text:
Why don't carrier proteins require energy to change shape?
I know that carrier proteins can be used for both passive and active transport, but I am referring to the facilitated diffusion aspect. Even though facilitated diffusion via carrier protein goes along the concentration gradient, the protein still must change its shape, from what I understand. Why does this process still not require ATP, and why does it require ATP to go against the concentration gradient in the same manner?

The carrier proteins that participate in passive transport do not require energy in the form of ATP molecules, which is the primary form of metabolic energy of the cell, but this does not mean that the transport process is energetically 'neutral'. Many proteins bind their ligands via hydrogen bonds, partial or full ionic bonds, van der Waals interactions, etc. These interactions build up a type of energy known as 'binding energy', which can be enough to induce a conformational change in the transporter. In addition, consider that a chemical gradient in itself is a form of energy, which effectively drives the movement of many solutes across the membrane. In fact, the gradient of a molecule can be used to transport another type of molecule, without using ATP. For instance, consider the Lactose permease. Its mechanism is, I quote:

Hydronium ions from the outside of the cell bind to a carboxyl group
  on the enzyme that allows it to undergo a conformational change. This
  form of lactose permease can bind lactose from outside the cell. The
  enzyme then everts and lactose is transported inward.

Below a diagram of this protein, with its ligands in the center:

That being said, some proteins that are involved in passive transport do not require conformational changes like these I described, because they are simply 'open' (like a tunnel), and the solutes can freely diffuse across the channel. This is the case, for instance, of aquaporines. The advantage of the carriers that need to change conformation is that the binding to their transported molecule implies a recognition mechanism, which gives high specificity, whereas the proteins that are simply 'open' are less selective and thus transport many different solutes. See, for instance, the central pore of an aquaporine:

Regarding your last question, the hydrolysis of ATP can release enough energy that (similarly to the binding energy described above) can induce a conformation change in the transporter protein (active transport). This is often used when going 'against' the gradient because, as I mentioned, the gradient in itself contains energy that if not used passively (as in passive transport) then it is not favorable to transport something against the gradient. Thus, an external source of energy is needed (ATP!).


text:
What was the evolutionary benefit of enclosing hemoglobin in cells?
The ancestral solution to oxygen transport is with hemoglobin (or, similar proteins) dissolved in blood (or, "hemolymph", but, basically, dissolved in water. ) What was the advantage of enclosing the oxygen-transport proteins in cells?

Hello, looks like this is your first question. Please notice that although I got your point and I think your question is good, you should do your own researches before posting here: this will not only improve the general quality of this SE, but will also make other expert users eager to answer, while short questions without references usually get no answer.Welcome to Biology SE by the way :)

Does this answer your question? Why isn’t Haemoglobin a plasma protein, rather than being encompassed by the erythrocyte?

@David what do you think yourself?

My angle is that, if you know, with certainty, the answer, then I'd like to hear it. If you just scan for something that "might" answer the question, you are no better than a search engine. If you know for a fact that a url you shared does answer it, then, good. In your opinion, does that url answer the question? Tumbisapichu suggested concentration as main factor. Sounds plausible. I've thought myself that oxidative stress might be it, ROS is in proportion to oxygen pressure, and I'd assume it is highest inside the oxygen transport cells, that also lack mitochondria (the main source for ROS)

The “does this answer your question” is the new and misleading auto-generated text when you flag a question as a duplicate. The point is not whether it answers your question, but that duplicate or similar questions are closed. I have no particular interest in the topic I just remember it coming up previously.

Well you flagged it as duplicate, so, you claim that it does answer the question. That the comment is auto-generated does not change that. Does it answer the question, in your opinion? What was the evolutionary advantage of enclosing hemoglobin in cells?

If you enclose the globin in a cell you can achieve a high concentration of the globin, which makes for a faster, readily usable pool available, and it is not subject to degradation (via proteases, or other mechanisms) as if it was just dissolved. In addition, all other functions of the globins (pH regulation, CO2 metabolism, etc) will be more tightly controlled if the globin is on the same site (i.e., inside a cell), instead of being mixed in a milieu. All of that has probably more to do with the evolution of the entire circulatory system, as a whole, and only sequentially as the 'enclosure' of globins in specialized cells. You can find some more details here.

If a higher concentration is the main benefit, is the primarily factor viscosity, that enclosed cells can have higher concentration without decreasing viscosity of the blood?

That's also a good point, but more than viscosity I'd say that a factor would me osmolarity. Dissolved proteins in a circulatory system make for higher osmotic pressure, which would need to be compensated.

Good point. My own analysis is that the cells then prevent endosmosis by tension in the cytoskeleton matrix. (I'd guess a way to compensate for the osmolarity is necessary, otherwise the cell would be in the same situation as a hyperosmotic blood. )

What is the scale of concentration increase, roughly? 10-fold? (albumin is 1/10th globin in red blood cells, guessed from that if osmolarity is main factor)

This might be informative: https://en.wikipedia.org/wiki/Mean_corpuscular_hemoglobin_concentration

have seen that, easily attainable. and albumin concentration is roughly 1/10th of MCHC

the hemocyanin concentration (or whatever pre-blood cell animals tend to use) is what it harder to find. if osmolarity was the main factor, I was guessing albumin could be a good estimate, that it is 1/10th of the MCHC. since roughly 50% of blood volume is red blood cells, concentration increase as advantage driving evolution of blood cells would be half of that, 5x. just guessing. do you know the scale of concentration increase?

Hmm, no I don't know.

here it looks like it is 9 g/L, 1/4th of that of erythrocytes. https://www.sciencedirect.com/science/article/abs/pii/0014489472901117. with 50% red blood cells in blood, that means concentration is only doubled.

my intuition was that blood cells protect against oxidative stress, primarily, by moving oxygen into the cell. they also die pretty quickly... that as endothermy evolved etc, and metabolic rates and oxygen consumption increased, it was necessary.

Also, hiding the Iron from invading bacteria is good. Free iron is a limiting factor for bacterial growth.

source: Stack Exchange

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

sort: votes


text:
How a person can transmit COVID-19 while his COVID-19 is still in incubation state?
A person with SARS 2003 cannot transmit that disease while his SARS is in incubation state but how a person with COVID-19 is transmitting COVID-19 even though his COVID-19 is in incubation period?

The incubation period is the time it takes from the infection of a patient with a disease until he develops symptoms. How fast this happens depends on the disease.
According to the references the main difference is that SARS 2003 replicates in the lung/lower airways, while SARS-CoV-2 also replicates in the upper airways and sheds high viral loads there early in the course of the disease.
Since both diseases are transmitted by droplets, it is much easier to have a sufficient viral load in infected cells from the upper airways compared to the lower ones.
References:

Severe Acute Respiratory Syndrome Coronavirus Infection of Human
Ciliated Airway Epithelia: Role of Ciliated Cells in Viral Spread in
the Conducting Airways of the Lungs
Virological assessment of hospitalized patients with COVID-2019

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


text:
Are specific primers or detectors, or both, used in COVID-19 tests?
I am trying to learn about the rRT-PCR testing procedure used to test for COVID-19, but I am slightly confused on one point. Are highly specific primers used with a non-specific detector, or are highly specific detectors used, or are both specific primers and detectors used? Some of the sources say that multiplex PCR is used, which indicates a specific detector, but as I am still a beginner on the subject, I am not sure. I would also really appreciate it if somebody could also point to a source that details the some of the testing procedures.
Thank you

It is often helpful to do a little background research using google before asking a question, or to link to specific sources that you need help with; e.g. It would help to know which sources you're looking at. Technical information on one testing procedure is available here (methods section): https://jamanetwork.com/journals/jama/fullarticle/2761044. The community has collected COVID-19 information here which may be helpful: https://biology.meta.stackexchange.com/questions/4035/information-about-coronaviruses-how-to-ask-and-external-resources?cb=1

When you run a PCR reaction, you are making copies of a DNA sequence of interest (cDNA in case of retrotranscription, since retrovirus have RNA as the genetic material). The sequence of interest is presumed to be in a sample, that you take from the patient, or some organism (I say 'presumed' because the PCR is precisely to confirm this). These copies are made by a group of 'generalist' enzymes, called polymerases, and by generalists I mean that they do not discriminate on which DNA sequence they are copying. But, they cannot copy DNA de novo (from scratch). The copying process needs to be 'primed' by a short sequence of nucleotides that is complementary to the DNA of interest. These are called primers, and they effectively serve as probes to target the copying of the specific sequence you need to amplify. And this is where scientists put a lot of care on: primer design. Bad primers will not be very specific, or will not be very efficient during the amplification process. As for the 'machine' that actually detects the copies, there are many variants. The most typically used in research and diagnostic laboratories, involves staining the amplified DNA with some molecule that binds nucleic acids (which there are many), and visualize it via DNA electrophoresis. What you visualize is a population of DNA copies (via the staining you make), so you need to know beforehand what to expect. For instance, do you expect a small fragment (a couple hundred basepairs) or a big one (a few thousands?). You have a 'ladder' (also called marker) that gives you a reference to compare, like in this image:

People know what to expect because they already know the DNA (or RNA) sequence they are amplifying (otherwise they could not have designed the target primers). They know the sequence because they've done some form of nucleic acid sequencing (labs, health institutes, and so, do this all the time and deposit the sequences in some platform, for instance GeneBank).
A 'positive' amplification will give you a band in the expected size range, and no other bands (because your primers are targeted for a particular DNA sequence). But as you mentioned, there exists also a multiplex PCR reaction. In it, you design multiple primers to target different sequences (using the same DNA sample -e.g. from a patient or organism-), but the verification process is basically the same. Here people are extra careful to avoid cross-interactions among the primers added to the reaction.
PCR is a family of techniques, not a single one. There are variations in the actual process, and also in the 'detection' (for instance, qPCR uses real time detection of copy numbers). But the general principle is the same: primers are specific, while the 'detection device' is not really.

Thanks for your answer. What I have seen is that gel electrophoresis is not used in covid testing. Instead, a dye is added which binds to the dna to be expressed, so you can monitor the fluorescence of the dye to determine the amount of dna present. These dyes can be made specific, like the TaqMan detector. Do you know if these specific dyes are used in addition to the specific primers you mentioned? Thanks

Dyes in general applications are not specific, that's why they are useful, otherwise you'd need to have one dye for each specific sample/sequence. Sometimes a dye is bound to a probe (like a primer), and thus made 'specific', but in reality is the probe which is specific, not the dye. And as I said, PCR and amplicon detection are a family of techniques, you'll find many variations and more sophisticated techniques appear all the time.


text:
Do PC-12 cells have to be stored in nitrogen?
My lab has been storing their PC 12 cells in the -80 freezer... upon arriving here and investigating a new project I see that it specifically stated to be stored in nitrogen vapor? Is this the absolute case or is -80 for short term storage okay as well?

The temperature at which nitrogen evaporates is about −195°C. Given the considerable difference in temperature between the current freezer and nitrogen vapor, I'm inclined to say probably not.
I suspect that it may be dependent on what exactly you are using the PC 12 cells for. Without knowing more detail about the situation, I would do my best to get ahold of some liquid nitrogen for your samples as soon as possible. When in doubt, it is always best to follow procedure.
Until you can acquire nitrogen, -80 is still far better than room temperature. Be sure to take note of the discrepancy in your notes and hope for the best.

From talk among the powers that be in my old lab, many of the common cell lines have become divergent anyway. I think HeLa cells were notorious for behaving differently in different hands due to different storage conditions and culture mediums.
PC12 cells were believed to be similar, so I think that whether or not it's OK will depend on what you want to do with them. If you want to set up simple assays for comparing the effects of small molecules, then you'll probably be fine (obviously note down the storage conditions when starting your cultures up again).
However, if you want to replicate a differentiation procedure from another lab exactly, then you should be replicating their conditions as exactly as possible. Therefore your -80 stored cells might not be OK for that.
So as Astrolamb said, have a go, see how they behave, but maybe be prepared to beg someone to give you some more if the -80 ones don't do what you want them to.

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


text:
need to identify species of this Leaf-footed bug?
I found this bug in Pune/India. I checked many species of leaf-footed bugs, but none of them is matching this one. It was about 3cm long. It was not showing any movement.

looks similar to some Leptoglossus species -- not sure if that genus is in India or not...

I think you are right, can you identify species?? @theforestecologist

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


text:
Help me identify species of fruit fly?
I found this fruit fly in Pune/India. It was about 1 cm in size. I explored info on several species in same region, but they were different in appearance, especially that black spot in middle of body.

No, it appears similar to fruit flies from Tephritidae family like Oriental Fruit fly @Remi.b

Indeed! I removed my comment! +1

This insect might be Bactrocera dorsalis.

It looks similar to this species based on the characterstic yellow spots, shape of the abdomen, as well as the light brownish orange stripes on the abdomen.
I had arrived at this conclusion by reverse-image searching the second picture that you have posted and observing the thorax and abdomen patterns. This image shows a very similar pattern as shown in your second picture:

The Wikipedia article has quite some stuff to say,

Bactrocera dorsalis is a species of tephritid fruit fly that is endemic to Southeast Asia, but has also been introduced to Hawaii, the Mariana Islands and Tahiti. It is one of the major pest species in the genus Bactrocera with a broad host range of cultivated and wild fruits.

Considering that you had found this insect in Pune, it makes a lot of sense to conclude that this is, in fact, the insect that you have found.

Do you know Indian flies well? Otherwise, it appears really premature to state "This insect is...". There are probably hundreds of related species in India, and the general color pattern are often very similar. I have an ok general knowledge of eg Swedish hoverflies (far from being a specialist), and based on this I would rather say that it is probably not B. dorsalis since too many small things that are often fairly stable seems not to add up. These include the posterior color of the scutellum, color of the femur towards the knee, distinctness of pattern etc. Might be a related sp. though

@fileunderwater I agree. There is black dot in middle of body which does not appear in any image of Bactrocera dorsalis.


text:
Help me identify this Beetle sp?
I observed many beetles like this in Pune/India in the beginning of rainy season. It was dark green in color with white spots and not too much shiny like many other beetles. Size is about 2cm to 3cm.

It is certainly a scarab, in subfamily Cetoniinae. It looks very much like a White Spotted Fruit Chafer, Mausoleopsis amabilis http://www.projectnoah.org/spottings/11819281

Thanks for above link from which I found this species (Protaetia alboguttata). It seems correct identification.


text:
Help me identify this fly species?
I found this fly in Bengaluru/India. It was larger than usual flies. It was more than 1cm in size, with black color which has blue shades in it. I managed to take just this one pic, then it flew away.

Based on the numerous strong bristles visible on the abdomen I suspect family Tachinidae; I don't know the Indian fauna, so I can't go any deeper.

yeah, you might be right ...


text:
Identification of Jumping Spider Species
I found this jumping spider (Salticidae family) in Pune/India. Most common species of jumpers in my region is heavy-bodied jumper (Hyllus semicupreus), but this is different species by observing body size and blue colored patch under eyes. Its size was about 7mm-8mm.


text:
What's the current conclusion about humans being omnivores vs herbivores?
What's the current conclusion about humans being omnivores vs herbivores?
And particularly, how is this relative to time? That is, is possible herbivoreness a "strictly" modern phase in human evolution? Or has it even occured yet?

The only people who claim that humans are herbivores rather than omnivores are basing that claim on ideology rather than science, since it is an observed fact that the vast majority of humans do eat meat when it is available.

do you have links to articles that claim that "herbivoreness a "strictly" modern phase" or any reference where you got this question?

@aaaaa I'm using it as a heuristic guess, since to distribute a diverse vegan meal to other than self-sufficient countries one needs some tech behind it, since stuff has to be transported around. Obviously herbivoreness might also be a location-dependent thing. In cold and short sunlight areas meat may have been one of the only foods available during e.g. winter months.

the guess should be based on something, and that is a lot of things to consider. I would suggest you start search on scholar.google.com for paper that studied some of that

Humans are omnivores as they can eat and digest meat. Early humans were hunters and gatherers and meat was a part of the menu from time immemorial. I don't know the exact technic term but some of our teeth were designed to handle meat (canines?). Sure, people can willfully limit their diet to plants only but from the biological point of view humans are omnivores.

some links to scientific literature would be good

I suggest you read this excellent review by Luca, Perry and DiRienzo:
Evolutionary Adaptations to Dietary Changes, Annu Rev Nutr. (2010) 30: 291–314.
I quote:

The evolutionary history of hominins has been characterized by significant dietary changes, which include the introduction of meat eating, cooking, and the changes associated with plant and animal domestication.
(...)
Meat is a critical food resource for modern human hunter-gatherers, along with plant foods (...) The earliest evidence for meat-eating in hominins dates to ~2.5 Mya.

There seems to be a scientific consensus about the fact that the human digestive system has evolved to consume both animal and vegetal foods.


text:
Is this spider venomous?
I found this spider in bathroom. Just wanted to know more about it.
Location : India(South India,Hyderabad)
Temperature : 30°C
Humidity : 74%

Hi Sumeet. Please provide an estimated size for your specimen. If you have additional photos, clearer photos of both the top/bottom of the spider are useful. Thanks!

I think with the legs, the length is around 4-5 inches.

Please [edit] your post to include the size information. Thanks.

perhaps 4-5 centimeters rather than inches?

Your spider shows an apparently large size, a large round cephalothorax, with smaller and thinner abdomen, very long and sturdy legs, with a long 'foot', and is a general brown color, with some darker markings on the legs.
This is consistent with one of the larger varieties of spider found in the warmer areas of the world, and trading under the name of Huntsman Spider, or Giant Crab Spider.  There are a number of species of these spiders in the family Sparassidae.
As it happens, the most common variety of Huntsman, Heteropoda venatoria, is found pretty commonly in southern India (reference link example included: http://www.southindianspiders.org/south-indian-spiders2.htm ), and I'm quite confident that this is what you have there.  Here is an example, from the US website Bug Guide, of this species:

Like almost all spiders, this spider is venomous, but like almost all spiders, its venom is not particularly troublesome to us humans.  A bite from a spider this big would be moderately painful simply from the large fangs, and the venom doesn't appear to usually add too much to it.  Here's a short but amusing discussion of such bites, from an Australian website: http://sciabc.us/IL2pR
These are sort of the spider equivalent of Geckos - commonly foraging in human homes for the various critters that like to make pest of themselves (cockroaches, mice, etc.) - but they never try to sell us insurance.

I don't know the species (could be a wolf spider), but I am certain they are not dangerous. I have seen these all over my bathroom, dining room and bedroom before. They are all over in South India. No one in my family seamed concerned by them. I am quite certain I even had one crawl on me once.

Hi J Houseman, and welcome to Biology SE! Please take the [tour] and carefully read through the [help] to learn more about the site, including How to write a good answer. In general, anecdotal comments such as yours can be added as comments if they are not chatty but instead provide insight. However, such anecdotal comments are unfit as answers because they do not provide reputable support (e.g., through links or citations) for claims made. As such, your answer will be downvoted and deleted. Please add support to your post to avoid this


text:
PCR not working
I am trying to check the integration of DNA into a very specific region of the E. coli genome, and for that I'm comparing via 2.5% agarose gel electrophoresis the length of whole cell PCR products (I'm expecting 120 and 242 bp bands).
Unfortunately, the last 3 PCRs were very unsuccessful, or should I say not interpretable, as only the non-consumed primers were visible (+ gDNA) and no 120 bp amplicons.

Those bands are 120 bp amplicons - Q5.

I wouldn't trust those fainted bands - Taq.
The ladder I used is 2-Log 0.1-10 kb.
Here's also the recipe for one 25 ul reaction:
- 5 ul polymerase buffer 5X
- 0.5 dNTPs 10 mM
- 0.25 ul of each primer 50 uM
- 0.25 ul polymerase (I tried Q5, Taq and Phusion)
- 1 ul template (bacteria)
- 17.75 ul H20
What could have possibly gone wrong? Am I misinterpreting the results? Am I adding too much template DNA? Is it possible for the primers to degrade after several freezings? Are there too many inhibitors inside bacteria?

First you should check that your annealing temperature is appropriate for the melting temperature of your primers. (and that the other PCR parameters such as extension temperature are appropriate for your polymerase)
Secondly, although most people will tell you it's not necessary, I've found that it can helpful to clean up the template DNA just a little. For bacteria, I would boil in water (put a colony into 20-30 uL) for 5-10 minutes, spin down the cell debris, and take 0.5uL of the supernatant.
Do you have a positive control? (try to amplify some other region of the genome that you haven't modified)
Of your other suggestions, I would say that primer degradation is incredibly unlikely.

No one can tell you exactly what went wrong, I'd check to see that your primers are the right sequence.  You can reorder them again, or reorder slightly different ones; primers are cheap, and come fast.

MgCl2 can also be the reason.i have tried titers of MgCl2 1.5 ,2,2.5,3 with all other conditions same and it worked


text:
A and AB blood types from B and O?
My grandma is O- blood type, my grandpa is B+, but my mother is A+ and my aunt is AB+.
Is that possible?
I've just looked at different sources like this and all of them are saying that from O and B, comes only B or 0, and A and AB are forbidden.
How can my mother be a child of my grandparents and how my aunt can be a child of my grandma at all? Or can we 100% say that they are not the real children of those parents, assuming that all blood types are correct?

maybe your grandmother is not really O negative or your grandfather is not B positive

Maybe, but I doubt so. Because my grandma was hospitalized (including surgeries) multiple times, and my grandpa was tested for his driving license.

It is correct that O- and B+ parents cannot produce biological children with A+ and AB+ blood groups, with the exception of a few rare edge cases.
Firstly, as noted in the other answer, your grandmother may have the Bombay phenotype. However, this is unlikely, due to the fact that she has been previously hospitalised and it was not noted.
Another unlikely possibility is that your grandmother is a genetic chimera. This means she would have two sets of genes, and her bone marrow hematopoietic cells had the O- genotype and phenotype, while her reproductive cells had an A allele.
If we exclude the rare edge cases, then it is strong evidence that your mother and aunt are not the biological children of your grandparents, and you should consider performing genetic testing to verify this if you wish.

Wouldn't a wikipedia link to genetic chimera be better than a link to a clickbait site?

@Pyritie I thought the "clickbait" site had more detail and was better as a case study, but the wikipedia page works too.

Assuming true paternity and correct ABO blood type detection, your grandma could likely have a Bombay phenotype (h/h blood group), which would make her blood look like the O type: http://www.ncbi.nlm.nih.gov/books/NBK2268/
This means that she would be double recessive to (and therefore lack) the H antigen, which is a precursor to A and B antigens. She would actually be AO or AA (genetically speaking) when it comes to the ABO group.
EDIT: As noted in the comments, this is indeed an extremely rare blood type, troublesome for transfusions, and should have been noticed prior to surgery. Other hypotheses are of course entirely plausible (another father, chimerism, etc.). But I think we can't discard it yet until the OP does some more extensive testing, as the transfusion issue could be handled by autologous blood transfusion or a very well stocked blood bank. Alternatively, the phenotype could be Para-Bombay, meaning that a little H antigen is produced and turned into A/B; this could be slightly more manageable for transfusions.
Sources:

http://www.bloodjournal.org/content/90/2/839.long
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658345/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658345/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652237/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159258/
http://www.jcbsonline.ac.in/Articles/jcbs%20-%201%20(3)_39-42.pdf
http://www.ijbti.com/archive/2016-archive/100023IJBTINS2016-suraci/100023IJBTINS2016-suraci-full-text.php

Maybe unlikely since, the OP mentions surgeries and Bombay blood is difficult to procure.

Isn't that actually like to say that my grandma group wasn't correctly determined? Or you meant that in the case of Bombay phenotype it's not possible at all to be correctly determined according to the ABO group?

@lalamer Someone with Bombay phenotype will appear as O in standard ABO testing regardless of their actual genotype. This is known as epistasis

Is there any other way except this Bombay phenotype?

@lalamer (and expanding on the comment by March Ho) ABO typing is firstly done with specific antibodies for A and B antigens (anti-A and anti-B), which induce clumping of the blood accordingly; i.e., A blood is clumped by anti-A, B by anti-B, AB by both, and O by none. If there is no H, then neither A nor B are produced or detected by the basic test; you would have to verify this by adding anti-H. An additional note: ABO and H are synthesized by two different enzymes encoded by separate genes (http://www.ncbi.nlm.nih.gov/gene/28 and http://www.ncbi.nlm.nih.gov/gene/2523).


text:
How are some people able to continue growing after reaching maturity?
This is technically a cross-post of a question posted last year concerning gigantism and how certain people are able to grow far past expectations after it's assumed they've reached maturity.
How are some people still able to grow after reaching adulthood? Someone gave the answer in the old post that epiphyseal growth plate closure is caused by testosterone and not growth hormones. Is it a lack of testosterone, or an excess of testosterone? If it's a lack, why are women usually shorter than men and stop growing sooner? If it's an excess, does that mean basketball players produce less testosterone than average height people?
There are a number of cases of pituitary gigantism out there, but these are the best examples of what I'm asking:

Väinö Myllyrinne was 2.22m at the age of 21 but is described as having "experienced a second phase of growth in his late thirties", attaining a height of 2.51m by the time of his death at 54.
Adam Rainer at the age of 18, he was only 1.22m. However, he had a growth spurt in his 20's, reaching a height of 2.18m at the age of 30 and 2.34m by the time of his death at age 49.

What could have caused these men to grow so much after modern medicine tells us our growth plates have closed? Is there a possibility of replicating their late growth for people who suffer from hereditary short stature or other growth-related problems? And would it be safe?
EDIT: Although my question is different in many ways, here is the original question.

Please [edit] your question and provide a link to the question you referenced in your first paragraph. Additionally, please provide links to verify the details you claimed about the two men in your post, preferably to reputable/scientific sources if possible.

Edited with information.

Usually the cause is 'acromegaly' but there are numerous possible causes.
It is impossible to start growing in length after your bones have matured too much. This is because of the 'Epiphyseal plate' this is a anatomical structure in bones that is necessary for length growth in bones and it degenerates at the start of adulthood.
The most common cause, although still not a common disease, for gigantism is acromegalia. It's cause is an abnormally high amount of growth hormone in the body which is most commonly caused by a hormone secreting tumor.
When the onset of this disease happens before the epiphyseal plates have degenerated it can cause them to stay active in which case the patient will continue growing.
Note: When the onset is after the degeneration of the disks it doesn't cause gigantism but it still causes a very recognizable change in appearance and the model for Shrek in the movie suffered from this illness.
Edit: Sorry, I didn't notice your subquestions initially. Yes, another possible cause in men is the lack of testosterone because this hormone is normally responsible for the degeneration of the plates in men.
Edit 2: In women estrogen is the hormone that is responsible for this, which explains why the length of men and women isn't dependent on testosterone in both cases

Please avoid having whole paragraphs bold, this is unpleasent to read and seen as yelling (as whole uppercase). Additionally: Most HTML commands do not work here, use the markup language of this page instead.

Thank you for the tips. How about just making the word edit bold?


text:
Image Dataset for Cardiac cells for Mus musculus?
I'm working on developing a transfer learning model to detect cells in a culture using microscopic images.
for that i require data set of images having microscopic images of various cell types. Is there any such database present? Any open source research work having  microscopic images of cardiac cells that can be used?

Sure help yourself with the broad institute image sets collection
Broad Bioimage Benchmark Collection - Annotated biological image sets for testing and validation:
https://data.broadinstitute.org/bbbc/image_sets.html
And the EMBL-EBI:
https://www.ebi.ac.uk/bioimage-archive/
No mouse cardica cells, but I am confident you can easily do transfer learning after training on those.


text:
How do researchers know that a species is at risk of extinction?

Recently researchers present evidence that the platypus is at risk of extinction.

Source
How do researchers know that a species is at risk of extinction?  I mean Earth is so large, said species could be deep in the Pacific ocean or somewhere else that has been thoroughly explored.

Habitat. (most) species can't live under your bed.

I can give some leads to those who can write a good answer: https://www.researchgate.net/publication/23311481_Quantification_of_Extinction_Risk_IUCN's_System_for_Classifying_Threatened_Species and https://www.iucnredlist.org/about/barometer-of-life and https://www.google.com/search?q=measurement+of+extinction+risk&oq=measurement+of+extinction+risk&aqs=chrome..69i57j33l4.3520j0j4&sourceid=chrome&ie=UTF-8

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, questions need to be narrowly focuses so that they are answerable on this site. This would need a book to answer in a non-trivial manner since different species have different requirements. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

The to assess the extinction risk of a species, Researchers first study the ecology and global populations of the species.
Then mathematical models are applied to  simulate the population dynamics and estimate extinction risk.
The results are collected in the IUCNs Red list.
https://www.iucnredlist.org/


text:
Is natural selection actually random?
In the Theory of Evolution, two main factors take place:
One is random, which are the different mutations that organisms' DNA suffer. This process adds genetic variability to a given population.
The other one is not random, which is natural selection. It is not random because it will only select  those organisms which are better capable of surviving to the conditions of their environment.
Most likely I am wrong and I would like to be corrected, but I was thinking that, since natural selection depends on mutations and the conditions of the environment, and since those conditions can be formed by random processes, wouldn't it make natural selection as actually random?
I mean, this is probably an over simplistic analogy, but take a group of mammals which suffer a great series of mutations in a short period of time, and separate into two species of mammals: one group of animals with hair and the other group has no hair at all. Suddenly, one day starts to snow. We could expect that the second group would most likely go extinct, while the mammals with hair would survive. Since the weather is based on random processes and since natural selection in this example would be based on the mutations that the animals suffered and the weather as well, wouldn't natural selection be a fundamentally random process?

Note that random processes can have systematic outcomes. E.g. random movement of gas molecules has a non-zero pressure as outcome. (Systems that do not behave in this way, i.e. where random processes do not have predictable systematic outcomes but the outcome stays unpredictable are called chaotic)

You are right in a sense. The processes which generate mutations in an organism are stochastic (not quite exactly random, but in most organisms they are effectively random for all intents and purposes). In terms of population genetics, it is considered that mutations occur randomly across the genome and have an equal probability of occurring at a given base pair.
The environment is also random/stochastic in the sense that it occurs mostly independent of mutations which have occurred. Whether or not it is cold one year is independent of the mutations which have occurred within an organism. (Actually that's not quite correct since organisms can generate their own environmental niches and evolve according to them, but I think that is beyond the scope of this question).
What is not random is how the frequency of genetic variants respond to different environments. This is natural selection. Over the long run, we expect genetic variants which increase the fitness of an organism within a given environment will increase in frequency and vice versa. There is a large body of theory and evidence which predicts how a particular variant may change in frequency in response selection of a particular pressure.
As @jamesfq correctly points out, a nice example of selection being non-random on the macro-scale is convergent evolution. For example, aquatic animals such as fish, certain mammals (e.g. Dolphins) and Amphibians and Dinosaurs have independently evolved streamlined bodyplans in order to conserve energy when moving through the water.

As an example of non-randomness, see examples of parallel evolution, where distantly-related creatures evolve similar forms because of environmental pressures.  E.g. Ichthyosaurs, dolphins, some sharks, and some fish all evolved similar body plans, even though creatures with very different body plans - plesiosaurs, rays - can be successful in the same environment.

Or as another example the very fact you can predict a hairy species to survive better in the cold makes it non-random.


text:
What external signals do tell catadromous fish to go from the sea to the rivers?
What signals do tell catadromous fish to go from the sea to the rivers? Is it photoperiodicity? Are there any other signals?


text:
Different BLOSUM matrices
What is the difference between different variants of BLOSUM matrices?
e.g What is the difference between BLOSUM 30 and BLOSUM 62?

Welcome to SE Biology. Please finish reading the Tour. You will often find that your questions have already been answered. For example, does this answer help you? If not, try to find the answer yourself first. Wikipedia is often the first place to look. If you still have difficulties with the explanations, then post them explaining your problem.

Thanks @David. I didn't see that. And could you please tell me are there specific instances I would use BLOSUM30 or BLOSUM62 ? Why should not I always choose BLOSUM90?

Thanks @mgkrebbs. I didn't see that. And could you please tell me are there specific instances I would use BLOSUM30 or BLOSUM62 ? Why should not I always choose BLOSUM90?

I'm afraid you don't seem to have understood. I asked you to finish the Tour which explains how this is a question and answer site building a library of answers to biological questions. We know you haven't done this because you haven't got the badge for doing so, and therefore there is no reason to believe you have looked at the existing answers that I and @mgkrebbs pointed to. Instead you appear to be hoping that someone will give you a personal answer to another (homework?) question, which reading those answers would give you. Please do as requested.

BLOSUM is a substitution matrix employee for protein sequence alignments, which are based on maximum identity percentage  of the aligned protein sequences used in calculating them. For example, BLOSUM30 would correspond to alignments with a maximum of 30% of identity, BLOSUM62, for a 62% of identity.
The type of matrix depends on the study your are doing. BLOSUM62 is the most widely used matrix for phylogenetic analysis. BLOSUM90 would return sequences with 90% of identity.
The percentage of identity is related to the phylogenetic distance, and this to the variations in the protein sequences,therefore BLOSUM90 cannot always be used. That is why you must take into account the type of analysis you are going to perform. (https://en.m.wikipedia.org/wiki/BLOSUM)

Thanks @Armand Could you please tell me are there specific instances I would use BLOSUM30 or BLOSUM62? Why should not I always choose BLOSUM90?


text:
Does DNA have a phosphate group or phosphoric acid?
I am confused about the structure of nucleotide of a DNA. I have seen that it has a phosphate group(PO₄³⁻) in some books but phosphoric acid(H₃PO₄) in other ones. Which one is right?

Check out this post and see if it answers your question. (https://biology.stackexchange.com/questions/3864/dna-as-an-acid). I will say, there is basically no circumstance in which the phosphate-group in a nucleic acid backbone will have a -3 charge, because two of the three available oxygens are utilized in the phosphodiester bond linking the sugar bases.

The phosphate ion has a negative formal charge and in an acidic solution its appears as a conjugate base of a phosphoric acid. That is the wey the phosphate group found in cells. The nucleotide synthesis can occur de novo or recovery ways. De novo way use phosphoribosyl pyrophosphate, which simple molecules such as amino acid, tetrahydrofolate and carbon dioxide are added.


text:
Why such diversity in sexual dimorphism in passerines?
In searching for info to answer my question, I’ve found a fascinating 1998 article  by Owens and Hartley from Proc. R. Soc. Lond. B. It reports such cool findings as that

When we break up plumage-colour dimorphism according to whether it is due to melanins, carotenoids or structural colours, we find that each category of plumage-colour dimorphism shows a different pattern of covariation. The correlation between overall plumage-colour dimorphism and the rate of extra-bond paternity is due to structural colours, whereas melanin-based dimorphism is associated with sex differences in parental care.

Intriguing, but not on point for my question; so I turn to StackExchange.
Is it known why, for example, northern cardinals (Cardinalis cardinalis) are essentially monomorphic in size but dimorphic in plumage color, American robins (Turdus migratorius) and blue jays (Cyanocitta cristata) are pretty much monomorphic for both traits, and the sexes in the brown-headed cowbirds (Molothrus ater) vary so in size and coloration that they could easily be mistaken for separate species?
Whether it involves caring for young or pair monogamy or whatever, how does one species arrive at a particular morphological-behavioral complex while another ends up someplace entirely different? Is that entirely a matter of evolutionary contingency?


text:
How can the pressure during contraction vary between the left and right ventricles?
After reading this passage from my physiology textbook (Vanders Physiology p. 384), I'm confused about how exactly the right and left ventricle can create markedly different pressures as they pump blood even if they have the same stroke volume, i.e. they push out the same amount of blood.

Typical pulmonary arterial
systolic and diastolic pressures are 25 and 10 mmHg,
respectively, compared to systemic arterial pressures of 120
and 80 mmHg. Therefore, the pulmonary circulation is a
low-pressure system, for reasons to be described later. This
difference is clearly reflected in the ventricular anatomy—
the right ventricular wall is much thinner than the left.
Despite the difference in pressure during contraction, however,
the stroke volumes of the two ventricles are the same.

How can two ventricles push the same amount of blood but at different pressures? I always assumed that pressure was created by a change in volume of the ventricles, and so I expected that if both ventricles have the same "change in volume" as they contract, they should also push out blood at the same pressures. Why is this not the case?

Pressure doesn't just depend on the characteristics of the pump — it also depends on the system that is being pumped into! Think about what pressure you would expect if you took the heart out of an animal and allowed it to pump in a bucket of fluid — now what is the pressure?

The key is vascular resistance.
Pumps like the heart don't move fluid, they exert force ("push") on it, increasing the pressure. The movement happens subsequently because there is somewhere for the fluid to go, so it moves down the pressure gradient from a place of high pressure to a place of lower pressure. If you clamped their outputs (increased resistance to infinity), neither ventricle would push any blood out.
We can say that the flow rate is proportional to the pressure difference and resistance:
Flow ~ ${\Delta}$P/R
If we assume that the two ventricles push out over the same time frame, you could easily get equal "Flow" with different "${\Delta}$P" if RLungs is different from RBody, and this is exactly the case: pulmonary vascular resistance is much lower than systemic vascular resistance. It's easier to pump the same volume through the lungs than through the rest of the body, so less pressure is needed.


text:
Garden Hose Analogy for Blood Vessel Resistance
I've been trying to reconcile the resistance component of Poisseuille's law with a mental analogy of a garden hose; specifically, I had assumed that the effects of reducing the radius of a blood vessel (of an arteriole in vasoconstriction for instance) would be the same as when you put your thumb over the opening of a hose, causing water to leave at an increased velocity. However, the law instead predicts that a decrease in radius like this would increase resistance, actually decreasing flow by a proportional amount equal to r^4. Why doesn't arteriolar flow actually end up increasing because of the pressure from the arteries, much like its "hose equivalent"? Does the hose analogy even work in this scenario? What am I missing that separates the two scenarios?

It comes down to the distinction between velocity and flow rate.
While you are right that the water would leave a an increased velocity if you put your thumb over the end of the hose, this is deceptive, because the water is exiting the closed system, so it can go absolutely anywhere.  So the fact that the velocity is increased could give one the impression that the flow rate is increased, but in fact it is the inverse.
Imagine that instead of putting your thumb on the end of the hose, you pinched the hose in the middle instead. This would result in the water flowing out of the end of the hose at a reduced flow rate (lower volume of water coming out per minute) and velocity (lower speed of the individual water particles).  Why?
It might help to take a snapshot of the place where you are pinching the hose.  the pressure behind the pinch zone goes up, causing the water to pass through the pinch zone at a faster velocity. However, because the hole is smaller, less water is able to pass through.  When it reaches the other side of the pinch zone, it slows down again because it has a very low pressure, and the smaller volume of water must fill the entire tube. However, because the flow rate was lowered because of the pinch zone, the amount of water at the end of the pinch zone is lower.  Consequently, the water flows slower and the flow rate is reduced simultaneously.
Another analogy that might help would be the comparison between a garden hose and a fire hose.  Let's say they have the same flow rate (same volume coming out of the hose per unit time).  You can immediately realise that for the garden hose to put out the same amount of water that the fire hose is putting out in a minute, the water would have to be flowing many times faster in terms of velocity.

Furthur reading

Grunwald JE, Petrig BL Riva CE, Sinclair SH. Blood velocity and volumetric flow rate in human retinal vessels. Invest. Ophthalmol. Vis. Sci. 1985;26(8):1124-1132. Available online: https://iovs.arvojournals.org/article.aspx?articleid=2159754
Baker M, Wayland H. On-line volume flow rate and velocity profile measurement for blood in microvessels. Microvasc. Res. 1974;7(1):131-143. Available online: https://doi.org/10.1016/0026-2862(74)90043-0

At a constant volumetric flow-rate, the product of velocity and vesicle cross-section area is constant.
In a real-life scenario, the volumetric flow-rate decreases when you hold your finger over the opening. So while water exits 'faster', at higher velocity, you would fill less bottles of water per minute.


text:
Effect of the Marcus Theory on Photosynthesis
As far as I know, the Marcus Theory explains the rates of electron transfers in reactions as a function of differences in free energy between the product/reactant's potential well.
Furthermore, there is the so called inverted region which is often said to be important to explain effects as the photosynthesis. Sadly, I do not see the connection here. The inverted region seems to reduce the transfer rate in the backwards reaction but not in the forwards reaction which creates a net reaction flux. But how can this be explained by the Marcus Theory? I tried to read several sources which claimed to talk about this online, but apparently missed the crucial point.

Please provide a reference link to the Marcus Theory. I have never heard of it myself, and suspect that very few on this site will have.

@David I am tlaking about this theory: https://en.wikipedia.org/wiki/Marcus_theory Do you think I should rather ask this question at the chemistry stackexchange?

Not sure. I'd wait a little to see if anyone answers.


text:
is this a soft coral on sand?

Was diving a few days ago at Jervis Bay (Australian East Coast - temperate). Water temp 20 degrees C, depth 5m. Spotted this creature in the sand. About 150mm high. It isn't sea-pen (Cnidarian) as it doesn't retract if touched and is wrong shape. Has polyps 20mm long all over stalk. Its soft. I've never seen one before. Took a few snaps as I was sure everyone else would say they knew what it is. No-one does. Is it a soft coral? If so, what's it doing growing on sand in temperate water. It looked quite healthy but we've never seen any others there.
I wish I'd taken better photos now :)

looks like a sea anemone to me.

But given that there are multiple polyps it could only be some sort of communal sea anemone.....and I can’t find any reference to anything that looks like that across half a dozen marine ID text books

Ok - found it. It IS a type of soft coral...and in fact is a type of Sea-pan that doesnt look like a pen and doesnt retract! From the family Veretillidae possibly Cavernolaria obesa (at least Ive found a photo of that organism that is remarkably similar).

@ScubaAl you can add that as answer and accept it.


text:
Does opponent process happen in the retina or in the brain?
I understand that both the Trichromatic Process and the Opponent Process take place in human vision.
Trichromatic Process is widely accepted to happen in the retina,
however I heard differing accounts of where Opponent Process happens - in the retina or in the LGN.

Opponent process happens BOTH in the retina, and in the brain (Lateral Geniculate Nucleus).
Here is the excerpt from Vision Science: Photons to Phenomenology by Stephen E. Palmer:
In the brain (LGN):

Physiological psychologist Russell De Valois (1965) and his colleagues (De Valois, Abramov, &
  Jacobs, 1966) measured responses in the LGN of macaque monkeys and
  discovered color-selective cells whose responses to wavelengths of
  light were incompatible with trichromatic theory but conformed roughly
  to the pattern predicted by Hering's opponent process theory. Some
  were excited by red light and inhibited by green (R+G- cells). Others responded in the opposite way,
  exciting to green and inhibiting to red (G+R- cells). In addition,
  they found cells that were excited by yellow and inhibited by blue
  (Y+B- cells) as well as ones showing the reverse pattern of responses
  (B+Y- cells). Together, these LGN cells can reasonably be interpreted
  as a neural implementation of Hering's opponent process theory.

In the retina:

Further research has shown that these patterns of response are also
  present in the bipolar and ganglion cells of the retina. Output of R+G- opponent cells can be derived by combining excitatory
  input from the L cones and the inhibitory input from M cones,
  essentially computing the difference between the output of these two
  cone systems (L - M).


text:
Identifying this winged ant with big hind legs
I found this walking across my floor not too long ago. I am not sure if it is actually an ant, I just chose the best words I could find for the title. It has wings, but does not seem to ever fly. It has antennae and the hind legs looks much larger than I've ever seen on an ant. Moreover, they seem to have a red tint. Any ideas?
Area: U.S. East Coast

Welcome to Biology.SE! That looks more like a wasp of some sort than an ant. Please [edit] your post to include an estimate of the size of this insect since that can be an essential clue for identifications. ——— If possible clearer, closeup photos of the creature from multiple angles would also be helpful. ——— Finally, please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Yes, that is a wasp. The legs are distinctive of that family, butI've forgotten the name.

I think it might be some kind of Conura. There are photos at https://bugguide.net/node/view/18810/bgpage which resemble yours. And according to that page it's in roughly the right area of America. But there are a lot of wasp species in the Conura genus and I don't know if other wasps in the chalcid family have those large hind legs. So... inconclusive.

The expanded hind femora are a feature of the Chalcididae as a whole, but are not unique to that family within Chalcidoidea (the related family Leucospidae also have them, but are much larger and might be mistaken for potter wasps at first glance [at least in North America]).


text:
Seeing new colours with new photoreceptors
If we developed new "eyes" that could see "non-visible spectrum colours" and connected them to our brains, would our brain be capable of identifying and interpreting those new colours? Is our brain hardwired to only de-encode information about RGB using our SML cones?
How is color information transmitted from the eye to the brain?
Our brain receives the information as an FM signal, but does that mean a different "carrier frequency" is used in the FM will the brain detect and interpret this new colour?
Cerebral activity during exposure to non - visible light
We lack the ability to see colours outside of the visible-spectrum due to a lack of photoreceptors.
https://www.quora.com/Why-cant-we-think-of-a-new-colour-Is-it-really-impossible-to-think-of-any-colour-that-doesnt-exist-right-now-Is-the-light-spectrum-the-only-possible-source-for-new-colours-or-might-there-be-something-else Note that this link states we can "imagine" new colours in a pseudo kinda way.
The two points I found online providing information about my question: Yes adding new photoreceptors/sensors to our eyes could be a way to see new colours and yes sending a different signal would seem to be the way to interpret a new "colour". But those answers only partly apply to whether it's actually possible and only narrowly approach this question.

"new eyes" = synthetically designed or robotic. I'm aware that the modulation of another animal's eye's wouldn't fit the bill and therefore we can't reliably transplant eyes from other creators to boost our vision capabilities. (e.g. Mantis Shrimp eyes would certainly be incompatible and require special vision processing capabilities http://phenomena.nationalgeographic.com/2014/07/03/natures-most-amazing-eyes-just-got-a-bit-weirder/ )

Each human optic nerve contains between 770,000 and 1.7 million nerve fibers, So it will be beyond human grasp to swap eyes in the near future, genetic eye and optic fiber development has to happen in the womb. Eye grafts require some kind of neural nanotechnology which is probably multiple generations away.
If you replace a human photoreceptor with another color, the result is: un-demonstrated/unknown.
Genetically engineered photoreceptor color swap (swap UV and blue)  which sends impulses to the same optic nerves as the previous color, may, and probably would work fine.
If you switch one eye to CMY and keep the other as RGB, it should have a usable result.
If you switch both eyes to CMY it's fine too, we would expect that there would be a fair vision perception, perhaps equivalent to RGB in clarity.
If you design a fetus with 4-5 photoreceptors and let it develop normally, It would have an unknown result. Perhaps the baby would have augmented vision, perhaps troubled. It's not know and many scientists would love to know the result.
I'd wager that a human with 4-5-6 colors of photoreceptors can be genetically engineered to see, within our lifetime.

Awesome, I believe that there is a man or woman who's been given a robotic eye (about 3 years ago) and it was very blurry and low saturation but the same colours as our SML receive. I just did a quick google and found about 5 links to different events claiming to be the first transplant and one really neat one to combat ARMD. I think that with Crispr being our modern DNA modifier would could eventually learn enough about DNA to design improved sight. But back to the question, yes certainly would be fascinating to know the outcome of "extra" or "new" colours.

@Tmanok If I get the reference correctly that was a photoreceptor chip grafted to the retina.

There be tetrachromatic humans already. https://web.archive.org/web/20120214002707/http://www.klab.caltech.edu/cns186/papers/Jameson01.pdf

Awesome John thanks for sharing!
@Ratchet Freak, yes there was a transplant of an entire bionic eye in colorado 2015, another in the UK but different operation and then a neat one for ARMD (AMD is the generally more accepted term) where they grafted an electrode array connected to a pair of glasses with a camera. I'm sure there have been more but when you read "first, first, first, first" all during different years it makes you think "first time using this method? Your title is misleading and earns a skepticism award".

Humans probably couldn't use UV photoreceptors, a study found that all animals that can see UV's, birds and some mammals, have eyes smaller than 5-7mm. https://io9.gizmodo.com/want-ultraviolet-vision-youre-going-to-need-smaller-ey-1468759573

There are two issues associated with "seeing extra colors". One is seeing parts of the light spectrum we currently do not see; for example, seeing ultraviolet or infrared light. Another is discriminating between different combinations of wavelengths, and perceiving more colors than we actually do.
Our color vision is based on three different receptors who are sensitive to different wavelengths; the brain infers color from the differences between how those receptors are activated. This allows to tell some combinations of wavelengths from others, but not all: we can tell red light from blue light, because the first excites the red-detecting cells a lot more than the two others and the second excites the blue-detecting cells a lot more than the two others, but we cannot tell yellow light from a combination of red and green light, because in both of those cases we have the red and green cells excited the same and the blue cells not as much. This is why our color vision is "three-dimensional", i.e. all colors can be generated from three basic ones.
Somebody who instead of a blue receptor had an ultraviolet receptor, would be able to perceive more wavelengths than we do, but they would probably see more or less the same colors - "ultraviolet" would be "blue" to them. There may be differences because the kind of combinations they ran into would be different - for example because they'd have a wider range between the "green" and "ultraviolet" sensors than we have between "green" and "blue", maybe more of the world would look cyan than it does to us.
To see additional colors, the same way that ordinary trichromat humans see more colors than color-blind people, and be able to discriminate between more combinations of wavelengths than we do now, we would need extra receptors. And that's where the questions arise of whether the brain would be able to handle the extra colors, or whether the optic nerve would transmit it as its own channel.
As it happens there are cases in humans where they have four different color receptors. The main case happens because the genes for some color receptors (red/green) are on the X chromosome, and in women one of their two X chromosome is inactivated in each cell, but which it is is random - meaning that if they have two slightly different versions of that receptor on their two chromosomes, some cells in the retina will have one and others the other - making two different color receptors in their eyes where other people have one.
It appears that most women with this conditions do not see more colors than others, which could be because the two receptors don't vary enough. But it appears that some rare cases do have better abilities to discriminate colors and a richer color experience, which suggests that human tetrachromacy is possible and already exists in a few rare individuals.
See also:
https://en.wikipedia.org/wiki/Tetrachromacy#Humans
https://theneurosphere.com/2015/12/17/the-mystery-of-tetrachromacy-if-12-of-women-have-four-cone-types-in-their-eyes-why-do-so-few-of-them-actually-see-more-colours/
https://theness.com/neurologicablog/index.php/tetrachromacy-in-humans/
https://www.researchgate.net/profile/Zoltan_Jakab/publication/254932347_Looking_for_potential_indicators_of_human_tetrachromacy/links/546c88c80cf2c4819f216fa5/Looking-for-potential-indicators-of-human-tetrachromacy.pdf
https://arxiv.org/abs/1703.04392
Enhancing human color vision by breaking binocular redundancy (this isn't about the abovementioned cases of tetrachromacy, but of people trying to induce tetrachromacy by stimulating the two eyes differently)
This paper gives a good general overview of color vision in the animal kingdom, and debunks some misconceptions (such that animals with a zillion color receptors see a bazillion more colors than we do - they actually process color very differently and the number of color receptors they have is related to that).
https://www.sciencedirect.com/science/article/pii/S0960982214013013
Another overview of human color vision:
https://www.imbs.uci.edu/colorcoglab/4-9.pdf
Human Potential for Tetrachromacy

Hi Rozenn, this makes perfect sense after having read about Mantis Shrimp perceiving very specific wavelengths of UV, although researchers have no idea why they have this innate need to see those wavelengths it can be assumed that they're related to something in their habitat and the fact that they filter out non-essential colours leads me to think that they are blocking out sun refraction underwater. Who knows, but do you'd think having photoreceptors that do not overlap with each other in the UV spectrum would be very odd- binary colour hue but with variable saturation in fact.


text:
Neurological response to food cravings caused by bacteria
Our microbiome (Kurzgesagt video) is thought to send our brain information to chose certain foods to eat over others and it's our increase in a certain type of bacteria that will form a stronger craving for whatever that bacteria happens to appreciate the most. I'd like to know more about how the brain makes those choices in relation to the bacteria, than in relation to a general reward (The brain receives dopamine for things that are achieved, how does bacteria affect that?). Do the bacteria affect the amount of dopamine released- if so then how are the neurons that appreciate that bacteria award, broken or less interested when another type of bacteria now wants a different type of food?
NOTE Neurons are formed when the brain "achieves something" like when bacteria are given the food they thrive on I suppose, so when another type of bacteria receives more food and takes over in your gut, how is it that your neurons are broken and seemingly replaced? I understand this is a stretch but bare with me I just spoke to a neuroscientist about a month back who informed me about the basics of this process.


text:
What is Balbiani's vitelline body function?
I tried searching on Google Scholar but I found little to no information about this Balbiani's vitelline body.
I don't even know why it is called vitelline...I've been taught that it can be seen under the electron microscope, is perinuclear, made of mitochondria and lamelle anulatae (I don't know what these are) and you can see it only in primordial follicles.
I initially thought it was involved in protein synthesis, but primordial follicles should be biologically quiescent until they 'wake up' and begin folliculogenesis.

Did you read this section in Wikipedia?

No, I didn't.I'm reading it now for the first time.So this vitelline body silences transposons?

We can close this question as solved.


text:
How much blood do we have when the heart first starts to beat?
How much blood do we have when the heart beats for the first time?
It should be between the third and fourth week of embryonic life.

Note: there is a heart "beat" but no pumping at 3-4 weeks. The blood vessels and chambers of the heart have not developed. The "beat" is just electrical activity in cells that will eventually become part of the heart.

From your comment I guess we don't even have blood at 4 weeks


text:
How do emus/ostriches/rheas have their upper leg connected to the rest of their body?
I'm working on a model for educational graphics of an emu in conjunction with other information, but there aren't a lot of great reference images. The thing that's most unclear is how the upper leg around the femur is connected to the rest of the body because it's always obscured by feathers.
Mainly, is the leg connected to the rest of the area around the hip only half way through the femur, at the distal joint of the femur, or past the distal joint of the femur to the tibia? Elephants seem to have the third option, while horses seem to have the second option, and wolves seem to have the first option, so there are many possibilities without a clear generalization.
Below are the three options with the red indicating how far up the body the leg is connected to the skin of the hip area.

Try typing "emu skeleton" into your search engine: https://www.google.com/search?q=emu+skeleton&sa=G&complete=0&hl=en&gbv=2&prmd=ivns&tbm=isch&tbo=u&source=univ&ved=0ahUKEwjy74zWsffYAhUC2WMKHWP9CQAQsAQIFA

I wish it was that brain-dead simple, but it would benefit you to know that bones aren't muscles and dermis tissue, so a skeleton doesn't tell someone how the muscles and dermis extend to connect to the rest of the body from the leg tissue, it's a supporting structure.

Well, googling for "featherless ostrich" does retry some results...

Tried that too, some of the first results were: a jumping featherless chicken, an owl chimera, a 3-headed camel, a t-rex, and an ostrich laying an egg.

@John Joe: Sorry, I wasn't clear on what you were asking.  Searching for "emu musculature" finds this: https://peerj.com/articles/716/ and this: http://onlinelibrary.wiley.com/doi/10.1002/(SICI)1097-4687(199810)238:1%3C23::AID-JMOR2%3E3.0.CO;2-O/full (which is paywalled, but you might find an online copy).


text:
Which nervous system is the Sensory system a sub-unit of?
I'm wondering about this because on one hand, the actual sensory information from something such as sight or sound transmits to the brain, which is part of the central nervous system.
On the other hand, the actual muscles that control eye movement but have absolutely nothing to do with processing incoming information are part of the somatic nervous system, meanwhile the actual motion of tissues within sensory organs can also be involuntary.


text:
Why did some animals evolve inward-slanted legs?
Something I noticed looking at reference images is some animals have legs that are slanted inward relative to the length of their body, like in the two images below. Why have animals evolved this instead of having their legs pointing more straight down like lions or elephants?

You picked the two habitual, upright, striding bipeds as examples.

So? The question remains the same.

I think @kmm is encouraging you to think critically about your question and giving a huge hint about the difference between the examples you came up with that have 'inward slanted' legs versus your counterexamples that do not.

No one teaches advanced mechanics until after calculus 3 or maybe 2, and frankly analyzing every possible force at every possible angle of three joints and a body with arbitrary self-locomotion and then guessing why something happened to coincidentally mutate that way is a nightmare for anyone, there's not much to critically think about unless you have a very accurate simulation set up. That's why the sources of answers to questions like these almost always originate from graduate researchers with extensive testing on live animals in motion or expensive robots.

Sorry no references other than illustrations for the moment.
If a running biped has it's feet further away from the line of gravity, then it's got less efficiency in forwards motion and more instability of the line of gravity falling left and right.
When you consider the kinetic downwards weight in kilos that goes into every step, a runner/sprinter who doesn't have aligned steps wastes a lot of energy.
here's are dinosaur footprints:
https://australianmuseum.net.au/Uploads/Images/7919/footprint%20comparisons_big.jpg
The hips joints tend to point sideways to give a strong musculature, lots of running muscle, and a wide base of more than 90 degrees, for a wide birth canal and other reasons.
So the tendency for efficiency of running bipeds is to have aligned footsteps and their hips tend to be a strong and wide base.
That's only the resting position, the walking angles actually vary a bit outwards and straight too, the knee goes outwards when it's rising.
https://cdn.pixabay.com/photo/2016/01/18/02/04/footprints-1145883_960_720.jpg
here is a comparison of ostrich and human bone angles: http://rsif.royalsocietypublishing.org/content/13/122/20160529


text:
Is there a name for the behavioral phenomena of when animals like ants sacrifice themselves?
Title says everything about the first question.
The second question is: does the special case when ants apparently explode, https://www.washingtonpost.com/news/morning-mix/wp/2018/04/20/meet-the-exploding-ant-which-sacrifices-itself-for-its-colony/?noredirect=on&utm_term=.b56b0100a88b have its own name or does it fall under the same previous term?

The term you're looking for is altruism. According to Wikipedia, altruistic behaviour "allows an individual to increase the success of its genes by helping relatives that share those genes." Someone correct me if I am wrong but this means that this behaviour evolved by natural selection because it ensures the survival of a species in most cases. The link about exploding ants is probably a nifty example of altruism.


text:
Is each blade of grass an individual plant or not?
Sometimes when I do gardening, I notice multiple blades of grass appear fused together at the root, yet still appear to be segmented. When I look at images, I get some that suggest each blade is an individual plant like this one, and I find ones that suggest they're fused together like this other one, and I wouldn't know if they're actually fused or if they just have a tendency to have seeds or roots distributed in a clumped manner as some survival strategy.
Should it be assumed that each individual blade of grass is a separate plant, or otherwise how many blades are part of the same plant?

Each blade of grass is part of the grass plant and may have multiple blades.  Clumping grasses, when mature, can spread producing multiple shoots with additional blades.  The number of blades would depend on the type of grass and individual seed, but the clumping grasses tend to produce 10-16 leaves/blades.

Source: Poaceae - Wikepedia

They are clones, technically a single plant, even if disconnected at some point. Usually they are connected through the root system, through a rhizome which will produce additional shoots that go up vertically above the ground. Once a decent root system has developed, new offshoots (of the same plant) will continue to grow vertically, even if separated from one another.
This is a bamboo grass,

In a bamboo forest (or any patch of grass), it is possible that entire groups of trees are actually just one plant.


text:
Classification of living organisms in kingdoms
What feature justifies the placing of prawns and grasshoppers in the same phylum

Is this a homework question?

Kingdoms represent phylogenetic relationship. As such there is no need for specific phenotypic features to group lineages together but only the recognition of their phylogenetic relationship. This being said, lineages from a certain kingdoms do share some phenotypic features.
As both the prawns and the grasshoppers belong to the kingdoms Animalia (aka. Metazoa), you can just look at the wikipedia article for animal and repeat the listed features. In short, they are both eukaryotic, multicellular, have motile cells and are heterotrophs.


text:
Causes of Back Dimples
What are the causes of the dimples commonly found above the buttocks?  They seem to be in line with the sacroiliac joints.  Do the joints have anything to do with them?

Back dimples or Dimples of Venus are created by a short ligament stretching between the posterior superior iliac spine and the skin. They are thought to be genetic.
Source and further reading: Kumar, Kanojia & Saili (2014) - Skin dimples

@Mesentery, thanks for editing. I took the image of Wikimedia without thinking that it might be deemed NSFW or inappropriate. Thanks again.


text:
Why don't water cuttings die of root asphyxia?
Root asphyxia happens when there is not enough oxygen available for the roots, for example when the soil is clogged with water.
However it is common to do water cuttings where roots directly develop in water.
In this scenario, how is it possible for the roots to develop in only water without asphyxia, but they die of asphyxia in waterlogged soil?

Look up dissolved oxygen in water. In mud, other organisms compete for O2.


text:
Where are eosinophils and basophils phagocytic?
It seems known that neutrophils circulate and are phagocytic within the blood stream, but I'm having trouble finding similar conconclusions about where eosinophils and basophils are phagocytic which are less common.

Eosinophils and basophils are broadly referred to as non-professional phagocytes, in that they can use phagocytosis, but don't primarily function like this. Rather, they tend to de-granulate to kill their targets. They lack the abundance of receptor complexes for efficient phagocytosis that professional phagocytes like monocytes and neutrophils express, like opsonin receptors.
There's some data to suggest that macrophages control non-professional phagocytes like epithelial and endothelial cells (ref), but it's a bit of a jump to generalize that to eosinophils and basophils.
My intuition is that these specialized types of cells uptake debris and extracellular antigen, since they do partake in non-professional class-II antigen presentation, rather than larger bodies or microorganisms like macrophages uptake.

Also to add to this - lets not forget that these cells can function differently in circulation, compared to when they enter in tissue. They look morphologically different, and often one can see phagocytic vacuoles present in the cytoplasms..meaning they probably do participate in some minor "cleaning up" , but like the above poster mentioned, primarily they release granules into the environment wherever they detect damage, or antibody reactions.


text:
What is the difference between how motor function is controlled in cerebrum vs frontal lobe?
At least according to wikipedia, the frontal lobe houses the primary motor cortex, but in a different article about the cerebellum, it says the cerebellum controls motor function. So, do both parts control voluntary movement at once? What's the difference in the roles these two parts play in movement?
https://en.wikipedia.org/wiki/Cerebellum
https://en.wikipedia.org/wiki/Frontal_lobe

The motor cortex, basal ganglia, and cerebellum all contribute to motor control.
Cortex stores movement memory, basal ganglia is responsible for "chunking", or segmenting the memory, and cerebellum compares cortex memory and current movement to correct for errors and to update perception of movement. So to answer your question they all control different components/processes of learned movements at the same time and in conjunction.


text:
What prevents platelets from clotting regular blood vessels?
Platelets clump together to initiate clotting, but, why don't platelets clot within healthy tissue and cause heart attacks all the time?

Platelets activate when the exposed collagen (which is normally present below the endothelium) at the wound site binds to the platelets, forming a plug. Other factors are also secreted which aid in stronger binding. A signaling cascade is triggered which then makes platelets release proteins called integrins, which help for tighter binding of platelets at the site. Activated platelets also release many stored compounds from their granules which initiate further signaling cascades to form a clot.
In a healthy tissue, there is no exposed collagen. Ergo, No clotting.


text:
How does an animal having toes create more friction than not?
I was looking at the morphology of different animals when I found that apparently part of the reason vertebrate mammals have toes is that they grip the ground. But, why is that better than having a solid foot with no toes if friction increases with the surface area in contact with the ground?

I would say that the premise that "the surface area of contact with the ground increases in case of solid foot" is incorrect.
In practice, the ground is very far from being even and flat, and the animals need to navigate themselves throughout different terrains that include very uneven ground, stones, growing & lying plants, etc. In that case, having toes, in general, offer an advantage of gripping to the ground (and increasing contact area in multiple directions) in a large set of terrains. Then, different animals will develop their toes in different shape/form tailored to the dominating usage (including, but not limited to gripping the ground).

I guess that would make sense. It seems like ostriches have flatter toes and seemingly not coincidentally, they run on flatter land, but so do lions and giraffes. But assuming that pattern, it would seem to suggest flat/solid feet are then more optimal for flat land, like how webbed feet are optimal for water, which, has a relatively constant density in an environment.


text:
Reflex muscular activity in three months old fetus

At the end of the third month, reflex activity can be evoked in
  aborted fetuses, indicating muscular activity

This quote is from Langman's Medical Embriology.
Have I misunderstood it or it is really talking about muscular reflexes in aborted fetuses?
Do we have any video proof or something like that?
How does it happen and why?
Why do we need a muscular reflex during prenatal life?


text:
Virus Mortality Selection
This question is related to the recent Wuhan outbreak. Currently, mortality rate for the virus is somewhere around 2-3%. This is much lower than say, SARS (9.5%) and MERS (34.5%).
As a thought experiment, the main cause of death of the above viruses tends to be pneumonia (direct and secondary). If pneumonia leads to a higher rate of infection, then (indirectly) would such a virus would become much more deadly over time?
Do viruses such as the coronavirus self-select for higher rates of mortality, e.g. by leading to pneumonia, thus causing more phlegm and coughing?
Related to the above, how quickly can such mutations arise?
Sources would be really appreciated!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular note that speculative questions (i.e. thought experiments) are not appropriate for this site. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Stack Exchange Biology does not have the remit or expertise to answer most questions about coronaviruses relating to the recent 2019-nCoV outbreak. A list of what are regarded as reputable external sources of such information has been posted on Biology Meta. Please consult that.


text:
What does T and the numbers mean in T coliphages?
I have searched a number of websites and articles relating to nomenclatures or phages but never found anything explaining what T in T-4,5,6.. Phages mean in the Coliphages. Also, what does the number mean? I have seen that many times, the T - even are grouped as one, why is it so?
Thank you.

The "T" stands for "Type" as in type 1, type 2 etc. To quote Wikipedia on Escherichia virus T4 (emphasis mine):

Bacteriophages were first discovered by the English scientist Frederick Twort in 1915 and Félix d'Hérelle in 1917. In the late 1930s, T. L. Rakieten proposed either a mixture of raw sewerage or a lysate from E. coli infected with raw sewerage to the two researchers Milislav Demerec and Ugo Fano. These two researchers isolated T3, T4, T5, and T6 from E.coli. Also, in 1932, the researcher J. Bronfenbrenner had studied and worked on the T2 phage, at which the T2 phage was isolated from the virus.[39] This isolation was made from a fecal material rather than from sewerage. At any rate, Max Delbrück was involved in the discovery of the T even phages. His part was naming the bacteriophages into Type 1(T1), Type 2 (T2), Type 3 (T3), etc.

It turns out Wikipedia is incorrect: The original use of Type as a designation for these viruses comes from a paper published in 1945 (PDF) by M Demeric and U Fano: BACTERIOPHAGE-RESISTANT MUTANTS IN ESCHERICHIA COLI Genetics 30:119. In this paper they collected phages from Luria (of LB/Luria Broth (actually properly known as lysogeny broth)) and Delbruck amongst others and collated them all for comparison. Delbruck references them in his review article (PDF, possible paywall, summary here), also from 1945.
I could find no evidence for why the phages were numbered as they were, though strains from Luria (actually previously from his supervisor as P28 and PC) were labeled T1 (Luria alpha) and T2 (Luria gamma), so it is possible that it was simply in order that they were received or possibly in order of discovery amongst the several groups working on these viruses.
The T-even phages were grouped because of structural similarities, and are now strains of the species escherichia virus T4 in the genus Tequatrovirus (see link for taxonomy).

Was the numbering done chronologically or based on some observation?

@Karthik, no idea, see revised post.


text:
Changes in DNA and forensic cases
If DNA changes over time, how is it that forensic DNA gathered decades ago can be matched to a person today for solving crimes?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular it is not clear what you mean by "DNA changes over time" — are you asking about mutations that accumulate in living tissue, or degradation of  specimens? ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

@Dirigible ?? DNA profiling is not based on sequencing at least until 2010, it is doing a fingerprint of the reaction product of a PCR+electrophoresis with specially designed primers targeting microsatellites https://www.yourgenome.org/facts/what-is-a-dna-fingerprint


text:
Can any molecule become a hapten?
Hapten are small-molecules, that can only become immunogenic when conjugated with a carrier protein. I was wondering if all small-molecules can become haptens (eg. by synthetic conjugation).
Given that lymphocytes are filtered by negative selection, I would expect that small-molecules that chemically mimic self-peptides would not work as haptens (at least not in the sense, that they could be detected by antibodies).
Are there any examples of small-molecules that have been tried as haptens but could not generate antibodies ?
Also is there any estimate of the ratio of naturally occuring haptens and synthetic haptens. I was investigating the IEDB (https://www.iedb.org/) as well as SuperHapten (http://bioinformatics.charite.de/superhapten/) but could not find a way to filter these two types of haptens.


text:
Can spike protein induced cell fusion be triggered by the mRNA vaccine?
The mRNA-based vaccines cannot lead to COVID-19 or its symptoms since they only lead to the production of the spike protein in the cell.
However, the spike protein itself can lead to cell fusion:
Quantitative assays reveal cell fusion at minimal levels of SARS-CoV-2 spike protein and fusion from without
Is this a potential risk of the mRNA vaccine ?
I could imagine, that the spike protein needs to be bound to the virus to induce this effect ?
I could not find any literature where the effect of the unbound spike protein is tested.

Why the down vote ?

The virus membrane anchored spike provokes virion-cell fusion, the cell membrane anchored spike provokes cell-cell fusion, when encountering ACE2. In most vaccines the 2P mutation greatly reduces this behavior (not in the AstraZeneca vaccine).

The mRNA vaccines encode a mutant version of the spike protein in which the structural transition needed to to fuse membranes is blocked. This was done to make the immune response focus on the pre-fusion state, which is much better for neutralizing the virus.
From https://cen.acs.org/pharmaceuticals/vaccines/tiny-tweak-behind-COVID-19/98/i38:

Fortuitously, Graham and a former postdoc, Jason McLellan, devised a solution to this problem before the pandemic. Through a bit of structural biology and persistent protein engineering, McLellan discovered that adding two prolines—the most rigid of the 20 amino acids—to a key joint of a vaccine’s spike protein could stabilize the structure’s prefusion shape. This 2P mutation worked in preclinical studies of Graham and Moderna’s MERS vaccine, so they applied it to Moderna’s COVID-19 vaccine.

I don't know if cells expressing wild-type spike protein would fuse into syncytia, but it seems very unlikely to happen with the vaccine spike.

Comments are not for extended discussion; this conversation has been moved to chat.


text:
Does estrogen have a more potent neural pruning effect in adolescence than testosterone?
I have read a study here which finds that female rats with their oestrogen inhibited had more neurones in a region of the visual cortex than intact female rats. To me, this suggests that estrogen may have a more potent neural pruning effect than testosterone, and that this may explain why female brains are on average slightly smaller than male ones. However, this study is A) not on humans and B) not on the whole brain. Further, the difference between average brain weight extends into childhood when sex hormones are low (but not non-existent. So, I wanted to know whether there was any consensus on the difference between testosterone-controlled neural pruning and estrogen-controlled neural pruning, and whether my conjecture is reflected by any evidence.


text:
Does antibodies get produced in female body against sperms?
Our immune system produces antibodies against any foreign particles entering our body.In female body  sperms are a foreign particle .Does females produce antibodies or some sort of chemical resistance against these sperms?If so how come sperms able to survive this?Is it because there a huge number of sperms entering female body?

https://en.wikipedia.org/wiki/Antisperm_antibodies Sperm can trigger antibodies production.Sperms are also killed by the low pH in the female genital tract


text:
Human Immune Response to COVID-19 Virus
I have tried to find an answer to this but have not found anything after multiple attempts.
The question on the table is if the human body is able to produce an immune response to the COVID-19 virus if one has been exposed? This would apply most specifically to persons that have been tested positive but have "survived" (i.e. not having succumbed to the serious lung complications that have caused deaths for some persons).
A follow on question that comes from this is if the human body is able to mount a suitable defense does the current practice of keeping people in quarantine for two weeks allow for this defense to reach full effectiveness?

I would think if you recover at all, that signifies some kind of immunity, short-term or not. Otherwise, the virus would just keep replicating, methinks.

We probably won't really know for certain until we have time to gather more data from survivors. However, infection with existing coronaviruses (including SARS-CoV, genetically very similar to the COVID-19 virus SARS-CoV-2; ref. https://www.nature.com/articles/s41564-020-0695-z) suggests that those who are infected and survive may develop temporary immunity (ref. https://www.statnews.com/2020/02/04/two-scenarios-if-new-coronavirus-isnt-contained/):

The toll of a seasonal-flu-like coronavirus also depends on immunity — which is also scientifically uncertain. Exposure to the four endemic coronaviruses produces immunity that lasts longer than that to influenza, Webby said, but not permanent immunity. Like respiratory syncytial virus, which can re-infect adults who had it in childhood, coronavirus immunity wanes.
“Everyone, by the time they reach adulthood, should have some immunity to some coronavirus,” said Tim Sheahan, a coronavirus researcher at University of North Carolina’s Gillings School of Global Public Health. But because it doesn’t last, older people can get reinfected. The elderly also have a higher death rate from coronaviruses such as SARS and MERS, a pattern 2019-nCoV is following.
“There is some evidence that people can be reinfected with the four coronaviruses and that there is no long-lasting immunity,” Dr. Susan Kline, an infectious disease specialist at of the University of Minnesota. “Like rhinoviruses [which cause the common cold], you could be infected multiple times over your life. You can mount an antibody response, but it wanes, so on subsequent exposure you don’t have protection.” Subsequent infections often produce milder illness, however.

It might also be possible that someone was infected with two different strains of SARS-CoV-2 and did not develop immunity from the first infection. But it could have also been a continuation of the first infection, or testing error. Without virus sequence data, it was not possible to determine what happened for certain (ref. https://www.wired.com/story/did-a-woman-get-coronavirus-twice-scientists-are-skeptical/):

What could be worse than getting the pneumonia-like illness now known as Covid-19? Getting it twice.
That’s what Japanese government officials say may have happened to a female tour bus guide in Osaka. The woman was first diagnosed with Covid-19 in late January, according to a statement released by Osaka’s prefectural government Wednesday. She was discharged shortly after, once her symptoms had improved. A subsequent test came back negative for the virus. Three weeks later she returned with a sore throat and chest pain and tested again. For a second time, she tested positive for Covid-19.
News reports detailing the case raised the possibility that people may not be developing immunity to the new coronavirus, even after they’ve recovered. But several infectious disease specialists say there’s not enough data to support that conclusion. Another possibility is that the virus subsided and flared up again. (Some viruses tend to do that.) Or the test was simply wrong.

If someone was infected twice, comparing the genomic sequences of the virus over time would have helped determine that with more certainty.

Macaque monkeys seem to develop immunity. If they try to reinfect the monkeys 28 days after the first time they are infected with SARS-CoV-2, same strain both times, they do not get sick.
https://www.livescience.com/monkeys-cannot-get-reinfected-with-coronavirus-study.html
(Not a link to the actual study.)


text:
Is touching or inhaling 70% isopropyl alcohol dangerous to humans?
I bought 99% isopropyl alcohol and made 70% alcohol + 30% water in small spraying bottles as a disinfectant.
I also read that this solution is safe and recommended by Apple for cleaning iPhones.
My worry comes from reading on the 99% bottle how extremely dangerous it is to humans. Basically touching, inhaling and of course consuming it is very toxic.
On the other hand 70% alcohol solutions are found in most hand and surface sanitizers which are usable against COVID-19.
So my question is: how much should I be afraid when cleaning surfaces with my small 70% spray bottle? Since alcohol evaporates, I'd be naturally inhaling it, I mean where else could it go in the air? I'm also just spraying it on a wipe to clean my mobile, not using a rubber glove for that.
What are the health concerns when using such solution?

If you're interested in the biological or health effects of various chemicals, try to look up the Safety Data Sheet, or "SDS" or "MSDS", for that chemical compound.
Going to your favorite search engine and plugging in your chemical of interest to the search term "SDS" or "MSDS" will almost always get you to some kind of answer — either what you're looking for has a safety data sheet or it doesn't!
In the case of 70% isopropyl alcohol, there are SDSs/MSDSs out there that will tell you what potential health effects are. Here's one example for 70% isopropyl alcohol:

Potential Health Effects
Eye: Produces irritation, characterized by a burning sensation, redness, tearing, inflammation, and possible corneal injury. May cause transient corneal injury. In the eyes of a rabbit, 0.1 ml of 70% isopropyl alcohol caused conjunctivitis, iritis, and corneal opacity.
Skin: May cause irritation with pain and stinging, especially if the skin is abraded. Isopropanol has a low potential to cause allergic skin reactions; however, rare cases of allergic contact dermatitis have been reported. May be absorbed through intact skin. Dermal absorption has been considered toxicologically insignificant. The cases of deep coma associated with skin contact are thought to be a consequence of gross isopropanol vapor inhalation in rooms with inadequate ventilation, rather than being attributable to percutaneous absorption of isopropanol per se.
Ingestion: Causes gastrointestinal irritation with nausea, vomiting and diarrhea. May cause kidney damage. May cause central nervous system depression, characterized by excitement, followed by headache, dizziness, drowsiness, and nausea. Advanced stages may cause collapse, unconsciousness, coma and possible death due to respiratory failure. Aspiration of material into the lungs may cause chemical pneumonitis, which may be fatal. The probable oral lethal dose in humans is 240 ml (2696 mg/kg), but ingestion of only 20 ml (224 mg/kg) has caused poisoning.
Inhalation: Inhalation of high concentrations may cause central nervous system effects characterized by nausea, headache, dizziness, unconsciousness and coma. May cause narcotic effects in high concentration. Causes upper respiratory tract irritation. Inhalation of vapors may cause drowsiness and dizziness.
Chronic: Prolonged or repeated skin contact may cause defatting and dermatitis.

Safety data sheets sound terrible! But in reality, people use rubbing alcohol with common sense, without putting into their eyes, without drinking it, etc.
Mainly the point of this answer is to help you find the answer for yourself, if you want to find out about this or other chemicals you might be worried about.