Dehydration Synthesis: Why does a monomer contribute a -H instead of an H atom? My Campbell's Biology 9th edition textbook says that a dehydration synthesis is a reaction in which water is produced while two monomers are joined together. Specifically, it makes the following statement:

  One monomer provides a hydroxyl group (-OH), while the other provides a hydrogen (-H).

Sorry if this is a silly question to ask, but what I'm wondering is how exactly a Hydrogen electron joined with a Hydroxyl will create H2O? Why isn't it a Hydrogen atom (1 proton and 1 electron) rather than just the electron which moves?

The dash ("-") does not represent a negative charge or an electron.  It simply indicates that the group of atoms ( -OH or -H ) are attached (covalently bonded) to other atoms in a molecule.  So they are saying one monomer (molecule) contributes OH to the reaction and the other H.  (A charge is indicated by a trailing superscript minus sign.)


Why is a membrane polar on the outside and non-polar in the inside? Why would the phospholipid bilayer want to be polar on the outside and non-polar in the inside? why would it not want to be the opposite?

Phospholipids in aqueous solution under the proper conditions organize themselves into micelles and other structures - the minimum energy state.  This allows the polar head groups to interact with water in the bulk solution, while the non-polar carbon chains are 'protected' from the polar environment.  Water is attracted to water, and the polar head groups are attracted to water, the non-polar carbon chains are excluded.
You can get inverse micelles in non-polar solvents.


What are tendons made of specifically From what I read on wikipedia they are made of collagen. Collagen is just a protein. Right? How is this collagen structured (I imagine like fibers). Aren't there cells in this fibers as well?

From this picture:

Is the pink stuff the collagen? and the purple stuff the tenocytes?

If someone can expand on this with a picture preferably, it would be great.

As you correctly say, tendons are made up of collagen fibers. Collagen is one of the most important proteins (or, to be more specific, family of proteins, as there are many types of collagen) forming connective tissue in the body.

Collagen molecules have a particular structure that allows them to form long fibers, composed by three different strands that form a triple helix. This is a schema of a collagen helix (each ball represents one aminoacid):

(source: Wikipedia)

These helices can then be bound together to form a collagen fiber, through the action of an enzyme called lysyl oxidase which binds two lysine residues from two different helices together (lysine is one of the aminoacids that makes up collagen).

Here is a scanning electron microscope of a collagen fiber:

(source: Science photo library)

Collagen is secreted out of the cells that produce it so, although there may be cells around the collagen molecules, it is important to understand that it is part of what is called the extracellular matrix, the extracellular structure that supports the cells in our body.

As for the photo you linked, it is an hematoxylin and eosin (H&E) stain of a tendon. Hematoxylin colours cell nuclei in dark blue, so the dark spots are definitely cells.
The pink "waves" are indeed collagen fibers, the cells are probably the tenocytes, the specialized fibroblasts of the tendon, which produce the collagen.


naturally occuring fatty acids The double bonds in naturally occurring fatty acids present in our body are in cis configuration while the enzymes for beta oxidation can act on trans double bond. Then what will be the significance of cis double bond in naturally occurring fatty acids? Why the naturally occurring fatty acids don't have double bond in trans configuration?

The diversity of fatty acids produced by an organism is limited by the diversity of enzymes which synthesize them. Unsaturated fatty acids contain carbon-carbon double bonds which do not isomerize. The capacity for humans to produce cis fatty acids is probably selected for because of their lower melting point which prevents arterial clogging. Cold blooded animals utilize cholesterol to increase membrane fluidity when their body temperature is low.


Did the Hela cells leave John Hopkins Did John Hopkins let people outside of the university use the Hela cell-line that was isolated from an immortalised cervical cancer?

Cultures of HeLa cells are used in many labs around the world, and were widely shared from very early on. From the Wiki:

  In the spring of 1953, a cell culture factory was established at
  Tuskegee University to supply Salk and other labs with HeLa cells.


What is the potential function of ultra-conserved elements in the genome? If selection pressure results in conservation of DNA sequences, what is the most plausible explanation for the existence of ultra-conserved elements (refs here and here) given that there hasn't been any significant validation of the functional significance of these elements other than a lot of bioinformatic analyses across different genome datasets? If these are of such high significance, does this mean that there is still some significant gap in our understanding of fundamental biology or is there another explanation? The second reference in particular show that there are UCEs shared between plants and animals, but are not syntenic (which is not necessarily a surprise) so it might suggest that at least a class of UCEs are associated with structural rather than functional elements.

It appears that there are at least several different 'classes' of ultra-conserved elements, based on the number of matching/identical bps, their spatial distribution across the genome and the species in which they exist. Even though there is probably no single explanation that would account for all the possible functions they can have, it is surprising that they are difficult to test functionally. This is again probably due to a lack of understanding about their properties and therefore no real method to validate their function. I think this is where we need to think outside the box to come up with the answer.

What would be the most obvious (and possibly not so obvious) function for UCEs?

Probably development, in particular transcriptional regulation.  To quote each link in turn,

  They are found in clusters across the human genome, principally around genes that are implicated in the regulation of development, including many transcription factors. These highly conserved non-coding sequences are likely to form part of the genomic circuitry that uniquely defines vertebrate development.

and

  [Highly conserved non-coding sequences] are significantly associated with transcription factors showing specific functions fundamental to animal development, such as multicellular organism development and sequence-specific DNA binding. The majority of these regions map onto ultraconserved elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments

Additionally,

  Here we report that 45% of these sequences functioned reproducibly as tissue-specific enhancers of gene expression at embryonic day 11.5. While directing expression in a broad range of anatomical structures in the embryo, the majority of the 75 enhancers directed expression to various regions of the developing nervous system.

These regions tend to be highly clustered in around 200 areas, and most of them are non-coding.  ncRNA is often regulatory, and those UCE clusters are associated closely with developmental genes.  That being said, not all of them are clustered near known genic regions, which might be a good indicator that there are heretofore unknown genes in those areas; UCEs might be useful for discovery.  And here's a paper trying to give a role to one in cancer.


In mitochondria, what is the mechanism by which electrons are transferred between different cytochromes? And how is the energy gained from the lowering of the "energy level" of the electron used to generate the chemiosmotic gradient?

All of the members of the Electron Transport System (ETS) are organized in "complexes", clusters of enzymes and other proteins. These complexes are in proximity to one another such that electrons can be passed between them. The different cytochromes, and other electron handlers, have different affinities (attractions) for electrons. Those at the beginning of the ETS have less affinity for electrons than those at the end. The reason the electrons move through the ETS is due to that greater attraction of electrons by the subsequent complexes in the pathway. These complexes are positioned with respect to one another so that no "short circuits" occur; the electrons skip no steps down the ETS. Finally, the "low energy" electron from the last complex is mopped up by that great electron-hog oxygen.

The energy lost by the electron as it passes between carriers is not directly harvested to pump protons. The importance of this "loss of energy" is that it makes the transfer of the electrons a spontaneous process insuring their passage down the ETS. Typical entry into the ETS involves NADH donating a hydrogen ion to the matrix and a pair of electrons to NADH dehydrogenase. The electrons are eventually transferred to the mobile coenzyme Q. This now attracts a pair of hydrogen ions from the mitochondrial matrix which then induces the operation of a proton pump. This pumps hydrogen ions into the inner-membrane space creating the electrochemical gradient.

So, in general the arrival of electrons, with the attendant hydrogen ions, changes the conformation (shape) of pumps which translocate the protons to build up the gradient. The electrons are ultimately passed on to oxygen, forming water with the help of some spare hydrogen ions. This removal of the electrons allows the ETS members to be receptive to another load of electrons from the NADH.

Reference 2nd paragraph: http://www.physiologymodels.info/metabolism/ETSOXPHOS/ets.htm
This is a good site to read more and view some diagrams, especially focus on the second panel, "Complex I".

Reference 1st paragraph: Molecular Biology of the Cell; Alperts, Watson, et.al.


Do sieve tube cells have any extrachromosomal circular DNA at maturity? In order to generate a tube system of low resistance, sieve elements lose most of their cellular components such as the nucleus, cytoskeleton, ribosomes, tonoplast etc.
Mature sieve elements contain structural phloem specific proteins (P-proteins), mitochondria, ER, and sieve elements plastids.
In plants, sieve tube cells lose their nuclei at maturity (just like our RBCs), and thus lose their chromosomal DNA, but they don't lose their mitochondria.
In eukaryotic cells Wikipedia has divided extrachromosomal DNA into three parts based on where it is seen (I guess):

Mitochondrial
Chloroplast
Circular

Sieve tube cells have mitochondrial extrachromosomal DNA at maturity, but I'm not sure about the existence of extrachromosomal circular DNA in these circumstances.
Do sieve tube cells have any extrachromosomal circular DNA at maturity?

This ref. says that the plastids and mitochondria are still intact.
Found by searching for "sieve cell development"
Neuberger, D.S., Evert, R.F. Structure and development of sieve cells in the primary phloem ofPinus resinosa . Protoplasma 87, 27–37 (1976). https://doi.org/10.1007/BF01623956
https://link.springer.com/article/10.1007/BF01623956


Can polystyrene sulfonate bind calcium or sodium in the gut? How? Polystyrene sulfonate is used as a potassium binder to treat hyperkalemia in traumatic rhabdomyolysis, acute and chronic kidney disease. It is listed as an ion-exchange resin that can also remove sodium or calcium from solution, but is also available in sodium salt or calcium salt form. How might this work?

Are you talking about Sodium Polystyrene Sulphonate (a.k.a SPS)?

If yes, then ...

Quoting from Chaitman, Dixit and Bridgeman (2016)

  Synthetic cation-exchange resins are insoluble polymers resembling a crystalline lattice. When placed in a solvent, this structure swells, allowing the exchange of ions between the reactive group on the resin (in the case of SPS, sodium) and ions dissolved in the solvent.

However, other cations like sodium and calcium ions can bind too.
As SPS moves through the intestine, sodium ions are released and exchanged for potassium ions.

References
Chaitman M, Dixit D, Bridgeman MB. Potassium-Binding Agents for the Clinical Management of Hyperkalemia. Pharmacy and Therapeutics. 2016;41(1):43-50.


Why can a zygote develop into all different types of cell, whereas a differentiated cell cannot? A cell formed by the fertilization between two gametes has all the DNA and can lead the development of a human person (or other animals in other species). But other cells in a human person has also all the DNA (like skin cells), yet they don't lead the development of organs, bones, etc. What is the difference between the zygote and cells from any part of the body from a developed person that one can lead to the development of a person and the others can't in spite of all of them have all the DNA? Does it have to do with the enviroment/surrounding those cells are in, is there any structural difference between the zygote and the other cells or how is it?

Developmental biology is a huge field that we are still working on a lot.

DNA is only half the story.  The other half is gene expression; what subset of the DNA a cell is using at any time.  Your lung cells have the gene for insulin, but in lung cells, that gene is dormant.

The short answer is that in general, a mature cell is using the subset of its DNA that it needs to do its job and can't just change its gene expression to become a different kind of cell.   Cells that do become less like adult cells and less specialized can become cancerous.


ID large-thorned plant growing in Turkey Can anyone identify this plant which is growing in a friend's garden in the Uzumlu area of Turkey. It has very large spikes/thorns. I'm told it doesn't have flowers or seeds so we are wondering how it propagates itself.

This is a palm (family Arecaceae). Many palms have spines; I'm no expert but it looks to me like it is a member of the Phoenix genus, perhaps a Cretan date palm (Phoenix theophrasti). Date palms do propagate themselves by seed (the pit of the date fruit). The palm in your picture, if a date palm, would be rather young, which could explain why it does not presently show flowers or fruits. Here is a photo of the spines and flowers of a Cretan date palm (by Wouter Hagens, from Wikimedia Commons):


How do processes of one osteocyte establish contact with processes of the adjacent cells within the mineralized matrix? Are the processes and canaliculi formed and contacts established after the osteocytes are embeded in the matrix or are they formed during the embedding process itself. Is there any evidence to suggest either?

Osteocytes attach to each other by cytoplasmic extensions through gap junctions [1]. The connections between these cells are formed since they were osteoblasts and osteoid-osteocytes (type II preosteocyte) [1]. Osteoblasts have a greater volume than osteocytes and the lack of extracellular matrix favors their adhesion. As they begin to synthesize extracellular matrix, their volume is reduced and this matrix takes space between cells, but with respect to the existent intercellular junctions around which matrix forms canaliculi.

"Osteoblast Organization" by Physio Muse - I drew this figure in drawperfect, printed to .pdf, and converted to .jpg
Previously published: Not published in any form, including not used on any website. Via Wikipedia.

Osteoblasts are connected via gap junctions mediated by connexin43 protein [2]. Mature osteocytes attach to the bone matrix by integrins (alphavbeta3) [3].

References:

Wikipedia contributors, "Osteocyte," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Osteocyte&oldid=618657480 (accessed July 27, 2014).
Civitelli R. Cell-cell communication in the osteoblast/osteocyte lineage. Arch. Biochem. Biophys. 2008 May 15;473(2):188-92. doi: 10.1016/j.abb.2008.04.005. PubMed PMID: 18424255.
McNamara LM, Majeska RJ, Weinbaum S, Friedrich V, Schaffler MB. Attachment of osteocyte cell processes to the bone matrix. Anat Rec (Hoboken). 2009 Mar;292(3):355-63. doi: 10.1002/ar.20869. PubMed PMID: 19248169.


Finding total concentration of enzymes Sorry if my question is very basic for biology majors because I am not. I am trying to build a mathematical model of a particular pathway using systems of differential equations and in order to reduce the number of parameters, I need to know the total concentration of multiple enzymes. How are enzyme concentrations usually reported in the literature so I can google it? Also, this does not seem to me to be a straightforward measurement for professional biologists, so how are enzyme concentrations actually measured or approximated? Thanks in advance!
I am interested in the following pathway:

Hi again TheLast Cipher,
Enzymes in a cell are usually semi-quantified by the: Western Blot technique.
But there are lesser known techniques.
E.g. For a Western Blot the unit of measurement is the color intensity of the enzyme band on the blot membrane.
If I were you I would look for journal articles covering your pathway of interest.
E.g. https://iubmb.onlinelibrary.wiley.com/doi/abs/10.1002/biof.5520320129
Covers the electron transport chain (Co-enzyme Q10)
If you can get through the pay-wall & read their results and you will find:

"Western blot analysis of membrane protein isolated from keratinocytes derived from one young and old donor. A representative picture out of five experiments is displayed."

Also they used and I quote:

"Arbitrary Units"

Maybe you could comment on which pathway and I can find some assisting material.


Why are antibiotics prescribed with a viral infection like a cold? I've heard both ways; people going to the doctor for a cold and then getting a prescription for antibiotics and those that go to the doctor and told they have ride it out because it's a viral infection.  Do antibiotics really help in true cases of a viral cold?

In general antibiotics don't help with viruses. However, sometimes a bacterial infection may follow a cold virus, so there might be some scenarios in which antibiotics would be needed. However in many cases it could be due to people demanding antibiotics from their doctor.

You can read more here (CDC site): http://www.cdc.gov/Features/getsmart/


Why is Ibuprofen contraindicated in asthma patients? So yesterday a patient showed up at the clinic with a massive swelling in his left face region. Upon examination it was found to be due to infected first premolar. Dentist recommended him to get the tooth extracted as the patient also had generalized attrition and abrasion. The patient was an asthmatic and diabetic on Ecosprin. The dentist while prescribing him medicines said that he won't prescribe him Ibuprofen as the patient was asthmatic. I have been looking for an explanation since then and Rang and DaLe have something to say about the isomers of COX enzyme. I am looking for a simple explanation.

Ibuprofen is an NSAID. So it acts by inhibiting COX (Cyclooxygenase) enzyme. What it signifies is that, if COX enzyme has been blocked, the PUFA (say arachidonic acid, here) will be converted to leukotrienes through lipoxygenase pathway.

Leukotrienes (LT) are of different types and have several target receptors; one of which is CysLT-receptors on bronchial smooth muscle. Once they are activated through LTD$_4$,E$_4$,C$_4$ , bronchospasm will occur. For asthma patients this is really fatal. So for them Ibuprofen is contraindicated.

Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5072955/
Lo, P.C., Tsai, Y.T., Lin, S.K. and Lai, J.N., 2016. Risk of asthma exacerbation associated with nonsteroidal anti-inflammatory drugs in childhood asthma: a nationwide population-based cohort study in Taiwan. Medicine, 95(41).


Can 1.5 gigabytes encoded in the human genome really account for the complexity of a human being? I read the human genome is 1.5 gigabytes in size. Thats actually not a lot; Photoshop probably takes more space. Mac OS takes 10+ gigabytes of space. Also, the genome is 1.5 gigabytes when counting base pairs as the alphabet, but the actual unit of information is a codon, which is made of 3 base pairs. That means that if the 64 codons are the alphabet, then the amount of information is (top of the hat calculation) 0.5 gigabytes. This is analogous to a "byte" in computer memory, composed of 8 bits. Byte -> codon, bit -> base pair.

Nevermind that some codons are start/stop signals and not part of a protein defining instruction. You can go further and say that the next level, formed by all the known proteins/chains of aminoacids, is a subset of all possible combinations of aminoacids, and forms a new alphabet. The language of proteins.

Anyway, a cell has 100 trillion atoms, and that structure is controlled by DNA containing 1.5 (or 0.5 depending on taste) gigabytes of instructions. That right there is pretty impressive. But then, the human body has 37.2 trillion cells, and you are telling me those 37.2 trillion cells, each containing 100 trillion atoms, are controlled by ~1 gigabytes of instructions? That doesn't add up.

In computers everything is 0 or 1, but after many layers that simple alphabet of {0, 1} can represent complex structures. I guess the same is possible with DNA, but I feel you'd need way more instructions to represent even the most basic of organs. So, I think I am missing something here. For basic structures, like tissue, veins, eyes, blood, hair; things that we share with animals, is that all encoded in DNA?

The complexity is rather enormous for a rather tiny amount of instructions, so there must be something else controlling organ and bone structure.

This is a VERY hard question to answer; I think mostly because it is very hard to think about how the DNA actually encodes information.

The first important thing to note (and also the only direct answer I can give to your question), is that

(Yes) the human genome does encode all information to make a human being, but only in the context of a cell/organism that can read this genome.

Transferring this to the computer code analogy this means that if the genome is the source code for a program (or rather a couple of them), then the operating system (and also the actual hardware) that executes this code is the cell itself and the two parts have to match up in order to work together.

This is essentially a hen/egg problem: without the cellular machinery to read and operate on the genome the organism doesn't work, but at the same time the genome is the source of the everything that reads it.
If one would put the human genome into another (not closely related) species (or the egg cell of one), this would not form a human being, because the organism/egg cell can't read the instructions properly. (This is also the reason why hybrid animals like i.e. mules are often sterile - the genomes of their parental species are similar enough to be readable and make a working animal, but there are already enough differences to introduce problems).

This brings me to what i think is the actual core of what you're asking:

How can so much complexity be encoded in so little space/bits/... ?

and I don't have a clear answer for that (and neither have I ever seen one). There are, however, a few things one needs to consider

Emergent behavior is when seemingly very simple and limited rules lead to very complex structures. This happens all the time in nature and our body plans are no exception, it is however very hard to see or understand and even harder to consciously design from scratch. Nowadays, machine learning algorithm can get complex results from initial simple instructions, but only because they run 'a couple' of optimization steps inbewteen - evolution has done the same thing for millennia.

A second thing to keep in mind, is that code can be re-used. Programmers already do that (a lot), but usually they try to keep the code readable and make a clean copy for a new purpose. Nature / the genome most of the time doesn't do that and its been re-using and re-purposing pathways on any level for millennia. The reason that arms and legs are built very similar, or that essentially all animals are symmetric is that it's just easier to (re)use the same set of instructions a couple of times with slight alterations than specifically writing everything down.

Finally (as almost always), Randal Monroe explained pretty well, why just knowing the 'source code' of the genome doesn't mean we actually understand how it's doing what it's doing:

This answer's gotten pretty long now and I'm out of time to add sources - if anyone feels motivated to add something feel free to make/propose edits.


What are these four large snails doing? Hiking in some hills near Taipei after a rain, I saw lots of large snails out and about. Here "large" means the shells are say 8 cm long, and the snail itself fully stretched out 10 to 15 cm perhaps.

At one point I saw a cluster of four snails stuck together in a confusing way. The one on the right was slowly climbing uphill, pulling the other three along.

What is going on here? I see some connections between some of the snails, but I can't really understand most of what I'm looking at here, nor why four snails would be stuck together sideways like this.

These are probably giant African snails, Achatina fulica, an invasive species of land snails. The two snails in the middle are mating using love darts. The other two may be waiting for their turn.

See also: Wikipedia - Achatina fulica


Irradiation positive effect on humans? In research paper Euphytica 135: 187–204, 2004 it is written that:

  434 mutant varieties of rice have been released with improved characters such as semi-dwarf height,
  early  maturity,  improved  grain  yield,  disease-  and
  cold-tolerance, and improved grain quality. Of these,
  225 (56%) were induced with gamma rays, 16 with X-
  rays, 7 with fast neutrons and 12 with other radiation
  sources

So I can see that irradiation may have positive effects on plants' genome.

Is there any information that mutations induced in this way in humans were beneficial for them? Can irradiation have positive effects on your body?

Regarding your first question, I don't know of any instance in which irradiation was used to select for a beneficial trait in humans. I italicized 'used' because I think that you could argue that naturally occurring sources of irradiation have led to the selection of traits that protect us from radiation damage.

That might sound like a bit of a circular argument, but keep in mind that in the case of the rice you mention, the discovery of beneficial traits came at the expense of a lot of dead rice that suffered deleterious effects of radiation. Unfortunately, the deleterious effects are a lot more likely to occur than than any really useful ones.

That leads to your second question. Conceivably, radiation could lead to a beneficial mutation. However, there are some pretty big caveats with that. First, in order for it to be beneficial, this hypothetical mutation would have to occur very early on in development, otherwise it would be limited to, at best, a handful of cells, probably in your skin, which would just get sloughed off anyway. So the second caveat is that in order for such a beneficial radiation-induced mutation to occur in the right place at the right developmental time, it would have to penetrate all the layers of your mother's genetic material that separate your fetal cells from the outside world without losing the energy needed to damage your DNA.

I couldn't tell you what sort of radiation might be capable of pulling that off with what probability of success, but my guess is that it's really unlikely.


Why do red blood cells contain haemoglobin and not myoglobin? So I am reading about muscles and I come across myoglobin. It has a much higher affinity for oxygen than haemoglobin. So why have animals evolved to have haemoglobin in red blood cells, rather than myoglobin, which would be much more advantageous?

Just to expand slightly on the answer by Jack Aidley:

Have a look at this section from Stryer's Biochemistry text book, particularly Fig 10.17, where you can see that haemoglobin has evolved to have a high affinity for oxygen at the O2 concentrations present in the lungs, but a low affinity at the O2 concentrations present in the peripheral tissues. This is achieved by binding oxygen co-operatively. This means that haemoglobin can release 60-70% of its bound oxygen. Under the same conditions myoglobin, were it be used in red blood cells as an oxygen carrier, would release much less.

Incidentally the Figure linked to shows a comparison between haemoglobin and a hypothetical protein which shows 50% saturation at the same concentration of oxygen but which binds oxygen non-cooperatively (like myoglobin).

A more direct comparison of haemoglobin and myoglobin  - found here -  is shown below:

edit added to respond to shigeta's response

I don't understand some of the statements from shigeta so here are my views - if I am wrong, I would (genuinely) like to be corrected, since I have to teach this stuff.

  ..."what is particularly useful about Hb's cooperativity is that the last oxygen is harder to pull off the Hb tetramer than the first."

This statement contradicts my understanding of the oxygen-binding behaviour of haemoglobin. In the deoxygenated state the protein is in the conformation known as the T (for tense) state, and this is a low affinity state. The binding of an oxygen molecule to one of the haem groups in one of the globin subunits of the tetramer increases the affinity, so that subsequent binding of oxygen becomes easier. The details of how this happens are still debated, but I think what I have said so far is accepted by everyone.

Here is an equation to represent the binding of the first oxygen molecule to the haemoglobin tetramer:

O2 + [Hb]4 <--> [Hb4]O2

If deoxygenated Hb has a low affinity for oxygen then that equilibrium must lie to the left hand side - in other words the right to left reaction (release) is faster than the right to left reaction (binding). This is not consistent with the idea that haemoglobin hangs on to its last oxygen.

  "The heart, which is the first organ in the blood cycle after the lungs uses a lot of oxygen - if hemoglobin were not cooperative, it might take all the oxygen from hemoglobin just after the beat when it uses oxygen when in distress, creating a block of hemoglobin which is completely without bound oxygen."

This is based on an erroneous view of the circulation - it implies that all of the blood passes through the coronary artery before getting to the rest of the body. Oxygenated blood leaves the heart via the aorta. Although it is true that the first branch off the aorta is the coronary artery, most of the blood doesn't enter this branch, but proceeds into the remainder of the circulation. In this sense the coronary circulation (by which I mean coronary artery>coronary veins - the heart's own blood supply) is in parallel with the rest of the circulatory system, not in series with it. At rest, just 5% of the heart's output goes into the coronary circulation.

According to this review, Regulation of Coronary Blood Flow During Exercise, (I am simplifying a lot here, but this statement does appear in the review and is not taken out of context): "Increased myocardial oxygen demands during exercise are met principally by augmenting coronary blood flow." At rest the heart is already extracting most of the oxygen from its blood supply (see here for some interesting data) so again there is no question of the heart extracting much more - it simply needs more blood, and of course the increased heart rate will contribute to this. There is also scope for directing a greater proportion of heart output through the coronary circulation, but I have been unable to find any quantitative statements about that. Interestingly, if you take a look at the data in the 1st table of the data here you will see that, at rest, 22% of the heart's output goes into the renal circulation, but that much less oxygen is extracted from that blood (about one ninth of how much is extracted from the blood going through the cardiac circulation). This represents a source of potential increased blood to be diverted to the heart at the expense of a reduction in renal filtration.

  "Also - Hemoglobin is pretty clearly an evolutionary adaptation where four myoglobins came together to form a cooperative oxygen binder, so at one time probably myoglobin was the oxygen carrier. There are some primitive animals which have no distinct hemoglobin, just myoglobin like carriers."

I agree it is clear that haemoglobin and myoglobin evolved from a monomeric myoglobin-like ancestor, and that the appearance of a tetrameric molecule created the potential for co-operative oxygen binding. I am not as convinced by the rest of the sentence. I think we have to agree first on what we mean by an oxygen carrier. What I mean is a protein that is a component of a circulatory system. I know of no evidence that a myoglobin like molecule could perform this function. This arises directly from the shape of a simple binding curve (a rectangular hyperbola). For the protein to be saturable at atmospheric oxygen concentrations it has to have a certain Kd, and this precludes significant release of oxygen at physiologically useful concentrations. You either have a protein which can unload effectively but will not ever become saturated with oxygen, or you have a molecule that is able to become saturated but cannot ever unload except at every low oxygen concentrations. That is the remarkable thing about haemoglobin - the appearance of cooperative binding allowed for a more switch-like interconversion between a high affinity state, for loading up, and a low-affinity state, for unloading.

Now, if you wish to include intracellular oxygen transport in your definition of "carrier" then we enter a whole other debate about the role of myoglobin, but I have gone on for far too long already, so I'll stop there.


Biological data source of trees I need some biological data for many types of trees, but I can not find good source of this on internet.
Where can I find following type of biological data of any tree:

Biological Profile
Taxonomy
Distribution
Cultivation
Edible Medicinal Parts
Phenology

The Ecological Data Wiki search for Woody Plants is a good start for some nice datasets. There is also the USDA Plants Database which has information for every plant in the U.S. Woody species are well represented with lots of species specific info. These can be downloaded handily with an R package.

Looking for occurrences? Put the species name into GBIF to get historical records of where and when a species was found. This has an R package as well.

Want distribution maps for all trees in North America? Someone has done that for you here.

Phenology? The National Phenology Network.

Edibility? I've never come across a specific data source for this. But the best reference I've used is the Handbook of Edible and Poisonous Plants of Western North America. It's an amazing book with years of research put into it. It does not have any pictures nor a key to identify plants, but it does have information on pretty much every plant in the Western U.S. at least at the genus level.


How do small birds survive the winter? I live in a region with cold winters (ca. -40 C) and many quite small birds (sparrows, crows, ducks) stay for the winter.

How can the birds survive this?

As I understand it, smaller bodies will be less able to produce and retain heat. Despite this, birds seem to cope much better than humans, sitting in the cold all winter and even swimming in cold water. In comparison, humans lose mobility in their muscles when cold, and can suffer severe frostbite causing them to lose fingers, toes, or limbs from relatively short exposure to the same conditions.

What specific adaptations allow birds to cope so well in these conditions?

There are a variety of physiological, anatomical and behavioral adaptations that keep birds warm in winter.

For starters, birds are endothermic ("warm-blooded"), similar to mammals. You suggested that the coats humans wear are superior to feathers as insulation. Yet some of the finest coats and sleeping bags were long filled with feathers (e.g. goose down). Animals that live in cold regions tend to have smaller extremities. For example, you probably won't find many long-legged flamingos or ibises in the Arctic during the winter (though food supply is another reason they couldn't survive there).

As someone else suggested, water temperature is a relative constant, which means water (or better yet, snow) can actually insulate animals from colder temperatures.

Countercurrent heat exchange is a strategy that helps endothermic animals conserve heat. The page I linked to is part of a book titled Animal Adaptations to Cold, which includes a chapter titled "Avian [Bird] Adjustments to Cold."


Is it possible to induce protein activation via frequency-specific mechanical waves? Would it be possible to induce shape changes in specific proteins by providing specific frequencies of mechanical waves in a thermostatically controlled environment such that those proteins may be activated without requiring regular ligand binding?

This should defentily be possible and most likely already exists in the form of touch or pain receptors.

In the case of mechanical nocireceptors, which sense pressure or other mechanical changes in the tissue to signal pain, it's quite likely that there are distinct channel proteins that can correspond to mechanical deformation/pressure/etc, but I couldn't find any specifically known protein.

Most touch receptors seem to be based on bigger structures made up by neurons, so I'm not sure if they have one specific protein that senses mechanical movement, but I also wouldn't exclude that option - especially since almost nothing is known about non-human/mammalian touch receptors.


What will happen to a neuron if I suddenly remove the pump but not the leaky Na+ and K+ channels? K+ is more abundant inside the cell and thus has a propensity to move outwards. It has an equilibrium potential of -80 mV. Na+ is more abundant extracellularly and thus has a propensity to move inwards. It has an equilibrium potential of 58 mV. The resting membrane potential of a cell is about -70 mV. So, K+ moves out (more towards its equilibrium potential) and Na+ moves in (more towards its equilibrium potential). The pumps throw out the Na+ and bring back in K+ thus maintaining their concentration and hence the membrane potential.

Now if I suddenly remove the pump from the cell, what would happen? Will the cell moves towards K+'s equilibrium potential or towards Na+'s equilibrium potential? I know that the answer is that the cell will discharge and have a membrane potential of 0 mv, but I don't understand why.

Both Na+ and K+ will move according to the electrochemical gradient. Given that K+ leaky channels are ever present, the cell is already around its K+ equilibrium. If you introduce leaky Na+ channel and remove the pumps, eventually the cell will be nothing more than a passive membrane and it will adopt the same concentrations of ions as the extracellular space, i.e., Na+ will pour in along its electrochemical gradient, after which K+ (formerly already at equilibrium) will start pouring out alongside its chemical gradient, due to the reduced electrical gradient because of Na+ coming in.


Action potential changes in low sodium concentrations but constant osmotic pressure If I bathe a squid axon in a fluid that has high sodium concentration , why does the duration of action potential decrease compared to a control experiment in low sodium bath but maintained at the same osmotic pressure with choline chloride? Why does the amplitude of action potential increase in the experimental set ?

In short-  In the experiment, when the neurons are bathed in low sodium fluid but constant osmotic pressure, amplitude of action potential decreased, but duration of action potential increased.

I wanted to validate this with Nernst equation and/or GHK equation .

The increase is action potential amplitude with high extracellular sodium ( more sodium influx,more depolarization ? ) is intuitive?
But again I am confused because the membrane is only slightly permeable to sodium such that increases in extracellular sodium won't really alter the membrane potential enough to generate an action potential.

Also how does the action potential duration decrease in high sodium ?

What should be done if I want to increase duration of action potential while keeping the axons in high sodium bath ?

  The duration of action potential is not the time to reach threshold voltage. It is the overall time the membrane stays depolarized.
  In other words, why are the axons slowly repolarized when bathed in low sodium concentration(and also maintained at constant osmotic pressure with choline chloride ) compared to high sodium bath axons that are rapidly repolarized ?

How do you think the answer would've changed if choline chloride was not used ?

High sodium extracellularly means an increased sodium concentration gradient across the membrane. This means there is a larger driving force for sodium to enter the cell once the sodium channels open at the start of the action potential, and hence a larger depolarization takes place increasing the action potential amplitude. The enhanced depolarization leads to an increased proportion of activated voltage-operated potassium channels that open upon depolarization. When more potassium channels open, more potassium will exit the cell, thereby repolarizing the cell to a larger extent, in turn stopping the depolarization step of the action potential faster. In all, the action potential develops quicker, as the depolarization is increased as well as the repolarization step, and hence the time it takes to execute an action potential is diminished.

Your subquestion as to the small sodium conductance is not valid, as during an action potential it is actually very high.

To increase the action potential duration you can increase the re-polarization step by increasing the extracellular potassium concentration, thereby diminishing the potassium concentration gradient and prolonging the repolarization step.


Why do we feel numbness and an electric sensation in our legs after standing for too long? We have all felt that numbness while standing immobile for a while.It gets difficult to walk.It can also happen if we are just putting some pressure on our legs
Why does this happen?

I'd like to know what specifically happens in the muscular tissue(if that's the origin of this sensation) for us to feel like this

This relates more to nerves than muscles. Each nerve has a small artery supplying it with nutrients and oxygen. A good example is the sciatic nerve, which is the largest nerve in the human body and requires a relatively large artery to supply it with blood:

http://article.sciencepublishinggroup.com/html/10.11648.j.ijcda.20150103.14.html

When we sit in a particular way that causes pressure over that nerve, or stand for a long while in a way that stretches the nerve, we effectively reduce or block its blood supply. This may result in temporary loss of signal leading to numbness, weakness or even temporary paralysis. If the pressure on the nerve is prolonged beyond a certain point, there will be irreversible necrosis of the nerve causing permanent nerve damage. An example of this is when a drunk person sleeps on the floor with pressure on the outside of the knee over the "Peroneal Nerve", causing "Peroneal Nerve Palsy" or "Zenker Paralysis".

https://en.wikipedia.org/wiki/Zenker%27s_paralysis

As for the electric sensation we might feel as a result of nerve damage, the answer is more interesting:

The transmission of signal in the nerves requires variable amounts of energy depending on the type of nerve fibre. Nerve fibres are mainly divided into "Myelinated" and "Demyelinated" ones, with further subdivisions. To put it simply, myelinated nerves have a coating of myeline formed by specialist cells called Schwann cells. Myeline allows the nerve fibre to act as a super conductor to transmit signal faster, but needs more energy to do so compared with demyelinated fibres, which are thiner, slower and more energy efficient.

One of the functions of the super-conducting large fibres is to modulate the pain signal. The damage or loss of these fibres results in "neuropathic pain", which is felt as sharp electric shocks or pins and needles along with many other reported descriptions. This is thought to be the result of the small pain fibres working uncontrolled, leading to the perception of pain without an actual painful stimulus. The super conductors "Myelinated Fibres" are much more vulnerable to injury due to reduced oxygen, while the smaller fibres, some of which conduct pain, are more resilient. This is why we might feel neuropathic pain as a result of reduction in signal rather than due to a painful stimulation. A good example is what happens in an auto-immune disease called Guillain-Barre Syndrome, where the immune cells attack and destroy Schwann cells, leading to significant neuropathic pains as a result of the loss of signal in the corresponding nerve:

https://en.wikipedia.org/wiki/Guillain–Barré_syndrome

Another common example is first degree burns, where the pain continues for a few days following a minor burn due to selective damage of the highly sensitive myelinated fibres leaving the non-myelinated ones intact. Pain improves gradually as the Schwann cells regenerate, improving the signal speed.


Steroid Hormone Signalling Can the lipid-soluble hormones (like steroid hormones) go inside every cell, as their particular receptors are located in the cytoplasm or nucleus of the target cells? Is there anything special on the membrane of the target cells which enables the steroid hormone to know that it has to enter that particular type of cells and avoid others?

(Peptide hormones function through cognate receptors located on the cell membrane of the target cell.)

Note: Since my area of expertise is with peptide hormones, I will offer a partial answer.

Steroid hormones are carried through the circulation by binding to globular proteins. When these hormones are released from binding proteins, the classical route of action is by free diffusion through the cell membrane. This diffusion is due to their aromatic structure. You rightly point out that the classical receptors of these hormones are found in the cytoplasm or nucleus. For example, estrogen signalling as a classic signalling template which has genomic (DNA) and non-genomic (protein) targets to exert its effects.

Non-canonical signalling can occur through at least one G-protein coupled receptor (GPCR). Unlike most GPCR's which are localized to the cell membrane, GPR30 appears to be localized to the endoplasmic reticulum, which means steroid signalling still occurs through canonical means and also this newer pathway.

Then again, there are also steroid effects that modulate ion channels, for example GABA receptors. These are not specific receptors where only a steroid hormone can have an effect, yet they can activate or inhibit the effects (along with other drugs).


Reason Non linear Lineweaver–Burk plot V vs S plot looks like hyperbolic but 1/V vs 1/S plot is not linear at all. Looks like some kind of exponential growth. What can be the reason?

The linearity of a Lineweaver–Burk plot assumes that your system follows standard Michaelis–Menton kinetics.

Not every enzyme system follows Michaelis–Menton kinetics with all the assumptions made in its derivation. There are a number of reasons for non-linear behavior, including cooperativity, substrate inhibition, substrate activation, limiting cofactors, isoenzymes, and non-steady-state kinetics.

Further reasons for a non-linear plot involve experimental issues. Depending on your experimental setup, you may not have accurately measured the initial rates of some of the faster conditions, which can lead to non-linearity of your Lineweaver–Burk plot. If you're operating under conditions which may lead to product inhibition, you might also see non-linear behavior.


Why are there few quail any more in the Northeast of the US? I currently live in southeast New Hampshire and was reading a history of my town and it describes the landscape as having a lot of quail and even partridges. The book said children going to school around 1920 would see lots of quail. The town itself has not changed much from 1920 except that there are fewer farms. The population is about the same. In fact, the population is probably lower now than it was in 1920.

I have never seen a single quail here, and certainly never seen a partridge. I have seen a pheasant on rare occasion. There are a lot of turkeys.

Is this like a Silent Spring thing, they all got killed off by DDT or something? Or is it because of insecticides killing all the crickets, maybe? I almost never hear crickets at night.

Work in the early 1990s (https://pubs.er.usgs.gov/publication/5210546) (https://www.nwf.org/en/Magazines/National-Wildlife/1993/The-Case-of-the-Disappearing-Quail) suggests development (curtailing habitat), climate crisis (and associated water loss), and decline in insect populations (reducing food supply) as possible causal factors.

Insects are an important energy source for birds, generally. They help pollinate plants, which help feed birds, and they are also a food source, themselves. Their loss (https://en.m.wikipedia.org/wiki/Decline_in_insect_populations) particularly hits bird populations hard. Unless we change our agricultural practices, it is predicted that most insects may be extinct within a century. This would decimate many forms of life (ourselves, included with quail and other birds) that depend on them.


How much DNA of mitochondrial origin is incorporated in main cell's DNA? And especially three points :

in which chromosomes is it located (especially for the human case) ?
how do we know about it ?
does the proportion and composition vary a lot from one eukaryot to another ?

Interesting question. I researched this a bit now and the phenomenon is termed "numt" for  "nuclear mitochondrial DNA". This term descrives the transfer of cytoplasmic mitochondrial DNA sequences into the separate nuclear genome of a eukaryotic organism. It seems that most of these sequences are inactive. This list at pseudogene.net has a large number of sequences in a lot of different organisms, for humans insertion between 0,2 and 14,2 kb are listed. Most of these sequences are detected in the deep sequencing projects underway these days and by comparative sequence analysis. An example is this paper, where they found mtDNA on chromosome 1 of homo sapiens, which was still part of the mitochondria in homo neanderthalensis.
For more information you can go to the list of papers I list below, this should be a good starting point:

http://www.ncbi.nlm.nih.gov/pubmed/11369110
http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0020273
http://www.ncbi.nlm.nih.gov/pubmed/15014143
http://www.ncbi.nlm.nih.gov/pubmed/18721785

The papers should all be accessible, if not, let me know.


Automatic cropping of collimated digital X-ray images Do you have any suggestions for a library which offers an algorithm to crop digital X-ray images automatically?

We receive full-size images (43x43cm) from a detector, independent of the collimator settings. If the collimator has been closed to 10x15cm, we need to crop this area. This should be done automatically, so that the user does not even see the full-size image because it contains a lot of information which is not needed.

Now we are looking for a good library which offers such an algorithm. This sounds like a simple task, but depending on the dose and the collimation, it can be pretty hard to detect the collimated area of the image. Therefore, we are looking for a professional solution rather than implementing it ourselves.

Any suggestions?

There is a software package ImageJ which can be used to what you are asking. Depending on your capability and the complexity of what you are doing you can either write a Macro in the program to crop images or you can extend the program in Java and write a custom plugin to do what you describe.

I used this program for years it is a very strong program.


How and where, in the human brain, are memories stored? Background
I am a computer programmer who is fascinated by artificial intelligence and artificial neural networks, and I am becoming more curious about how biological neural networks work.
Context & what I think I understand
In digesting all I have been reading, I am beginning to understand that there are layers to neural networks.  A front-line layer of neurons may receive, for example, a visual stimulus such as a bright light.  That stimulus is taken in by the front-line neurons, each of which produce a weighted electro-chemical response that results in a binary decision to pass an electrical charge through its axon to the dendrites of the tens of thousands of neurons to which it is connected.
This process repeats through layers channeling the electrical signals and focusing them based on their permutations until ultimately a charge is passed to a focused response mechanism such as the nerves that control shrinking of the pupils.
Hopefully I got that correct.
Preamble to the question ;)
Assuming that I am not completely off-base with my basic understanding of how a biological neural network operates, I am beginning to grasp how an input (stimulus) results in an output (response) such as motor movement or reflexes.  That would just seem to be basic electricity of open and closed circuits.
HOWEVER, what confuzzles me still is how a memory is stored.  The analogy to an electrical circuit breaks down here, for in a circuit I can't really stop the flow of electrons unless I dam up said electrons in a capacitor.  If I do that, once the electrons are released (accessed), they are gone forever whereas a memory endures.
So. . .
How the heck are memories constructed and stored in the human brain?  Are they stored in a specific region?  If so, where?

Unfortunately, we are all still "confuzzled" by how memory works. We are far from a complete understanding of how memory is stored and recalled. Nonetheless, we do know a little, so read on.

Your understanding of basic neural function is almost correct. First, an individual neuron will signal through its single axon onto the dendrites of many downstream neurons, not the other way around. Second, I am not sure what you mean by "focusing them based on their permutations," but it is true that neural information can undergo many transformations as it propagates through a circuit. Third, if there is a behavioral outcome of the network activity like a muscle response or hormone release, those effects are mediated by nerves communicating with muscles and hormone-releasing cells. I'm not sure if that is what you meant by "focused response mechanism."

Finally, as you have discovered, the analogy of neural circuits to electrical circuits is relatively poor at any reasonably sophisticated level of analysis. My opinion is that biological systems are often poorly served by being framed as engineering problems. Others will disagree with that, but I think understanding a biological system on its own terms makes many things much clearer.

The key thing missing from the electrical circuit analogy turns out to be one of the keys to understanding information storage in neural circuits--the synapse, the site where one neuron communicates with another. The synapse transforms the electrical signal from the upstream neuron into a chemical signal. That chemical signal is then converted back into an electrical signal by the downstream neuron.

The strength of the synapse can be adjusted in a long-term way by changing the level of protein expression--this is called long-term potentiation (LTP) or long-term depression (LTD). LTP and LTD therefore can regulate the ease with which information can flow along a particular path. As a basic example (that should not be taken too seriously), imagine a set of neurons that represents "New York City" and another set of neurons that represents "My Friend John." If you then happen to be in New York City with your friend John, both of those groups of neurons will be active and synapses between these two networks will be strengthened because they are co-active (see Hebbian plasticity). In this way, the idea of NYC and the idea of John are now bound together.

Where are these neurons that represent NYC and John? We are still not totally clear on this, and the question is complicated because there are many different types of memory. For instance, your memory of how to ride a bike (procedural memory) is not treated the same as your memory of what you ate for breakfast (episodic memory). However, a best current answer is that the hippocampus and its associated regions are important for the initial encoding of memories and the neocortex is where longer term memories are stored. There is substantial communication between these two areas so that memories can be effectively adjusted over time.

Update

In response to Jule's comment asking for some resources, I realize it is important to make the point that the Hebbian model I outlined hasn't been definitively shown. Like with all aspects of neuroscience, there is a lot of good work at the molecular and cellular level and good work at the behavioral level, but the causal link between the two is not so clear. Nonetheless, Hebb's idea is still the mainstream working model for how memory works. Some reading might include:

1) Neves, G., Cooke, S.F., Bliss, T.V.P., 2008. Synaptic plasticity, memory and the hippocampus: a neural network approach to causality. Nature Reviews Neuroscience 9, 65–75.
 A review on hippocampal memory and its relation to LTP/LTD and Hebbian theory. Notes the general difficulty of proving the theory and some ways for experiments to move forward.

2) Lisman, J., Grace, A.A., Duzel, E., 2011. A neoHebbian framework for episodic memory; role of dopamine-dependent late LTP. Trends in Neurosciences 34, 536–547.
 A review proposing an elaboration of the Hebbian model that includes neuromodulatory influence on plasticity and memory process.

3) Johansen, J.P., Cain, C.K., Ostroff, L.E., LeDoux, J.E., 2011. Molecular Mechanisms of Fear Learning and Memory. Cell 147, 509–524.. An excellent review on fear learning and memory with an extensive section on Hebbian theory.

4) Liu, X., Ramirez, S., Pang, P.T., Puryear, C.B., Govindarajan, A., Deisseroth, K., Tonegawa, S., 2012. Optogenetic stimulation of a hippocampal engram activates fear memory recall. Nature. A research article which is perhaps a realization of some of suggestions in the Neves et al review. They use light to reactivate a fear memory. This suggests that activation of the hippocampal network that was active during memory formation is sufficient to elicit the memory.


Why do some mammals not have testes in a scrotum? Coming from an evolutionary approach, Is the only purpose of a scrotum to regulate the temperature of the testes?

Knowing all mammals are warm blooded, shouldn't all mammals have testes in a scrotum?

Having descended testes is a derived characteristic within mammals; monotremes and the Afrotheria (including elephants) all retain the ancestral character state (Kleisner, et al., 2010)2. Among those mammals with descended testes, these can be ascrotal or scrotal. Testicular descent is hypothesized to have only occurred once within Mammalia, with the ascrotal Laurasiatheria. Descended ascrotal testes are found in cetaceans, phocid seals, hippos, tapirs, rhinos, and some bats. Descended scrotal testes are found in horses, pigs, camels, and Carnivora.

Since basal mammals would presumably have to regulate testicular temperature just as much as derived mammals, the temperature regulation hypothesis seems to not hold up. So the real question is: why have a scrotum? One hypothesis has to do with evolution of fast locomotion (e.g., galloping).

According to Frey (1991, 40)4:

  The strong flexions and extensions of the vertebral column during
  gallop should cause intense fluctuations of intra-abdominal pressure.
  Fluctuations of intra-abdominal pressure severely impede continuous
  flow of blood in the abdominal veins. Periodically reduced venous
  drainage resulting in fluctuations of intra-testicular pressure would
  impair the process of spermiohistogenesis, which is dependent on an
  absolutely constant pressure within the testis.

Chance (1996)5 suggests that the temperature hypothesis might represent a secondary adaptation:

  Because in the human male, scrotal testes function optimally at
  temperatures below that of the body, much speculation, and a
  considerable amount of research, has gone into attempting to see what
  (metabolic) advantage might accrue from this lower temperature,
  without considering the possibility that this is a secondary
  adaptation to an enforced external position.

Kleisner, K., Ivell, R., and Flegr, J. 2010. The evolutionary history of testicular externalization and the origin of the scrotum. J Biosci 35:27-37

Frey, R. 1991. Zur Ursache des Hodenabstiegs (Descensus testiculorum) bei Säugetieren. Z Zool Sys Evolut-Forsch 29:40–65

Chance, M.R.A. 1996. Reason for externalization of the testis of mammals. J Zool 239:691–695


Will "circus peanuts" biodegrade, and how? I have a compost barrel, and it is currently staffed by black soldier fly larvae. They eat pretty much anything, which is very satisfying to observe. I put a handful of the candy known as "circus peanuts" in there, and they haven't touched them so far. As you can see following the link, the ingredients are:

  sugar, corn syrup, gelatin, pectin, soy protein, food coloring, and artificial flavor

I assume these things are biodegradable, being "food", but if my star decomposers won't eat them, then what will? What can I expect to happen to these items in the compost heap?

As a follow-up question, was this a bad idea? Should I take them out and throw them away, so they can rot in a landfill instead?

Time answered this question. I didn't do anything to the candies, but moisture eventually worked its way in. After a week or so, they were showing definite signs of breaking down. After two weeks, I couldn't see a trace of them!


Is this a common garden spider? Spotted this outside my window today. Looks like an orb-weaver, but I can't tell whether it's a regular garden spider or not. What species could this be?

This picture was taken in Bangalore, Karnataka, India.

Looks like an orb-weaver ..

I agree! This spider definitely belongs to the genus Argiope, though, due to the angle of your provided image, it's difficult to be more specific than that (if I had to guess, A. anasuja).

The confidence in my genus suggestion comes from the stance the spider is displaying. Spiders within the Argiope genus carry a common nickname of "signature spiders", due to the fact that they'll intertwine additional webbing within their web, called stabilimentum, that, given the design of the support webbing and the spider's stance, will allow for the spider to appear much larger than it really is.

If you can provide an image that reveals the top of the abdomen, a more confident species suggestion may be possible.

  Is this a common garden spider?

From the looks of it so far -- yes, this is a common garden spider.


TFBS predictions for yeast and pombe? Are there any resources out there for TFBS (transcription factor binding site) predictions for the yeast (S. cerevisiae) and S. pombe genomes? Even if these are only de novo predictions, I would like to have access to them.

Try YEASTRACT http://www.yeastract.com/

  YEASTRACT (Yeast Search for Transcriptional Regulators And Consensus
  Tracking) is a curated repository of more than 48333 regulatory
  associations between transcription factors (TF) and target genes in
  Saccharomyces cerevisiae, based on more than 1200 bibliographic
  references. It also includes the description of 298 specific DNA
  binding sites for more than a hundred characterized TFs.


Strategy for tree and shrub identification I often find it difficult to identify trees and shrubs even though I have many handbooks and manuals on trees and shrubs in my area (New England). The typical problem is that the species is not in the handbook, or that it is very similar to many other species. For example, hawthorns have many different species which are very similar to each other and most books do not exhaustively list the different hawthorns and their distinguishing characteristics, instead just listing one or two of them.

Web sites are even more fragmented than books and are usually a lot less detailed than the books so even if I search around, the results are often useless.

Am I going about this wrong? What improvements can I make to my strategy for identify trees and shrubs?

Species ID books with pictures, or photos, will generally never be comprehensive enough to include all species, although with some there will be additional information it the text that will give details about other related species, varieties, hybrids or cultivars.

Importantly look for ID books that include an ID key, generally at the start, and learn how to use it. They are usually accompanied with a good explanation of how it works.

The key takes the form of

  Does it have this...?

  If it does go to [3]

  If it doesn't go to [7]

And so on, making successive distinctions until you end up with the species.

They can take some getting the hang of, and you need to know the botanical terms that they refer to.

Also importantly, if you don't already have and use one, you must have a decent hand lense, or magnifying loupe, that you take with you everywhere. Often the deciding features can only be properly be assessed when looking close up, and you need to get to know what the species you are familiar with look like under the lense.

An experienced ecologist friend, an expert in flora and fungi, has a couple of books that have no images in at all, it is just the species ID key, that he takes with him when he is surveying. Granted he already knows his species very well, but you can't remember everything all the time and so you need a book that can tell you the final distinguishing features, even if it is text.

But again a hand lense is a good place to start. My favourite is an Eschenbach 10/40 Pocket hand-held magnifier from Germany http://www.eschenbach.com/cdd40611-ceda-4188-a5c3-882565859296/products-hand-held-magnifiers-pocket-detail.htm

Someone gave this site http://dendro.cnre.vt.edu/dendrology/syllabus/key/key1.cfm?state=&zone= as a good resource for trees in the US


Why do neurons loose the potential to regenerate and reproduce in adult animals? I have read in several books that neurons in the central nervous system loose the power to regenerate after some developmental stage but why do they? Can we artificially induce regeneration?

To answer the first part of your question: In order to regenerate, the neurons need to divide. In order to do that they need to round up so that they can form a mitotic spindle that sorts the chromosomes and makes sure that each daughter cell gets exactly one copy of the genome. For most animal cells this genome sorting only works in rounded cells, which is why neurons need to round up before they divide.

However for a Neuron, rounding up would mean that the neuron needs to retract its axon as well as all its dendrites. To do so is physically impossible for most neurons simply because of the length and complexity of the axon and dendrites (the axons of human motor neurons can be more than a meter long). See also the image below.

Even if retracting the axon and dendrite network was possible, this would mean that the neuron would lose its function completely because it would lose all connections to other neurons and with them all information it has stored. Thus, from an evolutionary standpoint it does not make sense to regenerate a neuron once it has matured and started to form connections with other neurons.

That being said, despite the fact that matured neurons cannot divide any more, our brain and our nervous system retain a lot of regenerative potential:

Provided that there is little scarring at the wound, a nerve fiber (consisting mainly of axons of neurons) can regrow because the neurons don't necessarily die when their axon is cut and they can regrow a new axon. The main difficulty for regeneration in this case is for the axon to find the path to its destination. Therefore it is important that there is minimal scar tissue (glial scar) because scar tissue prevents regrowing axons from finding their path.
The brain retains some neural progenitor (stem) cells that are able to differentiate into new neurons even at old age (but not as many stem cells as other tissue).
When parts of the brain are damaged, other regions can often take over that functionality (for example by by rewiring their axons and dendrites) a process called neuroplasticity. For example, people can often re-learn to speak after a stroke.

As to the second question: Using stem cell technology it is possible to grow fresh neurons in cell culture. In principle, these neurons (or rather their progenitor cells that mature into neurons) can be implanted in order to regenerate nervous tissue in the central nervous system. However, this cannot solve the problem that once the neurons are dead, even a new neuron that replaces the dead one cannot recreate all the connections that the old one had.
Replacing neurons is like replacing the hard disk of a computer. All information is lost. Therefore, current research on the therapy of spinal chord injury focuses on the prevention of scarring in order to help the existing neurons to regrow the axons and reconnect the body with the brain.

Edit: added references.


Does documentation exist that shows the evolutionary connection between common horses and the okapi? I'm trying to put together some documentation on the relation between the common (modern) horse and the okapi. I've found a tree that shows that connection but it has no references. I'm hoping that someone has documented this connection somehow.

tolweb.org is your friend!

Because the okapi and the horse are not so closely related you will probably find several articles on the subject. Okapi belongs to the order of artiodactyla while the horse belongs to the order of perissodactyla. They are both mammals, eutheria, ungalata (superorder).

Here is the tree of the eutheria (within the mammals) from tolweb. You have approximatively 150 references. You can click on perissodactyla and artiodactyla and you will find 100 more references.

These two references may help you (I only read the titles)

Graur, D., M. Gouy, and L. Duret. 1997. Evolutionary affinities of the order Perissodactyla and the phylogenetic status of the superordinal taxa Ungulata and Altungulata. Molecular Phylogenetics and Evolution 7:195-200
Xu, X. F., A. Janke, and U. Arnason. 1996. The complete mitochondrial DNA sequence of the greater Indian rhinoceros, Rhinoceros unicornis, and the phylogenetic relationship among Carnivora, Perissodactyla, and Artiodactyla (plus Cetacea). Molecular Biology and Evolution 13:1167-1173


If a hand was suddenly chopped off while holding something, would the severed hand still hold a grip? This question was inspired by Star Wars Episode V: The Empire Strikes Back. In it, Luke Skywalker is battling Darth Vader in a lightsaber duel. Vader manages to win out and chops off Luke's hand, which is holding the lightsaber.

My question is: would his severed hand still hold a grip on the lightsaber? Or would it fall slack and lose grip, likely separating as it falls into the pit?

While this question is from a sci-fi series with a fantasy means of dismemberment, it might apply to other real-world situations (for instance, an industrial worker holding a tool while a piece of machinery accidentally severs his hand).

(Disclaimer: I have no personal or medical experience of cutting off hands, or any other body parts, so this is purely theoretical.)

It seems unlikely, since most of the muscles that provide the gripping force are in the forearm and are transmitted via tendons in the wrists. Try gripping something forcefully* and notice which muscles tense up, and how the tendons on the inside of the wrist transmit the force.  Cutting the tendons would eliminate the force.

Of course anyone who's done much fencing knows that you don't grip with too much force, because that interferes with the fine control provided by the fingers.


What is this insect in a cocoon climbing a web? I found this thing hanging from the framework of my garage yesterday:

The size of the object in the picture was about .75 inches tall by maybe a quarter inch wide. This was taken yesterday in a suburb of Jacksonville, Florida, US in late evening (8:30 pm?).

He was (apparently) using his mouth-parts to draw in what appeared to be a strand of spiderweb, and in about 10 minutes had drawn himself upward, towards the top of the garage framework, a total distance of about two feet.

An additional question would be what is that he's in, a cocoon? a piece of bark or something being used like a hermit crab uses a scavenged shell?

Any help would be appreciated!

That is, probable, a Psychidae (Lepidoptera), commonly known as bagworms. They build those "bags" with pieces of wood, twigs and leaves, and they protect them from predators and parasitoids. One possible species for Florida is this one: https://en.wikipedia.org/wiki/Evergreen_bagworm


Why doesn't infection with Clostridium Tetani immunize you? What Immunity to COVID-19 Really Means - Scientific American

  It is less clear what those antibody tests mean for real life, however, because immunity functions on a continuum. With some pathogens, such as the varicella-zoster virus (which causes chicken pox), infection confers near-universal, long-lasting resistance. Natural infection with Clostridium tetani, the bacterium that causes tetanus, on the other hand, offers no protection—and even people getting vaccinated for it require regular booster shots. On the extreme end of this spectrum, individuals infected with HIV often have large amounts of antibodies that do nothing to prevent or clear the disease.

Clostridium Tetani - StatPearls - NCBI Bookshelf

  It should be noted that infection with C. tetani does not provide immunity, and thus, all patients with the diagnosis of tetanus should receive immunization immediately with three doses of tetanus and diphtheria toxoid.

There is a big difference with tetanus compared with other infections. The amount of toxin that produces tetany is extremely tiny. Even a small infection that the immune system has yet to react to can be lethal.
To produce a long-lasting response against the bacterium would require a lethal number of bacteria.

Vaccination with the toxoid results in antibodies against the toxin, not the bacteria.


Why would taking antibiotics increase stamina and energy? I often hear that people who are taking antibiotics experience wild fluctuations between feeling full of energy and completely alert but soon after feeling impossibly fatigued and sick.

Does this have anything to do with the antibiotics being used by the body as anything? For example as a hormone or as a source of nutrition?  Is this this a reported side effect when used for other infections?

I have never heard about this phenomenon from my patients or professors at the Medical School, but this is a possible mechanism that comes to my mind.

One of the classification for antibiotics takes consideration the effect on bacteria. Two possible effects are either stopping the proliferation (and letting the immune system to kill those that are currently present in the body) or killing bacteria directly.

The second approach is obviously more effective but has one big disadvantage: massive death of bacteria leads to the massive release of their toxins that are normally trapped within they bodies (so-called endotoxins). The symptoms you describe as "impossible fatigue" match exactly the symptoms of bacterial intoxication -- and this can increase upon the antibiotics intake.

Depending upon the bioavailability and pharmacokinetics some antibiotics might not kill all bacteria "on the first run" and the symptoms of intoxication recur several times with decreasing severity of manifestations.


Output of clustalo on (1.2.1) on ubuntu 14.04 I am trying to align the following 8 sequences using clustalo on ubuntu terminal using the following command. But I am not getting the right output.

clustalo -i sequence.fasta -o output.clu

My input file issequence.fasta with 8 sequences I downloaded from BLAST

My output file output.clu

The output I was hoping for outputOnline.clustal

Also I would appreciate if some can tell me how to share this kind of data in a question because obviously the way I have done is doesnot seem appropriate.

You just need to specify the output format with the outfmt flag.

clustalo -i sequence.fasta -o output.clu -outfmt=clu

should give you the desired output.

How to share data?

Try using an abbreviated example which people can copy&paste, for longer data you could use something like http://pastebin.com/ but the URL might expire.

    gi|1709777|sp|P51780.1|PRIO_TRIVU MGKIQLGYWILVLFIVTWSDLGLCKKPKPRPGGGWNSGGSNRYPGQPGSPGGNRYPGWGHPQGGGTNWGQPHPGGSNWGQPHPGGSSWGQPHGGSNWGQGGYNKWKPDKPKT

    gi|1709773|sp|P52114.1|PRIO_MUSPF MVKSHIGSWLLVLFVATWSDIGFCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQWGKPSKPKT

    gi|1709774|sp|P49927.1|PRIO_PIG MVKSHIGGWILVLFVAAWSDIGLCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQWNKPSKPKT


Is this a variety of banana slug (Ariolimax columbianus)? (California) These very dark (dark grey to black) banana slugs are an anomaly. I live on the north coast of California and see many slugs every day. These particular slugs I find only on the west-facing headlands at the ocean. There is no cover from the sun since there are no plants taller than about a foot. Also these particular slugs are never longer than 2-1/2" to 3". Are they a sub species, a variety, or something else? Thanks for taking the time to answer.

Banana slugs are comprised of three species:

Ariolimax californicus
Ariolimax columbianus
Ariolimax dolichophallus

Ariolimax columbianus, or the Pacific banana slug is known to have black spots, sometimes so large as to cover their entire body (Source). This is certainly the genus of the slug you've shared.

At times, you could be seeing a Black slug which is well-established in Washington and Oregon. I only include this information as I have noticed this species occasionally in Southern British Columbia and wondered if it was the same species as the Banana slug. It isn't. The picture you've attached is not a Black slug (note the pronounced frills on the back of the Black slug specimen)


Do there exist publicly available Genome sequences of a family? I would like to explore the genome sequence of a publicly available genome sequences of a family (like mother, father, son, daughter...). If such human genome sequences are not publicly available at least any animal's family data is also OK. :)  I am not a biologist, but aims to just understand things more clearly.

I know that 1000 Genomes has sequenced Mother-Father-Child genomes from populations around the world (I think at least some of these samples were obtained from HapMap) and their data is publicly available by following the links in their website.


How does a pinched nerve cause pain (at the molecular level)? Is this due to pressure differentials in the surrounding tissue? (Is it possible to have a pinched nerve without compression of the surrounding tissues, and does this cause pain?)

What are the molecules/cell types involved in this process? Is the pain dependent on the compression of axons from mechanosensitive or nociceptive neurons?

Typically nerve compression or a "pinched" nerve is due to inflammation in the tissue through which a nerve passes. The gap is already quite narrow so any inflammation is quite potent. Inflammation causes you to feel things as more painful (hyperalgesia). In a similar way to how of you burn your hand then poke it, it hurts, when cells are damaged the receptors surrounding them are sensitised to be more reactive. Binding of many ligands involved in inflammation leads to higher than normal sodium influxes which means you feel pain as this impulse is sent. I could be a lot more detailed but not sure what level you want, however for much more detail see this review.


How evolutionarily conserved are UTRs? Coding sequences of genes have a certain degree of evolutionary conservation, so that comparisons based on sequences (BLAST, HMMER etc) can be informative. Generally speaking, the more two species are phylogenetically close to each other, the more their genes will be similar to each other. To add to that, different genes will have different degrees of sequence conservation - for instance, histons are very conserved and so on.

Do these considerations hold true for untranslated regions of genes (both 5' and 3')? To what extent can an alignment of UTRs be meaningful? Are there any very conserved UTRs as there are very conserved CDS? I know that there are some conserved motifs in 5' and 3'UTRs, but what about the overall sequence?

This is a question specific to the organism, assembly, and genes of interest to you. You can answer this yourself with a bit of elbow grease.

You could measure mean phyloP or phastCons conservation signal over UTR-annotated intervals, and compare it against the background mean conservation signal over random, mappable regions of the genome of similar length (i.e., calculate the mean and variance in UTR length and sample mappable regions of the genome for intervals with the same distribution).

At a very basic level, you could perhaps apply either the U-test or Wilcoxin rank-sum test, depending on your assumptions of dependence, whether your background does or does not include UTRs.

One source of phyloP and phastCons signals for various genomes and multi-genome alignments is UCSC Goldenpath. For example, here are phyloP 100-way alignments to hg38. You might get UTR annotations from Gencode, assuming you are working with human or mouse. To do interval overlaps and mapping/statistics operations, you might use gff2bed, bedops, and bedmap in the BEDOPS toolkit(*), and then use R to do statistical tests.

Disclaimer: I am one of the authors of the BEDOPS toolkit.


How does vasoconstriction retain heat? I am reading on vasoconstriction on wikipedia. The article states that:

  When blood vessels constrict, the flow of blood is restricted or decreased, thus retaining body heat or increasing vascular resistance.

Why/How exactly is the heat retained when blood flow is decreased? Isn't it the case that when things slow down they generally get colder?

Think of the body as a heat-sink. We can let off heat by using our fluid exchanges – namely, blood and sweat. When we exercise, sweat cools us off through evaporative cooling. When we’re not exercising or in warm weather, we’re generally not sweating, but we’re still exchanging heat with our surroundings – after all, the metabolism is still active, we’re still “burning energy,” and our skin never reaches air temperature nor does our core cool to the temperature of our skin (so some kind of heat exchange has to be happening). How can that be, when there’s no obvious mechanism to carry away our heat as in the case of sweating?
The answer to this lies at the heart of your question. Human thermoregulation is largely thanks to our blood flow and vasodilation:

“Skin blood flow in adult human thermoregulation: how it works, when it does not, and why.” Charkoudian. N. Mayo Clin Proc. 2003.
Cutaneous sympathetic vasoconstrictor and vasodilator systems also participate in baroreflex control of blood pressure; this is particularly important during heat stress, when such a large percentage of cardiac output is directed to the skin. Local thermal control of cutaneous blood vessels also contributes importantly—local warming of the skin can cause maximal vasodilation in healthy humans and includes roles for both local sensory nerves and nitric oxide. Local cooling of the skin can decrease skin blood flow to minimal levels.

In essence, your core “wants” to stay warm. If the air around your skin is comparatively warmer, cutaneous blood vessels will dilate to accommodate a higher flowrate, allowing more blood to engage in heat transfer. The opposite is true for air that is comparatively colder, and the relationships between cutaneous blood flow, sweating, and local skin cooling can be tested experimentally:

“Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans.” Wingo et al. J Appl Physiol. 2010.
In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34°C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20°C (2 sites) or maintenance at 34°C (2 sites). In both protocols, individuals were then passively heated to increase core temperature ∼1°C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 ± 1.2 vs. 1.0 ± 0.7 mg·cm−2·min−1·°C−1 for the effect of decreased skin blood flow, P = 0.01; 1.2 ± 0.9 vs. 0.07 ± 0.05 mg·cm−2·min−1·°C−1 for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 ± 0.4 vs. 37.6 ± 0.4°C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature.


The Evolution of Fruits I was cooking rice this morning and was fascinated by the color and it's sweetness and began to ask...

How did fruits evolve?
Did they come from a single cell?
Which cell?
How did that cell branch off from  the cell that became animals? Is there any evidence for this kind of thinking or just a lotta theories? How did we get rice, mangoes, beans, orange, coconuts, peanuts, apples, bananas, if there is no "Designer", where did ALL these come from and how did they evolve?

Fruit did not evolve from a single cell( except in the sense that plants did)  it evolved from seeds and their casing in angiosperms. Fruit is a means to disperse seeds. This will get you started on the different methods of seed dispersion.
https://www.britannica.com/science/seed-plant-reproductive-part

By enclosing their seeds in material animals want to eat, plants get animals to transport their seeds long distances and deposit them in a warm pile of fertilizer. Sugar is the easiest macronutrient for plants to produce so that is the what they pack their fruit with. animals tend to eat new growth which often contains seeds so it is easy to see how animals with seeds tough enough to survive digestion (which many seeds do) would quickly spread. Any adaptation that made animals more likely to eat these parts and spread their seeds would likewise spread.

I suggest familiarizing yourself with basic plant phylogeny first, since if you had you would know only one group of plants produce fruit, and so would not have asked half your questions. So please go do a few minutes of research and come back with a more coherent question.

If you want a complete retelling of the entirety of plant evolution you can do that yourself, show a little initiative and start here.

http://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-14-23

https://www.accessscience.com/content/plant-phylogeny/524400

Also rice is not a fruit. It is the plant's seeds you are eating, it did not evolve to taste good, you evolved to think it tastes good becasue it is nutritious, in much the same way meat tastes good. You are essentially murdering their offspring.

I also suggest learning what a theory is.


How long do Ziehl-Neelsen stained samples keep? I have acquired TB slides from my city's health center that are supposedly acid-fast bacteria (AFB) positive. However, when I took a look at it, I see basically no carbol fuchsin stains.
They were individually neatly folded in paper. When I opened them, the stains were slightly wet with immersion oil, facing down. So far, so good (page 6). I've been later informed that these samples were prepared Q1 2019. Based on my research, the staining solutions themselves last up to 12 months (page 33). I can't find any data on how long a stained sample would keep though.
Do they decolorize over time? I expected the AFB to be bright, or at least slightly pink, but I see no such thing. I do see bacilli, though all of them are nearly transparent/methylene blue in color.

Here are some sample images. The first 2 are how I expected AFB to look like, while the next 2 are what I captured (and I think should contain AFB). The last pic is a 10um/div calibration slide for reference.

This TB study might help you: external page
Briefly, they used 6 to 19 months old samples of mostly bad quality (due to their age). The last sentence of the quote below sounds promising though.

The 12,543 sputum smears stored at the national TB reference
laboratory for 6 to 19 months were stored at room temperature in a
wooden slide box without a cover slip. Most of them had lost their
stain reflecting the counterstaining with methylene blue. Restaining
of 436 doubtful slides by ZN gave disappointing results throughout [...]
After a 6 to 19 months storage of ZN stained sputum smears in a
non-air conditioned atmosphere, the bright red color of eggs due to
carbolfuchsin had virtually disappeared. [...] In such case, the ZN restaining of sputum smears allows to rediscover AFB that were discolored.

When I did this the last time, we used fresh and few months old samples which looked similar to the first of your images. Just have a look at the paper, I guess.


If the top epidermal layer is burned away, what is it replaced with? If the squamous (top) layer of epidermis, or skin, is burned or damaged in another way, will it then be replaced by the next layer of below?

Also, from where does the basal membrane originate? Does it regenerate from a different layer of cells?

The epidermis is a four- or five-layered epithelium. The top layers are squamous whereas the bottom ones are more columnar (http://en.wikipedia.org/wiki/Epidermis_(skin)). The lowest layer is separated from the dermis by the basal membrane (a.k.a. basal lamina, basement membrane).

The process of wound healing in skin is extremely complex and obviously depends on the individual wound and how many layers are destroyed. There is a lot of detail on Wikipedia: http://en.wikipedia.org/wiki/Wound_healing.

If the basement membrane is not disrupted, there are two main components as a rule of thumb: 1) outwards-inwards migration, i.e. cells surrounding a wound will migrate into the wound. 2) bottom-upwards differentiation, i.e. the bottom-most layer contains replicating cells which will differentiate and squamify to regenerate upper layers.

Something like this (picture modified from Wikipedia):

If the wound is bleeding, this means the basement membrane is disrupted and the dermis underneath is also wounded (the epidermis itself contains no blood vessels). In this case, the dermis needs to regenerate first, in a process which is probably similar as described above. Simultaneously, the bottom-most epidermal cell layer will proliferate to close the gap, and then deposit new basement membrane. Remember that the basement membrane is a mesh of proteins, not an actual cell layer.


Choosing the best assay for my experiment? Which of the following assays can be used to determine whether cell death specifically due to apoptosis has occurred in a given cell sample? Choose all that apply.

WST-1 Assay
Caspase Colorimetric Assay
Trypan Blue Staining

Which of the following assays can provide direct information about the plasma membrane integrity and/or morphological features of apoptotic cells? Choose all that apply

Annexin V-FITC / Propidium Iodide staining.
WST-1 Assay
Caspase Colorimetric Assay
Trypan Blue Staining
Wright Staining

My knowledge is very limited with these assays. I know Trypan Blue is used to measure a cell's viability, with dead cells stained blue. Wright Staining is used to study the cell's morphology and makes fragmentation visible. Caspase color and the WST assay seem very similar to me. Both measure cell viability with spectrophotometry.

Necrotic cells could be trypan blue positive. WST-1 Assay could reflect cell number by measuring mitochondrial dehydrogenase, therefore, you could not know how many cells die in dishes. When you define apoptosis in your experiment as caspase dependent cell death, measuring caspase activity is the best.

PS

Trypan Blue Staining actually is a method to see membrane integrity.


Barr body. How does it work? Barr's body is a spiral X chromosome. If I'm not mistaken, one random chromosome (a healthy woman) is inactivated in each cell. Which X chromosome is inactivated in a given cell is random. I've heard the example of a tricolor cat. The patched coloring is caused by the fact that  cells responsible for the color of each patch contain another inactivated X chromosome.

But what if a girl is a carrier of the Daltonism gene, why isn't she sick if a chromosome with this gene can be inactivated in some cells?

Like you said the sexual X chromosome inactivation is random in each different cell, this means women have some cells with the maternal x chromosome active and others with the paternal x chromosome active. Now if a woman carries the daltonism gene mutation (heterozygous for color blindness) she can actually manifest signs of the disease if the retinal cells randomly silenced the healthy x chromosome instead of the mutated one in more cells compared to the opposite pattern of silencing (meaning she can present daltonism out of pure bad luck).

It is worth mentioning that the magnitude of this disease will never be as strong as it presents itself in males since women (even the unlucky ones who present signs of daltonism) will always have the protection of a certain percentage of retinal cells with the healthy x chromosome active. The only way a woman could have classic daltonism to the same extent as a male is if she presents the color-blindness gene mutation in combination with Turner syndrome.

In conclusion recessive X-linked diseases aren't "everything or nothing" since woman could present signs in function to the number of cells that randomly inactivated the healthy X chromosome. They will fully express themselves in males all the time though.

References:

Scitable by nature education - Q&A

X chromosome inactivation - Nature education


What might earlier versions of caddisfly shelter-building behavior have looked like? The caddisfly has an amazing ability to build armor for itself by using a self-produced underwater glue to hold together pebbles: https://www.youtube.com/watch?v=Z3BHrzDHoYo.

How could this behavior and the ability to produce the glue have evolved? The survival advantage of the current level of the caddisfly's ability is clear, but how were the incremental stages advantageous? How could it have developed its armor-building ability without a strong enough glue? And how could it have developed a stronger glue without the armor-building ability that would make it useful?

My guess would be that before it was building a full shell like it does now, it started just by holding a pebble or two to itself. Then perhaps the bodily fluid that is now used as glue gradually increased in stickiness and helped the organism keep hold of the rocks or keep them together. It seems, however, like any modest amount of increase in stickiness that could occur due to mutations wouldn't have been enough to keep the rocks together.

Your intuition seems fairly correct. Mouro et al 2016 show some findings relevant to your question...

Caddisflies have been around for a very long time. Much of the fossil record of their existence is of preserved shelter cases rather than the insects themselves.
Early cases seem to be made up of more variety of materials, whereas selective cases made of very specific materials are observed more recently in the fossil record and today. This suggests that they first just collected random pebbles and organic materials, and later evolved more refined construction techniques.

As far as evolution of their silk, I think it's important to recognize that these insects are closely related to Lepidoptera, the moths and butterflies. Many Lepidoptera species, like caddisflies, spin silk cocoons as part of their development cycle, so it can be inferred that the silk and many of its properties precedes any construction behavior using other materials.

Mouro, L. D., Zatoń, M., Fernandes, A. C., & Waichel, B. L. (2016). Larval cases of caddisfly (Insecta: Trichoptera) affinity in Early Permian marine environments of Gondwana. Scientific reports, 6, 19215.