How do organophosphates affect kidney function?

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


Your image does not depict a predator, instead it's a scavenger. It's definitely a vulture, and by the looks of it a Griffon Vulture, which are a common siting in India.

The picture you provide is a bit grainy, and the apparently low-set sun colors the image somewhat yellow, but it does appear similar to below image of a Griffon vulture.

Griffon vulture. source: Vulture conservation in India and Nepal


What are the effects of combining rapamycin with dietary restriction?

To clarify; administration of rapamycin (a drug) to lab organisms (including mice [1]) extends lifespan. Similarly, restricting the intake of nutrients to the minimum without causing malnutrition also extends lifespan in lab animals (including primates [2]).

Rapamycin inhibits the mTOR pathway (mammalian Target Of Rapamycin) - specifically mTORC1 (Complex 1) - which influences protein synthesis, autophagy and inflammation (among others). Upstream factors of mTOR include nutrient availability and insulin signaling (see "Deconvoluting mTOR biology" for good review [3]).

It has been hypothesized that the lifespan-extending effects of caloric restriction (CR) are mediated by mTOR (one can see why - mTOR is affected by nutrient availability). In fact it may depend on the method of CR;

Greer et al [4] report that different methods of CR in C.elegans, for instance feeding them a diluted food source, or conversely feeding them on alternate days, do not necessarily require the same genetic pathways. Not only this but CR combined with a genetic mutant (eat-2) have additive lifespan-enhancing effects.

So whilst the evidence is not concrete, and I look forward to other studies in mammals similar to the one by Greer et al, it looks as though rapamycin and CR have similar but not exactly the same effects on lifespan; rapamycin specifically inhibits an individual pathway which is involved in many processes, and some of its effects are not necessarily desirable (e.g. rapamycin inhibits the immune system [5]). On the other hand, CR (most of the different types) seems to be mediated by mTOR - this difference is critical: mTOR is not necessarily inhibited by CR, it is just required for its effect.

Therefore combining rapamycin and CR is unlikely to have an additive effect as rapamycin may override any influence CR has on mTOR signaling, but I have not seen a study in which this has been tried. Combing different methods of CR (or developing drugs to do just that) may well have additive lifespan-enhancing effects.

Harrison DE, Strong R, Sharp ZD, et al. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature. 2009;460(7253):392-5.
Colman RJ, Anderson RM, Johnson SC, et al. Caloric restriction delays disease onset and mortality in rhesus monkeys. Science (New York, N.Y.). 2009;325(5937):201-4.
Weber JD, Gutmann DH. Deconvoluting mTOR biology. Cell cycle (Georgetown, Tex.). 2012;11(2):236-48.
Greer EL, Brunet A. Different dietary restriction regimens extend lifespan by both independent and overlapping genetic pathways in C. elegans. Aging cell. 2009;8(2):113-27.
Thomson AW, Turnquist HR, Raimondi G. Immunoregulatory functions of mTOR inhibition. Nature reviews. Immunology. 2009;9(5):324-37.


Why do I only breathe out of one nostril?

Apparently you're not the first person to notice this; in 1895, a German nose specialist called Richard Kayser found that we have tissue called erectile tissue in our noses (yes, it is very similar to the tissue found in a penis). This tissue swells in one nostril and shrinks in the other, creating an open airway via only one nostril. What's more, he found that this is indeed a 'nasal cycle', changing every 2.5 hours or so. Of course, the other nostril isn't completely blocked, just mostly. If you try, you can feel a very light push of air out of the blocked nostril.

This is controlled by the autonomic nervous system. You can change which nostril is closed and which is open by laying on one side to open the opposite one.

Interestingly, some researchers think that this is the reason we often switch the sides we lay on during sleep rather regularly, as it is more comfortable to sleep on the side with the blocked nostril downwards.

As to why we don't breathe through both nostrils simultaneously, I couldn't find anything that explains it.

Sources:
About 85% of People Only Breathe Out of One Nostril at a Time
Nasal cycle


I think what you are looking for can be found https://en.wikipedia.org/wiki/Lips#Functions_of_the_lips and https://en.wikipedia.org/wiki/Beak#Functions pretty easily.

To summarize, lips:

Mainly useful in mammals
Food intake
Articulation
Tactile organ
Erogenous zone
Facial expressions

Beaks:

Found in birds
Feeding
Defense
Manipulation of objects
Communication
Heat exchange


How does the blood of the veins in the legs get to the heart?

The veins in your legs have one way valves. These prevent blood from flowing down, but do not actively push it up. However, normal muscle movement from walking etc will squeeze the veins to push blood through these valves, and so it will work its way up to where negative pressure in your heart atrium can begin having an effect. This does however mean that blood accumulates from long periods of standing without movement, and so exercises are needed to prevent fainting, for example, for soldiers on parade (see Pathophysiology, Homeostasis and Nursing
By Roger Watson, Tonks N. Fawcett, Josephine N. Fawcett)


How do transgenic transformations cause off-target phenotypes?

The C.elegans used in the study you linked was originally made by Tissenbaum & Guarente using the gamma irradiation protocol.

In short, the protocol provides the injection of the desired DNA construct in the worm's gonad followed by gamma irradiation of the worms.

Upon radiation exposition, the genomic DNA of the worm will break at random sites and will undergo repairing by the appropriate cellular enzymes, during the latter stage the exogenous DNA can be integrated (ligated) into the genome. However, the genomic DNA can also acquire random mutations due to the radiation. This is how transgene insertions can cause off-target mutations in this case.

With other organisms or cells, the protocols are different. To engineer mammalian cells, for example, radiations are never used but still, you have to generate breaks in the genome to edit it. Depending on the method the "off-target rate" of a given experiment may vary, but it is never zero (not yet).


How do SDS-PAGE gels differ in a Bis-Tris system vs. a Tris-Glycine system?

SDS PAGE system rely on the fact that protein is denatured and surrounded by the SDS negatively charged detergent micelle.  This eliminates most of the charge and idiosyncratic solubility differences from one protein to another and gives a reasonable separation based only on size of the protein which is related to the size of the SDS micelle around each molecule.

Bis-Tris and Tris-glycine buffers have quite different charge shielding characteristics.  Bis (also known as 2-[Bis(2-hydroxyethyl)amino]-2-(hydroxymethyl)-1,3-propanediol) has a tertiary amine with a pKa of 6.46 and a pKb of 7.54.  glycine is a zwitterion at any pH between 2.3 and 9.6.  This creates a difference in the way that the buffer shields the SDS PAGE micelles from the rest of the electrical field, slowing down (probably glycine slows things down a bit) the time to resolution, but also giving the micelles more time to migrate.

So for SDS PAGE systems, the resolution of the gel has at least as much to do with the size of the gel pores (based on the acrylamide and bis-acrylamide percentages), the amount of protein you are putting into a given volume of loading well, and the size differences of the bands you are tying to separate. (you need to get pretty lucky to separate a 100.54 kda band from a 100.85 kDa band, but 1.5 to 1.8 kDa is easier 10 to 14 kDa is even easier). Also consider adjusting the current or voltage of the power supply.  The buffer system is only one consideration in planning your experiment and often not the primary factor of quality.


Normally, epithelial cells of mucous membranes express a chloride ion channel that allows movement of Cl- down its electrochemical gradient and out of the cell. This increase in extracellular electrolytes draws water out of the cells by osmosis, hydrating the mucus.

In cystic fibrosis, this protein is defective, most commonly caused by misfolding and subsequent degradation. Cl- cannot diffuse out of the cell and thus water is not drawn out, leading to thick mucus.

  ...given that CF changes the protein channels used for chloride ions to move through osmosis.

Water flows by osmosis, not ions.

  I thought osmosis was through a permeable membrane...

Osmosis does occur through permeable membranes, but large, bulk flow of water can be mediated by protein channels called aquaporins. Read more here.

  ...and active transport used a protein channel.

Active transport of solutes does use protein transporters, but they are not strictly "channels": "channel" is the term used for passive transport, also called facilitated diffusion when a channel is involved.


Is there a balance or feedback between O₂ and CO₂ in the atmosphere?

Yes, increase in CO₂ concentration increases the rate of photosynthesis in plants. The rate of photosynthesis is linealy proportinal to CO₂ concentration in range up to 225ppm  and  slowly increases range 225-650ppm.[Limiting Factors in Photosynthesis, Plant Physiol. (1984) 75, 82-86] (Now CO2 concentration is about 400ppm).
You can read more in Educational article on Nature journal website or in
More scientific review on the topic.


Identification of colorful jelly-like marine creature

You've found a sea anemone, a cnidarian of the Order Actiniaria. In this case, the anemone is closed and thus hiding its characteristic tentacles (likely as a form of protection while "out to dry").

I'm by no means an expert, but my guess is that you have a vertically striped species of the genus Diadumene  -- likely one of many morphotypes of the species Diadumene lineata. I've seen common names vary between "Striped Sea Anemone", "Lined Bead Anemone" and "Orange-Striped Green Anemone."

Here is a double stripe specimen from San Francisco, and below are two pictures from Ria Tan's Wild Singapore image collection:

Closed:

Open:

Without further information regarding size, color/length of tentacles etc., it will be hard for a non-expert like me to find a better answer.

According to the Wikipedia page, this species originated along the Pacific coast of Asia, but has spread more globally from attachment to ship bottoms, oyster shipments, and seaweed farming.

It appears from your picture, that you found your specimen out of water along the shoreline. Again according to the Wikipedia  article:

  Diadumene anemones display high tolerance to inter-tidal exposure and drying out in extreme summer heat


What are an internal and external exons?

Yes, the internal exons are those that aren't at the ends, which are often referred to as terminal exons1.

However, exons are sequences of nucleotides that are incorporated into the mature mRNA — i.e. they don't have to be (entirely) protein coding.

It is probably simplest to think of exons as being the transcribed regions that are not introns — i.e. they are the sequences that don't get spliced out during transcript maturation.

In other words, the 5'UTR is typically§ part of the first exon and the 3' UTR is typically§ part of the last exon.

§Note: I say typically, because sometimes introns are found within the UTRs2,3.

Reference:

1: Bolisetty, M. T., & Beemon, K. L. (2012). Splicing of internal large exons is defined by novel cis-acting sequence elements. Nucleic acids research, 40(18), 9244-9254.

2: Eden, E., & Brunak, S. (2004). Analysis and recognition of 5′ UTR intron splice sites in human pre‐mRNA. Nucleic acids research, 32(3), 1131-1142.

3: Paolantoni, C., Ricciardi, S., De Paolis, V., Okenwa, C., Catalanotto, C., Ciotti, M. T., ... & Giorgi, C. (2018). Arc 3′ UTR splicing leads to dual and antagonistic effects in fine-tuning arc expression upon BDNF signaling. Frontiers in molecular neuroscience, 11, 145.


Ephedrine or pseudoephedrine indirectly central alpha2 mimetic?

Anongoodnurse provide an excellent comment in other discussion about how to search PubChem.

Ephedrine is not alpha2 mimetic.
Pseudoephedrine is alpha2 mimetic, source:


Cancer and level of selection

Cancer results from the opposite action of different level of selection. There is selection on the population of multicellular individuals and there is selection on the population of cells within each multicellular individuals.

There is selection among cells within an individual for increase replication rate while there is selection among multicellular individuals in the population for controlled replication rate of their cells.

Major transitions

The passage from small unit of selection to bigger units is called a "major transition". Such transitions include the grouping of genes on chromosomes, the grouping of cells onto multicellular individuals, the grouping of multicellular individual onto colonies and, if there are several planets inhabiting life in the universe, then the grouping of life forms in every planet into a population of living planets. One can list other, more extreme or intermediate major transitions but there is quite a bit of debate on what really constitute a major transition.

Literature on the subject

  [I]s there any literature thinking about it this way?

The keywords that will help search further information are group selection, kin selection, major transitions.

I recommend having a look at Major Transitions In Evolution by Maynard Smith and Szathmary and also The Major Transitions in Evolution Revisited by Calcott and Sterelny which is a book made of many small parts, each written by a different author on these same questions of level of selection.

You might eventually have a look at Evolutionary Dynamics: Exploring the Equations of Life  by Nowak as well.

These discussions of level of selection include discussion of what an individual is and what level is most important. The extremely popular and well written books by Dawkins will also bring you some light on the subject. Consider The extended phenotype for example.

For more book recommendations in evolutionary genetics, please have a look at Books on population or evolutionary genetics?.

If you like the sensation of thinking of the entire earth as an individual part of eventually a larger group of living planet, then you'll maybe enjoy having a physiological / ecological view of this living planet earth with Gaia by Lovelock


I don't know if there is any "universal" virus that really gets into every cell type, but lentiviruses come pretty close. Lentiviral transfection vectors have been developed for a wide range of human (or mammalian) cell types, including immune cells and terminally differentiated cell types such as neurons and skeletal muscle.

But these are of course experimentally modified viruses that have been optimized in various ways for transfection; typically, the naturally occurring virus is much less efficient. I would guess it's unlikely that a natural virus can enter any (human) cell type, because this capability would be expensive for the virus to maintain, and there is probably little pressure to do so --- as long as the virus has a working route of transmission, via the airways for example, there is probably little benefit in being able to transfect other tissues.


Will sperm cells exhibit chemotaxis towards sucrose?

If you google "sperm chemotaxis sucrose" you learn some things of interest. Notably, wikipedia's article on sperm chemotaxis indicates that the important chemoattractants for sperm (the things that attract sperm via chemotaxis) are various signaling molecules given off the by the egg.

It is not clear why you would necessarily think that sucrose would attract sperm or that salt would repel them. In the first case (sucrose), it is not obvious why sperm would expect to see sucrose. If I remember correctly, sucrose is actually pretty rare in animal physiology except as an energy source in plants that animals eat; and sucrose is largely broken down into monosaccharides before it even leaves the small intestine, so it's not like it's circulating in the body. For instance, a lab protocol for studying animal sperm chemotaxis suggests adding sucrose as a densifying agent that doesn't interfere with chemotaxis, suggesting that sperm are pretty independent of sucrose. In the second case (salt), it is not obvious that sperm would necessarily avoid the things that kill them. Those things may be correlated with doing their job! Most sperm cells are expected to die in the human reproductive strategy.

In plain terms: there are huge numbers of sperm which are competing really hard with each other to find and fertilize an egg, not to find sucrose or to avoid salt. The chemotaxis that sperm exhibit will tend to help them accomplish this goal. So it seems (according to wikipedia) that they follow the signals that say 'egg', not the ones that say 'sugar'.

Update:
Sorry, only just saw update on Q. Thanks for the clarification- sounds like fun! I've been curious about the foldscopes.

If what you want is to do an experiment, then I think you've actually got a great start with knowing first that salt interferes with their motility. That is a control experiment, e.g. the very first thing you should do, to make sure that the world works the way other people say it should. (First rule of experimental science: never trust anyone!). Look up a protocol which suggests a sperm-inhibitory concentration of salt (ideally kosher salt, not table salt which has a bunch of other stuff like iodine in it). Put sperm in that concentration of salt and then also in a medium where they should show chemotaxis (the protocol I linked to could be helpful here). See if you can reproduce the salt inhibition, ideally in a medium that is otherwise identical to the medium that allows chemotaxis.

Next, try other stuff. Unfortunately, chemoattractants are probably proteins/small molecules you can't buy at the supermarket. But you could try to get creative. I can't ethically recommend that you try to find a human source, because that gets weird pretty quick, though it is the obvious suggestion (I assume you are talking about human sperm). Potentially there is an animal source for such things which isn't too expensive.

However, you could say to hell with chemoattractants and chemotaxis, and try to just understand sperm motility. You could try other osmotic shocks, with simple cheap chemicals like glycine. It looks like there is some literature that calcium ions affect sperm motility. Or you could play with pH, using vinegar or lye, or temperature. I bet that all of those affect sperm motility (probably for the worse). Or you could try the effects of various weird hippie herbs from the health food store. It sounds like you are just looking for an easy, fun experiment, and if that's your goal then I suggest you try a bunch of things and see what happens. That way you're more likely to find something interesting.

If what you want is a more elaborate experiment, then I think it is worth your time to sit down and try to read up on how sperm work, and then design an experiment that really clearly tests a hypothesis. I am not an expert here, but the Yoshida article I link to looks like it has a good literature review.

Hope that helps.


Do both TSG and Proto-oncogenes have to suffer mutations to cause cancer?

The typical idea is that several "hits" are required. The difference between proto-oncogene and TSG is mainly in their heritability - TSG mutations are usually recessive (because a heterozygote will still express sufficient suppressor, e.g. p53) whereas proto-oncogenes are dominant (if a consitutively active agent e.g. Ras is present, it doesn't matter if the other allele is under normal control).

A single "hit" in this way (TSG or proto-oncogene) may just cause the cell to die, which isn't a bad thing (in fact, TSG such as p53 often work by inducing apoptosis because proliferative errors make them accumulute). A tumour only results when a single cell accumulates sufficient mutations and genomic damage to gain a reproductive advantage over the cells in its vicinity.

However, you are asking about cancer, which is not simply a tumour. Tumours are any sort of abnormal growth, i.e. neoplasms, but they can be benign! This means they stay in their tumour capsule, do not grow at a fast rate and do not invade or metastasise other tissues. The distinct characteristics that define a cancer are very well-known and were published in a well recognised paper by Weinberg & Hanahan, 2002, "The Hallmarks of Cancer".

The six primary hallmarks of cancer. The first two are the ones most people know, but the other ones are just as essential for

Independence from external growth signals: Cancer cells produce their on autocrine growth factors or have mutated signal pathways active without GF receptor stimulation (Oncogenes).
Resistance to anti-growth signals: Cancer cells do not respond to growth-inhibitory factors from outside or inside (Tumour suppressor genes).
Evasion of apoptosis: Cancer cells resist signals which cause normal cells to die (apoptose) (these are also tumour suppressor genes).
Limitless replication / Evasion of cell senescence: Apart from stem cells, all normal cells can only replicate their genome a certain number of times before the ends of the chromosomes known as telomeres are too short, disintegrate and cause the cell to enter senescence or die. Cancer cells express telomerase, which extends telomeres and maintains replicative potential.
Sustained angiogenesis: Tumours and cancers form massive cell heaps. Tumours may stall growth because blood vessels do not grow into the heap and supply the cells with the nutrients needed to proliferate. Cancer cells have found a way to induce blood vessel growth (VEGF) and sustain it in order to maintain nutrient supply.
Invasion and metastasis: This is the crucial, most distinguishing difference between benign neoplasm (tumour) and malign neoplasm (cancer). Cancer cells degrade the extracellular matrix around them (by secreting metallo-matrix-proteases, MMP), which allows them to move away from where they are and invade into neighbouring tissues. They can also spill into blood vessels this way (especially if the neoplasm is well-vascularised thanks to hallmark number 5), where they can travel to other sites in the body and grow new cancerous tumours in other locations.

There are four more emerging hallmarks and enabling characteristics (immune evasion, inflammation induction, modification of energy metabolism, genomic instability), which allow better cancer growth and make a cancer more dangerous if it acquires them, but these are outside the scope of this answer.


First we must remember what a nucleosome is: a segment of DNA packed with proteins called histones. This is the initial step to turn the DNA a more compact structure. Citing the advantages of an extremely compact but flexible structure like chromosomes would make this answer a little longer (if you want, I can add them later), and to answer your question faster, we'd better keep moving on the discussion. Epigenetics and gene expression are so beautiful that they have many mechanisms to regulate or change gene expression, and you mention one, which is done by reversible covalent modifications on histones. Such modifications are executed by especific proteins, that can do methylation, acetylation, phosphorilation in some aminoacids of histones. When an aminoacid of a histone is linked with charged groups (e.g: methyl, acetyl) its charge is altered, and depending of the resulting charge (negative or positive), it can reduce or increase the afinity between the histone tail and the adjacent nucleosomes, and therefore, make the nucleosome more compact and less accessible or less compact and more accessible, respectively. But the main effect of these covalent modifications on histones is that the groups added to the aminoacids act like markers indicating for proteins involved in expression (like transcriptional factors and RNA polymerase) that some genes are switched on or switched off. The patterns of this modifications (which one repress or estimulate gene expression) is not completely understood yet.An example of how a certain region is chosen to be marked for expression or repression: Consider an organism that has received a repressed gene related to obesity from its parents and this organism is lazy, eats a lot, has a sedentary life. As a result of all this stimulation, the proteins responsible for altering the histones of the gene related to obesity can be activated or recruited by others proteins, and make covalent modifications in a way that the histones of that gene now are marked for it to be expressed. This organism can pass the new mark to the its children and they will have propensity to obesity due to the activated gene. (This final example was an experiment of epigenetics using rats, I saw a long time ago, so I can't remember the reference).And about if it's casual or not, the marks of regulation in a sequence of DNA can't be casual. For each one or two modifications of histones there is an enzyme that will only do its function if some event is already triggered or if it's triggered during the cell life depending on the environment the cell is exposed to. So millions of cells of a same tissue that have the same function would not have the same pattern of expression for the main genes related with that function by chance. Therefore, regulation of gene expression is very refined and histone marks are one of the many mechanisms that together dictate if a gene is repressed or expressed.


There are only 3 classes of fluorescent proteins proteins known I think.  Two of them are relevant to your needs maybe.

The first are usually called 'fluorescent proteins'.  These proteins are usually derived from the A victoria jellyfish.  Its entirely passive in its fluorescence, but has been tuned to many levels of quantum yield and color.

There was a new sort of fluorescent protein cloned recently from japanese eels.  It is activated by binding to bilirubin.  Its so new that its not likely to be available, but there you go.

The third class would be the luciferases.  They are luminescent, not fluorescent but in producing light involves binding from a cofactor called luciferase which is oxidized to produce their light.  This is not really fluorescence since the electrical stimulation that causes light production is not from incident light, but since what you are looking for might not exist I wanted to remind you of the luciferases, which bind their redox substrates to activate.  The luciferin molecule actually varies as there are several classes of luciferase.  I think Flavin and NAD are the most common substrates.


Why does photosynthesis occur even in blue light when the photocentres are activated in red light

While it is true that strongest activity of Photosystem I and II happens with 700nm and 680nm light, these are not the only wavelengths that can be used for photosynthesis.

The green color of plants comes from chlorophyll, which is the main light absorbing component in the photo systems. If chlorophyll had only a single absorption peak at 680-700nm, it would have a blue(-ish) color instead of a green one.

Looking at the absorption spectrum of chlorophyll (which wavelengths it can absorb how well), you can see that there is a a second peak around 400nm:

This both explains the results of Engelmann's experiment and the green color of chlorophyll (with both red and blue colors removed only green remains)

Picture taken from: http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ligabs.html


Textbooks tend to report structures as relatively static, whereas advanced biochemistry texts explore structural tautomerism. In essence, the histidine imidazole sidecvhain may move around it's protons and electrons when pH is roughly equal to pKa. Thus, the sidechain exists as two tautomers where the two nitrogens sort of "share" the double-bond character and the proton, like so:

And it's even more accurate to depict that the double-bond character is like so:


Why some traits are more desirable in the sexual selection?

There are two common explanations both are difficult to demonstrate. I personally favor the former but I will not claim it is the only explanation.

selection starts as either a random occurrence or as some initially beneficial trait (a slight increase in tail length may have been beneficial originally)
Then runaway selection takes over. Any increase also causes increased attraction because the evolved behavior of the desire in the females only functions as bigger is more attractive(or whatever=more attractive). This pushes further and further into absurdity becasue there is not behavioral regulation to say enough is enough. So any increase in the males increases attractiveness meaning any individual male with less can't reproduce in the current population of females no matter how beneficial to the individual male survival. Additionally no female will develop a favoring of smaller tail feathers becasue her smaller tailed offspring will not be able to find mates for the same reason. A positive feedback loop like this won't stop until it hits a point where the cost of tailfeather is more than the advantage of increased mating becasue the individual never lives long enough to mate.
By carrying a handicap the organisms shows it can withstand a greater burden and thus must be better.


Those aren't bees, they're a kind of paper wasp. As you observed, they start small and seem innocuous at first, but be warned, as the nests grow in size, the inhabitants become more protective of their nest and are more likely to see you as a threat to attack than as a peaceful cohabitant (at least this has been my experience.)

  Nest construction starts in late spring and continues throughout the summer. The last brood raised includes males and next year’s queens. Due to the importance of these reproductives, the worker wasps become very protective and aggressive toward those who venture too close to the nest this time of year.

Somehow we seemed to have a number of attractive habitats for paper wasps (and mud wasps) and had to deal with them when too large or in a dangerous place (e.g. in a door frame.). A honeybee relocation service will do you no good in this situation.

You have a few options to consider, I recommend sooner than later. First, at night and while wearing protective clothing and gloves, you can simply whack the nest off at the base and run away as quickly as possible); Plan/clear your escape route in advance! Stay away for a couple of days as it often takes this long for them to completely abandon the young inside. If these are bald-faced hornets, their sting is quite painful, much more so than a bee or a yellow-jacket.

Or, if this doesn't bother you (it does bother me), you can light the nest with a burning roll of paper (it is, after all, paper, and will burn quite rapidly. The 'good' part of this is that the flame usually destroys the wasps' wings as well, and they're less likely to be able to attack you. This is best done on a cool night after all or most activity around the nest has ceased. The fire flares brightly and burns the nest very quickly without setting fire to adjacent structures, but a fire extinguisher should be kept nearby just in case.

Third, you can buy a spray, but I found them to be ineffective against the kind of paper nest shown in your picture, because the envelope protects the wasps inside. I used up two large cans of foaming spray (in spite of hating insecticides, as it wasn't a spot I could safely whack) without any obvious result. I ended up doing multiple whack-and-runs.

Finally, you can hire a professional, something I never did in my 28-odd years of dealing with them, but which is often recommended.

Yes, it's probably poop.


How do you interpret this microbiology/ bacteriology research figure?

The short answer is that it looks like the colors are meant to represent different, partial copies of the bacterial genome in the process of being synthesized.

When bacteria replicate, they initiate replication at the origins of their chromosomes.  In fact, these origins can be replicated multiple times before it gets to the "end" of the bacterial chromosome (terminus). Looks like the stacking on the right figure shows this, with the colors just aiding in differentiating the partially replicated chromosomes. The coverage plot on the left shows how this might look based on read coverage from deep sequencing (again the colors just show different, partially replicated, chromosomes).


What is the motivation behind the CCA -> CCU modification between SARS-CoV-2 and the mRNA vaccine when encoding the signal peptide?

The other answer is a bit convoluted IMHO.
First note that as the article cited notes, that's not actually CCA -> CCU but CCA ->  CCΨ; they only used ASCII for convenience. Furthermore, these three all code for proline as the article also notes.
Second, Ψ stands for pseudouridine and it's the golden discovery of Kariko and colleagues (which made mRNA vaccines [more] practical) that you need to use as many pseudo-Us as possible to ensure that the exogenous mRNA doesn't get destroyed prematurely and/or triggers downregulation of transcription.
Third, that's not even pseudo-U that's actually used in the Pfizer vaccine but N1-methyl-pseudouridine (variously abbreviated as N1mΨ or m1Ψ), which is even more "potent" in these terms than even pseduo-U. (According to a book on RNA therapeutics, m1Ψ was actually discovered and is patented by Moderna circa 2012-2013, before any academic publications.) Actually a 2017 publication found that independently of reduced immunogenicity, m1Ψ seems to be more active "by increasing ribosome pausing and density on the mRNA":

We show that in addition to turning off the immune/eIF2α phosphorylation-dependent inhibition of translation, the incorporated N1mΨ nucleotides dramatically alter the dynamics of the translation process by increasing ribosome pausing and density on the mRNA. Our results indicate that the increased ribosome loading of modified mRNAs renders them more permissive for initiation by favoring either ribosome recycling on the same mRNA or de novo ribosome recruitment.

And more research on the latter aspect (2019)

Global incorporation of different modified nucleotides often (but not always) markedly changed mRNA expression. This effect was seen across numerous synonymous coding variants of multiple proteins, in several different cell lines, and in vivo. m1Ψ generally gave higher expression than U or mo5U for the same sequence. Biophysical studies revealed that m1Ψ and mo5U have dramatically different and opposite effects compared to U (stabilizing and destabilizing, respectively) on overall mRNA folding, nearest-neighbor base-pairing thermodynamics, and secondary structure pattern as mapped by SHAPE.

There could be additional reasons, but these are probably marginal.
Now, canadianer asks an astute question below (which was not asked by the OP), whether it's (still) preferable to do UUU -> UUC (which normally it is) if m1Ψ is going to be globally substituted for U anyway. I don't actually know the answer to that; Pfizer or Moderna might have researched it, but I haven't found any publication on the trade-off.
The actual reason for the latter (especially since UUC is about 3 times as inefficient as UUU) might be that real goal is to slow down the protein folding there. The WHO doc does say that the protein is folded in a particular way "to ensure the S glycoprotein remains in an antigenically optimal pre-fusion conformation". In general, there's a trade-off between the speed of translation and accuracy of folding. (ΨUU is actually twice as efficient as UUU already, even with naturally occurring pseudouridine. In fact UUU is one of the most common places where one finds a naturally occurring pseudouridine.)


A little digging on wikipedia seems to have answered my question. This picture of a 17 year cicada, Magicicada septendecim is pretty close to what I saw.

Furthermore, this seems to match the time and place, as the Kansas Brood of 17 year cicadas is scheduled to emerge this year and should appear in the Missouri-Kansas area. It also explains why I'm not familiar with these cicadas, 17 years ago I wasn't paying attention to them.


There are two relatively common contagious cancers: Tasmanian Devil Facial Tumor, and Canine Transmissible Venereal Tumor.  Both are truly contagious cancers, in that the cancer cells themselves are transmitted from one host to the next, and expand and cause disease in each successive host.  (There was also a contagious cancer of hamsters, which has long since gone extinct, and there are some transmissible tumors in clams and oysters; the latter don't have immune systems that are remotely similar to dogs, Devils, or humans.)

It's believed that one key aspect of the Devil Facial Tumor is that Tasmanian Devils are immunologically closely related.  Normally, cancer cells from one host would be a tissue graft in a different individual and would be rapidly rejected as with any allograft.  However, immunologically closely related individuals can tolerate each others' grafts, and it's believed that this is part of what allows the Devil tumor to spread -- a lack of genetic diversity among Tasmanian Devils.

  Major histocompatibility complex class I and class II genes have extremely low levels of sequence divergence in the devil population from the Tasmanian east coast (Siddle et al., 2007a, 2007b). ... The lack of diversity at MHC loci, coupled with weak responses of east coast devils to allogeneic mixed lymphocyte culture, has led to the suggestion that this population may be functionally identical at MHC loci, thus permitting the spread of DFTD as an allograft.

--Clonally transmissible cancers in dogs and Tasmanian devils

The genetic diversity explanation is widely accepted, but it hasn't been formally proven and there are a number of points that suggest that it isn't the whole story.  There are several other molecular features of the tumor that probably make it less immunogenic (see the review The role of MHC genes in contagious cancer: the story of Tasmanian devils) and the full story probably involves a combination of these things.

CTVT is different.  It's astonishingly ancient (it apparently arose in a dog, or a wolf, 11,000 years ago and has been passed from dog to dog continuously since), so it's obviously very successful at what it does, but it's not at all understood how it does it. Dogs are genetically pretty diverse and definitely don't tolerate arbitrary grafts from each other, so that's not the explanation. Lots of other possible explanations have been put forward, most of which point to various immunological features of the tumor; however, while that's clearly an important point, none of the things people have implicated are unique to CTVT -- tumors invariably have immune suppressive abilities and don't have the same ability to spread. (Going back to the Devil tumors, the low expression of MHC molecules on the cancer cells is probably a factor there too, but it's important to understand that low MHC expression is almost universal among tumors, including the vast, vast majority that can't transmit.)

Summary:

There do exist a very small number of truly contagious cancers.
The reasons for their transmissibility are not fully understood.
Genetic diversity and immune evasion are probably two of the causes.


How Do Adherent Cells In Culture Attach To A Plastic Dish?

I doubt that hemidesmosomes are much involved in 3T3 adhesion, just because they are characteristic of epithelial cells and fibroblasts are mesenchymal.

You're on the right track, though. It's going to be the same basic processes as adhesion to the extracellular matrix. The major factors will probably be integrins and focal adhesion assemblies.

You're also raising an important point for in vitro work, which is that adhesion to plastic is a very imperfect substitute for ECM, and this probably has implications for the behavior of the cells. If you're interested in ECM-dependent processes like migration, adhesion, and invasion, consider coating your plates with collagen or Matrigel.


Vitamins that could help "make us smarter"?

Are there vitamins that make us smarter?

Vitamins are micronutrients required in small quantities for normal human metabolism. Extra high (supra-physiological) doses do not generally result in improved performance. Of course, if one is deficient in certain vitamins (e.g. Vit B-1 deficiency causing Wernicke-Korsakoff encephalopathy), taking a vitamin can restore normal function. However, with adequate access to a normal diet, you are unlikely to be deficient. Commonly cited exceptions include:

strict vegans (Vit B12)
alcoholics (thiamine (B1), folate)
cultures highly dependent on maize as a staple (niacin (B3))

In people with a normal diet, taking additional vitamin supplements is usually not helpful.* (An exception may be Vitamin D depending on whom you talk to, but this is unrelated to cognitive performance.)

There have been scattered studies showing some benefit of various plant extracts and other “natural” substances. Studies such as this one about Bacopa monniera do demonstrate benefit. However, many such studies are of limited value due to sponsorship by the makers of supplements and publication in journals with questionable quality of peer review. This meta-analysis reviewing the effects of phosphatidylserine, phosphatidylcholine, citicoline, piracetam, vinpocetine, acetyl-L-carnitine, and antioxidants reached a more guarded conclusion:

  for most of the "brain-specific" nutrients we review, some mildly suggestive effects have been found in preliminary controlled studies

Note that most of the substances discussed thus far are not vitamins but rather amino acids, more complex plant extracts, or — in the case of caffeine — a synthetic crystalline xanthine alkaloid. These sorts of things are commonly included in supplements found at health stores. As for vitamins specifically, this large randomized controlled trial found no effect of multivitamin and mineral supplementation on cognitive function.

What component of Cognitive Supplements are active?

The answer is usually caffeine. Caffeine is cheap, widely available, and markedly improves short-term cognitive and physical performance. By modulating adenosine activity in the central nervous system, it improves alertness, prevents impairment in neuro-plasticity associated with sleep deprivation, potentiates synaptic transmission in animal models, and may slow neurodegeneration in certain disease states.

This review article looked at ”enhancement supplements” containing taurine, guaraná, ginseng, glucuronolactone, B-vitamins, and other compounds  as well as caffeine and concluded:

  there is an overwhelming lack of evidence to substantiate claims that components of [energy supplement drinks], other than caffeine, contribute to the enhancement of physical or cognitive performance.

To your question,

  Are these supplements safe?

You should look at the ingredients. If it is caffeine, the answer is: usually. However, it is not recommended for those with insomnia, anxiety, palpitations, or who are underweight. As for other components of these, you need to read the label and do your research. As mentioned in the footnote, vitamins themselves are not without the possibility of harm at supra-physiological doses. For other components the danger is likely uncertain and under-researched.

*For those interested in the vitriol around this subject, check out this series of editorials that followed the paper linked above. Quoting the first of these:

   In conclusion, β-carotene, vitamin E, and possibly high doses of vitamin A supplements are harmful. Other antioxidants, folic acid and B vitamins, and multivitamin and mineral supplements are ineffective for preventing mortality or morbidity due to major chronic diseases. Although available evidence does not rule out small benefits or harms or large benefits or harms in a small subgroup of the population, we believe that the case is closed— supplementing the diet of well-nourished adults with (most) mineral or vitamin supplements has no clear benefit and might even be harmful. These vitamins should not be used for chronic disease prevention. Enough is enough.


Stochastic parameters in population growth equations

Since you are asking for the biological interpretations about these parameters, it is important to realize that the model you are presenting is a non-dimensionalized version of this model:

$$ \frac{dx_1}{dt} =b_1x_1\Big(1- \Big(\frac{x_1 + \beta_{12}x_2}{K_1} \Big)\Big) $$
$$ \frac{dx_2}{dt} =b_2x_2\Big(1- \Big(\frac{x_2 + \beta_{21}x_1}{K_2} \Big)\Big), $$

which can also be written as:

$$ \frac{dx_1}{dt} =b_1x_1\Big(1- \frac{x_1}{K_1} - \beta_{12}\frac{x_2}{K_1}\Big) $$
$$ \frac{dx_2}{dt} =b_2x_2\Big(1- \frac{x_2}{K_2} - \beta_{21}\frac{x_1}{K_2}\Big). $$

This clearly shows how this competition model is merely the logistic Verhulst model, with an extra term attached. This extra term is simply describing to what extent each individual in "species" 2 is using up the resources of "species" 1 ($K_1$), where $\beta_{12}$ describes this relationship (~proportion of species 2 that is counted as species 1). The parameters in the model formulations above are also more easily interpreted in ecological/biological terms than the $a_{ij}$s in your model.

To go from this latter formulation to yours you substitute:
$$a_{11} = b_1/K_1$$
$$a_{12} = \frac{b_1\beta_{12}}{K_1}$$
$$a_{22} = b_2/K_2$$
$$a_{21} = \frac{b_2\beta_{21}}{K_2}$$

As you can see, this means that the $a_{ij}$s are composites of other parameters, and perturbing $a_{ij}$s could correspond to either $b_i$, $K_i$ or $\beta_{ij}$ being perturbed. It also means that perturbing e.g. $b_1$ in your model while holding $a_{11}$ fixed means that you are actually also perturbing $K_1$ to offset the change in $b_1$ (since $a_{11} = b_1/K_1$), which will introduce a positive temporal correlation between $K_1$ and $b_1$. This is a strong assumption to make. This also means that $a_{ij}$s are not strictly "interaction parameters" as you call them, but they include other aspects as well.

Since realistic cases and scenarios for perturbations may often be expressed in terms of the parametrization I give above (e.g. random fluctuations in population growth rate or carrying capacity), these relationships are essential to keep in mind.


What is the most appropriate way to normalize gene expression data?

Normalization of expression data is a big topic with new methods being published regularly. When approaching something like this you generally want look at people who have done similar things to what you've done, and then once you understand why they did what they did, you can ask what you need to do to answer your questions. Always keep your biological question in mind. For instance if you're measuring QTLs, you'll need to be a lot more careful than if you're just looking for genes effected by a knockout mutation.

In general you want to use quite different methods for RNAseq and Microarray data. The two data types follow completely different distributions (RNAseq gives you count data, microarray data gives you continous signals) and have different types of technical noise effecting them (GC content will effect both, but in a different way). Some methods can be used on both, but usually involve coercing the data into a different form (e.g. mapping counts to a normal distribution). The limma package for R can handle both, using different distributions, and is a good start. Newer, purportedly better methods exist for RNAseq, which I haven't personally used.


What species is this rabbit-like animal?

Thanks to @Satwik's tip about google image search, I was able to figure out that the animal in question is a Viscacha. Though the source answer is thanks to reddit, so take that as you will.

  Viscachas or vizcachas are rodents of two genera (Lagidium and Lagostomus) in the family Chinchillidae. They are closely related to chinchillas, and look similar to rabbits, apart from their longer tails


What is the population limit that makes consanguinity an issue?

I don't have a great knowledge in population genetics but I think your question can be answered by the relationship between loss of heterozygosity and the effective population size.

For an ideal asexually reproducing genetically diploid population, the heterozygosity is lost with increasing generations according to this equation:

$$H_t=\left(1-\frac{1}{2N}\right)^t H_0$$

where $H_t$ is the heterozygosity at the generation $t$, $H_0$ is the heterozygosity of initial population and $N$ is the population size.

If you analyse this equation then you'll note that heterozygosity exponentially reduces at rate inversely proportional to the population size.

For real populations you have to replace the population size with effective population size. Effective population size for a sexually reproducing population would be:

$$\frac{1}{N_e} = \frac{1}{4N_m} + \frac{1}{4N_f}$$

Where $N_e$ is effective population size, $N_m$ is number of males and $N_f$ is number of females.

You can find the derivation of these formulas in Principles of Population Genetics by Hartl and Clark.

Other than that, the probability of extinction is also higher, the smaller the population is.

When would consanguinity be an issue depends on other factors too such as initial heterozygosity, presence of deleterious alleles in the gene pool and other environmental factors. I don't think there is some kind of mathematical/practical lower bound. The minimum viable population is approximated using simulations.


This article has some good information. It's certainly more than I want to know about warts.

  Isolated warts may remain unaltered for
  months or years, or a large number of new lesions
  may develop rapidly in a short period of time. The
  development of warts is not predictable.
  Approximately 65% of warts disappear spontaneously
  within two years. The patient’s age and number of
  lesions do not seem to affect the prognosis.

There are many different types of warts and of HPV. Since warts cause a type of dysplasia their life cycle can be very variable and unpredictable.


Why did Darwin say "the misfortune to undertake"?

If you read the subsequent paragraph it is clear that he is speaking of the difficulty in drawing borders between species.

It is not possible to draw definitive species boundaries, especially if you follow species over time  rather than classifying organisms with a snapshot in time: these issues come up time and time again on this Stack. Some examples:

How could humans have interbred with Neanderthals if we're a different species?

Usage of "lineage" over "species"

Transitivity of Species Definitions

Because all species descend from common ancestors, there is a time at which any two organisms shared an ancestor. For related organisms, you can recognize that shared history, emphasize the similarity and at some point group two subspecies together as one species, or you can focus on differences and separate them. Whichever you choose, someone can argue that the species should instead be separated or grouped.

Ultimately, the distinctions are based on somewhat arbitrary decisions, and counterexamples are abundant whichever rule you try to use (for example, a rule that organisms that have viable offspring should be considered species renders many examples that one would argue should be separate species, and examples of individuals that should be one species that are nonetheless not able to produce viable offspring).

It's not so much the misfortune of the task being difficult but rather of it being not possible to come to a definitive answer.


Population Dynamics problem concerning Allee Effect

You're not interpreting that Wikipedia page correctly. That equation provides an example of the Allee effect, but is not exclusive.

The Allee effect occurs when the non-zero steady state of a system is not globally attractive, so that such populations may be stable at non-zero population levels for a long time, but are unable to recover once the population density drops below a certain threshold.

In terms of your problem, the tricky bit (conditions for global attraction) is done for you as it instructs you to find parameters so that $\frac{\dot{N}}{N}$ is maximum for intermediate (positive) $N$.

So when does $f(N) = r - a(N-b)^2$ have a maximum admitted at some positive $N$? This is a quadratic, so simple mathematics is enough.

$a>0$ is needed to ensure the parabola admits a maximum
$b>0$ is needed for the maximum is attained at positive $N$.
$r>0$ is also needed to ensure the maximum is positive. This is not clear from the information in the question, but the non-trivial steady states involve $\sqrt{\frac{r}{a}}$ and so $r > 0$ for these steady states to even exist.

So overall quite boring conditions and not a very satisfying question.

In general, a population $x$ with reproductive rate $b(x)$ and death rate $d(x)$ with dynamics $$\frac{dx}{dt} = x(b(x) - d(x))$$ displays the Allee effect if $b(0) < d(0)$. This is easy to prove with a basic grasp of ODE stability.


Does the cell have a mechanism to determine DNA sequence from protein?

"Reverse translation"

Translation is the process by which an mRNA is "translated" into a protein.

It is impossible to get the exact DNA sequence from the protein sequence because a large number different DNA strands could code for the exact same proteins. In other words, there is a loss of information in the translation process. See codon redundancy and I am not even talking about introns and UTR.

Now, it is theoretically possible to get one of the large number of possible DNA sequence from the protein sequence. I am not aware of any natural process that does this job.

"Reverse transcription"

Transcription is the process by which DNA is "transcribed" into a mRNA.

It is possible to get the DNA sequence from an mRNA. And it just so happen that such process does exist! A "reverse transcription" if you want. The enzyme that does this job is called reverse transcriptase. Reverse transcriptase is mainly found in retro-viruses but there are a number of non-retro viruses that have a reverse transcriptase.


From wikipedia > Golgi apparatus

  The Golgi apparatus, also known as the Golgi complex, Golgi body, or simply the Golgi, is an organelle found in most eukaryotic cells.

and further

  In plants, Golgi stacks are not concentrated at the centrosomal region and do not form Golgi ribbons. Organization of the plant Golgi depends on actin cables and not microtubules. The common feature among Golgi is that they are adjacent to endoplasmic reticulum (ER) exit sites.

and also

  The [trans Golgi network] may act as an early endosome in yeast and plants.

The dictyosome is a part of the Golgi apparatus. There is no english wikipedia for dictyosome but here is the french one


How different are tissue-specific fibroblasts from each other?

I have been told the normal fibroblasts are very similar all over the body. Is this really true?

No.

  Strong evidence indicates that fibroblasts in different parts of the body are intrinsically different, and there may be differences between them even in a single region [3].

They have morphological similarities, but they act differently (at least in cultures):

  Examination of skin and lung fibroblasts derived from the same human fetuses revealed significant in vitro differences. Fetal lung cultures had faster cell replication rates, greater [$^3H$]thymidine incorporation into DNA, higher cell numbers at confluency, smaller cell volumes, decreased cellular RNA and protein contents and lengthened in vitro life spans when compared with fetal skin cultures. In addition, these cell cultures had different responses to the addition of hydrocortisone to culture media [1].

They hardly adapt to a different serum (in vitro) [2]. Yet they have a great capacity to differentiate (in vivo):

  [...] fibroblasts also seem to be the most versatile of connective-tissue cells, displaying a remarkable capacity to differentiate into other members of the family. [...] “Mature” fibroblasts with a lesser capacity for transformation may, for example, exist side by side with “immature” fibroblasts (often called mesenchymal cells) that can develop into a variety of mature cell types [3].

References:

E.L. Schneider, Y. Mitsui, K.S. Au, S. Stuart Shorr. Tissue-specific differences in cultured human diploid fibroblasts. Experimental Cell Research. Volume 108, Issue 1, August 1977, Pages 1–6. DOI 10.1016/S0014-4827(77)80002-5
Zamansky, GLEN B., et al. "Adaptation of human diploid fibroblasts in vitro to serum from different sources." Journal of cell science 61.1 (1983): 289-297.
Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Fibroblasts and Their Transformations: The Connective-Tissue Cell Family. Available from: http://www.ncbi.nlm.nih.gov/books/NBK26889/


How does mad cow disease evade immune system?

Prions are proteins that we produced but that are misfolded and affect the folding of other proteins. As we produce these proteins, we don't recognize them as antigens. If we were to recognize our own proteins as antigens, then the immune system would constantly be fighting against ourselves. This is what is called a autoimmune disease.

While this was a simple explanation, the reality on how the immune system interact with prions might be a little more complicated. Bradford and Mabbot (2012) might be a good place to start for further learning


What is meant by the term synaptic targeting?

PSD-95 is a protein located in the post-synaptic region inside a cell. In fact it's named for this, "post synaptic density-95" referring to the dense appearance of the post synaptic area on an EM microscope and this protein's presence there.
"Synaptic targeting" in this context refers to how that protein gets to where it belongs (the synapse) in the cell, rather than just floating around in the cytoplasm by simple diffusion.


The definition of closed and open wounds is variable. In histopathological terms (i.e. looking under a microscope) it is usually defined that a wound where the dermis is affected is open. In this case an abrasion is an open wound. This puts it in the same class as cuts (incisional/lacerations), tears and punctures. Closed wounds on the other hand are when the dermis isn't affected, such as in a haematoma (blood collection under the skin) or crush injury (extreme force typically for a long period of time) and contusions (i.e. bruises).

Medically they may be divided by management. Where open wounds are wounds which are likely to be contaminated and need thorough cleaning and may need antibiotic cover whereas closed wounds are ones that are very unlikely to be. In this case, abrasions may be considered a relatively closed wound as not all the protective layers of the skin have been breached (the dermis is not completely breached). Thus the physical barriers are relatively intact and continue to offer us defense against bacteria and organisms.


Are there any known plesiomorphies of all living mammals relative to a newer trait state in all living reptiles?

The following article lists some distinctive skeletal differences in synapsids and sauropsids, and reptilia and non-reptilian amniotes:

    Sauropsida is defined as "reptiles plus all other amniotes more closely related to them than they are to mammals" (Gauthier, 1994). The characters supporting Sauropsida include the following:

  Presence of a single coronoid. Synapsids and the diadectomorph Limnoscelis have two coronoid elements. The coronoids are bones on the dorsomedial surface of the lower jaw.
  Supinator process parallel to humeral shaft and separated from it by a groove. In synapsids and diadectomorphs, the supinator process is strongly angled relative to the shaft.
  Presence of a single pedal centrale. Two centralia were present in the tarsus (ankle) of synapsids and diadectomorphs.

    Reptilia is defined as "the most recent common ancestor of extant turtles and saurians, and all of its descendants" (Gauthier et al., 1988). Characters supporting Reptilia include:

  Tabular small. The tabular (a bone on the posterolateral corner of the skull table) of early synapsids and diadectomorphs is large, but reptiles have only a small tabular, when it is present.
  Suborbital foramen present (Fig. 1B-D). The suborbital foramen is a small hole near the lateral edge of the palate, between the pterygoid, palatine, and ectopterygoid (or jugal, when the ectopterygoid is absent). This structure was not found in early synapsids and diadectomorphs (Fig. 1A).
  Supraoccipital anterior crista present. The supraoccipital of mesosaurs, synapsids, and diadectomoprhs lacks anterior parasagittal flanges. The supraoccipital of reptiles has a paired anterior parasagittal flange called an anterior crista.
  Supraoccipital plate narrow. The supraoccipital is a bone in the back of the braincase. The supraoccipital plate of mesosaurs, synapsids, and diadectomorphs is broad and extends farther laterally than the postparietal.

  Phylogeny and Classification of Amniotes, Michel Laurin and Jacques A. Gauthier


Human spine: Is the coccyx really fused?

The wikipedia article links to two papers. The first article has data for 120 pain-free and 51 affected patients with data on the number of coccygeal segments in each. We can back-calculate a reasonable approximation of segment distributions from their percentages:

1 Segment: 7%
2 Segments: 51%
3 Segments: 38%
4 segments: 4%

So 2 or 3 segments makes up almost 90% of the population. Given that only 7% of the subjects had single element coccyxes, I think it's safe to call the coccyx usually made of multiple elements.

Whether you refer to those multiple elements a single bone if largely a semantic argument. Since there is variation, it seems reasonable to call the collection 5 of variably fused terminal vertebrae the "coccyx".

As a practicing anatomist, I would say that there are 29 vertebrae, as in 29 vertebral elements (but you can't say 29 ossification centers, because each is made of multiple centers). These fuse into 24 free vertebrae, the sacrum (5 fused vertebrae) and one coccyx, which is variably fused.


To my understanding, a chromonema is the filament of DNA constituting a chromosome during interphase; its equivalent during DNA replication is chromatid. The plural of chromonema is chromonemata.

The chromatin is the form in which DNA is found within the nucleus of a eukaryotic cell, that is in complex with proteins such as histones.


There is a "anti-virus," although many call it a virophage.In 2008, a paper in Nature was published about the observations of a new strain of a virus known as Acanthamoeba polyphaga mimivirus. This virus mainly attacks amoeba. It was discovered in 1992. It was one of the biggest viruses ever found.Later, a related virus called the mamavirus was discovered. But, after observing this specimen under an electron microscope, scientist found tiny viral particles attacking the mamavirus. It was called Sputnik. The Sputnik virus hijacks the mamvirus's machinery and depends on the mamavirus to survive. It made scientists wonder if the mamavirus is a living thing.
Here is a picture of it attacking the mamavirus:

You can see small subviral particles attacking the bigger virus. That is Sputnik.
Note that it is a virus that coinfects other organisms but needs a virus infecting an organism to survive. According to Wikipedia:

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

It seems that there are more species of virophages, including one that infects the marine phagotropic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus and another one known as the Organic Lake virophage but not much detail is known about this virus.
Here is the link to the Nature article on the Sputnik virophage, published in 2008:
http://www.nature.com/nature/journal/v455/n7209/full/nature07218.html
It may be possible to synthesize one in the future. However using this to kill viruses would not make sense because the virophage technically still attacks the host of the virus it is hijacking, plus, from what I understand, it only uses the virus's machinery.
Hopefully this was helpful. If you have questions, you can comment on this answer...


Are new blood vessels able to deliver oxygen to hypoxic tissue before the establishment of blood circulation?

It is true that for long-term oxygen delivery the new vasculature must establish circulation. However, when the new vessels are starting to maturate they are filled with blood coming from the main vessel, which carries oxygen.

Since the endothelial cells of the new vessel derive most of their energy anaerobically through glycolysis (Quintero et al, 2006; Dagher et al, 2001; Krutzfeldt et al, 1990; Peter Fraisl et al, 2009), a metabolic mechanism  activated in critical microenvironments like hypoxic tissue (DeBerardinis et al, 2008), the oxygen in the lumen is free to be immediately delivered to the tissue.

Thus it is fair to assume that  at least for a short period of time the cells near to the new vessel are being oxygenated.

References:

Quintero, M., Colombo, S.L., Godfrey, A., and Moncada, S. (2006). Mitochondria as signaling organelles in the vascular endothelium. Proc. Natl. Acad. Sci. USA 103, 5379–5384.

Dagher, Z., Ruderman, N., Tornheim, K., and Ido, Y. (2001). Acute regulation of fatty acid oxidation and amp-activated protein kinase in human umbilical vein endothelial cells. Circ. Res. 88, 1276–1282.

Krutzfeldt, A., Spahr, R., Mertens, S., Siegmund, B., and Piper, H.M. (1990). Metabolism of exogenous substrates by coronary endothelial cells in culture. J. Mol. Cell. Cardiol. 22, 1393–1404.

DeBerardinis, R.J., Lum, J.J., Hatzivassiliou, G., and Thompson, C.B. (2008). The biology of cancer: metabolic reprogramming fuels cell growth and prolif- eration. Cell Metab. 7, 11–20.


Are wild cats the same species as house cats?

There are many definitions of species - look at the wikipedia page for an overview (this is a large and tricky subject). Some hybridization is not uncommon between "proper" species (often in narrow contact zones), also with fully or partially fertile hybrids. Definitions of species in these cases often comes down to genetic similarity/dissimilarity of populations. Even though hybridization is taking place it usually does so at very low rates, so the gene pools stay relatively distinct. The biological species concept (which is what you are referring to) is also problematic when it comes to e.g. ring species.

As for wild cats and domestic cats, my feeling is that modern evidence (e.g. molecular studies and phylogenies) places domesticated cats firmly as a subspecies of wild cats (Driscoll et al. 2007, 2009), with the domesticated cat as Felis silvestris catus. In the study by Driscoll et al. (2009), domesticated cats fall in the same mtDNA clade as F. silvestris lybica. However, domesticated cats were traditionally described as a separate species (by Linnaeus), and this has stuck and some still label them as separate species (as does Mammal Species of the World). I can imagine that some who argue for species status now might use a mixture of ecological, phenetic, and biological species definitions.

From Driscoll et al. (2009):

  In contrast, the world's domestic cats carried genotypes that differentiated them from all local wildcats except those from the Near East. Domestic cats show no reduction in genetic diversity compared with the wild subspecies (37), thus giving no indication for a founding genetic bottleneck. Multiple genetic analyses produced concordant results, in each case tracing the maternal origins of cat domestication to at least 5 wildcat lines (A through E, Fig. 2B) originating in the Near East. The domestic cat is referred to as a sixth subspecies, F. silvestris catus, although it is clear that domestic cats derive very recently from F. silvestris lybica (37).

   ... the vast majority of sampled domestic cats fall into the same mtDNA clade, which also includes F. silvestris lybica...

There is also evidence that hybridization can help adaptation by facilitating gene transfer (even though hybrid fertility/viability might be low), so you might want to check out e.g. results from the Heliconius Genome Consortium (2012).


What happens to H+ when Glycerate 3-Phosphate is converted to Triose Phosphate?

First off, I believe you have the production/consumption of the proton off, at least for the reaction with NADPH. Most reactions with NAD(P)H go like NADPH + H+ + (oxidized compound) --> NAD(P)+ + (reduced compound). In fact, in most reaction mechanisms the hydrogen that's actually on the NADPH is ends up covalently bonded to the reduced compound.

That said, acid-base reactions are some of the fastest reactions that can occur in the cell. The cellular environment is pH buffered, so any excess H+ ions would be rapidly taken up by the excess of buffering agents which are floating around in the cell. Likewise, when a hydrogen ion is needed in a reaction, it's pulled from the general pool of free hydrogen ions, and it is rapidly replaced from that same pool of buffering agents. As a consequence of this, it normally doesn't make much sense to talk about where hydrogen ions flow in the cell - there's just a general hydrogen ion pool which supplies and takes up any hydrogen ions that are needed/produced by the reactions in the cell.

The big exception to this is where hydrogen ion movement is restricted by things like membranes. The TCA cycle and the light-dependent reactions of photosynthesis being major examples of this. In those situations hydrogen ions are pumped across the membrane during the reaction, and there is a distinction between hydrogen ions "inside" and "outside" the membrane. But there isn't any distinction between any of the hydrogens on one particular side of the membrane.

The light independent reactions of the Calvin cycle, though, happen within the chloroplast stroma and don't pump hydrogen ions across the membrane. So the hydrogen ions generated/consumed by these reactions go into/come from the general stromal pool of hydrogen ions. Here they can be used by any reaction that requires/generates hydrogen ions - a major one of these would be the light-dependent reactions, which take hydrogen ions from the stroma and pump them to the lumen (and then release them back to capture the energy for phosphorylation). But the hydrogen atoms from the Calvin cycle enzymes aren't in any way "earmarked" for the light dependent reactions.


How does strength of a pulse related to EKG(ECG)?

Higher QRS complexes particularly in the lateral leads would suggest hypertrophy of the left ventricle. This in turn would suggest a stronger pressure is in place, although it is not known whether this is because it is required (incompetent valves) or a physiological response to exercise (where the volume is likely to actually be bigger).

Alternatively, if it really is just displacement of the brain you're interested in, why not use an EEG taken with an ECG and measure if there is a variation with each heartbeat. Then you can tease apart whether this is due to pressure or oxygenation or many other things.

Otherwise you could place something overlying the carotid which will loosely, but perhaps more accurately, reflect the pressure and one could potentially calculate the volume this way once enough other factors are known.


Is the structure of human brain white matter fixed at/near birth?

No, white matter structure is not fixed at a very early age. Although a person is born with most of the neurons they will ever have, those neurons must form connections between each other, via axons and synapses, and many of the axons become myelinated during this period. Although the number of neurons remains relatively constant, these processes lead to a substantial increase in overall brain volume. After a few years, there is then a period of synaptic pruning (https://en.wikipedia.org/wiki/Synaptic_pruning), in which many of those connections are rationalised. These processes explain many of the characteristics of human development.

For example, mammalian species can be characterised as precocial or altricial. A precocial species is one in which much of the brain's development has been completed in utero. This allows for a relatively sophisticated behavioural repertoire to be immediately available (think precocial = 'precocious'). For example, a foal is born and almost immediately is able to walk, follow its mother, and so on. Meanwhile, an altricial species like a human is born in a relatively helpless state, incapable of independent locomotion and with even very limited perceptual processes. It is the development of axonal and white matter pathways, with associated synapses, that allow learning and development of new skills in the post-natal period.

During this process, the brain is extremely flexible. For example, a baby can initially distinguish between the phonemes of any language. As its white matter connections develop in response to a lot of exposure to the language(s) in its home environment, the brain becomes more specialised. Eventually, past the pre-teen period, it becomes much harder to perceive and articulate subtle phoneme distinctions from other languages, and the acquisition of new grammars shifts from effortless and rapid, to slow and requiring formalised instruction rather than being spontaneous.

This shift to relative inflexibility reflects the second phase of white matter development (i.e. large-scale synaptic pruning). That is, in the first phase, there is widespread growth of connections between neurons via axons and synapses, along with myelination. In the second phase, the flexibility of this system is traded for the efficiency and focus of a brain that has learned what specific abilities it needs to have. This continues up until about age 10, at which stage 50% of the synapses present at age 2 have been lost (https://link.springer.com/referenceworkentry/10.1007%2F978-0-387-79061-9_2856). Learning is then no longer so rapid, but with specialisation and development, an adult is able to focus attention explicitly and maintain discipline towards achieving goals, where a child might get more easily distracted and seek novelty.

Synaptic formation and loss then continues throughout life, as the underpinning of learning processes, but no longer on the mass structural scale seen in earlier development.


I wouldn't bother trying to interpret press-release science that doesn't even contain a citation or link to the original research. However, I will try to address some of the other content of your question.

It is indeed true that many anti-anxiety medications, particularly the benzodiazepines, act primarily to increase GABAergic activity by potentiating GABA receptors.

However, it is also true that GABAergic activity is not some monolithic attribute of the brain. Different brain regions have different functions, and some brain regions are associated with behavioral or neurochemical inhibition of other regions. An increase in GABA activity in a brain region that tends to inhibit others could theoretically be anxiety-inducing rather than anxiety-calming, even if the overall effect of increasing GABAergic effects is anxiety-calming. Looking at GABA levels is also only one part of the picture, and it fails to tell you a) how often GABAergic cells are releasing neurotransmitter, and b) how sensitive post-synaptic cells are to GABA. The overall effect of GABA is going to be roughly proportional to (GABA concentration) * (how often GABA is released) * (sensitivity to GABA).

An extreme example of why this is important are the delirium tremens that occur if a severe alcoholic suddenly stops drinking alcohol. Alcohol also potentiates GABA receptors, and with long term use the brain compensates by reducing GABA production. However, this adaptation is fairly slow, and alcoholics who quickly stop drinking can have motor symptoms and seizures as a result (some other neurotransmitter systems are involved as well, though, so this is a bit of a simplification). The opposite could be true as well: it's possible that increased GABA concentrations could be because not enough GABA is being released or because postsynaptic receptors have been downregulated. It is quite possible that you could have more GABA but less GABAergic inhibition. This study didn't test levels of inhibition, just levels of GABA.

Lastly, eating GABA to make you sleep is a bit silly and is far removed from brain levels of GABA or inhibition in the brain - I am not aware of any study that shows that eating GABA makes you sleepy; companies can freely put it in a drink and make abstract claims that suggest it aids sleep, but that doesn't mean it actually does, a beverage like that isn't regulated the same way that pharmaceutical drugs are.

In summary: be very wary of attributing a complex behavioral outcome to one particular element in the brain.


Why does the refractory period of neurons only allow signals to pass in one direction?

The axon is an uniformly excitable structure; if you would stimulate an axon electrically somewhere in the middle, an action potential would be generated in both directions. Hence, an axon in itself does not have directionality.

Nonetheless, under normal physiological conditions, an axon  conveys action potentials from the dendritic region to the axon terminal, called anterograde signaling. The reverse direction, retrograde action potentials,  normally do not occur because signals arising in the dendritic region travel unidirectionally to the terminal. The reason why an action potential travels unidirectionally is because of the refractory period. Because the refractory period will cause the part of the axon that just generated an action potential to become unresponsive, the traveling action potential cannot generate another action potential in the retrograde  direction, because the only excitable region available is in the anterograde direction to the terminal (Fig. 1).

Fig. 1. Refractoriness. source: University of British Columbia

As an analogy, it's like a car driving across a road and throwing a temporary road block behind it that first has to be taken away before the road can be used again. This means that when a car leaves the parking lot and enters the road, it can never go back,  because it throws up road blocks that prevent it to return the way it came.


Can elements of one's environment act directly as hormones?

A hormone is defined as "a chemical released by a cell or a gland in one part of the body that sends out messages that affect cells in other parts of the organism" (I'm just taking Wikipedia definition).

Hormones work by binding to specific receptors present on their target cells so, if there is something in the environment that mimics the hormone, by binding to the same receptor they can act as hormones: these substances are called xenohormones and can often act as endocrine disruptors compounds (EDC), by acting on various organs in the body.

Probably the most known xenohormones are xenoestrogens that are been studied as possibly harmful for human health (e.g. linked to breast cancer), and as an environmental hazards, as they can, for instance, cause reproductive problems in fish.

Xenohormones are not necessarily bad, though. Some analogs of human hormones are used in therapy, having being synthesised specifically, for instance, to have higher potency then their natural counterparts.


What is the name of this bird from Tanzania?

That looks like a knob-billed duck.
Their range includes Sub-Saharan Africa, India, and Southeast Asia.

Picture source


What is the difference between effective and efficient selection?

You have a word problem here, not really biology.
Efficacy means "power to produce the desired result/effect"
Effective means "producing the desired result", stressing the ability to produce that result
Efficiency means "degree of being efficient"
Efficient in turn means "ability to produce desired result with little waste"
Efficacy and efficiency are not interchangeable as they have different meanings, albeit a subtle difference. You could on the other hand us efficacy and effective as synonyms, though properly the synonym of efficacy is effectivness.


Prader-Willi Syndrome and Angelman Syndrome?

Within that region, there are multiple genes.

  Although the same gene may control imprinting for both disorders, the
  gene(s) causing their phenotypes differ. AS results from
  underexpression of a single gene, UBE3A, which codes for E6-AP, a
  protein that functions to transfer small ubiquitin molecules to
  certain target proteins, to enable their degradation. The genes
  responsible for PWS are not determined, although several maternally
  imprinted genes in 15q11-q13 are known. The most likely candidate is
  SNRPN

From this paper: http://www.ncbi.nlm.nih.gov/pubmed/11180221


I have no idea how to start

You probably need an "identification key", or some kind of guide, that will help you identify the plant based on a series of questions or identification criteria.

To be able to use such keys or guides, you will need to familiarize yourself with technical vocabulary used in plant description. Some idea of the kind of ecosystem where the plant lives in would likely help too.

If the plant seems common, you will maybe find it on listings of common plants for your area.


Examples of animals with different number of chromosomes that can interbreed?

Such examples are not that rare: multiple species are polymorphic for supernumerary (B-chromosomes), others are known to show intra-specific Robertsonian polymorphism (fusions of acrocentric/separation of metacentric chromosomes).

One very well studied example, which covers both intra- and inter-specific crossings, are isopod crustaceans from the Jaera albifrons complex. They show Robertsonian variation (and additionally sometimes B-chromosomes):

different species in the same location normally have different chromosomal numbers;
on the macrogeographical level at least some species show certain gradients in chromosomal numbers;
sometimes the same variation can be observed on the level of local populations.

Hybrids between species are viable and not sterile, but rare in nature. Fecundity of hybrids is lower than that of the parental species, and this seems to serve as an additional post-zygotic mechanism of species isolation.

Crossings between specimens of the same species with different numbers of chromosomes do occur in mixed populations and are also possible for parents coming from different extremities of the above mentioned chromosomal cline. In the case of mixed populations frequency of these hetezygotes is less than expected by Hardy-Weinberg. Such offspring is fertile, and its lowered frequency is associated with higher incidence of abnormal meiosis.

On the cytological level (normal) meiosis in a heterozygote individual is remarkable in showing trivalents instead of bivalents for the polymorphic chromosomes:

(a metaphase with a trivalent in the center and two bivalents) (from Staiger & Bocquet 1956)

In addition, in four out of five species of the complex chromosomal sex determination is of the following uncommon type: males are homogametic with sex chromosomes ZZ, while females are heterogametic with ZW1W2 chromosomes. So, females normally have in total an odd number of chromosomes and in their meiosis one observes a trivalent similar to the one shown above: the metacentric Z-chromosome conjugates with the two acrocentrix W-chromosomes.

Some references available on-line:

Lécher & Prunus 1971 (in French)
Solignac 1981 (English, on isolating mechanisms in general)
Lécher et al 1995 (a review in English)
Kappas et al 2013 (a review in English - see pages 23-26)

These are highly relevant to the question, but not accessible on the web:

Lécher 1967 (Cytogénétique de l'hybridation expérimentale et naturelle chez l'Isopode Jaera (albifrons) syei Bocquet)
Lécher 1967 (Polysomie autosomique chez l'Isopode Jaera albifrons syei Bocquet)
Staiger & Bocquet 1956 (Les chromosomes de la super-espèce Jaera marina (Fabr.) et de quelques autres Janiridae (Isopodes Asellotes))


Where can I find a diagram of cortex connections?

The Human Connectome Project looks at imaging the functional pathways in the brain and might include some answers to your question:

http://www.humanconnectomeproject.org

Here is an article in Nature about the project:

https://www.nature.com/articles/mp201792


Proteins are made up of long chains of amino acids covalently joined together. The order of amino acids is the primary structure of a protein. In physiologic conditions, these long chains of amino acids fold into three dimensional shapes. The terms secondary and tertiary structure are used to refer to specific aspects of the three dimensional shape.
tl;dr what's the difference?
Both secondary and tertiary structure refer to the three-dimensional shape of a protein. Secondary structure is the regular repeating patterns, generally stabilized by hydrogen bonds between the NH and CO groups of the peptide backbone. Tertiary structure can be thought of as the way secondary structural elements fold together to create the overall shape of the protein.
Secondary structure
Secondary structure refers to regular repeating patterns stabilized by hydrogen bonding between the NH and CO groups of the peptide bond. Typically textbooks will focus on the $\alpha$-helix and the $\beta$-sheet.
Berg biochemistry has some useful diagrams demonstrating these secondary structures. The first is an $\alpha$-helix. The side-chains are represented by green balls here. Notice the orientation of the NH and CO groups, which stabilize this structure:

The $\beta$-sheet forms a very different secondary structure, but it's also stabilized by hydrogen bonding between NH and CO groups of the peptide bond.

Tertiary structure
Tertiary structure is the larger three-dimensional structure of a protein in its environment. It can be useful to think of tertiary structure as the way different secondary structural elements fold together to form the full, active protein. Notice in this figure, also from Berg, the way the elements of secondary structure (the $\alpha$-helices) fold into an overall three dimensional shape that can nicely cradle the heme group.


Can far-UVC light be safely used as germicide? (help understanding a paper)

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

There is another paper here that discusses using a similar frequency range of UVC radiation (207-222 nm) as a biocide:

  The biophysical reason is that, due to its strong absorbance in biological materials, far-UVC light does not have sufficient range to penetrate through even the outer layer (stratum corneum) on the surface of human skin, nor the outer tear layer on the outer surface of the eye, neither of which contain living cells; however, because bacteria and viruses are typically of micron or smaller dimensions, far-UVC light can still efficiently traverse and inactivate them.

Safety perhaps derives from the relatively exponential damage that far-UVC light can do to bacteria and viruses, while the layers and types of human cells that would get exposed are surface cells and mostly already dead or expendable. A 20% constant survival rate of vulnerable cells may be an acceptable trade-off, as those cells which are vulnerable would not typically be exposed (short of a wound or other exposed tissue, maybe), while the figure you cite suggests that you can raise the intensity of UV light linearly and kill exponentially more MRSA (or other disease-causing bacteria).


Are there axon branches that go up to cortex layer 1 and spread there?

Short answer: It depends on the layer.

Axons of some neurons in deep layers will project back to L1 (Brecht et al. 2003a, Oberlaender et al. 2011), but neurons of superficial layers extend their axons laterally (Brecht et al. 2003b).

Besides focusing on specific pyramidal cell sub-classes it's worth considering what proportion of inputs to L1 comes from intracolumnar or extracolumnar inputs. From the wikipedia article on the cerebral cortex:

  Layer I, the molecular layer, contains few scattered neurons and consists mainly of extensions of apical dendritic tufts of pyramidal neurons and horizontally oriented axons, as well as glial cells. [...] Inputs to the apical tufts are thought to be crucial for the ‘‘feedback interactions in the cerebral cortex involved in associative learning and attention. While it was once thought that the input to layer I came from the cortex itself, it is now realized that layer I across the cerebral cortex mantle receives substantial input from ‘‘matrix or M-type thalamus cells (in contrast to ‘‘core or C-type that go to layer IV).

Most of the inputs to layer 1 (L1) are indeed thought to come from the "non-specific" thalamus and other cortical areas, such as the primary motor cortex in the case of primary sensory areas.[citation needed] I am only aware of circumstantial evidence for the relative prevalence of thalamic inputs in L1. According to staining for different vesicular transporters of glutamate (type I is thought to label mostly cortical neurons in adult animals, type II subcortical), about half of the input to L1 is subcortical (Kubota et al. 2007). It's worth noting that the slender-tufted neurons described by Oberlaender et al. (2011) to project heavily in L1 are considered to be the main targets of the "non-specific" thalamus in the cortex (Brecht et al. 2003a). The extracolumnar origin of cortical inputs to L1 matches with the overall trend observed accross layers for the majority of inputs to come outside the cortical column (Stepanyants et al. 2009).


Are there any plants that parasitize on animals?

Yes! Here's a paper published August 2018
https://www.sciencedirect.com/science/article/pii/S0960982218308157


Why does the nerve action potential needs potassium?

The action potential is mediated by the opening of Na+ channels, which happens in the order of milliseconds (e.g., Aldrich & Stevens (1987)). Repolarization occurs through the opening of K+channels. Their opening is delayed by a few milliseconds (Purves et al., 2001) to allow Na+ to pour into the cell through Na+ channels. After that delay, the opening of K+ channels occurs also in the order of milliseconds. After these two processes are over, the membrane enters a refractory period, again on a millisecond scale. Then the membrane is ready for another action potential.

The Na+,K+-ATPase, on the other hand, has nothing to do in the action potential process as such. It operates much more sluggishly and it can by no means keep up with the rapid channel gating during action potentials. Instead, the Na+,K+-ATPase activity operates at the background to maintain the overall ion homeostasis. As an analogy, the power adapter of a laptop PC can never keep up with the processor speeds; instead, it functions in the background keeping the battery charged.

Then why two different ions? Because two different species of ions are necessary because they fulfill opposite roles in terms of polarization and reploarization.

References
- Aldrich & Stevens, J Neurosci (1987); 7(2): 418-31
- Purves et al., Reconstruction of the Action Potential. In: Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)


Telomere shortening is intrinsic to the process of replicating linear DNA (termed the end-replication problem). Adult stem cells that rapidly proliferate express the enzyme telomerase which is capable of lengthening shortened telomeres, thus allowing theoretically indefinite replication.

Further reading: Telomeres of Human Chromosomes


Why is EcoRI supplied with a unique buffer when it is allegedly 100% active in universal buffers?

Activity toward the desired substrate sequence is not the only concern in evaluating a restriction enzyme buffer system. In addition, you need to be concerned about so-called "star activity", or activity of the enzyme toward other, non-desired nucleotide sequences.

For example, NEB supplies an enzyme-specific buffer for it's standard EcoRI, even though it lists 100% activity in buffer #2 of NEB's standard buffer series. But at the very bottom of the page, there's this note: "May exhibit star activity in NEBuffer 2.1 or CutSmart Buffer."

Promega has a similar warning about it's "MULTI-CORE" buffer - even though EcoRI has 100% activity in that buffer. The MULTI-CORE buffer is not recommended due to star activity - cleavage at non-standard sites.

It's a little hidden on the product data sheet, but Thermo Scientific does have a mention of star activity in the standard "Tango" buffer, and mentions star activity with overdigestion in the standard "R" buffer. There's no warning about buffer "O", but given EcoRI's propensity toward star activity, I'm guessing this is part of why they recommend a unique buffer for routine usage. Given how frequently EcoRI is used in molecular biology, it's worth using a custom buffer to get the star activity as low as possible.

From canadianer: I contacted Thermo's technical support. Despite the fact that star activity is not listed as a concern for either 2X Tango or Buffer O in the product data for EcoRI, they say that it may actually show some star activity in these universal buffers which is why they continue to supply the unique buffer for this enzyme.


What are the appendeges behind a crane fly's wings?

They are the halteres. These structures help the flies to perceive body rotation and maintain balance.


what type of insect is this? is this a moth? (southeast asia - Malaysia)

Oleander Hawkmoth (Daphnis nerii)
Same fellow? (From oocities.org)

And a better picture from ukmoths.org.uk:

For more reading, here's a wiki article.


What is the oxygen carrying capacity of reticulocytes?

This was studied by Steve Fishbone et al and concluded that the Hb content of a Reticulocyte is slightly higher than that of a mature RBC. The CHr, which is the Hb content of a reticulocyte in CRF patients receiving Erythropoetin is around 27.5 +/- 2.5 pg

Ref: Fishbone S, et al. Reticulocyte Hemoglobin Content in the Evaluation of Iron Status of Hemodialysis Patients. Kid. Int., 1997; 52: 217-222


Is the "Manhattan Ant" a new species; still only found in Manhattan's Upper West Side?

Rob Dunn is a professor at North Carolina State University (though apparently taught at Columbia University at some point). I recall him mentioning this specific NY ant discovery to me 4-5 years ago. A better pop-sci article can be found here that suggests this discovery was circa 2012. Another related article can be found here.

You can find a few other papers regarding urban ant populations by Dunn and collaborator Amy Savage and others via Rob Dunn's website, (Ex: Savage et al. 2014 and Penick et al. 2015).

However, I could not find evidence in the few relevant papers I skimmed for the the so-called "Manhattant" or evidence of any publications formally introducing this as a new species.

Pećarević et al. 2010 ("Biodiversity on Broadway - Enigmatic Diversity of the Societies of Ants (Formicidae) on the Streets of New York City") lists a number of species found by Dunn and others in Manhattan, but again makes no mention of this specific discovery.

My conclusion is that since Dunn has not listed this as one of his many publications on his website it's either burried in another paper as an ancillary artifact, or, more likely, has not been formally described...

You could reach out to Rob directly [email | twitter], I suppose, and update us all on this question!


Where do lost membrane proteins go after exocytosis?

In the process of exocytosis materials which are about to be released are transported in small vesicles to the plasma membrane. The plasma membrane fuses with these vesicles and this sets the substances free on the outside of the cell. See the figure (from here):

The other possibility for transport vesicles is that they arrive at their target cell and either fuse with the membrane and release the transported substance into the cell or that they are taken up in another vesicle which is then targeted towards the endosome/lysosome. See the figure (from here):

It doesn't matter which way is chosen, the membrane of the vesicle is recycled either by integration into another membrane of by going through the lysosome.


This is a species of Hippobosca, looks like H. equina. There aren't too many species of this genus, so the species may be this one, which is rather common in Europe, Africa and parts of Asia - see https://www.biodiversidadvirtual.org/insectarium/Hippobosca-equina-Linnaeus-1758-img485046.html. Since you suggested it could be a tsetse fly, I assume you are in Africa. Hippobosca equina occurs in Africa as well. Other hippoboscids are not as strong fliers as Hippobosca species, which would explain its flying back to you over and over.