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Vero cells and Influenza
I am currently reading a paper regarding Influenza. In the paper they describe a mutant and a WT, and the differences in replication. They grow the two strains in Vero cells (kidney epithelial cells). Why do they grow them in Vero cells, when it is a respiratory disease?
Link for article: https://pubmed.ncbi.nlm.nih.gov/9878611/

In addition to @David's answer, the viruses in this paper were specifically grown in Vero cells because of their lack of interferon expression1,2, which the authors were looking at for examining functions of the NS1 fragment from influenza.
Normally, influenza viruses are grown on MDCK cells for propagation or (more commonly) in embryonated chicken eggs.  The authors propagated the viruses in eggs in this paper, as explained in the Materials and Methods. The authors also used HEK293 cells for transfection, which are used in co-culture with MDCK to generate genetically modified influenza viruses.
1: Diaz, M. O., Ziemin, S., Le Beau, M. M., Pitha, P., Smith, S. D., Chilcote, R. R., & Rowley, J. D. (1988). Homozygous deletion of the alpha- and beta 1-interferon genes in human leukemia and derived cell lines. Proceedings of the National Academy of Sciences of the United States of America, 85(14), 5259–5263. https://doi.org/10.1073/pnas.85.14.5259
2: Mosca JD, Pitha PM. Transcriptional and posttranscriptional regulation of exogenous human beta interferon gene in simian cells defective in interferon synthesis. Mol Cell Biol. 1986 Jun;6(6):2279-83. doi: 10.1128/mcb.6.6.2279-2283.1986. PMID: 3785197; PMCID: PMC367773.

@bob1 provides a specific reason for the use of Vero cells in this case, where the study concerns the behaviour of these cells in response to infection by influenza virus. However, it is worth pointing out that the implicit assumption of the poster — that one should grow a virus in the cells it infects in the wild — is questionable.
The problem has been historically that the cells a virus infects in the body cannot generally be grown in tissue culture — some kind of immortalized cell is needed. Originally — before tissue culture had been developed — viruses were passaged by inoculating eggs, and an answer I provided to another virus question goes into this area in more detail.
In summary, if you want to grow a virus to obtain large quantities of virus or its components you choose the best system available for doing that. If you want to study its pathology you inject it into a suitable animal model, or if you want to study how tissues respond to it, you choose a suitable cell line (as in this case). But the two things are generally quite different.

What about A549 human lung epithelial cells? I think that was the OP's point. A549 grows Influenza as well. Look at the link, and you'll see why they chose Vero.


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How many different smells can a human recognize?
How many different smells can a human recognize?
If the space of smells is not discrete, how many dimensions it has (for example, the space of colors is three-dimensional).

Another way to rephrase your question would be "how many different chemical receptors do we have in the nose?". Is it correct?

@Remi.b no, we have 4 types of photoreceptor cells, but our color space is 3-dimentional.

Here and here are posts on color perception by the way. Note: Your question might be a good fit for cognitive sciences also.

I really don't know much about this subject… Does it really make sense to talk in terms of dimensions? If we talk about color, then it might seem that there is only one dimension as any color can be define with only 1 number. Could you provide an in-depth explanation of how you apply the concept of dimension to visual perception (and other perception)? This might help.

"any color can be define with only 1 number" - this is not true.

@Remi.b http://en.wikipedia.org/wiki/LMS_color_space http://en.wikipedia.org/wiki/Young%E2%80%93Helmholtz_theory

All colors fit on a line from red to violet by decreasing wavelength. We see in three dimensions because we have three types of cones. Intermediate values on several axes allow us to infer the real value of the wavelength. That's why I thought we can reduce your question to the number of chemical receptor we have in the nose. Explain me what you think I am missing.

"All colors fit on a line from red to violet by decreasing wavelength." - no. For example, grey does not fit.

@Remi.b "That's why I thought we can reduce your question to the number of chemical receptor we have in the nose." - I already commented that we have 5 types of photoreceptors in the eye, of whom 4 participate in imaging, of whom only 3 participate in color vision. So the number of receptor types does not indicate the dimentions of the sensual space. For example, rod cells while being different from cone cells, give perception of white color, which also can be obtained with only cone cells.

3 participe in color vision and therefore our vision of color is in "3 dimensions". But anyway. I might not understand, I let other people trying to answer or to make sense of the question.

As nobody is suggesting an answer I'll give my guess that I already discussed in the comments and give some extra details about ongoing debates on the subject.
We'll start with the sense of color sight in order to make easier. One can argue that we see in 3 dimensions because we use three cells which level of activation inform the brain of the color. I guess that the whole 3D space delimited by the maximum level of activation of each three receptors can be used. Therefore, it is nothing else than the number of receptor that determine the number of dimensions in which we can sense. Now it is assuming that each receptor can send signal of different strength information of the intensity of the light or smell.
According to wikipedia. Mammals have about thousands of genes that code for olfactory receptors. Moreover, the question of how these receptors work is still debated

In mammals, each olfactory receptor neuron expresses only one functional odor receptor. Odor receptor nerve cells function like a key-lock system: If the airborne molecules of a certain chemical can fit into the lock, the nerve cell will respond. There are, at present, a number of competing theories regarding the mechanism of odor coding and perception. According to the shape theory, each receptor detects a feature of the odor molecule. Weak-shape theory, known as odotope theory, suggests that different receptors detect only small pieces of molecules, and these minimal inputs are combined to form a larger olfactory perception (similar to the way visual perception is built up of smaller, information-poor sensations, combined and refined to create a detailed overall perception).[citation needed] An alternative theory, the vibration theory proposed by Luca Turin, posits that odor receptors detect the frequencies of vibrations of odor molecules in the infrared range by electron tunnelling. However, the behavioral predictions of this theory have been called into question. There is no theory yet that explains olfactory perception completely.

Note: the two competing theories for color sights: Opponent process and Trichromacy
Hope this helps!
I think this question would also be a good fit for cognitive science beta.

"One color can be describe by one single value (it is unidimensional). This value can be the wavelength for example. " - this is wrong. You cannot describe all possible colors with a wavelength. For example, you cannot describe grey, white or magenta.

@Anixx Yes you're right. I updated my answer.

"Therefore, it is nothing else than the number of receptor" - As I already pointed out we have at least 4 types of receptors with different points of maximum. And to be precise there is also a fifth type. So the number of receptor types does determine the number of dimensions of the color space.

According to this wiki article we have 3 receptors for the color. But anyway, I don't know much, I suggest something as nobody is giving any answer. Sorry, I can't do better. I added, two wikipedia links that are competing theories of color vision.

unless you know beforehand the color space dimensions, you cannot tell which receptors are used for the color just by counting their types. We know that only three types of receptors participate in color vision BECAUSE our color space is 3-dimensional, not the other way around.

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Intermediate of Krebs cycle that can form Chlorophyll?
This was a question in a test in my school today.
Q) Which intermediate of Krebs cycle further can form chlorophyll?
A) Oxaloacetic acid
B) Citric acid
C) Succinyl CoA
D) Fumarate
Given answer was (C).
How can Succinyl CoA form chlorophyll? All I could find was related to porphyrine ring. Can anyone explain it or recommend a good source?

I think you will find my answer indicates what your teacher wanted. I would explain politely that the question was wrong as regards the porphyrin ring of chlorophyl for the reason explained by March Ho, and illustrated in my answer.

The standard treatment of this topic is covered in Section 24.4.3 of Berg et al., available freely online:
Succinyl CoA is a precursor for porphyrin in mammalian cells by condensing with glycine to form δ-aminolevulinate as shown in this diagram from that book:

This reaction is catalyzed by mitochondrial δ-aminolevulinate synthase.
To quote from that reference:

Two molecules of δ-aminolevulinate condense to form porphobilinogen, the next intermediate. Four molecules of porphobilinogen then condense head to tail to form a linear tetrapyrrole in a reaction catalyzed by porphobilinogen deaminase. The enzyme-bound linear tetrapyrrole then cyclizes to form uroporphyrinogen III, which has an asymmetric arrangement of side chains. This reaction requires a cosynthase. In the presence of synthase alone, uroporphyrinogen I, the nonphysiologic symmetric isomer, is produced.

This is illustrated in Fig. 24.35 of that section, which also shows that uroporphyrinogen I gives rise to protoporphyrin IX, the precursor of haem:

As regards the synthesis of plant chlorophyl (which also contains a porphyrin ring), the review quoted by March Ho contains the following statement:

The porphyrin ring with its conjugated double bonds is assembled in the chloroplast from eight molecules of 5-aminolevulinic acid…

(5-aminolevulinic acid is the chemically preferred name for δ-aminolevulinic acid.)
However the review goes on to explain that although 5-aminolevulinic acid synthesized in plant mitochondria uses the same pathway as mammals, that produced in the chloroplast and used for the synthesis of haem that gives rise to chlorophyl uses a different pathway, termed the C5 pathway, in which — as March Ho stated — glutamate is the precursor:

I suspect that the person who set the question is an animal or biochemist who thought he would try a variant of the standard question “which intermediate is a precursor of haem”, and ventured into waters where he was out of his depth.

Thanks for the explanation of what the question was intending to ask. Given that, it makes a lot more sense that the question referred to a specific molecule, since it was the molecule stated in the textbook.

This is a poorly set question. If any one member of the Krebs Cycle is used as the raw materials in a biosynthetic pathway, it will follow that all of the other members are also part of the same biosynthetic pathway, since they are part of the same cycle.
The full biosynthetic pathway of chlorophyll is a very complex process, and there are dozens if not hundreds of different steps and enzymes involved. This is one paper that attempts to cover the issue.
In short, the porphyrin ring region of chlorophyll is generated from glutamate, and the phytyl tail region of chlorophyll is generated via the phytol synthesis pathway, via the geranyl phosphate pathway

I think it is a poorly set question, but not for the reasons you state. It is fairly clear what is meant. I do feel a complete answer needs to point out the animal/microbial pathway for synthesis of δ-aminolevulinate, which, is what is causing the confusion. I feel a little bad about using your info on the C5 pathway of synthesis in chloroplasts in my answer, but I have acknowledged you and,  again, I feel it needs spelling out.

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Will eukaryotic RNA fold in the same way in prokaryotes?
As far as I know, there are no specific eukaryotic or prokaryotic factors that aid in RNA folding other than cellular environment (salt and ion concentrations, dissolved molecules, etc). Are there any factors to consider when introducing eukaryotic RNA in prokaryotes? Is it possible to predict the proper shape and folding upon introduction to a prokaryotic cell?

Interesting question. Ionic concentrations and temperature will certainly affect RNA folding. There may well be other constraints as well.

RNA chaperones will be different as well. I'm not sure how much the relevant ion concentrations vary, but Mg concentration is certainly a very important factor in RNA folding. And are you asking about secondary or tertiary structure by the way?

@MadScientist, in my specific case I was more interested in secondary structure, but an answer addressing tertiary would be ideal

Fast googling: http://www.nature.com/nature/journal/v505/n7485/full/nature12894.html#ref3 this might help

As you have mentioned ions and temperature affect RNA structure. There are also different types of RNA structures and their dependence on ions are different. Mg2+, as Mad Scientist mentioned, stabilizes duplexes; so do monovalent cations like K+ and Na+. However, Mg2+ favors duplex over quadruplex if the same RNA can adopt both these conformations.
Dependence on temperature is a trivial case.
Ions and temperature should be more or less same for prokaryotes and eukaryotes unless we are talking about extremophiles.
Apart from these factors I can think of two other factors that can cause difference in RNA structure between prokaryotes and eukaryotes:

Osmolytes
RNA binding proteins/chaperones (Already mentioned in comments by Mad Scientist)

Osmolytes
It has been shown that TMAO (Trimethylamine N-oxide) stabilizes RNA secondary structures. The metabolism of TMAO is different in prokaryotes and eukaryotes.
From this paper:

Although eukaryototes can endogenously produce L-carnitine, only
  prokaryotic organisms can catabolize L-carnitine11. A role for
  intestinal microbiota in TMAO production from dietary carnitine was
  first suggested by studies in rats; moreover, while TMAO production
  from alternative dietary trimethylamines has been suggested in humans,
  a role for microbiota in production of TMAO from dietary L-carnitine
  in humans had not yet been demonstrated30-32. The present studies
  reveal an obligatory role of gut microbiota in the production of TMAO
  from ingested L-carnitine in humans (Fig. 6c)

I cannot ascertain that this will affect RNA folding but is possible.
RBP
This is something that you can be certain about. Some RNAs require protein counterparts to adopt a functionally capable structure. In the absence of the protein they may not form the relevant structure. So if an RNA needs Hfq then you have to express it in the eukaryotic system where you want to use the RNA (and converse).


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Is there are practical lower limit to gene length in E. coli?
Question is rather self-explanatory.
Putting aside other post-transcriptional factors like rate of degradation of transcript, what is the smallest gene ever reported to have successfully been transcribed in E. coli or other similar prokaryotic systems? Why couldn't this gene be any smaller?
Note that in the context of this question, I am disregarding factors like promoters, operators and terminators. Also note that this gene does not necessarily need to code for a protein.

One example of short transcripts in bacteria would be transcriptional riboswitches when they are in the "off" state.

In terms of naturally-occurring "genes" I think that the record is probably held by the attenuator peptides.
In bacteria, the regulatory mechanism known as transcription attenuation involves the ribosomal biosynthesis of very short peptides. In the trp operon, where the phenomenon was first described by Yanofsky's group, the peptide, MKAIFVLKGWWRTS, consists of just 14 amino acids. Other examples, described subsequently, are of comparable size.
Now that I have written this answer, I have reread your question and I see that you are really interested in transcripts. In the case of the attenuators, the peptides are encoded by the 5' end of a much larger transcript, so they probably don't count for you.

Non-coding transcripts can be as small as 10-15 nucleotides. Once the RNA polymerase initiates, the DNA is melted and the transcription bubble forms. This region is about 10 nucleotides long.
But if you are asking the limit of mRNA length, then the answer is different. First of all, to get a protein, the ribosomes have to translate the transcript. To do that, they need some space to land on, and initiate the translation process. We know that ribosomes protect about ~30 nucleotides from  ribosome footprinting experiments
Moreover, bacteria wouldn't need to utilize the genomic space and the ribosome machinery to produce small peptides (even if the peptides were useful), since the small peptides are already around as the degradation product of other proteins. Hence, once you add 3 times the shortest produced polyaminoacid length to the minimum length required for the ribosome landing, you get somewhat physical (or let's say physiological) limit of the transcript length.


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What is the meaning of 'primary' and 'secondary' sympatric speciation in this paper?
Sympatric Speciation in the Genomic Era. Both terms are used throughout the paper.
I'm not able to make sense of these terms in the contexts used.
I've also heard the terms 'primary' and 'secondary' gene flow elsewhere on the same topic - are they related?
From the abstract:

However,  I  argue  that  genomic  studies  based  on contemporary  populations  may  never  be  able  to  provide  unequivocal  evidence  of  true primary sympatric speciation, and there is a need to incorporate palaeogenomic studies in  to  this  field. This  inability  to  robustly  distinguish  cases  of  primary  and  secondary divergence-with-gene-flow may be inconsequential, as both are useful for understanding the  role  of  large  effect  barrier  loci  in  the  progression  from  localised  genic  isolation  to genome-wide reproductive isolation. I argue that they can be of equivalent interest due to  shared  underlying  mechanisms  driving  divergence  and  potentially  leaving  similar coalescent patterns.

From the introduction:

Lastly,  I  consider  whether  primary  and  secondary  sympatric speciation represent a mechanistic dichotomy, I suggest that primary and secondary contact can leave a similar genomic signature, when speciation is driven by tightly clustered or  large effect loci. Arguably, the advent of affordable population genomic studies should place less focus on whether study systems result from primary or secondary contact and instead focus on the mechanistic aspects of the genomic architecture and making progress in identifying the conditions and processes under which natural and sexual selection can drive speciation, without extrinsic barriers to gene flow.

The paper is behind a paywall, which will mean that most readers cannot access it. Can you please extract some relevant fragments into your question?

Apologies, I've added some excerpts.

TLDR
Sympatric speciation and allopatric speciation with later migration into the same habitat were historically diffucult to distinguish without looking at palaeo-biological data. The paper argues that while palaeo-genetics has made this easier, it is still difficult to distinguish pure sympatric speciation (which it calls primary) and sympatric speciation with a geneflow from an geographically separated (allopatrically speciated?) subpopulation (which it terms "secondary sympatric speciation" or "speciation with secondary gene flow", "...with secondary contact" etc.).
Speciation
Speciation is the divergence of one species (with one gene pool) into two different species (with different gene pools). It is obvious that this will happen if subpolulations are geographically separated and continue to adapt to their local conditions (allopatric speciation).
However, Mayr suggested (back in the 1940s) that there is another type of speciation that happens while the speciating populations share a habitat, and, consequently, while gene flow between these subpopulations is maintained until the speciation process is complete. This requires strong selection pressure towards two different ecological niches each with their associated adaptations.
Empirical examples have been discussed and called into question again. One cool and frequently discussed example is that of the apple maggot in North America that has developed from the hawthorn maggot after the introduction of apples in North America.
Debate
Unequivocal examples for pure sympatric speciation are rare, leading to some debate about the merits of the concept. Sympatric speciation models (following Maynard Smith's models from the 1960s) as well as the reasons for skepticism towards them are illustratively explained for instance in this article (Felsenstein 1980), page 133-135.
The debate continues, today with additional, newer findings from genetics, palaeo-genetics, etc. This is what the article in the OP (Foote, 2018) was about. The pdf of the article (Foote, 2018) without paywall can also be found here. While Foote suggests that what pure sympartic speciation and speciation with secondary gene flow may never be unequivocally distinguished (without additional palaeo-genetic information), others are more optimistic, e.g. Richards et al. 2019 (without paywall on biorxiv). Coincidentally, Richards et al. have a very nice illustration (their Figure 1) that illustrates the issue the OP was asking about.

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How does pressure travel through the cochlea exactly?
I cannot find this answer anywhere.
What I do know is that the stapes pounds on the round window of the cochlea and this causes the fluid to move inside the cochlea itself, which has the three chambers (the scala vestibuli, the scala media, and the scala tympani), where the basilar membrane between the scala media and scala tympani is what fluctuates with pressure. This leads to the sound processing in the scala media and the organ of Corti due to the shearing motion of the hair cells against the tectorial membrane, and so on and so forth.
But I don't understand the pathway of the pressure. A lot of resources show the pressure wave moving front-to-back (towards the apex), making the basilar membrane move simultaneously. But at the same time, they also show that the full pathway through the cochlea goes front-to-back through the scala vestibuli, turns around at the apex, and then goes back-to-front through the scala tympani where the basilar membrane is located. So how can the basilar membrane be moving front-to-back when it's stretching along the latter half of this cochlear pathway, way over on the other side of the scala media?
Therefore I am unclear if (1), (2), or both of the following are true:
(1): Does the pressure somehow permeate through Reissner's membrane (between the scala vestibuli and scala media), move through the scala media (without disturbing any hairs in the organ of Corti), and then push on the basilar membrane from above, which would allow for this front-to-back wave motion?
(2): Does the pressure move the basilar membrane from below during its "return trip" going back-to-front through the scala tympani?

Short answer
The pressure wave through the scala vestibuli drives the basilar membrane response (BM). Your option (1) is correct, (2) is not. The pressure not really permeates or penetrates Reissner's membrane though; it is the pressure differential across the scala vestibuli and scala tympani that is the driving force for the BM movement.
Background
The most accepted way of viewing acoustic activation of the auditory system is the traveling wave theory (Fig. 1) as posed by the famous experiments of Georg von Békésy in the 1960's. These experiments showed, basically, that the basal part of the basilar membrane (BM) starts vibrating first (near the cochlear 'entrance' at the round window) and as the wave travels through the scala vestibuli, more apical parts get activated (Fig 2). This phenomenon explains the cochlear delay that's seen, i.e., that low frequencies tend to activate hair cells later than high-pitched sounds do (He and Ren 2013).
Reissner's membrane separates the scala vestibuli from the scala media. The traveling wave generates a pressure difference between the scala vestibuli and scala tympani. As you rightfully say, this pressure difference is established across Reissner's membrane and across the BM (Fig. 3). It is the movement of the BM that ultimately results in the sensation of sound (source: Ento Key). In fact, the movement of Reissner's membrane is comparable to that of the BM (Reichenbach et al., 2012). However, Reissner's membrane is not tuned and contains no neural elements involved in hearing. The stereocilia of the hair cells are embedded in the tectorial membrane. The shearing forces between the BM and tectorial membrane eventually result in mechanotransduction (Fig. 3). See Fig. 12.5 on this web page from Neuroscience online textbook for an informative video on the BM movement relative to the tectotial membrane.
The traveling wave is basically confined from base  to apex. Because of the tuning of the basilar membrane, high frequencies resonate the basal part (because the BM is stiff and narrow) and low frequencies the apical part (because the BM is wide and floppy). Each time a resonant frequency is met, the BM starts vibrating maximally and basically the frequency cannot go further and its energy is dissipated. Thus, along the way, sound traveling through the scala vestibuli  to the helicotrema (the boundary of the scala vestibulu and tympani) more and more energy is used up from the pressure wave. Thus, the basilar membrane is set in motion primarily by the pressure differences occurring in the scala vestibuli and by the time the traveling wave reaches the helicotrema no appreciable energy is left as all auditory frequencies have been filtered out. Remaining energy containing frequencies outside the audible range (roughly 20 - 20,000 Hz) continue to travel to the scala tympani (think of static pressure during a deep dive) and therefore the round window is necessary to act as a buffer (Robles & Rugggero, 2001).
However, there are other theories, notably one from Hermann von Helmholtz, a brilliant scientist of the 1800's that has revolutionized sensory sciences. It is called the 'sympathetic resonance' theory. I am not at all familiar with this theory, as it has been largely abandoned, at least as far as I know. The theory from Von Békésy assumes that the basilar membrane is a place-to-frequency converter that acts like a Fourier transformer, known as the place coding theory. Basically, the traveling wave dissects complex acoustic stimuli into different acoustic frequencies by menas of frequency tuning of the BM (Fig. 2). By contrast, Helmholtz assumed there are tiny tuned elements positioned in the cochlea that basically perform the Fourier transform (not shown here). If you wish to read more of the latter theory, I happily refer you to Bell, 2004).

Fig. 1. Traveling wave. source: NY University

Fig. 2. Basilar membrane movement. source: NY University

Fig. 3. cross section through cochlear duct. source: Psychology Wiki
References
- Bell, Plos Biology (2004); 2(10):e337
- He & Ren, Scientific Reports (2013); 3: 1874
- Purves et al. (eds), Neuroscience (2001) 2nd ed. Sunderland (MA): Sinauer Associates
- Reichenbach et al., Cell Rep (2012); 1(4): 374–84
- Robles & Rugggero, Phys Rev (2001); 81(3): 1306-43

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how do macrophages have the capacity to digest pathogen in opsonization
how do macrophages  have the capacity to digest pathogen in opsonization but not in the            first time when the pathogen is new  and they play the role of antigen presenting cells(APCs) first they digest polypeptide of antigen and then let the plasma cells first secrete an antibody and after that they can destroy antigens?

There are multiple mechanisms to induce phagocytosis by macrophages. One includes B-cell antibodies (specifically the Fc region) and another includes chemokines emitted by local cells that can also induce phagocytosis. I do not have my material with me at the moment, but the short answer is: Macrophages can do both. They can eat pathogens without antibody stimulation, but antibodies can also stimulate them into action.

It's a simple matter of ionic charge
Opsonization works because it is masking negative charge with positive charge. Phagocytosis works on positively charged things.
Your right though, the sequence seems odd.

First something is phagocytosed (by a macrophage or another monocyte-derivative, these are the APCs... but neutrophils, which are not APCs or monocyte-derivates also perform phagocytosis but they dot not have the MHC-II to be described)
then digested in endosome/lysosomal,
then presented on the MHC class II,
recognized by TCR on T-cell,
then much more complicated stuff to get to B cells to convert to plasma cells
plasma cells secrete the antibody, in order for opsonization of the pathogen to be phagocytosis more easily.

Yet it was the initial phagocytosis that led to this. A bit of a circle.
Here are three answers:

one is cytokines
another one is about how the TLR receptor mediates phagocytosis
a third is how complements act as opsonins

local presence of cytokines (ex. interleukins, interferon, TNF) from either innate or adaptive "immune system" (by "immune system" I mean immune cells other than macrophage, but also epithelium which secretes types of interferons) that lead to "signal transduction" ("signal transduction" is the intracellular chain reaction in response to the activation of the cytokine (or other ligand) binding to the receptor, too complicated for me to explain) that alters the behavior of macrophage to enhance phagocytosis.

On the other hand, PAMPs activate the TLR which could permit phagocytosis without prior activation from sources "other" than the thing being phagocytosis.
By "other" things I mean opsonins and cytokines.
PAMPs (pathogen associated molecular pattern) are things on the pathogen that are distinctively foreign to the host, like flagella or LPS [which is the outer membrane from gram (-) bacteria]
TLR is the receptor on the macrophage that recognizes PAMPs. I think that TLR simply enhances phagocytosis via signal transduction much like cytokines. As an interesting side note, the TLR is quite ancient in kingdom animalia, having it's origin in sponges  as close to the beginning as you get). Other aspects of the immune system evolved later on specifically in vertebrate. In fact the lymphocytes is unique to jawed vertebrate (aka absent in agnathans and invertebrate) and i don't know much about antibody production in non-mammals. Also in lower vertebrate and invertebrate, phagocytosis is done by hemocytes. In other words, the TLR is pretty fundamental as far as immune stuff goes, more so than cell types doing their things (ex. plasma cell making antibodies, macrophages doing phagocytosis).

But there is also complement mediated opsonization, primarily C3b but other complement proteins as well. Finally there are yet more (less important) opsonins, Mannose-binding lectin and C-reactive protein (CRP). all of these things are "Acute phase reactants" that are secreted by the liver under inflammatory conditions, mediated by cytokines. Complement is not always activated by the immunoglobulins.
Complement is activated by

classical pathway, again Fc region of antibody (IgG/IgM), just like antibody mediated opsonization. In addition, classical pathway can be activated by CRP binding to microbial polysaccharides

alternative pathway, which is the spontaneous hydrolysis of C3. Under normal (non-infected) circumstances, this is normally prevented by a variety of mechanisms.
activation by mannose binding lectin. MVL recognizes certain sugars that are found in certain positions that are unique to bacteria, fungi, viruses.

I'm saying all these things as explanations of human immune system. It's probably different in different animals, the more different the further away from human. The complement system has been discovered in primitive vertebrate (agnathans) and invertebrate (specifically in deuterostomes like protocordates and echinoderms) but there are variations.


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Why APC's present antigen to T cells?
the macrophages are pretty known well for antigen presenting process and to present the antigens which are bound to pathogens unlike exotoxins (which are free) the pathogen first should be digested and destructed and derive the antigenic portion and present it to T cells then stimulate the B cells to make antibodies. If the macrophages can destruct and digest the pathogen to derive the exact antigenic portion so then whats the need of humoral immunity to be activated because they have already destruct and kill the pathogen if your answer is that the pathogen gets knocked out quickly by antibodies for the second if they invade,so there are millions of other infecting agents every day         invading our body and are omitted by the first line defenses?

To answer your question properly would pretty much require giving an entire semester's course in immunology. As there isn't the time or space to do this here, my suggestion would be for you to read Janeway's Immunobiology This is the 5th edition, and from 2001 is likely very stale, as the current version is the 8th edition, and there have been many advances in immunology in the last decade and a half, but it is a start to your answer and will give you a better grounding.

Let's consider some situations real quick:
(1) A bacterial microbe enters through a fissure in the skin. What does an innate, systemic immune response look like? In short: it's lengthy, uncoordinated and has a lot of potential to damage tissue in the area of infection.
(2) A bacterial microbe enters the blood. The bacterium produces an AB toxin that enters cells and kill them.
(3) The host is infected by a helminth.
In situation 1: Innate immune responses are associated with the secretion of many cytokines and chemokines. Cytokines are associated with the inflammatory response, and chemokines are associated with lymphocyte trafficking. Inflammation and recruitment of lymphocytes, macrophages and the like are good for clearing the infection, but there's a lot of potential to damage the surrounding tissue. Effector cells from the adaptive response incl. humoral immunity don't elicit the same level of damage, and we can illustrate this in mucosal immunity. Since commensal (and some pathogenic) organisms are constantly stimulating mucosal immunity, there are (1) epithelial effector T cells, (2) plasma cells and (3) dendritic cells that make the response to these pathogens fast, efficient and little damage occurs to the tissue involved.
In situation 2: So let's say the pathogen has escaped the immune response, maybe it's encapsulated. There are AB toxins being produced that kill cells endocytosing them. What good will it do for a phagocyte to eat something that ends up killing it? Antibodies are particularly efficient for this extent because they can neutralize toxins they've encountered with the same fast, efficient response as we described above. This is achieved through antigen presentation. The host will then need to find other ways to clear the infection, however.
So: In situation 1 we illustrated that an innate, systemic response isn't always desirable due to tissue damage, and through the presentation to T cells by APCs, a later adaptive immune response mitigates this effect through formation of effector cells. In situation 2, we then illustrated that the first-line defenses can't always respond to the imminent threat for various reasons, which are overcome by the presence of effector cells.
Situation 3: This is the more complex concept. You have different subsets of CD4+ T cells that can be formed in response to the type of interleukin or cytokine that is present when the CD4+ T cells are being activated. This differentiation is driven largely by secretions of activated APCs! The APC performs this critical step based on what kind of receptors the specific types of pathogen are detected by. The differentiated CD4+ T cells, or T-helper cells of class: Th1, Th2, Th17, Treg, etc. each perform different roles which are effective in different situations. For example, you wouldn't see any benefit in throwing Th1 cells at a helminth infection, Th2 is the best effector for this. Treg cells are capable of abrogating autoreactivity, and Th17 cells are needed to assist B cell differentiation in response to antigen detection (which in the case of helminths, the B cell must class switch to IgE and this is stimulated by Th2 cells via IL-4).
Now, in situation 3, we've illustrated that CD4+ T cell intermediates are providing your overall immune response: flexibility, specificity, and checks/balances which are all-at-once critical to healthy functioning. I disregarded MHC-I responses and CD8+ CTL's because this is about APC-driven responses.

I did my best to provide something robust without going into deep detail, if anyone has a problem with the content let me know!

In nature and biology, the question of 'why something happens' is difficult to answer. Because, biological processes are 'not designed' to address a deficiency or fulfill be a need of the organism. On the contrary, biochemical processes undergo changes (induced or otherwise) leading to a number of new related processes which may confer advantages in altered environments. Therefore, to accomplish a task, every organism may use multiple pathways.
Eliminating a foreign molecule or an agent, is generally accomplished by a co-operative action of innate and adaptive mechanisms of immune system. Although innate mechanisms often can control propagation of some foreign agents, adaptive immunity and subsequent memory mechanisms of B and T cells are fast acting in subsequent exposures of many agents.

I'm not really sure this directly answers the question.  It gets to the issue of asking "why", I suppose, but that might be better phrased as a comment.


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Does repolarization of muscle fibers mean that the muscle bundle is relaxed?
If I flex my bicep and continue to contract it does it mean that the muscle cells are in depolarizing state and not repolarizing?

No, macroscopically human muscle works by oscillation. This means that when a muscle is contracted (isometric contraction), some fibers alternatively contract through the actin/myosin process while some others relax at the same time. The end result is that the muscle as a whole keeps the same length, although it still does consume energy to stay in that state. That is why you get tired after some time of isometric contraction. To directly answer your question, it means that muscle in isometric contraction state will have some fibers depolarized, and others in resting state at any moment.


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Is epimysium same as fascia?
I have read that epimysium is dense regular connective tissue made covering the a muscle like bicep brachi. at the same time we have fascia that is made of dense regular tissue and covers muscles. so are they same or different how can we describe it and differentiate it?

Epimysium is the specialized fascia located at the muscle.

Epimysium is a layer of connective tissue, which ensheaths the entire muscle. It is composed of dense irregular connective tissue. It is continuous with fascia and other connective tissue wrappings of muscle including the endomysium, and perimysium [1].

The fascia that covers muscle is named deep fascia:

The deep fasciae envelop all bone (periosteum and endosteum); cartilage (perichondrium), and blood vessels (tunica externa) and become specialized in muscles (epimysium, perimysium, and endomysium) and nerves (epineurium, perineurium, and endoneurium) [2].

References:

Wikipedia contributors, "Epimysium," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Epimysium&oldid=540536396 (accessed June 27, 2014).
Wikipedia contributors, "Deep fascia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Deep_fascia&oldid=593605746 (accessed June 27, 2014).

As I understand it epimysium is not only fibrous but also contains more elastic fibres than fascia. As such it is more 'loose' than the 'dense' fascia.  It lies immediately on the surface of the muscle (epi = on, mysium = muscle) below the fascia. The deep fascia which is denser lies on top of this.

Fascia is a widely used yet indistinctly defined anatomical term that is concurrently applied to the description of soft collagenous connective tissue, distinct sections of membranous tissue, and a body pervading soft connective tissue system. Inconsistent use of this term is causing concern due to its potential to confuse technical communication about fascia in global, multiple discipline- and multiple profession-spanning discourse environments. The Fascia Research Society acted to address this issue by establishing a Fascia Nomenclature Committee (FNC) whose purpose was to clarify the terminology relating to fascia. This committee has since developed and defined the terms a fascia, and, more recently, the fascial system. This article reports on the FNC's proposed definition of the fascial system.
Reference:
http://www.bodyworkmovementtherapies.com/article/S1360-8592(16)30259-5/fulltext

"A fascia"
A fascia is a sheath, a sheet, or any other dissectible aggregations of connective tissue that forms beneath the skin to attach, enclose, and separate muscles and other internal organs.
"The fascial system"
The fascial system consists of the three-dimensional continuum of soft, collagen-containing, loose and dense fibrous connective tissues that permeate the body. It incorporates elements such as adipose tissue, adventitiae and neurovascular sheaths, aponeuroses, deep and superficial fasciae, epineurium, joint capsules, ligaments, membranes, meninges, myofascial expansions, periostea, retinacula, septa, tendons, visceral fasciae, and all the intramuscular and intermuscular connective tissues including endo-/peri-/epimysium.
The fascial system interpenetrates and surrounds all organs, muscles, bones and nerve fibers, endowing the body with a functional structure, and providing an environment that enables all body systems to operate in an integrated manner.
Reference: http://www.bodyworkmovementtherapies.com/article/S1360-8592(16)30259-5/fulltext


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what these suffixes mean,-coel,-blast,-cyst?
in the connective tissue (Bones) we have 3 types  osteoblast, osteocoel,osteocyst what are they and why they differ.

have you tried searching the net for the answer. Wikipedia might be able to answer this question.

-blast : A precursor/progenitor/immature cell..
-coel : A fluid filled cavity...
cyst : A clump of cells with a defined boundary...

@WYSIWYG - even if it's short, please post answers to questions as actual answers. Comments should just be used to clarify the question, not answer it. See this meta topic for a discussion regarding this issue. Thanks!

@MattDMo: thanks for clarification.. I'll take care.. Since this question is closed, i won't be able to convert this one

You can easily search this on the web.
Osteoblasts are the immature cells of bone which are responsible for the production and mineralization of bone matrix.
Osteocytes are the mature cells of bone found in open spaces in bone called lacunae. The functions of osteocytes includes maintenance of bone and  calcium homeostasis.
Osteoclasts are responsible for removal of bone.
Source : Tortora and Derrickson


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How do insects recognize their host plants?
Many insects, like butterflies have specific host plants on which they feed or lay eggs. While researching about some butterflies, I found that they lay their eggs on certain specific plants and their larvae feed on the leaves of those plants. I wonderd how do they recognize those specific plant species:

Do they use visual cues to find or recognize these plants?

Or

Do they use chemical cues, like sensing volatile compounds released by the plants? I think this might be possible as I found many species of butterflies prefer plants of the citrus family which contain essential oils. Do they just sniff around following the trails of such chemicals to find the host plant,

Or

Is it the combination of both?

Yup, insect recognize their host by the combination of both visual cues and chemical cues.

@MaqsoodAhmad- Welcome. Answers should be backed up by credible sources, preferably journal articles. Unsourced one-liners are comments and I've converted it as such.


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Which bird species/families worm-dance and is this learned behaviour?
Today I saw a Herring Gull and a Common Gull (UK common names) "worm-dancing" on an area of wet grass. Worm-dancing is when the bird taps its feet on the ground rapidly in order to drum worms to the surface (that its a worm hunting behaviour might be conjecture, I'm not sure it's been proven).
Shortly after, a pair of Jackdaws landed and also began hunting, but without dancing. They walked over the area poking about in the grass, whereas the gulls stayed in the same place.
So my question is firstly, which species/families has worm-dancing been observed in, and secondly is this thought to be learned behaviour (this might be determined by it being a local phenomenon in certain populations)?
EDIT: Originally misidentified a common gull as a black headed gull (corrected above). Today I saw a black headed gull alongside the two larger gulls, and it was hunting like the jackdaws, not worm-dancing. There might possibly be a size/weight requirement to be able to worm-dance effectively, if we accept the hypothesis that it's a method of bringing worms to the surface.

Thrushes (Turdidae), like the Blackbird, don't actually dance, but they hop around when hunting worms. This might have the same effect as dancing.

Short answer
Sea gulls indeed tap the ground to surface earth worms, which is known as worm charming. Traditional human societies have practiced a similar technique known as worm grunting, involving vibrating the ground. Worm grunting is obviously a learned behavior passed down for generations in Florida. In other animals, such as gulls, I wasn't able to find evidence whether it is learned or innate behavior.
Background
From wikipedia:

Worm charming is especially [observed] among birds. The methods used vary; however, tapping earth
  with feet to generate vibrations is widespread. One common example is
  the "Seagull dance". The wood turtle also seems to be adapted for worm
  charming, as it is known to stamp its feet – a behavior that attracts
  worms to the surface and allows the turtle to prey on them.

It is popular belief says that the charming mimics the drumming vibrations made by rain and that worms are attracted by it. However, studies have indicated that the charm vibrations sound similar to those made by burrowing moles, a voracious worm predator and that the charming behavior of worms surfacing reflects an escape behavior of worms, namely the abandoning of their safe burrows to expose themselves to the real danger once surfaced (Catania, 2008).
The authors investigated the charming reaction of the worms by studying human-indiced charming, a technique used by fishermen. For generations, many families in and around Florida's Apalachicola National Forest have supported themselves by collecting the large endemic earthworms (Diplocardia mississippiensis). This is accomplished by vibrating a wooden stake driven into the soil, a practice called “worm grunting”. This worm grunting is obviously learned behavior.
However, I couldn't find evidence whether the worm charming in birds and turtles is learned yes or no.
Reference
- Catania, PLoS ONE 3(10): e3472

Do you have any information on which species/families practice worm-dancing, which was the main part of the question?


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What problem does kin selection solve?
I'm trying to understand what problem led to a development of kin selection.
The explanations I've found consist roughly of the following:

The existence of some altruistic and cooperative behaviors in social
  insects like honey bees, the phenomenon of sterile castes formed by
  non-reproductive individuals that leave no offspring and the suicidal
  role of these insects in defending the hive, were traits that natural
  selection could not favor. Kin Selection | Nectunt

What I do not understand: Why could natural selection not favor the phenomenon of sterile castes?
From the perspective of the sterile worker: Since it can't reproduce, no strategy will affect the number of offspring it has (will always be 0). So there is no conflict with natural selection.
From the perspective of the queen bee: Her offspring consist of sterile worker bees and a new fertile queen bee. The worker bees improve the viability of the next queen bee. This is consistent with natural selection.
Therefore, I can't see the relevance of the worker bee sharing lots of genes with its sister queen bee. This seems to be nothing but an ancillary effect of the mechanisms of evolutionary change.
Imagine, the queen bee could produce worker bees without a genome (like a robot), or a genome that is not related to its sister queen bee, those worker bees would still show altruistic behavior.
What am I missing?

Why natural selection leads to selfishness
Imagine a population of individuals. At a given locus, some individual carry the A allele and some others can the S allele (A for altruistic and S for Selfish). For simplicity, we will assume organisms are haploid. Individuals carrying the S allele are selfish and will take care of themselves only. The A allele are altruistic meaning that they produce behaviours (and non-behavioural phenotypes) that will reduce their fitness and increase the fitness of other individuals in the population.
As the altruistic behave as to reduce their fitness, they will be at a selective disadvantage and therefore, over time, only selfish individuals will remain.
How can altruism evolve then?
The study of the the evolution (and evolutionary consequences) of behaviour (and non-behavioural phenotypes) that affect the fitness of other individuals in the population is called social evolution. Social evolution is a wide field of knowledge and I will here attempt a very short summary of it so many concepts will be left out!
There are two main (non-exclusive) ways by which altruism can evolve:

Repeated interactions (False altruism)
Kin interactions (True altruism)

Repeated interactions
The concept is grounded within game theory. A good introduction to game theory is definitely out of the scope of this question but I just want to give a little bit of an intuition. I will over-simplified the concepts of game theory but you should definitely have a look at it. Those concepts are very enlightening for questions of evolutionary biology, economy, psychology, sociology and even philosophy.
If for example, the altruistic individuals are actually only altruistic to those
that have shown altruism in the past (via a Tit-for-Tat strategy for example or through the use of reputation), then altruistic individuals may end up have a higher fitness than the selfish individuals. Imagine for example that selfish individuals give nothing and receive nothing. Let's assume that all altruistic individuals, all make one good deed and receive one good deed. Giving a good deed comes at a cost of having, say 0.8 fewer offsprings on average. Receiving a good deed comes at a benefit of 1.2 extra offsprings. Overall and on average, each altruistic individual will produce 0.4 more offsprings than the selfish individuals and therefore, over time the whole population will become altruistic.
We often refer to these concepts as false altruism because altruistic individuals actually has a fitness increase over their life time. Let's now talk about true altruism where altruistic individuals really just give without receiving but yet, the allele coding for altruism thrives.
Kin interactions
Note first that any kin interaction follows within a give game theory scenario. As such kin interaction is just an add-on on what I discussed earlier. For those used to Hamilton's rule, please note that Hamilton's rule apply to Prisoner's dilemna (a type of game theory scenario) only.
So, imagine now that altruistic individuals are being altruistic with their family members (their kins) only (either because they direct their altruism or because there is a strong population structure). Note that such altruistic behaviour can pretty indirect as helping your partner (who we will assume is not part of your close family) will have for consequence that your partner may offer better parental care and therefore by being altruistic to your partner, you are actually being altruistic to you offsprings (which are your kins).
Because the kins of altruistic individuals probably carry the A allele, eve if the altruistic individual is experiencing a lifetime cost in fitness, the A allele may still thrive and the recipients of this altruism are likely also carrying the A allele. In other words, a truly altruistic individual is an individual that sacrifice itself for helping the allele A present in its kins to thrive. In yet other words, true altruism is when an allele is ensuring that copies of itself present in other individual will manage to get passed on.
And this is called Kin Selection. I can now clearly answer your question
Your question

What problem does kin selection solve?

Kin selection explains "true altruism"!
Only "true altruism" can yield to such separation of the reproductive task as that some individuals are perfectly steriles. In your post, you say

From the perspective of the sterile worker: Since it can't reproduce, no strategy will affect the number of offspring it has (will always be 0)

What is missing from this logic is that, 1) at a time workers could still reproduce and 'gave it up' and 2) in many (maybe most?) social species (honeybees, termites, ants and also in non-hymenopteran eusocial species), workers are still able to sometimes reproduce and are also able to overthrow the queen.

Found this: http://rspb.royalsocietypublishing.org/content/282/1803/20142886
"helpers do not necessarily improve their inclusive fitness by foregoing reproduction. These findings suggest the earliest evolutionary steps towards eusociality are most favored if mediated through maternal manipulation.“
That’s what I mean, if this can be achieved my maternal manipulation, then it seems to me to follow, that relatedness isn’t absolutely necessary.
But I’m starting to realize that I asked too broadly and should first read some papers. If I then still don’t get it, I'll post a follow up question.

Kin selection explains a violation of the assumption that individuals will always selfishly promote their own reproduction. (Lemmings jumping into the sea is a myth that does not happen). Every individual is supposed to work toward sending its own genes into the next generation. In your example, you say that the queen should just pump out workers to serve herself. And she does. But the workers are individuals too, with their own genes, and theoretically, should be selfish. However, in this case, due to honeybee reproduction and haplodiploidy, the workers are more than 50% related to their siblings. The math works out such that working toward the success of the colony is a more efficient strategy for promoting worker genes than if the workers were to try to reproduce on their own. Remember that one point in evolutionary time, these workers were reproductively capable, and gave up their own reproduction to serve the colony. So I think that what you are missing is that at some point in time, workers were once capable of reproduction, and gave it up. They were not always cogs in a machine.

"But the workers are individuals too, with their own genes, and theoretically, should be selfish." -> I addressed that: They are sterile, so the cost of their "sacrifice" is 0, which is consistent with selfishness.

"workers were once capable of reproduction, and gave it up." From the little I know, it doesn't like they were the ones who gave it up. It's more like it was taken from them.

They were not always sterile. They evolved from ancestors that were fertile. This is what breaks the rule.

It was not a conscious decision. Kin selection explains the math, and how such behavior could evolve without breaking assumptions about selfish reproduction.

And no, reproduction was not taken from them. Their genes still go forward into the next generation more efficiently than if they were laying their own eggs. It is a kind of decoupling of the individual from reproduction.

Both the worker bee and the queen bee evolved from the same ancestors. Natural selection started to favor individual bees that additionally laid offspring that behaved altruistically.
You say, every individual is supposed to selfishly promote its own reproduction. Yes, but only in accordance to its own power.
If I’m not mistaken, the behavior of a bee is genetically determined. So it’s outside the power of that bee to have more reproduction and the rule isn’t broken (only if you ascribe free will to the worker bee).

Let us continue this discussion in chat.

@KarlKjer Unlike you said "individuals will always selfishly" is NOT an assumption. It is a consequence of NS.

Individuals always acting selfishly to promote their own genes is absolutely an assumption that comes from natural selection, and is violated under the conditions we are talking about. Assumptions are fundamental units of refutation science. Things that are a consequence of a theory are still assumptions.

Well... I disagree with your definition of 'assumption'. If the consequences of all our models were to be called assumptions, then outside of the data themselves, nothing in science would not be an assumption which sounds pretty wrong. I am used to call an assumption, a belief that is not supported by evidences (or at least not necessarily always true in all cases found in nature)  on which a model is based. For example, HWr is based on an assumption of infinite population. However, the allele to genotypes frequencies resulting from the model is not an assumption.


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Using BLAST for molecular replacement in structural biology
This is my first time trying to do molecular replacement to solve a protein structure. I am using the NCBI blastp program to find suitable search models. When choosing a search model, I understand that sequence identity is the most important -- but should I also take into account e-values or query coverage (i.e, what % of my query sequence is in the alignment) or any other factors for the purpose of molecular replacement? Thank you for your help!

Identity, Similarity, E-value are the key numbers, for the prediction of the 3D structure of proteins. The Length of the query and selected results should also be close to each other.
E-value:
The first value to look at is indeed the E-value.
For the most accurate predictions, E-values less than $10^{-100}$ are of extreme importance While E-values ranging between $10^{-50}$ to $10^{-100}$ come as the second priority. E-values less than $10^{-20}$ or so, should not be trusted. (As you know the larger amount of E-value accounts for random hits which may not have any evolutionary background with your query)
Similarity and Identity:
The ranges for these amounts differ for each survey and should be assessed with other statistics. Needless to say, Identities below 5% for amino acid blasts and below 25% for nucleotide blasts are useless. For proteins identity above 25% is acceptable and 35-50% (and more) are of greater importance. Similarity plays a more important role in the overall shape and structure of the protein. "Total score" in Blast NCBI should suffice for these evaluations.
Length:
The sequence length of your results should be reasonably near to one another. For example, having a sequence of 600 amino acids as your query, the acceptable range for the selected results (to eventually predict 3D structure with) should be 600 $\pm$ 30. Five percent difference is usually enough. Deviation from this would result in extra 3rd and 4th structures induced by other subunits.
Other considerations: In the case that your organism is known, pick the sequences which share a common evolutionary history with your organism of interest See Tree of life. The number of subunits and Symmetry types might be useful in some cases. Avoid selecting ab-initio based 3D structures in your results all the time and focus mainly on X-ray diffraction-based structures. If you're using the PDB website for data retrieval, Refinement Resolution is also extremely important. Try both CIF and PDB formats as input, as the results may sometimes improve.
At last but not least, try blasting using curated databases. In blastp, refseq_protein , swissprot , pdb , refseq_select are ideal.
This is just a rule of thumb and should not be generalized as the exact numbers differ substantially from one query to another.


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Biochemistry - Plastic eating microbes at home
Is it possible for me to locate, without too much difficulty, and culture, at home, a bacteria (like yeast) on plastic?
I tried a similar process with yeast and I was able to culture it on extremely harsh medications at my home. However, I believe due to the lack of food they died.

Although you should be able to find bacteria that can grow on plastic, I think your criteria of 'not difficult to find' might be a challenging one to meet. Poly(ethylene terephthalate) (PET) is a commonly used plastic, and in 2016 Yoshida et al. discovered a species of bacteria, Ideonella sakaiensis, which can grow using PET as its carbon source. This study was significant enough to be published in the journal Science, and has since been cited over 700 times. Therefore, using impact as a proxy for 'difficulty', it could be said that this was a difficult bacteria to find!
In terms of how they did it, here is an extract from their paper:

We collected 250 PET debris–contaminated environmental samples including sediment, soil, wastewater, and activated sludge from a PET bottle recycling site. Using these samples, we screened for microorganisms that could use low-crystallinity (1.9%) PET film as the major carbon source for growth.

Similarly, only last year Espinosa et al. isolated a strain that was able to grow on Polyurethane, from their paper:

For the isolation of bacteria from soil, three samples from a site rich in brittle plastic waste (Paunsdorf, Leipzig, Germany) were used. ... 150 μL of the diluted soil solutions were added to agar plates containing mineral medium and different concentrations of 2,4-TDA (2, 5, and 10 mM) as sole carbon and energy source.

In both of these studies they isolated bacteria that could grow on plastic, rather than evolving bacteria to grow on it. These bacteria at some point did evolve to grow on plastic, so in theory you could probably evolve a strain that did as well, but it would be easier, although still difficult, to isolate bacteria that already grow on plastic.
EDIT: Adding information on Yeast to respond to question edit
Yeast are actually a member of the fungal kingdom, and are not a type of bacteria. What most people refer to as 'yeast' is a species of yeast, Saccharomyces cerevisiae, which is used in the brewing industry. As far as I am aware, no-one has engineered this yeast, or another yeast, to grow on plastic. However, in 2020 Chen et al displayed the enzyme, PETase, on the surface of the yeast Pichia pastoris. This is the enzyme that the bacteria I mentioned above use to degrade PET. This enabled the yeast to break down PET into other compounds, however the yeast cannot grow using these compounds. If you wanted to engineer a yeast to grow on plastic you would need more enzymes, such as a MHETase, to further break down these compounds into something the yeast can grow on.
As you are looking to use microorganisms to break down plastic for environmental purposes, Taniguchi et al., have written a review, Biodegradation of PET: Current Status and Application Aspects, which discusses the problem. This is from 2019, however, so doesn't include recent developments. You can read a news article from the Guardian, here, that discusses the impressive improvements made in 2020. A key thing to note about the most recent efforts is that they involve using the enzymes that degrade plastic, but not the microbes themselves.

Thank you so much for your response, I am also a new contributor so it was really helpful

Will it be possible to grow yeast to eat plastic? That's what I am trying to research as these researches do say that microbes are slow for now. Would it be possible to contact you?

By harsh chemicals, I meant, Calcarea hypophosphorosa, Budesonide, Alcohol solution, lactic acid capsules, etc. I also added some other substances for promoting growth - Vitamin E & B, Cod liver oil, milk, etc.

I would say that you should edit your original question to remove reference to harsh chemicals. This should probably be a separate question. You can also edit your original question to add your additional question about yeast, and I will edit my answer to reflect that. As for contacting me, this is not the StackExchange way as it hides information from the community (see here: https://meta.stackexchange.com/questions/431/any-way-to-send-a-personal-message-to-another-user).

Ohk I tried one option giving information in profile so you can contact me from there

@MikulRai To be clear, I agree with the link that moving questions to a private forum is not the best way to serve the community. If you have further questions you can post them and I can try to answer, or you can edit your original question. I've also suggested some edits to your question to make it clearer and I'll edit my answer once they're approved.

I understood your point, I wanted to ask for your recommendation to reduce the existing amount of plastic in the environment, according to my research there are major three ways: physical - burning without any harmful products, chemical - dissolving the plastics without any harmful by-products (requires advanced situation) and biological - microbes. Can you give your expert advise, please

I've edited my question to respond to the additional information you've provided. The key thing to note is that there is a difference between using enzymes from microbes to degrade plastic and actually growing the microbes on plastic. From my reading (I am not an expert in this area) it seems that most effort is being focused on using the enzymes, without actually using the microbes. Much like biological washing powder doesn't contain any live organisms, but rather the enzymes from them that can degrade the compounds that make clothes dirty.


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Can the fungal form of Malassezia morph into the fungal form of Candidia when feeling threatened? Resistance Mechanisms
Malassezia feeds on oils in the carbon chain 11-24 and Candida feeds on sugars. I recall learning that when these types of fungus feel they are under attack, they can morph. Does this mean they can change into each other? This question deals with resistance and strategies for overcoming resistance through combination therapies.
"Malassezia (earlier known as Pityrosporum) species form the cutaneous commensal flora, which are associated with varied clinical manifestations ranging from benign skin conditions, such as tinea versicolor, to fungemia in the immunocompromised host.[1] There are at present 14 described species, namely M. furfur, M. pachydermatis, M. sympodialis, M. globosa, M. obtusa, M. restricta, M. slooffiae, M. equina, M. dermatis, M. japonica, M. nana, M. capre, M. yamatoensis, and most recently M. cuniculi.[2] Owing to their lipophilic nature, they colonize the seborrheic parts of the skin and they sustain themselves by using the fatty acids present in normal sebum. They cause skin disease in certain conditions such as overgrowth, descent into hair follicles, or inflammation. Though, by definition superficial mycosis do not extend beyond the cornified epithelium, these organism are seen in the ostium, central and deep segments of the hair follicle in Malassezia (Pityrosporum) folliculitis. Malassezia infections can manifest as superficial localized or can cause systemic infections in immunocompromised hosts."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4533528/
"The genus Candida includes about 200 different species, but only a few species are human opportunistic pathogens and cause infections when the host becomes debilitated or immunocompromised. Candida infections can be superficial or invasive. Superficial infections often affect the skin or mucous membranes and can be treated successfully with topical antifungal drugs. However, invasive fungal infections are often life-threatening, probably due to inefficient diagnostic methods and inappropriate initial antifungal therapies. Here, we briefly review our current knowledge of pathogenic species of the genus Candida and yeast infection causes and then focus on current antifungal drugs and resistance mechanisms. An overview of new therapeutic alternatives for the treatment of Candida infections is also provided."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708393/
"CONCLUSION
Morphological transitions are commonly observed among diverse fungal species. These cellular responses are accompanied by equally profound changes in cell physiology and structure. As noted above, the highly regulated process of fungal morphogenesis represents an adaptive response to specific stresses encountered in various microenvironments, including that of the infected host. Therefore, morphological and physiological plasticity allows fungi to rapidly adapt to changing extracellular conditions. Species-specific signaling and morphological features appear to be a direct result of fungal attempts to survive as new microenvironments, and their particular cell stresses, were encountered (Hogan and Klein 1994; Newman et al. 1995; Batanghari et al. 1998; Sebghati et al. 2000; Gow et al. 2002; Brandhorst et al. 2004; Rappleye et al. 2004, 2007; Gantner et al. 2005; Nemecek et al. 2006; Gauthier and Klein 2008; Nather and Munro 2008; Mora-Montes et al. 2011; Wang and Lin 2012; Wang et al. 2012). The concerted action of morphotype and physiological changes in the context of a particular environment are therefore critical for successful fungal adaptation (Butler et al. 2009; O’Connor et al. 2010). Defining the cellular machinery controlling fungal morphogenesis offers unique insight into our basic understanding of fungal life cycles and pathogenesis."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315913/
"Therefore, morphological and physiological plasticity allows fungi to rapidly adapt to changing extracellular conditions. Species-specific signaling and morphological features appear to be a direct result of fungal attempts to survive as new microenvironments, and their particular cell stresses, were encountered"

The majority of fungi grow in one of two growth forms: either as rounded or spherical cells (yeast fungi) or as a polarised branching mycelium (filamentous fungi). Such fungi are found throughout the fungal kingdom and are termed 'dimorphic'.
http://www.davidmoore.org.uk/21st_Century_Guidebook_to_Fungi_PLATINUM/Ch05_01.htm
Candidiasis is a fungal infection caused by a yeast (a type of fungus) called Candida.
https://www.cdc.gov/fungal/diseases/candidiasis/index.html
Pityriasis versicolor is caused by a type of yeast called Malassezia.
https://www.nhs.uk/conditions/pityriasis-versicolor/
Malassezia (Pityrosporum) folliculitis is a fungal acneiform condition
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3970831/
Dimorphic means they can change from the fungal form of yeast to the fungal form of hyphae or filamentous fungi within their own species, not morph into another species. Its clear to me now.
Hyphae - Hypha. Hyphae are a highly polarized cell type and are the hallmark of the filamentous fungi, which make up the majority of known fungal species
https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/hypha


text:
Why can a gene lack of a binding site be expressed in skin cells?

In order for a specific gene to be expressed in the mammal’s cells, all of the gene’s binding sites must be bound by transcriptional activators. The mammal’s skin cells contain activators that bind to sites B, D, and E, while the mammal’s liver cells contain activators that bind to sites A, C, and E. (From Khan academy)

Why can both Gene 2 and Gene 4 be expressed in skin cells? I think Gene 4 can't since it doesn't have site E.

You understand this wrong: All present enhancers of a gene must be bound by a enhancing factor, not all factors of a certain cell types have to be bound. So when skin cells contain activators for B, D and E they can activate gene 2 and 4 of your example, but not gene 3 since the activators for A and C are missing.
So when you have a gene containing any combination of B, D and E, its activation in skin cells is possible according to this model. The same is true for any combination of A, C and E for liver cells. The special case would be a gene having E as the only enhancer as this could be activated in both, liver and skin cells.

This is the right answer, but enhancers tend to act in surprising ways.  The question works tautologically if you define expression as the highest level of expression, the binding sites as only those with an observed positive effect on expression, and ignore all other interactions.  Otherwise you could be in for surprises. :)

@MikeSerfas I know, I worked for quite a while on the regulation of gene expression and enhancers. Sometimes they bind coordinated, sometimes seemingly identical sites are only bound under certain conditions etc. This is a simplified example, for this purpose this should be fine I think.


text:
why can't we digest cellulose
I have a very tricky question....all the veg and fruit
cells contain cell wall and it is made of cellulose when we eat how our body digest though we
don't have the enzymes to breakdown 1-4 beta glucose sugar?

We don't digest cellulose; it just passes through us unchanged.

Related: https://biology.stackexchange.com/q/59205/24354

Humans, unlike cows for ex. don't have the necessary bacteria in their intestines that make the enzymes(cellulases) necessary to breakdown the 1-4 beta glucose bonds. So we cannot break down cellulose into its constituent glucose molecules as we do with starch. Therefore this is secreted as unbroken down chains of glucose called fiber.

tnx sir for your reply...but it didn't satisfy me i asked so how we can eat fruits and vegs they all got celloluse in thier cell wall

That's why I tried to explain that those parts of vegetables we can't digest are called fiber.

so then why in many biscuits and chocalate companies ads they say it fibers and etc if we can't digest it then why they promote it?


text:
Why the scent of mouth gets dirty after not eating for a long time?
After a long time of hard workout,not eating and nervousness makes your taste and scent of mouth very uncomfortable and bad why this happens and is there any way to prevent it?

This is caused by a build up of ketone bodies in your blood which lowers the pH of your body and can cause bad breath. Ketone bodies are a response of your body breaking down fatty acids for energy instead of glucose when in a low food intake (fasting) state. This is also true for morning breath since your body has been in a fasting state.
The way to prevent this is to eat the proper amount of calories needed for your body to function normally.


text:
Calculation of water potential
For a mesophyte growing in a moist soil, water potential of its root sap is -3 atm, then how to find the water potential of moist soil and leaf respectively?

I don't know if we can calculate the exact values. The only thing I can say is that the potential of the soil will be less negative than -3 while that of the leaf will be more negative.
You know that water travels from higher potential to lower potential. So, it will travel from a region of less negative water potential to a region of more negative water potential.

Could you please explain the reason behind your answer?

@Rudstar Yeah sure.. You know that water travels from higher potential to lower potential. So, it will travel from less negative to more negative.


text:
Have there been any macro-evolution experiements?
I'd like to start first by saying that I don't believe in creationism at all, nor any non-Darwinian-evolution explanation of the diversity of life on Earth. The theory, the fossil record, and the genetic, morphologic, and biochemical evidence are more than overwhelming in support of it.
Also, I understand that the term 'macro-evolution' is a "weasel word" invented by creationists to make a bogus distinction of two supposed kinds of evolution.
But for this question, I think the term is useful. I'm happy to take any corrections or qualifications in comments or answers.
I wonder if there has been any long-term experiment performed to attempt to induce 'macro' changes in a species-- something that would make this lab-based population considered to be a subspecies, or even a different species, if it were found in the wild.
I'm aware of the long-term E. Coli experiment that resulted in bacteria that developed mutations that allowed them to completely metabolize citric acid. I understand that's a change of a few genes (amongst other recorded changes).
What I'm looking for is something a little larger, more than a new protein. I was thinking something like 1. a new organelle, 2. a new type of cell or tissue, 3. a new organ, or 4. a new type of limb or radically different limb use (something like reptilian jawbones re-purposed in mammalian ears_.
I understand there are numerous incidents of organisms losing useless features, such as eyeballs in dark caves, flight ability, etc. For this experiment I don't think it's enough to show the loss of something-- genes turning off, but novel characteristics must arise. To rebut creationists, I think it's necessary to show 'new' information, not just loss of information (I'm speaking of the genes responsible for morphology).
With my laypersons' imagination, I was thinking of a species with a relatively fast reproductive cycle, put in an environment that had some selective pressures. Perhaps one without much room to fly, not enough food, but plenty of food in a water area where they couldn't normally get to it. Something that might encourage them to adapt to taking to water to exploit a new food resource.

The timescales over which your suggested changes could happen makes them infeasible to directly observe. Of course, there is plenty of indirect evidence to support the idea that such processes have already occurred. Also, science isn't concerned with rebutting creationists. We make observations and develop theories to explain them; that's it.

@canadianer If you know, what is a rough estimate for the time of any of these features to develop? I know there's not a (meaningful) average, and that no example would be representative, but any that you know of offhand would be informative to me.

@user151841 We could calculate an average (if if it would carry little info) if we could accurately define the evolution of a specific trait. But the question does not so there's really no way to answer it. I just tried to give a few examples that are of eventual interest. For more, we will need a more accurate question.

Would you accept Humanized mice that can be infected with the HIV or with Kuru or Creutzfeldt - Jakob brain homogenates and develop human prion disease? Wild type mice could not be infected with either the HIV virion or the misfolded human prion protein.

@Remi.b That is why I say there's not really a (meaningful) average. To take an example, we could say that, since it took ~ 10 million years from pakicetus to Mysticetes, two clearly different species, macroevolution can take about 10 million years (http://evolution.berkeley.edu/evolibrary/article/evograms_03) . Of course, tough, we want to find a shorter example in the interests of this experiment. But since the distinction between 'species' get fuzzier the more closely related populations are (subspecies, etc), finding the 'shortest' timeframe becomes more difficult.

@AMR Is that the expression of a protein on the surface of a cell that allows humanized mice to become thusly infected? If so, I'm looking for something that would involved the expression of multiple proteins to become a new organelle, cell, etc. as a outlined above. Creationists argue that human genetic experiments are examples of intelligent design, so I'm looking for something that's not consciously planned. While I somewhat agree with canadianer that it's not scientists' job to rebut creationists, somebody needs to fight back, and they are going to need the help of science to do so.

In order to have any chance at seeing what you want to see, you need lots of generations to do it, and about the most complex organism we will see this in, is the fruit fly. And there is no way of winning that argument. Logic cannot compete with magic in the eyes of a believer.

@AMR I'm more interested in convincing the uninitiated or the people who are up for grabs, such as a sixth grader who is in a school where creationism is taught next to evolution in a "science" class.

@ARM this article http://news.bbc.co.uk/2/hi/science/nature/4530959.stm says that the pygmy goby fish has a reproductive cycle of 59 days, which by my reckoning is 3 times as long as the fruit fly reproductive cycle (19 days http://www.orkin.com/flies/fruit-fly/fruit-fly-reproduction-rates-data/). That would turn a 20 year experiment into a 60 year experiment, which is still feasible, if we consider vertebrates more complex than flies.. The pitch drop experiment (https://en.wikipedia.org/wiki/Pitch_drop_experiment), while not as serious and maintenance-intensive, has been going for 98 years.

Issue with the question
The question of what is an evolved phenotype that is "seemingly significant enough to the layman to be called macro-evolution" is very unclear and it makes it hard to answer.
Most experimental evolution are performed on lineages that have very short generation time (for obvious reasons) and on these lineages it is hard to even imagine the evolution of something that a layman would consider to be "significant enough to be called macro-evolution".
The whole issue is that one will probably consider a change in phenotype to be "seemingly significant enough to the layman to be called macro-evolution" if it occurs on lineages that have long generation time and therefore cannot be observed within a lifetime.
The question interesting. However, I think the best one can do is to look at the wiki article for experimental evolution who already offer quite an interesting list of examples. I tried below to highlight a few cases of eventual interest

Long term artificial selection on "large living things"
If one wants to consider artificial on "large living things", then probably artificial selection on crops and cattle will be a good place to look at. I think I don't need to list and make extensive description of how artificial selection has changed their phenotypes (and genotypes). Consider the pigs, banana and corn as examples.
A few evolved features that has evolved in labs in small organisms
We have observed evolution of multicellularity form unicellular organisms, observed new metabolic pathways and change in ploidy level just to cite a few major things that we evolved.
Lenski experiments
The Lenski long term experiments is the longest in lab evolution experiment performed today. They made a lot of different observations and not only the case of citric acid metabolization that you mention. Note that being able to metabolize a new compound is a pretty considerable evolved feature that only those who can't go further than considering evolution of extra legs as something significant would fail to appreciate.
Drosophila and Waddington's experiment
If one must restrict I suppose that looking at experimental evolution on Drosophila would be our best bet.
Change in allele frequency through selection is a relatively fast process. Creation of beneficial variants through mutations is often the limiting process. Cases where very different phenotypes exist in natural population and selection over these phenotypes (change in frequency only) will probably not be considered to be "impressive enough". However, one can consider Waddington's experiments (and further experiments inspired by Waddington's work) as an example of experimental evolution where standing genetic variance existed before the experiment started but was hidden in the environment they experimented (the exact process here might well be too advanced for a layman). Waddington in his experiments showed one can evolve Drosophila to have a double thorax or lose their halteres in only 20 generations.
Other Drosophila experiments
We evolved Drosophila to live in hypoxic conditions. It took about 200 generations that is more than 4 years. We have also selected Drosophila for cognitive abilities and food preference (and many other things).
Note on the term "macro-evolution"
The term "macro-evolution" hasn't been invented by creationists. It has been invented a long time ago, in 1927 by a russian entomologist. T. Dobzhanski and E. Mayr (two famous evolutionary biologist) have used this term without ever quite defining it. Because the term was never correctly defined, the vast majority of evolutionary biologist have either criticized the term.
It is true that the term is now sometimes used by creationist as any poorly defined term is one of the finest solution to build questions that can't be properly addressed due its lack of clarity.


text:
Are transcription factors some kind of eQTLs?
Cause of working on Allele-Specific expression, working I am trying to know more about expression quantitative trait loci (eQTLs). based on definition, eQTLs are loci that control the expression level of other genes by Cis or Trans effects. Transcription factors are also proteins (product of genes) that control expression level of other genes. So the question is that, are transcription factors some kind of eQTLs? (or eQTLs are some kind of TFs?)

No, eQTLs and transcption factor are very different things.
Like you described TFs are proteins that control the expression level of genes.
eQTLs are nothing that is physically present in the cell. An eQTL is the conceptual influence of an allele-specific DNA locus (a SNP) on the expression of a certain gene. Explained with an example this means that some with the allele AA has a different expression in 'gene 1' than someone with the allele TT. The eQTL does not even imply any causality, merely statistical association of the allele state with a change in gene expression. (Of course one possible causation for the change in gene expression is that the allele influences binding of a TF to that locus.)


text:
Sitting in a closed room filled with regular air - for how long will the air last?
The question has implicitely a lot of variables attached to it:

volume of the room
activity
how closed the room is
size of the person (I'm 168cm long and 64 kg heavy)

That could probably be turned into some formula and I am interested in scientific insights.
But at the end of the day my question is actually of very practical nature. I have a small room - about 1m x 2m x 2.5m = 5m3 - and I would like to use it as super-quiet place for meditation, reading etc. - hence calm activities, no excessive moving around. To improve sound proofness I'll probably also increase the sealing of the door and there is no ventilation - no air exchange.
Now if I close the door - how long can I expect to stay there without the air quality deteriorating to a level where my mental processes start to be impaired by it?

Since you are considering to meditate in the room, without any excess of activity, you can consider the average resting O2 consumption, which is C = 3.5 mL/(min.kg) [1].
If we ignore the volume of your body, initially the room is filled with VO2(t0) = 0.21 * 5 = 1.05 m3 of O2.
With you breathing in the room, you can consider the volume of O2 in the room as a function of the time:
VO2(t) = VO2(t0) - C * M * t
where M is your weight in kg, and where C is converted to m3/(min.kg).
An oxygen defficient atmosphere is an atmosphere for which oxigen content is below 19.5 % of the volume [2]. An oxygen defficient atmosphere can be dangerous for your health. So in your case you need to find the value of t for which VO2(t) becomes inferior to the threshold Th = 0.195 * 5 = 0.975 m3.
So the maximum time you can spend in your room would be:
tmax = (VO2(t0) - Th)/(C * M) = 335 min = 5 h 36 min
Of course, this value is a bit surestimated, and you should leave the room before that time.

[1]  M. Kwan, J. Woo & T. Kwok (2004) The standard oxygen consumption
value equivalent to one metabolic equivalent (3.5 ml/min/kg) is not appropriate for elderly people, International Journal of Food Sciences and Nutrition, 55:3, 179-182, DOI:10.1080/09637480410001725201
[2] https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=12716

There is another problem: The rising concentration of CO2. If the volume of it get over 10 Volume% in the air, this is dangerous.

@Chris During respiration 1 mol of CO2 is produced for 1 mol of O2 consumed. Both gas being at the same pressure, we can consider that C is also the average CO2 production.

Not because the volume is getting bigger - CO2 in large concentrations is a problem for breathing.

@Chris Sorry I involuntarly send the comment above before it was finished. So, CO2 production is also a function of the time: VCO2(t) = C * M * t (initial amount of CO2 can be ignored). So VCO2 gets above 10% of the volume for t'max = Th(CO2)/(C*M) = 37h12min. t'max being superior than tmax, the first limitation is O2 depletion.

@Flo Can you check your citations for dangerous CO2 and O2 concentrations? 19.5% might be OSHA's suggestion for a safe environment, but the more severe effects of O2 require much lower concentrations; CO2 on the other hand can cause mental confusion well before 10%. That said, the estimation in the original answer is still reasonable and should provide a decent safety margin given the assumptions made.

The average untrained healthy male will have a VO2 max of approximately 35–40 mL/(kg·min). [1]
So even if we take minimum value, your consumption in a minute is 35x64 = 2.24Liters.
   But NOT all O2 is consumed since about 16% is exhaled along with 5% CO2.
So, Oxygen will get 50% by around 4 hours and I highly doubt if even 50% Oxygen is enough to breathe properly, you will feel suffocation much earlier. [2]
[1] Guyton, A.; Hall, J.E. (2011). "Textbook of Medical Physiology, 12th Ed.". pp. 1035–1036.
[2] https://www.princeton.edu/%7Eoa/safety/altitude.html


text:
Age-Dependent STD Infection
It seems that young females (comparing age 15 vs age 24) are 20x more likely to get chlamydia
from a single unprotected sexual encounter with an infected male.  What are the reasons for
this?  Are there other diseases with such extreme age-dependence?
Reference:

Estimating age-dependent per-encounter chlamydia trachomatis acquisition
risk via a Markov-based state-transition model.

The "Description of the analyzed data set" section seems suspicious to me:

In a nutshell, young women between the ages of 14 and 17 years old
were identified and recruited by the project.
...
At each follow-up visit during the study period, enrolled participants
underwent STI testing and treatment. Also at each follow-up visit, the
participants received follow-up interviews, in which they were queried
about the number of unprotected coital events since previous visit.
Most of the participations did not visit the clinic every quarter and left the project before its completion.
For our analysis, we collected 1173 quarterly test results from the
first 200 participants who were never infected and have completed at
least two follow-up visits. Their average enrollment age was 15 years
with standard deviation of 1.1 years.

It means that data is biased as for some reason most of girls were not able to participate in the study.
And I'm not sure about the correctness of your interpretation. I'd interpret it as "females are 20x less likely get chlamydia infection after being treated and warned about STD" as there were relatively continuous followed-up 15-17 y/o females and no older females. And I guess it was one of the goals of this "Young Women’s Project".

I'd like to simply ignore this paper too, but I'd also like to believe that the authors would have enough integrity to recognize and stop the error first!  I had thought there were other sources showing age-dependence, but now can't find them...

In this case the authors appear to imply that the mechanism is primarily the accumulation of partially protective immunity resulting from earlier infection.

From Table 1, we observed that 1) [p-bar] monotonically decreases as age
  increases; 2) [p-bar] decreases as q increases. [...]
The first observation support the concept that some degree of
  protective immunity against reinfection develops after first-time
  infection, although it appears to be partial at best [53, 54]. The
  second observation supports the concept that acquired protective
  immunity may restrict chlamydia replication in older persons [55].

There are quite a lot of diseases (infectious and non-infectious) with strong age-dependence - sometimes positively correlated, sometime negatively. For example, most severe disease associated with Plasmodium infection (such as cerebral malaria and severe malarial anaemia) occurs in infants and young children (source), while with chicken pox (varicella zoster virus) infection, adults and teenagers (or very young children) are more likely to develop severe disease and complications (source).