How are we able to selectively inflate our cheeks?

Muscles can only "pull" never "push" - that's just how they are organized at a molecular level. We can only push things because we use joints as levers: if you "pull" on the outside surface of your arms, you can push things out with your hands because that pull acts to extend the forearms.

It's not really possible to puff out your cheeks with muscle, because there is nothing floating in the space outside your face to pull against. Your cheeks puff up a bit when you smile, but I think you will agree that's a completely different type of "puffing" and comes from gathering up a bunch of tissue.

However, it's fairly simple to contract muscles in your face (specifically the buccinator) to prevent a cheek from bulging out by tightening the muscles in the cheek. The air pressure you are producing is pretty minimal, so it doesn't take much strength. The cheek bulges out when the muscles are relaxed, and doesn't bulge when the muscles are contracted.


How fast is water transported from roots to leaves?

You can find some answers for your questions in this paper (it is only for Ricinus communis, but you may follow the cited by from google and find for other plants):

http://onlinelibrary.wiley.com/doi/10.1046/j.1365-3040.2001.00704.x/full

velocity in the phloem (0·250 ± 0·004 mm s−1)
xylem in the light (0·401 ± 0·004 mm s−1), in the dark (0·255 ± 0·003 mm s−1)

Graphs on daily change are on the paper.


What direction is a sequence in databases written?

Directionality

It is indeed the convention to represent nucleic acid sequences in the 5ʹ to 3ʹ direction.

This is implied in the IUPAC/IUB document on Abbreviations and Symbols for Nucleic Acids, Polynucleotides and their Constituents, although not stated explicitly — presumably because this was written in 1974, before the large nucleic acid databases were established.

Strand

In general you can assume nothing about which strand a particular feature is located on. You need to refer to the context or documentation for the particular database that you are using.

I prefer the term ‘sense strand’ to ‘coding strand’ as explained in another post. However this only has meaning in a restricted set of circumstances relating to mRNA, particularly considering cDNA copies of eukaryotic mRNAs. Only if the context indicates that this is the case can you assume the strand presented as a ‘sense strand’.

The problem arises from the fact that for all (or almost all) genomes, different genes are located on different strands of the DNA — the chromosome has no unique ‘sense strand’ or ‘coding strand’. Thus, for DNA sequences in a database such as Genbank, the following are possible:

The DNA sequence presented does not encode protein or structural RNA.
The DNA sequence presented contains genes on both strands.

An example of the latter is given in the Sample GenBank Record which should be consulted to understand the feature annotation in DNA sequence entries in GenBank. This 5028 bp yeast chromosome entry encodes two genes. The first, AXL2, is annotated:

 gene            687..3158
                 /gene="AXL2"

The second, REV7, is annotated:

 gene            complement(3300..4037)
                 /gene="REV7"

This indicates that, when presented in the 5ʹ to 3ʹ direction, the gene REV7 lies on the complement of the strand presented.


When does a jalapeño begin to produce heat/capsaicin?

The reason the 'seeds' you ate weren't hot is because they're not seeds. What you thought are the seeds in the pepper flower are its anthers. The anthers are the pollen bearing parts of a flower. The unfertilized, and therefore undeveloped, seeds would be found in the flower's ovary which is at the base of the petals. The parts of a flower are labeled in this diagram.

I've tried both the seeds and the flesh of jalapeño peppers and noted the 'heat' in both but personally, I found the seeds a little hotter.


Are genes associated with obesity selected for?

This is called the "Thrifty Gene Hypothesis" which was first used to explain why diabetes is so common. Basically it suggests that these alleles would have provided some kind of advantage, over the other possible alleles at that loci, until the environment changed. Then the environment changed and the allele became harmful. Environments are always changing and therefore favour different alleles (variant of a loci).

I suggest the genes linked to obesity in the modern world would, if tested on the old world populations would have been linked to being of a healthy weight. Further, those without it may have been skinnier and more likely to suffer from the disadvantages of being in such condition.

However, this paper present some counter arguments to the thrifty gene hypothesis. Speakman suggests that the genes responsible spread via genetic (allelic) drift rather than by positive selection. It is worth remembering that drift is very poor at spreading new mutations through large populations so there are also weaknesses to his arguments.

One example of a change in the favoured allele caused by an environmental shift is the DDT resistance gene in Drosophila which was present in the population at very low levels for a long period of time. As an aside, it possibly remained this way because it was subject to sexually antagonistic selection - beneficial to females whilst detrimental to males. It then spread through the population when DDT pesticides were used because it obviously became highly beneficial.  Many other examples of environmental change leading to different selection are around, this is just one off the top of my head. Another is the Galapagos Finches in a drought in the late 20th century.

HTH, if not please ask more and if it does then please accept it!


How to correctly preserve organic matter with ethylene and polyethylene glycol?

I find that using mixture of PEG 400 and Ethanol 2:1 reduce the transparency. You also need to bake the pental in microwave 360w for 15 seconds. Still some small transparency but acceptable.


I think the order i,ii,iii should be correct, since the fall in temperature occurs after the heat loss exceeds production and will continue only till the temperature equals the ambient temperature. iv is the reason for i. Hence iv,i,ii,iii sounds pretty convincing to me.

With i,iii,ii,iv , the main problem is that there can not be any appreciable fall in temperature ii after the temperature equals the environmental temperature iii. And iv seems more probably to be the reason for i rather than the reverse


Does N1-methyl-pseudouridine occur naturally in any RNA?

N1-methyl-pseudouridine occurs naturally in the tRNAs of most archaea. It replaces the ribothymidine found in the TΨC-loop of eubacterial and eukaryotic tRNAs.

Although the enzyme responsible for the conversion of uridine to pseudouridine has been known for some time, it is only relatively recently (2012) that the gene for the methylation of the pseudouridine was reported in a paper, the introduction to which provides a useful background to the topic.
Original References
Pang, H. et al. (1962) J.Biol.Chem. 257 3589-3593
Gupta, R. (1964) J.Biol.Chem. 259 9461-9471


Why is a membrane polar on the outside and non-polar in the inside?

Phospholipids in aqueous solution under the proper conditions organize themselves into micelles and other structures - the minimum energy state.  This allows the polar head groups to interact with water in the bulk solution, while the non-polar carbon chains are 'protected' from the polar environment.  Water is attracted to water, and the polar head groups are attracted to water, the non-polar carbon chains are excluded.
You can get inverse micelles in non-polar solvents.


Why don't we hear ultrasonic sounds as aliased versions of the original signals?

Short answer
The cochlea is a tonotopic map with certain physically determined boundaries that determine the range of frequencies perceived. Ultrasonic soundwaves simply do not have a correlate on this map.

Background
The cochlea is a frequency analyzer that basically translates acoustic frequencies into a place-map. High frequencies are encoded basally (up to 20 kHz), low-frequencies apically (down to 20 Hz or so). Hence, it is pretty much a Fourier analyzing system (Fig. 1). This way of analyzing sounds is referred to as the place-coding theory of pitch. The place where a frequency is encoded is mainly dependent on physical characteristics of the basilar membrane in the cochlea. Every part is sensitive to a slightly different frequency then the next. This is caused by gradual variations in the stiffness and width of the basilar membrane, among other less important factors like hair cell length and so forth. The specific physical characteristics determine what specific resonant frequency a particular part of the basilar membrane has. Hence, incoming sounds are torn apart with standing waves, where each frequency results in a standing wave at a particular spot in the cochlea.

Fig. 1. Tonotopic map of the inner ear. source: Ternopil State Medical University

The frequencies mentioned are physical wavelengths of the acoustic air pressure differences entering the outer and middle ear. The cochlea translates these into fluid-based pressure differences. Hair cels in the cochlea pick up these fluid pressure differences and tranlate them into potential gradient differences.

The sampling rate of hair cells is pretty much infinite, as they work on a continuous membrane voltage, i.e., they are analogue.

The secondary neurons, the spiral ganglion cells, translate these voltage differences into neural spikes and lead them through the auditory nerve to the brain.

Neural spiking follows the acoustic frequencies up to, say 1 kHz (frequency following response). This phenomenon is referred to as the temporal code of pitch hearing. After that, the refractory characteristics cause single fibers to fire only to one in a few wavelength periods. So at the upper limit of hearing, say 20 kHz, a ganglion cell may only fire once every 20 wavelengths or so. No problem, as many others do the same thing. Stochastics cause the wavelength to be nicely encoded in a population of responsive fibers. Furthermore, the auditory cortex contains a tonotopic map, meaning that high frequencies are processed elsewhere then lower frequencies. In other words, the auditory nerve doesn't need to faithfully encode the incoming wave.

A nice example in this are cochlear implants; they stimulate the auditory nerve with electrical currents. The place of the electrodes determines the pitch, not their pulse rate (although it can have an effect).

Now why are you not hearing ultrasounds? Simply because the basilar membrane does not contain regions sensitive to frequencies above 20 kHz or so. This is referred to as the Greenwood map, which depends on species.


An issue in the question that I will ignore

You say

  Does the evolution head to some optimum that in future we will have only one species which will be superior to all other extinct form of life?

Firstly, it is a little bit weirdly phrased. By "superior" I suppose you would refer to a species that could outcompete all the other. This sounds very impossible to me firstly for simple ecological reasons. However, it would be a long answer to fully address this point and I don't feel like addressing (I might not be very much able to) in addition to the other questions.

Evolution vs Natural Selection

Just for a start. Evolution is way more than just Natural selection. There are plenty of other absolutely essential processes such as mutation and drift that are important to understand.

What is Natural Selection?

Natural selection is the process by which most fit individuals end up being at higher frequency in the population as a result of reproducing more and surviving better. Natural selection does not necessarily diminish the probability of a species to get extinct. It will not necessarily increase the ability of a species to compete another. It will not necessarily increase the rate of increase in the number of individuals in the species.

local vs global optima

Reading you post you seem to understand the concept of local vs global optimum (from algorithmic maybe). If selection alone was acting in the population and if mutations were feeding genetic variation to this population at a low enough rate, then population will ultimately reach a local optimum and will get stuck there forever. They would never reach a potential higher local optimum somewhere else. Drift may allow for such switch though, it is refer to "shifting balance theory".

Envrionmental change

The environment changes much faster at a local scale that you seem to think. When talking about environmental change for a lineage, we are not only talking about important ice age or current days global warming but we are talking about more subtle and more frequent changes. Imagine a species of unicellular living in a 50 cubic centimeter puddle. For them environmental change are drastic and frequent. So do population really have time to achieve any equilibrium. It is here a general question that comes in many field of evolutionary biology and also outside biology. Are the system that we study expected to be at equilibrium (in regards at some variables at least) in nature or are they never given the time to reach any equilibrium?

Mutations and drift

Mutation and drift are stochastic processes in evolutionary biology (among others). Mutations is the ultimate production of genetic variation. Most mutations are deleterious but not all are. The exact mutation (and mutational effects) and number of mutations that will occur in a population in a given amount of time is a stochastic process. Genetic drift refers to the random sampling of individuals that are chosen to survive. Drift is inversely proportional to the population size and you may want to have a look at this post to get some intuition for why this is the case.

How much fitness is lost du to ever occurring mutations?

As mutations are always occuring we might wonder how far is a population from its optimum due to these deleterious mutations.

Let's consider a very simple model.

Let $p$ be the frequency of the wild-type (not mutant) allele, $s$ be the deleterious effect of the mutation in the homozygote mutant and $h\cdot s$ be the deleterious effect in the heterozygote. The mean relative fitness in the population is

$$\bar w =  1 - 2 p (1-p) h s - (1-p)^2s$$

Let's define the mutation load $L$ as $1-\bar w$. As a consequence

$$L = 2 p (1-p) h s - (1-p)^2s$$

At selection-drift equilibrium the expected frequency of $p$ is $p=\frac{\mu}{hs}$, where $\mu$ is the mutation rate. As a consequence the

$$L = 2\mu$$
and
$$\bar w = 1- 2\mu$$

Let's assume that fitness effect at different loci are multiplicative (no epistasis). As a consequence an individual carrying $n$ deleterious mutations has a fitness of

$$\prod_{i=1}^n 1-s_i $$.

Let's further assume that all mutations have the same deleterious effect on fitness, that is $s_1=s_2=...=s_n=s$. Let $l$ be the number of nucleotides on which deleterious mutations can occur. Coming back to $w=1-2\mu$, we can say that over all loci in the genome the fitness is

$$\bar w = \prod (1-2\mu) ≈ e^{-\sum_{i=0}^l 2 \mu} = e^{-2\mu l} = e^{-U}$$

, where $U=2\mu l$ is the genome-wide deleterious mutation rate. According to best estimates, in humans $U≈2.2$ and therefore our load is $L = 1-e^{-2.2} ≈ 0.9$.

From this simple model, we would expect that 90% of the mean fitness of a population is lost due to ever recurring deleterious mutations. This sounds pretty big and suggest that we'll always be pretty far way from an actual optimum.


What is the viability of Intelligent Design as a supplement to chemical abiogenesis and Darwinian Evolution?

I think the issue with Intelligent Design is not so much that its patently proven wrong.  On the contrary, the problem is that it not a scientific hypothesis and so it really isn't a scientific question.

If I may, the basis of the scientific method, as formulated by Karl Popper, but commonly in use today, is that science is the putting forth of theories of cause and effect which are testable (or if we are being precise, falsifiable).

That is to say, you put forth a theory such as 'God/some diety figure made all living things' and then you perform an experiment which can differentiate whether the hypothesis or its null version (i.e. 'no intelligence is the source of life / biology is the result of accidents') is more likely true.

This question will not be testable in a way to answer enough of the reasonable skeptical questions ( or at least so far it has not).  Experiments have been tried, but they are often not acceptable to everyone.  For instance the idea that some biological structures such as the eye or the flagellar motor are too complex to have evolved through a typical Darwinian process which involves a series of small changes are almost biological theology - one can always hypothesize a more inhuman God (probably appropriate) who acts and 'thinks' in such an inhuman manner that anything you see could be created/inspired.  While I think you should feel free to believe either way, I also believe that this is not an argument that can be won or lost.  The tendency for any experiment to confirm both the hypothesis and its inverse seem inescapable.

That is to say, that biology and physics will ultimately fail where philosophy and logic also did in proving the existence of God, besides the less interesting truism that if God does exist, the deity is consistently elusive to proof.

On the other side of the coin, the proof that life has emerged from naturally occurring phenomena such as lighting strikes in a prebiotic environment are interesting since it shows that nucleotides and amino acids might have been available without metabolic pathways to synthesize them.  In its way, the molecular origins of life on earth is a question which is really testable only in theory.

Anyone who thinks they are going to re-create the event of the beginning of life itself is scientifically on thin ice - the prebiotic environment may have extended to the entire surface and atmosphere of the earth as well as down into mud and bodies of water and sat incubating for maybe hundreds of millions of years.  The idea that the fundamental moment of life generation is just going to show up on a well chosen set of conditions in a 500 ml flasks with some electrodes attached is an idea that workers in the field don't even entertain.

Until such an experiment produces life, the work will have to rely upon the idea that there was a moment in time where the necessary elements came together.

This being said, cosmology, biogenesis work has approached the moment of the genesis of life asymptotically with amazing clarity.

The RNAWorld hypothesis strongly supports the idea that an early biotic system might have been very simple - maybe only RNA and its four nucleotides.  Clearly after what Dawkins calls a replicator exists, then the pathway to living things as we know them is pretty easy to envision.

I should add that I'm not one of those people who think that science is everything - the trend that is impoverishing some humanities program is alarming to me.  Its just that some things are not science.


Are scientist able to correct mutiple gene defect in our body by using CRISPR

Certainly not yet - there is not yet any evidence that this can be used to correct specific deficiencies in an adult, though the in vivo applications are growing.

In particular, an exciting recent advance is the opportunity to better understand carcinogenesis by 'editing in' certain known mutations into a mouse, say, that should cause a cancer, and watching for when the cancer actually arises...


Why do flagella form a bundle only when they rotate counterclockwise during chemotaxis?

In principle this can happen, but you have to read up on flagellar dynamics and polymorphic transitions (Real-Time Imaging of Fluorescent Flagellar Filaments, Turner et al. 2000).

From Howard Bergs lab page:

  Runs can occur with filaments of any polymorphic form; although, the normal form predominates. For a cell to tumble, not every filament needs to change its direction of rotation. Different filaments can change directions at different times, or a tumble can result from the change in direction of only one.

If the whole bundle comes apart it can reform on either end of the cell body because E. coli has a random flagellation pattern (peritrichous) and thus no preferred direction of propagation of the cell body.

Also have  look here for some nice movies from the Berg lab.


What makes us all different and similar to some extent?

For ease of explanation let me first tell you that the "genetic makeup" is called "genotype" and that "how we look physically and psychologically" is known as "phenotype". These are not complete definitions of the terms but this should help you understand what we're talking about. I also apologise for the lack of detail or inaccuracies which many fellow contributors may find aggravating, but the question calls for keeping things down to the most important aspects :)

Do genes define how we look?

Genotype defines to some extent the human phenotype, but we don't know exactly to what extent regarding most aspects of the phenotype. This is called the "nature vs. nurture" debate and is concerned with the effects of genotype itself on phenotype vs. the effects of non-genetic influences after fertilisation (such as chemical surroundings during embryonal growth, experiences at young age etc).

Numbers of genes from males and females

Another misunderstanding is that a sperm carries a certain number of genes which it combines with a number of genes from the egg. While this is strictly true, the number isn't what matters because we all carry the same number of genes (*). The genotype doesn't depend on the number of genes, but rather, almost all genes exist in several variants within the human population. So the genotype is actually about which variants an individual carries, not about the number of genes. In biology, we use the term "allele" to refer to variants in this context. So in other words, each gene can have different alleles.

People with identical appearance

If two people have identical alleles for all genes (i.e. identical genotype), then they can indeed look almost identical. However, because of the vast number of genes and alleles present in the human population, it is practically impossible for the same alleles to come together in two humans. With only one exception: if two individuals result from the same combination of sperm and egg cell, they will be identical, and this is exactly what happens in monozygotic twins.

Similarities by geographical region

However, the total number of genes and alleles is limited (**). This concept is what people call the "gene pool" and is the reason why humans are still always humans and share certain similarities. In particular, for most of human history our geographical movement has been limited (most of the time), creating geographical "sub-gene pools" (to keep it simple). This is why people from the same geographical region are more likely to look similar; they have a higher chance to share the same alleles of genes that determine appearance. In terms of behaviour - to whatever degree genotype influences behaviour, peopel from the same geographical region will be more likely to be similar in these regards than people from different geographical regions. However, you can now hopefully understand why this "degree of similarity" is next to impossible to quantify (lack of knowledge: which genes determine what, how many alleles exist of them, how many people have which allele, how much and how far do people travel,...).

(*) Ok, not quite - it is possible for an individual to have the odd gene actually completely missing, but for the sake of simplicity we all have the same number.

(**) Again, not strictly, because new alleles and possibly even entire genes can result from mutation, but this is relatively rare and on the large scale you can work on the assumption that they are limited in number.


How is the gradient in density gradient centrifugation made?

Sucrose gradient separations are an example of a rate-zonal centrifugation technique (fair technical document on centirfugation separations). The idea is you layer lighter sucrose solutions on top of one another, for example, 35% at the bottom of the tube (the most dense zone) and 15% at the top band (the least dense zone). There might be 5 or 6 layers. You then layer the sample, which may contain cell lysate, at the very top.

This method is done on a centrifuge, and the idea is that in order to penetrate down to a more dense layer, the component of the lysate must exceed the density of the preceeding sucrose layer. Quite literally the dense components are pushing down through the sucrose layers. The method is suitable for organelles and proteins. The layering must be done deliberately and carefully, however, because the sucrose layers and sample will easily mix if they're disturbed. The same concept applies to ficol density gradient separations: If there's no density of solution below the sample for it to pass through, there's no separation.

On the other hand, the CsCl method is an example of an isopycnic centrifugation suitable for the separation of nucleic acids, see the above mentioned reference. This is because the DNA migrates to where the denisty of the DNA equals the density of the gradient, referred to as the neutral buoyancy or isopycnic point.


How do amino acids become attached to tRNA?

The process to which you refer is called tRNA charging and is catalyzed in the cytosol by a class of enzymes called aminoacyl tRNA synthetases.


These could be specimens of Omphalotus Illudens based on the orange/yellow color, the time of the year, their association with decaying wood (an oak in this case) and your location (eastern North America)

You can read more about these species in this reference: Messiah College


Action potential attenuation in unmyelinated axons vs demyelinated axons

Myelinated axons have schwann cells around them, electrically insulating the neuron axons except for gaps in the sheath which are called the Nodes of Ranvier. The insulation increases the speed of transmission of action potentials.

Without myelination conduction signals along the nerve can be impaired or lost.
There are some diseases E.g. Acute disseminated encephalomyelitis where myelination is lost.


How does methamphetamine (meth) damage neurons?

Nice question! I will directly begin with the process through which methamphetamine causes damage to neurons, putting in as much details as are known, and adding appropriate citations wherever required.

Methamphetamine (METH) is known to act by increasing concentration of dopamine in brain1. When excess of dopamine is produced, it causes oxidative damage to axon terminals2. This is because direct oxidation of dopamine leading to quinone formation3, iron-catalyzed dopamine metabolism via Fenton reaction4, and metabolism of dopamine by monoamine oxidase-A5 contribute to production of superoxide and hydrogen peroxide.

Methamphetamine is known to increase concentration of glutamate. This (supposedly) happens as: high concentration of methamphetamine D1-mediated striatonigral GABAergic transmission, which in turn activates GABA-A receptors in substantia nigra pars reticulata (SNr), leading to increase in GABAergic nigro-thalamic activity which increases corticostriatal glutamate release6 (since I can't explain all those terms in a single answer). Now, excessive glutamate activates the glutamate-activated NMDA and AMPA receptors which, in turn, increases activity of nitric oxide synthase7. Activation of nitric oxide synthase generates reactive nitrogen species which create an oxidative stress8.

Oxidative stress is further increased because of depletion of antioxidant enzymes due to methamphetamine itself9. Now, the oxidative stress has to be manifested somehow. This is done by lipid peroxidation and protein carbonyl formation10, and also by specific nitration and nitrosylation of proteins important for monoamine synthesis and release, including VMAT-2 and tyrosine & tryptophan hydroxylase7,11,12. Oxidative modification of these proteins restricts their activity and contributes to their degradation, thus playing a major role in neurotoxicity. Researches substantiate the significant contribution of oxidative stress to the neurotoxicity of substituted amphetamines antioxidant treatments have also been shown to be neuroprotective against the damage produced by methamphetamine or methylenedioxymethamphetamine13,14,15.

P.S.: oxidative damage is not the only way through which methamphetamine causes neurotoxicity. Other possible ways include altered metabolism16, damage to mitochondria17, peripheral organ damage18 due to oxidative modification of hepatocellular mitochondrial proteins19, activation of microglia in striatum, cortex and hippocampus20, etc. Also, cannabinoids are known to suppress inflammatory processes and damage during methamphetamine exposure21. But since this is out-of-scope for this question, I won't go into their details.

References:

 1. Cadet JL, Brannock C, Jayanthi S, Krasnova IN (2015). "Transcriptional and epigenetic substrates of methamphetamine addiction and withdrawal: evidence from a long-access self-administration model in the rat". Mol. Neurobiol. 51 (2): 696–717. doi:10.1007/s12035-014-8776-8. PMC 4359351Freely accessible. PMID 24939695.

 2. Schmidt CJ, Ritter JK, Sonsalla PK, Hanson GR, Gibb JW. Role of dopamine in the neurotoxic effects of methamphetamine. The Journal of pharmacology and experimental therapeutics. 1985;233:539–544

 3. Graham DG. Oxidative pathways for catecholamines in the genesis of neuromelanin and cytotoxic quinones. Molecular pharmacology. 1978;14:633–643

 4. Yamamoto BK, Zhu W. The effects of methamphetamine on the production of free radicals and oxidative stress. J Pharmacol Exp Ther. 1998;287:107–114

 5. LaVoie MJ, Hastings TG. Dopamine quinone formation and protein modification associated with the striatal neurotoxicity of methamphetamine: evidence against a role for extracellular dopamine. J Neurosci. 1999;19:1484–1491

 6. Mark K. A., Soghomonian J.-J., Yamamoto B. K., High-dose methamphetamine acutely activates the striatonigral pathway to increase striatal glutamate and mediate long-term dopamine toxicity. J. Neurosci. 24, 11449–11456 (2004)

 7. Eyerman DJ, Yamamoto BK. A rapid oxidation and persistent decrease in the vesicular monoamine transporter 2 after methamphetamine. J Neurochem. 2007;103:1219–1227

 8. Imam SZ, Islam F, Itzhak Y, Slikker W, Jr, Ali SF. Prevention of dopaminergic neurotoxicity by targeting nitric oxide and peroxynitrite: implications for the prevention of methamphetamine-induced neurotoxic damage. Annals of the New York Academy of Sciences. 2000;914:157–171

 9. Jayanthi S, Ladenheim B, Cadet JL. Methamphetamine-induced changes in antioxidant enzymes and lipid peroxidation in copper/zinc-superoxide dismutase transgenic mice. Annals of the New York Academy of Sciences. 1998;844:92–102

 10. Gluck MR, Moy LY, Jayatilleke E, Hogan KA, Manzino L, Sonsalla PK. Parallel increases in lipid and protein oxidative markers in several mouse brain regions after methamphetamine treatment. J Neurochem. 2001;79:152–160

 11. Kuhn DM, Aretha CW, Geddes TJ. Peroxynitrite inactivation of tyrosine hydroxylase: mediation by sulfhydryl oxidation, not tyrosine nitration. The Journal of neuroscience : the official journal of the Society for Neuroscience. 1999;19:10289–10294

 12. Kuhn DM, Geddes TJ. Peroxynitrite inactivates tryptophan hydroxylase via sulfhydryl oxidation. Coincident nitration of enzyme tyrosyl residues has minimal impact on catalytic activity. The Journal of biological chemistry. 1999;274:29726–29732

 13. Gudelsky GA. Effect of ascorbate and cysteine on the 3,4-methylenedioxymethamphetamine-induced depletion of brain serotonin. J Neural Transm. 1996;103:1397–1404

 14. Sanchez V, Camarero J, O’Shea E, Green AR, Colado MI. Differential effect of dietary selenium on the long-term neurotoxicity induced by MDMA in mice and rats. Neuropharmacology. 2003;44:449–461

 15. Fukami G, Hashimoto K, Koike K, Okamura N, Shimizu E, Iyo M. Effect of antioxidant N-acetyl-L-cysteine on behavioral changes and neurotoxicity in rats after administration of methamphetamine. Brain research. 2004;1016:90–95

 16. Pontieri FE, Crane AM, Seiden LS, Kleven MS, Porrino LJ. Metabolic mapping of the effects of intravenous methamphetamine administration in freely moving rats. Psychopharmacology. 1990;102:175–182

 17. Burrows KB, Gudelsky G, Yamamoto BK. Rapid and transient inhibition of mitochondrial function following methamphetamine or 3,4-methylenedioxymethamphetamine administration. European journal of pharmacology. 2000;398:11–18

 18. Smith DE, Fischer CM. An analysis of 310 cases of acute high-dose methamphetamine toxicity in Haight-Ashbury. Clin Toxicol. 1970;3:117–124

 19. Moon KH, Upreti VV, Yu LR, Lee IJ, Ye X, Eddington ND, Veenstra TD, Song BJ. Mechanism of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy)-mediated mitochondrial dysfunction in rat liver. Proteomics. 2008;8:3906–3918

 20. Pubill D, Canudas AM, Pallas M, Camins A, Camarasa J, Escubedo E. Different glial response to methamphetamine- and methylenedioxymethamphetamine-induced neurotoxicity. Naunyn-Schmiedeberg’s archives of pharmacology. 2003;367:490–499

 21. Yiangou Y, Facer P, Durrenberger P, Chessell IP, Naylor A, Bountra C, Banati RR, Anand P. COX-2, CB2 and P2X7-immunoreactivities are increased in activated microglial cells/macrophages of multiple sclerosis and amyotrophic lateral sclerosis spinal cord. BMC neurology. 2006;6:12


Why does the "all-or-none" principle hold true for only single nerve cell, and not a bunch of nerve cells?

The "all-or-none" principle refers to the roughly accurate concept that neurons fire all-or-none action potentials, individual muscle fibers contract fully or not at all, etc.

If you have a population of, for example, 5 neurons, the population response is no longer all or none, even if the individual units follow the principle. You could have 0, 1, 2, 3, 4, or 5 cells firing an action potential together (the definition of "together" is somewhat vague; depending on the location/function of a neuron you could consider spikes within 1 ms to be synchronous or you could consider spikes within 100 ms to be synchronous, for example). The more units you have, whether they are neurons, muscle fibers, etc, the more "smooth" the possible outputs are.

The reasons for different numbers of cells being recruited could be differences in thresholds, but it could also be from different inputs to each of the units, different firing histories of each of the units, etc. This arrangement allows for more "analog" responses both within the nervous system and at muscles, because the strength of a signal or the strength of a contraction can be regulated by how many neurons participate, or how many muscle fibers are contracted.

One everyday example of the importance of this system is your grip intensity when holding an object. If your grip was all-or-none, you would not be able to handle a disposable coffee cup without crushing it. By using a population response rather than a single neuron connected to all the fibers in a single muscle, the nervous system can control the strength of a muscle contraction. The same principle applies within the CNS, where population activity can encode seemingly continuous representations of features like colors, frequencies, sizes, etc, despite an underlying code that is all-or-none at the single unit level.


Why aren't animals diverse in phenotype?

In your question, your assumption that animal species are less diverse phenotypically than humans is wrong. I am sure you will appreciate @terdon's answer to this post and @rg255 answer to this post.

Don't forget that we are good at detecting differences among humans (because we evolved for this purpose). We are doing much worse at telling apart animals from other species just because we have not evolved for this purpose. This is the reason why we tend to see human faces when looking at clouds but we rarely see sheep faces! Several studies (here and here) showed that sheep are able to recognize each other (and we even know the number of neurones needed to remember one face). They are probably better at telling two sheep apart than telling two human apart.

Another interesting fact is the so-called cross-race effect. We, humans, are better at recognizing faces of people from our own ethnic group than faces of people from other ethnic groups. For example, a Japanese is very good at Japanese faces recognition but not good at recognizing European faces. Same is true the other way around.

As @user568459 said in the comments: some people are not able to recognize faces. This is due to a cognitive disease called Prosopagnosia (also called face blindness). Those suffering from this disease are not better at recognizing sheep faces than human faces.

  So consider the class of cats they are one type of species so why aren't they diverse in phenotype like us?

There is no good definition I think of what is phenotypic diversity (no accurate and objective index to measure it) but at first sight I would tend to think that cats are more diverse than humans. One of the main features one would probably raise when talking about human diversity is skin color. And in terms of color, cats are much more diverse than humans. You may think of an extraordinary diversity when thinking of Norwegian that are taller than Indonesian (I may not have chosen the two extremes) by several centimeters on average but think about cats! The average cat weight 4 to 5 kg but some cats weight less than 2 kg and some other (like the coon cat) weight more than 10 kg (World Record: 21.3 kg). Imagine a human ethnic group that would on average weight 5 times more than another ethnic group! And think also about cats' hair length or tail shape! Humans vary in terms of facial feature (lips size, nose shape, etc.) so do cats. Some look like their face was smashed against a wall while others have a long muffle. Again I welcome you to have a look to this post.

  how they can know each like a bird always brings food to his offspring and it can't make mistake by giving it to other offspring of it's own species?

As I said above humans evolved to recognize their own. Many species also evolved in order to recognize their own. In some species individuals use smell rather than visual features in order to recognize each other (odor is also a kind of phenotypic variation). But still some species are poor to recognize each other. For a bird, it seems rather easy to not feed the wrong individual as all their offspring are usually together in the same nest. However you might be interested the lifestyle of the cuckoo who parasites nests of other bird species. Cuckoos' babies and particularly the inner beak resemble to the babies of the species they parasite and often the parents (often the mother only is involved in feeding the young) get fooled and feed the cuckoo.

  So can i say they aren't diverse because of in their meiosis division their chromosomes don't cross over and random assort (alignment)?

No, you can't say that! Because they are diverse and because for many of the species you may think about, cross-over does occur. Their genetic diversity as well as their phenotypic diversity is as high than in humans. There is nothing extraordinary about humans (except their brain and the related fact that we predigest our food by cooking it) compare to other lineages. And there is nothing extraordinary to have one extraordinary feature (such as a big brain) that you can't find in other lineages! Many lineages are extraordinary in some sense.


Yes, treatment of thrombus can cause embolism. Hypertension favors hemorrhagic complications.

Thrombolytics:

Yes, they can cause paradoxical embolism, although it is a rare complication [1]. The most fearful complication of thrombolytic medication is major hemorrhage. And hypertension favors bleeding [2].

Catheter-directed thrombolysis:

Hypertension (more than 180 mmHg and associated with congestive heart failure) was found to increase hemorrhagic complications [3].

Angioplasty:

Angioplasty produces some embolic particles [4]. However, using embolic protection is disputed [4, 5].

References:

Liu YF, Bayliss M. Paradoxical embolism: a rare complication of thrombolysis. Emerg Med J. 2008 Mar;25(3):180-1. doi: 10.1136/emj.2007.053934. PubMed PMID: 18299379.
Meneveau N, Vuillemenot A, Bassand JP. [Complications of thrombolytic therapy in pulmonary embolism]. Arch Mal Coeur Vaiss. 1995 Nov;88(11 Suppl):1769-76. PubMed PMID: 8815838.
Agle SC, McNally MM, Powell CS, Bogey WM, Parker FM, Stoner MC. The association of periprocedural hypertension and adverse outcomes in patients undergoing catheter-directed thrombolysis. Ann Vasc Surg. 2010 Jul;24(5):609-14. doi: 10.1016/j.avsg.2009.12.011. PubMed PMID: 20413257.
Malik RK, Landis GS, Sundick S, Cayne N, Marin M, Faries PL. Predicting embolic potential during carotid angioplasty and stenting: analysis of captured particulate debris, ultrasound characteristics, and prior carotid endarterectomy. J. Vasc. Surg. 2010 Feb;51(2):317-22. doi: 10.1016/j.jvs.2009.08.063. PubMed PMID: 20006918.
Divani AA, Berezina TL, Zhou J, Pakdaman R, Suri MF, Qureshi AI. Microscopic and macroscopic evaluation of emboli captured during angioplasty and stent procedures in extracranial vertebral and internal carotid arteries. J. Endovasc. Ther. 2008 Jun;15(3):263-9. doi: 10.1583/07-2326.1. PubMed PMID: 18540698.


Is territoriality only the domain of the male of a species?

Absolutely not.  In many spiders and insects, the female holds the territory.  Many spiders for instance have much larger females than males - in these species the female can be > 10x bigger than the male and the male may not even eat during its lifetime.

Ordinary garden orb weaving spiders are this sort of animal.  Only the females even spin webs.

Another example is the Australian red back spider.

Quite often males are the 'disposable sex'.


Is autoclaving sucrose solution necessary?

I wouldn't autoclave this solution - sucrose will partly break down into glucose and fructose. A portion of the sugars will also caramellize and color the solution yellow to brown.

If you need the solution to be sterile, I would filter sterilize it, although this can be hard because of the higher viscosity of the sugar solution. If you haven't seen any negative effects of preparing the solution fresh with autoclaved water, I don't think there is any need to change your protocol.


Do alleles, by definition, code for the same trait?

I fear you won't get a definitive answer on this. A survey indicates both usages of trait all over the Internet. As a teacher, I generally used trait to apply to the gene. This made teaching the "central dogma" clear: DNA -> RNA -> protein -> trait. Of course this simplification gets added to later as the course progresses.

One interesting question this poses is in the case of skin color. Is that a trait? Last I read, at least four different genes interact to produce skin color.

I'd side with you on this but acknowledge the fact trait doesn't seem to have the consistent, well-defined meaning that allele does.

On the other hand, a visit to UC Berkeley's evolution site shows them applying trait to the variations due to allele combinations.

Hope that helps! :)


There doesn't seem to be a 3D structure of Osteopontin available, and after looking a bit at the literature about this protein I'm not really surprised.

Osteopontin is hypothesized to assume an elongated and flexible structure (Sodek et al., 2000). Flexible proteins are very hard to impossible to crystallize, typically the flexible parts are either removed or stabilized in some way. I'm not a crystallographer, but this protein doesn't look like it can be crystallized in the full form.

For NMR it is a bit on the large side, a full structure would likely be not feasible.

It also has extensive posttranslational modifications, which makes it much harder to produce in large amounts as needed for crystallography, and extremely expensive for NMR where you would have to isotope-label the protein as well.


Where can I find a transcriptome of a normal uveal melanocyte?

I can't find any transcriptome data, but I did find miRNAome data from GEO at NCBI and Array Express at EMBL.


Short answer
Appears to be an evening bat (Nycticeius humeralis) or little brown bat (Myotis lucifugus).
 Long answer.
You can see a list of common bat species in Georgia through the Georgia Department of Natural Resources. (A high-res image of a visual poster can be seen here).
According to Greenhall and Frantz (1994)1, three of the species found in Georgia are among the species most found in and around buildings: big brown bat (Eptesicus fuscus), evening bat (Nycticeius humeralis), and little brown bat (Myotis lucifugus)
Your image is relatively good, but it does not provide enough detail of key structures to definitively say which species it is. (see Morgan et al. (2019)2 for a key).
If we go simply based on size, the evening bat seems to be closest to your specimen:

E. fuscus is typically 4.1-5.1 inches in length (source), which is larger than your specimen
Your specimen is larger than a typical M lucifugus (1.8-2.3 inches, source).
N. humeralis is more similarly sized (average is 3.4 inches, source).

It appears that your bat has a broad nose, which would hint toward big brown bat (Eptesicus fuscus) or an evening bat (Nycticeius humeralis).
According to GeorgiaBiodiversity.com:

The evening bat is commonly confused with the big brown bat due to its fur color and broad muzzle. However, the evening bat is much smaller and does not have a keeled calcar. The evening bat's rounded tragus distinguishes it from all other small bats except the eastern pipistrelle, which has tri-colored rather than bicolored dorsal fur. The evening bat also has just two upper incisors instead of the four typical of all myotis.

Wait, keeled calcar? Huh?

A calcar is the spur of cartilage coming off the lateral side of the ankle of bats. The image below roughly dmeonstrates the difference between keeled and not keeled.

 Left is keeled; Right is not keeled. Source: Fig 12, Morgan et al. (2019)2
Your specimen does not appear to have a keeled calcar, which would suggest further that this is more likely an evening bat versus a big brown bat.
However, the little brown bat also lacks a keeled calcar....
Though many sources do not directly compare the little brown and evening bat, Morgan et al.'s (2019) key splits these species at the same step, suggesting they have much in common. Morgan et al.'s  differentiating characteristics for these species include:

Hair on hind foot extends beyond tips of claws; tragus long and blunt; underwing lightly furred to elbow: Myotis lucifugus (Little Brown Bat).
No long hair on foot; tragus is short, blunt and curved; underwing, muzzle, and uropatagium are hairless: Nycticeius humeralis (Evening Bat)

According to Greenhall and Frantz (1994)1,

[the evening bat] bears some resemblance to the somewhat smaller little brown bat (M. lucifugus) but can be identified by its characteristic blunt tragus.

To reiterate, the "sharply-pointed" tragus (source) of M. lucifigus and the presence of long toe hairs extending beyond the length of the toe claws (source) would both definitively point toward the little brown bat vs the evening bat. However, neither characteristics is really distinguishable in your photograph.
As such, I don't feel fully confident to rule one out over the other.
It's 3 am though, so perhaps I should stare at your image more in the morning after some rest...I'll update further if I notice anything definitive.

 1. Greenhall, A.M. and Frantz, S.C., 1994. Bats (Myotis lucifugus). The Handbook: Prevention and Control of Wildlife Damage, p.46.
 2. Morgan, C.N., Ammerman, L.K., Demere, K.D., Doty, J.B., Nakazawa, Y.J. and Mauldin, M.R., 2019. Field identification key and guide for bats of the United States of America. Occasional papers (Texas Tech University. Museum), 360.


It refers to organic carbon, i.e. the carbon present in proteins, carbohydrates and other molecules as consequence of the metabolism of living creatures. Carbon rich soil is an indication that microorganisms, insects, and worms are living in the soil. They are the basis for the soil ecosystem and boost the flow of nutrients that ultimately will support plant growth. A soil with low content of organic carbon indicates that it's a harsh environment where living organisms struggle.

Some articles on the matter:

https://en.wikipedia.org/wiki/Soil_microbiology
http://www.nature.com/nature/journal/v501/n7468_supp/full/501S18a.html
http://mbio.asm.org/content/6/2/e02527-14.full


Why should or shouldn't we allow the human body to take its natural course?

I am assuming that your question is: "why can a human intervention improve health?". Let me know if I misunderstood your question.

Why can a human intervention improve health?

Let's first avoid going into the details of your example. It is quite obvious that human intervention can often improve health in a way that your body alone cannot. To me, an intuitive way to classify the reasons why human intervention are important to improve health into two categories.

The body does not always react in an adaptive manner.

Example: Anaphylaxis is a serious and sudden allergic reaction that may cause death. An allergic reaction is what is happening when your immune system recognize a chemical as a infectious element while it is not. The reaction of the body is not adaptive and taking medication such as an anti-histaminic can force the body to stop this "stupid" reaction.
Note: There are reasons why the body cannot be always perfect but it is a bit long to make an overview here. There is stochasticity in the developmental processes, there is genetic variation for example due to always occurring deleterious mutations, there is also an arms race between parasites and host. This arm race leads parasites to take advantage of normal host physiological pathways. There are tons of other reasons that relate to the stochasticity and to the physic and physiological constraints of evolutionary processes.

The body sometimes cannot (physical constraint) produce the action that is required to be performed to improve health.

Example:  If you have an important wound, then a human-made compression can by far improve your chance of the survival. The body is not able by itself to simulate this external compression to prevent blood to exit the body through the wound.

You might easily find semantic issues with these categories though such as the question of cancer and its removal for example and some may argue against this categorization.

Dehydration and thirst

Your example would fall into the first category. It is not so uncommon that the body needs water while not causing thirst. Because after 50 years old, the sensation of thirst start to diminished, dehydration without the sensation of thirst is common among old people. Dehydration along with hyperthermia is a relatively important cause of death during hot weather in summer. It is especially true in old people as the sensation of thirst diminishes with age. Dehydration following diarrhea is also a common and important issue in old people sometimes leading to death.


It is hypothesized that exposure to and recovery from SARS-CoV-2 (as with other coronaviruses in humans) would generally result in short-term immunity to this strain, but we do not yet have data on this:

However, according to Dr Stephen Gluckman, an infectious diseases physician at Penn Medicine and the medical director of Penn Global Medicine, who spoke to the outlet, it seems likely that having the disease once results in immunity in most individuals - as is seen with other coronaviruses.
“Coronaviruses aren’t new, they’ve been around for a long, long time and many species - not just humans - get them,” he explained. “So we know a fair amount about coronaviruses in general. For the most part, the feeling is once you’ve had a specific coronavirus, you are immune. We don’t have enough data to say that with this coronavirus, but it is likely.”
This means that people who initially recovered are more likely to relapse rather than get reinfected with the virus.
According to one study, people with mild infections can test positive for the virus by throat swabs “for days and even weeks after their illness”.
But, that doesn’t mean it isn’t possible to contract the disease again, especially in those who are immunocompromised.
“The immune response to Covid-19 is not yet understood,” the Centers for Disease Control and Prevention (CDC) explains. “Patients with MERS-CoV infection are unlikely to be reinfected shortly after they recover, but it is not yet known whether similar immune protection will be observed for patients with Covid-19.”

Coronavirus: Can You Get Covid-19 Twice Or Does It Cause Immunity?

It is also hypothesized (in humans) that previous exposure to coronaviruses may enable immunity to certain other highly related strains:

These data indicate that challenge immunity to coronaviruses is strong, but highly virus strain-specific.

Virus strain specificity of challenge immunity to coronavirus., Archives of Virology (1989)

But these are all examples of adaptive immunity - not innate.


What made this small light weight bee hive-like structure?

This is a mantis (Mantodea) egg sack, or ootheca. The female mantis makes it in the fall and it will remain over winter until (juvenile) nymph mantises emerge from it in the spring.

The following site introduces how to raise mantises from eggs but also has some general background information including on how seasonal temperature changes can affect the ootheca:

https://www.keepinginsects.com/praying-mantis/caring-for-mantis-eggs/


That is a kind of honeysuckle. The picture below is for Japanese honeysuckle (Lonicera japonica), but your specimen is different in the way the flowers are arranged and that the distal-most paired leaves are clasping the stem.

It might be Lionicera periclymenum, or Lonicera etrusca (there are about 150 species of honeysuckle); L. etrusca is pictured below (the color is irrelevant) which is native to Europe.


There's an open access article "From vitamin D to hormone D", which explains the difference(s). Vitamin D is a family of substances, but for humans the most important one from this family is vitamin D3 aka cholecalciferol. "Hormone D" (1α,25(OH)2D3, the substance that normally regulates calcium etc.) aka calcitriol is closest to vitamin D3. So if one wants to be technical about it, the vitamin(s) and the hormone are slightly different substances. Vitamin D itself is more aptly called a prohormone (i.e. a hormone precursor):

Vitamin D[3] is not technically a vitamin, ie, it is not an essential dietary factor; rather, it is a prohormone produced photochemically in the skin from 7-dehydrocholesterol. The molecular structure of vitamin D is closely allied to that of classic steroid hormones (eg, estradiol, cortisol, and aldosterone) in that they have the same root cyclopentanoperhydrophenanthrene ring structure. Technically, vitamin D is a secosteroid because one of the rings of its cyclopentanoperhydrophenanthrene structure has a broken carbon-carbon bond.

The above view is also endorsed by Horst et al., but they have a much more detailed discussion, including the fact that in vitamin D poisoning, calcifediol (25(OH)D3)--an intermediate compound in the pathway between the vitamin and the hormone--can itself act as a hormone, i.e. it has some binding affinity to the calcitriol receptor, but only at at very high doses.
As for how the vitamin label came about, "historical accident" is one way to put it...

Considering the fact that now we accept that the biologically active form of vitamin D [what the other paper calls "hormone D"], namely 1a,25(OH)2-vitamin D3, is a steroid hormone, it is somewhat ironic that vitamin D, through a historical accident, became classified as a vitamin. It was in 1919/20 that Sir Edward Mellanby, working with dogs raised exclusively indoors (in the absence of sunlight or ultraviolet light), devised a diet that allowed him to unequivocally establish that the bone disease, rickets was caused by a deficiency of a trace component present in the diet. In 1921 he wrote, "The action of fats in rickets is due to a vitamin or accessory food factor which they contain, probably identical with the fat-soluble vitamin." Furthermore, he established that cod liver oil was an excellent antirachitic agent.
Shortly thereafter E.V. McCollum and associates observed that by bubbling oxygen through a preparation of the "fat-soluble vitamin" they were able to distinguish between vitamin A (which was inactivated) and vitamin D (which retained activity). In 1923 Goldblatt and Soames clearly identified that when a precursor of vitamin D in the skin (7-dehydrocholesterol) was irradiated with sunlight or ultraviolet light, a substance equivalent to the fat-soluble vitamin was produced. Hess and Weinstock confirmed the dictum that "light equals vitamin D". They excised a small portion of skin, irradiated it with ultraviolet light, and then fed it to groups of rachitic rats. The skin that had been irradiated provided an absolute protection against rickets, whereas the unirradiated skin provided no protection whatsoever; clearly, these animals were able to produce by uv irradiation adequate quantities of "the fat-soluble vitamin", suggesting that it was not an essential dietary trace constituent. In parallel studies, Steenbock and Black at the Biochemistry Department of the University of Wisconsin found that rat food which was irradiated with ultra violet light also acquired the property of being antirachitic. However, because of the rapid rise of the science of nutrition -- and the discovery of the families of water-soluble and fat-soluble vitamins -- it rapidly became firmly established that the antirachitic factor was to be classified as a vitamin.

As an amusing parallel to this, calcifediol was identified in 1968 as an active metabolite of the vitamin, but it wasn't until 1971 that calcitriol was properly identified as the metabolite that exercises the hormonal action under normal circumstances. (cf. DeLuca)


What are microRNA, siRNA and antisense RNA?

MicroRNA (miRNA) are gene-regulatory RNAs that are loaded onto the RNA-induced silencing complex (RISC) and interact with partially-complementary targets on mRNA to suppress protein expression.  The miRNA is originally double-stranded and composed of strands about 21 nucleotides long; on loading onto RISC, one strand is degraded and the other, the "guide" strand, is held on the surface of RISC where it can interact with mRNA. The targets recognized by the guide strand are most commonly on the 3'-untranslated region (UTR) of an RNA.  Binding can suppress assembly of an initiation complex on the 5' cap of an mRNA because the mRNA is bound into a circular shape at the initiation of translation, bringing the 3'-UTR and 5'-UTR close together.

If the RISC loads an RNA than then finds a perfectly complementary target, RISC cleaves the target RNA using the activity of one of the protein components of RISC called Argonaute.  This property is exploited experimentally by manufacturing small interfering RNAs (siRNA) intentionally targeted to particular target sequences.  Once loaded into RISC these siRNA might recognize and cleave their perfectly complementary target sequence within an mRNA (though there is a significant failure rate, so several sequences are often tried).  The siRNA will also have miRNA-like effects on some partially-complementary targets on various mRNAs, leading to the observation that a single siRNA sequence can modulate expression of hundreds of off-target genes.

Antisense is a nucleic acid strand (or nucleic acid analog) that is complementary to an mRNA sequence.  Antisense occurs naturally and can trigger RNA degradation by the action of the enzyme RNase H.  Originally natural antisense RNA was tried as a method for silencing a gene, but the poor stability of RNA in cells led to development of nucleic acid analogs that are more nuclease resistant and still activate RNase H (such as phosphorothioate RNA) and other nucleic acid analogs that bind to RNA and sterically inhibit processes without activating RNase H (such as 2'-O-methyl phosphorothioate RNA, Morpholino oligos, locked nucleic acids, or peptide nucleic acids).  These latter RNase-H independent oligos do not trigger degradation of mRNA but they can be used like molecular masking tape to block translation, alter splicing of pre-mRNA, inhibit activity of miRNA, block ribozyme activity, and interfere with various other processes that require some other factor to bind to a particular sequence on an RNA molecule.


Career advice for a bachelor of biology with russian STEM diploma

You have so many questions, and it seems like you have no idea what to do next. So you better ask Russian guys who are really into this as

Good FAQ with a lot of cases from real life:
https://vk.com/career_in_biology
More like Career in Biology 101:
https://vk.com/science_career (also they have a chat in Telegram)
Career adviсe and pretty decent list of positions: https://blastim.ru/
Winter biotech school (in my opinion you have good chances to get there as they do it for people just like you): https://vk.com/futurebiotech
Completeish list of biological summer schools where you can get hands-on experience: https://vk.com/coolresearch


What problem does the Dobzhansky-Muller Model resolve?

If reproductive isolation was to be caused by a single mutation, then the first individual to carry this mutation would likely have a very low fitness. At the extreme, in a purely sexually reproducing species without hermaprohiditism, this individual carrying the first mutation causing reproductive isolation would have no-one to reproduce with and would have a fitness of zero.

Hence, reproductive isolation is unlikely to arise from a single mutation as these mutations are unlikely to raise into appreciable frequency. Hence, Dobzhansky and Muller (and Bateson) created this minimalist model involving only two loci with negative epistatic interactions.


RNA-seq Data on domestic animal with different environment

There is something called GEO, which is maintained by the NIH and is a massive collection of data obtained from RNA seq, microarray, etc. experiments. One thing you can do is search for a paper that has done what you are looking for. The paper may have a GEO accession number, and you can use that number at the GEO website to find the data you want. You may also search GEO directly but Im not too familiar with it. It may just be easier to find a paper with a GEO accession number.


How can a three-base codon evolve from a two-base codon?

It is not suggesting a 2-base->3-base code in the way you are thinking, but of a non-coding, two-coding triplet pattern occurring first.

This means you would have 16 different coding sequences with 4 possible spacing bases in between.

Later, the spacing bases could become used as part of the code.

Does that make more sense?
Instead of AA,CG becoming AAT,CGT; AAX,CGX becomes AAT,CGT etc.

Its also likely that between 2 and 3 base codes a 2 base pyrimidine/purine system was used. Today the third base can often be switched for its pyrimidine/purine pair without changing the resulting amino acid.


Is newly produced sperm healthy if there was previous DNA damage?

Male gametes (aka sperm) is produced by meiosis of numerous germ cells (gametes precursors). It is unlikely that all germ cells have damaged DNA so the newly produced gametes should be healthy. This also implies that if the DNA inside the gametes was damaged after they were produced, then again, the new gametes will be healthy.

As a disclaimer, I am talking exclusively about damages to the DNA, it could very well be that gametes are unviable for other reasons than just spurious DNA (e.g. low mobility). In this case, viable gametes are unlikely to be produced unless the reason underlying the original production of unviable gametes is fixed (e.g. via medication).


How can dehydrogenation steps in some biochemical pathways produce ATP?

You have to consider the full redox reaction to determine if the reaction is favourable or not. It's not correct to think of enoyl-CoA alone as "higher energy" than acyl-CoA, because of the free energy difference $\Delta G$ of the half-reaction:

acyl-CoA  $\leftrightarrow$  enoyl-CoA + 2 $e^-$

cannot be determined without knowing what the electron acceptor is. You might be thinking of the enoyl group as "higher energy" because it is reactive towards H$_2$ (as in hydrogenation reactions), but that's not the relevant redox couple here.

In this case, we should consider the energetics of the entire process of electron transport, as shown in your diagram. Since the intermediates (FAD, ETF, quinones) all cancel out, the overall reaction without ATP synthesis is:

acyl-CoA + 1/2 O$_2$  $\leftrightarrow$  enoyl-CoA + H$_2$O

This reaction is highly favourable, with a $\Delta G$ of about -150 kJ/mol, because O$_2$ is a very good electron acceptor. (See this site for free energy calculations.) This is more than enough to drive ATP synthesis (about 45 kJ/mol).


Is it possible to sort droplets inside an oil phase with a FACS

It's possible that there's some specialized modified machine that can do it, but conventional flow cytometry machines can't do it. This article suggests one possible approach:

  Unfortunately, FACS instruments are incompatible with nonaqueous suspensions, so to sort a water-in-oil emulsion, it is necessary to carry out a further emulsification to produce a water-in-oil-in-water double emulsion. The resulting sample, now dispersed in an aqueous phase, is amenable to FACS sorting.

--One in a Million: Flow Cytometric Sorting of Single Cell-Lysate Assays in Monodisperse Picolitre Double Emulsion Droplets for Directed Evolution

There are also microfluidics machines that might be able to do it, but I think you'd have to build your own rather than being able to buy a solution (which would be expensive in any case, I think).


How is pain induced by blunt and sharp objects?

It is a simple matter of biology and physics actually:

Firstly, pain is caused by the simulation of cutaneous nociceptors in the body, beneath the skin and are activated when the sensation crosses a threshold.

  Nociception (also nocioception or nociperception) is the encoding and processing of harmful stimuli in the nervous system,[1] and, therefore, the ability of a body to sense potential harm. It is the afferent activity in the peripheral and central nervous systems produced by stimulation of specialized free nerve endings called nociceptors or "pain receptors" that only respond to tissue damage caused by intense chemical (e.g., chilli powder in the eyes), mechanical (e.g., pinching, crushing) or thermal (heat and cold) stimulation.[2][3] Once stimulated, a nociceptor sends a signal along a chain of nerve fibers via the spinal cord to the brain. Nociception triggers a variety of autonomic responses and may also result in a subjective experience of pain in sentient beings.[3] Nociceptive neurons generate trains of action potentials in response to intense stimuli, and the frequency of firing determines the intensity of the pain.[4]

From the wiki: https://en.wikipedia.org/wiki/Nociception

Now when you consider a knife, the surface area of the knife is small enough that it can cause damage. It's akin to holding a plastic sheet stretched tight and then piercing the sheet with the point of a knife. That is because the force is being transferred on a small point and hence easily extends the pain threshold.

However, when you consider a hammer, when the hammer touches you (lightly) you don't feel the pain because the force is spread over the larger surface area of the hammer and hence doesn't meet the threshold. However, if you hammer your finger in with force, the force being transferred is enough to shatter your bones, and in that case not only the cutaneous pain receptors activate, but the somatic receptors also activate, causing the feeling of pain.

TLDR: Knife has short surface area, and hence force transfer is over a small area, subsequently causing hurt. A hammer has a larger surface area, and hence unless more force is applied, the pain receptor threshold is not met and hence no pain.


Statistical method for characterizing the relationship between body mass and metabolic rate

Short answer: The results of the two approaches (linear versus non-linear model) do not match because the relationship between body mass and basal metabolic rate does not strictly follow a power law.

It is indeed the case that if the relationship between two variables follows a power law the two approaches should provide comparable results, but important differences could arise due to Jensen's inequality. In order to test whether the reported differences between the two approaches are due to Jensen's inequality or to some biological factor I obtained data from Kolokotrones et al. (2010) who have in turn taken them from McNab (2008). Kolokotrones et al. (2010) investigated the issue of whether a power law is appropriate by performing linear regression on log-transformed data but they did not attempt to fit the data with non-linear regression.

I've fitted a non-linear model of the form:
$$ B = \alpha M^b$$ , where $M$ the body mass (in grams) and $B$ the basal metabolic rate (in Watts),
which gave coefficients $\alpha = 0.005$ and $b = 0.87$.
I also fitted a linear model of the form:
$$ log_{10}(B) = blog_{10}(M) + log_{10}(\alpha) $$
which gave coefficients $ \alpha = -1.7 $ and $ b = 0.72 $.

It appears that the results of the two approaches are indeed different. Below I plot the results of the two fits. On the variables' original scale we see that the linear model fails to predict observations from species with large mass and that the non-linear model does much better in this respect (upper left). However, when we look at the two models after log-transform, it is clear that the non-linear model fails to predict many observations from species with low mass (upper right). Looking at the residuals of the non-linear model we see that the errors are multiplicative as the variance of the residuals is increasing with (log-transformed) fitted values (bottom left). This indicates that fitting with a linear model on log-transformed data is warranted. However, the plot of linear model's residuals over log-transformed fitted values (bottom right) confirms that the linearity assumption is violated. Thus, neither method is appropriate for this dataset and the quadratic term the authors of the cited paper added in the linear model fitted on the log-transformed variables appears to be warranted in order to account for the observed convexity.

We can conclude that for this dataset the results of the linear model approach do not match those of the non-linear model approach because the data do not strictly follow a power law. Rather, the megafauna appears to follow a different trend compared to smaller animals. Kolokotrones et al. (2010) found that adjusting for temperature improved the linear fit, in addition to the inclusion of the quadratic term. The resulting model was:

$$ log_{10}B = \beta_0 + \beta_1log_{10}M + \beta_2(log_{10}M)^2 + \frac{\beta_T}{T} + \epsilon $$

The R code used to generate the results for this answer along with the data used can be found in the following git repository in GitLab:
https://gitlab.com/vkehayas-public/metabolic_scaling

 References
Kolokotrones, T., Van Savage, Deeds, E. J., & Fontana, W. (2010).
Curvature in metabolic scaling. Nature, 464:7289, 753–756. https://doi.org/10.1038/nature08920
McNab, B.K. (2008). An analysis of the factors that influence the level and scaling of mammalian BMR. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 151:1, 5-28. https://doi.org/10.1016/j.cbpa.2008.05.008.


How does smoking, an environmental factor, cause cancer, fundamentally a genetic disease?

Because cigarette smoke contains many carcinogens.  Carcinogens can cause cancer by directly affecting the genome.  Wikipedia has a list of those present in cigarette smoke, which includes classics such as lead, benzene, and formaldehyde, not to mention radioactive polonium.


Yes, they are saturable, because they have a finite number of 'binding sites', depending on the particular example you are looking at. Then, once they join the substrate to be transported, they need to release it at the other side of the membrane, which takes time (in very short time scales, but time nevertheless). Therefore, the saturation rate and speed of transport depends on the number of transporters on the cell's surface, the gradient differential, and the number of binding sites.

Facilitated diffusion, which needs a transporter as you point out, is a form of passive diffusion, which implies that there is no energy cost to the cell to transport the solute (as opposed to active transport). This is the key difference: energy. It does not mean that it goes as fast as osmosis or any other type of passive diffusion/transport, because, the transport that goes across the membrane (small gas molecules, and other small molecules) will clearly be faster. Also, passive diffusion does not mean that there is no upper limit to diffusion, in fact, diffusion is always limited by the concentration difference of the diffusive molecule across the membrane, no matter if this is passive or active transport.

In short, it is simple/passive diffusion because it does not need energy. Whether is saturable or not is not what matters for this classification. In fact, all diffusion has a limit.


Do Asian koel males communicate through calls?

Still working on this question and the following are the findings:

The male bird when mimicked possibility mistakes the mimic as an intruder in its territory and so it gives louder & accelerated calls.

  The male while defending its territory gradually approaches its adversary, hopping from twig to twig calling loudly and displaying its threatening posture. ( B S Lamba (1969) )


The white things look like scale insects, you can scrape them (and their waxy fluffy coats) off the leaves.
If you can identify the plant, that would also help.
The gardening SE is also a good place for these questions.


It's a pied version of the Rock Pigeon (Columbia livia), aka Rock Dove. According to the Cornell Lab of Ornithology, the pied variety of Rock Pigeon is one of any color that has splotches of white on the body. I think that fits your bird very well. It's not a different species, but just one of several color varieties of Rock Pigeon.

If you are not familiar with Cornell's site and enjoy birds, their All About Birds site is very nice.


Texts usually have a verbal explanation of these kind of diagrams, so look in the text where it references Figure 17.5 and read the section before and section after.

That being said, if you start at the top with pyruvate, it enters the cycle where the curved circles touch on pyruvate dehydrogenase, which catalyzes its decarboxylation. That product then enters into the next cycle where the disulphide bond is broken and it is added to one of the sulfurs. Co-enzyme A then reacts with that and you get Acetyl CoA as a byproduct and dihydrolipoamide. The cycle continues and you get one hydride (I think) and one proton transfer to FAD and the reformation of the disulfide bond. You then have a hydride transfer to NAD+ and a deprotonation to regenerate FAD.

So each place a curved arrow touches another is what goes into the reaction and then following the split of the arrows is the product that comes out of the reaction. Where there are transfers to different circles means that there are different enzymes catalyzing the reactions.


Does loud music affect hearing and balance?

First off, there are many flavors of decibels, as it is a relative measure. For the sake of clarity I assume you are talking dB sound pressure level, or dB SPL, which is a unit of sound pressure relative to a standard sound pressure of 20 µPa and widely used.

The damaging effects depend on the sound pressure received by the ear. Whether this is a compound signal or a single source doesn't matter. Like whether you crash your car against a wall at 80 mph, or head's on against a truck both travelling at 40 mph - it doesn't really matter. It's the mechanical energy transferred to the hair cells that counts.
A one-shot noise... I don't really understand what you're aiming at, but as said above, it's the raw sound pressure that counts. Further, prolonged exposure is definitely more damaging than a short exposure. However, when the sound pressure is strong enough, e.g. a bomb blast which lasts just a fraction of a second, hearing can still be permanently lost provided the sound level is high enough.
According to the Ear Center of Greensboro, a rule of thumb is that the maximal safe exposure to sound of 100 dB is half an hour, and for every added 5 dB that time is cut in half. Thus, for 120 db that would add up to 7.5 minutes before permanent damage occurs. The safe loudness limit per day has primarily been established in terms of maximum sound levels for occupational exposures (i.e., sound exposure for 5 days per week, 8 hours per day). Likely it is dependent on where you live, but here in Australia, the Government has set the safe occupational limit to 85 dBA. The dB(A) is a weighted unit of loudness that is corrected for the hearing sensitivity of the human ear.
The labyrinth of the inner ear is a system of interconnected chambers and canals. The fluids in the cochlea (responsible for hearing) and vestibular system (responsible for balance) are indeed interconnected (fig. 1).

Fig. 1. The ear (upper panel) and structures of the inner ear (lower panel). Source: Washington University.

However, sounds enter the inner ear via the tympanic membrane that connects with low impedance to the cochlea, but there is no direct connection to the vestibular system. Hence, only very loud sounds may affect balance, but that are likely accompanied by mechanical blasts that will physically damage the delicate inner ear structures. Loud music of 120 dB will not damage the vestibulum.


It depends how you define an acid. For what it‘s worth, the chemical definition Google presents when I search is “a molecule or other species which can donate a proton or accept an electron pair in reactions”. On that basis the serine residue in the catalytic triad is acting as a weakly ionizing acid.

Of course in aqueous solution a free serine hydroxyl group is not acidic, but one of the important features of enzyme catalysis is that amino acid residues are operating in a different environment that can enhance their activity. One factor is the proximity of other residues. Another is the effective dielectric constant can be different in the hydrophobic interior of a protein which can exclude water molecules.


What equipment would one use to modify a virus?

I'm no expert at this and I would welcome any changes to this post. First you need to decide, what your target organism which you want to infect is (e.g. mammalian cells, bacterial cells) and based on that you choose your viral vector as listed in this article. Generally for mammalian cell stable transfection (usually you want the genetic materials you introduced to persist between cell divisions hence stable transfection) and transformation (just a general statement about changing cells as you have introduced, usually foreign genetic material but transformation is not necessarily the same as making something immortalised, which means the cells won't stop dividing i.e. becoming cell lines or in lay term cancerous) scientists tend to use lentiviruses, which are retroviruses, similar to HIV and they can even infect non dividing cells (so this should allow your imagination to run wild!). Once you have decided what the best viral vehicle for targeting your cells of interest is then you essentially transfect the plasmid DNA (packaging vector), which produces the virus protein package, into cells, whose job becomes to produce the virus as those cells have the required cellular machinery for this purpose. These cells are often 293T packaging cells. Along with the plasmid (circular) DNA, which produces the virus package, you co-transfect the packaging (e.g. 293T) cells with another plasmid, called lenti-vector, which does whatever you want it do, such as express a particular protein or microRNA or whatever but the idea is that stuff produces by the lenti-vector should not be toxic to the target cell (i.e. the cells you intend to target), unless thats what you want it to do.

Now as you can see, you can play around with two things here, first the packaging vector, to change the behaviour of the virus if you wish. And second the lenti-virus vector, to produce whatever you want it to! Once the packaging cells made your viruses, containing your lenti-vector, the virus get secreted into the media, which the packaging cells are in so you have to extract the media, congaing the virus, and concentrate the virus using centrifugation. Once you got the virus then you can use it to transform the (target) cells you wish.

For the lab based procedure of how you make the virus and what equipments you use and how to concentrate the virus then please see this link, although its a little technical. In this case, the packaging vector is fuGENE 6 and the lenti-vector or just plasmids of interests are listed (please not that I do not endorse any products mentioned here and I'm just using it as an example).

Now for making the packaging plasmid (making the virus), you often use the genetic materials from a virus and change it through a procedure called polymerase chain reaction (PCR). Same goes for the lenti-vector/plasmid as they are derived from somewhere and then change through time using PCR and restriction digests, which is an equivalent of genetic material cut and paste, to make the vectors and products of interest. Once all is done the the virus can infect the target cells and effect it based on its designed function (defined by the two vectors I described).

If the above response does not answer you question, since it is currently very broad, please make further clarification to the question so that I can modify my response accordingly.


Does one memory cell take part in different memories?

According to engram theory: Yes.

However, you need more than one cell to encode a memory engram.
The idea is that the combination of cells encodes the memory, not the cells themselves.

I am most familiar with the hippocampus, in which cells participating in the encoding of "concepts" like Jennifer Aniston, Bill Clinton or the Sydney Opera House have been found in humans Quiroga et al. (2008)


If a DNA letter is one of A,T,C and G, and there are 3 billion base
  pairs, why don't we say that there are 6 billion letters in the genome?

It is a convention, and stating the actual number of bases would not add any information, but would actually lead to more confusion. It's like saying

  I have six pairs of socks

vs.

  I have twelve socks.

It means bascially the same, but now one could assume that these twelve socks are not from actual pairs (e.g. twelve left socks). The same goes for DNA. Saying we have pairs of bases emphasizes the redundancy of the DNA double strand.


Optimization of E. coli growth in D₂O (heavy water)

It looks like you're very stringently avoiding $^1\mathrm{H}$. You may want to consider replica plating your transformations onto $\mathrm{D}_2\mathrm{O}$ plates (selecting for $\mathrm{D}_2\mathrm{O}$ tolerance earlier.)

I assume you're doing protein NMR and want "triple labeling." Depending on how specific your carbon labelling is, you may want to grow your starter cultures on triple labeled agal hydrolyzate (something like "Bioexpress.") You can buy some unlabeled stuff for fairly cheap (\$55 USD at CIL for 10 mL of 10X stock) and if your starters grow well you can spring for the same quantity of $^2\mathrm{H}$,$^{13}\mathrm{C}$,$^{15}\mathrm{N}$ for around \$405.


Does a gene that regulates itself necessarily be a transcription factor?

First of all you need to clarify what exactly is the output that needs to be regulated. We often say regulation of expression of a gene but what expression ultimately leads to is the activity of the gene (whatever it might be: enzyme based catalysis, cytoskeletal rearrangement, response to an extracellular signal). Activity of course depends on the expression level of the gene but it also depends on other factors such as covalent modifications, interactions with other genes (like dimerization) etc. Moreover, for genes which code for proteins, expression also has two stages.

Coming back to your question:

  If a gene is NOT a TF gene, can it regulate itself?

Yes it can. There are many modes of gene activity regulation as I already mentioned. Examples where a non-TF gene can regulate itself:

Feedbacks in cell signalling which happen via activity modulation by protein phosphorylation [1].
Regulation via post-transcriptional regulation via RNA binding proteins (RBP) or regulatory RNAs such as miRNA. MAPK signalling pathway has a feedback via the RBP, Rnc1, which upon phosphorylation binds to and stabilizes the Pmp1 mRNA. Pmp1 is a phosphatase which dephosphorylates Rnc1[2]. This loop contains regulation by both post-translational modification and post-transcriptional mRNA stabilization. There are many other examples involving RBPs. An miRNA, let-7 is post-transcriptionally regulated by Lin28 (promotes degradation) which in-turn is post-transcriptionally repressed by let-7 [3].

There are many examples of metabolic feedbacks too which operate via allosteric regulation of the enzyme activity.

If you are only interested in regulation of gene expression then you can ignore phosphorylations and allosteric regulation but there are several examples of post-transcriptional regulatory interactions which also contain feedbacks.

References

Dougherty, Michele K., et al. "Regulation of Raf-1 by direct feedback phosphorylation." Molecular Cell 17.2 (2005): 215-224.
Sugiura, Reiko, et al. "Feedback regulation of MAPK signalling by an RNA-binding protein." Nature 424.6951 (2003): 961-965.
Rybak, Agnieszka, et al. "A feedback loop comprising lin-28 and let-7 controls pre-let-7 maturation during neural stem-cell commitment." Nature Cell Biology 10.8 (2008): 987-993.


The number of drones in a colony may be hundred-thousand , i.e 15 % of the total population. The drones lack wax glands, pollen collecting-appartus and sting which is present in worker bees which make them completely dependent on the workers, transferring its genes to the next generation is the only contribution of the drone bees. Usually the drones do not mate with the queen of the same hive. The drones that are able to mate with the queen die shortly after mating due to breaking of bulb of endophallus(penis) inside the queen.

The rest, the survivors of the mating flight (mostly drones that could not participate in  mating) are not allowed to reenter the colony. They remain in the vicinity of the hive and eventually starve to death.

In hours of crisis when the colony needs to drop the expenditure of resources(food) the workers eat up larval drones or drive out the matured drones from the colony that eventually die due to the same reason.

Information taken from:

Wikipedia
Bees
The Backyard Beekeeper


Based on the location and image you provided, I suspect this spider to be Garden Orb-Weaver, belonging to the spider family Araneidae.

Just a side note: I used an app called iNaturalist to identify this spider. It is a helpful app to identify insects and plants.

Here is a similar image I found online:


How do bats distinguish between day and night?

Bats distinguish day and night the same way that other animals do, with an internal circadian clock and by environmental cues (dawn and dusk).

Most bats (over 1000 different species total) are nocturnal, meaning that they are out of their roost and foraging at night. This includes that vast majority of bats, which also echolocate. Some bats, notably pteropodid "Flying foxes" are diurnal, meaning they are active during the day and sleep at night, like humans. These bats are typically fruit-eating. There are, of course, exceptions, but these general patterns hold.

Bat Conservation International has good educational information about bats.


Is there a reference for the composition of viral genomes?

NCBI houses a collection of viral genomes at the aptly named Viral Genomes portal. They currently have 5921 viral genomes and by going to the previous link you can browse sequences from the major viral families.
If you have a nucleic acid or amino acid sequence it can be searched against NCBI's sequences here.
Uniprot also have a viral protein sequence annotation project which they describe as such;

The concept of this website is to associate specific knowledge for each virus family with viral protein and genomic sequences. All the available information is presented in a concise and accessible virus fact sheet, associated with the ordered list of reviewed entries. The site covers the whole known virosphere. The database section allows access to UniProtKB protein entries, as well as to specific virology databases.
Our efforts are currently directed towards viral ontology and reference strain annotation. A robust ontology will allow a more precise definition of the involvement of each protein in viral replication steps. The reference strain annotation will become the benchmark for each of the 334 genera.

Their work can be accessed through uniprot.org or through the project portal at; http://viralzone.expasy.org/


Can the negative afterimage appear only if there is light or is it possible in darkness?

Glutamate release from photoreceptors is inhibited by incident photons (ref). During photobleaching, assume that the effect of an incident photon drops to zero. The implication then is that if all light is removed subsequent to selective photobleaching, there will be no difference in activation between bleached photoreceptors and unbleached photoreceptors. This observation suggests that no afterimage will be visible in darkness.

But there might be rebound effects or other effects of light adaptation that will result in a perceivable afterimage in darkness. Certainly there are hallucinatory visual patterns than can be generated cortically, suggesting that a cortical afterimage could be generated in darkness.


Why does high EDTA concentration cause swelling of platelets?

As it's reported in an old 1968-article by J. G. White:

  Chelation of membrane calcium by EDTA appears to cause marked
  irregularities in the platelet wall and massive swelling of the
  canalicular system. Swelling of internal channals is the dominant
  alteration in EDTA platelets, and this change appears ultimately to be
  related to the breakdown of platelet granules.

Many articles followed the one reported above, but it seems that the main cause of platelets swelling in presence of EDTA is the reduction of calcium levels that causes a sort of platelet activation.

This acivation could also be linked to direct EDTA action as reported in this article by Golański et al.:

  The influence of EDTA on platelet membrane dynamics closely mimicked
  the alterations induced upon the interaction of fibrinogen with
  platelet GPIIb-IIIa. Thus, the EDTAK2-induced platelet activation
  might result from an interference with platelet membrane protein
  structure and conformation and possibly relate to an “unspecific”
  trigerring of a signal transduction pathway.

Anyway in normal conditions the laboratory platelet volume quantification using EDTA tubes seems not to be affected if executed in 1 hour since the collection (as reported in this article by Dastjerdi et al.).


which signalling pathway is involved in cancer?

The answer is b, as the mutation constantly activates the RAS protein. RAS is part of the MAP-Kinase pathway, constant signaling of it permanently activates this pathway and leads to changes in gene expression. See the image below:

If you are interested in more details, have a look at these papers:

RAS oncogenes: weaving a tumorigenic web
RAS mutations and oncogenesis: not all RAS mutations are created
equally


Fructose is absorbed by facilitated diffusion in the small intestine by the help of transport molecules GLUT5 or GLUT2.

Sources:

https://en.wikipedia.org/wiki/Fructose
http://diabetes.diabetesjournals.org/content/54/10/3056.long

The source you've mentioned (http://ncert.nic.in/ncerts/l/kebo116.pdf), says that certain monosaccharides, such as glucose, can be absorbed by simple diffusion, but it says nothing specifically about fructose.

In fructose malabsorption, in which the transporter GLUT5 is deficient, fructose absorption can be very decreased, which suggests there is probably no additional absorption of fructose by simple diffusion (PubMed).


The '75' of Sephadex G-75 refers to the water regain value, which is defined as the grams of water absorbed upon hydration of 1g dry powder, multiplied by 10 (see Reiland). Thus the water-regain value of Sephadex G-75 is about 7.5ml. This value refers only to the water contained
within the gel particles and not to the water trapped outside of the particles in a packed gel (Reiland). As a rule-of-thumb, the latter figure can be estimated to 50%.

So ... 1g of dry Sephadex will give about 15 ml of packed gel

From here: 1 g swells to 12-15 mL gel

Just a thought ...
Does alpha-amylase interact with Sephadex?  Maybe 'thinking' it resembles a substrate, and (reversibly) binding to it or otherwise interacting to cause effects in addition to gel-filtration ?


Is the information in the brain stored in the connections rather than neurons?

Is the information in the Brain stored in the connections rather than
  in the neurons ?

It depends on what information you are referring to.

The brain does not just store one type of information,the model of a grandmother cell and the model of an interconnected neuron network are 2 subsystems of a greater system working together perhaps in a competitive or complementary arrangement. The purpose of this system is to extract information from the environment and identify it again for the organisms benefit. 1.

So let's say we see something that will benefit us in the future or that we might want to avoid. This is a simplification, but as you see that something, neurons in your neocortex light up specifically in region V1 in the back of your head, they arrive there after a lot of computations along the way from your retina, but also project to other parts of your brain where they are perhaps processed consciously,they fire in an orderly fashion, in a map, this bouncing around of electrical signals represents your conscious, and unconscious processing of the image, so the information exists as a network of electrical signals. 2.

During recollection, ( there are different types of memories so the structure in charge could be the neocortex,basal ganglia, hippocampus or even a muscle)3. this same map ( or a smaller subset ) gets replayed. The mechanism(s) by which this information is first encoded and later retrieved is still not entirely understood, but it involves a map and a getaway or switchboard.4. This switchboard ties together different percepts ( a smaller network of electrical signals), so in a way the information is represented at the switchboard level, if you disable this switchboard, you can't make new memories or lose previous ones.

A grandmother cell in the scheme of what I just explained, is the result of another subsystem that helps recognize something. Once you successfully encode a percept ( thing we want to remember seeing) you might want to associate it with something ( good,bad,delicious,etc), at the top of a series of associations lies a grandmother cell, which in turn is a handy evolutionary way of signaling back to other systems when some previous information has been experienced. So in this way the information of whether a subset of relationships in between networks of electrical signals has been experienced and encoded lies here.

References/Sources:

The idea of grandmother cells and object recognition in general is summarized in the Object Recognition chapter of ( Cognitive Neuroscience,Gazzinga-3rd ed 222-225) along with the problems a grandmother cell introduces in object recognition (ie if you lose the grandmother cell you would lose all the information about your grandmother)
Koch( Quest for Consciousness-2004) chapters on vision provide a very readable account of how the information goes from retina to v1. Vision Science (Palmer) is a more thorough account.
The chapter on learning and memory (Cognitive Neuroscience) gives an overview.
(Gluck -2001-Gateway to memory) presents different models of this arrangement.


Are there fishes with a double circulatory system?

It seems that lungfish display the beginnings of a double circulatory system:


How non-invasive blood glucose concentration measurement work?

I'm not exactly sure how it is done non-invasively in the manner you describe but suspect that it has to do with IR absorption spectroscopy. Glucose has distinct bands in the near-IR frequency range. So by illuminating the ear lobe and the capillaries in the surface, picking off the refracted light, and spectrally analyzing you should be able to determine the amount of glucose relative to some reference calibration.

I worked for a start-up company that did this semi-invasively for glucose measurements in the ICU. We drew a small blood sample and optically analyzed it in a glass cell using a scanning interferometer - then returned the blood to the patient.

The optical method that draws blood probably is the best approach with regards to accuracy - where you would like to get within 10 mg/dL - but it also has its problems including response to 'interferents' in the blood that can pose as glucose not to mention high cost for the interferometer and fouling of the blood access system.