what these suffixes mean,-coel,-blast,-cyst?

You can easily search this on the web.

Osteoblasts are the immature cells of bone which are responsible for the production and mineralization of bone matrix.

Osteocytes are the mature cells of bone found in open spaces in bone called lacunae. The functions of osteocytes includes maintenance of bone and  calcium homeostasis.

Osteoclasts are responsible for removal of bone.

Source : Tortora and Derrickson


Is this aquatic plant duckweed or something else?

That looks very much like a duckweed.

The multiple roots rule out most genera within this group and so this is probably a Spirodela.

The apparently relatively large size and red undersides are consistent with this being Spirodela polyrhiza.

Picture by Christian Fischer available under Creative Commons Attribution-Share Alike 3.0 Unported.


Do there exist enzymes that can take up multiple cofactors to do different reactions?

It sounds like you are asking about what are commonly referred to as "multifunctional enzymes".

For a reasonably recent article covering this subject — see:
Cheng, X. Y., Huang, W. J., Hu, S. C., Zhang, H. L., Wang, H., Zhang, J. X., ... & Ji, Z. L. (2012). A global characterization and identification of multifunctional enzymes. PloS one, 7(6), e38979.

A specific example of such an enzyme is the fatty-acyl-CoA synthase from yeast — this enzyme catalyzes multiple reaction steps that use both NADP and Coenzyme A and also uses a third cofactor, FMN.

  The enzyme from yeasts (Ascomycota and Basidiomycota) is a multi-functional protein complex composed of two subunits. One subunit catalyses the reactions EC 1.1.1.100, 3-oxoacyl-[acyl-carrier-protein] reductase and EC 2.3.1.41, 3-oxoacyl-[acyl-carrier-protein] synthase, while the other subunit catalyses the reactions of EC 2.3.1.38, [acyl-carrier-protein] S-acetyltransferase, EC 2.3.1.39, [acyl-carrier-protein] S-malonyltransferase, EC 4.2.1.59, 3-hydroxypalmitoyl-[acyl-carrier-protein] dehydratase, EC 1.3.1.10, enoyl-[acyl-carrier-protein] reductase (NADPH, Si-specific) and EC 1.1.1.279, (R)-3-hydroxyacid ester dehydrogenase. The enzyme differs from the animal enzyme (EC 2.3.1.85) in that the enoyl reductase domain requires FMN as a cofactor, and the ultimate product is an acyl-CoA (usually palmitoyl-CoA) instead of a free fatty acid.

Source: https://www.ebi.ac.uk/intenz/query?cmd=SearchEC&ec=2.3.1.86


Initially I didn't like this question very much, but I changed my mind when I realized that there is actually ongoing research to do exactly what you propose in order to study just how long it takes to get maize from teosinte.
John Doebley at the University of Wisconsin-Madison has a project ongoing to breed 30 generations of teosinte to be more "corn-like" on a single parameter, the length of the lateral branches.
The first challenge is to find a strain that isn't already contaminated by modern maize - that isn't completely possible, but he selected a strain that has minimal hybridization. You would have to do the same.
Second, you have to plant someplace isolated to further prevent hybridization. Dr. Doebley has a plot in Hawaii for this purpose.
Note that even though this scientist is only selecting over 30 generations, he doesn't anticipate that much of a change (i.e., he doesn't expect to have anything like corn when he is finished), and he is only selecting on a single parameter and furthermore, this parameter was chosen specifically for being easy to score, showing a lot of variation in the existing population, and influenced by a known single gene. Many more generations would be expected to get a product like modern corn. And even domesticated corn has changed significantly over thousands of years of agriculture.
For this answer, I simply reference the project site that I linked above, but in case that link goes dead, here is some literature that the project cited directly:

Beadle, G. W., 1977  The origin of Zea mays, pp. 615-635 in Origins of Agriculture, edited by C. E. Reed. Mouton, The Hague.
Beadle, G. W., 1978  Teosinte and the origin of maize, pp. 113-128 in Maize Breeding and Genetics, edited by D. B. Walden. John Wiley & Sons, New York, NY.
Doebley, J., A. Stec and C. Gustus, 1995  teosinte branched1 and the origin of maize: evidence for epistasis and the evolution of dominance. Genetics 141: 333-346.
Doebley, J., A. Stec and L. Hubbard, 1997  The evolution of apical dominance in maize. Nature 386: 485-488.
Doebley, J. F., A. Stec, J. Wendel and M. Edwards, 1990  Genetic and morphological analysis of a maize-teosinte F2 population: implications for the origin of maize. Proc. Natl. Acad. Sci. 87: 9888-9892.
Iltis, H., 1987  Maize evolution and agricultural origins, pp. 195-213 in Grass systematics and evolution, edited by T. Soderstrom, K. Hilu, C. Campbell, and M. Barkworth. Smithsonian Inst. Press, Washington, D. C.
Wang, R.-L., A. Stec, J. Hey, L. Lukens and J. Doebley, 1999  The limits of selection during maize domestication. Nature 398: 236-239.
Wilkes, H. G., 1967  Teosinte: the closest relative of maize. The Bussey Institute, Harvard University, Cambridge.
Wilkes, H. G., 1977  Hybridization of maize and teosinte in Mexico and Guatemala and the improvement of maize. Econ. Bot. 31: 254-293.


Is it possible to label a DNA molecule using a radioactive sulphur?

Yes, it is possible, and indeed this was the standard labelling procedure used in early Sanger sequencing.

You synthesise DNA using a deoxynucleotide with a sulphur replacing an oxygen on the α phosphate as shown below. This phosphate forms the phosphodiester link in nucleic acids so the sulphur is incorporated.

The image is of dATPαS

response to David's comments

Please note that:

DNA does not normally contain sulphur.
This technique is for in vitro labelling of DNA; as far as I am aware it isn't possible to label with sulphur in vivo.


Introducing novel genes to an adult multicellular organism?

Short answer, in theory yes, in reality, at the current state of the art, no.

I guess you are speaking about higher organisms (such as mice or humans), if you are referring to small non-complex multicellular organisms then the answer is yes as far as you can transfect every cells with the system described hereafter.

The most promising technique is using the CRISPR/Cas9 system which has already been used to create all types of modified organisms but starting from the embryo. Here a good Nature reference http://www.nature.com/nbt/journal/v32/n4/full/nbt.2842.html.

There are no ways, at the moment, to transfect an entire organism with the full system. The most recent attempts I heard off is to target specific cells using an encapsulation techniques that only merges with the membrane of specific cells therefore delivering the CRISPR/Cas9 system in a targeted manner. This was in an attempt to knock-out a defined genomic regions in those specific cells, not to introduce a new gene.

I believe in the near future that this will be possible. Not necessarily every cells of an organism but at least some specific cell types.


Can the body of any organism on Earth live without impairment both in vacuum, and within Earth's atmosphere?

Remarkably, Tardigrades are multi-cellular animals which can survive the vacuum of space.


Why does underwinding create topological strain of DNA?

The double helical structure of DNA with ~10.5 bp/turn is thermodynamically favorable. Any perturbation from this results in strain. Thus, if DNA is under wound, it is favourable for it to adopt a negative supercoil to return to ~10.5 bp/turn.

That said, negative supercoiling and DNA melting are in fact in some kind of equilibrium. This is important for processes such as transcription and replication which require ssDNA.


Do RNA modification proteins bind to specific repeats on the RNA polymerase II CTD?

In attempting to answer questions about protein structure, the first port of call (which one might expect the questioner to have also visited) is the Protein Data Bank — the global repository of such structures. There one can search for RNA Polymerase II CTD, look for complexes with other proteins, find recent publications in which they are reported, and consult them to find the state of knowledge of a topic.
Knowing nothing of the protein in question, I adopted this approach, and after looking at a few proteins and a few papers the following points seemed to emerge.

The CTD has a series of 7-amino acid (heptad) repeats — in mammals 21 of these are consensus(YSPTSPS), and 31 non-consensus (K7, rather than S7).
Further heterogeneity is afforded by phosphorylation (especially) and also glycosylation and proline isomerization, together with modification of the lysine of the non-consensus repeats.
It is thought that different post-transcriptional modifications are responsible for differential activation of 5′-capping or 3′-processing enzyme activities.
The CTD is disordered (unresolved) in the crystal structure of RNA Polymerase II, indicating that in the protein itself it does not adopt a fixed structure.
There are no structures of the CTD complexed to proteins it activates, so the question cannot be answered definitively.
There are structures of proteins complexed to short peptides (10- to 19-mers) based on the repeating sequence. These suggest that the structure of CTD in the complexes may be a spiral bound by specific interactions in a groove. The spiral formation may involve hydrogen-bonded β-turn motifs. A deduced structure from one such study with a 10mer is shown, together with indications of specific protein–protein interactions.

(Phosphorylated 10mer based on CTD complexed to the conserved CTD-interacting domain of mRNA processing factors RPRD1 and 2 — Adapted from Ni et al., Nature Structural and Molecular Biology (2014) 21, 686–695)
Concluding Remarks
The question contains two invalid assumptions — that proteins that interact with the CTD should interact with a single repeat, and that repeat should have a compact structure. Nevertheless, the functionality of the repeats and whether there are multiple interactions are valid questions. It appears from discussion in the paper by Ni et al. that the interacting unit is a 24-mer that binds to a dimer of the interacting protein (CID), and they propose that for phosphatases (and I presume protein kinases)15 molecules interact with the CTD at once.
What the situation is with 5′-capping or 3′-processing enzymes is another matter. There will only be one mRNA emerging from the RNA polymerase, so multiple binding would appear to make no sense. How much of the CTD is needed as rope to attach the processing enzyme soap? Does the soap slide along the rope? One would hope that eventually such questions would be answerable by molecular visualization techniques (see e.g. this BioRxiv preprint).


Why is iodine used for metabolic hormones?

Classical thyroid hormones implement a very flexible signaling mechanism. Basically, they comprise two aromatic rings that are connected via an oxygen atom. Optionally, they may contain organic side chains and inorganic iodine atoms.

In the case of iodothyronines, which are represented e.g. by the well-known thyroid hormones T4, T3 and 3,5-T2, the side chain contains an amino group and a carboxylate group. Therefore, iodothyronines are amino acids. Up to four different hydrogen atoms (two at every ring) may be replaced by iodine atoms, and the resulting pattern of iodination determines their biological activity. Generally, iodination of the inner ring and deiodination of the outer ring results in high biological activity (e.g. in T3 and 3,5-T2), whereas iodination of the outer ring and deiodination of the inner ring delivers a receptor-blocking thyroid hormone (e.g. reverse-T3). There are three deiodinases encoded by the DIO1, DIO2 and DIO3 genes that catalyze the "step-up" and "step-down" reactions to active or inactive thyroid hormones, respectively. Multiple molecular processes are able to differentially upregulate and downregulate tissue deiodinases. Therefore, thyroid hormones are subject to both global and local control.

Removal of the amino group results in iodothyroacetates. Their biological effects are similar to those of iodothyronines, but in addition to nuclear receptors they also have a strong effect on membrane-bound receptors, which are only weakly activated by iodothyronines.

Thyronamines lack the carboxylate group. Their biological effect is different to that of iodothyronines and iodothyroacetates. By activating the membrane-bound TAAR1 receptor they have an effect that is in most respects antagonistic to that of classical thyroid hormones. Thyronamines seem to be most active in deiodinated state.

Summarizing, both organic and anorganic modifications are able to modulate the effect of thyroid hormones. This mechanism is a very effective way to encode a high  grade of information entropy in rather small molecules.

References

Gereben B, Zavacki AM, Ribich S, Kim BW, Huang SA, Simonides WS, Zeöld A, Bianco AC. Cellular and molecular basis of deiodinase-regulated thyroid hormone signaling. Endocr Rev. 2008 Dec;29(7):898-938. doi: 10.1210/er.2008-0019. PMID: 18815314

Engler D, Burger AG. The deiodination of the iodothyronines and of their derivatives in man. Endocr Rev. 1984 Spring;5(2):151-84. PMID 6376077.

Piehl S, Hoefig CS, Scanlan TS, Köhrle J. Thyronamines--past, present, and future. Endocr Rev. 2011 Feb;32(1):64-80. doi: 10.1210/er.2009-0040. PMID 20880963.


We know archea and eukarya are more closely related but endosymbiotic theory says eukarya have evolved from prokaryotes, justify the statements?

Actually endosymbiotic theory (we should write "Endosymbiotic theory of origin of eukaryotic organelles") suggests a theory about only the eukaryotic organelles (mainly Plastid-family and Mitochondrion).

I'll divide my answer into 3 parts:

# Theory of archaeal origin of the eukaryotic host.
* 1. How Archaea (Archaebacteria) and Eukaryotes shared a closest common ancestor
# Endosymbiotic theory of origin of Eukaryotic cell organelle.
* 2. How mitochondria originated?
* 3. How plastid was originated?

Please keep in mind, in origin and evolution of eukaryotes, origin of the host cell (and the nuclear genome) is a different event; and origin of eukaryotic organelles mitochondria and plastid is another different event.

Theory of archaeal origin of eukaryotic host

1. How Archaebacteria (archaea) and precursor of eukaryotes evolved from their nearest common ancestor.

It has been established (First by Carl Woese, mainly based on her prolonged researches on  rRNA sequences) (PDF) (REFERENCE-1 *) that Eukaryotic "host cell" (with the nuclear genome) shares the closest common ancestor with Archaebacteria, not the eubacteria.

Further reading: Relationships of Eukaryotes and archaea

Fig-1: Here the horizontal axis is the time axis.
(The small black balls here indicating many other possible extinct lineages (hypothetical, just todemonstrate how evolution works) )

On other hand, After the group bacteria (eubacteria) developed (better to say the precursor of bacteria further diversified, bacterial groups like proteobacteria and cyanobacteria developed. For bacterial phylogeny, see Wikipedia (image)

Endosymbiotic theory:

Now endosymbiotic theory tells that the origin of some eukaryotic organelles (at least Mitochondria and Plastid) were different and distant taxa from the eukaryotic cessls, and they came from outside and entered into the cell and formed symbiotic relation; and the endosymbionts gradually lost their free-living ability, were gradually became part of host cell. The peculiarity of this "Endosymbiosis" phenomenomenon in evolution is that; not only the "parent" taxa; but another "distant taxa" merge from side of the lineage. The concept is not only confusing but it was so shocking that when H. Margulis first proposed this hypothesis, the idea was rejected. Later on, genome-based research proven that the origin of mitochondria (and as we will see, plastids); were originated from mutualistic- symbiosis.

2. How mitochondria evolved in eukaryotes?

It has been suggested, the "precursor" of eukaryotes (which was descendant of closest-common ancestor with archaebacteria), the host cell, engulfed some aerobic eubacteria (perhaps allied to proteobacteria) those aerobic eubacteria gave rise to mitochondria. These derived protists were unable to photosynthesise. This endosymbiosis is very much similar to previous one.

Fig 2a: origin of the organelle mitochondria.

So our evolutionary tree now look like

Fig 2b: Origin of mitochondria in eukaryotes, placed in evolutionary tree.
The white balls here represent living and contemporary groups.
(Just like previous picture the extinct groups are hypothetical and representitive; but the relative positionsof clades for proteobacteria and cyanonbacteria is actual, and taken from from Prescott's microbiology **)

(A common example of intracellular endosymbiosis will help us to understand the theory-  we can still see such intracellular symbiosis in rhizobial bacteria colonising plant root/tissue; where we get both intracellular stage and culturable extracellular phase)

3. How Plastids evolved then?

From this group of protists, a certain group again engulfed a sort of eubacteria (allied to cyanobacteria). The cyanobacteria gave rise to plastids  , and photosynthetic protists.

There are disputes about whether plastid and mitochondra evolved simultaneously or at an interval. According to T. Cavalier smith they originated simultaneously, but according to other newer sources like this  and  this   , mitochondria appeared first.

Fig.3.a. one lineage eukaryote that already formed mitochondria, forming another association with a photosynthetic eubacteria.

It is not clear to me whether all eukaryotes (protists and their derivative higher plants, fungi and animals) had a plastid containing ancestor; or at least some non-photosynthetic protists came before origin of chloroplast (However just to mention, some of photosynthetic protists again evolved progeny with lacked  photosynthetic ability due to retrogressive evolution (degradation) of plastid, such as Helicosporidium sp. etc )

So our final evolutionary tree looks like

Fig.3b. Chloroplast originated similar way from eubacteria (bacteria)

REFERENCES:

BOOKS

* 1. : Molecular Biology, Author: R. F. Weaver, ED-5; Publisher: McGraw-Hill.

: Cell Biology: Concepts and Experiments. Author: Gerald Karp, ED6, Publisher: Wiley.

** 3. : Prescott, Harley, Klein's Microbiology; Edited by Willey, Sherwood, Wolverton, Ed7, MackGraw-Hill.

Papers and Reviews

Bacterial evolution, Author : Woese; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC373105/ ; PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC373105/pdf/microrev00049-0051.pdf
Endosymbiotic theories for eukaryote origin. Authors: Martin, Garg, Zimroski; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4571569/ , Pdf: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4571569/pdf/rstb20140330.pdf


How didn't large, highly active dinosaurs overheat?

There has been a long debate whether dinosaurs were ectotherms or endotherms but  most of the recent studies (hypotheses)1 show that they were endotherms. In one of the most promising recent studies (in 2011), a technique called clumped-isotope thermometry2 (which is based on a reaction involving the bond between carbon and oxygen; and used in paleoclimate reconstruction) is applied to bioapatite (a form of calcium phosphate in bones and teeth) which acts like a thermometer.

  The nature of the physiology and thermal regulation of the nonavian dinosaurs is the subject of debate. Previously, arguments have been made for both endothermic and ectothermic metabolisms based on differing methodologies. Here, we used clumped isotope thermometry to determine body temperatures from the fossilized teeth of large Jurassic sauropods. Our data indicate body temperatures of 36 to 38°C, which are similar to most modern mammals. This temperature range is 4 to 7°C lower than predicted by a model that showed scaling of dinosaur body temperature with mass, which could indicate that sauropods had mechanisms to prevent excessively high body temperatures being reached due to their gigantic size.

  Dinosaur Body Temperatures Determined from Isotopic (13C-18O) Ordering in Fossil Biominerals
  Robert A. Eagle, Thomas Tütken, Taylor S. Martin, Aradhna K. Tripati, Henry C. Fricke, Melissa Connely, Richard L. Cifelli, John M. Eiler
  http://science.sciencemag.org/content/early/2011/06/22/science.1206196
  (emphasis mine)

However, a study as of 2014 claims that dinosaurs were mesothermic3 (meaning the blood runs neither hot nor cold, a thermoregulatory strategy intermediate to cold-blooded ectotherms and warm-blooded endotherms) based on the metabolic rates of dinosaurs by looking at changes in body size as animals grew from birth to adults.

  In early depictions, dinosaurs lumbered slowly, dragging their tails. More recently, we have imagined them lifting their tails and running. The question boils down to whether dinosaurs had energetic systems closer to those of rapidly metabolizing mammals and birds, or to those of slower reptiles that do not internally regulate their body temperature. However, determining the metabolic rate of extinct organisms is no easy task. Grady et al. analyzed a huge data set on growth rate in both extinct and living species, using a method that considers body temperature and body size. Dinosaur metabolism seems to have been neither fast nor slow, but somewhere in the middle—so, dinosaurs did not fully regulate their internal temperature but they were also not entirely at the whim of the environment; neither slow goliaths nor supercharged reptiles.

  Evidence for mesothermy in dinosaurs
  John M. Grady1,*, Brian J. Enquist2,3, Eva Dettweiler-Robinson1, Natalie A. Wright1, Felisa A. Smith1
  http://science.sciencemag.org/content/344/6189/1268
  (emphasis mine)

As we covered the thermoregulation system of dinosaurs, we can start with the question "How didn't large dinosaurs overheat?". As explained above, whether they were endothermic or mesothermic, dinosaurs had mechanisms to regulate their internal temperature not to overheat. There are theories that say that some larger dinosaurs relied on shade and dense flora to keep cool or they might have migrated due to seasonal changes. Other theories claim that they used large surface area organs (like long necks and tails) as a heat radiator4.

One of the most plausible explanations is that large dinosaurs displayed tachymetabolism. Tachymetabolic animals have high resting metabolic rates, usually resulting in endothermy and homeothermy. Further explanation of how big tachymetabolic dinosaurs coped with high heat loads5:

  BIG TACHYMETABOLIC DINOSAURS WOULD HAVE COOKED IN THE HEAT

  Myth: Because tachymetabolic rates scale to W0.75, while surface area scales to W0.67, it is almost universally believed that big endotherms suffer serious heat stress in tropical climes. Big dinosaurs, sauropods especially, should have had low metabolic rates to avoid this dire fate (Martin, 1979; Regal and Gans, 1980; Spotila, 1980; Reid, 1984; Schmidt-Nielsen, 1984; Carroll. 1988; Alexander. 1989; Prothero, 1989: Russell, 1989). Alternately. tachymetabolic sauropods needed well developed cooling systems (Bakker. 1980, 1986).

  Figure 5 This plot shows the time it takes high level endotherms to overheat if they store all internal heat production and exclude external heat by allowing their body temperature to rise to maximum tolerable levels. The mass range approximates that of adult dinosaurs (including lagosuchians), with the highest masses of mammals also indicated: note that giant endothermic dinosaurs would have been more resistant to overheating than giant mammals! Energy storage capacity is in kcal assuming a 6-8°C rise in body temperature (up to 46.5°C), with 0.83 kcal/kg stored for each 1°C rise in body temperature; total active metabolic rates are either 2.0 times endothermic standard energy production/bout, or only 1.3 times normal standard metabolic rates due to suppressed levels of activity and/or standard metabolic rates. The results are in good agreement with thermal tolerances observed among large tropical endotherms.

  Reality: This is a major misconception (Costanzo and Paul. 1978; Paul, 1988a. 1990a). Many tropical mammals have reached from 1 to 20 tonnes, but no classic reptiles have done so, exactly opposite the predicted pattern. Elephants lack well developed evaporative cooling systems. Elephants living in treeless habitats do not drop dead from heat stroke, even in the most dangerous conditions of an extremely hot drought when it is not possible to dump excess heat by radiation or evaporative cooling in the first place, and shade is not available. Instead, large bull elephants have the highest survival rates under such circumstances, again opposite the predicted pattern (Owen-Smith, 1988). Field biologists have long known that endotherms from 100 kg on up use a classic thermal strategy in which their great mass is used to store a relatively low rate of internal heat production for most or all of the day, body temperatures are allowed to rise 3-10°C, and water loss is kept to a minimum (Schmidt-Nielsen et al., 1957; Taylor. 1969, 1970. 1972: Gordon. 1972; Finch and Rohertshaw, 1979: Schmidt-Nielsen. 1984). The built up heat is then unloaded into the cool night sky. This makes large endotherms practically invulnerable to over-heating under the harshest conditions, small endotherms must seek refuge or quickly die from heat stroke or dehydration. The large size of dinosaurs may have been an adaptation for better coping with high heat loads with a tachymetabolic level of heat production (Figure 5).

References:

1. The Evidence for Endothermy in Dinosaurs -
 Top Ten Hypotheses http://www.ucmp.berkeley.edu/diapsids/endothermy.html

2. Paleoclimate reconstruction using carbonate clumped isotope thermometry
(John M.Eiler) https://www.sciencedirect.com/science/article/pii/S027737911100268X

3. Why Dinosaurs Were Like Tuna, Great Whites, and Echidnas http://phenomena.nationalgeographic.com/2014/06/12/dinosaurs-tuna-great-whites-echidnas/

4. Sauropod Necks: Are They Really for Heat Loss?
(Donald M. Henderson)
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0077108

5. Dinosaur Studies - Commemorating the 150th Anniversary of Richard Owen's Dinosauria (By L. B. Halstead)

Further readings (supporting above theories or with different theories):

GEOL 104 Dinosaurs: A Natural History - University of Maryland -
Department of Geology -
https://www.geol.umd.edu/~tholtz/G104/lectures/104endo.html
Body Temperatures in Dinosaurs: What Can Growth Curves Tell Us?
(Eva Maria Griebeler)
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0074317
Ecology and Behaviour of Mesozoic Reptiles (by John L. Cloudsley-Thompson)
Dinosaur Paleobiology (by Stephen L. Brusatte)
The Dinosauria (edited by David B. Weishampel, Peter Dodson, Halszka Osmólska)
The Complete Dinosaur (edited by James Orville Farlow, M. K. Brett-Surman)
Encyclopedia of Dinosaurs (edited by Philip J. Currie, Kevin Padian)
Tyrannosauroid integument reveals conflicting patterns of gigantism and feather evolution (Phil R. Bell, Nicolás E. Campione, W. Scott Persons IV, Philip J. Currie, Peter L. Larson, Darren H. Tanke, Robert T. Bakker) - http://rsbl.royalsocietypublishing.org/content/13/6/20170092
Dinosaurs used nasal passages to keep brains cool - https://phys.org/news/2015-10-dinosaurs-nasal-passages-brains-cool.html


Do snail shells increase the number of rounds with age?

Yes. Once secreted the shell cannot increase in size, so that the growth of the body is accompanied by continuous growth of the shell, i.e. by the gradual increase in the number of the whorls.

This also means that the topmost whorls are the oldest and the aperture marks the front of the new shell.


Earliest ancestor of humans who could integrate into modern society

Interesting question.

The organism would have to be monogamous, that's for sure, otherwise it would be too competitive and it would be a beast - as chimps are. Chimps couldn't integrate into the modern society.

So, monogamy is the prime prerequisite as it's also prerequisite for intelligence. Bipedalism is another obvious prerequisite, as you need an organism with fine motorics of front limbs - and fingers.

For "modern language" you need high intelligence and the ability of abstract thinking. Same goes for reading and writing.

Humans split from great apes between 8 and 4 million years ago. Problem here is that every new piece of fossil of a human ancestor is classified as a new species, so there's very little we're certain of. I'd say the first organism capable of doing the above things existed around 200.000 years ago. Either homo erectus or, more likely, a Neanderthal.


Is Covid-19 likely to mutate into a deadlier form?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

Mutations are mostly deleterious to begin with. This means that mutant copies of virus only very rarely survive and proliferate. A virus that is deadlier will already be less likely to reproduce, having killed more hosts.

The current estimated mutation rate of the SARS-CoV-2 virus is 24 bases per year. Of those mutations, those to be most concerned about are those which would mutate the proteins specific to this virus. Vaccine development will aim to train the immune system to target those proteins, particularly the S or spike protein.

Mutations to those proteins can make potential vaccines less effective. This is why influenza ("flu") vaccines, which are produced ahead of the flu season, may not always line up against the more prevalent strains which result.

A recent comment was published in Nature, authored by life scientists and epidemiologists, which goes into your question in more detail, as regards to the novel coronavirus:

  In this case and that of SARS-CoV-2, mutations consume the narrative, even though individual mutations seldom become fixed during outbreaks nor modulate complex virological traits. Rather, mutation is a humdrum aspect of life for an RNA virus. Because these viruses employ an intrinsically error-prone RNA polymerase for replication, their genomes will accumulate mutations during every copying cycle. Moreover, these cycles can occur on the order of hours, ensuring that a diverse virus population will be generated within a single infected host. While this amazing capacity to mutate fuels the engine of evolutionary change, most mutations adversely impact some aspect of virus function and are removed by natural selection. (emphasis added)

Further, and more to the original point of your question:

  These warnings will probably not halt the question as to whether mutations will arise in SARS-CoV-2, enabling it to spread more efficiently between humans or generate a higher case fatality rate. In response, we can look to the 2002–2003 SARS-CoV epidemic. Large deletions in the open reading frame 8 (ORF8) region and mutations in the spike (S) protein were discovered during the early stages of the outbreak and eventually dominated the epidemic, suggesting that these were adaptations to humans12,13. Based on this observation, some hypothesized that virus genetic changes in part drove the SARS epidemic, but this claim is unsubstantiated14. So, could SARS-CoV-2 adapt in the same way? Yes. Will adaptation precipitate more deaths? Unlikely. (emph. added)


In Embryophyta (land plants), including bryophytes, the sporangium is usually a multicellular structure.

Perhaps you meant to ask about the number of spore mother cells (SMCs) in each sporangium? That varies across groups. In bryophytes, each sporangium has many SMCs, and accordingly produces a large number of spores. (Contrast this with angiosperms, where a megasporangium [called an ovule] has only one megaspore mother cell.)

References and further reading:

https://courses.lumenlearning.com/boundless-biology/chapter/bryophytes/

https://www.britannica.com/science/plant-development

Image attribution:
By LadyofHats. (Public domain;
https://commons.wikimedia.org/wiki/File:Hornwort_structures.jpg)


What is myopia?

Myopia, a.k.a. near-sightedness, is a refractory error. Refraction is the process by which the optical system focuses images of objects on the retina, which are then transmitted to the visual cortex of the brain to be interpreted as vision. The major components of refraction are the cornea, lens, and axial eye length (distance from the front to the back of the eye). The problem in myopia is that images are focused anterior to the retina, like this:

Causes of myopia

You ask

  I don't really understand the exact mechanism responsible for the transition from 1 [ciliary muscle spasm] to 2 [elongation of the eye].

Swelling or spasm of the ciliary body (the circumferential tissue inside the eye composed of the ciliary muscle and ciliary processes) can be seen after trauma or in inflammatory conditions. Contraction of the ciliary muscles causes decreased tension in the suspensory ligaments that connect the ciliary body to the lens. The results in the lens becoming more rounded and/or moving anteriorly. Both processes also bring the focal point more anterior, i.e. further in front of the retina, resulting in a configuration as in the picture above. You could call this "elongation of the eye" if you wanted. This 25 second video explains the process succinctly with pretty pictures.

Although interesting to think on, this is not the most common cause of myopia. Myopia is an extremely common condition, occurring in ~25% of the US population. Myopia can be classified as axial or refractive.

Axial myopia: The refracting power of the eye is normal but the length of the eye is too long.
Refractive myopia: The length of the eye is normal, but the lens refracts too much for a given axial length.

Both axial and refractive myopia are usually caused by failure of emmetropization, the process by which a normal eye has coordinated growth of its refractive components. This process takes place mostly during the childhood and adolescent years, which is why myopia most commonly develops during that time. There are certain disease conditions that increase lens power (e.g. osmotic effects in diabetes) or axial length (e.g. posterior staphyloma) that may also cause myopia at other points in life, but these are less common.

References:

1. Neil J. Friedman and Peter K. Kaiser. Essentials of Ophthalmology. © 2007, Elsevier Inc.

2. Albert, Daniel M., MD MS.Albert & Jakobiec's Principles & Practice of Ophthalmology, Third Edition. © 2000, 1994 by W.B Saunders Company, © 2008, Elsevier Inc.

Image from:
http://en.wikipedia.org/wiki/Myopia


Why does human chromosome 19 have the second highest number of protein-coding genes?

This Nature paper from 2004, by Jane Grimwood et al. goes at least a long way towards giving an answer to the question of the OP. In short: there were inordinately many duplications, especially during an event 30-40 million years ago, as well as during a much more recent event. These duplications are, uncharacteristically, predominantly intra-chromosomal rather than inter-chromosomal. Also, chromosome 19 contains a lot of immunoglobin-like paralogues: a type of gene for which it is clearly evolutionarily adaptive to undergo rapid duplication followed by random mutation, as they play a role in adapting to potential antigens.


Why is only one primer used for DNA sequencing instead of two?

The reaction for the Sanger sequencing reacting contains beneath the normal dNTP (which are needed to make most of the DNA) the dideoxynucleotides, which lack the 3'-OH-Group and which are labelled with a fluorescent dye. Once one of this nucleotides is incorporated, the chain reaction stops here, leading to a product with a specific length and a known (by the fluorescent dye) end base.

In theory this leads to products of a length primer + 1 ddNTP base, primer + 1 base + 1 ddNTP base, primer + 2 bases + 1 ddNTP base and so on. The sequencer seperates these bases by sizes and the sequentially reads out the fluorescent dye and translates this into a sequence of bases. See the image from the Wikipedia for illustration:

If you now add two primers (and of course have a double stranded DNA), this reaction will start from both ends of the DNA (always in 5'--> 3' direction) leading to two sets of marked DNA of the same size (so again the base + 1 ddNTP, base + 1 base + 1 ddNTP and so on). Since these are equal in size, you will always read out two bases at the same time and you will not be able to tell, which signal belongs to which strand. This looks like this (from here):


Why are hens so different from other birds?

Domestic organisms are bred to serve specific purposes for humans. Sheep are bred to produce wool; Cows are bred to provide meat and milk for human consumption; dogs are bred for service and companionship. Since domestic animal do need to survive in the wild in order to reproduce (ignoring feral animals, which is an interesting topic by itself), most of the other aspects of that animal relevant to its survival tend to be minimized.

So one could just as easily point out that there is no other animal that produces as much wool as a sheep, and yet producing copious amounts of wool isn't particularly useful to the animal itself (i.e. other than the fact that humans will tend to select good wool producers for breeding). So sheep are not particularly good at surviving in the wild, and yet they are incredibly successful as a species and are widely distributed, thanks to humans.

In short, domestic hens evolved to produce many eggs in their lifetime because over the past millennia since humans have started keeping them as livestock, humans tended to preferentially breed those individuals which produced more eggs and to eat those individuals which did not. Chickens tended to be kept in pens and guarded by humans or other animals, so the ability to defend themselves or flee from danger was not important to their survival, and in fact, those that did attack their handlers or escape were probably less likely to be bred.

This process is known as selective breeding or artificial selection.


What are sticky ends.
There is no substance that is attached making the DNA ends "sticky". What has actually happened is an overhang of at least a few nucleotides. Blunt ends are another kind of cut, but have no overhanging residues.

Why are sticky ends sticky?
Restriction enzymes usually cut these ends deliberately so that a four nucleotides are overhanging on the 5' end of the double strand. These are complementary to other overhangs and because they are less stable than a bound double strand region, and are able to hydrogen bond easily with complementary bases, they are easier to attach with a ligase.

Below is an image of the base pairs interacting via H bonds.


Is there a cheap and easy way to check for potentially unsafe UV exposure?

The instrument you are looking for is probably an UV-meter.


Sequencing a specific region of a genome

Yes, it is possible to sequence a specific region of the genome. The method, as you mentioned, is called targeted sequencing. Resequencing is basically sequencing something that has already been sequenced. This means that instead of assembling all of your sequence reads from scratch, you can just align them to the reference sequence (in your case, the entire human genome has been sequenced). Targeted resequencing means you're sequencing a specific region, such as a gene. This requires concentration of the specific DNA you wish to sequence and can be done by PCR amplification (using primers that flank your desired sequence) or hybridisation (using probes complementary to your desired sequence that are fixed to a surface), among other methods.

For information on methods for enriching a DNA sequence, give this a read:

Mamanova, L. et al. Target-enrichment strategies for next-generation sequencing. Nat. Methods. 7, 111-118 (2010).


Why the name coined for MARKUP LANGUAGE for SBML?

SBML follows in the same vein as XML, in that it provides a standardized and flexible method for structuring information. XML and its ilk aren't just for making web pages, they're for sending structured datasets between systems and programs (in fact, XML is a fairly common configuration format). Why? Because the structure makes parsing simple (well, simple-ish).

BTW, markup languages were not invented for the web, HTML was far from the first one. The origin of markup languages is typesetting and in fact one of the most common uses these days is still in writing papers (ask a local math/physics/CS person what he/she uses to write papers and the answer will be Latex...a markup language).

Edit: BTW, this really has nothing to do with biology and you could have at least read the wikipedia page on what a markup language is.


What's the minimum, if any, concentration of atmospheric nitrogen needed by plants?

Zero if you are supplying them with solid nitrates in their growth medium, plants can't use atmospheric nitrogen. Some soil bacteria can and create nitrates the plants can use but this can and often is supplied by other means.

But as Graham points out you will need another inert gas to fill in the atmosphere as high concentrations of CO2 or Oxygen are both toxic.


Determining if a Protein Model Contains a Backbone Clash

The way to check for steric clashing between any two atoms, backbone or otherwise, is to compute their Euclidean distance. If a and b represent two atoms (with a_x being the X coordinate of atom a and so forth), you can calculate their Euclidean distance as follows.

  d(a, b) = sqrt( (a_x - b_x)^2 + (a_y - b_y)^2 + (a_z - b_z)^2) )

So essentially the idea would be to calculate the pairwise distance between each of the backbone atoms. For any pair of atoms, there is steric clashing if the distance between them falls below a certain threshold. If I remember correctly, this threshold is the sum of the van der Waals radii of the two atoms.


How reversible is DAT upregulation from long-term ADHD medication use?

First the boring (but most important part) looking at the study:

It is important to critique the study design FIRST to see what kind of information we can actually obtain from this study. This is a meta-analysis of cross-sectional studies (meaning there is no record of change over time) that include a variety of age ranges of ADHD patients (some on treatment, some not) who were compared with age, gender and IQ-matched non-ADHD people to measure DAT levels in the stratum measured with PET and SPECT.

What they found:

There were very heterogeneous results from all the studies, there was no statistically significant difference between DAT in ADHD and normal (note that they use the word "trends"). The only thing statistically significant that they found was that there was a wide spread of DAT in the ADHD population, and that exposure to treatment accounted for half of this spread (variance).

What can we say about this?

This is not a very conclusive study, but studies like this are often necessary to merit doing higher resource intensive studies.  This study did not reach statistical significance in it's primary outcome, and on further search was able to only find a single outcome of significance. My summary of this would be: maybe this could represent a method of medication tolerance.

To answer your question
If hypothetically this was the cause and I had to make up a possible method of transcription control, I would say something similar to your answer. I would guess there is some transcription factor that is inhibited by dopamine in the cell. When there isn't dopamine (b/c it is being blocked from returning), it would somehow become active and start transcribing the gene for DAT.

Disclaimer
I am not a neurobiologist, this is my opinion after reading the article. Feel free to add to my comments

  Reference:

  Fusar-Poli, P., Rubia, K., Rossi, G., Sartori, G., & Balottin, U. (2012). Striatal dopamine transporter alterations in ADHD: pathophysiology or adaptation to psychostimulants? A meta-analysis. American Journal of Psychiatry, 169(3), 264-272.[Link]


Who is organizing the heartbeat and its roles in the body?

The Sinoatrial Node is a ganglion (clump of nerves) attached to the heart, which regulates heartbeat independently from the brain (http://en.wikipedia.org/wiki/Sinoatrial_node).

Heart rate can also be influenced by hormonal responses produced by the autonomic nervous system. To quote Wikipedia:

  While heart rhythm is regulated entirely by the sinoatrial node under
  normal conditions, heart rate is regulated by sympathetic and
  parasympathetic input to the sinoatrial node. The accelerans nerve
  provides sympathetic input to the heart by releasing norepinephrine
  onto the cells of the sinoatrial node, and the vagus nerve provides
  parasympathetic input to the heart by releasing acetylcholine onto
  sinoatrial node cells.

Source: en.wikipedia.org/wiki/Heart_rate#Physiology


Are all genes transcribed in differentiated cells?

No
Not all genes are transcribed, repressor proteins and nuclear receptors can bind the DNA preventing transcription of particular genes. Even things like histone regulation can prevent transcription. There may even be epigenetic regulation of transcription.

Source 1

Source 2


What is an "end-to-end fusion" in the context of telomerase?

An end-to-end fusion is the result of two chromosome ends fused together. This happens when telomeres (repeated sequences at the ends of chromosomes) lose their protective telomere-binding proteins. In mammalian cells, loss of TRF2 (telomere repeat-binding factor 2) leads to chromosome fusions.

Here is an example of how it looks with metaphasic chromosomes (the DNA is stained in blue and the telomeres are stained in pink; picture from Rai et al, 2016). The left panel shows normal chromosomes, the right panel shows end fusions upon depletion of TRF2.

What causes chromosome fusions in such situations is the DNA double-strand break (DSB) repair machinery, which is normally repressed by telomere proteins (mainly by TRF2; see van Steensel et al, 1998). In mammalian cells, telomere-binding proteins are collectively called the shelterin complex (they literally shelter chromosome ends; see de Lange, 2005).

Telomerase doesn't repress the DSB repair machinery directly. Because of the structure of telomeres (a single-stranded 3' overhang) and of the way replication is primed, linear chromosomes cannot be fully replicated and will gradually shorten at each replication. When telomeres become critically short, they don't recruit enough telomere-binding proteins and therefore fail to repress the DSB repair machinery. Telomerase, when expressed and activated, maintains the length of telomeres in replicating cells at each replication (by adding repeated sequences complementary of the RNA template that is a component of the telomerase holoenzyme), providing binding sites for telomere-binding proteins, and thus indirectly contributes to the repression of the DSB repair machinery.

End-to-end fusions cause problems in cells in part because fused chromosomes will likely not segregate properly during mitosis and meiosis. The resulting daughter cells end up with altered ploidies that can be severe enough to prevent cell viability.

de Lange T (2005) Shelterin: the protein complex that shapes and safeguards human telomeres. Genes Dev. 19: 2100–2110 https://doi.org/10.1101/gad.1346005

Rai R, Chen Y, Lei M & Chang S (2016) TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions. Nat Commun 7: 10881 https://doi.org/10.1038/ncomms10881

van Steensel B, Smogorzewska A & de Lange T (1998) TRF2 protects human telomeres from end-to-end fusions. Cell 92: 401–413 https://doi.org/10.1016/S0092-8674(00)80932-0


What flying insect is this? Resembles Wasp / Crane Fly / Moth?

Pselliophora laeta, a species of crane fly (Tipulidae) in the Ctenophorinae subfamily.

Route to discovery: Reverse image searching my own photo on Google led me to a matching image on Naturalista (Familia Tipulidae), and in-turn to iNaturalist, which showed me to Genus Dictenidia. Further Googling for "Genus Dictenidia" brought up many families of crane-fly, which I visually scanned until I spotted it -- Pselliophora! That led to Wikipedia, and to this image, which mentions its source to be whatsthatbug, where the discussion cites Pselliophora laeta on India Nature Watch.

--

Source: https://www.inaturalist.org/observations/299363
Observed: Thiruvananthapuram, India; Jul 28, 2012 5:13 PM IST

Mating Crane Flies from India

Source: https://www.whatsthatbug.com/2010/09/30/mating-crane-flies-from-india/
Observed: Mumbai, India; Sep 30, 2010 1:43 AM IST


Does adding antibiotic after 5-10 mins of innoculation affect the protein yield or growth?

That is not true. If you had forgotten to add the antibiotic before inoculation then you can add it before the bacteria starts growing. Make sure you add it when the bacteria is still in lag phase. If you add it later then it won't be effective as some non-resistant (non-transformed) bacteria would have already expanded their population. Ampicillin and kanamycin are best effective when the bacteria are growing. Even though these antibiotics are considered bacteriocidal, you would end up having unnecessary biomass in your culture.

So 5min delay for E.coli is not an issue. (I think this happens to all of us: forgetting to add antibiotic).


What's the maximum and minimum temperature a human can survive?

Hypothermia (when the body is too cold) is said to occur when the core body temperature of an individual has dropped below 35° celsius.  Normal core body temperature is 37°C. (1) Hypothermia is then further subdivided into levels of seriousness (2) (although all can be damaging to health if left for an extended period of time)

Mild 35–32 °C: shivering, vasoconstriction, liver failure (which would eventually be fatal) or hypo/hyper-glycemia (problems maintaining healthy blood sugar levels, both of which could eventually be fatal).
Moderate 32–28 °C: pronounced shivering, sufficient vasoconstriction to induce shock, cyanosis in extremities & lips (i.e. they turn blue), muscle mis-coordination becomes more apparent.
Severe 28–20 °C: this is where your body would start to rapidly give up.  Heart rate, respiratory rate and blood pressure fall to dangerous levels (HR of 30bpm would not be uncommon - normally around 70-100).  Multiple organs fail and clinical death (where the heart stops beating and breathing ceases) soon occurs.

However, as with most things in human biology, there is a wide scope for variation between individuals. The Swedish media reports the case of a seven year old girl recovering from hypothermia of 13°C (3) (though children are often more resilient than adults).

Hyperthermia (when the body is too hot - known in its acute form as heatstroke) and is medically defined as a core body temperature from 37.5–38.3 °C (4).  A body temperature of above 40°C is likely to be fatal due to the damage done to enzymes in critical biochemical pathways (e.g. respiratory enzymes).

As you mentioned burns, I will go into these too. Burns are a result of contact with a hot object or through infra-red (heat) radiation. Contact with hot liquid is referred to as a scald rather than a burn. Tests on animals showed that burns from hot objects start to take effect when the object is at least 50°C and the heat applied for over a minute. (5)

Freeze-burn/frostbite, which is harder to heal than heat burns(6) occurs when vaso-constriction progresses to the degree where blood flow to affected areas is virtually nil.  The tissue affected will eventually literally freeze, causing cell destruction. (7)  Similarly to hypothermia, frostbite is divided into four degrees (that can be viewed on Wikipedia).

As to the matter of global warming cooking us to death, I would imagine that it would be more indirect changes that got us first.  If the average temperature had risen  to the necessary 40°C to cause heat-stroke, sea levels would have risen hugely due to the melting of the polar ice caps.  Crops and other food sources would likely be affected too, therefore I don't think that global warming is overly likely to directly kill humans.


Lions

Lions are a classic example of cannibalism. To understand why this occurs we have to understand their mating system.

Males have a harem of females and males fight in order to access a harem (Note: females may also take part in the battle depending on which male they prefer). When a male takes over a new harem, he kills the young ones of the previous male if these young ones are still dependent on their mother. The reasons are:

The mother is not fertile while she is taking care of a young baby while the male would appreciate that the female is ready to raise his own kids.
The mother needs to invest quite a lot of energy to feed/milk their young while the new male would prefer this energy to be invested in his own offspring.

In short, a male kills the young ones when he takes over a new harem because these young ones do not carry his genes and prevent this new male to optimally pass on his own genes as the offsprings of the previous male consume time and energy from the females of the harem.

And well… once the offsprings are killed, it would be a shame to waste all this good and fresh meat. Better to eat them!

In the cases of lions, cannibalism does not result from food shortage but from "not wasting food". I think that the "not wasting food" hypothesis is the most explanation for cannibalism (I am not sure though). I guess that most often the "not wasting food" occurs after death due to competition as it is the case in lions.

Other Examples

There are many cases of cannibalism in the animal kingdom. Chimpanzees eating other chimpanzees and bear eating other bears. In the tiger salamander, there are cannibal morph and normal morphs. In this species cannibalism is very frequent as in nature one offspring over 5 is eaten through cannibalism (if I am not mistaken). Cannibalism is very common in prairie dogs as well (Reference). In Dragonflies cannibalism represents 95% of the total mortality (Reference).

Sibling sharks eat each other in their mum's womb. Here is a video on the subject. This type of cannibalism is called siblicide.

In Praying mantis the female may eat her mate after copulation. This is referred to as sexual cannibalism. The subject is slightly controversial, please have a look to the wiki article for more info.

In many species (including the dragonflies example above) the old individuals eat the young. This is referred to size-structured cannibalism.

Fillial cannibalism is a type of cannibalism when the adults eat their own offsprings as it is the case in the prairie dogs example I cited above.

Have a look to the Wikipedia links for filial cannibalism, sexual cannibalism and siblicide, they go further than my answer.


Why does Citric Acid occur in Citrus fruits?

Actually citric acid is not only available in citrus fruit but also in pretty much any living thing. it is an important intermediate in Krebs cycle, but I guess the main reason that it is available in high concentrations in citrus fruits is because citrate is an inhibitory compound for phosphofructokinase, that means it stops the glycolysis and hence it makes it hard for bacteria to use the fructose available in the fruit body.

Source:
 Stryer, Lubert; Berg, Jeremy; Tymoczko, John (2003). "Section 16.2: The Glycolytic Pathway Is Tightly Controlled". Biochemistry (5. ed., international ed., 3. printing ed.). New York: Freeman. ISBN 978-0716746843.


The helix shape of DNA molecule is a consequence of its secondary structure. This refers to the bases contained in the molecule which pair, thus determining tertiary structure [1].
Basepairing also occurs in RNA, so it can form a double helix. In fact, RNA is composed of short helices packed together [2]. Base pairs maintain DNA's helical structure no matter the nucleotide sequence [3].
A nucleic acid strand is composed of nucleotides joined together by covalent bonds between the sugar of one nucleotide and the phosphate of the next. Adenine pairs with thymine and cytosine pairs with guanine by hydrogen bonds and form the double-stranded structure [3]. Because covalent bonds are stronger than hydrogen bonds, the double helical structure of DNA is easily broken by heat [4], but the nucleotides remain bonded together.
Here is the tRNA molecule (you can see it has short helices):
"TRNA-Phe yeast 1ehz" by Yikrazuul - Own work. Licensed under CC BY-SA 3.0 via Wikimedia Commons.
Here is the DNA structure:
(source: wikimedia.org)"ADN animation" by brian0918™ - Own work. Licensed under Public domain via Wikimedia Commons.

References:

Wikipedia contributors, "Nucleic acid double helix," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Nucleic_acid_double_helix&oldid=609435163 (accessed June 26, 2014).

Wikipedia contributors, "RNA," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=RNA&oldid=612056511 (accessed June 26, 2014).

Wikipedia contributors, "DNA," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=DNA&oldid=611891356 (accessed June 26, 2014).

Wikipedia contributors, "Nucleic acid thermodynamics," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Nucleic_acid_thermodynamics&oldid=606379256 (accessed June 26, 2014).


Yes, Agrobacterium is indeed a very widely used vector in plants. So it wouldn't be wrong to consider bacteria as vectors. Just to add, it's worth noting that in recent times, bacterial vector options have been explored in the case of humans also, especially in the case of gene therapy for cancer treatment, though its success hasn't been demonstrated yet. Refer https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056088/ for more information on this.

To conclude, bacteria can be considered as a vector undoubtedly.


What causes REM atonia to be lost in sleepwalking?

There's an excellent, comprehensive review article on the entire process of REM sleep:

  Vetrivelan,R, Chang, C, Lu,J (2011). Muscle tone regulation during REM sleep:
  neural circuitry and clinical significance. Archives Italiennes de Biologie, 149 [DOI] [Free PDF]

Projections from the sublaterodorsal nucleus (SLD) of the Pons in the brainstem are responsible for the suppression of the spinal motor output/movement (for an anatomical schematic, see the article).

  Descending SLD glutamatergic projections activating the premotor neurons
  in the ventromedial medulla and spinal cord interneurons bring about muscle atonia and suppress phasic muscle twitches in spinal musculature.

Lesions in this area in rats have resulted in REM sleep without atonia.

  Many studies have
  suggested that the ventromedial medulla (VMM),
  which receives glutamatergic inputs from the SLD,
  may be the relay site for the pontine inhibitory area
  on spinal motor neurons

The SLD axons relay through the VMM, but also directly projects onto interneurons within the spinal cord, directly inhibiting their activation.

Most of the knowledge we have about this subject comes from animal studies, so it will take some time to verify whether these same mechanism and relays are the same in humans.

The area that is lending the most credence to these issues of REM atonia is not sleepwalking as much as REM sleep behavioral disorder (RBD).  In this condition, sufferers act out their dreams and generally lose atonia during REM sleep.

Evidence points to the fact that such behavior is often seen decades before such conditions as Parkinson's and Lewy Body dementia.

  Ferini-Strambi,L (2011) Does idiopathic REM sleep behavior disorder (iRBD) really exist?
  What are the potential markers of neurodegeneration in iRBD? Sleep Medicine 12, S43–S49 [DOI]

They summarized two studies which explored these anatomical changes:

  [Diffusion tensor imaging, a type of MRI scan] changes have been reported in the
  brainstem (pons, substantia nigra) as well as the fornix, the right
  visual stream, and the left superior temporal lobe suggestive of
  brain tissue disintegrity[1]

  significant decreases of [fractional aniosotropy] in the tegmentum
  of the midbrain and rostral pons and increases of [mean diffusivity]
  within the pontine reticular formation overlapping with a cluster
  of decreased [fractional anisotropy] in the midbrain [2]

So, the answer is, we don't know for sure, but we have some clues from the animal models as to what stages of the signals to suppress movement are interrupted.

[1]Unger MM, Belke M, Menzler K, et al.(2010). Diffusion tensor imaging in idiopathic
REM sleep behavior disorder reveals microstructural changes in the brainstem,
substantia nigra, olfactory region, and other brain regions. Sleep,
33(6),767–73.[FREE PDF]

[2]Scherfler C, Frauscher B, Schocke M, et al. (2011) White and gray matter abnormalities
in idiopathic rapid eye movement sleep behavior disorder: a diffusion-tensor
imaging and voxel-based morphometry study. Ann Neurol,69(2),400–7. [DOI]


What is the contribution of the cockroach to the ecological environment?

Short answer
Cockroaches are an integral part of the food chain.

Background
Cockroaches are an important source of food for a number of organisms, such as arthropods, birds, and mammals. As such, they are an important part of the food chain. Cockroaches also play an important role in nutrient recycling. Most species of cockroach are detritus feeders and with the help of endogenous cellulases play an important role in degrading plant material. Some species, such as Cryptocercus, feed directly on wood and play a major role in lignocellulose digestion in temperate forests.

Reference
 - Bell et al., Integr Comp Biol, 2008; 48(4): 541-3


Now  I cannot really tell the name of it without knowing more of its properties and characteristic features, e.g. size. (I am afraid I am not very good with faces, especially of microorganism :D)

But I am 90% sure it might be an
Oligochaete


Your view of the randomization of the parent traits seem a bit wrong and it makes the question a little unclear. But still, I think we can answer it...

The randomization happens at the moment of the creation of sperms and ovules. The two "randomizing processes" are segregation and recombination.


How useful are vitamin and trace element additions in E. coli culture medium?

Not sure that I have ever come across trace metals in recipes (I assume that you aren't referring to the Ca/Mg salts component of M9), but it is certainly the case that many K12 strains (e.g. C600, DH5α) require thiamine because they are thi mutants. This doesn't apply to BL21 since it is from a different lineage (it is a B strain). In a lab where several strains are being used it will always make sense to standardise on a universal recipe so that the medium available will suit all strains in use.

There is a useful list of E.coli genotypes here.


This specific experiment has not been done. Fusing cells is difficult and it also leads to polyploidy. Cells are immortalized by overexpressing oncogenes (or viral replication genes); for example HEK293 cell line was established by transforming embryonic kidney cells with adenovirus.

Now transforming a neuron would immortalize it but would also make it lose its function; for a cell like neuron, replication would compromise its activity for e.g. loss of established synapses. As mentioned in the comments by har-wradim, it was shown that transforming neurons with oncogenes leads to their de-differentiation. Another experiment of transforming neurons gave a contrasting result. Feddersen et al transformed purkinje cells in mice by expressing SV40 viral t-antigen from a purkinje-cell specific promoter and surprisingly it lead to degeneration of cerebellar tissue. Also have a look at this article.


How was the resemblance between apes and humans explained in pre-Darwinian biology?

The time before Darwinism, people believed life as an entity which is created rather evolved. But there were great biologists interested in the relationship between species, who deliberately thought of evolution ideas and some of them believed in ape-human similarities and placed humans and apes in same group.

In 1699, Edward Tyson, an English anatomist, dissected an ape specimen(chimpanzee) and showed that its anatomy closely approaches ours.But he didn't established any relationships between humans and apes. It was first done in 1738 by Swedish scientist  Linnaeus in his book Systema Naturae .After that in 1759, Lamarck, a French naturalist  who was Darwin's predecessor in general theory of evolution, stated that humans were derived from up-right walking apes.

  In 1759, just half a century before Darwin was born and precisely one hundred years before he published his famous book , "Origin of Species", Linnaeus, the great Swedish scientist, discovered that man was a mammal. He then placed man in the Order of primates, which means literary the first, or the highest,order of mammals.It comprises all the monkey like forms, including the man-like apes.
  Reference

References

Primate Evolution and Human Origins - Russel L. Ciochon & John G.Fleagle

Human Evolution: A Guide to the Debates - Brian Regal


Is extreme cladism a mainstream position in the species debate?

I've never heard of it, actually - though I can't speak for my professors or researchers I know, none have ever presented the Cladism argument as an argument for the delineation of species.

As far as I'm aware, the attempts to define a species fall along three lines:

The ability to produce fertile offspring in the wild.

Distinct physical characteristics.

An arbitrary amount of genetic divergence.


Is wiping with RNAse Zap enough to destroy RNAse activity?

It's hard to know what RNaseZap does since the ingredients list is a trade secret.  However, I expect it is a lot more than just detergent.  RNaseA is extremely hard to destroy; moreover it can easily renature once the denaturant is removed. Therefore, very minute quantities are sufficient to annihilate RNA experiments.  The historical method of purification was to boil solutions of it until all other proteins denatured and could be easily separated. I can personally attest that you can precipitate it in pure alcohols and it will spontaneously refold as soon as it is rehydrated.

I would not trust a simple detergent to get rid of it; you'll need something more volatile to be reliable.  A lot of "home made RNaseZap" recipes on the internet include hydrogen peroxide, which causes a variety of covalent modifications to the protein.  It also has the advantage of cleaning itself up (eventually turning into H2O).  The detergent is useful because you typically don't want any protein residue floating around your experiments, denatured or not.  If you have some dried RNaseA aggregates, it will also help break those up.

I work with RNaseA itself, so I can't personally vouch for the recipe below (since I'm not interested in destroying my sample), but it seems sound.  But if you have the cash to blow, just get the RNaseZap.  It's very widely used by RNA labs and you really don't want to chance a potentially expensive experiment on it.  Especially since you're constantly shedding tons of RNaseA from your skin, being sloppy will probably bite you eventually.

Mechanism of action for H2O2
plausible recipe


What bird is this (found at Alice Springs Desert Park in Australia)?

It is a Cisticola exilis as stated by @cezar
If someone has any objection please reopen this.


phylogenetic Independent contrasts with unresolved tree

Look also into PGLS. Either way, one thing you could do--it would be ugly--would be to set all branch lengths to 1. Additionally, you could smooth the tree with penalized likelihood, e.g. chronopl() function in ape package in R. Again, this is an ugly solution and look into PGLS (it won't solve the ugly phylogeny part).


Why do water molecules diffuse along axons direction?

The movement is just the thermal energy motion you describe, not due to any concentration difference.
The anisotropy is due to the geometry. White matter tracts are effectively a dense bundle of thick, fatty hoses. Water can freely move in the tubes but cannot move as freely through the dense walls, so you see more movement along the axon length rather than perpendicular to them.
You can read more at https://en.wikipedia.org/wiki/Diffusion_MRI


Why sister chromatids and daughter cells but not brother chromatids and son cells?

During the days when philosophers used to debate, they tended to regard  reproduction as a feminine trait. So naturally organisms/cells capable of producing offspring are also given a feminine trait. The parent cell is often called the mother cell, and the daughter cells are so named because they eventually become mother cell themselves.

I presume there exists a similar argument for sister chromatids, in that they are identical. When they separate, they are usually termed as undivided chromosomes.


Could humans breathe if the average methane content of the atmosphere increased to 1%?

Methane is biologically inert and can only act as an asphyxiant at high concentrations by displacing oxygen. An environmental exposure limit has been set at 5,000 ppm, though 10,000 ppm (1%) had no effect:

It is obvious that an exposure limit that presents an explosion hazard cannot be recommended, even if it is well below a concentration that would produce toxicity; thus, exposure limits should not exceed 5% by volume in air.
Animals exposed to methane at 10,000 ppm showed no toxic [effects]; an uncertainty factor of 2 is suggested to derive an EEL—5,000 ppm. There is no evidence that duration of exposure is important in methane toxicity.

Source: Methane in Emergency and Continuous Exposure Limits for Selected Airborne Contaminants Volume 1 (1984)


Is there evidence to suggest that sharks from prehistoric times live in the deep of the oceans?

No.

The article linked to is a hoax, and was debunked by Snopes.

The website is known for its hoaxes and satirical articles, and it states itself that its articles are faked.

  WNDR assumes however all responsibility for the satirical nature of its articles and for the fictional nature of their content. All characters appearing in the articles in this website – even those based on real people –  are entirely fictional and any resemblance between them and any persons, living, dead, or undead is purely a miracle.

The image of the shark was taken from a 2009 photograph of a great white shark caught in South Africa. The shark was reportedly 4.3m long, a normal length for a great white shark.

The large apparent size of the shark as compared to the fisherman is due to a trick of perspective. This article shows the shark in perspective in a second image, which clearly shows that it is not as large as it apparently is in the first image.


This looks like a pipefish, possibly a straightnose pipefish.

See also. But the size suggests a juvenile?


I have looked at this ECG using LightWAVE.

The first part is showing atrial fibrillation or flutter with variable conduction because:

arrhytmia
no P waves or coarse fibrillatory waves
tachycardia at about 95-100 beats/minute
can be seen better in V1

Sample from 00:00:40

The second part is showing premature ventricular contractions with trigeminy because:

different morphology of QRS - ectopic
wide QRS
two normal complexes followed by one ectopic
presence of the compensatory pause after PVC

Sample from 00:09:20

References:

ECG data: PhysioNET MIT-BIH Arrhythmia Database
ECG criteria: LearnTheHeart.com


Consensus codon optimization by organism

Try the Codon Usage Database at Kazusa. You can search by organism. The database contains 35,799 organisms and compiled from 3,027,973 complete protein coding genes (CDS's), but last updated in 2007.


Is an egg classified based on the species inside it, or by the species that laid it?

Species are generally defined in terms of populations (see e.g. the wikipedia page), and it is therefore relatively meaningless to talk about individuals as species. That species is defined in terms of populations is true for many species concepts, e.g. as groups that can produce fertile offspring (biological species concept) or as a evolutionary distinct lineage (phylogenetic species concept). The question is therefore somewhat ill-posed, since it is only framed in terms of individual parents and offspring.

A possible exception could be speciation in apomictic species or speciation events following a change in ploidy level, but this is mostly relevant for certain types of asexual species and probably not what you are after since you are talking about egg-laying animals.


Welcome to Biology.SE.

To my knowledge there is no good rule on how to name genes. The first person to name a gene or an allele is free to just pick up a that (s)he finds easy to remember and eventually intuitive. Sometime the author just picks a funny name. Here are a few examples from Drosophila melanogaster data base:

bag of marbles: involved in oogenesis, spermatogenesis.
breathless: involved in development of trachea.
buttonhead: regulates segmentation of the head.
dissatisfaction: involved in many aspects of sexual behavior.
hobo: a mobile genetic element.
Indy: for "I'm not dead yet"; this mutation makes the fly live twice as long.
windbeutel: German for "cream puff".

Did you suggest to name genes based on their sequence? Would be quite painful! One cannot name a gene based on its sequence as the sequence is way too long. The median gene length in humans  is 24,000 base pairs (Fuchs G et al. 2014). You just need to refer to a database to match a sequence to a gene name (see BLAST for example).

How could we improve this system?

Do you have any suggestion on how we should name genes? Should they be named in relation to the phenotype they affect or to the biological pathway that are involved in or maybe something else? The issue is that we often annotate and name a gene before knowing much about its effect.

Note that some genes have several names which is indeed confusing. Would be good to solve this a little bit.


From Illinois Wesleyan University:

  One way in which tardigrades have adapted to various types of
  environments, has been to reversibly suspend their metabolism. This
  state is known as cryptobiosis [ 'hidden life' (Clegg, 2001) ] and is a truly deathlike state.
  Metabolism lowers to 0.01% of normal or is entirely undetectable and
  the water content of the body decreases to less than 1%. [...]

  The most intensely studied type of cryptobiosis is anhydrobiosis, a
  form of cryptobiosis initiated by desiccation. [...] Anhydrobiosis is an almost complete
  loss of body water and the animal can stay in this state for an
  extended period of time. Tun formation, a vital part of the process [Fig. 1.],
  results in a body that is constricted and folded. The first step is
  invagination of the limbs, longitudinal contraction of the body, and
  infolding of the intersegmental cuticle. Wax extrusion covers the
  surface and may help to reduce transpiration (water loss by
  evaporation). The tun formation process requires active metabolism. [...]

Fig. 1. Tardigrade before and after entering the tun state. Note the decreased body length and infoldings. Source: Media & Society Journal.

Reference
- Clegg, Comp Biochem Physiol B Biochem Mol Biol (2001); 128(4): 613-24


What is the energy cost of an action potential?

There's a few [1, 2, 3] sources that claim it's on the order of $10^8$ ATPs per action potential. The first paper (which is a review that cites the second paper) also has some equations for converting from ATPs to free energy, although that's going to be very context dependent.

If you can't access the third paper, someone has helpfully entered the relevant figures into the bionumbers site.


Does pupil size affect image focus in persons with no lens?

Very nice question! You are right, in that small pupils will help to reduce the blurriness of vision caused by refractive errors.

Removal of the lens (aphakia) results in farsightedness. It is caused by a focus point that falls behind the retina as the absence of the lens prevents focusing of the image, causing a blurred image. The amount of blur is proportional to the pupil size (Colichia et al., 2008). See their figure 2 below:.

In the upper part you see a hyperopic eye, which has a lens that cannot accommodate sufficiently, comparable to an aphakic eye. the bottom part shows the result of when a pinhole is applied, namely a reduction of the blurred circle and improvement of the focus. This could also be achieved by having very small pupils such as when ambient light is very bright (and a characteristic of the Moken peoples when diving (Gislén et al., 2003). And indeed, under conditions of low lighting the pupil size will increase and hence blurring will be worse.


Ways to distinguish between purifying selection and selective sweep

Welcome to Biology.SE!

I actually recently went through the literature on this and similar subject, so I'll be happy to answer.

The answer will not be easy to formulate as a number of authors are working and arguing on the question. I will try to give a quick overview of methods.

Definitions: Background selection and selective sweep

First off, let's use the correct terms. As you decribed, both positive and purifying selection is reducing genetic diversity at nearby loci. When the reduction in genetic diversity is caused by positive selection, we call the process selective sweep . When the reduction in genetic diversity is caused by purifying selection, we call the process background selection.

What affect background selection?

Recombination rate
Strength of selection.

For a given neutral locus at distance $r$ centimorgans from a locus under purifying selection, the selective coefficient $s$ that is causing the highest decrease in genetic diversity is $s=r$ (Nordborg 1997).

Mutation rate
population structure

What affect a selective sweep?

Strength of selection
population structure
Number of loci involved under adaptation
Whether adaptation comes from de novo mutation or standing genetic variation

By the way, you might want to have a look at the terms 'soft sweep' vs 'hard sweep' in relationship to the two last elements of the above list and in relation to local adaptation.

How to disentangle Background selection from selective sweep?

There are a number of technics but again all of that is a work-in-progress. I would like to classify these methods into three themes.

Environmental covariate

This first element talks about disentangling local selection from background selection. It is maybe not exactly what you asked for but this discussion often comes to center stage in the literature talking about both.

If we assume to know the environmental variable causing the adaptation, then you can compare divergence between population present in different environments and those present in the same environment. If loss of genetic diversity is caused by local selection, then divergence should be higher between population occurring in difference environments. If loss of genetic diversity is caused by background selection, then all populations will show similar divergence. Bayesian Technics such as BayEnv2 (Gunther and Coop 2013) take advantage of this technic.

Among lineages comparisons

By comparing related species, it is possible to find out regions of low genetic diversity. If all related lineage show similar loss of genetic diversity irrespective to the existence of an adaptive event, then the loss of genetic diversity is likely caused by background selection.

From such methods (but I might not totally understand them, I should read the paper again), some authors (such as McVicker 2009) have build B-map and recently implemented in BayeScan (Huber et al. 2016; BayeScan is an Fst outlier method to detect local adaptation), that is map of the genome of the intensity of background selection measured by the B-value introduced by Charlesworth (history of the term reviewed in Charlesworth 2012)

Allele-Frequency-Spectrum

Both background selection and a selective sweep affect the Allele-Frequency-Spectrum as to cause an excess of rare alleles (Tajima's D < 0). However, the strength of the effect and the detailed effect on the Allele-Frequency-Spectrum is not quite the same and some authors have suggested to use such differences to disentangle the two.

Reading suggestions

There is a lot to read on the subject. I would recommend the recent special issue in Molecular Ecology DETECTING SELECTION IN NATURAL POPULATIONS including the review Haasl and Payseur 2016.


How many almonds a day can cause toxicity for vitE?

You can eat bags and bags of almonds every day for years and not be in any risk of vitamin E toxicity. There are many, many cases of adults consuming 500+ mg of Vitamin E every day, for years on end, with no signs of harm.

In general though, the max daily recommended value of vitamin E consumption is 1000mg. One cup of almonds (100g, or ~100 kernels) contains a little under 30mg of vitamin E. That being said, you can consume over 30 cups of almonds in one day before reaching the daily recommended limit.

You would have to eat tens of hundreds of thousands of almonds for there to be any kind of health concern.. at which point, you would probably suffer from other conditions than vitamin E toxicity.

You (should) have nothing to worry about.

EDIT: Here are a couple sources...

This page has everything about recommended limits, research that has been done, tables with daily limit values, etc.
US Department of Health and Human Services - National Institutes of Health

  Research has not found any adverse effects from consuming vitamin E in food.

This page contains basic nutritional facts for almonds. A 95g serving is about 90 whole kernel almonds. Nuts, Almonds - Nutrition Facts

  Serving size 95 g ... Vitamin E (Alpha Tocopherol) 24.9 mg


How does the size of insert affects the rate of Homologous Recombination in yeast?

As pointed out by aandreev, the greater the size of the insert relative to the flanks lower will be the recombination rate. This is because the donor DNA essentially becomes non-homologous. See the figures below:

  Figure1: Effect of insert size on recombination efficiency. Kung et al. (2013) Appl Environ Microbiol. Mar;79(5):1712-7

  Figure2: Effect of flank size on recombination efficiency. Kung et al. (2013) Appl Environ Microbiol. Mar;79(5):1712-7

However, you mentioned that you want to make gene knockouts. In this case you just need to make a small mutation (for example introducing a premature stop codon).

Use of genome editing tools such as Crispr-Cas, ZFN and TALEN increase the rate of transgenesis by introducing DNA double strand break.

These can also be used for making knockouts when NHEJ dominates over HR as the DNA repair mechanism. NHEJ is error-prone and can cause indels that can disrupt gene function.


How does the creative process of Biological Evolution work?

Your basic problem is indeed a fundamental misunderstanding of how DNA and by extension its evolution works. First of all, there is no such thing as "correct" or "error", there are only changes, some of them are better for the individual and some are worse. You also have a basic misunderstanding of the concept of information. An error does not decrease the amount of information, it just alters that information. For example, consider this sentence:

  The book is read

Say I make a simple error when I transcribe it:

  The book is red

The two statements contain the same amount of information. Nothing has been lost, only changed. But that change created new information. Now what if I try a different change:

  The book is rled

Now, this one is nonsensical, indeed, but how does that translate into DNA?

The computer analogy is a bad one. Programming languages have a very specific set of rules and anything outside those rules results in an error. For example, while this is a perfectly valid statement in many scripting languages:

print "Hello World"

This one is not:

priint "Hello World"

That, however, is not the way that DNA works. DNA is read in words of three characters, the codons. Every single possible
combination of those characters actually has a meaning. Therefore, a mutation like that above which would decrease the information content of the sentence (here, the gene) is not possible. Let's quantify. The DNA sequence consists of a long series of chemicals, commonly known as A, C, T and G. Since these are read in "words" of three "letters", this means you have:

$$4^{3} = 64$$

64 possible combinations. Of these 64, 61 are words with a specific meaning and 3, the STOP codons, are punctuation marks, full stops if you will. In other words, all possible combinations of letters have meaning in DNA.

Because all possible 3-letter combinations have meaning, no change will affect the information content of the "sentence". All it can do is change it. Now, changing the information can indeed result in "sentences" that make no sense. In the DNA world, this most often results in what are known as deleterious mutations. These happen all the time, but the result is usually a dead individual. Those with such mutations are not even born (speaking of mammals).

However, other mutations, such as the change from read to red that I mentioned before, can give rise to a change of meaning, this change, if it turns out that it makes the individual carrying it more likely to reproduce, will spread across the population and will be selected for. That is how new traits can arise.

In closing, another point that you have misunderstood is that evolution is not a path from the least to the most complex. In many ways it is the inverse. In fact, by any measure that counts, bacteria are far more "evolved" than humans for the very simple reason that the only way you can measure evolution is in terms of numbers of generations. Think of evolution as happening every time a species reproduces, this means that bacteria have had orders of magnitude more time to evolve than mammals have. Still, this is a useless comparison which is why nobody compares species by how "evolved" they are. For a discussion on that, have a look here.


After some Googling, it seems maybe this is a stinkhorn fungus, specifically Aseroe rubra.


Question about cell signaling pathways (RTK, Jak-Stat, SMAD, etc)

@Alexandria Jak/Stat are two families of proteins which mediate signals through phosphotyrosines.

JAK is a tyrosine kinase which binds to cell receptors and STAT is dimerized by JAK action.  JAK specificity seems to be your question.  A specific JAK protein (e.g. JAK1 or JAK2..) may mediate for different receptors in different cells.

There may be hetero- or homo-dimers of JAK, there may be more than one receptor in a cell using the same JAK enzyme, which may result in cross-talk between the two signals.  I think its a pathway dynamic that can vary quite a bit from one cell to another, depending on the receptor and cytokine environment the cell is seeing. JAK action can be modulated by any number of proteins which respond to other pathway signals or the cell state.  The diagram below from a review of heart muscle cell JAK action is not unusual nor is it complete.


What type of tree is this? (Coyote Hills)

I guess it is Schinus molle (Peruvian pepper)


Does minimizing hunger maximize weight gain?

Regarding the question in your title: minimizing hunger could be synonymous with leptin responsiveness. For example, leptin deficient or leptin resistant mice are known to become extremely obese - this is because leptin, the 'satiety' hormone, not only signals for you to stop eating, it also elevates the body's energy expenditure and stimulates thermogenesis.

An interesting strategy I've heard, though I don't know how effective it is, is increasing leptin sensitivity through the composition of your diet.

Another interesting element is that hunger, which is mediated by hormones such as ghrelin, decrease energy expenditure by multiple metabolic methods. So being hungry isn't always conducive to losing weight.

I believe most of the answer to your questions relies in these concepts. If you're talking about food distribution throughout your day, schedule it so that you're not very hungry for prolonged periods. Same with food type, eat foods that satiate for longer periods of time, unlike foods such as white rice.

If you want to read up a bit more, I suggest looking into AMPK, and the role these hormones and food composition has on it. AMPK reading


Why do viruses cause different symptoms?

every virus having differ differ spike proteins so they make infection  a particular type of cell ( just like HIV that only bind with CD4 type of receptor) and make effect. another fact is that every virus have different genomic marital so that have different codon and these different codon make different protein and that different proteins make different effect on host cell metabolism that's why different virus having different symptoms.


Oral polio vaccines are delivered in the site of the potential infection. You may think about them as about a realistic simulation of the infection. As it is not scientifically sound explanation, please see the answer about whether intramuscular vaccination leads to intestinal IgA secretion which protects against intestinal route of infection.
Oral polio vaccine (Sabina) contains attenuated (alive but weakened) polio virus, which can proliferate and compete in the environment with the really dangerous wild polio virus. That way also people which has not been  directly vaccinated may be protected - both by development of immunity after less severe infection, and by reduction of exposure to the wild virus.
The route of delivery is much more acceptable by children.


How to make GABA pass the blood brain barrier?

Short answer
Chemical reversible shielding of the aminogroup in GABA seems to be sufficient to get it into the brain as a Trojan horse.

Background

Given that you ask

  ...how to make GABA pass the blood brain barrier?

I assume that

You wish to elevate GABA by exogenously administering a compound;
That compound has to cross the blood-brain barrier (BBB) and physically turn into GABA;
A drug indirectly elevating GABA through unknown (e.g., GHB) or known mechanisms (Gabapentin) does not suffice your needs.
If you are happy with indirect actions, the links above will help you out. Now on to the real stuff :-)

GABA (Fig. 1) has 3 hydrophylic groups that may prevent it to cross the blood-brain barrier (BBB), namely a hydroxyl-, a keto- and an amine-group. The BBB generally only permits passive entry of small hydrophobic molecules. The amino-group in turn is also prone to de-amination by mono-amino oxidase inhibitors.

An often-used method to get drugs into the brain is shielding of pesky hydrophilic and/or fragile chemical groups by certain molecules that are irreversibly bound to them. A well-known example of shielding a fragile amino-group is the B-methylation of phenetylamine compounds into their amphetamine analogues. Alpha-amination to a methamphetamine further stabilizes the essential amino-group. Amphetamines and methamphetamines are way more stable in the brain than their phenetylamine precursors and likely enter the BBB also more swiftly because they are more hydrophobic by shielding the amino group (Shulgin, 1990).

However, those methyl groups are irreversibly bound, so it's not an option here, as apparently you wish to increase GABA, and not an active derivative of it.

Now, another way is using a Trojan horse method (Pardridge, 2006); by reversibly shielding the essential amine group the drug can enter the brain, where it is converted back to its original compound. Picamilon does the job here. Smarter Nootropics say;

  First developed in the early 1970s in the Soviet Union, picamilon (alongside phenibut) is an “enhanced” form of GABA that is capable of crossing the blood brain barrier when taken as a supplement.Inside the brain, picamilon is rapidly hydrolyzed into its constituent parts; niacin and GABA. Niacin helps to enhance brain blood flow through its vasodilatory properties [].

Fig. 1. GABA and Picamilon. source: Smarter Nootropics

Reference
- Pardridge, Discov Med (2006); 6(34):139-43
- Shulgin, PIHKAL, Transform Press, U.S. (1990)


The exposure to environentally occurring Mycobacteria causes a immune response to these (mostly unspecific, since no real infections occur). It seems that immunizations with BCG in these individuals is causing either no, or only a very attenuated immune response
This is shown in this ("BCG-induced increase in interferon-gamma response to mycobacterial antigens and efficacy of BCG vaccination in Malawi and the UK: two randomised controlled studies.") in which individuals with a high environmental exposure to mycobycteria showed only a very small response to this vaccination. If this natural level of immunity is enough to produce immunity to tuberculosis is unknown (and can not be tested for obvious reasons).

Another possibility is that the natural occurring immunity blocks the vaccine strains so they get eliminated before they induce an immune response. See here.
This is called the masking theory,if you want to read further, have a look at this three reviews, they give a good overview over the field:

TB vaccines: progress and problems.
A novel TB vaccine; towards a strategy based on our understanding of
BCG failure.
The success and failure of BCG - implications for a novel
tuberculosis vaccine.


What determines whether an action potential is inhibitory or excitatory?

Short answer
The physiological state of the postsynaptic cell ultimately determines the effect of an incoming action potential.

Background
An action potential occurring in a chemical synapse is neither inhibitory or excitatory. An action potential is a binary '1', an-all-or-nothing signal without any information, i.e., there is not a -1 or +1 action potential. Similarly, there are no excitatory or inhibitory neurotransmitters.

Notably, the principal excitatory neurotransmitter in the nervous system, glutamate, can have inhibitory effects dependent on the receptor activated. While most metabotropic glutamate receptors (mGluRs) and ionotropic AMPA and NMDA receptors are indeed all excitatory, the inhibitory glutamate receptors (iGluRs) are not (Cleland, 1996).

Conversely, GABA, the principal inhibitory neurotransmitter in the nervous system, can have excitatory postsynaptic effects. For example, hyperpolarized neurons may actually depolarize upon GABAA receptor activation, simply because the resting membrane potential is more negative than the reversal potential of Cl- (i.e., Cl- flows out of the cell due to the negative membrane potential) (Marty & Liano, 2005).

The existence of both excitatory and inhibitory glutamate receptors shows that it is the postsynaptic receptor that determines whether an action potential will inhibit or excite the postsynaptic neuron. The excitatory effect of GABAA activation shows that on top of that, even principal inhibitory neurotransmitters (GABA) with principal inhibitory receptors (GABAA) can excite a neuron dependent on its physiological state.

Besides chemical synapses there are electrical synapses. In these synapses action potentials are transmitted directly electrically through gap junctions. In this case, any action potential is excitatory as the signal will be carried forward if it is strong enough (Purves et al., 2001).

References
- Cleland, Mol Neurobiol (1996); 13(2): 97-136
- Marty & Liano, Trends Neurosci (2005); 28(6): 284-9
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates; 2001.


How do plants benefit from their seeds being buried?

Excellent question!

The main reason why us humans bury seeds seems to be to keep seed-eaters from finding them, though any historical evidence that could conclusively prove why we started doing that is probably lost to time, since we discovered agriculture before we began writing things down. Beyond that, you've rightly identified a number of advantages to burying seeds.

First, it may be helpful to note that no physical substrate is even necessary for plant nutrition. We can actually grow plants in mid-air, but for the fact that we would still need something to keep them still. Seeds will germinate if you simply spray nutrients at them - see aeroponics. This is because plants take in what would be soil nutrients via cation exchange and diffusion, as opposed to more a more active process like phagocytosis. By surrounding the seed with nutrient rich substrate, we inadvertently improved germination by exposing more of their surface area to nutrients.

As far as soil seeking behavior goes, Thomas Knight demonstrated that plants can actually find the ground by following gravity. He did this by sticking seeds onto a rotating disc to simulate gravity in another direction and germinating them there. The seeds responded by growing roots away from the center and sprouting stalk towards the center.

Of course, burying seeds too deep means that they may run out of energy before they can break the surface. However, it seems that many varieties of seed have a better chance of germinating in darkness.

Resources

On the Direction of the Radicle and Germen during the Vegetation of Seeds
A Reversible Photoreaction Controlling Seed Germination


Crassula tetragona, also known as mini pine tree (for its extreme use in bonsai technique), native to South Africa.

It is a succulent; a xerophyte (a kind of plant which needs very less water for survival), characterised with fleshy leaves developed due to evolution for storing water, this plant attains a height up to 3 meters.

Flowering in this plant usually take place in summer season, the flowers are yellowish orange and white.


Homology ratio comparison between different species

1.Is such an approach trying to quantify homology? Which i know is not correct as homology is qualitive measure.

A common approach to identify orthologs (homology between two genes resulting from a speciation event) it 'best bidirectional match': if you blast gene A (in species 1) against all genes of species 2 the best match is gene B, and if you blast gene B against all genes of species 1 the best match is gene A.

2.Can we compare the ratio of homology between the above 2 couples od species or such a comparison is biased?
3.Shouldn't the ratio of homology be proportional to the evolutionary distance of the organisms (according to conservation)?

Not necessarly. The fact that two genes diverged a very long time ago does not prevent them from being homologous. Homology is about shared ancestry (here of two genes) and not about evolutionary distance.
Could you clarify how you get the homologies? Did you compute them yourself (if so how) or did you use a specific database?