Is there a karyotype database for human cell lines?

As far as I know and have found, there is no one master database for karyotypes of all human cell lines. They are usually grouped into subsets either by some commonality (e.g. being cancers) or simply because of who/where they were developed and how they chose to share the line. Some good databases/resources are:

ATCC - A great repository that has cell line datasheets, references, images, and culturing info. I highly recommend using ATCC as your first stop when looking to learn more about a line.
NIGMS Human Genetic Cell Repository - A very robust repository that contains far more than just cell lines. It's good, but the wealth of info can be a bit difficult to sift through.
COSMIC - A great collection of info on cell lines and mutations found within them. Good if you want to look for/understand particular genetic aspects of a line.
Cellosaurus - A fantastic database on cell lines! I particularly like the info Cellosaurus hosts on different names and common misspellings of names for cell lines. It also provides info on hierarchies of cell lines- that is, when multiple cell lines are derived from a parent line. This is super helpful when trying to parse literature with confusing references to similar lines. It also provides references and cross-references. I cannot recommend this one enough.

To get back to your particular cell line, I have only been able to find one reference to a line called 'LG2'- even with the help of the resources listed above and PubMed, so I, unfortunately, can't give you much info on that specifically. If there really is so little info on this line, I would suggest contacting the source (colleague, lab, excel sheet associated with your storage system, etc.) for your cells to see what info they have. If you can't find anything that way, it may be best to just submit a sample for sequencing yourself and get that info out there.


Curling up is due to turgor pressure. Quoting from wikipedia

  Loss of turgor pressure in these cells causes leaves to "roll up" during water stress

More scientific reference , on morphology,  on mechanism, on development, some genetics and on physics.


What effect does the Barr body have, in relation to female Turner syndrome?

The reason is that X-inactivation is not complete (Carrell & Willard, 2005; Ahn & Lee, 2008), and as many as 15-25% of X-linked genes escape silencing (Carrell & Willard, 2005; Cheng et al, 2005). This means that some genes on the Barr body are expressed in XX-females, although often at lower levels compared to the active X-chromosome, and this is part of the normal gene dosage. The "purpose" of X-inactivation is usually dosage compensation, so that genes are expressed equally in males and females (and then actually upregulated in both sexes to balance autosomal genes, see e.g. Dementyeva et al, 2009). However, this is not true for all genes, and the ones that normally escape X-inactivation will be expressed in the incorrect dosage in X0 females. Some of these genes are thought to contribute to the symptoms of Turner syndrome.

It is also likely that the genes that escape silencing are involved in sex-linked traits, as stated in Carrell & Willard (2005):

  Such genes are potential contributors to sexually dimorphic traits, to phenotypic variability among females heterozygous for X-linked conditions, and to clinical abnormalities in patients with abnormal X chromosomes.
  ... ...
  However, as many of the genes that escape from inactivation do not have Y-linked homologues, strict dosage compensation may not be necessary for all genes on the chromosome. Such characteristic genomic differences should be recognized as a factor for explaining sex-specific phenotypes both in complex disease as well as in normal, sexually dimorphic traits.

Cheng et al (2005) also point out that the expression of the genes that escape silencing is tissue-dependent, which suggests that the role these genes play in the symptoms of Turner syndrome is also tissue dependent.


Do viruses compete with each other or even infect each other? (Virus vs Virus)

From what I understand virus on virus action is not particularly common but it isn't unheard of.

Consider the Sputnik virophage which

  reproduces in amoeba cells that are already infected by a certain helper virus; Sputnik uses the helper virus's machinery for reproduction and inhibits replication of the helper virus.

Also consider the Mavirus virophage, which

  is a double stranded DNA virus that infects the marine phagotrophic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus. Mavirus can integrate into the genome of cells of C. roenbergensis, and thereby confer immunity to the population.

As a last example, consider the Organic Lake virophage, which

  is a double stranded DNA virus that infects the marine phagotrophic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus. [...] [It] preys on Organic Lake phycodnaviruses, which in fact may rather belong to Mimiviridae than to Phycodnaviridae.

So yes, viruses do at least occasionally attack viruses and inhibit their infectious potential and grant a sort of immunity. I'm not aware of any applications of this in medicine for now but maybe somebody else can add something to this if they know.


Why doesn't the rest of the body have something like the "blood-brain" barrier to protect itself from pathogens?

There can be many reasons to why BBB-like barrier is not present in all the capillaries of the body. Let's talk about them one at a time.

Source

Blood-brain barrier has its own side effects. Some major side effects are cerebral edema (accumulation of excess water in the extracellular space of the brain, which can result when hypoxia causes the blood–brain barrier to open) and (possibly) Epilepsy. See this wikipedia article:

  Several clinical and experimental data have implicated the failure of blood–brain barrier function in triggering chronic or acute seizures. Some studies implicate the interactions between a common blood protein (albumin) and astrocytes. These findings suggest that acute seizures are a predictable consequence of disruption of the BBB by either artificial or inflammatory mechanisms.

Another problem is that BBB doesn't allow passage of drugs, diagnostic and therapeutic agents through it. Again, see this article:

  Overcoming the difficulty of delivering therapeutic agents to specific regions of the brain presents a major challenge to treatment of most brain disorders. In its neuroprotective role, the blood–brain barrier functions to hinder the delivery of many potentially important diagnostic and therapeutic agents to the brain. Therapeutic molecules and antibodies that might otherwise be effective in diagnosis and therapy do not cross the BBB in adequate amounts.

Now, if you want to know why the body doesn't have BBB-like barrier (not exactly BBB), then there are three parts of the answer.

These kinds of barriers are highly specialized for a particular organ or organ system, which may not be useful for another organ/organ system. Also, creating specialized barriers for all the parts of the body will take a lot of energy, cells and even more time to develop completely. Possibly, in the evolutionary course, body preferred to have phagocytic cells circulating in the body instead of having specialized barriers throughout the body.
These barriers might not be a total solution for immunity or restriction of pathogens. See this part:

  It is believed that latent HIV can cross the blood–brain barrier inside circulating monocytes in the bloodstream ("Trojan horse theory") within the first 14 days of infection. Once inside, these monocytes become activated and are transformed into macrophages. Activated macrophages release virions into the brain tissue proximate to brain microvessels. These viral particles likely attract the attention of sentinel brain microglia and perivascular macrophages initiating an inflammatory cascade that may cause a series of intracellular signaling in brain microvascular endothelial cells and damage the functional and structural integrity of the BBB. This inflammation is HIV encephalitis (HIVE).

Also, it is not necessary that those pathogens would infect only those tissues to which they reach via bloodstream. Pathogens like HIV cause infection in the blood cells. See this image from here:

  Once a person is infected with HIV, the virus begins to attack and destroy the CD4 cells of the immune system. CD4 cells are a type of white blood cell that play a major role in protecting the body from infection. HIV uses the machinery of the CD4 cells to multiply (make copies of itself) and spread throughout the body. This process, which includes seven steps or stages, is called the HIV life cycle.

Similar barriers are already present in many parts of the body. For example- Blood-Ocular Barrier, Blood-Testis Barrier, Blood-Thymus Barrier, etc. They may also have some loopholes. For example, see this article-

  Possible consequences of blood-thymus barrier failure are trophoblast-specific or tumor-specific antigens penetrate into the thymus, deletion or anergy of antigen-specific clones and acquired thymic tolerance induction.


This is some species of aphid.

Most people are familiar with the wingless stages of these insects that crawl on and eat plants. There are also winged 'alates'. For example, see the life cycle of the soybean aphid:

Due to the picture quality, I'm uncertain about the exact species. However, I can show you alates from some similar looking species:

Nasonovia ribisnigri (Currant-lettuce aphid)

 Source: influentialpoints.com

Aphis pomis (Green Apple Aphid)

 Source

Macrosiphum rosae (Rose Aphid)

 Source: Bernard Dupont

As you can see, these phenotypic characteristics (i.e., green body with black head, clear wings, black/green striped legs, green cauda and black cornicles) are present in numerous diverse species of aphids.

Perhaps you could comment on nearby crop plants or garden plants near your house or produce that you've recently purchased or brought into the house. Sometimes knowing possible host plant species can help narrow down possibilities.


Does natural selection apply to entire populations as it does to individual organisms?

Unit of selection

Your question is about the concept of unit of selection. Selection acts on any populations of things that have heritable features which explain at least part of the fitness variance in this population. The "things" can be genes, cells, organisms, groups of organisms, species, lineages, etc...

The standard is to view selection acting on population of individuals. But of course, selection can also act on populations of groups of individuals (or populations of populations if you prefer) or populations of species. When talking about selection on a population of groups of individuals, we talk about group selection (a concept very related to kin selection) When talk about selection on a population of species, we talk about species selection (or lineage selection).

Social evolution and altruism

An altruistic phenotype is defined as being a phenotype that is causing a decrease in the fitness of the carrier of the phenotype coupled with an increase in the fitness of one or more recipient individuals. Altruism can evolve at a level, only by selection applying at levels above it.

Imagine for example a population of individuals. If one individual mutates and as a result display a behaviour of donating food to the others. The cost for this individual is -0.5 and the benefit for the recipient is say 0.7. In absence of reciprocity, this mutation will not be passed on on future generations because  this individual carrying it have lower fitness. Therefore altruism should not evolve in this population. Imagine however if there are many populations and that some populations are altruistic and other aren't. Then, the altruistic population will likely outcompete the non-altruistic populations and therefore over time only the altruistic populations will remain.

It is by the way the existence of an altruistic behaviour that brought to wonder about the level at which selection can act.

The field that studies the evolution of such social phenotypes is called social evolution


Taxonomic classification is a large area of controversial debate. See for example Cavalier-Smith's system of classification, they described eight kingdoms, then six, then 7 kingdoms in subsequent publications.
Other (older) theories describe 6 kingdoms, two prokaryotic (Eubacteria and Archeae) and four Eukaryotic (Protista, Plantae, Fungi, Animalia) See image on Wikipedia's "Kingdom" explanation
The three domains Eubacteria, Archeae, and Eukaryota are less disputed.


If the average resting potential of a neuron is -70 mV, why is there such a high ratio of potassium ions inside relative to out?

Representative ion concentrations are shown in Fig. 1:

The membrane is mainly permeable to K+. Because the Na+,K+-ATPase pumps K+ inside of the cell, it tends to diffuse outward again, thereby taking positive charge outside the cell and making it negative inside (extracellular space is pretty much devoid of charge due to its vastness). Because the membrane is mainly permeable to K+, the membrane potential can be estimated using the Nernst equation by taking into account only [K+]:

This delivers about -90 mV, using the values in Fig. 1, which is quite close to the cell membrane resting potential.

However, other ions have some limited permeability too and especially Cl- also has quite a large leak current. To add the permeability p of the various ions (for K+ p=1, for Na+ p=0.04 and Cl- p=0.45) into the equation and take multiple ions into account, the Goldman equation is needed:

This equation yields closer estimates of the membrane potential than the Nernst equation taking only K+ into consideration. However, other factors such as buffer effects (Cl- is often buffered) as well as active transport mechanisms may alter the outcome of the Goldman equation slightly.


Depending on what you are trying to look at, for zooplankton you can take water samples and filter them through a 100-200um mesh and store them in glass or plastic bottles. For my research we used mason jars that were cleaned thoroughly. After filtering just submerge the biomass in 70-90% ethanol and they can be stored in a fridge for quite some time.

If you want to look at phytoplankton, you can look into using Lugols Solution for preserving your samples. The nice thing about using lugols is that it will stain the phytoplankton as well. Your best bet for these is to store in amber bottles and keep in cool dark place. Here is a decent guide on how to collect the samples and prep the solution.


What is the exact concept of "Repulsion" and "Coupling" (Genetics)?

I guess the confusion is stemming from trying to fit the phenotypic terms coupling and repulsion to their genotypic basis.

Coupling and Repulsion are both used considering the phenotypic profile of the progeny, and hence, takes into consideration only the distribution of the dominant allele. If, in the progeny of the test cross, the percentage of double dominant is less than that the average percentage of single dominant, that would be what we call repulsion, as in the two dominant traits tend to be separated. The opposite, percentage of double dominant being greater than the average of individual dominant, is coupling.

This said, it is clear what would be the corresponding genotypic states. If the chromosomal states are $Pr^+/Vg^+.. pr/vg$, coupling would be observed if the $pr$ and the $vg$ loci are linked, since for individual dominant phenotypes to appear, recombination is necessary which is rendered less probable due to linkage. A genotype of $Pr^+/vg..pr/Vg^+$ would result in the phenomenon of repulsion in a test cross. The case you cite, has the latter, and hence, we observe repulsion.

Now to your questions.

  Is "Coupling" an exact synonym of "Linkage" ? and is "repulsion" an exact synonym of "recombinant"? No-where I could yet found mention of it.

Neither. More accurate would be to consider both coupling and repulsion as consequences of linkage, differing in the configuration of the linked gene (see above).

  What are they telling as coupling-"phase" and repulsion-"phase"? Are there 2 different "step"s or "time-frames" or "generations"?

Although this is difficult to answer without knowing the context, I belive that the author here might be referring to the variable possible configuration of the alleles, as in, if they are in a coupling-phase, they are so oriented that the resultant progeny will show the coupling phenomenon. The phase may change to repulsion if a recombination event occurs. (again, see above.)

  Coupling and repulsion- are they indicating to a "phenomenon"? or the Genotypic "state"?

Not to argue much in this semantic mashup, they are best viewed as differing phenomenon (as in the different obtained progeny phenotypic ratios) resulting from varied genotypic states.


The ion concentrations are different inside and outside of the cell, allowing a potential.  The cell becomes even more polarized by the pumping out of H+ ions, making the cell even more negative (potential difference). Then this negative potential happens to cause voltage-gated channels to open and the uptake of potassium occurs. This will depolarize the cell (return it to the base potential difference).  It is usually very important for the cell to maintain the negative potential after it recovers. To combat the uptake of potassium, negative charges can be used to balance the increased positive ion influx so the resting potential is stabilized.

These mechanisms are usually mediated by special proteins that are regulated by actual electrical changes in the membrane.


Does extracted DNA degrade after a certain time period?

My rule of thumb for DNA samples (in TE or water) - if I have plans to use it that week, I store at 4C. If I plan on using it within a month, I store at -20C. If I'm not sure when I will use it, I keep multiple aliquots at -80C. DNA can degrade by acid hydrolysis in water, because of contaminating nucleases in the sample, and by multiple freeze/thaw cycles.


The mineral content in tap water differs from area to area as well as the source. The mineral content in bottled water is regulated by the companies that manufacture them, in particular the Mg and Ca content(reference).

  Death rates tend to be lower in areas with tap water containing higher
  levels of Ca and Mg. It has been shown that deficiencies in magnesium
  are capable of producing heart disturbances, including 215,000 fatal
  heart attacks in the U.S. each year, and as many as 20,000,000 fatal
  heart attacks worldwide (reference).

Different brands of bottled water will differ in their mineral content as well (reference). The place where you stay might be lacking in a particular mineral that your body requires which is why your doctor has specified the use of a particular brand of mineral water.


What species is this grey insect with red antennae and mouthparts?

It's some type of Reduviidae, or assassin bug - possibly a juvenile wheel bug.  Here's a few pictures of Floridan assassin bugs I've found just browsing the net:

Tagged as unidentified Reduviidae from Tallahassee

Tagged as assassin bug

Tagged as a Wheel Bug

Tagged as a wheel bug nymph

Bottom line:
Not an ant, for sure: it's almost certainly in the family of Reduviidae, possibly the subspecies of Arilus cristatus.


Turns out this is harder than it seems from just the picture...

The three candidates I think one could most argue for are:

Quaking Aspen (Populus tremuloides)
Paper Birch (Betula papyrifera)
Grey Birch (Betula populifolia)

Here is a picture of Populus tremuloides from the USDA:

Notice the smoothness of the above Aspen bark (identical to that of the picture in the OP's question). Now compare it to the peely nature of typical birch bark (here pictured B. papyrifera or paper birch):

Though not all birch species have peely bark: (my emphasis below)

Grey birch (Betula populifolia) typically remains fairly smooth. From Viginia Tech's tree guide:

  Bark: Reddish brown with numerous lighter lenticels on very young stems, later turning gray to white and very chalky; remains smooth and generally does not peel.

B. pendula (European white birch) bark is also described as being smooth and only somewhat peely. From Virginia Tech:

  Bark: Reddish brown with light lenticels when very young, later turning white, generally smooth but does peel a bit; the base of the tree develops thick bark which splits into narrow, vertical furrows which are nearly black.

However, the branches in the OP's picture are not drooping as is also common for B. pendula (AKA the European weeping birch). So this is not our tree!

Also, some sources describe paper birch as simply being smooth (vs. emphasizing the peeliness). See here for an example.

Here are images of European white birch (left) and gray birch (right) :

But Gray birch remains smooth, even at the base of the tree (though see here)...

Pay attention to the bottom of the trees in the OP's picture. The bark at the base of the trees is becoming furrowed:

Zoomed in OP picture:

This base furrowing is a characteristic of P. tremuloides:

According to the Virginia Tech Tree Guide (my emphasis):

  Bark: At first smooth, creamy yellowish-white to very light green; later developing thick furrows and becoming dark, especially near the base.

And according to The Sibley Guide to Trees  (my emphasis):

  Bark color from white to greenish, grayish, or bronze. Bark smooth, pale with dark scars that persist for many years; base of trunk becomes coarsely ridged grey on old trunks.

And from the NDSU Agriculture webpage (my emphasis):

  Bark Color - Varies from chalky white to olive-gray, and becomes rough furrowed on the lower trunk of mature trees.

[Note: I give all 3 sources to demonstrate the inconsistency in description of P. tremuloides bark color].

Here is a close-up of furrowed aspen bark from the USDA website (yes, this is still aspen):

However, this furrowing can also occur in paper birch.

From V tech (my emphasis):

  Bark: Reddish brown with light lenticels on very young stems; later turning chalky to creamy white, peeling in horizontal papery strips; brown to black and may be furrowed at base; orange inner bark.

From Field Guide to Trees of North America (my emphasis):

  Bark white papery; older trees have rough black bark near base.

I will comment that I have never seen paper birch with furrowed bark at the base. Further, I was unable to find visual evidence from any reputable sources by searching on Google.

So what about tree shape and form?

Again, according to The Sibley Guide to Trees:

  [P. tremuloides has a] single main trunk with relatively stout , jagged twigs (unlike more slender and graceful twigs of birches).

  [B. papyrifera] branches begin lower on trunk than in aspens; more graceful, ascending, and regular with slender straight twigs. Mature tree has oval habit, few strong branches, clumps of fine twigs in the crown.

  [B. populifolia has] typically multiple leaning, crooked trunks and narrow crowns. Bark of mature trunks grayish white, nonpeeling.

Citing a different source (Field Guide to Trees of North America) to address different language to differentiate the species:

  [P. tremuloides:] Small to medium-sized tree. slender trunk; pyrimidal to round crown of spreading branches with sparse foliage.

  [B. papyrifera:] Medium-sized tree. One to several slender, straight trunks; narrow to broad crown; branches upraised in youth, often becoming horizontal or drooping in age

  [B. populifolia:] Small tree. sometimes shrubby; One to several trunks; narrow, conical crown.

The smaller trees in the front left of the OP's picture demonstrate a more birch-like architecture and have branches growing along the stem as the description for B. papyrifera describes. These qualities are reduced or eliminated in the larger trees in the OP's picture.

For visual clarification, the typical pyrimidal crown shape of P. tremuloides is shown below (from Oregon State Department of Horticulture). The trees in this image appear more slender (pyrimidal) than the trees in the OP's image, but aspen trees can also have "round" crowns as stated above.

The following photo from Michigan State University Extension's Tree ID Key attempts to demonstrate a difference between paper birch and aspen crown coloration:

The crown branches/twigs visible in the OP's picture seem to be lighter colored, and so this line of evidence points to aspen.

Ok, so what about size? According to Field Guide to Trees of North America the typical sizes of the species under question are fairly similar, but with gray birch being smaller than the other two species:

Quaking Aspen (Populus tremuloides) = 30-70' tall, 1-1.5' diameter
Paper Birch (Betula papyrifera) = 50-70' tall, 1-2' diameter
Grey Birch (Betula populifolia) = 20-30' tall, 0.5-1' diameter

The relative sizes of the trees in the OP's picture don't seem to preclude any of these species.

Both birches and aspens develop yellow leaves in autumn, so this characteristic additionally is not useful for differentiating the two genera (or 3 species).

Though @fileunderwater is correct in stating that birches have horizontal lenticels that are helpful in identifying birch trees, the OP's image is far too zoomed out to make out any lenticels (even when zooming into the OP's picture). Those black spots are not lenticels; they are scars (generally from lost limbs). Regardless, other species (including some aspen species) also develop lenticels.

Here is a close-up of lenticels. The little slits are birch lenticels (here from B. papyrifera):

Names on files and webpages are notoriously incorrect so using that as a line of evidence is dangerous. I saw a number of misidentified species in pictures while I was searching myself.

So thus far it seems as though aspen is a pretty good choice, but paper birch could also be potentially correct. The distance of the picture makes this distinction difficult, but I will point to the two lines of evidence that have convinced me that some of the trees are in fact paper birches.

The girth and shape of the larger trees are more consistent with the growth form of birches vs. the usually slender, single-stemmed aspen.
In the OP's picture, you cannot see peeling or lenticels, but this might be due simply to the distance from the trees. However, you can see a brownish/orangish coloration on a number of the trees, which is consistent with numerous descriptions of paper birch trees that have already started peeling revealing brown/orange bark.

Conclusion = Hard to tell, and likely actually a mix of Paper Birch (Betula papyrifera) and Quaking Aspen (Populus tremuloides). I think you're looking at taller aspen and mostly wider paper birch.


Can proteins structure change depending of alimentation of an organism?

While it is theoretically possible for a protein to change size (based on length) because of nutrition, I don't think that's happening here.

You are right-- DNA encodes information that is transcribed to RNA which is translated into proteins. Proteins are made of a finite number of amino acids, which are the building blocks of proteins. Proteins can be modified (and can be cleaved to make the protein shorter), but I think this claim of "cow milk protein becomes longer" is a misunderstanding because there is not a single "cow milk protein", but rather many.

There are many different proteins in cow milk, and most of them are casein proteins. source

The milk protein likely at the root of this claim is beta-casein. It was a hot topic in the 1990s, because there are a dozen different variants of this beta-casein protein. Two of these variants are the most common in milk have been studied a lot: variant A1 and A2. The only way these are different is a single amino acid change at amino acid position 67 (remember that proteins are made of amino acids). Variant A1 has a histidine amino acid but variant A2 has a proline. What does that mean? That means that A1 can be cut (in your body) to produce a smaller protein bit (called a peptide). Because of the proline in the A2 variant, it cannot be cut like the A1 variant. The peptide resulting from the A1 getting cut is called BCM7.

In short:
beta-casein variant A1: can be cut to produce BCM7
beta-caesin variant A2: gets cut way less than A1 so way less BCM7 is produced.

So, what is BCM7? It had been reported to been linked to some different diseases but the European Food Safety Authority (EFSA) published this report which concludes that there is no link between BCM7 and non-communicable diseases. Despite this, there is still a lot of talk about A1 vs A2 in the dairy community. While websites such as this appear compelling, remember the EFSA report!

this paper is open source and has the information about these variants that is summarized above.

So what does all this have to do with "cow milk protein" changing size? Maybe more cows used as dairy cows have the A2 variant, which would not produce as much BCM7 (the small peptide). Since A2 is not cleaved to produce BCM7, it could be thought of as "longer"... at least relative to only a few thousand years ago.
The beta-casein A2 variant is thought to be the original version of beta-casein from undomesticated cows.

So, if this claim was originally about beta-casein, you can respond that "yes, the beta-casein protein can be thought of longer because it is not cut to produce the BCM7 peptide as much as the A1 variant is, but it is also the original beta-casein size." Whether it was 10,000 years ago or just now, the A2 beta-casein variant is the same size.

tl;dr / Good reading from the California Dairy Research Foundation.


How do plants maintain air spaces in leaves?

There has not been not much research on this topic, which has caused lack of definite answer. Sibbernsen et al, 2017 performed a study on response of stomatal opening on filling these air spaces with water. They suggest the existence of a vapor-phase signal (from water) that originates in the mesophyll and causes stomata to open in the light. In another research, Wiebe et al, 1976 were able to remove the air spaces with the use of paraffin oil which infiltrated the spaces. They show that leaf air spaces contain invaginations which are extensions of air space system and increase conductivity of CO2 to the chloroplasts which line these invaginations.

Stomatal transpiration gives a clue to this. When the stomata open, they expose the internal environment to the atmosphere. Due to this, the air spaces get filled with water vapors which, due to concentration gradient, flow outwards from the leaf. To maintain the inner water vapors, more water is evaporated from the nearby cells, which leads to more transpiration. This hints that some water is present all the time in these air spaces in the form of water vapors. However, when the concentration of vapors becomes high, the nearby cells might take in some water or the stomata might open to maintain the concentration. See this article for some details on this.

At last, there is Woolley et al, 1983 which concludes that the mechanism behind the maintenance of these air spaces is still largely unknown.


Why was the cackling goose split off as a distinct species from the Canada goose in 2004?

The "white-cheeked" geese have long been subject to taxonomic controversy. From the 1920s to the 1950s, authorities have classified them into between one and four species. Although Aldrich in 1946 asserted there was near-unanimous agreement among Arctic biologists that there were two species, from the 1950s Delacour's taxonomy was most often followed, which had one species (Branta canadensis) and twelve subspecies.(1)

What changed the consensus were DNA studies.  Mitochondrial DNA (mtDNA), which is passed on without recombination, showed distinct sequences supporting two species. One RFLP analysis of mtDNA suggested the split between these two species happened about one million years ago.(1)

The species divide mainly along size and breeding location lines.  The Cackling Goose (Branta hutchinsii) is smaller and breeds on the Arctic tundra. The (present) Canada Goose species (Branta canadensis) mostly takes a larger form and breeds mostly in non-tundra areas.(1)

(1) - Mlodinow, S. G., et al. "Distribution and identification of Cackling Goose (Branta hutchinsii) subspecies." North American Birds 62.3 (2008): 344-360.


I believe you speak of some species of Formica spp., such as Formica polyctena (nest example)

You should mind that (i) ants are not particularly noisy insects; (ii) ant nests are 3-dimensional structures within which ants are heterogeneously distributed. So considering a microphone somewhere on the nest where you happened to see more ants, mostly you will be picking up noises from foragers stumbling into debris while moving around. And that only when that region of the nest happens to be most active, which was your original concern. In case I am wrong and you're interested in some smaller ant species (e.g. Solenopsis fugax or Lasius flavus) then you will probably record few if any significant sounds resulting from ants' activities.

Thus my first advice if you're focusing on foragers moving around the nest surface is that you record them in the afternoon of your hottest days, particularly if they're refurbishing their nest or upon disturbance. If you leave the microphone for extended periods try to find out where most foragers are coming out from (and pray they'll not damage the equipment) and leave it there in the afternoon of a dry, hot day.

Now, I am not sure about your ultimate goal, but in case you want to actually hear the ants instead of their stumbling around, then you should focus on having a tiny (protected) microphone inserted into a nest chamber. It is hard to say when the insides of a nest of unknown species will be particularly active, but usually during a fair day, under the sunlight exposure following a wet night. Finding the best region to record ants stridulating inside their nest will depend on finding the best nest location(s) and equipment.

Good luck!


In germ cells telomerase enzyme is active and elongates telomeres, so youngsters are not born older than their parents due to telomeres.

Still, they do receive mutations, accumulated by their parents' germ-line cells, i.e. eggs and sperm. Most of the mutations occur upon division of the cell. Egg cells don't undergo many divisions - they are created in the course of embryonic development of a woman and then are spent one-by-one. At the same time, precursors of sperm cells divide constantly, thus accumulating mutations at a constant rate.

Got no time to look for a hyperlink, but I read that no matter what is the age of the mother, she gives 15 new single-nucleotide mutations on average to her offspring. Father gives about 10 mutations for each year of his life after reaching puberty, historically 70 on average. Out of those mutations most are neutral or silent (due to genetic code degeneracy), but on average ~1/70 leads to a change in aminoacid sequence of some protein, usually harmful.

So, although babies don't get older, but alas, they get uglier as generations pass :( Natural selection is what saves us from deterioration, so that the weakest are sentenced to childlessness.

EDIT:

Added a couple of hyperlinks as requested: decay of cognitive indicators of children with parent's age:
http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1000040

Another link: drosophila simulation of middle-class neighborhood (MCN) population, where each family has exactly 2 children, son and daughter, and no natural selection pressure is applied: such population rapidly deteriorates with fitness in wilderness decreasing by 2% per generation:
http://www.ncbi.nlm.nih.gov/pubmed/9371795


I think that it is termites larvae. For more info check this :  Termites follow the typical life cycle of insects that have a gradual life cycle: they begin as eggs, and then enter nymphal to adult stages. In termite development, newly hatched termites are sometimes referred to as “larvae,” which is not to be confused with the larvae of complete metamorphosis insects like flies.

Termite larvae typically hatch within a few weeks. They are approximately the same size as the eggs from which they hatched and are immediately tended to by worker termites. They often comprise a large part of a termite colony.

Similar to other insect young, termite larvae go through a series of molts, during which they shed their skins. From the larval stage, termite larvae may evolve into other members of the colony’s castes.

If you suspect you have termite activity in or near your home, contact a pest control professional. Termite damage can go undetected and result in significant financial loss from their damage. A termite inspector can inspect a home for signs of activity and conditions that are attractive to termites. They also can offer services to treat and protect the home from potential future damage.


Are the transitions between the different brain frequencies states easy to see on an EEG?

Delta/theta/alpha/beta/gamma are not different states and so there are no changes "between" them. These are terms used to label different bands of the frequency spectrum. Every EEG has energy in all of these bands. Brain state can change/be measured by the relative changes in different bands (either relative to each other, or in absolute power change over time), but there is always some energy in every band.
Here are some example spectra from different brain states (stages of sleep and anesthesia states) across different brain regions:

(from Banks, M. I., Krause, B. M., Endemann, C. M., Campbell, D. I., Kovach, C. K., Dyken, M. E., ... & Nourski, K. V. (2020). Cortical functional connectivity indexes arousal state during sleep and anesthesia. NeuroImage, 211, 116627. Disclosure: I am an author on this paper)
WS and WA refer to "wake" in the sleep and anesthesia experiments respectively; N1, N2, and REM are stages of sleep. S refers to sedated under anesthesia - subjects can still respond to commands, and U refers to unresponsive under anesthesia. These are actually not from EEG but from electrocorticography where the electrodes are placed directly on the brain, sometimes called iEEG, but there are a lot of similarities with EEG.
You can see that in all brain states, there is energy across all the frequency bands (identified with Greek letters), but there are changes with state. For example, delta has more power during N2 sleep across the brain. A trained eye could also easily pick this up in the time-domain EEG signal, but it's much easier to convert to the frequency domain like in this figure.
You'll notice that the energy decreases with increasing frequency. This is normal, and is typical of natural frequency spectra with certain properties, see Pink Noise; it's rare to ever have less power in the delta band than any other band, for example. You will also see that for the most part the spectra are gradually changing: there are few peaks in the spectrum, and it can be a bit misleading to refer to energy in a specific band or to compare between bands when there is no peak there. Some exceptions are that there is typically a peak in the alpha band for humans, especially with eyes closed. Hippocampus tends to generate rhythms in the theta band, and rodents have very large hippocampus relative to the rest of cortex, so you'll often see a theta peak in rodents especially during locomotion.
Lastly, these EEG differences are probably not the best way to discriminate between different brain states. There are lots of other measures that seem to do better. In the rest of the paper that I've taken this figure from, my colleagues and I use a specific measure called the weighted phase lag index which does a much better job at discriminating between putative conscious and unconscious states.


Is reverse senescence/"anti-aging" actually scientifically possible among humans yet?

Short Answer

You might be interested in learning about telomeres, telomerase, and telomerase gene therapy.

For example, Boccardi & Herbig (2012): describe a mouse study in which they used telomerase gene therapy to improve the healthspan and lifespan of mice by up to 24%.

As far as I know, we have no successful human trials of similar therapies that have targeted and succeeded at "decreasing the age" of humans.

However, this source does claim that a woman attempted to do so. I cannot substantiate these claims in any way, so I'm skeptical at best...

 Long Answer:

Telomere 101:

Telomere: non-coding nucleotide sequences on the tips of chromosomal DNA strands.

Due to the inability for DNA polymerase to replace RNA primers on the end of linear strands of eukaryotic DNA during DNA replication, ~50-100 base pairs are removed from the daughter strand from each replication event.

The "junk" (i.e., non-coding) telomere sequences (which could repeat 1000s of times) provide buffers against losing more valuable DNA when this happens. Eventually though, the telomeres run out, and replication events could lead to loss of coding regions of DNA...

According to Boccardi & Herbig (2012):

  As we age, telomeres in most of our tissues progressively become shorter and therefore likely contribute to the failure of our organs and tissues observed in old age. Supporting this are data demonstrating that healthy lifespan is positively correlated with longer telomeres in humans, and patients suffering from age‐related diseases and premature aging syndromes display shorter telomeres compared to healthy individuals (Zhu et al, 2011).

The enzyme, telomerase can replace these telomeres, but telomerase is really only active in stem cells and white blood cells, so most adult cells lack this regeneration ability.

This is where telomerase gene therapy  comes into play.

In the simplest sense, this approach attempts to artificially add telomerase to adult cells to essentially add back telomeres and potentially slow or even reverse the aging process.*

 *Note: As far as I know, we don't actually know whether short telomeres are simply an effect of aging or if they are actually the cause of aging (and ultimately death), so this gene therapy is running on an relatively unsupported hypothesis.

For example: Boccardi & Herbig (2012) "Telomerase gene therapy: a novel approach to combat aging".

They found that adding telomerase to 1 year old mice increased their lifespan by 24%.

 Credit: Boccardi & Herbig (2012):

As Boccardi & Herbig (2012) note, however, applied human studies are still a thing of the future.

  While these studies provide a proof‐of‐principle that telomerase gene therapy is a feasible and generally safe approach to improve healthspan and treat disorders associated with short telomeres, a clinical application in humans is likely still some time away.

However, this source does claim that a woman (Elizabeth Parrish, CEO of Bioviva USA Inc. -- notice the website :p) attempted to do so -- I cannot substantiate these claims in any way, so I'm skeptical at best...

Citations and additional suggested reading:

Boccardi, V. and Herbig, U., 2012. Telomerase gene therapy: a novel approach to combat aging. EMBO molecular medicine, 4(8), pp.685-687. read here
Campisi, J., Kim, S.H., Lim, C.S. and Rubio, M., 2001. Cellular senescence, cancer and aging: the telomere connection. Experimental gerontology, 36(10), pp.1619-1637. read here
Zhu, H., Belcher, M. and Van Der Harst, P., 2011. Healthy aging and disease: role for telomere biology?. Clinical Science, 120(10), pp.427-440.


It is an ormányosbogár species. :D
Curculionidae in Latin. I don't know the exact species, but it is common here in Hungary.

It is something like Mecinus janthinus, but it seems like shorter. Probably Mecinus pyraster or another Mecinus species.

Figure 1 - Mecinus janthinus - source

I think it is Sitophilus granarius aka. wheat weevil, but it is hard to decide because of the poor quality photo...

Figure 2 - Sitophilus granarius - wheat weevil - source


The scope of this question is too wide to be answered on Biology SE. However I will give you very brief answers to your questions (as I have rephrased them) and point you towards some sources of basic information on the Internet. After reading these you may wish to return with more specific questions. I have also briefly summarized some of the problems which it is useful to be aware of before reading details of specific approaches to gene therapy,.
Answers

(i) Some approaches involve attempts to replace a defective gene with
a functional gene or add the latter to the patient’s DNA. Others
involve drugs, often nucleic acid in nature.
(ii) Current efforts often have the more modest aim of ameliorating the disease, although there are also efforts to reverse the condition.
(iii) Gene therapy is not yet in general clinical use, although for some diseases (e.g. Severe Combined Immune Deficiency and Chronic Granulomatus Disorder) there have been reports of success in limited clinical trials.

General Reading
I am not an expert in this area, but by Googling for ‘Gene Therapy’ I came up with the following pages that you may find helpful.

Your Genome
University of Utah: Approaches to Gene Therapy
American Society of Cell and Gene
Therapy

You may also be interested to read about the currently controversial drug, Eteplirsen.
Problems in Gene Therapy
Rather than giving you details of technical approaches to gene therapy, for which you may not have the necessary scientific background, I draw your attention to some of the key problems and questions that have to be addressed in this area.

Does one need to counteract the harmful effect of a mutant gene product (e.g. sickle cell haemoglobin), or is it sufficient to produce a ‘good’ gene product to remedy a deficit?
Is it possible to target new cells or does one have to deal with existing mature cells?
(Some cells like blood and immune cells are constantly renewing themselves, whereas others like muscle turn over much more slowly. The latter are more difficult to deal with.)
How can the DNA (or drug) be deliverdd to the cell, and only to the appropriate cell. (A variety of delivery techniques have been employed in different circumstances.)
How can the therapeutic DNA be incorporated into the appropriate position in the genome, and how can one ensure that it is expressed, and that no other genes are affected. (Early attempts at gene therapy using in which DNA was inserted at the wrong position resulted in cancers. However technology here is moving rapidly.)


No, don't drink it... And here's why.

Ingesting lactic acid or for some reason having too much of it in your body can cause a variety of health problems ranging from mild to deadly. There are two types of lactic acidosis; the first is called metabolic acidosis and the second is known as respiratory.

Metabolic acidosis - which is what would be caused by ingestion - occurs when the fluids in your body build up too much of the acid and your kidneys can no longer keep up with the demand placed on them. Or they over respond and remove too much base from your body, leaving you acidic.

Respiratory acidosis is caused when your lungs cannot effectively remove CO2 from the blood. A buildup of CO2 leads to a more acidic body chemistry.

Regardless of what the cause of the acidosis was, you can expect some of the following.

Symptoms of metabolic acidosis:

~Rapid and shallow breathing

~Confusion

~Fatigue

~Headache

~Sleeplessness

~Lack of appetite

~Severe acidosis can cause shock, organ failure and even death

Diagnosis of acidosis:

A series of blood tests will check calcium, sugar and electrolyte concentrations in your blood.

My sources for this information:

Healthline

WikiPedia on Lactic Acidosis


Why would a bumblebee regularly hover over a arborvitae hedge?

Could actually be a male carpenter bee. They hover around like that waiting for females to pass by. If it is a male carpenter bee dont worry about it, they arent equipped with a stinger.


What is the tRNA gene copy variation between different yeast strains?

I'd take that computational angle and run the sequence data through tRNAscan-SE (Lowe & Eddy, Nucl Acids Res 25: 955-964). Ideally, you'd install this locally. This tool is what the UCSC folks use and it has been the best known, most widely used tRNA predictor for years. It's what we all used on Arabidopsis thaliana genome annotation back in the late 1990's.

There is also a genomic tRNA database that may have many of the predictions you seek, at least for some of your species/strains.


Why is it that cats can jump so high for their size, compared with humans?

There is not a linear relationship between the size of a muscle and its power. The cat weighs significantly less, but the decline in muscle power is not identical. If he weighs 20x less than you, but his muscle generate 1/5 as much force, he will still be able to jump way higher than you.


What is an example of a plant species that is a halophyte with seeds that germinate quickly?

It turns out that your research question about halophytes has been asked many times before. You should learn from your predecessors...

Seed germination in halophytes displays a high degree of inter- and intra-specific variability. However, Khan & Gul (2006) report that germination patterns respond to a number of environmental factors (including temperature, NaCl concentration, and presence of different regulating chemicals).

Their paper has over 100 citations, many of which cite germination studies of numerous halophyte species. I'd recommend you start your search there.

You'd also probably benefit by perusing the sources in Ungar (1978) and Panuccio et al. (2014).

Citations

Khan, M.A. & B. Gul. 2006. Halophyte Seed Germination. In Halophyte Utilization and Regional Sustainable Development of Agriculture. pp.11-30
Panuccio, M.R., S.E. Jacobsen, S.S. Akhtar and  A. Muscolo. 2014. Effect of saline water on seed germination and early seedling growth of the halophyte quinoa. AoB PLANTS 6: plu047
Ungar, I.A. 1978. Halophyte Seed Germination. Botanical Review 44(2): 233-264


Bioinformatics - DNA binding, sequence-specific protein data

You are seeking a database of transcription factor binding specificities. Some model organism databases (which are manually curated), such as Wormbase contain some of this annotation. I suggest you search PubMed for papers by Tim Hughes at the University of Toronto. He has published extensively on this topic over the past 5 years.  Papers he cites, and papers that cite him, will let you bootstrap your way in to the topic.


It looks like a carpet beetle larvae(Anthrenus verbasci) to me. This seems to fit considering you found it in your house, which is one place they are fairly common. I would not be able to tell you if you should be worried, I am not a biologist.


Why are new vessels more permeable in microvasculature?

In adult/pediatric humans, no they don't.  A good figure to get everyone on the same page was made by Cleaver & Melton:

It is important to note that:

  In fact, endothelial diversity is reflected by vessel size-specific,
  organ-specific and even age-specific differences. (1)

Developing blood vessels in the fetus can be a bit of a different story, and highlights the fact the one should loose the "inert plumbing" mentality of the previous century.  Modern research tells us that the epithelium is a very dynamic region that participates heavily with signalling.

When large vessels are growing the fetus, mesenchymal stem cells and neural crest cells are the normal precursors to pericytes, but depending on exposure the line between pericyte and smooth-muscle cell can be blurred (2).  I'm assuming it's beyond the scope of the answer to go into the signalling differences.

A good review of endothelium generation, and the surrounding tissue, can be found here.


Genetic Drift: Models, assumptions and empirical observations

This question has been around for a while, so I'll try to start with a partial answer.

The basic assumptions of the standard Wright-Fisher-Model are:

Constant population size $N$.
Discrete, non-overlapping generations.
Neutrality (e.g. all individuals are equally likely to reproduce)

I prefer looking at the model for haploid/chromosomes. If you bundle up chromosomes to polyploids, then you get the additional assumption of random mating, e.g. all pairs of individuals are equally likely to reproduce.

I might have missed something, but these assumptions should be sufficient to generate the Wright-Fisher-Dynamics: When we build a new generation, we have to fill $N$ spots again (follows from the first two assumptions). As each old individual is equally likely to reproduce (third assumption), e.g. to become parent of a new individual, we get the multinomial offspring distribution.

The main difference in the Moran model is that it assumes overlapping generations. Main assumptions here are:

Again constant population size.
Individuals reproduce at a constant rate.
Neutrality (however the Moran model can relatively easily be adapted to incorporate positive selection).

Every time an individual reproduces, another one instantly dies to maintain the constant population size.

Interestingly, the models have the same diffusion limit, e.g. they behave similarly for large populations (and identically for an 'infinitely large population'). If you trace the ancestry of a sample back in a large population, you will get close to Kingman's Coalescent under both models.

I think the two models exist more because of their distinct mathematical properties, than because one fits better to certain natural populations than the other. I'm not aware of any experiments that have shown how well they fit, maybe someone else can jump in here.


Enzyme Inhibitors: Using in vivo in yeast

This is usually the way this kind of inhibitors are used. There needs to be a way that they come into the cells (if they stay in solution and cannot reach their target they will be useless), but then they inhibit their targets.

What usually needs to be done is to determine which concentrations are needed in the cell culture (or the medium) to be effective for the inhibition but not to harm the cells. Therefore I usually use different concentrations of the inhibitor in culture and then measure the outcome.

To find the right concentrations, see if there are some recommendations from the manufacturers. Otherwise you will probably have to dig through Pubmed to find some starting point.


The psychologic and behavioral components of sickness represent a highly organized strategy of the organism to fight infection. Sickness is generally accompanied by fatigue, numbness, coldness, muscle and joint aches, and reduced appetite. These symptoms are not simply an effect caused by the pathogen. Instead, it now believed to be an active defense strategy of the body, referred to as “sickness behavior”. Sickness behavior is thought to be an adaptive response that enhances recovery by conserving energy to combat acute inflammation (Maes et al. 2012). It is triggered by the proinflammatory cytokines produced by activated cells of the innate immune system due to the presence of pathogens. These cytokines include mainly interleukin (IL) 1 (IL-1α and IL-1β), IL-6, and tumor necrosis factor α (TNF-α) (Dantzer, 2009; Plata-Salamán, 1998).

One of the sickness behaviors is a loss of appetite. Among a host of other effects, cytokines are believed to inhibit feeding by their actions in the hypothalamus. The hypothalamus is an important neural center that regulates food intake (Plata-Salamán, 1998; Meister, 2000).

I refer you to Maes et al (2012), Plata-Salamán (1998) and Dantzer (2009) for backgrounds and further reading, as cytokine immunology is highly complex and this answer is anything but complete.

References
- Dantzer, Immunol Allergy Clin North Am (2009); 29(2): 247–64
- Maes et al, BMJ (2012); 10: 66
- Meister, Vitam Horm (2000); 59: 265-304
- Plata-Salamán, Semin Oncol (1998); 25(1 Suppl 1):64-72


It looks to me like a cigarette beetle- they can infest many different types of products so I would definitely check everything carefully. Here's the link I used as a source, you can find more info here: https://www.orkin.com/other/beetles/cigarette-beetles/


Does the arrangement of amino acids in a protein matter for nutrition?

Arrangement of amino acids determines the protein structure which in turn can determine how easy it is to digest the protein. I cannot think of an example right now; never really checked if two entirely different proteins have identical composition. However, it is not really surprising. In chemistry, it is known that different isomers have vastly different physical properties.

So if the two proteins have different digestibility then they will have different nutritive values.

Regarding, protein digestion and nutrition. New proteins are built from individual amino acids and not pre-formed oligomers. Read about translation. So at some point the ingested protein has to be completely broken down into amino acids.


Decomposition Rate of A Body In A Wet Environment

It depends on the temperature of the environment as well. In the heat of summer and in a watery environment, I can verify through unfortunate personal reference that stuff can decompose very quickly. I honestly didn't look at the image, but judging by your description it can't have been there a year. There would be nothing left. Hungry bacteria and decomposers would have left nothing but bones by then. I would say your guess is more on target.


Why is it that I can understand speech through one ear better than the other ear?

I remember reading many years ago that this is normal...

Indeed, this is normal and quite expected: understanding one's voice is a brain task, not an ear (sensory organ) task, and if there is difference in the parsing capabilities between the left and the right hemisphere (which is the case, as we are going to see soon), the stimuli captured by the right ear will be treated differently from the stimuli captured by the left ear.

To understand what's happening here we have to know two things: the Wernicke's Area and Dichotic listening test.

The Wernicke Area, quoting Wikipedia, is...

  ...located in the posterior section of the superior temporal gyrus (STG) in the (most commonly) left cerebral hemisphere. It is involved in the comprehension or understanding of written and spoken language (in contrast to Broca's area that is involved in the production of language).

Thus, in most people, the left hemisphere is responsible for (most of) linguistic capabilities, both producing language (Broca's area) and understanding language (Werneck's area).

Now comes the dichotic listening test. In the dichotic listening test, two different stimuli are presented to each ear. The results of the test indicate that there is preference for the information captured by one of the ears.

According to Freberg (2010):

  Dichotic Listening Is Related to Hemisphere Lateralization for Language: When conflicting information is provided to the two ears, the person who has language lateralized to the left hemisphere will show a preference for the word heard by the right ear. The information presented to the right ear will reach Wernicke's area in the left hemisphere faster than the information presented to the left ear. (emphasis mine)

Here is an image explaining the test (click for a larger size):

As you can see, there is a advantage to the right ear. According to Hugdahl et al. (2003):

  In the present paper we report on speech perception in left (n=16) and right (n=10) frontal lobe nonaphasic patients compared with healthy controls (n=26). [...] The results showed significant differences between the left and right lesioned patients in their performance on the dichotic listening test. While the right lesioned patients and the control subjects had a normal and expected right ear advantage, the left lesioned patients performed almost at random with regard to the right and left ear stimulus. (emphasis mine)

Sources:

Freberg, L. (2010). Discovering biological psychology. 1st ed.
Hugdahl, K., Bodner, T., Weiss, E. and Benke, T. (2003). Dichotic listening performance and frontal lobe function. Cognitive Brain Research, 16(1), pp.58-65.


Is summation linear in a passive membrane?

For a membrane to satisfy the conditions for linear summation implies that when two EPSPs of amplitude $A$ and $B$ are summed at the integration zone, the resulting output signal will be of amplitude $A+B$. Since the signal dissipates due to time and length constants, increasing the delay between the two inputs means that the later input will be dissipated so $A+B$ will be smaller than it would have if the delay was shorter. Under this scenario, inputs $A$ and $B$ are still summed linearly. However, if the delay is shorter than the time constants or the inputs are delivered closer in space than the length constant, then you may get non-linear summation since the output signal at the integration zone will be larger than $A+B$.

Have a look here for more information (especially Figure 7):
Silver RA. Neuronal arithmetic. Nature reviews Neuroscience. 2010;11(7):474-489. doi:10.1038/nrn2864.


What gives diarrhoea caused by Cholera its milky colour?

The color of our feces is caused by the breakdown products of the hemoglobin, namely Bilirubin and Stercobilin, which depending on the concentration, cause a yellow to brown color. See here for details.

Since the amount of liquid lost by the cholera diarrhea with up to 250ml/kg bodyweight is really high, there is only very little to nothing of these breakdown products available in the feces. This causes an absence of color.


Why the total phosphorylation of certain neuronal proteins decrease during development?

Here are a couple Wikipedia articles that might help out:

Critical period - Critical period: the idea that certain types of plasticity in the nervous system occur only at certain "critical" times.

Long-term potentiation - LTP, talked a lot about in the paper you linked: it's a mechanism for strengthening of synaptic connections.

Synaptic pruning - # synapses/strength of synapses tend to decrease from adolescence to adulthood

The paper you linked talks a lot about the role of phosphorylated RIM1a in LTP. Without knowing more specifically about this protein, and from just a glance at the paper you linked, I'd suspect that RIM1a is phosphorylated during periods of increased LTP, particularly earlier in development, and as animals age and their brains go into the synaptic pruning phase, LTP is downregulated overall, and one of mechanisms could be the lack of phoshporylated RIM1a.


Indeed, good question. There's tiny bats, large bats, and so many different species of them! A clue can be found in the observation that each bat species is almost always restricted to a small geographical region. With this in mind, it has been shown that an animal lineage's ability to diversify quickly in new environments depends largely on its diet. Bats have an incredible variety of dietary sources. Plant nectar, insects (there's so many different kinds of insects...), blood-feeding, and more! So, as you can imagine, bat species are restricted because they have specialized diets and because they are very good at taking up new diets over evolutionary time. Unfortunately for them, it restricts them to a geographical location much of the time. Geographical restriction is always a good starting point for speciation events, and there have been many in the bat clade. But why bats, specifically, you might ask? Well - it is argued (below) that it is due to the characteristics of their skulls, rather than their wings.

Dumont, E. R., Dávalos, L. M., Goldberg, A., Santana, S. E., Rex, K., & Voigt, C. C. (2012). Morphological innovation, diversification and invasion of a new adaptive zone. Proc. R. Soc. B, 279(1734), 1797-1805.


Why is the ability to drink salt water so rare in land-animals?

According to an answer here there is around 356,000 km of coastline on the planet. If we take an average human walking speed of say 5 km/h then our 5 minute walk takes us 0.417 km inland - giving approximately 150,000 km^2 of land conveniently supplied with sea water.

Now according to this page the total amount of land area is around 150,000,000 km^2 which according to this page is covered by somewhere in the vicinity of 117 million lakes [I'm certain a large portion of them are more accurately described as puddles but well go with that number for now], that gives on average a fresh water body every 1.3 km^2.

If we simplify things and imagine dividing the land area into 1.3 km^2 grid with ~1.14 km the distance separating each watering hole meaning the furthest distance to a watering hole across all the earths land area (ON AVERAGE) is around 0.570 km or just under 7 minutes walk (using our previous 5km/h)

So according to my very very rough calculations only around 0.1% of the land area is located within 5 minutes of sea water while 100% is located within 7 minutes of fresh water! I don't think that extra two minute walk is going to be that much of an evolutionary drive for any species.


How detachment/separation works in biology?

Reproductive budding and what you call 'cellular budding' are really highly related processes. Budding as a form of reproduction essentially partitions protein aggregates and damaged cellular components into the host or mother and builds fresh or 'young' cells on the opposite side of a partition. To begin understanding this look at Saccharomyces cerevisiae (budding yeast) which forms protein rings (from the septin proteins) at the membrane, around the bud neck which separates the mother and daughter cells Hartwell 1971. This ring acts a partition that in part, withholds protein aggregates and certain proteins from diffusing from the mother to the daughter. This protein ring is an example of how cells limit diffusion of proteins and cellular components to the daughter cell. Another good example that comes to mind is Linder 2007, though it is done in E Coli, not budding yeast, where mother cells maintain protein aggregates and age, while the daughter cells are given fresh components and are therefore more fresh and 'young'.

Now like you mention, imagine this process in a multicellular organism to be fundamentally the same. At some point the multicellular organism will start an outgrowth of cells, while restricting what materials are given to the daughter cells to maintain their youth. And eventually a new organism will have been created. Some of the details will be different, but the fundamental process is is quite similar. In that you start with an old cell that creates a new cell from scratch, but rather than splitting all cellular components equally between mother and daughter, the daughter cells is made in peak condition while the mother cell retains much of the cell 'junk' like protein aggregates.

Hopefully that starts to answer your question.


What concentration of sugar is optimal for baker's yeast fermentation?

When glucose and fructose are fermented separately, the uptake profiles indicate that both sugars are utilized at similar rates. However, when fermentations are conducted in media containing an equal concentration of glucose and fructose, glucose is utilized at approximately twice the rate of fructose. The preferential uptake of glucose also occurred when sucrose, which was first rapidly hydrolyzed into glucose and fructose by the action of the enzyme invertase, was employed as a substrate. Similar results were observed in the fermentation of brewer's wort and wort containing 30% sucrose and 30% glucose as adjuncts. In addition, the high levels of glucose in the wort exerted severe catabolite repression on maltose utilization in the Saccharo~ myces uvarum (carlsbergensis) brewing strain. Kinetic analysis of glucose and fructose uptake in Saccharomyces cerevisiae revealed a Km of 1.6 mM for glucose and 20 mM for fructose. Thus, the yeast strain has a higher affinity for glucose than fructose. Growth on glucose or fructose had no repressible effect on the uptake of either sugar. In addition, glucose inhibited fructose uptake by 60% and likewise fructose inhibited glucose uptake by 40%. These results indicate that glucose and fructose share the same membrane transport components

References

D'Amore, Tony, Inge Russell, and Graham G. Stewart. "Sugar utilization by yeast during fermentation." Journal of industrial microbiology 4.4 (1989): 315-323.

Thirwell, A.J. and R.L. Busby. 1982. Liquid sugar as a brewing adjunct. Inst. Brew. Proc. Conv. (Aust. and N.Z. Sect.) 17:77 84.
, http://www.123HelpMe.com/view.asp?id=121963


Do creatures exist which can stop their hearing at will?

Yes
Many echolocating bats use the stapedius muscle to separate the inner ear bones
when they emit their call so they are not deafened by their own call. Their ears are highly sensitive to the very frequency they are making so they need a way to protect against it. They are only deafened for 2-8ms but that is enough to protect their hearing while still being able to hear any echo.
Source


Any food crops that could grow in a desert provided that they get fertilizer and water

Even if you have unlimited water available to the plants you'd still have to worry about the high temperatures and light levels of these areas. In the hot periods I would look into any plant that uses c4 carbon fixation like millet, sorghum, corn, sugar cane... In the cooler periods maybe look into rotating to a cool season legume crop like the cowpea that would help fix nitrogen. Another really important thing to do would be to find cover crops that will hold down the soil and build up some life in the otherwise sterile sands of the desert.


Heterochromatin binding sites position information

Have a look at these ChIP-seq data for HP1 in Drosophila: 1, 2 and 3. From ChIP-seq data you can find the distance between the TFBS peaks and the TSS of the gene.

You can also look for nucleosome positioning and DNAse hypersensitvity regions; for the former, I am sure that data is available for Drosophila.


How many times did photosynthesis evolve?

The emergence of photosynthesis has occurred rather independently in multiple organisms. One way of looking at this is to look at the taxonomic distribution of photosynthesis reaction centers, which points to 5-10 origins according to current data (mostly in bacteria). That number has some big error bars as we are talking about very deep, old branches of the tree of life.
There are other criteria that we could use- for example the evolution of carbon fixation. However, that includes also chemoautotrophy, and is thus a bit more expansive.
Note that by some definitions the acquisition of cyanobacteria in plants may not even represent an independent emergence of photosynthesis, as the cyanobacteria already did photosynthesis!
If your question is more narrowly "how many times did photosynthesis evolve in eukaryotes" (not bacteria or archaea), then you would also need to include animals that do photosynthesis in a way similar to (though I believe less efficiently than) plants. They seem to similarly use endocytosis to acquire photosynthetic machinery from photosynthetic cells that they eat.
Update
In response to comment from @shigeta, I'll add that the review that I link focuses on the reaction centers (RC) genes. They note that the RC genes probably had a single emergence, but that horizontal gene transfer is probably responsible for the current distribution of the organismal trait of photosynthesis:

Significant evidence indicates that the current distribution of photosynthesis in bacteria is the result of substantial amounts of horizontal gene transfer, which has shuffled the genetic information that codes for various parts of the photosynthetic apparatus, so that no one simple branching diagram can accurately represent the evolution of photosynthesis (Raymond et al., 2002).


Ribosomal RNA amount in a Drosophila cell

The protocol you are using will not only leave the sample with rRNA but also non coding RNA.

Many RNA protocols will separate mRNA by affinity of a carrier to the polyA tail.  This protocol references an older paper that estimates that only 5% of RNA is mRNA.  I'd be surprised if this ratio changed by more than 2-3 fold in drosophila.

I assume that %age is by weight but it could be a densitometry measurement which is similarly interpreted.


What species is this bushy thorny yellow-flowered angiosperm from Morocco?

I happened to come across a photo of a similar leafless shrub (without flowers) that also had 120 degree branches and looked thorny, or Spiny is probably a better description. It helped me to identify the plant in your photo as a Launaea arborescens. It is an unusual species of Chicory in the dandelion family, Asteraceae. Being tolerant of arid locations, it native to northwest Africa and southern Spain.

http://encyclopaedia.alpinegardensociety.net/plants/Launaea/arborescens

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

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


Strange Cordeyceps-looking Mushroom in Australia

You found a member of the stinkhorn family, The Phallales (in the family Phallacea), probably a Veiled Lady (Phallus indusiatus) or a Phallus multicolor (they have other names as well.) They are common in Asia, Africa, the Americas, and Australia. Don't eat them; they're attractive to dogs (lovely aroma!) and there have been dog deaths.

These fungi produce a spore slime which has an intense smell of rotting meat or sewage, which is why flies are attracted to them.

They are commonly found in rotted woody material.


A state of unconsciousness does not guarantee analgesia nor amnesia. Besides, a muscle relaxant is often paramount to prevent movements. The perfect general anesthetic would do all of this and have hypnotic, analgesic, amnesic and muscle relaxant properties. Such compounds do not exist, because each effect works on a different part of the brain or elsewhere.

In practice, therefore, multiple compounds are administered to obtain the desired effect. A cocktail anesthetic not only ensures all the desired physiological changes, it also reduces the chance of toxic side effects relative to giving one constituent in a large enough dose to encompass all the effects. And there lies an important point, namely anesthetic depth.

If anesthesia is deep enough, all effects may, perhaps, be reached to some degree with a single compound, but the dose likely becomes so high that the side effects become too large. An example in this realm is alcohol, which when consumed in copious amounts, may come close in reaching all desired effects at least to some degree. A related compound is ether. But even with ether, which has been used in early days of surgery, surgical stress caused patients to die intra-operatively due to cardiac hyperactivity. Surgical stress needs to be minimized and that's why an analgesic is needed in the cocktail.

Commonly applied anelgesics in the OR are opiates, such as fentanyl. Anelgesics are critical for invasice surgery, because the body reacts to trauma even when the brain cannot process the information to the degree necessary to turn it into a conscious experience.

For instance, a widely used cocktail is propofol-based anesthesia: A propofol injection might be used to start anesthesia, fentanyl (injectable) is used to blunt the stress response, midazolam (injectable) given to ensure amnesia, and sevoflurane (inhalant) during the procedure to maintain the effects.


How do circulating androgens contribute to higher rates of hirsuteness in some women?

This review may be of interest:

Sharma D, Shanker V, Tegta G, Gupta M, Verma GK. Clinico-investigative profile of patients of hirsutism in a tertiary level institution. Int J Trichol [serial online] 2012 [cited 2013 Feb 9];4:69-74. Available from: http://www.ijtrichology.com/text.asp?2012/4/2/69/96904

As for the genetic causes of hirsutism, researchers thought the number of CAG repeats in the androgen receptor gene might play a role, but there was no evidence to that effect, as of 2000.  I couldn't find any newer papers, but here you go: http://jcem.endojournals.org/content/85/4/1735.
This paper was cited by the previous review, but Sharma et al didn't read more than the title, because they cited Calvo et al as evidence for the role of CAG repeats in hirsutism.

tl;dr: read Sharma et al, and look up the references.


If nerve consists of many axons, where are then their soma located?

Neurons or nerve cells typically have a dendritic region, an axon and a cell body. The axon is also referred to as a nerve fiber. The axon is typically the longest structure, while the dendrites are mostly situated close to the cell body. See the following figure 1:

Schematic of a nerve cell. Source: Prof. Brown.

Axons often bundle into nerves. For example, the peripheral nervous system contains many nerves. The cell bodies of the neurons that feed their axons into a nerve are organized into ganglions outside the nerve (Fig. 2).

The peripheral nervous system and the location of the ganglia. Source: Miami College.


How is consciousness linked to the brain?

This question is difficult to answer and in the end, we'll just have to accept that we don't really know (at least for now). My own understanding is that what we call our consciousness is an emergent phenomenon, arising from the extraordinarily complex network of billions of neurons interacting with each other within the brain. Perhaps the rest of the cells in the body - everything that is interconnected - should also be included. This would mean that we are, indeed, "a mix of chemicals interacting with each other", but in my opinion, that does not make being any less meaningful.

As a side note, although this seems to imply determinism, the future behaviour of complex systems such as our brain, or better yet, the entire universe, is impossible to predict accurately with any computing device. We, as well as the universe, are the best simulators of ourselves.

I think it is really difficult to handle questions like this. To start with, how do you even define "consciousness"? Also, I don't think that such a discussion belongs to philosophy; surely any plausible explanation of conciousness must be rooted within the framework of science.


What's the difference between Cytoplasmic pool and Granular storage pool?

Neurotransmitters like dopamine are synthesized in the cytoplasm and then imported into synaptic vesicles.  When the neurotransmitters are released it is by a fusion of the synaptic vesicle with the neuron's cell membrane, emptying the contents into the synaptic cleft.  Re-uptake of the neurotransmitter back into the pre-synaptic neuron's cytoplasm is done by active transporters, in Dopamine's case by DAT.  The cytoplasmic pool refers to the dopamine in the cytoplasm, while the granular pool refers to the dopamine stored in the synaptic vesicles.


The quick answer is "both", but the stoichiometry is not 1-to-1. The stoichiometry of the calvin cycle doesn't add up when thinking about a single molecules making one "turn" of the cycle. There is only one carbon (CO2) added, but three carbons (in PGAL) leave, which obviously cannot work.

What's happening is that multiple molecules are processed at the same time. The cycle is of course just a set of enzymes that continually catalyze their reactions, so there are always lots of molecules available for enzymes act on, and the cycle doesn't "get stuck" just because things don't add up in a single turn. The "regenerating" steps between PGAL and RuBP produce 3 molecules of RuBP from 5 molecules of PGAL (15 carbons total). Carboxylating these 3 RuBP molecules adds 3 carbons, so that one PGAL molecule can leave the cycle.

The reason for this odd stoichiometry is that the cycle needs to turn 3-carbon sugars (PGAL) into 5-carbon sugars (RuBP), which is rather complicated. Several enzymes work together in a complicated series of reactions to achieve this. A good resource for learning about the details is the MetaCyc database, where you can explore all the molecular details of the pathway.


You have to design your primers properly. Usually, in real-time PCR, you don't choose a very long product. Ideal product size is 150-300.
Next, see what your NRTI is analogous to. For e.g. if I am using AZT (Azathymidie), I would place my reverse primer at or after the last T.

There are alternate techniques as well. You can use primer extension (radiolabeled) and then quantify different products by scanning the photograph. However, this technique won't be as  quantitative as real-time PCR.


Activated carrier molecules and their relationship to enzymes

I will focus on the meaning of ‘activated carrier molecule’ as descriptions of enzymes abound. In order to do that I need to introduce two other ideas first. I apologize to the purists for tailoring this to the level of the question.
1. Gibbs Free Energy in Biochemical Considerations
There are different ways of considering energy, and in chemistry one may be used to considering bond energy in relation to a particular molecule. However in biochemistry (which is what this question is concerned with) the focus is on the energetics of overall processes. For example “Are the reactions involved in the synthesis of glucose from pyruvate energetically favourable?" or “How can the synthesis of glucose from pyruvate occur if the overall reaction is not energetically favourable?” Likewise for individual reactions, such as the formation of peptide bonds between amino acids.
For considerations of this sort the thermodynamical concept (Gibbs) Free Energy (G) is most useful. This is because the change in free energy (ΔG) during a reaction (or other change of state) indicates whether a reaction can occur spontaneously. To quote from a useful section in Berg et al.

A reaction can occur spontaneously only if ΔG is negative.

So in the reaction sequence just mentioned, the overall synthesis of glucose from pyruvate (gluconeogenesis) has a positive ΔG and is energetically unfavourable, whereas that of the reverse process (glycolysis) is energetically favourable. And likewise peptide bond formation, not surprisingly, has a positive ΔG and is not energetically favourable.
2. How are Energetically Unfavourable Reactions Accomplished in Living Cells?
The question posed in the heading arises from the fact that gluconeogenesis and peptide bond formation occur in living cells, even though taken alone the core reactions that represent the processes are energetically unfavourable. The answer is given in the title of [section 14.1.1. of Berg et al.]

A Thermodynamically Unfavourable Reaction can be driven by a Favourable Reaction

As already stated, it is the ΔG of the overall process that is important, so if a reaction with a positive ΔG is ‘coupled‘ to one of negative ΔG of greater magnitude, the overall reaction can proceed. For example:
A → B           ΔG =  20 kJ/mol (unfavourable)
C → D           ΔG = –30 kJ/mol (favourable)
A + C → B + D   ΔG = –10 kJ/mol (favourable)

If reaction C → D proceeds alone, the free energy is liberated as biochemically useless heat. If it is coupled to reaction  A → B it drives the latter with the balance being lost as heat.
3. The Role of Activated Carrier Molecules in Energy Coupling
Clearly, any coupled reaction can cause water to run uphill, as it were. But in order to continue one needs to regenerate the starting molecules for the favourable reaction. It is more efficient to specialize this regeneration process by using a limited range of specialist reactions with a negative free energy change. One description of the substrates (reacting molecules) of such specialized favourable reactions is “activated carrier molecules”. Alberts et al. define them as:

Small diffusible molecules in cells that store easily-exchangeable energy in the form of one or more energy-rich covalent bonds. Examples are ATP and NADPH.

Berg et al. also use the term, but describe it in terms of the following examples:

ATP as an activated carrier of phosphoryl groups, because phosphoryl transfer from ATP is an exergonic process (i.e. has a negative ΔG)
Nicotinamide adenine dinucleotide (NAD+) is a major electron carrier in the oxidation of fuel molecules. (Although in this case it is the half reaction involving the oxidation of the reduced form, NADH — or NADPH as mentioned by Alberts et al. — that has a negative ΔG).
Coenzyme A… is a carrier of acyl groups (but it is the transfer of the acyl group of acyl-CoA molecules — e.g. acetyl CoA — with the generation of CoA that has a negative ΔG).

Examples of the participation of such molecules in metabolism can be found in the volume referenced, however I would emphasize that it is the specific reactions of these molecules involving the groups (or electrons) that they carry that is important.
And what about Enzymes?
As the poster stated “enzymes lower the activation energy for a reaction”. They are (generally) large proteins catalysts that have no effect on the ΔG, and they are unchanged at the end of the reaction.
Of course they are important for biochemical reactions, they participate in them, and provide binding sites to bring the substrates and activated carriers in juxtaposition so that they can react. But they couldn’t be more different from the small activated carriers.


Regeneration - or actions perceived as regeneration by popular culture - depend highly on age and specific type of cells (epithelial tissue cells are a fine example). But you can't regenerate a leg-bone once removed.

But to get a more specific answer you to make a more specific question and define the terms you're using.


In theory they're clones, but depending on the age of the strain(some strains are surprisingly old: ~40 years) there's variation inside strains.

The reverse is also true. Bacteria from a single species are isolated twice and named different things by different labs and the mistake can take years to even find, much less correct.


Complement factor c1q binds to the constant Fc portion of an antibody (Duncan & Winter, 1988). Indeed, the constant (Fc) tail of the antibody is where other proteins involved in immune responses typically bind, most notably the Fc receptors (e.g., Clynes et al., 2000) found on immune cells such as B lymphocytes. Fc receptors mediate the recruitment of immune cells to a site of infection. The primary role of the Fab region is antigen binding as it contains the highly variable antigen binding domain. See the following figure (from the site of Invivogen) for the Fab and Fc region showing the constant and variable regions of antibodies:

  Figure legend from Invivogen): The Fc region mediates effector functions, such as antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). In ADCC, the Fc region of an antibody binds to Fc receptors (FcγRs) on the surface of immune effector cells such as natural killers and macrophages, leading to the phagocytosis or lysis of the targeted cells. In CDC, the antibodies kill the targeted cells by triggering the complement cascade at the cell surface. I

The constant regions of antibodies are located on the heavy chain (CH1,2,3) and the light chain (CL). These constant regions are potential binding sites for other immune molecules as they are constant between antibodies, irrespective of the variable region in Fab. Most of the constant regions are found on the Fc region explaining its major role in binding other molecules involved in the immune response, including complement factor c1q. However, the constant regions in Fab (CL) may also provide binding sites for other proteins and indeed some bacterial compounds are known to bind to this region (Bouvet, 1994). However, I have not found evidence of c1q binding the Fab region.


Orange tipped plant found in Carden limestone plains of Ontario

It's an odd angle, but I think the plant/flower is an Indian Paintbrush (Castilleja coccinea). It is found in Saskatchewan, Manitoba, Ontario, and Nova Scotia.


What factors, other than its homochirality, make our "brand" of biology unique?

I think the opposite list---what features of life might be reasonably expected to be the same elsewhere---would be much shorter. Nearly every feature of life on earth as I can think of it is arbitrary in the particular molecules.

DNA. Why only 4 bases? Why the bases that we have (ACTG)? Researchers are able to create organisms with expanded DNA alphabets even here on earth (1). Even if you believe that some form of molecular mechanism of heredity is a requirement for life, there is no reason it need be DNA. And while there has been plenty of controversy about arsenic-based life here on Earth, I don't see why there couldn't be arsenic-based life elsewhere.
Ribosomes. Why a combination of RNA and protein? There is a lot in the overall architecture of ribosomes that is locked in due to historical/evolutionary contingency, not any necessary feature of life.
The Central Dogma. Biology as we know it has certainly made great use of the ability to make temporary copies of messages, but I don't see why life orbiting Alpha Centauri would have to have arrived at a similar solution.
Phospholipid membranes. You could make the argument that some degree of compartmentalization is necessary for life to occur (to reduce complexity and allow evolution via drift and small-number effects to generate change), but I don't think they need to be phospholipids. I can also imagine all life on another planet contained within viral-like particles with purely protein (or some other alien polymer) coats.
Genes. Depending on the level one is arguing I can see this going either way. If a gene is just a modular set of instructions for a limited number of components, then perhaps this will show up everywhere---life on our planet is surprisingly modular, and it is hard to imagine life on another planet being able to get by without some modularity (though of course it is possible in principle). But certainly nothing is inevitable about the details of gene organization into promoters, coding regions (why a 3-base code?), introns and exons (I'm still surprised these exist on our own planet), operons, etc.

I think you get the idea. In fact, it's really hard to envision any feature of life on earth that doesn't smack of contingency in some way or other. Astrobiologists have held on to water as an essential ingredient for life as we know it, but still, that's "as we know it."
I am really tempted to make some sweeping speculative statement about what features I might expect to be "inherent in all possible biologies" (a fascinating idea to think about), but that is way out of my depth. Right now I find it hard to come up with good candidates.
(1): Malyshev D et al. (2014). A semi-synthetic organism with an expanded genetic alphabet. Nature 509: 385-8.


A time-frequency graph also know as a TF distribution, is a spectrogram, a spectrograph, a sonogram, a waterfall display of sound. They are all different names for the same thing. They look like this:

https://www.google.fr/search?q=dolphin+spectrogram&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiD3vv-9cvdAhUCzhoKHf4jDM0Q_AUIDigB&biw=1429&bih=734

Just as white light contains many wavelengths of colors, sound energy contains bass, mids and high all in the same moment in time, a bit like a water wave has multiple wave sizes, sound energy is the same with sound pressure levels.

Modulation refers to the variation of a simple signal, like tarzan modulates his voice using a kind of tremolo effect, so does a car alarm, and a bird has very varied squeak effects with tremolo effects and also changes from squeaks into clicks into hisses, spectral changes in the timbral quality of the sound. Modulation is a scientific word for the variations of the amplitudes and frequencies of a communications signal.

They write about temporal modulation and spectral(pitch) modulation, it's just hte changes on the time-frequency graphs.

Modulation power spectrum is a relatively obscure field of bioacoustics, it attempts to generalize the fluctuations and patterns of loudness and squeak spectrums into another graph, which is a bit like a secondary time and freqency graph derived from the first sound time and frequency graph, else a 2D graph as in the illustrations, which show sound fluctuation prevalence as an average of the TF graph(a averaged sound fluctuation prevalence of the spectrograph). so, if tarzan's voice oscillates every 1 second, he has a major modulation at 1Hz spectrally, and a minimal amplitude modulation, and they will graph that as a peak as 1Hz on the MPS graph.

We can see on this image that The human speech spectrogram on the top left is mostly at 500HZ, with some S and CH sounds at 2000hz.

For the MPS of the human voice, they have correlated Spectral modulations against Temporal modulations. It is easy to see that the human voice mosly changes at arond 1HZ, same as tarzan's voice, because syllables and pauses take about .5 to 1 second (average words per minute of a human is about 50, average syllables per minute is about 120). So it is easy to see a temporal modulation peak at 1Hz.
The less clear thing is that it is plotted against spectral modulation, which is 2-3 octaves of change, an octave being a doubling of wave speed and frequency. So we can say that the main spectral modulations of the human voice occur over 2-3 octaves at a speed of about 1Hz.
There is a secondary peak, which suggest that there is a change of about 1 octave that occurs at about 200-300 HZ. That is the gruff buzz that you hear in your own man voice, it is about 150HZ and it has about .5-1octave, the base frequency of your voice being 150Hz and various 3rds adn 5ths of an octave, and another octave at 350Hz, seems to be visible from that graph.
tarzan voice: https://www.researchgate.net/profile/Alexandre_Hyafil/publication/283260815/figure/fig2/AS:293940512215079@1447092287682/A-Phase-Frequency-coupling-can-be-mistaken-for-Phase-Amplitude-Coupling-Top-curves-An.png

MPS seems to have been used to study neuron responses in psycho-acoustics.

Neurons interpret sounds using some kinds of complex time and freqency variation(modulation) recognition(resolution) and the researchers use MPS as they say it fits well with the neuron psychoacoustics study.

I would suggest that there are many other ways of measuring psycho acoustic nerve responses and bioacoustics than only MPS, it is an over simplification of sound analysis, and the Digital-Signal-Processing forum on this website will inform you that there are also 100ds of other maths and analysis algorythms that you can run on sound to study Time-Frequency Graphs, and to define sound in many different ways than MPS.

very pure sounds like sine waves make tight lines on a time frequency graph, noise makes very scattered signals at all frequencies, and sounds with many harmonic modes make nice ordered lines of smaller subharmonics that reflect the base frequency of a signal, which resemble echoes of the original sound in parralel with it, and that are on a different frequency.

Time frequency graphs are quite interesting to study and there are probably some studies of bird calls on YT: https://www.youtube.com/watch?v=_FatxGN3vAM


Can a human actually be "frightened to death?"

The people whom this happens to consider themselves average people.

The thought is that catecholamine surge caused by the event triggers some predisposition to cardiac arrhythmia - maybe inherited, maybe due to medicines.  People predisposed to this sort of arrhythmia probably do not know that is the case, and consider themselves to be average people.  It would seem that the victims of this are not average and have some sort of predisposition to that problem.  There is a lot of interest in figuring out who there people are in advance - not in the context of being frightening to death but in the context of SUDEP - sudden death in epilepsy.  Epileptic people sometimes just die, presumably for cardiac reasons, but there is no way of knowing who among this large group is at risk.

In the following abstract the frightening thing is being restrained.  Other circumstances that produce a catecholamine surge can do it too.

https://www.ncbi.nlm.nih.gov/pubmed/25628339

  Med Sci Law. 2016 Apr;56(2):85-90. doi: 10.1177/0025802414568483. Epub
  2015 Jan 26. Sudden cardiac death with stress and restraint: The
  association with sudden adult death syndrome, cardiomyopathy and
  coronary artery disease.

  Krexi L1, Georgiou R2, Krexi D1, Sheppard MN3. Author information
  Abstract OBJECTIVE: The aim of this study was to report on sudden
  cardiac death (SCD) during or immediately after a stressful event in a
  predominately young cohort. METHODS: This study used retrospective
  non-case-controlled analysis. A total of 110 cases of SCD in relation
  to a stressful event such as altercation (45%), physical restraint
  (31%) in police custody (10%), exams/school/job stress (7.27%),
  receiving bad news (4%), or a car accident without injuries (2.73%)
  were retrospectively investigated. The majority of the subjects
  experiencing SCD were male (80.91%). The mean age was 36 ± 16 years
  (range 5-82 years). Twenty-three cases (20.91%) were psychiatric
  patients on antipsychotic medication. RESULTS: Fifty-three per cent of
  cases died with a negative autopsy and a morphologically normal heart,
  indicating sudden adult death which is linked to cardiac
  channelopathies predisposing to stress-induced SCD. Cardiomyopathy was
  found in 16 (14.5%) patients and coronary artery pathology in 19 (17%)
  patients, with atherosclerosis predominating in older patients.
  CONCLUSIONS: This study highlights SCD during psychological stress,
  mostly in young males where the sudden death occurred in the absence
  of structural heart disease. This may reflect the proarrhythmic
  potential of high catecholamines on the structurally normal heart in
  those genetically predisposed because of cardiac channelopathy.
  Structural cardiomyopathies and coronary artery disease also feature
  prominently. Cases of SCD associated with altercation and restraint
  receive mass media attention especially when police/other governmental
  bodies are involved. This study highlights the rare but important risk
  of SCD associated with psychological stress and restraint in
  morphologically normal hearts and the importance of an expert cardiac
  opinion where prolonged criminal investigations and medico-legal
  issues often ensue.