what if there is a door for which our immune system has no key? And as a B cell matures, it develops the ability to determine friend from foe, developing both
  immunocompetence -- or how to recognize and bind to a particular antigen -- as well as
  self-tolerance, or knowing how to NOT attack your body’s own cells.
  Once it’s fully mature, a B lymphocyte displays at least 10,000 special protein receptors
  on its surface -- these are its membrane-bound antibodies.
  All B lymphocytes have them, but the cool thing is, every individual lymphocyte has
  its own unique antibodies, each of which is ready to identify and bind to a particular kind of antigen.
  That means that, with all of your B lymphocytes together, it’s like having 2 billion keys
  on your immune system’s keychain, each of which can only open one door.

This is what Hank said in Crash course. So the b cells, each are having several unique antibodies and I also saw that this is true for T cells too and the dendritic cells  look for a helper T cell that can bind the parts of the intruders which the dendritic cell has presented on its membrane.

my question is

What if there is no antibody in any cell against an antigen?

Does the immune system has antibodies against all antigens in the world?

What happens if an antigen came into our body which has no antibody matching for it?

The Native Americans and smallpox

First I want to note that some of the posted answers are not quite accurate. For example, smallpox ravaged the Native American population because they did not have high-affinity MHC molecules for it, which is an evolved trait. MHC molecules must be capable of binding to a large class of peptides, at least weakly, to allow their presentation. There are only a finite number of MHC alleles in a given individual, and they tend to represent the most commonly found classes of foreign organisms.

The Native Americans were equally capable of creating anti-smallpox antibodies as any European, but that process was significantly slowed down due to not having MHC alleles which promote the presentation of smallpox, allowing the virus to accumulate to lethal levels before a sufficiently mature immune response could be mounted. You can bet that the survivors were the ones with MHC alleles that promoted rapid recognition of the virus!

Somatic hypermutation and affinity maturation

The way antibodies work is, B cells undergo both genetic recombination and an intentionally increased mutation rate called somatic hypermutation. This results in a virtually uniform distribution of new antibodies. These new antibodies are actually pretty bad at binding antigens, and at best, only roughly approximate them. This is one reason the first exposure takes so long to eradicate. When an antibody that weakly matches is found and the number of B cells rise, some of them begin to induce additional mutations to their antibody, a process called affinity maturation. The mutations that result in breaking the antibody end up discarded (those B cells die), whereas those that have an even stronger affinity result in the clone of B cells being positively selected for. This goes on and on until the resulting clone of B cells produce extremely high-affinity antigens.

The result of this is that virtually any possible "door" will have a "key", even if it is poorly fitting. Over time (and subsequent exposures), the key is fine-tuned. The only way a persistent antigen could evade an immune response, short of interfering with the immune system is if the antigen is extremely similar or identical to a self-antigen.

Some pathogens can avoid an immune response in indirect ways, such as frequently changing exposed antigens either by switching genes or through rapid mutation, covering the cell surface with self-antigens or innate, non-protein material, tucking conserved regions that act as epitopes deeply inside a protein, releasing molecules that inhibit the immune response, etc.

Foreign antigens resulting in production of anti-self antigens

An interesting thing to note is that, even if the antigen is similar to self, it will still often be detected. This can be highly problematic because selection against anti-self antibodies occurs when the B cell is first developing, during somatic hypermutation, but not during affinity maturation. A weakly binding antigen that is similar to a self-antigen may then stimulate the production of anti-self antibodies since the antigen is different enough from self that B cells specific to it are not negatively selected, but similar enough to self that the changes in affinity maturation are sufficient to convert it into an anti-self antigen (in other words, an antibody x steps away from targeting self-antigens results in negative selection, but affinity maturation results in y changes to the antibody, where y > x). This is one reason why some viruses can trigger auto-immune diseases.

Answering your questions directly

  What if there is no antibody in any cell against an antigen?

If for some reason no antibody were even had the slightest affinity for an antigen, then there would be no problem, and a pathogen would trigger an immune response because of another antigen. If for some insane reason every single antigen on a pathogen (there are many) was not even slightly matched, then no humoral immune will be invoked. There still may be a cellular immune response (e.g. for viruses), and the innate immune system would still be active.

  Does the immune system has antibodies against all antigens in the world?

The immune system has antibodies that bind a wide range of antigens, albeit weakly, and with high overlap. As a result, you could say that all possible antigens that are not too similar to self are countered by antibodies with at least some level of affinity. There is only a finite number of possible antigenic peptides, and of those, all that's needed is a weak interaction to trigger a full-blown adaptive immune response.

It's like going to an ophthalmologist. They don't have lenses for all possible refractive indexes, but they do have enough samples that, by trying them out, you can see which ones improve your vision. Going through this process allows gradual improvement, and eventually they are able to proscribe a perfect match.

  What happens if an antigen came into our body which has no antibody matching for it?

A single antigen, as opposed to a pathogen with many antigens? Ignoring the cellular immune system, nothing would happen. It would be treated virtually identical to self-antigens (i.e. it would be ignored). Depending on how the pathogen behaves, it could be wiped out by the rest of our immune system, contained in a local cyst, or even result in a lethal infection.


Red and yellow insect found in kitchen in Conrad, Montana (USA) Beetle found in our kitchen in Conrad, Montana (USA) on 3/13/19:

This appears to be a stink bug in the superfamily Pentatomoidea of the true bugs (i.e., order Hemiptera).

Specifically, your specimen appears to be Perillus bioculatus or the two-spotted stink bug.

 Photo Credit: Margarethe brummermann (2008)

You can see additional photos including those demonstrating the species's various yellow vs red color morphs here.

According to the Integrated Plant Protection Center at Oregon State University [my emphasis and links]:

  Mature nymphs of the two spotted stink bug are about 8 to 9 mm long. Adults range in length from 10 to 12 mm. Nymphs may [be] pale yellow or reddishorange with a distinct black "Y-shaped" marking on the pronotum and two black spots on the thorax.

According to Wikipedia, this species is usually a beneficial predator (especially of the Colorado potato beetle), but early nymph stages feed by sucking on potato stems. The trade-off, I would guess, is worth it.

In fact, the color variation in this species (namely the shift from white/yellow to red) that my earlier link shows photos of is a result of a higher diet of potato beetles. [Source, taken from p 99 in McPherson's 1992 book The Pentatomoidea (Hemiptera) of Northeastern North America].

 Source: bugguide.net

Their range, according to bugguide.net is southern Canada, the U.S. and into Mexico.


Do plants absorb toxins from the soil? Consider a plant like Aloe Vera that grows up in a toxic environment where the concentration of pesticides, and materials like lead, mercury, cadmium, arsenic etc is very high(e.g. Marshland dumping yard ). Would that mean that the extract from these plants would contain all these toxic elements.

Not "all of them". But yes, plants suck up water from the soil, with everything dissolved in this water - nutrients, heavy metals, poisons. And also they breathe air, and absorb stuff via this route.

There probably are some toxins which will not enter the plant, because their molecules are too large and/or fragile. For example, should a plant root come in contact with snake venom, I cannot imagine that any venom will end up stored in the plant leaves.

Plants also have their own metabolism, so they will change/deactivate some toxins. I've seen claims that some plants "purify" formaldehyde, although I don't trust the sources enough to be sure of that.

But the smaller the poison molecule, and the less similar to stuff which is usually digested in nature, the more likely that it will enter the plant and stick around instead of being broken down. The heavy metals you mentioned are prime candidates. If they are present in the groundwater - or also lead from air pollution, before we banned leaded gasoline - they end up in plants, including food plants. And mushrooms are even more at risk.

Growing food near waste dumps is a known problem in farming, and sometimes makes the news, for example here:
http://bigstory.ap.org/article/mafia-toxic-waste-dumping-poisons-italy-farmlands


Prokaryotic Ribosomes During bacterial protein synthesis, when ribosomes attach to the cytoplasmic membrane and form a polysome, to what molecule are the ribosomes attaching? Is the polysome held to the cytoplasmic membrane by just a single connection between one ribosome and the particular attachment molecule?

According to Smith et al., 1978, bacterial ribosomes don't necessarily bind directly to the membrane, but through the nascent chain, in which case nothing is truly attaching to anything..


Relaxing Eyes when using Virtual-Reality-Glasses? Accommodation is the process by which the vertebrate eye changes optical power to maintain a clear image or focus on an object as its distance varies (eye focusing). For distant vision, the ciliary muscle must relax and the eye’s crystalline lens is stretched out.

When using a Virtual Reality Device (Occulus Rift, Samsung VR, Sony VR, Google Cardboard etc.) the eye has to focus on the screen that is only a few centimeters away from the eyes. I am aware of the Vergence-Accommodation Conflict. Yet I ask myself,

Is the ciliary muscle relaxed or contracted when looking at a (virtually) far distant object projected on the LCD of the VR-Device?

The eyes cannot focus on something a few centimeters away. The average maximum distance where the eye can still focus is 14 Diopters in young people (Duane, 1922) (approximately 7 cm in 8-year olds). The distance to the eyes of the display in a head-mounted display (HMD) is often less than this and hence the eyes cannot possibly focus on this. Instead, with the use of lenses, a virtual image is created at a virtual distance approximately a meter away (Fig. 1). In the Oculus Rift DK1, for example, the virtual screens were infinitely far away; in the Oculus Rift DK2, they are about 4.5 feet (1.4m) away (source: Immersive Computer Graphics). One meters is a comfortable viewing distance with minimal accommodation needed and hence little eye strain (source: Immersive Computer Graphics). At around 6 meters the eye is unaccommodated.

Fig. 1. Virtual image in a HMD. Left: eye failing to focus on a very close real screen. Right: eye able to focus on the virtual image of the same real screen created by an interposed lens. source: Immersive Computer Graphics

Reference
- Duane, Trans Am Ophthalmol Soc (1922); 20: 132–57


GHK Equation and Action potential Can GHK equation be used to predict the membrane potential even if the cell is not at resting state?
To say it again, can we use GHK equation at every moment during Action potential?
I'm confused because GHK equation is derived at the situation with total ionic current is zero, but is that true also during AP?

The GHK voltage equation also known as just "Goldman equation" is always valid for determining the voltage at which the net current is zero, given internal/external ion concentrations and their permeabilities. This includes times during the action potential, though the result you get from GHK will be changing faster than the actual membrane potential itself, since the change in membrane potential brings about changes in permeabilities.
It's still useful to think about this equation to determine in which direction the membrane potential is changing instantaneously: it will always be changing towards the equilibrium potential. You can also qualitatively estimate the relative rate of change: if the current voltage is very far away from the equilibrium potential, the voltage will change more rapidly than if it is close to equilibrium.
However, this equation is just a steady-state equation. It doesn't tell you how quickly you will get to the new voltage or exactly which ions will move. For this, you need some other equations and other parameters, namely the actual permeabilities (rather than relative permeabilities) of the ions and the membrane capacitance.
The GHK flux equation can help: this will give you the flux of each ion at a given membrane potential (Wikipedia shows how this equation is related algebraically to the Nernst equation, which in turn is equivalent to the Goldman/GHK voltage equation for a single ion). You can also think in terms of the Hodgkin-Huxley model and the simple differential equation for current.

In summary, with respect to your question:

Can GHK equation be used to predict the membrane potential even if the cell is not at resting state?

It can predict where the membrane potential is headed, but not what it actually is or how fast it's changing, and the voltage you get from GHK will itself change as membrane potential changes affect the parameters that go into the GHK equation itself.


PBS or TBS, where cannot use each buffers? As you know, Tris buffered saline and Phosphate buffered saline is multipurpose. For finding each buffer's use, there's so many use experiment for PBS and TBS. TBS uses for western blotting, and PBS uses for cell culture.

but some experiment never use PBS and some experiment never use TBS, I want to ask this situation which when you use TBE but never use PBS, and the opposite situation(use TBS but never use PBS), For example, When you western-blotting with alkaline phosphatase never use PBS and PBS-T. this case, phosphate inhibits AP, and amine-coupling with NHS-EDC, never use Tris buffer because it have primary amine.

I think you answered your own question.

The buffer used in a given experiment depends on the requirements and limitations of the experiment itself. You just have to look at the properties of the buffer, and if it is relevant to your experiment.

You just gave two great examples... are you just looking for more examples of experiments when one would not use phosphate buffer vs Tris buffer?

PBS is supposed to closely mimic/represent the osmolarity of a cell, and buffer from pH = 7.0 to 9.0. Tris also buffers around neutral pH. It is pretty cheap, but as you've stated, has primary amine groups that are nucleophilic and thus interfere with certain experiments like disuccinimidyl suberate crosslinking, etc.


Difference between protozoa, protists, protoctista? Are protozoa, protists, protoctista different classes of organisms or simply different names for the same?

These terms are all somewhat obsolete as taxonomic terms, but they may still be used to describe certain groups of organisms.

The term "protist" is used informally in two different ways.  One usage refers to the paraphyletic group consisting of all eukaryotes other than the animals, plants, and fungi.  The other usage is to refer to those eukaryotes that exist as independent cells or, if colonial, do not form colonies with differentiated tissues.

The term "protozoa" is used informally to refer to the "animal-like" protists, i.e. those that are non-photosynthetic and motile.

Wikipedia gives a good summary of how these terms were used historically.


Spider identification assistance Phoenix Anyone know what kind of spider this is? They seem to be in the walls of my house...

LocationL Phoenix, AZ, USA

That's a nice silhouette of a male Southern House Spider, Kukulcania hibernalis.  That bizarre body, with the gigantic, forward-projecting, 'jackknife' chelicerae is unique and unmistakable.  These are quite harmless spiders.  A link to some useful information is below:
https://bugguide.net/node/view/26400


Meaning of "external demands" in a paper describing the gut-brain axis From "Brain Gut Microbiome Interactions and Functional Bowel Disorders":

  In response to external and bodily demands, the brain modulates individual cells (ECC – enterochromaffin cells; SMC – smooth muscle cells; ICC – interstitial cells of Cajal) within this network via the branches of the autonomic nervous system (ANS) (sympathetic and parasympathetic/vagal efferents) and the hypothalamic pituitary adrenal (HPA) axis.

What is the meaning of "external demands"? What other possible demands can the brain strive to meet by modulating the activity of the neural network of the gut?

From the context, it seems to refer to those demands outside of the human body. i.e. perceptions of the external world. Examples could include a perceived threat, diunal cycles, or stress about that public presentation you're giving later.

If you are about to be chased by a dangerous predator, a sudden urge to poop would probably impair your chances of survival. Luckily, when our sympathetic nervous system kicks in, our GI motility slows down, so our body can focus on surviving the external threat and live to poop another day.


Is the human iris concave or convex? Most drawing and 3D modeling tutorials show the iris to be concave. But all the diagrams I Googled show the iris is at best flat, otherwise even a little convex (discounting the optical distortion in photographs). So is it concave or convex?

Edit: Just to be clear, the question only concerns the concavity of the iris. The reason I mention drawing and 3D modeling here is that because it's such a common practice to make the iris explicitly concave in a somewhat exaggerated way, which is at odds with countless profile diagrams of the eye that I could google.

For example, this video (at about 5:52) even says that "it is convex according to anatomical diagrams, but I like to draw it as if it is concave". Or in this video (at about 7:46), the modeler pushed the concavity of the iris quite far, it's like a deep indent.

Iris curvature seems to be dependent on the state and health of the eyes.

See Prevention of blinking alters iris configuration in pigment dispersion syndrome and in normal eyes :

  Initial iris configuration was concave in all eyes with pigment dispersion syndrome, whereas in control eyes it was concave in four eyes, planar in four eyes, and convex in two eyes.

Other resources :

Accommodation-induced changes in iris curvature

Ultrasound biomicroscopic analysis of iris profile changes with accommodation in pigmentary glaucoma and relationship to age

Quantification of Iris Concavity


Smallest unit on which selection can act Traditionally, the individual was considered to be the smallest unit on which Natural Selection (NS) acts. Today, we usually consider the gene as being the unit of NS. Of course, we should also consider all sequences that affect the fitness even though they are not genes (even though the do not code for polypeptide). And theoretically, any sequence of DNA does have an effect on fitness because it influences the time and energy for DNA replication (although it might be negligible). The decision of considering the gene as the smallest unit of NS seems rather arbitrary to me. We might as well consider a group of genes or a given exon of even a smaller sequence.

Here are my questions:

What factors influence the minimal size of a sequence to be considered as a unit on which NS acts? Mutation rate, generation time, selection differential for this sequence, recombination rate, ...?
Could we consider a nucleotide as a unit of NS? Why?
How does the quasispecies model fit into the question of what is the smallest unit of NS? (for those interested, you will also find a very good explanation of this model in Martin Nowak's book called Evolutionnary Dynamic: exploring the equations of life)
Is it worth talking about that? Is this question biologically relevant? Or is it rather a question based on a choice of definition such as "Is a virus alive?"

As I asked several questions, let me know if I should split my post into several. Otherwise, please do not hesitate to answer only very partially to this post!

UPDATE

Terdon's answer makes sense to me. I should be a bit more accurate in the reas of my question.  I read The extended Phenotype from Richard Dawkins quite a long time ago and if I'm not mistaken, Dawkins says the following things

A unit on which selection acts has to be:

active
germ-line
replicator

A replicator has the 3 following properties:

fecundity
longevity
fidelity while being copied

Therefore for fidelity to be respected a unit of selection has to be a sequence which is not too long, so that it is not too often modified by recombination or mutation. He argues in this sense.

He also argues that nucleotides are not possible unit of selection. Indeed, it is hard to imagine a nucleotide being an active replicator. The word active means that it influences its not probability to be replicated. I don't think a nucleotide can do such a thing.

Unfortunately I don't have the book with me right now and I can't check what I have said, give you a citation nor a more accurate a reference. If anyone has some citations from this book, it will be welcome for the discussion!

Thank you!

The smallest unit that can be selected is, of course, the single nucleotide. The most striking examples of this are Single Nucleotide Polymorphisms (SNPs), many of which confer selective (dis)advantages.

To take a simple example, imagine a SNP that introduces a frameshift mutation, rendering a gene incapable of producing its protein. If that protein is something relatively important like p53, the SNP in question will be lethal and will be selected against. So, to take your questions one by one:

What factors influence the minimal size of a sequence to be considered as a unit on which NS acts? Mutation rate, generation time, selection differential for this sequence, recombination rate, ...?

any sequence unit whose alteration can affect fitness is a candidate for NS.

Could we consider a nucleotide as a unit of NS? Why?

Yes, if it can affect fitness (which it can, see above) it can be selected for or against.

How does the quasispecies model fit into the question of what is the smallest unit of NS?

As far as I can tell, it is irrelevant. NS can act on any self-replicating entity as long as the process of replication can produce variation that can affect fitness. If I understand correctly, the quasispecies model simply posits a group of entities with a very very high mutational rate. However, the rate of mutation does not affect the smallest unit that NS can act on, as I said above, anything that can affect fitness will be subject to NS.

Is it worth talking about that? Is this question biologically relevant? Or is it rather a question based on a choice of definition such as "Is a virus alive?"

Yes, it is worth talking about it if you have the misconception that the smallest unit is a gene :). No, but seriously, it is an interesting concept and a very useful tool. The selfish gene hypothesis for example, helped us see the world of evolution in terms of sequences rather than species or individuals. NS did not change, our conception of it did.

These are all useful conceptual tools that allow us as scientists to understand complex questions. However, NS is not a directed or conscious process so it does not care or know what it acts on.

PS. Please do not confuse protein-coding sequences with genes. As I said in my comment, there are many genes that do not produce proteins (tRNA genes for example) and that was even before the waters were muddied in the past few years. The current definition of gene is something like:

  any nucleotide sequence with a job to do

Read the ENCODE papers for a more technical definition or take this one from wikipedia:

  A gene is a molecular unit of heredity of a living organism.

UPDATE: First of all, you have to remember that Dawkins wrote The Extended Phenotype more than 30 years ago, in a time when the only complete genomes available were those of a few viruses. The first bacterial genome was sequenced in the mid nineties and the first human genome draft human in 2000. It was a time when selection was seen as acting at the level of the individual, and the importance of genes was underestimated. Dawkins books were instrumental in bringing genes into the spotlight.

However, if he did argue that a nucleotide cannot be selected (I have not read this particular book) he was simply wrong. A nucleotide can indeed affect its chances of being replicated. Think about it, if you have a G at a given position in the genome, and that G is mutated to an A, then the chances of the original G being replicated are obviously very low. Therefore, the nucleotide 'affected' its chances of replication. Alternatively, a mutation of a single nucleotide in the promoter of a gene can also cause the entire gene not to be transcribed and, as I mentioned before, frameshift mutations can wreak havoc as well. All of these are down to single nucleotides.

In any case, our vision of what a gene is has changed enormously since Dawkins wrote his book, we understand the genome much better now, and we have realized that it is far more complex than originally believed. 30-year old literature about genes, even if written by such luminaries as Rihard Dawkins, should be taken with a pinch of salt today.


Which amino acids can be phosphorylated? Definitely serine, tyrosine, and threonine. What about aspartate and glutamate? I thought the O- on the carboxylic acid side group could be phosphorylated but am getting mixed responses to this. Any thoughts / any other amino acids I'm missing?

There's a Wikinome page called Phosphorylation of unusual amino acids describing phosphorylation of histidine, aspartate, cysteine, lysine, and arginine. Lysine and arginine are apparently phosphorylated on the nitrogens. I was a little surprised to see histidine and aspartate on the list, as histidine kinases seem to come up often in my area of research.
I'm also aware of at least one non-proteinogenic amino acid, creatine, which is phosphorylated by a dedicated creatine kinase. It functions as a sort of phosphate shuttle for rapid regeneration of cellular ATP from ADP in situations of high metabolic demand.
References:
Phosphorylation on unusual amino acids. (http://kinase.com/wiki/index.php/Phosphorylation_on_unusual_amino_acids)
PubMed Abstracts: https://pubmed.ncbi.nlm.nih.gov/?term=18558627%2C10772951%2C10698688%2C1654322%2C9553104%2C8577821%2C19498169%5Buid%5D
Guimarães-Ferreira L. Role of the phosphocreatine system on energetic homeostasis in skeletal and cardiac muscles. Einstein (Sao Paulo). 2014;12(1):126-131. doi:10.1590/s1679-45082014rb2741


Can anyone identify this spider? Found in Italy My cousin found this spider at his place. He lives near Milan, Italy, in a small town. It's a humid region, around there the are a lot of fields but it is a 15 km from the city. It's still hot in these days. He told me that in the picture it seems a little bit too yellow. In reality it is more of an orange shade. He has never seen anything like that around there. Any clues?

Judging by the photo and the web it may be an orb-weaver spider of the family Araneidae.  Orb-weaver spiders get their name from the circular webs they spin.  It's possibly an Araniella cucurbitina, also known as a Cucumber spider, which are commonly observed hanging head down in it's web.  Several photos can be found at eurospiders.com.


Is studying chemical and physical properties of chemical substances that make up organisms really a task of molecular biology? I have read in a high school textbook that (translated into English by myself): "Branch of science that concerns itself with studying chemical and physical properties of substances that make up organisms is molecular biology".

Is this statement accurate? From what I understand, molecular biology deals more with "biological processes at the molecular level", and so it would be biochemistry, or maybe even "standard" organic chemistry, that would study chemical and physical properties of such substances, not molecular biology.

If you look at the Google ngram for the term ‘Molecular Biology’ you will see that it first appears just before 1960, and it is relevant that the Journal of Molecular Biology was founded in 1959. It is not biochemistry — indeed the name was meant to indicate its difference from biochemistry, and I heard second-hand (so I cannot vouch for its truth) that Hans Krebs (Professor of Biochemistry at Oxford University at the time) referred to it as “biochemistry without a license”. What I can vouch for is that the contempt was mutual.

At the outset the term ‘molecular biology’ was used to combine two rather disparate areas of biological science that today we might refer to as Structural Biology and Molecular Genetics. The link between these was the work on the structure of DNA and proteins at this time,  and the molecular analysis of the genes that controlled the synthesis of proteins.

If you look at the definition in the short Wikipedia article, only Astbury — who worked on protein structure in Leeds — is quoted, but The Journal of Molecular Biology was initially almost the house journal of MRC Cambridge, the love-child of Crick and Perutz, as it were, with an emphasis on nucleic acid as well as protein structure, leading to the other side of the coin which was the genetic code, the lac operon and the study of bacteriophage.

Of course, terms change their meaning as science changes and what was once new and trendy becomes “yesterday’s girl”. It really doesn’t matter that much. Systems Biology anyone?


Dopamine and other neurotransmitter release during music listening I'm looking for any studies that show a positive curve in respects to music sessions in humans and neurotransmitter release (specifically dopamine, epinephrine, and serotonin.) Any direct links would be great as I attempted googling and cannot find any at all for some reason.

Here is an article I found on google scholar. It links an increase in 5-HT a serotonin neurotransmitter when listening to pleasant music.

https://link.springer.com/article/10.1007/s004060070031


Problem with bacterial transformation with electroporation I have a problem with a bacterial transformation of a yeast gene that I can not solve.

I isolated yeast DNA and did a PCR to get my product. I am using pCGCUm vector with a GFP construct. I digest both my plasmid and my product with SmaI and ClaI for 4h each. After that I purify the product from a gel and perform a ligation with high efficiency T4 ligase for 30 minutes at 22°C. Then I transform my electrocompetent cells with electroporation (2000V, 5ms), recover it in 0.5ml LB for 2h and plate it on LB-A plates.

First time I only did:

insert1
insert2
Empty vector

and it did not work (empty plates for insert and confluent growth (after 18h) of some weird colonies on EV).

I did the same ligation again and this time I included controls

This is what I did:

insert1
insert2
Empty vector
negative control (EK cells + electroporation)
positive control (EK cells + undigested vector)

Now I got:

insert1 (no colonies)
insert2 (big colonies a lot of them)
Empty vector (big colonies a lot of them)
negative control (EK cells + electroporation) (no colonies)
positive control (EK cells + undigested vector) (big colonies a lot
of them)

The negative control suggests that my competent cells are ok, at least they are not resistant to AMP.

What confuses me is that even with positive control I get some weird big colonies - if I got nice transformants here I would assume that either digestion of ligation was not successful, but now I doubt that).

Another thing that is weird is that now I got that colonies also on my insert2 plate.

The scan image of big colonies looks like that:

I have a question if anyone has had that kind of colonies? I was thinking of maybe having contaminated cuvettes for electroporation but I had them in 100% EtOH for 3 days and then dried in fume hood for 3 hours before electroporation.

I did try another transformation:

again with our electrocompetent cells
Cells form other lab
chemically competent cells I made

The good thing is that on chemically competent cells there is no weir colonies, however efficiency of transformation was very low, but still, I think it is ok - will confirm it in next day if I really got the right insert.

On the other hand my electroporation still did not clear out. I got colonies on both our cells and cells from other lab, however in much lower amount there. I will try to change the cuvettes and try to use different electroporator as this seems to be the only thing that could make problems - although I am still not convinced about that :)

Thank you for your help and I will report the progress so if somebody else will have that problem again he could maybe benefit from my findings.


In terms of Prions is there a possibility, that other proteins apart from PRPC could be misfolded This is as from research PRPC seems to be the cause of all Prion related diseases. Thank you

There are many prions other than PrP; it is often helpful to e.g. read wikipedia for these cases.
For example, there are many yeast prions that are not homologous to PrP https://en.wikipedia.org/wiki/Fungal_prion.
But even in humans there are a number of other proteins that form amyloids and are described as "prion-like" even though they aren't the canonical protein: https://en.wikipedia.org/wiki/Prion#In_other_diseases


Why does hair turn white but not skin? From my understanding melanocyte stem cells (McSCs) stop being produced and we have a finite reserve that gets depleted with time. They're at the origin of melanocytes that create hair and skin pigments. Our hair turns white when we don't have any more McSCs. So why does our skin stay the same color with aging?

The answer to this question has its reason in the hair cycle. Our hair goes through a cycle of growth. At the end of this cycle, the cells in the hair follicle die and have to be replenished before a new hair cycle starts, also the hair falls out eventually. See the figure from reference 1:

The replenishment process is done by to two cell types: Epithelial stem cells which replenish the hair follice itself and melanocyte stem cells (MCSC) which replenish the melanocytes in the follicle and produce the pigment of the hair.

The MCSC are located in the bulge region of the hair, to be able to successfully replenish the pool of pigment cells the MCSC need to do things: proliferate and also differentiate. Proliferation makes sure that there are enough cells in the bulge region to repeat this process in further hair cycles, while the differentiation generates the cells who actually produce the pigment. When the MCSC are lost, no further pigment producing cells and hence no pigment can be made.

It has now shown that with age this pool of MCSC is not replenished completely anymore, eventually resulting in the loss of the melanocyte stem cells. The reason that our skin does not become gray at some point is that this process doesn't happen there, so pigment cells are not depleted. Reference 1 summarizes this topic nicely, while reference 2 is the original paper.

References

Melanocyte Stem Cell Maintenance and Hair Graying
Mechanisms of Hair Graying: Incomplete Melanocyte Stem Cell
Maintenance in the Niche


Why does the sweat of children not smell like adults? My kids sweat plenty in this hot heat, but they don't smell afterward. I on the other hand need all kinds of deodorant. Why doesn't kid sweat smell?

There are two types of sweat glands: (1) eccrine sweat glands and (2) apocrine sweat glands.

Eccrine sweat glands are present from birth in humans and secrete sweat that is mostly water and functions in evaporative cooling.
Apocrine sweat glands are found in the armpits and groin regions and become active in humans at puberty (although the distribution appears to be broader fetally). These sweat glands secrete an oily substance containing lipids and proteins that through interactions with bacteria on the skin (e.g., bacteria digesting lipids), lead to the "smelliness" of adults (including body odor).

So it's not really the sweat that smells, it's the action of bacteria on apocrine sweat that becomes prevalent after puberty.


Why are chromatophore in phaeyophycae chloroplasts integrated within the endoplasmic reticulum? Why are chromatophore in phaeyophycae chloroplast integrated within the endoplasmic reticulum? While reading about phaeyophycae I came across this point, but couldn't figure out why and what could be the evolutionary basis for this?

Before explaining it, you need to know 2 things.

Fact 1:  a cell of an Eukaryotic organism; such as a higher-plant, an animal, or a fungus, is actually not a single cell, but mixture of cells from different distant taxa.

taxon-1. The main, host cell (probably came from an archaebacteria (archaea) ), whose 'own' genetic material is in its nucleus.

taxon-2. mitochondria (probably derived from an eubacteria (only 'bacteria' of modern use) allied to proteobacteria)
(found normally in all eukaryote, except a few )

taxon-3. Plastid (whose most-important form is chloroplast) (probably derived from an eubacteria, allied to cyanobacteria , i.e. blue green algae) (Found in higher plants, and so-called 'algae' ).

It is now very well-established that mitochondria and plastids are 'cell'-s, with their own genetic machinery (including DNA, whose sequence match not-with host-nucleus, but match to bacteria!! However, some of DNA was probably got mixed with host-DNA, via DNA-transfer). They are partially autonomous because they can synthesize some proteins (metabolic-machines) from their own genes. And such an organelle can arise from pre-existing such-organelle, and can-Not appear de-novo from host cell.

Plausibly, many-many-million-years ago,  the precursor of eukaryote , certain organism allied to archaebacteria, 'ate' (phagocyzed) these eubacteria , and instead digesting them, they involved in a mutually beneficial symbiosis. Gradually they get converted into some 'organelles' through millions of years.

This concept is known as 'Endosymbiotic theory of origin of eukaryotes' .

 Image from Gerald Karp.

(Initially it was unknown,and it was thought that chloroplast and mitochondria evolved by gradual complication of the main cell.  when Harry Margulis gave this as hypothesis, it was rejected because it was unbelievable. Later-on it was established as true)

However, this-type of endosymbiosis is also called 'Primary endosymbiosis', where a purely-single cell engulf another purely-single cell.

Fact 2: The group 'algae', named in a very early-stage of science, was a horribly 'hotchpotch' group (extremely polyphyletic or artificial). This group is a set of organisms which can perform oxygenic photosynthesis. But some of them are similar to plants (green algae), some are highly similar to some protozoan ('primitive animals'), for say, some euglenoid and dinoflagellate algae. There are lots of such close-related protozoans that can't photosynthesize and don't contain any chloroplast. Whereas, Blue-green algae (cyanophytes) (with a highly similar photosynthetic mechanism), is a bacteria.

It was an enigma for the scientists. How  a few members from separate groups can contain plastid? Could they separately evolved the same structure? Is it possible to coincide so-much convergent evolution? or if the common-ancestor of all of them, contained the plastid, then why that structure disappeared in so-many members?

This enigma was quite drastically cleared up after discovery of this past endosymbiotic mechanism.

It was then found-out that, the finest classification (excluding the chloroplast), which was showing the different groups under algae are highly unrelated; is true. Actually members from far-distant taxonomic groups, 'ate' some unrelated photosynthetic primary-endosymbiotic associations, and formed another association. Thus they all got the very-similar photosynthetic apparatus; though the hosts were unrelated. This was something very new-to science.

these 'another-association's, i.e symbiosis between impure cells, is known as secondary endosymbiosis.

It is assumed that, the trace of these secondary endosymbioses; left some remains as the plastid-coves' structure.

Here is a classification of algae, taken from Robert Edward Lee, Phycology, 4th edition, in a simplified diagram. 4 basic types of photosynthetic structure is found in algae, according-which the classification has been done.

 .classification of algae, by Lee.
(Representation concept courtesy- a note shared to  me by a college- friend several-years ago).

Now, How these structures exactly developed?

Each cell contains so-many membranes, that , practically we have poor way to determine from which-of the membrane of which symbiont; certain ultimate membrane came. There are controversies. Such as according to Lee (already mentioned book) and diagram used by Hans Walter Heldt, Plant biochemistry, (3rd edition, Academic press- Elsevier), the outer membrane of chloroplast came from the cell-membrane of host-cell (phagocytic vesicle's boundary). like
 (redrawn from Heldt)

Whereas some other source tells that, the outer cover of chloroplast came from "outer membrane" of cyanobacteria , (Since it is  a gram-negative eubacteria, so carries 2 membrane). (Wikipedia tells "The two innermost lipid-bilayer membranes that surround all chloroplasts correspond to the outer and inner membranes of the ancestral cyanobacterium's gram negative cell wall, and not the phagosomal membrane from the host, which was probably lost." https://en.wikipedia.org/w/index.php?title=Chloroplast&oldid=737014760#Primary_endosymbiosis).

However in my answer I've followed Lee (4th edn).

Answer:

step 1 : Origin of chloroplast, the primary endosymbiosis.

 Diagram from Lee.

(already discussed).

This step's product found in group 2 algae. (Glaucophyta, Rhodophyta, Chlorophyta) Higher-plants probably evolved from Chlorophyta (green algae) and they also contains this-sort of chloroplast.

Step 2:

Probable sequence of evolutionary events that led to a chloroplast being surrounded by a single membrane of chloroplast endoplasmic reticulum. Initially an isolated chloroplast was taken up by a phagocytotic protozoan into a food
vesicle, with the food vesicle membrane eventually evolving into the single membrane of chloroplast endoplasmic reticulum surrounding the chloroplast.
Diagram from Lee.

Products of this step found in Group-3 algae.

Step 3. Another event of secondary endosymbiosis.

The sequence of events that led to the evolution of algae with two membranes of   chloroplast endoplasmic reticulum.

Products of this-step found in group-4.

Diagram from Lee.

by the way, all these steps are assumptions by scientists.

There is another concept called tertiary endosymbiosis. When in certain step of  secondary endosymbiosis, a chloroplast (from certain-one cell out of 2) lost, it is called tertiary endosymbiosis.

  Reference:

  Phycology/ Robert Edward Lee/ 4th edition/ Cambridge University Press.
  Plant Biochemistry/ 3rd Edition, English translation/ Hans Walter Heldt/ Academic Press - Elsevier.
  Cell and molecular biology - concepts and experiments / 6 th Edition / Gerald Karp / Wiley.


COVID-19 deaths by year of birth? Are there (global, country, etc.) data of COVID-19 deaths (or hospitalization) by year of birth? I was able to found them only by "age group", the meaning of this being usually an interval of 5 to 15 years, but I'm interested in smaller intervals.
Why I am interested? We know that the severity of this illness increases with age, and in fact increases a lot with ages around 70. If this increasing is more o less locally constant (that is, the first derivetive does not vary much in any interval of a few years) or at least the second derivative is more o less locally constant, we can think that maybe age on its own is a factor risk. But if there is a rapid increasing in one, two or three (consecutive) years and then a smaller slope (that is, a sort of "jump"), it is possible that there are (instead/also) other factors: maybe an exposition of this aged people to something during their lives that younger people don't lived, or some other thing that we don't know yet. So we need to know with more detail ages of hospitalization, deaths, or other sign of severity.

Data are usually binned in broad age groups partly because that's all the detail that's useful in some context, and because access to more detailed data often involves access to strongly controlled, personally identifiable information.
This preprint (full disclosure: I'm a co-author) gives information in 2-year bins for COVID in Ontario, e.g. this graph of the fraction of known infections (KI) hospitalized, and fraction of hospitalizations that resulted in survival, by (2-year) age group.
It looks pretty smooth, although if you squinted hard you might be able to convince yourself there were some breakpoints, e.g. between [60-61] and [62-63] in hospitalization or between [62-63] and [64-65] in survival (although I doubt these impressions would stand up to a formal statistical analysis ...)


Use of western blotting I ran across this paper recently.

http://www.ncbi.nlm.nih.gov/pubmed/21151122

I am confused on their use of Western blotting. Their unmodified protein (no PTM group) has a band and their modified protein (succinylation of Lys) has no band, yet they use this as evidence of successful identification of the PTM. Can anyone see what they are doing here?

They are doing a peptide competition assay (see abcam protocol).

The antibody is incubated with a purified sample of the antigen and used in a normal Western-Blot of cell lysates. Any cross-reactivities of the antibody would still be visible as only the interaction with the epitope of interest is blocked. So all bands that disappear after such treatment are indicators for the substance that was used for blocking. A Western-Blot with non-blocked antibody is normally used for comparison.

In the experiment you mentioned, they vary the principle a bit, as they are comparing two blots - one blocked with a succinylated library, one with a non-succinylated one. As the band disappears after treatment with the succinylated library, they confirm that their antibody is specific against succinylated proteins - at least in these three cases.


How late in a human pregnancy can a zygote split? This page indicates that the first two days is "very early" for a zygote to split, and that conjoined twins are the result of an "extremely late" split:

  If the zygote splits very early (in the first 2 days after fertilization) they may develop separate placentas (chorion) and separate sacs (amnion). ... Most of the time in identical twins the zygote will split after 2 days, resulting in a shared placenta, but two separate sacs. ... Finally, the zygote may split extremely late, resulting in conjoined twins.

What I'm looking for is more specificity. At what time in the pregnancy does a split zygote result in twins who share a placenta and not a sac? What about conjoined twins (I'm most interested in the most common types of conjoined twins)?

Identical twins

Twinning occurring at the two cell stage or afterwards, up to and including the 16 cell stage, which translates to days 1 to 3 after fertilization, results in diamniotic, dichorionic twins.

Twinning at the 32 cell stage (day 4), up to  and including day 6 results in diamniotic, monochorionic twins. The majority of identical twins split at this stage.

Twinning from day 7 up to day 10 results in monoamniotic, monochorionic twins. This is rare and only accounts for about one percent of identical twins.

diamniotic: twins have separate amniotic sacs
monoamniotic : twins share one amniotic sac
dichorionic: twins have separate placentas
monochorionic: twins share the same placenta

Conjoined twins

This is where things get a bit fuzzy. While some sources say that conjoined twins occur when the twinning event takes place after day 10, others say conjoined twins are created when

  the twinning event occurs at about the primitive streak stage of development, at about 13–14 days after fertilisation in the human

It is very likely that because of the rarity of conjoined twins (one in 200,000 live births) there isn't enough data available on the very early embryogenesis.

Sources and further reading:

The embryology of conjoined twins

Twinning

Conjoined twins


Why are killer whales found in the Gulf of Mexico smaller than ones found in the Pacific? I recently found out that there are killer whales that live in the Gulf of Mexico, but they are smaller than killer whales that are commonly found in the Pacific Ocean. Why is it they are smaller in size?

Animals living in colder climate / environment are larger because this way they have better body surface / volume (mass) ration thus they're more resistant to cold. Animals living in warmer areas are smaller thus they have larger body surface compared to their volume(mass) to dissipate heat easier.
Check this wiki page for more details.


What are the uses of Helical Wheel Projections in Structural Biology? I have seen helical wheel projections used to illustrate amphipathic helices in proteins.  Are there any other uses for these models?

Helical wheel projections can be useful anytime you have a protein or peptide with one or more α-helical regions. They allow you to see whether any "property" is present along one side of a peptide. This can be useful in recognizing potential protein-protein interacting motifs such as leucine zippers.

The wikipedia article on "Helical wheels" also looks like a good place to start learning more about this.


Plant a whole fruit or only seeds? I'm trying to figure out whether it is better for the plant to reproduce by planting its whole fruits with seeds inside them, or picking the seeds out and planting them without the fruit. In my case it's chili pepper, but I'm also interested in other plants that reproduce through fruits.

I heard that the whole fruit concept is about providing the seeds with some energy in form of their shell (the fruit) to give them a head start in terms of initial growth into a seedling. Is that true? Do all seeds benefit from growing from inside its fruit, or is it not very significant?

I'd argue that this relates to species-specific strategies of seed dispersal, so the answer depends on which species you're asking about. Here's an answer for chili peppers, which I think illustrates how complex and idiosyncratic these strategies can be.
As I mentioned in this answer, the seedsavers' manual Seed to Seed has great info on most plants, including the genus Capsicum (chili peppers). They say to clean the seeds from the peppers, and then dry them thoroughly but not in direct sun.
The Tewksbury lab has done someone amazing work on Capsicum evolution and seed dispersal from a biological standpoint. As published in Tewksbury and Nabhan 2001 (behind paywall, but described well in this Science in the News article) Capsicum fruits have evolved specifically to be eaten by birds, who do not have the receptors that make the fruits taste spicy to us and other mammals.
Essentially then, what you're trying to do when you hand-germinate seeds is to mimic the process of the fruit being eaten and passing through a bird gut. Tewksbury and Nabhan found that seeds from fruits eaten by birds actually germinated at a slightly higher rate than their control group of hand-processed seeds. In contrast, seeds eaten by mammals (who in normal settings totally avoid these spicy chilis) were destroyed and did not germinate.
Seed dispersal mediated by birds and other animals is one way that plants can be motile.

 Tewksbury JJJ, Nabhan GPG. 2001. Seed dispersal. Directed deterrence by capsaicin in chilies. Nature 412: 403–404.

Whealy K. 2012. Seed to Seed. Chelsea Green Publishing (p. 152)


Do Blanding's Turtles die of old age? I have recently found articles and various claims that turtles (Blanding's turtles as an exact example) could possibly live indefinitely. http://discovermagazine.com/2002/jun/featturtle

This is said to be due to the fact that they

  don't senesce— deteriorate physically— as they grow old

I am highly skeptical of that claim, and on the other side are links such as this http://www.nature.org/ourinitiatives/regions/northamerica/unitedstates/indiana/journeywithnature/blandings-turtles.xml which say they can live up to 70 years (though in the actual article it says 70+)

I realize in the wild that predation, disease, and other causes other than old age could kill turtles, but my question is:

Can blandings turtles die of old age? If so, around what age would this be?

It looks like as in fishes, the lack of an intrinsic cause of death in turtles in general is seen:

  Like in fishes, the reptiles appear to show three types of senescence. The African skink, Mabuya buettneri, shows rapid senescence similar to death at mating observed in Salmon and marsupial mouse. Most of the lizards and snakes undergo gradual senescence comparable to the pattern exhibited by a majority of vertebrates. On the other hand, turtles, tortoises and crocodiles continue to grow throughout life and are thus credited with slow or negligible senescence.
  Patnaik 1994 Gerontology 40(2–4):200–20.

The main article by Congdon, the researcher who the Discover article profiles, also seems to be fairly definitive about this lack of senescence (or negative senescence?) in Blanding's Turtles specifically:

  Survivorship, reproductive frequency and size-adjusted mean clutch size were all higher in the Oldest age group compared to the younger age groups.
  Congdon et al 2001 Experimental Gerontology 36(4–6): 813–827


Will Fst (inbreeding coefficient) always be a value close or at 0 in asexual populations? FST is the average inbreeding coefficient of a total population. The equation is:
$F_{ST} = \frac{Var(S)}{Var(T)} $
$Var(S)$ = variance in the frequency of the allele between different subpopulations, weighted by the sizes of subpopulations
$Var(T)$ = variance of the allelic state in the total population
If $F_{ST}$ equals 0 that means there is no population differentiation and there is no heterozygosity in the population. The ceiling for $F_{ST}$ is one so there is population differentiation and the population is all heterozygotes.
If the population is asexual, meaning they are parthenogenetic, would $F_{ST}$ be at or close to 0? Can this not be assumed?
In the context of this question I am considering the whole genome or just one allele.

It depends on whether mutation exists. Generally mutation is happening in biology, but in its absence, yes it will be at or near zero:

Note that in the absence of any mutation, $F_{ST}$ would be defined but equal to 0, as all the genetic variance is within individuals and none between individuals and subpopulations.

From that paper, see this figure:

So, basically, the exact level of $F_{ST}$ in such cases will be controlled by the mutation rate. That figure shows a value above zero at 100% clonal reproduction because it does have a nonzero mutation rate. There is also nonzero migration between populations, so that will have the effect of reducing $F_{ST}$ somewhat. So here the value is controlled by those 2 factors. Another thing worth noting is that, if there is no initial variation between populations before the split, that will tend to increase $F_{ST}$. So it does matter how much variation exists overall.


Are there more than Five kingdoms? Is it true that scientists have disregarded their belief that there are five kingdoms and instead, they have theorized that there are multiple kingdoms?

Taxonomic classification is a large area of controversial debate. See for example Cavalier-Smith's system of classification, they described eight kingdoms, then six, then 7 kingdoms in subsequent publications.
Other (older) theories describe 6 kingdoms, two prokaryotic (Eubacteria and Archeae) and four Eukaryotic (Protista, Plantae, Fungi, Animalia) See image on Wikipedia's "Kingdom" explanation
The three domains Eubacteria, Archeae, and Eukaryota are less disputed.


Neuron Growth and Regeneration Are nerves and/or neurons able to grow and repair after damage, but not regenerate? Is this specific to humans? I have heard of people being paralyzed, but after much therapy are able to use their legs again. Is this just through the creation of new connections from healthy nerves, or is there nerve repair to an extent?

the following is true for humans, I dunno about other animals:
schwann cells in peripheral nervous system can rebuild a severed axon if the perineurium of the nerve fibers are sutured together ... the same is not true for oligodendrocytes in the central nervous system. Thus only peripheral nerves can regenerate and not nerves located in the central nervous system (ie. spinal cord or brain).

surgical nerve regeneration after a nerve is severed is not the only possible form of nerve regeneration, another example would be when the facial nerve is damaged by bells palsy and then it regenerates itself. so a fun example of what can go wrong is when some of the nerves switch when they regenerate, so your brain thinks it's doing one thing, but since the nerves switched when they regenerated, it does the other. The example would be "crocodile tears syndrome", it has nothing to do with crocodiles (thats just the name) but rather this is where the facial nerves salivation fibers get switched with the crying fibers... so when they eat they cry...

as for neuro-rehabilitation in people suffering paralysis, this is a broad question. As I understand it, if it's the spinal cord thats cut then it will never regenerate, but if its a nerve that left the spinal cord (a peripheral nerve) than it may possibly regenerate. Here are some specific conditions:

Also it could be a temporary thing like Guillain-Barré syndrome where the immune system (hyper sensitized by a previous campylobacter bacteria or CMV virus, or for some other reason) temporarily injures the peripheral nerves and then after about 2 weeks they recover)

also there is there are drugs and toxins which are temporary, so one your body metabolizes/excretes (bile or urine) it is gone: botulinum toxin (from bacteria Clostridium botulinum), curare (south american plant poison), the many chemically modified versions of curare produced by pharmaceutical used in surgery to relax the muscles, and the list goes on for drugs/toxins. Again, drugs/toxins are temporary.

Stroke, though in the central nervous system, might be able to be rehabilitated since maybe everything wasn't destroyed (even though what was destroyed was destroyed permanently), and the patient can salvage what is left and use their neuroplasticity to try and use their brains slightly differently to be able to recover.

ALS, affects the ventral horn of the spinal cord... this one is irreversible at least today.

there are many other causes of paralysis which may nbe reversible or irreversible

glossary

schwann cell= the fatty cell that wraps around an individual nerve in order to myelin ate it... myelination being the fatty insulating of axon so they send electric signals faster...

axon= a projection off of the cell body that sends an electrical impulse to the end of the nerve that ultimately communicates with the target nerve/muscle/gland/etc

perineurium= outside protective sheath composed of connective tissue covering many nerve fibers

oligodendrocytes= the equivalent of a schwann cell, but in the central nervous system, it myelinates many nerves, unlike the schwann cell which only myelinates 1 nerve.

nerve fibers= a collection of many nerves running together

facial nerve= facial nerve innervated the muscles of the face and there are 2 facial nerves, one for each side of the face. the facial nerve doesn't only do face muscles, but also taste, salivation, and tear formation

bell's palsy= when the facial nerve stops working and half the face gets droopy... there are a lot of possible causes, like virus bacteria, and many many noninfectious causes...


What kind of leafy house plant is this? I was given the plant as a gift.  Started out small and has grown to almost 6 1/2 feet tall and has sprouted off spring.

Original

Offspring:

Google reverse image search resulted in "Houseplant".  Not very helpful.

I have since removed the dead leaves from the plant.

I believe it's a Dieffenbachia, see also this question & answer from Gardening.SE:

https://gardening.stackexchange.com/questions/9765/what-is-this-thick-stemmed-houseplant-with-variegated-leaves

though I am not sure of the species, it could be Dieffenbachia seguine which shows a similar coloration and is one of the taller species (I believe some of the others stay bushy).

On the linked answer, @TeresaMcgH warns:

  By the way, one of the common names for this plant is "dumb cane" because the sap can cause numbness and swelling in the mouth and throat if ingested. So watch pets and small kids around it if you have such at home.


Help identifying leaf-like bone I found two of these objects near a creek in Missouri. They feel like they are made out of bone but they do not look like any bone I have seen before. They also appear as though the could be some sort of plant part. I am having a very difficult time identifying them and any help would be appreciated.

Those are isolated turtle bones:

Specifically, they are part of the carapace, or upper shell. The projections would articulate with the backbone. The "toothlike" structure at the other end projects down toward the margin of the shell.

Based on the size, and the fact that you are in Missouri, I'm guessing they are snapping turtle bones. Here's a photo of the inside of a snapping turtle shell:

They are a little hard to make out, but you can faintly see the marginal projections.


What is the difference between "Bisphosphate" and "Diphosphate" in biochemistry? I have often found bisphosphate compounds ( e.g. RuBP, RuBisCO, 2,3-BPGA etc.) and diphosphate compounds (e.g. ADP, GDP etc.) in biochemistry. They are commonly seen and are important compounds in both animals and plants but what is the basic difference between a bisphosphate and a diphosphate?

[Source:Wikipedia]

As you can see in the above structure of ADP(Adenosine di-phosphate), the two phosphate groups in the compound are directly attached to one another. So it is named as di-phosphate. [Source] You can see this table for more examples.

[Source:Wikipedia]

In this structure of RuBP(Ribulose-1,5-bisphosphate), the two phosphate groups in the compound are not directly attached to one another, they are attached to first and fifth carbon, meaning they are attached to different atoms. Therefore, it is named as bis-phosphate. [Source](2nd comment)


Pharmacologically, can tricyclic antidepressants have a side-effect profile similar to neuroleptics? Torticollis (wryneck, cervical dystonia) is a neurologic movement disorder causing involuntary muscle spasms in the neck. Often, neuroleptics can cause such a side effect.  I'm wondering if this condition could also be part of the side-effect profile of  tricyclic antidepressants, like amitriptyline.

Some potential indications:

Often the basal ganglia are associated with neurological conditions such as movement disorders. -> Do amitriptylines effect the basal ganglia?
Dressler and Benecke claim that "Of all patients treated with neuroleptics approximately 2 to 3% develop acute dystonic reactions within days of therapy initiation .When highly potent neuroleptics are used this rate may increase to over 50 %.Young men are at a particularly high risk. Cranial, pharyngeal, cervical and axial muscles are most commonly affected causing oculogyric crisis, grimacing, fixation of the jaw, retrocollis, torticollis or even opisthotonic posturing." -> Do tricyclic antidepressants operate similar to neuroleptics?
Geyer and Bressman claim that dystonia can be caused by certain drugs: "In addition to inherited forms of secondary dystonia (dystonia-plus syndromes and neurodegenerative diseases), a variety of acquired insults can cause secondary dystonia in previously unaffected individuals. Many cases are iatrogenic, resulting from drugs that block dopamine receptors; antipsychotic and antiemetic drugs are the most common culprits." -> even though amitriptyline doesn't seem to block dopamine, maybe there is some kind of connection?
Tricyclic antidepressants sometimes seem to be used to treat torticollis, so is the reverse effect of causing the condition also thinkable?

Torticollis can occur for several reasons, one of which is a side effect of certain drugs. Rather than highlight one specific drug it is perhaps better to talk about the mechanism of action by which this occurs.

Torticollis in a drug induced form is classed as an extrapyramidial side effect. Classically results from some medications which have anti-dopaminergic effects. The neurotransmitter dopamine is important for the regulation of movement. Different medications have different degrees of anti-dopaminergic effect. To complicate things further there are several different types of dopamine receptors and different drugs have different effects depending on their action on these receptors.

Classically drugs that have been associated with extrapyramidial side effects are some of the antipsychotics but there are case reports of this with trycyclics http://www.ncbi.nlm.nih.gov/pmc/articles/PMC489096/ however this appears to be a very rare, see http://www.sciencedirect.com/science/article/pii/S0924977X97004057.

The paradoxical treatment of torticollis might be dependent on the cause of the condition.  Tricyclic anti-depressants have anti-cholinergic effects, i.e. they block the effects of the neurotransmitter acetylcholine. This neurotransmitter works in opposition to dopamine in the basal ganglia (part of the brain responsible for movement control) as such might be used when the dystonia is as a result of doperminergic disregulation.

If you are at all concerned that you may be suffering side effects of any medication, then I highly recommend that you go and discuss this matter with your doctor. The above  is a simplified explanation of some of the reasons why these side effects may occur. It is not intended as information for the purposes of self diagnosis and treatment.


Are spiders part of the study of entomology? The definition of entomology says it is the science of studying insects.

I know spiders are not insects but does entomology include studying spiders as well?

Otherwise is there any name to the science of studying spiders (class Arachnida)?

Spiders are part of a taxon called Arachnida. Arachnida also contain scorpions, Oppiliones, acari, … The science of arachnids is logically called Arachnology

However, (wikipedia):

  Entomology (from Greek ἔντομος, entomos, "that which is cut in pieces or engraved/segmented", hence "insect"; and -λογία, -logia) is the scientific study of insects, a branch of arthropodology. In the past the term "insect" was more vague, and historically the definition of entomology included the study of terrestrial animals in other arthropod groups or other phyla, such as arachnids, myriapods, earthworms, land snails, and slugs. This wider meaning may still be encountered in informal use.

In other words, in the informal sense entomology include arachnology but the strict definition entomology does not encompass arachnology.

You will find here on tolweb.org more information about the systematics of Arthropoda


Why don't the apples seeds from grafted trees produce the same kind of apples? As Wikipedia says:

Grafting is a horticultural technique whereby tissues from one plant are inserted into those of another so that the two sets of vascular tissues may join together.
In most cases, one plant is selected for its roots and this is called the stock or rootstock. The other plant is selected for its stems, leaves, flowers, or fruits and is called the scion or cion. The scion contains the desired genes to be duplicated in future production by the stock/scion plant.

So why I don't get the apple-tree of the scion kind if I plant the seeds from an apple which has grown on such a tree? I would expect that the genes in the apple seeds must be the same. However if I plant the seeds, I have to graft the new seedling again.

The reason most apples are produced from grafted trees is that apples don't breed true.

In a large number of crops, you have "lines" of crops. Basically, if you breed two plants of the same cultivar together, their offspring are similar enough to both parents that it performs like the parents. The reason for this is that these crop lines have been interbreed with each other for long enough that the population is self consistent, and the important alleles are present in frequencies that mean all progeny are likely to inherit them.

However, the types of apples which are sold commercially are not from these sorts of cultivar lines. Instead, they've been obtained from "sports". That is, the chance production of either a particular hybrid gene set, or sometimes from random mutations that happened on an adult tree of another apple variety. For example, the Granny Smith occurred from a chance seedling which was discovered by Maria Ann Smith.

These apples don't necessarily have "consistent" alleles. For example, it may be heterozygous for certain genes. If you have Aa alleles at one gene, if you self-pollinate the plant, you're going to get a mix of AA, Aa and aa genes in the offspring, the last of these isn't going to be the same phenotype as the parent. Now recognize that this is happening at multiple genes across the entire genome, so there are many chances to get non-parent-like allele combinations. Add to this the issue of co-dominance, where the heterozygote has a different phenotype than either homozygote (that is, BB isn't like Bb), and the chances that an offspring has a gene with a non-parent like allele combination is pretty high.

There's a further complication that some apple varieties like Honeycrisp are self-sterile. Even if Honeycrisp could theoretically breed true, there's no way for it to fertilize itself, meaning that all fertilization events are hybridizations.

Now you can certainly grow apple trees from seed. The planted seed will grow up into an apple tree, but the chances are that the combination of alleles it received by random chance from its parents will not result in an genotype that produces any commecial apple phenotype. Instead, you're likely to get regression to the mean, meaning the apple tree will be like the ancestor of apples - a crab apple, or at least crab apple-like. - But there's a small chance that it will have commercial apple-like properties, which may or may not be like the parent. This is how new apple varieties are formed, after all.

The only way to guarantee that the genotype of an apple tree is close to the parent plant is to propagate it by cloning, and the easiest and cheapest way to clone trees (at least apple trees) is by grafting.

(As a final note, remember that the seeds get their genome from the flowers and the cells which produced the flowers. The genotype of the rootstock - grafted or not grafted - has no bearing on what genes are present in the seeds. You'd have the same issue with apples breeding true even if the parent tree was on its own rootstock.)


Can carnivores survive on a (processed) vegetarian diet? Why or why not? There are many differences in for example the digestive system between carnivores, herbivores and omnivores.

It seems that in certain kinds of species adaptability with respect to diet is possible. What I have heard is that it is impossible for carnivores to survive on a non-meat diet.

Therefore I wanted to ask: Is it really impossible for a carnivore to survive on a vegetarian diet, even when the fruits/vegetables/plants are processed? I could see how their digestive tract would not allow for them to survive on grass, but what about certain kinds of nuts, mushrooms, or even processed plant based foods?

If it is impossible to survive on these diets, why?(With respect to either causes in their digestive system or substantial differences between meats and any type of vegetarian food.

With arbitrarily broad meaning of "processed", yes. If absolutely nothing else, elemental purification and inorganic synthesis of something chemically resembling meat in nutrition is possible. Prohibitively expensive and stupid, yes, but possible. So then the question becomes exactly how much processing you need to do. Without clear bounds on that question and inadequate research on the metabolism of obligate carnivores, nothing closer than a broad stab at an answer makes sense. That said, here's a broad stab.

For instance, you'd probably need to synthesize vitamin D3, carnosine, DHA, and a handful of other things from plant extract, which is possible but difficult. Carnivores often have carnosine synthases, for instance. Cats have two distinct carnosine synthases. In terms of dietary sufficiency, that may or may not be enough. To be sure, you'd have to break it down to amino acids and build it back up again, essentially. Obligate carnivores are likely to have a number of other metabolic needs that aren't met with, for instance, pulverized soybeans. You're going to need at least one vat for fermenting raw amino acids into carnosine, and probably another for vitamin D3. Seawater microalgae contain lots of DHA, so that is probably something to look into. You could oversupplement alpha-linolenic acid instead of supplementing DHA, which might or might not work. There's not a lot of study into carnivore metabolism, so prepare to make some discoveries the hard way. Genetic studies can only take you so far, so don't try this on your favorite pet first.

In short: yes, you can raise carnivores on a diet made from plants and plant material. Rhetorical you, as in it is possible. It's probably not something you can do at home, even if you're wealthy.

(I'm assuming "feeding the vegetable matter to chickens" falls outside the domain of "processed" but it would be much easier than large-scale amino acid purification and fermentation.)


How does a woodpecker not give itself concussions? How does a woodpecker go about smacking it's head into a tree without killing itself?

Various features of brain,skull and beak anatomy help to achieve protection.
A paper was published in PLoSOne in 2011 on this very topic:
Why do woodpeckers resist head impact injury: a biomechanical investigation
There is also a very readable summary on the BBC website. I advise that you read the whole article, but here is a quotation which lists the main findings:

The team's simulations showed that three factors were at work in sparing the birds injury.
Firstly, the hyoid bone's looping structure around the whole skull was found to act as a "safety belt", especially after the initial impact.
The team also found that the upper and lower halves of the birds' beaks were uneven, and as force was transmitted from the tip of the beak into the bone, this asymmetry lowered the load that made it as far as the brain.
Lastly, plate-like bones with a "spongy" structure at different points in the skull helped distribute the incoming force, thereby protecting the brain.
The team stresses that it is the combination of the three, rather than any one feature, that keeps woodpeckers pecking without injury.


Is it possible to fuse DNA from two sperms into one sperm? Is it possible to fuse the DNA of two genetically different sperms into one singular sperm? In theory, half of the number of chromosomes in a normal sperm would come from one sperm and the other half could come from a separate sperm. In return, the fused sperm could fuse with a healthy egg cell for fertilization.

It would be theoretically possible to engineer such a cell, but something very similar can occur in nature, two sperm cells can fertilise a single egg cell, resulting in a fetus with DNA from both. See here


How do I put on a labcoat? Let's assume I am wearing a labcoat for two reasons:

Prevent the various bacteria, proteins, skin cells and substances on my clothes and my skin from contaminating my experiments.
Prevent various dangerous things from the experiment getting on me, and ruining my clothes or endangering my health (eg. toxic chemicals, pathogenic bacteria, ecotropic virus, etc)

A labcoat is an imperfect, but valuable barrier against such hazards. Perhaps a droplet of some Nasty Substance™ ends up flying towards my arm, but instead of getting on my exposed skin, hits my labcoat.

However, what happens when I take off my labcoat? My gloves, which have just been in contact with lots of Nasty Substance™, go through the sleeves of the coat, possibly smearing the substance all over the inside of the fabric. When I put on the coat again the next day, now my skin is in contact with these smears.

I could remove my gloves before taking off the labcoat, to avoid this smearing. But this time, I have to touch the labcoat with my bare hands as I remove it. Remember the Nasty Substance™ that was stopped when it splattered on the outside of the fabric instead of my skin? What if I know end up touching that?

I know that for truly dangerous conditions, there is specialized equipment and detailed procedure. Even at BSL2+, traditionally disposable labcoats are required, rendering the issue somewhat irrelevant. So let's assume the highest level below that, BSL2, as the context for answers.

In short, what is the correct way of putting on and taking off gloves and non-disposable labcoat when working in BSL2 conditions?

Wear two sets of gloves.  First, use nitrile gloves, not latex for this. 4mm or thicker is a specification I would recommend to avoid tearing.  Latex will bind too well to itself and tear easily with increased friction etc (same logic behind not using two condoms).  Also, use a coat with an elastic cuff on the sleeve.
So here's the breakdown

Put on first set of gloves
Put on coat over gloves.  Decon if needed for application.
Put on second set of gloves.
Science
Take off second set of gloves.
Decon as needed for your health
Take off coat
Take off first set of gloves

I can find sources for this, but I've been doing ABSL2 and BSL3 for a while, and they always go through this in safety training.

Edit: My internal nagging to site got the better of me, so some examples that recommend double gloving:

http://oehs.vcu.edu/chemical/labsafe/perchloricacid.pdf

https://extranet.fhcrc.org/EN/sections/ehs/hamm/chap3/section6.html

http://orsp.umich.edu/policies/um/committees/BRRC/ADDITIONAL_PRACTICES_revised_8_7_14.pdf

http://ehs.columbia.edu/carcmutguide.html

I could go on, but I think you get the idea.


Is natural selection actually random? In the Theory of Evolution, two main factors take place:
One is random, which are the different mutations that organisms' DNA suffer. This process adds genetic variability to a given population.
The other one is not random, which is natural selection. It is not random because it will only select  those organisms which are better capable of surviving to the conditions of their environment.
Most likely I am wrong and I would like to be corrected, but I was thinking that, since natural selection depends on mutations and the conditions of the environment, and since those conditions can be formed by random processes, wouldn't it make natural selection as actually random?
I mean, this is probably an over simplistic analogy, but take a group of mammals which suffer a great series of mutations in a short period of time, and separate into two species of mammals: one group of animals with hair and the other group has no hair at all. Suddenly, one day starts to snow. We could expect that the second group would most likely go extinct, while the mammals with hair would survive. Since the weather is based on random processes and since natural selection in this example would be based on the mutations that the animals suffered and the weather as well, wouldn't natural selection be a fundamentally random process?

You are right in a sense. The processes which generate mutations in an organism are stochastic (not quite exactly random, but in most organisms they are effectively random for all intents and purposes). In terms of population genetics, it is considered that mutations occur randomly across the genome and have an equal probability of occurring at a given base pair.
The environment is also random/stochastic in the sense that it occurs mostly independent of mutations which have occurred. Whether or not it is cold one year is independent of the mutations which have occurred within an organism. (Actually that's not quite correct since organisms can generate their own environmental niches and evolve according to them, but I think that is beyond the scope of this question).
What is not random is how the frequency of genetic variants respond to different environments. This is natural selection. Over the long run, we expect genetic variants which increase the fitness of an organism within a given environment will increase in frequency and vice versa. There is a large body of theory and evidence which predicts how a particular variant may change in frequency in response selection of a particular pressure.
As @jamesfq correctly points out, a nice example of selection being non-random on the macro-scale is convergent evolution. For example, aquatic animals such as fish, certain mammals (e.g. Dolphins) and Amphibians and Dinosaurs have independently evolved streamlined bodyplans in order to conserve energy when moving through the water.


law of independent assortment Self fetilization of F1 dihybrids, following independent assortment of alleles result in:

a) 3/16 Tall-rounds ; 3/16 dwarf-wrinkled
b) 9/16 Tall-wrinkled ; 3/16 dwarf-round
c) 9/16 Tall-round ; 3/16 dwarf-round
d) 3/16 Tall-wrinkled ; 3/16 dwarf-round

This question was asked in MCAT exam in Pak for which I'm preparing this year.... no genetic arcitecture was mentioned in question... The above mentioned is original format of question.... in ans-key, the ans is D but I am confused why it can't be C.

In real life, round and tall are dominant traits in pea plants, which would make C and D both correct.  I don't think people are expected to memorize the traits of pea plants, so the question ought to tell you somewhere which traits are dominant.  There must be an error in the question as printed.


What's the difference between releasing hormones and tropic hormones? I've been reading my textbook and two terms have appeared that, after a bit of looking, I still can't seem to be able to distinguish. Here's what the textbook says (McGraw Hill Bio 12, 2011):

  After receiving signals from various sensors in the body, the
  hypothalamus secretes what are referred to as releasing hormones,
  which often travel to the pituitary gland. The releasing hormones
  stimulate the pituitary gland to secrete hormones that act on other
  endocrine glands. Hormones that stimulate endocrine glands to release
  other hormones are called tropic hormones. (pg. 394)

From the work I've done, it all seems to indicate that releasing hormones regulate the secretion of other hormones, and that tropic hormones target and stimulate other endocrine glands (to release hormones). And yet my textbook appears to use the terms separately later on as if they're related rather than identical (e.g.: "the pituitary gland is controlled by the hypothalamus via releasing hormones and it secretes tropic hormones" (pg. 396)). So are they identical? And if not, what distinguishes between them?

The releasing hormones could also be considered tropic hormones, and indeed they fit the definition as you noticed, but aren't usually named as such.

The special thing about the ones your textbook is specifically highlighting as releasing hormones is that they communicate from the hypothalamus to the pituitary through the hypophyseal portal system, vessels that travel directly from the hypothalamus to the anterior pituitary.

Therefore, they aren't really released into the broader circulation (they can get there, but they'd be in too low a concentration). They are easily identified in a list of hormone because they all share a naming convention where they are called "____-releasing hormone" and their primary function is to cause the pituitary to release whatever is in the "_____".

In terms of overall neuroendocrine function, the "releasing" hormones all cause release of tropic hormones, which in turn cause release of hormones that affect other tissues.

Therefore, the sequence is releasing -> tropic -> non-tropic. They could have been named something else, like "primary tropic" and "secondary tropic" but this terminology keeps them separate as "tropic hormones that cause release of other tropic hormones."


Does anyone know what type of Cocoon this is? I am really concerned with this since I've never seen a cocoon this color before and can't find it anywhere on the internet. I found it just laying on the ground not attached to anything, but it seems to be alive because when you touch it, it will wiggle abit. Any answers are appreciated.

I think I may have found your cocoon: it appears to be a Magpie Moth (Abraxas grossulariata) cocoon:

According to UK Moths, it's common in the UK.


Are there fungi that are directly beneficial for humans? It is well known that the human body benefits from a lot of different bacteria - and indeed wouldn't be able to survive without them.

Are there fungi that are beneficial to humans, or even needed directly for surviving?

Saccharomyces boulardii.

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

S. boulardii is a yeast, closely related to S.cerevesiae (if not the same organism).  There is a lot of solid data showing use of this fungus as a probiotic can help treat or prevent intestinal infections.

Systematic review with meta-analysis: Saccharomyces boulardii in the prevention of antibiotic-associated diarrhoea.

  RESULTS:  Twenty-one randomised controlled trials (4780 participants),
  among which 16 were new trials, met the inclusion criteria for this
  updated systematic review. Administration of S. boulardii compared
  with placebo or no treatment reduced the risk of antibiotic-associated
  diarrhoea (as defined by the study investigators) in patients treated
  with antibiotics from 18.7% to 8.5% (risk ratio, RR: 0.47; 95% CI:
  0.38-0.57, number needed to treat, NNT: 10; 95% CI: 9-13). In children, S. boulardii reduced the risk from 20.9% to 8.8% (6
  randomised controlled trials, n=1653, RR: 0.43, 95% CI: 0.3-0.6); in
  adults, from 17.4% to 8.2% (15 randomised controlled trials, n=3114,
  RR: 0.49, 95% CI: 0.38-0.63). Moreover, S. boulardii reduced the risk
  of Clostridium difficile-associated diarrhoea


On average how many genes / alleles do people share? I am curious about how much more a child can be alike to one parent than the other. If a child were to inherit all the alleles that are shared between both parents from one parent, but inherit all alleles from the other parent which the first parent doesn't possess, wouldn't this make the child genetically more uniquely similar to the second parent?

This question would be aided by understanding of how many alleles on average a person already shares with another person. Taking into account regional areas probably yield more similar people, I would imagine the average couple would share more than two randomly chosen people on the planet.

I will attempt to answer the question. Allele is defined, in simple terms, variation of a given gene, e.g. through deletions, SNPs etc. Humans are diploid organisms, meaning we have two sets of chromosomes, one from mother and one from father. Now since we have two sister chromosome, we can only have (share) two alleles of a given gene (one from mother and one from father) unless there are multiple copies of a gene or chromosome, which is mostly observed in disease conditions but that's not what we are talking about. Now since every humans have SNPs at roughly 1 every 1000 base pair, there are genetic variations between sequences of genes between humans, although there are some hot spots, which are more varied and some genes are very highly conserved due to their critical function such as cytochrome C. This just means that parents of the child you are describing (if not related to each other) are not likely to share the exact same, sequence wise, genetic code for a given gene selected at random.

The inheritance of a given allele of a gene on a chromosome happens through independent assortment (a process which happens maternally and paternally), meaning a child (offspring/zygote) would get one copy of a gene/allele (from the possible two that each parent themselves have) from maternal and one copy from paternal side at random. This is one source of genetic variation in a zygote. The other source of genetic variation is gene cross-over (through homologous recombination) meaning bits of the maternal or paternal chromosomes swap at gamete stage before the gametes are fused together to form a zygote, which makes the offspring unique and no offspring alike (except MZ twins but thats another discussion). This overall means that you can inherit a maximum of two alleles of a given gene (assuming again the parents of the child are not closely related) and even then the sequence of the offspring genes are not likely to be exactly the same as their parents, which makes every human unique. But saying that, you have a much higher gene sequence match to your parents than any other non-related human selected at random.

One thing worth noting here is that mitochondrial genes, are inherited exclusively from you mother (through the egg) and males inherit the Y chromosomes paternally so there are circumstances I guess you could say you inherit certain gene/alleles paternally or maternally.

What I speculate you might be thinking about is how many homologues (similar versions) of a given genes humans have and I think the average in the human genome is 3 but do check this! Flies (Drosophila) tends to have one, which is why its such a great model organism to study genetics and genetic interactions with as you do not tend to get redundancies.

I hope this answers your question


Disadvantages of unihemispheric sleep Is is well known fact that marine mammals and some birds can sleep with one brain hemisphere at a time, since it's essential for their survival.

However, at least in my opinion, such mechanism would give significant advantage to many other species (e.g. to antelops) because it helps avoiding predators.

While answers to this question explain why sleep is necessary, animals with unihemispheric sleep mode does not seem to suffer from any of mentioned drawbacks of non-sleeping (except maybe increased energy consumption).

Are there any particular disadvantages of unihemispheric sleep versus "normal" sleep?

EDIT: I've stumbled upon the following paper:  Rattenborg N., Amlaner C., Lima S.. 2000. Behavioral, neurophysiological and evolutionary perspectives on unihemispheric sleep. Neuroscience & Biobehavioral Reviews 24: 817–842, which discusses several possible reasons for absense of unihemispheric sleep in most mammals, but does not present any evidence to support their hypothesis. The main reason (from authors' point of view, at least) is the need for very loose coupling of both hemispheres to allow them sleep independently, which might negatively affect overall brain effectiveness.

  Along these lines, sleep may play a role in integrating the
  functions of different brain regions. Thus, BSWS1 in terrestrial
  mammals may be superior to the BSWS in animals with USWS2
  because it allows integration within and between hemispheres, rather than
  just within a particular hemisphere.

  ...

  Specifically, the reorganization of the central nervous system
  required for USWS may interfere with other adaptive brain functions,
  such as integrating the functions of both hemispheres.

  1 Bihemispheric Slow Wave Sleep; 2 Unihemispheric Slow Wave Sleep

They also argue that the unihemispheric sleep might have been present in first mammals, but wasn't giving any advantages on first stages of evolution.

However, this paper was published more that 10 years ago, so there might have been some advances in the field since then.

I thought this was an interesting subject and I had some time to do a little search around today.  I can't find anything better than the review you point out. All I can do is add a few interesting notes since 2001.  Nothing really turns over Rattenborg et al.

Sleep is itself a poorly understood process and most of the theories of the necessity of sleep can teeter precariously with discoveries like this report that baby dolphins and killer whales and their mothers simply don't sleep at all for the first few months of life.

The Rattenborg review is only guessing, but I think its clear that there is a cost to unihemispheric sleep, even if we don't know what it is.  Cetaceans and birds and perhaps reptiles having unihemispheric sleep are all cases where there are perpetual and strong selection forces that maintain the ability in these animals.  Without constant predation experienced by tasty ducks or the vagaries of being an air-breathing underwater mammal, animals quickly lose their ability to sleep with one half their brain, one assumes because the ability to maintain it is particular and easily lost with variation.  Modelling work of the hemispheres in sleep indicates that the connections between the hemispheres are modulated between the two modes of sleep - there may be advantages to such brain structures for instance.

This blog post is a good read though and a bit more recent, though most of the references are from before 2001. Dolphins do use both hemispheres to sleep, but just not very often (about 15% of the time), indicating there is some advantage even for these animals.  Seals may alternate between bi and uni-hemispheric sleep when they are on land and at sea.

If you were wondering if there was something you were missing - I'd say no.  At the time of this writing THIS web page is the sixth hit on a google search for the term 'unihemispheric sleep'....


Melanistic Snow Leopards? Are there any confirmed cases of melanism in snow leopards? I am aware that melanism is much more common in Jaguars and Leopards, both often called black panthers, but I cannot seem to find any info on melanism in snow leopards.

I'm not aware of any confirmed cases of melanism in snow leopards either.

There are some relevant studies on the evolution of melanism on Felidae. Melanism seems to occur only in two extant species of the genus Panthera (Panthera onca and Panthera pardus). There is a direct correlation between melanistic colorations and enviroment (especially humidity):

  Moist forests (especially in Southeast Asia) presented very high
  frequencies of melanistic leopards (e.g., 39 of 71 individuals [55%]
  in Southeast Asia), and more than 80% of the black animals in our
  database, a fivefold increase relative to the expected number based on
  the overall number of records. Furthermore, we found no confirmed
  melanistic leopards in the Middle East, Arabian Peninsula, Central
  China, and Russian Far East, nor any mention in the literature as to
  the presence of melanism in these regions, indicating that this
  polymorphism is really absent from these areas. Overall, there was a
  significant reduction in the frequency of melanism in some biomes that
  consist of open habitats or temperate forests. There thus is a clear
  pattern in which melanism tends to increase in tropical/subtropical
  moist forests and decrease in open/dry or temperate habitats

References:

https://www.sciencedirect.com/science/article/pii/S0960982203001283
https://www.intechopen.com/books/big-cats/ecology-and-evolution-of-melanism-in-big-cats-case-study-with-black-leopards-and-jaguars


Are nosebleeds unique to humans? Are there other species that get nosebleeds? If so, do they occur for the same reasons that humans get nosebleeds? How would an animal stop a nosebleed?

Cats, dogs and other animals can suffer from epistaxis.  The causes differ depending on the animal.

  foreign things in the nose, abscess, cancerous growth, snake bite, some poisonings and diseases especially in the trachea and lungs and anthrax. Sometimes excessive sneezing or coughing can result in nose bleeding as well. All animals are susceptible to get nose bleeding.

They would need to see their vet or owner to get it treated.

https://www.thevillager.com.na/articles/7474/Dealing-With-an-Animal-Bleeding-From-the-Nose/


What is the meaning of a 1,4 bond between sugars? I don't know how to express my question. I want to know what are bonds like 1.4 bond between molecules. I've read somewhere like the amylase enzyme can break 1.4 bond. I want to know what are these bonds and what are their benefits and where  can I find more info about them?

Amylase breaks the bond between two sugar molecules in a chain (the chain is called starch).

The type of bond is called a glycosidic bond which is just a covalent bond between sugar molecules.

The "1.4" bond you are talking about is normally written "1,4" or "1-4"; you could interpret it as "1 to 4" because it is referring to a bond involving the first and fourth carbons of the sugar (they aren't bonded directly, there is an oxygen in between); they are just numbered that way so that (bio)chemists can talk about the molecule - see this other Q&A from Chemistry about the numbering of the carbons of glucose.