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Are gene variants at different loci also called alleles?
I think the title says it. I always read that alleles are gene variants at a given locus, which confuses me. Thanks!

I really hate that term "allele" and avoid its usage as much as possible :P I feel it is a prehistoric term which I don't know for what reason is still in use. I generally use "allele" only to differentiate maternal and paternal copies; I call gene variants as paralogs. Many people call paralogs as alleles too if they are quite identical.

@WYSIWYG Are you referring to e.g. "functional" alleles (alleles defined by functional differences) vs. alleles as DNA-sequence variations?

@fileunderwater As I said, the term confuses me a lot. So I restrict my usage to paternal/maternal copies.

EDIT:
Short answer : Yes: "allele" is a synonym for "gene variant", irrespective of location (locus).
Background
Original answer: From About Education I found this definition for an allele:

An allele is an alternative form of a gene (one member of a pair) that is located at a specific position on a specific chromosome.

EDIT:
Hence, two alleles are located at the same locus, but are situated on a different chromosome.
ADDITION EDIT: Given the many high-quality comments (and the downvote) I erased the concluding sentence of my first attempt and I will elaborate below:
Feero et al. (2010) gives the following more elaborate definition of "allele" (text relevant to the question is bolded out):

Specific locations in the human genome where differences between individual people
  are found are generally referred to as variations, and the term “normal” or “wild type” is often used to refer to the most common variant at a location in a given population group. In its simplest form, the variation has two different spellings, referred to as “alleles.” If the frequency of the minor allele is greater than 1%, such variants are called polymorphisms. The word “mutation” is generally reserved for changes in DNA that are believed or known to be pathologic [...] or for changes that are [very] recent (e.g., not inherited DNA changes).

Hence, from my understanding, the original quoted definition from About Education still stands.
As to the critical comments placed by the PO, @fileunderwater and @WYSIWYG:
(1) [...] what is a copy or a variant of a gene at a different locus on the same chromosome? - That is a very interesting question, and I think Feero et al. (2010) deals with that simply by saying

In its simplest form, the variation has two different spellings, referred to as “alleles.”

In other words - perhaps the gene duplication is a step too far for this terminology. And in fact, although I regret having to cite wikipedia here, it does provide a very enlightening sentence:

[...] [A]t the gene locus for the ABO blood type [...] classical genetics recognizes three alleles, IA, IB, and i, that determine compatibility of blood transfusions. Any individual has one of six possible genotypes (IAIA, IAi, IBIB, IBi, IAIB, and ii) that produce one of four possible phenotypes [...].

Hence, what this implicitly tells us is that an allele is, as Feero et al. (2010) also says, simply a gene variation.
This means that it basically boils down to what is a "chromosome locus"?
An article by Proulx & Phillips, 2006 entitled "ALLELIC DIVERGENCE PRECEDES AND PROMOTES GENE DUPLICATION" mentions:

[...] [H]eterozygotes at a single locus are broken up by segregation, whereas for duplicate loci an individual can carry copies of alternative alleles at separate
  loci.

Hence, what the authors implicitly say is that an allele is a gene variation and that a locus is a fixed position on a chromosome. Hence, a gene duplication means 2 loci that can carry the same or a different allele. This should answer
(2) Are the alleles at the two duplicated loci then named differently, even if their DNA sequences are identical (as well as the protein they might be coding for), namely no, an allele has a name (e.g. IA) that remains unchanged when duplicated. The locus is then different for the duplicate, but the name of the allele stays the same (as an allele is, by definition, simply a gene variant wherever on the chromosome).
(3a) [...] two versions of a gene at two different loci are alleles (not paralogs)?: yes
(3b) What about the same identical version at two different loci: same allele or not? yes, same allele, allele has nothing to do with locus. Just a gene variant. Where ever.

Reference
Feero et al. N Engl J Med 2010;362:2001-11
Proulx & Phillips. Evolution 2006;60:881-892

Ok, but what is a copy or a variant of a gene at a different locus on the same chromosome?

Is this really the case when you have recent gene duplications, so that a species e.g. has two loci with the same gene (paralogs), and still only two versions of this gene irrespective of loci (so two alleles at one loci duplicated to two original alleles found at two loci)? Are the alleles at the two duplicated loci then named differently, even if their DNA sequences are identical (as well as the protein they might be coding for)? Mostly a question on naming convensions I guess, but I'm curious.

@user14860 If they are the result of duplication they are called paralogs.

@WYSIWYG Ok, so saying that two versions of a gene at two different loci are alleles (not paralogs)? What about the same identical version at two different loci: same allele or not?

@fileunderwater Can be called. But it is confusing; there should be a term that explicitly means homologs at the same locus in the homologous chromosomes.


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Questions on DNA damage
I'm not strong in biology, so bear with me on this:
I've been reading that as we age, our DNA is damaged by internal (e.g. errors during replication) and external (e.g. sun damage or radiation) factors.

If you take, say, an 80 year old, can you find DNA in their body that's the same as when they were a newborn? What kind of cells would have undamaged DNA?
Is DNA damage distributed evenly across the body or will some parts have more damage than others?
Is there any published data on how much DNA damage an average person accumulates over their lifetime? I'm not sure how this can be quantified, but I'm wondering if there has been any study on gauging damage.

Since errors frequently occur during cell division, I guess cells that divide less frequently (e.g. mature neurons do not divide at all) will probably have less damage. Some cells not only divide fast, but also become polypoloid (e.g. liver cells), so these cells probably can tolerate a lot of mutations.

Also, this new article may be of interest DNA mutation clock proves tough to set. Apparently, rates with which mutations accumulate over human generations may be fluctuating!

Excellent question!

You would definitely be able to find quite a few sequences of DNA that are undamaged (in fact most of them would be undamaged), but it is very unlikely that any cells in his/her body would have a perfect copy of the entire original genome.
I'm sure that cells closer to the skin (exposed to more radiation) would have more mutations, but beyond that most everything depends on where you live, your habits, etc. (if you're a smoker you will obviously have more mutations in your lung cells).
Under regular circumstances (low levels of mutagens), about 3 nucleotide mutations occur in the human genome per cell per division (DNA replication) (from http://www.ncbi.nlm.nih.gov/books/NBK26881/). The rest of the math would be a very rough estimate, seeing as you'd need to make a lot of assumptions (cell division rate average, other mutagens an organism may encounter, life span, the list goes on), but however you want to do it, there's the number you need to start with.

I hope this helps.
CDB

Hi. Thanks for your answer. Regarding the first question, is it possible to use multiple DNA samples and compare them to one another to derive the entire original genome? The goal would be to identify damaged sequences and replace them with the undamaged ones from other samples since I assume a single block of DNA is unlikely to be corrupt in every single sample. I think a similar concept is implemented in cryptography and data storage in computers to achieve integrity.

@Mark13426 Sure. See e.g. this PLoS Computational Biology paper and references therein. Often the aim in these studies is to map cell lineages rather than infer the genotype of the fertilized egg, but the information is there if you wanted to do it.

I'm not sure how you would identify which sequences were the original, undamaged sequences unless you had a reference (such as a map of the organism's genome when it was an embryo), but it would be very possible to retrieve an entire complete and undamaged genome from perhaps only a few hundred cells if you could identify the original DNA. May I ask what your project is regarding? It sounds very fascinating!

@CDB It's not generally true that cells closer to the skin have more mutations; what matters more than e.g. UV exposure is the number of cell generations that a cell goes through. Intestinal epithelium turns over rapidly and can have up to an order of magnitude greater number of cell generations than other tissues, resulting in a higher number of accumulated mutations over the lifetime.

Very true, however skin cells would be much more prone to mutations from radiation and radiation is a much more deadly mutagen than just mistakes made inside the cell itself seeing as radiation actually destroys the nucleotide.

@Mark13426 I apologize, I just realized something that you said in your comment. Comparing the cell genomes themselves to find the original genome without a map of it would be possible. It would just be very extremely difficult.

@CDB Regarding radiation leading to higher rates of mutation in epidermis than in more rapidly proliferating tissues: is do you have evidence for that, or is that just a hunch? Because in mouse, it goes in the opposite direction. And liver tissue, with its high exposure to mutagens, accumulates vastly more mutations than epidermis.

Thanks both of you. I'm not involved in any project. Over the last year, I've been interested in the study of aging. The older I get, the more I think about death, so I have a personal interest in why we age and whether it's preventable. With regards to genome preservation, I've been asking myself whether it makes sense to get my genome sequenced (not sure if this is commercially possible) and use the data in the future if future medicine can take advantage of it. Sounds like genome reconstruction is difficult, so why not map out whatever I have now while I'm healthy? Sorry, if I sound silly.

You've asked a number of questions here, but yes -- mutation rates have been studied extensively in humans as well as in model organisms. And as you suggest, they vary substantially across tissues. One starting point to read about how mutation rates are measured and how they vary across species, tissues, etc., is a 2010 Trends in Genetics review by Mike Lynch. See particularly Table 1.

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A study claims that the consumption of fish increases the likelihood of getting skin cancer, does this have any relation to their omega-3 content?
A study claims that fish consumption increases the likelihood of getting skin cancer.
Since another older study claimed that omega-3 consumption increases the likelihood of prostate cancer is there any evidence that omega-3 is at least partly responsible for the increased likelihood of cancer assuming that the result of the first study is accurate?

The study doesn’t mention fish (that I saw on glancing at it) at all. How did you jump to fish? Also, can you support your statement about omega 3 fa? There’s a good chance you missed something. Thanks.

There are academic-ish articles that you could have referenced such as this which suggest a link, but with indeterminate cause as far as I can tell (they guess it's toxin contaminants).

The summary article states Data showed that the risk for developing SCC and BCC was associated with a higher intake of polyunsaturated fats. While the risks of SCC, BCC, and melanoma were associated with a higher omega-6 fat intake, omega-3 dietary fat intake was found to be associated with risk of BCC but not with SCC or melanoma. No other fats were associated with melanoma risk.

Honestly spoken, I doubt the results of this study and there are a few reasons for this. To start with, we have to recognize that the authors did quite a lot of work to exclude bias and false conclusions. They did their study as a prospective study which means they collected the data first (questionnaire on eating habits) and watched the people afterwards to see the outcome. This avoids wrong conclusions or bias in terms of what has been eaten. Also, the sample size is sufficiently large, which is often problematic in such studies.
To categorize the results: In this study, the effect size was not very strong, the hazard ratio was 1,22 (with a 95% CI = 1.11-1.34 ) meaning a 22% higher risk of developing melanoma. The absolute lifetime risk for developing melanoma in the US for white skinned people is about 2,6%, putting a 22% increase on top would translate in a absolute risk of around 3,2%.
However, some points are to be criticized, some mentioned by the authors. First, this is a study which relies on a self-reported questionnaire on their fish consumption in the year before and then tracked the participants for 15 years. This is not very hard data, since I would probably misjudge the amounts of the different stuff I ate and drank over the course of the lase year. Additionally it does not factor in changes in lifestyle (some people may become vegetarians, I personally ate a lot more fish when I lived close to the sea since it was easily obtainable and so on).
Then there are factors which are a lot more important for developing melanoma. This includes exposure to UV radiation (sun and sun tanning booths), mole count and if you are lightskinned/have red hair. For the later the absolute risk for getting melanoma is about 400% higher than for people with dark hairs. Also the UV exposure: The study did not ask for the personal habits on UV exposure (meaning working outside a lot like gardening or other outdoor activities or using tanning booths), they calculated the UV associated risk by the median UV radiation based on the place of living at the beginning of the study. As far as I can see they did no further correction for places of living for the following 15 years which might have brought a much higher (or lower exposure). Not correcting for these importants factor contributing to the development of melanoma is very problematic and can skew the whole statistic. What happens if the group of "fish related melanoma" contains disproportionately many redhaired people?
Some points are just curious. The authors distinguished between canned tuna, fried and non-fried fish and found a correlation to the development of melanoma only between non-fried fish and canned tuna. This is an observation for which they do not really have an explanation.
Additionally the median age in which melanoma where first detected was 70,1 years, according to the American cancer society this age for the whole population is around 65 years of age. This might not be significant but is at least odd.
The authors themselves speculate about some toxins like arsenic, mercury or polychlorinated biphenyls which have been connected to melanoma in recent studies, but fail to explain why this would not cause problems with fried fish.
Taken together, this is a relatively weak link which is not supported by strong indications while there are other, strong causes of disease which have not been analyzed further. If there is such a link, I think this is a very weak and not very important one.

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What is the oxidation state of iron at the photosynthetic reaction center?
Is the iron at the reaction centre  in the $3^+$ or $2^+$ oxidation state?
For instance, 1AIG is $2^+$ or, perhaps it will depend upon charge separation state? I checked the PDB: some are $3^+$ while some are $2^+$.

At what reaction centre?

The question needs more information. The pH is critical to the answer.

Iron in these complexes is used to transfer electrons and so can exist in both oxidation states.

in chlorophyll it is Mg but in RC it is iron. I am asking the role of Fe. I don't care about Mg. I am not doing catalysis. By the way, what is the role of Mg?

How will PH influence the oxidize state? Just the normal living plants and bacteria. I saw in PDB various molecules. They marked out whether they are 3+ or 2+ ......I think they did not specify the PH?

Iron is fixed at the RC. It is not moving. It cannot transport electrons.

no....in the reaction center of (bacteria)  light harvesting antenna

Is there anything interesting about Fe in cytochromes?

@latra yes, Fe in cytochromes is also fixed, but it also functions to transport electrons. Like cytochrome c oxidase, or generally, all cytochromes in electron transport chain in respiration.

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How likely is rabies virus will enter the body through this kind of imperfect human part when you perform this "experiment"?
First, let's not confuse my question with typical skin peel when your body part slip on a road and get that typical red colored skin due to blood. It's not like blood is flowing, but clearly red area is visible due to some upper skin damage. This often happen when you fall from motorcycle and friction between your body part and the road (especially when you're not wearing riding gear).
Example
I read somewhere that skin abrasion is considered open wound which definitely can cause rabies spread if it came in contact with virus.

My question is more about non bloody/reddish skin imperfection of any human body part for some reason. The similar peeling can occur for many other reasons. E.g. when hands or even toes have been wet for long time then the palm or finger tips, toe skin is more likely to peel if someone manually tried to peel it.
Important thing is - it usually doesn't cause any noticeable pain or blood.
Here is an example that will clarify a little:
Example
It's like the skin is peeled (manually or through some disease). There's no blood though as upper layer usually doesn't cause pain.
But unlike this palm skin if someone tries to peel the opposite side of their palm (I mean the skin where there are hairs on skin i.e., the back side of hand), it is more likely to give pain and cause red area/blood.
So the focus of my question is around an imperfection of a skin which doesn't have blood and pain.

Here's the thing I'm curious about:
Suppose a dog has rabies virus in its saliva. And we collect the sample in a glass. And then make a contact (like submerging for few minutes) with the saliva with the human part.
In simple terms, that particular part of human body has touched that saliva.
Now I'm interested in knowing how likely is rabies virus will enter the body through this kind of imperfect human part when you perform this "experiment"?

Why am I interested in knowing this?
I belong to a developing country where education system is not good enough. So you can't expect a college professor in average college to answer you about this. And top colleges need high skills. I want to educate myself and people around me. Most people around me know that you can get rabies only when a dog bites you and a lot of blood is flowing. Which I think misses a lot of information or it is incomplete.

What I've studied so far is this:

Rabies virus can spread through bites (which is easy to understand because wound is deep)

It can spread through wounds which are deep or at least have blood (I'm really not sure if my example is considered a wound or not )

Saliva of a dog will contain the rabies virus after the incubation
period (read here) But in my question, let's assume dog saliva
contains the rabies virus

Example of a few skin problems I read here: https://www.healthline.com/health/skin-peeling-on-hands (I could not add it to my question because it was marking it spam)

You asked this question a few months back. This is a medical question, as it concerns your skin lesions. We cannot predict how likely it is in every situation; strange things can happen, but usually don’t. How likely is it that someone will be killed by a stone gargoyle breaking loose from an old building a moment before they walk by? Highly unlikely but it has happened. The CDC has a lot of good information on rabies which might reassure you. No one, though, can predict with any accuracy a one-off event.

@anongoodnurse where did I say "my skin" or "your skin"? If someone asks a question about skin, human gut, immune system, cell, human muscle, baldness, retina etc. (which of course are posted here usually) that doesn't make it "my" or "your" body part. It's a general question.

Secondly, I tried my best to edit this question after moderators and others suggested me to edit it. I might have not done better editing but I still think it's definitely not asking for personal medical advice now.

If we were not aware of your previous question, the present question (which contains long passages verbatim from the personal medical question you asked), maybe this would “fly”.  However, the problem exists that this is a thinly veiled personal medical question. At least you have your answer.

@anongoodnurse okay. The thing is I did not try to hide my past history. It's public. But I really don't think dragging my past history into this separate question to prove it a personal medical question is a "Be nice be respectful policy". That is what close votes and down votes are for.
And why do you think there haven't been many personal medical questions already haven't "flown"? Or won't fly in the future?
Irrespective of the past, my whole intention was to get educated and educate people around me on this topic.

There is a whole lot of difference between developed countries and developing countries about rabies. People here aren't aware of many basic things about rabies. People "assume" a lot of things without facts.

If asking this question helps to gain knowledge to someone, I really don't think it's a bad thing.

One thing I would point out is that no one in their right mind would collect the saliva of a rabid dog then submerge their broken skin into it. So what, exactly, are you educating the public about? Have you seen this done? Have you tried to talk people out of this? The answer given, which is rock-solid, concerns people who have come into contact with dogs they have assumed to be a non-risk for rabies, and paid the ultimate price for their mistake. The scenario you propose is unfathomable…

…and if it leads you to try to spread false information about the risk of rabies from objects in the environment, that is not educational, it’s the opposite: it’s misinformation. There are orders of magnitude between the solid answer and the risk of contracting rabies from an object outside where a rabid dog may have wandered .

@anongoodnurse that is the worst argument. If you think everything could and should be prevented only when it realistically happen, that isn't how someone educated always. Prevention is better than cure and there's a far big difference of importance between experiment and accident. I am not spreading false information, you are trying to prove my question is far worse than actually it is.

Your logic is worse. It is like blaming Louis Pasteur too by trying to experiment to find cure rather than naturally waiting and getting infected by rabies and then find a cure.

Finally, I never tried to spread false information. I tried to investigate facts. Do you see difference? Please read my old history and this question again. You're stuck with my old history. There's no point in argument. I rest my case.

I don't think anyone can give a good estimate for the risk from such exposure, but it is not zero. From “Scratches/Abrasions without Bleeding” Cause Rabies: A 7 Years Rabies Death Review from Medical College Shimla, Himachal Pradesh, India:

We investigated 19 deaths due to rabies in the past 7-year period. Of these, five were caused by “scratches/abrasions without any bleeding” and no postexposure prophylaxis (PEP) was sought. All injuries were caused either by unvaccinated pups below 3 months of age or by stray unvaccinated dogs. Four deaths were of patients who received proper wound care along with minimum 3 doses of intramuscular rabies vaccination, but rabies immunoglobulins (RIG) were not given or were not available. In eight cases, no PEP was sought as the patients were either not aware of its need or the PEP facility was far away or the PEP cost was not affordable or deceased believed that pups below 3 months of age do not carry a risk of rabies. In one case, the patient was bitten by a cat 2 years back. Majority patients belonged to rural and remote areas. Five of the deaths in our study were because of not seeking prophylaxis as abrasions/scratches without bleeding were not thought to carry a risk of rabies. In the Philippines, a rabies death review of 1839 patients demonstrates that all deaths were due to dog related injuries including bites and scratches.1 In Iran[2] four people having scratches on their hands were infected with the saliva of rabid animals and died due to rabies, there was no history of bites. In our death review also, deaths caused by “scratches/abrasions without blood” amply demonstrate the ability of the rabies virus to enter nerves through dermis due to broken skin and its capacity to cause rabies.

So, clearly, bleeding at least is not necessary for infection. My guess would be that many skin conditions would provide the virus enough access to susceptible cells that infection could result. Personally I would seek treatment after any exposure to potentially infected saliva, even on completely healthy skin.

Thanks. That is helpful information. I wonder why some users are reluctant on sharing information on this topic. I know it's not easy to answer but not every answer needs exact and 100% fool proof facts right?

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Do humans have any biological adaptations to eating cooked food?
Humans have been cooking food for at least tens of thousands of years. The presumed reason why cooking took root in nearly all human cultures is that cooked food is easier to digest. However, cooking food can also generate toxic compounds such as polycyclic aromatic hydrocarbons, which would not be found in the uncooked version of the food. Considering that humans have been eating cooked food for such a long time, I am wondering whether humans evolved any adaptations to eating cooked food, e.g., that certain types of foods, when cooked, are more toxic to our closest relatives (great apes) than they are to humans, because we have more ability to metabolize the toxic compounds.

I'd say that tens of thousands of years is too short a time on an evolutionary timescale to develop any adaptations. On the other hand, social learning did take place, in teh sense of learning of what can and cannot be eaten, how it should be cooked, etc. One could thus make an interesting study of how local cuisine has evolved via selection (what is available and edible), random drift (accidental trials and ideas whiel cooking), and other evolution-like forces.

@Vadim its really not, just look at the evolution of lactose tolerance in human populations that kept cattle.

Fair point. Indeed, if domestic animals had enough time to evolve into new species, so could humans. It is still not clear what are the evolutionary pressures here: I'd rather expect more random drift than adaptation.

Humans are incredibly good at processing maillard compounds, which include both beneficial and mildly toxic byproducts of cooking. Humans are better at breaking them down than other animals. This is presumed to be an adaptation to eating cooked food. Malliard reactions are also a good indicator of when most plant and animal products are safest to eat via cooking, (browning) which may explain why humans on average show a preference for them or even adaptations to detect them. we are also learning that one place animal testing may be problematic is in dietary tests becasue of this.
extra reading on hominid adaptations to diet

Adaptation implies selection. In other words, the claim is that those uncapable of digesting cooked food would have lesser chances of survival. On the other hand, more random drift is quite possible. A somewhat similar case is the increase of the number of women in need of cesarian section - it is not a adaptation to an evolutionary pressure, but result of removing such a pressure.

@Vadim no a trait to be better at doing something is also is also an adaptation. very few adaptations have lethal alternatives, they are just better than the alternative. humans are better at digesting cooked food than any animal tested, due to known unique enzymes, that is adaptation. https://onlinelibrary.wiley.com/doi/abs/10.1002/evan.21498

https://en.wikipedia.org/wiki/Adaptation
What you are saying that people became better at digesting cooking food (adapted) without any insensitive to do so. What could be an adaptation is if people began using cooked food, because they are better at digesting it. Also, the link that you provided emphasizes the role of the gut mircobiome, which is in a big part acquired during lifetime (apart from what we get at the birth, which is still not genetic).

@Vadim NO, incentive does not mean do it or die. incentive or in biological terms "advantage" comes from well having an advantage.  If Jon is better at digesting cooked food that Bob he has a distinct advantage, he is getting more nutrients and fewer problems from the same foodstuffs. Cooking was a part of the hominid diet long before Homo sapien evolved. Also only one link refers to gut microbes, that is the one that lists many factors.

advantage in evolutionary terms means producing more offspring - either by living longer or by doing it more frequently or in bigger numbers. If Bob produces as many miserable Bobs as Jon happy Jons, neither has particular advantage.

@Vadim if you don't understand how greater resource access constitutes an advantage I can only suggest you ask a few questions about evolution. This is pretty basic evolutionary biology.. To use an very basic example, why do herbivores have longer guts than carnivores?

I understand how greater resource access can be an advantage, but it doesn't mean that it always is. I am simply trying to help you clarify things. Your argument about humans being able to digest cooked food better is a solid one, but it needs to be correctly interpreted from the evolutionary standpoint.

There seems to be evidence that cooked food intake regulates different genes than raw food in mice. Apparently these genes also tend to be human specifically expressed (more precisely, their overlap is more than expected by chance) [1]. While this is not a dramatic finding, it does show association between cooked food and genomic changes that evolutionary adaptation implies.
As for toxicity of certain edible foods to non-human primates, I do not know the answer but I would not expect toxicity. Rather, high metabolic demand of humans might have required more protein based diet which is safer when cooked.
1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860691/


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If the human atlanto-axial joint is pivotal only, what accounts for the craniums additional degrees of freedom?
The atlanto-axial joint is supposedly a pivot joint. I assumed it would be considered a ball-and-socket joint, based on a) the physical shape of the dens, and b) the degrees of motion of the cranium relative to the spinal column.
A pivot joint is distinct from a typical ball-and-socket joint because it only allows for a single degree of freedom; yaw - to rotate about it's own axis or diameter, like a spindle. A typical ball-and-socket joint allows at least one additional plane of limited movement.
I can think of (or observe) at least three degrees of freedom of the cranium, relative to the spinal column; pitch & roll. Pitch allows you to direct your gaze from the ceiling, to the floor. Roll allows lateral movement in a similar manner, so you can point your left ear to the ground, and then your right.

The additional degrees of freedom are provided by the entire cervical spine, rather than the atlantoaxial joint alone, which is the joint between C1 and C2. What you're describing as roll (when you point one ear to the ground), is provided by contraction of the sternocleidomastoid. The sternocleidomastoid muscle pulls the mastoid process (behind the ear) down and in, toward the fixed clavicle and sternum.  The joint that provides lateral flexion in response is the entire cervical spine.
Here you can see the sternocleidomastoid muscle (the SCM):

And here, a drawing with a reasonable approximation of the way the cervical spine responds to lateral flexion (due to contraction of the SCM). I can't find a good c-spine film at the moment to demonstrate it in a human person, rather than an artists imagination. But this drawing is accurate to my recollection. You can see the space between C1 and C2 on the right is quite limited (that atlas and the axis are in close apposition). C2 and C3, as well as the other cervical vertebrae, have more space between them on the right:


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How old would seashells be if I found them 9 ft deep 30 miles from the ocean while digging a pond in North Carolina
 This is a picture of some specimens that I found while digging a pond. I'm 30 miles from the coast in Wilmington, North Carolina and dug down about nine feet past the blue clay and hit a layer of seashells.

This Wikipedia page might interest you.

this is probably a better fit for the earth science stack, since this is really a question about stratigraphy.

I'm not familiar with the area at all, but it looks like Wilmington is one of the coastal cities in southern North Carolina (NC):

Image attribution: Rcsprinter123, CC BY 3.0 https://creativecommons.org/licenses/by/3.0, via Wikimedia Commons
As NC seems to be basically a highland of the Piedmont and Appalachian ranges caused by a geologic fault line with a slope towards the coast followed by lowland flat areas, what you are likely seeing here is remnants of a historical sea-level change.
There's what seems to be a good summary of the geologic history at North Carolina Seagrant University, from which I take the following.
About 200 million years ago, the Atlantic ocean started to form of the Eastern coast of the USA and deposited marine sediments that vary in depth from a few feet (~1-2 m) deep to about 10,000 thousand feet (~3,000 m) deep  at Cape Hatteras on the Outer Banks. Since then the land has risen and fallen a few times, resulting in quite a range of environments, from terrestrial to marine and back again. These should all be represented in the rocks below you by the fossils present.
The rocks will range from hard sandstones and mudstones in the deeper parts to quite soft friable sediment in the shallower bits. The clay overlaying will be alluvial/fluvial deposits since the most recent sea level dropped or the land rose in relatively recent times.
You are seeing some of these historical sediments. As you are only about 30 miles (50 km) inland and the terrain seems to be fairly flat, the sediments will be quite deep below you. The ones on the top will be the more recent ones and might be quite soft in terms of rock that they are in. They should all be fossil bearing if they are oceanic sediments, as yours seem to be.
I can see remnants of some type of mollusc (a snail) in the top, followed by some what is probably coral on the right. You also have a one half of a scallop shell (these are bivalves, so one top and one bottom shell. The top half of the shell is usually the flat one. You also have a shark tooth. Given the size of the shark tooth, I suspect that it is from Otodus megalodon, the giant well known "Megalodon" shark which was the subject of the dramatic movie The Meg.
As this species of shark lived between 4 and 23 million years ago, that gives you some indication of the age of the sediments in which you are digging.


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Book request: systematics and evolution of vertebrates
Would you recommend any good vertebrate systematics & evolution book?
The main goal is to teach a Master's level class - mostly focused on amphibia, reptiles and fish.

I'm tempted to recommend Alfred Romer's The Vertebrate Body , but it's quite out of date now.

If nobody is able to offer recommendation on Biology.SE, you can look at reviews on Amazon by search Vertebrates Evolution. This book has many good reviews for example

I really like Liem et al.'s Functional Anatomy of the Vertebrates: An Evolutionary Perspective.


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Purpose of K+ channels in action potential
I understand that they serve to repolarize the neuron after the Na+  influx. What I don't understand is why this is important.
Meaning, let's say all the K+  channels disappeared. So now the potential is up near +50 mV about. It doesn't go back down quickly, because the K+  channels aren't there. Instead, we have to wait until the Na+/K+  pump can restore the proper intra-/extra- cellular balance between them. And then the neuron can fire again.
I can see that it will take longer for the potential to be restored. But don't we have to wait until the Na+  concentration is restored before we can fire again anyway? If we don't wait, wouldn't that interfere with maintaining sufficient/proper extracellular Na+ concentrations (which I would assume would have other effects)? And the same amount of time will be needed for the Na+ balance to be restored.
So what do we really gain by having a way to restore the charge differential?

Great question! However, your question is based on some misconceptions about what polarization means and how ion movement is involved, as well as the difference between equilibrium and the time it takes to get there. That's okay - it's a mistake that many many people learning about neurophysiology make, including instructors.
Na+/K+ concentrations actually change very very little during an action potential. The Na+/K+  pump establishes the concentration gradient, not the resting membrane potential. The resting membrane potential is caused by the concentration gradient plus the relative permeability of different ions via the Goldman equation: specifically, that permeability to K+ is much much higher than Na+.
When you open voltage-gated Na+ channels during an action potential, the relative permeability to sodium increases dramatically, so the new "equilibrium potential" is closer to the reversal potential for sodium (again, use the Goldman equation). There will be a net flow of ions (mostly Na+ coming in) until that new equilibrium potential is reached.
However, voltage-gated Na+ channels inactivate quickly, so that equilibrium isn't really reached. Instead, as the Na+ channels close, the new equilibrium potential is back near the original resting potential (for a third time, use the Goldman equation), because the primary permeability is to K+ through leak channels, and therefore the net current flow direction changes.
Okay, so what's the need for the voltage-gated potassium channels in all this? Well, the rising phase (sodium phase) of the action potential is fast because there is a really high conductance to Na+ so lots of Na+ can flow quickly in. In comparison, there is a lot less conductance of K+ through the leak channels. If all you have are leak channels, it takes a long time to return to rest. Equilibrium potential is just that: the equilibrium. It takes time to get to equilibrium. Voltage-gated K+ channels speed up that return to rest.
What if you had no K+  conductance, including no K+ leak channels? Well, then it doesn't matter at all what the relative concentration of K+ is inside and outside the cell: check the Goldman equation! You can't really have no conductance to anything at all, but if there is no dominant ion then the membrane potential will be something around zero. In that condition, the charge imbalance of the Na+/K+ pump process can contribute a couple mV, but nothing more than that.
All that said, to address your specific questions:

I understand that they serve to repolarize the neuron after the Na+ influx. What I don't understand is why this is important.

It's important for speed and for the minimum refractory period between action potentials. Nervous system activity would slow way way down if action potentials could only occur every 100 ms.

Instead, we have to wait until the Na+/K+ pump can restore the proper intra-/extra- cellular balance between them. And then the neuron can fire again.
But don't we have to wait until the Na+ concentration is restored before we can fire again anyway?

Na+/K+ pump is only needed to maintain ion balance over a very long term. On the time course of a single action potential, the concentrations of Na+ and K+ do not change appreciably. That's not what repolarization is.

So what do we really gain by having a way to restore the charge differential?

Speed!
You can also see my answers on some related questions:
Why is it possible to calculate the equilibrium potential of an ion using the Nernst equation from empirical measurements in the cell at rest?
Why does K+ moves out of the cell?

Dude, leaving something for me too! +1 anyways...

Seems like you've pitched your answer at a higher level since its becoming difficult to get your point (that too, without any diagram/graph/equation!). Don't worry for answer length if longer only means better. Everyone knows that the question is quite broad ;)


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Major groups of photosynthetic prokaryotes
According to Stryer there are four major groups of photosynthetic prokaryotes, i.e. Table 19.1
Bacteria Photosynthetic electron donor $\ce{O2}$ use.
Green sulfur $\ce{H2}$, $\ce{H2S}$, $\ce{S}$ Anoxygenic.
Green nonsulfur Variety of amino acids and organic acids Anoxygenic.
Purple sulfur $\ce{H2}$, $\ce{H2S}$, $\ce{S}$ Anoxygenic.
Purple nonsulfur Usually organic molecules Anoxygenic.
Cyanobacteria $\ce{H2O}$ Oxygenic.
Do each groups belong to a different genus?

To answer your question, yes they are all in a different genus, but that’s really specific.  If you are wondering about their fundamental differences, they fall into a few different groups.
Green sulfur bacteria usually falls into the phylum Chlorobi
Green non-sulfur bacteria falls into the phylum Chloroflexi (Part of the terrabacteria superphylum)
Cyanobacteria is a phylum in itself but also falls into the terrabacteria superphylum.
Both, Purple sulfur/non-sulfur bacteria are all proteobacteria.
Now, pay attention here, as linking these could be somewhat confusing sometimes.  But now we can link together their relationships.
Green sulfur bacteria (Chlorobi) falls into the FCB superphylum, meaning that it is a gracilicute.
Purple sulfur/non-sulfur bacteria (Proteobacteria) are also gracilicutes.
Green non-sulfur bacteria (Chloroflexi) is part of the terrabacteria superphylum.  Terrabacteria are not gracilicutes.
Cyanobacteria is also in the terrabacteria superphylum. (Again, not a gracilicute.)
Now that we know this, we can reasonably assume that both purple sulfur/non-sulfur bacteria are related to green sulfur bacteria, as they are both gracilicutes.  Also, we can conclude that the non-gracilicute green non-sulfur bacteria and Cyanobacteria are more closely related to each other than they are to the latter mentioned bacteria.
Here’s another cool fact, some Deinococcus-Thermus bacteria (members of the terrabacteria superphylum along with Cyanobacteria and Chloroflexi) have been found to carry the bacteriophytochrome photoreceptor (BphP) which absorbs red light.  Interestingly, Deinococcus-Thermus are non-photosynthetic, but these photoreceptors are found in photosynthetic Chloroflexi as well. This indicates that the deinococcus bacteria likely diverged from chloroflexi at some point but still retained the BphP.
Hope this helped!

Genus is the classification one more general up from species.  Two species in the same genus will be pretty similar - for example wolves and coyotes.  Two things with radically different energy metabolism systems will not be in the same genus.  In fact these different modes of metabolism mean that the creatures using them are so different from each other that they are categorized in different phyla (phylum being the second division after kingdom). Humans are in phylum Chordata with frogs and fish.  Prokaryotes using such different modes of energy metabolism will not be closely related at all.

phyla! so high? need to go to so high level so that they are together?

Is there a website or something that I can determine from the name to know whether does two species are together?

Sure.  Wikipedia has them all.  For example the (super cool!) green sulfur bacteria.  https://en.wikipedia.org/wiki/Green_sulfur_bacteria


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Why is cartilage replaced by bones in a vertebrate adult?
Why is cartilage present in a vertebrate embryo replaced by bones in an vertebrate adult even though cartilage can also provide me the structural framework like as in Chondrichthyes and they seem to do well with it as Sharks are members of Chondrichthyes which are some of the most fearsome creatures of the world.

Short answer, cartilage can't provide the same support as a bone,  bone is stronger and stiffer.
Sharks may be big but they have pathetically weak bites for their size and that even when they partially ossify their jaws. They just can't fully ossify the tissue. The main swimming action of "fish" works even with flexible connections because each muscle is linking to the next linearly, the cartilage and collagen is mostly subjected to tension. But things like jaws and limbs need to withstand shear forces and withstand flexion, which cartilage sucks at, but bone is quite good at. It is not coincidence that the first bones evolved in jaw.

Bones are complex organs, made of more than just a structural element. Cartilage is just a tissue, usually devoid of nerves and blood vessels.
Chondrichythes live in water (ἰχθύς ichthys is Greek for 'fish'); the difference in specific gravity and buoyancy is considerable, and cartilage is not robust enough to mechanically support your body out of the water.
Vertebrates have evolved to have a bone marrow, which is part of the bone. If the structural element of the bone (the dense mineral matrix) was replaced by cartilage only, then the hollow structure would make things even worse.
Additionally, cartilage has about the same density as water (Pan et al, 2016) whereas dense bone is 60-90% more dense, which means extra weight pulling aquatic animals down.

Bones evolved in fish that lived in the same water as sharks, so the mechanical argument doesn't hold. Maybe land vertebrates would be hindered (but there are plenty of insects, etc. that do just fine).

@kmm The mechanical argument only means that "if you live on land and have a significant mass, then you need bones", it does not mean that "if you have bones, you cannot live in the water". There is no contradiction here :)

Then I don't understand the point you are making in the 2nd paragraph with respect to the poster's question.

It's an example of why in certain contexts, vertebrates (like you and I) have a biological advantage because they have bones instead of cartilage. Which contributes to explaining why the presence of bones has been maintained in aerial vertebrate lineages. It does not explain everything but it explains why vertebrates are ecologically successful on land (which is where the majority of described vertebrates species live) so that helps answer the question

bone marrow is unrelated to bone, marrow actually evolved before bone. https://www.ncbi.nlm.nih.gov/pubmed/3636583


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Thermophilic yoghurt bacteria survivability in the gut
Would they mostly not simply perish since they need much higher than body temperatures to thrive? Are mesophilic ones (such as kefir) much better at that and thus have better probiotic functions?

I had magnesium supplements for a while because i was deficient, but their alkaline pH upset my gut and I had gas. Afterwards, I tried all kinds of cheese and yoghurts, olives and whatever fermented food i could find. They had nearly zero probiotic action. one day i had fermented taboulet salad from a pack that had puffed up from fermentation. I was completely better for a week, Since then i decided that cheese has very little probiotic effect and that a soup that was purposefully left on the counter for days until it goes biological has incredible probiotics.

Milk contains no cellulose and plant matter, so if you eat plants, a fermented equivalent of milk, unpasteurized/fermented plant matter, should logically provide probiotics more adapted for humans. Milk products are a good contribution to diet but it's a myth that they are contain a suitable mix of probiotics for all people, they are probably most effective for digesting protein. cheese yeasts can thrive between 0-43 degrees and diverse cheeses contain a bigger diversity of species.

I have been questioning the usefulness of commercial yoghurts stored, sold and served chilled. And @comprehensible, your point well taken, unless there is a lactose and caesin rich diet, these poor mircrobes will only starve and suffer in the gut if they had not already died of cold.


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What kind of snake is this
Found this outside on patio in northern Virginia, Ashburn area, September 2018. It's about 12 inches. Is it a water snake or rattlesnake?

It looks like an Eastern Hognose Snake, which is characterized by an upturned nose and high likelihood of playing dead.
These are described as variable in coloration:

"Two color phases are common in Virginia: (1) a patterned phase (79.6%, n = 98), characterized by a series of 19-27 (average = 23.2 ± 2.4, n = 12) black or dark-brown blotches along middorsal line, with alternating black spots on sides; body color consists of varying combinations of gray, tan, pink, yellow, orange, and red; venter of body and tail immaculate cream to dark gray;"

If you replace the tan in this image (www.virginiaherpetologicalsociety.com) with gray in yours, I think the pattern match and overall body form are very similar:

Another characteristic of Hognoses is their tendency to flatten their necks in a cobra-like fashion when they feel threatened. This is visible on both the picture in the question, and in the answer.


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Why does menthol clear a stuffy nose?
I've looked all around online for an answer to this. Some sites say menthol causes blood vessels in the nose to constrict, some sites say it causes blood vessels to expand. Many sites simply say it's a remedy, but with no explanation.
And if it does cause the constriction or expansion of blood vessels, what's that got to do with making the stuffiness go away?

Wow, you aren't kidding about the different answers online.  To add to the confusion here's an answer from the Mayo Clinic saying that menthol tricks the brain into feeling like you are breathing through an unclogged nose.  https://www.mayoclinic.org/diseases-conditions/common-cold/expert-answers/nasal-decongestant/FAQ-20058569

Menthol is stimulating action potential at cells which are inducing thermoception. As far as I have found out it does not have any effect beyond that. The patients only feel like they can breath better while it could not be proven that they actual do.
https://www.ncbi.nlm.nih.gov/m/pubmed/18702906/
The blood vessel thing : In general "cold" is a cause for vasoconstriction - that might lead to the conclusion that menthol is doing the same. I have no experental background on that but - after online research :-D- it seems like that menthol causes vasodilatation.

+1 for the correct answer. Fyi: If menthol caused vasodilation, there would be an increase in stuffiness, which is not the case. One can decrease nasal stuffiness with vasoconstrictors, like phenylephrine hcl. The reverse holds as well.


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Is this plant Yucca filamentosa color?
I am trying to find the name of this plant for a while. The closest I got is Yucca filamentosa color. The leaf blades are near 4-5 inches and are almost thin(without pulp). Please help me in identifying it.

Location: Hyderabad, India.

Yucca mostly has smooth leaf  and this has spine shaiped leaf.  Yucca ussaly dont have so wide leaf. (https://www.swcoloradowildflowers.com/White%20Enlarged%20Photo%20Pages/yucca%20baccata.htm) here is some pictures of semi desert yuccas

No, not the Yucca baccata . I was thinking Yucca filamentosa color guard(http://www.missouribotanicalgarden.org/PlantFinder/PlantFinderDetails.aspx?kempercode=d184). As per the wide part, the leaf blades in my picture are around 4 inches wide.

You know i am not professional botanic so i hope you will get proper answer for this question.  But i think that yucca has smooth leaf without pulp(mostly), but agave has spike shaiped leaf with pulp.

Thanks for mentioning the pulp part. The plant that I uploaded has almost no pulp in it's leaves.

I found out the picture that I posted belongs to  Furcraea foetida 'Mediopicta'. It belongs to "Agave" family like L.Diago suggested in comments.


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How is CO2 and O2 separated in our body during gas exchange?
https://www.msdmanuals.com/home/lung-and-airway-disorders/biology-of-the-lungs-and-airways/exchanging-oxygen-and-carbon-dioxide
The image in the above link shows that CO2 and O2 both pass through the same membrane but still CO2 is exhaled and O2 is taken in the body.
Why doesn't the CO2 mix with O2 and stay in the blood ?
Why is only CO2 passed out through the membrane?

You actually inhale and exhale both CO2 and O2, what changes is the relative amounts of each.
Besides tiny percentages of various gases and non-gas particles, air contains primarily nitrogen (78%) and oxygen (21%). Carbon dioxide makes up roughly 0.04% of the air you inhale.
By the time you exhale, that air now contains about the same amount of nitrogen, but the amount of oxygen has decreased to around 15% and the amount of carbon dixoide has increased by about a hundred times to around 4%.
On the level of individual cells, both gases pass through the membranes in both directions, what matters is how much passes in each direction. As @porkchop explains, that depends on the relative concentrations. When it reaches the lungs, blood has relatively high CO2 and relatively low O2, compared to the outside air that you inhale. As long as the air stays inside, the two will equilibrate. There will be some molecules going each direction - some CO2 molecules will go into the blood, but many more will leave it and go into the air, and some O2 molecules will go into the air, but many more will come from the air into the blood. As a result, the net flow is CO2 going out of the blood, and O2 into the blood. Diagrams usually only illustrate the net flow.

But if the CO2 attains equilibrium shouldn't there be 5 % of CO2 also stay in the blood and shouldn't the concentration increase with time?

5% isn't an appropriate way of describing it because blood isn't a gas, it's a liquid with CO2 solved in it. But yes blood leaving the lungs should have about the same "CO2 content" as exhaled air, and as it runs through the body it accumulates more CO2. There can be conditions under which more CO2 accumulates throughout the body than the blood can get rid of in the lungs (i.e. suffocation), and we also have a programmed responses to that condition (gasping).

But we don't suffocate frequently, right? But still CO2 is accumulating in the blood.

Blood is never completely devoid of CO2, but that doesn't mean the baseline increases over time. How much CO2 is left in the blood when it leaves the lungs depends on the concentration of CO2 in the inhaled air. As long as that's constant, the blood will always end up at the same baseline CO2 content after undergoing gas exchange.

@poin yes. But CO2 in blood is also being converted to carbonic acid and eventually bicarbonate, so the chemistry is a bit more complicated

@Poin Don't forget about the breathing part: blood and lung gas match in the lungs, then you breathe out the lung gas and bring in new gas that matches the outside air, then diffusion happens again until they match and so on. If you stop breathing yes, CO2 continues to accumulate in the blood and lungs and you asphyxiate.

It all comes down to concentration gradients. In deoxygenated blood, which is what enters the lungs, the O2 concentration is relatively low and the CO2 concentration is higher than that of ambient air. On the flip side, the air that we breathe in has a higher concentration of O2 than deoxygenated blood. The alveolar membrane is thin enough that the gases can diffuse across this gradient almost instantly. And just like that, you have oxygenation of blood, and removal of CO2.


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Can anyone identify this species of spider?
These spiders are all over everything on my padio in New Hampshire. Can anyone help me identify what they are?

How big are they?

They look like acari: https://en.wikipedia.org/wiki/Acari

They are approximately 1mm in total size leg to leg. I am suspecting that they are some sort of mite, but they don't seem to bite, or be in the tick family (at least not human blood suckers).

Pretty clearly mites, not spiders, but unfortunately I'm not a mite guy.

It depends upon the environment or surrounding

Based on your area and this pest control site I believe that the bugs in your picture are not spiders, they are clover mites. I have found that some clover mites are a darker brown color and also slightly larger. This image gives a better view of the features of a clover mite, including the longer pair of front legs and oval shaped body:  Clover mites don't pose a threat to people or animals as they live off of either plants or fungi, but smashing them can leave stains on furniture and clothing.


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Remove the baby from the womb
Is it possible to remove the baby from the womb of a mother to cure the baby of a tumor and putting it back in the womb to be delivered naturally (the baby is 6 months)

Welcome to Biology S.E.! Can you clarify where the tumor on the baby is? Fetal surgery is definitely a thing; however, I would tend to think that a doctor wouldn't want to operate if it weren't a threat to the baby's life. If you have any questions about what kind of questions you should ask or how to ask them, please feel free to visit the Help Center, here https://biology.stackexchange.com/help.

I would think it would be nearly impossible to remove the fetus from the womb, as it is connected to the placenta, and thus to the mother.  While I'm not a surgeon, I would think using minimally-invasive techniques would give a greater chance of success. See e.g. the Wikipedia article on fetal surgery https://en.wikipedia.org/wiki/Fetal_surgery or any other of the ~3.7 million hits on "surgery "in utero"".


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Mendelian dominant trait involved with Hypodontia
If the absence of teeth is a dominant trait, then why is it not seen in generations? My teacher taught that absence of teeth is a mendelian dominant trait, but why don't we see this trait if it is dominant?

Hypodontia isn't a single gene phenotype, but a poli-genic mechanism involved with epistatic phenomenons and environmental scenarios.
The trasmission isn't clear till now, but when you're talking about a poli-gene phenotype isn't so easy to describe the way in which the trasmission is performed. You could find every info about this disease here, in a meta-review study:

Note also that if there was indeed a dominant allele for hypodontia, then if the frequency of this allele is low enough, you would still not see it (or only very rarely).


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A cure for radiation exposure?
Some of the greatest inventions of my lifetime have been from looking at nature and copying. I found out tadigrades in outer space have the ability to repair their own DNA when exposed to radiation thousands of time higher than what it would take to kill a human being. Can the tardigrade's genome be mapped and the section of DNA responsible for repairing radiation damage be duplicated? Would that be a good thing? Could a stem cell with that section of DNA make our astronauts safer?

Would that be a good thing?

Recent research from the Samson lab at MIT suggests that there are side effects from amplifying the DNA repair mechanism.
Hyperactivity of a base-excision repair (BER) protein called AAG in mice caused a positive feedback loop in DNA repair signaling that triggered macrophages to attack retinal cells, leading to a cycle of increased inflammation, photoreceptor (PR) necrosis, and ultimately blindness.
From the linked paper:
In this study, we demonstrated that programmed necrosis and subsequent inflammation are important mediators of AAG-dependent alkylation-induced PR cell loss in male mice... We showed that PR cells present necrotic morphology and oxidative DNA damage after the induction of PR cell death with alkylating agents; furthermore, we observed that PARylation in the PR nuclei is associated with the release of HMGB1, increased macrophage infiltration, and elicitation of an inflammatory response.
Another research project looked at a DNA repair protein called ATM in mice, where hyperactivity or overexpression may be implicated in Alzheimer's and Huntington's diseases. Knock-down mutants show reduced expression of this protein and reduced neural damage.
Ignoring the larger ethical questions of splicing genes into human beings, and the technical questions of how to get said genes inserted, transcribed, and translated in the right place at the right time in the right way, it would likely require considerable study to see what the systematic effects might be from expression of tardigrade or other organisms' DNA repair genes in humans.
At the very least, these papers suggest that the biology is complex enough that turning up the dial on repair machinery could cause serious health problems downstream, as much as it might confer greater protection from radiation or other environmental damage.

My first thought is that, if we were able to introduce such a mechanism, we'd essentially stop natural mutations and therefore natural improvement and diversification of our species. Perhaps, this would only be useful for Human 3.0.
(Tardigrades have ~1300 known species and been seen in fossils as old as 530 Myr.)


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Large black caterpillar, cocoon, moth - Los Angeles
This is my first visit here, probably the first of many, since I have many species to identify!
The first is a regular resident of my back yard in the Los Angeles neighborhood of Mt. Washington. It's a large black caterpillar that comes out at night to feed on what I assume is native flora. I have seen as many as five or six at a time in a good (wet) year, but the last couple of years have literally seen only one at a time. Note the ant in the lower left for scale:

A couple of years ago, I brought one home and kept it in a terrarium until it pupated and hatched.  I have a picture of the cocoon, but can't post more than 2 links right now. It was dark brownish-red, with strands of silk that looked to anchor it to the ground, with the empty body on top.
It turned into this very pretty moth:

Unfortunately, it beat up its wings a little, as it took me some time to realize it had hatched. It was released at night.
I had a possible ID at one point on another website, but I didn't follow up with them, and have a lot of trouble searching there for my old thread. Found this place, and thought I'd give it a shot. As I say, I have many more species questions, but I'll just start with this one. Many thanks in advance.

Based on the image of the moth, I think this is a Painted Tiger Moth (Arachnis picta). See the image of the moth from the Wikipedia (you can even see the yellow color at the head region):

An image of the caterpillar can be found here, but this is less decisive.
It also fits with the geographic location where you found the moth, see here.

That was fast! Thank you! The location does fit, because that's the same one! Tha'ts the page I couldn't get back to, and couldn't remember the possible species they had mentioned. Thank you very much.

@Chris - You do realize you used the OP's own photograph as a source, right?

@anongoodnurse I see different images in the question and my answer.

@Chris - You linked to the OP's photograph as a source for your answer. Still, it worked out well for the OP sice he had been searching for it.

Yes, it did work out well! They are cropped differently, so it wouldn't be immediately apparent that it's the same picture. Thanks again.

@anongoodnurse Now I got it, strange coincidence.

@Chris - I did upvote you, btw, regardless. Good answers are good answers.


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How would you identify the independent variable in an experiment where it isn't specified?
I know that the above question is broad, but I specifically want an answer in terms of the following investigation - all of question 3 (ONLY) of this paper.
The independent variable, according to this mark scheme is the presence of hidden food in the cage to which the rats are released. How am I to identify this if it's not stated that the investigation investigates the ability to learn with the presence of hidden food.

Please include the question from the external site. There are good reasons to do this. The main one is: once the link breaks, your question is worthless. I'm voting to close this question as unclear because even though I have read the exam question and helped to edit the previous version of this question, you still do not have a specific question. Are you asking "what is an independent variable"? I sympathise with your question. It's a poor exam question in my opinion.

@James, it does indeed indicate that. The exam question claims that the difference in the percentage of mice in group P and Q who found food in the second experiment was due to the fact that the group P mice had to look for food when they were released the into the cage the first time around. In the first version of the question, I had completely missed the fact that there IS indeed an independent variable in this question. I deleted the other question. I am absolutely baffledas to how one can note the independent variable in this investigation when the question does not state it at all.

Yet, we seem to be required to notice such an independent variable. How? That's my new question, and it's completely different from the previous one. Does that make the question more specific? :)


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Solving Hardy Weinberg problems
I really fail to understand Hardy-Weinberg equilibrium and can't find an easy enough source of information.
Can you help me to understand Hardy-Weinberg equilibrium?
My goal is to be able to solve the following kind of problem

In a population with two alleles for a certain locus, B and b, the allele frequency of B is 0.7. What is the frequency of heterozygotes if the population is in Hardy-Weinberg equilibrium?

Homework questions are off-topic, so I rephrased your question to make it more general and ask for a tutorial rather than asking for the answer to a specific question. Feel free to roll back if you don't like the edit but the post will likely be closed if you do

Do you want a method to solve the questions or you want to understand the mechanism?

That's perfectly fine with me!

The one thing about Hardy-Weinberg Equilibrium you should understand; this is the null-hypothesis for evolution. It's important not when it's correct, but when and how it's incorrect for a population. Deviations from HW are how populations genetics are measured. As such, it's a simple mathematical model for the random distribution of alleles.

Here is a tutorial to perfectly understand Hardy-Weinberg Rule! If you feel like you just need a brief reminder, you can skip the text until the section In short... and try out the exercises just to check your understanding.
Terms you should know a priori
I will not define the following terms, so make sure you understand them

locus
allele
(relative) frequency
Homozygosity and Heterozygosity

What is the Hardy-Weinberg rule?
Hardy-Weinberg rule (HWr) describes a relationship between allele frequency and genotype frequencies. I will present the maths later.
Alleles and Genotypes frequency
Let's assume we have a bi-allelic (two alleles) locus. The possible alleles are called A and B.
Notation for genotype frequencies
Note that I will use a slightly unusual notation on purpose.
Let $f_{AA}$ be the frequency of the homozygous individual caring the allele A on both haplotype (both chromosome). Let $f_{BB}$ be the frequency other homozygote. Let $F_{AB}$ be the frequency of heterozygote which inherited the A allele from the mother and the B allele from the father. Finally, $F_{BA}$ is the frequency of heterozygotes which inherited the B allele from the mother and the A allele from the father.
Most of the time people write $f_{AB}$ (or similar notation) to designate all heterozygotes irrespective of whether the A allele comes from the father or the mother. In this answer, I make the difference of which parent gave which allele. I will instead note $f_{het}$ the frequency of all heterozygotes. Therefore $f_{het} = f_{AB} + f_{BA}$. Similarly, I will note $f_{hom}$ the frequency of all homozygotes. Therefore, $f_{hom} = f_{AA} + f_{BB}$.
Notation for allele frequency
Unlike the above, I will use a class notation here.
Let the frequency of the A allele be $p$ and the frequency of the B allele be $q$.
All genotype frequencies must sum to 1
Of course, if you add up the frequency of all types of individuals in a population, you should reach 1 (or 100% if you prefer). Per consequence,
$$f_{AA} + f_{AB} + f_{BA} + f_{BB} = f_{hom} + f_{het} = 1 $$
is our first important result.
Problem 1

There is 20% of heterozygote in the population, what fraction of the population is homozygote?

Answer: (hover to see the answer)

 $f_{hom}=0.8$ (or $f_{hom}=$80%)

Problem 2

There are 10% of AA individuals and 15% of BB individuals in the population, what fraction of individuals are heterozygotes

Answer:

 $f_{het} = 0.75$ (or $f_{het} =$ 75% )

All allele frequencies must sum to one
The same is true for the allele frequency, they must sum to one. This is even easier than before. Using the above notation it means:
$$p + q = 1$$
You will note that an obvious consequence of this result is that $1-p = q$ is also true. This is the second important result.
Problem 3

The frequency of alleles which are the A allele is 0.3. What is the frequency of the B allele?

Answer:

 $q = 0.7$

Hardy-Weinberg equilibrium
Let's now talk about HWr.
HWr assumptions
HWr makes a number of assumptions that I will not detail them here. Please have a look at the post Assumptions of Hardy-Weinberg rule for more information.
HWr exercice without explanations
Here are exercises that one may consider they come too early in my explanations. Don't worry too much if you can't solve them but please take the time to try solving them. Please do not try to apply known formulas about HWr, only use your logic and the above formulas (allele frequencies must sum to 1 and genotype frequencies must sum to 1)
Problem 4

In a population, one observes that 20% of the population is homozygote for the A allele and that there are no heterozygous individuals at all. What is the frequency of the A allele?

Answer:

 $f_{A} = 0.2$

Below is a drawing of the population (assuming N=20 individuals) to help understand the answer.
AA | AA | AA | AA | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB
Problem 5

In a population, one observes that all B alleles are present in heterozygote only. The frequency of heterozygotes is 0.1. What is the frequency of the A allele?

Answer:

 $f_{A} = 0.95$

The hard part here is to first calculate $f_{B} = 0.05$. Let's draw the population (assuming only N=20 individuals) and that will likely help you out.
AA | AB | AA | AA | AA | AA | AA | AA | AA | AA | AA | AB | AA | AA | AA | AA | AA | AA | AA | AA
HWr formula
As said above, HWr describes a relationship between allele frequency and genotype frequency
Without much explanations, here are these relationships
$$f_{AA} = p^2$$
$$f_{AB} = pq$$
$$f_{BA} = pq$$
$$f_{BB} = q^2$$
Therefore,
$$f_{hom} = p^2 + q^2$$
$$f_{het} = 2pq$$
To build your intuition, you should try to consider for yourself extreme cases where one allele is fixed (fixed=reached a frequency of one). For example, what are the expected genotype frequencies when

$p=1$ and $q=0$?
$p=q=0.5$?
$p=0$ and $q=1$?

How HWr is often expressed
Mixing up the idea of the above relationships and the fact that all genotype frequencies must sum up to one, one can also write
$$p^2 + 2pq + q^2 = 1$$
As by definition $q = 1-p$, it is also common to replace write
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$
Why do these relationships make sense?
Problem 6

Imagine you are drawing alleles in a population of alleles like you would draw cards from a deck of cards! You draw a single allele. If the frequency of A allele is $p$, what is the probability of drawing an A allele?

Answer:

 $p$

Similarly, the probability of picking a B allele is $q=1-p$.
Problem 7

Ok, now. Assuming that the fact that you already drew an allele does not change the allele frequency in the population (because the population is very large), what is the probability of drawing two A alleles in a row?

Answer:

 It is $p$ for the first draw and $p$ for the second draw. The overall probability is therefore $p \cdot p = p^2$

Here we go! You just solved why $f_{AA} = p^2$. You can apply the exact same logic to find out $f_{BB} = q^2$.
Now the probability to first draw a A allele and then a B allele is $pq$. Therefore, $f_{AB} = pq$. The probability to first draw a B allele and then a A allele is $qp=pq$ as well. Therefore, $f_{BA} = pq$.
Exercise
Problem 8

In a population with two alleles for a certain locus, A and B, the allele frequency of A is 0.7. What is the frequency of heterozygotes if the population is in Hardy-Weinberg equilibrium?

(You will note I renamed the alleles to match my above notation)
Try to solve this problem yourself now!
Answer:

 It is a given that $p=0.7$. The question is what does $f_{het}$ equals to?
 Let's start by calculating $q$. $q=1-p=0.3$.
Then, let's calculate the the genotype frequencies.
$f_{AA} = p^2 = 0.49$.
$f_{BB} = q^2 = 0.09$.
$f_{het} = 2pq = 0.42$.
Here we go! We've got the answer. Let's make sure the answer makes sense by summing up the genotype frequencies to ensure we get 1.
$f_{hom} = f_{AA} + f_{BB} = 0.58$
$f_{hom} + f_{het} = 0.42 + 0.58 = 1$
All good!

Problem 9

At a bi-allelic locus, the allele A is dominant over the allele a. The phenotype associated with the dominant allele is present in 10% of the individuals of the population. What is the frequency of the allele A?

Answer:

 The genotypes coding for the phenotype associated with the dominant alleles are AA and Aa. Therefore, $f_{AA} + f_{Aa} = 0.1$ and therefore, $f_{aa} = 0.9$.
 The frequency of the allele a is $p = \sqrt{f_{aa}} = \sqrt{0.9} ≈ 0.95$.
 To conclude the frequency of the allele A is $q = 1 - p = 1 - \sqrt{0.9} ≈ 0.05$

Problem 10
You will find a HW problem involving selection at this post.
Problem 11
You will find a HW problem involving a population of triploids individuals at this post.
Problem 12
You will find a HW problem for sex-linked loci at this post

In short...
Here is a summary for a bi-allelic locus
Allele freqs sum up to one
$$p + q = 1$$

Genotype freqs sum up to one
$$f_{AA} + f_{AB} + f_{BA} + f_{BB} = f_{hom} + f_{het} = 1 $$
You will note that most often when people write $f_{AB}$, they just mean $f_{het}$ and therefore don't make the distinction between $f_{AB}$ and $f_{BA}$.

Hardy-Weinberg rule
Note that Hardy-Weinberg rule holds only under a number of assumptions (such as random mating, panmictic population, no selection, ...) that I have not detailed here (see Assumptions of Hardy-Weinberg rule for more information).
$$f_{AA} = p^2$$
$$f_{AB} = pq$$
$$f_{BA} = pq$$
$$f_{BB} = q^2$$
Therefore,
$$f_{hom} = p^2 + q^2$$
$$f_{het} = 2pq$$

Putting all together
The whole thing put together is often expressed as
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$

Has anyone else explained it so nicely ever on this site? Awesome answer, +1! I read once that if allele frequency changes over time, it means evolution is taking place. And thats where this rule is used. Would you explain it a bit too? :)

@another'Homosapien'  if allele frequency changes over time, it means evolution is taking place yes, this is true by definition of evolution.  And thats where this rule is used. I don't fully understand what you mean. Actually in the assumptions for HWr to hold perfectly (and not just as an approximation), it is required that there is no selection and no drift (infinite population size) which pretty much mean no evolution. I think it would be worth to make a post on the assumptions underlying HWr. I'll be happy to start (but not tonight!).

I meant this is the application of this rule: making population studies at different times to measure change in allele frequency. I think I can ask a question about that...surely not tonight! But I'll ping you there :)

@AlwaysConfused Yes, I think it was the first time I used it. I kinda failed for several lines answer such as the last answer. If anyone manage to implement spoil-protection for problem 8, that'd be great!

@Remi.b So HW's frequency is relative frequency?

Yes, it is a relative frequency, also called proportion, very often (always in population genetics) just called frequency. It indeed has nothing to do with the definition of frequency as used in wave physics.

Lets say there are 2 alleles. One of them is represented by B and other by b. Both will have some frequency at a specific time in a population. Now, frequency is number of that allele divided by total alleles. So, if frequency of B is, say X, the frequency of b is Y=(1-x). It would be because whatever alleles are not B are, for sure, b.
That gives us our first equation,
X+Y=1
Now, let us consider all the genotypes. There is BB, Bb and bb. Now, considering each of the 2 homologous chromosomes, there can be any 2 randomly selected alleles in a population. Here we are selecting an organism randomly. There can be no bias in selecting. This is one of the essential features of HW equilibrium. There is no selection pressure.
So, for B to be on the first chromosome (of the 2), the probability is x. So is for the second chromosome. So to have B on both, that is BB genotype, the probability is X x X = X^2.
Similarly for bb genotype, it would be Y^2.
Now, for heterozygous, there are 2 possible scenarios, bB and Bb.
For case 1: probability would be X x Y
For case 2: probability would be X x Y
So in both cases it is same, that is XY. So total would be 2XY.
So, lets add all the genotypes. The total should be 1 if all are included.
So,
X^2 + 2XY + Y^2 = 1
That gives our second equation. Now, whatever you have to find, you must find either X or Y first.
When you find one, you will get other by subtraction. When you have that, you can find whatever frequency is asked by putting values in second equation.
Allele B's frequency is 0.7. So allele b will be 0.3 (1-0.7).
By this you get the value of B (frequency of dominant allele) and b (frequency of recessive allele).
Now we put the values in the formula B^2+2Bb+b^2=1.
Here 2Bb is the frequency of heterozygous. So 2x0.7x0.3=0.42.

@cell0 watch the use of articles here. This does need editing, but be careful. Because "frequency" is a term in a mathematical expression, the use of articles is not going to be standard.


text:
Variations in action potential threshold and temporal coding
I would like to ask a few questions about things I'm not sure I understand in a paper Action potential threshold of hippocampal pyramidal cells (...).
(1) At the start the paper considers the possibility of irregular firing patterns of action potentials may be an argument to hold that the information processed by the CA1 neurons is a temporal code. I think it is hard to see the relation of final results (see the abstract) with these initial considerations. Do the results support the temporal coding hypothesis of CA1 neurons? How?
(2) At the end of the first page it says the following: "significant variations in action potential threshold would have implications for the precise timing of action potentials since the probability of initiating an action potential could not be predicted by only fluctuations in the membrane potential".
Does this mean that they aim to explain the irregular patterns by means of the fluctuations in the threshold?
I also don't see how from "the probability of initiating an action potential could not be predicted by only fluctuations in the membrane potential" follows that "significant variations in action potential threshold would have implications for the precise timing of action potentials".

It's very hard to read what you have written here. Can you take some time to edit your post?

@BryanKrause My apologies. I tried to rephrase it, I hope it's slightly more clear.

Hi,
For what I read, the objective of the paper is in fact to study the neural code using methods that study the membrane threshold changes (as you said). They mention both rate and temporal code in the introduction and they do give more emphasis to the temporal coding because it explains better the irregularities of the neuronal transmission.
They did find some correlations between changes in the threshold, which influences the iniciation of the action potential, and the timing and rate of the firing or the firing pattern. That means that the firing pattern influences the iniciation of the action potential even if in an indirect way (which is by influencing the membrane threshold). Saying that the pattern of firing is important it means that the timing is also important, instead of only the rate the firing. Because this is the major difference between both neural codes theory, it does support more the temporal code.


text:
Will a store bought cabbage kill my Pieris brassicaes?
About 4 days ago I found a large amount of caterpillars (Pieris brassicae) in my radishes, I took them aside for seeing how they grow and I am out of radishes to give them. I bought a cabbage in the supermarket to give them as food but I am concerned it could be GMO anti pests which to my understanding could kill the caterpillars.
I took one of them aside and it is happily eating the cabbage, if this cabbage is designed to resist pests how long would it take for the caterpillar to die since she started eating?
Thank you so much for the info :)

I wasn't aware GMO cabbage was available at grocery stores. A quick search for GMO cabbage gave some hits for a scorpion venom gene being added to cabbage, but I couldn't find anything suggesting it was being sold for food yet. Do you have more information?

Can you please provide some more information on the GMO cabbage?

I am not sure the cabbage has gmo, but I naturally think it might have because usually chains like LIDER (Chilean Walmart) where I bought the cabbage works with massive producers. any ways… the caterpillars are still eating and are not dead yet hehe :)


text:
What physical force attracts the anti-codon on tRNA to the codon on mRNA during translation?
What physical force attracts the anti-codon on tRNA to the codon on mRNA during translation? I know that these two bond together, but what actually makes the tRNA move through the cytoplasm to the mRNA on the ribosome?

Diffusion is the obvious answer. tRNAs bind to elongation factors which mediate the former's entry into the ribosome. I don't know if the cell possesses some mechanism to localize these molecules to sites of high protein synthesis, but it's certainly not outside the realm of possibility.

None, simply the brownian motion in action. @canadianer not impossible and I also never heard of such mechanism. Based on this paper, Figure 2D suggests cytoplasmic regions enriched in tRNAs (protein synthesis hotspots perhaps). Could also be background noise though.

As with many processes in cellular biology, nothing really moves anywhere, attracted by specific force. What that means, is that any molecule has a chance to interact with any other molecule, say, bind to it. Only force that is acted is electrical force of attraction of negative charges to positive ones.
Due to diffusion and temperature fluctuations, molecules wander around, bumping in each other. Sometimes, two complimentary molecules will bump into each other in a very desirable, energy-efficient orientation. Their atomic-scale interfaces (with tiny charges on it) will find each other as neat as hand finds glove of the right size/orientation neat and comfy. That is the way, for example, tRNA finds slot on ribosome/mRNA complex to plug into. just simple key-and-lock, or hand-and-glove model, that's all there is. And beauty is that you can try computationally calculate probability and energy of different interactions from molecular 3D structures.
Now, there are many tRNAs, but Glycine-tRNA will bind tightest to glycine-codon/ribosome complex. There is a chance that Alanine-tRNA will get in that spot, but that chance is very little compared to chance of proper interaction. Also, because interfaces of Ala-tRNA and Ala-codone don't match exactly, molecular vibration due to heat (temperature) will destroy this complex quickly. This allows specificity.

The Ef-Tu has an affinity for a factor binding site in the A-site of the large ribosomal subunit. When the anticodon of the tRNA binds tightly enough to the mRNA during translation, two adjacent adenines in the 16s rRNA of the A site crosslink (via hydrogen bonding) the grooves formed by the correctly paired tRNA, increasing the affinity for correctly paired tRNAs. I think those physical interactions are important as well. - From Molecular Biology of the Gene, 7th ED., by Watson.

In short, electrostatic forces and mechanical forces. Electrostatic forces are responsible for the classic Watson and Crick base pairing that is de facto  what brings together codons and anticodons. Mechanical forces are involved in the displacement of the pairing and the shift of the RNAs. The ribosome's subunits literally grab and move both messenger and tRNAs.

I wanted to illustrate the process I explained in a comment on aandreev's answer with some images, I just copy/pasted the actual text sections, however.
From comments:
The tRNA is bound to an elongation EF-Tu (which is also bound to GTP). The Ef-Tu has an affinity for a factor binding site in the A-site of the large ribosomal subunit. You have an anticodon triplet on the tRNA, and a bend in the 3D structure of the anticodon loop gives you wobble base pairing on the last nitrogenous base. When the anticodon of the tRNA binds tightly enough to the mRNA, two adjacent adenines in the 16s rRNA of the A site crosslink (via hydrogen bonding) the minor grooves formed by the correctly paired tRNA. These adenines don't differentiate between G:C or A:T pairs, just the tightness/correctness of the tRNA binding.


text:
What does saying a phylogenetic tree is 'well resolved' mean?
I'm not sure what 'resolution' means in the context of phylogenies.

It means incomplete separation or a failure to split into two groups unambiguously.
There are multiple ways to estimate the resolution of a phylogenetic tree; involving an index to measure the likelihood of observing the phylogenetic tree that you derive relative to those produced by drawing species at random, for instance, or permuting species to produce a null distribution.
A badly resolved tree should show up in sets of randomly generated trees far more often than well resolved ones.
See http://onlinelibrary.wiley.com/doi/10.1111/j.2041-210X.2012.00196.x/abstract

I think PO asks what well - resolved means

My bad, well spotted, Alice.


text:
What makes a good phylogenetic tree?
How can one improve a phylogenetic tree? If one was to make the 'golden standard' of phylogenetic trees, what features would it have? Would it be highly reliable, well resolved etc? What other features are important to aim to maximise when it comes to improving phylogenetic trees?

Can you please merge your two questions into one as these are highly connected? Addtionally you may want to work on your attitude. No one here is obliged to answer, so you probably want to cut down the use of ASAP. Additionally: How does your own research look like, what have you found out?

I've found that a phylogenetic tree is an estimate of the true evolutionary relationships between species.Thus, we cannot really measure a tree's accuracy because we don't know the 'true value' i.e.what the actual pattern of evolutionary relationships is.I'm aware that trees which are well resolved,constructed using multiple genes & with high reliability/repeatability(indicated by high bootstrap values)are considered to be better than others but I'd like some references to back up my inferences since I'm doing a final year project.An objective list of what makes a good phylogeny may not exist

A 'good' phylogenetic tree would be completely refined, properly binary, have high bootstrap support for all its branches, and reconstruct clades we think exist with high support values.
Generally high support values(there are other methods besides bootstrapping but that is a question for another time) is a measure of a good tree. There are other concerns, for example a tree that has no felsenstein zones is probably better than one that has lots.
We can know a lot more about trees than you suppose, though. Through simulation studies we can create datasets with a known phylogenetic history and then see how well the methods reconstruct the history. There are still problems(errors in the model used, just random error, ILS, HGT, other things) but mostly that kind of study tells us what good phylogenies look like.
It's very easy to generate a lot of different phylogenies. Using different methods, different models or approximation schemes, different genes or sequences from each species, or simply bootstrapping "new" samples from your existing dataset. A phylogeneticist usually has dozens of trees to choose from, which is a sort of crude bootstrap method itself. If trees look similar, they're probably pretty good. If they don't, you have a problem.

Would you please elaborate on what it means for a tree to be 'completely refined'? I am interested, but unfamiliar with what you're referring to here.

Some methods represent uncertainty by producing internal nodes that have more than three connections, essentially saying "all these groups are about the same amount similar, I can't figure out their arrangement". Finding an arrangement that has fewer of these internal nodes contains more information, and is called a 'refinement' of the tree. The 'star tree' where everything is connected equally is the least refined tree, and contains no information. The 'fully refined' tree is properly binary and has the maximum information.


text:
Why is down syndrome more common than other trisomies?
Why is Down syndrome more common than say trisomy 18? Is chromosome 21 easier to replicate? Or is it because those babies are more viable?


text:
How do I measure fermentation rate?
I'm doing a lab soon and I need to find a way to measure fermentation rate to a relatively high degree of accuracy without using a specialized sensor. It should ideally be done with easy to find tools at home or in the classroom.

http://www.freecontentweb.com/content/measuring-rate-alcohol-fermentation-yeast-cells Perhaps

@CMosychuk I'm not quite sure how there measuring it, I got lost when they said "its distance to the baseline water level." The difference of what to the baseline water level?

Your setup is essentially like this. You have the fermentation occurring in one tube. The CO2 travels through tubing to another tube that was inverted with water in it, and the other end of the tubing fed through the bottom. The CO2 will force with water level in the inverted tube down so more CO2 = lower water level. If you take readings over time, you can measure the relative rate per unit time.

Here is a more simple figure!

@CMosychuk I'm not sure I can do exactly that but I may be able to do a variation.


text:
Tensile strength of collagen?
Really specific question, but what is the average tensile strength of human collagen, type I? I've tried looking for it online, and either my google-fu skills are weak, or I'm just unlucky. Also, is there a specific database for mechanical protien data, or do I just have to look up each protien's tensile strength individually?

Measuring mechanical properties of proteins is REALLY hard, because you either need to measure individual proteins (which is afaik only possible with an atomic force microscope) or you need to assemble purified protein into a larger complex that is normally measureable, however single purified proteins often don't from physiological complexes.

@Nicolai, I'm specifically interested in scleroprotiens, but i don't know if that helps?


text:
Understanding the picture of a synapse
I need help to see exactly what is going on here. According to the textbook here is shown a synapse, but I cannot quite see the things the textbook says are there.
From what I understand: (1) At1 and At2 are axons?, (2), The black thing on the bottom left is a dendrite?, (3) s1 and s2 are post-synaptic densities?
Is there more to see here that I am missing?

The word is "synapse" not "synapsis" - and yes, those are the major features to see. Note that is probably more correct to say those are axon terminals, hence the "at". All the spherical objects inside the axon terminals are vesicles. I think this question should probably be closed, though, because you don't have much of a question: the textbook is telling you what's in the picture.

Does the book have another diagram or picture of a synapse from a different angle? Or a picture that shows synapses within a larger context? Would be worth adding to this post if so.

You can tell that the structures labelled At are axons, or rather axon terminals, due to the presence of the synaptic vesicles.
I think this is a fine photo that's a bit more a clear representation:

Source
PSDs are really just protein aggregates that are thought to facilitate neurotransmitter trafficking. So the structures here make sense. At least, they make sense if you know the tissue you're running in TEM, and you understand that how you cut the samples for microscopy affect the way they end up looking. My only assumption that Den is a dendrite is knowing that axon terminals synapse with other dendrites: they're receiving structures. I'm also somewhat sure the cell body from which the dendrites extend have that characteristically large nucleus.
The other understanding is that these pictures are just snippets of a larger image and you only get used to identifying structures through practice and experience. Rather, the author wants you to see this section and for lack of context has identified the structures for you.


text:
What is head of a bone?
For most of the long bones head is the proximal end, but for metacarpals and Ulna, head is the distal end. Why are their distal ends called as heads?
What's the criteria for calling an end as head end?

Why voted to close? I have searched on internet but could not find any literature about it, all I see is " head is usually the proximal end" .So I asked it here. What should I mention in the section MY attempt in the question?

Because it's easy to google, but I'm answering it anyway.

Here is a head and a neck:

Anatomy is fairly straightforward. regarding individual long bones, "heads" are curved ends of bones distal to a narrowing called a neck of a bone. Take the radius:

See how the radial head (curved) is just distal to a narrowing (neck)?
The ulnar head, though, is at the opposite end, because the proximal end isn't rounded, but the distal end is.
Metacarpal heads are distal (see blue area):

The humeral head is probably most obvious:

So, the head of a long bone is not determined by the position (it can be proximal or distal) but by the contiguous shapes.

When will you answer about chassaignac's tubercle?

@JM97 - I don't appreciate your pushiness. I would have thought you'd have accepted that I'm no longer involved in that thread. You're welcome for my answering this, btw.a completely voluntary activity.

You were the only person to say that you know about it, so i was eager to know about that.

I'm curious, do bones have two necks or only one neck, proximal to the head, in that case?

@DavidCian - Yes, only one.


text:
What kind of spider is this and is it dangerous?
Found this spider on my couch the other day in Steubenville, Ohio. The spider is about 1 - 1.5'' (2.5 - 4 cm) long. The spider looks brownish in the image, but tends to a pale yellow color in reality.

It's not a brown recluse, the pattern on the head and the shape of the abdomen are wrong.

That looks like a good ol' wolf spider.  Call him spiderbro and leave him to hunt down obnoxious insects.

It looks like a member of the Thomasidae (crab spiders) To properly identify spiders to genus or species I would have to see the eye pattern. It is harmless, Dangerous spiders in Steubenville are unlikely

its face would have helped a lot

That's a nice female Nursery Web Spider, related to the Fishing Spiders.  They're rather pretty animals, and like almost all spiders, quite harmless to anything that's too big to eat.  The very rectangular cephalothorax ('head' end) pattern and the simple wavy line down the abdomen are the key clues for this one.  They also like to sit with the front legs arranged in pairs.
https://bugguide.net/node/view/2919/bgimage


text:
What moth is this?

Location: Rural area near the Western Ghats, Kerala, South India.
Date: Sometime in December, 2016
Climatic Conditions: Humid, frequent rains.
Brief Description:
Couldn't have been bigger than an inch. Took the picture at night. Has characteristic orange stripes across wings and dorsal thorax. A pair of black dots present on either wing; one pair located on the distal region of the wings and another (less conspicuous) pair located on the proximal region of the wings (laterally over thorax). No immediate/visible response when I shone a flashlight at it (eventually moved the torch up to the antennae, still no reaction).

That is a red striped tiger moth. An initial search hasn't found a picture I'm sure is redistributable, so I've linked a Google image search instead.
The number of spots on the wing seem variable. The pictures show examples with four and six spots as well as two spots.
Later:
As discussed on the Physics Stack Exchange chat, this is probably Cyana perornata.