What does the presence of 6 molecules of water in this equation indicates to?

This reaction only means complete oxidation of glucose to 6 molecules of carbon dioxide and 6 molecules of water.

Reaction presented in question is very generalized, but the presence of six water molecules only means complete cellular respiration. Check out the actual biochemical pathways which take place to oxidize one glucose molecule.

And other options do not represent the complete cellular respiration, so there will not be formation of six water molecules, only option C means complete oxidation of glucose.

Via: https://en.wikipedia.org/wiki/Cellular_respiration

Water molecules shown by solid blue arrows.

During glycolysis, One glucose molecule releases two water molecules. This is the 9th step  of glycolytic pathway controlled by Enolase. Two water molecules are produced because two reactions are taking place.

(Image source:  https://johncarlosbaez.wordpress.com/2016/01/08/glycolysis/)

During Citric acid cycle, 2 water molecules are used in two enzymatic reactions performed by  Fumarase and Citrate Synthase. And Aconitase performs the  isomerisation of citrate to isocitrate so it has no net effect on water molecules. So, 4 water molecules are used here.

(Image Source: http://www.biosciencenotes.com/citric-acid-cycle/)

During Electron transport chain, 12 water molecules are produced due to oxidation of NADH (FADH2).

As electrons in this chain are passed, they move from higher to lower energy state, and release energy. Some of the energy is used to transport hydrogen ions across the membrane. This creates electrochemical gradient. And electrons are transferred to molecular oxygen to form water.

This makes net total of 10 water molecules. But 4 water molecules during cellular respiration are used in substrate level phosphorylation. Check out its explanation here   (Via : https://onlinelibrary.wiley.com/doi/pdf/10.1016/0307-4412%2895%2900140-9)

(Image Source: https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/oxidative-phosphorylation/a/oxidative-phosphorylation-etc)


Do antioxidants interfere with chemotherapy?

Since it's a very broad argument I'll try to summarize in a few sentences.

First of all the sentence:

  Since most of the chemotherapy drugs kill cancer cells by damaging their DNAs by means of free radicals. So antioxidants, which will detoxify free radicals, should theoretically decrease the efficacy of the chemotherapy.

is a bit inaccurate as of today. The chemotherapy today uses the "classical" chemotherapy drugs which IN PART use the mechanism of free radical but there are a lot of mechanism such as microtubule damage and so on which do not depend on free radical toxicity. Today there are also a lot of biological drugs and inhibitors of tyrosine kinase inhibitor which use a completely different pathway.

You cite a paper from 2007, a bit dated, I cannot access full text because it's an abstract. It seems it's not performed in a systematic manner (it's a not a systematic review or meta-analysis) and is published in a journal of alternative medicine. Maybe there are more recent paper but unfortunately at the moment I cannot have the time to check.

Finally you are comparing the effects of a chemotherapy drug administered usually in high dosage to the use of antioxidant which I cannot recall are sold as drugs used regularly, so it's a potential interesting biological question but practically it's a bit difficult to compare the oxidative effect of a cancer drug with the effect of an antioxidant one in real patients since I don't think there are randomized controlled clinical trials comparing chemotherapy to antioxidant alone.


The mutation rate per haplotype per site is $\mu = 10^{-5}$. Assuming diploidy and a population size of $N=5000$, the population wide mutation rate per site is $10^{-5} * 5000 * 2 = 0.1$.

$0.1$ is hence the probability that a mutation occurs a at a given site (in the whole population). For 10 sites the probability that a mutation occurs at at least one site is $1 - (1-0.1)^{10} = 0.65$.

The probability we are aiming for is 0.95. So let's write the equation

$$1 - (1-0.1)^{x} = 0.95$$

, where $x$ is the number of sites we are looking for. You just have to solve for $x$ now and round up to the larger integer.


Is hunting animals, crafting and attacking/defending from enemies intellectually equivalent to learning quantum physics?

Addressing some assumptions/presumptions apparently present in the question (this might be too long for a comment):

First, natural selection has not stopped. The sexual selection might be more active than ever, so there is ongoing "pro-fertility" selection and some segregation "pro-smarts". Not every member of contemporary potplation is capable, even with unlimited attempts at education, of doing something useful with quantum physics.

Second, surviving in the wild and fighting enemies are competitive enterprises. Which means that the task is of potentially unlimited difficulty: the better you are at survival, the more you procreate, the more pressure you put on limited resources of the environment, to harsher climates you spread. With enemies, especially those evolving along with yourself, this unlimited competitiveness is even more obvious.

So, the question could possibly be framed differently: how hard our ancestors, living in nature, made the intellectual part of the task of competing with each other? Apparently, about that hard.


Why is the inside of a cell negatively charged

Net Potential on a cell surface is always measured in comparison to the extracellular media...so it is a relative parameter. So inside of the cell membrane is negative implies that there is more negative charges inside or more positive changes outside compared to the respective opposite side of the membrane. As we do not deal with the "absolute potential" we need not calculate the values of them.

K+ concentration is more inside the cell compared to outside...but there are other ions in and outside cells...e.g. Na+, Ca+,  proteins, Cl- etc...all of them together determine the potential difference across cell membrane.


How host defends against S. pneumoniae capsule?

According to the two papers listed below, this is mostly done by a neutrophilic inflammatory response. The response is regulated by mechanisms of the innate immune system and is mediated by receptor like TLR2, TLR4 and SIGN-R1.

Role of Dectin-2 in the host defense against Streptococcus
pneumoniae infection
Dectin-2-dependent NKT cell activation and serotype-specific antibody
production in mice immunized with pneumococcal polysaccharide
vaccine.

There are a few papers which go deeper (reviews, so you will probably have to go through the reference lists):

Mechanisms of host defense against infection with Streptococcus
pneumoniae.

This paper mentions specific antibodies later on in the reaction and finally the opsonization by immune cells.

These two papers tal specifically about pneumolysin:

Pneumococcal virulence factors and host immune responses to them.
Pneumolysin as a vaccine and drug target in the prevention and
treatment of invasive pneumococcal disease.


By what physiological mechanism do we not feel microbes (bacteria, etc.) living on our skin?

Ask yourself, what benefit would it have?

Keep in mind you will always bee covered in them, this is the state you evolved in. Thus sensing them would serve no purpose, and sensory organs are expensive in terms of resources so why would we evolve a useless sense?


I'll try to approach this topic academically and undogmatically since skepticism is essential to scientific discourse. However, bear in mind that as of $2009$, $97\%$ of scientists believed in evolution (Pew Research Center, 2009). Although I can't find how many scientists were surveyed, nor what disciplines they studied.
I've not given many citations, since I'm questioning the counter-arguments to evolution, and not necessarily providing my own specific claims. I'll also avoid discussions in comments since this could be a contentious topic.
1. Missing Links
In theory, if there aren't fossil records forming a complete chain of species from early hominids to humans, then this could cast doubt on the theory of evolution. But the fossil records are convincing and there are many of them (Wikipedia, n.d.). Also, if there truly is a missing link and there is no relation between humans and early hominids, then why do their skeletons look so similar? And why did humans suddenly come into existence? Is there a better rational or empirical explanation?
2. Skepticism of Existence of Fossils
One could propose that there are no fossil records, or that they have been faked. But why would anyone want to make any fake fossils or lie about them? What possible conflict of interest would they have, and why would this benefit them? Why would tens of thousands of scholars want to support this theory? How does this explain how scientists are still discovering new fossils? If anything, a paper that shows that evolution is false would be groundbreaking and give instant publicity to whoever publishes it.
3. Inaccuracy of Techniques: Radiocarbon Dating
A variety of scientific techniques have been used to garner information about the fossil records. One such technique is radiocarbon dating, which tells us how old the fossils are. If this technique is inaccurate, we could be wrong about the fossils and they might not form a chain that leads from early hominids to humans. But the technique is broadly accepted. Also, how would this explain the fossils - why would humanoid fossils with such odd shapes occur at random points in time? The shapes of these fossils don't look like typical human mutations.
4. Skepticism of Age of the Earth
Another counter-argument proposed to evolution is that the age of the fossils doesn't allow for their beliefs of the age of the earth. But the age of the earth is accepted by the geological community to be ca. $5\;\mathrm{bn}$ years old (Wikipedia, n.d.).
5. Summary and Micro/Macroevolution
A related counter-argument to evolution that I'd like to cover, but isn't directly related to the accuracy of fossil records is that of microevolution vs. macroevolution. Some people argue that we can only see evolution on minute scales, and not on large scales. But then if a population does have small-scale changes, and there is a higher probability individuals with certain adaptations surviving, then wouldn't these micro-effects sum, over millions of years, to produce large-scale effects?
In my opinion, the counter-arguments for the fossil records of the fossil records for evolution are rather flimsy, which suggests that evolution is the best explanation we currently have for the evidence we've observed.


Is it possible to have a random un-mutation of genes?

A large part of the body of your question seems relatively unrelated to the main question which is a little confusing. I will focus on the question

  Is it possible for there to be a random un-mutation of genes?

Yes, these are usually called reversed mutation. It is quite common though that a second mutation at a distinct locus may reverse the phenotypic effect of a first mutation. This is called a compensatory mutation.


Are there more/less favourable phases of menstrual cycle to donate blood?

1)

Hormones involved with Menstruation (FSH, LH, Estrogen, Progesterone, etc.) will vary depending in concentration depending on the time-frame:

You are correct in saying that not much blood is actually lost in the menstrual fluid: Less than 80mL (80cc), although the blood's origin is ultimately the circulatory system. Does it affect the quality of the blood? No. Usually not enough iron is lost during menstruation to make a difference between being able to donate blood and not donate. However, women who bleed heavier than the average can experience anemia (iron deficiency) - although anemia attributed to menstruation is often misdiagnosed gastrointestinal issues (up to 86% error rate).

One thing to consider is that common pain medications can affect blood content, and thus a woman taking aspirin cannot donate platelets for 5 days after she stops, and a woman taking NSAIDs (like Ibuprofen) cannot donate for 2 days after she stops.

2)

  ...the combination of blood loss from periods and donation will make iron deficiency anaemia more likely, particularly if the periods are heavy or prolonged. This effect can be minimised by taking supplemental iron.

In general, as long as the woman feels well or the pain is controlled, she is perfectly capable of donating as long as her iron levels reach the minimums. The blood makeup is not significantly different, although hormone and iron levels will minimally fluctuate.

  As always, this response is based upon information during some light research. I am not a doctor, and the information presented in this response may be modified later to increase accuracy or remove errors upon the discovery of new information.


IMPORTANT EDIT : In your particular case, if you are working with bacterial genes, splicing is not an issue since bacteria do not have introns. I am leaving the information here since it may be useful to someone else. However, I recommend you focus on the UTRs since they are probably what is causing you problems.

There are three things that could be causing you problems. I will briefly touch on each one. I will talk about all genes, bear in mind that bacteria have no introns so any discussion of splicing and/or introns and exons is not directly relevant to your problem.

1. UTRs

Untranslated Regions (UTRs) are sequences at the beginning and end of a gene that are not translated into protein. UTRs are regions that are part of the original genomic sequence, they are also part of the mature mRNA (indeed, UTRs are sometimes modified by splicing events, they are exons not introns) but they do not get translated into protein. To illustrate, have a look at this simplified representation of an mRNA molecule:

Only the green exons will make it into the final protein. Introns are spliced out and UTRs are not translated.

Therefore, if you translate the entire gene, you will not get the correct protein.

2. Reading frames

Genes are read in words of three letters (the codons). The sequence ATGTGTACCTGA has six possible reading frames (three on each strand) which can be read and translated as follows:

5'3' Frame 1

    ATG TGT ACC TGA
     M   C   T  Stop

5'3' Frame 2

    a TGT GTA CCT ga
       C   V   P

5'3' Frame 3

    at GTG TAC CTG a
        V   Y   L

3'5' Frame 1

TCA GGT ACA CAT
 S   G   T   H

3'5' Frame 2

t CAG GTA CAC at
   Q   V   H

3'5' Frame 3

tc AGG TAC ACA t
    R   Y   T

DNA is double stranded. The sequence of one strand is complementary to that of the other, therefore if you have one strand you can infer the sequence of its complementary one. Genes can be found on either strand, the two are equivalent biologically. However, sequencing projects choose one of the two strands (randomly) and call it the plus (+) strand and then save all sequences with respect to that strand. This means that sometimes the genomic sequence that you download from a database might be the complement of the actual sequence you are looking for.

3. Names

I once heard someone say in a conference that

  Biologists would rather share a toothbrush than a gene name.

While that might be a little exaggerated, naming conventions vary between research communities and species and databases. So, are you sure that you have downloaded the correct gene? Where did you get it from? How did you identify it? Does the sequence also contain up/downstream regulatory regions, promoters, enhancers and the like? If you post the exact sequence you are attempting to use I can give you more specific help.

For example, the first 20 hits when searching for the E. coli DNA Polymerase 3 in ncbi's nucleotide database, are whole genome shotgun sequences. These do not correspond to the gene sequence you are looking for. They are huge pieces of the genome (or even the entire genome) that will contain your gene and many others. Look at the Tools section below for suggestions on extracting your gene from the whole genome.

4. Splicing (irrelevant to bacteria)

Another possible problem is splicing. Lets start with the basics, the process of producing a eukaryotic (bacteria have no introns) protein from a genomic sequence is summarized in the image below (modified slightly from here):

Transcription begins at the transcription start site (TSS) but not all the transcribed sequence is translated into protein. First, the introns are spliced out of the mRNA to produce the mature mRNA (other things like capping and poly-A addition also occur but are not relevant here). So,the mature mRNA contains the exons of the coding gene. This means that a linear translation of the gene's sequence will not correspond to the protein produced. You will need to take splicing into account.

Also, bear in mind that splicing will change the reading frame.

Now, if the sequence ATGT were spliced at, for example, AT/gt (most splice events cut/join at GT/AG sites) and joined with the sequence agATTATT, the resulting (spliced) sequence would be (the splicing process will remove the gt from the first sequence and the ag from the second):

ATATTATT

As you can see, the reading frame has now changed. Where before, in the first reading frame, we had the codon ATG, the canonical translation initiation codon, we now have ATA which codes for isoleucine (I). I hope that is clear,  the main point is that splicing can change the reading frame.

5. Tools

OK, that was the background. Now, what you will need to do is use existing programs that model splice sites and can correctly align a protein sequence to genomic DNA. My personal favorites are exonerate and genewise. On a Debian-based Linux distribution, you can install them with this command:

sudo apt-get install exonerate wise

Then, to align the protein to its gene do:

exonerate -m protein2genome -n 1 prot.fa dna.fa > out.txt

or

genewise -pep -pretty -gff -cdna prot.fa dna.fa > out.txt

In my experience exonerate is (much) faster but genewise is a little more accurate. I usually use exonerate if I am dealing with a whole genome and genewise if I only have a few kilobases of sequence. Both are very good and both will be able to align a protein to its genome of origin.

I will not explain all these options because that is beyond the scope of this site. Have a look at their documentation (which is quite good and clear) and if you still have problems, you could ask a question on our sister site, Bioinformatics Stackexchange

Alternatively, you could link your web application to the ucsc genome browser BLAT service. Click here to see the results when aligning the human
DNA-directed RNA polymerase II subunit RPB1 protein.


How does the body respond to blood donation; are there any possible risks?

My answer below directly (and solely) addresses what I think is the main gist of the question: Are there any adverse effects on one's physiology as a direct result of donating blood?

Blood donation, at the amounts typically taken (200~500mls), will not harm you. A healthy human being produces approximately 100,000,000,000 (one hundred billion) NEW hematopoietic cells DAILY to replenish short-lived blood cells and platelets. All of these ultimately derive from the hematopoietic stem cells residing in the bone marrow within one's long bones.

As you can appreciate, with such a huge amount of turnover daily, the body is constantly churning out new blood cells. Thus, any depletion in blood cells one will experience as a result of blood donation is a fraction of what will be lost normally in daily homeostasis anyway and thus will not affect a healthy individual.

And then there are the knock-on benefits suggested by epidemiological studies, some of which are alluded in this layman article: http://news.health.com/2014/06/13/4-unexpected-benefits-of-donating-blood/

[source: I'm a hematologist]


How does Sanger sequencing resolve two bands with equal size?

It happens if your sample contains a mix of two DNA molecules, with different bases at a certain position.

In your case, you would have a mixture of ACTGGCTA and ACTGTCTA.

In real life, the "double band" would be half as intense as the other single bands, as the signal is "divided by two".


Claudia's dad is not a taster, so he is tt. He passes one allele on to his daughter. Since he is homozygous, he can only pass t. Claudia is a taster, so she must have the dominant allele from her mother, who is also a taster. Thus, Claudia is Tt.


Short answer
The textbooks are right; the receptor part of sensory neurons is always considered to be the dendrite. Axons are nonetheless an integral part of some receptor types to send the signal to the brain. Other, more specialized sensory cells do not have an axon and therefore rely on secondary neurons to send the signal to the brain.

Background
There are three types of sensory cells, namely those with free nerve endings, those with specialized dendritic structures, and specialized receptor cells that synapse directly onto a secondary neuron (Fig. 1).

Fig. 1. Types of sensory neurons. Source: Premed HQ.

Sensory neurons with free nerve endings have an exposed dendrite that functions as receptor. Examples are nociceptors (pain receptors) and hair follicle receptors.
Other sensory neurons are complex cells that feature a dendritic region specialized for a particular receptor function. Examples are the Pacinian corpuscle and olfactory neurons.
The most common receptor type are specialized receptor neurons that have no axon and need a secondary sensory neuron to send the signal to the brain. Examples are the photoreceptor cells in the retina, the hair cells in the cochlea and Merkel cells.


Let's review drug administration routes, and see for yourself:

transdermal/ionophoric: expensive, unreliable release concentrations (which makes it expensive because of the extensive research needed for controlled release), noticeable to others ("why do you have that skin patch, mom?" Er...)
Sublingual: quite similar to oral route, however absence of first pass hepatic metabolism can result in completely different blood concentrations between the two routes. Impairs speech. Could cause mouth irritation (quite disabling). Requires patient compliance.
intravenous: quite unpractical in outpatient settings. Invasive measure.
intramuscular/intradermal: hurts. As all things using a needle. Usable, but impractical in the outpatient setting. Can lead to skin lesions (insulin injection in diabetes, for example)
rectal: culturally unacceptable to some, unreliable release.
vaginal: similar to rectal, but only for women obviously
spinal/epidural: very invasive, only in inpatient settings.
topical: usually only acts locally, can cause discomfort (eyes)
oral/enteral: well known pharmacokinetics, mostly invisible to others, practical in the outpatient setting, requires limited patient compliance, well known excipients. Of course there can be secondary effects, but that is the case for all administration routes. Most common side effects are abdominal discomfort and nausea, but no one can see you in the water closet. Plus people are used to see pills as medication, something which might not be the case for other routes, depending on the cultural background of the patient.

This answer is of course somewhat subjective, however the importance of the patient's perception and his/her view of what the administration route implies socially cannot be overemphasized.


how body doesn't make antibodies against adjuvants of vaccine?

Basically, this is what is happening when you receive a vaccine.

Immunoglobulins are being made agains protein adjuvants such as flagellin
Some of the adjuvants based on endotoxins such a lipopolysaccharides are not proteins. While there are some immunoglobulins produced that detect these molecules, the majority detect proteins
Most antibodies are produced against the functional conformation of the protein, so its tertiary or quaternary structure. When polypeptides are loaded into MHC II, it is a small piece of the primary sequence of amino acids. This is used to activate CD4+ helper T-Cells.
Vaccine is given in one of three ways; subcutaneously, intramuscularly, or orally (including nasally). Most antibodies circulate in the blood until they leak out of the blood vessels at the site of an infection. Also free antibody have half-lives of between 7 to 21 days, so even if there had been IgG in the tissue from a prior inoculation, it is unlikely that any will be at the site of the new inoculation without an inflammatory response taking place.

Oral vaccines will encounter IgA molecules in the mucus, so if they were made from a prior immunization, they could opsonize the vaccine, however, it is likely given in a high enough dose that some of the vaccine will reach the antigen presenting cells.

When delivered subcutaneously or intramuscularly, the vaccine will first be encountered by the innate immune system, even if adaptive immune cells were activated in previous rounds of vaccination. It is very unlikely that IgG will be encountered at the site of the inoculation, as IgG circulates in the blood and only ever really gets into the site of inoculation or infection after the innate immune cells have initiated an inflammatory response leading to the permeabilization of the blood vessels, allowing other immune cells and immunoproteins access to the site of the infection. Either way, APCs will be taking up the vaccine before the antibodies against them can neutralize them.

It is also likely a good thing that there are CD4+ cells in circulation that recognize a sequence of the adjuvant. If the B cell phagocytoses the vaccine and adjuvant, such as with a flagellin fusion vaccine, because there was specificity for an epitope on the target protein (vaccine), then even though the B cell is not making an antibody to the adjuvant, putting the adjuvant sequence on the MHC II means that it can be activated by a helper T-cell that recognized the adjuvant polypeptide, even if there is no T-cells that recognize the vaccine.


How do you find probabilites of carrying an X linked recessive disease in a blank pedigree given only one phenotype?

Assume the disease is rare. The parents of the affected male are thus probably X/Y and Xc/X. Their daughter (the sister of the affected male) has a probability of 1/2 of being a carrier (Xc/X). Her daughter also has a 1/2 probability of being a carrier. Her son has a 1/2 probability receiving the mutant X chromosome. Therefore, the probability that the son is affected is 1/2 * 1/2 * 1/2 = 1/8.

I can’t right now, but I’ll try and make it clearer with a figure tomorrow.


Do non-migratory canada geese still exhibit migration behaviors?

The answer is yes, also sedentary geese do use migration patterns (V-formations). When they move from roosting place to feeding areas (or vice versa) geese always tend to fly in formations. I speak for personal experience of resident and wintering birds in Europe and America.

They do so because they save energy as explained here: http://jeb.biologists.org/content/128/1/445.short and here: http://www.nature.com/nature/journal/v413/n6857/full/413697a0.html

The second study also show how not all the positions in the formation are the same regarding energy expenditure. The one closer to the front of the V shape need to flap the wing more often.

Have fun


What is this black and white worm in a white case?

This is just a larva of a moth from the Family Tineidae, most probably Phereoeca uterella (known as plaster bagworm or household casebearer), or Tinea pellionella (known as case-bearing clothes moth).

As you can see, the larva of this moth...

  ... constructs a protective case from silk and camouflages it with other materials such as soil, sand and insect droppings. (from Wikipedia)

Here is a better picture of Phereoeca uterella, from the entomology deptartment of the University of Florida:

Here is the imago (adult), for comparison:


What is the main general difference between Mitosis and Meiosis?

If the question is about the one and only most important difference between mitosis and meiosis, then the answer "meiosis reduces ploidy" is probably correct. But if the list of important differences is open, it would be critical to add that mitosis generates identical cells (identical to each other and any ancestral cells, barring rare new mutations), while meiosis generates genetic diversity by creating cells, which are all different from each other and from any ancestral cells. It does so by independent segregation of homologs and by crossingover within chromosomes.


General overview.
Each toxin and poison probably have their own evolutionary "arms race". Generally, an organism contains a compound that is a bit harmful to other species. As a predator or prey species becomes tolerant to low doses of this compound through natural selection, the compound efficacy could be increased (again by natural selection) on a molecular level, or at a dosage or concentration level.
Below are a few examples of where this has become the case, and some more general examples of how venom evolved in the first place.
Examples.
California Newt.
These newts contain tetrodotoxin (you may be familiar with this from the fugu fish). It is preyed on by a species of garter snake. This is a textbook arms race as the garter snake is naturally selected to have beneficial alleles that are tolerant to the toxin.
Dart Frogs.
The golden dart frog Phyllobates terribilis contains enough batrachotoxin to kill 10 people. That is apparently overkilling for any predator it would surely have to face especially given that the only animal alive that is immune to the poison is the frog itself. However, the snake Liophis epinephelus can tolerate massive doses of batrachotoxin (although I've heard it gets pretty poorly after eating a frog, rather understandably). These two species are locked in an arms race that drives the frogs to produce an unbelievably fatal cocktail and the snakes to become ever more tolerant.
Snakes.
Modified sweat glands evolved to damage the prey as much as possible for immobilisation, partial digestion, or defence. There are textbooks about snake venom and toxins. Here is a neat article I found with a cursory search or if you want to sink your teeth into the topic (heh.) check out this article.
Long story short: venom sacks are modified saliva glands from non-venomous snake ancestors. The diagram shows generally just how modified these apparatus have become!

Platypus
Let's not forget the weird and wonderful monotremes. It's hard to pinpoint exactly what drove the platypus to develop venomous barbs on its elbow (last time I looked into it, it was still disputed if they were for defence or hunting).

But what we can learn from this is that venom can independently evolve. Although the venom producing proteins are different, they produce the same venom as some snakes.


Can you identify this (possibly waterstoring) plant?

It is an Euphorbia leuconeura (Madagascar Jewel), which is native to Madagaskar. The leaves and the thick (waterstoring) stem with a narrow base is very typical.

The plant is cool in the sense that it easily produces seeds (also as potted) which it can shoot away from the plant. I've had it myself and you can sometimes hear seeds hitting the window or floor. Even if it is easy to grow and to reproduce it is actually considered threatened in its native habitat (IUCN Red-listed as Vulnerable) due to habitat loss

The flowers are very small and found directly on the stem, see below:

(picture from Wikipedia)


Would humans eventually evolve to fight off fatal diseases if we didn't treat/vaccinate for them?

Sure.

When the Europeans settled the Americas, 90%+ of the native American inhabitants were wiped out due to diseases like smallpox that the Europeans clearly had developed resistance to. Clearly, the surviving native americans had resistance, and the Europeans had gone through some similar event previously in history.

The bubonic plague that was the cause behind the black death wiped out large percentages of populations, but selected for survivors with resistance:

Black Death Left a Mark on Human Genome

Caveats:

Often evolving to fight off disease involves mass death, like with >90% of the native american population dying.
There is always the chance that a future pandemic can come that human biology fails to simply evolve a resistance for and gets wiped out.
The Earth is changing rather quickly. The past is not a guarantee for the future.


Why doesn't infection with Clostridium Tetani immunize you?

There is a big difference with tetanus compared with other infections. The amount of toxin that produces tetany is extremely tiny. Even a small infection that the immune system has yet to react to can be lethal.
To produce a long-lasting response against the bacterium would require a lethal number of bacteria.

Vaccination with the toxoid results in antibodies against the toxin, not the bacteria.


How are drugs distributed in regards to bone marrow?

How are drugs distributed into any tissue, and what affects it?
Note that there are no general answers, and that this is highly dependent on the drug in question.
Active or passive transport
Is your drug a substrate for any uptake or efflux transporters that may affect the distribution?
Solubility
Lipophilic drugs will generally have a greater volume of distribution, as there is more passive diffusion into tissue.
Blood flow
How much drug is presented to the area in question? Tissue with greater perfusion (e.g. kidneys) will have a greater exposure to the drug. Look up the well-stirred model.
Relating this to the blood marrow
So what should you research in order to answer your question?

What are the physiochemical properties of the drug in question? How are these compared to other drugs where the bone marrow is a target?
Is the drug a substrate for any relevant transporters in the tissue of interest?

You should also look up if there are any physiologically-based pharmacokinetic (PBPK) models for your drug or drugs with similair physiochemical properties. Some of these are free, and allow you to make general assumptions about the distribution of the drug.


TL;DR: Living fossils are the children of long-dead fossilised creatures that were good at being alike, other animals are the children that were good at being different.

The boring answer is that living fossils are around because nothing has happened to make them go extinct.

The more exciting answer is a tale of intrigue and lies stretching back hundreds of millions of years:

The lie that is the 'species'

The notion of a species is, of course, a lie. It's a useful lie, and one without which the equally useful field of taxonomy would be impossible, but a lie all the same. Every living thing is ultimately a unique individual unto itself. We group these individuals up and call them things, according to things that are more or less arbitrary, and we arrange these groups into bigger groups and fill books upon books with this method, because it makes it super easy to get a good overview of how life developed.

However, if we want to understand the details, we have to see past species, and look at the lineages.

The shark, our ancestor1

One such lineage that is of interest is that of the shark. Sharks are ancient: They are roughly as old as plants, and older than almost all land fauna. They are vicious, unrelenting killing machines, and all but perfectly suited for being this, with their sleek shape, their conveyor belts of teeth, and rough skin. At some point way back when, however, the lineage of sharks split in two: One branch that leads to fish, amphibians and eventually dinosaurs, squirrels and dolphins, and one that leads to sharks. The forebear to all these things were the early cartilaginous fish of the Cambrian ocean.

To answer the question as posed, we have to compare the success factors of the two lineages.

Why sharks are still around as living fossils

The real answer here is that, in a very real sense, they aren't. Modern sharks are no more alike their long-dead forebears than squirrels are. However, the biological niche inhabited by sharks (apex predator) is a successful one, and sharks, already existing in this niche, have had successful children, made more successful by being superficially and behaviourally alike to their parents, and so, the modern shark presents as a living fossil.

Why shark contemporaries are not still around as living fossils

The real answer here is that, in a very real sense, they are. Morphological differences aside, squirrels are no more different from their long-dead forebears than sharks. Rather, crowded niches have made generation upon generation of increasingly squirrely animals more successful by being superficially and behaviourally different from their parents, and so, modern squirrels have arisen.

Edit: Footnotes:

The shark is not in fact our ancestor, rather Cambrian early jawed fish are. The image of a shark is however far more evocative and easier to talk about.


It's probably an adult varied carpet beetle (Anthrenus verbasci). They are quite small and commonly found in homes. Here's one of a number of images available on Wikimedia:


Given the presence of a petiole and postpetiole, this is most likely a winged ant (drone or queen), such as this similar one here:
https://bugguide.net/node/view/57281


Importance of germline and somatic genomic mutations to the purpose of treatment in cancer

A) There isn't really a fixed hierarchy that is applicable across the board - alterations are often binned into actionable targets and non-actionable ones. In terms of customised cancer vaccine for immunotherapy (Eg - www.sciencemag.org/news/2017/04/personalized-tumor-vaccines-keep-cancer-check ) , more antigenic mutations tend to be prioritised.

B) Sometimes there are reasons to prioritise mutations over others even for small molecule targeted therapies. For example, one would want to target mutations that are clonal rather than subclonal where possible, so that the bulk of the tumour, rather than a small fraction of the cells in it, are targeted. Alternatively where one has, for example, a resistance mutation arising from prior therapy (You see this with EGFR T970M mutations) it is an indication for next generation EGFR inhibitors that specifically hit the resistant mutation.


Does H. pylori have paracellular activity?

I found no evidence for paracellular movement.

Some notes of mine

  Mucinase $\to$ lophotrichous flagella $\to$ Transcellular (actin fibrils, tails) movement
  ICF Vacuolating cytotoxin (VacA) $\to$ altered T-cell function $\to$
  damages epithelial cells, disrupts tight junctions and causes
  apoptosis.

I think the latter point makes transcellular momevment possible.
I see no way how paracellular movement would be possible.


Aseptic technique: a single technique, or any technique fulfilling criteria, or collection of said techniques?

This is primarily a linguistic question and I am answering it on the basis that it will be migrated to Stack Exchange, English Language and Usage.

The question is whether, in the context of a report describing (otherwise unspecified) student work, the phrase “aseptic technique” can be used without an article, or whether it requires the definite or indefinite article. This is a question of meaning and usage, and, without using any technical grammatical terms, can be answered by anlysis of scientific publications and by analogy.

“The aseptic technique” (definite article)?

The definite article would normally be used in this type of situation if reference was to one specific clearly defined technique. As an anlogy I would take ‘The Heimlich manoeuvre’ (where ‘manoeuvre’ occupies an analagous position to ‘technique’. Clearly the phrase does not refer to a standard defined procedure like the Heimlich manoeuvre, but merely that the work was performed asceptically (i.e. under sterile conditions). So in this context the definite article is certainly not necesary. In some circumstances employing sterile conditions requires satisfying certain enumerated criteria (example below), in which case the definite article may be used.

“An aseptic technique” (indefinite article)?

I think that this is possible but not obligatory. The use of the indefinite article indicates that the asceptic technique used was one of several possible. Although sometimes this would be used in the context of a limited number of items, this is not a necessary requirement. Analogies with a different adjective would be “she executed the dive with a graceful technique”. Here, the article is (almost) obligatory, but less so in the case of “she showed superb technique in executing the dive”.

“Aseptic technique” (no article)?

As the last example shows (“she showed superb technique in executing the dive”), omitting the article is perfectly acceptable in analagous phrases. I would say it is perfectly acceptable in this case.

The arguments above are only useful to the extent that they reflect actual practice. A quick internet search brought up an interesting example in which both no article and the indefinite article were used in the same text. This is the entry for Asceptic Technique on a website called Healthline.

The second paragraph omits the article:

  Aseptic technique is a method designed to prevent contamination from microorganisms.

But when it gets down to specifics:

  According to The Joint Commission, there are four chief aspects of the aseptic technique

So unless your friend was referring to ‘The Joint Commission’ (which I doubt) there is nothing wrong with that sentence of her lab report.

Other Professional Examples

ThermoFisher Scientific — no article

  Aseptic technique, designed to provide a barrier between the microrganisms in the environment and the sterile cell culture, depends upon a set of procedures to reduce the probability of contamination from these sources

Nuffield Foundation — indefinite article (implied by use of ‘any’)

  There are some general rules to follow for any aseptic technique.

ANTT — definite article used in reference to a specific named technique

  Aseptic technique is the most commonly performed infection prevention procedure in healthcare; it is also probably the most critical. This article looks at the Aseptic Non Touch Technique (ANTT) model for reducing healthcare-associated infections

(You could argue that the definite article refers to the model, rather than the technique, although I think if you omitted ‘model’ you would be left with an example like the Haemlich manoeuvre. In any case the English in this article is appalling — “infection prevention procedure” gives a foretaste of the stylistic horrors that follow.)


Fraction of naive T-cells in CD4+ T-cells isolated from whole blood?

Stemcell Technologies has a really good wall poster for this. You can enumerate roughly 80,000 to 760,000 naive CD4+ T cells from peripheral blood per mL. This is 1-10% of leukocytes.

One of the things you need to remember about memory cells is that they do circulate, but it follows that among the circulating subsets of memory cells, they highly express markers for lymph node localization such as CCR7 and CD62L. Their presence in the blood at a given time is influenced by a number of factors including disease state.

Likewise, effector cells are programmed to localize within infected or distressed tissues through the actions of chemokines and chemokine receptors. The presence of effectors will depend on the same sort of factors, and as effector T cells, they are typically either made anergic and die by apoptosis or differentiated into memory cells.


Which of Perutz et al's protein structures other than 3₁₀ helix were correct?

I think you've got the list of good predictions from the Bragg, Perutz, and Kendrick paper.  And the 310 helix was not really right either - it did turn out to show up occasionally in protein structures though.

At the time all of these secondary structure elements were well evidenced from noncrystalline diffraction data and small molecule crystal structures. Examples being collagen from hair and spider silk fiber diffraction patterns. Fiber diffraction of hair, whose ordered structure consists mainly of alpha helices somewhat aligned to the fiber axis (along the length of the hair) or the mainly beta sheets which constitute silk.

Because it was known that these substances contain mainly protein, building models which would show how regular peptide polymers would produce these patterns.  This happened in chemistry and physics departments worldwide.  The paper you cite is representative to the field.

Pauling caused a splash in the spring of 1951 by publishing descriptions of the alpha helix and the beta sheet (both parallel and antiparallel).  The main advantage that Pauling had was that he had studied the structure of simple di-amino acid structures (notably glycyl-glycine) and understood that the peptide bond had some double bond like properties which prevented it from rotating freely.  As the discoverer of valence bond theory, which united quantum mechanics and chemistry and established the basis for at least most organic/biological chemical structures Pauling must have been practically alone in this insight at the time.

This next set the stage for the dramatic race to discover the structure of DNA. If you read Watsons' memoir, he describes how the MRC in Cambridge was still feeling the heat,  competing with CalTech and Pauling.  He and the young lab there was holding their own against the MRC Cambridge with its multiple nobel laureates; a lab which had established the relationship of x-ray diffraction and chemical structure (the notes on chapter 7 are interesting - follow the link).

Looking back on it, Pauling's main advantage was that he understood the peptide bond better than the rest of the world. By the time DNA was being resolved, the conformations of organic molecules were understood by many and the playing field should have been more level.  I'm not sure I buy the arguments that Pauling would have got the structure without seeing the diffraction patterns and even then maybe not. I might not give such strong credence to the idea that Pauling would have gotten the DNA structure so quickly if he had been able to travel.

Of course Perutz and Kendrew verified the peptide alpha helix themselves when they solved the first crystal structures of hemoglobin and myoglobin, having the final say.  The structures contain a small amount of 310 helix but are otherwise full of alpha helices.  I'm not sure that the secondary structure was entirely confirmed until the 1958 when myoglobin was resolved.


Are left-handed people more likely to be colorblind?

In research literature, colorblindness and handedness appear to be correlated through male-ness.

Genetic causes of colorblindness are on the X chromosome, which explains why males are much more likely to suffer from colorblindness than females, as high as 16x more likely for red-green colorblindness.

Handedness is a complex polygenic trait governed by dozens of genes. A recent paper, Brandler et al., PLOS Genetics 2013, studying handedness implicated genes in chromosome 10.

However, males appear to be 25% more likely to be left-handed than females.

I wasn't able to find any studies directly addressing whether or not handedness is correlated with colorblindness, but it appears that if the only thing you tell me is that you are left-handed, then I can guess that you are more likely to be male than female, which means you are more likely to be colorblind than a person picked at random. So yes, a correlation appears to exist through maleness.

However, it's possible that being left-handed is conditionally independent of being colorblind given that you are male. In which case, for males, there may not be a correlation between left-handedness and colorblindness - there haven't been any studies addressing this question that I have seen.

To put this another way: if you tell me that you're male and left-handed, then insufficient scientific studies exist for me to guess whether or not you're more likely to be colorblind or not.


The insulin receptor is a glycoprotein. This is discussed, albeit briefly, in both papers for the structures you mentioned and the glycosylation is visible in the structures themselves. You can get more info in the following paper, among others:

Sparrow LG, Lawrence MC, Gorman JJ, Strike PM, Robinson CP, McKern NM, Ward CW. 2008. N-linked glycans of the human insulin receptor and their distribution over the crystal structure. Proteins 71(1):426-439.


Is there a name for the evolutionary loss of vestigial structures?

This phenomenon can be (and has been) described as regressive evolution (the loss of a phenotypic trait). There are several reasons why this occurs:

Neutral mutations which become fixed through genetic drift.
Positive selection of regressive mutations that are beneficial.
Pleiotropic antagonism: positive selection for one trait may have the consequence of disrupting another trait which isn't strongly selected for.

The eye degeneration example you chose is a good one because it is well studied in cavefish (which evolved from sighted surface fish and have degenerate eyes). Normal eye development is under the control of the Pax6 transcription factor. Expression of another transcription factor, Shh, reduces Pax6 expression. Shh expression along the embryonic midline is responsible for splitting the eye field bilaterally. Overexpression of Shh in surface fish leads to eye degeneration and, indeed, it was found that cavefish have an expanded Shh expression pattern.

Cavefish have also undergone a behavioural shift to bottom feeding and have become less aggressive to focus more on finding food. As it happens, the expanded Shh expression also causes a widening of the jaw and amplification of taste buds, both of which aid in scooping and sampling the river bottom. Furthermore, increased Shh expression during brain development influences a decrease in aggressiveness and a shift to foraging behaviour.

This is an example of pleiotropic antagonism: positive selection for jaw enhancements and behavioural changes via expanded Shh expression, which increase fitness in cave environments, can explain why the eye degenerated.


I don't think the microtubules shorten. The disassembly of tubulin (dynamic catastrophe) happens from its + end which in this case is protected by the kinetochore proteins. The separation of chromatids, I guess, happens via a dynein (and in some cases kinesin) mediated movement.

The wikipedia article on kinetochore is quite detailed and you can have a look at it.


Neurons generally have one axon, because of the way it sums potentials from its dendrites. Right at the axon hillock (the little area where the axon protrudes from the soma), all the potentials are summed together. Now, you have to consider that what is actually summed here is dependent on the shape of the neuron, potentials lose amplitude as they travel towards the axon hillock. If there were multiple axons protruding from different sites, they would send out different signals and compromise the computational integrity of the neuron.

Instead of having multiple axons, a neuron simply branches its axon with axon collaterals. This way, all post synaptic sites are receiving virtually the same message.


Meaning of Allele

The word "allele" is often used with two slightly different meanings in biology.

The first, probably more appropriate usage is the one in Remi.b's answer: an allele is a variant of a gene in a population; there are many many possible alleles for a given gene, depending on the length of the gene, though typically only a few are common in a population and even fewer may be known.

The second use of the word "allele" is to mean "copy" of a gene; because those copies can be different, in this context an allele is a potential variant of a gene in an individual. For a diploid organism like a human, you might say that an individual has "two alleles" but what you really mean to say is that individual has "two copies of a gene, which could be the same or different alleles." The relationship between the two copies is called zygosity. I'd argue that this is a slightly sloppy use of the term, but nonetheless it is common and if you understand the meaning it is still clear.

Genes for hemoglobin

For hemoglobin, there are at least 3 important genes: two each encode alpha subunits, and the third encodes the beta subunit (there is also a delta and gamma subunit, but we can omit discussion of those for now).

For the beta subunit, each individual has two copies of the gene, which in human populations are typically thought of as one of two population alleles: either a normal allele or an allele associated with sickle cell anemia. Individuals with two of the sickle cell alleles will have sickle cell anemia.

For the alpha subunit, each individual has two copies of two different genes. There are alleles for each of those genes that produce non-functional products. Individuals with alleles that produce non-functional alpha subunits, for either gene, have Alpha-thalassemia. The severity of Alpha-thalassemia depends on how many alleles are present across the two genes that do not product functional alpha subunits.

Why 4 alleles for hemoglobin??

I suspect if you read somewhere that there are "4 alleles" for hemoglobin, that source was probably talking about Alpha-thalassemia in particular, in which case there are indeed 2 copies of 2 different genes so that an individual has four possible alleles. The severity of Alpha-thalassemia depends on the total number of defective alleles across the two genes, where having 4 defective copies is fatal, and having just 1 defective copy is not noticed clinically.

In the population, however, it is likely that there are actually many other alleles for each gene. For the purpose of describing disease, however, we can group these into "functional" and "non-functional" and say that there are two population alleles for each of these two genes.


Is it possible to perform selection of plants without seeds?

Most commonly by breeding with a related plant - if there is one. Mutagenesis is an old technique that technically can work.

If one part of the plant has mutated, of course you can take cuttings or plant tissue culture samples.

strawberries can be bred and characteristics selected for.
https://en.wikipedia.org/wiki/Breeding_of_strawberries

A good example of a difficultto breeed plant is bananas
See
http://www.promusa.org/blogpost363-Who-s-breeding-bananas


Why is Mus Musculus a good model organism?

Mice are mammals, like humans, so their proteins tend to show more homology with human proteins than non-mammalian options. They are also actually more closely related to humans than cats or dogs due to the relatively recent (~80 million year) separation of lineages that led to modern rodents and primates.

Mice breed fairly quickly year-round and have relatively large litters. Laboratory strains are also quite tolerant of research lab conditions.

Mice are inexpensive to keep: they are small, require little food and care, etc.

People tend to have less opposition to research in mice due to their status as pest species.

Many genetic tools are available for mice, which makes them better models for the next generation of science, which means there are more genetic tools available for the generation that follows, etc. There are now many specialized mouse lines, some for particular diseases, some for particular techniques, etc.

Mice are well-studied, so experiments in mice can be easily compared to other experiments, and there are a lot of standards for protocols. Most experiments are done on inbred mice, which have the advantage of being nearly genetically identical to each other, so experiments done in different labs are done in (nearly) genetically identical subjects which can help with reproducibility and comparisons across studies (though there are also downsides to inbred animals; see below).

None of these factors make mice perfect model organisms. Many successful experiments and treatments in mice have not translated to human outcomes. Laboratory mice are typically highly inbred and may display characteristics thought to be "normal" that are actually the result of genetic drift, founder effects, etc. These can include preferences for alcohol, tendencies toward obesity, poor immune systems compared to wild mice, etc. Some get particular tumors early. Some have seizures. Some lab mice are blind at birth or shortly after. Others have hearing problems.

References

Abolins, S. R., Pocock, M. J., Hafalla, J. C., Riley, E. M., & Viney, M. E. (2011). Measures of immune function of wild mice, Mus musculus. Molecular Ecology, 20(5), 881-892.

Beck, J. A., Lloyd, S., Hafezparast, M., Lennon-Pierce, M., Eppig, J. T., Festing, M. F., & Fisher, E. M. (2000). Genealogies of mouse inbred strains. Nature genetics, 24(1), 23.

Battey, J., Jordan, E., Cox, D., & Dove, W. (1999). An action plan for mouse genomics. Nature genetics, 21(1), 73-75.

Gordon, J. W., Scangos, G. A., Plotkin, D. J., Barbosa, J. A., & Ruddle, F. H. (1980). Genetic transformation of mouse embryos by microinjection of purified DNA. Proceedings of the National Academy of Sciences, 77(12), 7380-7384.

Justice, M. J., & Dhillon, P. (2016). Using the mouse to model human disease: increasing validity and reproducibility.

Kurien, B. T., Gross, T., & Scofield, R. H. (2005). Barbering in mice: a model for trichotillomania. Bmj, 331(7531), 1503-1505.

Lynch, V. J. (2009). Use with caution: Developmental systems divergence and potential pitfalls of animal models. The Yale journal of biology and medicine, 82(2), 53.

Martin, B., Ji, S., Maudsley, S., & Mattson, M. P. (2010). “Control” laboratory rodents are metabolically morbid: why it matters. Proceedings of the National Academy of Sciences, 107(14), 6127-6133.


Are the y-axis values informative when performing biolayer interferometry?

From the linked article:

We found that hACE2 bound to SARS-CoV-2 SB and SARS-CoV SB with respective equilibrium dissociation constants of 1.2 nM (Figure 2A) and 5.0 nM (Figure 2B).

An equilibrium dissociation constant (commonly called Kd) represents the propensity of a complex to dissociate into its constituent pieces.  A smaller value represents a smaller propensity to break apart, i.e. a stronger interaction.
So, yes, considering only the data presented, domain B from the SARS-CoV-2 spike protein shows a slightly higher affinity for hACE2 than the equivalent domain from SARS-CoV.  Note, however, that the authors are careful with their wording, and state in multiple places that the relative affinities of the homologous domains are comparable.

The SARS-CoV-2 SB engages human ACE2 (hACE2) with comparable affinity to SARS-CoV SB from viral isolates associated with the 2002–2003 epidemic (i.e., binding with high affinity to hACE2).

What's more telling are the binding constants (kon and koff) given in Table 1:

$$\begin{array}{c|c|c|}
\text{} & \text{SARS-CoV-2 S}^{B} & \text{SARS-CoV S}^{B} \\ \hline
\text{K}_{D} \text{ (nM)} & 1.2 ± 0.1 & 5.0 ± 0.1 \\ \hline
\text{k}_{on} \text{ (M}^{-1} \text{s}^{-1}\text{)} & 1.4 × 10^5  (2.3 ± 1.4 × 10^5) & 1.4 × 10^5  (1.7 ± 0.7 × 10^5) \\ \hline
\text{k}_{off} \text{(s}^{-1}\text{)} & 1.6 × 10^{−4}  (1.7 ± 0.8 × 10^{−4}) & 7.1 × 10^{−4} (8.7 ± 5.1 × 10^{−4}) \\ \hline
\end{array}$$
Values reported represent the global fit to the data shown in Figures 2A and 2B and the averages obtained from five (SARS-CoV-2) or four (SARS-CoV) replicates carried out with different protein preparations are shown in parentheses.

Note that Kd is the reciprocal of the association constant, Ka, which is equal to the ratio of the binding constants.
$K_{a} = \frac{k_{on}}{k_{off}}$, $K_{d} = \frac{k_{off}}{k_{on}}$
Since the values given for kon derived from the global fit are the same for SARS-CoV-2 and SARS-CoV, the observed difference in Kd is due to the different values of koff.  So, at equilibrium, SARS-CoV-2 SB and SARS-CoV SB will associate with hACE2 at the same rate, though SARS-CoV SB dissociates faster.


histones in the Hershey / Chase experiment

It's true that eukaryotic chromosomes have histones associated with them. But the DNA in the Hershey-Chase experiment was viral, no histones.


Why are the bodies of the Risso's dolphin covered in scratches?

[ From Jefferson et al. 2015, Marine Mammals of the World, 2nd edition, p 212: "At sea, the best identification characteristic is the coloration and scarring. Adult Risso's dolphins range from dark gray to nearly white, but are typically covered with white scratches, spots, and blotches. Many of these are thought to result from the beacks and suckers of squid, their major prey, but others may be caused by the teeth of other Risso's dolphins. If fact, this species is the most heavily-scarred of all the dolphins." ]


What is the most-stable gene identifier?

Maintaining IDs consistency is a common problem. I've never seen any reasonable solutions for it and don't believe that there are any. However, there are a few shortcuts.

You can create an extra table with aliases for later renamings and refer them to original ids. Pros - it is flexible. Cons - maintaining is exhausting and you need to figure a way to explain to users why they input one id and receive other.
The solution is pretty obvious - if you'd like to have "a single unique identifier for each human gene that will remain stable for many years" you can just take a snapshot of current state of any database you like and don't touch it for many years. You can release version-specific releases of your database and specify versions of reference database you use. E.g. "Glioblastoma_drug_perturbation_2016_(GRCh38_ENS87)".


Vo2 of the brain is 21% of Q=13% or of the entire blood?

TL; DR 21% of the whole body.

The VO2 numbers add up to 100%. You are looking at the way six major compartments of the body split the oxygen consumption. The brain takes 21% of the whole oxygen brought into the body by the arteries.

The Q numbers add to 100% too. The brain takes 13% of the blood coming out of the heart.

The picture is meant to contrast high-flow and high-metabolism organs. The kidneys take 20% of all the aortic blood, but use only 7% of the oxygen consumed in the body. The coronaries take 4% of the blood leaving the ventricles, but use a large 11% of the oxygen take in by the whole body.


The definition on the Wikipedia page you recite uses the language 'no protein coating' as opposed to 'protein coating'.
A protein coating would make it a virus.
No protein-coating would make it a Viroid.
As far as we know DNA Viroids do not exist. But this is an advancing field of research and it depends on what structure of genetic material you are referring too.
The general different types of genetic material include - but are not limited to:
Single-stranded DNA (ssDNA),
Double-stranded DNA (dsDNA),
Single-stranded RNA (ssRNA),
and double-stranded RNA (dsRNA).
There is more information on Classes I and II DNA viruses here:
https://www.ncbi.nlm.nih.gov/books/NBK21523/
If there were no DNA viruses without a protein coating - what is the reason?
Viroids only infect plant cells.
It may be that Viroids route of entry via microscopic junctions between plant cells (Plasmodesmata) are only large enough to fit single stranded genetic material. Therefore allowing ssDNA and ssRNA, but not dsDNA and dsRNA to act as plant cell infectious agents.


Do Fatty Acid Synthase Inhibitors Selectively induce Apoptosis in Cancer cells without inducing the same in healthy human cells?

I found this reference: "Inhibition of fatty acid synthase (FAS) suppresses HER2/neu (erbB-2) oncogene overexpression in cancer cells".   Cerulenin is not a magic bullet, but in some cases it may help.


Bat is the other basement creature that comes to mind. It looks like a match as explained in this and several other videos - https://www.youtube.com/watch?v=897Fb9ndids


Does amount of sperm affect fitness of baby?

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


Is the nuclear envelope present in G1 of interphase?

To answer the question about nuclear envelope in G1 phase, yes it exists. The nuclear envelope is reformed at the end of Telophase after the 2 copies of the DNA are pulled apart, but before the two daughter cells are separated by cytokinesis. We can see the new nuclear envelope in these images:

Image from here

Nuclei visible near end of cytokinesis, centrosome still visible. Image from here.

As for how DNA gets into the nucleus without cellular division I don't have a good answer and I'm not sure anyone does right now. The nuclear envelope is a major barrier for non-viral gene delivery.


Doubt on genomic code for nucleosome positioning?

Dyad is the centre of the DNA that is wrapped around the nucleosome core (It basically is the centre of symmetry of the nucleosome). It is a common practice to set it at 0 thereby making incoming DNA half, negative and outgoing DNA half, positive.

By oscillations the authors mean that there is a periodic repeat of A/T dinucleotide. IMO it is actually not correct to call it oscillation which is mostly used in a time course dynamical sense.

I guess this is what is meant by the 3-nt moving average:

You have conditional dinucleotide probabilities for each position (As shown in the figure). Now you calculate the A/T dinucleotide probability which is:  P[A/T] = PAA + PAT + PTT + PTA

Now you find the moving average for 3 steps:

MA(n) = (1/3)×(P[A/T](n) + P[A/T](n-1) + P[A/T](n-2))

where n is the nth position of the DNA


If a blocker prevents repolarization, will the neuron be stuck in a depolarized state forever?

The voltage-gated potassium channels are there only to swiftly repolarize the membrane potential. Ultimately it is the Na,K-ATPase that has to pump the various ions back where they belong (Na out, K in), also when potassium channels are active. So when the potassium channels are blocked, the Na,K-ATPase will restore the membrane potential, albeit in the order of seconds instead of milliseconds.


What are these little creatures on the fish?

Though it's hard to say exactly what you're talking about based on the image, that cod appears to have several sea lice on it:

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

Sea lice are common parasites of fish.


Antibacterial soap impacts on septic system?

The quick answer is: Yes, it can cause harm.
Think about it...The septic system (both the tank and your "drain field") rely on bacteria, and antibacterial soap is not designed to kill only specific species of bacteria. In other words, antibacterial soap can kill a whole range of bacteria, and that certainly includes the bacteria needed in your septic system.
According to University of Arizona Cooperative Extension (Farrell-Poe, 2018):

The use of “antibacterial,” “disinfectant,”or “sanitizing” products in the home can and do destroy both good and bad bacteria in septic treatment systems. “Normal usage” (according to directions) of these products will destroy some beneficial bacteria. Fortunately, the normal bacteria population within the septic system is sufficient and adequate to quickly recover. Significant treatment problems, with conservative use, should not occur. Excessive use of these products in the home can cause significant and even total destruction of the bacteria population. Normally, the use of any single product or single application will not cause major problems.
However, the accumulative affect of using too many such products and excessive application may cause serious problems and damage to the septic system.
It appears that some alternative systems may be more affected by “antibacterial” products than other systems. Additional and more conclusive research is needed.

You can find additional info about antibacterial agents in septic tanks as well as discussion about the effects of the common antibacterial agent, triclosan, on septic tanks here: Svenningsen et al. (2011) and Kirjanova et al. (2014).

 Works cited:
Farrell-Poe, K., 2018. Antibacterial Products in Septic Systems. The University of Arizona Cooperative Extension fact sheet
Svenningsen, H., Henriksen, T., Priemé, A. and Johnsen, A.R., 2011. Triclosan affects the microbial community in simulated sewage-drain-field soil and slows down xenobiotic degradation. Environmental pollution, 159(6), pp.1599-1605.
Kirjanova, A., Rimeika, M., Vollertsen, J. and Nielsen, A.H., 2014. Retainment of the antimicrobial agent triclosan in a septic tank. Water science and technology, 70(4), pp.586-592.


Examples of heterologous expression in human cell beside viral expression

Expressing GFP in human cell lines for research purposes is an extremely common example of heterologous protein expression.

For research purposes, it's usually unnecessary to optimize codons for increased expression, especially since using more efficient enhancers and promoters produces a far greater improvement in expression levels than codon optimization which is non-trivial and species-specific.


Definitions of robustness and canalization

As canalization is defined in your question (also in wikipedia) it means robustness.

Semantically it is possible to differentiate the two.

Robustness of a system refers to its sensitivity to perturbations. In other words small differences in parameters would not affect the steady state of the system (parameter changes in a physically plausible range would not lead to bifurcations).

By system I mean a set of entities connected to each other in a defined fashion. For example an ecosystem in which different species are connected to each other by interactions of the food chain. At steady state a system configuration (for instance- 10 foxes, 100 rabbits, 10000 grasses, 1000 honeybees etc) remains constant over time (that, however, doesn't mean it is static). Or in case of development a system may be the body defined by a set of certain phenotypes.

Canalization/channelization refers to mechanisms that make the system follow a certain trajectory. So if you see it mathematically canalization keeps the trajectory dictated by a  given set of eigenvectors. In case of development you may call mechanisms such as dosage compensation, functional compensation by isoforms, parallel metabolic flux channels etc as canalizing mechanisms.

So in contemporary usage we can call a system robust (a property of a system) whereas we should address mechanisms that help to preserve trajectories as canalizations. The final aim of canalization is to render robustness to the system but it is not the only mechanism that is responsible for robustness (for e.g. the steady state may just be independent of certain parameters).

Robustness is a property of the system and is dependent on how the different entities of the system are coupled and what their interaction parameters are (rates etc).

You should note that these are parlances that are adopted by different groups in the scientific community and may perhaps mean the same thing- this is merely my attempt to remove redundancy of terms by the means of semantics.

Now, plasticity is a different concept altogether. Plasticity is in a way opposite to robustness. This means that the qualitative nature of the system can change if certain parameters are tweaked. However, the system should still maintain its stability. In a stable system mild perturbations from steady state will result in system going back to that steady state - like a ball in a well. However, a system may inherently allow for multiple steady states (like switches), and depending on certain parameters the system can be in either of the states (but if pushed too far then the system can go to another stable steady state). This is called multistability.

NOTE: some people also use the term plastic to mean "responsive". The above definition may not be exhaustive or the most perfect.


Either you can cut out the fungus and get away with it, or the fungus will rapidly overgrow your plate regardless.  You might as well try to cut out the fungus.  If it overgrows your plate the experiment with that plate is done.

This is why you should have parallel plates for this sort of experiment.  There is a saying: don't put all of your eggs in one basket.  The reason is that if you sit on that basket all eggs are broken.  If you are counting on just one plate for your experiment and you sit on it, or it gets overgrown with fungus you must start over.

The other reason to have several parallel plates going is that you can average the spore count.  One plate might have more or less for some random reason, like fungus.  But if you have several and average them out you will reduce noise.


Lateral, axional and temporal resolutions for imaging in vivo

The lateral and axial resolution depends on the numerical aperture of your objective (lateral = lambda/2NA; axial = 2lambda/NA^2). You can improvee the axial resolution with FLI by using a confocal approach or with 2-photon microscopy (2PM). In 2PM you need absorption of two infrared photons to get emission. The probability of 2 infrared absorption depends quadratically on the excitation intensity. Therefore, fluorescence is restricted where the illumination beam is focused which give a better sectioning. An advantage of 2PM is the higher penetration depth and reduce phototoxicity. Indeed you can use 2 infrared photons to excite fluorophore which required visible excitation.

Temporal resolution depends on the area you want to measure and the integration time.

Resolution is limited by the diffraction. In the best case with the 3 imaging techniques you mentioned you can get ~200-300 nm in lateral resolution and 500 - 800 nm in axial resolution
Higher resolution can be achieved by using super resolution techniques. They are separated in two groups. The first one exploid the photo-physical properties of the fluorophore to excite and de-excite it. This allows to resolve sub-diffraction areas. This is the case STED (Stimulated emission depletion) microscopy or SSIM (saturated structured illimination microscopy). The second group use the fluctuation of the fluorophore emission to localize it better. It includes techniques such as STORM (STochastic Optical Reconstruction Microscopy, PALM (Photo-Activated Localization Microscopy) and SOFI (super-resolution optical ﬂuctuation imaging).


Tracking of oxygen molecules in glucose oxidation

I think this experiment (PDF file) will help you understand the basic concept about the fate of oxygen in aerobic respiration. Basically the result is:

The oxygen of respiratory carbon dioxide is in exchange equilibrium with body water.
Utilized molecular oxygen is converted to body water.

In respect to calculation of electrons donated to oxygen, just calculating how many NADH2 and how many FADH2 is reduced in how many steps during ETC will be able to answer your question.


Proline Iminopeptidase v Proline Aminopeptidase

There are two related enzymes that cleave an N-terminal residue. Enzyme 3.4.11.9 cleaves any residue from a peptide when the next residue is proline. Enzyme 3.4.11.5 cleaves an N-terminal proline from a peptide. Unfortunately, it appears that both are sometimes referred to as proline aminopeptidase. However, only 3.4.11.5 is referred to as proline iminopeptidase.

The vendor should certainly specify which enzyme they are offering.


To explain it briefly:

Lets take a human as example, you are diploid and you have a pair of 23 chromosomes (= total 46) and the sex chromosomes which I will exclude for this explanation.

Your gamete is haploid and has therefore only one of the two paired chromosomes. So for every chromosome pair there are 2 possible chromosomes. So in total you have 223 possibilites to arrange chromosomes. The gamete from the sexual mating partner also has 223 possibilites to arrange chromosomes. So in total a new diploid organism has (223)x(223) possibilites. So unique.

However, it is always the chromosomes of the parents. So yes, parents influence the children because the genetic information of the children can be found in one of the two parents.

Furthermore you have recombination, but you already asked another question about this. So I will not expand this answer.

There are relevant articles in Wikipedia on genetic recombination and meiosis that I would recommend.


Although the photos are less than ideal, and I can't see any flowers or fruit, I can clearly see that the leaves are "evenly pinnate" and rounded distally (not pointed). The wood structure also looks bumpy.  Given Israel as the neighborhood, it is likely to be a carob tree (Ceratonia siliqua) which is native to the Mediterranean region.  This tree is sometimes mistakenly called a "locust" tree.  See Links below.

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

http://tree-species.blogspot.com/2008/04/carob-tree-ceratonia-siliqua.html


How does glucose uptake happen in the various tissues of the body?

As far as I am aware, all tissues have glucose transporters, but there are many different types with varying tissue distribution. A short review in Biophysical Reviews (2016) by Navale and Paranjapei is freely available and provides a summary with links to original papers.
In short, there are two types of glucose transporter, those involving sodium symport (SGLTs) and those operating by facilitative diffusion (GLUTs). The review lists six SGLTs and mentions thirteen GLUTs, belonging to three different structural classes.
The tissues specifically mentioned in relation to one or more of these transporters include:
For SGLTs — small intestinal cells, proximal tubule of nephron, intestine, testes, uterus, lung, brain, thyroid, kidney, liver, uterus, pancreas.
For GLUTs — pancreatic beta cells, liver, kidney, brain, heart, skeletal muscle, adipose tissue, small intestine, testes, placenta.
I reproduce below a table from Chapter 6, Insulin and Sugars, in Gerald Litwack
Human Biochemistry (2018). The chapter is available if you belong to an institution with a subscription to Springer publications.


Why do flipped cockroaches sometimes lose their heads?

In all likelihood, it is your cat who crunches the cockroach's head once it catches it and/or finishes playing with it.

Ants do eat bugs but they are usually not so selective that they'll carry off the head alone. With more manageable insects, they carry the whole thing off; otherwise they take it apart and carry it away in pieces if they're interested in it as a food source.

If you watch a cat with a mouse, chipmunk, bird, large insect, etc, they often seek to kill the animal with a throat or nape bite if they are done 'playing' with it. I've found headless prayer mantises and other large insects in my garage many times, and have seen my cats beheading them.

The techniques that cats use to kill prey vary with prey size


Lewontin's recipe

A very nice way to consider natural selection is through the lense of Lewontin's recipe. Evolution of a given trait (tail length for example) through natural selection occurs whenever the three following conditions are met:

There is variation for this trait in the population

This variation is caused by mutations

Part (or the totality) of this variation is heritable

Heritability is the part of the variance in a trait that is explained by genes. It can be measured as a parent-offspring correlation.

The variation of this trait is correlated with fitness

loosely speaking, fitness is an index of both fecundity and survival

You can take two minutes to think about how logical it is that changes in frequency of variants (natural selection) occurs whenever these three conditions are met. You can imagine any objects you want (pencils of colors for example) and simulate these three steps:

Variation

different pencils have different colors

Heritability

simulate that your pencils reproduce (asexual reproduction is conceptually easier to understand) and offsprings have similar (or even the same) color than parents

Correlation between trait and fitness

Pencils of different colors have different fitness.
For example each red pencils create two red pencils the next generation while blue pencils do not manage to replicate at all.

You can quickly see how the red pencils become more frequent in your pencil population through time. If you wait long enough your pencil population will be totally composed of red pencils. And you'll need to simulate a mutation in order to create a blue pencil. I think you understand the how different are the roles of mutations and natural selection in evolution with this example.

Genetic Adaptation During Lifetime of a multicellular organism

For a beginner in evolutionary biology, saying that a multicellular individual's genome does not change during its lifetime might be considered satisfying. In reality it is slightly more complicated. Two elements that are mostly influent very early in the lifetime of an individual have to be considered.

While most mutations occurs during reproduction, some mutations does also occurs during body growth or stated differently during cell reproduction (Mitosis). In consequence, some pairs of your cells share exactly the same genome while other pairs of cells have a sligthly different genome.
Moreover, once some mutations had occurred within the development of an individual, these mutations might influence the fitness of the cells and therefore some alleles (variant of a gene) might raise in frequency while others decrease in frequency (Natural selection). It is important to understand that this process of natural selection select for cells that have a higher fitness and therefore do not necessarily select for the cells that allows the individual to increase its own fitness.

I don't fully understand what you mean when saying: "But does evolution work by some primitive genetics-engineering too?" Could you try to rephrase this question?

Please, let me know if I answered your question!

Note:

Here is a good way to understand the difference between "gene" and "allele". A gene might be a called the "eyes color" gene for example, while the three alleles of the "eyes color"  gene might be callsed "blue eyes", "brown eyes" and "green eyes". In this sense, the alleles are the different variants of a gene. Mutations increase the number of alleles and natural selection reduces the number of alleles by selecting for the allele that cause its holder to have the greatest fitness. If you understood that, it is already good!

Note: Natural selection does not necessarily reduce the number of alleles, several alleles might be kept (polymorphism) in certain "types" of natural selection (frequency dependent selection and overdominance (heterozygote advantage), fitness varies in space and/or time, selection acts on different levels). The "type" of Natural selection that reduces the number of alleles after some time is called directional selection.


Yes, cell membranes are highly permeable for water. While diffusion through the membrane is possible (description, and some science), it is most effective through water channel proteins (aquaporins). The different expression levels of aquaporins in different cell types result in differences in the permeability.

And yes, the tissue fluid has to be isotonic to the cell interior. The water balance in the body is therefore highly regulated. If not enough water is available, the blood osmolarity (ratio between solubles and water) increases. This is sensed in the hypothalamus (an area in the brain which is a major player in hormone regulation) and results in production of the hormone vasopressin. This will not only increase your thirst (and therefore add more water to the system) but also regulate aquaporin expression, improving reabsorbtion of water in the kidney (nicely shown here, actual science here). Urine production is of course also important in the response to drinking too much, which can be harmful as well..

If tonicity is deregulated, this has serious consequences for the body (some more science). For example, mutations in vasopressin or kindney aquaporins can result in very similar phenotypes, characterized by dehydration because water levels cannot be properly regulated (even more science).

edited for more explanation, because people complain when I give short answers to short questions ;)


Can anyone identify this dragonfly spotted outside of Boston, MA?

It is a male Green Darner.

Pretty common in general, especially in the US.


Looks like it is Phytolacca dioica.  I found this by searching your first image in a phone app called Pl@ntNet (PlantNet).  Looking at Wikipedia confirms the ID.

Interestingly, you said the fruit was sweet.  The North American relative Phytolacca americana is extremely poisonous.  A brief search suggests your species is possibly poisonous, with reports about the leaves more common than the fruit.


Identifiying a conserved residue in multiple PDB structures

My approach to this problem would be to use VMD (Visual Molecular Dynamics), where you can load multiple PDBs, perform structural and/or sequence alignment and analyse residue conservation within one program.

VMD is a powerful molecular visualization program for displaying, animating, and analyzing large biomolecular systems using 3-D graphics and built-in scripting. It is probably an overkill for what you want to do, but I find it rather intuitive to use and powerfull. I also has an amazing documentation and many step-by-step tutorials, starting from this basic introduction.

What you will specifically need for your problem is a MultiSeq 2.0 plugin that you can find under Extensions->Analysis->MultiSeq in new versions of VMD. It is a bioinformatics environment that allows you to load, display, and analyze both sequence and structure data for your proteins within a few mouse clicks. It also has a great set of tutorials to help you start! What you might find interesting for comparing many similar protein structures is an option to create, view and manipulate phylogenetic trees.

Here is step by step tutorial on comparing structures and sequences with MultiSeq.

Here you can find original publications for both VMD and MultiSeq:

VMD:

  Humphrey, W., Dalke, A. and Schulten, K., VMD - Visual Molecular
  Dynamics., J. Molec. Graphics, 1996, 14:33-38.

MultiSeq:

  Roberts, E., Eargle, J., Wright, D. and Luthey-Schulten, Z.,
  MultiSeq: Unifying sequence and structure data for evolutionary
  analysis. BMC Bioinformatics, 2006, 7:382.


Why is prothrombin time used to monitor warfarin and not activated partial thromboplastin time?

This article tells that warfarin can prolong aPTT too.
Now look at the image below

It is almost 5 days and some extra hours when anticoagulant effects start, during which we give heparin, also called as heparin bridge.

But in that case, warfarin usually takes a few days to be considered effective enough to stop administering patients heparin with it; wouldnt all the affected factors be depleted enough by that time to also affect aPTT?

PT is used as a standard measure not just for initiating but also for monitoring  warfarin therapy using the INR(international normalised ratio) because it gives the earliest result(as half life of factor VII is shortest) to start another treatment according to guidelines, when INR is altered beyond normal range

Warfarin affects factor VII, which is the initiating factor (tissue factor aside) for the extrinsic pathway, which is why it affects PT more?

Well I might not have any sources to answer that, but I can try to deduce answer by some logical arguments. In intrinsic pathway there is multiplication of factors, for eg. Factor XII activate factor XI and factor XI activate factor IX but by this time more and more factor XI are getting activated thus causing more interaction with whatever factor IX is left in blood(factor IX is less here due to warfarin) so no relative profound anticoagulant effect of warfarin is present. But in case of extrinsic pathway factor VII is the intiating factor and is already less due to warfarin, and there is no such factors multiplying before that to cause their maximum interaction and therefore activation of factor VII so relatively more profound anticoagulant effect is present.


Why is it desirable to couple chemical production to growth?

When designing new metabolic pathways for chemical production, one has to keep in mind that the purpose of it is to get scaled up (i.e. to reach industrial size).

From the industrial point of view, the faster/simpler a process is, the better. Growth coupled chemical production means that only one step is necessary in order to produce the desired product (before downstream processes). Otherwise, one would have to produce the biomass first (growth step) and then to proceed to the chemical production step. One step is cheaper and faster than two, not mentioning the intermediary steps that could be necessary (cells washing, centrifugation, filtration ...).

The main drawback of growth coupled chemical production is that the final yield ($mol_{final~product}/mol_{substrate}$) is hindered by biomass production. This can be a real issue if the substrate is expensive.


When can a virus modify DNA in every cell of a living organism?

The answer depends on two factors:

The type of vector (virus) you are using
How well your vector can be integrated.

The bottom-line is that there is no guarantee the vector will work even if you start from the embyro.

As far as I know, the problem of using vectors in general is that the vector you are using might not be integrated into the genome of the host. (Not necessarily get into the DNA, but just keep replicating during each S phase.) Therefore doing it earlier gives you a better chance to actually get them in the organism.

For example, there is a linear vector used in C. elegans that was injected into the oocyte even before fertilization. The cell later treats the vectors as broken DNAs and linages them so they could be pull to one side of the cell during mitosis. However, the huge chunk of vector DNA is mosaic. (i.e. only some of the cells in that worm have the vectors.) Other vectors like engineered HIV have better chance to integrate themselves.


What percentage of Americans have Native Indian ancestry?

I found some averages from 23andme on sciencemag. It doesn't state the figures for all americans, although it says that 8 percent of white americans have some native american ancestry, afro-americans have on average 0.8%, and latino have 18% native american ancestry.


Is there a scientific name for the field of study focusing on the hemispheres of the brain and their control of opposite sides of the body?


I will be doing my own whole genome sequencing soon. The best reputable company I've found is Veritas. For 999 dollars and at a pretty decent depth (30+ reads).  They will produce a canned report of diseases and traits similar to cheaper alternatives, but also for another $100 will provide you a complete Variant File.

My understanding is that they will only use your data after anonymization for scientific endeavors, but I still need to finish reading the fine print. See here under privacy.  Good luck!

p.s. I also would skip exome and go with WGS since the price has come down. More and more diseases and traits are being linked to variation in intergenic regions of DNA.


Genotypes of gametes produced by an F1 individual?

Gamate is a haploid germ cell produced by either male or female parent. In your question,two homozygous dominant and recessive parants produce RY and ry gamates respectively. F1 would have four types of gamates if we think about their genotype.They should have any one of  RY, Ry, rY, ry as their genotype.
RY and ry are parental gamates. They have the genotype of the gamates that F1's homozygous parents produced. Other two are recombinant genotype. Since they behave independently, you can go with mendelian genetics and draw a punnett squre.write RY Ry rY ry horizontally and vertically then get the F2 cross genotypes. Dominant genotypes will determine the phenotype.


I think @fileunderwater is definitely right, these are psocids (of the family Psocoptera, AKA booklice).

Specifically, the body shape looks very similar to that of Dorypteryx domestica or some closely related species.

See here for an additional photo.

According to this site, the species is present in many countries including Poland.

The source cited at this site (Kučerová 1998) mentions that this species can be brachypterous (i.e., having very reduced wings. I can't tell from the quality of the photo whether your specimens has tiny wings or not. Your top picture looks like it might.

Citations:

Kučerová, Z. (1998). Wing polymorphism in Dorypteryx domestica (Smithers) (Psocoptera: syllipsocidae). Insect Systematics & Evolution, 29(4): 451-57.


Is the "freeze response" really a remain of our reptilian past?

Freeze response is also a part of the fight or flight response. See this paragraph below from Wikipedia:

The fight-or-flight response (also called the fight, flight, freeze, or fawn response in post-traumatic stress disorder, hyperarousal, or the acute stress response) is a physiological reaction that occurs in response to a perceived harmful event, attack, or threat to survival.

This, being enough of a definitiin, does not explain the point in your question i.e. how could the freeze response help our ancestors in some dangerous situation (and thus become evolutionarily helpful)? Its actually quite simple. Let me first explain how the fight and flight responses would've helped us.

For the fight response, imagine a simple situation: a small animal (say, cat) runs towards you to attack you. Now, fight response immediately turns on. Hormones in your body tend to make you feel more powerful and aggressive, so that you easily fight off the cat and make it run away. This would be helpful for someone who would've otherwise done nothing and simply get a couple of injuries from a notorious cat.

In flight response, imagine a simlar situation: you are being attacked by a larger animal (say, bear). You know that you just can't fight with it, but if you run fast enough, you can outrun that bear. Now, flight response rapidly takes over. Hormones, like adrenaline and nor-adrenaline, tend to get more blood to your legs (so that you can run faster), dilate your pupils (so that you can see everything more clearly), etc., everything required for a faster sprint. This would be beneficial for someone who would otherwise not run away and reach a near-death situation.

So, how does the freeze response help? Consider another (last one) situation: you're being attacked by a lion. In this case, you know that you can neither fight with an angry lion nor outrun it. What should you do? One immediate idea would be to play a dead man's role in front of the lion so that (maybe) it will leave you. Of course, it doesn't pay off everytime, but surely it does, sometimes. And in such a case, this would be better for someone who would otherwise either try to fight with the lion or to outrun it. And, obviously, it is a better option for many other organisms too. So it indeed seems that this response developed much earlier in time, maybe even long before first chordates appeared.
With the above part explaining why it is beneficial, one part still remains i.e. how does it work? For this, see the paragraph below:

Studies show that particular connections from the periaqueductal grey (brain region located along the spine) to the pyramis at the base of your skull are integral to the freeze response. When these connections are activated, it causes the body to freeze. They can be activated by things that are actually dangerous and by things that aren’t, so even irrational fears can cause us to freeze. While giving a presentation, you might not actually be in danger, but your body responds like it is and causes you to clam up.

Below are images of the periaqueductal grey in spinal cord and pyramids in brainstem to help you understand their locations.

To conclude, freeze response is not a mere "remain" of our reptilian past, it is still beneficial for us.
References:

https://en.wikipedia.org/wiki/Fight-or-flight_response
https://www.psychologytoday.com/blog/evolution-the-self/201507/trauma-and-the-freeze-response-good-bad-or-both
https://joyable.com/blog/fight-flight-freeze/
https://www.slideshare.net/mobile/dr_ansari2000/the-brain-stem-ii
http://slideplayer.com/slide/4637165/


Why does our visible range not include infrared or UV radiation?

Usually we don't ask why in biology because the explanation is always the same, it was good enough for survival. But here are a couple of explanations.
The radiation peak from the sun is in the visible range of the spectrum, between 400nm-700nm with the highest point around 550nm as can be seen here or calculated from Wien's law and the sun temperature.
That's why photosynthetic pigments use the visible spectrum and following them the rest of the ecological system.
Our retina blocks most of the UV light and water absorbs the lower part of the IR, illustrated very nicely in this article, figure 1.
It is true that materials on earth emit more radiation in the IR than in the UV-visible spectrum due to their temperature but:

most objects have the same temperature approximately
the soil emits a lot of radiation
the radiation from the sun in the IR is high compared to the radiation of earth. This is the best graph I found, emphasizing the great difference between sun & earth intensities
in the IR range there isn't a lot of variance in the wavelength intensity and therefore it is less useful.
Notice how uniform the IR reflection is from this leaf spectral signature

To summarize:

UV light is dangerous so we filter it out and not use it
IR light is uniform and not useful
Visible light is the peak of sun emission and therefore the most efficient range to use