Is heat released during work due to ATP breakdown or a increased blood flow?

Is heating of a body the result of increased blood flow or extra energy from ATP?

It is mainly because of the breakdown of ATP (Adenosine Triphosphate, a type of nucleic acid with an Adenosine base, a Ribose sugar, and 3 Phosphate groups), alternatively and more formally known as ATP Hydrolysis. During hydrolysis by water, ATP splits into Adenosine Diphosphate (ADP) and an inorganic Phosphate (Pi), releasing some energy. I'll explain more below how exactly this works.

How or why does ATP Hydrolysis release energy?

If you take a look at a diagram of an ATP molecule, you'll notice that it has 3 phosphate groups, each with a Hydroxyl group (-OH) that has a net negative charge due to Oxygen being highly electronegative and hogging electrons from the Hydrogen bonded to it. Consequently, you have 3 molecules with slightly negative charges attached to each other. If you've ever played with magnets, you'll know that like charges repel. So overall, the ATP is highly unstable because of these repulsive forces that are situated so close to each other. When the bond between the 2 inorganic phosphates is broken, a large amount of energy is released. Here's a diagram from Campbell's Biology 9th ed (note that the Hydrogens in the phosphates are not shown for simplicity):

When the last phosphate is broken off, you are left with one molecule of Adenosine Diphosphate (ADP) and an inorganic phosphate group (Pi). Energy has been released. However, this is not the entire story. Generally speaking, ATP Hydrolysis does not occur without another component: an endergonic process. An endergonic metabolic process is any which requires energy input in order to proceed. Think of it with the following analogy: imagine a ball trying to roll uphill by itself. At the bottom of the ramp, the ball is very stable and has low potential for performing work. But uphill, the ball would have a higher potential energy. It is impossible for the ball to roll uphill from a state of low energy to a state of high energy. Thus, we first need an input of energy--say the mechanical energy of our hand pushing the ball--in order for it to move up.

Our endergonic process (such as in protein synthesis by a ribosome or the phosphorylation of glucose in glycolysis, the first step of cellular respiration) requires some energy input from ATP in order to proceed in an exergonic manner--that is, in order to release energy without any help. With our analogy, this is like pushing the ball to the top of the ramp and then letting go, allowing the ball to roll back down from a state of very high potential energy (and therefore instability) to a state of low energy. The energy that we had to input from ATP is known as "activation energy", because it's literally energy that we need in order to unlock or "activate" an endergonic pathway.

Example of ATP Hydrolysis releasing heat:

When you have an infection in your body, your hypothalamus will raise the body's set temperature point to induce shivering. Shivering consists of many muscle contractions, all of which require hydrolysis of ATP. The result is a release of a large amount of heat that increases body temperature to a point at which pathogens cannot survive.

What about blood flow?

Blood flow does not actually produce heat by itself, but it can direct heat to the surface of the skin, such as when the body needs to cool down. The main source of heat in the body remains the ATP.

EDIT: much of the information here can be reviewed in this wonderful YouTube video by Andrew Douch


What does it mean if gene A is epistatic to gene B? Does this simply mean that gene A masks the phenotype of gene B when expressed?

Yes.  Note that this does not say anything about mechanism. If A converts 1 to 2, and B converts 2 to 3, then A is epistatic to B, but A is also upstream of B.  In a signaling pathway, say B inhibits A and prevents it from signaling. A mutation in B allows A to signal. A mutation in A means there is no signaling. Mutations in both A and B means there is no signaling: A is epistatic to B, but A is downstream of B.

An epistasis group is a group of genes in the same pathway.  Knocking out any combination of these genes will not result in a more severe phenotype than knocking out the most "sensitive" of these genes (the single mutant with the most severe phenotype).


Do lunar rhythms have impact on human biology, if so, how?

The moon doesn't have a direct effect on metabolism. Nor does it affect menstruation (an archaic theory existed which claimed so!!). The lunar effects are due to its gravitational field which is known to affect tides (Spring tides and neap tides).
Even on a daily basis if you might have observed the sea advances into the beach in the night and recedes in the day. This effect is also because of the lunar gravity.

The abstract of the article, that you mentioned, says that moonlight may have some effect on certain organisms; I am highly skeptical about that.

I think it is just the tidal patterns that might affect the behavior of marine/coastal organisms. I am also slightly skeptical about whether the currents produced by lunar gravitation would be deep enough to affect benthic life. In that case even the heating effect of the sun can produce sea currents. Perhaps it can also produce an upward current because of differential heating.


Do people who have been blind all their lives dream?

Yes, they do. A blog post on the National Geographic website describes the results of a study about how blind people dream.(1) The participants who were born blind did not report any visual impressions. Among those who previously had sight, the number of visual impressions reported decreased with the time since loss of sight.

  Just as there are many ways to take in the world, there are many ways
  to dream about it. Blind people dream, just as they live, with a rich
  mix of sensory information.

  About 18 percent of the blind participants (both congenital and
  later-onset) reported tasting in at least one dream, compared with 7
  percent of controls. Nearly 30 percent of the blind reported smelling
  in at least one dream, compared with 15 percent of controls. Almost 70
  percent of the blind reported a touch sensation, compared to 45
  percent of controls. And 86 percent of the blind reported hearing,
  compared with 64 percent of controls.

  (...)

  Despite these sensory differences, the emotional and thematic content
  of dreams isn’t much different in the blind and the sighted. Both
  groups reported about the same number of social interactions,
  successes, and failures in their dreams. They had the same
  distribution of emotions, and the same level of bizarreness.


Is there a protein in the eye that gets kinked by photons and shipped down to the liver to get un-kinked?

The protein is called rhodopsin and the bit that gets kinked up is called retinol.   Normally when light hits it, it does trans to cis isomerization at the 11th carbon.  'kinks up' is a pretty apt way of describing it.

I'm not familiar with the shipped down to the liver part, but I'm guessing that the photo reaction of the retinol with itself or the protein must occasionally make the rhodopsin-retinol complex unfunctional - perhaps by the double bonds cross linking to other atoms in the retinol or to the protein.  As I understood it the retinol just straightens out again.  This reference shows that in the presence of rhodopsin, 11-cis retinol will become all trans again normally.

There should be enzymes in the liver that can recycle some messed up retinol configurations.  Its probably not the main route through your body. Retinol is stored in the liver from dietary intake, and then shipped via retinol binding proteins to the eye. So that is the organ which is the source of retinol in the human body (and probably most animals).  It should catch damaged retinols and refurbish them the same way it does those taken in via the diet.


Fibonacci sequence in nature, truth or just wishful thinking?

As far as I remember, Fibonacci patterns emerge in plants from hormone gradients. I.e. an apical meristem forms a leaf where the auxin concentration is highest, and already existing leafs lower auxin concentration, leading to some negative feedback.

See e.g.
http://www.sciencedirect.com/science/article/pii/S1360138507000581

or http://en.wikipedia.org/wiki/Phyllotaxis


Some hypnotics — the active component of sleeping medications — act as central nervous system (CNS) depressants, which in turn depress breathing or respiration, especially when mixed with other drugs, such as alcohol.

If your breathing slows sufficiently and is arrested, as can be caused by an overdose of CNS depressants, your vital organs will be starved for oxygen, which in turn can lead to brain damage and — ultimately — death.


Can PCR duplicates have complementary sequences?

The standard directional Illumina library prep protocols that are used at the facility in my building follow the schematic below:

So, I guess this provides a potential technical explanation for your stranded duplicates, with the broad simple answer being it depends on the protocol used to make the libraries.


difference between trisomy and partial trisomy

Any organism with a partial polyploidy has got some tissues with a different number of chromosome set, unlike the rest of cell tissues.
These situations are often consequences of meiosis error and are more common in plants than in any other organism.


Not less efficient, but introns are under less selective pressure than exons. Exons actually encode the protein. A single bp insertion will ruin a mRNA encoding a protein by causing a frame shift in how the sequence is read.

However the same is not true for introns. 1bp insertion even if the intron has function such as transcription or translation factor regulation has a higher chance of not damaging anything important. Simply because such factors are spaced apart and the space is not really important.

http://www.nature.com/scitable/topicpage/rna-splicing-introns-exons-and-spliceosome-12375
https://www.ncbi.nlm.nih.gov/pubmed/17570818


Can we develop a nucleos(t)ide analogue to cure rabies?

In theory that would be possible, as you mentioned the rabies virus does have its particular polymerase, and adequate inhibiting substrates could possibly be found.

On the other hand, the current immunoglobulin and vaccination post-exposure scheme is quite effective, and the incidence of rabies in developped countries is pretty low; so it's unlikely an inhibitor could profitably be developped to the market.  That means rabies-directed nucleoside analogues are not priority target for pharma companies, IMO the biggest obtacle.

Here are some of the technical hurdles a drug candidate would have to overcome, as a nucleoside analogue :

Affinity to the viral polymerase : too low an affinity makes competition with the native substrate difficult
Rate of conversion to triphosphate form : a low affinity of the host nucleoside kinase to the analogue can cause a inadequate concentration of active triphosphated inhibitor. Some virus (HSV) have their own kinase that may be less selective, though that doesn't seem to be the case for the rabies virus.
Selectivity for the viral polymerase (versus the host replication/transcription machinery) : a cause of cytotoxicity and, generally, adverse effects.
Pharmacokinetic problems : the analogue has to be able to be taken in through nucleoside transporters (facilitated transport into the cell), or go through other means of active transport, as that kind of compound is usually quite hydrophilic. One could also use the usual prodrug tricks to pass the membrane (see CP-4055 or sapacitabine). This may be particularly problematic for acute-stage rabies, as there would be the blood-brain barrier to pass.

Some additional perspectives on the development of nucleoside analogues

Advances in the development of nucleoside and nucleotide analogues for cancer and viral diseases -- (http://www.nature.com/nrd/journal/v12/n6/full/nrd4010.html)

Discovery and development of clofarabine: a nucleoside analogue for treating cancer -- (http://www.nature.com/nrd/journal/v5/n10/full/nrd2055.html)


There are two reasons for this:

Nasal mucus helps warm inhaled air before it reaches the lungs. In cold weather, the mucus tends to dry out, so the membranes increase their production.
At the same time, exhaled air is warmer than the surrounding air, so it contains more moisture than the outside air can hold. This moisture condenses around the tip of the nose.

Explanation found here.

So there's no particular advantage to getting a runny nose; it's just a normal reaction occurring in extreme conditions.


It looks to be a bush cricket of the Leptophyes genus.  Possibly Leptophyes punctatissima, also known as the speckled bush cricket - not sure if the one in your image is speckled or not.  It is endemic to Europe and can be found in the UK.

Photo source: Wikimedia commons - Leptophyes_punctatissima


Which bacteria have the highest mutation rate?

You seem to be assuming that mutation rates are somehow constant over evolutionary time. They are not. Mutation rates will change according to the stresses a species is subjected to. If you take a bacterial population and place it in a stressful environment (high/low temperatures, oxidative stress, lack of nourishment or whatever) you are likely to see an increase in the mutation rate.

That said, this review and references therein might interest you:

E. Denamur and I. Matic,Evolution of mutation rates in bacteria,Molecular Microbiology 60(4), pages 820–827, May 2006


During the time when you are not drinking water you still loose some water to sweating and urine. Sweating is (especially in hot climates) an important function of the body to maintain the body temperature in desired range. If this water is not replaced, the body gets dehydrated. This induces a reaction which reduces the activity of the "body thermostat" to tolerate a higher body temperature without excessive sweating to maintain the fluid balance of the body.

When you start drinking again after this the dehydration period, the body starts sweating to regulate the body temperature again, since now the loss of water is not critical anymore for the body. For a detailed discussion (including further references) have a look at this publication:

The effect of water temperature and voluntary drinking on the post
rehydration sweating


What is possibly wrong in my gel electrophoresis when I didn't see bands of DNA ladder on gel?

Possibly You don't mix ladder containing microtube by Sampler. You should slowly Fill and emptying Sampler for several times when pick it for use, mix it well, but do it without creating a bubble.one more thing, check your ladder by "NanoDrop"


What is the role of acetylcholine in blood pressure regulation?

I hope this answers your question:

So the heart is an electrically excitable tissue: it pumps due to action potentials that start  from specialized heart cells called nodal cells and these nodal cells spread the action potential to surrounding heart cells. These nodal cells are found throughout the heart and they make up what's called the conducting system. These nodal cells don't need neural or hormonal input for them to spread action potentials, they have this mechanism to spontaneously start action potentials on their own called a pacemaker potential, BUT they can be influenced by neural (think sympathetic and parasympathetic) or hormonal input. These external inputs change the frequency (the pace) of the heart beat by influencing the pacemaker potential of the nodal cells.

The sympathetic nerve fibers send out epinephrine which cause the pacemaker potential to occur at a faster rate, that's why during exercise (when epinephrine is released... hopefully) the heart beats faster. Parasympathetic nerve fibers send out acetylcholine which causes the pacemaker potential to occur at a slower rate, thus slowing down the heart. What does this mean in regards to the cardiac cycle? It influences how much blood (the volume) is ejected during the cycle. The volume of blood that is ejected from the ventricles, called cardiac output (CO), which is also how many liters/min, is determined by 2 other factors: stroke volume (volume of blood ejected during each ventricle during systole) and heart rate (CO = HR x SV). And therein lies a part of the answer to your question: when heart rate decreases because of parasympathetic stimulation, cardiac output should also decrease, granted stroke volume stays constant.

I unfortunately do not know how acetylcholine affects blood pressure. I've read a paper of how acetylcholine induced relaxation in hypertensive rats, but I'm not sure of the mechanism, like how it affects systolic or diastolic BP.


Statement 1 is true and Statement 2, false.

B cells, in the absence of antigenic stimulation express surface receptors(B-cell receptors or BCRs), which look like normal secreted antibodies (but these are membrane bound and not secreted). What is amazing is that each B cell at a particular time expresses the same B cell receptor - same as in, all receptors produced off one B cell are of the same type, say, antigen A. Now, another B cell produces another type of receptors, say, those which detect Antigen B. There is not just one BCR on the B-cell, but many - just like any other cellular receptor.

Now, there are many B cells in the body. Very much like antigen A and antigen B, there so many more antigens that our body can produce antibodies against. (The source I quote below says $\ 10^{12} $) It is a wrong notion that just one little B cell is doing that all. There are specific B cells for each specific antibody.

Each B cell isn't necessarily producing a unique antibody, but yeah, specific. It isn't unique since there must be a few more similar B cells producing the same receptor against antigen A. So it is not just one single B cell producing antibody against 'A'.

How does the body produce so many types of specific proteins?

Being proteins, they must be encoded by genes. B-cells while maturing, undergo a recombination (shuffling) of their immunoglobulin genes which leads to this differential expression of receptors, hence the diversity.

For further reading on genetics of immunoglobulins and the generation of diversity, I'd suggest - http://www.ncbi.nlm.nih.gov/books/NBK26860/


Is there an optimal illumination level for human habitats/workplaces?

It seems there has been some work done on too much light affecting human health, but in regards to lack of darkness at night, rather than too much during the day. Without the appropriate amount of darkness at key times melatonin production and the major clock regulator or SCN can be disrupted and lose sync with the peripheral clocks. See here [1] for a comprehensive article with loads of information and other links to studies done on this topic.

This part in particular illustrates some of the problems associated with too much light:

"Overexposure to sun-mimicking light is also believed to play a role in the increase of insulin resistance, type 2 diabetes and obesity in developed countries (where round-the-clock illumination is more prevalent). Some research also shows that too much sun-mimicking light ups our craving for carbohydrates.

Before humans started cultivating grains, carbohydrate energy was available only from spring to fall. In response, our bodies evolved to stock up on carbohydrates during the growing season to prepare for winter, when no carbohydrates were available. In turn, we didn’t crave carbohydrates in the winter. All that changed with the light bulb, write T. S. Wiley and Bent Formby, PhD, in Lights Out: Sleep, Sugar and Survival (Atria, 2001)"

This might be a bit off topic but check out http://www.lightingdeluxe.com/workplace-lighting-ergonomics.html and the HSE has some info on what the required lighting conditons in the workplace should be [2]. They only mention lighting conditions with reference to reducing levels of stress in the workplace though.

Also not directly related but pretty cool; an article in Science from 1998 found that light shining on the back of the knees may be able to regulate circadian rhythms [3].

[1] http://experiencelife.com/article/light-rhythms/

[2] (scroll to the lighting section) http://www.hse.gov.uk/humanfactors/topics/lighting.htm#lighting

[3] Wright, K.P. Jr. & C.A. Czeisler. Absence of circadian phase resetting in response to bright light behind the knees. Science 297, 571 (July 26, 2002).

or if you don't have access http://www.genomenewsnetwork.org/articles/08_02/bright_knees.shtml


Is probability for double crossing over included in distance cM? [task]

Centi-Morgan (cM) is based on observation not precise measurements. Now since double crossing-overs (and actually any arbitrary even number of crossing-overs) revert gene combination to the parental type, resulting lower recombinant frequency. So in your case since the chance (or the frequency if you wish) for double COs is 0.6%, you have to subtract this from parental genotypes and add it to the recombinants.


Why must gene entrapping constructs be integrated into introns and not exons?

I don't know that they must integrate into an intron. It seems perfectly reasonable that they could also integrate into an exon, as long as the reporter is in-frame. There is obviously an element of chance in that, and so the advantage of integration within an intron is that splicing will ensure that the reporter is translated correctly. Intragenic regions are also more abundant in the genome and so insertion is more likely. They discuss the advantage of this design in the original paper:
Gossler A, Joyner AL, Rossant J, Skarnes WC. 1989. Mouse embryonic stem cells and reporter constructs to detect developmentally regulated genes. Science 244:463-465.

...ES cells permit selection for rare-occurring integration events, which allowed us... to design and use a "gene trap" vector. The vector contains the lacZ gene, lacking a promoter and translation initiation signal, inserted in frame into the homeobox exon of the En-2 gene such that a splice acceptor is placed at the 5' end of lacZ. Integration of the construct into introns of genes in the correct orientation should create a spliced lacZ fusion transcript and a functional fusion protein when the reading frame is maintained. Evidence for this came from experiments in which a construct lacking the 5' En-2 splice acceptor yielded 12-fold fewer lacZ-expressing transformants than the construct carrying the splice acceptor.

Exonal insertions by gene traps have been reported:
Song G, Li Q, Long Y, Gu Q, Hackett PB, Cui Z. 2012. Effective Gene Trapping Mediated by Sleeping Beauty Transposon. PLS One 7.

Insertion of a trapping cassette into an exon or an intron of transcriptional active loci can generate a fusion transcript that contains the upstream exon and the reporter/selectable marker.
...
Eighteen transposition events were obtained from distinct cell colonies. Blasting the human genome in the NCBI and ENSEMBL database... indicated that seventeen of them landed in an intron and one of them integrated in an exon at active genomic loci. These data are in consistence with the fact that exons and introns comprise 1.5% and 24% of human genome, respectively.

See here for further reading.


How migration creates Linkage Disquilibrium

Imagine one population is fixed for A1 at locus A and for B1 at locus B. Here is a representation

--- A1 --- B1 ---

Another population is fixed for A2 at locus A and for B2 at locus B. Here is a representation

--- A2 --- B2 ---

Further imagine that the recombination rate between loci A and B is 0 $(r=0)$. Any migration rate will cause some individuals --- A1 --- B1 --- to be present in a --- A2 --- B2 --- population (and/or vice-versa). So linkage disequilibrium is complete.

If the recombination rate is in between 0 and 0.5, then there will be some level of linkage disequilibrium at equilibrium that can be calculated for a specific demography (incl. migration rate).


Do viruses linger/passively transport or attack the body at once?

Different viruses have different "modes of attack". Also, it depends on what you mean with "attack".

As a really short introduction to what viruses are, they are very unlike your body cells or bacteria. They are literally (usually) just genetic information with a kind of shell. The shell allows them to penetrate cells, where they then use the cell itself to produce more viruses. That's all they do, reproduce.

So, what do I mean with different "modes of attack" - well, different viruses lead to different things. For example, infections with Herpes simplex are often asymptotic and many people have no idea that they are infected. If you get the flu, however, you will notice.

Every virus that can infect humans will try to spread as soon as it enters the body. It won't linger around and wait - HIV directly targets immune cells, herpes directly targets nerve cells. The reproduction does takes time, but if they start reproducing and the immune system can't destroy them immediately symptoms can follow soon (think influenza) or late (HIV/AIDS). With most viral infections, the immune system at one point catches up and destroys the virus.

  Like is it improbable I have inhaled a virus if I do not feel pain in my lungs?

I'm going to assume you mean either the virus responsible for colds (rhinovirus) or the flu (influenza) here. No, it's perfectly normal to be exposed to either of these viruses without noticing anything. Many people come into contact with infected people without ever showing any symptoms, because their immune system takes care of the infection before any symptoms show up. If it does show up, it will be within a matter of days, though. The flu virus won't stay in your lungs for weeks waiting, it has no way of doing that (viruses are... very simple in that regard).


When it comes to displaying color, most organisms use chromatophores. Chromatophores are pigment-containing and light-reflecting cells, or groups of cells. Chromatophores reflect the color that they look like.

Chameleons also use chromatophores. The outermost layer of the chameleon’s skin is transparent. Beneath this layer are the chromatophores. The deepest layer contains melanophores, which are filled with melanin. Above that layer are cells called iridophores, which have a blue pigment that reflects blue and white light. Layered on top of those cells are the xanthophores and erythrophores, which contain yellow and red pigments, respectively.

For a chameleon to change color, it must expand or contract certain chromatophores depending on the signal of the nervous system. The expanded chromatophores block the contracted ones and the color of the expanded chromatophores determine the color of the chameleon. For example, to make the chameleon green, the iridophores and xanthophores must expand, and melanophores and and erythrophores contract.

Reference

WIRED - How Chameleons Change Colors

More to read
This Nature article provides a detail description and explanation of how this occurs - Photonic crystals cause active colour change in chameleons


What do the numbers in Photosystem I P700 and Photosystem II P680 stand for? Is it the optimum wavelenght? The maximum wavelenght?

I'd first like to briefly mention what the P700 and P680 refers to. These are the reactions centers of the photosystems. The Photosystems are where the light is absrobed and converted to the form of electrons. The light is absorbed by the chlorophyll molecules and the energy is transferred to the reaction center which transfers that energy into an electron from a water molecule. Tha elecron is transport tmake ATP and NADPH, which is important for carbon fixation.

The numbers specify the wavelength of light that the reaction center are most reactive to, and therefore, the wavelength where they absorb the most light. That's what's meant by the maximum absorption. So everybody is right, your teacher, the textbook and Wikipedia. They just say it differently.


These are probably giant African snails, Achatina fulica, an invasive species of land snails. The two snails in the middle are mating using love darts. The other two may be waiting for their turn.

See also: Wikipedia - Achatina fulica


Discrepancy in time for genetic differences between human and chimpanzee to accumulate

Good literature work here and good question +1! In short, your main mistake was that you based your calculations on a single site and not on the whole genome. More info below.

Genome-wide vs sites specific mutation rate

The statistic of $10^8$ generations that you computed is the average rate of fixation of new neutral mutations per site. As considered the genome-wide statistic between humans and chimpanzee, you have to scale your predictions up to the entire genome. There are about $3 \cdot 10^{9}$ nucleotides in either the human of the chimp genome. That would result in a genome-wide mutation rate of $U ≈ 2 * 10^9 \cdot 10^{-8} = 20$  (the two is because mammals are diploids). Hence, the rate of fixation of 0.05 generation.

So, the expected time it would take for $30 \cdot 10^6$ new mutations to fix would be $30 \cdot 10^6 \cdot 0.05 = 15 \cdot 10^5$ generations. Because, such mutation can happen in either lineage (humans or chimps), we have to divide this number of 2 leading to $7.5 \cdot 10^5$. With a generation time of 20 years, that would take $1.5 \cdot 10^7$ years or 15 million years.

15 million years? Why not 6-8 million years as expected from fossil records?

Most of the discrepancy is probably due to vague approximation made in the computation. For example, you assumed a mutation rate of $10^{-8}$ while in reality, the average mutation rate is rather twice as large (Nachman et al., 2000, Kong et al., 2012, Wang et al., 2012, Rahbari et al. 2016).

Doubling this mutation rate would divide by 2 our expectation of 15 million years leading to an expectation of 7.5 million years that perfectly match the fossil records!

There is however another source that may cause an overestimation of the time needed... You assumed the absence of incomplete lineage sorting or in similar words, you assumed that the standing genetic variance in the ancestral population negligibly affected divergence among the two lineages. However, these discussions are for another time!


Why are so many spermatozoa produced when only one of them fertilises the ovum?

Short answer : Sexual selection with sperm competition

However this answer will vary depending on which species you are referring to. When female mates with multiple males (like in many insects), sperm competition increases male's chances of getting his genes forwarded to next generation. When there is not much rival competition with other males (like in humans) this has correlation with mate guarding behavior and quality of sperm.


Thanks all for your comments guys. I tried purifying using PCR purification kit. I could recover 120 ng of purified fragment from 500 ng. It is ok for my further work.


Specificity of Protein Kinases in Signaling Pathways..?

Phosphorylation requires a nucleophile and hydroxyl oxygen acts like one. Serine, theronine and tyrosine get phosphorylated on the free OH group in their side chains.

Nitrogen, in some cases also can act as a nucleophile. In case of histidine, the imidazole nitrogen is phosphorylated during bacterial chemotaxis signaling. As far as I know eukaryotes do not have an enzyme for histidine phosphorylation.

Carboxylic groups in glutamate and aspartate can technically be phosphorylated as it happens in case of phosphoglycerate. Glutamate is phosphorylatyed by the enzyme glutamine synthase during the synthesis of glutamine. Same happens in the case of aspartate during aspargine synthesis. However, this is a reactive intermediate and the phosphorylation is not stable like that of hydroxyls.

Other amino acids do not have such nucleophilic groups to render an attack on the phosphorous atom in phosphate- so they are not phosphorylated.


What's the state of the art in designing and creating your own life forms?

The problem is of course very complex so take my answers as simplifications.

Most transgenesis so far has been done on unicellular beings (bacteria, yeast), which we can change as much as we want fairly "easily", plants, insects and some mammals. Notably, for the latter case, mice are the species which has been used the most for transgenesis, as they are cheap (compared to, say, using pigs), do not take lots of space, have big litters and a quick reproductive cycle (~20 days). Aside from mice we've seen GFP rats, pigs, dogs, cats, sheep and probably there is more, but I will mostly restrict my answers to mice (as far as I know there are big technical difficulties in applying transgenics procedures to something bigger than a mouse, but to be honest I could not explain you the details on this as I have never done it).

  What features can be easily inserted into almost any organism easily?

Well, essentially, it is easy to give rise to monogenic traits (i.e. traits that depend on a single gene). Generally speaking, when you want to have more traits, or need more than 1 gene to have the trait you create single transgenics and then breed them together.

So, if your phenotype depends on the presence of gene A and B you will generate a (mouse) line expressing A, one expressing B, you breed them together and, if you are lucky, a part of the pups will be expressing both.

  Next, I imagine that to design and create an artificial life-form will consist of three steps: 1. Figure out which proteins will give rise to those feaures, 2. Design a genome that will express those proteins in the right quantities and 3. Implant that genome into a cell and actually let the being grow.
  Is the above sequence of steps correct, or am I missing something?

No, that is not how it is done!

There has been, to my knowledge, only one (very impressive) attempt to do that, a project led by Craig Venter at Celera Genomics. The project resulted in the creation of the first synthetic life form, named Mycoplasma laboratorium (see also the original paper on Science). Doing this for a multicellular being is, presently, science-fiction.

What normally you would do is to insert or remove just the piece of DNA you need in the genome.

There are different approaches to do that: for instance, you can start from embryonic stem cells, from fertilized oocytes or from spermatozoa.

This is the general process for making a transgenic mouse:

Source: https://web.archive.org/web/20161212170103/http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/T/TransgenicAnimals.html

Now, depending on how you inject your gene you can distinguish between transgenics and knock-in mice. In a transgenic mouse you insert the gene somewhere in the genome and, although there are method to understand where it ended up you generally do not know.
Knock-in animals, instead, target a specific region of the genome. This is usually used in order to change an existing gene, to improve its function or to remove its function (knock-out animals). This process, called gene targeting relies on the biological process called homologous recombination.

So, why don't we just synthesize a new genome each time?
Aside from Venter's dream, the process would:

have incredibly high cost
be extremely complicated technically
be extremely long (mostly for reason 2)
suffer from the problem that there is so much we do not know about genome regulation in a bacteria, let alone in a mouse! You have to think that the genome is not just a series of genes one after another: there is a big part of regulatory regions that define things like the 3D form of the genome, which determines when and how much genes are accessible for transcription, when and where they are activated and so on. Also, more and more attention is now drawn to something called epigenetics marks, modifications of the DNA, or its associated proteins that can also modulate its transcription.

  What is the cheapest experiment you can perform at your own home without access to a biology lab which involves changing the genome of a living organism in a way that's functionally visible? (An arbitrary example: Can you create an apple that's blue in color with a budget of $500? By create, I mean you should be able to hold the blue apple in your hand.)

Quick answer: no you cannot.

Health authorities will be not very happy if you start to produce transgenic organisms in your garage
The sole cost of the reagents which you will need to create the transgene will be >$500. You would then need various machines (e.g. a thermocycler, probably a spectrophotometer, a hood, etc etc.).
I personally don't have a clue how one creates a transgenic plant, but I suspect it is not much easier than an animal. And definitely you don't want a mouse colony in your garage, do you?

An easy experiment you can do is extracting (fairly unpurified) DNA with stuff you have at home. More than that it gets really complicated.


Looks like they do.

What We Know and What We Do Not Know about Dragon Trees?

  Numerous phytochemical studies of resins from the Dracaena species
  resulted in the isolation and subsequent identification of sterols
  [135–138], steroidal saponins [110,138–141], lignans [138], and
  terpenoids [131,135,142–144], flavonoids (recently reviewed by Sun et
  al. [129], bioflavonoids [145,146], carotenoids [109,138], and
  aromatic compounds [107,147–151].

Citations are behind a paywall but apparently carotenoids are in the sap.


Can assimilated energy be simply lost from a trophic level?

In this diagram, since this is the only loss between trophic levels (along with  respiration and NA within each trophic level), NU represents dead organic matter, that is not transferred along the food chain. In other words, this represents dead leaves that are not eaten by herbivores, hares that die of old age and not predation, and foxes that are killed by falling rocks. So NU is the amount of energy that goes directly into the  decomposer community (another flow to decomposers is coming from matter that is excreted by herbivores and predators), since this diagram only includes primary producers, herbivores and predators.

NA, on the other hand, represents energy that is consumed by the next trophic level but not assimilated (Not Aassimilated). So this represents faeces etc.


How would a herbivore's digestive tract differ from a human's?

It depends on the method of digestion the herbivore utilizes and what they eat, grasses, leaves, fruit, or nuts . Ruminants are only one form of herbivore. A wonderful introduction to the various methods can be foundd here. http://vetsci.co.uk/2010/05/14/comparative-digestion/#
For comparison gorilla which are far more herbivorous than human have a much longer small intestines which is one reason they need a much wider trunk. They also of course need larger teeth with thicker enamel and much larger jaw muscles to chew the tough plant fibers. Not so much more complex digestive systems just bigger/longer.


This is the cannon bone of an adult artiodactyle.. The size points towards sheep or goat.


What is the name for the opening in the mouth for the nasal passages?

From what I understand from your comment is that you are asking for opening which connects the nasopharynx to oropharynx.

This opening is is connecting two parts of pharynx , acting like a bridge therefore it was named as Pharyngeal/Nasopharyngeal isthmus.

According to this site:

  isthmus of pharynx

  Type:Term

  Definitions
  1. passage posterior to the soft palate by which the nasopharynx and oropharynx communicate (i.e., the junction of nasopharynx and oropharynx), closed during swallowing by elevation of the soft palate and contraction of the posterior fascicle of palatopharyngeus (muscle), forming a Passavant cushion.

  Synonyms
  isthmus pharyngis , pharyngeal isthmus

Source of image: Textbook of Anatomy: Head, Neck, and Brain : Vishram Singh


Do Penicillin based antibiotics affect birth control?

Evidence on the association between antibiotic use and combination oral contraceptive (COC) failure remains controversial, with recent studies reporting no evidence to support decreased effectiveness of birth control with the use of antibiotics except rifampin and rifabutin.
The reasoning is antibiotics might interfere with the effectiveness of COCs by decreasing steroid hormone’s plasma concentrations by hepatic microsomal enzyme induction or inhibition, interference with enterohepatic circulation of
COC metabolites, interference with absorption from the GI tract, competition between two drugs for the same metabolizing enzyme, alterations in plasma protein binding, induction of an opposite physiologic effect, or increased urinary or fecal excretion of the contraceptive.
As you stated, the strongest evidence is for rifabutin and rifampin: a significant decrease in the hormonal levels was noted in women taking rifampin even after a single dose.  Dirithromycin slightly decreased plasma ethinyl estradiol levels, with questionable clinical importance. A recent study in the Netherlands did find a relationship between the use of antibiotics and breakthrough pregnancy in a population-based prescription database; also, individual patients do show large decreases in the plasma concentrations of ethinyl estradiol when they take certain antibiotics, notably tetracycline and penicillin derivatives.
Because of earlier studies, anecdotal reports, and the above (it's not possible to identify whose levels will drop with antibiotic use), a cautious approach is advised. Physicians and pharmacists (80-90% of both) still lean towards believing that broad-spectrum antibiotics decrease the effectiveness of COCs, and continue to advise the use of back-up contraception.
The tide is shifting, however, as new studies come out. Here are a few excerpts of recent studies:

Available scientific and pharmacokinetic data do not support the hypothesis that antibiotics (with the exception of rifampin) lower the contraceptive efficacy of oral contraceptives. (J Am Acad Dermatol 2002;46:917-23.)

Since dermatologists treat acne with antibiotics, and a significant percentage of these patients are young women of child-bearing age, they certainly have a vested interest in knowing if this is true.

Rifampicin and griseofulvin induce hepatic enzymes and do appear to have a genuine interaction with the COCP, leading to reduced efficacy. The situation with the broad-spectrum antibiotics is less clear. There are relatively few prospective studies of the pharmacokinetics of concurrent COCP and antibiotic use and few, if any, demonstrate a convincing basis for any reduced contraceptive efficacy.
We did not find an association between concomitant antibiotic use and the risk of breakthrough pregnancy among COC users. However, due to limited power and potential carryover effects, findings from this study cannot rule out an elevated risk of COC failure among antibiotic users. (2011)

So, the answer is (except with your noted exceptions) the penicillin-class antibiotics probably do not interfere with effectiveness of COCs. However, one unwanted pregnancy is one pregnancy too many, and the use of a back-up method is not a huge deal (just ~14 days).
Until more and larger studies demonstrate a lack of interaction between most antibiotics and COCs, this will likely be the advice people continue to receive. When you look at the risk to benefit ratio of back-up, it's probably the wisest course for people prescribed a short course of antibiotics. It is more significantly problematic for people prescribed continuous antibiotic use for acne, Crohn's and other conditions/illnesses.
Oral contraceptive efficacy and antibiotic interaction: A myth debunked
Interaction between broad-spectrum antibiotics and the combined oral contraceptive pill: A literature review
Antibiotics and oral contraceptive failure — a case-crossover study
Are antibiotics related to oral combination contraceptive failures in the Netherlands? A case-crossover study
Drug interactions between oral contraceptives and antibiotics.
Survey of pharmacists and physicians on drug interactions between combined oral contraceptives and broad-spectrum antibiotics.


For lift-to-drag ratio (so, hydrodynamic efficiency), high aspect ratio semi-lunate tails are most efficient-- leading edge suction is implicated in their ability to produce lift (which provides the thrust for high economy swimmers) while minimizing drag. Convergence of multiple animals (tunas, swordfishes, jacks, pomfrets, whales, ichthyosaurs, etc.) on that tail shape is considered indirect evidence of it's hydrodynamic benefit. So, for speed and energy economy, a tuna like tail, independent of orientation in the water.

NB: other aspects of morphology and physiology are also very important in predicting performance, and a semi-lunate tuna-like tail has often coevolved with these other traits.

More info:
http://rspb.royalsocietypublishing.org/content/280/1756/20122071.short
http://jeb.biologists.org/content/213/1/89.short
https://academic.oup.com/icb/article/24/1/107/104211/Body-Form-Locomotion-and-Foraging-in-Aquatic


How to determine externally that a whale is a mammal?

A whale has a horizontal tail fin which is a typical feature of mammalian marine animals see link. Mammalian sea animals typically have a vertical movement of the tail fin for swimming. Fishes like sharks have a vertically oriented tail fin and move it side-ways for locomotion.


Can someone help me to identify what kind of pear is this?

Plu Code 4413 is a bosc pear (a cultivar of Pyrus communis).

From the PLU search tool available via the International Federation for Produce Standards

FYI: take a close look at the pear you're holding in your picture:

Pera canela, meaning "cinnamon pear" in English, is in reference to its color. From Wikipedia:

  Famous for its warm cinnamon color


This is hard to answer since we don't know the exact conditions you chose, as these are rotation speed (or better g), how long you spun them down and also if you used a cooled centrifuge or not. It's also important how gentle you resuspended the pellet.

However, I would plate these cells, no matter what happened since you are at the last step of the procedure and have nothing to loose. Do the usual dilutions you use for plating your cells and then add another plate with undiluted transformation mix. If you have only very few surviving cells after your mistake you might get your clones on this plate. If it doesn't work, you will have to repeat the transformation.


Dreadnoughtus: Why are new taxa named using Dog Latin?

There is an International Commission on Zoological Nomenclature, to which submissions for new organisms' names is strongly recomended. The discoverer does have some leeway within this system if there is no Latin name that well-describes this species. Your example is one of many.
Chapter 31, for example, clearly states:

31.1.1. A species-group name, if a noun in the genitive case formed from a personal name that is Latin, or from a modern personal name that is or has been latinized, is to be formed in accordance with the rules of Latin grammar.

Examples. Margaret, if latinized to Margarita or Margaretha, gives the genitives margaritae or margarethae; similarly Nicolaus Poda, even though the name of a man, if accepted as a Latin name, gives podae; Victor and Hercules, if accepted as Latin names, give victoris and herculis; the name of Plinius, a Roman, even though anglicized to Pliny, gives plinii; Fabricius and Sartorius, if treated as Latin names, give fabricii and sartorii, but if treated as modern names give fabriciusi and sartoriusi; Cuvier, if latinized to Cuvierius, gives cuvierii.

31.1.2. A species-group name, if a noun in the genitive case (see Article 11.9.1.3) formed directly from a modern personal name, is to be formed by adding to the stem of that name -i if the personal name is that of a man, -orum if of men or of man (men) and woman (women) together, -ae if of a woman, and -arum if of women; the stem of such a name is determined by the action of the original author when forming the genitive.

Example. Under this provision, the species-group names podai from Poda, victori from Victor, and cuvieri from Cuvier are admissible. The names puckridgei and puckridgi may be formed from Puckridge.

Similar rules apply for genus and family names.
Since your example was a new genus and species, it didn't "fit" into previous categories (in the future, if and when similar discoveries are made that shed light on the genus' relation to others, the name can and will be changed accordingly, with or without the authors' approval).

According to the research team that discovered the taxon, the genus name Dreadnoughtus "alludes to the gigantic body size of the (which presumably rendered healthy adult individuals nearly impervious to attack)" and to the two dreadnought battleships of the Argentine Navy, the ARA Rivadavia and ARA Moreno. Thus, the genus name also honors the country (Argentina) in which Dreadnoughtus schrani was discovered. The name of the type species, schrani, was given in recognition of the American entrepreneur Adam Schran for his financial support of the project. - Wikipedia

A "good" or "useful" taxon is commonly taken to be one that reflects evolutionary relationships. Since this one does not, in a few decades, this name may well be gone.


Why deoxyribose for DNA and ribose for RNA?

Nice question which leads to the fundamentals of DNA and RNA.

DNA (Deoxyribonucleic acid) is the core of life in Earth, every known living organism is using DNA as their genetic backbone. DNA is so precious and vital to eukaryotes that its kept packaged in cell nucleus, its being copied but never removed because it never leaves the safety of nucleus. DNA directs all cell activity by delegating it to RNA. RNA (Ribonucleic acid ) have varied sort of biological roles in coding, decoding, regulation, and expression of genes. RNA carries messages out of the cell nucleus to cytoplasm.

  The structure of RNA nucleotides is very similar to that of DNA nucleotides, with the main difference being that the ribose sugar backbone in RNA has a hydroxyl (-OH) group that DNA does not. This gives DNA its name: DNA stands for deoxyribonucleic acid. Another minor difference is that DNA uses the base thymine (T) in place of uracil (U). Despite great structural similarities, DNA and RNA play very different roles from one another in modern cells.

  http://exploringorigins.org/rna.html

RNA has three main characteristics that differs it from DNA

RNA is very unstable and decomposes rapidly.
RNA contains Uracil in place of Thymine
RNA is almost always single stranded.

DNA and RNA use a ribose sugar as a main element of their chemical structures, ribose sugar used in DNA is deoxyribose, While RNA uses unmodified ribose sugar.

Ribose and Deoxyribose

  From the fig above we can see that the principal difference between
  the two molecules is the presence of OH in ribose (2' tail) and absence
  in deoxyribose. There is a difference in one Oxygen atom as the name
  stands de-oxy ribose. Both Ribose and deoxyribose have an Oxygen(O)
  atom  and a Hydrogen (H) atom (an OH group) at their 3' sites. The OH
  groups are very reactive in nature, so the 3' OH tail is required for
  phosphodiester bonds to form between nucleotides in both ribose
  and deoxyribose atoms.

Answer

DNA is such an important molecule so it must be protected from decomposition and further reactions. The absence of one Oxygen is the key for extending DNA's longevity. When the 2' Oxygen is absent in deoxyribose, the sugar molecule is less likely to get involved in chemical reactions( the aggressive nature of Oxygen in chemical reactions are famous). So by removing the Oxygen from deoxyribose molecule, DNA avoids being broken down. In an RNA's point of view the Oxygen is helpful, unlike DNA, RNA is a short-term tool used by the cell to send messages and manufacture proteins as a part of gene expression. Simply speaking mRNA (Messenger RNA) has the duties of turning genes ON and OFF, when a gene needed to be put ON mRNA is made and to keep it OFF the mRNA is removed. So the OH group in 2' is used to decompose the RNA quickly thereby making those affected genes in OFF state.

Finally, the ribose sugar is placed in RNA for easily decomposing it and DNA uses deoxyribose sugar for longevity.

  References

  Flesh and Bones of Metabolism -  Marek H. Dominiczak

  Genetics For Dummies -  Tara Rodden Robinson


Is it possible to have cancer and normal blood count at the same time?

Cancer doesn't have to have a profound effect on the blood. Remember that a cancer generally starts off as an abnormal tissue growth or a neoplasm. As the tumor progresses into a malignancy, it has the potential to gain or lose functions, develop new cell types that shouldn't be present in a given organ, invade other tissues, etc. Because of this, in some cases of cancer patients may be subject to paraneoplastic syndrome, or cross-reactivity between something the cancer is doing and the normal tissues.

In the above-linked source, some hematologic paraneoplastic syndromes include (1) eosinophilia, commonly associated with a number of cancers, (2) granulocytosis, often associated w/ lung cancer, (3) Pure Red Cell Aplasia, commonly associated w/ thymomas. The list goes on, but in some cases blood testing is capable of assisting in diagnosis, especially in cases where cancer of the blood is the culprit (very obviously). To also be kept in mind, they note paraneoplastic syndrome only affects around 8% of all cancer patients.

In other cases, you'll be monitoring treatment. As we know, chemotherapy is destructive, and can cause a depletion of platelets or neutrophils, damage organs, etc. Complete blood count (CBC) testing will help oncologists monitor treatments in cancer patients.

Being said: Because individuals with a tumor/cancer may fall within normal ranges in a CBC test, and because these tests must be analyzed scrupulously due to several factors that influence them such as diet, multiple tests are often needed to arrive at a meaningful conclusion. On the basis of cancer itself, however, if it's a solid mass lodged in the liver for example, it's completely possible that blood counts are normal. What you may find, however, are biomarkers in the blood that are saying "hey, the liver is being damaged or dying" such as the enzyme aspartate transaminase. If the tumors are currently small, you may not find anything meaningful in blood tests, or that the blood is "normal." (the possibilities aren't exhaustive)

As a matter of real data I was able to find, Spell et al. was at least able to find some efficacy in CBC testing for colon cancer, to 84% sensitivity and 88% specificity, but you should suspect that individuals may still be asymptomatic under such tests regardless.


Do Vaccinium membranaceum plants need a minimum amount of darkness per 24 hours?

Some plants are long day plants -- they require a certain number of days longer than a certain number of hours.

Some plants are long night plants -- they need nights that are longer than a certain number of hours.

See this for more details: http://www.biology-pages.info/P/Photoperiodism.html

Other plants are day neutral.  They bloom when triggered by other stimuli such as it being warm enough.

If you don't care if they bloom or not, then you can give them 24 hour light.  They should grow somewhat faster.

However, you may need to check what triggers them into dormancy.  E.g. Spruce start going into dormancy when days get shorter than about 10 hours (Varies by species, and provenance)  Reforestation growers trick them into going dormant in August with black tarps in mid afternoon.  They can then plant them with minimal stress, and they take off in the spring.


Is a nature possible where animals do not kill each other?

No, even herbivores will eat other animals, and predation goes down ot the cellular level.  Also something has to be ating your dead and will have a huge evolutionary pressure to evolve toward predation with no predators present.

Animals by definition have a much better profile of nutrients for other animals.

Deer routinely kill and eat birds, eggs and even dead rabbits. In nature food is food and evolution does not care where you get it from. Carnivores will and have evolved from an herbivorous ancestor when no carnivores are present.


Why do plants need oxygen through their roots?

Plants need oxygen but don't have a heart

Complex animals all have a circulatory system of some sort to get oxygen throughout the body for respiration. Plants also do respiration even though they are net producers of oxygen through photosynthesis.

Plants also have a bit of a circulatory system, but for the most part it isn't nearly efficient enough to deliver oxygen everywhere in the plant: plants don't have anything like circulating hemoglobin-filled cells we are familiar with in vertebrates, and although fluids flow in plant circulatory systems, they aren't circulating quickly like you are familiar with in your own body. This means that plants need to get oxygen near to where it is needed.

Roots, in particular, consume oxygen

The problem of a plant not getting enough oxygen through its roots isn't because the whole plant gets oxygen through the roots, it's because the roots themselves need oxygen to function. Roots do a lot of 'heavy lifting' in a plant, literally: they are pumping ions across membranes to pull in water, to concentrate other nutrients that the plant needs for survival and growth, and to pressurize the plant enough for those nutrients to make it up into the leaves. Those processes take energy, and in turn they need oxygen.

Additionally, photosynthesis isn't taking place in the vicinity of the roots: plants are both taking in CO2 and releasing oxygen from their stomata in the leaves and stems.

If roots cannot get enough oxygen, for example due to overwatering, the roots themselves are damaged, and this harms the plant as a whole.

Adaptations

Because there are always exceptions in biology, it should be noted that some plants are indeed adapted to wet environments and have better systems for promoting the diffusion of oxygen including increasing the amount of air space in the roots, where oxygen diffuses more quickly than through aqueous media. Other plants use fermentation in their roots to survive temporary hypoxia.

References

Colmer, T. D. (2003). Long‐distance transport of gases in plants: a perspective on internal aeration and radial oxygen loss from roots. Plant, Cell & Environment, 26(1), 17-36.

Drew, M. C. (1992). Soil aeration and plant root metabolism. Soil Science, 154(4), 259-268.

Justin, S. H. F. W., & Armstrong, W. (1987). The anatomical characteristics of roots and plant response to soil flooding. New Phytologist, 106(3), 465-495.

Laan, P., Tosserams, M., Blom, C. W. P. M., & Veen, B. W. (1990). Internal oxygen transport inRumex species and its significance for respiration under hypoxic conditions. Plant and Soil, 122(1), 39-46.


What is an effective method for putting on blue rubber butyl stoppers?

From what I can tell from this machine (https://www.youtube.com/watch?v=TwRtsAG5Oy4), the blue caps are put on the bottles first, then a loose version of the aluminium neck seals are put around the top of the capsule, which is then pressed in the machine to seal the lid hence if you use many gas sampling techniques, it might worth investing in purchasing a similar machine/technology to seal your samples, which would be the most efficient in the long run.

EDIT: as pointed by @user137 there are also hand crimping tools, which you can use, which are considerably cheaper, which as @user137 pointed out, can be found here


I am thinking it is the skeleton of a colonial large polyp stony coral. I am not certain, but I suspect a species of the Favia genus. Most likely one of these two species (see links for info and pictures):

Favia lizardensis
Favia rosaria


How is sugar in fruit metabolized, or digested and used?

Do you mean fructolysis?

Here what I found on the textbook  by John L. Tymoczko:

Fructose can take one of two pathways to enter the glycolytic pathway.Much of the ingested fructose is metabolized by the liver, using the fructose 1-phosphate pathway. The first step is the phosphorylation of fructose to fructose-1-phosphate by fructokinase. Fructose-1-phosphate is then split into glyceraldehyde and dihydroxyacetone phosphate, an intermediate in glycolysis. This aldol cleavage is catalyzed by a specific fructose 1-phosphate aldolase. Dihydroxyacetone phosphate continues into stage 2 of glycolysis, whereas glyceraldehyde is then phosphorylated to glyceraldehyde 3-phosphate, a glycolytic intermediate, by triose kinase. In other tissues, fructose can be phosphorylated to the glycolytic intermediate fructose 6-phosphate by hexokinase.


Significance of synthesis of D-glucose in plants..?

Synthesis from chemicals in organisms is fundamentally different from laboratory synthesis of chemicals. In the latter, more than one chemical species or other unwanted byproducts are usually formed, whist living organisms use enzymes, that are often stereo-specific. This means that they usually can bind, in the case, produce, only one stereo-isomer.

To produce both forms they would need double sets of enzymes.

It makes sense for animals, bacteria, protozoa, etc. to digest whatever comes, so less specific enzyme, but since plants will only access the glucose they themselves formed use of a stereo-specific enzymatic pathway probably enables a more efficient metabolism.


Are there any benefits/disadvantages/traits from having a permanent lower core temperature?

Yes absolutely. Body temperature is associated with basal metabolic rate which is linked to life-span/body mass. Keeping your body at temperature is responsible for the majority of your caloric burden majority of your caloric burden, and having a lower resting temperature would mean you require fewer calories to survive. Higher body temps are thought to have been a defense against parasite infection, so reductions in body temperature might leave you more susceptible to disease, however a paper came out recently discussing falling body temperature in the US and its implications, and I think it addresses many of your questions in detail in the discussion.
Edit: To elaborate on that elife paper, they've identified a small reduction in average body temperature overtime using military medical records going back to the civil war. They postulate that the reductions they observe are due to improvements in healthcare and a potential decrease in chronic inflammation in the population which increases your body temperature.


Minimal viable EEG equipment for dissertation research on BCI / BMI

I have been working with BCI since some time and would recommend you to try these ones. They all have been widely used in MS/PhD research and their results are more or less accepted everywhere:

Emotiv
NeuroSky  (Starts from 99$)
g.tec (Most accurate/Expensive one - not recommended for startups)

P.S: Last, but not least, feel free to have a look at BCI Competition datasets. I remember I used them in my semester project. Plus, if you are interested in getting the dataset of invasive BCI, I can provide you the email of respective research as well. Best of luck in your Research!!


How much shorter is the short arm of a chromosome? And why?

It varies from chromosome to chromosome and from species to species. In some cases, both arms are roughly the same length. In some cases, one arm is so short that it is almost inexistant. For chromosomes with equal length arms, of course the terms p and q do not apply.


Is there a difference between drinking water straight from the tap compared to leaving it to sit?

If you are speaking especially of the stomach, it actually makes no difference because the extremely low pH of the stomach allows very few bacterial organisms to survive. Often, Helicobacter pylori can however be present. Whether dissolved oxygen makes a difference to it is, to my knowledge, unknown. However, pure water does not stay long inside the stomach and passes almost immediately through to the intestines in most cases, so I doubt it would make that big a difference.

Now, it seems you are actually referring to the intestines in your question. Well, in fact the bacteria that inhabit the gut are almost exclusively limited to the colon and to a limited extent to the distal part of the ileum (small intestine). The stomach and almost all the length of the small intestine are sterile. Water absorption takes place in the jejunum (proximal part of the small intestine), which is a sterile region proximal to the locations colonized by bacteria. In conclusion, the oxygen content of tap water will not influence the bacterial flora simply because it does not come into contact with those bacteria.

BTW, the major difference between tap water that you leave sitting and the one that just came out of the tap is the chlorine concentration (decreases with time). Of course this will favor microorganism development, since it is precisely one of the reasons why we put chlorine in the water in the first place...


Books on machine learning applications in Biology

At NIPS 2016 most ANN implementations I saw were related to biology were trained on imaging data, thus the kind of comprehensive book you are looking for probably doesn't exist yet.

However, if you utilize the search feature on Amazon.com you'll find:

Neural Networks for Applied Sciences and Engineering: From Fundamentals to Complex Pattern Recognition

Artificial Neural Networks (Methods in Molecular Biology)

and this, which seems to best meet your need:

Neural Networks and Genome Informatics, Volume 1 (Methods in Computational Biology and Biochemistry)


Why is the ability of a virus to get crystallized considered as a "Non living feature of a virus"?

Crystallization involves removing extraneous molecules, so that remaining molecules — here, virions, or virus particles — can form a crystalline or ordered structure. https://en.m.wikipedia.org/wiki/Crystallization

As far as cells go, cellular proteins can be crystallized (some more easily than others), as well as nucleic acids, but having those crystals alone is not sufficient for life. You need an input of water, energy, etc.

Making crystals from the constituent parts of cells would effectively kill that lifeform. On the other hand, you can take virus crystals, add a bit of disorder, and they will "wake up" and regain their infectious properties.

Viruses sit on a fine line of what constitutes life. To some extent, the discussion is philosophical in that definitions are chosen and the subject either meets those criteria or not, and some criteria are a bit more arbitrary than others.

Some have argued that viruses in infectious virion form are life, at the stage when infecting a cell and redirecting its machinery to make more virus particles. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2837877/

Over the decades, biology has shifted from a study of cells in Petri dishes, or monks growing peas, to a more abstracted investigation into information science and related fields and subjects: mathematics, entropy, statistics, physics. That perspective started with scientists like Schrödinger, Turing, and Von Neumann, and it continues in the modern day with work by Dawkins, England, and others.

Viruses have and continue to shape the evolution of life around them. In a way, they are frozen information, and the definition of life may be changed over time, as we gain a more broader picture of how things work.


How can low cholesterol cause mortality?

What you have asked for is a causal answer to correlated findings. There is no cause-effect evidence (at least from my searching) showing low cholesterol will indeed cause stroke. Associations like this are dangerous in the sense that we shouldn't think that one causes the other. But, we can speculate on how they are linked, which is always fun.

I'll be going off my understanding of cholesterol transport and will include the reference at the bottom. Essentially, cholesterol is used in the cell membrane to change the permeability of the membrane. The more cholesterol, the less permeable the membrane is to water. However, this also changes the physical properties of the cell membrane, making it more rigid and structured. If I had to guess (which is again PURE SPECULATION) I would think that decreasing the cholesterol to the point of a dangerous level would increase the cell permeability of vital cells, the most sensitive would be neurons who depend on ion based signaling to perform primary functions. Since ions are very small and easily pass through the membrane if the membrane is leaky, they might be the first indicator that the something is wrong and the membrane isn't strong enough. Again, purely speculative with no evidence. An experiment one could do is examine the amount of cholesterol required in a cell to keep ions from crossing the membrane and see if there are any other effects that occur within or around the cell before ion passing. If you aren't in this type of research yourself, maybe you can fund it!

Source= Cassarett and Doul's Essentials of Toxicology. Textbook, 12th edition


Are amino acids of viruses L or D enantiomers?

Viral amino acids would almost exclusively be L-enantiomers considering they use host cell resources and machinery to build their proteins and the host cells are built on L-enantiomers.

With that said, you could always have nonstandard exceptions as xusr mentioned, if a virus somehow requires oxidase for example.


What does common viruses found in the body weigh?

Viruses, in general, are obligately pathogenic i.e. they don't usually co-exist (as commensals or symbionts) with our body cells. Their mechanism of survival involves usurping of the host cell machinery to produce their own proteins and genetic material. However, as pointed out in the comments, there are some viruses such as the GBV-C which can infect the host but seldom cause any disease. Moreover, this virus has been shown to have a positive effect on the innate immune response and inhibitory effect on HIV [1].

(Also, have a look at: Do beneficial viruses exist? If so, what examples are there?)

In our genome, here are some remnants of viruses that had infected our ancestors long back in past. A prominent example is that of retrotransposons. Retrotransposons are DNA sequences that constitute a significant part of our genome and they are structurally similar to the genome of retroviruses (like HIV). Retrotransposons had been considered junk DNA in the past but recent studies have shown that they do play some important roles in our body. For example, L1 retrotransposons cause somatic diversity (genetic diversity at the cellular level) of neurons and may possibly contribute to increasing the plasticity of our brain[2,3]. Retrotransposons can also regulate gene expression[4].

Other than that, there may be infectious viruses that are present in the body but are dormant. These may become active later (when the conditions are conducive) and cause the disease in that individual or spread to another person.

You can perhaps calculate the weight of these viral remnants (retrotransposons). It won't provide any great insight to anyone. You just have to calculate the percentage of genome these DNA sequences occupy and multiply it with molecular weight of the genomic DNA and total number of cells in the body. I'll leave that exercise to you.


Calcium concentration in activated dendritic spines?

An earlier source for an estimate of ${[Ca]_{i}}^{+2}$ in spines comes from hippocampal slices of P13-P19 rats (Majewska et al. 2000). The resting ${[Ca]_{i}}^{+2}$ in this paper was ~80 nM and a back-propagating action potential (AP) elicited a response up to ~250 nM (change of ~170 nM). They included $F_{min}$ and $F_{max}$, the minimum and maximum fluorescence signal from a single AP, as parameters in the equation they used to estimate ${[Ca]_{i}}^{+2}$. This paper may be where the models you mention got their numbers from.

The resting ${[Ca]_{i}}^{+2}$ estimated in Sabatini et al. (2002), where they also used rat hippocampal slices from P14-P20, matches that found in Majewska et al. as it was ~70 nM. For the estimation of the evoked change in ${[Ca]_{i}}^{+2}$ after a single AP they used the maximum fluorescence increase from trains of action potentials at 62.5 Hz and 83.3 Hz as a parameter in their estimator equation, assuming that the calcium indicator was fully saturated at those stimulation frequencies. Their estimate for the change in ${[Ca]_{i}}^{+2}$ per AP was about 530 nM. They then reasoned that the buffering properties of the calcium indicator itself could reduce the change in ${[Ca]_{i}}^{+2}$. Thus they loaded several different calcium indicators with different affinities and at different concentrations, in order to manipulate the $\kappa_b$, the buffer capacity, of the calcium indicator. They observed a very strong linear relationship between $\kappa _b$ and the change in ${[Ca]_{i}}^{+2}$. By extrapolating from a linear fit on these data, they concluded that in the case where there was no calcium indicator in the cell —i.e. when $\kappa _b = 0$— the change in ${[Ca]_{i}}^{+2}$ per AP would be approximately 1 $\mu$M.

So the difference between these studies is that in Majewska et al. they used the maximum observed fluorescence of the calcium indicator in their data after single APs, whereas in Sabatini et al. they attempted to saturate the calcium indicator with high-frequency trains of APs. Furthermore, in Sabatini et al. they attempted to account for the buffering capacity of the calcium indicator itself, thus arriving at a more unbiased estimate.

Reassuringly, later work from the Yuste lab (the same lab as in the Majewska et al. study) could replicate the results of Sabatini et al. when they used similar methodology (Cornelisse et al. 2007). Their estimate for $\Delta{[Ca]_{i}}^{+2}$ for a single AP was also ~1 $\mu$M.


Can you please give a direct quote? I am pretty sure your textbook did not say exactly what you said!

  When DNA polymorphism occurs mutations can take place.

In genetics, polymorphism just refer to the existence of genetic variation among individuals in a population (often referring to a specific locus).

Mutations is the ultimate source of polymorphism. It is not polymorphism that allow mutations to occur.

  If these mutations occur in the germ cell and do not destroy its capability to reproduce, it is said it might move on to the next generation.

Indeed!

  My book says it might lead to allele sequence variation.

'allele sequence variation' is just some kind of another generic term for polymorphism. For this expression to make sense to you, you should start by looking up the definition of allele


Effect of paracetamol or any antipyretic tablets

This is a controversial topic. I co-authored a paper that drew on this research to make conclusions about population-level effects. The only situations I can recall where antipyretics have been shown to be clinically beneficial is in severe cases where inflammation itself is causing neurological damage (e.g., acute brain injuries); results for e.g. infectious diseases are ambiguous. In our paper, we summarized previous research on the costs and benefits of fever suppression as follows (our summary may be slightly biased in the direction of "fever suppression is bad" ...)

  Previous investigations of the effects of fever suppression have focused on the clinical benefits and costs to the individual [8,9]. The adaptive value of fever [10–13] is well known to immunologists; for example, Janeway's Immunobiology [14, p. 110] notes that ‘At higher temperatures, bacterial and viral replication is less efficient, whereas the adaptive immune response operates more efficiently’. Others argue that the adaptive value of fever arises instead from activation and coordination of the immune response [12]. By contrast, a common view in the medical community, as expressed for example in Harrison's Principles of Internal Medicine, is that the ‘treatment of fever and its symptoms does no harm and does not slow the resolution of common viral and bacterial infections’ [15, p. 107] ...

References from this section:

  Mackowiak PA. 2000 Physiological rationale for suppression of fever. Clin. Infect. Dis. 31, S185–S189. (doi:10.1086/317511)
  Eyers S, Weatherall M, Shirtcliffe P, Perrin K, Beasley R. 2010 The effect on mortality of antipyretics in the treatment of influenza infection: systematic review and meta-analyis. J. R. Soc. Med. 103, 403–411. (doi:10.1258/jrsm.2010.090441)
  Kluger MJ. 1991 The adaptive value of fever. In Fever: basic mechanisms and management (ed. Mackowiak PA), pp. 105–124. New York, NY: Raven Press Ltd.
  Hasday JD, Fairchild KD, Shanholtz C. 2000 The role of fever in the infected host. Microbes Infect. 2, 1891–1904. (doi:10.1016/S1286-4579(00)01337-X)
  Blatteis CM. 2003 Fever: pathological or physiological, injurious or beneficial? J. Thermal Biol. 28, 1–13. (doi:10.1016/S0306-4565(02)00034-7)
  Simon HB. 2003 Hyperthermia, fever, and fever of undetermined origin. In Infectious diseases: the clinician‘s guide to diagnosis, treatment, and prevention. (ed. Dale DC). New York, NY: WebMD Professional Publishing.
  Murphy KM. 2011 Janeway‘s immunobiology, 8th edn. New York, NY: Garland Science.
  Dinarello CA, Porat R. 2008 In Harrison's principles of internal medicine (eds Fauci AS, Kasper DL, Longo DL, Braunwald E, Hauser SL, Jameson JL, Loscalzo J), 17th edn, p. 2958. New York, NY: McGraw-Hill.


Which plants are healthy to keep in the bedroom at night?

There exist a diversity of flora you may select relative to the antigen or noxious chemical you seek to reduce.
Pursuant to the British Medical Bulletin, the critical indoor pollutants are the polycyclic aromatic hydrocarbons like furanes and benzenes, ethanal (formaldehyde) and carbon monoxide. Depending upon which gaseous or volatile compound you seek to reduce in your household, you may select Chrysanthemum morifolium for the reduction of ammonia gas, xylene and alternative respiratory irritants; Chlorophytum chomosum for formaldehyde; and Dracaena genus concerning and trichloroethylene.

If you should suffer any infestation of Penicillium mould, then it is advised that one tackle the source of the infestation directly - areas rich in cellulose and moisture.

Further information regarding is available from the following links:

9 Air-Cleaning plants that are almost impossible to kill, https://greatist.com/connect/houseplants-that-clean-air

British Medical Bulletin, https://academic.oup.com/bmb/article/68/1/209/421251


Looks like the larvae of an elephant hawk moth (Deilephila elpenor).

 Green Variant. ©2005 Henk Wallays  (CC BY-NC 3.0)

In the Sphingidae family (like the snake-mimic caterpillar in this post).

Description: typically brown-gray color with black dots along length of body. Young larvae are yellowish-white or green, but some mature larvae also can be green colored. Fully-grown caterpillars reach 7.62 cm in length.

Have a backward curving spine or "horn" on the final abdominal segment.

 D. elpenor color variation. Source: A.R. Pittaway & I.J. Kitching

Range: Most common in central Europe and is distributed throughout the palearctic region.

Habitat: variety: including rough grassland, heathland, sand dunes, hedgerows, woodland, open countryside, and even urban gardens.

Source: Wikipedia


Online resource for downloading gene variant data?

Seems your variants are all possibly harmful mutations to human genes, in that case ClinVar can be quite useful, it returns hits to all your variants except L747_T751delinsP. I have never used the ClinVar API so I'm afraid I can't vouch for how easy to use that is.

When ClinVar doesn't have the variant (or info about it) you need you could search EBI to see if other sites have information for this variant, when queried with L747_T751delinsP EBI actually shows us that it has been entered into Reactome twice. (welcome to the mess that is sequence annotation!).

This might be outside of your scope but if you have an interesting variant that you cannot find information on you could try to find the most similar (known) variant using BLAST.


Does vitamin D affect melanin concentration?

Darker skin, as opposed to common belief, probably did not develop as cancer protection. Cancer is usually something that attacks the body in a subsequent life. Even pale individuals under the sun are likely to survive far beyond their reproductive era before they are wiped off by skin cancer.

Instead, it is believed that folic acid manufacturing is the highest selection pressure causing darker skin. Folic acid (vitamin B9) which is used all over the flesh, especially during pregnancy and childhood, will decompose in sunlight.

So the skin tone tries to discover the ideal equilibrium between vitamin D and minimal folic acid breakdown.

As a consequence, if you genuinely have enough vitamin D in your diet, there is no need for lighter skin (and further proof for the vitamin-d hypothesis). That is why the Inuit have lighter skin than expected for their extreme location: the intake of vitamin D is large, so the folic acid part of the equation "wins" and pale skin is not preferable. This is why Inuit individuals do not need so much sun.

Source:

scienceline.org/2007/06/ask-dricoll-inuiteskimos/

pnas.org/content/107/Supplement_2/8962


Are there eukaryotes with fully working mitochondria but without mitochondrial genes?

No there aren't any organisms with fully functional mitochondria which (the latter) do not retain the minigenome.

On whether it is theoretically possible to transfer all the mitochondrial genes to the nucleus:

Perhaps it is possible and mitochondria may work just like lysosomes and ER, but I think that the responses will be greatly delayed. At present there are no mathematical models that can provide a better understanding of that possibility. Nonetheless, some studies have shown that chloroplasts and mitochondria also have redox dependent gene regulation by which the expression of some components of the ETC is regulated by the redox state of the quinone. This helps in optimization of the ETC; if all genes were in the nucleus then this would not be possible. This pheonomenon is, however, better studied in chloroplasts. See this review.


Mathematical Modelling of Natural Selection

Mathematical and computational modeling of evolution is a huge field. To start you off with some broad strokes, there are two main approaches to evolutionary modeling with their own communities: frequency-independent and frequency-dependent models. Of course, in a real biological setting, the truth lies somewhere in between, but models are idealizations of key principles, and so the two extremes are good to study.
For frequency-independent selection, they key concept is the fitness landscape -- a way to map each genotype to a fitness. The population then lives in this landscape and agents with higher fitness reproduce better and so the population slowly movers over the lattice. Under reasonable macroevolutionary assumptions such as very rare mutations and asexual populations, the population will tend to be homogenous and can be just modeled as a single point in the fitness landscape with properly chosen selective sweeps to move the point from vertex to vertx (Gillespie, 1983; 1984).
The most popular concrete approach for frequency-independent selection is [Kauffman's NK model of rugged fitness landscapes] (Kauffman & Weinberger, 1989; Kauffman, 1993). Computer simulations tend to favor this sort of model. Wilf's model would be an NK model with K = 0, and fitness of 0 for incorrect letters and 1 for correct letters (to get the shorter walk). Related questions:

Is local equilibrium a reasonable assumption for evolutionary processes?
Structure of fitness landscapes in the NK model

The frequency-dependent selection approach is dominated by evolutionary game theory. A typical question for this field is the evolution of cooperation, and the most basic approach is to use replicator dynamics and look at evolutionary stable strategies. However, the field is in general saturated with all kinds of exciting models (both analytic and computational). A very friendly book-length intro is Nowak's Evolutionary Dynamics. For a genetle intro and connections to evolutionary psychology look at the slides in this post. A brief and sophisticated introduction aimed at mathematicians can be found in Hofbauer & Sigmund (2003). Related questions:

Sources for Algorithmic Evolutionary Game Theory
Why is 'Grudger' an evolutionary stable strategy?
How exactly are game theoretical evolutionary models described during implementation for computer simulations?
When does weak selection produce qualitatively different results from strong selection?

References
Gillespie, J.H. (1983). A simple stochastic gene substitution model. Theor. Pop. Biol. 23, 202.
Gillespie, J.H. (1984). Molecular evolution over the mutational landscape. Evolution 38, 1116.
Hofbauer, J., & Sigmund, K. (2003). Evolutionary game dynamics. Bulletin of the American Mathematical Society, 40(4), 479-519.
Kauffman, S. (1993). The origins of order: Self organization and selection in evolution. Oxford University Press, USA.
Kauffman, S. & Weinberger, E. (1989) The NK Model of rugged fitness landscapes and its application to the maturation of the immune response. Journal of Theoretical Biology, 141(2): 211-245
Nowak, M. A. (2006). Evolutionary dynamics: exploring the equations of life. Harvard University Press.


Why is leucine amino acid used the most in proteins and tryptophan the least?

This is a guess.

Tryptophan is a bulky amino acid. Having a lot of if would make the protein bulky. It is anyways hydrophobic and cannot be present on protein exteriors; high tryptophan may distort hydrophobic core possibly because of its bulkiness and ability to form pi-stacking interactions.
However, tryptophan is an essential amino acid and cannot be made de novo in humans. Indeed, it has only one codon perhaps because of its limited usage.
Nonetheless, tryptophan, despite its low abundance, is important in stabilization of protein structures such as β-hairpin [1] and it is also required for synthesizing serotonin.

Leucine is present in the hydrophobic core and β-regions. It also surrounds active sites which causes exclusion of water; this in turn facilitates catalysis by allowing polar residues to bind to the substrates [2].

I don't have any comment on why not isoleucine or valine instead of leucine.


Gene distance and Recombination Frequency: Mechanism

The genetic phenomenon referred to as recombination reflects the process of crossing over which occurs during meiosis. Crossing over creates an exchange of genetic information between homologous chromosomes. To a first approximation cossing over events take place at random positions along the aligned chromosomes. Consequently the further two loci are apart, the more likely that there will be a crossing over event between them. Thus the recombination frequency can be used to measure the distance between two genetic loci (or genes).

Supplement added in response to comment from OP

An analogy

Imagine a piece of string. It has 6 marks on it (1-6 on the diagram) which divide it into 7 intervals (A-G). We are going to cut the string at one of the marks. We throw a die to decide which position to cut.

What is the probability that our cut will separate A and G? It's 100% since all single cuts will do this.

What is the probability that our cut will separate A and D? It's 50% since single cuts at 1,2 or 3 will do this.

What is the probability that our cut will separate A and B? It's 16.7% (1/6) since only a cut at position 1 will do this and the probability of throwing a 1 on our die is 1/6.

Think of the intervals (A-G) as genes and the cut sites (1-6) as possible crossing over events. If two homologous chromosomes are going to undergo a single crossover somewhere at random, then the closer together are the genes (intervals), the less likely is it that the crossover (cut) will take place between them. This assumes of course that the site of crossing over is chosen at random.

In the model presented here, if the order of the letters was scrambled and didn't know what it was but we were told the frequencies of occurrence of the separation of the intervals with random cutting we could deduce the order of the letters.


No there is no membrane that separates the nucleolus from the rest of the nucleus. The nucleolus is an aggregate of all kinds of molecules involved with ribosome assembly like: precursor and mature rRNA, Small nucleolar RNAs, rRNA-processing enzymes, ribosomal proteins and partly assembled ribosomes (but no fully functional ribosomes)

Aside from all these protein and RNA there are indeed regions of the chromosome called Nucleolus organizer regions (NORs) present in the nucleolus. These NORs are located near the tips of the short p region of chromosome 13, 14, 15, 21, and 22. During interphase these regions decondensate due to proteins like nucleolin and are thus open for transcription. Many of the protein I mentioned are needed to form or present in the aggregation that is the nucleolus.


Why don't we find animal corpses and skeletons all throughout the woods?

Large predators can break up the bones to get at the marrow. This disperses the skeletons. But for the most part, bones are a good source of calcium, and are eaten by rodents. You can see evidence of this when you come across the gnaw marks that rodents make on the plastic boards made from recycled milk cartons. As for the reason that human skeletons are particularly resistant to this destruction, I have only a guess. Perhaps the first stage of destruction, the dispersal by large predators, is less common because these predators have been trained to avoid humans. I would also guess that many murder victims are concealed by the murderer.


Can frequent ultrasound diagnostics be harmful?

Ultrasound is considered a safe procedure (reference) which is accepted by the WHO as well (reference). There have been studies however, that show the link of ultrasound treatment to some undesirable traits.

Ultrasound could be possibly linked to a decrease in body weight on birth of infants (reference).

Frequent use of ultrasound may influence babies scanned to grow up left handed (reference)

A significant migration of neurons (change of neurons from their rightful area) has been observed in mice on exposing them to ultrasound at the prenatal stage. (reference).

A study has found detrimental affects to the brains of mice on exposure to ultrasound in the fetal stage (reference).

So based on these papers, I wouldn't call them a 100% safe but these tests all relate to repeated usage of ultrasound imaging. Ultrasound usage sparingly and on valid medical indication should not be a matter of concern.


Creating a cell, not from another cell. Will it be possible?

Many of the parts of a cell, which perform its basic functions, such as transcription, translation, DNA replication, etc. have been already isolated and successfully recreated in a test tube. So if we obtain a complete list of all the parts we need and know how to make those parts and mix them together, we can make a cell from scratch.

However, this will probably be very time-consuming and costly and will serve no other purpose than showing that it can be done. It is much more time- and cost-efficient to create a genome only, transplant it into an existing cell, and wait for the cell to replicate and synthesize new molecules until it changes in a way that completely fits the new genome.


Are gizzard muscles voluntary or involuntary?

Involuntary. The gizzard, like our stomachs, works unconciously. However, chickens do choose to peck up stones to help along the process, whether that is by instinct or otherwise. (I raised chickens a long time but a proper reference is below)

This book on commercial poultry raising says involuntary


Does "squinting" make you concentrate better on a logic test?

The phenomenon in question is probably related to people with uncorrected/undercorrected myopia.

This "ancient" phenomenon is called stenopeic slit effect (a case of pinhole effect): when the person squints the visual acuity becomes better because of smaller blur circles: the "slit" between the eyelids is the key point improving blurring.

One can check if it works by creating slit in paper or plastic:

Some "charlatans/witch-doctors/quacksalver/etc" can "treat" refractive error with pinhole/stenopeic glasses:

It is known that children with refractive errors have attention issues because they cannot see the objects sharply (this is why they can be mistakenly diagnosed with ADHD), thus your concentration improvement related mostly to your vision improve and not a better "understanding".

If you mean by squint using mimic muscles and corrugator muscle the answer should point out that not a "squint" improves your concentration, but your attempt to improve your concentration causes this type of "squint".


You can search by traits (mostly diseases) for genome wide association, in these databases:

Gwasdb2
Human genome variation Database: it also links to a Copy number Variation (CNV) database.


Are there hybrids that emerge as a new species?

Yes, this is called hybrid speciation.

  Hybrid speciation is a form of speciation wherein hybridization between two different species leads to a new species, reproductively isolated from the parent species

There has been a fair amount of work on hybrid speciation (see here). Hybrid speciation is often thought to be more frequent in plants than animals. In ferns for example, we estimate that 7% of species emerged through hybrid speciation (Otto and Whitton 2000). Typical cases of hybrid speciation include changes in ploidy levels (examples include sunflowers). Hybrid speciation also occurs in animals such as the lonicera fly to cite just an example.


Why is the current Ebola outbreak different from previous outbreaks?

This is too long for a comment, so I put this in here: The main reasons are sociological. From the data I have read so far, this outbreak (actually these are two independent outbreaks, one in West-Africa and another one -not connected- in the Democratic Republic of Congo) is not exceptionally deadly in terms of Ebola. The death rate is about 60% which is extremely high compared to other diseases, but Ebola had reached up to 90%...

I think the main differences are that this outbreak struck in a much more populated area which has a very poor health care system (if you can call it like this at all). Then it happened in a border region, I recall reports about a traditional funeral of a Ebola victim which infected visitors, some of them crossed the border afterwards.

Then it was completely underestimated in the beginning, because a lot of cases stayed unknown. This led to a wider spreading as people who got sick infected relatives and medical personnel subsequently. And although the reaction has been powered up a lot since then, it is still not adequate to contain the outbreak.

Former outbreaks happened in rural areas which where easier to contain with a smaller number of personal, which is not possible this time. If you want to read further about this, I recommend the blog of Tara C. Smith which has been doing research about Ebola for some time and also worked in crisis response teams.
Especially interesting are these two:

A historical perspective on Ebola response and prevention
Addressing more Ebola myths


Yes, it is true.

Prairie dogs

Prairie dogs for example are known for frequent infanticides.

Many other species kill their babies too

But of course, such behaviour also exists in other lineages such as grey langurs, gerbilles, lions, giant water bugs and Bottlenose dolphins (just to cite a few examples).

How does that evolve

It will be impossible to provide a complete universal explanation to this behaviour because the evolutionary processes causing this behaviour varies from lineage to lineage. For examples, in lions, only males kill young of the females that are still nursing and they do so when taking over a new harem only. In prairie dogs, mothers cause infanticide preferentially on others' babies but also on their own babies.

Going into the details of how such behaviour evolves in every specific lineage would probably require writing an intro on kin selection and other fields of evolutionary biology which is way too much for a single post. You may want to have a look at the wikipedia article infanticide for a start.

  Shouldn't the fact that they kill their own lineage make them nonviable?

Of course, they don't kill all the babies. Only a fraction of them!


Antigen Antibody reactions during blood donation

The key feature of type O blood as "universal donor" is that the incoming red blood cells have neither A nor B antigens and so the resident antibodies (anti-A , anti-B) will not react with them. Since transfusions are carried out with packed red blood cells the plasma antibodies of the donor don't matter - they will not be introduced into the recipient.


Impact of Terminator Efficiency in Genetic Constructs

To add to gaspanic's answer, not all terminators work equally well under all conditions. So if terminators weren't characterized in the organism or tissue you are working in the efficiency might be different. Additionally, though rarely people might be looking to design with a leaky terminator mimicking bacterial use of leaky terminators to use one DNA sequence to create two mRNAs of different length.
[Edit] Sources for further reading
Example of terminator efficacy differences between different species
Example of terminator differences between tissues
Terminator Attenuation - stopping of termination only sometimes
Leaky stop codons as a molecular tool


It might work, many cyanobacteria are reported to be phototaxic. https://www.pnas.org/content/115/52/E12378