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Paper saying that humans and animals are (mostly) the same age
I'm brazilian and today I've came across this news published in a religious brazilian site. It's about a recent study that says that 9 to 10 species on Earth today, including humans, came into being 100,000 to 200,000 year ago.
Also, according to the site, that study supports what the bible says about the origins of life.
I'm pretty sure it's creationist rubbish, but I couldn't understand the conclusion of that study. So, I wish someone would explain to me that conclusion in lay terms. And, taking the opportunity, I'd also like to know if the paper is peer-reviewed and realiable.
Thanks in advance.
Source: https://phys.org/news/2018-05-gene-survey-reveals-facets-evolution.html

What is exactly the claim that you want to have it confirmed or not? Can you please clearly write out a clearly defined claim for which we could work on to write an answer. For the moment, I am afraid the question is unclear.

I didn't ask for a confirmation of a claim but for the conclusion of the study (if there's one). I think my questions are pretty clear.

Do you want us to copy-paste their conclusion? Have you read their conclusion (see their section Summary and conclusion). Was there anything specific that was unclear to you from this section?

To answer your side question... Yes, the paper Stocker and Thaler (2018) has been peer-reviewed. It is published in the Journal of Human Evolution, which a journal of average to low impact.

The conclusion is too technical for my level of english. I'm not a scientist, but I like science, so I decided to try this board expecting that someone could explain that conclusion in plain terms. And to say whether the paper is reliable.

Is your question Can you please summarize in lay terms Stocker and Thaler (2018) for me?, then? If yes, you might want to clarify this in your post. You might want to add your level of knowledge in evolutionary biology too. For example, the paper talks about mtDNA, incomplete lineage sorting, genetic drift and population bottleneck. Do you know those concepts?

Can you just say if that study brings any implication to the evolution theory?

They key qualifier is living species, many living species have relatively recent origins, that is exactly what you would expect in an ever changing ever evolving biosphere. That is like stating that most cars on the road are less than ten years old, OK, but that's not really a surprising statement. If you plotted a bell curve of how old all current animal species are the bulk would be fairly recent geologically speaking. Species have a lifespan. The average lifespan of a mammal species is around a million years so simple statistics will mean most living mammal species will be less than half that. No one is surprised when you say most of the data points in a randomly distributed set fall within one-two standard deviations.
In fact based on back of the envelope calculations, if the average lifespan of a species is ~ 1 million years, and  we assume they are randomly distributed, (they are not, extinction events exist which would shorten it), then just based on the 68–95–99.7 rule, 95%  of living (at or below the mean) species should be less than 320,000 years old.
Now the paper itself is meaningless, it's justification is largely circular: define species based on mitochondrial mutation rate, (which of course is a time based calculation), then use that definition to say most species fall within a certain time period. You can change the number of mutations in your definition of species to fit your conclusion. Even a species has existed a single unfractured population for millions of years will count as a recent species by that definition. It is circular reasoning, made worse by using mitochondria, which are not undergoing recombination so variance is basically only controlled by generation time. If a population splits into two or remains a single population its mitochondrial variance will remain largely unchanged. Interestingly they exclude the groups (plants, fungi, ect) in which mitochondria undergo recombination.
Really the only conclusion you can draw from the article is  most journalists don't understand statistics or genetics.

I like the cars on the road analogy. If you used the same logic as the paper you'd be concluding that the automobile was invented sometime after 2000.


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Help identifying a moth
It looks like it might be an emerald moth but its hard to tell from the discoloration in the wings and it is too high up for me to get a better look.
When: July 23rd 2018
Where: Central Illinois

It looks like an Imperial Moth (Eacles imperialis):

Source: https://www.butterfliesandmoths.org/species/Eacles-imperialis
As shown on the distribution map at this link, they can be found in central Illinois.

source: Stack Exchange

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

sort: votes


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Mendelian dominant trait involved with Hypodontia
If the absence of teeth is a dominant trait, then why is it not seen in generations? My teacher taught that absence of teeth is a mendelian dominant trait, but why don't we see this trait if it is dominant?

Hypodontia isn't a single gene phenotype, but a poli-genic mechanism involved with epistatic phenomenons and environmental scenarios.
The trasmission isn't clear till now, but when you're talking about a poli-gene phenotype isn't so easy to describe the way in which the trasmission is performed. You could find every info about this disease here, in a meta-review study:

Note also that if there was indeed a dominant allele for hypodontia, then if the frequency of this allele is low enough, you would still not see it (or only very rarely).

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


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Neuroscience - A neuron with two types of synapses (electrical and chemical) at the same time
I learn that the nerves from the Peripheral Nervous System can carry signals from and to other organs of the body.
I'm wondering if A Single Nerve carries
1) Only chemical signals
2) Only physical signals
3) Both of them at the same time
4) It can occur either of the case below, either (1), (2), or (3)
Thank you!

Homework questions (or homework like questions) are off-topic here unless you have shown your attempt at an answer (for more information see our homework policy). Can you show your attempt at an answer?

When you say "nerve" this refers to a bundle of axons from many different neurons, but I suspect what you actually mean is a single neuron.
Synapses occur at the ends of axons. Almost all axons branch to some degree, so there are many of these endings, and they fairly exclusively end in chemical synapses.
However, the actual propagation of the signal down the axon is electrical.
Electrical synapses ("gap junctions") also occur in vertebrate nervous systems, but they do not necessarily involve the ends of axons contacting dendrites of other cells. Rather, electrical synapses tend to be between dendrites of different cells, or between a dendrite and the somatic region of another cell, or between axons of two different cells.
The neurons that make electrical synapses also typically make chemical synapses in other places - sometimes they make these electrical synapses with the same cells they make chemical synapses with.
Note that these rules are different in invertebrates, and in general the distinction between axons and dendrites in invertebrates is more complicated.
There are other places besides the CNS with gap junctions/electrical synapses as well, including in the enteric nervous system and in the heart.

Draguhn, A., Traub, R. D., Schmitz, D., & Jefferys, J. G. R. (1998). Electrical coupling underlies high-frequency oscillations in the hippocampus in vitro. Nature, 394(6689), 189.
Galarreta, M., & Hestrin, S. (2001). Electrical synapses between GABA-releasing interneurons. Nature Reviews Neuroscience, 2(6), 425.
Traub, R. D., Bibbig, R., Piechotta, A., Draguhn, R., & Schmitz, D. (2001). Synaptic and nonsynaptic contributions to giant IPSPs and ectopic spikes induced by 4-aminopyridine in the hippocampus in vitro. Journal of Neurophysiology, 85(3), 1246-1256.


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Unknown plant, can anybody identify this plant?
Location: Western Germany
Can anybody identify this plant from Germany ?

This is Phytolacca esculenta, Asian pokeweed. Because the flower stalks (berry) are standing upright, and not hanging. The berries are also closer together compared to P. americana.
Despite the name 'esculenta', this plant is also poisonous.

https://m.wikidata.org/wiki/Q17244662

Ah yes right, oversaw this fact. Thank you very much RHA!!!

@nkell13s if you think this answer is better, consider accepting this answer (the check sign).

And just FTR, it becomes a pest quite easily. Seeds are dispersed by birds and other animals. It has tubers which can grow quite large, and regrowth can occur even from parts of the tuber from my experience.

Looks like Phytolacca americana
Better known as pokeweed, Phytopacca americana is native to the western US but naturalized in Germany and other European countries. The “berries” are quite distinct.

And it is quite poisonous!  The unique color to the berry pigment is due to a class of compounds called betalains, specifically betacyanins.

You are totally right, thank you very much ! Pretty interesting plant though

I think you are right this is Phytopacca, but it is another species. See my answer below.

@RHA oooh, good call - you should get the check


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How is the mechanism that reads dna passed?
DNA is how a species stores genetic information. Somehow the body needs to know what to do with this information. somehow the "machinery" that translates the DNA into proteins needs to be passed along with it.
Could this machinery also be encoded within the DNA? Or does it come automatically from some physical/chemical properties of dna? Or is it already present within the sperm/egg?
I am thinking if the dna somehow contains information on how to build the machinery to interpret it, we might be able to get a whole new understanding of how it works.

Welcome to SE Biology. Please read the Help on how to ask a question here. You are expected to demonstrate that you have done your own research before asking.Yours is a basic question that is covered in many biochemistry and biology texts, such as Berg. Please do some reading and then If you have specific questions post them here, explaining what you do not understand. Text book explanations of basic ideas in a subject are likely to be far more useful than the short answers here.

well, i come from a computer science background. biology is not my usual area of expertise so I don't know the right technical terms to put into google....

Ok, but if I posted a similarly naive question on Stack Overflow, I would be treated much more severely. Computing Scientists entering bioinformatics have to take the trouble to educate themselves in molecular biology. I mentioned one good biochemical resource. NCBI bookshelf also has older versions of a couple of outstanding Molecular and Cell Biology texts: Lodish et al. and Alberts et al. Use them!

Your question is very general, but it has a simple answer.
Yes. The protein machinery which interacts, reads, structures and manipulates the DNA strands is coded for in the DNA.
By way of example: one enzyme which opens the double helix is called DNA Helicase B. Once a DNA strand is accessible, another enzyme 'reads' (transcribes) DNA, called RNA Polymerase. In humans, the gene which produces helicase B is found on chromosome 12. The gene which produces one of the subunits for RNA polymerase is found on chromosome 10. These genes are essential for life; they are found in all organisms, perhaps excluding viruses, which hijack a host cell's machinery to duplicate their own DNA.
You may have also noticed that DNA by itself cannot 'read itself', it requires machinery in the form of proteins. How the first-ever replicating gene arose is an open question today. A likely candidate for the first ever gene, or unit of inheritance, is a kind of molecule called RNA, which is capable of storing information as well as catalyzing reactions (functioning as an enzyme).

The machinery that manipulates and read the DNA (e.g. helicase, rRNA and RNA polymerase) is itself coded in the DNA.
Now, of course, if you put an individual DNA in a bowl of water, that won't be sufficient to create a new organism. An egg (ovule + spermatozoid) is not just DNA and a membrane. It contains a lot of stuff that was already present in the ovule is still present after the spermatozoid made its entry. There is already a lot of nutrients and a lot of proteins, including those needed to manipulate and read the DNA.

Somehow the body needs to know what to do with this information.

No.  That's not how it works.  Chemicals interact with other chemicals according to their shape.  Chemicals do not "know" anything.

somehow the "machinery" that translates the DNA into proteins needs to
  be passed along with it.

Well, yes, in that when an organism divides, or makes a gameme, it doesn't make an empty cell with DNA floating alone.  The gamete or new organsim also gets the contents of the cytotol of the parent cell, which includes a bunch of of proteins.


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Why and how does falsifying sensory information work?
Some context, before the question:
Whenever I have a craving to binge on something sugary, I just prepare a cup of extremely bitter green tea (with 3 bags of tea) and I imagine myself binging on something sugary, but at the same time I take a gulp of this bitter stuff and let that sit in my mouth for a few seconds.
The very next moment, I immediately notice that the craving comes down and after a few more sips the craving completely goes away. I feel nauseous if I think about something sugary for another day.
Actual question:
Why and how does this work? Even though I consciously know that I am fooling myself, with a false sensory perception, why does my brain associate sugary treat to be revolting and poisonous(cause of nausea)?

I'm voting to close this question as off-topic because, IMO, the question belongs to psychology.SE

@Remi.b I don't understand why does it belong in psychology. I am seeking to know why is sensory perception ignored for evolutionary knowledge on bitterness.

I might be misunderstanding your post then. I don't see the word "evolution" in your post (excluding the tag) and the only answer for the moment does not talk about evolutionary biology but about psychology and cognitive science. I am not sure what you would mean by "evolutionary knowledge". Maybe, you could try to clarify your post but it might be problematic as it already received an answer.

These are learning phenomena you describe. I'll try to explain a simple way to think about this.
By default, sweet foods are appetitive and, for instance, strongly bitter foods are aversive. However, it is possible to condition yourself to associate a stimulus, no matter how it presents originally, with a different valence (appetitive or aversive).
There are several well understood forms conditioning can take. I list a few here, and some subtypes. They are described well on Wikipedia:

Classical conditioning
-- Serial application of classical conditioning can be called second-order conditioning.
-- You can also condition yourself through self-evaluation, called evaluative conditioning
Covert conditioning is a technique more than a type of conditioning, it may directly apply to your question. It involves the use of imagery.
Operant conditioning

Operant and classical conditioning are the two major paradigms to know. Classical or Pavlovian conditioning involves pairing an "unconditioned" stimulus with a neutral "conditioned" stimulus. Operant conditioning involves providing a feedback, usually a reward or punishment, to reinforce learning.
You can self-learn or condition yourself. This does not mean necessarily it is intentional or conscious on your part, often things can be subconscious or unconscious. For instance, if you associate eating crisps with watching a movie, watching movies without crisps can become uneasy, in spite of the fact that watching a movie was originally a pleasurable activity. In a neuroscience seminar involving conditioning in fruit flies, I once recorded a saying which captured the spirit of the experiment quite well: An expected reward, not experienced, can feel like a punishment, and vice versa. Rewarding yourself after doing chores can also be a easy and practicable way to build good habits with doing chores.


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Preprocessing microarray data to detect increased male expression variance due to dosage compensation?
I am currently working with a dataset from a large microarray experiment where one of the aims is to look for evidence of the predicted doubling of variance in expression on the X chromosome in hemizygous males relative to females due to dosage compensation.
Speaking broadly, the experiment uses a controlled breeding scheme in Drosophila to generate individuals that are heterozygous or hemizygous for different known X chromosomes (the autosomal genotype is also controlled). I then want to use a genewise linear modelling approach to estimate additive genetic variance for gene expression for each gene in males and females. The arrays involved are Affymetrix GeneST arrays.
My initial inclination was to preprocess the array data using RMA, in my case from the oligo package in R. A fundamental part of RMA preprocessing implementations is a log2 transformation, and of course this has desirable properties for most gene expression analyses. However, it is apparent that the variance-stabilizing properties of the transformation have some undesirable consequences when looking for the sex differences in expression variance across samples that I am interested in. A toy example showed that variance in log2 expression is the same whether or not males show dosage compensation, obscuring the very signal I am interested in.
I would like to retain the benefits of the preprocessing steps (e.g., background correction), but I wonder if anyone can weigh in on the best way to avoid the log2 transformation’s effect on estimates of variance. Is it appropriate to simply take the antilog of the expression matrix after RMA preprocessing or is there another approach/package I should look into instead?

I would probably be able to answer if I knew what exactly the "expression matrix" contained, and exactly what you take the logarithm of. In general, I would need to know exactly what information you have, and what the algorithm does. If you don't get an answer here. It may be your best bet to go to Cross Validated Stack Exchange and ask. Although, they would not need to know all the biology you've written here, and like I, they would need more precisely what data you have, and you want to achieve mathematically.


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Can immunity to diseases vary by populations?
A common explanation for the massive population decreases of isolated societies upon contact with Europeans during the Age of Discovery is that the natives lacked immunity to newly introduced diseases.
What does this actually mean?
Is it just a shorthand for "the adult population was not subjected to these pathogenes during childhood and is therefore more susceptible to them" or is there maybe a certain genetic component to it?

This is a very interesting question. 1) You might want to narrow your question down to a single disease (such as smallpox for example) because otherwise the question might be too broad. 2) You might also want to consider the possibility of a cultural difference in response to specific diseases. Maybe in Europe, the people knew how to deal with a specific disease they were used to encounter (quarantine, specific treatments, ...) but the native, having never encountered this specific disease, did not know how to deal with it.

Related posts: Why was disease transfer to the Americas one-way? and Why Can't The Immune Systems of Uncontacted Tribes Handle Our Common Colds?. This second post might actually be a duplicate. You might want to address this other post in your question.

@Remi.b I'm a complete layman and really wouldn't know which disease would be suitable for narrowing down the scope though.

@Remi.b I don't think this is a duplicate. This question, to me, focuses on the heritable vs. non-heritable factors in susceptibility in general. The proposed duplicate, to me, reads as a question about how the common cold can be relatively innocuous in one population but fatal in another. That's a different question entirely (and is poorly answered right now). Both are questions about host-pathogen interactions on a population level, but I read them as very different.

It would also help to consider the response of European populations to newly-introduced diseases.  For instance, bubonic plague killed tens of millions of Europeans in several episodes.  Yet now it's endemic amoung rodents in the western US, yet only about 10 human cases per year are reported: https://www.livescience.com/51792-plague-united-states.html  Similarly the Antonine Plague (either smallpox or measles).

Is it just a shorthand for "the adult population was not subjected to these patogenes during childhood and is therefore more susceptible to them" or is there maybe a certain genetic component to it?

It's a little of both. You can read some of the math behind this in Infectious Diseases of Humans: Dynamics and Control, by Anderson and May.  Chapter 2 gives an overview. The behavior of an epidemic depends a great deal on the specifics of the host-pathogen interaction, but generally you can say that the epidemic curve in a a naive population will have a larger and sharper upswing than in a previously exposed population. You can attribute some of this different behavior to lack of adaptive immunity in the adult population. Again, depending on the pathogen, you can also attribute some of this different behavior to lack of selective pressure in the naive population on highly variable loci involved in the immune response.
To address more directly what seems to be your primary question: yes, there is a genetic component to the susceptibility of a host (e.g., a human) to a pathogen (e.g., a microbe that can cause disease).
Non-heritable aspects:
There are certain aspects of what we call the adaptive immune system in jawed vertebrates that are not directly heritable. You are a jawed vertebrate, and the DNA in each of your B-cells and T-cells that produces B-cell receptors (BCR) and T-cell receptors (TCR) goes through a number of changes outside of the germ line. You can read about these changes in, for example, How the Immune System Works, Chapter 3, by Lauren Sompayrac. It's an excellent introduction if this is new to you.
In addition to the exact set of BCRs and TCRs in the pre-immune state, your current repertoire of cells and molecules is determined by your history of exposure. While some of this can be vertically transmitted, the majority of it is not. This is one of the reasons why, when you look at this repertoire, much of the variability is attributable to non-heritable factors. A not insignificant proportion is attributable to heritable factors, though. So if TCRs and BCRs are not encoded in your germ-line, and your environment obviously has a strong influence on your current immune state, where does the heritable component come from?
Heritable aspects:
All of the other proteins involved in the immune system response are encoded in the germ line, and are thus heritable. Some of them are highly variable, and since they are very important they are under strong selective pressure. You can see important changes in the population distribution of these loci over a relatively small number of generations. There are many other heritable components of an individual or population's susceptibility to infectious disease. There is a great deal of work on this. Casanova has a great article about this in PNAS, which I've linked to in another answer to a related question. A more traditional review of his is here. Of course, he's not the only one working on this. I just like the way he writes. Here's a good one by Baker and Antonovics.
A simplified and speculative example
Re: your comment about measles in the Polynesian islands, we don't have scientific consensus about the relative importance of non-heritable and heritable factors for this particular case. Instead of getting into the nitty gritty details, I'll walk you through a hypothetical:
Imagine an isolated population with a lot of variability in germline genes that code for a special protein that helps their immune system mount a full response to viruses.
A very nasty, very contagious virus is introduced to this previously isolated population. The characteristics of the population help determine the outcome of their interaction with this new virus. Here are 3 important characteristics:

Because nobody has ever been exposed to this virus, nobody has neutralizing antibodies or the rapid immune response that happens the second time you're exposed to a pathogen.

Some versions of that special protein with all that variability don't do a good job of helping the immune system mount a response to this new virus.

Luckily though, some other versions of that special protein with all that variability do an especially good job of helping the immune system mount a response to this new virus.

Because of (1) the disease spreads broadly throughout the population. Because of (2), a specific group of people get especially sick, die, and (because they are dead) don't reproduce, and don't pass on their version of the gene that codes for special protein. Because of (3) a specific group of people do very well, are only sick for a little while, and do an especially good job at generating long lived immunity, and (because they are alive and well) reproduce a lot, and pass on their version of the gene that codes for that special protein.
The epidemic is eventually controlled. Years go by, and the virus starts circulating again.
Now the characteristics of the population are quite different, so the dynamics of the host-pathogen interaction will be different.
Many of the people that were alive during the first epidemic now have neutralizing antibodies and a memory response, so this second epidemic will not spread as quickly or as broadly. This is a non-heritable factor. Previous exposure to the virus has changed the repertoire of cells and molecules in people's blood.
Among the younger generation, more of them have the helpful version of the special protein that helps the immune system generate a response, so not as many of them will die. This is a heritable factor. Previous exposure of the population to the virus has exerted selective pressure, changing the frequency of the helpful and unhelpful alleles in the population.

Thank you. I'm still having trouble reconciling my (naive!) ideas of how evolution works with the phenomenon at hand. Say, after 40% of Polynesians were wiped out after the first wave of (e.g.) measles, were the surviors genetically "hardier" to the germ? I understand that most likely the best answer is "go read a textbook" (thank you for the references), but maybe you could address this point (more).

@TNierath It's very plausible that those who survived were genetically more resistant to measles (on average). Don't think of this as an on/off switch, more on a gradient. People can be more likely to survive for many reasons. Perhaps some people had stronger lungs (partially for genetic reasons, but also partially due to non-genetic reasons). Perhaps some people had a stronger immunity system. All kinds of factors can be involved, and all these factors may influence how much at risk any individual is.

@TNierath I've added a hypothetical example that may help you understand.

Thank you again for taking the time. I understand the evolutionary logic (I think), but have trouble with some of the terminology and concepts: What are germline genes and how are they different from other genes? The "same" protein can have varieties? Are proteins themselves uniform across human populations and only differ in their varieties coded by genes? What is a "memory response"?

@TNierath Germline genes are passed on to your children. My first paragraph on non-heritable factors talks about how some genes involved in the immune response are changed outside the germline, so can't be passed on to your children. Variability is what makes evolution work. Genes are not uniform across human populations, they are variable. The proteins they code for are not uniform either. Different versions of a gene (and the protein it codes for) are called alleles. Small differences in a protein may not have an impact in certain conditions, but will in other conditions. This is an example

@TNierath the memory response is a specific property of the adaptive immune system. When you're exposed to a pathogen the second time, your immune system remembers it and can mount a quicker more effective response.

@De Novo Ah yes, so the "germline" is what laymen usually just think of as "genes" (information transferred to offspring). I assume there must be utility in making a conceptual distinction between "having antibodies" and having a "memory response", but that it may nevertheless not be esp. relevant in the current context?

@TNierath yes. Having antibodies can be just a passive response. You've already made them. This can be helpful for neutralizing and preventing an infection. A memory response is more than just ongoing production of antibodies. It's reactivation of memory cells, and a rapid increase in many different effector mechanisms of the immune system.


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Why do alpha-gal allergies only occur after a tick bite if alpha-gal is already present in red meat?
I just read an NPR article about allergies to red meat being caused by tick bites. That stood out to me because I thought allergies are triggered by an initial exposure to some allergen. In this case, the allergen is alpha-gal, a disaccharide found in cell membranes of most mammals; humans and apes are a notable exception. The article explains that ticks might cause this allergy by transferring alpha-gal from other animals to us when they feed on our blood.
However, we also are exposed to alpha-gal every time we eat red meat. How are we protected from allergic reactions when we eat red meat but not when we eat peanuts? Why does that protection fail after alpha-gal is exposed to our bloodstream?

Please give the full chemical name for the compound you refer to as alpha-gal. This is not a common abbreviation.

@David Gal is the standard abbreviation for galactose, per IUPAC.

@canadianer — The question referred to alpha-gal which is not, but in any case glc is the IUPAC abbreviation for glucose but it would be strange to use this. My point is that for optimal communication (and especially in titles) abbreviations should only be used if they are widely known (that is what I had intended) and really necessary.

@David the allergy itself is known by clinicians as alpha-gal syndrome. A common (but unclear) name would be meat allergy. I think the title is clear to people that are familiar with it.

In order for the immune system to respond to an antigen, beyond recognition of that antigen, there needs to be a signal that there is something wrong. Co-stimulation can take a few different forms, but it requires the involvement of more than just one arm of the immune system, and generally helps prevent our immune system from what I like to call the Dr. Strangelove effect (a psychotic lone general can just decide that there is a problem and launch an attack). Here, costimulation might be from (or downstream of) the tick bite and other invaders associated with the tick bite, or from an allergy to peanuts. You can read about this in the first chapter of Sompayrac's How the Immune System Works, as well as the first chapter of Abbas Basic Immunology.

Does the immune response also vary by the route that the antigen enters the body? I'm speculating here, but if the GI tract is less prone to triggering immune responses, that could explain why we're okay with eating alpha-gal but not if alpha-gal gets in our blood. While it's possible that the tick bite itself is a source of some costimulating substance, I also read that immune responses against alpha-gal may also play a role in rejection of pig tissue implants. I can't imagine that a similar response would occur if we ATE that tissue.

@BatWannaBe yes, mucosal exposure is less immunogenic, and eating pork is different from having a porcine valve. Costimulation is a requirement, though, however the antigen is introduced.


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What is this insect or worm?
I found it on the cedar siding of my home in Houston, Texas.
It was quite small, I'd estimate 1cm in length. I did not observe it move up or down the side of the house, but when I touched it gently and it did bend over.

Some species of Eupithecia perhaps. A type of moth, the larvae tend to resemble twigs. According to this relatively old text, Eupithecia miserulata is the most commonly distributed species in Texas, but I'm sure identifications stem largely from expertise and adult specimens, both of which I lack. The larvae for E. miserulata don't seem to visually match what you have, there.
In essence, though, it's a caterpillar that will turn into a moth.

I looked up some images and it definitely looks similar, thank you. Quite a strange looking caterpillar


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Does amount of sperm affect fitness of baby?
If there's a 3 day ovulation period in which to have intercourse, would it be better (to create a more fit/healthy baby) to have sex once and ejaculate more sperm than have sex three times with reduced sperm count?
You would think that the more sperm ejaculated at once would result in much more competition to reach the egg, leading to a more fit spermatozoa, and presumably a more fit baby.
If the egg is fertilized during a lower level ejaculation, a less fit spermatozoa can fertilize the egg since there's less competition. Meaning a less fit baby?
Keep in mind I'm NOT asking about the chance of getting pregnant, I'm talking about the fitness/health of the baby. Obviously having sex once instead of three times decreases the chance of getting pregnant.

Expecting competition between spermatozoa to make the child "more competitive" (or "fit") is like expecting that somebody winning a singing competition could be advantaged for winning a Nobel Prize.
The child doesn't use the genetic information which regulates the shape of the spermatozoon or the motion of its tail, hence maybe some future Nobel Laureates could be awful at swimming as spermatozoa.

Sperm actually survives for ~5 days so it really should not matter much.

@The_Vinz This is only partially correct since overall sperm fitness does inversely correlate with complications during early embryonic development, which in turn correlates with later life outcome in a variety of ways.

You are arguing that Usain Bolt is not as good a runner than a child who is the fastest among a mob of her classmates?

I can see where you're coming from, and keep in mind I am no expert in the area, but have you considered that there may be many, perhaps important factors at play than if the sperm had many competition or few? Take the parents genetic and epigenetic profile for instance, meaning not only what the mother and father could each pass on, but whether or not what they pass on will be active or not. And to use your own example, the fittest sperm, who outperformed the larger group; say it required more energy and thus produced more ROS, with which to damage to it's DNA, than the winner in the smaller group - which would be weaker and which stronger? Say the health of the sperm which fertilises the egg could not be influenced by you in any practical way, which method would you choose then?


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True examples of common variation due to Mendelian Inheritance
Classic examples of mendelian inheritance are genetic diseases such as sickle-cell anemia, Tay-Sachs, cystic fibrosis, and xeroderma pigmentosa. For some of these diseases, it is believed that they evolved because the genes gave a beneficial effect that outweighed the rare occurrence of the disease (e.g sickle cell and protection against malaria).
However, all of these are examples of uncommon phenotypes, usually less than 1% of the relevant population (where it is most common) has those diseases. I'm interested in examples of mendelian inheritance where variation is common (all of the relevant phenotypes have, say, >5% frequency or something like that).
Consider eye color. In European populations both blue and brown eyes are common phenotypes. Many people have probably experienced a typical high-school class of biology, where this was introduced as an example of mendelian inheritance with brown eyes being dominant and blue eyes being recessive. However, modern studies (for example, genome-wide association studies) show that things like eye, hair and skin color are all polygenic traits. See for example (Sulem, ..., Stefansson, 2007).
Throughout the years I've heard of other traits that some said were examples of mendelian inheritance. Being able to roll the tongue, for example. This question was inspired by this recent question where absence of teeth (Hypodontia) was taught to the OP as an example of a dominant trait. The current answer says that hypodontia is probably an example of a polygenic trait that interacts with certain environmental effects. This got me wondering whether there even are examples of common mendelian variation.
I don't quite know the best way to phrase it, but my question is the following:

Are there any examples of human phenotypes that are due to mendelian inheritance where all of the phenotypes are common?

Take eye color as an example again. By common, I mean that both blue eyes and brown eyes are common (over, say, 5% in for example Sweden). On the other hand, for example Tay-Sachs disease occurs only about 1 in 3,500 among Ashkenazi Jews where it is most common, according to Wikipedia. Way less than even 1%.
Preferably I want it to be verified by modern genomic studies (such as GWAS) that it is an example of mendelian inheritance. If such an example does not exist, then I will accept any answer that provides modern, relevant scientific literature that explores this topic. For example, it might explain why we would not expect to see common variation due to mendelian inheritance.

Generally, you don't need a GWAS to detect Mendelian traits (though it can and will quite reliably, precisely because those genes are Mendelian). That's why common Mendelian traits were identified before GWAS.

@kmm Fair enough. But there were also traits that were claimed to be Mendelian, and after GWAS were discovered to not be. (Though, to be fair, that could simply be bad practice by the people who claimed that, and perhaps it was not consensus.) But you're right. It doesn't have to be GWAS evidence. Just simply some good evidence that is consistent with modern findings.

GWAS aside, what you are asking for isn't clear to me. If I understand correctly, you are looking for phenotypes that are Mendelian (i.e., not complex traits), but which also have common alleles (I imagine 50:50 would be ideal).

@kmm Well, for example take any population, say The Netherlands. Imagine if a person from this population could either have blond hair or dark hair. Both phenotypes are fairly common. Then imagine if it were discovered that blond/dark hair was Mendelian, then that would be a nice example (It happens not to be the case; hair color is actually polygenic). Now I want to know if there are any examples like that. Sure, I guess 50:50 would be great, but I would be satisfied with, say, 95:5 or 90:10. (If you wish, you can edit my question to make it more clear)

Depending on how broadly you want to bin a phenotype, and what you mean by "all the phenotypes", hemoglobin disorders are among the most common mendelian traits. In Cyprus, for example, I believe around 17% of the population is heterozygous for a hemoglobinopathy.

@DeNovo I think that could be made into a satisfactory answer. This question has been open for long, and your example seems fine to me.

Earwax consistency is an example of a monogenic trait with dimorphic phenotypes in humans -- "wet" and "dry" -- where both phenotypes are globally common, though allele ratios are highly variable between human populations.  The population genetics and molecular basis of this trait are discussed at length by Dr. John H. McDonald as part of a series on the myths of human genetics (archived version here).  I reformat his discussion in my answer.

In The dimorphism in human normal cerumen, Matsunaga summarizes 30 years of research into the earwax of Japanese families, with two major observations:

Dry earwax parents never have wet earwax children, suggesting the genetics underlying the wet phenotype are dominant to those underlying the dry phenotype.
Because the allele for wet earwax is relatively rare in the sampled families, it is likely that most wet earwax parents are heterozygotes.  Following from this, if the trait is monogenic with two allele variants, we expect a 3:1 ratio of wet to dry children in wet × wet parent crosses, and a 1:1 ratio of wet to dry children wet × dry parent crosses.  Indeed, this is observed.

$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 35 & 12 \\ \hline
\text{w×d} & 205 & 195 \\ \hline
\text{d×d} & 0 & 634 \\ \hline
\end{array}$$
These results were later corroborated in Native Americans --
Cerumen in American Indians: Genetic Implications of Sticky and Dry Types
$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 32 & 6 \\ \hline
\text{w×d} & 20 & 9 \\ \hline
\text{d×d} & 0 & 42 \\ \hline
\end{array}$$
And in a different Japanese cohort --
Distribution and inheritance of earwax types: a study on inhabitants in Awa District, Chiba Prefecture
$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 27 & 3 \\ \hline
\text{w×d} & 137 & 109 \\ \hline
\text{d×d} & 0 & 345 \\ \hline
\end{array}$$
In the early 2000s, the molecular basis of human earwax consistency was elucidated in three major publications.

Toshida et al. mapped a single locus on chromosome 16
Yoshiura et al. identified a SNP at position 538 in the coding region of ABCC11.  At this site, G corresponds to a wet earwax phenotype, whereas A leads to a dry earwax phenotype.  A less common allele representing a deletion of 27 nucleotides in exon 29 also yields a dry phenotype.
Toyoda et al. found that the 538G>A transition encodes arginine in place of glycine, resulting in a loss of glycosylation in the mutant protein, leading to deficient cellular localization, rapid degradation, and loss of function.

To directly address your question,

Are there any examples of human phenotypes that are due to mendelian inheritance where all of the phenotypes are common?

I point you to the tables above, as well as Table 1 from Cerumen Phenotypes in Certain
Populations of Eurasia and Africa, which shows that the frequency of the dry allele ranges from 59% to 89% across diverse human populations --

To conclude, human earwax consistency is a dimorphic trait controlled by a single gene, where both phenotypes are common across human populations.

Thank you for the answer (upvoted and accepted), and nice site that "Myths of human genetics" by Dr. McDonald.


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which of these fields will cure aging?
life extension is expected to happen as a result of breakthroughs in tissue rejuvenation, stem cells, regenerative medicine, molecular repair, gene therapy, pharmaceuticals, and organ replacement. Which among the seven fields is more likely to achieve that goal in the foreseeable future?

I'm voting to close this question as opinion based. It's an interesting question for discussion, but doesn't fit the SE model.

Not even opinion based, as any answer would require a crystal ball :-)

If we knew that, then we'd just emphasize research in that area, and reduce the effort in the other areas. Qualified opinions in the matter differ, and in the end they could all be wrong!

I think the structure of this question could be less opinion based as De Novo stated above. But a recent article published by mayo clinic will help shed light on the question. Falls under the category of regenerative medicine I believe.
Senolytics Article
EDIT:
 Since links are apparently a taboo, here is the paper. Educational on current research and methods on an 'aging cure'.
Xu, Ming, et al. "Senolytics improve physical function and increase lifespan in old age." Nature medicine (2018): 1.

We frown upon link-only answers at StackExchange as a whole and here at Bio specifically because they are likely to degrade over time and not exist anymore, making your answer meaningless. However, I would also consider whether this question should be answered at all, since fortune telling is not all that scientific.


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Why ketoacidosis is less common in patients of Noninsulin Dependent Diabetes Mellitus?
The other day my teacher said ketone bodies are mostly formed when insulin is less and NIDDM type diabetes mellitus has less chances to grow ketosis. https://medlineplus.gov/ency/article/000320.htm
P. S. I had read the difference between the type 1 and type 2 diabetes.

Did you read this already? If so, could you please edit your post and explain, what remains unclear? Do you know the differences between Type 1 and Type 2 diabetes mellitus (formerly called insulin dependent or non-insulin-dependent)?

btw: there is a  diabetes-mellitus tag, while your editing your question, you should add this one :)

@Marzipanherz I don't think that Wikipedia article is very helpful in answering this question. The answer is certainly not obvious (or fully understood), and it's not really addressed there. In type 2 diabetes, insulin fails to work at some sites but not at others.

@DeNovo I agree that Wikipedia doesn't cover everything. However, in this case the article is more informative than the article linked by the OP. With my above comment, I was trying to figure out, how much background knowledge the OP has, since this isn't clear to me from the question. And I think, knowing this enables us to write an answer that is helpful for the OP.

@Marzipanherz The difference between the two types are clear, not wholly though, as you can see this question arising.

This is a good and important question. The answer is not obvious, or necessarily well understood. Hyperglycemic crises occur in both Type 1 and Type 2 diabetes. In type 1 diabetes, the crisis is more likely to be diabetic ketoacidosis (DKA). In type 2 diabetes, it's more likely to be something called hyperosmolar hyperglycemic state (HHS), though type 2 diabetics can develop DKA, especially later in the course of the disease. Both can be brought on by similar precipitating events (for example, infection) in an individual who has had diabetes for a very long time (and this is where we often see these patients now -- pneumonia or the flu in an older diabetic). With type 1 diabetes, though, it can be how diabetes is discovered in a young, otherwise healthy individual.
The key difference between type 1 and type 2 diabetes is that type 1 is an absolute loss of insulin production, typically due to autoimmune destruction of the cells of the pancreas that produce insulin. Type 2, on the other hand, starts as insulin resistance. In fact, insulin levels may be high early in the course, but the tissues do not respond appropriately.
Insulin actions in glucose and fatty acid metabolism
Broadly, a key role of insulin is to respond to increases in blood glucose by shifting energy metabolism from fatty acids to glucose.
In a healthy individual, insulin is secreted as blood glucose rises, and causes peripheral tissues, especially fat and muscle, to take up and use glucose. It also causes the liver to release less glucose into the bloodstream from glycogen stores and gluconeogensis, and instead to store it (in glycogen).
At the same time, since there is plenty of glucose available, insulin diverts fatty acids to fat cells, promoting their storage in and inhibiting their release. Insulin indirectly prevents fatty acid catabolism in the liver by promoting its storage in fat cells, but also directly inhibits liver ketogenesis, a process by which byproducts of fatty acid and protein catabolism are converted to ketone bodies that can be used by, among other tissues, the brain.
Impaired insulin signaling
In both DKA and HHS, despite high levels of blood glucose, the muscles, fat cells, and liver act as if the organism is starving. In response to this state, counter-regulatory hormones (catecholamines, cortisol, glucagon, and growth hormone) are released. The liver releases glucose from glycogen stores and generates even more glucose from other metabolites through gluconeogenesis.
The difference between DKA and HHS is how lipid metabolism is regulated. It is unclear why, exactly, in HHS insulin fails to regulate glucose metabolism but seems to succeed in suppressing lipolysis and ketosis, but that is the current hypothesis. In DKA, fatty acids are released from adipose tissue and delivered to the liver, where massive unregulated lipid catabolism and ketogenesis occurs. In HHS, the existing insulin seems to be effective at suppressing lipolysis and ketogenesis.
You can read more about the pathophysiology of both these diabetic hyperglycemic crises in this excellent review.

Are cells completely resistant to insulin? I construe if there might be some, albeit reduced action of insulin on adipocytes suppressing lipolysis.

@user73023 that's the theory. If this answered your question, you should mark it the answer by clicking the gray checkmark next to it (it will turn green). If it was helpful, and you have the upvote privilege, you should upvote it. See someone answers


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Frequent urination caused by sound of running water
I urinate at sound of running water when I brush my teeth or wash my hands . This only happens when I am home

Very simply put, its the power of suggestion. You urinate, flush, wash your hands umpteen times together each day. So when you hear the sound of running water, you naturally feel the need to urinate.
Apparently, the sound of running water also help patients with lower urinary tract symptoms urinate (reference)


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Confusion about a gene's description
I have a very basic biology question. I am reading the description of gene FAM166A here, and I have no idea what "sequence similarity 166" means. What does 166 stand for, what is this gene's sequence "similar to"? And what does member A mean?

Family membership is probably referring to something similar to this: https://www.ebi.ac.uk/training/online/course/introduction-protein-classification-ebi/protein-classification/what-are-protein-families. I'm not sure how the sequence similarity is scored, though.

Oh okay, then this gene named FAM166A is member A of the protein family with ID 166 where each family is determined based on sequence similarity. Thanks!

The FAM symbols are defined in the HUGO Gene Nomenclature Committee guidelines.
The FAM symbol is an anonymous and temporary identifier that is given to groups of poorly characterised genes which share more than 40% amino acid sequence identity (see Section 4.1).
There are two human genes/proteins in the sequence similarity 166 group; FAM166A and FAM166B. These have some sequence similarity (more than 40%) but  function of this similar sequence is currently unknown. Once further characterisation has been performed for any FAM group they will likely receive more meaningful names.


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Identification of a beetle found in a basement in Virginia, USA

Beetle found in basement in Alexandria, VA, USA
Approximately 5cm (2 inches) in length.

That is a female Eastern Hercules beetle. Dynastes tityus https://bugguide.net/node/view/4462 Family Scarabaeidae, Subfamily Dynastinae. One of the largest of the beetles in the South-East U.S.


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Are Measles patients infectious until death?
I'm examining a dataset of a measles outbreak, and for each patient I have the date of first appearance of symptoms $t_1$, date of appearance of rash $t_2$, and if applicable, date of death $t_d$. According to the literature, patients are infectious for one day before appearance of symptoms, and up to about 4 days from appearance of rash, so the interval of infectiousness is approximately $\left[t_1 -1, t_2 + 4\right]$. After this, most of the time their symptoms gradually abate and they get better.
However, if a patient dies, presumably they remained sick until they died. If $t_d$ is like, 10 or 15 days after $t_2$, are they infectious during all of this period? Or is it reasonable to conclude that they're infectious for the same length of time as everyone else, and the symptoms that kill them are non-infectious complications?

The characteristic rash of measles is itself an immune response, and is a good marker for progression of the immune response. Patients with immunodeficiency can  have a much more limited or even absent rash. In most patients, if it's been 4 days since the appearance of the rash, and they have improvement in fever, runny nose, and conjunctivitis, without a productive cough, they probably aren't infectious. If you have that data (fever and mucous membrane inflammation), I'd pay attention to that as well as the time since the appearance of the rash. A sick patient with measles should be kept in respiratory isolation regardless, but if you're looking at modeling disease transmission, you can follow the symptom progression.
As far as death is concerned, there are several pathways. Measles can cause a poorly understood immunosuppression and immune dysregulation, which certainly contributes. The most common cause of death is pneumonia (often secondary pneumonia), but early diarrhea can be a major cause in malnourished children. Otherwise immunosuppressed individuals (e.g., HIV, and primary immunodeficiencies) can develop a fatal measles encephalitis (a brain infection). Some deaths result from a fatal post-infectious autoimmune syndrome.
Some of these individuals are probably still shedding virus (diarrhea, primary measles pnuemonitis or encephalitis), many of them aren't (secondary pneumonia and autoimmune cases).
Many texts focus on vaccination and the current epidemiology of measles in developed countries, but Cecil Medicine has a very good chapter (375) on the clinical manifestations of measles. There is an interesting article in Lancet Infectious Diseases about the US army outbreak in 1917-18 that is a good example of the interaction of measles with other respiratory pathogens.


text:
what's the species identification of that camponotus queen
City: Antalya, Turkey
Date: July 27 night
Specific location: I found it in the middle of the city

In what kind of environment / ecosystem did you find them?

antalya, turkey ... summer +40 celcius, winter 10 celsius on avarege. seaside , and haliday city. There mediterranean coast. if you write antalya on google picturen you may see . :)

I meant "micro-environment" (I should have been clearer). In the middle of the forest in the shade of large trees, right up on the beach, in the middle of the city, in houses as pest, etc...

sory :) . I found it in the middle of the city. when I dronk a cup coffee she drop my table on the July 27 night .


text:
Simulating DNA sequences in R with a given value of $\theta = 4N_{e}\mu$
This might not be the most appropriate site to be asking such a question, but perhaps someone has a solution.
My question is: is there an R package or function for simulation of DNA sequences of a given basepair length generated according to a prespecified value of the population mutation rate $\theta = 4N_{e}\mu$, where $N_{e}$ is the effective population size and $\mu$ is the per-generation mutation rate
I have real sequence data from GenBank, but I would also like to simulate some random DNA sequences according to a coalescent process.
Essentially the function would output the generated aligned DNA sequences as a FASTA file.
I have been rather unsuccessful in tracking down a suitable package, as most only output generated phylogenies.

@Remi.b Thanks. I'll do some sleuthing. If I don't come across anything, I will code it myself, or use SimBit..

There are a number of tools but I don't know any that comes with an R library. They are usually all called from the command line. I don't either of any that produce FASTA file. SimBit (my own software) can produce vcf files which can easily be converted into FASTA with PGDspider.
However, if your simulations are so easy, you might not need these individual-based softwares. Just write the code yourself. It might only be take a few tens of lines. Here is a simple example
freq = 0.1 # initial frequency
N = 1000   # Constant population size
mu = 1e-7  # mutation rate

for (generation in 1:nbGenerations)
{
   # Drift
   freq = rbinom(1,N,freq) / N

   # Mutations
   oneWayMutations   = rbinom(1,N*freq,mu) / N
   otherWayMutations = rbinom(1,N*(1-freq),mu) / N
   freq = freq - oneWayMutations + otherWayMutations
}

If you need something more complex (such as several loci), then you should probably use one of the existing individual-based software. See the post Sequence evolution simulation tool

What is the 'freq' variable in your example?

'freq' is the frequency of a one allele at a single bi-allelic locus. If you want several linked loci, then you'll have to use some individual based software, such as SimBit, Nemo or SFS_code for examples. See edit in the post.

Thanks! I just came across @EliKorvigo 's post, as it was recently commented on.


text:
Which strange fruit is this?
Yesterday, my brother brought a strange fruit resembling Lychee (but much bigger in size). Here is a pic of it:

When cut it, it had smell like banana and fibers were like of the chicken meat, though taste was more or less like banana (sorry have no pic of that).
Can someone kindly help me identify it?

As a complete sidenote, go search for "durian". It is a different kind of tropical fruit that you might not know about and it's fascinating. Especially how the taste/smell of it is commonly described.

The meat-like texture of jackfruit has led some people to use it as a meat substitute for vegetarians/vegans (though of course it's not really comparable in terms of macronutrients.)  See here, for example.

As a sidenote where are you from? This fruit and variants of it is pretty popular in S. Asia.

@J.E I don't think it's a durian according to wikipedia articles.

@AnonymousI yes, you are completely right, but that's why I used words such as "complete sidenote" and "different kind of fruit".

Yep, I've noticed that before I even started the comment but somehow unconsciously I wrote it anyways. My apologies for the mistake.

This appears to be a jackfruit. Jackfruit are a large, tropical fruit, commonly reported as smelling similar to banana.

Oh yeah!! Yes it is what it pretty much looked like from inside. Thanks a lot! I have seen it for the first time in my life.

Jackfruit are famously reported to taste like Wrigley's Juicy Fruit. Both seem to contain a lot of isoamyl acetate, as do bananas. So this all adds up.


text:
Why don't acacia trees prefer increasing tannin levels in their leaves rather than leaving them high?
According to this article, the Acacia tree has a chemical defence system which leads to the release of ethylene in the surroundings when a herbivore grazes on it. This leads to an increase in tannin concentration in the leaves not only in the plant where the herbivore is grazing but also in the acacias surrounding 45m.
The question is, what prevents acacias to store tannins beforehand? Wouldn't the giraffes totally avoid them then?  Tannins aren't poisonous by themselves (correct me if wrong).

I was unable to find the original research article. A link would be really appreciated

The original article doesn't seem to be online. A summary of the findings was in the Scientific American in 1990. A thesis by a student of van Hoven's seems to cover it (THE INFLUENCE OF PLANT TANNIN ON THE FEEDING ECOLOGY OF GIRAFFE (GIRAFFA CAMELOPARDALIS)) but only the abstract seems to be online and the thesis is in Afrikaans.

Usually the answer to these sorts of questions is that generating the toxic substance (tannins) is metabolically costly, so it's bad for the plant to produce the toxin when it's not needed. When the plant is threatened by browsers, it's beneficial to turn on the production until the threat goes away.


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How does 2,3 biphosphoglycerate works to release oxygen bound to the hemoglobin?
I read on Wikipedia that 2,3 BPG binds with the deoxygenated state of hemoglobin and helps in stabilizing it. It was also written that it helps release remaining oxygen from the hemoglobin. How?
https://en.m.wikipedia.org/wiki/2,3-Bisphosphoglyceric_acid

Possible duplicate of Effect of 2,3-bisphophoglycerate (2,3-BPG) on haemoglobin

You've answered your own question. The association/dissociation of oxygen is an equilibrium reaction. If you stabilize one state, you move the equilibrium to that state. 2,3-BPG helps release oxygen from Hb exactly by binding and stabilizing deoxy-Hb.

From more mechanistic point of view, 2,3-biphosphoglycerate contains 2 negatively charged phosphate groups, which interacts with positively charged groups of each beta-chain within deoxyhaemoglobin decreasing the oxygen affinity (see good old Stryer Biochemistry)

If I understand your question, you want to know, HOW the 2,3-biphosphoglycerate helps release the oxygen from the heme. In addition to other factors like the blood temperature, the pH, and the ambient pCO2, it modifies the heme oxygen affinity. It binds, using salt bridges to lysine and histidine of deoxygenated heme subunits and, by this, changes the deoxygenated heme's conformation. The so modified heme conformation renders the (oxygenated) heme-oxygen bond instable. The altered heme subunit conformation cannot hold the oxygen atom anymore, which dissociates from the heme subunit and diffuses to the mitochondria, thus allowing for ATP production. This process is called "the hemoglobin oxygen affinity is being reduced" and one of the promoting factors of this process is 2,3-DPG.

This looks like an informative answer, but it would be made more helpful for others if it cited sources or linked materials.

Comment to M.P.'s note from Aug 25, at 22h14

Comment to M.P.'s note from Aug 25, at 22h14. From my point of view, the 2,3-DPG does not stabilize the hemoglobin but the oxygen's affinity to hemoglobin, as is stated in the original Q and also in the first A to the original Q, This is far from being the same thing. My intention was to draw attention to this fact, which was incorrectly stated in the original Q and also in De Novo's upvoted answer. The source of my A (answer) is : https://en.m.wikipedia.org/wiki/2,3-Bisphosphoglyceric_acid

It's helpful to have these sources in the answer. I don't take a position on the subtleties of deoxy Hb stabilization mechanism, but if these subtleties exist, it's handy to have very clear visuals or explanatory references, e.g. slides 15-20 or so of this presentation. Wiki is also generally fine, your page looks reasonable, though I don't see any notable distinction between the answers. The important thing is to have all this stuff in the answer itself.


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Why are only few cigarette smokers prone to cancer?
It's tacit that only a few populace of smokers get cancer. What spares the others from it or what specifically cause cancer in those populace? See this Washington Post Article

Those 5% are unlucky to have incurred a genetic mutation which survived. Cells have protective measures against cancer. So a cancer cell which has survived has very likely multiple mutations (e.g. 3 mutations in a same cell is unlikely than 1 mutation in a single cell). Also this 5% of smokers has a subset of mutation not caused by smoking + random mutations.

Where did you read that statistic? It does not appear in the article you link.

Consider that only 16.666% of Russian Roulette https://en.wikipedia.org/wiki/Russian_roulette players die on the first round :-)

Cigarette smokers are most certainly prone to cancer. See Cecil Medicine, Chapter 183, on the epidemiology of cancer, exposure to tobacco is the most important environmental risk factor for cancer development, at least in the US:

Exposure to tobacco is the single largest cause of cancer in the United States... All forms of tobacco can cause cancer. Cigarette smoking causes cancer of the lip, oral cavity, nasal cavity, paranasal sinuses, pharynx (nasal, oral, and hypopharnyx), larynx, lung, esophagus (squamous cell and adenocarcinoma), stomach, colorectum, pancreas, liver, kidney (adenocarcinoma and renal pelvis), urinary bladder, uterine cervix, and myeloid leukemia.

Cancer may be identified or the cause of death in fewer smokers than might be expected, though, because smoking is an even greater risk factor for cardiovascular disease, and death due to cardiovascular disease.
Cancer is an unlikely phenomenon in an individual cell, but becomes  more likely at the organism level, and even more likely over time. Though tobacco may be the most important environmental risk factor for cancer, age is actually a stronger predictor of cancer (see again, Cecil Chapter 183. Autopsy studies give us a quite remarkable example, this one shows incidental prostate cancer in nearly 60% of men over 80 who died from other causes. That figure is not out of the ordinary. Live long enough and you are likely to develop cancer.
Death due to heart disease may account for the lower than expected rates of cancer diagnoses and deaths in smokers. Nothing prevents cancer as well as dying from something else. And as discussed in the blog in the Washington Post you linked to, up to 2/3 of smokers die from smoking related causes

+1 for "Nothing prevents cancer as well as dying from something else"

I've edited the question and removed the 5% part :-)

@user73023 thanks! I took it out of my answer as well.


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Help me identify this fly species?
I found this fly in Bengaluru/India. It was larger than usual flies. It was more than 1cm in size, with black color which has blue shades in it. I managed to take just this one pic, then it flew away.

Based on the numerous strong bristles visible on the abdomen I suspect family Tachinidae; I don't know the Indian fauna, so I can't go any deeper.

yeah, you might be right ...


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Sample suggestions for phase contrast microscopy
I am a non-bio student working on an academic paper recently and would like to have some sample preparation for phase contrast microscope.
For it to work, I imagine the sample to be:

Transparent;
Easy to obtain from daily stuffs;
Easy to slice and prepare (i.e. approachable to people untrained in bio).
Best dimension around 10 micros, and is well seen under x100.
Preferable to be seen dynamics at room temperature.

My current thoughts are:

Human: oral cheek cells, red blood smear, sperm.
Plants: onion surface cells.
Others: yeast, pond water.

Any further suggestions (especially dynamic ones)? Thanks!

Since phase contrast microscopy is a rather old technique, you might find a book on microscopy with sample preparation protocols in the library of your institution. And here a protocol from the web https://www.education.ie/en/Schools-Colleges/Information/Curriculum-and-Syllabus/Senior-Cycle-/Syllabuses-and-Guidelines/lc_biology_support.pdf

@fabianegli Thanks for the helpful link. Though I would prefer easier ways (instead of following the protocols) to prepare the samples, so as to save time and funding. The samples are for demo usage, so protocols are beyond sufficient.

Do you want to prepare the samples at the time of the demo or should they be stored days/weeks/months/years before the demo? Dynamic samples are normally wet samples and they have to be prepared fresh. For demo purpose, I would not take any body fluids, since you work with glass (danger of cutting the skin, including oral cheek skin) and the combination can pose a serious rick for infections. Also a blood smear is looked at when it is dry and would thus not be dynamic.

@fabianegli Thanks for the reply. The samples should be prepared at the time of demo. That’s exactly the reason why I would like an “easy-to-obtain” sample, especially for the dynamic ones. For now I have already tried on blood smear and oral cheek skin, they look good! However I should still need some suggestions for dynamic samples.

Any green, soft leaf from a non-toxic plant is a good start. Cut a thin slice from the leaf (either to look at the cross-section or the surface). Try different leafs with different colors - there might be colors in the cytosol and/or in chromoplasts.
Concrete example for dynamic structures:

Elodea leafs: they consist of only two cell layers and can be looked at under the microscope without further preparation. Keep the the leaf in water and cover it with a cover slide before looking at it under the microscope and add water when it starts drying out. The green chloroplasts in the plant cells are moving around as long as the cell lives.

You might find Elodea either in a pond or in a store selling aquarium fish and the like. You can keep Elodea alive and grow it in nutritious water at a sunny place.


text:
Help! What kind of bug is this?
Please help identify this little bug and how I make them go away.

Where did you find it? Is it a pest? How many do you have? Where do you live (country, type of ecosystem)? What is the approximate size? Any other info (behaviour, what they feed on, etc..)

If you can get a clear photo showing the antennae it would help; at the moment I suspect family Anobiidae (order Coleoptera: beetles I'm sure of), but seeing the antennal segmentation (we can't with this photo) would help with my suspicions.


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How to categorize non-coding sequences in the genome?
I'm trying to wrap my head around the diversity of functions in a genome. Obviously, you've got coding and non-coding regions. But within "non-coding" regions, it seems to be a "wild west" to me. Transposable elements, SINEs, LINEs, transposons, retrotransposons, introns, promotors, etc. Have we annotated genomes enough to have a comprehensive list of the types of non-coding sequences?
It'd be really helpful for me to have a list of the types of non-coding sequences and sub-categories (where relevant). Wikipedia seems to break out a list but the figure on the same page for the human genome doesn't match. Can anyone provide a good reference for how to categorize non-coding sequences?

Is this the Wikipedia article, you are referring to? Which figure is the one that doesn't match?

No, I was referring to "Genome" https://en.wikipedia.org/wiki/Genome#Eukaryotic_genomes but I had just found this page which is helpful. Thanks.

thanks for adding. However, I think the figure and text do align. The text says Noncoding sequences make up 98% of the human genome and the figure says that 2% are Protein-coding genes. Everything else is non-coding :)

Check out the Sequence Ontology, for one approach to categorizing sequence features.  Alternatively, you could download a GFF3 file for the hg38 assembly of the human genome (for example from the ENSEMBL website.  One of the columns in that file contains feature types.

Here's my likely over-simplified and incomplete categorization I could come up with. Please, for those more informed, please edit!
Noncoding sequences can be broken up into the following categories:
1. RNA genes (genes that produce tRNAs, rRNAs, miRNAs, etc.)
2. Introns and untranslated regions (UTRs)
3. Cis- and trans-regulatory elements
    3.1. Cis-regulatory elements (CREs)
        3.1.1. Promoters
        3.1.2. Enhancers
        3.1.3. Silencers
    3.2. Trans-regulatory elements (genes for transcription factors)
4. Repetitive elements (repeated sequences, repeats)
    4.1. Long terminal repeats (LTRs)
    4.2. Variable number tandem repeats (VNTRs, tandem repeats)
        4.2.1. Satellites
        4.2.2. Minisatellites
        4.2.3. Microsatellites (short tandem repeats, simple sequence repeats)
    4.3 Transposable elements (TEs, transposons)
        4.3.1. Retrotransposons (Class I TEs)
            4.3.1.1. Short interspersed nuclear elements (SINEs)
            4.3.1.2. Long interspersed nuclear elements (LINEs)
        4.3.2. DNA transposons (Class II TEs)
    4.4. Telomeres
5. Pseudogenes


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Why there are no RBCs in lymphatic vessels?
I know the following.

Leukocytes (white blood cells) are made in the bone marrow, and naive leukocytes go to the blood vessels. So, leukocytes mainly exist in blood vessels.
Endothelial cells wrapping the capillaries have some gaps, but too narrow for RBCs or leukocytes to leak out (or for bacteria to invade. So, bacteria go to lymphatic vessels).
When leukocytes are needed (like when some foreign molecules invade), leukocytes such as macrophages get out of blood vessels to the tissue of interest by the mechanism of  extravasation.

My question is, why there are no RBCs in lymphatic vessels? Is it because they cannot do extravasation, while leukocytes can?

That's exactly right


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A synthetic sieve organ known as kliver?
in this video at 5:28, the narrator talks about a "vat-grown all-purpose sieve organ" called Kliver that would do away with both liver and kidney transplant. But i don't seem to find online resources about the same. Is that terminology popular in scientific literature, and if so, how would synthetic biology accomplish that? articles about the same will also be appreciated.

This term is used in this book (Synthetic Biology, The National Academies Keck Futures Initiative, p.43). This book is a summary of several interdisciplinary team discussions during a  conference held in 2009.
One...

[...] team considered building artificial organs. Engineered to be hypoallergenic, these could allow for a mass production of personalized organs. Their novel and broad functions could also be useful for medical testing. In a single artificial organ, one might screen potential drugs for both toxicity and permeability.
For instance, group members proposed the idea of a "kliver", a kidney-liver hybrid. An independent "kliver" could help filter bio-compounds out of drinking water.

There are some more paragraphs revolving around the question how to build a "kliver" and a final paragraph concluding that enough necessary building blocks were available and researchers could start working on it:

Potential building blocks might be mammalian and microbial cells and their products, such as slime, fibers, small molecules and proteins. The cells might be engineered to hold new electrical, mechanical, and chemical powers.
  [...]
  Cells would be programmed to degrade their organs and DNA if they began to invade other organisms or the environment. A genetic "kill switch" aims to stop contamination or infection.

Summarising this, I wouldn't call it a "popular term".

PS: to share some Google-fu: the book popped up when searching  for "kliver kidney liver"

How would synthetic biology accomplish this?

We already have a synthetic kidney. We've had it for over 50 years. It prolongs life, but still not very well. Transplant, with all its challenges and complications, does much better.
The liver is much more complicated, and I would be very suspicious of anyone who thinks of it as primarily a sieve or detoxifying organ being able to build a synthetic liver. It certainly does some of those things, but it does much more, playing an important role in digestion, metabolism, protein synthesis, excretion, and the immune system. See Cecil Medicine Ch. 148 for an overview.   There's a reason we don't yet have a synthetic bridge to transplant for liver failure. I wouldn't rule it out, but I think you'd need to be able to build a synthetic liver before you could build a synthetic kliver.


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HLA typing between siblings to identify a genetic disorder
If a patient  suffering from a complex array of signs and symptoms for a disease and is having an 8/8 loci match with his sister who suffers no such symptoms can you conclude that the disease is an X-linked recessive disorder? Can u rule out autosomal dominant disorders and autosomal recessive disorders from the diagnosis?

No, you can't conclude that.
First of all, two siblings being HLA identical tells you very little about the rest of their genome. HLA genes are closely linked, and each haplotype is transmitted in mendelian fashion as a single gene.  For non-linked genes (on other chromosomes, or further away on chromosome 6), they are as or nearly as likely to have the same genes as non-HLA identical siblings.
Further, the disease of interest may (is highly likely to) be multigenic and have incomplete penetrance. The heritability of common disorders generally varies from 20-80% (Cecil Medicine Chapter 41, the Inherited Basis of Common disorders).

Technically, there is a small chance of recombination within the HLA (MHC) region, so haplotypes are transmitted in a mostly-medelian fashion.


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Visual and clear example of the idea that "animal doesn't need to understand the evolutionary function of its actions"
This is a question about education. I am trying to come up with a very visual and clear example, to explain a particular concept in evolution.
The concept I am trying to explain is,

the fact that an animal does not need to understand why it's doing something in order for that behaviour to be selected

(by "why" I mean, the evolutionary/functional role of that behaviour, the reason why it increases the animal's fitness).
Students who don't yet intuitively understand evolution, sometimes mistakenly think that in the theory of evolution, animals need to understand why their behaviour is leading to offspring in order to do that behaviour. (they might say: "the bee looks for flowers because it wants to feed his children", although bees (probably) don't actually make this computation, but simply act on stimuli).
(Note by the way that this is not simply about anthropomorphization: e.g. humans also don't need to understand what sex is for, in order to produce offspring).

What I'm looking for is an example of an animal, and a behaviour that is characteristic for that animal, that very clearly shows this principle:

It should be clear and intuitive, that the animal doesn't understand "why" it's doing what it's doing, because to reason about this would clearly be too complicated for the animal (I don't think the bee example really satisfies this).
It should be visual, and memorable.

I may give an answer at some point. But what you're referring to is the distinction between ultimate and proximate explanations for a phenomenon. You can see the Wikipedia article for one example. This is also widely discussed with many examples in many books on animal behavior, for example in chapter 3 ("Hormones and Neurobiology") in the book "Principles of Animal Behavior" by Lee Alan Dugatkin. This part is actually in the free preview of the book on Amazon, so you could look there.

@Eff, I would say that the category I'm referring to is an example of a ultimate and proximate explanations, but that concept is far more general. In any case, thanks for the comment :).

just use things that don't have a brain like trees.

@John, that would actually not bring the point accross, since people would retain the intuition that it holds with things that have brains

if you can show how it works in plants you can only explain it works the same in animals. Trying to use an animal as an example has a big problem, if the person does not know basic evolution they will have no idea of what an animals brain is or is not capable of. You are expecting two vastly different levels of biological knowledge from the student.

Use human behavior, they're human, do they understand why they like salty foods or why thiols smell bad to them. These behaviors still work even when you have no idea why you are doing them.
Using humans circumvents the problem of them not understanding animal behavior, which they already have to do to grasp your explanation for animal behavior. Using any other animal requires them to understand that animals mind which an entry level student will not, however as humans they can assess their own knowledge directly.

It's very hard for people not to see volution in actions of external entities. Thus, use the students themselves: choose a completely autonomous motor function like the contraction of the pupil in different lighting to give them the opportunity to observe themselves during an involuntary act.


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How do the chromosomes arrange themselves after fertilization in humans?
In human reproduction the male produces sperm containing 23 chromosomes and the female has the oovum containing 23 chromosomes , so after fertilization the zygote contains 46 chromosomes. What I want to know is , how do the chromosomes identify each other and pair up,  fir example say ,how does chromosome '1' of the male pair up with chromosome '1' of the female to make set '1' of the zygote?

I don't understand your question. 23 chromosomes from the mother, 23 from the father and they combined in 23 pairs of chromosomes. What exactly is unclear to you? Maybe you'll want to watch an introductory class about genetics such as e.g. the series of lectures from Khan Academy

Do want to know, how for example the male and female chromosome 1 "find" each other and pair up in the zygote?

Yes that 's right , what I am asking is that after fertilisation how do the chromosomes find each other and pair up.

After fertilization the diploid cells divide by mitosis.  Chromosomes don’t need to pair with their partner during the eukaryotic cell cycle.  After S-phase each chromosome has been duplicated (so there are 46 + 46 = 92).  The two daughter chromosomes resulting from semi-conservative DNA replication are held together at one point: their centromeres. In M-phase two microtubules from opposite poles of the mitotic spindle will attach to the kinetochore that assembles at those centromeres.
Nowhere in this process is the maternal chr1 required to interact with the paternal chr1.
The pairing that you are refering to takes place much later after the new primordial germ cells haved developed into the germline, leading to meiosis.  The molecular details of homolog pairing during meiosis are best understood in the model organism C. elegans where each chromosome has specific cis-acting sequences that are recognized by different trans-acting factors that lead to recognition and then pairing, followed by synapsis, and eventually crossing over.


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Are there any plants that parasitize on animals?
It seems, fungi often infect animals, while plants it seems, never. Is it because the cellulose cell walls make them incompatible with animal tissue?

The question in the title differs from the one in the post. Can you please pick one of the two questions only?

The threshold between parasite and predator is somewhat blurry. Would carnivorous plants be a good example? The only true good example coming to my mind are plants that get insects to carry their pollen but don't give them any nectar as reward. There are also plants that lure insects in but imitating a potential mate and then just use these insects for pollen transportation again. Are these good examples or did you mean endo-parasites only?

Why would they? They evolved to become phototropic.Although carnivorous and protocarnivorous plants exist for survival advantages.Can you be a bit more specific so that it's easy to relate?

Boundaries between parasite and symbiotic are also fuzzy. What about the algae that are symbiotic with sloths? Molecular evidence for a diverse green algal community growing in the hair of sloths and a specific association with Trichophilus welckeri(Chlorophyta, Ulvophyceae)

Well...there is the Venus Fly Trap.

I am voting to close as unclear as long as the OP has not address the difficulties of definitions of ecological interactions and has not addresses whether the presented examples would answer the question or not.

Helicosporidium https://doi.org/10.1371/journal.pgen.1004355

Yes
Acrochaetium spiculiphilum is an marine endozoic parasite on sponges.
It is a Biliphyte algae and thus a plant.
https://www.cambridge.org/core/journals/journal-of-the-marine-biological-association-of-the-united-kingdom/article/abs/observations-on-an-endozoic-red-alga/A2486145D3811B18BCC65A81B24ADA56

Yes! Here's a paper published August 2018
https://www.sciencedirect.com/science/article/pii/S0960982218308157

No, ans the abstract says, the parasitic plant attacks the insect-induced tumors of the other plants. In other words, plant tissue.

Link-only answers are generally not acceptable on Stack Exchange sites. The link may change or become unreachable in the future, and without a summary of what the link contains this answer would be useless. Please summarize what is in the link (don't just copy and paste) and use the link solely for reference. If you remove the link and the answer cannot stand on its own, it is not a good answer.

Could you please summarise the relevant content of that paper? Posts should be self-contained and not rely on a link only, because the link might get broken.


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What type of bug/insect is this?

I found this bug on the bedsheet and can’t figure out what it is. Can anyone help?

Could you please edit your question and add the size of that insect as well as a geographical location and season?

It looks very much like a webspinner, Order Embioptera. But many geographic locations would rule that out. I have never heard of these entering homes. I can assure you that it is not a bedbug.

Using my browser's zoom function to magnify the photo we have lets me confirm the order as given (and as the animal has wings, we can be pretty sure it's a male); going to family might be possible for Gina if she still has the specimen, but identification further than that may not be possible -- turning a search engine loose on the order name and "Ross" will (I believe) eventually turn up a notice to the effect that the specialist just named has over 1000 species not yet formally named in his collection ...

It looks like a species of earwig. I get them inside my house at certain times of year or after it rains. As far as I know all species are harmless but I would double check that.

Could you please explain, why you think this was an earwig? For example, the wings of earwigs in my area have quite degenerated wings, not such prominent ones as in the given picture. But this might be different for other species. Would be nice, if you could clarify this.


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Using distilled water on sterile swab for collecting microbes on solid surfaces
I was wondering if it is acceptable to use distilled water on a sterile swab for the collection of microbes on a solid surface. - in this case, Salmonella and Shigella.


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How many teeth can "African wild dogs" have?
The New York Times article In Mozambique, a Living Laboratory for Nature’s Renewal discusses reintroduction of what the article calls only "African wild dogs" into Gorongosa National Park in Mozambique.
I was taken aback by the "smile" of one of the dogs shown below. Though I'm not particularly familiar with canine dental situations, this looks like an awfully large number of teeth. Is there a known limit to the number of teeth wild African dogs (or any canine) can have?

above: "A wild dog in Gorongosa. One pack has been reintroduced, and a second will be brought in next year.CreditBrett Kuxhausen/Gorongosa Media, via Associated Press" Cropped, from NYTimes.

above: "Wild dogs, apex predators missing from Gorongosa National Park for decades, have been reintroduced and are slowly making a comeback, part of an ongoing experiment in reviving the park ecosystem after years of devastating war.CreditBrett Kuxhausen/Gorongosa Media, via Associated Press" From NYTimes.

I found conflicting information on different websites with a humanima article stating that they have 4 toes and 40 teeth (reference). However, multiple sources state that they have 42 teeth (reference 1, reference 2 and reference 3) with the different teeth being (i= 3/3; c=1/1; p=4/4; m=2/3) x2. I did search for official journal publications but could not find any.
However, since more sources state that there are 42 teeth, I am led to believe that 42 is the right number rather than 40.

Wow, thank you for the thorough and well-supported answer! Viewed top-down, human molars are roughly squarish. I'm having difficulty understanding from the photo in the question how each half of each jaw could only have ten to twelve teeth, unless some of them are extremely elongated along the jaw (front-to-back). Is that what's going on here?

@uhoh That seems to be the case. Here are some images of the skull. http://skullbase.info/skulls/mammals/african_wild_dog.php

Super, and yikes! Thank you for the additional info.


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Butterfly/Moth identification: Puppa is half green, half brown, and 1,5cm long, found in Upper Austria
Question: What butterfly is going to evolve out of the puppa illustrated in the attached picture?
Characteristics: Puppa is half green, half brown, and 1,5cm long
Further details: I don't know if this is relevant we found it on our mint plant, presumably it has eaten its leaves along with the lice on it.

Did you pull it out of the silk in the photo to take the picture?  If so, it is probably a moth species. You will probably need to wait for it to emerge to identify it.

@user22542 No i did not pull it out of the silk, no person did. However we had severe rain once in a while in the last 1 and a half weeks and I was not present at the spot where the plant stands, hence I cannot tell if it had an impact


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Devonian Fish Diversity--What Would it Have Looked Like?
For 70 million years, the oceans, lakes and rivers of the world teemed with seven groups of fish:

Placodermi

Acanthodii

Agnatha

Chondrichthyes

Sarcopterygii

Actinopterygii
Now two of those groups have been extinct for hundreds of millions of years, but they were still a pretty big deal back then.
So by using modern fish as analogies, which niche(s) did which group of fish occupy during the Devonian Period?

A fascinating question, I wish I had time to delve into it, but it seems I am not the only one unable to do it justice at the moment.


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Oak processionary or what else?
We have those caterpillars with some sort of webbing on stinging nettles below some oaks.  Photographs I found in Wikipedia look quite hairier with long white hairs but maybe it's the molting level?
Or those guys are something less notorious.  This is in Germany, Northrhine-Westfalia.

And here is a video in case it helps.

Looks more like aglais io, the European peacock.  At any rate, oak and stinging nettle leaves are quite too dissimilar to make a crossover of comparatively specialized caterpillars likely.

Totally agreed!


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Why aren't all infections immune-system resistant?
It's been less than a century since the widespread use of antibotics started, and already we're seeing bacteria that have evolved immunities to the antibotics we use.
On the other hand, we've been using immune systems to to fight bacteria for millions of years, and bacteria evolve much faster than humans do.  Why have bacteria not evolved immunities that let them completely overwhelm our immune systems and kill us all?

First of, not all infections are mediated by bacteria and not all bacteria are infectious. Also, not all parasitic bacteria lead to a strong infection or important health problem that cause any non-negligible selection pressure. Following the implicit logic of your post I will talk about infectious bacteria which cause "noticeable harm".
The mistake in your thinking is in the sentence

bacteria evolve much faster than humans do

While it is true that the mutation rate of base pair is higher and that the generation time is lower, the statement bacteria evolve much faster than humans do is made way too general and lead to your mistake here.
Infectious bacteria are selected to deal with the host immune system and the host is also selected to deal with the the parasite. Both virulence and penetrance evolve in this evolutionary arms race.
The evolution of host-parasite interaction is a very large field of study and it would take several books (and several books have been written on the subject; see this Amazon search) to summarize it. For some theoretical insights into the evolution of host and parasites, you might be interested in the book by Martin Nowak Evolutionary Dynamics: Exploring the equations of life
You will also note that a parasite does not have any "direct interest" in killing (or even harming) its host (thanks @jamesqf for his comment). You might want to have a look at the post Why do parasites sometimes kill their hosts?

Consider that an infection which kills off all its hosts is committing suicide :-)  From an evolutionary viewpoint, the ideal of bacterial survival would be to not harm the host at all, or even to benefit it - and indeed, there are many such bacteria living in your digestive system.

I'd like to add to @Remi.b's excellent answer with a few additional points
To quote Lewis Thomas in Germs

Disease usually results from inconclusive negotiations for symbiosis, an overstepping of the line by one side, a biologic misinterpretation of borders.

The human host is a complex ecosystem. Many "pathogens" live quite happily in one compartment, having co-evolved to the point where detection and attack by immune system mediators doesn't happen (the microbe avoids it) and is unnecessary (attacking the microbe provides no benefit to the host). For example, enterobacteriaceae have a capsule that allows them to avoid binding of IgA in the gut (see Murray Medical Microbiology, Chapter 30). Disease occurs when that otherwise commensal microbe is introduced to a compartment where it doesn't belong. Here, as it often is, disease may not be beneficial for either the host or the pathogen.
Two other small points to consider:

Antibacterial resistance is not new. The spread is new. In fact, resistance genes have been around for at least tens of thousands of years (see my answer to another question)
Again, a (human) host is a complex ecosystem. It is not an arms race between two species. A successful microbe must negotiate for space and resources with many other species, and may, in fact, be a host itself.

Every pathogen is resistant to immune responses. That's why they're pathogens. "Normal" bacteria, that don't have resistance adaptations, are immediately destroyed by immune responses; that's why we're not immediately infected by the vast cloud of microbes that surround us.
Individuals with weakened immunity (such as AIDS patients) are infected by microbes that normally aren't considered pathogenic. Such microbes don't have most of the immune-resistance armory that true pathogens or even opportunists have; but even they have some immune resistance capacity, as proven by the fact that even AIDS patients aren't infected with, say, plant viruses or the billions of soil bacteria that surround us, but that lack immune resistance altogether.
Although all pathogens and opportunists have immune resistance, few if any have complete immune resistance. Why not? Because the selective pressure on hosts to develop and maintain effective immunity is extremely high. Those hosts that failed to protect against some form of infection are probably extinct.

Immune-system resistance is especially difficult due to how immunity works.
First, I make 2 assumptions in my explanation:

the pathogen isn't specially designed to dodge the immune system and it isn't able to hide dormant in cells
the immune system is healthy and normal

When a pathogen is present, the immune system samples pieces of it (epitopes) and works on "randomly" putting together antibodies that bind to that epitope. Once a match is found, the qualifying antibody proliferates and is deployed in full force. Each copy of the matching antibody binds to the offending pathogen on contact with good probability - think of it as a microscopic football tackle. Cell-like pathogens (bacteria, fungi, and protozoa) thoroughly covered in antibodies can't consume nutrients, attack cells, and in extreme cases they can't excrete toxins because exocytosis proteins are blocked in antibodies. Viruses covered in antibodies have their surface structures blocked, thoroughly preventing binding to host cells.
The only reason why antibiotics are "easy" to gain resistance to by comparison is that they don't change on their own. The ones most vulnerable to resistance rely on tricking bacteria into eating them (endocytosis), which quickly selects for bacteria that work around the vulnerable protein channel. In other cases, bacteria develop something that inactivates antibiotics.
There has recently been work on antibiotics that force their way into bacterial cells, effectively punching large holes in the membrane. These would be difficult to develop resistance to, especially if they operate via electrical potential or grab onto a wide variety of bacterial epitopes.
Additionally, bacteria would be in a lot of trouble if humans developed antibiotic-generator implants that work as a secondary immune system. Consider a technology that scans for pathogenic bacteria, builds computerized 3D models of them, and then uses a biochemical 3D printer chip to construct custom antibiotics after preliminary safety checks to verify that the custom antibiotic in question wouldn't have dangerous side effects.

This answer has a number of misconceptions and speculation with no references.

Prove it. Your accusation provided no references. At least I'm contributing. How do I (or anyone else for that matter) know that you aren't #FakeNews? If you want to fact check, post a link in a comment and prove me wrong. Don't just downvote with no source, that's effectively trolling and abuse of the system.


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What is the equation and mechanism of Hopkins-Cole Test reaction?
The Hopkins-Cole reaction or glyoxylic acid reaction, is a chemical test used for qualitative detecting of tryptophan in protein solutions.
tryptophan + glyoxylic acid + sulfuric acid  >  violet product
I know the chemical formulas of reactants, but I could not find the product formula and a mechanism for the reaction.