of ethanol and two moles of carbon dioxide, producing two moles of ATP in the process.

from: http://en.wikipedia.org/wiki/Ethanol_fermentation
Anaerobic bacteria follow this path because fermentation of ethanol does not require oxygen. This byproduct is secreted from the cells. In natural environments ethanol either dilutes in the media bacteria live in or can be taken up by acetic acid bacteria and used as an energy source.

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Fats as energy source
As we know that the preferred source of energy for our body (source) are carbohydrates but heart muscle is an exception and need some explanation for this exception, that why the preferred source of energy for  or cardiac muscle are FATS?

What is the source of this claim?

http://www.ncbi.nlm.nih.gov/books/NBK22436/ (point no. 2, last paragraph)                                                                                2. William's Basic Nutrition and Diet Therapy by Staci Nix , 13th edition. Chapter no. 2 Carbohydrates, page no 22.

Nice question! I've found a great article about fatty acid metabolism in heart muscle in healthy and disease conditions. As it is stated in this paper long chain fatty acids are utilized through beta-oxidation to meet the high energy need of continuous contraction. Beta-oxidation of long chain fatty acids produce far more ATPs than glucose. According to wikipedia:

For an even-numbered saturated fat (C2n), n - 1 oxidations are necessary, and the final process yields an additional acetyl CoA. In addition, two equivalents of ATP are lost during the activation of the fatty acid. Therefore, the total ATP yield can be stated as:
(n - 1) * 14 + 10 - 2 = total ATP or 14n-6 (alternatively)
For instance, the ATP yield of palmitate (C16, n = 8) is:
(8 - 1) * 14 + 10 - 2 = 106 ATP

While a single molecule of glucose produces 36 ATPs (under aerobic conditions)
Thus use of fatty acids (fats) in cardiac muscle is beneficial because of their higher energy concentration. Also it is noteworthy that this does not occur in isolation, so this is a response to contractile work and other competing energy sources (such as glucose, lactose etc). Also excessive uptake and beta-oxidation in disease conditions can even endanger cardiac functions. See details in the linked paper.


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Any good website/book to understand protein folding and enzymes?
I'm looking for a good, understandable and simple explanation about protein folding, mechanisms and function, and their relationship with enzymes.
I understand that the protein is a polypeptidic chain, I know its composition, but the part that I really can't figure out is "the folding of proteins", I mean "How a straight polypeptid chain turns into a complex folded structure?"

Could you please specify what is you are looking for exactly?

As I wrote down, I'm searching for a good resource that explains how proteins fold (Mechanism), and causes of proteins folding.

Have you tried googling or wikipedia? There are many levels of explanation and they require different levels of knowledge. If you want to start from the very beginning try searching for university textbooks or as I said try wikipedia. If you're a biology student then you can go for articles maybe.

I'm a beginner. I've checked many websites and books and I always find high level explanations that I can't figure out yet.

I see. Well then, what are the things that you can't figure out? I not trying to screw with you, but protein folding and enzymes in general are large topics, it takes books to explain everything, so if you can share what you already understand and what you cannot understand then we can help you more by explaining the things you need.

I understand that the protein is a polypeptidic chain, I know its composition, but the part that I really can't figure out is "the folding of proteins", I mean "How a straight polypeptid chain turns into a complex folded structure?". That's my question for instance.

https://www.youtube.com/watch?v=O5gN-IK6uKs
Khanacademy has a lot of resources for just about anything

Okay, so for introduction the 4 levels of protein structure (each level influences the levels after it):

primary (1st): the order of amino acids.
secondary (2nd): alpha-helicies and beta-sheets
tertiary (3rd): complex 3d structure
quaternary (4th) : 3rd+ non-protein elements (ions, co-factors etc)
and / or multple subunits interact. Not every protein has this kind
of structure.

I think the first does not need any explanation.
The secondary structure is where amino acids form 2D structures: alpha-helices or beta sheets. From wikipedia on a-helix and b-sheet

The alpha helix (α-helix) is a common secondary structure of proteins and is a righthand-coiled or spiral conformation (helix) in which every backbone N-H group donates a hydrogen bond to the backbone C=O group of the amino acid four residues earlier (i+4 \rightarrow i hydrogen bonding)
The β sheet (also β-pleated sheet) is the second form of regular secondary structure in proteins. It is less common than the alpha helix. Beta sheets consist of beta strands connected laterally by at least two or three backbone hydrogen bonds, forming a generally twisted, pleated sheet.

Pictures are from here, that is a great site that explains basic protein strucutre in a quite understandable way.

These secondary structures are important because they can from motifs with specific functions like DNA binding, interaction surface with other proteins. The aforementioned wiki sites have detailed info. These secondary structures and motifs serve as building block for higher order functions. Between motifs "loose" non-structured parts can be found to allow for flexibility.
Tertiary structure:
This is the level where complex 3D geometric structure is defined. The aforementioned 2D structures are packed into domains - a single functional element of a protein. A single protein can have multiple domains and the relative position of these domains result in the tertiary structure. The domains themselves are connected with loose regions that do not show any high order structure and provide flexibility between the domains. Flexibility is necessary for conformational changes.
The quaternary structure is where non protein elements and / or multple subunits are involved. For example the positioning of the heme group in hemoglobin. Or when monomers from dimers, trimers etc. so in general when mature proteins get together to form a larger complex.
Here is a great image about the different structure levels:

source: https://dopeahmeanbio.files.wordpress.com/2013/03/333.gif
So now onto the "how" part :)
As I mentioned in the beginning all levels influence the levels after it. So the amino acid sequence predestines the 2D structures to be formed. The secondary structures themselves are formed by amino acid forming hydrogen bonds with each other. This process occurs "naturrally", so by the inherent properties of the amino acids. At the third level disulfide bonds stabilize the structure. This is also a naturally occuring event. Also binding ions, co-factors, etc also stabilizes the protein strucutre.
The folding process can also be supported by chaperon proteins, These proteins can actively "twist" the polypetide chain using ATP as energy source. They can "sense" if there are hidrophobic amino acid chains facing the outer surface of the protein, a thing usually avoided because these amino acids need to face inner surface of the protein where they can avoid water - this is energetically better. This signal (outward facing hidofobic AAs) indicate that either the protein is un/misfolded or it is damaged because of for example heat - that denatures ("unwinds") proteins.
Finally the wiki page on protein folding if you need more. I hope this helps.

This is not a book / website recommendation but I hope it helps :)

Finally, an awesome explanation. Thanks dude :)

IMO, this is by far the best introduction to enzyme mechanisms and protein folding, by a leading researcher in the field.
Structure and Mechanism in Protein Science: A Guide to Enzyme Catalysis and Protein Folding
by Alan Fersht

For basic knowledge I would recommend the 5th edition of "the cell" and "Lehninger Principles of Biochemistry" 6th edition (3rd and 4th chapter). Even Lippincott's Biochemistry (chapter 2) and Biochemistry by Stryer (6th edition, chapter 2) is good. You can find the 5th edition of Stryer here http://www.ncbi.nlm.nih.gov/books/NBK21154/
If you have access to a library you could try out the latest editions. If not older editions are available online. Protein folding should be among the first few chapters.

All the information can be found here:
http://www.ncbi.nlm.nih.gov/books/NBK21054/
The whole book is there, you simply have to search whichever part interests you or you can also find the paper version in a library. The part on protein structure is Chapter 3.
It's a textbook used in some biochemistry and cell biology introductory courses at my university, so it will cover the basics as well as some more detailed things.


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Why do we get tired
At the end of a day full of work, it is general for people that their eyelids start to feel heavy. Laziness takes over and  we begin to yawn. We all know that we're tired at that time, but why people get tired?

I took the liberty to remove all personal references to yourself to avoid being flagged as personal medical question. Please feel free to revert my edit at any time if you wish.

Also in this question the regulation of sleep is quite well answered and in your case I'd look for the homeostatic regulation of sleep (that is the accumulation of adenosine in the brain due to the depletion of energy sources in neurons after a long period of wakefulness).
http://biology.stackexchange.com/questions/28123/length-of-sleep-time/31305#31305

Muscle fatigue

google that

It is yet to be discovered by scientists. But there is a new study that finds that brain cells called astrocytes supply the urge to sleep by releasing adenosine a chemical known to have sleep-inducing effects. The chemical accumulates in the brain during waking hours, eventually helping to stimulate the unique patterns of brain activity that occur during sleep.
You can find more about it in this link bellow  http://healthysleep.med.harvard.edu/healthy/matters/benefits-of-sleep/why-do-we-sleep


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what is linkage disequilibrium supposed to measure?
During reading about genetics I came across with the term of linkage disequilibrium, and I do not really understand what it supposed to mean. What is linkage disequilibrium? My current understanding that it is "deviation from independent assortment",

@Corvus - you were right, I totally mixed the two things..thx for pointing that out.  This is a good sign that I should go to sleep, I had a long day and its almost midnight.

@poka.nandor I know the feeling! Cheers.

Cagliari -- this is false. The definition of linkage  disequilibrium involves nonrandom association between alleles at different loci. One cause of linkage disequilibrium is physical linkage like you describe, but linkage disequilibrium can exist without physical linkage, Eg due to natural selection.

Linkage disequilibrium refers to a situation whereby two or more alleles, from different loci, segregate non-randomly. Therefore we have a statistical association between this two alleles.
The linkage disequilibrium can be used in gene mapping, because we assume that these loci are in the same region on the chromosome. The more often they appear together, the more they segregate non-randomly, the closer they should be on the chromosome.
http://www.researchgate.net/post/What_is_the_difference_between_Linkage_Equilibrium_and_Linkage_Disequilibrium


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Earth's history: The Great Oxidation Event and the 'Boring Billion'
From what I understand the 'Great Oxidation Event' occurred around 2.4 billion - 2.3 billion years ago, when cyanobacteria flooded Earth’s atmosphere with oxygen.
The 'boring billion' period was around 1.8 billion years ago, during which it is thought not a lot changed on planet Earth. Low oxygen levels were thought to be 1-40% of modern oxygen levels during this time.
Why did the atmosphere go from 'flooded with oxygen' to 1-40% of modern oxygen levels. Was it because during the Mesoproterozoic era, the rate
of burial of decaying organic carbon matter under marine sediments
flatlined?

Your question probably arises from a misunderstanding regarding the 'flooding' metaphor. I would not assume that 'flooded Earth's atmosphere with oxygen' means a lot of oxygen in the first place ... the metaphor means that oxygen levels rose from basically absent to noticeable.
If you look at the history of oxygen in Earth's atmosphere you see a general trend of gradual increase with a 1GY lasting stationary phase (Holland (2006), picture taken from above linked Wikipedia article - red and green lines are upper and lower estimates, respectively):

After initial atmospheric oxygenation about 2.5 GYa, Earth's oxygen sinks (mainly the oceans, after that landmasses and the ozone layer) were filled and buffered atmospheric oxygen levels, keeping them low. Once those sinks were saturated (approx. 850 MYa), the atmosphere started to oxygenise rapidly.
The constant (or as discussed below: drop in) oxygen concentration is caused by these sinks. The oxygen that is produced by photosynthesis was just not available to Earth's organisms as it was not atmospheric.
As @GerardoFurtado points out in the comment, modalities of the stationary phase are still debated. A review by Lyons et al. (2014) presents evidence that after the initial increase in oxygen levels, a drop in atmospheric oxygen preceded the stationary phase (see their Fig. 1, blue boxes). This does not change much as the newly inferred stationary phase, though probably a more fluctuating stationary phase than suggested by Holland (2006), is still higher than before the great oxidation event and lower than at present.
The major conclusions remains the same: There is evidence that the seemingly slow evolution 2-1 GYa was probably caused by oxygen limitation and oxygen levels were buffered by oxygen sinks. The change of oxygen concentration was determined by both the rate of oxygen production and the rate with which oxygen is stored in those sinks; the interplay of those rates caused the oxygen concentration to remain constant, drop or occasionally even rise, i.e. fluctuated.

@GerardoFurtado: Thanks for pointing that out. I do not think this changes much but incorporated a recent review that supports the claim of dropped oxygen levels and discussed this a bit.

Maybe the introduction of any amount of oxygen altered the availability of nutrients.  The oxygen producers had evolved in low / no oxygen conditions and it was only when they reached critical mass that the great oxygenation event could occur.
Once it did occur, nutrients that had once been soluble and available were in short supply: specifically iron and reduced nitrogen.
Fe2+ is soluble and so before the oxygenation event there was probably a fair bit sloshing around.  Once oxygen came the iron turned to Fe3+ and was much harder to come by.  https://www.princeton.edu/~cebic/ironIIvsIII.html
Iron is still growth limiting in large areas of open ocean, as evidenced by this experiment supplementing the open ocean with iron.
http://www.nytimes.com/2012/10/19/science/earth/iron-dumping-experiment-in-pacific-alarms-marine-experts.html
Nitrogen is the other nutrient whose availability would have changed.
The ancient enzyme used by nitrogen fixers is poisoned by oxygen and once oxygen was around, the activity of these organisms no doubt plummetted and with it, availability of reduced nitrogen.  Lack of iron would be a double whammy for the nitrogen fixers in which the enzyme requires iron.
So: maybe the boring billion occurred because oxygen-induced nutrient starvation handicapped proliferation of organisms, and with low proliferation you have fewer chances to evolve something new.


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What is the difference between a response element and a enhancer?
I have been confused as to the difference between a response element and an enhancer.
Wikipedia has the definition of response element as the following:

Response elements are short sequences of DNA within a gene promoter region that are able to bind specific transcription factors and regulate transcription of genes.

Wikipedia's definition of enhancers:

In genetics, an enhancer is a short (50-1500 bp) region of DNA that can be bound by proteins (activators) to increase the likelihood that transcription of a particular gene will occur.[1][2] These proteins are usually referred to as transcription factors.

They seem almost the same. What are the main differences?
The only difference I can see is that response elements can both halt transcription or allow for it. While enhancers only promote transcription if the transcription factor is present.
Is this the difference between the two, or is there something else that differentiates them?

Enhancers specifically bind transcription factors in an effort to obtain robust rates of transcription, in a very general fashion and may be upstream or downstream of a promoter. Remember that you don't need to receive a signal to produce housekeeping genes, regulated by general transcription factors, because they're always needed (in part). A response element can enhance or repress transcription depending on the stimulus.
Vitamin D response element (VDRE) is a fair example: In response to your extracellular calcitriol or 1,25(OH)2D, the vitamin D receptor will complex with a number of proteins that bind at the VDRE, controlling transcription of various vitamin D-controlled gene targets.

Vitamin D activity is mediated through binding of 1,25(OH)2D3 to the vitamin D receptor (VDR), which can regulate transcription of other genes involved in cell regulation, growth, and immunity. VDR modulates the expression of genes by forming a heterodimer complex with retinoid-X-receptors (RXR).

Source: http://www.wikipathways.org/index.php/Pathway:WP1531
And just as well, other promoters such as that for pro-parathyroid hormone contain VDRE sequences that suppress it's transcription (ref).

I had the notion that transcription factors binding to enhancers can also have a ligand binding domain. Which would mean that it would be activating depending on a stimulus. If my notion is correct, what then differentiates them?

Essentially your RE is always in the promoter, and the action can be bidirectional, either activating or silencing, based on the same stimulus across genes that contain that RE. You enhancer can be anywhere and always up-regulates in response to any number of variables that site reacts to.

You know it just cant be miles away from the TSS because it still needs to interact, so when I say anywhere I mean not just in the promoter.

A response element is a DNA sequence that binds with a set of one or more transcription factors/cofactors/factors  in order to regulate transcription. A response element is usually specific to a given stimulus that a cell needs to respond to.
A promoter is a sequence of DNA located nearby a gene and contains one or multiple response elements and up-regulates transcription
Once a promoter’s response element is binding with factors and is beginning to be set up for its role in transcriptional up-regulation of the nearby gene, the response element of another, second sequence of DNA (typically farther away from the gene than the promoter) has its own response element that in turn begins to bind with its own factors.
The factors of this other, second sequence interact directly or indirectly with the promoter’s factors to enhance the promoter’s transcriptional up-regulation to the gene. This other, second sequence is called an enhancer.


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What is the difference between transverse section and longitudinal section?
Can anyone explain the difference between transverse and longitudinal section?
Or are they the same?

One passes through long axis of the body while other is perpendicular to it.

For an animal with bilateral symmetry, a longitudinal section is parallel to the anterior-posterior axis (labelled central axis in the image below). Sections through or parallel to either the sagittal or coronal (also called frontal) plane are longitudinal. A transverse section is perpendicular to the anterior-posterior axis and is also called a cross section.

image source


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What prevents a pregnant woman's immune system from recognizing her fetus as nonself (and attacking)?
I'm familiar with the scenario of Rh- mother with Rh+ fetus having complications (more so after her first child), but that's not what I'm curious about. I want to know mechanistically why a pregnant woman's body does not display a reaction similar to what we see with rejection from a mismatched organ transplant. On the most basic level, I feel as though the fetus should be recognized as "nonself" due to paternal genetic contribution.
I feel as though if this mechanism could be understood, it could be harnessed for other situations (e.g., organ transplants).

Right now I don't remember the full story, but part of it is that pregnant women are somewhat immunosupressed and there is something like a layer of NK cells around the placenta making sure nothing attacks it. Not very practical to adapt to organ transplants.

There's a Wikipedia page: http://en.wikipedia.org/wiki/Immune_tolerance_in_pregnancy

Just so that someone answers this question so that the moderators have less work to do:
The fundamental reason why embryos don't get massacred by the maternal immune system is because of the placenta and several of its functions. Three mechanisms are:
1) Secretion of neurokinin B, which is also secreted by parasites to avoid detection of the host.
2) The placenta has developed immunoevasive actions from a virus. It creates a syncytium to limit transaction of mobile immune cells.
3)It only allows specific antibodies,(IgG) to enter and bind infection. (IgG being the only isotype here).
Yay  for biology


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Question about cell signaling pathways (RTK, Jak-Stat, SMAD, etc)
I am in an embryology course right now and we've just started covering cell-cell communication in development. We were talking about the roles of the various cadherins and their discoveries but we got to cell signaling pathways and in reading my textbook I'm finding myself confused by these pathways-- some of those that are mentioned include Notch, Wnt, FGF, TGF-beta, RTK, Jak-Stat, SMAD, integrins, PTHrP, Hedgehog, Discoidin domain receptors 1&2, and the unfolded protein response (UPR).
I know the RTK pathway and I know the SMAD pathway, but the others just seem to be specific ligands that are using these pathways -- is this correct?

In contrast to each and every one that I listed having its own distinct pathway.

Not sure what you mean. Notch has its own pathway, as does wnt and tgf-beta. Don't remember the other off the top of my head. Why don't you check them out on kegg?

see my comment on the post below -- I could have done a much better job saying what I was confused about in writing this question.

@Alexandria Jak/Stat are two families of proteins which mediate signals through phosphotyrosines.
JAK is a tyrosine kinase which binds to cell receptors and STAT is dimerized by JAK action.  JAK specificity seems to be your question.  A specific JAK protein (e.g. JAK1 or JAK2..) may mediate for different receptors in different cells.
There may be hetero- or homo-dimers of JAK, there may be more than one receptor in a cell using the same JAK enzyme, which may result in cross-talk between the two signals.  I think its a pathway dynamic that can vary quite a bit from one cell to another, depending on the receptor and cytokine environment the cell is seeing. JAK action can be modulated by any number of proteins which respond to other pathway signals or the cell state.  The diagram below from a review of heart muscle cell JAK action is not unusual nor is it complete.

With the exception of Jak/Stat, all of the proteins you mentioned are ligands and/or receptors. When a ligand binds to a receptor, it induces one or more cell signaling pathways, which are dependent on intracellular proteins being activated via association with the receptor, then going on to activate other proteins in a signaling cascade that eventually results in the cell doing something - usually involving regulating gene transcription to make proteins that effect the change - such as altering the cell's developmental fate to become more specialized, for example.
Jak/Stat is an example of a cell signaling pathway, that is also fairly straightforward to understand. Various members of the Jak family are loosely associated with a variety of receptor proteins. When those receptors are activated by a ligand binding to them, Jak becomes activated and recruits various members of the Stat family of transcription factors. The Stats become activated and dimerize (form doublets), then translocate to the nucleus and bind specific promoter regions of DNA. They then recruit the rest of the DNA transcription machinery to transcribe these target genes. The gene products then help effect the cell's response to the original stimulation - the binding of the ligand to the receptor.

Thank you, but I do understand that -- I suppose I didn't write my question very well and I was initially confused because my book explains the receptor tyrosine kinase (RTK) pathway in the context of the fibroblast growth factor family of paracrine factors, because the FGF receptors are RTK's. I was wondering how much of this "sharing" takes place -- how many of these ligands use the RTK pathway? My book implies that quite a few do, but isn't explicit about which.


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Simple diffusion of lipid-soluble molecules through phospholipid bilayer -- does anything get "stuck" in transit?
It's a pretty elementary concept, and when I first learned of it I don't think I had the foundations to even think of such a question, but I found myself the other day thinking about the amphipathic nature of the phospholipids in the plasma membrane and why it might be that lipid-soluble molecules don't stay in between the layers (of the bilayer).
I know that simple diffusion is a response to a concentration gradient, but consider a case where equilibrium is being restored and lipid-soluble molecules are diffusing from whatever extracellular matrix through the membrane and into the cytosol. Towards the end of this process, when equilibrium is nearly restored and the last few molecules are making their way into the cell, the rate of diffusion for these last couple molecules will be slower than those that diffused when the concentration difference was greater. Since the polar heads on the outside and inside of the bilayer are hydrophilic but the inner part, where the fatty acid tails are, is hydrophobic, what drives a molecule to leave the cozy, accepting, lipophilic environment of the middle (of the bilayer) to cross through the cytosolic-side rejecting polar heads and enter the cytosol?
I understand that initially these molecules were moving into the cell in response to a difference in intracellular vs extracellular concentration, but I'm asking whether we would ever see a case where the gradient is nearly zero and a molecule in transit simply decides to reside in between the layers instead of crossing all the way into the cell; as if moving through the cytosolic polar head side is not worth the effort to reduce a nearly-zero gradient to zero.
Please ask me if I can clarify my question in any way -- I'm finding it difficult to phrase. I asked my professor (who has her doctorate in toxicology & pharmacology) and she understood what I was asking but didn't have an answer.

I'd say it's certainly possible, but I doubt it would be for very long. I cannot think of a single concentration gradient that's at equilibrium for every long with respect to cells. They are always quickly restored to some imbalance, so as soon as the cell starts to restore the imbalance, the molecule/atom would be urged to choose a side.

I think, given Alan's answer the question you might be asking is something like
'do compounds become concentrated in the lipid bilayer', as opposed to achieving high concentration inside the cell after diffusing through the membrane as he describes.
This could certainly happen (if that's what you're thinking), but usually won't for I think two reasons.
The first is that any molecule that would not soluble in the interior of the cell is going to have a correspondingly small not going to be found in the blood or lymph, tissue, ocean or other milieu the cell is living in, which will be mostly water.
You might well ask whether there are cases where the compounds in question might be available in low concentrations around the cell and over time accumulate in the lipid bilayer. This slow concentration model probably happens, but there is a compensating mechanism - the lipid bilayer is taken into vescicles and degraded, to be replaced by newly synthesized such that membrane components renew themselves.  This process includes the cell engulfing by endocytosis and specifically turning over membrane proteins.
The turnover rate for most cells is on the order of days, some of the best numbers for this are behind a paywall, but a reference to synaptic membrane turnover shows some components turn over varying between 6 and 24 days.  Different components such as cholesterol, phosphatidylcholine and phosphatidylethanolamine have differing rates of turnover.
So between these two effects, the concentration of 'permeant molecules' would be low for most cases.

is "permanent molecules" a typo -  permeable molecules?

its at term they used on wikipedia - it seems like a conventional term for the standing concentration in the membrane..

Just checked - is it "permeant"?

Thank you -- I wasn't thinking about turnover and synthesis of new membrane lipids, and this is exactly what I needed. I thought for sure that at least theoretically a molecule could remain in between the bilayers, but I agree that the amount of this occurrence is relatively insignificant.

I interpret your question to refer to the movement of a lipid-soluble molecule that is therefore able to diffuse into cells down a concentration gradient. I think that you are asking whether as the gradient collapses, some of these molecules would "stay in the bilayer".
You are thinking about the diffusion process in the wrong way. There will always be a pool of these molecules in the bilayer, and these will be continually exchanging with molecules in the two aqueous phases on either side of the membrane. The net flux which results in diffusion in any particular direction will be the  movement that results from these equilibria. Diffusion isn't a directed process in the way you define your question.

My diagram shows on the left the progress towards equilibrium and on the right the situation where it has been reached. Note that at equilibrium, because it is lipid soluble, the molecule is at a higher concentration (larger typeface) than it is in either aqueous phase. And - importantly, molecules will still be moving into and out of the bilayer at both faces.
Added later:
A classic example of a lipid soluble molecule able to diffuse in this way is oxygen. According to this paper, at physiological temperatures, and at equilibrium, the concentration of oxygen in a bilayer will be approximately 3x that in the surrounding fluids.


text:
Is there a term that distinguishes extracellular "transport" proteins from membrane-bound "transport" proteins?
I've been researching genetics and biochemistry in my free time and I've noticed that proteins such as albumin and apolipoproteins that facilitate extracellular transport and proteins such as GLUT1 which transports glucose across the cell membrane or MFSD12 which transports cysteine into the melanosomes of melanocytes are all referred to as "transport proteins" or "carrier proteins". Maybe its just my opinion as a layman but as far as I can tell these are two distinctly different processes, I don't see the logic in referring to these by the same name. One is a protein bound to a membrane that facilitates diffusion across that membrane and the other is a protein that spends the majority of it's lifetime shuttling molecules around outside the domain of any cell.
I'm wondering if maybe there is a set of terminology that distinguishes between the two?

The short answer to this question is NO.
To understand the reason one needs to appreciate certain things about proteins and about research into them. A primary objective in research into proteins is to understand how their structures determine how they work, not to classify them by function. Of course, assigning similar proteins to groups and using phrases to describe them is helpful, but as science progresses broad categories may be found to be invalid or unhelpfully wide, and even when valid it may be more helpful to consider narrower categories, with the practitioners being aware of the overall picture.
I have given introductory lectures on proteins to undergraduate students, and would list some of the diverse roles they can play. I might have said something like “some catalyse reactions, some play a structural role, some transport substances across membranes, others carry molecules from one location to another…”. For stylistic reasons I have used two different verbs “transport” and “carry” — and if I wanted to make headings for a list I might use “carrier proteins” and “membrane transporters”, but these are not official categories and others might use other descriptions.
As @bryankrause commented, “carrier transport proteins” such as apolipoprotein, albumin, zinc carriers, haemoglobin etc represent very diverse types and are generally not considered together after first introduction. The term “carrier protein” has problems as it may be mentally associated with “acyl-carrier protein”.
As for the “membrane transporters” it is instructive to look at the index to the respected text, Berg et al. Biochemistry — Chapter 13 which considers such proteins under the title “Membrane Channels and Pumps”. This has a subheading “Many molecules require protein transporters to cross membranes” but  then proceeds to use specific terms for different classes like “ion channel proteins”, “secondary transporters”, “ion pumps”.
In conclusion protein researchers tend to focus mainly on descriptive phrases and precise specialist sub-categories when talking about functional groups. The nearest thing to biological taxonomy is perhaps structural classifications such as SCOPe.

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


text:
Is this a texas sage?
So for a project in one of my classes we must identify two monocots and two dicots growing at our school. We've managed to identify all but one:

So more information:

My school is in southern nevada
It's about one foot tall
It's growing with joshua trees and oak trees and some rosemary.

Update: I think it's a texas sage, but I'm not completely certain, verification would be nice.

The link doesn't work for me. Looks like that link is private, and I cannot access it.

@TwistedGenes Thanks for informing me, I've posted the image

That's a good guess, but I doubt it is Texas sage or Leucophyllum frutescens -- which is a common urban landscape shrub in the USA southwestern deserts.  L. frutescens is more upright and bushier, and in particular, much grayer than the plant in your picture.  Can you provide better/more pictures, from different angles, and especially pictures of any flowers that might be present?


text:
What is this Las Vegas area weed?

This is a picture I took of my mystery weed out by Pittman wash in Henderson NV earlier this year. From my experience this last year, I assume that the plant turns red later in the year and loses the bottom leaves. The plant typically seems to grow no more than half a foot tall but can grow a couple feet wide at or near the top.
Edit: I wasn't able to get a background but here are more pictures

The spindly nature of those stems makes it hard for the camera to find a focal point.  Maybe try getting down low and have the camera focus on the basal leaves, and if the depth of field is good we'll be able to see the stems as well.  If you are taking photos with a phone be sure to sit down (for steadiness) and tap the image where you want it to focus -- sometimes they need a little guidance!

@BryanHanson Thanks, I'll take a better picture when I get a chance later today.

If there’s a lot of that plant around, you might pick one of the stems, and bring it home and photograph it on a neutral surface. Might be easier to get focused there.

@BryanHanson idk if these are better but I picked one and took some pictures.

Those are helpful, thank you.  Not a lot of plants generally w/o any leaves (ignoring the tiny basal leaves that are probably from when it sprouted).  Someone will know this plant, I may have time later to dig through some field guides.

Alright, after a lot of searching, I have a proposed ID: Eriogonum deflexum known commonly as skeleton weed or little desert trumpet.  I feel pretty confident of the genus, less so on the species (there are several close candidates).  The family is buckwheat or Polygonaceae.
This plant has basal leaves as yours does, has pretty much leaf-less stems and relatively infrequent flowers, which look quite a bit like your picture.  Reading various descriptions it seems the plant is somewhat variable, it often looks like your pictures but sometimes has more flowers and sometimes the plant is more dense, rounded, shrubby and taller (it probably depends on the moisture and soil quality).  It is a desert species, preferring scrubby areas and washes, widely distributed in Western US deserts.
CalPhotos has a picture which looks to be a good match (credit: Jean Pawek; also, CalPhotos has many other photos).  This photo by Hank Jorgensen looks like a good match too and shows flowers which look similar to yours.
If you see the plant again, bring a picture on your phone and check the flowers carefully. Also the leaves should be hairy/wooly.

Yes, the leaves are frequently wooly. Thanks!

Great! I've been semi-obsessing about this!  Found it by browsing a field guide to San Diego county plants and fortunately it was there.


text:
what is the poison in chinaberry?
I was trying to look up what the poison in Chinaberry is, however, with the exception of a couple related compounds was able to find no information on the poison. What chemical makes up the Chinaberry poison, and what is this chemical's concentration and LD50, if known?
Edit: The Chinaberry I am referring to is Melia azedarach

Which chinaberry do you mean? https://en.wikipedia.org/wiki/Chinaberry_(disambiguation)

@jamesqf I am referring to Melia azedarach, I was not aware that there are multiple plants by that name.

The toxin is Meliatoxin, in a class of toxins called tetranortriterpenes.
I found this here.  Bold emphasis mine.
https://wagwalking.com/condition/chinaberry-tree-poisoning

What is Chinaberry Poisoning? The chinaberry tree is a member of the
mahogany family that is native to Australia, China, and India. These
deciduous trees sprout delicate light purple flowers in the spring,
which develop into yellow, berry-like fruits in the summer. They were
transported to North America in the early 1800’s as an ornamental
plant, but has escaped into the environment and is considered an
invasive species in several southern states. It produces a potent
insecticide which utilizes a tetranortriterpene neurotoxin known as
meliatoxin. This insecticide is found throughout the plant’s bark,
leaves, and flowers but is found in the highest concentrations in the
ripe fruit. If you suspect that your pet has consumed any of this
plant, contact your veterinarian immediately. The chinaberry tree, or
Melia azedarach, is a deciduous tree that produces a potent
insecticide which utilizes a neurotoxin that can prove detrimental to
your pet if ingested. Symptoms of Chinaberry Poisoning in Dogs
Symptoms of chinaberry tree poisoning occur most often from eating the
ripe fruit, however, the bark, leaves, and flowers also contain
smaller amounts of the toxic substances. Symptoms usually begin within
just two to four hours from ingestion. Abdominal pain Blood in stool
Colic Constipation Death Depression Diarrhea         Excessive
drooling Heart attack Hyperactivity Lack of coordination Loss of
appetite Muscle rigidity Seizures Slowed heart rate Stupor Vomiting
Weakness Types
The scientific name for the chinaberry tree is Melia
azedarach, and it belongs in the mahogany family.

From another source
http://www.sciencedirect.com/science/article/pii/0031942283830398

Toxic tetranortriterpenes of the fruit of Melia azedarach . .Peter >B.Oelrichs. Michael W.Hill. Peter J.Vallely. John K.MacLeod. .Tadeusz >F.Molinski
Show more https://doi.org/10.1016/0031-9422(83)83039-8Get rights and
content Abstract Four new tetranortriterpenes, meliatoxins A1, A2, B1
and B2 have been isolated and identified as toxic constituents of the
fruit of Melia azedarach L. var. australasica. Toxicity and
pathological results confirm that the meliatoxins are responsible for
most but not all of the symptoms resulting from the ingestion of whole
fruit.


text:
What is this mushroom?
I found a singular mushroom in my back yard,  It is jet black, seems to have gills and looks somewhat like a flower do to it's upturned-ness. Sorry for not having spore colors, but I didn't want to disturb it. I will post a picture soon. I found this mushroom at 4/11/15 and it disappeared the next day. I'm just south of San Antonio.

picture + geographical location + micro-environment are necessary info

Welcome to Biology S.E.! If you need any assistance, please visit The Help Center. Please do edit this by adding a picture as soon as you can. Also, as @AliceD said, it would be very helpful to have the general location and climate the mushroom is growing in.

May be http://www.mushroomdiary.co.uk/2011/11/blackening-waxcap/ . If you are looking for an answer, here is a hint, it's black because it may had a disease called black inking.

@DevashishDas isn't the stem a bit to tall and the cap to small to be a blackening waxcap?

@tox123: Yup. Then maybe be a mushroom with the disease. But something is wrong. you are sure its a mushroom?

@DevashishDas Yes it had gills and looked like it had the texture of a mushroom.

It has gills? Are you sure it's not a fish?

The mushroom suggestive for one of the inki ones of Coprinus family, especially Coprinus comatus. The black color can be very intensive in some stage of their development, since it is a part of the spread mechanism.
"Members of the genus Coprinus have been collectively known as the "inky caps" because of the curious character of autodeliquescence of their gills-- in other words self-digestion to release their basidiospores. Most of these species have gills that are very thin and very close to one another, which does not allow for easy release of the spores. Moreover the elongated shape of mushroom does not allow for the spores to be shot off the basidia and get caught in air currents as in most other mushrooms. Coprinus species "compensate" for this by a sequential maturation of the spores from the bottom of the gill towards the top. After the spores have matured and been released, the gill tissue digests itself and begins to curl up, allowing easy release of the basidiospores above. In other words, the digestion opens up the fruiting body so that spores from further up the gills become exposed to the air and a clear path of spore release. The self-digestion continues until the entire fruiting body has turned to black ink. In the olden days this ink was actually used for writing. The self-digestion is also a way of releasing the spores over a longer period of time, and allowing the release of spores from very closely spaced narrow gills borne inside a longitudinally tall pileus. If any Coprinus species are collected for eating or for scientific study, they must be cooked or dried right away, since the self-digesting enzymes seem to kick into high gear after the mushroom is removed from its substrate. They're pretty easy to find too-- the genus name Coprinus gives you a pretty good idea where to look for these mushrooms-- in dung or very rich organic soil."
examples:
1.

2.

3.


text:
Help identifying tiny jumping bug
I've found a few of these bugs hanging out on my desk. There aren't many. Maybe 5-10 at any given time. Are they a type of springtail? I couldn't find an image in searching that made me say, "That's it!"
Any help is appreciated!
Thanks!

Welcome to SE Biology. Could you edit your question to include a location? It may help with the identification.

Related to: Bug Identification: Tiny Bugs in Fairport NY, What are these tiny, swarming, jumping bugs?, Can Anyone Identify This Insect?, Taxonomy: Categorising Collembola, What kind of small insect is this?, Unknown aquatic larvae

Those are springtails. Order Collembola. You can find yours here on BugGuide. https://bugguide.net/node/view/258362

Thanks for confirming. Now to figure out how to get rid of them! :-)

@Mattaton do you have a plant that you water frequently nearby your desk? They probably come from that. They're not harmful and if it really annoys you, just water less frequently.

@tox123 Nope, no plant and no moisture that I can find. My office is in a basement, but there's no noticeable humidity. Might see about getting a dehumidifier, just in case. Not really sure WHY they're hanging out here.

@Mattaton they might just be lost. They live in soil and dark conditions, so it's possible that there may just be a way into your basement from surrounding soil.


text:
GWAS: why is replication in another cohort so crucial?
Almost all the landmark GWAS (Genome-Wide Association Studies) reviews agree that, for a GWAS finding to be valid, it needs to be replicated in an independent cohort. What exactly is the rationale behind this? Is this criterion still valid even when the objective is looking for genes to do functional studies, instead of a clinical perspective of searching for susceptibility loci? Considering the difficulty in replicating some phenotypical characterizations in a large numbers of subjects, for a biologist this whole thing seems irrelevant.
Consider the following scenario: Suppose I have 5000 phenotyped individuals with a budget to genome-wide genotype them all. The phenotyping requires state-of-the art methodology with immense costs, and the cohort was phenotyped through another grant. What would be the point of dividing my cohort to two as a discovery and replication groups, other than to save money in exchange for stat power. To this, add the subsequent functional studies on the associated loci, what would the point in genotyping a few SNPs in 500 more people be? If one can indeed find that additional cohort, wouldn't it be a better option to combine any available cohorts in a meta-analysis, rather than using them for replication?

Think of it like this, if the study can't be replicated in an independent cohort, what does that mean for your results in terms of applicability?

Great question. The answer is non-random technical biases correction. Will expend on that in an answer as soon as I find some time. You are not supposed to divide a genotyped cohort in two, by doing so you might correct for population structure (and not really as you can correct for it anyways using a simple PCA based on the genotype) but definitely not for technical biases. Population might also be a reason but it is not the principal one (population specific SNPs are informative).

As an elaboration of my comment.
Summary: Replication is required in GWAS studies to account for non-random technical biases.
An example of such bias is, for example, a chip used for genotyping giving consistently incorrect genotypes for a locus. In this situation adding more subjects will not correct for this effect and therefore the only solution is to genotype additional subjects with another method (e.g. another chip or experimental protocol). Another source of non-random technical bias is at the phenotype measurement level. You might want, if possible, to measure the phenotype using other techniques to make sure that bias will be corrected.
A replication cohort does not need to be huge and the actual size needed will largely depend on the effect size of the SNP seen in the discovery cohort. A "power-to-detect" calculation would help in predicting the cohort size needed. For a SNP to be significant, it must pass Bonferroni correction but as you can run a statistical test at the candidate site only the correction will be usually not very astringent (i.e. you might run association tests on "only" a few dozens or hundreds SNPs).
Historically GWAS replication was also required to correct for population structure but as the tools evolved substantially (e.g. the use of principal component analysis) and the cohort sizes are now substantially bigger compared to the first GWA-studies, this is less a concern. What was required is to sample independently other subjects from either the same or a different population.
For your situation what you could do is to split your cohort into a discovery and a replication panel, genotype your subject in the replication panel using an independent technique, eventually do the same with the phenotyping and replicate you candidate SNPs. The replication panel needed is usually must smaller than the discovery cohort for the reasons stated in the previous paragraph.
For your last question about the meta-analysis. Yes this could also be a way to go but be careful that you will still need a replication cohort to validate SNPs found this way therefore resulting in the exact same problematic you described.
I hope this help!

As with all serious scientific result GWAS results need to validated by others. In this case it think is extremely important because these studies link mutations to diseases or in more general given genotypes to phenotypes, thus pointing out possible causes. So validating these results with the use of independent "samples" is indeed crucial. But as I said all serious (noteworthy) scientific finding should be reproducible.
Edit: the point in it is randomness and sub sampling. Such large cohort should not come from a small sub-population but many regions of the world, and by randomly dividing your individuals to two or even more groups you ensure that other background effects such as local gene allele variation frequencies, life-style differences etc average out. Imagine a scenario where you have 90 individuals in 60 of them you can link the genotype to the phenotype. that is 2/3 of the individuals. But if you take 3 sub samples of 30 individuals and get 7/23 , 17/13 and  6/24 (not linked / linked), that is 76.6% (23/30) , 43.3% (13/30) and 80% (24/30). From these you can get tbe same average of 66.6% but with standard deviation (15,5), and confidence interval not just a number.

Let me elaborate the question: Suppose I have 5000 phenotyped individuals with a budget to genome-wide genotype them all. What would be the point of dividing my cohort to two as a discovery and replication groups, other than to save money in exchange for stat power. To this, add the subsequent functional studies on the associated loci, what would the point in genotyping a few SNPs in 500 more people be?

Also, in the above scenario, where SNP chips costs much less compared to phenotyping individuals, wouldn't it be a better option to combine any available cohorts in a meta-analysis, rather than using them for replication?

It's not really due to population and sampling but rather technical biases. As you pointed out at such large population size (>5000) you are not expecting to get so much variation due to local population variation or sampling biases. Also reviewer don't ask you to replicate your results in another population but rather another cohort (could be the same population "type"). Last point, no you don't have to run a GWAS on people coming from all over the world, you can run a GWAS in a very specific pop if you want and replicate the discovered associations in a replication panel from the same pop.

I agree, yet I wanted to give a 'general-view' answer on doing paralells, rather than focusing the actual GWAS (as it is like any other experiment from this point of view) I totally agree with your last point, but again my aim was to emphasize the positve effects of diving your sample into sub groups.


text:
Monozygotic vs Dizygotic heteropaternal superfecundation
Update: I had a wrong assumption.

After triple checking, I now see that how ordinary monozygotic twins arise is 1 sperm and 1 ovum and then later the zygote splits up.

(1.1. and that that phil and lil from rugrats are opposite sex and identical twins is actually an extremely underrated genetic miracle, possibly giving more credibility to the rugrats theory/hypothesis. There's also semi-identical twins in a song of ice and fire - though i guess not game of thrones -, Ben 10, legend of korra, KND, baka to test, and i think samurai jack, etc)

Honest to God, what i weirdly remembered was that ordinary 'monozygotic' twins arise from 2 sperm 1 ovum and then this 'zygote' or whatever of 2 sperm and 1 ovum splits up into 2 zygotes i.e. the splitting up of the 'zygote' is a natural consequence from that 2 sperm have fertilised 1 ovum. From what I weirdly remembered, it would be natural to ask what if the 2 sperm were from different males.

(2.1. Additionally, the Phil and Lil thingy is not really a genetic miracle since all you need is a 22X sperm and a 22Y sperm to fertilise 1 ovum. Damn television. i really thought opposite sex identical twins were not that rare.)

However, apparently it is possible for 2 more sperm to fertilise 1 ovum, in a case called semi-identical twins or something, but there are apparently only 2 reported cases.

New question: Okay in the unlikely event that what would be semi-identical twins would arise from sperm from different males, well, then what?

From wikipedia:

Homopaternal superfecundation refers to the fertilization of two separate ova from the same father, leading to fraternal twins;6 while heteropaternal superfecundation is referred to as a form of atypical twinning where, genetically, the twins are half siblings.

There doesn't seem to be a distinction between heteropaternal superfecundation occurring with two ova and with one ovum. How will monozygotic heteropaternal superfecundation twins look like as opposed to dizygotic heteropaternal superfecundation twins and to identical twins?

Are/Were there real life cases of monozygotic heteropaternal superfecundation?

The heteropaternal superfecundation selected cases given on wikipedia seem to be for dizygotic. I tried looking up on google, but I've found so far only dizygotic.

Have you thought about how many chromosomes your one zygote with heteropaternity would have?

@mgkrebbs No. The extent of my familiarity with genetics is what I learned in a non-elective class in secondary school. Thanks for commenting. Please enlighten me. But I do remember the 22X, 22Y stuff I guess. What's the difference if the 2 sperm are from the same father vs from a different father?

A normal singleton child is a result of the fertilization of an ovum (with 23 chromosomes) by a sperm (with 23 chromosomes). After fertilization, the cell (with 46 chromosomes) is called a zygote.  All normal human cells (other than ova and sperm) have 46 chromosomes.
Monozygotic twins (identical twins) occur when the set of cells resulting from the early divisions of a single zygote separate into two groups.  Each of these two groups of cells proceed to form a normal embryo, with resulting (if carried to term) in twins.  Since these twins came from the same zygote, they have the same 46 chromosomes and so are essentially genetically identical.
Now how could this monozygotic process occur with two fathers being involved?  Only by having two separate sperm combine with a single ovum.  This would result in the zygote having 69 (3x23) chromosomes.  This could happen, but would be an extreme case of aneuploidy (abnormal number of chromosomes). Such a genome is massively defective due to the presence of too many gene copies, and the embryo (whether singleton or twin) will be spontaneously aborted.  Only a few kinds of aneuploidy can result in a viable fetus, almost all having only a single extra chromosome (one of the smaller ones); the most common case is having 3 copies of chromosome #21, which results in Down Syndrome.
So, monozygotic heteropaternal superfecundation has not been observed because the resulting pregnancy is very unlikely to go to term. (It's just as unlikely when the two sperm are from the same man.)

thanks. i apparently remembered my biology/genetics from secondary school wrong. i updated question. follow-up 1: but your answer is still the same...right?

follow-up 2: do you really mean 'the resulting pregnancy would never go to term' rather than 'the resulting pregnancy has never in human history been recorded as having gone to term' ?

Never say "never" with biology - yes, there have been a very few reports of twins apparently resulting from two sperm entering an ovum. In the well documented 2019 report, the result was twins who were both mixtures (chimeras) of cells derived from both sperm, some XX and some XY.  They hypothesize that an initial 3-way division separated the 2x69 chromosomes into 3 cells with 46 chromosomes each. I've softened the wording in my answer above.

right i never said 'never happened' i said 'never...been recorded'....anyway thanks for answering and thanks in particular for putting up with my wrong assumption about monozygotic twins


text:
How should one interpret heritability? Is it related to $R^2$?
From Wikipedia:

Heritability estimates are often misinterpreted if it is not understood that they refer to the proportion of variation between individuals on a trait that is due to genetic factors. It does not indicate the degree of genetic influence on the development of a trait of an individual. For example, it is incorrect to say that since the heritability of personality traits is about .6, that means that 60% of your personality is inherited from your parents and 40% comes from the environment.

So what is the plain english interpretation of heritability?
Is it supposed to be the genetics version of $R^2$? If so, please explain it to me anyway because I forgot my statistics.

I found this so from what I understand, one might say:

If height is estimated to be 80% heritable, and if we get 10 people, get their heights and then compute the variance, we say that around 80% of that variance is likely due to genetic factors while the remaining 20% is due to other things.

Such interpretation of heritability seems to work for non-categorical traits. What about categorical or binary traits?
Hair and eye colour is categorical (I think?). So what, we assign a number for each colour and then compute the variance?
ADHD is binary (I think?). Do we assign 0 for not having and 1 for having then compute variance?
I seem to recall regressing binary or categorical variables needs some kind of adjustments and hence interpretations of estimates (such as intercepts or slopes) may be different.

Also, the book linked above says

heritability represents the degree to which the variance in a trait is attributable to genetics in the population on average

Combining that with the Wiki paragraph above, I don't think someone saying

Eye colour is around 98% heritable. I have brown eyes. Therefore, around 98% of the reason why I have brown eyes is genetics.

is far off from saying

If we have a million people who near-identically flip a million near-identical coins a hundred times, and we compute the average of the coin flips that turn out to be heads to be 58.6, then the probability that you will flip heads when you near-identically flip this near-identical coin is around 58.6%.

Is it? (Of course 'near', 'around', etc are not always used similarly...lol)
So yeah, technically the 60/40 interpretation in the Wiki example is technically wrong but practically it's around 60% $\pm$ some standard deviation?

Possible duplicate of Why is a heritability coefficient not an index of "how genetic" something is?

@Remi.b $R^2$ is there?

No, it is true that the other post does not explicitly talk about the relationship between heritability and it's measure in parent-offspring regressions... I haven't decided yet how I would deal with that. I might retract my vote close soon but I must read your edit first :)

I would advice that you restrict your question to the regression interpretation of heritability and ask separately about the heritability of a non-quantitative trait.

Heritability (as shown a long time ago by Galton) is the slope of the parent-offspring regression. However, I don't understand it well enough for the moment to formulate an answer. +1 btw

@Remi.b Are you sure it is slope? Since it is a ratio of variances, it sounds closer to an $R^2$, though some manipulations might give you slope

Yes I am pretty sure. I would expect both the slope and the $R^2$ to get closer to 1 as heritability increases. I would vote to close as too broad until you reduced you post t only a single question (currently you talk about the interpretation of heritability as a regression and about the case of non-quantitative traits). Note that you might want to talk about which regression (which variables) you are referring to.

@Remi.b approaching 1 through values from the left? Anyway, go ahead and close for now, I guess. I'll split up and edit later on. Thanks ^-^

What do you mean "approaching 1 through values from the left"? If you agree that the question should be closed, you should probably just delete it (or vote to close as duplicate).

@Remi.b I'll edit it later. I'm asking if you mean for both slope and R2 that we have 0.8, 0.9, 0.99, 0.999, etc rather than 1.1, 1.05, 1.01, 1.001, 1.00001, etc or 0.9, 1.1, 0.99, 1.0001, 0.999, etc

Yes from the left. You should not have a slope steeper than 1 and it makes no sense to have a correlation coefficient greater than 1. You seem to describe the dynamic of a system (especially when seeing to hypothesize cyclic behaviour) though and I don't get it.

@Remi.b R2 and correlation coefficient I get. But why can't we have a slope steeper than 1? Is it a bio thing? I seem to recall slopes steeper than 1 in areas outside bio

Yes it is a bio thing! For a parent-offspring regression, only sampling error could cause slope to be higher than 1. In the whole population the slope is bounded between 0 and 1. We will have to delete all these comments once you've edited your post.

@Remi.b Thanks! ^-^ What am I supposed to do again? Not really into Bio SE hehe

The post Why does the slope of parent-offspring regression equals the heritability in the narrow sense? can help. Otherwise, I would recommend you having a look at the section on quantitative genetics of Gillespie's book.


text:
What would sanitiser fail to do that detergent and warm water would do in cleaning glasses frame that isn't 'visibly soiled'?
Update (from comment):

It's certainly possible that the manufacturer had that in mind when making their cleaning recommendation, but I'd like to think they would specifically warn against it if it was a common issue.

For an arbitrary glasses frame, specifically the earsocks, can regular alcohol/sanitiser replace detergent and warm water? Apparently some brands of glasses frames recommend really detergent and warm water. I mean, with alcohol and sanitiser, am I perhaps killing only 99% of the germs instead of 99.9% of the germs? (If we wanted planes to be safe "with statistical significance" that is 99% confidence level we'd have between 400 and 2500 crashes a day.)
I couldn't find any videos for this on youtube. Most of what youtube gives is cleaning ears or cleaning the lenses.
Edited to add: I got the following with my new glasses.

Kind of a hassle to do the recommendation especially that I've never cleaned glasses frames in my 13 years of wearing of glasses, except when they were, to borrow a term from WHO, 'visibly soiled':

Clean your hands by rubbing them
with an alcohol-based formulation,
as the preferred mean for routine
hygienic hand antisepsis if hands
are not visibly soiled. It is faster,
more effective, and better tolerated
by your hands than washing with
soap and water.

• Wash your hands with soap and water
when hands are visibly dirty or visibly
soiled with blood or other body fluids
or after using the toilet.

Alcohol is a substitute for soap and water for hands that are not 'visibly soiled'. Is there perhaps some kind of substitute for glasses frame?

Did your recommandations specifically mention killing germs? Because glasses have special coatings that may be damaged more with one cleaning product than the other.

Are these recommendations specifically for the purpose of decontaminating or santizing your glasses, or for removing the oils and debris of everyday use? In my experience, ethanol doesn't do a great job of removing oils or drying clear. Most hand sanitizer has additional additives that may leave even more residue. Also, soap or detergent and water is effective against a much broader range of germ, as there are many on which alcohol sanitizers have little to no effect.

@Cell Thanks. Edited to add details. Kind of a hassle to do the recommendation especially that I've never cleaned glasses frames in my 13 years of wearing of glasses, except when they were 'visibly soiled'. Actually now I'll edit to add more details about 'visibly soiled'.

@MikeyC Thanks. Edited to add details. Kind of a hassle to do the recommendation especially that I've never cleaned glasses frames in my 13 years of wearing of glasses, except when they were 'visibly soiled'. Actually now I'll edit to add more details about 'visibly soiled'.

At least as I read those instructions, the purpose of cleaning is to remove accumulated dirt, dust, and natural skin oils, not to kill bacteria.  AFAIK hand sanitizer - a product I was entirely unaware of until the recent COVID-19 pandemic - is not designed for cleaning.

@jamesqf Ah so hand sanitiser(/alcohol?) would kill bacteria but wouldn't necessarily remove dirt, dust or oil?

@BCLC: Yes - or so I'd suppose from what I've read about the product.  As I said, I've never actually used it myself.

@jamesqf i mean in general with sanitiser/alcohol on hands, tables or glasses frames they kill bacteria but do not necessarily remove dirt, dust or oil?

@BCLC:  Once again, I DON'T KNOW for sure.  I've never used the stuff, and had never even heard of it before the COVID-19 panic buying caused it to become news.

Ignoring any possible impact alcohol-based solvents might have on the material or coating of frames, alcohol won't really remove anything it dissolves unless it is rinsed or at least thoroughly wiped off. When the alcohol evaporates, it will leave behind a residue containing anything that was dissolved in it. That's why your hands sometimes feel sticky after applying that gel hand sanitizer. The gelling agents don't evaporate with the alcohol, but instead remain on your skin.
But since this is the Biology stack, so I'll try to provide a more biological answer.

What would sanitizer fail to do that detergent and warm water would do in cleaning glasses frame that isn't 'visibly soiled'?

While alcohol based sanitizers are effective at killing most pathogens, it's typically on par with a soap and water scrub. However, for the purposes of sanitation (which seems to be the only reason you'd need to clean frames that are "not visibly soiled") there are several indications for which alcohol based sanitizers are considered ineffective and inferior to soap and water. This is generally because of the specific physiology or life cycle stage of certain organisms which allow them to be resistant to the biocidal effects of alcohol. Common examples include Cryptosporidium, a water-borne protozoan parasite, norovirus, a non-enveloped intestinal virus that spreads notoriously fast in hospital environments and on cruise ships, and almost all endospore-forming bacteria, like Clostridium perfringens and Clostridioides difficile. In the lab, we actually use alcohol to isolate live bacterial spores from the vegetative components of a culture. It has also been reported that alcohol based sanitizers are more likely to cause allergic reactions (e.g. contact dermatitis) from skin exposure.
Most of these statements can be referenced in this open-access article on PubMed, with links to primary sources if you're interested in following up more.
Gold NA, Mirza TM, Avva U. Alcohol Sanitizer. 2020 Jun 24. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513254/#

Thanks MikeyC! So actually alcohol or sanitiser may be harmful to the frame? ('Ignoring any possible impact alcohol-based solvents')

I only mentioned it because the possibility had been raised in some of the comments and the previous answer. It's certainly possible that the manufacturer had that in mind when making their cleaning recommendation, but I'd like to think they would specifically warn against it if it was a common issue.

MikeyC, GENIUS. thanks. i added part of your comment to an update to the question post

The earsocks on Oakley brand sunglasses are made of a proprietary hydrophilic rubber called Unobtanium 1.  From what I can find, Unobtanium is likely a styrene copolymer 2, possibly a formulation called Kraton G 3.  Polystyrene is insoluble in water, but soluble in ethanol and 2-propanol (isopropanol) 4, which are the most common alcohols used in sanitizers.
So, as suggested by @Cell, soapy water is likely recommended by the manufacturer because it is unlikely to damage the glasses, whereas alcohol-based cleaners may degrade the soft rubber components.

https://www.oakleyforum.com/threads/how-to-restore-old-unobtainium-that-has-gone-sticky.10821/
https://www.oakleyforum.com/threads/rubbers.21973/page-2
https://kraton.com/products/KRATON_G.php
https://www.bangslabs.com/common-solvents-and-non-solvents-polystyrene

Thanks Dirigible! So actually alcohol or sanitiser may be harmful to the frame? ('whereas alcohol-based cleaners may degrade the soft rubber components.')


text:
In what way is ADHD genetic?
According to Psychcentral depression, bipolar disorder, ADHD, schizophrenia and autism are traceable to the same inherited genetic variations
According to AsapSCIENCE, depression could be genetic due to a variation in the serotonin transporter gene. Having at least one short seems to give some kind of genetic predisposition to depression.
So what's the analogue of the serotonin transporter gene in ADHD? Is there a dopamine transporter gene?
Double posted on Cognitive Sciences Stackexchange

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4264104/ The diagnosis is observational. One misconception that people have is that a given genotype will, in 100% of cases produce a phenotype. So even if the genetic marker(s) has(have) been identified, it doesn't mean that the expression patterns of a person will be such as to produce the phenotype.  There will be a predisposition, but it is possible that a heterozygote allele could rescue the normal phenotype. It is also possible that even homozygotes will not manifest the phenotype if the deleterious gene is not expressed.

@AMR For a lay person pls? 'There will be a predisposition' --> How? I'm guessing the serotonin transporter gene is what gives a predisposition for depression. What about for ADHD?

I'm voting to close this question as off-topic because it's cross posted and answered on CogSci.SE:http://cogsci.stackexchange.com/questions/12311/what-is-the-underlying-genetic-basis-for-adhd


text:
What is this insect? Found in Peru
I took the pictures today in Cusco Peru. It is the third insect of its class in a month. I never see it before. I thought that it is a wasp, but I think it's really thin to be a wasp. It's about 4 or 5cm.
I want to know what kind of insect is and if it's dangerous. Thanks!

Very good picture for identification, even I am not the one who can answer here.

Yeap! Very good quality of photos.

http://www.nhm.ac.uk/resources-rx/files/keys-for-nocturnal-workshop-reduced-109651.pdf

So that looks to me like the Ophioninae family of wasps, genus Ophion. I'll query the list of known species to try to find a more direct match.

Some evidence exists which notes Ophion may sting when threatened, but at the same time (and I don't have the reference ready) it's believed that the sting contains no toxin.
As for a positive identification, it's difficult without examining the the features of the wasp extremely close up. Identification keys exist here.

It seems, that I haven't found more direct match, as you promised in your answer. Nor, you haven't answered OP, whether it can be dangerous. An edit would be nice, to clear these things (i.e. remove promise for searching for more details). Thanks!


text:
Which white beans have phosphatidylserine?
Many articles online say that plant foods are poor sources of phosphatidylserine, except for white beans, which have 107 mg per 100 g.¹ ² ⁴ Honestly though, I think they might just be repeating a claim from Wikipedia, which cites "Souci SW, Fachmann E, Kraut H (2008). Food Composition and Nutrition Tables. Medpharm Scientific Publishers Stuttgart." I wasn't able to find this source freely available online. Examine.com mentions that "Phosphatidylserine (PS) is found in Soy Lecithin at around 3% of total phospholipids"⁵, citing https://www.ncbi.nlm.nih.gov/pubmed/18846580.
I haven't been able to find any (reliable) sources that say which kind of white bean is being referred to here: is it navy beans, cannellini beans, great northern beans, runner beans, or marrow beans? There are some that say navy beans,³, but I believe that information is derived from the Wikipedia article on phosphatidylserine, plus some speculation based on what the writer of the article thinks "white bean" refers to.

Use sci-hub to get the article? You probably know this by now though since this question is old.


text:
Recommend good conversational books to learn about cell and developmental biology or biochemisty?
I'm an engineer by training and teaching myself the basics of cell and developmental biology. I'm using Scott F. Gilbert's Developmental Biology and Alberts' Essential Cell Biology right now, and they are both great resources.
Can you recommend good books on similar topics that are written in a non-textbook format?
EDIT: For example, I found books like The Greatest Show on Earth, Extended Phenotype, and Nature via Nurture really useful to learn about the basics of evolution while I was reading Watson's Molecular Biology of the Gene. Are there similarly well-written books for cell biology, developmental biology, or biochemistry? I know this sounds broad, but I'm not asking for textbook recommendations. I'd like to read something that isn't a textbook alongside my current studies.
SECOND EDIT: I'd be like to extend this question to recommendations of broad review articles in Cell and Developmental Biology too. For example 'How do cells know where they are?' is an excellent article on different strategies cells may use to assess distance in a developing embryo.

Cell Biology, Dev Bio and Bio Chem are three very vast topics. I presume you want a book separately for each one ?

Yes, that's what I meant.

The two textbooks you mentioned are some of the best. Gilbert's is quite technical and assumes you have some background in molecular biology.  It might be prudent to get a more introductory textbook in that case.

Since when are book requests too broad?

I don't find Gilbert's book hard to peruse at all since I've read Watson's Molecular Biology of the Gene. When I read Watson's textbook, books like The Greatest Show on Earth really helped put things in context.
While I think Gilbert's Dev Bio is an excellent textbook and well-written, it has a great deal of detail. I would also like to read something that distills the key concepts. This is where something written in a non-textbook format would really help.

For Biochemistry:

For Molecular Genetics:

For Developmental Biology:

That last one, Life Unfolding, is really cool and I think exactly what you're looking for.

Endless Form Most Beautiful: The New Science of Evo Devo introduces the reader to several classic embryology experiments and some key principles too.
I'll edit this answer when I find more books or reading material of this nature.

Please try reading 'Principles of development' by Lewi Wolpret. This book explains the general concepts in develpmental biology beautifully. Invertebrate models like dorsophilia and zebrafish are used as examples to simplify the concepts in developmental biology.

The Machinery of Life by David S Goodsell

I just picked this up and haven't actually read through it yet, but it looks amazing. Very well illustrated with drawings and molecular models. It's also not overly technical. I don't have much to say in the way of a review, but there's plenty on Amazon. It sort of seems exactly like the book you're looking for.

Would you consider the New York Times a suitable level of detail (while admittedly not a book)? If so then you may want to peruse this collection:
http://topics.nytimes.com/top/news/science/topics/biology_and_biochemistry/index.html
You will have to be selective.
This was my first hit in Google searching for 'lay articles on biochemistry.' I would recommend my own textbook but it is aimed at 3rd year undergraduates, and would probably contravene the Biology SE rules.

Thanks a lot for the NYT link. However, those articles are based more on relaying findings than explaining key principles.


text:
Does the species of snake that eats Amphidromous inversus have chiral dimorphism?
From what I read at Schilthuizen and Davison (2005), Amphidromous inversus is a species of snail that occurs in 2 forms that are nearly mirror images of each other occurring in nearly equal proportions. I don't see any way that could be evolutionary stable if it was only eaten by snakes with a symmetrical jaw because then the snake species would evolve to be ambidextrous and then the snails would lose the selection pressure for being the rarer form but retain the selection pressure for the more common form. I can't find the information anywhere on the internet of what the snake species that eats that species of snail looks like. Have observations shown that that species of snake has a chiral jaw and occurs in 2 forms that are mirror images of each other in nearly equal proportions?

I don't know much about this particular species of snake but here are some info that may help.
What do we mean by right-handed snakes?
I doubt that in this context a snake could be ambidextrous. What they call handedness in these snakes (Pereatids) concerns the density and size of teeth on each side of the jaw (pictures from Hoso et al. (2010))

This asymmetry helps them to forage on snails.

Here is how they describe the snake feeding behaviour.

The Japanese pareatid, P iwasakii, strikes an exposed soft
  part of a crawling snail from behind at a determined leftward angle
  to grasp the ventral shell surface with the upper jaw and the soft
  body by inserting the mandibles into the aperture. The snake then
  extracts the soft body by alternately protracting and retracting the
  asymmetric right and left mandibles.

On the figure below, the individual on the left is sinistral and the individual on the right is dextral. Note by the way that snails of different chirality have a hard time to mate together.

"Right-handed" snakes can easily forage on dextral snails (the most common and ancestral form), while they have a hard time to forage on dextral snails. Hoso et al. (2010) reports a survival probability of 0% for dextral snails and 87% for sinistral snails.
Left-handed snakes
Hoso et al. (2007) report that "left-handed" snakes have never been found in south-east Asia. This is surprising as noted by Hoso et al. (2010). Even in areas where sinistral snails are relatively common, all snakes were "right-handed".
They do not suggest any potential explanation for this lack of "left-handed" snakes but one could speculate that "handedness" in snakes might be under other selection pressures than those related to foraging. It is also possible that intermediate forms are deleterious and that mutation of large enough effect are rare. It is possible that the genetic variance for handedness is just not present. It is possible that even if in some areas there are more sinistral species of snails than dextral species, the abundance of dextral is still higher and therefore, there is no selection for switching to being right-handed.


text:
How do poikilotherms thrive in a wide range of core temperatures?
What is it about the metabolism of a poikilotherm that enables them to adapt to the surrounding temperature?

I guess the answer lie mainly in (1) they stop all activity outside their comfort zone, (2) they spend time to control their internal temperature through behaviour (sun bathing or sun avoidance typically) and (3) their biological pathway are relatively not too sensitive to temperature change. I am not sure (3) is really a thing!

Do they thrive in a much wider range of temperaures than usual but regulate their temparture to within that large range by controlling where they go?

I do not understand your question. Could you specify what you mean by "what is it about ..."? Metabolic reactions are chemical reactions and therefore not extremely sensible to temperature changes, unless you are looking at reaction rates. You do not need special adaptations to being poikilotherm as this is life's (and dead matter's) status quo. This means that the metabolism of poikilotherm animals reacts (more or less, see Remi.b's comment) passively to temperature whereas homoiotherm animals have an actively reacting metabolism that creates it's own constant temperature.

I'm not an expert in this topic but I have read a reasonable amount on animal thermal regulation, especially in insects, so maybe I can give some insight into your question.
First of all, an important thing I learned is that one must differentiate poikilotherms from homeotherms and endotherms from ectotherms.
According to Randall et al (1997):

Endotherms are animals which generate their own body heat through metabolism, while ectotherms have a hard time generating enough body heat to maintain their physiological functions, as they have low metabolic rates.
Homeotherms are animals which are able to maintan their body temperature at a more or less constant rate, while in poikilotherms body temperature fluctuates more or less with the environmental temperature.

This a somewhat troubling classification. Insects, for example, are considered ectotherms/poikilotherms, but they may show a condition called heterothermy: they are (most of the time) ectotherms, but they may be able to generate heat through some metabolic activity, and in this situation, they are showing endothermy. This happens quite often in winged insects, which may raise their body temperatures by flapping their thoracic muscles which move their wings. They may also ventilate themselves using their wings, lowering their body temperature, which (I'm not sure about this) may be considered an endothermic behaviour, as they are lowering their temperature in spite of the ambient temperature. Bees and wasps are even able to control their nest temperatures when the whole colony uses their wings to heat or cool their nest. So classifying animals in one of these categories is not so straightforward, but I'm just pointing this out because this is important. I don't think this invalidates your question, so I will talk about poikilotherms/ectotherms for now on.
One important thing to know about these animals is (Randall et al 1997):

Often, ectotherms have low rates of metabolic heat production and high
  thermal conductances-that is, they are poorly insulated. As a result,
  heat derived from metabolic processes is quickly lost to cooler
  surroundings. Accordingly, heat exchange with the environment is much
  more important than metabolic heat production in determining an
  ectotherm's body temperature. On the other hand, the high thermal
  conductance allows ectotherms to absorb heat readily from their
  surroundings.

As for how they control their temperatures...well, there are lots of mechanisms. I'll state some of them.

As Remi.b stated, behaviour is an important mechanism of temperature regulation in poikilotherms/ectotherms. This happens with basking/avoiding sunlight (as previously said), but also happens in the example of wing flapping I mentioned. Another interesting behaviour mechanism for temperature control is microhabitat selection: desert ants, for example, may face soil temperatures as high as 70° C when searching for food. They lower the harmful effects of such a high temperature by standing high on their legs and/or climbing onto small grasses or rocks which they find through their way. This may seem useless to us, but it plays a big difference between life or death for them (Marsh 1985).
Some animals have antifreeze substances in their blood which prevents them from freezing to death (see Randall et al 1997). This is common in arthropods.
Colour may play an important part in temperature regulation, as lighter body colours make the animal absorb heat less quickly than darker colours.
Some bumblebees may heat up by producing heat at the cost of ATP (a clearly endothermic characteristic) (May 1979).
Body size plays a huge part in body temperature regulation, not only in endotherms, but in ectotherms too. Lighton et al (1994) demonstrate that bigger workers from a species of ant called Veromessor pergandei can withstand dessication from higher temperatures for longer than smaller workers (and they show only a few milimeters difference in their sizes).

Well, as you may see, I don't think there is a straightforward answer. The way I look at it is that, as almost anything in biology, different organisms may show different strategies of coping with thermoregulation. I suggest you take a look at the following book if you want to know more or if I haven't quite answered your question (and the articles I have cited are the ones below):
Book: Randall et al. 1994. Eckert Animal Physiology: Mechanisms and Adaptations. W. H. Freeman  and Company.
Journal articles:
May, M. 1979. Insect thermoregulation. Annual Review of Entomology.
Lighton et al. 1994. Is bigger better? Water balance in the polymorphic desert harvester ant Messor pergandei.
(The name of the ant above changed, that's why I called it Veromessor pergandei)
Marsh, A. C. Microclimatic factors influencing foraging patterns and sucess of the thermophilic desert ant, Ocymyrmex barbiger. Insectex sociaux.

I want to know how they thrive in a wide temperature range and don't want an explanation of how they avoid extreme temperatures outside that large range to be instead.

I have some ideas on your comment, but first I must understand something: you're stating poikilotherms are able to withstand a wider environmental temperature range than homeotherms, is that so? Why do you think that? I see no reason for that being true (if you've read it somewhere please tell me where, because I'd like to know if I'm wrong).
Also, the mechanisms I talked about are not necessarily ways of dealing with extreme temperatures only, they are, most of the time, ways of coping with a temperature range.

I once saw a page that mentioned the word poikilotherm and described what it was that I can't find anymore then I searched for the Wikipedia article https://en.wikipedia.org/wiki/Poikilotherm.

What the article says is "A poikilotherm is an organism whose internal temperature varies considerably". That does not mean that poikilotherms can withstand wider environmental temperature ranges than homeotherms. If a poikilotherm is in an environment in which the temperature ranges from, say, 10° C to 30° C, its body temperature will vary acordingly (10° C-30°). If a homeotherm is in the same environment, its body temperature will be always, say, 28° C, independently of environmental temperature. But both of them can thrive in that environment.

I fixed the title of the question to be what I meant it to be all along.


text:
Do blood vessel walls have blood vessels in them?
If so, do those blood vessels have no walls because they don't need them because they're in the same tissue as that of a blood vessel wall? Are the cells alligned diffently at the edge of the blood vessel than in the rest of the blood vessel wall? Do blood vessels in blood vessels have an outer wall defined a sudden change in orientation of the cells?

This question is not very clear. The oxygen just diffuses into the cells of the blood vessels. What is confusing?