Why would a single celled organism evolve to be multi-celled? I read a story this week on Richard Lenski who has been 'evolving' E. coli for more than 50,000 generations now.  One comment I read was from someone who doesn't accept Evolution who pointed out that we haven't seen a single celled organism 'evolve' into a multi-celled organism.  Another person responded and said that a bacteria is not going to evolve into something that isn't a bacteria.

So, if Evolution created single celled organisms and then multi-celled organisms how might that change have happened?  And is it possible to recreate that set of driving forces to make a bacteria something other than a bacteria?

To that end, what advantage does being multi-cellular have over being unicellular (if that's even a word)?

How did multicellularity evolved?

It is an ongoing field of research - Some insights about the origin of multicellularity

This is a big ongoing field of research. To start with an example, there was relatively recently (2012) an important article by Ratcliff et al. that shows that yeast can quickly evolve multicellularity under selection on the speed they sink to lower water layers. This article is one among many others and is far from being able to explain everything we would like to understand about the evolution of multicellularity. Typically, I think that this yeast species had a multicellular ancestor and we might think that this species would already have fixed alleles (=variants of genes that is fixed meaning that the whole population is carrying this variant today) in the population predisposing this species to easily (re-)evolve multicellularity. Also, they may have kept some standing additive genetic variance in their genome from their past and they would therefore very quickly respond to selection as they don't need de novo mutations. (Sorry if this last sentence was slightly technical).

One of the first traits that we usually refer to when talking about the evolution of multicellularity is the presence of sticky proteins allowing individual cells to paste to each other.

Some insights about the evolution from simple multicellular to more complex multicellular

Then, we could talk about more complex multicellular and argue how do these simple multicellular evolve into some more complex organisms. A common argument is that multicellular can have specialized cells are very could at doing what they're doing as they are specialized. Also, some level of complexity is thought to have raised due to the fact that multicellular organisms tend to have smaller population size than unicellular (see Lynch and Conery, 2003). It is important not to confuse evolution of complexity with the evolution of multicellularity although these two notions are somehow related.

What do you mean by multicellularity?

The evolution of multicellularity can be discussed in the context where sister cells form an organism together or when unrelated cells (among the same species or even cells from different species) come together to form an organism. Also, the multicellularity can be discussed at a different level depending on how we want to define multicellularity. Is a stack of cells reproducing individually, working for their own benefit a multicellular? Do we need a division of labor? Do we need a division between germline (reproductive caste) and soma line (non-reproductive case)?

How many times did multicellularity evolve independently?

Some people consider that there are multicellular bacteria (biofilms) but we will avoid discussions that are based on limit-case definitions. Let's talk about eukaryotes. Most Eukaryotes are unicellular and multicellularity evolved many times independently in eukaryotes. To my knowledge, complex multicellularity however evolved only (only?) 6 times independently in eukaryotes.

Metazoa (animals)
Ascomyceta (fungi)
Basidiomyceta (fungi)
Viridiplantae (green plants)
Florideophyceae (red algae)
Laminariales (brown algae)

Model organisms and interesting cases to study multicellularity

There are a bunch of specific clades that are particularly interested in studying multicellularity because they present transition states. For example Volvox is a chlorophyte genus and the species in this clade present different stages of multicellularity; Some species are exclusively multicellular, some form small groups, some create big colonies, some have some division of labor and some even have separation between the germline and the soma (Some castes don't reproduce). (ref1, ref2, ref3, ref4, ref5, ref6). Yeasts are also a good model organism for studying the evolution of multicellularity.

The eucaryote that became the modern organelle mitochondria, combined with procaryotes. This probably occurred as a result of the mitochondria being absorbed by the parent cell but not destroyed as it usefully created energy rich ATP molecules using Oxygen and Water through respiration.

These were the first Eukaryotic cells, they went on to become Eukaryotic, multicellular life.

Various benefits to Eucaryotes becoming multicellular include:

The volume to surface area of a cell gives cells a natural size of a few micrometers. Larger single cells find it increasingly difficult to absorb enough nutrients or oxygen for the volume of there cytoplasm.

Amoebas can be larger due to being so irregular in shape, this ensures that so nowhere inside the cell is it too far from the cells surface. Various more spherical centimetre scale single celled life also exists in nutrient rich parts of the deep ocean, such as the Valonia Ventricosa.

https://en.m.wikipedia.org/wiki/Valonia_ventricosa

Another advantage is that structures can form between cells, outside of the cell walls, that can still be protected inside the creatures body. Such a connective network in animals called the extracellular matrix.

https://www.khanacademy.org/test-prep/mcat/cells/cytoskeleton/v/introduction-to-cytoskeleton

Note that creatures like the sea sponge are multicellular, but do not have distinct areas of the body such as organs in the same way as animals do.

"The genes I discuss in my article were not present in the common ancestor of all life on Earth. They do not exist in bacteria, for example. They do not even exist (as far as scientists know) in sponges. Only after the ancestors of cnidarians and bilaterians diverged from sponges did they emerge." (A planet of viruses, Carl Zimmer) This is the quote I could find, as I remember, relating to "bodybuilding" in many creatures, but not the sea sponge.


How does the immune system distinguish between a TH1 and a TH2 response? Hello and thanks for taking the time to read my post.

I know that naive T-Cells (T0) can be induced to become mature T-Helper cells (TH1 or TH2)
by induction with either IL2 or IL4.

IL2+  TH0 -> TH1   Humoral (antibody-mediated)
IL4+  TH0 -> TH2   Cell Mediated response

But what I would like to know is the causal chain that creates the IL2 and IL4 cytokines.

The reason I ask is because one clinician has reported that Azythromycin(an anti biotic) is useful in treating COVID-19(a virus) disease and was wondering if the immune system might become confused about whether should develop a TH1 or TH2 response.

If you can provide me with any help I would greatly appreciate it

Thanks in Advance
Michael Mckeon

From what I have read, the Stage 3 differentiation depends on the surrounding cytokine environment. IL-2 does not specifically promote T-Cell differentiation, it is a general growth factor which promotes proliferation, and is secreted by both profiles.

Differentiation of T-Cell into Th1 is controlled by Interferon Gamma, the production of which is stimulated by IL-12, which is secreted by many APCs (upon stimulation by IFN Gamma produced by cells, in a self-feeding loop). IFN Gamma also suppresses IL-4 production.

Th2 cells are promoted by IL-4. It is not exactly known which cell initially produces IL-4, but it could be basophils. IL-4 then acts in a self-promoting loop, which encourages T-Cells to produce IL-4 as well as other effector cytokines, and also stimulates IL-10 production, which suppresses production of IFN Gamma and IL-12.

Thus, each pathway is self-promoting and suppresses the other pathway, ensuring that the immune response is set in stone.


How does injecting low doses of allergens cure allergies? Allergy shots (aka. allergen immunotherapy) help people adapt to allergens by injecting a gradually increasing doses of one or more allergens.

Does this procedure tell the body that this allergen is safe and there is no need to mount a response to it? In other words, does this mean that there will be no reaction at all rather than just a reduction in the allergic reaction.

But are there ways to tell the body that this allergy is safe and there is no need to amount a response to it?

Yes, that's what allergy shots (Exposure Therapy) does. Exposure Therapy is an effective, albeit sometimes imperfect, method of letting the body know that a substance is common and that it shouldn't mount a response to it. Over time the body re-calibrates itself to accept the allergen, although in some cases it's never fully accepted.

A complete "cure" can be attained via allergy shots, but the extent of the therapy's success will rely almost exclusively on the individual's immune system. Some people can be cured completely, others will never be cured.

  If not, why not?

There will probably not be a general "allergy" cure anytime soon because we're still not 100% sure why the body responds in such an overprotective matter sometimes and not others. Even if we fully understood at some point, there are many ways which the immune system can go awry that result in allergies.

There isn't a single, double, or triple point of failure along the line - just about any immune cell, whether Mast, Eisonophile, T-Cell, T-Reg, B-Cell, etc. can misidentify a substance and contribute to an allergic reaction (although some are more likely candidates than others). More than that, just about any substance can become an allergen for people. There's a well-studied case of a woman who became allergic to Copper because of repeated exposure via an early version of IUD that she had implanted.

So with nearly every immune cell capable of mounting a response, and nearly anything in the world capable of provoking a response, the best route - at least thus far - has been repeated, increasing exposures to teach the body what is "OK" and what isn't. The absolute best way to avoid allergies later in life is to simply promote outdoor playtime and a widely variable diet to children while the immune system is operating at peak efficiency and learning capability.

Immune Amnesia

I have a speculative idea of how someone might start to turn off allergic reactions in the immune system.

I've read that the measles virus can cause "immune amnesia".

If biologists had a deep understanding of why this happened, then maybe they could use that understanding to wipe of immune memories that cause allergic reactions.  Maybe they could use a genetically modified measles virus, maybe something else inspired by this.

I'm sure someone else must have thought of this before, but I haven't seen anything when I searched.

I think it would be an interesting beginning for a research project.  But I'm not a biologist, so I wouldn't really know.


Are there examples of encryption in nature? There are examples of mathematics in nature such as Fibonacci number, fractals, etc.  Are there examples of encrypted information?

What I am looking for is a pattern that seems random on the surface, but once you put it through a "decryption" process, it is actually something else.  Not patterns that seem random because they are complex.

One example that comes close is DNA.  But I see DNA as a form of encoding, not encryption.

One example is in the development of the immune system. V(D)J recombination, antibody production, and T-cell receptor production generates a specific "key" that, in most cases, can only be bypassed by that individual's molecular inventory.

In that sense, parasites, mutualists, and commensalists could be viewed as black, white, and grey hat hackers, respectively.

Another example is the organism-specific tRNA synthase inventory and the matching tRNAs.

Interspecies communication at the human level obviously includes cryptography, it could be surmised that most animals and plants probably do some version of communication and hence, some cryptography (as all have predators.) The aforementioned viral example seems very apt, also interesting might be communication within a larger group, biofilm exhibiting herd-like communication in the presence of complex predators or anti-biotics for example. If whales communicate in the ocean, perhaps bacteria and viruses communicate and encrypt non-chemically in biofilm and hosts.


There are small parts between Genes in an Operon that does not encode for any amino acids. What is the purpose of these parts? What is the purpose of these parts in the translation process ?
Picture to demonstrate below :

The regions between the genes on a prokaryote operon are transcribed into the messenger RNA  but are not translated into proteins.  Because they are not translated, they are characterized by the general term UnTranslated Regions (UTRs).  A typical operon having two genes is shown in this diagram from Wikipedia:

The UTR which occurs between the protein-coding genes contains the sequence for a ribosomal binding site (RBS) in the transcribed mRNA.  An RBS is a site where a ribosome can attach to the mRNA so that the Start codon of the following gene is in the correct position to begin translation of the protein.  (Of course, the 5' UTR preceding the first gene also has an RBS sequence.)  An RBS contains a particular nucleotide sequence to match up with a complementary sequence of the ribosomal RNA of the ribosome; this sequence is known as the Shine-Dalgarno sequence.

(Note that these inter-gene UTRs are not called introns; introns occur only in eukaryotes and occur within a gene, between the Start and Stop codons.)

Not sure about the role in this particular case of lac operon but normally such noncoding sequences in eukaryotic system (intron regions) have some regulatory roles, may be on the same gene or other genes located elsewhere on the chromosome. For example intron 3 of gene A may act as an enhancer sequence of gene B located 500 bp downstream of gene A

In this case the operon is producing three different proteins, if there were no gaps then a fusion protein may have been produced which is not desired


Lotka-Voltera predator prey model isocline? In lotka voltera predator prey model, why do we get a straight isocline with variable prey/predator population for single value of corresponding predator/prey?

I understand that we get the prey isocline by the equation

N1=prey population ; n2=predator population

What I don't understand is why we are getting variable prey population on isocline for same value of predator population. Shouldn't the prey population be also constant?

PS: I picked the graph image from the internet so the symbols are different. Sorry.

I think your issue is mainly with the interpretation of the isoclines.

If you assume this standard predator-prey model:

$$\frac{dN_1}{dt} = rN_1-pN_1N_2$$
$$\frac{dN_2}{dt} = apN_1N_2-mN_2$$

you get the isoclines:
$$ N_2 = \frac{r}{p} $$
$$ N_1 = \frac{m}{ap}$$

with the first isocline referring to prey and the second to predators. These isoclines mean that the population growth rate of prey and predators (respectively) will be zero exactly at these isoclines (as well as at the point N1=N2=0). Since the isoclines, for this partuicular model, are fixed values and not functions of N1 and/or N2 they will be strait lines. Also, in a sense, you should view the isoclines as the borderline case where population growth rate shifts between a positive and a negative value (ie a growing or a decreasing population). The isoclines are not giving you the population size of the prey at a certain predator population size (which you seem to be implying with "...why we are getting variable prey population on isocline for same value of predator population"), but the locations in the plane where the population growth rate (for either prey or predators) is zero.

A graphical view of only the prey isocline (with some color coding) can be:

This means that the prey population (blue) is growing (arrows to the right) below the blue prey isocline, so there if a "flow" to the right there, while it is declining at predator population sizes above the isocline (arrows to the left). So basically, for all predator population sizes (N2) below isocline the prey population will grow, and for all N2 above the isocline the prey population will decline. In reality the rate of increase/decrease differs depending on how far from the isocline you are (so arrows should be of different lenghts), but to simplify the issue and to show the general principle I'm just showing the direction of flow here.

The same picture for the predator population is:

Here the predator population (orange) is declining to the left of the orange predator isocline (arrows down) because there is too little prey to sustain the population, and increasing to the right of the isocline (arrows up).

If you combine these you get this, with the black arrows showing the overall direction of the combined population trajectories:

I hope this clarifies the issue a bit. Otherwise, please comment and hightlight what parts you find unclear.

Also, the dynamics of this Lotka-Volterra model also means that populations that start exactly at the intersection of the isoclines (i.e. both N1 and N2 will lie at that point) will stay there, since that is an (unstable) equilibrium point. Populations that are started anywhere else in this plane (except for cases where N1 and/or N2 is zero), will follow an oscillating population trajectory, that will not change if there isn't any external pertubations (environmental changes, input/output through immigration/emmigration etc). Therefore, the combined trajectories of N1 and N2 will form an ellipse in the plane, until they are perturbed (by something outside the current model), when they will then settle at a new ellipsis. For examples of the ellipses, see this phase-plane graph from Wikipedia, with initial values as points:

However, also note that changing the model, i.e. to include a logistic component to the prey population, will completely change the population dynamics.

I am going to try and cover the math with a few more words, to show that your intuition is in fact, correct (which with math, is not always given).

In the differential equation you wrote $$ \frac{d N_1}{dt} = r_1 N_1 - p_1 N_1N_2 \;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;\;     (1) $$
the numbers $r_1$ and $p_1$ are simply constants that give a strength of coupling, between the change of a variable (the left-hand side) and how this change is computed (the right hand side).
Would you set $p_1=0$, then the resulting solution of (1) would be an unhindered exponential growth. If we go and increase $p_1$ to $p_1>0$, then we increase the "efficiency of conversion from $N_1N_2$ into negative $N_1$", or more simply put "the predators become more efficient at hunting".

Hence, intuitively, as the predators become more efficient, by increasing $p_1$, the prey population cannot grow exponentially grow to infinity any more. It must now level off (as the solution of (1) will show you, if you keep $N_2$ constant, see also the logistic function "In ecology: modeling population growth").
And the stable value towards which it is leveling off, is given by the requirement $\frac{d N_1}{dt} =0$, which leads us to the isocline $0=r_1-p_1N_2$.

Now, coming back to your question, it is important to notice that by requiring $\frac{d N_1}{dt} =0$, we have already set $N_1=const.$, we just have no means yet to compute this value.
 So the prey population is in fact constant! And the predator population that can live off this unknown value is given by the ratio of prey multiplication vs. hunting efficiency, which is the isocline.

As a last comment, it is strange that an equation for $N_1$ turns out to give us the most  information about $N_2$, but that's how it often is with coupled differential equations.


No bands show up in gel electrophoresis, not even marker I haven't seen any gel lanes in neither my PCR samples nor the marker itself when photographing them.  This is not my first time performing 1.2% agarose gel electrophoresis.

I see gel lanes when I take the gel out the apparatus, but when I go to photograph them:  nothing shows up.  I only let the samples "run" for 30-40 minutes (when I ran for an hour, the bands almost ran off the gel).

Tried using different markers:  no luck.

Re-added some more EtBr to better stain the gel:  no luck.

I am also keeping the lights off in the dark room, so I do not think I am exposing the film to light early on (errors still a possibility though).

What could I be doing wrong?  Am I taking the film out too early?

What I can quickly think of is that you were running the gel incorrectly: instead of from - to + direction,  You ran it the other way around and your DNA went out of the gel. Another thing might be that the UV light was not turned on or is broken.

May your gene of interest will not be cloned perfectly that is the reason, make sure that first you have to run pcr well accourding to your sequece then run the gel


Is viral single-stranded RNA in the absence of reverse transcriptase infectious? In a medical microbiology textbook I'm reading (Murray et al, 1994), the authors state the following:

The retrovirus genome has a 5' cap and is polyadenylated at the 3' end. Although the genome resembles a messenger RNA (mRNA), it is not infectious because it does not encode for a polymerase that can directly generate more mRNA. The genome consists of at least three major genes that encode for the enzymatic and structural proteins of the virus: gag (group-specific antigen), pol (polymerase), and env (envelope). At the end of the genome are long terminal repeat (LTR) sequences

From this, I interpreted that because viral RNA doesn't encode an RNA polymerase, it is not itself infectious. However, if a cell were to be injected with retroviral single-stranded RNA alone, wouldn't this RNA be translated into proteins (including reverse transcriptase) as if it were normal mRNA into a protein? If this were correct, then the single-stranded RNA has all the information in itself to propagate the virus. Single-stranded RNA needs to be reverse-transcribed into the host's DNA before being transcribed into mRNA that can be translated.
Is there something different between viral RNA and the mRNA transcript that makes one translatable and the other not?
Source: Murray, Patrick R et al, Medical Microbiology (1994), Second Edition.
EDIT/UPDATE
I contacted the author of this chapter (Dr. Ken Rosenthal) and gained some more insight into how this hypothetical (injecting plain retroviral RNA into a cell) would play out. His answer is that yes producing new viruses possible but not probable. The reasoning for this is as follows:

The main reason that a new virus would likely not be created is that for the genome to make a new virus, reverse transcriptase is needed. Without reverse transcriptase, cDNA can't be made. Suppose that a ribosome was able to make reverse transcriptase with naked retroviral RNA and this newly made reverse transcriptase stayed near the ribosome. It would have difficulties making new cDNA from the original RNA template. One of those challenges is that cDNA synthesis needs a specific primer on reverse transcriptase.
The translated retroviral RNA would likely be degraded due to their finite lifespan in the cytoplasm.
There would need to be enough viral proteins translated to form a capsid. This would be unlikely considering the lifetime of the RNA in
Even if there were enough proteins in the cytoplasm, these proteins would then have to remove the RNA from the ribosome to encapsidate it. This is also unlikely.

Considering this, the microinjection of naked retroviral RNA would be an inefficient process to cause an infection.

In RNA viruses with a single-stranded genome, this RNA can be positive or negative sense. Positive sense RNA is directly translatable by a ribosome, while a negative strand RNA cannot be directly translated and therefore non-infectious. It either has to be converted to a positive strand RNA with the help of an RdRP (RNA-dependent RNA polymerase, carried in the virion) or reversely transcribed into a DNA which then serves as the template for generation of translatable mRNAs. In either case, this RNA is non-infectious in absence of the necessary proteins.
Note that positive strand RNA has to be propertly capped in order to be translatable. This is also not always the case - some viruses generate or steal the cap from the cellular mRNAs once uncoated in the cell.
Another aspect worth mentioning is that positive-sense retroviruses usually code for their genes in multiple reading frames and make heavy use of splicing to produce their proteins. Thus, directly translating their positive sense RNA is not sufficient for infection.
From Chapter 3 in Viral ecology:
For plus-strand RNA viruses except retroviruses, translation of the viral RNA
follows immediately after uncoating. The viral RNA extruded from the capsid is then
used by the host translation machinery for directing protein synthesis (Fig. 9).
For all other viruses, whether of DNA or RNA genome, the step immediately following
uncoating is either transcription of the genome yielding functional mRNAs or
reverse transcription of vRNA yielding proviral DNA (retroviruses).

References:

Viral Ecology
Principles of Virology

As far as I can understand, the poster is concerned about the statement:

Although the genome resembles a messenger RNA (mRNA), it is not infectious because it does not encode for a polymerase that can directly generate more mRNA.

I find this a somewhat unfortunate aside as the infectivity or not of viral RNA “injected into a cell” has no physiological relevance, and would advise the student to focus on the essential details of the actual viral life cycle rather than on this sort of thing.
However, the point it would seem that the poster and the other answer misses is that numbers count. A virus (or viral RNA) needs to generate enough progeny for infection to overwhelm antiviral defences. This entails there being sufficient mRNA generated from the genomic RNA (or DNA) for translation into protein.
In the case of ‘normal’ RNA viruses (i.e. non-retroviruses), this involves an RNA-dependent RNA polymerase, which has to be virally coded as the host cell does not have such an enzyme. Retroviruses, however, produce multiple mRNA molecules from an integrated DNA genome (integrated through the RNA-dependant DNA polymerase — reverse transcriptase) by using the cell’s DNA-dependant RNA polymerase, not from replicating the transcribed mRNA.
All viruses rely on host protein synthesizing systems to translate their mRNAs. But a single retroviral RNA that can act as both mRNA or (part of) the genome can only generate enough coat proteins etc. to encapsulate it (or enough reverse transcriptase to reverse copy it). A situation unlikely to cause retroviral RNA to be infectious in this hypothetical situation. I imagine it is this that the authors of the text have in mind.
The student of this subject would do well to distinguish the different transcriptional enzymes involved in viral replication and learn to refer to them by their full names.
Reference: Coffin et al. Retroviruses (1997), available on NCBI Bookshelf


Cell division - meiosis Really confused. How many chromosomes pairs do humans have in their sex cells? How many single chromosomes do humans have in their sex cells?

Terminology is what is holding you back.
What chromosome implies depends on context, i.e. is it replicated or not.

In Meiosis. Gametes arise from Germline cells that have 23 PAIRS of chromosomes. That means, that while there are 23 different chromosomes they come in doubles/pairs. This is the typical X like shape we think about when we hear chromosomes.
Another way, chromosome can means either 1X or 2 single chromatid

MEIOSIS I -- 23X chromosome pairs are duplicate and end up as 46X chromosome pairs (46 pairs of X OR, 92 separate chromatid)

These 46X are divided equally among two daughter cells just like in mitosis. Where now each daughter cell receives 23X = 23 pairs.

MEIOSIS II. The daughter cells in end of Meiosis I divide without DNA replication and the 23 pairs are split among 2 new cells. So now each new daughter cell (in total 4) has 23 individual chromatid (individual chromosomes)
and these are the gametes.

When the gametes fertilize to form a zygote, the zugote product ends up 24X each.

Each X contains, 1 chromatid (|) from the father and 1 chromatid {|} from the mother.

Haploid means once copy of each chromosome.
23
Diploid means two copies chromosomes or 23X

Ref
- Allison Q.N,.(2015), Freeman Biological Science.


Advantages of pain sensation? The hazards of congenital insensitivity to pain (CIP) are well-known.

This question is about the obverse: what selective advantage, if any, does the normal sensation of pain confer? I'm thinking of severe pain such as that associated with back injury, burns, and some intestinal problems in which the pain seems to serve no function other than to incapacitate.

A related question is whether there is a spectrum of sensitivity to pain, ranging from CIP to heightened sensitivity, what the distribution looks like, and whether this is a genetically plastic trait (like color perception)? If the distribution were sensitive to selective pressure then naively I would guess it serves our needs well, but we spend a lot of our collective time trying to dial it back, hence my question.

Yes a range of pain exists. This can be seen probably in your friends who all probably have a completely different threshold for pain. When doctors ask patients to rate their pain it's usually to establish a baseline so after treatment we can see if there's a decrease. The different thresholds have so many factors from general health to receptors to brain activity to emotional state. You name it! Often just focussing on a pain makes it more painful.

It's definitely an unpleasant sensation pain but it's our way of our body saying "hey, you need to pay attention". Usually the response required is rest or to identify what might be there causing the pain. For example pain means we will withdraw very quickly from a hot surface. Doesn't even require the brain as it is a reflex arc which minimises the time we spend burning that part of our body. And as it continues to hurt we use the arm less letting it recover and protecting it from infection by doing so.
As these hazards of being cut, burnt, bit, knocked, fractured are very common there is a survival advantage to be the individual that is alerted to these hazards and take the necessary actions. Particularly in children where pain is necessary as it makes the baby know it needs to eat (or the mother) or that something isn't a good idea (putting hands on something hot).

However as you say there are times when the pain itself is more crippling than anything else and in that situation we have a problem. Childbirth, backache and in cancer or in tension headaches are just some examples. As being able to feel pain is pretty much required for a long life, the disadvantage of having pains like the above is less and doesn't outweigh the benefits. Pain is always going to be necessary. They also usually don't interfere with reproduction and so genes are passed on.

In terms of inflammation, the purpose of pain is to force the organism to rest the area that is inflamed. Thus promoting healing. In terms of chronic pain, this is the same thing. However I think that if the pain will not cease regardless of protection of the affected area, and say if the underlying cause of the pain is ultimately fatal, then the pain is subordinate. The phenotype is already being selected out.

I think the concept shows a lot of parallel to the underlying concept of hypersensitivity (allergy).

Remember that over generations as all different things that can cause and prevent pain in our bodies are evolving, So too is the pain mechanism itself evolving.


How did butterflies evolve to have eyes on their wings? Some butterflies, such as the UK native Peacock butterfly (Google Image Search) have markings on their wings that look just like eyes, complete with a white fleck to imitate a convex, transparency effect, as though the "eye" is reflecting sunlight.

Presumably, this pattern is designed to deter prospective predators, because the predator will see a creature with massive eyes looking at them and think twice before attacking.

But how did the pattern evolve?  Was the first one a fluke / a genetic mutation that happened to work, or is there another explanation?

For possible bonus points, is there any way of telling when this occurred, and therefore making a guess as to which creature's eye is being imitated?

You're correct with the genetic mutation bit. A basic explanation would be:

Some gene or genes became mutated that lead to the coloration you see, and the end result was that the butterfly or butterflies with the mutated gene were able to produce more offspring or offspring which survived better than the eyeless versions.

There are ways of dating genetic mutations by comparing one organism's genes to another, but accuracy can be an issue without some significant genomic study to confirm mutation rates and other aspects.

However, the butterfly wouldn't be purposefully imitating another creature's eye. It may be by chance and/or predator behaviors that the eyespots look like the eyes of another creature, but the adaptation wasn't a willful act. It was a random genetic mutation or mutations that lead to beneficial coloring, and the eyespots may have improved over time as more mutations occurred.

I read above ;

''Some gene or genes became mutated that lead to the coloration you see, and the end result was that the butterfly or butterflies with the mutated gene were able to produce more offspring or offspring which survived better than the eyeless versions.''

But, for the genes to mutate randomly, an eye would not form, but a mess.
Further,  how strange it is, that neither the butteryfly nor the genes are able to see this manifestation. Yet any preditors, from above sees it clearly.

To apply that this random mutation and natural selection, makes up everything that we know, is in itself blind and calls for an eye.

I will state, it is positive variation and nothing more nothing less.
No lifeform goes downhill in terms of evolution. Random anything would render any 'random' lifeform , lifeless.


Effects of lactic acid ingestion What would happen if I drink lactic acid?

I use lactic acid to clean an espresso coffee machine and I wonder what injuries could occour drinking it.

No, don't drink it... And here's why.

Ingesting lactic acid or for some reason having too much of it in your body can cause a variety of health problems ranging from mild to deadly. There are two types of lactic acidosis; the first is called metabolic acidosis and the second is known as respiratory.

Metabolic acidosis - which is what would be caused by ingestion - occurs when the fluids in your body build up too much of the acid and your kidneys can no longer keep up with the demand placed on them. Or they over respond and remove too much base from your body, leaving you acidic.

Respiratory acidosis is caused when your lungs cannot effectively remove CO2 from the blood. A buildup of CO2 leads to a more acidic body chemistry.

Regardless of what the cause of the acidosis was, you can expect some of the following.

Symptoms of metabolic acidosis:

~Rapid and shallow breathing

~Confusion

~Fatigue

~Headache

~Sleeplessness

~Lack of appetite

~Severe acidosis can cause shock, organ failure and even death

Diagnosis of acidosis:

A series of blood tests will check calcium, sugar and electrolyte concentrations in your blood.

My sources for this information:

Healthline

WikiPedia on Lactic Acidosis


Why does heating kidney beans at a low temperature potentiate the toxicity of phytohaemagglutinin? I recently found out that red kidney beans contain a relatively high amount of the toxic lectin, phytohaemagglutinin.
An article on phytohaemagglutinin on the FDA website states:

Several outbreaks have been associated with "slow cookers" or crock pots, or in casseroles which had not reached a high enough internal temperature to destroy the glycoprotein lectin.
It has been shown that heating to 80°C may potentiate the toxicity five-fold, so that these beans are more toxic than if eaten raw.

What I do not understand is how the toxicity could increase if the beans are cooked at lower temperatures in a crock pot. I would understand if the toxicity remained the same (that is, not be deactivated), but I thought a toxin is nonliving (i.e., unable to grow and reproduce) since it is not a bacteria?
I know nothing about biology, so I am utterly confused.

I am a Snr lecturer and a PhD candidate. Currently, I am putting my theses together. My research area involve in part the kinetic degradation of lectins in neglected and underutilized legumes. I  also looked at the possibility of using irradiation to produce complexed degraded starches  to inactivate lectins during low temperature extruder cooking.I observed in some of the extruded samples that lectins have actually potentiated up to about 50%. I was confused. I know lectins are proteins so they are supposed to denature when heated. I was looking around to see whether someone has made similar observation and I saw that indeed somebody has reported similar observation. I was so over joyed but it was short lived-no explanations were offered.  I now offer a possible explanation. Yes, lectins are proteins(or glycoproteins) and like most proteins their tertiary and quaternary structures are 3D. So the 3D forms have a couple of smaller subunits, woven together into the giant super structure(lectin). In the 3D form, most of the binding sites are "buried" or not fully exposed. It is possible that these smaller units have binding sites for carbs and are best positioned to present their ligands for  exposure and maximal binding when the 3D structure begins to "melt down". This melt down occurs at low temperature when denaturation has actually started.  Thus, the greater the exposure  number of subunits bearing the binding sites, the greater the potentiation. My work used low temperature extrusion cooking and the observation occurred in the extrusion cooking.

I just hope this suggestion is adequate. That is indeed the explanation I am going to offer for my observation anyway. Wish me best of luck!

Bye!