What is the role of triton in buffer for western blot assay? What is the role of triton in buffer for western blot assay?
I understand it has to do with preventing non-specific binding of the antibody.

That's exactly it. Triton is a detergent and incorporating it just makes it a little more difficult for everything to bind. Here's how I imagine blocking buffer working:

PBS/TBS: buffering pH

milk/BSA: uniformly interacting with the entirety of the blot. The idea is that these will a) adsorb to the parts of the blot that don't already have much sample in them (since "empty" areas of the blot would otherwise adsorb the detection antibody/ies (this is a source of nonspecific binding).

Triton (or, more commonly, Tween-20): OK, now think about what's on your blot. Your antibody will have weak interactions with just about anything there. A detergent interacts with everything it touches (antibody and adsorbed proteins on the blot) to reduce binding affinity in lots of these interactions (although, some interesting counterexamples can be found here), thereby making the less-favorable binding even less favorable, decreasing the chances of your detection antibody retaining these weaker (off-target) interactions. The preceding article also suggests that the use of nonionic detergents lowers the signal intensity of the Western (and to a different degree across proteins).


What is this creature? I found this small creature in my water bucket which i filled from my water tank. I would like to know what kind of creature I have found here.

Features which ought to help for identification:

Size = 1 cm
2.Transparent or semi Transparent
4 thread like legs
6 tentacles
2 black dots possibly eyes
It can swim
Triangular tail (Fish Like)
Found in Karachi City, Pakistan.

It's almost certainly a crustacean of the order Decapoda. The long antennae, fan-like tail and long legs are dead giveaways.

You said you it came from a water tank, so I assume it's a species of freshwater crayfish.

Type "crayfish" into Google images and you'll see lots of pictures, though yours appears to be more translucent.


Why are bald heads so "shiny"? Why do males with baldness have  shiny skin on their head, whereas we don't experience such "shiny skin" in other parts of body without hair.

Think of what happens when you don't wash your hair for days. It gets oily and greasy. This oil-like substance on your hair is called sebum and mainly works as a lubricant . The Sebaceous glands responsible for excreting sebum don't stop working when the hair follicles attached to them do. The result is a "shiny" head.


How are cyclic hormones characterized? I have a question regarding the description of a subset of peptide hormones, called cyclic hormones. Two examples of cyclic hormones would be somatostatin and melanin-concentrating hormones. I know the definition is not applied based on observations of oscillations in biologic levels of the hormones, rather, it is applied to the structure. These hormones possess a single disulfide loop, giving them a cyclic (circular) topology.

My question relates to the chemical definition of cyclic in this context. Does the word cyclic imply any chemistry that forms a single loop topology, arising from any kind of chemical bond (e.g., C-C bonds in carbon rings, or S-S bonds in these hormones). Or, does the word cycling only apply to S-S bonds in the context of these hormones?  I have not seen it defined in the literature, and my inclination is that it is more a definition of topology than any specific chemistry.

If you look in the results section of this paper on somatostatin-14, they explain that s-14 "is a fourteen residue peptide hormone where Cys$^3$ is disulfide bonded with Cys$^{14}$ to form a cyclic structure.

So your inclination is correct. The structure is cyclic and it is the cyclic structure which is responsible for the terminology. I don't know if there are exactly analogous structures with other than disulfide bonds but they would be cyclic for the same reason.

Another paper at page S1 talks briefly about the linear version of the same hormone, contrasting it with the cyclic form, again confirming that it is the structure that gives rise to the name, and not some other property.

It is the second reference that I think also answers the broader question: 'cyclic' is generic usage to describe a (simple or) complicated molecule containing a cyclic structure of joined atoms. Yet another paper (abstract) talks about cyclic vs. branched in a general way with respect to somatostatin and others:

"The aim of this contribution is to offer an unambiguous and general nomenclature system that enables researchers to represent all cyclic and branched homo- and hetero-detic peptides in a coherent manner in one-line text - as long as their as constituents can be represented in (three)-letter codes."

In this somewhat dated paper containing proposed IUPAC nomenclature for cyclic organic compounds, in cases in which there is a question whether a molecule is cyclic or not the prefix "cyclo-" enters the formal name. But in the title the origin of the issue is clear: "Nomenclature for cyclic organic compounds..." and again confirms that the usage is not based on the elements bonded but the ringlike structure.

There is a paper in which 'heterocyclic' (vs. 'carbocyclic') is used as a subclass of cyclic to refer to rings containing other than carbon. But the term cyclic applies to both.

Finally there is discussion of 'cyclic peptides' (wiki entry) generally which are classified 'according to the types of bonds that comprise the ring.' But they are cyclic because of the circular molecular structure notwithstanding considerable variation in the atoms (or multiplicity of bonds) comprising the ring.

Biochemistry has inherited much nomenclature from organic chemistry, and informal usage in textbook organic chemistry is that ringlike structures are called 'cyclic' whether they are comprised entirely of carbon or contain another element (typically N,O,S, etc.); for example 'cyclic ethers'--oxacyclopentane is a cyclic molecule containing oxygen.


Can VMD change its cartoon representation for secondary structure according to trajectories? I am using VMD to visualise the secondary structure of protein.

The trajectories are from my Gromacs simulation. Firstly I use File - New Molecule... to load the protein.gro file. Secondly I use File - Load Data into Molecule... to load my protein.xtc trajectories.

Then I use Cartoon to visulise the structure. As I drag the time frames, all the secondary structures (e.g. alpha-helix, beta-sheet) keep the same. But I am pretty sure some of them are changing, as I look into the Timeline analysis for secondary structure.

So how to use VMD to see the secondary structures at different time frames?

Thanks a lot for @Stefan's help! It finally works! So follow Stefan's guide, and replace the molid with the number under the ID in the VMD Main.

As Martin pointed out, VMD doesn't update secondary structure content over the course of an MD trajectory. You can easily do this in VMD by using the SSCache script:

http://www.ks.uiuc.edu/Research/vmd/script_library/scripts/sscache/sscache.tcl

I believe it ships with the newest versions of VMD, actually, but I'm not exactly sure; even if not, you can easily source it:

Extensions > Tk console (in the console, type source Downloads/sscache.tcl (or where ever you've saved the script)). Once you've sourced the script, the easiest thing to do would be to load your topology and trajectory and (in the Tk console) issue the command start_sscache molid, although I advise having a look at the examples and options in the script.


Cross section through the right arm question Is the largest drawn vein on first attached pictue v. brachialis or did they make a mistake and it's actually v. basilica?

Picture 1: Cross section through the right arm (source: Thieme, General Anatomy and Musculoskeletal System, p. 296)

Location of sectional plane (picture 1):

Picture 2: A similar drawing from Sobotta (source: Sobotta, General Anatomy and Musculoskeletal System, p. 240) :

Based on the location of that cross section in the upper arm the vein in question appears to be the basilic vein. The basilic and cephalic veins are the largest veins (most of the time) in the upper arm. Here is a nice diagram from wikipedia that shows both. The cephalic vein is much more superficial than the basilic vein, as you can somewhat appreciate in the diagram below.

I think the label "brachial vein" is probably an honest case of mislabeling.

This is another figure that supports that vein in the image in the question as the basilic vein as well:

From this image (Gray's Anatomy), you can appreciate that the basilic vein is the large and deeper vein that runs near the brachial artery. In the case of many arteries and veins there are similar names, but that does not appear to be the case in this instance.

Clinical Correlate: In vascular and/or transplant surgery, when making an arteriovenous fistula for dialysis access (for kidney failure), there are a number of common routes of access. Two of the most common are the (1) brachiocephalic fistula, which is formed by surgically connecting the brachial artery to the cephalic vein, and (2) brachiobasilic fistula, which is created by connecting the brachial artery to the basilic vein. Some additional information and a picture can be found in this open access article from Maya et al entitled Outcomes of Brachiocephalic Fistulas, Transposed Brachiobasilic Fistulas, and Upper Arm Grafts .


Why is E.coli used as a model? Is there a reason for the choice of E.coli as a model for many bacterial systems? Other bacteria such as B.subtilis are also used, but why is E. coli preferred?

Short answer. It was discovered pretty early (late 1800's). It is easy to get (you probably know where it comes from), purify, grow and is not virulent. E.coli spreads very rapidly (30 minutes division rate).

Why this one in particular and not another similar bacteria? Well you have to choose something at some stage and usually the more an organism is used the most valuable it becomes which means that more and more scientists will start to use it creating a loop which favors certain organisms, like it happened with E.coli.

E.coli started to be studied because Theodor Escherich wanted to prove the "germ theory of disease" which led him and later other scientists to work with E.coli and everybody uses it today.

By the way, the mouse model is actually quite interesting. Started by breeding huge amount of mice for selling them as pets.


How can octopus walk if muscles can only contract? From this video it is evident, that octopus can make tentacles push:

https://youtu.be/zaE-LwDowcU

How is it possible, if it is said, that muscles can only contract?

What types of muscles can distract?

Kier and Smith wrote a paper on how tongues tentacles and trunks worked. It explains in detail exactly how their legs (and our tongues) elongate, shorten and move about without any bones for support. It's called muscular-hydrostat.

Movement of the limb actually depends on which muscle is being contracted. If it's contracting the muscles longitudinally it will make the limb short and wide, while if it contracts laterally it will cause the limb to extend and be short and thin.

If you watch the video carefully you can actually see the changes in thickness of the limbs as the lateral muscles release and the longitudinal muscles contract so the octopus can move its leg forward.

If you want to see it work in person, go into the bathroom and move your tongue around and watch in the mirror. It uses the same mechanics to move your food around your mouth, lick your teeth, help you get that bit of food that is stuck up against your gum, and who can forget rolling the tongue into a cylinder or making tongue clovers.


What is the most condensed form of (stored) energy used in biology? When considering how organisms store energy for later use, I was wondering what substance known in Biology is best for compacting the most energy in the smallest space(volume-wise).

With my (limited) knowledge, I would guess that it would be what we would normally call "body fat". However, I know I am probably not aware of most forms of stored energy, and I considered that perhaps substances like egg-whites may potentially contain more energy in the same amount of volume.

So, the question as in the title: What is the most condensed form of (stored) energy used in biology?

Alternatively, if there is no known "best": What would the leading competitors be?

The best ratio between weight and energy content (and of course also stability) has indeed fat. It's energy content is more than twice as high as for carbohydrates (sugars).
See this table from here on the energy contents:

This is the reason why animals which hibernate or migrate fed up to build up fat resources before the winter or their journey. With carbohydrates they would need more than the double amount of stored carbohydrates to get the same energy. Proteins are approximately on the same level as carbohydrates.

If you look on this problem not by energy per mass but volume per mass, fat still wins. For this we need the density of protein (muscles in this case) and fat. Paper 1 (see reference below) say that the human muscles have an average density of 1.06g/cm³. Paper 2 lists a density of 0.92g/cm³ for fat. So fats (this is practically only valid for the human body, but should be in the same range for other animals) are about 15% less dense than muscles. As the energy density per weight is about double as high for fat, this compensates for the lower density.

Carbohydrates are better, but are still not as good as fat. It's a bit hard to find specific densities for carbohydrates in the human body, so let's use Glycogen (which is a widely found carbohydrate used for mid-term storage of energy) for this purpose. Paper 3 lists a density for Glycogen between 1.40–1.62 g/cm³, so fat has only 55-65% of it's density. Since the energy density of fat is about 2.25x that of carbohydrates, fat is still better.

If you look at ATP in comparison, it has relatively little energy to provide. ATP delivers about 32.3 kJ/mole (with 507.18 g/mole this make around 64 J/gram) per phosphate released from the molecule, which is 128 J/gram if both phosphates are released. This is approximately 300x less energy per gram than fat. This makes sense, since fats are completely oxidized (down to water and carbon dioxide), while in ATP only the phosphate bonds are broken. ATP acts as an energy carrier in the body and not as an energy storage molecule.

References:

Specific Force Deficit in Skeletal Muscles of Old Rats Is Partially
Explained by the Existence of Denervated Muscle Fibers
Association of adiponectin and resistin with adipose tissue
compartments, insulin resistance and dyslipidaemia
Shifts in the Distribution of Mass Densities Is a Signature of
Caloric Restriction in Caenorhabditis elegans


Why doesn't water enter my body through my anus or genitals when swimming? So when we swim, we can make water not enter through our nose and mouth, simply by holding our breath. However, the mouth and the nose aren't the only cavities. What about the anus and the genitals? They obviously can't "hold breath", so how do they stop water from entering?

I thought the reason is gravity, but then, people would be killed when diving because your butt is facing up, against the gravity.

Another explanation might be that the internal pressure is higher than the external one, but I fail to recall any organ that creates the pressure..

For the same reason that when you urinate or use the toilet, you have to exert pressure and urine or faeces just does not simply leak out when you stand up. The urethra seals shut when the urethral sphincter muscles relax. Similarly Sphincter ani externus muscle seals shut in the anal canal when there is no antagonistic force. So water can't just simply enter our body in such huge quantities that we die. It is possible to get more water through your anus with some pressure which is what happens when you get an enema.


How are whole Haplotypes for Sequencing isolated? Is it possible to reliably isolate and amplify DNA from individual sperm and/or eggs (from a fish)? I'd imagine that the small amount of DNA would make the PCR a bit wacky. We've considered irradiating sperm and attempting to create haploid females via gynogenesis, but I was wondering if there was a faster and easier method that could utilize gametes directly.

If your aim is to isolate the two haplotypes (chromosomes) maybe you should try flow cytometry. You might read this paper http://www.ncbi.nlm.nih.gov/pubmed/21181533 by Dolezel which is leader in the field, at least for plant chromosomes. I'm pretty sure that the applicability of the method depends on the physical properties of the chromosomes you have (especially their size distribution).


If an organism is supported only by cartilage, does it have an endoskeleton? Lamprey and sharks lack bones, but does this mean they are not classified as having an endoskelton? Does an organism need bone to be considered as having an endoskeleton?

From wikipedia

  An endoskeleton (From Greek ἔνδον, éndon = "within", "inner" + σκελετός, skeletos = "skeleton") is an internal support structure of an animal, composed of mineralized tissue.

Cartilage is a mineralized tissue so it counts as a skeleton from this definition. A bit further in the wikipedia article it says

  The vertebrate endoskeleton is basically made up of two types of tissues (bone and cartilage)


determining genome-wide exogenous binding of pathogens to host genome? I've read this paper where they specifically modify a region in the rice genome to ablate the binding site of a pathogen, Xanthomonas oryzae, and disrupt the hijacking of a gene network in the rice genome to the advantage of the pathogen.

It's an interesting concept but left me wondering how one would determine de novo the binding of these pathogen effectors into the host if one didn't know them. What would be the steps to determine where are the pathogen's TFs binding the host genome?

Edit: there is the possibility of not knowing which proteins bind to the host genome, so what would be the way of developing the antibodies in this case?

Reference:

 Li T, Liu B, Spalding MH, Weeks DP, Yang B. 2012. High-efficiency TALEN-based gene editing produces disease-resistant rice. Nature biotechnology 30: 390–2.

The techniques used to do this are ChIP-seq and ChIP-chip.

Basically, you

let the pathogen bind to the (highly replicated) DNA
cut up the DNA into little random pieces by sonication
enrich (“pull down”) the pathogen-bound DNA fragments by using a known antibody which binds to the pathogen
sequence the thus enriched DNA
map the sequenced fragments back to their original location on the genome.

Wikipedia has a nice picture explaining this process in a little more detail:


Super-resolution imaging in vivo Are there any microscopy modalities or techniques for in vivo imaging at higher resolutions than the diffraction limit?

I was looking at this list: Super resolution microscopy, but they don't talk about in vivo imaging.

Any superresolution techniques relying on stochastic sampling (e.g. PALM, STORM) is extremely difficult to accomplish in vivo, as the tissue would be moving (e.g. due to respiration) and this would hinder a lot the reconstruction of the image.

Apparently it may be possible to do it with STED but I could not find the related paper*, although the same authors recently published some interesting work on living brain slices.

* Note that the images in that article come from this paper, which is not done in vivo.

Thanks to @vkehayas for pointing out that in vivo STED has been done for instance here Nanoscopy in a living mouse brain


What made this tiny honeycomb-like structure? I found this on the ground in Maryland.  I believe the twig is from a tulip poplar tree.  The structure looks like a tiny honeycomb except that the cells are individual tubes rather than a true hexagonal honeycomb shape.  It's one layer deep and wraps completely around the branch.  I assume it was made by some tiny insect, but what?

Many insects lay eggs in tight clusters; because of the shape of the eggs (like honeycomb cells themselves), the cluster looks a bit like a honeycomb.  If you had a high quality macro shot, the eggs might be easier to identify definitively.

Newly hatched Beet Armyworms:

Wheel Bug (Arilus cristatus) Eggs:

  Wheel bugs are common in eastern North America, but are confirmed to occupy areas of Mexico and Guatemala.

With wheel bug for size:

My guess is that you found a cluster of Wheel Bug eggs.

  Females lay eggs at a low elevation on trees, bushes, twigs, and other objects.[5] Secreted glue serves as an adhesive which maintains the cluster formation of the eggs. - Wikipedia


What are the pros & cons of site-directed mutagenesis? What are the alternatives? For a lab course we have been assigned to "remove a stop codon, using mutagenesis, that is in the middle of a gene in order for the full gene to be expressed. This will then fluoresce."

To do this we are considering site directed mutagenesis, which can replace the stop codon, however is this a good method? Are there any alternatives to SDM using Quikchange that are better? What are the pros and cons of the SDM we are thinking of performing? To see if we succeeded we will then use DNA sequencing and gel electrophoresis.

Our overall plan looks like this:

Gathering plasmids from E. coli
Gel electrophoresis of the plasmid DNA
Perform the mutagenesis using Quikchange
Transformation by heat-shock
PCR
Use a lac promoter to produce the gene protein

One issue I could think of was, how do we make sure the primers carrying the mutation don't anneal to each other due to their complementarity?

Is overlap-extension a good alternative? Are there any advantages to using transposon-based or point-directed mutagenesis?

Thank you!

SDM will be the perfect tool for this mission, unless the plasmid in question is very large (20+ kb).

When you have performed the SDM, digest the products with dpnI to remove the original plasmids, transform e.coli and use a selective media matching your plasmid. Only bacteria with the plasmid will then be able to survive and form colonies, pick several colonies and perform a miniprep for each and sequence the area of interest. You can use the rest of the miniprep with the correct plasmid for transformation and expression. So skip step 5.


I just saw this bird outside my apartment. Anyone know what it is? (Texas, US) Saw this bird outside my apartment in College Station, Texas  and have never seen anything like it before!
It is about the size of a hand.

It is American Woodcock, Scolopax minor.

  Superbly camouflaged against the leaf litter, the brown-mottled American Woodcock walks slowly along the forest floor, probing the soil with its long bill in search of earthworms. Unlike its coastal relatives, this plump little shorebird lives in young forests and shrubby old fields across eastern North America. Its cryptic plumage and low-profile behavior make it hard to find except in the springtime at dawn or dusk, when the males show off for females by giving loud, nasal peent calls and performing dazzling aerial displays.

The newborns are even more camouflaged in downs.

References:

Audubon
All about birds


Actual determination of the DNA sequence in the shotgun approach? I'm studying bioinformatics and I'm confused by shotgun sequencing. In Sanger sequencing we break up the DNA and use ddNTPs in order to determine the exact position of each neucleotide. How exactly does shotgun sequencing help us determine the sequence structure?

If we break up the sequence randomly and then stitch it back together by looking at the overlapping parts, how does that tell us what order the nucleotides are in? How exactly are the nucleotides read so that shotgun sequencing helps us?

The question appears to confuse the method of identifying and determining the order of bases in a fragment of DNA — Sanger* sequencing, Maxam–Gilbert or more modern ‘next generation’ methods — with the strategy for selecting fragments to analyse and reassemble into the larger contiguous sequence from which they were derived, of which shotgun sequencing is one.

Shotgun sequencing is a strategy in which the selection of fragments to sequence is random, the method of sequencing is a matter of choice (it was often the Sanger method when it was first developed), and the assembly is done by computer programs that identify matching stretches. (It fails — or is not completely successful — if by chance the fragments do not cover the whole DNA with suitable overlaps or there are certain types of repeated regions.)

Shotgun sequencing should be contrasted with what might be called ordered sequencing strategies in which one generally starts with a restriction map of the whole DNA and initially selects specific fragments to clone and sequence (by whatever method seems best). On the basis of the sequence of the fragment one can choose to sequence further from a position within the already sequenced fragment, and this procedure repeated. Here there is no apparent assembly step as this is inherent in the choice of fragments to sequence. (This is much slower than shotgun sequencing, and cannot be automated so that it is much more expensive. However, it is more precise.)

Coda

Part of the confusion may arise from the fact that modern automated methods of sequencing genomes are designed to work on a mixture of many uncloned fragments of DNA, so inherently involve the shotgun sequencing strategy. They tend to employ technologies other than the classic Sanger method. If a ‘manual’ clone-based ordered sequencing strategy is required to ‘finish’ missing or ambiguous regions of a genome, this would most employ the Sanger method of determining the sequence. Hence, the contemporary writer might employ what is, in fact, a misleading contrast.

*Fred Sanger was an eminent Nobel laureate, so his surname is capitalized.


Do DNA viroids exist? Viroids are described as short circular ssRNA with no protein coating.
Are there any analogous infectious particles that contain DNA instead of RNA?
If DNA viroids do not exist, is there an obvious reason for this?

The definition on the Wikipedia page you recite uses the language 'no protein coating' as opposed to 'protein coating'.
A protein coating would make it a virus.
No protein-coating would make it a Viroid.
As far as we know DNA Viroids do not exist. But this is an advancing field of research and it depends on what structure of genetic material you are referring too.
The general different types of genetic material include - but are not limited to:
Single-stranded DNA (ssDNA),
Double-stranded DNA (dsDNA),
Single-stranded RNA (ssRNA),
and double-stranded RNA (dsRNA).
There is more information on Classes I and II DNA viruses here:
https://www.ncbi.nlm.nih.gov/books/NBK21523/
If there were no DNA viruses without a protein coating - what is the reason?
Viroids only infect plant cells.
It may be that Viroids route of entry via microscopic junctions between plant cells (Plasmodesmata) are only large enough to fit single stranded genetic material. Therefore allowing ssDNA and ssRNA, but not dsDNA and dsRNA to act as plant cell infectious agents.


Do fish break a water molecule to absorb oxygen? How do fish separate oxygen from H20 & consume it? Do they break the water molecule and absorb  the oxygen only?

The answer to this, I reckon, is that they don't.

They use molecular oxygen (O2) dissolved in the water for respiration, where it acts as a terminal electron acceptor, just as we use molecular oxygen in the air for respiration. We can speak of the water as being oxygenated.

Water is split in photosynthesis, where reducing equivalents from water are used to reduce NADP+ (giving NADPH).

One of the great discoveries of biology, IMO, is that the oxygen formed in green-plant photosynthesis comes from water, not CO2.

Tricarboxylic Acid Cycle (Krebs Cycle) Rant

Despite claims to the contrary, most infamously by Racker (1976, pp 28 - 29) and Wieser (1980), but also by Madeira (1988) and Mego (1986) for example, water is not split in the tricarboxylic acid cycle (Krebs Cycle). Banfalvi (1991) also sails pretty close to the wind on this one.

That is, reducing equivalents from water are not passed down the respiratory chain, or in any way used to make ATP, or are in any way a 'source' of free energy.  Such claims, IMO, are nonsense.

The definitive answers to the Wieser (1980) paper are given by Atkinson (1981) and Herreros & Garcia-Sancho (1981). Both of these articles are models of clarity, and categorically refute the claims of Wieser (1980).  Nevertheless, as shown by the references above, the controversy surfaces periodically.

The only sources of reducing equivalents in the TCA cycle are carbon compounds, and the only electrons passed down the respiratory chain are those 'held' in C-H and C-C bonds (Herreros & Garcia-Sancho, 1981).  An ionization is neither an oxidation nor a reduction (see Atkinson, 1981) and neither is a hydration. Adding water to (say) a double bond does not make the compound any more oxidized or reduced.  As far as oxygen and electrons are concerned, and to generalize from a biological point of view, what is has it holds - except in photosynthesis.

As you may have guessed, the splitting of the water in the TCA cycle is a pet rant of mine.  Thanks for the opportunity of airing my views!

Edit 3

Found this one when searching Google (Brière et al, 2006).  In an invited review for the American Journal of Physiology (Cell Physiology) at that!

  Finally, TCA cycle should also be considered as a water-splitting process generating oxygen for acetyl-CoA oxidation [they quote Wieser]

So now the TCA cycle is producing oxygen from water.  Wonders will never cease!

(end edit)

(end rant)

Edit 2

As rwst and Alan Boyd have drawn attention to, the concentration of dissolved oxygen in water is all important, and varies with (for example) temperature.

In air-saturated buffer at 25oC the concentration of oxygen (O2 molecules) is about 0.24 mM (0.24 μmoles/ml, or about 0.474 μg-atoms of oxygen per ml). [Chappell (1964)]. This figure decreases with increasing temperature.

Great question, BTW.

References

(Apologies for the incomplete Atkinson and Herreros & Garcia-Sancho references. I have a photocopy of these papers but have been unable to trace the full source. They are both in the 'Letters to the Editor' section of the February 1981 edition of Trends in Biochemical Sciences. They do not appear to be in Pubmed, or anywhere else on-line.  Has anyone ever seen these references quoted, or can provide me with a full source?.  I'll update if I find anything)

Atkinson, D.E. (1981) TCA Cycle Confusion.  Trends in Biochemical Sciences (February 1981 edition; full ref to follow)
Banfalvi,G. (1991)  Conversion of Oxidative Energy to Reductive Power in the Citrate Cycle. Biochemical Education, 19, 24 - 26  [see here] (pdf apparently free to all)
Brière, J.J., Favier, J, Gimenez-Roqueplo, A.P. & Rustin, P (2006) Tricarboxylic acid cycle dysfunction as a cause of human diseases and tumor formation.  Am J Physiol Cell Physiol, 291, C1114-20. [Pubmed]  [pdf]
Chappell (1964) The oxidation of citrate, isocitrate and cis-aconitate by isolated mitochondria. Biochem J., 90, 225-237.[pubmed]  [pdf]
Herreros, B. & Garcia-Sancho, J. (1981) TCA Cycle Confusion.  Trends in Biochemical Sciences (February 1981 edition; full ref to follow)
Madeira, V.M.C. (1988) Stoichiometry of Reducing Equivalents and Splitting
of Water in the Citric Acid Cycle.  Biochemical Education 16, 94 - 96 [pdf] (apparently free to all.)
Mego, J.L. (1986)  The Role of Water in Glycolysis Biochemical Education,  14, 130 - 131. (see here)
Racker, E. (1976) A New Look at Mechanisms in Bioenergetics.  Academic Press, New York.
Wieser (1980) Textbook Errrors: The splitting of water by the tricarboxylic acid cycle.  Textbook error or textbook omission? Trends in Biochemical Sciences, 5 (Issue 11), 284. [see here].  [pdf], apparently free to all.

Edit 4

I have not been able to locate the exact reference for the incomplete Atkinson and Herreros & Garcia-Sancho references cited above but, in response to this great question, I have put a copy of a very bad scanned version here

Another great reference to this controversy which I should have quoted is the
following:

Losada, Manuel
. (1978) Energy-Transducing Redox Systems and the Mechanism of Oxidative Phosphorylation. Bioelectrochemistry and Bioenergetics, 5, 296-310 [Science Direct].

The following is the relevant section, for those who do not have access:

A more complete version of the Racker reference quoted above by Losada (1978):

However, pyruvate has only 4 hydrogens to donate to 2 oxygens and with a P:O ratio of 3 should therefore yield only 6 molecules of ATP (Table 1.2). Where are the other 6 hydrogens coming from so that 15 ATP can be formed? The answer to this question gives us what I think is the key to the puzzle why nature has designed the complex acrobatic scheme of the Krebs cycle. Its major purpose I believe is to increase the energy yield by catalyzing cleavage of water.

There are three steps at which water enter the Krebs cycle. - one at the transformation of fumarate to malate an the other two somewhat more indirectly during the utilization of acetyl-CoA and succinyl-CoA. In the course of the Krebs cycle the hydrogens of these water molecules are separated from oxygen and are donated to DPN or to a flavoprotein (e.g., succinate dehydrogenase) and then transported via the oxidation chain of mitochondria as electrons and protons as we shall discuss later.

[Racker, E. (1976).  A New Look at Mechanisms of Bioenergetics, pp 5-6, Academic Press].

IMO, the last sentence of this quote is complete rubbish. (For DPN, read NAD. DPN, or diphospo-pyridine-nucleotide (or something close), is an old name for NAD)


Does light from the left visual field reach the temporal left retina? A diagram of the visual pathway is shown here. Light from the left visual field reaches the left nasal retina and the right temporal retina. On the other hand light from the right visual field reaches the right nasal and the left temporal retina.

The optic fibers from the nasal parts of the retina cross, whereas the fibers from the temporal hemispheres don't. This configuration leads to the projection of the left visual field to the right occipital cortex and vice versa.

My question is, why can't light from the left visual field reach the temporal left retina and vice versa? I have illustrated this in the picture below with blue arrows.

Obviously, if it would, it would interfere with the normal pattern of projection. Now my question is what prevents light from the left field of view reach the left temporal retina? Or is there some overlap between the visual fields?

There is overlap between the left and right visual fields, as shown in Fig. 1. This overlapping part is referred to as the binocular field of view. The monocular field of view (FOV) is 160o (w) x 175o (h), and the binocular FOV is 200o (w) x 135o (h). The region of binocular overlap is 120o (w) x 135o (h) (Kolb, 2016). The visual disparity in the binocular FOV of the both retinal projections forms one of the most important depth cues that allows us to estimate the distance of objects.

Fig. 1. The left and right visual fields have an overlapping area, the binocular visual field. source: Harvey Mudd College

Fig. 2 below shows why only a certain part of the visual fields overlap. Firstly, the retina has a finite size and secondly, the anatomical location of the pupils restricts the angles of the visual field. The most eccentric parts of the left visual field simply cannot reach the temporal left retina (and vice versa), because the angle of the pupil with respect to the retina simply doesn't allow for it. The same holds for the most central part of the left FOV, which cannot reach the nasal part of the right retina; it can only project to the the temporal right retina because of the restrictions due to the localization of the pupil, the retinal size limitations, as well as the nose blocking a certain part of the FOV.

Fig. 2. The left and right visual fields have an overlapping area, the binocular visual field. source: Ohio State University

Reference
- Kolb, Facts and Figures concerning the human retina. In: Kolb et al (eds). Webvision, The Organization of the Retina and Visual System. Utah University (2016)


Is there a reliable estimate of the number of cells on Earth? A quick Google search didn't turn up any reliable sources. An awkward Cosmoquest thread gives a rough estimate of 10^25 to 10^32, but this is just a bad extrapolation of the number of cells in a human body. Also, I recently learned that we don't even know the number of cells in humans to good precision.

Has anyone ever made a serious attempt to figure this out? If not, does anyone here want to make a quick calculation?

Okay so I looked around a bit, and there are surprisingly few papers related to this question.

This paper is the best I cold find, but it's almost 20 years old. There's also this one, which slightly updates the other one, but they both focus on bacteria. For those the total number is estimated to be somewhere in the range of $10^{30}$.
For humans the latest published number is $3.72 \times 10^{13}$, so even with a few billion in total ($10^9 \times 10^{13} = 10^{22}$) we probably don't even matter for the total cell count. Since smaller more abundant animals have a much lower number of cells, they probably don't matter either.

Now to the only thing I'm not sure about: plants

The number of plants on earth is really elusive, only more elusive is the number of cells per plant. This study claims around 3 trillion ($10^{12}$) tree's on earth. Since tree's are bound to have (many) more cells than humans, we're probably getting closer to the number of prokaryotic cells by now (I guess the number of 'tree cells' will be somewhere around $10^{27}  - 10^{30})$.
So far I didn't find anything about grasses or other plants (neither numbers nor cell counts), so it's really hard to say whether these matter or not.
This study seems to give an average number of cells per growth ring in tree's, but I'm not sure how to get a number of cells / tree from that.

In total the estimated number of bacteria ($10^{30}$) is probably a good measure for the number of cells on earth. Even if plants manage to come to that level, the order of magnitude will probably not change (by much).


Help with gene linkage and mapping! Here's an interesting question I've been trying to figure out:

My annotations are in red. So far, I've figured out:

We know 630 colonies survived when plated with ACD antibiotics...meaning they picked up the a/c/d resistance alleles, but remain wild-type for the b allele. The genotype would be "a b+ c d". Because SO MANY (630!) colonies seemed to inherit a/c/d together, and b completely separate from them, I would say b is the gene quite distant from the 3 other genes.

However, I've unsure about how to proceed and determine the probably order of the 3 others genes: a, c, and d.

Here's my hunch: B--------------------C-D-A.

I'll explain:

Well, I looked and saw 942 (many!!!) picked up A/D together. So A/D are probably adjacent.
Then, 786 (many, but fewer) picked up C/D together. So C is further from D than A is far from D. The question becomes: is it "C---A-D" or is it "A-D---C"?
The insight comes in with 640 (still fewer) picked up A/C together. That means A is actually quite FAR from C, because more distance = more recombination events that could split them up. So between the "C---A-D" or "A-D---C" listed above, it's more likely "A-D---C".
Okay! We know B is far from the other ones, BUT is it like "B-------ADC", or is it like "ADC-------B"? Well, let's look: picked up B/C together is 51, but picked up A/B together is only 46. That means A is a little FURTHER from B than C is further from B, since 46 < 51.

This led me to my proposed answer: that the order is "ADC---------B", or if you just flip it around, its equivalent: "B---------CDA".

How's my reasoning? This stuff can be pretty confusing; am I approaching it from the right angles? Thanks so much; really appreciate it!

I think your reasoning is sound and your ordering very likely, but I wouldn't feel comfortable with deciding the side B is on. Actually, it's more than that: I think that by using basically the same number (~40) for everything that includes B, they want you to come to another conclusion.

Unlike eukaryotic cells undergoing meiosis, there is no crossing over in bacteria taking up DNA from the surroundings. Therefore, it shouldn't be possible for the cell to inherit A, B and C but not D, which is in the middle. Simply, from my understanding of the "experimental" setup, they added antibiotics A, B and C, so they have to assume the bacteria are wild type for D. However, it's basically for sure that those ABC-resistant colonies are also D-resistant.

Still, your reasoning is correct: comparing BC and AB should give you the side B is on, since the break could have been inside of the 3-gene cluster. However, the numbers are very close, and the "AB" and "BC" phenotypes are probably ABCD anyway, making the small difference even less meaningful (the true AB and BC are lost because they are mixed with the many ABCD).


The meaning of and standards for "specimen numbers" I just read here:

  For example, in the research collection of the Natural History Museum in London, there is a bird specimen numbered 1886.6.24.20. This is a specimen of a kind of bird commonly known as the spotted harrier, which currently bears the scientific name Circus assimilis.

I am wondering what exactly that number 1886.6.24.20 means and how to find out more information. It seems it is structured to give some significance, such as perhaps year.month.day.incremented number. Wondering if this is unique to the Natural History Museum in London, or if this is how everywhere does it. By everywhere, I mean every museum. That is, wondering if there is a standard of some sort on how to number specimens.

In this case, your suspicion of year.month.day.sequential number is correct. The NHM specimen page has an image of the collector's notes:

On line 20, that specimen of Circus assimilis is accessioned, with a note on the right that it is the type for that species.

Generally however, there are no standards for specimen numbers in museums. Many museums that I have studied in have several different numbering or ID systems in use at the same time. Importantly, each specimen is accessioned under the system used at the present time. Sometimes these are later renumbered, sometimes not.

Even in the NHM, there are different schemes in use. Megalosaurus bucklandi, the first described species of dinosaur, is specimen PV OR 2482.

The NHM has 80,000,000 specimens. I'm sure that those doing the cataloging at the start couldn't have imagined the collection would grow to that size, so planning ahead for a single numbering scheme wouldn't even have occurred to them.


How can you explain the origin of life out of nonliving matter (abiogenesis)? According to biochemist Robert Shapiro, the "primordial soup" theory is as follows:

Early Earth had a chemically reducing atmosphere.
This atmosphere, exposed to energy in various forms, produced simple organic compounds ("monomers").
These compounds accumulated in a "soup", which may have been concentrated at various locations (shorelines, oceanic vents etc.).
By further transformation, more complex organic polymers – and ultimately life – developed in the soup.

From: en.wikipedia.org/wiki/Primordial_soup

I don't understand how in step four life forms out of nonliving organic polymers. Could you explain this process? Can it be reproduced in the lab?

Louis Pasteur already disproved Spontaneous Generation: The law of biogenesis

Welcome to Biology.SE!

Your question has nothing to do with evolutionary biology

Evolutionary Theory does not explain the origin of life just like the Theory of Gravity does not explain the diffraction of light! In other words, explaining the origin of life is not within the scope of evolutionary biology. You should edit your title. But still, your question is within the scope of Biology so that your question is totally on-topic. This question would probably also be on topic on Chemistry.SE.

Some other posts may interest you

You may want to look at other posts on this site. This post for example explains what are our issues in order to select which of our hypotheses really explain the origin of life. This post, this one may eventually interest you as well.

Your question might be too broad. You may want to start with some introductory readings

Abiogenesis is not my field and I know very little about the origin of life. But at first sight, I am a bit afraid that your question is too broad and inaccurate and a good answer would ask for writing a lot. This post will give some good source of reading to further your knowledge. It may be good to start there and come back to this site with a more accurate question.

Hope I could help you a bit.


Are human eyes equally sensitive to AC, and DC lamps? Definitely anecdotal.

This friend is hypermetropic, and uses reading glasses. He doesn't have major issues facing car headlights, or using a torch (the one with a bulb - not a white LED). Yet place him in front of a TV/Computer screen, and he'll develop an ache in the eye sockets in no time.

I understand an electric torch, an incandescent bulb, a car lamp are all DC types, whereas a TV/Computer screen is fast changing AC.

Are human eyes equally sensitive to light from an AC, and a DC lamp?

Let's not confuse the type of power of a light emitting device with the type of light it produces.
This question is not about AC or DC current. It is about flicker frequency, light wavelength and their biological effects.
Flicker frequency
The term "ache in the eye sockets" probably refers to asthenopia.
Human eye cannot detect flicker with a frequeny above 75 Hz. But many computer displays have a refresh rate of 60 Hz [1]. Out of focus and  low refresh rate monitors are known to cause eye strain and asthenopia [2], favored by existing hypermetropia (and other vision issues).

Visual discomfort has been related to 1) the presence of flicker; the possibility to regulate, 2) brightness, 3) height; and 4) inclination of monitor. Asthenopia has resulted statistically correlated to the presence of flicker and to the impossibility of regulating height and inclination of monitor for both sexes. The possibility to regulate monitor brightness has not determined a reduction of visual discomfort either in men or in women [3].

Wavelength
Eye sensitivity is different (see spectral sensitivity):
"Cones SMJ2 E" by Vanessaezekowitz at en.wikipedia / Later version uploaded by BenRG. - Based on Dicklyon's PNG version, itself based on data from Stockman, MacLeod & Johnson (1993) Journal of the Optical Society of America A, 10, 2491-2521d http://psy.ucsd.edu/~dmacleod/publications/61StockmanMacLeodJohnson1993.pdf (log E human cone response, via http://www.cvrl.org/database/text/cones/smj2.htm)
Transferred from en.wikipedia to Commons by User:Richard001 using CommonsHelper.. Licensed under CC BY-SA 3.0 via Wikimedia Commons.
Light color and color contrast matter:

The study results showed that both visual acuity and the subjective visual fatigue were significantly affected by the color of light [4].
Images with excessive energy at medium spatial frequencies (Fernandez and Wilkins, 2008 Perception 37 1098-1113), or that have high color contrast and little or no luminance contrast (Wilkins et al, 2008 Perception 37 Supplement, 144-145) appear uncomfortable or aversive and can induce headaches in hypersensitive observers. Such stimuli are uncharacteristic of natural images [...] [5].

Blue light can also reduce melatonin levels and affect sleep and mood (the studies don't have a strong conclusion though):

Melatonin concentrations after exposure to the blue-light goggle experimental condition were significantly reduced compared to the dark control and to the computer monitor only conditions. Although not statistically significant, the mean melatonin concentration after exposure to the computer monitor only was reduced slightly relative to the dark control condition [6].
All light is not equal: blue wavelengths are the most potent portion of the visible electromagnetic spectrum for circadian regulation. [...] evening use of amber lenses to block blue light might affect sleep quality. Mood is also affected by light and sleep; [...] At the end of the study, the amber lens group experienced significant (p < .001) improvement in sleep quality relative to the control group and positive affect (p = .005). Mood also improved significantly relative to controls [7].

References:

Wikipedia contributors, "Flicker fusion threshold," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Flicker_fusion_threshold&oldid=615159751 (accessed July 29, 2014).
Wikipedia contributors, "Asthenopia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Asthenopia&oldid=617227613 (accessed July 29, 2014).
Rechichi C, Scullica L. [Asthenopia and monitor characteristics]. J Fr Ophtalmol. 1991;13(8-9):456-60. PubMed PMID: 2081858.
Lin CJ, Feng WY, Chao CJ, Tseng FY. Effects of VDT workstation lighting conditions on operator visual workload. Ind Health. 2008 Apr;46(2):105-11. PubMed PMID: 18413962.
Juricevic I, Land L, Wilkins A, Webster MA. Visual discomfort and natural image statistics. Perception. 2010;39(7):884-99. PubMed PMID: 20842966.
Figueiro MG, Wood B, Plitnick B, Rea MS. The impact of light from computer monitors on melatonin levels in college students. Neuro Endocrinol. Lett. 2011;32(2):158-63. PubMed PMID: 21552190.
Burkhart K, Phelps JR. Amber lenses to block blue light and improve sleep: a randomized trial. Chronobiol. Int. 2009 Dec;26(8):1602-12. doi: 10.3109/07420520903523719. PubMed PMID: 20030543.


Lifespan of helper T cell CD4+ cells or helper T cells are produced in Thymus. How long these cells live? For example, RBC live for 3-4 months.

I will respond with a "story-like" approach. You may already know some info but I want to be sure I can help you fully understand!

Unlike RBC, you are born with all the CD4+ (or Th, as I refer to them) you will ever need in your lifetime in the primary organs of the immune system -- they are already specialized and ready to be used, and this has taken place in the thymus. On the other hand, RBC get renewed through erythropoiesis every ~120 days.

In utero, the thymus and bone marrow (primary organs) now supply secondary organs (lymph nodes, the spleen, the MALT) with the various cells they’ve made (B&T). However, only 5% leave the thymus, as 95% are recognized as "anti-self" and are killed. So this would be the first "killing" of Th cells. B cells live in the peripheral layer, while T cells live in the deep lymphoid tissue and the lymphoid dullet.

The dendritic cell will "wander" into the lymph node, carrying the fragment of antigen presentation on the MHC class 2 molecule-Dendritic cell resides between the B cell area and the T cell area. Now, the first specific thing occurs in the immune response, when the T cell receptor attaches to the antigen and tells cell says to make antibodies.

Now -- as of here, we have a lot of Th (and B) cells doing nothing while the antibody is being produced. Some of the Th will be killed, while some will serve as "memory Th cells" so that the next time such an antigen is present in your body, the response will be quicker. At this point, it's hard to distinguish which Th cells are dividing, and which are dying. The average lifespan has been reported to be >17 years.
 Source: https://www.ncbi.nlm.nih.gov/pubmed/24492253

I hope I have been able to help.


Why Is Action Potential Propagation Not Described by Telegrapher's But Cable Equation? In modelling the propagation of action potential in an axon, why is the partial differential equation the cable equation rather than the telegrapher's equation? The difference between the two is that the former does not have inductance while the latter has. Does an axon not have inductance whether it is myelinated or unmyelinated? This is related to my previous question. There the only answer I obtained attributes this choice not to experimental evidence but the deficiency on the part of biologists in mathematical sophistication in dealing with the complication of electromagnetism arising from including inductance.

I am the individual who answered your earlier question.  The answer remains much the same.  The Cable Equation is inappropriate.  It was developed originally as the Heat Equation of Thomson,  While Thomson disowned its application to the axon as a cable, Herman continued to promote the solution within the Biology community.  The problem is the Cable Equation requires as an initial condition that the stimulation of the cable continues until the signal reaches the terminus of the axon by conduction (diffusion).
When exploring the myelinated axon, the Telegrapher's equation must be used.  The formal name for this equation is the General Wave Equation, GWE, of Maxwell. It involves an initial condition that is much more lenient.  The stimulus must only be applied to the axon for long enough to ensure the desired full waveform is represented. Thus the GWE involves propagation and not conduction (or diffusion).  See section 7.4 of Chapter 7 of "Processes in Biological Hearing," PBH, on my website.
Cole & Baker, "Longitudinal Impedance of the Squid Giant Axon", Journal of General Physiology, (1941) vol 24(6) pp 771-783 present their initial measurements of inductance within the large axon of a small squid.  This axon generated "swim waveforms" and not "Action Potentials" as currently defined.  The inductance is much smaller in a non-myelinated axon than in a myelinated axon.  It remains calculable in either case.
I have reviewed the two papers by Lieberstein & Mahrous you cited for my benefit.  The authors are apparently two very good mathematicians without much knowledge of biophysics or the biophysics literature.  They quote a diffusion velocity from Hodgkin & Huxley (1952) that is several orders of magnitude slower than the phase velocity along an axon that is very well documented by Cole and more recently by Smith et al.  I have uploaded a more complete analysis in Section 9.1.1.4.3 of the above citation to chapter 9 of my work, 9SignalTransmission.pdf.
These two papers should not be relied upon until reviewing Section 9.1.1.4.3


How many birds in this population would be expected to have either red or white feathers? Question: The red and white feather pattern of a  bird is determined by a gene that has two alleles, band R and W,which show codominance.  Some birds have completely red feathers (RR),some parrots have completely white feathers (WW), and others have red and white feathers (RW).In a population of 630 birds that is at Hardy-Weinberg equilibrium, 202 parrots have completely red feathers. How many birds in this population would be expected to have either red or white feathers?

Is this question asking for what is the carrier proportion-2pq? The answer is supposed to be 321 but I keep getting 309. I did 202/630= p^2=0.32= 0.566. Then q=1-0.566 =0.434. Then I did 2(0.434)(0.5662)= 0.49. Then I multiplied 0.49 x 630 to get 309. If any one can point out what I did wrong I would really appreciate it!!

The solution

$$p^2 = 202 / 630 ≈ 0.32$$
$$p = \sqrt{202/630}$$
$$(1-p) = 1 - \sqrt{202/630}$$
$$(1-p)^2 = \left(1 - \sqrt{202/630}\right)^2 ≈ 0.188$$

There is a fraction of $202 / 630 ≈ 0.32$ of red birds. There is a fraction of $\left(1 - \sqrt{202/630}\right)^2 ≈ 0.188$ of white birds. There is therefore a fraction of $0.32 + 0.188 = 0.508$ of birds that are either all white or all red. In a population of 630 individuals, it therefore represents $630 * 0.508 ≈ 320.53$. A result that is apparently rounded up at $321$ in your answer key.

Your mistake

You computed the number of birds that have both white and red feathers (WR) while the question was asking for either red or white feathers. You calculated the expected number of heterozygotes instead of calculating the expected number of homozygotes.

Of course the number of heterozygotes and the number of homozygotes should add up to the number of individuals in the population ($321 + 309 = 630$).


During what phase is the cell polyploid? During what phase is the cell polyploid? Why is it polyploid at this point--what has happened to create this state and why is it important to the process?

I assume that you mean phase of cell division. First off all i will write down a definition of word polyploid. Polyploid is cell which has two or more pairs of homologus chromozoms. There are two basic types of cell division are meiosis and mitosis

Technicly you can say that in reduction meiosis when chromozomes go from diploity to haploid state (which is first anaphase in this process), but ussually polyplidy occure when something goes wrong in cell division.

The major cause of polyploidy is found to the non disjunction of sister chromatids during the meiotic recombination events. Prior to meiosis chromosome numver doubles followed by chromosome separation during gamete formation (anaphase).
Artificial generation of polyploidy have been found to be useful both in research as well as economic purposes. Colchicine, the chemical which inhibits formation of spidle apparatus is widely used.

Unfortunately colchicine is only used in mitosis. Result of this process is new cultivars of plant specious.


Engineered CD8 T-cell therapy for HIV infection CD8 T-cells are effective in controlling HIV during the early phase of the infection. However by the time, the virus mutates and develops an evasion mechanism against CD8 T-cells.
Since cancer cells also develop immune evasion mechanisms, and scientists are using several technics to block those mechanism, i think it would also be possible to control "viral escape".
I made some research regarding HIV immunotherapy, however the only thing i found was antibody based immunotherapy.
My question is, would it be technically possible to engnieer custom CD8 T-cells which will targed HIV infected cells ?

People in the comments suggest that this would "Drive the patient into AIDS sooner", or that this will be ineffective because of dormant virus.  Neither is correct.

The question is asking about engineering CD8 with engineered T cell receptors specific for HIV.  This is a logical approach, and multiple groups have tried it:

In Vivo Suppression of HIV by Antigen Specific T Cells Derived from Engineered Hematopoietic Stem Cells
Reconstitution of anti-HIV effector functions of primary human CD8 T lymphocytes by transfer of HIV-specific alphabeta TCR genes
Development of CD8+ T cells expressing two distinct receptors specific for MTB and HIV-1 peptides
T-cell engineering by a chimeric T-cell receptor with antibody-type specificity for the HIV-1 gp120

A brief search on Pubmed will turn up many other articles. Some of these approaches have entered clinical trials; for example:

Redirected High Affinity Gag‐Specific Autologous T Cells for HIV Gene Therapy

The problem with this approach is not that it will "drive the patient into AIDS sooner".  A strong CD8 T cell response controls HIV well, and although it might be one contributor to CD4 T cell loss it's no longer believed that it's a major cause, especially in the early stages of HIV infection.

The general problem with CD8 control of HIV is that the virus is capable of mutation to avoid control by CD8s. Essentially, every case of HIV is effectively controlled by the CD8 T cell response in the early stage of infection, but the virus then mutates and escapes control, then the CD8 response adapts and controls the virus once again, and the virus mutates and escapes ... This can and has been tracked in many patients, showing repeated rebounds of the virus in the blood correlated with CD8 changes.

Better CD8 control of HIV is linked to a broader CD8 response -- that is, attacking many viral proteins, so that viral escape requires multiple simultaneous mutations (exponentially more difficult for the virus).  (Alternatively, the CD8 response can attack a small number of proteins that are very constrained, so that the virus can't successfully mutate them.  However, for reasons related to MHC restriction, that seems to only work in a small minority of people.)

An engineered CD8 T cell response will inevitably be to one or a small number of viral proteins.  That's conceptually similar to the natural situation following HIV infection, meaning that the outcome could be the same -- viral mutation and immune escape.

Because engineering the TcR means you can pick your targets rationally, you might be able to do better than the natural situation, but it's not obvious.  Overall, the fact that groups have been working on this approach for decades, without a breakthrough cure yet, suggests that it might be useful but isn't going to be a slam-dunk.


Assays for detecting RNA binding with protein In a project I'm working on, we are designing a system where specific RNAs bind to proteins - an important part of this is to test whether the RNA binds when we modify the proteins in some way. What assays are there to test whether a specific (or non-specific) RNA is binding to a protein?

I would reccomend an electrophoretic mobility shift assay (EMSA), one procedure for which can be found here.


Predictive Single Nucleotide Polymorphisms (SNPs) for Bipolar Disorder Are there any validated SNPs that are either predictive of developing bipolar spectrum disorder or are associated with its pathophysiology?

Yes, there have been a variety of studies that do association analysis of variants with bipolar disorder. Here is a recent one that validated 11-30 variants depending on how you count.
However, in these kinds of analyses you should be somewhat cautious as the associations are extremely weak (as they generally are for complex traits in humans):

Eight of the 19 variants that were genome-wide significant (P < 5 × 10−8) in the discovery GWAS were not genome-wide significant in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity.

The statistics of how you interpret such variants are rather dodgy/uncertain, so I would put very little stock in any particular variant. Maybe if you take the genome-wide significant variants only and added them all up you might start to get a little predictive power.
In terms of other more speculative observations (again from the abstract of that study):

The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling. Bipolar I disorder is strongly genetically correlated with schizophrenia, driven by psychosis, whereas bipolar II disorder is more strongly correlated with major depressive disorder.

I would suggest reading that paper and finding some further citations from it if you are interested in more detail.


An over-simplified model of cell division and its relation to stem cells I am a mathematician, and I decided to try to model cell division with math and see what conclusions came out of it. I had some questions concerning stem cells that came up in the model.

In an extremely simplified model of cell division, each cell decides what cells it will divide into with no output from the outside workd, including from neighboring cells. I also assume the time frame is small enough that cells do not die, and that there are only finitely many 'programs' telling different cells how to divide.

Given these assumptions, I came to the conclusion that one of two things could happen:
1. The number of cells grows exponentially, or
2. Most cells will never divide into other cells.

In fact, if growth is going to remain constant (e.g. 300,000,000 cells per month, every month in a sample), then eventually there will be two kinds of cells:
1. Normal cells, which never divide, and
2. 'Starter cells', which divide into normal cells but NEVER create other starter cells. The number of starter cells is eventually constant.

I hypothesized that these starter cells would eventually be far outnumbered and become a very small part if the body proportionally. I hypothesized that hair follicles, nail roots, growth plates, and bone marrow contained starter cells. I further hypothesized that these are adult stem cells.

  Question 1: Is this what stem cells are? Are they the cells that divide to create other, non-dividing cells?

After this, I realized that if the starter cells die, they would not be replaced under my model, because no cell is allowed to divide into new starter cells. I hypothesized that stem cell transplants fail because the host body kills off stem cells one by one and they can it be replaced. I also hypothesized that in the host, outside signals like hormones (which weren't allowed in my model) tell the body to create new stem cells as needed.

  Question 2: Do stem cell transplants fail because isolated stem cells do not replicate themselves?

Finally, I noted above that the alternative to a bounded amount of stem cells is exponential growth, where stem cells divide into stem cells.

  Question 3: Do embryo stem cells divide into other stem cells exponentially? Is this why embryo stem cells are easier to work with?

Thanks for your time. Even answers like "no, this is obviously wrong because ..." would be appreciated.

You have a few misconceptions about stem cells, I will try to explain where they are.
First of all, cells are not independent. They influence each other with signals and secreted messenger substances. If you look at a human embryo the state of totipotency (where all cells can differentiate into each cell type of the body) ends after 3-4 days when the blastocyte has developed. This structure already has a differentiation into a inner cell mass (embryoblast) and a outer cell layer (tropoblast).
If all cells would simply divide on their own, this would rather look like bacteria dividing in culture media, but not as a forming, multicellular organism.

From these few cells in the beginning all cell types of the body have to develop (around 200, if I remember the number correctly). To reach this, the pluripotent stem cells need to proliferate and differentiate (develop into more specialized cell types) quite a lot. So embryonic stem cells do proliferate. Adult stem cells are not proliferating at the same rate a embryonic, but they still do. A good example are the melanocyte stem cells (which are already pretty specialized as they can only further differentiate into melanocytes) which replenish the melanocyte population of the hair bulb at the beginning of each hair cycle. Differentiated cells can divide as well, when necessary, think only about wound healing.

Question 2: Stem cells (especially adult stem cells) need very defined living conditions. This includes specific signalling molecules (Oct or nanog are examples for that) to stay stem cells. If this signalling is missing (and it does in the normal human body) then these cells either differentiate or (more likely) die.
The only stem cell transplant which takes place regulary is the transfer of hematopoietic stem cells to leukemia patients. There the problem is to keep the immune system from atacking these cells as foreign.


What are the evidence that all life today descended from a common ancestor (LUCA), and which organisms (if any) challenge the concept? If I understand correctly, the concept of the LUCA (last universal common ancestor) is based on the hypothesis that archaea and bacteria share common ancestry.

In the realm of mathematics, the same discoveries have often been made more than once, in different places. Sometimes (like with calculus) these independent discoveries were made almost simultaneously. Sometimes the discoveries appear to  be totally unrelated (Hipparchus affirmative compound propositions before 100 BC, and David Hough's work on inserting parentheses in 1944).

If "life" started on Earth in some kind of primordial soup, it is conceivable that it started not once but many times, in different places and at different times.

How strong is the evidence that bacteria and archaea do not represent quite separate discoveries of "life", which (because of the nature of the chemical substances that they use) happen to share a number of features, such as DNA?

It is quite likely (but impossible to study) that the first stages of life originated more than once. However, the evidence that all currently existing life originated from the same population is very strong.

On the most basic level, many of the basic building blocks of life, RNA, DNA, amino acids are chiral, which means they come in multiple forms, but for the basic processes in nature, always the same one is chosen. For example, the DNA double-helix is almost always right-handed in nature,
see also here. If there were multiple origins of archaea and bacteria, we would expect some to pick another form, if not other molecules. In addition, many crucial proteins such as DNA- and RNA- polymerases are very similar between all species, the probability that they would have originated independently is simply minuscule.


Comparing SIFT and PolyPhen to other methods I'm looking for a database of nsSNP (non synonymous single nucleotide polymorphisms) and their effects. As I understand, the common methods to predict this are SIFT and PolyPhen, and I want to compare them to other methods.

The database needs to list the old sequence and the new one (or that I'd be able to infer that somehow), and their effect (whether harmful or not).

What are my options?

I will strongly suggest you:

PredictSNP: It's the best tool for nsSNP detection as it compares and throw out result from all the tools available.

http://loschmidt.chemi.muni.cz/predictsnp/

Paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3894168/


Can humans' ability to dive with only breathing modifications tell us anything about our evolution? Can humans' ability to dive with only breathing modifications tell us anything about our evolution?

For example, it is possible to imagine a human anatomy that would be destroyed by the pressure of a few meters of water, and yet humans can, with scuba apparatus dive to several hundred meters.

This is not a complete answer to your question, but your question prompted me to research the Mammalian Diving Reflex, which is used, according to the article, as a survival mechanism rather than assisting us in day to day functioning.

Looking at the evolution of the diving reflex, and how it appears in varying degrees in all mammals, suggest that it has been around for a long time, this article suggests for over 125 million years.


Swing bucket for PCR I see a swing bucket rotor for PCR trips and don't know what step is using? What difference if I use fixed - angle? In addition, Which step I can use swing bucket instead fix - angle in molecular biology (Example: extraction, purification,..) to improve centrifugation efficiency?

For a PCR preparation, swing bucket or fixed angle does not make any differences. The only thing you want is that everything is soluble, in the same volume, and homogeneously mixed.

The main difference between swing bucket and fixed angle is how the pellet will be formed in the tube. Depending on the type of extraction or purification you are doing it would be advantageous to have a large pellet on the side (fixed angle) or at the bottom (swing bucket).

This article explains it in much more details if you are interested: https://handling-solutions.eppendorf.com/sample-handling/centrifugation/this-and-that/detailview/news/when-to-use-a-fixed-angle-rotor-or-a-swing-bucket-rotor/


Tiny huntsman found in Czechia? I found this spider today and I'm curious to know what it was.

Discovered today at 14:27 CEST, about 200 meters from Hamr pond, Prague, Czech Republic. It may have been carried all the way from the pond.
Body length cca 5mm (cf. photo #2 - reference object is a 5 CZK coin, 23mm in diameter according to Wikipedia)

Initially swept off my shoulder (white T-shirt), to which it succeeded in attaching, and began descending on a thread. After it was placed on a small ledge, it began climbing the adjoining wall. After some convincing to stay in place (using my finger as an obstacle and a little physical contact with its legs), it lifted its four front legs, so I left it alone.

I didn't manage to get good sight of its eye pattern, but it did appear to be consistent with the eye pattern of huntsman spiders - the sides of its face were black with a brighter region between. I was unable to determine the quality of its eyesight either, though it did not object to placing the coin nearby to it.

Wikipedia page on huntsmen living in Europe lists nine species, but none of those that had photos included matched in appearance.

The spider in question is actually Xysticus Cristatus, also known as the common crab spider.

From Wikipedia:

  The adult female reaches a length of 8mm and the smaller male 5mm. The colour varies from light cream, dark brown to greyish with a dark triangle on the carapace which ends in sharp, defined point. The abdomen has a broad middle band fringed by two darker rows of triangular marks which extends back to about two thirds of the carapace length from the posterior row of eyes. ... Active adults have been recorded from February to December, with a peak of male activity in May and June. ... The species has a Palearctic distribution, being found throughout Europe, including Iceland.

Arachnology.cz provides several photos of the species. The image below is a perfect match.

Copyright by Rudolf Macek; published at https://www.arachnology.cz/druh/xysticus-cristatus-800.html; page viewed in May 2019


Is molecular oxygen (O₂) consumed in any process (in humans) other than acting as an electron acceptor for the ETC? I know that molecular oxygen (O2) serves as the electron acceptor in Complex IV of the electron transport chain, which maintains the proton gradient that produces ATP for, as far as I know, every cell in the human body.

Is this the only reason we need molecular oxygen for life, or are there other vital functions (i.e. necessary for life) that molecular oxygen serves within the human body?

Edit

For clarification, there are probably well over a million oxygen-containing compounds, from water all the way up to the largest proteins, which perform repeatable roles in basically every system of the body. But in cases where oxygen is exhausted, specifically consumed requiring a continuous supply of new oxygen, what roles does oxygen serve with the exception of serving as electron acceptor in Complex IV of the electron transport chain?

Molecular oxygen also has roles in antimicrobial defense1,2. Specifically macrophages use O2 to create cascades of reactive nitrogen intermediates (RNI) and reactive oxygen intermediates (ROI; aka ROS) — these compounds have antimicrobial effects.

The RNI cascade starts with nitric oxide (NO) and is catalyzed by a nitric oxide synthase, which converts arginine and O2 into citrulline and NO.
The ROI cascade starts with superoxide (O2•-) and is catalyzed by a NADPH oxidase, which transfers an electron from NADPH to O2 creating superoxide.

Figure 1 from2 gives an overview of these reactions:

Legend for figure 1:

  ROI and RNI production in mammalian cells via phox and NOS: parallel but connecting paths. Nitroxyl anion (NO−), a one-electron reduction product of nitric oxide (•NO), is unlikely to arise from •NO under physiologic conditions, but is considered by some investigators to be a primary and more toxic product of NOS. Reaction of RNI with cysteine sulfhydryls can lead either to S-nitrosylation or to oxidation to the sulfenic acid, as well as to disulfide bond formation (not shown), all of which are potentially reversible. Peroxynitrite anion (OONO−) and peroxynitrous acid (OONOH) have distinct patterns of reactivity, but for simplicity, the text refers to both as peroxynitrite. OONOH spontaneously decomposes via species resembling the reactive radicals, hydroxyl (OH•) and/or nitrogen dioxide (•NO2). When L-arginine is limiting, NOS can produce superoxide (O2⨪) along with •NO, favoring the formation of peroxynitrite.

References:

1: Weiss, G., & Schaible, U. E. (2015). Macrophage defense mechanisms against intracellular bacteria. Immunological reviews, 264(1), 182-203.

2: Nathan, C., & Shiloh, M. U. (2000). Reactive oxygen and nitrogen intermediates in the relationship between mammalian hosts and microbial pathogens. Proceedings of the National Academy of Sciences, 97(16), 8841-8848.


What is this furry, long-limbed, presumably tree-dwelling creature? Can anyone identify the species below? I believe the picture was taken at the Museum Of Zoology in Cambridge so maybe someone cleverer than me could narrow it down using their collections search.

Of the species I know, it looks most like a tarsier to me. Is there any relation?

It looks like a taxidermic specimen of a gray slender loris (Loris lydekkerianus), but it does look pale in color. The lack of color distinction in the fur may be because it is a non-living specimen. The links below may be helpful with more detail.

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

https://www.shaldonwildlifetrust.org.uk/page/grey-slender-loris.html

https://www.youtube.com/watch?v=yU3n0BlUP0A


Do trees have no set lifespan and
"quite"immortal? Many trees survive centuries and die only in disasters like
storms and lightnings or infections. So do they have no set
life span? Are they exceptionally resistant to genetic
mutations and have very less cell cycle regulations which
keep them 'forever young'?

There are certain annual(eg.peas) and biennial plants(eg.carrot) also which die at fixed times.

But for perennial plants :

From this

  Trees endure as long as they do basically because they're
  nonhierarchical organisms. In animals, all vital functions are
  controlled by the central nervous system, the guiding element of which
  is the brain. When the brain dies, so does the animal. By contrast,
  vital functions in trees are decentralized. A large part of the tree
  can die, and indeed routinely does die, without killing off the tree
  as a whole. Most of a mature tree is dead except for a few layers
  under the bark.....

  All trees die eventually, of course. Four thousand years is old
  compared to the life spans of gossamer creatures like ourselves, but
  in the context of geologic time it's the blink of an eye. As they get
  older trees become more susceptible to disease, pests, and other
  perils, and inevitably these take their toll.


Which restriction enzyme would i use? Plasmid pBr322 includes two genes that confer antibiotic resistance: a gene for ampicillin and  a gene for tetracycline. The cutting site for the restriction enzyme BamH1 is in the middle pf the tetracycline resistance gene. The cutting site for the restriction enzyme Pvu1 is in the middle of the ampicillin resistance gene.

If you were using a cell culture plate that contained ampicillin, which restriction enzyme (BamH1 or Pvu1) would you use to cut the plasmid and excise the gene you wanted to insert?

Attempt:

I would assume you need to use Pvu1 since the cutting site is in the ampicillin resistance gene, but the correct answer is BamH1. Why?

Any help would be awesome! Thanks!

Remember than Pvu1 cuts in the middle of AmpR, and when you insert your gene you'll be disrupting its function, meaning that any transformed colonies will no longer be able to grow on Amp-containing media. This is why you want to cut with BamH1 - the disruption to the TetR gene is irrelevant, and it leaves Amp resistance in place.

The point of growing on antibiotic-containing media is to select for cells that have taken up your plasmid - cells that haven't can't grow.


How plausible would it be for animals to normalize the birth of monozygotic twins in their reproductive cycles? I'm currently trying to develop the world of a sci-fi story I'm working on, and a concept I've thought of adopting with the environment and characters is a common breeding system where identical twins (or sometimes not, asymmetric twins from the same egg have also been under consideration) are a commonplace byproduct of the world's evolution.

I'd like to know the plausibility of this. My idea is for two twins to be born with natural, pheromonal connections between each another. The sexual organs of the twins would be the same, thus preventing immediate inbreeding. I'd also envisioned [most] twins consistently having lifelong reliance on one another. i.e. I also want to know how reasonable it would be to expect them to coordinate efforts in the acquisition of food and evade potential predators. As for mating, I thought if they shared the exact same DNA there would be less ingrained concern over which gets to spread its genes. Would this be accurate?

Thanks in advance for anyone that tries to answer me. I'm doing what I can to keep things in the realm of reality, so it'd be much appreciated to know whether or not the universe I'm creating has a strong enough footing in the real world.

As a whole, your question is opinion-based, speculative and not really suitable for Bio-SE.  However, several of the building blocks that you describe have a reasonable biological foundation, which might be useful to know.

For instance:

There seems to be a genetic component To monozygotic twinning (see e.g. ghr.nlm.nih.gov). This means that the trait could, very hypothetically, be selected for, and a population with a higher level of monozygotic (identical) twins could develop (ignoring other possible detrimental effects). Different frequencies of MZ twins is also know from castle breeds and other species.
The level of shared genes is the driving force between kin selection. This is part of the explanation  for the reproductive system in social bees (and other eusocial insects), where (usually) a single queen reproduces and her workers (all sisters), which are 75% related to eachother due to the haplodiplod genetic makeup, all work towards the common "goal" of producing new sister queens (which will then be 75% related to all the workers).
This gives some (again, very hypothetical) basis for your idea that "...they shared the exact same DNA there would be less ingrained concern over which gets to spread its genes".
Monozygotic twins often describe an especially strong sibling bond, which lends support (again, very hypoythetically) to your idea of "...expect them to coordinate efforts in the acquisition of food and evade potential predators.". There is also some research to back this up (e.g. Fortuna et al. 2011. Twin relationships: A comparison across monozygotic twins, dizygotic twins, and nontwin siblings in early childhood), but there are also studies that indicates that monozygotic twins show similar sibling behaviors as other types of sibling pairs (see e.g. Mark et al. 2017. Using Twins to Better Understand Sibling Relationships). This is not a field I know well and there is most certainly many more relevant sources to look at.

The introduction to Mark et al (2017) contains many references on MZ twins that should be relevant to your "thought experiment", e.g.:

  ...Fraley and Tancredy’s (2012) later work, which suggests that twin children rely more heavily on their co-twin for safety and security than do non-twin siblings.


Is the water transpired by plants pure H₂O, or does it contain trace minerals? I'm considering the idea of drinking water that I trap from what is transpired by trees.

Interestingly, is this water a fairly (or maybe even extraordinarily) pure form of H₂O, a remarkably pure by-product of the respiration / evapotranspiration processes - so does the process give off a fairly distilled form of water into the atmosphere - or is there actually a fairly measurable amount of trace elements that also are transpired in that water through the leaves?

A second complication which would be good to clarify, is that even if minerals / other chemicals are excreted along with the H₂O, would condensing that water in a water trap still only collect the pure H₂O anyway?

It will depend a bit on the specimen of tree / plant that is doing the transpiration. Minerals will typically stay behind during evaporation, but volatile compounds (think the minty smell of Eucalyptus) would evaporate at the same time as the water, and might condense (in some concentration) at the same time as well; this will depend a bit on the temperature of the leaf, the relative humidity of the air (lower will favor evaporation - higher means there is a lot of moisture already in the air, and you don't necessarily know where it came from) and the temperature of the surface used for condensation (lower condensation temperature will trap things besides water).

Note - this is more a physicist's answer than a biologist's... betraying my background here.


Why are fungi and algae microbes? Both fungi and algae have very small cells but so do most animals. Yet both of them are visible to naked eye just like other organisms.
Why do we call them as microorganisms then ?

Because both of those produce single-cells able to viably survive and grow on your own. For example, take a fungal spore and it can grow into a full fungus given enough food. I assume algae cells are the same way. In a single-cell form, fungi and algae qualify as self-sufficient microbes.

Animal cells are typically specialized and dependent on a support framework. Usually, a single animal cell left out on its own is largely doomed.


What is a "tool strain"? When a biologist is talking about a genetically engineered mouse strain which is a "tool strain", what does that mean? What is the exact definition of a tool strain? What is the difference between a tool strain and any other mouse strain?

Also, how are tool strains connected to recombinase techniques? Does using a recombinase automatically create a tool strain? Or are the properties "tool strain" and "recombinase containing strain" independent from each other?

If it is important, the context is mouse (and possibly other animal) strains used in cancer research.

It would help if you could keep the explanation high-level. I only have high-school biology knowledge and I am trying to make sense of the requirements for a software application for use by biologists.

Until a better answer shows up...

A tool strain appears to be a mouse strain that is useful for making recombinant mice.  It has genes inserted into its genome to make detection of your manipulations easier.  In this case several phenotypes (luciferase, human SMN) can be observed as well as a tetracenomycin resistance marker is in place so that offspring with the gene can be easily estimated.

  These Tg(SMN2)89; Smn1+/-; Tg(SMNΔ7)4299; ROSA26rtTA; "old" Luci-TRE-SMN mice allow high levels of both luciferase and full-length human SMN expression to be regulated by the addition/removal of doxycycline. These may be useful as a fluorescent reporter and/or Tet-On/Tet-Off tool strain for doxycycline-inducible rescue of Type II (moderate) proximal spinal muscular atrophy (SMA).


What are the best plants to cultivate yeast from? I know that cultivating yeast from potatoes yields a good brewing yeast and that forms of wheat make good baking yeast, however; I have not seen much information on other useful plant yeast cultures. What are some of the other plants that offer potentially useful yeast cultures?

*edit : corrected my error in thinking yeast was produced by plants due to a answer given

Yeast colonize the surface of many plants — for example they are a typical part of the normal surface flora (microbiome) of fruits such as grapes1 and pears2.

As you can see from the second reference, yeast can compete with other microorganisms to delay rotting of the fruit.

You might also find the "Uses" section of the wikipedia article on yeast and this article on winemaking to be of interest.

References:
1: Zahavi, T., Droby, S., Cohen, L., Weiss, B., & Ben-Arie, R. (2002). Characterization of the yeast flora on the surface of grape berries in Israel. VITIS-GEILWEILERHOF-, 41(4), 203-208.
2: Benbow, J. M., & Sugar, D. (1999). Fruit surface colonization and biological control of postharvest diseases of pear by preharvest yeast applications. Plant Disease, 83(9), 839-844.


Identification of a small to mid-sized, yellow moth species found in India at monsoon season I am from India and it's monsoon here. What is the name of this insect?

Description:

Length: ~4cm
Width: ~2.5cm
Color: yellow, almost uniform across the wings. Slightly darker, dandelion yellow across the body.
Small black dot in the middle of each large wing.
White, speckled iridescence on wings.
Short antennae.
Longer than average hair for moths.

This is likely a member of the Nygmiini moths. The Nygmiini are a tribe of tussock moths of the subfamily Lymantriinae (formerly called the Lymantriidae) of the Erebidae family

A specimen that closely resembles yours can be seen here, and copied below:

I have not found a definitive species for you, but will keep looking. I'd advise you try to do the same given this information.


Are Schwann cells the sole source of myelination in PNS? Are Schwann cells the only source of myelin for axons in the peripheral nervous system, or are there other neuroglia or other processes that result in myelination of PNS axons?

Schwann cells seem to be the most common type of glial cells outside of CNS, and the myelinating Schwann cells are the only known source of myelin in PNS. Other types of neuroglia in PNS, for example non-myelinating Schwann cells and astrocytes-like cells do not seem to take part in myelination, neither in CNS nor in PNS.


Common ancestry of our cells to the first unicellular cell If we start the chapter of life with low fidelity self replicating RNAs forming exactly identical copies of themselves,  which then later evolved to form the first primordial basic cells which further reproduced, and formed identical daughter cells and so on ... besides mutation and other factors that might affect gene expression, our genome must still be derived from the very first RNA strand.
So is it too far fetched to say that in our bodies, our cells are the primordial cells themselves, as reproduction happens either by mitosis and meiosis (which keep the integrity of the first cell genome besides factors like mutation, etc.)?

What it seems you're struggling with here is a lack of clear definitions.
Yes, the unity of core cellular mechanisms implies an unbroken line of descent back to the origins of life. But that does not in any way mean the cells are actually the same. I think that you would find it instructive to learn about the puzzle of the Ship of Theseus, which is the essence of the issue you are dealing with. In short, once changes can happen (e.g., mutation, as you note), it's possible to have both continuity and a fundamentally different item.
Beyond this, it's also worth noting that at every step we are dealing not with individuals but populations, even likely back into the murk of abiogenesis (when the populations would be various chemicals and protocells of some sort), and that genomes are also modified in a much wilder variety of ways, e.g., all the various forms of horizontal gene transfer.


Can a person be infected with Polio even after vaccination in childhood? We know that a person develops antibodies by active immunisation after the administration of vaccines (either in dead form / live attenuated form). Is there any chance of developing the same disease in immuno compromised persons after reaching adulthood?

Short answer: Yes.

Slightly longer answer:
Recall how a vaccine works - it introduces an antigen to the body, which provokes the body to produce antibodies towards that antigen.

Antibodies, simply explained, call upon the remainder of the immune system to fight off a potential infection of foreign body. If there is no immune system to mobilize, the infection would most likely run its course. However, the immune system would have to be sufficiently weakened in order to not be able to fight the infection.


Why did a lot of common insects evolve such a thin waist? Something that doesn't quite make sense to me is why lots of insects like ants, bees and wasps have a such a small petiole when it connects many major organs to the rest of their body from a suddenly much wider abdomen.

Normally from an engineering standpoint, you don't increase the width of a cantilever from a joint because the torque applied to a joint already increases with the length of an overhanging segment, so increasing the width would only multiply the torque that joint or opposing segment needs to balance.

It could have something to do with ants being so small that large  torque isn't an issue in proportion to their body size, but if it wasn't, then why do their legs also get thinner as they measure further in length from their body?

This thin waist is called petiole (aka.  wasp‐waist).

How many times did the petiole evolve?

  Why did a lot of common insects evolve such a thin waist?

Reading this question make it feel that you are assuming that several lineages evolved this petiole independently. It would be wrong. The petiole evolved once only and all the species that are having a petiole today (ants, bees, wasps, ...) are descendent of this lineage that evolved this petiole.

The taxon of all these species having a petiole is called Apocrita, which is a suborder of hymenoptera. You can learn much more about the phylogeny of these taxons in Rasnttsyn and Haichun (2010).

Why did it evolve?

The early lineage who evolved this trait where parasites (or even parasitoids at that time, I am not sure). This lineage was laying their eggs in tree trunk (or maybe already in other insects larvea if they were already parasitoids). The constriction that is the petiole allowed these individuals to have greater maneuverability for depositing their eggs accurately (Peters et al., 2017; Wilhelmsen et al., 2010).

The evolution of this petiole greatly affected the future evolution and diversification of Apocrita as things like stings and even maybe eusociality. From Peters et al., (2017)

  The evolution of the wasp waist, a constriction between the first and the second abdominal segment greatly improving the maneuverability of the abdomen’s rear section, including the ovipositor, was a major innovation in the evolution of Hymenoptera that undoubtedly contributed to the rapid diversification of Apocrita