I am not 100% sure that I understand the question, but I am going to try to answer, based on the following assumptions:

The "number of 3 and 4 node motifs" is not very clear. If I understand correctly, it should be a quantity determined in large part by the degree distribution. You could rewire your network to lose all information about the TRN other than degree distribution and this number is probably very similar (or it is a quite weird network, which would make me suspicious of the data).
Therefore, the number of such motifs of size $k$ is not particularly interesting biologically, specifically due to technical issues such as incomplete ascertainment of edges, etc. The true network may have many more edges, and this will change this number, so the degree distribution is not itself interesting- it is in fact the thing you want to control for.
Therefore, when you compare with randomly generated networks and find different numbers of motifs of $k$ nodes, I suspect the random networks were generated with a different degree distribution. (It is pretty easy to generate networks of the same degree distribution, using e.g. the rewire() function in igraph)
Therefore, I interpret the question to be more specifically: "Among all 3 and 4 node motifs, a subset are overrepresented in my TRN compared to randomized graphs of the same degree distribution. What are some ways to interpret these motifs?" This is the kind of question that is traditionally asked with TRNs in my experience.

As an example of how other groups have analyzed TRN motifs, I suggest looking at Figures 5 and 6 of this paper. For instance, the "feed-forward" motif is overrepresented for links involving some TFs. I believe that it is standard to compare motif distributions to other biological networks, such as the C. elegans neural network. There are references in the Cell paper that could probably help you out further. The wikipedia article on network motifs also looks to have some information, and there are other resources on the internet if you google.

While there is not necessarily a strict biological interpretation of such motifs, they nonetheless can be informative in identifying specific patterns peculiar to different TFs or master regulators.

Caveat
It is possible that I have misunderstood the question or made bad assumptions- my graph theory is superficial. But if I am wrong and you are actually interested in the simple number of motifs of size $k$, that observation is of interest as a "I have a weird graph" theoretical problem, not as a "this is biologically interesting" problem. As a biologist I would care much more about which specific motifs of size $k$ you have, rather than the summed count of all motifs of size $k$.

On the other hand, forgetting about motifs for a moment, a "weird" network could be quite topologically interesting biologically. For instance, do your different clustered components associate with different pieces of biology, like sugar metabolism vs. morphogenesis? That would be expected, but it has very little to do with motifs- they may just be a side effect of that functional topology. In that case, it would be not only degree distribution but also that topology that you would have to control for to make interesting statements about motifs.

good luck!


Why is Artemisinin Compound Therapy preferrable over Artemisinin therapy with regards to drug resistance?

The idea is rather simple. When an antibiotic is used, it becomes a driver to select for a mutant that has resistance towards the antibiotic. Let say the probability for that happening is P1 (Lets say 1 in 10, 0.1).

When you use two antibiotics with different modes of attack, the probability of acquiring resistance to both is P1 x P2. (Let say P1 =0.1 and P2 = 0.15). So P1 x P2 = 0.1 x 0.15 = 0.015

Hence the probability of becoming resistant to both antibiotics at the same time is very much lower. And as the antibiotics are always used together, the time a bug needs to develop resistance to the therapy becomes longer. The duration which you can use the drug is increased.


How to determine the direction of regulation of a gene by comparing gene expressions?

If you have control expression values $c$ and e.g. disease expression values $d$, you take the ratio: $\frac{d}{c}$. If this is greater than one, it's up-regulated. Usually, the log-ratio is computed: $log\frac{d}{c}$. Now, if this is positive, the gene is up-regulated.

Gene expression values are usually measured genome-wide and then normalized before computing the ratios. So you rarely deal with individual raw expression values.


Non-fatal / low-harm measurement of Drosophila traits

You could do negative geotaxis (climbing) assay, (larval or adult) locomotion assays, % brain vacuolisation (after the flies die), maze tests. There are probably much more but these are all I can think of that are no-lethal and can be applied to males and females and some larval work too.

You could maybe consider doing starvation assays and longevity in some of your populations.


Troubleshooting bioconjugates migration in a SDS-PAGE gel?

The first step in troubleshooting is to run controls - run lanes with your protein input alone, and the conjugate alone (you may need to play with the type/percentage of the gel if the conjugate molecule is much smaller than your target protein - attaching biotin to a 50 kDa protein, for example) to see if the smear shows up. Depending on the type of conjugation you're using, the number of acceptor sites on the substrate, and the time and conditions of the conjugation reaction, you may be adding a highly variable number of conjugate molecules to your substrate. For example, when I first started working with adding fluorophores like Alexa and DyLight dyes to antibodies, the fluor/protein ratio was highly variable from reaction to reaction and between antibodies in the same reaction.

This is most likely what is happening in your case - the number of conjugate molecules being added to each substrate molecule is highly variable. If you haven't already, I'd suggest getting in touch with your conjugation kit vendor's tech support, as they likely encounter this problem all the time. You may need to change the type of conjugation chemistry, get a higher-quality conjugate, or purify the substrate before and/or after the reaction. One of the solutions to my antibody labeling problem I mentioned above was to purify the reaction products through a size-exclusion column. This had the dual effect of separating out the un-reacted antibody and fluorophore, and allowing us to pick different fractions of the conjugated product and decide which were best for our needs.


why did capacity of regeneration decreased in evolution?

Evolution made life more and more complex. The more complex the "bodyplan" of an organism became, the more different tissues and cell types it has, the more difficult it is to regrow them.
For example a sponge has about 3 different cell types. If you take a small piece of a sponge, these 3 cell types well still be present and once they grow they can form a whole new sponge.
The more complex you go, the more different cell types you need, and thus the harder it becomes for a few cells to represent a full organism.

It also has to do with symmetry. Sponges have none, cnidarians have radial symmetry, mammals bilateral. To put it simple: if you slice a piece out of a jellyfish like you would out of a pie, it's easy to imagine it can 'close' itself with new tissue coming out of the border tissue, because it's the same tissue as the one you removed. If however you cut of a foot of a human, the cells of the leg won't produce new foot cells, because they are (a lot of different) 'leg cells'.

As for the lizards, they can "regenerate" a tail but it is never the same tail as before, it will always be shorter than the one they lost. Also the tail is still pretty 'simple' (if you can put it that way). If you would cut of a lizards leg it would not regrow...

I hope this has somewhat answered your question!


Difference between AjuA and ajuA in biosynthesis

It's just the nomenclature:

  Bacteria: Gene symbols are typically composed of three lower-case, italicized letters that serve as an abbreviation of the process or pathway in which the gene product is involved (e.g., rpo genes encode RNA polymerase). To distinguish among different [but related genes], the abbreviation is followed by an upper-case letter (e.g., the rpoB gene encodes the β subunit of RNA polymerase). Protein symbols are not italicized, and the first letter is upper-case (e.g., RpoB).

[source]

You can check out the Wikipedia article on Gene Nomenclature for more information.


When I took Microbio we had a entire lecture on this. My professor's view was that they do not survive due to the pH of the stomach.  He told us that there are microbiologist on both sides as to whether they do make it to the intestine (or enough of them to make much difference) or that they do survive and help. I have added a link below to a article by the American Society of Microbiology. Here it is saying that it may be helpful, but that more studies are being conducted.

http://cmr.asm.org/content/16/4/658.short


The source of ABA for inducing stomatal closure in the detached leaves?

I think that ABA could be one of the player involved on the stomatal closure in detached leaves. In fact originally it was think that ABA is the main player on abscisic leaf but this in correct only for a small number of plants. Moreover ABA is produce in terminal buds to slow down the plants growth and prepare it for the winter (it is also produce in response to water depravation by roots). So probably ABA could also migrate in leaves and provoke the stomata closure.
This is what wikipedia suggest by looking on Abscisic acid.

ABA was originally believed to be involved in abscission. This is now known to be the case only in a small number of plants. ABA-mediated signaling also plays an important part in plant responses to environmental stress and plant pathogens [...].
Abscisic acid owes its names to its role in the abscission of plant leaves. In preparation for winter, ABA is produced in terminal buds.This slows plant growth and directs leaf primordia to develop scales to protect the dormant buds during the cold season. ABA also inhibits the division of cells in the vascular cambium, adjusting to cold conditions in the winter by suspending primary and secondary growth.

By digging more on internet I found that abscission (the shedding hence the dropping of the plant leaves) occurs after the senescence of the leaf. In fact, before the leaf falling, the plant draws resources out of leaves and degraded the chlorophyll. This will cause also the change of colour (the leaves are green thanks to the presence of chlorophylls).
Finally I think that the stomata closure is also due by the darkness and the senescence. In fact the open or close state of stomata is mediate by guard cell and their state (swollen guard cell stomata is open, shrunken guard cell stomata is closed. Those state are influenced by Temperature, Darkness, Photoperiod, pH and also ABA. Hence when the plant start to take out nutriments from leaves, on leaves there will be a rise on pH and a diminution on water contents that will provoke the closure of stomata. Those two image could maybe help 3.

Hope my answer will help.


What are examples of genes succesfully reproducing in ways that is in conflict with helping the individual creating offspring

The prototypical example of this is t, whose existence was predicted by Robert Trivers and featured prominently in the Selfish Gene.  The current dominant point of view in evolutionary biology is that genes act in their own interest and even the 'self' is just a manifestation of the gene's reproductive properties.

t is a locus in some male mice. The t gene characterizes very well the selfishness of a selfish gene.  While most paternal genes are found in 50% of offspring, t is found in over 3/4 of offspring.  Somehow it manages to reproduce at the expense of the other loci in the male mouse.  t itself is not known to convey any advantages to its host organism.  the males tend to be smaller and sometimes even reproductively disadvantaged.

Does that go some way to answering this question?

Animal behavior such as cheating or adopting are often interpretable as reproductive advantages.  Killing the best and brightest definitely are to the advantage of those who are doing the killing.  This SNL Skit has always said it best to me. "... and now I am smart!".  Such kill offs so rarely include killing one's own offspring.  I'm not sure they can be called in conflict with reproductive advantage.  EO Wilson's essay "On Human Nature" does a reasonable case for saying that wars and famines are in fact produced by evolutionary advantage, however cruel and ugly they may be.


Screen brightness for reading in dark room

Not an answer, but just a suggestion:

If you are in a position where you must read off of a computer monitor without ample ambient light, I'd suggest you try setting your monitor/reader/whatever to have a dark background and light/wight text so it doesn't feel like you're staring into the sun.


Why do rabbits often have white hindquarters?

Apparently the most noticeable research on this subject of a rabbit's white behind has been done by Dr Dirk Semmann of the University of Goettingen. He proposes that

  these spots actually confuse predators because of their very
  noticeable nature. By focusing on the bright spot, the would-be
  predator ignores the larger body of the animal. Then, when the rabbit
  executes a sharp turn, the spot disappears and the predator has to
  readjust to focus on the camouflaged coat, losing vital seconds
  (reference 1, reference 2).

It could be the same reason for the white behind of a deer. As to why deer flag their tails, there is a paper on the subject which lists 4 possible reasons for the behaviour.

1) Flash behaviour

2) Alarm Signal

3) Cohesive signal

4) Detection signal

More can be read about it in this paper.


Purpose of intensive protein synthesis in G1 phase of mitosis

The G1 phase of eukaryotic cell cycle is part of interphase, which is when the cell is replicating its DNA ready for division. To understand the need for intense protein synthesis, we first need to understand how DNA is organised during mitosis.

Before DNA is condensed into chromosomes ready for nuclear division it is in the form of chromatin, a long fiber-like structure inside the nucleus. In order to condense into chromosomes, this chromatin must undergo a process of coiling and folding in order to create the chromosome 'X' structure we are familiar with.
A major part of this DNA 'miniaturization' is the folding of the double helix around proteins called Histones - this creates new structures called nucleosomes.

In order to fully condense the roughly 3 meters of DNA in the average human cell down to a singular chromosome, millions upon millions of these Histone proteins are required.

And that answers your question; intense protein synthesis during the G1 phase is required in order to produce the extremely large amount of Histone proteins that are needed for packaging DNA into chromosomes ready for cellular division.

As for carbohydrates, these are constantly being processed by the body in order for the production of ATP for use as energy. The use of said energy for mitosis is a just another constantly required use of ATP within the body. Therefore there isn't any noticeable increase in carbohydrate processing/production, as it is happening regardless of the cell's stage in its cycle.

-See the image below (from shmoop.com) that explains the process of getting DNA into a chromosome.


There are multiple answers to this question depending on who you ask (meaning, what their field of expertise is).

The biological dark matter from the wikipedia article in question seems to mean sequence from metagenomic samples which was not assigned to any of our commonly known domains of life. That might not necessarily mean that it does not belong to them. Sometimes it is hard to decide where a small particle of sequence informations belongs to, because it does not match anything we know. Still, it might be from a perfectly "normal" bacterium. Or it might be a result of sequencing errors.

Additionally, depending on how you assign a taxonomy to the sequence, there might be cases where there are so many different possibilities for where this sequence came from (because it is very conserved in a lot of different organisms, even from different domains of life), that this sequence will not get any taxonomy assigned. Not because there is none, but because we cannot safely decide which it is.
Some people also speak of this information as "dark matter".
There is for example this project which specifically is designed to study the dark matter we can (or at least for some reason do) assign to be microbes, but not more specifically.

Basically, any decision of where to place potential dark matter sequence is guided by our previous knowledge about the domains of life and the genomes of all those organisms. This knowledge is very incomplete.

I am sorry this answer lacks some more nice sources. Most of the information is based on my knowledge as a person working with datasets that might include "dark matter", if I would call it that. (I call it "not assigned sequence".) I don't have the time right now to add more sources, but if needed I can maybe add some later.

Edit:
As a fast add-on after re-reading your question: How much of the sequence is unassigned for example if one would study your gut depends a lot on what is actually there in you gut that we know, how diverse the community in your gut is, what database is used for comparison and how old this database is, how the data is preprocessed and analysed, and so much more. But yes, there is still a lot of genomic information in nature that has not made it into any database.


Disadvantage of using Drosophila for breeding experiment

All options given have advantages but become disadvantageous depending on experiment you are trying to do. Here question is asked for "breeding experiment". In these experiments it is very important to keep track of genetics. If females mates with males of some undesired genotype, it will ruin your experiment objective.

As option (c) is 'mating soon after emergence of flies' , females and males from same vial (which is generally maintained as single genotype) will start mating soon. Generally this time period is 4 hours. Drosophila melanogaster starts mating after 4 hours at room temperature. This is the precise reason in Drosophila, virgin collection is done within 4 hours of eclosion.

Imagine you want to set up cross between wild type and some mutant. You will grow them initially in separate vials. Now for crossing , assume you need females from wild type and males from mutant. In this step it is important that females should be virgin else it will be difficult to track your genotype later on. Now if Drosophila starts mating soon after emergence of flies, it is disadvantage for your breeding experiments.

Note: There is sperm competition but that is special case


Short answer
The pain withdrawal reflex can only be suppressed when touching something painful on purpose. Deliberate, conscious contraction of the extensor muscle before reflex initiation can prevent the contraction of the flexor muscles once the reflex is started.

Background
The pain withdrawal reflex arc (Fig. 1) receives input from sensory neurons that enter the dorsal part of the spinal cord via the dorsal root of the spinal nerve and synapse onto interneurons within the spinal gray matter. The interneurons in turn synapse onto motor neurons, which send axons that exit the cord via the ventral root. They conduct information to the muscles. The resulting withdrawal reflex is initiated by activating motor neurons of the flexor muscles (agonist), and simultaneous inhibition of the motor neurons to the extensor muscles (antagonist). This loosening of the antagonist while the agonist is being contracted is referred to as reciprocal inhibition (Crone, 1993). More important to the question is the fact that the motor response is well under way before the signals responsible for the conscious sensation of pain (which exit the reflex pathway in the spinal cord) ever reach the brain (Cornell University).

Fig. 1. Schematic of the pain withdrawal reflex arc. Source: Washington Uni.

Hence, the reflex pathway is initiated even before we are aware of any pain. The only possible way to suppress a reflex that is faster than perception is to start counteracting the agonist (flexor) before the reflex is initiated, i.e., by contracting the antagonist (extensor) before touching the painful object.

Reference
- Crone, Dan Med Bull (1993); 40(5): 571-81


Did we first have swimming birds or flying birds?

Flying came first, as far as we know. The earliest known bird (currently), Archaeopteryx lithographica, already had aerodynamic feathers (Feduccia and Tordoff, 1979). The Solnhofen Limestone, where it was discovered, is ~145 million years old, so we can place the "when" flight evolved to greater than or equal to that time.

Gansus yumenensis is regarded as the earliest aquatic bird and is dated from ~120 million years ago. The Hesperornithiformes are the sister taxon of Gansus (less derived) and also aquatic. However, they date from ~85 million years ago. It is not clear whether the ancestors of Hesperornithiformes were also aquatic. Because they branched off the main line of birds before Gansus, these ancestors would likely predate Gansus, but those relatives have not yet been discovered.


That is a silverfish, order Zygentoma (also known as Thysanura). Likely genus Lepisma (family Lepismatidae). Zygentoma are insects, and are the sister taxon to Pterygota (winged insects)


Are the asymmetrical positions of owl ears consistent across species with this trait?

This is a good question indeed. If owls with asymmetrical ear canal openings have different arrangements, it would suggest that the asymmetry has evolved more than once and arrived at different solutions.

The Cornell Handbook of Bird Biology (2nd ed.) states that the Boreal owl right ear is positioned higher than the left. Ornithology by Frank B. Gill (2nd ed.) states that the barn owl left ear is higher than the right. If both of these reports are accurate, then we have two species that differ.

The Wikipedia entry on Sound Localization in Owls (section 3) also suggests that the asymmetry of different owl species may be a product of convergent evolution:

  For example, in barn owls (Tyto alba), the placement of the two ear flaps (operculi) lying directly in front of the ear canal opening is different for each ear. This asymmetry is such that the center of the left ear flap is slightly above a horizontal line passing through the eyes and directed downward, while the center of the right ear flap is slightly below the line and directed upward. In two other species of owls with asymmetrical ears, the saw-whet owl and the long-eared owl, the asymmetry is achieved by different means: in saw whets, the skull is asymmetrical; in the long-eared owl, the skin structures lying near the ear form asymmetrical entrances to the ear canals, which is achieved by a horizontal membrane. Thus, ear asymmetry seems to have evolved on at least three different occasions among owls.

(Emphasis added)

I presume the source of the Wikipedia information to be from Konishi, Masakazu and Susan F. Volman, 1994, though it is not cited in the relevant paragraph.

Perhaps some other ornithological journals will have more specific information, perhaps even allowing us to trace these separate evolved structures. It may even become a great thesis project!


What is the attachment after this gene name, following the comma: SULF1,hCG18956?

Here, hCG stands for "human Celera Genome". hCG-prefixed protein and gene descriptors are used as a last resort for genes which are found only in Celera's database.

See for example http://www.ncbi.nlm.nih.gov/protein/119619226 , the gene you referred to as "hCG1809003". As the entry says, this was submitted by Celera in 2005 as a putative gene, after being found by "conceptual translation", that is, scanning the Genome Project data for start and stop codons. It is likely this gene has yet to be found as RNA or protein - because the only references for that gene are Celera's submission and the Genome Project paper. Nevertheless, Celera's sequencing (and microarray!) software and chips still look for it.

Your two example genes eventually made it to GenBank. The first example even has a proper name and function assigned - sulfatase 1. Many genes remain in hCG limbo.


You could upregulate the transcription of the receptor gene you are interested in. More receptors being produced = more receptors being expressed on the cell's surface.


Writing methods section on PCR amplication in a paper

Here's my take, just a few minor changes which are shown in bold (I have also changed ,to . for decimal numbers and added a few spaces where needed):

  PCR Amplification and sequencing

  A PCR reaction for sequencing was performed using universal primers ITS5: F:
  (5’TCCTCCGCTTATTGATATGC3’) and ITS4:R: (5'TCCGTAGGTGAACCTGCG C3'),
  including 5.8 S rRNA region (White et al. 1990). Amplification condition
  was performed in a 25 ml reaction volume and consisting of 10 µL
  nuclease free water, 12.5 µL Taq green master mix, 0.5 µL forward
  primer, 0.5 µL reverse primer, 0.5 µL DMSO, 1µL template. PCR was performed using a Biorad PCR machine. The thermal cycle was
  programmed for 90 s at 95 °C for initial denaturation, followed by
  35 cycles of 30 s at 95 °C for denaturation, 30 s at 55 °C for
  annealing, 90 s at 72 °C for extension, and 5 min at 72 °C for the final extension.
  PCR products were examined by electrophoresis at 100 V for
  30 min in a 1% (w/v) agarose gel in 1 x TAE buffer. The marker
  used a 1 kb DNA ladder. The electrophoresis gel was soaked in ethidium
  bromide for 30 min then examined in UV light.


What are some (bioinformatic) methods to characterize potentially novel gene transcripts?

It sounds like you have considered most of the obvious alternatives (and thank you for clarifying the question).  I suppose the first question in an alternatively spliced transcript with a retained intron is whether the open reading frame of the protein is maintained.  If there is a termination codon that now becomes in-frame due to the intron then the protein would ordinarily be truncated.  The mRNA could also get targeted for degradation due to the nonsense-mediated decay pathway (i.e., from introducing an early stop-codon).

If the alternatively-spliced transcript lacks any significant ORFs, or if there is an ORF but no suitable translation initiation codon then you have entered the realm of non-coding RNAs, of which there are two loose categories, microRNAs (there are several classes) or long non-coding RNAs.  most miRNAs have recognizable sequence motifs, may be contained in mir-Base, and may be complementary (in part) to a regulatory target elsewhere in the genome. lncRNAs are less well-defined. Perhaps the best criteria are transcripts that are stable enough to be detected, but lack noticeable protein coding features.  I don't even think there is a consensus on the minimum length of a transcript to be considered an lncRNA.

What sort of databases have you searched? For example the ancient dbEST contains all kinds of short cDNA reads from all over the planet, dating back to 1992 (or so).  Evolutionary conservation of exons and splice-sites, or reading frames can all be used to support the hypothesis that a transcribed region has a biological function.

For a really deep fishing expedition you can use tblastn, etc. to take a potential translated ORF and search all 6 conceptually translated reading frames of all the sequences in a database--it takes longer, and there can be many spurious matches that you have to search through, but if you are studying something that has never been annotated it might be worth considering.

RE: folding RNA (secondary structure) every sequence can be folded into some kind of structure (try it and see), but structurally conserved compact loops typically fall into one of a small class of selected families (like GNRY). Stems are easy to find, but if the single-stranded loop is huge, how likely is that structure to fold up in real time?

RE: TFBS not clear to me at all what you mean by this. Transcription factors bind dsDNA not ssRNA. There are families of protein domains that bind RNA but not typically with such sequence-specificity.  So unless this alternatively spliced transcript is being transcribed from some type of alternative promoter, I am not sure where you would even be looking for TFBS.  It's true that some large introns can indeed contain regulatory regions for the gene as a whole (cf. immunoglobulin heavy chain enhancer is conveniently stored in an intron), but it is not clear to me if that would have an affect when transcribed into RNA.

I do like your idea that a retained intron could now contain a binding site for a regulatory miRNA, but if I understand the theory this would lead to the transcript being degraded--so it would be more difficult to detect.


It would be interesting to see a picture of your centrifuge, which you appear to have built in a few days.
Centrifugation simply accentuates the effects of gravity, and since bacteria are denser than aqueous solutions they will move to the bottom of the sample to form a fairly tight pellet.
The conditions for your centrifugation will depend very much on the design of the centrifuge since as well as the rotational velocity, the radius of rotation is also important.
I found a suggestion on the internet to use a relative centrifugal force (RCF) of 12000 g for 2 minutes (I must admit that from memory I always spun slower and for longer than this suggests). Anyway...

using RCF = 1.12 * 10-5 * r *N2
r = radius of rotation
N is revolutions per minute
and plugging 12000 g into that, for a rotational radius of 10 cm, I get 3300 rpm.

Don't know if you can manage that with your machine, but as I say, a lower RCF with a longer spin will probably be ok as long as you can dilute the yoghurt sufficiently to reduce viscous drag. Of course if you have access to any microbiological growth media you could grow a standard liquid culture by inoculating some sort of broth with a small amount of yoghurt.
Try a Google image search for hand powered centrifuge to get an idea of what has been used in the past.
after comment from Mad Scientist
see here for a typical large table top centrifuge maximum RCF is 3120 g at 4600 rpm. You can certainly pellet bacteria in something like this in tens of minutes.


How do enzymes not change the overall energy change of the reaction they're catalysing if they lower the activation energy?

You're on a valley on one side of a mountain (representing some fairly stable state of your reactants), and you'd like to go to a town on the other side at a lower elevation (representing another stable state for your products, at lower energy than your current state: this is an energetically favorable reaction).
You can go over the mountain: high activation energy to climb up to the top, then you go down the slope to eventually get down to the town.
You can go through a pass between mountains instead: much lower activation energy to get over the pass, then you eventually get down to the town.
Whichever path you choose, you're at the same elevation (energy, $\Delta H$ compared to where you started), with the same products (your location in space), but if you took the pass you've gotten there via a different chemical route that was easier to achieve energetically at the peak.
Enzymes let you take the path through the pass rather than over the top of the mountain. They don't change where you started from or where you're going, so they don't change the overall energy of the reaction.


Why are potassium channels slower than sodium channels?

Short answer
The activation kinetics of Na+ channels are faster than K+ channels.

Background
Voltage-dependent channel gating basically occurs through three possible states of the channel: open, closed and inactivated (Fig. 1).

Fig. 1. Gating of a voltage-activated sodium channel. Source: Balseiro Institute.

Basically, ion channels are protein pores in the membrane. Upon depolarization, the pore opens, which is a process with fast kinetics in Na+ channels and slower kinetics in K+ channels (Lacroix et al, 2013). K+ channel activation is in the order of 6 times slower than Na+ channel activation. The slower inactivation of K+ channels allows sufficient Na+ to flow in the cell for the depolarization phase of the action potential to develop (Fig. 2).

Fig. 2. Action potentials and underlying Na+ and K+ currents. Source: Dundee Med Student Notes.

After opening, the channel is inactivated, which can occurs through a physical "protein-plug" as shown in Fig. 1, or through conformational changes in the pore. This inactivation again is fast in Na+ channels leading to a transient spike in the action potential, and deactivation is slower for K+ channels (K+ channels do not inactivate, but rather deactivate). This inactivation step results in the refractory period of a neuron (silent period after firing). The channel is then de-inactivated and converted to the closed state, after which the channel is again ready to participate in another round of firing.

Note that neurotransmitters do not activate voltage-gated channels directly. Neurotransmitters can activate ion channels, but those are ligand-gated ion channels, such as the nicotinergic acetylcholine receptor, AMPA receptor or NMDA receptor (Purves et al., 2001).

References
- Lacroix et al, Neuron (2013); 79(4): 651-7
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)


Why are there still useless traits/mutations in our body

Natural selection "selects" the trait that is less advantageous and removes/ reduces its frequency. It is like a filter paper. All solids are filtered out of mixture while clear liquid is collected. So if there is a difference in fitness of organisms by variations in traits, then only they are SELECTIVELY removed. Now, if a person without an earlobe would have had an increase in fitness, it would have had eliminated over time. And it might (I said might) be that there IS some pressure but it might be so slow that we can not realise it. But in case of earlobes, evolution will be evident in the case of elephants and Jackrabbits.


Why is it possible to make yoghourt with lactose-free milk?

Conversion of lactose to galactose and glucose is a part of the bacterial metabolism of lactose. So digested lactose would work.

In fact, it should work for all kinds of 6-carbon sugars as lactic acid is produced from pyruvate (end product of glycolysis). See Wikipedia:lactic acid fermentation.


It's a BLACK KITE (Milvus migrans). I bet you took the pics this summer because the great majority of the population is in Africa at the moment.

It is a black kite because:

rather uniform dark brown color
squared tail (it form a shallow v during gliding)
uniform underwing color and lighter head is a shared with marsh harrier but the absence of darker patch around the eye, the dark shoulder and 6 digitated primaries assure us is a black kite.

Here is a picture for reference:


What is the mechanism behind plants losing their leaves?

The process of a deciduous plant losing its leaves seasonally is known as abscission. It occurs when a layer of cells known as the abscission zone elongate and weaken, causing the leaf to fall off. It is mediated mainly by the hormones auxin and ethylene.

The functional purpose of abscission is to remove leaves when they are no longer producing a net gain of biomass. Leaves decrease in productivity during drought, decreased day length, and when under the effect of herbivory.

In some species (according to the day-length source), "When the daylength exceeds a certain 'critical' duration, growth may be
maintained continuously for at least 18 months under favourable temperature conditions, e.g., in Liriodendron tulipifera, Robinia pseudacacia". So, to answer your final question, some deciduous species (but not all) may indeed retain their leaves if they are grown in favorable conditions. One reason why not all deciduous trees retain their leaves even in favorable conditions is that internal ageing can also induce abscission: "In such species, growth is determined primarily by the endogenous ageing process and is only modified by environmental factors, including daylength"


Isopropanol precipitation of DNA - duration and magnitude of cold storage

For the precipitation you use different reagents: First you add salt under slightly acidic conditions to make sure that the DNA precipitates in a less polar environment. This is achieved by adding alcoholes like ethanol or isopropanol.

It is commonly thought that a incubation at low temperatures enhances the results, but this is interestingly not true. There is a paper from the Bethesda Research Laboratories which is called "Ethanol Precipitation of DNA." which analyzes these relationships (temperature, time and alcohol concentration) in great detail, its definitely worth reading.

Figure 1-3 from this paper shows the influence for Ethanol (but I am pretty sure that this is not much different for isopropanol):

I would prefer ethanol precipitation to ispropanol whenever possible. Isopropanol co-precipates salts, so you have to wash a few times with 70% ethanol and it is less volatile than ethanol, so the drying step takes longer. Its also less effective cleaning organic compounds like phenol away and sometimes the pellets are harder to see.

On the other it can be useful when you have to deal with large volumes, since you only need 0,7 volumes of isopropanol compared with 2,5 volumes of ethanol.

Precipitations with Isopropanol are usually not incubated but centrifuged directly after mixing. Here is a protocol from my lab (which originally came from Qiagen, if I remember correct):

Adjust the salt concentration, for example, with sodium acetate (0.3
   M, pH 5.2, final concentration) or ammonium acetate (2.0–2.5 M,
   final concentration).
Add 0.6–0.7 volumes of room-temperature isopropanol to the DNA
       solution and mix well.
Centrifuge the sample immediately at 10,000–15,000 x g for 15–30 min
   at 4°C
Carefully decant the supernatant without disturbing the pellet.
Wash the DNA pellet by adding 1–10 ml (depending on the size of the
preparation) of room-temperature 70% ethanol. This removes
co-precipitated salt and replaces the isopropanol with the more
volatile ethanol, making the DNA easier to redissolve.
Centrifuge at 10,000–15,000 x g for 5–15 min at 4°C
Repeat the washing and centrifugation steps once more.
Carefully decant the supernatant without disturbing the pellet.
Air-dry the pellet for 5–20 min (depending on the size of the
pellet).
Redissolve the DNA in a suitable buffer.


Probability of Extinction under Genetic Drift

update

The answer is here!

Original comment/answer

Kimura and Ohta (1969) showed that assuming an initial frequency of $p$, the mean time to fixation $\bar t_1(p)$ is:

$$\bar t_1(p)=-4N\left(\frac{1-p}{p}\right)ln(1-p)$$

similarly they showed that the mean time to loss $\bar t_0(p)$ is

$$\bar t_0(p)=-4N\left(\frac{p}{1-p}\right)ln(p)$$

Combining the two, they found that the mean persistence time of an allele $\bar t(p)$ is given by $\bar t(p) = (1-p)\bar t_0(p) + p\bar t_1(p)$ which equals

$$\bar t(p)=-4N\cdot \left((1-p)\cdot ln(1-p)+p\cdot ln(p)\right)$$

This does not answer any of the two questions!

This answer gives...

the average persistence time

but not...

the probability of fixation rather than extinction if we wait an infinite amount of time

neither...

the probability that the allele get extinct over a period of say 120 generations.

Can someone improve this answer?


Does the mesoderm evolve from the ectoderm or the endoderm?

In human,the mesoderm doesnot develop from the endoderm or the ectoderm.It develops from epiblast of the bilaminar germ disc stage.

During the week 3 of development, the epiblast of the disc invaginate and divide rapidly to form the cells of the endoderm.The division is rapid enough to replace the hypoblast layer.

Even after the endodermal layer has formed, the epiblast continues to divide at the region of the invagination.The divided cells migrate between the epiblast(soon to be the future ectoderm) and the newly formed endoderm to form the mesoderm.

REFERENCES:

Langman's Medical Embryology (13th edition) T.W. Sadler
website


This is because rabies is a viral infection of nervous tissue that propagates through peripheral nerves into the brain and causes brain tissue inflammation (encephalitis).

As long as the virus is in the brain there is no way to get rid of it. The main trade-off here is that everything that would kill the virus will be as (or even more) aggressive against the brain tissue, and impairment of the latter will lead to really heavy deficits in vital functions like breathing and thermoregulation.

The first manifestations of rabies are those due to brain damage. This means, the virus is already there and the brain is already fatally damaged.


Is there a command line molecular cloning tool?

Making maps of plasmids Annotating plasmids with common features

Plasmapper works through commandline

  Finding restriction sites

Simple regex searches can do that

  Mapping Sanger sequencing reads

BLAST will do it.

  Showing sequence, reverse complement of the sequence, translations in
  different frames

EMBOSS has a collection of tools for these things. (getorf is a tool for finding ORFs)

  Designing primers for specific applications (such as
  Gibson cloning)

Primer3 works through commandline

You can just download the entire EMBOSS collection. It has many useful tools.


Can anyone identify the worm in this video clip?

I think it's a Gordian worm or more accurately known as Spinochordodes tellinii . Good music for a parasitic event like that by the way. Nematomorpha is the phylum.

If your a molecular guy, check out Spinochordodes tellinii and the WNT pathway, pretty cool stuff.


Why is traditional rank based taxomomy considered by some as logically inconsistent with phylogenetic knowledge?

You can find discussions of problems with rank-based taxonomy in light of phylogenetics in Ereshefsky 1994, de Queiroz 1996 and Ereshefsky 2002. To summarize, the main problems they identify are:

It's hard to define what exactly an "order", "family" or "genus" is; in particular, taxa at the same rank aren't always comparable. For example, order Hymenoptera, which evolved 250 million years ago and consists of over 150,000 species, with order Carnivora, which evolved 42 million years ago and consists of "over 280 species".
Not enough ranks: NCBI recognizes 29 higher taxa for Homo sapiens. That would require dozens of sub-and-super ranks to render into Linnaean taxonomy.
Names based on ranks: current nomenclature allows certain ranks to be identified by their ending, for example names ending in "-ini" refer to tribes (e.g. Hominini, Canini). If one of these tribes turns out to be non-monophyletic, it may have to be moved to a higher or lower rank to keep its monophyly -- which would have to be renamed, increasing confusion.
Redundant taxa: take division Ginkgophyta. It contains a single class, the delightfully named Ginkgoopsida, which contains a single order, Ginkgoales. In the Linnaean hierarchy, each of these taxa contains the next one along, but in terms of monophyly, they are exactly identical to each other, as they share exactly the same most recent ancestor.


How does air pass through when we breathe through the mouth?

The oral cavity and the nasal cavity merge into the trachea which yield to the lungs. As a consequence one can breath in and out through the nose or the mouth.


"Recurrent" might be the term you are looking for, i.e.:

running or turning back in a direction opposite to a former course —used of various nerves and branches of vessels in the arms and legs

https://www.merriam-webster.com/dictionary/recurrent

If you observe a recurrent network within a single pair of neurons, you could also refer to this as a reciprocal connection, in that a pair of neurons are both post-synaptic and pre-synaptic to each other.

More generally, you could also talk about feedback as a general motif in neuronal circuits.

The function of recurrent connections likely depends on the specific network you are talking about, but they can be used for predictive coding, pattern generation, computation, and more. In organisms with 'simple' nervous systems like C. elegans, however, these connection patterns can be even more complex, because they have evolved to perform a lot of behavior with very few neurons.

Try searching Google scholar for recurrent neuronal circuits for some more information.


What are most common natural causes of death?

The WHO has data from 2002 where they have classified and counted causes of death. I have treated the following as natural causes:

Cardiovascular disease (29.34%)
Infectious & Parasitic disease (23.04%)
Cancers (12.49%)
Respiratory disease (6.49%)
Perinatal conditions (4.32%)
Digestive disease (3.45%)
Neuropsychiatric disorders (1.95%)
Diabetes (1.73%)
Genitourinary disease (1.49%)
Maternal conditions (<1%)
Congenital abnormalities (<1%)
Nutritional deficiencies (<1%)
Endocrine disorders (<1%)
Neoplasms (<1%)
Musculoskeletal disease (<1%)
Skin disease (<1%)

I treated the following as non-natural causes:

Intentional injuries
Non-intentional injuries

The sum of the groups explains 96.7% of deaths. I think the remaining 3.3% would be other or undetermined causes, and rounding errors in the data. The natural causes accounted for 87.9%, and non-natural causes were 9.1%. The most common causes were cardiovascular diseases, infectious/parasitic diseases, and cancers.

It is difficult to assess how natural the cause of deaths are. For example, many cancers, cardiovascular, and respiratory diseases are more common in obese people and smokers (often self-inflicted damage), nutritional deficiencies are often caused by failing welfare and social systems.

Additionally, among the recorded causes of death in England and Wales in 2011, of the total 484,367 deaths recorded, 17,590* deaths were from extrinsic sources (accidents, homicides etc.). This is around 3.6% of deaths. In this data, the most common causes were cancers (29.6%), circulatory diseases 28.8%, and respiratory diseases (14.0%).

According to the CDC, in 2013 there were 2,596,993 deaths in the US, and 92.5% were of natural causes. Of those, the principle causes were heart disease (24%) and cancer (23%). There's a good table at the bottom of this site.

Rates of natural and non-natural causes of death will likely vary greatly by country given different health risks (e.g. malaria in Africa vs Europe), health care services, extrinsic risks (e.g. traffic accidents in Sweden vs India).

$*$ The table in the article features a potential mistake, it seems the columns are incorrectly labelled


Why does the number of mutations per individuals follow a Poisson distribution?

A Poisson process follows these postulates:

$\lim\limits_{h\to0+}\frac{P(N_h=1)}h=\lambda$  i.e. the probability of occurrence one event in a very small interval of time is equal to the macroscopic rate or intensity ($\lambda\,$).
$P(N_h\geqslant2)=o(h)$ i.e. the probability of occurrence of more than one events in an infinitesimal interval is essentially zero.
Events are independent.

If you consider a single individual (for simplicity assume a single cell), then the DNA will undergo mutations at some fixed rate (which we assume to be uniform for all loci). Now each mutation event is independent of the previous event and in a very small interval of time the chance of two or more mutations is negligible. Considering all these facts and assumptions, it can be said that mutation in a single cell would behave like a Poisson process.

From the Poisson postulates you can derive the expression for the Poisson distribution which describes the probability of $k$ number of events in a given time interval, $t$. Hence, the number of mutations in an individual for a fixed time window ($t\,$) follows a Poisson distribution.

$$P(N=k)=\frac{(\lambda t)^k e^{-\lambda t}}{k!}$$

You can find the derivation of Poisson distribution from the postulates from many sources. I referred to this book:

Hogg, Robert V., and Allen T. Craig. Introduction to mathematical statistics. New York: Macmillan, 1978.

EDIT

The effect of deleterious mutations, in the mentioned section of the linked paper talks about Muller's ratchet that describes the accumulation of deleterious mutations and its effect on the population (i.e. extinction). Like any mutation event, accumulation of deleterious mutations will also follow Poisson distribution. Muller's ratchet just says that beyond a tolerance limit, deleterious mutations will cause extinction of asexually reproducing organisms. Perhaps if each deleterious mutation had a strong effect on the fitness, then sampling from the population may lead to non-Poissonian estimates.


Can Leptospirosis be spread through human urine

It can be spread from human to human through urine but it is very rare seeing as we are relatively clean creatures (most of the time) and our excrement hardly ever comes into contact with other individuals without first being purified.

Sources:

Leptospirosis
CDC: Leptospirosis infection


Is Ellman's reagent specific for low molecular weight proteins and thiols?

It's specific for thiols in general. If the contaminating proteins contain solvent accessible thiols, DTNB will react with them.


Why are minor introns bounded by nucleotides AT-AC, where T is not normally in RNA?

It is not unusual for RNA sequences to be reported with T instead of U; the writer is reporting the cDNA sequence instead of the RNA sequence.  In RNA at the boundary of the minor intron, there is a uracil.  In the following page, the writers follow the oft-used convention of describing RNA with T instead of U (writing the cDNA sequence).  https://en.wikipedia.org/wiki/Minor_spliceosome


Is there any difference between strain and mutation/mutant?

You can think of "strain" roughly analogous to how you would think of "breed" in the context of dogs or horses.
There might be some key mutation that identifies members of a strain over non-members, but you would expect to find other genetic differences as well. "Strain" for a virus is not referring to a particular mutation but to the viruses on one side of some fork in their evolutionary history.


How does a polymerized TruSeq adapter affect sequencing reads?

In short, you stand to lose information from your library due to the length of the fragments you're sequencing.

When you set up your sequencing run, you'll set the parameter for the number of sequencing cycles, which will determine the length of the reads to be sequenced. The longer the fragments contained in your library, the less they'll be fully sequenced.

A good idea would be to sequence your suspected polymerized fragments to verify that primer polymerization is really occurring. Just send your sample for normal sequencing, as you would for plasmids and PCR fragments.

If your primers are polymerizing because of inefficient design, you should fix this before loading your library into the Illumina device. If the primer-dimer effect comprises a significant portion of your library, this will only get amplified during the run and can definitely lead to a significantly less complex library. Sequencing a low-complexity library is a really expensive mistake whose one guaranteed result is to enrage your advisor and make him/her loudly question your competence. Trust me.


Confusion over role of current/potential in Nervous system?

Current flow is the movement of charged particles (ions in this case). The membrane potential is the charge difference across the cell membrane. Usually there is more negative charge inside the cell than out, so the membrane potential is said to be negative. When ion channels open, typically positive ions (Na+, K+) will flow into the cell as they are flowing from a medium that is approximately uncharged (extracellular space) into an environment that is highly negatively charged. By analogy, the positive ions can be viewed as water flowing down a gradient (waterfall). Electrical activity is not a flow of electrons per definition, especially not so in nervous tissue where it is ions that move (it is indeed electrons in electric circuits and the likes). During an action potential, therefore, it is not electrons that are moving across the cell membrane, but ions, most notably Na+ and K+, but also Ca+, Cl- among other charged particles.


Do insects' muscles become stronger with exercise?

There are instances of insect muscle growth in response to increased use. The flight muscles of the tsetse fly (Glossina morsitans) have been observed to grow at a faster rate when subjected to enforced exercise (Anderson and Finlayson, 1976). Also larger mandibular adductor muscles (which power the feeding apparatus), and associated head capsule have been noted for caterpillars and grasshoppers feeding on particularly hard grasses (Bernays, 1986). However these examples occur immediately post-eclosion (i.e. after emergence as adults), and during immature stages respectively. Insect muscle typically grows during larval/nymphal (immature) stages, and often for a brief period at the start of adulthood - known as the teneral period. During immature stages, insects typically have a flexible membrane to allow for tissue growth and expansion, this can also be the case during the teneral period, before the inflexible exoskeleton has fully hardened. However at full maturity, insect growth is limited by the rigidity of their exoskeleton.

As far as excessive exercise is concerned, that some insects may be weakened permanently may be more to do with the fact that their life strategy is different to ours. Due to the vast number of offspring per adult, and subsequent low survival chance of any given individual, there could be an evolutionary advantage for individuals pushing themselves to possibly deadly extremes. This could lead to many deaths, whilst retaining a viable population and thus accelerate the emergence of a population of fitter individuals.

References

Anderson, M. & Finlayson, L.H., 1976. The effect of exercise on the growth of mitochondria and myofibrils in the flight muscles of the tsetse fly, Glossina morsitans. Journal of Morphology, 150(2), pp.321-326.
Bernays, E.A., 1986. Diet-Induced Head Allometry among Foliage-Chewing Insects and its Importance for Graminivores. Science, 231(4737), pp.495-497.


How does GTP help in the step of codon recognition?

GTP based structural changes (even motor actions) are very common in biological systems. For e.g. G-proteins, Rab-GTPase (vesicular transport), Ran-GTPase (Nuclear export/import).

So all these GTP-bound proteins make use of an intrinsic or assisted GTPase activity to convert GTP to GDP. This conversion causes change in the structure of the associated protein. Going back to the GTP bound form requires proteins called GEF (Guanine nucleotide Exchange Factors).

So in the case of translation elongation, the elongation factor is a GTPase which changes confirmation upon GTP hydrolysis. This confirmational change twists the tRNA so that the bound amino acid moves closer to the peptidyl-transferase center (if P-site is in the left then the amino acid is bound to the rightward CCA tail of tRNA. The twist causes the amino acid to move leftwards- towards the P-site).

You can refer books like Genes by Lewin for details.


What's the name of this colorful tiny spider?

It seems a lot like the 'jade jumping spider'.
The jade jumping spider scientifically known as Siler semiglaucus has been observed primarily in Asia. I notice that the legs and abdomen have similar patterns to this species. As for the feelers and head I'm not so sure, but the dark hair on the front legs makes me more convinced of my guess. Perhaps look at different species that share the same genus to see if there is any other species that looks more similar to your observation.

If you're still not convinced, as a last resort, perhaps take a look at the peacock spider also known as Maratus volans. It's a long shot but maybe you see connections that I couldn't catch from the photo :).


What is the difference between endomysium and sarcolemma

Just to illustrate Gerardo's answer, this picture is provided. The endomysium as you see is a layer of connective tissue which surrounds the individual muscle fibres (cells) (in between one muscle cell and the next) but each muscle cell in particular is lined or covered by a plasma membrane called the sarcolemma.


How does "be altruist to those who are similar to you" evolve?

This is an important question in evolutionary biology, but you need to distinguish the biological terms 'altruism' vs 'cooperation'.

Altruism in biology means giving up your chance to reproduce so that someone else can more readily.  This is not like a gorilla troop, where only one male breeds, and the rest contribute to mutual security.  A more typical example is a honeybee or an ant, where the vast majority of the hive have no ability to reproduce at all.  This happens in animals, but is relatively rare. Its causes are currently the subject of intense debate but as far as I know, the only cases are where you do this for others who are genetically similar to you.   That logic sort of plays out as you say: "My brother has kids, why do I need to have any? I'll just help out a little bit there."

Cooperation includes forming groups for mutual safety and increased competition for food resources are why you might vote or schlep down to the DMV to get a drivers license when simply getting in your car without might be just as good most of the time.

Cooperation is incredibly common in biology.  It even happens between species.  A dolphin helps a ship navigate submerged rocks, symbiotic bacteria in our gut help us digest food, but also get enough to live and reproduce.  The benefit is always win-win in such situations.

To understand how cooperation occurs spontaneously, one of the best experiments to look at is the Prisoners Dilemma experiment.  If individuals are in a situation where you are likely to see each other again later (like a society).  The most successful ones are the ones who treat each other reasonably well, even if you do look out for less reliable types.  Why do people from Northern climates have strong hospitality traditions?  "Today you (are in trouble) tomorrow me."  As the saying goes.

There are individuals who are not cooperative, but the selection forces are positive enough that those folks will regularly disappear from the group, while more cooperative types will become more numerous.

This is a significant selective pressure that you can train robots with very simple reward mechanisms to cooperate.  http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.144.2881


Why is the variance of the Wright-Fisher model not equal p(1-p)/(2N)?

The binomial variance $2N p (1-p)$ is for the number of individuals $n'$ carrying the allele in the next generation. The frequency of the allele in the next generation is $p'=n'/(2N)$, so its variance is $$\text{Var}[p'] = \text{Var}[n'/(2N)] = \text{Var}[n']/(2N)^2 = p(1-p)/(2N).$$


I'm trying to identify this salamander-looking creature I found in my house today in Coos Bay, Oregon. It is about 2" long. What is it?

That is definitely a lizard, not a salamander. Salamanders don't have scales. It is a Northern Alligator lizard, Elgaria coerulea, in the family Anguidae.
https://www.inaturalist.org/check_lists/9307-Reptiles-of-Oregon
https://en.wikipedia.org/wiki/Northern_alligator_lizard


Why are the fertility rates of large predators kept low?

This question can be tackled in several ways, and also seems to contain a couple of misconceptions about ecological processes (e.g. problematic group-selection ideas and how species 'fit' into the ecosystem).
However, I think it is most usefully answered from the perspective of life history theory and the evolution of life histories (see e.g. Roff, 2002 and Fabian & Flatt, 2012 for background), and at its core this question is dealing with tradeoffs between e.g. fecundity and mortality.

All organisms act under a limited energy budget, and when they spend energy on some activities that will limit what they can spend on other activities.
This lies at the core of life history tradeoffs.
If organisms use resources to produce or raise offspring, this can therefore have consequences on growth, maintenance (e.g. disease resistance), predator avoidance and many other traits and behaviours, which all affect fitness.

With regard to your question, there is a well-known tradeoff between survival and fecundity (an intraindividual effect), which has been shown both between individuals within species and across species.
As with almost all species traits, there is also variability between individuals within populations, so that some have higher fecundity than others, but may then also suffer lower adult survival rates (maybe under certain environmental conditions).
Therefore, there are certainly already "mutation(s) that increases fertility among the predators" within populations.
The reason that fertility is not continuously increasing over time, is that this would have negative fitness consequences overall.
So the reason that the (average) life history traits within a particular species are what they are, is that they are the result of the evolutionary pressures that the species have been experiencing over evolutionary timeframes, acting on the entire life history.

To be sure, hypothetical mutations/changes in life history traits that would increase fecundity with no negative tradeoffs whatsoever for either parents or offspring (i.e. no negative fitness consequences) would definitely increase in frequency.
From the perspective of life history theory, everything else equal, selection will maximize the survival function, $l(x)$ (survival to age x) and the reproductive function, $m(x)$ (number of offspring at age x), while minimizing maturation age.
However, tradeoffs between these functions (directly or indirectly) and between generations will prevent these from being optimized one by one.

Population growth in long-lived predator species is usually also very sensitive to changes in adult survival rate (Caswell, 2001).
This result comes from analysing stage or age structured population models, and is the result of a life history strategy with high adult survival rates, fairly high age of maturation and relatively low fecundity.
To increase fecundity in this situation with negative effects on adult survival will risk adult death and therefore loss of many future years of reproduction.
These kinds of results and models are often used to identify which life history traits and stages to target in conservation actions, but can also be used to understand evolutionary processes, since population growth rate can be used as an overall measure of fitness.

It should also be added that many other ecological processes must be considered.
For instance, large predators often care for their young for quite a long time, since their hunting/foraging behaviours are complex, and it takes a long time for young to learn how to hunt successfully by themselves.
This means that adults need to bear not only the direct cost of producing offspring, but also to support them until they are self-sufficient.
For an extreme case, look at the Orangutan (not a predator, but still) where the young stay with their mother and nurse for up to 5-6 years (sometimes more).
To increase fecundity in such a situation will put a large strain on adult mothers.
You also need to consider trade-offs between offspring number and offspring "quality", which have been demonstrated in many species (an intergenerational effect).
This means that an increase in fertility can result in lower offspring survival over longer timeframes, with overall negative effects on fitness.

Finally, life history evolution is a large and complex field, and these are just a couple of examples and suggestions for why the situation isn't as simple as your question makes it out to be.
Environmental variability and the predictability of the environment are other factors that I haven't considered at all, but are both important processes when you try to understand life history evolution.
This question can also be approached from a more theoretical perspective, but without a background in life-history evolution I think it is more useful to start reading about different processes and tradeoffs, and then later if you are interested to go into the theory for a deeper understanding.


V(D)J recombination on homologous chromosome

There are two alleles (variants of the same genetic region) for the Ig and TCR loci, one on each chromosome. The cell will try first with one allele to obtain a productive arrangement, and then with the other. If the cell fails on both alleles, the cell undergoes apoptosis. If at least one allele has a productive arrangement, the cells move on to selection.

Groups are still uncertain, however, how the cell chooses which allele to initiate recombination on, and ruled out parental imprinting as a culprit last year (1).

To be certain, the regions are the same, though not the same sequence. However, mechanisms during recombination ensure that recombination events among individual cells result in robust junctional diversity and a suitably diverse repertoire of immature antibody or TCR sequences (example).

In activated B cells, however, class switching and somatic hypermutation can result in gross changes to the Ig locus not seen in immature or pro-B cells.


How many teeth can "African wild dogs" have?

I found conflicting information on different websites with a humanima article stating that they have 4 toes and 40 teeth (reference). However, multiple sources state that they have 42 teeth (reference 1, reference 2 and reference 3) with the different teeth being (i= 3/3; c=1/1; p=4/4; m=2/3) x2. I did search for official journal publications but could not find any.

However, since more sources state that there are 42 teeth, I am led to believe that 42 is the right number rather than 40.


If overcooked hard boiled eggs show these green sulfide rings, why do scrambled/fried eggs not show this?

Scrambled eggs can change color, but you perhaps haven't run into a batch that shows discoloration. It is the same chemical reaction:

Why Scrambled Eggs Turn Green
When serving a large group, a buffet can provide enough food for everyone without the need to spend all of your time in the kitchen. Breakfast is a fairly simple buffet to set up, but there are special challenges when it comes to scrambled eggs. When scrambled eggs sit for a while, they tend to turn green or gray. This is a chemical reaction that happens as hydrogen sulfide in the egg white reacts with the iron in the yolk to form iron sulfide.

Via: https://living.thebump.com/lemon-juice-keep-raw-eggs-turning-green-cook-them-8383.html


Which are the most important carcinogens in tobacco smoke?

This is not an easy question - as tobacco smoke contains something like 5000 different chemical components, from which 70-100 are carcinogen. The list includes: Oolycyclic aromatic hydrocarbons (PAHs), N-nitrosamines, aromatic amines, aldehydes, volatile organic hydrocarbons and metals. I haven't found articles which specifically concentrate on the carcinogens in saliva, but my guess would be that you find them all because of the "application route" of the cigarettes.

Most of these carcinogens first need to be processed from the livers cytochrome P450 system to reach their carcinogenic potential. The enzyme complex converts these substances into forms which can then covalently bind to DNA.

A list of several different of the carcinogens can also be found in the Wikipedia. For further information see the references.

References:

Hazardous Compounds in Tobacco Smoke
How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis
for Smoking-Attributable Disease: A Report of the Surgeon General.
Tobacco Smoke Carcinogens and Lung Cancer


What are the effects on hearing of in ear headphones?

The main effect on hearing is the volume of the sound. Both the intensity and duration matter. However, it seems like hearing loss from personal music players is not as prevalent as from other causes like gunfire or occupational noise exposure (see also here).

The specific problem with in-ear headphones is people tend to listen to them louder than other types of headphones, here is an example study that shows this result.

So, in summary, there isn't anything wrong with in-ear headphones if you listen at a low volume, but be wary that peoples' tendency is to listen louder with in-ear headphones, and you already mentioned liking loud music. The volume is going to be your problem.

Be very wary with your hearing though: once you have lost hearing, there is no way to get it back at this time. Hearing aids only temporarily compensate for the loss. You might be okay now but regret a lifetime of noise exposure by the time you are an older adult.

References:

Clark, W. W. (1991). Noise exposure from leisure activities: a review. The Journal of the Acoustical Society of America, 90(1), 175-181.

Hodgetts, W. E., Rieger, J. M., & Szarko, R. A. (2007). The effects of listening environment and earphone style on preferred listening levels of normal hearing adults using an MP3 player. Ear and hearing, 28(3), 290-297.

Mostafapour, S. P., Lahargoue, K., & Gates, G. A. (1998). Noise‐induced hearing loss in young adults: The role of personal listening devices and other sources of leisure noise. The Laryngoscope, 108(12), 1832-1839.


Your sugar substrate was sucrose. Yeast cells metabolise this by secreting an enzyme, invertase, which splits the disaccharide into glucose and fructose both of which can be fermented by yeast to produce CO2.
According to this site

Equal Original (blue packaging)  is a zero calorie sweetener that contains aspartame and acesulfame potassium as its sweetening ingredients along with a bulking agent.
Equal Original PACKETS:
dextrose with maltodextrin, aspartame, acesulfame potassium

This agrees with what you say - that the sweetener that you used contained dextrose - and leaves me very confused. Dextrose is another name for glucose so how can this contain zero calories?
The answer lies in the legal definition of zero calories  = less than 5 calories per serving (presumably per package in this case.) So let's assume that by adding two packs you were adding 8 calories equivalent of glucose.
Calorie content of carbohydrate = 4 calories per gram
Two packs could contain 8 calories = 2 g glucose.
The molecular weight of glucose = 180
therefore 2 g = 2/180 moles
if completely fermented to CO2 each mole -> 6 moles CO2
12/180 moles CO2 = 0.75 litres of CO2.
I conclude that there is enough glucose in two packets of Equal to generate a reasonable amount of CO2.
Yeast cannot ferment maltodextrins. It is possible that aspartame (aspartyl-phenylalanine-methyl ester) could be metabolised, but I think the dextrose/glucose solution is the best explanation.
EDIT:
I meant to say, just to illustrate that this is a significant amount of glucose, standard rich yeast medium is 2 g glucose /100 ml (2 % w/v).
EDIT #2 My back-of-an-envelope calculation has a fundamental error in it, but luckily I am the first to spot it. If glucose is being used fermentatively, then only one third of the carbon will end up in CO2, with the remainder going to ethanol. This means 0.25 litres instead of 0.75 litres. Yeast is so oriented towards fermentation that even in the presence of oxygen the fermentative pathway will dominate.


I hate to sound rude, but you could easily answer this yourself with even the most minimal look into well-tabulated demographic information, rather than highly non-representative observations. About 13% of Japan's population is 0-14 years old, the third lowest fraction in the world. (https://data.worldbank.org/indicator/SP.POP.0014.TO.ZS ; easy to find with Google)  The fraction of the population over age 65 is 28%, the highest in the world. (https://data.worldbank.org/indicator/SP.POP.65UP.TO.ZS?most_recent_value_desc=true) The population density is high, so you'll certainly see more kids than in many other countries, though not proportionally more. I will leave it as an exercise to look up the numbers for Tokyo itself.


Blocking buffer

Once the proteins in the gel have been transferred to the nitrocellulose membrane it is necessary to coat the rest of the surface of the membrane with an unrelated protein. This is necessary because all proteins will bind non-specifically to the nitrocellulose. Once the membrane has been blocked the only way that antibiody proteins (the probe) will bind to the membrane is via the transferred proteins that they recognise. The usual source of a blocking protein is defatted milk powder, i.e. casein, although some people use (or used to use) bovine serum albumin.

Secondary antibody

In a typical blotting experiment you expose first with a primary antibody directed against the protein of interest, for example this might be an IgG raised in a rabbit. Then in a second step you add a secondary antibody which will bind to the first one - in this case this might be goat ant-rabbit IgG (i.e. anti-rabbit IgG raised in a goat). Why is this done? The secondary antibody is in the form of an antibody-enzyme conjugate, typically with horseradish peoxidase, and the final development of the blot detects the presence of the conjugated enzyme.

Why use a secondary antibody? Two reasons: - firstly, there will sometimes be a degree of amplification if more than one secondary antibody molecule binds each primary antibody molecule; but more important is that it means that it is not necessary to produce an enzyme conjugated form of every primary antibody, which is time-consuming and quite tricky. So in your work you may be studying several different proteins using Westerns, but you will be able to use the same secondary antibody to detect all of them.

Pore size

That should be 0.45 - 0.5 µm. Pore sizes are measured in micrometres.


Can roots have cuticle, especially aerial roots?

According to this article, Selaginella aerial roots have a thick root cap that possesses a cuticle. Roots that have breached the soil do not have cuticles.


What is the primary energy source for sprouting plants?

This depends largely on the plant, some seed stores can last a very long time, but a few general trends can be discussed.

sprouting plants run off stored carbohydrates in the seed, they are using respiration, photosynthesis begins as soon as they are able and they will switch over to it as quickly as possible it is however gradual as the plant never stops using respiration it just starts using photosynthetically produced sugars instead of stored ones. The stored energy will run out so the faster a plant can stop relying on it the better, so even a small production is helpful, you yest it is a gradual process, even if it is a fast gradual process ins some plants.


What's seen when stress echocardiography shows ischaemia? Can this happen without angina?

A number of things can be seen. Ischaemia is typically caused by the narrowing of blood vessels that prevents perfusion (blood flow) to the heart or other organs. When the heart muscle doesn't get enough oxygen, the walls of the heart might not "beat" (i.e. contract) properly. We observe this and thus can tell if a coronary artery is reduced or blocked or fine. It doesn't give absolute numbers of how blocked it is, although observation of the way the muscle moves can give some indication. Contrast can further allow us to visualise the wall with more detail, giving a clearer indication of coronary artery disease in the vessels that supply this part of the heart.

Pain is caused when the heart muscle is really suffering, which doesn't occur unless the vessels are seriously blocked. They're so great that even if about 70% of the artery is blocked there is almost no effect including chest pain. In fact it is silent, which is quite worrying also. However, when the heart is most stressed, we can potentially detect decrease in perfusion from small changes in the contraction of the heart.


How to choose right volume of DNA and SYBR Green

I had to look it up online, but I eventually found here an important information: the detection limits of SYBR Green.

  dsDNA at 300nm transillumination: 60 pg
  Oligonucleotides at 300nm transillumination 1-2 ng

You should first check the size of your DNA of interest, and from its size figure out its approximate molecular weight (for example using this online calculator). Then, you should check that 1000 nmoles of your DNA corresponds to a mass greater than 60 pg. If not, you should increase the amount of DNA in your assay accordingly until the mass introduced in the assay exceeds the detection limit of SYBR Green.

Now, do you know the concentration of your DNA? In other words, how did you choose to use 3 uL of DNA? How do you know that these 3 uL contain enough material? (1000 nmoles as in your protocol, or better, that this is higher than the detection limit in terms of mass).

Also, did you use the 1000X stock solution of SYBR Green without intermediate dilution? If so, the final concentration of SYBR Green is much larger than the final 1X you want, in both of your samples:

sample 1: 5 uL of 1000X SYBR Green in a total volume of 3 + 5 + 27 = 35 uL means that the final concentration is 1000X * 5 / 35 = ~143X.
sample 2: 5 uL of 1000X SYBR Green in a total volume of 3 + 5 = 8 uL means that the final concentration is 1000X * 5 / 8 = 625X.

What you need is either use 1 uL of 1000X stock solution of SYBR Green + whatever amount of DNA that will be above the detection limit + buffer to adjust the volume to 1000 uL final (which will bring the SYBR Green to 1X final), or make an appropriate intermediate dilution of SYBR Green so that its final concentration is 1X by following the sample preparation as described in your question.

The sample preparation you describe here yields a composition that is way off the one suggested by your protocol, at least for the SYBR Green. Until you try again with proper final concentrations, do not conclude that it didn't work. :-)

Good luck with your project.


What type of movement is "spontaneous movement" if it isnt reflex movement and it isnt purposive movement?

Although I can't read the original article in Czech, from their abstract it is clear that all they mean in differentiating spontaneous versus induced movement is whether the experimenter manipulated the uterus to induce a movement. Movements they observe could still be reflexive, they make no distinction of the type of movement (and do not intend do) except indicating whether the movement was purposefully caused by the experimenter.


Effect of zero selection (pressure) on the population health

I need to point out one thing, natural selection does not bring species to perfection.  The best mutant may not be selected for many reasons.

When you have no selection pressure then you have neutral evolution concurring and what takes over instead of natural selection is genetic drift.  Genetic drift is just sample error.  Say you have 1,000 individuals in a population and all of those individuals reproduce, in the next generation all the genotypes would be in the next population.  Now imagine if you only had 10 individuals in the population and only 5 of those individuals were randomly selected to produce 10 individuals in the next generation (the parents die every year).  There is no selection pressure but just by chance some individuals reproduce and some don't.  If you do this over and over again what you will see is that some genes become fixed in the population, meaning that there is no other genotype in the population.

This fixation at small population sizes can occur with either beneficial or deleterious mutations.  Obviously if a mutation is very deleterious the individual will die but slightly deleterious mutations can become fixed in the population as well.

There is an entire field of biology devoted to this study.  It is called population genetics.  The probability for fixation for an allele is its proportion in the population.  This proportion can be calculated by 1/2N, where N is the population size.


What is the significance in an alpha-helix being right-handed or left-handed?

Some experimental and modelling observations suggests, folding energy for right handed in more favorable. You can find more detailed answer to this question here.


In our 23 chromosome pairs, do the 2 members of the pair have distinct or virtually identical sequences?

Homologous chromosomes (those that are paired up), excluding the sex pair are almost identical in size, shape and genes (members as you called them) present in them.
Genes determine traits and each homologous chromosome controls the same traits. The level of identity of a gene inside a population varies between genes. There are very conserved ones that do not change even between humans and yeast and others that vary alot event inside a species. This changes can be small in sequence length, a simple base (letter) swap or one deletion, and have a huge effect on the traits. This is how chimps and humans are very different but share 98.6% of their genome and humans are very similar and share 99.9% of their genome.
In summary, on the bigger scale homologous chromosomes are very similar (size, shape, traits inside), on the smaller scale homologous chromosomes have small changes that affect greatly.
EDIT: elaborating on when recombination occurs.
The zygote do not recombine the chromosomes it gets from it's parents. Each parent chromosomes recombine in the first step of meiosis. We do not expect them to be identifcal on the gene level (or the SNPs level). Each chromosome represent each paren't genetic material.
Lets look at parents A chromosomes
parent a Paternal: a-b-c-d-e                       parent b Paternal: a-B-c-D-e
parent a Maternal: a-B-C-D-e                   parent b Maternal: a-b-C-D-e
possible recombination  (a)                       possible recombination (b)
(a-I) a-B-C-d-e                                         (b-I) a-B-C-D-e
(a-II) a-b-c-D-e                                         (b-II) a-b-c-D-e
Now the child can be any of the 4 possible combinations (and obviously all other not shown). Let's say (a-I) and (b-II). This chromosomes do not recombine until they get to the meiosis stage.


Why is DNA replication  performed in the 5' to 3' direction?

Prof. Allen Gathman has a great 10-minutes video on Youtube, explaining the reaction of adding nucleotide in the 5' to 3' direction, and why it doesn't work the other way.

Briefly, the energy for the formation of the phosphodiester bond comes from the dNTP, which has to be added. dNTP is a nucleotide which has two additional phosphates attached to its 5' end. In order to join the 3'OH group with the phosphate of the next nucleotide, one oxygen has to be removed from this phosphate group. This oxygen is also attached to two extra phosphates, which are also attached to a Mg++. Mg++ pulls up the electrons of the oxygen, which weakens this bond and the so called nucleophilic attack of the oxygen from the 3'OH succeeds, thus forming the phospodiester bond.

If you try to join the dNTP's 3'OH group to the 5' phosphate of the next nucleotide, there won't be enough energy to weaken the bond between the oxygen connected to the 5' phosphorous (the other two phosphates of the dNTP are on the 5' end, not on the 3' end), which makes the nucleophilic attack harder.

Watch the video, it is better explained there.


What is the copy number of a given gene in GRCh37?

A very naive approach would be to simply ask how many copies of the sequence in question are in the hg38 sequence, at some level of homology. You could do this using a tool such as BLASTN (which has a web interface that you can use to search against a human genome) or, if you have the sequences downloaded somewhere where you can work with them, using a tool such as minimap2 (which will be faster) as long as you're comfortable using command-line tools.
If you choose to do this, you will have to be comfortable setting thresholds for what counts as a copy of the gene in question.
A more involved solution would be to obtain DNA sequencing reads for the sample you're interested in and use them to quantify the copy number of the gene based on the number that map to a given sequence of interest. An older approach would be to use microarrays.
I am guessing that since you are interested in the reference genome that you are not interested in going to that kind of trouble.
Is this a homework question? If so, you should add the "homework" tag.


Yes, glycocylation is same as glycosylation. You can check out following links which explain glycocylaion same as post translational modification named glycosylation.

https://www.semanticscholar.org/author/Haudhiya/93411308

https://grantome.com/grant/NIH/R01-DA004166-05

https://quizlet.com/137217422/lecture-10-a-biochem-final-flash-cards/

https://books.google.com/books?id=3RbT3cpdCc0C&pg=PA508&lpg=PA508&dq=glycocylation&source=bl&ots=qIwbK6-ZdP&sig=ACfU3U18W_rG0D53R67_fzAywtMXGye5NA&hl=en&sa=X&ved=2ahUKEwjKrvfJp_foAhW3knIEHWLVB8gQ6AEwFnoECGQQQw#v=onepage&q=glycocylation&f=false


Why there is Cp/Ct (crossing point) value for negative sample in COVID-19 RT-PCR?

PCR is highly specific (meaning it amplifies only the DNA the primers bind to), so the results in general are good. But: Due to the exponential nature of amplification, even very small mispairings can lead to the amplification of a very small amount of DNA and subsequently to a fluorescent signal. There are basically two ways of getting this amplification (except from the desired one): Contaminations and primer self-amplification. The first one should be clear, the second one happens when primers are able to bind to themself (or the complimentary one). This usually shows up late in the PCR, which is the reason why you assign a Ct-value to it after which you do not expect any meaningful amplification result anymore.

Depending on the method, you extract all RNA from your sample and translate it into cDNA. However, for the amplification in the PCR you need primers that fit to this cDNA. And since these primers have been proven to be highly specific (meaning: they bind absolutely no other sequence, not even from closely related viral species) we can be sure that any signal which is about the criteria mentioned in 1. comes from viral RNA and shows an infection. See the reference for one of the often used PCR tests.

Without seeing the curve, I cannot say anything specific about it. In general a real-time PCR curve follows a sigmoid shape. This gives some information about the way the reaction progressed over time. If it looks differently, something may have either happened to the reaction or to the sample. It may contain a PCR inhibitor, the sample can be contaminated or something else. I wouldn't trust such a result and repeat it with a new sample.

Reference
Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR


Is there an antagonistic association between Penicillium and Aspergillus?

It is hard to find any articles on the association between Penicillium and Aspergillus species, although they are both considered two of the most common mold species found indoors.

  In this study, the most prevalent spore types detected in both the indoor and outdoor air samples were generally from the Penicillium/Aspergillus group [...] these ﬁndings are qualitatively similar to those observed in other geographical locations, conﬁrming the ubiquitous nature of these fungi.

Although these genera seem to be found commonly, it also has to do with environmental factors, and the relative humidity of the area as well.

  Geographical location, climate, and short-term meteorological
  conditions are responsible for outdoor types and levels of fungal
  spores.

As for the association and apparently colonization/opportunistic behaviour of the genera, it seems like there are not any associations between the two, unless perhaps environmental conditions are subject to changing, and different mold species have different moisture/temperature thresholds, although again these mold groups tend to be generalists and do well at a wider range of environmental conditions than other fungi.

  A laboratory procedure was developed in which viable peanut seeds were wounded and inoculated with field soil containing natural populations of fungi, then incubated under different conditions of seed water activity and temperature. [...] A. parasiticus colonized peanut seeds at lower temperatures than A. flavus, and cool soil temperatures relative to temperatures of aerial crop fruits might explain why A. parasiticus is found mostly in peanuts.

  Other fungi, dominated by the genera Penicillium, Fusarium and Clonostachys, colonized seeds primarily at water activities and temperatures suboptimal for section Flavi species and A. niger.

  Eupenicillium ochrosalmoneum frequently sporulated on the conidial heads of section Flavi species and showed specificity for these fungi. The inoculation of wounded viable peanut seeds with soil containing natural populations of fungi provides a model system for studying the infection process, the interactions among fungi and those factors important in aflatoxin formation.

Any associations with different fungi species and their different structures, including, for example, with the conidial heads of Aspergillus seem to be currently under study:

  The genus Penicillium comprises species that mostly colonize plant matter. However early reports suggest that several species are capable of parasitizing Aspergillus and sporulating on the conidial heads of the host. More recently Eupenicillium ochrosalmoneum and E. cinnamopurpureum, [...] have been observed sporulating on the heads of Aspergillus species belonging to section Flavi during the colonization of peanut seeds.

  Little is known about the host specificity underlying these Aspergillus-Penicillium associations. [...] all species spread across Aspergillus colonies by means of aerial hyphae that grew from head to head. Additional studies are required to clarify whether Eupenicillium and Penicillium species are parasitic or simply epibiotic on their hosts.


How did the moray eel evolve a pharyngeal jaw?

well considering jaws originally evolved from the first set of gill arches and eels still have gill arches, so it's not that much of a stretch. Most fish gill arches already have muscle attachments that aid in swallowing and breathing. Many bony fish already have  pharyngeal teeth to aid in swallowing (they teeth prevent the prey from being pushed back out of the mouth by water pressure. Moray eels have a much more direct mechanism becasue they live in burrows and can't fold the gill arches out to generate suction and pull food down the mouth as other fish do. So instead the muscles pull the arches backwards and the shape pulls them together pulling food down the gullet.

it has actually happened independently in cichlids and something similar happened in Snakes and Mosasaurs


It appears that little is known regarding how water is detected in mammalian mouth and throat. However, a recent study published in Nature Neuroscience(1) showed that acid-sensing taste receptor cells (TRC) participate in taste responses to water.

First, the team screened knock-out mice in order to identify which TRC were involved:

  They used genetic knockout mice to look for the cells, silencing different types of TRCs, then flushing the rodents’ mouths with water to see which cells responded. “The most surprising part of the project” was that the well-known, acid-sensing, sour TRCs fired vigorously when exposed to water, Oka says. When given the option of drinking either water or a clear, tasteless, synthetic silicone oil, rodents lacking sour TRCs took longer to choose water, suggesting the cells help to distinguish water from other fluids.(2)

Then, the acid-sensing TRCs thus identified were artificially activated using optogenetics techniques:

  They bred mice to express light-sensitive proteins in their acid-sensing TRCs, which make the cells fire in response to light from a laser. After training the mice to drink water from a spout, the team replaced the water with an optic fiber that shone blue light on their tongues. When the mice “drank” the blue light, they acted as though they were tasting water, Oka says.(2)

Source:

(1) Zocchi, D., Wennemuth, G., Oka, Y., The cellular mechanism for water detection in the mammalian taste system, Nature Neuroscience 20, 927–933 (2017) doi:10.1038/nn.4575

(2) Scientists discover a sixth sense on the tongue—for water, Science


Interpreting graph of mitosis and meiosis

I believe III → IV is mitosis and VII → X would be meiosis. As Jam explained in comments below, the stationary points of the graph (II → III or VI → VII ) do not count as part of either process.


Take a look at the paper by Ojasoo et al. [1] It reports the relative binding affinity for a wide variety of steroids for the AR, PR and GR.

Nandrolone (19-nor testosterone) does not have any affinity for the GR, but is a potent activator of the AR. However, it does have some affinity for the progesterone receptor (does this matter for your research?). Additionally, nandrolone bound to the AR also binds estrogen response elements (does this matter for your research?).

5a-DHT also is a potent AR activator with no affinity for the GR. Do note that a metabolite of 5a-DHT has significant affinity for the estrogen receptor, might that matter for your research.

You might also use a strong GR antagonist in conjunction with an androgen which also has some affinity for the GR. Then you can simply use methyltrienolone, as commonly used as AR ligand.

On a sidenote: do note that androgens usually only lead to significant dissociation of a GR ligand for the GR at very high concentrations. Therefore, androgens most likely act as GR antagonist by heterodimer formation of the AR with GR [2], as well as through squelching [3].

References

Ojasoo, T., et al. "Towards the mapping of the progesterone and androgen receptors." Journal of steroid biochemistry 27.1 (1987): 255-269.
Chen, Sei-yu, et al. "Androgen and glucocorticoid receptor heterodimer formation A possible mechanism for mutual inhibition of transcriptional activity." Journal of Biological Chemistry 272.22 (1997): 14087-14092.
Zhao, Jingbo, et al. "Oxandrolone blocks glucocorticoid signaling in an androgen receptor-dependent manner." Steroids 69.5 (2004): 357-366.


Is the quality of sleep dependent on sleep duration?

Sleep duration certainly affects the quality of sleep, but it is nowhere near a simple correlation. It is just one of many factors, and these factors don't work in isolation. Statistically speaking, it's a multivariate model - and one which includes a differential equation, because the way sleep duration affects your sleep today depends on the sleep quality (and also the sleep duration) from yesterday. For example, if you go several day with too little sleep, but keeping firm going-to-bed and waking-up times, the ratio of your sleep phases changes significantly, giving you much more deep sleep. This is what compression therapy is based on.

And beyond that, the way you feel upon waking is also dependent on sleep quality in very complicated ways, and other factors (for example the synchronisation of the time at which you woke with your circadian cycle) play a much larger role than the sleep quality you got. Also, there are some unexpected effects, where getting too little sleep making you feel good - it's a kind of lightheaded, giddy state, somewhat comparable to having had a small glass of champagne.

So yes, there is a dependence, but you cannot expect that having had lots of sleep will make you feel good in the morning.


What kind of beetle has fuzzy orange antennae and can flip its head down for digging?

I'd guess that the beetle you found was of the genus Nicrophorus ,family Silphidae . They are commonly known as Burying beetles and are true to their name

was this the beetle you saw?


How do tight junctions in stratified squamous epithelia affect nutrient supply?

Tight junctions function to occlude the baso-apical flow of small molecules. However, tight junctions do not always completely seal a cell's lateral surface. In addition to regulating diffusion, tight junctions promote cell polarity. Establishment of polarity and prevention of water loss are the major roles of tight junctions in stratified squamous epithelia.

In simple epithelia, transcytosis allows the flow of molecules through a cell with tight junctions. However, stratified squamous cells do not use transcytosis for nutrient supply.

In the stratum granulosum, skin cells lose their nuclei and become non-viable. In the stratum lucidum, an oily layer is produced by exocytosis.

It is the loss of nuclei, organells, production of an oily layer at the stratum granulosum and lucidum that contributes most to the death of skin cells, not the limits of nutrient diffusion.