Intrinsic apoptosis in erythrocytes With a lack of mitochondria, can red blood cells perform intrinsic apoptosis and do they have another way of generating cytochrome c to attach to a CARD domain and assemble the apoptosome?

Or are they dependent on killer lymphocytes to bind via the fas ligand and activate procaspase 8 or 10 in extrinsic apoptosis? Do red blood cells even have fas ligand receptors for this process?

Or is there an entirely different method for red blood cells?

Red blood cells (RBCs) don't have nuclei in mammals, so they are usually considered to be pretty inert compared to other cells.

They do have some biochemical activity, and evidently there is some mechanism for cell death  in RBCs when they are induced to degrade or infected by pathogens.  I found this reference that shows caspases -8 and -3 are evident in mature RBCs.  Several other components of the cell death pathway are not evident.

At this time the authors speculate that they don't activate to induce cell death.

It seems that over the broad field of disease research 'apoptosis' and 'cell death' are used equivalently even when the well known apoptosis pathway is not involved.


Can viruses pass through sweat pores? I have read somewhere that viruses and other microbes can not penetrate skin but what about sweat pores? Can viruses pass through these pores?

'Pore' is a confusing term. Sweat is produced in sweat glands, and subsequently excreted through a duct, as indicated in the image below (sudoriferous ~).

In short, viruses cannot enter the body through these glands because the glands don't really open up into the body, but instead the inside of the sweat gland is lined with sweat-producing cells (fig 2 and 3).

A passive protection mechanism preventing infection is similar to the mechanism by which the bladder is guarded from infection through the urethra: even if some malignant agent were to enter the sweat duct, it is simply pushed out by the excreted sweat.

Figure one: Sweat glands in skin. Source: wikimedia commons.

(source: uwa.edu.au)

Figure two: Slide of sweat gland. Tightly packed secretory cells dump sweat into the lumen through exocytosis (see fig 3). Source: University of Western Australia.

Figure three: Exocytosis. The lining of the sweat gland contains cells producing sweat through exocytosis. Viruses and other pathogens cannot simply enter these cells, and also cannot 'slip in between' the cells. Source: wikimedia commons.


A missing endogenous retrovirus in humans, but present in gorillas and chimpanzees? I have read an article about an endogenous retrovirus called PtERV1. It is present in gorillas and chimps, but is missing in humans (original study here).

According to the article, this retrovirus is very similar to HIV. And all of us (gorillas, chimps and humans) have a protein called TRIM5α to fight against PtERV1.

Nearly at the end of the article the author says: currently, there is no explenation for why the endogenous retrovirus (PtERV1) has never entered the human genome.

Is that a typo? Isn't a missing endogenous retrovirus just basic heredity? Especially because humans have the TRIM5α protein against PtERV1 just like gorillas and chimps, which indicate that we used to have it, but we lost it due to how heredity works.

Or did the author meant something deeper that the average user would not understand without a lot of pre-knowledge about genetics?

I think your question boils down to:

Why do modern chimpanzees contain endogenous PtERV1 whereas humans do not?

This is discussed in the original research article:

Kaiser SM, Malik HS, Emerman M. 2007. Restriction of an Extinct Retrovirus by the Human TRIM5α Antiviral Protein. Science 316(5832):1756-1758.

PtERV1 was active after the phylogenetic split of humans and chimpanzees, so any infection would be from separate events. In other words, the endogenous virus was not inherited from a common ancestor:

  Comparison of individual PtERV1 proviruses in gorilla and chimpanzee genomes suggest that this virus was active 3 to 4 million years ago, after the separation of chimpanzee and human lineages.

They hypothesize that modern humans evolved from ancestors that were protected from PtERV1 by TRIM5α:

  Although we cannot rule out the possibility that PtERV1 never infected human ancestors for other reasons, our data do suggest the possibility that TRIM5α was fixed in human populations because of its ability to confer protection against PtERV1 and that modern humans have descended from ancestors who resisted infection.

This does raise the question of why humans were not infected whereas chimpanzees were, despite both containing PtERV1 restricting TRIM5α. This seems to be out of the scope of your question, but they do talk about it in the article if you're interested.


Can a new plant grow from half a Succulent leaf? Succulents like Crassula ovata can be propagated by simply tearing a leaf from the stem and putting it into soil. The leaf will usually grow roots and additional leaves from the calloused wound, and eventually become a full Crassula plant itself.

Now I only have half of a leaf left, the other half got rotten, and dried out. In particular, the part of the leaf that was attached to the mother plant is missing. The remainder is about 3/4" long.

Is it still possible to grow a new plant from just this part of a leaf? Or is it at least necessary that the part of the leaf that was attached to the stem is still present?

After waiting for a while, I am finally able to answer this question myself:

A part of a Crassula leaf is still able to grow roots and new leaves, even if the part that attached the leaf to the mother plant is missing.

I have tried this out myself. I left the half-leaf depicted in the question on top of soil, watered it occasionally, just to keep the soil humid, but not wet. After roughly 5 weeks the leaf grew a first root from the calloused end. For the photo I have flipped the leaf around, to better show the first root.

In the following month, it grew more roots, and after about a month, the first new leaves started to appear.

At this point there is little doubt that a full plant can grow from this, given the right treatment. It is not different any more from full leaves growing new plants.

Update (June 2018): The plant is now 2 inches tall, and doing well.


How do CAM plants keep stomata closed by day and open at night? I understand how plants open stomata, with the H+ ion removal and the resulting K+ ion influx in the guard cells to induce turgor (wikipedia article here), though not how this process relates to presence/absence of light.

However, I don't understand how CAM plants manage to keep their stomata closed during the day and how it relates to CAM photosynthesis (if at all). I know that malate ions are involved in the opening of the stomata in C3 plants, could the malic acid production in CAM photosynthesis contribute to this?

So my question is: How do CAM plants induce closing of the stomata and what signal triggers this?

As others already say in comments, the complete answer to this question is still unknown. However, the basic mechanism has been understood and has been summarized in the following diagram (from Wikipedia):

As you see, the mechanism is regulated by temperature instead of presence of light, keeping in mind that high temperatures are generally observed during the day and low tempertures at night. Temperature regulates, at the expression level, the activity of an enzyme PEP-C kinase. This enzyme phosphorylates PEP carboxylase (or PEPCase in short), which increases its activity. So lets see what happens when temperture is high:

During day:

high temperature inhibits expression of the enzyme PEP-C kinase, which decreases the activity of PEPCase.
activity of PEPCase is further reduced by an enzyme PEP-C phosphatase (this enzyme is active all the time, but its effect is reversed by PEP-C kinase).
due to respiration and photosynthesis, the amount of cytoplasmic malate is reduced (malate is converted to pyruvate to yield NADPH for photosynthesis, and pyruvate is used up in TCA cycle, whose by-product, $\ce{CO_2}$, is used up in calvin cycle).
due to this, malate is released from vacuole into the cytoplasm. This malate is not only used up in photosynthesis and respiration, but also further inhibits activity of PEPCase and expression of PEP-C kinase.
because PEPCase is inhibited, it results in depletion of malate in cytoplasm as well as vacuole.

During night:

at night, stomata open leading to increase in amount of $\ce{CO_2}$. Also, low temperature is unable to inhibit expression of PEP-C kinase.
when activity of PEPCase increases, PEP is converted to malate, which is then transported into vacuole. Also, increased concentration of $\ce{CO_2}$ increases photosynthesis.

Where is light required? As already said, the exact mechanism is still unknown. The mostly accepted mechanism is potassium ion pump hypothesis, but problems arise when we think about the initiation of this process in CAM plants. There are many hypotheses regarding this, and I will follow the one presented by Lee, 2010. Lets begin with the diagram (don't pay attention to the spellings):

initial stomatal opening is mediated by phytochrome in guard cells. The $\ce{H^+}$ pump in guard cells is also activated by darkness.
the maleic acid synthesized in other cells is also transported to the vacuoles in guard cells. There, the intracellular $\ce{H^+}$ (from maleic acid) is exchanged for intercellular $\ce{K^+}$.
increased concentration of $\ce{CO_2}$ also regenerates glyceraldehyde-3-phosphate and ribulose-1,5-bisphosphate, which lead to formation of sucrose via calvin cycle.
this sucrose is again transported to vacuole of guard cells, adding up to osmotic pressure. However, the major effect comes from maleic acid.
increased $\ce{CO_2}$ concentration and increased activity of PEPCase (as already explained) form malate and lead to further increase in the osmotic concentration. All this causes stomata to open.
during the day, malate is decarboxylated to pyruvate (as already explained), leading to decrease in osmotic pressure and thus, closing of stomata.

I hope this makes the concept more clear, but bear in mind that the above mechanism could later prove to be wrong as further studies on CAM plants help to find out the actual mechanism.


Thermodynamics of spontaneous protein folding: role of enthalpy changes I'm trying to get clear why protein folding occurs spontaneously.

$$\ce\Delta G=\Delta H-T\Delta S$$

According to thermodynamics the ΔG should be negative for a process to occur spontaneously.
When a protein folds the ΔS (Entropy) is decreasing, because the protein gets more ordered. However I think the forming of the bonds (disulfide and other weak interactions) counterbalance this unfavourable rising entropy by forming an enthalpy (ΔH) which thus would result in a negative ΔG.

However I saw some other explanation online which didn't apply the Gibbs free energy formula to the protein but instead to the water. Because the water is more ordered when the protein is unfolded it would be favourable according to the second law of thermodynamics to fold the protein because after folding the water molecules can move more freely --> higher entropy -->negative ΔG --> spontaneous folding.

So my question is which of these two (or maybe both) are the cause of the spontaneous folding of proteins?

Summary

The first explanation is commonly encountered.
The second explanation cannot be correct, as it stands, as it ignores the free energy change in the protein.
A modification of the second explanation (perhaps what was intended) is that it is necessary to consider the protein folding and change in the water as being coupled, in which case the overall free energy change — the sum of the two considered separately — is the determinant of protein folding. The assertion would then be that a negative free-energy change in the water system is the deciding factor. This view has been persuasively advocated on the basis of experimental measurements.

Free energy change in individual transformations

It is standard practice in biochemistry to consider the Gibbs Free Energy of transformation of the sort A → B in isolation in determining whether it will proceed spontaneously. A chemical reaction for which ΔG is negative may generate heat (i.e. have a negative enthalpy change (ΔH) ) which affects its aqueous surroundings, but it seems justified to consider the reaction in isolation as there is no sense that the change in the vibration of the water molecules is driving or coupled to the reaction.

This approach has been applied to the structural change of protein folding with the conclusion (consistent with the first explanation) that the change in enthalpy (ΔH) is sufficient to produce a negative ΔG and hence drive protein folding (Citation 1, below).

Free energy change in coupled transformations
Many biochemical changes involve transformations which individually have a positive free energy change, but are made possible by coupling to another reaction with negative free energy change, of greater magnitude:

  A → B , ΔG1 = +x

  C → D , ΔG2 = –y

If y>x and these two reactions are coupled (generally through a complex reaction path on an enzyme) , then we have:

  A + C → B + D , ΔGoverall = –ve

See also Berg et al.

Although one can reject the second explanation in the question as it stands because it ignores the free energy change in the protein folding, perhaps it was intended to mean that the folding of the protein (A → B) should be considered as coupled to the change in the environment of the water (C → D), and that the negative ΔG for the aqueous environment made a greater contribution to the overall ΔG than that for the protein folding.

Is it valid to consider these two systems as coupled? In the original version of my answer I argued against this point of view, but am no longer convinced by my own arguments. The water environment is clearly essential for the hydrophobic effect — the burying of the hydrophobic residues in the centre of the protein away from the water. This is evident if one considers the same protein in a hydrophobic environment such as a cell membrane — it would not fold. In membrane proteins it is hydrophobic residues that are exposed to the lipid bilayer and it is their interiors that sometimes have hydrophilic channels.

So in this coupled system, what is the determinant of the negative free energy change? Minikel (Citation 2, below) asserts that there is no net enthalpy change for the protein folding, and it is the entropy effect on the ΔG for the aqueous environment that drives the folding. He indicates that this view is supported by differential scanning colorimetry and, although he doesn’t cite references, there is a recent (if rather complex) review of this topic by Christopher M. Johnson.

Citation 1: Assertion of role of ΔH of protein

The following explanation, taken from Essential Biochemistry, treats the protein folding in isolation and asserts that change in enthalpy is sufficient to produce a negative free energy change:

  The folding of a protein also provides an example of the "ΔH" and "–TΔS" terms competing with one another to determine the ΔG of the folding process. As described above, the change in entropy of the protein as it folds is negative, so the "–TΔS" term is positive. However, in addition to entropic effects there are enthalpic contributions to protein folding. These include hydrogen bonding, ionic salt bridges, and Van der Waals forces. An input of thermal (heat) energy is required to disrupt these forces, and conversely when these interactions form during protein folding they release heat (the ΔH is negative). When all of these entropic and enthalpic contributions are weighed, the enthalpy term wins out over the entropy term. Therefore the free energy of protein folding is negative, and protein folding is a spontaneous process.

Citation 2: Rebuttal of role of ΔH of protein and assertion of role of water

The following explanation, taken from on-line lecture notes of  of Eric V. Minikel of Harvard University, rebutting the point of view above:

  An incorrect and simplistic view of protein folding is as follows. An unfolded protein has high configurational entropy but also high enthalpy because it has few stabilizing interactions. A folded protein has far less entropy, but also far less enthalpy. There is a tradeoff between H and S here. Note that because ΔG = ΔH - TΔS, increased temperature weights the S term more heavily, meaning that higher temperature favors unfolding.

  That entire explanation only considers the energy of the protein and
  not that of the solvent. In fact, hydrophobic domains of a protein
  constrain the possible configurations of surrounding water (see
  explanation above), and so their burial upon folding increases the
  water’s entropy. Moreover, it turns out that the hydrogen bonding of
  polar residues and the backbone is satisfied both in an unfolded state
  (by water) and in a folded state (by each other). Therefore enthalpy
  is “zero sum,” and protein folding is driven almost entirely by
  entropy.


Do human somatic cells have 46 chromosomes all the time? As far as I know, a human somatic cell has the cell cycle:

Interphase and Replication (mitosis). In interphase, the cell has 2 growth phases (G1 + G2) and a synthesis one (S phase being in between G1 and G2). After G2 ends, the cell will start entering mitosis.

Until the S phase, the cell has only 23 chromosomes right? And only after the DNA has duplicated the number of chromosomes doubles (to 46).

Please correct me if I am wrong? And will the cell in the G0 phase (after duplication and before G1) have 23 or 46 chromosomes?

Humans have 46 chromosomes, 23 come from the mother and 23 come from the father. I think The easiest way to remember this is to think of the sex chromosomes--if you are male, you have one X chromosome from your mother and one Y chromosome from your father. During S-phase, the cell will make another copy of the X chromosome and the Y chromosome, so you will (technically) have 4 sex chromosomes in the cell before it divides, although you only have 2 UNIQUE sex chromosomes. After division, each daughter cell will have 2 sex chromosomes (one X and one Y). The same holds for all the other chromosomes.

So, to answer your question, yes, in G2 phase, you have double the amount of chromosomes in your cell (46*2 = 92), but you only have 46 UNIQUE chromosomes in your cell.

EDIT: As many people have pointed out, there are examples that do not conform to this rule. For example, both skeletal and liver cells can maintain a second copy of their chromosomes (making them 2n). This, however, is the exception. In my opinion, it's more valuable to know the basic rules that govern chromosomal number.

As an exercise I'd suggest to think about what it means that a cell has '2n' chromosomes? What happens if a germ cell obtains 2n chromosomes and passes that to a viable offspring? Is that offspring now '2n', or do they just have double the number of chromosomes as the parent? When does a duplicated chromosome become an it's own chromosome and not just a "duplicate copy"?


kcat in uncompetitive enzyme inhibition Why doesn't $k_\text{cat}$ change in uncompetitive inhibition, given the fact that uncompetitive inhibition lowers the enzyme–substrate complex efficiency (which is the reason for lowering of $V_\text{max}$ as well)?
Source of information: https://youtu.be/0ZiCqwtFMTs

Short answer
It all depends on how you look at $k_\text{cat}$ and enzyme concentrations

Long answer
The effect of an uncompetitive inhibitor on $k_\text{cat}$ can be interpreted in two ways.
Interpretation 1:
This is followed in the lecture series mentioned in the question.
See the video https://youtu.be/rNBEUGYu034 from 7:37 to 11:01 minutes. The instructor says:
... the turnover number basically describes the ability of that active site to actually transform the substrate molecules into the product molecules per unit time. Now because when the inhibitor is not bound to that particular enzyme-substrate complex, the active site's ability or efficiency to change that substrate to the product doesn't actually change, we see that the $k_\text{cat}$ value in uncompetitive inhibition also doesn't actually change...
Mathematically, $k_\text{cat}=\frac{V_\text{max}}{[\ce{E}]}$ (where $[\ce{E}]$ is the concentration of enzyme, excluding that which has been inactivated by inhibitor). Now, uncompetitive inhibition reduces both $V_\text{max}$ and $[\ce{E}]$ by the same factor. Thus $k_\text{cat}$ remains unchanged.
Interpretation 2:
Some people do things differently. They regard $k_\text{cat}$ as $\frac{V_\text{max}}{[\ce{E}]}$, where $[\ce{E}]$ is the total concentration of enzyme in the mixture (including inactivated forms). In this treatment, the uncompetitive inhibitor reduces $V_\text{max}$ but $[\ce{E}]$ stays the same. Thus $k_\text{cat}$ is reduced.
Qualitatively, the enzyme in the mixture is now a combination of active and inactivated forms, and thus has lower "efficiency" overall, i.e. lower $k_\text{cat}$.


Examples of chromosome fusions One of the best "smoking gun" pieces of evidence of humans' close relation to chimpanzees, gorillas and orangutans is that human chromosome 2 is a fusion of two primate chromosomes, with a double telomere in the middle and a centromere on each side. This fusion, which occurred some time after our MRCA with chimpanzees, was an accident with no evolutionary importance, but it happens to provide extra support for our common ancestry with other African apes. In theory, such fusions could be so commonplace that they can be used to infer much of the family tree of life on their own. I'm sure they're nowhere near that common, but this got me thinking: are there any other examples of species with chromosome fusions (or splittings?) that betray their closest relatives?

You can go to ensembl.org and look up synteny between closely related organisms, like rats and mice.  Below is one example: rat chromsome 1 is made up of all of mouse chromosome 7 and 19, plus parts of 17, 10, and a smidge of 13

https://uswest.ensembl.org/Rattus_norvegicus/Location/Synteny?db=core&r=1%3A126594509-126694509&otherspecies=Mus_musculus


Can you please identify this mosquito-like insect? I've seen these insects before (here in Cambridge, UK) and thought that they were probably mosquitoes, but they don't make the annoying noise that mosquitoes do (they fly similarly, but silently):

I also noticed that they are perhaps slightly larger than mosquitoes (maybe 12mm long) and don't have the long mouth which mosquitoes use to sting you.
Sorry for the poor photos, I don't have a camera with a macro lens anymore, and it's night-time. It's casting a strong shadow as you can see in the second photo.

It is most certainly a fly from Chironomidae, which belongs to the same suborder (Nematocera) as Mosquitoes (Culicidae). They have an overall resemblance to mosquitoes, but lack the large sucking mouthparts, and often have the large feathery antenna that are seen in your pictures. Some species are found in large swarms in early spring (but also later in the summer). Larvae can be found in most freshwater, and are called bloodworms due to red colour (high in hemoglobin, adapted to live in oxygen-poor sediment environments)
I doubt that the exact species can be determined from these pictures though.


Is it possible to produce a tangible mass of DNA/RNA using a PCR reaction? A Polymerase Chain Reaction (PCR) is a method of amplification which enables one to produce many copies of a certain DNA/RNA strand for many applications (as described in the link above).

I have never seen the actual process and the resulting PCR solution, but according to Wikipedia, the volume of the solution is of the micro- to milliliter magnitude.

I was wondering: if this process were allowed to continue on and on, while supplying all necessary nucleotides and other materials, to the magnitude of, say, liters - could we end up with a tangible mass of DNA/RNA? In other words, will we be able to extract from the solution a solid mass of DNA/RNA that is visible to the naked eye? If yes, can we predict the physical characteristics of such mass?

PCR amplifies only DNA not RNA.

A PCR reaction is typically within the  micro liter volume, and can go down to the nano liter volume for qPCR. The maximum volume of a PCR tube is 200 microliters. The maximum volume a 96 well thermocycler can handle per well is usually 100 microliters. So the maximum amount of reagent volume one thermocycler can handle at a time us 9.6ml

I have never seen anybody scale a PCR to mili liter volume, as that would be rather expensive and excessive.

However if some some reason, somebody did do as you say, yes it is possible to obtain visible quantities of DNA. (Removal of impurities would be required first... ie unreacted dNTP, primers) And given that we can obtain visible quantities of DNA by extracting DNA from bacteria or salmon sperm.. I am sure a chemist somewhere would be able predict the physical properties of that DNA mass.


Are homozygous carriers of the CCR5-Δ32 allele fully immune to all known strains of HIV? Or is there documented evidence of even one homozygous carrier contracting HIV and staying infected?

I would say no.
Some HIV strains are X4-tropic and not R5 tropic. That means that the virus uses the CXCR4 coreceptor and not the CCR5 coreceptor for entry into the CD4-positive cell.


Number of spindle fibres during Metaphase? During metaphase, the chromosomes are arranged on the equatorial plate and are attached to spindle fibres. After S phase, can the cell be said to attain the configuration of 4n?

Also, during metaphase, since two spindle fibres (one from say right centriole and other from say left centriole) are attached to one tetrad, so can it be said in a well defined pattern that for a human being, 46*2=92 spindle fibres are formed in order to proceed with mitosis? Also how would the number vary in case of Meiosis I and Meiosis II?

The number of spindle fibres is actually more than total number of kinetochore pairs. The fibres attached to kinetochores are called K-fibres and the others are called polar fibres. I cant surely say that there is exactly one K-fibre per kinetochore but as per its definition and from the microscopic images you can conclude that there is one per kinetochore.

In a normal mitotic metaphase there are 2n kinetochore pairs, and as you rightly calculated, there will be 96 K-fibres.

In meiosis-I there is a tetrad which has 2 kinetochore pairs but the ones in sister chromatids behave as a single unit. So there would be 23 fibres.

The fusion of kinetochores of sister chromatids is relaxed in meiosis-II and again a separation would require 23 fibres.

Please have a look at this article. Molecular biology of Meiosis nicely explained:
http://www.sciencedirect.com/science/article/pii/S0092867403000837

More about K-fibre formation:

http://link.springer.com/article/10.1007/s00412-005-0028-2/fulltext.html


Competition in DNA hybridization to RNA After we separate the two DNA strands, what makes one of the two strands combine with the labelled mRNA strand instead of the old complementary strand?

In this type of experiment the concentration of the mRNA will be greater than the concentration of the starting DNA.

When the DNA strands separate, the DNA and mRNA will be in competition for the complementary strand. Using really high concentrations of mRNA compared to the DNA will give it advantage to recombine with a higher frequency and give a higher ratio of the DNA-mRNA combination.

It is all a question of ratio.


How cotranscription events affect splicing? I want to know how and how often does cootranscription takes place? Can transcription regulators influence splicing during cotranscription?

Co-transcriptional splicing (CTS) is very widespread. Different studies (which are done on different cell types) report different frequencies of CTS. Most of them report a frequency of ~0.8 in different cells except for mouse liver which was reported to have a frequency of 0.45
This is the article that summarizes these different studies.

Can transcription regulators influence splicing during cotranscription?

Yes.. including factors such as nucleosome positions.. this post may be helpful.


How are physiological reversal potentials (or ion concentrations) of neurons measured? Patch clamp electrophysiology experiments typically use an intracellular solution that mimics the ionic concentrations of neuronal cytosol. At the same time, the extracellular solution is meant to mimic cerebrospinal fluid. If these two sets of ion concentrations are similar to their in vivo physiological values, then one might expect a patch-clamped neuron to also have physiological ionic reversal potentials. If, on the other hand, they are dissimilar, then we might expect the behavior of the patched neuron (for example its intrinsic excitability or synaptic currents) to be different from the behavior of the same neuron in vivo. In principle, one would like to use solutions that are as close as possible to physiological for this type of experiment.

My question is: how do we know what these physiological values (concentrations or reversal potentials) really are? It is easy to find these values in a textbook, but I would like to know what original research was performed to determine these values in the first place.

In many patch clamp experiments, the solutions are designed to set the reversal potentials to non-physiological values, or are otherwise constrained by the practicalities of the experiment. Let's consider these issues to be outside the scope of this question.

There are various methods to determine the intracellular ionic concentrations. One method is to register action potentials by the fowling method: inject a Voltage Active dye VAD (something like a -2di Anepp or s similar dye) into the cell or tissue and using an Optic Mapping System register the Action potentials and then determine the intracellular ionic concentrations by Nernst equations.

We could also register Action potentials by "ion-sensitive glass electrodes method" by introducing ion-sensitive glass electrodes directly into the interior of the cells. The problem with these electrodes is that they cannot register very low ionic concentrations especially of Calcium. And so the above method is superior using  VAD.


protein-binding sRNAs I am actually a computational biologist, pardon me if my question description is a bit off-note, my curiosity is driving me on

A bit of background and context:
In bacteria, a regulatory protein termed CsrA binds certain structures in the UTR regions of genes and prevents their translation. These structures are short hairpin-like and all have AGGA nucleotides in the exposed part. There are sRNAs that isolate the protein from its targets, a common feature of these sRNAs is that they have several repetitive hairpins that more or less display AGGA nucleotides in the exposed part. So basically, the sRNAs mimic the structures on the targets of the proteins and that makes them potent competitors for protein binding against the genes actually targeted by the protein. By relying on this mimickry the sRNAs bind CsrA, isolate it from its targets and remove its suppression on gene translation.

My question: Are there any other examples that illustrate similar mechanisms of analogy/mimickry of sRNAs to bind protein?

What I tried
I've skimmed through a lot of literature to identify other similar systems in bacteria where sRNAs have conserved repetitive structures but to no avail. I hope someone with deeper experience directs me to such examples in any living organism, preferably bacteria but I am open to suggestion.
I found CRISPRs but these are  DNA based, I have come across few other cis-acting sRNAs which target mRNAs and aren't protein-binding. So could it be the case that sRNA mimickers aren't very pervasive in bacteria after all ?!

The sRNA mediated regulation in bacteria operates via diverse mechanisms. This case of sRNA competing with a mRNA for a protein is a passive kind of regulation. This might be good for finetuning but may not be very efficient. It is much better to actively regulate a mRNA by direct binding. Also, it will work only if the concerned protein is in limiting concentrations.

I haven't come across any examples of what you are interested in. There may be one similar situation in case of a eukaryotic system. miRNAs can be titrated away by long RNAs that bear multiple binding sites for that miRNA, thus making the miRNAs unavailable for binding to the target mRNA. These long RNAs are called ceRNA (competing endogenous RNA) or miRNA-sponges (this term is mostly used if the RNA is exogenous). However this is not really a protein-RNA interaction even though RISC complex contains proteins.


Amber eye color in Neolithic Africa Given what we know of the genetics of eye color and their historical distribution, is it possible or at least plausible for a person born in the Horn of Africa during the early Neolithic (ca. 9000 BCE), assuming no recent ancestors from outside this area, to have had amber eyes (or in general anything other than brown?) If so, would one or both parents need to have that color as well, and what of siblings?

I know that today there is much less isolation and much more crossing of genetic lines, so that pretty much any combination of skin and eye color is likely possible, but no doubt it was different back then.

There are two possibilities: First, that an individual develops a mutation de novo and is the first to carry it.
When we talk about recessive expressed allels, than both parents need to have a copy of the allel, otherwise it will not show up in the kids. In this case a mixed population of siblings is to be expected (some carrying both recessive allels, some only one).
However, its most likely, that the eye color at this time was brown. As far as I know, there has been no evidence so far from ancient DNA that this has been different.

The oldest DNAfrom Europe, which has been analyzed and which showed a difference for the eye color comes from Spain (La Brana-Arintero site in Valdelugueros) and is about 7.000 years old. See this report about it. This individual is thought to have an "african" type of pigmentation but blue eyes. The original publication is called "Derived immune and ancestral pigmentation alleles in a 7,000-year-old Mesolithic European."

Another paper claims that the blue eye color comes from a mutation which occured in a gene called "OCA2" in the black sea region some 6-10.000 years ago. See here: "Blue eye color in humans may be caused by a perfectly associated founder mutation in a regulatory element located within the HERC2 gene inhibiting OCA2 expression"
.


Why is FAD, rather than NAD+, reduced in the succinate dehydrogenase reaction of the Tricarboxylic Acid Cycle? FADH2 is produced in the conversion of Succinate to Fumarate in the tricarboxylic acid cycle. Why is this so? Why not NADH?

In general, $\ce{NADH}$ and $\ce{FADH2}$ are coenzymes. The structure of the main part of an enzyme determines which coenzyme or which prosthetic group will work with the concerned enzyme. Unlike most other TCA cycle enzymes, Succinic Dehydrogenase involves the participation of $\ce{FAD}$ rather than $\ce{NAD}$ and that is a consequence of its specific structure.

Another possible reason might have to do with the energy gap available. The conversion of succinate to fumarate liberates less free energy as compared to other oxidation reactions. Ususally, the steps which are coupled with NADH reduction have a free energy change of about $\Delta G=-100$ to $-150~ \pu{kcal/mol}$ but the conversion catalysed by succinic dehydrogenase has a free energy change of $ -80~ \pu{kcal/mol}$ (rough figures) and hence releases less energy. It therefore might not be feasible to couple with $\ce{NADH}$ reduction but it would be favourable (thermodynamically) to couple with an easy-to-reduce (since the reduction potential is higher and hence reduction is more favourable) and hence less energetic molecule $\ce{FADH2}$.

Apart from structural and thermodynamic requirement, one last possible reason might be that succinic dehydrogenase is a part of the mitochondrial membrane and involved in the Electron Transport Chain. Here, flavin molecules are excellent electron transporters (in comparison to nicotinamide based reductants) and therefore it might be more profitable to use a flavin based reductant to later facilitate easy electron transport and proton transfer.
Again all these are probable reasons and I dont know for sure.


How to obtain virus samples? I'm trying to observe the behavior of simple viruses in different environments. I'm just looking for simple viruses like the common cold and the flu virus nothing major. Is there a way to obtain them?

First of all, cold and flu viruses are not 'simple viruses', and they are not harmless. They kill tens to hundreds of thousands of people every year.

Secondly, this would depend highly on the risk group that the virus falls in. The NIH sets strict guidelines on who can handle infectious agents. Unfortunately, I can almost guarantee you that no one is going to give you even risk group 1 plant viruses, and they are certainly are not going to give you cold or flu viruses. Risk groups range from 1 to 4. To handle risk group 2 viruses, for example, you are expected to do so in a BSL-2 or higher laboratory, and anyone maintaining stocks of virus is going to do a hefty check of you and your 'facilities' before shipping you anything.

Furthermore, even if you did obtain the virus, you would need to store it or maintain stocks of the virus in tissue culture. Its not like you can just get an eppendorf tube of virus in saline and expect it to survive in your refrigerator at home, and its not like companies are shipping virus willy-nilly to anyone.

That being said, and at the expense of sounding self-righteous, there is really no reason for you to obtain virus particles. You should start by getting a book on virology and reading it. There is plenty of learning material both visual and written out there, and all I will say is if you don't already know how to culture virus or where to obtain it, you shouldnt be doing so, and no one is going to give it to you.

CDC Biosafety in Microbiological and Biomedical Laboratories: http://www.cdc.gov/biosafety/publications/bmbl5/BMBL.pdf

WHO Laboratory Biosafety Manual: http://www.who.int/csr/resources/publications/biosafety/en/Biosafety7.pdf

NIH guidelines recombinant nucleic acids: http://osp.od.nih.gov/sites/defaul/files/NIH_Guidelines.html

I think its great that you are interested, and it sounds like you are interested in histopathological changes caused by virus, so I have included some nice histo pictures below

Syncytia (Herpes Simplex Virus type 1)

Clearer example of syncytia

Characteristic owl-eye (Cytomegalovirus)

Distemper virus inclusion body

Coronavirus particles with 'crown' of surface glycoproteins

Budding HIV virus particles from the plasma membrane

Bacteriophage T4 escape by lysis

Papillomavirus

Rous-sarcoma virus

Tobacco mosaic virus


Can anyone identify this insect from India? Found this bug in Chennai. Curious to know what kind it is. Does it pose any danger?

This is definitely a bug - as indicated by the characteristic body form and the segmented (it should be five) antenna. My guess here is that this is Nezara viridula, also known as the "southern green stink bug" or the "southern green shield bug".

See this image (from here):

Besides being a pest for agriculture, they are harmless and not toxic, although they can spread a stinking substance when threatened, hence their name. You can find more about them here and here.


In a sugar such as a disaccharide are both ends of the sugar known as reducing ends? For example, in maltose (a disaccharide of glucose monomers) are both of the ends either side able to be opened to form an aldehyde group?

No, in dissacharides the reducing end is situated only on one monosaccharide which is having free anomeric carbon. This carbon does not take part in glycosidic bond formation and can form open chain.

Check out:
https://chem.libretexts.org/Courses/Sacramento_City_College/SCC%3A_Chem_309_-_General%2C_Organic_and_Biochemistry_(Bennett)/Text/14%3A_Carbohydrates/14.6%3A_Disaccharides


Why is fructose not glucose the main energy source of sperm? The seminal fluid contains fructose as the main energy source for the sperm and not glucose.

  Why is fructose and not glucose the primary energy source for these
  sperm, since glucose is the preferred energy source for most other
  tissues?

I have been searching this for a while and I got something of an answer, which I am posting below.

There are primarily two advantages of using the polyol pathway and aldose reductase to produce fructose from glucose via sorbitol:-

1) Quoting the book here,

  Seminal fluid contains up to 11 mmol/L (200 mg/dl) of free fructose.
  It is the major energy source for the sperm cells in their
  all-important race for the ovum. The advantage of fructose over
  glucose may be that many bacteria, which compete with the sperm cells
  for the available nutrient, prefer glucose to other energy sources.

Thus, to avoid other competitive bacteria and cells from utilising the energy source of sperm, fructose is used as the energy source since the bacteria prefer glucose.

2)Another reason is that the metabolism of sorbitol into fructose is energetically efficient way (no ATP required) as compared to glycolytic conversion of glucose into fructose(G$\rightarrow$G6P$\rightarrow$F6P$\rightarrow$F). Tapping the polyol pathway is energetically preferred to metabolizing fructose produced during glycolysis.This is only to show the possible evolution of the polyol pathway once the advantage of using fructose as the energy source was established. It does not explain why the fructose was advantageuos but just that if it was advantageous, the semen-producers would develop the currently existing machinery to produce fructose as the exclusive source of energy.

Hence, sperms (seminal secretion) contains fructose as the primary energy source and not glucose.


Why does hair know when it needs to stop to grow I'm still not quite sure if head hair grows endlessly, or if it stops at some point, but that's not the question.

When the hair on my leg grows, it obviously doesn't grow endlessly, but it also stops at some point. I learnt that hair is dead matter, so why does the body know that my hair reached maximum length, and realizes I cut it when I did?

That's an awesome question! Let me help you rephrase, as I don't have a direct answer; why does hair stop growing at certain lengths, and differentially at various locations on the body?

There are three stages to hair growth:

Anagen phase- growth
Catagen phase- transition
Telogen phase- rest
(then falls out!)

You're asking why and how the anagen phase stops, or more concisely, what processes cause anagen phase to cease and proceed to transition to a degenerated rest.

The indirect answer I have for you is this: there doesn't exist a definitive mechanism for how the the telogen phase is induced- that is to say that the process by which the hair-producing follicle "turns off" it's cycle to come to a halt has not yet been fully elucidated in the literature and remains a discovery to be made.

I hope I've helped you understand your targeted question


What happens with the nitrogen in blood in membrane oxygenators? The air we breathe consists of about 80% nitrogen and 20% oxygen. The oxygen gets diffused into the blood and CO2 out of it, the nitrogen does mostly nothing, as there isn't a partial pressure of nitrogen between the air and your blood.

In membrane oxygenators the blood flows arround small tubes which contain pure oxygen. The oxygen diffuses in your blood en the CO2 diffuses in the tubes, basically doing the same thing lungs does. However, since it's pure oxygen that flows through those tubes, the nitrogen in your blood should get diffused into the tubes.

So is this what happens? Does the nitrogen simply diffuse untill there's nothing left? Isn't that then bad for your body if all the nitrogen is out? Or can't nitrogen pass through the membrane the tubes are made of? Or does it differ wether you use 'true' membrane of microporous membrane?

It gets diffused out, like you expected.  Grist (2013) writes about this in relation to "the bends," which has already been mentioned by user1136.  He writes:

Cavitation of blood containing normal oxygen and nitrogen levels by mechanical heart valves after implantation generates bubbles that can be detected in the brain using transcranial Doppler ultrasound (2). These bubbles are mainly nitrogenous. Nitrogen is less soluble in water than oxygen. So during excessive turbulence, temperature changes, or pressure changes, nitrogen is the first gas to come out of the solution. (Ask any knowledgeable diver about the physiology of the bends.) We know these bubbles are mainly nitrogen because when the nitrogen in the patient’s blood is off-gassed by breathing 100% oxygen, the cavitated bubbles go away. In one study, the administration of 100% oxygen by facemask reduced the cavitation generation of GME by 98% (3). [Emphasis added]

Can't say it a lot better than that and the rest of the article.  When people are breathing de-nitrogenated air, it simply results in nitrogen being diffused out of the blood.  So yeah, basically the amount of N2 goes down to 0, at least if they are on it for long enough.
As for it being bad for you, not really, at least not perceptibly: though nitrogen is critical for body function, it's practically useless to the body in the N2 form; it has to be "fixed" to a more reactive form such as ammonia / other nitrogen oxide.

Sources

Grist G. 2013. Oxygen or Nitrogen: Which Is the Lesser of Two Evils? J Extra Corpor Technol 45(1): 61-63.

Sprent JI, Sprent P. 1990. Nitrogen fixing organisms: Pure and applied aspects.


Processing of speech/non-speech sounds in the human brain I have a ""which came first: the chicken or the egg?"-kind of question regarding the processing and understanding of speech / non-speech sounds in the human brain.
I'm wondering whether speech and generic non-speech sound processing in the human brain are somehow related and whether one of the two is used as a "basis" mathematically speaking or a reference to understand the other.

Most people use "His voice/It sounds like .." to describe sounds/human voices, besides, we are able to tune out and block any non-speech acoustic activity surrounding us if we are not in a conversation which suggests that we have a special sensibility for hearing speech (or maybe our language or just our names if someone is calling us).

I've read an article which states that :

  Knowledge of our mother tongue acts as a sort of auditory "template" that influences the way we perceive the sounds of other languages (scientists call this "native listening").

Hearing other languages differently than its native speakers is easy to grasp but is there any research that studies the difference in brain activity when speech / other sounds are heard and whether there is something special about hearing speech in particular.

"I'm wondering whether speech and generic non-speech sound processing in the human brain are somehow related and whether one of the two is used as a "basis" mathematically speaking or a reference to understand the other."
They both have in common acoustic energy - whose rate of change is information in itself. The mathematical basis of choice to compare each against the other, I think, is in how each relate that energy to the brain response - aka the forward model of the stimulus-response relationship.
In auditory studies you often get the (spectro)temporal response function (S/TRF) to estimate an approximate "summary" of this relationship. Note that traditionally, this is done independently, that is, either energy from speech or from other types of sound are separately investigated.
"is there any research that studies the difference in brain activity when speech / other sounds are heard"
There is a history of work contrasting the differential encoding of natural versus artificial sound classes (check out foundational work by Theunissen and colleagues). At these scales (neurons or neuron groups), the differences can be rather stark and happen in birds and mammals alike.
If you are more interested in these coding rules regarding "brain activity" at a larger scale, there are local-field-potential studies (e.g. Gaucher et al. 2012 J Physiol-Paris) that also relate mathematically to the S/TRF. However they are most likely invasive animal studies. Also I don't recall if they contrast speech S/TRFs versus other sound's. If you want something closer to human cognition, probably you might want to look at EEG or MEG studies also.
It turns out that finding similarities can be a bit harder than finding out the differences, maybe because the sounds are so different themselves. The mathematical relationship cannot escape this fact, and may then give distinct S/TRF patterns in return.
In a pre-print that seeks out similarities across stimulus types it is reported that certain information about the acoustic energy changes, in particular temporal onset edges, can be coded by the human auditory cortex, be it from speech, or music, or something else, in a more or less generalizable format across classes, at least qualitatively.  https://www.biorxiv.org/content/early/2017/07/27/168997


What is the human energy consumption by organ? The human brain uses about 25% of the human body's metabolic energy. How are the other 75% spent, in terms of portioning to its various systems?

I thought this could be answered by a simple search, but I can't find the answer after searching very hard. I only got dieting advices.

I am envisioning the best answer to look like

Percent of basal metabolic rate by organ (BC Campus Open Education):

Liver and spleen : 27%
Brain: 19%
Skeletal muscle: 18%
Kidneys: 10%
Heart: 7%
Other tissues (lungs, intestine, skin, bone, fat tissue, glands...): 19%

Basal metabolic rate by 1 kg of specific organ tissue (kcal/kg of organ/day) (Table 5 from American Journal of Clinical Nutrition, 2010):

Heart: 440 kcal/kg
Kidneys: 440 kcal/kg
Brain: 240 kcal/kg
Liver: 200 kcal/kg
Skeletal muscle: 13 kcal/kg
Adipose tissue: 4.5 kcal/kg
Residual tissues (lungs, intestine, skin, bone...): 12 kcal/kg


How compelling is the hypothesis that dinosaurs were killed by toxic plants? A friend of mine has recently told me that dinosaurs were "killed by flowers". I was a bit surprised and so I googled. And I did find a lot of recent articles in popular media on this topic, probably based on this. To me it doesn't sound convincing at all, but I'm an outsider. Does anyone think that there's more to that than just a usual journalistic overhype?

Things in the paper that strike me as suspicious
Associating toxic plant defenses with the Cretaceous

Although there continues to be uncertainty about precisely when plants
first evolved toxic defenses, this period of angiosperm proliferation
would seem to be a strong candidate case. (pg 50)

Against this Gleadow and Moller (2014) discuss Cyanogenic glycosides (CNglcs), a class of organic compounds that can kill overgrazing herbivores from cyanide poisoning,

CNglcs are unusually widespread in the plant kingdom. They are found
in the oldest of terrestrial plants (the ferns) and in gymnosperms and
angiosperms.

Similarly, poisonous terpanoids are found in the Ginkgo; Proanthocyanidins, of which oak or wine tannins are a member, is found also in maritime pines; etc. There doesn't appear to be a strong link between angiosperms and chemical defenses against herbivory in plants.
Claiming that the angiosperm proliferations and extinction of dinosaurs are linked in time

The relative co-occurrence of angiosperm proliferation and the
disappearance of the dinosaurs has not gone completely unnoticed.(pg 50)

The diversification of angiosperms occurred starting about 112 MYa for the Monocots, and 100 MYa for the Eudicots, according to De Bodt, et all (2005). From Figure 1 of that linked paper, we can see that both branches of the Angiosperms were approaching their modern diversity by 90 MYa; a time still 25 million years before the extinction of the dinosaurs. 25 million years ago, our nearest ancestor hadn't diverged from the line that would lead to Old World Monkeys, and was probably arboreal. Evolution can do a lot in such a time. Calling these two events linked in time is suspicious, at best.
Using crocodilians as a test case for taste aversion

Since crocodilians are descendent from the same creatures that gave
rise to dinosaurs, this creates the opportunity to evaluate the
tenability of the proposition that dinosaurs went extinct due to an
inherent inability to learn to avoid eating toxic plants.

Reptilian cladistics are far from settled, but I would suggest that crocodilians diverged from dinosaurs by at least the early Triassic. They are almost certainly more divergent from all dinosaurs than birds. Here is what the authors have to say about birds.

However, in contrast to caimans, birds are in fact capable of forming
learned food aversions. (pg 51)

That seems to really undermine the argument here.


How long to regrow hair? This is one of the questions I wasn't exactly sure where to post. Basically, I want to make an X-Men parody, and for the part of Professor X I need to shave off my hair. Now I have a simple french crop, not really long or anything, but I was wondering if there's an estimate for how long it would take me to regrow my hair. Again, sorry if this is the wrong site, but I just thought "human body", so I guess it fits.

According to https://en.wikipedia.org/wiki/Human_hair_growth:

Scalp hair is known to grow between 0.6cm and 3.36cm per month. The growth rate of scalp hair somewhat depends on age (hair tends to grow more slowly with age), sex, and ethnicity. It was previously thought that Caucasian hair grew more quickly than Asian hair and that the growth rate of women's hair was faster than that of men.
However, more recent research has shown that the growth rate of hair in men and women does not significantly differ and that the hair of Chinese people grew more quickly than the hair of French Caucasians and West and Central Africans.

Depending on your age, follicle-condition, nutrition or possible inhibiting factors it can vary how long it will take until your hair has grown back to the previous length.


Understanding recombination scoring in family pedigrees I am having some problems understanding recombination, and I am not sure what element I am missing here. This figure is an example from my text book. The pedigree belongs to a family with an autosomal dominant disease, typed for a marker with alleles A1-A6.

So, all meioses are phase-known, meaning we know which combination of alleles was inherited from each parent. Apparently this leads us to be able to unambiguously score III1-III5 as non-recombinant (N) and III6 as recombinant (R).

This is were I get lost, I don't understand how it is possible to unambiguously score each individual as N or R. Also, if the disease is dominant, how is it possible that III6 is affected, as both alleles originate from the both unaffected I1 and II2?

EDIT: Blue colour in the pedigree means the person is affected by disease, white symbolizes unaffected individuals. I believe the red stars symbolizes that the person carries the disease gene. That would mean blue corresponds to not carrying the disease gene. If this is the case The red colour of III2 is a fault in the figure.

Ns are not non-recombinant at the genomic level. What you know is that they do not show recombination events at the risk allele locus as subjects carrying the marker A1 show signs of the disease and similarly healthy subject do not carry the marker A1. Hence they are called non-recombinant. On top of that 3rd generation subjects (excepted III6) show combinations of alleles reflecting inheritance of one allele from each parent.

What is very important is that A1 is not the allele, it is the marker for the risk allele. This means that A1 is not directly the allele but a region of DNA close to the allele provoking the disease, sufficiently close to be co-inherited most of the time with the disease allele.

For III6 you actually know that a recombination must have happened as this subject obviously carry the risk allele (shows the disease) yet not the marker associated with it, therefore a recombination event happened between the marker and the disease allele.


Why is 'Grudger' an evolutionary stable strategy? I am currently reading 'The Selfish Gene' by Richard Dawkins, which I am sure many here have read. The topic are evolutionary stable strategies (ESS) regarding cooperation.

I apologise for the long question. If you are already familiar with the topic and Dawkins' model of Cheat, Sucker and Grudger: my question is, how can Grudger be an ESS if it could be invaded both by Suckers (because they have no disadvantage against Grudger) and Cheats (because a Cheat minority is unlikely to meet the same Grudger twice, turning Grudger into Sucker effectively)?

More detailed:

The model

Near the end of chapter 10 (p 185 in my version), Dawkins uses a model of birds who clean each other of parasites, therefore helping in survival (as cleaning themselves they cannot reach every spot of their body). He defines three different behaviours for the model:

Sucker - birds who indiscriminately help and clean other birds
Cheat - birds who let others help them but never do so themselves
Grudger - birds who help others and remember who they helped. If the same bird does not help them later (reciprocate), they will not help that bird again.

Claim: Cheat and Grudger are ESS

He claims that both Cheat and Grudger in themselves are ESS - that is, if all birds behave this way, none of the other behaviours can develop because they will be immediately penalised by lower chances of reproducing.

The part that makes sense: Suckers is not an ESS, Cheat is

Sucker is of course not an ESS. If all birds were Suckers, any Cheat that developed would have a huge reproductive advantage and Cheat genes would overtake the population.

Being an ESS makes sense for Cheat. If all birds cheat, nobody will ever be helping each other. A minority of Suckers would be spending all their time helping and not getting anything in return, Cheats have the advantage and Suckers die out again. Grudger would be unlikely to meet a Cheat who they helped before again, so they too will spend all their time helping and die out again.

The part that confuses: Grudger is an ESS?

But Dawkins also claims that Grudger is an ESS, and he seems very confident in that. Now I don't consider myself enough of a smartypants to claim that he's wrong, but I don't understand how Grudger can be an ESS. If all birds behave in this way, and for any reason some Sucker developed - the Sucker would have no disadvantage. All birds would still always be helping each other, so nothing would stop the Suckers from propagating equally well as the Grudgers, invading the gene pool. That's already the ESS broken, but even further, the presence of Suckers would mean that if Cheats came up, they would have a realistic chance of surviving - Grudgers would shun them after having helped once, but if the number of Suckers is large enough, Cheats will have an advantage.

Moreover, back to the initial setting of Grudgers only - if a Cheat developed, he would be unlikely to meet the same Grudger twice, receiving the benefit all the time but never paying the cost. He would have an advantage and spread Cheat genes.

The problem

I'm not familiar enough with how these kinds of models are calculated in order to state chances that Cheats will take over completely, but however I think of it Grudger does not seem to be an ESS to me.

Does anyone have an explanation why Dawkins is so sure that it is? Seeing as in nature we do see patterns like Sucker and Grudger all the time, I must be missing something important here.

Unfortunately it is not necessary to invoke group selection to answer this question.  This is one of the reasons that Dawkins likes this discussion so much - he does not believe in group selection and so the discussion in SG does not invoke group selection.  ESSs are described in the book as the product of direct competition or interaction between genes.

ESSs in this case, can be described in terms of game theory.  In the famous Prisoner's Dilemma experiment, Grudger is similar to tit for tat, which 'won' the competition in the original Axelrod contest.

To see how this works you make a simple win/loss game matrix:

     G        NG
G    win 1    win 3
NG   lose 3   lose 1

if you are groomed you win 1, if you are groomed, but you don't have to groom - even better win 3 (say)
If you groom but are not groomed, lose 3
If neither of you are groomed, you both lose 1

one might argue the exact proportions, but the point is that getting some thing for nothing is better than reciprocating, and getting nothing for your efforts and time are a loss, because you could have been getting groomed by someone else. As you can see cheaters end up in the top row all the time.  grudgers end up along the diagonal, and once in a while in the lower left, Suckers get stuck in the lower left a lot whenever there is a cheater around.

now run this encounter over and over.  A behavior which scores negative the more times you run is not stable - they are going to disappear from the population, at least if this disadvantage is real

It has more than one stable outcomes in populations, a population that is full of Grudgers will all groom each other as before you know everyone, you assume they will reciprocate.  Everyone wins!

Any invading Cheaters will quickly be at a disadvantage, in that they will not be groomed more than N times where N is the number of grudgers in the community.  Note that there is an equilibrium here - the Cheaters may exist in a small number - when N is large enough for a cheater to get enough grooming to make a 'living'.

Suckers can also exist within a population of grudgers, but a population of Suckers where Cheaters show up are quickly sucked dry by the cheaters over several generations where you tally up 'points' and give more, healthier offspring to high scorers.  They are not ESS stable.

Cheaters are also stable - nobody ever wins, but they don't lose big either and any invading grudgers can't get groomed.


Plant with purple/white/yellow flower This plant popped up as a volunteer in a flower box in Winnipeg, Manitoba.
It is roughly 6-inches tall by 6-inches wide.
What is it?

The plant is Convolvulus tricolor, the dwarf morning-glory. It belongs to the family Convolvulaceae.Blue, white, red and pink flowering cultivars of this plant are available$^1$. It is a annual/perennial growing to 0.3 m (1ft) by 0.2 m (0ft 8in) at a medium rate$^2$.

Image source
References:

Plantasm

PFAF database


What roles do circular connection structures play in the brain? Most neural network simulations are strictly linear, one reason being they don't want to deal with circular connections (and infinite feedback loops if you dont have the right mechanisms). You can deal with them at the cost of some efficiency, but I'm curious about whether in the real brain, circular connections play an important role, or are they really not necessary?

To be clear, I mean any structure where you have a Neuron A, Neuron B, and Neuron C (or a thousand more) and the structure is similar to A > B > C > A or generally at some point Neuron A ends up having a path where its own output can lead back to itself.

What roles do circular connections play in the brain? Or more simply: Are they useful and what are a few reasons why?

'Circular connections', as you refer to them, are super common in the nervous system. This motif usually referred to as feedback connections, and serves a variety of roles.

Connectivity studies can be broadly grouped in to those that look at brain areas, and those that look at individual neurons (usually within a single brain area).

My background is more the latter, so that's what I'll focus on.

Firstly, your question misses an important distinction: inhibitory neurons. So if neuron C was inhibitory, we would have a negative feedback loop, a classical circuit that can be used to produce a homeostatic like signal, keeping a system within certain bounds; a delayed feedback loop can also act as a 'signal terminator', allowing an action to be stopped once it reaches a certain threshold. Lastly, under some circumstance, feedback loops can produce oscillations, which are applicable to a number of tasks.

But more generally, recurrent connectivity is hugely important in the cortex. The majority of inputs to neurons come from neighbouring excitatory neurons (see https://www.ncbi.nlm.nih.gov/pubmed/7638624), and if A connects to B then B is more likely to connect to A than by chance (see http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1054880&tool=pmcentrez&rendertype=abstract for a really nice study on this).

So why? For a variety of reasons. Networks with feedback mechanisms can do more, is the basic answer; from negative feedback for homeostasis, to persistent network states. My personal feeling is that too much of computational neuroscience models a network as an operator - it takes an image, say, and outputs what it thinks the image is. And whilst that is important, it's not what the brain is. We need to maintain a constant internal model of the world around us, rather than going 'that thing is a cat. That thing is a burger'. Perhaps recurrent activity maintains the cortex in a certain state - knowing that the cat is there - and inputs serve to move the state so that we can update our internal models when the sensory environment changes.


Can skin become denser? I heard that after injury or repeated damage bone becomes denser, can skin become denser as well?

The structure of skin (epidermis) can change with damage, when the skin is broken the body repairs this partly by recruiting cells called fibroblasts. These fibroblasts lay down collagen fibres to repair the skin. These fibres a normal component of skin are not as neatly arranged as the original fibres and may also higher in number leading to 'denser' skin. This is essentially what a scar is. In some cases the above process can go awry forming what is known as keloid scars.

The other thing that can happen with repeated pressure exposure the skin can become callous, this is when there is thickening of the outer layer formed of cells called keratinocytes increase in number due to recurrent damage. These form typically on pressure points such as balls of feet.


Can plants absorb organic compounds? Plants are autotrophs, meaning that they grow by building organic matter out of inorganic compounds (and energy).
Is it then also true that plants are generally not capable of absorbing organic compounds? There are certainly some plants that can do it, e.g. carnivorous plants absorbing amino acids of their (dissolved) prey. But what about, say, the common sunflower on my balcony?

Yes plants can absorb organic compounds..For example plants can absorb citric acid

Due to citric acid’s ability to chelate metals and be absorbed by plants, it is hypothe-sized that exposure to it will increase the ability of wheat-grass  to  absorb  macro-  and  micro-nutrients,  as  well  as  heavy metals, from soil.

Citric acid chelates absorption
Also plants have the ability to absorb and release sugars.

Plant roots are able to absorb sugars from the rhizosphere but also release sugars and other metabolites that are critical for growth and environmental signaling. Reabsorption of released sugar molecules could help reduce the loss of photosynthetically fixed carbon through the roots

Monosacharid absorption activity
I'm sure there are other examples, feel free to edit the answer.


Time taken for species to become endemic Is it known how long species take to become endemic? I know from examples such as Canada which have no endemics following the end of glaciation that the process must take at least 10 thousand years, but this merely demonstrates endemism must take a longer time. Has any technique been developed that provides some measure of the time needed for species to become endemic?

I am especially interested in the rate of endemism on a small and extremely isolated island such as St Helena.

From wikipedia > endemism:

  Endemism is the ecological state of a species being unique to a defined geographic location, such as an island, nation, country or other defined zone, or habitat type.

There is therefore no time component to it. If a species is found only in Canada, then it is endemic to Canada. If it is found only in your garden, then it is endemic to your garden. No matter the duration in which the species has been found in this specific location.

That being said, in conservation biology, it is common to oppose endemic species with invasive species. An invasive species

Wikipedia > invasive species

  An invasive species is a species that is not native to a specific location (an introduced species), and that has a tendency to spread to a degree believed to cause damage to the environment, human economy or human health

As the linked wikipedia page explains the concept of invasive species (or if you prefer the concept of non-endemism) is open to a lot of critics and is in no way well defined. There is no time limit under which we would stop considering an invasive species as invasive. It is rather the ecological impact of this species that will people to call it invasive or endemic based on purely subjective notions.


What kind of owl does this moth look like? I found this moth and I noticed that it looked like an owl to me and remembered something about how some moths camouflages look like predictors?  What kind of moth this is and what owl does this moth resemble? Would this moth be a newer species than other moths because it came after the owl? The wing span is 5.5 inches across. The eyes of the wing are transparent allowing light to pass through like reflecting eyes.

North American Great Horned Owl

First of all what a nice foto!

I think this is Antheraea polyphemus. According to Wikipedia, the moth has an average of 15 cm (6 in).

The purplish eyespots on hind wings give its name - from the Greek myth of the Cyclops Polyphemus.

And about the defence strategy it's quite interesting. As a green caterpillar, it is camouflaged by its color. However, if it's noticed then it starts to do pose like Sfinx to look less like a caterpillar, if it's still attacked by threat then it is started to make a clicking noise with its mandibles - sometimes as a prelude to or accompanied by defensive regurgitation of distasteful fluids.

When threatened, adult Polyphemus flip the front wings forward and also often flap the wings exposing the large hind wing eyespots - possibly to startle potential predators. The eyespots are possibly to protect an adult from Blue Jay.

The pattern on the hind wings of the polyphemus moth resembles that on the head of the great horned owl (Bubo virginianus).


Where does female ejaculate actually originate from? It's common knowledge that it's released via the urethra, but where does it originate? If it doesn't come from a part of the clitoris, then why is the clitoral glans called the clitoral glans? How does it travel from the originating spot to the urethra?

According to this article female ejaculate is produced by the Skene glands.


Do ant pheromones indicate the direction to go? I know that ants communicate with pheromones but I am wondering if these pheromones can indicate in which direction to go. For example the ants leave pheromones to indicate a food source and when they find food they eventually create a "highway" of ants running to the food.

If I disturb the ants while they're going to the food source in such way that they don't know anymore in which direction is the food will they choose a direction randomly (nest or food) or will the pheromones also indicate in which way to go to get the food?

@shigeta is correct.  Trail disruption is actually a method of controlling ant populations.

For an example, see http://www.ncbi.nlm.nih.gov/pubmed/20077128


What are some possible causes that might explain why the global temperature has remained relatively constant in the last decade? First - I do not know if this is the best site to pose this question.  However, stack exchange does not appear to have an ecology sub-site. That said, this appears to be the most appropriate place post this question.

Consider this chart:

The chart was retrieved from here here.

I am curious as to whether anyone has any thoughts regarding this trend - note, however, that this is one chart among several that I came across on reputable site. All seem to depict this observed "capping" effect between roughly 2000 and 2010+. Unfortunately, I don't have much to offer right now since I am still looking into it.

Any input is appreciated.

Not my field but I have a couple of thoughts:

According to your link, the blue line represents the change in the trend and the red bars are the temperatures. These have not remained that stable, it is the bar that gives that illusion:

A much more important point are the grey bars extending above and below each year's value. This is the range of uncertainty, the actual values could be anywhere within the range of those bars. Notice how the uncertainty decreases the closer you get to the current date.

I think a lot of the stability you observe is probably due to the line hiding the detail and the far lower precision of the older measurements.


Parameters of Variant calling analysis What is the good or stringent parameter for variant calling?
At present using the DP > 10 and Q > 30 for Variant calling. Is it ok?

We will be needing some additional information to answer your question more completely:

What sequencing platform are you using? Illumina HiSeq/MySeq; Ion proton

What type of sequencing (as noted by @CMosychuk): Exome or Whole Genome?

What type of variant caller (as noted by @CMosychuk): Unified Genotyper; Haplotype Caller; TVC

The QUAL metric is heavily dictated my sequencing depth, so if you use 30 (phred-scaled), that would be an accuracy of 99.9%.

The typical QUAL metric used by most sequencing studies is 20 so using 30 may cause accumulation of false negatives. But again, depends on the type of sequencing and platform used.


The Fish-Tetrapod Transition, evolution of the "elbow" in Stem Tetrapods The Acanthostega and Tulerpeton limbs seem to form "elbows" in an axis perpendicular to the flexor and extensor plane of the fin. They seem to "flex" their "elbow" forwards, pre-axially. And, I assume, keep it permanently "flexed", a bit as if their humerus, ulna, and radius has been one single "V-shaped" bone. This adaptation positions the primordial hand forwards. Is this pretty much correct? Why I wonder, I always understood elbows as bending in the flexor/extensor plane, but in the first terrestrial life it seems to be in the pre-axial/post-axial plane. That probably has implications for how limbs continued to evolve, and for the embryogenesis of limbs in mammals like humans. I found that interesting.

The current research doesn't venture many details on the elbows/radius/ulna and locomotion biomechanics.
For the moment they just say the elbow was "slightly flexible" and that the bones were transitioning towards a round shape.
You can research deep into the resources and will perhaps find more.
Here are a resource which give context, found via "locomotor performance in stem tetrapods"
https://www.researchgate.net/publication/236460049_Historical_Perspectives_on_the_Evolution_of_Tetrapodomorph_Movement
There's also a 3D study of the legs here: https://www.researchgate.net/publication/227857349_Three-dimensional_limb_joint_mobility_in_the_early_tetrapod_Ichthyostega
https://sandykawano.weebly.com/locomotor-biomechanics-for-moving-onto-land.html


Is the xylem like a tissue paper? I am a 5th grader learning about the plant transport mechanics and I learnt that the xylem is made up of dead cells.So if water travels up the xylem and water travels only 1 way, is it like how water travel up a tissue paper?

I'm in year 5 too; and (with a bit of help of my dad) I have some bits of answers (my challenge of the day).

A paper tissue is principally made of cellulose. And cellulose is a polar molecule. And so is water. So, the paper will easily absorb water.
See these short clips [1] for water polarity and here for cellulose [2].

In plants, xylem vessels are also made of cellulose and that helps the small molecules of water to stick to the vessels walls.
Think of it as a lot of tiny drinking straws made of wood.

There are at least two reasons why water manages to 'climb up' from the roots to the leaves through the xylem.

During the day, when the sunlight is available, water will be consumed by the leaves during photosynthesis [3]. For each molecule of glucose, 6 molecules of water are needed.
So the water already present from the xylem in the leaves needs to be replenished by water (sap) from the twigs, which is replenished by the water from the xylem in the branches,... And so on, till the water is pulled from the roots.[4]
Remember little molecules of water cling to each other because they are polar.  This is why they tend to pull each other up, as they are consumed in the leaves [1'].

And this is why it is important that both the water molecule and the cellulose molecule are polar.  If H2O would be like CO2, there would be no vascular plants as we know them.

But there is no sun, so no photosynthesis, during the night.
Then the stomata, which are holes used by vascular plants to "breath" (
transpiration), are usually closed.
There is also another reason why water moves up the xylem. Here it is.
Roots not only 'pump' water, their role is also to capture nutrients.
These nutrients are like salts, not table salt, more like ions (potassium, phosphorus, zinc, mangnese, etc) which are needed by the plant cells.
So the water is a bit more 'salty' inside the roots.  Water outside the roots tends to try to diffuse into the roots in order to compensate the relative saltiness [5].
This in turn pushes the water from the root below the ground towards the branches.[4]

What is remarkable is that the whole cycle of water is passive, the plant does not spend energy to move the water 'upwards' to the leaves.

Here are a few sources which I can recommend and from which I learned most of these things. Crash course biology.
They talk fast but it's quite funny.

[1] water polarity: 'Water - Liquid Awesome: Crash Course Biology #2'
https://youtu.be/HVT3Y3_gHGg?list=PL3EED4C1D684D3ADF&t=171
[1'] To picture molecules of water pulling one another up the xylem... well:
https://youtu.be/IlmgFYmbAUg?t=154 (Monkey chain in Madagascar 3)

[2] cellulose: ' Plant Cells: Crash Course Biology #6'
https://youtu.be/9UvlqAVCoqY?list=PL3EED4C1D684D3ADF&t=255

[3] Photosynthesis ' Photosynthesis: Crash Course Biology #8'
https://youtu.be/sQK3Yr4Sc_k?list=PL3EED4C1D684D3ADF&t=75

[4] For a simple presentation of xylem, I use Simple English in
https://simple.wikipedia.org/wiki/Xylem_vessel
and 'Vascular Plants = Winning! - Crash Course Biology #37'
https://youtu.be/h9oDTMXM7M8?t=373

[5] Osmosis (water compensating solutes) "In Da Club - Membranes & Transport: Crash Course Biology #5"
https://youtu.be/dPKvHrD1eS4?list=PL3EED4C1D684D3ADF&t=148

Ian (and dad <= all errors and approximations are his :) ).


Which Receptors are Involved in the antidepressant effects of SSRIs? From what I've read the major receptor subtypes involved in the antidepressant effects of SSRIs are:

5-HT1A
5-HT2C
5-HT3
5-HT6

Please cite journal articles to back up your claims, I don't want any piece of information to be unverifiable.

You're right, those are all important! There are several good reviews on the mechanism of action antidepressants. I like Molecular Pharmacology, by Nestler, or even Principles of Neural Science, by Kandel. I think a textbook is going to be your best bet, in terms of getting up to speed here, as this is largely an already-researched issue, but here are some good review articles as well:

Bonhomme et al., 1988
Charney et al., 1981
Norbert & Esposito, 1998
Spencer, 2012

If you have a more specific question, let me know!


What kind of weird little insect is this? What kind of insect is this?

I found it in my work room.

I live in the city of São José dos Campos, São Paulo, Brazil

This is probably a nymphal stage of a stink bug (aka shield bug).

Based on the roundness of your specimens, I'd suspect that they represent possibly the 1st or 2nd instar development stage.

I am unsure of the species currently, though I suspect this is an image of the adult (wrongfully labeled as a "bed bug" at its source):

 Source: Shutterstock

I will dig into the Brazilian fauna to see if I can get you a species...


Strange Exoskeleton Found in Maine: What is It? There is a gall like object or exoskeleton attached to a plant stem I have found. At first I thought it was a cicada but it is not. The object cannot be identified by me. Attached are some pictures of it. Could you identify it?

It seems to me the ootheca of a mantis before larvae eclosion. You can read more about it here.

.jpg


How does valerian make you calmer? Why do Valerian pills make us calmer? What is the mechanism behind it?

I understand how artificial tranquilizers work. Do valerian pill have similar chemical components?

Short answer
Valerian preparations contain many compounds, but it is not known which may be responsible for its sedative effects. It is likely that there is no single active compound and that valerian's effects result from multiple constituents acting independently or synergistically (source: NIH). Overall, I think it is safe to say that valerian's sedative properties are related to its GABAergic properties (Yuan, 2004).

Background
The constituents of the volatile oil obtained from the rhizomes (underground stems), and stolons (horizontal stems) of Valeriana spec are variable due to  the variability in genetic make-up and environmental factors impinging on the batch of plants used (source: NIH).

The major constituents include the monoterpene bornyl acetate and a variety of sesquiterpenes including valerenic acid.

Some of the sesquiterpenes have been shown to have a direct action on the amygdala, which is a brain structure in the limbic system. The amygdala is responsible for feelings of fear and anxiety. Valerenic acid has been shown to inhibit the breakdown of GABA in the brain, resulting in sedation. GABA is the principal inhibitory neurotransmitter in the nervous system.

The non-volatile monoterpenes known as valepotriates possess sedative activity, but their mode of action is not clearly known. The valepotriates themselves act as prodrugs, and are transformed into homobaldrinal which has sedative properties.

Extracts of valerian roots contain substantial amounts of GABA which could directly cause sedation. However, whether GABA reaches the central nervous system is debated.

Another compound present in extracts is a lignan, hydroxypinoresinol, and it binds to benzodiazepine receptors, which are GABAA receptors and the target of benzodiazepines, i.e. tranquilizers and sedatives (Houghton, 1999).

References
- Houghton, J Pharm Pharmacol (1999); 51: 505-12
- Yuan et al., Anesth Analg (2004); 98(2): 353-8


Under what circumstances will a human neuron divide? I read somewhere that a mature neuron loses its ability to divide, except for very specific situations. I was unable to find the description of those situations. What are they?

(I'm sorry I'm not saying where I read that, but I simply can't find it.)

Mature, differentiated neurons do not divide (undergo mitosis), but apparently there is a small population of self-renewing neural stem cells in adults that can produce new neurons. Neurogenesis predominantly occurs in the subventricular and subgranular zones of the brain.

Peripheral nerves can regenerate along its axon as long as the endoneurial tube and the Schwann cells are intact. Here's a picture of a neuron regenerating.


Alternate genetic codes in newly sequenced organisms Variations of the standard genetic code are pretty rare, but as the cost of high-throughput genome sequencing continues to drop, there is a greater possibility of discovering additional exceptions. That being said, there is a clear emphasis in genome projects on nucleotide (genome and transcriptome) sequencing, with much less (if any) effort put into proteomics work (correct me if I'm wrong there).

Let's assume we're sequencing the genome of a new organism and we're focusing completely on genome and transcriptome sequencing--no proteomics. Let's also assume this organism has slight variations to the standard genetic code. Would it be possible to annotate this genome (for protein-coding genes) completely incorrectly since the gene prediction software does not take into account these variations, or would it be pretty obvious? What would you expect to see in this case?

If the organism uses an alternative code, the predicted protein sequences would always include the same type of amino acid substitution errors. This pattern should become apparent when you compare the proteins to other organisms.
In reality, the most common alternative code uses UGA for tryptophan instead of the usual stop. If you make the mistake of using the standard code for these genomes, the predicted genes would become highly fragmented so it is almost impossible not to notice.


What is this beetle and what are the strange antennae for? I found this wonderful creature in my yard (I live in the south of France) last night:

It was about 2-3cm long, with a hard carapace and wings. It also made loud hissing noises when agitated. I am curious as to what species this is, I'm quite surprised I'd never seen it before cause the beastie is quite large and last night I found it because of the noise it was making. It was upside down and hissing like a kettle.

More than the specific species' name, I am curious as to what the large antennae are for. Does their shape and size somehow increase the beetle's sensitivity to whatever stimuli these are atuned to?

Alan Boyd's comment below helped me along a bit. I seem to have found a close relative of the ten-lined June beetle (Polyphylla decemlineata) pictured below (image source)

From the pattern on the elytra (hard upper wings), it looks like you might have a beautiful male Polyphylla fullo. Compare your photos with the P. fullo in this illustration, or photos on the Wikipedia page.

edit to fully respond to the comments:

I suspect you're right that the antennae plates in your picture are just tightly closed up, giving a different appearance. Here's a photo I took of a related species where you can see both appearances of the antennae.

And I think that Alan Boyd is correct about the antennae being used as chemoreceptors to locate females. The wikipedia page on the Ten-Lined June Bug also mentions both of these points.


What is the location of the Hypoglossal nerve? I kind of know where the hypoglossal nerve is located when I look at the diagram, but I'd like to know how far is the nerve from the skin and where is the closest area to the skin before and right after it's branching?

Is there any video or schema showing the location of the Hypoglossal nerve relative to skin and not the skeleton?

From this pic. I can't really tell the closest location of being able to detect the nerve near the skin.

The following image of a cadaver shows the hypoglossal highlighted:

 Source: StudyBlue

You can see the flap of skin/muscle that has been removed to get an understanding of the thickness of tissues separating the nerve from outside the body.

Additionally, here is an image showing a person receiving an operation. You can see the relative depth of the nerve fairly well:

 Source: Cambridge University Press


Conjugated deoxyribonucleotides I'm currently learning about using PCR techniques to make fluorescently labelled DNA probes, and the textbook mentions "conjugated deoxyribonucleotides"

Can someone explain what these are? Nothing too in-depth and detailed. Just a decent description/explanation so I can get somewhat of an understanding.

To "conjugate" means to join or couple something together. Deoxyribonucleotides are the "letters" of DNA - A, T, C, and G. In biology/biochemistry, when you conjugate something you chemically modify it by adding something to it. Given the context of your question, the conjugated deoxyribonucleotides are fluorescently-labeled — a fluorescent dye has been covalently attached to it.


Is there a mechanism by which mammals lose interest in a partner after mating? I'm reading the book called "Cupid's poison arrow", which revolves around a rather simple assumption: most mammals, including humans have a genetic program that is responsible for ever increasing dissatisfaction with a mate after intercourse with orgasm.

The book proceeds to give a number of examples, here's what I remember:

Coolidge effect, where libido is revived upon exposure to a novel, receptive partner.
Male rate copulating on average 8 times with a receptive female before losing interest
Sexual satiety setting off a 14-15 day hormonal cycle where [a male rat] would lose all interest in a partner

The book contains a large amount of anecdotal evidence of humans experiencing negative outlook on their partner after orgasmic intercourse, with more intense intercourse producing more intense dissatisfaction.

The author proceeds to formulate a hypothesis that humans and other mammals have a genetic program that fosters sepratation between mates and seeking of a novel mate as a mechanism to promote more genetic diversity in offspring (as opposed to monogamy)

Is there a scientific basis for such claims -  do mammals have a mechanism that draws them apart after intercourse or sexual satiety is achieved?

Well from what I have been taught, and have studied, is that multiple partners for men does not equal more of their DNA persisting, because they are needed to provide for the offspring. So if they impregnate 10 different females and don't stick around, that really doesn't help them pass on their DNA because most would die. So having a family with the same partner does ensure more offspring survive. Humans are picky selecting their mate for the reason of wanting to get the best genetic combination possible to have the most offspring survive. A human child takes a lot of effort to raise to reproductive age, we aren't like some animals who are off and running. So our bodies invest a lot in making sure that happens, being flooded with bonding hormones after sex, women's bodies changing to nurse (and then not being able to hunt/gather/protect themselves) etc. So there is a hormonal cascade that happens to ensure you are going to stick around after mating.

I am really talking about our ancestors, but obviously some of their behavior has carried to us.

However having multiple partners DOES benefit the female. Males can't tell they are the father to a child until much later, after they have supported the pregnant mother, etc. Females can then have their DNA pass on in multiple combinations to ensure survival of more children. Pubic hair in women is thought to have evolved to hide any physical evidence of a recent mating with different males outside of the family. And if current statistics say anything - just as many women cheat on their spouse as men. And when cheated on women want to go after the other woman, because that's our competition and they may be taking the mate we worked so hard to get.

Humans are hard to compare to other animals because we can manipulate so much of what happens to us. But if the ultimate goal is to ensure the passing of DNA then that hypothesis (to me) doesn't fit with humans.

But then again, I am a woman and therefore could be biased haha. If you read an animal behavior textbook it will go into this in in detail, and state it much better than I can, and with supporting scientific evidence. As a biologist the term "anecdotal evidence" makes me cringe :)


Ways to monitor enzyme kinetics with very fast time resolution? I'm interested in any way to do time-resolved study of enzyme kinetics.  I am studying some physical variables that may affect kinetics, but I want to study how quickly they take effect, and how long the effect lasts.  The time scale of interest is milliseconds or less, so the typical spectrophotometric methods (which usually look at absorption change over fairly long times on the order of minutes) won't work.

Luciferase activity can be monitored by tracking the light emitted, and this has potentially very high time resolution as the time between reaction and light emission is on the order of microseconds.  However luciferase is a bit of an odd model, as it is not part of normal metabolism or signalling in most organisms.

Is there a way to track enzyme kinetics of any other enzymes with a similarly fast time resolution?

EDIT Just discovered one name for what I'm looking for: "transient kinetics".

Some ATPases can work with MANT-ATP or similar fluorescent ATP analogs that change their fluorescence properties upon protein binding as well as hydrolysis of their phosphate group. This has been used frequently (see here or here) to study enzyme kinetics on fast timescales.


Do white Australians have a distinct look? Background
I've heard from many people working in tourism or similar industries that, white Australians can be recognized as Australian solely by their facial features. Being Australian myself I've heard variants of the claim quite often and lean towards the claim being at least, a possibility.
While it's true that people tend to see patterns when there are none or incorrectly attribute, why they correctly recognize something. I don't necessarily think that is the case here. Australians don't tend to dress in a distinguishing way when overseas, and people have recognized them before hearing them speak. Given the extent to which I hear this claim made, I can't completely dismiss it.
Examples of claims
This article from an Australian newspaper in 1943 interviews an artist who when asked if Australians have a racial type, says he thinks that it was generally possible to distinguish an Australian [from other Caucasians] due to differences in the nose and differences in the jaw.
Googling for terms like "look Australian" returns examples of the claims strewn around the internet, such as this forum thread and this blog.
Also of note is the art project to show the average face of Sydney, of which the following quote is relevant:

In many cases, however, the likeness is so strong that it's possible
to guess the nationality just by taking a cursory glance at the photo.

Reasons for thinking it may be possible
I'm fairly ignorant when it comes to biology, although there are a few reasons I think this might be possible. The (relatively) small gene pool from when Australia was colonized could have led to features from a small group being inherited in a large population.
There seems to be some evidence that environment can play a large role in influencing genetics more so than ethnicity. I can't find the paper investigating that, although will update this question if I am able to.
It seems possible to me that facial features belonging to the original colonists could have spread through subsequent populations, becoming a defining characteristic for some Australians.
I don't think most immigrants are relevant to this question as they will not have inherited distinguishing features (if they exist), nor will they or their parents/grandparents have been able to be influenced by the environment - if that is even a relevant factor.
So...
Do a significant number of white Australians, excluding 1st or 2nd generation immigrants, have distinct facial features unique or generally only found in Australia?
Is it reasonable that some white Australians could be recognized as Australian, going only by facial features?

Yes, it is possible (on some average basis, i.e. with chance better than random).

Take a look at average women faces from 41 different countries (AFAIK created with Face Research software; sadly no picture for Australia). Clearly, even from small and nearby European countries you can spot differences (which work on the average). I guess the case of Austriala vs other countries isn't an exception. Similar face averages are also on the project Face of Tomorrow.

However, when dealing with a single subjects it it may be not a reliable method to tell of his/her nationality or country of origin, as:

even within an relatively isolated group there is variance in genotype and phenotype,
people do move (especially now) and do mix (so unless you are comparing isolated islands you should't expect to have homogenous genotype).

Moreover, when identifying a person we may (even subconsciously) look at different features (including clothes, accent, behaviour, context, ...).


Colorado potato beetle diet The Colorado potato beetle is best known for being a potato pest. However, I've just learned that it originates from Northern America and the potato itself comes from South America.

So the question is, what did potato beetles eat before they were introduced to potatoes?

They ate other Solanaceae species.  This University of Florida info page gives an excellent overview of the species, including its hosts (emphasis mine):

  Potatoes are the preferred host for the Colorado potato beetle, but it may feed and survive on a number of other plants in the family Solanacae, including belladonna, common nightshade, eggplant, ground cherry, henbane, horse-nettle, pepper (rarely), tobacco, thorn apple, tomato, and its first recorded host plant: buffalo-bur.

The naming history is a bit weird — being neither originally from Colorado or associated with potatoes — but hey, that's science.


What’s the name of this insect that looks like a leaf? I found it in Taiwan Found it in a tea plantation. It can jump.

It appears to be a Tituria planata nymph.

The adults look like this:

At first I thought it was a treehopper, but it turns out that it was a leafhopper (they are similar but different).

Tituria planata is one of the most common leafhopper species in Taiwan.

https://www.inaturalist.org/observations?place_id=7887&taxon_id=49025&view=species

Image source 1

Image source 2