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Are androgenic-anabolic steroids a form of gene editing?
Is taking AAS a form of gene-editing? Steroids alter genes in some way since they allow people to build more muscle than what's naturally possible -- so they sort of "break" natural genetics somehow.
Given this, would this be considered a form of genetic-engineering on living humans/etc.? What about relative things like myostatin-inhibiting to prevent muscle growth cell limitation or HGH use?
In summary: does the use of AAS/performance enhancing drugs/etc. constitute gene editing? If not, why -- and if so, why and how is it comparable to things like CRISPR and stem-cell/etc. methods?

Steroids are not a form of gene editing
A gene is a sequence of DNA. Gene editing means changing this DNA sequence, kind of like changing the letters in a book.
Essentially all drugs, steroids included, affect the body without changing DNA sequence. Often they bind to a protein, which is the product of a gene, and alter its function. Steroids bind and alter the activity of transcriptiton factors, which are kind of like switches that turn certain genes on and off.
If gene editing is like rewriting a book, taking a drug would be like changing how, when, or where someone reads from the book, without altering the text itself.
If you are interested in how all of this works, you can check out some great free online courses like this:
https://www.khanacademy.org/science/biology#intro-to-biology


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Flower Identification: Pyrenees, France
I'm trying to identify the white flowers in this photo. Location is in the Pyrenees mountains near Luz-Saint-Saveur in France. The image was shot in early September of this year. Any help is greatly appreciated!
Robert

source: Stack Exchange

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

sort: votes


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How do opportunistic infections affect an immunocompromised or AIDS patient?
I mean, everyone knows that AIDS patients don't die of the HIV infection, rather the opportunistic infections. But if HIV only affects T lymphocytes, and destroys them, then that means only cell mediated immunity and humoral immunities are affected (since B cells need helper T cells to be activated).
The body should still be producing other types of leukocytes like neutrophils and macrophages, which should eliminate most bacteria. So does HIV infection render the mononucleaf phagocytic system useless as well? If yes, how so?

Clinical diagnosis of AIDS in a person infected with HIV is based on the following criteria:

A CD4+ T-cell count below 200 cells/µl (or a CD4+ T-cell percentage of total lymphocytes of less than 14%)

OR

The patients has one of the few "indicatory" diseases that strongly suggest severe immunodeficiency. See the list of this diseases here. Usually they have fatal consequences.

As we can observe, there are mostly fungal and viral infections that live inside the host cells or (in case of tuberculosis) diseases caused by intracellular bacteria. They can be overcame only with working mechanisms of cellular immunity. Other mechanisms are simply too slow, not specific or not precise enough.
Another issue is an impairment of the immunological surveillance and much higher risk of cancer in individuals diagnosed with AIDS. Precise elimination of malignant cells is fully dependent on cellular immunity.
[EDITED]
For further reading, recent paper analysing the most common causes of death in patients with AIDS in the era of anti-retroviral therapy.

First, without support and amplification from the adaptive immune system, the innate response is less efficient.
Second, virtually every pathogen, whether obligate or opportunistic, has mechanisms that allow it to evade or subvert the innate immune response. That's why AIDS patients are susceptible to pathogens (including opportunistic pathogens) but are still not infected with non-pathogens, such as environmental agents or pathogens of, say, plants or insects even though we're constantly soaking in those non-pathogen microorganisms. Those agents don't have the needed ability to avoid innate responses.
So even in AIDS patients, innate immune responses are helpful, it's just that they're not enough, on their own, to prevent infections by pathogens with ways of evading innate immunity.

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


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How and why did bats and dolphins develop echolocation?
By how and why, I mean, what factors pushed them to develop echolocation and how did the intermediate stage (before a full-fledged echolocation system was developed) look like?

There should be echo locating birds, but they perhaps don't have the right vocal and auditory structures. For dolphins, perhaps their eyes can't point forward while swimming fast, plus they stir sand and hunt in dark and low visibility waters. water's awesome transmission of high frequency sound is a factor. All animals can echo locate, like blind people do, evolution just has to increase high frequency hearing and chirps. Mammals tend to be nocturnal prior ot KT boundary and have good vocal and auditory structures by default.

@com.prehensible Is that an answer disguised as a comment ;-)

echolocation likely evolved very differently in each group you may have better luck spitting this into individual questions.

There are many conditions in which echolocation has evolved, and bats, dolphins, and even some birds (oilbirds) have evolved the ability to echolocate with different anatomical structures. Echolocation is a great example of convergent evolution, where a very similar feature is developed through very different stages in different taxa. Stephen Rossiter (from Queen Mary University of London) has uncovered that both bats and dolphins have similar mutations in a unique protein called "prestin", that increases hearing sensitivity. This could be a key step in developing the ability to echolocate.
Before a fully fledged echolocation system developed, fossil odontocetes seem to have developed high frequency hearing and sound production structures (for more details see research by Travis Park, Erich M. G. Fitzgerald, Alistair R. Evans http://rsbl.royalsocietypublishing.org/content/12/4/20160060 DOI: 10.1098/rsbl.2016.0060).
Instead of anatomical limitations (eyes on the side of the head) driving the development of echolocation, it seems to have evolved because it gives predators a competitive edge over visually oriented predators.

Simple echolocation is fairly widespread and varying levels of quality exist
This specifically addresses what the intermediary forms look like.
Mammals posses some nice preadaptations for echolocation. external ears for gathering sound, a three bone middle ear which creates an amplifier which means mammals can hear both weaker and a wider range of sounds. It also means the brain has to be able to do more processing of sound due to distortion and frequency shift. Even humans can perform very limited echolocation with training due to this.
Old world fruit bats don't use full fledgedly echolocation like other bats and dolphins. First the sound is created by their wings not their vocal cords, it is a side effect of their wing beat. Second it is functionally rather poor not giving a very detailed image, as noted in this study they cannot detect small objects or judge distance very accurately unlike other bats. The study also have a lovely table showing how many other animals have primitive forms of echolocation, including shrews, rats, and swiftlets.

re: mammals possess some nice preadaptations for echolocation, here's a human mammal example. The voiceover is incorrect when it says this is the only example of a person who sees with echolocation. There are others.


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In men, why do over 80% of sperm have abnormal form?
Here is the percentage of normal forms among fertile mens according to the centile (Source: Cooper et al. 2010):

2.5: 3%
5 (below this is Teratozoospermia): 4%
10: 5.5%
25: 9%
50 (median): 15%
75: 24.5%
90: 36%
95: 44%
97.5: 48%

Men who have less than 4% of their sperm that have normal morphology are diagnosticated with Teratozoospermia (also called Teratospermia) and are likely to be infertile, though technically 5% of fertile men have Teratozoospermia.
I read on the internet that abnormally-shaped sperms are bad and useless because their abnormal shape prevents transport through the cervix and/or prevents them from adhering to the ovum.
But I think that if they were really that bad, Mother Nature would not have engineered the average men with 85% of their sperm abnormally-shaped.
And I also heard that even animals have a big fraction of their sperm that are abnormally-shaped.
So, in men, why do over 80% of sperm have abnormal form?

Why do you think it has an adaptive purpose? Not all traits have been selected for. For example, forming abnormal sperm might be a high probability event, and so ejaculating a large number of sperm may have been selected for to counter that. Of course I do not know if that is what happened, but I am illustrating how not all traits are adaptive.

How is a 'normal morphological form' defined? For most other medical reference values one would take exactly a distribution like that to have 'normal values' in the first place.

@NatWH: True this is a possibility, but I think it's unlikely because more than 80% of failed creations is really high, it's so high that this cause a significant fraction of men to be infertile.

@James: This question is a general question, it's answers are just general possibilities. My question is a precise question about a precise topic and needs a precise answer. E.g. answering "maybe there is a tradeoff" would not be an acceptable answer, but answering "there is a tradeoff which is that the abnormal sperm have the advantageous function that ... something" could be a correct answer.

@Nicolai: A normal morphological form is a form which can reach and penetrate an egg. An abnormal form is a form which cannot. Normal sperm have an oval head with a long tail. Abnormal sperm have head or tail defects, such as a large or misshapen head or a crooked or double tail.

@Aero that was the purpose of my hypothetical example - if the proportion of malformed sperm is high, then one way to deal with that is to produce huge numbers of sperm, and hope that the 20% still represents a large enough fraction to fertilize the egg.

@Aero: "normal morphological form is a form which can reach and penetrate an egg" sounds more like what you wish Cooper 2010 was reporting about rather than what they actually were able to report about. As Nicolai shows below, they are actually compiling data about lab microscopy about sperm appearance, not about whether sperm actually reached and penetrated ova.  So you shouldn't assume that the median man has semen with only 15% of the sperm present capable of fertilizing an egg just because of that report.

The way the winds are blowing, this question is about to get closed as a duplicate of a question that doesn't talk about sperm at all.  This might be able to be headed off by changing the headline to drop the evolution/purpose aspect, as e.g. "Why do over 80% of sperm have abnormal form?".

@mgkrebbs: Done.

@NatWH: 1% of men have 100% abnormal forms, so even producing huge numbers of sperm won't increase the number of normal forms. Based on the many articles I just read, it seems that abnormal forms can in some men still possibly fertilize the egg but that it's just much less likely for an abnormal form to succeed compare to a normal form.

What do you mean with 'why'? These edits take out the evolution aspect,but replacing it with 'why' makes it unclear. Why, as in, what are the underlying mechanisms? Or why in terms of the evolutionary benefits? The latter makes it a dupe.

So I've dug a bit into how a 'normal morphological' form is defined and characterised, since assessing morphology into 'normal' and 'not normal' is always a very tricky thing.
Looking into the method section of the source you cited, we get:

All laboratories generating the data analysed here used standardized
  methods for semen analysis [...] The various editions of the manual provided similar
  methods for assessing sperm concentration, motility and morphology but
  provided different criteria for categorising morphology.

So the  problem begins already with the fact that there is not one, but multiple different recommended practices.
(For anyone interested the different staining methods used were: Bryan–Leishman [B], DiffQuik [D], Haematoxylin and Eosin [H], Papanicolaou [P], Quickdip [Q] and Shorr [S]. Of thses H, S and P were used for generation of the 'normal morphology' reference set).
Clearly this problem was also obvious to the authors, so they tried to restrict the data they used:

Although all centres reported using WHO procedures, the recommended
  methodologies have changed over time, and many centres have
  experienced difficulties with the subjective assessments of
  morphology. Data on normal sperm morphology were only included if
  results were reported as determined according to the so-called
  ‘strict’ (Tygerberg) method (WHO, 1992, 1999).

Fortunately these WHO guidelines are available on Google Books and they require the following points to met (most of which were defined by 95% confidence intervals of control samples):

head length 4.0-5.0µm
head width 2.5-3.5µm
head length-to-width ratio 1.5-1.75
well defined microsomal region compromising 40-70% of the head area
mid piece should be slender, <1µm
[mid piece should be] 1.5x size of the head
[mid piece should be] axially attached to the head
Cytoplasmic droplets should be less than half size of the head
Tail should be [...] approximately 45µm long

Plus one very important sentence:

This classification scheme requires that all 'borderline' forms be considered abnormal

This sentence is important, because it means that each criterion stated has to be fulfilled for a single sperm to classified as morphological normal.
If we take only the numeric requirements (which should cover ~95% of the normal value distribution for a healthy population) and assume that they are not correlated, this means that for any given single healthy sperm we have a $0.95^9 = 0.63 = 63\%$ chance that it is within the 95% interval of all defined parameters.
This means that applying this strict categorisation scheme should even for a 100% healthy population only result around 63% sperm cells categorised as morphologically normal (ignoring that the parameters are probably not interdependent which would make it a bit better).
If we now take into account that the analysed samples were probably not 100% healthy cells and remember that the (reported) difficulties of assessing morphology, I think that the reported values for 'morphological normal' are not as quite as unexpected as they might seem.
Note: all bold highlighting in the quote blocks was added by me.

Biological evolution occurs when there is a change in gene frequencies over time (as I recall).  There are two components, or elements, required for this process:

genetic variation, which provides the raw material
natural selection, which results in the genes from the most successful reproducers being transferred to subsequent generations

The data you present support the hypothesis that “normal” sperm morphology in human males is not a strongly selected trait (because otherwise “normal” sperm would be more prevalent). Period. Full stop.
Any attempt to answer the “Why” part of this would have to be a conjecture, and ultimately untestable on an evolutionary scale.


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Difference between NCBI's /genomes and /1000genomes
Wondering what the difference is in the data hosted here:

ftp://ftp-trace.ncbi.nih.gov/1000genomes
ftp://ftp.ncbi.nih.gov/genomes/

Also (sidenote), would be interested to note what the difference between ftp-trace and just ftp is. But there is probably over 1TB of data in /genomes, and I assume something of "a thousand genomes" is in /1000genomes, but I'm not sure what data exactly. Would like to know what is i thse two folders, and where the 1000genomes data is exactly. It looks like /1000genomes/ftp/data/ has "sequence data", but I'm not sure how that compares to the /genomes list of species names (and I'm also not sure what "sequence data" entails exactly).

The simplest difference is the scale and range. The aim of 1000 genome project was to provide comprehensive library of human genetic variation. DNA of individuals coming from different ethnic groups, geographic locations were sequenced and the results of the study were published here.
Genomes from NCBI come from different organisms and the number of sequenced individuals differ between species (including human). This database is constantly growing. Detailed description can be found here.

In fact these two things are very different and I would say quite opposite.
NCBI genomes are collection of information on genomes of various species including sequences, maps, chromosomes, assemblies, and annotations. Basically it's a catalog of reference genomes.
1KG is a catalog of human genetic variations from a genome-wide association study.


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Why is a hippo so big if it has round about the same genes as a mouse
My science teacher told us that all mammals have round about the same number of genes. This confuses me, since there are very big and very small mammals. Where do genes come from and why do animals have such large differences in size between one another even if they have around the same amount of genes?

@stormy The comments are not a place to talk about pet theories, especially those unrelated to the question. Please only use comments to improve questions and answers.

@stormy Science isn't based on what you find fascinating, it is based on empirical observation. Plant DNA does not have 99% of the information that human DNA has, nor 99% of what a bacterium has.

Genes are the "plans" for proteins in an organism; in turn, those proteins do all sorts of things, catalyzing chemical reactions and making up much of the structure of an organism.
A hippo is much bigger than a mouse, but it isn't that much more complex: both are going to have the same sorts of organs like a heart, lungs, kidneys, liver, brain. If you look at an individual cell from each animal from the same tissue, they will probably look almost identical! They are going to have similar metabolic pathways, etc. Their genes will be different, because some differences in proteins are necessary to build organisms of different structure and size, but the number of genes doesn't have to vary much, the hippo just needs to produce a lot more of the gene products, not have more plans.
A hippo will of course have way more genetic material, because it also has more cells and there is a copy of the DNA in every cell, but what your teacher is talking about is the number of genes within each cell.
Ultimately, genes come from evolution. You can read more about the basics of evolution somewhere like Berkeley's Evolution 101.

@stormy Ok first, what does 'asteroid mimi' have to do with this answer? Second, if organisms didn't evolve, why are all organisms different? Third, DNA that'll never be used? Fourth, how can a virus seed life with DNA?


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Can a cancerous cell from outside cause cancer in a healthy person?
If a cancerous cell enters the body of a healthy person from someone else's blood or something, will that healthy person get cancer? In human beings.

Yes it can.  See https://www.livescience.com/63596-organ-donation-transmitted-breast-cancer.html

@sterid those case involve immunosuppressed patients with end organ failure. This question is about what happens when a healthy person is exposed to cancerous cells

Can a cancer cells from someone else's body cause cancer in a healthy person?

No. Cancer cells from another person cannot cause cancer in a healthy person. The rare cases of transmissible tumors all involve unhealthy or not yet developed persons.
Transmission of tumor cells from one individual to another happens, but is quite rare, and in all cases involves some compromise or reduced development of the immune system. Though tumor cells do metastasize in an individual, when this occurs, tumor seeds must be able to evade the immune system and find an environment suitable for adhesion and replication. Tumor associated cells (non cancerous cells that regulate the microenvironment to make it favorable for growth and replication) are discussed in this seminal paper on cancer biology by Hannahan and Weinberg.  There are similarities to infectious processes, but cancer is not measles. Tumor cells don't shed in comparable numbers, aren't adapted for immune escape in a separate host, and don't express appropriate adhesion proteins for portals of entry on a new host or readily induce tumor associated niches in a new host. The cases where person-to-person transmission of cancer via tumor cell inoculation does occur seem to demonstrate more how cancer cells are not infectious agents.

Donor-related tumors in transplant patients occur in immunosuppressed patients, but are still rare. The low frequency of transmission seems to be due, in part, to screening. The fact that we see this at all demonstrates the significance of transmission route and immune escape.
Maternal-fetal, and in utero twin-twin seem to be exceedingly rare, but have occurred, again, demonstrating the existence, but poor efficiency of transmission. Here, the fetus has an undeveloped immune system. I would not consider this case to be cancer cells causing cancer in a healthy person.
Inoculation of volunteers with tumor cells in a problematic series of experiments at Sloan Kettering in the 50s, transplantation of tumor cells into patients with other cancers, resulted in growth, recurrence after excision, and death in some cases. Transplantation into healthy volunteers (yes, they did this) resulted in nodules that spontaneously regressed. This experiment has since been interpreted as evidence for immune system control of transplanted tumor system in healthy individuals, as compared to growth and progression in a receptive niche in a cancer patient.

So person-to-person transmission of cancer cells is rare and requires an immunosuppressed or undeveloped host, or a host who already has cancer. There are no documented cases of person-to-person transmission to a healthy individual, and documented cases of failed transmission despite a surgical attempt. This is because, unlike an infectious microbe, in a healthy individual, there is not a suitable receptor for adhesion at an exposed or accessible site, a suitable environment for replication, and adaptations for immune escape by tumor cells in the original host are not effective in a new host.
As a side note, there are contagious cancers in other species, but this doesn't seem to be particularly relevant to a question about whether cancer can be transmitted between two humans. Many cancers have transmissible risk factors (e.g., human herpesvirus-8, hepatitis B and C viruses, human papilloma virus 16 and 18, and others)

@Chris I don't believe I have that privilege (moving other people's comments to chat). Feel free to move the whole series of comments to chat if you think they belong there.

Comments are not for extended discussion; this conversation has been moved to chat.

I thought about you guys moving to chat. Anyway, the chat link is above.

The last sentence in this answer seems to refute the others.  If the introduced cancer cell contains a cancer-causing virus then the answer is 'yes', my cancer cell could give you cancer.

@aml good instinct, but that doesn't happen to be the way it works. The virus is the risk factor, not the cancer. If you want to ask a separate question about that, I'd be happy to answer in detail. I'll just give you an example here: blood exposure could, for example, expose someone to HBV, and they might develop cancer 30 years later, but it would be the extracellular HBV, not any cancerous cell that was responsible. The foreign cancerous cell would be rapidly killed by the healthy host's immune system.

@Chris Actually the system gives an Option for the OP or others commenting to move it to chat when it gets quite long. When they do not, I think mods are notified.

@DeNovo Yes, IIRC if there are 7-8 comments between two users within quick succession, it prompts......

If I recall, only one in around 10,000 cancer cells that break off from their primary tumor and get sucked into the lymphatic system survive the trip to the subclavian veins. It's likely that far fewer cancerous cells would survive if they carried significantly more non-self antigens as would be the case with foreign cancer cells.

Before OP edited his/her question, it was a little unclear whether the question was only about humans. The following answer is more general than asked as it also considers cancers in non-humans

Most cancers are not transmissible but some are. We call them (clonally) transmissible cancers.
Transmissible cancers
The most famous case of transmissible cancer is the Devil facial tumour disease in Tazmanian devils. Other cases of transmissible cancers exist in Syrian hamsters, dogs (CTVT), and some bivalves. No such transmissible cancer is known to exist in humans.
Transmission of viruses inducing cancers
There are cases of cancer caused by viruses. Those viruses are transmissible and hence it looks like the cancer itself is transmissible. In humans, this is for example the case of Kaposi's sarcoma-associated herpesvirus.
Transmission via transplant
Finally, there are cases of cancer that can be transmitted to a new person via a tissue transplant. In humans, Kaposi's sarcoma is (again) an example.

Kaposi's sarcoma is not a transmissible cancer. It has a transmissible risk factor, HHV-8, but this is definitely not an example of cancer cells from one person causing cancer in another person. The cancer cells are not the transmissible agent (unlike the transmissible cancers in nonhuman animals). The special cases of Kaposi sarcoma transmission after transplant definitely don't involve healthy recipients. These patients are immunosuppressed, and the cells are, well, transplanted.

@DeNovo You're right. I actually made reference to transmission of Kaposi's sarcoma indirectly via the transmission of a herpesvirus. I clarified that. Thanks. I added the idea of transmission via transplant. If I am not mistaken Kaposi's sarcoma is known to be "transmissible" via both transplant and virus transmission. Please correct me if I am wrong.

Thanks for editing. I'm removing the downvote. I'm not going to upvote because I don't think this directly addresses the question about what happens when cancerous cells enter the body of a healthy person.

The answer states that different cancer types may be transmissible but I think this is wrong, or at the very least misleading. In reality the transmissibility mostly isn't a function of the cancer, it's a function of the host organism. Tasmanien devils have transmissible cancer due to a recent population bottleneck that reduced genetic (and thus immune factor) diversity. Same for transmissible dog cancer cases.

@KonradRudolph both the immune characteristics of the animal and the cellular behavior and genetic characteristics of the neoplasm are important here. I think it is correct to say that only a few types of cancers are transmissible. Tasmanian devils have a wide variety of neoplasms, but only DFT is transmissible.

The answer is no.
From molecular/mechanistic point of view cancer cell itself is not a self-maintaining and independent creature. Even assuming its infinite potential to renew and grow, it still needs constant nutrients supply and tailored microenvironment to survive. Therefore, there is a growing number of attempts to therapeutically target tumour cells niche, see: Joyce JA, Cancer Cell, 7(6), P513-520, 2005 and Belli C. et al., Cancer Treat Rev. 2018 Apr;65:22-32. To overcome this limitations, Cells can undergo epithelial-mesenchymal transition, which allows for migration outside the primary location and is crucial to initiate metastases.
Another important issue is the major histocompatibility complex, which allows to identify and eliminate cells, that contains foreign antigenes. Also, constant immune surveillance in immunocompetent individuals leads to elimination of potential cancerogenous cells. Therefore, patients with immunodeficiencies (eg. with AIDS or on prolonged pharmacological immunosuppression) have significantly higher risk of developing infection-related cancers, such as cervical cancer (HPV) or Kaposi Sarcoma (HHV-8).


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Mutation rate and Evolutionary rate?
What is the difference between then?I have read some jobs that describes analysis about mutations rates and another ones with evolutionary rates.I want to know the diferrence between then.

this answer may be helpful: https://biology.stackexchange.com/a/76988/42697

Mutation rate
A mutation rate is a rate at which mutation occur. It is typically expressed as number of mutations per site (per nucleotide) per reproduction event. In humans, the average mutation rate per site per reproduction is of the order of $10^{-8}$.
When a mutation occurs, it will exist in only one copy in the population. This mutations might, over time, reach a higher frequency and even eventually reach a frequency of 1.0 (we talk about "fixation" then) but most mutations will never reach a high frequency and just disappear in the coming few generations whether or not the selection was deleterious.
Evolutionary rate
The term "evolution rate" has no commonly agreed upon definition. Depending upon your definition the mutation rate will be more or less correlated with the evolutionary rate.
Phenotypic evolutionary rate
Evolution rate might refer to phenotypic evolution. The Darwin (named after Charles Darwin, obviously) is a common unit to measure phenotypic evolution. Other unit of evolutionary rate could consist at measuring how much time it take for the mean phenotypic trait to change by one standard deviation of the original phenotypic distribution.
Genetic evolutionary rate
One can also consider genetic measure of evolutionary rate such as the number of neutral substitutions in a lineage per unit of time. With this definition, the difference between the mutation rate and the evolutionary rate become a little more blurry as the expected substitution rate at neutral site is equal to the mutation rate.
Always cite your source!
You say

I have read some jobs that describes analysis

Please, always include your source. There is no way to give any information about what they mean by these terms without having a look at the original paper.
Related post
The post Are we “more evolved” than present-day bacteria? is somewhat related.


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Why green light is good for our health?
I have a knowledge that when you woke up and see green light it increases your sight power. How it does so?

Any more specifics or evidence for that claim?

http://applications.nam.lighting.philips.com/blog/index.php/2015/08/06/the-subconscious-effect-of-colored-lighting/

There's nothing in there about green light increasing sight power, or about green light and waking. It reduces glare and provides good contrast for red objects, but it doesn't make your eyes any more powerful.


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Can someone help me identify this insect
We found this insect in the basement of a friends house. It is about 1 inch in size. My friend lives in Canada

Can you please give more information (e.g. size, where do you live, better picture, did you find just one or were there many,  ...)

It is about 1 inch in size, they are located in Canada, I have another picture but it is a further away one. They only saw one in the basement.

I actually feel for this guy stuck to the duct tape.  I am a bit different, I admit.

He was found in a basement furnace room that is usually quite dark. There was recently a worker down there and he was the one that brought him upstairs on the tape. From there they didn't want to touch it since they didn't know what type of insect it was.

This guy looks very close to one of the variants of the very dangerous Triatoma.
I'm not sure what you should do in Canada about those guys, but in Brazil you should report them to your Disease Control Center. Triatoma has a very nasty bite and it can trasmit the Chagas Disease.
It is a bit weird to find this one in Canada - they are usually found in tropical places.

Why the downvote? Did I miss something?


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How do longleaf pine trees adapt to the florida keys rainforest?
I know that longleaf pine trees can be found in rainforests, but I can't find anything.

This question is way too broad! Can you please let us know what exactly you are interested of? What species? What forest (Canada type of rainforest or Brazil type of rainforest)? What evolutionary event? Are you looking at current rainforest trees that have broad leaves and are evergreen or trees that had broad leaves that have now evolved toward needles or whatever?

I have to whine a bit.  I am sure this question's wording has been changed...as have lots of questions after the fact after answering.  Is there a way to tell?  I surely do not remember pines, I do remember broad leaf plants in the rain forest.

Conifers have evolved to handle cold winters, not rain forests per se.  What the heck does 'long leaved conifers' mean?  White pine with long long needles?  How about Ponderosa or Jeffery Pine?  Conifers aren't meant for tropical or subtropical regions.  Perhaps the monkey puzzle tree might qualify? Conifers evolved to be able to hold onto their 'leaves' by thick epidermis resistant to freezes.  There are even hardier deciduous conifers.  Why would my answer be voted down?

This is sort of a too broad question but here are a few ideas.  The second most fragile part of plants are the leaves. In the latitudes and elevations that experience freezing, plants have learned to abscise their leaves and go dormant for the winter season.  Conifers have thick, waxy, very thin leaves that most conifers do not need to shed.
In a rainforest there is no danger of too cold temperatures.  That is why there is an abundance of broadleaf trees and plants in the rainforest.  Most of our indoor plants are tropical rainforest species.
There is also an awful lot of rain in a rainforest. There is a problem with leaves covered with water, as it inhibits the absorption of CO2.  Beneath the leaf, O2 is released as a by-product of photosynthesis.  Broad leafed plants that have adapted to an environment with lots of rain, little wind, and being crowded together have leaves designed to 'wick' the rain water off the leaf to run down the midrib and off the pointy tip or lobed or curled under leaf margins.  This clears off the water and allows the plant to take up CO2, or it would not be able to do photosynthesis to make its own food for energy.
The other cool thing I can remember, is that broad leafs of plants are able to 'adjust' to the light. Similar to a 'solar sail' in outer space. If in full sun, those leaves get thick and stay smaller.  If in shade, very normal in a rainforest, those leaves can thin and get larger in order to capture as much light as possible.
A better wording for your question would be, 'why is there an abundance of broad leaf species versus conifers in a rainforest'?  If I've been able to translate your question correctly?
Hope this helps.


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What are the effects of enzyme exposure to high temperatures?
Question: After enzymes are exposed to high temperatures and undergo denaturation, then returned to their optimal temperature and renatured, can the enzyme's active site return to it's original shape and will it function at the same level of efficiency as it did before being denatured and renatured?
Some background I wrote to the question:
I am just beginning to learn Cell Biology, I hope what I've written is correct.
When you raise the temperature of an enzyme, at first it will increase the efficiency of the enzyme's activity, but eventually as the temperature rises, the enzyme with stop functioning and undergo denaturation, which means that the 3D formation of the protein is unraveled, so it doesn't function anymore. From what I've managed to research, the high temperature changes the shape of the active site in the enzyme, which is what allows the enzyme's activity in the first place.
I know that some proteins cannot be renatured (like adding heat to an egg will fry it and there is no way to unfry it), but some can be renatured (like heated milk, when it cools down the protein bonds will reestablish themselves).
But will the enzyme's active site return to it's original shape and manage to function at the same level of efficiency as it did before? Or is the damage permanent?

Possible duplicate of How does temperature influence the rate of protein degradation?, How is the rate of transcription influenced by temperature?, and Influence of temperature on protein binding and decay rates.

The answer is that it completely depends on what specific enzyme you're talking about; some of them will and some of them won't. What you wrote is correct, that increasing temperature of most enzymes (although there are exceptions) will increase their activity to a certain point, after which the proteins lose their 3D structure and become unfolded.
Upon cooling, it all depends on whether the enzyme can re-fold by itself or not. Some proteins when heated form aggregates, which are more stable than the original conformation, and so generally won't refold with cooling. Some proteins are able to fold into proper conformation by themselves, while other require assistance from chaperone proteins in order to fold correctly. Many of these chaperones are called heat-shock proteins, which are upregulated in response to thermal stress. That points to the fact that many proteins can't just refold on their own, and require help to regain their original conformation from these HSPs.
So the real answer is that it all depends on the specific protein. It also depends on how much you heat the enzyme, and how much of its 3D structure you affect, if you only partially denature an enzyme, it's more likely to refold than one that's been completely denatured. However, if you want an answer about enzymes in general, I'd say that most enzymes after denaturation aren't able to refold properly and regain their enzymatic activity, so the damage is permanent.

Thank you so much! Your answer really helped and gave me some more knowledge to use, to do further research into the matter.


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Question: What is CINWntUp and CINnormL?
What is CINWntUp and CINnormL?
I read a paper that uses this two things as classes but Im not sure what they represent. I imply that CIN is referring to Chromosomal instability but I don't know what WntUp & normL refer to. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214593/)

From the paper:

The dataset contains six colon cancer subtypes: class 1 = CINImmune-Down (116 samples), class 2 = dMMR (104 samples), class 3 = KRASm (75 samples), class 4 = CSC (59 samples), class 5 = CINWntUp (152 samples), and class 6 = CINnormL (60 samples).

CINWntUp and CINnormL are therefore two classes of colon cancer. You are correct, CIN is for chromosomal instability; WntUp refers to upregulation of Wnt, a signalling pathway involved in some cancers and named for a Wingless/Integrated phenotype in fruit flies and the homologous gene in vertebrates. normL stands for "normal-like."
See the original paper describing these classes:
Marisa, L., de Reyniès, A., Duval, A., Selves, J., Gaub, M. P., Vescovo, L., ... & Kirzin, S. (2013). Gene expression classification of colon cancer into molecular subtypes: characterization, validation, and prognostic value. PLoS medicine, 10(5), e1001453.


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What is the meaning of a 1,4 bond between sugars?
I don't know how to express my question. I want to know what are bonds like 1.4 bond between molecules. I've read somewhere like the amylase enzyme can break 1.4 bond. I want to know what are these bonds and what are their benefits and where  can I find more info about them?

Amylase breaks the bond between two sugar molecules in a chain (the chain is called starch).
The type of bond is called a glycosidic bond which is just a covalent bond between sugar molecules.
The "1.4" bond you are talking about is normally written "1,4" or "1-4"; you could interpret it as "1 to 4" because it is referring to a bond involving the first and fourth carbons of the sugar (they aren't bonded directly, there is an oxygen in between); they are just numbered that way so that (bio)chemists can talk about the molecule - see this other Q&A from Chemistry about the numbering of the carbons of glucose.


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Could a mammal convert ingested dissolved CO2 to usable energy?
I'm trying to find out if it's possible that a mammal could orally ingest dissolved CO2 and convert it to energy for body heat, organ function, etc.
Unfortunately, most of the scientific sources I've been able to find talk instead of CO2 gas inhaled by mammals. All the sources speaking to orally ingested dissolved CO2 begin their argument with the assumption that all of it is converted to (and expelled as) gas in the digestive tract, but they never bother to prove that or cite anything.
It seems like this would rarely be observed in nature, and therefor not really be studied or documented, so I'm curious what degree of chemical or biological certainty there is about this, and what research has been done.

As a new contrbutor you are welcome to SE Biology. However I would suggest that you be polite in your criticism of the sources you have read. It is fine to say "they do not prove…", but "they do not bother to prove…" is derogatory. Admitedly you do not name them so they won‘t be offended, but the principle of polite and objective scientific argument is the same. And people in glass houses shouldn‘t throw stones — you haven‘t cited your sources, which we might have expected and would have strengthened your question.

No.
What is lacking from the question is a logical framework for the possibility suggested — that carbon dioxide can be a source of energy — and I suspect that this is because it lacks a clear chemical conception of what energy is and how it is formed in living organisms.
The generation of energy in a biological context can be considered as the consequence of a chemical reaction or physico-chemical process which involves  a negative (Gibbs) free energy change. For use by the cell (except in exceptional circumstances like heat generateion) the energy released in this process must be used to drive the thermodynamically unfavourable formation of a molecule (e.g. ATP) in which this can be ‘stored’. The stored energy is used when the hydrolysis of ATP is coupled to a thermodynamically unfavourable biological reaction or change, hence providing the ‘energy’ for it. This topic is covered in most biochemical texts, e.g. Berg et al..
So if carbon dioxide were to be a source of energy, it would have to undergo some reaction with a negative (Gibbs)free energy change. Other carbon compounds that are sources of energy are so by virtue of their ability to be oxidized (again see Berg et al.). However, as has already been mentioned in a comment, carbon dioxide is the most oxidized form of carbon and so cannot generate energy this way:

So unless the question could proposes another chemical or physico-chemical in which carbon dioxide could participate that has negative (Gibbs)free energy change, there is no reason to consider the postulate.

Finally, some sense.  The question as worded is just not going to be answered directly.  Just a no suffices.

Thanks for your answer. One quick follow-up: Is it possible that the microbiome of a mammal's digestive tract could produce glucose if it comes into contact with dissolved CO2? Meaning the ingested CO2 contains no usable energy, but the act of ingesting it results in the production and consumption of usable energy inside the mammal? And is there anything other than the microbiome that might be able to do this (like something else being consumed together with the CO2)?

@Adelmar — No. As has been mentioned, photosynthetic organisms use carbon dioxide to make glucose, and carbon dioxide is fixed in gluconeogenesis, but these processes require energy in the form of ATP derived from other processes to do this (and I don't think there are any photosynthetic organisms in the human microbiome).  You don't say why you have this idea. The only related thing I can think of is the way the ATP synthase of Ureaplasma urealyticum utilizes a pH gradient it generates from hydrolysing urea to ammonia in the bladder. But dissolved carbon dioxide is acidic.

There isn't any biologically useful energy in CO2. In fact, humans and all other animals produce CO2 as a waste product at the end of metabolism specifically because it is low-energy. You don't need to ingest it or breath it in as a gas, and if you didn't breathe it out you would die.

You're kind of just saying "no" here, and the statements about CO2 in waste and the necessity of ingestion/exhalation aren't really relevant to the question. I'm hoping for more specifics than this.

@Adelmar What sort of specifics? I included those other facts because it didn't seem from your question that you realized CO2 was a low-energy metabolic waste product, and because you were talking about the possibility of differences depending on ingestion versus inhalation of CO2. Those don't matter, because there is already dissolved CO2 being produced all over.

@stormy That isn't relevant here; also, even photosynthetic organisms do not use CO2 as energy.

Bryan, without CO2 those plants will not have ANY energy to use to MAKE their food, carbohydrates that plants have to have to survive.  Period. What are you saying??

@stormy Yes, petroleum is high energy. When you burn petroleum, you release energy by turning the hydrocarbons back to low-energy carbon dioxide. The reaction is "Hydrocarbons + O2 -> CO2 + Water + Energy". Plants do not use CO2 for energy, they use the sun for energy. They store that energy by taking low-energy CO2 and making it into high-energy molecules like carbohydrates.

Bryan oh my.  YES the plants use sunlight, turning that sunlight into carbohydrates that the plant can use for growth, reproduction and repairs.  If you think for one moment photosynthesizing chlorophyll can make carbohydrates WITHOUT CO2?  You are absolutely wrong.  Without CO2 that photosynthesis will not happen at all!  To include chemistry such as nitrogen , phosphorous, potassium minute amounts of boron, calcium, iron, sulfur, magnesium, manganese...at least 13 different micro chemicals.  Otherwise, photosynthesis does not work does not make energy usable to plants.

@stormy Did I say plants didn't need CO2? I said CO2 is not the source of energy.

About this unit
There's a lot of carbon in your body - in DNA, proteins, carbohydrates, fats, and other key biological molecules. How did that carbon get there? Drumroll... photosynthesis! Learn how plants and other photosynthetic organisms use light energy to make sugars from carbon dioxide and water, bringing both chemical energy and readily usable carbon into Earth’s global ecosystem. excerpt from https://www.khanacademy.org/science/biology/photosynthesis-in-plants

Without CO2 and macro/micro chemicals there is no making of an energy source to support life.

Plants without CO2 as well as O2 for the roots, the rest of the chemistry will not be able to use sunlight for energy.  Animals certainly are unable to harness the energy of the sun directly either.  What is more important?  Sunlight or chemistry?  BOTH are critical to convert the energy of sunlight to something usable by plants and animals.  Critical, just as much as sunlight.  Why are we arguing? Sunlight alone will not be usable to any life form, that is why we have so many processes to take the energy of the sun to convert it usable.  Petroleum, is sunlight captured because of CO2 +

CO2 does not yield any biological energy.
Living things can oxidise compounds like glucose and drive ATP synthesis from it.
This energy keeps us alive by not letting us fall into a state of equiibrium(death).
If mammals had any speacial complexes that converted light into chemical energy in their digestive systems they would have been able to derive energy from ingested CO2.
We don't even have any reactions in our metabolism that oxidise inorganic minerals(like chemosynthetic bacteria) to drive carbohydrate synthesis.
So I don't think mammals can convert ingested CO2 into useable energy.


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How do you write genotypic and phenotypic ratios?
If two homozygous recessive parents are crossed, I know that all of the offspring will be homozygous recessive as well. Would you write the genotypic ratio as 0:0:4 then and the phenotypic as 0:4? (Does order matter? i.e. compared to 4:0)
Also, if the results are 2 homozygous dominant and 2 heterozygous, is it necessary to put the zero for recessive (2:2:0) or would 2:2 be fine?

I don't think there is formal notation for those ratios.
One would note that perfect dominance and recessivity, perfectly discrete phenotypes without pleiotropy and without environmental variance is extremely rare and these examples are pretty much only encountered in intro classes but never in the real life. There is hence, for the phenotypes at least, really no need for any formal notation here.
That being said, out of clarity, I would definitely prefer 0:0:4 (genotypes) and 0:4 (phenotypes) over 4 (for either genotype or phenotype) and I would definitely prefer 2:2:0 over 2:2


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Why in the Electron Transport Chain does PS2 go before PS1?
Why in ETC does PS2 go before PS1?

It's just because PS2 was discovered before PS1.

If your question is related to numbering, the photosystems were named in the order of their discoveries not participation.
In cyclic ETS PS-II doesn't participate at all.
PS-I would have gone first if PS-II was named PS-I.


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Fluoroquinolone mitochondrial and genomic DNA adduct
What could be possible consequences of covalent bond mitochondrial and genomic DNA adduct by Fluoroquinolones, our study was done by Fluoroquinolone Toxicity Study NFP. All 50+ participates who took Ciprofloxacin and Levofloxacin were positive. In vitro study showed DNA adduct after 3.61 min. We are FQAD victims not scientists. We would like to know what may be consequences of DNA adduct.

As a new user you are welcome to SE Biology, however you should be aware that there are a couple problems with your question that might have been avoided if you had taken the tour and read the help on answering questions. The first is to express yourself clearly — 'mt' and 'n' should be written in full in the title for clarity and to help indexing. The second is that questions here should be self-contained. Nobody should have to go to another site or download material to understand your question.

Sorry David, I did remove the link. Thank you.


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What are these bladder snail parasites?
I collected some bladder snails several months ago. While checking them out one day, I noticed that they were now infested with worm-like ectoparasites.
Appearance and behavior
Here's a picture of a snail with a bunch of the worms hanging off of it's head, where they tend to congregate. I've also circled one of the worms crawling along the glass.

I sampled some of the worms and took a look at them under a microscope. Here's a video ("Video 1" below) I recorded of one of them crawling around. They have some notable characteristics.
First, they appear to have some sort of sucker mouth.

Second, they have some interesting "legs" tipped with hairs (?) at the ends of their tails. Here's a short video ("Video 2" below) of a worm writhing around that shows them off a little better than pictures do. They appear to be in pairs of two.

Animated clips from the linked videos:

 Video 1 (left) and Video 2 (right)
The length of the worms ranges from 1-5 mm (edit: they get larger; see below).
Update: After keeping infected snails for a while longer, I believe that these worms only parasitize bladder snails when the worms are young (within the aforementioned size range). Larger, adult worms appear to be free-living and growing up to 1-1.5cm, and will actually crawl away when snails disturb them. Here is a picture of an adult specimen (along with some smaller ones), no microscope required:

Here's a much better picture of the hair-like legs, of which this adult specimen has numerous pairs:

Lastly, here's a very interesting detail: These worms are highly specialized, and do not seem to affect ramshorn or pond snails, which I have numerous of in the same tank, in the slightest. It's only the bladder snails that end up infested.
Location
These snails were gathered in Canada, in a still-water area connected to the Oldman River. The river is accessible by cows and deer.
Reproduction
I have witnessed the snails shedding tons of cercariae into the water, which eventually disappear after a couple of hours (reinfect the snails?). I'm not sure if those are related to this worm, or if the snails are also infected with some other type of fluke.
Update: I now believe the aforementioned cercariae are unrelated to the worm in question. I managed to record an adult worm releasing numerous live young, which resemble tadpoles (trochophores?):

I've recorded a video of the worm giving birth that can be viewed here (left image below). The young seem to be stored in chambers inside of the parent, and then are pumped through the body and out the back end. While the young appear to be still in the video, some of them are quite active (right image below).

My theory at this point is that the young penetrate snails, grow inside of them, emerge and hang onto the host for a while, and then eventually dismount as free-living adults. Adult worms seem to be independent, while smaller worms hang off of the host the snail (feeding off of it?) until they're large enough to live freely.
Treatment
I would like to eliminate these worms if possible (I can't gather more snails any time soon, and they eventually kill off smaller snails). My first attempt was dosing with praziquantel, which is supposedly effective against flukes while being snail-friendly. Unfortunately, three days later, one of the snails died, and the worms appear to be unharmed.
Update: I gathered some more snails, and attempted praziquantel once again. While it did not harm the snails, it also continued to be ineffective against the worms. I have been experimenting with Seachem ParaGuard, and the results seem to be positive for minor infestations, but not against fully mature worms.
Conclusion
After some research, my best guess is that they're trematodes from the class Digenea-- They appear have sucker mouths, can parasitize snails exclusively, can have a free-swimming form, and can shed cercariae. That said, I'm not terribly confident, and would ideally like to be able to identify them more specifically.

Hi welcome to Bio.SE! This is a very well thought out and well written question that shows prior research effort on your part and provides useful pictures and specimen characteristics (including size and your location). These are all excellent qualities we hope to see in all of our questions! Thanks. Unfortunately, I find it unlikely that anyone here will know this answer. My hope is that my bounty (though little, given how unlikely I think a good response will be) will attract someone to dive in and do a little more research for a good answer. We'll see. Good luck!

Thanks a lot! If no one here can provide an answer, I'm not sure where else to turn. Anything to narrow it down a bit would helpful. I've been trying to find any parasitic worms that feature these "legs" (or even what the proper term for them is if not that), and so far my search has been futile.

I would guess the pseudopod/protoleg looking structures and the mouth parts should be the most helpful in narrowing this down...

The oral sucker and association with snails almost certainly makes this a trematode (aka fluke). The cercaria life stage usually has one or more tails, which I don't see on your specimen. However, I don't know of any adult flukes with the leg-like structures seen in your images (though this old drawing identified as Phyllodistomum americanum appears somewhat similar)

This is single handedly the best series of updates I've ever seen on a Stack Exchange post anywhere. Bravo, mate! your answer is much more possible now, I'm sure (though I admittedly don't know the answer). I am not an expert in these things so I'll have to do a bit of digging/thinking etc. -- which will take time when I can find some -- but I will try to see if I can help you with this. If you don't get an answer from me within the next few months, ping me. Boy, I hope you get a great answer for this post!

Could it be the rat lungworm which has a primary intermediate host in snails: Angiostrongylus cantonensis

I have finally figured out what these are, and it turns out I greatly misunderstood their relationship with snails.
These worms are annelids of the genus Chaetogaster, specifically Chaetogaster limnaei limnaei.

Source: Page 653 of "Fresh-water biology" (1918)
Ch. l. limnaei is unique in its genus in that lives on the bodies and in the shells of snails, including Physa spp. like the Physa acuta snails in question. While the relationship was originally thought to be parasitic by early researchers, it turns out that it's actually commensalistic (or even mutualistic in some scenarios).
From this vantage point the worms feed on various microorganisms, such as rotifers and algae, and small particles stirred up by the host snail scavenging for food. They also feed upon the cercariae and metacercariae of fluke species that parasitize the snails, even able to protect the snails from getting infected in the first place.
That said, it's not all good-- Snails with heavy infestations of Ch. l. limnaei have been shown to be less active, spending more time in their shells rather than out and foraging for food (Stoll et al., 2013). Additionally, worms have been experimentally shown to consume tissues of their hosts when food is low or nonexistent (Stoll et al., 2013).
To respond to a few points from the question:

These worms are highly specialized, and do not seem to affect ramshorn or pond snails, which I have numerous of in the same tank, in the slightest. It's only the bladder snails that end up infested.

Ch. l. limnaei is not restricted to bladder snails, and will happily live on pond snail and ramshorn species. It's possible that the bladder snails had more severe fluke infestations which the worms found preferable.

My theory at this point is that the young penetrate snails, grow inside of them, emerge and hang onto the host for a while, and then eventually dismount as free-living adults. Adult worms seem to be independent, while smaller worms hang off of the host the snail (feeding off of it?) until they're large enough to live freely.

This worm is able to reproduce both asexually through budding, but also sexually as shown here. Sexual reproduction often occurs in the winter, where the worm lives freely and reproduces sexually before returning to snail hosts in the spring.

I would like to eliminate these worms if possible

I found a blog post by someone struggling with the same problem:

One day (do not know it exactly, probably few months later) I noticed that all worms disappeared. I did not know why they were gone.
Later I found the reason in the 1974 thesis. Chaetogaster limnaei limnaei is highly sensitive to temperatures above 24 °C. Such a temperature reduces or completely eliminates these worms. Therefore, If you transport worms from their natural environment to your tropical aquarium, there is no need to worry. If you have aquaria with aquarium heater, they are bound to be killed by high temperature. Worms are killed in summer heat as well.

This seems to be accurate, as with the onset of the summer heat, I no longer have any of these worms present on my snails. Now knowing what they were, it almost feels like a shame-- They were protectors, not foes.
References

Density-dependent relationship between Chaetogaster limnaei limnaei (Oligochaeta) and the freshwater snail Physa acuta (Pulmonata)

Awesome job -- glad you figured this out!! Great answer to your wonderful post. I'm glad you're the one to figure it out, too, so you could come full circle with this. Bravo. (Also, very interesting to learn about the ecology of this organism -- thanks!)


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Why is free ribose not reduced to deoxyribose rather than the reduction occuring on ribonucleotides
I cannot understand why deoxyribonucleotides are not synthesized directly from deoxyribose, but ribonucleotides have to be synthesized first, and only then can deoxyribonucleotides be synthesized.

Clarification
I assume that question is posed in the knowledge that ribose is an intermediate in the dark reaction of photosynthesis and can be synthesized in the hexose monophosphate shunt in animals. Hence I assume that the question is not why ribose precedes deoxyribose in the metabolism of mammals and other living things. Rather, the question would seem to be why ribose is not converted directly to dexoyribose, but only after ribonucleotides have been formed (in the ribonucleotide reductase reaction).
Possible Answer
Question as to why a metabolic pathway has one form rather than another can sometimes have a chemical explanation, but in this case I suggest answers can only be speculative.
Thus, one possible answer could be:

There is no need for free deoxyribose in the cell, and that if free
  deoxyribose were produced there would be potential competitive
  inhibition of enzymes that catalyse reactions involving ribose.

If an ‘RNA world’ preceded the modern ‘DNA world’, then one could argue that:

The simplest way for the shift from an RNA genome to a DNA genome would by the introduction of a
  specific reaction for the reduction of the ribose in nucleotides. The
  fact that the base that differentiates DNA from RNA — thymine —
  is also synthesized as a nucleotide (see my answer to this
  question)
  is consistent with (but does not, of course, prove) this idea.


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How are we able to selectively inflate our cheeks?
First an observation - I noticed that I can not inflate my cheeks with my mouth open. This means that inflating cheeks is not a muscle property and that only pressure of air from lungs trapped inside my closed mouth is responsible for any inflation. Also, once inflated I can move my tongue anywhere and still retain the inflation. This means that tongue is also not responsible for air regulation inside mouth.
Moving on, we all know that we can either inflate both our cheeks, or we can inflate only cheek from one side or we can inflate *portion of face between lips and chin* (I don't know what it is actually called). Put simply, we have complete control over which part of my face would I like to inflate.
I don't understand how this is possible without muscle control? Air has tendency to occupy all space therefore my entire cheeks should get inflated without me having any control whatsoever, but as it turns out I can control and redirect the air to apply pressure only at a particular cheek without any help from tongue. How?

Why have you concluded that not being able to inflate your cheeks with your mouth open means the muscles of your mouth and face are not involved in control the space available for inflation?

I was convinced that facial muscles could only produce inflation and not contraction (mostly because we never feel contraction). A naive conclusion on my part as evident by Bryan's answer.

Muscles can only "pull" never "push" - that's just how they are organized at a molecular level. We can only push things because we use joints as levers: if you "pull" on the outside surface of your arms, you can push things out with your hands because that pull acts to extend the forearms.
It's not really possible to puff out your cheeks with muscle, because there is nothing floating in the space outside your face to pull against. Your cheeks puff up a bit when you smile, but I think you will agree that's a completely different type of "puffing" and comes from gathering up a bunch of tissue.
However, it's fairly simple to contract muscles in your face (specifically the buccinator) to prevent a cheek from bulging out by tightening the muscles in the cheek. The air pressure you are producing is pretty minimal, so it doesn't take much strength. The cheek bulges out when the muscles are relaxed, and doesn't bulge when the muscles are contracted.

Perfect. Just one follow up. When my mouth is closed and cheeks not inflated, are my cheek muscles still contracted? I ask this because when I then attempt to inflate my one cheek I do not notice any significant feeling on my other cheek of contraction or whatever. Is it because muscle contraction is so insignificant that I did not feel it, or because my facial muscles were already contracted before I attempted inflation.

@Sarthak123 I think you would get your answer reading about muscle tone. In general, though, you don't really feel muscle contraction except when it is unusually forceful (especially a cramp), and even then you may also be feeling the movement of other tissues rather than the force of the muscle itself. Think especially about all the muscles in your back and core that maintain your posture: you probably don't ever notice them and they are doing a lot more work than your cheek muscles would be.

While it's true that we don't have facial muscles to actively move our cheeks, we DO have muscles to put them under tension (I don't which specific ones that are though).
If we apply both air pressure from our lungs and tensions to (selected) cheeks, we can thereby control which regions to inflate.
As an anecdotal note: building up and using this tension is especially important for musicians playing wind instruments


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Is there any known reason why 6 leg mammals are only found in mutations?
Taking a look in internet you can find photos of mutated mammals with 6 legs. Some cows with legs in unnatural positions were shown in website versions of widely known newspapers (you can easily guess here that if the animal gets his additional legs in the back or another unuseful position why a mutation like that wont spread, but the point here it's 2 additional legs in mammals do appear occasionally) . Also there are some dubious photos of sheeps with appparently functional 6 legs, these ones are dubious and hard to confirm if real, some clearly fake but the dubious ones are there and make you wonder. Insects have 6 legs, there are confirmed mutations of mammals with 6 legs, then why did it never appear a mammal species with 6 legs. Is there any known reason why 6 leg mammals are only found in mutations? (how about size and enviroment, is there any reason in those for them not to get 6 legs?)

What make you thing that those cases are caused by mutations (in other words than leg number has a non-zero heritability) rather than some other developmental defect?

If stability is the goal, more legs tend to be better. However, having lots of legs also comes with a cost: they take energy to build and use, have extra weight, etc, and they don't really add any speed.
Insects are incredibly successful and likely evolved from many-legged ancestors, losing legs for efficiency but stopping at six. For small creatures with exoskeletons like insects, having fewer than 6 legs means too much loss of stability, because they rely on a tripod of 3 legs while moving the other three.
However, mammals and the vertebrates in general are larger and don't have exoskeletons and can use balancing and moving strategies that insects cannot. Further, they have evolved with four appendages since before they walked on land.
For a 6-legged vertebrate to evolve, there would need to be a selective advantage for having 6 legs versus 4; since vertebrates get along just fine with 4 legs, adding two more isn't likely.
I would also add that just because you can observe mammals with more than 4 legs does not necessarily mean that is a heritable trait. It could instead be caused by environmentally-induced errors in development. I think for the cases you mention this is probably most likely.

Lanham, U. N. (1951). Why do insects have six legs?. Science, 113(2945), 663-663.

Also worth pointing out that many insects have adhesive feet, and more feet allows for more adhesion. An ant with 6 legs sticks to a wall 50% better than an ant with 4 legs. Water skimming insects, too, spread the hydrophobic force over all their legs, and might fall through the surface of the water with fewer legs.

@NuclearWang Good point. Although larger mammals like OP is thinking of are certainly too large to achieve some of those feats that could benefit from extra limbs, other vertebrates have done so by having longer toes rather than extra appendages (like the Jesus lizard).


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denovo 2Gb whole genome sequencing on a small sequencer
What are the limitations of using Illumina's smaller sequencers (e.g., iSeq100, miniSeq) to do de novo whole genome sequencing on an organism with a larger genome (~2Gb)?
Naively, it seems even if I am only able to do 5Mb worth of sequencing per 24 hour run on these sequencers, after about two years of running the thing continuously, I should be able to have enough reads to be able to assemble a de novo genome sequence of a larger eukaryote (downstream bioinformatics concerns aside). Yet clearly the sequencers are never marketed like this and I'm struggling to understand why.
I am interested in GWAS on non-model vertebrates if that matters. That time frame doesn't seem crazy, as some field experiments take several years before something is publishable.

Yet clearly the sequencers are never marketed like this and I'm
  struggling to understand why.

You don't see why two years of instrument reagent costs for a single project might be considered prohibitive?


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How does heat stress kill plants?
It is known that many plants typically die when exposed to temperatures of 40 to 50°C (I believe, these figures relate to exposure times of ~1–2 hours). When a plant is heated, what is the mode of action at the cellular level that results in the death of the plant? What are the main mechanisms involved?
P.S. I have read that at high temperatures plants synthesize heat-shock proteins, so I am not sure if this plays a role in the death of the plant. Another obvious effect following heating is the damage/denaturation of some chlorophylls (but a plant should be able to survive the loss of some photosynthesis; e.g. detaching leaves will not kill a plant).
Any explanation is greatly appreciated.

High temperatures cause 'global' damage, i.e. damage to pretty much the entire plant, everywhere, in every cell. One of the most major mechanisms is denaturations of proteins in the cell; proteins misfold, aggregate, lose their structure and function, and cannot sustain the variety of metabolic and other activities in the cell. Heat shock proteins are proteins responsible for stabilizing or re-folding proteins that denature. They are expressed as a last line of defense, which can only partial protect or rescue the plant from accumulating proteinaceous debris and temperature-related damage.

And perhaps I should add that if you cause such widespread protein dysfunction, you obviously and adversely affect cell signaling, transport of metabolites, the ability of the cell to regulate its own behavior, or multiply, or generate energy, regulate water content, fight off microbial pathogens, let alone sustain the catabolic, long chain of reactions required for photosynthesis and growth. The list is very long if you go into molecular detail. And on the cellular level, plant cells survive by maintaining gradients and compartments which require a positive energy balance to upkeep.

At roughly 95F/35C the rate of carbon fixation saturates and remains fixed to higher temperatures because of state recovery in RuBisCo. In other words, the rate of photosynthesis is saturated (or maxed out) above 35C or so. However metabolic reaction rates continue to increase with increasing temperature, o the plant consumes more carbon than it fixes when temperatures are above 35C or so. Tissues need oxygen, but the solubility of oxygen in water declines with increasing temperature. Diffusion of oxygen in water increases with temperature which leads to oxygen starvation with increasing temp.

Distributed storage and parallel redundancy means it takes a lot. There are pathogens (cankers) that clog the phloem - when it girdles a trunk, roots die once their carbohydrate stores are exhausted (months) and the plant dies quickly afterward. Other pathogens clog the xylem - death follows rapidly because transpiration leads to desiccation. Application of artificial auxins and cytokinins and other phytohormones can affect phytotoxicity and kill plants. Most herbicides are artificial auxins.


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What is the purpose of the AraC gene in pGLO?
The AraC gene activates in pGLO from my understanding in the presence of arabinose. Arabinose is present as a metabolite from other metabolic in the e.coli cell. Is it that there's no termination marker, so transcription continues to the GFP gene?
In addition, does AraC contain parts that are encoded 5'->3' and 5'->3'?

The AraC gene can activate GFP expression, because the GFP in the pGLO plasmid has the negative inducible pBAD promoter:
In the absence of arabinose an AraC protein dimer binds the promotor region, but does not activate transcription. When arabinose is present, the protein binds in a different way, which allows the downstearm gene (here GFP) to be produced.
According to this plasmid map I found the AraC and GFP genes are in different orientations (and facing 'away' from each other), so transcription of AraC wouldn't run over into GFP even without a terminator present.


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What are the fibers and small droplets on the surface of dividing HeLa cells in the figure?
I did some literature searching but could not find any info probably because I did not know how people name them.

The figure is from the wikipedia entry HeLa

They are microvilli and blebs.


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Relationship between inbreeding and sterility in humans
In general, inbred individuals tend to be at increased risk of sterility as shown in cows (Gonzales-Recio, 2007) or in leghorns (Nordskog and Cheng, 1988) for examples. I only have very quickly looked at a few abstract but it seems that this effect is a bit controversial in humans with two studies showing a negative relationship between consanguinity and sterility (Rao and Inbaraj, 1979; Bittles et al., 2009) and one showing a positive relationship (Ober et al., 1999).
What is the relationship between the inbreeding coefficient $F$ and the (relative or absolute) risk of sterility in humans?
For a definition of the inbreeding coefficient, please see here, here and there or just google inbreeding coefficient.
I am looking for some function, linear or not, that describes the probability of being sterile ($P_s$) as a function of the inbreeding coefficient $F$ in humans. I am aware such measure might differ among human populations but I'll be interested in whatever we can find.

I'd note that two of the three human studies you cite re: inbred individuals are at increased risk of sterility actually show the opposite. The 1999 Ober study demonstrates decreased fecundity (not sterility) in a subset of Hutterite women, but generally, larger population based studies (Bittles is a good example) show the opposite (no decrease in fecundity, or general production of offspring). The concerns that do hold up are increased rate of major birth defects and childhood death. Once these individuals in these communities reach reproductive age, if anything, they produce more offspring.

@DeNovo Oops! Indeed! +1. I rephrased my post.


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Is there an Exit site (E-site) on the eukaryotic ribosome?
One of my professors mentioned something about the e-site (the exit site for the t-RNA) on a eukaryotic ribosome.  There was a student in the class who objected, saying that there is no e-site on eukaryotic ribosomes; it only exists on prokaryotic ribosomes.  I've tried to find some reliable source to figure out who's right, but to date the only thing I've found is an obscure sentence in a wikipedia article, which doesn't look all that official.
Is there indeed an e-site on the eukaryotic ribosome?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3331703/#s4title

http://case.edu/med/coller/Coller%20C3MB%20Lecture%201.pdf

@theforestecologist — citing a peer-reviewed publication is acceptable evidence because the references therein can be followed up. Citing somebody's lecture notes is not.

Both are acceptable. Just like citing Wikipedia is acceptable here. However, I agree that a peer-reviewed publication is often an optimal resource.

Why not do the research yourself? Download a free copy of pymol and start looking at ribosomes from the pdb database... You might want to compare bacterial and eukaryotic ribosome structures. Try identifying the A,P and E sites. It will be a nice little project and you will learn a lot doing it

@theforestecologist — Depends what you mean by acceptable. WIkipedia may not necessarily be correct, but its virtue is that it is correctable. Someone's lecture notes are surely no more likely to be correct than the professor of the question.

@David I mean that all those source types are allowed to be used on biology stack exchange without closure or deletion,and their use need not be challenged every time they're used here. If you find something to be wrong in a cited source, please point it out to the poster (or downvote the post accordingly) and include (and by all means suggest the use of) more reputable sources to support your challenge. If you have additional comments or opinions about the use of such sources, please write a [Meta] post about it. Thanks

Prelude: Thinking about protein synthesis
I remember the time when there were only two sites on the ribosome, and when it became clear there were more, I resented the need to make my lecture notes and my contribution to a venerable text book more complicated. So I am neither a devotee nor an expert on the exit site, but if asked to guess who was right (even if, or especially if, the student was supported by Campbell’s Biology as @CSharp informs us) I would put my money on the ‘professor’. Why? Because protein synthesis and the ribosome are so ancient that although there have been changes in eukaryotic proteins synthesis, something so fundamental as the sites for the fundamental process would not change.
Answer
Yes, Virginia, the eukaryotic ribosome does have an exit site.
The evidence
Although editions of the venerable text book no longer appear and my research no longer impinges on protein biosynthesis, I still collect papers on the subject with my bibliographic software. The latest relevant publication I have is by Khatter et al. from Nature in 2015, entitled Structure of the Human 80S Ribosome.
As not all list members have access to Nature, as a subscriber I have taken the liberty to reproduce a a section from the abstract (my emphasis) and a pertinent illustration:

Here we report the near-atomic structure of the human ribosome derived
  from high-resolution single-particle cryo-electron microscopy and
  atomic model building. The structure has an average resolution of 3.6A
  ̊, reaching 2.9A ̊ resolution in the most stable regions. It provides
  unprecedented insights into ribosomal RNA entities and amino acid side
  chains, notably of the transfer RNA binding sites and specific
  molecular interactions with the exit site tRNA.

The cryo-EM map and atomic coordinates have been deposited in the EMDB and Protein Data Bank under accession codes EMD-2938 and 4ug0, respectively.
I admit I haven’t researched and rehearsed the evidence, but I think that would be another question.

Here is an open access source for structural information regarding the eukaryotic ribosome, figure 3 in particular seems to contain the answer to the question being asked. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3331703/

No. According to page 369 of the 9th edition of Biochemistry by Campbell:
"The structure of the eukaryotic ribosome is different in that there is no E site, only the A and P sites."

Welcome to SE Biology, Unfortunately Campell is a general biology text book, not a more specialist biochemistry or molecular biology text, which is where you are likely to find a better coverage of ribosomes. I do not have a copy of Campbell but I see from Amazon that it is now in its 11th edition, so perhaps this mistake (see my own answer) has been corrected now.

Down voted due to low information content in the answer. You refer to a book which state the structure is different, but you do not go into much depth of how they are different. Also, how old is the book...

@CSharp Welcome to biology stack exchange! We appreciate your well-cited answer. I just wanted to ensure you that the downvotes you are getting on your answer appear to be due to the accuracy of your source and not the quality of your answer. Even downvoted answers like this are sometimes useful as they clarify a common misconception or point out inaccurate, commonly-used sources. Please don't be discouraged, and I invite you to check out our [tour] and welcome you to continue posting here. Thanks!

Further to the remark from @theforestecologist, although I think your answer incorrect I did not downvote you because you provided support for your conclusion. You were just unlucky to hit a mistake in a text book. One wonders whether that same mistake provoked the original controversy.


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Is there a feasible way to create a large number of long random DNA strands?
Suppose I want to create a large number of random DNA strands (maybe a million, or a billion, or even something close to all $4^N$ possible sequences of $N$ base pairs).  Is there an experimental way to do this?

Please do not add inappropriate tags to attract the attention of more people. It is abusing the system. I have removed both them and your aplpologia.

I'm curious, why do you want to do this?

Chemical DNA synthesis has you covered for short DNA strands.
It's possible to just use an equimolar mixture of all 4 bases when you do chemical synthesis, which results in random sequences. (This is most often used to generate barcoded primers).
The main problem with this approach is that:

chemical synthesis is not super efficient, anything above ~1-2kb will likely not be possible
If you work with a fully randomised sequence it becomes much harder to do quality control of the product (you can't sequence it).

You can also easily even calculate the probability of generating all possible sequences for a given strand length and yield.


text:
What species is this aromatic plant found in a mountainous region of Greece?
This plant was found in the Taygetos mountains, Greece, and had a lemony smell.
Small plant about a foot high.
The shiny recurved leaves are reminiscent of rosemary, and the dry seed-heads seem rather distinctive.
Any ideas of Genus or species most welcome!

The seed pods look like delphinium or a weird dwarf lilium species. Perhaps it is a mountain Lilly species. google lens said lilium and perhaps a weird heather variant. http://www.flora.dempstercountry.org/V.B.28.Ericaceae/Phyllo.empe/Phyllo.empe.pic1.jpg

@LifeInTheTrees - neither of the plants you mentioned are aromatic.

@anongoodnurse I had another look at this and now I'm pretty sure it's a Hypericum..

After taking another look at this, I think it's almost certainly a Hypericum species. Compare with Hypericum empetrifolium.
The fruit of Hypericum are very distinctive:
https://www.inaturalist.org/observations/104581263

The narrow revolute leaves of H. empetrifolium are also unlike other Hypericum species:
https://www.inaturalist.org/observations/69680320

Geographic distribution seems right:
https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:433403-1

A type of greek lavender with no blossoms anymore?
https://www.florealpes.com/photos/lavandulastoechias_5.jpg?PHPSESSID=0a72039f5036d91c7df80dd406b795b0

The desiccated seed heads seem like nothing that would come from a lavender flower though..


text:
For a luekemia patient - how does the chemotherapy fixes the bone marrow to not produce immature cells
For ALL patient this link says 90% of the children are cured.   It has high survival rate. From what I understand is that - luekemia is type of cancer where the immature cells does not turn into mature cells. How does the chemotherapy with other drugs - fixes the bone marrow immature cells defect?
What are the survival rates for acute lymphoblastic leukemia?
About 98 percent of children with ALL go into remission within weeks after starting treatment.
About 90 percent of those children can be cured. Patients are considered cured after 10 years in remission.

Chemotherapy in general works by killing (hopefully all) cancerous cells, while leaving the patient / healthy cells alive.
The drugs used for this usually are in principle toxins/poisons, but are more deadly to cancer cells, since these cells are growing very quickly compared to healthy cells. This general strategy is true for a lot of different types of drugs (and cancers). However, because the drugs are still generally toxic they are hard to dose correctly and also the reason why chemotherapy often has quite strong side-effects.
Additionally cancer can quickly evolve to gain resistance to specific drugs, which is why nowadays often a combination of multiple drugs at once is used.
In leukemia - which is a form of cancer where the blood and immune cell precursor cells in the bone marrow become cancerous - additional ways of selectively killing the cancer are radiation therapy (of the affected bones) and in some cases complete bone marrow transplants (which have their own issues, so they are not usually  used as first option).


text:
Are modern gene-editing techniques capable of creating genetically-superior versions of humans?
Can we alter the DNA in, say, a small-framed, low muscle mass male to those of elite bodybuilders?
Can we alter the DNA sequence that stops balding and hair loss? How about the genes responsible for bone metabolism, hormonal profiles, and the entire endocrine/hard tissue foundation of humans?
Can we alter the genes responsible for looks and alter them so they make an ugly personal hotter?
Basically, summarize this to: "Can gene editing create genetically-advanced versions of ourselves?"
Uglier prettier? Shorter taller? Weaker to stronger? Slower to faster? Dumber to smarter?

Please don't flag this as "vague." I make it clear by labeling "genetically-superior" as basically "any advancement of one's current genetics and gene expression to a superior level" as previously explained.

For example, genes limit muscle growth and can make what is known in gym culture as a "hard gainer" or "non-responded" AKA someone who works out and does not make much progress due to genes. Superior version of this would be one extending this possibility or altering it to a more fashionable and fulfilling extent where muscle building genes are then more comparable to elite-genetic bodybuilders or at least closer to this goal. Same with genes and hormones, soft/hard tissue, looks, and all the way to intrinsic, internal abilities like learning ability, intelligence and etc.

When you say alter the DNA, do you mean at adult age or at the stage of the zygote?

@Remi.b Adult age I mean.

Short answer is clearly "No", then. You might want to read about 'gene therapy' to see what we can do and what are the classical difficulties of such therapies.

So I guess the only way people can be stronger and prettier would be surgery and drugs....

How about eating healthy, and having a healthy level of physical activities?!

@Remi.b Eating healthy and going to the gym doesn't make an ugly face sexy.

You said "stronger and prettier", not pretty face. You can definitely get stronger through the appropriate physical activity 2) healthy lifestyle improves skin and eyes appearance.

@Remi.b Yeah, I don't doubt it's possible to improve somewhat, but often it's not enough if you don't have the genetics in the first place. What I mean is that all the health/exercise in the world won't make an average, plain person to be more beautiful -- only cosmetic surgery and etc. has a better shot at that.

No, this is still science fiction. There have some of experimental efforts to correct very simple, monogenic, diseases. Some of experiments seem to have helped the patient, many were ineffective, and some killed the patient or gave them cancer. Gene therapy in humans in still in the very early experimental stage. On top of that, the traits you are talking about are almost certainly governed by multiple genes, and the genetic networks are "incompletely understood", to put it mildly.

Is there a such thing as "beauty genes?" Are people born to be potentially attractive determined by genes -- or is physical attraction a combination of genes and environment? Some people not born goodlooking cosmetically achieved some level of "beautification" so it's a complicated issue I get, yeah.

@FullofPowers Clearly children tend to look like their parents, so much of our appearance is determined by genetics, However, the details involve the interaction of hundreds of genes and gene regulatory regions. Even the genetics of something as straightforward as height is still poorly understood. Something as nebulous as beauty is going to be even more difficult to analyze.

So it's possible that one can predict a threshold or range of attractiveness potential genetically?

@FullofPowers , no, that's not what I wrote. It's even more complicated then height, because unlike height which is an objective measurement, beauty or attractiveness have strong cultural components.

I don't know about that. It's pretty clear that beauty is very objective, even if also somewhat subjective too.

Look for example at people popularized in the media (celebrities, models, etc.); those non-famous who are regarded as attractive more so than others; those who live better lives due to their appearance; etc. It's hard to argue that beauty is "very subjective" when we can measure down all of the so-called factors that influence facial beauty in males and females, even if slight subjectivity always exists.

For example, AI can already look over pictures of people and make smart "guesses" as to which are more attractive based on symmetry, face shape, facial balance/proportions, EME angle, FWHR, feature shape, etc.


text:
What does the concept of information mean in biology?
We use a lot of borrowed analogies from other sciences; linguistics, computational sciences but what do we really mean, mean with information in living systems?

bioinformatics can be a research topic.

The word "information" is not borrowed from any other science, it is borrowed from the English language. The genetic code, for example, was deciphered before most University Computing Science departments were established. This question is both basic and wide. I would start by reading about the genetic code, which is used to encode a certain subset of genetic information. If your background is such that you can't understand the Wikipedia entry or other web accounts, you need to buy and read a molecular biology text.


text:
How exactly does heterozygous sickle trait help patients survive malaria
Heterozygous sickle cell anaemia trait is known to increase the survival rate of carriers to malaria attacks. How does a recessive gene not expressed in the phenotype allow for such an advantage? Is the red blood cell of a recessive carrier structurally different from that of a non-carrier?

Sickle cell anemia is characterized by the formation of sickle shaped red blood cells rather than the usual biconcave ones. For a double recessive homozygous genotypic person, i.e. an infected person, this causes severe lack of oxygen diffusion into the RBCs because of defective haemoglobin production.
In case of a carrier, he/she carries the gene for the defective version of haemoglobin but does not show the symptoms for the disease.
The malarial agent, Plasmodium uses haemoglobin, or more specifically haem as its main nutrient source The defective sickle haemoglobin induces the expression of heme oxygenase-1 (HO-1) enzyme in hematopoietic cells (those which produce erythrocytes, for example marrow of long bones). Carbon monoxide (CO), a byproduct of heme catabolism by HO-1, prevents further accumulation of circulating free heme after the infection by Plasmodium. This decreases the pathogenicity of the organism and prevents the disease from occuring.  Moreover, sickle haemoglobin inhibits activation and/or expansion of T lymphocytes (specifically CD8+T cells), which recognize the antigens expressed by Plasmodium and hence do not attack it. This is an immunoregulatory effect that does not involve the heme oxygenase enzyme.
This leads to the carrier person having innate resistance to malaria (or at least Experimental Cerebral Malaria )
And no, the RBC itself is not structurally different. Though there might be some
sickle shaped RBCs in the blood, their number is very less. The major difference comes from the haemoglobin in the red blood cell.
Here is the original paper which explains the phenomenon in detail.


text:
Do we know which traits reside in which chromosome? If not, how about the next 10 years?
Assuming we develop a technology that allows us to make human gametes (sperm & eggs) combining chromosomes from different persons. Thus we take 1st chromosome from 1st person, 2nd chromosome from 2nd person, 3rd from 3rd etc. Afterward we combine them and make a gamete (sperm or egg)
Do we know which traits reside in which chromosome in order to make that technology useful? If we don't know now, how about in next 10 years.
The only thing I could find is that we know which chromosome hosts genes for certain diseases.
P.S.
This question was originally asked on world building where it was closed as off-topic.

We know the location on the chromosomes of most of the genes in the human genome. You can go to the UCSC or Ensembl genome browsers and look up the positions of most of the genes, and many other features of the human genome.
There may be some genes we haven't recognized yet, but the real issue with what you are asking is that biology typically isn't as simple as "one gene" = "one trait".
The simplified picture is that one gene is the recipe for one protein, but even that isn't strictly true. We now know that one gene may make several variations on a protein through a process called splicing. Furthermore most "traits" will arise through the interactions of dozens of proteins. On top of that there is the issue of which proteins are produced when, and in which cells. Some of this is controlled by regulatory regions, and we're still very much at the beginning of finding all the regulatory regions and how they work together.
To give you an idea of how complex this is: human height is known to be strongly heritable. We've identified about 400 regions of the human genome (genes and regulatory sequences) that have a significant effect on height. However, taken together, the variation in human height explained by these 400 regions explains only about 20% of the observed heritable variation. In other words there is a great deal about the genetics of height that we simply don't understand yet.
There have been experimental efforts to treat simple genetic diseases in humans by substituting or adding "healthy" versions of genes into people who have a non-functioning copy of some critical gene, but we're many decades away from creating whole gametes by cut and pasting multiple genes together. There is considerable ethical and political opposition to the development of such techniques.


text:
Examples of striking/pedagogic large dataset analysis in biology
This question belongs in "Cross-Validated" as well as "Biology"
I am looking for example datasets that I could use both for teaching and for my personal training, that would be good examples of very successful applications of in silico data analysis tools.
I am interested in tools like: k-means or hierachical clustering, principal component analysis, generalized linear models, or basic machine learning like class discovery & prediction.
Of course, if the data is available, that would be even better, but a simple figure in a paper would work as well.
What I mean by good is "fairly unambiguous and demonstrative", ie. the results could be, for example, a dichotomy of the dataset into two or three groups that make sense from a biological point of view (e.g. different tissues of the same organ, different times in cell development...).
A good example would be, for example, this figure:

(From Handschuh et al, Int J Oncol (2017) Copyright Spandidos Publications)
Rows are genes (microarray expression analysis) and columns are healthy (HV) or cancer patients (AML); clustering makes two large clusters appear.
It is a really good example because we can easily check that the two clusters match the two types of patient samples, which makes this clustering a good, pedagogic case study.
In other words I am looking for striking examples of how the visualized data makes perfect sense, if properly analyzed.


text:
What happens when the bacteria in the petri dish lack nutrients for long time?
If I put some E.coli in a petri dish filled with limited nutrition in room temperature and forget them for months or years. What will happen in the final after they overgrowth and used all nutrition left? Will they die or just stop dividing?

They will die, eventually.
The requirement for energy is a thermodynamic constraint; maintaining cellular structures, repairing molecules that spontaneously damage etc takes some energy, and E. coli is not able to reach a level of quiescence sufficient to survive for years. However some cells might survive longer than expected if they enter low-metabolic activity states; that would not be enough to survive years in a petri dish, though.
Note that other species may be able to survive, through special stress-induced processes such as sporulation or cryptobiosis.