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Could you force meiosis in a cell that normally uses mitosis
I've read in the red queen something that suggests the DNA repair mechanisms are better in meiosis than they are in mitosis.
I was wondering if occasionally we could force some of our cells that use mitosis to use meiosis so as to clean up mistakes in our DNA.

It is not clear from your question if you understand the basics of mitosis and meiosis, especially the differences of outcomes of the two processes. Your question will have higher chance of being answered if you explicitly state what effort you have made to answer it yourself.

How would meiosis "clean up mistakes" in DNA?

@forest I would assume he is talking about gene conversion during meiosis and the hypothesis/theory stating that crossing-over has evolved from a DNA repair mechanism.

it isn't going to help somatic cells to undergo meiosis, because at the end they would be haploid and not really capable of doing good somatic cell stuff... ie. if you were heterozygous for something that was a autosomal recessive disease ... half of the cells would end up with it... also if you were male (human) half of your cells would have a Y chromosome and half would have an X... in general in higher animals the gametophyte generation doesn't do a lot of living on its own.

@BagiM, yes I was sort of referring to the hypothesis you refer to. I was just reading "the red queen" and saw reference to the idea that germ cells had a better DNA repair mechanism that regular cells during meiosis and was wondering there might be some way to get somatic cells to occasionally use a better firm of DNA repair. I realize the haploid problem Grady mentioned. I'm not tried to get somatic cells to use meiosis exactly. Was just wondering if we could somehow encourage cells to us a better DNA repair mechanism. I am a physicist. I have cancer and am interested improved DNA repair.

@chemong In normal body cells there already is Homology directed repair. If I remember correctly it is active in G2 phase where sister chromatids can serve as a template for reparation. The gene conversion would not do much good in multicellular organism because it would introduce genetic diversity of individual cells (in some cells allele A gets converted to B, in others B to A). Genetic diversity is a base of natural selection and I fear the whole thing would kickstart cancer instead of preventing it.


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Can cerebrospinal fluid pass through the pia mater or ependymal cells of the ventricles?
During a lecture, a professor commented that the cerebrospinal fluid and interstitial fluid of the brain parenchyma have similar composition because they can exchange with one another. This struck me as surprising because I was always under the following impressions:

pia mater is essentially impermeable to fluid (therefore CSF from the subarachnoid space could not penetrate it to be in a passive exchange with the underlying brain tissue)
the ependymal cells of the ventricles (besides the choroid plexus where blood is 'pushed' through) is impermeable to fluid...i.e. CSF cannot leave the ventricles to be in passive exchange with the surrounding brain tissue.

Could someone please confirm if these two impressions are correct, and, further, if they are correct, could someone confirm the accuracy of the professor's claim and by what means it is true?

Both the blood brain barrier and the blood CSF barrier tightly regulate the CNS fluid interstitial fluid environment of the CNS. You, however, are talking about a different barrier, the barrier formed by the pia mater, sometimes called the brain/CSF barrier. This barrier is less well studied. It does appear to prevent transport of particulate matter and red blood cells, but allow the passage of immune cells and small molecules. In addition to your professor's statement that the composition of CSF and brain interstitial fluid is similar, intrathecal injection directly into the CSF in the subarachnoid space provides an effective way to deliver drugs with CNS action, suggesting the pia mater does not effectively restrict small molecules (see Goodman and Gilman's The Pharmacological Basis of Therapeutics Ch 2).

Well then, an even better question is, "Okay, so it makes it past the pia mater. How does fluid then make it past the glia limitans?"

@S.Cramer there's definitely a good question in there. I'd recommend writing it up and asking it. You would, of course, want to phrase it more specifically than "How does fluid make it past the glia limitans?"

source: Stack Exchange

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

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Inheritance of partly genetic conditions
Suppose Anne has a condition like OCD, that has a significant genetic component. Neither of Anne's parents have OCD, though. Does this mean that each of Anne's OCD genes were carried by at least one of her parents?

You should read the post Why is a heritability coefficient not an index of how “genetic” something is?

Many things are possible theoretically. Consider the following hypothetical example for illustration. Imagine, if you had two genetic variants A and B affecting a trait with the following probabilities
AA: 5% chance of having OCD
AB: 10% chance of having OCD
BB: 20% chance of having OCD
In this case, clearly having OCD has a genetic component, and yet no matter which genes a person has (and its parents had), it is possible for that person to get OCD. Probabilistically, however, they have increased risk if they inherit certain genetic variants over others.
In practice, most common psychatric disorders tend to be highly polygenic. I have answered a similar question (Q: Bipolar disorder genetics) of yours which may be relevant again.

This is a correct answer and could be improved with a reference. I realize this is basic textbook level information, but that makes the reference easy. I'd suggest wherever you learned about this, or possibly Thompson & Thompson Genetics, Ch. 8. There is a discussion about this here. Feel free to contribute!

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


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What is the fastest way to crystallise lysozyme (for student course)?
High school sudents are going to visit my university and I plan to demonstrate crystallisation of lysozyme. I ordered pure lysozyme from VWR. I can easily crystallise this within 15 min in batch (4% w/v NaCl, 35 mg/mL Lysozyme dissolved in 0.2M NaAc). However, as many different student groups will go through this experiment sequentially, it is preferable that it takes even less time (5 min waiting time maximum). I can of course try to optimise this on my own, but I am wondering if anyone has experience with the absolute fastest way lysozyme forms crystals in a batch setup (to save time and chemicals).
In summary: What are the most optimal buffer/pH/lysozyme concentrations that will give crystals (in a batch experiment) within a very short timeframe (<5-6 min)?

I think you have better chances to find an answer here than on [chemistry.se]. Your question is on-topic on both sites.

Check this out https://hamptonresearch.com/product_detail.aspx?cid=28&sid=173&pid=524

Cool, I could try this out and report back

I don't have an expertise in this field but don't you think 15min is quite fast? Most biology protocols take much longer. I have seen protein-crystallography people waiting for several days to get their protein to crystallize.

Yes it is, my PhD-project crystal normally take about 3-4-day. However, lysozyme is insanely easy to crystallise - and this is for a open research day with high-school student that have a very limited time to conduct the experiment. I just think its interesting to get the absolute optimal way of doing this fast. The answer may be that its not possible in less than 15 min (but I dont know).

Perhaps you could start a new crystallization with each group (every 5 min) and then show them the results of previous groups. Each group could then be able to observe what is happening at 0, 5, 10 and 15 min.

One try would be to see if also for lysozyme a powder of previously generated lysozyme crystals would nucleate and hence speed up the crystallization if added to lysozyme solution.


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3D Cellular Model
I'm learning biology on my own and it's pretty hard to understand all processes inside a cell from the side of chemistry and physics and in some cases pointless to bring a complexity instead of abstraction.
I just curious to know if we have some open-source projects that provide 3D
program models of a cell? I mean not just like study model that shows cell organelles and their names but I want something that shows real cellular processes like (1x1 or close to it) real model of a living (in program) cell with some types of abstraction levels.

I don't know of such resources but certainly there are good animated videos of different cellular processes. Khan Academy would be a nice place to look for video tutorials. I also would want to add that a full computational model of an entire cell would be quite complex and I haven't come across any (the closest to complete was that of M.genitalium and it was not intended as an educational resource but a research project instead).

Not of a complete cell, that would seriously overload even most powerful animation software/hardware you could build, not to mention there are gaps in our understanding of the cell. Understanding a cell purely through chemistry is possible if a bit masochistic, sooner or later you are going to need to approach it from a different direction to get the whole picture. There is so much complexity in a modern cell that sooner or later you have to start looking at the emergent characteristics. Don't believe me check out this chart of just the common metabolic pathways in a human cell, you are looking a 3.5 billions years of kluges, breathtaking elegance, rube goldberg monstrosities, and duck tape solutions all layered and tangled into each other, messy doesn't begin to describe it.
But there is several places creating models of individual processes, modeling each individual atom. These will let you at least understand hte chemistry of the components.
www.dnalc.org is focused on nucleic acids and their interactions.
Their work is related to Harvard's biovisions program which uses XVIVO. which is a much rougher but larger scale approach and may be the closest to what you want.
Cambridge MRC has a more diverse selection with better visualization of the actual chemical interactions.
Swissmodel by the Swiss Institute of bioinformatics focuses on protein modeling and has a free to use program and database.
There is even a wikipedia database Protepedia
Image from www.dnalc.org animation

I'm sure others on the site could list a dozen other such programs/databases.

@user237650 Thank you, that should have fixed it.

The complete function of a cell is something which is still quite beyond our current knowledge and understanding. Many gaps remain that prevent us from building such a complete model, and also from engineering an artificial object that would reproduce some basic function of a living cell.


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Tillers and stolons in grasses
In many grasses, tillers develop roots at their nodes etc.. Those roots can hit the ground and subsequently anchor in the soil, so eventually the tillers end up like something that is very hard to separate from stolons (I often see this in Agrostis gigantea).
Are there objective criteria for separating tillers and stolons at all times?


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Neuronal membrane resting potential for large cells
I'm reading Medical Physiology by Boron and Boulpaep (a really terrific book). In the chapter Electrophysiology of the Cell Membrane, section Membrane Potential Is Generated by Ion Gradients, Not Directly by Ion Pumps, the text reads:

It may seem that the inside negative Vm originates from the continuous pumping of positive charges out of the cell by the electrogenic Na-K pump. The resting potential of large cells -- whose surface-to-volume ratio is so large that ion gradients run down slowly -- is maintained for a long time even when metabolic poisons block ATP-dependent energy metabolism. This finding implies that an ATP-dependent pump is not the immediate energy source underlying the membrane potential.

I totally get the main takeaway, that Vm results from the net accumulation of ion gradients, rather than the immediate consequences of the ion pumps. But I'm unclear on the phrase large cells -- whose surface-to-volume is so large that ion gradients run down slowly.
Presumably a cell with a large surface-to-volume ratio, like a long thin neuron, would have many ion channels which leak constitutively. So I'd expect the net ion conductance to be high, and gradients would run down quickly. But that contradicts the book's run down slowly point, so I'm confused.
Does passive diffusion play a role here? A long, thin cell would have slow passive ion diffusion, so is that why Vm would run down slowly?
Am I overthinking this?
What is the authors' point here?

In a typical neuron at rest, potassium is high inside the cell and low outside, with the opposite true for sodium. The membrane is mostly permeable to potassium. Let's ignore the other ions.
The resting potential in this situation will be something like -70 mV. Rest means that the net current flow is zero; however, there is still current: potassium is flowing out of the cell and sodium is flowing in. Therefore, if we turn off the sodium-potassium pump, over time, the concentration gradients will slowly equalize.
The authors are making an assumption that the current is roughly a function of membrane surface area: more membrane = more current. However, the "reservoir" of concentration imbalance is a function of volume: a bigger cell has more total potassium ions than a smaller cell.
Therefore, in a large cell, if the membrane potential is mostly driven by the concentration gradient, and it takes a long time for the concentration inside to equalize with the outside because the current is small relative to the volume, the membrane potential will only change slowly if you use a toxin to stop the sodium-potassium pump.
I don't think the authors are really intending to say anything special about large cells versus small ones, they are just setting up some assumptions under which their argument about the resting potential is going to be most evident. This is a bit like in a physics textbook where you read something like "assume a uniform spherical baseball."
The claim they are making: "the membrane potential is because of the concentration gradient, not the action of the pump itself" is true for all cellular membranes, not just in large cells. This particular piece of evidence they are referring to, however, is going to be most obvious in a large cell. That's all.
If you tried to do this experiment in a very small cell by turning off the pumps and watching the membrane potential, you might erroneously conclude that the pump was responsible for the membrane potential, but this would be a false conclusion caused by the concentration gradient equalizing too quickly. Instead you should test it in a big cell to see the effect more clearly.
In my personal opinion, this is not the best evidence to explain this feature, but it's a hard concept for many people to grasp and I suspect the authors of your text approach it in several different ways to find one that sticks.

I also thought about a large spherical cell, and had the authors stopped there, the point would have been clear. Given that spherical area grows at $O(r^2)$ and volume grows at $O(r^3)$, the resting dynamics of a large cell would be rate-limited by the small number of open membrane channels compared the huge number of intracellular ions. And if that's correct, they probably meant to write, "whose surface-to-volume ratio is so small"... Might just be a typo.

@user50080 Oops, I hadn't even read the quoted passage clearly. Yes there is definitely a typo, they mean to say "whose surface-to-volume ratio is so small" or conversely "whose volume-to-surface ratio is so large", I think they caught up with the cell being large and the ordinary way to arrange these things is "surface-to-volume ratio" and made a mistake. The meaning is more clear from the rest of the text.


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Is there any way bicondylar/bigonial, bizygomatic or bitemporal breadth can change in adults?
Without cosmetic surgery or etc., are there any cases/example wherein a human adult has had a change in significance regarding these regions of the face? I have seen many anecdotes where people have asserted that certain things (not surgery) like diets, drugs, or etc. has affected these regions.
Is this possible and what are any such means in which these regions of the face can change?
This isn't a personal medical question as this is widely applicable and generic to any human adult.

Possibly many things can affect the morphology but the question is whether they are controllable in any manner like a surgery. Can you please elaborate your question and try to keep it to the point such that it can be answered in a few paragraphs?

There's no way I can think of to better word/organize the question -- it's as simple and straight as I can get it.

Acromegaly (pituitary gigantism) is a disease that causes enlargement of the bones of the face.  There is interest in computerizing facial measurements to catch subtle enlargements and prompt testing for the disease.
https://www.researchgate.net/publication/261409008_Three-dimensional_facial_analysis_in_acromegaly_a_novel_tool_to_quantify_craniofacial_characteristics_after_long-term_remission

Sixteen patients in remission of acromegaly for over 24 months (50 %
  male, mean age 56.0 ± 10.7 years, mean body mass index 29.3 ± 5.5
  kg/m(2)) were compared to 16 matched control subjects. A 3D cone beam
  computed tomography scan and 3D stereophotograph of each individual
  were acquired and analyzed using 3D cephalometry. In addition to an
  accurate quantification of the classical craniofacial characteristics,
  3D cephalometry, shows that many typical soft tissue deformities
  persist, even after long-term remission. Furthermore, we found that,
  compared to controls, the patients in remission of acromegaly have a
  wider face at the level of the zygoma and longer maxilla (p < 0.05)

Apocryphally, enlarging hat size goes along with acromegaly.

Pagets disease of bone causes enlargement of the skull and also an increase in hat size (so bitemporal dimension); the hat size increase was one of the chara eristics first described in the disease.

Thalassemia is a group of blood diseases characterized by ineffective red blood cell production.  The body compensates by making more marrow anywhere it can.  Some people wind up with expanded bones in the skull or maxilla as a result.

https://www.slideshare.net/ismahharon/thalassemia-is

These are all systemic diseases that affect the bone.  Of course one can have a tumor of bone (primary or metastatic) that expands it and changes the shape of the face or the head.


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Using spp. for taxa other than Genus
Can spp. be used for taxa other than genus ? For example Noctuidae spp. meaning certain genera in the Noctuidae family.

eric I think this is an interesting question, but I'll suggest you modify a bit: You ask" "...meaning certain genera...". "Spp." would still likely refer to species and not genera in the application you're asking about.


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How does fluid pass through the glial limitans into the subarachnoid space?
I have often heard that the cerebrospinal fluid (CSF) and interstitial fluid (ISF) are in free exchange. Because the CSF eventually drains (predominantly) into the dural venous sinuses, ISF's ability to access the subarachnoid space actually allows the brain to eliminate metabolic waste products that would otherwise remain the parenchyma. ISF presumably accesses the subarachnoid space, mixes with the CSF, and eventually, through arachnoid granulations, drains via the dural sinuses.
While that is fine and dandy...there are two layers that the ISF must first pass in order to access the subarachnoid space: the glial limitans and the pia mater.
How does ISF pass through the foot processes of astrocytes, which comprise the glial limitans? Does the H2O remain largely in the parenchyma while waste metabolites are selectively transported across the astrocytes and into the small spaces between the glial limitans and pia mater?

Excellent question. This is an active area of research.
The glia limitans defines the external most layer of brain parenchyma. Previously thought to primarily be a barrier against migration and growth of neural cells out of the brain parenchyma during development, recent work has characterized its involvement in regulating the immune environment of the CNS. A 2017 JCI paper demonstrated that the tight junctions of the glia limitans are inducible in mouse in response to inflammatory cues. You may find the associated editorial helpful. In addition to demonstrating a dynamic role for the barrier function, you can see that tight junctions are not the standard state, and the typical state allows passive diffusion as well as active transport of small molecules between the CSF and brain ISF, but the question is not fully resolved.
Importantly, this is mouse data, and mouse data in particular cannot fully resolve questions about human astrocytes.


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What is this Peacock-like creature?

In the below picture I believe  bird in the foreground is a female. The one that opens the wings is the male.

Please [edit] your question and give us some more details. How big is this animal? Where did you see it? What sort of habitat? Most importantly, what makes you think that isn't a peacock?

It looks like male Great Argus (Argusianus argus) displaying to a female. The circular markings on the male pheasant's secondaries are pretty distinct. The specific epithet argus refers to a hundred-eyed giant from Greek mythology.

I think you're right, the answer could be improved with a link of some sort & a note to the effect it's a species of pheasant wouldn't hurt either :)


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From refseq ids to Go term Ids
I have a list of Refseq accession numbers such as :
YP_009448812
YP_009448725
YP_009448701
NP_659591
around 10 000 acc_numbers...

and I'm looking for a tools in R or Python in order to get the corresponding Go term ids.
I tried the packages (org.Mm.eg.db) and (GO.db) but it does not work.
> Term(names(get(get("YP_009165174", org.Mm.egREFSEQ2EG), org.Mm.egGO)))
Error in .checkKeys(value, Rkeys(x), x@ifnotfound) :
  value for "YP_009165174" not found
> Term(names(get(get("YP_009448701", org.Mm.egREFSEQ2EG), org.Mm.egGO)))
Error in .checkKeys(value, Rkeys(x), x@ifnotfound) :
  value for "YP_009448701" not found
> Term(names(get(get("NP_659591", org.Mm.egREFSEQ2EG), org.Mm.egGO)))
Error in .checkKeys(value, Rkeys(x), x@ifnotfound) :
  value for "NP_659591" not found
> Term(names(get(get("YP_009448812", org.Mm.egREFSEQ2EG), org.Mm.egGO)))
Error in .checkKeys(value, Rkeys(x), x@ifnotfound) :
  value for "YP_009448812" not found

Does anyone have an idea? Thank you for your time. I cannot find a egREFSEQ2EG for viruses.

I've had very good experience with the biomaRt package (R, bioconductor) when it comes to mapping of different databases. If I don't forget about it, I can post an answer with code tomorrow.

Ok thank you for your time then. The proteins are from Acc_number  types and from virus organisms. The idea is to get the corresponding Go terms Id of these refseq Acc_numbers IDs in order to perform a Go term analysis.

So, I've looked a bit into this and the way you want to do your analysis won't work as you planned it. The main reason for this is that the GO database does not contain any virus species (as fas as I could see). The existence of the species you want to analyse in the database is important, because you need to have a background or reference gene set in order to perform enrichment analysis. Even if you're just interested in the IDs and want to perform the analysis by yourself, this means that you're unlikely to find anything for your genes/proteins in the GO databases.
Your best alternative is to use other annotation databases and either rely on their annotation or map their annotation to GO term ids (here is a list of all databases that allow this).
Your best bet for this is probably the UniProt database, since that should have entries for most of your proteins (though not all will have annotated GO terms). UniProt also offers an ID mapping tool that should be able to convert your RefSeq IDs to uniprot IDs, and also comes with an API for python. Do note that some of your IDs (the YP_ ones) are provisional RefSeq entries and the webpage tool only finds them in the 'UniParc' database (not UniProt KB).
Once you have the the UniProt IDs you should be able to map the available GO terms from there (see the last entries of the first link above).

Allright, thank you very much for all these informations!! It will be very useful for my project. Have a lovely day.


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True or False: Endocytosis delivers vesicles directly to the cis face of the Golgi complex
Does anyone know the answer to this question, and also the explanation of to why this is True or False?
I know that Endocytosis is the process of uptake of materials into cells including microorganisms, solute particles, and food particles from the ECF. The Golgi Complex is the trafficking directory organelle of the cell which vesicles enter in the cis face and exit in the 'rougher' trans face. It adds tags to vesicles for target compartments. Proteins come from the rER wrapped in vesicles and directed to the Golgi Complex.
In my knowledge the membrane bound or secreted proteins are directed to the rER first, thus I am half certain that this question's answer is False.

I've added the [tag:homework] tag to your question, since that seems appropriate (even if the question you got was not meant as homework). However, I do think you're providing your own thoughts and tenative answer on the question, so I don't understand the close votes.


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Toxic Metals and Oxidative Phosphorylation
I was reviewing the toxicity of certain toxic metals, specifically cadmium and their effect on Oxidative Phosphorylation and Cellular Respiration, I have found that metals such as cadmium inhibit certain antioxidant enzymes such as catalase, resulting in oxidative stress as a result of excess of Reactive Oxygen Species or free radicals, I also have come across information that states that toxic metals can bind to the mitochondria and interfere with oxidative phosphorylation, possibly in the electron transfer change or in another way. I was wondering if anyone is aware of the other ways in which cadmium interferes with oxidative phosphorylation as it bonds with the mitochondria, or if attaching to antioxidant enzymes IS actually binding to the mitochondria.


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Branch taking over a tree trunk
I stumbled upon a birch growing in sandy soil in a coniferous forest in central Russia.
It looks like over time the tree trunk got bent towards the trail and one of the branches became the new trunk as it now grows straight up, whereas the old trunk is pointing sideways.1
The tree isn't dead, I visited that place during summer time and it was covered with green foliage.
I'm wondering what's the name of such phenomena, how common it is and what usually causes the tree "to change it's mind"?

1. I apologize in advance if the terminology I'm using is inaccurate, so feel free to edit my question.

This phenomena has elements of what,  in the UK, are termed Phoenix Trees, however this term, and the term Phoenix Regeneration, is more often used when describing characteristics of ancient and veteran trees.
The principles that underlie what the photo shows is that new growth on trees will always grow strongest where there is the most light available, and so in this case as the trunk has become bent towards the canopies, and the shade, of neighbouring trees this branch has become the part of the tree to encounter the most available light.
It is possible to find many trees in a woodland that may show elements of this phenomena; your photo is of a tree that is on the more extreme end of the spectrum for a tree that is still standing. It has developed a different 'dominant' stem to the one it 'started' with.
It is probably not now possible to discover what has happened in the past to cause this tree to bend over in this way; it could have been perhaps a heavy build up of snow or ice at a particularly vulnerable point in its growth, or more likely one or more other trees, or a part of another tree perhaps falling in such a way to knock into it and stay in that position long enough for this tree to adopt this shape in its trunk. If this was the case it may be that the tree/s that fell into it has since been cleared, or decayed away if it was a dead tree or branch.
Often trees that are completely blown over can remain alive because enough roots remain in the soil for it to survive. When this happens the branches on the trunk start to grow upwards into the new space and light that has been created by the tree itself falling. Over time the result is a tree where the main trunk is lying on the ground but the canopy is now a series of branches at right angles heading straight up.
The name for a tree that continues to live and grow after it has fallen over is a "Phoenix tree", named after the mythical bird that regenerates itself after catching on fire; it rises from the ashes.
This term is often applied to old trees, but it could, and does, also be used to describe any tree that has fallen over but continued to grow.
References can be found in Natural England's excellent publication on Veteran and Ancient Tree management
http://publications.naturalengland.org.uk/publication/75035
For example in Chapter 2 "What are Veteran Trees and why are they important?" Section 2.3.4.6 (page 21) of Veteran Trees: A guide to good management
Old trees may fall over completely and then re-grow or collapse and layer well away
from the original base. This is characteristic of lime, willow, alder, black poplar, medlar
and bird cherry but can occur in any species. A particularly notable example is the
Tortworth Chestnut.

The term phoenix regeneration has been applied to trees that have fallen over, or
split apart, and successfully continued growing.

Nice name for these kind of trees, was new to me (+1). Could you add a reference for it? that would make it awesome.

@RHA Thanks, I have added a reference for the term Phoenix regeneration and have also added that the term is commonly used in the UK. I didn't know that there is a date tree that is commonly known as a Phoenix tree, so that could be confusing.


text:
Does the preservation fluid (ethanol or formaldehyde) leach heavy metals from mollusc tissue?
In a thread on researchgate, the concern was raised that long term exposure to unbuffered preservation fluids such as ethanol or formaldehyde may leach heavy metals from biological samples due to a reduction in the fluid's pH. Can anybody tell me if this also applies to mollusc samples? I would assume that carbonate shells function as a pH buffer and thus keep the fluid's pH relatively stable over a long time.
Edit: Link to the researchgate thread. No research articles were mentioned in that thread.


text:
Does spinal cord have pain receptors?
I understand that the brain itself does not have pain receptors, so when the brain is damaged or cut, there is no experience of pain. For example, surgeons can operate on the brain while a patient is awake without causing pain.
How about the spinal cord? Are there pain receptors in the spinal cord? Will damaging the cord itself cause a feeling of pain?

I'm voting to close this question as off-topic because it's the same as this question https://biology.stackexchange.com/q/81524/107

@kmm that question has no upvotes or accepted answers. This question is slightly better worded than the one you linked. I think this one should be left open.

That question should be edited and thus proposed for reopening, not posed as a new question.

This is a difficult and subtle question for many reasons. The primary issue here is that there is a difference between "does the parenchyma of this central nervous system structure have nociceptors (or, in fact, any peripheral receptors)" and "can the parenchyma of this central nervous system structure detect direct stimulus". There is also the issue that pain is not a sensation, so much as an associative cortical event. So this is a hard question to answer completely, as it is phrased, but it is also difficult to expect someone to understand this after, even a few hours of undirected research

tl;dr
Like the brain, the receptors commonly called 'pain' receptors aren't in the spinal cord itself, but they are present in the meninges around the cord, and damage to the cord can be perceived as pain in particular because it can increase activity in the pathways carrying 'pain' information to the brain.
Details
Nociceptors, often called pain receptors, are peripheral structures that sense and transmit noxious stimuli to the central nervous system. The cell bodies of afferents from these receptors are found in the dorsal root or trigeminal ganglion. The receptor structures themselves (the afferent terminal of these neurons) are not found in the parenchyma of any central structure, though they do innervate the meninges of both the brain and spinal cord. Despite the lack of peripheral receptors of nociception, damage to the spinal cord is often associated with increased activity in the tracts that carry nociceptive information.
This may be beyond the question you're asking, but I would note that the IASP defines pain as:

a sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

Pain is probably best understood less as a sense that nicely maps the external environment to a conscious representation of that environment, and more as an emotional need state, like hunger. Many different receptor structures and nerves can transmit a signal that can eventually be interpreted as pain, and in fact pain can be experienced without any physical peripheral input at all (as the IASP definition attests). This is one of the reasons nociceptors are typically not called pain receptors by people who treat or study pain.


text:
Why are tardigrades so rare?
If tardigrades are so resilient and nearly immortal, why are they so rare when looking at samples of a pond or lake, where tardigrades should thrive?
I've met people who've been studying protozoa and metazoa in nature all their life and have only seen tardigrades once or twice!

They're not, they're ubiquitous.

From wikipedia > tardigrade

[Tardigrades are] considered cosmopolitan and can be located in regions all over the world.
Tardigrades are often found on lichens and mosses. Other environments are dunes, beaches, soil, and marine or freshwater sediments, where they may occur quite frequently (up to 25,000 animals per litre). Tardigrades, in the case of Echiniscoides wyethi,[20] may be found on barnacles.[21] Tardigrades can be often found by soaking a piece of moss in water.

Tardigrades are, in fact, very common. See the simple video how to observe tardigrades. If the people you've met have rarely seen tardigrades, it is probably because they are not looking for them.

"If the people you've met have rarely seen tardigrades, it is probably because they are not looking for them" [+]


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What evolutionary advantage do viruses have in host specificity?
Warning: I have almost no knowledge of biology past the high school level.
Viruses generally have three components: the DNA, the virus protein coat, and an outer membrane "decorated" with these surface marker glycoproteins. I am thinking that a virus would want to infect as many hosts as possible, so that it would reproduce as much as possible, why would a virus just infect one group of organisms.
What evolutionary advantage do viruses have in host specificity?

Tell me if there are issues with this question, I will reply as soon as possible

It is true for any living creature, that it would be great for it if it could thrive in all environments. Any creature would do better if it had a greater ecological niche while remaining as competitive in each of these niches. However, competition, predation and other biotic and abiotic factors lead species to specialize in specific niches. Of course, some species are more generalist and some are more specialist but I won't go into these details.
When it comes to parasites, such as viruses, the story is the same. A host is an environment. Being less specific would be great but the immune system is no easy detail to get around. Viruses are often quite specific to a given species, just because it evolved to be efficient for a given host but tend not to be that efficient in other hosts.
Note that parasites are not only species specific but also often tissue specific and specific to the specifics genetics of the host (e.g. malaria).
Somewhat related posts:

Why do parasites sometimes kill their hosts?
Why aren't all infections immune-system resistant?

Thank you @DeNovo for helpful comment

Good answer. I'd note that, not only are viruses often specific to a given species, they're often quite tissue specific.  I think there are several Q/A pairs that may relate to this question. The one you linked, and also this, though asked about bacteria. The basic question (why doesn't some group of organisms just take over everything everywhere) is very similar.

Thank you! Helps the day before my bio test ;)

I would more specifically address the advantage/benefit, in that even though a virus may be host specific (or not, since it really doesn't matter in terms of gain), even the most virulent of viruses throughout history have not killed off entire species, save the 'virus' of being man (whole other story), yet for some reason some within a species survive! They may have a specific protein, are a carrier - the list is long and not entirely understood. In any case, they often handoff whatever adaptable mutation they have to their offspring, thereby making them immune to such viruses. Survival of the fittest?

Viruses infect a cell via a receptor. Without the specific receptor infection is not possible. A virus will mutate to enter a cell via another receptor (HIV-2). So, I say viruses are receptor specific.


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Is it possible for human body to convert carbohydrates to protein?
Is it possible for human body to convert carbohydrates to protein to build muscle for example?
EDIT: I read in many articles that you should eat more than 1.5 gram protein for each 1 kg weight of your body to gain muscle, but I see some bodybuilders that I know they don't eat that much of protein but gain muscle and have muscular body. So it was interesting to me to ask this question here!

Welcome to Biology.SE. Your question could be interpreted a number of ways. In particular, it sounds like nutrition and bodybuilding question, but could be a biochemistry question. Could you edit your question to clarify what kind of answer you're looking for?

In short, no, because proteins contain nitrogen, and carbs do not.

@swbarnes2: So body can not add this nitrogen or combine carbs with something that can add this nitrogen to them and make protein?

Just to further clarify my comment, the answer depends a great deal on what you mean by "carbs" (glucose? bread?) and "is it possible"

@DeNovo: Thank you for remark. I want to know, if is it essential to eat 1.5 or 2 grams of protein(especially whey) to build extra muscles or it's just advertising tricks and a person with normal diet(without eating extra whey powders or eating 10 eggs per day) can make extra muscles if he just eats more food(I mean he just increases his normal diet whatever he was eating before, not only increasing protein)?

It sounds like you're looking for an answer that is more suited for fitness.SE. The biology stack would be more suited for this question if it was about biochemistry. I'd note that, re: the biochemistry question, in addition to @user1136's comment, a glucose load is associated with increased activity in protein anabolic pathways. This may be because of the insulin response.

@DeNovo: No I am not looking for workout advices! I asked here to see the scientific view of this, if is it possible or not!

Some amino acids can be synthesized from carbohydrates if nitrogen and any other necessary mineral elements are present. But some carbohydrates have to be ingested.

@Tak: Do you know those amino acids that can be synthesized from carbohydrates are enough to making new muscles or building new muscles need other type of amino acids that can't be reached by carbohydrates syntheses?

Essential amino acids cannot be synthesized from carbs, but non-essential amino acids can be synthesized. Intermediates from the citric acid cycle or pyruvate can be used to synthesize at least 11 kinds of non-essential amino acids. They will be incorporated into muscle, but you need all the essential amino acids available in order to produce complete proteins that will build muscle tissue. Proteins are made from the entire repertoire of amino acids, and I don't think there exist any (perhaps very, very few, none to my knowledge, *I've checked the literature) that are made from only non-essential acids.

PS. I'm sorry the question is on hold @user145959, there are poorly behaving regulars and/or mods here, and one that is blindly downvoting every post of mine. The question can humans convert carbohydrates to protein is a biology question, one asked very frequently in biochemistry classes; it is definitively not a homework question, the questioner has repeated that they are interested in a scientific verdict. It's clarified that you specifically want to know whether anabolism is taking place... And people are still voting to close the question. Come on guys, what are you doing?

@SPr re "Come on guys, what are you doing": I would encourage you to open a meta discussion. re: downvotes, I'd encourage you to not take downvotes personally, but consider them to be feedback about your answers. I don't think you have a serial downvoter. I downvoted this one, and haven't recently downvoted any other answers of yours. I downvoted because the OP isn't asking about biochemical carbohydrates, but nutritional "carbs", which usually include carbohydrates AND protein. That and the lack of references led to my downvote. I should have made a comment when downvoting.

@SPr on reflection, my downvote reasoning doesn't make a lot of sense. I'll remove it. I'm not going to upvote, though, since it doesn't have any references and doesn't seem to address the question, which is essentially "what should I eat in order to bulk up", not "what are the biochemical pathways from which glucose can contribute carbon to amino acid synthesis".


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How do you dilute forward and reverse primers for a master mix?
I apologize for the very naive question, but I'm just starting out in a high school biology lab and I am very confused.
If I have stocks of 100μM for forward and reverse primers separately, I can dilute them to 10μM very easily. But what if I want to make a master mix? I have 1000μL of 10μM for each primer, forward and reverse (not mixed). Would I just add 500μL of my forward primer and 500μL of my reverse primer for a mix of 1000μL in  which both concentrations are still 10μM?

Would I just add 500μL of my forward primer and 500μL of my reverse
  primer for a mix of 1000μL in which both concentrations are still
  10μM?

No.  Diluting your 10μM solution in half will half the concentration.  Mixing equal parts of 10μM primer will make a master mix where each primer is 5μM
But in general, primers are added to these reactions in great excess, so 5μM of primer might be okay.

The question also states that they have 100 uM stocks of each primer. In that case, they can make their master mix (with 10 uM of each primer) using those stocks.


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Cadmium Poisoning and Toxicity Mechanisms
Is anyone aware of the toxic mechanisms of specific instances in which cadmium ions can interfere with cellular functions resulting in acute cadmium poisoning?

What have you found in your own attempts to research the question?


text:
What exactly does the phrase "chimerical sharing" mean in this abstract?
The Gizmodo article Australian Siblings Are Semi-Identical Twins, Some of the Rarest Humans Ever links to the new paper in NEJM Molecular Support for Heterogonesis Resulting in Sesquizygotic Twinning Gabbett et al. N Engl J Med 2019; 380:842-849 DOI: 10.1056/NEJMoa1701313.
The abstract of this paper says:

Sesquizygotic multiple pregnancy is an exceptional intermediate between monozygotic and dizygotic twinning. We report a monochorionic twin pregnancy with fetal sex discordance. Genotyping of amniotic fluid from each sac showed that the twins were maternally identical but chimerically shared 78% of their paternal genome, which makes them genetically in between monozygotic and dizygotic; they are sesquizygotic. We observed no evidence of sesquizygosis in 968 dizygotic twin pairs whom we screened by means of pangenome single-nucleotide polymorphism genotyping. Data from published repositories also show that sesquizygosis is a rare event. Detailed genotyping implicates chimerism arising at the juncture of zygotic division, termed heterogonesis, as the likely initial step in the causation of sesquizygosis.

There are several terms I am trying to understand here:

sesquizygosis and sesquizygosity: A postulated form of twinship, in which individuals share between 50 and 100% of genetic identity by state (number of shared alleles).
heterogonesis: The assortment of two or more paternal genomes into distinct cell lineages after polyspermic fertilization of an ovum.
juncture of zygotic division (?)
chimerism

So far I understand that the chimerism means for each fetus, some cells have a distinct genome from other cells, and sesquizygosity means (at least) that there is DNA present from more than one sperm.
But I don't understand what "...chimerically shared 78% of their paternal genome..." means exactly when speaking about twins. What does chimerical sharing mean in this case? Are we talking about four genomes (two genomes in each of two fetuses)? If so, how does that comparison reduce to a single value of 78%?

Heterogonesis \ he-tə-rō-gō-ˈnē-səs \
The assortment of two or more paternal genomes into distinct cell lineages after polyspermic fertilization of an ovum.

Visual Representation:

This term — chimerical sharing seems to be used only in this study as a google search did not return any other results. So, it is not a standard term. I believe what they mean by this term is that the twins shared x% of the paternal genome but the sharing is not homogeneous for each cell. In other words each twin has some cells with genetic material from sperm-1 and the others with genetic material from sperm-2.
If the two sperms were genetically identical, then you would not see any chimerism. Let's now consider only one allele as a marker of paternal parentage. So, there will be two populations of cells for each allele.  If both populations are of the same size then you would have 50% chimerism in a single individual (i.e. the allele frequency). The percentage of chimerism may be different between the twins.
Now, there may be several genomic regions at which the paternal-genomes differ. Since the paternal chromosomes would not be symmetrically partitioned between the blastomeres, the different genetic markers (alleles) are likely to have different extents of chimerism.
In this study they measured the frequencies of a few SNPs that were informative for deducing the parentage.

Analysis of SNPs from twin amniotic fluid and parental blood showed
  that 265,489 maternal and 179,205 paternal SNPs were informative for
  parent of origin.

They noted that ~78% of the paternal SNPs were found in both the twins.

Of these, the twins shared 265,400 maternal and 139,155 paternal SNPs,
  which makes them 100% maternally identical and 77.7% paternally
  identical.

Note that this is just a qualitative test for the presence or absence of the alleles. This does not say anything about the extent of chimerism of different alleles. (There are some figures in the supplementary data for the frequencies of different SNP but they are not in a tabular form and hence difficult to deduce).

I appreciate the help, the edit has thrown me off a bit. When I read "...if both types of cells are in equal numbers then you would have 50% chimerism in a single individual." should I understand "50% chimerism" to refer to fraction of cell types, fraction of cell numbers, or fraction of genome that is chimeric?

@uhoh In that case I meant the fraction of cellular genotypes in the individual.


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Why does B12 deficiency enlarge red blood cells?
I'd like to know why B12 deficiency enlarge red blood cells

Welcome to Biology.SE, Adriana. @SPr has shared a reference with you that may answer your question. If not, it may help to know more about what you understand and what you don't. See the help center article on how to ask a good question

The technical term for enlarged blood cells is macrocytosis (macro means large, -cyto- means cell).

Macrocytosis due to vitamin B12 or folate deficiency is a direct
  result of ineffective or dysplastic erythropoiesis. These important
  vitamins and cofactors are required for normal maturation of all
  cells. Marrow erythroblasts are no exception. When either of these two
  factors is deficient, RBC proliferation and maturation result in large
  erythroblasts with nuclear/cytoplasmic asynchrony. These abnormalities
  are caused by a defect in DNA synthesis that interferes with cellular
  proliferation and maturation. RNA synthesis and cytoplasmic components
  remain relatively unaffected. The marrow is hypercellular with all
  forms of the myeloid cell line being increased and erythroid elements
  being dominant on the marrow aspirate smear preparations. The
  erythroblasts become large, oval shaped and contain a characteristic
  immature, lacy nucleus. These bone marrow features are called
  “megaloblastic” and are highly suspicious of a vitamin B12 or folate
  deficiency. Megaloblastoid (megaloblastic-like) abnormalities of the
  marrow are frequently seen in other hematologic disorders not
  associated with vitamin B12 or folate deficiency, (e.g.,
  myelodysplasia and leukemia) and a careful examination of the bone
  marrow is necessary to make this distinction.

Source: Megaloblastic Anemia and Other Causes of Macrocytosis
Erythropoiesis simply means the process of red blood cell production.
Erythroblasts are immature red blood cells that still have a nucleus. Mature red blood cells lose their nucleus before they enter the bloodstream to become active oxygen carriers.

I'm not the down voter, but I suspect this may have been because your answer is mostly a reference with a small glossary. Your answer is correct, and I think better than an explanation with no reference.

Indeed, why paraphrase when another has said it more accurately and concisely? I'll happily add that B12 is additionally known to affect epigenetic mechanisms as a coenzyme of methyltransferase that methylates, demethylates and remethylates various biological molecules including DNA. B12, and DNA methylation status, is important for structural stability of regions of chromosomes such as centromeres and subtelomeres. Medically it may explain why B12 deficiency affects pregnancy, and from a molecular point of view, why DNA synthesis is affected globally across the entire body!

that was perhaps an indirect way of saying I personally think your answer could be better (as a response to this basic question) with more than just a reference and a glossary. But I didn't think it was worthy of a downvote, specifically because it was correct and referenced.

Other things that compromise DNA synthesis also produce macrocytosis - nucleoside analog chemotherapy / antiviral therapy are good examples.

@SPr has given you a good reference in his answer. I thought I'd add some context to it.
The basic problem here is that red blood cells need B12 in order to synthesize DNA. Red blood cells live for about 4 months, and have to constantly be replaced, so when you have a problem with B12, this is one of the cell populations that will be affected. The problem here is actually the anemia. It's not that the cells are too big, but that there aren't enough of them (see the linked reference, as well as Robbins and Cotran Pathologic Basis of Disease, Ch 13, subsection "Anemias of Diminished Erythropoiesis"). The size itself helps identify why there aren't enough of them, distinguishing this anemia from other anemias that cause cells that are smaller than normal.
The mechanism in lay terms (which hasn't entirely been worked out, again, see both the article and Robbins), is that a problem with DNA synthesis causes the cells get larger before they divide. So you have fewer, larger cells. Because it's a universal problem with DNA synthesis, red blood cells aren't the only cells affected.

@user1136 that is a good question. Perhaps you could ask it? I'd be happy to answer.

@user1136 I'm not sure what the purpose of your comment is, but perhaps we can chat about it


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Why are restriction sites palindromic in nature?
Any restriction site given in any fragment of DNA or vector molecule is a palindrome. eg restriction site for the endonuclease EcoRI is
5'...GAATTC...3'
3'...CTTAAG...5'

Clearly, this is a palindromic sequence. Why is that?

I was going to answer this question, covering what I regard as a key point that other answers ignored. However as this is a duplicate I have answered it on the original. You may be interested to look at it there.

Not all restriction sites are palindromes : https://en.wikipedia.org/wiki/List_of_restriction_enzyme_cutting_sites:_E%E2%80%93F#Whole_list_navigation
EcoRI: GAATTC (note that this is not 'palindromic' in the usual sense (e.g.'anna', GAATTC read backwards actually gives CTTAAG), but only if given the G-C A-T binding)
The double strand of DNA is composed of one strand in direction 5'-3' and another into the other direction (3'-5'). Restriction enzymes tend to be homodimers, thus would bind to both sides of the double strand, expecting the same recognition sequence. But as one strand runs into the other direction, the strands need to be palindromic to form a double strand.

EcoRI has a palindromic recognition site in the sense of the term used in molecular biology. Perhaps I'm not understanding your point.

@canadianer  my point is that someone asking this question possibly is not well versed in molecular biology, and might thus be only privy to the non-m.-b. sense of the word: 'Palindrome' = 'A Word that looks the same, if the order of  characters is reversed'

You really need an example of the structure of a complex to justify and explain your answer better. What is the point of. binding to both strands?

bukwyrm gives a good answer for "Why" palindrome: to cut both strands. To expand the evidence, apart from clear demonstration of the current utility of restriction enzymes (they cleave recognized nucleotide sequences), the best proof indicating their evolutionary persistence is the relative lack of palindromic sequences in genomes of a wide variety of organisms.1 The idea is that the presence of endonucleases with palindromic recognition has caused organisms with such patterns to lose out to those that lack the patterns over time.

Thank you so much! I had found out lately too!

So that these enzymes can recognize the sequence on the both strands. It's the mechanism bacteria have evovled to degrade the only double stranded RNA and not single stranded.

Welcome to Biology.SE, Sujeet. Your answer could use a little more detail, and ideally a reference to an authoritative source.


text:
How do we feel sensations from a tooth surface that is made up of enamel?
If enamel does not have any sensory receptors, how do we feel the tactile sensations when we touch our teeth with an object/finger nail?

How do we feel the tactile sensations when we touch our teeth

The same way you feel tactile sensations when you tap a bicycle helmet on you head: the motion (or vibration) is transferred through the material to your head & the nerve endings in your scalp the same as tapping a tooth sends vibrations to the nerves in & at the base of the tooth.


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Can anyone identify this creature that looks like a stick?

This thing was on me. I thought was a stick until it moved. It had a black worm like thing come out one end and stood up and thats how it moved. It would stick to fabric also. In Louisiana

Looks like a terrestrial Caddisfly, the order of Trichoptera. Please add the location (country) were you found it, we might be able to answer your question.

It may be a Caddisfly (Trichoptera). Though my guess is a moth (Lepidoptera). Specifically one of the Psychidae family, also known as "bagworm moths." They are common pests in most parts of the world and while they're typically seen fixed in place they spend much of their life mobile. Both of these groups spin a case from silk and attach detritus to the outside so without a better look at the resident insect it is basically impossible to distinguish them from a photograph. However, as a general rule (with some exceptions), Caddisfly larva tend to be aquatic.
Here are a couple of links to descriptions of the groups (with pictures!) as they appear on BugGuide:
Psychidae
Trichoptera

Hi David, and welcome to Biology.SE. Answers in general should include supporting reference(s). Species identification answers in particular are best with a representative picture of the species for comparison as well. For a good example of how to answer a species-identification question, see these answers by @theforestecologist

Knowing the location, I think you are right this is a bagworm. In North America there is only one terrestrial Trichoptera and that species looks different.

@David. Welcome to Bio.SE! As De Novo mentioned, please add some support (preferably from a reputable source!) to strengthen your answer. I agree that this is likely a bagworm (see previous posts on the subject here and here). It's very unlikely to be a trichopteran larvae outside of an aquatic setting.

This is a clothing moth.  Casebearing clothing moth. The larvae wraps itself in a fabric or cotton like cocoon and feeds on soiled clothing or anything made from animals. The worm like larvae will emerge from the cocoon

Welcome user70847. This answer could be improved by the addition of one or two references, even a picture showing the clothing moth - as answers here are expected to explain why they are correct and be supported by references where possible. Please take our [tour] and refer to the [help] for our guidelines. Enjoy the site.


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Do mutated c-sis oncogenes only affect cell growth?
Since c-sis regulates only cell growth, a mutation there should only lead to an out of control growth of the cell, but the cells would still be mature, since c-sis does not regulate the function or maturing of the cell.
However a mutation in c-sis leads to cancer, and cancer is not just cells that grow out of control, but also don't performe their function (are not mature). Can someone explain how a c-sis mutation still leads to cancer please?

Hello and welcome to Biology.SE! Currently, the title of your question is quite broad, but the content of your question seems to focus on the c-sis oncogene. Are you expecting an answer only for the c-sis oncogene? If so, please be sure to edit the title of your question to reflect that.

Any oncogene that regulates growth only, I used c-sis oncogene as an example because that is the only one I know that has this function. I changed title, thanks for the feedback!

Cancer is not a disease like the flu or E. bola, where there is a single quick and easy cause for the disease which you can locate and describe in a single sentence.  Cancer consists of malignant cell growth, it is true, but why are the cells growing out of control?
The fact is that there is not one single cause.  At some point along the way, some cell experience a mutation to some gene which resulted in a slightly higher rate of proliferation than normal.  However, this in and of itself is not even enough to produce a tumour.  It simply gives the cells a higher number of daughter cells, and consequently, a higher risk of having more mutations.
At some point, one of those daughter cells acquires a mutation which results in higher levels yet of proliferation, or a mutation which encourages angiogenesis, or (in the case of epithelial cells, for instance) a mutation which allows the cell to escape typical anoikis pathways and perhaps perforate its basement membrane without dying.
Even the process of metastasis requires multiple mutations to happen, and yet if a tumour does not metastasize, it is typically regarded as benign.  The point is, cancer is not caused by a single mutation to an oncogene or otherwise.  It is caused by an accumulation of mutations which permit the cells to proliferate much faster than normal, to recruit the body's resources, and to live in tissues all around the body.
In the case of the particular gene that you mentioned, the exact role of the c-sis oncogene in cancer prevention is still unclear; in fact, according to the OMIM page,

The protein product of the c-sis gene has not been identified.

...though the gene is very similar to platelet derived growth factor genes, some of which have been identified as mitogenic factors.  Theoretically, therefore, it is possible that a mutation to the c-sis results in excessive mitogenic stimulation, resulting in an increase in cell division and proliferation.  But that last sentence is speculation, not hard science.
TL; DR:
We don't know, but it's possible c-sis encourages faster cell division.

Sources:

Platelet-derived growth factor, beta polypeptide; PDGFB on OMIM.org
Josephs SF, Guo C, Ratner L, Wong-Staal F. 1984. Human-proto-oncogene nucleotide sequences corresponding to the transforming region of simian sarcoma virus. Science 223(4635): 487-491.


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Help identify this vertabrae found on Costa Rica beach

I was walking down tamarindo beach in Costa Rica today and came upon a really LARGE section of vertabrae.. I matched it against a crocodile a shark , whales, a horse, a cow, a snake even ... any ideas ? It naturally doesn't have another piece beyond the two transgressors bones ... I'm stumped... joined just to ask this... and also I think I found footprints in lava immortalized..  in the same area yesterday... thats a diff post tho w video .. I found the footprints in lava yest.. and went back today to see if I could find them again.. I didnt.. but found this instead... Note : I found another vertabrae about 1/5 its size about 15 ft away .. not sure if same animal
Any guesses?

Looks the same on the other side.. trying to upload more pics

It looks like a tuna/ sea bass / barracuda. may be worn away so we don't have all of the spine.


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Alcohol effect on heart and vascular system
How does alcohol weaken heart muscles and why does it increase blood pressure both temporarily and long term? Is the long term effect due to increase of plaque or is it due to other effects?

The actual mechanism through which alcohol increases blood pressure is poorly understood (1,2). However, there is a mountain of evidence that shows that there is a strong correlation between alcohol intake and hypertension (small, infrequent amounts may have positive effects whereas excessive consumption has very negative effects (3)).
Back to the underlying mechanisms however, there is a good paper by Kazim Husain, Rais A Ansari, and Leon Ferder, which presents all the possible mechanisms that may contribute to alcohol-induced hypertension. The core ideas are as follows:

Mechanisms of alcohol-induced hypertension. CNS: Central nervous system; SNS: Sympathetic nervous system; RASAS: Renin-angiotensin system and aldosterone system.
Image taken from: Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention
Central nervous system in alcohol-induced hypertension

[..] greater effect [of] alcohol on systolic blood pressure compared with
  diastolic blood pressure may indicate an imbalance between central
  nervous system factors influencing cardiac output and the peripheral
  vascular effects of alcohol

Baroreceptors in alcohol-induced hypertension

Alcohol diminishes the baro (presso) reflex by interacting with receptors in the brain stem, i.e. nucleus tractus solitarii and rostral ventrolateral medulla.

Sympathetic nervous system in alcohol-induced hypertension

Several studies reported increased sympathetic nervous system activation and discharge of sympathetic amines after alcohol consumption.

Renin-angiotensin-aldosterone system in alcohol-induced hypertension

The serum levels of vasoactive substances such as renin-aldosterone have been reported to be affected by alcohol ingestion in vivo or ethanol in vitro.

Cortisol in alcohol-induced hypertension

Certain studies have implicated the role of cortisol in alcohol-induced rise in blood pressure. Potter et al have reported a significant rise in plasma cortisol levels following alcohol consumption and a drop in plasma cortisol levels when alcohol intake was discontinued.

Increased intracellular calcium and vascular reactivity in alcohol-induced hypertension

Rats treated with ethanol showed constriction of blood vessels due to greater shifts in the binding of the calcium ion (Ca2+) in arterial and arteriolar smooth muscle cells causes increased sensitivity to endogenous vasoconstrictors.

Endothelium and oxidative stress in alcohol-induced hypertension

Imbalance of specific endogenous vasoconstrictor such as angiotensin II, endothelin-1 and nor-epinephrine and vasodilator nitric oxide (NO) may also play an important role in alcohol-induced hypertension. Alcohol stimulates the release of endothelin 1 and 2 from vascular endothelium in a dose dependent manner. Alcohol also increases the angiotensin II levels in the blood and vessels. Endothelin 1 and 2 as well as angiotensin II are known to be potent vasoconstrictors of the blood vessels.

References:

Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention
Saunders et al 1981 - Alcohol-induced hypertension
Grønbæk et al - 2009 - The positive and negative health effects of alcohol‐ and the public health implications


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About embryonic and genetic evidence of evolution?
My question here is about evidence for evolution from Embryology and from Genetics.

Mammals do have similar Embryos, but is it the case that for each species there is an embryonic development that occurs in earlier species, has such relationship been observed?
What I mean for example if we generally conceive of having species$Sp_1,Sp_2,...,Sp_n$ where each $ Sp_{i+1}$ being evolved from $Sp_i,$ then is it the case that the embryonic development stages of $ Sp_{i+1}$ contains some of the embryonic development stages of all of its ancestor species.

Similar question to 1 but regarding Genetics, is it the case that every species has a genetic thumbprint of its ancestors that lie there in the non-functional sections of its DNA, i.e. is it the case that all the genetic history of our evolution is recorded in the non-functional section of our DNA. So do human DNA have some portions of the DNA of some dinosaurs for example?

In short: Yes and Yes

"ALL the genetic history", most definitely not, genes mutate and get recycled or lost. There is some genetic history of our evolution, and comparing it to other organisms can yield much more.

You seem to want to use LaTex formatting in your post. That's great for having nice layout. Just wrap your format in $ to have it Latex (MathJax actually) format. For example,  $Sp_1$ is displayed as $Sp_1$

Question 1 asks whether ontogeny recapitulates phylogeny. It is striking that the when observing e.g. human embryo development, the embryo seems to go through stages that its ancestral species would go through, but where those 'lower' species would terminate at a specific stage. In other words, embryonic development seems to recapitulate a species' evolutionary lineage.

This is the recapitulation theory, which is outdated and incorrect, but a great example from the history of science. The most prominent of these was Ernst Haeckel's biogenetic law and the Meckel-Serres Conception. There were many problems with this, especially because they focused on noting similarities rather than differences, and several exceptions exist to the rule. They were not very scientific. It also incorrectly presumes that complex organisms have more predecessors. However, it is a compelling piece of evidence to elegantly show that evolution acts incrementally on existing embryological processes.
Question 2 asks whether there is evidence of ancestral DNA in our genome. The answer is yes. Where to begin? We share almost all of our genes with close relatives (e.g. chimpanzees and bonobos) and progressively fewer with more distant relatives. 50% of a banana’s genes (and indeed most other plants') can be found in the human genome. But remember, logically, that doesn't necessarily mean that 50% of human genes are found in bananas, though, because of the way divergence works. The human genome also contains a record of many viruses that have inserted themselves over tens of millions of years. Though they are not ancestors, they have been added 'horizontally' as opposed to the 'vertically' that ancestor DNA is modified over a species lineage.
It's very possible to answer your questions from many, many different angles, and present countless pieces of evidence in favor, but I think this should suffice.

S Pr's answer is very good, I'll just elaborate on a few points.
1) Evolution acts incrementally on existing embryological processes -> the insight here is that organisms don't come out fully formed, they develop. When we say a gene, say, "codes for" a tail, it doesn't make a tail magically appear: its action happens during the organism's development, where it acts on the development process such that the adult organism will have a tail.
This means that when organisms change over time via evolution, the way these changes are actually implemented are as changes to an existing development process; obviously the development process isn't going to be reset each time. So for example, it might make sense that since snakes don't have limbs as adults, they should never have limbs at any point in their development because what would be the point? But they evolved as a variation on organisms that did have limbs, and whose embryological development included the development of limbs. Evolutionarily speaking there's little reason why you should change that by preventing the development of limbs at stage 0, as opposed to, say, halting their development at stage 10 and destroying the limb buds. Either way you end up with a limbless adult snake! On the other hand if you destroy the limbs at stage 10, you're hardly going to have them come back at stage 19. In other words, you can end up with a pattern of later evolutionary changes happening later in development on average even if the changes occur at a random point in development, simply because a change at one stage of development also changes the later stages, but keeps the earlier stages intact. So earlier stages are more likely to be unchanged on average, i.e. similar to how they were in the ancestors. In practice the changes don't happen randomly in the development process of course, which is one reason "ontogeny recapitulates phylogeny" actually has tons of exceptions. This textbook "Developmental Biology" has a cool companion site with a chapter that discusses the history of the idea. This Wikipedia page also discusses some evolution in the view of evolution and development, talking about the "hourglass model" vs the "funnel model". The funnel model is this idea that the earliest stages are most similar to ancestral forms (and thus similar between related species), but the hourglass model points out that actually there is one specific stage (the "phylotypic stage") that stays similar between species, but there are differences both in earlier and in later stages.
2) There is no such thing as "dormant" DNA. There is active DNA (that codes for genes, regulatory regions, etc) and non-functional DNA. Non-functional DNA can be a few mutations away from being functional, and thus become functional as a result of chance mutations, but "dormant" suggests regions of DNA that are deactivated with the intent of reactivating them in the future; this isn't a process that occurs in evolution, which has no such future-looking intent.
Now it is the case that a) all DNA is subject to mutation, and b) we have a whole lot of DNA, and the mutation rate is quite low. This means that a lot of DNA is indeed more or less the same as it was in our faraway ancestors. Having said that, non-functional DNA is less likely to remain the same than functional DNA is, because nothing prevents mutations to those parts from being passed down through the generations. The DNA sequences that are the most unchanged ("conserved") are those that are used in such basic functions of life that they evolved very early in the history of life, and any change to them kills the resulting organism, which means that natural selection will make sure they don't change, or change very little. Here is a paper "The Genetic Core of the Universal Ancestor" that looks at such DNA sequences that are the same in all organisms ("universally conserved") to infer what genes the common ancestor of all living things had.
Finally, while this does mean that humans share a lot of their genome with dinosaurs, those shared genes mostly come from the fact both humans and dinosaurs share genes with their common ancestor, which was one of the earliest reptiles. Dinosaurs are not ancestors to humans.

On the upside those changes in nonfunctional portions also get passed on and make for a better measure of relatedness, since selection is not really doing much with them.

Question 1

Mammals do have similar Embryos, but is it the case that for each species there is an embryonic development that occurs in earlier species, has such relationship been observed?

Technically, we do not observe much from the embryology from ancestral lineages. They don't exist anymore, so we can't make many observations from their embryology. The question is rather whether related lineages have similar embryogenesis.
The answer is yes. Mammals develop like mammals, birds develop like birds, angiosperms develop like angiosperms. For example, in all protostomes (insects, spiders, crustaceans, molluscs, ...), the blastopore becomes the mouth while in all deuterostomes (sea urchins, sea cucumber, vertebrates incl. birds, mammals, turtles, lizards, sharks, etc...), the blastopore becomes the anus.
Question 2
Genetics is our main tool for inferring our phylogenetic trees. So, it makes more sense to ask whether other things match the genetics than the other way around. But yes, things match. Fossil records, ontogeny, phenotypic variation and genetics. Everything match to tell a similar story of the phylogenetic relationships among species.

The important thing about "ontogeny recapitulates phylogeny" is that it is not true,  There was an idea that it perfectly replicated phylogeny, which is were the phrase came from, but that proved false pretty quickly. The phrase has hung around because ontology can provide a lot of useful information about phylogeny.

@John I did not know that it used to mean more than it does today. Thanks for your comment.


text:
Why doesn't alum coagulate my cyanobacteria?
My collected rainwater has a pronounced blue-green tint which I believe to be due to the presence of cyanobacteria.
I have been trying to remove the cyanobacteria using aluminium sulphate, but it doesn't seem to work.
Would anyone like to suggest why?

Do you have a good microsocope with which you could confirm the identity of the microscopic organisms?

Thank you for replying.  Unfortunately I didn't see your response for some reason.
I have come to the conclusion that the problem organism is not cyanobacteria.
I will ask another question to clarify the issue.


text:
Can an importin without any cargo pass through the NPC?
Can an importin (nuclear import receptor) without any cargo pass through the Nuclear Pore Complex (NPC)? If it can, wouldn't it be a waste of energy to have the 'unloaded' importin enter the nucleus and then binding to GTP?


text:
How many phosphates are in the 5' end of a DNA strand?
I know that the pyrophosphate of a NTP is hydrolysed so that it can create enough energy for the synthesis of DNA. But if we want to get specific we can know for sure that the 3' end of the DNA strand has got one phosphate because the phosphate is having a bond with another nucleotide. But what could be the reason for the 5' end to have only one phosphate and not 3? Could it be the energy providing or that the structure has to be consistent or something else that I can't think of?

The DNA polymerase can only extend a primer and therefore almost all lifeforms have a primase (which is a type of RNA polymerase) that synthesizes RNA primers at the replication origins that the DNA polymerase can extend.
As you guessed, the 5' end would indeed have a triphosphate.

Organism            Template Sequence        Primer Synthesized
Herpes simplex-1        3′-GPyPy                 pppPuPu
T4                      3′-TTG                   pppAC
T7                      3′-CTG                   pppAC
E. coli                 3′-GTC                   pppAG
S. aureus               3′-ATPy                  pppAPu
S. aureus               3′-ATPy                  pppAPu
A. aeolicus             3′-CCC, CCG, CGC         pppGG, pppGC, pppCG
B. stearothermophilus   3′-ATPy                  pppAPu
Human                   3′-PyNN                  pppPuNN
Calf                    3′-PyNN                  pppPuNN

Initiation sites used by primase from different sources. Pu = purine, Py = pyrimidine, N = any base ppp = the triphosphate on the 5′-end of the primer. Those bases that are required but do not code for a base in the primer (“cryptic” nucleotides) are underlined and in bold.
Kuchta and Stengel (2010)

In the final stages of replication, these RNA primers are removed by RNAseH and DNA polymerase I in bacteria and the gaps are filled by the latter (Cooper (2000) The Cell). In eukaryotes, the primer is removed by the action of Fen1 and Dna2 exonucleases and the gaps are filled by DNA polymerase δ (Burgers 2009).
In PCR, it is quite straightforward: the product will have whatever 5' modifications the primers have (usually none).


text:
Why does atheroma contain thromplastin/tissue factor?
From my understanding, when the endothelial lining of arteries is damaged, atheroma is formed at the site of the damaged area. If the atheromas is ruptured, thromboplastin contained in atheroma is released into blood stream thus thrombus is formed after atheroma gets ruptured - this phenomenon is known as atherothrombosis. As a result, atheroma is characterised by its thrombogenic activity.
My question is, how come atheroma contains thromboplastin thus when it is damaged, thrombosis occurs? What was the source of this thromboplastin? Was it in the bloodstream? If thromboplastin was always present in the blood in which it entered into the atheroma during the formation of atheroma, why don't thrombosis occurs at the start when endothelial lining of the artery is damaged (without the need for an atheroma to rupture)?
I've read a couple papers and watched some videos on this topic. I've put one of my research below for reference to back up 'my understanding'.

Rupture of the fibrous cap will typically release all the semiliquid
  material from the central portion of the atheroma. Because this
  material contains thromboplastin, it will trigger blood clotting, and
  a thrombus will develop at the site of intimal ulceration.

Tissue factor is present in subendothelial tissue and leukocytes - in this case this would be within the atheroma since the atheroma consists of damaged endothelium.
Tissue factor's presence in the subendotheilum in general implies that whenever the endothelium is damaged, tissue factor is released which promotes clotting at that site. Clotting starts after an atheroma ruptures because up until that point all the tissue factor is encased within the atheroma, protected from direct contact with the bloodstream - there is still no superficial injury to the endothelium to expose the underlying tissue factor that would signal the clotting cascade to begin. Therefore, clotting only starts after the atheroma ruptures and all the tissue factor stored within the atheroma is released into the blood vessel.
It is worth noting here that in homeostasis without any injury, the coagulation cascade and fibrinolytic pathways (the clot-lysis or pathways) are both active, but they balance out each other's effects. Disruption of this balance due to pathology, injury, or other insult causes an imbalance between the two pathways which the body seeks to rectify. The imbalance is what leads to clot lysis (in the case of wound healing - after the wound has healed) and clot formation (in the case of a new injury).
Sources:

https://www.ahajournals.org/doi/full/10.1161/01.CIR.94.6.1226
https://www.ahajournals.org/doi/full/10.1161/01.CIR.96.2.396
https://ascpt.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1752-8062.2011.00351.x


text:
Where do the lysines come from during ubiquitination?
I know that Ub forms an isopeptide bond with lysine, but where do the lysine come from?
Are they just always available for the Ub to find to during the ubiquitination process? Is there a free lysine available on each of the additional Ub added to the chain? After the first Ub is added onto the target protein, does the E2/E3 complex still have to bind each time a Ub is added to the chain?

The Wikipedia article on Ubiquitin gives a pretty good answer to your questions. Look at the referenced articles if you want to get more detailed answers.

Are they just always available for the Ub to find to during the ubiquitination process?

Yes, This [Ubiquitination] process most commonly binds the last amino acid of ubiquitin (glycine 76) to a lysine residue on the substrate.

Is there a free lysine available on each of the additional Ub added to the chain?

Ubiquitin has seven lysines and each one of them can be bound to the N-terminal glycine of the next ubiquitin.

After the first Ub is added onto the target protein, does the E2/E3 complex still have to bind each time a Ub is added to the chain?

Yes, but this is more complicated than the general mechanism. A poly-ubiquitin chain can be attached just like a single ubiquitin or one more ubiquitins can be conjuated to an exisiting ubiquitin-protein complex. See for example Brown et al and David et al.


text:
Electron Transport Chain Proton Pumping into the Intermembrane Space
In regards to the electron transport chain, I know that complex I pumps 4 H+, complex III pumps 4 H+, and complex IV pumps 2 H+, but where do these numbers come from? If someone could explain this, that would be great. For example, I'm confused at how 4 H+ are pumped when only two enter complex I via NADH + H+.


text:
What genes in a plant determine whether a stem is erect or climbing?
I was randomly reading this Wiki article on Jasmine and this question crossed my mind after reading the following lines:

Jasmine can be either deciduous (leaves falling in autumn) or evergreen (green all year round), and can be erect, spreading, or climbing shrubs and vines.

How can a plant be both erect and climbing at the same time?
I have looked for genetic mechanisms related to this, correlating environmental or other stimulus with this phenomenon, but have not found a satisfactory explanation.
So how does this occur?


text:
Why both forward and reverse primer are added in asymmetric PCR?
If the purpose of Asymmetric PCR is to amplify single targeted strand of dsDNA then instead of adding just one primer for targeted strand why do we add both forward and reverse primer? Upon addition of only one type of primer won't we will get linear amplification of that strand?

The other primer is at least 30 times less. I suppose this is done for amplifying the template to a certain extent. If you have a pure template (i.e. the exact length as the final product) of good enough concentration then the other primer is not required at all.

I'm not 100% sure about it as I haven't done it personally and I couldn't find any material on this topic. So it is just a guess.


text:
How to interpret this PubChem record of L-Alanine
Using the PUG service from NCBI, I am retrieving 3d structure data for a molecule.
Raw data here.
I am trying to understand this record, specifically for the purpose of rendering in a 3D coordinate system using threejs.
Could anyone please assist in understanding this information.
Due to the large size of the json response and as I am using javascript, I have constructed some Typescript types that describe the shape of the data to assist the discussion. I have specific questions, which are stated below.
//// Root Object
interface JSON_Response {
    PC_Compounds: PC_Compound[];
}

//// Compound Object
// must stand for PubChem Compound
interface PC_Compound {
    id: ID;
    atoms: {
        aid: number[];
        element: number[];
    };
    bonds: {
        aid1: number[];
        aid2: number[];
        order: number[];
    };
    stereo: Stereo[];
    coords: Coords[];
    props: Data[];
    count: Count;
}

//////// Sub-types described below

Atoms
The atoms object has two arrays; 'aid' and 'element'.In the above JSON response, these arrays are both of length 13. The data for L-Alanine shows it has 13 atoms. I am correct in saying that the numbers in the 'element' array are corresponding to Atomic Numbers? And these atomic numbers are assigned to ids from the corresponding indexes in the 'id' array?
Bonds
What are aid1, aid2, and order? These arrays are 12 entries each so each must represent 1 bond between two atoms. But what do the number values correspond to? How should they be interpretted?
Coords
In the coordinates object,
interface Coords {
    type: number[];
    aid: number[];
    conformers: [
        {
        x: number[];
        y: number[];
        z: number[];
        data: Data[];
        }
    ];
    data: Data[];
}

The x, y, & z arrays are of length 13. Am I correct in saying that these represent the x, y, and z coordinates of atoms in the corresponding index of the above elements array?
Data
Data Object seems to be part of a esoteric system for attaching arbitrary data to the object. If anyone has any pointer on this it would be greatly appreciated.
interface Data {
    urn: {
        label: string;
        name: string;
        datatype: number;
        release: string;
        version?: string;
        software?: string;
        source?: string;
        parameters?: string;
    };
    value: {
        sval?: string;
        fval?: number;
        slist?: string[];
        fvec?: number[];
        ivec?: number[];
    };
}

stereo
seems to describe planes of rotation
//// Compound sub-types
interface Stereo {
    tetrahedral: {
        center: number;
        above: number;
        top: number;
        bottom: number;
        below: number;
        parity: number;
        type: number;
    };
}

interface ID {
    id: {
        cid: number;
    };
}

miscellaneous chemical information
interface Count {
    heavy_atom: number;
    atom_chiral: number;
    atom_chiral_def: number;
    atom_chiral_undef: number;
    bond_chiral: number;
    bond_chiral_def: number;
    bond_chiral_undef: number;
    isotope_atom: number;
    covalent_unit: number;
    tautomers: number;
}

In addition, if anyone has any techniques or advice on how to extract meaning from the response data from PubChem, if they could please post below it could come in handy for me or some other person working on this.

The PubChem format description is not that easy to find:
https://www.ncbi.nlm.nih.gov/IEB/ToolBox/CPP_DOC/asn_spec/pcsubstance.asn.html
And the ASN file linked here:
https://pubchemdocs.ncbi.nlm.nih.gov/data-specification

I am correct in saying that the numbers in the 'element' array are corresponding to Atomic Numbers?

Yes, 1 is hydrogen, 6 is carbon, 8 is oxygen, etc.

And these atomic numbers are assigned to ids from the corresponding indexes in the 'id' array?

in your example, "atoms": {"aid": [1, 2, 3,  ...,  13], "element": [8, 8, 7, ..., 1]},, the the ID of the first atom would be 1 and element 8 (oxygen), the third atom: ID 3 and element 7 (nitrogen).

Am I correct in saying that these represent the x, y, and z coordinates of atoms in the corresponding index of the above elements array?

Yes

What are aid1, aid2, and order?

aid1 and aid2 are the atom identifiers. order is the bond type.

These arrays are 12 entries each so each must represent 1 bond between two atoms. But what do the number values correspond to? How should they be interpretted?

For example aid1 = [1, 2], aid2 = [3, 4], order = [1, 2] would mean a single bond between atom 1 and atom 3 and a double bond between atom 2 and atom 4.
Good examples of implementations:

PubChemPy
pubchem_2d_structure_json_to_svg.py


text:
Can Dpn1 digest hybrid PCR product with only one methylated strand?
In Site directed mutagenesis using PCR, after a cycle we obtain a hybrid molecule with one parental strand and other newly synthesized unmethylated strand. This is followed by Dpn1 digestion. Does this digestion just cut the parental strand leaving behind single strand of newly synthesized product?
Does this means that Dpn1 can use ds methylated DNA( both strands methylated) as well as ds hybrid DNA (with one methylated strand and other unmethylated strand) as substrate?

According to the NEB website FAQ, yes, it can, but less efficiently.
"DpnI cleaves hemi-methylated dam sites 60X more slowly than fully methylated."


text:
Is there any independent non-DNA based information system in the cell
The information in protein is not neccessarily independent of the genome as the information of amino-acid sequence comes directly from the  genome. The process of post-translational modification may be another candidate but the main players in this process are proteins so its not clear whether this process is totally determined by genome (total DNA-based information) or some portion of it comes from a different source.
Obviously the external world is a source of information but I am interested in internal sources.

What do you mean by "information system"? Information per se is defined only if there is a sender/receiver or rather a transmission process. In evolutionary terms, information is something that is heritable, e.g. is stably inherited from parent to offspring cell throughout an indefinite number of reproduction steps. Do you mean this latter interpretation?

yes, the latter.

According to the comments, the question is about inheritance systems of cells. The "mainstream" information storage and inheritance system is of course DNA (and RNA in some cases). However, there are additional and parallel inheritance systems even within a single cell (not to mention in multicellular organisms). These form a subset of epigenetic inheritance methods and - as expected - are less precise than the information copying mechanisms of polynucleotide replication (in eukaryotes) and certainly more limited in the amount of information that can stably maintained throughout generations. This was explored in detail by Eva Jablonka and Marion Lamb (among others) in a few books and many papers:

Jablonka, E. & Lamb, M. J. 1995. Epigenetic inheritance and evolution: The Lamarckian dimension. Oxford University Press, 346 pp.
Jablonka, E. & Lamb, M. J. 2006. Evolution in four dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life. MIT Press, 472 pp.
Jablonka, E. & Szathmáry, E. 1995 The evolution of information storage and heredity. Trends in Ecology and Evolution, 10, pp. 206-211.
Maynard Smith, J. 1990 Models of a dual inheritance system. Journal
of Theoretical Biology, 143, p. 41-53.

“An epigenetic ineritance system (EIS) is a system that enables a
  particular functional state or structural element to be transmitted
  from one cell generation to the next, even when the stimulus that
  originally induced it is no longer present. In other words, EISs are
  the systems that enable the transmission of various phenotypic
  expressions of the genetic information in an individual.” (Jablonka & Lamb 1995, p. 80.)

Epigenetic inheritance methods include the following systems that could in theory code for information that is potentially inherited from parent to daughter. The list is far from being exhaustive.

DNA methylation: a methyl group added to a gene's promoter represses its transcription. Methylation is heritable: when DNA replicates, methylation carries over. There are other chromatin-marking methods that are inherited.
Steady-state inheritance system: "the inheritance of functional states through self-sustaining metabolic networks, maintained by positive feedback." (Jablonka & Szathmáry 1995 TREE) The cytoplasm itself is also inherited by the daughter cells, but any information "stored" in the cytoplasm cannot effectively be "replicated" from cell to cell.
Structural inheritance system: 3D structures of the cell provide the template for similar structures to assemble, e.g. "transmission of cytoskeletal organization and of cortical organization" (Jablonka & Szathmáry 1995 TREE).
Symbionts and parasites (bacteria, viruses, plasmids, etc.) that can replicate within the cell (so that when the host divides, both daughter lineages receive the partner). Note, however, that if the parasite is too virulent then it is expected that horizontal transfer is more emphasized than vertical "inheritance".
Prion proteins. Prions are proteins that may exist in several distinct conformations, and at least one of these conformations is capable of replication by forcing its alternate conformation (and therefore alternate function) on the normal physiological form of the protein (both having the same amino-acid sequence). See Shorter, J. & Lindquist, S. 2005. Prions as adaptive conduits of memory and inheritance. Nature Reviews Genetics 6, p. 435–450.
...

How is DNA methylation "non-DNA based"?

@David Well, strictly speaking, it is. But a crucial difference compared to standard DNA-encoded genetic information is that heritable information is not encoded in the nucleotide order of the polynucleotide chain. On the other hand of course, (almost) everything is DNA-based when talking about biology (on Earth at least).


text:
What's the plant name? It is climber or creeper plant..like money plant...help me finding its name...it has seven to five lobes

It is climber or creeper plant..like money plant...help me finding its name.

Please add the location where you found it (country, state or city), and something on the habitat (forest, garden, wasteland in a city etc.). Only a leave is a bit difficult... Might be Bryonia

To add to @RHA's comment, when you add to the question, do it with an [edit] rather than in the comments. It may be useful to review the tag information at [tag:species-identification].


text:
Why do stem cells injected into muscle become muscle cells?
In this article published in Science Daily, researchers injected teratoma-derived stem cells into mice with muscular dystrophy, and the stem cells regenerated 80% of the lost muscle. But what is the mechanism that results in their becoming muscle cells, rather than any other type of cell?
I'd have to assume some sort of cell signaling is responsible for this directed differentiation into muscle cells, so what is it? Can it be reproduced in vitro?

Looking at the paper itself, we find that they prepared the stem cells to have myogenic (muscle-specific) properties. They first injected stem cells into the irradiated (which kills muscle stem cells) muscles of immune-deficient mice. This resulted in tumor growth (teratoma - a stem cell derived tumor, where different kinds of tissues are spontaneously formed. Growing in a muscle environment increases the chance of muscle tissue formation.). The tumor cells, which expressed muscle-specific markers, were isolated from the other tissues and then used for regeneration of an injured muscle.
In their teratomas they checked for cells expressing α7-integrin and vascular cell adhesion molecule-1 (VCAM-1), which are markers expressed in satellite cells (muscle stem cells). These factors were expressed in about 10% of the fraction that did not show any hematopoietic and endothelial markers (meaning: there were a lot of other tissues formed as well). They also showed expression of Pax3 and Pax7, which are muscle-specific transcription factors, important for differentiation of myogenic progenitors. These cells were therefore already muscle-specific cells before they have been transplanted for regeneration.
The researchers did, in fact, do in vitro and in vivo differentiation experiments. For in vitro differentiation they subjected their muscle-marker expressing cells to a myogenic medium. This mimics the muscle environment and enables cell differentiation signaling. Here is an example protocol how this can be done. Then they transplanted their muscle stem cells into a muscle and they also managed to differentiate in vivo and regenerate the injured muscle.
The entire process of pluripotent stem cell to muscle cell differentiation can be performed in vitro, but seems to be tricky (1,2). Medium factors or genetic activation of transcription factors can activate different steps in the differentiation cascade.