text:
How do the anti-D antibodies help prevent Hemolytic Disease of the Newborn? And why do they not act like the maternal antibodies?
I understand that this question has been asked a few times in the past, but the answers there didn't really explain to me why the Anti-D antibodies we introduce are able to prevent the hemolysis of foetal RBCs, and why they aren't identical to maternal antibodies.
As I understand it, HDN is caused when, after the first pregnancy, the mother's body makes antibodies to the D antigen of an Rh+ve foetus, and in subsequent pregnancies, these antibodies cross the placenta and destroy the foetal RBCs.
How do the exogenous anti-D antibodies help prevent this?
Regarding what I didn't understand:
Why is the administration of exogenous Anti-D not harmful to the foetus?

This is exactly what the makers of RhoGAM suggest, saying that the amount of antibody administered at 28 weeks into the pregnancy is sufficient to block any Rh antigen on Red Blood Cells that escape into the mother's blood, but insufficient to cross the placenta and be a problem. At this time the child will be large enough that any RhoGAM that does cross the placenta will not kill enough Red Blood Cells to harm the child.

I thought that the problem was the maternal antibodies crossing the placenta, how does blocking antigens of foetal RBCS leaking into maternal blood help? Isn't it the leaking of maternal blood into the foetus which lets the Anti-D antibodies attack the D-antigen and cause erythroblastosis?
And either way, don't the maternal antibodies do the same thing as RhoGAM, i.e. attaching to the D antigens?

If other questions relate to yours, or other references you've read elsewhere on the internet, it's helpful if you cite and link to these answers and explain what they've said and where you are stuck exactly.

Thanks, edited.

I think the key to your questions is to note that antibodies are only one part of the problem in HDN.
Yes, they are the direct cause of HDN, but the problem is the development of immunity, which will persist. Once the mother becomes sensitised to Rho(D), she will not only be able to produce anti-D, but she will also have primed her whole adaptive immune system against that antigen (e.g. there will be antibody-producing plasma cells, as well as memory B-cells etc.). Once the immune system is primed to respond to an antigen, it does so vigorously, with the second-time response being typically stronger than the first. So the chances are that if response occurs, a lot of antibodies will be produced. And she will likely react in each subsequent pregnancy. One immunity develops, it is a path of no return (and the treatments are supportive rather than preventative, unlike anti-D).
The rationale for giving anti-D antibodies is to allow them to bind to and mask the antigen and thus 'hide' it from mother's immune system. No antigen = no sensitisation.
I was hoping that the antibodies given in anti-D have an isotype that doesn't allow them to cross the placenta, but this is not the case. Turns out that anti-D preparation is actually IgG, which is the only isotype that is capable of crossing the placenta.
I think that the likely explanation for why it works is that it is the dose that makes the poison. Giving just the right amount of the anti-D means that the foetal antigens can be mopped up, but that the amount that might reach the foetus will not be sufficient to cause too much problems.

Why the Anti-D antibodies we introduce are able to prevent the hemolysis of foetal RBCs?

Because they bind to the antigen (foetal Rho(D)) and hence 'hide' it from mother's immune system, so she does not produce a fierce storm of her own antibodies (in the amount that would harm the foetus).

Why the Anti-D antibodies we introduce aren't identical to maternal antibodies?

They are identical to what the maternal antibodies would be. In fact, anti-D (e.g. rhophylac) is human derived from donor plasma (i.e. people who have been sensitised against Rho(D)). The main differences are that the amount of antibody is likely to be different and that mother's immune system does not become primed to attack RhoD.


text:
What is a (preferably) flying carnivorous insect that hunts adult fruit flies at a rate that doesn't threaten extinction?
I am forming an experiment, where I will be forcing evolution on Fruit Flies
(Thanks rogue ant) The experiment goes a bit like this;
I will be forming an ecosystem where every abiotic factor is perfect for the fruit fly, and is supporting its growth and species prosperity. everything down to temperature and humidity, however every biotic factor is trying to kill the fruit flies.
If anybody knows of a species that would work for this, or has miscellaneous tips, or ideas, please let me know.

You could also test whether the lab strain of flies have lost any predator avoidance behaviours compared with wild-sourced flies.

Good idea! Will surely look for changed behaviour patterns.

Biotic fruit fly pathogens / predators.
You don't need every single one for a basic project.  Here are 2 types.
Parasitoid wasps
Parasitoid wasps lay eggs in larva.

Drosophila in the wild suffers massive mortality from the attacks of
parasitoid wasps. As many as 80% of Drosophila larvae in natural
environments may be killed by wasps that lay eggs in them. These eggs
hatch into larval wasps that devour the fly larva from within. Adult
wasps then emerge and mate, after which female wasps search for new
hosts in which to begin the cycle anew.

source
Earwigs, spiders and ants oh my!
Predation on Drosophila suzukii within Hedges in the
Agricultural Landscape

When we exposed D. suzukii pupae in dry and humid hedges, we found
that on average 44% of them were predated within four days. The most
common predators in the hedges were earwigs, spiders, and ants.

There are lots of other mortality causes for fruit flies - fungal infections, bacterial infections, mites, viruses.  But as far as predation these will do.  The parasitoids for the larva and the 3 predators for adults.
Plus those 4 insects will make a sweet icon.

While I appreciate the contribution, I was mainly looking for something that preys on the adult flies. I will edit the post to mention this, Thank you though!

source: Stack Exchange

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sort: votes


text:
Primer design for site-directed mutagenesis
In our practical course about modern cloning methods, we performed point mutations on a promotor via site-directed mutagenesis.
As far as I understand that method you need forward and reverse primers with a partial overlapping sequence to perform point mutations. For deletion and insertion you need forward and reverse primers with a back-to-back orientation.
In the practical course, we already performed that step of the mutation. However, after taking a closer look via CLC workbench where we performed that reaction in silico, I saw that our used primers had no overlapping sequences. Instead our forward and reverse primers had a back-to-back orientation.
Our mutation did work out.
Therefore, I was thinking that point mutation via SDM is also possible with back-to-back primers. However, I did not find any source that can prove that theory of mine.
So I am hoping that someone with more experience than I have, could help me out.

It would be useful it you could make an example drawing/figure to explain what you mean. I'm currently having a hard time understanding your question.

Thank you for your comment! I now edited my question and included some screenshots of my analysis in the CLC workbench. Even though I found the solution now, do you understand what I meant?

Yes, I understand now. Since you have no primer overlap, you probably used 5' phosphorylated primers, amplified the entire plasmid, and then ligated the resulting PCR product to create the new, mutated plasmid. You might want to remove your edit from the question and instead post it as an answer. Also, you did not perform permutations, you inserted mutations. Permutations is something different.

Try this tool for primer design. Yes, you can always do it by hand, but this NEB tool is a great guide.  It is especially efficient when using NEB's QuickChange kit because of reagent optimization done by the company. https://nebasechangerv1.neb.com/

I found the answer! Apparently, it is possible to perform a site-directed mutagenesis with back-to-back orientated primers.

In that picture, the green mark represents a part of the lacZ gene. There, we performed a point mutation by using the forward primer "Cand2 M5 Fwd" and the reverse primer "Cand2 M5 Rev". The forward primer is in fact longer: it includes the purple highlighted part as well. There we exchanged some nucleotides.

In this picture, some nucleotides in the once highlighted part are now exchanged. I was confused as I was tought that the primers should have a partial overlapping sequence with each other. But now as they are back-to-back orientated and have no matching sequence with eacht other, I discoverd that it is possible to perform point mutations like this in a template sequence.

This doesn't really answer your question though. Like I pointed out in my comment to your question, my guess is that you used phosphorylated primers and then went through a ligation step to seal the plasmid before transformation into bacteria. But whether that's what you actually did or not is not clear from your answer.

Hello there! Maybe you understand something wrong. We indeed used back-to-back primer which were phosphorylated and then ligated the plasmid with the wanted mutations. However, with my question I was focusing on the POSSIBILITY to use back-to-back primers for point mutations. Maybe I misunderstood that in class, but I thought you have to use overlapping primers. Therefore, I was very confused as I saw our in silico experiment and reached out to get an explanation from more experienced people (my prof didn't answer my mail...).

Got it. Thing is that in traditional site-directed mutagenesis (with homologous primers) you don't use phosphorylated primers, nor do you depend on a ligation step. Two completely different methods.

Hi there!
Thank your for your response. Do you mind telling me more about this? Is there a possibility to write something like a private message?

There is not, but you can look for the QuikChange method.

Just thought i'd clarify for anyone who is reading this.

Typically site directed mutagenesis uses two complementary, overlapping primers which each contain the mutation desired in the plasmid.  then PCR will generate the entire plasmid.
There is a second method with only one primer for each desired mutation.  The primers are phosphorylated by a kinase enzyme to make the primers work to accept ligation.
This requires a high fidelity polymerase because PCR is copying the entire plasmid else unwanted additional mutations will occur.  This sounds simpler but you have to sequence the mutation sites of several colonies to get full results.

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Color of the Fur coat of Polar bears
Recently I was playing a quiz and a question was asked about the color of the fur coat of a polar bear. To my surprise the answer was black. I thought it was yellowish white or creamy. Why so ?

The fur coats of polar bears are in fact clear tubes - not white fur as is often believed. It is their skin that is black, to absorb the most warmth from the sun (and the clear tubes allow the majority of the light to pass through to the skin).
I recently watched the BBC's Frozen Planet TV series (with David Attenborough), where I heard the above answer. If you haven't already, I recommend watching it.

Also the tubular hairs, like a hollofil padding, are better insulators than solid hairs so they keep more heat in the bear.

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text:
How do carrier RNAs increase yield in sequencing experiments?
I would like to know how carrier RNAs increase yield in RNA/DNA sequencing experiments. Is their main function in the precipitation steps of each protocol (i.e. small quantities are difficult to precipitate and the carrier RNAs add material), or do they have a role at other stages in the process as well?

What kind of sequencing methods and which step in the method are you talking about? In many cases, carrier is added to visualize precipitates and/or get efficient precipitation.

If you are adding phenol-chloroform extracted tRNA then that is a carrier for the precipitation steps. Some people use linear acrylamide for the same purpose.

Thank you for the information, but this does not answer my question. Are carrier RNAs used at other steps in preparation for sequencing?

I've used glycogen for this too.

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text:
Just how light-sensitive is ethidium bromide?
One lab I was in was paranoid about keeping it in a foil-wrapped conical tube; my current lab leaves it out on the bench (and it works fine for staining gels). It's the same company/concentration in both cases, but this second lab uses it up much faster.

Good question.
I found this reference in "Molecular Biology: A Project Approach"

A phenomenon called photobleaching occurs when ethidium bromide (EtBr) -stained DNA is illuminated by ultraviolet light.... This decreased fluorescence is presumably due to the dissociation of ethidium bromide from the DNA.

Ethidium bromide fluoresces when it is in a hydrophobic environment, such as when its stuck between two base pair stacks in DNA- water quenches its fluorescence.
I also found this article citing the fact that sunlight can break down EtBr but only when a catalyst of iron and titanium dioxide is there to catalyze the reaction.
A lot of the original characterization of EtBr as a stain is very old, so I couldn't access it directly online... It looks like the compound itself is pretty stable, but UV can, somehow interact with it when its bound to DNA to bleach it out.

Thanks. So on the bench in its bottle, ethidium bromide shouldn't be light-sensitive, unless there's iron and titanium dioxide contamination (or some hydrophobic substance)?  (also, could you link to the article? I'm pretty sure I found it earlier but I can't find it anymore)

I should think not. Eppendorf tubes are UV absorbant anyway.   I added a link to the article - thought I had it there.. (UV reference: http://www.eppendorfna.com/int/index.php?l=131&action=support&sitemap=4.1&productpage=41&catalognode=28832)

In my current lab we just leave the bottle out (but use it up pretty quickly as we have 20+ people). But we do buy 5 bottles at a time and leave them in the same spot as the bottle that is in use (inside a hood, with the light always turned on) and we've never had a problem with degradation/expiration


text:
How was the diversity between ethanol fermentation and lactic acid fermentation evolved?
Quite simply, some organisms metabolize glucose under anaerobic conditions via Glucose->(2) Pyruvic Acid->(2)Ethyl Alcohol. Some organisms, however, metabolize to lactic acid.
When did such a process (lactic acid) arise biochemically from its related (ethanol) fermentation, and how was it selected for? i.e What were the advantages?
Also, can someone create the glycolysis or fermentation tag?

First, it is not clear from the physiology or biochemical information alone to determine what evolved from what. The intermediate pyruvate is always there, so lactose dehydrogenase (LDH) and pyruvate decarboxylase (PDC) could have each evolved anytime, and there are good reasons for both:

LDH: the reaction pyruvate + NADH/H+ = lactate + NAD+ + 25 kJ/mol is highly exergonic, i.e. produces heat
PDC: the reaction pyruvate = acetaldehyde + CO2 (and with ALD present) acetaldehyde + NADH/H+ = ethanol + NAD+ where ethanol is poisonous to other species

Add to it that there are organisms like Sch. pombe that have both enzymes, so can do both reactions, your questions should be rather:
How has the enzyme LDH evolved?
The enzyme is similar to malate dehydrogenase, both form a family. They belong to a group of enzymes that all have a NAD(P) binding domain, so it's not too far-fetched to state that LDH and MDH evolved from another enzyme with NAD(P) binding domain.
http://www.ebi.ac.uk/interpro/IEntry?ac=IPR016040
How has the enzyme PDC evolved?

Protein sequences of pyruvate decarboxylase (PDC) derived from cloned
  yeast (Saccharomyces cerevisiae) and bacterial (Zymomonas mobilis)
  genes were compared with each other and with sequence databases.
  Extensive sequence similarities were found between them and with two
  others: cytochrome-linked pyruvate oxidase from Escherichia coli and
  acetolactate synthase (ilvI in E. coli; ILV2 gene in S. cerevisiae).
  All catalyse decarboxylation of pyruvate using thiamine pyrophosphate
  (TPP) as cofactor. General overall similarity suggests common ancestry
  for these enzymes.

cited from abstract of
Green, Jeremy. "Pyruvate decarboxylase is like acetolactate synthase (< i> ILV2) and not like the pyruvate dehydrogenase E1 subunit." FEBS letters 246.1 (1989): 1-5. http://www.ncbi.nlm.nih.gov/pubmed/2651151?dopt=Abstract


text:
Why do COVID19 serology tests focus on the nucleocapsid while vaccine efforts focus on the spike?
When I look at the specification sheets for many of today's serology tests like the new Roche test or the Abbott test, they use a nucleocapsid antigen in the test, looking for anti-nucleocapsid antibodies. Given that these tests seem to have high sensitivities toward past infection, it suggests that recovered patients seem to reliably generate an immune response to the nucleocapsid.
At the same time, a lot of the research into vaccines focuses on the spike protein: Moderna is developing a vaccine based on an mRNA coding for the spike protein, CanSino and Oxford combine an adenovirus carrier with a SARS-CoV-2 spike, and so on. I'm having trouble finding any vaccines that target the nucleocapsid peptide.
I'm having trouble understanding this difference. Is it the case that recovered patients reliably produce antibodies to both viral components, but the nucleocapsid is better for testing due to cross-reactivity or other concerns? Or does a natural immune response target the nucleocapsid, while scientists think that the spike is a much better target because it's directly expressed on the cell surface or for some other reason?

N is highly antigenic because N-Elisa works and shows an early and high Ab load. N is hidden inside the virions and  infected cells so it is unclear how anti-N Ab might be useful. The antigen presentation and B-cell maturation (as described in the books) doesn't depend on if targeting the antigen will be efficient. Emphasizing neutralizing antibodies is probably deserved but they are not all, most antibodies simply tag and opsonize the virions and infected cells for destruction by immune cells. S accumulates on the surface of virions and infected cells, a perfect marker

The vaccines will be directed towards a protein/epitope of the virus that creates the most robust immunogenic response, in which the defense system will create an array of antibodies to confer immunity, those antibodies will have to NEUTRALIZE the virus upon entry.
In the case of SARS-CoV-2, the majority of research shows that neutralizing antibodies are directed towards the S1, S2 and RBD proteins which are all part of the S protein.
In this same line, the fact that the body creates antibodies directed towards other components of the virus doesn't mean that they are protective. So creating a vaccine towards those components wouldn't be useful at all.
The reason why those serologic tests target the N protein is probably due to the fact that is highly antigenic. But I'm sure I've seen tests that also target the S protein.

Can you please provide citations for the claims that (1) antibodies directed toward the S protein are neutralizing and (2) the N protein is highly antigenic?


text:
Variance of Stochastic Growth Rate for Average Population Size Over Time
I'm interested in calculating the variance of the stochastic growth rate for the average population size over time,
$$\ln \beta = \lim_{t\to\infty}\dfrac{1}{t}\ln V[N(t)]$$
which shows that the variance of $N(t)$ grows at a rate $\beta$.  The equation to compute this is given in the book "Matrix Population Models" by Hal Caswell.  The variance can be calculated as,
$$\beta = \lambda_1^{(\bf{B}_2)}$$
where $\lambda_1$ is the dominant eigenvalue,
$$
\begin{align*}
\bf{B_2} &= \bf{F_2}[\bf{P}\otimes(\bf{I}\otimes\bf{I})]\mathrm{,} \\[1em]
\bf{F}_2 &= \mathrm{diag}({\bf A_1 \otimes A_1, \ldots, A_k \otimes A_k})\mathrm{,}
\end{align*}
$$
$\bf A$ are the population projection matrices of dimension $s$ from $k$ independent environments, $\bf P$ is the column-stochastic transition matrix of dimension $k$, and $\bf I$ is the identity matrix of dimension $s$.  I tried doing this in R using the goldenheather (Hudsonia) example from the Caswell book that can be loaded into R as follows,
library(popbio); library(Matrix); data(hudsonia)

I ended up with a value for $\beta$ of 0.9366351.  This cannot be right, the variance is way too high.  I must be doing it wrong, or perhaps there is a mistake in one of the equations (very, very likely the former).
Here's my code (if it helps),
s = NROW(hudsonia[[1]])
k = length(hudsonia)
P = Matrix(1 / k, k, k)
I = Diagonal(s, 1)
F2 = bdiag(lapply(hudsonia, function(i) kronecker(i, i)))
I2 = kronecker(I, I)
P2 = kronecker(P, I2)
B2 = F2 %*% P2
lambda(B2)


text:
Why do I want to urinate when I touch water?
I've noticed that whenever I come in contact with running water (especially when I do my dishes), I have a desire to urinate. A quick Google search (link,link) gave me few different hypotheses:

Cold diuresis. Being in contact with cold water reduces temperature on the skin, which then constricts blood vessel to reduce heat loss, thereby increasing blood pressure and prompting the bladder to release excessive fluid.
Afferent innervation. I wasn't able to comprehend all the details of the process, but it seemed like this hypothesis is pertaining to the nervous system than circulatory system, hence different from first hypothesis.
Learnt psychological response. Second article linked above argues that this is a conditioned reaction, where even the sound of tap water triggers the desire to urinate. While it did not mentioned specific details of how this happens, I'm also assuming that this hypothesis is different from aforementioned hypotheses, because this hypothesis sounds more like a psychological response than biological reaction.

Which one of these hypotheses accounts for the desire to urinate when in contact with water? How exactly does it happen? If there is any other reason, feel free to add in the answer.

All three are probably contributors to some degree, although the third is a learnt psychological one and not physioly as you said.

@comprehensible I find it a little hard to believe in the first hypothesis. It's bewildering to me that such a limited time of exposure to cold water in a small surface area (hands) will result in such a drastic change in blood pressure that will prompt bladder to release excessive fluid. Is there any studies done for this?

@comprehensible I'll also be interested to see why the people will learn to have desire to urinate at the sound of tap water. Is there any reason that for that?

The blood pressure is a direct response to your body being supported by gravity, or when it is weightless in water and in fact your upper body pulls upwards. It would be interesting to see when the pee reaction arrives, because, it's normally strongest above the groin up to the solar plexus, the visceral nervous response. There are some more answers here. https://www.quora.com/Why-does-swimming-make-you-need-to-pee

Your point, and the article that I've linked to, seems to point to the case when the body is submerged in water. I guess this does not fully answer my case of washing hand, but your point certainly is true to body in swimming pool.

I came to this thread while I was doing some google search about the first theory because this applies to me. I have noticed that if I come into contact with cold water, I feel the sudden need to urinate. This is the reaction of my body and I don't have control over it. My body does not react the same way with hot water. This could be a complex mixture of biology and neurology (speculating). Some years back at the college, I learnt that part of the waste (e.g. salt) that comes out in the urine, also goes via the sweat through the skin pores. So the more we sweat, the less we feel the need to u

FIRST PART:
I am writing this answer with an analogy.I have analogised your question to a childhood habit developed by our mothers-when she would want us to urinate all she had to do was to take us to the toilet and make a "siiii" "siii" sound to mimic the sound of running water(more or less)
Since I have analogised in that way I think the third hypothesis (referred in your question)is more apt.
SECOND PART:
What fascinated me more about your  question was your comment-"I'll also be interested to see why the people will learn to have desire to urinate at the sound of tap water. Is there any reason that for that? – Hosea Jul 14 "
Indeed there is because we still have our mirror neurons
[SOURCE]
What I wanted to understand is if mirror neurons contributed to Pavlovian reflexes.The answer was yes
Furthur I could find out from sources that the micturition process has centres in the brain stem which are controlled by higher centres in the brain.One of them was the "medial frontal cortex".
Read the following article:

The Pontine micturition center (PMC, also known as Barrington's nucleus) is a collection of neuronal cell bodies located in the rostral pons in the brainstem involved in the supraspinal regulation of micturition. When activated, the PMC relaxes the urethral sphincter allowing for micturition to occur. The PMC coordinates with other brain centers, including the medialfrontal cortex, insular cortex,hypothalamus and periaqueductal gray(PAG). The PAG acts as a relay station for ascending bladder information from the spinal cord and incoming signals from higher brain areas.[source]

From the outline in the following lines I could conclude that there are mirror neurons in this region which 'may' be involved in the micturition control:

Yoshida et al. [26] recently recorded from neurons in the medial frontal cortex, some of which selectively responded to self or observed actions within a social context
[source]

Although research has confirmed that mirror neurons contribute to Pavlovian reflexes no such pathway has yet been discovered which can directly help us to confirm  and understand its relation to urination urge in contact with water.

I asked my doctor about this issue. I had noticed the effect after age 65 and I remember my mother putting my younger siblings when they were just a year or two old, on her insteps as she sat down, and imitated the sound of running water - like a half whistle - soothing sound. And pee came. Now when I do dishes, I immediately feel to pee although I did not really want to before. I know this happens to most older folks. My doctor said maybe it is nerve anticipation that activates the urethral muscles, and too, maybe the instinct of a baby in the womb of the mother surfaces again. I did not quite get that part. I think it is a psychological thing where we respond to brain-nerve-urethra instinctive coupling, something we have no control over. I have started to empty my bladder before going to do dishes. When you shower, it is natural to pee when the water hits you, even if you had no urge to pee before. This is no fancy explanation but I just thought it might contribute.


text:
Which organism can point us to the evolution of sight?
I'm trying to identify the basic biological mechanisms for sight.
Could you help me with identifying any organism that has the most basic ability to see objects?
Most importantly, creatures like dogs, cats, insects are able to not just see light, but are also able to identify objects and other living beings. I feel that an organism could be classified as "being able to see" if it can identify objects and movement and use its "visual sensory organ" to help it move around, locate food, identify species of animals, differentiate between living and non-living and escape predators if any.
Even if an organism can see just black and white or the most basic perception of sight, it would qualify for what I'm searching for. Is there any such known organism that has such a basic visual perception and has the way its eye+brain perceives images, been studied?
I'm not referring to the kind of "photosensitivity" that plants have. Detecting the presence and direction of light is not sufficient.

Could the downvoter please explain why this is a bad question?

"less evolved" does not mean anything. Instead you can ask "What was the first lineage to evolve the ability to detect electromagnetic waves?"

It doesn't make sense for an organism to be "less evolved" because every organism has been equally subjected to billions of years of evolution.

Which is the least evolved organism that can see?

The term less evolved does not mean anything. Instead one can ask

Which lineage was the first to evolve the ability to see?

And by "see" of course, I mean detect electromagnetic waves. Seeing does not imply color vision and does not imply accurate vision.
It will be hard to tell really which lineage came up with vision first. But I am sure you'll be interested to know that some cyanobacteria are able to detect electromagnetic waves (reviewed in Nilsson and Colley 2016).

Thanks Remi. You've linked to an excellent article. They conclude that "Both photoreception and vision thus have multiple origins", and "The ‘simplest’ organisms with real eyes are warnowiid dinoflagellates".


text:
Genotype-Phenotype databases?
Beyond the Stanford HIV database, what other databases out there provide a dataset linking virus/bacterial genotype to quantitative phenotype? I'm looking for high quality datasets to test machine learning pipelines. My own searches usually yield only databases that curate mutations related to drug resistance class ("resistant, possibly resistant, susceptible), but not quantitative information in a standardized form like the Stanford database.

There are thousands of phenotypic variables. The most commonly documented is that of growth rates (or colony size). Also you can have 2^n genotypes for an organism with n genes, assuming there are only two alleles of a gene. Whole genome single and double knockouts experiments have been donee for yeast and E.coli, afaik, but I am not aware of a database. These experiments just measure the growth and fitness.


text:
Ribosomal DNA references sequences
I'm having a bit of trouble with searching for this piece of information. I'm doing a study related to phylogenetic susceptibility of hosts to pathogens (based on a recent Nature publication), specifically to flu. This requires knowing the reference 18S ribosomal DNA sequence for chickens, wild ducks, horses, pigs and humans (amongst others). Is there a resource that enables us to easily download these?

I presume you have tried the usual sources (NCBI, ensembl etc ?)

Yes, I have tried the usual sources, my biggest question was whether they had a "reference" genomic 18S rDNA sequence, or if the NCBI sequences themselves were reference sequences.

Considering the chicken is sequenced, I'd say that its the same thing. tbh I am not too sure of what exactly you ant, but for ll intent and purposes, you'll be using the sequences from below for your analyses

For birds you can start by searching 18s in http://birdgenenames.org/cgnc/
But generally NCBI Nucleotide database, should provide you with all information and accession numbers. See this broad search: http://www.ncbi.nlm.nih.gov/nuccore/?term=18S+ribosomal+RNA+gene
Adding species specification and other parameters, you might find what you are looking for. For example, see chicken 18S ribosomal RNA gene

I may be jumping the gun here, but assuming that you haven't searched NCBI or ensembl, I'd do that first.
Essentially all genomic information is maintained by a collaboration between US NIH, EU EBI and Japan. All databases are synced to each other, and hence the data should (theoretically) be the same (in practice it never is). I'd suggest you pick one server and stick to it.
In my lab we prefer to use NCBI, but that differs from lab to lab.
You can search NCBI by following the tutorial here (http://www.ncbi.nlm.nih.gov/guide/howto/find-published-info-gene-sequence/) or ensembl bu following the tutorial here (http://www.ebi.ac.uk/training/online/course/ensembl-browsing-chordate-genomes/how-search-ensembl)
A sample search for chicken gives you this (http://www.ncbi.nlm.nih.gov/gene/100861561) with three entries for genomic dna and one for mRNA. I'd choose a complete sequence over a partial sequence.
You might also want to look up in their help the meaning of cds (coding sequence; you'll encounter it)


text:
What is the creature on the cover of the fourth edition of 'Dinosaurs: A Concise Natural History'?
I have yet to receive my copy so apologies if this is explained in the book - what is the creature on the cover of the fourth edition of 'Dinosaurs: A Concise Natural History'? It looks like a bird with bat wings (picture below). Could anyone put this in context and suggest why it may have been chosen as the cover image?

It appears to be of the family Scansoriopterygidae.
This dead-end family in evolutionary terms, thrived in woodlands at some point between 153 and 165 million years ago. They ranged in size between small red-squirrels and large grey-squirrels, all having bat-like wings with no developed flight feathers as found in later species such as the well-known archaeopteryx.
They are thought to be marginal flyers or incapable of sustained flight, most likely gliding between trees as flying squirrels do now.
The most recent media sensation (such as it was) was of a discovery of the simply named Yi qi, the first dinosaur ever found with bat-like wings.

That fossil find—announced in 2015 by study co-author Xing Xu, the
IVPP's deputy director—reshaped how scientists understood the
evolution of flight.

This seems to justify its inclusion as a cover illustration.
There's a rather splendid illustration in National Geographic, but I'll not reproduce it here as per their wishes. (Link will try to sell you a subscription, no affiliation with myself), however a related species Ambopteryx longibrachium is reproduced here with attribution:

Ambopteryx longibrachium. Artwork by Chung-Tat Cheung / Min Wang / Institute of Vertebrate Paleontology and Paleoanthropology / Chinese Academy of Sciences. 2022, Smithsonian, fair usage.

Amazing - I had no idea


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Distinguishing between yeast and bacteria
Can hematoxylin stain be used to tell apart yeast and bacteria cells
Are there any other method to tell apart yeast and bacterial cells?
I know hematoxylin stains histone protein but I am not sure how does it affects the bacterial cell so not sure if it will be full proof method to tell them apart( and it’s given that the cell I have is yeast cell or a bacterial cell)
Other method to tell them apart  I thought of is through microscope I think there will a size difference in yeast cell and bacteria cell but are there any other morphological features which can be used to tell them apart
So my first thought was to use a stain which only stains nucleus through which I came came across H&E staining but was not sure what affect it has on bacteria and I also saw other alternatives for hematoxylin but not sure about their affect their affect on bacteria for that I am thinking of setting up control (as stated in comments) will this be sufficient there may be other variables need to be taken into account?
And for antibiotics I was thinking was using a mixture of them but then I came across an answer in research gate saying chloramphenicol is used
So my main question is are the above stated method sufficient to distinguish between bacteria and yeast or are there any other efficient ways to distinguish them?
And the hematoxylin one too

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. Please see our homework policy for more information.

Now is it fine?

Better, but it still needs work. What actual research have you done - web searches, literature searches through Google Scholar or your university's library, looking through microbiology textbooks? Have you simply searched for how to tell the difference between bacteria and yeast in the lab? What did you find when you did that? What do you still have questions about? Keep in mind that there are (roughly) two major kinds of bacteria - Gram positive and negative - and they have different types of cell walls. Also, remember that different bacteria range in size from tiny to gigantic.

So I am thinking I might not need to know how hematoxylin affects bacteria as I will stain the given sample in hematoxylin. And take a yeast cell and a bacteria cell  and stain them and compare these cell with the sample(which might be bacterial or yeast). And on comparison I make sure which cell is given in sample. This way there’s no need to know hematoxylin affect on bacteria

And also using antibiotics I have heard that chloramphenicol usually kill multiple bacteria but there might be some chances of survival is using a mixture of antibiotics recommended or chloramphenicol will be sufficient on its own

You should indicate whether you mean any possible yeast and bacteria, or specific ones of interest. Why are you trying to do this?

You should also include details of the research that you have done with references - in the body of the question. Comments are not permanent and should not be used as a substitute for editing the question with the relevant details.

I have made changes now is it fine


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What is this small white insect on my plants?
Environment
I have a large amount of plants in an old industrial loft apartment.
I live in Rochester, New York.
I ship plants in from across the US, often exotic ones.
Observations
A few months ago, I noticed that two of my Sarracenia plants in my carnivorous plant bog were not growing anymore. Upon cutting them out as to not disrupt the live sphagnum moss grow medium, I noted that one of the insects in question had burrowed its way down into the core of the plant. I assume this to be the cause of the growing issue.
Today I noticed that one of my grape plants and Colocasia plants were covered in these bugs at different stages of growth. They range from white specs to ~3mm with the tail thing.
These insects appear sedentary. I have never seen one move, except when I cut the one out of the center of the plant.
Here is a picture of the bug, which was difficult to get due to the size.

Research
I looked through a variety of different "common insect" sites as well as some insect identification sites but I was unable to find anything remotely similar.
I have only elementary knowledge of insects. Any pointers in the right direction would be appreciated.

Mealybug; don't know much about them.


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How are cotyledons able to affect the structure of plants?
How are cotyledons able to affect the structure of plants? I am asking in the context of leaf venation, root and stem structures.

Did you Google this? It's a basic in botany. If you have an intro Biology textbook, it will be there. See what you can find, and if you have a specific question, edit your question to include the information that confuses you. Thanks.

@anongoodnurse Yes, I did. The question is not only about what are they-- which I can find out but more about how they can affect the structure of plants: this is something I wasn't able to figure out. I have edited the question to make it clearer. I hope this helps. Thank you : )

This is still basic plant biology, one of the first things one learns about plants: are they monocots or dicots? As I said, if you have an intro Biology text, it's there. And it's everywhere on the internet. This is an answer you can find for yourself if you look and read. Getting answers fed to you cuts down on your work but doesn't help you in the long run, which is why we require evidence of an attempt to answer a question on this site.

Cotyledon is a structure of embryos of seed-bearing plants. During seed germination, cotyledon is raised up above the soil and turns green temporarily. They temporarily carry out photosynthesis for net food production for a few days during which the plant's leaves are still underdeveloped, unable to carry out photosynthesis at sufficient rate.
After the leaves become maturely developed and start carrying out photosynthesis, producing food at sufficient rate, cotyledons fall off onto the soil. They are decomposed by putrefying bacteria in soil and converted into nutrients, which dissolve in soil water and can be absorbed into plant.
Edited to add: To answer the question "how are cotyledons able to affect the structure of plants?", we have to clear up some ambiguities within the question itself.
Your question is, "How are cotyledons able to affect the structure of plants?". Instead, you may want to ask, "What is the effect of cotyledons on plant structure?" and "how do cotyledons affect plant structure?" The former ask what the effect is, and the latter ask to explain the process of "affecting". These two questions might be what you want to actually ask.
In Biology, when you are relating two concepts to each other, you have to know what they mean. Visually, you are trying to fill out the gap between the two:
$$\text{cotyledons}\rightarrow\dots\rightarrow\text{plant structure}$$
However, the ambiguity lies in each of the two concepts. What attribute of "cotyledons" are you referring to? What "plant structure" are you referring to? By "cotyledons", are you referring to "the development of cotyledons during seed germination"? This was what my previous effort was trying to answer. By "plant structure", do you mean "dry mass"?
Another way to think about it, when you ask "how does $X$ affect $Y$?" very often $X$ is an explanatory variable (or independent variable), while $Y$ is a response variable (or dependent variable). "cotyledons" and "plant structure" are not variables themselves. Variables are attributes which varies. For example, when you simply say "eye" is the variable, it is not clear how it varies because it is simply a body part. However, "eye color" is a variable because it varies - brown, blue and green. To apply the same logic, how does "cotyledon" vary? How does "plant structure" vary?
I really wish to know what your motivation for the question is. If it is a homework, it is implicit and please ask your teacher to clarify. If it is out of curiosity, target what you are truly asking. The question is simply too ambiguous to answer.

I have edited this. I hope you can understand what I am trying to ask :)

Do you mean "how does removal of cotyledons affect structure of vascular bundle development"? The most ambiguous part of your question is still "cotyledon". Do you mean the size of it, or simply the presence of it?

I assume I correctly imply your question. After removal of cotyledons, the young seedlings cannot carry out photosynthesis for food production at sufficient rate for a period of time as the leaves are still underdeveloped. In this period, food is continuously mobilized for growth and development of seedlings without replacement. This leads to net food consumption. With limited availability of food in seedling, it will soon enter food shortage and eventually deplete its food.

Without enough food (to provide energy and building materials), growth and development is stunted to conserve food for survival. With stunted growth and development of vascular bundles, they appear shorter and thinner than those in seedlings with intact cotyledons.

I think - perhaps - you're reading too much into this question; it's not sophisticated enough to be probing the depths of energy production/genetic expression/other. i think it's asking the difference between monocots and dicots, but the wording is poor. That's just my opinion. It's great that you're teaching, and trying hard to understand the OP, but we tend not to answer such basic questions, especially when no research effort is shown.

I just wish I could help. The question is simply too ambiguous to answer. I recall the OP said they are a high school student and usually high school curriculum emphasizes energy usage in seed germination. That's why I chose to answer the question like so.

"I just wish I could help." That's perfectly understandable, and laudable. I didn't mean to minimize cotyledon's ability to supply energy. Just thinking out loud. Botany was one of my favorite Biology courses, and I have a ginkgo tree because it's a monocotyledonous tree (which is cool!), but I couldn't elucidate the precise mechanisms responsible for vascular tissue patterning.


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How similar are Circulating Tumor Cells and Cancer Stem Cells?
Circulating Tumor Cells (CTCs) are linked with metastasis and their presence can be used to indicate the onset of metastatic cancer. Likewise, the Cancer Stem Cell (CSC) hypothesis suggests that tumorigenic stem cells are the source of cancer. However, microscopy experiments and cytometry have suggested that the morphology of CTCs and CSCs are quite different. Essentially, we have not been able to find Circulating Cancer Stem Cells (asides Myeloma since they are circulating anyways).
My question is how similar are these cells? If they are different, is relapse caused by the CSCs from the primary tumor or CTCs in metasises that have become CSC-like?

There are several competing models of metastasis, and this question does go right to the differences between them.
The primary thing to remember about CSCs is that all evidence suggests that they are a tiny, tiny subset of tumor cells.
CTCs, meanwhile, consist of whichever cells manage to acquire the right combination of motility, invasiveness, and resistance to anoikis (apoptosis caused by lack of attachment to neighboring cells or extracellular matrix).
So, one possible explanation is that CTCs are drawn from the whole population of tumor cells, and that CSCs therefore make up a very small, nigh-undetectable subset of CTCs-- but that this is the subset that ends up founding the distant metastases while the rest of the CTCs get cleaned up by the immune system or lie dormant in the target tissue. You could call this the stochastic model: CSCs form some small, randomly determined fraction of the CTCs, but they preferentially survive and found secondary tumors.
Another model posits that the cells undergo substantial changes in phenotype driven by responses to their microenvironment. CSCs, like normal stem cells, presumably require a pretty specific niche to maintain their stemness. CTCs, meanwhile, acquire their invasiveness and anoikis-resistance in response to conditions in the tumor, such as hypoxia. So, another possiblity is that, in response to stimulus from the microenvironment, a cell with the potential to be a CSC undergoes some phenotypic changes and becomes a CTC. It circulates for a while, finds a target tissue, extravasates, invades the target microenvironment, then starts re-setting up the microenvironmental niche to re-establish its stem-like properties. Call this the dynamic hypothesis: it's a single potential CSC the whole time, but it looks like a CTC while it's circulating and like a CSC only in its niche.

Actually people have been able to isolate circulating tumour cells that show the phenotypic hallmark of a CTC - the ability to give rise to an entire tumour and successfully implant in serial transplantation / dilution assays.
See http://gut.bmj.com/content/early/2016/07/25/gutjnl-2016-311447.full
There is also some elegant work in mice showing that you can trace metastatic populations derived from clusters of polyclonal cancer cells in circulation and through to eventual metastasis, showing that circulating tumour cells with stemness certainly exist at least in model organisms.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4763783/


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are female bonobos "always" pregnant?
Given that bonobo chimps are more sexually active then humans, are the females almost always pregnant? if not how not?
also are they so sexually active in the wild as well or is it just in captivity?

In most species, females are pregnant as often as they can be. Since the availability of sex is rarely a limiting factor, it seems likely that female bonobos are as "always" pregnant as other chimps and socially living primates. The actual rate of pregnancy will be hormonally limited by things such as reduced fertility during lactation and so on.

I think this is normally true for humans - we only need to have sex once a month to make this true - not nearly as often as bonobos.


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Do cells know or imagine how each part of the DNA influences body structure and function? How else would evolution happen in specific ways?
Consider how an octopus looks at a rock and it's entire body blends in to resemble the rock. Consider how insects evolved to resemble leaves or twigs. Even frogs, butterflies and other creatures evolved similarly. When the Pakiectus slowly evolved into the dolphin, there would have been a conscious observation made by the creature, that it could swim better if it had appendages similar to the fishes it saw around it. Or, it could have simply been a realization of how it was able to push water better, when its phalanges were held together tightly. Consider how the nostrils of the whale and dolphin moved to the top of the body. Or even the transition from fins to limbs. In blind cave fishes, 'master switch' genes triggered their blindness. Perhaps light signals are required to keep such genes active. Finch beak sizes evolving rapidly, were theorized as an extra-genetic mechanism (epigenetic changes, that are independent of changes in the DNA sequence).
For the body to evolve a specific type of adaptation, there has to be some kind of knowledge within the cells or the neural network, about which specific part of the DNA to alter or silence, in order that the progeny would have a certain specific type of an altered body shape or function. Even if there's no specific knowledge, there could be a trial and error way of slightly tweaking some known part of the DNA to try and achieve the desired change in body structure or function. Or, the imagination of the creature would have some way of expressing a desire for what kind of change it wants to achieve, and that conveys a signal to perhaps a stem cell that's capable of 'visualizing' and altering cell structure and function. For this, the cells or body would need some kind of a database and 'thinking' function which can bring about such specific changes.
Is there some kind of a "research and development department" in certain cells or a network of cells, which allow it to observe the cause-and-effect of various molecular interactions, and allows it to design molecular and bodily architectures? I would assume that such mechanisms would be capable of manufacturing specific types of molecules. How else would Conus geographus know how to use insulin to disable fish? How else would sea creatures figure out that they could use the oxygen from air to adapt to become land creatures? How else would snakes evolve venom, and termites evolve enzymes to digest wood? How were redox centers designed to allow electrons to jump in a specific direction (3:48 of the video), and how were the F1 F0 ATP synthase designed like a motor and 'placed' at a specific point in the cell to perform a specific function?
There has to be some kind of programming or intelligence outside the DNA, which allows a broader scale visualization of the environment and the body. The intelligence takes decisions based on that. Axon guidance proteins are one such example, where a precise decision is taken for neural connectivity in a jungle of neurons. Could such intelligence be a part of the cytoplasm (because I've only known of cells being created from cells, but never independently appearing into existence. Even viruses need cells to replicate)? Is there any current knowledge that provides pointers regarding this?
ps: Before 1982, conventional thinking was that bacteria couldn't survive in the stomach's acidic environment. But H.Pylori did, and was discovered. Louis Pasteur speculated that rabies could be caused by an extremely small pathogen. Later, viruses were discovered. Cholera was discovered by the initial inference that brewery workers weren't contracting cholera. This process of questioning and inference is what takes science forward. Please don't stomp down my questions just because it does not fit the current hypothesis of mutations. If anything, you should agree that the scientific community is yet to discover a lot more intricacies about cellular function.

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.

The short answer, is that there is no current knowledge of any coding or intelligence outside the DNA.
The long answer (see chat) is that some scientists speculate on cellular intelligence and the ability of the network of individual entities to store memory via the network (see this, this, this, this, this and this. Plus a wiki for some other references). However, as per current knowledge, a cell just follows the "instructions" it's given in the transcribed portion of its DNA. There is some study ongoing regarding epigenetic changes  which may influence evolution too (changes in gene function and expression patterns that are independent of mutations in a gene’s DNA sequence, yet these changes may still be inherited).
[community members: please feel free to edit this answer if you feel any information is lacking]


text:
When is wing growth in the bat complete and how soon can bats fly after wing growth is complete?
I was reading this paper by Cretekos et al (2008), in which they state that wing development in the bat is not complete until after birth - the wing continues to elongate postnatally.  This would suggest that bats are unable to fly immediately after birth, and a brief web search confirms this.
However, I would like to know:

When is wing growth (by which I simply mean outward growth or extension) complete?
When are bats able to fly?  (Are there other developmental processes that take place after wing extension that delay this process?)

The ability of the forelimbs in bats (as well as in other tetrapods) to grow depends on the proliferation activity and ossification of cartilage in growing zones of the bones. Adult bats do not grow (as is the rule for mammals) and wing parameters (wing span and area) show growth curves with more or less pronounced plateau, which asymptotically leans to "adult" values. (This reflects progressive ossification of the cartilage.) As one could intuitively expect, variability in wing relative parameters decreases with age, meaning that juveniles before their first flights show more diversity in wing shapes than flying juveniles and those, in turn, approach gradually the narrow variability of these parameters of the adults.
Juvenile bats start performing their first short flights even before weaning. The main requirement for the flight ability per se is a certain threshold value of wing loading. Sustained flights start roughly half-way to maturity and correlate with the emergence of the above mentioned plateau on the growth curves. The flight abilities improve together with aerodynamic characteristics of the wing: duration of flight increases, beat frequency decreases, but beat power increases etc.

Some references:

Jones (1967)
Buchler (1980)
Hughes et al (1995)
Isaac, Marimuthu (1997)


text:
If human CD8 T cell was injected intravenously into someone could it destroy the orexin receptors in the hypothalamus?
It seemed to have worked in mice https://www.pnas.org/doi/epdf/10.1073/pnas.1603325113
It seems like CDT worked its way into the mouse’s brain and destroyed the orexin receptors. Could this happen in humans too? Destruction of orexin receptors is what is believed to cause narcolepsy.
I want to test it in humans.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Welcome to Biology.SE. The answer would seem to be 'yes', which suggests that you might want to reformulate your question. Questions that ask "could this happen" or "is it possible" often aren't a good fit here since they tend to generate opinions. It might help to tell us why you care (context often helps clarify what sort of answer is useful). Please take the [tour] and consult the [help] starting with [ask] for details.

Okay thanks, I edited my question, hopefully it fares better.

Uhh, please don't test in humans?
O

Why would you want to do this? In addition to appearing to suggest something that would be extremely unethical (if not outright illegal), it sounds completely unproductive (and needlessly baroque if you do actually want to harm someone). I'm going to assume you aren't actually as monstrous as this makes you sound, but please take a step back and make sure you are expressing yourself clearly!

Uhh, please don't test in humans?
But conceptually, it should be about the same in humans.
That Bernard-Valnet PNAS paper presents evidence that these autoreactive CD8+ T-cells can trigger a narcolepsy-like phenotype in rodents, and it's widely accepted that a traumatic brain injury (TBI) can (probably pretty rarely) cause narcolepsy.
So, widespread death of orexinergic neurons probably can cause narcolepsy.
But it's not know whether that's a common cause.
An underlying cause (pathogenesis) could result in both idiopathic narcolepsy AND loss of orexinergic neurons.
In fact, Bernard-Valnet et al. say the same:

it is currently unknown whether autoantibodies precede or are the consequence of brain tissue destruction in narcolepsy

Though you might be able to give your human experimental subjects a long-term or permanent neurological disorder, it might not be the most useful model.


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Poison of the Japanese Tree Frog
The Japanese Tree Frog (Dryophytes japonica) (EN / JP) has a poison on its skin that can even make you loose your eyesight, if you touch your eyes, after touching{NOTE}. I found quite a couple of site stating that you must be careful with the poison of the frog. But I could not find any site that states what exactly that poison is.
{NOTE} Stated by

Wikipedia JP:

手で触る分には問題ないが、傷ついた手で触ったり、触った手で目や口を擦ったりすると、激しい痛みを感じ、目に入った場合は失明することもある。
(google translate:) There is no problem with touching it with your hands, but if you touch it with your injured hand or rub your eyes or mouth with your touched hand, you will feel severe pain, and if it gets into your eyes, you may lose your eyesight.

Japanese blog

触った手で目や鼻、口などの粘膜に触れると、最悪の場合失明する恐れがあります。
(google translate): In the worst case, you may lose your eyesight if you touch the mucous membranes of your eyes, nose, mouth, etc. with your hands.

And various other blogs, which don't necessarily add much value to this list

Question: What is the poison the Japanese tree frog uses on its skin?
If possible, please add a reference.
Why do I want to know this?
I'd ultimately like to know how dangerous it is to keep the frog around:

Can I eat vegetables the frog touched?
Do I need to boil the vegetables before eating?
Can I wash the poison away with water?
Do I perhaps not need to worry, because the poison evaporates very quickly?
What happens, if the frog touches my clothes from the inside and I take on these clothes?

I can only start answering these questions if I know what exactly the poison of the frog is.

Have you tried asking a zoology professor at your university? (presumably you are in Japan if these are your concerns).

Welcome to Biology.SE. Please [edit] in sources for your claim about these amphibians having a toxin that can cause blindness. A cursory check found no corroboration for this claim. Please see the [tour] and consult the [help] starting with [ask] for details about how to use this site.

@DKNguyen I'm not a student; so no prof here.

@DarkTrick I'm not assuming you are. I'm literally saying to find and e-mail a professor out of the blue and ask. I guess I should have said "your local university" rather than "your university".

@tyersome I added two sources. Sources on this are 1) generally in Japanese and 2) generally blog post-like sites. I'm aware that those are unreliable. If the frog has not the claimed poisonous effect, knowing that the information spread is a false claim, is also an important insight.


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Is there any evidence that mammalian ears can act as thermal receptors?
Some snakes have a "pit organ" capable of sensing infrared radiation. The structure is similar to a primitive pit eye. Snakes are cold-blooded and their prey is generally warm-blooded, so it is obviously a useful organ to possess. The need for mammals to possess such an organ is not so obvious.
Many mammals such as rabbits, deer, bats, etc. have large ears with a parabolic form, presumably designed to reflect short wavelengths (high frequencies) into the ear canal. The inner surface is usually smooth with some protection provided by sparse hairs.
I understand that large external ears can be involved in thermoregulation, but that is not the question.
The parabolic form can also be quite useful reflecting and concentrating infrared radiation. To be effective, the external ear would have to have a smooth inner surface and to stay relatively cool. The heat-sensing nerves, if they exist, would have to be concentrated near the enterance to the ear canal. Again it would be helpful if these nerves could be kept relatively cool, perhaps on a projecting fold of flesh.
Mammals are relatively warm which already makes thermal sensing much more difficult.  Humans can easily sense the difference between facing a warm pavement versus a cold sky, though I doubt that our ears play much of a role. But could, for example, a rabbit, in the pitch dark, sense the stealthy approach of a predator or sense the entrance to its own warm burrow, just based on the thermal signature picked up by its ears?
[edit] There is a structure called a tragus in bat ears. It is described as playing an important role in echolocation, but it's also in the right position to be a thermal sensor.
Flying insects will be warm compared to their surroundings and the bats external ear may be quite cool.
[edit 2] Vampire bats have thermal sensors that are used to locate hot areas (blood close to surface) on their prey. But these seem to be concetrated in the nose-leaf and not particularly near the ear orifice.

It doesn't seem likely given the distances over which the distances surface mammalian prey and their predators operate. The most likely candidate would seem to be mice given the common environment that they operate in with snakes equipped with such senses. However, mice have no need for it since as prey, mice neither hunt nor could they use such a sense as a defense against snakes.

@DKNguyen Agreed. It's difficult to identify exactly what might drive the evolution of such a capability in mammals.  But even a mouse might find it's useful to sense its thermal surroundings in the dark while not making any noise. It would be easy to check to see if there are thermal receptor neurons clustered close to the opening of the ear canal.

Unfortunately usefulness doesn't seem to be sufficient criteria for evolution. Many things are useful. It would be useful if mice could also fly or breathe underwater, for example. But evolution seems to prioritize necessary and even already present but not too much of a hinderance over useful.


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How to induce a steady increase in cyctoplasmic [Ca2+] in HEK293T cells? And is there any simple marker/method to confirm it?
We are trying to find out whether increase or decrease of cytoplasmic calcium concentration affects the interaction of two proteins, using co-IP in HEK293T cells as a readout.
In different forums and papers I have found that to increase cytoplasmic Ca2+ levels in non-exciteable cells, there are three major categories of compounds. Ionophores (A23187, Ionomycin), Agonists of InsP3-PKC signalling (carbachol, ATP) and SERCA inhibitors(Thapsigargin, CPA).
However, different papers and different people on use  different concentrations and durations of treatments. Since a lot of the drugs generate rather transient spikes, I realize that the timing is crucial here. Since, we do not have the resources for the optimisation of [Ca2+]-sensing dye imaging, I am also wondering whether there is a simpler way of roughly assessing [Ca2+], perhaps by by analyzing a marker protein/RNA using Western Blot or qPCR?
Thanks a lot!

As far as I know, microscopy (be it with dyes like fluor or with genome-encoded calcium indicators) is really your only good bet, especially for getting quantitative sensitivity, which I think is what you're looking for. Changes in cytosolic calcium are incredibly dynamic both in time and space, which is something to consider when asking how calcium affects your two proteins.
I do know of an example where investigators transferred cells to buffers with different Ca2+ concentrations and permeablized them with a mild detergent to raise calcium levels (Borges-Pereira et al 2015). I'm not sure if that would work for your system, but it's worth taking a look, as I think it raises the levels pretty gently and steadily, and you have a better idea of what your intracellular concentration is going to be without directly visualizing it. Considering you won't be able to tell the Ca2+ concentration at any given time without microscopy, things like SOCE and intracellular chelation rates might be important, so you'll want to watch out for when after treatment you start your assay, perhaps trying a few different time points
Hope that was of some help!


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Why are RNA nucleotides added first, only to be replaced by DNA nucleotides during DNA replication?
I am not asking why RNA primer needs to be added, but rather why RNA nucleotides are added as a primer by Primase and replaced by DNA polymerase I? It seems very inefficient to first insert RNA nucleotides and then add DNA nucleotides when you could have evolved to just add DNA nucleotides directly, without having to add RNA nucleotides.
Perhaps, it is an evolutionary remnant? Proof that DNA arised RNA? What do you guys think?

Does this answer your question? What is the function of the RNA primer in DNA replication?

Welcome to SE Biology. At root, your question is a good one, but I have voted to close it as a  duplicate for the following reason. You say you are not asking why an RNA primer is needed, but that is the self-same reason why the primer is RNA and needs to be replaced. In short only DNA-dependent RNA polymerases (of which primase is an example) can operate without a primer —DNA polymerases cannot. If they could there would be no need for a primer, the lagging strand could just be copied. WHY this difference is a matter for conjecture. The answers in the original question only make suggestions.


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Why are animal's whiskers in a square lattice?
I was observing my cat up close when I noticed his whiskers were in a square lattice as a novice mathematician, took notice of it and wanted to know if any other animal had this peculiar feature, so I went onto my phone and choose a random animal that I knew had whiskers (which was the sea lion), and to my surprise, it had the same grid-like shape of my cat's. This seemingly insignificant question was turned into a very real question that I had no answer to. Plus, the only place where I saw someone mentioning it was on Wikipedia, where it said: "…they form an ordered grid of arcs (columns) and rows…" However, this is the only sentence (besides the caption of the image that the sentence refers to) that takes notice in this lattice, so I'm wondering why (maybe because of evolution?) all whiskers are in this shape.

The question of "why" can have different meanings for different people. You may find an answer by studying how the whiskers develop. Evolutionary explanations are intriguing but hard to prove. You can also look at their functionality.

We know that some nocturnal species use them for navigation. In the case of mice or rats, the tips of the whiskers of a row reach forward, beyond the nose, placed on the same plane. So it helps the animal predict what is coming next as it moves forward. The physical properties of an obstacle appear as a series of row-wise stimuli.

The brain of these species (e.g. the barrel cortex) is certainly set up to process stimuli row-wise, with increased inter-row connectivity and activation flowing row-wise.

Being more specific about what you mean would help, I certainly would not describe whiskers as being in a lattice, they rarely cross over each other. what about the whiskers is in a lattice? maybe include an image.

Whiskers in cats are like little tuned sensory apparatuses that let them feel/handle what they're eating up close, since they don't see very well up close. It could be they're organized in a sort of matrix to get a better feeling of what's close. I personally see rows, and then the two whiskers that are apart (further up the cheek). Also the whiskers in the hind legs can convey meaningful information about the environment before deciding to, for example, perform a jump.


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What is "Correlation of growth" according to Darwin and was he correct about it according to modern science?
What are the views that modern biologist have on Correlation of growth? I need some clarification on statement that I'm gonna mention below as well that is it reason to that as mentioned here: "The gradually increasing perfection of the human hand, and the commensurate adaptation of the feet for erect gait, have undoubtedly, by virtue of such correlation, reacted on other parts of the organism."
Quote mentioned above can be found here: Can be found here

@JiminyCricket. Sure, please find it here: https://www.marxists.org/archive/marx/works/1876/part-played-labour/index.htm

@JiminyCricket. Done !

I suggest that you look into spandrels.

[...] correlation of growth, as Darwin called it. This law states that the specialised forms of separate parts of an organic being are always bound up with certain forms of other parts that apparently have no connection with them. Thus all animals that have red blood cells without cell nuclei, and in which the head is attached to the first vertebra by means of a double articulation (condyles), also without exception possess lacteal glands for suckling their young. Similarly, cloven hoofs in mammals are regularly associated with the possession of a multiple stomach for rumination. Changes in certain forms involve changes in the form of other parts of the body, although we cannot explain the connection. Perfectly white cats with blue eyes are always, or almost always, deaf. The gradually increasing perfection of the human hand, and the commensurate adaptation of the feet for erect gait, have undoubtedly, by virtue of such correlation, reacted on other parts of the organism. However, this action has not as yet been sufficiently investigated for us to be able to do more here than to state the fact in general terms.

Much more important is the direct, demonstrable influence of the development of the hand on the rest of the organism. It has already been noted that our simian ancestors were gregarious; it is obviously impossible to seek the derivation of man, the most social of all animals, from non-gregarious immediate ancestors. Mastery over nature began with the development of the hand, with labour, and widened man’s horizon at every new advance. He was continually discovering new, hitherto unknown properties in natural objects. On the other hand, the development of labour necessarily helped to bring the members of society closer together by increasing cases of mutual support and joint activity, and by making clear the advantage of this joint activity to each individual. In short, men in the making arrived at the point where they had something to say to each other. Necessity created the organ; the undeveloped larynx of the ape was slowly but surely transformed by modulation to produce constantly more developed modulation, and the organs of the mouth gradually learned to pronounce one articulate sound after another.

First, the term correlation of growth is not often or frequently or widely used in biology. In my career I've know of no reference to it. That's why I preface with a comprehensive quotation to give readers a context of what is meant!
Second: if by correlation of growth, you mean that some trait is concomitant with another trait simply out of evolutionary contingency, then absolutely yes, modern biology would very much support this "correlation". However, it is stated above as a "law", and there exist countless instances in which traits are lost or gained in evolution. Mutations may produce gain- or loss-of function enzymes (genes), for instance. These enzymes possess chemistries hitherto unknown by the ancestral enzymes (genes) and so would violate a correlation with all other traits. It sounds more like a broad pattern or principle of thought than a biological law.
However, the idea that specialized traits are bundled together into organisms, and that organisms may only propagate into the future as lineages, is absolutely in line with modern biology. Thus, the expectation that unconnected traits, such as number of toes and number of ears, co-exist in a lineage for a while, is sound. It is also a little trivial too. At least for the vast majority of cases, in mammals*.
*Plasmid horizontal gene transfer in bacteria and other such things, again, would violate the notion that traits are "bundled" strictly within organisms and are only shared by descent... so I would rather mention that it'd be wiser not to think of it as law but rather as a matter of guiding principle.


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Are there any Biology research classification systems?
There are research classification systems for mathematics (MSC) and physics (PACS and subsequently PhySH) which help the researchers to navigate through codes composed by letters/numbers made by associations that specialise in those pieces of human knowledge. Are there any classification systems of research in Biology?

You need to explain what sort of classes these systems produce, who operates them, and in what circumstances, as they do not immediately convey anything to me.

These classes are made by big associations in a try to make a classification of a piece of human knowledge, for example in the case of Mathematics the American Mathematical Society has made an effort since the last century to classify all the Mathematical research areas into a "simple" system of classes where one can access all areas of Mathematics just by a system of numerical/letter codes.
These classes are usually updated from times to times due to human knowledge evolution.

I discourage people answering in comments, but when the answer is a simple 'no' it is difficult to provide rigorous documentation in support. There are obviously different disciplines that lead to different academic departments, and British and (I imagine) US grant authorities divide biology up for the purposes of targeting resources and assigning experts, but trying to make a classification would be like trying to catch a greased piglet.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.


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Vertebra identification
What type of vertebra is this? It was found on a beach in Corea, Maine.

Definitely mammalian and quite large; my very much a guess is seal. Any chance you could post a photo looking straight down from above with the vertebra in the orientation you have in your second photo

Thanks, I added suggested picture.


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Fly identification (Michigan)
Recently we've seen lots of this small fly in our house in Michigan. They are smaller than regular houseflies and don't have the distinctive green/blue sheen that houseflies have. I assume they bite, because at least once I've killed one and it spewed red (which I assume was blood), although I haven't actually been bitten by one to my knowledge.
The fly is about 8mm in length. They tend to sit on walls or ceilings without flying a lot, and they're not difficult to kill, i.e., they don't immediately fly off when approached unlike a regular house fly.
Is it possibly a cluster fly?
Here are two images. The first image is a live fly, the second is dead which is why the wings aren't flat to the body.

Some insects have internal body fluid and organs that can appear reddish upon disruption of the exoskeleton (aka - squishing). I wouldn't be so quick to assume it's blood.

@MattDMo Fair enough but then wouldn’t all of them behave the same way when crushed? I’ve killed quite a few and only one had that result.


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Does human brain produce nicotine?
I had a discussion with a high school student about the effect and production of nicotine. He mentioned that nicotine is naturally produced in our brain so when the person takes to smoking, the brain stops producing its own nicotine and starts craving it from an external source. According to him, this is how nicotine addiction develops. How true is this?
The students also claimed that nicotine in cigarettes is harmless. I have already seen the answer about how toxic it is to humans, but I would love to know:

What's the lethal dose for nicotine via ingestion (not inhaling)?
How does nicotine compare to other toxic substances - for example, cyanide or any other known poison? Is it more toxic or less toxic?

THANK YOU

No, the human brain does not produce nicotine. The brain has nicotinic acetylcholine receptors, but the endogenous agonist for these receptors is acetylcholine, not nicotine; they aren't named "nicotinic" because they are for nicotine but just because nicotine happens to act on them. Many other human receptors are named similarly, based on discovering the molecular basis for sensitivity to exogenous compounds.
The human LD50 for nicotine is reported between 0.5-13 mg/kg depending on age and other factors, but LD50 is only appropriate for evaluating acute toxins; many substances, including nicotine, are most often encountered in small chronic amounts, but concentrated availability of nicotine in insecticides or vape juice can be a plausible source for sufficient doses for acute toxicity. Studies of nicotine toxicity in relationship to smoking are going to be based on much smaller doses over many more administrations.

Thank you very much for your answer. Could you please provide some info on your educational background? I want to show your answer to my students and I don't want them to say "you cannot believe random people on the Internet". Thanks one more time.

@treehugger My educational background shouldn't be relevant; I do have a PhD in a biological science but I could also say I'm an astronaut and the head of state of a major country; since I am ultimately a person on the internet you should use other information to decide whether to believe me. Your question is fairly basic, so I've left some links to Wikipedia articles. Of course, Wikipedia is not an ideal source, but you can follow sources on each of those linked pages to reputable scientific publications.

@treehugger I understand, I'm just trying to give you another perspective. As a scientist, I'd much prefer a ninth grader learn how to find and evaluate scientific information from credible sources rather than appeal to authority of an individual. They should learn to be skeptical of their own intuition, skeptical of unsourced claims, skeptical of sources with other motives or unclear provenance, and learn about how scientists themselves reach their conclusions. All those skills are much easier to learn as a high school student than as an adult - we adults tend to be quite stubborn.

No nicotine is a special type of drug which is never secreted by the brain. Each person has their immunity -- it's based on what amount you take and how your body responds towards it because for some there is a small amount require to become toxic but for some, it can't. As compared to cyanide it is less toxic because cyanide is very harmful

Needs a citation.

The answer is poorly written. Needs links and references.

https://cvi.asm.org/content/11/3/563

It is a good link and there is a lot of explanation and a lot of knowledge in it


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Polymerase Cycle Assembly (PCA) is not working (Only primrs in EF Gel)
Helllo All !
I am working trying to assemble dsDNA fragments (for further golden gate domestication) via polymerase cycle assembly (PCA). After designing the required oligonucleotides with overlap regions. (Image of the design provided below).
Using
NZYProof Green mastermix x2  25 uL
Inner Oligonucleotides 2 uL of 1 uM stock
Outer Oligonucleotides 2 uL of 100 uM stock
Initial denaturation 95 ºC 2 min
Denaturation 95 ºC 30 sec
Annealing 62 ºC 30 sec
Extension 72 ºC 30 sec
Repeated by 25 cycles
Final extension 72 ºC 2 min

After performing the following protocol (based on This one) with a high fidelity polymerase mastermix, the EF gel of PCR products only shows a single "band" corresponding with the oligonucleotides introduced in the reaction.  (Ignore the blurred EF gel, it was imaged quite a long time after running the gel).

Any idea of what could actually be going wrong? Should not I observe at least some faint higher molecular weight amplicons?
Thanks in advance for your answers!
Jorge.
UPDATE: Regarding the length of overlap regions, the design considers different overlap sequences length in order to achieve roughly the same Tm for all the overlaping regions. Tm of every overlap has been calculated using the online NEB Tm Calculator tool, and all of them are in the range of 61-63 °C (Considering a Q5 mastermix, which is the closest HiFi polymerase to the one we are currently using )
UPDATE2: After trying the PCA procedure with a "touchdown" approach (reducing annealing temperature gradually after 3 succesive cycles, most of the assemblies has started to show distinctive bands of the desired lenght in the EF Gel. Annealing is a crucial parameter for PCA.

I just ran the red/right gray primer overlap sequence (gtgaggacgaaacagcctctacaaataatt) through the NEB Tm calculator at https://tmcalculator.neb.com/#!/main and got a predicted Tm of 68C.

Yes! That's actually right. The provided image is the only PCA assembly which features a weird overlap of higher Tm. However the remaining ones (the other two lanes of the EF Gel) are other sequences where all the overlaping regions are between 61 to 62 ºC of Melting temp.

I suspect mispriming due to annealing temp being too low compared to predicted melting temp of overlap regions. As the protocol in your link notes:

(3) Choose annealing temperature wisely. We recommend to use the same
as min_Tm by Primerize design, which is usually between 60-64 °C.
(4) Check PCR product on 4% agarose gel. If assembly is unsuccessful
with shorter mis-priming products, we suggest try raising the
annealing temperature to reduce mis-priming. Alternatively, splitting
the assembly into separate sub-pools (i.e. primer 1-4 and primer 5-6)
and do an additional round of full assembly (see below).

At first glance, the sample assembly in the linked protocol uses overlap regions of similar length (presumably of similar predicted melting temp as well), while your overlaps vary substantially in length (esp. red primer and bottom right gray primer).
Using the NEB Tm calculator page ( tmcalculator.neb.com/#!/main ), I got the following predicted Tms:
left gray/red primer overlap sequence (ctttccggtctgatgagt) Tm 61C
red/right gray primer overlap sequence (gtgaggacgaaacagcctctacaaataatt) Tm 68C
green/left gray primer overlap sequence (gctcgtataatgtgtggaag) Tm 60C
Based on the much higher Tm of the red/right gray overlap, I'd retry your reaction with annealing temps of 65C and 68C.

Thank you for your advise Armand, we will try to do it this way and check the resutls. However, still being strange for us not to find any other product of higher molecular weight than of the primers by themselves.

There may be a more general issue with your PCR reaction. It may be helpful to do a positive control reaction where you are doing traditional PCR, with 2 primers amplifying a segment from a template. The linked protocol also suggested breaking the reaction down into 2-primer segments, then doing a final reaction to assemble those overlapping segments. I agree that not seeing products in any of your reaction lanes suggests it's not just an issue with one sequence.

I've had experience in the past with impure primer preps that inhibited the reaction, manufacturing residue on wells that inhibited the reaction, and so forth.  Positive control reactions that let you verify the reaction components and conditions are all working can help troubleshoot more quickly.

Actually, we have already tried to perform other PCR amplifications and those reactions were succesful. Seems that it is not an issue of the PCR mix or impurities within the tubes. We have also performed a "PCA" with only 2 overlaping primers, and the results were similar to the ones posted here. I am starting to think that our HiFi Polymerase buffer leads to lower melting temperatures compared with NEB Q5 (closer to Phusion polymerases), so maybe trying with a Toucdown PCA could worh it.

Also could be that the resolution of EF gel is not enough and the "blurred spot" are multiple bands. We are going to try running the products again on a well performed 4% agarose gel and see the results. We are also planning to perform a second PCR only with outer primers using the former PCR product as template and see if some amplification occurs.  We will keep this thread updated.    Thank you for all the wise advise Armand!

It seems like you've got things covered -- good luck! I know how frustrating it can be when a supposedly simple reaction doesn't work.


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Why do eyes feel exhausted after reading on a computer screen for a long time?
Similar question before closing this one was: Question.
The answer holds true for most of the observations, but my observation differs from what is described in that question. Even if we consider that tiring eyes is due to the constant focus which creates stress in the ocular muscles, the extent to which eyes feel tired in the case of books/physical paper is lesser than that of display appliances.
Even if I keep screen brightness comfortably low, still there is a slight stress build up, which does not happen when I read a newspaper or something similar physically?
What is the exact attribute of computer displays which causes this? We have come a long way from those CRT displays and current imaging technologies offer realistic and immersive experience. Is it the refreshing frequency, which of the display which causes this stress?

Welcome lousycoder. Please take our [tour] and refer to the [help] for guidance. It's unclear to me if this will stay open as it's possibly just the wrong side of off-topic. I'd be interested in the answer anyhow. Not voting to close.

@ARogueAnt. The previously answered question has mostly answered my question. Could you please share why reading books is not tiring as watching displays even though both of them could be as near as 30-50 centimeters to the eyes.

If the nominated duplicate doesn't completely answer your question, you can [edit] and make it clear in what respect that's the case, it'll then enter the reopen review-queue.