Can humans ever directly see a few photons at a time? Can a human see a single photon?

A single molecule of rhodopsin (actually the cis-retinal bound to it) can and actually does react to one photon (Purves et al. Chapter: Phototransduction in Neuroscience).

  It has been estimated that a single light-activated rhodopsin molecule
  can activate 800 transducin molecules, roughly eight percent of the
  molecules on the disk surface. Although each transducin molecule
  activates only one phosphodiesterase molecule, each of these is in
  turn capable of catalyzing the breakdown of as many as six cGMP
  molecules. As a result, the absorption of a single photon by a
  rhodopsin molecule results in the closure of approximately 200 ion
  channels, or about 2% of the number of channels in each rod that are
  open in the dark. This number of channel closures causes a net change
  in the membrane potential of about 1 mV.

Photoreceptor cells continuously secrete the neurotransmitter glutamate in dark; with light exposure glutamate release would reduce. This leads to activation of the next line of cells (bipolar, horizontal cells and retinal ganglion cells).

   Modelled relationship between glutamate release and rod membrane potential.  From Witkovsky et al. (1997).

From this model (Witkovsky et al. 1997) it appears that for a change in glutamate release rate, a larger change in membrane potential is needed. Moreover, the depolarization of the photoreceptors has to be sustained for a while so that downstream cells can react (light absorption is much much faster than biochemical processes). The lifetime of an activated rhodopsin molecule is ~40ms in mice (Gross and Burns, 2010) and ~400ms in salamanders (Lyubarsky et al., 1996). We can assume that human eye is more similar to that of mice. There are approximately 40,000,000 molecules of rhodopsin in a rod cell (BioNumbers). The most sensitive of retinal ganglion cells need ~0.04% of rhodopsin molecules per rod cell to be activated (Takeshita et al., 2017).

  (b) Absolute threshold of On and Off retinal ganglion cells

  Both On and Off RGCs carry rich information about the weakest light
  signals. Off cells are somewhat more sensitive than On cells but have
  a higher error rate in their gap-based coding. The absolute threshold
  for primate On and Off parasol cells in a two-alternative
  forced-choice task is extremely close to the limits posed by the
  quantal nature of light: On parasols reach 75% correct choices at a
  light level corresponding to approximately 0.0008 R* per rod per flash
  (mean, n = 6) and Off parasols at a light level corresponding to
  approximately 0.0004 R* per rod per flash (mean, n = 5).

A single activated rhodopsin molecule would be 0.0000025% of the total. This would be insufficient to activate an RGC.

So, I can make a reliable guess that you cannot actually "see" a photon although one of the retinal photoreceptor cells can sense it. However, I'm still looking for a solid reference that says how many photons are needed (and for how long) to produce a visual response.


Why HIV need integrase enzyme to integrate their DNA into host cell?

During gene transfer by microinjection the DNA has at least some fragments of identical DNA sequence to the host genome. Usually DNA that is used for microinjection will have flanks on either side identical in sequence to two nearly situated, sometimes adjacent blocks of DNA sequence. This allows homologous recombination to occur which engages proteins already present in the host cell: https://en.wikipedia.org/wiki/Homologous_recombination

In case of HIV, there are no fragments of identical sequence flanking the genome of the virus, so no homologous recombination can occur, therefore integrase is necessary. Furthermore, integrase inserts viral genome into random parts of the host genome unlike homologous recombination, which would always localize that viral genome into the same spot each time.

Now, this is my wild guess, as I couldn't really find any evidence in the literature but I'd say it gives the virus certain advantage. Site-specific insertion could be easily inhibited in the course of evolution by mutations within the host genome and eventually the virus would be eliminated. This is not the case with random allocation, as no mutations in the host genome will ever substantially change the probability of integration.

Here is a good review on the process of DNA integration regarding HIV: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3385939/

Let me know if this helps, confront your opinions with what I think.

Cheers,

Krzysztof


As Christiaan already pointed out, this depends on the pharmacokinetic and pharmacodynamic parameters. The effective drug concentration depends on the drug-receptor association constant and the drug degradation constant (for a highly simplified model). The degradation/removal depends on the abundance of the enzyme catalyzing this reaction.

Ethanol is primarily thought to cause intoxication by activation of GABAA receptors. However, only a very specific subclass of these receptors are activated at the levels of alcohol that one consumes during "social/moderate" drinking. Others require very high alcohol concentrations (Hanchar et al., 2006). Basically alcohol is not a very specific agonist/antagonist of any neurotransmitter or neuromodulator receptors. In other words, it does not have high affinity to any of these receptors. There is no answer to "why". I would guess that since ethanol is a very common molecule (and is also used as energy substrate by some organisms, to a certain extent), high sensitivity to ethanol would have been evolutionarily selected against.

  Although many proteins show changes in their function at very high
  alcohol concentrations (>50 mM), the molecular basis for behavioral
  alcohol effects at low to moderately intoxicating doses experienced
  during social alcohol consumption remains elusive (1). GABAA receptors
  (GABAARs) and the inhibitory GABAergic system have long been suspected
  to be targets for acute alcohol effects (2–4). For example, the GABAAR
  agonist muscimol potentiates the sedative actions of alcohol, whereas
  the opposite effect, a reduction of ethanol (EtOH)-produced sedation,
  is detected with the GABAAR blockers picrotoxin and bicuculline (5).
  Although most GABAAR subunit combinations can be activated by high
  (anesthetic) alcohol concentrations (6), only very specific GABAAR
  subunit combinations (containing the δ as well as the β3 subunit)
  exhibit dose dependencies that mirror blood alcohol levels that are
  associated with mild to moderate intoxication in humans (7, 8) (≈3–30
  mM, because the legal drinking limit is 17 mM or 0.08%).

  From Hanchar et al., 2006

Other psychoactive drugs are highly specific and have high affinity to their corresponding receptors. For example, caffeine acts on the adenosine receptors at µM concentrations (Daly et al., 1983). This is because of caffeine's high affinity to these receptors.

Moreover, ethanol is readily metabolized to acetyl-CoA by alcohol dehydrogenase and aldehyde dehydrogenase enzymes which are quite abundant in the body. Some people who have mutations in these enzymes leading to their reduced activity, "get drunk" and experience hangovers even with a low level of alcohol consumption.


This is a beetle from the family of the "longhorned beetles", since you found this beetle in India, I think this is Acanthophorus serraticornis

See the images for comparision (from here and here):

There is not much information online, but some can be found here and especially  here in this scientific article. The larvae of this beetles are considered a pest, as the bore into wood.


Is there an example of a species wherein the female lays eggs in the male?

Yes.

Pipefish & Seahorses to name two.

Both widely mentioned in many wildlife programs as being an example of what you've asked.


How do t-lymphocytes become mature if thymus has lost its function?

A few points, I'll expand on this later and add references if I have time:

The thymus starts degenerating at puberty but continues to function in thymocyte maturation for decades, albeit at a lower level
Many mature T cells can live for years
Through homeostatic proliferation, peripheral T cells maintain their population size
Immune surveillance generally decreases with age

Note that extended lifespans and homeostatic proliferation (points 2 and 3) don't contribute to TCR diversity but only maintain the existing repertoire.


What did we learn with Nazi human experimentation?

Basically nothing.  The Nazis did unfathomably terrible things of little value, and they did it poorly.

This* is a fascinating, albeit long, read.  It goes through some of the ethics of the data, but first lists some more of the "experiments" the Nazis performed.  To add to your list: high-altitude, sea water potability, tuberculosis, poisoning, artificial insemination, and numerous woundings.  They also did terrible things to twins.  Aside from being torturous and cruel, the "experiments" rarely if ever used anesthetics and were usually designed to kill the prisoner.

The article goes on to list a few case studies where some of the Nazi works came up and could have been considered, but were repeatedly shot down.  It then details a number of reasons why the "experiments" were worthless.  In particular,

"[I]t is doubtful that physiological responses of the tortured and maimed victims represented the responses of the people for whom the experiments were meant to benefit."
Nazi "researchers" were racists who were looking to validate their own beliefs.  No good science comes from that.
The results weren't ever actually published.
The "data" are inconsistent.

The article moves into ethical arguments and hypotheticals, but ends up saying theoretically some of it could be considered, or that "Absolute censorship of the Nazi data does not seem proper, especially when the secrets of saving lives may lie solely in its contents."  It's a complicated scenario where that would arise.

Editing a few years later to add this discussion from the NY Review of Books.  It's a little removed in tone, and is over-generous as regards the intent of the Nazi torturers, but makes the interesting point that one good thing to come out of the experience was the first codified guidelines for human experimentation:

  As part of the judgment, the court issued the celebrated Nuremberg Code in 1947—the first, shortest, and in many ways most uncompromising of the major ethical codes and regulations for the conduct of medical research on humans. Although the code had no legal authority in any country, it had great influence on ideas about human experimentation, and subsequent international codes and legislation.

In particular, the concept of "informed consent" is directly traceable to the Nuremberg Code:

  The first provision of the Nuremberg Code is unqualified: “The voluntary consent of the human subject is absolutely essential.” No exceptions are permitted... Furthermore, the code is clear that consent must be given by subjects who are fully informed.

*I should note that the article is from a Jewish law website, so some may discount that as not a perfectly neutral source.  Which is silly.


Does the second law of thermodynamics cause aging?

Second law of thermodynamic and ageing

The second law of thermodynamic applies to closed system. Organisms are not closed system. The second law of thermodynamic is a fundamental principle of our universe and any biological processes do follow the principles of physics. However, stating that biological ageing is (partially) caused by the second law of thermodynamic suggests a big misunderstanding of what the second law of thermodynamic is.

To have a better understanding of the second law of thermodynamic, check up the wikipedia article or one of the many other sources of information on the subject and ask questions on Physics.SE if needed.

Ageing and its evolution

The evolution of ageing (or senescence) is a big subject and has already been subject of a large number of questions on Biology.SE. Have a look at the questions tagged . Below are two examples of post that will interest you:

Why do we age? or Do we have a theory of senescence?
Why does evolution not make our life longer?

There is also a wikipedia page on the evolution of ageing.

Note btw that biological immortality and negligible senescence do exist.


Why do depleted blood veins seem to appear near the surface (or skin) more frequently than blood vessels and arteries?

Short Answer:

The veins you see are special veins right at the surface; major arteries are typically much deeper in the tissue.

Longer Answer:

Great question. Usually veins and arteries come in more or less one-to-one pairings, traveling side-by-side (often nerves accompany them as well). Both types of vessels tend to be fairly deep, because, as you note, damage to blood vessels can be quite problematic.

However, superficial veins, the ones you can typically see right under the surface of the skin, are different. They don't have a direct artery pairing, and they are not the only venous drainage from the areas distal to them.

Instead, superficial veins have a known purpose in temperature regulation. When core temperature is high, the superficial veins are relatively dilated to allow temperature exchange between the blood and outside. When core temperature is low, the superficial veins constrict to cause the blood to flow deeper and retain heat.

A nice side benefit to these superficial veins is that, because they aren't completely necessary for circulation, they can be harvested as surrogate vessels to divert around a blocked artery, like in coronary artery bypass grafting. The saphenous vein from the leg is often used. Superficial veins can also be removed for cosmetic reasons.

References

Webb-Peploe, M. M., & Shepherd, J. T. (1968). Responses of the superficial limb veins of the dog to changes in temperature. Circulation research, 22(6), 737-746.


Welcome to Biology.SE!

About your title

Let me first react to your title: Viruses selected by evolution.

Evolution is any process of genetic (and eventually phenotypic) change in a population through time. Selection (Natural Selection for example) is one of such process. Genetic drift is another such process. So, evolution doesn't select viruses unlike your title suggests. Viruses are selected and therefore evolution occurs. When saying "viruses are selected", it means some viruses have a higher fitness (fitness is a function of both survival and reproductive success) than others.

Species interactions

Generalities

Species interact. Species actually interact a lot. One can classify species interactions into categories. Here is a table of possible biological interactions (comes from wiki), where a + indicates "beneficial", a - indicates "detrimental" and a 0 indicates it has no effect on fitness.

Note about symbiosis - comes in reaction to @Gerhard's comment

Different authors use the word symbiosis differently. From wikipedia:

  The definition of symbiosis is controversial among scientists. Some believe symbiosis should only refer to persistent mutualisms, while others believe it should apply to any type of persistent biological interaction (i.e. mutualistic, commensalistic, or parasitic).4 After 130+ years of debate,5 current biology and ecology textbooks now use the latter "de Bary" definition or an even broader definition (i.e. symbiosis = all species interactions), with the restrictive definition no longer used (i.e. symbiosis = mutualism)

Blurry limits

Generalities

It may seem pretty obvious that two species should have either one type or another type of interaction. However, the reality is often more complicated than that. An interaction might fall under one set of environmental conditions and fall under another category under another set of environmental conditions. In addition to that, it is not uncommon that due to selection on the host genes due to the presence of a parasite, the host evolve so to tolerate the presence of the parasite up to the point of actually having a lower fitness in the absence of the parasite.

Example

Parasites often have different life cycle of alternance of generation. That is a parasite sometimes need several hosts such as the parasite causing malaria for example that need both mosquitoes and a primate.

Consider for example a snail which is infected by a parasite. Let's assume (I think it is a real world example but I am too lazy to find out a reference) that the parasite need the snail to be eaten in order to reproduce in the body of the predator. In order to improve the chance of its host to be eaten the parasite is selected so to diminish the thickness of the snail's shell. In response to that, there is selection (which intensity depend also on the proportion of infected snails in the population) for having thicker shells. But now, snails that are not infected have shells that are so thick that the can't move as fast as they'd need to forage. So, by the end infected snails may have a higher fitness than non-infected snails. And therefore the interaction between the snail and its parasite is not a parasitic interaction anymore but a mutualistic interaction.

Can viruses have non-parasitic relationship with their host?

Well... why not? There is nothing so fundamental about viruses that would prevent them to have mutualistic relationship with their host. Actually I am aware of a few relationships. For example, female parasitoid wasps (parasitoids: parasite that kill their host). parasitoid wasps lay their egg in other insects larvea (host), the egg (and later the larvea I think) develop in the larvea (host), eat the larvea (host) and once the host is dead, the individual metamorphose to its adult form and fly away to find a mate a parasite the next larvea. Some lineage of those wasps have viruses in their ovary that infect the host to reduce the immune defence of the host to protect the growth of their egg (Flemming and Summers 1991). This is an example of mutualistic relationship between the wasp and the virus.

Sequencing to know if the plants are infected

You said

  they collect samples of plants and somehow by analyzing their DNA notice that these plants are all infected by some kind of virus

Most likely, they make a PCR (amplification of DNA, that is increasing the number of copies of a given DNA sequence) on viral DNA and look for a signal. In other words they are not sequencing (=reading) the plant DNA but only seeking for viral DNA. If they find viral DNA, then the plant is infected if not, the plant is not infected.

What is unclear to me from your text

From your post, it is unclear to me yet how your "family member" plans to decide the type of interaction there are between viruses and plants. Knowing the frequency of infected plants won't tell you much about the interaction between the plant and the virus.

They will likely have to make growth experiment and try to measure the fitness of infected and non-infected plants.

EDIT - Following the first comment

Knowing that every plant individual is infected doesn't tell much of the virulence of the virus. The frequency of infected is not an information that can help understand the "type of biological interaction" (paratism, mutualism, etc..). One will need to actually make growth experiment and measure fitness (or measure phenotypic traits that are known to be good proxy for fitness).

  One question about your answer is : can we really speak of a virus as a species and especially does your table really apply in this situation ?

The concept of species is not a natural category. It is a man-made, unclear, sometimes useful, category. Typically, it is hard to even talk of species for organisms that don't have sexual reproduction (which is the case of viruses). I wrote this other answer today about the concept of species, you may want to read it. Here is another post on the subject. Btw, talking about semantic issue, viruses are often not considered as alive. All those semantic issues don't have any impact on our understanding of biological processes.

But yes, the table applies to viruses as well. This table is indifferent to the concept of species. Consider just two genotypes (two individuals), one plant and one virus, the existence of the virus has (or has not) an impact on the fitness of the plant (and vice-verse) and therefore, you can classify the relationship between those two genotypes (individuals) into one category of the table. As a reminder, the nature of those relationship may depend on the environment. Typically, a photosynthetic endosymbiote might be very beneficial to the "host" if there is some sunlight but might be quite detrimental in the absence of sun light.


Identification of Bug/Insect (with picture)

It is a cockroach, probably a German cockroach nymph.

Cockroaches are well-known pests. According to the Wikipedia link above, there are about 4600 species of cockroaches, 30 of them are associated with human habitats. Cockroaches are extremely resistant and are able to survive in a wide range of environmental conditions.

@PhysicalFatness pointed out that German cockroach nymphs look very much like your picture and it is likely the species that you've found. Don't be fooled by its name German cockroaches are found all over the world, not only in Germany.


What are the differences in ultrastructure of cilia and flagella?

Perhaps you mean that flagella spin to provide locomotion whereas the cilia tubules themselves beat.  the flagellar motor vs the fixed anchored structure of the cilia...


Microwave ovens can indeed kill bacteria in food by heating them to high temperatures. For example, this article found that microwave heating could kill all of the Salmonella bacteria in a chicken thigh sample:

  The effect of microwave heating on Salmonella Enteritidis inoculated
  on fresh chicken was investigated using a microwave oven (800 w) to
  determine the destruction of Salmonella Enteritidis isolated from
  chicken carcasses, in relation to the time of heating at two power
  settings: high (power level 10) and medium (power level 6); The
  relationship between heating time and temperature was also been
  studied. The destruction was 6.4 log cycles at time 95 sec for the
  high power level, and 5 log cycles at time 140 sec for medium power
  setting. After 110 sec for higher power level, no survival of
  Salmonella Enteritidis was detected in samples (100g), but at 140 sec
  for medium power level, these food pathogens were still present.

However, the main issue is balancing the amount of microwave exposure. Heating the food for too long will result in the food becoming dehydrated or burned, and heating it for too short a period of time will result in food poisoning.

This paper shows that insufficient microwave exposure can and will lead to food poisoning if there is a large amount of bacteria inside the food:

  Leftover samples of a savoury rice dish consumed by all six ill
  persons contained 6×103/gm Salmonella enteritidis PT4. The rice salad
  comprised boiled rice, raw carrots, eggs, cheese and curry powder. The
  curry powder and remainder of the pack of six eggs were negative on
  microbiological analysis. The rice dish had been prepared by heating
  in a 500 W microwave oven with a rotating turntable on full power for
  5 min.


What is the adaptive significance of temperature dependent sex determination?

To my knowledge, it is still mainly unclear what are the enviromental factors that would promote Environmental Sex Determination (ESD; incl. TSD) vs Genetic Sex Determination (GSD; incl. with and without sexual chromosomes).

Environment variability and Climate change

Generally speaking it is thought that in variable environment, GSD might be more beneficial as an ESD mechanism could lead uneven sex-ratio and hence lower fitness (Pen et al., 2010).

Climate change can be very detrimental to species that use ESD. A sudden climatic change can cause a population to have a highly biased sex-ratio to the point where persistence is not possible anymore (Boyle et al., 2014).

Differential fitness variance among sex

On the other hand, ESD can allow parents to decide the sex-ratio of their offsprings (Randy, 2005).

Consider for example a case where sexual selection lead to a much high variance in fitness among, say, males than among females. Note that parents fitness and offspring fitness is correlated (because an obvious genetic correlation but also because some environmental correlation). In such case, parents that have a low fitness would prefer to produce females (that despite being unhealthy / ugly will still manage to have a decent fitness) while parents with high fitness would prefer to produce males (because very healthy / good looking males will have a very high fitness).

Charnov and Bull model

In Charnov and Bull (1977) own words (taken from their abstract)

  We propose that labile sex determination (not fixed at conception) is favoured by natural selection when an individual's fitness (as a male or female) is strongly influenced by environmental conditions and where the individual has little control over which environment it will experience. Our argument also applies to sex expression in hermaphrodites

According to wikipedia, there are a number of evidences for this model in the literature. I let you go through the cited papers for more information about what is the logic behind this hypothesis!

Evolutionary constraint

Changes in sex determination systems has not evolved that many times (in Reptilia at least; Jansen and Phillips, 2006; see this post for definition of Reptilia). It can be hypothesized that there might be a strong evolutionary constraint (see also phylogenetic signal) and hence looking for adaptive reasons for its evolution might be a moot point.


Is there any kind of immortality in plants?

I can find no examples of immortal plants, but then again immortality is rather hard to prove, it's rather like trying to prove that space will never turn in to a pony - as long as time exists it could still occur, only if you go beyond the end of all time would you be able to say that it has or has not happened but then time would no longer exist and nor would space/the pony.

However, for examples of long lived plants it is perhaps best to look at trees - there are some species that live a long time and they can easily be aged. Here is a list of oldest known trees. It is difficult to tell how old these trees can become, and thus whether they are "immortal", because anything that lives that long is likely to encounter sources of extrinsic mortality during it's lifetime - predation, deforestation, extreme weather, erosion, natural disasters, contaminants, humans, disease, parasites etc. (rather than intrinsic dying of old age).

A lot of plants go through some kind of apoptosis, where cells are programmed to die. Plants such as annuals, biennials etc. die after a few months or years in a programmed way. It is difficult to say whether long lived species of trees would do the same after a few thousand years of life, because we just don't get to see many reach that stage of life, or if the mechanisms causing it have been suppressed (which could explain their long life).

Luke has posted a very thorough answer on the cellular and genetic aging of plants here. And to quote him:

  "...it seems to me likely that plants may also have enhanced maintenance
  against other cellular stresses than DNA damage, such as build-ups of
  aberrant proteins. It therefore appears that in a protected
  environment some plants could live indefinitely"

Wikipedia has some very good pages on the evolution of senescence & aging. This article has also a good section on plant aging and I hope you can access it.

and finally, if you want to have a laugh, take a look at this entry on plant immortality and aging from creationwiki.org...

  "Plants are actually or potentially immortal organisms that will live
  indefinitely provided their environmental requirements are met. In
  striking contrast to plants, humans and animals have a maximum life
  expectancy regardless of whether their needs are fulfilled. Although
  it is true that some plants grow as annuals, all plants are actually
  perennials by nature, and have adapted to a programmed life cycle in
  some instances to match growing seasons. Otherwise, plants only die
  because of biochemical starvation or disease. If their physical
  requirements are met, plants will grow indefinitely."

Some great clear science there, well done creationists... but it's just plain wrong.


Cyanobacterial photosynthetic oxygen yield

This is a study on the O2 production rate of one of the fastest growing species of cyanobacteria. The theory is not just someone's idea, it's a conclusion made from trends which were discovered during the course of conducting countless experiments.


Does the formation of water inside the mitochondrial matrix help contribute to the proton gradient during the electron transport chain?

Your description of it is largely correct, but the electron transport chain does not simply "dump" charged oxygen ions in the mitochondrial matrix. Instead, cytochrome C oxidase (complex IV) binds the O$_2$ molecule to one of its heme groups, and the reduction O$_2$ + 4 H$^+$ + 4 e$^-$ $\rightarrow$ 2 H$_2$O occurs at the heme group before water is released. Some more details on the enzyme is found here and here (or in any biochemistry book).

In theory you're right that producing water in the mitochondrial matrix would dilute the H$^+$ concentration there a little (along with the concentration of everything else). But this dilution is negligible: the mitochondrial matrix has pH $\approx$ 7.8, which is the same as a H$^+$ concentration of about 15 x 10$^{-9}$M, while the concentration of water (yes, there is such a thing ;) is 55 M. So adding a water molecule has virtually no effect compared to removing a proton.


Pink growth (aka pink slime) in bathtub or shower

I live in St. Louis, MO and get this in my bathtub over time, but not in my other sinks. I actually think @Christiaan is correct here, but with a few additional observations:

I don't think it's bacteria. When dry, it's not slimy, nor does it grow back quickly when wiped away. It feels much more like a mineral deposit.
It was no longer pink when using a different shampoo. Upon returning to an older brand, the color returned to pink.
It's only directly around the drain, it isn't on the walls or anywhere else.

These lead me to think it's a mix of mineral deposits from the hard water and potential reactions with certain soaps/shampoos, at least in my case. These are only based on my own observations though, there very well could be a pink bacteria/fungi that tends to inhabit damp areas.


Why have parasites not evolved to be harmless?

There are actually many examples of viruses that have integrated into the human genome and were rendered harmless, perhaps even helpful.

This New Scientist article referencing this Nature article describes endogenous retroviruses, which are ancient viruses which have integrated into the human genome.

  About 9 per cent of our genome is thought to have come about this way.
  Until recently, these viral relics were largely dismissed as inactive
  “junk” that ceased to have any impact on their host many thousands of
  years ago. The discovery that HERVK, the most recent ERV to make
  itself at home in our DNA – probably around 200,000 years ago – is
  active in human embryos challenges that notion.

  Joanna Wysocka and her colleagues at Stanford University in California
  made the unexpected find while they were analysing gene activity in
  3-day-old human embryos, which are bundles of eight cells. Besides DNA
  from the parents, they found genetic material from HERVK. “The cells
  were full of viral protein products, some of which had assembled to
  form viral-like particles,” says Wysocka.

  Further experiments revealed that the virus appears to produce a
  protein that prevents other viruses penetrating the embryo, suggesting
  it protects the embryo from dangerous circulating viruses, such as
  influenza. It also seems to play a crucial role in the genetic
  activity of the embryonic cells, helping to genetic instructions to
  the cellular protein factories.

Additionally, the endosymbiotic theory is also another possible example. It is thought that mitochondria and chloroplasts are previously free-living, possibly parasitic organisms that ended up integrating into the host cell and living as an organelle.

In short, parasites absolutely can and do evolve into harmless versions of themselves. There are already discovered examples, and as the human genome is better understood, doubtlessly more would be discovered.


Through which mechanisms did the Drosophila Histone Cluster evolve?

This is the best review I have seen with a comprehensive discussion on gene duplication and amplification mechanisms (and it is also quite recent). It seems like there may be no definitive answers to your question in the literature--perhaps because of a paucity of viable experimental models that would allow one to test various hypotheses.

Also @canadianer is quite correct. Most metazoans with sequenced genomes have some kind of clustering of their histone genes (as well as multiple copies). In Drosophila embryogenesis the early zygotic cell-cycles are extraordinarily brief, on the order of 20 min as I recall, which means the fertilized egg is essentially a bag of DNA polymerase replication complexes.  Therefore there is a very high demand for histone proteins.  The gene amplification you describe is one way to achieve high concentrations of histones in a short time-frame.

Note that not all metazoans undergo this rapid burst of synchronous nuclear division, and therefore not all species have such a high copy number of core histone clusters.


Can mitochondria with "depleted" mtDNA reproduce?

Can mitochondria with "depleted" mtDNA reproduce ?

If by depleted, you means reduced number of mtDNA copies, then yes, as long some copies still remain, these can be replicated.

Mitochondrial genome is replicated asynchroneously from nuclear genome [Bogenhagen, 1977], through a particular process (review [Holt, 2012]), and is present in multiple copies. These copies can be different, due to mutation.

Mitochondria do not "reproduce" in the common sense, as they do not undergo mitosis, but have a fission and fusion mechanism (review [van der Bliek, 2013]). The fission products get their half of the mtDNA copies at random when the two mitochondria separate.

Mitochondria with depleted mtDNA can (and do, according to your image) undergo fission.

  passing on the damage from breaks in the DNA?

There are DNA repair mechanisms for the mitochondrial genome. In this case, the mechanism of choice to repair double strand break is  microhomology-mediated end joining (MMEJ) [Tadi, 2016], that try to align the ends of the DSB through use of 5-25 bp homologuous sequence. This ususally results in the deletion of some material near the break.

The resulting mutation is conserved, and passed on through replication of this particular mtDNA instance. The mitochondria will contain a mix of mutated and non-mutated mtDNA from now on.

  Or is the mitochondria and cell doomed?

One could say a particular mitochondria is "doomed" if there is no [viable] copy of mtDNA; if it is not able to maintain adequate internal membrane potential, it will try to fuse with other working mitochondria, or be eliminated through autophagy/mitophagy.

The cell itself could be "doomed" if there are not enough mitochondria left to meet energetic demands. (or, through mitochondria-induced aptotosis). Some particular human cell type have hypersensibility to fluroquinolones (tenocyte, chondrocyte, osteocyte), with increased cell death, but other types have not manifested this behaviour. [Barnhill, 2012] The reason for this sensibility/resistance is not elucidated.


What is the term for a given interpretation of a fossil record?

The term you are looking for is reconstruction (as in
Forensic facial reconstruction).

You can find it used on the wikipedia articles for Fossil cave and for Transitional fossil or in the post In reconstructions, how are various shapes of facial features determined from skull only? for examples.


Why do people cut back on kilo-calories?

The calorie is a unit of energy. Our body uses the energy found in food to create ATP (a molecule that is handy to deal with energy) with the help of oxygen (that we breath in). ATP can then be used for plenty of tasks such as importing ions through a cellular membrane or more ultimately walking, talking, warming up your body, etc...

Saying that some food contain 100 calories (not kilo-calories) does not mean that it will heat up 100 grammes of our body water by one degree (Celsius). It only means that we are ingested the same amount of energy than the one that is needed for warming up 100 grammes of water by 1 degree (Celsius).

You might to have a look at CrashCourse video on ATP and respiration.


I've been working on fruit flies now for 7-8 years, including a lot of large mating and courtship assays. I believe what you are seeing is the male (identifiable by the black end of the abdomen and different shape) approaching a female. Judging by the extension of the male's right wing in the second still image, he is making a brief courtship attempt, but its very difficult to be certain of that from these images. The female then extends her ovipositor.

I believe that this could be one of two things:

A mate rejection behaviour by females - she actively made the movement to stop the males advances
The female was simply preparing herself for oviposition - the male just happened to approach her

I've seen it happen enough times both with females subject to courtship and females not subject to courtship to think that either of those is plausible for what is happening in your clip. Given the possible courtship by the male and the following text & videos from a recent paper I would say it is option 1, a mate rejection.

  "Recently mated females reject courting males through a variety of actions such as decamping, flicking their wings, kicking the approaching male, or extrusion of the ovipositor [8]. Thus, copulation switches female behavior from acceptance to rejection." - Kimura et al. 2015

and

  "Under natural conditions, the recently mated female occasionally extends the ovipositor straight along her body axis (anterior-posterior axis) toward the courting male (Fig 1A, S1 Movie), who usually positions himself behind the female [21]. During the ovipositor extension, the female abdomen was width-compressed throughout its entire length. We refer to the ovipositor extension as mating-type extrusion when it was protruded horizontally along the female body axis. A mated female that has found a suitable site for oviposition will lower and bend her abdomen downward and insert the ovipositor into the substrate before performing movements to expel an egg that is inserted into the substrate (Fig 1B, S2 Movie) [9]. Unlike the extrusion for rejection, the female narrowed the abdomen only at its posterior part." - Kimura et al. 2015

In figures S1 and S2 you can see those two behaviours very clearly in videos.

Note, I came to my answer before finding this Kimura paper so that's two lines of independent evidence (my experience and their paper). I hope it answers your question.


Is there a comprehensive database of fossils (with images) online?

No. Museums are the traditional repository for fossils, and the process of "digitizing" their collections is slow and labor intensive. Often, the museums only aim to digitize what me might call the "meta-data" associated with the fossil, as was done here:
http://ucmpdb.berkeley.edu/cgi/ucmp_query2?admin=&query_src=ucmp_index&table=ucmp2&spec_id=V8111&one=T

A truly comprehensive database is not feasible in the near future. A single photograph likely would not be sufficient to characterize the fossil -- the interesting components of fossils are often microscopic. For example:

http://www.pnas.org/content/99/14/9117.full.pdf

Even taking a single photograph can be very labor intensive, and fossils can be fragile. Proper photo-documentation would probably require multiple images. More generally, a comprehensive database would probably need to include non-photographic data relating to the fossil -- such as chemical composition of non-visual imaging techniques (X-ray, IR, UV, etc).

For the foreseeable future, "comprehensive" collections will be housed in museums without full digital representation. The only way to know how comprehensive these collections are is to ask the museum curator, who will be aware of the scope and limitations of the collection.


How is the growth of benign tumors suppressed?

The primary difference between a benign tumor and a malignant tumor is that the former cannot metastasize; therefore they remain within the tissue boundaries.They grow slowly and are are not very de-differentiated thereby retaining some of the tissue organization.

Another point to be considered is that benign tumors do not cause vascularization (formation of blood vessels in the tumor tissue; triggered by secretion of VEGF), which also limits its growth.


What does the term 'modified residue position' in phosphorylation mean?

You are correct, the 368 stands for the position of the amino acid in the protein's sequence - this particular serine is the 368th residue in the protein counting from the amino-terminal end.


This is a "click beetle" (Coleoptera, Elateridae). They have this name because of the loud click sound they produce. They are related to fireflies (Lampyridae), and some click beetle species are themselves luminescent.

According to the link above:

  A spine on the prosternum can be snapped into a corresponding notch on the mesosternum, producing a violent "click" that can bounce the beetle into the air.

I don't know about those North American beetles, but in South America I've seen click beetles jumping more than 30cm in the air.

Here is a photo of a click beetle in Montreal, from the Pest Control Canada website, which looks like your specimen:

Unfortunately, the entomologist that identified the animal in the photo above didn't narrow it down to Genus or Species.


Does the amplitude of action potentials vary among species?

Does the amplitude of action potential in animals differ from the amplitude of action potential in humans?

Surprisingly, they don't!

The current model that's used to describe biophysical neurons is the Hodgkin-Huxley model, and one of its fundamental assumptions is that, action potentials (APs) are electrical events consisting of a large transient change in membrane polarization (typically around 100 mV). (source)

The reason for this can be seen when quantifying the absolute value of peak conductance during an AP, specifically when considering the average membrane resistance with respect to peak conductance. The following graph is from the original publication by Huxley & Hodgkin, just here, and it illustrates this principle.

This model applies to virtually all excitable cells, and therefore, AP amplitude values aren't specific to the organism. Consider the following table which lists AP measurements amongst various animals, and pay notice to the values in the highlighted column. As can be seen, amplitude values remain fairly consistent across all animal types, hovering right around 100mV. (source)

And then, regarding humans, just as you stated, the resting potential of a neuron is ~ -70mV. When excited, the membrane potential rises to ~ +30mV.

  Most cells in the body make use of charged particles, ions, to build up a charge across the cell membrane. ... The exact value measured for the resting membrane potential varies between cells, but -70 mV is most commonly used as this value. ... The change in the membrane voltage from -70 mV at rest to +30 mV at the end of depolarization is a 100-mV change.

(source)

If you're well versed in math, you can directly compute the ~100mV change in membrane potential using the Goldman/Hodgkin/Katz equation, given that inter & extra cellular ion concentrations are known.


What role does a protein's size have on protein-protein interactions?

Protein interactions occur mostly (if not all) through residues that are on the "surface" and exposed to the milieu in which they exist, be it cytoplasmic or extracellular. So, a naive thought would be to guess that a greater surface area means a greater swathe of exposed regions and probable interacting parts. One protein can bind many others, even simultaneously, through different such interaction surfaces. However, other factors also determine whether a given set of two proteins interact, most important being where they localize in a given cell. If one protein is nuclear but the other on the plasma membrane, it is highly unlikely that they ever interact even if thermodynamics highly favors complex formation. Interaction between two proteins also depends on their respective conformations, which can further be regulated by events such as post translational modifications (eg., phosphorylation by a kinase), bound nucleotide state (eg., GTP vs GDP in a G protein). Last, scaffolds can also sequester and organize protein clusters together spatially and increase the probability of them interacting. All put together, I think it is highly unlikely that just looking at 3D surface area of a protein will say much about its "interactability" with other proteins.


Are there diseases for which a placebo treatment is state of the art?

Doctors sometimes use "open-label placebos" - substances that have no known physiological effect on the treated disease, but have been associated with symptoms improvement in some studies. Open-label means doctors openly tell people it's placebo. The example is treatment of irritable bowel syndrome.

Doctors use not only fake drugs, but also real drugs as placebos. There are some doctors who don't have a courage to say they don't know how to help, so they just prescribe "something" (a real but ineffective drug) in the hope they will convince someone that they provided some help.

Prescribing "placebo treatments": results of national survey of US internists and rheumatologists (BMJ, 2008)

  Prescribing placebo treatments seems to be common and is viewed as
  ethically permissible among the surveyed US internists and
  rheumatologists. Vitamins and over the counter analgesics are the most
  commonly used treatments. Physicians might not be fully transparent
  with their patients about the use of placebos and might have mixed
  motivations for recommending such treatments.

There is a common practice to prescribe:

Vitamins or antibiotics for common cold, flu and other viral infections (Montana DPHHS ; JRSM Open)
Antipsychotics, antidepressants and sedatives for personal problems that can't really help to solve those problems
Various drugs for fibromyalgia

The seeming effect of placebo can discourage a person to seek for the real treatment.


How do I find samples/patients in TCGA (the cancer genome atlas) that had radiation therapy?

The process is slightly painful but here is how you do it.
Go to UCSC Xena, then launch the browser, hit the Visualize tab, pick your cohort of interest, then in the next menu pick phenotype, and then type radiotherapy in the box and pick the radiotherapy related columns you want. Then, once it has loaded the annotation bar, you can hit download and the downloaded spreadsheet will have this information along with the TCGA barcodes. As for clinical data, https://www.synapse.org/#!Synapse:syn7343873/wiki/412112 is a very good pancancer source.


Could the proteome of E. coli be fluorescently labelled?

One at a time, you could potentially label all of them.

If you're asking how many proteins you could label at once, your biggest limitation is probably your microscope. In order to distinguish between different types of proteins you need different color fluorescent labels (dyes, fluorescent proteins, etc). Even the fanciest fluorescent microscopes tend to be set up to excite/record labels in <10 distinct wavelengths.

In practice I've only seen experiments where there were tracking 3 distinct types of proteins at one time.


Is the PCT of the nephrons of the kidneys of marine vertebrates to minimize the natural tendency for exosmosis?

First off, I agree with @WYSIWYG - marine life has adapted to conserve water, not electrolytes. Osmosis in sea water draws water from the body and hence their problem is to keep the water in, not the salts.

Osmoregulation in marine mammals is accomplished mainly via differences in hormonal regulation of the kidneys. The histology and morphology of the kidneys are different, but the adaptations have more to do with adaptations to diving/pressure than anything else. Instead, most marine mammals take care not to drink too much sea water and obtain their water from metabolism and foods (Ortiz, 2001).

Reference
- Ortiz, J Exp Biol (2001); 204: 1831-44


Vitamins — how did they get their names?

They were more or less named in the order that they were found.  Letters F-J are skipped because many of those were reclassified or later found not to be vitamins.  The K comes from the German word for Koagulation because the vitamin is involved in the coagulation of blood.

The discovery dates of the vitamins and their sources /
Year of discovery   /Vitamin    Food source

1913 Vitamin A (Retinol) Cod liver oil
1910 Vitamin B1 (Thiamine)   Rice bran
1920 Vitamin C (Ascorbic acid)   Citrus, most fresh foods
1920 Vitamin D (Calciferol)  Cod liver oil
1920 Vitamin B2 (Riboflavin) Meat, dairy products, eggs
1922 Vitamin E (Tocopherol)  Wheat germ oil, unrefined vegetable oils
1929 Vitamin K1 (Phylloquinone)  Leaf vegetables
1931 Vitamin B5 (Pantothenic acid)   Meat, whole grains, in many foods
1931 Vitamin B7 (Biotin) Meat, dairy products, eggs
1934 Vitamin B6 (Pyridoxine) Meat, dairy products
1936 Vitamin B3 (Niacin) Meat, grains
1941 Vitamin B9 (Folic acid) Leaf vegetables
1948[42] Vitamin B12 (Cobalamins)    Liver, eggs, animal products

There are many different B vitamins, water soluble, because many vitamins previously given different letters where later found to be part of the B complex. For example H is now B7.  Additionally, many letters, such as P, are no longer classified as vitamins.

More information can be found on this Wikipedia page.


What is the expected effect of pH on the activity of a fungal pectinase?

I actually doubt that the pectinase has such a broad pH range in which it works optimally. Searching the web I found two figures which support my doubts:

The first is from an article ("Immobilization of pectinase by adsorption on an alginate-coated chitin support") which compares the activity of native and immobilized pectinase under different conditions. The second is from the datasheet of a company which sells the enzyme. Both show an activity over 50% roughly between pH 3.5 and 5.5 but not at higher or lower pH values.


Why people still die after eat them even boiled to 100 oC, but why?

Well not all toxins are protein based. Some are just small molecules that fit into some vital protein in your body, causing  it to stop and death not long later. Some are cyclic peptides and are not denatured by heat. The peptide is simple, and has many carbon bonds to stablize its structure (it is a ring and has carbon bonds linking internally) https://en.wikipedia.org/wiki/%CE%91-amanitin

  Or is there any absolute temperature and time to kill most type of protein ?

Autoclaving.. 134 °C (274 °F) for 18 minutes in a pressurized steam can destroy prions. And prions pretty tough. https://en.wikipedia.org/wiki/Prion


These are not gene ids, but groups of orthologous genes -- try to search for the ids on Google, I can find this page http://cegg.unige.ch/orthodb6/fasta.fasta?ogs=EOG6STSR2&swaptree= and thus you should be able to download the sequences and ids from OrthoDB.

Note that, strictly speaking, the are no Ensembl ids for Drosophila, only FlyBase ids that are also used by Ensembl.


How many virus infections does the average human have?

Ignoring short-term (acute) viral infections, so only considering persistent viruses, probably on the order of 5-10-ish.  There are 8 human herpesviruses known, of which 6 (herpes simplex I, EBV, CMV, VZV, HHV6, and HHV7) are very common in humans, generally infecting 50-90% of a population.  There are over 50 strains of human adenoviruses, but only a few are very common and persistent; hAb2 and hAd5 are probably the most likely.  Then there may be a human papilloma virus or two persistently infecting many people, though the prevalence is lower than herpes or adenoviruses.  So, it's reasonable to assume that most people have somewhere around 5-10 persistent viral infections.

If you add in acute infections, and ask about all exposures during one's life, you're probably looking at thousands or tens of thousands of viruses, but the questions about what's a different virus and what's an "infection" become trickier.


Why do Mangoes have a single large seed, and not multiple small ones?

It is an interesting question and it applies to other fruits with big seeds as the avocado as well. It is very likely that these fruits evolved to be spread by large animals (like big birds or large mamals) which existed for a relatively long time, but are extinct today. These animals swallowed whole fruits and excreted the seeds afterwards (most of these seeds are slighty laxative) together with dung to support the growth.

They are called "evolutionary anachronisms" and there is a very interesting book about them, called "The ghosts of evolution: nonsensical fruit, missing partners, and other ecological anachronisms." (which can be found as a PDF online)
Two interesting articles about this phenomenon can be found here:

The Trees That Miss The Mammoths
Anachronistic Fruits and the Ghosts Who Haunt Them


Is there any reason to use an upright microscope over an inverted microscope?

As already mentioned in the comments, cost is one of the primary reasons when you're looking at simple light microscopes. Inverted scopes have more complex optics, along with the convenience factor of being able to examine larger samples, generally having a more stable frame, etc. All this leads to higher cost.
An advantage I can think of for smaller upright scopes is the ability to use them as a dissecting scope, where the sample is opaque and you need to see it from above. Another advantage is this:

Many fluorescence microscopes are upright, as there is a significant amount of extra equipment that needs to be mounted in addition to the eyepiece, including lasers, stage motors, and cameras and other detectors. This can take up a lot of room, and for convenience's sake it's often easiest to mount it up top where it is accessible.


What is the most recent non-primate ancestors of humans?

According to the Tree of Life, tree shrews (Scandentia) are the sister group to Primates. So Scandentia are the most closely related extant mammals that are not Primates. Here's an image:


Alternatives to trypsin for cell detachment?

Lets make this a proper answer: There are a few possibilities to detach adherent cells without Trypsin.

PBS/EDTA: Integrins and Cadherins play an important role in the adhesion and also in maintaining cell-cell contacts. These function of these proteins depends on Calcium2+ ions, so EDTA will chelate them and make them unavailable. First remove the culture media, rinse the cells with warm PBS to get rid of most ions and then incubate them for 5 min (the time needs to be optimized for each cells line) in PBS with 10mM EDTA in it. The cells either detach themself, can be washed of the surface with a pipette or can be gently knocked off the surface (this works only in tightly closing flasks). Centrifuge the cells shortly to pellet them and get rid of the PBS/EDTA and take them up in fresh medium.

Wash cells of the surface: Some cell lines are so loosely attached (which makes working with them pretty hard), that they can simply be washed off the surface. To do so, use the pipetboy to get some medium and then pump it out again against the cell layer. You can see the cells disappearing from the surface and the medium (or the PBS) get more cloudy.

Knock off cells: To do so, you take the flask with medium in one hand and knock it gently 4 or 5 times against the palm of the other hand. The cells should come off then and can be centrifuged down to separate from the medium. Alternatively you could replace the medium first and then knock them off. This method is not recommended for very sensitive cell lines.

Besides these methods, there are a number of commercial products available which claim to be better than the classical Trypsin/EDTA method and to be less harmful for the cells. Since I haven't tested them, I cannot say anything about them. In my experience Trypsin and the methods described above work perfectly.


What is the chemical composition of an egg shell?

It's the same stuff that makes up most sea shells, calcium carbonate, $CaCO_3$.

Incidentally, this explains why egg shells dissolve in vinegar (acetic acid which, since it is an acid, provides the Hydrogen ions in the reaction below):

$CaCO_3+ 2H^+ -> Ca^{2+} + H_2O +CO_2$

This simple reaction (which is what would happen in your stomach as well) produces water, calcium ions and carbon dioxide, none of which are particularly harmful.

The specific reaction with acetic acid is

$CaCO_3 + 2CH_3COOH → Ca(CH_3COO)_2 + H_2O + CO_2$

which also produces calcium acetate.

Anyway, there is nothing particularly toxic about $CaCO_3$, it's basically chalk. I wouldn't recommend eating a lot of it but you shouldn't freak out if some falls into your omelet either.

However, don't forget that an egg has exited a chicken's anus (well, cloaca) so their shells are likely to have come into contact with feces and they are porous so they are not necessarily the cleanest thing around. This is just not because of any chemical toxicity.


Read "supply" as "carry action potentials to." When the action potential reaches the junction with the muscle (i.e., the neuromuscular junction), neurotransmitters are released into synapse. A similar membrane depolarization occurs on the muscle cell, ultimately leading to contraction.

Nerves visible to the naked eye are actually bundles of individual axons (hundreds, thousands, or tens of thousands of axons). Nerves have the appearance of branching because the individual axons that travel to muscle fibers don't all go to one muscle.

For example the oculomotor nerve branches:

So what you see as the oculomotor nerve is really a collection of neurons. Some of these carry action potentials to the ciliary muscle and some to the sphincter pupillae. These are the parasympathetic components. There is a completely separate set of neurons (but still contained in the same nerve) that carry signals to the extraocular muscles.

This is really basic material that your professor should have explained to you.


How does Line Integrate work on a laser scanning confocal microscope?

Most microscope software provides options for line average or line integrate as a function that helps the signal to noise ratio when taking an image.

Averaging sums the lines and then divides by the average number. Integration sums the lines without dividing.  They're functionally the same thing just with different scales.

  I assume it involves summing pixel intensity and operating on that somehow, but it simultaneously is able to reduce noise in the system so I am not sure what else it is doing.

In terms of shot noise, both have an equal reduction.  If you are averaging over extremely dim signals at low gain (particularly those averaging less than 1 DN per pixel), integration can save you signal from being rounded down to zero.


There is previous research for that field of macroevolution.... Horse shoe crabs change slowly and tropical fish change fast.

You are right, it's not just random variation, it's fine tuned by DNA transcription processes which are too developed to be random, so the complexity of the processes leads scientists to think "WTF" regarding epigenetics, transgenerational phenotypic plasticity, paramutation, genetic drift, DNA mutation types, Specifically: "no systematic cross species studies of variation have been conducted (most focus on model organisms)", because the topic is so intense.

You don't have to change the DNA code of alleles to go from a chimpanzee to a human, most of the changes come from pre-existing genes that are varied to produce different results.

The texts for macroevolution fine-tuning of variability talk about: variability, gene flow, constriction, epigenetics, of traits of adaptive significance, of DNA mutations, their mathematical measurement... it can be summarized by this statement:

" variability has been a dilemma of evolutionary biology. Considering the pattern of increased genetic variation associated with environmental clines and heterogeneous environments, selection in heterogeneous environments has been proposed to facilitate the maintenance of genetic variation. No comprehensive models have been developed, likely due to the genetic and environmental complexity of this issue. " ref

Many books are devoted to the subject, so there is lots to read through, and there are mutation-control systems that fine tune variability, so it gets complex:

"... Epigenetic modifications, such as; DNA methylation, together with covalent modification of histones, are thought to alter chromatin density and accessibility of the DNA to cellular machinery, thereby modulating the transcriptional potential of the underlying DNA sequence" ref

There are genetic switches, which vary which DNA sequences are expressed by different species... Humans and chimps are 98% the same, and genetic switches can change the species selectively without having to change the DNA itself... "regulates when and where genes are turned on and off and how much protein they produce. The regulatory machinery works when proteins called transcription factors bind to specific short sequences of DNA that flank the gene, called transcription factor binding sites, and by doing so, switch genes on and off." ref

sharks ahve less less variability than humans and 1.5 times bigger genome...
"The researchers found that the white shark genome contained a lot of genes responsible for maintaining genetic stability — things like DNA-repair genes and tumor-suppressing genes. And when the researchers compared the white shark's stability genes with analogous genes in other vertebrates, they found small changes in the gene sequence that suggest a specific pattern of evolutionary adaptation for these genes in white sharks."

Only a few epigenetic processes for transgenerational epigenetic inheritance have been discovered, which vary species traits independently of the DNA sequence, so we don't even know how they compare between animal families.


Are there any examples of proteins with no or minimal sequence identity, but highly similar structure?

This paper published last year, address the answer for your question, about computational methods, they mention 3 principal algorithms for structural alignment
of proteins:

Structural alignment directly at the level of C atoms.
The second class of algorithms first uses the SSEs (Secondary Structure Elements) to carry out an approximate alignment, and then uses the C atoms.
The final class of algorithms uses geometric hashing.

And finally you could find useful this paper for an example of this kind of analysis with structural analyses of metabolic families.

References:

 Venkateswaran JG, Song B, Kahveci T, Jermaine C. TRIAL: a tool for finding distant structural similarities. IEEE/ACM transactions on computational biology and bioinformatics / IEEE, ACM 8: 819–31.
 Marsden RL, Ranea JAG, Sillero A, Redfern O, Yeats C, Maibaum M, Lee D, Addou S, Reeves GA, Dallman TJ, et al.. 2006. Exploiting protein structure data to explore the evolution of protein function and biological complexity. Philosophical transactions of the Royal Society of London Series B, Biological sciences 361: 425–40.


What is an adjective that describes the property of conferring fitness?

Terms

A trait variant that is associated to a higher fitness than another variant is said to be beneficial or sometimes adaptive. On the other hand, a trait variant that is associated to a lower fitness is said to be deleterious or sometimes maladaptive.

"beneficial / deleterious" vs "adaptive / maladaptive"

The terms are very similar but I would tend to think that there are tendencies of using either "beneficial / deleterious" or "adaptive / maladaptive" depending upon the specific context.

These terms can also be used when talking about genetic variants and not only phenotypic trait variants. In evolutionary genetics, the terms "beneficial / deleterious" are used more often than "adaptive / maladaptive".

Also, in general, the terms "adaptive / maladaptive" are often used in absence of variation for the trait in question in the population while the terms "beneficial / deleterious" are most often used when there is variation in the population.

Note

Note that trait X is a trait that confers fitness does not make much sense as is explained here.


Why does drinking milk lead to increased fractures?

The authors suggest a reason in their abstract:

  Given the observational study designs with the inherent possibility of residual confounding and reverse causation phenomena, a cautious interpretation of the results is recommended.

There are variables they haven't measured that lead to the observed patterns. A simple one is that the respondees to the initial survey are self-selected (they return the survey). What if milk-drinkers are more likely to respond? Even if the base rate of fractures remains the same, then there will be an apparent association of fracture with milk consumption.

They also discuss physiological reasons, which is the subject of a different answer.


Are there any parasites that alter human behavior in a self destructive way?

There is a link established between Candida and Aspergillus fungal infections and mental illness of schizophrenia and depresssion. Over prescriptions of antibiotics and use of antibiotics in cattle ranching, subject people to excessive antibiotics. This causes a die off of natural gut flora and consequent fungal overgrowth.
Fungal metabolites (aflatoxins) have been linked to anorexia,depression and schizophrenia. Pubchem lists lists behavioral acute anorexia for aflatoxin G1.
Research published in Journal of Antimicrobial Therapy, suggest that some SSRI antidepressants have an antifungal effect.
Ethyl alcohol (alcoholic beverage) is a fungal metabollite of brewers yeast that is well known to impair human behaviour in a negative way.
I have been unable to find any research into using antifungal agents to treat mental illness.

A fungus that thrives in soil, contaminates grain, is distilled into a beverage that causes drunk driving and death, and returns the host to the soil has also completed its life cycle. Similar to the ant example in your question.


How are bones growing, if bones are not connected to the brain?

The developmental growth of bone tissue is hormonally controlled. It is, as far as I know, not under direct neuronal control. Before reaching adolescence, the long bones (mainly in the arms and legs) grow in the epiphyseal plate, the area of the bone where cartilage is formed and ossified on the diaphyseal side, thereby lengthening the bone. The longitudinal growth of long bones continues until early adulthood at which time the chondrocytes in the epiphyseal plate stop proliferating and the epiphyseal plate transforms into the epiphyseal line as bone replaces the cartilage (boundless website). The growth and stop of growth in adulthood is hormonally controlled. Bone tissue growth is controlled by various hormones including parathyroid hormone and growth hormone.

Growth hormone (GH) is secreted by the pituitary, in turn controlled by the hypothalamus in the brain. So although the brain is involved, it is not directly involved, in that it regulates growth, and cessation of it through hormone release. Growth hormone is probably the most important hormone and is released by the pituitary, but parathyroid hormone released by the thyroid, among other hormones, may play a role as well.

Edit: Your question implies bone growth, which at first seemed to point toward developmental growth to me. However, there is also the more dynamic control of bone mass due to the forces that act on them in everyday life, referred to as bone mass accrual. This process is controlled by the sympathetic and parasympathetic system (Bajayo et al., 2012):

This system acts through direct neural innervation of bone tissue and stimulates bone formation when needed (after imposed strain on the skeletal system), but by default stimulates the breakdown (resorption) of bones to salvage its components for other uses (use it or loose it principle). So yes, the skeletal system is directly connected to the brain (with credits to @anongoodnurse).


What are some online databases that I can search to find the pathways for sythesis of Lignin, Cellulose, GAX?

The other big metabolic database site besides Kegg is MetaCyc which certainly responds to searches for lignin and cellulose.

The problem with lignin is that it is a very complex molecule, so in both Kegg and MetaCyc there are a many reactions involved in its synthesis. Cellulose is less complex and I have no idea what GAX is, despite an internet search. If you are so new to biochemical reactions and metabolic pathways that you cannot handle the results of a MetaCyc search on lignin you should easily be able to find articles devoted specifically to cellulose and lignin, perhaps using Wikipedia as a start.


Alpha and beta brainwaves are just two of several arbitrary, named frequency ranges for a brain-wide phenomenon. See Types of Brain waves. These so-called brainwaves are big electrical events that sweep across the entire brain.

My recommendation for electrode placement is based on my engineering experience. Pick any location on the scalp. You could start with the temples. Take your measurements. Then move the electrodes to a different location and repeat the measurement. Continue this experimentation until you discover by observation which location yields the best results. When you have finished with the experiment, you can post your experimental results on SE Biology and answer your own question.

I suspect that electrode type and method of contact (dry versus conductive gel) will be more significant than actual placement on the head.


What is the chemical process involved in human hairs changing colour after sun exposure?

Melanin is the main compound responsible for the color in hair. It is synthesized from the amino acid tyrosine. The absorption of tyrosine is around 280nm, which is a shorter wavelength than humans can see. Tyrosine can not absorb or preferentially scatter visible light in order to appear colored. It appears colorless as it scatters visible light equivalently. After tyrosine is synthesized into melanin, a pigment is formed which can be seen. Melanin scatters and absorbs light preferentially, it appears non-white.

The absorption of melanin is in the visible spectrum. This means it can absorb and scatter light in the visible spectrum differentially.

As your hair is exposed to sunlight, melanin begins to break down into lower molecular weight compounds which have their own absorbance spectra. The different forms of melanin and carotenoids in your hair can be oxidized by sunlight, giving hair a spectrum of possible colors.

Pigment in bleached hair has been oxidized into products absorbing light primarily outside the visible spectrum. White hair appears so because it lacks compounds which preferentially scatter and absorb light in the visible spectrum.


The least complex animals with ability to dream

Since mammals all share the same neural structures it is quite likely that most non human species dream, but as yet, the simplest animal I could find that has been scientifically demonstrated to dream is the rat, as proven by Massachusetts Institute of Technology (MIT).

MIT not only established that rat were capable of dreaming about the events they had experienced while awake, but that the content of the dreams could be manipulated with audio cues the rats had been trained to respond with in a specific way.

Sources:

http://en.wikipedia.org/wiki/Brain#Mammals

http://web.mit.edu/newsoffice/2012/neuroscientists-achieve-dream-engineering-0902.html


In relation  to angiospermic megasporogenesis, archesporium cell is the precursor of Megasporocyte.

  Archesporium is defined as   the cell or group of cells from which spore mother cells develops

  The megasporocyte is the cell(or the tissue) which directly produces
   the megaspores.

In most angiosperm, the nucellar tissue within the ovule first differentiates into a single archesporial cell, the ancestor of the Megaspore Mother cell(MMC). In certain species, this archesporial cell may itself act as the MMC undergoing meiosis to produce the megaspores. in such cases, the archesporial cell and the megasporocyte (another name for MMC) is the same.

But in some species, the archesporial cell first undergoes a periclinic division producing two cells which further produce the parietal layer (covering of the megaspore) and a single sporogenous cell. This cell acts as the MMC, and is the megasporocyte.

Thus the archesporial cell may or may not be the same as the megasporocyte. It could be the ancestor of megasporocyte.


First, before talking about fruits, let's remember that fermentation is an energetic metabolic process where there is no net oxidation of the substract. Bacteria, fungi, animals like you and me and even plants can use fermentation in different occasions. Plant cells, like fungal cells (and unlike bacteria and animal cells) perform alcoholic fermentation. So, there is no need of a fungal contamination to make a plant tissue producing ethanol.

But, of course, the presence of fermenting fungi, particularly yeasts, can make alcoholic fermentation much faster and noticeable. Several fruits contain what is called "ambient yeasts" (differing from "cultured yeasts", which we add to the fruits latter) covering them, and I believe the most famous example are grapes. Grapes are covered by several genera of Ascomycota (like Candida and Pichia), which can lead to alcoholic fermentation of the fruit. These species are different from Saccharomyces cerevisiae, the most common "cultured yeast" (and the one used in winemaking), but they can produce ethanol the same way.

This "natural fermentation" of grapes is known for a very long time, and it's probably one of the first cases of natural alcoholic fermentation known by civilized man.

EDIT: references for alcoholic fermentation in plant cells:

http://www.plantphysiol.org/content/149/2/1087.full

  Under oxygen-limiting conditions, pyruvate can either be converted into ethanol by pyruvate decarboxylase (PDC) and alcohol dehydrogenase (ADH) or to lactate by lactate dehydrogenase.

http://www.plantphysiol.org/content/100/1/1.full.pdf+html

  During the early hours of germination [...] seeds rapidly generate high respiratory quotients and exhibit increased ADH2 activities and active alcoholic fermentation.


When physical damage to the cells occur a biological process called inflammation occurs. When inflammation occurs, white blood cells are rushed to the area in order to fight off any bacteria or harmful waste leakage from damaging the cells further. In order to get the white blood cells to the site of damage faster, the body induces a process called vasodialation where the arteries are expanded and blood is rushed to the site. This causes the site of injury to swell and redden, two signs of inflammation. The white puss that forms comes from the white blood cells. The white blood cells release chemicals that kill of bacteria and waste in the area and forms a white pus that will eventually harden or break through the skin to be exerted. If the site of impact begins swelling within a matter of hours, it is likely acute inflammation is occurring and the body is rushing blood to the site. However, if swelling occurs on a more rapid time scale it is more likely that this fluid is from the damage of the impact itself and the cells and capillaries are leaking blood and extracellular fluids (What is Swelling?).

In short, when you bump your head your body is trying to fight off further injury and infection by inducing the inflammatory response. It is also leaking fluids due to the impact and may result in rapid swelling at site of impact. The symptoms you discuss are due to inflammation and are a normal process of your body's defense mechanism. Hope this helps!


The white circle in the center is a bone, probably the femur. The muscles are covered with an external later of fascia, the epimysium (here's a question with some information). These layers separate muscles from each other, and often fat will also deposit in the spaces between muscles, which is what the white lines between muscle bellies are. There is also some cutaneous fat.

This is probably a section through the thigh, possibly a pig (though it looks a little too red). Regardless, the muscle will have the same basic layout as the image below of a pig thigh from pork.org, even if your image is from some other mammal.

You have to rotate your image clockwise about 45 degrees to get them to match up. The back of the thigh is at the top of the image.


What is a good review book/source for microbiological diagnosis?

I would suggest:

Koneman's Color Atlas and Textbook of Diagnostic Microbiology

by Elmer W. Konema


Most people most of the time live in the environments that have lower temperatures than it is their normal body temperature (36-37 °C). And most people sweat sometimes at these temperatures.

In the summer, when it is 30 °C and you wear only swimming trunks, even light walking can make you sweat. The same can occur in the winter when the ambiental temperature drops below 0 °C and you wear warm clothes. This is because the muscles, when working, can generate more heat than you need and sweating is the way to get rid some of it.

When you eat food and the food is broken down to release energy, some of this energy will be released as heat. If the food generates more heat than your body needs, eating foods, especially ones high in protein, can make you sweat.

Some people get sweaty after eating certain spicy foods. This is called gustatory sweating, which is not related to food combustion, but it is a neurological phenomenon.

Capsaicin in red hot chili peppers can also trigger heat generation and sweating.

Drinking alcohol dilates the blood vessels in your skin, which results in increased flow of warm blood through your skin, which can signal the thermoreceptors in your skin to trigger sweating.


Unknown plant, please help me identify it

It appears to be a cultivar of Jujube (Ziziphus zizyphus) also known as Chinese date - https://en.wikipedia.org/wiki/Jujube
This is based on JimN's correct observation. I looked at a few dozen images of Ziziphus Zizyphus - both fruit and leaves. They appear to be identical. The fruit tastes as described. The fruiting progression matches the description in Wikipedia.


Can inverted microscope also be phase contrast microscope?

Definitely true, an inverted microscope is one where the optics are positioned below the specimen, and the light source above, providing an optimal situation for looking at a live culture. The Phase rings that shift the light come soon after the light source. For phase, the orientation doesn't matter, just the order:

Upright microscope

Orientation:

(top)eye--->objective--->specimen--->phase--->light source

order:

eye-->Phase compatible objective-->specimen-->phase disk-->light source

Inverted microscope

Orientation

(top)light source--->phase--->specimen---->Objective--->eye

order

eye-->phase compatible objective-->specimen-->phase disk-->light source

Not all microscopes have phase no, they are an important and expensive addition to a microscope. Adding phase not only required the phase disk but also a phase compatible objective.


Answer is, obviously, yes.

Primerbank

Here. You can search primers using accession number or Gene-ID


Generally, sorbitol is one of those 'old tricks' in the book which is thrown into cultures or buffers for several reasons. Here are a few that I have heard of:

Bacterial cultures (e.g. E.coli BL21) that are optimised to express (produce) protein, because sorbitol is thought to increase the expression of soluble protein. I have even heard of people (who work with very difficult proteins) that add to a final of 0.6M sorbitol in their culture media (note that the cultures grow very slowly).
In buffers intended for proteins, as it is thought to increase the solubility (i.e. avoid aggregation), similar to other sugar such as glycerol or osmolytes such as betaine.
Sorbitol is considered (chemically)  to be relatively inert, and many will therefore prefer to add sorbitol over e.g. glycerol or sucrose as a stabalizating agens when they work with proteins.
When you work with glycoproteins, you are generally depending on the addition of some sugar to stabilise the protein of interest - both during isolation, purification and analysis/testing.

The last point here could answer you question, as immunoglobulins are glycoproteins, you are generally depending on a high concentration of some sugar - such as sorbitol - to work with these proteins (i.e. antigens and antibodies) in e.g. immunoprecipitation.
I don't believe that sorbitol is a crowding agent - as this would perhaps facilitate aggregation, the opposite of the intended purpose. Adding crowding agents it typically done in protein crystallography with the addition of various PEGs to 'get the' proteins to form crystals. Instead, I think that sorbitol may (somehow) interfere with the proteins solvation shell - in the same way that is speculated for osmolytes (e.g. betaine or various sugars); however, this is something that I dont know much about and should be investigated.


How do antibiotics create drug-resistant strains

There is no such thing as a "stronger" or "weaker" strain until the bacteria are treated with antibiotics.

It is true that potentially antibiotic-resistant mutants will still occur whether or not treated with antibiotics.

However, the mutants would not be "stronger" without the antibiotic use, so there is no selective pressure for them to survive to any greater degree than the wild-type. Without the antibiotic, something else will kill that mutant bacteria, meaning that the mutation ultimately did not make it any stronger.


Looking for a gene in my raw genetic data. What are the possible causes for this?

Let's set things straight. The genomes of humans are highly similar and in general everyone shares the same genes. SNPs, or Single Nucleotide Polymorphisms, are single basepair positions in the genome in which there tend to be differences between people. This means, that instead of measuring the whole genome sequence for a person, which is very expensive and difficult, we can just examine a subset of the genome (the SNP positions) and capture most of the unique characteristics of that genome.

23andMe do exactly that. They measure a large set of SNPs (but not all of them), and thus give you some useful information about your unique DNA sequence. So you would need to look in the output given to you by 23andMe and see if they measure the SNP in question (rs35705950).

What do SNPs have to do with genes then? Well, if one of these SNPs occurs inside a gene, it could affect the gene, for example by producing a slightly different protein that could lead to some phenotype. So, studies link SNPs to different phenotypes such as disease or hair color. Usually the link is not one-to-one, but given as a probability.


Evolution of Upside Down Catfish (Synodontis nigriventris)

Well, I haven't managed to find many studies that explores this but I suspect that their coloring was a result of their upside down swimming rather than the other way around.
They evolved from benthic (bottom-living) creatures that ate off the ground and would have had mouthparts evolved for that. So in order to feed at the surface they would have to turn themselves around. The areas that they lived in may have changed to have poorer benthic food quality making surface feeding more advantageous. They also do this for aquatic surface respiration in hypoxic (low oxygen) waters.

Check out "Chapman, L. J., Kaufman, L. and Chapman, C. A. (1994). Why swim upside down? A comparative study of two mochokid catfishes. Copeia" for more information.


Can electricity be harvested from the soil around plants?

Electricity may be indirectly generated from plants through the use of a microbial fuel cell, in which biologically-catalyzed chemical reactions are used to drive an electrochemical cell.

A non-technical description of the technology can be found here.  The basic idea is that plants produce organic compounds, which are broken down by soil microorganisms to produce carbon dioxide, electrons, and hydrogen ions.  Ordinarily the hydrogen ions and electrons combine with oxygen to form water, but there are various ways to divert the electrons to travel through an electrical circuit before the oxidation reaction takes place.  This flow of electrons (electricity) can be used as a power source.

This technology is still in its early stages but the process has been demonstrated in some laboratory proof-of-concepts:

Strik, David P. B. T. B.; Hamelers (Bert), H. V. M.; Snel, Jan F. H.; Buisman, Cees J. N. (2008). "Green electricity production with living plants and bacteria in a fuel cell". International Journal of Energy Research 32: 870–876. doi:10.1002/er.1397.
De Schamphelaire, Liesje; Van den Bossche, Leen; Dang, Hai Son; Höfte, Monica; Boon, Nico; Rabaey, Korneel; Verstraete, Willy (2008). "Microbial fuel cells generating electricity from rhizodeposits of rice plants". Environmental Science and Technology 42 (8): 3053–3058. doi:10.1021/es071938w.

The E-Kaia company has not released enough information to say whether their product is in fact a plant microbial fuel cell, a simple earth battery, or a mere scam.


codon optimization / enzyme active site improvement

Kind of an old post, I'm surprised it doesn't have an answer yet.
There's no reason why you couldn't modify the RNA or cDNA directly, you just have to splice the gene correctly to make the changes you want. You're absolutely right that even a single amino acid change can have a huge difference if it's in the right spot.


Resilience to the neurotoxins of Indian King Cobra

Well, turmerin, the compound in turmeric has been medically proven to help neutralize venom from King Cobras in snakes (reference1, reference2). It has also been used in ayurveda for snake bite treatment (reference) The alcohol I guess is just used to help ingest the turmeric and act as a pain reliever, though it strangely seems counter-productive since most snakebite help guides advice against the consumption of alcohol after getting bitten (reference1, reference2) due to its blood thinning properties.

Having said that, I guess personally, I would go for anti-venom rather than ingest turmeric. As a quick remedy until you get the anti-venom you should be able to depend on turmeric.


The justification is simple.

The bones of the ear [ear ossicles] do not articulate with any other bone of the skull hence it is not considered as a part of the skull, similar is the case with the hyoid which is attached to the tongue.These bones have been placed under the group of associated bones.


Usually I had no problems with RNA extractions - from various cultured cells as well as a number of different tissues from mouse. If I look at your protocol this is pretty much the same as the one we used or the one recommended here for zebrafish embryo. This protocol "Purification of RNA Using TRIzol (TRI Reagent)" seems also interesting.

What can happen is a contamination by phenol or carbohydrates, then we usually used the protocol below to clean up the sample. You can also use column based methods, but they are more expensive.

add 1/10 vol of NH4OAc (5M), 2.5 volume 100% cold EtOH (100%) and 10µg
glycogen (for total RNA we usually didn't use any co-precipitation
agents) and mix well
incubate 30 min at -80°C
centrifuge 20 min at 12000g at 4°C and remove the supernatant
wash with 75% ice cold EtOH
centrifuge 5 min at 12000 g at 4°C and remove supernatant
Re-suspend the pellet in RNAse free water (can take some time)


Those are isolated turtle bones:

Specifically, they are part of the carapace, or upper shell. The projections would articulate with the backbone. The "toothlike" structure at the other end projects down toward the margin of the shell.

Based on the size, and the fact that you are in Missouri, I'm guessing they are snapping turtle bones. Here's a photo of the inside of a snapping turtle shell:

They are a little hard to make out, but you can faintly see the marginal projections.


Determine whether aromatics originate from polyketide or shikimate pathway

Aromatics that stem from the Shikimat Pathway result in a structure like this

Whilst aromatics originating from the Polyketide Pathway have an alternativ structure in the distribution of the OH groups.


Do fledglings die if they are not fed constantly?

Depends on the species and their age. All birds have fat reserves that can keep them alive for a relatively long time. It's when fledglings are left for many hours or days that one should start worrying about their survival.
The following link explains more detail on how frequently birds must be fed, even if in your case I suppose you aren't the one feeding them:
https://birdwatchingbuzz.com/how-often-should-you-feed-a-baby-bird/
In my experience some species of birds might become less afraid if you leave food or water stations for them.


Why doesn't the cell membrane just...break apart?

The membrane bilayer is held together by hydrophobic forces. This is an entropy driven process. When a greasy or hydrophobic molecule is suspended in water, the water molecules form an organized "cage" around the hydrophobic molecule. When two hydrophobic molecules come into contact, they force the water between them out. This increases the entropy because the freed waters don't need to be organized into the cage. Lipid bilayers have many many many hydrophobic lipids that squeeze out a lot of water and greatly increase entropy. The polar phosphates allow the water to interact with the surface of the membrane, without a polar head group the lipids would form a spherical blob instead of a membrane.

Read this section on wikipedia for more.


Why is PEG important for efficient yeast transformation?

http://www.protocol-online.org/biology-forums/posts/26634.html

I found this link - it says 'we don't really know'.  It says PEG binds DNA, I assume shielding the membrane from its negative charge and allowing internalization to happen.

I would guess that the amphipathic nature of PEG, being partly hydrophobic, also helps soften up the membrane.  Interestingly, if you increase the PEG concentration beyond the limits, it decreases the efficiency of the procedure.


Interdependency between organsims on our planet and its relation to ecosystem?

The problem is not really that we don't understand some stuff (lthough this is certainly true) but that an ecosystem, or the biosphere is a highly complex network of interactions. This network is continuously displaying some chaotic (determinist but not foreseeable) behavior. In such a system it becomes very hard or practically impossible to predict what the impact of a change (even a minor one) might be. To illustrate, one could say that killing half of the world's lions might cause the population of rabbits in Norway (!) to increase but killing two thirds might cause the same population of rabbits to decrease. Note: Stuart Kauffman wrote some articles where he argues that life is a system which is always balancing between chaotic dynamic and non-chaotic dynamic. Today, many conservation biologists use the tools of graph theory (network analysis) in order to get a better understanding of how things are influenced by a minor change.

But defending an endangered species like the pandas or elephants is certainly much more a matter of ethics than of human security faced with environmental shifts. I would guess (a reference on how the world's money is spent on conservation action would be interesting) that an important part of the money  spent on programs for the defense of endangered species are for ethical reasons, just because these species are big, clever, sing well or display nice colors.

There are many false reasons in ecology (in the political sense of the word) where people act for their ethics rather than to defend humans from environmental change. (I don't mean that ethics is stupid, or that only defending the environment for the benefit of the human species should be considered). You may already have heard "the amazonian forest is the lung of our planet" suggesting that this forest produces lots of $O_2$. This is completely wrong! Cutting down this forest would not change much in terms of either $O_2$ or $CO_2$ levels (except if the wood is burned!).

So to summarize I would say:

We spend quite a lot of money defending species for ethical reasons rather than to protect humans from environmental shifts.
Changing a little thing might affect the world-wide biosphere in a way that is practically impossible to predict.


Are there any species whose descendants can meet their ancestors from 100 generations back?

Yes, cryopreservation works quite well for many species, including multicellular animals. So you can freeze the ancestor and wait until the descendant is there, then unfreeze them. A good recent example in the news would be the Siberian worms that woke up after being frozen in permafrost for a very long time.
Cryopreservation is routine in laboratories, to freeze ancestors and compare to descendants; see the Long Term Evolution Experiment. It doesn't work well for every organism of course. In principle it might work for humans.
Some bacteria will sporulate, and in spore form they can persist for thousands of years theoretically. They don't even need cryopreservation. There are other organisms that do something similar as well.


How do nerve impulses travel so quickly?

There is a large gradient created by selective permeability of Na channels and as you're probably aware the speed of diffusion is proportional to the electrochemical gradient.

Very small numbers of ions actually cross the membrane during depolarisation and subsequent AP events.


Bison humps are made of muscles, huge muscles. According to this and this pages bisons use their heads for snowplowing. This hump provides head support. It seems that also other animals have structures like that: giraffes, rhinoceroses, elasmotheriums,... this list can go on since this structure should be homologous of other animals'. From this page rhino humps made from muscles, nuchal ligament, fat, and dermis. And from the page, probably fat quantity depends on the nutritional state of animal.

I searched nuchal ligament, the remarkable structure of hump according to rhino page. This is a ligament spans from upperback vertebra to neck vertebra and to skull. Can be found on humans too. Also muscles of hump should be homologous to humans' notice that vertebras have spines not just for supporting ligaments they also for muscles. Human skeletons just don't have vertebra with long big muscle connection points and huge neck/back muscles connecting huge bones, this is why we don't have a hump or an obvious large hump. And I think even camels do have slighly bigger muscular humps but theirs are covered with big fat hump.

Bison skeleton and elongated spines supports huge muscles and ligaments.

Horse's nuchal ligament

Human nuchal ligament

Human nuchal ligament drawn with red lines and muscles (bison hump also consist of muscles).

Giraffes' this is an energy saving feature. Giraffes don't need to use muscles to hold their neck. They just use when flexing their necks down, when drinking water etc.

According to Wikipedia, for an alternative hypothesis Ouranosaurus have a hump. (Other hypothesis is display sail or termoregulation sail of course. Also spinosaurus have this kind of alternative hypotesis but this hypothesis not accepted much as sail. and spinosaurus' spine different from bisons. Bison spines concentrating at shoulder but spinosaurs' not at the shoulder. You can find spinosaurus info from this page.)