text:
Microarray data and analysis tools
Microarray has various uses, and to analyse the data a main function classification is used. There are many methods used to classify the data but what are the best and most frequently used methods? Are there any well-known, web-based tools for microarray analysis?  Where can I find datasets of gene expression profiles, where I can find and understand the matrix of the dataset?

try the bioconductor package.

Sebida and DGRP have data available

Come to think of it most or all gene expression data has to be deposited online - try looking at the gene expression omnibus. And I echo recommending bio conductor (in R)

This is a fairly broad question and a book or two will give a more complete answer.  I'm assuming you are interested in expression microarrays.  Genotyping microarrays are also very popular these days and are quite different though.
Where can I understand the matrix of the dataset ?
This is a little unclear as a question, but I'll start with a numerical description.  Microarray data is reducible to a one dimensional array of intensities.  As a vector of numbers, each representing the amount of a given species of RNA in a sample, it has many interpretations.  Most of what is said here applies to RNASeq data too.
These numbers are sequence dependent - that is, they should not be interpreted as an absolute count of a specific mRNA in the sample, so comparing two entries in the vector (e.g. "gene A has 10% more RNA than gene B") will probably not be useful.
For this reason, microarray experiments are typically done as difference experiments, where two or more conditions are compared, producing a matrix of numbers, where N rows represent N experiments, and the M columns each represent a probe set / gene.  The transpose of this matrix is also common.
**Methods to classify microarray results. **
Taking the matrix of data, there are many ways of interpreting data in matrix form and most of them have been tried credibly with microarray data.
The most common are to take a set of probe sets whose biological action are related (e.g. all in a metabolic pathway and display them as a heat map where the columns have been clustered by a distance based algorithm to produce a tree, where neighbors have the greatest numerical similarity.

For purely numerical methods, Principal Component Analysis is often used (despite the fact that this is not a great method), but Self Organizing Maps, neural nets and just about any machine learning algorithm have been used.
Most common method by far though, is Analysis of Variants (ANOVA), where the probe sets/ genes have been scored by their greatest to smallest variance.  The most common case of this is a two condition difference experiment where the largest differences are taken as results.  This is not a great experiment, but the data is not super cheap to produce.
**Microarray data repositories **
Gene Expression Omnibus (GEO) is a highly regarded repository for microarray data, with over a million sets of data. They also have some tools, see below.
EMBL ArrayExpress claims to have slightly more data than GEO (1.2 M assays).
There are many many specialized microarray websites, mostly focusing on a particular organism (E coli for instance) or problem (like cancer).  Google is pretty helpful for this sort of thing once you have the right keywords.
**Web based tools for microarray analysis **
There are several tools you will use for microarray analysis and there are lots of websites for different aspects of this data.  I'm going to cite a couple, but the most commonly used tools are command line tools like R/bioconductor or the software that comes from the array manufacturer.
GEO2R is a great tool to browse expression data experiments.  It does a simple version of ANOVA and will really help you find some cool biology quickly.
VAMPIRE is a web analysis suite for microarray analysis.  Scaling the data into numbers from images to intensities to data analysis to compare several arrays.  Its probably one of the most comprehensive analysis sites out there.

"Principal Component Analysis" not "Principle Component Analysis". It analyses principal components. Misspelling it may demonstrate why you find it a problem, because you need to understand the principles behind the principals.

I don't see why you would not  be predisposed to using PCA but yet pre-disposed to accepting proximity clustering and self-org maps. It doesn't matter which chicken lays the egg. They are chicken eggs.

I don't it is a discussion we should indulge in, in this comments section - but in short, the people using it (in the link you provided) may not understand the meaning of "principal components".


text:
Number of dopaminergic neurons in VTA
Do you know an authoritative source for the approximate number of dopaminergc cells in the ventral tegmental area (VTA)?
Ideally I would like to know this for mice, rats, as well as humans, but one species alone would be a nice start. I have looked for this via google scholar and pubmed, but found nothing.

Integrating the information from @WYSIWYG's excellent answer, it appears the dopaminergic neuron count lies at:

4k for mice - Triarhou, 1988
10k for rats - German and Manaye, 1993
250k-440k for humans - Rice et al, 2016

Approximately, 250000-440000 neurons in Humans (Rice et al., 2016).

The substantia nigra/ventral tegmental area (SN/VTA) complex is a
  heterogeneous collection of dopaminergic cell groups that extends from
  diencephalic to mesencephalic territories in many vertebrates,
  including rodents, non-human primates, and humans (Puelles and Verney
  1998; see as reviews Smits et al. 2006; Smidt and Burbach 2007; Smits
  et al. 2013). The SN/VTA contains the largest number of dopaminergic
  neurons in the brain (see as reviews van Domburg and ten Donkelaar
  1991; Haber and Fudge 1997; Nieuwenhuys et al. 2008), with average
  estimates ranging in most studies from approximately 250,000 –
  440,000 dopaminergic neurons within the complex (Bogerts et al.
  1983; Hirsch et al. 1988; van Domburg and ten Donkelaar 1991; Damier
  et al. 1999a; Kubis et al. 2000).

Thank you. Any ideas about the other species?

@TheChymera no idea. I'm also relying on Google scholar and pubmed. I have no expertise in this field.

source: Stack Exchange

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

sort: votes


text:
Multiplex PCR, shorter amplicon inhibiting longer amplicon?
I want to run multiplex PCRs for my genotyping, with a primer pair targeting my construct and a primer pair targeting some housekeeping gene (sort of a built-in control).
I designed the control amplicon to be very short (I tested 3 primer pairs with ~120, 85, and ~50bp amplicons respectively). The main rationale behind this being that usually my amplicons are ~200-400bp, and I want something clearly distinguishable, but shorter rather than longer (I want to keep my options open for longer target amplicons).
In any case, regardless which control primer pair I use, whenever I try to multiplex I only end up seeing the shorter amplicon. See the gel picture below for an example (lanes: 1-ladder, 2,3-target+control, 4,5-control, 5,6- target).

I see that lanes 2,3 have a very faint additional smear compared to 4,5, but I want a band for my target amplicon. Also, my shorter bands are quite blurred.
Also, just for reference, my amplicons do not overlap at all.
So, I guess my questions are:

Why is the longer band disappearing?
Why is the shorter band so blurred?
What can I do to prevent this form happening?

How far are the construct and the housekeeping gene from each other? If they are close there might be transcription interference occuring.

As long as the amplicons do not overlap, I don't see how there could be any direct interference. In any case, they do not overlap and are on different chromosomes.

Overlap is not necessary for transcription interference to occur, but since your genes are on different chromosomes it should not be the case. Did this setup worked before or this is the first use of these set of primers?

What are the $T_m$ of these primer pairs? If one primer pair is significantly more stable at a given temperature, it could explain your results.

58-60°C for all primers. All 3 PCRs are run under the same conditions - would you say that there is no polymerase left to be recruited by the less stable primers?

50bp amplicon is not a good idea.. They will look like primer dimers.

True, I guess that can become problematic if I ever end up using dimerizing primers. Still, the same problem happens with 120 and 85bp.in fact,the figure you see here is 85bp

It turns out that the $T_m$ was in fact the issue, or rather, that the computation algorithm overestimated the $T_m$ of the primer pair for the longer amplicon (or underestimated that of the shorter one). At any rate, it seems that at 60°C the shorter amplicon primers hijack the polymerization mechanism.
Setting the annealing phase temperature to 55°C solved my issue, and now I consistently get better results:

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


text:
How do bees and wasps react to carnivorous plants?
I seem to recall that bees and wasps have alert pheromones, so that if a few of them are killed or attacked in the proximity of others, they will attract backup.
I assume it's pretty straightforward how this would work out if I were to start swatting bees next to their hive, but how does it work if they're killed by... a plant?
Would the bees try to sting or choke the plant? And if it doesn't work would they ever give up?
Would they alternatively realize it's a plant and therefore can neither be compelled to move nor harmed by venom? If so would they be aware they can do more damage to it with their mandibles than with their stingers?
Conceptually, I guess the experiment would be pretty easy — placing an array of carnivorous plants right in front of a beehive — except my carnivorous plants are still very small and rarely eat, and I don't own bees and don't have any wasp nests in the area.
Has anybody tried this or observed it in the wild?
I'd also be curious whether it's any different for e.g. Venus flytraps and pitcher plants. The former would likely get filled up rather fast if swarmed, whereas the latter could be able to swallow a large part of a hive. Also, venus flytraps actually move, so perhaps that might trip off the animal-pattern-recognition of the insects whereas a pitcher plant might more readily be identified as a plant.

There is a rather easily discovered Reddit thread about "bees stinging inanimate objects" where pest exterminators have chimed to say that bees do sting anything they perceive as a thread whether animate or inanimate objects, and that only when stinging mammals do they lose their stinger since mammal muscles contract upon stinging causing the stinger to become lodged. They claim when other things are stung they are either too hard or the stinger can be pulled out. I have not checked the veracity of these claims.

I'm not going to directly answer your question (which I think is an interesting one) because I do not have the data. However, I do want to share some anecdotal experience with you. (As such, my answer should not be accepted, but rather supplemental.)
Insects trapped by plants appear to be just that: trapped by a plant. They react much differently in a flytrap, for example, than in the palm of a hand. In other words, their reaction seems much more passive vs aggressive -- even when I've seen this happen to hymenopterans. It's almost as if they view the situation as a part of their surroundings shrinking around them vs some form of aggressor trying to "eat" them.  It's actually quite interesting that insect brains seem to interpret the entrapment as an unfortunate stochastic act of their environment vs an intentional form of aggression.
You can watch Venus flytraps eating yellow jackets via this YouTube video: Venus Flytrap Eats Wasps || ViralHog.
Notice two things:

To my point, take a look at the 3:30 minute mark. Two yellow jackets are trapped, and they both struggle to get free. But at no point do I see any signs of a stinger. In other words, these yellow jackets never try to attack their entrapper.

Related to your specific question: no other individuals are reacting when one of their own is trapped. (admittedly, this is away from the nest, and hive-mentality protective behavior while foraging is different vs protecting young of the hive)

Thank you, this is in fact very interesting, though I'm unsure much can be concluded from it. I also see no stinger, but the abdomen movement around https://youtu.be/FMMNPKyaedo?t=212 looks like it might be trying to sting. Indeed no backup comes, but as you say, this might be because it's not close enough to the hive.

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


text:
What is a set of chromosome and what is a pair of chromosome
What is the definition of set of chromosomes? Does it differ from pair of chromosomes?

Yes those two expressions refer to different things.
Set of chromosome
The term "set of chromosome" refers to ploidy number. A haploid has one set of chromosome, a diploid has two sets of chromosomes, an hexaploid has six sets of chromosomes.
In humans, each set of chromosome is made of 23 chromosomes (22 autosomes and 1 sex chromosome).
Pair of chromosome
A pair of chromosome refers to the two homologous chromosomes in a diploid individual (one chromosome from each set for a given chromosome number).
Source of information
If the above is unclear, then you should have a look at any intro course to genetic such as these courses by Khan Academy for example.

Plz clarify this a bit more. 1- Does each set of chromosome come from mother and father in a PAIR of chromosome?  2- Chromatid - a single chromosome in a newly copied pair - Do Two Chromatid contain the Identical DNA  sequence ?

Yes, although most of the time, we don't know which chromosome of a pair comes from which parent (we don't know which chromosome of a pair belong to which set). 2) Yes. There are many related posts to this second question of yours. E.g. see What are homologous chromosomes? or Chromosome and chromatid numbers during cell cycle phases. Feel free to open a new post if you've got more questions.

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


text:
Is it safe to look at infrared LEDs?
What happens if one looks directly at infrared LEDs? Sometimes I see this kind of LED at night as red dots and I'm also courious about it.
I was wondering what would happen if one looks directly to these LEDs, because we see them everywhere like in remote controls, CCTV cameras, sensors, etc.
What is the difference between infrared and visible light to our eyes?
(I mean why is it impossible to look directly to visible light while we can look to infrared?)

LED: Light-emitting diode

Infrared wavelengths are EM waves of longer wavelengths than visible light. Also, visible waves are more energetic than IR waves.
Because of this, Visible light has the ability to excite organic receptor molecules in our eyes called Rods and Cones. These molecules stimulate cell responses and in turn excite cell responses in our nerves called an Action Response. Still unclear to most scientists is how the brain composes these action responses into an image, though a great deal of research is being done to date.
The reason why "nothing happens" when we aim infrared lights into our eyes (which I still wouldn't suggest) is that the photoreceptor molecules that we use to see don't have the necessary bonding configuration to accept the energy from these impinging EM waves.
 However, don't go thinking that nothing happens. Infrared radiation is a type of radiation that is usually a measurable heat source. IR is one of the broader parts of the EM spectrum. My point is to say, that when you "radiate" some thing with an IR source:
1) You don't know if it is also radiating other EM waves unless you know the specs.
2) You're still exciting molecules with that energy even if it isn't causing a seen effect. I highly doubt anything will happen unless you have a very high powered IR source. You shouldn't really ever focus high power lasers of any source onto your body, because higher intensities could inflict damage.

To Learn more about IR radiation:
http://coolcosmos.ipac.caltech.edu/cosmic_classroom/ask_astronomer/faq/radiation.shtml
IR (InfraRed)
EM (ElectroMagnetic)

I was aware that it's not a good idea to aim a source or IR directly to the eyes. Sometimes I see in the street CFTV cameras at night and I can clearly see the IR LEDs as red dots, how could this happen as IR is not seen?

As I mentioned, You never know if a source is only radiating one wavelength. The red exists because those "IR LEDs" also have radiation that is in the visible spectrum.  Red (visible) light is closest to IR radiation in the EM spectrum.  See the spectrum here. This only applies for radiation that is being emitted not detected. http://www.pion.cz/_sites/pion/upload/images/a14cf10a5583d19f7cfdebd63cf64382_electromagnetic-spectrum.png

Wait, wait wait wait. Those CFTV camera's have a red light only to let you know that it's recording...The outgoing red light has nothing to do with the light that is being absorbed, aka the IR light. The IR light for the camera is generated from your body, as thermal radiation.

I added a picture of the IR LEDs as I mentioned in the comments to better illustrate the question. The red dots aren't of the LED that indicates that the device is powered on.

This is an old question, but those IR LEDs are actually Near IR, just below the visible light cutoff. The ones that make a faint visible red are probably around 800 nm. There are others around 900 nm that don't make any visible light.

Hi, I work with desktop devices that features IR audio distribution. I am supposed to keep the devices in front of me, such that the 4 ir emitters used for audio distribution is in direct contact towards my face, neck and shoulder. The problem is, after this project, i am sometimes feeling itching feeling in my one eyes as long as i am sitting with this device. Can you advise on this ?

here's a similar question. some studies say that it may cause cataracts if you see enough of them, also the eye may receive a lot of a wavelength while dilated. that's a technical thing about sunglasses, if a sunglass dilates your pupil but IR flashes through the seams, technically it's not perfect. Could there be any effects from low powered infrared being used to track eye movements long term?


text:
Diffusion approximation to genetic drift
I am reading from the classical textbook Principles of Population Genetics, Hartl and Clark (pdf here).
Introduction
Let $f(p,x,t)$ denote the distribution of allele frequency $x$ at time $t$ knowing that at time $t=0$ the frequency was $p$. One can model the change in this distribution with time using the Kolmogorov forward equation
$$\frac{\partial f(p,x,t)}{\partial t} = -\frac{\partial [M(x) \cdot f(p,x,t)]}{\partial x}+\frac12\,\frac{\partial^2[V(x) \cdot f(p,x,t)]}{\partial x^2}$$
where $M(x)$ is the "drift parameter", which represents natural selection (thus, in the absence of the selection $M(x)=0$), and $V(x)$ is the "diffusion parameter", which represents genetic drift. The diffusion parameter is $V(x) = \frac{x(1-x)}{2N}$, where $N$ is the population size.
Question
Why is it true that $V(x) = \frac{x(1-x)}{2N}$?
I welcome intuitive explanations and mathematical proof.
Thoughts
I would think it derivates from the Wright-Fisher model of genetic drift where the distribution of allele frequency at the next generation is given by a binomial distribution.

What is the definition of N in V(x)?

$N$ is the population size. Thanks for noticing. Question edited.

It does indeed proceed from the Wright-Fisher model, specifically from its diffusion process approximation.
If the population is size $N$, then at generation $t$ the number of alleles is $A(t)$, and so the frequency of alleles is $x(t) = A(t)/(2N)$, assuming the diploid case. Then Wright-Fisher says that:
$$ A(t+1)\mid A(t) \sim \text{Bin}(2N,x(t)) $$
So the distribution of the next generation's count, given the last one, is binomially distributed (under random mating).
One can find that, for a binomially distributed random variable $b\sim \text{Bin}(m,p)$, the mean and variance are given by:
$$ \mathbb{E}[b]=mp\;\;\;\;\;\;\&\;\;\;\;\;\;\mathbb{V}[b]=mp(1-p) $$
Thus, we get that
$$ \mathbb{E}[A(t+1)\mid A(t)] = 2N x(t)
\;\;\;\;\;\;\&\;\;\;\;\;\;
\mathbb{V}[A(t+1)\mid A(t)] = 2N x(t)[1-x(t)] $$
Applying $x(t)=A(t)/(2N)$, we see that
\begin{align}
\mathbb{E}[x(t+1) \mid x(t)]   &= \frac{1}{2N}\mathbb{E}[A(t+1)\mid A(t)]= x(t) \\
\mathbb{V}[x(t+1)\mid x(t)] &= \frac{1}{(2N)^2}\mathbb{V}[A(t+1)\mid A(t)] = \frac{x(t)[1-x(t)]}{2N}
\end{align}
using the fact that $\mathbb{V}[cX]=c^2\mathbb{V}[X]$.
We can relate this to forward Kolmogorov as follows. Recall that the binomial distribution can be approximated by a normal distribution, with mean $\mu$ and variance $\sigma^2$ given by the mean and variance of the binomial. This tells us that: $$ x(t+\delta t)\mid x(t) \sim \mathcal{N}(x(t),(\delta t)x(t)[1-x(t)]/(2N)) $$
The properties of the normal distribution then imply that $$ \Delta x_t=x(t+\delta t) - x(t)\sim\mathcal{N}(0,\sigma^2(x_t)\delta t) $$
where $\sigma^2(x_t) = x(t)[1-x(t)]/(2N)$.
This implies the following equality (in distribution):
$$ \Delta x_t = \sigma(x_t)\Delta W_t $$
where $\Delta W_t\sim \mathcal{N}(0,\delta t)$. As $\delta t\rightarrow 0$, we get a stochastic differential equation,
$$ dx_t = \sigma(x_t)dW_t $$
where the solutions are Markov random processes (unlike e.g. ODEs where there is only one solution and it is a deterministic path; think of it as a noisy ODE), specifically in this case an Ito diffusion. Note the SDE has no $dt$ component since the increment mean was $0$. If we then consider the density function for the random process $p(x,t)$, it must satisfy the Fokker-Planck (Forward Kolmogorov) equation: $$ \partial_t p(x,t) = -\partial_{xx}[p(x,t)\sigma^2(x)/2] $$
which gives a probability distribution over the allelic frequency value at each time point (given some initial value I've not specified here).
Note that $V(x)=\sigma^2(x)$.

In terms of intuition, I'm not really sure. Essentially $V(x)$ measures how much perturbation in the allelic frequency you can expect to happen each generation due to purely random effects, i.e. genetic drift. Notice that there is no perturbation when $x=0$ or $x=1$, i.e. no random changes can happen if no one or everyone has the allele. Notice also that this variance is exactly the variance of a Bernoulli distribution. It's like we've distilled the individual-level model to a population-level model that simply looks at the frequency of the binary choice of allele presence, I guess.
The variance (noise) is maximal when the frequency is $1/2$. It's sort of pushing the allele away from the middle, by increasing noise when one goes there; one might expect that (if run long enough) any such model will hit and get stuck at $0$ or $1$ (not sure if this is true).
I looked a bit if there were any other interesting interpretations of the sde considered here (e.g. in physics), but couldn't find any. Basically, it would be equivalent to a heat equation, spreading under some potential function controlled by $\sigma$.

Your question is closely related to this one. My answer largely follows Tataru et al, Statistical Inference in the Wright–Fisher Model Using Allele Frequency Data.


text:
What if $rB=C$ in Hamilton's rule?
Hamilton's rule states that if $rB>C$ then a gene giving altruistic behaviour will increase in frequency in the population. What would happen if $rB=C$? Will an individual perform the altruistic act?

Why has this been downvoted?

@Biogirl How have you tried to analyse the problem? Also, I rephrased your Q to better fit with a standard way of stating Hamilton's rule.

Could you edit your title so it doesn't have dollar signs in it please.

I agree with @Amory in the sense that Hamilton's rule is not a rule that applies to each specific individual and explain their behavior (or other traits). The Hamilton's rule describe the direction (and not the dynamic) of how a social traits evolve. A social trait is any trait which does not only affect the fitness of its carrier but also affect the fitness of other individuals in the population. Theoretically, all (or almost) traits are actually somehow social traits.
$RB>C$ is a simplistic way of looking at Hamilton's rule which might bring you to some confusion. This formula makes more sense to me by replacing $B$ by $\frac{dw(x,y,z)}{dx}$ and $C$ by $\frac{dw(x,y,z)}{dy}$. $w(x,y,z)$ is the fitness function of a focal individual expressing trait $x$ and interacting with an individual drawn from a subpopulation expressing trait $y$ (expected value of the probability distribution of trait expression of individuals in the subpopulation) in a population expressing trait $z$ (expected value again). In the particular case where there is no population structure $y$ equals $z$. $\frac{dw(...)}{dx}$ describes the partial derivative of the fitness function according to the variable $x$.
Therefore the Hamilton's rule can be rewritten as:
$$R\cdot\frac{dw(x,y,z)}{dx}>\frac{dw(x,y,z)}{dy}$$ where $R$ is the coefficient of relatedness which can itself be expressed as a correlation between the variables $x$ and $y$.
Altruistic behavior evolves if (but not "if and only if") this rule is respected. Hope this reformulation of Hamilton's rule helps a bit understanding it.
In the special case where $R\cdot\frac{dw(x,y,z)}{dx}=\frac{dw(x,y,z)}{dy}$ then, the trait of interest is not selected (neither counter selected). Therefore the trait will evolve under genetic drift alone. While the allele frequencies are modified by drift, the Hamilton's rule might (or might not) differ from the equality and then the trait would not be neutral anymore.

I loved your answer !

"Hamilton's rule states that if rB>C then a gene giving altruistic
  behaviour will increase in frequency in the population."

To start here are some examples of how Hamilton's Rule works...
In a population of four individuals a pair of adults mate. A first unrelated male (r=0) is genetically coded to help raise their offspring by an allele (selfless) at the "sociality" gene. A second male, also with r=0, has a different allele (selfish) at the same locus which makes him not help with offspring care. The pair raises 4 offspring if they go it alone, and 10 if another male helps. By helping, a male sacrifices his ability to mate so produces no offspring. Going it on his own he would produce 4 offspring.
By helping, when r=0, a male passes on no copies of his genes to the next generation (fitness = 0, no offspring in the next generation have genes that are identical by descent [ibd] to his), by being selfish he passes on 4ibd copies of half of his genes (fitness = 2 = 4*0.5). Thus the male carrying the selfish allele should do better and genes promoting social behavior should not evolve in the population because 0*(10)<2 (by helping he sacrifices the fitness score of 2, this is the cost).
Now with related males, say the father's brothers. This time the males will on average be related to the offspring of the pair with a relatedness coefficient of r=0.25. With the same results of helping and selfish behavior, genes for social behavior should evolve because 0.25*10>2, the selfless male has more IBD genes in the population than the selfish male. The next generation would have many individuals in it with the selfless allele.
Hamilton's rule is used to estimate whether "selfless" type alleles will spread through a population, to do so there must be some sort of relatedness within a group otherwise r=0 so rB will never be greater than C. In populations where relatives stay together there is more chance that altruistic behavior will affect a relative, when relatives can't/don't disperse away from each other much then genes promoting altruism should evolve. In more fluid societies they should not be as common.
Hamilton's rule is not definitive though. The closer that rB and C are to each other, the weaker selection will be at driving out alleles which reduce fitness, that is because the gain of having the correct allele is so marginal. For example, if r=0.5, B=100, and C=49, then selfless alleles are 2% fitter than selfish alleles. In comparison, if we keep r=0.5 and B=100, but change C to 40, then the rB>C still holds and selfless alleles have more strongly favorable selection (they are 25% fitter) so will spread more rapidly. If C=0 the behavior is likely to evolve because r=0 is unlikely in a population (even if you only include polymorphic loci).

"What would happen if rB=C? Will an individual perform the altruistic
  act?"

Whether animals can use Hamilton's rule to decide behaviors plastically is different application of the equation in Hamilton's rule. It is a similar concept, but evolution does not happen with the individual; the genetic makeup of an individual will not change as a result of selection. However, ignoring the definition of how Hamilton's rule is used you could use the same equation to estimate likely behavioral outcomes when an individual is given a choice. Here is an example where an individual is given the option to give or keep food and can judge relatedness, it is a very simplified model.
Example: A locus has two alleles G and g. Individuals can then be GG, Gg, and gg and each genotype has an easily discernible unique trait. Thus when a GG individual meets a GG individual it knows it is perfectly related, r=1. For Gg r=0.5, and gg r=0. When the individuals meet our focal individual (GG) has the option to either provide something for the other one or not provide (let's say give it some food).
For our GG individual the cost of providing the food to the other is the energy it took to find the food, say 50 calories. The benefit to the recipient is the energy within the food, lets say 120 calories. Thus we can say, GG should give the food to the other individual if the other is GG (because 1*120 > 50) or Gg (0.5*120 > 50) but not when it is gg (0*120 < 50). If we reduce the value of the food to 80 calories it becomes that GG should not help Gg (0.5*80 < 120).
There are a few limitations to consider...
Firstly, how well can an individual quantify relatedness? Just using Wrights Coefficient of Relatedness we would come out with roughly accurate measures on average. But there is variability due to mutations and the second law of Mendelian inheritance; independent assortment.
Secondly, how well can an individual judge benefit of its actions? The effect on the recipient is likely to be complex, it could have serious knock-on effects such as increased fitness later in life, longer lifespan, the action might reduce predation risk for the recipient that day etc..
Thirdly and similarly, how well can the provider judge the cost it incurs? If it is giving away food, it does not know if and when it will actually find it's next food item, foraging might cause it to be predated upon, and it might lose out on a mating opportunity if a receptive mate comes by while it is foraging etc..
When rB truly equals C (unlikely due to the complex nature of r, B and C) or is approximately equal, then the individual will be less likely to make the correct choice. When it is obvious that the cost is large and benefit is small it is more likely to make the correct decision. This is analogous to the ability of selection to drive out the incorrect allele as outlined above.
This is a rewrite of a previous answer made after some thinking and I think it provides a much better answer than the previous incarnation which I have deleted

Thanks for such a wonderful answer ! Actually, this question arose because there was this question : If an individual with an alternative of rearing its own 1 offspring or rearing its cousin's offspring,what is the minimum no. of offspring its cousin should have ? I know that 1own off. = 4 cousin off. So should the minimum no of offspring be 5 or is 4 an apt answer ?

@biogirl Well I guess you could always say that an individual might choose to help regardless of the benefit due to its lack of ability to differentiate, but that would be a risky idea! I'd suggest explaining 3-5 offspring. Such that at 5, given the individual can distinguish relatedness, costs and benefits quite accurately, that it would be altruistic. At 3 it should behave selfishly. And at 4 it theoretically could choose either strategy with no adverse effects. As long as you show your working (0.254=1, 0.253<1, and 0.25*5>1) and explain those three you should nail it on the head.

As far as I understand it, Hamilton's "rule" isn't really meant to apply individually, it's meant as a way of thinking about kin selection and altruism that can be reduced to individual cases.  The reality is that B and C can rarely, if ever, be easily measured or determined.  If the two sides were equal then who knows?  You'd have to observe it.  Presumably it would split 50-50.  Or maybe laziness takes over.  Or maybe some species are inherently altruistic.  That being said, exact equality is a near-impossible occurrence in the wild, and B and C are movable targets, so you'd have to measure it, which is, as stated, very, very difficult.


text:
What do "reduced antipredator defense" and "reduced antipredator vigilance" mean?
The book BIOMAT 2010 (International Symposium on Mathematical and Computational Biology, edited by Rubem P. Mondaini) mentions the terms reduced antipredator defense and reduced antipredator vigilance.
Can you help me to make sense of them?

Do you mean "What is the definition of RAD? and What is the definition of RAV?"?

@Remi.b Yes. Where they are seen and what are those effects.

Where did you first encounter these terms? In the book you're citing? Does the book attempt at defining these terms at all?

@Remi.b Yes, in the book. Not defined those terms.

I edited your question. Feel free to rollback (or to further edit) if you don't like my edits. I would suggest that you make an attempt of what you understand of these terms so far. I personally have never encountered them before but I am not an ecologist.

A quote placing terminology into context is helpful

When groups of prey use certain mechanisms to defend against predators, those mechanisms are known as antipredator defenses. For example, groups of tuna and starlings flock together to confuse predators. A reduction in this defense would be 'reduced antipredator defense'.
Groups of prey also exhibit shared antipredator vigilance, as in certain members of a group will look out for predators to protect the group. This is seen most predominantly in meerkats. A reduction is said vigilance would be a 'reduced antipredator vigilance'.
With reference to the Allee effect, which is what you appear to be reading about, this reduced antipredator defense and vigilance can significantly effect the population and the population growth.
Some related links:

On the ecological mechanism of the Allee effect.
Vigilance, predation risk, and the Allee effect in desert Bighorn sheep, a recent research paper.

Please explain in more details the term reduced antipredator vigilance. I understand the term 'reduced antipredator defense'

I think it's a good answer, but basing questions entirely on Wikipedia is not preferred, given its dynamic contents. Your info used may be gone from your link tomorrow.

Alright, I will find different sites to validate this information. Thanks!

@user1942348 Reduced antipredator vigilance would mean that the group of prey would not be able to detect the predator as well as earlier. This can be due to increased ability of the predator to hide and camouflage or isolation of prey from the predator for some time
Here is a link you might want to look at : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1559846/

@malharkhushu Thanks a lot. Would you please give some examples where it is seen?

If (hypothetically) meerkats are taken to islands without predators for many generations, they would eventually forget to be vigilant about predators. When put back into a normal condition, they would not be able to detect and avoid predators. This was also seen in dodos, who could not survive when external predators were brought onto their isolated islands. There are quite a few more examples, but I can't remember any off hand. If I remember more, I will be sure to tell you


text:
Why do we feel cold on having fever?
Why do we feel terribly cold on catching fever of any sort, however our body becomes hotter?
Why is it that a rise in temperature makes the sufferer feel colder? Also, sweating symbolises betterment of the conditions. Why?
{This question has been asked with reference to personal experiences}

Body temperature results from a balance between the heat generated by our cells and the heat “lost” to the environment. Heat created by our cells comes from the energy used to keep us alive. Heat is lost through our skin and the air we breathe out. Human beings have an average temperature of 98.6 degrees Fahrenheit. The brain monitors body temperature and controls our bodies to keep our temperature within the normal range.
If you get a fever when you’re sick, it’s because your brain has told your body to get hotter. It directs the body to make a number of changes to correct the imbalance. Those changes include increasing heat production within the body (by shivering, for example) and reducing heat loss to the environment. Heat loss is reduced by decreasing blood flow to the skin.

Why are some fevers also accompanied by chills and shivers...like, the malarial fever...?

@Shamayeta: same reason, body try to heat up by shivering.

@Devasish Sir: My bio book refers to HAEMOZOIN that is responsible for the shiver during malaria. How does haemozoin work to raise the body heat?

@Shamayeta: Can you ask this as a separate question, it's long answer.

@Devasish Sir: I shall be doing it.


text:
What does salt do to styes?
Styes formed in the eyes are cured by dabbing at them with lukewarm water(I saw this being done many a times as a home remedy.) At times, common salt is added to the water before dabbing. My mother says, NaCl hastens the healing process; why is it so? What does salt do to cure the styes faster? Can salt be used for treating other eruptions anywhere else?

Same reason as this http://biology.stackexchange.com/questions/189/why-does-salt-water-help-sore-throats

Is there no difference between the cause for sore throat and that for sty formation? I guess there is. So, I wonder how the reasons for salt healing both can exactly be the same. Anyways, thanks a lot.

Stye is caused due to infection by micro-organisms. So the same theory applies. Salt water does not discriminate between organisms

authors: วันชัย แสนหวู่


text:
Why does crying lead to a running nose and reddened nose tip?
Why do we have a running nose for quite some time after crying? It persists even after we stop crying. Why is it so? I have faced this always. Also, why does our nose redden on crying for long?

When you cry, you produce tears, which come out of your tear ducts. These are not only open to the eyes but also have a connection to your nose, see the image below:

A part of your tears runs through this connection and mixes with the mucus which is present in your nasal system making it thinner and allow it to flow more easily. If the tear flow is prolonged, the nose will produce more mucus and make your nose running for a longer time. The nose appears redder because the blood flow is increased. This is partly due to the production of more mucus and also because you repeatedly touch the nose when using a handkerchief.

Thank you for the explanatory answer. The diagram proved to be of immense help.


text:
Synthetic life creation - status of attempts
First I apologize for my incorrect English and for lack of modern knowledge regarding the subject (I studied biology a long time ago).
I'm interested to find out:

if there were successful attempts of life creation from conditions that we suppose were dominant on early Earth
if there were not, are such attempts still being conducted?

To clarify, by "life creation" I mean the accidental creation of entire organism in conditions of organic compounds, water, electricity, radiation etc. being present (Abiogenesis).
If this is already answered here, I'm sorry for asking, I have researched this, this, this and this question with no luck.

You might be interested in this answer: https://biology.stackexchange.com/a/56363/6307

There have been lot's of attempts, no success so far, a few groups are still working on. However, many steps forward have been done in the last decades.
Starting from the Miller experiment which demonstrated that the building blocks of life chemistry can be obtained starting from fairly simple chemical compounds. Following, Luisi and Szostak showed that 1) nucleic acids can polymerize without the help of enzymes and 2) autocatalytic micelles form spontaneously in many different conditions. It is also important to remember the work of Otto that showed how different molecules can self-replicates.
There are many more examples reported in the literature, still, the complete "creation" of life from matter has not been yet accomplished. However, the results from the experimental work done so far suggest that it is only matter of time and lots of combinatorial work. Unfortunately, there are little to no investments in this field. It's very hard to get the funds needed to start an international cooperation (like the one made to sequence the human genome or to build the CERN's Large Hadron Collider) with the goal of actually making life in the lab. I think that the work of a few (uncoordinated) groups will not get to the goal in the next few years.

I would add that even these more basic results have really shown that abiogenesis is feasible. It is definitely feasible to show in a lab that certain steps are possible given certain conditions (like polymerization of nucleic acids). What isn't feasible is doing the experiment on whole-earth scale and waiting for potentially millions of years. It's really frustrating that some people take the infeasibility of that last step and conclude "oh so life must have come from a Creator!" That isn't what it means at all.

I agree. But I also think that it is possible to do it in the lab without having to wait millions of years. Actually, I hope that the pressure set from creationists will move some billionner to put money into this research. Is one of the great question of biology, is still lacking the final prove and it worth a Nobel price once solved. We can definitely do it, it's really just matter of money/organization.

Maybe, but if that attempt fails it doesn't prove anything, so really the experiment is quite flawed - probably one of the reasons there isn't much support for it.

I see lot's of support already from all the experiments reported in the literature. Surely it's not easy to solve, but again founding the Higgs boson wasn't easy as well, and same you can say or the first Human Genome. Now it's routine. Soon or later it will be routine also to create life in a lab.

I think that's a cool thought, but I'm skeptical. I think it is more likely that we will find life on another planet than create it here truly from scratch. I think we will continue to fill in some of the puzzle pieces here, though. The problem is that for those other projects you can engineer solutions that still answer the original question, like producing particles that are otherwise near infinitely rare to occur naturally. For abiogenesis, if the whole point is to say 'early earth could create life from scratch' you are sort of cheating if you add anything to the system.

@BryanKrause you say: 'early earth could create life from scratch'. My view of abiogenesis is more general: any complex mixture of chemicals, with enough energy and time, will tend to form complexity. Chemical complexity leads eventually to Life (the is, chemistry at the nth power). In this sense, there is nothing to "add to the system". It's just matter of finding the way of repeating the process in a controllable and repeatable way. I would expect different biochemistry evolve every run even if the initial conditions are the same. Eventually, some of them will evolve Life.

But you are assuming that that can happen on an experimental scale in a lifetime. The actual hypothesis is that it occurred at least once on a global/geological spatial/temporal scale. If you want to just say "tend to form complexity" we have already seen that to some extent.

Yes, I think it can happen on an experimental scale in a lifetime. Under controlled conditions, reaching a self-reproducing protocell should be doable. Then having that protocell evolving into some bacteria-like life form may take ages. But yes, I am speculating on that.

I find your speculations correct. However, there is a problem coming out precisely from running the experiment with a different outcome each time. See, scientists expect falsifiability of their experiments, it's heavily expected that if you run an experiment over and over again you should get the same result every time you run it. But it's not what you expect, or more likely shouldn't be what you expect when you run experiments for the creation of life-here one must expect that different outcome every time it's run and that destroys falsifiability.

That field of highly complex chemistry may indeed be the only case in science where you would expect to have unexpected result and that hampers your data analysis. If you produce different biochemistry each time you run the thing what about your statistics or any other interpretation of your data? Can you imagine doing the math of a different outcome of a highly complex experiment already? Do you think anyone could get enough funds to support such an endeavor? I highly doubt it, not with what we currently have as hardware and funds, at least.


text:
Plants anti-aging process
Every cell has its division limit. But plants cell looks like don't have it (like Sequoia sempervivens D.). I searched a little for it but what I have found didn't help to answer my question. I found a paper http://epsce.com/wp-content/uploads/2016/02/EMBRYONIC-PLANT-EXTRACTS-EXTEND-THE-HAYFLICK-LIMIT.pdf, which states that plants cell have something call EPE. Which seems to me like super telomerase ( Just kidding don't take it seriously).
My question is: How do plants slow their aging process? Have they different limits for cell division? Are phytohormones related to this phenomena?

I am not so big plant fan. So sorry if is just basic questions for you guys.

Can anybody even tried to answer this. I am really curious about aging process in plants. Any articles about it might help too.

Sequoias are perhaps not the best example.  Consider clonal organisms like the quaking aspen (Populus tremuloides), one grove of which is estimated to be about 80,000 years old (and some suggest much older): https://en.wikipedia.org/wiki/Pando_(tree)

Wow didnt know about it. And now the question about aging is much more interesting!!

Check this paper, it is a great starting point! https://www.sciencedirect.com/science/article/pii/S1568163713000615?via%3Dihub


text:
E. coli not growing in liquid medium
We are regularly doing bacterial transformation and subculture from plate to liquid media to extract DNA. This usually goes very well and is straightforward, but occasionally, the colonies that grew well on a plate, will not grow in liquid culture (with the same antibiotics that were in the plate). This has happened now to three persons on multiple plasmids.
For example, I was trying to ligate an ampicillin resistance gene (with its promoter) inside pENTR4 plasmid (already with Kanamycin resistance). My plate and LB both contained the two antibiotics, but the colonies only manage to get slightly turbid at a 16h timepoint.
Phage contamination is very unlikely, and the effect cannot be due to a toxicity of the inserted fragment, as both insert and vector have been grown in these same bacteria multiple times without problem.
Help?
EDIT1 - We use Carbenicillin in place of ampicillin in the plate, but not in the liquid media.
EDIT2 - After managing to grow some colonies in liquid, I managed to get a small amount of the plasmid (profile was good; concentration = 70ng/ul). The weird thing is that when I retransformed this DNA in Stbl3 bacteria, I had absolutely no trouble. Do you think the bacteria stock could be responsible?

Did you change your batch of antibiotics, or media recently?

Simplest explanation is something is culture tubes or media prep bottles that inhibits growth (detergent residue?). But lots of people have seen what you describe if the colony-bearing plates have been stored too long at 4 C. One way to test (besides comparing media +/- drugs) is to "patch" out colonies on a new gridded plate--you may do this routinely, lots of people do. So either after finding cfu patch candidates to a master grid, or, when you innoculate the tubes for mini-preps, also patch out the cfu on a fresh plate. If the patched grid plate grows but the culture doesnt, voila

In very rare cases patching shows healthy tiny lawns with pin-prick holes from phage contamination. Also, if it is phage contamination from a lytic phage, in my experience the broth will clear and accumulate a small stringy clot of lysed cell debris, that floats. What if there was a non-lytic phage like M13? Sounds like you are carefully considering the "obvious" reasons.  There definitely ARE toxic inserts that are virtually impossible to propagate in regular E. coli, but then you would only find transformants without inserts (typically), but that is fortunately a pretty rare occurrence

The antibiotics are stocks stored at -20C, and they have been used simultaneously by a colleague of mine that had the same problem on some of his vectors (2/8). Since we have used the same type of tubes successfully, I doubt it could be the reason.

did you try positive control transformation? Of some test vector, like pEGFP-type

also your incubator might not work, sometimes people switch temperature for no reason or turn shaker off (maybe your outlet has timer that goes off overnight :)

This transformation was done with my colleague; we did the thing together. In his plasmids (stuff he received as is from another lab and transformed directly in bacteria) two out of eight presented the same problem as mine. The others grew perfectly. It was done in commercial DH5a bacteria that we had just bought. The temperature and rotation were fine.

how big/numerous are the colonies on the plate?

The colonies were small to average in size. It made no difference overall.

Which strain of E.coli are you using?

And about your insert, do you have the terminator as well? Because on your post you just mentioned promoter and AmpR

I'm not sure about the terminator as it is not labeled...

I think there is more than one possibility for this.

Plates bearing colonies are stored for too long in 4C(as @mdperry suggested). This causes the colonies to lose the plasmid over-time as the antibiotic in the plate gets degraded over-time. There is a study on this and I've shared the link. (http://homepages.bw.edu/~mbumbuli/biotech/colin/index.html).
The insert is toxic to cells and promoter is not strong enough. There is a leaky expression causing cells to die.
Check the competent cells and their storage condition as it would greatly affect the efficiency of transformation. Do a mock transformation with plain plasmid without insert and spread them on an antibiotic plate.


text:
Looking for good reference book in molecular biology
I am starting to work in molecular biology/ molecular genetic and I am looking for a really good book containing the main concepts and mostly the more recent techniques.
I would be interested in a book that has also protocol examples and examples on how to apply the different techniques.
My focus is on bacteria and fungi.
Any suggestion?

Usually questions asking for book recommendations are considered 'opinion-based' if specific details are not mentioned.

These always have a place at my library
HF Lodish, Berk, Arnold, and S. Lawrence Zipursky. Molecular cell biology. Vol. 4. New York: WH Freeman, 2000.
Alberts, Bruce, et al. "Molecular biology of the cell." Garland Science, New York 4 (2002)(the first few editions had James Watson himself as the editor)
Brown, Terence A. Genomes. Garland science, 2006.
For basics. I would recommend staring with Brown, and going on to Bruce Alberts and then Lodish. That's the way I learnt it.
For a really nice book with pictures (yes, we all like those) you might want to look into Lippincotts illustrated reviews (biochemistry, cell and molecular biology and the like). They are also quite good.
For a specific emphasis on techniques, I'd  recommend this:
Sambrook, Joseph, Edward F. Fritsch, and Tom Maniatis. Molecular cloning. Vol. 1. No. 7.58. New York: Cold spring harbor laboratory press, 1989.
(You can read the contents here http://www.molecularcloning.com/)

Thank you very much. I am actually a PhD. So I need to refresh my knowledge and get update with more recent molecular/genetic techniques

@efrem Updated my answer with a bookset on cloning.

Brock's Microbiology is a great book when you are interested in unicellular organisms.
From the publishers's website (Pearson):

The authoritative #1 textbook for introductory majors microbiology, Brock Biology of Microorganisms continues to set the standard [...]. This book for biology, microbiology, and other science majors balances cutting edge research with the concepts essential for understanding the field of microbiology, including strong coverage of ecology, evolution, and metabolism. The Fourteenth Edition [...] pay[s] particular attention to molecular biology and how the genomic revolution has changed and is changing the field.

If it's techniques you are interested in, Weaver, now in its 5th edition, has (had) a strong emphasis on recent experiments from the literature, and he is constantly updating the book. We used  to use it for a variety of courses.


text:
Enzymatic error rate
I am aware that each enzyme generate a certain amount of misproducts.
This is well documented, for example, for the DNA polymerase.
I am interested in enzyme involved in biochemical processes, so for example methytransferase, oxidoreductase, carboxylase and so on.
I have been looking for any reference that could report the error rate or the amount of misproduct for any of these enzymes, but I was not successful.
Does anyone know a reference reporting the error rate, or any other information about the misproduct generate by these enzymes?
EDIT
I will try to clarify a bit better my question.
Let's assume that we are considering an enzyme that add a methyl group to a molecule, we can choose propionic acid for example.
In theory the correct product would derive from the addition of a methyl to the C3.
For the biochemistry study we know that the activation energy is decreased by an enzyme for example by orienting the molecules in the right way to react with the second molecule.
Therefore, if the enzyme in question will not be able to orient the molecule in the right way there is a certain probability that there will be a mis-product.
For example the methyl group could be added to the C2 and not the C3. Now. the probability for this process is quite low, but it cannot be excluded from happening.
My question is, if there is anything known about this type of error rates in the different type of enzymes.
I hope this make things a bit more clear
EDIT 2
Lets consider the imagine below that was taken from here

In B you can see the interaction of the active site of the enzyme with a substrate (for the example it does not matter if it is the real substrate or an inhibitor). I would say that among al possible interaction that this active site can make with substrates there are some much more likely than others. An hypothetical chart could be created considering the free energy of the complex enzyme-substrate, higher the free energy lower the stability.
Therefore among all possible enzyme-substrate combination we will have just few possibilities that have a low free energy. In the first place we will find the "correct" substrate, then we will find eventual competitors and other molecules that have similar chemical features as the substrate. Even though with low probability these interaction, enzyme-competitors, will happen.
This might led to the formation of "unwanted product" that I refereed to in my question as "misproduct".
I am interested in reading some paper that are considering thie phenomenon and also quantify its rate. I am also curious if this phenomenon can happen with different rates in different enzymes.

I think these enzymes are different. There is one chemical reaction that they catalyze and thus this will take place or not. This is different for the DNA polymerase where 4 different nucleotides can be incorporated (which raises the possibility for some errors).

There can certainly be enzymes other than polymerases that catalyze errant reactions. Aminoacyl tRNA synthetases immediately come to mind as an example. Some even have proofreading mechanisms to correct errors.

DNA pol only appear different because enzyme is influenced by template strand, in a sense. Chemical reaction catalyzed is still a chemical reaction

please let us know if you find answers sufficient. I think that question is important

If you ask references for all the enzyme then I am afraid that this question would be closed as broad. I am giving you one example and the basic idea behind the problem. You can search for the other cases.

I think you should clarify what you mean about error: a.) the enzyme uses a different substrate and the result is a different end product b.) the enzyme uses the same substrate and the result is a different end product. I think b.) is unlike, but I may not know everything about enzymes.

@WYSIWYG I ask for some reference that consider the issue I indicate as example. It would be really helpful to have a suggestion as hint

@efrem I don't know an example from from the back of my head. Have to look for it. In general what you are asking is unlikely because it is rare that a same molecule will have many similar groups where the reaction is supposed to occur.

First it is important to define what actually an error is. What you call misproduct is actually a right product for a different substrate. The enzyme has a low specificity; but you won't say hexokinase is error prone because it has wide substrate specificity. The question is — is specificity critical?
Coming to the example of DNA polymerase, you should note that DNA polymerase only adds a nucleotide to the DNA strand. Here the template DNA strand acts like a co-enzyme and it is the template DNA that provides specificity to the reaction. In this case the specificity is really critical and there are mechanisms that help in ensuring that.
Other enzymes also make errors and the probability of making errors depends on different parameters. Take the example of restriction enzymes that are supposed to cut at a specific site. When this specificity is lost we say that the enzyme is showing a "star activity" i.e. non-specific cleavage. This depends on different parameters such as buffer composition, enzyme concentration etc.
In general specificity is provided because of high affinity of binding towards one molecule compared to the other. These binding reactions are second order — a high affinity substrate will bind to the enzyme even at a low concentration, however if you increase the concentration of the low affinity substrate or the enzyme, then at some point the rate of binding may be significant enough to create a "wrong" product.
Sometimes there are cases where the enzyme can bind to a wrong substrate but cannot create a product. This is the typical case of a competitive inhibitor. It is also possible that a certain molecule is good at binding but the conversion rate is slower.
To conclude, these kinds of "errors" happen with many enzymes but it is very critical in case of DNA polymerization. You can get information on star activity of restriction enzymes (just google it).

Rubisco is an enzyme that is involved in the biochemical process of carbon fixation in photosynthesis, but also has an economically important error (photorespiration) which incorporates the wrong molecule (oxygen) into RuBP, therefore wasting the energy captured by the plant and producing toxic downstream products.
Rubisco's error rate in carbon fixation ranges from approximately 1:10 to 1:80.

Thank you very much for your answer. However, the paper you refer to neither contains the information about the error rate nor the table. Did I miss something or you took these data somewhere else?

@efrem Rubisco makes an error when it incorporates oxygen instead of carbon, and therefore the error rate is Vc/Vo.

Chris is right here, polymerases are generating sequences,  the enzymes your asking about do a single type of reaction, so you would be assessing its activity not its fidelity. A good resource I've found for looking at qc data for enzymes like these are just the product inserts from the manufacturer. NEB for example generally seems to provide sufficient qc data in my opinion. For example:
https://www.neb.com/~/media/Catalog/All-Products/B2D1E3A4F480489EAD7A1CD43E164DA0/Datacards%20or%20Manuals/M0233Datasheet-Lot0031209-1.pdf

DNA polymerase does single type of reaction too, namely, creates covalent bond between dNTP and DNA, releasing diphospate group $PP_i$

Since chemical reactions are governed by quantum physics, there is a whole lot of products that can come out of mixing together several multi-atom molecules. And all of those will have non-zero probability of occurrence. But this probability is extremely low at normal temperatures, so you don't see those products.
Enzymes lower activation energy and so increase chance of reaction, but only for certain substances and products (spatial position of reagents can influence outcome). In case of DNA replication, when wrong nucleotide is inserted, it happens because enzyme/template nucleotide complex has not enough specificity. All 4 nucleotides have rather high chance of participating in the reaction (but errors are still on order of $10^{-6}$ and lower).


text:
How to determine if this blood disorder is recessive or dominant?
This question is from "Concepts of Genetics," Klug & Cummings, 10e.
"Thalassemia is an inherited anemic disorder in humans. Affected
individuals exhibit either a minor anemia or a major anemia.
Assuming that only a single gene pair and two alleles are
involved in the inheritance of these conditions, is thalassemia a
dominant or recessive disorder?"
I know from a quick Google search that the disorder is recessive, but how would I come to this conclusion based on the question alone?
Edit: I've spoken to my professor, and he shared his opinion that is essentially the same as canadiener's answer. Thanks to everyone that replied!

I would say neither, as ">either a minor anemia or a major anemia" implies two phenotypes. This is co-dominance if I am not mistaken. Dominant would mean always major anemic (either homo or heterozygous) when affected, recessive would mean only major anemic (homozygotic). Perhaps the geneticists among us can look into this?

I was under the same impression about codominance, but the text splits up inheritance patterns by the usual dominant/recessive in one chapter and all the modified patterns in another. This question is listed in the first of these two, so I assume I'm given enough info in this chapter to be able to answer, but I just don't see the reasoning.

no answers in the back o/t book? ;)

Not for this one, unfortunately. Only evens get answers >_<. I'll consult the professor when I can.

don't forget to answer your own question then :)

I think in general, we prefer to use "incomplete dominance" when the heterogeneous phenotype is in between the two homozygous conditions, and "co-dominant" when the het show both distinct phenotypes.  If a red and white flower cross yields pink flowers, that would be incomplete dominance.  A and B blood types having an AB child is co-dominance.  But these terms don't really tell you much about the underlying molecular genetics

Given that this is a text book question about classical genetics, you can safely disregard any reality about the disorder.
I'd argue that the two alleles show incomplete dominance. The mild anemia, which is intermediate between healthy individuals and those with severe anemia, can be attributed to heterozygous individuals. In this case, the expression of the functional allele is not enough to compensate for the nonfunctional allele, producing the mutant phenotype.


text:
Why are plants classified in living things?
@Volunteers Beware that I am none of the biological magnates. Nor a philosopher. This is just a sign of curiosity. And, I want only an intuition that enables me to see the difference.
As far as I know, the growth of the plants and their metabolism is induced by Chemical laws and physical laws (govern matter and energy). Whatever, absorbing sunlight, photosynthesis, pollination etc are persuaded by physical and chemical laws. And, it is not surprising because all matters experience Physical and Chemical laws. The Food going upward in a plant is illustrated by Capillary Action. Pollination is influenced by wind and like that.
In my opinion, the chief thing which differs us from non-living things is the existence of 6 senses. At least, (various) animals have some of these. But as far as I know, plants possess none of that. So, after all, why are they classified in group of Living things? (Or, why plants' behaviour is not classified in Physics and Chemistry in stead of Physiology?)

First of all, plants do have all "feelings" in terms of their ability to response to environment . By your definition bacteria are dead, because they don't have a nervous system, but that is a very metazoa-centric view of life. There are many scientific definitions of life. I prefer a physics-inspired definition: life is a self-organizing self-reproducing system. Plants perfectly comply with this.

Please read the Wikipedia article about life.

Plants can sense IR light and adapt their above-ground growth accordingly. Chemoreceptors underground do the same thing for root growth. A plant is a living thing that senses, responds to the physical stimuli sensed, grows, reproduces and dies. The latter are referred to as the reproductive cycle. Never seen inanimate matter do all these things..

I'm voting to close this question as off-topic because it is philosophy and a mere attractor of philosophical debate.

The definition of life is definitely a question of philosophie. In the past however, we did make the effort to answer these questions by mainly focusing on describing the lineages of interest and not commenting too much on the philosophy part of the question. This question is similar to previous question about why viruses are not alive except that it is a lower level question. I think that it can be answered by listing a few life-sounds-alike properties of plants (as I tried to do).

Short Answer
Yes, plants are alive!
How to define life?
It is up to anyone to define what is living and what is not. In other words, the definition of what is living is arbitrary. Viruses are a common limit case (see the post why-isnt-a-virus-alive?).
What are plants able to do?
Now coming to plants, everyone seem to agree quite well on whether plants are alive or not. I think that you misunderstand what plants really are and that  brought you to eventually consider them as non-living. Here is a short list of things you might want to consider about plants.

Plants have DNA (plants often have very large genomes compared to animals).
Plants reproduce
Plants evolve (wiki > Evolutionary_history_of_plants)
Plants grow
Plants have a rich and complicated physiology and metabolism (wiki > plants_physiology)
Plants interact with other individuals of the same species and different species.
Plants can communicate (chemical cues) with other plants.
Plants are made of cells. Their cells contain a nucleus and a mitochondrion (just like animals). They also have other double-membrane organelles than mitochondria.
Plants are more closely related to animals than they are to bacteria. Animals are more related to fungi than they are to plants. (Explore the tree of life by yourself on tolweb.org)
Some plants also consume organic material (wiki > carnivorous plants)
Plants get diseases such as all kind of infection and cancer (wiki > Lists_of_plant_diseases)
Plants can be parasitic.
Some plants are motile (SE post > are-there-any-motile-plants)
Some plants are symbiontic (including endosymbiontic) and some are parasiti

Sensing
You seem to consider senses as an important distinction between living and non-living things. Note that the 6th sense that we attribute to humans have a pretty bad semantics and one could count more or fewer senses. Anyway, plants have tons of sense. They are able to sense:

chemicals
gravity
light
moisture
infections
temperature
oxygen and carbon dioxide concentrations
parasite infestation
disease
physical disruption
sound
touch

Conclusion
It would actually be quite complicate to find a definition that is not based on phylogeny or structural differences that would allow you to exclude plants but nothing else from the realm of what is considered alive. So, Yes plants are alive!


text:
What is an auditory upward sweep?
I was reading an article in nature communications, when I came across this sentence: "The ‘match’ rule was indicated by either a blue circle or a auditory upward sweep".So I tried googling what was an upward sweep, and came across this: "natural and complex vocalizations consist of basic elements such as upward sweeps, downward sweeps, constant frequency components, amplitude modulations..." I don't understand this. Can someone explain what is an upward sweep?
Here is the link to the article: http://www.nature.com/ncomms/2013/131128/ncomms3878/abs/ncomms3878.html,
But I think you have to pay to view the whole article, so here is another link that discusses the findings of the article:
http://www.uni-tuebingen.de/en/landingpage/newsfullview-landingpage/article/von-wegen-spatzenhirn-wie-nervenzellen-schlaues-verhalten-bei-rabenvoegeln-ermoeglichen.html

You should provide a link to the article.

Yes definitely include the article link. It sounds to me that the authors used a sound that started at a low frequency and increased in pitch over time.

It just means a sound that starts at a low frequency and goes up to higher frequency like a whistle sound. Perhaps someone can give you an example sound file and/or a spectrogram representation of it.

Copied from my comment:
It just means a sound that starts at a low frequency and goes up to a higher frequency like a whistle sound. Perhaps someone can give you an example sound file and/or a spectrogram representation of it.

http://jn.physiology.org/content/jn/94/2/1299/F2.large.jpg


text:
With the 5$ covid19 test - an antigen test - , would trials (most likely) be independent?
Actual question
What would typically cause antigen tests to give a false positive or false negative and would these causes be typically independent (if we run the test twice it won't automatically fail twice) or would such tests typically fail in the same manner and thus consistently give the same result for the same person? Or is this completely different from antigen test to antigen test and nothing can be said in general?
I hope this question is narrow enough, and I totally accept an answer of 'nothing can be said in general'.
Background
Abbott’s BinaxNOW was recently approved by the FDA. These are the false positives and false negatives rates given by Abbott:

Abbott says that the test correctly diagnoses a coronavirus infection 97.1 percent of the time, and correctly returns a negative result 98.5 percent of the time.

Therefore, the probability that one has the disease given that they test positive is - if I didn't make a naive mistake in my application of Bayes theorem and assuming 1% of the population currently has it - only 39%. This obviously is... pretty bad.
The useful thing about Bayes theorem though is that we can also calculate the chance of actually having Covid19 if we take the test twice assuming that both trials are independent (97%).

Your interpretation with Bayes therom is likely on point, and this is a problem with broad testing of populations with low underlying rates. It's easy to find scenarios where are test is returning more false positives than true positives, even with what seems like a good specificity values around 99%. My intuition tells me that this might not be independent, and that retesting a false positive would yield similar result, since a false positive is likely the result of non-specific binding to similar antibody. But they say that immunology is the place where intuition goes to die.

I don't know enough immunology to answer the question properly, but here's a cool article that goes through the numbers and talks about when it's useful vs. when it's harmful (https://blogs.sciencemag.org/pipeline/archives/2020/08/27/thoughts-on-a-new-coronavirus-test-and-on-testing)


text:
Is bacterial resistance caused by underdosing?

The phenomenon of antimicrobial resistance caused by overuse of antibiotics was predicted as early as 1945 by Alexander Fleming who said "The time may come when penicillin can be bought by anyone in the shops. Then there is the danger that the ignorant man may easily under-dose himself and by exposing his microbes to nonlethal quantities of the drug make them resistant."

Source: https://en.wikipedia.org/wiki/Antimicrobial_resistance#History
Obviously quotes from the history section are hardly authoritative, but I just wanted to check that although his prediction was correct, the mechanism that caused it was misunderstood at that time? My own understanding would be that resistance is about random bacteria being resistant and those bacteria thriving because all other bacteria were killed.

In a 2017 analysis in The BMJ, Martin Llewelyn and colleagues addressed the question of whether it is good to advise people prescribed antibiotics to "finish the course".1 I've copied their key takeaways below, but I encourage you to read the full article as they present a convincing argument that overtreatment is more dangerous than undertreatment in regards to the emergence of resistant organisms.

Patients are put at unnecessary risk from antibiotic resistance when treatment is given for longer than necessary, not when it is stopped early
For common bacterial infections no evidence exists that stopping antibiotic treatment early increases a patient’s risk of resistant infection
Antibiotics are a precious and finite natural resource which should be conserved by tailoring treatment duration for individual patients
Clinical trials are required to determine the most effective strategies for optimising duration of antibiotic treatment

References

Llewelyn MJ, Fitzpatrick JM, Darwin E, SarahTonkin-Crine, Gorton C, Paul J, Peto TEA, Yardley L, Hopkins S, Walker AS. The antibiotic course has had its day. BMJ. 2017 Jul 26;358:j3418.

You have to either subscribe (157 dollars per year) or  buy  the  individual  article (£30 / $37 / €33 (excludes VAT)) to read it in full. Regarding 'finishing the course'. Can we trust our doctors to prescribe a course that is commensurate with the illness the antibiotic is designed to treat? If so we should finish the course. If not, how do we decide when to stop? When we feel better? I recently had an abscess on my gums (ew). By day 3 (of a 7 day course) the pain had disappeared. Would it have been a good idea to stop then?

@Naj -- Here's a PDF hosted elsewhere. My answer addresses the question of antibiotic use in regards to antibiotic resistance, not in regards to disease treatment. Always take your medication as it is prescribed.

Hi, thanks, read the PDF. Of course, I acknowledge that your answer is about antibiotic resistance. However, the linked article does say the following (addressing my concerns about how you know when you're actually cured, as opposed to just 'feeling better') : "Outside hospital, where repeated testing may not be feasible, patients might be best advised to stop treatment when they feel better, in direct contradiction of WHO
advice." and "Research is needed to determine the most appropriate simple alternative messages, such as stop when you feel better."


text:
Oral allergy syndrom, continuation of continuous consumption of allergen
Wikipedia states on its page that

In addition, patients are advised to avoid the triggering foods, particularly nuts.

And same thing goes for webmd.com

The basic rule: If a food makes you uncomfortable, don’t eat it.

So two very related questions flow from this:

Does continuous consumption cause such an allergic reaction to become stronger?
And if that is the case, by what mechanisms does that happen?

And if possible at all, I would greatly appreciate it if you could keep the explanation to like a first year bachelor level (as in, anything a first year bachelor student would be capable of comprehending, not necessarily things that a first year bachelor student is typically taught) O:) . Anything beyond that I am likely to not understand even if I do take my time. And this is my first question on biology.SE so I hope I did everything correctly.

When you ingest an allergen for the first time, your body produces many of an antibody called IgE with specificity toward that allergen. These IgE antibodies bind to mast cells, and basophils. When you encounter more allergen, they bind to these IgE on the surface of the mast cells and basophils, causing them to release a host of chemicals like histamine. Massive amount of histamine are the cause of anaphylaxis, so when more allergen interacts with more and more IgE, the situation worsens. The following figure is a detailed mechanism,

Source
We can also see, though, that histamine released is a function of total allergen, and eventually reaches a maximum regardless of allergen present,

Source
Here they're showing histamine release vs allergen concentration while investigating allergic rhinitis.


text:
Mechanism of antiperistalsis
What is the mechanism of antiperistalsis that occurs during vomiting? Why the peristaltic waves normally don't propagate in anal to oral direction? Please give logical explanation with authentic sources. :)

What is the mechanism of antiperistalsis that occurs during vomiting?

Emetic agents in the bloodstream stimulate chemoreceptors in area postrema and nucleus tractus solitarius [1].
Nucleus tractus solitarius is connected to motor neurons in ventral medulla and hypothalamus [1].
Esophageal and gastric peristalsis is inhibited. Small bowel peristalsis is reversed. Esophagus and stomach don't have antiperistaltic movements [2].

Why the peristaltic waves normally don't propagate in anal to oral direction?

Because of the mechanism of descending inhibition. Distension of the esophagus and intestine causes a reflex action that leads to circular muscular contraction just above the bolus/chymus. Longitudinal muscle also contracts (shortens) [3].

Reference:

Hornby PJ. Central neurocircuitry associated with emesis. Am. J. Med. 2001 Dec 3;111 Suppl 8A:106S-112S. PubMed PMID: 11749934.
Brizzee KR. Mechanics of vomiting: a minireview. Can. J. Physiol. Pharmacol. 1990 Feb;68(2):221-9. PubMed PMID: 2178746.
AUMSA. Digestive Physiology. May 2012. CC-BY-SA-3.0


text:
Do hot drinks cool you down?
It is quite the old wives tale that drinking a hot drink cools you down. If you don't really think about it it does seem somewhat logical: increasing temperature will cause your body to try and cool down faster. This is of course flawed by the fact that you have increased your temperature before cooling it back down again.
I have had a bit of a look, but have been unable to find any evidence that addresses the fact that drinking a hit drink may make you feel cooler after sweating a little bit, rather than actually changing anything about your net temperature. Basically, is the 'cool down' just the placebo effect (you feel cooler because you think you feel cooler), or is there any evidence for a 'real' effect of hot drinks cooling you down? Or is there evidence that hot drinks do nothing at all except heat you up a bit before you come right back to the same temperature?

A Study by Lee & Shirreffs addresses this question.  Unfortunately I only have the abstract, but it's enough to summarise from:
Method

Three groups exercised by  cycling before being given water at either 10°C, 37°C or 50°C.
They then continued to exercise until exhausted.
Mean skin temperature, core body temperature and heart rate were measured throughout.

Results

Mean skin temperature was highest in the hot drink category - half a degree warmer than in the cold group.
There was a heat difference between the two outlying groups of 33kJ.

Irritatingly the pre-drink temperatures are not included in the abstract so it's hard to compare the effect that the drinks have had.  Certainly the hot drink has warmed skin temperature above the thermoneutral group but I suppose that could be due to increased vasodilation leading to better core heat dissipation (as you suggest).
In absolute terms, you are warmer than you would have been after having a neutral or cold drink, however it could be that you feel cooler as your hotter skin loses heat energy at an increased rate due to the greater gradient.

References

 Lee JKW, Shirreffs SM. 2007. The influence of drink temperature on thermoregulatory responses during prolonged exercise in a moderate environment. Journal of Sports Sciences 25: 975–985.

n.b. I got to that article on p4 of a pubmed search for hot drink - others might want to start from after there as there was nothing really before :)

They should've done a perceived temperature as well...

Another study found that hot drinks caused more sweating, and if the sweat was able to completely evaporate the net result was greater cooling than with cold drinks.  However, under real-life conditions sweat often does not fully evaporate, so the relevance of this finding is doubtful.


text:
What is the reason behind more severe proteinuria in nephrotic syndrome than in nephritic syndrome?
Why is there less protein loss via urine in case of nephritic syndrome than in case of nephrotic syndrome?

It is to do with the extend of the damage to the glomerulus. In nephrotic syndromes the glomerulus is damaged so that there is death of the podocytes. This happens to sufficiently high number of podocytes so that large proteins such as albumin and clotting factors can leak out causing large proteinuria. Damage to the basement membrane may also occur, such as in minimal change, where there is a loss of charge on the basement membrane.
In nephritic syndrome the damage is as a result of inflammation which does not lead to the same structural damage as in nephrotic syndrome, therefore there is not leakage of protein to the same degree.


text:
Do spouses begin to share genes over time?
I apologize if this hypothesis sounds strange by I was wondering if any research had been done on a phenomenon which I've seen and have corroborated with many other - the idea that over time spouses tend to start looking similar to each other.
My hypothesis is that this is really a one-way street with the wife tending to look more like the husband. The reason being that after coitus her body is flooded with his genetic material which may lead to some mixing of DNA outside of the egg. Furthermore once the woman is pregnant she enter into a symbiotic relationship with an organism whose DNA is approximately 50% foreign. Her body must then adapt to the presence of that new genetic material.
I realize this may sound strange and Lamarkian but I was curious if the phenomenon itself had been investigated.

While battling between Lamarkians and Darwinists, this sure has been investigated some time. The answer is: no. There are a lot of factors beside genes that can be a reason for this. First of all: our psychological reception of spouses. I, for example, tend to see similarities developing in people and their dogs over time. I am very sure they never ever share genetic material.

@skymninge i can show you images of couples you've never met. At their wedding they look a certain way, 20 years later they look strikingly similar to each other. From what I understand genetic change within one's own lifetime has not really been conclusively resolved.

I did not say, that I don't see those similarities. I see them quite often, EVEN between people and their dogs. But I would never account them to a genetic cause.

Microchimerism (Mc) is an interesting concept, and

refers to the harboring of a small number of cells (or DNA) that originated in a different individual. Naturally acquired Mc derives primarily from maternal cells in her progeny, or cells of fetal origin in women.

In women, it has nothing to do with transfer during/after sex but rather is due to the presence of the developing fetus.  There is definite long-term persistence of microchimerism, although not much is yet known about its effects.  Here is a nice and free review from 2010 dealing with the subject.  Most if not all of the effects have to do with immune function, in particular autoimmunity.  It is definitely not a mechanism by which couples begin to look similar.  That is social, in particular a result of living in the same environment with similar activities and tastes.  Male contribution to cellular content in the embryo is almost nil, as sperm die and the transcript count in the successful sperm is puny compared to the egg.  Most RNA content in the embryo is maternal until it switches to embryo.

Terrific, this is just what I was looking for. Very helpful and very interesting.

@user4481 There was an interesting article in Scientific American called " Your cells are my cells " by J Lee Nelson.Just google the title.

The actual article is behind a paywall, here's a pdf.  It's a great summary for sure.


text:
Is it a medical condition to not able to recall the word in a language while having a conversation
While having a conversation it happens to some peopl that clearly they know there exists a perfect word to be used but can not recall it during the conversation in real time and hence forced to use some other word which may not be so perfect.
But after the conversation is done they will be able to recall it. This happens very frequently to some people. Is this some kind of medical condition. If yes what is the name of this condition called as. ?

Welcome to Bio.SE! Thanks for your question. Self-help questions are strongly discouraged, so as to stimulate folks to seek professional help where necessary. Please remove any self-reference, otherwise the question may be closed. Secondly, it may be wise to post this question on Cognitive Sciences.SE as it may attract more attention there.

@ChrisStronks Thanks. Removed the self references

Have you read anything about any kinds of memory loss? Most accurately: maybe it is an illness, maybe it isn't.

@anongoodnurse Or may be it is a resultant of cannabis :P

The phenomenon you describe is known as tip-of-the-tongue phenomenon, where you know there is a word, and you feel it's "right on the tip of the tongue, but doesn't come out".
The phenomenon is normal and tends to worsen with age. Only in case it becomes so strong that it seriously interferes with daily life, it can be considered a medical condition (anomic aphasia) that may be indicative of damage to the brain, such as stroke, head trauma, dementia, or tumor.


text:
GWAS: matched-pairs and logistic regression
Logistic regression is a common analysis tool used for GWAS when your response variable of interested is qualitative. It comes as one of the standard tools in most GWAS packages (e.g. PLINK).
Most logistic regression models for GWAS would be setup as:
$\log{\frac{P(Y=1)}{1-P(Y=1)}} = \beta_0 + \beta_1*X$
Where $X$ is number of copies of the minor allele for a particular SNP of interest and $Y$ is disease stuatus. However, suppose that my case-control data is matched (In my case matched by age, BMI, reported ethnicity, and distance to procurement site). I don't think standard logistic regression (as I have outlined above) is valid. What does everybody do? I don't see options for this in packages like PLINK.
I also posted this question on (http://www.biostars.org/p/81394/) before I realized they were no longer part of stackexchange.

My first thought was to suggest a mixed effects model, so I will describe that first. But having had a Google there are models known as "Conditional logistic regression" models in which you can include any data structure as a covariate, which may be more appropriate, but I cannot vouch for them as I haven't used them. I would suggest reading the documentation.
Mixed effects models
I only know how to do this in R (stats language - www.r-project.org), but if you're using PLINK (so presumably also UNIX) R is pretty straightforward.
There are a couple of packages available for mixed effects models, my personal preference is function lme in package nlme (CRAN link). This type of model allows you to specify 2 types of independent variable (e.g. age, BMI, ethnicity... in your case);

Fixed effects - such as age, sex (something that is a phenotype of the samples),
Random effects - such as batch or other "technical" consideration,

This means you can format a model as you would before, but include an additional "random effects" term for your "matched" variable;
model = lme( fixed= outcome ~ exposure + covariate1, random= 1|matched )

.
Conditional logistic regression models
In the survival package for R there is a function called clogit (CRAN link) which seems to do exactly what you want. Although I have never used it myself.
From what I can gather this allows you to run a logistic regression with an additional covariate strata(matched), so your model may look like
model = clogit( outcome ~ exposure + covariate1 + strata(matched) )

.
Disclaimer!
This may not be exactly what you are after, as I'm not familiar with your data, so I would suggest heading over to https://stats.stackexchange.com/ as well, and searching for questions about regression analysis and paired observations - if none answer your question then ask a fresh one.

Thank you Luke. I'm quite familiar with R, and I figured either a mixed effects model or conditional logistic regression would be needed. I was just not seeing those in the basic GWAS packages...so I was wondering if I was missing something. Thank you!

@Benjamin I find that the published packages are only so useful - they're great for performing simple analyses via an established pipeline - but there is no substitute for creating an analysis that actually fits your data. Unless there truly is an established, published method, it is better to adapt one to your specific situation - all experiments are different and have their own considerations!


text:
Henrietta Lacks Cell Line - Immortality
I'm a newbie in biology and medicine. I understand that Henrietta Lacks provided the cells that formed the HeLa cell line with which much research has been done. Henrietta Lacks died of cancer. If we assume that she did not have cancer, every cell in her body could divide for an infinite period of time, and she never sustained any trauma ever, would Henrietta Lacks have been immortal?
Thanks,
mj

This doesn't seem to be a question about Biology?  Or is your question more generally, if someone's cells could "divide for an infinite period of time" would they be immortal.  HeLa cells worked in tissue culture (TC) because of her cancer, and indeed new primary cells must be "immortalized" before they can be used in TC.  https://en.wikipedia.org/wiki/Biological_immortality

I'm curious about this from a biological perspective.

Immortality does not exist and has never existed.

No, there was nothing special about Henrietta Lacks, apart from the fact that her cells have been used for so many years (without her knowledge or consent, by the way). She was not immortal, her tumor cells were. The HeLa cell line comes from her cervical cancer cells. The rest of the cells of her body were not immortal any more than yours or mine are.
Such immortality is a classic characteristic of cancer, in fact it is a hallmark of tumor cells. Normal cells die when they are told to, apoptosis (programmed cell death) is a normal part of a functioning, healthy organism. Tumors are collections of cells that replicate uncontrollably and do not do what they're told, including dying like good little soldiers.
That is why we often use tumoral cells for cultures, since they have been immortalized, it is relatively easy to keep them alive in the lab. This means, essentially, that they produce an enzyme called telomerase which lengthens telomeres. In normal cells, the telomeres get shorter with each round of mitosis and when they get shorter than a certain threshold, they are targeted for apoptosis. Cancer cells are protected from this by the telomerase and can therefore undergo many more rounds of reproduction.
So, the cells are not special because of the person they came from, they are special because they are cancer cells.

This is very interesting because I have the same understanding: "cancer cells are "immortal" in the sense of permanent division". So HeLa cells are not very specific. But sometimes, Henrietta Lacks is presented as a unique discovery. Why is that? Is it because her cells were the first to be cultivated?

@totalMongot if you have a new question, please ask it separately, but no, there was nothing unique about Ms. Lacks beyond the uniqueness of every human being. The only reason she is well known is because eher cells were used (stolen, actually, but that's another story and easily googleable) and have been used ever since.

Ok thanks, this confirms my general understanding. Any person with a cancer pathology could have provided those cells

I believe your question is unclear, but if am I am understanding the question as:

If H.L., or anyone, did not develop cancer, was never introduced to any physical insult, would they be immortal?

The answer is no, they would not.  When we talk about aging in biology, we use the technical term senescence.  Without a cancerous influence normal aging would occur, and cell division would be halted by a number of factors.  One of the best researched causes of aging is telomere shortening.
The reason that HeLa cells can be passed indefinitely is that they are immortalized.  You can only get a few passages (allowing the cells to grow out from one plate to the next) out of primary cells directly from a human.  This varies some based on the cell type, but is a good rule of thumb.  The basic rule as to how often this can be done is described as the Hayflick limit.
So no, free of cancer and all insults may mean you lead a long life, but you will most certainly not be immortal.