text:
Where would vegetarians/vegans get a substitute of hemo/myoglobin from?
As far as I understand, there is a difference in the iron absorbed from meat than from other sources like grains and vegetables.
If this is the case, is it possible that not ingesting the hemoglobin and myoglobin found in meat leads to some kind of deficiency in a protein or iron itself that creates some symptoms similar to anemia, like fatigue or headaches? Or, is the iron found in non-meat products just as viable as that found in meat-based products?

Your two questions seem unrelated. How is your question on whether non-consumption of myoglobin from meat cause anaemia related to iron content in vegetarian food? Plus, there are other iron containing proteins in the animal body and there are excellent plant-based sources of iron. Your question is not clear to me.

I can't take your comment seriously because if you had any knowledge on the subject, you would know your question doesn't make sense, you don't understand the subject well enough to understand what I asked.

The following informations is taken this source. It also lists some references. If this doesn't answer your question let me know in the comments.
Iron is found in food in two forms, heme and non-heme iron. Heme iron, which makes up 40 percent of the iron in meat, poultry, and fish, is well absorbed. Non-heme iron, 60 percent of the iron in animal tissue and all the iron in plants (fruits, vegetables, grains, nuts) is less well absorbed. Because vegan diets only contain non-heme iron, vegans should be especially aware of foods that are high in iron and techniques that can promote iron absorption. Recommendations for iron for vegetarians (including vegans) may be as much as 1.8 times higher than for non-vegetarians.
Some might expect that since the vegan diet contains a form of iron that is not that well absorbed, vegans might be prone to developing iron deficiency anemia. However, surveys of vegans have found that iron deficiency anemia is no more common among vegetarians than among the general population although vegans tend to have lower iron stores.
The reason for the satisfactory iron status of many vegans may be that commonly eaten foods are high in iron.For example, you would have to eat more than 1700 calories of sirloin steak to get the same amount of iron as found in 100 calories of spinach.
Another reason for the satisfactory iron status of vegans is that vegan diets are high in vitamin C. Vitamin C acts to markedly increase absorption of non-heme iron. Adding a vitamin C source to a meal increases non-heme iron absorption up to six-fold which makes the absorption of non-heme iron as good or better than that of heme iron.
Fortunately, many vegetables, such as broccoli and bok choy, which are high in iron, are also high in vitamin C so that the iron in these foods is very well absorbed. Commonly eaten combinations, such as beans and tomato sauce or stir-fried tofu and broccoli, also result in generous levels of iron absorption.

These numbers for spinach are based on an ancient typo, compare also the actual values i.e. on wikipedia. The actual difference between spinach & steak would only be around 1.7x

Okay, so the iron in non-heme sources is less absorbed, but enough of it can still be consumed to match exactly what one would absorb from a quantity of meat. So the source doesn't make a difference as long as a sufficient quantity is absorbed in the end?


text:
What are these insects
I am conducting research and these insects were found on my biological sample (sections of pig's femora placed in an artificial water setting).
My location: Mississauga, ON
What species of insects are these?

Please provide the following to receive an answer: Where are you? Where did you collect these specimens? What is your "biological sample"? What sizes are the specimens?

Were they alive or dead? Do you have photos showing the entire insect larvae (i.e. including not only its head/thorax, but also abdomen and posterior end)?

The small one was alive, but the larger one was dead as the samples were placed in a freezer.

source: Stack Exchange

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

sort: votes


text:
Is it normal to see yeast cells stacked in the Z axis when counting yeast?
I just got started with yeast cell counting and was surprised to observe yeast cells that are at different z axis depths at 400x. That is, by adjusting the focus (not the x/y stage) I can make some cells go into view as others go out (there is some overlap in some cases but not always).
Is this normal? It means that I will have to count at probably 2 different depths which I haven't seen anyone else talk about. I had assumed everything would be visible at a single depth.
It is possible I did something wrong like not properly seating the cover slide. My filling technique, based on some videos I watched, was to breathe on the cover slide and the hemocytometer, place the cover slide on and slide it around a bit, and then touch the dropper to the edge of the slide to fill the chamber (I did not observe any obvious overflow/overfill).

Did you wait for the cells to settle or did you look immediately after loading the volume?

I looked immediately but I also looked over different time periods--probably up to 10 minutes... and did not notice any change in stacking.  I did however notice that the yeast cells start dying off over time with the stain creeping into formerly live cells--so I'm not sure I'd want to wait very long either.

That sounds very odd. Yeasts are very hardy and in my experience I can dilute them 1:100 in sterile water and let them sit for an hour on the bench but I never observe a significant drop in colony forming units, let alone observe them dying under the microscope.

I should mention the yeast were not that healthy--I was just using an old sample to test the technique--that may explain why they seemed to die quickly.  I did counting more recently on a healthy sample and did not have any issues (and there was only negligible Z axis stacking for a couple budding cells).  I'm guessing I didn't properly seat the cover when I had the problem originally.

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


text:
Why is the capirally electrophoresis rarely carried out?
I'm a student at the university in Japan.
I search details and advantages with each electrophoresis.
I think the capirally electrophoresis has much nice method at the points of resolution, rapidity and so on. However, just my thought, there are not very many of papers using it.
I have asked at a Japanese site (not professional one), and the answer is on cost. But no sites explain so.
Please give me a help for this confusing.
Thank you for your reading.

Are you asking why capillary electrophoresis is rare compared to normal agarose gel electrophoresis?

Can you also clarify what kind of analytes you are interested in?

For WYSIWYG; It is protein. Our laboratory studies it. Except of me, however, none knows capirally's in detail. So the more you teach me, the happier I am.

For user137; I was going to search in terms of PAGE, but agarose is also OK because I could get few data about the capirally electrophoresis.


text:
Why do our bodies maintain blood pressure but not the flow rate?
This might be a silly question but i'm not not clear
I'm always told that blood pressure is homeostatic parameter and can't not be changed but isn't what important is the flow rate to the organs? why not maintain flow rate
Doesn't having enough blood flow to the organ already satisfy our bodies to function properly or do pressure play any role? what happens if blood flow is constant but blood pressure drop below normal
there's some case when one have blood lost , pressure drop and our bodies respond by constricting artery and that results in decreased cardiac output.Isn't that worst? decrease cardiac output just to maintain blood pressure
Forgive my little understanding out this I know my thought is kind of logically wrong but please help me understand. thank you

A constant blood-flow would not be advantageous to organisms with a varying activity level. The blood supplies (mainly) oxygen to the tissues and the supply of course needs to match the requirements. Organisms rely on a number of mechanisms to ensure this match, one of these is to increase the blood-flow (heart-beat). But flow through a (blood) vessel relates directly to the pressure and inversely to the cross-sectional area of the vessel, so if the flow is increased, the organism must accept either a higher blood pressure or expand  the blood-vessels. Of course, it is in reality a compromise of both mechanisms.

Hi FrankS. Welcome to [biology.se]. Your answer is good but if you could expand a bit on the activity part, it would be great.

What I mean by "activity" is primarily muscle work. If you exercise the muscles work harder, which requires more energy and oxygen. Also for homeothermic organisms, producing more heat to keep warm in a cold environment means higher metabolism and thus higher oxygen consumption. Constantly keeping the blood/oxygen supply at a high level is not an economical solution in a competitive nature where food is scarce.

I'm always told that blood pressure is homeostatic parameter and can't not be changed
Homeostatic doesn't mean it is constant. It means if it goes high or low it tries to revert back to equilibrium.If you check your blood pressure it doesn't show 120/80. What you call normal is the statistical average of all.
Other questions I do not know the answer.

By regulating the pressure the body is regulating the flow rate. Pressure is the driving force for flow and as shown in this equation below (called the Hagen–Poiseuille equation) pressure drop and flow rate are related to each other for laminar flow in a cylindrical tube. So its impossible in your scenario to keep the flow rate constant but reduce pressure drop for the same size blood vessel.
{\displaystyle \Delta P={\frac {8\mu LQ}{\pi R^{4}}}}
You are right that flow rate is the key parameter because it's important to deliver adequate oxygen to all the tissues in the body or they'll die.

But if your pressure drop.flow rate drop yes but doesn’t further constrictinf the vessel with drop the flow rate even more as the flow is restricted because of more resstance? Why do our body constrict the blood vessel when pressure drop just to increase pressure but reduce flow rate?


text:
Understanding the derivation of the Nernst equation
I am trying to understand how the Nernst equation can be derived and am mostly referring to the explanation given in the book Theoretical Neuroscience by Dayan and Abbott.
Given we have a concentration gradient and consider only Potassium, the overall approach to derive the Nernst equation is to find the equilibrium state where the flow of ions out of the cell and the flow of ions into the cell due to diffusion are the same. For the flow of ions we find the following two expressions:
$$
F_{out \rightarrow in} = \gamma [K^+]_{out} \\
F_{in \rightarrow out} = \gamma [K^+]_{in} \cdot exp({\frac{q V}{k_b T}})
$$
In these two formulas $\gamma$ is some complex factor that we don't know that e.g. encodes the number of channels but it does not matter since it will disappear when we equate both equations. $[K^+]_{out}$ is the concentration of potassium ions outside the cell and $[K^+]_{in}$ is the potassium concentration inside the cell. $V$ is the difference in electrical potential between the inside and the outside and $T$ is the temperature.
The reasoning given by Abbott and Dayan is that the flow of ions from inside the cell to the outside needs to overcome the energy barrier of the electrical gradient. Only ions that have sufficient thermal energy can do so, this is why the Boltzmann factor appears. The flow of ions from the outside to the inside does not need to overcome such a gradient. It is therefore proportional to the concentration of the outside.
The last part is where I struggle. Don't we need to account for the fact that positively charged ions are pulled into the cell due to the potential difference. Am I wrong in claiming that there is an electrical field that will increase the number of ions traveling into the cell?

This is not how I would approach thinking about the Nernst equation; check the derivation on Wikipedia I find it very straightforward: https://en.wikipedia.org/wiki/Nernst_equation

Unfortunately, I am not really familiar with electrochemistry and cannot follow the employed formalism on Wikipedia. Do you think the more physical approach presented in the question is not rigorous?

I think it's probably perfectly rigorous (though I suspect there is a hidden simplification in there), just not a direction I've approached it from before and I don't have Dayan and Abbott in front of me, though I trust them and typically recommend their book as a starting point for those interested in theoretical neuroscience. See also http://www.columbia.edu/cu/biology/courses/w3004/Nernstequationderiv.pdf or https://onlinelibrary.wiley.com/doi/pdf/10.1002/9781118687864.app1


text:
Is feeding birds only after a snowstorm helpful or harmful?
We had a very rare snowstorm here which left the ground covered in 8" of snow and trees covered in snow and ice. It'll likely all melt away in the coming days as we have sunny days and temps rise above freezing.
I noticed some birds poking around the snow on my back deck, so I cut up some raw untoasted walnuts and almonds into small pieces and and scattered them out on the deck and have seen a number of small birds stopping by to feed.
I travel away from home a lot and can't reliably keep a bird feeder stocked, so I'm wondering if this temporary food source is helpful or harmful to the birds since I'm not going to keep it up after the snow melts.
My concern about harm is about causing them to change their behavior and training them to keep looking for food on my deck after I stop feeding them in a few days. I'm assuming that the raw nuts I'm feeding them won't cause any harm even if it's not a well balanced diet, but I don't really have anything more suitable.
I don't know what type of birds they are, they are around 3" high, typical Pacific Northwest birds, I guess.

[pets.se] may be better place for your question. It should be on-topic here too. Can you please add some information on what kind of birds are these. That would be an important factor.

Pets stack exchange specifically excludes wild animals: not livestock, wildlife, and pests in and around your home.  I don't know what kind of birds they are, but I added some photos. Based on this  and this answer, Biology seemed to be an appropriate place to ask.

it's helpful if you give them healthy food which strengthens them, i.e. natural oily foods like seeds, veg oil and natural whole carbs. oil is the most energetically dense and digestible fattening form of food and in the antarctic a cold guy can eat an entire bar of butter without noticing it. birds like vegetable oils, peanuts, seeds. they had it a bit hard with h1n1 virus, it can help to mitigate the effects of man's destruction on them. it also artificially selects certain birds for favorable survival treatment in the cold spells.

@com.prehensible please don't answer in comments. If you think you know the answer then please post one with suitable references.

Feeding for a short period should be helpful, not harmful to the birds, particularly if it is during or following a cold storm.  (Ground feeding birds, such as the Junco or Towhee shown in your picture have particular difficulty after a storm covers the ground with snow.)  A concern people have with feeding is that feeding will create a dependency of the birds on the artificially supplied food.  The worst case of this would be expected to occur during fall migration, where an unusual supply of food might delay birds from migrating, which may be detrimental if they cannot survive the colder weather they may encounter because of the delay.  Other than that period, short term feeding should not be problematic since the birds will not develop a strong visiting habit over a short period.
Dependence on human feeding was studied by Brittingham and Temple in an article "Does Winter Bird Feeding Promote Dependency?".  This study evaluated chickadees in two areas, one which had supplemental food available for a year.  The next year, without food available for either area, showed no difference between the resident birds of the two areas.  Although they didn't test suddenly discontinuing food in midwinter, they do comment on that scenario:

We did not test what happens when feeders are removed unexpectedly from a site in the middle of winter, but we suspect that this would not be as detrimental as is typically thought. In winter, a natural food patch may disappear suddenly as a result of a winter snow or ice storm or the foraging activities of other flock members. As a result, chickadees apparently track a number of food patches at all times and sample a number of areas continuously no matter how abundant food is in any one patch. This strategy is necessary for surviving in an unpredictable and fluctuating environment. People consider bird feeders to be a very predictable food source, but in terms of evolutionary time, they have only been available for a very short time. For birds, they are probably no different than any other food patch.

Thank you, that's exactly the kind of information I was looking for. I was told by someone that I shouldn't have started feeding them since now they are hooked on using me as a food source and I need to keep it up all winter, but I feel more confident now that just feeding them while there's significant snow cover is better than not feeding them at all.

It does help them if they have proper feed:
quote:

studies have shown that birds making it through the winter in better physical condition see those benefits carry over into the nesting season.
  Bird feeding produces significantly earlier egg laying dates, larger clutches of eggs, higher chick weights and higher overall breeding success across a wide range of bird species2,6.

https://blog.nature.org/science/2015/01/05/winter-bird-feeding-good-or-bad-for-birds/

I clarified my question that my concern is more about feeding them only for the few days while the snow is on the ground, not general long-term feeding.


text:
Can a bumblebee hive be positioned high above the ground?
We'd like to set up a hive for bumblebees and I wonder if it can be positioned high above the ground, for example on a balcony.
As bumblebees usually nest in holes in the ground, I'm somewhat concerned if they'd find the hive comfortable and be able to navigate back to it.

Depends on the species. Some bumblebee species makes nests in bird boxes high above ground.


text:
PCR Mastermix Preparation
I am currently preparing a PCR mastermix for the first time, and have a few questions regarding the distribution. I am trying to amplify a specific gene cluster in a sample of DNA so I can use it in a cloning vector; however, I am not sure how many separate PCR reaction mixtures I should prepare in my mastermix for this purpose? Also, what is the purpose of a negative PCR reaction mixture (withouth the template DNA), as I saw a procedure recomend making one. Should I prepare the same number of negative reactions as positive, or should I prepare only 1?

A PCR Master Mix is just a way to speed up your pipetting. Instead of preparing 10 different reactions of 20ul each (for example) you prepare one reaction of 200ul and then you split it into 10 tubes. This also reduces distraction errors (it is less likely to forget to pipet once 100ul that 20 times 5ul). Also, less plastic (pipet tips) is used.
Some tips:
Given the error of some pipettes, it's generally good to count for an extra reaction every 10. For example, if you need to run 10 PCR, make a Master Mix for 11.
If you are planning to run the same PCR on different templates (which is often the case) then you don't need to add the template in your Mix.
Negative and positive controls should always be included.
The negative control of a PCR reaction is often done by substituting the template DNA with water. The negative control should not show any amplification band. This guarantees that you don't have DNA contaminants in your mix and that you primers do not amplify each other.
A positive control is a reaction that is expected to work. In this case, if your positive control shows amplification but your sample don't, you know it is not because of some component in the reaction behaving unexpectedly (Polymerase, buffer, etc..).
Let's make a practical example.
Let's say I want to amplify the same target sequence from 10 different DNA samples.
The 1X reaction looks like something like:
**PCR 1X**

Template     1ul
Primer F     1ul
Primer R     1ul
H2O         10ul
MgCl2        2ul
dNTPs        2ul
Buffer 10X   2ul
Polymerase   1ul

Now, considering the positive and negative controls, and 10% extra volume, I would prepare a Master Mix for 13 reactions. Of course, the template must be excluded.
**Master Mix 13X:**

Primer F     13ul
Primer R     13ul
H2O         130ul
MgCl2        26ul
dNTPs        26ul
Buffer 10X   26ul
Polymerase   13ul

Now aliquot 19ul in the 12 tubes, add 1ul of the right template to each of them (in the C- just add 1ul H2O) and run it!
There are cases in which you may want amplify different targets sequences from the same DNA. In this scenario, you want to include the template in the Master Mix, since it is the same for all the reactions, but you want to add the primers separately since each reaction will contain a specific set of primer to amplify a specific sequence.

Great answer! One comment: I'd say the biggest reason for using a master-mix is to reduce pipetting error due to multiple operations (pipetting 10ul once has less error than 1uL 10 times) and due to small volumes (relative error is much larger at the low end of a pipette's range).

Agree, although it's your responsibility to check the pipettes are in perfect condition.

There are four things you can change depending on how much DNA you need to insert into the cloning vector:

(i) amount of PCR reaction mixtures ("how many tubes")
(ii) concentration of template DNA ("how much template DNA in a tube")
(iii) how many cycles ("how many times will you amplify your template")
(iv) how efficient amplification is ("how efficient is amplification") i.e. ideally each cycle exactly doubles your DNA, but in practice it's almost double or sometimes substantially lower than double

Remember, 1 tube after 10 cycles ideally contains exactly as much DNA as 2 tubes after 9 cycles. Usually changing the number of cycles is the way to go. You don't need that much DNA for vector insertion, I would go with a single tube to begin with.

How much DNA do I need?

We can't help you with determining how much you need, but see how much you need for inserting into the vector; make an excess using PCR, check to see whether the PCR worked on a gel (size purification) and measure the concentration of your product. Then you take the appropriate amount for making your vector.

Negative PCR control?

Negative control is a control reaction that contains all essential components of the amplification reaction except the template. This enables detection of contamination due to contaminated reagents or foreign DNA. Here you should see exactly no PCR product - if you do, you'll have to troubleshoot your reagents!

How many separate PCR reaction mixtures I should prepare?

If you're just amplifying DNA, one tube should be enough to see clear bands on a gel. In other cases, for instance with quantitative PCR (which you aren't doing), you'd prepare replicates, so you have a negative tube, and let's say 3 experimental tubes (technical replicates) so you can average across them for better accuracy and reliability.
When preparing a master mix, e.g. for 10 reactions, prepare it as if you were making 10% more reactions (11 reactions) so that you can comfortably pipette everything. You need 100mL of a solution for an experiment? Make 110mL. This is general good lab practice - always make a slight excess of master mixes.

The number of reactions you set up depends on a lot of parameters. To answer this question you'd need particulars about the source of template DNA, melting point of primers, the taq you are using and the size of the product you want to amplify. All of these will dictate how you optimize your PCR. Have a look at the below reference
http://cshprotocols.cshlp.org/content/2009/4/pdb.ip66.abstract


text:
What is the overall end result of proteins and enzymes binding together?
My rudimentary understanding is...

a gene gets transcribed to mRNA
that mRNA is sent off to the ribosome
that ribosome pumps out whatever proteins are coded by that gene
each protein floats around in the cell until it encounters an enzyme that it fits into, and along with other molecules that may have floated into the same enzyme a chemical reaction occurs and one or more products are formed.

I'm assuming "products" are either new protein molecules or maybe the amino acids that made up the original input proteins. What I don't understand is what the overall end result of these reactions are. So there's a reaction, but what does that mean? How does that reaction, lets say, result in some physical attribute of the organism?
Any examples would be helpful.

Your question is a bit broad. Even though someone answered your question to your satisfaction, your question itself seems to ask for the entire molecular biology behind life. Can you please rephrase your question to make it precise while keeping the current answer relevant to it?

@Mowgli has been kind enough to answer this question, but it shows a basic lack of knowledge about proteins and enzymes that any answer here would not be able to remedy. You need to read about proteins in a standard text book of biochemistry or molecular biology, written and illustrated in a professional manner. There are some old editions (all you need) of very reputable books online at NCBI Bookshelf, where you can search for these terms. Alberts et al. might be suitable.

At a high level, points 1 to 3 are reasonably correct, but 4 is only a special case.
Say we're at end of point 3. You get a protein. Some proteins are enzymes (the majority of enzymes are proteins), others are not. Example of proteins that are not enzymes would be, for example, hemoglobin, which is "just" a (very high-tech) carrier.
Now, each enzyme catalyzes (at a very high level) one reaction, which may or may not involve other proteins:

Reactions without protein other than the enzyme: for example, the cleavage of sucrose into glucose and galactose (two small sugars) performed by an enzyme called sucrase. Such reactions can assemble, cut and modify small molecules or large organic molecules that are not proteins (for example, starch, which is a large polymer of sugar, or even DNA itself)
Reactions mediated by enzymes, that act on non-enzyme proteins: for example, your digestive enzymes can cut proteins from food into building blocks (amino acids) that your body can use to build its own proteins. Similarly, some proteins can ligate proteins together, or add things on them (the proteins on the surface of cells are commonly modified with small sugar chains that control their activity).
Enzymes that catalyze reactions that involve other enzymes: since enzymes are proteins, they can be the target of other enzymes. A very well described example is the cascade of enzymes called kinases. When a cell is stimulated by a hormone, a kinase gets activated by addition of a small phosphate group. Once it is activated, the kinase phosphorylates (i.e. it adds a phosphate group on) another type of kinase, which phosphorylates yet another type of kinase etc; that's a way to amplify small signals.

So the overall result of an enzymatic reaction, regardless of whether it acts on other proteins or not, is usually either

The conversion of a molecule into some other molecule (1 to 1)
The assembly of several molecules into a larger, new molecule (N to 1)
The separation of a large molecule into smaller fragments (1 to N)
The transfer of a fragment of molecule on another molecule (N to N)

Examples of these four types of processes when enzymes act on other proteins:

1 to 1: a "protein disulfide isomerase" can rearrange the topology of the so-called disulfide bridges, that connect cysteine amino acids together in the target protein. This allows a misfolded, non-functional protein to turn into a functional molecular machine.
2 to 1: a "ubiquitin ligase" can covalently attach small proteins (ubiquitin) to old, broken proteins and target them for recycling, thereby preventing the accumulation of dysfunctional proteins in the cell.
1 to 2: a "protease" can cut another protein into two smaller proteins
2 to 2: a "protein kinase" removes the phosphate from a small molecule called ATP, and sticks it on another protein

Thank you for the thorough answer. Are the physical attributes of an organism the result of enzymes manipulating molecules? So for example, is some enzyme responsible for glueing molecules together to pump out hair? nails? etc.. I'm trying to relate what's happening to some higher level biological process.

@offbynull physical attributes or phenotypes are governed by a lot of molecules and all of them have been formed because of the action some enzyme or the other (for e.g. RNA polymerase is needed for the expression of all the genes). So your statement is correct but is gross oversimplification of the biology.


text:
Open database of whole slide digital pathology images
I am looking for sequential image sections (stacks) of biological structures (such as liver, kidneys etc.) that I can download and use. Most of the pathology images I have found are either one image or 3-4 sections. I am looking for >50 sections to test some code.
Is there a public repository for this kind of data?

you could try the new Google tool https://toolbox.google.com/datasetsearch - it's searching for open scientific data. You might also find something here: https://github.com/sfikas/medical-imaging-datasets

thank you. Unfortunately i could not find any stacks or sections in the sites you recommended. I am looking for series of images (stacks or sections), it seems that those are not widely available.


text:
Genetic Inheritance
With suppression in mind consider the following in a system that requires two genes (and their products) to produce a function or phenotype:
The products of the two genes are both necessary and sufficient to produce the phenotype (fluorescent flowers). Call the genes A and B and the mutant forms a and b. What would be the ratio of phenotypes of the progeny if a heterozygous plant AaBb were allowed to self pollinate? The genes are not linked.
Now you take a plant that is aaBb and you mutate it, then allow it to self pollinate and find that one of the progeny has the fluorescent flowers. When you allow this progeny plant to self pollinate you get a ratio of 3 progeny with fluorescent flowers and 1 without. That is not the expected ratio for a reversion of the "a" gene.
When you cross this plant with the original AaBb plant you get a ratio of 3:1 also.
Propose an explanation.

Explanation? You are trying to cheat on your homework. Do it yourself!


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

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

It does look somewhat like a Tarsier. I looked a second on the wikipedia and the closest thing I could find was the Tarsius fuscus. I don't believe this is what you're looking for, but if it helps you in anyway to get to the goal of identifying it, I thought I would just leave this comment.

@Eff Thanks! The limbs look a lot more similar to tarsius fuscus. Looking at their collection, they only have one species from the tarsius genus, tarsius tarsier, which does not look like it matches the photo above. If that's correct, I wonder why it looks so different? Bad taxidermy?

Yeah it was the limbs that looked alike... But I really can't tell. I'm not the one to ask for these questions. I really don't have much expertise on phylogeny. I just thought that a very slight chance of helping was better than none, so I posted the comment. I upvoted question. Hope you get help!

It looks a lot more like a loris to me. There are 10 loris species. Not sure which one this is.

I just looked at the museum list for loris and tarsier. I think the one closest fitting is probably the Red Slender Loris (Loris tardigradus).

It looks like a taxidermic specimen of a gray slender loris (Loris lydekkerianus), but it does look pale in color. The lack of color distinction in the fur may be because it is a non-living specimen. The links below may be helpful with more detail.
https://en.wikipedia.org/wiki/Gray_slender_loris
https://www.shaldonwildlifetrust.org.uk/page/grey-slender-loris.html
https://www.youtube.com/watch?v=yU3n0BlUP0A

thank you! if it's a loris then according to their collection it's either a red slender loris or a Bengal slow loris. Both specimens are hundreds of years old, might the fur discolour in that time?

@Michael If you look at their collection, there is only one mounted loris skin. All the Nycticebus cougang specimens are wet (in fixative) or bones. So, if it's a loris and it's listed in their collection, it's a red slender loris.


text:
How can twins be born months apart?
How can twins be born months apart? What is the science behind it?

Well once the womb is open... But just google it and you'll see that it's very rare but it happens that there are a few days of interval !

In vitro fertilization creates twin embryos.  One is implanted & carried to term, the other is frozen, and later thawed and implanted.


text:
Obtaining protein atomic co-ordinates from dihedral angles
https://en.wikipedia.org/wiki/Dihedral_angle#/media/File:Protein_backbone_PhiPsiOmega_drawing.svg
I've been reading on Protein Amino Acid Sequences and their 3D structure. It seems that the 3D structure is encoded by the three torsion angles as shown above. My professor said there is a 1-1 encoding between 3d cartesian coordinates and the torsion angles, but I cannot find any way to do this either in pyrosetta or biopython. Is there any formulas/packages that would be of use for this conversion?

Do you want to calculate the dihedrals from the coordinates? That's easy enough - use something like dang http://kinemage.biochem.duke.edu/software/dang.php. For the other way round, see https://www.rosettacommons.org/content/conversion-dihedral-angle-representation-cartesian-representation

Welcome to SE Biology. If your professor said really said that (and I imagine he qualified it in some way), he should be fired; and you should reconsider whether angles alone can determine (not encode) a structure in which there are different amino acid residues with bonds of various length. Do you actually have any imput data for the program you can't find? You should ask yourself what is the experimental data in the real world that would need computer processing. Are there experimental techniques for determining dihedral angles, or are they deduced from the determined 3D co-ordinates?

As I indicated in my comment:

You need the amino acid sequence and values for bond lengths before you could determine the atomic co-ordinates from the dihedral angles.
Originally the dihedral angles are calculated from the experimentally atomic co-ordinates (with the help of the sequence), so that what you propose is in its nature an academic exercise.

There is, however, a situation in which I have — in effect — done that, in exploring the structures that would be produced if the dihedral angles were varied. Rather than a command-line tool, there is a graphical tool that allows you to vary the angles interactively and see the results. This is the excellent Ramachandran Plot Explorer (Rama) by Bosco Ho. And yes, it can also generate the co-ordinates — you can save the results in PDB format to reopen or to visualize with other protein graphic software, such as JSmol.
The only problem is that the last version of this software was released in 2006, and is not 64-bit, so it will not run on the next version of Mac OS X (no idea about Windows). Bosco’s blog is still active, so perhaps he could be persuaded…


text:
Can PCR detect phosphorylated protein?
I'm trying to detect the level transcriptional protein inside cells. However, the cells contained both of this protein that is phosphorylated and not phosphorylated. Can RT-PCR detected the level of both of them? If yes can it detect them separately?

Have you thought at all about what PCR measures? Maybe even from Wikipedia if you've forgotten?

No. PCR (and quantitative PCR, or qPCR) rely on primers. They will amplify DNA flanked by primer regions, and this 'multiplied' DNA will be detected (and quantified).
PCR can be used to detect DNA. Reverse transcription followed by PCR (RT-PCR) can be used to indirectly detect RNA. Neither method is used to detect protein abundance, or post-translational protein modifications such as phosphorylation. This is because the modifications are not inherently encoded* in the nucleic acid sequence. They occur only on the protein level. Also, the abundance of a transcript tells you very little about how much protein will actually be produced from it, and how long this protein will remain in your biological system. A single mRNA can result in two very differently-modified proteins, and PCR would not be able to distinguish between an mRNA producing one kind or another. Also, phosphorylation is often a temporary modification, it's good to remember that.
*unless you have transcript variants (that produce protein isoforms) which omit or gain sequences that are modifiable, in the environment of a specific biological system.

It is up to you whether or not you answer a question, but I do encourage you to read the help section on answering entitled "Answer well-asked questions". @Bryan_Krause wrote a comment encouraging the poster to think about what PCR does. You told him. Which response will most help him develop as a scientist?


text:
What is the importance of alkaline condition in biuret test?
Biuret test aims to quantify the amount of protein in a given unknown sample. Biuret agent contains copper sulphate, sodium potassium tartrate and Sodium hydroxide. Coppper ions form the complex of purple colour. Sodium hydroxide is added to make the solution alkaline. Why is it needed to make the solution alkaline?

In the Biuret reaction, copper forms a complex with the nitrogen of the peptide bond, that looks like this (Structure 61 from the paper below):

A strong base is necessary to provide the conditions for deprotonating these nitrogen atoms and have the conditions to form the complex. If you want to read this in detail, have a look at this publication:

Coordinating properties of the amide bond. Stability and structure of
metal ion complexes of peptides and related ligands


text:
Do all cells of a plant contain chloroplasts?
If the answer is no, then how do plant cells tell whether they need to keep chloroplasts or not? What kind of signals are used, and how are chloroplasts eliminated?

Not all cells of the plant contain chloroplasts, but they all contain some form of plastid. When the plant is its development state, they contain proplastids which may turn into chloroplasts if the cells are exposed to light. Other forms of plastids may play a role in storing lipids, amylum or proteins and they form because there is a lack of light (these are present mostly in roots). Chloroplasts are not eliminated from the cell.
 Here you have a helpful wikipedia image:

This is a very general explanation though and you should look more into hormones and specific triggers for the formation of chloroplasts.
Article talking about chloroplasts biogenesis

It's interesting that proplastids sort of differentiate. Chloroplasts are often compared to and suggested to have evolved from cyanobacteria. Do you know if cyanobacteria also change their morphology in response to light? The article you provided doesn't address it.


text:
Would our body adapt to changes that are not in our DNA?
If a person was to undergo a treatment or surgery at a very young age, that significantly reduced their final height, would the rest of their body adjust to the sudden change? If not; because our arms’ length is very similar to our height, would this give the person arms that weren’t proportional to the rest of their body?

It will be hard to discuss for the specific example you consider, mainly because it is unclear how would you treatment affect the person's height.
That being said, yes, our bodies can change in function of the environment. This is called phenotypic plasticity

Phenotypic plasticity refers to some of the changes in an organism's behavior, morphology and physiology in response to a unique environment.

Here the term environment does not only refer to outside temperature or other obvious environmental factor. For example, one can ask whether the size of a vein can react plastically to the blood flow. Here, blood flow is the environmental factor toward which, the plastic response is mediated.
Note that some plastic responses are adaptive and some are not. Note also that there are a lot of related terms (developmental flexibility, acclimation, polyphenism, developmental selection, ...) in the field of plasticity and different authors sometimes use these terms with slightly different definitions which can make everything a bit confusing.

+1 One note which might not be obvious to the OP. There are limits on the plasticity. A human somehow reduced to the size of a mouse would be very unlikely to survive, for example.


text:
What is the most frequently occurring health problem of rodents caused by the usage of pesticides on the agricultural fields in the United States?
For centuries the mankind has used pesticides to protect its crops but within the last century the pesticides have become more artificial and toxic. It is a well known fact that most of the pesticides can have fatal consequences, when one consumes them to much, as different studies have shown links between the pesticides and different diseases like cancer, ADHD and also different birth defects. People today are more aware about it and try to eat more organic food, but the pesticides are still in constant use and therefore it is still a threat to animals, who are in direct contact with the pesticides.


text:
How many "primary colors" can we smell?
There are many more that three visible wavelength in the visible EM spectrum, and yet we can model any color using only three primary RGB wavelength. Perception of an arbitrary color is equivalent of perception of a linear combination of only three fixed wavelengths that correspond to Red, Green, and Blue.
On the other hand, as far as I know, there seem to be no auditory "primary colors": you cannot fool an ear into believing that it hears an arbitrary frequency by starting with a small finite number of primary frequencies.
The question is about human olfactory sense: is it possible to fool the nose into believing it smells an arbitrary odor by offering a combination from a small collection of "primary smells"?


text:
Question regarding when it's a homoplasy in a phylogenetic tree
If you have 2 organisms that both come directly from the same common ancestor on a phylogenetic tree, and that common ancestor does not have trait "x", is it possible for both of its direct descendants to develop that trait "x" independently, and would that be an example of a homoplasy?

Can you draw what you are describing?

Phylogenetic tree vs first generation offspring
Please note that on a phylogenetic tree, the time scale is big enough so that the generation time is completely undistinguishable. Hence, questions of first generation offspring won't rise. Also, in practice when reconstructing a phylogenetic tree, our level of accuracy does not allow us to distinguish exactly at what generation did specific mutation occur.
Rephrasing your question
The term homoplasy is typically used in the context of phylogenetics. Also, most of the time the term homoplasy refer to phenotypic trait and not to genetic sequence but I will not go into these specific complications here. The term is also mainly used in intro textbook and not so much in the peer-reviewed literature. In all cases, one can define the concept of homoplasy as a shared trait that is caused by a mutation that is not identical by descent. In other words, if in two lineages/individuals that share the same trait, the trait is caused by the same mutation(s) (same, not only by its state but by descent), then the shared trait does not represent a homoplasy.
With this, I can rephrase your question as

If two siblings share a (heritable) trait that the direct parent does not have, are the traits identical by descent?

If two siblings share a (heritable) trait that the direct parent does not have, are the traits identical by descent?
Well.. it depends as to whether the mutations happened happened twice independently in the two different gametes or if the mutation happened once in the (germ line) lineage that gave rise to these gametes in the parent body.
The second is much more likely. Because, it is very unlikely for the same mutation to happen twice independently in two different gametes for the same individual and much more likely that the mutation happened once in a cell that gave rise to the two gametes, it is very much more likely that the shared trait among the two offsprings is caused by a mutation that is identical by descent. Hence, not a homoplasy.

editted I think I did a poor job of explaining my question and for that I apologize, let me rephrase it. I am trying to take a tree that is in a state of synapomorphy and turn it into a tree that is not. So can I create the condition of a homoplasy simply by moving the introduction of a trait to the branches that come off after the common ancestor instead of before the common ancestor?

did you see my most recent comment?

I did but did not quite understand it so I ignored it. If you could maybe make a drawing in the post, that might help.


text:
Animal with "advantageous" trait in a environment where the trait is never utilized (high cold tolerance in mild climate) - natural selection occur?
If you were to put an animal with a certain type of seemingly advantageous "trait" into an environment where the trait was not necessarily needed, ex: Putting an animal with a high tolerance for cold into a mild climate, what kind of natural selection occur? Balancing?

It becomes redundant and has no positive selection pressure, so it becomes vestigial, become intermediary performance, changes in quantity to something useful but less adapted to the extreme, and may even disappear, although highly useful genes tend to stay hidden in the chromosomes for many millions of years rather than just disappear.

Recipe for selection
There is selection on a specific phenotypic trait if and only if

There is variance for this trait in the population
This variance is, in part at least, explained by genetic variance
The trait covaries with fitness

The first two points can be reduced to a single point by stating "The trait has some non-zero heritability in the population". For more information about heritability, please have a look at Why is a heritability coefficient not an index of how “genetic” something is?.
This recipe is often called Lewontin recipe.
Applying the recipe to your case
So, in the model you consider, some individuals are cold tolerant and some aren't, so the first point is checked!
We will assume that the difference in cold tolerance is caused by genetic differences. Second point is checked.
Does the trait covary with fitness? As you defined that, in the environment considered, being cold tolerant does not have any impact on fitness, then no, there is no covariance between the trait and fitness. The third point is not checked and therefore, there is no selection happening.
Are you sure there is no cost to being cold tolerant?
Note, btw, that it is not rare to observe (or at least to assume) that some adaptation such as cold tolerance would come at a comparable cost when the environment is warm enough.
For example, increased cold tolerance might be mediated via anti-freeze proteins. The production of such proteins might be costly for the individual. In such case, we would have a covariance between fitness and the trait (cold tolerant individuals would have lower fitness that individuals that are not cold tolerant) and hence selection should act as to reduce the frequency of individuals that are cold tolerant in the population (always assuming an environment that is warm).
What else could cause the frequency of cold tolerance to evolve?
In absence of selection, the frequency of cold tolerance individuals might still evolve in the population. Things like genetic drift, selection at linked site or selection at correlated trait or migration can typically affect this frequency.

What if I were to phrase the question, "after putting them into the mild climate, would you expect positive, purifying, or balancing selection to occur?" Thus making you choose one? Or is there no grounds for any of the three?

Real world example - Primates' ability to synthesize vitamin C (clearly a good thing for most species) held no benefit to species that ate a very fruit-rich diet, and the vitamin C synthesis pathway gradually accumulated mutations and become non-functional.

@iayork - and would that be a kind of "selection" on the gene?

@biostudent4451 it would be the absence of selection, allowing random drift leading to mutational inactivation (possibly also some negative selection reducing metabolic costs but I don't know if that's been demonstrated)

@BioStudent4451 would you expect positive, purifying, or balancing selection to occur? I would expect, no selection. Hence none of the three you mention (assuming mild climate and not fitness trade-off of any kind).


text:
human sight at 1000x while looking into the mirror
I noticed that my eyeballs have the ability to see in what appears to be 1000x.
Setting the conditions: Look into a mirror while in a well lit room. (for me the lighting in my living room as opposed to the bathroom was not as direct and offered a better focus)  Position your face with your nose touching the mirror. Look at the twinkle of light that reflects off your eyeball. Stay focused on that twinkle with both eyes. Now, pull your face away from the mirror in order to focus your vision.  Position that twinkle of light directly to the center of your eyeball.
At this point that twinkle of light starts to look like a patch of cells under a microscope.  My left and right eye are different images.  My question: Am I looking at the cellular array that makes up my retina?   Eric McBrearty

What color and shape is the image? Red equal spaced cells? A different visual effect at 1000x is If you look up into the blue sky long enough, and with enough attention, you should be able to see tiny blue-white dots flashing around the sky.The phenomenon was so well-known that it acquired the nickname "blue-sky sprites," and they're actually white blood cells moving through your eye.

Not sure why this is gathering close-votes as "personal medical question". This is a common phenomenon that many people have noticed and has a non-personal  answer to it. com.prehensible alludes to a similar phenomenon in his comment above. I vote to keep open, and I hope someone takes the time to write a good answer here :)


text:
Projects in DNA Computing
I am physicist and have recently heard about DNA computing. I want to work in this area.
I want your ideas on a "feasible but new project" (maximum time I can put on the project: 6 Months ), I can work on.
(I have already heard about songs, image storage on DNA and don't want to repeat the same process for some other song or image).

DNA computing is a branch of computing, not biology. I am voting to close as off-topic.

Note that asking for research ideas is likely to be close as off-topic even when asked on the right SE site. If someone has a good novel idea for a research project she/he would probably not give it away to a random stranger.

Hi @ParasKoundal and Welcome to Stack Exchange. SE is a bit different than some other sites, questions need to be fairly specific and have factual answers. "What do you think..." questions will usually be closed quickly. Specific questions about the chemistry of DNA computing might theoretically be on-topic in Chemistry SE but I don't see any there yet. There are several SE sites related to computing and math and physics as well. In fact there are almost 200 Stack Exchange sites to choose from. Have fun!

You mostly need to learn which machines and what budget permits a certain type of program in DNA form. you can try biostars forum. https://singularityhub.com/2018/07/24/dna-computing-gets-a-boost-with-this-machine-learning-hack/#sm.001305vt3155je0yvct1toklipjuy


text:
Spine found on the beach
Can someone please tell me which animal does this spine belong to? I found it today on the beach..

Where in the world is this beach located.


text:
The organisms of the same species with a different number of chromosomes
I am looking for some specific creatures. The organisms of the same species that have different chromosome numbers. Just like male grasshopper (23 chromosomes) and female grasshopper (24 chromosomes).
(Please disregard any disorders such as Trisomy 21 in humans or other disorders in other organisms.)

Well this applies to many, many species of insects.  While a few different sex determination systems are at use in insects, including xy (fruitflies), xo (grasshoppers), and zygotism (ants), all of them other than xy involve differing chromosome numbers between males and females.  xo is the system you discuss in your question, where females have an extra x chromosome and males don't, with no equivalent to the y chromosome present.  In this case, females always have one more chromosome than males.  In zygotism, the sex determination system seen in ants, bees, and most wasps, males are haploid (possessing only one copy of each chromosome) and females are diploid (possessing 2).  This means that females have twice as many chromosomes as males.  Interestingly, it is this odd form of sex determination that appears to have driven the evolution of these species into eusocial insects.  If two sister bees share the same mother and father, they each got half of their mother's DNA and all of their fathers DNA, since he is haploid.  That means that they share 50% of DNA in common with their mother and any children they might produce but 75% in common with eachother.  Due to this genetic eccentricity, a bee gets more of her DNA out there by protecting and helping her mother push out more sisters than she would by having children of her own.
Outside of the insect world, we have other mechanisms for inducing chromosomal differences that are not related to sex determination.  You mentioned trisomy but this is really just the tip of the iceberg.  Polyploidy, mutations resulting in more than 2 copies of one or more chromosomes, and anuploidy, the deletion of one or more chromosomes, are very rare in humans, with trisomy 21 being the only really publicly well known example, but common in some other species.  Ferns and other simple plants regularly duplicate all of their chromosomes, resulting in triploid and quadroploid offspring that are still viable and able to produce children of their own.  Mice are also very susceptible to this type of mutation, to the point that there are currently 97 separate populations of the common house mouse characterized by various chromosomal eccentricities.  Here is a rather interesting study on this tendency in the common house mouse.
Chromosomal variation in the house mouse

haplodiploidy is the term for organisms in which one sex has half the chromosomes as the other sex.

Well. Can we come to this conclusion? "In normal circumstances (by ignoring chromosomal abnormalities), organisms of the same species with the same sex must have the same number of chromosomes."


text:
Why the position of facial organs is the same for almost all animals on Earth?
I was questioning myself on why the position of facial organs (eyes, nose, mouth) is the same for almost all animals on Earth ? Is it because of a common ancestor in evolutionary history ? We don't see animals with a mouth on the forehead and eyes on the chin. This face pattern looks universal, is there some biological cause behind, natural selection?

There is more diversity than you seem to acknowledge. Consider octopuses, spiders, sea stars, slug, etc... Also, how you define these organs is up to subjectivity. For example, insects have amazing chemical sensory organs on the legs but you probably will not want to call these organs noses, just because it is not in the middle of the face.

That being said, the question of how much of it is due to common ancestry and how much of it is due to some selective pressures is still of interest. It appears for example that a head like structure appeared several times in independent lineages if I am not mistaken.

If those organs were elsewhere, wouldn't you just call that area the "face"?

Maybe I misused some of my words and I know my statement don't apply to all animals, but for example if you take a human, a bear, a squirrel, a tiger, a goat, etc.. the head structure looks similar (eyes on top, nose below and then the mouth). I know that I simplify a lot but it's to be able to easily explain my question.

@Remi.b ...and you're not mistaken. The Berkeley site on evolution cites cephalization (nerve cells becoming more and more clustered during each generation of a group) as one recurring evolutionary trend. I heard in a lecture that bilateral symmetry facilitates this, resulting in polarization. It is also facilitates survival that latter sensory organs (such as "eyes" or "noses") begin developing around that proto-brain, as to make signalling faster. That's why many animal lineages have "faces", but not due to common ancestry.

@PeculiarVale, then you're referring to mammals in general, and I can identify two reasons. The first is common ancestry, and the second is constraints. Mutations rearranging facial features seldom confer any real advantage to survival. We can see some "extreme" transitions in the fossil record, such as the evolution of cetaceans, where the nostrils gradually moved from the beginning of the snout to the top of the head.

@Jagoe Thank you for your answer, actually cetaceans seems to be a very good example.
And so, is there a constraint reason that could explain why mammals usually have eyes above the mouth ?

Most mammals live on land where obstacles to vision come from below (eyes up top see over barriers) and food tends to be low rather than high. Selection pressure would have to outweigh those simple facts.   Mammal eyes are in very different spots though. For a cat or human the eyes are in the front to assist depth perception. For a cow they are on the sides so they can see predators from any direction.


text:
Has an ape ever drawn/painted something?
I know there are plenty of examples of apes making paintings and drawings, but has there ever been a recorded case of one representing something in their art?

Welcome to Biology S.E. if you have any questions, please visit the help center! Just out of curiosity, have you done any research on this topic? And if you have, could you share some of the results of that research in your question?

You meant a non-human ape of course.

Yes. The objective clarity of what constitutes representation is not certain, but here: https://www.youtube.com/watch?v=nSHQyLsPm4Q you can see something relatively convincing. The elephant really slays this, but your question is about apes; I don't know how species-specific you intend to be. I find that non-biologist laypersons assume that finding humanoid traits necessitates searching in human-like animals. Often not so! In fact, I wouldn't be surprised if someone came up with an octopus capable of a transformative masterpiece.

The elephants in those attractions paing the same thing every time: https://en.wikipedia.org/wiki/Animal-made_art#Painting_elephants So it's not clear that the animal is representing something (from its own mind), as opposed to the trainer doing that through the animal.

Part of the problem is ascertaining whether something is representative, outside humans primate lack the fine motor control needed to make realistic art. And normally you cannot ask them what something is. individual chimps and gorilla have painted or drawn and clearly take pleasure in the activity without any reward.
However there is one way in which the ape could tell us what their art is, some chimps and gorilla know sign language.. Both Koko and Micheal the gorilla sometimes named their paintings, this is by no means conclusive but the combination of colors and titles is suggestive of a the art being representational. however no exhaustive study of their art has been done to determine if this is cherry picking the data.
Likewise chimps who both know sign language and paint like Washoe, will title their art and when later asked identify them as the same title. More notably some claim their art patterns to their art, when asked to paint a dog for instance Washoe produces similar shapes each time. However again these are interpretations by keepers not independent studies, which it should be noted would be very difficult given the language skill of the animals. But like all behavior science, conclusiveness is nigh impossible to achieve but they are certainly suggestive even if they must be taken with a huge grain of salt.
It is also worth noting apes there is a notable difference between self motivated and reward motivated "artists" those prompted to paint for a reward show significantly less care, planning, or evaluation but just make something quickly then demand a reward.
Sauce
Source 1
Source 2
One of the first studies on the subject, which I desperately wish was available online.


text:
Are there any natural cases of direct translation of DNA to protein?
I'm aware direct translation of DNA to protein (without the need for RNA) has been observed in test-tubes using e-coli. (Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC219759/)
I wanted to know whether there have been any natural cases for this that have been observed. And suppose there aren't, would it be theoretically possible in a cellular environment?

Please provide a reference for your assertion. But in any case the answer is NO. Why do you think the complex system that exists developed?

I have edited the post to provide a reference.

OK. You should consider whether the technology used in that work over 50 years ago was able to demonstrate and compare it with your assertion.

I'm aware that RNA is of course an essential role in molecular biology for almost all complex systems as far as I know. Its importance to biology is unquestionable. However, the reason I asked this question in the first place was from reading Crick's Central Dogma of Biology article (https://cs.brynmawr.edu/Courses/cs380/fall2012/CrickCentralDogma1970.pdf). In it, while he ruled any transfers from Protein to nucleic acids impossible, he argues that while there is no evidence for direct DNA to protein translation nor is it impossible either.

But that was 60 years ago. It’s of historical interest — no more. Do you realize how little was known at the time?

I seem to remember that paper coming up here in a previous question. Is there some person or source still churning it up? You might try to check. Otherwise I may respond with a history lesson sometime in the next few days.

https://www.sciencedirect.com/science/article/pii/S0006291X09009127?via%3Dihub  It cannot just be historical interest alone; this 2009 paper shows researchers attempted (though also failed) direct DNA to protein translation. Still, the abstract does mention "the question still remains whether or not DNA could be directly translated into protein".  So it cannot be of historical interest alone if a study in 2009 attempted this.  Surely it's still an open question? Although I suppose the evidence renders it very unlikely.

@neuro Why does it matter to you? What thing are you trying to get at by studying this? Even that 2009 paper is essentially throwing it away. It's an open question only because you cannot prove a negative scientifically. It's a possible, but low-probability poorly-supported alternative to an RNA-world hypothesis.

@BryanKrause  I was just curious. Central dogma of biology interests me. But yes, the overall consensus seems to be that in vivo dna to protein direct translation is highly unlikely, if not impossible.

Ah thanks for this @David . This post unintentionally seems to be a duplicate of that previous post. But your answer  on that post was what I was looking for anyhow. Thanks again.

No problem. Your post was expressed in different terms and had a different focus, but most of the problems around it are discussed there and in another post mentioned in a comment. Regarding The Central Dogma, I have an answer to a question on that, referencing the original 1956 formulation. 1956 — Transfer RNA wasn't discovered until 1965! What Crick was doing was emphasizing that you couldn't get back to NA from protein, but not ruling out other possibilities which might be possible in principle.


text:
Influenza infections and drug design
Why is the neuraminidase used as a target for drugs against influenza virus instead of haemagglutinin? Is there some basic reason that this will make a more effective drug?

Can you add any research you've already done on this?

It's not that people didn't want to use hemagglutinin as a target for antivirals, it's that they haven't been able to get the antivirals through the approval process yet. There are a number of experimental inhibitors (see for example Progress of small molecular inhibitors in the development of anti-influenza virus agents) but the approval and licensing process is slow and difficult.


text:
How do scientists determine the nature of ions passing through a channel/carrier/pump?
The NCE (Sodium Calcium Exchanger) transports 3 Na+ inside the cell for 1 Ca2+ outside.
How did we figure this out, and other mechanisms of this sort?
If it were a protein, we could tag it with GFP. But they're ions.
Looking at potentials isnt very informative either I guess; both K+ and Na+ have the same charge.
What is done, experimentally?


text:
Must I HPLC-purify my PCR Primers for amplicon sequencing with PacBio SMRT?
I would like to order some primers for amplicon sequencing. I am using universal tag primers (unusually long 30-mers recommended by PacBio for SMRT, both F&R) + barcodes (16-mers).   The resulting order of 192x46bp oligos is prohibitively expensive, because of the recommended HPLC purification. The increased expense is related to purification and to the increase in minimum scale (amount) required for ordering.   My question is this: what are the worst-case scenarios (and likelihood thereof) if I do not HPLC-purify primers for PacBio SMRT sequencing?  I am generally looking to make the process of sequencing heterozygous RT-PCR products less expensive, so additional advice in that vein would be terrific, especially from experienced users.  Additional, minor and clarifying side-questions. The PacBio recommended primer, the Universal Tag 30-mer primer seems a bit long to me, and possibly unnecessarily so. Does anyone know why they would insist on a 30-mer? It's a bit irritating that there is no specific reason given, and combined with the unnecessarily long symmetric 16-mer barcodes, and 5’-block (5’ NH4-C6), they are pushing up the cost for little transparently good reason. Perhaps I am wrong. Any offered reasoning on these points would be appreciated.

I am at the same stage as you right now. I am assuming that you are planning a 2-step amplification: first one with the universal primer and second one with the barcoded primers. So, this has been my rationale and experience on this.
HPLC purification
If you are generating your own primers and not buying the plate from PacBio it is better to get HPLC purified oligos. The idea behind using HPLC purified primers is that the oligo synthesis may produce truncated products (primers with deletions usually towards the 5' region) in little concentrations. According to IDT, each base addition has an approximate error rate of 1%.  Therefore, longer products have a higher probability of deletions; the number of expected errors would be 0.01 × length of the primer. For a 46nt primer (16nt barcode + 30nt universal sequence), the percentage of deletion-free products would be ~63% (Poisson probability of no deletions). So, you can expect 27% truncated products with approximately 1.2 deletions per product†. Therefore there is some likelihood that the truncated products may mess up your barcode. However, the probability of the deletions specifically in the barcode regions would be less than this estimate.
5' NH4-C6 modification
This modification makes prevents the ligation of the PCR products. You generate the final library by re-amplifying the PCR products of universal primer, with the barcoded primers. The product will also contain a little amount of the template, which you do not want to be ligated to the sequencing adapters. Again, this would be very less: for example if you take 2ng of the template and your yield is ~1.5µg (I typically get this much yield even with a colony PCR of 25 cycles) then the template contamination is less than 0.2% (ideally you should calculate this with number of molecules instead of mass but since the template and product would have almost equal molecular weight you can use the latter also).
Why 16-mer barcodes
You can use shorter barcodes too but you should make sure that they are different enough such that any sequencing error would not make it difficult for you to distinguish between your barcodes. PacBio has an error rate of 13% for a single read; it reduces if you do the Circular Consensus Sequences (0.13^n where n is the number of rounds). When you have a large number of samples then it is better to use longer barcodes as you can reliably distinguish between different samples. They also recommend that the barcoded primers have a 5' phosphorylation. This will further increase your cost. The 5' phosphorylation will increase the ligation efficiency. It is technically possible to use polynucleotide kinase to phosphorylate the products but the efficiency of T4-PNK varies with the 5' base (Houten et al, 1998). In this case I would recommend pre-phosphorylated primers.
Why 30-mer universal primer
I don't have a good knowledge about this but I guess the reasons have to probably do with the molecular biology rather than the data analysis part of it. Demultiplexing can be done manually and it is not very difficult. Technically, a 20nt sequence should also suffice (usual length of PCR primers). Under usual circumstances, I don't think you are going to save a lot by using a 10nt smaller primer. The total length of primer (universal sequence + the template specific sequence) may go down from ~50+ to ~40+. Many oligo-synthesis services have an upper bound for HPLC purification; they would PAGE purify the longer ones. For example, the company that I order from has a cutoff of 50. So, longer primers have to be PAGE purified which would reduce your yield and increase the price. But usually you can negotiate with the company to allow your 1-5nt longer-than-cutoff product to be HPLC purified.

Summary
Some of these modifications would just improve the efficiency marginally and may be skipped if your data is not likely to be affected by a slight drop in efficiency.
So this is my final recommendation:

HPLC purification: not necessary but recommended for long primers (at least the barcodes)
NH4-C6 modification: not necessary
5' phosphorylation of barcoded primers: recommended
Length of universal primer sequence: can possibly be shortened by 10nt but probably that is not likely to reduce the cost significantly.

However, you can significantly reduce your cost by asymmetric barcoding. For example, if you have 100 samples then the minimum number of barcode primers needed would be 20 (10 pairs). You can shuffle the forward and reverse primers to create 100 combinations.

† Explanation of the error rate probability
Let $\lambda$ be the error rate per base (0.01) and $N$ be total number of bases (46). The error will follow Poisson distribution and the probability of errors would be:
$$P(X=k)=\frac{(\lambda N)^k e^{-\lambda N}}{k!}$$
For zero error i.e. $k=0$ the probability would be simply $e^{-\lambda N}$ which would be ~0.63
The mean number of deletions for the 27% that contain errors would be (see zero-truncated Poisson distribution):
$$E(X|X>0)=\frac{\lambda N}{1-e^{-\lambda N}} \approx 1.25$$

Thank you! I will accept and close this--great answer. But I should mention that I am still not clear on why 30-mer is necessary. I know it's proprietary, but the question is whether we can use something entirely different. The only reason for adhering to using a 30-mer is if the software that demultiplexes and removes primers must have the specified 30-mer. Else, I don't see why a shorter primer we designed (for 3'-RACE) would not perform better. I simply don't understand and cannot seem to find how this works in any of their many, many manuals. Anyway, it ought to be a separate question!

@Plantaloons I have edited my answer to discuss that point. However, it is still my guess and I can't say anything conclusively.

@Plantaloons I also have updated some of the calculations regarding HPLC purification.

What a terrific answer! Thank you very much.


text:
Is the strength of presynaptic stimulus on the postsynaptic neuron affected more by the dendrites, or the cell body?
Is the strength of presynaptic stimulus on the postsynaptic neuron affected more by the properties of the dendrites & axon terminals, or the cell body & axon?

Two years ago I asked a question here and learned that neurons do have a bias, and that various factors affect that bias, and now I'm trying to learn more specifically, how much of the strength of the the strength of a synapse, i.e. the size of the effect of a presynaptic stimulus on the postsynaptic neuron is dependent on the properties of each individual axon terminal / dendrite terminal, vs how much is dependent on the properties of the axon or cell body.
And do the properties of each individual axon terminal / dendrite ending vary diversely, even among dendrites of the same neuron, or do individual dendrites and axon terminals of the same neurons typically have similar properties?

I think this question is far too broad. You are better off thinking about what actually happens in neurons postsynaptically rather than trying to think in terms of what's "more important"  A or B - that sort of question isn't really answerable.

It depends on the type of axon, of course.
In Axosomatic synapses the properties of dendrite is not important, but for Axodendritic synapses, the properties of post syn. dendrite is more important as the amplification and other processing happen there. However, Soma is much nearer to Axon hillock, so changes by Soma wouldn't be declined as the impulses won't. It may be depended on neuron properties itself and so that's wrong to generalise!


text:
Diffusion to center of the cell
I have been researching about the ratio between cell membrane surface area and volume.
Obviously, when the volume increases faster than the surface area, and up to a certain point, there is comparatively less membrane for substances to diffuse through and comparatively more organelles that need these substances.
http://scienceline.ucsb.edu/getkey.php?key=5203
The resource above says that "These nutrients then need to get to the center of the cell."
My question is: why do the resources get depleted before they reach the center of the cell? Aren't all the important organelles in the center anyway? For example, wouldn't the glucose go to the center of the cell, and not be used up "on the way"?
And just to be clear, the "center of the cell" refers to organelles like the mitochondria, nucleus etc?

The center of the cell in this case is a way to say "the nutrients arrive to every part of the cell", and should not really be taken literally as "the center". If the cell is modeled as a sphere, with the nutrients diffusing in from the outside, the whole sphere would be filled with nutrients when the nutrients "arrive to the center". Figure 1 shows how the nutrients would diffuse from the outside layer further in. It is like saying the whole glass would be filled when the water "arrives to the top". It does not particularly mean that the vital organelles are in the center, but is just used to illustrate the fact that nutrients diffuse into and can reach all parts of the cell.

Figure 1: an illustration to show how nutrients would diffuse from the outside to the center of the cell, filling the cell with nutrients. This image is trying to model a cross-section of a circular cell. The nutrients would for example enter from around the green layer, and gradually get to the middle/center dark blue area.
Resources may get depleted before they reach the "center" of the cell because of the rate of diffusion, and also because metabolic processes may convert the resources into other molecules (e.g. converting glucose into ATP; glycolysis happens in the cytoplasm, and can happen in any part of the cell. If that particular glucose molecule is used up, then it will not be able to travel to the center).
Moreover, the "important organelles" are not in the center in particular. If you have seen an image of a typical plant cell for example, most organelles are around the walls of the cell (Figure 2).

Figure 2: a typical plant cell electron micrograph.
Also, you must remember that the Surface Area to Volume ratio is also a restriction for the effective diffusion of waste substances out of the cell. The small volume / big surface area is not only because nutrients have to diffuse in, but also because waste products (like CO2) must be able to diffuse out of the cell, through the membrane.


text:
Has human skin pigmentation adaptation and evolution ceased?
Before asking this question read

Why human skin colour disprove natural selection?
Does darker skin color make it easier to live under sun?

though neither posed the same question or provide the answer to the present question.
In Modern Human Diversity - Skin Color published by The Smithsonian National Museum of Natural History the document in pertinent part states

As early humans moved into hot, open environments in search of food
  and water, one big challenge was keeping cool. The adaptation that was
  favored involved an increase in the number of sweat glands on the skin
  while at the same time reducing the amount of body hair. With less
  hair, perspiration could evaporate more easily and cool the body more
  efficiently. But this less-hairy skin was a problem because it was
  exposed to a very strong sun, especially in lands near the equator.
  Since strong sun exposure damages the body, the solution was to evolve
  skin that was permanently dark so as to protect against the sun’s more
  damaging rays.
...
The darker skin of peoples who lived closer to the equator was
  important in preventing folate deficiency. Measures of skin
  reflectance, a way to quantify skin color by measuring the amount of
  light it reflects, in people around the world support this idea. While
  UV rays can cause skin cancer, because skin cancer usually affects
  people after they have had children, it likely had little effect on
  the evolution of skin color because evolution favors changes that
  improve reproductive success.
There is also a third factor which affects skin color: coastal peoples
  who eat diets rich in seafood enjoy this alternate source of vitamin
  D. That means that some Arctic peoples, such as native peoples of
  Alaska and Canada, can afford to remain dark-skinned even in low UV
  areas. In the summer they get high levels of UV rays reflected from
  the surface of snow and ice, and their dark skin protects them from
  this reflected light.

Cases: Lighter skinned populations who migrated to tropical regions (for example, Mennonites in Belize, Boers in South Africa, Belgians in Congo (DRC)) and darker skinned populations which migrated to non-tropical regions (for example Africans in Britain, Africans in the northern U.S. States and Alaska, and Africans in Canada), where the diets of the populations take on the diets which in part led to the specific pigmentation, and the sun applies the same amount of light (UV; other spectrums) to the population as the population where darker or lighter skin adapted, or evolved.
Given the parameters provided, a lay person might conclude that they should be able to migrate to a specific tropic or non-tropic region of the world, take on the diet which led to the melanin production and skin pigmentation which the article states influences adaption or evolution, and over N fixed generations, or an unknown period of time, though eventually, their skin pigmentation will adapt or evolve to the population planners' desired pigmentation; that melanin production and skin pigmentation is not fixed, that evolution and adaptation as to skin pigmentation is continuously ongoing in the human population on Earth circa 2019 CE - and the claim is capable of being reproduced, observed and objectively measured using the scientific method.
Have any scientific studies been performed which substantiates or refutes by observable measurement the theory or claim that environment and diet have an effect on melanin production and skin pigmentation within the scope of any timescale ("One generation, two generations, ten generations, 10-20 generations")?

I downvoted because this question, despite its length, seems to strongly misunderstand evolution and because I suspect it is not asked in good faith. See a good reference on basic evolution like https://evolution.berkeley.edu/evolibrary/home.php

@BryanKrause Gather what evolution and adaptation are. Have no "faith" in anything. The question asks for facts: have any studies been performed to substantiate the claim presented as to melanin production and diet having measurable impact and influence over skin pigmentation; which obviously can be proven true and correct or false by examining the cases provided as example at the question.

"In good faith" is a phrase not related to the typical meaning of "faith" as religious belief. Saying I don't think your question is in good faith means I think you're probably asking it because you want to infer something about race, rather than having any actual interest in human evolution.

The claim is that melanin production may have been selected against in higher latitudes and selected for in lower latitudes. The evidence is that populations near the equator tend to have darker skin than those far from the equator, across multiple continents.

@BryanKrause Am fully aware that "race" has absolutely no basis in science and "it is a made-up label", etc. Do not self-identify with any fictitious "race". Am asking about the actual science. Yes, have an interest in evolution, though am not compelled to agree with every assertion made under the banner of evolution or adaptation. "The evidence is that populations near the equator tend to have darker skin than those far from the equator, across multiple continents." Is that true for Mennonites in Belize?  The question is: Is that process ongoing right now?

@BryanKrause Just re-read your comment and noticed the "may have been" ("used to say that something is possible or probable" http://www.learnersdictionary.com/qa/comparing-may-and-might). Does that intend to relegate the theory of human skin pigmentation adaptation and evolution proffered at the linked publication as just that: Merely a theory that has not been proven by way of the scientific method?

@guest271314 Are you asking whether, today, people with lighter skin have a lower fitness in areas where the solar radiation than people with darker skin (and similar questions for other UV and diet environments)?

Most evolution pressure has been divided by 10, maybe 50 recently due to medicine and life conveniences. good sunguards and no need to spend days out finding food makes white people able to live in the tropics, who have a max sun time of 1 hour, and very dark people can live without much sun thanks to vitamine D. Same goes for most other wild traits.

The originally linked page contains a bibliography: http://humanorigins.si.edu/evidence/genetics/human-skin-color-variation/bibliography

@Remi.b The question is clear. Am asking if the claim is measurable right now. If the claim of skin pigmentation being the result of diet, tropical or non-tropical residence is true and correct then the Mennonites in Belize and Dutch in Congo (DRC) and Boers in South Africa must be adapting and evolving darker skin in real-time, right now, and that adaptation must be observable and measurable. Similarly, the dark skinned people who migrated to Nordic countries, or Minnesota, Alaska, Canada, and so forth must be adapting and evolving lighter skin. If false, neither is measurable right now

@tsttst Which link in the bibliography provides a study which presents evidence that skin pigmentation adaptation and evolution is occurring right now?

You keep repeating “in real time, right now” which is at the best vague, and at the worst nonsense. “Real time” is a computing expression generally taken to mean “in a period of time that would not entail an unacceptable wait for the user”. “Right now” suggests today or even within the hour. Until you replace this by something more precise — e. g. 10-20 generations — I shall have to vote to close your question as unclear.

@David The question is clear. The conjecture that you are contriving does not make the question unclear. Yes, real-time in the computational manner that you gathered as a reference. Yes, "right now" does means today and tomorrow. Again if the claim is true that measurement must be possible, today, particularly as to the cases cited at the question. If in fact the claim is true even from one second to the next the claim must be measurable 10-20 generations are not necessary. The actual question asks if any studies have been performed which publish evidence to substantiate or refute the claim.

Pardon me, but “right now” and “in real time” qualify the studies you ask about in the question in your last sentence. This is not clear and would take little effort to clarify, assuming you are clear yourself about the timescale. Are you?

@David A cursory definition of "adaptation" "a change or the process of change by which an organism or species becomes better suited to its environment." Any timescale must be capable of being applied to the subject matter. If in fact the claim is measurable, from one second or one year to the next. Are Mennonites in Belize becoming darker and Africans in Scandinavia becoming lighter second by second, year by year, decade by decade, generation by generation? What terminology do you suggest to overcome what you interpret as being unclear to you about the terms "right now" and "real time"?

I told you. One generation, two generations, ten generations, 10-20 generations. You choose, it's your question. Evolution questions actually bore me, and I just check them for trolls to see if they need a close vote. In your case the question was so long I looked to the end to see if there was an actual question there. There was, but the "right now in real time" stuck out like a sore thumb. Comments on SE Biology are not for discussion but for asking for clarification or suggesting improvements in a question, and that is what I did. Take my advice or leave it, but that's enough.

@David Updated the question. Does that satisfy the criteria for substitution of "right now in real time"? Used your own suggestions. Am asking if any scientific study has vetted the claim by way of empirical evidence. If the theory was true in some arbitrary period of the past the theory must be true from that arbitrary past date through to and including 2019 CE, and must be true for any moment in time that a scientist decides to capture the raw data to vet using the scientific method.


text:
Spider found in bathroom can’t identify

Found this spider in my bathroom on the wall by the door. Near Houston, TX.

Almost certainly a spider belonging to the genus Scytodes. It largely resembles the species S. thoracica with very similar markings to the picture above. It is a common spider in the United States, and is often found in houses.

Hi@ShroomZed and welcome to Bio.SE. Thanks for providing an answer to this question! However, if you check out our guide for writing good answers, you'll see that we really are seeking answers that *provide, cite, or link-to support for their answers. In this way, we cut down on misinformation while simultaneously providing easy access for further learning for the OP.  Please consider adding [reputable] support for your [seemingly valid] answer, and you'll almost certainly receive more positive attention (i.e., up votes). Thanks!


text:
Can nervous disorders be cured? Will enough research be the answer?
I have searched every nook of the internet and I couldn't find a clear and to-the-point answer. Well my story is that I am a young BSc student who wants to do research on neurological conditions because as far as my knowledge goes neurologists cannot do anything about ANYTHING, things like dementia and brain damage lead the person to become completely destroyed and then eventual death is what every doctor has to see. As of current.
So I am asking if we can develop eventually effective treatments for let's say OCD or Alzheimer's? Or that will never happen because of other factors in the ecosystem and it's the rule of the nature that some people are just unfit to survive? If that's possible, and about to happen in my life time -- i.e., I can contribute -- I am in. I am gonna get a doctorate in one of the life sciences and start doing something. Like discovering genes, or understanding the pathophysiology, or discovering drugs, whatever I am competent in and able to. I just cannot see people suffer like that.

Yes, levodopa type treatments for parkinsons.
epilepsy:
In 2017, 116 children were randomly assigned to undergo epilepsy surgery or receive medical treatment. After 12 months, 77% of the children who had undergone surgery were seizure free compared with 7% who received medical treatment.
Check news and histories of advances in neuroscience and neurology.
Every year drugs improve, it's best to stay objective in the face of mind dysfunction, meditate.

But will enough research lead to such advances that neurological conditions will be cured? If not, can the patients be significantly benefited in the near future? Thanks in advance.
Edit : I'll try to stay objective my best.


text:
Flying insects on olive tree
They may be responsible for why the leaves are drying out.
Location is in West Europe.
Their size may be 0.5 cm to 1 cm

Please update with your location, approximate size of the insect, and a better image (i.e., a close-up image) to receive a proper ID. Currently, I don't think anybody can provide an accurate sub-family identification. You can use the edit button below your post to update your question directly. Thanks.

done @theforestecologist

Maybe some sort of olive fruit fly

They look like three different kinds of insect. I have no identification for any of them.

All of the insects in the uppermost photo are parasitoid Hymenoptera; the smallest (and uppermost) may be from superfamily Chalcidoidea; the other two appear to be members of superfamily Proctotrupoidea (and may represent different families from that group: the elbowed antenna of the second reminds me of the family Diapriidae; the straight antenna of the third recalls Proctotrupidae).


text:
Fruit identification - What is this green long fruit?
I found this fruit in the South of France, but I have no Idea what it is. It's a green, hard fruit. I tried to cut it to see the inside (on the following pictures).
It fell from a big tree, but I don't remember much information about it.

Thanks in advance!

Do you have a photo of the plant?

Reminds me of Theobroma cacao, which almost certainly wouldn't grow that large (or at all?) in France (I wouldn't think). I'm not sure if any other Malvaceae plants grow similar fruits. I'll admit that the seemingly-circular stipule scar on the stem is reminiscent of a magnolia, but I don't know of any with a fruit like that. Overall, I ca't say I know European flora all that well...Can you provide more information (location, tree photos) and perhaps more pictures (seeds, tree leaves, etc.)?

Could it be a Ceiba speciosa pod? We have a lot of Silk Floss trees near where I live and they grow these types of pods. When they are fully developed, they burst open and are filled with cotton-like floss and dark seeds. I have never seen an unripe one opened up, but it definitely looks like the ones on the trees. The trees themselves are easily identifiable as well. They are large with greenish trunks that have thorns growing along the surface. Also, if you had previously seen the tree with large pink-purple flowers, that would be a good indication.
https://en.wikipedia.org/wiki/Ceiba_speciosa

Please provide some reasoning with support.

I agree that the OP's specimen looks like a member of the Malvacaea and could very well be Ceiba speciosa. The OP's lack of more useful pictures and your (now improved) post still do not have me convinced, however. I find it strange that the OP mentioned but I don't remember much information about [the tree], when the trunk of C. speciosa would be quite memorable I believe.  I'd recommend finding an image of C. speciosa fruit to include in your answer and adding some indication about how such a tropical fruit could be found in France. Both would strengthen your answer. Thanks!

Thanks, it totally looks like Ceiba Speciosa ! I really don't remember the trunk tought, I think it was partially hidden behind a wall. But I've seen another specie of Ceiba ("Ceiba Insignis") in the same town, so it makes sense.


text:
Why do the RNAseq reads map to only a certain region of a viral genome?
I am looking at RNAseq data and mapping them to 3 RNA segments from Cucumber Mosaic Virus.
I trimmed the adapters from the fastq files and converted them to fasta, which I searched against a virus database using BLASTN.
The results were confusing:
The reads align to one RNA segment (RNA 1 segment) of this virus but not the other segments. I looked in my BLAST result file the qseqid of this RNA segment of this virus and compared with the ids in my fasta file.
I copied this sequence and I did a NCBI BLAST which gave to me the same result. These 3 segments are in the capsid together, so they should be together. I am sure that they are in this NGS file.
What parameters should do I change?

I have edited your question. Can you please confirm if this is what you meant? Add more details; for example, length of the reads, number of reads and percentage of reads mapping to your RNA 1 segment, where are other reads mapping etc.

Also, you do not generally use BLAST for aligning short RNAseq reads. Try other NGS aligners like Bowtie or STAR (since this is a viral genome you may not need splice site aligners like HISAT).


text:
What is the name of the wrinkles occurring in people's lips?
I was wondering if there is a name for the wrinkles occurring in people's lips.
Just curious.

What research of your own have you tried performing to answer this question? We ask that all question askers perform their own research before posting . Thanks.


text:
Can you name this plant that likes shade on Asturias?

This was located in the Turón valley on Mieres, Asturias, Spain. Usually, I find this plant in shadowy, not too illuminated spots, although I'm not sure if that's important or simply coincidence. This picture is from yesterday 16th February 2019. The plant is lower than knee high, so let's say a maximum of 30cm tall maybe.

You have found a helleborus, possibly helleborus viridis.
https://en.m.wikipedia.org/wiki/Helleborus_viridis

Seeing that there's even a common name for it in Asturian (yerbunegru) I think you identified it perfectly :D Thank you


text:
What bird is this (found at Alice Springs Desert Park in Australia)?
I was reviewing photographs of the animals we found on our trip to Australia during the past September and I cannot find what is the bird in the picture. It was found inside Alice Springs Desert Park, so it has to be a native bird, same as all the others.

Could anyone please help me?

I'm tempted to say it could be a golden-headed cisticola (Cisticola exilis), but it's a difficult angle to clearly see the head.

Thank you @cezar it totally looks like this one, the habitat matches and I've searched in several photos on flicker and google and it seems like the bird :)

It is a Cisticola exilis as stated by @cezar
If someone has any objection please reopen this.

Thanks and sorry @theforestecologist I'll take that into account next time!


text:
Do you know which is this small flower in Asturias?

Was located in the Turón valley on Mieres, Asturias, Spain (https://goo.gl/maps/BMwyfWtiSdw). Found it at 900 meters of altitude. The plant is just about 8 cm high maybe. All the ones I've found were alone. Just one flower from a couple of leaves.
Kind of reminds me of a Cyclamen?

It is an Erythronium lily commonly called a "dog's-tooth-violet" or "trout lily". I see that one of the species Erythronium dens-canis is found in Spain, being native to Europe. Most of the Erythronium species are native to North America. The foliage is very attractive and they are commonly grown as ornimentals. The flower in your photo is just opening. I have included a few links that better describe these lilies.
https://en.wikipedia.org/wiki/Erythronium
https://en.wikipedia.org/wiki/Erythronium_dens-canis
http://www.srgc.org.uk/bulblog/log2008/160108/log.html


text:
Nerve/muscle fibre depolarizaitonand repolarization balance
if continously sodium is pumped in during depolarization and pottasium is pumped out during repolarization, eventually there will more sodium and less sodium inside. How the does the fibre/cell return to the balance?