Think of the body as a heat-sink. We can let off heat by using our fluid exchanges – namely, blood and sweat. When we exercise, sweat cools us off through evaporative cooling. When we’re not exercising or in warm weather, we’re generally not sweating, but we’re still exchanging heat with our surroundings – after all, the metabolism is still active, we’re still “burning energy,” and our skin never reaches air temperature nor does our core cool to the temperature of our skin (so some kind of heat exchange has to be happening). How can that be, when there’s no obvious mechanism to carry away our heat as in the case of sweating?
The answer to this lies at the heart of your question. Human thermoregulation is largely thanks to our blood flow and vasodilation:

“Skin blood flow in adult human thermoregulation: how it works, when it does not, and why.” Charkoudian. N. Mayo Clin Proc. 2003.
Cutaneous sympathetic vasoconstrictor and vasodilator systems also participate in baroreflex control of blood pressure; this is particularly important during heat stress, when such a large percentage of cardiac output is directed to the skin. Local thermal control of cutaneous blood vessels also contributes importantly—local warming of the skin can cause maximal vasodilation in healthy humans and includes roles for both local sensory nerves and nitric oxide. Local cooling of the skin can decrease skin blood flow to minimal levels.

In essence, your core “wants” to stay warm. If the air around your skin is comparatively warmer, cutaneous blood vessels will dilate to accommodate a higher flowrate, allowing more blood to engage in heat transfer. The opposite is true for air that is comparatively colder, and the relationships between cutaneous blood flow, sweating, and local skin cooling can be tested experimentally:

“Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans.” Wingo et al. J Appl Physiol. 2010.
In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34°C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20°C (2 sites) or maintenance at 34°C (2 sites). In both protocols, individuals were then passively heated to increase core temperature ∼1°C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 ± 1.2 vs. 1.0 ± 0.7 mg·cm−2·min−1·°C−1 for the effect of decreased skin blood flow, P = 0.01; 1.2 ± 0.9 vs. 0.07 ± 0.05 mg·cm−2·min−1·°C−1 for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 ± 0.4 vs. 37.6 ± 0.4°C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature.


The flux control coefficient measures the relative change in the steady state pathway flux in response to a relative change in enzyme activity. Mathematically it is defined according to:
$C^J_{e_i} = \frac{dJ}{de_i} \frac{e_i}{J}$
Because enzyme activity is proportional to enzyme concentration, the flux control coefficient is often define with respect to the enzyme concentration, $e_i$.
This can be also expressed in log form:
$C^J_{e_i} = \frac{d\ln J}{d\ln e_i}$
It can also be expressed approximately as a ratio of percentage changes:
$C^J_{e_i}  = \frac{J\%}{e_i\%} $
This definition makes it easy to measure. For example, if the activity of a given enzyme is changed by a factor of 1.5 which results in a 1.25 fold change in the steady-state flux, then the value of the flux control coefficient is approximately 1.25/1.5 = 0.83. Because flux control coefficients are measured using relative changes, the coefficients are dimensionless.
Flux control coefficients are useful to gauge how much a given enzymatic reaction influences the flux in a pathway.
For further information I recommend the following paper:
Kacser, Henrik, James A. Burns, H. Kacser, and D. A. Fell. "The control of flux." (1995): 341-366.


If potassium ions were alone inside and outside of the cell, they would be tended to diffuse along out of the cell due to high gradient inside. Because of potassium ions have positive charge, potassium lose would cause negativity inside. Within a few seconds, potential loss would rise enough to be able to stop potassium exit out of the cell. Because against decreasing concentration gradient, there would be reverse direction electrical gradient increase so these forces have to be balanced somewhere. For a large mammal nerve cell , needed potential gradient is about-94 millivolts.

We can assume similar concepts for sodium ions also. This time direction will be outer to inner side of cell. And this makes a positive potential (about +61 millivolts) due to gaining positive ions .

When we calculate total diffusion potential for only one ion, Nernst equation is used. For ions more than one we have to use Goldman equation, which is more complicated , instead.
Goldman equation consists of three factors:

Electrical charge for each ions.
Permeability for each ions.
Concentrations inside and outside of the cell for each ions.

Major factor on this resting potential is membrane permeability. For potassium ions, membrane permeability is about 100 times more than sodium ions. Because potassium leakage channels makes potassium leakage more easier than sodium. When we put this factor on Golman equation, we find resting potential about-86 millivoltes which is closer to potassium diffusion potential.
(source:Wikipedia)
(source:KhanAcademy)


This doesn't take much effort to answer!  Googling "HIV mosquito" brings us straight to this blog post, which gives three main reasons (along with more details, links to other resources, etc.):

Only saliva is injected into humans when a mosquito bites and thus HIV positive blood that a mosquito may have previously ingested is never transmitted to other humans.
Unlike mosquito borne diseases, HIV is unable to replicate within the mosquito's gut and therefore is broken down.
HIV circulates in human blood at a far lower level than would be necessary to create a new infection.


In the context of twin studies, what do 'unique environmental factors' and 'shared environmental factors' refer to?

Shared environmental factors are those shared by the twins: uterine/prenatal environment and then the home environment and other environments both twins are raised in or remain in together. Unique environments are any environment not shared by the twins - they generally appear later in age.


By what mechanism does an obstructed bile duct cause excess fat in the stool?

The function of bile produced by the liver and concentrated in the gall bladder is to aid in fat digestion.  Bile acts as an emulsifier to allow the fat to be packaged into small droplets, micelles.  The breakdown of fats into small micelles greatly increases the surface area for lipases produced by the pancreas have to act on.  These are then absorbed across the intestinal wall.

Bile breaking down large fats into small micelles

If this first step of bile production and transport is lacking (due to liver dysfunction or obstruction anywhere in the biliary tree), the fats are not packaged into micelles and are consequently very hard to digest.  They pass through the entire alimentary canal virtually undigested causing steatorrhoea, fatty, bulky and foul smelling stool.

The Biliary Tree


To close this, we're now reasonnably sure that they were carpenter ants or a close relative. One more clue is that they infested the wood close to a window receiving sunshine and were much more active when it was warm there. Thanks to @user137.


Does pepsin enzyme digest other enzymes like other pepsin molecules

Pepsin does cleave itself (Ingram, 1951) - this is termed autolysis. Pepsin (and other proteases) act on proteins with the right amino acid sequences. Pepsin prefers to cleave at phenylalanine, tryptophan or tyrosine residues (Lehninger, A. Principles of Biochemistry).

* Pepsin can also cleave inactive 'zymogen' enzymes to activate them. One of these zymogens is pepsinogen (an inactive form of pepsin itself). So you could argue that pepsin is cleaving itself here but I personally wouldn't, since pepsinogen isn't really pepsin.


N is the IUPAC code for any nucleotide, so in DNA sequence an N signifies any one of the four bases could be in that position.

The {4} means 4 of the previous character in the pattern, or NNNN. In Perl regular expressions \d{4} means match 4 digits in a row, so the notation is quite similar.


By reasoning, we can make the following distinction:

the trigeminal nerve is a cranial nerve.
the 2 others are peripheral
nerves.

Cranial nerves take their origin into their respective nuclei, and bypass the dorsal columns (main spinal tract for sensory information). Peripheral sensory nerves stem from the spinal roots, and from there go up through the dorsal columns. This would bring you to the thalamus, where all sensory information is regrouped. However, somatosensory information from the face and the rest of the body happen to travel through different thalamic nuclei (ventroposterolateral for the body, ventroposteromedian for the face, If my neuroanatomy is not too far behind me...). This leaves us with the internal capsula (fibers that link the thalamus to the cortex), but I do not think much signal integration occurs there.

In conclusion, the first anatomical level of convergence between the 3 above-cited nerves would indeed be the somatosensory cortex.


Natural athletes have to deal with MSTN gene.

  The MSTN gene provides instructions for making a protein called myostatin.

  This protein normally restrains muscle growth, ensuring that muscles do not grow too large.

Just look at the top natural athletes. There are a lot of them who train for 20+ years and still can't be as large as those athletes who take steroids. Here are some examples of professional natural athletes(Bobby Pandour, Georg Hackenschmidt)

With steroids you can exceed all natural limits up until your body meets its boundaries, often accompanied by serious health issues.


If a given DNA oligo is an aptamer, will the corresponding RNA oligo with the same sequence be an aptamer aswell?

There is at least one known case where both the DNA and RNA versions of the same aptamer sequence bind the same target (Lauhon and Szostak, 1995).

But you can't generalize this, there are two differences in structure between RNA and DNA, the Uracil/Thymine change and the missing 2'-OH in DNA. Those differences can affect the binding and overall structure of the aptamer.

It is possible that the RNA version of a DNA aptamer binds the same ligand, but this won't be always the case.


Does human behaviour that is caused by inheritance depend on the environment and lifestyle in general?

I feel that 99% of the time that someone asks "are human unique concerning ?", the answer is nope. There's nothing exceptional about humans in this respect.

Rephrasing your question

Your question can be rephrased

  Is heritability sometimes different from 0 or 1 for humans too?

If you do not understand well why this is a good rephrasing of your question, then you should definitely have a look at this post.

Is heritability sometimes different from 0 or 1 for humans too?

Yes, humans are not exceptional in this regard. In humans, other animals, plants, fungi, bacteria, archeabacteria and for any other living things, any behaviour (and any phenotypic trait in fact) can have a heritability that differs from both 0 and 1, or in other words, there can be for any trait both genetic and environmental variance underlying phenotypic variance in the population.

In fact, very few traits that have a non-zero genetic variance has no environmental variance. Have a look at the post List of heritability estimates in humans? for a list of traits on which we measured heritability.

ADHD

The difficulty with a trait like ADHD is that the methodology to measure it vary a lot from one country to another or even from one practitioner to another. But yes, for ADHD too, there is both genetic and environmental variance underlying the observe phenotypic variance (Thapar et al., 2000).


How does the zygote divide much faster than other cells?

A zygote generally has a lot of nutrients, essential biomolecules like RNA and proteins and cytoplasmic organelles for rapid division. So the cell does not grow and divide but rather undergoes "cleavage" (there is no G1 phase of cell cycle). However, it still undergoes DNA replication. And yes, DNA replication is fast because it is initiated at once from several parts (origins of replication) of the long DNA (it still takes a few hours† ).

 † See:

Confusion about the duration of different phases of the cell cycle such as G1, G2 & S
Time spent in phases of cell cycle


Head transplant feasibility - Project HEAVEN-GEMINI

I have the impression that the MNT article is significantly over-stating the potential of this technique, at least with current technology. The mouse work by Xiaoping Ren (see this 2014 paper) seems to have a very steep death-curve post-surgery:

  Forty Kunming mice and forty C57 wild type underwent the
  AHBR  procedure.  After  transplantation,  18  mice  survived
  for 3 h after the ventilator was disconnected.

There are no details in the paper about how long the most robust mouse survived for post-surgery. I would guess that it is not an impressive number, otherwise the authors would include it. Alternatively, the 18 surviving mice may have been euthanased after three hours - the paper does not make this clear, but it is common to have a predetermined time-limit for euthanasia in experiments where animals are expected to suffer from an irreversible treatment.

  During these 3 h, the mice
  awakened and displayed normal cranial nerve function and
  characteristic responsiveness (blinking, whiskers moving, etc.).
  After the mice awoke, electroencephalogram (EEG) recordings
  were  made  directly  from  the  cortex  of  the  transplanted
  Cephalons (Figure 3). Because blood supply was maintained at
  an adequate level during surgery by anastomosing the donor
  and recipient carotid and jugular vessels, the intra- and post-
  operative EEG and ECG show electrophysiological activity.

This sounds a lot like a 'no' to 'can this technique be used to substantially extend human lifespans?', on current technology. If a human trial is approved, and is as successful as the mouse trials, the recipient will likely be dead within hours. If they survive for several hours, the level of motor control that can be expected in that time is likely restricted to unconscious motor tics (cf whisker twitching and blinking).


How many SARS-CoV-2 viruses in circulation at the moment? Mass?

Based on all species of viruses, Everyday you breathe in 100 million viruses. There can be 1mn+ viruses per ml of blood of patients. Covid-19 diameter = 125 nm.

Perhaps it's wrong, the maths would go something like this:

1mn * 1000ml * 5liters * 400k patients = 2^12 - 2^13 sars2 viruses.

total volume of viruses =  2^13 viruses / 1^15 viruses per cm3 = 0.02 cm3

(10^7 nanometers per centimeter, 125nm diameter, gives, about 10^(5*3) viruses per cm3.)

Weight of all the Covid Sars 2 in the human population = a raindrop or a teaspoon of hydrocarbons/mayonnaise, probably less than a teacup.

Perhaps i am wrong, it's reasonable to think that the people with major symptoms contain about 1 ml of virus. 20k x 1ml = 20cm3


Number of beneficial mutations cataloged?

That would be hard to say because really beneficial mutations become well distributed through the genome.  Basically the differences between us and chimpanzees are a catalog of all the beneficial (or completely neutral) mutations since the ~4.7 M years since we diverged from each other.

Separating them from changes which have no special effect would be difficult too, but more to the spirit of your question, its difficult to explain what many mutations do, unless they cause significant changes in something we can observe in the individual (like height, weight, big nasty claws, etc).

For some more specific examples you can look at Online Mendelian Inheritance in Man.  Some mutations which are useful sometimes might be related to skin color for instance (really helps when there is a lot of sun about) or lactose tolerance (a variation which is popular amongst europeans who have been drinking dairy milk for thousands of years).


Comparing BLAST and the Smith-Waterman algorithm

So I got this answer from my lecturer:

Since Smith-Waterman algorithm is based on DP, we will get the best performance on accuracy, but there is a change that the homologous sequence is not with the highest probability (so better matching sequences will be "hidden" behind worse ones).
Since blast is based on the heuristic approach, it overcomes the disadvantage described above, by adding biological information, and therefore make it more accurate from biologist's perspective.


What impacts on metabolism are likely from the 6x increase in water consumption by Americans at restaurants since the 1950s?

As mentioned by nico in his comment, this infographic is very misleading in that it presents quite uninteresting data in a way as if it was a sensation.

It claims the average meal drink has been soda which has increased by 6 times in size. Then it claims most of the volume is water. This is of course true. But while a substance solved in water barely increases its volume, it can still make a difference - soda and water are completely different things and the important statistic to look at here is not the amount of water drunk, but rather the fact that it is soda. Where I live, soda usually contains around 27g of sugar per 240ml (8oz) which is 9% of the GDA. So according to this data, people consume half their energy needs of that day with the drink they get in their restaurant meal.

The other statistic is about calories per ounce of the food. What sense does a statistic about that make? The only relevance of the calorie density of food would be the effect on how well it is digested, and for that only a calorie number isn't really helpful. The relative ratios of fibre, carbohydrates and fats would be much more useful in that case. The only interesting statistic here is that meals have almost doubled in size. The fact that the volume of meals has increased much more hints that there is a higher portion of less calorific foods, such as salads.

Impact on metabolism? Hard to say, this is a statistic about what people eat at restaurants, which is not really something that you expect to reflect their refular diet. It doesn't tell you anything about their general lifestyle, which would be the relevant statistic for effects on metabolism. If you only look at restaurant meals, those could look really unhealthy but on the larger scale, people balance it out in their every day diet and general lifestyle. If you had an additional statistic that shows that people actually eat a significiant amount of meals at restaurants, and they're the kind of meals described by the infographic you gave, that would have some implications.


Problem with joining the gene of interest into the open plasmid when their lengths are not the same

From your question I suspect that you are thinking of DNA as being a very rigid molecule — it isn't.

Double stranded DNA is reasonably flexible and a useful mental model would be to think of this as being like tying the ends of two pieces of thin wire together to make a circle.

Double stranded DNA can make a closed circles smaller than 250 bp long1,2 and I don't think there is any known upper limit — for example there is a known circular bacterial chromosome 14,782,125 bp in length3.

A typical plasmid can accommodate inserts of any size up to total size of around 50 kb, but plasmids that are more than 20 kb are very difficult to work with and may require special transformation techniques.

References:
1: Thibault, Thomas et al. “Production of DNA minicircles less than 250 base pairs through a novel concentrated DNA circularization assay enabling minicircle design with NF-κB inhibition activity.” Nucleic acids research vol. 45,5 (2017): e26. doi:10.1093/nar/gkw1034
2: Shore, David, Jorg Langowski, and Robert L. Baldwin. "DNA flexibility studied by covalent closure of short fragments into circles." Proceedings of the National Academy of Sciences 78.8 (1981): 4833-4837
3: Land, Miriam et al. “Insights from 20 years of bacterial genome sequencing.” Functional & integrative genomics vol. 15,2 (2015): 141-61. doi:10.1007/s10142-015-0433-4


Factor V is indeed mainly produced in liver (Wikipedia), which releases it into blood plasma.
But platelets are also an important source of factor V and "may account for "~25% of the circulating factor V" (ref 1)
Platelet factor V is synthesized in megakaryocytes (ref 1), which of course are the bone marrow cells responsible for the production of platelets.
The following reference gives a much more detailed explanation of factor V
Reference (available as free pdf)
Factor V Is Complexed with Multimerin in Resting Platelet Lysates and Colocalizes
with Multimerin in Platelet α-Granules *

Catherine P.M. Hayward
Emilia Furmaniak-Kazmierczak
Anne-Marie Cieutat
Michael E. Nesheim
John G. Kelton **
Graham Côté

Journal of Biological Chemistry (1995) Vol 270, pp19217-19224


Reliable recipe to make DIY yeast slants

Yeast grows very well in liquid. The initial innoculum from the store will visible grow (“prove”) in warm water with a little sugar.


Do spring varietes of cereals have a process of vernalization?

The answer depends to some degree on what you mean by "some process of vernalization". As far as I know, the difference between winter and spring varieties is a matter mostly of how strong the response is, not whether the response exists.
One paper writes in the abstract:

Wheat cultivars are classified as two general types: winter wheat with variable low temperature requirement for a proper flowering time (vernalization) and spring wheat without the requirement, based on their qualitative vernalization requirement. Winter wheat cultivars are classified as three types, weak winter, semi-winter and strong winter, according to their quantitative vernalization requirement to reach a vernalization saturation point or achieve the maximum vernalization effect.

The difference is not whether vernalization exists as a process, so much as whether it is required for timely reproductive transition.
See the figure below (from this paper), showing spring (LEG) and winter (MIR) varieties of wheat after various vernalization periods. Basically, even the spring variety has a weak vernalization response; it's just much less notable than the strong response of the winter variety.

With legend:

Frost tolerance (LT50), apical development (DC = decimal code) and days to heading of ‘Mironovskaya’ (MIR) winter wheat and ‘Leguan’ (LEG) spring wheat plants during 12 weeks of acclimation at 2 °C and two photoperiods, 16 h (long day) or 8 h (short day). Vertical bars indicate LSD0·05 and asterisks indicate that the plants had not reached heading by 100 d.


What does it mean for a chemical pathway to be conserved?

A conserved pathway is a pathway that exists in a variety of species, by virtue of that pathway being conserved throughout the evolution of those species. A pathway must by neccessity have appeared for the first time in one particular species. If that species gives rise to new species, but the pathway in question is identical or very similar in all the new species, it is sensible to say that pathway has been evolutionary conserved. This may imply that the pathway in its conserved form is important for the fitness of those species.

For some examples, here is a page on evolutionary conserved pathways in Drosophila: http://www.sdbonline.org/sites/fly/aimain/aadevinx.htm


Why does looking at bright light trigger sneezing in some people?

You are talking about the photic sneeze reflex.

The mechanisms are not entirely understood, but it affects 18-35% of the population.

According to Wikipedia (although this passage is not sourced):

  The probable cause is a congenital
  malfunction in nerve signals in the
  trigeminal nerve nuclei. The fifth
  cranial nerve, called the trigeminal
  nerve, is apparently responsible for
  sneezes. Research suggests that some
  people have an association between
  this nerve and the nerve that
  transmits visual impulses to the
  brain. Overstimulation of the optic
  nerve triggers the trigeminal nerve,
  and this causes the photic sneeze
  reflex.

And, it could  be advantageous:

  On the other hand, some people with
  the trait feel that it is
  advantageous. In the event that nasal
  discomfort occurs, but to an extent
  that is insufficient to induce a
  sneeze, intentionally seeking and
  finding a light source facilitates the
  sneezing process and is in turn a mode
  of relief.

Also, anecdotally, as I too photosneeze, I can see an advantage: should the atmosphere become weaker in the future, and allow more light to enter than we are accustomed to, it would discourage looking directly at the sun.


Why are there so many sex determining systems in animals

Could not fit in a comment…

I don't quite know how to answer. I think that the only answer one could give is why not?. Various mechanisms may evolve under different life-history, different environment, different ecological strategy, different mutations occuring,..

In some species (including some amphibians) the evolution of sex determination system is highly dynamic and switch back and forth between one system and another.

I highly recommend the book: The Evolution of sex determination system (2014) that will give you a very good theoretical understanding of how sexual determination system evolve and make a complete review of empirical studies on the evolution and mechanisms of sex determination system. I think it is the only book existing on the subject.


Could a prolonged amount of Antibiotics severely affect the digestion Gut Microbiota?

Yes, even if you will not kill ALL the bacteria in your gut, you can mess up your flora pretty badly by using antibiotics for prolonged time.

For how long? It depends from person to person, from antibiotic to antibiotic.

Similar to Crohn's disease? Some symptoms like abdominal pain, diarrhoea and weight loss can occur in case of messed-up flora like in Crohn's disease (and many other diseases!).


How is an RT-PCR representative of the RNA contents in a cell?

It isn’t really clear exactly what the questioner is asking, but…

...one way of thinking about this is to ask how likely is it that a low-abundance RNA will be absent from the sample taken from the preparation of RNA. This would make the sample non-representative at the qualitative level.

The question states that 12,000 ng of RNA is isolated. Since nothing else is specified I assume this is total RNA. A rough estimate of total RNA per eukaryotic cell is 20 pg.

This means that the preparation came from 6 x 105 cells. (I’m assuming 100% yield, but this won’t really affect the conclusion.)

Now assume that a low-abundance mRNA is present at 10 copies per cell. The total RNA preparation therefore contains 6 x 106 copies of that low-abundance mRNA.

We take a sample of 1,000 ng from the total 12,000 ng. In other words we take 1/12th of the preparation of RNA. If that RNA preparation contains 106 copies of the low abundance mRNA how likely is it that we happen to take a sample which contains no copies of that low abundance mRNA? Here my maths fails me, but intuitively I say that the probability is very very small.

Now, if there are 1,000 different low-abundance mRNAs in the cell the probability of missing each of them is very very small, but the overall probability of missing one of them is 1000 x very very small, so maybe very small.

I'll continue thinking about how to calculate the value of very very small, but if anyone wants to help out - thanks in advance!


Can spike protein induced cell fusion be triggered by the mRNA vaccine?

The mRNA vaccines encode a mutant version of the spike protein in which the structural transition needed to to fuse membranes is blocked. This was done to make the immune response focus on the pre-fusion state, which is much better for neutralizing the virus.
From https://cen.acs.org/pharmaceuticals/vaccines/tiny-tweak-behind-COVID-19/98/i38:

Fortuitously, Graham and a former postdoc, Jason McLellan, devised a solution to this problem before the pandemic. Through a bit of structural biology and persistent protein engineering, McLellan discovered that adding two prolines—the most rigid of the 20 amino acids—to a key joint of a vaccine’s spike protein could stabilize the structure’s prefusion shape. This 2P mutation worked in preclinical studies of Graham and Moderna’s MERS vaccine, so they applied it to Moderna’s COVID-19 vaccine.

I don't know if cells expressing wild-type spike protein would fuse into syncytia, but it seems very unlikely to happen with the vaccine spike.


Selection of recombinant host by color selection method

The Z gene you are talking about should be lacZ that encodes the $\beta-$galactosidase, which is made from $\alpha$ and $\omega$ peptides. Neither peptide is functional by itself.

$\beta-$galactosidase will cleave the glycosidic bond in X-gal and form galactose and 5-bromo-4-chloro-3-hydroxyindole. The latter product then dimerizes and oxidizes to 5,5'-dibromo-4,4'-dichloro-indigo, an intense blue product that is easy to identify and quantify.

Next, you should check out the genotype of your bacterial strain because they typically have only the $\omega$-peptide encoded in its genome. Thus, the enzymatic activity of the $\beta-$galactosidase is only recovered when the $\alpha$-peptide is in the environment, and the process is called $\alpha$-complementation.

Two commonly used strains for cloning and expression in E. coli are Dh5$\alpha$ and TOP10.

The genotype for Dh5a is like this:

  F– Φ80lacZΔM15 Δ(lacZYA-argF) U169 recA1 endA1 hsdR17 (rK–, mK+) phoA
  supE44 λ– thi-1 gyrA96 relA1

Here, lacZΔM15 indicates that the M15 segment is lost from lacZ, and the mutant protein will only have the $\omega$-peptide.

The genotype for TOP10 is like this:

  F– mcrA Δ(mrr-hsdRMS-mcrBC) Φ80lacZΔM15 ΔlacX74 recA1 araD139 Δ(ara leu) 7697 galU galK rpsL (StrR) endA1 nupG

Again, you will notice lacZΔM15, which is still a non-functional peptide segment after all.

Finally, to your question. Even if the there is no glucose as primary energy source in the medium and only X-gal is present, the operon of your host bacteria(I suppose it's E. coli) cannot produce the functional $\beta-$galactosidase on its own. Moreover, the recombinants, with the vector sequence encoding the $\alpha$-peptide disrupted, will not exhibit $\alpha$-complementation. No color reaction then! :D

Reference:
1.Genotypes of Invitrogen™ competent cells - TOP10, retrieved from: https://www.thermofisher.com/cn/zh/home/life-science/cloning/competent-cells-for-transformation/chemically-competent/top10f-genotypes.html.
2.Genotypes of Invitrogen™ competent cells - DH5a, retrieved from: https://www.thermofisher.com/us/en/home/life-science/cloning/competent-cells-for-transformation/chemically-competent/dh5alpha-genotypes.html.
3. Langley, K. E.; Villarejo, M. R.; Fowler, A. V.; Zamenhof, P. J.; Zabin, I. (1975). "Molecular basis of beta-galactosidase alpha-complementation". Proceedings of the National Academy of Sciences of the United States of America. 72 (4): 1254–1257. doi:10.1073/pnas.72.4.1254. PMC 432510 Freely accessible. PMID 1093175.
4.


Any protein which enters the secretory pathway will proceed via vesicular transport to some point on that pathway. That includes lysosomal proteins, integral plasma membrane proteins and secreted proteins (also, not on your list, resident proteins of the ER, Golgi proteins, some endosomal proteins).

Cytoskeletal proteins are cytoplasmic: I suppose you could argue they are 'transported' sometimes, e.g. tubulin treadmilling, motors etc., but no vesicles are involved. Nuclear proteins enter the nucleus from the cytoplasm through nuclear pores. They have nuclear localisation signals; vesicles aren't involved. Mitochondria, chloroplasts and peroxisomes all have their own protein import systems with associated unique signals; again no vesicles are involved.


Are there animals which can see movements better than shapes or colors?

I think "movement-based vision" is perhaps a bit of a misnomer. Ultimately, all vision is contrast-based, depending on integrating signals from ON and OFF bipolar cells. It seems that this notion of so-called "movement-based vision" is derived from work on toad vision and feature detection. In this case, it's more the downstream processing that results in different behavior based on the shape of the stimulus and the direction that it moves. The simple sensing of visual stimuli does not seem to be motion-based.

So, aside from evolutionary inference, we would have no way of knowing whether Tyranassaurus rex had such behavior. As for the chickens, it's possible but I would be skeptical of such a system discriminating between immobile food and hand pouring food. I would chalk that up to a simple behavior of associating seeing you with getting food.

One interesting note: many, many species have reflexive responses to moving visual stimuli. The first is called the optokinetic reflex, in which the eyes reflexively track contrast-based movement; and the second is the optomotor response, in which the head or even the whole body move in response to a moving stimulus. Thus it is safe to say that for many (most?) species, motion detection has a strong influence on the visual response...but again, I remain hesitant to use the phrase "motion-based vision".


Can wood frogs who have frozen and thawed remember their past lives?

Wood frogs are highly philopatric to their breeding ponds. And the fact that they return to the same pond after multiple winters, would indicate that, at the very least, they must retain at least some spatial memory after freezing.
It is worth noting that a frozen wood frog is not nearly the same scenario as a butterfly metamorphing. Butterfly metamorphosis involves complex reintegration of all bodily systems, whereas frog brains do not reform during the winter--they just cease neurological activity. Even frog metamorphosis is less complex since much of the chondocranium and brain morphology is retained from tadpole to frog.
I know it wasn't the original question, but it is relevant to note that tadpoles seem to retain their personality through metamorphosis (see Wilson & Krause, 2012; Koenig & Ousterhout, 2018), which also seems to indicate that they have neurological stability.
References:
Wilson, A. D. M., & Krause, J. (2012). Personality and metamorphosis: is behavioral variation consistent across ontogenetic niche shifts? Behavioral Ecology: Official Journal of the International Society for Behavioral Ecology, 23(6), 1316–1323.
Koenig, A. M., & Ousterhout, B. H. (2018). Behavioral syndrome persists over metamorphosis in a pond-breeding amphibian. Behavioral Ecology and Sociobiology, 72(12), 184.


Your question is not directly related to Liebig's Law of the Minimum. Instead you ask about a conditions under which the Law holds according to your quote.

From the quote it is clear what is in steady state: it is the total amount of energy and material. If the the amount of energy and material flowing into a system equals ("balances out") the amount of energy and material leaving the system, the total amount in the system does not change, that is, it is in steady state.

This does not mean that other quantities in the system are necessarily in steady state. For instance, the species composition of a bacterial community may fluctuate or evolution may cause the community to change.

An example of the sort of systems we are talking about here is the chemostat. A chemostat is a device for culturing microorganisms. It consists of a culture vessel connected to a feed bottle. A solution of nutrients (the growth medium) literally flows from the feed into the chemostat. Microorganisms in the chemostat will grow and reproduce (if the concentration of nutrients is sufficient). A mixture of microorganisms, unused nutrients, and byproducts of growth leaves the chemostat in the effluent flowing out of the outflow of the vessel. The rate at which this happens is the same as the rate at which medium flows into the vessel. Typically, after a while the concentration of microorganisms and the concentration of nutrients in the chemostat and effluent do not change anymore (if the inflow is constant, that is). The chemical conditions in the chemostat have then become static (hence "chemostat"). The concentration of nutrients and microorganisms are then at steady state.

In the case that the microorganisms are phototrophic, the nutrients may be inorganic and energy is added to the system through light. The light absorbed may then be considered as the energy flowing in, and the energy flowing out is then the chemical bond energy in the organic material that make up the microorganisms and the byproducts, and heat.

Chemostats are culturing devices, but are also models of natural systems such as lakes or ecosystems.

Liebig's Law of the Minimum says whichever resource (nutrient of light) is in short supply determines the growth rate of an organism. For instance, if nutrient concentrations are in ample supply but light levels are low, changing the nutrient concentrations will not change the growth rate of the organisms, however, changing the light levels will. The quote of Odum suggests the Law only holds under steady state conditions, but I do not understand very well why this would be so.


What is immunopanning (vs. immunoprecipitation and FACS)?

Immunopanning is essentially an immunoprecipitation (IP) of cells using an antibody immobilized to a solid surface, like a cell culture plate. Conventionally, an IP is performed using small agarose or magnetic beads (~50 to 150μm in size) conjugated to an antibody or Protein A/G, and can pull down individual proteins, protein complexes, and/or nucleic acid complexes.

Cells are much larger than protein complexes, obviously, and for the most part much smaller than beads, but they can be damaged during a traditional IP, so immunopanning utilizes a single solid surface coated with the specific antibody or cell-surface protein ligand of choice. In this article (free PDF here), retrograde axonal transport was used to selectively label specific populations of neuronal cells with the extracellular portion of cholera toxin β (CTB) adsorbed to fluorescent beads, then the cells were purified using an immobilized anti-CTB antibody.

Fluorescence-Activated Cell Sorting or FACS is another way to purify cell populations. Cells are labeled with a fluorescent marker (either conjugated to an antibody specific to an extra-cellular epitope, via absorption as in the example above, or by expression of a fluorescent transgene like GFP), then scanned in a flow cytometer. Cells which match certain parameters or "gates" in the machine's software are then diverted into a separate collection chamber, allowing for the generation of a quite pure cell population.

However, as the authors point out in their paper above, FACS requires an expensive piece of equipment (can be over US$100,000), can be harsh on the cells, and is dependent on the availability of an antibody to a cell surface marker specific to the desired population of cells. Immunopanning is much less expensive, is more gentle on the cells, and in the authors' case was really the only choice for purifying their cell population of interest, as no specific biomarkers were available. It certainly won't replace FACS in the long run, but is another tool for investigators to use when studying specific cell types.


In my understanding you cannot skip the tree construction, since there is no guarantee that the pairwise distances are compatible with a tree, even for non-ultrametric trees. That is, to create a pairwise distance matrix that reflects patristic distances between tree leaves you need to create a tree first. Even without the ultrametricity condition.

The complicating factor here is that distance matrices compatible with trees must also respect distances to unobserved internal nodes...
This blog post about how to make a tree ultrametric might be relevant.


Expression of red and green fluorescences in the same tissue

These images are not typically taken using color cameras. They are taken using grayscale cameras, using filters that allow the excitation wavelengths to hit the sample and the emission wavelengths to go to the camera.

For visualization, these black and white images are often put into the red or green channel in a digital image (TVs and computer monitors make color by mixing different amounts of red, green, and blue light: RGB). If you have red and green together that shows up yellow to a human eye, but that doesn't mean any yellow light is involved: it's just perception.

If you don't see yellow in these images it's because the red and green emission were not in the same place.


The biological environment in every cell and tissue of your body is an extremely complex, tightly controlled system. There are tens of thousands of genes in a typical eukaryotic genome, and depending on tissue types and environmental conditions, these genes are turned on and off in a very controlled manner. There is regulation at every point in the flow of genetic information: nucleosome disruption to expose DNA; RNA transcription from the DNA; protein translation from the RNA; and in some cases, additional modifications of proteins or intermediate mRNAs. At early stages in development, regulation of RNA and protein levels is even more crucial than, say, when an organism is fully developed and healthy.

All living organisms share some basic building blocks--DNA, RNA, and proteins work pretty much the same in all of life (there are a few rare variations of the genetic code but the basic premise is identical). However, the way that specific genes, transcripts, and proteins work together to sustain life varies widely between different organisms.

For a very rough analogy, imagine you want to bake a batch of cookies. Then consider the three following scenarios.

You look at two different recipes for chocolate chip cookies. They will have some slight differences, but they will share a lot in common. If you put the ingredients for both recipes in one bowl, it's likely you can still come up with some pretty good chocolate chip cookies in the end.
You look at two different recipes: one for chocolate chip cookies, and one for chocolate muffins. There will be some big differences in these recipes, but combining all the ingredients and baking, you still might be able to come up with something edible (and maybe even tasty).
You look at two different recipes: one for chocolate chip cookies, and one for French onion soup. If you combine the ingredients from these recipes and try to cook or bake them, there is no way you will come up with something that anyone would want to eat.

The first example we can relate to two individuals of the same species mating. Of course there is natural variation in the population, but this doesn't typically lead to lethality during development. The second example we can relate to individuals of two related species (such as a horse and a donkey). Sometimes these matings can produce viable offspring, although these offspring are often sterile. The third example we can relate to individuals of two very divergent species (such as donkey and dog in your original question). The biological systems inside donkeys are just so different from those inside dogs that this mating cannot produce a viable offspring.

Admittedly this is a rough analogy, but hopefully is sheds some light on the issue.


Biodiversity is the opposite of monoculture, and we know that one possible consequence of monoculture is disease transmission -- bananas being the modern poster child for monoculture leading to disease spread.

The concept seems to have been most clearly presented in

Schmidt, K.A. & Ostfeld, R.S. Biodiversity and the dilution effect in disease
ecology. Ecology 82: 609–619 (2001)

  A community of abundant alternative hosts with reduced competence mitigates Lyme disease risk in this system by decreasing the average infection prevalence of ticks. When alternative hosts have net negative impacts on the most competent reservoirs, via competition and predation, the dilution effect is compounded. We believe this dilution effect to be a general phenomenon of disease ecology because the majority of vector-borne zoonoses are characterized by the fea- tures necessary for it to occur.

There are many articles following up on this one, such as Declining ecosystem health and the dilution effect:

  The “dilution effect” implies that where species vary in susceptibility to infection by a pathogen, higher diversity often leads to lower infection prevalence in hosts. For directly transmitted pathogens, non-host species may “dilute” infection directly (1) and indirectly (2). Competitors and predators may (1) alter host behavior to reduce pathogen transmission or (2) reduce host density. ... Our study provides further evidence for dilution effect ...

However, not all agree that this is a general or even a real effect.  For example:

  How changes in biodiversity alter the transmission of infectious diseases is presently under debate. Epidemiologists and ecologists have put a lot of effort to understand the mechanism behind biodiversity–disease relationship. Two important mechanisms, i.e. dilution and amplification theories have in some manner made it clear that biodiversity and disease outcome have an intimate relationship.... We suggest a multidimensional approach whereby the same disease system needs to be studied in different ecological zones and then the effect of biodiversity on disease outcome needs to be ascertained. Nonetheless, caution is to be taken while jumping to any conclusion as biodiversity–disease relationship is a multifactorial process.

--Does alteration in biodiversity really affect disease outcome? – A debate is brewing

The book seems to be making the specific claim that biodiversity reduces transmission of avian influenza, and without a reference I can't evaluate that, but I couldn't find any articles supporting the claim. I'd be skeptical about that claim without some good  evidence, because avian influenza viruses are exceptionally good at crossing species barriers, so biodiversity should be much less of an obstacle for them than more species-constrained pathogens.


One possibility is PTB Diagnostic ECG database here.
However, its AAMI verification is still under process here.
Some ECHO findings also there.


Difference between ‘tagging’ and ‘conjugating’ a fluorochrome to an antibody?

Conjugated and tagged mean the same thing here, although I would advise against using tagged here.

In the context of antibodies, tagging means the addition of a (short) peptide sequence to a protein. Either to do something useful (degradation tag, HHHHHH-tag) or just as an epitope for an antibody.


Do the majority of fish lack scales on their heads?

I certainly agree with your general observation, but not being an ichthyologist, I can only offer a partial answer, based on a particular family of fish. Within the family Tripterygiidae, most species lack scales on their head, or have highly modified types of scales. A comparative study of 48 species showed that only 2 have "normal" scales of their head (Jawad, 2005).

  The squamation pattern of the bases of the fins
  varies among species. The head is usually devoid of scales
  except for two species that have squamation with body-
  type scales (Matanui bathytaton (Hardy, 1989) and
  Norfolkia clarkei). Several species have head ctenoid scales
  modified into tiny spicules of different shapes (Acantha-
  nectes rufus Holleman & Buxton, 1993, Apopterygion
  oculus Fricke & Roberts, 1994, Axoclinus carminalis,
  Ceratobregma acanthops, Cremnochorites capensis, Ennea-
  nectes boehlkei Rosenblatt, 1960, Forsterygion malcolmi
  Hardy, 1987, Forsterygion varium (Forster, 1801), Karalepis
  stewarti, Matanui bathytaton, Norfolkia clarkei, Notoclinops
  caerulepunctus Hardy, 1989).

So far, I haven't found a broader comparative study, to support your general question. Someone more knowledge in the area and the literature can perhaps offer a more general answer. This is at least an indication that your observation might be correct.

Reference
Jawad. 2005. Comparative scale morphology and squamation patterns in triplefins (Pisces: Teleostei: Perciformes: Tripterygiidae). Tuhinga 16 (1), 137-168


What is the difference between myopia and hyperopia?

Short answer
Myopic eyes can still focus on nearby images as the lens needs to relax a bit more than in a normally-sighted person. However, objects far away cannot be focused, because in a complete relaxed state (for distant objects), the lens focuses the image in front of the retina. Hyperopic eyes cannot focus on nearby objects as, at a certain close distance, the lens reaches maximum accomodation (maximum roundness) and objects cannot be focused any longer.

Background
Myopia or near-sightedness is a condition of the eye where the light that comes in does not directly focus on the retina but in front of it, causing the image that one sees when looking at a distant object to be out of focus, but in focus when looking at a close object. Often the eye ball is too long, or the cornea has too much curvature (Web MD).

Hyperopia ("over-measured sight") or farsightedness, is a defect of vision caused typically by the eyeball being too short, or a lens that cannot accomodate/become round enough. It causes difficulty focusing on near objects (wikipedia).

Source:Monroe Publishing


What is the difference between floral primordia and floral buds?

A primordium (plural: primordia) is the first recognizable manifestation of a biological structure. In the case of a flower this will be a small meristematic bump typically at the periphery of a shoot apical meristem.
In contrast, a flower bud is generally used to describe the entire structure including the meristem and any associated structures (such as bracts) that can develop into a flower. This structure often goes through a period of dormancy.
Another way of saying this is that, in the context of a flower, a primordium is a group of meristematic cells that has not yet formed any lateral structures, while a bud contains a meristem and its associated lateral structures. Note however, that I believe I've seen bud used as a synonym for primodium in some cases.
Another difference is that primordia are (usually) microscopic structures, while buds are (usually) macroscopic (visible to the unaided eye) structures.


Apparently poly(ethylene oxide) is a biologically interesting polymer, with minimal protein interactions.

The apparently means that I haven't tried it myself, but my polymer teacher told us so.

http://www.sigmaaldrich.com/materials-science/material-science-products.html?TablePage=20204110

http://en.wikipedia.org/wiki/Polyethylene_glycol

Nomenclature seems to favour poly(ethylene glycol). I prefer poly(ethylene oxide), because then I know from what monomer the polymer was synthesized.


Can Phosphogycolate buildup in a plant kill it?

Phosphogycolate can break down enzymes needed in the Calvin Cycle along with other enzymes in a plant so that is a yes.l.


Where can I find trees preserved for hundreds of years?

Yes, this occurs fairly regularly in Alaska and British Columbia (and probably other places with low-elevation glaciers that interact with forested zones) where climactic oscillations have led to rapid advance and recession of glacial extent.

In Glacier Bay, Alaska, for instance, there are a number of interglacial stumps (you can see a few sites marked on this map). These stumps represent a forest that was established in the ice-free interim period between the Last Glacial Maximum (10,000-15,000 ya) and the "Little Ice-Age" (~500 ya). Thus, these trees have been preserved under the ice for a few hundred years and have only been uncovered recently (<100 ya). Many of the glaciers in Southeast Alaska are receding, so new stumps are being exposed every day.


Is there anyone discovered new drugs by actively create mutations in drug-producing organism?

I'd say this is possible, but not really practical. Mutating genes by UV light is not that hard, it's just the screening for the (new) compounds that makes it difficult. You would probably be better of creating diversity using established chemical methods.

Usually UV mutagenesis is done for whole organisms, but some people probably also tried this for single genes (even though they'd hit the whole genome). This is the easy part; you could get an enormous amount of diversity with very little work. Even though mutations that change enzymatic products are probably much more rare than mutations that change substrate specificity or product chirality, people find those mutations (example from the top of my head: p450 hydroxylation patterns, although they probably used targeted mutagenesis).

Determining if a specific compound is produced by an organism is also not very hard. You break all the cells, put the solution on a column and check with your favorite analytical method whether or not your compound is in there. Checking for new compounds is much harder. You need better analytical methods such as MS/MS as you don't have analytical standards, and the adapted molecule might not even be detectable with the analytical method you used for the starting molecule. We are very good at detecting needles in haystacks, but determining if there is a needle, a stick, or maybe a piece of hay from another species in the haystack is much harder. You'd already have to predict what kind of altered molecules you expect to find.

When you have successfully done all this, you have identified a single new molecule. Nowadays, people use libraries with >100,000 compounds to screen against their disease protein of interest.

The idea of mutating enzymes to produce new products is not that strange, people work on this, publish, find a lot of interesting things and we learn a lot about enzymes. As an approach for drug discovery this approach is just not high-throughput enough.


Cyanidioschyzon merolae seems to be an example of such algae. Cryptomonad, aka Cryptophyceae also lacks cell wall.

I think, problem you encounter is that most studies are concerned with structure and function of cell walls, as such knowledge can be used in biotech industry. Hence, you will not find answer by looking for "algae without cell wall".

As a suggestion, I would point to this evolutionary study on development of plants: Evolution and Diversity of Plant Cell Walls: From Algae to Flowering Plants. Seems like trying to look through evolutionary trees might give you more examples.


Non-coding DNA correlation with rate of evolution

Whether or not species with less non-coding DNA evolve faster, the assumption that this could be explained by their genomes being more susceptible to mutation would seem to me to be based on a false premise.

Let us examine the logic of the assumption by making an analogy to drawing of tickets from an urn in a lottery. If you buy one ticket (coding region), and only one ticket is drawn (there is a single mutation) from the urn (the whole genome), the probability of winning (your gene suffering a mutation) decreases as the number of tickets (the size of the genome) increases.

So the question is “does mutation follow this model?”, i.e. are the number of mutations in a genome independent of its size? To answer this, let us look at two examples of known mechanism of mutation.

Misreading during DNA replication: Here (and in other types of misreading) the error frequency is, quite logically, related to the number of bases replicated i.e. it has a specific (if very low) value of n per 1,000,000 bases — not n per genome.
UV radiation: Here the source of the radiation is external and its flux will be proportional to the area it strikes — hence the larger the target area the more interactions with thymine causing dimerization. Although our linear-centric view of DNA tends to ignore its area, the larger the genome, the larger the target. The only way I can see the non-coding DNA buffering the coding DNA from radiation is if it somehow formed a protective shell around the latter. I know of no evidence that this is so.


I understand haplogroup as the group of people that share the same given haplotype for a region of the genome.
A haplotype is the readout of the DNA sequence for a part of the genome in one of the two copies that diploid organisms have. If you start reading the DNA sequence for a given point in the genome from one of your copies and someone else's copies, it will coincide up until a point where there is a change. It is more probable to have longer identical haplotypes if the two people that are compared are related. The closest the relation, the longer their haplotypes will be identical. What breaks haplotype identity are recombination events that happen in the germinal line in the previous generation, and mutations that happen both in the germinal line and the soma (the rest of your body) along time.


Monochromator in fluorescence microscopy

Zeiss LSM780 uses essentially monochromator to spread all fluorescence across 34 detectors for multi-spectral acquisition. It is used to detect autofluorescence, unmix closely positioned emission spectra (unmix GFP and YFP for example) and to measure precise spectral peaks with ~1nm resolution.

Monochromator is useful when you need to transform frequency domain information into spatial domain. In fluorescence microscopy we usually collect light from wide bands of well-separated GFP-like proteins, so that filters make more sense. We usually don't detect 1-nm wide lines or plot spectra. LSM780 does allow all that, if you need to.

You can use spectral imaging, but for that you will have to either scan for very long time, or spread signal onto array of detectors.


It isn't a butterfly, it's a saturnid moth -  Samia canningi, also known as the wild eri silkworm moth.

There is a good image on Flickr here, and some more information here.


Is the golden ratio of anatomic measurements universally beneficial for sexual reproduction?

I have some insight into this from an engineering perspective. Years ago, I worked on some computational and search algorithms which used a growth factor to determine how far to widen a search space, or how much more memory to allocate. For some of these algorithms, I ran a series of random trials to search for an optimal growth factor and found that for some, that optimal factor approached 1.618. Completely outside the realm of biology, this golden mean popped up as the most efficient growth factor for some of my algorithms.

Over the years since then, I have recognized that this is an optimal factor for various engineering problems (although in practice I often find it more trouble than it's worth to explain to colleagues why they want to use it). So, I have gradually come to believe that this is why we see this ratio all over nature, in the way seashells grow, the proportions of various body parts, the arrangement of seed structures, etc. It appears that natural processes have ultimately led various lifeforms all over our world to tend toward this ratio to optimize their own functions.

The fact that we find this ratio "beautiful" is a far more fascinating study of what appears to be a meta-adaptation. Consider all of the various ways that the recognition of this ratio is important beyond just sexual reproduction. When we select our food, choosing vegetable or meat specimens which exhibit this ratio most perfectly is more likely to lead us to the healthiest food. Choosing to take shelter under the more "beautiful" tree may also be a good bet that it is the more stable, healthy tree. Making tools, clothing, or structures with this ratio may serendipitously lead us to better formed products. We don't have to find this ratio more beautiful to look at, but because we do, it leads us to better choices in a variety of odd ways. So, those of us whose brains appreciate these things thrive a little more.

Your question was not about underlying causes, but about statistical prevalence. I don't know the answer to that. And I think it would be very difficult to obtain those numbers accurately for another loosely related reason. The human brain is very attuned to finding patterns, and the human brain likes to find this ratio. Taken together, this presents a huge bias for any researcher trying to objectively measure the frequency of this ratio in nature.

However, once we understand that this ratio is the solution to a variety of engineering problems, it becomes clear that it is an indicator of optimization, or proximity to perfection. And even if we cannot say how many species are able to recognize, appreciate, and seek after this ratio, we can say that those who do will most likely find it a beneficial adaptation.


Role of the pupil response in night vision

Short answer
Pupil responses have little effect on dark adaptation. It is the retinal processes that govern the bulk of the dynamic range of the eye's light sensitivity.

Background
You are referring to dark adaptation of the eye, which is, according to the Universty of Calgary:

  This change is called dark adaptation and refers to the process by which the eye becomes more sensitive to light under conditions of reduced illumination. [C]ones are primarily responsible for resolving fine detail (acuity) and colour vision in good light, while rods allow us to see more effectively in dim lighting conditions. The recovery of sensitivity in dark adaptation involves the regeneration of photoreceptor photo-pigments as well as neural changes.

See figure 1. The rods are way faster in gaining sensitivity than the photon-hungry cones.

In a typical clinical setting for diagnostical purposes of e.g. rod function, a typical dark adaptation period is about 20 minutes or so, which fits the below graph quite well. At the end of dark adaptation, the eye is about 100,000 times (i.e., 5 log units) more sensitive than it was at the beginning of the test, a level called dark adapted sensitivity (Universty of Calgary).

In contrast, the pupil response has only a minor effect on light sensitivity in  dark adaptation. It does change its diameter in the dark for sure, but the amount of light that passes through doesn't change too drastically. Pupil diameters range between about 2 and 8 mm (Spector, 1990), say a factor of four. In terms of surface we are talking about 3 and 50 mm2, respectively using (pi*r2), hence a factor of 16, as opposed to 5 orders of magnitude in the process of retinal adaptation.

Fig. 1. Light sensitivity adaptation of rods and cones. source: Uni Calgary

Reference
- Spector. The Pupils. In: Walker et al. (eds.) Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd ed. Boston: Butterworths (1990)


How to compare diversity between different ecosystems?

Have a look at the Wikipedia page on Diversity Index

Here are the indices that the wikipedia page describes

"True Diversity" Index
Species Richness
Shannon Index
Rényi entropy
Simpson index
Inverse Simpson index
Gini–Simpson index
Berger–Parker index

The article also links to related concepts such as

$\alpha$ Diversity
$\beta$ Diversity
$\gamma$ Diversity
Isolation Diversity
Relative Species Abundance

The literature is important on the question of measuring species diversity, ecosystemic function diversity and genetic diversity. What you want to use very much depends on your interest. Just to cite one other example: In the conservation literature, total sum of branch length over a phylogeny is sometimes used as measure of diversity and is sometimes used for prioritize populations (see for example Curnick et al. 2015). This method implicitely assume that more distantely related branches have different ecosystemic functions and keeping many of these functions is good for conservation purpose.


How statistically significant was the "sweaty T-shirt" experiment?

First, let's consider the original Wedekind et al (1995) study.

Sample sizes seem reasonable, if the effect is not very noisy:

  [...] 49 female students (average age: 25.2 years, s.d. = 4.0) and 44 male students (average age: 24.7 years, s.d. = 2.6) [...]

... and the statistical design accounts for individual differences in a fairly robust way:

  [...] women were asked to rate the odours of six T-shirts each, three of them worn by men who were dissimilar to the rating woman's MHC (average number of dissimilar HLA-antigens = 5.9, s.d. = 0.26), and three worn by men who were more similar to it (average number of dissimilar HLA-antigens = 2.7, s.d. = 0.74). We tried to present every T-shirt as often to MHC-dissimilar women as to MHC-similar women (average difference of presentations to thc two groups: -0.02, s.d. = 0.73). The presentation was random in every other respect [...]

Rather irritatingly, although the study design involved asking women to rate at least three attributes of the smells (sexiness, pleasantness, and intensity) the study performs a bait-and-switch in its results:

  The scores for sexiness are not shown in the figures as they were highly correlated with pleasantness (all scorings: r = 0.85, n =  294; for women who do not take the pill: r = 0.87, n = 186; for women who take the pill : r = 0.83, n = 108, p always << 0.001)

This is a bait-and-switch because even if A correlates with C, and B correlates with C, we do not know that A and B correlate with each other. Of the three measured attributes, 'sexiness' arguably has the most direct bearing on mate-choice. Because analysis for 'sexiness' is not presented, the paper ends up telling us much less than it could have about the relationship between MHC relatedness and mate choice.

The results for 'pleasantness' and 'intensity' look like this:

One further piece of analysis is presented: some number of the female subjects seem to have reported that particular smells reminded them of their partner or ex-partner; or reminded them of family members. Mentioning that a shirt smelled like a partner or ex-partner happened more frequently for MHC-dissimilar shirt smells (~17% vs ~9%; p = 0.038, two-tailed Fisher exact test). Oddly, no written response-collection is described in the methods, so I can only assume that these assessments were ad-hoc.

If this was all of the analysis that had been done on the topic, my assessment would be: this is amongst the many published research findings that are probably false. My main concerns would be that

Not all of the collected data are presented;
The most directly-informative contrast is not shown;
No adjustments for multiple comparisons are made on the statistical tests;
The data that are shown are very noisy, and sample sizes are not huge, raising concerns that the tests are underpowered;
The authors conduct tests based on data-collection which is not detailed in their methods, raising concerns about p-hacking.

And now, the 2005 paper!

Right off the bat, this paper cannot possibly replicate the findings of the Wedekind (1995) paper, because Wedekind et al found significant preferences for dissimilar MHC odours in women not taking the pill, and significant preferences for similar MHC odours in women taking the pill. In this study:

  [...] we did not distinguish between, in our statistical analysis, women who were taking oral contraceptives from women who were not.

  [...] Nine female participants (31.03% of female subjects) were taking oral contraceptives.

Sample sizes are smaller than Wedekind 1995 in terms of number of participants, but larger in terms of number of contrasts, because this experiment had two different sample types (sweat odour and urine), and had men smelling women as well as women smelling men. Within-individual effects are not modelled, so there is a potential for (e.g.) a small number of generically good-smelling individuals with rare MHC alleles at the population level to bias the analyses - whereas this potential bias was accounted for in Wedekind by performing within-individual correlations. The sample-sizes look like this:

The analysis was a series of Chi-squared tests, for data collected in four different sessions: one with men smelling female urine, one with men smelling female body odour, one with women smelling male urine, and one with women smelling male body odour. All chi-squared tests returned non-significant results with the exception of women smelling male body odour, for which the Chi-squared table looks like this:

So, this study didn't find the same result as the Wedekind study, but then, it couldn't find the same thing as the Wedekind study because of the way the analysis was performed, so that is no surprise. The authors claim that they found a significant effect of MHC relatedness on odour perception, but only in the proportions in the hard-to-interpret 'indifferent' response category. I am inclined to disagree. The authors presumably conducted 16 contrasts (a test of independence and three goodness-of-fit tests in each of four treatment types), and found one instance of p < 0.05. I would argue that the one 'significant' result is best explained as a failure to account for multiple comparisons.

Ending notes

If these two papers were the only things that had been published on MHC-directed mate preferences in humans, I would be far from convinced that the claimed effects were real.

however...

These are far from the only papers on the subject of MHC-driven mate-choice in humans. Wedekind and Füri (1997) conducted an analysis with very similar experimental design to Wedekind et al (1995), but arguably better statistical analysis, and found the same direction of association as Wedekind et al (1995), albeit still with a fairly high noise-to-signal ratio. Subjectively, this goes a reasonable distance towards making me think that the findings of Wedekind et al (1995) were not just a statistical fluke. I'm still not utterly convinced, but certainly more convinced than I would be if Wedekind's final paper on the topic had been the 1995 publication.

MHC-driven mate-choice has also been investigated using facial preferences and mate choice surveys. The combined evidence (across odour preference, facial preference, and mate choice surveys) is reviewed in Havlicek and Roberts (2009).


I want to understand a mechanism how at the first times when the life began on earth evolution helped the new species to arise through selection while the same organism also continued to live as not evolved.

Well, this beginning is not grammatically correct so it is hard to make much comments on it.

  If natural selection favors survival of the fittest, [..]

Selection is the process by which fitter individuals increase in frequency in the population. survival of the fittest is a layman phrasing of the process that is natural selection. Natural selection therefore does not favour survival of the fittest, but it is represented by the phrasing survival of the fittest.

  [..] th[e]n why after a living evolves to a new fittest form, the older form still exists

It does not. The older form is called an ancestor. The ancestor does not exist today. If there was a speciation events, then the ancestral lineage would have giving rise to more than a single lineage today. Some of these modern lineages may 'look more' like the ancestors than others but it does not mean that any ancestor still exist.

For example, the chimpanzee is not an ancestor of humans. Chimpanzees (and bonobos) and humans share a common ancestor that is about 8 millions old. To consider another example, humans and an oak tree share a common ancestor. This ancestor was neither a human, nor an oak tree. This ancestor lived about 1.6 billions years ago.

If you want to know why I am using term 'lineage' rather than 'species', you can have a look at this post

See below linked Biology.SE posts for more information

  the older form still exists while it should be counted as unfit for survival and extinct

Don't forget that different lineages may (and will be at equilibrium due to the competitive exclusion principle) be adapted to different ecological niche. As such, one lineage will not necessarily outcompete the other one.

Source of information on StackExchange

There is a lot you can learn on the subject. You should start with an introduction to phylogenetics such as the one provided in the post

Why do the ancestors of birds still exist?

You can also have a look at

Extinction of species

You should also have a look at

How does Darwinian Evolution work?

Reading your post, it sounds like you may have too a pan-selectionist view of evolution. Related to this point, you might want to read

Why don't mammals have more than 4 limbs?

Source of information external to StackExchange

Understanding Evolution is a good introductory course to evolutionary biology.

Response to comment

  Thank you for the very descriptive answer, as you have figured out easily I am very new to evolution. I will read the references you have provided carefully

You're welcome!

  is after evolution of a specie through natural selection,

This show again that you have too a pan-selectionist view of evolution.

  unfit ancestor extinct and this is explained through phylogeny ?

From wikipedia

  Phylogenetics is the study of the evolutionary history and relationships among individuals or groups of organisms (e.g. species, or populations).

A phylogeny is a tree of life of a given taxon. For example here is a phylogeny of placental mammals.

To be able to fully answer your own question, you need to understand the relationships between lineages and therefore you need to have some understanding in phylogenetics.


How exactly are gaps defined in genomics?

You're not wrong but gap can mean more than that. A good recent reference is this paper: Genetic variation and the de novo assembly of human genomes.

Essentially, a gap occurs if something happens in our genome that can't be explained by uniformity. Since our genome is highly complicated, you can expect gap is also more than just mis-sequencing. The gap you mention is the sequence-coverage gaps mentioned below.

This paper has a section about the types of gaps.

1. Sequence-coverage gaps

Sequencing gaps occur, under the simplest condition, where no sequence reads have been sampled for a particular portion of the genome.

2. Segmental duplication-associated gaps

Over one-third (206/540) of the euchromatic gaps in the human reference genome (GRCh38) are flanked by large, highly identical segmental duplications.

3. Satellite-associated gaps

These include short and long runs of tandem repeats designated as short tandem repeats (STRs; also known as microsatellites), variable number of tandem repeats (VNTRs; also known as macrosatellites) and Mb-sized centromeric satellite repeats.

4. Muted gaps

Muted gaps are defined as regions that are inadvertently closed in an assembly but that actually show additional or different sequences in the vast majority of individuals

5. Allelic variation gaps

Some regions of a genome also show extraordinary patterns of allelic variation, often reflecting deep evolutionary coalescence.


The answer that you link to provides a pretty good overview of what it might take to clone an extinct organism from preserved tissue and what some of the challenges are. I won't repeat that answer, but in a nutshell, two big obstacles are incomplete sequences and a host womb.

To get at your question of whether this preserved "chunk" of flesh will lead to the cloning & revival of extinct species...you're a little late to the game. :-)

In 2003, researchers used preserved DNA to revive the Pyrinean Ibex, a goat native to the Iberian Peninsula, that had recently gone extinct. The results were mixed. The experiment worked, in the sense that the scientists were able to successfully bring a recently extinct animal to term, but unfortunately, the revived goat only lived for a few brief minutes, due to developmental abnormalities. It's important to note that this was achieved using DNA that was even better preserved than that of the cave lions in the Mirror article.

So, will the DNA found in the cave lion cells lead to successful cave lion revival? If such a revival occurs, I'm betting that it will be due to advances in how the ancient DNA is integrated with reference DNA and in how fertilization and implantation are carried out, more than on the quality of the found DNA.


Exposed collagen at the site of vessel damage simultaneously initiates plates aggregation and the clotting cascade. So, when the wound is sealed and no more collagen is exposed, which is the main factor to activate the cascade, the blood clothing cascade stops.


Does the new virus tree of life change their position between living and non-living things?

The definition of life is a question of philosophy

The definition of life is a question of philosophy and not of biology. However, because discussing it often require some knowledge of biology and because it is so common for the general public to misunderstand that the definition of life is not of biological interest, the question has already been addressed on this biology.SE. Please have a look at:

why-are-viruses-considered-microbes and why-isnt-a-virus-alive.

Why would the tree of viruses affect our definition of life?

It is impossible to say much without a link to the original claim. I will need to speculate on what the authors of this claim first meant.

A tree of viruses gives a visual representation of a feature that we tend to associate to living things only, that is they evolve and speciate. Of course, we did not need to build a tree of viruses to understand that they evolve and speciate but a visual representation can sometimes offer an emotional response that will push some to prefer considering viruses as living things. In consequences, it is possible that the vision of this tree affect the emotional aspect of what we define as "living things" and might push the community to expand their standard definition to include viruses. Again, it is important to understand that the definition of life really has absolutely no impact on Biology.


What would be the best dredging/trawling tools to collect macrofaunal priapulids?

My first question would be is there any external indication of them such as air holes or anything else that you can assess from the surface?  I would think that if there is, you could use transects and a quadrat.  If you need to dive for them you can obviously make a weighted quadrat by filling pvc pipe with sand and gluing it together.  Then take an area and lay out transects and and randomly choose different lengths along each transect to put the quadrat down and that will give you an estimate of density.  If you actually need to extract them from the mud, I imagine that varies by species and you could make due with a grab sampler of the right size, something on the small end I would imagine.  That way you aren't dredging up tons and tons of mud to sort through.  If they are even rarer than I imagine, you could just lay out transects and swim them until you see something and do away with the quadrat.  Hope this helps.


T cells are not transferred. Vaccines induce the host to expand their own T cells that are responsive to the antigens that are given.


I don't think it's wise to use a spectrophotometer for this experiment, as it is a total count, i.e. it can't distinguish between dead and alive cells very well, and so she might not see a clear difference between her treated and untreated algae. If she has access to a haemocytometer and a good microscope, then she can count the living cells directly, and calculate the cells/ml using a simple formula.

This paper has a nice overview of how to count algae using a haemocytometer, and if her species of algae can swim, then she would need to use the iodine solution mentioned in here:

http://weis.science.oregonstate.edu/files/weis/Protocols/Symbiodinium/Cell%20Counts.pdf

I hope this helps!


Do cell membranes have more phospholipids in one layer than in the other?

Yes there is a difference in the number of phospholipid molecules because of the curvature. This is very evident when there is a lot of bending as in case of exocytosis (see here) but otherwise I do not think there would be an enormous difference in the number of phospholipids between inner and outer surface of the bilayer.

Assumptions:

Cell is spherical
Cell diameter = 1µm (overall)
Thickness of bilayer = 6nm
Width of a phospholipid molecule = 1nm

Difference in circumference of outer and inner layers = 2π(6nm) ≅ 37.7nm

So approximately 37 more phospholipid molecules in the outer layer in this cross section of the cell. This is just 0.6% of total number of phospholipids in the outer membrane.

I don't think fluidity will be compromised because of this - only if a layer is overpacked will the fluidity be affected.


coenzymes are factors that bind to the enzyme so that enzyme can show its activity. In this case conversion between Ran GTP and Ran GDP are caused by hydrolysis and phosphorylation reactions. Ran GEF and Ran GAP are not binding to Ran GTP or Ran GDP.


I dont think this would be possible from the simple idea that all cells need energy, and if there's no nutrient flow, then how would the cells inside the detached body part stay "alive".  Doctors can currently reattach body parts right now if it's within a certain amount of time, but no animal yet can just reattach at will.


Transformation of a multicellular organism

Your inference is basically correct. The Agrobacterium acts as a vector for a plasmid containing the genetic construct one wishes to introduce into the plant genome. A medium containing a large number of bacterial cells transformed with this plasmid is injected into plant tissue, and the plasmids enter plant cells where parts of their DNA are integrated into the host genome. The overall effect of this is that there is localized integration in the areas where the Agrobacterium was introduced. A nice visual illustration of this comes from a paper from our lab where my colleagues introduced the genes for betalain biosynthesis into the tissue of Nicotiana benthamiana: in Figure 3 you will see only a localized area of cells around the injection site gain the ability to produce betalains.
You can find a nice review of the whole process of transformation with Agrobacterium here.


A botanist at a local university says it is most definitely Crown Gall.

He didn't provide any other information than that, so all I can do is quote Wikipedia:

  Agrobacterium tumefaciens (updated scientific name Rhizobium radiobacter, synonym Agrobacterium radiobacter) is the causal
  agent of crown gall disease (the formation of tumours) in over 140
  species of eudicots.

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


How to find conserved residues across species?

I'd perform a bigger alignment using clustal or mafft or something. Pairwise alignments will give you a lot of noise from random chance and the set of pairwise alignments will be really large. Multiple sequence alignment will detect smaller conservation signals.

Compare against several species of yeast and maybe other mammals for context. When the alignment is done, perhaps draw it? I like logos for vertically large alignments.


There is no fundamental difference between viral RNA and and native cellular RNA other than the sequence of RNA bases in them.  The sequence differences are not biochemically apparent in the RNA, only in the protein products produced from the RNAs.

Regulation of native RNA is done in a huge variety of ways (nothing in the cell is designed; everything is ad hoc, so any random happenstance can become established).  Native regulation is essential, otherwise runaway production will happen leading to cell death or to cancer.

Much, if not most, of the native regulation is done by regulating transcription of DNA into RNA. Once the RNA is in the cytosol, little further regulation is done, so viral RNA in the cytosol has the run of the cellular protein factory.  But at least some viruses have acquired further advantages which help their RNA out-compete the native mRNAs for use of the protein machinery (see, e.g., Hijacking the translation apparatus by RNA viruses)

So it is not really an easy thing to "label a sequence of RNA as dangerous simply because it is unregulated" as the wide range of normal RNAs in the cytosol does not provide a basis for determining if any are "unregulated" and the cell cannot be protected in that manner.

Self-assembly is widespread in normal cellular functions as well as in viral production.  The molecules involved have long-honed attractive points for their mate molecules, and in the jiggling molecular soup of the cell the molecules can soon bump into each other and join up.  Thanks to the virus's uncontrolled production, new viral particles have plenty of component molecules available for this assembly.


Biological basis of the science fiction story "The Dipteroid phenomenon"

After some research, it appears that the phenomenon being discussed was the consumption of Diptera flies by the dung fly, Scatophaga stercoraria. This paper describes their inability to sexually mature without consuming prey (for which Musca domestica flies were provided).

  Male  Scatophaga  stercoraria must prey on other Diptera before they
  display sexual behavior, develop  the  accessory cells  of  their  ejaculatory ducts, and
  achieve  full elongation of  the testes. The corpus allatum also becomes enlarged
  after predation and is  necessary for  the onset of sexual behavior and development
  of reproductive organs. The complex diet consumed  during predation apparently
  cactivates the corpus allatum, and the hormone released acts  independently on
  organ growth and sexual behavior.


The shape, colour and scales on the hat suggest something in the genus Coprinus.

Some species are edible, but it is not recommended to have them with wine.
I would not advise you to eat them without further live identification by someone knowledgeable. Photo identification is not reliable.


Why is it better to drink room temperature water instead of cold water?

Your teacher was passing on a myth.

This false belief might be related to the equally false belief that hot exerted horses should not be fed cold water. It could also be down to someone downing a big glass of ice-cold water in one go as a child, get a brief stomach ache and spin a health-advice on it.


How is the concept of species defined in asexual organisms?

There is no taxonomic category called "asexual organism". It is rather a phenotypic trait of scattered occurrence.

However the absence of sexual-reproduction in a group of organisms sometimes causes problems in scientific classification. This caused development of the artificial-group fungi-imperfecti (or deuteromycota) at one time, for fungal strains which lack sexual reproduction.

Bacteria and archaea (prokaryotes) are not known to show sexual reproduction. However  they  show  some gene transfer processes like conjugation and transformation; but this is not the same as sexual reproduction because cell fusion does not take place.


How would you use readthrough as part of a genetic circuit design?

Readthrough has already been used to implement transcriptional NOR gates, wherein tandem input promoters express a repressor that represses an output promoter. (First time I recall here: 21150903, used widely here: 27034378, roadblocking modeled here: 32141239.) An advantage of this design is that the repressor need only be encoded in DNA once, which can significantly reduce the DNA footprint of the design and the likelihood of recombination if the repressor's DNA sequence is long (e.g., protein-based repressors). OR gates have similarly been implemented as two tandem promoters expressing a common output gene. (An alternative NOR design—which is common with repressors with short DNA sequences (e.g., sgRNAs)—is to duplicate the repressor and express it separately from both input promoters. This approach circumvents the roadblocking and input asymmetry that can occur with tandem promoters.)
Readthrough has also been used with antisense promoters to tune gene expression (see 26769567). In these designs, an input promoter must read through a downstream antisense promoter, and the strength of the antisense promoter can be used to tune the response of the input promoter.
Another application that comes to mind is encoding the relative ratio of expression of multiple genes by separating them with weak terminators (e.g., to achieve X-fold expression of the first gene relative to the second). This begins to evoke an operon, as jakebeal notes. The closest example I can think of comes from this paper: 23727987, although they actually used readthrough to address the inverse problem of characterizing terminator strength.


Queller's 1985 version of Hamilton's rule

It is just worded a little wierdly in my opinion. The key line in the paper is: 'Fitness components are also defined for all individuals, for example, $C$ is defined, even for a non-altruist, as the cost it would incur if were altruistic.'

Essentially, if it doesn't matter what individual you are you always pay the same cost, then $C$ is a constant. This is pretty much the definition of a constant! The expectation of a constant is just the constant, $E(C) = C$.

The reason it works is that to find whether or not the cost is realised, Queller simply multiplies by the focal individual's phenotype value $P$, which is either 0 or 1. So either the individual pays the cost or it doesn't.


Why does black and yellow indicate danger?

First of all, great question! What you describe here is known as aposematism. Aposematism is the adapation of warning signals against the predator. This word is used for any sound, coloring, and odor used as a warning signal. Of course, for this question the focus is color.
Honest indications
Animal coloration is usually an honest indication of their noxiousness. The brighter they are, the more noxious and toxic they are (http://rspb.royalsocietypublishing.org/content/276/1658/871). In the linked article, there are many references one this positive correlation of toxicity of prey to predator and the brightness of the coloration. In the article they use mathematical models to support the mathemstical evidence. But one thing is for sure: bright colors do mean the prey is armed with defenses, whether the correlation is positive or not.
Why then is it black and yellow?
The conspicuousness of the coloration is very important because it is important to see from a far away distance. The reason colors like yellow and black are used is because (http://rspb.royalsocietypublishing.org/content/279/1728/417):

— They provide high contrast against the background (e.g. red/yellow against green foliage), which promotes detection.
— They are resistant to shadows (which are rich in blue-UV), and to changes in illumination (e.g. black should not change during day, whereas white could become ‘pink’ at sunset and sunrise). Therefore, they provide a reliable signal under varied habitats and light conditions.
— Yellow/red and black has both high chromatic and luminance contrast.
— Such colours may allow distance-dependent camouflage if yellow/red and black ‘blend’ to an average colour that matches the background at a distance when predator vision is no longer sufficient to discriminate individual marking components.
— Such colours are distinctive from profitable species.

What about the combination of black and yellow?
In the same article, they mention that:

Many warningly coloured prey have markings comprising repeated pattern elements. Such arrangements in signal structure may increase redundancy in the signal but improve the likelihood that the strategic component will be detected by the receiver. In addition, repeated elements may be rare in many natural environments, thus increasing conspicuousness of the prey animal. Simple pattern components (such as stripes and spots) may facilitate detection and also speed up avoidance learning if they are easier to memorize.

The research seem to show that the patterns, such as the stripes, lead to increased avoidance, but it is not sure whether or not it is due to the stripes itself or due to the constrast of the black and yellow.
I hope I have answered your question and if you have any questions, feel free to ask in the comments.


I am no mycologist, but I think it looks like the false death cap, Amanita citrina var. alba.

I'm basing this mostly on color, size, and the universal veil remnants on the cap.  Here is a picture for comparison:

  Amanita citrina is now known to contain the toxin alpha-amanitin;
  however, if eaten in normal amounts it is considered the concentration
  is so low that it is unlikely to have any significant effect on a
  healthy adult. Of far greater risk is the possibility of confusion
  with one of the deadly Amanita species such as the Deathcap, Amanita
  phalloides, or the Destroying Angel, Amanita virosa. For this reason
  our advice is not to eat Amanita citrina, whether it is raw or cooked

Source: First-Nature


How to convert enrichment/depletion to frequency for comparing deep sequencing to sequence profile?

Although the question is kind of confusing at some places, what I understood is that you are trying to compare the relative amino acid enrichments in the two datasets.

As far as I know, you could construct the protein sequences from directed evolution experiment (presumably a time series data. Please clarify that.) and make a multiple sequence alignment (MSA) of that. In order to construct the sequences, there would be some technical procedures that would depend on the type of deep sequencing data you have. Factors such as the read length, protein length and coverage would need to be taken into consideration.

You could similarly make MSA for second datasets too.

Then using tools such as Rate4site (https://www.ncbi.nlm.nih.gov/m/pubmed/12169533/) you would be able to get evoutionary rates per site from MSAs. Then compare the evolutionary rates per sites for two datasets by correlating them.

If the correlation is high, the enrichments in both datasets are similar, otherwise not.


Fish "coming back to life" after being frozen

I have no idea what's the real reason for the survival of the poor fish, but I would guess this is all in the timing. I know for certain ;-) that one can submerge a hand in liquid nitrogen for a short time or in general one can pour liquid nitrogen on the skin with no harm done whatsoever.

The reason is that the difference in temperature that interface (-180 deg C or so for liquid nitrogen and 20-30 for the skin surface) is so large that nitrogen vaporizes instantly and does not penetrate/affect the tissue. The demonstrator could have pulled the fish with bare hands.

I think that for the goldfish the time was too short and while it was cooled/shocked a bit, it might have been too short to do any serious damage. But -

As a scientist, I can't help but notice that we don't really know the condition of the fish before or after the liquid nitrogen 'treatment'. We only see it flapping for a few seconds when back in water. I wonder what happened to the eyes and the mouth, both quite sensitive tissues for such a shock. Also, the water the fish was in was a factor probably, providing additional buffer between the fish and the liquid nitrogen.

Last but not least, the ethical committee quite certainly did not approve that demonstration.


How do marine mammals and penguins maintain bone density?

I wouldn't refer to it as "bone loss" but more as bone strength. Lifetime swimmers spend a lot of their time in the water. As in water yes they are almost "weightless" and their bone strength will decrease because it has gotten used to the "low" gravity. Now in the case of penguins and other Marine mammals, they have adapted to the force that the water applied to them.

Here is a link to a picture of penguin's flipper.


There are two possible ways to perform refractive operation: first,  to perform the procedure on the cornea, the second - to exchange the crystalline lens with the artificial one.

The second approach is extremely rare, because the lens (1) is inside the eye and (2) it allows us to accommodate (=change the focus of vision). Thus, this method is relevant only to extremely high myops and people who have some degree of cataract (the clouding of the lens).

In "classic" myopia the eye is larger than "normal" one, and the lens thickness is less relevant in the terms of treatment.

Back to LASIK - the operation is performed on the cornea: for myopic eye the corneal thickness should be reduced, for hyperopic eye there are other protocols (special thickness reduction).


How can I set micropipette volume with decimal separators, for example 109.5 in p200?

It doesn't make sense to set volumes of decimals of microliters with a P200, since usually the accuracy of these pipettes is in the order of a few microliters. So even if you set your pipette at 190 uL, you may still dispense a volume ranging from 187 to 193 uL. For a P1000, due to higher volumes the inaccuracy is of course higher, usually +/- 10 uL or more. Some brands are more accurate than others, like Eppendorf or Finnpipette. I suggest you check the specs of your pipettes and see how much accuracy you can achieve.


Your description is correct. Most genes do not show complete dominance as outlined in Mendelian genetics and inheritance is almost always more complicated than a simple 1 gene/2 allele system. The mutation you're studying is classified as autosomal dominant but even heterozygotes may not display the phenotype. The proportion of the population that has the mutation AND displays the mutant phenotype is called the penetrance and, for DYT1, has been estimated at around 30%.

http://www.omim.org/entry/128100?search=Dyt1&highlight=dyt1


My assumption is that if you're sweating excessively, you could also be suffering from a condition called hyperhidrosis. This is a condition whereby your hands and feet sweat excessively. I would suggest that you try looking into using a solution like an iontophoresis machine to be able to treat this condition. I too have suffered from sweaty hands for a long time, and after trying different options, I found that using an iontophoresis machine provided me with the best results.