What's the mechanism or structure responsible for new species genetic code generation? I always had this question in mind. I think, If humans find answer to it then we can trigger the next evolution of human specie.

What is the mechanism or structure responsible for evolution ? I don't mean the nucleus and the genetic code. because it's the consequence (the result) of evolution.

I mean all that I found right now as studies materials, treat only the consequences of the evolution, similarities between ancestors and descendants..etc

But what process triggers this evolution ?
For example, the birds ancestor (which couldn't fly ), how did his cells generate genetic code to build new proteins needed to build new protein structures and organs and also to keep this evolution's result for next generations ?

Is there any current research on this matter ?

Thank you All for your explanation, but they treat only the case when there is only a certain length ADN chain and this chain will change in time to produce let's say "more effective population ".

but if we say that all the species came from one cell. than this cell had necessarily less ADN then we have now (for ex: it doesn't have yet ADN to code for hemoglobin and other complex proteins)

So my question was Where did the new ADN came From ?

This question came to me, when we were studying bacteriology and one bacteria had all my attention, it's the staphylococcus, they produce a coagulase that trigger the coagulation process to stop the blood stream so the phagocytes and immune cells can't reach there position.

Random mutations ? well random process can have some result in variation and deletion of existing species, but not in building new ADN chains.

don't tell me that the staphylococcus acquired the ability to produce this protein randomly, because if we do some math, the ADN is a base 4 code (there is 4 bases) and to produce an amino acid we will need 3 bases, so for 30 A.A protein we have only one chance in 4 power 90 without adding the random length and the random 3 dimensional structure, I know, even if there is billions of staphylococcus that will mutate all the time there will be nearly 0 chance to produce a protein that can action exactly with the prothrombin.

that's only for one protein.

I Know I have moderate knowledge in biology but I don't believe that errors in a code (mutations) can make it "better" or produce functioning mechanisms that can interact with other organisms, because if we say so, then we are just insulting our intelligence as human being, because we are saying that random process is making organisms that we, with our brain can't reproduce, the proof is we are still using antibiotics and didn't make our immune system more effective.

I strongly advice to have a look at an introductory source of information on evolutionary biology (such as Understanding Evolution by UC Berkeley). It will give you much more information.

Locus and Allele

Here are two definitions to start with:

A locus is a location on a chromosome. This location can be of any size. It can be a single nucleotide, a codon, a whole gene or even longer.
An allele is one variant at a given locus. When considering relatively short loci (say 1 nucleotide or 1 base pair (bp)), then the majority of loci have only one allele.

What is evolution?

Evolution is defined as any change in allele frequency in a population over time.

There are a number of "forces" that affect evolutionary processes. I picked the 3 most commonly considered: Mutations, Natural Selection and genetic drift

Natural Selection

Natural Selection is the process by which variants of genes called alleles are selected and therefore increase in frequency. This selection result from a differential reproductive success.

Natural selection occurs whenever the three following conditions are respected

Individuals in a population varies in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

In such situation natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.

You may want to have a look at this post (although it might be too advanced) to understand the concept of heritability.

Mutations

In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen that other but in any case the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of "if a trait would be beneficial"), then a mutation will occur to make this trait existing is wrong. Note that most mutations are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to raise in frequency in the population.

Mutations can be a simple a "small change" such as nucleotide substitution, an nucleotide insertion and deletion or can be a "bigger change" such as a chromosomal duplication/deletion, a whole genome duplication and the duplication/deletion of a long sequence.

Mutations create the genetic variance on which natural selection selects the best variants. As a consequence natural selection decreases the genetic variance while mutations increases genetic variance.

Genetic drift

If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency deterministically. An intuitive explanation of what is genetic drift can be found on this post. It will also allow you to understand why small population undergo more random change in frequency of their genes than are big population.


Is life expectancy linked to intelligence in animals? For example, animals that live only a few days or a few years are often not very intelligent. In contrast, the most intelligent animals seem to live longer.

Is this true? Are there any studies to prove or disprove this statement?

Limiting the conversation to mammals, and taking relative brain size as a proxy for intelligence (which, of course is not necessarily "true", but at least is quantifiable), the answer is yes: body-size relative  brain size correlates with   body-size relative longevity in mammals.

  using a global database of 493 species, we provide evidence showing that mammals with enlarged brains (relative to their body size) live longer and have a longer reproductive lifespan (González-Lagos et al.).

They present data by species in the paper, which is available free online, but so as to have something on SE, I've mocked up a chart based on the averages they give for each mammal order:

 González-Lagos C, Sol D, Reader SM. 2010. Large-brained mammals live longer. Journal of Evolutionary Biology 23: 1064–1074.


Hardy-Weinberg principle The following paragraph on Wikipedia about the Hardy-Weinberg principle is bothering me.

It should be mentioned that the genotype frequencies after the first generation need not equal the genotype frequencies from the initial generation, e.g. f1(AA) ≠ f0(AA). However, the genotype frequencies for all future times will equal the Hardy–Weinberg frequencies, e.g. ft(AA) = f1(AA) for t > 1. This follows since the genotype frequencies of the next generation depend only on the allele frequencies of the current generation which, as calculated by equations (1) and (2), are preserved from the initial generation:

Why is it so that the genotype frequencies are dependant on the previous generation, but not in the case of the first as compared to the inital generation?
https://en.m.wikipedia.org/wiki/Hardy%E2%80%93Weinberg_principle#math_1

I can't think of a more succinct way to phrase it than the explanation in your post.

"...the genotype frequencies of the next generation depend only on the
allele frequencies of the current generation..."

The genotype frequencies still do depend on the initial generation, they just depend on the allele frequencies of the previous generation, not the genotype frequencies. For example, an initial generation consisting of only (XX) and (xx) genotypes will produce F1 offspring with (XX), (Xx), and (xx) genotypes through random mating. Since the (Xx) genotype frequency was 0% in the initial generation, and >0% in the subsequent generations, it can't be equal that of the initial generation. But it will still be a function of the relative frequencies of the two alleles in the population, (X) and (x).


What kind of spider is this from Sydney, Australia? I was cleaning the pool when this guy crawled on my foot. I hit him away and noticed a bite mark. I managed to snap a photo of him.

I went to the doctor because I was worried it was a funnel web and she told me to just keep an eye on it, ice it and take anti histamines if it itches.

I have a tiny bit of tenderness in my foot.

Good news is that this is definitely not a funnel web spider (Atracinae), which, by the way, is not that dangerous✻.

The image doesn't have a good resolution, but that seems to be a spider from the Family Lycosidae, known as wolf spiders, more specifically Venatrix pictiventris.

Here is an image for comparisson:

Source: http://www.findaspider.org.au/find/spiders/497.htm

This is the distribution of Venatrix pictiventris in Australia, going from Tasmania to Queensland, with most observations in New South Wales:

✻ I advocate for the protection of sharks, spiders, snakes, bats etc. So, whenever I can, I try to demystify arachnophobia. People love saying that the funnel web is deadly and so on, but for you to have a better idea, moths (e.g. Lonomia) kill more people than spiders.


What exactly is a centimorgan? Centimorgan's aren't physical distances. The analogy that I could come up with is if you had an array with 10 items,

A = [a, b, c, d, e, f ,g ,h ,i ,j, k]

The distance of a in the array is closer to b than k, ie A[0] is closer to A[1] than A[10] so that the centimorgan of A[0] and A[1] is less than A[0] and A[10]?

I personally like to talk in Morgan (M), instead of centiMorgan (cM), because the Morgan has a more intuitive meaning than one-hundredth of its value.

Morgan

If two loci are at distance 1M, it means the expected number of cross-over happening between these two loci is 1. If they are at 0.1M, then the expected number of crossover is 0.1. If they are at 1.4M, then the expected number of crossover is 1.4.

centiMorgan

As the typical distance of interest is much lower than the Morgan, we typically talk in centiMorgan.

Rate of recombination

If in a given meiosis, there is 0 crossover between two loci, then the two alleles from the same haplotype will end up in the same gamete. If there is 1 crossover, then the two alleles from the same haplotype end up in different gametes. If there are 2 crossovers between two loci, then the two alleles from the same haplotype will end up in the same gamete.

In short, if the number of crossovers between two loci (which expected value is the number of Morgans) is even, then the two alleles from the same haplotype will end up in the same gamete.

At very low Morgan (say 0.000001M), the probability of having an odd number of crossovers is low and the recombination rate is therefore low. As the number of Morgans increases, this probability of having an even number of crossover approaches 0.5. The recombination rate can therefore never be greater than 0.5.

Physical distance

Note that as the recombination rate per nucleotide varies throughout the genome (and among genders and among lineages), the distance in Morgan between two loci is not a simple function of their physical distance in number of nucleotides. The two are obviously correlated though.

Human genome

In the human genome, the average per nucleotide recombination rate is of the order $5\cdot 10^{-8}$ (Wang et al. 2012). This means that 1 cM is about 1.5 millions of nucleotides.

Highly Related posts

This question has actually been answered several times already. You'll find more information, some drawings and some math at the posts

Recombination frequencies
Genetic linkage greater than 50 centimorgans

For a more introductory post, have a look at

Why do we need two markers to measure a recombination rate?


Did migratory birds' ancestors live in the places of migration? I was studying birds' migration as a type of instinctive behaviour. But my textbook points out that other than for warm climate and easy food, migratory bird migrate to places where their ancestors lived.

Is it a real point? Or the writers just made it up.

Edited for a different consideration: Do birds migrate to and from zones defined only by ecological and climate choice, or do they evolve to migrate away to and from an ancestral home?

Later studies of migration searched for evolutionary definitions of bird migration as opposed to ecology/geography definitions which were the initial focus. Various theories of evolution and migration have been developed, although ice ages and climate change make the definition of a bird ancestral land vague.

If you search google for "sister taxa, migration, evolution" you will find a lot

A study for American Thrush species starts with previous research:

range expansion and speciation for the
evolution of long-distance migration. In brief,
resident, tropical species expand their ranges
into the seasonal subtropics. Further range
expansion into temperate areas due to competition
and other selective pressures creates a partially
migratory species. The partially migratory
birds continue to expand into higher latitudes,
where they breed successfully; migratory behavior
becomes fi xed (Stiles 1980).

It's results for the thrush are very complex, and you can see the map and the conclusions at the end, which state that:

The migratory species tree does not have a clear single ancestor.
The ancestor's range was probably very widespread, over 1000ds of
kilometers.
They migrated by stepping stone, rather than by diet
constraints of being frugivorous versus insectivorous.

http://www.sonoma.edu/users/g/girman/outlawetal2003.pdf
also
http://www.bioone.org/doi/abs/10.1642/0004-8038%282007%29124%5B410%3AASROMM%5D2.0.CO%3B2?journalCode=tauk

The data is erased in history, the migration routes and maps are very complex, the ancestral homeland shifts as forests and boreal ranges change latitude, so it's a balance in between the ability for birds to have fixed ancestral lands, given their great mobility, and the speed of their evolution. For the moment there are some theories on mechanisms and causes for selection by migratory advantage which are not general enough to apply to many clades of bird.

for precise and recent return to homeland:

Yes it's absolutely true, that many birds return to the exact same nest in Europe for example after wintering in Africa, and they also return to the same cliff/forest as where their parents were born, and some species vaguely follow the flocks very broad zones:

One study showed that most swallows returned to the same colony, with 44 per cent of pairs reoccupying the same nest. “This is remarkable given the length of a swallow’s return migration from its wintering grounds in South Africa,” says Rob Robinson, associate director of research at the BTO. Robinson has studied this iconic species’ unusually strong nest-faithfulness, a phenomenon called natal philopatry.

https://en.wikipedia.org/wiki/Philopatry


What is this row of pits along the "upper lip" of theropod skulls? Consider the row of pits visible in the "upper lip" area (and to some extent, the "lower lip" too) of this T-Rex skull at the Palais de la Découverte, Paris (picture from Wikipedia):

I noticed similar pits in a Deinonychus skull a few weeks ago when I visited the American Museum of Natural History in New York:

What are they?

They are called Nutrient Foramen which are innervation of blood vessels and nerves, you see the same thing in reptile and bird skulls (mammals tent to pack it all into one or two large openings). They feed blood vessels and nerves to the gums, lips, and face.

Dinosaurs do seem to have more of them, but size making them more noticable is also a factor. The increase in dinosaurs may be involved with pressure sensitive scales as seen in crocodiles or alternatively something like lips, or both. Here is a great article on them. Paleontologist are hampered here becasue the related animals are birds (who have beaks) and crocodiles (which are entirely scaly). So it is hard to pin down exactly what a dinosaur oral facial anatomy would look like.


Why magnesium ion is needed for activity of G-proteins? I was studying about G-protein coupled signaling sysytem, somewhere they have mentioned about need of Mg$^{2+}$ for acticty of G-protein and related it to increase of cyclic AMP production. On further reading I came to know that the said ion is related to GTPase activity of G-protein, but how does it relate to incresed cyclic AMP production?

Ion can change secondary structure of an enzyme. Magnesium ion is coordinated within certain domains (for example, EF-hand motif) and makes them more ordered. Usually it happens via hydrophilic shell of residues embedded into a hydrophobic one (https://www.pnas.org/content/87/15/5648).

You can reverse it by adding a chelator (EDTA, for example) and protein is more disordered which can affect it's activity.


What kind of detergent should I use in cell culture laboratory for cleaning purposes? I work on establish a cell culture laboratory in the company where I work. All equipment are new and I want to clean lab before I start to work with cells. Is there any special detergent for cleaning cell culture lab?

I can't tell if you're asking about glassware or work surfaces (hoods, benches etc), but...

We use regular old dawn dish soap in my lab because what's more important than the soap you use to wash you're glassware is the water you use to rinse it.  We teach our undergrads the 3-rinse-rule.  After soaping, every item gets 3 rinses with normal tapwater (or until no more suds forms- whichever comes last) followed by 3 rinses with deionized water.  We have DI water on tap which makes things easier.  I remember rinsing some glassware with acetone or other solvents in organic chem lab, but you shouldn't need to do anything like that for TC.

The same principle holds true for work surfaces.  After cleaning, decontaminate with 70% ethanol, 10% bleach, envirocide or any other BSL2 recommended cleaner.


Why do fishes have both a gustatory and an olfactory system? I would like to know if there is a reason why fishes (and many aquatic species) have both an olfactory and a gustatory system. As far as I know, in all fish species the chemoreceptors, organs and neuronal pathways are different for taste and olfaction, but why is it an asset to have two distinct sensory systems for chemical compounds in an aqueous medium ?

For terrestrial animals it makes sense to separate information stemming from remote sources mediated by volatile molecules and from the oral cavity, where the molecules are everything one can find in food. But in aqueous medium this distinction is far less obvious, especially when one considers that in some species there are taste receptors located on the body surface (lips, barbels).

I've read a few articles and this thread describing the physiological and neurological aspects of this separation, but it's not answering my question (and it actually aroused my curiosity even more).

In addition to olfactory and gustatory, fishes have two more chemoreceptor systems, solitary chemoreceptor cells and free nerve endings (Finger TE 1997). Asking why do they have all these chemorecepor systems is 'little bit' difficult in the light of evolution. But we can definitely look at this question by using some comparative studies. Hence, this answer will not give you answer to 'why' but will give you enough information to understand roles of these systems.

Reference provided by you explains much of the mechanism of olfactory and gustatory system. I will highlight the important difference between these mechanisms.

In olfactory system, signal is directly detected and transmitted to Central Nervous System (CNS) by neurons of cranial nerve I (Liu and Zhang 2019)
In gustatory system, signal is first detected by specialized gustatory cells and then transmitted to CNS via cranial nerve VII (Purves D et al 2001)

As both of them have similar function, it has been difficult to assign specific function to specific system due to lack of robust behavioral assays (Hara TJ 1994)*

Nonetheless, there are following functions in different kinds of fishes are preferred by one system over another,

Hara TJ 1994 comment that spatial feeding behavior is supported by olfactory system in contrast to gustatory system which helps in consummatory feeding like turning, biting, snapping and mastication**
Morais s 2016 suggests, olfactory system is involved in kin-nonkin recognition, prey–predator interactions, and territory or homing recognition because it is less plastic while gustatory system only plays a role in feeding behavior.
Discrimination of Pheromones is done by olfactory system (Lastein et al 2014)

From reading all these papers, I can 'guess' answer lies in the physiology of these sensory systems. Following conclusion is mine and I am no expert to tell whether this is correct. So just take it with pinch of salt :)

Fish has to survive in the water which is filled with tons of different chemical signals. So it has to distinguish these signals from each other. Many functions might not need very careful separation of signal (e.g. searching for resources) while other might need (e.g. which resources to eat). Some functions might need quick response (e.g. presence of predator) while other can be delayed for short time (e.g. migration). If you give responsibility to one system to perform all these functions simultaneously, it might get confused when multiple important signals arrive. From this I can speculate that this would have put some selection pressure during evolution so that there are multiple chemosensory systems.

From the literature cited above it looks like, Olfactory is less plastic and less sensitive than gustatory and hence involved in functions where you need little sensitivity to distinguish between multiple signal. While gustatory is involved where you need more specific selection of chemical signal.

*I could not get any recent paper directly comparing these two systems in fish. My hope is now we will be in more favorable place to perform some complex behavior experiments. **I did not understand difference between these behaviors conceptually, but you can look it up if you are interested.


Can oral baking soda effect tumor cells in mice Could anyone explain me please, how exactly (according to research article in Cell journal) adding the baking soda in drinking water can influence the acidity of tumor cells? What about homeostasis and ph buffer systems?

In this article in Cell, discussed in this news source, in addition to a number of experiments with cell lines, a live mouse model with xenograft tumors was used to show the effect of oral bicarbonate on tumor acidification, and support the in vitro results re: the effect of tumor associated acidification on the circadian clock.

How is it possible that oral bicarbonate could make tumors in these mice less acidic? Wouldn't the physiological buffer system prevent any changes to the pH in tissues?

What can oral baking soda do?
If your question is (which I don't think it is):

Does baking soda cure cancer?

The answer is that there is no support for that statement.
If your question is:

Can oral bicarbonate alter the pH of tumors in a mouse model?

The answer is yes.
This effect has been observed in this mouse model and replicated many times
This is an effect that has a been used for a while, and was first demonstrated in this 1999 article in the British Journal of Cancer.  The addition of bicarbonate increases the buffering capacity in the live animal model, preventing the acidification of the tumor. It does not increase the pH of other tissues.
How does this work?
The idea here is not that adding a base increases blood or tissue pH directly, but it increases the amount of a physiologic buffer in a situation where that buffer has been depleted or is insufficient, allowing a better response to a pathologic excess of acid. Your question suggests you believe that an oral acid or base load will not change the pH of body tissues. This is true in normal physiology because there is a robust system of buffers. The primary extracellular buffer actually is bicarbonate. However, in diseased states, the buffer may become depleted or be insufficient. Oral (as well as intravenous) bicarbonate therapy is used in humans in several disease states, including certain forms of metabolic acidosis (Cecil Medicine, Ch 63, 120) and kidney disease (Ch 124, 128, 132). What is happening in these cases, and in the mouse model, is not a change in pH from the normal set point, but an increase in buffering capacity that allows the pH to return to the normal set point.
I would caution, though, that just because oral treatment is used in certain specific forms of acid base pathology, however, does not mean that there is support for the various forms of quackery that use arguments about flushing acids from your body, or using alkaline water as a general health tonic. It does address the question about whether it is very strange that orally administered buffer would impact a tissue with excess acid. It's not (strange).
The effect of changing the pH in the tumor microenvironment
The effect in the study behind the article you referenced, as well as others, is an increased sensitivity to cancer chemotherapy in otherwise resistant tumors. This is not horribly surprising, and doesn't mean by any stretch that baking soda cures cancer or that, e.g., an acidic diet causes cancer.  Other studies, including this one (also in this very particular mouse model), show decreased invasion and metastases, also presumably because of the increased buffering capacity (and decreased acidifcation of the tumor and tumor microenvironments), so there may be other possible effects.
There has been a good deal of interest since 1999 in human studies adding bicarbonate to other treatments, but none have been published that I'm aware of, though I haven't checked the clinical trial registry.
EDIT:
On checking the clinical trial registry, on first glance it looks like some safety and tolerability studies have been completed, but it would take a fair amount to do a full analysis of what has been done and what hasn't. Maybe someone else wants to do it and include it in an answer? I'm fairly certain I would have seen and remembered an article showing that bicarbonate cures cancer in humans, though, so I don't think that's on the list :)


Why does hair thicken and become more rough after a razor shave but not after one using a trimmer? If a razor cuts only the hair, then how does hair thicken and become more rough with a razor shave and not after one using a trimmer? If both are used for hair removal, why is there a difference in hair growth?

I have been using a trimmer for 1 year, but the growth of hair remained unchanged.  When I started shaving with a razor, the hair growth thickened.

Hair does not grow back thicker when it is cut. This is somewhat of an optical illusion because when you shave with a razor it leaves the top of the hair flat rather than pointed so it appears thicker. For instance see this picture:

As you can see the hair is tapered at the top and when cut loses this taper to leave a large cross-sectional area. I would say that for your question with with the trimmer that it is probably cutting the hair further up the taper where the hair is 'thinner' to begin with. A razor cuts closer to the base and thus gives a thicker appearance.
Evidence: http://www.scientificamerican.com/article/fact-or-fiction-if-you-shave-or-wax-your-hair-will-come-back-thicker/
http://www.sciencedirect.com/science/article/pii/S0190962299701817


Why does enteral carbohydrate yield higher energy than parenteral? The following is written in a well-known textbook of surgery:

  Each gram of enteric carbohydrate provides 4.0 kilocalories (kcal) of
  energy. Parenterally administered carbohydrates (eg, intravenous
  dextrose) yield 3.4 kcal/g

What is the explanation for this?

Parenteral carbohydrate is usually dextrose which is actually D-Glucose monohydrate. Monohydrate implies coupling with a water molecule, such that 1 gram contains a lower relative component of glucose, resulting in a lower kcal yield.


will a plant grow faster if it is exposed to concentrated sunlight? I know that plant grow faster depending on the hours of sunlight it has, but what happens if i put a giant mirror focusing light to the plant?.

Will the growth rate be limited by the damage the sunlight produces, or will it be limited by the speed of the photosythesis?

In nature, there is often ample sunlight available to plants. From this NIH page:

  However, even at the maximum light intensity encountered by photosynthetic organisms (tropical noontime sun, ≈1.2 × 1020 photons/m2/s), each reaction-center chlorophyll a absorbs about one photon per second, which is not enough to support photosynthesis sufficient for the needs of the plant. To increase the efficiency of photosynthesis, especially at more typical light intensities, organisms utilize additional light-absorbing pigments.

In other words, plants are not entirely photosynthetically efficient and do not typically use all of the light available to them. From Wikipedia:

  Photosynthesis increases linearly with light intensity at low intensity, but at higher intensity this is no longer the case (see Photosynthesis-irradiance curve). Above about 10,000 lux or ~100 watts/square meter the rate no longer increases. Thus, most plants can only utilize ~10% of full mid-day sunlight intensity.


Can DNA fingerprinting tell you if someone has been genetically engineered? I am writing a fictional novel about an extensively genetically engineered man, unbeknownst to him, who gets into trouble on a regular basis. The man is physically large and strong, very fast (tiger-like hand speed), and he has exceptional sensibilities such as night vision, hearing and smell. The FBI gets some of his saliva from a crime scene and creates a DNA fingerprint from it.

My question/s is: could the technicians/scientists who perform the DNA fingerprinting procedure for the FBI be able to tell that this man is different from other humans? Would it be possible for someone to be human and have a different number of chromosomes? Does all DNA fingerprinting appear as bar codes and mean nothing until compared to a sample?

Please forgive my ignorance on the subject. Thank you for any input.

Chris

Could the technicians/scientists who perform the DNA fingerprinting procedure for the FBI be able to tell that this man is different from other humans?

If by different you mean genetically engineered, it depends on whether the loci tested have been engineered to such an extent that they are substantially different from other humans in order to arouse some kind of suspicion. There are other tests could be done that would show, at the least, that this individual's genome is abnormal.

Would it be possible for someone to be human and have a different number of chromosomes?

Yes, this is called aneuploidy and is the cause of many genetic disorders. Fingerprinting would not detect this.

Does all DNA fingerprinting appear as bar codes and mean nothing until compared to a sample?

DNA fingerprinting looks at sequence length polymorphisms and essentially tells you the length of certain regions of DNA in an individual. In fingerprinting, samples are compared to see whether DNA from two samples come from the same individual. A single sample obviously wouldn't work for this, but that doesn't mean it would tell you nothing.


How to interpret this PubChem record of L-Alanine Using the PUG service from NCBI, I am retrieving 3d structure data for a molecule.

Raw data here.

I am trying to understand this record, specifically for the purpose of rendering in a 3D coordinate system using threejs.

Could anyone please assist in understanding this information.
Due to the large size of the json response and as I am using javascript, I have constructed some Typescript types that describe the shape of the data to assist the discussion. I have specific questions, which are stated below.

//// Root Object
interface JSON_Response {
    PC_Compounds: PC_Compound[];
}

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

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

Atoms

The atoms object has two arrays; 'aid' and 'element'.In the above JSON response, these arrays are both of length 13. The data for L-Alanine shows it has 13 atoms. I am correct in saying that the numbers in the 'element' array are corresponding to Atomic Numbers? And these atomic numbers are assigned to ids from the corresponding indexes in the 'id' array?

Bonds

What are aid1, aid2, and order? These arrays are 12 entries each so each must represent 1 bond between two atoms. But what do the number values correspond to? How should they be interpretted?

Coords

In the coordinates object,

interface Coords {
    type: number[];
    aid: number[];
    conformers: [
        {
        x: number[];
        y: number[];
        z: number[];
        data: Data[];
        }
    ];
    data: Data[];
}

The x, y, & z arrays are of length 13. Am I correct in saying that these represent the x, y, and z coordinates of atoms in the corresponding index of the above elements array?

Data

Data Object seems to be part of a esoteric system for attaching arbitrary data to the object. If anyone has any pointer on this it would be greatly appreciated.

interface Data {
    urn: {
        label: string;
        name: string;
        datatype: number;
        release: string;
        version?: string;
        software?: string;
        source?: string;
        parameters?: string;
    };
    value: {
        sval?: string;
        fval?: number;
        slist?: string[];
        fvec?: number[];
        ivec?: number[];
    };
}

stereo

seems to describe planes of rotation

//// Compound sub-types
interface Stereo {
    tetrahedral: {
        center: number;
        above: number;
        top: number;
        bottom: number;
        below: number;
        parity: number;
        type: number;
    };
}

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

miscellaneous chemical information

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

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

The PubChem format description is not that easy to find:
https://www.ncbi.nlm.nih.gov/IEB/ToolBox/CPP_DOC/asn_spec/pcsubstance.asn.html

And the ASN file linked here:
https://pubchemdocs.ncbi.nlm.nih.gov/data-specification

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

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

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

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

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

Yes

  What are aid1, aid2, and order?

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

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

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

Good examples of implementations:

PubChemPy
pubchem_2d_structure_json_to_svg.py


Western blotting questions? everyone. I've just been introduced to the procedure of Western blotting from my reading, though I'm not entirely sure about some points. I'd appreciate it if someone could help me with this.

What exactly is the function of the blocking buffer?

Why does one need a secondary antibody?

When discussing nitrocellulose membranes, say of a 0.45 5m pore size, what does 5m refer to?

Blocking buffer

Once the proteins in the gel have been transferred to the nitrocellulose membrane it is necessary to coat the rest of the surface of the membrane with an unrelated protein. This is necessary because all proteins will bind non-specifically to the nitrocellulose. Once the membrane has been blocked the only way that antibiody proteins (the probe) will bind to the membrane is via the transferred proteins that they recognise. The usual source of a blocking protein is defatted milk powder, i.e. casein, although some people use (or used to use) bovine serum albumin.

Secondary antibody

In a typical blotting experiment you expose first with a primary antibody directed against the protein of interest, for example this might be an IgG raised in a rabbit. Then in a second step you add a secondary antibody which will bind to the first one - in this case this might be goat ant-rabbit IgG (i.e. anti-rabbit IgG raised in a goat). Why is this done? The secondary antibody is in the form of an antibody-enzyme conjugate, typically with horseradish peoxidase, and the final development of the blot detects the presence of the conjugated enzyme.

Why use a secondary antibody? Two reasons: - firstly, there will sometimes be a degree of amplification if more than one secondary antibody molecule binds each primary antibody molecule; but more important is that it means that it is not necessary to produce an enzyme conjugated form of every primary antibody, which is time-consuming and quite tricky. So in your work you may be studying several different proteins using Westerns, but you will be able to use the same secondary antibody to detect all of them.

Pore size

That should be 0.45 - 0.5 µm. Pore sizes are measured in micrometres.


Identify orange-brown, teardrop-shaped insect in central Europe that was found indoors TL;DR Can someone identify the species of the insect in below picture? Editing of the wording of this question (if possible) to make it easier to find by using search engines is welcome.
I caught this insect and was wondering what species it was:

Here a milimeter-scale and an USB-plug next to it to allow to estimate the size (sorry that they are so unsharp but I hope it is sufficient to get the size):

I was not able to find it by reverse image search or by searching for some keywords using google. I also checked some questions here but did not find any that seems to be about such an insect.
Following description/keywords are added to help someone searching for such an insect to find this using word-search. If someone can formulate this more search-engine-friendly to make this more likely to be found, please edit or add a comment so I can edit it:

Teardrop-shaped
six legs / 6 legs
two antennas / 2 antennas
orange-brown / brown-orange
size about 3mm / 3 millimeters / 0.11811 in / 0.11811 inches (I hope my calculation from mm to in is correct)
if touched by glas or paper, it remained motionless for about 1 to 2 minutes
no wings / not airbourne / walking
able to walk up walls
it was found indoors
the region is central Europe

Many Thanks in Advance.

I think it may have been a tick of some kind, one that had already fed and was round (hungry ticks are sort of flat).  I couldn't say exactly what species.
I'm not sure, but that's the only thing I can think of that matches this photo.  I'm no professional, so another person here may be able to do better.
Ticks have eight legs (they're vaguely related to mites, and, even more distantly, to spiders), so I was puzzled at first by you saying it had six legs, but possibly what you thought were its antennae were its other pair of legs?  (Ticks have no antennae).
https://en.wikipedia.org/wiki/Tick


How to attract spiders to my house? I've been living in my apartment for a year now, and noticed something lately. During spring and summer I have quite a lot of midges indoors, and even now there are some. But there are no spiders! So my question is a bit of the opposite of what all spider/house related articles are about: how do I get more spiders to my house?

Some info about my place: I live in a 40 year old apartment in Rotterdam, Netherlands on the second floor. It's always between 17 and 20°C, and the place is poorly isolated; plenty of cracks for visitors to crawl through. Also, I usually have a window open a bit. I have quite a lot of plants, and an aquarium, so I guess air humidity is relatively high. There is a large backyard with lots of weeds and some trees, however people use it for dumping old furniture so it is not a real garden (it's most likely the source of the midges).

Can I do something to stimulate spiders to come to my house?

Spiders are naturally attracted to areas where preys are abundant, insects are primary source of spider prey. So you must create proper environment for insects in your home,  lights to attract nocturnal insects, flowers to attract butterflies and moths are attracted towards decaying vegetation(It may make your place smelly). Once insects are abundant then spiders are attracted towards these areas. Some parasitic wasps are predator to spiders like those belonging to Ichneumonidae, try to avoid these species. Also you can collect spider eggs and place it inside your home, so they will hatch out in your place.Some times you can see web full of spider nymphs, take it out and place it in your home.
Attracting spider to home can be achieved through buying some spider traps like poison free spider glue, which contains pheromones. Spiders are attracted to it and they will stick on them and eventually die, so you need to be careful and use the phenomenal effect of the spider trap to attract spiders or it will be dead and become useless.
The analysis revealed that the wasp spider pheromone is methylcitric acid trimethyl ester, a derivative of citric acid.
Some other techniques to attract spiders

An unspecified Cheiracanthium species is attracted to the smell of petroleum and has caused problems by weaving webs inside the canister vent of particular models of Mazda vehicles, resulting in blockages and build-up of pressure that could potentially cause fuel leakage from the fuel tank and an increased risk of fire. Mazda issued a voluntary recall of Mazda 6 models built between 2010-2012, to fit them with software which would alert drivers if problems were developing.
Reference

A spider that preys on the malaria-carrying mosquito is attracted to the odour of people's smelly socks, say scientists.
Reference

Eugenol baited traps we found seven individuals of two species of Thomisidae. In contrast, with the control traps, no Thomisidae were caught . Since Thomisidae were caught only in traps baitedwith eugenol, whereas no crab spiders were attracted to control traps, we postulate that eugenol served as an attractant for these spiders.
Reference


DNA replication and combination "Each gamete is genetically unique because the DNA of the parent cell is shuffled before the cell divides. This helps ensure that the new organisms formed as a result of sexual reproduction are also unique."

Then why do we say that the DNA of the parent influences the characteristics of the child while the DNA of the child is formed as a combination of shuffled up nitrogenous and phosphate bases?

To explain it briefly:

Lets take a human as example, you are diploid and you have a pair of 23 chromosomes (= total 46) and the sex chromosomes which I will exclude for this explanation.

Your gamete is haploid and has therefore only one of the two paired chromosomes. So for every chromosome pair there are 2 possible chromosomes. So in total you have 223 possibilites to arrange chromosomes. The gamete from the sexual mating partner also has 223 possibilites to arrange chromosomes. So in total a new diploid organism has (223)x(223) possibilites. So unique.

However, it is always the chromosomes of the parents. So yes, parents influence the children because the genetic information of the children can be found in one of the two parents.

Furthermore you have recombination, but you already asked another question about this. So I will not expand this answer.

There are relevant articles in Wikipedia on genetic recombination and meiosis that I would recommend.


Converting miRNA names I need to convert all of my microRNA names e.g. hsa-miR-30e-5p to e.g. entrez gene IDs, ensemble IDs or another ID. Does anyone know a good ID conversion tool for microRNAs?

(I managed to convert it to miRBase ID e.g. MIMAT0000692, but David does not recognise them apparently)

It seems there're no ids for a mature sequence. You better search for a parent sequence ids. You could check, but it also seems that HGNC ids are -miR-30E- part.
So you could try Ensemble search (you should input names in 'Filter'-'GENE' section) or use Genenames. As you see, it has API, and you could use it programmatically with HGNC ids.


Redheads and pain receptors I remember reading this in a biology textbook, and decided to do a little digging. Redheads have a lower sensitivity to some pain and a higher sensitivity to other compared to people of other colored hair.

Sciencenordic.com and webmd.com note that redheads have a higher sensitivity of pain when it comes to dentistry, yet can tolerate more pain subcutaneously. According to the Journal of the American Dental Association, redheads require more anesthesia due to some mutation in the MC1R gene. What mutation could account for this difference, could this be a point mutation or nonsense mutation?

Source: http://www.webmd.com/pain-management/features/whats-your-pain-tolerance?page=2
http://sciencenordic.com/redheads-feel-different-kind-pain

I think it's best to break this question up in to two parts:

What mutations account for red hair and fair skin in humans
How might these same mutations affect pain sensation

MC1R variants & red hair
The MC1R gene encodes a transmembrane receptor protein (belonging to a very common family of receptors), called melanocortin 1 receptor. It also has another name describing its best known role in the body: 'alpha melanocyte stimulating hormone receptor'.
This receptor binds ligands - both agonists and an antagonist - outside the cell, and passes signals to the pigment-producing pathways in melanocytes; activation favours eumelanin (brown) production over pheomelanin (red).
Common MC1R variants are all single point mutations which cause an amino acid substitution and reduce/impair the normal function of the receptor - i.e. loss-of-function mutations. E.g. Arg151Cys, Arg160Trp, Asp294His, the most common variants in european red-heads probably arose ~80,000ya in a eurasian population, and have a reduced ability to activate adenylate cyclase inside the cell.
How & why could the same mutations affect pain sensation?
Genetic linkage, or dual role of MC1R?
Firstly, it is possible that MC1R variants are linked to a mutation at a separate nearby gene; the two making a haplotype.

In this diagram, mutation A might be a red-hair MC1R mutant, and mutation B might be some other pain-sensitivity mutant. Through random effects on small populations, group Hg B might have 'seeded' the european population, say; meaning that the two mutations are inherited together in that population. If the two loci are very near, their linkage is less likely to be disturbed by recombination.
This is an obvious possibility whenever two seemingly unrelated traits co-occur.
However, there's good reason to believe that this case is due to a dual-role of MC1R...
Arguments against linkage; for dual role of MC1R: The existence of many different haplotypes in redheads argues against linkage, if this pain sensitivity effect is found across all/many redhead haplotypes, and not in wildtype MC1R europeans.

Indeed, this study shows that europeans with 2 MC1R mutant variants (homozygote or compound-heterozygote) have increased pain tolerance to electric shocks compared to people with 1 or more functional copies of MC1R. The second panel shows that a mu-opiod analgesic (morphine) has greater effect on those with no functional MC1R. The effect coincides with presence of functional MC1R, not a particular haplogroup.
MC1R is also expressed in a region of the midbrain responsible for pain modulation. This region produces endogenous opioids to control pain. As far as I can gather, researchers are trying to work out what exactly it does there.
The study by Mogil et al suggests MC1R in the brain somehow counteracts pain inhibition by the opioid receptors, and so MC1R mutant redheads have more effective ex/endogenous opioid pain inhibition, which reduces noxious pain.
This study found that redheads are slightly less susceptible to pain-sensitisation by capsaicin.
Whereas this study found a contradictory result, that redheads are more sensitive to thermal pain and that lidocaine is less effective for them. (This study didn't genotype the subjects, and red-hair may be caused by mutations in other genes.)
Overall, the number of subjects in these studies (both humans and mice) is fairly small; and the science of MCR pain modulation seems early-days.
But at least we can answer your question: the mutations apparently responsible for red hair and altered pain sensitivity are amino acid substitutions in MC1R causing loss-of-function variants.
The fact that MC1R probably has totally different roles in the brain and in the skin is an interesting general point of biology.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1288200/ < about the evolution of MC1R mutant variants.
http://www.ncbi.nlm.nih.gov/pubmed/10403794/ < about the mechanism of loss-of-function
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1736101/pdf/v042p00583.pdf < evidence of increased pain tolerance & greater morphine effectiveness
http://www.scandinavianjournalpain.com/article/S1877-8860%2810%2900111-4/abstract < evidence of resistance to hyperalgesia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1692342/ < evidence of decreased pain tolerance & lesser lidocaine effectiveness


Does evolution produce organisms perfectly adapted to their environment? I have this biology assignment with this chosen topic. I have no idea where to start researching. I have studied the mechanisms and theories of evolution. I just don't know which relates to the topic. The task is to persuade an audience of one side, either yes evolution produces perfectly adapted organisms or no evolution does not produce perfectly adapted organisms. I have started research on the blind spot of the vertebrate eye and that might be case scenario for the topic. If you have anything to add at all that would help me complete this project. It is much appreciated. Thank you in advance!

You should most definitely have a look at a very introductory course to evolutionary biology such as evo101 for example.

  Does evolution produce organisms perfectly adapted to their environment?

There is a lot to say about this question. The question is very broad and cannot be fully answered in a single post. The very very short answer is "no". I will very briefly develop this "no" below.

Concept of perfection

There are semantic (and hence philosophical) issues of the concept of perfection in this question but I shall not go into these issues. Typically, in the fact of sexual selection (and other arms race), the concept of "perfection" becomes very unclear (see S Pr's answer).

There is variation in populations

Evolution is all about genetic variance in populations. The fact that variance exists makes that necessarily there is no notion of perfectly adapted for a population (or for a species) as not all individuals are the same!

"Drivers" of evolution

Evolution is a change in allele frequency over time. There are a number of drivers of such changes, including natural selection, genetic drift and mutations.

While natural selection is a deterministic process, genetic drift and mutations aren't. There is hence constantly departure from a "hypothetical perfect" caused by genetic drift and mutations.

Mutations, while being a "random process" (see Are mutations random?), most mutations are deleterious, hence constantly inputting "imperfection" into populations.


Are all single-celled organisms Bacteria? I read that "Bacteria are one-celled organisms that can multiply by division", are all one-celled organisms bacteria or are there any more narrow definitions?

No, many unicellular organisms are not bacteria. Examples include (but certainly not limited to); some fungi, chlorella algae, and archaea.

Bacteria are one of three domains in the classification of life. You can find more about the bacteria domain at the wikipedia page (It's a long and complex history which is hard to summarise here) and about the domains here. This last defines bacteria loosely consisting of "prokaryotic cells possessing primarily diacyl glycerol (DAG) diester lipids in their membranes and bacterial rRNA, no nuclear membrane, traditionally classified as bacteria."

The composition of lipids in their membrane (DAG-esters) differentiates them from another major class of prokaryotes — Archaea, which have isoprenoid lipids in their membranes.

Initially Archaea was called Archaebacteria. Because of significant differences, including the membrane composition, they are now grouped into a different kingdom.


Complementarity of cDNA Strictly speaking, what is the definition of cDNA?  This confuses me, since usually it is said to refer to DNA that is complementary to mRNA.  Is this correct?  Is it restricted to mature mRNA?

I also find directionality very confusing.  As I understand it, mRNA has a sequence equivalent (less introns, after splicing) to the so-called 'coding strand' of DNA.  Does this mean that cDNA made from mRNA, at least before treated with a DNA polymerase, is also complementary to the original genomic DNA?  Is this the better definition (I have seen this used as well, though the first definition seems far more common).

Lastly, as I understand it each chromosome has a forward and reverse strand, defined by convention, but that the 'coding' strand of a given gene is random.  This seems counter-intuitive... is it just because both strands are equivalent?  Does it introduce complications in terms of the cell 'knowing' which strand is the coding strand for a gene?

The most upvoted reply to this question (http://www.biostars.org/p/3423/) confused me even further.  I feel the same way as 'Onefishtwofish' does, in the replies.  Can anyone clarify?

It's a good question and has confused me as well.

A standard definition of cDNA is that it is a double stranded (ds) product of mature mRNA. I suppose it is possible to get a nascent RNA strand copied into cDNA, but I've never heard of that being done.

Because cDNA is dsDNA, the original strand is made from your mRNA as the complementary strand, but then you dispose of the RNA and make the second strand to get a stable, reproducable molecule. The total dsDNA molecule is what we refer to as cDNA (not a single strand of this material).

consider this simplified DNA molecule:

ATG-INTRON-CTCTAG

TAC-INTRON-GAGATC

this could be transcribed into the following mRNA (corresponding to Met-INTRON-Leu-Stop):

AUG-INTRON-CUCUAG

before nuclear export the intron is removed, making mature mRNA:

AUGCUCUAG

you make cDNA from this:

ATGCTCTAG

TACGAGATC

So, you have both a coding and a complementary strand in your cDNA.

As for directionality on the chromosome, genes can be in either direction (meaning that they can use either strand as the coding strand), but remember that the forces that contribute to transcription are just locally determined (assembly of transcription factors, etc) and pay no heed to what direction they're going or strand they are on relative to any other gene. The strands are labeled as positive and negative, but that's just a reference for orientation. A good place to browse the human (or other species) genome is the NIH's map viewer. Click on a chromosome to see the genes mapped to it. Note the column labeled 'O' is for orientation.


Chlamydomanas are present in Kingdom Protista or Plantae? Chlamydomonas, Chlorella are present in Kingdom Protista as well as  Plantae under division algae.

In which kingdom they correctly belong to?

It is generally accepted now that Chlorophyta are Plantae (see here). They are more closely related to plants than any other group of organism. Protist is a kind of basket term for any eukaryotic unicellular organism that is not an animal, fungi or a plant which is a rather exclusionary definition.

Personally, I think the kingdoms are pretty 'macro' oriented and do not really capture the diversity well of unicellular organisms. If you want to see a bunch of elderly scientist shout at each other over what appear to be arbitrary distinctions, I highly recommend attending the taxonomy session of any unicellular conference


Facultative anaerobic organism While I was studying Cellular Respiration: Harvesting Chemical Energy, I found this question:

An organism is discovered that consumes a considerable amount of sugar, yet does not gain much weight when denied air. Curiously, the consumption of sugar increases as air is removed from the organism's environment, but the organism seems to thrive even in the absence of air. When returned to normal air, the organism does fine. Which of the following best describes the organism?
A) It must use a molecule other than oxygen to accept electrons from the electron transport chain.
B) It is a normal eukaryotic organism.
C) The organism obviously lacks the citric acid cycle and electron transport chain.
D) It is an anaerobic organism.
E) It is a facultative anaerobe.
Answer: E

I wonder why the answer is E not D. How can I know that it is a facultative anaerobe? Do anaerobic organisms die in air?

There are organisms with anaerobic metabolism that tolerate oxygen: aerotolerant anaerobes.  "Anaerobic" refers to the metabolic system.  You cannot be sure of oxygen tolerance based solely on metabolic system.

Factors influencing the tolerance of anaerobic bacteria to oxygen

Here is why this is a facultative anaerobe.

This organism does not gain weight when denied air.  One concludes its metabolism is less efficient.

  Curiously, the consumption of sugar increases as air is removed from
  the organismʹs enviroment

Anaerobic metabolism uses sugar less efficiently than aerobic metabolism in organisms that can use both methods. This means oxidative metabolism is the preferred method.

So:  this is a facultative anaerobe because it can get by using anaerobic metabolism, but two pieces of information show that for the organism, anaerobic mode is less efficient than aerobic metabolism.  Brewers yeast is such an organism.


Variation in deathstalker scorpion I recently encountered a (probable) deathstalker scorpion in the Negev desert in Israel:

However, when trying to identify this species I found that in many/most photos of the yellow scorpion the final segment before the stinger was dark or even black (see the wiki link for examples) i.e., not yellow, as shown in the photo.
Is a black/dark pre-stinger segment an indication of some sort (perhaps venom?), or is it an indication of a separate species, or other? Clarification on this matter is most welcome.

Update - I contacted an Israeli PhD from Haifa University who wrote the following:
"...looks like Andrtoctonus amareuxi (also referred in the past as Andrtoctonus amareuxi hebraeus, Israeli fat-tailed scorpion (קטלן עברי)
the genus common name is fat-tailed scorpion... The color of the last segment of the abdomen before the stinger is not a very good sign alone for species identification, as it is variable in the population and also found in at least 2 other genera/species (in the genus Buthus and in some species of the genus Compsobuthus). Anyway for sure it is not the deathstalker which is easily identified by a marking on the prosoma, behind the central eyes, that looks like a lyre  and the ridges on the abdomen..."

According to the Israeli Scorpions Field Guide, deathstalkers can have also pale metasomal segment V, so a black one isn't a sure identification sign although it is very common among deathstalkers. The characteristic of the Israeli deathstalker are 5 ridges along its back. The species of deathstalker in the Negev (and Israel) is Leiurus hebraeus.


What is the proper format for genus and species names in latin? When using the latin nomenclature for a fish in printed materials (such as Sander vitreus for walleye), what is the correct capitalization of each word?

In this example, should 'S' be uppercase only, or both 'S' and 'V' be upper/lower case?

The correct latin nomenclature is Sander vitreus, with the genus capitalized and the species name in lowercase.  This is known as binomial nomenclature.

  Carl Linnaeus chose to use a two-word naming system [...] binomial nomenclature scheme, using only the genus name and the specific name or epithet which together form the whole name of the species. For example, humans belong to genus Homo and their specific name is sapiens.  The first letter of the first name, the genus, is always capitalized, while that of the second is not, even when derived from a proper noun such as the name of a person or place.

Some scientific naming conventions:

Classification example (for Homo sapiens):


Very introductory online source of information in evolutionary biology We receive quite a lot of questions from layman in evolutionary biology in this site that are sometimes difficult to answer just because there is way too much to say. Why don't human keep evolving? is a perfect example. I often want to give some pieces of information and link to a good source of information for them to get introductory knowledge in evolutionary biology.

Obviously nobody that ask a question on a Stack website want to read an answer of the kind You should read that book!. It is often not really pleasant to read a book, it takes time and the OP that get this answer will likely just forget about their question.

What are the best online resources that offer a very introductory understanding in evolutionary biology?

Either a written course of videos such as Khan Academy videos would do (I haven't watched the evolutionary biology section of Khan Academy though and can't really judge of how good it is).

At least online, I think the single best introductory evolution resource is the Evolution 101 tutorial at UC Berkeley's Understanding Evolution project. The site has been designed by some of the top evolutionary biologists and evolution educators in the country, and does a very good job presenting a basic overview of how evolution works.


What neurons make up the CNS? I generally see it written that there are three types of neurons, classified by projection: (1) sensory neurons, (2) interneurons, and (3) motor neurons. Now, in the CNS, I don’t think there would be sensory or motor neurons, seeing as they connect the PNS to the CNS. Does that mean, then, that all the neurons in the CNS are interneurons? I remember my biology teacher telling me not all neural pathways involve interneurons, so that suggests to me that the CNS consists of other neurons as well. What neurons would these be, if they are existent?

Short answer
Sensory neurons are invariably considered to be located in the periphery. Interneurons and motor neurons are part of the CNS.

Background
There are various classifications possible to categorize neurons.

One classification is the one you mention (Furness, 2000), which is a broad classification based on where the neuron projects to. It divides all neurons in:

Sensory neurons (feed information to the central nervous system (CNS));
Interneurons (are stimulated by sensory neurons and/or other interneurons);
Motor neurons (feed information from the CNS to the periphery).

Sensory neurons are invariably considered to be part of the peripheral nervous system. Their cell bodies are located in the periphery. Their projections may feed directly into the brain. For example, olfactory sensory neurons directly project onto the olfactory bulb in the brain.

Motor neurons include the motor neurons controlling muscles. Their cell bodies are located in the spinal cord, which is the CNS, but not the brain. Here the terminology becomes confusing, as this functional classification uses overlapping terminology with the projectional classification. That's why I, personally, prefer to talk about efferent fibers (away from CNS) and afferent fibers (to the CNS). Especially because motor neuron implies something motoric. In case of neurons driving glandular secretion this is counter intuitive. Efferent and afferent fibers are essentially the same names for motor neurons and sensory neurons. One way or another, motor neurons controlling muscles have their cell bodies in the spinal cord and hence are part of the CNS.

Interneurons are invariably located only within the CNS. Interneuron is also a confusing term, because often they are implicitly considered to be inhibitory. Often they are, but they don't have to be. In the classification scheme discussed, most CNS neurons can indeed be classified as interneurons. For example in the neocortex, 70–80% of the neurons are excitatory pyramidal cells, while the remaining 20–30% are inhibitory interneurons (Markram, 2004). The spinal cord also contains interneurons.

In all, most interneurons are located in the CNS, but not all CNS neurons are interneurons, because motor neurons are part of the CNS too. I agree with 243's answer that the classification scheme is most appropriate for the relatively simple neuronal circuitry characteristic of the spinal cord.

References
- Furness, J Autonom Nervous Syst (2000); 81: 87–96
- Markram, Nature Rev Neurosci (2004); 5: 793-807


What happens to the excess immune cells or WBC in our body? When we have an infection our immune system produces a large amount of white blood cells (WBCs) in our body to fight against the pathogen or parasite. My question is after the immune response has finished fighting the pathogens, what happens to the excess cells and antibodies that presumably are no longer needed? Will they disintegrate themselves, is there a final step in the immune response to dispose of these cells, or are excess of these cells and proteins present as if they are not in excess (they are filtered no more so than when at normal levels)?

The process you are asking about is called the termination of the immune response, and for a long time it was not studied very much for some reason, with scientists preferring to analyze initiation instead. However, this has changed in recent years, and while we still don't know a good deal, the picture is much clearer than it had been a decade or three ago.

Here is a special edition of Immunological Reviews focusing on termination of the immune response. While the site says you need to pay to access each article, they're actually available for free in PubMedCentral, so just look it up there for access. For a very brief overview, this section of the Wikipedia article on inflammation lists some of the mechanisms involved.

In regards to your question about immune cells and antibodies, a couple of things happen. First, the vast majority of responding cells are either "turned off" or directed to commit suicide (apoptosis) by a variety of signaling mechanisms, such as anti-inflammatory cytokines like IL-4, IL-10, IL-13, and IL-35, along with other molecules like TGFβ and IL1RA, soluble receptors to pro-inflammatory cytokines like TNFα and IL-6, or through "death receptors" like Fas/CD95 and others. However, some cells are prompted to turn into long-lived memory cells, which are able to be quickly activated upon re-exposure to antigen, in many cases completely clearing it without the need for a full-fledged immune response (such as one generating fever and sickness).

As for antibodies, like most circulating serum proteins, they are metabolized mainly in the liver and can be excreted via the kidneys. Their half-lives vary by isotype, but can be as long as three or more weeks. This is assisted by FcRn, the neonatal Fc receptor, which recycles antibodies back into circulation, protecting them from breakdown:

FcRn: the neonatal Fc receptor comes of age
Derry C. Roopenian & Shreeram Akilesh
Nature Reviews Immunology 7, 715-725 (September 2007)
doi:10.1038/nri2155


What's the difference between life expectancy of cigarette smoker and general population? Some say that smoking cigarettes will shorten lifespan. By how many years is the lifespan of a typical smoker shortened? What are the common cause(s) of death among smokers? Are there any known statistics for cigarette smoking and life expectancy?

The difference in life expectancy between smokers and non-smokers appears to be at least 10 years on average, in a survey of American adults between 1997 and 2004.

The same paper lists causes of death (higher among smokers than non-smokers, as measured by hazard ratio), although this is not exhaustive: lung cancer, other cancers, ischemic heart disease, stroke, other vascular disease, and respiratory disease have an adjusted hazard ratio of 1.7 or more, with 94% of lung cancer deaths attributable to smoking among female smokers, and 93% to smoking among male smokers.

If you have access, you will probably find Table 2 (hazard ratios) of interest.

Figure 2 shows the survival probability:


What is this insect? And does it eat aphids on plants? I found this insect that looks like a praying mantis on my plant which was infested with aphids. I sprayed neem oil and most aphids died, even one of these praying mantises did. But here in this picture is one and I want to know if it is going to eat the aphids so I can stop spraying neem and killing every bug in the process.

The insect is around 2 centimeters long.

This is in a hot and humid area in the middle east. The plant, I guess, is from the jasmime family. It produces small scented roses (hasn't flowered yet due to the aphids problem).

Based on the head morphology and the upper limb visible on the first picture, I would say it looks like a mantis. The length of the abdomen also confirms the same.

The internet is also full of several non-scientific sources that seem to confirm they eat aphids. Animals will normally learn to avoid bitterness in food as it's a sign of toxicity. I haven't found a lot of information about how bitter are aphids, however mantis are sit-and-wait predators, so they will try most things that crawl their way. Judging by the following pictures (and the article linked at the end), I would say it's very likely:

  Indeed, catching every prey would be a beneficial strategy because of uncertainty in encountering another prey due to a sit-and-wait strategy. By holding prey with its forelegs and gradually eating the prey by chipping away at it, the mantis has enough time to find edible parts of prey and reject unpalatable parts/prey (Reitze and Nentwig 1991).

Sources:

https://en.wikipedia.org/wiki/Mantis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5882761/
https://praying-mantis.org/what-do-praying-mantis-eat/


Are males taller than females in humans? Is there any scientific evidence that in humans males are taller than females? And if so, what is the reason that they are taller (please include genes or hormones that accounts for human growth and how they are affected in males and females)?

Are males taller than females?

Best data I could find come from the Statistical Abstract of the United States (1999) > Section 3. Here is a table reporting the percentage of the male and female population which height is lower than a given threshold

Note that this data collection was done among students in US universities and is therefore not representative of the whole world or even the whole country.

Does height follow a bimodal distribution?

A difference in height between males and females is often used as a classical example in introductory statistic class to exemplify a bimodal distribution as seen in this picture

and on these (a priori fake) data

However, Schilling et al. 2002 argued that while the difference in mean height between the sexes is real, this difference is too small relative to the variance in height within each sex to be clearly depicted on a graph.

Note that I found this non-peer-reviewed paper which shows real data that display a truly bimodal distribution of height.

Genetics of height

The question why are they taller? is very broad. I will just focus to give you some hints about the genetics of height in humans. First, you want to make sure you understand the concept of heritability.

Evoy and Vissher 2009 report a heritability coefficient of 0.8. This estimate is impressively high - only a few phenotypic traits have such high heritability. They also review articles discussing that 50 loci are correlated with variation in height (actually, today, more than 500 loci are known to contribute to height, see the link in AlexDeLarge's comment to this answer). However, these loci are not sufficient to explain the whole heritability observed (common missing heritability issue). Yang et al. 2010 provide evidence that the remaining heritability is due to incomplete linkage
disequilibrium between causal variants and loci of weak effects. In short, height is a highly polygenic trait.

Related post

You should have a look at Is there a genetic reason explaining the difference of the height of male and female? for more information.


Can a blood type O be born from AB and A parents? I have a basic understanding of genetics, and I'm really puzzled by this. My grandma's blood type is A (I don't know if it's heterozygous or homozygous) and my grandpa is AB. Yet my mother is type O.
Grandma says that my mom is 100% my grandpa's child, so how did it happen?
I have a few hypotheses regarding this. Either my grandma is lying, which I find to be really implausible, or there's some genetical anomalies either in my mom or my grandparents.
I suspect that grandma is heterozygous, having the IAi genes for blood type, and grandpa has a weird case of IAIBi alleles, coming either from a failed disjunction which caused both alleles for A and B to be present in one sperm cell, and the i allele to be present in the egg, resulting in the IAIBi genotype. Then, when grandpa had my mom, both i alleles got combined and out came my mom with O type.
My other hypothesis is that mom is heterozygous, either IAi or IBi, but the dominant allele underwent a deletion (or something else) and was inactivated, and as such only the recessive allele remained, giving her type O blood.
Could I get some insight on how this happened? I can't seem to find anything related to it on the internet.

The ABO blood type is controlled by a single gene (the ABO gene) with three types of alleles inferred from classical genetics: i, IA, and IB. The IA allele gives type A, IB gives type B, and i gives type O. As both IA and IB are dominant over i, only ii people have type O blood. [1]
So from this standpoint, normal Mendelian genetics cannot explain the blood-group 0 offspring, given the AB parent.
However, besides errors in testing, the (pseudo?) 0-bloodgroup could be explained by the Bombay phenotype. I don't know the incidence rate in your region, so I can't comment on the likelihood.
To give theoretical background, this would be considered a pseudo 0-phenotype, as the individual genetically does not need to be ii. Instead, the individual lacks another effective enzyme that is required for the A or B alleles to be effective; the blood-type specific sugars (N-Acetylgalactosamin|Galactose) cannot be attached to the red blood-cell membrane, as the anchor of these sugars (called H-substance) is not present.
Finally, to address your hypothesis of a gene-duplication followed by a gene knock-out: There is no need for a preceding duplication. The more probable cause is a single point mutation (or multiple) near the active center of the inherited A/B enzyme, or a nucleotide insertion/deletion in its coding region, causing a frame-shift. A completely (not partially!) inactivated A/B enzyme would effectively represent a novel 0-genotype.


Do cell walls prevent cancer? To my knowledge plants do not have an uncontrolled growth disease similar to cancer. Is the function by which they avoid uncontrolled growth related to their cell wall and preventing damage to DNA/RNA? Is their telomerase special in some way in that it does not indefinitely replicate?

Plants do have uncontrolled tumorous growth. Though in almost all known cases, it is pathogen induced; such as in the case of the bacterium- Agrobacterium tumefaciens. Viruses can also induce plant tumors. Theoretically, the cell wall will pose a mechanical barrier to cell division. Also, cell wall synthesis is an extra biochemical step during cell division. Surely, the presence of a cell wall will disallow any metastasis if it might occur. There is an old article which says that cell wall structure differs between the normal plant tissue and the crown galls (tumor). However, this is with respect to Agrobacterium adsorption sites.

I am not aware of any natural plant tumor or the role of telomerase in plant tumorigenesis. However, there is one paper that says that telomerase dysfunction leads to disorganized growth.


What exactly is neuroplasticity, and can it be demonstrated with a simple experiment? As far as I know, neuroplasticity is about restoring brain functions by moving some functions to other still functional. Neuroplasticity is more prominent in children than in adults.

What are other examples of neuroplasticity that are unrelated to pathologies? Can it be demonstrated by a simple experiment outside the laboratory? Are learning, or simply the getting used to new things examples of neuroplasticity?

For example, after wearing red-cyan goggles, I see a color mismatch for some time after I take off the goggles. Is it related to neuroplasticity or some other thing?

Your question is basically a matter of defining brain plasticity or more broader, neuroplasticity. According to a well-cited paper in Brain (Cramer et al., 2011) neuroplasticity is defined as:

  [...] the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections.

Hence, the term can be, and indeed is used very broadly. A more elaborate definition in the same article should answer you question as to whether learning and habituation can be considered to be associated with neuroplasticity:

  Neuroplasticity can be broadly defined as the ability of the nervous system to respond to intrinsic and extrinsic stimuli by reorganizing its structure, function and connections; can be described at many levels, from molecular to cellular to systems to behaviour; and can occur during development, in response to the environment, in support of learning, in response to disease, or in relation to therapy. Such plasticity can be viewed as adaptive when associated
  with a gain in function [...] or as maladaptive when associated with negative consequences [...]

Your vision example, however, is more appropriately referred to as adaptation. Although it strictly spoken falls under the above definition of plasticity (...reorganizing its... function,  color adaptation is (at least in my opinion) too short-lived (minutes) to be associated with plasticity.

Lastly, as to experiments - Although learning a chunk of material from a textbook as a homework assignment is definitely related to plasticity, it cannot be seen as proof; it is the result of neuroplasticity. Experiments showing plasticity can and have been done with imaging (most notably fMRI) or with electrophysiological approaches (patch clamp studies showing long-term potentiation reflecting learning). These techniques cannot be applied outside the laboratory, as they require advanced and pricey equipment, careful experimental design, and not least importantly ethical clearance.

Reference
 - Cramer et al., Brain 2011;134:1591–609

Further reading
 - Color adaptation: What is the science behind the   inaccurate perception of colors?


What factors must be taken into account for the maintenance of the immunogenicity of ovalbumin antigen? What factors must be taken into account for the maintenance of the immunogenicity of ovalbumin antigen?

If the ovalbumin is aggregated, could we inject it for induction of immune reponse?

Ovalbumin is frequently used in immunology to induce an immune response (see some publications about mice and ovalbumin here.
You usually inject it together with an adjuvans to enhance the reaction. The factors that must be taken into account for its maintainance are the same as for the other antigens, so you should boost this "vaccination" from time to time.


In what circumstances does a mammalian egg copy its DNA? In the 2nd episode of the new Cosmos series, the host Neil deGrasse Tyson shows how the white-furred bear could have evolved (reasonable scientific speculation, of course).

If you haven't seen that episode, here's the link. Great show, by the way.

So, it shows the bears eggs, and then goes on to show how there can happen an error in the DNA copying, that leads to the brown pigment production malfunction. Here's an excerpt from the subtitles text:

- great bears roamed the frozen wastes of Ireland.
- This might look like an ordinary bear,
- but something extraordinary is happening inside her.
- Something that will give rise to a new species.
- In order to see it, we'll need to descend down to a much smaller scale, to     the cellular level, so that we can explore the bear's reproductive system.
..
- Those are some of her eggs.
- To see what's going on in one of them,
- we'll have to get even smaller.
- We'll have to shrink down to the molecular level.
..
- When a living cell divides in two,
- each one takes away with it a complete copy of the DNA.
- A specialized protein proofreads to make sure
- that only the right letters are accepted
- so that the DNA is accurately copied.
- But nobody's perfect.
- Occasionally, a proofreading error slips through,
- making a small, random change in the genetic instructions.
- A mutation has occurred in the bear's egg cell.
- A random event as tiny as this one can have consequences on a far grander scale.
- That mutation altered the gene that controls fur color.
- It will affect the production of dark pigment in the fur
- of the bear's offspring.

From my (not professional but kind of passionate amateur) knowledge of biology, I I was under impression that all of the mammalian eggs are present at birth. But the story depicted in the show involves the (erroneous) DNA copying. I see dissonance there, and I'd like to solve it.

The writers of the show may have been somewhat imprecise either by accident or intentionally to avoid excessive details.

There are several different stages of egg cells, with distinct names for each and for the process that leads from one to the next. The whole process of egg cell creation is called [Oogenesis].1 To quote Wikipedia:

  Oogenesis starts with the process of developing oogonia, which occurs
  via the transformation of primordial follicles into primary oocytes, a
  process called oocytogenesis.[4] Oocytogenesis is complete either
  before or shortly after birth.

To our current knowledge all primary Oocytes are present at birth. The next stage in the maturing process is called ootidogenesis, which produces an ootid.

  The succeeding phase of ootidogenesis occurs when the primary oocyte
  develops into an ootid. This is achieved by the process of meiosis. In
  fact, a primary oocyte is, by its biological definition, a cell whose
  primary function is to divide by the process of meiosis.[8]

  However, although this process begins at prenatal age, it stops at
  prophase I. In late fetal life, all oocytes, still primary oocytes,
  have halted at this stage of development, called the dictyate. After
  menarche, these cells then continue to develop, although only a few do
  so every menstrual cycle.

  Meiosis I of ootidogenesis begins during embryonic development, but
  halts in the diplotene stage of prophase I until puberty. The mouse
  oocyte in the dictyate (prolonged diplotene) stage actively repairs
  DNA damage, whereas DNA repair is not detectable in the pre-dictyate
  (leptotene, zygotene and pachytene) stages of meiosis

DNA replication is completed before Meiosis occurs. So oocytes do not replicate DNA after birth, but they do repair DNA to fix mutations that may occour after birth but before conception. If DNA repair fails, then mutations may persist. So the show would appear to be wrong about egg cells copying DNA in an adult bear, but right in that mutations might occur during its lifetime affecting its offspring.


What kind of bird species is this? Every now and then I got a glimpse of this bird which I'm pretty sure is not native to Northern Germany where I live. There are at least three of these birds around but I usually only see something quick and green somewhere in the trees. I finally managed to get some decent pictures so I'm hoping someone can tell me what kind of bird this is. I'm curious what biological niche this bird is likely to fill and which native species it might compete with.

Almost definitely (I'm not a regular birder) European Green Woodpecker (latin name: Picus viridis) and it is native to your area according to its species distribution map.

  "Green woodpeckers are the largest and most colourful woodpeckers
  native to Britain. They are easily recognised by their laughing
  ‘yaffle’ call, which they use to demarcate their territory. They also
  drum on trees, though the sound is not as resonant as that made by the
  other two British species (the greater and lesser spotted
  woodpeckers). Green woodpeckers survive on a diet of insects and have
  a particular fondness for ants. They return day after day to their
  favourite ant hill to feed." - BBC nature


Why is it cool near the trees? I can understand that trees produce oxygen in daylight but why is the area with vegetation much cooler than the environment's temperature?

Why it can feel chilly close to trees in the evening:

Water coming out of Stomata vaporises, reducing the surrounding temperature.
There is normally no direct sunlight reaching the ground beneath the tree, hence the moisture content of soil is higher, giving it the "chilly feeling"
If there is other vegetation (e.g. grass) growing beneath the tree, then point the first point is repeated for the other vegetation, consequently the combination of point 1 and 2 decreases the temperature noticeably.

An empirical study that estimates the cooling effect of trees from evapotranspiration can be found in Konarska et al (2016). Transpiration of urban trees and its cooling effect in a high latitude city.. In the study, they specifically find a cooling effect at evenings, but less so during nights and at daytime:

With an estimated night-time latent heat flux of 24 W m(-2), tree transpiration significantly increased the cooling rate around and shortly after sunset, but not later in the night. Despite a strong midday latent heat flux of 206 W m(-2), a cooling effect of tree transpiration was not observed during the day.

Why is it more noticeable during the summer?
If the temperature is warm, the atmosphere has a greater capacity to hold water in its vaporous state than if it was cold.
Relative humidity
The ratio between the actual amount of water vapor present to the capacity that the air has at a particular moment. For any given temperature, the air has a particular capacity for water vapor. If that capacity is exceeded, the excess spills out as liquid water.


16s rRNA Sequencing From Gut Microbiome (stool) Do I extract RNA or DNA from gut microbiome (stool samples) if want to do 16s rRNA sequencing?

In general, you extract DNA, then PCR out the 16rRNA coding regions and finally sequence them.
Here some links

http://press.igsb.anl.gov/earthmicrobiome/protocols-and-standards/16s/

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0068739

https://support.illumina.com/content/dam/illumina-marketing/documents/products/other/16s-metagenomics-faq-1270-2014-003.pdf


What species of bird is on this coin? What species of bird is depicted on this coin?

http://www.artic.edu/aic/collections/citi/images/standard/WebLarge/WebImg_000100/139651_846511.jpg

Thanks in advance for your help!

It said to be an eagle.

It looks like a Ptolemy V (204–181 BC):

http://www.bonanza.com/listings/-DD-G-068-Ptolomy-V-Octadrachm-COPY/16293418?gpid=21297750541&gpkwd=&goog_pla=1&gclid=CMWBpbOaxrUCFYx_Qgod6TsA9w

it looks to be a pretty standard motif of that era:

From: http://www.worthpoint.com/worthopedia/alexander-iii-great-336bc-greek-coin-150614256

I agree that this is not really a biology question.. but what the hey.


Chemoautotrophy in large organisms? The major nutritional mechanisms include chemoautotrophy, heterotrophy (including parasitism and saprotrophy) and photoautotrophy. All of these modes of nutrition developed first in prokaryotic ancestors, and gradually, through the course of evolution, these prokaryotes formed complex eukaryotic, multicellular organisms. Some of these complex descendants (the majority of Kingdom Plantae) possessed the photoautotrophic mode and some (the majority of Kingdom Animalia, some of Kingdom Protista & Kingdom Fungi) possessed the heterotrophic mode.

My question is, since all the three modes developed quite early in evolutionary history, why didn't any chemoautotrophic multicellular, eukaryotic organism develop? (Or, if they did, why did they not form a wide-diverse group as the organisms with other two modes of nutrition did.)

(One possible reason could be lesser availability of chemoautotrophic substrates, but I have no proof, nor any argument to support this.)

I've been thinking about this question for a few days and along the lines of @ThomasIngalls comment, the simple answer is that cooperation between organisms has such a huge advantage in selection that any chance a eukaryote would become a chemautotroph would simply not adapt fast enough to compete with those that are already holding these niches.

The chemautotrophs I'm aware of are usually archaeabacteria.  They are optimized to grow slowly and have a large number of genes that can break down the unusual chemical compounds to grow in an inorganic often anoxic environment.  These bacteria have genes evolved from the chemautotrophic earliest days of life on earth.  They live deep within the earth, under ground, in volcanic vents.  There are animals that live in some of these environments, but its simply too easy for these to use the bacteria that are already growing here readily rather then re-evolve the genes to do it by themselves.

Eukaryotes are already symbiotes - they used bacteria to create ATP and photosynthetically fix carbon to the extent that they absorbed them as mitochondria and chloroplasts respectively.  If eukaryotes were under a tremendous amount of selective pressure, some of them might absorb symbiotic chemautotrophs, but without such pressure, it doesn't happen when you are competing against plants with roots and animals that eat for their energy.

Forming systems of organisms is much more stable than having individual species that can do it all.  This question is actually similar to other questions that ask why we don't have metal armor, run as fast as cheetahs, etc.  Evolution doesn't actually create super animals that are completely self contained.  The ones that reproduce the best are the ones that can actually spread out the risk of survival and contribute to an ecosystem.

It kind of makes me think of human beings - the only superorganism on the planet in this regard.  We don't really need to compete against any organism - we are in fact killing most of them out there without really thinking about it.  That might now turn out to be good for us long term.


What would happen if we had a device that produced oxygen inside of our lungs? Hypothetically speaking, suppose there is a device that produces a limitless supply of oxygen. The device is inhaled by a human and is resting inside the (a) lung.

What would hypothetically happen if this were possible?

You might need to narrow your parameters a bit.

Just things to consider:

Our lungs are not hollow organs that can accommodate an oxygen producing machine. They are basically narrow tubes that get smaller and smaller until they end in a tiny balloon-like structure - about 700 million of them. Where would the machine go?
100% oxygen is toxic to the lungs, as it is to many other things as well.
How would the oxygen diffuse to all the other areas of the lung that need oxygen? Diffusion is a complicated process in a structure like the lungs.
from what would it produce oxygen? For example, would it extract it from water? How would the body deal with the loss of moisture from the air in out lungs? Where would the excess hydrogen go?
Hydrogen is highly flammable around 29%. Would we become fire-breathing?
How would the machine not hyperinflate and thus injure the lung?
How would we get rid of CO2? We would still have to breathe in and out.
Etc.


Which of the three is true for insulin receptors? I have seen the following question in a Cell Biology exam:
Which of the following is true"

Insulin has an hydrophobic Signal Peptide and the insulin receptor does not have an hydrophobic Signal Peptide

The insulin is coded by two genes, the insulin receptor has an hydrophobic sequence in the middle of the protein.

Receptors in the ER bound the SRP that is bounded to the insulin receptor, SRP is made of RNA and proteins.

I think that (1) is the right answer. However, people I talked with thought (3) is the right one.
I think 1 is right because I have never seen anywhere that insulin receptor has a signal peptide so I assumed it does not have.
I also think that SRP is a part of the insulin receptor, which is located on the ER (and not bounded to the ER by receptors), this is why I thought (3) is not the right answer.
Am I right, or did I miss anything?

Signal recognition particle (SRP) receptor, also called docking protein, is a dimer composed of 2 different subunits that are associated exclusively with the rough ER in mammalian cells. The surface of the rough endoplasmic reticulum (often abbreviated RER or Rough ER) (also called granular endoplasmic reticulum) is studded with protein-manufacturing ribosomes giving it a "rough" appearance. so i don't think (3) is the right statement.
the insulin receptors is made up of two hormones, insulin and glucagon, are at the center of this signaling system. there is no such things as hydrophobic sequence in the middle of the protein i believe.
also, Insulin is a peptide hormone produced by beta cells of the pancreatic islets and and insulin receptors doesn't have an hydrophobic signal peptide. so i think (1) is the correct answer.
Edit :
https://en.wikipedia.org/wiki/Signal_recognition_particle_receptor
https://www.healthline.com/health/type-2-diabetes/insulin#Function1
www.news-medical.net/health/What-is-Insulin.aspx


What does it mean when you "extract the filtrate with ethyl acetate three times?" "The fermentation broth (600 mL) of each endophyte was filtered, and the filtrate was extracted three times with ethyl acetate at room temperature and further concentrated in vacuo to give dried residues prior to antimicrobial assays"

This procedure is referring to chemical extraction, which is a separation process used in chemistry (and biochemistry) to isolate compounds of interest by using two immiscible phases in which the compound of interest has differential solubility.

For example, in a liquid-liquid extraction, often one of the phases contains a polar solvent like water, and the other phase contains a nonpolar solvent like oil. Water and oil won't mix, but after stirring them together and waiting some time, the more polar molecules in solution will tend to concentrate in the water, and the less polar molecules will tend to concentrate in the oil. Because the phases are immiscible, it is relatively straightforward to separate them once equilibrium has been reached.

Ethyl acetate is a fairly non-polar molecule often used in organic extractions. In the process that you described, the result will be that non-polar contents of the fermentation broth will be extracted into the ethyl acetate, and hydrophilic contents will remain in the aqueous phase.

Because this process is never 100% efficient (the efficiency will depend on the concentrations of the solutes and relative affinity for the two phases), it is often repeated several times to improve the extraction.