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What animal has the longest juvenile period?
I just heard the following complaint from a comedienne.

Humans are the only animal that is completely useless for the first twenty five years of life.

Obviously this is just a joke but it is true that primates and especially humans do have profoundly long juvenile periods compared with most animals. It's got me wondering whether humans really do spend the most time in sexual immaturity.
Unfortunately I have found this question hard to search because Google thinks I'm asking about the longest gestation period (which seems to be a much more popular question). To be clear, I am not asking about the longest gestation period.

As you indicate in your question, the average age of sexual maturity is probably the best way to approach this, since immaturity is usually how juveniles are defined. Age of puberty is also different in boys and girls (the same goes for many animals), and has also decreased in the 21 century. However, as an historical average for humans 15 years is probably fair, even though there is a lot of variance. That is high compared to most animals, but there are some that have similar or higher ages of maturation, e.g.:

Cicadas in the genus Magcicada, which can have a 17 year life cycle
Elephants reach sexual maturity at about an age of 8-15 years, but usually dont start to breed until they are at least 18-20 years (see e.g. elephantsforever.co.za and Association of Zoos and Aquariums). Males mature and start reproducing later than females, and in practice it is mostly older bulls that reproduce.
The Nile crocodile, which reach sexual maturity at at an age of 12-16 years (largely dependent of body size though).
Some species of Tortoise reach maturity at ages 13-16 years (e.g. Gopherus
sp, see Germano, 1994), and, again, which is largely due to body size and growth rate. Captive bred individuals can mature more quickly.

As you can see, there is a difference between sexual maturity and reproductive age. To actually be able to reproduce, especially in some male mammals, you often need experience and size, which means that reproduction is delayed in practice. Whether this period from sexual maturity (with respect to producing mature eggs/sperm) to reproductive age should be defined as least partially as "adolescence" will affect how humans compare to other animals. In my examples, I have focused on sexual maturity (which usually has less variation between individuals).
For other examples, you might want to look at insects other than Cicadas that have delayed larval stages. This does for many woodliving beetles, where development times can be very variable, and under poor conditions take up to 20-30 years. This is usually not the norm though.
When searching for other examples, use the terms "age of maturation, "reproductive age", "sexual maturity" etc, to focus on sexual maturation and not gestation.

This article provides general facts about Tuataras, one of which is:

Tuataras reproduce slowly. They take 10-20 years to reach sexual maturity. Males can mate every year, but females breed every two to
five years. It takes the female between one and three years to provide
eggs with yolk, and up to seven months to form the shell. Then it
takes an additional 12 to 15 months from copulation to hatching,
possibly the longest incubation rate of any reptile.
A male tuatara named Henry, living at the Southland Museum and Art
Gallery, became a first-time father at the age of 111. He fathered 11
babies with a female named Mildred, believed to be in her seventies.

Those creatures are therefore one of the many that can be added to the list of the above answer.

Welcome to Bio.SE. Please [edit] your post to include a citation to a reputable source that supports your claim. Without it, your post will likely be downvoted or deleted. The goal here is to compile accurate and supported information about biology, as the internet already has too much misinformation. Please take out [tour] and visit our [help] for more information about how we work. Thanks.

The Greenland shark (Somniosus microcephalus) has been reported to need at least 156 ± 22 years reach to sexual maturity1. This is also thought to be the vertebrate with the longest lifespan.
Reference
1: Nielsen, J., Hedeholm, R. B., Heinemeier, J., Bushnell, P. G., Christiansen, J. S., Olsen, J., ... & Steffensen, J. F. (2016). Eye lens radiocarbon reveals centuries of longevity in the Greenland shark (Somniosus microcephalus). Science, 353(6300), 702-704.


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What is the protocol for extracting Protease Onion?
I am Investigating the protease concentration in certain fruits and vegetables. I am unable to find the protocols for the extraction from onions. I want to purify my protein using the ammonium sulphate (salting out) followed by dialysis. I am specifically concerned about the mass of ammonium sulphate that is required and the amount of water I should dissolve it in.

If no protocol exists, you would typically increase ammonium sulfate in stepwise amounts and assay for activity. You can somewhat purify your protein this way. Or you could just add some arbitrary amount like 75% and see what happens. I use this calculator.

source: Stack Exchange

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why prokaryotic ribosomes have 30s and40s subunits and eukaryotic ribosomes have 40sand 60s subunits?
Ribosomes are protein factories of cell and are composed of two subunits; one smaller and other larger unit I want to know that why ,ribosomes of eukaryotes have a 40s and 60s subunit and prokaryotic ribosomes have 30s and50s subunits ?If we combine 30s and 50s subunits shouldn't it be 80s ribosome instead of 70s ribosome .

What exactly is your question? Are you asking why there is difference between prokaryotic and eukaryotic ribosomal subunit masses? Or do you simply wanna know why these numbers dont add up?

I want to know why these numbers donot add up?I know that difference in their masses is due to difference of masses of their proteins.(of subunits).

Mass and sedimentation-coefficients are not the same thing, although related.

I think I can get the point after your second comment.
Not only protein composition, but rRNA composition and sequence length of Bacterial and Eukaryotic ribosome is very different. And the difference of sequence lengths (and hence mass) in both take part in the difference.

The S units are an artifact of the historical way these RNAs were characterized, based on the rate at which they sediment in an ultracentrifuge. S stands for Svedberg, which is a non-metric unit that measures sedimentation rate, based on size and shape. Larger molecules sediment slower. A better way to refer to ribosomal subunits is by calling them large subunit (LSU), and small subunit (SSU), because ALL ribosomes consist of one SSU and one LSU. Even the 5.8S is simply a part of eukaryotic LSU. Put subunits together and the shape changes, so it they would not sediment at a rate equal to the sum of each subunit.

You mean sedimentation depends on shape of subunits as they combine they slightly change their shape and will now sediment at 70s instead of 80s?

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Is it possible to make a cancer cell that doesn’t encode any neoantigens?
The cell still has mutations, but those mutations only occur in the noncoding sequences, such as promoters, which drives over expression of proto-oncogenes and downregulation of tumor suppressor genes. So the cell will proliferate uncontrollably, but won’t express any neoantigens.
Will such cell be invisible to our immune system?

Immunosurveillance of cancer cells is predicated upon multiple "signals" derived from the cancerous cells and their microenvironment.
I should point out tumor mutational load (Figure 1). A sort of take-home point here is that certain indications have less mutations and thus less neoantigens than others. You also have to take into consideration the stage of the tumor, though. Stage IV tumors have amassed more mutations than stage I/II.

Figure 1. Mutational prevalence by indication. A higher prevalence predicts a higher neoantigen frequency or mutational load for that cancer histology. (1, 2)
It's interesting to point out the bottom part of figure 1 where the authors of a separate review note for us where it's believed the disconnect between traditional checkpoint blockade immunotherapy and CAR-T immunotherapy exists. Just to educate a bit on the subject, checkpoint blockade targets T cells, the drivers of antigen-dependent cell killing. T cells naturally infiltrate the tumor as it develops and attempt to mount an attack. One of the methods tumors use to evade T cell killing is through persistent antigen, expression of inhibitory receptors and secretion of inhibitory molecules. Checkpoint blockade immunotherapy uses antibodies against the inhibitory receptors such as PD-1 (Opdivo, Keytruda), it's ligand PD-L1, CTLA-4 (Yervoy), Tim3, Lag3, and so forth. This attempts to lift the dampening effect these receptors have on T cells so that they may resume killing. The T-antigen-dependent paradigm is also supported by such publications which look at checkpoint blockade in the setting of clonal T cell diversity and confirm that (1) a diverse repertoire of T cell clones result in successful checkpoint blockade, and (2) enrichment of certain clonotypes within the repertoire, presumably the antigen-specific clonotypes, further indicates a response (3).
So below that are indications circled in red, notably the histologies with a low neoantigen frequency. The idea behind CAR T cells is that I can take advantage of T cell biology, notably that T cells recognize antigen with a receptor and kill the target cell. So just backing up to checkpoint blockade immunotherapy real quick, say a patient has melanoma which can consist of 1000s of mutations and 100s of neoantigens. There is a greater chance that an infiltrated T cell has specificity for any particular antigen. So how about a glioblastoma patient? They may have 10-20 neoantigens, or as you said they may have no neoantigens, at least none that their T cells are specific against. So checkpoint blockade may not be so effective. CAR stands for chimeric antigen receptor. It's essentially a monoclonal antibody against one target connected to a linker connected to the intracellular domain of a T cell receptor. Hematologic malignancies such as NHL like diffuse large B-cell lymphoma are commonly targeted for a B cell receptor known as CD19. So all you have to do is make your CAR CD19 specific and transfect the T cells with it in place of their own T cell receptor or TCR. So the basic process behind CAR is I isolate your T cells as with leukapheresis, lentivirally transfect with my anti-CD19 CAR, expand, and infuse. There are two CD19 CAR T products with great response rates on the market (Kymriah, YESCARTA). The whole reason these are good is because we can direct them to whatever antigen we want (of course be careful about self-antigens, see autoimmunity).

Figure 2. Schematic of CAR T cell therapy. (4)
The CAR T approach is in fact because the neoantigen load is low or non-existent, which is problematic for un-modified T cells, and thus problematic for standard-of-care treatments like checkpoint blockade.
As such, there are other ways, and other cells that can handle some of the abnormalities presented by tumors as a whole. This includes the presence of danger/damage-associated molecular patterns (DAMPs) and the regulation of surface receptors, for example, NK receptor ligands such as MIC.
The way DAMPs work is that a milieu of molecules are secreted by cells that are damaged or transformed, signaling cells of the innate immune system. One of the issues is that the DAMPs promote an inflammatory environment. This means that yes, you get immune cells checking out the situation, but that some of these are good immune cells and some are "bad" (myeloid-derived suppressor cells (MDSC), tumor-associated M2 macrophages (TAM), or T-regulatory cells (Treg)). These dampen the immune response both through inhibitory cytokine release like IL-10, and expression of inhibitory receptors like PD-L1.

Figure 5. The molecules secreted by the inflammatory tumor microenvironment both help and hurt the immune response. (5).
And then the idea behind NKR ligands is pretty straightforward: Natural killer (NK) cells patrol your body routinely for abnormalities and are licensed to kill cells that are abnormal. For example, all nucleated cells express class I major histocompatibility complex (MHC-I) on their surface. Some receptors like MIC are also present on the cell surface that engage receptors on the NK cells like NKG2D in distress. So what do cancers do? They sometimes express truncated and thus inactive MIC, express no MHC but also express inhibitory receptors to NK cells, and so forth.
Everything is summed nicely in the following figure on cancer immunoediting (Figure 7). Note that while things are working normally, the immune system can handle the tumor load. As the scales tip, and this could be for example, your T cell response edits out an immunoantigen but doesn't take care of the whole tumor, resulting in growth that those T cells no longer respond to. As this happens, the cancer becomes increasingly invasive.

Figure 7. Cancer immunoediting. (7).
So just to clarify at the end, there probably isn't a case where the immune system isn't responding at all unless you had chemotherapy that destroyed your immune system. Inflammatory environments alone are sufficient for your immune cells to at least check out the tumor. In fact, and I cant find the paper now but I'll try, investigators even found naïve T cells in the tumor microenvironment simply due to the inflammation. We could also get into "hot" and "cold" tumors, but that's out of scope here (take-home point, cold tumors aren't inflamed and are known to contain less immune infiltrate). I used immunotherapy as a vehicle to get my point across, note that this answer isn't about immunotherapy but rather about immune escape and mutational load theory.

Let me know if something doesn't make sense. There are a lot of caveats to the system that were cut out for brevity, like a formal definition for T cell repertoire diversity, for example.


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Firing rate of retinal ganglion cells
I have few questions about the firing rate of retinal ganglion cells.
1) How to explain the baseline firing rate if either the entire receptive field is stimulated or there is no light stimulus at all? That behaviour means that the intensity of light does not have any effect if the entire receptive field receives the same stimulus. I don’t understand how horizontal cells let that possible.
2) When the on-center is stimulated, the firing rate is maximized at the beginning and it diminishes with time to reach the baseline rate. Why does the firing rate decrease? What is responsible for that?

3) Is it possible to have a simple mathematical model of the process with an artificial neural network?

It's best to limit one question per question, especially when they are not closely related (Q3 here, e.g.).

1) This is a bit simplified; in reality, flashes of light or dark that cover the whole receptive field do influence the firing rate somewhat, just not nearly as much as an on-center stimulus for an on-center RGC. Your textbook is using a bit of an idealized interpretation to convey the concept of center-surround organization. I'm not sure what your confusion related to the horizontal cells is, however.
2) This is usually called "adaptation" and is a general principle in nervous systems (particularly on the sensory side). Multiple systems influence adaptation, including depletion of neurotransmitter-containing vesicles, metabotropic receptors activated by high concentrations of neurotransmitter that have opposite-sign effects to ligand-gated receptors, feedback systems that suppress the potency of second-messenger systems, accumulation of extracellular inhibitory neurotransmitters, etc. For the eye, there are additional sources of adaptation that come into play, depending on the experimental paradigm.
Without knowing the exact paradigm your textbook is meaning to indicate, it's probably more important at this point to just recognize adaptation as a normal aspect of sensory processing. The specific mechanisms can be understood later.
3) Yes - but you don't need to go to anything as complex as an artificial neural network. Basic image filters like the Laplacian of Gaussian (LOG) filter are basic approximations of center-surround organization in the retina.

Thank you very much for your answer! Retina horizontal cell article on Wikipedia says that horizontal cells allow eyes to see under different light conditions. So I deduced that they are responsible of the "adaptation" you are talking about. That's right?

@ardayigit That's an incomplete explanation from Wikipedia then about the role of horizontal cells. They can have some role in adaptation, but there are many other mechanisms for adaptation and horizontal cells also have a role in making center-surround organization more robust.

so many cells are involved in adaptation. I can not say if it is done by photoreceptors, bipolar cells, etc.


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How do gain-of-function alleles help with problems caused by genetic redundancy?
Genetic redundancy masks the gene functions (eg it masks diverse functions of the tumor suppressor gene). I have read on the internet that gain of function alleles can solve a such problem caused by genetic redundancy and would like to know how.

Genetic redundancy can be a problem when studying knockout or hypomorph mutations of genes, or analogues such as exogenous RNAi. The redundancy can consist either in incomplete knockout (the genome contains more than one copy of the gene but only one copy is mutated) or functional redundancy (different genes doing more or less the same thing). If you try to figure out what a gene does using a loss-of-function allele, the other copies or redundant genes may weaken or completely mask any phenotypic manifestation of the lost gene function.
Gain-of-function alleles can be useful in such a situation. A gain of function means the gene product does something different, or something additional to its normal function. Even if there are "healthy" other copies of the gene or redundant genes around, the modified function of the introduced allele will interfere with the normal behaviour of the molecular pathways it partakes in, and thus cause a phenotype.
A classic example are constitutively-active alleles. Imagine for example a tumour suppressor with a mutation that prevents it from being degraded (but imagine you don't know this gene is a tumour suppressor yet). Let's say there are other tumour suppressor genes around, so if you knock out your gene of interest, the cell behaves as normal - loss-of-function isn't useful to study what the gene does. Now, if you introduce this constitutively-active mutant variant that doesn't get degraded, it causes too much suppressive activity and drives the cell into complete cell cycle arrest, regardless of the other redundant genes being around. Based on this phenotype, you could infer that the gene is probably a tumour suppressor.


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Which plants are healthy to keep in the bedroom at night?
I know that there are no plants which release oxygen in the dark (Can plants produce oxygen at night (without light)?).
I also know that some plants can clean toxic agents from the air (Nasa Clean Air Study).
Are there any plants which have health-beneficial properties specifically at night, i.e. in the dark?
Assume, if you'd like, that 12 leprechauns bring the plants to your bedroom the moment you turn off the lights and place them outside your house when you turn on the lights in the morning. Can bedroom plants still be beneficial to your health in this case? If so, which ones and why?

...leprechauns?

@Dubukay The reason I bring up leprechauns is that I have noticed many autistic people are active on SE. These people malfunction when you leave any room for interpretation. E.g. if I had only said 'at night' instead of 'in the dark', they would complain that artificial light could still result in photosynthesis. This is obviously besides the point and, to non-autists, need not be made explicit. Therefore, I used a tongue-in-cheek method to make such nuances explicit here.

Why have some people -1'ed? The question is well posed, has references and fits within the scope of this SE. If you -1'ed, explain yourself.

There exist a diversity of flora you may select relative to the antigen or noxious chemical you seek to reduce.
Pursuant to the British Medical Bulletin, the critical indoor pollutants are the polycyclic aromatic hydrocarbons like furanes and benzenes, ethanal (formaldehyde) and carbon monoxide. Depending upon which gaseous or volatile compound you seek to reduce in your household, you may select Chrysanthemum morifolium for the reduction of ammonia gas, xylene and alternative respiratory irritants; Chlorophytum chomosum for formaldehyde; and Dracaena genus concerning and trichloroethylene.
If you should suffer any infestation of Penicillium mould, then it is advised that one tackle the source of the infestation directly - areas rich in cellulose and moisture.
Further information regarding is available from the following links:
9 Air-Cleaning plants that are almost impossible to kill, https://greatist.com/connect/houseplants-that-clean-air
British Medical Bulletin, https://academic.oup.com/bmb/article/68/1/209/421251

Thanks, but this is not what I was asking.

As far as I understood the question, this answer should be perfectly suitable (though lacking references to substantiate the claim of those plants doing what is claimed). If not this, what are you asking for?

@Armatus Wow, seriously? My question, so obviously, is not about reducing toxins in general. In fact, I preface my question by stating that I am already familiar with the air-cleaning capabilities of some plants. I am not looking for more references about that. As stated multiple times in my question, I am interested in the effect of plants specifically at night, i.e. in the dark. I even wrote an entire story about leprechauns in the hope to make this more clear, with a further explanation in the comment.

While I think you should rethink your communication strategy, I see your point. As a suggestion, when you know what kind of information you're not looking for, it generally helps to specify that in your question.

@Armatus I fully agree with your last sentence, that is why I started with those 2 points which I already knew. But it seems that wasn't clear enough. Unrelated: please use the @[name] in your comments, such that I get a notification about comments directed at me.


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A Brain Implant improves memory--but how?
https://www.nytimes.com/2018/02/06/health/brain-implant-memory.html
A new therapy could improve memory by "sending electrical pulses to aid the brain when it is struggling to store new information." I'm trying to figure out how this works physically, in terms of how it actually helps the brain. I would imagine that it has something to do with the neurons getting past the threshold for firing a signal with more ease, but is this because the threshold is suddenly lower because of the presence of the current, or what?
Could anyone provide me with an explanation of the science behind this in lay terms?
Many many thanks

From what I understand, when we learn we go over things quite a few times, this is so that our brain goes over the memory cells where we store that information with electrical impulses. Thus when an electrical impulse travels over some branches they strengthen the branches, (I don't know the science behind this). This is what helps us memorise data. So if we ran lots of Impulses over the branches it could help strengthen them or fry your brain, just saying try this in a safe environment such as a lab and not in a homemade electric chair. Also like you said it helps them run easier over the brain which makes it a lot easier to remember things.
Hope this helps,
IbnJalal

Answers here need to be referenced and based on scientific information, not just ad hoc hypotheses


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What type of fish is this- Cabo San Lucas, Gulf of California side

Can anybody tell me what this fish is?  Caught in Cabo last week, actually closer to San Jose, with a Joe's Flies 1/4oz spinner.  Cool looking fish for sure, just can't seem to find it online of what it is??

We need a picture...

That is a giant hawkfish, Cirrhitus rivulatus. It is identified by its unique markings from other species in the same region. This individual looks slightly young to me from the size, however it is most certainly this species. Giant hawkfish on mexican-fish.com

Cannot thank you enough!  You look to be exactly right!

@BrettNelson No problem. If you think the answer is correct you can also accept the answer but no need to.


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How does cell detect if a RNA polymerase II is stalled during transcription and in turn deploy the proper transcription-coupled repair factors?
When a segment of the template strand of DNA is damaged due to factors such as UV radiation, a lesion is created that would effectively block the passage of RNA polymerase II during transcription.
When such stalling occurs, a mammalian cell would usually deploy various transcription-coupled repair factor, such as the XP group of proteins to give provide a proper basis of the lesion and to orient other enzymes in. The endonuclease would cut out the damaged bases, and the DNA polymerase and DNA ligase would, respectively, add the new bases and correctly anchor them onto the template strand.
I fully realize that during the process in which the RNA polymerase II was stalled to the arrival of the transcription-coupled repair factors, some sort of cell signaling must have occurred. However, I could not find any sources that would tell me the specificity of such phenomenon. Therefore, I hope this forum could explain such matter.
Thank you very much!

The beauty of RNA polymerase II is its faculty to act like a sensor towards damage to genetic data. The response of the RNA molecule is variable on the type of DNA lesion which presents itself.
DNA lesions may be a consequence of ultraviolet radiation, or through the metabolic by-products of oxidative free radicals. These specific faults within the lesion, it is hypothesised, are respectively detected by the RNA pol II molecule by interaction with its active site.

Some examples of different genetic damage to bases
In the example you provided, namely, RNA is limited fully or partially from transcription elongation, this is detected as an inhibition of the active site. This could be caused by presence of cyclobutane which distorts the shape of the DNA molecule such that it prevents further RNA synthesis.
Therefore, in the incident that RNA pol II is fully stalled, the first co-factor to commence the signalling process is Transcription factor II H, which repositions the polymerase molecule away from the site of damage. Although it is not fully known, this allows the XPG, having certain endonuclease properties  to excise the faulty bases (thymine dimer, for instance).
In order to fully repair the molecule, DNA polymerase uses translocation to reinsert the correct complementary bases. PCNA, proliferated cell nuclear antigen, may be used as a DNA clamp to increase the processivity, ability for multiples catalyses without leaving the substrate, of DNA polymerase. Then protein complexes XPD operates as a ligase.
Therefore TC-NER, transcription-coupled repair, is believed to begin at a blockage of the active site of RNA pol II!
Best regards
More information regarding this hypothesis and function may be found from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4984683/ and https://www.ncbi.nlm.nih.gov/pubmed/11245433


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Why are worker ants not clones of the queen?
Currently worker ants of most species share only three quarters of their genetic code. It seems like worker ant clones would be better, as it would remove all genetic conflict of interest between them. Then they would be like our body cells. Only queens (and possibly males) would be produced sexually.

Yes, worker ants have a relatedness of 0.75 between each other (haplodiploid with shared parents).

why has evolution not produced perfect X can usually be answered by the correct mutations have not occured. evolution is about jury rigging good enough not perfection.
you are assuming ant are free to change how related they are, they aren't, they cannot rebuild their reproductive system from scratch they can only modify what they have.

Hypothetically, there could be disadvantages to making worker ants clones of the queen. In that case, an unfertilized queen could start a colony. Even if that colony was successful, how could the queen produce a new queen and new colonies? If we assume parthenogensis could answer those problems, then we would probably see much less genetic diversity over time, which could potentially lead to massive die-offs if the genetically homogenous ant population couldn't handle some new pathogen or environmental change. Forcing queens to mate before forming a colony ensures greater genetic diversity.

You are assuming my question is rhetoric, when you say "you are assuming ant are free to change how related they are". There is no such assumption in my question.


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Why does Anti-A antibodies make type-A blood type clump?
A-type blood has B-antibodies; it also clumps anti-A antibodies are inserted. Why is that? The blood has no antibodies against the A-antibodies to make clump in this way.

When an antibody meets its antigen it will bind it. So if you add anti-A antibodies to A blood, these antibodies will bind the red blood cells. Because of its Y-shaped form, each antibody can bind two epitopes. These can be located on the same red blood cell, or on two different. If they are located on two different, this leads to cross-linking of two blood cells. Since this happens many times, the blood cells will clump. The whole process is called hemagglutination.
See the image (from here) for illustration:

The so-called ABO blood grouping is based on the antigen-antibody reaction, where anti-A antibodies circulating in the plasma will bind to cells possessing antigen-A and cause clumping, or agglutination. A deadly situation since the red blood cells will be unable to circulate.
A person's blood group is designated according to the antigens found on the surface of their red blood cells. Type A blood means type A antigens are on the surface of the red blood cells. Type B - the same. Type AB - the same. Type O blood means there are no type-A or type-B antigens on the red blood cell's cell membrane/surface, theoretically making them the universal donor of red blood cells, but not their plasma if it contains anti-A, or anti-B, or both anti-A and anti-B antibodies, that can bind to their pair antigen type.
Persons of type-A blood mean that their red blood cells exhibit the antigen-A on their red blood cell membranes/surfaces, hence these persons can safely have anti-B antibodies circulating in their plasma to avoid agglutination. Type-B blood therefore means that the plasma may have anti-A antibodies safely.
Blood matching is further complicated by various blood antigen systems that have been found to be clinically significant, for example the Landsteiner blood antigens.

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filtering variant list according to target regions
I have a variant list in VCF file for a particular disease, I want to filter these variants according to exonic regions in a BED file using a Perl script. How I do this?

Sounds more like a question for Stack Overflow to me.

I'm voting to close this question as off-topic because it is not a question about Biology.

Don't reinvent the wheel.  Use BEDTools.
And no one on any Stack Exchange board wants to write you a perl script.

As a fuller explanation, use bedtools with the intersect command:
bedtools intersect -u -a variantList.vcf -b exonicRegions.bed > filteredVariants.vcf

While this should work, if your vcf version is giving you trouble use vcf2bed to convert the vcf to a bed file, then intersect directly.


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Using proportion or a diversity index when dealing with just two strains
I'm looking at diversity maintenance in an experimental system consisting of just two strains. I have count data. I can calculate their proportions and I can use that data in my statistical models, or I can calculate Shannon or Simpson diversity, and use that data.
My question is: When dealing with just two strains, is it really necessary to use a calculated diversity index, or will proportions do just fine?
The benefit of using proportions is that it's a more accessible metric - not requiring any (albeit fairly basic) knowledge of diversity indices and how they alter the data.
Having calculated Shannon, Simpson, and proportions, and run all three through my models, it makes no difference which I use - the data are quite emphatic. My slightly educated instinct is, in this case, to use the most simple metric, but I'm looking for some opinions on the case.

Extended upon the suggested statistic
The proportion $p$ is definitely not a good measure of diversity. A proportion of 0 or 1 both indicates no species diversity as only one species exist. If one species, never reach a frequency of 0.5 in your data it might be reasonable though. Otherwise, something like $p(1-p)$ could be a statistic of interest.
If you're willing to use $2p(1-p)$ (instead of the above $p(1-p)$) as index of diversity, then you could make the point that it can be easily extended to $S$ species with $1-\sum_{s=1}^S p_s^2$, where $p_s$ is the frequency of the species $s$ by analogy to the genetic diversity within populations (see Nei 1973).
Note that these statistic will be sensitive to the sample size. For example, if you sampled only one individual, then this individual can only belong to one species and your measure of diversity can only be zero. You might want to compute an unbiased estimator for this statistic.
Your goal is to reduce the reader's cognitive load
Your goal is to use a statistic that will communicate easily. If your readers are going to be very much used to Simpson's or Shannon's indices, then even a mathematically simpler index might end up leading to an extra cognitive load onto the reader.
IMO, it will be hard to give a more definite answer without knowing 1) who are going to be your readers (which journal are you aiming to publish in) and 2) what are the exact data manipulation and interpretation you are aiming to do based on your results. For example, if it makes the comparisons among graphs easier by using a simpler statistic over a more complicated once, then choosing the simpler statistic is a good idea.
Good statistical analysis
In any case, it is essential that you to try out (and you did) different measures of species diversity and make sure that your conclusion is robust to these different measures and explain in your methods that the chosen statistic won't matter. That will make your point and your choice of statistic much stronger.


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Do ovaries produce estrogen before menarche?
It is traditionally taught that estrogen is produced by the granulosa cells of the follicle. But before menarche, where does the estrogen come from? Is it from the thin layer of granulosa cells lining the primordial follicles?
The adrenal zona reticularis produces androgens physiologically. Are they converted to estrogen? If yes, by whom? If not by the ovary, would the levels of estrogens be same in prepubertal boys and girls?
More importantly, are there estrogens in a girl before menarche? If yes wouldn't they cause endometrial changes?

It would be better to break this into two individual questions.

@Polisetty one possibility-pre pubertal FSH release follows a circadian rhythm and this concentration is so little that only very sensitive methods could detect this rhythm...as menarche approaches the frequency and amount of FSH release increases & hence also oestrogen...so endometrial changes would not be possible before menarche.


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Is it possible to Interpret Nerve Signals As to Where They Are Going In The Human Body And What Their Task Is?
I have recently watched some anime, (yes, anime, probably a huge cause to lots of questions asked on the internet), and it got me thinking. We can intercept nerve signals throughout the body, but could we interpret their task, as to whether they are meant to contract or relax a muscle, and their destination, as to which muscle they are meant to travel a signal to.
Extra Inspiration:
I have seen an article by Chris Brooker about the theory of intercepting optical nerves to benefit augmented reality, so it got me thinking, what if we could intercept all nerves in one go, the brain, but I realised, that's a stupid idea, they travel to the brain all over, so the next best location was the Central Nervous System (The Spine).
On top of Anime super inspiration, and some articles which helped further my theory, I thought more and more about how nerves travel around the body as impulses, so I theorised maybe they use different currents or charges to travel to different parts of a body, which brings me to my conclusion, is there anyone who would be willing to carry this experiment out? And then give me the results? If this is true we may be able to make a huge breakthrough in the virtual department, even if incorrect it can still be a starting stone for a new hypothesis.
However this entirely bases on the idea that all nerves start from one point on the cns, however the start to this would be to gain a test subject and patch a circuit into a nerve. on the circuit would be an ammeter and a voltmeter, and then have the subject move the muscles connected to the nerve.
The second step would be to find a lone point in the cns where all nerves touch or cross paths to identify the Sweet Spot (( ͡° ͜ʖ ͡°) I named it myself) and differentiate different nerves for different purposes.
Keep in mind this would be no small discovery, this would help engineer a better future in the virtual department, however this is only a small part to this, imagine being able to truly see or hear without the help of heavy machinery, or be able to walk with actual legs again, or be able to play catch with family again as this would engineer the greatest part to prosthetic engineering where we could actually move lots of different gears as if we contracted or relaxed a muscle.
If my hypothesis is completely off as my science is incorrect than please let me know. I currently do not have the facilities to go further into this as I am still in High School ((̿▀̿ ̿Ĺ̯̿̿▀̿ ̿)̄), and am busy with studies, but I hope I am correct and thus would have contributed to science which can help thousands of people everyday.
Please contribute to this topic even if it is criticising it.
Thanks,
IbnJalal

you've done a lot of thinking about that, and the wording is informal, talking about animes, high school. you should prepare yourself to know that this is a relatively formal science forum, where people prize concision and prior research for the wording of questions. sounds like, once you have armed yourself with lots of knowledge you will be contributing to science of many people.

I agree with previous comment from com.prehensible but I would like to change the emphasis ever so slightly.
Its great that you 1. get inspired by experiences you find in the world 2. you think about them and 3. you reach out to other people to check if your ideas are correct. This is basically how any scientific project starts.
I don't think that an informal tone is detrimental to serious and precise scientific discussions on any topic, quite the opposite, so I wouldn't worry about talking about animes or high school. Ask away and as you talk more and more with people with the same interests your language will automatically change to reflect more precise and specific objects/subjects.
Nonetheless, and to the point of the previous commenter, I'll try, instead of general statements of form, to point out some specific things you might want to look at in order help you think about your question:

A precise statement of your hypothesis is a must. You almost make a precise hypothesis about different charges and currents. A lot is known in terms of neuronal communication, both at the single cell level as at the group level. I would start from the wiki entry on action potentials it might help you understand exactly how neurons "talk" to each other. Also it might be useful to have a more specific insight on how these cells are physically organised. Again the wiki on the CNS is a good place to start.
You should have a specific idea of a particular experiment that would allow to you to test your hypothesis. Thinking about the experiment will require you to know what is possible and what is not. Usually animes, movies, and books are quite a bit more advanced in terms of what is nowadays possible, hence the word "fiction" in science fiction. Thinking of an experiment also allows you to operationalise your hypothesis, which is science speak for deciding exactly what you will measure and how. This will tell you if you can answer your question as you stated it and is super important to plan an experiment.

If you have these 2 things i.e., a good idea and a doable experiment that would answer your question the hard part is done!
Well... then you will probably need time and money, but that is a different problem altogether...
Answering your question though, yes, it is possible to interpret nerve signals, both in terms of their targets or downstream areas, as in terms of information content they might relay in order to accomplish a particular task. There is a whole field of Neuroscience that studies neural coding and its trying to solve how neurons transmit messages to each other or how they can encode information in general. However looking at the signals by themselves is usually not enough and people are very careful about the particular behavior that is going on while these signals are being recorded, basically it turns out that one needs context to properly interpret the messages that are intercepted.
Good luck :)


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Is it possible to be allergic to the yolk of an egg but not the egg white?
At lunch one day, my friend had a hard boiled Easter egg. When he pealed it he squeezed the yolk, or yellow part, of the egg out. I asked him what on earth he was doing and he said, "I'm allergic to the yellow part of the egg not the white." I was very confused by this, he also sad he was allergic to tomatoes but could still eat pizza with sauce on it, apples but only the skins, and some other strange things. I didn't think this was possible at all. Can anyone explain this and tell me if it's even possible to be allergic to one part of an egg and not the other, or is it all in his head. If this is possible, is there an actual name for this condition?

It's plausible, on first thought, if the yolk contains different antigens than the white or the antigen in tomatoes is heat labile.

This isn't really a biology point but I've known a few people who use "allergic" as a shorthand for any similar condition (e.g. lactose intolerance) so your friend may not necessarily have an allergy (in the sense of an antibody mediated reaction)

The protein composition of the egg white and egg yolk differ appreciably. Hence, it is plausible for one to countenance symptoms of indigestion when consuming the egg yolk as opposed to the albumen, egg whites. It is important to stress that your friend may only an indigestion towards egg yolks as opposed to an immune response to an antigen.
If we consider the protein family, the egg yolk comprises a family of phosvitins, a group of highly phosphorylated proteins capable of mustering iron and calcium metal cations - serving a role in embryo development.
These are primarily absent from the albumen which comprises (with an unexpected name!) a highest percentage of suspended ovalbumin, ovotransferrin and ovomucoid. As demonstrated by the American College of Allergy, Asthma & Immunology, it is feasible to suffer an intolerance towards the egg yolk and yet suffer no gastro-enteric indigestion to the egg whites.
More information regarding the American College is available from: https://acaai.org/allergies/types/food-allergies/types-food-allergy/egg-allergy
Your friend evidently does not suffer a severe anaphylactic shock after consumption of the egg yolks otherwise he/she may be adverse to both the egg whites and egg yolk. In conclusion, it is possible that he/she may simply have a mild intolerance towards certain proteins in the egg yolks.


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Why is it that guttation is most commonly observed in the morning?
Knowing that guttation occurs through a plant's hydathodes due to root pressure forcing liquid water out of the leaves, I am curious as to why so many small drops of water are observable on plants in the morning. Could this potentially have to do with the moisture in the air at night vs day? Since humidity tends to increase at night?
Thanks in advance!

Perhaps you are thinking of the atmospheric phenomenon called dew, which is not caused by plants, or limited to them: https://en.wikipedia.org/wiki/Dew

I don't think so, these are two different phenomena as guttation is water coming out of the plant while dew is condensation of air on the plant! But perhaps their cause is related.

I understand the difference.  What I'm saying is that dew is a far more likely explanation for those small drops of water you observe, especially if they are on things other than plants.

You should add an image if you're trying to convince us that you're talking about guttation vs just dew formation.

I am asking due to a specific question brought up in a lecture, where the professor gave us a prompt of "why is guttation observed most commonly in the morning?". Here is a picture of the slide as well as the portion of my textbook discussing this phenomenon, I am confident I am speaking of guttation. https://imgur.com/a/Pdk7g

@jamesqf I know it's just anecdotal evidence, but I have a Monstera deliciosa in my room and I see it guttate way more in the morning, sometimes by night, never by day. In this case, it just cannot be dew.

Guttation is commonly seen at night and early morning. Plants release excess of water via the guttation. During day time as the transpiration rate increases, excess of water is released via transpiration and hence guttation decreases. Also due to high temperature these small droplets are quickly evaporated during day time.

A stable mass of air holds, more or less, a fixed amount of water vapor. As the air is cooled it reaches the point where water will begin to condense (form a cloud) - this is the dew point. If this amount of moisture is fixed, the relative humidity (rH) decreases with increasing temperature, meaning the air could hold more water vapor if there were a source for additional water vapor - like from a plant leaf, say.
The relative humidity is generally maximum at night (just before the dawn, to borrow a phrase). Hence little if any moisture evaporates from the leaf.
Plant roots actively load mineral salts into their cells which creates an osmotic potential that draws in water. This can create a 'root pressure' that forces water out vein ends on the edges of a leaf. During day time, the relative humidity is generally low and any water presented as guttation evaporates before it is easily noticeable. At night and early morning, the relative humidity tends to be close to the dew point, so the guttation doesn't readily evaporate.
There is a bit more to this in terms of movement of water thru the xylem  and how this reduces the 'root pressure' seen at the leaf edges when the stomata are open. Stomata tend to be closed at night (when it is dark), so there is very little or no transpiration occuring at night (independent of rH) - hence root pressure is 'fully' expressed at the leaf margins --> guttation possible.

The stomata are mostly closed at night and early morning. Early morning rising temperatures cause efflux of H2O from the hydathodes while stomata are still closed, and by the time the stomata are opened, the efflux switches to the shorter route through the stomata.

Hello! I fear that your answer isn't really different from the Jim Young one, and, as such, it may attract downvotes. If you like it (as it seems) go upvote it :) and elaborate on something that has not already covered by existing answers (for instance none of the answers provide references).


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What species is this blue and white bird?
I want to know what kind of species this bird is

Please add your location, where you got the birds, and an approximate size of the birds. A better photo would also be helpful

The bird in the photo appears to be a white faced "variety" of Lovebird - Genus Agapornis - mainly identified by beak and nares not being visible (cere skin and nostrils not visible). The exact species is uncertain due to ease of hybridization between species and the availability of many color varieties.  The links below may be of further help.
https://en.wikipedia.org/wiki/Lovebird#Species
https://www.agapornidenclub.be/eng/?page_id=2


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What is the meaning of "leukemic cell recovery" in an abstract?
An article abstract:

Significant predictors of treatment outcome are poorly defined for patients with T-lineage acute lymphoblastic leukemia (T-ALL). A high WBC at diagnosis, which has traditionally been a predictor of poor response in T-ALL, has considerably weakened prognostic significance in the face of modern, more intensive chemotherapy. To test the hypothesis that bone marrow stroma-supported leukemic cell recovery might identify children at high risk for relapse, we measured the ex vivo recovery of T-ALL lymphoblasts from 29 newly diagnosed patients using a stromal cell co-culture assay. In all cases the T-ALL lymphoblasts showed an increase in recovery of T-ALL cells (RTC), ranging from 4 to 343%, in comparison to samples maintained without stroma. Since we were blinded to patient outcome in this case-control study, we then correlated patient outcome with RTC. The RTC for 18 patients in complete continuous remission (CCR) for greater than 4 years was stochastically larger than for the 11 patients who eventually relapsed (P = 0.011, by the two-sided Wilcoxon test). Furthermore, 100% of patients with an RTC of more than 26% had a CCR greater than 4 years while 78% of the patients with an RTC of less than 25% relapsed within 4 years. This is the first report to show that higher lymphoblast recovery may predict a more favorable outcome for children with T-ALL. A prospective study is needed to test whether stroma-supported leukemic cell recovery might serve as a basis for assigning risk-adjusted therapy.

What is the meaning of recovery here? It puzzles me as a non-native speaker of English. Do the authors simply mean "the number of cells that survive"? Or is there some "recovery process" - if yes, what is the nature of this process?
P.S. The question arose from a question asked by a fellow translator. She translates a text in which T cells transduced with gene for a receptor against leukemic cells are co-cultured with such cells, after which

"T cells transduced with the receptor markedly reduced leukemic cell recovery".

The translator has trouble understanding how to put it in Russian, because translating "recovery" verbatim would imply some process in which a cell recovers, say, from injury.
Is "recovery" just "the percentage of cells that survived, relative to the overall number of cells"?

I don't think this is a great place to ask, unless a bona fide hematologist answers, and who can assure that? The term is confusing. In your place, I would check with a hematologist. It's not a common term.

TL;DR: Yes, it's just percentage of cells that survived. With the caveat that the assay doesn't give information on how much the number of cells is influenced by survival, dying, or growth rate.
"Recovery" in this context means "cells found after X amount of culture time". Generally speaking, recovery often refers to putting something in a program/dish/liquid/organism and seeing how much is still left after some processing/treatment/culture. For example, if I give a 1-year-old child 10 porcellain plates to play with, I might be interested in what percentage I can recover after 2h of play time. Of course in the context of cell culture, that percentage can be above 100% if the cells multiplied in the meantime.
As the methods of the article describe, the culture assay consists of first growing a single layer of stromal cells (HS-5 cells) on a culture plate for 24h. These cells provide support for the actual cells of interest. The researchers then spread 5.0 × 105 viable T-ALL lymphoblasts isolated from a patient sample on the stromal cell layer. They do this twice* for each sample, in one case collecting the cells after 1h (which isn't usually enough time for human cells to do anything), in the other case collecting them after 72h of culture (which is enough for healthy cells to grow substantially). Then they use flow cytometry to quantify how many T-ALL cells are now in the culture after that time has elapsed.
This helpful graphic is from the paper. The word "cells" in the formula refers to T-ALL cells.

The percentage of recovered T-ALL cells (RTC) was calculated by:

Essentially, what the authors here studied is whether the likelihood of a T-ALL patient to relapse might be related to the ability of their cancerous cells to survive or grow in a culture dish coated with stromal cells.
The quote from your colleague would mean that the T cells were surviving/growing less or dying more if they were transduced with the receptor.
*rather, four times. Twice for 1h and twice for 72h collection. At least this is what "in duplicate" implies.

Why do the authors use ex vivo instead of in vitro for their culture? I found the term ambiguous, and only used 13 times (can't remember exactly) on Googling with Scholar. But nice answer.

In my understanding, ex vivo is a subclass of in vitro, although it's not something I would associate with primary culture of lymphoblasts...

Thanks. My understanding of ex vivo is, say, bone marrow. But if it's cultured, it's not ex vivo (it's been grown.) Anyway, I didn't have full access, but thought the paper was not without ambiguities. Again, thanks. (btw, the term I found ambiguous was leukemic cell recovery). For a cancer so well studied, to find it so few times was interesting.


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What is C-terminal tryptic peptide?
A biologist wrote to me:
... C- or N-terminus,... For example, a C-terminal tryptic peptide like AGWRGSDSHSR, would be...
I don't have any idea what that is. When I google the term ("C-terminal tryptic peptide"), nothing obvious came up. What's that? Why AGWEGSDSHSR is a "C-terminal tryptic peptide"?

Did a biologist really write this to you? Seems strange as it's clearly not your field. But really how do you expect a decent answer unless you give us the full text and context of what appears to me as a quite bizarre communication.

Its quite simple if you look at the basics! Lets have a look at the sequence you give:

AGWRGSDSHSR

Write that in 3-letter terms1:

Ala-Gly-Trp-Arg-Gly-Ser-Asp-Ser-His-Ser-Arg

Pay attention to the C-terminus. The last amino acid residue in the sequence is Arginine. Now, its well established that Trypsin cleaves a polypeptide after (i.e. towards the C-terminal side of) Lysine and Arginine2.
Thus, C-terminal tryptic peptide is the peptide that remains after a polypeptide has been treated with Trypsin.

Its just about getting the clues @smallchess

Ah, so it refers to where the peptide was cleaved, not where the peptide was located on the original protein. Unintuitive for me :)

@armatus haha I've been working on peptide sequencing for a while now, so I got the point there ;)

Why the downvote? I get that the question is pretty naive, but is there something wrong in the answer?

Trypsin does not cleave at the "carboxy-terminus" of any amino acid, as that term is used to designate one end of a protein (that with a free alpha-COOH). I also do not believe "C-terminal lysis by trypsin" means anything, or if it did it would mean the removal of the C-terminal amino acid, which is here not the case. Your answer does not represent usage and is clearly wrong.

@david I agree with you in that I should have framed my sentences more carefully since there are terms which represent something but are used to mean something else. I've edited my answer. Does it make sense to you now?

@xusr yup I get what you mean, so I edited the answer a bit to make it clearer :)

Downvotes are free that is why instead of giving input to improve the answer people go around anon downvoting.

@ronisaiba TBH I quite agree with you. Most of the time David has something to say about my answer, I see him talking like "here's a -1 and a comment for you". AFAIK what SE encourages is "all right you touch the correct point, lemme just edit these finer details to make it more presentable". Downvotes on answers do give -1 to downvoter though :/

Unless your corespondent is off their rocker (or I am), this is rather unambiguously referring to the peptide released from the C-terminal end of a polypeptide by tryptic digestion.
This means that the final arginine in your sequence would have been the C-terminus of the original polypeptide, not the trypsin cleavage site. It also means that your sequence was preceded by R or K.

Quite, which is why it looks like some sort of homework question, with the R in the sequence as red herring.


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Calculate growth rate of a population by Leslie matrix
We can calculate growth rate of a population by calculate the dominant eigen value of a Leslie matrix. What does this growth rate mean? I think that the growth rate N(t+1)/N(t) is depend on the age structure of N(t)? If the growth rate of a population is less than 1, will the population go extinct?


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Is it Bufo bufo?
I find a couple of frogs. It was cca. 4inches long and 2inches wide. Photo was taken in Prague, Czech republic, middle Europe.. Same zoomed.

Just want to be sure, guys.

I suggest this is definatly a toad. Thank you guys anyway.

Yes, this is almost certainly Bufo bufo.
It has the stocky figure and the warty skin, ruling out the true frogs.
It lacks the stripes of B. calamita or Pelobatus fuscus.
It is brown without the green colors of Alytes obstetricans.
A red yellow or red belly is not visible at the photos, but I assume you would have noticed it if it was present (ruling out Bombina sp.).
See here for some pictures of European toads (not complete and in Dutch, but pictures and latin names are clear.
Finally: a city like Prague lacks specific habitats of the more rare species.  Common toad is the most likely to be found there.


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Are there any known rules that neurons always follow while transmitting/receiving signals?
I'm new to neurobiology so I don't know much about it. However, I have worked on artificial neural networks. Man-made AI networks all follow a handful of simple rules.
I was wondering if biological neurons also have a set of predictable rules?
E.g
What does a neuron do if it does not get stimulated/receives no signal for a long time. Will it die ... or try to find new connections that might send signals?
What does a neuron do if it is over-stimulated?
What does a neuron do if it receives a signal -> does it broadcast it to all of its connections, or only 1. Does it have a preferred output path for any incoming signals.
Can a neuron send out a new signal without having received a signal from anywhere else.
How does a neuron know if it has done his job "well". How does it get positive feedback.

Short Answer:
"Always" is always a dangerous term in biology.

Longer Answer:

What does a neuron do if it does not get stimulated/receives no signal for a long time. Will it die ... or try to find new connections that might send signals?

What neurons do when they aren't stimulated depends on the neuron and phase of development. Typically, thresholds for spiking will decrease, but it's also normal for cells to atrophy and die: neuronal death is a critical part of development, and loss of synaptic connections and some neurons is the most obvious feature of human brain development during adolescence, rather than birthing new neurons or growing new synapses.

What does a neuron do if it is over-stimulated?

Overstimulated neurons may die, they may also reduce the efficacy of their inputs either by increasing their thresholds or reducing synaptic weights by removing postsynaptic receptors. Calcium is an important mediator of these signals - you could read about its role in long term depression for example (this has nothing to do with 'depression' in mental health, just reduction in synaptic weight). There are also short-term effects that limit overstimulation of particular pathways, with many acts on the pre-synaptic rather than post-synaptic cell. Neurotransmitter is held in vesicles, and after release, there are fewer vesicles available for the next release event. Presynaptic terminals also often have autoreceptors that cause negative feedback and limit subsequent transmission.

What does a neuron do if it receives a signal -> does it broadcast it to all of its connections, or only 1

Of all your questions, "does it broadcast it to all of its connections" has the simplest answer: biological neurons almost always broadcast to all of its forward connections in response to any sufficient input (just like most artificial neural networks). However, the release probability at any one synapse is typically <1. Therefore, a given cell can make much higher-fidelity (and also higher-amplitude) connections with another cell by the number of contacts. If a typical cortical neuron makes only one synaptic contact with another cell, there will be a high rate of failures of transmission between the two cells. It's common for stronger connections to involve up to hundreds of individual contacts, just between two cells.

Can a neuron send out a new signal without having received a signal from anywhere else

Some neurons are spontaneously active. There are various types, but the most familiar are the ones thought of as intrinsically oscillating. An example are the sinoatrial node cells of the heart (although these are not really neurons, they act a lot like neurons; there are similar cells that are neurons that control respiration). There are also some CNS cells.

How does a neuron know if it has done his job "well". How does it get positive feedback.

This question is the most complex of all the questions you asked, entire textbooks and journals are needed to answer it, and it isn't at all possible to answer here. I'll just say that many of the learning rules used in artificial networks are not biologically plausible, they are simply computationally efficient. Biological neural networks use a lot more recurrent activity than artificial ones do, and a lot of the feedback like this occurs within that recurrent network. Biological networks are also built to do a variety of computations, and learning rules that apply in one may not apply in another. For example, pattern separation versus pattern completion require completely different learning rules.
However, the very general principle of updating synaptic weights in response to errors or outcomes does hold between artificial and biological networks.


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How big is a baby's stomach?
There is a lot of contradictory information on baby feeding volumes on the internet. A common claim is that a baby's stomach is the size of a hazelnut or small marble, with a volume of 5-7 ml. But this seems confusing on two counts -

Breast milk contains approximately 0.7 cal per ml, so feeding 6 ml eight times per day would only provide the baby with 33 calories, which doesn't seem enough.
A typical marble is 1/2 inch (1.25 cm) in diameter, which means it has a volume of about 1 ml, not 5-7 ml as claimed.

Are there any authoritative sources on the size of a baby's stomach?

I am voting to have this migrated to biology.se

At 1 month it's 80-150 mL. https://www.lllc.ca/thursday-tip-newborns-have-small-stomachs

That site does not look particularly authoritative...

@Chris Very happy to have this migrated to biology.se if that's the most appropriate place for it

I am migrating this, they may ask for specifics on age of child. I also removed the "how much can they eat", as that is highly variable by bebby.

The first 30 days involve rapid growth, but generally, fall within a standard proximal range of 5 - 7mL on day one. By day 3 the stomach has expanded vastly to nearly 23 - 27 mL. From this point on, growth and size to age ratio will vary a bit.
https://themomivist.com/2016/10/10/the-newborn-stomach-size-myth-it-is-not-5-7ml/
Here's a link to an article that has some efficacy. Many hospitals and physicians use different techniques and believe differently on this particular subject. Considering the laws surrounding experimentation on fetus and children, the "Size" of the stomach debate only has efficacy if we were able to case study THOUSANDS of infant stomachs which isn't likely to happen anytime soon. I hope the link helps and maybe points you in the right direction. There really is no 100% correct way to answer this as the studies surrounding it just don't have any weight to them.

Infant stomach capacity:

At birth: 5-35 mL
1 week - 1 month: 60-120 mL
6-12 months: 210-240 mL

Sources:

http://alabamapublichealth.gov/Staging/test/perinatal/assets/StomachCapacity.pdf
https://www.ncbi.nlm.nih.gov/pubmed/23662739
http://www.dhss.delaware.gov/dph/chs/files/neurobehavioralapproach.pdf

Remember that the human uterus is about the size of a fist.  That doesn't mean it can't be stretched.  Plenty of babies are perfectly capable of eating and holding down an oz of formula shortly after birth.
This overview of the research says between 10 mL and 30 mL
http://www.infantmentalhealth.co.za/files/Bergman_2013_stomach_capacity_feed_interval.pdf


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Will the N- or the C- terminal soluble domain be on the extracellular side?
Here is a homework question

A single-pass transmembrane protein is destined to be transported to the plasma membrane. In the wild-type protein, a lysine flanks the transmembrane domain on the N- terminal side, and a glutamic acid flanks on the C-terminal side. Both the N- & C-terminal soluble domains carry sequences that can by glycosylated by oligosaccharyltransferase.
After the protein is transported to the plasma membrane, will the N- or the C- terminal soluble domain be on the extracellular side?

My answer is

N-terminal with lysine will be towards the extracellular side and C-terminal will be towards the cytoplasm.

Does this seem right to you?

I made a major edit to your post. Please roll back if you don't like the edit. If you agree with the edit, take advantage of it to learn how to ask a good question on Biology.SE (explicit title, highlight the quotation, clearly specify your question, etc...). You should try to add why you think your answer is right.

Hints: 1. Consider the structures of lysine and glutamate. What's the main difference between the two amino acids? 2. What are the rules governing how proteins are trafficked to the cell membrane? When a protein is synthesized, where is it processed and what does this involve?

Well I know that lysine has a overall positive charge and glutamate has an overal negative charge. So just considering there charge, does the more positive one (lysine) on one side of the transmembrane protein face the extracellylar space?

At the moment this is at risk of closure - I think it can stay open, but only if you add an explanation of why you think that is the answer...

Luminal/cytoplasmic orientation of single-pass transmembrane proteins is mostly dictated by positively charged residues residing on the cytoplasmic side (positive-inside rule) and negatively charged residues being suppressed on the cytoplasmic side/preferred on the luminal side (negative inside depletion/outside enrichment rule).
Since your molecule has a positively charged Lys residue on its N-terminus and a negative negatively charged Glu residue on its C-terminal side your protein would most likely acquire a type II integral membrane protein topology, i.e. the C-terminal part would be directed towards the extracellular space while the N-terminal part is in the cytosol.
Further references can be found here:
Baker JA et al., Charged residues next to transmembrane regions revisited: “Positive-inside rule” is complemented by the “negative inside depletion/outside enrichment rule” BMC Biol. 2017 pubmed
Ott CM and Lingappa VR, Integral membrane protein biosynthesis: why topology is hard to predict. J. Cell. Sci. 2002 pubmed

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!


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Ratio boys:girls born - how to explain?
My son studies genetics at school right now and they have been covering gender. It's well known that slightly more boys are born than girls. However, originally there's an equal number of sperm cells with X and Y chromosomes. From what I've read it sounds that fertilization is affected by different factors but it seems that on average it's about equally likely? At school, they told them that more fertilized female "embryos" die than male?? Could it be true? Question: Do you know how it happens that there is an equal number of X, Y-carrying sperm cells, but more boys are born?

This page has quite a nice overview of the topic: https://en.wikipedia.org/wiki/Human_sex_ratio#Factors_affecting_sex_ratio_in_humans but as far as I know, it's not well understood.

The hypothesis that male embryos are more viable seems reasonable, but I've not seen any data to back that up. Also, it's purely speculative but you could imagine how particular proteins expressed with X or Y chromosomes could change how an embryo develops, which in turn could change how viable the embryo is.

The Y chromosome is smaller than the X. So sperm carrying the Y chromosome are very slightly lighter, and faster. I'm not an expert on this, but I wonder if it might be a possible reason.

@Jam That link says that sex ratio decreases as the father gets older. Maybe older men have a higher proportion of defective Y chromosomes? That could cause a greater number of male embryos to fail and bring the male to female ratio down.

This post seems to adress the question https://biology.stackexchange.com/questions/27582/why-do-we-have-more-male-infants-born?rq=1


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What is the death mechanism of an electrocuted Mosquito?
While using the Electric bat, does the mosquito get killed by primary electrocution, or it secondarily by burning?


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Do sea sponge cells transfer nutrients to each other?
Does a sea sponge cell transfer nutrients or energy to their neighboring cells or is their only symbiotic relationship that they are connected to each other forming a structure?
The sea sponges that I'm talking about are the ones that can be broken apart and naturally reassemble themselves.
YouTube of the sea sponge I'm talking about.

yes choanocytes handle the bulk of sponges digestion and transfer nutrients to other cells. in some species Amebocytes also perform a similar function.


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determining horizontal gene transfer between two genomes?
I want to determine if there is horizontal gene transfer between two genomes, in particular I was to use the parametric methods described in wikipedia since I would most likely struggle to understand the phylogenetic methods fully.
The two genomes in mind would be Lactococcus lactis and  Lactobacillus helveticus since they are used in the process of cheese making and therefore would be in close enough proximity/environment to argue for tentative events of HGT. (Correct me if I am way off base here in my line of thought...)
Could I just access representative genomes for each from NCBI and calculate/determine the various genomic signatures that are indicative of HGT via the previously mentioned parametric methods(Nucleotide composition, oligonucleotide spectrum, structural features, etc...)?
Or would the genomes need to be rendered and sequenced from a confirmed source where they are both located/habituated to properly argue for HGT?(In which case I believe NCBI does not have this data readily available?)

Since the parametric model is applied to only a single genome to see if there is evidence of recent HGT via a change in the average content in coding regions, it will not tell you from where the HGT came from, just that a HGT likely occurred in an area of the genome. Since you are trying to specifically see if there was a HGT between L. lactis and L. helveticus you would have to run a parametric analysis on both, find a HGT candidate on one of the genomes and then find that sequence as a non-HGT candidate on the other genome and via BLAST.
These papers give a good argument to why to use genome signatures instead of GC content as a parametric method of detecting HGT.
Review from where most of the Wiki figures came from
Genome signature paper
Newer Genome signature paper


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What is the difference between alarmones and riboswitches
An Alarmone is an intracellular signal molecule that is produced due to harsh environmental factors. They regulate the gene expression at transcription level. A riboswitch is a regulatory segment of a messenger RNA molecule that binds a small molecule, resulting in a change in production of the proteins encoded by the mRNA, it works as a way to sense eviromental changes.
I've been reading some papers ("ZTP 5-Amino 4-lmidazole Carboxamide Riboside
S-Triphosphate): A Proposed Alarmone for 1O-Formyl-Tetrahydrofolate  Deficiency" , Bochner 1982; "An Ancient Riboswitch Class in Bacteria Regulates Purine Biosynthesis and One-Carbon Metabolism" Kim 2015) which study how ZTP can bring changes upon 10f-THF deficiency. Bochner (1982) through several experiments proposes ZTP as an alarmone for 10f-THF; some assumptions of Bochner might not have been entirely correct and a later paper fails to replicate some experiments. Later Kim (2015) propose ZTP as a riboswitch.
I'm not fully aware of the differences between the concept of "alarmone" and "riboswitch". Seems to me that both Bochner and Kim propose virtually the same thesis.

I don't really consider myself qualified to answer, but sounds to me like alarmone is a functional category whereas riboswitch is a structural category. Thus, they're not mutually exclusive - a riboswitch can act as an alarmone but not all riboswitches do, and vice versa an alarmone might be a riboswitch but not all alarmones are. At least that's my impression.

Your first paragraph answers it!

First time I actually hear the word alarmone so bear with me okay?
"An Alarmone is an intracellular signal molecule that is produced due to harsh environmental factors. They regulate the gene expression at transcription level" <- this probably refers to activating/inhibiting transcription factors and stuff like that. Looking at bit further into the wikipedia article from whence you copied the description, we see that ppGpp is considered an alarmone.
According to the wikipedia article on ppGpp (https://en.wikipedia.org/wiki/Guanosine_pentaphosphate) we see e.g. this line "When (p)ppGpp associates with the promoter it affects the RNA polymerase enzyme's ability to bind and initiate transcription", so this alarmone can act by inhibiting RNA polymerase's ability to bind to the promoter.
A riboswitch on the other hand is a structural element INSIDE an RNA molecule that causes a conformational change upon binding a ligand. This conformational change then has an effect on transcription or translation etc. Thus, an alarmone could probably bind to a riboswitch to exert its effect, but a riboswitch is a quite specific thing.
You can read about some of the mechanisms in the wikipedia article https://en.wikipedia.org/wiki/Riboswitch
So basically, think of alarmones as signalling molecules and riboswitches as structural elements in transcripts that regulate gene expression upon ligand binding.


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How does the human body power itself?
This query can be divided into sub-queries:

What form/s of energy does the human body "run" on?
Why/for what are these particular forms of energy required?
From what can these types of energy be derived?
How efficiently (less waste) does the body use energy?

Looking for a simple, effective answer with little to no jargon (distinction between pertinent use of terminology and showboating).

This question is very broad, and you can easily google part of it and show your research. If you narrow this down and add your research, I'd be happy to withdraw my close vote  and my downvote, and even to answer it.

If you had read the info about this site you would have seen that is for students of biology. Biology is a specialised subject with its own language. This is not jargon but a vocabulary to describe specific entities and concepts not encountered by the layman. To suggest its use is "showboating" is insulting to members of this list. If you have such a detailed list of informational requirements you need to learn some metabolism from a standard text, or find a website that provides a naive account of such processes, replete with half truths and false analogies.

The question is broad and can hardly be fully answered in a single post. I will be very brief hoping it will help you and push you to seek for more knowledge.
Humans, like all other animals (or almost all) are chemo-organotroph. This mean we get our energy from the food we eat and we release this energy through oxydation. It is therefore chemical energy that we're using. We are then storing this energy into another chemical called ATP. Note that not only humans use ATP but any living thing on earth uses ATP (or GTP I think). ATP is then used (ATP loses one phosphate group and becomes ADP) to perform specific action (such as the use of a trans-membrane pump or the contraction of a muscle fiber).
You should have a look at wikipedia > Primary nutritional groups as well as  wikipedia > chemotrophs and eventually this post.
For more information, please consider having a look at wikipedia and if you can't find feel free to ask your question in a new post. Always attempt to narrow your post down to a single, clearly defined question.


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Do chromosomes change with time?
An offspring is 23 chromosomes of mother and 23 of father, if one of the mate learns say music after the birth of their first child— will their second offspring have better music skills than former? about my knowledge of biology, so far I read about DNA, Genome, chromosomes and genetic engineering, I am an engineer by profession.

You might want to read about epigenetics

@Remi.b — But the Wikipedia article you cite is a mish-mash of misleading nonsense.

Short Answer: Probably, at least a little, much research still needs to be done.  For a great paper on this see here.
Your question can be answered in two parts:

Can Epigenetics be inherited - The answer to the simple question in your title, do chromosomes change with time, is yes.  There are copying errors, and carcinogenic mutations that can permanently change cells' genomes.  Less permanent is epigenetics, which are temporary chemical modifications to the DNA which changes how it is expressed. The epigenetics of the cell may change for various reasons from the cell undergoing mitosis to a wildly changing diet.  However, when sperm and egg cells are formed these epigentic modifications are typically wiped from the genome in order to remove any possible damaging marks.  However, there is a growing body of literature which states that some marks escape the purge and change the characteristics of the progeny.  Studies include scare-treating mice, 1836 famine, fatty rats, human psychological changes.  While the exact genes causing the change is unknown, there is clearly a strong correlation
Can Music Skill be Captured in Epigenetics - Music skill is to difficult to measure biologically, but likely has some links in speech skills, which would be captured in the brain, and muscle skills.  While there is some evidence for there being an muscle epi-memory, brain epigenetic inheritance is more tenuous (although see this exciting paper on RNA causing memory changes through epigenetics).  I would say the general scientific consensus is that there is some relation between epigentics, and memory, and music skill - there is a great deal of work still to be done.

Until recently, the answer to your question would have been a definitive "no", because is smacks of the rejected Larmarckian ideas of the inheritance of acquired characteristics. And the example you provided, about musical skills, that would be "no" as well from a genetic perspective, although the hearing of music around the house may have cultural impacts on the second child. However the new field of epigenetics has revealed that DNA methylation, over the course of ones life can influence offspring of future generations. There was a community in Sweden that took very detailed health records over generations. The effects of a famine in 1836 showed up in the grandchildren of the survivors. It is further explained here: https://io9.gizmodo.com/how-an-1836-famine-altered-the-genes-of-children-born-d-1200001177

Still smacks of Lamarckism, and there is absolutely no evidence or intellectual framework for acquired music skills being associated with methylation of genes, this changing the musicality of an individual, or being responsible for musicality in offspring.

No, it was a good question. The Swedish study was rejected for years, with the simply statement that what had been observed could not be. The question was not about music, but about change in inheritance over time. Music was just an example.

The question has obviously been asked by an outsider. I think a good answer should start with an introduction to epigenetics.

Can you provide an instance of a mammalian gene that:
(a)  is normally unmethylated at some site but has been shown to be demonstrate changed expression following methylation at this site (even just turned off or on),
and
(b) this specific methylation has been demonstrated to be induced by some environmental stimulus,
and
(c) methylation at this site following the said stimulas has been shown to be passed on to the offspring,
and
(d) the offspring have been shown to exhibit the changed gene expression resulting from the methylation?


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Why are there so many species of large predator on the African savanna?
On the tropical grasslands of Africa, there are loads of large carnivores. Lions, cheetahs, leopards, hyenas and wild dogs are all found, sometimes, in the same place. I was wondering, why is it that there are so many species of large predator in the same place? Wouldn't competition drive all but one species to extinction?
Obviously, this means that each of the predators fills a special niche. So, could anyone tell me what these ecological niches are? What makes the position in the food web of lions, leopards, cheetahs, hyenas and wild dogs different to eachother?

I am not sure but you might overestimate the density of large predators in the African savanna. 1) The savanna covers a very large territory in Africa 2) how many large predators are there? Lion, cheetah, hyena, African wild dog. Looking at a list of apex predators, it does not obviously occur to me that more of them are present in the African savanna than elsewhere.

Note that it is possible that humans have less impacted the African savanna, than say, the European forests, leading to more extinction of apex predators in European forests, than in the African savanna.

@Remi.b Well, there are places, like the Serengeti or Kruger, where you could go on a safari and see all of them, wild, in a day. If they all occupied the same ecological niches, all but one species would die out. So I'm wondering what makes each of their roles unique.

I am playing the devil's advocate but don't get me wrong, I think the question is interesting. You say they all occupied the same ecological niches They are likely not actually. It is not because they live in the same geographical space and all predate that they share the same ecological niche. They might differ because prefer to predate on one or another prey species, or because one target babies, the other adults, because one needs more water than the other, because one needs more shade than the other, etc ...

North American had bear, puma, wolves, coyote, and at one time cheetah and lion, africa does not look all that special.


text:
Correct structure of RNA
Of the 2 figures, which is the correct structure of RNA,
This is the link :  1: https://i.stack.imgur.com/IYgyv.jpg
Sorry, the figure is not to scale.
If there's any problem with the question please inform me.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. It is also bad practice to have figures as part of the question as they are inaccessible to partially sighted people. In addition the figures are incomprehensible and neither represents RNA.

Both figures include A,G,T,C.
Those are abbreviations for the bases adenine, guanine, thymine and cytosine.
RNA does not contain thymine, but its unmethylated form uracil, abbreviated with an U.
Thus, none of the structures represents RNA.

Please do not answer homework questions where the poster has made no attempt to research the question himself.

As Marzipanherz said, RNA does not contain thymine. Furthermore, none of those resemble any kind of RNA structure you usually see, for example two dimensional secondary structures showing watson-crick basepairing such as this example:
http://www.rna-seqblog.com/wp-content/uploads/2014/02/secondary1.jpg
Familiarize yourself with RNA by e.g. reading the wikipedia article or something https://en.wikipedia.org/wiki/RNA
After you've done this, you can e.g. go to the vienna webserver http://rna.tbi.univie.ac.at/cgi-bin/RNAWebSuite/RNAfold.cgi and predict secondary structures of your own RNA sequences.

Please do not answer homework questions where the poster has made no attempt to research the question himself.


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Why can I raise my left eyebrow independently from the other but not the right?
I've seen the same question on other forums, but have not come across any definitive explanation.  The non-cited answers seem to fit into three categories:

It is due to greater muscle dexterity on one side of the face.
It is a result of being either left/right brained.
It is genetic.

Perhaps it has to do with a combination of these three, or none of them at all.  Some have even said that with practice they have been able to raise both independently from the other.  Why is this so?

The muscle responsible for being able to raise both eyebrows is one and the same (m. occipitofrontalis). You can not raise one eyebrow because the whole muscle is connected to both eyes. It is possible that one side is not connected or less connected but that's usually not the case and such a person would not be able to raise both eyebrows at will.
What happens in almost all people is that they are not raising one eyebrow, but instead keeping one eyebrow down and raising both at the same time thus giving the impression of only raising one. There are various muscles that are able to lower the eyebrows.
So if one person is "not able" to raise one eyebrow, it actually means that they are not able to keep the other side down.

This doesn't answer the question.

Then the original question thus boils down to why some people can keep the other eye brow down and others can't? If you could expand on this and answer OP's question, that would really help. And adding sources to your statements will help improve this post further.

I googled this because: I have a very expressive face and started noticing (perhaps with age, I'm 36), that one side of my face appears more droopy, or sulky, than the other. This lead me to wonder if it's because I raise my eyebrow on the left side of my face quite often and generally have more expression on that side of my face. More expression, more flexion, this more muscle-work. I tried raising just my right eyebrow and realized I cannot, or at least not without raising both. This bothered me and I wanted to know why, hence my Google search. I chose not to believe the answer to this query and started training myself to make little independent movement of my right eyebrow, watching myself on my phone. Within a few minutes I realized I can close my left eye and raise my right eyebrow, seemingly independently. That become a vision that I could see. I opened my left eye and repeated the vision, but in reality. I can now move my right and left up and down eyebrows independently.

Welcome Osiris. Please take our [tour] and refer to the [help] for guidance. You seem to be suggesting that practice helps. You'd need to support any claims with references from credible sources. The rest of your post seems to be more suited to being a comment. You'll be able to leave those once you've gained sufficient reputation.

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


text:
I am trying to identify this plant
I am trying to identify this medium arching shrub growing to about 1.5m high x 2m wide in the subtropical climate of the Mt Coot-tha Botanic Gardens in Brisbane, Australia. Unfortunately there was no label with it. The inflorescence is about 3cm across, a greenish yellow, and made up of many tentacle-like florets.  I don't think it is an Australian native plant.

Best I could find is Maclura pomifera, but no pictures of this exact stage of development

Opposite, pubescent leaves with acuminate tip and truncate base. White stipule in background. Inflorescence appears to  be a compound cyme? Not sure if those are strange pubescent petals
(unlikely?) or sepals or bracts in 7s. Initially made me think of Hamamelis flowers, but the yellow "tentacles" are not ribbon-like enough to be any Hamamelis I know or could find. Hmmmm

@theforestecologist could it be Listea glutinosa? It is native to Australia.

@trinitrotoluene doesn't look the same to me. E.g., leaf base and flowers look different. http://www.geocities.ws/wessaaliens/species/laurel.htm

@theforestecologist yeah you're right. I hadn't properly seen the leaf bases. Maybe op could post some more pictures from different angles.

See if you can find any pieces of fruit under the tree. some photos of the bark and the tree/shrub total shape would be help too.

Finally, I found the info about this plant:
Common name: Buttontree
Botanical name: Terminalia pendula
Family: Combretaceae (Rangoon creeper family)
Flowering: June - September
Buttontree is a moderate sized tree with small leaves, which fall early in the dry season. Before falling the foliage of these trees turns a beautiful yellowish red. The leafy branches are pendulous and hang down gracefully. Leaves upto 3 cm appear in nearly opposite pairs. Tiny yellowish green flowers occur in spherical heads about 1 cm wide. Protruding stamens are prominently visible like a fuzz on the round heads. Fruits are sort of circular, clustered in round heads.
Source: Terminalia pendula - Buttontree

This appears to be incorrect. You could try to update with explicit evidence, but I'm not convinced your species is correct

You can try google searching the species, you will get the same result. Also, I reconfirmed my answer with my Botany Professors and its correct.

I agree that Terminalia is incorrect. At a minimum, Terminalia lacks the long sepals(?) of this plant. Terminalia flowers also have a long style, while this plant has essentially no style.

It's hard to find a match. Based on the shape, margin and venation of the leaves it could really be Terminalia but I think we need more information.