text:
Can different cell lines of same type symbolise samples from different patients in ChIP-seq?
Can I simulate different patients by using different cell lines of the same cell type and from the same tissue? Can I also study apoptosis in an immortalised cell line?
I have a gene X (transcription factor) which from wet lab experiments induces apoptosis in  cell type A (endothelial cells) and proliferation in cell type B (smooth muscle cells).
I want to address this differential behaviour using ChIP-seq of antibodies against gene X.
I do not have enough patient samples and I wish to purchase immortalised cell lines to perform ChIP-seq with 4 biological replicates per condition: untreated control and over expression of X.
I plan each biological replicate to be a different cell line of the same cell type and preferably the same tissue. Is it possible to have such?
I will also be very grateful if anyone provides me a link or good article containing the best practices in planning for a ChIP-seq experiment.
Thanks in advance.

It is difficult to say anything conclusively unless we know what kind of cells you are talking about.

@ WYSIWYG Thank you for your response. I will use microvascular endothelial cells from the skin and or lungs.

Can you please [edit] your question to add this information? And do you plan to use cell lines like lung/skin cancer as a proxy?

@WYSIWYG  Please I am completely new to Chip-seq and I do not properly understand the meaning of "proxy" in this context. But I think I will only be using non-cancerous cell lines from the skin or the lungs.

I used "proxy" in a general sense. Using something in place of the other (a substitute that is expected to represent the original condition). In your case, the cell lines being proxy for the patient samples. There are commercially available human microvascular endothelial cells. Are you planning to use them?

Again, I would point out that it would be difficult to say anything conclusively unless we know what the patients really suffer from and whether the experimental model replicates these disease conditions accurately. A general answer would most probably be "no" as we can expect that most cell lines would not properly represent the actual condition. In some cases, however, the cell lines can be a good model. So, as I said before, it is difficult to comment without knowing more details.

@WYSIWYG  Thanks a lot for your response. Yes I plan to use commercially available human microvascular endothelial cells from the skin or the lung. Could you please recommend for me a link  or links where I could find such cells? I need 5 different human skin microvascular cellines  per treatment condition (untreated and overexpressed). I have been searching the internet but I cannot find the number I want.

Moreover, I think you are asking multiple questions here. First is whether cell lines represent the patient conditions reasonably well. Second is whether different cell lines derived from the same tissue are more or less similar (and if they are available commercially or otherwise). The last part about ChIP-seq guidelines is somewhat off-topic. There are plenty of articles available on this topic.

Regarding purchasing the cells: I have no experience on this topic but google gives me many hits to vendor websites: Lonza, Thermo and some other smaller companies.

@WYSIWYG  Thanks a lot for your elaborations. In addition to having a better understanding, You answered all my questions.


text:
Why do Guinea Pigs chirp / sing?
Ok, so this appears to be quite a mystery. Me and my girlfriend have 2 Guinea Pigs, 1 male and 1 female.
My girlfriend once picked up the female one and took her outside into our garden. The Guinea got scared for some unknown reason and jumped out of my girlfriend's arms and fell down hard.. That night, the female Guinea woke us up with some very strange sounds. She sounded like a chirping bird.
Since then, she sometimes repeats these sounds (most often at night, but not always). Mostly, we are puzzled as to why as there is often no apparent reason for her sounds. Also, when she makes the sounds, she appears to be in a trance-like state, making no movements at all.
Looking for the answer online I found many discussions on the subject like this one or this one. Mostly, the sounds (and the often mentioned trance like behavior) appear to be interpreted as either (1) alarm sounds, (2) loneliness sounds or (3) happiness sounds.
There are also recordings of it one Youtube, like this one.
What I was wondering:
Does anybody know about some actual research that has been committed on this subject? If so, what were the results?
I'm just so very curious to find out!

Today's night my guinea pig did the same chirping sound, as you explained early. I got really scared, i did not know what to do. I almost felt like his going to die. Then when i stept out of my bed, those chirping noises magicaly stoped. So i got to him, turned on the light, and i tried to make him calm. I got to bed, and after 2 minutes or so, i heared the same exact sound, repeating over and over again. It really sounds like a bird or fire alarm. Now i decided to move my guinea pig in my room, so if he does it, i could easely calm him down. Now i'll get some good sleep. By the way, as soon a

I found this question very interesting so I did some research. Here's a brief summary of what I've found:
Researchers have found that there are 11 different call types. Some of these include a "sharp alarm cry", "sociable clucking", chutter, whining, purring etc. Using body position and behaviour, researchers attempted to associate these vocalizations with behaviour. Some vocalizations had no apparent associated action including what researchers designated the "chirrup" ( I think this is similar to what your guinea pig might have emitted.)
For more information you can read the results section of this paper by Berryman. You can find a full description of each of the 11 calls and their assumed cause or purpose. Some involve social interaction, reproduction, and distress. Much of the research regarding Guinea pig vocalization involves communication and response between mothers and pups.
In short, it seems as though this chirping behaviour your Guinea pig is exhibiting is normal, but not of any known cause.

Plus one and labeled as solved for the extensive reply and link to comitted research. Sadly though that they have not yet figured out it's cause, as I am almost sure the sound does indeed have a function.. almost all the sounds they make have a quite clear purpose, as you'll notice if you ever have them as pets. But with this sound, the entire behaviour changes (the trance thing). I even read somewhere that someone who had a chirping pig noticed how all her other pigs would group up and get into the trance state all together to become hyperactive afterwards.. mysterious sounds they remain...

Yes, a lot of vocalization seems to involve communication with offspring. With your Guinea pig, it could be a misdirected maternal instinct. The paper I cited was from 1975, so it is possible that other researchers have suggested a reason or cause for the vocalization though I did quite an extensive search on scholar.google.com and couldn't find anything else!

Hmm, maybe there is also confusion on what sound should/could be labeled as a chirp with Guinea Pigs. In this more recent article (2013) the chirp is described as: Chirp is an isolated brief acoustic impulse with a harmonic structure accompanying the calming of an animal in comfortable conditions. But this does not at all seem similar to the singing bird like sounds that our own Guinea makes at night (and some others as well as I read on Internet forums) that sometimes can go on for up to 20 minutes or more..

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Ventricular Filling : Systole or Diastole?
As the Blood goes down from the Atrium to the Ventricles:

The Tricuspid Valve ( Right Atrioventricular Valve)
Bicuspid Valve (Mitral Valve )

The atrial pressure is INCREASES WHEN ATRIA ( THE ATRIA CONTRACTS AT THIS STAGE/ATRIA SYSTOLE) Thus:

fills the ventricles with blood ( blood goes down from the atria to the ventricles)
The Tricuspid/ Bicuspid valves OPENS since there is a higher pressure of Atria than the Ventricle

Questions:

Is the Ventricular Filling, (When Blood from Atria fills the Ventricles) itself a DIASTOLE or SYSTOLE
So during the Ventricular Diastole
Ventricular Filling is Diastole?? ,
Is it when VENTRICLES are filled with blood :

it increases THE PRESSURE IN IT SO THAT IT MAKES A
  (** VENTRICULAR DIASTOLE /VENTRICULAR CONTRACTION **)

I also saw in here that:
" The P wave represents the atrial electrical depolarization. This phase is ventricular diastole. During filling, pressure within the right atrium increases, pushing blood across the AV valves into the right ventricle."
I'd also like to clarify:

Shouldn't it be  WHEN IT FILLS THE VENTRICLE is filled,
     THE PRESSURE GOES LOW in atria gradually within the???
    I get it that the atrium has a HIGHER PRESSURE BEFORE FILLING and it makes the (TRICUSPID AND BICUSPID) valve OPEN

Kindly clarify through diagrams and steps, I'm somehow confused. Thank you!
You can kindly watch this short clip of video and this may help me clarify things:
http://highered.mheducation.com/sites/0072495855/student_view0/chapter22/animation__the_cardiac_cycle__quiz_1_.html

https://www.sciencedirect.com/topics/neuroscience/cardiac-cycle

Ventricular diastole is a period in cardiac cycle during which the ventricles are filling with blood. During this period, the atria are contracting and the ventricles are relaxed.
The diastole consist of this: atrioventricular valves open, atria contract (atrial systole), blood flows from the atria to the ventricles, the atrioventricular valves close.
When the term systole or diastole is used without saying is it atrial or ventricular, it means it is ventricular. For example, systolic blood pressure is the blood pressure during ventricular systole and diastolic during ventricular diastole.

According to what i've read and during ventricular filling the valves open because of there is  lower pressure in the ventricles, however the atria contracts  only on the later stage of ventricular filling it does not take most part of the ventricular filling

There are detailed graphs available, if you are interested in the exact timing of all events of the cardiac cycle.

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


text:
About cell membrane; action potential and resting potential
Ion X is negatively charged and more concentrated inside than outside the membrane potential of a cell
therefore Ex (equilibrium) is positive. Ion X is unknown.
Why is the equilibrium positive?

Assuming this is a homework assignment, we do expect OP to show prior research effort. At the very least you can provide the meaning of the acronyms used and a plausible way how you think the problem should be tackled. Good luck!

Possible duplicate of If the average resting potential of a neuron is -70 mV, why is there such a high ratio of potassium ions inside relative to out?

(note: the question isn't an exact duplicate, but otherwise it should be closed as a "homework" problem due to low effort; the principles addressed in the other question should help the OP, however)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Need / consumption of magnesium
Does doing sports makes a human require more magnesium and – if any – how strong is this effect?
Do athletes take magnesium supplements (e.g. pills of magnesium carbonate) because they build muscles and therefore need more of it as their muscle masses increase, or is magnesium consumed by muscle activity (e.g. by causing a chemical reaction which the human body can't undo so it has to excrete the reaction product and get new magnesium from food)?

@Xaqron You should post that as an answer.

Strenuous exercise apparently increases urinary and sweat losses that may increase magnesium requirements by 10-20% according to this paper.

Is magnesium stored in muscles / do you need more when gaining muscles?

@UTF-8: You are correct. Please check here for more info.

I don't see how the linked page says anything about where magnesium is stored or whether you need more of it if your muscle mass increases.

@UTF-8: Your assumption is true and the like contains a table for magnesium needs in different ages/gender. According to table 0.5 gr/day is maximum someone may need.

Sweat and kidneys remove magnesium.  Some foods and medicines retain potassium. Exercise will move salts indiscriminately.  Kidneys try to keep a balance.


text:
What fills the space between the alveoli in the lungs?
Do the lungs just consist of a large tree of alveoli, covered by the pleura, like this picture:

Or are they found "inside" the sac that is the lungs? If it's the later, what fills the space in-between the alveoli and forms the walls of the lung?

Alveolar tree is like a bunch of grapes. If you put a bunch of grapes into a plastic bag and put this bag into another bag, you can imagine how the lungs are covered.
Alveoli form the surface of the lungs. There is a membrane called visceral (or pulmonary) pleura that covers the alveoli and this membrane continues into another sheet called parietal (or thoracic) pleura that covers the inner side of the thoracic wall. The space between the membranes is called pleural space.
Here you can see how visceral pleura continues into parietal pleura:

Picture 1. Pleural space (source: sdstate.edu)

Picture 2. from page 1117 of "Cunningham's Text-book of anatomy" (1914) (source: Flickr)

Oh, so aside from the pleura, there is nothing else covering/containing the alveoli? It's just alveoli that are then immediately covered by the visceral pleura?

@Dahen Yes, alveoli are immediately covered by the visceral pleura. The image you pasted may mislead you into thinking that alveoli are very individual and scattered, but they are actually packed together and form a smooth surface similar to the liver (see the real lungs without pleura).

One nitpick. I usually encourage students not to think of a pleural sac as a bag containing a lung, but rather a bag containing the pleural fluid, which is smashed in between the lung on one side and the chest wall on the other. The part of the bag that touches the chest wall is parietal. The part that touches the lung parenchyma is visceral. Using the bag of grapes analogy, you'd put water in the bag, then press the bag up against the grapes without ever putting the grapes inside the bag.

That does make it easier to visualize, thanks!

I agree with Jan's answer generally, but thought I'd clarify a few points.
What fills the space between the alveoli in the lungs?
As Jan says, alveoli are packed together. In most cases, the thing next to any particular alveolus is another alveolus. In this case, the space between them is the alveolar wall, which (generally) consists of a pneumocyte and capillary (endothelial cell) with a shared basement membrane. You can see this in the following slide from Yale.

Alveolar sacs can abut other elements of lung parenchyma, including bronchioles, smooth muscle, nerves, and pleura. In this figure from Ross Histology, Ch. 19, you can see an alveolar sac adjacent to visceral pleura.

The relationship between lung parenchyma and pleural sac
I would encourage you to not think of the visceral and parietal pleura as two different bags, both of which contain the lung parenchyma (bag in a bag analogy). There is only one bag (per lung), and the only thing inside of it is the pleural fluid. The alveoli and associated parenchymal tissues are on the outside of the pleural sac just as much as the chest wall. They are just on opposite sides of the sac. This ubiquitous figure illustrates the relationship. The fist represents a lung, the ballon represents the pleura.

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


text:
In the PR segment of an ECG, how come there's no current flowing?
I don't really know how to phrase the question, but to put it as clearly as I can, I don't get why it is the P wave "flattens down" when the atria have completely depolarized. I get that the charge is uniform across the atria, but the ventricles are still polarized (and therefore of a different charge compared to the now completely depolarized atria), wouldn't this create a difference in charge and therefore a voltage to produce a current? I think this GIF can help explain my question better:

At frame 12:

I don't understand why there's no current flow and no deflection on the ECG leads despite the charge difference. Rather, why does the GIF deal with the current and charge difference in the atria and ventricles separately? I thought this all might be because of the fibrous cardiac skeleton, which acts as an electrical insulator, but that doesn't make complete sense either; sure it prevent current flow within the heart, but it wouldn't influence current flow outside of it, right?

I'd suggest reading the rest of the Wikipedia article on EKG rather than focusing on the particular cartoon you are using right now, because that cartoon does not depict the dipoles that are measured.
The key interpretation that you are missing is that the signals measured are not voltage differences between intracellular compartments of the heart (like between the atria and ventricles, or between the depolarized and polarized part of one compartment), but a moving dipole created during polarization changes.
As the atria depolarize, there is a wave of negative extracellular charge as positive ions enter cells, creating a dipole: there is more negative charge at the most recently depolarized point than ahead of the wave where cells haven't yet depolarized. This is the signal you measure. If you were to pause this process at any moment, those extracellular charges are free to move and the potential dissipates quickly.
There is too much conductivity in the extracellular space for the dipole to be maintained without the rapid polarization changes that occur when ion channels open. You can think of this as a high-pass filter; the amplitude of the dipole measured would approach zero as the speed is reduced regardless of static differences in intracellular voltage measured against some reference.
This is what happens during the brief "pause" between atrial and ventricular contraction: there is still a dipole, but it is much smaller as it travels through the AV node than in the muscle and would only be measurable from local electrodes. You begin to see the signal again once the ventricles contract.
http://umdberg.pbworks.com/f/Hobbie-EKG-1.pdf may also be useful.


text:
Can an organism process H₂O into H₂O₂?
In an answer to a recent question on Worldbuilding, I suggested that an organism convert $\ce{H2O}$ into $\ce{H2O2}$. I suggested a few processes that yielded the desired final result ($\ce{2H2O \rightarrow H2O2 + H2}$ and $\ce{H2O + O3 \rightarrow H2O2 + O2}$). I noted that both were mere guesses. The feasibility of it was debated because hydrogen peroxide is a rocket fuel and contains a lot of energy (I heavily modified the answer and set it on an entirely different track after another mistake was pointed out).
Could some process similar to this ever happen in an organism?

Hydrogen peroxide as a reactive oxygen species (ROS) is a highly problematic molecule for the processes inside of cells (it can spontaneously oxidize and damage cellular components). With Catalase, organisms have a very effective enzyme which degrades the peroxide into water and oxygen.
However, although the molecule is problematic, it is still produced by organisms in traces. For its production by the NADPH oxidase, first NADPH is oxidized and superoxide is formed. The reaction looks like the following:
$NADPH + O_2 \rightarrow NADP^+ + H^+ + O_2^-$
In a second step the superoxide dismutase uses two molecules of superoxide and H+ to generate H2O2, the total reaction (which is divided into several steps) looks like this:
$2O_2^- + 2 H^+ \rightarrow H_2O_2 + O_2$
H2O2 is then usually degraded by the catalase (or used in immunological processes like the respiratory burst).

Actually, there's a lot of animals, plants and microbes can do it. However, it is just an Intermediate process in general. Here's a strong example. In the condition with the absence of catalase, glucose oxidase can catalyze glucose + H2O + O2 become gluconic acid + H2O2. Another process can also generate H2O2 catalyzed by Ero1.

Would it be possible to add a source to your answer? It helps with people finding material to pursue more reading about it.

Shan, C., Yang, H., Song, J., Han, D., & Niu, L. (2009). Direct electrochemistry of glucose oxidase and biosensing for glucose based on graphene. Analytical Chemistry, 81(6), 2378-2382.
Shu, S., Ju, G., & Fan, L. (1988). The glucose oxidase-DAB-nickel method in peroxidase histochemistry of the nervous system. Neuroscience Letters, 85(2), 169
Umana, M., & Waller, J. (1986). Protein-modified electrodes. the glucose oxidase/polypyrrole system. Analytical Chemistry, 58(14), 2979
Wilson, R., & Turner, A. (1992). Glucose oxidase: An ideal enzyme. Biosensors and Bioelectronics, 7(3), 165-185.


text:
What are the side-effects of long-term liquid breathing?
I just saw a recent Physics question that mentioned liquid breathing (which I had never heard of before) and I started to wonder about its long-term effects. Let's imagine a person underwent liquid breathing for some wacky reason - see the Wikipedia page for some starters - for a long time, maybe a month. What would begin to happen to them? Would any effects be reversible?

I'm pretty sure this has never been done long enough to really know the long term effects of liquid breathing. While the perfluorocarbons used for this aren't considered very toxic, exposure to such large amounts for such a long time could cause some toxicity.

Although I don't believe it's being done anymore, there were studies in respiratory care involving partial liquid ventilation. The perflurocarbons, besides offering a good interface for the perfusion of oxygen, provided a surfactant effects, prevening the alveoli from otherwise collapsing. Search the journals 'Chest' and 'Respiratory Care' for partial liquid ventilation.

Can anyone give a reference to liquid breathing done on an awake animal (or human)?  The only cases I have seen have been animals, in which case I think the prolonged anesthesia is going to be more of a problem.

It depends on the mechanical properties of the liquid you use. If you can find a suitable liquid, i.e. one that has fairly low density and viscosity, and is non-toxic even when inhaled in copious ammounts, then you can have a human "breath" in this fashion for a pretty long time, probably. Of course, these requirements aren't at all easy to fulfil and I'm sure are not the only ones. Also, "getting it right" would require a tremendous amount of trial and error, which is costly (and probably unethical, even in animal studies) and offers very little (if any) benefit, because we already have plent

I vaguely recall David Blaine (a celebrity illusionist/escape artist) considering this to complete a long submersion trick, but he dismissed the concept and commented that the process would intensely painful [Citation needed]. Still unsure if this has ever been attempted by a fully awake human without anaesthetic.

Overview.
This is a very interesting question. The ideas behind this have been around for a while and the methods are covered in great detail elsewhere.
The overall answer to the hypothetical question is rather surprising. There may be actually potential benefits to perpetual liquid ventilation for people with certain diseases. Trials so far have not found side effects in fluorocarbon liquid breathing.
So lets talk about the history of liquid breathing and case studies, then we will move onto the hypothetical situation of liquid breathing indefinitely.
A great review (Shaffer et al, 1992) covers the field in great depth.
@MCM pointed out in the comments that my original answer did no emphasise that animal diaphragms are not powerful enough to move the liquid in and out of the lungs. I should mention now that the below cases all use ventilators to pump the fluid into and out of the lungs. The difficulty of breathing this without a ventilator is emphasised by David Blaine at 4:54 in this TED talk who said it was like trying to breathe with an elephant standing on your chest.
Case studies.
As early as the 1920s, poisonous gas research that lead to the infamous mustard gas found that lungs could tolerate large quantities of saline briefly without damage.
Animals.
Kylstra, the first pioneer introducing the idea of land animals breathing liquids (Kylstra et al., 1962), found mice could withstand 4 hours of 160 atmospheres of pressure.
Clark found that mice and rats could breathe oxygen bubbled silicone oils and survive for a few hours after emersion.
In 1965, he discovered that the fluorocarbon known as FC75 not only supported respiration during total immersion but the mice survived indefinitely in apparent good health.
The most recent study I can find is the partial use of fluorocarbon liquid ventilation in adult respiratory distress syndrome (ARDS) of rabbits. The same improvements in breathing were not observed in saline liquid breathing or conventional ventilators.
Humans.
In humans PFCs were first used successfully in 1989 for the ventilation of young infants near death.

Marked improvement in lung compliance, without a compromise of cardiovascular status was noted in all three patients.

All three infants died of their severe preexisting respiratory complications, but the trial showed liquid breathing can support gas exchange in humans. However developing lungs of infants cannot rely on mechanical ventilators for prolonged periods as nearly a quarter of premature infants of those that do later developed chronic breathing problems.
Biomedical application.
There are a fair few researches and doctors who believe fluorocarbon liquid ventilation has some advantages over gas ventilation. It reduces stress at the area of interfacial surface tension in the distressed, surfactant-deficient lung. This would be ideal and appropriate for ARDS in human adults. A more sophisticated use would be using fluorocarbons as a drug delivery system straight to damaged lung tissue.
(All the above can be found in the 1992 review. There is also data on the different properties of suitable FCs)
Real world potential.

Is perpetual liquid breathing possible? ...And healthy?

So this is where we stand with the case studies; mice can breath liquids indefinitely and stay in good health, rabbits with ARDS survive where breathable gas would not help, and there is a contingency in the biomedical community that it can be better than gas ventilation for medical treatment. To me it seems that there is nothing to suggest a fully grown adult would suffer from breathing liquids. The inertness of the fluorocarbons implies any toxicity would only reveal itself in a timescale of years, and everything else about the compounds pose no danger and may make gas transfer across the lungs easier.
This relatively modest success is perhaps no surprise. The exchange interface of our lungs relies on a mucous (liquid) so the gases can permeate the lung tissue. Expanding on that idea should certainly not rule out the possibility of liquid breathing.
The biggest drawback, besides the cost of a long term experiment and being dependent on a mechanical ventilator, is that these are very small case studies of success. Given the massive amounts of unknowns (particularly for long term studies), switching to  purely liquid ventilation in an adult human could have unforeseen risks and would be considered dangerous by any ethics board (or insurance company)!
On a lighter note, here is a YouTube video of what Maddie, a biology podcaster from the BBC, had to say on the matter of living in total submersion. Lots of skin problems, risk of infection after a few days etc.
Again, a very interesting, albeit understudied, topic!

@HDE226868 -- One thing that absolutely must be said that wasn't addressed is this: All of those human studies used external pumps to move the fluid. Mammalian diaphragms are not designed to move a liquid medium more than a handful of times. They will literally tear themselves to shreds very, very quickly.


text:
Why is the human ear most sensitive to 4000 Hz tones?
Human hearing sensitivity is dependent on frequency, which can be visualized by equal-loudness (iso-loudness) contour plots. An example is given below (Taken from here).

This plot shows that a tone with around a 4 kHz frequency (minima above) needs the least amount of actual energy in order to be percieved well as compared with a tone of any other frequency, while on the other hand it shows that tones of frequencies below 100 Hz and above 19 kHz need to have a lot of energy for us to percieve it.
My question is, how does one explain the clearly uniform/persistent fluctuations in these iso-loudness contours? Why are our ears most sensitive to 4 kHz tones, and why is there a "shoulder" in the contours at about 7 kHz? My first guess would be for proper perception of human speech - but the characteristic frequency of human speech is around 80 - 260 Hz!

EDIT:
My question is similar to this previous question, but it is a bit different in detail (they are only concerned with the overall dip, whereas I'm concerned with the dip, the shoulder, etc.). Moreover, that question has no accepted answer.

Uhp,... my question may be a duplicate of http://biology.stackexchange.com/questions/26067/why-do-humans-hear-better-between-2khz-and-5khz.

So many evolutionary "why's" questions around. Really hard to answer..

@LiuTianyi They're easy to answer! It's just that they're hard to answer with objectivity or empiricism... ;)

Close-voters - I don't see reason why this question is pob?

You started with an erroneous teleological argument: that the ear should hear best at the frequencies of the human voice. Teleological arguments are usually wrong. Who knows why  the ear evolved this way? (Also note that it was very likely pre-human.)

@Christiaan - Your own answer (which is good, btw) demonstrates why this question is POB: "But this is entirely and purely speculative and remains an unreferenced statement for which I do not wish to be held repsonsible in any way." One can explain the mechanics, as you did, but the why cannot be explained except possibly by a forensic anthropologist.

@anongoodnurse - that makes sense I guess... Speech understanding does come to mind in this regard I guess, as speech was probably a pretty important factor in who we are know. I might add something along those lines in my answer to clarify. Thanks for your comments.

@Christiaan - Speech recognition comes to mind to me, too, but in a slightly different way: I see hearing loss charts all the time (we do drivers' physicals in the oc med section) and am amused at the fact that men lose hearing in the higher frequency ranges of women's voices. :) Evolution?

@anongoodnurse hahaha whoooo that's a really nice perspective to explain the evolutionary beneficial role of presbyacusis :-D The survival of men kind :-)

The frequency-selectivity of loudness perception was first shown in the 1930s, when Fletcher and Munson published a set of curves showing the ear's sensitivity to loudness compared to frequency. These equal-loudness curves, as shown in the question above, are now known as Fletcher-Munson equal-loudness contours.
One straightforward physical explanation is the fact that sounds with frequencies around 4 kHz are amplified in the middle ear canal through the process of resonance. In effect, they are perceived 10 to 20 dB louder than other audible frequencies. The pinna also affect resonance and hence the outer and middle ear together join forces to create humps and bumps in the equal-loudness curves.
The evolutionary reason why 4 kHz, and not, e.g. 0.5 or 8 kHz, is difficult to pinpoint. First I can clarify some misconceptions in the question, before getting back to the question proper:

Firstly, you mention that the "characteristic frequency" of a human voice is between 80 and 250 Hz. You are referring to the fundamental frequency; the characteristic frequency is a measure used in electrophysiology to determine the frequency-specificity of inner-ear neural structures.
Secondly, the fundamental frequency does not determine the frequency-selectivity of speech understanding. A useful picture is given below in Fig. 1, which shows which frequencies convey which speech components.

Fig 1. Frequency dependence of speech components. source: The Essential Guide to Hearing Loss
It becomes apparent from Fig. 1 that consonants (f, s, h etc.) are higher pitched than vowels (a, o, u etc.). Arguably, consonants convey most of the word information. Indeed, speech understanding is generally less affected by removing the vowels than by removing the consonants. One may deduce from all this that high-frequency hearing (say 2 - 8 kHz) is most important to understanding speech.
And then, to get back to your evolutionary motivation behind the Fletcher-Munson equal-loudness contours, it may, purely hypothetically be so, that our ancestors with a middle-ear resonance around 4 kHz were advantaged over those that had resonances elsewhere in the audible frequency range, if any, because of an enhanced perception of the spoken word. But this is entirely and purely speculative and remains an unreferenced statement for which I do not wish to be held responsible in any way.

+1 - Really nice answer. A question, though (and I truly don't know the answer to this, whereas you might): do you think this frequency range evolved with language, or do you think it was there in primate ancestors?

@anongoodnurse see Figure 5 here of the chimp audiogram compared to the human: http://onlinelibrary.wiley.com/doi/10.1002/ar.a.20117/full Chimps appear to have a pronounced insensitivity where humans have their best hearing. This is also consistent across studies, albeit very low sample sizes: http://laboratoryofcomparativehearing.com/uploads/Chimpanzee__Pan_troglodytes_.pdf


text:
Human Papillomavirus E7 (HR HPV16)
So there's a protein that binds to E7 viral protein, I want to remove a sub domain of the protein to see which exact domain the E7 binds to.
What is the procedure for this?
Edit: I believe the virus is HR HPV16. I need to know a method/procedure that can allow me to delete/mutate the NLS, CXXC ,BAH1 and BAH2 domains in the enzyme DNMT1

Welcome to SE Biology. Unfortunately your question is unclear as it stands. What virus are you talking about? When you say you want to remove the subdomain are you talking about work with the gene or the protein? And what do you mean by "What is the procedure?" How much work have you already done? What research have you done? We need to have that sort of information if we are to try and help you.

Thank you David :D I believe it is the HPV E7. And I am talking about work with the protein. I'm actually a bit confused myself. I will update as soon as I get more information

Oh and David, I sent you an email regarding further information on this. I hope you don't mind.

Please do not send me personal emails. This is a question and and answer site. When someone makes their first post, it is flagged to older members of the list so that they can make suggestions, if necessary, for improving it. That is what I did to prevent your question being rejected and to incease the chances of your getting an answer. I personally shall not be answering as this is not my field of expertise.

Ahh I see. I apologize


text:
I found this strange tooth in Galveston, Texas. What does it belong to?

I found this on May 7, 2017, on Bolivar Peninsula in Galveston, Texas. What's not visible are the treelike rings inside the tooth and what looks like a tiny interior porous center. It looks like it was considerably larger but broken off.
We're all taking bets on what it is!

Hi welcome to Bio.SE! Neat tooth! :). Could you please include an image from the top of the tooth if possible? Thanks!

Will do! It will just be a little later this afternoon.

My dentist said it was human's lower right first molar. I think it's starting to look like cow.

You should probably find a new dentist if they think that came from a human.

I'd agree that it looks bovine but there is a lot of homology in teeth so I wouldn't be confident in that determination, might at least be a ruminant though. See here for some bovine molars.

Sure, wishful thinking, but for its size it could be densiovan which would be awesome ... :D

@BryanKrause I agree that your cow tooth link looks very close.

@Bryan I think it has something to do with Bison. This link will take you to some fossil forums.

@Tytoalba Why do you think it is a fossil rather than a relatively modern tooth?

I didn't mean it is a fossil, I found these forums discussing about bovine (Bison) teeth, which can shade some light on this specimen. @BryanKrause

@Tytoalba Got it. I don't see a single tooth on there that is definitively attributed to a bison that looks like this one, though, is there an example I missed? I think it's more likely to be from common domestic cattle. People raise quite a few cattle in Texas, and there aren't very many bison there these days.

I didn't do a thorough research and I see it lacks the prominent stylid of a Bison. Never mind.

This discussion might help: http://www.nhm.ac.uk/natureplus/message/57652

This is a cow tooth. Your image matches above image.
https://www.flickr.com/photos/61377404@N08/12300347505

I agree with this answer. I grew up on a cattle farm and saw these quite often. But it would be important to know if cattle were ever raised on Bolivar Peninsula. It seems quite small.

It looks like a bison tooth
Just saying btw if u have any other bones post them in thefossilforum.com(gives little bit of help with fosills and bones)
How i identified it just search on tooth of random animal maybe you/ll see the answer somewhere

Most likely a horse tooth. Check out this image from Wikipedia.

It doesn't look anything like any of the teeth in that horse's mouth. Compare to my link for a bovine molar in the link in the comments above.


text:
Is this woodlouse or bed bug?
I have found 3 of these things in the main bedroom within 4 days of each other. A little freaked out, can someone advise if these are woodlouse or bed bugs? and now just added another pic (first pic?) which seems to be an entirely different bug? Carpet beetle? ...that I just found in a cupboard?
I have found 3 of these things in the main bedroom within 4 days of each other. A little freaked out, can someone advise if these are woodlouse or bed bugs?

Welcome Jax. Which photo are you referring to? The reason I ask is that you seem to have 4 photos of 3 different creatures. Could you add that detail, bearing in mind we answer single focused questions one per post, and tell us whereabouts in the world you are.

Apologies, the top pic and creature was one I discovered this morning after I made my original post. I think the first pic is a carpet beetle? the 2nd pic, did wonder if that was a moth as it looks different, this was in a draw. Last two are the main ones that I was finding and my main concern as I found two on Friday and another last night. These are the ones that I am hoping are woodlouse and not bed bugs, but I am not sure?

To add, I'm in London, UK.  and sorry I didn't realise you are meant to have single focus questions. To be honest I thought pics 2-4 might be all the same, but your suggestion 3 different types made me question the one from the draw which I think could be a moth.

The insect on the first image is a ladybeetle, likely the Asian ladybeetle (Harmonia axyridis), a species which is well-known to enter buildings, especially for overwintering.
The subsequent photos likely depict the larvae of a carpet beetle - compare to this answer here.

You say the subsequent pics show larvae beetle, but when I look at that link, it looks like the one from the first pic?  Can someone clarify what the bottom two pics are? i.e one on the wall and one of the grey fabric

@JaxConrad The bottom two are very likely carpet beetle larvae. Google "carpet beetle larvae" (without quotes) and click on the tag underneath, images.


text:
What are the advantages of using interphase cells rather than metaphase cells for gene mapping purposes using FISH?
I have been told that interphase cells are better for gene mapping purposes than metaphase cells but don't know why.

Can you give more information about what kind of mapping is being done? Do you have a reference for the claim?

Clones of human DNA were used for FISH. I don't have a reference for the claim, but please could you suggest some advantages of using interphase cells rather than metaphase cells for gene mapping.

Already good to know the question is about FISH. You should edit this info in your question. Have you read the wikipedia on FISH? There seems to have quite a bit of info already that may well help you.

Thanks for your reply. The wiki page describes the process of FISH but doesn't address advantages of using interphase instead of metaphase cells.

In metaphase, chromosomes are at their highest level of condensation. FISH relies on being able to dissociate the two strands of DNA to anneal a sequence-specific probe. So, my guess is that it is technically easier to achieve a good FISH staining in interphase, when chromosomes are much less densely condensed. There might be other reasons I am not aware of (I am not a geneticist).


text:
Which cancers are routinely treated with anti-angiogenic therapy?
I have been asked to discuss 2 of these cancers and how the therapy is used. I understand angiogenesis and its role in tumour progression, but need some help in explaining how the therapy is used.

Welcome to Biology.SE. You might want to consider giving more work on your future post. For example, spelling correctly the very concept you are interested in would be the least you should do! Make sure to always read at least the wikipedia page when there is one and make sure to let us know what you found, what you understand and what you don't understand.

Assuming you meant "Angiogenesis" instead of "Antiogenesis"...
From wikipedia > angiogenesis inhibitor

Angiogenesis inhibitors were once thought to have potential as a "silver bullet" treatment applicable to many types of cancer, but the limitations of anti-angiogenic therapy have been shown in practice.2 Nonetheless, inhibitors are used to effectively treat cancer, macular degeneration in the eye, and other diseases that involve a proliferation of blood vessels

You should definitely have a look at this webpage form the National Cancer Institute.

Angiogenesis plays a critical role in the growth and spread of cancer. A blood supply is necessary for tumors to grow beyond a few millimeters in size. Tumors can cause this blood supply to form by giving off chemical signals that stimulate angiogenesis. Tumors can also stimulate nearby normal cells to produce angiogenesis signaling molecules. The resulting new blood vessels “feed” growing tumors with oxygen and nutrients, allowing the cancer cells to invade nearby tissue, to move throughout the body, and to form new colonies of cancer cells, called metastases.
The U.S. Food and Drug Administration (FDA) has approved bevacizumab [a angiogenesis inhibitor] to be used alone for glioblastoma that has not improved with other treatments and to be used in combination with other drugs to treat metastatic colorectal cancer, some non-small cell lung cancers, and metastatic renal cell cancer


text:
Why doesn't chloride cause high blood pressure?
Assuming osmotic pressure is the (main?) culprit, why isn't the chlorine ion loose in your body after eating salt considered equally responsible for hypertension?
I have searched Google and Wikipedia, and cannot find an answer.
I have looked here at Stack Exchange, too.
Why is it that you always hear about how bad 'sodium' is for your diet, but every sodium cation comes with a chloride....
Could someone point me to an article, at least?

I made an important change to your title: chlorine -> chloride. The latter is the anion in salt, which is presumably what you're interested in. The former may cause high blood pressure via a horrific death.

what have you done to answer this question? this will inform community on how to help you

What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Not every sodium comes with a chloride ion.  For instance sodium bicarbonate (baking soda), sodium nitrate (in preserved meats), monosodium glutamate (Chinese food), and many more that are used in food (or sometimes medicines).

Boy, so many people are obsessed with how much OPs research..

Osmotic pressure is not the main mechanism of sodium-induced high blood pressure.

high dietary salt raises cerebrospinal fluid [Na(+)]. This leads, via the Na(+)-sensing circumventricular organs of the brain, to increased sympathetic nerve activity (SNA), a major trigger of vasoconstriction

How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension.


text:
Could cyanobacteria thrive with very high CO2 concentrations and almost no oxygen to start with?
Has there been research to see if cyanobacteria could live in high levels of CO2, like in the atmosphere of Venus ?
Because cyanobacteria caused the Great Oxygenation Event one might expect that they could !

Yes, there has been research. This paper asks and answers your question!
Here is the abstract of the paper. I highlighted the sentence that answers your question.

Cyanobacteria and similar organisms produced most of the oxygen found in Earth's atmosphere, which implies that early photosynthetic organisms would have lived in an atmosphere that was rich in CO2 and poor in O2. We investigated the tolerance of several cyanobacteria to very high (>20 kPa) concentrations of atmospheric CO2. Cultures of Synechococcus PCC7942, Synechocystis PCC7942, Plectonema boryanum, and Anabaena sp. were grown in liquid culture sparged with CO2-enriched air. All four strains grew when transferred from ambient CO2 to 20 kPa partial pressure of CO2 (pCO2), but none of them tolerated direct transfer to 40 kPa pCO2. Synechococcus and Anabaena survived 101 kPa (100%) pCO2 when pressure was gradually increased by 15 kPa per day, and Plectonema actively grew under these conditions. All four strains grew in an anoxic atmosphere of 5 kPa pCO2 in N2. Strains that were sensitive to high CO2 were also sensitive to low initial pH (pH 5–6). However, low pH in itself was not sufficient to prevent growth. Although mechanisms of damage and survival are still under investigation, we have shown that modern cyanobacteria can survive under Earth's primordial conditions and that cyanobacteria-like organisms could have flourished under conditions on early Mars, which probably had an atmosphere similar to early Earth's.

Thomas, D. J., Sullivan, S. L., Price, A. L., & Zimmerman, S. M. (2005). Common freshwater cyanobacteria grow in 100% CO2. Astrobiology, 5(1), 66-74.

I like this exobacteria theory question because they implement a strategy for answers that may go against or for the idea of out of space terraforming. Simply providing detail won't be enough in this case. Cyanobacteria are not very durable in Venus atmosphere. The temperature of Venus is of much higher average and they will be feeding of the atmospheric pollution as well causing an oxidative affect on the cell when too much co2 gives off oxides. But more importantly hydrogen buildup in the protein folds could cause inhibitory stress (prevents binary fission). So no I would not use Cyanobacteria as a space project. But please go against me if I'm false.

Thank you for your answer. Temperature would be no problem, at a height of 55 km, it is 27$^0$ C with a pressure of 0.5 atm. How does CO2 give of oxides ? And the hydrogen build up, is that caused by the splitting of water or the exposure to H2SO4 ? Some cyanobacteria can withstand acidity ! https://link.springer.com/article/10.1007%2Fs00442-011-2200-0

To simplify, nitromethane gives off nitrogen oxides and hydrogen carbide when in contact with nitrogen and co2. Acidity is not a problem true. But oxygen may be used up with the introduction of Cyanobacteria. Look up photosystems for more information. I am happy that I could be of help.

Thank you for the information, but there is no nitromethane in the atmosphere of Venus. And didn't you know that cyanobacteria produce  oxygen ? https://en.wikipedia.org/wiki/Cyanobacteria

Allow me to describe what I meant,

C+2H2SO4->CO+2SO2+2H2O, now add nitrogen,H2NO3+CO2->H2CNO2+O2.

I forgot to mention that iron oxide on Venus surface is harmful to Cyanobacteria.

Thank you again, but in my  original question i asked for research done


text:
Could biofilms float and survive in the sulfuric acid clouds of Venus?
The atmosphere of Venus is composed of 96.5% carbon dioxide, 3.5% nitrogen, and traces of other gases, most notably sulfur dioxide.
The main cloud deck is located in the 48-70 km altitude range and is composed mainly (75-96%) of sulfuric acid droplets, with a temperature of 27$⁰$C and a pressure of 0.53 atm at 55 km.
But to put the acidity into perspective, the mass loading of the droplets is 10 mg/m$³$, while the density of CO$_2$ at that altitude is about 950 g/m$³$.
Despite these harsh conditions for life, could biofilms float and survive there when certain bacteria species producing hydrogen could live within them ?
Nostoc commune for instance,is a  colonial species of cyanobacterium which forms a gelatinous mass for protection and can withstand acidic exposure and other extreme conditions like desiccation and high and low temperatures.
In addition the cells contain pigments that absorb ultraviolet radiation, which enables it to survive high levels of it, and in some cells nitrogen-fixing occurs.
There are also bacteria, like Enterobacter aerogenis, which produce hydrogen, and when it could live inside the gelatinous mass it could provide  the necessary buoyancy to float within the clouds of Venus.
Assuming the biofilms could be provided with the necessary trace elements, could they be airtight to some degree, to even float in the air with gas vesicles for buoyancy ?

potentially of interest Is it known how some heat-resistance Bacillus spores repair their DNA after having been heated to 420 °C?

I have pondered life on Venus.  I think the biggest problem would be lack of free water.  The atmosphere is thick and under high pressure, and polar CO2 and H2SO4 like to bind with water.  There is no water there.  Mass action would pull water out of any concentration of water (like a Nostoc blob) and into the waterless density of the adjacent atmosphere.  It would be like putting a Nostoc in a tub of salt grains.
Dessication would be the biggest problem.  The other problem related to lack of water is its requirement for photosynthesis.  If you had a photosynthetic organism there would be CO2 in abundance, but green algae type  photosynthesis also requires water as a raw material:  CO2+H2O+ light -> O2 + CHO (carbohydrate).  If you have only the water you brought with to Venus, with no prospects of replenishing it, you will run out quick.
You would need an organism that is not only durable, but had the metabolic chops to either pry H2O off of H2SO4 or use sulfur as its reducing agent instead of water.  Purple sulfur bacteria can do sulfur chemistry like this but they like starting with reduced sulfur, not H2SO4.  Purple sulfur bacteria need water as a solvent inside the cells just like we do.  But maybe something that can handle H2SO4 can make water out of it also?

Although not much, there's some water in the atmosphere of Venus, 20 ppm, and the acidic droplets contain up to 25% water. Indeed, dessication would still be a big problem, but the main question for me is if a biofilm could really float in the atmosphere with hydrogen producing bacteria within it ?

@Conelisinspace - such a feat would be easier on Venus than Earth.  CO2 is a big molecule and atmospheric pressure aside, CO2 is denser than our N2+O2 atmosphere.  If a critter could produce an H2 bubble inside its shell (made of elemental polymeric sulfur?) it might be buoyant enough to float!  We are converging on WorldBuilding Stack here which suits me fine.

Where, I might add, your speculations would get a lot more enthusiasm than is apparently the case on Biology stack.

Lucky me that you appear enthusiastic enough ! It could be that my speculations could already have been tried out in the laboratory, i like to know if it's really possible.  So there are bacteria that produce hydrogen from glucose, so there have to be also cyanobacteria to nourish them. Now i think about aerogels ( https://en.wikipedia.org/wiki/Aerogel ) to hold the different bacteria species and the necessary trace elements and the produced hydrogen , be made airtight  outside with the extracellular, acid, sulphated polysaccharides.


text:
Infection treatment without anti-biotic
When we have some bacterial infection, say throat infection (pharyngitis) we take antibiotics as treatment. I was wondering how throat infection was treated when there was no antibiotics at all, before 1940's I think.
Throat infection is just example, It can be post surgical operation, urinary track infection etc, basically anything where we use antibiotics currently. So in a way replacement of antibiotic tablet when antibiotic wasn't available.

https://health.howstuffworks.com/wellness/natural-medicine/chinese/how-to-treat-a-sore-throat-and-stress-with-traditional-chinese-medicine.htm

The use of antibiotics to treat pharyngitis is either useless or unnecessary in most cases. (See e.g. Wikipedia article ) Such use of antibiotics has contributed to the rise of multiple drug resistant bacteria. Did you do any research of your own before posting this question?

I'm voting to close this question as off-topic because, although answers might provide information to contemporary biologists about medical practice in advanced industrial societies in the early twentieth century, this is not within the remit of SE Biology.

@David: I researched and only found out that , during some infection people used to have several cuts on the body, which will lead to blood loss and might kill the bacteria. and thought this is not the answer that I expect. I mean slitting body for just throat infection??

Interestingly, treatment of mild pharyngitis before the advent of antibiotics wasn't too different from what it is today - it was (and still is) mostly symptomatic. First of all, viral pharyngitis, which is quite common (Hidreth et al., 2015), is not affected by antibiotics (no viral infection is), and they are not indicated in such situations. Second, mild and self-limiting bacterial infections, including pharyngitis, most often do not warrant prescription of antibiotics, as this leads to the growing problem of antibiotic resistance, which, according to the World Health Organization is "one of the biggest threats to global health." Many guidelines can be quoted, urging clinicians to prescribe antibiotics sparingly, but pharyngitis is so common (literally everyone has had it, multiple times) that one can simply turn to one's own experience - simply put, when you have a mild case of soar throat, your doctor doesn't give you antibiotics (if you even bother going to the doctor about it), most often you are advised to take only symptomatic medications (many of which are OTC). These most often include compounds with analgesic, antiseptic, and/or anti-inflammatory properties. Interestingly, such compounds were widely available long before the advent of antibiotics and even the pharmaceutical industry itself.
Menthol, for example, is a selective agonist of κ-opioid (Galeotti et al., 2002) and a modulator of GABBAa receptors (Watt et al., 2008), thereby eliciting analgesic and anaesthetic effects, respectively. Moreover, by disrupting bacterial cell membranes, menthol (and similar compounds, such as thymol, for example), elicit antibacterial activity, as well (Trombetta et al., 2005). Thus, wild mint, peppermint, and thyme are much more often indicated in cases of soar throat than antibiotics! Their use in the form of infusions and decoctions likely predates most, if not all, modern countries. Moreover, the analgesic and anti-inflammatory properties of willow bark, which are due to the salicylic acid contained therein, were known to Hippocrates (Norn et al., 2009), quite possibly dating back much earlier. Furthermore, it is known that caffeine potentiates the analgesic effects of many nonsteroidal anti-inflammatory drugs, including salicilic acid (Granados-Soto and Castañeda-Hernández, 1999). Unsurprisingly, this combination is often found in many modern drugs (many OTC), being marketed all over the world. Whether this effect was known before the advent of the pharma industry, however, is hard to say. Willow bark has been used as an analgesic and anti-inflammatory medication since ancient times, but coffee was brought to the West in the XVI century.
This is only a handful of traditional medications for pharyngitis, and I'm sure many more can be found, as well as many other treatments for many other conditions. The point is that treatments of mild pharyngitis were available before the advent of antibiotics, as a matter of fact, many of those treatments are still first-line therapy in most cases, even to this day.

"In those times". 1940s US and Western Europe? Have you actually done any research on the history of medicine?

Yes, I have, and the question referred to the entire period of human history before the 1940s, all over the world. What makes you think of the US and Western Europe specifically?

The question obviously relates to North America and Western Europe (and Australia etc) because that is where antibiotics were introduced. If you make statements about the properties of herbal medicines, please back them up with references in reputable peer-reviewed journals. You cite nothing in support of the statements you make.

No, it is not obvious that the question refers to a specific place because it simply doesn't, that's entirely your own (mis)interpretation. Nowhere does it refer to a specific place, it asks what people used before the introduction of antibiotics, i.e. it applies to any place people live. Asking for references is a fair comment, of course, and I will gladly provide references after a proper lit search, I'm just not going to do it around midnight.

I'd save your efforts. If this question is about the history of folk medicine it's off-topic here. In fact, if it's about the history of medicine, rather than science, it's off-topic. Answers about analgesics, anti-inflamitory drugs, innate or herd immunity etc. might be relevant if they related to mechanisms. But I don't see you going in that direction.

I was simply answering the question but you make a good point that I should make my answer more mechanism-oriented. I will try to find the time tomorrow  to improve and substantiate my answer, hopefully turning your downvote into an upvote.

@Stefan: Exactly!. my question is not location specific. Its for entire world.

@Stefan.. Thanks for the info but It was for  antibiotic in general. Updated my question.

http://www.eliava-institute.org/?rid=6
Bacteriophages. Institute in Georgia

Please do not post link only answers.


text:
Family eye genetics
Both my parents have brown eyes.  My older and younger siblings have brown eyes.  I have green eyes.  Is this genetically possible?  Back in 1962, this was questionable and led to family problems, which have long since been resolved.

Of course it is possible. Your parents obviously have two different allels for the eye color (heterozygous), one recessive for green/blue eyes and one dominant, for brown eyes, which is expressed in this case beacuse dominant allel determines eye color if present.  You and your siblings have inherited one allel from each parent. Your siblings have inherited at least one dominant (brown) allel from one of the parents, so they have brown eyes as well. You have inherited recessive allels for green eyes from both of them (homozygous). The chance to inherit two recessive allels in this case were 25%. I hope this helped you a bit :)

@TamaraSpipka do you have any reason to think that eye colour genetics is that simple? In fact it does not seem to be that easy Zhu et al. (2012)

There are at least three major effect QTL according to Mengel-From et al. 2009

I agree with you that it is not that simple, especially because there are more complex eye colors besides clear brown, green or blue. But the color example in the question and the question itself were very simple: 'Is it possible?' and it was quite explicable in the simple way. Don't you agree with this?

I would tend to agree it is possible (although I'd love to have a reference for it) but I disagree with the explanation provided.


text:
Costa Rican Centipede Species
What species of centipede is this?
Found it 3 miles from San Ramón, Costa Rica

I appreciate the coin for the scale but honestly, I have no idea what the diameter of a 500 colones coin is :D


text:
Polyploidy, or why plants of different species can produce fertile offspring hybrids more frequently than animals?
This site says:

Plants hybridize much more frequently and successfully than animals do. [...] Chromosomal doubling (polyploidy) occurs more frequently in plants and facilitates the fertility of the hybrid offspring.

Outcomes of the successful hybridization of different species of plants (i.e. yelding fertile offspring) can be easily observed in agriculture - for instance, Triticum aestivum is 6n, while Triticum durum is 4n. The latter comes from the hybridization of two plants from different genera (!). So it seems to me that not only can plants hybridize more easily, but also that the evolutionary distance between the parents can be greater than in animals.
As far as I know, the preferred animal strategy to have fertile hybrids is to go partheno/androgenic (for example in Phasmida).
My question is:
Why can plants produce fertile hybrids more often than animals? What constraints are present in animals and absent in plants?
To my knowledge, polyploidization is the main mechanism by which this is achieved. If this is true, then my previous question can be rephrased as why does animal polyploidization occur more rarely?
I'm not entirely sure about my assumptions, so feel free to correct me, of course with references.

While I do not know if there is a definitive answer to this question, I suspect that at least part of the answer can be found in the fact that animals typically have much more complex and delicate mechanical interactions in their bodies than plants.
From a mechanical perspective, plants are pretty simple. They move, but generally quite slowly and via very simple mechanical principles, and the interconnection between different tissues and organs is mostly via chemical and fluid flow.  Many plants are also highly flexible in their size and also change their size by orders of magnitude even after sexually mature.
Animals, by contrast, are often ferociously complex and intricate systems of joints and complex and highly differentiated organs. They also tend to have a well-defined typical size of mature individuals, which doesn't vary all that much compared to plants.
When you have a change in ploidy, a major effect is to multiply or divid the levels of gene expression, based on the change in number of copies.  Where that interacts with the processes of morphogenesis, it will thus often have radical effects on the size or growth patterns of the effected tissues or organs.
With a more intricately connected and scale-sensitive system like an animal, it seems then unsurprising that such changes might be much more difficult to survive.


text:
Succulent Plant identification
Can anyone identify this succulent plant?
Location: Tamil Nadu,India

This looks possibly like a species of Sansevieria, also known as Snake Plant. Perhaps Sansevieria parva or Sansevieria dooneri. Parva is usually much darker in colour than dooneri, but it's difficult to tell in the photo. Both are perennials that can be found in India.


text:
What is this whitish jelly-like substance on a branch?

I came across this whitish jelly-like substance hanging on a fallen branch. I assume it was growing there and I feel like it might be a fungus or algae of some sort, or maybe an egg sack. I was hiking in a mountain rainforest in Hawaii. The area I found it was shady with adequate indirect sunlight, about 65-70°F at the time. There weren't any others nearby and it was the only one like it that I happened upon during the hike. What is this and if it is living, how does it grow, how does it live?

It is obvious, by the values, that the temperatures you give are not in Celsius degrees, but it would be nonetheless better to add the units.

Looks like a Tremella fuciformis, which is actually a sort of yeast that produces jelly-like fruiting bodies. AKA the white jelly mushroom.


text:
Furry Bug that swarms only certain plant
What is this strange bug?
It swarms only on one certain plant with trumpet-shaped red flowers (in the picture the flowers are all shriveled and the leaves are in the foreground) and totally coats it until the bush dries up. It spreads very rapidly but only to this particular plant - will not touch any other. The bugs don't noticeably move, giving the impression that the whole bush has developed white fur.
Picture taken in Israel:
EDIT:
Here's a closeup of a single specimen (taken from one of the leaves in the foreground):
And it seems the plant is a hibiscus:
http://homeguides.sfgate.com/hibiscus-leaf-87355.html

almost certainly a scale insect (or, less likely, some kind of aphid). Can't seem to get the picture to zoom on my phone, so I can't really see the white fuzz too well...

They are some kind of mealybug.

@Karl Kjer I think you are correct! https://en.wikipedia.org/wiki/Mealybug#/media/File:Mealybugs_feeding_on_hibiscus_plant.jpg

As indicated in @KarlKjer 's comment, this insect is a Pseudococcidae, or commonly known as Mealybugs. The exact species is difficult to find due to picture quality.

Mealybugs are insects in the family Pseudococcidae, unarmored scale insects found in moist, warm climates. Many species are considered pests as they feed on plant juices of greenhouse plants, house plants and subtropical trees and also act as a vector for several plant diseases.
Mealybugs occur in all parts of the world. Most occur naturally only in warmer parts, and get introduced into greenhouses and other buildings in cooler countries. It is unlikely that any live in the Arctic or Antarctic, except perhaps in buildings.

Considering that Mealybugs are found basically anywhere on Earth, it's not a surprise to have found them in Israel.


text:
How does cell detect if a RNA polymerase II is stalled during transcription and in turn deploy the proper transcription-coupled repair factors?
When a segment of the template strand of DNA is damaged due to factors such as UV radiation, a lesion is created that would effectively block the passage of RNA polymerase II during transcription.
When such stalling occurs, a mammalian cell would usually deploy various transcription-coupled repair factor, such as the XP group of proteins to give provide a proper basis of the lesion and to orient other enzymes in. The endonuclease would cut out the damaged bases, and the DNA polymerase and DNA ligase would, respectively, add the new bases and correctly anchor them onto the template strand.
I fully realize that during the process in which the RNA polymerase II was stalled to the arrival of the transcription-coupled repair factors, some sort of cell signaling must have occurred. However, I could not find any sources that would tell me the specificity of such phenomenon. Therefore, I hope this forum could explain such matter.
Thank you very much!

The beauty of RNA polymerase II is its faculty to act like a sensor towards damage to genetic data. The response of the RNA molecule is variable on the type of DNA lesion which presents itself.
DNA lesions may be a consequence of ultraviolet radiation, or through the metabolic by-products of oxidative free radicals. These specific faults within the lesion, it is hypothesised, are respectively detected by the RNA pol II molecule by interaction with its active site.

Some examples of different genetic damage to bases
In the example you provided, namely, RNA is limited fully or partially from transcription elongation, this is detected as an inhibition of the active site. This could be caused by presence of cyclobutane which distorts the shape of the DNA molecule such that it prevents further RNA synthesis.
Therefore, in the incident that RNA pol II is fully stalled, the first co-factor to commence the signalling process is Transcription factor II H, which repositions the polymerase molecule away from the site of damage. Although it is not fully known, this allows the XPG, having certain endonuclease properties  to excise the faulty bases (thymine dimer, for instance).
In order to fully repair the molecule, DNA polymerase uses translocation to reinsert the correct complementary bases. PCNA, proliferated cell nuclear antigen, may be used as a DNA clamp to increase the processivity, ability for multiples catalyses without leaving the substrate, of DNA polymerase. Then protein complexes XPD operates as a ligase.
Therefore TC-NER, transcription-coupled repair, is believed to begin at a blockage of the active site of RNA pol II!
Best regards
More information regarding this hypothesis and function may be found from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4984683/ and https://www.ncbi.nlm.nih.gov/pubmed/11245433


text:
Is cruelty a human instinct?
I had started studying human behaviour and human instincts a few months ago, earlier the question was raised after seeing human behaviour with animals (his prey). Animals hunt their prey for eating, on the other hand, I have seen kids stone pelting at street cats and dogs. Again human approach towards life is more than survival, it is dominating his peer beings. Can I call this behaviour of mankind as a cruel? If so, is it instinctual?
I am very sorry for the late response. Hope this clears the question.

Can you expand a bit? As it stands, you only have the title question. To be able to talk about these things from a scientific point of view, it is important to define exactly what you mean by "cruelty", so that is can be viewed as a behaviour without all the negative connotations (as much as possible...). After that, it might be possible to draw comparisons to other species closely related to humans, as well as looking at results from neurobiology and psychology.

What made you think people are generally cruel? What cruelty even is from your POV?

I have edited the description, please revisit the question. @fileunderwater

I have edited the description, please revisit the question. @rus9384

It sounds like a philosophical question, but it also has evolutionary roots. All species are instinctually selfish, in that there is a drive to move their genes into the next generation. So misbehaviors (like "cruelty") should be held in check, because they are likely to be punished in a social species. We evolved as a social species that lives in family groups, with a high probability of meeting nearby family groups repeatedly. If you are cruel to your neighbors, you would expect to meet the points of their spears sometime in the future. This expectation of future encounters with neighbors can explain altruism as well. But its a balance. If cruelty to your neighbors is in your long term selfish interests, then you would expect it to be instinctual, just as you might expect kindness to be. Its all about different strategies to send our genes forward. As a side issue, chimps, our close relatives exhibit violence to their neighbors (but bonobos, equally close, are much less violent).


text:
Will a dog develop similar feelings with a robot as like human?
I think we are connected to the world by Biochemistry first and then physical and verbal interactions. If a robot feeds a dog regularly, pampers it and cuddles it regularly, would it develop the same feeling to the dog as it would have developed with a human?
A sci-fi robot like Ultron from Avenger movie.

Somewhat of a bad question due to being vague about the type of robot. Are you referring to modern-tech robots or sci-fi robots with human intelligence more than sufficient to ace the Turing test? Is the robot you have in mind specifically designed to look like a human?

chemistry first and then physical and verbal interactions. This is unclear. You are probably not using the terms "chemistry" and "physics" as used in science. So please define them.

the same relation is unclear. Will the dog have the same feeling of awe when thinking of the algorithm that is governing the robot's behaviour. No, it cannot understand it. Will the dog appreciate the presence of the robot. Yes, eventually. It also appreciate its bed and many other objects though.

I'm voting to close this question as off-topic because it is not about biology but about pet psychology. Also, the question is unclear and any answer would necessarily be drawn from opinion rather than evidence.

Assuming you mean a robot "designed to be human" (that means human-like behavior patterns, human-comparable intelligence, being self-aware and able to learn), then from the dog's perspective, the only significant difference is the differing smell.
There is no scientific evidence for mystical or metaphysical "connections to the world".
From the dog's perspective, the defining factors are:
Owner's behavior (petting, feeding, walking, training, rewards for good behavior or learning tricks). In this case, the robot is no different from the human.
Owner's speech (voiceprint). There's evidence that dogs understand human speech to some extent (https://www.independent.co.uk/news/science/dogs-can-understand-human-speech-scientists-say-a7216481.html). Given how adaptable organic brains are, I assume a dog would be able to adapt to even a synthetic (digitally altered) voiceprint over time or one that spoke in a conspicuously robotic manner (for example: "Temperature alert. Please fetch an external cooling fan./Your assistance above your designated specifications continues to be noted." instead of "It's getting hot in here. Grab a soda from the fridge over there?/Good dog!"
Owner's scent. The only real difference from a dog's perspective. A robot would lack the distinctive scent cues from a human, except if the robot was designed to produce those as well. Even if those aren't present, a dog should be able to adapt to a robotic owner's distinctive smell (plastic with motor oil and a hint of ozone).

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!


text:
HELP! How will pH 14 affect enzyme structure?
If a substance is very alkaline/ basic, e.g. a pH of 14, does this mean that there are near to zero H+ ions (or it is possible to have such a situation where there are zero H+ ions and it is still alkaline) or does it mean there are lots of OH- ions relative to H+ ions? If so, how will this affect enzyme structure in very alkaline/ acidic conditions?

pH can go more than 14, also probably better off on chemistry

I'm voting to close this question as off-topic because it is a chemistry question (see chemistry.SE) and not a biology question.

pH is most definitely a chemistry question. Acids and bases are chemistry, pH is crucial for many many chemical reactions that have absolutely nothing to do with biology. It's not much relevant to today how the idea initially spread.

This is a very chemical explanation. Here goes.
$\ce{pH = -log[H+]}$
$\ce{pOH = -log[OH-]}$
$\ce{pH + pOH = 14}$
Therefore, at a $\ce{pH}$ of $14$, $\ce{pOH}$ is zero, so there is 1 mole of $\ce{OH-}$ and $10^{-14}$ moles of $\ce{H+}$ in a liter of your substance.

Yes, in a simplistic model; although "in a mole of" should be "in a liter of".

Please do not answer (or up vote) chemistry questions on biology.SE. Off-topic is off-topic.

I don't think it's too off-topic as he said something about enzymes at alkaline environments, but it doesn't seem like he researched a lot before hand, as the very definition of pH involves the concentration of H+.


text:
Is a wild-type strain more "fit" than its mutant strains?
Question's context
In the context of a presentation on mathematical models for antibiotic-resistance bacteria research, someone mentioned that wild type strain (WT) are expected to be more fit than mutant strains.
Assume that there is one WT introduced to an environment E (no drugs present), and consider the WT mutates, yielding a certain number of fit-enough mutant strains.
Question
Is WT expected to be the ONLY strain to persist in the long run?
How common is this scenario?
What about co-existence?
Examples and references for beginners will be very appreciated.
My context:
Please note that this may be a very naive question, and I may even be using the wrong terminology, given my background on mathematical modeling and a very, very basic knowledge on evolution.
Thinking about dynamical systems, I would have guessed that coexistence would be possible, so I didn't understand how strong was such an assumption.

I will assume the mutation is not under some kind of balancing selection such as negative frequency dependent selection. As fitness is conditional upon the environment, I will assume a constant environment (heterogeneous environment can also lead to balancing selection).

Is WT expected to be the ONLY strain to persist in the long run?

Yes. In fact, even if the mutation was beneficial, as it starts out at low frequency it still has a low probability to actually fix (fixation = reaching a frequency of one).

How common is this scenario?

Mutations happen constantly. For example, every new human baby carry something like 10-100 new mutations that were not present in any parent. Most mutations are neutral or deleterious, only very few are beneficial. New mutations have a low probability to reach fixation even if the mutation is beneficial. The exact probability depends upon the selection coefficient $s$, the dominance coefficient $h$ and the effective population size $N_e$.

What about co-existence?

In absence of balancing selection (or frequent recurrent mutations) and assuming that ressources are limited, then one strain will necessarily end up fixing. Note that this is also true under genetic drift only and does not even require any selection.

Examples and references for beginners will be very appreciated.

Evo101 is a very short, very easy introduction to evolutionary biology. You should probably have a look at it.
Then, for something a bit more advanced, and because your background in mathematical modelling, I recommend having a look at the book Population Genetics: A Concise Guide by Gillespie
For more book recommendations, please have a look at the posts

Books on population or evolutionary genetics?
Text Book Recommendation: Organic Evolution

Perhaps you can add that fitness is conditional.


text:
Insertion of an additional base at start codon make the protein still functional?
So the question is if:
a deletion of a codon for the amino acid lysine (AAG) is more or less likely to cause nonfunctionality of the protein than:

Insertion of an additional base (C) within the start codon for this protein
Mutation of the stop codon (TAG) to an arginine codon (CGC)

My attempt at an answer:

Not more likely. Since the insertion of the “C” base is done at the very start, the reading frame could be shifted and the sequence would remain the same after the first base. Since the most common start codon is “ATG”, the “C” would not affect it and the “reading” of the sequence would start after the “C” and at “ATG”
More severe as the stop codon is what signals that the translation of the sequence has ended, so if the stop codon got modified then the sequence would continue into the untranslated region. More peptides would be added to the sequence which would only stop when the next stop codon is reached. If the next stop codon is relatively close and the length if similar to a normal protein then it would still be functioning. But most cases it would continue for a considerable length and cause it to be non-functional

I think the question is fairly confusingly worded, so good job on your attempt based on that.

If a C is inserted within the start codon, I presume that is referring to making a sequence that was originally ATGXXX and making it either ACTGXXX or ATCGXXX. Either insertion means the start codon will be missing completely. This is going to either cause no protein to be made whatsoever, or for the beginning of the protein to be severely truncated or completely frameshifted if there is another open reading frame created downstream. This is going to be magnitudes more serious than a deletion of 3 bases corresponding to a lysine.
I think your answer here is fine - lots can happen with a missing stop codon. If there happens to be another stop codon in the same reading frame shortly downstream, then the effect could be not that severe, but if not it could result in a substantial additional peptide chain added to the end of the protein, which could cause all sorts of issues with folding, and the mRNA may not even be functional and be degraded.

Again, this question isn't worded in the best way, but I think the general principle it is trying to convey is that whole missing codons do a lot less damage to the structure of a protein than mutations that affect the reading frame or the stop/start codons, because they affect only a single amino acid. Of course, it could turn out that that amino acid is crucial to the structure of the protein, but the question is about what is most "likely."

I would interpret "within the start codon" as meaning changing ATG to ACTG or ATCG or ATGC.  All of which are going to destroy the start codon, which is likely to ruin the protein.
Whereas adding extra amino acids at the end might not affect the protein function of the rest of the protein.  Protein functions tend to be based on domains, and adding more amino acids to the end might not disturb the structure, and therefore function, of the domains that belong to the protein.

There can be nonstop decay if there is no downstream stop codon.


text:
Why is there a carbon atom without a greek letter in protein residues?
For protein residues I know that $C\alpha$ denotes the first carbon atom attached to a functional group. Each subsequent carbon is given a corresponding greek letter ($\beta, \gamma, \delta$) except for one. For example, each residue in a PDB file has a list of atoms that looks something like this:

ATOM     32  N  AARG
ATOM     33  CA AARG
ATOM     34  C  AARG
ATOM     35  O  AARG
ATOM     36  CB AARG
ATOM     37  CG AARG
ATOM     38  CD AARG

(A,B,G,D are stand-ins for the greek letters). Why is there just a plain C in this list? What is significant about that carbon?

In your context, the "plain-C" labelled carbon is the carbon atom in the carbonyl ($\ce{C=O}$) group.
In organic chemistry, the alpha carbon is the carbon immediately adjacent to a functional group. In general, the greek letters in alphabetical order denote the distance in increasing order from a functional group.  The $\ce{C_\alpha}$ in the case of amino acids is alpha carbon with respect to both the amine and carbonyl.

The edit seems to have spoiled your answer. I imagine you can easily edit it to fit the new question that does not mention the phantom C'.

@David Done....


text:
Are there any proven ways to increase the rate of bone remodeling in humans?
I'm not asking for anything specific -- just wondering if there's any data, studies, or etc. that show a possibility in increased bone resorption and turnover (bone remodeling/Wolff's Law) from certain procedures (whether it be diet, supplementation, drugs, surgery/experimentation, exercise/habits, etc.)
For example, comparisons between studies of people that show bone remodeling faster under different circumstances that can prove a specific method one can use to apply
By "increase" I mean anything that allows the human skeleton to be replaced faster some way

How can I clarify to make it sound as if I'm not asking for something specific then?

There, I clarified -- check the new title.

The main factors affecting bone remodelling are the person's age, and the load applied on the bone. It is known that in relation to fracture healing, younger children remodel much faster and more effectively. This allows surgeons to accept very displaced fractures in young children without having to restore original anatomy as remodelling will take care of that naturally. Here is an example:
http://www.brokenarmanswers.com/arm-still-crooked-cast-comes-off/arm-fracture-remodeling-children/
The reason is that bone absorbs in areas under less loading, and forms along load lines. The shape of bones therefore follows the shape and alignment of surrounding muscles, which apply some form of load even at rest due to muscle tone. The process of bone absorption and formation is much more efficient and faster in younger people and becomes slower with age. This also explains why bones become osteoporotic in people who can't weight-bear for a lengthy period of time, or in astronauts who spend long periods in zero gravity.
A well known method to accelerate fracture healing is to load the fracture as early as possible. This is the main principle of the dynamic compression plates where the holes of the plate are designed as oval rather than circular, so that when an off-centred screw is tightened, it pulls the plate in a direction that results in compressing the fracture to promote bone healing. Here is an illustration to demonstrate this technique:
https://www2.med.wayne.edu/diagRadiology/RSNA2003/Compression_Plates_Overview.htm


text:
How much generation of hamster's family it takes to get first bad mutations
So if I have two humsters and they start to reproduce themselfs then how much generations of hamster's family it takes to get first bad mutations?
The info here does not help to find answer https://www.reddit.com/r/askscience/comments/32x33j/how_do_animals_like_hamsters_and_snakes_avoid_the/
Thank you!

I think you're more likely to see problems related to recessive alleles than mutations. If the hamsters keep inbreeding, the odds of getting a hamster with two copies of bad recessive genes goes up, so you're more likely to see genetic diseases based on that instead of new mutations. But I don't know anything about the frequency of hamster recessive alleles, so I can't estimate the odds of seeing a genetic disorder in each generation.

@user137  Good point about recessive alleles!

Is the question aimed only at mutations (which involve changes in individual genes), or also at genetic changes  including recombination and crossover which only involve changes in gene frequency and location?  Both types of changes occur in every generation. Changes due to recombination and crossover are more likely to be harmful when both parents have a larger number of "bad" recessives.

Everybody carry deleterious mutations anyway
Your two hamsters most definitely already carry a number of deleterious alleles at segregating sites (segregating sites = polymorphic sites). Also, I will not talk about inbreeding depression in your population coming from only two individuals which will be very important but I will only answer your specific question. In short, I will assume your are not interested in segregating sites...
Probability of an offspring to carry a new deleterious mutation
The vast majority of new mutations are deleterious (Shaw et al. 2003). I don't know of estimates of mutation rate in hamsters but in mammals (and in all eukaryote species anyway generally speaking; e.g. see this post and this post or directly bionumbers#mutationrate), the genome-wide mutation rate is of the order of 1 to 100 mutations per offsprings.
If the couple of hamsters have $x$ offsprings, then the probability to have at least one new mutation in at least one offspring is given by the cumulative exponential distribution
$$P = 1-e^{-U x}$$
, where $U$ is the genome-wide mutation rate. With $U=50$ and $x=1$ (one offspring), this probability is $P = 1-e^{-50} = 1 - 1.9 \cdot 10^{-22} ≈ 1$.
In short
In short, to a fair level of approximation, every new offspring carry at least one deleterious mutation that was not present in either parent.


text:
Can anyone tell me what this is?
On my one plants, this green worm is all over it, with white and yellow cocoons on the Leaves.

Where is the worm again? Do you have any pictures?

looks like a cocoon. Without the location and a picture of the actual worm, this is like searching for a needle in a haystack.

Please add your location, size of the white and yellow masses in your picture, and info about the green worm (size, pictures would be very helpful). Thanks

The green worm is inside the cocoon, I'll see if I can find one.  Leduc, Alberta, Canada

There is the worm, can't post anymore of them cause of size limit

You should keep the first picture of the worm and the old picture of the cocoon! as @theforestecologist said, we could need the size of the worm and cocoon.

Would it help to have a ruler in the picture so u can see wat the size of it is?


text:
What's the evolutionary reason behind feeling 'sorrow'?
As it's established that life's design is a product of evolution, what advantage does emotions like sadness play in the life of an individual/species ?

Do you really think you there is a concrete evolutionary advantage to every human emotion? And if you do, do you think that anyone knows for certain what it is. All you will get is subjective speculation. This is a question and answer site, not a discussion site. I have voted this off topic.

@david yes every emotion had better have an evolutionary advantage otherwise it is is really difficult to explain why humans have it.

@John — So there is no such thing as a neutral mutation being propagated? Yes the things that make us human attract us to others and we mate with them. Is that anything more than common sense. Except in Sparta or in Gengis Khan's army...

Won't answer your question, but if your name is an indication of another problem I may be able to help you there.

Basic emotions like sadness are wide spread basic behavior in multiple species, with strong  effects on behavior, they are not neutral effects, drift will not explain them.

I‘ll answer from a perspective I‘ve been studying in Psychology, but can‘t provide sources. If this is not within the scope of this SE, I‘d kindly ask to either add appropriate sources to my answer or close it.
Sorrow is an emotion that has specific cues and expressions like tears, distinct micro-facial cues (which are stable over practically all cultures according to studies of Paul Ekman et al.), a general tendency to withdraw from social settings.
This can be understood as communicating to other members of your group the need for consolation and social closeness, which would count as an evolutional gain.
Update:
I found an extensive article on the subject: http://www-personal.umich.edu/~nesse/Articles/Nesse-EvolutionBereavement-2005.pdf

First sadness and sorrow are not necessarily the same thing. Many consider them quite distinct and thus have different functions.
In the case of sadness it is currently believed that sadness functions to drive you to change disadvantageous behavior. Example 1. Bob insults Betty, Betty will not talk to Bob, Bob feels sad and depressed about this and learns to stop alienating potential mates and allies. Example 2. Lela the wolf takes too long to in sneaking up on what would be easy prey and the prey wanders off Lela feels sadness, a negative stimulation, at the loss and the behavior leading up to it and quickly learns to sneak faster. Source
Sorrow on the other hand is a bit more difficult because it is not clear what you mean by sorrow. Separation sorrow may function to maintain connection in anticipation of the return of a partner or ally. Source Michi's anwer explores some other possible advantages in more intelligent social species. This a a far more tentative explanation than sadness which is not surprising as we see signs that sorrow exists in far fewer organisms and thus is far more difficult to define or study.

This is just a thought......... overtime the animal brain has developed and became more sophisticated. Included in this process has been the development of emotions, such as love, need to perpetuate the genetic line, ability to feel a sense of loss and hence, sorrow and the need to belong. This emotional growth has contributed in no small way to the ongoing perpetuation of the species.  The ability to experience a variety of emotions enables us to feel both wonderful highs but also mind numbing lows. If we were incapable of feeling emotions and never knew was it was like to be happy or sad our subconscious yearning to perpetuate the species might not be so strong. In other words, I think there is a direct link between our capacity to feel and the innate need to perpetuate the species. If animals, including humans, didn't experience a range of emotions why bother to perpetuate the species?

We represent a science stack and thoughts or opinions are not really what we're after - we ask answers to be properly founded and backed up by references.


text:
complete DNA transfer across different organism zygotes
Consider we have a monkey zygote (i.e. single cell just fused) and a tiger zygote. If we extract the nucleus of monkey zygote and place it into tiger zygote where nucleus of tiger zygote is already removed. Is there any chance of zygote to survive and finally turn into a monkey offspring ? I tried Google for any such experiment ever conducted but seems like biology is googol to Google, no close result at all.
For more clarity it can even be considered all chromosomes transferred  instead of nucleus.
As far as I think this could be possible as all 20 amino heads must be present in zygotes of both the mammals and thus synthesizing protein should not be a problem. However I can't say anything about their respective immune system response.
This question came to my mind considering Darwin hypothesis/theory(interpret as you wish) of evolution, where even if some mutation changes the DNA sequence how much chances are there for a completely new organism if cells don't support growth natively.

Unfortunately the answer is no. Similar experiments of cross species nuclear transplants into enucleated oocytes have been attempted. Rat nuclear transfer into activated denucleated mice oocytes, rabbit oocytes etc.
The primary stumbling block appears to be incompatibility between mitochondria proteins derived from the donor nucleus and proteins derived from the host mitochondria. Mitochrondria proteins are encoded from two DNA sources, the genome within the nucleus and the genome within the mitochondria. While mammalian mitochondria proteins are very similar, there are differences. These small differences between species appears to be enough to kill a developing embryo if there is a miss match.
Attempts have been made to replace both host nucleus and host mitochondria. However complete replacement of host mitochondria has not been successful. Partial replacement of host mitochondria (mouse oocyte as host and rat nucleus with rat mitochondria as donor), appears to marginally prolong the life span of embryo. But death is still the outcome.
PS: nuclear transfer between subspecies and very closely related species does produce viable clone.  Coyote (Canis latrans) using dog (Canis lupus familiaris) oocytes. (Bos gaurus) adult nucleus donor cells and bovine (Bos taurus). My guess is that if a hybrid is possible between the two species, nuclear transplant between the two species should be possible

Can you provide me some pointer to any such research. google sending to animal cloning even when I use words cross species nuclear transplants.

https://www.ncbi.nlm.nih.gov/pubmed/21556135 Here is a started article.

The fertilized tiger ovum probably has some tiger mRNA in its cytoplasm already, those are not going to interact properly with the monkey DNA.  That is going to be a problem long before there is any development of the immune system.

Doesn't mRNA has same structure across multiple eukaryotic cells? I don't know specific exception but heard there are exceptions.

"Structure" isn't enough.  Lots of genes are controlled by mRNA binding to matching sequences upstream.  If those sequences don't match well enough, the cells won't develop correctly.