Where can I find the metabolic network for the human erythrocyte?

The model used by Jamshidi et al. can be found in the BioModels database with acession no. MODEL1103210001  http://www.ebi.ac.uk/compneur-srv/biomodels-main/MODEL1103210001

A more recent model has also been described in Bordbar et al. iAB-RBC-283: A proteomically derived knowledge-base of erythrocyte metabolism that can be used to simulate its physiological and patho-physiological states. BMC Systems Biology 2011, 5:110 The model file in SBML format can be downloaded from the Additional Files section (http://www.biomedcentral.com/1752-0509/5/110/additional) or BioModels (http://www.ebi.ac.uk/compneur-srv/biomodels-main/MODEL1106080000).


How do I prepare a PDB for submission to the Protein Data Bank?

These two links go through the specifications required for the PDB format:

Link1: http://deposit.rcsb.org/adit/docs/pdb_atom_format.html

Link1 primarily goes through the specs. required if you say have a NMR file you would therefore require the MODEL statement. It also goes through other statements such as when to use TER and how each ATOM line should look etc...

Link2: http://www.wwpdb.org/documentation/format33/v3.3.html

Link2 goes through the other statements such as HEADER, REMARKS and TITLE


Why people fear GMOs? Can't we map a plant composition?

People are not always rational when it comes to what they eat, especially when the compounds that make up the food have long, arcane-sounding names.

It is indeed possible to analyse the amino acid composition of a food substance. However, this has no bearing whatsoever on the safety of the food product.

For example, the following are two truncated protein sequences. One of them is a fragment constituent of cobra venom, the other is a fragment of harmless DNA polymerase. Without looking up or otherwise referring to the PDB IDs, it is not obvious which is which, even to an experienced molecular biologist.

  3HRZ:A|PDBID|CHAIN|SEQUENCE
  ALYTLITPAVLRTDTEEQILVEAHGDSTPKQLDIFVHDFPRKQKTLFQTRVDMNPAGGMLVTPTIEIPAKEVSTDSRQNQ

  1KLN:A|PDBID|CHAIN|SEQUENCE
  VISYDNYVTILDEETLKAWIAKLEKAPVFAFATETDSLDNISANLVGLSFAIEPGVAAYIPVAHDYLDAPDQISRERALE

Furthermore, even if scientists can prove beyond reasonable doubt that the two products are chemically identical, people will still irrationally purchase them. A clear example is the different prices commanded by "natural" versus "artificial" flavourings, as seen in this Scientific American article.

  Consumers pay a lot for natural flavorings. But these are in fact no better in quality, nor are they safer, than their cost-effective artificial counterparts.


What will happen if a scorpion pierces itself?

Scorpions are immune to their own venom (reference) as has been said in some studies as well (reference) But some other studies and eye witness accounts have referred to the contrary.

  in an experiment a scorpion, Bulteus australis, was killed by an
  injection of the same venom as its own (reference).

So, it should be safe to say that there is a very low chance for a scorpion to be affected by its own venom. It is said that

  Mutations in the scorpion’s own membrane protein genes make the
  arachnid immune to its own venom (reference).

A scorpion could die quickly if venom is injected into its brain (nerve ganglion). Larger species inject a higher amount of venom to overcome the smaller ones and should have specific neurotoxins if smaller scorpions are their prey to disable them (reference).


Do phagocytes need antibodies to be able to engulf pathogens (to function)?

Phagocytes don't necessarily need antibodies to recognize intruders, i.e. by presence of non-self sugars. Additionally, phagocytes can aid amplification of effective anti-bodies by presenting degraded pathogens to the adaptive immune-system. I found this concise summary of the innate immune system, that I would strongly recommend to read!
Now to your more specific question: Detection of viruses. You have to consider, that viruses are highly optimized to evade the innate immune system:
Viruses can happily replicate and mutate without proof-reading without negative consequences and with relatively low conceptual constraints, as they are so simple, compared to cells. This is why the innate immune-system is prone to miss viruses (at least those, that are optimized for a certain species). Imagine how big of a genome you would need to cover all possible viral substances by at least 1 innate gene! Read about hyper-mutation to understand the role of antibodies to detect even these highly evasive viruses.


What happens during kefir fermentation process?

Well essentially the added Lactobacillus species ferment lactose and other sugars to lactic acid, thus lowering the pH of the product (they take up lactose use it as an energy source under anaerobic conditions and secrete lactic acid). This gives the kefir and other fermented milk products their sourness. Also the lower pH prevents many other bacteria from growing in the product so this is also serves as a natural preservation method. Further more the low pH can denature some of the protein in the milk/kefir resulting in a more solid form. Many of these Lactobacillus species or their relatives are natural part of our gut flora.


Is the human biological clock genetically programmed or learnt?

Short answer
The biological master clock is neurologically and genetically hardwired. The biological clock is not affected by learning. Instead, it is constantly entrained mainly by daylight.

Background
The biological clock is hardwired in the human body and can be traced back to the master clock in the suprachiasmatic nuclei (SCN) of the hypothalamus (Fig. 1).

Fig. 1. The SCN is entrained by environmental light captured by the retina in the eyes. Source: Neuroscience News.

The SCN is an intrinsic oscillator that governs sleep and wake timing, rhythms of temperature, hormones, mood and cognitive acuity etc. etc. These rhythms are entrained to 24 hours by the environmental light-dark cycle primarily via a subset of photosensitive retinal ganglion cells that project directly to the SCN (Fig. 1). Using hormones and neuronal signals, the SCN entrains peripheral clocks of similar molecular mechanism present in many tissues (Pagani et al., 2010).

In humans and other organisms, the timing of 24-hour behavior is governed by the period length of the circadian oscillator. This period is approximately, but not exactly, 24 hours long (circa diem), and ranges from 23.47–24.64 across people (23 hours 28 min to 24 hours 38 minutes) in laboratory conditions (Pagani et al., 2010).

Why is it circa diem and not exactly 24 hours? Note that the absolute length of a day depends on the definition used. For example, one complete rotation of the earth around its axis (the sidereal day) actually takes 23 hours, 56 minutes and 4.1 seconds. The solar day is 24 hours and is defined by the time it takes the sun to make an apparent circuit across the skies. More importantly, there is apparent solar time, sometimes called true solar time, which is determined by the daily apparent motion of the observed sun. It is based on the interval between two successive returns of the sun to the local meridian. The length of a solar day varies throughout the year, and the accumulated effect of these variations (equation of time) produces seasonal deviations of up to 16 minutes.

The length of a day can also be defined in the number or hours from sunrise to sunset, which varies where you are on earth. At the equator every day of the year is exactly 12 hours long. At 50° latitude (e.g., England & Canada) the longest day is 16.5 hours and the shortest day 7.5 hours. At 35° latitude (e.g. many US states and Greece) the longest day is 14.5 hours and the shortest day 9.5 hours. Given that light is the most effective way to entrain the circadian rhythm, it is obvious why the absolute length of the intrinsic circadian rhythm is not important. As long as it is circa diem, it will do.

Reference
- Pagani et al., PloSONE (2010); 5(10): e13376


Does every wave length of UV kill bacteria?

The CDC's disinfection guidelines lists UV radiation between 328 and 210nm as effective for disinfection, with a maximum of bactericidal activity occurring between 240-280nm. At this wavelength DNA damage (Thymine dimers) is induced with a high rate.

Due to practical reasons UV light is mostly used to disinfect water, if used in rooms there is some effectiveness against microorganisms in the air and some on surfaces, but on one hand the effectiveness is reduced  by square with the distance from the UV source and on the other hand you need completely empty surfaces where nothing casts shadows. The other problems are plastic materials which may get damaged by repeated UV exposure.

Have a look at this reference (only available via Google Books): "Principles and practices of disinfection, preservation and sterilization." and this subchapter.


Is there a physiological difference between love and infatuation?

Assuming that our emotions are the psychological manifestations of chemical changes in our bodies (an assumption I have no trouble with but one that others may take umbrage at), any emotion will be different.

If your brain can distinguish between two emotions, then the underlying chemistry through which these emotions are expressed will be different.

This is not to say that we, as scientists, can quantify this. Definitely not today at any rate. Simply that there will almost certainly be a physiological difference between any emotional state that can be differentiated by your brain. Otherwise the brain would not register different emotions.

UPDATE:

Human language has different words for different feelings. There is often a type of feeling "continuum" with different words representing different ranges on this scale. For example:

Adoration--->Love-->Infatuation-->Affection-->Indifference-->Dislike-->Hate

How you decide to qualify an emotion you are feeling is more a question of semantics than biology. The point I am making here is that each point on that scale (and every point in between that we haven't explicitly assigned a word to) will represent a slightly different mix of various chemical signals in your body.

If your question is more about the English language words love and infatuation, their definition and distinguishing between them, try posting on English.SE.


How does extracellular potassium ion concentration and calcium ion concentration affect the excitability of a cell?

If extracellular $Ca^{2+}$ concentration increased, it makes the extracellular membrane more positive then it used to be, then it would take the membrane potential to lower level then the excitability of the cells will be decreased

if extracellular $K^+$ increased more than the concentration inside the cell than it will make the $K^+$ on extracellular space move inside the call down the concentration gradient, it would take the potential membrane to higher state make it easier to reach the threshold (easier to be excitable)


Madrid, Noise by the river: Bird or cricket?

In this case i am going to agree with AliceD, because I live in Greece and here we hear cicadas everywhere. But in Madrid, there is a other kind of cicada that its "song" is more noisy and more deep.In this video you can hear how your cicada sings.https://youtu.be/mah26og11ms


Will dissolved proteins pass through a 0.2 micron filter?

Many proteins will pass through a 0.2 micron filter. If the proteins aggregate or if they stick to the filter material because it is charged, they may not.

Barring the above, a 0.2 micron filter will allow proteins up to 200kd to pass through.  There are some proteins that are larger.

Editing with some source material.

Nice Presentation on Pore Sizes and Membranes Here

Graphic from that presentation:


Do lysosomes play any role in cell division?

It is actually not completely correct to include it as a fact in textbooks. The main cause of it is that there is not much research on this topic. See this article for reference. According to Allison and Mallucci (1964), during cell division, lysosomes either released an unspecified activator or some hydrolase that inactivated a repressor. Apart from this, Allison and Paton (1965) showed that treatment of human embryonic lung cells in tissue culture with photosensitizing agents allowed high frequency of chromosome breaks on irradiating the cells with light from a high intensity tungsten source. They claimed that these effects were observed only at lysosomal sites, from which they concluded that a cytoplasmic event was giving rise to structural alteration in chromosomes. This event was suggested to be release of deoxyribonuclease from the lysosomes. However, Chevremont et al, 1959 showed different results through their experiments. They grew mammalian cells in tissue culture in the presence of acid deoxyribonuclease. This treatment inhibited cell division, but allowed DNA synthesis to proceed and did not appear to alter the nuclear DNA. Hence, the contribution of lysosomes in cell division is not yet completely established and still comes under debate.

So, it should not be considered a total false, but is also not reliable enough to be printed in textbooks. Overall, we don't yet know whether lysosomes do play a role or not.

References:

TUATARA: VOLUME 18, ISSUE 1, JULY 1970
THE LYSOSOME
ALLISON AC, MALLUCCI L. LYSOSOMES IN DIVIDING CELLS, WITH SPECIAL REFERENCE TO LYMPHOCYTES. Lancet. 1964 Dec 26;2(7374):1371–1373.
Nature 227, 707 - 708 (15 August 1970); doi:10.1038/227707a0;
Chromosome Breakage by Deoxyribonuclease;
GILLIAN R. PATON & A. C. ALLISON
CHEVREMONT M, CHEVREMONT-COMHAIRE S, BAECKELAND E. [Action of neutral and acid desoxyribonucleases on living somatic cells cultivated in vitro. III. Histoautoradiographic study after incorporation of tritium-labelled thymidine]. Arch Biol (Liege) 1959 Oct-Dec;70:833–849.


What is Environmental Robustness? Is it different from plasticity?

I think robustness and plasticity are different concepts, although related to each other.

I would define plasticity as the property of a system to adapt to external changes. As defined in the wikipedia page for phenotypic plasticity:

  Phenotypic plasticity is the ability of an organism to change its phenotype in response to changes in the environment.

I think this definition agrees with the one in your question.

Robustness in biological systems, however, is defined as (wikipedia article):

  Robustness of a biological system (also called biological or genetic robustness) is the persistence of a certain characteristic or trait in a system under perturbations or conditions of uncertainty.

From this article three references are cited, all of which give some definition of robustness in their introductions/abstracts:

Felix and Wagner (Heredity 2008):

  Robustness, the persistence of an organismal trait under perturbations, is a ubiquitous property of complex living systems.

Kitano (Nature Reviews Genetics 2004):

  Robustness is a property that allows a system to maintain its functions despite external and internal perturbations.

Stelling et al. (Cell 2004):

  Robustness, the ability to maintain performance in the face of perturbations and uncertainty, is a long-recognized key property of living systems.

All these definitions imply that robustness is the ability to remain unperturbed under external or environmental perturbations. In a sense this looks like the opposite to plasticity, which is the ability to change under external perturbations. Personally, I think that robustness is accomplished because biological plasticity allows organisms to compensate (with some limits) the external perturbation in order to maintain their state.


(Why) are polar bears more common in Labrador than in southern Greenland?

I think the lack of sea ice coverage would point you somewhere- even with the maximum sea ice coverage picture, the SW corner of Greenland has next to none, which may impact the carrying capacity for both bears and prey animals on that narrow strip of land between the ice cap and the sea- less space and less things to hunt, less ways to get around, etc. And then there's not much continental shelf over there, either.

Labrador is surrounded by more continental shelf, which might contribute to higher levels of sea ice at high levels and greater seasonality. Might lead to more prey?

This article might get you somewhere:Polar Bears in a Warming Climate


Polydactyly can be dominant or recessive. that is

A single copy of the mutation/s involved result in the phenotype
vs
Both copies of the gene must be mutated to result in the phenotype

When two random people who don't have polydactyly nor a family history of polydactyly have a child, there is around 1/548 (0.18%) chance that child will be polydactyly because the parents were carriers without knowing it, and a 1/11.7 (8.54%) chance the child is a carrier of a single copy

If the aunt's polydactyly is Dominant, then your friend's father hasn't inherited it (he isnt polydactyly) and just has the normal population chance of being a carrier.

In the case of Dominant polydactyly, assuming your friend has a partner with no history of polydactyly, your friend and her partner have the same chance as average of a polydactyly child (1/548)

If the aunt's polydactyly is recessive, meaning she has two copies one from each parent (you friend's grandparents), there is a 1/130 (0.76%)chance your friend's child will have polydactyly (4.2 times more likely), and a 1/4.5 (21.4%) chance of being a carrier (2.6 times more likely)

I'll quickly go through the working/
if you're interested:

Given that the grandparents are both carriers (needed for the aunt to have two copies), then your friend's father has a 2/3 chance of being a carrier of a single copy (1/3 chance no copies, 0/3 chance having two copies because he isn't polydactyly).

Your friend's mother has the usual 1/11.7 chance of being a carrier.

The chance of your friend inheriting a single copy is (chance passes from father) + (chance passes from mother) - (chance of getting two copies)

=0.6600/2 + 0.0854/2 - (0.33*0.0427)

=0.3727 - 0.0140

= 0.3586

35.9% chance your friend carries one copy

Your friend has 1/2.8 chance of carrying and 1/5.6 of passing it on

Friend's partner has the 1/11.7 chance of being a carrier and the 1/23.4 chance of passing it on

Therefore their child has

=0.1793*0.0427 (chance friend passes on * chance partner passes on)

=0.0076

=1/130 chance of having two copies, having polydactyly

=0.1793 + 0.0427 -(0.1793*0.0427) (chance any copies - chance two copies)

=0.2143

=1/4.7 chance of one copy a 2.5 times increase risk


Why is blood pressure higher the more distal an artery is?

Because of reflected pressure waves and the stiffness of the blood vessel.  The forward pressure wave from the heart travels much faster than the blood itself and is reflected at areas of tapering and branching.  This backward wave slows the forward flow of blood, and at the same time, when it meets the next forward pressure wave, that forward pressure wave is augmented...so higher pressures distally...And now you know, and knowing is half the battle...


Why is the liver the only internal organ of the human body to regrow?

Maybe it is due to two factors:

The liver is one of the few solid non-tubular organs. If a tubular organ is damaged, all the layers that composes it must regenerate. This layers usually have different cell types, which is always nasty for regeneration since some of them may be formed by specialized tissue (for instance, myocytes are very difficult to regenerate. If the organ has a muscle layer, such as the esophagus, regeneration will be more difficult). Furthermore, damage in a tubular organ usually involves perforation, which will disrupt its function even if the injure isn't big.
Hepatocytes are pretty undifferentiated cells. They are basically enzymatic sacks with some vacuoles and mitochondrion, but they remain as your typical animal cell. They have a regular nucleus, they don't have any cytoskeletal adaptation and their vacuoles don't compose the most part of their cytoplasm (in a healthy liver). Cells with so little morphological specialization usually regenerate with no problem. Plus, the liver itself is constantly exposed to chemical damage due to toxins, drugs and other chemical compounds that may be present in the diet. This situation is special and don't apply for any other organs, with the exception of the kidneys (which, in fact is a very complicated tubular organ).


When is the second polar body extruded from the egg nucleus?

As stated in the answer by @CDB, these polar bodies don't last too long, and the second polar body which forms as the result of meiosis II, extrude only after fertilisation. The secondary oocyte is arrested in metaphase II until it becomes fertilised, so meiosis II can only by completed after ovulation and fertilisation (see e.g. UNSW Embryology: Meiosis at https://embryology.med.unsw.edu.au). This means that meiosis II, which actually forms the second polar body, occurs as a result of fertilisation. The secondary oocyte becomes a mature oocyte (ovum) by the expulsion of second polar body into perivitelline space.

The metaphase arrest is caused by the presence of two types of cytoplasmic activity
1. MPF - maturation promoting factor
2. CSF - Cytostatic factor that inhibits APC/C

  Only when MPF is present, stabilized by CSF, and active will the M phase persist. However, this complex is very sensitive to calcium, such that a rise in calcium tilts the equilibrium away from complex synthesis towards destruction.

Capcitated spermatozoa that have undergone an acrosome reaction is capable of fusion and Calcium mediated calmodulin is required for this process. When fusion happens spermatozoon ceases to move and the nuclear with parts of mid piece and tail passes to the ooplasm. So sperm initiate Calcium release at fertilisation this helps in the completion of the 2nd meiotic division.
For further detail on these processes you could read the article Penetration, Adhesion, and Fusion in Mammalian Sperm-Egg Interaction
Increased Calcium activated Calpain (calcium dependent cysteine protease which causes CSF to disappear thereby activating APC/C which in turn causes dissociation of MPF. This results in completion of 2nd meiotic division.

For further details I recommend you to read Johnson and Everitts Essential Reproduction (6th edition), cell cycle chapter in The cell by Bruce Albert (5th edition)

  During oocyte–sperm fusion and second polar body expulsion, the cytoplasmic contents of the sperm cell membrane (now fused with the oocyte membrane) pass into the oocyte cytoplasm. Between 4 and 7h after fusion, the two sets of haploid chromosomes each become surrounded by distinct mem- branes and are now known as pronuclei (see Fig. d). The male is usually the larger of the two. Both pronuclei contain several nucleoli. During the next few hours, each pronucleus gradually moves from its subcortical position to a more central and adjacent cytoplasmic position. During this period, the haploid chromosomes synthesize DNA in preparation for the first mitotic division, which occursabout 18–24h after gamete fusion. The pronuclear membranes around the reduplicated sets of parental chromo- somes break down (see Fig. e), the mitotic metaphase spindle forms and the chromosomes assume their positions at its equator. The final phase of fertilization has been achieved: syngamy (or coming together of the gametic chromosomes) has occurred. Immediately the first mitotic anaphase and telophase are completed, the cleavage furrow forms, and the one-cell zygote becomes a two-cell conceptus.


Physiology of tricuspid and bicuspid(mitral) valves

During embryogenesis at the level of an atrioventricular canal there is so called endocardial "cushion" tissue. This tissue bulges to the left side more than it does to the right and contribute to the fusion of the valvular ring to a one leaflet, while from the remaining part of the ring develops the second leaflet:

AVEC = atrioventricular endocardial cushions

As has been stated, the cushion tissue bulges more to the left, thus on the right side where the tricuspid valve is forming the leaflets does not "merge" and develop into three-leaflet valve.

Interestingly, this left side "suture" might sometimes fail to develop with resulting three-leaflet mitral valve.


Frequency of dominant phenotype (Hardy-Weinberg)

p = p(a) = 0.6

q = p(A) = 0.4

Frequency of homozygous recessive, aa = p2 = 0.36

All other genotypes have dominant phenotype therefore the frequency of the dominant phenotype is 1-0.36 = 0.64

(Frequency of homozygous AA = q2 = 0.16

Frequency of heterozygous Aa = 2pq = 0.48)

And if you want a deeper explanation you really should study this answer by Remi.b


That depends on the status and activity of the cell. Red blood cells purge their nuclei and DNA contents and continue to perform their function quite well, though they lose their ability to split and form new cells (i.e. are terminally differentiated). Most cells, however, require the genome to transcribe and translate genetic information into protein to maintain their metabolic and functional activities. As you say, DNA would also be required to divide and build new cells, so that would be one major downside of removing all DNA. Adding exogenous proteins or amino acids will not help with ensuring correct protein production and maintenance, because proteins are coded for by mRNA which act as mobile transcripts of DNA. They are dependent on DNA transcription, without which they cannot exist. Proteins do not spontaneously form. Long story short, DNA is almost always absolutely essential, and it is the case that if you removed the nucleus from most cells, they would die very shortly thereafter.


Why have people much more different cells than rice plants, while they have roughly the same number of genes?

Actually, rice has about twice as many genes than humans (you can check yourself on bionumbers). But who cares? It is not because two species have the same number of genes that they would look alike. Human and rice have quite different genes. Numbers in themselves do not matter.

Consider the situation where Paul has twice the number of clothes in his wardrobe than Jack, it does not necessarily mean that Paul and Jack dress up differently. Conversely, when playing poker, Paul always has the same number of cards in his hands than Jack, yet their hands may well be very different.

Generally speaking 'higher plants' tend to have way more genes than 'higher animals'. There are several hypotheses for that. Plants are more often polyploid and therefore have more neofunctionalization. Also, plants don't move. It is not impossible that they would need more genes to cope with a more varying environmental conditions.


What was the breakthrough behind the “sudden” feasibility of mRNA vaccines in 2020?

Answering my own question after reading the 2018 Nature review article “mRNA vaccines — a new era
in vaccinology”
The resources and motivation engendered by the COVID-19 pandemic are a major factor in the development of the first mRNA vaccines approved by national governments. However, before the COVID-19 pandemic, there were recent advances in mRNA vaccine pharmacology, which made everything possible.
Introduction
The Nature review points out that it was not a single breakthrough, but a lot of research that was conducted during the last couple of years.
Demonstrations of protective immune responses by mRNA vaccines against various infective pathogens were published in recent years. In the first one, published in 2012, direct injection of non-replicating mRNA vaccines was shown to be immunogenic against various influenza virus antigens in multiple animal models1. Since then, several studies on animals, and in some cases, healthy human volunteers, have managed to induce protective immunity against rabies2,3, HIV-14,5,6, Zika7,8,9, H10N8 and H7N9 influenza10, and other viruses.
The authors of the review, which was written before the COVID-19 pandemic, believed that “mRNA vaccines have the potential to solve many of the challenges in vaccine development”. Therefore, had the pandemic not happened, it is likely that we still would have seen effective mRNA vaccines being developed, albeit at a slower pace.
Recent technological advancement has largely overcome the main challenges in the development of mRNA vaccines.
The Challenges
1. Instability
Protein expression after the vaccine is administered might be insufficient if, for instance, the half-life of the vaccine is too low, or if in vivo mRNA translation is insufficient11,12.
2. Inefficient in vivo delivery
mRNA vaccine delivery is tricky. For instance, mRNA can aggregate with serum proteins and undergoes rapid extracellular degradation by RNases. Therefore, formulating mRNAs into carrier molecules is often necessary, and delivery formulations need to take into account factors such as the biodistribution of the vaccine after delivery, mRNA uptake, and protein translation rate13,14.
3. Safety
The complexity of modulating the immunogenicity of the mRNA used in vaccines can potentially lead to unwanted stimulatory effects on the immune response15,16,17.
The Recent Advances
1. Optimization of mRNA translation and stability
Sequence optimization techniques such as replacing rare codons with more frequently used synonymous codons18, as well as enrichment of G:C content16, have been examined for increasing in vivo protein expression.
2. Progress in mRNA vaccine delivery
There are numerous delivery methods for mRNA vaccines that have been examined in the literature. In recent years, the limitations of some of these, such as using physical methods (e.g., electroporation) to penetrate the cell membrane, were demonstrated19. On the other hand, progress was made toward the increased efficacy and reduced toxicity of other delivery methods such as cationic lipid and polymer-based delivery13,16,20,21.
3. Modulation of immunogenicity
Recent studies have demonstrated that the immunostimulatory profile of mRNA can be controlled more precisely using a variety of techniques. These include chromatographic purification to remove double-stranded RNA contaminants, the introduction of naturally-occurring modified nucleosides to prevent the activation of unwanted innate immune sensors, and complexing the mRNA with various carrier molecules (this includes novel approaches to adjuvants that take advantage of the intrinsic immunogenicity of mRNA)15,17,22,33.
Apart from the advances in techniques such as purification and the introduction of nucleosides, there was also an improvement in the understanding of when these techniques should be used, based on factors such as the mRNA platform used, RNA sequence optimization, and the extent of mRNA purification under consideration16,24.
References

Petsch, B. et al. Protective efficacy of in vitro synthesized, specific mRNA vaccines against influenza A virus infection. Nat. Biotechnol. 30, 1210–1216 (2012).
Schnee, M. et al. An mRNA vaccine encoding rabies virus glycoprotein induces protection against lethal infection in mice and correlates of protection in adult and newborn pigs. PLoS Negl. Trop. Dis. 10, e0004746 (2016).
Alberer, M. et al. Safety and immunogenicity of a mRNA rabies vaccine in healthy adults: an open-label, non-randomised, prospective, first‑in‑human phase 1 clinical trial. Lancet 390, 1511–1520 (2017).
Pollard, C. et al. Type I IFN counteracts the induction of antigen-specific immune responses by lipid-based delivery of mRNA vaccines. Mol. Ther. 21, 251–259 (2013).
Zhao, M., Li, M., Zhang, Z., Gong, T. & Sun, X. Induction of HIV‑1 gag specific immune responses by cationic micelles mediated delivery of gag mRNA. Drug Deliv. 23, 2596–2607 (2016).
Li, M. et al. Enhanced intranasal delivery of mRNA vaccine by overcoming the nasal epithelial barrier via intra- and paracellular pathways. J. Control. Release 228, 9–19 (2016).
Pardi, N. et al. Zika virus protection by a single low-dose nucleoside-modified mRNA vaccination. Nature 543, 248–251 (2017).
Richner, J. M. et al. Modified mRNA Vaccines protect against Zika virus infection. Cell 168, 1114–1125.e10 (2017).
Richner, J. M. et al. Vaccine mediated protection against Zika virus-induced congenital disease. Cell 170, 273–283.e12 (2017).
Bahl, K. et al. Preclinical and clinical demonstration of immunogenicity by mRNA vaccines against H10N8 and H7N9 influenza viruses. Mol. Ther. 25, 1316–1327 (2017).
Weissman, D. mRNA transcript therapy. Expert Rev. Vaccines 14, 265–281 (2015).
Sahin, U., Kariko, K. & Tureci, O. mRNA-based therapeutics — developing a new class of drugs. Nat. Rev. Drug Discov. 13, 759–780 (2014).
Kauffman, K. J., Webber, M. J. & Anderson, D. G. Materials for non-viral intracellular delivery of messenger RNA therapeutics. J. Control. Release 240, 227–234 (2016).
Guan, S. & Rosenecker, J. Nanotechnologies in delivery of mRNA therapeutics using nonviral vector-based delivery systems. Gene Ther. 24, 133–143
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Kariko, K. et al. Incorporation of pseudouridine into mRNA yields superior nonimmunogenic vector with increased translational capacity and biological stability. Mol. Ther. 16, 1833–1840 (2008).
Thess, A. et al. Sequence-engineered mRNA without chemical nucleoside modifications enables an effective protein therapy in large animals. Mol. Ther. 23, 1456–1464 (2015).
Kariko, K., Muramatsu, H., Ludwig, J. & Weissman, D. Generating the optimal mRNA for therapy: HPLC purification eliminates immune activation and improves translation of nucleoside-modified, protein-encoding mRNA. Nucleic Acids
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Gustafsson, C., Govindarajan, S. & Minshull, J. Codon bias and heterologous protein expression. Trends Biotechnol. 22, 346–353 (2004).
Johansson, D. X., Ljungberg, K., Kakoulidou, M. & Liljestrom, P. Intradermal electroporation of naked replicon RNA elicits strong immune responses. PLoS ONE 7, e29732 (2012).
Schlake, T., Thess, A., Fotin-Mleczek, M. & Kallen, K. J. Developing mRNA-vaccine technologies. RNA Biol. 9, 1319–1330 (2012).
Reichmuth, A. M., Oberli, M. A., Jeklenec, A., Langer, R. & Blankschtein, D. mRNA vaccine delivery using lipid nanoparticles. Ther. Deliv. 7, 319–334 (2016).
Fotin-Mleczek, M. et al. Messenger RNA-based vaccines with dual activity induce balanced TLR‑7 dependent adaptive immune responses and provide antitumor activity. J. Immunother. 34, 1–15 (2011).
Rettig, L. et al. Particle size and activation threshold: a new dimension of danger signaling. Blood 115, 4533–4541 (2010).
Kauffman, K. J. et al. Efficacy and immunogenicity of unmodified and pseudouridine-modified mRNA delivered systemically with lipid nanoparticles in vivo. Biomaterials 109, 78–87 (2016).


spinal cord lesion and result in somatic sensation

This is a classic Brown-Sequard syndrome well- studied in the field of neurology. To answer your question, you would need to know what tracts are being severed and what sensations each tract is responsible for. A clean R hemi-section of the spinal cord at the level of T6 would affect the 1) R lateral corticospinal tract, 2) R spinothalamic tract, and 3) R dorsal columns.

The R lateral corticopsinal tract is an upper motor neuron (UMN) pathway, which relays messages from your brain to the periphery. If severed, it would lead to paralysis of muscles below the lesion on the ipsilateral side. This would result in UMN signs such as increased reflexes, increased spasticity, and muscle weakness.
The spinothalamic tract is a sensory pathway connecting peripheral sensations and bringing them up to the brain. Specifically, it communicates sensations of pain, temperature, and gross touch. If severed on the R side, these sensations would be lost on the contralateral side a few levels below the site of the lesion. The reason for this is due to the decussation, or crossing over, of the tract at or slightly above the level of entry of the nerve fibers into the spinal cord from the periphery.
The dorsal columns are similar to the spinothalamic tract, except the sensations communicated are vibration, fine touch, and proprioception. If severed, this would cause loss of these sensations below the level of the lesion but on the same side. A patient would not be able to balance himself/herself without support.

Regarding what areas of the body would be affected based on a lesion in T6, C1, or L5, just as mentioned by jonsca, one would need a dermatome to understand what areas of skin sensation would be affected, and know the nerve root origins of different nerves of muscles. A great book to read to locate these answers in a table format is Neurology BluePrints.

Otherwise, feel free to open any Neurology textbook for a reference, and look for Brown-Sequard Syndrome to read in more detail.


Components of the concept of Developmental Noise?

There are two good papers on this that I like a lot:

Noise in Gene Expression: Origins, Consequences, and Control

Cellular decision making and biological noise: from microbes to mammals.

I think they can tell you better than I can, but the major other source of noise is extrinsic noise. Extrinsic noise typically is taken to means two things (both of which are related):
1. Physical noise from the environment that affects biological processes (thermodynamic fluctuations, for example)
2. Intercellular heterogeneity caused by, for example, unequal division. This is also related to cells not being "well mixed" - essentially, molecules found inside of cells are not evenly distributed throughout it.

There may be other kinds of noise, but I think extrinsic is really the main one you should think about.


What kind of reverse transcriptase is used in qRT-pcr is there a standard like taq dna pol is used for qPCR

M-MuLV (Monoley murine leukemia virus) reverse transcriptase

Some RT enzymes are engineered to remove the RNAseH domain so that template RNA persists for more rounds of RT.

  Is it possible to use a biologically active Telemorease Elongation Reverse Transcriptase (TERT) in the place of the Reverse Transcriptase

Perhaps it can catalyse an RT reaction in-vitro. But commercial enzymes need to be efficient and I think using TERT won't be that advantageous.


Would it be possible to force the pineal gland to release dimethyltryptamine on command?

According to this page the release of DMT upon death is speculative and its presence has so far been confirmed in rodents brain and human melanoma cell line SK-Mel-147. DMT is also produced in humans; however, its production and purpose in the brain has yet to be proven or understood (http://en.wikipedia.org/wiki/Dimethyltryptamine). Hence from what I have gathered on the matter DMT has not yet been proven to get secreted from human pineal gland and its command based secretion is yet to be discovered.


There are two things happening: First melanin absorbs the energy from the UV radiation and releases it as infrared energy and thus protects the cells in the skin. This happens in all people, the deeper the skin color is, the better is the protection.

What is different between people is the amount of pigment they produce, the number of melanocytes is approximately the same. This depends on their genetic backgroud and is influenced by mutations in the pigment production pathway. As this is relatively complex, there are numerous positions which can influence the ability to tan, so I will only name a few.

The rate limiting enzyme for the pigmentation is Tyrosinase which catalyzes the first step of the melanin biosynthesis and oxidizes the amino acid tyrosine into DOPA. Without tyrosinase humans are not able to make any pigment at all which causes albinism. This is pretty drastic and doesn't happen too often. See reference 1.

Other possibilities are mutation in the signalling towards pigmentation, more specifically mutations in the MC1R gene which encodes on of the receptors. These mutations affect the ability to tan and are associated with red hair color, pale skin and freckles (most of the red-haired people carry at least one mutation in their MC1R gene). See reference 2.

Then there are mutations in the tyrosinase gene, which results in an enzyme with a lower processing rate. Because of this, less pigment can be made as the amount of materials is limited. See references 3 and 4.

The diversity of the human pigmentation is influenced by all these (and much more) genes. Have a look at references 5 and 6 for details.

References:

Analysis of tyrosinase mutations associated with tyrosinase-related
oculocutaneous albinism (OCA1).
Red hair is the null phenotype of MC1R.
Mutations at Critical N-Glycosylation Sites Reduce Tyrosinase
Activity by Altering Folding and Quality Control
Mutational mapping of the catalytic activities of human tyrosinase.
Molecular genetics of human pigmentation diversity
The genetic architecture of normal variation in human pigmentation:
an evolutionary perspective and model


Identification of Bioluminescent Species in South Carolina Marshlands

Confirmed by a number of locals later on to be a small species of pistol shrimp. It was a pretty cool phenomenon.  Thanks for the help here.


Chills down the spine with certain music?

It is called a frisson, and actually, there has been a study about it, available here.
The frisson is kind of the same you get from cold weather, fear, or... well, other things not suitable to discuss if not knowing how old people reading this might be.

Actually, they found that this works best if you include familiarity. In their case, asking study participants to bring their favourite emotional music, in you case hearing it played by your brother.

How this evolutionary came by is unclear. But as it resembles the shivers you would call "a tingling sense of danger" it might stem from a reaction to uncertainty or at least unclear danger. In this case, it is meant to enable you to concentrate on whatever is coming, and maybe (but that's one of my own theories) this is how it came to connect to pleasant emotions as well: You want to be able to concentrate, delve into the emotion. This could explain, why it works best with familiar pieces: you already know that you want to listen closely.


Can Cas13 be used with multiple crRNAs in the same reaction?

Answer is no. Because each CRIPSR-Cas(xx) system works as a ribonucleoproteic complex, so they needs to be loaded with a crRNA in order to be working. Functionality is guaranteed while each of the Cas endonuclease domain is associated with a crRNA. You maybe could use multiple Cas13 with multiple crRNA.
In molecular diagnosis is common to use orthogonal CRISPR enzymes with different crRNA, as can be seen in this original research.


Nice question! Many vegetables taste bitter because they contain compounds known as phytonutrients (Greek phyto = "plant"). There are more than 2500 phytonutrients known, and the most important (and common) ones are categorized as1:

Carotenoids: they are the ones that give red/orange/yellow color to some vegetables. They are mainly antioxidants, but some of them, like $\beta$-carotene and $\beta$-cryptoxanthin, are good for eyes as they can be converted into vitamin-A, whose derivative forms a part of phototransduction cascade.
Ellagic acid: it is found in a number of berries, such as strawberries, raspberries, pomegranates, etc. and has been shown in vitro to be helpful in slowing the growth of cancer cells and aid liver in neutralizing cancer-causing chemicals.
Flavonoids: they are found in a large variety of plants and constitute a large number of phytonutrients. Some flavonoids, like catechins, hesperidin and quercetin are very good for health. For example, see this answer for effects of catechins on the body.
Resveratrol: it is found in grapes, red wine, etc. and shows antioxidant and anti-inflammatory effects. Some researches have also concluded that it may reduce risk of heart disease and certain cancers.
Glucosinolates: these are found in cruciferous vegetables, like sprouts, cabbage, etc. and help checking formation and growth of cancer. This is the one we're talking about, so I'll continue about this below.
Phytoestrogens: they can exert estrogen-like effects on the body because of their structure, and even block body's natural supply of estrogen. Isoflavones can also reduce risk of endometrial cancer and bone loss in women. They are also found in a large number of plants, including soybeans, oats, barley, rice, apples, carrots, etc. (see full list here).

Another category, alkaloids, has been discussed by @WYSIWYG in their answer. These are all made naturally by plants as a part of their defense mechanism against insects and pests. This, in part, explains why they are bitter.

Coming to main point, glucosinolates are organic compounds that are responsible for bitter taste and pungent smell of many cruciferous vegetables. They are derived from glucose and amino acid, and contain sulfur and nitrogen as constituents. When they are cooked, chewed, or otherwise damaged, an enzyme myrosinase cleaves the glucose molecule, while the remaining molecule converts into isothiocyanate, thiocyanate and nitrile2, which cause the bitter taste and pungent smell (think of the isocyanide test you performed in grade XI and the smell it produced ;) The reaction looks like this:

source

A special glucosinolate, sinigrin, has been shown as responsible for the bitterness of Brussels sprouts and cauliflower3. Also, high concentration of glucosinolates are toxic to humans as well as other animals, though tolerance levels vary even within the same genera (Acomys cahirinus and Acomys russatus)4. So, that partly explains why these compounds are bitter.

Talking about the anti-cancer properties of glucosinolates (going a bit off-topic just so that you know why these are good for you), two of the main compounds that are responsible for such effects are sulforaphane and indole-3-carbinol. Sulforaphane (in which R- becomes C5H11OS- in R-NCS), for example, is derived by the action of myrosinase on glucoraphanin (again, a glucosinolate). It has been shown to have anti-cancer properties. For example, Li et al, 2010 have shown that sulforaphane prevents breast cancer by inhibiting breast cancer stem cells and downregulating the Wnt/$\beta$-catenin pathway (yeah, there is something like cancer stem cell!). In another research, Hsu et al, 2011 showed that sulforaphane prevents prostate cancer by inhibiting HDACs (histone deacetylases, which interfere with normal functioning of tumor suppressor genes) and DNA methylation. This example was just to mention about the anti-cancer properties of glucosinolates in general.

Another class of compounds, called cucurbitacins, are produced in plants of Cucurbitaceae family. Unlike phytonutrients, cucurbitacins are considered a type of steroid since they are derived from cucurbitane and stored as glycosides5. Their derivatives are also found in other families like Rubiaceae, Rosaceae and even some marine mollusks, and, much like glucosinolates, they are also produced for defense against herbivores.

However, it is not sure whether only glucosinolates are the only compounds responsible for bitterness of vegetables. A study suggests that increased levels of calcium can also be responsible for bitterness of vegetables6, although its evolutionary cause and mechanism of action are unknown yet. Also, it may even depend on the person(!). If you are a supertaster (which has high chances to be true if you're woman or from Asia, South America or Africa), you will tend to be highly sensitive to bitterness of Brassica oleracca cultivars, such as kale, Brussels sprouts or cabbage7,8. Sensitivity to coffee, green tea, mushrooms, etc. is also known to increase. You can view a full list on Wikipedia.

References:

 1. Phytonutrients - WebMD

 2. Burow, M; Bergner, A; Gershenzon, J; Wittstock, U (2007). "Glucosinolate hydrolysis in Lepidium sativum--identification of the thiocyanate-forming protein.". Plant molecular biology. 63 (1): 49–61.

 3. Van Doorn, Hans E; Van Der Kruk, Gert C; Van Holst, Gerrit-Jan; Raaijmakers-Ruijs, Natasja C M E; Postma, Erik; Groeneweg, Bas; Jongen, Wim H F (1998). "The glucosinolates sinigrin and progoitrin are important determinants for taste preference and bitterness of Brussels sprouts". Journal of the Science of Food and Agriculture. 78: 30–38.

 4. Samuni Blank, M; Arad, Z; Dearing, MD; Gerchman, Y; Karasov, WH; Izhaki, I (2013). "Friend or foe? Disparate plant–animal interactions of two congeneric rodents". Evolutionary Ecology. 27 (6): 1069–1080.

 5. Jian Chao Chen, Ming Hua Chiu, Rui Lin Nie, Geoffrey A. Cordell and Samuel X. Qiu (2005), "Cucurbitacins and cucurbitane glycosides: structures and biological activities" Natural Product Reports, volume 22, pages 386-399

 6. Tordoff MG, Sandell MA. Vegetable Bitterness is Related to Calcium Content. Appetite. 2009;52(2):498-504. doi:10.1016/j.appet.2009.01.002.

 7. Dinehart, M.E.; Hayes, J.E.; Bartoshuk, L.M.; Lanier, S.L.; Duffy, V.B. (2006). "Bitter taste markers explain variability in vegetable sweetness, bitterness, and intake". Physiology & Behavior. 87 (2): 304–13.

 8. Drewnowski, Adam; Henderson, Susan Ahlstrom; Levine, Alisa; Hann, Clayton (2007). "Taste and food preferences as predictors of dietary practices in young women". Public Health Nutrition. 2 (4).

 9. Li Y, Zhang T, Korkaya H, et al. Sulforaphane, a Dietary Component of Broccoli/Broccoli Sprouts, Inhibits Breast Cancer Stem Cells. Clinical cancer research : an official journal of the American Association for Cancer Research. 2010;16(9):2580-2590. doi:10.1158/1078-0432.CCR-09-2937.


That is an Oleander Hawk Moth, Daphnis nerii. Order Lepidoptera,family Sphigidae. https://en.wikipedia.org/wiki/Daphnis_nerii


Why Only DNA can Contain Hereditary Material?

I think any discussion of this question can benefit from a historical perspective. For a long time, it was in fact believed that proteins was the hereditary material. The Nature Scitable page on the discovery of DNA (1) starts with the following passage:

  In the first half of the twentieth century, Gregor Mendel's principles
  of genetic inheritance became widely accepted, but the chemical nature
  of the hereditary material remained unknown. Scientists did know that
  genes were located on chromosomes and that chromosomes consisted of
  DNA and proteins. At the time, however, proteins seemed to be a better
  choice for the genetic material, because chemical analyses had shown
  that proteins are more varied than DNA in their chemical composition,
  as well as in their physical properties.

While perhaps easy to dismiss in hindsight, it is possible to understand the reasoning of the day. The "central dogma" of molecular biology, that genetic information flows from DNA to RNA to proteins was only described later, and explained how the production of complex proteins consisting of 20-odd amino acids can be directed by a polymer consisting of only four nucleotides. This allows great complexity and variety in phenotypes while maintaining simplicity of the genetic material. The central dogma also facilitates the seperation of the use (through protein expression) and storage (as DNA) of genetic material.

As Watson and Crick noted in their famous paper, the double helix of DNA, when discovered, immediately suggested how the genetic material could be elegantly copied. While the more complex structure of proteins would likely require a more complex copying mechanism, the specification of amino acids through three-nucleotide codons in DNA allows the regularity of the DNA material to be retained for easy replication while allowing complex proteins to be produced.

However, even though DNA is the primary genetic material today, the situation may have been different at the time life first appeared. According to the RNA world hypothesis, RNA may have been the original genetic material and that DNA is a variation of RNA, not the other way around as it is commonly seen.

For a fuller historical perspective, I recommend the book "What is Life?" by Erwin Schrödinger, which was written before the discovery of DNA as the genetic material.


Skeletal muscle has got many many peripheral nuclei. What does "peripheral" mean here?

'Peripheral' in this context refers to the position of the nuclei within the skeletal muscle cell.  They are in the periphery (outer part) of the cell body rather than central as in most cell types.  More specifically, they are "subsarcolemmal", i.e. just under the sarcolemma, the cell membrane of the muscle fiber cell (source):

(Image from Wikipedia)

The many nuclei of a skeletal muscle cell are spaced out along the length of the cell (source 1, source 2).


How do catenanes form when DNA replicates?

The first DNA circle is double-stranded. If you could melt the double-helix completely you would not be able to pull the two stands apart without breaking the sugar-phosphate backbone of at least one of the two strands. This is a topological problem, the two strands are linked to each other.

Now consider DNA replication. In the simplest example there is a single origin of replication and there will be two replication forks proceeding around the circular genome in opposite directions. This is exactly what happens during DNA replication in the bacterium E. coli.  The DNA double helix of the parental molecule "melts", the RNA primers are synthesized by primase, and the DNA polymerase complexes initiate synthesis. Behind each replication fork there are now two hybrid DNA strands, each with a parental strand, and a new daughter strand.

Thus far no sugar-phosphate bonds have been cleaved. When replication is done each daughter ds DNA helix will have a single-stranded nick at the origin, and another one at the site where replication terminated, but those will be quickly repaired by DNA polymerase I and DNA ligase. Even if those two repair enzymes were inhibited, and you could somehow melt the DNA strands of both the daughter chromosomes, you would only be able to pull out the new DNA molecules (with the nicks), the two original parental strands are still topologically linked.

To resolve two concatenated DNA circles you need to make a double-stranded break in at least one of the ds circles. This  enzymatic activity is provided by a class of enzymes named Type II DNA topoisomerases.


Why are particulate matter toxic to humans?

Particulates can accumulate in the aveolae in the lungs. This leads to inflammation and tissue damage and scarring. This reduces the available surface area for gas transfer. Low level exposure over long periods is harmful. Asbestos workers are well known to get sick, but miners can get black lung or silicosis from inhaling mining dust, and farmers can get lung disease from inhaling dirt that gets blown up as dust. This damage usually isn't seen until they are in their 50s or 60s.


Why do I have a lot in common with my mother?

In this answer I mainly repeat the comments!

There are several reasons why you might share some traits with your mother.

genetic (see below)
epigenetic
environmental influence while being in the womb
environmental influence up to the time you were 4 years old
the two environment were not so different (maybe because your adoptive parents wanted to follow the will of your mother or just because by chance your adoptive parents have similar behaviour that your mother)
multiple testing issue (see below)

These reasons can be classified into three categories:

environmental variance
genetic variance
poor observation (statistic mistake)

The phenotypic variance in a population is influenced by the environmental variance + the genetic variance + the variance due to the interactions between the environmental and genetic variances. The heritability can be calculated as the part of the phenotypic variance which are genetically determined. Such calculations make sense only for populations not for a given parent-offpsring pair.

genetic: It does not make sense to ask whether the variance of a trait is dominant or recessive. It makes sense to say that "liking pink" is dominant over "liking blue". Therefore, you should tell us what is the variant of a given trait that you share with your mother. In such case we might tell you if this variant is dominant or not over the other variants. But of course, this works only for traits that are at least slightly genetically determined. liking a color will certainly not have a strong genetic variance for example. And even if a trait is 100% genetically determined, complex genetic architecture might make it hard to answer. For example a given variant might be dominant in a given genetic background but recessive in another. Finally, I should say that it costs to perform the necessary study (Genome Wide Association Studies) to know exactly the part of the variance of a given trait that is genetically determined. And of course, such studies depend on the population we look at.

Multiple testing issue: Without realizing, you actually looked at many different traits. You might have looked at your favorite color, your favorite beer, the way you wash your teeth, the sport you practice, the color of room, whether you are calm or impulsive, etc... You might not have paid attention only to things that match but you would have found as many similarities (not the same ones though) with any other human on earth.


How does Bernoulli’s Principle apply to the cardiovascular system?

Bernoulli's principle can be a little tricky when applied to the cardiovascular system, but it still holds true across the entire system. You mention a good point that the relationship doesn't seem quite right at the aorta or arteries, because of the constant fluctuation of pressure between systolic and diastolic without a significant change in diameter of the vessel. Remember that this is due to the pulsatile flow of blood from the heart, and has nothing to do with Bernoulli's principle. If the flow was constant (i.e. not pulsatile) then the pressure would be constant as the diameter of the vessels is constant. As the diameter of the vessels begins to decrease the velocity would increase to maintain a constant value.

As you mention, Bernoulli's principle describes how the product of area and velocity of flow must be constant across a system. When the total surface area of the system increases, the pressure decreases as well as flow. It is important to remember that even though the capillaries are so small and individually high resistance (which you would think according to Bernoulli's principle should increase the velocity), you are effectively adding an innumerable number of these very small resistors in parallel (not in series) and the resistance overall (and subsequently pressure + flow) decreases greatly.

When adding resistance in series the total resistance is additive and it adds up quickly! $$R_{Total} = R_1 + R_2 + R_3$$
While resistance in parallel adds the reciprocal of the resistor, meaning that as more resistors (or capillary pathways) are added the total resistance continues to decrease because of the following relationship: $$\frac{1}{R_{Total}} = \frac{1}{R_1}+\frac{1}{R_2}+\frac{1}{R_3}$$

The parallel resistance stuff was difficult for me to grasp when I was a student, because it never seemed to make sense in my mind that the resistance significantly decreased when you added all these small capillaries. One of my physiology professors described it well when he said, "Think of adding resistance in parallel, in the way that capillary beds and other vessels are in the cardiovascular system, like giving the blood another place to go." If the blood has more places that it can go, then it's easier to see why resistance falls so much when you add a bunch of extra places for the blood to flow.


Do epigenetics determine the proteins a cell produces and therefore it's function?

Short answer: Yes, epigenetics play a role in determining gene expression, therefore protein expression and function.

Lifestyle factors like diet, smoking, alcohol consumption, and stress can change one's epigenome. A historical example of this might be the Dutch Hunger Winter of 1944-45; there is evidence that after the parents' generation suffered during World War II, the children who were conceived during this time and exposed in utero to famine had different epigenetic marks than their siblings who were conceived not during the famine.

Epigenetic regulation is also essential for cell differentiation in vivo and in vitro. Embryonic stem cells undergo many changes to their epigenome in order to become mature cells. One interesting example for further reading is the transcription factor NeuroD1, which binds to targets in the DNA to cause widespread changes in gene expression that are specific to neurons, and commits cells to a neuronal fate. It doesn't bind to thousands of neuronal genes; instead, it causes a "ripple effect" thanks to epigenetic mechanisms.

Longer answer: Epigenetic marks are added to the genome for many reasons, including the two you just listed, and I think it is helpful to understand what happens at a molecular level in order to understand "why" we have them and to better visualize what the epigenetic marks ("tags") are. This might help you to think of better examples on your own.

DNA spends most of its time wrapped around proteins called histones. A complex of DNA and histones is called a nucleosome. DNA-in-nucleosomes is called chromatin. Chromatin can then either be "loose" (called euchromatin) or "compact" (called heterochromatin). There are more detailed ways to define how accessible chromatin is, but this is the basic idea. Intuitively, loose chromatin is more easily accessible and the genes there can be transcribed actively. Compact chromatin is less active.

The looseness of chromatin is determined by how closely the nucleosomes interact, which is controlled by the histones' molecular properties. Whether or not the histone proteins interact to make the chromatin compact, or repel each other to make the chromatin loose, depends on what modifications they possess. These modifications are added by histone-modifying enzymes.

Histone-modifying enzymes are regulated by transcription factors (i.e. during the process of differentiation) as well as signals generated by extrinsic factors (i.e. during the organism's lifetime). The balance of activating and silencing activity is what adds and removes these marks to give a cell its individual epigenome.

So, in simple terms, epigenetic marks determine how accessible different parts of the DNA are, and a whole lot of factors (like cell identity and lifestyle) can determine where those epigenetic marks are.


Definition of "structural underdominance"?

I understand heterozygote inferiority (also underdominance or heterozygote disadvantage) as the opposite of heterozygote advantage, that is, lower fitness of the heterozygous genotype than either homozygote (as reference, see Hedrick, 2009, p. 119). I haven't seen the term structural underdominance before. However, heterozygote disadvantage can sometimes be seen in species/subspecies hybrids and also chromosomal heterozygotes (see Hedrick, 2009, p 140), and this might be what the term structural underdominance is describing (structural as in chromosomal). This can then lead to unbalanced gametes with low viability, which means low fitness compared to homozygotes. The quote you have included also talks about plant hybrids, which makes this explanation likely, and it also makes sense since they mention artifical doubling as a solution. If I have understood the process correctly, chromosomal doubling should lead to better pairing of chromosomes and lower risk of unbalanced chromosome translocations.

Also note that Hedrick labels heterozygote disadvantage as an unstable equilibrium (p. 140ff), but I haven't looked more closely at the dynamics behind this.


Terminology question: the scope of an allele in an organism

If I were discussing a SNP of FOO that gives rise to foo in a tumor
  cell of an organism, I wouldn't say that the organism has foo, but I
  might say that the tumor has it.

You can call it a somatic mutation. See this paper. They report such mutations in cancer.

You can use the term like this:

  Carcinoma tissue had a somatic mutation in XYZ oncogene, thereby making it constitutively active.

  If I were discussing a chimeric or mosaic organism in which some
  fraction of the chimera had foo and the other fraction had FOO

In this case you can say:

  The organism is chimeric for gene-X, expressing variants X1 and X2

From this article:

  Effects of AngII-Infusion Into LDL Receptor−/− Mice That Were Chimeric
  for AT1a Receptors


Do IgM and IgG differ for different infections?

IgM (Immunoglobulin M) is the first antibody to appear in response to an antigen. It can be produced by the fetus and cannot be crossed by the placenta.

Typically one might test IgM to diagnose hereditary and acquired IgM immunodeficiencies or diagnose Waldenstrom macroglobulinemia. It can serve as the earliest Ig serologic diagnosis of infectious disease.

Lab tests for IgM may be increased in liver disease, chronic infection, hyper IgM syndrome, and secondary to nephritic syndrome; Waldenstrom macroglobulinemia, lymphoma, CLL, multiple myeloma (rare), Schnitzler syndrome, cold IgM antibody agglutin, and MGUS.

Lab tests for IgM may be decreased in protein-losing syndromes, non-IgM myeloma, and infancy/early childhood.

IgG (Immunoglobulin G) activates complement and fights infection. IgG represents 70-80% of the total serum immunoglobulins in normal adults. It exists in four subclasses (IgG1, IgG2, IgG3, and IgG4). IgG1 predominates as 65% of the total IgG. IgG of maternal origin provides passive immunity to the neonate. It is transported across the placenta.

Typically one might test IgG to diagnose IgG myeloma, diagnose hereditary and acquired IgG immunodeficiencies, and provide a serologic diagnosis of infectious diseases and immunity.

Lab tests for IgG may be increased in multiple myeloma, solitary plasmacytoma, MGUS, lymphoma, CLL, sarcoidosis, cirrhosis, autoimmune diseases, parasitic diseases, chronic infection, and intrauterine contraceptive diseases.

Lab tests for IgG may be decreased in protein-losing syndromes, pregnancy, non-IgG myeloma, Waldenstrom macroglobulinemia, primary immunodeficiency states, and agammaglobulinemia (if combined with other immunoglobulin decreases).

Sources:
https://5minuteconsult.com/collectioncontent/2-152356/lab-tests/immunoglobulin-m-igm
https://5minuteconsult.com/collectioncontent/2-152354/lab-tests/immunoglobulin-g-igg


Welcome to Biology.SE

Fields of interest

The assignment you have to write has a little bit to do with Biology and a little bit to do with Philosophy! The question of what is alive and what is not depends on the very definition of what is a living thing and this question is not of interest to biologists but only to philosopher.

How to nail this assignment

Therefore, for your assignment you will need to understand what a mitochondrion is (the Biology part) and to understand how do the different definitions of life apply to the mitochondrion (Philosophy part although you will need some knowledge in Biology to understand the relevance of these definitions).

What is a mitochondrion?

This question is too broad and cannot be answered here. Make sure to have a look at the wikipedia page. In short:

mitochondrion contain DNA
mitochondrion is the result of a bacteria that has somehow been internalized into a bigger cell (it is a symbiont). This is why today mitochondrion contain DNA. It is therefore not exactly an organelle like others. Note that plants, in addition to having mitochondrion, they have plasmids that are also consequences of a similar process of internalizing other form of life.
mitochondrion DNA evolve (of course)
mitochondrion are basically the energy factory of the cell.
mitochondrion are not able to live by themselves outside a living cell (to my knowledge).

Definitions of life

It is important to understand that the definition of life has absolutely no impact on biology and is nothing but a question of nomenclature.

There are a lot of definitions and I can't cover all of them here. You might want to have a look at this wiki page. The previous link lists the most common properties we think about when thinking about the definition of life.

Homeostasis: Regulation of the internal environment to maintain a constant state; for example, sweating to reduce temperature.
Organization: Being structurally composed of one or more cells — the basic units of life.
Metabolism: Transformation of energy by converting chemicals and energy into cellular components (anabolism) and decomposing organic matter (catabolism). Living things require energy to maintain internal organization (homeostasis) and to produce the other phenomena associated with life.[49]
Growth: Maintenance of a higher rate of anabolism than catabolism. A growing organism increases in size in all of its parts, rather than simply accumulating matter.
Adaptation: The ability to change over time in response to the environment. This ability is fundamental to the process of evolution and is determined by the organism's heredity, diet, and external factors.
Response to stimuli: A response can take many forms, from the contraction of a unicellular organism to external chemicals, to complex reactions involving all the senses of multicellular organisms. A response is often expressed by motion; for example, the leaves of a plant turning toward the sun (phototropism), and chemotaxis.
Reproduction: The ability to produce new individual organisms, either asexually from a single parent organism, or sexually from two parent organisms,"with an error rate below the sustainability threshold."

Related questions

The question of whether viruses are alive is a very common one. Here are two Biology.SE posts on the subject:

why-isnt-a-virus-alive
changing-the-definition-of-life


Awesome question! The immune system detects the presence of non-self using MHC and T cells and the lack of self using NK cells. The placenta first of all doesn't display MHC so T cells can't detect it, and expresses NK inhibitory receptors which stop NK cells killing it. Furthermore, the immune system isn't able to get to the foetus so it isn't able to activate against these antigens nor produce the antibodies which require T cells to be activated first, which then activate B cells. This is because the placenta is a syncitium, thus no spaces between cells for immune cells to slip through (a mechanism used by viruses). The placenta also secretes Neurokinin B, this makes it hard for the immune system to see the baby, and is a mechanism used by parasites. There are T reg cells which act to supress an immune response.


Is it possible for a parasitic wasp to alter the behaviour of its host after emerging from it?

The species of wasp in the video you link to is Cotesia glomerata. Furthermore, there is at least one other species, Glyptapanteles, which parasitizes other caterpillar species in the same way and induces the same behaviour in its host.

I'm not sure which virus it is.

http://www.newscientist.com/article/dn14053-zombie-caterpillars-controlled-by-voodoo-wasps.html?feedId=online-news_rss20

Is it possible? Of course, you have an example! Though, there is a small caveat. Some of the offspring sacrifice themselves to induce the behavioral change after the rest of the brood has emerged.

Is it common among parasitic wasps? No. While injecting offspring into host species is a common theme for parasitic wasps, and while there are a handful which somehow induce behavioral changes in the host animals - continuing the manipulation after leaving the host animal is extremely rare among parasites in general.


Is ability to easily pollinate desirable?

Yes, the fact that pea plants were easy to pollinate was desirable and helpful in understanding the effects of Mendelian factors (genes) but for the proper study of the factors expressed CROSS POLLINATION of homozygous plants having different phenotype and genotype ( e.g. cross between RR and rr) was preffered rather than self pollination.


Human disease and associated phenotype database?

It seems to me like you're effectively wanting to make a decision matrix.

So... As said above, ICD and SNOMED CT going to have codes for your diseases and symptoms. I'd lean toward SNOMED CT due to the way it organises concepts. Essentially from broad to specific. That way users can enter very specific symptoms, and your matrix only needs to have symptoms as specific as is required.
For example you can say "vomitting" is a symptom of "alcohol poisoning" in your db. And if a user enters "projectile vomitting" the SNOMED structure recognises this as a type of vomitting.

However - Symptoms don't make the disease, and most diseases have a huge array of 'possible symptoms' (Which is why SNOMED CT doesn't have such relationships). So it's not an easy undertaking. Hence why those who've made such db's (as you've linked to) are reluctant to share their IP, at least without $$$.

If you're going to make your own, here's some tips.
Consider:

only diseases relevant to your use case - eg. Aged care doesn't require paediatric disorders;
exclude non-specific symptoms;
rank your symptoms by frequency - eg. 60% of pregnant women have morning sickness, where as 100% have an HCG > 10*

Hope this helps. And good luck.

edit- there is a similar thread on LinkedIn

*fabricated statistic :).


How do cockroaches resist the effects of ionizing radiation?

Off the top of head as a medical professional I can imagine the following mechanisms (everything is just speculative reasoning):

Insects don't have blood. Instead, they have hemolymph whose primary role is not oxygen transport (they have an additional tracheal system for this purpose), but rather that of nutrients. Thus they don't need (and don't have) an intense proliferation of blood cell precusors -- these (bone marrow, spleen) are the most susceptible to radiation in a human and animal body.
Insects have a rather primitive immune system that is mostly humoral[a]  and much less cellular[b] compared to the immune system of animals and humans. This eliminates the next common weak place in the body: lymphatic nodes, thymus, again spleen and bone marrow etc.
Insects have generally a much primitive and in many cases also rather decentralized nervous system: the ganglia are organized in a sort of a cord and even though the capital ganglia are usually larger, these dominance is not as prominent as in case of CNS and PNS in animals and humans. Therefore this system is much more tolerant to losses.

1.-3. Therefore, the only sensitive part of insects is the intestinal epithelium which gets renewed on a regular basis (similar to that of humans, also a known target of radiation), but...

Insects (and generally the arthropodes) are known to have exoskeleton. This potentially serves as a good "armor" for vulnerable intestine cells, filtering out the most heavy particles (like alpha- and in some respect also the beta-particles).
EDIT: This seems not to be real protection, see the discussion in comments.

Therefore it is not a surprise that insects generally show much higher resistance against radiation.

EDIT:
As it was correctly added in the comments, there are also gamets, that are most sensitive to radiation (because they bear only the half of the normal genetic information and cannot repair mutations). Even though the lesions in gamets do not lead to immediate death, the potential sterility can easily cause the extinction.

However, cockroaches (and insects generally) are known to be r-animals, meaning that they favor the quantity (r) over quality (K) of their off-spring. This strategy is optimal when dealing with radiation-induced changes in gametes: the high number of offsprings compensates for the genetic imperfections in gametes.

[a] -- meaning that is has secreted peptides in their hemolymph that protect them
[b] -- there are phagocytes, somewhat similar to tissue magrophages in humans, but the rest of the cell chains in immune response in vertrebrates, like T- and B-cells, are completely missing. Those are responsible for the mediation and amplification of the immune response in vertebrates and are the cells that are most susceptible to radiation damage.


There are metanephric diseases, which refer to the location of pathologic tissue relative to the main kidney mass, but unless someone with more expertise wants to weigh in, I don't think that kidneys themselves are called metanephric.

There is also a developmental stage of the kidneys, in which they are referred to as metanephros. Perhaps you're thinking of that?


Does a virus that spreads more rapidly have less chance to evolve?

Any evolutionary process has two components to it:

generation of genetic diversity in a population, and
shifts in the distribution of genetic variants under selective pressure.

For a virus like SARS-CoV-2, every infection results in a vast amount of replication, some of which will be variants generated through imperfect replication. Thus, the more rapidly a virus is spreading, the more opportunity it has to generate genetic diversity. Conversely, if there's not many infections going on, then there won't be much evolution because there won't be much diversity generation.
With regards to selection, the more actions that we take against the virus (e.g., mask wearing, social distancing, vaccination), the more selective pressure that it is under, since these actions differentiate between strains that are more or less effective in evading them. If the pressure goes too high, however, this breaks down. With highly effective countermeasures (e.g., rapid vaccine distribution while not letting our guard down), then there won't be much evolution because most variants won't have an opportunity to infect any new host: each new generation of infections will be driven more by countermeasure failures unrelated to viral efficacy, and thus there will actually be little effective selection.
The highest opportunity for evolutionary change, then, is with poorly coordinated countermeasures. This produces an intermediate rate of spreading, with both much viral replication and many opportunities for selective pressure on infections.  It's really much the same as the problem with stopping a course of antibiotics prematurely, only on a societal rather than individual scale.
Bottom line: countermeasures are still a good idea, even when potential evolution of variants is included. People and governments that don't take the problem seriously, however, are threats to all the rest of us.


Why do mammalian red blood cells lack a nucleus?

Red blood cells are initially produced in the bone marrow with a nucleus. They then undergo a process known as enucleation in which their nucleus is removed. Enucleation occurs roughly when the cell has reached maturity. According to one research (Ji, et al., 2008), the way this occurs in mice is that a ring of actin filaments surrounds the cell, and then contracts. This cuts off a segment of the cell containing the nucleus, which is then swallowed by a macrophage. Enucleation in humans most likely follows a very similar mechanism.

The absence of a nucleus is an adaptation of the red blood cell for its role. It allows the red blood cell to contain more hemoglobin and, therefore, carry more oxygen molecules. It also allows the cell to have its distinctive bi-concave shape which aids diffusion. This shape would not be possible if the cell had a nucleus in the way. Because of the advantages it gives, it is easy to see why evolution would cause this to occur. However, since little is known about the genes the control enucleation, it is still not a fully understood process.


What will happen if a foetus is Rh- and the mother is Rh+?

Nothing. Rhesus incompatibility results when people who are Rh- develop antibodies against Rh+ blood after exposure. People with Rh+ blood do not show any such reaction to Rh- blood.

In a way, it's comparable to blood types in that regard. People with the blood group O can develop antibodies against type (for example) B blood. People with type B don't develop antibodies against type O blood, and can thus receive blood donations of type O.

Also, rhesus incompatibility during pregnancy is only a concern in second or subsequent pregnancies (or after miscarriages). The antibodies develop through the blood being "mixed" during the birth (or miscarriage) and are then an issue if the next fetus also has Rh+ blood, which is just assumed if the father is Rh+ or has an unknown blood type to be on the safe side, and can be addressed medically.

  Injections of a medicine called Rh immune globulin can keep your body from making Rh antibodies. This medicine helps prevent the problems of Rh incompatibility. If you're Rh-negative, you'll need this medicine every time you have a baby with Rh-positive blood.

-What is Rh Incompatibility

Also, as you can read in my answer to a similar question about blood groups and pregnancy
How does a fetus retain a blood group different from its mother? the maternal and fetal blood usually only mix during birth due to the placental blood barrier. If you are wondering whether the fetus should have a reaction, the immediate functions necessary for that don't develop until more than six months after birth.


Rotting is a biochemical reaction: basically catabolism (breaking down of complex compounds to simpler compounds). Cellulose or lignin or any other structural polysaccharide will not undergo spontaneous hydrolysis. This reaction is catalyzed by enzymes produced by the microorganisms like fungi and bacteria (the term for these decomposers is saprophyte). Saprophytes prefer to grow in humid and warm environments.

So the primary role of humidity is to promote the growth of decomposers. Simultaneously it provides the water required for the hydrolysis.


Why is human vision restricted to 400-700 nm?

Short answer
The visible spectrum has the highest energy in sunlight at the earth's surface, explaining the gross location of the visible spectrum in life on earth. The specific frequency range varies across species and can be explained by species-specific survival strategies.

Background
When you look at the solar light spectrum at the earth's surface the visible spectrum has the highest intensity (fig. 1).

Solar irradiation. Source: University of California.

So it makes sense to use the range of frequencies that is represented most in sunlight as a starting point.

Then the question becomes, why do humans utilize approximately 400 to 700 nm, and not infrared or UV? That can be explained because we do not need it. Our range has been hypothesized to be related to foraging behaviors and our visual system is particularly sensitive in the frequency range of the coloring of (ripe) fruits, which is thought to have been of great benefit to our hominid ancestors (Osorio & Vorobyev, 1996).

Why then do animals extend their vision into UV? Many fish, amphibian, reptilian, avian, and some mammalian species use UV vision. Many birds can identify UV-reflected nectar and berries, and UV-reflecting plumages in birds, and scales in fishes are used for recognition (Shi & Yokoyama, 2003). Moreover, some arthropod species are know to use UV vision to reduce light-reflection distortions under water, such as in the mantis shrimp that features 12 photoreceptor types (as opposed to four in humans) (Thoen et al., 2014).

Why then do animals extend their dynamic range into the infrared? A notable beneficial effect of perceiving infrared is the detection of body heat. The generation of heat is accompanied by the generation of infrared light. The detection of this emitted light is highly useful for nocturnal predators, like the rattle snake (Hartline & Newman, 1982).

References
- Hartline & Newman, Sci Am (1982); 246(3): 116-27
- Osorio & Vorobyev, Proc Roc Soc B (1996); 263(1370)
- Shi & Yokoyama, PNAS (2003); 100(142003): 8308-13
- Thoen et al., Science (2014); 343(6169): 411-3

Further Reading
1. Is our color vision calibrated to sky, vegetation, and blood?
2. Is there a physical reason for colors to be located in a very narrow band of the EM spectrum?


Genetically speaking, are dogs exactly similar to humans and chimps both?

Dawkins is overgeneralizing.  Genetic distance is a fairly new field, and a heated topic, since your answer depends upon which genes you are comparing.  If you picked ONLY strongly-conserved genes for your genetic distance comparison, then you'd find that humans, bonobos, dogs, mice, mosquitos, shrimp, and bakers' yeast are all equally distant (and that the distance is small).  But if you pick ONLY very weakly-conserved genes for your genetic distance comparison, you can get crazy results -- humans are more closely related to yeast than to horses, for example.  (Creationists have had a heyday making fun of some early genetic distance studies that, in retrospect, had poorly-chosen genes.)  So biologists doing genetic distance comparisons try to pick genes that are common to many species, and that have some drift to them, but not so much that the answers are obviously goofy.  Another problem that has arisen is that sometimes an entire gene in several species appears to have been obtained from a very dissimilar species, in a different phylum or kingdom even.  (Current theory is that this is the work of viruses.)  The "tree of life" paradigm might need to be changed to the "web of life."  Needless to say, there's still a lot of argument about which (and how many) genes to pick for genetic distance studies.


Who compared developmental biology to crystallography?

The idea to compare biologic cells and crystal is mostly related to a German physiologist Theodor Schwann (1810-1882):

His work "Microscopic researches on the Conformity in Structure and Growth Between Animals and Plants, 1839 relates to this idea.

  He believed that new cells form principally outside pre-existing
  cells, and wanted to draw an analogy to crystal formation.

another source:

  The cell is the unit of structure, physiology, and organization in
  living things. The cell retains a dual existence as a distinct entity
  and a building block in the construction of organisms. Cells form by
  free-cell formation, similar to the formation of crystals (spontaneous
  generation).

(other related scientists are Schleiden, Virchow, Muller).


No, the human brain does not produce nicotine. The brain has nicotinic acetylcholine receptors, but the endogenous agonist for these receptors is acetylcholine, not nicotine; they aren't named "nicotinic" because they are for nicotine but just because nicotine happens to act on them. Many other human receptors are named similarly, based on discovering the molecular basis for sensitivity to exogenous compounds.

The human LD50 for nicotine is reported between 0.5-13 mg/kg depending on age and other factors, but LD50 is only appropriate for evaluating acute toxins; many substances, including nicotine, are most often encountered in small chronic amounts, but concentrated availability of nicotine in insecticides or vape juice can be a plausible source for sufficient doses for acute toxicity. Studies of nicotine toxicity in relationship to smoking are going to be based on much smaller doses over many more administrations.


Why use two stop UGA codons instead of one in the spike protein mRNA for the BioNTech/Pfizer SARS-CoV-2 vaccine?

The two stop codons are obviously to prevent read-through of the termination codon.  Why this should be necessary is not clear to me, but the following may be relevant:

The synthetic mRNA differs from the natural mRNA in a particular respect that is easier to explain with reference to the transcript map of the virus, below.

The two ORFs 1a and 1b are translated directly from the virus RNA as polyproteins, which are subsequently cleaved, but the proteins at the 3′ side of the viral RNA are transcribed into a series of nested mRNAs, each starting from a different 5′ position immediately preceeding the gene that will be translated. These mRNAs also retain RNA corresponding to the remaining genes (coloured grey, and not translated because of the monocistronic translation of eukaryotic mRNA) and the common 3′ polyA tail. The synthetic mRNA for the spike protein (S) lacks the RNA for the non-translated genes, and has the polyA tail near to the stop codon. Hence the secondary structure near the stop codon in the synthetic mRNA may well differ from that in the natural mRNA and possibly influence the likelihood of readthrough.

The stop codons used in this artificial mRNA are not UGA but 1-Me-ΨGA, as U is replaced by 1-Me-Ψ (1-methyl-pseudouridine*) in they synthetic mRNA to prevent degradation. As the anticodon is recognized by a termination factor — not a tRNA anticodon — the interaction with 1-Me-ΨGA may possibly be poorer than for UGA.

Footnote
*The structural relationship between uridine, pseudouridine and 1-methyl-pseudouridine is shown below. The NH and CO involved in base-pairing are similar in each case.
The sequence is generally written with Ψ, rather than 1-Me-Ψ, for compactness.


Looking at the container from the side, it's probably a situation like this:

There might be some clear plastic wrap around the entire thing as well that you would need to cut/break.


The meaning of and standards for "specimen numbers"

In this case, your suspicion of year.month.day.sequential number is correct. The NHM specimen page has an image of the collector's notes:

On line 20, that specimen of Circus assimilis is accessioned, with a note on the right that it is the type for that species.

Generally however, there are no standards for specimen numbers in museums. Many museums that I have studied in have several different numbering or ID systems in use at the same time. Importantly, each specimen is accessioned under the system used at the present time. Sometimes these are later renumbered, sometimes not.

Even in the NHM, there are different schemes in use. Megalosaurus bucklandi, the first described species of dinosaur, is specimen PV OR 2482.

The NHM has 80,000,000 specimens. I'm sure that those doing the cataloging at the start couldn't have imagined the collection would grow to that size, so planning ahead for a single numbering scheme wouldn't even have occurred to them.


You are absolutely right in that there will be immune reaction against proteins that are not naturally present in the body.

However, hemophilia is not caused by complete lack of protein. It is due to loss of function of the clotting factors due to mutations. The proteins are still present, but they do not have the ability to bind and/or activation of their catalytic function. So, there will be no immune activity against exogenous clotting factors given to hemophiliac patients.


Why are peas in mendelian genetics different?

You are confounding the concept of dominance with the one of high frequency. The dominant phenotype might be at lower frequency than the recessive phenotype.

Dominance

  Dominance in genetics is a relationship between alleles of one gene, in which the effect on phenotype of one allele masks the contribution of a second allele at the same locus

Trait frequency

Let's imagine a case where A is dominance and a recessive. Let, $f$ be the frequency of A alleles in the population. The frequency of individuals that have the dominant phenotype is the frequency of AA individuals plus the frequency of Aa individuals. Under Hard-Weinberg assumptions, the frequency of individuals having the dominant phenotype is therefore

$$f^2 + 2 f (1-f)$$

The frequency of individuals having the recessive phenotype is $(1-f)^2$.

If

$$f^2 + 2 f (1-f) < (1-f)^2$$

reorganizing the in-equation yield to

$$f < 1 - \frac{1}{\sqrt{2}}$$

So under the condition that $f < 1 - \frac{1}{\sqrt{2}}$, the dominant phenotype is present at lower frequency than the recessive phenotype.

If the calculations were unclear to you, then you should have a look at the wikipedia article of Hardy-Weinberg principle.


Did human hairs actually evolve from scales?

From a little research I have been able to find some of the hypotheses and speculations but no papers expressly confirming or denying the matter.

One theory displayed in "The evolution of mammalian keratinized structures" (abstract only) is that mammalian hair developed along the following pathway:

Hair follicles develop between reptilian like scales.
A granular layer formed in the pilosebaceous canal (see diagram of modern human skin)
The granular layer extended into the epidermis.  I read this as the point where scales started to more resemble mammalian skin.  It is suggested that this was as a result of a need for increased flexibility and agility.
Hairs began to protrude through the follicles (as seen in rat tails today).  Adaptations to organisms living in cold conditions led to the production of wool to help conserve heat.

So this paper would suggest that hair production evolved separately from but parallel to the movement away from reptilian scales.

"Some Speculations on the Evolution of the Vertebrate Integument" (Paul F. A. Maderson) suggests an entirely different origin of hairs.  He proposes that hairs ultimately evolved from sensory appendages that were involved in the detection of temperature in early synapsids.  The extension of these micro-limbs into hairs was selected towards as a result of their thermally insulating effect by-product rather than for their sensory role, however.


It's the common Prunus padus, which flowers with its strong scent now in many parts of Sweden (including my yard). At least if you are referring to the common species found in the wild (there are planted domesticated varieties as well). It is common across many parts of Europe though, and not only the Nordic countries, and can be found in Asia as well.


How genetically similar are worker ants from the same colony?

Relatedness of ants within a colony vary from species to species (as different species may use different mating systems) and from colony to colony. I will consider a basic (simplified) model of a honeybee colony and describe it a little bit to try to address your question.

Simplified Model of an ant colony

There is quite a lot of diversity in mating systems among ant lineages. See for example the amazing case described in Fournier et al. 2005 (which is quickly summarized at the end of this answer). I will assume a general and simplified model below.

In general, a queen can have several mates. The queen is storing the sperm of these males in her spermatheca. As you noted, the queen is diploid while the males are haploids. The queen will use the stored sperm for all of her life. Each egg that is fertilized will give rise to a worker. Although, a worker does not reproduce (in our simplified model), a worker is still considered a female for morphological reasons. At some point in the life of the colony, some larvea that could have become workers are fed with royal jelly and they will then develop into queen. These queens will fly away to mate with multiple males and make up a new colony. The queen also produce males. The males are haploids. The queen only uses her own gametes to make up a male.

Relatedness

In our simplified colony, a male has no father and has the same mother than any other male and any other worker. Two workers may or may not have the same father. Let's imagine to simplify the story that the queen mated with a single male so that all the workers have the same parents (they are sisters).

queen-worker: 1/2
worker-worker: 1/2

This relatedness decreases with the number of father. At the extreme when there are an infinite number of fathers, the relatedness between two workers drops down to 1/4.

queen-male: 1/2
male-male: 1
male-worker: 1/4

The calculation of relatedness is a little bit problematic when comparing individuals that differ in ploidy (queen - male comparison for example).

Consequences of these relatedness

The fact that the workers are more closely related to their sisters than to their brothers have been suggested to cause a queen-worker conflict for the sex-ratio. Indeed if workers are more closely related to their sisters than to their brothers we might think that they would tend to bias the sex-ratio of the colony toward more sisters to a degree that would not be optimal for the queen. The degree of relatedness between workers depends on the number of fathers. There more fathers there are, the lower is the relatedness among workers and the lower is the incentive to bias the sex-ratio. As a consequence, while the queen would wish a sex-ratio of 0.5, the workers will deviate this sex-ratio toward more workers with a strength that is decreasing with the number of father.

Personally, I have some trouble with these predictions (that I won't express here) but empirical evidences (Chapuisat et al. 1997; Passera et al. 2001) support that the sex-ratio differ depending on the number of fathers (and therefore on the worker - worker relatedness).


Gradual slowing breath, its effect on health

You can try as much to slow down your breathing but the body will speed it up if it requires. What you've probably done is relaxed and just basically meditated. It's not the breathing but the relaxing yourself to slow your breathing and the focus which has refreshed you. I say conduct some experiments, like listen to calming music and relax and don't monitor your breathing and see if you feel the same.

//updating answer

Slowing your breathing builds up the carbon dioxide in your body. This is bad for the body so it forces you to breathe. In fact our breathing is seriously tightly controlled so that our body tightly controls the carbon dioxide (or more correctly the pH) in our blood. There are some groups of patients in which permanent slow breathing exists. In these people their carbon dioxide climbs and the kidneys have to compensate.