text:
Why reaginic antibodies are absent in these types of syphilis?
According to Textbook of Microbiology and Immunology
2e, Subhash Chandra Parija, pg.no; 375

These(reaginic) antibodies do not appear in early primary syphilis, latent acquired syphilis of long duration, and late congenital syphilis. Therefore, Venereal Disease Research Laboratory (VDRL) and other tests may show false negative reactions during these conditions.

Isn't latent syphilis detected by presence of reaginic antibodies? Then why is it said that it does not appear in long duration?
Why antibodies are not produced in late congenital syphilis?

To make the diagnosis of syphilis, the most common tests fall in two categories :

Non-specific tests like VDRL test & Rapid Plasma Reagin (RPR) test : those detect antibodies against cardiolipin, present in the treponema but also in our cells.
Specific/treponemal tests like TPPA/TPHA & FTA-ABS : antibodies titers against antigen specific to T. pallidum are  measured.

Non-specific titers decrease when antigenic stimulation ceases : either when syphilis is cured (no more treponema), or in the late stage where the number of bacteria present in non-immune-privileged zone is low (treponema is almost eliminated except in the central nervous system, eyes, testis where it is protected from immune response).
Specific titers fall very slowly if at all, once they are acquired.
Thus in late stage syphilis we get the following : VDRL- TPHA+, a source of confusion since this can also indicate old/cured syphilis.


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Mechanism by which hypokalemia reduces insulin secretion
Is there any known mechanism by which hypokalemia reduces insulin secretion?

This video explains a mechanism, but its inherently wrong because ATP dependent K+ channels will allow movement of K+ from inside of cell to outside.

tl;dr
Hypokalemia hyperpolarizes membranes by increasing the $K^+$ gradient, making $\mathcal{E}_K$ and consequently $\mathcal{E}_m$ more negative. This makes any signaling event controlled by depolarization less responsive.
It's complicated, but we can understand the effect by looking at $K^+$ alone
Good catch. Yes, the video (and diagram) are incorrect. The electrophysiology of pancreatic $\beta$-cells is still an area of active research. Your textbooks (e.g., Costanzo Chapter 9, under Regulation of Insulin Secretion) will tell you that an increase in the $\frac{[ATP]}{[ADP]}$ ratio closes ATP-sensitive $K^+$ channels, which depolarizes the membrane. This is, in large part, correct, but not thoroughly understood, and not only by decreasing the $K^+$ conductance of the membrane. Further work in the years since that linked article supports the importance of a $Cl^-$ gradient and anion current, but $K^+$ conductance is still involved, and probably still underlies the mechanism through which hypokalemia reduces insulin secretion.
Membrane potential is determined by the concentration gradients and permeabilities of ions
The membrane potential of the pancreatic $\beta$-cell, as with the neuron, is determined by both concentration gradients and permeabilities of the membrane to ions. I'm sure the OP understands this, but for the general reader, you can read about this basic principle in any neuroscience or physiology textbook. You can calculate the membrane potential using the Goldman equation or chord conductance equation. Both are representations of the same principle, but I think the chord conductance equation is more intuitive. We'll simplify for our purposes to.
$\mathcal{E}_m  = \frac{g_{i}}{g_T} \mathcal{E}_i + \frac{g_{j}}{g_T} \mathcal{E}_j + \frac{g_{k}}{g_T} \mathcal{E}_k + ... $
Here, for ions i, j, k, ..., the membrane potential is equal to the sum of a series of terms for each ion, with each ion term being a product of the equilibrium potential of that ion ($\mathcal{E}_i$) and the portion of the total conductance across the membrane that the conductance of that ion represents. Conductance can roughly be understood as permeability. More open ion channels means a greater permeability/conductance to that ion.
Short term changes in membrane potential used in signaling are accomplished by changing the conductance of the membrane to specific ions. If the $\frac{g_i}{g_T}$ increases for ion i, the membrane potential moves closer to the equilibrium potential for ion i.
The concentration gradient determines the equilbrium potential
Each ion has an equilibrium potential, a membrane potential at which the net current of an ion across the membrane is 0. From the Nernst equation, we can say:
$\mathcal{E}_i \propto log_{10}\frac{[I]_{out}}{[I]_{in}}$.
Here $[I]_{out}$ is the concentration of the ion outside the cell, and $[I]_{in}$
is the concentration inside the cell. We've eliminated the proportionality constant because, in physiological conditions, it's constant, it's different for pancreatic $\beta$-cells (vs. neurons), and it's not relevant to our discussion (since we're not going to make any calculations with real numbers. If you are very careful, you'll notice the log term has outside concentration on the top, inside concentration on the bottom. You may find the Nernst equation written with a negative proportionality constant and with the inside concentration on top. These are equivalent because of how logs work.
Changing conductance, or permeability, changes the membrane potential
When you increase the conductance of a membrane to a particular ion, the membrane potential moves closer to the equilibrium potential for that ion. This is why in the neuron, for example, increasing the conductance of the axon membrane to $Na^+$ causes depolarization. The equilibrium potential $\mathcal{E}_{Na}$, is positive. The resting membrane potential is negative. Higher permeability to $Na^+$ moves the membrane potential closer to $\mathcal{E}_Na$.  Similarly, increasing the conductance of the axon membrane to $K^+$ (after the membrane has depolarized) repolarizes and then hyperpolarizes the membrane. $\mathcal{E}_K$ is negative (more negative than resting membrane potential). Higher permeability to $K^+$ moves the membrane potential closer to that large negative $\mathcal{E}_K$.
Increasing the permeability of pancreatic $\beta$-cells to $K^+$ hyperpolarizes the membrane
I'm using examples of the neuron because this is typically where these concepts are most thoroughly taught, but lets try to apply our understanding to the pancreatic $\beta$-cell. Concentrations, permeabilities, and membrane potentials are a little different, but not that much. Resting membrane potential for a $\beta$-cell is about -60mV. Threshold potential for $Ca^{++}$ release (which leads to insulin secretion) is between -50 and -40 mV. (Refer to my earlier linked articles). I don't have an exact number for $\mathcal{E}_K$, the equilibrium potential of $K^+$ in $\beta$-cells, but it is more negative than the resting membrane potential of that cell. We know this because (as is demonstrated in the linked studies), the OP is correct, increasing the conductance of the membrane to $K^+$ causes a net $K^+$ current out of the cell, rather than in, moving the membrane potential to a more negative state (hyperpolarizing the membrane), similar to what we see in neurons.
Decreasing the permeability of pancreatic $\beta$-cells to $K^+$ DEPOLARIZES the membrane
As discussed in Constanzo Chapter 9, ATP-sensitive $K^+$ channels close (not open) in response to an increase in the $\frac{[ATP]}{[ADP]}$ ratio. This decreases the $K^+$ conductance of the membrane, allowing the membrane potential to move closer to other equilbrium potentials (e.g., $\mathcal{E}_{Na}$, which is positive). With $\mathcal{E}_K$, which is more negative than the prior membrane potential, contributing less, the membrane potential becomes less negative, or depolarizes.
You can use a less mathematical reasoning to work out what happens when the $K^+$ conductance decreases as well. Close a $K^+$ channel and positive ions that would have moved out of the cell stay inside the cell, making membrane potential less negative, depolarizing the membrane. This is effectively the same as bringing positive ions inside the cell.
When the membrane depolarizes, $Ca^{++}$ is released, which causes secretion of insulin.
Hypokalemia
In hypokalemia, outside concentrations of $K^+$ decrease. This has an effect on the equilibrium potential, $\mathcal{E}_K$. From the Nernst equation above, we can look at the log term to see how $\mathcal{E}_K$ changes when $[K^+]_{out}$ decreases. The fraction $\frac{[K^+]_{out}}{[K^+]_{in}}$ is less than 1 in all human cells (there is more $K^+$ inside the cell than out), so the log term is going to be log(some number between 0 and 1). You can work this out using a calculator, but in this domain (0-1), the log is negative. It is larger and negative the closer you get to 0, smaller (but still negative), the closer you get to 1. If this behavior is unfamiliar to you, I encourage you to explore it with a calculator.
If you decrease the numerator in the log term ($log_{10} \frac{out}{in}$), as we do in hypokalemia, you get a larger negative number. This doesn't change the net direction of flow, or current for $K^+$ at levels that occur in the cell. It's still net out. $\mathcal{E}_K$ is more negative than it would otherwise be, so why doesn't decreasing conductance/permeability by closing the ATP sensitive $K^+$ channels do the same thing and depolarize the membrane?
Closing ATP sensitive $K^+$ channels in the setting of hypokalemia does cause depolarization, but not enough. You have to go back to the chord conductance or Goldman equation and consider the effect of $\mathcal{E}_K$ on the membrane potential before the ATP sensitive $K^+$ channels are closed. With a more negative $\mathcal{E}_K$, the chord conductance term $\frac{g_{K}}{g_T} \mathcal{E}_K$ is more negative, and the overall $\mathcal{E}_m$ is more negative. Global hypokalemia effectively hyperpolarizes the membrane, not just in the pancreatic $\beta$-cell, but everywhere. This is an important principle for understanding the consequences of hypokalemia, not just in insulin secretion, but in all settings. As a rule, excitable membranes are sluggish in hypokalemia (except Purkinje fibers). This is why, for example, it causes muscle weakness.

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Why warfarin is given as racemic mixture?
Warfarin is administered as a racemic mixture of S- and R- warfarin.
S- warfarin is 3 to 5 times more potent than R- warfarin.
So, what's the logic behind giving a mixture of it? Isn't administration of only one form gives more predictable results?

In general, it's more difficult to produce a specific stereoisomer of a compound than it is to produce the racemate. Producing a pure S- or R- sample of a particular compound requires either enantioselective synthesis, or racemic synthesis followed by a purification step such as chiral chromatography. This tends to be expensive - especially for an older drug like warfarin where it would likely imply either chiral purification (throw away half your product) or redesigning the synthesis to be chiral.
For some drugs it makes sense to do this - some reasons might include adverse effects of the undesired stereoisomer, or taking a drug that's about to go off-patent and re-branding an enantiopure preparation for further patent protection. I think the latter is what happened with Citalopram -> Escitalopram (Lexapro) although this is speculation.
Most likely in the case of warfarin there is no strong argument for producing a pure enantiomer. It has been off-patent for a while, there likely aren't major adverse effects related to the less potent isomer, and most likely economics dictate that producing and selling the racemate is cheaper / more profitable than retooling to produce and sell an enantiopure version. That latter option would only make sense if they could sell the pure S-warfarin for enough to recoup the development / purification costs, and this is unlikely for a drug with such a long history of use in its racemic form.

Another "evergreening" example is omeprazole --> esomeprazole

I wasn't even aware that esomeprazole was a thing :)

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Etymology of vimentin
What is the etymology of the intermediate filament , Vimentin?

According to this paper:

From the Latin word vimentum, used to describe arrays of flexible rods,both ordered ones (e.g.,latices,filigres,and wicker-work) and non-ordered ones (e.g.,brushwood).

Vimentin:

Filigree art:

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Junk DNA and "random" mutations
I'm somewhat irritated by "mutation" generally being described as a fully random factor in evolution: pure randomness does not seem like something that can survive in a long evolutionary process.
And some basic evolution in some long-lived organisms appears to happen in quite fewer generations than one would consider plausible considering just natural selection over an unbiasedly mutated genetic base.
So I'm wondering whether there have been attempts to view mutation itself as a process influenced by evolution.  For example, couldn't "junk DNA" result in a susceptibility to certain mutations that is determined by environmental factors, like amount and constitution of nutrients, ambient temperatures and others.
The overall discussion of mutagenesis I can find focuses entirely on "damage", again basically assigning all mutations a negative or at least undirected character (like more mutations occuring under stress, with the "aim" being more likely to have more random mutations where one offspring might be more successful than the stressed parent by chance).
In a similar vein, I don't see not much of anything about evolution and competition of gametes: how different environmental factors influence which of an abundance of eggs mature and which of the (asexual) male gamete reproduction mutation in the testes will be favored over time or under environmental conditions.
Basically all of evolution and natural selection seems about how to survive into fertility and select a partner, and that's it as genes are constant apart from random cosmic radiation or toxic substances.
I think that this kind of viewing the message in the DNA as isolated from its medium just does not sound like something that would survive billions of years without something less random replacing the pure randomness.
So are there any major studies trying to figure out whether certain mutations leading to better adapted phenotypes occur in a non-random manner (namely not just affecting mutation rate but also direction) in response to environmental circumstances?

I'm a bit unclear what your question is. Are you asking what the general mutation rate is of genomic DNA, if anybody has looked at this, and if certain base pair changes are more common than others?

Welcome to Biology.SE. There is a mixture of different concepts in your post, most of them seem to be a little unclear to you. I recommend that you take some time to follow some introductory course to evolution. Understanding Evolution for example would be a good fit.

I am voting to close as the question reveals several misconceptions that cannot be fully addressed in a post (although I gave it a short try).

Biology SE is not the place to come and just throw out an opinion like this, if you have a proper biology question then please focus on that. The effect of a mutation is random - a species cannot will itself to produce a mutation with specific effect

I agree with the above. Mutations are random. Selective pressure provides direction.

"pure randomness does not seem like something that can survive in a long evolutionary process." This is the "argument from incredulity". Just because it doesn't seem that way to you doesn't mean it isn't that way.

"that's it as genes are constant apart from random cosmic radiation or toxic substances." That's totally wrong. Genes mutate without external influences like radiation or toxins--in fact they mostly mutate without these, due to occasional replication errors. It's incredible how little the DNA machinery screws up, but it's not perfect, either.

pure randomness does not seem like something that can survive in a long evolutionary process.

I think this is because you don't quite understand (no offense) the interplay between mutations and natural selection. You should have a look at Understanding Evolution.

The overall discussion of mutagenesis I can find focuses entirely on "damage"

This is because the vast majority of mutations are deleterious (=damaging). But obviously, not all mutations are deleterious, otherwise no adaptation would be possible (only purifying selection would occur).

In a similar vein, I don't see not much of anything about evolution and [..]

I don't understand this paragraph.

Basically all of evolution and natural selection seems about how to survive into fertility and select a partner [..]

No! There is much more to evolution than that. Note that the semantic of evolution and natural selection is wrong as they are used in your sentence. Again, check out an introductory course.

I think that this kind of viewing the message in the DNA as isolated from its medium

No! The environment is a fundamental tenet in evolutionary biology. The association between genotypes to fitness is a function of the environment as well.
Are mutations random?
The mutation rate varies dramatically among species and along genomes (roughly speaking from $10^{-2}$ to $10^{-10}$). For example microsatellites (repeated sequences) are highly mutable. Note also that the probability of a given nucleotide to mutate depends also on the exact nucleotides that are around it (Rob Ness; Personal communication). The mutation rate is also a plastic trait (and is therefore under selection) in some species (of plants typically). The environment affect the mutation rate and the environment can be chosen by some species (avoidance) or even constructed in some species (niche construction). In multicellular organisms, the age of the father correlates with the number of new transmitted mutations as well. However I have never heard of any studies showing such behaviours in order to affect the mutation rate. Epigenetic changes (does not concern all species) can also the mutation rate and even into what new nucleotide the old nucleotide will be mutated into (with a given probability). Mutations are more likely to be transitions than transversions. If a specific region is under environment-depend selection, then a mutation that would allow to drastically increase the mutation rate at this nucleotide whenever the organism has a low fitness (or even whenever the trait of the organism is unfit for the specific environment) could reach fixation. This process (and maybe others I am not aware of) are I think encapsulated within a hypothesis called (and it is a horrible name as it can yield to confusion) adaptive mutation hypothesis. But really don't start studying any field of science by jumping into an advanced subject (or even worst, a controversial subject). You should start with an introduction.
However, the impact on fitness (and on phenotype) of a new mutation is essentially random. An organism has absolutely no way to know what protein will be caused by a given new mutation. Selection then select upon the variance created by the mutations, the variance decreases and adaptation occurs. The impact of new mutations seem to follow more or less two weighted gamma distributions (added to which a bump of probability density for lethal mutations).

The studies you cite seem focused on short-lived organisms with a high reproduction rate.  I did explicitly mention longer-lived specimens.  Some correlations like a higher male birth rate for older first parents are well-known and not attributed to destructive mutations.  It's also established that the number of birth defects for old fathers is not explainable by mere random mutation but rather by higher competitiveness in replication of gametes with a certain defect inside of the testicle issue.  But all of that is always focused on defects and not on correlation with desirable features.

I don't actually cite any studies. Not all what I am talking about is specific to short lived vs long lived organisms. I don't fully understand why the short-lved vs long-lived distinction metters for your question but I guess I don't really understand the question.

I think I am also confused about the low level of understanding of evolutionary processes that your post shows and am even more confused now that I see that you actually have some knowledge...but in the same time things like number of birth defects for old fathers is not explainable by mere random mutation but rather by higher competitiveness in replication of gametes with a certain defect inside of the testicle issue really doesn't seem to be related to the question. Also I don't understand the use of the concept of "junk DNA" in your title. I guess I just don't understand the question.

junk DNA is an obvious contender for contributing to tertiary molecule structures and/or hydrogen bonds that make the neighboring non-junk DNA more or less susceptible to certain environmental influences.  Those can be either direct influences of factors like acidity or other ion concentrations, temperature, viscosity, osmotic pressure or more specific organic substances potentially generated by the body itself in response to external stimuli.  When people "turn grey with grief overnight" (no, hardly overnight) does the responsible change in body chemistry also affect gene mutation?

Did you hear about the historical Luria-Delbrück experiment where they demonstrated that in Escherichia coli mutations conferring resistance to antibiotics are essentially random?
Also, discussions and some references on the phenomenon of (directed) adaptive mutagenesis, which I think you are asking about, is mentioned in the Wikipedia article. But I don't know much about the debate.

Most antibiotics are essentially "random" environmental factors since the substances in question don't as a rule occur in massive amounts in nature (penicillin being a notable exception).  Escherichia coli also is not exactly a higher organism with slow reproduction and long life.

As Rémi.b, I don't see why slow reproduction and long-life are relevant for your question. You seem to be surprised about mutations appearing quickly, but a mutation can and does actually appear in one generation because it appears in an offspring. What takes time then is just the "propagation" of the mutation to the population through successive new offsprings, but this has nothing to do with the complexity or life expectancy of the organism.

Also, whether an environmental factor is "random" or predictable is independant from whether the mutations that occur in an organism experiencing those factors would be random or targeted, so I don't see the relevance here either.

slow reproduction and long life are relevant for the question since there is not much of a necessity for adaptive genetic changes bypassing the selection process of phenotypes when phenotype selection already happens fast enough to follow typical environmental changes.

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Is it possible to amplify every single piece of DNA through PCR?
Is there a way to perform non-specific PCR amplification for the purpose of amplifying every piece of DNA present?

what is the source of DNA? If minor variation is not a problem, then you can just grind more tissue/culture volume to extract more DNA. All cells in your body and most cells in cultures have (almost) the same DNA

actually, that is how RNAseq works. A lot of DNA is produced from RNA, then fragments of DNA have adapters (know short sequences) added to its' ends, and then those DNA fragments are amplified with PCR

Are you asking about whole genome amplification?

Ah, thank you, that was what I was looking for.

In short; Theoretically yes.
In practicallity no.

I agree with this opinion.
But, there are some methods to do so.
Ligating both ends with specific tags to amplify DNA fragments with the tag specific primer set. If you have different length of DNA fragments in original sample, PCR products could be biased.

In short; Theoretically yes.
In practicallity no.
Non-specific PCR require random primers to anneal to a target sequence to initiate replication during PCR. Theoretically this should anneal to every combination of bases and therefore allow the amplification of all DNA (or at least in a fragmented form).
Practically, all the primer combinations will have different primer annealling temperatures due to the differential base composition, making the amplification of fragmentation inconsistent, and in others down-right impossible.


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Time required to evolve advanced chromatophores in octopuses and squid?
Do we have any idea how long it took primitive Coleoida to evolve from non-color changing organisms to color changing organisms?  Granted, not all coleoidans can change color (vampire squids are good example), many of them do.
(Coleoida is the subclass below Cephalopoda that includes all squid, cuttlefish and octopuses.  Nautilus' are excluded.)

Here is a print screen from oneZoom.org.

Coleoida include decapods and octopods, both of which have chromatphores, so their MRCA (which lived 330 millions years ago) probably did as well. Coleoida is a sister group to the nautiloids. They branched +400 millions years ago. Together they form the group of cephalopods. As nautiloids do not have chromatophores, the evolution of chromatophores probably occurred in between these two nodes (between MRCA of cephalopods and MRCA of coleoida). In other words, it occurred at some point during a period of about +70 millions years.


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Can epigenetic structures carry a trait?
Can epigenetic structures cause a trait to manifest in a person if the trait is not already in the DNA? In all my readings I have yet to find a definitive statement that it is impossible.

I'm not an expert on this and it's really complicated, so I'd rather not give an answer. But take a look at research on transgenerational epigenetic inheritance TEI. By chance I read the abstract of a paper today that might be of interest for you as well. Rawlik et al. conclude that differences in DNA methylation patterns in humans are mainly driven by genetic differences in cis - so the differences is actually 'DNA-driven'.

Yes, epigenetic changes does affect the phenotype. This is here the whole interest behind epigenetic. Environmental variation (incl. parental care) affect epigenetics which in turn affect the phenotype (incl. behaviour) of an individual. It is pretty much clear from the wikipedia definition of epigenetics

Epigenetics studies stably heritable traits (or "phenotypes") that cannot be explained by changes in DNA sequence.

The term "phenotype" (or "phenotypic") is actually present 3 times is the first small paragraph of the wikipedia article.
For example, you can read here on wikipedia an example of a study showing that maternal care affect epigenetic variations which in turn affects stress level later in life as measured by HPA.

Please forgive my ignorance, but is the quote you cite equal to "Epigenetics studies stably heritable traits that cannot be explained by DNA"?

Replace "DNA" by "DNA sequence" or "amino-acid sequence" and you're good. The term epigenetics is typically poorly defined but most often we are thinking of methylation occuring directly on the DNA (hence the importance of saying "DNA sequence" and not just "DNA") or on histone tails. The definition as presented might also make some people in the field of niche construction unhappy but this is a story for another time. You should have a look at this post for more information


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Want to identify plant and flower

This plant is hardly 40/50 days old and given to me in seed form claiming to be hibiscus plant seed.I m not sure that it s hibiscus plant.. Please identify.

Definitely not hibiscus.

Please state where in the world this plant is located, or native to. There are lots of yellow flowers in the world.

I agree with @WYSIWYG. No way this is hibiscus. Can you provide more details? e.g. undershot of leaves, texture of plant/leaves (are they fuzzy? prickly? ), size.

Good resource: http://midatlantichikes.com/floraandfauna/yellowflowers.htm


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Is a nightly curfew an effective intervention strategy for limiting the spread of an infectious disease?
The governing bodies of several geographic areas hit by disease outbreaks will sometimes impose a nightly curfew on their citizens, restricting or limiting the ability of their citizens from going outside during certain hours of the night (or day). As I write this, several United States local or state governments are implementing such strategies in March 2020 to contain the COVID-2019 coronavirus pandemic (Puerto Rico and Hoboken, New Jersey both have nightly curfews as of March 15, 2020).
My question is: does any data exist showing that these measures are effective, or counter-productive? My intuition is that a nightly curfew could actually accelerate the spread of an infectious disease, because citizens who have to leave their homes to do errands are all obligated to do them during a shorter time-window, thereby raising the number of people present in public places at any one time. I couldn't find any published research directly assessing the effectiveness of nightly curfews as an epidemic response strategy. (I only found articles such as this one discussing the failure of nightly curfews in Liberia during the 2014 Ebola epidemic, but those caused public rioting and low compliance). Considering how common this is frequently mentioned and attempted as an intervention strategy, what were the results? Is there any published data from real-world examples, or even results from model simulations?

I'm voting to close this question because it was cross-posted to Medical Sciences.

Cleaned up the comments since they are rather moot now that the question is closed; the discussion can continue on Meta. My personal view is this question is on-topic both at Biology.SE and MedicalSciences.SE, but I'm strongly opposed to cross-posting. A mod at MedicalSciences says it's fine there, so I'd rather close here and instead direct people to https://medicalsciences.stackexchange.com/questions/21448/is-a-nightly-curfew-an-effective-intervention-strategy-for-limiting-the-spread-o


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What is the role of lamellar bodies in lung cells?
Lamellar bodies have been found to be secreted in lung cells many of their associated proteins have been identified. What is the current consensus or research on the function that these lamellar bodies play in lung?
(Sourced answers, please)

Little too broad! Can you narrow it down?

@DevashishDas is it? The answer can just be a few words. Even if you asked me, what is the role of RNA in the cell, I could answer with a few key words even if the full explanation would take a whole book

Well, The paper published in Nature 2003:

Despite two decades of progress in understanding the role of LGs and
their contents in epidermal barrier function, almost nothing is known
about the mechanisms responsible for the assembly of these unique
organelles.source: http://www.nature.com/jid/journal/v120/n4/full/5601763a.html

Since then the word "Lamellar Granule" appeared only 5 more times in journals:

1: Sando GN, Zhu H, Weis JM, Richman JT, Wertz PW, Madison KC.
Caveolin expression and localization in human keratinocytes suggest a
role in lamellar granule biogenesis. J Invest Dermatol. 2003
Apr;120(4):531-41. PubMed PMID:
12648214.
2: Akiyama M. The roles of ABCA12 in epidermal lipid barrier formation
and keratinocyte differentiation. Biochim Biophys Acta. 2014
Mar;1841(3):435-40. doi:
10.1016/j.bbalip.2013.08.009. Epub 2013 Aug 15. Review. PubMed PMID: 23954554.
3: Sakai K, Akiyama M, Sugiyama-Nakagiri Y, McMillan JR, Sawamura D,
Shimizu H. Localization of ABCA12 from Golgi apparatus to lamellar
granules in human upper epidermal keratinocytes. Exp Dermatol. 2007
Nov;16(11):920-6. PubMed PMID:
17927575.
4: Lee WS, Oh TH, Chun SH, Jeon SY, Lee EY, Lee S, Park WS, Hwang S.
Integral lipid in human hair follicle. J Investig Dermatol Symp Proc.
2005 Dec;10(3):234-7. PubMed PMID: 16382672.
5: Kelsell DP, Norgett EE, Unsworth H, Teh MT, Cullup T, Mein CA,
Dopping-Hepenstal PJ, Dale BA, Tadini G, Fleckman P, Stephens KG,
Sybert VP, Mallory SB, North BV, Witt DR, Sprecher E, Taylor AE,
Ilchyshyn A, Kennedy CT, Goodyear H, Moss C, Paige D, Harper JI, Young
BD, Leigh IM, Eady RA, O'Toole EA.  Mutations in ABCA12 underlie the
severe congenital skin disease harlequin ichthyosis. Am J Hum Genet.
2005 May;76(5):794-803. Epub 2005 Mar 8. PubMed PMID: 15756637; PubMed
Central PMCID: PMC1199369.
6: Ishida-Yamamoto A, Deraison C, Bonnart C, Bitoun E, Robinson R,
O'Brien TJ, Wakamatsu K, Ohtsubo S, Takahashi H, Hashimoto Y,
Dopping-Hepenstal PJ, McGrath JA, Iizuka H, Richard G, Hovnanian A.
LEKTI is localized in lamellar granules, separated from KLK5 and KLK7,
and is secreted in the extracellular spaces of the  superficial
stratum granulosum. J Invest Dermatol. 2005 Feb;124(2):360-6. PubMed
PMID: 15675955.

According to the last mentioned paper[6]:

LG(Lameller granule) constitute a specialized secretory system within the epidermis.

LG are seen as isolated oval-shaped granules in post-embedding methods, whereas they appear as parts of beaded tubular structures in cryo-ultramicrotomy

Result highlights the biological significance of LG in regulation of protease activities.

LEKTI labels were aggregated and not evenly distributed throughout the LG system, indicating the heterogeneous nature of the LG  (Ishida-Yamamoto et al, 2004).

Biologically active fragments derived from LEKTI are released extracellularly (Bitoun et al, 2003).

LEKTI labels were seen in the extracellular spaces in the superficial granular layers and the first cornified layer with release from the apical side of upper granular cells. Aggregates of LEKTI immunolabels were also closely associated with the TGN46-positive trans-Golgi network .

Double labeling with antibodies to glucosylceramide, a well-known LG molecule, showed that each occupies a distinct domain of beaded tubular structure

The ultrastructural localization of LEKTI was compared with that of KLK7. As reported previously (Sondell et al, 1995; Ishida-Yamamoto et al, 2004), KLK7 was localized in the LG system but was not co-localized with LEKTI within keratinocytes.

This finding suggests that LEKTI is expressed and released earlier than its target proteases, which is consistent with a role in preventing premature proteolysis of extracellular matrix proteins or cell surface adhesion molecules, and in controlling the timing of desquamation.

Source: [6]. http://www.nature.com/jid/journal/v124/n2/fig_tab/5602696f4.html

(source: nature.com)

Caption: Lympho-epithelial Kazal-type-related inhibitor (LEKTI) is
transported through the lamellar granule (LG) system. Post-embedding
immunoelectron microscopy using Lowicryl HM20 resin (A, D) and a
cryo-ultramicrotomy method (B, C, E). (A, B) LEKTI signals (black
arrows) are detected in the LG using polyclonal antibodies against
D8–D11 in (A) and D1–D6 in (B). Note that LG are seen as isolated
granules in the post-embedding method (A), but appear as beaded
tubular structures in the cryo-ultramicrotomy (B). Lamellar internal
structures are seen in both methods (white arrows). (C) LEKTI is
secreted from the apical side of upper granular cells (arrows). d,
desmosomes. Polyclonal antibody to D8–D11 and desmoglein 1 monoclonal
antibody were used and were labeled with 5 and 10 nm immunogold,
respectively. (D) LEKTI antibody to D8–D11 labels are closely
associated with those of the TGN46-positive trans-Golgi network. (E)
LEKTI (monoclonal antibody, 5 nm gold labels) and glucosylceramides
(GlcCer, 10 nm gold labels) are localized within the same continuous
beaded tubular structure of the LG system.


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Can insects feel pain?
Insects do have a nervous system, even if it isn't nearly as complex as that of other animals. Can insects or other arthropods sense pain? Does their aversion to harmful stimuli suggest that they can 'feel' pain in the sense that other animals seem to?

This question has been asked in different forums and many of the answers say that there is no nociception in insects. This book, however claims that Drosophila do have heat induced nociception and is mediated by TRPA ion channels. Also, there is a gene called painless whose mutation causes loss of nociception.


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Why violets die in closed space?
I'm going to engage into making florariums (a garden in the bottle). I've heard, that violets die in closed space. Do anyone have an idea, what is the reason for that? Lack of oxygen or CO2 or moisture control issues?

We also have gardening and landscape SE. You can consider posting this there.

I believe it is because of the violets' propensity to collect mould. They seem to like warm, humid space, but in a closed-air type system, it is a breeding ground for mould.
There could be another reason as to why they die, but I would assume it would be an infection.

Hi!  Welcome to the site! It would improve your answer if you add some reference/source for your answer.

Thank you for your answer. As far as I know, violets perfectly exist in +20C, is it to warm to breed mould? If that's the point, I guess violets could grow in closed space, provided the mould is tackled (i. e. by chemicals).


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what is the effect of soda water on digestion?
what is the effect of soda water on the process of digestion? As it has been seen that after drinking soda the process is increased...I just want to know that what is the chemistry behind this?

do you have source for this observation?

What should happen? It can be slightly acidic due to carbon dioxide which reacted that way. But the stomach is orders of magnitudes more acidic, which makes sure, that the CO$_2$ is removed from the solution.

Soda, anything carbonated causes bloating, which stretches the stomach. Mechanoreceptors in stomach detect the stretching resulting in parasympathetic innervation to GI smooth muscle. This causes an increase in GI motility.

what about chemistry?

I think unless your talking about caffeinated drinks, or drinks that contain a chemical that affect the nervous system, it's negligible. carbonated liquids are acidic, but like @chris stated above, it's moot compared to the pH of the stomach.

Due to presence of hydrogen ion in soda water ,H+ ion Concentration in stomach is increasing (common ion effect) it helps in digestion.

Please extend your answer and provide reputable support for your claims. Unfortunately, failure to do so will result in downvotes or deletion. Please see our [help] page about writing good answers. Thanks!


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What causes Paresthesia (Pins and Needles) at a cellular level?
I've looked it up in plenty of places like the Wikipedia page and such, and it is clear that the most common cause of Paresthesia is either a fair amount of pressure on a specific patch of skin causing lack of blood flow to the specific nerve endings in that limb (not to be confused with a stop in blood flow to the limb altogether) or a much stronger amount of pressure on that patch of skin for a shorter amount of time. This, although the most common cause, is not nearly the only one, which could be anywhere from simply sleeping on the wrong side of the bed to a lethal injection. I'm wondering what happens to the nerve cells that are affected at a cellular level, and what causes it at a cellular level. The level at which pounds per square inch aren't what is being noticed.

Underneath the superficial layers of your skin there are receptors which sense pressure, temperature and pain. These receptors are part of the peripheral nervous system which senses stimuli and they take the message conveying details about the stimulus to the somatosensory cortex of the brain. Here is where the perception of pain, burning, pressure etc is ultimately made. To take the simplest example, if you stop blood flow for a short amount of time in a limb, these receptors are activated, and will send signals to the brain that are interpreted as tingling or numbness. With more severe pain, different receptors are activated which , again, project to the same brain area but a different message is read out. If the pressure from one limb is removed, the receptors will go back to normal function as blood flow is restored.
https://en.wikipedia.org/wiki/Nociceptor
http://www.scholarpedia.org/article/Mammalian_mechanoreception

The main reason I asked this question was to hopefully get an understanding as to whether it would be possible to stimulate a group of these cells in the peripheral nervous system to induce the feelings of tingling numbness from outside of the skin using a form of directed energy such as directed sound or a laser. The problem with finding the right kind of stimulus is that I don't know whether the cells send out an electrical signal back to the brain or some sort of chemical signal. Do you know if it's possible, and if so with what kind of stimulus?

This would in theory be possible. You would have to create a stimulus which matches the response profile of the receptor you want to target. The signals to the brain are electrical-- between cells-- but locally release of chemicals can triggers the electrical signals. For example during injury, the body can release certain chemicals which can numb pain at the release site and your brain perceives this as "reduced pain". A lot of sensations can be felt outside the skin already. If you think about sensing a hot oven just by going close to it or air pressure from a blow-dryer on your skin.

So without considering something which would cause excessive nerve damage or that would last longer than a common case of paresthesia, what kind of stimuli could stimulate the nerve clusters through the skin in the same way as stopping blood flow. While I was reading about the sensation, I saw somewhere that it could be triggered with an excessive amount of vibration like in the case of motorcycle riders while they grip their bikes over jumps, which is known as, "cyclist's hands". This is why I'm thinking a directed sound device could create the vibrations with a high enough frequency.


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What, if anything, would prevent flying fishes evolving to be capable of extended flight?
This extraordinary video documents a flying fish gliding above the surface of the sea for nearly two minutes. Occasionally it uses its tail for added impetus.
It is possible to imagine a fish gliding like this for longer and longer. However it would still be gliding. Is there any physiological reason that these animals couldn't evolve to flap their 'wings' and even learn to soar?
Another consideration is why this should happen. As I understand it, the behaviour is an adaption for escape from predators.  They do not fly in order to catch prey. What prey might they hunt in the air in the ocean?
Questions

Is there any physiological/anatomical dead-end that would prevent flapping/soaring from evolving?
Is there any adaptive reason that flapping/soaring should evolve?

The first problem is that they have gills and cannot filter oxygen out of the air... so they wouldn't get very far before suffocating. Second would be that  the mass to surface area of wings. Birds wing bones are very porous, so there is very little mass with a rather large surface area. Also they likely do not have the same type of muscle development. The flying fish generate most of there propulsion form their tails, not their side fins. Also birds tails are parallel to the ground which provides stability in flight while the fish are perpendicular, which helps with water propulsion.

I think this would be a better fit on World Building. The question is extremely broad and hypothetical, and is difficult to answer given the scope of this site.

Maybe I'll ask for it to be moved.


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Why don't snails run out of slime?
I understand that land-snail-slime and slug-slime are made of mucus.

Externally, one kind of mucus is produced by the foot of the gastropod
and is usually used for crawling on.
https://en.wikipedia.org/wiki/Snail_slime

Travelling on a trail of mucus seems very expensive. How do snails manage to replace it so abundantly without ever running out? Do they ever run out - if so, what happens to them?

Cool info here: https://www.google.com/search?q=mucus+slug+dry+weight&oq=mucus+slug+dry+weight

Why don't you run out of mucus when you have a bad cold?

@jamesqf  If a human produced mucus in the same proportion to body size as a snail, they would dry out within minutes. Also a lot of mucus from a cold gets swallowed and so is recycled.


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Phylogenetic algorithms: How to interpret multiple ML trees from the same dataset?
There's still something that confuses me about how many of these algorithms work, and how results are presented in the literature.
Let's consider a Maximum Likelihood based algorithm like MrBayes or RAxML: Users set a random number seed which generates the starting tree. For many of our datasets, different seeds which result in different ML results, as the algorithms are initialized with different trees.
I'm not entirely sure how one is supposed to interpret this, especially as my experience with ML methods is that the initial step is irrelevant to the global/local min/max in parameter space----the chains just take longer to converge.
How should one interpret these results? Are users to run 1000s of trees at different parameter values, and then chose the most optimal likelihood value? That seems rather ad hoc, as does bootstrapping, etc.
Is the dataset fundamentally flawed?

MrBayes is definitely not doing maximum likelihood, as its name suggests.

@kmm Was trying to make this question relevant to several algorithms, and failed. Thanks for the help! I'll try to edit

In short, you have chosen two examples that do not use maximum likelihood as you know it in other contexts. In most statistical contexts, the ML is a single number which can be calculated analytically, so it it always the same for a given data set. This is not the case for either MrBayes or RAxML but for different reasons.
MrBayes
The likelihood criterion in MrBayes is the marginal likelihood of the posterior, given effectively the data conditioned on the priors. This likelihood comes from a stochastic MCMC sampling of the parameter space. If all is well behaved, then the chains and/or runs will converge in the same general location. But then the different possible topologies need to be summarized in some way.
RAxML
RAxML generates essentially random starting trees by random sequence additions to build up trees. The subtrees are then rearranged to find a "best" tree. Again, different starting points may lead to different best trees. But if all goes well, analyses will end up with the same tree. This process is described in this chapter.
In both cases, if you start in a different place, you may end up in a different place. There may be many trees that are, within some criterion, equally likely. If you are familiar with parsimony methods, the analogy is that of multiple equally parsimonious trees.

I'm not sure I follow this: "If all is well behaved, then the chains and/or runs will converge in the same general location. But then the different possible topologies need to be summarized in some way." (1) If the chains converge in the same general location, wouldn't the topologies be equivalent? (2) How would one summarize the different topologies---consensus trees?

Also, " There may be many trees that are, within some criterion, equally likely. If you are familiar with parsimony methods, the analogy is that of multiple equally parsimonious trees." How does one proceed in the literature then? Do you report all equally likely trees? Use (again) consensus tree methods?

Rather than there being a single tree with the highest (maximum) likelihood, there are a family of trees that are all possible, just some more likely than others. The topologies don't have to be equivalent. A consensus tree is the summary of those trees considered most likely or credible (in the Bayesian sense). Yes, you would report the consensus tree (or as many as you want).


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How exactly are gaps defined in genomics?
My understanding is that when sequencing a genome, "gaps" refer to fragments which were not sequencing in the sequencer.
Is this correctly? What are there other meanings to the term "gap"?

You're not wrong but gap can mean more than that. A good recent reference is this paper: Genetic variation and the de novo assembly of human genomes.
Essentially, a gap occurs if something happens in our genome that can't be explained by uniformity. Since our genome is highly complicated, you can expect gap is also more than just mis-sequencing. The gap you mention is the sequence-coverage gaps mentioned below.
This paper has a section about the types of gaps.

1. Sequence-coverage gaps
Sequencing gaps occur, under the simplest condition, where no sequence reads have been sampled for a particular portion of the genome.
2. Segmental duplication-associated gaps
Over one-third (206/540) of the euchromatic gaps in the human reference genome (GRCh38) are flanked by large, highly identical segmental duplications.
3. Satellite-associated gaps
These include short and long runs of tandem repeats designated as short tandem repeats (STRs; also known as microsatellites), variable number of tandem repeats (VNTRs; also known as macrosatellites) and Mb-sized centromeric satellite repeats.
4. Muted gaps
Muted gaps are defined as regions that are inadvertently closed in an assembly but that actually show additional or different sequences in the vast majority of individuals
5. Allelic variation gaps
Some regions of a genome also show extraordinary patterns of allelic variation, often reflecting deep evolutionary coalescence.

The word ‘gap’ can be used both loosely and in specific genomic contexts, as listed by @Student T. The usage that seems to relate to your question — Sequence Coverage Gaps — is quite nicely illustrated in the Wikipedia entry on ‘Contig’. I reproduce, below, a modified form of a (public domain) illustration from it.

The sequences of the ‘contigs’ (see legend) are known completely as the ‘reads’ (solid blue arrows in legend) overlap, even though the ‘fragments’ (see legend) contain unsequenced regions. However because the length of the fragments can be determined roughly (e.g. by gel electrophoresis) — here fragment 5 is the key — the two contigs can be assembled into a ‘scaffold’ with a gap of (approx.) known length. I have marked this as ‘Gap’ in green.

Thanks for the explanation. Please also check my answer.

Nice categorization @Student T! I've modified the opening para of my answer to relate it to yours. I think it's worth keeping as it goes into more detail on sequence coverage gaps and introduces some other relevant terms.


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Why use RRBS (reduced representation bisulfite sequencing) instead of general BiSeq?
My understanding is that RRBS is used for certain cases. For example, WGBS (whole genome bisulfite sequencing) is limited by repeated sequences.
However, many papers seem to use both techniques.
What are the reasons researchers would use RRBS instead of WGBS?

The use of RRBS instead of WGBS is mostly about coverage vs. cost.
To confidently call methylation status at a cytosine residue, you need to have at least 10x sequencing coverage at that particular residue (ENCODE standards require at least 10x coverage for RRBS and 30x coverage for WGBS). To perform whole-genome bisulfite sequencing (WGBS) on large genomes (e.x. mammalian genomes) is very expensive if you are trying to achieve the 10x coverage requirement.
The principle behind RRBS is to improve the sequencing depth of cytosine-rich areas by enriching your sequencing library with CpG-dense regions of the genome. This is accomplished through the use of CpG-specific restriction enzymes like MspI, which recognizes 5'-CCGG-3'.
In RRBS, the entire genome is cleaved using MspI, leaving at least two cytosines per cleaved DNA fragment (one cytosine at either end of the MspI-MspI fragment). Sequencing libraries are constructed from size-selected MspI DNA fragments, bisulfite conversion is performed, and the converted library is sequenced. Specialized software is needed for alignment and analysis of the converted genome (e.x. Bismark, methylKit).
One of the major limitations of RRBS is that you will sequence only CpG-rich regions of the genome. Also, since the library is size-selected after MspI digest but before adapter ligation, you will never sequence any MspI fragments outside of your size-selection range (~40-250 bp).
I have analyzed both types of data and found that the RRBS data was very unsatisfying and didn't answer our research question. WGBS, though extremely costly, is a better option for a comprehensive cytosine modification profiling. There are publicly available RRBS and WGBS datasets at https://www.encodeproject.org/.
I must mention a critical limitation of both techniques in that neither RRBS nor WGBS can distinguish between the type of modification (methylation, hydroxymethylation, carboxylation, etc) present at a particular cytosine residue. RRBS and WGBS, which rely upon the ability of certain modifications to protect cytosines from deamination, can only be used to determine whether cytosine residues are modified or not.
Further reading:
I would suggest following this link for an exceptional technical and practical article in which the authors compared RRBS to WGBS: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026711/
A more technical guide to RRBS: http://www.bioinformatics.babraham.ac.uk/projects/bismark/RRBS_Guide.pdf

can you add some references for others to understand your answer better? it would improve your answer - thanks


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Why is chronic lymphocytic leukemia (CLL) most common leukemia in the West but so rare in Asia?
In "Advances in Chronic Lymphocytic Leukemia" (2013, Edited by Sami Malek), several times it is stated that CLL is very common in Western countries.
However, it is quite rare in Asia. (I do not have data regarding other regions in the world.)
Why would this be? I am familiar with cancers being related to lifestyle, which varies by country. (The obvious example would be how countries with high rates of smoking have higher rates of lung cancer.)
Do we have any reasons why this is? Thanks for any help.

This paper should help get you started. The exact reason is not yet known, but is most likely related to germline genetic differences between the two ethnic groups, as Asian immigrants to the US continue to have a low incidence of CLL.
References:

KAWAMATA N, MOREILHON C, SAITOH T, et al. Genetic differences between Asian and Caucasian chronic lymphocytic leukemia. International Journal of Oncology. 2013;43(2):561-565. DOI:10.3892/ijo.2013.1966.
American Cancer Society: What are the risk factors for chronic lymphocytic leukemia?


text:
Can sexual selection operate in temperature dependent sex determining organisms?
Or more broadly, are distinct forms of genetic inheritance (ie. sex chromosomes) needed for sexual selection?
My thinking was that since there are no sex determining loci, there could not be linkage to mutations that are subject to sexual selection.
Given the large sexual dimorphism in crocodiles (wikipedia), I would expect sexual selection is acting in crocodiles, but how are those phenotypes heritable if there are no sex chromosomes?
I know the sexual dimorphism could be due to differences in gene expression, but that still leaves me with a chick-egg problem. What causes the differences in expression?
I'd like to know if there are any studies that have looked at this kind of question.

Sexes are required for sexual selection, not sex chromosomes

Can sexual selection operate in temperature dependent sex determining organisms?

Yes! Crocodiles are indeed a good example as the sex in determined by the temperature (ref) and they have some traits evolving through sexual selection (ref).
I think you went almost all the way to the answer in your thoughts. Let's categorize things a little bit and talk about Genetic Sex Determination (GSD) and Environment Sex Determination (ESD) separately; that might help.
Note that ESD and GSD are two extremes of a continuum present in nature. Note also that I will talk about sexual dimorphism only and not specifically about sexual selection. Of course sexual selection is one process that can yield to sexual dimorphism. You can replace "locus involved in sexual dimorphism" by "locus involved in selection selection" in what follows and that will work as well expect that we will lose some generality.
Genetic Sex Determination (GSD)
Physical linkage
Indeed if you have sexual chromosomes, then you can have loci sitting on those sexual chromosomes that are affecting only one sex and therefore have genders with different appearances.
Gene expression
As you noted as well, those genes causing sexual dimorphism can also be sitting at different position in the genome and be regulated (directly or not) by the sex determining locus.
Environment Sex Determination (ESD)
If there is no genetic variance for sex but the whole variance is exclusively environmental (ESD), then phenotypic differences between males and females are just determine by whatever environmental variable (temperature for example) is used. In other words, you can have loci being under antagonist selection pressure between the two sexes that is regulated (more or less directly) by the temperature.
In short, you can have sexual dimorphism in ESD just like in GSD that...

the causal agent of the sexual dimorphism is not the sex determining locus but some environmental variable.
sexual dimorphism cannot occur through physical linkage (as there is no genetic variance to determine the sex) but only through regulation of expression.

I recommend this book (although a little expensive).
Do males of all sexual species have Y chromosomes is a somewhat related post but might be too introductory for you.
Here is a nice figure from Bachtrog et al. 2014 that offers an idea of the diversity of sex determination system (thanks @rg22)

See the tree of sex (mark Kirkpatrick,  Judith mank, Doris Bachtrog and many more) for a good figure on the diversity of sex determination systems

http://bbrowse.biol.berkeley.edu/treeV2/files/slide1.jpg


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How do biologists quantify "gene expression" in experiments?
I've read papers which contain statements such as "control of gene expression is critical in biological processes".
How exactly does one quantify "gene expression"? Isn't gene expression an umbrella term describing all of the mechanism by which DNA is synthesized into an organism's phenotype?

probably with SDS Pages. At least I assume this. And by comparing one Page with the other one from another e.g. plant part. Often this is also done using GFP proteins or other marked proteins and quantifying those ones using microscopes... doing westernblots or just coloring the material at defined time points (which will kill the material most probably but also gives an insight)... is it something like this what you are asking? The methods?

@TheGreenOne Yes, the methods and the quantifiable features they used (from let's say, phenotypes, or perhaps something related to mRNA) to measure this. The question is a bit general, I know.

Gene expression involves RNA synthesis (or Transcription), NOT DNA synthesis.  The study of DNA synthesis is usually called DNA Replication.

There are several techniques. Possible duplicate of http://biology.stackexchange.com/q/8153/3340

The primary product of protein coding genes are mRNAs.  When we talk about measuring gene expression we want to assay the steady-state levels of a specific mRNA within a cell.  This is usually accomplished by starting with a large number of cells and harvesting all of the mRNAs from all of the cells.  One way to measure the expression level of just one gene's mRNA is to perform a Northern Blot.  Other sensitive methods include: an S1 nuclease protection assay, an RNAse protection assay, and a primer extension assay.
Microarrays have also been used extensively to measure expression levels of thousands of genes at the same time in a single experiment.
With the advent of RNA-Seq methodology it is possible to count the number of transcripts in an experiment (if you have a sequenced reference genome)

According to next generation data:
I was never working directly with mRNA but what I got from the bioinformatician was something like this: you extract your mRNA, sequence it, filter it according to the quality & length, assemble it and what you then have is something like "transcripts". Those you are counting: xy of transcript1 & yx of transcript2. You are further looking for isoforms and in the end you are correcting this counts according to the initial reads which you computed. Comparing the transcripts to a control you can measure if its up or downregulated (setting the reads of the control as "zero" like 1234 reads of one transcript are normal..... in sample 2 you have 5000 reads of this transcript... the gene seems to be upregulated). As far as I know is is approximately the way how gene expression approximations / quantifications are made.


text:
How does one apply Bayesian inference to quantify a read the deeper you sequence?
For NGS sequencing technology, the "deeper" you sequence given fragments, the more certain you are of what is being sequenced. This sounds like a simple application of Bayes's Rule.
What is the normal approach in the field to quantify one's level of certainty in NGS sequencing with Bayesian methods? There is also a statistical question here in terms of how one aligns reads, etc.

This is a very broad question. There are possibly a thousand ways by which someone can apply bayesian inference to NGS data.

@WYSIWYG I'm happy to delete the question. Could you refer me to techniques used now?

You can have a  look at some of the RNAseq quanitification methods. There, one of the problem is to find out where exactly does a read come from (when there are many homologous regions). Bayesian methods are applied to infer the location of the read given its counts. From this the overall gene expression is estimated.

@WYSIWYG Sorry to be lazy, but the names of these methods?

I have a reasonable level of familiarity with Bayesian methods, but not so much with NGS. If you can explain the question better I might be able to add something here.


text:
Are "constraint trees" in phylogenetic analysis cheating? How can I correctly use them?
How do phylogenetic experts evaluate results which use constraint trees? Are there examples in the literature where phylogenetic experts detail how they use constraint trees?
Here is my problem. I have 500 samples. These are five different "categories" of species A, B, C, D, E, 100 samples each.
Category A: A1, A2, A3, ..., A100
Category B: B1, B2, B3, ..., B100
Category C: C1, C2, C3, ..., C100
Category D: D1, D2, D3, ..., D100
Category E: E1, E2, E3, ..., E100

There are two classes of which these "categories" fit in: Class 1: A and B, Class 2: C, D, and E.
For the purpose of this discussion, let's say A=whale, B=dolphin, C=mouse, D=gerbil, E=hamster
When I do the analysis, there are some problems. The output tree resolves the samples into two classes which meet my expectations; it splits the samples into two groups: ( A & B) and ( C & D & E ). That's great. However, it doesn't resolve the species into separate categories, e.g. it mixes together "whale" samples with "dolphin" samples, and mixes together all the individual C, D, E . I see
(A1, B3, A27, B23, B2, A2, A3, A4, ....), (C3, C5, D72, D3, E1, E2...).

This would mean whale1 is more evolutionarily "related" to dolphin3 than whale 27.
I try to use a constrain tree instead to constrain each of these groups, using the form
((A1, A2, ..., A100), (B1, B2, ..., B100), (C1, C2, ..., C100), (D1, D2, ..., D100), (E1, E2, ..., E100))

Sure enough, my tree now resolves each "category" A, B, C, D, E into a distinct category.
Question 1: Isn't this cheating? I feel like I stipulated "resolve the tree in this manner I expected" and RAxML output that.
Question 2: How do I evaluate whether this is correct?
Question 3: For experts, could direct me to published literature which used this approach? Which papers used RAxML constraint trees?
Thanks for any help. I'm happy to clarify things.

I understand where you are coming from when you say that it feels like cheating. However, there are a coupled of things to keep in mind. First let's consider why your tree topology might not reflect concordance with intuition/species trees:
1) Presence of artefacts such as long-branch attraction
2) Lack of sufficient phylogenetic signal/presence of non-phylogenetic signal (due to, for example, convergent evolution in the sequences)
3)Horizontal gene transfer (unlikely in animals).
4) Incomplete lineage sorting/deep coalescence (hemiplasy).
Only in the case of 3 and 4 does your tree reflect true relationships among taxa that genuinely differ from the species tree. Cases 1 and 2 are artefactual. In cases 3 and 4, it would not be appropriate to use a constraint tree to get a species-tree concordant topology because the resultant topology would not reflect the 'true' relationships among taxa (i.e. would be 'cheating'). In cases 1 and 2, I would argue that it is appropriate to use a constraint tree to get the species-tree concordant topology (depending of course on what you want to use the tree for) because you know that the your current topology is species-tree discordant because of artefacts and is therefore not reflective of the 'true' relationships among taxa. Of course, you are unlikely to know a priori what factors (1-4) are causing your bad topology (though you can do some tests for long-branch attraction for example -- see Cladistics 21 (2005) 163–193).
What you can do is test whether the log-likelihood of your non-constrained tree and your constrained tree differ significantly. You can use tree topology tests such as the  Kishino and Hasegawa (KH) test. I don't know about RaxML, but IQ-TREE has excellent topology testing: http://www.iqtree.org/doc/Advanced-Tutorial. If your constrained topology is significantly different (statistically) from the ML topology, then you probably should not use the constrained tree. I am by no means proficient in phylogenetics concepts so I would take my advice with a grain of salt, hopefully some of the other members can illuminate the issue a bit further.


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How do catenanes form when DNA replicates?
So I am taking a course in DNA replication and repair. And we are talking about catenanes forming when DNA replicates (two circles of dsDNA interlinked) How is this possible?

The first DNA circle is double-stranded. If you could melt the double-helix completely you would not be able to pull the two stands apart without breaking the sugar-phosphate backbone of at least one of the two strands. This is a topological problem, the two strands are linked to each other.
Now consider DNA replication. In the simplest example there is a single origin of replication and there will be two replication forks proceeding around the circular genome in opposite directions. This is exactly what happens during DNA replication in the bacterium E. coli.  The DNA double helix of the parental molecule "melts", the RNA primers are synthesized by primase, and the DNA polymerase complexes initiate synthesis. Behind each replication fork there are now two hybrid DNA strands, each with a parental strand, and a new daughter strand.
Thus far no sugar-phosphate bonds have been cleaved. When replication is done each daughter ds DNA helix will have a single-stranded nick at the origin, and another one at the site where replication terminated, but those will be quickly repaired by DNA polymerase I and DNA ligase. Even if those two repair enzymes were inhibited, and you could somehow melt the DNA strands of both the daughter chromosomes, you would only be able to pull out the new DNA molecules (with the nicks), the two original parental strands are still topologically linked.
To resolve two concatenated DNA circles you need to make a double-stranded break in at least one of the ds circles. This  enzymatic activity is provided by a class of enzymes named Type II DNA topoisomerases.

Thanks for clearing that up for me, any good videos that show this in action?

When replication is done each daughter ds DNA helix will have a single-stranded nick at the origin-can you substantiate your claim with reference?

Do you have access to a recent biochemistry or molecular biology textbook? DNA replication requires a newly synthesized RNA primer, and that primer has a 5'-triphosphate.  When DNA polymerase completes the synthesis of the new daughter DNA strand, then DNA polymerase I uses its 5'-3' exonuclease activity to degrade the RNA primer (also called nick-translation).  When that is finished the daughter strand is not a covalently closed circle.  The enzyme DNA ligase (plus ATP or NAD) is required to 'heal' that nick and repair the sugar-phosphate backbone.


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Types of heparin
My textbook(biochemistry 4th edition, U. Satyanarayana) says that the following structure is of heparin
and it's name should be D-Glucuronate 2-sulfate, N-sulfoglucosamine 6-sulfate.
 I searched on internet but could not find this kind of heparin.
So could anyone give credibility that this structural compound is heparin?
Atlast what is the criteria that determines whether the compound is a heparin?

Why downvotes? Am I wrong?

This structure is exactly the same structure as found on wikipedia at the very top the page. Other variations are also shown elsewhere on that page.
Perhaps you are being misled by the presence/absence of hydrogens on the sulfate groups? The way your textbook shows it is a more physiologically relevant way as those groups would be deprotonated in normal biological conditions, but this doesn't really change the chemical structure. Heparin is normally administered as a salt.
Further, heparin is a polysaccharide chain of varying lengths (more information on that same wikipedia page) - it doesn't really make sense to say that heparin's chemical name should be "D-Glucuronate 2-sulfate, N-sulfoglucosamine 6-sulfate" - this is the name of only one disaccharide in a long, long chain. Your textbook doesn't say that either, the little "n" in the lower right corner is very important and indicates a chain of unspecified length.

on what basis we classify those(other variations)  as heparin?

Wikipedia shows iduronate on the very first pic while the book depicts glucuronate.

Sorry, you are correct; if you read more on the wikipedia article it mentions  the composition of heparin which includes both - it really doesn't matter much which are depicted. Heparins are just glycosaminoglycans of a variety of subunits - there is no one specific chemical called "heparin" but they all have roughly the same biological function - welcome to biology :)

This link might help you sort out some of the details in terms of where the boundaries are between heparins and similar compounds.


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Chief Sensory Cells
What makes the second order neurons of posterior grey horn of spinal cord to be called as "chief" sensory cells?
Why don't we call 1st order, or third order neurons or other second order neurones in different part of spinal grey part as "chief" ?

Eh, searching on Google a bit, this terminology seems limited to two Indian sources: one textbook and one study guide, and isn't used anywhere else. There is a different area called the "chief sensory nucleus" which is separate. It just seems to be an attempt by those couple sources to refer to the cells which aren't one of those other categories. It isn't meant to indicate some special significance for those cells versus cells at other hierarchical levels, rather simply trying to classify different cell types within the spinal cord.


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A limit to birds affinity for high vantage points
Birds seem to have a natural affinity for high vantage points, including power wires, the tops of trees, and the sides and tops of buildings.
However I presume the top of the Burj Khalifa is not packed with birds, flyover video of cities full of skyscrapers suggest this would not be the case.

Q: Therefore, is there a cap, if so at what height, where higher is no longer better? Perhaps the birds vantage point is reduced by going higher.

Related, but I feel different: Why do crows sit on treetops even when it is cold?

Not all birds do this.  For instance, the quail I can see outside my window right now like to stay on the ground, and hide in tall grass.  Ducks and geese seldom land anywhere but water or flat ground.  Hawks & eagles may perch/nest on the sides of cliffs or steep slopes (and I've encountered them flying several thousand feet AGL).  As mesam22 says, it's all about evolutionary niches.

Birds find their niches based on many reasons. Their choice is based on primarily resource availability, predation risk, and competition. Keep in mind there are variations among species, most birds like to forage for food at a hight safe enough to avoid ground predation, at the same time to be able to see and find food without much competition. Therefore very high altitudes do not seem beneficial for food resources and its a cost in energy, thus reasonable altitudes are preferred. But again many variations depending on species and location.

Could the majority of birds fly to the top of Burj Khalifa?

wow, Excelent point as well. ("Most birds fly below 500 feet except during migration." - https://web.stanford.edu/group/stanfordbirds/text/essays/How_Fast.html) Thats 1/5th as far.


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How distantly related are eusocial insects? Aren't members of a species much more related than 1/4, 1/2, or 3/4?

Possible Duplicate:
How many genes do we share with our mother?

I went to a lecture that talked about the behavior of social insects in terms of their relatedness of genes. For instance, workers were 3/4ths related to each other, so it was in their gene's interest to care for each other instead of having their own, half-related offspring.
However isn't it the case that members of the same species are much more related than 1/2 or 3/4s? I've read that we share anywhere from 95-99% of our genes with chimpanzees. Also I believe I've read (perhaps in Pinker) that we share some 60% of our genes with daffodils.
So when they talk about the relatedness of social insects, and they say it's 1/2 or 2/3 or 1/4, aren't they really talking about the 1% to 5% of genes that are in play in sexual reproduction within the species? In other words, aren't I 97% + 1/2 * 3% related to my sister, assuming human beings share 97% of our genes?

I guess the issue is that related is a generic term that can induce confusion without a proper definition.

In evolutionary genetic comparison, you are talking about members within species. They will share almost all genes, because if they didn't they would belong to a different species.
However, within species there exist different versions of the same genes, called 'alleles'. When we say that you are 0.5 related to each of your parents, we mean that statistically, 50% of your alleles should be those which your father has, and 50% of your alleles are those passed down from your mother.
Eusocial insects have different mechanisms. Bee males are produced without fertilisation, meaning that they only have one copy of each bee gene. When the male produces sperm, it only has this one set, so all sperms end up carrying the same set of alleles.
Females on the other hand have the normal double set, with two different versions of each gene. So if you look at one gene, half of the female's egg should have one version and the other half should have the other version. All females of one hive are produced by the same queen and the one male that she mated with. Remember, the male only has one set, so the versions coming from the male are the same in all female offspring.
This means a female's genes are made up of: 50% from the father (these are the same across all females) and 50% from the mother (where half the females have one version and half have the other version). Statistically, this means that looking at one gene, there is a 75% chance that two bees will have the same version of that gene.

So it's not only the selfish gene, but also the selfish allele?

Yes, evolutionary biologists tend to talk about genes when they mean alleles. (Usually because what they are saying goes for both genes and alleles; the 'relatedness' is an exception to that)

So in biology, there is gene competition between species, and allele competition within species?

That sounds possible to me, but I think that's another question which I'm not very confident about.

The part that is probably specific to this question is that some species of insects divide their population in the reproducing individuals, that are usually diploid and the working individuals, that are sometimes haploids, meaning they only have one copy of their set of chromosomes. This means that the workers have about half the amount of DNA material compared to reproducing individuals, although they share that copy in full with the diploid individuals.
There are variations of this mechanism in different species. Some species keep the copies but epigenetically "shut down" one of the copies. Others shed specific bits of the genome in the somatic cells. Sometimes this loss of DNA is not perfect, so different parts of the genome are lost just by chance.
We humans don't lose any material at all, we just epigenetically "shut down" one of the X chromosomes in XX individuals -- females.


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What does "melanistic phase" mean in regards to black jaguars?
From Black Jaguars in Belize?: A survey of melanism in the jaguar, panthera onca by John R. Meyer:

There occurs in jaguars, as well as in leopards (Panthera pardus), a melanistic phase which has been much sought by zoos for exhibition purposes. This color phase was relatively difficult to acquire until the 1970's, by which time a few zoos, among them the Jacksonville Zoo, had begun to breed them regularly.

And likewise on the Wikipedia page for Black Panther:

This "black cougar" was most likely a margay or ocelot, which are under 18 kg (40 lb) in weight, live in trees, and do have melanistic phases.

I don't understand this term "melanistic phase", which makes it sound like the jaguar has a period of time in which it is black.  However, it looks like it means something else, i.e., along the lines of What does phasing mean?, but I don't really understand that.
What does "melanistic phase" mean in regards to black jaguars?

I think it is coming from color phase (see meaning 2: https://www.merriam-webster.com/dictionary/color%20phase or meaning 1: http://www.dictionary.com/browse/color-phase)

In this context, "phase" means the same thing as "color phase". Here's the definition from Merriam-Webster:

1: a seasonally variant pelage color
  2: (a) a genetic variant manifested by the occurrence of a skin or pelage color unlike the wild type of the animal group in which it appears (b) an individual marked by such a variant

So it sounds as if "phase" originated in the case of animals that spent a season with a particular pelage (meaning "fur, hair or wool"), such as the snowshoe hare, which is brown in summer and turns white in winter, and the term then began to be used for animals that might be a different color from other individuals of that species. If the alternate color was caused by a recessive allele, most offspring of that individual would have the wildtype color unless bred with another double-recessive individual, and alternate offspring might spontaneously be born to wildtype heterozygous individuals, so pre-Mendel biologists might have seen it as a "phase" between wildtype generations.
As you can see from the illustrations on the snowshoe hare Wikipedia article, "morph" is much more commonly used today for this kind of visible variation within a species. Wikipedia has a fuller description of the nomenclature of this and related terms.


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Alfred Jost's rabbit experiment: how did he actually do it?
I was watching a Crash Course on Biology YouTube video by Hank Green: Great Glands - Your Endocrine System.  Hank humorously describes a sex determination experiment by Alfred Jost as follows (beginning at time 9.17 in the video):

So, he, ah, very carefully... very, very carefully (and this is a little disturbing) removed bunny embryos from their mother, and then, also very carefully, removed the part that would become the ovaries or the testes from the bunny embryos.  And then, also very carefully, he put the embryos back in the momma rabbit.
What Jost found, after the bunnies were born, was that the ones that he performed the surgery on turned out to be girls.  So, in the absence of gonads, and therefore hormones that specifically instructed the development of testes and the growth of a pee-pee and a deep bunny voice, he discovered that the default setting for mammalian embryos is "make it female".

Q: How did Alfred Jost actually perform this experiment?
Essentially I'm after a less superficial description of how Jost implemented this experiment in practice.
I did a bit of Googling; what I found was consistent with Hank's description, but still omits a description of how Jost excised rabbit embryo gonads (instead just asserting that he did it).

I assume the procedure is very similar to castration or spaying practiced on fully developed animals, but done very carefully. The harder part of the operation would be removing the embryo and putting it back without damaging it too much to keep growing.

Check out Fig. 7 in the document at http://ipubli-inserm.inist.fr/bitstream/handle/10608/4343/MS_1991_3_263.pdf . The caption says: "Castration of a 23 day fetus. [Mother's] womb is open, the rear end of the fetus is pulled out, a flank incision is performed, and the testicle, located on the mesonephros, is exposed, then cut. After bilateral testicular removal, the fetus is re-placed in the womb. [..] For ease of explanation, an older fetus is in fact shown."

I don't read French, so I might be missing it, but I can't find any photographs, just some diagrams of the reproductive organs.

sorry, link fixed now

That looks a lot more complicated than when I used to castrate pigs. Thanks for clarifying that.

The picture I indicated shows only the castration of the embryo. Mother's oophorectomy is not described in the above link, and must be trivial. For completion, here's a rat oophorectomy: http://www.nature.com/protocolexchange/protocols/2152


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Familial Hypercholesterolemia
Why does Familial Hypercholesterolemia shows autosomal dominant pattern?
Let us take that there is mutation in LDL receptor gene, it is said that:

The LDL receptor gene is located on the short arm of chromosome 19 (19p13.1-13.3).[6] It comprises 18 exons and spans 45 kb, and the protein gene product contains 839 amino acids in mature form. A single abnormal copy (heterozygote) of FH causes cardiovascular disease by the age of 50 in about 40% of cases.

Shouldn't the expression of the other normal allele mask the effect of abnormal allele by producing the receptor protein?
So, why does this disease show dominant pattern?
Is there anything extra?

Source: https://en.wikipedia.org/wiki/Familial_hypercholesterolemia

Why does the cell not up regulate the expression of normal allele?

According to Wikipedia : Up-regulation occurs, for example, when a cell is deficient in some kind of receptor. In this case, more receptor protein is synthesized and transported to the membrane of the cell and, thus, the sensitivity of the cell is brought back to normal, reestablishing homeostasis.

So, why does cell not produce LDL receptors by up regulation?

Let us continue this discussion in chat.


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Why do nerve fibres rotate?
Background: Lemniscus (Latin lēmniscus, ribbon) is a strap of second order nerve fibres which twist as they ascend to the brainstem.

Why do these these nerve fibres rotate?
 What could be the functional significance of such rotation?
I think that rotation is somewhat less beneficial because firstly it causes increase in length thereby increasing the conduction time , secondly it may decrease structural integrity of such a bundle of axons.

Why downvote????

I didn't downvote, but I think you are overestimating the amount of twisting that occurs, it isn't going to affect length substantially. If you mean the quarter-turn twist that makes caudal inputs turn lateral and rostral inputs turn medial then indeed this is a very minor twist. Not everything in biology is significant in terms of function, often things are significant for development; a slight twist might help to coalesce the fibers. I'd also say that the structural integrity argument makes no sense, think about how a rope is constructed via twisting smaller fiber strands for strength.

Okay. Does this make any functional significance just like decussation?

It is probably relevant for the orientation of the homunculus in, for example, the VPL of the thalamus, but I think it's more an issue of it being important that there is a spatial organization of the fibers, rather than any particular orientation being important.


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Understanding Enzyme saturation curve

From the above picture it can be seen that, in the region "B" the activity of enzyme is not proportional to the substrate concentration.
Why don't we achieve enzyme saturation linearly? Why do we go through that curved phase( region B )?
Why don't all enzyme gets saturated at a point?

The binding of substrate S to enzyme E is an equilibrium which means that there will always be some free enzyme (V is proportional to ES). Section A of the line isn't really linear at all.

At very high substrate concentration, the process will become diffusion limited. At that point adding additional substrate will no longer improve enzyme effectiveness, thus we get a curve and not a straight line as the enzyme concentration is constant.


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Why difference in degree of folding in a cell?
For a cell to maintain constant volume, input should be equal to output of substances.

My question is, if the basolateral membrane, by less folding can attain the same rate of transport as of the apical surface with microvilli, then why do cells produce more foldings (microvilli)?
Why is there a difference in degree of foldings on each side?

This is not my area of expertise, but assuming that the concentration gradient is significantly different on each side of the cell, there should be different transport rates over a given membrane surface area simply from the different diffusion rates. Throw in varius pumps and transporters, which can differ in localization and numbers and there should be no reason to assume identical transport rates in the membrane. Therefore I would suspect that the increased surface area on one side serves to maximise passive absorption while the other side acts as an active transporter expending energy.


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Microalbuminuria in inflammation of urinary tract

Albumin is excreted into urine (albuminuria) in nephrotic syndrome and in certain inflammatory conditions of urinary tract.$^1$

How is inflammation in urinary tract related to increase in albumin excretion? I know that microalbuminuria will result when albumin filtered is greater than its absorption( which takes place in nephron, not related to urinary tract).

My attempt : After some research I found this, which states cause of microalbuminuria in children may be causing infection in glomerulus, leading to increased permeability of glomerular basement membrane.
So, will it be correct to say that UT inflammation is not causing directly microalbuminuria?

UT infection in glomerulus causes inflammation of Glomerulus which causes increased permeability of glomerulus that directly cause increased filtration  of albumin. So, more is excreted as well.

in a nut shell, its indirect effect?

Direct effect.  Inflammation caused increased permeability which itself means protein filterablity.

inflammation is in ut which is not a place where filtration takes place. re read my question.


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Special visceral efferent
Why are special visceral efferent nerves are named as such?

They are supplying motor impulses to muscles of pharyngeal arch, which are both skeletal(facial) and visceral(laryngeal) 1, so why only visceral in name?
Why the name special?

I tried wikipedia but didn't find any information.

What nerves are you referring to specifically as special visceral efferent? The link you include only has the text "special visceral efferent" once that I can find, in the table at the top.

@kmm 5, 7 ,9 , 10 and 11c most probably.

I find this https://www.ncbi.nlm.nih.gov/pubmed/8109195 suggesting to change the terminology.

Why they are special?

They are also called Branchial efferent.
They are special because they supply striated muscles derived from Branchial arches.
https://en.m.wikipedia.org/wiki/Special_visceral_efferent
Like Mandibular nerve, nerve of 1st arch supply muscles of mastication and motor nuclei of facial nerve, 2nd arch, supply facial muscles and Stylohyoid.

Special Visceral Efferent (SVE)
  These fibres innervate certain striated muscles with a special embryological origin.
  They are referred to as the branchiomeric muscles.
  Structures that develop into gill arches in fish develop instead into various structures near or in the head and neck (muscles of the face, larynx and pharynx).
  Although these muscles are identical to normal striated muscle, neurons for branchiomeric muscles have a distinctive location in the brainstem.

..

Why only visceral?

This term is quite ambiguous. That's why some scientists prefer term Branchial efferents. https://en.m.wikipedia.org/wiki/Special_visceral_efferent
The nerves supply striated muscles(also called skeletal, though most facial muscles have no skeletal support).
These do not supply any smooth muscle of viscera (laryngeal muscles are striated too).
But, still they are called visceral.
Well, that is because the muscles supplied are actually mostly to various viscera.
Larynx is a viscera. Pharynx and palate are viscera too. All these are supplied by 5 , 9 and 10th nerve.(Nuclei - motor nuclei of 5th, Nucleus ambiguus for 9 and 10th)
 Nerve to stapedius is muscle of middle ear, again a sensory organ.
So, the word viscera was added.
Facial muscles and sternocleidomastoid and trapezius are of course not supplying organs(viscera). That is why some say branchial efferent to remove ambiguity.
Branchial efferent represents muscles derived from branchial/pharyngeal arches. That's what is important about these nuclei.

@Charles I dont know of text for sure. But,  that is what are proffessors at college told us.


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Why metacarpus is considered hand proper?
This textbook states

The hand (or manus) consists of the following parts: (a) wrist or carpus, (b) hand proper (or metacarpus), and (c) digits (thumb and fingers).

How could I justify why are digits not considered as hand proper? Hand is a prehensile organ and digits are of primary importance for prehension. So then how could metacarpus be considered as hand proper?

Proper in this instance means the main body of the hand, the part that has no other identifier. the fingers and wrist have other terms to identify them, the hand proper does not. If I say the the hand you are not sure whether I mean the hand as a whole or that part in particular so it is called the hand proper. Its an old usage of the word, but that is common in anatomy text.
From webster it is the 6th definition. Proper: strictly limited to a specified thing, place, or idea

If you define a hand as a prehensile organ, try grasping an object with just your fingers(digits). Try that action without your thumb.
You cannot make a firm grasp of anything without using your metacarpus. Most people don't hold thing using just their fingers. In effect your prehensile organ known as the hand is incomplete is you include only fingers. The metacarpus are involved in the grasping action.
Finally what amounts to a hand has already been defined. So metacarpus is considered part of the structure that we call a "hand".

But why the adjective "proper"?

There is possibility to grasp objects only with fingers but it's impossible to grasp objects only with metacarpus. So why is it still considered as hand proper?


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How pulmonary vasculature removes embolism?
This book says:

Pulmonary vasculature removes emboli before they reach into systemic circulation.

I can speculate that if the emboli are made of fat or clot then our body could degrade it but how does it removes air emboli?
Wikipedia without any citations just states:

Gas bubbles arising from decompression sickness are generally formed in the venous side of the systemic circulation, where inert gas concentrations are highest, the bubbles are smaller at first and they are generally trapped in the capillaries of the lungs where they will usually be eliminated without causing symptoms.

Could anyone provide a reliable source for it or a satisfying explanation?

Diffusion is the primary job of the lungs, so it's easy to see why this would happen more easily there; size is also a factor. In fact, large air emboli will eventually be removed from the right atrium if they spend significant time there just because gasses diffuse into liquids. (Breathing 100% O2 will help decrease the size of the embolus by speeding up nitrogen diffusion.)

So we can say that the air inside the microbubble will diffuse into atmosphere through alveoli ?

Yes, that is safe to say. It's also safe to say that the gas will simply diffuse into the blood stream (the lungs are very blood-vessel rich) and go the route of all gasses in the blood stream.


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Essential fatty acids function
Why are essential fatty acids so essential? I know that if taken less then it would cause diseases, but what metabolic role do they play? Are their importance is just because of their structural role?

''Please add details to narrow the answer set or to isolate an issue that can be answered in a few paragraphs.''

Essential fatty acids consist of two main EFAs - Omega 3 (Linoleic acid) and Omega 6 (Linolenic acid).
These two play vital roles in the following:

Growth and development
Brain functioning
Skin health
Hair growth
Metabolism
Reproductive system health
Cell membrane integrity.

The fact that are bodies can't make them makes them very important in our diet. They are most important in our cell membranes.
Omega 3 is an amazing anti-flammatory. It does this by blocking the inflammation pathways in the cell.
We need more Omega 3 than 6 - about a ratio of 2:1.
This is a pretty good page if you want more information.

thanks, but how do they achieve those functions?

@JM97 editing...


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Location of male and female reproductive organs in fern (prothallus)
I can't seem to find an authoritative answer to this anywhere else online.
Basically, my school text-book says the antheridium (male organ) is located on the lower surface of the fern prothallus and the archegonium (female organ) is located on the upper surface of the fern prothallus.
Another (somewhat unreliable) book mentions that both the antheridum and archegonium are located on the "ventral side". With regard to plants, I'm not quite sure what "ventral" is...is it the side that's in contact with the soil/substratum (i.e- the "lower" surface)?
Besides, which source is right? Or are they both wrong?

The acchegonium and antheridium are NOT found on the 'mature' plant, but on a gametophyte that grows from the spore. This is well illustrated in the "Petersons Field Guild to Ferns", https://www.amazon.com/Peterson-Field-Guide-Ferns-Northeastern/dp/0618394060 Click through the 'Look inside' pages and find the 'Life Cycle of a Fern' for details.