text:
How to identify active protein in a complex mixture?
I am trying to figure out how to identify which protein in a complex mixture is producing a certain effect.
There is an assay for the effect, so anything (a fraction of the mixture) can be tested on microplate.   The part of the mixture producing the effect is pretty definitely a protein (or has a protein component).
Unfortunately, the mixture is serum... which contains >10,000 proteins and peptides, some in tiny amounts and some in huge amounts.
There is not enough information to go the other way, ie guess what is producing the effect and test that by itself (or remove it from serum and test the depleted serum as a confirmation).
There is also no possibility to use affinity (use a receptor as bait, etc) because many components of serum stick to the cells in the assay (or, practically to any cells).
I need a way to narrow this down from "serum" to one specific protein (or a handful), but how?

Liquid Chromatography may help

@leonardo: It is endogenous to serum (maybe only sometimes).  Samples are from animals not cell culture.  Thanks...

This is a classical protein purification problem - you have to find ways to fractionate your mixture so that each fraction can be assayed for the activity you are interested in. When you find the active fraction you then subject that to a different type of fractionation.
Salting out
The solubility of proteins is affected by the ionic strength of the buffer. If the ionic strength is raised above a critical value (which is a characteristic of an individual protein) the protein  will precpitate, usually without being denatured. By doing a series of such precipitations at increasing ionic strengths a protein mixture can be fractionated according to this property. The salt used is ammonium sulphate, because of its very high solubility. You can find more details at this Wikipedia page (ammonium sulphate precipitation).
Ion exchange chromatography
Proteins have different intrinsic charges, and the net charge on a protein will vary with pH. This property is exploited in ion-exchange chromatography. In this technique the protein mixture interacts with a solid matrix carrying fixed charges. Under the correct conditions your protein plus others will bind to the matrix, while lots of other proteins won't. That's already a purification step, but you can then treat the matrix with buffers of increasing ionic strength. Weakly-bound proteins will be eluted from the matrix first, and as the ionic strength of the elution buffer increases proteins will elute in order of strength of interaction. By performing this procedure with the matrix in the form of a chromatography column and collecting eluate fractions you can achieve another step in the purification of your protein.
Size exclusion chromatography (gel filtration)
This technique is used to fractionate a mixture of molecules according to size. In this case the solid matrix that is used is charaterised by pores of a specific size. Proteins that are too large to enter the pores will pass through quickly;  small proteins will spend a lot of time moving in and out of the pores and so will pass through slowly; and proteins of intermediate size will spend some time in the pores. Essentially the average time spent passing through the matrix will depend upon size. Read more here.
These are just three of the possible fractionation procedures - others, including  hydrophobic interaction chromatography are described here). The key point to grasp is that using any one of these techniques will give you your protein in a fraction which also contains other proteins, but if you apply them sequentially you will progressively remove contaminants because each approach is based on a different physical property of proteins, and your target will have a unique combination of these properties.
At each step you will be assaying fractions to locate the protein of interest, and also running fractions on  SDS-PAGE to get a feeling for the number of proteins left. If you have an assay that lends itself to measuring some kind of unit of activity (as you would with an enzyme), then by also measuring the protein content of the active fraction you can express the purity as a specific activity (units of activity per mg protein). At each step in your purification this specific activity should increase because you recover most of the activity, but discard a lot of the proteins that were present in the previous material. The increase in specific activity can be used to assign
a purification factor to each step. A useful purification step will give a reasonable yield in combination with sigificant purification.
Finally, what order to do these steps in? I've listed them in a logical order - salt precipitation is a low-tech method that can give a quick first step and which has the advantage that it concentrates the target protein (since the precipitate is redissolved in fresh buffer). Size-exclusion chromatography doesn't deal well with large amounts of protein so is best left until later. However, protein purification is a craft, and an expert will use the available techniques according to the exact nature of the project.
UPDATE
From the tone of your original question I had inferred that you were a beginner, but from your comments, apparently not, since you are thinking in terms of mass spec as an endpoint.  A starting concentration of pg/mL is quite a challenge, and clearly you are never going to have enough material to see your molecule on standard gels.
Here are a couple of thoughts on aspects of your problem.
It seems that  in trying to purify minor components of serum a good starting point is to deplete the serum of its major proteins. This is a link to an imunodepletion product, and here is a related product from Biorad (no connection with either company and no recommendation implied).
I also found these papers which may be of interest. (Incidentally I think you'll find that each of the techniques I described is still used, perhaps just with modern instrumentation.)
Li,J et al. (2012) Purification, identification and profiling of serum amyloid A proteins  from sera of advanced-stage cancer patients. JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES 889: 3-9
Fertin, M et al. (2011) Strategy for purification and mass spectrometry identification of SELDI peaks corresponding to low-abundance plasma and serum proteins. JOURNAL OF PROTEOMICS 74: 420-430
Finally, a quick look at the Wikipedia page on plasma reveals that brain natriuretic peptide seems to be present at the levels that you are considering  perhaps you should look for papers describing its purification.
Other than that I think you have to hope that a proteomics expert will come by and give you an expert answer.

Alan, Thank you, excellent answer.  Could you possibly direct me to a paper where someone else tackled a similar problem using modern techniques?  (in serum samples)

Alan, Part of what makes this one tough is that the level of what I'm looking for is probably pg/ml (by analogy with other proteins likely to be similar), whereas the total protein content of serum is ~70mg/ml.  It seems I need a total purification factor of tens or hundreds of thousands, before it is even possible to try to identify this using mass spec.

Answer extended somewhat in response to your comments.


text:
Mechanism of DNA gyrase inhibitor
Why DNA gyrase inhibitor, such as Nalidixic acid and Norfloxacin, do not stop gyrase from cutting DNA helix but only prevent them from decatenation replicating DNA?

Crysallographic studies do not exist for this yet. It has been predicted by computational methods that quinolones bind to DNA-gyrase complex and stall the enzyme at that step.

I didn't really answer the question.. If no better answer comes up then I'll find details and post it as answer

This might be a good article to read: http://www.ncbi.nlm.nih.gov/pubmed/24497635
Robert Kerns's lab has been doing a lot of work on fluoroquinolines, so look into his other work as an entry to the literature. And apparently X-ray crystals have been done for at least parts of this complex. There is some evidence for fluoroquinolines binding to DNA, then moving into the protein as it moves along the DNA.

source: Stack Exchange

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

sort: votes


text:
How to measure trajectory regularity?
I have two animal running trajectories. A regular one with repeated back and forth running between point A and B, like the one on top in the figure. The other one is very irregular, animal paused and turned around a lot in the middle. Is there any algorithm to measure the regularity of a trajectory, like repeated activity on the top? And compare the extend of regularity between the two trajectories? Thanks in advance.

are you trying to see if an animal runs in the same pattern over and over again? I know there are computer programs that use a camera to watch a mouse and plot its movement over time. This is used to measure mouse activity when you can't have a human watch it 24/7. You might be able to overlay the paths and get an average and standard deviation, but I don't really know much about it.

In the world of physics, you can distinguish between random motion (e.g. thermal Brownian walk) and directed motion (called ballistic: think of a cannon ball) by studying the mean square displacement of the object: you'll be able to fit this displacement as a function of time by a linear law if it is random, and by a quadratic one if it is directed. Exponents in between will give you an indication of the degree of randomness. The advantage of this (even if it is not specialized for your case) is that there's a large body of work using this, including for living organisms.
Note also that if your motion is as in the first case above, you'll have ballistic motion for times smaller than the travel time from left to right, and diffusive (random) for times larger than that. This has been used e.g. to analyse the run-and-tumble motion of bacteria who have a short-time ballistic motion and then after some time tumble to explore another randomly-chosen direction.
Example of this type of coexistence of two regimes:

In the field of biophysics, much of this was initiated by Howard Berg and coworkers
In your first case, you'll have an initial ballistic regime and then something that plateaus (because you stay between A and B). The transition time-lag will be the travel time between A and B.
In your second case, you'll be able to characterize the random walk: if the animal is aiming at going from A to B but randomly errs for short times, you'll have a short-time diffusive behaviour, and an intermediate time ballistic one. (And then again a plateau, as in the first case and for the same reasons). If the animal reaches B by mere chance, on the contrary, you'll have a diffusive regime only before this plateau.

I guess what you suggested is more applicable in 2-D situations. In my case, displacement in Y-axis is very small most of the time.

@sgyf: It is valid in any dimension. Use only the x-direction displacement if y-direction is irrelevant.

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


text:
Do butterflies pass over migration patterns to their offspring?
So, earlier, I read online (http://io9.com/butterflies-remember-a-mountain-that-hasnt-existed-for-509321799) that Monarch butterflies veer east during their southward migration to avoid a mountain that no longer exists. If this is true, how do butterflies know to continue avoiding the "mountain" after countless generations, and does it have to do with evolution? Do other animals have similar abnormalities in their migration routes?

here's the original paper - I couldn't find support for this hypothesis in the paper but that was only a quick skim read (and the manuscript only features one brief reference to lake superior) http://jeb.biologists.org/content/199/1/93.full.pdf

If you think about it, monarchs must have a pretty strong genetic component to migration since often they only make one round trip at most in a lifetime. But its not as simple as passing a map in the DNA.
If a mountain springs up on the route, the 'common sense' of the butterflies are still operational and they will tend to find their way around it.
The paper discussed here is older.  More recent Monarch butterfly migration  of some genetics that have been done shows some traits that are related to migration patterns by sampling over many butterflies whose patterns vary tremendously.
Glancing over the paper, I'd say that there may be some 'muscle' memory in migration, but probably the mechanisms encoding the route of migration are not yet discernable.  This is far from something we understand well.
The insect is following patterns of behavior but doesn't turn into a robot just because its migrating.  Migration patterns are probably linked to a series of environmental cues.
Changes in climate or shifts in magnetic fields can change migration patterns. Butterflies would be very different than say migratory birds in terms of the social and environmental markers for migration.

I think it depends on the route taken and which population you're talking about (western vs. eastern US), but my understanding is that both migration directions are multi-generational, so any individual is not necessarily covering the same ground as its parents did.

Thanks for the review @MattDMo I can't find any reference of Monarchs living longer than 8 months.  I just re-reviewed several sites. post a link?  the wikipedia article seems to refer to the fact that Monarchs have mulitple breeding waves (called generations) over the year where their lifespans can vary tremendously (4 wks <-> 8 mos).


text:
Description of the paramaters in the packing parameter?
For a phospholipid, the critical packing parameter is given by:
$$P=\frac{v}{a_0l_c}$$
And I know that

$v$ is the volume of the hydrocarbon tail.
$l_c$ is the critical length of the hydrocarbon chains.
$a_0$ is the optimum surface area of the head group.

But what do these actually mean?
For example what is the volume of the hydrocarbon tail, since it can't be simply the volume of all the atoms that make it up else this would be negligible? What is the critical length of the hydrocarbon tail? And What is the optimum surface area of the head group?

Following image from (Salim et al 2014) will makes thing clear to you,

When they say volume, it is volume of shape of lipid. Shape can be determined by many factors as described here. Following is modified images from (Sprong et al 2001) which will tell you how change differ in general. Here are examples of few common lipids.

+1 Wrt the second figure: perhaps you can also say what these phospholipids are (expand the abbreviations). It would be useful.

LPC: lyso-Phosphatidylcholine, PC : Phosphatidylcholine  and  PE: phosphatidylethanolamine


text:
Does our immune system react on all bacteria?
In our body we carry a lot of bacteria. Some of them are bad for our health, but others are beneficial. For example bacteria may protect us against other pathogenic bacteria.
But is our immune system reacting to all bacteria, i.e. the good and the bad, or does it selectively target the bad? If yes, how does it differentiate between beneficial and pathogenic bacteria?

I believe we have commensal bacteria on and inside our body that are considered part of the innate immune system. And those flora can try to predate on the foreign flora that try and attack us.

@RoSiv I think the question is why our immune system doesn't attack those bacteria which help us i.e. although they're considered part of innate immune system, what differentiates them, from pathogens, for our immune cells?

Just because there's no answer here after 9 hours, yes the immune system would typically lash out at everything. Commensals have ways of redirecting all that anger, however, and I'll provide two reference here and here that outline some ways they accomplish this. In short: they resist some mechanisms and exert influence on others.

I don't have time to answer right now, but do some reading on immune tolerance and the microbiome. There is a lot of work going on right now to try and understand the exact details of this very process, and it's not yet clear how exactly it happens across the board. Basically, though, we and our microbiome have evolved together over millions of years, and can signal back and forth to each other. It also involves some specialized immune cells, and very complex reactions between many different species of microbiota. You could also look up "biofilms" if you're interested in that aspect.

Perhaps you should have a look at this review. It is quite extensive and relatively recent as well (2014). I am myself reading it; if you end up reading it before me then you may ask specific questions about the article.

I've found too that CD4 T-cells can become regularity suppressor T-cells that suppres effector T-cells. See at 1:17 https://www.youtube.com/watch?v=xDvQI9ynl1Q

The immune system is capable of recognizing pathogenic ("bad") bacteria, either by components of the innate (non-specific) or adaptive (specific) immune system. Pathogenic bacteria will have antigen on their surface that mark them as 'foreign', leading to an immune response targeted to the bacteria. In contrast, the immune system tolerates the normal flora of the body. The precise role that the human immune system takes in tolerating and regulating the populations of the normal flora is not known, it is currently a hot area of research.
Current research suggests that microbiota induces host immune tolerance to commensal bacteria directly via a microbe-associated molecular pattern (MAMP) and polysaccharide (PSA) signalling. The immune system continuously monitors the resident microbiota, and certain antimicrobial mechanisms are constitutively engaged to prevent overgrowth of the colonizing microbes: this maintains what is loosely called immune homeostasis. The mechanisms that control (intestinal) tolerance include those that:
1) minimize exposure to and 2) immune recognition of intestinal microbiota, and 3) those that down-regulate immune responses through intra-cellular and inter-cellular mechanisms.
Research has shown that he tolerance of the normal microbiota of the gut seems to require an extensive network of regulatory immune cells including Tregs and (tolerogenic) dendritic cells.
Thymus-derived Tregs were discovered by Dr. Leszek Ignatowicz to be a crucial  player involved in "educating" the immune system about the diverse bacterial colonies in the intestinal flora of mice. In response to the diversity of gut bacteria found in the gut, the Tregs express a 'repertoire T cell receptors' (TCR) that recognize the antigens characteristic of individual bacterial colonies in the gut. Upon engagement of these receptors, Tregs suppresses the adaptive immune response, specifically through the release of immune-modulatory cytokines such as interleukin-2. Moreover, it was found that gut bacteria can also be recognized and protected by a distinct innate lymphoid cell population (ILC) in the intestinal lining of mice. These cells behave like antigen presenting cells, and can recognize and present antigens from gut bacteria through the major histocompatibility complex class II (MHCII). But rather than activating CD4+ T lymphocytes through MHCII engagement, these ILC works by suppressing CD4+ T lymphocytes through MHCII engagement. CD4+ T lymphocytes are involved in clearing pathogen/bacteria, and thus the suppression of CD4+ T lymphocytes is involved in the immune-tolerance of normal flora.
http://www.sciencedirect.com/science/article/pii/S2352345X14000083
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007055/


text:
Why does the nerve action potential needs potassium?
When looking at the action potential generation I do not understand why potassium is needed. I know that potassium is used to repolarize the cell. But why are sodium channels and/or sodium pumps not used to push the cell back into its resting potential?
For example in this video at minute 2:00, sodium is pumped in, and potassium out of the cell. But both are positive ions. You get a less negative membrane potential but wouldn't it go faster if the potassium ions stayed in the cell?
Has potassium an extra property compared to sodium that makes it especially suitable for the repolarization step?

The action potential is mediated by the opening of Na+ channels, which happens in the order of milliseconds (e.g., Aldrich & Stevens (1987)). Repolarization occurs through the opening of K+channels. Their opening is delayed by a few milliseconds (Purves et al., 2001) to allow Na+ to pour into the cell through Na+ channels. After that delay, the opening of K+ channels occurs also in the order of milliseconds. After these two processes are over, the membrane enters a refractory period, again on a millisecond scale. Then the membrane is ready for another action potential.
The Na+,K+-ATPase, on the other hand, has nothing to do in the action potential process as such. It operates much more sluggishly and it can by no means keep up with the rapid channel gating during action potentials. Instead, the Na+,K+-ATPase activity operates at the background to maintain the overall ion homeostasis. As an analogy, the power adapter of a laptop PC can never keep up with the processor speeds; instead, it functions in the background keeping the battery charged.
Then why two different ions? Because two different species of ions are necessary because they fulfill opposite roles in terms of polarization and reploarization.
References
- Aldrich & Stevens, J Neurosci (1987); 7(2): 418-31
- Purves et al., Reconstruction of the Action Potential. In: Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)


text:
How can fresh cavities form at the margins of sliver amalgam fillings on teeth?
Silver amalgam fillings predominantly contain silver a known bactericidal agent and mercury which a known toxin and has bactericidal property. So how is it that the plaque bacteria survive near the filling margins and produce fresh caries?


text:
What is a lip? (upper lip and lower lip)
Everyone knows what a lip is but I'm asking from a technical and anatomical standpoint.
Actually what we call "lip" is "vermilion" in medical terminology. But I want to ask if my understanding is right or not regarding to surface anatomy of the lip.
Lip consists of two parts called upper lip and lower lip. And upper lip and lower lip consists of two parts: skin (cutaneous) part and vermilion part  (vermilion is a special kind of skin also but we do not call it skin).
Thus:
Lip = upper lip (upper cutaneous lip + upper vermilion) + lower lip (lower cutaneous lip + lower vermilion)
This is a diagram that depicts the upper lip portion:

Source: http://elementsofmorphology.nih.gov/anatomy-oral.shtml

Questions:
Am I right so far? Did I miss any points?
Is the term "upper lip" ever used for the skin (cutaneous) part only? (especially in surgical terminology and reconstruction surgeries)
Are the "upper cutaneous lip" and "lower cutaneous lip" terms established terms in medicine? Are there any other names or latin names for those?  (I also see the usage of "cutaneous upper lip" and "cutaneous lower lip")

Don’t forget the part of the inside of lip where the skin texture changes to smooth wet surface. In cosmetic procedures this is call the wet - dry border.

Source

The upper lip extends from the base of the nose superiorly to the nasolabial folds laterally and to the free edge of the vermilion border inferiorly. The lower lip extends from the superior free vermilion edge superiorly, to the commissures laterally, and to the mandible inferiorly. Around the circumferential vermilion-skin border, a fine line of pale skin accentuates the color difference between the vermilion and normal skin. Along the upper vermilion-skin border, 2 paramedian elevations of the vermilion form the Cupid bow. Two raised vertical columns of tissue form a midline depression called the philtrum. The philtrum is located between the paramedian elevations of the vermilion and the columella above. The labiomental crease passes horizontally in an inverted U-shape across the lower lip, which intraorally corresponds to the depth of the gingivolabial sulcus.

This includes vermilion as well. Dont forget the mucous part inside mouth.

This whole is lip.
As for upper cutaneous lip or cutaneous upper lip, it wont matter, both are same and are used interchangeably. And quite frequently
used is upper cutaneous lip.
As for latinisation, you can use labium for lip, no such specific word for upper or lower lip, is know to me. But, you can try superior cutaneous labium and inferior cutaneous labium, if you want.

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


text:
How does the mechanism which controls blood pressure in the brain work?
I know that pressure is sensed in the skin by mechanoreception mediated by skin receptors. Static pressure stimuli are mainly sensed by slow-adapting fibers connected to receptors like the Merkel discs. Vibratory stimuli are sensed by rapidly adapting receptors like the Pacinian corpuscle.
Blood pressure is also sensed by the body and the brain regulates blood pressure by influencing the peripheral nervous system that can increase or decrease the blood output of the heart.
How are blood pressure differences in the brain sensed and how do these receptors mediate cardiac activity? Are blood pressure differences in the brain sensed by rapidly adapting receptors akin to Pacinian corpuscles?

I've added background to the question and I vote to re-open.

Blood pressure is sensed in blood vessels by baroreceptors. Baroreceptors are stretch-sensitive nerve fibers located primarily in the aortic arch and carotid sinuses. The baroreceptors send afferent fibers via the glossopharyngeal nerve to the nucleus tractus solitarii in the dorsal medulla in the brainstem. From there, efferent cardiovascular neurons send projections to the medulla and spinal cord. There are also stretch-sensitive receptors in the heart and pulmonary vessels, called cardiopulmonary receptors that use the same nerural connections as the baroreceptors.
The baroreflex loop results in activation of sympathetic or parasympathetic fibers to the heart, the smooth muscle of the peripheral blood vessels, and other organs such as the kidney to maintain arterial pressure at normal levels.
In a simplified scheme, increased pressure stimulates baroreceptors, which attenuates the sympathetic outflow to the peripheral vessels and the heart, restoring pressure to normal levels. The parasympathetic influence will dominate which is mediated by acetylcholine. Conversely, a decrease in pressure relieves the baroreceptors and increases sympathetic outflow. Sympathetic activation causes a release of noradrenaline that leads to vasoconstriction and increased cardiac output and hence an increased blood pressure (see Fig. 1).

Fig. 1. Control of blood pressure. Source: Human Physiology (2011).
Reference
- Cougias et al., Med Sci Monit (2010); 16(1): RA1–RA8

With regard to blood pressure in the brain, note that besides the general baroreceptor in the aorta at the output of the heart, there are two at the carotid sinuses.  The latter are in the neck just under the head and sense the pressure of the blood flowing into the head, providing close control of the blood pressure in the brain.

The control mechanism in the brain for blood pressure is a endocrine hormone named ADH.  This stands for AntiDiuretic Hormone.  This hormone is produced by special nerves in the hypothalamus and stored in the posterior pituitary gland.  ADH is stimulated by increased blood solute (particles like ions and other molecules) present or decreased blood volume level.  When you have adequate hydration, this hormone is actually inhibited.  On a very elementary level, it works by stimulating kidney tubule cells to reabsorb water rather than eliminate it.  Some drugs also interfere with ADH, most commonly ethanol (drinking alcohol).
Edit: Forgot to add that ADH is also known as Vasopressin, and is also responsible for constricting the blood vessels.

Although AVP may affect blood pressure (does it?), its primary role is in fluid balance by affecting kidney function. And if EtOH affects AVP, it should also affect blood pressure according to your reasoning? Could you add some references to back your answer up? I don't buy it :-)

Fluid balance is the primary regulator of blood pressure.  EtOH most definitely affects blood pressure, as it is a CNS depressant.  ADH is also known as vasopressin, and is the main control for blood fluid, and solute levels which in turn is responsible for the mineralcorticoids (renin-angiotensin) synthesized in the Adrenal Cortex.  The method I've explained is how the brain regulates blood pressure.  What Christaan posted is how blood pressure is locally mediated. -- Edit: Maybe balance is the wrong word - but rather Fluid Volume regulation. --Edit2: ADH inhibitors exist to modulate bp.


text:
What species is this worm?
I was at the park lying on the grass and its the third time I have seen them, I used to think they were parasites when I was like 7. It is the very small brown worm on the green leaf. It moves by squiggling. It comes in different colors but same size.
http://postimg.org/image/ea3x2nw95/
http://postimg.org/image/zfawh9pr1/

Location, time of year, and description of the habitat/vegitation are going to help.

Location: local park in Miami. Also found in trees as one spontaneously fell on my finger and squiggled on it mildly fast when I was 7, in Honduras. Time of year is both summertime/late spring. Lots of leaves

"Brown string" and "on the green leaf" are of little help for me at least: where is it?

to be honest, I cant find it.. edit the picture on paint and add a red circle around the worm.

And please use the add image button. Do not use third party sites. This one actually is blocked in my lab for some reason (Not your fault actually. My sysadmin needs to be boiled in hot oil. Nonetheless it is better to use the approved image uploader)

For me it looks like an inchworms which are the larvae of geometer moth or Geometridae.
By your picture it is almost impossible to see of which type it is.
I took picture of one in Switzerland (but likely not the same as yours).

Full resolution here: https://flic.kr/p/utFsiU

Is this what you mean?

It's pretty hard to tell from this photo, and I'm no entemologist, but to me, it looks like it may be a wireworm, a larvae of a click beetle. This is a diverse group, so I think it would be pretty difficult to give a specific identification. (More images)

It was attached to the edge of the leaf. It's not on a leaf.


text:
Why is peripheral vision not bleached by daylight?
In daylight, rods are known to be bleached: we have to wait some time after going into darkness before scotopic vision becomes effective. But, as I understand, peripheral vision is also mostly due to rods, since away from the fovea, cone density rapidly declines.
But I wonder then: if rods normally saturate in bright light, why does peripheral vision still work in daylight?

Short answer
In photopic lighting, peripheral vision is mediated by cones.
Background
The rods are indeed saturated at daylight, and even at twilight (source: Nature). However, the cones are active and although their density in the periphery is low, they are still present (Fig. 1). Hence, peripheral vision in photopic lighting conditions is mediated by cones. Because of their low density in the periphery, however, visual acuity is low (Kolb, 2012).

Fig. 1. Rod & cone densities in the retina. (Kolb, 2012)
Reference
- Kolb, Photoreceptors, In: Webvision: The Organization of the Retina and Visual System. Utah University

This seems to contradict this answer, which doesn't appear to rely on scotopic vision to explain its point. Is it wrong?

@Ruslan For primates, AliceD's answer here is better. See also Stabell, U., & Stabell, B. (1976). Absence of rod activity from peripheral vision. Vision research, 16(12), 1433-1437. and Stabell, U., & Stabell, B. (1982). Color vision in the peripheral retina under photopic conditions. Vision research, 22(7), 839-844.

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


text:
Need Help Identifying this Critter (Insect?)
This creature is hanging out on my kitchen window. I live in Western Maryland, US, near the Potomac River. The creature is about 3 inches long (measured from tip of mandibles to tip of tail). Does anyone know what it is? Is it dangerous? Rare? I've been living here about a year and have never seen one before.

It looks like an adult Dobsonfly (Corydalidae), where the adult males have huge pincher-like jaws. Apparently, the jaws are the result of sexual selection and, even though they look scary, males cannot use them to bite.
I'm only vaguely familiar with the group though, and cannot say what species this is.

(Picture from bugguide.net)


text:
What causes the tonotopic organization of the inner ear?
I'm trying to understand why tones are registered in the way that they are in the inner ear, i.e., why are high pitched sounds sensed at the base of the cochlea and low frequencies in the apex? I've been unable to find out the specifics of this tonotopy, but as far as I can gather this is due to the physical properties of the basilar membrane.
But what exactly are those physical properties? Does the basilar membrane vary in size and stiffness along its length, so that each bit has its own resonant frequency, or is there something else going on?

The frequency tuning in the cochlea is due to a number of factors.

The primary factors of cochlear frequency tuning are generally ascribed to the passive physical characteristics of the basilar membrane (BM), which OP already identified in the question - The BM is wider and more flexible at the apical end (low-frequency region) and narrower and stiffer at the basal end (high-frequency region). Like the strings on a guitar, stiff and thin cords produce high-pitched sounds, while loose and thick cords produce low-frequency sounds. The stiffness of the BM gradually decreases from base to apex, while its width gradually increases along that length, thereby creating the gradient of characteristic frequencies of the basilar membrane (Purves et al., 2001) (Fig. 1).
Another factor that may play a role is the length of the stereocilia. Stereocilia are the mechanotransductive hairs that give the hair cells their name. In the inner hair cells (IHCs) the stereocilia are mechanically deflected when a sound wave eneters the cochlea. That in turn leads to neurotransmitter release from the IHC and that in turn stimulates the auditory nerve. The stereocilia increase in length towards the base of the cochlea. Longer stereocilia respond most optimally to longer wavelengths (lower frequencies). Hence, stereocilia length also provides another mechanical gradient that facilitates frequency decomposition in the cochlea (Snow & Wyckam, 2009).
A last factor is more physiological in nature; the frequency tuning of the cochlea is much sharper than can be explained on the basis of the passive membrane properties of the BM. For example, studies in dead cochleas show a shallow tuning of the BM, while the tuning in alive cochleas is much sharper. Hence, it is thought that an active mechanism has to be at play. Generally, the outer hair cells (OHCs) are attributed this function. OHCs start to increase and decrease in length when the BM moves in response to sound. They are thought to amplify the BM response to sound. If these OHCs only amplify a very narrow set of frequencies and not others, they may indeed be capable of sharpening the tuning curve of the associated nerve fibers, but the exact mechanism behind this is unknown (Purves et al., 2001).

Fig. 1. Frequency tuning along the basilar membrane. source: Purves et al., 2001
References
- Purves et al. (eds.) Neuroscience 2nd ed. Sunderland (MA): Sinauer Associates (2001)
- Snow & Wyckam, Ballenger's Otorhinolaryngology: Head and Neck Surgery, John Jacob Ballenger (2009)

To add to Christiaan's answer, the length of the hair cells also changes along the basilar membrane. They are longer and floppier near the apex. There are many levels of mechanical interaction occurring--the basilar membrane vibrates, the outer hair cells change length and articulate with the tectorial membrane which is also moving, the displacement of the fluid beneath the tectorial membrane causes inner hair cells to depolarize, etc.
Also, if you're asking for an ultimate 'why,' high frequencies are more quickly attenuated so it would make sense for them to be represented at the base, right at the point of transduction from the middle ear. Interestingly, I believe the cochlea grows out from that point during development (e.g. the apex moves out/up/around) but low frequency hearing is the first to mature.
Edited to add sources:
Change in length of hair cells, see table 2: http://upcommons.upc.edu/bitstream/handle/2117/26076/MorellUltrastructure2014_final+proof.pdf;jsessionid=82346B40F24139DA94D7217DCA227C18?sequence=9
Discussion of attenuation by frequency: https://physics.stackexchange.com/questions/87751/do-low-frequency-sounds-really-carry-longer-distances
Cochlear growth: http://onlinelibrary.wiley.com/doi/10.1002/dvdy.10500/pdf


text:
design and assessment of qPCR primers for COVID19
I read the False Negative of qPCR test for COVID19 is high compare to CT scans.
https://pubs.rsna.org/doi/10.1148/radiol.2020200642
I was curious if experts can comment on why and what makes it difficult to design more accurate PCR given the genomes is out there.

The WHO's primers are compatible with every sequences found so far, when the PCR fails it is because the sample doesn't contain enough viral genomes (here the probe https://blast.ncbi.nlm.nih.gov/Blast.cgi?CMD=Get&RID=607FNKGR01R )

what do you mean by compatible ? every test as sensitivity and specificity. here is the question, given the high match on blast - what makes it to have low specificity ? it is clear in the paper and other papers these pcr tests suffer from high false negative :)

Compatible means the forward and reverse primer (20 nt each) bind to the ends of the target 100 nucleotides subsequence of the viral genome (and its minus sense copy) and this subsequence contains the probe (25 nt). When extended by the TaQ polymerase the probe releases its quencher so that its fluorescent end produces light which is detected by the fluorometer. If some mutations appear in those three 20 nucleotides subsequences the PCR will stop working or it will be much less efficient and the WHO will have to make new primers with more diversity


text:
Question about radiation and how it affects biological systems
I'm doing research on the effects of radiation, and specifically UV, X-Ray and Gamma radiation, on biological systems at the cellular level and beyond. I understand that radiation types can be classified by their wavelength, with the gamma radiation being of the shortest wavelength and thus highest energy.
How does this measure of wavelength relate to the unit rads, or radiation dosage? And how do they both affect the survivability of cells? I can understand that the lower the wavelength, the higher the energy and it will affect the cells more adversely at those levels, but how does rads relate to that?

The absorbed dose describes the amount of radiation absorbed by an object or person, i.e., the amount of energy that radioactive sources deposit in materials through which they pass. The units for absorbed dose are the radiation absorbed dose (rad), or better: the gray (Gy) unit.
One gray dose is equivalent to one joule radiation energy absorbed per kilogram of organ or tissue weight. Rad is the old and still used unit of absorbed dose. One gray is equivalent to 100 rads.
1 Gy = 100 rads
Equal doses of all types of ionizing radiation are not equally harmful. Alpha particles, for example, produce greater harm than do beta particles, gamma rays and X rays for a given absorbed dose. Alpha radiation is the most dangerous because it is easily absorbed by cells. Beta, gamma an X radiation are not as dangerous because they are less likely to be absorbed by a cell and will usually just pass right through it (source: BBC).
To account for this difference, radiation dose is expressed as equivalent dose in units of sievert (Sv). The dose in Sv is equal to absorbed dose" multiplied by a radiation weighting factor (WR - see Table 1 below). Prior to 1990, this weighting factor was referred to as Quality Factor (QF).
Note that the heaviness of the alpha particle makes its penetration rates very low. Hence, it will not easily penetrate through the outer layers of the skin.

Table 1. Recommended Radiation Weighting Factors. source: Canadian Centre for Occupational Health and Safety
Now to your question:
Ionizing radiation has more energy than non-ionizing radiation. Ionizing radiation can cause chemical changes by breaking chemical bonds and damage living tissues.
Shorter wavelength UV begins to have enough energy to break chemical bonds. X-ray and gamma ray radiation, which are at the upper end of the EM spectrum, have high frequencies (~100 billion billion hertz). Radiation in this range has high energy and it can strip electrons from an atom or even break up the nucleus of the atom.
The process in which an electron is given enough energy to break away from an atom is called ionization. It results in the formation of two ions: the molecule with a net positive charge, and the free electron with a negative charge. Each ionization releases a large amount of energy which is absorbed by the surrounding tissues.
There are three main kinds of ionizing radiation:
Alpha particles, which include two protons and two neutrons; beta particles, which are essentially electrons; and gamma rays and x-rays are photons. Alpha particles, beta particles and neurons are not part of the EM as they are energetic particles as opposed to pure energy bundles (photons) (source: ARPANSA Australia).
So in the EM realm, frequency is proportional to energy and hence to tissue damage (Fig. 2) and hence to rads.

Fig. 2. EM spectrum. source: ARPANSA


text:
How can a tongue-biting parasitic arthropod become a fully functional tongue?
From wikipedia:

The parasite Cymothoa exigua [consumes a fish's tongue and] then replaces [it] by attaching its own body to the muscles of the tongue stub. The fish is able to use the parasite just like a normal tongue.

Wikipedia says that it replaces the host's tongue and becomes fully functional. But how does the arthropodic parasite reattach the nerves of the fish, such that the fish can assume control of it? Am I misunderstanding something?

Short answer
There is no evidence whatsoever that the parasitic arthropod Cymothoa exigua develops itself into a functional tongue. Instead, it consumes the fish's tongue and occupies the freed buccal space to continue feeding onto the fish's blood or mucus.
Background
The linked wikipedia page that states that Cymothoa exigua arthropods form fully functional tongue-replacements refers to Brusca & Gilligan (1983) to back up that claim. While the journal is credible, the article itself is a theoretical work. The authors base their conclusion that the tongue replacement is functional on the relatively healthy condition of just 2 specimens of fish. They reasoned that, because the parasitic arthropods were relatively large, the fish had to be hosting them for quite a while. In turn, given the relatively healthy condition of the fish, the authors reasoned the arthropodic tongues may actually have had functionality. In the figure below taken from Brusca & Gilligan (1983) the parasite does indeed look much like the normal tongue.

Source: Brusca & Gilligan (1983).
However, there is no mention whatsoever that the parasitic tongue taps into the nervous system and I have not found any literature supporting such a claim. Further, Brusca & Gilligan (1983) specifically say that:

[...] we propose [that] a fish with an 'isopod tongue' [is] not feeding as efficiently  as a non-parasitized fish, [but] feeds more efficiently than a fish with no tongue at all [...]

The authors' claim is much more nuanced than the blunt conclusion as drawn in the wikipedia page that it is a fully functional tongue; while the effects on its host may be relatively mild, it may not replace all, or even any, physiological functions of the normal tongue.
Reference
- Brusca and Gilligan, Copeia (1983); 3:813-6

Just to add to Christiaan's excellent answer: The authors of his cited study state:

[the tongues] replacement by a parasite would not appear to be a complex phenomenon.

Implying that this is a very basic process, according to what they observed.
To answer your question as it was posed:
Wikipedia states the tongue becomes fully functional. The authors of the study quoted by Christiaan also state two further pieces of information which may be of benefit to you.

It [the tongue] is primarily a mechanical device to hold prey ... in the roof of the mouth while being processed.

[the parasite] attaches to the remaining tongue stub.

I suppose that with 'fully functional' you mean innervated. However, the parasite merely has to perform a basic mechanical function, and may be directed by the remaining stub (though that is my own inference).


text:
Does evolution head to some optimum?
Currently we have many species which are "good enough" for current environment, some species emerge, another die. So let's say that they could be close to some local optima. Does the evolution head to some optimum that in future we will have only one species which will be superior to all other extinct form of life?

The environment is highly variable thus it is unlikely (I'm going to say impossible) that a single species would be the best in all possible environments. Species do often exist close to a "local optima" - see fisher's geometric model of adaptation - there's a recent paper showing that it seems to be a good model for real world adaptation

The question is unclear in many ways. First, you seem to be assuming that all species are evolving in the same fitness landscape, when all species (and populations) exist in their own fitness landscape. Second (assuming that a global optima really exists), why would this imply that all species but one should go extinct? Third, other species (the entire foodweb) constitutes "the environment" for a particular species, which means that the environment is never stable (since all species evolve).

Fisher's Adaptive Hypersphere model proposes a single adaptive peak with a range of genetic configurations that could bring the population closer to optimum.

According to Orr (1998), the inclusion of drift in the model adjusts the expected sizes of mutations that become fixed. Early in adaptation, fixed mutations are predicted to be larger on average than those fixed later.
Tenaillon (2014) discussed simulations of adaptive walks within the geometric model, w/ the dynamics of adaptation and the phenotypic effect of mutations.
An increase in E. coli fitness over 10,000 generations was documented by Lenski & Travisano (1994) indicates "yes" to your question

An issue in the question that I will ignore
You say

Does the evolution head to some optimum that in future we will have only one species which will be superior to all other extinct form of life?

Firstly, it is a little bit weirdly phrased. By "superior" I suppose you would refer to a species that could outcompete all the other. This sounds very impossible to me firstly for simple ecological reasons. However, it would be a long answer to fully address this point and I don't feel like addressing (I might not be very much able to) in addition to the other questions.
Evolution vs Natural Selection
Just for a start. Evolution is way more than just Natural selection. There are plenty of other absolutely essential processes such as mutation and drift that are important to understand.
What is Natural Selection?
Natural selection is the process by which most fit individuals end up being at higher frequency in the population as a result of reproducing more and surviving better. Natural selection does not necessarily diminish the probability of a species to get extinct. It will not necessarily increase the ability of a species to compete another. It will not necessarily increase the rate of increase in the number of individuals in the species.
local vs global optima
Reading you post you seem to understand the concept of local vs global optimum (from algorithmic maybe). If selection alone was acting in the population and if mutations were feeding genetic variation to this population at a low enough rate, then population will ultimately reach a local optimum and will get stuck there forever. They would never reach a potential higher local optimum somewhere else. Drift may allow for such switch though, it is refer to "shifting balance theory".
Envrionmental change
The environment changes much faster at a local scale that you seem to think. When talking about environmental change for a lineage, we are not only talking about important ice age or current days global warming but we are talking about more subtle and more frequent changes. Imagine a species of unicellular living in a 50 cubic centimeter puddle. For them environmental change are drastic and frequent. So do population really have time to achieve any equilibrium. It is here a general question that comes in many field of evolutionary biology and also outside biology. Are the system that we study expected to be at equilibrium (in regards at some variables at least) in nature or are they never given the time to reach any equilibrium?
Mutations and drift
Mutation and drift are stochastic processes in evolutionary biology (among others). Mutations is the ultimate production of genetic variation. Most mutations are deleterious but not all are. The exact mutation (and mutational effects) and number of mutations that will occur in a population in a given amount of time is a stochastic process. Genetic drift refers to the random sampling of individuals that are chosen to survive. Drift is inversely proportional to the population size and you may want to have a look at this post to get some intuition for why this is the case.
How much fitness is lost du to ever occurring mutations?
As mutations are always occuring we might wonder how far is a population from its optimum due to these deleterious mutations.
Let's consider a very simple model.
Let $p$ be the frequency of the wild-type (not mutant) allele, $s$ be the deleterious effect of the mutation in the homozygote mutant and $h\cdot s$ be the deleterious effect in the heterozygote. The mean relative fitness in the population is
$$\bar w =  1 - 2 p (1-p) h s - (1-p)^2s$$
Let's define the mutation load $L$ as $1-\bar w$. As a consequence
$$L = 2 p (1-p) h s - (1-p)^2s$$
At selection-drift equilibrium the expected frequency of $p$ is $p=\frac{\mu}{hs}$, where $\mu$ is the mutation rate. As a consequence the
$$L = 2\mu$$
and
$$\bar w = 1- 2\mu$$
Let's assume that fitness effect at different loci are multiplicative (no epistasis). As a consequence an individual carrying $n$ deleterious mutations has a fitness of
$$\prod_{i=1}^n 1-s_i $$.
Let's further assume that all mutations have the same deleterious effect on fitness, that is $s_1=s_2=...=s_n=s$. Let $l$ be the number of nucleotides on which deleterious mutations can occur. Coming back to $w=1-2\mu$, we can say that over all loci in the genome the fitness is
$$\bar w = \prod (1-2\mu) ≈ e^{-\sum_{i=0}^l 2 \mu} = e^{-2\mu l} = e^{-U}$$
, where $U=2\mu l$ is the genome-wide deleterious mutation rate. According to best estimates, in humans $U≈2.2$ and therefore our load is $L = 1-e^{-2.2} ≈ 0.9$.
From this simple model, we would expect that 90% of the mean fitness of a population is lost due to ever recurring deleterious mutations. This sounds pretty big and suggest that we'll always be pretty far way from an actual optimum.

The short answer is NO.
Here, very briefly (since it would take to much to properly analyze all the aspects of this topic), is why:
First of all, the environment is constantly changing so there will be no such thing like 'the end of evolution'. Even if you try to stabilize the environment artificially (a lab setup) the organisms will continue to interact each other, mutations will occur, new stuff will evolve anyway. (here one example https://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment)
Moreover, each environment is made up by sub-environments (niches) that can be colonized by different organisms each of them will tend over time to adapt to their niche while competing with all the other organisms in the nearby environments but no organism will ever be the fittest for all those niches.
Zooming into molecular evolution, there are some enzymes that have reached "perfection" in the sense that they can catalyze a certain reaction at the maximum speed possible (https://en.wikipedia.org/wiki/Diffusion_limited_enzyme). However, even in these cases, such enzymes are well fit to their local environment (the specific cell type) and they will not work as well (or at all) in different conditions. So, even if they may perform a reaction perfectly, they may always evolve. For example, they may change substrate specificity of temperature stability or they can evolve different reaction mechanism.


text:
How does the brain know what to remember and what not?
People remember some information for example when learning for an exam, or remember to go to a shop after work etc., but we don't remember usually much other stuff like people passing us, what was the weather some days ago etc. How does the brain know what to remember and what not, how does it filter important information from not important?

Look at https://en.m.wikipedia.org/wiki/Engram_(neuropsychology).              Totaly anecdotally i would imagine that there is a thershold level/s of excitation of certain neuron to network (check out Jennifer Aniston neuron study) which leads to an imprinting of a memory trace. How you recide to recall would be interesting001

The body of work on this topic huge, so I'll just try to mention a few things.
On the cognitive level, one possible answer is salience (also see here for an article specific to the visual system). You can think of this (in a somewhat circular answer) as the thing that makes certain stimuli stand out from others. Salient stimuli capture bottom-up attention. Another possible answer is top-down attention. This is where you actively/deliberately pay attention to something.
In terms of mechanism, we have to think about different types of memory. For example, there are separate long-term and short-term memory systems (among many other distinctions). In general, there are hypothesized gating mechanisms that determine the information that can enter memory. The gating systems are controlled by some signal that says 'store this information' or 'ignore this information'. Different memory networks can have different gating systems.
There's a lot of work looking at neuromodulators as gating signals. Dopamine and acetylcholine are some prominent examples. For example, people have found that dopamine can modulate synaptic plasticity (the strengthening and weakening of connections between neurons, which is thought to be a primary mechanism of long term memory storage). It can also cause cortical remodeling. For just a couple examples, see:

Zhang et al. (2009) Gain in sensitivity and loss in temporal contrast
  of STDP by dopaminergic modulation at hippocampal synapses.
Bao et al. (2001) Cortical remodelling induced by activity of ventral
  tegmental dopamine neurons.
Froemke et al. (2007). A synaptic memory trace for cortical receptive field plasticity.

On the behavioral level, stimulating the dopamine system can induce particular forms of learning (which you can think of as a form of memory). For example, if you stimulate the dopamine system, an animal may tend to repeat the behavior that led to the stimulation. A pathological version of this is thought to be what happens during addiction with certain classes of drugs that stimulate the dopamine system (e.g. cocaine, but not lsd).
Interestingly, many of the same mechanisms appear to work across species, from sea slugs to humans). Although,sea slugs can't remember going to a shop after work.

Well I have a theory; I think that when we see at something or some event, our brain processes this information in two separate parts. One of them is composed of the objects on which we are focusing. That part is saved in our memory and we know about it. all other objects from that scene on which we are not focusing our attention, are handled by sub conscious part of our brain. And these are also stored in our memory but we dont know about them.
So memory in brain can be considered as a book with events as its contents. Those events on which we focus are placed in the index of this book. Other events are also stored in the book but are not in the index. When we try to remember something our brain checks the index to fetch the relevant information. So even though majority of stimuli received by brain from our senses are stored in brain, we only perceive to remember those events of which we have created an index ( focused stimuli )


text:
Are there examples of animals being sexually attracted to another species more than to their own?
I just thought that from the perspective of a female domestic cat, a male bobcat probably looks like the archetype of a perfect mate. As tall, strong, muscular and mighty as it possibly gets. Clearly preferable to any of these boring male domestics.
Has anyone ever done any research on this topic, like presenting a male cat and bobcat to a female in heat and scientifically evaluating her response? (I'm not exclusively asking for cats and bobcats, but for any type of animal, and I'm just using the cat-bobcat-example to better explain the question.)

Here are a few examples. All are open to debate as to whether it answers your question.
Zoophilia in humans
When asking of example of a "species" that does something, it is easy to forget about the diversity of behaviours among individuals of that species. It raises the question of how frequent must the behaviour be in that species to accept that the species is representative of this specific behaviour. Many might be tempted to disregard humans as examples thinking that zoophilia (sexual fixation of a human on non-human animals) is very rare but the reality appears quite different.
The Kinsey reports (1953) estimated that 8% of men and 3.6% for women had sexual interaction with animals at some point in their lives. More recent studies tend to find somewhat similar results (of the order of a few percents). These numbers seem to go way higher for people living near farms. Although these numbers seem debated, the Kinsey reports (1953) estimated that 40–50% of people living near farms have had sexual interaction with animals at some point in their lives.
Given the prevalence of zoophilia, I would argue that humans could be considered an example of a species where (some) individuals are sexually attracted to individuals of another species.
Many animals have sex with about anything
In my life I have seen many dogs, rabbits and bulls attempt to have sex with inanimate objects. If a dog can be sexually aroused by a pillow (poor pillow), then I am pretty sure it can be sexually aroused by individual of another species.
Here is a picture of a moose trying to mate with a statue of a bison

Note btw that I am talking here about animal species that have a very high cognition, so below is a funny example with a beetle.
A tragic love story
In Australia, a species of Buprestidae (family of beetles) called Julodimorpha bakewelli has gone through an important decrease in population size. The blame is on people throwing their empty bottles of beers on the side of the road. Why? Males are attracted by the brown shiny color of the females and it turns out that many glass beer bottles have this same exact color. Hence, males started to spend all their time mating with beer bottles rather than with females causing a decrease in the species population size.
Sure a beer bottle in not another species but it shows how individuals of a species can be more aroused by something else than individuals of its own species (and the example is funny; the study won the IgNobel prize in 2011).
Amazon Molly
The Amazon molly is a fish species in which there is no males. All Amazon mollies are females. However, the amazon mollies need sperm to reproduce. How is it possible?
The females have to seek for sperm in a sister species in order to activate the development of the eggs. They mate with males of this sister species but don't use the genetic material of the father from the sister species (otherwise they would not be two different species). The amazon mollies are therefore only sexually aroused by individuals of another species. See Kokko et al. (2008).

Not to mention all those flowers mimicking female insects to attract pollinators...

Not just flowers some predatory insects so it as well.


text:
How exactly does symbolic language for apes work?
I'm talking about the panels with lots of colored symbols on them you sometimes see in documentaries and the like. Apes point at the symbols in a specific order and in this way can communicate with humans.
I already googled around a lot, but wasn't able to find any detailed explanation on how exactly the language works (meaning of all the symbols, grammatical structure of the language and so on). It might just be because I don't know what words to use for my search, so can anyone with more expertise in the field point me in the right direction?

The best article I found was this one. In it it says among other things that:

Kanzi, an unusually intelligent Bonobo chimp trained at Georgia State
University, was remarkable in that he learned to use around 200
symbols on a portable electronic symbol board, a computer with buttons
in the shape of absolute arbitrary symbols rather than manual signs.
More interestingly, Kanzi learned how to use this board while watching
his foster mother, Matata, being taught by traditional reinforcement
methods. So Kanzi did learn how to use arbitrary symbols without being
taught, although he did observe direct reinforcement of each symbol
during the process and the symbols were taught one at the time.
The
evidence for the mastery of syntax is not so convincing. While
chimpanzees can learn to order their symbols to get what they want, it
is not clear that they have mastered syntax. The reason is that when
they initiate communication, even adult chimps often abandon the order
they have learned and phrases such as, "Fight mad Austin," a famous
utterance of Kanzi's friend Panbinisha. Here the order doesn't seem to
matter. Apparently Panbinisha was trying to express, "there was a
fight at Austin's and someone (Austin?) was mad". It is interesting
that even human children simply don't make such errors once language
acquisition begins, and certainly adult speakers would never utter
such strings. Notice it lacks any morphemes (-ing, at, I, she, -ed),
the hallmarks of grammar.

The trainer of Kanzi has published some materials but I do not know if they are available free online. You could probably send her an email and ask. The article goes on to state:

The maximum number of lexeme symbols (simple nouns, verbs, and
adjectives) is interesting, too. The brightest chimpanzees master
fewer than 200 of these symbols by adulthood. Human children know
about 50 by the time they are 18 months old, when they begin learning
nouns, verbs, and adjectives at the rate of about 5 per day. So the
maximum achievement in symbol acquisition among other primates is more
than matched by human children before the onset of language
acquisition. In fact, the type of phrases spoken by chimpanzees and
gorillas also resemble those spoken by children before they acquire
their first language: "give orange" or "give Bobby orange" (without
the pronoun me) are common expressions of children before the onset of
language learning around the age of two.
The results suggest that
while chimpanzees and gorillas are far more intelligent than anyone
had imagined during the first half of this century, they are not
capable of human language. Rather, they have a primitive version of
the semantic ability children use before that explosion of
language-learning around the age of two.

At least according to that article there is not much of a grammatical structure at all. The apes does not so much care about the order of the words either, even if the can learn a certain order, especially if they get something to eat if they do it right.


text:
Why does sex last so long?
I wonder why (especially human) sex lasts longer than just a few seconds?
My thought is that the shorter it takes a man to ejaculate, the lesser is the risk that he gets interrupted by a rival or a predator. Therefore, men who ejaculate quickly get an evolutionary advantage in the long-term.
But, as human sex lasts several minutes, I'm obvioulsy wrong with my argument. Anybody knows why?

there is probably an element of recreation into your procreation argument, which can contribute towards this.

If male sexual performance / stimulation / duration affects females in terms of things related to fertilisation (immune systems, gene expression etc.) Then there is possibility of selection for duration

I think it is rather a cultural thing to prolong ejaculation.

For a great many men, sex does not last longer than just a few seconds. This seems as good an explanation as any I've ever seen.

It's also entirely possible that there are physiological constraints on the reproductive system as it happened to evolve that necessitate a certain minimal duration of sex.

@anongoodnurse "A few seconds" is below the 2.5 percentile as estimated here. The median they obtained was 5.4 min.

@har-wradim - 500 couples (250 men) is not many for a study. Even if it were that low (which I seriously doubt), multiply the number by all men having intercourse and that is still a great many men.

@anongoodnurse Why should we multiply? The question addressed was about boundaries of the norm and how to define pathology. What's the base for your pessimistic claim? By the way, those observations are also related to seaotternerd's idea: "a few tens of seconds" is physiologically possible, but for modern humans it is certainly not normal.

Females might select males who are more durable in sex. Or maybe men who were more durable in sex had a direct advantage, like better semen or maybe causing female orgasm (which is said to upsuck semen into the cervix). But as humans lived in societies, the scenario of being interrupted by a predator was minimal. By a rival... well, probably cheating was not a common thing. Or maybe strict monogamy was not so common.

There are plenty of animals with brief procreative periods, as you suggest. In chimps, sex takes 10 to 15 seconds - much less time than humans. So the question is really why have humans evolved to be different?
I don't think any of the answers based on fitness are particularly compelling. It's not like sex feels like running a marathon or less physically fit people can't manage to ejaculate in their partners so it seems unlikely that the lengthy sex act serves to distinguish fitter individuals.
Instead, I think the difference probably lies in the pair-bonding role of sexual activity. Humans form unusually long-lasting, typically monogamous or largely monogamous, bonds that function to provide the support needed during the lengthy childhood that humans undergo. The prolonged, and highly pleasurable, sex act likely functions to help maintain these bonds in order to keep the couple together and provide the stable support needed to maximise the chances of successfully raising a child to adulthood.
Unfortunately, to the best of my knowledge, there is no high quality empirical evidence that would convincingly answer the question so any answer must be somewhat speculative.

I'm going to give a tentative answer full of speculation and guesswork, but it's too long to fit in a comment so here goes.
Sex duration is possibly a sort of human reproductive handicap. Sexual arousal can soften the cervix, increasing fertility during lengthy sex sessions. Lengthy sex exposes them couple to predators and takes time and energy, so if you have the calories to burn you are probably a better mate.
The more orgasms a male has had in the recent past the longer the average sex session takes to ejaculation. This kind of makes sense as an adaption strategy to different frequencies of sexual intercourse (if less sex happens it's more important to ejaculate quickly, if more sex happens you want to get as much fertility out of the sperm you produce as possible).
Comparing testicle size and penis size to other primates, humans have a large penis and relatively small testicles(compared to chimps, say) which implies we spend more energy on the sex and less energy on the ejaculation than chimps. It also implies a lower sexual frequency or smaller ejaculate sizes or larger vaginal depths or really a number of other things.
The whole system kind of makes sense. Long sex durations are a sexual handicap system to show the fitness of partners, which are rewarded with slightly higher fertility. The whole post-sex evolutionary mechanism thing is a layer on top of the underlying mate selection which is beyond the scope of a book, nevermind a stack exchange answer.
That's probably at least a little bit wrong. The handicap principle isn't super well accepted as a general evolutionary principle, even though it explains some things.

-1. For the handicap principle to be valid, potential partners should have a way to distinguish the duration of sex length prior to mating. This doesn't appear to be possible. If partners are unable to distinguish the length prior to mating, no sexual selection takes place.

I think you misunderstand. The selection is performed by the cervix, not by the partners. Longer sex durations (weakly) imply a higher sexual frequency and that in turn (weakly) implies higher fitness. A partner that has a great deal of sex is a good partner, because your offspring are likely to have a great deal of sex. If a sex act lasts a long time, the cervix is interested in increasing the per-sperm fertility for this surprisingly lengthy sex act.


text:
In which of the following diseases structure of haemoglobin produced is normal but their amount reduced?
The options provided are-

Chronic blood loss
Sickle cell anaemia
Haemolytic anaemia
Thallasaemia
Transfusion reactions
               -

*Q-15: pg-785; **Review of Medical Physiology - William F. Ganong;    International 22nd Edition***
Here, the answer provided is (4), i.e Thallasaemia...
My point is that, Thallasaemia is essentially a genetic defect resulting in mutation of either alpha or beta or both the chains, thus rendering the structure of haemoglobin fragile....the disease as far as I know don't cause any reduction in blood volume...
According to me option (1) i.e chronic blood loss is more feasible as in case of diseases resulting from nematodes like Hookworm (Ancylostoma duodenale)....
So, where am I wrong???

It's a misleading question, and I agree that Thallasemia is the wrong answer.

1, 5 and sometimes 3 too (based on what is causing hemolysis) can be correct @anongoodnurse

You are correct, Thalassemia is the wrong answer.
In Thalassemia and Sickle Cell Anemia, the structure of Hemoglobin is altered.

Chronic Blood Loss: Here the hemoglobin and packed cell values will be low, however there is no alteration in structure of either RBC or Hemoglobin
Hemolytic Anemia: This is a host of conditions which can cause hemolytic anemia. Some mechanisms where Hemoglobin structure remain normal would be:

The structure of RBC membrane is altered, this will make RBCs less maleable and cause early destruction - Example: Spherocytosis
G6PD Deficieny - In this the deficiency of G6PD will decrease the ability of Red Blood Cells to handle oxidative stress and when subjected to sudden oxidative stress, hemolysis will occur. Here the structure of both RBC membrane and Hemoglobin are normal.

Transfusion reaction (I am talking about only hemolytic transfusion reaction, there are other transfusion reactions too): Here the problem is the host reaction to transfused Red Cells. The host was initially severly anemic (Therefore low Hb) for which transfusion was done, now the host immunity is reacting against transfused RBCs which have normal Hemoglobin, resulting in reduced RBC counts and Hemoglobin. So this too can be taken as a correct answer as the end-result will be severe normochromic normocytic anemia.

Well-formulated answer+1


text:
Are brassica oleracea cultivars the same species?
I used to think Brassica oleracea cultivars (e.g., kale, cabbage) were different species originating from the same species Brassica oleracea.
But it seems I were wrong, right?
If so can we breed two different cultivars with each other, e.g., cabbage + cauliflower?

Cultivars are, per definition, the same species of plants. Animal breeds are the same species too, think of the bewildering phenotypical variety of dogs for example; they are still the same species, i.e., Canis lupus.
To your question - Yes, cabbage, broccoli, cauliflower, and Brussels sprouts are the same species.
Hybrids of these plants are called cultivars; broccoli and cauliflower yields broccoflower for example. However, I wasn't able to find evidence of a hybrid between cabbage and cauliflower - a cabbaflower?

These are the same species. There are people working on new cultivars. This species can also cross with some of the other brassicas - search for 'The Triangle of U' for further information on interspecific hybrids in this group.


text:
Why are local field potentials generally band-pass filtered?
I was wondering what the rationale was behind low-pass or band-pass filtering in local field potential measurements?
It seems to me that we could potentially filter out potentially valuable information by filtering procedures.
Is there a physical limitation for this that would not allow to measure, say, the responses in a frequency range of 0 to 5 kHz?

There is no physical limitation whatsoever on the frequency band you wish to record, other than the hardware limitations on the sampling rate.
Often electrophysiological recordings suffer from noise (mainly in the high-frequencies) and drifts in the baseline (low-frequency range).
In the end, you wish to filter out as much noise as possible, without throwing away the baby with the bathwater. In effect, prior knowledge about the frequency range of the responses of interest are vital. Anything outside that range can, and likely should be filtered out.
For example, FFT analysis of EEGs mainly focuses on bands limited to the frequency range of 1 to 50 Hz. The mains frequency is 50 or 60 Hz, often imposing sinusoidal noise when the room is not shielded. Hence, what reason would there be not to use a low-pass filter with a cutoff around 50 Hz to get rid of it?
Lastly, offline filtering methods are aplenty. My personal preference nowadays is, is to collect the raw data and filter offline. That way you have the baby and the water, and you can focus, with trial and error, on where the baby is and where the water.

Coming to my rescue once more!

This is a nice answer. I remember an EE prof. who said a lab procedure they used to give grad students required them to recognize that noise from florescent lights would ruin their results unless filtered.


text:
Why is stimulation of nerve tissue with a negative pulse called "cathodic" stimulation?
By definition, the cathode is defined as the terminal through which current exits a polarized device. But in the context of neuromodulation, such as spinal cord stimulation, deep brain stimulation, the "cathodic" pulse refers to a negative current pulse that elicits action potentials. A negative current is by definition a current flow that enters the electrode.
Can anyone explain where this terminology comes from and help me resolve this apparent contradiction? It's driven me mad for the past years.

The answer to your (excellent) question is a matter of definition, which has its roots in the 18th century.
A cathode is the electrode where conventional positive current leaves a current source. Conventional current is positive, due to historic reasons. Around 1750, Benjamin Franklin described the flow of current between wool and wax after electrostatically charging the former. He defined the flow of current as being positive, flowing from the surplus side (which he defined as positive) to the current sink (defined as negative). This unfortunate choice is sometimes referred to as the Franklinian approach to electricity, and is still widely used today to describe electronic circuits and referred to as the conventional flow notation (Fig. 1) (Efron, 1960).

Fig. 1. Franklinian approach: the conventional flow of current still in use today for electronic circuits. Source: All about circuits.
The electrical current was only later found to consist of negatively charged particles, namely electrons. The work of Luigi Galvani on electrical stimulation in frog muscles around 1780 and the invention of the electric battery by Alessandro Volta in 1800 eventually led to the discovery of the electron in 1897, attributed to J.J. Thomson and his work on cathode rays shown in Fig. 2. As the figure shows, the true flow of electrical current is the reverse, namely an electron current flowing from from negative to positive. In the meantime, however, the convention of positive current flowing from the positive pole (cathode) to the negative (anode) was already established. Note that this holds for a discharging device. In a charging device, such as the battery, the cathode is negative, and the anode is regarded as positive.

Fig. 2. Cathode ray showing electron flow. Source: TutorVista
Hence, in a stimulating (discharging) device, the cathode is in truth negative, because it is the source of negative current (electrons). Cathodic stimulation therefore means electrical stimulation with a negative current. A cathodic pulse is therefore injection of a negative current pulse.
Reference
- Efron. Chapman & Hall London, Rider Publisher New York (1960)

Thanks for this @Christiaan . You write that the positive pole is the anode, is this a typo (in all my electronics courses, confirmed by Wikipedia, the cathode is the positive terminal)?. I do however understand what you mean. This leaves me to assume that in biology or neuromodulation, the cathode is defined as the terminal through which the "charge" leaves the device? In this case it would indeed be the negative terminal. So basically, in electronics we still use the conventional definition of current flow, whereas in biology we use a more accurate, charge based definition?

@Moppentapper No worries, and yes, it was a typo - and corrected. And yes, your comments are correct. In Bio the 'real' situation is used, because it is important to know what really happens in a prep; negative current has often opposite effects over anodic stimulation.

Excellent @Christiaan thanks so much. It's incredible how simple things are made confusing when different conventions are used!


text:
Is an athlete's heart rate after exercise greater than a non-athlete
I was just wondering
And if it is greater or lower how does this benefit an athlete
Also what is the averaged number of heart beats per minute

Do you mean for example a) if a trained 5 k runner and a regular person both ran 5 k in the same time, or b) if a trained athlete and a regular person both exercised as hard as they can. For your second part, do you mean are people with lower natural heart rates more/less able to become athletes? Also for your third part, do you mean resting heart rate?

If they both ran througsame distance

For second part if persons with a lower heart rate better abled to become athletes and for the third part the resting heart rate

The answer is that resting heart rates vary a lot.  Typical rates can be found with Google.  For an active person or athlete, capacity increases with training (that's what training is FOR), so (all else being equal) doing the same distance/time causes less increase in pulse rate.

@ user21887- The Heart can only endure a certain amount of pumps and then it fails, So speeding up the limited amount of pumps just for exercise is only shorting your life expectancy in reality.

@ user21887- Look into how many deaths occur in Soccer from heart failure, Those guys were in absolute great shape, How did they have a heart attack? They used up there limited heart pumps from years of extreme exercise and died a rather premature death in my eyes. If only they knew it was self involuntary.

Whilst exercising, the heartbeat of a non-athletic individual is faster than that of an athletic individual. The untrained heart beats faster, but less efficiently than that of an athlete. Both the maximum, and the resting heart rate of an athletic individual are lower than the average heartbeat. In a non-athletic individual, the heart rate when resting is about 60 to 90 beats per minute, whilst in athletes it can drop below 40 beats per minute.

When you exercise, the heart works harder when other muscles in the body pump more blood back to the heart. The major muscles of the legs have large veins that will fill during the relaxation stage of the movement, and the muscle contraction in the active movement pushes the blood back into the circulatory system. Increasing blood flow triggers a faster heartbeat. Because the heart muscle of conditioned athletes enlarges and strengthens, the hearts of athletes pump more blood per beat. 1


text:
How are smell and taste in fish differentiated?
The senses of taste and smell in different fish classes are described as two distinct senses; smell is mediated by the nasal openings, and taste by epithelial taste buds.
They are both forms of chemoreception and therefore it is not clear to me what intrinsically defines them as two distinct senses. The more so because reception of chemical substances is mediated by water.
What defines them as different senses? Is it only the difference of receptors that defines them as two distinct senses, or are there other reasons to differentiate them?

One difference is that they are controlled by different parts of the brain. But both are GPCRs and perhaps have common evolutionary origins. I am in a hurry now so cant look up the answer but I can point you to this article that talks about functional difference between olfactory and gustatory response towards the same chemical.

@WYSIWYG - I hve waited a month before answering, but I am assuming you have other priorities now as a mod. I hope you don't mind me taking this opportunity to answer this interesting question  :)

@AliceD No problem at all. You can add my comment in your answer if you want. That article was not accessible to me then.

Short answer
One way to distinguish between the olfactory and gustatory system in fish is by their  anatomical differences. For example, olfactory receptors are clustered in the nasal region, while gustatory receptors are scattered in the head region and beyond. In turn, olfactory information is sent via a single cranial nerve to the brain, while the gustatory system includes three cranial nerves.

Background
The olfactory and gustatory system both receive their inputs through chemoreceptor cells. The chemoreceptor proteins in both systems are G-protein coupled receptor systems. However, the olfactory and gustatory systems are anatomically separated.
The olfactory end organ is in fish comparable to that in humans, namely sensory epithelia situated in nostrils. The olfactory receptor cells form axons that are grouped into the olfactory nerve (cranial nerve I). The nerve innervates the olfactory bulb, where its axons synapse onto mitral cells. Mitral cell axons group into the olfactory tract that projects to the telencephalon in the brain.

Schematic of olfactory system of a fish (not all structures shown). Source: Global Warming Australia.
The gustatory end organs are less well anatomically localized. The taste buds can be found in various structures including gills, barbels, fins, oral cavity and pharynx, dependent on the species. Unlike the olfactory system, gustatory information is transmitted to the brain via three separate cranial nerves: facial (cranial nerve VII), glossopharyngeal (cranial nerve IX) and vagal nerve (cranial nerve x). Normally, the facial nerve innervates taste buds on the extraoral surface, the glossopharyngeal on the anterior part of the oral cavity, and the vagal nerve on the pharynx. The facial and vagal nerves respectively terminate in the facial and vagal lobes in the medulla. The glossopharyngeal nerve terminates in a dorsal medullary region between the facial and vagal lobes.

Reference
- Hara, Rev Fish Biol Fisheries (1994); 4: 1-35


text:
Are aquatic filter feeders effective at cleaning water to a safe level?
I've been raising Daphnia magna cultures over the last few months as feedstock for freshwater aquarium fish. From my reading, Daphnia feeds on bacteria and single-celled algae, as well as other small crud suspended in the water column.
Practically, yeast or soy flour can be suspended in water and poured into a tank containing a population of Daphnia, and the critters usually clear the water in a few days. The clarity of the resulting water is quite impressive. Which leads me to...
My question: How effective are these types of organisms at removing harmful bacteria and substances from a volume of water? Lets say you only needed a few gallons of clean water each day, could you have a tap that drew from a tank containing a dense culture of Daphnia, and use that water as drinking water?
I've not found information that studies the quantities of bacteria in the water column before and after introduction of Daphnia or other filter feeders.
P.S. I thought about posting this question in the Sustainability SE but figured I'd get more accurate information here.

Great question. +1. I slightly edited your post. It was great, but I thought to add a link to wikipedia and do some formatting. I removed the cooking part, because boiling water to cook typically kills all microorganisms in the water anyway. It's definitely on topic here.

My answer from the top of my head is that they will not be very effective at cleaning the water. One reason is that if the substances and organisms are harmful to the filter feeder as well, they will avoid eating them or they will die from them or have their health reduced. In either case they will be filtering less.
Another reason is that if you use the tap and replenish the water with new contaminated water regularly, the filter feeders will probably not filter all water in the tank, and the outflow from the tap will still contain the contaminant. This is certainly the case if the tank is also the culture vessel for your filter feeders. In this case, the tank has come close to being a continuous culture. There are decades of science (including R* theory) which show that resource levels in such systems settle at a positive level (and you propose that the harmful micro-organisms are used as resource or at least eaten in proportion to the resource if the filter feeder cannot be selective). This positive level will then thus also be present in the effluent from the tank (your tap water).
An alternative is to grow the filter feeders in a dedicated tank, and than add them later in high concentrations to your drinking water. This would not be efficient because you need to feed your filter feeders with something.
Finally, the harmful substances may be absorbed by the filter feeders, but also be excreted, in which case the will end up in your drinking water anyway.
For getting rid of the harmful micro-organisms, it is probably more efficient to boil your water!

Great links and information, thanks. I clearly have more reading to do. I suppose a common example of a functioning chemostatic continuous culture system would be a biofilter for a common aquarium, where ammonia-enriched water is fed into an environment full of bacteria that metabolize the ammonia into nitrites and nitrates?

Yes. Continuous cultures (e.g. chemostats) have a continuous supply of resources (nutrients/food), as opposed to batch cultures, in which resources are added in batches. Because continuous cultures are easier to model, lots of theory is derived from them. Batch cultures come close to continuous cultures if resources are added often in small batches, as opposed to rarely but in large batches. So chemostat theory may apply to batch cultures as well.


text:
What is the fastest marine mammal?
When I did a research, most of the sources say that orca is one of the fastest. But I could not find a source that says it is actually the fastest.
Some sources say that Dall's porpoises rival orcas in speed. And there are other kinds of porpoises and dolphins that comes into question.
Is there any scientific research with measurements? Or does anyone have any detailed knowledge about this topic?
(Also it would be nice to know top 10 fastest marine mammals, so the question becomes: what are the fastest marine mammals?)
Note: This scientific research might be difficult to conduct also so you can explain the situation as well.

This article by R. Aiden Martin doesn't have citations, but is a great read with a lot of detail on observations and mechanics of animals moving in water. If you trust the numbers the author gives, the top 10 marine mammals in terms of speed (in mph = 1.6 km/h) are:

Dall's Porpoise (Phocaenoides dalli), leaping   34.5 mph
Killer Whale (Orcinus orca)  34.5 mph
Shortfin Pilot Whale (Globicephala macrorhynchus)   30.4 mph
Blue Whale (Balaenopterus musculus) 29.76 mph
Fin Whale (Balaenoptera physalus)   25.42 mph
California Sea Lion (Zalophus californianus)    25 mph
Pacific Spotted Dolphin (Stenella attenuata)    24.7 mph
Common Dolphin (Delphinus delphis)  23.6 mph
Bottlenose Dolphin (Tursiops truncatus) 17 mph
Pacific Whitesided Dolphin (Lagenorhynchus obliquidens) 17 mph

As noted in the article, higher estimates of speed for, for instance, the common dolphin may be in fact records of them 'surfing' on the bow wave of boats (not propelling themselves through the water).

It's interesting that the common dolphin is 23.6mp/h here, and 39mp/h in @jarlemag's answer. I have a feeling the fastest marine mammal might depend on who is the observer and how the measurement is made!

According to the MarineBio conservation society, the fastest marine mammal is the Common Dolphin, with a top speed of 64 km/h. That places it just above the Zebra on the Wikipedia list of fastest mammals. (I wasn't able to find a primary source for this immediately, so take it with a pinch of salt.)

Thanks. I don't know how I missed that. It would be nice to find out top 10 also.

Interesting factoid! Incidentally this is dwarfed by the fastest fish. The sail fish for example can get up to 110km/h!

Dall's porpoise and orca are the two fastest cetacean species (whales, dolphins, and porpoise), but Dall's porpoise reach those speeds during shorter sprints while orca can sustain those speeds over longer durations.  Dall's porpoise are known for their "rooster tail" splash as they sprint to approach a ship to bow-ride.  The speeds provided by Oreotrephes look reliable as they are similar to speeds described in the Encyclopedia of Marine Mammals (Editors W.F. Perrin, B. Wursig, J.G.M. Thewissen, 2002).  Some of the speed research on smaller dolphins comes from systematic studies of trained dolphins while values for wild animals come from radio-tagged animals, theodolite tracking, or measurements of boat speeds for ships traveling at a similar speed to whales.

Hi and welcome to Bio.SE. Thanks for posting. However, please provide support/citations for your claims. Unsupported posts (or posts mentioning but not fully citing sources) come across as opinions and are best reserved for comments. We have high expectations of good answers on this site to help avoid the spread of misinformation. Please consider revising your answer to provide some sort of support to attract more positive attention and to better (and more accurately) inform our future visitors. Thanks!


text:
Why do humans cook animal meat
Why do humans "need" to cook animal meat?
It seems there's an aspect of safety to it: are other animals (eg, house cats, dogs) not vulnerable to the same diseases we get from modern food processing of meats?
But it also seems there's something else to it: is raw animal flesh is harder to digest for us, no matter how fresh or processed?
I've read so many conflicting things about it, like how cooking is really a way to avoid disease, but that the human body is capable of processing protein from raw meat just the same. An example is how other countries eat raw meats that Americans would not. But then I've also read things about how cooking meat is what allowed humans an energy advantage early in our development as a species (I'm not clear how more calories are "unlocked" by cooking) or how denatured protein plays some role in usability. I also know that my person experience with raw meats doesn't help me understand it, because sushi seems to be fine but raw eggs will upset my stomach.

Possible duplicate of Why cooked food considered nutritious if proteins decompose at much lower temperatures?

Because in general (sushi &c excepted), it tastes a lot better?

Humans do not "need" to cook food, but in general cooking food facilitate digestion and absorption of nutrients.
Heat cause denaturation of proteins. Once denatured, proteins are more susceptible to the enzymatic digestion. Thus, more nutrients are absorbed. There are also macroscopic phenomena in play, for example, a cooked piece of meat is more tender than the raw one, making mastication easier and less energy consuming.
The fact that you may feel your stomach upset because of raw food is probably due to the fact that you were never used to it. Your intestinal flora has been selected during the year to deal with the food you usually eat, any "new" food may cause the same symptoms. Humans that eat regularly raw food will not feel the same way.
Generally speaking, cooking food help killing bacteria, so your body does not need to deal with lots of infections that would occur otherwise. This, on the other side, makes your body weaker compared to the one of a wild animal, for example, that is used to deal with such bacteria. Of course, many animals also die because of food poisoning or food-related infection, only the "stronger" survive so there is a strong selective pressure in wild animals to have "a strong digestive system" (and a strong immune system as well). This selective pressure is less pronounced in modern human society but it is still present in less modernized areas.

Taste is relative. Some likes raw food more than cooked one.