What is the function of dreaming? Does a particular hormone secretion interfere with dreaming? Why do some people dream more?

Dreams are hallucinations that occur during certain stages of sleep. They’re strongest during REM sleep, or the rapid eye movement stage, when you may be less likely to recall your dream.
Research is yet to reveal the true reason of dreams. But we know for sure it is not one reason.

Speculated Reasons:

1. Dreams as fight-or-flight training

One of the areas of the brain that’s most active during dreaming is the amygdala. The amygdala is the part of the brain associated with the survival instinct and the fight-or-flight response.

One theory suggests that because the amygdala is more active during sleep than in your waking life, it may be the brain’s way of getting you ready to deal with a threat.

2. Dreams as memory aides

One widely held theory about the purpose of dreams is that they help you store important memories and things you’ve learned, get rid of unimportant memories, and sort through complicated thoughts and feelings.

Research shows that sleep helps store memories. If you learn new information and sleep on it, you’ll be able to recall it better than if asked to remember that information without the benefit of sleep.

How dreams affect memory storage and recall isn’t clearly understood yet.

3. Creative times!

One theory for why we dream is that it helps facilitate our creative tendencies. Artists of all kinds credit dreams with inspiring some of their most creative work. You may have awakened at times in your life with a great idea for a movie or a song, too.
Without the logical part of the brain working, emotional and illogical thoughts take over your mind!

Eectroencephalography (EEG), electro-oculography (EOG), and
electromyography (EMG) are used to monitor neurological data from the brain to reveal information about neurological activities in the sleeping brain.

Here is a scientific literature (pdf) you can go through for in-depth study ( this link leads to ResearchGate page, you can read it there or download the pdf) :
https://www.researchgate.net/publication/281071308_The_Role_of_Dreams_in_the_Evolution_of_the_Human_Mind


Are there dangers to Teflon and aluminium cookware?

The US Department of Health and Human Services has a nice set of factsheets on aluminum. In brief, and to specifically answer your questions, they point out that:

Aluminum occurs naturally in air, water, soil, and plants.
The amounts of aluminum that we encounter in pots and pans are considered to be safe for healthy people. Cooking acidic foods in aluminum pots increases the amount ingested, but is still considered to be safe; and it still represents many times less aluminum than in over-the-counter antacids, which are also considered safe.
Much of the aluminum we ingest leaves ones body naturally through the digestive system (that is, feces), and is not taken up into the bloodstream. The small amount of aluminum that makes it to our bloodstream is mostly quickly eliminated in urine. Those with kindey problems may not process this bloodstream aluminum as quickly.

Nonstick pan coatings are a little more difficult, probably because they're so diverse. Cookware isn't even mentioned as a source on the factsheet for perflouroalkyls, the chemical which has been mentioned in connection with nonstick pan health issues. The US Environmental Protection Agency FAQ says:

  Consumer products made with perfluorochemicals include some non-stick cookware ... Consumer products made with fluoropolymers and fluorinated telomers, such as Teflon and other trademark products, are not PFOA. PFOA is used as a processing aid in the manufacture of fluoropolymers and can be also be produced by the breakdown of some fluorinated telomers [NB. I assume they mean overheating nonstick pans]. The information that EPA has available does not indicate that the routine use of consumer products poses a concern.


Can twins that develop in separate sacs but share the same placenta be identical?

they were both in different sacs when developing but shared the same
placenta

This suggests that they were monochorionic diamniotic twins, which would mean they are monozygotic, i.e. identical.


How to translate a blood type used in Eastern Europe?

It is a direct correlation between the ABO blood groups and the Roman numerals.

 O: I

 A: II

 B: III

AB: IV

This numeric system was pioneered by Jan Jansky of Czechoslovakia in the early 20th century. Apparently it is still used in some former Soviet states.

Erb IH. 1940. Blood Group Classification (A Plea for Uniformity). Can Med Assoc J 42(5):418-421.


Can retroviral delivery systems "overwrite" genes?

Retroviruses, such as HIV, have a genome that is composed of RNA.  Once inside the host cell, that RNA is reverse-transcribed into DNA; it is that DNA which is inserted into the host genome.  All retroviral genomes are integrated through insertion; there is never any replacement.

Some retroviruses do, however, disrupt normal gene function.  Mouse mammary tumor virus (MMTV) or Human T-lymphotropic viurs (HTLV) will often insert inside or near host genes termed "oncogenes," that, when disrupted, can lead to cancer formation.1,2  Viruses could cause up to 15% of cancers in humans.3  So, no actual genetic replacement, but there can definitely be genetic disruption and a deleterious functional change.

This ability, to insert new genes, has recently been touted as a new way to cure many diseases.  Here's the most recent case, where the researchers used a retroviral backbone to insert a functional gene into some children; i.e., genetic engineering (Side note: Every time you see an article saying how scientists used HIV to cure a disease or something, this is what they mean.  It's akin to calling dental X-rays "giant death lasers that fight cavities.").  With luck we will get better and better at it, but right now it's only successful in limited cases for very specific diseases; massive genetic engineering of humans is still far off (unless you count bone marrow transplants).


How does the stem-loop cause intrinsic transcription termination?

There are two mechanisms of transcriptional termination in prokaryotes.  The one shown here is "rho-dependent" because it involves rho, a DNA-RNA helicase that loads on and unwinds the RNA from the DNA, terminating the elongation by the polymerase.  Check out [1] which shows a model for how rho multimers move through the RNA.

The other mechanism involves just a hairpin. The paper [2], especially Page 23, part C, shows how "rho-independent" or "intrinsic" termination works.  Basically, the hairpin slows down the polymerase and destabilizes the transcription bubble, allowing the intrinsically-weaker A:U bonds to fall apart.

There is no requirement for a hairpin in rho-dependent termination, and I think the movie is mixing them up.

 Geiselmann J, Wang Y, Seifried SE, von Hippel PH. 1993. A physical model for the translocation and helicase activities of Escherichia coli transcription termination protein Rho. Proceedings of the National Academy of Sciences of the United States of America 90: 7754–8. [pdf]
 Datta K, von Hippel PH. 2008. Direct spectroscopic study of reconstituted transcription complexes reveals that intrinsic termination is driven primarily by thermodynamic destabilization of the nucleic acid framework. The Journal of biological chemistry 283: 3537–49. [pdf]


The is something called the Pressure Stiffening Effect (turn on a coiled garden hose and watch it try and uncoil for instance), pressure in the fluid filled xylem stiffens the root, making it harder to pull out, Roots are rarely completely vertical or straight to pulling them from the soil generally involves them flexing, which the stiffening pressure resists. its the same reason an Inverted Y of steel can anchor in soil but an inverted Y of rope will not, the steel resists bending thus you have to displace all the soil above it to remove it.


How to clone and sequence a gene transcript of unknown sequence?

Perhaps you can draw inspiration from classic paper on lambda cloning:  Maniatis T, Hardison RC, Lacy E, Lauer J, O’Connell C, Quon D, Sim GK, Efstratiadis A. 1978. The isolation of structural genes from libraries of eucaryotic DNA. Cell 15: 687–701.

Try selecting tissues from the animal which you think is "enriched" (i.e. highly expressed) for the specific gene you're looking for. This might take a little bit of guessing. For example, if gene A is very highly expressed in tissue B, then you can "assume" most of the mRNA transcripts will be for that of gene A. Do a RNA purification, RT-PCR, and clone the cDNA into lambda vectors and pick plaques. With a little bit of luck, you'll be able to identify the gene by cloning, hybridisation, and subsequent chromosome "walking" to determine it's structural origin.

This was done back in the day to identify novel genes way before genomics, sequencing, or even PCR!


Calcium for Humans: Supplements vs Fortified Sources

This is close to a personal medical question, so I'll try and be vague and avoid advice.

There's nothing inherently bad about calcium supplements, and those links and thousands of others that are easy to find tend to all say that same thing.  Basically, for typical people on a typical diet, enough calcium is supplied through food that supplements are unnecessary.  The problem arises when people take too many supplements, such that their intake is significantly higher than the daily recommended intake.  These people can experience a number of symptoms, including kidney and heart failure.  Fortified food and supplements are, as best as I can tell, no different, except that food is simpler route for intake with built-in limit-setting.  That is, you can easily pop five calcium pills (BAD IDEA) but nobody is ever going to drink five containers of fortified soy "milk" on a whim.

My go-to example is that of astronauts.  Astronauts who are in space for extended periods of time must take calcium supplements, in addition to a strict exercise regimen to help stem the tide of bone loss.  Bone loss still occurs, however, because they can only take so much calcium before it starts to cause serious heart problems.  There's nothing inherently wrong with calcium supplements but for most people they are completely unnecessary.  You should talk to your primary care physician and perhaps a dietician.


Organisms that contain rare chemical elements

All the elements you mention (B, Fl, Si, V, Cr, Se and Ti) are listed as (probable) essential trace elements in humans by the World Health Organization. The WHO document "Trace elements in human nutrition and health" mentions a host of studies addressing the functions of these elements in species ranging from bacteria and plants to primates. The following list provides some of the functions these trace elements have in humans:

Boron - essential for cell membrane characteristics and transmembrane signaling (Nielsen, 1991);
Fluoride - necessary for the prevention of caries and it is associated with bone health (WHO);
Silicium - probably essential for healthy connective tissue and bone (WHO);
Vanadium - possible role as an enzyme cofactor and in hormone, glucose, lipid, bone and tooth metabolism (WHO).
Chromium - essential trace element that potentiates insulin action and thus
influences carbohydrate, lipid and protein metabolism (WHO);
Selenium - essential component of one of the antioxidant defense systems of the body (WHO);
Tin - expected to have a function in the tertiary structure of proteins (WHO).

References
Nielsen, FASEB 1991; 5: 2661-7
WHO, Trace elements in human nutrition and health 1991


Is Richard Dawkins's interpretation of the theory of evolution circularly?

The following is more an extended comment than an answer...

Why the question is off-topic

Your question has actually nothing to do with biology. You are looking for a purpose behind the existence of organisms. Science does not care about purpose, nothing has a purpose, everything just happen mechanically. If the theory of evolution gives you a bad feeling, then I am sorry for you that it does but that point is not to be discussed on a science forum. I am voting to close for this reason.

Tautology

Please note that evolution is the science that has for goal to explain the change in allele frequency through time. The process studied is a continuous succession of reproduction and therefore in some respect a repetitive process but it does not make the explanation of how change in allele frequency occur a tautologic explanation. You will note by the way, that evolution does not explain the origin of life, this is the role of another of field of biology that we call abiogenesis.

Did you say Dawkins's theory of evolution?!

I often get a little mad when people write Darwin's theory of evolution thinking this is a modern concept. But writing Dawkins's theory of evolution is even worst. Dawkins is foremost a popular science communicator, so there is really no such thing as Dawkins's theory of evolution. Dawkins was also a researcher before and he brought some knowledge that allowed to grow our theory of evolution which we call the modern evolutionary synthesis (some argue that we should rename it Extended evolutionary synthesis in the light of recent discoveries).


What are the reasons that soap has so different smell and flavour?

It is possible for a substance to not smell very much, but to taste very strongly - chili peppers are a great example. They (in my experience) have a rather weak spicy odor, but the taste is much much more intense. In the case of soaps, very small amounts of essential oils are used to give soaps their odors. You may be able to slightly taste them were you to eat some of the soap (definitely NOT recommended!), but the major taste you'd experience is the actual soap - the saponified surfactants that do the cleaning.


Based on the fruits, leaves and tendrils, it looks quite like Bryonia dioica (which is toxic). It is almost certainly something from the same family (Cucurbitaceae, which often make such tendrils and usually have similar leaf shapes) and could even be the same genus, Bryonia, which is present in the Mediterranean region (there's even a cretica species). Based on images found on the internet, leaf shape seems variable (more or less indented).


Short Answer

Yes, you could hear, but it would be harder to localize sounds.

Longer Answer

The "ear" from a biological perspective includes the inner ear which is all of course necessary for hearing.

The external part of the ear is called the pinna/pinnae (plural), and yes, you can hear without pinnae; that's essentially what you do when you use in-ear headphones since they project right into the auditory canal and don't use the pinnae at all.

However, the pinnae are important both for collecting sound (therefore increasing the amplitude) and for sound localization, because they both shape the volume of sounds depending on direction (you can localize continuous sound by turning your head back and forth) and have a vital contribution to the head related transfer function that is crucial for localizing sound in elevation.

Sound localization experiments that use in-ear headphones sometimes first record the head-related transfer function with a microphone in the ear to then apply this filter to sounds that are played. This varies somewhat from individual to individual and captures the unique shape and position of the pinnae.

Note that sound localization is not only important for knowing where sounds are coming from, it can also be important to identify and pay attention to auditory objects, especially in noise, like one person talking in a cocktail party.

Algazi, V. R., Duda, R. O., Duraiswami, R., Gumerov, N. A., & Tang, Z. (2002). Approximating the head-related transfer function using simple geometric models of the head and torso. The Journal of the Acoustical Society of America, 112(5), 2053-2064.

Batteau, D. W. (1967). The role of the pinna in human localization. Proc. R. Soc. Lond. B, 168(1011), 158-180.

Brungart, D. S., & Rabinowitz, W. M. (1999). Auditory localization of nearby sources. Head-related transfer functions. The Journal of the Acoustical Society of America, 106(3), 1465-1479.

Hofman, P. M., Van Riswick, J. G., & Van Opstal, A. J. (1998). Relearning sound localization with new ears. Nature neuroscience, 1(5), 417.

Wenzel, E. M., Arruda, M., Kistler, D. J., & Wightman, F. L. (1993). Localization using nonindividualized head‐related transfer functions. The Journal of the Acoustical Society of America, 94(1), 111-123.


Why does my grass luminesce when I step on it?

If it were fireflies or glow-worms, you would have seen them pretty quickly with your searching and collection of grass. I would guess that this is some kind of bioluminescence caused by bacteria or Dinoflagellate.  I have seen this effect when walking on wet sand at the ocean. It is quite fascinating and fun to watch. According to wikipedia, bioluminescent bacteria and Dinoflagellate can exist in fresh water. The moisture in your yard might be enough to support their growth.

https://en.wikipedia.org/wiki/Bioluminescent_bacteria

https://en.wikipedia.org/wiki/Dinoflagellate :

  The luminescence occurs as a brief (0.1 sec) blue flash (max 476 nm) when stimulated, usually by mechanical disturbance. Therefore, when mechanically stimulated—by boat, swimming, or waves, for example—a blue sparkling light can be seen emanating from the sea surface.[66]


A feedback loop is a network structure in which the gene is able to regulate itself via a single path.

$A\rightarrow B\rightarrow C\rightarrow A$

Interactions can be called positive or negative depending on their effect on the downstream gene. If a gene A represses another gene B, then it is a negative interaction; when it activates then the interaction is positive.

If you multiply the signs of all the interactions in the path from gene-A back to itself you will get the sign of the loop.

So a positive FBL will result (in the above example) if :

A activates (+) B; B activates (+) C; C activates (+) A
A represses (-) B; B activates (+) C; C represses (-) A
A activates (+) B; B represses (-) C; C represses (-) A
A represses (-) B; B represses (-) C; C activates (+) A

Any other combination of interaction will result in a negative feedback loop.

Differences are based on their properties. I'll mention two main unique properties of each.

PFBL

Switching circuits
Hysteresis

NFBL

Expression control (feedback control)
Oscillations

Similarity: well, nothing more that they both are called feedback loops and the topology is similar (just the nature of interaction is different).


Does DNA polymerase always go the same direction?

Summary:
In bacteria or organisms with only one well defined replication origin and a circular chromosome, yes for a given DNA region the same strand is replicated discontinuously.
In high order animals, which replicate chromosomes using several origins of replication (ori), this is less clear as the way ori are recognized is still not fully understood but seems to involve DNA structure. Chromatin structure is dynamic which means ori are also likely dynamic which results in defined regions of the DNA not likely to always be replicated discontinuously from a well defined strand (i.e. DNA replication might not always start at the exact same sites).

First off, as you probably know, DNA is always transcribed in a 5' to 3' direction. The why is nicely answered in this post.
DNA replication forks start at replication origins. Replication origins are recognized by origin recognition complexes. The way DNA replication occurs is by having two DNA polymerase complexes traveling in opposite direction (i.e. two bidirectional replication forks) from the origin as shown in the following schema:

This means that given constant origins of replication in an organism (like bacteria which usually only have only a single origin of replication) and given the DNA is replicated in a 5'-3' direction, same strands will be replicated discontinuously from the origin (i.e. in the schema, the bottom one on the left and the top one on the right). A global view of the replication at the chromosome level in bacteria is shown here below:

Now for more complex organisms, the origin of replication is not a single site but rather multiple ones across chromosomes (30'000-50'000 ori in humans). Where does DNA replication starts exactly, this is still not fully understood. DNA sequence is likely to play a role but no highly conserved consensus sequences were found and it is believed that origins of replication are linked to the structure of the DNA instead. In essence the chromatin structure is what seems to dictate where DNA replication starts and as the chromatin structure is dynamic within a cell, it is likely that origins of replication are also dynamic therefore making the identification of the discontinuously replicated strands very difficult (Méchali M, 2010).
Finally if you wonder what happens when two replication forks collide, well the answer is simple, replication stops and the two DNA polymerase complexes leave the DNA.


Did the Britons 100 years ago have different intestinal flora and fauna?

Who said they did not have the same problems? I'm sure they did and I'm sure most of them had horrible diarrhea.

A quick google search brought up Man and Microbes: Disease and Plagues in History and Modern Times, by Arno Karlen which states that

  In 1817, when the first cholera pandemic began [...]. In Calcutta and Jessore, cholera killed 5,000 British soldiers within weeks

However, those who survived would get used to it eventually. Cholera is much more serious than simple dysentery of course but its main symptom is also diarrhea.

The locals of wherever you happen to be are used to the pathogens that are common in the drinking water. If I am not from a place and drink water with new pathogens, I will be sick. I will also, however, eventually get over it and my body will be used to them. Depending on the details, either because I have developed an immunity or because I have developed the necessary intestinal fauna to deal with it.

So while the intestinal fauna may indeed have changed over time, this has absolutely nothing to do with what you're asking. First because your assumption is wrong (the British were subjected to the same health issues as modern Europeans visiting Asia) and second because people adapt.


How do I deal with sticky and viscous samples from cell lysates?

Yes, it is the genomic DNA that is causing you trouble. Although a brief 1000g spin should bring it all down, the pellet is never tight and you almost always are going to pull up some gunk with the clear supernatant. A better solution is to include a quick sonication step (5-10s) before the 1000g spin. That way, the DNA is sheared and it should pellet better. It has worked for me most times. Also, remember to use a reasonable volume of SDS buffer when you lyse the cells. Too little buffer and its always going to be hard. For comparison, I use about 200ul per 1ml culture pellet and this volume works well for both pre- and post-induced cells.


I am sure you have done it; just a note to others: do a PCR screen to
ascertain that the plasmid is there.
For minipreps you generally do not need a starter culture.
If you have screened your clones and now just want to amplify and keep the plasmid for cloning purposes then go for a maxiprep with 200-400ml cultures.
Do not overgrow the cells, your extraction becomes difficult and you would get even worse yields. Just set up a huge culture and pool the cells before extraction. Always seed and harvest cells that are in exponential growth phase.
If you need to screen the plasmid for clones or something then do a colony PCR, keep the colony inoculated in a small culture (make a temporary glycerol stock if your screening is taking time). If screen is positive then incoulate the starter culture for maxiprep/gigaprep culture with this stock.


This refers to haplotype phase (aka gametic phase). This essentially means knowing which allele belongs to which copy of the chromosome, or alternatively, which alleles appear together on the same chromosome.

In short-read sequencing, for example, it is difficult to resolve the haplotype of two heterozygous SNPs if they have not been covered by the same read. If you observe A/a and B/b, you do not know whether you have AB + ab or aB + Ab. So you would say you do not know the phasing.

See the Wikipedia links for more information.


what is the exact definition of entdothelial cell fenestrae?

Fenestrae are basically holes within the cytoplasm of the squamous cell, that allow the transmission of macromolecules, therefore, according to the two options you've provided, your second example is the correct one.


How long does foreign DNA stay intact in human blood?

The De Vlaminck Lab has extensively studied the origins of circulating cell-free DNA (cfDNA) in human plasma and its utility in detecting infections and organ injury.1,2  Concerning your question of parasite DNA detection and parsing signal from noise, I don't think you'll find a better resource than their 2020 publication in Microbiome.3
If the (uncited) claims on their website are to be believed, cfDNA from all sources is cleared within one hour after release into the blood.

Our research pursues technologies and applications of cell-free DNA in infectious and immune-related disease. The great promise of cfDNA in diagnostic medicine derives from i) its abundance: 10-100 billion molecules of cell-free DNA can be isolated from just 1 mL of plasma. The combined DNA sequence of these molecules is sufficient to cover the human genome 1,000 to 10,000 fold. ii) Its origin: cell-free DNA is derived from dead cells and comprises rich information about cells in the blood and any vascularized tissue that can be accessed noninvasively. iii) Its short lifetime: cell-free DNA is cleared from the blood within 60 minutes. Cell-free DNA therefore provides a very dynamic window into health.

References

Burnham P, Kim MS, Agbor-Enoh S, Luikart H, Valantine HA, Khush KK, De Vlaminck I. Single-stranded DNA library preparation uncovers the origin and diversity of ultrashort cell-free DNA in plasma. Sci Rep. 2016 Jun 14;6:27859.
Cheng AP, Burnham P, Lee JR, Cheng MP, Suthanthiran M, Dadhania D, De Vlaminck I. A cell-free DNA metagenomic sequencing assay that integrates the host injury response to infection. Proc Natl Acad Sci U S A. 2019 Sep 10;116(37):18738-18744.
Burnham P, Gomez-Lopez N, Heyang M, Cheng AP, Lenz JS, Dadhania DM, Lee JR, Suthanthiran M, Romero R, De Vlaminck I. Separating the signal from the noise in metagenomic cell-free DNA sequencing. Microbiome. 2020 Feb 11;8(1):18.


The statement in your first paragraph is correct: for yeast to ferment a carbohydrate it must be fed into the glycolytic pathway which, in the case of oligomers of glucose (e.g. mannose) simply means breaking the oligomer into its constituent glucose monomers using a single enzyme. This is similar to how yeast processes sucrose: the disaccharide is hydrolysed by invertase to release glucose (fed directly into glycolysis) and fructose (fed into glycolysis via fructokinase).

A separate mannose pathway would require a completely new set of enzymes that somehow processed mannose in a stepwise fashion without breaking the glycosidic bond linking the two monomers - I'm sure that you can see that this is a much less likely option in terms of the evolution of yeast metabolism.


How does a thymidine block halt DNA synthesis?

Excess thymidine in a mitotic cell generates negative feedback on the production of deoxycytidine triphosphate from cytidine-5'-phosphate. Excess quantities of deoxyadenosine and deoxyguanosine also block progression through S-phase. However, as a reagent for the control of replication timing, thymidine has been found to work best as its blocking activity can be applied and reversed more consistently.

Xeros N. (1962) Deoxyriboside Control and Synchronization of Mitosis. Nature 194: 682-683.


Biopython and the other bio-programming languages typically have examples of how to do this kind of thing.

For example here is some python code for calculating some of these:

http://biopython.org/w/index.php?title=ProtParam&redirect=no

Many of the propensity scales are in this database:
http://www.genome.jp/aaindex/

And there are also biojava classes for accessing these. Essentially you will need to know what these physicochemical properties are and get access to a scale for converting the letter to a numerical value.


Horizontal gene transfer versus convergent evolution

Without any molecular evidence you could infer convergent evolution if the species being compared shared a common ancestor that lacked the trait in question.

With genomic and developmental data you would measure the degree of similarity shared between the relative factors in each species. Little or no similarity indicates convergent evolution.

Horizontal gene transfer is predominantly found in bacteria. Although there are examples of limited gene transfer in eukaryotes, the donor is almost always bacteria. And there are currently no known cases of multi-gene transmission of complex networks.

It is interesting to contemplate how a full network might be transmitted horizontally. Horizontal Network Transfer would first require a mechanism for segregating the relevant genes from the rest of the genome. It would also require invasive machinery that allows the large amount of foreign genetic material to bypass the host's defense systems. Furthermore, integration of a foreign network is increasingly more difficult with the more genes you transmit due to positional and regulatory effects of the host genome. And on top of that, it is highly unlikely that a full complement of genes involved in a complex developmental process would function in any way resembling eye or wing development. These networks have been coevolving within massively complex genomic environments for hundreds of millions of years. Expressing a large network in a foreign cell would likely prove toxic.

A looser definition of HGT might include bioengineering, specifically stable transgene integration.


Is it possible for a human to wake up in a wrong way?

I did a quick search and found some research in this area. Sleep inertia is the technical term for feeling groggy for a while after waking up.

In a review article by Patricia Tassi, Alain Muzet (Sleep inertia. Sleep Medicine Reviews. Volume 4, Issue 4, August 2000, Pages 341–353), they define sleep inertia as

  Sleep inertia is a transitional state of lowered arousal occurring immediately after awakening from sleep and producing a temporary decrement in subsequent performance.

and also says,

  Depending on the studies, it [sleep inertia] can last from 1 min to 4 h. However, in the absence of major sleep deprivation, the duration of sleep inertia rarely exceeds 30 min.

Same article reviews several studies (first report in 1964) on sleep inertia relating to sleep stages:

  Abrupt awakening during a slow wave sleep (SWS) episode produces more sleep inertia than awakening in stage 1 or 2, REM sleep being intermediate.

So yes, sleep stage seems to correlate with "waking up in the wrong way" as @CactusWoman suggested.


How are single-stranded binding proteins removed from the lagging strand during DNA replication?

Actually, there has been some evidence that the SSBPs keep the bases facing outwards so DNA polymerase can still replicate the lagging strand with the SSBPs on them. There has also been other evidence that they can pop off spontaneously.

You can learn more about this by watching the lectures on https://www.edx.org/course/molecular-biology-part-1-dna-replication-and-repair


Identification of fuzzy insect in Pennsylvania

This is the nymph of a bug (Hemiptera) from the Genus Arilus, probably Arilus cristatus, also known as "wheel bug".

Here is another image of it, for comparison:

Source: http://bugguide.net/node/view/288330

And here is the adult:

Source: https://en.wikipedia.org/wiki/Wheel_bug


Estimation of cell count of E.coli culture

You start with $10^6$ cells. After 30 min they double, so there are $2⋅10^6$ cells. After another 30 minutes they double again, so there are $2⋅2⋅10^6$ or $2^2⋅10^6$ cells. After three doubling periods, the number of cells is $2^3⋅10^6$. Doing this, the equation for exponential growth should become evident. All you must do now is determine the number of doubling periods in 12 hours.


This will be a complete answer, but it's got code, so it won't work as a comment. Working backwards from rtree(3), here's a way to build a phylo object from component parts, which might be helpful:

children <- c(5, 1, 2, 3)
parents <- c(4, 5, 5, 4)
x <- matrix(c(parents, children), ncol = 2)
tr <- list(edge = x, tip.label = 1:3, Nnode = 2)
class(tr) <- "phylo"
plot(tr)

Doing the same with your children and parents, doesn't work, however.

children <- c(1, 2, 3, 4)
parents <- c(1, 1, 2, 2)
x <- matrix(c(parents, children), ncol = 2)
tr <- list(edge = x, tip.label = 1:3, Nnode = 2)
class(tr) <- "phylo"
tr

Gives

Error in if (tabulate(phy$edge[, 1])[length(phy$tip.label) + 1] > 2) FALSE else TRUE : missing value where TRUE/FALSE needed

I don't know hot to make the edge list conform to the expected order for a phylo.


How do I change bond colors to something besides a different hue in Coot?

You could try other visual differences, like make what you're interested in ball-and-stick, and everything else wireframe, like in this example:

.

.... Because, from: http://www.ysbl.york.ac.uk/~lohkamp/coot/doc/coot-python.html

  procedure: hilight_binding_site (imol, centre_residue_spec,
  hilight_colour, radius): hilight-colour is specified in degrees (round
  the colour wheel - starting at yellow (e.g. 230 is purple))

It looks from this like you only get to choose Hue (color_map_rotation) and not Saturation or Lightness, even with the script interface.

However, text can be full RGB

  3.28.3 (set-font-colour red green blue)

  where:

  red is an inexact number green is an inexact number blue is an inexact
  number


What causes knuckle "popping" and the feeling of relief that comes from it?

Nobody really knows where it comes from. The currently most popular theory is that pulling the joint apart leads the gases in the joint's cartilage to accumulate and form a bubble which then pops when you let it spring back. The only thing that has been researched is whether it has an effect on the joint, but people who do it regularly don't seem to have any problems with their joints more than anyone else (I'll find the reference once I have time). Apart from that it's hard to get funding for this kind of research because it has little practical use.

Relief like feeling? That must be subjective to you, I used to do it every now and then but I don't remember getting any relief from it. In that case, it's probably the same relief as other people get from picking their nose, their ears, biting their nails, etc. It's called compensation reaction.


Does RNA-LPX expression of antigen by DC induce only T-cell with that antigen specificity?

The OP (me) was unclear whether or not the new therapy had to ultimately present antigen specific to a particular naive T-cell. The answer is yes: Each T-cell is specific for a single antigenic determinant. An antigenic determinant is a small portion of an antigen, such as a certain sequence of amino acids in a protein, that the immune system (a T-cell receptor in this case) recognizes as non-self or altered self. The antigenic determinant is also known as an epitope. Typically an antigen has many different epitopes, each able to react with a specific antibody or T-cell receptor (when presented with MHC).

The confusion arose from the description of the RNA as encoding "mutant neo-antigens" (among other possibilities, e.g., viral or endogenous self-antigens). At first glance this seemed to imply that a tumor antigen constituting a novel polypeptide antigen ("mutant neo-antigen") was able to induce T-cell response (effector and memory T-cell responses) in the absence of any T-cells with a T-cell receptor specific to that neo-antigen. That would not be possible.

Through somatic gene rearrangement in development, T-cell receptors (TCR)  have a wide range of antigen specificity, such that each T-cell has a unique receptor on its surface able to recognize foreign protein antigen associated with MHC molecules. Some estimate that human TCR and antibodies can respond specifically to 10 million different antigens.

Apparently the distinction is made between classical tumor-associated antigens that typically constitute autoantigens (which may appear frequently on the surface of cancer cells in conjunction with MHC and therefore generate some antibody response, possible ineffective) and neo-epitopes, the latter being the result of the estimated 25 – 30% of antigenic mutations (mutations not normally found in the genome) in tumors that could be made to induce immune response on the single- or poly-epitopic level. It appears that autoantigens are more modified normal protein that tend to appear somewhere in the disease process on a particular class of tumor than the result of entirely novel mutations. Since tumors usually have tens to hundreds of non-synonymous mutations, the mutanome of a tumor provides many possible targets for custom poly-epitope vaccines for each individual patient. Coding messenger RNA (mRNA), i.e., synthesizing mRNA to encode multiple transcripts for synthetic poly-epitopic nucleotide sequences, is an attractive antigen delivery format.

In order to locate a sequence that would be likely to act in this capacity (that is, to select tumor mutations likely to exhibit immunogenecity), an approach like the following serial selection has been suggested: (1) next generation sequencing (NGS) of an patient's individual tumor mutanome and patient genome (2) identify triplicate sequences present in the tumor mutanome but not in the patient genome, i.e., identify the mutations in the tumor that distinguish it from normal self (3) identify those mutations that are likely to code for a protein (4) identify those mutations that are likely to cause a non-synonymous protein change (5) identify those mutations meeting all the previous criteria that a predicted to be in a peptide presented on tumor MHC. An example quantifying this selection process is that of the murine B16F10 melanoma mutanome: The NGS exome profile (coding exons) predicted 12,842 mutations; 3570 of those predicted as somatic mutations; non-synonymous mutations 962; mutated peptide predicted to bind MHC 462; 50 of those selected for testing and of those 50, about a third of those tested strongly immunogenic when encoded to RNA and transfected to dendritic cells, i.e., inducing strong T-cell response. As a test of actual anti-tumor effect, mice were immunised with the encoded mutations identified and achieved complete tumor protection and survival in 40% of the group, compared with death of all control group animals.

Generalizing, a poly-epitopic vaccine formed from a tumor mutation should be selected to be specific to the tumor and not in the patient germline genome, to occur in a protein-coding transcript, to cause a change in protein sequence and that protein be expressed in tumor cells. In order for the mutation to induce a robust T-cell response, the mutation-containing epitope must be presented on the patient's MHC molecules in the dendritic cells during vaccination (and at least one T-cell must possess a receptor specific for one of the epitopes) and in the tumor cells for recognition (on the surface of the tumor cells). With the patient HLA haplotypte, MHC-binding epitopes can be predicted with computer algorithms. The immunogenecity of the computationally predicted epitopes can be tested in vitro with T-cell stimulation.

One of the challenges to RNA delivery has been degradation by ubiquitous extracellular RNAses. The study noted [Systemic RNA delivery to dendritic cells] solves that issue by protecting the RNA with lipid carriers to form RNA-lipoplexes (RNA-LPX). This has the additional adjuvant effect (the RNA-LPX) of triggering interferon-a (IFNa) release by plasmacytoid DCs and macrophages in a manner similar to early phases of viral infection.


There are a lot of approaches to this kind of problem. Starting with the simplest approach I think you'd benefit from using a K-means classification, with K=2 (or higher numbers to address @Luigi's concerns about model bias.) Once you've defined the geometric center of each population, you can treat them as foci, and use the equidistant points between each focus to define the boundary of interest. That does import another assumption (that the boundary is equidistant to the two points).

A more sophisticated way to divide two clusters is with a support vector machine but because this is a machine learning approach, you'd need to manually annotate a number of training data sets as "group 1" or "group 2." But after training, the SVM will define the optimal boundary (hypersurface) between these groups.

The two types of approaches (clustering versus machine learning) differ in where the manually-imported assumptions lie. One can combine them fruitfully -- using K-means to define the populations and SVM to define the dividing boundary.


Almost certainly not the pituitary proximity hypothesis. Simple counter-examples include the adrenal gland (ACTH-cortisol axis), liver (GH-IGF1 axis) and  the gonads (LH/FSH axis).


Can two protein secondary structures "overlap" in the PDB?

TLDR; Answer: You could consider this particular residue to belong to both structural elements, but it's a tricky call and depends on the method of secondary structure assignment.

Ambiguous secondary structure allocation comes up fairly often. Whilst obviously, not many people will be able to use this protein specifically, the below approach could be useful for other proteins.
Default pymol assignment
In PyMol I used fetch 1ae9 and highlighted M at position 255 on the A chain in red. I can see why this isn't a satisfying representation: the beta sheet allocation is very short, and the residue in question is clearly the beginning of a helix.

DSS is more conservative
To run a more conservative secondary structure allocation run dss in pymol (watered down dssp). This reveals that the beta sheets were actually quite putative.

We can see why when we look at the stick model (below). There are only a few (2-4) residue pairs in proximity that would be available for hydrogen bonding, even assuming all 4 form H-bonds, calling this a bona fide beta sheet could be seen as a bit generous.

Dual assignment can be okay.
Looking at this example (1ae9), we see the potential for H-bonding with another putative beta sheet, as well as a backbone angle that starts to form a helix. It's a classic case of ambiguous dual assignment. @AlexanderDScouras draws a reasonable conclusion that both is okay and to directly answer the question: dual assignment is possible, and allowed. I would prefer to rule out beta sheets in this particular case, but on the condition that one highlights that there is plenty of hydrogen bonding in the hairpin loop.
So long as it's reasonable.
So long as you can reasonably justify the assignment it's probably okay. You can manually assign any residue and secondary structure.
# set residue 155 to be alpha-helical
alter 155/, ss='H'

# update the scene in PyMOL to reflect the changes.
rebuild

Evidence is always a good idea to support manual assignments. A quick and thorough way would be to run the sequence through a few secondary structure predictors, or use the genesilico metaserver to save yourself some hassle (you'll need an account) (this does feel like going back a step since you now have a structure, so exercise caution - if the sequence prediction doesn't look correct according to the structure, it's probably not). Another method as suggested by shigeta is running this through a Ramachandran plot (RAMPAGE is a favourite).

If it's very very unclear then discuss it thoroughly and clearly whenever this part of the protein is relevant. These secondary structure assignments have somewhat arbitrary cut-offs after-all, and when things get near the thresholds, it's important to approach the situation with clarity and specificity.

Ramachandran plot image source: By Dcrjsr - Own work, CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=9105708


Parallel DNA double-helices with Watson–Crick base-pairing: Why do they not occur?

“The only specific suggestions that I could find was because of the DNA replication process and…”

No. The explanation can have nothing to do with DNA replication. If the structure does not exist, you can’t replicate it, if it does, Nature will evolve a mechanism. (The related SE question, mentioned by @Gilleain, asked whether it could still replicate if it were parallel, i.e. using the enzymes that have evolved for parallel DNA.)

  I know that parallel DNA helices exist…

Let us clarify this first. Perhaps the most extensive parallel duplex DNA, the structure of which has been determined, is that described by Parvathy et al.. The two parallel strands of this are shown below:

The following points should be noted:

This parallel DNA (and the shorter examples that preceded it) is not a pure stretch of complementary base pairs.
It is stabilized by what the authors refer to as “CC+ clamps” at either end. One is left to conclude that without these the duplex would not form.
All the complementary base-pairs are of the type AT (actually reverse Watson–Crick base pairs). Presumably GC base-pairs would have destablized the structure.

(You can inspect this structure in three-dimensions here. Choose ‘Licorice’ style and colour ‘by chain’ and notice the non-planarity of the three base ‘pairs’ at each end.)

So although the question refers specifically to parallel DNA helices with Watson–Crick base pairs, it should be recognized that extended parallel DNA helices composed of any kind of complementary AT and GC base pairs are not found, and the question applies equally well to them.

  “In the diagram if we were to flip one of the strands while keeping the other same, hydrogen bonding is still possible”

The diagram in the question is two-dimensional; DNA is three-dimensional. It is only by considering the three-dimensional structure of DNA can you approach this question.

So how would one do that? One must consider the free energy of alternative structures in the relevant millieu to determine which will occur (i.e. be more thermodynamically stable).

This will tell you whether single DNA strands with parallel sequences will form a double-stranded (ds) structure or not.
This will tell you whether ds-parallel DNA is more or less energetically stable than a ds-antiparallel DNA. Hence, even if both can form (which I doubt, without some special circumstances*) the lower thermodynamic free energy of the anti-parallel dsDNA would give organisms adopting it an evolutionary advantage.

And the answer to the question?

It seems unlikely that one single factor is responsible or it would have been pointed out in elementary text books such as Berg et al..

To answer would require a complete theoretical analysis of the structure or structures. First one would have to build a model of a proposed parallel structure that could accommodate Watson–Crick base pairs. This in itself is a problem because there are likely to be many alternative structures. Perhaps there are computer programs that can find the structure with the lowest energy. This would be calculated in the classic manner, calculating the positive contribution of hydrogen bonding (which depends on distance and angle), ionic interaction etc.*  against the negative contribution of charge and steric repulsions.

*Etc? The two-dimensional diagram fails to consider the contribution of base stacking (how could it?), which contributes to a considerable extent to the stability of nucleic acid helices, as the original cover design of Stryer’s Biochemistry is a constant reminder:


Crossing or decussation is a lot more robust against wiring errors than their seemingly simpler same-sided wiring counterparts. See here for the research carried out to establish this and for more detail.


It's an Epiphyllum Oxypetalum. Epi is greek for around (epi-center) and phyto is plant, epiphytes are plants that live on other plants, for example rainforest plants that grow on the canopy of tall trees.

There are lots of hybrids and lots of colors.


What happens to plants if they are exposed to "sunlight" 24h a day?

This review (from 2011)1 states that it depends on the plant species and cultivar.

  Some continuous light (CL)-grown photosynthetic organisms show
  increased productivity. However, CL also induces negative effects in
  several plant species. The most visible CL-induced negative effects
  are leaf chlorosis and necrosis. CL also lowers photosynthetic
  parameters ... The CL-sensitive species include eggplant, geranium,
  some onion species (Allium fistulosum), peanut, some cultivars of
  potato, tomato, and even lichens (Xanthoria parietina) and mosses
  (Pleurozium schreberi and Ceratodon purpureous).

Among the plants that have better yields under continuous light are lettuce, roses, some potato cultivars, some algae.

The reasons why some plants can be damaged under continuous light aren't completely clear (at least they weren't in 2011). One of the problems is carbon imbalance. Leaves produce too much sucrose and other organs such as roots are not able to process it fast enough. This leads to high sugar concentrations and can cause leaf senescence. Continuous photosynthesis also results in more photo-oxidative damage and plants that better detoxify reactive oxygen species have less negative effects from continuous light.

So look for research on the particular species you want to grow or just experiment with different light conditions.

 1. Velez-Ramirez, A.I., van Ieperen, W., Vreugdenhil, D. and Millenaar, F.F. 2011. Plants under continuous light. Trends in plant science, 16(6):310-318.


Why's there no vaccine against Respiratory Syncytial Virus (RSV)?

In answer to the specific question,
This paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741363/ is the one the review was talking about.

The epitope that is targeted (the F protein) varies between strains, so a produced vaccine would only work on that strain. The protein (an obvious vaccine target) was selected because it exists on all strains, and is needed for the virion to fuse with the human cell.

In the vaccine The F protein epitope is fused with an immunostimulatory particle to get a good immune response. That's why they mention "prefusion" and "postfusion". There is confusion in the terminology because the F protein is so-named because of its role in fusing the virion to the cell.


Why are our bodies created to itch when histamine is released by our immune systems?

Scratching is getting potentially poisonous or at least irritant substances out and removes lodged insects like ticks.

Removing subcutane parasites like scapies mites is not feasible without scratching yourself bloody.

I don't see how "scratching them clearly doesn't help us survive".  Behaviors and skin reactions evolved way before our modern hygiene and parasite cures.


There is a really good discussion of this in Chesson & Kuang Nature 2008, they propose a way to measure niche complementarity accounting for competition and predation.


Here is a good write-up for NASA of human needs in space, which applies to other planets, too.

Here is a table of contents with links to chapters that discuss relevant information for you.

The source is described so:

  Space Settlements: A Design Study, provides information on space
  settlement development and education and assists teachers and students
  in the NASA Ames Space Settlement Design Contest. The design study was
  the result of a 10 week program in engineering systems design held at
  Stanford University and Ames Research Center in the summer of 1975.
  Participants included professors, technical directors and students in
  a variety of disciplines from physical science and architecture to
  engineering and social science. The goal (see preface) was to
  construct a vision of how people might sustain life in space in a
  large colony.


What can give rocket salad (Eruca Sativa) a fish smell?

Complete guess - the arugula could contain or be decomposing into amine-containing compounds (known to have a fishy smell).

https://en.wikipedia.org/wiki/Amine#Physical_properties


Do residue sequence numbers in PDB files correspond to the positions in the backbone?

The residue numbering convention in the PDB is more-or-less entirely up to the depositor of the structure. While generally speaking sequential numbers are next to each other, there is no guarantee of that fact.

For example, the PDB allows for what are called "insertion codes", which are extra residues which interrupt the regular sequence progression. For example in the PDB entry 1IGY in between residues 52 and 53 on chain B is residue "52A". Normally, these insertion codes are used because the depositors want the numbering scheme to correspond with some external numbering standard, and there are extra residues (e.g. from affinity maturation) which would throw off this numbering.

Alternatively, the depositor might choose to mix up the numbering significantly. An example of this is the PDB entry 4OO9, which is the transmembrane domain of human mGlu5 with a lysozyme insertion to help crystallization. The mGlu5 is numbered from chain A from 568 to 832, but between residues 678 and 680 are residues 1002 to 1162, representing the inserted lysozyme. (So it goes 677, 678, 1002, ...)

Ultimately, the only reliable way to tell if two residues in the PDB which are sequential in numbering are actually sequential polymerically is to actually look at the coordinates and see if they're in a bonding configuration. There may be some information about "out-of-order" residue numbering in the header lines, but that's not always clear. Usually you have to deal with such situations on a case-by-case basis.


Reverse evolution to gain back lost traits

Back evolution

Evolution do not strictly keep a history of how they were before. There is no way for a population to specifically produce mutations to reverse previously fixed mutations in order to evolve back in time. This has sometimes been called Dollo's law but very few people actually use this term today.

Note however that a population may have kept pseudogenes or specific developmental pathway or case of atavism that make the evolution of some traits similar to previously existing trait "easier". A very nice example of such mechanism is the case of Membracidae (treehoper).

Example of Membracidae

insects have evolved flight once. The first flying insect had 3 pairs of wings, one pair on each of the 3 segments of the thorax. Today, there exist no insects with 3 pairs of wings. In all lineages descendent of this flying ancestor many have no wings and many have 2 pairs of wings only. Here is a schema showing a typical insect with 2 pairs of wings.

As you can see there is no pair of wings on the first segment of the thorax (called prothorax) as it has been lost through evolution. Note that the diptera (true flies) have lost a second pair of wings (the one on the metathorax which has been replaced by halters).

Membracidae (treehoper) is a family of wingless insects. They use previously existing developmental pathways and previously existing genes (Prud'homme et al. 2011) for developing wings on the protothorax but instead of making wings, they make all kind of funny shape for defense purpose. Here are a few examples


One olfactory acuity rating method that has found acceptance in some studies (despite the commercial-sounding name) is based on "Sniffin' Sticks,"

"a test of nasal chemosensory performance that is based on penlike odor-dispensing devices. It is comprised of three tests of olfactory function: tests for odor threshold, discrimination and identification. Previous work has already established its test-retest reliability and validity in comparison to established measures of olfactory sensitivity. The results of this test are presented as a composite TDI score--i.e., the sum of results obtained for threshold, discrimination and identification measures."

In the paper from which this abstract portion was taken$^1$, subjects were assigned a score based on their thresholds, ability to discriminate, etc., and the findings were said to be internally replicable (consistent from one test to the next).

This is probably not the only rating available but it has been used on other studies and seems to be taken seriously by M.D.s and others who measure such things.

There is no absolute measure of olfactory acuity. People are classed as 'anosmic' if they do poorly enough on the test but that doesn't mean they have no sense of smell (although that might be the case). Likewise people who get a high TDI score are--by definition--people who got the "Sniffin Sticks" right. They might be poor at discriminating a good coffee from a bad one based on smell.

The test seems to do what it was intended to do: quantify relative olfactory acuity in a replicable way.

An earlier study is somewhat reserved. From an abstract: "It is concluded that ‘Sniffin’ Sticks’ may be suited for the routine clinical assessment of olfactory performance."

$^1$ Eur. Arch. Otorhinolaryngol. (2000) 257(4):205-11. Multicenter investigation of 1,036 subjects using a standardized method for the assessment of olfactory function combining tests of odor identification, odor discrimination, and olfactory thresholds. Kobal et al.


Might be a red palm weevil

Rhynchophorus ferrugineus

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


What advantages do birds gain when they mimic other bird species calls in the wild?

There are a number of reasons birds will mimic other birds mostly for deception, but not always.

Impressing a mate: Songs are a large part of bird courtship behavior, and a more varied song that includes different mimicked tones can help attract a better mate. Because mimicked tones are learned, a bird with more vocal variety is demonstrating its intelligence, ability to survive, and other characteristics a mate would find desirable.
Safeguarding Food: Using a hawk or owl call, or the sound of a cat, dog, or other predator, is an effective way for a bird mimic to claim a food source. When it utters such a call, birds monopolizing feeders or nearby bushes, trees, or other feeding spots may scatter, letting the mimic take advantage of a less crowded food source.
Defending Territory: Songs are crucial for many birds to claim territory, and adding mimicked tones into the song can demonstrate the resident bird's strength. Extra sounds may also trick other interested birds into believing that there are far more birds in the region than there actually are. The newcomers may then simply move along rather than challenge the resident mimic bird.
Social Acceptance: Baby birds learn many songs from their families and other birds of their species, and if mimicked sounds are included, young birds will learn them as part of their initial repertoire. This helps birds fit in with their flocks, which will also help them eventually defend their own territories and attract mates. Many pet birds that mimic speech are doing so for social acceptance, as they consider humans to be their flock.Bird to bird mimicry
I have personal experience with one of these where a Blue Jay would come to our feeder imitating the screech of a hawk and all the other birds would scatter so he/her had the feeder to themselves.


Why does all life use the same macromolecules in their genetic code?

Preamble
Any answer regarding the origins of our biochemical evolutionary origin will be reasonably speculative given that this is a very hard question to scientifically test and this field is generally understudied to say it is pretty much the most fundamental biochemical question. But there are a few reasons why RNA makes sense as the prime genetic molecule compared to other established macromolecules present in the primordial soup, and also there are good reasons why DNA superseded it as genetic storage for most cellular organisms.
In summary, the alternative abundant polymer macromolecules that came from the primordial soup aren't as versatile as RNA, and over time DNA was used more over RNA due to it being a more reliable information storage molecule.
We must remember though that the conditions that lead to the genesis of RNA is a much tougher question. There are an unfathomable amount of combinations of chemicals that could have facilitated an evolutionary process. @WYSIWYG made an excellent comment regarding why this is an almost impossible question to answer definitively:

...Why is there a phosphodiester backbone used rather than
ether, amide, carboxyl ester or any other kind of linkage? Or why
purines and pyrimidines, why not naphthalene ring heterocycles? Why
imidazole, why not oxazole or furan? You cannot reason this out in a
reverse manner.

Therefor in this answer we will be discussing RNA and other bio-polymers that were established in abundance from the very early primordial soup, not the original genesis of such biochemicals. What made each of them good vessels for an evolutionary process?
A genetic code macromolecule needs the following features:

Stable.
Variable structure.
Expandable.
Replicable.

RNA has all these and doesn't rely on a biological system for reproduction of the RNA molecule.
RNA world.
Let's not forget that DNA is probably not the first one along and there was an RNA world before the cell as we know it. Even today many viruses particularly make use of ssRNA.
RNA was a good molecule because it was a polymer made of 4 base monomers that could bind with other polymers to make any array of compositions of the base components and was spontaneously replicable. This allowed a primordial form of molecular evolution as we know it today. It is able to carry more varied information than other abundant macromolecule polymers.
RNA can also carry out functions in a similar way a protein might, including catalysis. No known sugars or other macromolecules are able to demonstrate the same level of variability and versatility as RNA, although deoxyribosymes have been artificially designed in laboratories.
This probably gave it a good chance at establishing itself as the first molecule to trigger biogenesis, and this lead to nucleic acids being established as the fundamental molecule of molecular evolution.

DNA chemical structure.
Eventually RNA evolved into more complex structures and DNA broadly superseded RNA as a storage device for genetic information in cellular organisms primarily due to the increased stability DNA offers over RNA. If we take a look at DNA specifically we see a very good data storage mechanism for a couple of reasons.

Intra-strand hydrogen bonding and different chemically structured sugar group makes a more stable overall structure.
More rigid grooves allow proteins to bind at particular sites.
Again, it's a polymer of variable composition.

Alternative coding macromolecules.
What are our other options from the biological polymers?

Carbohydrates. The glycocalyx coats most cells in our body, and clearly sugars (specifically polysaccharides and glycoproteins) are an expandable, information rich molecule. However it relies on proteins for assembly in the same way proteins do, so it never really got the chance to be that prime molecule.
Lipids. A brilliant expandable polymer, and many are spontaneously expanding in the right conditions, but generally lipids cannot carry as much "information" in the polymer (pretty much just varying lengths of CH2 groups).
Proteins. Too complex and not spontaneously replicable. They rely on other systems for production (except in some rare examples, although they arguably still rely on a complex biological system).


Can a drug induce specific mechanism of resistance in tumors?

Yes.

There is a lot of literature on cancer evolution and now several countries have genome sequencing programs for "pharmacogenomics", for example Genomics England, specifically to see which cancers are likely to evolve resistance to which drugs.

One small detail is that mutation exists before treatment in a subset of the cancer population —as happens with evolution normally. That mutation is neutral for the fitness of the cancer before, but is advantageous during treatment.


Does a walk after a meal help with digestion?

apparently walking helps in the movement of food into the stomach and improves digestion. Also helps in decreasing blood sugar after meals, which decreases cardiovascular risk and potential signal diabetes by helping muscles absorb glucose in the blood. Here is the link to a study done comparing the results of walking after food and after a drink. Also a study was conducted where when people with Type 2 diabetes took a 20 minute walk just 15 minutes after eating, their post-meal blood sugar levels were lower than if they had walked before dinner or not walked at all. Here is the link to another similar study.


See UN > stats Down Syndrome per country.

What the data says

I have not made a proper statistical test (as I am too lazy to reformat the data in anything convenient to perform a statistical test) but the prevalence seems to be consistently around 0.12499% all around the world with very very little variance. I doubt there is any significant difference in the frequency of birth that have down syndrome.

As @Markonionini rightly noticed, these estimates of prevalance are slightly far fetch extrapolation and the UN specifically advice to consider them with caution. It is probably the best data we have though.

The hypothesis seems improbable to me

Do you have any good rational behind your hypothesis? Down Syndrom is typically caused by de novo mutations and not due to standing genetic variation (Veltman and Brunner 2012) so your hypothesis seems rather implausible to me.


How do lipid-soluble substances diffuse through the cell membrane?

See this paragraph and image from The Cell: A Molecular Approach. 2nd edition.:

  During passive diffusion, a molecule simply dissolves in the phospholipid bilayer, diffuses across it, and then dissolves in the aqueous solution at the other side of the membrane...Passive diffusion is thus a nonselective process by which any molecule able to dissolve in the phospholipid bilayer is able to cross the plasma membrane and equilibrate between the inside and outside of the cell. Importantly, only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates (Figure 12.15). Thus, gases (such as O2 and CO2), hydrophobic molecules (such as benzene), and small polar but uncharged molecules (such as H2O and ethanol) are able to diffuse across the plasma membrane. Other biological molecules, however, are unable to dissolve in the hydrophobic interior of the phospholipid bilayer. Consequently, larger uncharged polar molecules such as glucose are unable to cross the plasma membrane by passive diffusion, as are charged molecules of any size (including small ions such as H+, Na+, K+, and Cl-). The passage of these molecules across the membrane instead requires the activity of specific transport and channel proteins, which therefore control the traffic of most biological molecules into and out of the cell.

As shown in above paragraph, molecules have to dissolve in phospholipid bilayer to diffuse through it. But since the hydrophilic part is already interacting with water, so dissolving is mainly for the hydrophobic part. Now, since hydrophobic part is non-polar, so it can dissolve only non-polar substances (like dissolves like). Thus, small gases like O2, CO2 and non-polar molecules like benzene easily dissolve in hydrophobic part and diffuse through it. Also, molecules like water and ethanol can also dissolve in it in small amounts due to their small size and very less polarity. That's why only some molecules of water can diffuse passively, large amount of water would require aquaporins. Now, since bigger molecules like glucose have large size and high polarity, they cannot dissolve in the membrane and thus require transmembrane channels even for diffusion. Similar case is with ionic substances too: they require ion channels for their diffusion.

Hope this helps. Comment below if you have any further doubts.


How do scientists decide which version of a polymorphism is the main one?

[..] G is the default and C is the polymorphism

An allele (or just a nucleotide variant) cannot be "the polymorphism". There is polymorphism, if a given locus (or just a given nucleotide position) is polymorphic, that is, if as this position, there are different variants existing in the population. Therefore, an allele cannot be called polymorphism, only a locus can be called to be polymorphic and if a locus is polymorphic, then there is some polymorphism in the population.

I have never of people talking about the main or default variant. Do they use this word in the article you link? If yes, can you please indicate where?

Commonly, people talk about the wildtype versus the mutant variants. In this case, the wildtype variant is just the most common variant. Rarely I have seen people referring to wildtype variant when talking about variants that are at low frequency because the mutant is increasing in frequency and slowly reaching fixation. In such case, the wildtype mutant would correspond to the original variant at an arbitrary time point in the past but would not depend on the frequencies observed today.


Molecular Cloning- Blunt end restriction endonucleases

To know if the ends are compatible see compatible cohesive ends (isoschizomers) from NEB website.

If you are unsure then do a blunt end ligation. For blunting a sticky end (From the comments):

Use Klenow or Pfu polymerase (or any proofreading/high fidelity polymerase).

You can use Taq if you intend to to a TA cloning.


Material recommendation: molecular biology for mathematicians and computer scientists

I have also come from purely non-Bio background (I am a Software/Electrical engineer who didn't study Bio even in his high-school).
As others have pointed out in comments above that Molecular Biology is a vast field. But if you want resources covering all the basics of Genetics/Molecular Genetics, then I can easily recommend the following to anyone (which are both easy to understand and very authentic ones):

Nature Scitable
Genetics by PS Verma, Agarwal, S Chand.

There are other books like this one but they all are on bioinformatics/advanced and expect some knowledge of Molecular Biology. My recommendation (proved one) are above two. Best of luck!!


I work with membrane proteins and in my experience some proteins can be frozen and thawed without any problems, other proteins just don't like that. It's linked to the stability of the protein. If you really need to freeze the protein you may think about playing around with different detergents to see if you can improve the stability of the protein.

General rules:
- freezing membrane proteins at -80°C without glycerol
- avoiding protein freeze-thaw cycles, making aliquots before freezing
- keeping them at 4°C only for short term use
- after concentration always spinning the protein (10 min at 100k for example) to precipitate aggregated material. Aggregation causes aggregation, so you want to get rid of it.


The DNA sequence "TATATATA" contains 4 repeats of the 2-mer "TA" and because these repeats are adjacent to each other, they are tandem repeats. The pattern of  nucleotides is repeated and the repetitions are next to each other.

This is what both the Wikipedia and the Simmons definitions are trying to communicate.  The statement you quote from Benson'a paper can be taken to mean the same thing (except for "approximate"), but might also be construed as saying the collection of all contiguous repeats is one tandem repeat, but that is not what was intended.

So, the oriC sequence has 4 tandem repeats of one kind (9-mers) and 3 tandem repeats of another pattern (13-mers).


What is a regulable promoter? And how does one regulate it?

Regulatable promoter means that the expression of the gene downstream of this promoter can be either induced or repressed. Met3 is an example of such regulatable promoters and it is regulated by the addition of methionine to the media. In yeast, Met3 gene encodes for ATP sulphurylase, an enzyme in the methionine biosynthetic pathway. Upon the addition of methionine, the gene driven by Met3 promoter is repressed, as its expression level is reversely correlated with the concentration of methionine added to the media (Figure from this paper):


Caterpillar(?) in Leaf Cocoon identification - Missouri

This is the larvae (caterpillar) of a bagworm moth (family Psychidae).

 Source: Wikimedia Commons; Credit: Bernard DUPONT

From Wikipedia:

  The caterpillar larvae of the Psychidae construct cases out of silk and environmental materials such as sand, soil, lichen, or plant materials.

There are about 240 genera, so I will leave IDing to lower taxonomic levels up to you. However, based on the striations of the caterpillar and your lcoation, the Evergreen Bagworm Moth doesn't seem like a bad guess...


From the picture, it looks like Cacatua sulphurea

[Source: Wikipedia]

  The yellow-crested cockatoo (Cacatua sulphurea) also known as the lesser sulphur-crested cockatoo, is a medium-sized (approximately 34 cm long) cockatoo with white plumage, bluish-white bare orbital skin, grey feet, a black bill, and a retractile yellow or orange crest. The sexes are similar.[Source]

Habitat and ecology:

It mostly inhabits evergreen, deciduous, monsoon and semi-evergreen forests.
It nests in tree cavities or a pre-existing hole made by any another species.(Nandika et al.)
Observations made on Masakabing Island suggests that it's favourite diet include male fruits of Artocarpus communis, flowers and fruits of Cocos nucifera, Young leaves and flowers of Ceiba petandra, mangroves and male fruits of Brassus sudaica.(Metz et al.)
It mostly nests on C. nucifera, A. communis, C. petandra, Tamarindus indica and Avicennia sp. (Nandika et al.)
[Source]

Why it is not Cacatua galerita?

The plumage is different and the skin around the eyes are more white. [Source: In description part]
In the picture of the OP there is a blue ring over the eyes and it is also known as blue-eyed cockatoo. [Source: In the description part]


Why would the stroma have a higher pH during photosynthesis?

Energy from an electron transport chain is used to actively transport protons from the stroma to the thylakoid lumen. Thus the lumen has a relatively higher proton concentration and therefore a lower pH than the stroma.

Higher [H+] means lower pH.

Lower [H+] means higher pH.

Keep in mind that the flow of actively transported protons from the stroma to the lumen is against their concentration gradient. There wouldn't be a net flow of protons this way without active transport.


How can someone share 50% of their DNA with their parents yet all humans share 99.9%?

It will be clear with a simple analogy.

You are 50% related to any one of your parent

Let's say you don't have any biology books. You have two friends, Alice and Bob. They each give you a copy of the book Campbell Biology. You now have two Campbell Biology. You have received 50% of your Campbell biology books from Alice and 50% from Bob.

Similarly, you inherit 50% of your DNA from your mother and 50% from your father. You are related at 50% to any one of them.

Two randomly sampled individual are 99.9% identical

Now consider the list of all the copies of Campbell Biology in the world. As there exist different editions, all Campbell Biology won't exactly be the same.
Let's say you randomly sample two Campbell Biology from around the world and you align them letter by letter. What is the expected fraction of the letters that will be identical? If, for example you find the two sentences

  Selection is a fitness variance associated to a genetic variance among individuals in a population.

and

  Zelection is a fitnezz varianze azzociated to a genetic varianze among individualz in a populazion.

There are exactly 9 mismatches out of 99 characters, that is a 90% similitude.

Similarly, if you randomly sample two humans, align their DNA (a DNA sequence look like ATTTCGCTGTCGAATCGATCGGTA), you'll find that the fraction of mismatch is lower than 0.1%. Therefore, we all share 99.9% of our DNA.

Of course, alining DNA sequences (or normal sentences) is not quite that easy as some sequences (or sentence) can have more nucleotides (or letters) than others but I won't go into the details here.

How do these two measures relate?

Let's say that instead of giving you a book, Alice actually produced a copy of its book and gave it to you. The book you have received from Alice (that is 50% of all your Campbell Biology books) is 100% identical to Alice's book in term of mismatch.

Similarly, the 50% of your DNA that you inherit from your father (or mother) is 100% identical to the copy of the genome found in your mother.

Note however that

Your mother probably made between 10 and 100 mutations when copying her DNA so that the DNA you received from your mother is not exactly 100% identical to your mother's DNA

Similarly Alice could have miscopied her Campbell Biology book that she passes to you

Your mother actually recombined her two haplotypes

Similarly Alice actually had two different editions of Campbell Biology and she mixed them up a little bit before copying the resulting book!


Membrane potential after exposure to glutamate

I believe C is also correct. The excitatory neurotransmitters open $\ce{Na}$ channels which makes the cell membrane more permeable to sodium as compared to potasium and therefore the equilibrium membrane potential would be much closer to the nernst potential for sodium. Now, since the concentration of sodium outside is much greater than inside, the nernst potential for sodium is positive with respect to the inside of the membrane. This makes the overall potential also positive.

If you want further clarifications regarding the calculation of the equilibrium and the nernst potential across the membrane, feel free to ask.

ADDENDUM

The approximate concentrations of sodium and potassium inside and outside a cell are :-
$$\ce {Na+_{in}}=10 \text{mmoll}^{-1}$$
$$\ce {K+_{in}}=105 \text{mmoll}^{-1}$$
$$\ce {Na+_{out}}=140 \text{mmoll}^{-1}$$
$$\ce {K+_{out}}=5 \text{mmoll}^{-1}$$

The Nernst potential is given by $E=-\frac{RT}{nF}\ln\frac{\text{in}}{\text{out}}$

Which for the given concentrations comes out to be $+67.7mV$ for sodium and $-78.1mV$ for potassium. During a sufficiently strong action potential, the relative permeability of sodium with respect to potassium becomes $10$. Using the GHK equation(ignoring the contribution of chlorine) gives us a net potential of $+47.5mV$.

The graph of the action potential clearly indicates that at the peak of the AP, the membrane potential is positive. Source : Graph of action potential


There seems to be some solid evidence that transcription promotes mutation because the untranscribed strand is able to form secondary structures which expose bases to chemical mutagenesis.

Here is a recent paper about transcription-associated mutagenesis:

Kim H et al.(2010) Transcription-associated mutagenesis increases protein sequence diversity more effectively than does random mutagenesis in Escherichia coli. PLoS One 5(5):e10567. doi: 10.1371/journal.pone.0010567.

From the abstract:

  During transcription, the nontranscribed DNA strand becomes single-stranded DNA (ssDNA), which can form secondary structures. Unpaired bases in the ssDNA are less protected from mutagens and hence experience more mutations than do paired bases. These mutations are called transcription-associated mutations. Transcription-associated mutagenesis is increased under stress and depends on the DNA sequence. Therefore, selection might significantly influence protein-coding sequences in terms of the transcription-associated mutability per transcription event under stress to improve the survival of Escherichia coli.

The authors cite a number of papers in their introduction which document the phenomenon that you could follow up. Just in case the focus on a bacterial system puts you off, the Kim et al. paper has in turn been cited in:

Wright et al. (2011) The roles of transcription and genotoxins underlying p53 mutagenesis in vivo. CARCINOGENESIS 32:1559-1567

Abstract in full:

  Transcription drives supercoiling which forms and stabilizes single-stranded (ss) DNA secondary structures with loops exposing G and C bases that are intrinsically mutable and vulnerable to non-enzymatic hydrolytic reactions. Since many studies in prokaryotes have shown direct correlations between the frequencies of transcription and mutation, we conducted in silico analyses using the computer program, mfg, which simulates transcription and predicts the location of known mutable bases in loops of high-stability secondary structures. Mfg analyses of the p53 tumor suppressor gene predicted the location of mutable bases and mutation frequencies correlated with the extent to which these mutable bases were exposed in secondary structures. In vitro analyses have now confirmed that the 12 most mutable bases in p53 are in fact located in predicted ssDNA loops of these structures. Data show that genotoxins have two independent effects on mutagenesis and the incidence of cancer: Firstly, they activate p53 transcription, which increases the number of exposed mutable bases and also increases mutation frequency. Secondly, genotoxins increase the frequency of G-to-T transversions resulting in a decrease in G-to-A and C mutations. This precise compensatory shift in the 'fate' of G mutations has no impact on mutation frequency. Moreover, it is consistent with our proposed mechanism of mutagenesis in which the frequency of G exposure in ssDNA via transcription is rate limiting for mutation frequency in vivo.


What was the evolutionary benefit of enclosing hemoglobin in cells?

If you enclose the globin in a cell you can achieve a high concentration of the globin, which makes for a faster, readily usable pool available, and it is not subject to degradation (via proteases, or other mechanisms) as if it was just dissolved. In addition, all other functions of the globins (pH regulation, CO2 metabolism, etc) will be more tightly controlled if the globin is on the same site (i.e., inside a cell), instead of being mixed in a milieu. All of that has probably more to do with the evolution of the entire circulatory system, as a whole, and only sequentially as the 'enclosure' of globins in specialized cells. You can find some more details here.


Asexual Reproduction Of sponges through endogenous or exogenous budding?

I would say that the quoted sentence from the Wikipedia gemmule article is wrong.  The first sentence of the containing paragraph says:

Asexual reproduction in sponges occurs via budding, either by external or internal buds.

At face value, the two sentences together imply that sponges can reproduce by external budding, but that the external budding "reproduction" does not produce "new sponges"(!). Note that the most recent edit to the article (on 10 March) was by an anonymous user who changed the sentence you quoted from "Both types" to "Only endogenous types", so this was a somewhat recent corruption.


What are the evolutionary explanations for why women are weaker than men (on average), and is this difference adaptive?

All of the theories surrounding this fact are speculative; it would be difficult to prove "why" men are, on average, stronger than women.

One contributing theory is Female-Choice - basically that women had (or has) the ability to be more selective when it comes to choosing a mate. Over time men will reflect the preferences of women (taller than them, stronger than them, facial hair qualities, etc.). This is superficially supported by casual studies like this study from OkCupid where the "attractiveness" curve for men is down-shifted, meaning women think the average man looks below average in attractiveness and implying those who are viewed as average ( actually the top 20% of men or so) would have better reproductive success. Men, in the same casual study, had a nearly perfect bell-curve associated the attractiveness of women, implying that men are excellent at deducing whether a women is below average in attractiveness, average, or above average in attractiveness.

Another contributing theory is Male-Male Competition. Basically men, at some point (and still might) compete with other men to win over women. The bigger, stronger man would presumably win in a fight and eliminate his competition - directly preventing the production of offspring by the weaker male. The male-male competition also holds true in a more speculative theory in that the winners of wars literally raped their way to reproductive success.

It is worth noting that men, on average, are only about 30-40% stronger than women due to the larger muscle fibers in men (as cross-sectional area determines muscle strength, not volume). With training the difference (kg for kg) is reduced to 15-20%.

Ultimately why women are weaker than men (or men are stronger than women - whichever way you prefer to put it) doesn't have a solid answer beyond "because the stronger, taller men have reproduced".


What's the explanation for those shivers/shudders that happen at random times?

It is just like a muscle spasm but generated from your nervous system. If the problem persist you are lacking in a certain vitamin that your body needs to function correctly.


Do humans sneeze or cough in their sleep?

Sneezing does not occur during REM sleep, due to REM atonia.(1)

The coughing reflex is  also suppressed during sleep, but coughing may still occur occasionally during sleep. (2).


Why does my anti-ubiquitin antibody visualization not work on my PAGE gel?

There are stable ubiquitinated proteins in mammalian cell lysates even if active proteosomes exist in cells.

First, you might want to make sure that the antibody is applicable to WB.

Then, you would ask if your WB system using the antibody works. You could optimize the condition using just 1D SDS-PAGE followed by WB.

For the condition for isoelectric focusing, when focusing is completed, you get very high electric resistance, so you might want to monitor current after you change the voltage to 700 V. Current decreases gradually, and get stable at some level. But I do not know you can see stabilization by 700 V.

You also might want to check if major proteins such as actin form spots nicely at the expected pI. That could tell if forcusing is completed roughly.


Short answer
Human females do not benefit much from an extra cone class, as color discrimination is hardly affected in most tetrachromats. In fact, tetrachromats often show increased error rates in their color discrimination. In dichromatic New World monkeys the heterozygous females do functionally benefit from their extra cone as they gain trichromatic vision.

Background
Anomalous trichromats have all of their three cone types to perceive colors, but one type of cone perceives light slightly out of alignment. There are three different types of effect produced depending upon which cone type is affected.

The different anomalous conditions are protanomaly (reduced sensitivity to red light), deuteranomaly (reduced green sensitivity - the most common type) and tritanomaly (reduced blue sensitivity - extremely rare). People with deuteranomaly and protanomaly are collectively known as red-green colour blind and they generally have difficulty distinguishing between reds, greens, browns and oranges. They also commonly confuse different types of blue and purple hues. Red and green cones are indeed coded on the X-chromosome.

One source of variation is the very common Ser180Ala polymorphism that accounts for two spectrally different red pigments and that plays an important role in variation in normal color vision as well as defective color vision. The most common source of variation is the existence of several types of red/green pigment chimeras. The red and green-pigment genes are arranged in an array on the X-chromosome with one red-pigment gene followed by one or more green-pigment genes. Recombination events have given rise to red/green hybrid genes and deletion of the green-pigment genes. Only the first two genes in the tandem are expressed. The severity of red-green color vision defects is inversely proportional to the difference between the wavelengths of maximal absorption of the photopigments encoded by these two genes.

Females who are heterozygous for red and green pigment genes that encode three
spectrally distinct photopigments have the potential for enhanced color vision, as they are effectively tetrachromats (Deeb, 2005, Neitz et al., 1991). However, sensitive color-contrast testing on 43 tetrachromats has revealed that most of these females have no deviating color-discrimination whatsoever. 8 subjects showed relatively small effects, while only one showed a clear increased sensitivity in a narrow range of frequencies. It is believed that the human visual system is not plastic enough to cope with the extra spectral input. In fact, in the group there was an overall increase in error rates on some color tests (pseudoisochromatic plates, and Nagel anomaloscope color matching) (Jordan & Mollon, 1993).

In New World Monkeys, however, the situation is different. Squirrel monkeys are basically a dichromatic species, but two-thirds of the females are heterozygous, and gain trichromatic vision by expressing two of three possible alleles coding for pigments in the middle- to long-wave range of the spectrum. X-chromosome inactivation serves to segregate the alternative allelic products in different subsets of cones. The visual system of the heterozygous female is apparently plastic enough to take advantage of the presence of three classes of cone, because heterozygous monkeys have enhanced color selectivity in the red-green range that are impossible for all males and for homozygous females. This advantage perhaps enables the heterozygote to judge better the ripeness of fruit, or to find fruit or conspecifics (Jordan & Mollon, 1993).

Note that the emergence of trichromacy in humans and some other primates was the result of the red/green gene duplication. Trichromacy in primates was evolutionary selected for likely because of the enhanced capability to discern (ripe) fruits (Lucas et al., 2003). It has nothing to do with sex-differences, because not many human females benefit from tetrachromacy in terms of enhanced color vision.

References
- Deeb, Clin Genet (2005); 67: 369–377
- Jordan & Mollon, Vis Res (1993); 33(11): 1495-1508
- Lucas et al., Evolution (2003); 57(11): 2636–43
- Neitz et al., Science (1991); 252(5008): 971-4

Further reading
- Is our color vision calibrated to sky, vegetation, and blood?


Does zygosity have meaning for mitochondrial variants?

You abosolutely can have mixed populations of mitochondria in a cell (it is in fact very common). Therefore when you sequence the mtDNA you will get a completely variable percentace of reads containing a variant from close to 0% to 100% (there is a lower limit based on the quality and read depth of the sequencing data).

You can't consider the variants to be heterozygous or homozygous as conventional zygosity doesnt apply. Heteroplasmic and homoplasmic are the terms which are used.


Can we say the 'goal' of Mullerian mimicry is a 'decrease in the number of sacrificed indivials'?

What is Müllerian mimicry?

Proposed by Fritz Müller, is when two or more species, which are both unpleasant to eat, poisonous, toxic, harmful etc. have similar colouration and patterns. A key point to note is that they have common (shared) predators. A classic example is the Heliconius genus of butterfly.

Why does it evolve?

The argument you make is kind of along the right lines, but it is a group selection argument, and is worded slightly badly as it insinuates that evolution is a goal driven process. I will use a toy example/thought experiment to explain why it's evolution is adaptive.

In this example there are three species of butterfly are toxic. We will call these species Butterfly-1, Butterfly-2, and Butterfly-3 (yeah, I'm not feeling very creative today). We also have a predator, a bird which likes to eat butterflies. We will call this species Bird.

Butterfly-1 and Butterfly-2 are very different to look at; they have different colours, shapes, and patterns. An individual Bird then eats one of Butterfly-1 and becomes sick. That individual learns to avoid Butterfly-1. Our Bird is then hungry again, and eats Butterfly-2, and again gets sick, and learns to avoid Butterfly-2. Two individuals die before Bird can learn to avoid both species.

Butterfly-1 and Butterfly-3 are very similar in appearance; they have similar colours, shapes, and patterns. An individual Bird then eats one of Butterfly-1 and becomes sick. That individual learns to avoid Butterfly-1, but also to avoid the similar looking species Butterfly-3. Likewise, if it eats a Butterfly-3 then it learns to avoid both Butterfly-1 and Butterfly-3. This is Müllerian mimicry. Survival is higher in one or both species because of more rapid learning by predators, fewer individuals will die compared to the non-mimicry scenario.

The essence of this is captured in the following statement from this paper:

  "Müller provided what could well be the first formal mathematical model to support an evolutionary hypothesis. Following Müller’s original argument (1879), let $a_1$ and $a_2$ be the numbers of two approximately equally unpalatable (or otherwise defended) species in some definite district during one summer, and let $n$ be the number of individuals of each distinct unpalatable species that are killed by predators during a season before their distastefulness is generally known. If the species are distinct in appearance, then each species would lose $n$ individuals in the course of educating predators. If, however, the two species were exactly alike in appearance, then the first species would lose only $a_1n/(a_1+a_2)$ and the second would lose only $a_2n/(a_1+a_2)$. Under these conditions, a mimetic mutant of species 1 that perfectly resembled species 2 would tend to spread from extreme rarity"

Note that there may be caveats and complexities which I haven't discussed, this is a simplification to try and explain the general reasoning


If women need more dietary iron than men, then do blood donors also?

This can indeed be an issue.  Frequent blood donors are known to get low on iron, which begins to result in fatigue, even before it starts resulting in low hemoglobin and anemia.

The cause is simple: like you pointed out, the loss of blood results in the loss of iron, and it takes the body a certain amount of time to rebuild the iron store.

As for your second question, the "newly created blood" will be low on iron until the body can absorb enough iron to replace that which has been donated.  Even on iron supplements, it can take up to half a year to rebuild the iron stores of the body to where they ought to be.

Sources:

Frequent blood donors risk iron deficiency, Miriam Shuchman, MD
Iron Deficiency & Anemia Treatment, Webmd.com


Why do genes, encoding the same proteins and in the same conditions, have different expression?

If I understand your question and graph correctly, your Y-axis is log(x/REF), where REF is some external standard. Your "Ref" on the x-axis you expect to be the same as REF, so that log(Ref/REF) "should be" zero, but you find it is not.
However, it looks like the mean(log(Ref/REF)) is still approximately zero. This is what I would expect: values that deviate a bit from perfectly 0, but having an average around 0 (and this average should approach 0 the more samples you have per the law of large numbers). You don't expect to have zero variance in data like this, which is why you repeat the experiment a number of times. You'll notice you have variance in all of your categories.


Where is the H+ ion in this step of glycolysis coming from?

Although texts such as Berg et al. tend to refer to inorganic phosphate, $\ce{P_i}$,  as orthophosphate ($\ce{PO4^{3-}}$), the term inorganic phosphate is used because in aqueous solution at pH 7.6 several phosphate species exist, the predominant one being $\ce{HPO4^{2-}}$. If this is regarded as $\ce{P_i}$, then it is the source of the $\ce{H^{+}}$, and the equation balances.

Note added by David:

On checking I find, in contrast to Berg, Lehninger’s book defines $\ce{P_i}$ as monohydrogen phosphate ($\ce{HPO4^{2-}}$), and Fersht actually writes the equation of the reaction (16-1) with $\ce{HPO4^{2-}}$ rather than $\ce{P_i}$.


How come our thyroid glands don't suffer awful mutations (or do they)?

Radioactive does not mean much in and of itself, your bones are radioactive (potassium), just being radioactive is not enough to do any damage.  It needs to be the right type of radiation and have high enough intensity before it can start damaging DNA and thus cause cancer. Second the amount of iodine in the body is miniscule, the aforementioned radioactive potassium in your body is orders of magnitude larger (if there is any radioactive iodine present at all which is unlikely).

On top of this remember we are surrounded by low dose radiation all the time so our bodies have evolved ways to handle minor damage.http://imgs.xkcd.com/blag/radiation.png


I did an agar gel electrophoresis but I could not see DNA, why?

One common reason you can't see your DNA is because you didn't put any EtBr / GelRed into your gel. Do you have enough PCR product to run it on another agarose gel?


How does one identify a seed's species & variety?

Yes, their name are "molecular marker". Every gene carrying a phenotype, quantitative or qualitative, is identified as an allele of every gene encoding for proteins.
In order to identify a phenotype using just infos gained from DNA, you'll need a previous library made by these gene regions, were every polymorphism between them is associated with a phenotype. For example, a kind of marker used for this kind of work is SSR , or "Simple sequence repeats" : it is made by a simple sequence of DNA interspaced between two other region. The number of repeats of the internal sequence could be associated with a phenotype.

So, by a simple PCR you could amplify this regions:

And by a electrophoresis you could see how much repetitions are in your band, using just the molecular weight.
Here is an example of SSR used for phenotype/genotype screening