Why dogs move their noses when smelling?

The dog's ability to smell the world around him and to interpret these odors depends on a complicated chemical sensory system. First of all, it possesses mobile nostrils, that help to determine the direction of the smell. Then comes sniffing, the ability to disrupt the air with a regular pattern of breathing that, through laboratory testing, is structured in a series of 3 to 7 snorts. Most of the sensory organs of the dog's nose, the septal organ, are probably responsible for the outbreak of sniffing behavior.

The air is scented, it passes over a bony structure called "projection sub-ethmoid", that man does not possess, and nasal membranes that cover it. The area above the protrusion is not sweep, when the dog exhales air and it allows olfactory molecules to settle and accumulate.

When a dog breathes normally, air is introduced into the nasal passages, it continues its way to the lungs. The action of smell allows air to remain "at rest" in the nasal passages. The intricate complex surrounds the maxillo-turbinate bones of the skeleton provides that the nasal membranes are capable of creating models of air flows odors that lead content in the air to hit the regions of the olfactory receptors.

The odor molecules disintegrate and are concentrated in the nasal mucus that adheres to the receptor cells. Once the mucus, load odor, adheres to the microscopic hairs of receptor cells, the chemical signal odor turns into an electric signal and is sent to the cerebral cortex and the limbic system, ie, the part of the brain that regulate behaviors feeding, drinking and sex. Small molecules stimulate the olfactory nerve of smell. Big odor molecules stimulate the trigeminal nerve, one of the largest nerves of the skull, and the volatiles of sex hormones probably stimulate the vomeronasal organ, the other part of the anatomy of the dog that does not exist in primates.

http://www.ucsuggiatevedano.it/l-olfatto

EDIT @ kmm

Their nostrils can move, like the eyes to focus and channel the light energy. Or the highly mobile ears of many predatory animals, including cats and owls, which can rotate, also independently one from the other, not only to improve the perception, but also to identify the direction of the sound.

The principle is the same as the frontal binocular vision, which allows us to calculate the distance.

EDIT II @ terdon

When the dog sniffs, "taste" a smell with a series of inhalations shorter and faster than normal, as we do when we feel a bad smell, breathes quickly several times to understand what smell is that.
Of course we are well-educated people and we do not do this in public. But the gesture is the same. =-]

EDIT III @Petr

"Smell is the ability to detect and discern the odorous emanations from the air. The snuff is the ability to intercept and discern the odorous emanations from the ground. They act with a pattern of regular breathing and is structured in a series of one / three smells accompanied by a series of three / seven snuffs.
The behavior is controlled by the organs of sense of smell nasal septum."
(Section 3.3.3.4.1 and the following)

http://www.fongaros.it/ana2.pdf
http://www.cacciapassione.com/cani-e-cacciatori/1956-olfatto-del-cane-tutta-questione-di-naso.html

The dog is able to absorb the chemicals present in the air, thanks to the characteristics enjoyed by its olfactory cells. To further stimulate their sense of smell to the dog no choice but to expand with some emphasis their nostrils sneaking in a strong "suction" of odors. The air will be retained more or less long and the dog will recognize odors also very weak.

http://www.ucsuggiatevedano.it/l-olfatto
http://en.wikipedia.org/wiki/Olfaction

The nose of the dog is also called truffle, at its end there are the nostrils or the cavity, through which sucks air, and the vibrissae, equipped with sensory hairs. The dog's nose is particularly sensitive, is equipped on the inside of an organ said "of Jacobson", which allows to perceive any kind of substance, able to distinguish between a million of specific molecules, over that of perceiving pheromones, i.e. substances that indicate important information about the physical and mental state of others like it.

http://www.comeaddestrareuncane.com/blog/tag/cani-molecolari/

In the dog, the surface of the olfactory mucosa varies between 70 and 150 cm2 - in this tissue the number of olfactory receptors varies from 250 to 280 million - In 1962, Becker et al. showed that dogs are able to recognize substances in dilutions from 1/100 to 1/10.000.000.
- http://milano.corriere.it/milano/notizie/cronaca/12_febbraio_19/cani-olfatto-parere-esperto-1903358352720.shtml

Have you noticed how a dog sniffs the urine of a female "tasting it"? It is the same action that makes the viper when it follows the track of the mouse: it evertes the tongue and carries on it the odorous particles in the buccal cavity, and this organ has a function in the middle between the olfactory and gustatory ones. "Pointing dogs" is as pointing "the wild" taste the smell.
"Eat the scent", in the jargon, because savored, not only in terms of smell, the smell of the wild. The Jacobson's organ is then a second organ capable of perceiving odors, the first we've said is represented ciliated epithelium of the mucous membrane of the nose.
But there is a third organ called the "Rodolfo-Masera" which also serves to sense the emanations chemical (not yet known which), that way you could explain a specialization of these organs to perceive certain groups of biochemicals than others.
- http://www.laciotola.net/Cani/la-funzione-olfattiva-del-cane.html


Do blind birds bob their head when they walk?

The forward thrusting movement so peculiar of pigeons and other fowl (Fig. 1) while walking is thought to be related to shifting the visual field. The less visible backward motion of the head is thought to be related to fixating the field of view (Dunlap & Mowler (1931).

According to the meticulous observational study by Dunlap & Mowler (1931), blindfolded pigeons stop making head movements altogether while walking. They stop their forward thrusting motion, the backward motion as well as more random scanning head movements. Hence, the authors conclude that the forward and backward jerking movements are related to vision, and not to hold their balance or whatsoever.

Fig. 1. Snapshots of a pigeon walking. The head thrusts forward in the middle frame. source: Dunlap & Mowler (1931)

Reference
- Dunlap & Mowler, J Comparative Psychol (1931); 11(1): 99-113


Is there any evidence that sexual selection may lead to extinction of species?

TL;DR:

There is a dearth of actual experimental evidence. However:

there is at least one study that confirmed the process ([STUDY #7] - Myxococcus xanthus; by Fiegna and Velicer, 2003).
Another study experimentally confirmed higher extinction risk as well ([STUDY #8] - Paul F. Doherty's study of dimorphic bird species an [STUDY #9] - Denson K. McLain).

Theoretical studies produce somewhat unsettled results - some models support the evolutionary suicide and some models do not - the major difference seems to be variability of environmental pressures.
Also, if you include human predation based solely on sexually selected trait, examples definitely exist, e.g. Arabian Oryx

First of all, this may be cheating but one example is the extinction because a predator species specifically selects the species because of selected-for feature.

The most obvious case is when the predator species is human. As a random example, Arabian Oryx was nearly hunted to extinction specifically because of their horns.

Please note that this is NOT a simple question - for example, the often-cited in unscientific literature example of Irish Elk that supposedly went extinct due to its antler size may not be a good crystal-clear example. For a very thorough analysis, see: "Sexy to die for? Sexual selection and risk of extinction" by Hanna Kokko and Robert Brooks, Ann. Zool. Fennici 40: 207-219. [STUDY #1]

They specifically find that evolutionary "suicide" is unlikely in deterministic environments, at least if the costs of the feature are borne by the individual organism itself.

Another study resulting in a negative result was "Sexual selection and the risk of extinction in mammals", Edward H. Morrow and Claudia Fricke; The Royal Society Proceedings: Biological Sciences, Published online 4 November 2004, pp 2395-2401 [STUDY #2]

  The aim of this study was therefore to examine whether the level of
  sexual selection (measured as residual testes mass and sexual size dimorphism) was related to the risk of extinction that mammals are currently experiencing. We found no evidence for a relationship between these factors, although our analyses may have been confounded by the possible dominating effect of contemporary anthropogenic factors.

However, if one takes into consideration changes in the environment, the extinction becomes theoretically possible. From "Runaway Evolution to Self-Extinction Under Asymmetrical Competition" - Hiroyuki Matsuda and Peter A. Abrams; Evolution Vol. 48, No. 6 (Dec., 1994), pp. 1764-1772: [STUDY #3]

  We show that purely intraspecific competition can cause evolution of extreme competitive abilities that ultimately result in extinction, without any influence from other species. The only change in the model required for this outcome is the assumption of a nonnormal distribution of resources of different sizes measured on a logarithmic scale. This suggests that taxon cycles, if they exist, may be driven by within- rather than between-species competition. Self-extinction does not occur when the advantage conferred by a large value of the competitive trait (e.g., size) is relatively small, or when the carrying capacity decreases at a comparatively rapid rate with increases in trait value. The evidence regarding these assumptions is discussed. The results suggest a need for more data on resource distributions and size-advantage in order to understand the evolution of competitive traits such as body size.

As far as supporting evidence, some studies are listed in "Can adaptation lead to extinction?" by Daniel J. Rankin and Andre´s Lo´pez-Sepulcre, OICOS 111:3 (2005). [STUDY #4]

They cite 3:

  The first example is a study on the Japanese medaka
  fish Oryzias latipes (Muir and Howard 1999 - [STUDY #5]). Transgenic males which had been modified to include a salmon growth-hormone gene are larger than their wild-type counterparts, although their offspring have a lower fecundity (Muir and Howard 1999). Females
  prefer to mate with larger males, giving the larger
  transgenic males a fitness advantage over wild-type
  males. However, offspring produced with transgenic
  males have a lower fecundity, and hence average female
  fecundity will decrease. As long as females preferentially
  mate with larger males, the population density will
  decline. Models of this system have predicted that, if
  the transgenic fish were released into a wild-type
  population, the transgene would spread due to its mating
  advantage over wild-type males, and the population
  would become go extinct (Muir and Howard 1999).
  A recent extension of the model has shown that
  alternative mating tactics by wild-type males could
  reduce the rate of transgene spread, but that this is still
  not sufficient to prevent population extinction (Howard
  et al. 2004). Although evolutionary suicide was predicted
  from extrapolation, rather than observed in nature, this
  constitutes the first study making such a prediction from
  empirical data.

  In cod, Gadus morhua, the commercial fishing of large
  individuals has resulted in selection towards earlier
  maturation and smaller body sizes (Conover and Munch
  2002 [STUDY #6]). Under exploitation, high mortality decreases the
  benefits of delayed maturation. As a result of this,
  smaller adults, which mature faster, have a higher fitness
  relative to their larger, slow maturing counterparts
  (Olsen et al. 2004). Despite being more successful
  relative to slow maturing individuals, the fast-maturing
  adults produce fewer offspring, on average. This adaptation,
  driven by the selective pressure imposed by
  harvesting, seems to have pre-empted a fishery collapse
  off the Atlantic coast of Canada (Olsen et al. 2004). As
  the cod evolved to be fast-maturing, population size was
  gradually reduced until it became inviable and vulnerable
  to stochastic processes.

  The only strictly experimental evidence for evolutionary
  suicide comes from microbiology. In the social
  bacterium Myxococcus xanthus individuals can develop
  cooperatively into complex fruiting structures (Fiegna
  and Velicer 2003 - [STUDY #7]). Individuals in the fruiting body are
  then released as spores to form new colonies. Artificially
  selected cheater strains produce a higher number of
  spores than wild types. These cheaters were found to
  invade wild-type strains, eventually causing extinction of
  the entire population (Fiegna and Velicer 2003). The
  cheaters invade the wild-type population because they
  have a higher relative fitness, but as they spread through
  the population, they decrease the overall density, thus
  driving themselves and the population in which they
  reside, to extinction.

Another experimental study was "Sexual selection affects local extinction and turnover
in bird communities" - Paul F. Doherty, Jr., Gabriele Sorci, et al; 5858–5862 PNAS  May 13, 2003 vol. 100 no. 10 [STUDY #8]

  Populations under strong sexual selection experience
  a number of costs ranging from increased predation and
  parasitism to enhanced sensitivity to environmental and demographic
  stochasticity. These findings have led to the prediction that
  local extinction rates should be higher for speciespopulations
  with intense sexual selection. We tested this prediction by analyzing
  the dynamics of natural bird communities at a continental
  scale over a period of 21 years (1975–1996), using relevant statistical
  tools. In agreement with the theoretical prediction, we found
  that sexual selection increased risks of local extinction (dichromatic
  birds had on average a 23% higher local extinction rate than
  monochromatic species). However, despite higher local extinction
  probabilities, the number of dichromatic species did not decrease
  over the period considered in this study. This pattern was caused
  by higher local turnover rates of dichromatic species, resulting in
  relatively stable communities for both groups of species. Our
  results suggest that these communities function as metacommunities,
  with frequent local extinctions followed by colonization.

This result is similar to another bird-centered study: Sexual Selection and the Risk of Extinction of Introduced Birds on Oceanic Islands": Denson K. McLain, Michael P. Moulton and Todd P. Redfearn. OICOS Vol. 74, No. 1 (Oct., 1995), pp. 27-34 [STUDY #9]

  We test the hypothesis that response to sexual selection increases the risk of extinction by examining the fate of plumage-monomorphic versus plumage-dimorphic bird species introduced to the tropical islands of Oahu and Tahiti. We assume that plumage dimorphism is a response to sexual selection and we assume that the males of plumage-dimorphic species experience stronger sexual selection pressures than males of monomorphic species. On Oahu, the extinction rate for dimorphic species, 59%, is significantly greater than for monomorphic species, 23%. On Tahiti, only 7% of the introduced dimorphic species have persisted compared to 22% for the introduced monomorphic species.

  ...

  Plumage is significantly associated with increased risk of extinction for passerids but insignificantly associated for fringillids. Thus, the hypothesis that response to sexual selection increases the risk of extinction is supported for passerids and for the data set as a whole. The probability of extinction was correlated with the number of species already introduced. Thus, species that have responded to sexual selection may be poorer interspecific competitors when their communities contain many other species.


First of all, if you want 90% identity, you can discard this hit. None of the HSPs pass that threshold. What's more, since you're working with proteins, there are no splicing issues involved and you should be able to get a single HSP spanning most of the query and subject sequences. Assuming, of course, you have a true homolog.

In your output, I see many small, overlapping HSPs, most of which have low identity. I can't be sure without seeing the sequence but it's a safe bet that what you have there are low complexity/repetitive regions and that's why you have so many separate HSPs. The only half way decent one starts at position 630 of the query sequence and is only 595 residues long, less than half your query protein. Either you have a very diverged N-terminal region or your HSP is just a conserved domain. Again, I would need to see the actual sequence alignment to be sure but that doesn't look like a true homolog (assuming your species are reasonably close which they must be if you're using a 90% identity threshold).

So, always assuming that your species are close enough to expect decent homologs, I would simply ignore the shorter HSPs and deal with those that represent more than, say, 80% of my query's length at >=90% identity. Shorter hits will most often be conserved domains or repetitive/low complexity regions. The thresholds you choose depend on the species you are studying.

If your species are not that close, don't use BLASTP at all. Instead, you can use something like hmmer. Collect a set of homologs from various species for each of your query proteins, build a matrix using these and use that matrix to search your database. You could also use Selenoprofiles which uses a similar approach.


Assuming that you are asking about E.coli cells being made competent for transformation using plasmid DNA, an answer is cached here from this source:

  Hanahan, D. & Bloom, F.R. (1996). Mechanisms of DNA transformation. In F.C. Neidhardt (ed.). Escherichia coli and Salmonella : Cellular and Molecular Biology. (pp. 2449-2459). Washington D.C., United States: ASM Press.

The source (and it is perhaps worth emphasising that Hanahan is/was a transformation guru) states that treatment with divalent cations can achieve 10% of cells rendered competent, whereas treatment for electroporation can achieve transfer into 95% of cells.

This information was, of course, published in 1996 so it is conceivable that advances have been made in the case of the former method.


Can someone please explain the following jargon to a layman

So I can definitely explain what "inhibits" means and what that implies, but I think the answer as to what apigenin is actually doing to testosterone levels is somewhat complicated. I wasn't able to find a study looking at steroid levels in vivo following apigenin administration, so this is based solely on a quick look through the biochemistry and cells biology available.

17β-HSD is an enzyme that catalyzes a reaction (meaning it makes the chemical reaction happen more quickly than it would by itself) that converts androstenedione to testosterone. If it is inhibited, that means that the enzyme is no longer able to catalyze the reaction. Therefore, inhibition of this enzyme should prevent the synthesis testosterone, and reduce its levels, since less testosterone will be made.

On the other hand, aromatase is an enzyme that converts androgens, namely testosterone and its aforementioned precursor androstenedione, into estrogens. So, one would expect inhibition of this enzyme to lead to increased testosterone levels, as less testosterone and androstenedione would be converted to estrogens, meaning more testosterone and its precursor are left unchanged.

So, it seems we have some competing actions. Based on the paragraph in your question, apigenin's IC50 for 17β-HSD is 0.3 μM, and its IC50 for aromatase is about 2.9 μM. That means that when the concentration of apigenin is 0.3  μM, the enzyme activity of 17β-HSD is cut in half, but it must be at a concentration of 2.9 μM to do the same to aromatse's activity. So, it is about ten-fold more potent at inhibiting 17β-HSD than aromatase, at least in the assays used above. That would suggest that at concentrations significantly below 2.9 μM, apigenin would inhibit 17β-HSD but not aromatase, resulting in a decrease in testosterone. However, once concentrations became sufficiently high to allow for inhibition of both enzymes, things would get more complicated. Depending on the relative amounts of both enzymes, how much access apigenin was able to get to each, and what the cellular steroid composition was prior to inhibition, you could imagine relative testosterone levels to go either up or down. However, I would be inclined to suspect that testosterone levels would in fact decrease in the long run, since eventually existing testosterone stores would be depleted, and the inhibition of 17β-HSD would prevent the creation of new testosterone.

However, if we look at the paragraph in the article immediately following the one you quoted, there is a summary of a study done in cells that found that apigenin actually increased testosterone levels by blocking the TBXA2 receptor. This inhibited a signaling cascade that normally decreases testosterone synthesis, so the end result was an increase in steroidogenesis/testosterone production.

So, I suspect things are actually somewhat complicated and the best way to know would be to test in vivo


İrreversible dopamine antagonist vs. Dopamine agonist

No. Irreversible antagonism is, by definition, inhibition that cannot be reversed by the agonist. Let me summarize the basics. You can read about this in Goodman and Gillman's The Pharmacological Basis of Therapeutics, Chapter 3, but there are many basic biochemistry textbooks that will cover the same ground.

When an interaction between a ligand and a receptor is said to be reversible, it means that it can associate to form a ligand receptor complex, and then dissociate, leaving the system with free ligand and free receptor. In the most general case, when the ligand is bound, it changes the conformation and activity of the receptor, and when it dissociates, the receptor returns to its original conformation and activity. The effect of the ligand in the biological system is related to the proportion of bound receptors.

Irreversible ligands typically involve covalent bonding (e.g., aspirin, alkylating agents). When the ligand interacts with the receptor, it irreversibly alters the conformation and function of the receptor. Cell or tissue function is only returned to the free receptor state when the particular receptors that have had a ligand receptor interaction have been degraded and replaced by a new receptor.

One of the ways to test whether an interaction is reversible is to try to reverse it. Let's look at how you would do this.

Start by looking at the effect when an agonist binds. The agonist is reversible. When you add it to an assay that contains the receptor, it associates and dissociates from the receptor, but at any moment, some proportion of receptors is bound to agonist. This binding produces an effect you can measure. The effect is related to the overall proportion of receptors bound to agonist at any given time, which is related to the concentration of the agonist. When you increase the concentration of an agonist, more agonist binds and you can measure a greater effect. In this figure from Goodman & Gillman Chapter 3, you can see the log concentration of the agonist on the x axis and the effect measured in an assay on the y axis:

Now consider the effect of an agonist in the presence of an antagonist. Classically, a competitive reversible antagonist binds the same site as an agonist. When the antagonist is bound, it doesn't allow the agonist to bind. So run the same experiment as you did above (by increasing the concentration of the agonist and measuring the effect), but start with a solution that contains some fixed concentration of antagonist. Because an antagonist is competing for those same binding sites, there will be fewer receptors available for agonist binding, fewer receptor/agonist complexes, and a smaller effect.

If the antagonist is reversible, though, you can still get the same effect you got in the first experiment. You just have to increase the concentration of the agonist until it binds the same proportion of receptors. Since both agonist and antagonist are constantly associating and dissociating with the receptor, increasing the concentration of one of them will out compete the other.  In this figure (same source), you can see that in the presence of an antagonist (here, i, for inhibitor), it requires more agonist to get the same effect, but the maximum effect is still the same.

If the antagonist is irreversible you can't get the same effect you got in the first experiment, even by increasing the concentration of the agonist. The receptors have been permanently altered by the presence of the antagonist, and whatever portion of them had some interaction with the antagonist will either not bind the agonist, or will not produce an effect when bound. What you see in the assay here is that increasing the agonist concentration in the assay may increase the measured response, but you are unable to reach the same maximum response. Note here, the figure describes a pseudo-irreversible inhibitor (antagonist). This is just a term for an irreversible inhibitor that doesn't covalently bind the receptor, but has a strong enough affinity for the binding site that, based on the measurements, it looks like it covalently binds. Effectively, the inhibitor is going to sit there on the binding site until the receptor is degraded and will not be outcompeted by the agonist.


is it possible that there is no gene at a locus?

Like you said in your question - "locus" means location.  A locus may be anywhere on a chromosome - an entire "gene" coding locus, a non-coding locus (junk DNA), a regulatory sequence locus (example - the promoter region of a gene), or just a single nucleotide locus (SNP) etc.  A "locus" is the location of interest on the chromosome.

Yes, it is also possible that any genetic "locus" may be absent if it has been lost by a "deletion".  A deletion is a type of mutation.  They might be a single nucleotide deletion or a very large deletion of thousands of nucleotides. Genetic deletions can happen in several natural ways (a DNA repair error for example), and by other mechanisms, but also through "man made" genetic manipulations.


What is the maximum potential sucrose concentration of plant sap? What keeps plants below this potential?

As the concentration of sugars in the sap increases, so does viscosity. At high viscosity, the sap will not flow at a sufficient rate to provide nourishment to the different plant tissues.

In addition, there are limitations to concentrating the solutes in the sap. As the sap becomes more concentrated, the plant would be working against a osmotic gradient to further increase that concentration. That energy cost may be too great.


This is actually not easy - for the first one I am sure that is a caterpillar from order Orgyia and the family Erebidae, but since there is a vast number of different caterpillars on all continents, I am not sure which one it is exactly.
If you look at this image (from here), you will see a striking resemblance:

A lot more information on these moths can be found here.

The second one is most likely Trabala vishnou ssp. guttata, see the image (from here) for comparision:

There seems to be very little information available, some on the Wikipedia page.


Will dead cells in culture media have any significant impact on Live cells during incubation?

I'm not sure if this is linked to the actual dead cells, but I've found that not changing the media on plates while trying to generate lines from primary cultures can lead to contamination. Again, I haven't determined if this is because there are dead cells available for contaminants to derive nutrients from, or if it's just because changing media removes contaminants before they can grow too much. You might want to keep that in mind, though. I've found that changing media every 3 days is good enough.

Also, it depends on what you want to use your lines for. If you're hoping to study cell signaling or polarization (like if these are immune cells), it may be a problem, as the dead material will activate immune cells, and alter their signaling patterns. This has less to do with your worry about overall growth and more about you developing a good model for whatever you're doing.

To be fair, these signaling shifts can modulate proliferation in culture, but that's really going to vary from cell type to cell type. Sorry for being a bit vague! It's just that all cells are different- I happen to work with immune cells that are fairly finicky. There are other types that are a lot more robust, however, like fibroblasts, that you could probably spit on and they'd be fine.

If changing the media every 3 days really is too cumbersome, you could try splitting off small subcultures and doing a mini-experiment to see if changing the media vs not impacts confluence after a week or so? That would tell you how flexible your cells are when it comes to this.

Edit: Here are some publications that discuss the effects of dead cells in culture and differences between cell types. I also recommend that if you're using a cell line, looking up information via the ATCC website and reading their datasheet and some of the top references they site that likely describe how the line was isolated and best practices for culture.

"Inhibitory effects of persistent apoptotic cells on monoclonal antibody production in vitro" - a good example of how a lack of dead cell removal in vitro can impact cell function/phenotype and highlights the differences between different cell types.
"Cell death in mammalian cell culture: molecular mechanisms and cell line engineering strategies" - a good review that touches on the actual molecular mechanisms to which I was alluding. I particularly recommend reading the section "Induction of cell death in mammalian cell cultures", as it summarizes and links to several primary resources that show how increases in cell death can affect things like productively, growth, and cell number. It also does a good job of touching on the different kinds of cell death, which is important to understand but may be a bit too in-the-weeds for the original question.
"Links between metabolism and apoptosis in mammalian cells: Applications for anti-apoptosis engineering" - similarly good as the previous source, but looks at it through a more metabolic lense, which I think is helpful when considering the realities of cell culture.


Can/Do any spiders "release" their own web in the presence of a threat?

Building a web costs a lot of energy. From Wikipedia: "It is common for spiders to eat their own web daily to recoup some of the energy used in spinning. The silk proteins are thus recycled." https://en.m.wikipedia.org/wiki/Spider_web


Is there any virus that contains both DNA and RNA in its genome?

Here is the results summary of the study that describes the discovery of DNA:RNA hybrid virus:

  Results
  Bioinformatic analysis of viral metagenomic sequences derived from a hot, acidic lake revealed a circular, putatively single-stranded DNA virus encoding a major capsid protein similar to those found only in single-stranded RNA viruses. The presence and circular configuration of the complete virus genome was confirmed by inverse PCR amplification from native DNA extracted from lake sediment. The virus genome appears to be the result of a RNA-DNA recombination event between two ostensibly unrelated virus groups. Environmental sequence databases were examined for homologous genes arranged in similar configurations and three similar putative virus genomes from marine environments were identified. This result indicates the existence of a widespread but previously undetected group of viruses.

And here is the link to the paper:

https://biologydirect.biomedcentral.com/articles/10.1186/1745-6150-7-13


A good choice is the IgG/anti-IgG pair for cheap, easy to demonstrate/work with system. E.g. Goat-IgG coupled with donkey anti-goat IgG.  Just about any antibody supplier will have these.
These type of systems are the basic primary/secondary antibody bindings routinely used in immuno-assays, blotting etc. These may be mouse IgG coupled with a labeled anti-mouse IgG for example.
Reference
Wilson MS, Nie W. Electrochemical multianalyte immunoassays using an array-based sensor. Anal Chem. 2006;78(8):2507-2513. doi:10.1021/ac0518452


Was Dr. Livesey's treatment a valid one in the Treasure Islands?

The procedure described here is called venesection. It is no longer standard of care, but was when Treasure Island was written.

Here is an excerpt from the first edition of Cecil's Textbook of Medicine (1927):

  During the acute apoplectic attack the following therapy may be employed: The patient should be put to bed with the head elevated. If he has fallen to the ground the clothing around the neck must be loosened. Difficulty in swallowing contraindicates the administration of nourishment by mouth. An enema may be given. When the face is puffy, the pulse full and strong, and there is reason to suspect hemorrhage, venesection is advisable. It should be employed only for plethoric individuals, not for patients who seem asthenic or arouse suspicion of thrombosis. Usually 250 to 300 cc. of blood are removed.


Detecting Calcified stones and cracks in tooth

Cracks on your teeth are hard to detect if they are cracks on the mesial or distal surfaces (surface of the tooth closest to and farthest from the midline respectively) through x-rays. Please check this link for illustrations and very good explanations from the University of Maryland dentistry department. The different methods on the detection of cracks as well as the uses of radiographic evidence can be found in this link.

Now pulp stones can be identified through x-rays unless they are too small or not too dense. There has been researches done specifically using radiographs for detection like "A radiographic assessment of the prevalence of pulp stones in Australians". It could also be human error that your doctor was unable to detect it. A small explanation on pulp stones can be found here.


How can I tell if a certain marker is useful to date a phylogeny?

Speed of Sequence Divergence

You need to use a sequence which diverged only little among most closely related lineages in your tree and diverge quite a lot among most distantly related lineages. In other words, you need a sequence that diverge at a rate that is convenient for your needs.

If you investigate a young tree (a tree which MRCA of all lineages lived recently) you need a sequence that diverge quickly through time. If you investigate an "old tree" (a tree which MRCA of all lineages lived a long time ago) you need a sequence that diverge slowly through time.

Selection

Selection is affecting how fast two sequences diverge. But because selection is specific to the environment experienced by the individuals in each lineages, it can be more difficult to use sequences under selection as a molecular clock (exception of highly conserved selection which are under purifying selection used for very large trees). So we use neutral sequences.

Rate at which mutations fix

Let $u$ be the mutation rate for the sequence of interest and $N$ be the population size. The number of new mutations per year is equal to $2Nu$ (assuming a diploid population). Now, knowing that the sequence is not under selection, the probability of reaching a single mutation to fix (=to reach a frequency of 1 in the population) is $\frac{1}{2N}$ (see this post for a very introduction to why the probability of fixation is inversely proportional to $N$). As a consequence, the rate at which mutations fix is $2 N u \frac{1}{2N}=u$. In other words, the rate of mutation fixation is the mutation rate (for neutral sequences).

Rate at which mutations fix and sequences divergence

The term, sequence divergence is not clearly define. Typically, one would mean "average number of pairwise differences". Assuming that each new mutation that fixes occurred at a new locus (infinite allele model), then the number of pairwise differences between two lineages is the addition of the number of mutations that fixed in each lineage, that is $2u$. Always under the infinite allele model, the probability of the average number of pairwise differences to equal k is given by a Poisson distribution.

Wrapping up

  how can I tell if a certain protein would be a good phylogenetic marker

The sequence

has to be neutral (it makes things easier)
has to have a mutation rate of the right order of magnitude (it improves accuracy of the estimate and therefore improves statistical power)


Purpose of the conversion of 3-PGA to G3P in the calvin cycle?

Nice question! To see what trouble that extra oxygen can cause, lets get to the core of the reaction i.e. Calvin-Benson cycle; one step at a time. To start with, have a look at the detailed Calvin-Benson cycle (following image taken from here):

As becomes quite clear from this image, the actual use of Glyceraldehyde-3-phosphate is at the step of formation of Fructose-1,6-bisphosphate. Yet, we don't know why we cannot use 3-Phosphoglycerate instead at this step. For that, lets go a step further and see how the concerned enzyme, fructose-1,6-bisphosphate aldolase/phosphatase (aka aldolase), works.

Since the full article is behind a paywall, lets get a sneak peak into it. See this image1:

Pay attention to the steps where G3P enters i.e. steps between b and c. Even without entering into details of the mechanism, we get two factors which can prevent 3PGA from being utilized in this reaction:

Steric Hindrance: replace the terminal -H with -OH of G3P in the first image in your mind. You can clearly see that this would cause some steric hindrance and prevent formation of covalent bond between DHAP and G3P.
Formation of Geminal Diol: again, replace the terminal -H with -OH, but this time in the second image, in your mind. You get geminal diol in the resultant molecule, which is famous for its reactivity and instability. Thus, by adding 3-PGA instead of G3P in the reaction, we might end up with unstable molecules that cleave themselves up. I hope this is what you were looking for.

Reference: Juan Du, Rafael F. Say, Wei Lü, Georg Fuchs, Oliver Einsle Active-site remodelling in the bifunctional fructose-1,6-bisphosphate aldolase/phosphatase Nature 478, pages 534–537 (27 October 2011)
doi:10.1038/nature10458


Are there adaptations in tropical fish to compensate for less oxygen in water?

Fish that live in cold water for most of the year actually have particularly strong hypoxia-tolerance adaptations, i.e. from summer heatwaves and algal blooms, compared to fish that are better oxygenated by waves and flowing rivers.
Goldfish and other fish are able to rapidly change the surface area of their gills in less than a day.
Carp, killifish, goldfish and oscars have 2/3 times as much glycogen in their bodies than river fish i.e. rainbow trout.
There's a lot of research into the biochemistry of fish's oxygen response, i.e. gene expression changes, things like decreased expression of genes involved in the citric acid cycle.
Probably you will find most of the information on the wiki page, there are also summaries of current advances in the field.
On coral reefs, oxygen is a limiting currency for all the fish and zooplankton. The reading suggests to me that hypoxia adaptations depend mostly on heatwave events and low current waters vs rivers and coastal waves than by tropical vs pelagic and temperate regions.


In myosin II are regulatory and essential light chains calcium binding proteins or sites of phosphorylation?

The answer is both, the regulatory light chains , regulate myosin by phosphorylation which  can be dependent or independent of $\ce{Ca^2+}$.

Medical Physiology:

  The activity of the myosin regulatory light chain is in turn regulated through phosphorylation by $\ce{Ca^2+}$ -dependent and $\ce{Ca^2+}$ -independent kinases.

Source claiming calcium is essential for phosphorylation in tarantula skeletal muscle:

  Contraction is modulated in many striated muscles by $\ce{Ca^2+}$-calmodulin dependent phosphorylation of the myosin regulatory light chain (RLC) by myosin light chain kinase.

Calcium independent phosphorylation of regulatory protein by MLCK4:

  We find that MLCK4 is also expressed abundantly in cardiac muscle, and structural analyses indicate that it is a $\ce{Ca^2+}$/calmodulin (CaM)-independent kinase, in contrast to $\ce{Ca^2+}$/CaM-stimulated cMLCK.


In a lab there are so many ways of doing this. However, at home is a little tricky. This is what I would do:

Keep your bacteria in a liquid media.

Liquid Media: make the media out of NaCl and AS CLEAN AS POSSIBLE (distilled if possible) water (concentration 18g NaCl / L). Place a sample of the bacteria into the solution. Freeze solution with bacteria (-20 degrees C if possible). Take out when wanted.


What is the name of the property of viruses can activate a second time, with different symptoms?

Viral latency is the best term to use for viruses that can lie dormant.

I have not come across a specific term for latent viruses that recur with different symptoms. This is probably because "different" is very subjective. Many pathogens can cause several different forms of disease depending on factors such as the route of exposure (i.e. where and how the pathogen got to its destination). Obviously the latent infection has a different pathophysiology to chickenpox. Due to its latency in dorsal root ganglia, shingles typically results in a localised rash, but there are less common disseminated forms of shingles that can look very similar to chickenpox.


How can Chronic myeloid Leukaemic drugs reduce the production of the Philadelphia genotype?

The key is that TKIs, such as Imatinib, are a therapy rather than a cure
Per Wikipedia, Imatinib acts as a competitive inhibitor of the otherwise constitutively-active BCR-ABL fusion protein, rather than the fusion gene.  By binding the kinase domain, BCR-ABL is unable to phosphorylate downstream effectors that result in unchecked proliferation.  As long as a patient continues to take Imatinib, BCR-ABL activity should be blocked.

In the past few years (i.e, long after imatinib's discovery) there has been a lot of research into exactly how hematopoetic stem cells, which reside in the marrow and create leukemic blasts, work. Most HSCs remain in a quiescent state, but it's not particularly well-known how frequently they turn over.  Recent CML studies have shown that after ~5 years, a large portion of CML patients can safely taper the the drug.  Presumably this is related to HSC turnover, but frankly as a leukemia molecular biologist rather than a physician, I'm not the best font of clinical knowledge.


Are trees the only source of large amounts of oxygen?

71% of the earth's surface is taken up by water. Not surprisingly therefore, the seas are an important source of oxygen. National Geographic claims that photosynthesis by phytoplankton (mostly single-celled phototrophs, such as cyanobacteria, green algae and diatoms) account for half of the earth's oxygen production. The other half, they claim, is produced on land by trees, shrubs, grasses, and other plants.

The Ecology Global Network takes it a step further and claims that all marine plants (including phytoplankton) together produce 70 to 80 percent of the oxygen in the atmosphere.

Based on these reports, hence, marine phototrophs account for 50 - 80% of the earth's oxygen production.

With regard to terrestrial oxygen production, NASA reports that 30% of the land is covered by trees, and as much as 45 percent of the carbon stored on land is tied up in forests. So on land, trees are definitely large contributors to oxygen production.


Statistical Analysis for Blood Sugar Measurements

It would help to see your plots. The way I would imagine to present this data is not scatter plots but line plots:

(Each line would have a confidence interval/standard deviation from your different test subjects. This is just a schematic representation. Color represents different experimental conditions. Let me know if I misunderstood your experiment.)

Now, what is your actual question? Your hypothesis? You want to know if the time or height of the peak of blood sugar levels is different between the different fiber levels, right?

So, why not measure this? At what time do you find the peak for each subject and experimental condition and what's the blood sugar level at that time point? Your null hypothesis would be that there is no difference between the test conditions.

Here some mock data show the data spread from your 5 test subjects of the peak height measurements in the 4 different test conditions. Now you reduced your data to a question, where you could use a statistical test to see if you can reject the null hypothesis.

One thing you could do is to perform an ANOVA with e.g. Dunnett's post hoc test to compare your fiber conditions to the control condition

A problem with that is that your conditions are not really independent. And your actual question is not if any of these conditions is different. Your hypothesis would rather be if there is a relationship between fiber content and peak height/delay (null hypothesis would be: there is no relationship).

Here is the same mock data in a scatter plot (color represents test subjects, they overlap, but let's assume there are 5 data points for each condition) with a trendline showing, that with increasing fiber content there is a reduction in peak height:

You could therefore try a correlation analysis and test the statistical significance of your correlation coefficient.

As you see, the statistical analysis very much depends on your hypothesis and how you analyse your raw measurements. I hope, I have correctly identified the issue and this helps you with your analysis.


I assume that your are looking for human data. Take a look at these papers:

Human Cancer Protein-Protein Interaction Network: A Structural Perspective

From the abstract:

  Protein-protein interaction networks provide a global picture of cellular function and biological processes. Some proteins act as hub proteins, highly connected to others, whereas some others have few interactions. The dysfunction of some interactions causes many diseases, including cancer. Proteins interact through their interfaces. Therefore, studying the interface properties of cancer-related proteins will help explain their role in the interaction networks. Similar or overlapping binding sites should be used repeatedly in single interface hub proteins, making them promiscuous. Alternatively, multi-interface hub proteins make use of several distinct binding sites to bind to different partners. We propose a methodology to integrate protein interfaces into cancer interaction networks (ciSPIN, cancer structural protein interface network). The interactions in the human protein interaction network are replaced by interfaces, coming from either known or predicted complexes. We provide a detailed analysis of cancer related human protein-protein interfaces and the topological properties of the cancer network. The results reveal that cancer-related proteins have smaller, more planar, more charged and less hydrophobic binding sites than non-cancer proteins, which may indicate low affinity and high specificity of the cancer-related interactions. We also classified the genes in ciSPIN according to phenotypes. Within phenotypes, for breast cancer, colorectal cancer and leukemia, interface properties were found to be discriminating from non-cancer interfaces with an accuracy of 71%, 67%, 61%, respectively. In addition, cancer-related proteins tend to interact with their partners through distinct interfaces, corresponding mostly to multi-interface hubs, which comprise 56% of cancer-related proteins, and constituting the nodes with higher essentiality in the network (76%). We illustrate the interface related affinity properties of two cancer-related hub proteins: Erbb3, a multi interface, and Raf1, a single interface hub. The results reveal that affinity of interactions of the multi-interface hub tends to be higher than that of the single-interface hub. These findings might be important in obtaining new targets in cancer as well as finding the details of specific binding regions of putative cancer drug candidates.

Tools for protein-protein interaction network analysis in cancer research

From the abstract:

  As cancer is a complex disease, the representation of a malignant cell as a protein-protein interaction network (PPIN) and its subsequent analysis can provide insight into the behaviour of cancer cells and lead to the discovery of new biomarkers. The aim of this review is to help life-science researchers without previous computer programming skills to extract meaningful biological information from such networks, taking advantage of easyto-use, public bioinformatics tools. It is structured in four parts: the first section describes the pipeline of consecutive steps from network construction to biological hypothesis generation. The second part provides a repository of public, user-friendly tools for network construction, visualisation and analysis. Two different and complementary approaches of network analysis are presented: the topological approach studies the network as a whole by means of structural graph theory, whereas the global approach divides the PPIN into sub-graphs, or modules. In section three, some concepts and tools regarding heterogeneous molecular data integration through a PPIN are described. Finally, the fourth part is an example of how to extract meaningful biological information from a colorectal cancer PPIN using some of the described tools.


You would be amazed at the vocal abilities of the lyrebird.  A car alarm is easy for them; they can mimic much more complicated sounds.

Here's a snippet from a David Attenborough BBC documentary on YouTube (which includes the car alarm example, among others).  They are so skilled, it's hard not to think this video is fake.


Origin of human intelligence and thought

How is

"we don't descend from any Chimpanzee or Orangutan because, if we did, they would also have the cognitive thinking ability that we have"

not equivalent to

"We are not related to the chimpanzee or orangutan because, if we did, they would also have [the same amount of body hair]/[the same sized mouths]/[the same muscular strength] that we have"

?

Any related species are going to differ in some respects (otherwise they would not be different species, after all), and it is plain to see that intelligence is one of the ways in which species can differ.

Regardless of that (if your friend thinks intelligence is special in a way that hairiness is not), you can make your argument even while sticking to talking about intelligence, and there is no need to go into the reasons for changes (increases) in intelligence to see that.

To make the point with your friend, it might be best to point to two different animals that

she recognizes as related, and that
she also recognizes as having different levels of "cognitive thinking ability".

In light of such an example, her argument falls flat (unless she further considers only human thinking ability special, in which case you will have a harder time!)


Can platypuses communicate via electroreception?

Electrocommunication is used by weakly electric fish only and it is limited to aquatic environments where the electrical conductivity of the medium allows to transmit electric signals. The best studied fish species that use this communication method are The African Mormyriformes (which comprise the Mormyridae or elephantfish and the Gymnarchidae with Gymnarchus niloticus as the only species) and the South American Gymnotiformes (or Neotropical knifefish).[1]

The mammals that are capable of electroreception use it for passive electrolocation which means locating the prey by detecting the weak electric fields of the prey with electroreceptors. These mammals are the three living species of monotreme; the Australian duck-billed platypus (Ornithorhynchus anatinus), the Australian short-beaked echidna (Tachyglossus aculeatus) and the Western long-beaked echidna (Zaglossus bruijnii) of New Guinea; and more recently discovered, the Guiana dolphin (Sotalia guianensis) from the cetacean order.[2][3]

Note: Electroreception was reported in star-nosed mole, Condylura cristata, based on limited behavioral data (Gould et al., 1993) but the theory remains unexplained physiologically.[4]

The electrosensory system of platypus (and probably other mammals) is evolved independently and the electroreceptors belong to the trigeminal system. The physiology of the electosensory system of mammals reveal why they can't use their electroreception for conspecific communication.

  In African mormyriform and South American gymnotiform fishes this sense has evolved to an additional active system using an electric organ as a source for a.c. impedance measurement of the environment and for communication. All electroreceptors found in fishes and amphibians that do not have electric organs are of the ampullary receptor type and probably form part of the acoustico-lateralis system. In contrast, the electroreceptors in platypus belong to the trigeminal system. Their sensitivity to d.c. as well as to high-frequency pulses [2] contrasts with the mostly d.c. or lowfrequency responsiveness of ampullary receptors, which are less well-adapted to detect rapid muscle action potentials.

  Langner, Gerald & Scheich, Henning. (2009). Electric Senses in Monotremes: Electroreception and Electrolocation in the Platypus and the Echidna. 1056-1060. 10.1007/978-3-540-29678-2_2919.
  https://www.researchgate.net/publication/299656487_Electric_Senses_in_Monotremes_Electroreception_and_Electrolocation_in_the_Platypus_and_the_Echidna

References:

1. Map of Life - "Electrolocation and electrocommunication in weakly electric fish"
http://www.mapoflife.org/topics/topic_578_electrolocation-and-electrocommunication-in-weakly-electric-fish/
January 24, 2018

2. Passive electroreception in aquatic mammals.
Czech-Damal NU, Dehnhardt G, Manger P, Hanke W.
https://www.ncbi.nlm.nih.gov/pubmed/23187861

3. Electroreception in the Guiana dolphin (Sotalia guianensis)
Nicole U. Czech-Damal, Alexander Liebschner, Lars Miersch, Gertrud Klauer, Frederike D. Hanke, Christopher Marshall, Guido Dehnhardt, and Wolf Hanke
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248726/

4. Edwin Gould, William McShea, Theodore Grand; Function of the Star in the Star-Nosed Mole, Condylura cristata, Journal of Mammalogy, Volume 74, Issue 1, 19 February 1993, Pages 108–116, https://doi.org/10.2307/1381909

Further reading:

1. Electroreception (edited by Theodore Holmes Bullock, Carl D. Hopkins, Richard R. Fay)

2. Neurobiology of Monotremes: Brain Evolution in Our Distant Mammalian Cousins
(edited by Ken Ashwell)

3. Sensory receptors in monotremes ( Proske U, Gregory JE, Iggo A.)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1692308/

4. Electroreception in monotremes (John D. Pettigrew)
https://jeb.biologists.org:2083/content/jexbio/202/10/1447.full.pdf

5. Perceiving in Depth, Volume 3: Other Mechanisms of Depth Perception (By Ian P. Howard)

6. Electroreception and Electrogenesis (James S. Albert and William G.R. Crampton) http://www.ucs.louisiana.edu/~jxa4003/Albert%20PDF%27s/Albert-Crampton-Electroreception-proofs.pdf


Does tremor frequency generally increase as Parkinson's disease progresses?

Frequency of tremor typically remains constant for the person. Levadopa (sinemet) does not change the frequency.

Typically the tremor frequency will be in the range from 3Hz to 7Hz.  There is a common phrase when dealing with PWP (Person With Parkinson's Disease). If you have seen one PWP, you have seen one PWP.

Currently I am part of a study by the Micheal J Fox Foundation using Pebble Watches and Smart phones to monitor PD.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1014720/
Hughes AJ, Daniel SE, Kilford L, Lees AJ (1992) Accuracy of clinical diagnosis of Parkinson’s disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry 55: 181-184.

https://blog.getpebble.com/2014/08/25/mjff-intel-parkinsons/


What are the mechanism binding histone code with alternative splicing?

According to literature, histone marks seem to be affecting splicing both directly and indirectly.

The indirect regulation appears to be due to biophysical hindrance, where a certain chromatin structure would cause Pol-II slowdown, allowing the splicing machinery to do its job.

The direct regulation seems to be essentially dependent on H3K36me3 and H3K4me1, marks that are recognized by MRG15, which in turn recruits the splicing regulator polypyrimidine tract-binding protein to splice sites.

Ref: Luco, R. F. et al. Regulation of alternative splicing by histone modifications. Science 4 Feb 2010


Where to find E.coli gene expression data?

There are some databases in which you can search for E.coli gene expression data:

GenExpDB: E. coli Gene Expression Database
Many Microbe Microarrays Database (M3D): A resource of microbial
gene expression data
Stanford MicroArray Database (use the search tool to find relevant organisms)
Colombos (COLlection Of Microarrays for Bacterial OrganismS)
ArrayExpress

To find out about the purpose and the conditions of the experiments behind this data sets you will have to read the respective publications.


Can a broken thumb/finger bone not require realignment of the bone?

Yes. You can figure that yourself if you look a bit at the types of fractures on Wikipedia, the Bone Fracture page:

  Other considerations in fracture care are displacement (fracture gap) and angulation. If angulation or displacement is large, reduction (manipulation) of the bone may be required and, in adults, frequently requires surgical care.

  [...]

  Other types of fracture are:

  Complete fracture: A fracture in which bone fragments separate completely.
  Incomplete fracture: A fracture in which the bone fragments are still partially joined. In such cases, there is a crack in the osseous tissue that does not completely traverse the width of the bone.
  [...]

Incomplete fractures and fractures with less or no displacement may heal correctly in some situations without needing realignment.


I think the asymmetry allows for a stronger selection process.  Sperm competition is a powerful force in evolution.

This is useful since sperm vary wildly in quality - for healthy human males only 50% might not be normally motile. Other animals can have a higher percentage, but there are always a significant number of floaters... This means that the fertilization via sperm takes out a lot of the less functional sperm.  Since these are in many cases the same genes we use as diploid organisms later, sperm competition really tames a lot of problems which might be produced in meiosis.

Many animals have multiple mating events from multiple males at just about the same time - when the female is in heat.  This gives a larger role for sperm competition - literally different sires are competing as sperm to fertilize the egg.

In females it is a different process of choosing the cells.  Ova are mostly eliminated in women by the time they reach reproductive age.  I think that this is not well understood biologically... references are hard to find.

The differences in the morphology and roles of the gametes, which goes back to the most primitive of animals has a strong role in selection of healthy offspring through a diverse set of mechanical and biochemical conditions experienced during fertilization.

Added Note: I ran across this reference for how ova are selected for presentation by the ovaries.  Its not really a review, but maybe a lead reference on how selection works in the female reproductive system - its also picky:

  In mammals, ovarian folliculogenesis is a process regulated by complex networks composed of various endocrine, paracrine and autocrine factors that interact coordinately.

Its no cake walk to being an egg either...


Difference between Trophic and Tactic movements

I think that you got a bit confused about terminology. In fact Chemotrophic is an organism that obtain energy by organic or inorganic molecules.
In your case I think that you want to know the difference between Chemotropism and Chemotaxis.
Chemotropism

Chemo-tropism is the growth of organisms (or parts of an organism, including individual cells) such as bacteria and plants, navigated by chemical stimulus from outside of the organism or organisms part [...]
An example of chemo-tropic movement can be seen during the growth of the pollen tube, where growth is always towards the ovules.

Chemotaxis

Chemotaxis (from chemo- + taxis) is the movement of an organism in response to a chemical stimulus.Somatic cells, bacteria, and other single-cell or multicellular organisms direct their movements according to certain chemicals in their environment. This is important for bacteria to find food (e.g., glucose) by swimming toward the highest concentration of food molecules, or to flee from poisons (e.g., phenol). In multicellular organisms, chemotaxis is critical to early development (e.g., movement of sperm towards the egg during fertilization) and subsequent phases of development (e.g., migration of neurons or lymphocytes) as well as in normal function.

Hence, to sum up (Chemo)taxis is the physical movement of a cell (or an organism) in response to a (chemical) stimulus, as done by the Antherozoids that are attracted towards Archegonia.  However (Chemo)tropism is the growth on organism toward a (chemical) signal, like done by Spermatophytes where pollen tube moves (so it growths) towards the Ovule.
Hope this explanation help you to clarify.


Can I figure out the identity of my grandparent from this information?

One of my potential grandfathers had blue eyes, so if it had been him my mother would have received two blue eyes genes and have blue eyes.

No, this does not necessarily follow, because eye color genetics are more complicated than just one dominant-recessive gene. See, for example this article from a someone at  Stanford University on How Blue Eyed Parents Can Have Brown Eyed Children. It isn't common, but apparently it does happen.

Solving your inheritance just based on eye color with 100 percent certainty is not possible.


Atmospheric gas changes, and their effects life

The Earth is blue (at least the non-land mass) because of the light our atmosphere refracts from the sun. A planets color is primarily determined by distance from sun, not from gas components.

Most gas does not refract light. Therefore a planet's gaseous composition can not be identified based on color.

To elaborate on your primary question, gas composition balance is essential to most life on Earth. Carbon dioxide, for instance, is responsible for photosynthesis occurring in plants. Different concentrations will affects photosynthetic rates. Another example is that CO2 levels, CO levels, and hexa-fluoro-carbons affect the amount of heat trapped in this planet.

Gas composition is highly delicate and must stay in balance to preserve life on Earth.


As MattDMo suggested, this is a hawk moth.  Given your location and season, this is why I thought it was either the Impatiens hawkmoth (Theretra oldenlandiae) or the  White-edged hunter hawkmoth (Theretra lycetus).  And finally, why I now think it is the Brown-Banded Hunter (Theretra silhetensis).
Brown-Banded Hunter Hawkmoth
The Theretra silhetensis exhibits a solid white line along the upperside of its abdomen, and more of a faded banding pattern on the forethat corresponds with your picture.  These moths are also common in India.

It is differs from T. oldenlandiae in being very much paler in color
and with white line down center of abdomen.

When it comes down to it, that solid single white line is the biggest indicator it is a T. silhetensis over a T. oldenlandiae or T. lycetus.

While my final answer is the brown-banded hunter hawkmoth, below are the original two species I suspected it was and why.  I've included them below simply for reference / alternative comparisons.
Impatiens Hawkmoth
Theretra oldenlandiae was my original instinct, since it is a more common in your area and the banding/stripe pattern matches to a T.

But, upon closer inspection, there are two things that don't quite align:

Your Specimen exhibits pink suffusion, especially on the back edge of the fore wing.
Your specimen has a single dorsal line, not two.

For these two reasons I think it is not the Impatiens Hawkmoth and thought it was more likely the...
White-edged hunter hawkmoth
Theretra lycetus is not as common on the T. oldenlandiae for your location, but the pink suffusion supports this idea.  See below for a picture:

This still doesn't explain the double vs. single white stripe along the upper abdomen.  Which is why I know believe it is the...

As an aside, this could be an example of polymorphism vs. identifying characters. Welcome to the world of taxonomic lumpers and splitters...


What is the difference between DNA vs RNA Editing in the context of gene therapy?

There are several differences, both mechanistically and functionally.

DNA edits are heritable by the daughter cells and are therefore permanent whereas RNA edits are not.
The type of Cas protein used in the editing process for DNA and RNA are different.
In the paper that you linked the authors have fused an RNA editing enzyme (ADAR) with dCas13 (a variant that does not cleave the target). So the CRISPR-Cas system directs ADAR to the sites on RNA that need to be edited. Usually when editing the DNA with CRISPR-Cas, people rely on the ability of the complex to cleave the DNA. This double strand break may be then repaired using different pathways (NHEJ and HR) during which editing happens. See these posts for more details:       How is the type of genetic manipulation determined in CRISPR-Cas9?       Mutations/deletions with CRISPR       How does NHEJ cause indels?
It is also possible to edit DNA in a way that does not involve cutting of the DNA. These techniques use similar principle as in the case of RNA editing described in the paper that you linked (see the abstract and introduction of this paper). However, if you cut the RNA, then it will be completely degraded instead of being repaired.


Creating a Phylogenetic tree using DNA sequences

There is no single mathematical measure of relatedness.

In the context of phylogeny, you need a model of evolution in order to be able to evaluate some relatedness between your strings of nucleotides. Then you would have various option for how to build a tree so that it reflects this relatedness. See for instance the wikipedia page about computational phylogenetics: https://en.wikipedia.org/wiki/Computational_phylogenetics.

Through what kind of historical process were your sequences generated ?
If there is no historical process underlying the generation of your sequences, then it is not meaningful to build a phylogeny with them. You can still define distances between them and use clustering techniques to build a tree, but that tree will not be a phylogeny.


Not in general -- there can be linkage disequilibrium among the loci. For instance, say that there are two di-allelic loci, $A/a$ and $B/b$, and that the frequencies of the $A$ and $B$ alleles are both $1/2$ and that they have the same effect on the trait, with no dominance. If all haplotypes in the population are either $Ab$ or $aB$ (with no $AB$ or $ab$ haplotypes), then the genetic variance at each locus is high, but the total genetic variance for the trait is 0!


NCBI E-utility to Find Shortest Citation Path Between Two Publications

I'm going to pursue Neo4j. Example usage, similar to what I'm looking for, is given here. (per a tip from the blog's author in response to my cross-posting on biostars)


What microscope/magnification would I need to observe P. Acnes bacteria?

I agree with canadianer that chemical tests are generally more useful for identification.  However, morphology does help and some staining techniques can be useful for identification (the Gram stain is the obvious one).  If you are looking for a microscope, look for a nice scope with a 100x oil-immersion objective and a 10x ocular lens (12x would be OK too). Zeiss, Nikon and Olympus are some old names that make good scopes - and there are more.


Identify this insect, found in Central Vietnam, with long antennae, black wings, and red body

This is a male scale insect, which are Hemipterans from the superfamily Coccoidea.

The one in your photo is probably from the Genus Drosicha. Here is the Wikipedia page for Drosicha corpulenta.

Here is an image, for comparison:

Here is another one, with black antennae, like yours:

There is no doubt that your specimen is a male because sexual dimorphism in Coccoidea is huge. Have a look at the females of Drosicha:

In conclusion, determining the exact species here is very difficult. However, we can be sure that the Genus of your insect is Drosicha.


What happens when the congenitally blind brain receives visual input?

Short answer
Congenitally blind people can regain visual function at a later age.  However, the longer they were blind for, the lesser their visual function will be and the longer it takes for them to rehabilitate. Immediately after receiving first eye sight, the visual experience of congenitally blind people is not comparable to that of normally sighted people. They may need months of rehabilitation training to make sense of their newly acquired sight, especially when they were blind for many years.

Background
There are various treatments for blindness to date. Since you mention technology in the question, visual prosthetics come to mind. Visual prosthetics already exist, and there are at the time of this writing two retinal implant systems commercially available; the Argus II and the alpha-IMS (Stronks et al., 2014). Retinal implants are used to provide a crude form of vision to those with severe retinal degenerations, such as end-stage retinitis pigmentosa. However, visual prosthesis technology is still in its infancy and at the time of this writing, only people that lost their vision later in life are implanted. So there is as yet no data available on your question whether congenitally blinded people can benefit from it.

However, from a related technology, cochlear prostheses, we know that the earlier a congenitally deaf person is implanted, the better the result is. Early-implanted folks can learn to understand speech, and develop speech relatively normally. Nowadays infants as young as 3 months receive cochlear implants. Early implantation is critical, because the brain is plastic. When the auditory cortex is not used due to sensory deprivation, it will quickly be taken over by other cortical areas. Once this cortical recruitment progresses for too long, a person can never gain functional hearing at the level reached by early-implanted people (Teoh et al., 2012).

Very likely the same holds for visual prosthetics. A congenitally blind person should be implanted as soon as possible after birth. This, because it is known that cross-modal plasticity results in the visual cortex being recruited for tactile and auditory processing. As with the auditory system, once this restructuring progresses long enough, my educated guess is that a person will never be able to develop functional vision comparable to an early implanted subject. And this is the reason why at present, only the acquired blind receive retinal implants.

For example, a case report of a subject who was blind for over 50 years regained his eye sight after corneal surgery. Although the subject did develop visual function after the surgery, visual performance remained greatly compromised. This was particularly evident when the tasks targeted finer levels of perceptual processing Siki et al., 2013).

Important clues are being obtained in the "Project Prakash", an ambitious project to provide opthalmological support to the people in poor, rural parts of India. Routine cataract surgeries have been performed in people with cataracts, including in people with congenitally present cataracts, where the lenses in the eyes were opaque from birth. Older kids, like teenagers, that were blind from birth typically show non-functional vision after the bandages are removed after surgery. It is thought that these first moments for the newly sighted are blurry, incoherent, and saturated by brightness, akin to swirls of colors that do not make sense as shapes or faces or any kind of object. However, after months of rehabilitation, they do develop functional vision. The lower-level markers of visual function never reach normal values. Specifically, they continue to suffer from poor visual acuity - the gold standard to assess visual function. Nonetheless, some higher-order aspects of vision do seem to be improving. Within a week to a few months after surgery, the children can match felt objects to their visual counterparts (source: The New Yorker, August 28, 2014).

References
- Siki et al., Iperception (2013); 4(8): 498–507.
- Stronks et al., Expert Rev Med Devices (2014); 11(1):23-30
- Teoh et al., Laryngoscope (2004); 114(9): 1536–40


Proteinuria is the presence of proteins in urine. Refractory means "persistent" or "stubborn", but in medical terms it means resistant to treatment or cure.


How can I purify RNA after gel electrophoresis to remove residual acrylamide?

If you don't want acrylamide in your preparation, don't use it, as you will always have some carry-over in the solution. And you will not get rid of it completely, as it at least partly co-precipitated with the nucleic acids (it's used as a co-precipitation agent for this purpose).

I think the best solution is to use chromatography, either size-exclusion or charged resins. See these two papers for more information:

Large-scale preparation and purification of polyacrylamide-free RNA
oligonucleotides
Rapid, non-denaturing RNA purification using weak anion-exchange fast
performance liquid chromatography


Are there terrestrial plants that thrive on sea water?

The University of California, LA mentions some genera and species of salt-loving plants (halophytes):

The genus Atriplex (Family Chenopodiaceae), saltbush, is found worldwide along saline shorelines. On the surfaces of the leaf are vesiculated trichomes (hairs). Each trichome has a stalk and a balloon-like tip, the bladder cell. The leaves use the bladder cells to excrete salt.

Coastal saltbush. Source: Enviro Active Australia.

Excreting salt glands occur in numerous unrelated plant groups, including grasses that live in alkali sink and salt pans and in warm temperate to tropical salt marshes (Sporoboleae, Chlorideae, and Aeluroideae (Family Poaceae)). These include such well-known tidal saltmarsh plants as the cordgrasses (Spartina alterniflora, S. patens), alkali grass (Puccinellia phryganodes), saltgrass (Distichlis spicata), and shoregrass (Monanthochloe littoralis). Short, two-celled trichomes have evolved as collecting chambers for salts, from which salts are excreted through tiny pores.

Cordgrass in the Chesapeake Bay. Source: Chesapeake Bay Program

Frankenia (Family Frankeniaceae) is a genus found both in coastal salt marsh and inland saline habitats. Saltcedar (Tamarix, Family Tamaricaceae) grows around the world in arid and semiarid regions. All of these taxa have salt glands, i.e., trichomes, in which salts are accumulated and excreted.

Several common mangroves secrete salts from leaves. So much crystalline salt can occur on the leaf of black mangrove, Avicennia germinans, that it appears whitish. Aegialitis annulata is a salt-excreting mangrove of Family Plumbaginaceae, a group in which other species are salt excreters in salt marsh and oceanside (Limonium and Armeria) or have chalk glands and live in dry, alkaline habitats.

Black Mangrove. Source: PlantDex.

Halophytic succulence is demonstrated in many genera of plants that inhabit saline environments, such as the mud flats of coastal salt marsh, but also is commonly observed on the leading edge of vegetation on coastal beaches, i.e., in strand vegetation. Common examples of succulence can be found in Family Chenopodiaceae: Allenrolfea, Arthrocnemum, Halimione, Nitrophila, Salicornia
Suaeda.

Succulence (fleshiness) also occurs in other famous and widespread species, such as Batis maritima, Sesuvium portulacastrum, Trianthema portulacastrum, and many Old World species of Zygophyllum. True succulents in the ice plant family, Aizoaceae, are also commonly found in saline habitats: Aizoon and Mesembryanthemum. By depositing salts in vacuoles, the toxicity is partitioned from the cytoplasm and organelles of the cells. As in Atriplex, salts are removed from the plant when the leaf of stem segment is shed.

Halophytic succulent Trianthema portulacastrum. Source: Altervista.

Among the halophytes, the seagrasses, which are submerged plants of shallow marine meadow, have salt tolerance, because the osmolality of cytoplasm is adjusted to match the osmolality of the seawater, so that desiccation of the plant does not occur. This contrasts the strategies of excluders and succulents, which are primarily salt avoiding mechanisms, attempts to reduce salt concentrations within the cytoplasm of photosynthetic cells.

As to why some shores may be devoid of plants, it may have to do with extreme temperatures, lack of nutrients, phytotoxic material etc.


How does decreasing surface tension of lipids help to emulsify them?

There appears to be either a typo or transcription error in your textbook.

According to this Nuffield Foundation and Royal Society of Chemistry article

  Molecules of most detergents and soaps are long chain hydrocarbon
  molecules with an ionic group at one end, usually carrying a negative
  charge, thus making it an anion. This charge is balanced by the
  opposite charge of a soluble cation, for example Na+. The long
  hydrocarbon chains do not interact well with water molecules, and many
  of them are effectively ‘squeezed out’ to the interfaces between the
  water and the air or the glass sides of the beaker. The effect of
  these molecules on the water surface is to considerably weaken the
  forces between water molecules there, thus lowering the surface
  tension.

Soaps, detergents, and bile (all examples of amphiphilic compounds) act to reduce the surface tension of water, not the lipids.


How to predict Protein-Protein Interactions from a pair of gene symbols?

This may or may not be possible, depending on what proteins you are considering. Generating a PDB file means predicting the structure of the protein. There are no methods for predicting protein folding accurately from plain sequence data, so you will need some experimental data on the structure of your proteins.

If your proteins have not been structure determined, the next best thing is some kind of homology model, that is, a prediction of your protein structure based on a known structure of a homologous protein. These can be more or less accurate, depending on how close the homolog protein is. If specific domains are interacting, it may be enough to create a model of the domain only.

There are online tools available for homology modeling, for example swiss-model from the expasy site. This is not an automated process though --- creating an accurate model requires some skills. You should read the publications describing these tools and make sure you understand the process and error souces, and perhaps contact an expert if in doubt. Good luck!


What makes a 'sense'? Is fatigue (tiredness) a sense?

To me, the defining characteristic of a sense is that it assimilates information from the external environment for your body to use if necessary. This is also the way the textbooks I've taught from treat it.  Thermoception senses external temperature, your body evaluates and, if need be, you take action. Equilibroception senses gravity to help you evaluate your orientation with respect to the Earth.

Proprioception is a hard one to categorize. Some of what is classified as such seem to rely on only internal sensors such as how much a muscle is stretched. Other aspects of proprioception rely on muscle tension which would indeed be affected by gravity and qualify proprioception as a sense by this definition.

I would say fatigue is not a sense because it is based on internal messages. How about a "sense of hunger"? I'd again say no, hunger is also the result of internal messages. Your sense of smell can lead to hunger but the information gathered was odor, not hunger.


What determines when a virus becomes a "new strain"?

I don't know if this is a comprehensive enough answer, but viruses are taxonomically broken down into order (-virales), family (-viridae), subfamily (-virinae), genus (-virus) and species. This system was developed by the ICTV and is concurrently used with the Baltimore System.

A lot of species contain variations called virus strains. There are two types, serotype and genotype.

In serotypes, the differences are detected by variation in antigens. Genotypes are detected by differences in genome sequence.(1).

The reason a vaccine is difficult to create for the common cold, or upper respiratory tract infections is not only because of the frequency of mutation but also due to the large number of serotypes present.(2),(3).

Virology: Principles and Applications - Carter.
Princuples and Practice of Infectious Diseases - Mendell, et al.
E.g. Olszewska, et al. Development of vaccines against common colds. Br Med Bull. 2002. 62(1):99-111.


How to generate simulated mass-spectrometry data for phosphorylated proteins?

I know this is a two years old question... but I recently developed a web application which could be useful for you:
Prot pi

The Protein tool lets you simulate the mass spectrum of the intact protein, while the Peptide tool gives you the fragment ions of peptides. Modifications can easily attached to every site you want.


The worker ants give water to the other ants in the nest. Also, they get most of their hydration out of the food anyway.
Here is a blogpost with some references and nice humour about it.


where to find the relative frequency distribution of synonymous codons

The phenomenon of using different codons with different probabilities is called codon usage bias. How the different codons are used is sometimes pretty different between species and requires some care. This is especially true when you want to overexpress sequences in bacteria to produce protein, which may need codon optimization to ensure an optimal codon usage (otherwise rare tRNAs can slow down the translation process). There is a database (based on the NCBI Genbank) which gives you the codon probabilities for different species:

Codon Usage Database

Additionally, these papers might be interesting:

Synonymous codon usage in bacteria.
An evaluation of measures of synonymous codon usage bias.

Regarding your second question, I don't think (and I haven't found any evidence either) that the codon usage is dependent on the neighbours.


why prokaryotic ribosomes have 30s and40s subunits and eukaryotic ribosomes have 40sand 60s subunits?

I think I can get the point after your second comment.

Not only protein composition, but rRNA composition and sequence length of Bacterial and Eukaryotic ribosome is very different. And the difference of sequence lengths (and hence mass) in both take part in the difference.


How do biological communities at deep-ocean hydrothermal vents migrate between vents?

I did some research on the topic and came accross this paper by Johnson et al. I am not a zoologist, so everything I write here is taken from the references paper.

The authors used genetics to estimate gene flow between different populations of limpets Lepetodrilus fucensis which is considered to be an endemic hydrothermal vent animal. They used a mathematical demographic model "isolation with migration" to estimate the migration of the animals across different biotopes.

The vents are distributed along the ridge segments and can be seen as small islands isolated by tens of kms from each other along the same ridge segment and thousands of kilometers between distinct ridges.

The results suggest that there is certain migration between the adjacent vent locations, that means that the flora of one vent can indeed survive the distance towards the next most proximal vent.

So, from now on is my pure speculation. Since the distance between single vents along the same ridge segment seems not be to so high we can suggest that these organisms are capable to resist the pressure and temperature on the ocean bottom while travelling from one vent to another...


Why does it hurt the next day after doing significant exercise?

Unlike the conventional wisdom, the pain you feel the next day (after a strenuous exercise) has nothing to do with lactic acid.

Actually, lactic acid is rapidly removed from the muscle cell and converted to other substances in the liver (see Cori cycle). If you start to feel your muscles "burning" during exercise (due to lactic acid), you just need to rest for some seconds, and the "burning" sensation disappears.

According to Scientific American:

  Contrary to popular opinion, lactate or, as it is often called, lactic acid buildup is not responsible for the muscle soreness felt in the days following strenuous exercise. Rather, the production of lactate and other metabolites during extreme exertion results in the burning sensation often felt in active muscles. Researchers who have examined lactate levels right after exercise found little correlation with the level of muscle soreness felt a few days later. (emphasis mine)

So if it's not lactic acid, what is the cause of the pain?

What you're feeling in the next day is called Delayed Onset Muscle Soreness
 (DOMS).

DOMS is basically an inflammatory process (with accumulation of histamine and prostaglandins), due to microtrauma or micro ruptures in the muscle fibers. The soreness can last from some hours to a couple of days or more, depending on the severity of the trauma (see below).

According to the "damage hypothesis" (also known as "micro tear model"), microruptures are necessary for hypertrophy (if you are working out seeking hypertrophy), and that explains why lifting very little weight doesn't promote hypertrophy.

However, this same microtrauma promotes an inflammatory reaction (Tiidus, 2008). This inflammation can take some time to develop (that's why you normally feel the soreness the next day) and, like a regular inflammation, has as signs pain, edema and heat.

This figure from McArdle (2010) shows the proposed sequence for DOMS:

Figure: proposed sequence for delayed-onset muscle soreness. Source:
 McArdle (2010).

As anyone who works out at the gym knows, deciding how much weight to add to the barbell can be complicated: too little weight promotes no microtrauma, and you won't have any hypertrophy. Too much weight leads to too much microtraumata, and you'll have trouble to get out of the bed the next day.

EDIT: This comment asks if there is evidence of the "micro tear model" or "damage model" (also EIMD, or Exercise-induced muscle damage). First, that's precisely why I was careful when I used the term hypothesis. Second, despite the matter not being settled, there is indeed evidence supporting EIMD. This meta-analysis (Schoenfeld, 2012) says:

  There is a sound theoretical rationale supporting a potential role for EIMD in the hypertrophic response. Although it appears that muscle growth can occur in the relative absence of muscle damage, potential mechanisms exist whereby EIMD may enhance the accretion of muscle proteins including the release of inflammatory agents, activation of satellite cells, and upregulation of IGF-1 system, or at least set in motion the signaling pathways that lead to hypertrophy.

The same paper, however, discuss the problems of EIMD and a few alternative hypotheses (some of them not mutually exclusive, though).

Sources:

Tiidus, P. (2008). Skeletal muscle damage and repair. Champaign: Human Kinetics.
McArdle, W., Katch, F. and Katch, V. (2010). Exercise physiology. Baltimore: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Roth, S. (2017). Why Does Lactic Acid Build Up in Muscles? And Why Does It Cause Soreness?. [online] Scientific American. Available at: https://www.scientificamerican.com/article/why-does-lactic-acid-buil/ [Accessed 22 Jun. 2017].
Schoenfeld, B. (2012). Does Exercise-Induced Muscle Damage Play a Role in Skeletal Muscle Hypertrophy?. Journal of Strength and Conditioning Research, 26(5), pp.1441-1453.


Which are the best apps and websites for insect identification?

There are not many beginner-friendly apps that I am aware of. However, there are a few websites you can use.

BugGuide has a relatively nice picture-based search system. You will also gradually learn to easily identify various characteristics of an insect, thus making your search easier.

Insect identification is more beginner-friendly and more suitable to your kids.

You can also ask either here, or perhaps in the reddit community if you have trouble identifying a particular bug.

If they become interested I would recommend searching your local book store or library for a good field guide (depending on your location). Entomology can be a fun excuse to get out of your house and learn something in the process.


We found a very similar skull on a beach near Richardson Bay, Lasqueti BC. Decided it was a seal skull (locals agreed)
See harbor seal skull: http://www.skullsunlimited.com/record_species.php?id=4726


Is every neurotransmitter receptor an ion channel?

is every neurotransmitter receptor also an ion channel?

No.

There are two general types of receptors for neurotransmitters, ligand gated ion channels and receptors that activate second messenger systems, for example, G protein coupled receptors. They are sometimes referred to as ionotropic and metabotropic receptors. This figure from Principles of Neural Science, Ch. 10 illustrates the difference nicely:


What does the term "relay competent" mean?

If you read the lines immediately following your quoted line (on p.391, left column, last paragraph in the linked article) it becomes clear what relay competent means (and I quote):

  As a result, the cells sense and move toward a source of cAMP, and they relay the signal as well by secreting cAMP. [..] After about 8 h of starvation randomly located cells, called pacemakers, begin to emit cAMP periodically (Raman et al. 1976), the chemotactically competent cells move toward these pacemakers, and eventually the entire population forms a mound-shaped aggregate of up to 105 cells.

In other words, starvation makes cells move toward cAMP by chemotaxis, and  makes them secrete cAMP as well, which factually relays the cAMP signal back to other cells that are also attracted to cAMP due to starvation.


Has the human body the greatest total length of nerves of all animals?

There is no reason to believe that total nerve "wiring" (or combined length) does not increase with the size of the animal, although the number of neurons in the brain (and the number of connections they make via dendrites) matters as well.

Animals with long necks, legs and tails have long nerves. Ancient sauropods may have had the longest nerves (referring not only to nerve bundles but single neurons) in history. Their brains were not as large compared to their body size, however, as humans.

But whales - the largest animals on earth - do have larger brains. Modern cetacean brains are among the largest in both absolute size and in relation to body size of all mammals. The brain of an average adult sperm whale weighs 8 Kg; by comparison, the average adult human brain weighs about 1.3 Kg.

Blue whales are the largest animals in existence today. With a large brain (3.6 Kg) and a long body, I can't see a particular reason to believe that the total amount of "wiring" in a blue whale doesn't exceed that present in a human.

[Normal weight of the brain in adults in relation to age, sex, body height and weight]
Normal organ weights in men: part II-the brain, lungs, liver, spleen, and kidneys.
Cortical complexity in cetacean brains


What is the difference between "gene delivery" and "gene therapy"?

Citing wikipedia:

Gene delivery is the process of introducing foreign DNA into host cells.
Gene therapy is the therapeutic delivery of nucleic acid polymers into a patient's cells as a drug to treat disease.

In other words, 'gene therapy' refers to the use of 'gene delivery' for therapeutic goals.


Is it possible to consciously increase or decrease your own heart beat?

Yes, you can decrease your own heart rate very simply by stimulating the vagus nerve in what are called 'vagal maneuvers'. If you stick your thumb in your mouth, wrap your lips tightly around your thumb, and blow on your thumb like you are blowing up a balloon, you will stimulate the vagus nerve and decrease HR. This technique is often used clinically, and is termed the 'valsalva maneuver'. The vagus nerve runs posterior to the oropharynx. Blowing on the thumb increases pressure in the chest cavity and stimulates a parasympathetic response. Another technique is carotid sinus massage, which works in a similar way, by modulating vagal tone. Many other techniques exist. Another is the result of the 'mammalian diving reflex', which slows heart rate in response to immersing the face in cold water.

Vagal maneuvers https://en.wikipedia.org/wiki/Vagal_maneuver

Carotid sinus https://en.wikipedia.org/wiki/Carotid_sinus

Carotid sinus massage http://www.ncbi.nlm.nih.gov/pubmed/3985038

http://medical-dictionary.thefreedictionary.com/carotid+sinus+massage

Vagus nerve https://en.wikipedia.org/wiki/Vagus_nerve

Valsalva maneuver (see section on heart, where tachycardia means high heart rate) https://en.wikipedia.org/wiki/Valsalva_maneuver

WebMD on decreasing HR http://www.webmd.com/heart-disease/atrial-fibrillation/tc/vagal-maneuvers-for-a-fast-heart-rate-topic-overview


How to replace intron region in a plasmid?

Your strategy would work, but if possible you might be better off using XmaI rather than SmaI, as the latter is a blunt-end cutting enzyme.
Furthermore, your strategy would not replace the entire gpdA promoter, if that's what you're after. You might wanna refer to their paper, where it's clear from Fig. 1 that the promoter region is much longer than the region between SalI and SmaI:


Are genotypes with the same two alleles equivalent even if the alleles come from different parents?

If you have genomic imprinting then $k^n=m^2$ (with k=m and n=2 because of diploidy) is correct as inheriting a from the father and b from the mother (i.e. ab) is not equivalent to inheriting b from the father and a from the mother (i.e. ba). For 3 alleles (a,b,c) you have 9 possible genotypes (aa,ab,ac,ba,bb,bc,ca,cb,cc).

Under no genomic imprinting, ab and ba are equivalent. This is equivalent of calculating the number of elements of a triangular matrix which is $\frac{(m+1)*m}{2}$. So for m=3, you have 6 possible genotypes (aa,ab,ac,bb,bc,cc), for m=4 you have 10 possibilities (aa,ab,ac,ad,bb,bc,bd,cc,cd,dd) etc...

I hope this helps. Your formula is actually equivalent.


How closely related are two parasites Giardia intestinalis and Trichomonas vaginalis?

Basically, Giarda is a an Excavates while Trichomonas is a Cercozoa meaning a Rhizaria (Chromealveolates in the broad sense as noticed by @har-wradim in the comments (now deleted) because Cercozoa are neither Chromista nor alveolata). Because the very basis of the tree of eukaryotes is still unresolved (eukaryotes), the most recent common ancestor of these two species is just an old eukaryote! In other words, these two species are not more closely related than are related a cat and a chestnut tree!

The links yield to Tolweb.org which shows you the phylogenetic tree and allows you to explore the relationships between organisms. Have a look to eukaryote tree especially to see the positions of the Rhizaria and Cercozoa.


What is the role of a chemotroph in an ecosystem?

Chemotrophs are usually found in extreme environments where they can be the source of all energy for the ecosystem also called the primary producers. Deep-sea hydrothermal vents are a great example of a chemotroph primary producer and support the growth of large eukaryotes like the tubeworms (Below). The chemotrophs supporting life at the vents can oxidize Sulfur to create ATP.

But chemotrophs don't just have an impact on these small ecosystems, they are actually responsible for earth-scale geochemistry affecting all life. (Cool paper on that here). The reason why chemotrophic bacteria are usually not found in "normal" environments with algae is simply competition. A heterotroph using hydrocarbons will occupy a niche faster and more efficiently than any chemotrophic bacteria.
You are definitely right on the Mars soil question, where chemotrophic bacteria could be used to fix carbon or nitrogen and solubilize nutrients for future plants on mars. But maybe some cool chemotrophs are already living there!


What are differences between formation of embryonic disc in chick and mammal embryo?

Embryonic disc forms on top of yolk during cleavage on chicken embryo, while between amniotic sac and yolk sac inside blastocyst after implantation on human embryo.

Some further processes take place on and in the embryonic disc: specifically these here during the week 3.

Embryonic disc formation includes still during the 3rd week of development:

Formation of the primitive streak
Genesis of the germ layers
Genesis of the notochord

Formation of the primitive streak: The process of primary neurulation appears to be similar in chick and mammalian. The embryonic disc becomes oval and then pear-shaped, the wider end being directed forward. Near the narrow, posterior end, the primitive streak makes its appearance and extends along the middle of the disc for about one-half of its length from migrated ectoderm cells.

Genesis of the notochord: “The notochord extends beneath the neural tube from the base of the head into the tail.” - As the mesoderm develops between the ectoderm and endoderm it is separated into lateral halves by the neural tube and notochord.

Figure 2: Neurulation. NB the use of neural groove is correct. Notochord is below neural groove. - Genesis of germ layers here: from a flat thing to a developed one.

Figure 3: Genesis of notochord and primitive streak. Yolk-sac surrounds notochord and primitive streak.