In gel electrophoresis, the gel is the mechanism by which macromolecules of different sizes are separated. By loading the gel with amino acids (or proteins or DNA), you start all of the samples equally, and then push them through a gel using a salty buffer solution that is electrified.

The gel has a certain concentration of a polymer (commonly agarose or polyacrylamide) that acts as a mesh that slows your macromolecules down. So, after running a gel for a certain amount of time, molecules of different sizes will have traveled different distances. This can be visualized by different methods (ethidium bromide for DNA and antibodies for proteins, commonly) after further preparation.

So, the amino acids in question should not be dissolved in buffer, as this would result in loss of sample.

Edit:

Regarding the last point: when loading samples on a gel, they must first be dissolved in some loading buffer that will help the sample settle into the well and not diffuse out. I took your mention of "buffer" in the original question to be the running buffer for electrophoresis, which you should not dissolve your sample in. I am also unfamiliar with analyzing amino acids by electrophoresis, and I do not know if there is a specialized loading buffer that kind of analysis would require. A quick look didn't uncover anything, but you might be in a better position to answer the loading buffer issue.


Plant growing very rapidly near my house

It looks like a young Empress Tree (Paulownia tomentosa)

Native to China, it is an invasive species in the USA. looks beautiful when full grown however


Which kind of drugs get absorbed through epidermis?

According to a review (Prausnitz2004), marketed drugs with a dermal route of administration tend to fulfil the following criteria :

Small molecular size (< 500 Da)
High lipophilicity
Small required dose (up to ~milligram)

This is a consequence of the structure of the skin (with a lipophilic stratum corneum, and low diffusion speed) and practical concerns (everything else equal, a higher dose would need more surface area).

Beyond "pure" diffusion, there has been much work on improving drug delivery through other means : chemical enhancers (ethanol or DMSO being classical member of this class), medical devices (microneedle patch, ultrasonic device), and other more exotic methods mentionned in the paper.

These criteria are also mentionned in (GoodmanGillman2006, chapter 26), with emphasis on concentration gradient being the driving force behind diffusion across the skin. This chapter also contain a list of commonly used transdermal/dermatological drug, and their use.


How do sharks and other fish conserve and gain water in marine environments?

The mechanisms of osmoregulation is different for sharks (and other elasmobranch fishes) and teleost fishes.

In Elasmobranchs the body osmolarity is maintained equal to the seawater by Na⁺ Cl⁻ and urea. Toxicity because of high concentrations of urea (strong chaotrope) is counteracted by high levels of trimethylamine oxide (TMAO). So, the elasmobranchs do not need to drink water to prevent dehydration. But sometimes they do drink water for adapting to different salinity levels [1].

Teleost fishes, however, need to drink water in order to prevent dehydration. Initially Na⁺ and Cl⁻ are absorbed in the esophagus via cotransporters (Na-Cl/Na-K-Cl), thereby reducing the osmolarity of water. The cells that absorb Na⁺ maintain its low concentration by pumping extra Na⁺ in the Extracellular fluid, using Na⁺/K⁺-ATPase. Cl⁻ is also exchanged with Bicarbonate (HCO3⁻) via anion exchangers [2].

.


Why do mice have a higher metabolic rate than humans?

In endothermic and ectothermic animals, ie. warm and cold blooded animals, metabolic rates are inversely proportional to size of the organism.

  Quoting from https://www.biog1445.org/demo/04/metabolicrate.html

  This is because smaller animals have a higher surface-to-volume ratio,
  thus a larger relative heat loss to the environment per unit time. To
  maintain a constant body temperature despite rapid heat loss across a
  body surface, a small animal must oxidize food at a high rate. Because
  the relative amount of food consumed and the pace of digestion,
  respiration, and so on must rise with decreasing body size, there is a
  lower limit on the size of endotherms. The smallest mammals are
  shrews, which weigh only about 4 grams. They must eat nearly their own
  body weight of food every day, and starve to death is just a few hours
  if deprived of food.

This is shows that smaller animals, like mice have a much faster metabolic rate than that of larger animals like humans or elephants.

When talking of within the cell, the mitochondrial content of a muscle cell of a mouse would be increased to produce more energy from one feeding than that of a human. This is because cells themselves increase the number of mitochondria based on the requirement of the body, thus a muscle cell of a human has more mitochondria than a neuron, since muscle cells have to utilize much more ATP to function. This phenomenon, known as mitochondrial biogenesis would be observed in mice vs human cells.
In mice, having more mitochondria would be an evolutionary advantage, as only those producing the optimal amount of energy would be able to survive the loss of energy to the surroundings and the process of natural selection would leave mice with relatively larger numbers of mitochondria in their cells.

(For more info)
https://en.wikipedia.org/wiki/Metabolic_theory_of_ecology
http://www.sciencedirect.com/science/article/pii/S0378111900005825


Which part of human body sustains most pressure when standing up straight?

It is logically clear that the ankle could only partly be analyzed in the group of joints that are below its height. There is no direct way to measure the pressure on ankle joint (on talus bone), but from the logic it is clear that it should be the point of highest pressure in the group of points lister in the question, however the pressure is distributed through the other joints of the foot.

Below are the graphs of pressure distribution according to surfaces (not joints). From the graph we can conclude that part of the pressure experienced by ankle joint distributed tangentially to metatarsal region and other surfaces.

Indeed the highest pressure in standing person in on feets. The term you are asking about is foot pressure distribution (FPD).

In we assess the FPD dynamically, in younger persons the FPD is nearly equivalent between calcaneus region and metatarsal region, while in older persons the FDT in calcaneus region is higher than metatarsal pressure.

During stance:

Foot pressure distribution. A. Maximum pressure distribution on all sensors during stance for one subject. B. The nine anatomical masks superimposed on the insole (MC = medial calcaneus, LC = lateral calcaneus, MA = medial arch, LA = lateral arch, MT1 = first metatarse, 3 = second and third metatarse, 4 = fourth and fifth metatarse, H = hallux, and T = toes).

Pressure distribution by anatomical region. Normalized maximum pressure distribution for the young (white bar) and elderly (black bar) group for each anatomical region (medial calcalneus mask p = 0.0001, lateral calcaneus mask p = 0.03):

source article, you can find much more using FPD as a keyword.


Where does the term "cos site" come from?

"Cos" is the abbreviation of "cohesive end site". This is a speciality of the lambda phage which has to be linearized to fit into the phages head, but circularizes in the host cell. To achieve this, it has the cohesive (or sticky) sites at each end.
See here and also the publication by Allan Campbell on "Bacteriophages".


Pharmacokinetics: why do certain drugs follow zero-order kinetics?

Basically any compound in concentrations sufficient to saturate its metabolization machinery will show zero-order pharmacokinetics. This reflects the fact that metabolization is taking place at full speed while facing a comparatively enormous amount of substrate (just as @WYSIWYG pointed out). This effect can also be shown in vitro with pure substrate/enzyme solutions.

But the above is a rather simplistic model, valid only in specific situations.

Most of the time in humans, zero-order kinetics stem from the fact that liver enzymes are saturated. However, for most drugs the redistribution phase is much more important than metabolization/elimination in defining the duration of effect. A good example of that would be sodium thiopental. As a single iv bolus dose, it will induce loss of consciousness for a short time due to redistribution. However, continued infusion will allow blood and tissue concentrations to equilibrate, and then the metabolization/elimination rate will become much more prominent in defining the duration of effect. And as sodium thiopental happens to have zero-order metabolization kinetics in continued infusion, it will take you a loooooooooong time to wake up! This is why in human pharmacology, we use context sensitive half-life to better represent drug kinetics.


This is of course a controversial topic with there being supporters for both methods of slaughter. First of all, The research paper that you have mentioned is a highly cited one and it is the foremost study that supporters of exanguination use to support their method of slaughter. However, the author himself (Wilhelm Schulze) has stated and I quote

  "objective results presented for the captive bolt application in sheep
  indicates that the captive bolt device used is suspect" and that these
  initial "scientific findings and the results presented are only a very
  first contribution" and that they "need to be followed as a high
  priority by further investigations in the continuation of the
  scientific clarification of the issues of loss of pain and
  consciousness during slaughter of this kind with and without stunning
  using the same experimental approach with a representative number of
  grown cows of various breeds." (reference)

Since stunning methods have advanced (reference) from the time this paper was published (1978), it would probably be a bit unfair to hold onto this paper as proof for supporting exsanguination. Moreover, in another study, in which measurements were done with an electro-corticogram it was found that

  Captive bolt stunning followed by sticking one minute later resulted
  in immediate and irreversible loss of evoked responses after the stun.
  Spontaneous cortical activity was lost before sticking in three
  animals, and in an average of 10 seconds after sticking in the
  remaining five animals. The duration of brain function after shechita
  was very variable, and particularly contrasted with captive bolt
  stunning with respect to the effects on evoked responses. These were
  lost between 20 and 126 seconds (means of 77 seconds for somatosensory
  and 55 seconds for visual evoked responses) and spontaneous activity
  was lost between 19 and 113 seconds (mean 75 seconds) after slaughter (reference).

The two questions that have to be answered in exsanguination are

-- Does the neck cut cause pain?

-- How long does it take for the animal to lose enough blood for insensibility to occur and for any perception of pain or suffering associated with slaughter to disappear?

With regard to pain, in the process of cutting the major blood vessels leading to and from the brain a number of other tissues are also severed by the extensive neck cut including muscle, skin, sensory and motor nerves etc. There is a chance that this might cause significant shock and fear to the animal. The time to lose consciousness is highly variable in  exsanguination. (reference)

Very good arguments are presented in this article and I highly recommend that you go through it.


I think you are reading too much into that statement. The proper reading of that statement is to add on the implied "..compared to other nuclei." That is, what defines a nucleus, in most cases, is some shared similarity in connectivity. That does not mean homogeneity.

I also think your reading of the second statement is incorrect; it does not suggest that there are "simple and complex" nuclei as two distinct categories, rather it is indicating that "complexity" varies, and gives a couple examples; essentially, it is exactly saying that you should not assume homogeneity.

I don't think it makes much sense to think in terms of "number" of nuclei, and anyways, nuclei can be somewhat arbitrary. For example, take the auditory thalamus: the medial geniculate nucleus (MGN). The MGN is typically divided into three parts: the dorsal, ventral, and medial divisions. Someone chose to call them all the medial geniculate nucleus, based on gross appearance, but with more functional understanding we can classify each part separately. Should this be one nucleus or three? It really doesn't matter, it's just semantics and terminology to get people talking about the same structure. In one context, it makes sense to talk about the whole MGN, in other cases it makes sense to differentiate between MGv, MGm, and MGd. You could call them subnuclei, or nuclei, or whatever you want. Most people choose to just be consistent with the terminology used in their field for historical reasons because it doesn't matter.
I don't really think it makes sense to think of in terms of prototypes; nuclei are different from each other.
Again, you'd have to first define simple and complex. I don't think there is meaningful dichotomous distinction.


Where does the additional 1 proton cost of oxidative phosphorylation come from?

The energy required for the ATP production by ATP synthase is obtained from movement of ions (H+ or in some cases Na+) downstream of their potential (proton motive force). I guess, there is no exact stoichiometric exchange as in case of ion pumps. The rotation of the motor is generated by the movement of protons through a channel. The H+/ATP ratio is estimated using biophysical/biochemical techniques.

Brand and Lehninger (1977) estimated this ratio to be greater than 3.

Turina et al. (2003) recalculated this ratio using constituted liposomes and their estimate is  3.9 ± 0.2.

This is an excerpt from a more recent study on chloroplast ATP synthase by Hahn et al (2018).

  The symmetry mismatch between the 14-fold Fo rotor and the
  near-threefold F1 head means that the number of c subunits rotating
  past subunit a to generate one ATP is not an integer. cF1Fo requires,
  on average, 4.67 c subunits, or protons, to produce one ATP. The
  nearest integral numbers of c subunits per step would be 4, 5, and 5,
  equivalent to rotation angles of 103°, 129°, and 129°. Surprisingly
  however, the three conformations are separated by rotations of 103°,
  112°, and 145°, or 4, 4.4, and 5.6 c subunits (fig. S5C). This means
  that the position of the c subunits relative to subunit a in the three
  conformations differs.

The structure and efficiency of chloroplast ATP synthase may be a little different but what I want to emphasize is that there is no exact exchange of protons and ATP.


High sequence similarity but start codon isn't methionine

There are alternative start codons to AUG used in prokaryotes: GUG and UUG. Those still match the initiation tRNA and encode N-formylmethionine. The rare start codons are matched by wobble pairing.


Pituitary giants - is the fusing of growth plates dependent on amount of growth hormone in blood?

Gigantism is caused by too much growth hormone (GH) and causes increased growth in kids (healthline website). After adulthood, increased GH leads to acromegaly which leads to continuing growth of fingers, feet, forehead, jaw, nose, and lips (UCLA Health website). Note that structures like the nose and ears also keep on growing in healthy folks.

Hence, GH does not prevent closure of the growth plates, which happens normally as far as I am aware.

Taking GH during childhood will likely lead to gigantism, and to acromegaly in healthy individuals.

EDIT: In answer to the QUESTION EDIT: the comment by @Raoul is interesting here, as the first guy Bernard Coyne was an eunich. Perhaps that was why his plates never fused as he will have had no testosterone production. I couldn't find specifics in the other 3 cases, but my guess is they are also exceptional cases (otherwise they wouldn't have made it in the record books). As to the question title I dare say that GH is not involved in plate fusion.


Alright, after a lot of searching, I have a proposed ID: Eriogonum deflexum known commonly as skeleton weed or little desert trumpet.  I feel pretty confident of the genus, less so on the species (there are several close candidates).  The family is buckwheat or Polygonaceae.

This plant has basal leaves as yours does, has pretty much leaf-less stems and relatively infrequent flowers, which look quite a bit like your picture.  Reading various descriptions it seems the plant is somewhat variable, it often looks like your pictures but sometimes has more flowers and sometimes the plant is more dense, rounded, shrubby and taller (it probably depends on the moisture and soil quality).  It is a desert species, preferring scrubby areas and washes, widely distributed in Western US deserts.

CalPhotos has a picture which looks to be a good match (credit: Jean Pawek; also, CalPhotos has many other photos).  This photo by Hank Jorgensen looks like a good match too and shows flowers which look similar to yours.

If you see the plant again, bring a picture on your phone and check the flowers carefully. Also the leaves should be hairy/wooly.


The probability of indirect human fertilization (follow-up)

Safer sex techniques are more risky.  Perfect condom use is associated with around a 2% pregnancy rate within a year.  According to that, even sterilization has a 0.1% (male) or 0.5% (female) rate.  Combining techniques is, of course, safer.  "Indirect," as you proposed in the other question, will border on an infinitesimally small chance, as answered there.


How do you obtain specific mRNA transcript levels for comparison from a Hi-Seq dataset?

It's going to be hard for you to generate an RPKM or RPM value without % aligning to the genome, or the transcriptome.  Your read counts will have no context.


How are the wings of birds, pterosaurs and bats related to each other?

Here is a discussion of homology and analogy that clearly presents bat and bird wings as an example of analogous organs:

http://amrita.olabs.edu.in/?sub=79&brch=16&sim=132&cnt=1

You are right however that bat, bird and pterosaur wings are homologous in a sense, as they have similar underlying structure and a common evolutionary origin - the front limbs of tetrapods.

One could perhaps say that bat, bird and pterosaur wings are homologous organs as front limbs, but analogous organs as wings.

This page has pictures of the skeletal structure of each:

http://www.ucmp.berkeley.edu/vertebrates/flight/converge.html

As you can see, they are similar front limbs - made of a common set of bones and muscles. But those bones have been arranged into wings in different ways: Pterosaurs have a lengthened pinky finger maintaining a flap of skin that makes up the wing; bats have three lengthened fingers with a flap of skin around them; and birds have small, fused finger bones with the surface of the wing being made up of feathers.

And it is in fact the case that as far as their evolutionary history goes, bat, pterosaur and bird front limbs have a common origin in the front limbs of tetrapods, but have separate independent origins in terms of how those front limbs evolved into wings. Or put another way, the common ancestory of bats, birds and pterosaurs had front limbs, but those front limbs weren't wings.

Compare with the "wings" of flying fish, which does have a common origin with that of birds/bats/pterosaurs: both developed from the pectoral fins of their bony fish common ancestor. Obviously they became wings independently, and they also have a very different evolutionary origin as "limbs". On the other hand when you look at the wings of insects, there is no common origin between those and the wings of vertebrates at all. The common ancestor of insects and vertebrates had no limbs at all, not even bones or an exoskeleton. Both lineages developed limbs and hard support structures independently, and then adapted some of the structures they had for flight.

Interestingly it seems a book recently came out on the flight of bats, birds, pterosaurs and insects: On the Wing: Insects, Pterosaurs, Birds, Bats and the Evolution of Animal Flight by David E. Alexander. It could be an interesting read to anyone interested in the question. Here are some reviews of the book:

http://www.bioone.org/doi/pdf/10.1642/AUK-15-210.1

https://academic.oup.com/icb/article/56/5/1044/2420642

ETA: If you want to bend your mind a bit around the question of homologous vs analogous organs (or homology vis homoplasy), look at these two questions from the sidebar:

The pectoral fins of a whale and a shark. Are they analogous organs?

How large is the range of 'same origin' when determining whether two organs are analogous or homologous?

Which ask similar questions you did, but of the fins of whales vs the fins of sharks. And that's a funny one isn't it! Because where in the pterodactyl example we have a common ancestor who had front limbs but didn't have wings, in that case the common ancestor of whales and sharks did have pectoral ("chest-level") fins, that the fins of whales and sharks descend from! So, homologous? But the fins of whales spent so much of their evolutionary history not being fins at all that it does make one want to say the homology is at the "front limb thingy" level not the "fin" level. I mean, as far as evolutionary distance goes, the wings of flying fish and of bats are actually more closely related to each other than the fins of whales and of sharks are!!! (the evolutionary history there goes: jawed fish (Eugnathostomata) -> cartilaginous fish (Chondrichthyes; led to sharks) and bony fish (Osteichthyes; led to flying fish, bats and whales).

99% of the "shark-fin-like" appearance of whale fins developed long, long after their split from the shark lineage; and I don't know what the front fins of the jawed fish common ancestor was like but it's possible it looked different from whale/shark fins too, so the some of the "whale-fin-like" appearance of shark fins may also have developed independently after the split.


Can I dry digested protein sample over weekend in a vacuum concentrator?

If your sample dried in the speed-vac then it should not cause to much damage to the sample. But if Speed Vac stopped and there was some liquid left, then incubation at room temperature would result in hydrolysis and sample degradation ( also depends on the pH, neutral would be slower). Also you would have modifications to the amino acid side chains like oxidation and deamidation


Why does a worm's skin need to be wet for oxygen to diffuse across it?

The quick answer: When the skin dries, the lipids in the cell membranes of the skin tissue undergo a phase transition which makes the membranes less permeable for oxygen.

Explanation: The lipids of the cell membrane can exist in different phase states. In the liquid disordered phase the lipids are relatively flexible and mobile, making this phase more oxygen permeable compared to the liquid ordered phase, in which the lipids are more rigidly packed.

The phase transition temperature of lipids increases upon dehydration (another reference), meaning that at the same ambient temperature, a dry lipid membrane is in the liquid ordered state and a wet lipid membrane is in the liquid disordered state.

Therefore, a dry cell membrane is less oxygen permeable than a wet one.


If the process of evolution is driven by completely random process...

It's not.  The evolution of "better" protein (and other) molecules happens because of selection, a very non-random process.  The repeated selection of better molecules, and then of the variants of the better molecules, repeated many times, will lead to "good" molecules (in the sense that they work better for their producers).


Do you know which is this small flower in Asturias?

It is an Erythronium lily commonly called a "dog's-tooth-violet" or "trout lily". I see that one of the species Erythronium dens-canis is found in Spain, being native to Europe. Most of the Erythronium species are native to North America. The foliage is very attractive and they are commonly grown as ornimentals. The flower in your photo is just opening. I have included a few links that better describe these lilies.

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

https://en.wikipedia.org/wiki/Erythronium_dens-canis

http://www.srgc.org.uk/bulblog/log2008/160108/log.html


Is it ok for Chili pepper plant's fruits to fall into its soil?

As @MCM says, the capsaicin molecule isn't intrinsically damaging - its effect upon us is mediated through the TRPV1 (Transient Receptor Potential Vanilloid 1) receptor in the membranes of cells whose function is to sense noxious stimuli such as heat. The binding of capsaicin to this protein causes transmembrane movement of Ca2+ ions which depolarises the membrane, triggering an action potential - a signal to the brain. Heat has the same effect on the TRPV1 protein. In this way the presence of capsaicin mimics the effects of heat, causing a painful sensation.

Have a look at this SE.Biology question.


Are all action potentials the same shape and amplitude when graphed with respect to time?

Short answer
Action potentials differ in shape between neuronal cell types, and action potentials may even change shapes during action potential propagation within one and the same axon.

Background

  Once an action potential is sent from a given neuron down the axon, does the shape and amplitude remain constant as it is propagated?

Although the textbooks will typically say action potentials are transmitted without their amplitude being changed this claim is theoretically virtually impossible due to the many variables encountered in and around the axon. For example, axons in the sciatic nerve may extend to a meter and it is virtually impossible to keep the exact conditions along that length exactly identical. The amplitude of the action potential is mainly dependent on the influx of Na+. Slight variations in membrane potential, concentration of sodium, or channel (subtype) densities may therefore change the amplitude. In addition, temperature affects action potential amplitude (Hodgkin & Katz, 1949) and slight temperature differences along long axons may therefore be expected to alter amplitude. Likewise, shape may alter as well. For example, glutamate released alongside axons of hippocampal pyramidal neurons results in widening of action potentials (Sasaki et al., 2011).

  Do all action potentials have the same amplitude and shape?

Therefore, given the answer under question 1 no, they do not have to. Even a propagated action potential in a given axon may change amplitude and shape, as said. Most notably, different neuronal types may in fact be classified according to their action potential morphology, such as the various neuronal types in the dorsal root ganglia of the spine that can be differentiated based on their duration (Villiere & McLachlan, 1996).

References
 - Hodgkin & Katz, J Physiol; 109: 240–9
 - Sasaki et al., Science 2011; 331: 599-601
 - Villiere & McLachlan, J Physiol 1996; 76: 1924-41


I did a quick lookup on google for "hyphal compartments" and the number of online texts/books/citations using this term is quite meagre to say the least. One of the images that I found was this-

And I have reached to the conclusion that--
Hyphae cells (only in septate species) are known as hyphal compartments.
Quoting from wikipedia (read if you don't know about septate and coenocytic varieties of hyphae)

A hypha (plural hyphae, from Greek ὑφή, huphḗ, “web”) is a long, branching filamentous structure of a fungus, oomycete, or actinobacterium.In most fungi, hyphae are the main mode of vegetative growth, and are collectively called a mycelium.
A hypha consists of one or more cells surrounded by a tubular cell
wall. In most fungi, hyphae are divided into cells by internal
cross-walls called "septa" (singular septum). Septa are usually
perforated by pores large enough for ribosomes, mitochondria and
sometimes nuclei to flow between cells. The major structural polymer
in fungal cell walls is typically chitin, in contrast to plants and
oomycetes that have cellulosic cell walls. Some fungi have aseptate
hyphae, meaning their hyphae are not partitioned by septa.
Hyphae have an average diameter of 4-6 µm.


Is there a relationship between efficiency of cellular metabolism and warm-blooded-ness?

While heat is lost during glycolysis, a lot more heat can be lost during chemiosmosis.  This is the movement of H+ (protons) across the inner mitochondrial membrane.  The energy potential of having a greater concentration of H+ on one side of the membrane usually powers ATP synthesis through ATP synthase.  In mammals, however, special proteins called uncoupling proteins (UCPs) can make the membrane 'leaky' to H+, so the energy is lost as heat, instead of being used to make ATP.  This is called non-shivering thermogenesis, and usually happens in brown adipose tissue (because fatty acids are used to enable UCP production).

It is not that glycolysis in ectotherms is less efficient (as far as I'm aware), but that ectotherms have different levels of different types of UCPs. Some UCP genes may have their expression altered in response to colder conditions (e.g. UCP2 and 3 may be upregulated) or the genes may not be present at all (e.g. UCP1 is not present in birds and crocodiles).

A better summary of UCPs in reptiles etc. can be found in this abstract:

http://rspb.royalsocietypublishing.org/content/275/1637/979.long


Temperature Tolerance In Relationship To Body Temperature

Things other than the temperature that could affect whether or not the coat is necessary: Is it raining? a wet dog will get cold quicker. How long/thick is the fur? thin coats of fur will be less efficient at keeping the dog warm than thick. Is it windy? Wind blows warm air out of the fur. How big is the dog? Size & body fat will affect the rate of heat loss. How active is the dog? A dog doing lots of fetching will keep warmer than a dog ambling along the pavement.

Clues as to whether the coats are necessary: Is the dog shivering? if yes, give it a coat. Is the dog panting? yes, take the coat off before you bake the thing!

this probably does not fully answer the question "If the temperature outside is 45°F who would feel colder?" but as requested by the OP I have posted my comments as an answer. I would expect a dog without a "doggy sweater" to be better able to cope with the cold than a human not wearing a "people sweater" or any clothes, just like the dog, if you want to make it a fair test!


DIY extraction and long term storage of human DNA sample?

If you have access to a centrifuge, either spin columns or phenol:chloroform will give very pure, high-quality DNA. Even with dirty methods, you can re-extract the product several times, to sacrifice yield for purity. Just be very clean. Whatever method you use should remove salts and proteins, which are the major contaminants. I won't go too much into how to extract DNA, as that's a whole separate question - but the most important thing is that purer is better.

You should resuspend in Tris-EDTA. Tris buffer maintains pH at slightly acidic (best for DNA) and EDTA chelates metal ions which can catalyze oxidative damage of DNA. Very pure distilled water works too, but if you get contaminants they will do more damage.

Afterwards you can store the DNA for quite some time provided it's frozen. At -20C you can store DNA for years. It may not be perfect quality when you pull it out a decade later, but most of it will be good, and I'm sure it will be okay if you use a good sequencing method (and I'm sure sequencing technology will advance more in 10 years than the degradation of your DNA). The good news is that you can simply store it in your freezer, and it will be okay. -20C particularly is not hugely important, you can probably get away with -10C or so - the crucial thing is for it to be frozen, not liquid (this vastly reduces diffusion).

If you want to do it like a pro, you would put it under -80C. This is considered very safe for multiple years. You can do even better by precipitating it with ethanol, and then storing at -80C. In my opinion, this -80C is overkill - DNA is fine, for the most part, stored at -20C and even 4C, especially if you work reasonably clean and contamination-free. If you had some extremely valuable, very sensitive DNA, sure, do the -80. But just personal sequencing/genotyping? Just extract a bit extra DNA  (a couple micrograms).

The really safe method is liquid nitrogen, which stops practically all chemical activity. Higher temperatures are too cold for most DNA-damaging reactions to proceed at a significant rate, but the molecules still move around. At -200C, they stop dead. But, once again, overkill unless you are saving very critical DNA for centuries later.

Source.

Three simple things I can recommend that are less obvious: First, do not handle your sample with hands, even gloved. Use some kind of plastic tweezers. Hands are warm and will locally warm up the sample. I would go as far as to put the sample tube in another box so that there is no direct contact. Second, avoid freeze/thawing. Whatever your storage system is, make sure it is very reliable. Third, wrap it in something opaque, to minimize light exposure.

Note as per Chris's comments: Always consult the MSDS of the substances you work with and take appropriate safety precautions! Always make sure to receive proper training before working with hazardous materials, and never purchase illegal contraband without appropriate authorization!


It looks like an Eastern Hognose Snake, which is characterized by an upturned nose and high likelihood of playing dead.

These are described as variable in coloration:

  "Two color phases are common in Virginia: (1) a patterned phase (79.6%, n = 98), characterized by a series of 19-27 (average = 23.2 ± 2.4, n = 12) black or dark-brown blotches along middorsal line, with alternating black spots on sides; body color consists of varying combinations of gray, tan, pink, yellow, orange, and red; venter of body and tail immaculate cream to dark gray;"

If you replace the tan in this image (www.virginiaherpetologicalsociety.com) with gray in yours, I think the pattern match and overall body form are very similar:


What is the oval shaped bone in the heads of some fishes?

I am a professional fish biologist and those are otoliths; I have aged thousands of them. They are primarily used in maintaining equilibrium, hearing, and balance. The details of the shape of the otolith can vary between species but generally look very similar. They are located in the skull of the fish, usually at the back.

Here is an image of other otoliths:
Photo source: Examples of common fish otoliths found at archaeological sites in Florida. Images from the Florida Fish and Wildlife Conservation Commission http://www.flickr.com/photos/myfwc/sets/72157625872804969/

Otoliths are calcium based structures located within otolithic organs (the sacule, lagena, and utricle) and make up the inner ear of boney (teleost) fishes. They come in pairs and there are three of them: Sagittal (within the saccule), lapillali otoliths (within the utricle) and asterisci (within the lagena). They are made of calcium carbonate and are generally composed in two different crystalline formations, aragonite and vaterite; crystalline form and amount depend on the otolith and stress induce metabolic processes. Otoliths are formed as the fish grows. In periods of fast growth (warmer months) the otolith forms faster and in periods of slow growth (colder months) the otolith forms more slowly. Given the cyclical pattern of warm and cold months in the year, the otolith form annuli (growth rings); annuli can be used to age fish just like rings on a tree. Additionally, they are metabolically inert and cannot be reabsorbed as calcium reserves like other boney structures in the fish; thus, they are a permanent record of the fish's age. This permanent record can also be used to evaluate the life history (i.e., movement patterns) using trace element analysis.

Specifically, how do they work/help the fish? Within the sacule, lagena, and utricle the otoliths are suspended in endolymphatic fluid within their respective organs. The organs have hair-like sensors in them that detect vibration or movement of the otoliths within, triggering an associated nervous stimuli. The nervous stimuli are then interpreted as movement and orientation.

Here are some sources:

https://dfo-mpo.gc.ca/science/aah-saa/otoliths/info/introduction-eng.html

https://en.m.wikipedia.org/wiki/Otolith#Description

https://www.sciencedirect.com/topics/earth-and-planetary-sciences/otolith

https://www.daf.qld.gov.au/business-priorities/fisheries/monitoring-compliance/monitoring-reporting/commercial-fisheries/species-specific/estimated-fish-age

This book is also an excellent resource for a much more in-depth look:

https://fisheries.org/bookstore/all-titles/professional-and-trade/55078c/


How does amiodarone act as an alpha and beta blocker?

Amiodarone inhibits sodium, potassium and calcium currents. Its major antiarrhythmic properties are thought to be related to prolongation of the
action potential duration. Amiodarone also exerts an antiadrenergic
effect by non competitively inhibiting alpha- and beta-receptors (Ghuran & Camm, 2000).

Alpha blockers relax certain muscles and help small blood vessels remain open by antagonizing norepinephrine's tightening effects on the muscles in the walls of smaller arteries and veins, which improves blood flow and lowers blood pressure (Mayo Clinic). Beta blockers decrease the effects of epinephrine (adrenaline), reducing heart rate and reducing its force, thereby reducing blood pressure. Beta blockers also help blood vessels open up to improve blood flow (Mayo Clinic).

Alpha-adrenergic receptors and Beta-adrenergic receptors are G-protein coupled receptors (Wallukat, 2002). Hence, they do not form channels and your notes are incorrect. The ion currents are mediated by channels, though.

References
- Ghuran & Camm, J Clin Basic Cardiol (2000); 3: 206
- Wallukat, Herz (2002); 27(7): 683-90


Why can't you taste food when you have a cold?

This German review supports common wisdom that the sense of taste is predominantly informed by the sense of smell. For instance, common advice to children taking "nasty" tasting medicines is to plug one's nose. Any condition that blocks olfaction, such as sinusitis from flu or other sinus infections, or blocking nasal airflow, will decrease or block olfaction and as a result, the majority of taste.

Hüttenbrink KB. [Disorders of the sense of smell and taste]. Ther Umsch. 1995 Nov;52(11):732-7. [Article in German]


Why does gaining a hydrogen in biology considered reducing a molecule?

Hydrogen can accept electrons or donate them, so it can get a bit confusing. For instance, hydrogen donates electrons from a reducing agent. For example, in biology, consider cellular respiration. A co-factor will carry electrons often by reducing an atom with a nitrogen.

Consider NADP+ to NADPH.

The nitrogen atom on the Pyridine group has an oxidation state of +1. When it picks up a hydrogen, to become NADPH, the oxidation state will go to 0 by gaining electrons brought by the hydrogen. Although the hydrogen doesn't bond to the nitrogen directly, it breaks the double bond on the para carbon (The carbon on which the new hydrogen is attached) at the top of the ring, and thus distributes the electrons to the nitrogen.

EDIT -
Hydrogen comes from some reducing agent, not a free hydride I'm sure.


Does low gravity exposure to early stages of human fetus have potential to unloc unused genetic information from earlier stages of evolution?

No
The question itself does not even make sense, we do not hold onto much unused information, there is nothing to unlock. Unused genes mutate and get co opted for other purposes. We have about a hundred new mutation per generation. Much of so called junk DNA is actually just used for other purposes besides coding for proteins.

Will a colony evolve differently sure, any isolated population evolves along its own lines but it will happen at evolutionary speeds.


Is designing alien life still just science fiction?

The answer to this question can go as far as anybody's imaginations. So I'll just tell why the answer is what it is, and try to include scientific facts (possibly with references) wherever possible.

Simple Answer: Designing alien life forms on the basis of current theoretical and practical knowledge of science (if this is what you mean) is still, and seems to remain, a field of science fiction only.

Why? Because, simply, the proposed organisms can be as many as you can count. The point is that, even if this field comes under the category of science, it will remain as large as the universe itself, because there are literally no boundations and limitations to speculation and imagination. Only recently have researchers agreed that discovering organisms similar to humans is much much less than any layman thinks. Actually, there is even a formula for it, known as the Drake equation after Frank Drake who proposed it. The equation is:

$N = R^* \times f_p \times n_e \times f_l \times f_i \times f_c \times L$

where:

$R^* =$ the average rate of star formation in our galaxy
$f_p =$ the fraction of formed stars that have planets
$n_e =$ the average number of planets per star that can potentially support life
$f_l =$ the fraction of those planets, fl, that actually develop life
$f_i =$ the fraction of planets bearing life on which intelligent, civilized life has developed
$f_c =$ the fraction of these civilizations that have developed communications i.e. technologies that release detectable signs into space
$L =$ the length of time over which such civilizations release detectable signals

Obviously, this answer comes out to be very small, meaning that intelligent life is very difficult to find. But that doesn't mean finding life is difficult. And this claim gets even more support when scientists find water on mars and even mercury! Now, to give a bit of knowledge, this field is not really limitless; there are (at least) two limits (i.e. I'm not including more). The first limit is source of liquid water$^*$. Now, knowing that water is easy to be found almost anywhere, this does not seem quite a difficult one. Another one is source of energy. Now this is a difficult one. The problem with discovering life (in near future at least) is the area in which we are searching. Most of the searches (by telescopes of course) are being conducted near red dwarf stars. There are quite some reasons for it:

red dwarf stars are quite stable
they have very long life
they are pretty less shiny (making observations easier)
they may be home for many super-Earths

But being less shiny also poses a problem: too less energy for life. Red dwarf stars emit most of their radiation in the infrared portion of spectrum, which is pretty useless for plants (on Earth at least). Now, to survive in a red dwarf system, plants need to capture infrared light. Thus, the speculated plants in red dwarf systems will be pitch black just to absorb more energy. Also, red dwarf stars are pretty lightweight, as less as 7.5% of sun. This means they have less gravitational pull i.e. they will have much lighter planets in their Goldilocks zone. Now, much lighter planets means much less gravity on planet's surface. Thus, the speculated plants in red dwarf systems will be a lot higher than plants on Earth. But, less gravity also means much less density of air even on surface. Now, you can interpret it yourself. And, not just to surprise you, there would be absolutely no surprise if in future a satellite discovers silicon-based life, because it is really possible for life to emerge from silicon instead of carbon!

$^*$why I am continuously saying liquid water has a reason. Water is actually one of the very few candidates that can serve the purpose of maintaining life forms. Its one of a handful of liquids which are liquids at desired temperature. As one might think, life cannot survive below a certain temperature, simply because below that temperature, the liquid itself would absorb all the metabolic heat from organism and evaporate. So, it is quite relevant to say liquid water here.

What I meant to say is that there are technically no boundations to designing alien life forms, as long as you talk about the whole universe. So, this does not really count as science. After all, if you search science definition on Google, you get this:

  the intellectual and practical activity encompassing the systematic study of the structure and behaviour of the physical and natural world through observation and experiment.

This does not include imagining alien life forms in any way. So, I do not think this subject would ever be considered as scientific by the scientific community. Mostly, scientists are not indulged in this kind of work because they like to observe and interpret natural phenomena rather than imagining them. Scientists make laws from nature rather than applying laws on nature. Still, there are some scientists who take this matter seriously and publish scientific papers about it. I could find only one (PDF) related to this point. You might get some more on the internet.

In the end, if you think about how plants would look on a planet in a red dwarf system, you might end up with this:

Bonus: Dawn space probe from NASA has detected organic materials on Ceres(!) Now, what kind of organisms would you expect to see there based on our current knowledge about Ceres?


The term "cortical circuit" refers to the generalization that the neocortex is a uniform structure. For the most part, the outer sheet of the brain (the neocortex) is the same structure of neurons all the way around the brain.  It consists of the canonical six layers and it generally looks something like this.  Different research will emphasize different aspects of the circuit.

Anyway, it's quite an interesting evolutionary step for mammals.  The neocortex.. or "associative cortex" as it's sometimes called... is a very dexterous structure.  Someone born without sight will still make use of their occipital lobe to process nonvisual sensations.

Of course, as a I qualified above, it's not strictly true that the neocortex is uniform all the way around; there are exceptions.


Why are skin tactile receptors considered to be phasic receptors?

Short answer
Slowly adapting mechanoreceptors in the skin mediate the perception of static pressure stimuli, while rapidly adapting skin receptors mediate swiftly changing (e.g., vibratory) stimuli.

Background
There are various skin receptors. Hairy skin, such as that encountered on the arm, contains at least four specialized mechanoreceptors, namely Pacinian corpuscles, hair follicle receptors, Ruffini endings and tactile discs. They can be roughly distinguished by their adaptation rates, namely fast adapting (Pacinian corpuscles and hair follicle receptors) and slowly adapting (Ruffini endings and tactile discs). Rapidly adapting receptors generate robust responses to vibratory stimuli, but respond weakly to static pressures. The opposite is true for slowly adapting receptors (Kaczmarek et al., 1991).

Hence, the static pressure is faithfully registered by static pressure receptors, while the phasic receptors are specialized in vibratory perceptions.

Static receptors fire a continuous train upon a continuous pressure stimulus, phasic receptors do so only at the start and the end of a static pressure stimulus. Hence, when there is a fast vibrating stimulus (say 200 Hz), then the phasic receptors will also fire action potentials each time at onset and offset of a pressure phase, thereby faithfully representing the stimulus. Here follows a picture of various skin receptors and their responses to a static pressure stimulus. Note that only the slowly adapting receptros show a rocust response:

Source: Michael Mann

Reference
Kaczmareck et al., IEEE Trans Biomed Eng 1991;38:1-16


Why do DNA and RNA have the functions they have?

DNA is more chemically stable than RNA, which makes it ideal for long-term storage. RNA viruses like HIV have a short lifespan and must replicate to survive, which is why they can get by with a less chemically stable genome.

RNA is a useful format to transcribe since it has multiple forms and functions (e.g. rRNA, mRNA, tRNA, siRNA, snRNA, miRNA, etc.). RNA can sometimes function like a protein in which it carries out cellular actions without needing to be translated. It has been hypothesized that RNA were the first molecules as precursors to life since they can function for both storage and action. The theory is that RNA was the first molecule but was then able to be translated into proteins (which were more variable/useful) and able to be stored as DNA (which was more stable as a storage medium).


Disease causing variants and Hardy-Weinberg Equilibrium

Hardy-Weinberg law makes a series of assumptions. One of them is the absence of selective effects. As you talk about disease, this assumption of neutrality is obviously not met.

At the moment of fecundation

Imagine for example that at the moment of the fecundation, the genotypes AA, Aa and aa are at Hardy-Weinberg equilibrium. Let x be the frequency of the allele A at the moment of fecundation, the frequencies of the genotypes AA, Aa and aa are $x^2$, $2x(1-x)$ and $(1-x)^2$, respectively.

After selection

As all genotypes aa die off, you're left with the A allele being at frequency $y=2x^2 + x(1-x)=x(1+x)$ and the frequencies of the genotypes AA, Aa and aa are $\frac{x^2}{x^2 + 2x(1-x)}=\frac{2x-2}{x-2}$, $\frac{2x(1-x)}{x^2 + 2x(1-x)}=\frac{x}{2-x}$, and $0$, respectively.

Expressing the genotype frequencies in terms of the new allele frequency

You can as well plug $y$ into those genotype frequencies to get the expression in terms of the genotype frequencies at birth ($y$; after selection). It gives you $\frac{1-\sqrt{4 y+1}}{\sqrt{4 y+1}-5}$, $\frac{2 \left(\sqrt{4 y+1}-3\right)}{\sqrt{4 y+1}-5}$ and $0$ for the genotypes AA, Aa and aa respectively. So, obviously, it is not at Hardy-Weinberg equilibrium.

Assumptions

You can make some more interesting calculations by leaving out the assumptions that all aa genotypes die at birth and you could use a Leslie matrix to describe the probability for an individual of each genotype to make to the next age. I also assumed that the a is completely recessive. You might want to release this assumption as well by computing the death of a fraction of the Aa genotypes.


Yup. Radiation induced secondary cancers exist and vary in their site of incidence and risk of incidence based on the site of treatment. In breast cancers treated with radiation, for example , there is upto a 3 fold increase in relative risk relative to the general population for leukaemias within five years and 1.5 times the relative risk for secondary lung cancers within 15 years.

The literature also reports 1 in 10 malignancies as being of a secondary nature, and radiotherapy amongst others is probably responsible for a fraction of those.

Despite this risk, radiotherapy is very often worth using because without it the risk of dying from the primary cancer is vastly greater than the risk of a secondary malignancy from therapy, and secondly, unlike systemic chemotherapy, the side effect profiles of radiation are more tolerable and localised.

It is also possible to "shape" fields of irradiation to maximise the dose delivered to the tumour and to minimise exposure to normal tissue; this is called intensity modulated radiotherapy (IMRT).

Also, a lot of the cancers radiotherapy is used for occur in older people, and the benefits of saving someone from their primary tumour again outweighs the risk of secondary malignancies later on. It is especially of concern in paediatric patients because that brings with it the risk of secondary malignancies in middle-age, but advances in intensity modulation I think has the potential to minimise that risk.


The center of the cell in this case is a way to say "the nutrients arrive to every part of the cell", and should not really be taken literally as "the center". If the cell is modeled as a sphere, with the nutrients diffusing in from the outside, the whole sphere would be filled with nutrients when the nutrients "arrive to the center". Figure 1 shows how the nutrients would diffuse from the outside layer further in. It is like saying the whole glass would be filled when the water "arrives to the top". It does not particularly mean that the vital organelles are in the center, but is just used to illustrate the fact that nutrients diffuse into and can reach all parts of the cell.

Figure 1: an illustration to show how nutrients would diffuse from the outside to the center of the cell, filling the cell with nutrients. This image is trying to model a cross-section of a circular cell. The nutrients would for example enter from around the green layer, and gradually get to the middle/center dark blue area.

Resources may get depleted before they reach the "center" of the cell because of the rate of diffusion, and also because metabolic processes may convert the resources into other molecules (e.g. converting glucose into ATP; glycolysis happens in the cytoplasm, and can happen in any part of the cell. If that particular glucose molecule is used up, then it will not be able to travel to the center).

Moreover, the "important organelles" are not in the center in particular. If you have seen an image of a typical plant cell for example, most organelles are around the walls of the cell (Figure 2).

Figure 2: a typical plant cell electron micrograph.

Also, you must remember that the Surface Area to Volume ratio is also a restriction for the effective diffusion of waste substances out of the cell. The small volume / big surface area is not only because nutrients have to diffuse in, but also because waste products (like CO2) must be able to diffuse out of the cell, through the membrane.


does the amount of blood circulate in a body is same before and after amputation?

The kidney regulates the amount of blood being produced and removed from/recycled in the body. Even if somehow the body lost no blood when it lost the limb, the kidneys would remove the excess blood as it filters.

I think the misconception in asking this question is that the body knows how much blood to produce for the body. Yet, that isn’t the case, it just regulates the amount based on different signals it gets from the blood.

More info: https://www.ncbi.nlm.nih.gov/m/pubmed/17630596/


What prevents platelets from clotting regular blood vessels?

Platelets activate when the exposed collagen (which is normally present below the endothelium) at the wound site binds to the platelets, forming a plug. Other factors are also secreted which aid in stronger binding. A signaling cascade is triggered which then makes platelets release proteins called integrins, which help for tighter binding of platelets at the site. Activated platelets also release many stored compounds from their granules which initiate further signaling cascades to form a clot.
In a healthy tissue, there is no exposed collagen. Ergo, No clotting.


How is Coenzyme A Transported to the Matrix?

Zhyvoloup et al. (2003) J Biol Chem 278: 50316-50321; emphasis mine:

  CoA synthase is localized on the mitochondrial outer membrane.
  Moreover, we demonstrate for the first time that phosphatidylcholine
  and phosphatidylethanolamine, which are the main components of the
  mitochondrial outer membrane, are potent activators of both enzymatic
  activities of CoA synthase in vitro. Taken together, these data
  provide the evidence that the final stages of CoA biosynthesis take
  place on mitochondria and the activity of CoA synthase is regulated by
  phospholipids.

https://www.ncbi.nlm.nih.gov/pubmed/14514684


Does DNA polymerase I require a $3^\prime$ end?

DNA Pol I does require the 3' end of a previous nucleotide to initiate elongation.

Regarding Okazaki fragments, this is accomplished by the annealing of small RNA primers to the lagging strand part of a replication fork. DNA Pol I extends the lagging strand off of the 3' end of those primers, generating the Okazaki fragments. The RNA primers are later removed, leaving gaps between Okazaki fragments, which are later filled in through the combined actions of DNA PolI and DNA ligase.

In the case of telomeres, the final RNA primer can't be filled by DNA Pol I because polymerase requires a free 3' hydroxyl for the attachment of the first DNA nucleotide. After removing out the RNA primer, the first DNA nucleotide would need to be attached to the DNA nucleotide preceding it, which is not found in the case of the final primer on a telomere, since it's all the way at the end of the linear strand.

In this case then, DNA Pol I removes the RNA primer is removed by DNA pol I but cannot replace it with DNA, leaving a gap (step 6 in the following image).


What does C. Elegans sense when touched?

In short, you are correct. You touch the skin, and that compresses mechanoreceptors, which then generate a cascading neuronal response.

As far as the actual neurons, it really depends on the type of touch. For example, a well characterized type is gentle mechanical stimuli, which can involve ALM, AVM, PLMs, and PVM, depending on the response (Will Schafer's review doi:  10.1007/s00424-014-1574-3).

Those gentle touch receptors (TRNs) are in the hypodermis, and they have specialized mechanotransduction (MeT) channels along their neurites. It's the altering of those channels that causes receptor activation and the whole downstream behavioral response (summarized from the scientific reports paper below).

So, in summary: mechanoreceptor neurons are activated, and those produce a response. By "response" I mean that those mechanoreceptor neurons activate some interneuron pathways, which in turn activate motor neurons, which make the worm do stuff.

There are many other mechanosensation mechanisms, and WormBook is the place to see a ~comprehensive review of those.

The actual mechanical mechanism/way that MeT channels are activated is a great enough question that a recent paper was published in Scientific Reports to address it. That paper is DOI:10.1038/s41598-017-12190-0 (Elmi et al. Determining the biomechanics of touch sensation in C elegans).

They introduce the paper reiterating what I summarized above.

  [...] touch sensation can be considered as a chain of events initiated
  by the spatiotemporal distribution of mechanical loads applied to the
  skin, which result in stresses that deform the skin’s surface,
  sub-layers and underlying mechanoreceptors. In response to the
  transmitted mechanical energy, the mechanoreceptors activate a
  neuronal signaling network that encodes the physical contact as
  information which we perceive as ‘touch’.

Elmi et al. set up a clever assay to look at how the worm's body changes. The body is pretty elastic (up to 16 micrometers) and there's some imperfect skin displacement because the body isn't perfectly cylindrical.

They used that data to build a preliminary model of the different layers of a worm body, and then they validated and tuned the model. It's a cool paper (with some math/physics, which from your profile it looks like you might appreciate).


Chapter 31 in the Voet and Voet biochemistry book (I have the 4th edition) link has a rather extensive explanation on this subject. It is rather pricey but you can find a copy of this one in nearly every university library. It generally is a good resource if you want to know more about the DNA or Protein structure of a basic process


I think your getting confused. Your assuming that it's actually the heat or cold that creates the feelings of pain.

  I was very surprised. cold is just atoms moving slower.

Pain is a warning mechanism, stop doing that or you'll hurt yourself. It is not caused by the atoms in your nerves moving faster or slower in response to heat. Your nerves are triggered by a stimulus that could cause harm to your body and react by passing a pain signal to your nervous system. The heat (or lack of it) does not transmit up your nerves.


ID Request: What is this frog? Eastern Long Island, NY USA mixed hardwood forest

It is hard to tell exactly from the photos, but given the location and time of year, it is either a juvenile green frog (Rana clamitans) or juvenile bull frog (Rana catesbeiana).


How can (or did) Deinococcus radiodurans continue to evolve after developing resistance to mutation?

According to the "Functional adaptation" section of this webpage, Deinococcus radiodurans uses repair proteins to stitch up DNA after radiation damage. Meaning, after a burst of radiation, the DNA will be in pieces and the repair proteins put it back together. It seems like this mechanism would not come into play during other forms of DNA mutation that happen during replication, such as point mutations or inversions.


Possible combinations in the Meiosis' Telophase 1

Failure to properly separate homologous chromosomes during meiosis, either by including an extra copy of a chromosome or including zero copies of a chromosome, causes gametes that are 'aneuploid', and as a result, a zygote that results from that gamete will have an extra or missing chromosome as well.

For humans, most aneuploidies are completely fatal at some point of early development, so there is not an associated genetic disorder in live births.

One common aneuploidy that is not fatal to the embryo is an extra copy of chromosome 21; this causes Down syndrome.


We have to consider the main function of lignin in xylem vessels, which is providing mechanical support for the plant. For the parts of plant above the ground, the stem where the xylem is located has to counteract the gravitational force pulling the plant down. Here's where lignin comes in to strengthen the xylem to support the plant. Remember that this is for many land plants.

Compare this to creepers, vines and aquatic plants. Lignin is absent or only present in small amounts as for creepers and vines, they have another external support, while for aquatic plants, it's weight is distributed on the surrounding water apart from the stem.

Now we can liken the case for aquatic plants to the xylem vessels in the roots of land plants. The roots of land plants are firmly anchored in the soil, and the plant's weight is distributed along the roots and soil, not just on the central root (for tapped roots). Hence there is not a need for lignin in roots of land plants.

And yes there are perforations in lignin as mentioned by @Always Confused, hence water can still enter the xylem vessel even when lignin is waterproof.


Is there any biosafety level scale for plant pathogens?

Plant pathogens are not a health hazard to the experimenters. However, they can pose health hazards to plants and cause damage to ecosystem. There are plant biosafety levels: BL1-P up to BL4-P (also sometimes abbreviated as BSL-1P and so on). The four levels have an increasing order of stringency of containment. Containment of plant pathogens (also seeds and pollen) is the primary concern, not exposure to them.

From NIH guidelines:

  For research involving plants, four biosafety levels (BL1-P through
  BL4-P) are described in Appendix L, Physical and Biological
  Containment for Recombinant or Synthetic Nucleic Acid Molecule
  Research Involving Plants.  BL1-P is designed to provide a moderate
  level of containment for experiments for which there is convincing
  biological evidence that precludes the possibility of survival,
  transfer, or dissemination of recombinant or synthetic nucleic acid
  molecules into the environment, or in which there is no recognizable
  and predictable risk to the environment in the event of accidental
  release.  BL2-P is designed to provide a greater level of containment
  for experiments involving plants and certain associated organisms in
  which there is a recognized possibility of survival, transmission, or
  dissemination of recombinant or synthetic nucleic acid molecule
  containing organisms, but the consequence of such an inadvertent
  release has a predictably minimal biological impact.  BL3-P and BL4-P
  describe additional containment conditions for research with plants
  and certain pathogens and other organisms that require special
  containment because of their recognized potential for significant
  detrimental impact on managed or natural ecosystems.  BL1-P relies
  upon accepted scientific practices for conducting research in most
  ordinary greenhouse or growth chamber facilities and incorporates
  accepted procedures for good pest control and cultural practices.
  BL1-P facilities and procedures provide a modified and protected
  environment for the propagation of plants and microorganisms
  associated with the plants and a degree of containment that adequately
  controls the potential for release of biologically viable plants,
  plant parts, and microorganisms associated with them.  BL2-P and BL3-P
  rely upon accepted scientific practices for conducting research in
  greenhouses with organisms infecting or infesting plants in a manner
  that minimizes or prevents inadvertent contamination of plants within
  or surrounding the greenhouse.  BL4-P describes facilities and
  practices known to provide containment of certain exotic plant
  pathogens

  Section III-D-5-a. BL3-P (Plants) or BL2-P + biological containment is recommended for
  experiments involving most exotic (see Section V-M†, Footnotes and
  References of Sections I-IV) infectious agents with recognized
  potential for serious detrimental impact on managed or natural
  ecosystems when recombinant or synthetic nucleic acid molecule
  techniques are associated with whole plants.

  †Section V-M.  In accordance with accepted scientific and regulatory practices of the discipline of plant pathology, an exotic plant pathogen (e.g., virus, bacteria, or fungus) is one that is unknown to occur within the U.S. (see Section V-G, Footnotes and References of Sections I-IV).  Determination of whether a pathogen has a potential for serious detrimental impact on managed (agricultural, forest, grassland) or natural ecosystems should be made by the Principal Investigator and the Institutional Biosafety Committee, in consultation with scientists knowledgeable of plant diseases, crops, and ecosystems in the geographic area of the research.

These descriptions refer to plant experiments in greenhouses. When working with plant pathogens in a lab (in vitro culture or on whole plants in incubators), similar guidelines should be followed.


Cyanide binds cytochrome oxidase so as to prevent the binding of oxygen. Electron transport is reduced to zero, and none of the oxygen breathed in can be used. Cytochrome oxidase is one of a superfamily of proteins which act as the terminal enzymes of respiratory chains, so if the cyanide is binding to the cytochrome then it inhibits the process and making it dangerous. Another example I would give rotenone which binds competitively.


It has been demonstrated that there are common patterns of microbiome composition evolution during life. In general, the diversity of microbiota composition of fecal samples is significantly higher in adults than in children, although interpersonal differences are higher in children than in adults. Much of the maturation of microbiota into an adult-like configuration happens during the three first years of life.

As the microbiome composition changes, so does the composition of bacterial proteins produced in the gut. In adult microbiomes, a high prevalence of enzymes involved in fermentation, methanogenesis and the metabolism of arginine, glutamate, aspartate and lysine have been found. In contrast, in infant microbiomes the dominant enzymes are involved in cysteine metabolism and fermentation pathways

evolution of the vertebrate gut microbiota :

Multi-cellular eukaryotes have existed for at least a quarter of Earth's history, or 1.2 billion years. Thus an already long history of interaction between multi-cellular lifeforms and microbial communities preceded, and likely shaped, the evolution of the vertebrates. The legacy of ancient associations between hosts and their epibiotic microbial communities is evident in the present day effects that the gut microbiota exerts on host biology, ranging from the structure and functions of the gut and the innate and adaptive immune systems, to host energy metabolism. Host responses to microbial colonization are evolutionary conserved among diverse vertebrates including zebra fish, mice and humans

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664199/

"the human body is made up of about 10 times more microbial cells than human cells . Further, there may be millions more microbial genes than human genes in this human+microbiome system (which is often thought of as a human ‘superorganism’), and it is the ways in which these microbial genes interact with the human host that describe their ultimate role in our health. Scientists now believe that infants are sterile (meaning free of microbes) in the womb and receive their first inoculum of microbes from the mother during natural childbirth. This inoculum goes on to colonize the newborn and initiate a succession of events leading to the development of the child’s own microbiome. The newborn relies on this maternal vaginal microbial inoculum and the additional inoculum of microbes from mother’s breast milk for microbial colonization of all exposed surfaces in and on the infant’s body (e.g., oral, nasal/airways, gut, urogenital, skin).2 This is a dynamic process in which microbial abundances increase from effectively zero at birth to over six orders of magnitude (that’s more than a million times!) within just the first few weeks of life, with wide swings in the microbial membership of these communities until the microbiota largely stabilize in composition and numbers after approximately three years of life."

http://www.actionbioscience.org/genomics/the_human_microbiome.html

you can read about Gastrointestinal Tract Microflora here:

https://www.ncbi.nlm.nih.gov/books/NBK7670/

and normal flora :
https://www.ncbi.nlm.nih.gov/books/NBK7617/


Stomach Virus : How does it affect the bacteria of the intestines?

No, since the pH and the conditions are different in the different compartments (stomach, small intestine, colon) of the bowel.
See this figure (taken from this website) for the differences:

There are not that much bacteria in the stomach, so even even nothing else than acidic stuff comes out, the bacteria are not affected. And even when you have a severe diarrhea, there are still enough bacteria left to keep it colonized.


Why isn't there 1' to 2' direction or something else except 5' to 3' in dna replication?

[Source]

DNA is a polynucleotide. The above structure is of a nucleotide which has three components, a nitrogenous base(yellow), a pentose sugar(purple) and a phosphate group. These nucleotides form phosphodiester linkages to form a polynucleotide.

[Source]

These phosphodiester linkages are formed between 3' and 5' carbons of the pentose sugar which is shown in the above image.

[Source]

The end of DNA having a free phosphate group at 5' of pentose sugar is known as the 5'-end of DNA, and the end of DNA having a free hydroxyl group at 3' of pentose sugar is called the 3'-end of DNA.

Here, you can play with the DNA.


It seems like you suffer from a misconception. "The left eye sees more of the left side of an object..." is not how distance perception works. Otherwise we wouldn't be able to estimate the distance from flat objects, such as traffic signs and shooting targets.
The actual mechanism is parallax estimation, or Binocular disparity. In a nutshell, the closer an object is to your eyes, the bigger the difference of its position on the left and right eye's retina will be.
You may perform a simple experiment: find a place where several parallel wires hang in the air: a train line or aerial phone/power line. Look at the wires normally, and they will appear just as black lines in the sky, with no distance perception. Now tilt your head to the side, and you will instantly gain a feeling which one is closer, and which one is further away. Why the difference? Because any shift of a horizontal wire gives the same picture, meanwhile for vertical wires the difference is obvious.
When you close one eye, your brain loses the ability to estimate parallax. However, it is left with several options:

Visual cues. If one object overlaps another, it's obviously closer. If two objects look the same but one is smaller, it's probably further away (or a child). If you know the expected size of an object (a mountain/a horse/a fly), you may get the feeling of distance as well.
Focusing distance. When you focus your eye on a near and far object, the feelings are different.
Memories. You remember what you've seen with two eyes.

Of these, only (3) depends on previous binocular vision. (1) and (2) are available even to those who were born with one eye. However, parallax estimation is much faster and more precise. With a single eye you will be able to hit a fly on the wall, but catching it in the air will be extremely difficult.


What is the name of this strange white caterpillar?

It is hard to be sure without clearer pictures, but that looks like something in the genus Eriocampa and it could be a Butternut Woollyworm (Eriocampa juglandis).
Picture taken in Kentucky from BugGuide.net © 2015 by dan40165:

These are the larvae of a sawfly (so not technically a caterpillar) and are about 1 inch long.
You can learn more about this particular species here. To narrow down the exact species it would be helpful to edit more information into your post including the types of plants in the area.


Does one neurotransmitter travel all the way through the nervous system?

You've got a few things mixed up here:

A signal may travel down a pathway, passing through several neurons (e.g. around 4-8). However, this signal is not always in the same form: From one end of a neuron to the other, it is merely an electric potential which travels down the neuron's cell membrane (from the dendrite to the axon hillock, where the cell decides whether to carry the signal on; if yes, a new potential is sparked to travel down the axon).

When the potential reaches the end of a neuron, i.e. an axon terminal, it causes exocytosis of neurotransmitter. The signal has become chemical now. This diffuses through the synaptic cleft to the next neuron, where it acts on ion channels in the membrane to cause a new electric potential.

So the actual distance a neurotransmitter travels is only the distance between the two membranes at the synapse, i.e. the synaptic cleft. This is only about 20-40 nm wide, so it's fairly rapid :)


I am pretty sure that this is an oil beetle (also known as blister beetle) of the family Meloidae. In this special case this is probably the violet oil beetle (Meloe violaceus), although this does not completely coincide with the size you mention. The slightly different color is probably caused by the different lighting.

See the image from this Wikipedia for comparision:

Be careful with them, as they can secrete a poisonous substance making blisters on the skin (hence there name) when they feel attacked. For more information see also here.


Plasmid addiction system in high-copy number plasmids

According to the review by Kroll J, Klinter S, Schneider C, Voß I, Steinbüchel A. Plasmid addiction systems: perspectives and applications in biotechnology. Microbial biotechnology. 2010;3(6):634-657. doi:10.1111/j.1751-7915.2010.00170.x., there are high-copy-number Plasmid Addiction Systems (PAS), "specifically the addiction system depending on plasmid‐borne ORT utilizing the lac repressor."

  The lac repressor protein (LacI) binds to the lac operator (lacO) and therefore represses the expression of the kanamycin resistance gene. When IPTG is available as an inducer, LacI is titrated by lacO, and the E. coli cells were able to grow in media containing kanamycin due to expression of the corresponding resistance gene. The same result was obtained when high‐copy‐number plasmids harbouring lacO were used for ORT. In this case the plasmid was stably maintained over 72 generations (Williams et al., 1998).

ORT = operator repressor titration

ORT is one of the three main groups of PAS.


Is life expectancy linked to intelligence in animals?

Limiting the conversation to mammals, and taking relative brain size as a proxy for intelligence (which, of course is not necessarily "true", but at least is quantifiable), the answer is yes: body-size relative  brain size correlates with   body-size relative longevity in mammals.

  using a global database of 493 species, we provide evidence showing that mammals with enlarged brains (relative to their body size) live longer and have a longer reproductive lifespan (González-Lagos et al.).

They present data by species in the paper, which is available free online, but so as to have something on SE, I've mocked up a chart based on the averages they give for each mammal order:

 González-Lagos C, Sol D, Reader SM. 2010. Large-brained mammals live longer. Journal of Evolutionary Biology 23: 1064–1074.


How can I predict DNA binding affinities from a protein sequence?

Those that come up from a Google search ("predict DNA binding from protein domain tool") seem pretty well suited to your question.

BindN
DNAbinder

Depending on your computational/statistical know-how you might also find these papers relevant

Huang et al, Predicting and analyzing DNA-binding domains using a systematic approach to identifying a set of informative physicochemical and biochemical properties
Gao et al, A threading-based method for the prediction of DNA-binding proteins with application to the human genome


Can DNA base pairs go through each other?

The base pair you are describing is only stable if each base is part of a macromolecular polymer, a polynucleotide. Specifically the DNA strands need to be oriented in an anti parallel alignment, and there will be a chain, or string, of base pairs (imagine the rungs of a ladder).
Remember, individual hydrogen, or H-bonds, are one of the weakest molecular interactions that we can detect. So the scenario you propose, where one single base forms a Watson-Crick base pair with its complementary base, free in solution, is so unstable as to be undetectable.

Once the base pairs are formed in a DNA double helix (think of a flexible ladder where one end is fixed and the other end has been twisted through several clockwise revolutions) then there are many other energetic contributions that stabilize the base pairs. For example, the electrostatic repulsion of the anionic phosphates in the sugar-phosphate backbone drives the two strands apart.  The hydrophobic stacking interactions of the pi bonds of adjacent bases also makes a major contribution to the stability of the helix, and permits the H-bonds to be more stable in this context.

Finally, the fact that base pairs are only stable in polynucleotides means that if you melt a single base pair, the sugar phosphate backbones will topologically prevent any other melted base pair from "passing through" the first one.


Why do larger diameter myelinated axons have greater conduction velocities than small diameter myelinated axons?

Why should the action potential in Axon B traverse the distance X1 to X2 more quickly than in Axon A?

The larger the diameter of the axon, the less the longitudinal resistance, so the current can propagate along the axon more easily.

Shouldn't the increased capacitance of Axon B (due to its increased diameter) increase the time it takes for the action potential to travel between the two points?

Both, the capacitance and the number of ion channels increase quadratically whit the diameter. So the increase in capacitance is compensated by an increase in total ionic current.

Wiki cable therory


This is some species of Ground Beetle (family Carabidae); the trochanter of the hind leg (just before and somewhat overlapping the femur) and the threadlike antennae helps point to that group.  The book The beetles of northeastern North America by N. M. Downie and Ross H. Arnett (Sandhill Crane Press 1996; now out of print but in at least some libraries) may help with a species identification (fair warning: the keys are not profusely illustrated).


How can bats hear such high frequencies?

Short answer
Echolocating bats have relatively large sensory epithelia in their inner ear, that may correlate with their high upper frequency limit of up to 200 kHz. The basilar membrane is thinner and stiffer, possibly allowing it to decode higher frequencies.

Background
In terms of the place theory of hearing, the cochlea acts as a frequency transformer, where high frequencies are encoded basally, and low frequencies apically. The cells responsive to sound, the hair cells, are located along the basilar membrane (BM). Going from base (high frequency) to apex (low frequency), the BM becomes wider and less stiff, making it more susceptible to encode low frequencies apically. Note that sound is encoded as a travelling wave, where the point of resonance of a particular frequency corresponds with the characteristic frequency of the hair cells (Fig. 2).

Fig. 1. Rolled out cochlea. Source: New York University.

Fig. 2. Travelling wave and resonance frequencies along the basilar membrane. Source: University of Minnesota.

A study in Microchiroptera species revealed that the basal part of the basilar membrane was relatively narrow and stiff, which increases the resonance frequency of the basal part of the BM and hence may allow it to encode higher frequencies in these bats (Pye, 1966).

Because the high frequencies are encoded basally, it would be tempting to speculate the basal region would be enlarged in echo locating bats. Although this is true in some species, it may have more to do with frequency sensitivity than the upper limit of hearing, simply because a larger surface of the BM allows for more exquisite resolution of the BM. Although there is a tendency for larger BM lengths in echolocating bats, it is not consistent (Davies et al., 2013).

The human BM is 33.5 mm, while the BM of the bat with the highest frequency limit known (200 kHz, Hipposideros bicolor) is only 9.13 mm. However, compared to that of acoustically unspecialized mammals of a similar body size, e.g. Sorex araneus (BM length 4.4 mm) and Mus musculus (BM 7.0 mm) it is relatively long. However, as said, other bats with lower upper-frequency limits have longer BM lengths, e.g., Pteronotus parnellii (13.2 mm) and Rhinolophus ferrumequinum (16.1 mm). Indeed, the BM length has been correlated both with an extension in frequency range as well as enhanced frequency resolution (Dannhof & Bruns, 1991).

References
- Dannhof & Bruns, Hear Res (1991); 53: 253-68
- Davies et al., Front Zool (2013); 10: 2
- Pye, J Morph (1966), 118: 495-510


Do camels have nucleated RBCs or enucleated RBCs?

Camel RBCs are anucleate [1, 2]. The dark structure seen in microscopic images is not nuclei but a network of microtubules called the marginal bands. Marginal bands cause these RBCs to adopt an ellipsoid shape. The unique shape of these RBCs possibly allows them to survive osmotic stress and is probably advantageous to a camel under extreme dehydration.

References:
[1] Cohen, William D., and N. Barclay Terwilliger. "Marginal bands in camel erythrocytes." Journal of cell science 36.1 (1979): 97-107.
[2] Long, Charles A. "Evolution of function and form in camelid erythrocytes." Actas de The 2007 WSEAS International Conference on Cellular & Molecular Biology, Biophysics & Bioengineering. 2007.


Can I grow unlimited stem cells from limited embryonic stem cells?

Like I said in my comment stem cell culture is a very difficult process, and while people have been doing research on this for about two decades there is still a lot we don't know about stem cells. Additionally working with (human) stem cells can cause a lot of ethic problems and is therefore under strict regulations in most countries.

In principle stem cells will continue to divide until they get a signal o differentiate. In normal embryo development some cells start producing these signals at different stages, and the complete interaction of different signals allows the formation of the organism.
In cell culture one has to make sure that exactly the right signals (which are mostly growth factors) are present in the culture medium, since stem cells can easily die if they do not get any signals.

I don't have any detailed experience or knowledge in working stem cells, but a quick literature search turned up these two papers, which should provide you a good starting point. There's likely a lot more research out there you can look for.


Was life less colorful before color vision evolved?

It is likely that the world have been less colourful before colour vision evolved, though that is my opinion, I will now back it up a little.

Certainly some of the colour we see in nature serves a function outside of the use of visual stimuli. For example plants have green leaves because of the way that functions with photosynthesis - it absorbs enough energy whilst not so much that the leaves burn. For more on the green leaves in plants see this classic Biology SE question with it's very good answers. Other examples could include functions such as thermal regulation or light contrast for camouflage (if anyone has other valid examples then please comment and I'll add them in).

However, there is likely to have been an increase in the prevalence of colour in nature since the evolution of colour vision. Colour is used as a visual stimulus in numerous ways. My first example is flower colouration. Flowers use coloured petals as a stimulant to attract pollinators. Another example is the use of colour in mate attraction. Peacocks tails, the orange bills of blackbirds, and the brightly coloured cichlid fish. All of these examples take advantage of colour vision, without it they simply wouldn't be as discernible from less colourful variants and given the cost of producing them it is unlikely they would evolve as often as they do. A third example is camouflage, the most striking example I can think of is cuttlefish which match themselves very well to their background.

Although I haven't provided direct evidence that the world was less colourful I have provided a potential theory. Hopefully the examples I've presented have convinced you that my theory of the world being less colourful, even possibly only marginally less so, is not developed without thought.

I will point out it is entirely possible the world was equally or even more colourful before - no colour vision would allow colours to drift around more, selection on colour in the context of camouflage would reduce the variety of colour we see as selection would favour colours matching the surroundings (if camouflage was necessary to survival in a grass environment we would expect most things to look quite green). To this end, I don't think we can currently answer your question firmly but we can put out theories as to how it would have been.


Do "transcription factor binding site" and "operator" mean the same thing?

As you no doubt know, the term operator was coined by Jacob and Monod as part of the formalism they developed to explain the properties of certain mutants in the lac operon in E. coli. In physical terms it is indeed the site of binding of a transcription factor, the lac repressor.

My understanding is that technically it is best to restrict the use of this terminology to bacterial systems in which the idea of an operon is useful. I don't think it would be wise to extend it to cover any site in eukaryotic DNA where a transcription factor is shown to bind.


Do birds require cilia for left/right symmetry during their embryological stages?

Here is a paper that talks about left-right patterning across bilateral organisms, discussing both Xenopus (frog) and chicken.

It looks like it may be hard to generalize, but the answer appears to be "yes" for Xenopus and "no" for chicken (see e.g. Figure 2, and text immediately following).

However, it looks like the question of what exactly is going on in chicken is not well understood, according to this other paper. Chickens do have lethal ciliopathy mutants homologous to mutants causing left-right defects in other organisms, but these mutants appear to have normal left-right asymmetry development in chicken.

It is also not clear that the requirement of motile cilia for left-right asymmetry is generalizable within clades though, as pigs have apparently also lost the dependence on cilia for L-R, whereas mice and humans do require cilia for L-R. It appears that pig and chicken have dispensed with cilia by the same histological mechanism (see image below, Figure 7 of first paper).

I do not know whether the mechanism has been investigated in other birds.

Hope that helps.


How the chaotropic agents help in purification of DNA molecule?

Chaotropic agents are cosolutes that can disrupt the hydrogen bonding network between water molecules and reduce the stability of the native state of proteins by weakening the hydrophobic effect. a chaotropic agent reduces the amount of order in the structure of a protein formed by water molecules, both in the bulk and the hydration shells around hydrophobic amino acids, and may cause its denaturation (biochemistry).
A chaotropic agent is often used in DNA isolation. It's purpose is

a. To degrade membrane lipids

b. To destroy the endoplasmic reticulum

c. To degrade mitochondria

d. To limit the amount of magnesium salts in the lysate

e. To destroy the three dimensional structure of proteins

To make it simple, a chaotropic agent destroys the 3D structure of a protein, thereby leading to subsequent protein degradation. It serves as a proteinase enzyme, cleaning the cellular proteins in your DNA isolation and purification process.

http://www.hindawi.com/journals/bmri/2009/574398/

http://www.ncbi.nlm.nih.gov/pubmed/16152629


copper vs aluminum, what's the safest for health?

Assuming the answer can't be C) Stainless Steel I would go with Aluminum.

The USDA specifically mandates (1) stainless steel 300:

  "Milk contact surfaces shall be made of stainless steel of the 300
  series, equally corrosion-resistant non-toxic metals or heat-resistant
  glass."

Is the copper tinned?  From what I can tell after reading some old sources (2) un-tinned copper will be corroded by milk.  You have the advantage of a cool temperature lowering contamination risk (3), but many states following the FDA specifically removed the allowance of tinned copper (Sec. 22-201).

While the effects of life long dosing of Al are becoming more and more clearly tied to Alzheimer's (4), the effects build up over time.  Copper has a tendency to be more acute (5) and pronounced (6, 7), and further it can tasted in low amounts  and discolor the food (8).  It can be said that water flows through Cu pipes, but soda is put in Al cans.

The research for this has been quite enjoyable, and led to things I didn't even think of.  A alternative cleaning site has even recommended using milk to clean Cu pans.

Again so my final recommendation is to follow USDA guidelines and use stainless steel, but my second choice would be Aluminum.

Citations:

(1) USDA. 2011, July. Milk for Manufacturing Purposes and its Production and Processing.

(2) US DOC. 1917, April. STRUCTURE OF THE COATING ON TINNED SHEET COPPER IN RELATION TO A SPECIFIC CASE OF CORROSION. Technologic Papers OF THE Bureau of Standards.

(3) COMMITTEE ON COPPER IN DRINKING WATER, NATIONAL RESEARCH COUNCIL. Copper in Drinking Water. NATIONAL ACADEMY PRESS. 2000.

(4) Walton, J.R. Aluminum Involvement in the Progression of Alzheimer's Disease. Journal of Alzheimer’s Disease 35 (2013) 7–43. DOI 10.3233/JAD-121909

(5) Reilly C. The dietary significance of adventitious iron, zinc, copper and lead in domestically prepared food. Food Addit Contam. 1985 Jul-Sep;2(3):209-15.

(6) Conor Reilly. Metal Contamination of Food:
Its Significance for Food Quality and Human Health. Pg 50. John Wiley & Sons, Apr 15, 2008

(8) ibid pg. 16

(7) Lee A. Price, et al. Chronic copper toxicosis presenting as liver failure in an Australian child. Pathology. 1996, Vol. 28, No. 4 , Pages 316-320 (doi:10.1080/00313029600169264)


Insertion of an additional base at start codon make the protein still functional?

I think the question is fairly confusingly worded, so good job on your attempt based on that.

If a C is inserted within the start codon, I presume that is referring to making a sequence that was originally ATGXXX and making it either ACTGXXX or ATCGXXX. Either insertion means the start codon will be missing completely. This is going to either cause no protein to be made whatsoever, or for the beginning of the protein to be severely truncated or completely frameshifted if there is another open reading frame created downstream. This is going to be magnitudes more serious than a deletion of 3 bases corresponding to a lysine.
I think your answer here is fine - lots can happen with a missing stop codon. If there happens to be another stop codon in the same reading frame shortly downstream, then the effect could be not that severe, but if not it could result in a substantial additional peptide chain added to the end of the protein, which could cause all sorts of issues with folding, and the mRNA may not even be functional and be degraded.

Again, this question isn't worded in the best way, but I think the general principle it is trying to convey is that whole missing codons do a lot less damage to the structure of a protein than mutations that affect the reading frame or the stop/start codons, because they affect only a single amino acid. Of course, it could turn out that that amino acid is crucial to the structure of the protein, but the question is about what is most "likely."


After puzzling over this for a while I think I have the answer . It's nothing to do with protein A or protein G. I think that whoever wrote your study materials meant Ag which is a common abbreviation for 'antigen'. I guess this was in the context of immune responses, or strain typing.

Looking back over your last few questions, it seems that you are at the mercy of a teacher who specialises in ambiguity.


Short answer
Yes, taste sensations can be generated electrically. However, we cannot taste electrons themselves, as taste-receptor proteins on the taste receptor cells are not activated by electrons. Instead, electrical currents stimulate taste receptors directly by depolarizing the cell membrane, without the need of activation of the proteins that normally bind ions or molecules.

Background
There is a medical device called the BrainPort that electrically stimulates the tongue (Fig. 1.) The device is marketed as an electrotactile vision substitution device. Basically, it captures images of the outside world with a glasses-mounted camera and these images are translated into electrical stimuli presented on a 20 x 20 electrode array. That array is embedded in the tongue display unit (aka intra-oral device, IOD). The IOD is worn on the tongue.

Fig. 1. BrainPort V100. source: TuWindowsMundo

It typically generates electrotactile sensations, like champagne bubbles. However, some subjects do report metallic taste sensations when using the device. In fact, Lawless et al. (2005)* investigated the electrically evoked metallic-taste in response to anodic stimulation of the tongue directly and confirmed the anecdotal reports obtained with the BrainpPort device that electric stimuli evoke metallic-taste sensations.

Physiologically, taste receptor cells sense certain compounds (salts, acids etc.) due to activation of receptor molecules on the cell's surface. In turn, activation of receptor molecules depolarizes the cell membrane which eventually lead to neurotransmitter release and activation of secondary neurons that transmit the signal up to the brain (Fig. 2). Electrical stimuli bypass the receptor molecules and directly depolarize the taste receptor cells.

Given the anatomy of the taste receptor system in the tongue (Fig. 2), I am inclined to believe that the taste receptors are stimulated directly, and not the secondary neurons, because they are situated in deeper layers.

Fig. 2. Neural pathway of the taste buds on the tongue. Note that the secondary neurons transporting the taste information to the brain are situated in deeper layers than the taste buds. Source: Universe Review.

Note that taste receptors do not sense electrons. Rather, larger ions or molecules may stimulate them and cause a depolarization of the receptor cell, in turn activating the secondary neuron via a chemical synapse.

Reference
- Lawless et al., Chem Senses (2005); 30(3): 185–94

Acknowledgment
*Credits for the Lawless et al. (2005) reference go to @CMK


What is full form of r and K in r-selection species and K-selection species?

This article discusses the origin of the terms. They come directly from the equation used to describe population dynamics. As Canadianer mentioned the Wiki also covers it quite well.

"r" stands for "rate" {growth rate}, r strategists have a high r value and a low K value. They grow fast but most die.

"K" stands for Kapazitätsgrenzen which is german for capacity limit, now called carrying capacity, K strategists have a low r and a high K. They grow slow but more survive.