Infer gene frequency within a species over time I was reading Karlsson et al. (2014) and I came into this:

  A selected variant that increases rapidly in frequency in the past ~250,000 years can be detected as an unusual reduction in genetic diversity.

I realised that I do not know how to infer a specific allele frequency over time within a given species.

I tried to googled some keyword but was flooded by other concepts. Could you please direct me to some appropriate documentation/kewords?

There are really two ways to infer past genetics.

Sample the past.

Only really works if you have well-preserved uncontaminated archaeological samples, but works surprisingly well, considering. The accuracy and completeness goes down fairly quickly as you go back in time but thousands of years to hundreds of thousands of years is roughly possible. You won't have many samples so it's hard to say anything about population genetics. Don't do this. It doesn't work very well and it's very hard.

Molecular clocks.

Same-sense mutations that affect nothing accumulate in genes over time as they're passed down. Genes that have a distant common ancestor are more different than genes that are just a generation or two apart. This is essentially how phylogenetics works as a whole, but you can use age differences between nearby genes to detect selection in this way. If gene A is nearly identical in every individual in a population, but gene B has thousands of pretty distinct variations, it's clear gene A does something important and has been powerfully selected for. Don't just count the number of kinds of alleles for gene A, calculate the average relatedness between all the alleles you find. If the relatedness for gene A is much lower than for other genes, gene A is being selected on. This is what the text means by 'reduction in genetic diversity', bringing down the average relatedness.

You can't work out allele frequencies at arbitrary times in the past without a time machine(even ancient sampling, you can't really be sure you're getting an accurate sample of the historical population), but phylogenetics can hint at what happened by detecting the signatures of evolution.


Do pet animals and humans perceive good and bad smells differently As the title says, just wondering if there is a difference in what animals like dogs and cats perceive as good smell vis a vis humans. Example : Smell of some flowers - great . Fart smells - bad.

TL; DR Mostly no.

On a molecular basis, cats' and dogs' noses look quite similar to ours. Most of what we know about smell comes from studies on non-human mammals, and is supposed to apply to humans too. So, big similarity, but...

Cats and dogs distinguish far more kinds of than humans. It's likely they know more kinds of bad smells and good smells, possibly including from things that we think lack odour.
Many animals also have a working vomeronasal organ, that is, a sensing organ similar to the olfactory mucosa we use for sensing common smells. The vomeronasal organ detects pheromones, the smell-like signals used for communication between animals. We, humans, are at least deficient, if not completely unable to use the vomeronasal organ and pheromone signals. It is debatable whether animals conflate regular smells with pheromones. Pheromones are very efficient in conveying information about potential sexual partners, rivals, and so on. So these are a completely different set of bad and good smells, available only to animals. That is, if we can call those sensations smells, a big if.
On the other hand, humans evaluate smells culturally. Some people learn to enjoy offensive smells that people from other cultures carry on disliking. Since dogs have limited ability to manipulate smells and to convey information to another dog, I doubt they can form these cultural constructs of smell. We sense sensuality in a perfume; the dog senses a bunch of pungent flowers, neither good, nor bad.


How does de-myelination occur in multiple sclerosis? From what I understand, only the oligodendrocytes are affected in multiple sclerosis, and they are attacked by T cells which cross the blood-brain barrier. This leads me to two questions:

How is the blood-brain barrier affected in MS that allows T lymphocytes to cross the barrier?
Why do the T lymphocytes attack the oligodendroccytes? And when they do, what is the mechanism for de-myelination?

Thank you in advance!

T-cell migration to the brain is very limited and occurs at a very low level in healthy conditions, however during diseases the number of T cells passing through the blood-brain barrier is elevate due to increased expression of traffic signals and adhesive molecules.
I've found two good articles on how T-cells migrate through blood-brain barrier:

J Neural Transm (2006) 113: 477–485
Molecular mechanisms involved in T cell migration across
the blood–brain barrier, B. Engelhardt

and
 D. W. Miller, “Immunobiology of the blood-brain barrier.,” J. Neurovirol., vol. 5, no. 6, pp. 570–578, 1999.

During T-cell maturation, those that react too heavily to antigens of the body are killed to avoid having T-cells that would kill the body's own cells. But in rare cases this process fails and auto-reactive T-cell get released from the thymus (This short paper is good for starters). So the (simplified) reason why T-cells attack oligodendrocytes is that they falsely recognize them as pathogens, and therefore kill them. The loss of oligodendrocytes results in loss of myelin sheats.

Also in this paper (it holds many info on demyelination and multiple sclerosis) it is shown that even non-specicfic T-cells can open the way for antibodies through the blood-brain barried, and this results in extended demyelination.


Why are the posterior and anterior inferior temporal cortex called area TEO and area TE respectively? I don't understand why you would call them that. How did these names originate/where did these names come from?

These are very old names for primate cortical areas, originally from the anatomist Constantin von Economo and also used by von Bonin and Bailey (1947) (where the TEO region name seems to originate).

Like Brodmann areas these regions were defined by cytoarchitecture well before most functions were determined.

I discovered another work that I can access from 1935, Rose (1935) that is quite helpful for the TE terminology. From Rose it is clear that von Economo labeled areas in the temporal lobe TA, TB, TC, etc. up to TH. So they seem to be simply "temporal"+letters of the alphabet. Rose refers to "Area temporalis propria" as area TE, comprised of Brodmann areas 21 and 20; Rose calls Brodmann 21 "TE1" and Brodmann 20 "TE2" which are separated based on the size of layer 3 pyramidal cells.

As far as the TEO terminology, Boussaoud et al (1991) write:

  In their study of  the cytoarchitecture of  macaque cortex, von Bonin and Bailey ('47) labeled this region with a question mark on their section drawings but showed a photomicrograph through the region that they labeled  “TEO.”

This is the best evidence I can find that the TEO name a) originated with von Bonin and Bailey, and b) that the further origin or meaning of the name is unclear; it's just a label on a photomicrograph that wasn't even used in the drawings by those authors who instead used a ?. I suspect further authors preferred the TEO terminology rather than confusingly referring to "area ?" and yet they felt like giving credit to von Bonin and Bailey for their work on the macaque cortex.

It's unclear to me whether TEO is meant to be an acronym; "temporal" is part of the name, but whether O stands for a word (perhaps occipital, as it is toward the occipital lobe?) or if it is actually the number 0, or a non-English word (possibly German or Latin?). However, when more modern neuroscientists refer to area TE and area TEO, they are simply intending to refer to "area TE and area TEO in the von Economo/von Bonin & Bailey terminology."

Other terminology, such as referring to posterior or anterior inferior temporal cortex, may seem more descriptive but there isn't anything inherently wrong with referring to the older names as long as people know what area you refer to. TE and TEO are clear, short names that have been used for decades, whereas inventing a new acronym like PIT or AIT would be unfamiliar at this point.

References

Boussaoud, D., Desimone, R., & Ungerleider, L. G. (1991). Visual topography of area TEO in the macaque. Journal of Comparative Neurology, 306(4), 554-575.

Rose, M. (1935). Cytoarchitektonik und Myeloarchitektonik der Großhirnrinde. Handbuch der Neurologie, 1, 588-778.

von Bonin, G., & Bailey, P. (1947). The neocortex of Macaca mulatta.(Illinois Monogr. med. Sci., 5, No. 4.).

von Economo, C. F., & Koskinas, G. N. (1925). Die cytoarchitektonik der hirnrinde des erwachsenen menschen. J. Springer.


Known MicroRNA - Gene Systems? Have there been any experimentally-verified systems of microRNAs targeting a gene set (e.g., in cancer, perhaps)?

Yes. Below is a link to a review of ncRNA (non-coding RNAs) and their role in disease. There are many examples in this review in all sorts of diseases, one of which is miR-200, which is thought to play a role in some cancers.

There are also some tables in the paper that list the miRNA and the disease they are linked to. They also have a reference for each one, so you could read more about that particular miRNA and its function, including the gene it regulates.

http://www.nature.com/nrg/journal/v12/n12/full/nrg3074.html

Im not sure if that article is open to the public or not. If you cant access it you could always check out the wikipedia entry for miR-200

http://en.wikipedia.org/wiki/Mir-200


Are bronchioles and alveoli covered by respiratory epithelium? Which parts of respiratory apparatus are covered by respiratory epithelium and which are covered by other kinds of epithelium?

From the nose to the pharynx and larynx: stratified squamous epithelium

From the end of larynx to the bronchi: pseudostratified columnar ciliated epithelial cells.

From the small bronchi cartilage is being replaced by elastic tissue.

Bronchioles: ciliated simple epithelium with club cells (known as Clara cells). Also they lack cartilage and glands.

Alveoli are covered with squamous alveolar cells which form the wall (also known as type I pneumocytes). They also contain great alveolar cells (which produce surfactant) or type II pneumocytes and macrophages.

From http://en.wikipedia.org/wiki/Respiratory_tract , http://en.wikipedia.org/wiki/Pulmonary_alveolus and http://en.wikipedia.org/wiki/Pharynx


Why does the PR form of phytochrome exist? I know how it gets converted because PR is more stable and when there is neither red or far red light PFR naturally converts to PR. But what is the point of it? If PFR is the biologically active one why didn't evolution just make one pigment, PFR. At night neither is active so PR again has no point, in the morning PR gets converted to PFR. So why do we need a PR?

First off, "evolution" doesn't necessarily lead the most efficient system for anything - it works with what we already have.  Once something has evolved, it might not go away, if there is no particular harm to having it around. You might take a look at the evolution tag, as other people have asked similar questions about the "usefulness" of biological mechanisms and molecules.
Aside from that, having both isoforms is important for the detecting the color of light. When Pr absorbs red light, it gets converted to Pfr, and when Pfr absorbs far red light, it gets converted to Pr.  The ratios of Pr to Pfr allow plants to determine light levels and adjust their growth accordingly:

Sunlight has a R:FR ratio of 1.2

Light under a canopy of leaves has a R:FR ratio of 0.13

Light under 5 mm of soil has a R:FR ratio of 0.88

A higher proportion of FR light allows plants to detect when they are
shaded. Plants adapted for growth in full sun will display greater
stem elongation when they are transferred to shade.  They also develop
smaller leaves and less branching.  This change is due to greater
proportion of Pr to Pfr.

Seeds of certain plants require red light for germination; FR light inhibits germination.  Many small seeds with low amounts of storage reserves (such as lettuce) show such a red light requirement.
If these seeds they are buried below the level of light penetration in the soil, they do not germinate.
If they are shaded by a leaf canopy, causing a high proportion of FR, germination is inhibited, [as] Pfr is required for germination.

Source: Missouri Botanical Garden


Is Nerve Growth Factor (NGF) commercially available? I'm curious if NGF, or Neurotrophins in general is available commercially. Can I order it online? If not, what are the medical/biological reasons. Does it breakdown quickly after synthesis/capture? Is it a regulated protein?

recombinant human NGF is available for purchase.  You might not be able to buy it without some sort of a research lab affiliation.

http://products.creative-biolabs.com/symbolsearch_NGF_1.htm


How is phenol antiseptic? What makes phenol an antiseptic, is it because of its acidity which may increase the proton concentration at cell membrane? I am unable to figure out the exact mechanism.

The main reason for phenol being antiseptic is it's effect on proteins which it denaturates. It also causes leakage of cellular membranes. See the paper in reference 1 for some details and a load of references. They say in the section on phenol:

  Phenolic-type antimicrobial agents have long been used for their
  antiseptic, disinfectant, or preservative properties, depending on the
  compound. It has been known for many years (215) that, although they
  have often been referred to as “general protoplasmic poisons,” they
  have membrane-active properties which also contribute to their overall
  activity (120) (Table (Table22).

  Phenol induces progressive leakage of intracellular constituents,
  including the release of K+, the first index of membrane damage (273),
  and of radioactivity from 14C-labeled E. coli (242, 265). Pulvertaft
  and Lumb (386) demonstrated that low concentrations of phenols
  (0.032%, 320 μg/ml) and other (nonphenolic) agents lysed rapidly
  growing cultures of E. coli, staphylococci, and streptococci and
  concluded that autolytic enzymes were not involved.

Reference:

Antiseptics and Disinfectants: Activity, Action, and Resistance


If two definitive ovums are fused will they form an organism? Pretend that somehow in a laboratory two definitive ovums (finished 2nd miotic divisions) are
are fused together. Will they form a new species?

No, it is not possible. The reason is the genetic imprinting, which takes place on the parental DNA in the egg and the sperm. Here small modifications are added to the DNA which marks them as silenced. So some genes are expressed from the mother (while the fathers copy is not expressed) and vice versa.

There are even genetic diseases which are caused by imprinting. One example is the loss of a gene region on chromosome 15. Depending in which copy its lost, either the Prader-Willi Syndrome or the Angelman Syndrome occur. PWS is inherited via the father, Angelman via the mother. Another interesting article on imprinting can be found here.

If you combine two eggs, some genes, which are not imprinted in the father, will not be expressed in the developing embryo which will finally lead to death of it. However, researcher deleted the maternal imprinting in mice and mimicked the from the father and made off-springs from two mothers possible. This is something which is ethically very problematic in humans. The article can be found here:

Birth of parthenogenetic mice that can develop to adulthood


Are there certain symmetric-pair muscles that are slightly bigger and NOT due to handedness? Ok, hear me out, I was just thinking about an article in Nature I read in the past titled "Scrotal asymmetry in man and in ancient sculpture"$^{\dagger}$ and more recently an entire medical textbook detailing everything about hands wherein the author accounts the different types of blood vein topology categories there are in humans, and he touches on handedness too. The part about handedness stuck with me, and I began to notice (looking in the mirror, etc.) that my right neck muscles are slightly larger than the left ones, but so is my friend's who is left handed. I thought this might be due to handedness not translating to chewing behavior (chewing on the right or left predominantly). Anyway, all this is building up to my main question which is this:

  Is there something about our anatomy (organ placement, vein topology, etc.) that makes certain symmetric-pair muscle groups unavoidably asymmetrical or is it just handedness or the environment?

$\dagger$ Heard about it here: https://www.youtube.com/watch?v=Xyquv6SsLWg&t=0m56s

There are many variables that could affect the answer to this question. Such as what activities you partake in.

For example, I am a hockey player at the he varsity level in high school. I have noticed that my entire right side is more toned, muscular, and flexible (especially my right latisimus dorsi and deltoid). It just so happens that I rely on my right side for energy and strength more than my left when it comes to shooting pucks and just playing the game.

Typically what we see in humans is the dominant side of their body will tend to show more hypertrophy than the non-dominant side. When you look at a human anatomically, their dominant side shoulder will be bigger and will rest lower when relaxed. Even small things like sleeping habits can effect the visual difference of you symmetry. I will agree though that it is odd that your friend noticeably has more hypertrophy in his neck muscles on one side but is dominant on the other side. This could be due (but not limited) to small habits not taken into account. Like I mentioned before, sleep habits, any motion with the neck in a specific way, chewing could maybe be a factor, or (maybe not likely) a genetic mutation.

This is an interesting topic and I urge you to maybe look at some more people for evidence that dominance has a role in it. 2 people is maybe not enough evidence to really back up a claim you're going to make.

Hope this helped!

-Sartoaster


Why does high EDTA concentration cause swelling of platelets? According to this textbook, high ( >2mg/ml of blood) EDTA concentration causes swelling of platelets which lead to their fragmentation.

I know that high concentration of EDTA increases plasma osmolarity which leads to cell shrinkage , as is the case in all other blood cells, but why does it have opposite effect on platelets? Why osmotic effects aren't seen in platelets?

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

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

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

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

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

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


Can primers for PCR be duplicated? Complete beginner question here, don't laugh:
If I have some primers that have been synthesized, and I am close to running out of them, is there any way to duplicate them / amplify them / synthesize more of them myself? I don't know the sequences.
Or is my only option to buy more?
Thanks

Short answer: You need to buy some more, but you need the sequence also for ordering.

Long answer: The Taq polymerase needs a piece of DNA (or RNA) to prime the reaction and be able to enlarge the DNA chain, this is why we use primers in the first place (also to ensure reaction specificity to the region we want to amplify). To enable the reaction you would need a primer complimentary to the one you used of about the same length (or at least not much shorter), so this actually doesn't really make sense, because you would have to have a primer to make your primer. Since primers are cheap today, order some more.


Can bacteria pick up lethal plasmids? I am sorry if this question is too general, and does not have any concrete answer.

I was explaining to my non-biology-background friend about plasmids and how they are picked up by bacteria from the remains of other dead bacteria during stressful conditions. This is when this question arose:

Why would bacteria pick up plasmids released from the dead bacteria, as this means that these plasmids either did not help it survive in those conditions, or could have in fact been the cause of their death? This also lead to the question of whether plasmids can be lethal? (I believe there could be, for example plasmids which are translated into proteins which are endonucleases which would probably kill the bacteria, yet I am not sure).

Moreover, if this sort of plasmids exists, then why could we not engineer them specifically and use them as medicine as an “antibiotic”?

The ability of bacteria to take up intact environmental DNA is called natural competence.

One problem with trying to take advantage of this in a therapy is that it is not very efficient. Importantly, natural competence is regulated and tends to be activated when bacteria are already stressed. This is also likely part of the answer as to why a bacterium would take up DNA from the outside: if they are already in bad shape, they don't have much to lose. Bacteria growing in non-stressful conditions are less competent, and possibly negligibly so.

Ween et al 2002 compared competence in two bacterial strains, one with a "normal" regulation of competence. At most bacterial concentrations, the "normal" strain showed less than 1% transformation, and this is still in sort of an ideal laboratory condition, where the culture medium is flooded with plasmids. There wouldn't be a feasible way to even approach delivering that much plasmid DNA into a human.

Ween, O., Teigen, S., Gaustad, P., Kilian, M., & Håvarstein, L. S. (2002). Competence without a competence pheromone in a natural isolate of Streptococcus infantis. Journal of bacteriology, 184(13), 3426-3432.

The other big problem is you are working directly against selection pressures. In the case of a plasmid that improves survival (say, one containing a gene that confers antibiotic resistance in the presence of that antibiotic), then the population will more quickly increase the expression of that plasmid, as bacteria with it grow and reproduce while other bacteria die. However, if you have a lethal plasmid, all the bacteria you are able to transform simply die. They don't spread the plasmid by reproducing, and as they die the non-transformed bacteria will continue to reproduce.


What is this pink-flowering plant found in Shanghai, China in March? This plant appears to have fleshy protrusions resembling flowers growing out of its stem (although I am unable to identify them as such).

Does anyone know the identity of these plants?

I think this is the Chinese Redbud (Cercis chinensis), see this image (from here):


Trade-offs between phage and yeast displays? If you wanted to test a peptide you designed, you can do a phage display or a yeast display experiment to assess binding affinity.

What are the trade-offs between these two methods?

I've heard anecdotally that yeast display is more sensitive and closer to human cells?

According to Creative Biolabs, the primary differences are:

  In the screening/panning step, yeast display is suitable for Fluorescence Activated Cell Sorting (FACS), allowing to sort out antibodies with desired binding properties
  precisely. However, the affinity of antibodies to antigens in phage
  display can only be roughly stratified (sorted into categories of goodness) by adjusting the washing buffer
  compositions.
  Owing to its eukaryotic expression system, yeast displayed antibodies can be correctly folded and modified, such as [...] to be closer to their native structure in mammals
  compared to the antibodies expressed by E.coli in phage display.
  The diversity of yeast displayed antibodies may be lower than phage (107-109 for yeast, up to 1011 for phage), due to the low
  transformation efficiency of yeast.
  Due to the many more copies of antibody on yeast surface (104-105) than phage, it is possible to select out low affinity antibodies
  according to antibody avidity with yeast display system.


Why do bacteria die in a high sugar content environment? I was reading some questions in the test bank. Then in Chapter 27, I wonder why the answer is A. (undergo death by plasmolysis). Is the high concentration of sugar that kills them or the effects of sugar on bacteria?

  Reece et al. Campbell Biology Test Bank. 9th ed. Boston: Benjamin Cummings / Pearson, 2011: 563.

In (very) short: enzymes are necessary for life. Cytoplasm is necessary for enzymes to function. Water is necessary for cytoplasm to exist. Cells have osmotic membranes.

Given a cell in a solution (even a goopy one, like jam) with a very high concentration of sugar, water will move along a gradient of low to high sugar concentration, in other words, water will move out of the cell and into the jam, thus stopping all major activity in the bacterium (basically stopping it from reproducing, if not exactly killing it. The killing actually comes from heating the jam and canning it while still hot enough to kill most bacteria.)

Plasmolysis: The shrinking of protoplasm away from the cell wall of a plant or bacterium due to water loss from osmosis.


constitution of read and gene region (IGV) I work with fastq files containing NGS reads for some human DNA regions. The reference genome is hg19. I had two fastq files (pair-ended). I generated alignment BAM files. I used "bwa" and samtools to find a possible target gene region (chr7:55,242,376-55,242,574,). This corresponds to a region of the EGFR gene.

Here is a screenshot of the gene region

And here is a screenshot of the primer region

I also have a list of primers and reverse primers:

FORWARD
1. TTGCCAGTTAACGTCTTCCTTCTCTCTCTG
2. CCCTTGTCTCTGTGTTCTTGTCCCCCCCA
3. TGATCTGTCCCTCACAGCAGGGTCTTCTCT
4. CACACTGACGTGCCTCTCCCTCCCTCCA

REVERSE
1. GAGAAAAGGTGGGCCTGAGGTTCAGAGCCA
2. CCCCACCAGACCATGAGAGGCCCTGCGGCC
3. TGACCTAAAGCCACCTCCTTA
4. CCGTATCTCCCTTCCCTGATTA

And I have some adaptors

ADAPTORS 1
AAGACTCGGCAGCATCTCCA

ADAPTORS 2
GCGATCGTCACTGTTCTCCA

I have to answer to the following questions:

1) What is the constitution of each read (adaptor+primer+amplified region)?
The forward primer is obvious and corresponds to the first primer of the list

TTGCCAGTTAACGTCTTCCTTCTCTCTCTG

So why do we have the three other forward primers? I don't understand. And what about the correct reverse primer?

It seems to be the complementary sequence of the end region

GAGAAAAGGTGGGCCTGAGGTTCAGAGCCA

Finally which adaptor is used?

Is [ADAPTOR1 - PRIMER1 - AMPLIFIED REGION] the correct answer? Are there other possibilities?

2) % of reads that map the human genome? what about the unmapped?

Can you please give me some clues about how to answer this question.

I just need some clues I want to do it by myself.

Thank you very much for your help.

You have asked quite a few questions here. I will try to answer a subset of them.

To answer your question, I started by going to the UCSC genome browser, and selected the BLAT from the tools dropdown menu. Then passing your primer sequences as queries, we can clearly see where they map to the reference genome.

Looking at the figure above, I can guess that your data comes from a targeted sequencing experiment (exome, or gene panel, etc); where you have primers around each exon of EGFR on two strands, on 5' end of exon sequence on each strand (think about DNA polymerase acting in PCR to amplify the number of DNA molecules before sequencing).

Regarding the adapter, I am not sure which read you are referring to. Can you clarify please?

About percentage of mapped vs unmapped reads, you can use bamtools.

Example Usage:

/user/me/src/bamtools/bin/bamtools-2.3.0 stats -insert -in my-sequence-file.bam

Example output:

Total reads:       103277668

Mapped reads:      90088436     (87.2293%)

Forward strand:    58136735     (56.2917%)

Reverse strand:    45140933     (43.7083%)

Failed QC:         6529806      (6.32257%)

Duplicates:        0    (0%)

Paired-end reads:  103277668    (100%)

'Proper-pairs':    87439672     (84.6646%)

Both pairs mapped: 87910438     (85.1205%)

Read 1:            51638834

Read 2:            51638834

Singletons:        2177998      (2.10888%)

Average insert size (absolute value): 6317.39

Median insert size (absolute value): 301


Modern views on the correspondence of moles In his Memoirs, Casanova wrote:

In the midst of the dimple which added such a charm to her chin Esther had a little dark mole, garnished with three or four extremely fine hairs. These moles, which we call in Italian ‘neo, nei’, and which are usually an improvement to the prettiest face, when they occur on the face, the neck, the arms, or the hands, are duplicated on the corresponding parts of the body. I concluded, therefore, that Esther had a mole like that on her chin in a certain place which a virtuous girl does not shew [...]
I then explained to her the theory of the correspondence of moles on the various parts of the human body, and to convince her I ended by saying that her governess who had a large mark on her right cheek ought to have one very like it on her left thigh.

Does contemporary biology/medicine support this law? Are there publications on it?

There are a lot of different types of moles out there, and while there are correlations in locations of some classes based on their nature, there is nothing like the correspondence described.

There is, however, a long history of attempting to attribute meanings and patterns to moles, however, since essentially random phenomena like this tend to engage our human biases for pattern-making.


Why cannot there be multiple sources for same species origins? We often associate Africa as the geographical location of the origin of humans. Why cannot there exist multiple geographic locations of origin (given same environmental conditions)?

The same argument exists for other species as well. So what is the basis of the common ancestor (from single geographical location) theory?

Please give me references so that I can read more on this subject.

This is a very fundamental, and in my opinion, interesting question. You might not find many sources that directly cover this question because it is hard to test. If speciation did happen in two separate locations and the resulting species were so similar that they could breed with one another and not the original species, how would we be able to tell if the species originated in separate locations and that the new species didn't just travel to the new location? Below I'll try and explain why it's safe to assume they probably didn't have different locations for speciation.
Thought Experiment
Here is what happened in hypothetical land. Species X exists in happy land. Individuals of X then move to water land. Some more individuals from X move from happy land to H2O land (very similar to water land). Species X undergoes speciation in water land to species Y and speciation of X also occur in the H2O land to species Z.
Can Z and Y be the same species with different origins where the niche conditions are the same?
As you can imagine, the longer after geographical isolation the more mutations occur and the less likely it is that the new species will be able to breed successfully with similar species.
Although the two environments may seem identical, ecology is notoriously complex and chaotic, and so in reality as far as ecology is concerned, they are very different environments. Even the slightest difference between niches will naturally select different traits that could make Z and Y sexually incompatible.
Furthermore, when dealing with the geographical origin, you must assume that there was geographical isolation between the two speciation event locations. Since there is typically no contact between Z and Y species, there is no selective pressure to remain genetically compatible and given enough time, they will become unable to breed.

Humans
There is a contentious claim that ancient humans bred with chimpanzees after both speciation events from our common ancestor to humans and chimpanzees. Broadly I think this has now been dismissed. However, it is reasonably well accepted that in a more recent "Tolkien-esque" world humans bred with Neanderthals.
But ultimately I don't think there is a single example (I am thoroughly open to being proven wrong!) in the natural world of two similar geographical isolation events driving exactly the same species to evolve and both versions of the new species are more genetically similar to one another than they are to the origin species. The odds are just too slim even if to us the conditions seem identical.


Why does increased humidity decrease coronavirus "survival"? All news I can see scientist telling that the SARS-CoV-2 virus survive more in cold and dry weather. I can understand cold as hot weather will desiccate virus, but why dry  weather.

Would not dry weather dry droplets of saliva sooner also desiccate virus, would not humid weather support virus?

I found an answer to this mystery in the literature, but it is a somewhat tentative explanation from a relatively recent (2012) paper by Yang et al. In a nutshell, [respiratory] viruses do worse in small droplets compared to large/unconstrained ones. Even being "totally" dry is apparently somewhat better for them than being trapped in a small droplet. So you get a V (or U)-shaped survival curve as a function of relative humidity.

There appear to be three regimes of IAV [influenza A virus] viability in droplets, defined by humidity: physiological conditions (∼100% RH) with high viability, concentrated conditions (50% to near 100% RH) with lower viability depending on the composition of media, and dry conditions (<50% RH) with high viability. This paradigm could help resolve conflicting findings in the literature on the relationship between IAV viability in aerosols and humidity, and results in human mucus could help explain influenza’s seasonality in different regions.
[...]
After release from the respiratory tract, where RH is ∼100%, a respiratory droplet shrinks by 40–50% in diameter at RH below 90% due to evaporation [16]–[18]. As a result, concentrations of solutes in the droplet increase by up to 15 times, and solutes such as salts (e.g., sodium chloride (NaCl)) that are harmless at physiological levels may become harmful to the virus. For example, avian IAV has been reported to be less stable at salinities greater than 25 g L−1 [19]. Evaporation induces changes to IAV’s microenvironment inside droplets that may affect the virus’ viability, and the toxic effect of solutes may be enhanced at lower RH due to higher concentrations that result from greater loss of water.

Yang et al.'s paper has been positively cited in a couple of subsequent reviews  Lowen and Steel (2014) and Paynter (2014)
So it seems to be a fairly credible explanation as far as influenza is concerned. Paynter's review also discusses similar observations on RSV:

One study examined the effect of humidity on RSV survival in 1 μl droplets of tissue culture medium on polythene at room temperature. Over the first 5 h, RSV survival was highest at the highest humidity, while over the next 67 h, RSV survival was highest at the lowest humidity. The explanation of these findings may lie in the droplet drying time in this study. Droplets exposed to 77% RH were still wet at 18 h (no data were given for drying times at 32% or 52% RH). The relatively high survival at higher humidity over the first 5 h was probably due to the fact that the droplets remained wet in these conditions. The survival over the final 48 h (when all droplets were dry) was progressively reduced with increasing humidity. Consistent with this explanation, only 1% of RSV was lost over the 72 h when stored in liquid culture medium, and in addition, the authors noted that RSV survival was increased with increased droplet size. Similarly, in another study the survival of RSV on countertops was reduced if the virus was in droplets that were dried quickly. These results are consistent with the studies examining influenza survival on surfaces, suggesting that while the virus remains ‘wet’ in droplets, high humidity prolongs its survival, by reducing evaporation.

There might be more recent advances in this area though, especially regarding mechanisms of the "middle regime".


Are these cats calico? Calico cats are cats that have 3 fur colors and are always female or males two X chromosomes.
I've seen many cats that will have 2 fur colors (one of them is usually white) and another, third, color which is a darker shade of one of the other colors. As exampled in the pictures below (taken from the internet). Are those considered Calico cats?

(source: mirror.co.uk)

I think you are misunderstanding "color" here. When applied to cats, it doesn't literally mean a color shade as used in color theory, but "coat color" which can in fact also be a "coat pattern".

The cats above are two-colored, not three-colored. One color is white. The other color is what is called "tabby" in English and is a pattern of dark spots arranged in regular stripes on a lighter background. These spots are not considered a third color in cats.

This is a calico cat. Her three coat colors are white, orange, and grey tabby. See how the orange and grey are irregularly interspersed, this is the pattern of paternal and maternal chromosome expression on her body. Again, the grey and black patches within the tabby part are regularly placed. They don't make two separate colors, grey and black, but a single coat coloring, grey tabby. There are also other color combinations in calico cats, for example white-orange-black, and they are more straightforward to recognize.


What could humans do to "see" what dogs smell? We're able to see a lot of things using computers that we can't see normally: yellow-green, UV light, X-rays, etc. What do we have that harnesses the ability to "see" what dogs smell (e.g., harnessing a dog's sense of smell to detect cancer and so forth)?

NMR spectroscopy is a technology that is used to identify molecules. So-called "NMR spectra catalogs" document the spectra of various known compounds. Acquiring these spectra requires purified samples, expensive equipment, and time. In addition to making next-generations of this technology into something that would be practical for realtime "smelling", you'd have to match up catalog entries with what dogs actually respond to. That's going to take a fair bit of work.

There's some literature online about growing olfactory sensory neurons in a Petri dish (with difficulty). If we can learn how the signaling pathways work for "odorant detection" for specific odorants or "fragrances" that we already know dogs perceive, perhaps we could genetically engineer a cultured neuron cell to "light up" a fluorescent marker or issue some other signal that is perceptible to humans, whenever some dog-specific odor wafts in. I suspect this would be more realistic than "tabletop NMR" in our lifetime.


Aging and death of perennials Perennial plants species generate a new plant annually from the same parent root stock. At the end of the year that new shoot withers and dies, to re-appear the next year. Hence, the above-ground parts of perennials obviously age and die, but what about the rootstocks?

Are the rootstocks from perennial plant species immortal, or do these rootstocks age and die as well?

The issue is based on your perception of what an individual ought to be. The concept of individual is actually often hard to apply in biology and therefore is the concept of ageing. In other words, the wish to categorize is a rather human tendency but it may fail to make objective representation of biodiversity. The book The Major Transitions in Evolution Revisited makes a very good job to explain the difficulties to deal with the concept of individual in biology.

You seem to be happy to consider an offspring be a different individual if you can still perceive the parent individual. In bacteria, both resulting cells could be considered as offspring and therefore new individuals. Note however, that asymmetrical division bring some more blur into these categorizations.

Note also that single cell bacteria do age. See the wikipedia article on bacterial ageing. You might also want to have a look at the wikipedia article on biological immortality as well as the posts Why is the Hydra Biologically Immortal? and Do crocodiles age?.


Is copy number variation dynamic? Is there any evidence showing that copy number variation changes over time? I'm wanting to model interactions in expression level as a dynamic bayesian network, but an assumption my approach will need to make is that it is static.

Your question could be phrased more specifically to avoid ambiguity, but rephrasing it the way that I suspect you mean it, ("Is there any evidence showing that [the rate of] copy number variation changes over time?"), then yes, there is indeed.

The rate depends on many factors including which mechanism and which organism and which region of the organism's genome and as @Michael wrote, also what scale (et. al.) is under consideration too.

So your assumption that the rate is static should probably be stated explicitly.

Nature Reviews Genetics 10, 551-564 (August 2009) | doi:10.1038/nrg2593


Can P. falciparum and other malaria parasites be cultured and genetically engineered? I'm not a parasitologist, and I was wondering about the current state of malaria research. For instance, is it possible to culture P. falciparum? Are there techniques for genetic manipulation, editing or transfection (analogous to in vitro cell culture) ? Are there any major limitations to studying these parasites in culture?

Yes it is possible to culture plasmodia but they don't grow in a simple constituted medium. Usually RPMI supplemented with serum and erythrocytes is used for growing plasmodia ex-vivo. This article discusses the issues related to plasmodial culture in detail. The authors say that sometimes a certain growth stage (in particular gametocyte) is lost on prolonged cultivation.
In the same paper it is discussed that the exo-erythrocytic (liver stage) plasmodia can be grown on cultured hepatoma cell lines.

Several transfection methods also exist. However, culturing is not a mandatory prerequisite for transfection. Usual methods like electroporation work for a wide spectrum of cell types (in-vivo electroporation is also becoming popular). You can refer to this article for a summary on different transfection methods for plasmodia.

A major limitation, in my opinion would be that the different life stages may not be reproduced in a single culture (as you can see that each stage thrives in a very different type of milieu).


Is there any way to differentiate between a contractile and a non contractile vacuole by observation alone in any given organism I have read about distinguishing them using osmotic experiments in books and here as well.
But is there any thing common (on a biochemistry level) from which I can tell if a vacuole is contractile or non contractile irrespective of the organism taken and only by observing?

Contractile vacoules are usually surrounded by distinguishing structures

  The contractile vacuole has several structures attached to it in most cells, such as membrane folds, tubules, water tracts and small vesicles. These structures have been termed the spongiome; the contractile vacuole together with the spongiome is sometimes called the "contractile vacuole complex (CVC). The spongiome serves several functions in water transport into the contractile vacuole and in localization and docking of the contractile vacuole within the cell.

This type of arrangement is not common in non-contractile vacuoles like gas, sap or food vacuoles.


How are presynaptic burst firing signals transmitted post-synaptically? Neurons can exhibit burst firing and this presynaptic process basically results in a flurry of action potentials being fired in a short time window.

I'm, however, wondering how these signals are further relayed once they synapse onto other neurons? Specifically, does each action potential in the burst volley generate another post-synaptic action potential, or is the bursting somehow averaged to then transmit either one or no action potential post-synaptically depending on long the burst train was?

Short answer
It depends.

Background
It all depends on the neuronal circuit and neurotransmitter system under investigation. For example, raphe neurons release 5-HT in a burst-like fashion onto cortical dendrites. However, the postsynaptic effect is inhibitory, so no action potentials there (Gartside, 2000).

Intracortical recordings in the rat have shown that each action potential in a burst resulted in neurotransmitter (glutamate) release and subsequent excitatory postsynaptic currents (EPSCs) and potentials (EPSPs) (Williams & Stuart, 1999). So that would positively answer your question, at least in this specific neuronal circuit.

Reference
- Gartside, Neurosci (2000); 98(2): 295-300
- Williams & Stuart, J Physiol (1999); 521(2): 467–82


Are there any proven ways to increase the rate of bone remodeling in humans? I'm not asking for anything specific -- just wondering if there's any data, studies, or etc. that show a possibility in increased bone resorption and turnover (bone remodeling/Wolff's Law) from certain procedures (whether it be diet, supplementation, drugs, surgery/experimentation, exercise/habits, etc.)

For example, comparisons between studies of people that show bone remodeling faster under different circumstances that can prove a specific method one can use to apply

By "increase" I mean anything that allows the human skeleton to be replaced faster some way

The main factors affecting bone remodelling are the person's age, and the load applied on the bone. It is known that in relation to fracture healing, younger children remodel much faster and more effectively. This allows surgeons to accept very displaced fractures in young children without having to restore original anatomy as remodelling will take care of that naturally. Here is an example:

http://www.brokenarmanswers.com/arm-still-crooked-cast-comes-off/arm-fracture-remodeling-children/

The reason is that bone absorbs in areas under less loading, and forms along load lines. The shape of bones therefore follows the shape and alignment of surrounding muscles, which apply some form of load even at rest due to muscle tone. The process of bone absorption and formation is much more efficient and faster in younger people and becomes slower with age. This also explains why bones become osteoporotic in people who can't weight-bear for a lengthy period of time, or in astronauts who spend long periods in zero gravity.

A well known method to accelerate fracture healing is to load the fracture as early as possible. This is the main principle of the dynamic compression plates where the holes of the plate are designed as oval rather than circular, so that when an off-centred screw is tightened, it pulls the plate in a direction that results in compressing the fracture to promote bone healing. Here is an illustration to demonstrate this technique:

https://www2.med.wayne.edu/diagRadiology/RSNA2003/Compression_Plates_Overview.htm


what kind of lizard is this Found on ground by house in residential neighborhood in Fort Pierce FL. looks mature maybe 17".

Nice find. It's a common basilisk or jesus christ lizard, distributed throughout central america, they grow to 27 inches and can run on water, the male is bigger than the female:

https://travel.mongabay.com/colombia/images/colombia_1513.html


Does creatine-phosphate (CP) supplementation regenerate NADH? I have the following facts:

It is possible to convert ATP <-> creatine vice-versa. (ref - non scientific)
CP supplementation protects against metabolic syndrome. ref1 ref2
Fructose digestion depletes NADH via TG synthesis. ref

I assume that CP supplementation regenerates not just ATP, but NADH, if it is depleted, and so it restores the redox balance in the liver. Both ATP and NADH are similar energy storing molecules, so I guess there is a biochemical pathway which converts ATP to NADH, or there is a pathway, which regenerates NADH using CP. Am I right, if so, which pathway is it?

note:

I might be wrong. From one of the references:

  Taken together, this study provides direct evidence that creatine reduces lipid accumulation in hepatocytes by the stimulation of fatty acid oxidation and TG secretion.

So maybe ATP is enough to prevent TG accumulation in the liver.

Creatine itself is never converted into ATP. Creatine-phosphate on the other hand can donate its phosphate group to ADP, phosphorylating to form ATP and creatine. This is a buffer system for high-energy phosphates, and is very important in organs with rapid ATP turnover, notably muscle.

The mechanism of the findings described in the papers is not fully understood yet I think. But it is not via ATP, because the supplementation is not creatine-phosphate, but creatine itself, which does not yield ATP.

Regarding NADH: ATP is very different from NAD/NADH in terms of molecular structure, and the two are not interconverted by any pathway that I know of. (Probably this is not what you meant, but just to be clear.) But it is certainly true that reducing power in the form of NADH can be used to phosphorylate ADP into ATP; this is the task of the mitochondrial respiratory chain, where NADH is oxidized to NAD by complex I. On the other hand, I am not aware of a physiologically relevant process that uses ATP to reduce NAD into NADH.

The liver is a main site of synthesis of creatine itself, and this syntesis consumes methyl groups donated by the S-adenosylmethionine system. The authors of your ref1 seem to suggest that reduced synthesis of creatine following supplementation is a possible mechanism. Similar effects have been observed with choline supplementation, but again this effect is not well understood and a current research topic. A recent review is found here.


What effect does ambient temperature have on the cardiovascular system? I am sorry if this is not appropriate for this site, but I think it fits so I am asking it here:

I went for a run yesterday, and it was about -8⁰C.  I was wearing a couple pairs of shorts, a t-shirt and a long sleeved shirt, which is not that much, so I went with the idea that I would warm up a lot while running.  After running for a while, I found that I was tired and out of breath much earlier on then I would normally be.  It raised the question:

  How does decreasing the ambient temperature affect the cardiovascular system?

There were two things I could think of that might directly affect it.  (1) The fact that my body's metabolism has to work to heat itself, and this takes energy.  However I am not sure how much of a role this plays since running warms you up anyway.  (2) The air being so cold, and entering the lungs, I imagine my body has to work much harder in some way to deal with it.  What exactly happens here, and how is the process different from breathing at 25⁰C?

Also, how much faster would we expect a runner to be able to finish a 10km run when it is 25⁰C outside versus -5⁰C outside?

In relation to the cardio vascular system a combination of adrenaline from exercise and the bodies natural response to the cold causes constriction of blood vessels in the skin and extremities. This helps to reduce heat loss.

The movement from running increases the amount of cold air that runs across your body and into your lungs, which would offset the effect of heat generated from running. According to the article about Thermoregulation in cold conditions on Wikipedia, the offset is great enough to make shivering while standing still a better way to keep warm.


What's the best way to measure/calculate the size of a light beam at the sample of a microscope? I am using a microscope with an LED derived light through the epi-fluorescent port of a microscope.  I know that the "field of view" for a given objective is equal to the field number/magnification but I don't know that this is the actual area of illumination on the sample.  In my case, I am using a 40x objective with field number 26.5.

Secondly, if I were to use a pinhole filter between the light source and the back of the objective would this limit the area of illumination so long as the pinhole was smaller than the f.o.v. dimension?

I would be grateful for any answers, most of the information I can find on beam size at sample is related to spot size calculations of resolution.

Well you can always use a piece of white circular paper and draw the outline of the light onto it since it should be visible. This is a quick and dirty method that can be improved by taking a photo of the light with a camera if you have one and then comparing the distance of the edge of the paper measured with a ruler to that of the circle of light.


In what ways, if any, does administration of rapamycin *not* mimic calorie restriction? Numerous sources like this say that rapamycin increases lifespan. And mTOR antagonism appears to be a large part of this (mTOR antagonism also appears to be a large part of calorie restriction's mechanism too).

Is the effect of calorie restriction equal to that of rapamycin treatment or are there differences?

Rapamycin specifically inhibits the mTOR pathway (mTOR = mammalian target of rapamycin), which has numerous downstream functions including protein biogenesis, regulation of cell cycle, immune function and apoptosis. The upstream effectors of mTOR include growth factors and amino acid availability, so you can certainly see that the lifespan enhancing effects of caloric restriction will be (at least in part) mediated by the mTOR pathway.

But there are key differences. mTOR also receives signals relating to DNA damage and inflammatory changes (to name just 2) that are essential for healthy survival. So any direct inhibition of this pathway will affect all the functions - I can't find the reference now, but I have definitel read in one of the numerous rodent studies that rapamycin treated mice have reduced immune function (i.e. the lifespan increased effects can only be seen in a controlled lab environment - in the wild mTOR-inhibition to this degree would be a disadvantage).

I think therefore it is fair to say that the effects of caloric restriction on longevity are mediated by mTOR, but administration of rapamycin is not an equivalent treatment.

Update

Really great review came out last month (http://www.ncbi.nlm.nih.gov/pubmed/22500797) - I recommend you give that a skim if you want detail!


What does NaOH do for the plating of Bacillus subtilis? A book called Molecular Biological Methods for Bacillus called for plating Bacillus subtilis cells on LB-agar plates with the following components:

  A general-purpose medium containing per litre:

  Bacto-tryptone 10 g

  Bacto-yeast extract 5 g

  NaCl 10 g

  1 M NaOH 1.0 ml

  Autoclave (151b/in^2, 30 min). For LB agar plates solidify with 1.5% (w/v)
  agar; for LB overlay use 0.7% agar.

The first three components and their corresponding amounts are the same as what I normally work with, but I usually add distilled water for plating E. coli instead of NaOH. According to Wikipedia's entry on lysogeny broth, NaOH can be added to adjust LB's pH. But the protocol here mentions nothing of that sort. In other protocols of the book, at least it would say "adjust to pH -- with 10 M NaOH" or 1 M NaOH, etc. So if it is not to adjust the pH for the growth of Bacillus subtilis, what other purpose does NaOH do for the bacteria?

Also, I usually autoclave my LB or LB-agar for 2 hours instead of 30 minutes. Would autoclaving at 2 hours instead of 30 minutes affect NaOH?

I think NaOH is added to bring up pH not to get too acidic. I feel autoclaving LB or LB-agar for 2 hours is too long. During autoclaving, some components are gradually degraded.


Why are there no marine birds? Walking  by the lake and watching the ducks the other day a thought struck me; there are lots of aquatic birds but all remain at least somewhat terrestrial, nesting on land.

Why is it that no birds have taken the evolutionary route of the dolphins and whales and returned to the sea?

Is there something in avian biology that means this is not possible?

Apart from one isolated group of birds in Australia (i.e., mound nesters found in Australia that use external heat for incubation - see link), all birds incubate their eggs (see link). All species that returned from land to sea have retained their reproductive cycle (marine mammals still give live birth and suckle their young) and still rely on air for oxygen intake. Extrapolating this mammalian evolution to birds would result in a creature that returns to sea, with all ties to land cut off, but that still has to incubate their eggs under water. As they would still rely on air, this is not very feasible as they would need to go up often to breath. This would leave the eggs vulnerable to predation. Even worse, it would leave the eggs at the mercy of a relatively cold ocean cooling them down quickly. Incubation means that the eggs are pretty much kept at body temperature which is difficult in the sea regardless of breathing parents. In all, while there may be certain benefits of underwater life for birds, it will require some drastic evolutionary changes in terms of the reproductive cycle. A more parsimonious way of colonizing the sea is to go back to land once and a while to lay eggs, incubate them, and raise the young until they are sea-worthy, like penguins do as @MattDMo mentioned.


What stops telomerase? The telomerase is an enzyme that adds telomeres.

What stops the telomerase from adding too many telomere sequences ? What's the regulating mechanism ?

Telomerases are tightly controlled on all level: Expression, post-translational modifications and by external factors. I think for this the external factors, a protein class called telomeric proteins. They bind to the end of the telomere and regulate the telomerase.

The figure is from this paper, which looks into the topic quite extensively:

Regulation of telomerase by telomeric proteins.


Two different Leucochloridium infected snails - different species? In the last three days, I have found two snails infected by some species of Leucochloridium. I found them in my garden in the south-west of Sweden. Now I'm wondering if they are the same species or not.

One has broodsacs with green stripes and looks like a typical Leucochloridium paradoxum, and the other has brown stripes, which makes me think it's a Leucochloridium variae, but I've seen it mentioned that their appearance can vary.

Update: I have learned that there is only one (documented) species of Leucochloridium in Sweden, so maybe I should close this question, but I would still like to know if there is a way to tell the difference just by appearance.

And here they are in animated form in case that is helpful:

An intriguing question. Because I have not conducted any formal research into the parasitic family of Leucochloriidae, I shall hazard two options which would not require genomic sequencing.

Principally, as you suggested, observing the banding of the broodsacs is one critical means to distinguish members of this genus. The study entitled 'A
REVISION OF THE FAMILY LEUCOCHLORIDIIDAE POCHE (DIGENEA) AND STUDIES ON THE MORPHOLOGY OF LEUCOCHLORIDIUM PARADOXUM CARUS' describes its broodsacs 'typically' to have green banding with dark brown and black spots. On the grounds that this indicator is liable to being variable, the next procedure may yield greater accuracy.
The secondary host of most Leucochloridium species, including paradoxicum, is an adult bird ranging from crows to finches in which the larval mircidia enter the bird's tract and develop into distomes through consuming the snail's infested tentacle. Moreover, if possible, determining the secondary host of the parasite may assist your taxonomic identification: the Leucochloridium often gives its host's left tentacle the resemblance of a maggot, attracting the American Robin, for example.
Ultimately, analysis of the distomes produced in the secondary host phase could allow you to discriminate at the specific level.
Information regarding Leucochloridium variae, available from: http://eol.org/pages/849160/details
The cruel world of parasites


What are blood group determinants? I am trying to understand if they are the same as the blood antigens. The books I have tried to read say something about them being the antigens on the surface of the red blood cell.

Blood group A expresses A antigens and anti-B antibodies etc etc, see the next figure:

Taken from the wikipedia entry on blood groups.


Keyword based literature search I understand this is not a biological question but this is often a problem whenever I look for literature.

How to look for a reference for some fact based on keywords. For instance you know about a fact such as - Cell signaling responses are faster but short lived compared to transcriptional responses. How to find the literature which actually says this. I often end up getting irrelevant results.

In other words, how to represent a fact using appropriate keywords. Is there an algorithm which can generate synonymous statements [like MeSH terms in pubmed] and search for those.
Or is there any way of setting up a hierarchical search.

PS: If someone finds a reference for "Cell signaling responses are faster but short lived compared to transcriptional responses" then please let me know

I think the statement above is slightly misleading. There are many many types of cell signalling, anything from RTK (at the cell surface or when its endocytosed), to steroid receptors, which operate on different time scales and produce different results depending on the type of signalling. Also it depends on what you are measuring/defining as a signal/response in lets say "cell signalling" because you could define cell signalling response as protein phosphorylation at any point in a signalling cascade or it could be the transcriptional activation itself (consider the MAPK pathway in Drosophila, at which point do you consider a response is produced? when Raf is activated? or when transcription factors such as pointed bind to their ETS binding site and start to transcribe as measured by luciferase? as you can tell the time difference between the two is quite large, well as far as I know after RTK activation in Drosophila it takes ERK 20 minutes just to translocate to the nucleus). A cell signalling response could also constitute changes in the rate of cell migration, cell shape etc, which can either be slow or fast depending on the signal in question. so I think the above question needs major rethinking and redefining.

Now getting back to your questions about key search terms, in my experience, over time you just end up developing a knack for what you consider to be key words after you carefully define the question and think bout its different aspects. A rule of thumb that I use is typing at name of proteins (e.g. JNK or RAS etc) or processes (transcription, phosphorylation etc) and use a word like rate, time-scale, half-life, turn-over or something like that if its measuring changes in time you are interested in. Just play around with words.

Also as a general advice you don't have to reference every snippet of every fact like "water is liquid at RT in standard atmospheric pressure" etc. References are meant to be there to acknowledge the work of others like "how DNA was discovered" so that people can't just lift paragraphs or pages out os someones research without acknowledging them and passing it as their own work.

Hope this helps.


Does anyone know what kind of caterpillar this is? I was out hiking, and was walking along the side of a road, and saw this little guy on some gravel. Hes a light blue/grey color, hairy, spotted with red,and looks like he has horns and a tail. I've been trying to search for what species it is. If anyone knows, please share!

(Click to view full image)

Looks similar to a Rusty Tussock Moth (Orgyia antiqua) caterpillar, but you might want to check the bugguide page for the species, or submit your photo there for a second opinion.


How do organophosphates affect kidney function? Many organophosphates, besides inhibiting acetylcholinesterase, can also permanently inhibit the enzyme neuropathy target esterase, leading to nerve damage. NTE also happens to be found in the kidneys, and is involved in osmolyte production. Have organophosphates been known to affect kidney function through the inhibition of NTE in the kidneys? If so, how?
Source:
Gallazzini, M., & Burg, M. B. (2009). What’s New About Osmotic Regulation of Glycerophosphocholine. Physiology, 24(4), 245–249. doi:10.1152/physiol.00009.2009

One article suggests that NTEs in kidneys are important for regulating NaCl concentrations, whereby if increasing concentrations of NaCl are sensed in inner medullary collecting duct cells transcription of the building blocks of NTEs are increased to decrease this NaCl. If NTEs are inhibited due to being irreversibly bonded with moieties of organophosphates at their active sites then this would mean that the kidneys would lose their mechanism for controlling how much salt is excreted from the body.
Gallazzini, M., Ferraris, J. D., Kunin, M., Morris, R. G., & Burg, M. B. (2006). Neuropathy target esterase catalyzes osmoprotective renal synthesis of glycerophosphocholine in response to high NaCl. Proceedings of the National Academy of Sciences, 103(41), 15260 LP – 15265. https://doi.org/10.1073/pnas.0607133103
This loss of chloride and sodium, I posit, would then have a knock-on effect on the concentration gradients maintained in the kidney as necessary for effective absorption and excretion of other ions. My guess is that hyponatraemia would be one of the direct results of the presence of organophosphates in the kidneys.


From what kind of insect might these eggs be Does anybody know what kind of insect might have laid these eggs:
The photo was taken a few days ago in Limburg, Belgium near a pasture with some goats.

Those are likely moth eggs... moths have a tendency to attach their eggs on metal screens that you might have in your windows or doors.
Here is a video of a moth laying eggs on glass:
https://www.youtube.com/watch?v=L2zf1J8CZdg
Here is a video of a moth laying eggs on a metal screen:
https://www.youtube.com/watch?v=qKHReVNAMYw
Here are photos of eggs on a wire fence, believed to be moth eggs:
https://www.whatsthatbug.com/2013/09/19/possibly-moth-eggs-deer-fence/
And another example of moth eggs on a metal wire:
https://hardtocomebylifestyle.wordpress.com/2014/08/31/moth-eggs/


What is the purpose of back-crossing mice for multiple generations? Occasionally I will come across articles that refer to back-crossing mice of one strain onto the background other another strain (e.g., C57Bl6). They do not explicitly state the purpose for doing so, but I can infer that the change of strain is to relate their findings to what is already known using the new strain (e.g., C57Bl6). Usually the back-crosses are performed for 5-10 generations. Is this to try to remove (epi)genetic variation from the original strain relative to the new strain, or is it more about normalizing expression of a particular allelic variant (e.g., knocking-in a transgene)?

Depending on the exact goal of the experiment, the researchers may back-cross both to smooth out genetic variation between individuals and to potentially normalize expression of a transgene, although once you get past the chimeric stage gene expression should be fairly stable. In my experience, back-crossing allows you to generate a genetically-altered mouse that differs as little as possible from a (generally well-characterized) parent strain, except at the locus of the genetic manipulation. This way, any differences in phenotype can more easily be explained by the knockout/knockin/transgene/what-have-you, and not by any variations in background genetics.

As an example, C57BL/6 mice, being inbred, have a number of well-known mutations, deficiencies, resistances, etc., and for one reason or another have become one of the most popular and most-characterized mouse strains in biology, so there is a great interest in continuing research using a well-known historical model with so much extant experimental data. These mice are quite different from the 129 strain, which are frequently used to make initial genetically modified strains due to the large number of embryonic stem cell lines available, and other technical reasons which allow for the relatively easy generation of transgenics, etc. However, for various other reasons, 129s aren't used as often in the type of studies that BL/6s are, so it's preferable to create the mutation in a 129, then back-cross it onto a BL/6 background. Both of these strains are quite homogenous from one individual to another (each sibling is practically a twin of the next), but once you start breeding 129s to BL/6s you can generate all sorts of genetic heterogeneity due to random cross-overs and all the other things we like to talk so much about around here when it comes to mutations and meiosis. As anyone who has worked with genetic diseases in humans will readily tell you, it can be extraordinarily difficult to nail down specific genotypes that lead to specific phenotypes when there are so many other confounding factors present. Backcrossing a mutant 5, 10, or even 20 or more generations back onto a reference strain is one of the best ways we have at the moment of controlling for all the genetic variations that are introduced when two inbred "tool" strains are bred together.

And now, cute pictures :)

129 mouse

C57BL/6 mouse

both images from Charles River


Transverse diffusion of lipids in red blood cells The membrane of a human erythrocyte has polarity:

Phosphatidylethanolamine and phosphatidylserine are predominantly on the inner side.
Phosphatidylcholine and sphingomyelin are predominantly on the outer side.

Although these can diffuse in the lipid bilayer, they stay on only one side of it. How is this sidedness preserved?

There are two reasons for the asymmetry for the lipid composition of membranes in cells usually.

The first which was mentioned by @Superbest is proteins which are called 'flippases' which describes three broad categories of proteins which facilitate the translocation of the lipids through the membrane, despite the fact that they all have polar or even charged head groups.

This is not really an answer to your question here though - they will have little to do with asymmetry of lipids in erythrocytes I think because the these proteins will only allow lipid diffusion to equilibrium on either side of the membrane.  To force an energetically unfavorable mixture of lipids they would require the use of energy.  While some lipid translocases can force the composition to change against the equilibrium, these seem to require ATP and human erythrocytes do not have mitochondria.

The second, probably better answer is that the lipid composition of a membrane at equilibrium is dictated by of the curvature of the membrane.  The outside of a membrane takes lipids with larger head groups and shorter or fewer chains, the interior will compose more of lipids with smaller head groups and longer and more aliphatic chains.
This capacity of a lipid to take up a greater volume in its head group vs its non-polar end is called its 'intrinsic curvature'.

Erythrocytes have some cytoskeletal structures such as ankyrins which give the cell its characteristic curvy 'dented lozenge' shape, which must also drive some of the lipid composition in some parts of the cell.


Spatial learning in microorganisms Has there ever been an experiment performed that demonstrated a form of 'spatial memory' in a unicellular organism?  I'm imagining something analogous to the classic 'rat in maze' experiments, but obviously on a much smaller scale.  Possibly even something as simple as following a concentration gradient, but choosing to go either upstream or downstream based on some sort of prior reward in a similar circumstance.

To build on busukxuan's answer, there are a lot of single-celled organism responses that kind of resemble memory:

Slime mold uses an externalized spatial 'memory' to navigate in complex environments - essentially, a slime mold leaves behind a trail, which it then avoids, allowing it to avoid where it has traveled in the past.

If you apply a periodic stimulus to Physarum, it will anticipate the next stimulus: Popular, openly accessible summary Paywalled journal article.

If the amoeba Dictyostelium sees an increasing cAMP gradient, it will follow that gradient - and then be less sensitive to a reversal in the gradient: Cellular memory in eukaryotic chemotaxis

In fact, even bacteria have some memory - they can figure out whether or not they are going up a chemoattractant gradient by making a comparison with the signal they observed a few seconds ago: Temporal comparisons in bacterial chemotaxis


Henrietta Lacks Cell Line - Immortality I'm a newbie in biology and medicine. I understand that Henrietta Lacks provided the cells that formed the HeLa cell line with which much research has been done. Henrietta Lacks died of cancer. If we assume that she did not have cancer, every cell in her body could divide for an infinite period of time, and she never sustained any trauma ever, would Henrietta Lacks have been immortal?

Thanks,
mj

No, there was nothing special about Henrietta Lacks, apart from the fact that her cells have been used for so many years (without her knowledge or consent, by the way). She was not immortal, her tumor cells were. The HeLa cell line comes from her cervical cancer cells. The rest of the cells of her body were not immortal any more than yours or mine are.

Such immortality is a classic characteristic of cancer, in fact it is a hallmark of tumor cells. Normal cells die when they are told to, apoptosis (programmed cell death) is a normal part of a functioning, healthy organism. Tumors are collections of cells that replicate uncontrollably and do not do what they're told, including dying like good little soldiers.

That is why we often use tumoral cells for cultures, since they have been immortalized, it is relatively easy to keep them alive in the lab. This means, essentially, that they produce an enzyme called telomerase which lengthens telomeres. In normal cells, the telomeres get shorter with each round of mitosis and when they get shorter than a certain threshold, they are targeted for apoptosis. Cancer cells are protected from this by the telomerase and can therefore undergo many more rounds of reproduction.

So, the cells are not special because of the person they came from, they are special because they are cancer cells.


Most suitable biodiversity index I am conducting an investigation into the effect of two different grass management techniques (grazing vs. machine-mowing) upon floral biodiversity.

I have collected my data and now need to process it in a way that will yield meaningful and valid results. My data is in the form of 25 samples per area with %-abundance measured for each species in a 0.25m2 quadrat.

I am currently using a non-standard diversity quantification technique, called Disney's index (which I have been led to believe is named eponymously after R.H.L Disney, however I am unable to find any references describing this), in which we assign each species a weight based on percentage abundance, as follows:

We then use these weights to calculate the index as follows (i.e. by computing the sum of the weights of the species, over the number of species):

I want to know if this is the best possible diversity index I could use for this type of analysis, or whether there are others which I should be considering.

Thanks in advance!

It sounds like you are interested in beta diversity which is the change in taxa composition (i.e., alpha diversity) between plots.  There are a number of approaches to calculating beta diversity and the correct choice generally depends on the question(s) you are trying to answer.  The most common approaches are very well described in this paper:

Anderson, M. J. et al. 2011. Navigating the multiple meanings of Beta diversity: a roadmap for the practicing ecologist. Ecology Letters 14:19-28

P.S. I am not familiar with Disney's index so I cannot comment on its merits.

P.P.S. You may also be interested in this question.


Major groups of photosynthetic prokaryotes According to Stryer there are four major groups of photosynthetic prokaryotes, i.e. Table 19.1

Bacteria Photosynthetic electron donor $\ce{O2}$ use.

Green sulfur $\ce{H2}$, $\ce{H2S}$, $\ce{S}$ Anoxygenic.

Green nonsulfur Variety of amino acids and organic acids Anoxygenic.

Purple sulfur $\ce{H2}$, $\ce{H2S}$, $\ce{S}$ Anoxygenic.

Purple nonsulfur Usually organic molecules Anoxygenic.

Cyanobacteria $\ce{H2O}$ Oxygenic.

Do each groups belong to a different genus?

To answer your question, yes they are all in a different genus, but that’s really specific.  If you are wondering about their fundamental differences, they fall into a few different groups.

Green sulfur bacteria usually falls into the phylum Chlorobi

Green non-sulfur bacteria falls into the phylum Chloroflexi (Part of the terrabacteria superphylum)

Cyanobacteria is a phylum in itself but also falls into the terrabacteria superphylum.

Both, Purple sulfur/non-sulfur bacteria are all proteobacteria.

Now, pay attention here, as linking these could be somewhat confusing sometimes.  But now we can link together their relationships.

Green sulfur bacteria (Chlorobi) falls into the FCB superphylum, meaning that it is a gracilicute.

Purple sulfur/non-sulfur bacteria (Proteobacteria) are also gracilicutes.

Green non-sulfur bacteria (Chloroflexi) is part of the terrabacteria superphylum.  Terrabacteria are not gracilicutes.

Cyanobacteria is also in the terrabacteria superphylum. (Again, not a gracilicute.)

Now that we know this, we can reasonably assume that both purple sulfur/non-sulfur bacteria are related to green sulfur bacteria, as they are both gracilicutes.  Also, we can conclude that the non-gracilicute green non-sulfur bacteria and Cyanobacteria are more closely related to each other than they are to the latter mentioned bacteria.

Here’s another cool fact, some Deinococcus-Thermus bacteria (members of the terrabacteria superphylum along with Cyanobacteria and Chloroflexi) have been found to carry the bacteriophytochrome photoreceptor (BphP) which absorbs red light.  Interestingly, Deinococcus-Thermus are non-photosynthetic, but these photoreceptors are found in photosynthetic Chloroflexi as well. This indicates that the deinococcus bacteria likely diverged from chloroflexi at some point but still retained the BphP.

Hope this helped!


What stops the coagulation process? Whenever there are minor/major injury to blood vessels, the platelets, fibrin, thrombin, etc. are recruited. They then seal the wound and block bleeding.

What tells them that their job is done?

Exposed collagen at the site of vessel damage simultaneously initiates plates aggregation and the clotting cascade. So, when the wound is sealed and no more collagen is exposed, which is the main factor to activate the cascade, the blood clothing cascade stops.


Is evolution a fact? Richard Dawkins in one of his videos says that Evolution is a fact and not just a theory.

He goes on to say that man and chimpanzees both evolve from apes.
Is this correct (Is evolution a fact and did humans & chimps evolve from apes)?

A tiny bit of terminology

Fact

In popular culture, the term fact means "something that is true". I would consider a theory as being the closest concept in science to what is called a fact in the population culture.
In natural sciences, the term fact is rarely used but would have the same meaning than the one in popular culture. The reason we are not often using this concept is that in science (nor in any other field of knowledge) one can never definitely know the truth. We can only have evidence that are congruent with a hypothesis or body of statements. In such case we talk about theory (see below).

Theory

In popular culture, "theory" is used to mean what the natural sciences call a "hypothesis."
In the natural sciences, a theory is a body of thoughts/statements that is very well supported by loads of evidence. In science, a theory is not a hypothesis. For example: Theory of evolution, Theory of general relativity, transition state theory, etc. Note by the way that various definitions of theory are in use (ref.). The below answer respects the definition that I gave above.

The scientific terminology presented above is actually a matter of philosophy and not science. If you need more information about the definitions of "theory", "fact" and other related terms, you may want to ask on Philosophy.SE. Stephen Jay Gould summarized the concepts of theory and facts nicely when saying

  [..] facts and theories are different things, not rungs in a hierarchy of increasing certainty. Facts are the world's data. Theories are structures of ideas that explain and interpret facts.

In the answer below, I am using the scientific terminology.

Your questions

  Is evolution true?

Evolution is what is called a theory in natural science (The Theory of Evolution a.k.a. modern evolutionary synthesis), and it is extremely well-supported. Evolution is NOT a hypothesis. In other words, we have a lot of supporting evidence that living beings have evolved and are evolving.

  Did both humans and chimpanzees evolve from apes?

Humans and chimpanzees are apes (great apes to be more accurate). Both humans and chimpanzees evolved (and are still evolving) from a common ancestor who already was a great ape. We have a lot of evidence to support this common ancestry.

What does the theory of evolution say?

Understanding Evolution (by UC Berkeley) is a short and introductory course to evolutionary biology. Of course, there exist other good sources of information online such as Evolution and the tree of life by Khan Academy.

We have a number of posts providing book recommendations for

General biology (Books for beginners and Introductory biology text for an outsider)
Intro to evolutionary biology (Text Book Recommendation: Organic Evolution and Introductory books about evolution)
Intro to evolutionary genetics (Books on population or evolutionary genetics?)

You will also find a lot of introductory posts on biology.SE such as for examples:

Why do some bad traits evolve, and good ones don't?
Is there a biological mechanism for evolution encoded into our DNA?
Does it make sense to classify all humans in a single species?
Why is a heritability coefficient not an index of how “genetic” something is?
How could humans have interbred with Neanderthals if we're a different species?
If dinosaurs could have feathers, would they still be reptiles?
Why does evolution not make our life longer?
Why don't mammals have more than 4 limbs?
How to define “evolution”?
How did some humans evolve to be white?
Who are humans' closest relatives, after primates?
Did cats evolve from monkeys ? or vice versa?
Why do the ancestors of birds still exist?
How does Natural Selection shape Genetic Variation?

What are the evidence?

Demonstrable and repeatable examples of evolution lists sources that list evidence. There are probably thousands of pieces of evidence listed in total, all explained in lay terms with links to the original article. Of course, this is just a small sample of the evidence we have.

The post Is there any biological evidence that is not suggestive of or seems to disprove evolution? might be of interest too.

Thanks to @CortAmmon's comment for correcting a very poorly phrased sentence.


Can someone ID this moth seen in Bellandur, Bangalore? Picture taken near Saul Kere. You may need to zoom in.

It's the Indian Lily Moth
(https://en.m.wikipedia.org/wiki/Polytela_gloriosae).


Is it possible for any animals today to have more than one brain? Is it possible for any organisms in the animal kingdom to have more than one brain?

To some degree the answer depends on your definition of what counts as a brain.

Bilaterally symmetrical organisms tend to have some level of cephalization, which involves the concentration of sensory and inter-neurons at one end of the organism (the head).

This aggregation of neurons at the head is typically more complex than aggregations of neurons elsewhere in the body and so it gets designated as a brain whereas the others are designated as ganglia (if they are outside the central nervous system or nuclei if they are within the central nervous system).

In vertebrates, cephalization is very well developed so the brain is typically much more complex than the ganglia (although the enteric nervous system is pretty awesome, its not the brain). However in many invertebrates, the ganglia at the head of the organism (its brain) is not much more complex than the other ganglia around the body.

For this reason, many invertebrates can survive decapitation (at least for a while) and some like the flat worm, can famously survive and regenerate their head after decapitation.


Are there any photosynthetic catalysts in use other than chlorophyll? When I search for catalysts other than chlorophyll on Google, I only get references to artificial photosynthesis. When I look up photosynthesis, I see accessory pigments mentioned, but it appears that the chlorophyll family is crucial.

These chlorophyll variants all have the chlorin (not to be confused with chlorine) ring in common.

Are there any photosynthetic organisms that do not use a chlorin derivative? Why is chlorin so predominant?

There are photosynthetic organisms that use retinal-rhodopsin complex. However, the mechanism of photosynthesis is different in these organisms than those that employ chlorophyll dependent photosystems. In these organisms, the light causes the rhodopsin-like membrane proteins to pump proton out of the cell and create a proton gradient which in turn is used by the ATP synthase to make ATP.

See this post too Why are there no known photosynthetic archaea?

This mechanism of "photosynthesis" is not as efficient as the chlorophyll dependent one (page 22, Baltscheffsky, 1997†). Moreover, it does not produce NADPH.

† Baltscheffsky, Herrick. Origin and evolution of biological energy conversion. New York etc: VCH, 1996. Print. ISBN: 978-0-471-18581-9


How much influence does toxoplasmosis have on personality and intelligence? Latent toxoplasmosis affects up to 1/3 of the human population and up to 40% of the population in Australia.  I have heard that latent toxoplasmosis has many significant undesirable effects on personality, such as decreased novelty-seeking behaviour, and decreased intelligence quotient.

While these changes are statistically significant, I'm wondering if anyone knows the magnitude of these personality and cognitive changes, since a statistically significant result doesn't necessarily imply that there is a large difference in personality between those who are infected and those who aren't infected.  Also, can one succeed in an academic career path if one becomes infected with toxoplasmosis?

I believe its the other way around - humans may engage in riskier and more novel behavior when infected... which is the most interesting part of the story.  Its not cut and dried, but I think its quite possible that risky behavior increases.

T. gondii is a parasite whose typical life cycle includes both mice and cats as hosts.  The transmission involves the mice being eaten by a cat.  Mice infected with T gondii will tend to lose some interest in being sheltered in close spaces and wander out into open spaces.  They also lose their fear of cats.   That is a permanent change even if the mice are cleared of the parasite.

Other animals, such as humans are secondary hosts - they can become infected by handling or close proximity to cat feces, who have a nearly 50% (45.6%) infection rate themselves. As a result toxoplasmosis is very common in humans.

Toxoplasmosis has been found to increase novelty seeking and increases risk seeking behavior at least in men.  Its been shown to contribute to higher automotive accident rates, schitzophrenia and suicide.

  Thus, the men were more likely to disregard rules and were more expedient, suspicious, jealous, and dogmatic. The personality of infected women, by contrast, showed higher warmth and higher superego strength (factors A and G on Cattell's 16PF), suggesting that they were more warm hearted, outgoing, conscientious, persistent, and moralistic. Both men and women had significantly higher apprehension (factor O) compared with the uninfected controls.

The correlation between toxoplasmosis and lower intelligence is a matter of debate, at least in this review I cite.  Its still not clear whether it is a sociological correlation - do smart people just handle their cat poo more carefully or not at all? This more recent study shows that some factors might make infected humans more intelligent and some researchers see toxoplasmosis as a transformative factor in humans ability to generate and use technologies.

I do see those links suggesting less risky behavior too.  Some say that the increase in traffic accidents is related to lower muscular coordination for instance.  There is evidence on both sides, but looking at what T gondii does to mice, I would bet that some risk behavior will increase.  As such, I'd guess that researchers as such might have a slightly higher rate of toxoplasmosis, but maybe you will do a study and help figure this out!

That being said - anyone who tries to link a single phenomenon; host-parasite interactions; a drug; a gene; a mutation to a phenotype with a simple description is definitely oversimplifying.  The mapping from biological activity to english (or any other language) is hopefully conscious of the caveats of such talk.


Who are these biologists? I know the third one in the front row is James Watson.

Does anyone recognize the others?

Front row, left to right; Victor McKusick, Maurice Wilkins, James Watson, Walter Gilbert and John Kendrew.


What's so special about Chassaignac tubercle? 1-How does massaging of carotid artery at chassaignac tubercle( anterior tubercle of transverse process of C6 vertebra ) can relieve the symptoms of Supraventricular Tachycardia?

My attempt: I think by massaging carotid artery we are somehow stimulating the satellate ganglion present at level of c7. Or, I think, by massaging the carotid artery we are increasing BP, thereby affecting the baroreceptors and somehow this relieves the symptoms of supraventricular tachycardia.

2-Why can't the same massage be done at level of other cervical vertebrae?

The reason massaging the carotid artery can relieve symptoms of supraventricular tachycardia is because by massaging the artery, as you point our yourself, you artificially increase BP within the carotid artery, this activates a reflex (via the glossopharyngeal nerve) that lowers bloodpressure by reducing the heart rate via the vagus nerve, by increasing the refractory period of the AV-node, so the heart rate drops.
It should be noted though, that it can be a bit dangerous to play with these reflexes in some patients, especially because massaging the carotid arteries can lead to an embolism in older individuals with atherosclerosis, or in some patients, it can lead to asystole or ventricular fibrillation (i.e. cardiac arrest).
It's not really about which vertebra is at the level you are massaging, rather it's about being near the carotid sinus, which is where the baroreceptors are located, and that might vary between individuals and how you position the head etc.


Do electron microscopy change the structure of the specimen due to the vacuum step? Since specimens have to be prepared using the vacuum, would the pressure change affect the structures of the specimen?

There are several different ways to deal with the difficulties of imaging biological samples in vacuum. I'll go over the ones I'm familiar with.
TEM - plastic sections
The water in the specimen is gradually replaced with a resin which then solidifies, and slices about 100 nm thick are cut from the specimen and put into the TEM column at high vacuum. The chemical composition of the specimen is radically altered, but the shape of cells and even the arrangement of organelles inside can be preserved if the treatment is done well. Here's a representative image for this technique from http://www.cellimagelibrary.org/images/7722. You can see the endoplasmic reticulum with ribosomes and mitochondria.

TEM - CryoEM
The specimen is cooled so fast that the water in and around it solidifies without forming ice crystals, which would otherwise disrupt membranes, etc. The specimen is nearly identical to its natural state. These 'vitrified' specimens can be put directly into the microscope column, but they need to be maintained at liquid nitrogen temperatures. The size of specimen that can be cooled rapidly enough is limited to about 300 microns thick. A standard TEM beam doesn't penetrate well through samples more than about 200 nm thick; cryo specimens can be cut similar to plastic sections (though it's much harder than at room temperature), or by focused ion beam milling. Here's a representative image from https://www.pnas.org/content/117/16/8941 showing flagellar motors:

Environmental SEM
Larger specimens can be imaged without dehydration or coating in an environmental SEM (ESEM). This microscope has a high-vacuum chamber for the electron gun and lenses, and a low-vacuum chamber containing the specimen and detectors. This method can image larger samples, up to about 10 mm, close to their natural state, but isn't as high-resolution as the TEM methods. Here's an image from https://forschungsinfrastruktur.bmbwf.gv.at/en/fi/fei-esem-xl30-scanning-electron-microscopy_540 showing a small fish, you can judge for yourself how well the structure is preserved:


estradiol hormone role Increasing estradiol (E2) hormone from ovarian follicles prior to ovulation has been hypothesized to play a critical role for induction of pheromones. These pheromones render females sexually receptive to males to facilitate mating. An investigator performs experiments in sheep in which females are gonadectomized, then treated with E2 or vehicle alone and allowed to breed. What can be the hypothesis

The experiment is easy to design: Measure the concentration of the pheromones in the test sheep versus the control sheep and see what the outcome is. Further compare the reaction of the male sheep on both, control and treated sheep. Ideally you treat both animals with some kind of treatment to avoid an influence by the application method of the estradiol. Also blind the researchers to avoid their influence on the experiment.
The hypothesis would be: Has estrogen E2 an influence on the pheromones in female sheep and do these pheromones influence the male sheep.


What is the minimum eye? What is the minimum eye which confers some evolutionary advantage?

By minimum I mean anything less than this has no advantage whatsoever and therefore is not favored by natural selection.

By eye, I mean not just a light sensor but also infrastructure which converts the light stimulus into an advantageous response.

Ideally would like a clear unambiguous before/after case especially on the infrastructure between the mutated protein and the cell's response mechanism which translates this into a survival advantage.

(I assume Opsin proteins floating around the cytoplasm by themselves confers no advantage without some kind of other infrastructure)

please also provide an estimate of the number of coordinated DNA base pairs which needed to change to confer this advantage so that a proper probability estimate can be done.

I think that you are expecting for some complicated system while such things are not necessarily involved. You basically just need a protein that is light-sensitive and some cascade of signal transduction. A light-sensitive protein is just a protein which conformation is changed in the presence of photons of a given wavelength. This cascade of signal transduction can be very standard. It doesn't need to be anything extraordinary.

Consider a mutation that turns a given protein into a light-sensitive protein. Such mutant protein could easily still activate the same cascade (and eventually regulate the expression of the same gene) and may eventually be beneficial. A visual signal (presence/absence of photons of a given wavelength) directly affect the conformation of the protein which in result can activate a whole cascade. The cascade doesn't need to have evolved after the protein had acquired the ability to response to photons. You may want to dive into the details of how the structure and function of the opsin proteins.

This article describes how an ancestral non-light sensitive protein (coded in GPCR gene. The proteins are also called serpentine) evolved into a light-sensitive protein (opsin). The article also link to other articles that discuss this transition.

There are several types of light-senstive proteins in different kingdom, including plants and bacteria that don't have nerves.

You can learn more about the cascade of transduction on wikipedia (here or here for example). You may want to learn more about opsin proteins and learn more about light-sensitive proteins.

Wikipedia page: Evolution of eyes > Early Eyes will probably interest you as well. Depending on the definition you use for "eye" (note, "eyes" have evolved independently 50 to 100 times), Planarian might be a good example of a species that have a primitive eye.