Why are bats the source of dangerous coronavirus pandemics?

The preponderance of links between bat and human pathogens has led to a debate about whether bats disproportionately contribute to emerging viral infections crossing the species barrier into humans (26–30). Given the diversity of the Chiroptera order (Figure (Figure1),1), we may simply see more bat viruses because there are so many (>1,300) species of bats (31). However, even when accounting for the fact that they make up ~20% of extant terrestrial mammals, bats are overrepresented as reservoir hosts of pathogens with a high potential for spilling into human populations (32, 33). In fact, no known predictors that have been described to impact the likelihood of crossing the species barrier, including reservoir host ecology, phylogenetic relatedness to humans or frequency of reservoir-human contact, explain this pattern (32). Thus, why bats are such a frequent source of pathogenic human viruses remains a tantalizing mystery.

--Going to Bat(s) for Studies of Disease Tolerance

Other references that debate whether bats are special, generally conclude that they might somehow be, and argue about causes, include

Brook CE, Dobson AP. Bats as ‘special’ reservoirs for emerging zoonotic pathogens. Trends Microbiol. (2015) 23:172–80. This may be the best of the group, going into more detail and including more recent data
Dobson AP. Virology. What links bats to emerging infectious diseases? Science (2005) 310:628–9.
Wang LF, Walker PJ, Poon LL. Mass extinctions, biodiversity and mitochondrial function: are bats ‘special’ as reservoirs for emerging viruses? Curr Opin Virol. (2011) 1:649–57.
Olival K, Epstein JH, Wang LF, Field HE, Daszak P. Are bats exceptional viral reservoirs? In: Aguirre AA, Ostfeld R, Daszak P, editors. editors. New Directions in Conservation Medicine. Oxford, UK: Oxford University Press; (2012). p. 195–212.
Luis AD, Hayman DT, O'Shea TJ, Cryan PM, Gilbert AT, Pulliam JR, et al. . A comparison of bats and rodents as reservoirs of zoonotic viruses: are bats special? Proc Biol Sci. (2013) 280:20122753.


Is it plausible that strict lockdowns made it more likely for the new variant of COVID to have emerged?

While I get your intuition, the hypothesis seems implausible

Emerge of new CoV variants should be considered proportional to the
current spread of the virus. Each virus has a certain mutation rate that surely does not depend on lock-downs.
It seems implausible to interpret
lock-downs as physical limitations to viral spread, that could potentially be
overcome by any mutation.
Even if CoV magically learned to
teleport to different households, such an ability would always represent immense advantages; an advantage that does not need lock-downs to be effective
Lastly, the differential viral competition is neglectable so far; we are at 6 of 100 thousand infected persons. So basically a 0% chance that a virus would infect a person who has acquired an immunity due to a previous CoV infection. In your model this person, who is immune, further would need to NOT be immune because quarantine prevented the (previous) infection.


Definition of nucleotide-associated proteins and RNA-polymerase associated proteins

In short:

Nucleotide-associated proteins are DNA-binding proteins that bind DNA. RNA-polymerase associated proteins bind RNA-polymerases and are required for its functionality.

In more detail:

DNA-binding protein is a higher level term that comprises all proteins that bind to DNA. These can be seen as nucleotide-associated proteins as they interact with the nucleotides in the DNA strand, even though I did not hear people use that term very often. There are two types of binding:

Non-specific DNA-binding proteins that do not bind to specific sequences DNA sequences, e.g. structural proteins.
Specific DNA-binding proteins that bind to specific DNA sequences, e.g. transcription factors. These proteins mostly have specific DNA binding motifs like zinc fingers or helix-turn-helix motifs.

RNA-polymerase (RNAP) associated proteins are different from that. RNAP itself is a DNA-binding protein, but proteins binding to RNAP are necessary for it to be fully functional. The fully functional RNAP then is a holoenzyme. For example RNAP II requires an initiation factor called sigma in bacteria and several general transcription factors and regulatory proteins in eukaryots.


Looks like you may have Monilinia fructigena, brown rot, or at something similar (possibly also called brown rot, but from a different species). This pattern isn't special to quince, but to this fungus.
The formation of these rings is called "zonation", and the concentric rings are from areas of growth that are primarily spore-forming versus not.
Hall (1933) gives an extensive description of the different factors necessary for observing this growth pattern, but ultimately the key factor is light. Patterns of light-and-dark conditions while the fungus spreads causes alternating phases of growth, with one phase comprised of more sporulation.
Another source: https://www.cabi.org/isc/datasheet/34747

Byrde, R. J. W., & Willetts, H. J. (2013). The brown rot fungi of fruit: their biology and control. Elsevier.
Hall, M. P. (1933). An analysis of the factors controlling the growth form of certain fungi, with especial reference to Sclerotinia (Monilia) fructigena. Annals of Botany, 47(187), 543-578.


What is the need for lobules in (human) testicles?

The structure of the testes as with many other organs in living things has all to do with form, function, and efficiency. The testes are extremely efficient sperm producers, with on average 1,500 sperm cells being produced per minute in the average human male. If the testes were just an open space of fluid with free-floating sperm producing germ cells, it would not be as nearly an efficient design, not to mention the waste caused by an inability to sort through sperm producing cells and the cells they produced.

According to this site, each lobule in the testes contains about 1-4 seminiferous tubules, each an average of 50 cm in length. Like many structures in the human body, intestinal walls, nephrons in kidneys, etc, the complex structures and organization of the cells that have a specialized function involves increasing access to the inputs and outputs of their function and increased surface area to increase that function.

This site has a helpful graphic showing the structure of the seminiferous tubules that are wrapped up in each lobule. The germ cells which split and create sperm cells are lined along the wall and when the new sperm cell they produce have developed enough, the sperm cell is released to be moved through the tubule where it can be prepared and developed further. This complex structure allows for uniform, controlled, and efficient production of sperm, essentially, a sperm factory running with an assembly line, and is a design that nature has kept and improved upon for millions of years.


Some physical methods of sterilisation are in hospitals

Steam autoclaving
Dry heat – thermostat
White light / UV light sterilization

where continuous UV light has poor penetration.
UV radiation heat is absorbed by proteins and nucleic acid.
All micro-organisms contain tehm.
They inactivate the DNA.
There will be electronic and photochemical reactions by

photolysis
loss of colony-forming ability
enzyme inactivation
destruction of nucleic acid.

  If I shone a UVC lamp (11W) on something (say for example a plastic
  phone case) for an hour, would that kill off a noticeable amount of
  bacteria?

Direct answer: Not all bacteria, but some.
UV light has poor penetration so it will not expose all bacteria.
Most prevalent bacteria there

streptococci,
staphylococci and
some others.

I estimate that the majority of the bacteria will remain because the light cannot reach each corner of the object.
In clinics, many hours and high temperatures are used to kill bacteria.
UV light is not efficient there.
I think the problem is that you cannot reach each corner of the object.
The high temperature and disinfectants can then again reach the clinical instruments throughly.
Manual work is however still needed.

You can then take examples of bacteria.
Search their corresponding temperature ranges.
The survival can also be dependent on the nature of the light of the bulb.
Each bacteria has an individual structure.
We can manipulate the environment to make bacteria more vulnerable to the heating i.e. to change the structure of the bacteria.
We can increase the duration of the heat exposure to make kill of the bacteria more effective.


Trying to identify an Ontario bird photographed in Spring in the Don Valley

Based on the location, timing and picture, this bird is a female Red-winged Blackbird (Agelaius phoeniceus)

In the spring in Ontario, it would be unlikely to have juveniles around, as breeding has just begun unless this photo was taken near the end of Spring. Male Red-winged Blackbirds would be in their dark black plumage with the yellow/red wing patch. Here is a photo of a pair with the male on the left and female on the right.

You can find more information about them here


Does my nearsightedness come into play when creating light outlines in the distance?

Not likely.  The afterimage you see when you close your eyes is an effect dependent upon which light-receiving cells in the retina (rods and cones) saw light when your eyes were open.  The blurry image you saw when your eyes were open has the same size and shape as the afterimage you see when you see when you close your eyes.  Because the afterimage has less detail, perhaps you would be less distracted by detail and be able to pay more attention to shape, but it seems unlikely that would noticeably help your idea of the shape.


Antisense, promoter replacement and when possible tetracycline allows one to titrate of gene expression
http://www.springerprotocols.com/Abstract/doi/10.1007/978-1-59745-321-9_20#


Have there been any studies on 'surf balls'? (not related to surfing)

These surf or beach balls are made of plant material throughout the structure. They form by wave action along beaches. As the naturalist at Wilderness State Park, the campers and I discovered over 30 of these balls along the beach the summer of 2017.  In previous summers we had found 0. Lake Michigan and Lake Huron were at record levels during the summer of 2017, the highest since 1998. This may explain the formation of these grass balls in abundance. We found some of the balls still in the water, in a depression, just offshore. Others were rolling in and out with the waves. Some had been deposited on the shore and were filled with large quantities of sand. I shook out nearly a cup of sand from one ball. I dissected one surf ball and found predominantly roots and grasses. I will continue to investigate the species of plants that form these curious creations and try to discover the secret to their formation


Can a bacteriophage be used to treat bacterial diseases?

Yes, this is possible and is researched as an alternative to antibiotics. It has been used experimentally before antibiotics became widely available. Research was abandoned when antibiotics became widely available. See for example here and here for reports on this.

Today bacteriophages are researched for the treatment of bacteria which have a lot of resistances against antibiotics like Mycobacterium tuberculosis, Enterococcus faecalis, Staphylococcus aureus, Acinetobacter baumannii and Pseudomonas aeruginosa. See the references for more details (the first article also contains a nice historic overview of the field):

Bacteriophage Therapy
Bacteriophages: an appraisal of their role in the treatment of
bacterial infections
New ways to treat bacterial infections


How do kidney cells excrete their own wastes?

I checked my anatomy notes and online figures about the kidney. There is no mention about dedicated arteries for feeding kidney cells. So it does not work the same way as the heart does, where there is a dedicated coronary artery. The kidneys use the same blood vessels for filtering and for nutrition/waste transport purposes too.

Figure 1 - kidney anatomy - source

Figure 2 - nephron anatomy - source

The urea is created from NH4+ and HCO3- in the liver (mostly) and the kidney because of blood pH regulation purposes. It neutralizes the HCO3- created by the lungs from CO2 and OH-.

  The urea cycle (also known as the Ornithine cycle) is a cycle of
  biochemical reactions occurring in many animals that produces urea
  ((NH2)2CO) from ammonia (NH3). This cycle was the first metabolic
  cycle discovered (Hans Krebs and Kurt Henseleit, 1932), five years
  before the discovery of the TCA cycle. In mammals, the urea cycle
  takes place primarily in the liver, and to a lesser extent in the
  kidney.

  In chemical terms, urea synthesis is an irreversible, energy driven
  neutralization of the strong base HCO3- by the weak acid NH4+, and the
  average daily excretion of 30 g of urea is equivalent to the disposal
  of about 1 mol of HCO3- per day. Thus, a major function of hepatic
  urea synthesis is to effect this neutralization, without which the
  body would otherwise be confronted by a major load of alkali.

  Urea is excreted by the kidney, and is normally present in plasma and
  body fluids at a concentration of 3.0–6.5 mmol/L.

wikipedia - Ornithine cycle
Textbook of Hepatology - Ammonia, urea production and pH regulation - Dieter Häussinger
1984 - The role of ureagenesis in pH homeostasis

The kidney reabsorbs urea in order to concentrate the urine:

Figure 3 - nephron with material transports - urea resorption at the end of the urine creation process - source

  About 40% of the urea filtered is normally found in the final
  urine, since there is more reabsorption than secretion along the
  nephron.

wikipedia - Renal urea handling:
2007 - Critical Role of Urea in the Urine-Concentrating Mechanism

The kidney secretes the urea to the urine, but it absorbs more by the reabsorption than it secreted.

  The kidney freely filters urea at the glomerulus, and then it both
  reabsorbs and secretes it. Because the tubules reabsorb more urea than
  they secrete, the amount of urea excreted in the urine is less than
  the quantity filtered. In the example shown in Figure 36-1A (i.e.,
  average urine flow), the kidneys excrete ∼40% of the filtered urea.
  The primary sites for urea reabsorption are the proximal tubule and
  the medullary collecting duct, whereas the primary sites for secretion
  are the thin limbs of the loop of Henle.

Medical Physiology by Walter F. Boron and Emile L.

So if we are talking about urea, then it is secreted to the urine. If we are talking about other waste products, then e.g. CO2 is certainly handled by the veins.


In the process of photosynthesis light is used as as a source of energy to generate sugar from carbon and water. A by-product is oxygen.

This process can be broken into two cycles: light reaction and Calvin cycle. In the light reaction energy from photons is transformed into usable energy and reducing agents (ATP, NADPH) and water is used as a source of electron, this results in the release of oxygen. In the Calvin cycle this energy coins are used to produce the actual carbohydrates.
There are three known wide-spread mechanisms of photosynthesis: C3, C4 & CAM
One can think of C3 as the "common" system and C4 & CAM as adaptations.
The CAM adaptation is a way to overcome dry, hot climates. The problem is that photosynthesis requires CO2 but opening the stomata allows water to escape. This is not acceptable. CAM plants separate the time of acquisition of CO2 and the actual fixation. They open the stomata at night, allowing oxygen to get out and CO2 to get in but fix the carbon, and thus create the oxygen, during the day.
Although the Calvin cycle is not light dependent it needs substrates created in light conditions so it will not work in the dark under normal conditions.
This article has assimilation curves depending on temperature in different CO2 concentrations. You can use the above equation to estimate grosso modo the amount of oxygen released. They also supply graphs of oxygen change inside a bag following several hours.

Please remember that the amount of oxygen is less important that the concentration, especially compared with CO2


I would link your data with the ENCODE dataset. This dataset provides locations of TFBS. It is also accessible via the UCSC genome browser.

For the actual question TFBS are located pretty much everywhere, including exons (as described here), introns and of course intergenic regions (e.g. enhancers, silencers, control locus regions - here a reference).


Cloning a coding gene into a non-expression vector

In principle, you can amplify any gene with PCR and then clone it into a vector of choice. However, it is often not as easy. Most things can be done with expression vectors, but sometimes it is easier to clone a sequence first and then subclone it.

Some sequences are hard to amplify, especially when they get long or very long. Amplifying 2,5kb can be tricky, digesting and subcloning such a piece might be easier. Additionally yields of PCR can be low, while you get a lot of DNA from a miniprep.

You might want to introduce additional restriction enzyme recognition sites (one can easily be done via PCR, but more again is tricky), linker or additional tags, which are not present in all expression vectors. Then it is easier to simply do a first cloning step into the non-expression vector and then take the complete insert into the expression vector.


What kind of viruses can be found in sperm?

Those are some viruses that can exist in sperm :

Zika : Zika and Sexual Transmission
Ebola : How Long Does the Ebola Virus Survive in Semen?
Hepatitis C : Hepatitis C virus detection in the semen of infected patients
Human papillomavirus infection (HPV) : Correlation between HPV sperm infection and male infertility
Herpes simplex : Detection of herpes simplex virus DNA in semen of men with genital HSV-2 infection
Hepatitis B : Effects of hepatitis B virus on human semen parameters and sperm DNA integrity


Why are children more active than adults?

This is a great question!
As I see you are new and you have explained within the comments above that you haven't studied biology much I will keep the explanation short and sweet.
Young children have fatigue resistant muscles and they also recover faster from high intensity workouts when compared to adults. Children have also been found to use more aerobic respiration when compared to adults during high intensity workouts. This means the child will feel less fatigue and so can continue exercising for longer. As the muscles also recover faster, the child is able to get up and start exercising again much faster than the adult as they will still be recovering.
Aerobic fitness at the muscle level decreases however once the child reaches adulthood and this explains why children have more energy and can play/exercise for much longer. They experience less fatigue and recover faster.
I hope this answers your question.
References:
https://www.frontiersin.org/articles/10.3389/fphys.2018.00387/full


What is the minimum number of chemical elements required for life on earth? Does it vary between kingdoms?

If we change the question to "what is the minimum number of elements common to every form of life?", my lists would be as follows. (I am not considering either viruses or prions to be 'alive').
The following elements are surely common to all forms of life (List 1):

H (1), C (6), N (7), 0 (8), Mg (12), P (15), S (16) [#7].

In addition, the following elements are very likely to be common to all forms of life (List 2):

Na (11), Cl (17), K (19), Ca (20), Fe (26), Cu (29), Zn (30) [#7].

If we broaden things to include elements occurring in any form of life I would add (List 3):

B (5), F (9), Si (14) [!Seemingly], V (23), Cr (24), Mn (25), Co (27), Ni (28), Se (34), Mo (42), Cd (48), Sn (50) [!Maybe], I (53) , W  (74) [#14].

No element in either list has an atomic number greater than 74 (Tungsten). (In the list given by Frieden (1972), the highest is I (53)).

For List One (and as pointed out by @bob1), H (1), C (6), N (7), 0 (8), S (16) are all present in proteins. P (15) is present in ATP and NAD. We must surely also include Mg (12), as the true substrate of almost all ATP-requiring enzymes is a complex of Mg++ and ATP. I can't see that any element can be removed from this list, but it could be argued that we need to add some from List 2.

For List 2, Fe (26) is present as haem in haemoglobin and the cytochromes, and (not necessarily complexed to heme) in other components of the electron transport chain. It might be possible that anaerobic life is possible without iron, in which case Fe (26) needs to be demoted to List 3 (but I doubt it). Zn (30) occurs in many enzymes (including yeast and liver alcohol dehydrogenase). It might be possible for a life form to exist without requiring Zn, but I don't know of any examples.

If we restrict consideration to plants, then Mn (25) needs to be promoted to List 1 (Mn is an essential component of Photosystem II, the enzymic system responsible for the 'splitting' of water in photosynthesis). As life as we know it would be impossible without PS, Mn (25) should possibly be in List 1 without qualification.

List 3 will probably always be contentious, but here are my thoughts:

B (5) is present in boromycin the only naturally-occurring compound containing Boron (as far as I am aware). It has long been considered essential for some plants, but this is contentious. See The importance of boron in biological systems and Boron: the essential element for vascular plants that never was
Edit B (5). @john has pointed out that B is required by some cyanobacteria, and has provided the following reference: Boron Requirement in Cyanobacteria. Its Possible Role in the Early Evolution of Photosynthetic Organisms.
The authors (Bonilla et al.) point out that B is a trace element that "although required in higher plants, has no role in animals or fungi". They suggest that B (possibly as boric acid?) can stabilize membranes by forming cis-diols with glycolipid -OH groups, a role previously suggested to account for B requirement in plants. (References to the original plant research may be found in Bonilla et al.).

This, I think, justifies B being included in List 3: required for some forms of life (but not a minimum requirement for life).

F (9) occurs in fluroacetate (See also The natural production of chlorinated compounds by G W Gribble)

Si (14). A paper in Science in 1972 suggests that Silicon is an essential element for the chick (news to me!). Frieden (quoted below) has this to say: "Possible structural unit of diatoms; recently shown to be essential in chicks. "

V (23). Occurs in haloperoxidases (See Coordination environment changes of the vanadium in vanadium-dependent haloperoxidase enzymes.  The vanadate ion is very similar to phosphate. See The role of vanadium in biology)

Cr (24) Whether Chromium is an essential trace element is controversial. It may play a role in insulin action (see Wikipedia) but this is not universally accepted (the Wikipedia article gives a good summary of the current position). Some bacterial can reduce chromium but this seems to be a detoxification mechanism (See also Chromium: is it essential, pharmacologically relevant, or toxic?). Frieden states "Essential in higher animals; related to action of insulin." but this, it appears, is still controversial. Possibly Cr (24) needs to be deleted from List 3.

Co (27) is a component of Vitamin B12

Nickel (28). Urease, the first enzyme crystallized (by Sumner in 1926), an accomplishment that played an essential role in establishing that enzymes are proteins, was shown in 1984 to contain Nickel (see Urease (Wikipedia))

Se (34) Selenium (as selenocysteine) is directly incorporated on the ribosome into some enzymes (SelenoCys is considered "the twenty-first amino acid")

Mo (42) is a component of quite a number of enzymes, including xanthine oxidase and is often associated with a pteridine cofactor.  See Molybdenum and Molybdenum-Containing Enzymes

Cd (48) A carbonic anhydrase from the marine diatom Thalassiosira weissflogii contains cadmium. It is thought that in oceans depleted of Zn, diatoms can use Cd as a zinc substitute. (See Biochemistry: a cadmium enzyme from a marine diatom and
Structure and metal exchange in the cadmium carbonic anhydrase of marine diatoms)

Sn (50) There have been some reports that Tin is an essential trace element for rats and humans (see Case study: bioavailability of tin and tin compounds and Frieden (quoted below)), but the evidence appears to be very scanty. Tin probably should be deleted from List 3.

I (53). Iodine is known to be a component of the thyroid hormones

W (74) Tungsten The first enzyme to require tungsten, a NADP-linked formate dehydrogenase from Clostridium thermoaceticum was purified and characterized in 1983. Since then a number  of tungstoenzymes (at least ten) have been identified, including acetylene hydratase. In many cases (and in a similar fashion to molybdoenzymes), W is often bound to a pterin cofactor. (See Tungsten in biological systems)

I think The chemical elements of life by E.Frieden, published in Scientific American in 1972, is still relevant, and I have relied heavily on the table on p55 of this publication in compiling the above lists
I haven't considered Sr (38), Nb (41), Ba (56) or Ta (73) but from Tungsten in biological systems  it appears that there is a case for these elements to be included in List 3


Identify this mite from Rajasthan (India)

Hi it definitely looks like a red velvet mite.  They often are called "rain bugs".  They are of a variety of species and sizes and can be quite large - up to 1 or 2 Cm. These links might help.

https://study.com/academy/lesson/red-velvet-mite-facts-life-cycle-diet.html

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

https://www.youtube.com/watch?v=OtHYSIRCZ1c


Why does mud therapy work by some pain related diseases?

The answer on the linked question is apt: transdermal administration of medications or other compounds include exclusively lipophylic compounds, i.e. uncharged 'fatty' materials, such as nicotine, opiate-bases and steroids. Minerals, like those found in clay, are highly hydrophylic and are therefore unlikely to be taken up by the skin.

A search through a bunch of articles makes me believe that mud therapy has mainly a thermal effect, i.e. a mud pack heats the underlying tissue and thereby relieves muscle spasms and pain (Espejo-Antúnez et al., 2012; Liu et al., 2013).

References
- Espejo-Antúnez et al., Rheumatology (2012); 258: 1-10
- Liu et al., J Int med Res (2013); 41(5): 1418–25


What is the source of the fat in adipose tissue?

The proximal source of adipocyte lipids is mainly fatty acids from circulating lipoproteins (1) after hydrolysis by lipoprotein lipase (LPL).

LPL is activated by ApoC-II, which is present in hepatic-originating VLDL and IDL lipoprotein, but also chylomicron of direct dietary source. Insulin, secreted after meals, stimulates LPL production by adipocytes.

Thus the ultimate source of these lipids is both hepatic lipogenesis (from other substrates like glucids) and dietary fats.

Lipid transport in blood, for reference purpose (Michal G. Schomburg D., Biochemical Pathways, 2012)


Can a second mass extinction by microbes happen?

First of all, let’s consider your Methanosarcina scenario in specific.
Methanosarcina with those properties are still around. So, there is no reason to expect that introducing some ancient Methanosarcina into a suitable environment today would do very much – as they should already be there. Any existing (large-scale) environment providing a niche for Methanosarcina should already be occupied by it as it only needs a single organism to get there by chance at some point.
Moreover, there must be some reason why our atmosphere stopped being filled with methane by Methanosarcina.
For example some prerequisite resource could have been depleted, some other organism evolved that consumes this methane or controls the Methanosarcina population by feeding on it.
Whatever this reason is, we should expect that it still applies: A required resource would still be gone and a second organism controlling this activity should still be around (or resurface together with the Methanosarcina in question).
In fact, the hypothesis you mention maintains that the nickel required by Methanosarcina to produce methane was available in huge amounts due to specific volcanic activity at that time.
Finally, the current ice masses of the Earth are much younger and have not been around since the Permian period.
In general, if geologically cryostoring microbes were relevant, climate change should be the least of our worries as drilling a hole into the ice or local geologic activity could suffice to bring back a few individuals – which is all that would be needed.
Now, what about unfreezing microbes in general?
Due to lack of fossils, we have little knowledge about microbe extinction, except that it does happen.
However, my ecological intuition is that microbes either lose their niche to a fitter alternative (which either be more apt at causing problems or avoid them resurfacing) or survive in small amounts (ready to occupy their niche if it should resurface).
Microbes are considerably different from higher, sexually reproducing life forms here as it only needs a single individual to revive the species and individuals can survive for a long time in adverse conditions, not only by sporulation but also because they need little energy to maintain their state.
Finally, if a niche for disastrous microbes exists, there is the constant risk that it will be filled by some ordinary microbes evolving, which brings us to the next point.
Something that is conceivable to happen is that some microbes spontaneously evolve to fill a big niche and have some disastrous by product leading to a mass extinction.
It is hard to estimate this risk, but as far as I know, there is no historic precedent after the evolution of higher life forms.
(As elaborated above, the Methanosarcina hypothesis for the Permian extinction features additional factors.)
However, I consider it unlikely that climate change increases this risk.
While climate change undoubtedly has disastrous ecological consequences, tilting individual ecosystems, I don’t see how it creates some fundamentally new environment (that wasn’t already there in similar form somewhere else on the planet) that would stimulate a spontaneous disastrous microbial evolution.


According to this paper:

  From the Latin word vimentum, used to describe arrays of flexible rods,both ordered ones (e.g.,latices,filigres,and wicker-work) and non-ordered ones (e.g.,brushwood).

Vimentin:

Filigree art:


Are chromosomes from each parent split between gametes with equal probability (esp. in humans)?

Other answers are correct in their own terms, but because of homologous recombination during meiosis, the idea of maternal and paternal chromosomes becomes meaningless. Any chromosome in a gamete will be a mosaic of the maternal and paternal versions. In this sense the chromosome is not the unit of inheritance.


GO is based on experimental evidences; biomart is quite good. GO:0006383 seems to be the right tag.

If you want to use the ChIPseq data then you can do this:

Map the ChIPseq reads to the genome. If you already have the tracks
then you need not do the mapping. You would have the position of the
reads in the genome.
Now count the number of reads mapping to each geneic region. The gene boundaries can be obtained from a GTF file.
Optional: Normalize the reads with the length of the gene.
Find the difference between the number of Pol-II and Pol-III reads for each gene.

By doing this you still won't be able to say that "gene-x is transcribed by pol-III". All you can say is that "pol-III binds to that geneic region". If there is an even distribution of the ChIPseq reads along the gene then you can assume that there is an active transcription and the polymerase is not merely stalled. You can also do a CLIP (Crosslink-Immunoprecipitation) of Pol-III followed by a RNAseq. This will enable you to find RNAs transcribed by pol-III (this is a better way than ChIPseq but I don't think anyone has done it yet; so no ready data).


The number of fat cells, or adipocytes, in adult bodies remains constant. Therefore, consuming more fat only increases the size of the fat cells not the number. After reaching the age of about 20 years the average number of fat cells is closely related to body mass index.

On the other hand, the adipocytes in children increase in number as more fat is consumed. This explains why people who became fat as children have a harder time shifting their weight as adults.

A study on obese adults who went through surgery to decrease the amount of food intake showed a reduction in their body weight by 18%. While the average size of the fat cells decreased, the number of fat cells remained the same.

This doesn't mean that the same fat cells are active throughout your lifetime. Adipocytes normally die off and are replaced by new cells. One study shows that fat obtained from liposuction of people who were exposed to radioactive materials from atomic bombs in the Cold War showed a decrease in radioactive material stored in the cells which indicates replenishment of fat cells over the years.

So when adults intake excess fat, their fat cells increase in size. The average number of their fat cells is correlated with body mass index. However, when children eat excess fats they exhibit an increase in the number of fat cells.

For more information see: http://www.nature.com/news/2008/080505/full/news.2008.800.html


How to grow fibroblast colonies from single cells?

This should be relatively straight forward. Sort the cells into single wells so all descendants are clones of the sorted cell and let them grow until they are dense enough to be transferred into a bigger plate (probably 48 or 24 well). Continue this process until you can go into big cell culture flasks or plates and make sure that you freeze away a number of aliquots as a backup if something goes wrong. Expand the cells further until you have enough cells to do an analysis.

Keratinocytes need some time to get highly proliferative (around a week or so) and if you don't grow them on a layer of feeder cells, usually also need a special conditioned medium. See the references below (if you have trouble accessing the papers, let me know).

What often also helps is the use of conditioned media. I know this from other cells in the skin which often don't like to grow (at least not as primary cells) unless you use conditioned media. For this, take of the media from the same sort of cells (here it would be keratinocytes) before it is completely used (typically yellow if the media contains pH indicators), centrifuge it to remove any cell debris and then mix it with fresh media to let your cells grow. You might need to experiment a bit with the mixing ratio between the "used" and the fresh media, but 50%:50% is usually a good starting point.

References:

Isolation and cultivation of human keratinocytes  from skin or
plucked hair for the generation of  induced pluripotent stem cells
Culture techniques for human keratinocytes
Improvement of human keratinocyte isolation and culture using
thermolysin


There are many questions in your question. I'll try to answer each question pointwise.

  Which flags are used by the enzymes in the process of making the
  centromere to tell them that it is the right spot

There are some centromere associated repeats in the DNA which mark the site for centromere assembly. There is no particular consensus sequence of this repeat. However, this study says that in certain cases stable chromosomes are formed in the absence of centromeric repeats.

  are the sister chromatids physically intertwined around each other for
  the purpose of joining, or are they simply adjacent?

They are joined by proteins called cohesins. Cohesins looks like rings which form around the sister chromatids. During anaphase, the anaphase promoting complex (APC) activates an enzyme called separase, which in turn degrades cohesin.

  what in the centromeres do the spindle fibres attach to, and how do
  the tips of the growing fibres notice it to head it its general
  direction?

Centromeres serve as a site for the assembly of kinetochore. Kinetochore is a multi-protein complex which forms contact with the spindle fibres (specifically, K-fibres. Refer this previous post). An essential component of kinetochore is the motor protein dynein which makes the kitetochore to crawl along the spindle fibres, towards the pole. The wikipedia article on kinetochore is quite descriptive and you can refer that for details.


Is there a database for immunoglobulin domain structure?

There are a number of databases that exist, though the one you would want to use will likely depend on what you need it for. The one that's recommended at my university is IgBlast, associated with The National Center for Biotechnology Information (NCBI), however I've seen IMGT as a recommended source, as well; it seems to have a wider array of tools. That being said, I can't say which you might find more beneficial, as I'm uncertain as to how you'd be using the resource.


How do we predict the lifespan of dinosaurs?

Your first question appears to be answered (tentatively, at least) in the article you linked to...

  "Traditional" estimates based on slow, reptilian growth rates,
  combined with the enormous size of dinosaurs, led scientists to
  conclude it could be up to several hundred years. However,
  palaeontologists today believe that dinosaurs grew much more quickly,
  rather like birds and mammals.

Then...

  Dinosaur bones grew like those of other vertebrates, by adding new
  bone matter to the outside of the bone. Because of annual variation in
  temperature or the availability of food, periodically bone growth
  would slow down, and a thin layer of a vascular bone would form a ring
  or "growth line" in much the same way that tree trunks do. By taking
  thin slices of bones, these rings can be viewed under a polarised
  light source. Counting the rings can give an idea of the dinosaur's
  age at death.

Theoretical ages of some specific species are given in various articles, including Wikipedia and LiveScience.

The infamous T. rex theoretically reached adulthood at the age of twenty (similar to humans) and reached an age of at least twenty-eight years. I think most contemporary animal species mature much more quickly than that...but few approach T. rex in size. The hypothetical ages given for some of the smaller dinosaurs appear to be more in line with modern living species.


How does DNA damage cause ageing in yeast?

In eukaryotic cells there is no difference between a mother and a daughter cell - the later is an exact copy of the mother cell. This is true for yeasts as well for example for human cells. The only thing that happens over time is that the telomeres at the end of the chromosomes get shorter (unless the cell has an active telomerase which most cells doesn't) and it reaches the Hayflick limit where every further division will lead to a shortage of coding chromosmal regions and thus cause problems. If cells do not acquire any other chromosomal damage and have enough ressources, this would be the limit for their lifetime.

Of course there are DNA damages occuring over time. Most of them are either repaired by the highly efficient DNA damage repair system of eukaryotic cells, which consists of different checkpoints during the cell cycle. These checkpoints are located at transition between the different  phases of the cell cycle. If a DNA damage is identified, the cell cycle is stopped to enable a DNA damage repair by special proteins and to prevent that damaged cells undergo mitosis (here the G2-M checkpoint is important). This works schematically like in this figure (from the Wikipedia article on DNA repair):

If the DNA damage cannot be resolved, cells will either go into senescence (basically go into a permanent dormant state) or undergo apoptosis. If there are damages which are (for whatever reasons) are either not spotted or occur during the repair of DNA double strand breaks by non-homologous end joining, these are then replicated and inherited by further generations. Unless these errors occur during the replication process mother and daughter cells are genetically identical.

So eukaryotic cells acquire DNA damage over time (one of the reasons why late pregnancies pose a greater risk than early), but we are different from yeast in one point: Yeast has an active telomerase, which is not active in most of our cells (mainly except in stem cells). If the cells collect too much chromosmal damages than they will die.

The references listed below go deeper into the topic and are interesting to read.

References:

Negative regulation of yeast telomerase activity through an
interaction with an upstream region of the DNA primer
Cell cycle control in the kidney.
The evolution of diverse biological responses to DNA damage:
insights from yeast and p53
DNA damage and decisions: CtIP coordinates DNA repair and cell cycle
checkpoints
Cellular Responses to DNA Damage: One Signal, Multiple Choices


Judging by this image in wikipedia, I would say Theae folium is another name (probably a name in another language) for Camellia sinensis


Why does low sequence diversity cause sequencing problems

I think the problem is more that the software has a hard time identifying individual clusters if way more than a quarter of them are lighting up for a given base.  If you have more diversity in the first few cycles, when the cluster coordinates are being identified, I think this is less of a problem.


Do animals exhibit handedness (paw-ness?) preference?

Short Answer
Yes. handedness (or Behavioral Lateralization) has been documented in numerous vertebrates (mammals, reptiles and birds) as well as invertebrates.

This includes domestic cats (see Wells & Millsopp 2009).

 Long Answer
There have been numerous studies that have documented behavioral lateralization in many groups of animals including lower vertebrates (fish and amphibians), reptiles (even snakes!), birds and mammals. More recent work (e.g., Frasnelli 2013) has also shown that lateralization can also occur in invertebrates. In other words, "handedness" (or pawedness, footedness, eyedness, earedness, nostriledness,
toothedness, breastedness, gonadedness, etc.) occurs rather extensively across the animal kingdom.

These studies suggest that the evolution of brain lateralization, often linked to lateralized behaviors, may have occurred early in evolutionary history and may not have been the result of multiple independent evolutionary events as once thought.

Although this view of brain lateralization as a highly conserved trait throughout evolutionary history has gained popularity, it's still contested (reviewed by Bisazza et al. 1998; Vallortigara et al. 1999).

Note: Laterality of function may manifest in terms of preference (frequency) or performance (proficiency), with the former being far more often investigated.
And no, right-handedness is not always dominant.
But Why?

One hypothesis is that brain lateralization was the evolutionary result of the need to break up complex tasks and perform them with highly specialized neuronal units to avoid functional overlap (i.e., to account for "functional incompatibility").

In humans, many hypotheses have been developed including: division of labor, genetics, epigenetic factors, prenatal hormone exposure, prenatal vestibular asymmetry, and even ultrasound exposure in the womb.

Snake studies (see below) have suggested lateralization behavior can be dictated by environmental conditions (specifically, temperature).

Other work (Hoso et al. 2007) suggest that lateralization could be the result of convergent evolution. In this case, snakes developed feeding aparati that allow them to better consume more-common dextral species of snails.

Note: dextral (meaning "clockwise") is a type of chirality -- another form of "handedness"

Reviews:

Lateralization in non-human primates: McGrew & Marchant 1997.

Lateralized behaviors in mammals and birds:
Bradshaw & Rogers 1993; Rogers & Andrew 2002.

Lateralized behaviors in lower vertebrates: Bisazza et al. 1998; Vallortigara et al. 1999.

Some Examples:
Invertebrates

Some spiders appear to favor certain appendages for prey handling and protection (Ades & Novaes Ramires 2002).

Octopi (or octopodes) preferably use one eye over the other (Byrne et al. 2002; with seemingly no preference for right/left at the population level: Byrne et al. 2004) and also apparently have a preferred arm (Byrne et al. 2006).

Fish

Preferential ventral fin use in the gourami (Trichogaster trichopterus). [Bisazza et al. 2001].

Preferential eye use in a variety of fish species [Sovrano et al. 1999, 2001].

Amphibians

Lateralization of neural control for vocalization in frogs (Rana pipiens). [Bauer 1993].

Preferential use of hindlimbs (Robins et al. 1998), forelimbs (Bisazza et al. 1996) and eyes (Vallortigara et al. 1998) in adult anurans.

Snakes

Preferential use of right hemipenis over left under warm conditions. [Shine et al. 2000].

Coiling asymmetries were found at both the individual and population levels. [Roth 2003].

Birds

Tendency for parrots to use left-feet when feeding. [Friedmann & Davis 1938].

Mammals

Pawdness in mice. [Collins 1975].

left forelimb bias in a species of bat when using hands for climbing/grasping. [Zucca et al. 2010]

Behavior experiments show domesticated cats show strong preference to consistently use either left or right paw and that the lateralized behavior was strongly sex related (in their population: ♂ = left / ♀ = right). [Wells & Millsopp 2009].

Non-human Primates

Posture, reaching preference, tool use, gathering food, carrying, and many other tasks. See McGrew & Marchant (1997) for review.

Citations

Ades, C., and Novaes Ramires, E. (2002). Asymmetry of leg use during prey handling in the spider Scytodes globula (Scytodidae). Journal of Insect Behavior 15: 563–570.

Bauer, R. H. (1993). Lateralization of neural control for vocalization by the frog (Rana pipiens). Psychobiology, 21, 243–248.

Bisazza, A., Cantalupo, C., Robins, A., Rogers, L. J. & Vallortigara, G. (1996). Right-pawedness in toads. Nature, 379, 408.

Bisazza, A., Rogers, L. J. & Vallortigara, G. (1998). The origins of cerebral asymmetry: a review of evidence of behavioural and brain lateralization in fishes, reptiles and amphibians. Neuroscience and Biobehavioral Reviews, 22, 411–426.

Bisazza, A., Lippolis, G. & Vallortigara, G. (2001). Lateralization of ventral fins use during object exploration in the blue gourami (Trichogaster trichopterus). Physiology & Behavior, 72, 575–578.

Bradshaw, J. L. & Rogers, L. J. (1993). The Evolution of Lateral Asymmetries, Language, Tool Use and Intellect. San Diego: Academic Press.

Byrne, R.A., Kuba, M. and Griebel, U. (2002). Lateral asymmetry of eye use in Octopus vulgaris. Animal Behaviour, 64(3):461-468.

Byrne, R.A., Kuba, M.J. and Meisel, D.V. (2004). Lateralized eye use in Octopus vulgaris shows antisymmetrical distribution. Animal Behaviour, 68(5):1107-1114.

Byrne, R.A., Kuba, M.J., Meisel, D.V., Griebel, U. and Mather, J.A. (2006). Does Octopus vulgaris have preferred arms?. Journal of Comparative Psychology 120(3):198.

Collins RL (1975) When left-handed mice live in righthanded worlds. Science 187:181–184.

Friedmann, H., & Davis, M. (1938). " Left-Handedness" in Parrots. The Auk, 55(3), 478-480.

Hoso, M., Asami, T., & Hori, M. (2007). Right-handed snakes: convergent evolution of asymmetry for functional specialization. Biology Letters, 3(2), 169-173.

McGrew, W. C., & Marchant, L. F. (1997). On the other hand: current issues in and meta‐analysis of the behavioral laterality of hand function in nonhuman primates. American Journal of Physical Anthropology, 104(S25), 201-232.

Robins, A., Lippolis, G., Bisazza, A., Vallortigara, G. & Rogers, L. J. (1998). Lateralized agonistic responses and hindlimb use in toads. Animal Behaviour, 56, 875–881.

Rogers, L. J. & Andrew, R. J. (Eds) (2002). Comparative Vertebrate Lateralization. Cambridge: Cambridge University Press.

Roth, E. D. (2003). ‘Handedness’ in snakes? Lateralization of coiling behaviour in a cottonmouth, Agkistrodon piscivorus leucostoma, population. Animal behaviour, 66(2), 337-341.

Shine, R., Olsson, M. M., LeMaster, M. P., Moore, I. T., & Mason, R. T. (2000). Are snakes right-handed? Asymmetry in hemipenis size and usage in gartersnakes (Thamnophis sirtalis). Behavioral Ecology, 11(4), 411-415.

Sovrano, V. A., Rainoldi, C., Bisazza, A. & Vallortigara, G. (1999). Roots of brain specializations: preferential left-eye use during mirror-image inspection in six species of teleost fish. Behavioural Brain Research, 106, 175–180.

Sovrano, V. A., Bisazza, A. & Vallortigara, G. (2001). Lateralization of response to social stimuli in fishes: a comparison between different methods and species. Physiology & Behavior, 74, 237– 244.

Vallortigara, G., Rogers, L. J., Bisazza, A., Lippolis, G. & Robins, A. (1998). Complementary right and left hemifield use for predatory and agonistic behaviour in toads. NeuroReport, 9, 3341–3344.

Vallortigara, G., Rogers, L. J. & Bisazza, A. (1999). Possible evolutionary origins of cognitive brain lateralization. Brain Research Reviews, 30, 164–175.

Wells, D. L., & Millsopp, S. (2009). Lateralized behaviour in the domestic cat, Felis silvestris catus. Animal Behaviour, 78(2), 537-541.

Zucca, P., Palladini, A., Baciadonna, L. and Scaravelli, D. (2010). Handedness in the echolocating Schreiber's long-fingered bat (Miniopterus schreibersii). Behavioural processes, 84(3): 693-695.


Relation between respiration and concentration of citric acid

This image is a bit misleading since both ways seem to be the reversion of each other, but in fact they are not (although the same metabolites are used).

Reaction A takes only place in gluconeogenesis which makes glucose from other metabolites (coming from the metabolism of fatty acids for example) and this pathway is only active when there is an abundance of energy present in the cell. Citrate activates the Fructose-1,6-bisphosphatase. The gluconeogenesis takes only place in liver and kidney.

Reaction B takes place in glycolysis and is the rate limiting for the whole pathway. It takes place when glucose is taken up and then used for the production of energy. The Phosphofructokinase (PFK) is inhibited by signals of excess energy as ATP (which is an allosteric inhibitor of PFK) as well as citrate and NADH/H+. While citrate is a weak allosteric inhibitor on its own, it acts as a strong inhibitor together with ATP. This makes sense since both molecules are indicators of free energy metabolites in the cell.
See these two publications for details:

"Allosteric regulatory properties of muscle phosphofructokinase."
Effect of citrate on the activities of 6-phosphofructokinase from
nervous and muscle tissues from different animals and its
relationships to the regulation of glycolysis.

If there is an excess of AMP/ADP then the enzyme is activated and phosphorylates Fructose-1-phosphate.


Hemithea maybe, is as close as I can figure, although since there is so much variation between them it is very hard to tell.


Identifying a shrub with unusual "many shoots" growth behavior

Possibly an example of a "Witch's Broom."

Witch's Broom is a deformity in plants (typically woody species) which typically causes dense patches of stems/shoots to grow from a single point on the plant. The name comes from the broom-like appearance of the stems.1

Witch's broom may be caused by many different types of organisms, including fungi, oomycetes, insects, mistletoe, dwarf mistletoes, mites, nematodes, phytoplasmas, or viruses.2

Sources:
1. Wikipedia
2. Book of the British Countryside. Pub. London : Drive Publications, (1973). p. 519
 Image1. Gardeningknowhow.com
Image2. Iowa state University


What causes paresthesia from compression?

Seems like it results from a loss of blood flow as the Vasa Nervorum is compressed. Vessels, like arteries or tubules within the kidney, are compressible since they have a vacuous lumen, while an axon is cellular and resists compression. I was thrown off a bit by an answer by a Bryan Krause to this question here, Neurons during Numb feeling, "the feeling of paresthesia is not from loss of blood flow", but, seems like that person was wrong.


Is there any small animal that can jump over a meter high/long?

no animal smaller than 5 cm can jump higher than 1 meter. grasshoppers and locusts have wings which supposedly disqualifies them. https://www.guinnessworldrecords.com/world-records/highest-jump-by-an-insect.
The immense mechanical power that would be required for any animal to jump so high with such a small size is unbelievably high which is why they have developed different evolutionary adaptations. not to mention that the terminal velocity of such a small creature is very low so a jump would quickly become a fall due to the air molecules slowing them down. https://www.youtube.com/watch?v=f7KSfjv4Oq0


Here's the issues with your well considered project:

1/ Temporal datasets to proportion trees: That's probably the most absent thing in species measurement. You'd need data sets of time for beetle species, for mammals, plants in millenia and million years. 90+% of that information is absent.

2/ Genetic proximity to arrange trees. Scientists publish their genome studies into the ToL project. There is lots of distance data to compare all animals.... Genetic distance doesn't graph easily because on the same tree, some distances can be 500 times longer than others. On a tree of 20 extant species, you will have branches 5mm long and 5 meters long, half the the species are on your screen and the other half are higher than the ceiling. It's best to represent them with another symbol, else interactive 3D trees where you can switch compact/large views and the tree zooms out crazily, it's illustrative and cool, else use a weighted proximity length which is 1+ similarity/50, that doesn't really work either. either way, I couldnt find a way of clearly displaying that info on the tree.

Phylogeny trees don't lend themselves well to being informatively measured. You start by thinking "Oh I could find a pretty way of doing that" then when you apply the datasets, your trees become uncontrollable and jumbled up because of exponential branch lengths.

I programmed phylogenetic trees based on the 81MB ToL tree of life project to represent many millions of species, to do 3D physics trees and HTTP lookups to provide wiki texts and images for all species. There is www.biostars.org a very kind and helpful bioinformatics forum for postgrads that do trees all day.

There are many (dozens) of informative tree graphics programs coded by academics, to visualizw and analyzw species data, arranged into different trees and sorting through them.


Yes, it is. Dolly died of cancer in early years. Length of the telomeres depends on the donor tissue: "In Dolly's study, the animal produced from fetal tissue appeared to have telomere lengths non-distinguishable from normal controls, while the other two, including Dolly, which originated from adult cells, were found to have shorter telomeres." (Xu & Yang, 2003) This statement doesn't mean that embryonic cells are the only cells able to maintain telomere length.

This also doesn't mean, that offspring of animals cloned from nuclei with shorter telomeres, inherits this shortedness: Miyashita et al, 2011

The Xu & Yang, 2003 review is pretty old, you can find newer articles on the topic.


Are there any examples of information compression in nature?

Preliminary Remarks

Many of the posts to this list about biological information (usually equated to DNA) from mathematical and informatics scientists start from what I regard as false premises, especially that the genome is similar to that man-made artefact, the computer. This post does not explicitly make that assumption, but I think it important to address the difference between computer systems and biological systems before considering possible examples of what is requested.

Do biological systems need to compress information?

Although one can argue that not all biological information resides in DNA (or RNA, in the case of organisms with an RNA genome) I suspect the poster was thinking of that, and that is what I shall restrict myself to — i.e. to genetic information. (Other answers may quite validly address other types of information.)

The point, at least historically, of compressing digital information on computers is space limitation. Lossless compression involves re-coding the information in a more compact form. For example, instructions in the PostScript language can substitute ‘d’ for draw, ‘s’ for stroke. Gif or tiff image compression can substitute 20x(256,0,0) for repeating (256,0,0) — a red pixel — twenty times. Such compressed information must generally be decompressed when it is used (e.g. when the gif file is displayed in a web browser).

I find it difficult to think of any compression/decompression of this type in biological systems, and I would point out that genome ‘space’ is generally (but see below) not a limiting consideration in biological systems. One example of this is the fact that many organisms (especially plants) are polyploid — that is they have multiple (apparently unnecessary) copies of the complete genome. Another example is that the genomes of mammals contain at least some DNA that can be regarded as unnecessary. Although there are arguments about ‘junk’ DNA having a function, it is difficult to argue that processed pseudogenes and SINES and LINES are necessary. However genome ‘space’ has not eliminated them.

Where space or size is a problem, there Nature often uses other solutions than compression. For example the genomes of RNA viruses are thought to be restricted in size because of the occurrence of slow non-enzymic alkaline hydrolysis of RNA. Influenza virus, for example, has a genome consisting of several shorter (less vulnerable) RNA segments, which may be considered as a solution to this problem.

However, here are a couple of possible examples, although not with the sort of compression used in computers.

Possible example 1: Antibody Genes

To put it in simple terms, the genome has the potential for expressing millions of different antibodies, but the immune system requires that antibody-producing cells only produce one type. Instead of having millions of antibody-producing genes, only one of which is expressed, there is a much smaller number of segments of the genes, from which each of the two antibody chains are combined in a process called recombination. This is illustrated below for the heavy-chain genes where combination of one of 250 V-regions with one  of 20 D-regions with one of 4 J-regions, giving 20,000 possibilities. The resulting heavy chain can combine with one of 1000 different light chains, giving twenty million possibilities. (The diagram and data are old, but the principle holds. See, e.g. the Wikipedia entry.)

Of course, there is an alternative, and converse, way of thinking about this. Rather than the existence of 500–600 genes being a way to compress 20 million, one can regard the existence of 500–600 being a wasteful way to encode only protein.

Possible Example 2: Alternative splicing of pre-mRNA

This is similar in principle to the first example, although the mechanism is different. Most of the protein-coding genes of higher eukaryotes are built up of two components — exons, which encode sections of the protein product — separated by introns, which do not. Both these components are present in the initial RNA transcript, but the introns are removed from this (spliced out) to produce the mature mRNA, which is translated into protein. An advantage of this arrangement is that there are alternative ways for the splicing to occur, involving removing some of the exons (as well as the introns). This can lead to different protein products, in some cases just two, in others dozens.

So one could regard this similarly as a compression mechanism — or alternatively as an example of wasted space in the genome occupied by the introns.

Possible Example 3: Read-through and frame shift proteins

Certain mature mRNAs have the potential to encode more than one codon by the processes of read-through or frame shift. In brief, a protein of 100 amino acids will have a mRNA with a stop-codon 300 nucleotides after the signal for the start of translation. However in a few cases (and most notably with small bacterial RNA viruses) the structure of the mRNA near the stop codon is such that in a certain percentage of cases a tRNA will misread the stop-codon, resulting in continued translation, producing a longer protein of different function.

Similarly, certain mRNAs have a structure at a certain point that encourages the tRNAs to continue reading in the wrong phase (missing a base or starting a base too early — I forget) so that the continuation of the protein has a completely different amino acid sequence.

There is an old review of this topic in Current Opinion in Cell Biology.

Although this is technically a way of compressing two proteins into one, its rarity makes it difficult to regard its biological rationale as being compression.

&c.

No doubt there are more examples. I had toyed with considering Wobble as a way of saving space for tRNA genes, but have probably written enough.


Why don't myopic people see the world upside-down?

You have misinterpreted the nature of the light rays shown in the diagram in the question.  The two rays are representing light coming from the same (distant) point in the environment, that is, some small feature on an object is reflecting (or emitting) light in slightly different directions and reach the eye separated by a small amount (less than the width of the pupil).  The rays are almost, but not quite, parallel.  The two rays, coming from the same point, should be focused on the same point on the retina (as are the red rays corrected by the external lens).  The spread of the uncorrected rays in myopia or hyperopia sends them to different places of the retina, causing the image to be out of focus, not upside down.

The path of light from an entire scene can be illustrated like this:

As this diagram shows, the image is upside down for all of us, in focus or not.  That the image top is at the bottom of the retina is not especially important -- the cells doing the interpretation could have been located physically located anywhere as needed.


A quick diagram to point out to people who may not know what Eustachian tubes are (#2).

In order for the aromatic molecule to reach the olfactory bulb, it would first have to get through the Tympanic Membrane (#22) [a.k.a. - Eardrum]. The Tympanic Membrane is water/airtight unless pierced.

So, while it's plausible that an aromatic molecule could travel through the Eustachian tubes and enter the pharynx areas, there isn't any way to get into the middle-ear in the first place unless the Tympanic Membrane has been compromised.

In a healthy and intact individual, the answer should be No.


Are there any intersections between the biochemical pathways of uracil biosynthesis (or metabolism) and methionine degradation in eukaryotes?

No, I don't think there are any intersections, and I can't see how uracil metabolism would have any influence upon methionine degradation.

Methionine degradation is shown in Figure 1 below. The end product is succinyl CoA which is fed into the TCA cycle. The only obvious by-product is cysteine which doesn't have any connection with uracil biosynthesis.

Uracil biosynthesis (as UMP) is shown in Figure 2: it is built from CO2 and NH3. Uracil degradation produces CO2 NH3 and aspartate.

There are certainly no shared intermediates in these pathways, and I can't come up with any convincing indirect connections either.

Figure 1. Methionine degradation

Figure 2. Uracil biosynthesis


This appears to be a "Monkey slug" caterpillar (Phobetron spp) of the family Limacodidae (or slug moths).

According to these sites (here and here), caterpillars of this type are commonly referred to in Portuguese as "Lagarta-Aranha" (or "lesma-macaco") [literally, "spider caterpillar" and "monkey slug" in English].

The most common Phobetron species I can find in Brazil is Phobetron hipparchia.

The caterpillar of this species appears to be quite variable (ranging from browns to reds in color) as is made apparent by here, here, and here

 Phobetron hipparchia  (Source: http://caterpillars.unr.edu/)


Is there a biophysical causation from local field potential (LFP) to spikes?

I am not sure that kind of action would be a "significant influence", but the general understanding is that LFP and spike frequency are inter-correlated (1, 2). An interesting recent publication on the topic (3), however, doubts this correlation as the nature of LFP recording and signal processing might introduce some artifacts to the recordings.

It would be interesting to see a correlation between the spike shapes and LFP, but I failed to find a relevant paper here.

References:

 Belitski A, Gretton A, Magri C, Murayama Y, Montemurro MA, Logothetis NK, Panzeri S. 2008. Low-frequency local field potentials and spikes in primary visual cortex convey independent visual information. The Journal of neuroscience : the official journal of the Society for Neuroscience 28: 5696–709.
 Rasch MJ, Gretton A, Murayama Y, Maass W, Logothetis NK. 2008. Inferring spike trains from local field potentials. Journal of neurophysiology 99: 1461–76.
 Zanos TP, Mineault PJ, Pack CC. 2011. Removal of spurious correlations between spikes and local field potentials. Journal of neurophysiology 105: 474–86.


ID large-thorned plant growing in Turkey

This is a palm (family Arecaceae). Many palms have spines; I'm no expert but it looks to me like it is a member of the Phoenix genus, perhaps a Cretan date palm (Phoenix theophrasti). Date palms do propagate themselves by seed (the pit of the date fruit). The palm in your picture, if a date palm, would be rather young, which could explain why it does not presently show flowers or fruits. Here is a photo of the spines and flowers of a Cretan date palm (by Wouter Hagens, from Wikimedia Commons):


What slope do I need to prove a hypothesis?

You will get a much more complete answer on a statistics forum, or by simply consulting some basic tutorials on linear regression.

But a little intuition should tell you that setting a cutoff on the value of the slope does not make sense. For instance, suppose you measured heart rate in beats per second instead of beats per minute. All the y-values would be 60x lower, your slope would be 60x lower, but intuitively, nothing should change about your interpretation.

When you calculate your linear regression, you'll be able to obtain a correlation coefficient and a p-value, which tell you how well your data fits the line and the probability of obtaining such a result if there was no relationship between the data. These will be based not on the slope, but rather on how well your data fit the line and the number of points you have (the more data you have, the more confident you can be of the effect).

But you will never prove your hypothesis. The best you'll be able to say is "if my hypothesis were false, the probability of obtaining the result I got is less than X%". The clearer your data, the smaller X will be.

You would also do well to consider sources of systemic bias, not just statistical power. For instance, could the music affect the accuracy of the measurement? Do you always gradually increase the tempo of the music, or do you randomize the order? Just some examples off the top of my head, I'm sure you can think of others more relevant to your setup.


What is the smallest visual unit perceptible to the human eye, like a pixel? (esp. in visual static)

The human eye has two types of sensors that become stimulated when wavelengths of visible light (photons) hit the pigments in these sensors. They are known as 'rods' and 'cones'. Rods detect the brightness of light, cones detect the color. There are three different cones in the human eye: red, green and blue. Each cone reacts to the corresponding waves of light. When they are stimulated due to their corresponding wavelengths, they send a signal that travels through the optic nerve to the visual cortex at the occipital lobe.
individual cones don't have different levels of stimulation and always send the same frequency, it's the lack of the stimulation of other cone types that causes certain colors to appear.
in short:

signal or photon of the appropriate wavelength I suppose.
rods for brightness, cones for color.
probably not since the cones are microscopic and tightly packed, too close and too small to see what each cone is literally receiving. The moving static you're seeing is called phosphenes and is comprised of the inherent electrical charges the retina produces both during resting state and with the eyes open. they're just easier to notice when your eyes are closed. Try covering your eyes and you may get static just like when you close your eyes.

The electrical charges get sent to the visual cortex. that's where your brain processes the image. Here's an diagram of how the rods and cones send their electrical signals to the optic nerve (the optic nerve is the [4] label).

Here's a diagram of how those signals travel to the visual cortex:


Limitations of the Self-Incompatibility Mechanism in Plants

Herrera, Sara et al. 2018 suggest that there are at least 33 S-alleles in apricot.

I believe some species of Brassica have at least 60 S-alleles identified.

However, there are dominance relationships among these alleles, so I don't think you can directly extrapolate from the number alleles to to the rate at which non-self pollen will be excluded.  The frequencies of the different alleles within a population will clearly also affect this calculation.

In addition, different individuals with the same S-alleles are more likely to be closely related, so I would hesitate to classify this as a limitation of the system.

Ref: Herrera, Sara et al. “Identification of Self-Incompatibility Alleles by Specific PCR Analysis and S-RNase Sequencing in Apricot.” International journal of molecular sciences vol. 19,11 3612. 15 Nov. 2018, doi:10.3390/ijms19113612


Since I apparently don't have enough reputation to comment, I'll post this as an answer and let someone move it.

Firstly, try to ensure that the order of the arguments are correct. You should be typing bowtie2 -f -x $TARGET -U $TARGET -S $TARGET.sam, since bowtie2 (as with many other programs) can be a bit picky about the argument order.

Secondly, it's usually advisable for the example input to include lines that are causing the problem (since it's apparently not complaining about the lines you posted, we can only assume that it's aligning them).

Thirdly, you'll typically only get those warnings if they're true. For example, if you were to grep -A 1 -w GACACTGTTCATGCTGGTGTCGCTGTCGGGCATTAT $target then my guess is that you'd find it to have no remaining sequence. Presumably these are the result of you trimming adapters or something like that, so just have your trimmer discard really short results (they won't align meaningfully anyway).


Chickens roosting, is it sleep or torpor?

When birds sleep, they do experience NREM sleep [1]. Furthermore, Kavanau (2002) concluded that NREM has evolved in warm blooded animals [2].

  Birds provide a unique opportunity to evaluate current theories for the function of sleep. Like mammalian sleep, avian sleep is composed of two states, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep that apparently evolved independently in mammals and birds. Despite this resemblance, however, it has been unclear whether avian SWS shows a compensatory response to sleep loss (i.e., homeostatic regulation), a fundamental aspect of mammalian sleep potentially linked to the function of SWS. Here, we prevented pigeons (Columba livia) from taking their normal naps during the last 8 h of the day. Although time spent in SWS did not change significantly following short-term sleep deprivation, electroencephalogram (EEG) slow-wave activity (SWA; i.e., 0.78-2.34 Hz power density) during SWS increased significantly during the first 3 h of the recovery night when compared with the undisturbed night, and progressively declined thereafter in a manner comparable to that observed in similarly sleep-deprived mammals. SWA was also elevated during REM sleep on the recovery night, a response that might reflect increased SWS pressure and the concomitant 'spill-over' of SWS-related EEG activity into short episodes of REM sleep. As in rodents, power density during SWS also increased in higher frequencies (9-25 Hz) in response to short-term sleep deprivation. Finally, time spent in REM sleep increased following sleep deprivation. The mammalian-like increase in EEG spectral power density across both low and high frequencies, and the increase in time spent in REM sleep following sleep deprivation suggest that some aspects of avian and mammalian sleep are regulated in a similar manner [3].

From the Abstract and reference [3] above, we see that EEGs have been taking on birds and show that birds enter REM and SWS similarly to mammals.

In response to Chris Stronks, researchers have also studied chickens see Evolution of Sleep: Phylogenetic and Functional Perspective by Patrick McNamara, Robert A. Barton, Charles L. Nunn. In the section for REM sleep in birds, the studies were conducted on pigeons and chickens see pages 204-205.


I assume, you mean by "producing DNA" Neanderthals had larger brains than us. Basically, this is possible and generally, brain size correlates with body size. What you may ask here is: Can our brain size to body size ratio increase? Probably yes... I can't think of a reason, why not?

But please please be aware of that intelligence, does not have to correlate with brain size. e.g. elephants and humans. There may be some limits of the smallest possible brain size for certain mental tasks and skills. But wiring and plasticity is probably more important than the bulk size.


Can erythrocytes Function without plasma?

Erythrocytes need more than just glucose in order to function and, they also need a extracelullar medium who shares the same osmolarity, so placing your red blood cells into a medium that solely has glucose will be problematic. If you solely want to evaluate the lactic fermentation carried out by erythrocytes on a short period of time, then you can add the blood plasm on your centrifuge tube (which will be in the superior layer) to the newly separated erythrocyte fraction. This way, we make sure your extracelullar medium not only has every metabolite needed, but is also isotonic with respect to your erythrocytes. If you're planning on evaluating this pathway for a considerable amount of time (days, perhaps), then you, most likely, will have to prepare a solution with glucose that is isotonic with respect to your red blood cells.


The main reason is because the genetic differences between individuals of the same species are tiny. For the vast majority of studies, they can simply be ignored.

Differences between individuals are usually (not always, but mostly) differences in SNP genotypes. These are single nucleotide differences which, while they can have phenotypic effect, don't really affect the ability of sequences to align. Sequence alignment software is designed to be able to deal with such small differences. For example, consider these two random sequences:

>seq1
ACCTTGCATCGGATCGAATTCGCGTTAGCGATCG
>seq2
GCCTAGCATCGGACCGAATTCCCGTTAGCAATCG

If we align them, we will get:

seq1            ACCTTGCATCGGATCGAATTCGCGTTAGCGATCG
seq2            GCCTAGCATCGGACCGAATTCCCGTTAGCAATCG
                 *** ******** ******* ******* ****

As you can see, despite the small differences in sequence, the two can be aligned very well. The same is true when you look at real data. My haemoglobin gene, for example, will align perfectly well against both yours and the one in the reference genome. In fact, they will almost certainly be identical or, at best, have a couple of different residues.

So, when doing work that is not about studying specific polymorphisms, we need a representative genome. Anyone's will do, unless they have a particularly serious mutation such as a chromosomal translocation.


Is the missing "life-ingredient" in today's Earth's existence the reason why we cannot recreate life?

Three important concepts about abiogenesis
Let's start with three important concepts
Definition of life
You'll need to give a good definition of life, because biologists actually don't have one (it is a matter of philosophy to define life, not biology).
Time it took for life to emerge
Life as we know it emerged only after a huge period of time (hundreds of millions of years), which we obviously cannot reproduce in a lab.
Current competition
Even if some kind of protolife would appear at some point, it would still have to face the competition with its veteran partners. Hypothetical protocells would be eaten by some microbe with no doubt.
Panspermia
The idea of panspermia (the hypothesis that the life may have appeard in outer space or in another planets, and then "contaminate" the Earth) has been on the scene in many forms for quite a long time. Regularly we hear of some study which proposes that life, or at least some key biomolecule, may have formed in asteroids, comets, in Mars or somewhere else. They're quite interesting, mainly because they suggest more than one way that life may have appeared.
Molybdenum
While molybdenum is rare in the Earth, it still exists and so the study doesn't deny the posibility that life may have formed in the Earth. Nowadays, molybdenum is used by many organisms as part of the core of some key enzymes, such as nitrogenase (the enzyme complex that catalyzes the conversion of molecular nitrogen into nitrate). Molybdenum has very interesting catalytic qualities and may have been a key factor for the origin of life.
Phosphorus on Mars
However, those studies say that Mars has higher concentration of phosphorus, which is one of the main components of life, and that was pretty rare in the early Earth. The hypothesis is interesting but, without experimental data, it is only that. The authors suggest that nowadays those phenomena may happen in Mars, so the hypothesis may be confirmed in a few years as the exploration of the Red Planet continues.


Would a vial of anticoagulated, warm blood attract mosquitoes?

According to wikipedia they locate "prey" by detecting CO2 and some other compounds, so I don't think mosquitoes will actually find the blood unless they're accidentally right on top of it.

And for your reason: if you have the equipment to regularly draw some blood, keep it at 37 C and have some anticoagulants on hand, you might be better off using some tried and true anti-mosquito tech (nets, insecticides, preventing them to breed in the local area).

Or maybe this: https://en.wikipedia.org/wiki/Mosquito_laser


When does meiosis occur in flowering plants?

In case of male gametophyte (in angiosperms), meiosis ends before the formation of the pollen tetrads which in turn marks the end of cell division in anthers and petals (Li and Johnston, 1999). However, the same study reveals that the relative timing of pollen tetrad formation with respect to floral development (abbreviated as RAFT), varies between different plants. Despite the variation, they seem to form three clusters with mean RAFT at 0.45, 0.62 and 0.73.

In case of the female gametophyte, the megasporogenesis happens inside the ovule (Yadegari and Drews, 2004). Therefore, ovule should have formed before the onset of meiosis. I could not find a detailed study on the timing of the megasporogenesis.


I have never performed an AMOVA myself and I don't know what a genind object is. But ...

Error

Typically, "error" can also be called "residuals". In other words, it is the sum of squared deviation between the data and the regression line (just like in any regression model). You might want to learn a little bit about regression and ANOVA to understand your AMOVA.

Fst definition

From Nei 1973 (very good paper, I recommend reading it),

$$F_{ST} = \frac{H_S-H_T}{H_T}$$

, where $H_S$ is the average subpopulation variance in allele frequency and $H_T$ is the total variance in allele frequency.

What you probably got from the AMOVA output

You should have these info in your AMOVA output. If it only give you the total variance and the between group variance (which is what is used for the F-test), then just remember that the among variance is the total variance minus the between group variance.


Proteins in water vs proteins in crystal

Protein crystals are not like crystals of more commonly found substances like salt [NaCl] or diamond [carbon only.]  These materials do not include other atoms in their crystal structures.  For instance, a crystal of NaCl will contain sodium ions and chloride ions.  X-ray crystallography of that material will, after mathematical processing, show electron density peaks of two varieties, each easily distinguished by intensity as either a sodium ion or chloride ion.  Any other electron density peaks will be few and far between, as well as clearly identifiable as an interloper.

Because most proteins have hydrophilic regions on the exterior surface of the structure, crystals of proteins actually contain a considerable fraction of water molecules within the crystal itself.  These water molecules are part of the crystal because they are interacting with those hydrophilic residues on the tertiary surface of the protein, both by hydrogen bonding, in some cases, and less specific polar interactions in other cases.   This is at least one of the reasons why obtaining a crystal of any random protein is not at all a routine endeavor.  The large proportion of water in these crystals make them very fragile once they do form, as well as not necessarily likely to form in the first place.

If you go into the technical literature to look at the electron density maps that the more commonly diagrammed structure maps are derived from, you'll be able to actually trace water molecules surrounding the individual protein molecules.

In fact, in the days of development of protein crystallography, assigning correct specific atoms to the various electron density peaks was a decidedly non-trivial task.

Effectively, despite being a crystal, the microenvironment experienced by the protein within the crystal is very much like that in an aqueous environment.  The hydrophobic interactions & hydrophilic interactions will not be very different from those in solution.

That is, the crystalline state achieved is not, in fact, "a complete change of surrounding environment" to use the phrase that you've used in your post.


Is bacillus strain 2-9-3 really 250 million year old?

Disclaimer

I was unaware of 2-9-3, but performed a simple internet search which brought up a an open-access paper from 2001 refuting the claim, and nothing more recent, suggesting that the refutation was valid. I mention this both to make it clear that although, like the poster, I am not an expert in the topic one can get considerable mileage through standard search techniques. (I do acknowledge that it does help if you know you can get access to papers through a University Library, open-access or not.)

Refutation

The claim was actually made nearly two decades ago in a paper by Vreeland et al. in Nature 407, 897-900. The date is relevant because at that time full-length sequences of bacterial genomes were only just appearing.

The paper refuting the claim is entitled “The Permium Bacterium that Isn’t” by D.Graur and T.Pupko and was published in the journal, Molecular Biology and Evolution 18 1143–46 (2001).

The authors put forward various indirect arguments for doubting the claim but they based their refutation on sequence comparison between so-called Bacillus permeans (2-9-3) and other bacteria. The first argument was that the 99% similarity of B. permeans to a contemporary halophilic bacterium, previously known as Bacillus marismortui, subsequently renamed Salibacillus marismortui, implied a relatively recent divergence from the latter. To rebut the argument that S. marismortui had also been trapped in salt for millions of years until recently a comprehensive comparison with other bacteria was conducted resulting in the phylogenetic tree shown below which was incompatible with the bacterium having not evolved in the last 250 MYr:

An independent analysis by Nickle et al. in Journal of Molecular Evolution 54, 134 (2002) came to a similar conclusion.

I am not expert enough to judge the methods of determining rates of evolution and relative distances between species, but it would appear that they are accepted by those in the field.


Oh my. Do the authors provide any support for this claim? More importantly: what is their affiliation with creationist organizations? Well, back to science.

First, a note about your question. It might seem that you have sketched out two scenarios, but for the biologist, they are equivalent. We know two things: life exists, and life adapts. Yes, the specific circumstances on Earth have made life possible, and subsequently, life has adapted and fine-tuned itself to those circumstances.

Now to answer your question.
I really like the visual representation of the Life Timeline on Wikipedia. 4.1 billion years ago, earliest life appeared on Earth. At that time, all oxygen on the Earth's surface was bound in chemicals like CO2, iron oxide, etc. We are unsure whether the earliest life-forms originiated in the ocean, but we know they ended up there one time or another. The absence of athmosphetic and water-dissolved oxygen of course meant those first life-forms were anaerobes (lived without oxygen). In fact, oxygen was extremely poisonous for our teragrandparents. (We are the ~ 10^12th generation of life.)

So, aquatic life has existed without oxygen, and still exists, whether the solvabily of oxygen is 'perfect' or not.

Another fun fact debunking your chemistry authors statement: water oxygen saturation doesn't reach 100% at all times (linked article provides lots of great information about dissolved oxygen and life, by the way). Lots of life-forms requiring oxygen hence live in a world where the solvability of oxygen is even more than perfect. Furthermore, life exists (but doesn't thrive) in low-oxygen conditions (e.g. pubmed:9510533).


Actually No.

Amazingly there is this paper published on the motions on Ants which says:

  The isotropic distribution of average speed appears as a surprising
  result since it would be expected, for instance, that ants progressing
  uphill should be slower than when moving downhill. For instance, Seidl
  et al. found lower speeds on steeper inclines in desert ants moving
  uphill, but indicate that desert ants progressing downhill displayed
  high velocities [42]. This is in contrast with our finding with Lasius
  niger in the present set-up where the velocity showed no dependency to
  the walking direction, even for the steepest inclination. However,
  Wohlgemuth et al. report, also in the desert ant, that speed was
  reduced in both their uphill and downhill channels (+540 ) compared to
  their flat channel, thereby excluding metabolic cost as a reliable
  means to gauge walked distance on various inclines [28]. In an attempt
  to determine the effects of inclination on the gross metabolic cost of
  locomotion in leaf-cutter ants, Holt & Askew report that ants
  travelled the fastest on a horizontal plane, and indeed moderated
  their speed with the inclination, both on the incline and the decline.
  They suggest that ants adapt their behavior so as to keep their
  metabolic rate constant despite changing mechanical demands.

Source: How Do Ants Make Sense of Gravity? A Boltzmann Walker Analysis of Lasius niger Trajectories on Various Inclines


Why cooking make foods , e.g rice, vegetable etc, soft?

Short answer Hydrolysis

Cooking shortens many molecules, particularly carbohydrates and proteins although almost anything long is affected. By heating them in a aqueous environment (many foods supply their own water) we are inducing billions of hydrolysis reactions. This chops up long polymers into shorter ones.For proteins heat also causes them to unwind which makes them easier to digest.  In effect we are outsourcing a major portion of the digestion. This is why cooking is believed to have evolved as a behavior in the first place – it greatly increases the nutrient availability of the food by putting it in a much more easily digested state. Without heat the number of hydrolysis reactions is negligible, although a few things like extreme PH or infusion of enzymes can be substituted for heat.

For most edible molecules shortening them also makes them softer (most macronutrients are polymers, after all) which is an additional benefit. This is also why there is a balance in cooking, cook too long or at too high a temprature and you start to get lots of other kinds of reactions that produce new indigestible molecules. Cook too short or too low a temp and you get few hydrolysis reactions and it essentially does nothing. Hydrolysis is one of the reasons cooking will also dry out foods, since water is being used up in hydrolysis.


From Wikipedia (emphasis mine):

  Mucins are a family of high molecular weight, heavily glycosylatedproteins (glycoconjugates) produced by epithelial tissues in most animals. Mucins' key characteristic is their ability to form gels; therefore they are a key component in most gel-like secretions, serving functions from lubrication to cell signalling to forming chemical barriers.

The "ability to form gel" is the key here. Also from Wikipedia:

  Gels are defined as a substantially dilute cross-linked system, which exhibits no flow when in the steady-state. By weight, gels are mostly liquid, yet they behave like solids due to a three-dimensional cross-linked network within the liquid.

So, a gel (and mucins are no exception) is composed of a liquid trapped in a 3D net, much like a sponge. This is the "mucin net" your book is referring to.


Due to its coloration, shape and tarsal formula (5-5-4) I think that a Meloidae(Blister beetle) of the Pyrota genus is likely. You can see several examples of species in this genus from a basic google search. Meloidae has about 2500 species world-wide though, and there might be similar species in other genera. Here is an example of Pyrota bilineata, just for comparison.

(picture from http://bugguide.net/node/view/918423/bgpage)

You probably need somebody more knowledgeable on Indian beetles for a proper species determination though, but hopefully my suggestions can serve as a starting point.


Do beavers' tails hurt from being dragged?

No, it does not, otherwise beavers wouldn't walk with their tails dragging. Here is a picture of the bottom of a beaver's tail:

Found here
and here is a closeup (probably of the top, but they're very similar):

Royalty-free stock photo from Dreamstime
As you can see, the skin looks almost like reptilian scales. It is likely highly-keratinized and is quite thick, as you can see below. Innervation is probably net very close to the surface, like callouses we develop on our hands and feet, so it doesn't hurt to be dragged over sharp surfaces like rocks or thorns. Here is a cross-section of the thick part of the tail close to the body:

Source: Cannundrum blog


Why don't most animals have "heads" in the middle of their bodies?

We generally define a "head" as something that comes at the top/front of the body. I think that, we're likely to ignore examples of animals with nervous systems / sensory systems not at the top/front of their body as "animals without heads" rather than "animals whose heads are not at the top/front". For example, sponges and jellyfish.
Some animals who do, arguably, have heads, have their heads in the center of their bodies:

Image by james_michael_hill (CC BY-NC-ND 2.0)

The evolutionary - developmental roots of head position (or having a "head" at all) go very deep (although despite this, some organisms, like the starfish above, shifted evolutionarily and shift developmentally from bilateral to radial symmetry).


The meaning of the $\alpha$ helix and $\beta$ sheets in proteins

The answer is very simple. As described in the accepted answer to the related question about alpha-subunits vs alpha-helices the alpha- and beta- are arbitrary names. It could easily have been 1 and 2 or A and B based on ordering of letters or numbers; indeed, there are "type I" and "type II" turns.
The history, from the wikipedia page on alpha-helices says:

In the early 1930s, ... William Astbury initially proposed a kinked-chain structure for the fibers. He later joined other researchers (notably the American chemist Maurice Huggins) in proposing that:

The unstretched protein molecules formed a helix (which he called the α-form)
The stretching caused the helix to uncoil, forming an extended state (which he called the β-form).

(Emphasis added). In other words, he named the "α-form" first, and considered the "β-form" to be an uncoiled form of the first one. These names later became "α-helix" and "β-sheet". It could easily have been the other way around.
Indeed there are other types of helix; the 310 helix and the π-helix. If either of these had been discovered first, perhaps they would be the alpha-helix. Of them all, the 310 helix has the most 'logical' name as:

the helix has three residues per turn, and ... has 10 atoms in the ring formed by making the hydrogen bond

so if we followed a similar naming scheme, the alpha helix would be a 3.613 helix. Admittedly this is a bit of a cumbersome name.
As well there are the alpha sheet - a sheet made of helical strands - and the beta helix - a helix made of strands. For both of these, the "alpha" and "beta" part of the name has been chosen because of the naming of the original structures they are related to.


Is oxygen's paramagnetism biologically relevant?

It sounds a bit like chem exam question to be honest... Or at least the answer does... namely that O2 being paramagnetic creates a "spin barrier" that prevents most organic compounds from reacting fast with atmospheric oxygen:

  The magnetic properties of O2 are not just a laboratory curiosity; they are absolutely crucial to the existence of life. Because Earth’s atmosphere contains 20% oxygen, all organic compounds, including those that compose our body tissues, should react rapidly with air to form H2O, CO2, and N2 in an exothermic reaction. Fortunately for us, however, this reaction is very, very slow. The reason for the unexpected stability of organic compounds in an oxygen atmosphere is that virtually all organic compounds, as well as H2O, CO2, and N2, have only paired electrons, whereas oxygen has two unpaired electrons. Thus the reaction of O2 with organic compounds to give H2O, CO2, and N2 would require that at least one of the electrons on O2 change its spin during the reaction. This would require a large input of energy, an obstacle that chemists call a spin barrier.

(quote from McQuarrie and Simon's (free) textbook Physical Chemistry: A Molecular Approach).


What is the name if this glittery fly seen in Pittsburgh?

Looks like a green bottle fly.

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

Might be a Common Green bottle fly.

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


Name of scientist who discovered lifesaving drug and chose not to patent it?

Dr Jonas Salk or Dr Albert Sabin who did not patent their respective polio vaccines. There are some more such researchers so I am not sure who exactly you are looking for but this would be a start.


T-Cell Motility: does motility require direction specific actin polymerization?

It's understood at least that leukocyte motility is dependent on cytoskeleton remodeling and actin dynamics. In the blood, as the T cells tumble past the activated endothelium of an affected site, they're grabbed by selectins and integrins expressed on the endothelial surface. These are often illustrated as the adhesion and rolling phases of T cell migration.

Chemokines, which normally form a gradient for T cell chemotaxis, induce changes in the cellular morphology that promote migration into the surround tissues. The cells polarize into a force-generating lamellopodium with a leading edge in the front, and a uropod in the back. It appears as though actin polymerizes in the lamellopodium and juts the cell out toward the direction of the signal, and the uropod contracts in a myosin-dependent manner, releasing molecules bound there, thereby allowing the cell to tug in the direction of the lamellopodia (1, 2).

The mechanism has in fact been characterized by leading-edge redistribution of chemokine receptors such as CCR5 and CXCR4, which may have to do with actin/myosin dynamics and lipid rafts. This makes the receptor distribution asymmetric as well, and so a weaker response to the chemoattractant in the back end of the cell. The best way I could describe it is using the formation of the cSMAC in T cell receptor biology (Figure 1) (3). The SMAC is basically a synapse formed during T cell activation where receptors are concentrated to a particular area where the T cell is meeting the APC.

Figure 1. TCR-mediated cytoskeletal remodeling

The way the authors describe it is the downstream signals from the TCR localize actin pathway molecules to the site of signaling, and causes cytoskeletal remodeling at that particular site.

Studies in neutrophils have shown that polarization leads to a frontness and backness to the cell, regulated by different proteins and inhibit the formation of one another. This is a good paper to read through on that matter, though it's a tougher read in my opinion: https://www.researchgate.net/publication/8957894_Cytoskeletal_remodeling_in_leukocyte_function