text:
Do axonal conduction delays have a function?
I'm reading about mathematical models of biological neural networks, which can be grouped into two categories:

The model accounts for the fact that a signal takes time to travel from the excitatory to excited neuron
The signal is modeled as if it travels instantaneously between neurons

I'm trying to understand whether a signal delay is introduced for the purpose of realistically modelling a neural network, or whether it has other functional roles in the model. So by function I mean a role in the information-processing capacity of the network that extends mere physical limitations of axon signaling. I'm referring specifically to their function in biological neural networks
Here are three distinct cases that I expect the answer should fall under, to further illustrate what I mean by function:

They don't, signal delays are a mere physical necessity of biological neural networks, irrelevant for the information-processing aspect of their operation. The differences between delay durations are primarily due to the fact that low reaction times are metabolically expensive and spatially-inefficient and are thus reserved for specialized purposes such as reflexes, instead of having a wider functional role as a parameter.
They do, signal delays are fundamentally required for neural networks to process spatio-temporal patterns. However, the differences between the durations of delays are unnecessary to explain any fundamental internal property and are still due to external factors.
They do, and the differing durations themselves are operational parameters, i.e. the function of a sub-network can only be fully understood if the ratios of the delays in signal transfers are taken into account.

It's unclear from your question whether you are asking about the importance of timing delays in biological systems, or about the purpose of timing delays in artificial neural networks.

@BryanKrause I've edited in a clarification, this has to do with biological neural networks, and of course mathematical models of them, not the classical broader computer science concept but continuous-time numerical simulations

Your point #1 is correct, signal propagation is not instantaneous in real physical world. But for some models it is "good enough" to approximate action potential to go through axon in an instance.
There is also biological role of signal propagation timing. One example, is classic Hebbian learning model. Based on "fire together - wire together" idea, connected neurons that become active relatively close in time, will increase synaptic connectivity, illustrated here:

General temporal dynamics are present in both models, and Hebbian learning is achieved via a simple rule dz(i, j)/dt = x(i)*x(j), where z is connection strength and x is the activation. That rule perfectly approximates Hebbian learning through time for neurons i and j without there being a need for a signal delay between them. Axonal delay is far from the only source of temporal dynamics in networks

@jcora i though that delay is driving learning, but source of the delay is unspecified. It can be regulated on different levels, including axonal propagation speed.

See also this paper from Izhikevich in which he claims that the conduction delays can be instrumental in timing-based assembly formation, memory encoding and recall.

@aaaaaa that paper is likely exactly what I needed, will report back when I check it out:)

@jcora .paper was not my suggestion :)

ah right I see haha, well than ty @vkehayas


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How do chemists calculate the existence of billions of organisms?
So the packaging of Bio-Cultures Complex says that it contains a minimum of a billion viable organisms per capsule.
How has such an estimate been drawn?
Have they counted a smaller amount and then multiplied it?

Aren't you just describing statistical sampling?

Have you mistaken chemists for chemists?

It says a "a billion viable cells". The viable is important because it tells you that they employ a method that determines whether the cells are alive or dead. Most likely they did a simple colony count.
The approach is simple, you take bacteria in suspension, serially dilute them in order to reduce the concentration to numbers that can be counted, and then spread onto a solid media plate (usually containing agar) and leave for 1-3 days (depending on organism) and count the number of colonies produced. You can then multiply up this number by the amount you diluted by to get the number of viable cells present in the original.
A billion is not a lot of bacteria. You can expect 100-1000 billion cells per ml in an overnight culture of these bacteria.
Looking at the product description, it specifically mentions CFUs (colony forming units) so I think we can be pretty sure that this is the approach they are using.
(Note that this is standard microbiological technique rather than something chemists would be doing)

Welcome to Chemistry! Take the tour to get familiar with this site. Mathematical expressions and equations can be formatted using $\LaTeX$ syntax.

This more a question of Biology than Chemistry, but we have a similar problem when determining particle size distributions.
The principle is always the same: the suspended particles or cells are passed through a capillary tube and than some measurement is done. This can be with light, an electrical field, etc. When a particle passes, there is a change in the variable and  a counter is stepped. It can be designed to determine the size also.
The most usual instrument for counting organisms is a Coulter counter.
Knowing the volume that has passed through the counter and the number of organisms you know the concentration. Then you can calculate the content in any other volume.
Edit
To distinguish between living and dead cells, stains are used.
There are several types but they relay on cell membrane integrity.
If the membrane is broken, the organism is not viable, but the stains can enter the cell.
They than bind to intracellular molecules (DNA, proteins,...) giving an intense color or fluorescence.
On the membrane there can also be some of the molecules, but then the color is much less intense.

Okay so it uses measurement instruments, rather than the human eye.

This method could not distinguish viable and non-viable cells.

@mavavilj In the good old days the sample was put on a slide with a square grid. Then the cells in a predetermined selection of the squares were counted and the total extrapolated.

@Aidley Fluorescent stains are added if the living and dead cells must be distinguished

@RaoulKessels: Living vs. dead is not quite the same thing as viable vs. non-viable. Whether the makers of these pseudo-scientific bio-capsules know or care about the difference I don't know, but I find it more likely that they're use standard microbiological techniques to count CFUs. Also, for live/dead staining, wouldn't you need a Flow Cell Cytometer rather than a Coulter counter?

I have just given you the point of view of a Chemist. For a more Biology based opinion you might have more success at Biology Stack Exchange. Further, I am not going to judge how companies that I do not know are performing their analyses and if they are science oriented or not.

source: Stack Exchange

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sort: votes


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What is the coefficient of relatedness between a queen bee and her daughter if the male that mated with the queen was the queen’s own son?
What is the coefficient of relatedness between a queen bee and her daughter if the male that mated with the queen was the queen’s own son?
The answer should be 0.75, but I keep getting 1 because 0.5(queen-daughter) + 0.5(queen-male) * 1(male-daughter) = 1.
1 also makes sense because all of the daughter's genes come from the queen. However, I do understand that there is a chance that the genes inherited from the daughter's mother and father may overlap. How is that calculated?

When dealing with haplodiploidy (male are haploids and females are diploid as it is the case in bees), there are several ways at looking coefficient of relationship and the coefficient of relationship between A and B may differ from the coefficient of relationship between B and A. Considering (male-daughter) as being 1 is the source of your issues

I misread it as Rotatedness, and I thought that scientists had figured out that bees signal to each other at N degrees between queen bee and her daughter if the male that mated with the queen was the queen’s own son. that was funny.

Remi, I understand what you’re saying and also that bees are haplodiploids. I thought that when tracing from Queen—>male—>daughter, I’d consider them in the same order that they appear. So regarding queen-male, queen has 1 of male’s genome. Regarding male-daughter, the male has 1/2 of daughter’s genome, on average.

See the answer to this question: How to calculate relatedness in haplodiploid organisms (mainly full sisters and full brothers)?

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Can an RNA anneal to its complementary (not reverse) sequence?
Say I have a target RNA strand:
5'--AAUGGCCCUUUAAA-->3'
I know that this strand will readily anneal to the sequence
3'<--UUACCGGGAAAUUU--5'
which is the reverse-complement. I'm wondering if this strand will also anneal to it's "forward" complement, namely:
5'--UUACCGGGAAAUUU-->3'
?
In other words, can RNA form parallel helix structure?

Possible duplicate of why is DNA antiparallel? Can it be parallel?

No. The 5' end has to anneal to the 3' end of the other strand. Here your 5' end is AAU and the 3' UUU, so you can see that U will not pair with U.

It is, of course, a matter of opinion, but my opinion is that if this question can be answered in two lines it is a poor question for which the poster shows no evidence of having done any research himself. (It may even be a homework question.) I would say that this comes under the category of questions that should be ignored and the poster encouraged to do some research of his own as this site requires.

@charlesdarwin why is that?

@mike-flynn, I don't really understand your comment. In a double-stranded DNA helix, if you move along the helix, one strand goes in the 5'-3' direction and the other strands goes in the 3'-5' direction. So, if you want to pair 5'--AAUGGCCCUUUAAA-->3' and 5'--UUACCGGGAAAUUU-->3' you have to flip one over, align them and check that all nucleotides are complementary. When you flip over 5'--UUACCGGGAAAUUU-->3'  you get 3'-UUU...5' and you can stop here because you see that the third U does not match the U in 5'--AAUGGCCCUUUAAA-->3'.

@charlesdarwin, I'm talking about paring without flipping them over. Taking two free floating RNA strands that are complementary only in parallel direction (5' to 3'), will they form a helix. Can helices form with 5' ends going together towards 3' ends - or why not? That is my question. I don't think you have to "flip" them over as you say, I don't think that's chemically necessary.

@mike-flynn I think they do need to be parallel to pair up.

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text:
Spread of a benign virus in a population over time
This is a somewhat difficult (for me) population dynamics question and I wonder if someone with experience in this area could suggest a reasonable approach?
My simplifying assumptions: As a gross oversimplification, let p(k) be the world's population at generation k, and assume a smooth exponential curve that models p(k) from $k=0$ at 10,0000 B.C.E to generation $k=600$ in 2000 C.E. A generation is 20 years, and in acc. with this Wiki there are about 4 million individuals at $k=0$ and 6070 million at $k=600.$
(Of course the exponential model is bad, as world population growth appears to have been sluggish before recorded history.)
Now assume a benign virus infects 120 individuals in $k=0.$ It benignly infects all individuals who have at least one infected parent. Perhaps unimportantly, it also continues to infect 30 new individuals per million in each generation (because its found in the soil), but would not infect those already exposed.
Call infected individuals II and non-infected NI. They are indistinguishable without clinical tests--which are not done, since the virus is harmless. Since II individuals are almost certain to mate with NI individuals, in earlier generations, the number of II will grow very quickly. For a time the growth rate of II will exceed that of p(k). At some point it will be unlikely that an II individual will encounter an NI mate, however a few NI persons will still pair with NI mates--for a while.
My question is, after 600 generations, what is a reasonable estimate of the percentage of II in the population? Is is possible that there would be any NI individuals left? Or would we have some sort of dynamic equilibrium between II and NI in which (I think) the former would strongly dominate?
FWIW, the population growth model is $p(k)=4e^{0.012 k}$ with $p(k)$ in millions.

For simplicity, I denote the population of non-infected individuals by $N$ and the infected ones by $I$.
Model without soil infection
As your phenomenology is generation-based, the best approach would be to make an iterative population-based model. Let’s first forget about the new infections by soil. I will first give you the equations and then explain them:
$$
\begin{alignedat}{3}
 N_{k+1} &=       &   &g \frac{N_k}{N_k+I_k}N_k &   =~& g \frac{N_k^2    }{N_k+I_k},\\
 I_{k+1} &= g I_k &~+~&g \frac{I_k}{N_k+I_k}N_k &~=~& g \frac{2N_kI_k+I_k^2}{N_k+I_k}.
\end{alignedat}
$$

$g=\left(\frac{6070}{4}\right)^\frac{1}{600} ≈ 1.012$ is the growth rate per generation.
$\frac{N_k}{N_k+I_k}$ is the likelihood a given non-infected individual to mate with another uninfected one.
Now, we have $N_k$ such individuals and they multiply by $g$ and thus the next generation of non-infecteds is $g \frac{N_k}{N_k+I_k}N_k$.
Infected–infected matings produce infected offspring regularly, accounting for the $gI_k$ term.
$\frac{I_k}{N_k+I_k}$ is the likelihood a given non-infected individual to mate with an infected one.
Now, we have $N_k$ such individuals and they multiply by $g$ and thus the next generation of infecteds gets an additional $g \frac{I_k}{N_k+I_k}N_k$ individuals.
Sanity check:
$$g \frac{N_k^2}{N_k+I_k} + g \frac{2N_kI_k+I_k^2}{N_k+I_k} = g (N_k+I_k)$$

Model with soil infection
Now, let’s add the soil infection to the model.
It simply means that each generation another $\frac{30}{1000000}N =: rN$ individuals get subtracted from $N$ and added to $I$:
$$
\begin{alignedat}{3}
 N_{k+1} &= g \frac{N_k^2    }{N_k+I_k} &~-~& rN_k,\\
 I_{k+1} &= g \frac{2N_kI_k+I_k^2}{N_k+I_k} &~+~& rN_k.
\end{alignedat}
$$
Result
With this it is easy to insert your initial conditions and run a simulation, here in Python:
# Parameters
g = (6070/4)**(1/600)
r = 30/1000000
K = 600

# Initial Conditions
I = 120
N = 4000000-I

# Iterate
for k in range(K):
    N,I = (
            g*N**2/(N+I)-r*N,
            g*(2*N*I+I**2)/(N+I)+r*N
        )
    print(k,N,I)

It shows that there are no non-infected individuals left after 600 generations. In fact, $N$ drops below 1 after generation 17.
On equilibria

Or would we have some sort of dynamic equilibrium between II and NI in which (I think) the former would strongly dominate?

No, there is no mechanism that somehow favours the non-infected population.
But this doesn’t exist:
The infected population gets to grow as fast as the non-infected on its own plus infecting parts of the offspring of the non-infected.
In fact, as described in the other answer, we can look at the evolution of the fraction $n$ of non-infected individuals in the model without soil infection:
$$n_{k+1} ≡ \frac{N_{k+1}}{N_{k+1}+I_{k+1}} = \frac{g \frac{N_k^2}{N_k+I_k}}{g (N_k+I_k)} = \left( \frac{N_k}{N_k+I_k} \right)^2 ≡ n_k^2 $$
The only way that some non-infected individuals survive is if they multiply faster than they are infected, i.e., if:
$$g \frac{N_k}{N_k+I_k} = g n_k > 1.$$
Since $\lim_{k→∞}n_k=0,$ this does not work even with an absurdly high growth rate.

To many, many decimal places, the percentage of II in the population is 100%.
To answer this you need to make some assumptions about mating structure. I assume mating is panmictic here for simplicity. Ditto sex ratio, but I'm assuming equal number M/F (and equal risk of environmental infection). Finally, I’m assuming NI and II are at equal risk of soil-borne infection (and infections to II are simply wasted), rather than the environmental reservoir somehow seeking out a fixed proportion of NIs, which I think is probably what you meant. I’m also applying the soil-acquired infection to generation 0 here (so they have a chance to become infected before they mate). Finally, II and NI are more traditionally called $I$ (for infectious) and $S$ (for susceptible) in this type of model, so I've followed that convention below.
Unless I’m missing something the population size makes no difference: the chance of a child acquiring infection does not depend on the number of children, and the background rate of environmental infection is proportional to population size, so it all cancels out. I'll therefore stick to proportions from here on, which means $I$ and $S$ are proportions below, not absolute numbers.
Each generation, the proportion of matings between two $I$s is $I^2$, between two $S$s is $I^2$, and between an S and an I is $2·S·I$. So the proportion of Is in the next generation is $I^2 + 2·I·S$. Or, more simply, $1-S^2$.
So:

$S(0) = \frac{3,999,850}{4,000,000} = 0.9999625$
$S(1) = S(0)^2$
$S(2) = S(1)^2$, which is ${S(0)^2}^2$

More generally,
$S(n) = {S(0)^2}^n$
So at generation 600:
$S(600) = {S(0)^2}^{600}$
$2^{600}$ is a very large number. So it shouldn’t be too surprising that everyone is infected by this point.
We can mess around (technical term) with the equation:
$S(n) = {S(0)^2}^n$
...to solve for (for example) how many generations it takes for 50% of the population to be infected:
$$\begin{alignat}{1}
0.5 &= {0.9999625^2}^n \\
\log(0.5) &= \log(0.9999625)\times2^n\\
\frac{\log(0.5)}{\log(0.9999625)} &= 2^n\\
\log_2\left(\frac{\log(0.5)}{\log(0.9999625)}\right) &= n
\end{alignat}$$
So 50% of your global population is infected by generation 15, only 300 years into the simulation.

however a few NI persons will still pair with NI mates--for a while

The probability of anyone ($S$, or $I$) mating with an $I$ individual is directly proportional to the $I$ proportion of the population, so the chance of this happening just keeps going down faster and faster.

Both answers here are fine. I am upvoting this and accepting the other (would accept both if I could). A small nitpick is that while you don't mean to say that the number of I gets bigger than the population, you don't explain how growth slows as the number of I gets significant, unless I am missing it.


text:
Why doesn’t a basic side chain (R group) of an amino acid form a peptide bond in protein biosynthesis?
Why doesn’t a basic side chain (R group) of an amino acid form a peptide bond in protein biosynthesis?
Consider lysine, for example, why can’t its side-chain amino group, –(CH2)4–NH2, form a peptide bond with the carboxyl group of the other amino acid? Is it due to orientation alone are their other properties involved?

Welcome to SE Biology. I have edited your question. Please do not make statements about "nobody being able to tell you something". It is untrue, irrelevant and appears to be an attempt to draw attention to your question. If nobody is able to tell you I suggest you try to find out for yourself. If you read the Help on asking questions you will see you should show your research when posting. Do you know about protein synthesis on ribosomes and their peptidyl transferase activity? Research this first and then ask for help if you still need it.

Possible duplicate of Why don't amino acids get linked in the functional groups of acidic and basic amino acids?


text:
How to find out the when we had a common ancestor with a particular animal
For example, Jordan Peterson claims that human and lobsters have a common ancestor X million year ago. I wonder, how does he know it?
I'd be so delighted to visit a website, where I could select two currently existing species and it'd show me how many years ago they had had a common ancestor. Does anything like this exist? Do we at least have a database, so I, as a web programmer, could create this kind of website?

This post will interest you: The best free and most up to date phylogenetic tree on the internet?

TimeTree [http://www.timetree.org] is one site that allows you to look at times from divergence of various taxa. Their FAQ describes how they calculate the times by pointing to this paper: Tree of Life Reveals Clock-Like Speciation and Diversification, but in general they used standard molecular clock approaches. You ask about downloading their database: they say

The TimeTree Database data is currently not available for download. Methods for making these data available in the future are currently under discussion.


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How are mitochondrial ATT (Ile) start codons translated as Methionine?
In some vertebrate species, some mtDNA start codon sequences are ATT but these are translated as Methionine rather than Isoleucine. What is the mechanism for this non-standard translation?
The main example below is in a bird, blue crane (NCBI Genbank excerpt below). The NCBI data give the standard note on completion of the stop codon but there is no note about modification of the start codon. We have confirmed this ATT start codon from PCR-Sanger sequencing an independent sample. There are similar cases in other vertebrates (Aves, Squamata, Amphibia) such as ND2 in Goggia geckos (example 2 below, also independently confirmed by Sanger sequencing. In this genus the start codon DNA varies from ATT to ATA or ATC: 50/59, 6/59, 3/59). I think I have seen this in other mtDNA genes. In many other birds and reptiles ND2 starts with ATG.
Are these modifed post-transcription to ATG? If so how?
Could they reflect a variant of the mtDNA code where AUU = Met? Or where any AUX codon is recognized as Met.
Example 1. ND2 from Blue Crane (NCBI Genbank refseq excerpt)
LOCUS       NC_020572              16696 bp    DNA     circular VRT 18-APR-2013
DEFINITION  Anthropoides paradiseus mitochondrion, complete genome.
ACCESSION   NC_020572
VERSION     NC_020572.1
DBLINK      Project: 193816
            BioProject: PRJNA193816
KEYWORDS    RefSeq.
SOURCE      mitochondrion Anthropoides paradiseus (blue crane)
  ORGANISM  Anthropoides paradiseus
 gene            3970..5008
                 /gene="ND2"
                 /db_xref="GeneID:15088361"
 CDS             3970..5008
                 /gene="ND2"
                 /note="TAA stop codon is completed by the addition of 3' A
                 residues to the mRNA"
                 /codon_start=1
                 /transl_except=(pos:5008,aa:TERM)
                 /transl_table=2
                 /product="NADH dehydrogenase subunit 2"
                 /protein_id="YP_007624320.1"
                 /db_xref="GeneID:15088361"
                 /translation="MNPHAKLIFLTSLVLGTTITISSNHWMSAWAGLEINTLAIIPLI
                 SKSHHPRAIEAAIKYFLVQATASALVLFSSMINAWSTGQWDITQLNQPMPCLLLTTAI
                 AMKLGLVPFHFWFPEVLQGSSLTTALLLSTVMKFPPITILFLTSHSLNPALLTSMAVA
                 SAALGGWMGLNQTQIRKILAFSSISHLGWMTIIIMYSPKLTLLTFYLYSLMTITVFLT
                 LNTTKALKLSTMMITWTKIPTLNATLMLTLLSLAGLPPLTGFLPKWLIIQELTKQEMT
                 TAATIITMLSLLGLFFYLRLAYYSTITLPPNSTNHMKQWHTDKSTNTLIAIFTSLSAL
                 LLPLSPMILTII"

 3901 agtagagtca gctaaaaaag ctatcgggcc cataccccga aaatgatggt ttaacccctt
 3961 cctctacta**a tt**aacccaca tgcaaaacta atcttcctca caagcctagt cctagggaca
 4021 accattacaa tctcaagcaa ccattgaata tcagcctgag caggcctaga aatcaatact
 4081 ctcgccatta tccccctcat ttcaaaatcc caccacccgc gagccatcga agccgcaatc
 4141 aaatatttcc tagtacaggc aaccgcttca gcactagtcc tcttctcaag tataatcaac
 4201 gcatgatcta caggacaatg agatattacc caattaaacc aaccaatacc atgcctttta

Example 2. ND2 in Goggia (Gekkota, squamata) NCBI nucleotide locus ref.
LOCUS       KF666817                1424 bp    DNA     linear   VRT 09-SEP-2014
DEFINITION  Goggia lineata voucher MCZ R184778 NADH dehydrogenase subunit 2

The key point in understanding non-AUG start sites in mRNAs is the nature and role of the initiator tRNA.
There is a special initiator met-tRNA which differs in structure from all the elongator tRNAs in such a way that it — and only it — is recognized by the IF-2 type initiation factors (and not by the EF-Tu/EF-1 elongation factors). In a complex with the initiation factor and GTP it can bind to the ribosome at the P-site. Normally the ribosome will also be interacting with an AUG codon at the P-site, but in some cases it is not, so that initiation may still occur.

Thus, the initiating amino acid is always methionine, regardless of
  the codon, because methionine is the only amino acid with which the
  initiator tRNA can be charged.

In the case of bacterial mRNAs, it has long been known that about 10% start with other codons, predominantly GUG. This can be explained by their relative position to the ribosomal binding site on the mRNA — the Shine and Dalgarno sequence. I imagine this is what happens in mitochondria.
In the case of eukaryotic cytoplasmic mRNAs, an initiator met-tRNA complex normally scans from the 5ʹ-end, initiating at the first AUG or first the first AUG in an ‘appropriate context’. The precise definition of an appropriate context is unclear, and on can imagine that in some cases such a context pauses the ribosome at a non-AUG codon, at which initiation begins.
References
“The Biochemistry of the Nucleic Acids”, 11th edition, Chapter 12 (1992) RLP Adams et al. — this has all the older original references, but not the recent ones.
Wikipedia entry on Shine and Dalgarno sequence.
Eukaryotic scanning model: Hinnebush review (2011)
Initiation in prokaryotes and eukaryotes Londi review (2015)
Related SE Biology Answer on initiation and elongation met-tRNAs (by me)


text:
Can you use a microscope without an eyepiece?
Can you use a microscope without an eyepiece?

Do you mean without a camera too and looking straight into the tube?

yes I do mean that.

Yes, sort of. I tried it just now - take the eyepiece out and look down the tube.  However, the view area is smaller, and you lose the magnification of the eyepiece.

Yes, you can. I have a microscope where the data can be transferred to a screen on a computer instead of going to the eyepiece. This microscope has both an eyepiece and the option to redirect the image to a screen. However, I also have a microscope with a screen only. So, I suppose you can have a microscope without an eyepiece.
I have never come across a microscope that has neither an eyepiece nor a camera but I don't know whether it's possible or not.

You might want to edit your answer to address the OP's answer to my comment under the question.

Surely you have taken the eyepiece (or the camera) out of your microscope?  I think with most the eyepieces just slide in - mine works that way.

@jamesqf I have not taken the eyepiece out. It arrived without an eyepiece, just with a screen.

A microscope composed of a single lens is called a simple microscope. In fact you can use an objective or just the eyepiece, as a magnifying glass. Antonie van Leeuwenhoek's microscope's were simple microscopes.

Source: Wikipedia
In contrast, compound microscopes (by far the most common type nowadays) are composed of two or more lenses. I would argue that their benefits compared to simple microscopes include:

Multiplicative magnification arising from the combination of lenses.
Ease with which the objectives can be interchanged independently of the eyepiece offering different magnifications.
Easier to achieve an ergonomic design.
Advanced illumination setups, such as phase contrast.
Cheaper to provide stereoscopic vision and achieve parfocallity with two low-magnification lenses that are able to be focused independently than having two high-magnification lenses.
Some eyepieces additionally correct for aberrations.


text:
If longer wavelength color is perceived faster by human, what about non-spectral color (black)?
Related to human vision, I read the hypothesis about how longer-wavelength color is perceived faster by human eye than shorter-wavelength color source : A Brief Classification of Colour Illusions. But what if the other color is a non-spectral color like, black ? Black is achromatic color, it's the absence of colors and has no wavelength. Does this perception hypothesis still apply ?
Because I've been doing a color comparison by putting a layer of colors on top of each other. In this case I tried with black - green (~549nm) and black - yellow (~570nm), and it seems like black is always dominant against other colors. But I can't find any scientific reference for this. The closest I found is the hypothesis I mentioned before. Any suggestion ?

It would be helpful if you provided a citation for your claim about faster longer-wavelength perception. It's also not at all clear what you mean about putting a layer of colors on top of each other. If you are talking about absorbance, then yes of course, black is always going to dominate because it absorbs everything else. It doesn't matter what other color is there, when you see an object that has color that's based on the light reflected off of it. It has nothing to do with perception speed.

Hi, I've updated my question. So I've been doing some kind of experiment by putting a different color pattern for each eye to see. Because human vision will see the scene from 2 eyes as a whole one, so they will perceive these 2 colors overlap with each other. What I'm trying to find out is the information about color perception according to human vision. In case if there's black in the pattern, why is it always dominant when it's overlapping with other colors ? I hope I explain clearly.

Might be nice to post some of those illusion pictures; I have an idea of what you are talking about now thanks to the link you provided, but previously it was unclear from the text. Thanks for the edits

Thanks ! I'm not sure to put one of that illusion picture. I'm afraid it will mislead because what I've been doing is quite different. Not some kind of optical illusion.

Oh okay - still it might be helpful to show what you're doing. After all, I thought you were creating illusions similar to what was on that page. It's going to be hard for someone to help you with a hypothesis if they don't know what phenomenon you are trying to hypothesize about.

That link is not about perceiving some colors faster than others, so that reference is misleading, or distracting at best. What do you mean with faster? Quikcer, or perhaps better?

I couldn't find any mention of wavelength-dependent latencies in perception


text:
Question about Racemic Mixtures in Miller-Urey Experiment
I'm studying the Miller-Urey Experiment for my Biology class, and a significant point made by my professor was that Miller made a 50/50 racemic mixture of chiral monomers.
However, life is homochiral.
I'm trying to draw some significance out of Miller and Urey's experiment. Could life have started in multiple various places (because all you need for life to start is some organic molecules), so you could have developed various chiral forms of polymers (like amino acids), but one chiral form dominated and thus natural selection favoured that one form?
Thank you!


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What determines the reversibility of cell of G0 phase in cell cycle?
From Weinberg's The Biology of Cancer: A cell that has been recently formed by mitosis must decide whether it will once again initiate a new round of active growth and division or retreat into non-growing state G0. This decision is strongly influenced by mitogenic growth factors in the cell's surroundings. Their absence or presence of anti-mitogenic growth factors will trigger the default decision to proceed from mitosis into the G0 quiescent state.
Withdrawal from the cell cycle into G0 is often reversible (cell can re-enter into active growth and division), however some cells irreversibly leave the cell cycle (such as neurons).
Here comes my question : What determines in the cell whether the cell will go to reversible (quiescent) or irreversible (senescent) state of G0? I have found that it has something to do with the amount of RNA (low RNA content in reversible), but I do not understand why low RNA content means that the cell should proliferate again. And are there any other criteria that determine whether the cell will go to quiescent or irreversible state? (I am looking for exact molecules and mechanisms, the more into detail the better !)

The answer is quite complicated. One of the major issues in understanding what factors drive senescence vs quiescence has been the absence of a clear, uniform molecular definition of senescence. That said, multiple tumour suppressors, including p16 (and the other genes that occupy the INK/ARF locus) , as well as TP53, can modulate the expression of senescence associated transcriptional programmes.
Additionally, epigenetic remodelling, including heterochromatinisation at E2F target genes (which are a major driver of cell cycle progression through the S phas) , is also known to be a feature of senescence.
A very good starting point to survey the literature surrounding the topic is https://www.nature.com/articles/nrc3960?message-global=remove


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How much Open Access Data is there in genetics?
Type of data of interest
I would like to consider

Genetics data (SNP, microsatelites, whole genome sequencing, RFLP, ...)
Genetic - phenotype data (disease-related data, QTL, etc...)
Sequence annotation and function
Transcriptomic data

I would like to include data on any living thing (including data from fossils) and not only human data. To avoid issues of semantic I would leave out epigenetic data.
Question
How much (in bytes) of such data is available in Open Access online?
Difficulties
I realize getting to such estimate might be hard and the estimate may be very inaccurate. Also, the format used for storing these data will definitely affect the relationship between information content and storage usage. But if someone can give just a rough order of magnitude, a vague intuition, it would already help. Is it a few terabytes or a few petabyte or even more?
I would welcome as well a detail of how you got to this estimate. I am particularly interested in what fraction of it is human data (if you happen to get to such fine detail).

Despite all your tags, I rather think this is off-topic for biology. Regardless, I would imagine that if you checked how much NCBI has in GenBank that would give you the order of magnitude you need.

Functional annotations etc will be negligible, as the size of largest databases (e.g.: Interpro, or EBI GTX) only is 100GB. For sequences, it depends, if you save difference to references. Otherwise you can extrapolate from NCBI statistics - as also noted by David -, that - depending on sequence complexity - you'd be in double digit petabytes ( https://www.ncbi.nlm.nih.gov/genbank/statistics/ ) ; note that sequencing information is small compared to image-based biological data, and the - open / not licensed - image information contained in old books and texts could easily exceed petabyte

Can you clarify which type of data you are looking for and what for?
There are lots of public databases with all sorts of information. And obviously most of it is redundant.
Coming back to you question I'd say there is much more data publically available that not even the most powerful supercomputer would be able to handle. But as I said, it depens on what you want to do with it.

@aLbAc I don't intend to do anything with these data right now. My question comes out of curiosity mainly. I was just trying to get an appreciation of how much data we are producing and storing in genetics.

The answer is "huge amounts" and increasing exponentially with the new generation of high througput sequencers.

It is difficult to answer this if we include all NGS and microarray data on the genome and gene expression. In addition to reference sequences, databases with expression  data are growing exponentially as well. Separate projects such as TCGA, ENCODE, FANTOM, HapMap, and various biobanks also have massive data repositories. As such, any answer would be outdated very quickly.

I'm voting to close this question as off-topic because the answer to this question will change over time.


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What Evidence Do We Have For the First Mammal?
Edited for a less broad question, I've retained my original question in the event anyone wants to try to answer it
Narrowed down question
According to evolution we should all share common ancestors, straight to the very first cell. I am trying to find evidence for these ancestors. So therefore as a start, what fossil evidence do we have for the first official mammal to roam the earth? What was the defining moment and change from whatever it was before to a mammal?

Original question
I'm just doing some research for my biology class and I was wondering
what evidence we have for the elusive "change of kinds" question? And
for clarification, I define kinds as the branches of life (essentially
birds, reptiles, mammals, amphibians, fish, etc etc). Do we have
evidence for the common ancestors that link the vastly different
species we have? Because obviously a human, tortoise, jellyfish, and
say tarantula are vastly different, each their own distinct "kind",
but according to evolution there should be common ancestors and many
distinct species leading up to them. We all came from one thing. Man
and primates came from one thing. Mammals came from one thing. Where
do we get that distinct change of a kind, from say a fish to mammal?
There should theoretically be tens of thousands of in between links
and species that were what led to everything today, correct?
Therefore, we should have mountains of fossil evidence to support it,
yet from what I've researched I've found very lacking evidence and
generally just see posts insulting creationists and skimping the
question. So by asking the question myself hopefully I'll get a
legitimate and clear answer that is the truth.

Yes there is tons of evidence, including whole living groups of species as well as fossil missing links. Every time science finds one of these "missing links", though, creationists pop in and say "oh well what about the link between that and (other group)" - it's really quite frustrating. Try an academic source on evolution like https://evolution.berkeley.edu/evolibrary/home.php

We indeed have thousands (in fact, probably hundreds of thousands) of evidence. Note that fossil are not the only source of evidence for such common ancestry. We also have genetic data, phenotypic, biogenographical and geological data that all agree on the same general story. The question is very broad though and it is hard to know exactly what study you would like to hear from. You might want to have a look at this post who list to thousands of studies explained in lay terms.

For a short and easy introduction to evolutionary biology, you might be interested in having a look at Evo101 by UC Berkeley

Because of the phrasing of your question (usage of the expression "change of kind"), you might want to have a look at this related post.

I entirely understand the theory behind evolution and that's why I question it. You all have mostly disregarded my question. Microevolution is certainly proven, but do we have proof for macroevolution is perhaps how it should have been phrased? If we have hundreds of millions of years, we should see thousands of distinct "in-between" species that we do not have today. Where is the fossil evidence for that? Can someone give me a direct link?

I am voting to close as too broad. If you can somehow narrow your question down (such as asking for specific type of evidence for a species lineage), then I would be happy to vote to reopen it.

@Timble Can you please tell us more precisely what fossil you are looking for. If you can pinpoint to a specific fossil, we would be happy to try to look for evidence of such fossil. For example, would a dinosaur fossil answer your question? Would fossil records of early eukaryote answer your question? Would bacteria fossils answer your question? Would fossils of early mammal answer your question?

Alright, what is fossil record for the common ancestor that all mammals share? What was the very first mammal that all mammals evolved from?

@Timble Great! That's a question sufficiently well defined to be answered. If you can edit your post so that this becomes your question, we will happily attempt to find evidence of fossils of early mammals.

Please take no offense but when you say I entirely understand the theory behind evolution, I doubt this is in anyway true given the phrasing of your question. Note that as a researcher in evolutionary genetics, I would not have the confidence to say such thing as " entirely understand the theory of evolution" because it is such as vast field of knowledge. Also, the fact that you seem to consider fossils as being the only source of evidence make it feel that you don't understand the extend of methodologies by which we gather evidence in evolutionary biology.

Apologies. When I said that, I meant that I understand the basics of evolution. I understand the theory of it, things that are better suited for their environment tend to survive those that aren't, things evolve through natural selection. A single celled organism through random mutations eventually created life as we know it today. I didn't mean that I know all the ins and outs of it. My knowledge of evolution is purely high school level and relatively low, but I'm better trying to understand it. Thanks for being patient with me :)

I made an edit (feel free to roll back if you don't like it) and I am rectracting my close vote. Thanks. I shall come back to your question tonight (or at least in the coming days) if it has not been answered yet.

Remi.b alright great, thank you. And also in response to what you mentioned in a previous comment that I neglected to respond to... obviously other evidence is great, but if it's not backed up by physical fossils, in my opinion it means and proves very little. And I'm just saying, that logically, there should be billions of fossils of unknown species buried on earth from the "in-between" species that were in the process of evolving into the next great things.

@Timble Not all dead animals fossilized. In fact very few do. So don't ever expect a billion fossils! Early mammals were rather small and mainly restricted to areas that are less likely to provide good fossils. But don't you worry, I am sure we have at least a dozen of good quality early mammal fossils.

You should not be looking for Mesozoic mammal fossils, as they are already Mammals, defined by 3 small inner ear bones, derived from jawbones of their ancestors. You should be looking for synapsid mammal ancestor fossils. Things like Pelicosaurs and cynodonts. What you see here is a transition from slow moving early creatures to dog-like predators that were built for running, and likely homeothermic (and fur-covered), but not yet defined as mammals because they did not yet have the characteristic ear bones.  There are hundreds of these transitional fossils.

iayork I have looked at it, but I'm looking for fossil evidence. Very few of the the pages on that wikipedia bit had any fossils. The couple that did were blurry and grainy. Where did the discovery of these animals come from? How do we know they're the links in this tree? When I looked at the individual animal pages and even when I looked it up seperately, it was very lacking in references or history. I'm not opposed to believing it, I simply believe there should be more fossil evidence than there is.

That monotremes, marsupials and eutherians all share these three inner ear bones (hammer, anvil and stirrup that we learned in elementary school), then it is likely that the single species that gave rise to all mammals had these inner ear bones too. The transition from say Dimetrodon to this common ancestor was gradual, but there are lots of fossils in the synapsid lineage.

@Timble The idea that there is some sort of conspiracy over missing fossils is a lie that is commonly spread by creationists. Fossils are exceedingly rare. Nonetheless, there is ample evidence of gradual change over the synapsid lineage, leading to modern mammals.  https://www.fieldmuseum.org/fossil-non-mammalian-synapsid-collection-field-museum   http://www.truthinscience.org.uk/evolution-synapsids

Part of the problem is that defining the exact point at which a "change in kind" took place, or even whether it did take place, is essentially a human construct, while evolution is continuous.  Take for instance the people who say that birds are dinosaurs, denying that a "change in kind" took place.  Or even that all dinosaurs were one kind, rather than (at least) two distinct sorts (saurischians & ornithischians, IIRC).

@jamesqf To piggyback on this comment, consider something much more recent that changes over time and see how difficult it is to detect a change in time, for example, when was the first baseball game played? There are points in history where you can identify the first time "base ball" was mentioned in a newspaper, or the first team that charged admission to watch their baseball game. There are more recent times when modern rules came into effect (e.g., the 'dead ball era'). It's clear baseball is played now. It's clear baseball wasn't played in the far past. Saying "first" mammal is difficult.

@Bryan Krause: Or consider the evolution of the telephone, from a wooden box that hung on a wall, like this: https://en.wikipedia.org/wiki/History_of_the_telephone#Early_commercial_instruments to a flat rectangular box that you can hold in your hand, and which shows pictures.  But they're all "phones" :-)

Obviously, it's impossible to point to "the" earliest mammal; dividing lines are pretty much arbitrary. However, a reasonable representative of a very early mammal or very late mammaliaform is Arboroharamiya jenkinsi, described in A new arboreal haramiyid shows the diversity of crown mammals in the Jurassic period, from roughly 155-160 million years ago.  That shows a number of fossils, including this quite nice one:
The supplementary information shows some cranial features, including this:

A related species from roughly the same time period, Haramiyavia clemmenseni, had CT scanning done on this fossil mandible:

yielding images like this:

Similarly, the euharamiyidans were either very early mammals or very mammal-like cynodonts, which are known from a number of quite nice fossils including these three (described in Three new Jurassic euharamiyidan species reinforce early divergence of mammals):

Good answer +1. It would be nice to have an estimate of how old these fossils are.

It is a mistake to think that there was ever a "first" mammal.  There were only animals that were more mammal-like or less mammal-like. To ask what was the first mammal is like asking who was the first tall person.  What is "tall"?  "Mammal-ness" is on a continuous spectrum just as "tallness" is. All we can do is acknowledge transitional forms like those mentioned by @iayork.


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At what g force do bacteria start to pellet down a tube?
I am working with C. elegans and bacteria and I want to get rid of the bacteria they eat by centrifuging the worms without centrifuging the bacteria. I am using a g-force of 600 and the bacteria sometimes still centrifuge down. What g-force would be ideal to pellet the worms but not the bacteria? Does this depend on the bacterial species?

Have you tried using Ficoll to separate them?

no, how does it work? The wikipedia page mentions its use for blood cells separation.


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How much pressure can human withstand if inner and outer pressure is balanced?
I know human can't dive too deep because there's pressure difference between inside and outside of the body. But how much pressure can human withstand if human is breathing components that is surrounding him?
So I have two questions:
1.How much pressure can human handle if he is surrounded by regular air (also breathing air)? 2. How much pressure can human handle if he is floating in oxygen-rich liquid and breathing it at the same time (Liquid Breathing, Wikipedia)?
There's a similar question, but it doesn't have answer that fully satisfies me. Highest Pressure Human Body Can Survive In?

Welcome to Biology Stack Exchange. The physiological responses to breathing 'regular air' under pressure are very well understood (a good answer could be based on medical studies of regular SCUBA divers), whereas the liquid breathing techniques are extremely experimental and under-studied, so any answer would have to be very hypothetical. I suggest splitting these off into two separate questions, because the answers will be basically unrelated.

Most issues with typical diving technology involve compression/dissolution/ or expansion of gas. But for extreme depths, if you assume you can eliminate issues related to gases, there is virtually no limit as long as the rate of compression allows (fluid) equalization of pressure through the cell walls. Too rapid compression/expansion can result in similar affects as exposure to hypotonic/hypertonic solutions - crenation or rupturing effects. The bulk elastance of water - very 'stiff'


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Do Marsupials have a standard classification system for their blood groups?
I've seen a limited amount of animal blood groups listed...like dogs, cats, horses, etc. But what blood types do marsupials have?
To clarify, what I want to know is if the species has a classification system similar to the ABO blood group? For example: Blood Type A, Blood Type B, etc.
Or in the case of Dogs, the classification system is labeled as: Dea 1.1, Dea 1.2, etc.

I'm interested in this myself, as we are developing a school program on genetics and would like to include this info if it is available. A quick Google search comes up with the Wikipedia page that includes dogs, cats, horses etc. that you mentioned, plus a couple of research papers on the grey opossum and a 1960 article on koalas. I suspect that this won't change unless a large number of people start to keep marsupials as domestic pets, and the inevitable large number of injuries or operations requiring blood transfusions by the local vet.


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What does ensemble-based model of enzyme mean?
I am reading Pan et al. (2000), a paper about dihydrofolate reductase (DHFR).  They claim using a ensemble-based model of DHFR.
What is a ensemble-based model?

Can you please link to the paper? Does DHFR means "Dihydrofolate reductase"?

@Remi.b,yes it is dihydrofolate reductase, I edited the question to add the link

An 'ensemble' is a set of related models of a structure.
For example, conformational ensembles describe the structure of flexible proteins. There is a database of such structures here : http://pedb.vib.be/.
When NMR is used to determine a structure, the result is an ensemble of structures (see this paper for a comparison with crystallography). However, it is possible to see multiple structures for crystallography as well. This paper on "Accessing protein conformational ensembles using room-temperature X-ray crystallography" describes limitations to the idea of crystal structures having one unique structure.

Does that mean: using a ensemble-based model of DHFR is using one conformation of DHFR (e.g. there might be multiple DHFR forms in E. coli, and the study used one of them)?


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Sickle cell life span
How long do sickle red blood cells "live" before being broken down in phagocytosis?
I had trouble doing a normal search as it brings up life span of those inflicted with the disease. Also, I have been doing a semester long assignment, where we are delving into all aspects of this disease, and I have 20 sources so far and still haven't come across the answer.

Try changing the order of the words. :) lifespan of rbcs in sickle cell anemia

A better title would be "Lifespan of sickle cells" (fewer words and no abbreviations). I'd change it myself, but am voting to close as there is no indication of which of the many sources on sickle cell anaemia the poster was unable to find the information in.

Hi Brittt,. welcome to Bio.SE. Please share a few of the sources you've already read to indicate to the community that you've done your own prior research. This will likely stave off a full close vote.

Sickle cells usually die after about 10 to 20 days, compared to normal red blood cells, which live an average of 120 days. The bone marrow can't make new red blood cells fast enough to replace all the dying ones which causes anemia,low blood count that results in fatigue,shortness of breath and related symptoms.As the cells are made normally but die too rapidly,this is termed as haemolytic.

Welcome to Biology SE! Although this could potentially answer the question we prefer to have answers backed up by references. Un-referenced answers may be challenged or flagged for deletion.


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Using nanodrop for analysing biological samples other than nucleotides
I am a 3rd timer postdoctoral fellow with some experience in molecular biology and biochemistry, but major skills in Zoology and Natural History. I am studying some natural extracts, and isolating compounds.
Some biological samples come in limited amounts (e.g. invertebrate haemolymph), hampering analytical methods that rely on larger amounts. For instance, establishing UV-Vis spectra of extracts is a usual non-destructive method for approaching unknown samples and estimating general parameters, done with a spectrophotometer.
The microvolume-scaled spectrophotometer system popularly known as 'Nanodrop' has been around labs since almost two decades now. Its use has been usually limited to fast purity & concentration estimations for DNA & RNA in molecular biology labs.
I am considering using the nanodrop to estimate parameter of other biological and chemical samples. The manual says most commonly used solvents are compatible with the system. I have however yet found no-one else who has tried using Nanodrop for different applications.
Please, anyone here who has experimented using a Nanodrop system with other biological samples and extracts could comment on the experience?

The Nanodrop is a generic UV-visible spectrophotometer. According to the manufacturer, the latest model can measure absorbance from 190 to 850 nm. Its dynamic range is also very good: from about 0.1 to about 60 in absorbance. Therefore, as long as you don't use an incompatible solvent, you can measure anything that absorbs in this wavelength range. I use it very often for purified proteins. It also works well for turbid suspensions (like bacterial cultures; reading optical density at 600 nm gives an idea of turbidity).
It is easy to use, and of course the low volume requirement is a big advantage. One drawback is that it won't let you fine tune certain parameters like a "real" spectrophotometer would allow (bandwidth, gain, etc.). But you can definitely get decent spectra for characterization of mixtures and concentration estimation of pure samples.

'you can measure anything that absorbs in this wavelength range' -- Yes, I have been trying out for the first time recently. But have you officially done it? My peers seemed revolted as they state a nanodrop should be used only for DNA/ RNA/ protein standards. They sounded so dogmatic.

Yes, I have measured absorption of fluorescent dyes that is nowhere near absorption wavelength of proteins or nucleic acids.
Using a Nanodrop only for proteins and nucleic acids seems like a lab policy (in my opinion, too strict and not justified), but it is definitely not a technical limitation of the instrument.

I used the Nanodrop for the measurement of the absorbance at 600 nm of bacterial cultures, as well as nucleic acid preparations. However, I switched to using another spectrophotometer (Spetrophotometer, Ultrospec 2100 pro, UV/Visible Spectrophotometer, Amersham Biosciences) for my bacterial cultures because I trust it more due to using a cuvette containing 1 ml of bacteria instead of just 1 microlitre of culture.

In fact some nanodrop models do have a special pedestal for measuring OD600 of microbial growth. I ought to have mentioned that in my brief intro for the question. My main issue is, as soon as I mentioned to peers I'd be using nanodrop with other biological samples they got revolted, stating 'a nanodrop should be used only for DNA/ RNA/ protein standards'. I was wondering why they sounded so dogmatic about it, and how readers would receive if I employed it otherwise.

Maybe some people measure their sample and retrieve afterwards and you are contaminating the system. They might be concerned that their sample gets contaminated?

Perhaps. Nanodrop is naturally unstable, and people may blame anything for a weird result. But if samples are soluble in compatible solvents, I see no logical point, and they really declared they believe it is designed solely for nucleotide analysis (which is not what it says in the manual).

After completing my tests, I have decided to come back to answer my own question.
A Nanodrop machine has served my purpose quite efficiently, as far as I can judge. I used have used it to evaluate the degree of purity of a natural alkaloid extract from insects, using synthetic alkaloid analogues as controls. See our published paper discussing the method here, along with raw data.
We have noticed no alterations nor cross contaminations to colleagues' DNA/RNA samples running in parallel, highlighting on the fact that I properly cleaned the equipment between use.
Therefore, yes: I recommend using the Nanodrop as a cheap & quick method to scan biological samples, provided chemicals and solvents used in cleaning the pedestal are compatible with the manual.
Hope this discussion help others dare!

@WYSIWYG I reckon we did what you describe, no? On using synthetic compounds as standards and doing a wavelength scan?

Sorry. I did not see it. Also, if you use the "UV-Vis" mode (I have nanodrop 1000), you can choose two wavelengths (in other assays, the wavelengths are fixed). I assume you used that.

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


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Why do mitochondria have a phospholipid bilayer?
So, a thought came up and I couldn't find all that much info online, so I thought I'd ask some professionals here!
The endosymbiont theory states that: mitochondria came to be ingested by bigger prokaryotic cells about 1.8 bYa, and by chance of luck came to a mutualistic relationship.
Now, mitochondria are said to have been archaea, right? But the mitochondria in our cells have phospholipid bilayers, with ester bonds in them, like all eukaryotes, but when you look at archaea, you see that they have monolayers because of their ether bonds, with rings and all sorts of branching, which is what gives them that extremophile-acclaimed resistance.
Question is if the endosymbiont theory is so widely accepted and mitochondria are meant to be archeae, why do they not present a monolayer with ether bonds?
Thanks for your time!

Only some archaea have a monolayer others have a bilayer, and the monolayer is believed to be a derived adaptation for extreme environments.

@xusr — I was going to make the same point, suggesting the poster change his question to why don't eukaryotes have an archae-like cell membrane. But rather as a joke. If you think about it, eukaryotes are assumed to have evolved from prokaryotes but in either case they don't have a cell wall. So the enclosing structure of eukaryotes evolved from that of their prokaryotic ancestor at some time. Anyway, that's a separate question.

I think there is a typo or a misconstruction in the sentence before the one I take issue with. "The endosymbiont theory states that: mitochondria came to be ingested by bigger prokaryotic cells ". Whatever was ingested was not a mitochondrion, but a prokaryote that became a mitochondrion. You should tidy this up.

I think the question is based on a false premise:

Poster: Now, mitochondria are said to have been archaea, right?
Me: Wrong, I’m afraid.

The closest bacterial relation of mitochondria is  Rickettsia, an alpha-Proteobacterium (see Lang et al. for a review). Rickettsia is a eubacterium, not an archaebacterium.
The confusion is probably due to misreading one of the two alternative theories of the origin of mitochondria. This is the theory that the host for the original mitochondrion was an archaebacterium (rather than a primitive nucleated eukaryote). In both theories this host aquired a eubacterium related to Rickettsia, which gave rise to the mitochondrion.

Ah, great reply! The actual misunderstanding had come from one of my teachers actually (actually just a PhD who got to give us a few lectures), you cleared it up!

@FedericoParravicini — Don't be too hard on your teachers. It's easy to make a mistake, especially if the main focus of your lecture is elsewhere, or even to trip over your tongue (a verbal typo). What I would recommend is to use web resources to check these things. I prefer text books to random websites or Wikipedia, as they are integrated and subject to editorial review and often well illustrated. If you don't have access to a good library try NCBI Bookshelf, which has old editions of some reputable texts such as Berg, Alberts and Lodish et al.

During the process of phagocytosis, the host membrane surrounds the food. So in this case, these bacteria were surrounded and encased in the host membrane, which pinched off internally, and became the outside membrane of the mitochondria.


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how origin of koi carp is different from goldfish
where did koi-carp originate? how are they different from goldfish? Wikipedia say that goldfish originated by genetic mutation but what about koi-carps?


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Why ambidextrous persons are so rare?
According to this article, only about 1% of all humans are ambidextrous:

About 90 percent of people are right-handed, says Corballis. The
  remaining 10 percent are either left-handed or some degree of
  ambidextrous, though people with "true" ambidexterity—i.e., no
  dominant hand at all—only make up about 1 percent of the population.

Less dominance is observed in other animals, as indicated by this article:

Bill Hopkins, at the Yerkes Regional Primate Research Center in
  Atlanta, USA, has made even more contentious claims in recent years,
  asserting that his captive chimpanzees exhibit a 70% right-handed
  preference for many tasks requiring manual dexterity, a rate that
  rises to almost 98% for very specific tasks, like the precise over-arm
  throwing of objects. However, for everyday food-related tasks (like
  cracking nuts or digging out honey), the rate remains closer to 50-50.

I am wondering if there is any theory that explains why ambidextrous persons are so rare. As a totally layman when it comes to biology it seems that this would require a more complex brain to wire all the complexity to both members and this would be rarely justified (virtually all tasks can be done without being fully ambidextrous).
Question: Why are ambidextrous persons so rare?

Speculation: Left-right hemisphere competition and dominance became more pronounced as our brains evolved to do more and more cognitive work. Hand dominance increased as a side effect and there was never any selective pressure to maintain ambidexterity.

It would be interesting to know whether, and to what degree, it is simply a matter of training.  That is, once a child displays handedness, perhaps in early writing or ball games, it is encouraged to practice doing things with the dominant hand.  But from my own experience, when one temporarily loses the use of that hand (as with a broken wrist), it is possible to learn to do many things adequately well with the non-dominant hand.

While not specifically answering why ambidextrous persons are rare, one potential explanation is that mixed-handedness and/or ambidexterity seems to be related to adverse effects. For instance, some studies have shown that mixed-handedness (which might not be exactly the same as ambidextrous, depending on how you define the terms) is related to ADHD symptoms (e.g. Rodriguez et al. 2010) and patients with schizophrenia have an overrepresentation of mixed-handedness (Green et al, 1989; Orr et al, 1999) and ambidexterity (Crow et al, 1996).
A potential reason for the adverse effects seems to be that mixed-handedness and ambidexterity is related to delayed or weakened dominance of one cerebral hemisphere, which is important for language development (see e.g. Crow et al, 1996). See also this quote from Intelligence and the ‘Intelligence Quotient’ (Crow, 2001 from Encyclopedia of Genetics):

Handedness, reflecting cerebral dominance, is a trait that is associated with quantitative variation. Whether this variation is a correlate of human cognitive ability, as would seem plausible if it underlies the specific characteristic of language, has been much debated, but it now appears that lesser degrees of lateralization (‘hemispheric indecision’) are associated with delay in the development of verbal, and also nonverbal, ability (Crow et al., 1998). Thus it appears that lateralization is associated with significant variation in the rate at which words acquire meaning, and that this variation reflects a dimension that is specific to Homo sapiens.

This is not my area of expertice thought, and others more knowledgeable about the field can maybe expand on this or explain more in detail.


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What are these colonies on my Bacillus pumilus lawn?
I am growing Bacillus pumilus and I have plated some on agar plates. Now I can see some colonies on top of the lawn.

Does anybody know what they could be? A contaminant? Bacillus pumilus? I have observed some people growing Bacillus pumilus, and the colonies they streaked looked different than mine. Could it be that B. pumilus has several colony phenotypes?


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After the primer is removed from the leading strand, how does DNA polymerase I add dNTPs without a 3'-OH?
I have a question about replication in prokaryotes. I learned in school that:

DNA polymerase needs 3'-OH to add a dNTP.
The chromosomes of prokaryotes are usually circular.
The primer in the leading strand (of course the primers in the lagging strand too) is removed by the 5'→3' exonuclease activity of DNA polymerase I.

It makes sense that on the lagging strand the primers are removed and then replaced by new dNTPs using the 3'-OH of the previous Okazaki fragment. However, for the primer on the leading strand, there is no Okazaki fragment upstream and thus no 3'OH that DNA polymerase can use for polymerisation.
How is the primer replaced by new dNTPs on leading strand?

It seems you're asking about the leading strand, but you may have made a typo that made it unclear what you are actually asking. I tried to clarify your question, but please roll back the edit if it changed the meaning.

@canadianer — I think you must be right. I have had to scrap my answer which assumed the lagging strand, because the question makes no sense for the leading strand where the primer is the growing DNA chain which is not removed.

@David Sorry for making your original answer obsolete. However, the leading strand does have a primer at the origin of replication that needs to be removed. The gap can be filled using the upstream Okazaki fragment as a primer. See this image for example.

@canadianer — No problem about my original answer. And you're right, but I wasn't thinking about the ori. I doubt the poster was either, but I guess I should update my answer to cover that. That way it will be of some value. Tomorrow perhaps.

@canadianer — where was your figure from? I have now  extended my answer and should acknowledge the source.

@David Nice update. The image is from the following website: http://www.mun.ca/biology/scarr/iGen3_03-09.html

Can someone please explain what they mean by stating that the RNA primer on the leading strand does not need to be removed? I mean it is an RNA hybrid. The DNA pol cannot initiate replication by itself and can only elongate the primer. Thus primer removal is required. I have the same question as the poster and haven't found a satisfactory answer as yet. If someone does, pls do share.
Thanks!

@SarveshAnandas — If you are referring to the statement in my answer you should comment on my answer, not the question. But I would read that answer again, where I first talk about the situation at the replication fork (where the leading strand is not being primed by RNA) and then consider the case of the origin of replication (where it is and needs to be removed).

The leading strand post-initiation
First consider the DNA replication fork after initiation has occurred.
The 3′-OH primer on the leading strand is the 3′-end of the strand of DNA being synthesized in the 5′ to 3′ direction (circled in the diagram below, modified from Berg, Biochemistry). It is not removed because there is no need to do so. (The primer on the lagging strand is only removed because it is RNA.) So the problem posed in the question does not arise.
Remember that the reason for Okazaki fragments is that there is no DNA 3'-OH primer for the lagging strand, so a temporary RNA 3′-OH primer is generated instead, RNA polymerase — unlike DNA polymerase — is able to copy DNA without a primer. There is no such problem for the leading strand.

The leading strand at the origin of replication
As @canadianer points out in a comment, the remarks above do not apply to the initiation of DNA replication, the single instance where the leading strand must have an RNA primer. In the case of prokaryotes such as Escherichia coli replication proceeds in both directions so that a short time after initiation one has a replication bubble as shown in the figure below (adapted from Russel, iGenetics) :

It can be seen that, at the origin, the 3′-OH of the DNA from the lagging strand of the other direction of replication (boxed in red) can act as a primer for the DNA synthesis function of DNA polymerase I, after its exonuclease activity has removed a nucleotide from the start of the RNA primer on the leading strand.
References
Berg et al. Ch.27
The Cell, Ch. 5
Sandwalk: Blog page
Footnote
There was a typo in the original question which caused confusion about which strand the poster was concerned with. This answer assumes the leading strand.

I am very sorry for my late response, and I guess someone already modified my question, but indeed my question was how the primer on the leading strand at the site of initiation could be replaced by a DNA fragment when there is no 3OH' (on the lagging strand, the 3OH' of an okazaki fragment just behind the primer can be used), but as you say, we have a 3OH' from the lagging strand which results from the replication in the opposite direction!!! Wow, that was very interesting. Thank you.

However, I still have a small question if you allow me. I thought that the leading strand starting from the Ori would continue until the very end (when two forks meet) without any addition of another primer, so I'm confused about the first diagram. Does it mean that during the replication in procaryotes (my question has been always the case on procaryotes), on the leading strand, far from the initiation site, a few primers are added and in this case they are DNA primers? Or the explication with the first diagram is a general description of the replication in eucaryotes? Thank you so much.


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Gene terminology - is one gene a concrete, single physical sequence?
Suppose you have two identical copies of the same, coding nucleotide sequence (e.g. two copies of BCL2 - a random gene I found on Wikipedia).
Could you say that these are two genes (i.e. the name "gene" refers to a specific, physical sequence, and where there are two of them, you have two genes, even if identical)? Or just two molecules of one gene (in the same way that when you have two molecules of carbon dioxide, you can't say that they are two carbon dioxides)?

You should familiarize yourself with molecular genetic terminology by reading some of the literature. It differs in many respects from chemical terminology, and the gene was defined in non-chemical (genetic) terms before its chemical nature was determined. Search especially for "gene duplication" to see how this is referred to. Then come back with more specific points if this does not answer your question. (And "two molecules of one gene" means absolutely nothing.)

'just two molecules of one gene'.
They are the same gene. Gene is more of an abstract concept. We say for example that humans have ~ 20,000 protein-coding  genes. It does not mean that we have only 20,000 molecules, one for each gene. We have many more molecules of course. What we mean is that we have 20,000 different entities, each coding for a specific type of protein. If you have two molecules of a sequence in a tube, it becomes questionable whether these sequences can be thought of as genes. I would say that those sequences lose their 'genicity' or their property of being genes because they are not coding for anything in a tube. They lack the cellular machinery that makes them code for something. I would just say you have 2 nucleotide sequences of the gene BCL2 but not that you have 2 copies of the gene BCL2. It's maybe just a personal difference I see though.

A gene is more a functional unit in the genome. As such if you have, say, 5 sequences of the same gene, you will say that you have 5 copies of this gene but you won't say that you have 5 genes. If you say that you have 5 genes, then we would think that you refer to 5 different loci (locus = position in the genome).
Note that if you are not familiar with the term allele, then you will want to check it out. An allele is a variant of a gene. Again, an allele is more the information in the sequence than the sequence itself (a gene is typically a coding region). Therefore, if you say that at gene BCL2, there are 4 alleles in the populations, that means that there are 4 possible variants in the population, not that the whole population is made of only 4 physical sequences of this gene.


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Is there any research on wolf and bobcat interactions?
I'm studying interactions between North American predators, specifically wolves, coyotes and bobcats.
There's evidence from data I've collected from game cameras that suggests a significant interaction between wolves and bobcats. However, I haven't found published literature or reports on interactions between these two carnivores besides a paper by Stenlund (1955) that suggests bobcats may benefit from scavenging wolf kills.
Does anyone know of any publications in peer-reviewed literature, government reports or even reliable observations from biologists in the field on interactions between wolves and bobcats?
Thank you!

In Sweden, no clear evidence have been found for interactions between wolf and European bobcat (Lynx lynx), see Wikenros et al, 2010. There, they have studied effects of wolfs on the survival of Lynx kittens, spatial movement of Lynx and Lynx' homerange size. The study finds no significant difference in any factor with/without wolves. They also speculate that the reason for a lack of interactions is that the two species use quite different main food resources (at least in Scadinavia); Lynx being specialized on Roe deer and wolves having wider preferences, but mostly Moose.
You should also look at the report Meta-analysis  on  the  effect  of  competition  between  lynx  and wolf on their diets (Lelieveld, 2013 which might provide more information. From reading the abstract, the report indicates no effects on wolves but that Lynxs might change their foraging behavior.


text:
Is the axon part of a Schwann cell or no?
Whenever I see diagrams of a neuron, it always shows the Shwann cells around the axon, but it doesn't seem as though anything distinguishes whether the axon is a component of the Schwann cells or not, or whether it's a component of the cell body itself (whatever that's called).

Your question isn't very clear, I think you have a bit of confusion in your use of terminology.
The axon is a part of a neuron, it's membrane is continuous with that of the cell body (also referred to as the 'soma'). Schwann cells are not neurons, they are a type of glial cell found in the peripheral nervous system. Schwann cells wrap their membrane around the outside of the axon to insulate it; this process or the presence of this insulation is called "myelination" and allows for faster transmission via saltatory conduction.
Cells that provide a similar function in the brain and spinal cord are called oligodendrocytes.

I think the fact that you just answered my question in detail proves it was clear enough. I asked if the axon is part of the Schwann cell, you clearly indicated "no" by explaining that the Schwann cell merely wraps around it and that the axon itself is an extension of the neuron. But despite that misunderstanding, thank you.


text:
How does the body regenerate nerves?
If neurons come from neuroblasts which come from neuro stem cells that are embryonic, how is it possible for an adult to regenerate nerve tissue? Are neuro stem cells created during later stages of life, and, if so, where? Or is it solely a finite repository of stem cells somewhere?


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Are mutations the cause of alleles?
For example, some leopards have a mutation which causes black fur. So Black fur and normal fur colour (orange-white) are both alternate forms of the same gene, right? So does that mean that mutations cause alleles?
Thanks

That's correct. Alleles are alternate forms of a gene that occur at the same locus and arise by mutation.
Another example might be sickle cell anemia where a SNP (a single base change) is the cause of the disease.

Not correct. Alleles can be identical. They are just copies of the same gene. You get one copy from Mom, and the other from Dad. Alleles need not be alternate forms. Mutations cause variation.

@KarlKjer OED: "Allele: Each of two or more alternative forms of a gene that arise by mutation and which may be found in the same position on a homologous chromosome." Can you point to a source that unambiguously uses 'allele' in the sense that you are suggesting (i.e. as a synonym for 'copy')?


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HOW is the Gallbladder attached to the liver
The gallbladder’s function is to store bile from the liver which is delivered through the cystic (bile) duct.  The cystic artery is also connected to the gallbladder to deliver blood.  (Correct me if I am wrong about any of this.)
However, when I was watching a gallbladder surgery video on YouTube, in the process of removing the gallbladder the surgeon clips the bile duct and artery which I understand but he/she also cauterises the gallbladder off the liver.  I also understand that The cauterisation is to prevent bleeding.
BUT the question is WHY is the gallbladder attached to the liver in the first place?  WHAT purpose does being attached to the liver serve? Does it provide stability? Because I always thought the gallbladder just sits beneath the liver.  Most importantly, HOW is the gallbladder connected to the liver?  (This maybe be more of a chemistry question), what bonds is it connect through, what/which biomolecule connects it and why is it that biomolecule/ bond that is used.
As watching the video,  I also noted that the surgeon didn’t clip the cystic vein, or even mentioned it.  Maybe I am wrong and he/she did clip the cystic vein but I didn’t see, would you also be kind enough to explain to me why the surgeon didn’t clip the cystic vein or if he did why it wasn’t pointed out.  Also tell me more about the cystic vein where is it located because it’s very hard to find clear diagrams with them...(is it because it’s small)

Hi welcome to Bio.SE! Posts should not contain multiple questions. Please remove the final paragraph of your post as it has nothign to do with the main question. You may opt to post it as a secondary question in a separate post.

1. Gallbladder attachement to the liver
In this video (check from 55 sec on), you can see that the gallbladder is covered by a thin sheath that wraps the gallbladder; the sheath extends to the liver and intestine and thus keeps the gallbladder in place. The sheath is a part of the abdominal membrane (peritoneum) that covers most of the abdominal organs. You can see that the surgeon is cutting the sheath.
2. The Cystic Vein: The Significance of a Forgotten Anatomic Landmark (PubMed Central)

...there is no cystic vein per se, but the venous drainage is
  through the bed of the liver [between the attachment surfaces of the
  gallbladder and liver]...however..Gray's
  Anatomy of the Human Body...describes cystic veins which join at the
  neck of the gallbladder to form either single or double cystic veins
  which flow along the cystic duct and upward along the hepatic
  ducts.

there are also accessory ducts (Luschka) that can connect to the gall bladder directly. Not all bile enters the gall bladder through the common bile duct. These additional ducts need to be sealed to prevent bile being leaked directly into the body cavity.

@John, that's a valuable info.


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When does genetic randomization happen?
When two parents (regardless of species) reproduce in sexual reproduction each offspring is generally a random combination of genetic traits from each parent. Their developed traits then depend on the expression of each of their genes per established genetic combinatory science. All well and good.
Now my question - when does the actual randomization of genes for a given offspring happen? Does it happen when the individual sperm and egg cells are formed, or does it happen when they combine?
So does every one of a female's eggs have the same genetics, and every one of a male's sperm have the same genetics, and when the two combine it is randomized to form the zygote?
Or is each egg unique and each sperm unique, and already "pre-randomized", and the combination to form the zygote is then a straight-forward addition?
Or is it some variation or combination of those two options? Maybe the answer actually even differs across species, or across plants vs animals, or fish vs mammals, or something?

Randomization is the act of making random. I have corrected one clear misuse. While an enquiring mind is to be commended, it's owner should learn how to find the answers to its questions himself using the sources available on the internet if he does not have access to a University library. And, indeed, that is what SE Biology expects of posters (see the Help). Google for NCBI Bookshelf, where you can find older editions of standard textbooks in cellular and molecular biology. If these do not answer your question, then post citing the information provided and how it is deficient. Have fun!

Randomisation happens in the forming of the the egg and the sperm. In a first approximation, the egg and the sperm receive a random single chromosome of each of the chromosome pairs during meiosis.
More randomisation happens due to the possibility of crossing over when homologous chromosomes exchange chromosome parts.
EDIT: In terms of the question, bothe the egg and the sperm are pre-randomised.

Your view of the randomization of the parent traits seem a bit wrong and it makes the question a little unclear. But still, I think we can answer it...
The randomization happens at the moment of the creation of sperms and ovules. The two "randomizing processes" are segregation and recombination.


text:
What do memory cells actually do?
So I know that memory cells "remember" the most efficient way to kill a pathogen should it show up again... but what is the mechanism by which memory cells become activated by the second contact with a pathogen? How do they interact with the other immune cells to enhance immunity?
For example: phagocytes engulf pathogens and plasma cells release antibodies, but what do the memory cells actively do?

I think memory cells will efficiently do clonal expansion so that it can produce immune cells which can actually remove the pathogens quickly compared to the first time as it now remembers the method it used before.

Can you provide evidence for why you think this? Unsourced or opinions can/will be challenged.

Sure, I read it from Immunobiology: The Immune System in Health and Disease. 5th edition.

On the first entry of a pathogen a division of B cells produce memory cells that remember the details about the pathogen to protect the body during it's next entry.
On the second entry of pathogen, the memory cells get activated and activate the remaining cells of immune system to kill it.

This is basically a part of Secondary immune response which lasts longer than primary immune response( the response where the memory cell encounters the pathogen for the first time).

The process of activation of memory cells is still unknown and scientists are working on it.
The Secondary immune response makes a person immune to various diseases. That's why, a person surviving disease like Chicken pox, Small pox, Measles, etc. gets lifetime immunity to such diseases.
The concept of vaccinations are also based on the concept of "memory" of our immune system.

One the first entry of a pathogen some B cells produce memory cells that remember the details about the pathogen to protect the body during it's next entry. The process of activation of memory cells is still unknown and scientists are working on it.

Edited the answer. Hope you understood the answer.


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What is the point of storing biological samples in Trizol/TriSURE before RNA extraction?
The Wikipedia article on Trizol says that it helps break the cells and maintain RNA integrity during homogenisation of samples. Does anybody know by how much Trizol improves RNA integrity compared to homogenisation without it? If somebody is extracting RNA from tissues without first storing them in Trizol, can you please tell me about the quality of your RNA?

These reagents denature RNases to protect RNA from degradation.


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Plant determination: Lilium monadelphum versus L. szovitsianum
Lilium monadelphum, L. szovitsianum and L. armenicum belong to group of yellow flowering Lilium species and they are both often cultivated.
These species come from Caucasus area, so the first two are both described in the Flora of SSSR (4th volume). However, I find the dichotonic key description incomplete, and, based on the key, I am not able to clearly distinguish these species. Lilium armenicum is described by some authors as a variety of L. szovitsianum or as a subspecies of L. monadelphum.
What are your experiences with determination of these species?


text:
Does imprinting occur at different life stages?
For example, consider the offspring of a bird species. Can offspring get imprinted by other individuals of the same population at various life stages (e.g., hatchling, nestling, fledgeling, juvenile)?
If you have any literature, please send the links.


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IgA-s in an immune system vaccined intramuscularly against Hepatisis A
As IgA are immunoglobulins associated with secretion and mucosis membranes, I am interested whether after intramuscular vaccination with Hepatitis A vaccine IgA antibodies will be produced by the immune system before an actual infection?
Also, would they be secreted into breast milk, intestine lumen etc. before the infection coming in a traditional (gestational) way?
Or does it take to have the antigen presented at the mucosis mambrane to start IgA production or secretion?

Antibodies are produced after exposure to cognate antigen.
Remember that B cells start off expressing membrane IgM and/or IgD. IgA requires class switching recombination at the B-cell receptor locus to the IgA isotype. Further differentiation of the B cells to antibody-secreting plasma cells results in soluble IgA production and immunologic memory to the antigen. Whether you'll get IgA, IgE or IgG antibodies against the vaccine will largely depend on the signals they get in the muscle, however (Figure 1). I think IgG is largely a result, since the tissue antiviral response is often interferon gamma (Figure 2).
The importance of intramuscular vaccination is outlined here, just in case it wasn't apparent.

Figure 1. Activated helper T cells that can recognize the same antigen mediate the class switch by providing co-stimulatory signals and cytokines. Source

Figure 2. Class-switching continued. Source: Parham, The Immune System, 4th Ed.

Then I see it is unlikely to have IgA produced after vaccination, am I right? As a side note - the linked paper seems to compare only muscle/fat injections, but no oral delivery.


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Lipid Diffusion
Epithelial cells in the small intestine absorb lipids through simple diffusion but how does diffusion of lipids occur in the first place if they are insoluble in water? I thought that substances need to be dissolved in order to have concentration and therefore a concentration gradient?

Insolubility means they don't dissolve in water and may self-associate. That doesn't mean they cannot exist in aqueous environments. I'm not sure this question is clear enough to answer accurately.

Do you actually have a reference that supports your understanding as being correct?

http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_lipids.html     "The major products of lipid digestion - fatty acids and 2-monoglycerides - enter the enterocyte by simple diffusion across the plasma membrane. A considerable fraction of the fatty acids also enter the enterocyte via a specific fatty acid transporter protein in the membrane." Essentially I would like to know if a non-soluble substance could diffuse in water because my current understanding is that only dissolved substances can.


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Why it is important to vaccinate a human newborn within 24 hours since birth?
In Poland a newborn has to be vaccinated within 24 hours against hepatitis B and tuberculosis.
As I understand it is good to be vaccinated against both, I do not see the need to hurry so much.
Hepatitis B is transmitted sexually or by blood. The former vector is definitively unsuitable for a newborn, and the latter... Well, I do hope so far all Polish hospital adapted to Ignaz Sammelweis advice on antiseptics.
In case of BCG vaccine against tuberculosis (containing alive bacteria) there would be an additional risk if the newborn's immune system were in any way impaired which is unknown within first 24h. It is not that tuberculosis is common disease in Poland - is endemic (probably due to the obligatory vaccination indeed).
What possible biological benefits are there to vaccinate a newborn so early? Especially which of them prevail over possible risks of BCG vaccination?

What is the route for maternal to child hepatitis b transmission?

@GrahamChiu possibly, but if the mother is positive, then child shall be rather given antiglobulin as it takes time to build active immunity

Well, in the Netherlands we don't vaccinate so early and AFAIK we don't vaccinate children against heb. B and tuberculosis at all. So it is not that important. I can only guess that they do it because they are afraid the mother might carry hepatitis B.

And how long is hbig effective for?

@BenBolker agreed

@GrahamChiu I guess no longer than transplacentally transmitted IgGs, which I estimate to be at least several months ($T_{\frac{1}{2}}$ is about 1.5 month). The problem is that AFAIK children of HepB+ mothers are not given antiglobulin as there is no HepB screening at all.

Since another posted answer addresses HepB vaccination at least as effectively as I would have, I'll say something about first-day scheduling for BCG, which is consistent with WHO guidelines (emphasis added):

In countries with a high burden of TB, a single dose of
  BCG vaccine should be given to all infants as soon as
  possible  after  birth.  Since  severe  adverse  effects  of
  BCG vaccination are extremely rare even in asymptomatic,  HIV-positive  infants,  all  healthy  neonates
  should be BCG-vaccinated, even in areas endemic for
  HIV ...

(it goes on to discuss recommendations for symptomatic HIV-positive infants. I didn't look at the details of the Polish vaccine policies, but I'd be extremely surprised if there weren't an exception/variation for newborns who are known to be immunocompromised. We can argue about the frequency of newborns who are immunocompromised based on factors that are unknown before birth [i.e. not based on known factors such as genetics, mother's condition, etc.] ...)
I'm admittedly speculating a bit here, but based on what I've read it seems that the main reasons for "as soon as possible after birth" are (1) to allow for development of immunity and (2) logistics, i.e. increasing the actual coverage achieved.
Development of immunity: it takes time for immunity to develop, so the issue is not that babies will be exposed to Tb in the hospital, but that they may be exposed before the vaccine has taken effect. Gaisford and Griffith 1951 quote Wallgren (1950) as saying that effective immunity may be delayed by 10-12 weeks. More recently, Saroha et al 2015 say

BCG vaccine induces delayed type of hypersensitivity reaction and cell mediated immunity (CMI) in the host 4–8 weeks after immunization.

Logistics: Oberoi et al. 2017 report on changing scheduling of BCG vaccination in Indian clinics:

Rescheduling of BCG dose, from twice weekly to daily, the coverage of BCG and OPV zero dose increased from 54% (in 2014) to 78% (in 2015), and a marked increase from 8.2% to 42.9% was noted for the birth dose of hepatitis B.

Is Poland a high-incidence Tb country?

Tb incidence in Poland in 2016 was about 18 per 100,000: based on this map, that's about twice the level of most Western European countries (and more than triple the rate of Canada, which is what's referenced in the link you give above about dangers to immunocompromised people), but half to a third of levels in the former Soviet Union ...
The World BCG Atlas shows that vaccine policies follow a similar geographic pattern - BCG is used in Eastern but not in most of Western Europe

the rate of adverse advents following BCG vaccination in Poland is low and hasn't changed much after changes in timing of vaccination:

It is generally estimated that local adverse reactions usually occur at the rate of 0.1 to 0.5 per 1000 vaccinations, and serious disseminated complications occur at rate of less than 1 in a million vaccinations

Some research studies suggest that delaying vaccination for a few weeks may have different (better or worse) effects (e.g. here, here).

There has been a long standing shortage of bcg which is diverted for bladder cancer use rather than vaccination here in NZ.

In the US, infants are vaccinated against Hep B at birth and again a month or two later as well, because of the risk of maternal transmission. If the mother is known to be HepB positive, HBIG will also be administered.

Perinatal HBV transmission can be prevented by identifying HBV-infected (i.e., hepatitis B surface antigen [HBsAg]-positive) pregnant women and providing hepatitis B immune globulin and hepatitis B vaccine to their infants within 12 hours of birth.

The reason for the HBIG is obvious, but it doesn't last for life. Therefore, the vaccine and its booster.

Hepatitis B virus (HBV) infection in a pregnant woman poses a serious risk to her infant at birth. Without postexposure immunoprophylaxis, approximately 40% of infants born to HBV-infected mothers in the United States will develop chronic HBV infection, approximately one-fourth of whom will eventually die from chronic liver disease.

In countries where HepB is not prevalent, there is little cause to immunize at birth. However, it is too common in the US.

Preventing perinatal HBV transmission is an integral part of the national strategy to eliminate hepatitis B in the United States. National guidelines call for the following:
  - Universal screening of pregnant women for HBsAg during each pregnancy
  - Case management of HBsAg-positive mothers and their infants
  - Provision of immunoprophylaxis for infants born to infected mothers,   including hepatitis B vaccine and hepatitis B immune globulin
  -Routine vaccination of all infants with the hepatitis B vaccine series, with the first dose administered at birth

The risk of HepB vaccine is low. The seriousness of the disease is high. It is not only the mother who might be a carrier. There are many unidentified carriers in the US. That makes the risk-to-benefit ratio low. Driving your newborn home in an automobile is probably more of a risk than the vaccine, but most people do so anyway, and do so many, many times over the course of the baby's life.
In the US, we do not routinely vaccinate against TB, so I cannot address that issue with any degree of expertise. The risk-to-benefit ratio is not as low as for HepB. It is given to children who are continuously exposed to someone (say, a parent) with active TB, or in certain communities where TB is very prevalent. Obviously, if the risk of SCID (severe combined immunodefficiency) is high, the risk of the vaccine is much higher, and some infants have died from it.
Discussing the risk to benefit ratio of all infant vaccines is too broad for this venue.
Separating Fact from Fiction in the Newborn Nursery: Hepatitis B Vaccine for Newborns
The benefits and risks of bacille Calmette-Guérin vaccination among infants at high risk for both tuberculosis and severe combined immunodeficiency: assessment by Markov model

I guess that also risk of HepB infection within first months of life is also lower than of a car accident due to its way of transmission. Of course given that we trust our healthcare to follow antiseptic guidelines, which was not the case in early 90' in Poland (as it was common practice to use dry-air autoclaves that time, which AFAIK do not inactivate HBV).


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Simple Autosomal Recessive question by a novice genetics student
How do you figure the percentage of offspring that will be a carrier of an Autosomal Recessive gene when the FATHER is the recessive carrier and the MOTHER is not affected (normal, no recessive)?  Thank you for your assistance.

Do your cross diagram and multiply the correct combinations together:
Father: Rr
Mother: RR
Since it's autosomal:
Chance of getting R from father: 50%
Chance of getting r from father: 50%
Chance of getting R from mother: 100%
You're looking for the chance of receiving Rr, which requires r from the father and R from the mother.


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Ingestion of cellulose digesting prokaryotes?
If humans digest cellulose digesting prokaryotes,  can  we start digesting cellulose like cows?

How would we get the three additional stomach chambers, and the time to eat this stuff?