What is the conical mouthpart of a soldier termite and what does it do? I'm trying to get a visual understanding of termite anatomy and I'm getting quite confused on the protruding mouthpart area (it looks like a beak) located between the pincers.

What does it do / what is it for? It does not look like a chewing mouthpart.

Further, is it related to the mouthparts of the worker / females termites?

Oddly enough, I found "Conehead" termites with what appears to be a far more profound version of this part (though it might not be) and again I see no purpose for it.

Is there a place on the internet where the breakdown of termites can be found? This would be very useful.

What is between the pincers?

This is actually the termite's labrum. Its quite big in termites. Does not have value in telling male from female.


Basic Local Alignment Search Tool (BLAST) Why would BLASTP (Basic Local Alignment Search Tool) be a poor tool to search for motifs in protein sequences?

Because it has a poor statistical model. It's basically a local alignment tool aided by a fixed-length k-mer index. It estimates homology in terms of sequence identity and while this is often enough to find homology in relatively conservative sequences, the heuristic scoring model doesn't really allow to search motifs. A motif in terms of bioinformatics can be seen as a series of state-switch events, hence you need a model that estimates similarity in terms of likelihood of observing such a sequence of state switches under  your prior state-switch matrix (inferred from a training sample). These models are known as Markov models and people usually utilize Hidden Markov Models to find motifs. There are good popular tools, such as HMMER

EDIT as per OP's comment

  As motifs are locally conserved regions & BLAST also performs local
  alignment then why it should not be able to search for motifs?

A motif is not just a "locally conserved region", it's a specific sequence profile. BLAST doesn't extract any sequence profiles, it wasn't created for that. Given a pair of sequences it simply shows you similar patches. Hence BLAST is simply not the right tool for the task. They made PSI-BLAST for that very sake.
Moreover, many motifs comprise amino acids or nucleotides that can be quite separated in a primary sequence and only get close in a folded (secondary or tertiary) structure. Here your definition of "locally conserved region" fails as does BLAST.
As I've already mentioned, BLAST performs a heuristic local alignment, that is it assumes that two related sequences must contain at least one common k-mer (word) of specific length. This, given a precomputed word index, significantly increases performance in terms of speed and RAM consumption. But similar motifs can be present in non-homologous sequences or in highly divergent sequences that hardly evince any homology, and BLAST won't find anything at all.

BlastP carries out a search for sequence similarity to infer function by comparing an unknown sequence with a sequence that has already been annotated with a function, but structurally similar proteins with different sequences can have the same function because function can be mimicked if the replacing amino acid falls into a similar category as the substituted amino acid. The four major categories of amino acids are: negative charged, positively charged, polar and hydrophobic.

Proteins have many shapes, while the double helix in DNA is the form in which DNA is most often found. Therefore, the structure of DNA is not as important for function as the structure of proteins are for protein function. So you need a tool that can compare the three dimensional shape of one protein to another (in addition to sequence comparison) to make an estimate of how likely there is going to be a similarity in function. The Research Collaboratory for Structural Bioinformatics offers a tool that can compare proteins by sequence as well as by structure. The following screenshot shows the options for comparison under each of these two categories:


Why are antibiotics prescribed with a viral infection like a cold? I've heard both ways; people going to the doctor for a cold and then getting a prescription for antibiotics and those that go to the doctor and told they have ride it out because it's a viral infection.  Do antibiotics really help in true cases of a viral cold?

In general antibiotics don't help with viruses. However, sometimes a bacterial infection may follow a cold virus, so there might be some scenarios in which antibiotics would be needed. However in many cases it could be due to people demanding antibiotics from their doctor.

You can read more here (CDC site): http://www.cdc.gov/Features/getsmart/

Antibiotics kill bacteria, not virus! So it's just plain wrong. If a bacterial infection appears after the cold, then the antibiotics should be prescribed because of the bacterial infection, not because of the cold. There is a serious concern about misuse of antibiotics promoting hyper-resistant bacteria through natural selection, but doctors keep ignoring alerts from WHO and prescribing antibiotics without even knowing the bacterial strain. It's absurd that a doctor should prescribe an antibiotic just because "the patient needs to get some medicine to be happy". In this case he/she should prescribe a placebo, not a real antibiotic (and there's still the point that killing most bacteria in our body destroy one of our defensive lines against pathogens). Confirming this point, according to American Medical Association, medical error is the third death cause in USA. So in many cases, yes, it might just be a medical error.


How can one relate in vitro studies of caffeine (dose expressed as concentration) to dietary intake of caffeine (dose in mass)? Having difficulty making the data in the below charts to apply to daily life. What is the right interpretation and implementation? How are the “in vitro” results of the below charts relevant to levels that cells would experience "in vivo" after the consumption of caffeinated beverages?

Link to the medical research article which the two above charts were taken from

In the mentioned study, they tried to support the evidence from earlier studies in which caffeine consumption was associated with skin aging and slow wound healing:

  Our research confirms our earlier observations that caffeine may have
  an adverse effect on the wound healing process, as well as on the
  aging process, of the human skin.

...and by "earlier observations" they mean another in vitro study.

In the study, they used 1, 2 and 5 mM caffeine solutions. 1 cup (~250 mL) of brewed tea can contain 95-165 mg caffeine (source), which makes it 2-3.4 mM, so much like the solutions used in the study. When you drink 1 cup of coffee (let's say, 2 mM caffeine solution), the caffeine, which is water- and lipid-soluble (StatPearls), will be dissolved in the body water and fat, which can together make ~50 kg in a 70 kg person. So, you would need to drink ~200 cups of coffee (~20 g caffeine) in ~2 hours (caffeine half-life is ~5 hours - source) to achieve 2 mM caffeine solution in the skin cells.

I haven't found any actual human clinical trial in which caffeine consumption would be associated with adverse effects on the skin. In a recent review: Coffee consumption and health: umbrella review of meta-analyses of multiple health outcomes (BMJ, 2017), they don't even mention skin or wound healing and regular drinking of 3-4 cups of coffee per day was not associated with an increased risk of various health conditions (except in pregnancy).

Tar86, on the chemistry site, stated that: “they work in concentrations, not total dosage”. If this is a correct judgement, which it seems to be, then a 1mM caffeine concentration containing 194mg caffeine needs to be reduced, because in the test they use a much lesser volume of solution then the basic unit of one litre.

The culture dishes they used hold only 3.5 ml each.

In each dish was poured a 1ml mixture of 100000 cells in growth medium. Leaving space for 2.5 ml caffeine solution.

2.5 ml is only 0.25% of the base unit of 1 litre. This turns out to be about 0.485 mg pure caffeine. (0.25/194; or 1/776; or 0.13 %)

There is 17% protein in a human body. In an 80 kg person that equals to about 13.6 kg protein. Collagen makes up 30% of that protein, which equals to about 4 kg collagen. So, there is in an 80 kg body about 4 kg collagen. That is 1/20; or 5%.

One cup of a 250 ml cup of coffee at 1mM concentration contains 48.5 mg caffeine.
If a double doze, or 97 mg caffeine is ingested only 5%, or 4.49 mg, will reach the collagen. This 4.49 mg of caffeine will be distributed over 4 kg of collagen, becoming 0.00112 mg caffeine per mg collagen.

There are 37.2 trillion cells in the body. And in each culture dish 100000 were plated in a 1 ml growth medium. That is, each culture dish contains 1/372000 of all the cells in the body.

The answer seems to be dependent on:

The number of cells in 1 mg of collagen in the human body

The toxic impact levels of caffeine on human body cells.


What are the differences between carnitine forms? I've heard of L-carnitine, acetyl L-carnitine and L-carnitine L-tartrate. What form(s) occur in meat? What form does the human body manufacture?

Is L-carnitine just a shortened name for L-carnitine L-tartrate?

Carnitine tartrate is a salt between carnitine (cation) and tartrate (the conjugate base of tartaric acid, anion). So in this case, tartaric acid is not covalently bound to carnitine.

The salt formulation is a little tricky, because carnitine is itself a zwitterion at physiological pH (it has both a positive and negative charge) and so is overall uncharged in pure form. I think the tartrate salt is formed because tartaric acid is more acidic (first pKa = 2.89) than the carboxyl group of carnitine (pKa = 4.09), which leads carnitine to become protonated and therefore +1 charged in a concentrated mixture. The formulation sold by Lonza (which seems to be a major provider) appears to be a ratio of 2 cartinine (68%) to 1 tartrate (32%), which would indicate that tartrate acts as a -2 anion in this mixture (this is a bit surprising as the second pKa of tartaric acid has pKa = 4.40, but maybe I'm missing something).

You can recognize that this is a salt from the naming: the form tartrate indicate a conjugate base of an acid (as in lactate, acetate), and when used in a two-component name like carnitine tartrate (or, sodium acetate) refers to a salt. On the other hand, a carboxylic acid covalently bound to another group is given the suffix -yl, so tartryl carnitine would indicate tartaric acid bound to carnitine, as in fatty acid oxidation.

Carnitine is a molecule that allows transport of carboxylic acids (including fatty acids) across mitochondrial membranes and is involved in fatty acid metabolism. Like many biomolecules it exists as the L-enantiomer in the cells. It can be coupled to any carboxylic acid and in that case is called acyl-carnitine. L-Carnitine L-tartrate is a drug formulation and is a mixture of L-carnitine and L-tartarate (tartarate is not covalently coupled to tartaric acid).


Do proteins contain phosphorous? If its true then how alfred hershey and martha chase used the statement that proteins do not contain phosphorous? I hv heard about phosphorus that it is a constituent of certain protein, although we know that no amino acids have phosphorus... and if its true then how Alfred hershey and Martha chase experiment got acclaimed whose base of the experiment was that "protein doesn't have phosphorus"??

Yes some of the proteins contain phosphorus but in the experiment (Hershey and chase experiment) they used bacteriophage it's protein sheath contains carbon,hydrogen,nitrogen and sulphur while the DNA in the bacteriophage contains carbon,hydrogen,nitrogen and phosphorus(in the acid) so they selected this for that experiment moreover sulphur is absent in the DNA but phosphorus is not so one can conclude that DNA is the thing that was transferred
Reference:NCERT

It is true that no amino acids contain phosphorus, but due to post-translational modifications some proteins can be phosphorylated. In addition, there are enzymatic proteins such as glycogen phosphorylase b, which are relatively inactive protein, and the change to the active forms (glycogen phosphorylase a) can be carried out by the action of phosphorylase kinase (Lehninger. Principles of Biochemistry. 5th Ed.)


Why do smaller mammals move intermittently? I was watching a nice little video on youtube but couldn't help but notice how snappy smaller animals such as rats and chipmunks move. By snappy I mean how the animal moves in almost discrete states pausing between each movement.

Is this a trivial observation or something inherent in the neuro-synapse or muscular make-up of these animals?

Short answer
Intermittent locomotion can increase the detection of prey by predators (e.g.  rats), while it may lead to reduced attack rates in prey animals (e.g., rats and chipmunks). It may also increase physical endurance.

Background
Rather than moving continuously through the environment, many animals interrupt their locomotion with frequent brief pauses. Pauses increase the time required to travel a given distance and add costs of acceleration and deceleration to the
energetic cost of locomotion. From an adaptation perspective, pausing should provide benefits that outweigh these costs (Adam & kramer, 1998).

One potential benefit of pausing is increased detection of prey by predators. Slower movement speeds likely improve prey detection by providing more time to
scan a given visual field.

A second plausible benefit is reduced attack rate by predators. Many predators are more likely to attack moving prey, perhaps because such prey is more easily detected or recognized. Indeed, motionlessness (‘freezing’) is a widespread
response by prey that detect a predator.

A third benefit may be increased endurance. For animals moving faster than their aerobically sustainable speeds, the maximum distance run can be increased by taking pauses. These pauses allow the clearance of lactate from the muscles through aerobic mechanisms.

PS: If you mean with 'snappy' not only that small animals move intermittently, but also 'fast', then Remi.b's answers nicely covers the story why small critters are quick. Basically, it comes down to Newton's second law, namely acceleration is inversely proportional to mass (a = F/m), but the size of muscle power is not. Hence, bigger animals have more mass and need a lot more force to build up to accelerate at the same speed. That build up of force needs time (ever witnessed the vertical lift-off of a space shuttle?) Hence, small critters accelerate quicker and allow them to move 'snappy'.

Reference
- Adam & kramer, Anim Behav (1998); 55: 109–117

From the systems theory point of view it is because they have a lot less inertia, so their feedback systems operate much more rapidly, with a 'snap' action.


How do T-cells determine which cells they've already inspected? From what I understand, T-cells are constantly traveling in the body, inspecting cells by looking for antigens. If they're self antigens, then the T-cell doesn't attack, whereas if they're non-self, they attack. My question is how does a T-cell know when it just inspected a cell? Does the T-cell leave something behind on the cell to mark it as checked or does the cell itself present something on its surface to indicate that it has just been checked? If there is no such system, then what prevents the T-cells from being stuck in a loop, and just inspecting the same cell over and over?

Your question spans two activities of T-cells that are related to each other: migration and activation. T-cells that usually stay in lymphoid organs migrate to non-lymphoid organs with different mechanisms for each T-cell subtype. When migrated to non-lymphoid organ, the T-cells move through the organ looking for infected cells.

Migration

As you can see in the image below, there are many mechanisms for moving T-cells across the endothelial layer.

The main idea for all three mechanisms is that the tethering of the T-cell to the endothelial layer is weak. Because of the weak interaction, the blood flow causes the T-cell to move across the endothelial layer while still being attached to the endothelial layer. This is known as rolling. Other stimuli (usually chemokines) such as CCL21, CCL25, or ICAM 1 are needed to induce T-cell to migrate across the endothelial layer. This is important because these chemokines are expressed where there is inflammation. For example, there is a correlation between CCL25 level in the gut and inflammation in the area.

T-cells express α4β7 integrin or CCR7 that bind T-cell to the endothelial layer. Central memory T-cells and naive T-cells express CCR7 and CD62L and thus reside preferentially within the secondary lymphoid organs. Effector memory T-cells bind to gut endothelium with α4β7 integrin, CCR9, and LFA-1.

CCL21 is expressed by both stromal cells of lymph node paracortex and endothelium of lymphatic vessels to assist migration of activated dendritic cells and naive and central memory T-cells to lymph node respectively. Dendritic cells are professional antigen-presenting cells (APCs) that migrate to lymph node where it can interact with T-cells more efficiently.

T-cell activation

One important concept to take away from T-cell activation is that there needs to be direct contact between MHC complex and T-cell receptor (TCR).

T-cells that have moved into the lymph node interact with dendritic cells, which have high MHC complex concentration on their cell surface. This leads to subsequent activation of the T-cell leading to release of cytokines such as IL-2 leading to proliferation of activated T-cells.

The activated T-cells now are able to freely move across the endothelial layer of non-lymphoid organs to infiltrate and look for infected sites. (Naive T-cells enter endothelial layer of non-lymphoid organs as well but this is chemokine independent nad thus not a reaction to inflammation).

Sources:

Difference between naive T-cells and memory T-cells: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782715/

Dendritic cell's role in immune response: http://lab.rockefeller.edu/steinman/dendritic_intro/immuneResponse

Memory vs naive T-cell migration:
http://www.nature.com/icb/journal/v86/n3/full/7100132a.html

Dendritic cell and role of CCL21:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078419/

Naive T-cell non-lymphoid organ infiltration: http://onlinelibrary.wiley.com/doi/10.1002/eji.200535539/full

CCL25 and inflammation relation:
http://www.sciencedirect.com/science/article/pii/S0896841116300014

T-cell does not inspect any cell until the cell shows a piece of the "non-self" antigen on it by the MHC.

The helper T-cell connects with the antigen which is on the cell's surface. The T-cell sorts the cytokines that activate the cytotoxic T-cell to divide and form a colony of cytotoxic cells. The colony of cytotoxic cells then attack the "non-self" antigen expressing cell.


What kind of event would cause the current Mitochondrial Eve to be replaced by a new one? Apparently all living humans are matrilineal descendants of a single woman who lived 200.000 years ago. She is called Mitochondrial Eve.

But at the time she lived there was a different matrilineal ancestor that all living humans shared. And between then and now I imagine many other women have been Mitochondrial Eves of the human population that lived at a particular time.

What I'm wondering is what kinds of events would cause a different, more recent matrilineal ancestor to become the Mitochondrial Eve of all living humans?

One scenario I can image is that the human population is on the brink of extinction and literally only a few people survive. Because there are so few people alive, I imagine that the chance that they share a more recent matrilineal ancestor is high.

Are there other scenarios possible? Does the chance of a new Mitochondrial Eve emerging decrease if the human population is large (billions) instead of small (hundreds or thousands)? Suppose that the human population will not decrease, is it likely future human populations will ever have a different Mitochondrial Eve than the current population? Does it depend on the amount of people that migrate?

The same questions could be posed for Y-Chromosomal Adam and the most recent common ancestor of all humans, I guess...

One possible scenario would be that a particular woman develops a mutation rendering her much more 'fit' (in the evolutionary sense) than her peers. For the sake of argument, lets take the very simplistic case of an X-linked recessive mutation causing the women who bear it to have say 10 children at each birth. If this mutation is then transferred to the offspring, it will very quickly spread across the entire population.

If this continues for a few generations, the crushing majority of the earth's population will be the descendants of that one woman who carried the original mutation, she would be the new mitochondrial Eve.

I want to stress that this is nothing but a very simplistic thought experiment. Such a mutation is i) very unlikely, probably impossible, ii) likely to render the carrying individual less fit rather than more as each birth would be exhausting, increasing the chances of dying during child birth.

Update:

I have specified that the mutation has to be X-linked and recessive. This means that it will only present a phenotype in women who are homozygous for it, women both of whose parents carried the mutation. This is because, as mgkrebbs very correctly pointed out in the comments below, otherwise her sons would mate with women who are not their sisters and their children would have the mutation but not her mDNA. If the phenotype is only expressed when the mutation is homozygous, only women whose mother carried the mutation (and Eve's mDNA) would show it and only then would a new mEve arise.

What would need to happen for a single woman's mitochondrial genome to be in all living humans ?

All other women would suddenly or gradually need to be eliminated from the gene pool.   No other woman could enter the gene pool of this future humanity.  So the most likely scenario is one where we would have to be reduced to a single woman at some point.

Genetic isolation was brought up, but the words 'all living humans' doesn't really say 'isolation'.  In isolation, there are other people still carrying on somewhere else.   Here we are talking about only isolation in the sense that the breeders are the only ones left to reproduce.

Even so, any human woman will still be descended from MEve.  That original Eve would still be the mitochondrial Eve, though the genomic record pointing to her would have disappeared.

A completely New Eve could happen if there were a woman unrelated to MEve were to come along, and her offspring were so much more successful than all other women that over time only this woman's daughters were chosen as mothers.  She would be incredibly successful- like all her children were 6'6" and much smarter, attractive etc etc, then the rest of the gene pool could dwindle leaving only 'new Eve'.  This could happen say if we got some Neanderthals going.  They don't seem to be particularly likely to take over though.

This is similar to the scenario where one female lineage simply out-competes all other female lineages to assume the mantle of M-Eve.  This seems less likely to me.  This lineage would have to enjoy an advantage would have to out-weigh all over variants that exist at the time and would ever emerge over the following generations before our new M-Eve's final domination. Given the number of genes and possible variants, in the entire genome, that is statistically really improbable.

As far as a new Y Adam, this sort of thing nearly happened for men.  Just to remind, the Y chromosome is transmitted exclusively from father to son, so a Y Adam would be the only ancestor of all men on the face of the planet.

A national geographic sponsored survey of genomes found that in central asia 8% of all men have the same Y chromosome.  Over all humanity, 0.5% of all men have the same Y chromosome.  The genetics point to the Mongol Warrior King, Genghis Khan whose campaigns across Asia to the doorstep of Europe included him bedding with one or more different women from the conquered peoples every night, one of whom is reputed to have killed him.  Not incidentally killing many men too, eliminating much future competition for his progeny.

Still, all this is a mere fraction of the sort of effect you are talking about.  100% replacement by a single individuals descendants is hard to imagine in less than an extinction like scenario.  Or a new race of superbeings coming from a single individual.  Hard to imagine given the billions of people on the face of the planet now.

Its a little easier to imagine in the case of a new Adam only because a one man can have hundreds or even thousands of offspring in his lifetime.  Even then, Male psychology seems to bring it up more than is rational. Its still extremely improbable (not going to happen).

Its also worth noting that few species have been able to come back from such a small gene pool and number...

Here's a tree of human Y chromosomes. You can see that fat grey blob which are descendants of GK.


unknown bird in Long Lake Michigan......chocolate brown head and neck, charcoal body and tail, ivory wings, top and bottom light chocolate head and neck w/ charcoal body and tail. the wings are ivory white, top and bottom from the body outwards. the colors are clear.....not mixed with other colors. no stripes or spots, etc. slightly smaller than a robin.

That's a very interesting set of colors.  Unfortunately nothing springs out at me, although I can think of a couple of birds that might sort of (maybe) match.
First, common pigeons come in all sorts of colors and patterns, and it's possible that yours is one.  On the other hand, common pigeons tend to be very familiar to most of us, so I don't think you'd be asking about that.
Second, there is a tern that is moving through the area about this time of year, that might fit:  Black Terns can have a lighter wing.
Here's a link and a representative photo:
 https://www.allaboutbirds.org/guide/Black_Tern/overview

There is another, even better possibility, if your bird is ternish:
The White-winged Tern (formerly White-winged Black Tern) is an uncommon late-summer wanderer through much of the region.  Here is a link and a representative photo:
https://avibirds.com/white-winged-tern/

Could it be any of these? These are all iNaturalist observations around the Long Lake, MI.


Why does something taste less sweet after eating something else that is sweet? Why does something taste less sweet after eating something else that is sweet, especially if you don't drink water in-between.

It's a general flaw (IMO bad design) in organic/neural sensor frameworks where inputs tend to be measured relative to previous experience rather than absolute quantitative.

This happens with weights as well. There have been plenty of experiments where people are asked to pick up a heavy weight and then a light weight, then record/estimate the perceived light weight. The next day, they pick up a medium weight and then the same light weight and record the perceived light weight.

The 2nd recording turns out "heavier" because of relative perception.

Suggestion: Computer-mediated nerves designed to measure in absolutes.


If a woman was fertilized with her own DNA, would it be her clone? Several questions:

1) Can human DNA fertilize an egg, without having been naturally packaged in a sperm cell?
2) If a female had her ovum fertilized with her own DNA, would the fetus be her clone?
3) If this technology of fertilizing ovum from arbitrary samples of human DNA were effective, would males be unnecessary for reproduction of the human species? (No political implications, just a thought experiment.)

Thank you for your insight!

1)
In principle yes, you could in theory use micro injection to inject haploid DNA into the egg. I don't think this has been used in practice though. However Dolly the sheep was created by exchanging haploid nucleus of a sheep egg with a diploid nucleus from a mammary gland cell.

2)
Not necessarily, DNA is packaged into chromosomes and diploid cells have two copies of the same chromosome (with the exception being the sex chromosomes MALE:XY FEMALE:XX). Remember that gametes are haploid (single copy of each chromosome) and that homologous recombination occurs during gamete formation, therefore the chance of obtaining two identical sets of haploid DNA that also match the females is extremely low, unless all chromosome pairs are completely identical.

3)
In principle yes. I could imagine that DNA extraction from eggs could be used for artificial fertilization and the result of that would be a race of all females.

No it is not possible. For fertilization only DNA is not required. Sperm is necessary for fertilization because it provides centriole also for cleavage of zygote as ovum does not contain centriole.


How strong of an electric field is dangerous to adult humans? Given that "a potential difference is introduced over the membrane, the associated electric field induces a conformational strong in the potassium channel" is required for our muscles to move, how powerful of an electric field is required to cause our muscles (including the heart) to fire irregularly?  How much stronger would it have to be to kill someone?

https://biology.stackexchange.com/a/53330/7973

https://en.wikipedia.org/wiki/Voltage-gated_ion_channel

(No, I'm not an "electrosensitive" afraid of cellphones or high-tension wires.)

Thanks

Research published by WSU Professor Emeritus of Biochemistry and Basic Medical Sciences, Dr. Martin Pall, bears directly on your question about potassium channels.

https://www.researchgate.net/project/microwave-frequency-radiation-acts-via-voltage-gated-calcium-channel-activation

He has concluded that weak EMFs cause cascading health impacts that derive from false electrical signaling of voltage-gated ion channels, and that these impacts include heart disease and the dreaded social bugbear elctrosensitivity (microwave disease).


Critical discussion: Gene expression and systems biology allows us to understand the control of complex traits I'm having a bit of trouble tackling this question. Any help on what I should write about or the points I should mention would be much appreciated. I keep seeing articles about eQTL and QTL are these relevant as well?

Turns to be too long for a comment.

If you are looking for explanation of the title/question, than it is following (roughly).

If we get information about gene expression from all different cell types, and extract also interactions between those genes (if a gets higher then b gets lower), this will allow studying multigene traits. E.g., life quality, height, mental disabilities, cardiovascular risks etc. Thing is that for most health problems that stem from single gene variation we already know named gene, or can easily find it out.

More complex issues are often hidden in statistics, links are not so clear. So, for example, autism is described by genetic variations (so far) only in less than 30% of cases or so. In other cases there is no genetic predisposition or strong evidence. Mainly that is so because many genes interact to produce final trait or illness. Looking with microscope one gene at a time will not provide information about it.

You should look into multi-gene traits, maybe pick your favourite illness (e.g. autism) and see how it is hereditary (tip: not fully). Whole-genome sequencing is important tool in tracing such issues because it gives wide overview and a lot of genetic information about patient.


Having a lot of trouble identifying this insect It was found in central Alabama

Other's are right, some genera in the subfamily Reduviinae, I don't think it's an adult though. Very close to this.


Does DNA have the equivalent of IF-statements, WHILE loops, or function calls? How about GOTO? Does DNA have anything like IF-statements, GOTO-jumps, or WHILE loops?

In software development, these constructs have the following functions:

IF-statements: An IF statement executes the code in a subsequent code block if some specific condition is met.
WHILE-loops: The code in a subsequent code block is executes as many times as specified, or as long as a specific condition is met.
Function calls: The code temporarily bypasses the subsequent code block, executing instead some other code block. After execution of the other code block the code returns (sometimes with some value) and continues the execution of the subsequent block.
GOTO-statements: The code bypasses the subsequent code block, jumping instead directly to some other block.

Are constructs similar to these present in DNA? If yes, how are they implemented and what are they called?

Biological examples similar to programming statements:

IF : Transcriptional activator; when present a gene will be transcribed. In general there is no termination of events unless the signal is gone; the program ends only with the death of the cell. So the IF statement is always a part of a loop.
WHILE : Transcriptional repressor; gene will be transcribed until repressor is not present.
There are no equivalents of function calls. All events happen is the
same space and there is always a likelihood of interference. One can
argue that organelles can act as a compartment that may have a
function like properties but they are highly complex and are
not just some kind of input-output devices.
GOTO is always dependent on a condition. This can happen in case of certain network connections such as feedforward loops and branched pathways. For example if there is a signalling pathway like this:  A → B → C and there is another connection D → C then if somehow D is activated it will directly affect C, making A and B dispensable.

Logic gates have been constructed using synthetic biological circuits. See this review for more information.

Note

Molecular biological processes cannot be directly compared to a computer code. It is the underlying logic that is important and not the statement construct itself and these examples should not be taken as absolute analogies. It is also to be noted that DNA is just a set of instructions and not really a fully functional entity (it is functional to some extent). However, even being just a code it is comparable to a HLL code that has to be compiled to execute its functions. See this post too.

It is also important to note that the cell, like many other physical systems, is analog in nature. Therefore, in most situations there is no 0/1 (binary) value of variables. Consider gene expression. If a transcriptional activator is present, the gene will be transcribed. However, if you keep increasing the concentration of the activator, the expression of that gene will increase until it reaches a saturation point. So there is no digital logic here. Having said that, I would add that switching behaviour is possible in biological systems (including gene expression) and is also used in many cases. Certain kinds of regulatory network structures can give rise to such dynamics. Co-operativity with or without positive feedback is one of the mechanisms that can implement switching behaviour. For more details read about ultrasensitivity. Also check out "Can molecular genetics make a boolean variable from a continuous variable?"

In addition to the excellent WYSIWYG answer, there are some programming-like constructs at the lower level:

FUNCTION CALL - replacing a single sub-unit inside a complex protein, assembled from multiple sub-units, each encoded by separate genes. This can also be seen as COMPOSITION, another programming concept.
IF - alternative splicing, a piece of DNA (exon) may be included or not included into transcript that encodes the final protein.


Why does the protection afforded by some vaccines last longer than for others? After reading an answer to the question of How Do White Blood Cells Learn? Or Do They?, I came to wonder something. Specifically,

  The effect of this is that every new B and T cell that your bone marrow makes will recognize a unique, random protein sequence, and you will have billions of these cells floating around in your blood circulation at any given time. These cells however will only float around in circulation for a short period of time before dying and being replaced by other cells with new random sequence receptors.

Assumption: What I gather from this (and the remainder of the answer) is that basically, a vaccine "teaches" the existing white blood cells in your body; eventually, these cells will  be purged, so you will no longer be immune.

However, many vaccines seem to only be once-in-a-lifetime, or at least require a vaccine only once per decade (or less).

Some examples would be the Varicella vaccine, which can last up to 20 years, the Tetanus vaccine, which recommends a booster every 10 years, and the HPV vaccine, which lasts 5-6 years. Durations also vary with Hepatitis, Influenza, Polio, and numerous other common vaccines.

I would assume that, regardless of what a cell has "learned," it is purged with the same likelihood as any other cell; yet, it seems that some "learned" defenses can be retained longer than others. In essence, my question is: Why do some vaccines take longer to "wear off" than others?

(Note: This question is not a duplicate of Why do I need a flu shot every year, while many other vaccinations last years or even a lifetime?; I understand that some pathogens can mutate, so immune cells are of no use against mutated strains since they were not vaccinated against the mutation.)

The first thing I want to make clear is that, the B and T that "will only float around in circulation for a short period of time before dying and being replaced", are not the ones that have already learned to recognise a certain diseases (or vaccine) but rather the naive cells that haven't yet done so. This is also made clear later in the same answer you cited:

  As these injected protein sequences circulate through your blood they
  will eventually bump into a B or T cell that has a receptor that
  recognizes them. When this happens, the B or T cell will now start to
  divide and give rise to long lasting memory cells that express the
  exact same receptor and will therefore recognize the exact same
  protein sequence again in the future. These cells will float around in
  your blood for most of your life and make you 'immune' to the
  recognized pathogen.

In order to understand why some vaccines hold for your whole life, while some need a booster every few years we need to look at the life time or recycling of those memory cells, which stay in your body for much longer than the naive immune cells.

Now we come to the actual answer(s) to your question and there multiple  factors that (can) have an influence on this:

Initial strength of the immune response: Every vaccine (and/or disease) evokes an immune response with a different strength. Generally the stronger the first response is, the more memory cells will be created initially (those actually don't have correspond to the same molecular memory either, they might recognise different aspects of the vaccine/disease) and with more cells available it will take longer until none are left
Natural exposure: memory cells start proliferating when they encounter the molecule (protein/virus/bacteria) which they have 'memorised', if there is an acute infection they will do so a lot in order to produce a lot of antibodies against it. However, even a very small amount of virus/bacteria, that wouldn't actually make you sick, will allow induce them to proliferate and preserve their numbers. Therefore memory cells against a more common or prevalent disease should be more stable in your body, than ones against a very rare one.
There very likely more factors that either I or the whole scientific community don't really know about. Cellular systems and the immune system in generally are rather complicated ...

This issue is deep but one answer is bacteria/virus genetic variability. Some organisms have the ability to change their DNA in just a few generations (for example the influenza virus which requires a new vaccine every year). When you take a vaccine for influenza virus you expect that will protect you in a short period of time (winter season) because this virus is a nasty one, i.e it has the ability to present antigen variability due to mutation/constitution of its DNA and antigen is the source of power of vaccine (a vaccine assumes the organism has a antigen that could be a protein or other biomolecule that is relatively fixed between generations and is specific to that organism) so the vaccine loses its effect because the organisms are no longer susceptible which causes immune response to be weak (no longer recognizes the organism as it recognized) and you get sick. If the organism has slow mutation/variability the vaccine will last longer because the antigens are present for a longer period of time but eventually you will need to get another vaccine years later (for example tetanus).


Teens concerned about impregnation through clothes Dry Humping, is:

  dry humping is the process of two people repeatedly moving up and down and back and forth on top of each other fully clothed( or missing various pieces, but the penis must not come in contact with the vagina with out some sort of fabric separating them ex: boxers,panties, or even sheets!!)

We all know that the basic rule for impregnation is that the sperm must come in contact with the egg, and even be able to fertilize it. While sperm can get through clothes, semen (but this is yet been proven or disproved) gets stuck, thus the sperm dies.

What is your opinion about this? If two people are on top of each other, fully clothed, and the male comes to ejaculation, is there any chance that pregnancy can happen, in the realistic and biological look at it (and not some probability or statistical way)? What advice should be given to teens on the matter?

I am a computer scientist with no biology knowledge, and am very interested in getting the opinion of biologists.

But since I know that the stackexchange community likes to see work done before asking questions, I did my own research (I am used to googling code and algorithms):
Very few research has been done on the subject. There is one shining research that  concluded, as I recall, that:

  If the underwear is completely saturated with semen, and is in direct contact with the woman's vagina, pregnancy is possible statistically, but highly unlikely.

If there has been an ejaculation by the male, and semen is present, there is a chance of getting pregnant. Period. Teens really need to know that.
I think you may have your terms confused - semen is the overall fluid released during an ejaculation, sperm are the cells with tails that are produced in the testes and fertilize the egg. At any rate, according to the WHO, a normal sperm count is over 15 million per milliliter, with some counts much higher (>50e6/ml ), and an average between 20 and 40 million. The volume of the ejeculate tends to be anywhere from 1-6 ml. If you take a healthy young male at the peak of his reproductive capabilities, this equates to a very large number of sperm being released during a sexual encounter. All it takes is for one to reach an egg and fertilize it. Sperm are very very small, much smaller than the pore size of average fabric, so clothing will do very little to stop them. The female is likely sexually aroused during this activity as well, and produces additional fluids and lubricants that promote the survival and motility of sperm, among other things.
So, it depends on many factors. If both parties are fully clothed (at least 4 layers of clothing between their respective reproductive organs) and there is a minumum of soaking through, the chances of pregnancy are correspondingly quite low. On the other hand, if only one partner is wearing just their underwear, it's essentially like there is no clothing present at all, and the relative chances go up significantly.
Safe sex practices can't be emphasized enough to young people, as education and awareness is so much better than ignorance and myths. Even aside from pregnancy, if condoms are not utilized properly to contain all the semen there is the chance of sexually-transmitted diseases, ranging from herpes and gonorrhea to AIDS. None of these require penetration to be passed along, and one might argue that the additional presence of potentially irritating fabrics could open up raw areas or cuts and enhance their transmittal.

Take home message
Now, all this being said, the chances of impregnation through clothing without direct penetration of the penis into the vagina is quite low compared to "typical" unprotected fully-penetrating intercourse, especially depending on where the female is in her fertility cycle. According to this study, a woman's most fertile day is two days before ovulation (as had been postulated before), and the chances of pregnancy on that day are about 25% (assuming penetrating intercourse). Overall, the chance of pregnancy throughout the month is about 5%.
I don't have any hard numbers on the pregnancy chances when one or both partners have at least some clothing on, as obviously it will vary greatly depending on who is wearing what, the volume of ejaculate, contact time after ejaculation, etc. Just for fun, let's assume it's 100 times lower. That means the chances of impregnation two days pre-ovulation would be 0.25%, or 1 in 400. While rather low, this is still a non-zero chance.
Condoms are about 98% effective if used properly during penetrative vaginal intercourse. Various other birth control methods such as contraceptive pills, intrauterine devices, implants and injections are quoted as being 99% effective on their own, although they do not protect against sexually transmitted diseases. I'm certainly not one for preaching abstinence, but done properly it should be 100% effective. Ultimately, it is up to both partners to decide what their risk tolerances are, together. It is much better to seriously talk about it beforehand than to be panicked and unsure afterwards.

Hopefully this addresses your concerns, please leave comments if you have additional questions.

It is effectively impossible to get pregnant by dry-humping because the conditions that would have to be met for sperm to pass through multiple layers of clothes, survive on skin, find the vaginal opening, survive in the vaginal environment and finally impregnate an egg are simply unrealistic.

The barrier of clothing that we can assume present during 'dry humping' is significant. Semen begins to die as soon as it begins to dry out and any clothes you're wearing are likely to draw water away from the sperm cells through adhesion of water to the fabric. One layer is absolutely not "like there is no clothing present at all".

Assuming some sperm cells made it through all that and onto skin, their motion isn't directed towards the vaginal opening, so a sizable fraction will be literally lost at that step. Skin is also a toxic environment on its own, so these improbable sperm have a very limited time to find their way.

That last battle buddy team of sperm has very little chance of surviving the vaginal environment. A lot of sperm need to enter the vaginal environment together to ensure that just a few survive.

As far as dry humping is concerned, there's no realistic reason to worry about pregnancy.


Polymorphism in cnidarians? To me, the phenomenon of polymorphism in cnidarians is particularly troubling. I gather that it essentially refers to existence of various different forms or  kinds of individuals, i.e. zooids and polyps in one species. But when we refer to the cnidarian Physalia, as an animal, aren't we actually referring to a colony of individuals? Physalia consists of several "entities" including gastrozooids, dactylozooids, and the float, and since each of these is a distinct "organism", therefore is what we refer to by saying Physalia is actually a colony of phenotypically distinct forms of the same species?

Therefore, can "animals" like Physalia or Gorgonia or Pennatula be thought of actually as "colony-beings" which always contain several individuals in group?

It seems like your question might contain two separate and linked issues, both of which are perhaps equally confusing and equally interesting. They're both really discussion questions in a sense, but they've also both been dealt with in the literature in thoughtful ways, so here's a stab at an "answer".

Issue One: how does your species concept deal with polymorphism?

This may depend on which species concept you're using. And, to some extent, the choice of which species concept you use depends on what kind of organism you're dealing with (for instance, organisms that reproduce asexually have a whole different set of issues and challenge several species concepts).

Various papers by Kevin de Queiroz deal very well with species concepts. In 'The General Lineage Concept of Species'  (which is also summarized on this page), he argues that although there are many different species concepts that can be better applied to different situations, they all share the basic tenet of defining a "segment of a population-level lineage". In other words, each concept is attempting to put a continuum into slightly different categorical bins, but they all recognize the existence of the same continuum (the lineage). (Also see his 'Species Concepts and Species Delimitation'.)

I think most species concepts have no trouble dealing with polymorphism because the different morphs are all part of the same lineage, that is, "a series of entities forming a single line of direct ancestry and descent" (de Queiroz 1999).

Issue Two: how does your concept of the individual organism deal with colonialism?

In 'Does Biology Need an Organism Concept?'  Pepper and Herron make a similar point to that of de Queiroz. They argue that multiple definitions (concepts) exist, and that these concepts all attempt to categorically bin what is in fact a continuum. Like de Quieroz, they argue that most definitions recognize the same underlying continuum, and that the difference is in the categorical bins.

In the case of the organism concept, this continuum is based on two criteria: increasing genetic homogeneity, and increasing physiological integration.

So, for instance you could have two organism concepts (in the picture below, lighter yellow and darker yellow) that agree that Physalia falls in the same location along these axes, but disagree on exactly where to draw the boundary between their "multiple organisms / colony" zone (yellow), and their "individual organism" zone (white).

I'll finally get to my point, paraphrasing both de Queiroz and Pepper and Herron. For both concepts of the species and of the organism, arguing about whether one concept is better than another is endless (especially on a site that aims at answers rather than discussion). However, recognizing that there are different concepts, understanding that what these concepts do is to bin the same continuum in different ways, and being clear about which concept you decide to use is very useful.

While refering to an animal say Physalia, we refer to its massive type colony, containing many zooids. Among the zooids, a large cup shaped float is seen, which is bright blue in color and remains above sea water normally. On the undersurface of float many gastroaooids, gonozooids and dactylozooids are present. The colony thus shows a high degree of polymorphism.
This is all I know and thus the reasoning seems to be absolutely correct...


Does genetic morbid obesity exist? With the acceptance of being a little overweight

I hear of people saying they were born morbidly obese and it was genetically passed on. I'm aware being so obese leads to countless health issues, yet we have people defending fat shaming and the likes. Is the excuse of having 'obese' genetics scientifically justified? Do people have genetics that make them ridiculously fat? Alongside, would this simply be down to the diet of the person from a young age?

Thanks.

It is certainly a very difficult question to answer.

There are some genetic disorders that can predispose individuals for becoming obese: https://www.ncbi.nlm.nih.gov/pubmed/18230893

There are also evidence of epigenetic influences on obesity: http://www.nature.com/nrendo/journal/v12/n3/full/nrendo.2016.18.html

Typically each case of obesity is caused a combination of both genetics, epigenetics and lifestyle: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873060/

However also keep in mind that obesity is a fairly recent problem and as such the genetic changes are likely minimal between the 1980 and 2008 populations sampled by WHO: http://www.who.int/gho/ncd/risk_factors/obesity_text/en/
A doubling in the prevalence of obesity in the two populations are most likely caused by changes in lifestyle and the availability of food, rather than genetic changes as the time frame is so short.

So to sum up: Morbid obesity caused by currently unfavorable genetics exists but is very rare. People can be genetically and epigenetically predisposed for developing obesity, which when combined with certain lifestyles can further increase the risk of becoming obese.

It's a myth that obesity is mostly caused by genes. Yes, there are many genes that predetermine your apetite but when a baby is born obese, it's not a matter of genes but a matter of the mother's health and diet. And because till the birth, the fetus shares a single bloodflow with the mother, it gets everything the mother has in her blood. Thus, some babies are born obese, some are born addict.

Indeed, there are papers showing that there's a higher chance for the newborn to die during birth, even though you can't always say what was the main cause of death (also it depends on what you connect with obesity).


What is the name of this insect? Is it venomous or possess any threat to human life if someone gets stung? I found it in Northern part of India, on a mango tree. When I intended to move it away from home, it seems to bite like a snake with front part lifting like a king cobra.

This insect is 6-7 inches long, 1-2 inches wide, and appeared during summers.

That looks like some kind of lappet moth caterpillar. Although I am no expert in them, especially not species that would appear in India. But hopefully my answer gives you the right direction of research.

You can see some visually similar observations on iNaturalist:

https://www.inaturalist.org/observations/42382365
https://www.inaturalist.org/observations/40958993
https://www.inaturalist.org/observations/40137289


How do I tell if the mosquitos in my New York City apartment can carry Zika? The species that carries Zika, A. aegypti, is unlikely to be found in New York. However, the related species A. albopictus is prevalent and quite concerning. So this question is focusing on A. albopictus (if I may editorialize I would suggest leaving the title closer to the real question of interest, and disambiguating the species as the first step in resolving it).

According to the CDC

  Zika virus is transmitted to people primarily through the bite of an infected Aedes species mosquito (A. aegypti and A. albopictus).

I understand New York has IIRC the aegypti species and Zika has appeared.

My apartment gets mosquitos rather randomly every couple months. Understandably I want to figure out how much effort I should put into preventing or getting rid of them. I can describe their behavior here and maybe that's enough information. If not, do I need to get out a magnifying glass or sequence DNA? (Which I did once in college but I wasn't very good at it).

Their behavior:

I get "bursts" of them at random times in the year - more in the warm months but also in November. We had a warm winter but this still surprised me.
They seem to bite me at night but I've never had a mosquito bite on me. I've had mosquito bites from being bitten by mosquitos before, so unless I've developed a resistance to that in the last few years, that's strange.
I haven't found any evidence of standing water nearby. They don't hover around my sinks or toilets. I read once the Zika carrying strain is on the hardy side and can live off of moisture in walls so this is troubling.

If you're curious my preferred life hack is keeping my living room slightly warmer than my bedroom. And also, you know, killing all of them.

So, are these behavior traits useful? Can I identify them as opposed to other New York inhabiting mosquitos? Is a DNA test necessary?

This is a reasonable question, and I was surprised to find that official information on whether Aedes aegypti is present in NYC isn't very clear. I personally would have thought that NYC was quite far beyond the range of Aedes aegypti (the 'yellow fever mosquito', believed to be the main vector of Zika virus in the ongoing emergence event in South America), and the New York City Department of Health apparently agrees with me:

  Aedes aegypti has not been found in New York City.

...(emphasis theirs) which seems pretty clear cut. However, the CDC recently published a map claiming that NYC is within the potential range of Aedes aegypti.

It's not really clear exactly what they mean by this. From the webpage:

  The new estimated range maps have been updated from a variety of published and unpublished sources.
  These maps show CDC’s best estimate of the potential range of Aedes aegypti and Aedes albopictus in the United States.
  These maps include areas where mosquitoes are or have been previously found.

A related species, Aedes albopictus, is sometimes found in NYC during the summer and is probably capable of transmitting the strain of zika virus currently circulating in the Americas (see for example this recently-published experimental infection study). Aedes albopictus has been the major vector in some previous zika outbreaks in other parts of the world.

(Edit (14th June): A group of mostly-CDC entomologists just published a map of locations where Aedes aegypti and Aedes albopictus have actually been collected between 1995 and 2016 here, and there's an NPR article explaining why the maps are different here).

Whether the density of this species or the temperatures are sufficient to sustain transmission for any length of time in a climate like that of NYC is a more complicated story. The CDC even adds:

  Maps are not meant to represent risk for spread of disease.

But you've asked whether the mosquitoes in question can carry zika, not whether they're likely to be good at it, so I'll leave it there. The short answer is that if they're Aedes mosquitoes, then they might be able to.

So how do you know if they're Aedes mosquitoes? Aedes are visually quite distinctive; they have black bodies with white stripy abdomen and legs:

(Image taken by Muhammad Mahdi Karim; details and license here).

Aedes are also generally day-biters, so if you're getting bitten at night that makes me suspect you've got something like Culex mosquitoes instead (which might be able to spread West Nile virus, although that's a different story). These are dull brown.

If you do find you have Aedes and you'd like to try to identify them to species level, you could collect some dead ones and look at their thorax. If you take some photos and post them here as a species-id question you'll probably get an answer pretty quickly, but this figure illustrates the difference between aegypti and albopictus:

(Image from WHO (1995) Guidelines for Dengue Surveillance and Mosquito Control, Second Edition)

There are better images here but I think these are under copyright.

You're very much out of range of Aedes Aegypti, which is the primary carrier of Zika. Albocitus is a much more theoretical carrier, whose potential for spreading disease is much less. There have been no locally acquired cases in the mainland US this year. The odds of a New Yorker being the first to catch it are ridiculously long.


Need help identifying this wasp/hornet I am currently on holiday in southern France and have noticed that the house we are staying in has somewhat of a hornet/wasp problem.

Is there anybody that can help in identifying it? My best guess is a European Hornet but I'm no expert so may be wrong.

Below are some pictures. Sorry they couldn't have been of any clearer quality, they were taken through a window, and I didn't particularly feel like going out to get any closer because I've heard that some hornets can be quite aggressive even if unprovoked.

From what I saw, it has visible fur, and is around 2cm in length. The feature that led me to it being a Hornet is that the waist gets smaller before the abdomen.

This looks like a European hornet Vespa crabro to me. Wasp-like appearance, red on head and thorax and base of the abdomen. And the legs are red/dark, not yellow.

Picture from wikipedia

Hornets can be aggressive, especially if you come near the nest. Usually, European hornets are actually not really interested in people (unlike other wasps). But if there are many around your house, it is likely the nest is near, so be careful and perhaps contact the owner of the house.

It is quite possible that what you are dealing with are Asian Hornets.
This is a link to an article that helped me answer your question.

http://www.telegraph.co.uk/news/worldnews/europe/france/6049302/Tourists-warned-as-Asian-hornets-terrorise-French.html


Stem Cell Replication Reading from the internet, I've come across quotes that said stem cells have the potential to replicate indefinitely. However, there are other sources that say cells that are specialised will have their telomeres shortened each time the cell undergoes cell division until it renders them unable to reproduce.

I would like to ask if stem cells that replicate in terms of self-renewal will have their telomeres shortened as well to a point where they can only renew themselves a set number of times before they cannot undergo cell division anymore.

Thank you.
[P.S. I'm no biology student, just a curious person seeking answers, hence do forgive me if this is supposedly a basic question. I've tried looking online for answers but it seems quite difficult to get a satisfactory or targeted answer.]

Telomere shortening is intrinsic to the process of replicating linear DNA (termed the end-replication problem). Adult stem cells that rapidly proliferate express the enzyme telomerase which is capable of lengthening shortened telomeres, thus allowing theoretically indefinite replication.

Further reading: Telomeres of Human Chromosomes


Why people like to see pornographic scenes, but do not feel the same about eating scenes? This question may seem funny, but I think biology must have good answers.
I think no more explanation is needed.

I really thought about this and searched for an answer, but there is nothing yet.
If you know some thing about or have some thing which may lead to good answer(s) please express.

Also, do animals portray the same behavior in such situations?

For these two phenomena to create the same feelings all of the time, the physiology that engenders these feelings would have to be the same.  All I can do is point out that these have been separate and distinct even in yeast and bacteria and invoke a likelihood argument.

The impulse for hunger is almost as old as living things.  In bacteria, cyclic Adenosine mono phosphate (cAMP) mediates hunger, though this does not appear to be universal.

Sexual reproduction appeared much later - in the single celled eukaryotes mating factors for instance are mediated by the MATa/alpha receptors.

In animals like C elegans the differences persist (hunger, mating).  This is not a precise argument, but there is the entropy argument - the odds of these 2 signals evolving together biochemically or genetically is quite unlikely given how separate they have always been.

That's not to say that eating food can't create a sexual arousal, but it does not do so all the time.  The sexual response appears to be plastic and adaptable to nearly any sort of stimulus.  The fact that in primates and many other animals, the pleasure stimulus is related to both mating and eating might make them seem like similar impulses, but when you go deeper it doesn't seem plausible.  So the two could hypothetically create the same feeling, but if you are asking why doesn't it usually... then there are lots of reasons why.

I find it helpful to reverse the question and ask - what would happen to a species where you could suppress the mating impulse by eating?  Probably not an adaptation that would survive long.

People can satisfy their sexual urges on their own (that is, without a sexual partner) through masturbating. They cannot satisfy their hunger on their own (that, without food).

I suppose people could eat one food while looking at another kind of food pretending that the food they are eating is the one that they are watching, but where's the fun in that?

Having sex with an attractive person is an indicator of biological desirability ----- namely that another human being wants you in the way you want to be wanted due to your accomplishments or social status. Thus, people watch or read porn to satisfy their need to be accepted or to make them feel as if they are such a person with accomplishments or social status or to compensate for things not going their way in life and subsequently masturbate to such porn.

As for hunger, a better analogy for porn would be taking those kind of drugs that make you feel less hungry.

So yeah, for sex, people watch porn. For hunger, people do not compensate for their inability to eat by looking at food that they cannot have. They would probably take drugs or something. I'm not quite sure if such a thing exists, but I swear one of my grade school teachers said that there was some kind of drug that makes people stop feeling hungry.

I think a better analogy for looking at food they cannot have is looking through pictures of a lustful or romantic interest with his/her romantic partner.

This may sound like a stupid answer that is more philosophical than biological from some loser with 1 reputation. I request commentary along with any downvotes.


Does evolution go only in one direction? In this video Richard Dawkins talk about intermediate fossils. He describes how the whales were evolved from a common ancestor who lived on land.

But his theory sounds more like a devolution. I thought evolution was coming from the sea to the land and then to the skies. Are there more examples where species evolve back and forth between the ocean and land or skies?

Does evolution go only in one direction?

No, it does not. There is no such thing as a goal of evolution at making things fly or at making things intelligent or whatever. There is no intrinsic directionality.

In short the reasons are 1) Evolution is much more than just natural selection 2) natural selection does not systematically select for a specific trait. Some traits are advantageous under some ocnditions, some other traits are advantageous under other conditions.

I won't talk more about the mechanisms of evolution here as it would take a whole book. Instead I will recommend a source of information for you to further your knowledge.

Source of information

As your question is very introductory and shows misunderstanding, you might want to have a look at an intro course to evolutionary biology such as for example Evo101 by UC Berkeley.

Devolution

Note that this term is rarely used in the scientific literature (actually I think I have never encountered it in the scientific literature). From wikipedia:

  In modern biology the term [devolution] is meaningless: evolutionary science deals with selection or adaptation that results in populations of organisms genetically different from their ancestral forms, where evolution has no intrinsic directionality. The discipline makes no general distinction between changes leading to populations of forms less complex or more complex than their ancestors, and in such terms the concept of a primitive species cannot be defined.

The question is a bit unclear

There is a slight issue with the question as it is not that easy to categorize all animals as living strictly in the water, on land or in the sky. Note that almost no living things live strictly in the sky without ever touching the ground. Here are a few examples of limit cases

oysters
dragonflies (larvea live in the water, adult fly)
flying squirrels
Most ducks (spend much time on water but nest on land)

As a consequence the question is very undefined

Examples of potential interest to you

The question is undefined but here are a few examples of cases anyway that will interest you. For simplicity, I will reduce my list to animals only and will not consider similar cases in procaryotes, and non-animal eukaryotes such as plants and fungi.

Whose ancestors were terrestrial

Cetacea (blue whale, orca, dolphins, ...)
Sirenia (dugong and manatees)
Pinnipeds (sea lions, sea leopards, ...)
Monotremes
Marine iguana (and other swimming lizards)
Beavers
Otters

Whose ancestors were flying

Penguins
ratites (Ostrich, emu, kiwi, ...)
dodo
Many birds are able to stay for relatively long period under water when hunting for fish.
Ants and other non-flying hymenopterans.
Ground beetles and other non-flying beetles
water beetle

Again, categorization is not that easy. I just want to highlight the water beetle as example where the ancestor was marine, then terrestrial, then flying, then non-flying and finally living in the water again.

Related post

How many times did terrestrial life emerge from the ocean?

Evolution helps an organism to be successful in the environment in which it lives. In this case, the organism evolved to suit it's aquatic environment. So there's nothing called devolution. For example, the cave  proteus is blind while it's ancestors weren't. It does not mean that it has devolved. It doesn't require well developed eyes in a dark cave. So it has evolved to suit it's environment. Same case here.


Is there a way to know how many sodium channels are active (conducting) at a given time in the brain? I was doing some reading about anti-epileptic sodium channel blockers, then wondered how many sodium channels are actually conducting (actively passing ions) at any given time, that is, in an "average, awake" brain?

Unfortunately, there is no way to know how many sodium channels are active (or even present) in one person's brain due to the extremely high variability of channel and neuron density in a population and the lack of methodology around quantifying total number of healthy active synapses (1). Diseases like epilepsy can occur due various points of the sodium signaling process going wrong. It could be sodium channels are deformed and not accepting the proper signal, it could a low density of channel proteins, or it could be damage to the neuron themselves (2-4). No one has examined the "normal/healthy range" of sodium channels in the brain. When categorizing sodium channel deficiency scientists will often compare the number of sodium channels in a healthy brain vs. a disease brain using bioluminescence imaging or some other visualization technique. Bioluminescence specially quantifies the number of active sodium channels by binding causing healthy sodium channels light up and then quantifies density by the brightness of the synapse. This is not a direct quantification of the number of proteins, but I can not think of any technique that allows you to count the number of proteins on a cell without damaging the cell. I'm sorry this isn't technically an answer to your question, but hopefully it provides some helpful references to understand molecular brain protein imaging.

Principles of Neuroscience
Low Sodium Channel Density and    Epilepsy
Sodium Channel Mutations and Epilepsy/ Other Nervous    System Disorders
Neuropathy and Sodium Channel Related    Diseases

This is a difficult question because we are talking about properties of channels-molecules which can have stochastic opening and closing rates. The question is made even more difficult by the fact that there are multiple types of sodium channels. One can begin to quantify this by recording from many many cells in the awake animal using in-vivo electrophysiology by washing in sodium channel blockers and looking at sodium currents. Conversely you can start doing antibody staining for sodium channels in a brain area -- then take acute slices from that area and do single-channel recordings so you have some sense of number* probability of opening.


Why can't we call dog breeds different species? I understand this question might fall into opinion based, but I'm trying to write it so that it meets the "Many good questions generate some degree of opinion based on expert experience" part and not get closed.

A closed creationist question about directly observing the evolution of new species made me think about just declaring dog breeds as new species just to provide an answer to that question. Turns out I'm not the first one to think of it, and to be honest I probably read that article and forgot about it.

That article quotes geneticist Jerry Coyne as saying:

  “If somehow the recognized [dog] breeds existed only as fossils,
  paleontologists would consider them not one species but
  many—certainly more than the thirty-six species of wild dogs that live
  in nature today.”

There is also this question about breeds of dogs being different enough they can't breed. The answer posted to that question discusses attempts to breed beagles with irish setters, and having great difficulty.

I'm aware that the commonly used definition of different species is individuals who can't interbreed and make a fertile offspring. However the Scientific American article I referred to above mentions that animals are often classified as separate species because they are separated by a geographical barrier, and if they could mingle they would make fertile hybrid offspring. The same articles mentions fruit fly research that bred two different species of fruit fly and made fertile offspring, even though they would never interbreed in the wild.

This is speculation, but let's imagine taking an island and putting several breeds of dogs on that island. Many of those breeds would easily interbreed and create mutts. But I'm pretty sure there would some sorting, the large dogs like st. bernards and great danes aren't going to easily interbreed with tiny dogs like chihuahuas. If we came back to this island after 50 or 100 years, we'd probably see small dogs and large dogs (assuming the island had decent ecological niches for both sizes of dogs to survive in)

Creationists like to ask why we haven't observed the evolution of a new species and don't want to listen to arguments about the fossil record or DNA sequences. If we just define some dog breeds as different species, we'd have an easy answer. I think some dogs would at least come close to meeting that definition for these reasons:

Dog breeds with large size differences would have great difficulty breeding.
Some pairs of breeds seem to have trouble interbreeding (Beagles + Irish Setter).
Some animals recognized as different species can create fertile hybrid offspring.

So why don't we recognize some dog breeds as different species?

I don't enjoy the idea of comparing people to dogs, but this is a bit akin (please note the bit) to asking if people who are genetically short (or "little people", both proportionate and disproportionate dwarfism), pygmies, short people, normal sized people, tall people, very tall people, and people with acromegaly (gigantism) can be called different species. I compare because it's fairly clear to most individuals that we are all the same species: homo sapiens. About breeding, it is very likely that a reproductive specialist would be quite concerned (I certainly would be) about a woman with drarfism carrying the child of a very tall person (who had very tall parents), but not the opposite pairing.

Below is a photograph of the wedding of Tom Thumb and Lavinia Warren. That union produced no children. Her bridesmaid Minnie, (her sister), who was only 27 inches tall, also married a little person (Edward Newell). She became pregnant with a normal-sized child, but died during the birthing of a 6 pound baby (her baby died as well).

Are they a different species? No. A paleontologist (a good one) would be able to tell that the bones of a little person was actually of the same species based on certain conformations, just as I believe paleontologists today could distinguish prehistoric small cats from very large cats. Size matters, but not nearly as much as the type and distribution of teeth, the shape of the jaw, etc.  In other words, I strongly disagree with the following:

  If somehow the recognized [dog] breeds existed only as fossils, paleontologists would consider them not one species but many—certainly more than the thirty-six species of wild dogs that live in nature today.

That statement is based on a fairly profound error in thinking: a cognitive bias that is mistrustful of science in general due to a lack of familiarity with the rigors involved in the scientific methods of paleontologists in particular. I say this without rancor or animus of any kind; where I settled down (in the deeply religious region), the vast majority of my children's friends' parents are creationists, and the vast majority of our friends are fundamentalists. We argue about science all the time; I know the basic arguments. I'm familiar with their websites. I personally find myself in the camp of Christian thinkers like geneticist Francis Collins, M.D., Ph.D., the director of the Human Genome Project, who understand genetics and find no threat to their faith in evolution or science. (E.g. Creationists reject all science which indicates the age of the Earth is >~6000 years.)

The truth is that the definition of a species is not that easy, even for prokariotes. Difficult as well is a pure definition of life.

Finally, about size. The domestic dog exhibits greater diversity in body size than any other terrestrial vertebrate. This is due to a small number of (or perhaps even a single) alleles: the IGF1 Allele. It's hard to argue difference of species on the basis of a small number of alleles: we allow much more variability for other alleles without wanting to classify as different species: eye color, hair color, hair length, straight vs. curly coat, degree of tail curl, ear morphology, etc.

A Single IGF1 Allele Is a Major Determinant of Small Size in Dogs
Lessons learned from the dog genome
A species definition for the modern synthesis
Single-Nucleotide-Polymorphism-Based Association Mapping of Dog Stereotypes
Canine Genetics Facilitates Understanding of Human Biology
How many species of prokaryotes are there? (PNAS)
Ernst Mayr and the modern concept of species (PNAS)
Hybridization, ecological races and the nature of species: empirical evidence for the ease of speciation
Is it Useful to Have a Clear-cut Definition of Life? On the Use of Fuzzy Logic in Prebiotic Chemistry

I don't think taxonomy works as precisely as one would hope...NOT that they don't have standard approaches but they are often working with inadequate information.  Rightfully, if a population of chuahuahuas and St Bernards lived side by side in the wild, they would, from a biological standpoint be considered a different species because they could not interbreed.  IT would be physically impossible.  And, in short time, behaviors of both would tend them to start staying away from each other.  NOT that evolution works preemptively, but as behaviors vary...those tiny dogs that simply stayed away from the massive males would tend to survive (NOT die in child birth) while those that inadvertently got pregnant by the massive male DID die in childbirth...any inherited tendency toward the safer behavior would be selected for.  The "example" of dwarfism...when it is known, does not apply to finding fossils in rock strata.  Through testing and actually experience we know very small people can interbreed with very tall people.  Often the pregnancy doesn't end well.  But for now and for reasons other than pure science, no one is considering re-naming human taxonomic groups...and they shouldn't IMHO.   But with dogs, with sometimes completely different structures and sizes of skulls and other body parts and the recognition that the massive dog's fetus would not life and be birthed from the tiny dogs womb would incline them to be described as different species.  Size AND VARIATION in structure does matter in taxonomy.


How come large herbivores have such thin legs? Edit:
This question is very similar to this and related to this one (though the latter focuses on homology instead of scaling laws). However, the answer to this question is far more comprehensive, in particular it offers a plausible explanation why horse legs evolved as they did (vs human or even rhino legs).

Large grazing mammals such as horses, moose, and cows tend to have relatively thin legs despite being up to ~1000kg. For example, this rider's and her horse's legs appear to have about the same cross-sectional area both for below and above the "knee":

If this horse is 500 kg (a mid-range mass for horses), each leg would have to support 125 kg, compared to only 37.5 kg for a 75 kg adult. Why don't we see a corresponding difference in cross-section?

Elephant, rhinoceros, &c all have much thicker legs in proportion.  The answer, I think, lies in the fact that the animals you mention all evolved as cursorial animals (that is, they run to escape predators).  Less mass in the lower leg means it swings easier, so the animal can run faster.

There are two things you're apparently not noticing in that picture.  First, the the horse's lower leg is almost entirely bone (and some tendon), and it's bone that does the supporting.  The propulsive power comes from the large muscles of the hip, thighs, and shoulders.

Second, the lower part of the leg (with the white wrappings) is not anatomically equivalent to the human's lower leg, but to the bones of the hand and foot.  You can see this if you look closely at the rear leg in that picture.  The femur, equivalent to the human's thigh, ends at the knee just above the belly line.  Then the tibia extends about halfway down, ending at another joint which you might think is the knee, but which is called the 'hock' in horse-speak.  The white-wrapped part is a metatarsal, equivalent to human foot bones, then there pastern bones equivalent to human toe bones, ending in the hoof/toenail.

So consider that you can, if reasonably fit, walk around on tiptoe without crushing your foot and toe bones, then imagine the end result of your ancestors having done this for the last several tens of millions of years :-)

PS: With horses, there is some effect from human selection, too.  Racing & show breeds tend to have thin lower legs, draft horses & working breeds have proportionately thicker ones.  My first horse, a thorobred/arab mix, had legs about as thick as my wrists (granted, I'm a fairly muscular guy); my current mustang, about the same height & weight, has legs about twice as thick.

You're assuming that horses and cows are still subject to Darwinian evolution.  In fact breeding of domestic animals has mostly been controlled rather carefully by humans, to breed for characteristics which we feel are favourable, even if those characteristics are detrimental to the animal's survival in the wild.

This became most obvious in the Agricultural Revolution, with selective breeding work pioneered by Robert Bakewell and others, where animal size increased dramatically.  African cows today give you an idea of how big cows would have been before this breeding effort, but even they are the product of thousands of years of fairly selective breeding.

Horses are a similar case.  Genghis Khan's Mongol warriors used ponies of around 12hh, and these would have been relatively wild animals.

Fragility of limbs is just one way modern animals are rendered less fit in the wild, of course.  Many breeds of domesticated animals have problems giving birth without assistance, or have genetic defects which can cause the animal distress or reduce its lifespan.  These issues are usually tolerated or managed somehow, because humans prioritise the desirable features of the breed.


Could humans theoretically see infrared better than regular light? I have noticed that in infrared film, people's eyes reflect that light within their eyes much like nocturnal animals (and many other animals for that matter) do with regular light. I know that this is in order to maximize their night vision capabilities by reflecting more light onto the retina.

My question is this: If a human had the nerves in our eyes to process infrared light, would someone with these 'special' eyes be able to see better than someone with 'regular' eyes? What would they see? What about in low-light conditions?

...Infra-red illumination of the eye produces the 'bright pupil' effect

Source: http://www.museumsandtheweb.com/mw2003/papers/milekic/milekic.html

(most of the way down the page)

No, retina doesn't have or has too few infrared receptors.

Practical example: most remote controls use IR LEDs (infra red light emitting diodes) to send commands to a receiver device. So take a remote control, keep pressing a button and look at its front. Do you see any flashing light? Now take a camera (phone camera, photo camera or video camcorder) and look with it at the remote while pressing a button. Now you see it producing white light. The camera sensor detects IR. That is how night vision in cameras work.

What you read in that article is about how light is reflected by the eye (the pupil). There is nothing to do with the retina which is on the 'back wall' of the eye ball.

Infrared light is emitted by warm things, like our head.  We'd be detecting it ambiantly all the time.  That's why animals that can detect infrared are not warm-blooded.


Why are some neurones unmyelinated? As far as I am aware, most of the central nervous system consists of myelinated axons and most of the peripheral consists of unmyelinated.

What is the reason for this?

Would it not be more efficient to have them all myelinated?

In this answer I'm building off of @Fizz's pointer to the nice paper by Laurence Knowles, "The Evolution of Myelin: Theories and Application to Human Disease" [1].

First -- I just want to point out that your question is adaptationist, which means that it assumes that myelin is on some axons and not on others for a reason. Whereas maybe evolution just hasn't gotten around to it yet, even though myelinating all axons would actually be beneficial.

That said, here are two of the main downsides of myelination:

It might cost energy. This one is a bit controversial, but at least one study has found [2] that while myelin decreases the energetic cost of firing an individual action potential, the whole apparatus involved in myelin (e.g., in the CNS, the oligodendrocyte, its processes, and the sheath itself) actually costs more energy than it would cost to just open all of those ion channels without saltatory conduction.
Myelin and its associated oligodendrocytes/Schwann cells take up space. This is likely to be especially important in areas of the nervous system where there are a lot of neurons packed into a small area.

So from the adaptationist perspective, the question is whether the benefits of myelinating an axon, such as increased conduction velocity, increased conduction fidelity, axon protection, and supplying the axon with nutrients, are worth the downsides of taking up space and possibly increasing net energy use.

http://www.ashdin.com/journals/JEM/235996
http://www.jneurosci.org/content/32/1/356

Myelinated neurons are neurons whose axons are surrounded by myelin; the myelin has has an insulating effect and allows the axons to conduct neural impulses faster - but at some metabolic cost, so neurons are not myelinated unless there is a significant advantage to they're being able to conduct faster.


Can you help with insect identification? (Outback Australia) This was in my child's shoe that was left outside. They got it out of the shoe and it went on the wall where they measured it. The body is approx 3 cm and from head to tail it's 6 cm. Any help would be greatly appreciated!

We are in central Australia in the Outback.

This is a member of the family Anostostomatidae, but given its sex is unlikely to be placed further (many Orthoptera are best identified on the basis of males, including this family).  There don't seem to be internet-based identification tools for the group (but the page http://bie.ala.org.au/species/urn:lsid:biodiversity.org.au:afd.taxon:a8042a0a-f34e-4ae3-ab86-5306b9176774#gallery shows a number of specimens and living examples, the latter usually taken only to family); Chapter 5, "Australian king crickets: distribution, habitats and biology (Orthoptera: Anostostomatidae)" in the book The biology of wetas, king crickets and their allies appears to be the best option I've seen that might allow a further identification.

Looks like a king cricket, Anostostoma australasiae

http://www.qm.qld.gov.au/Find+out+about/Animals+of+Queensland/Insects/Grasshoppers+Crickets+and+Katydids/Common+species/Giant+King+Cricket#.WIs179XRU0M


What biological specimen is this? Seed? Excrement? Fungal form? Hundreds of these 1-3 mm "seeds" have been found a couple of times this summer on my deck shaded by a large oak tree. But, they are not seeds with typical seed parts.  Too small to be pollen or spores.  I am baffled. They each have one or more deep crevices or slits longitudinally. Structurally, they appear to be composed of tiny (almost microscopic) wood chips. (Though I am sure this is just the appearance they have.) The first time I found them was after a rain and they had absorbed water and swelled to twice or three times their size and had become gooey and almost gelatinous to the touch. Almost looked like hundreds of little piles of brown poop on our deck. This time the weather was dry and they look as pictured in the photo.  I swept up hundreds in a four-foot diameter area.  Another area of the deck had a similar amount.  None on the rest of our deck or any noticed in other areas under the oak tree. My biologist friend was also baffled.  Please help identify

All right, I'll say it if nobody else will.  Insect feces.  The "wood chips" you saw are bits of your oak (or some other over-hanging tree) that have graduated from the arthropod digestive tract, so to speak.  The pellets soak up water because the bugs are on a tight water budget and extract all the water before making a deposit.  Never heard of a gall infestation that produced feces like this, but who knows?  Look for dieing, deformed, or discolored leaves.  Look for bugs on the tree and on fallen leaves.  On the 2nd page of the document linked below is a larger specimen of what you are getting.  http://collier.ifas.ufl.edu/CommHort/CommHortPubs/Stained_sidewalks_under_Oaks.pdf

Since these pellets are found under oak trees, I researched further and found a possible answer on the internet in a different location.  Apparently, they are "galls" caused by insects disturbing the leaf structure of the oak trees.
https://ask.extension.org/questions/157218
Not sure, still, what exactly is raining down in the pellets.  Is it just dead plant material or is it something reproductive for the insects?  I am very familiar with the ping pong ball "galls" that sometimes fall from these trees.
Once they get wet and then dry again, they eventually become very powdery and crumble into dust.


Why do some viruses cease being a problem even though no vaccine or cure is found? No vaccine or cure has been found for SARS-CoV or MERS-CoV yet the world is not too concerned about them. How can it be? Did all people who had those viruses die or do viruses just randomly decide to stop being infectious at some point?

Infections spread in a population when the number of new infections caused by an infected person is greater than or equal to 1.

If each infected person spreads the virus to less than 1 person, eventually no one will be infected, without a need for any sort of cure. Of course, the longer a deadly infectious disease spreads in a population, the more people will die during this process. Ideally you want to get the number of transmissions as close to zero as possible as quickly as possible.

SARS and MERS are each a bit different, but share some similar characteristics. Compared to COVID-19 caused by SARS-CoV-2, both are more severe in a larger fraction of the people infected (note: all three viruses are closely related betacoronaviruses). This made it easier for public health officials to identify and isolate infected individuals.

The MERS virus is really not gone at all: it lives on in animal reservoirs, like camels (so it is primarily only a concern in places where those reservoirs live). Cases continue to occur sporadically. However, MERS is usually not that transmissible between people, having a natural transmission rate that is already less than 1: that means that most people who get it get it directly from an animal, and don't continue to spread it to others besides occasional infection of individuals with close-contact, like a family member. There have been exceptions where isolated incidents involved substantial human-to-human transmission. Some of these incidents were associated with "super-spreaders": particular individuals who got infected and spread the virus to way more people than the average. See https://wwwnc.cdc.gov/eid/article/26/2/19-0697_article for more.

SARS caused by the original SARS-CoV virus indeed seems to be gone, with no cases reported since 2004. The elimination of SARS from the human population occurred via controlling the human-to-human spread through isolation and contact tracing. See https://apps.who.int/iris/handle/10665/70863 for a report on the epidemic and how cases and spread in different locations were handled.

Viruses don't have any agency: they can't decide to do anything. However, humans can, and our best response to outbreaks of novel diseases is to trace the spread and try to limit transmission as much as possible.

One more effect: a pathogen that is both deadly and highly contagious either triggers strong response (when we talk about humans, human pets, cattle, etc) or simply wipes out the population it infects (and disappears with it).

This creates a strong selection pressure over the pathogen. In order to successfully spread, it either becomes less deadly, or less contagious, or both. The generations of the pathogens change quickly and mutation rate is usually high, so the pathogen (given time and groups of hosts to infect) will react to the selection pressure.

The groups, once survived the less-deadly version of the pathogen are at advantage - they are most probably immune also to the original. The pathogen is also at advantage - it gets less organizational reaction (quarantines, vaccines, etc) and more hosts to infect (because survived hosts reproduce and the new hosts are not immune).

p.s. a second-order of the same effect is the pathogen becoming less dangerous only to minors of the host. We all know a lot of examples.


How does a baby deer stand the day it's born? I know most creatures take time to learn some things.

Birds take some time to fly.
Human beings take some time walk or stand.

But in the case of the deer species, it's different. It can stand the same day it's born. Why is this so?

If you compare placental mammals in how much time they need to start walking, you'll see that deer are no exception. Humans are an exception.

Hypothesis of Obstetrical Dilemma

The hypothesis of Obstetrical Dilemma states that humans are born premature. We very much think this is because if we were to be born more developed (like other mammals), our big brain would not be able to make its way through the pelvis. Also, bipedalism leads to a narrower pelvis making the passage of the big brain even more problematic. For this reason, human babies are very dependent on the care of their parents for a long time. This hypothesis is called the Obstetrical dilemma (see Rosenberg 1992, Weiner et al. 2008 among many other papers as well as several books such as Ancient Bodies, Modern Lives for example).

Counter arguments to the Hypothesis of Obstetrical Dilemma

Note however that this hypothesis comes with a few potential contradictions, such as the fact that human gestation is no shorter than the gestation of humans' sister species. Indeed, in chimpanzees, for example, gestation lasts 243 days on average against 280 days on average for humans. These counter-arguments can be found in Dunsworth et al. 2012.

Thanks to @MattThrower and @AdamDavis for their helpful comments.

On a practical note not previously mentioned: If deer couldn't walk very soon after birth, they would be very vulnerable to predators, as would their parents who would have to remain nearby to take care of them.  This is true for many creatures - even for predators themselves, if you think about it.