Is the son of a couple engaged in farming better suited to the same profession unless he receives a couple of recessive alleles from both parents?

Not everything is coded in the genome, environmental cues play a very important role in shaping who you are. Profession is just one of those things that is not encoded in genes.
Many people do not continue doing the job of their parents, but they do very well in life.
Also note that, aside from the fact that there is no "agriculture" gene, having a recessive allele does not mean you will miss a certain phenotype.
What is true is that someone who has higher education will probably be more keen to have their kids studying. On the contrary, the kids of someone who is a poor farmer and is barely able to provide for his family will probably not have the opportunity of going to school (let alone university) and therefore will continue to work the land. It has nothing to do with genetics.

  Generally there is a lot of unscientific information floating around about these matters. One of the grapevines is that it is genetically better for one to marry outside their caste to create diversity(?). Is such a thing true?

Continuing to reproduce in the same group of people will limit diversity in the genome, and create an accumulation of mutations, which is generally a bad thing. That is why it is very common to have particular illnesses in closed communities.

For instance Amish people have an higher incidence of genetic disorders such as Ellis-van Creveld syndrome (a form of dwarfism)

From The Gene for the Ellis–van Creveld Syndrome Is Located on Chromosome 4p16 - Ruiz-Perez et al., Nat. Genetics 2000

  Autosomal recessive transmission of the disorder is supported by
  multiple affected siblings with unaffected parents in families with
  known parental consanguinity. The largest known pedigree segregating
  with EVC is that reported by McKusick and his colleagues in the Old
  Order Amish (McKusick et al., 1964). The prevalence of living persons
  affected with EVC among the Lancaster County Amish was estimated to be
  2 in 1000, whereas the frequency of occurrence among live births was 5
  in 1000. McKusick et al. estimated that the frequency of heterozygous
  carriers in the Old Order Amish is as high as 13% (McKusick et al.,
  1964). All cases of EVC in the Amish at that time were traced to a
  common founding couple, Samuel King and his wife, who immigrated to
  Pennsylvania in 1744.

This is a well known effect, called the founder effect.

As for India, a study on the genetic behind casts has been done a couple of years ago.

Reconstructing Indian Population History - Reich et al., Nature 2010

From the paper:

  Haldane wrote 45 years ago that “if inter-caste marriages in India become common, various… recessive characters will become rarer”. However, it has not been generally appreciated that this applies to groups throughout India, and not only to groups in the south where consanguinity is common. We hypothesize that founder effects are responsible for an even higher burden of recessive diseases in India than consanguinity.
  To test this hypothesis, we used our data to estimate the probability that two alleles from a group share a common ancestor more recently than that group’s divergence from other Indians, and compared this to the probability that an individual’s two alleles share an ancestor in the last few generations due to consanguinity. Nine of the 15 Indian groups for which we could make this assessment had a higher probability of recessive disease due to founder events than to consanguinity, including all the Indo-European speaking groups.
  An additional reason why some diseases are expected to occur at elevated frequencies in India is shared descent from a common Indian ancestral population. An example is a 25 base pair deletion in MYBPC3 that increases heart failure risk by about 7-fold, and occurs at around 4% throughout India but is nearly absent elsewhere.

They conclude that:

  We have documented a high level of population substructure in India, and have shown that the model of mixture between two ancestral populations ASI and ANI provides an excellent description of genetic variation in many Indian groups.
  [...]
  By showing that a large proportion of Indian groups descend from strong founder events, these results highlight the importance of identifying recessive diseases in these groups and mapping causal genes.

It is very important to understand that this results in no way show a genetic basis for the existence of casts, which remain purely social entities. They rather show that an environmental constraint can influence the distribution of genetic traits, due to a restriction in the possibility of mixing genes in the population.


Why do Indian Major Carps spawn in running water?

Some fish spawn in running water for a simple reason: There eggs need oxygen and survival rate will be low under hypoxic conditions. Running water has a much lower change of becoming hypoxic than standing water, so that is why many fish spawn in running water. Some fish of standing water, like sticklebacks, wave fresh water over the eggs to achieve the same.

How they sense oxygen level is another matter. In fish, the neuroepithelial cells (NEC) have been implicated as the major oxygen sensing cells. See wikipedia above and specifically this if.you want to know more.


Can you use images taken at different exposure times in western blot image analysis?

Generally no, you can't directly compare them and you can't easily compare across gels. I have done many hundreds of western blots, a large proportion of which were for quantitation, and in general quantitation on western blots is difficult (because of inconsistency run to run) and not highly quantitative - a 2-fold change is detectable and probably real, but a 10% change - unlikely to be real.
If you want a real example of how to compare and observe this (works with the Bio-Rad system or others where the transfer is in the same space) - run exactly the same amount of protein on two identical gels, place them both into the same transfer tank. Compare protein stain on the membranes after transfer. The one closest to the black terminal will have stronger staining = better transfer.
However, what you can do is convert the numbers you get into a relative expression on each of the blots and then use those numbers for comparison.
For example you compare expression of protein X to a normalizer (often B-Actin) and get fold-change data out of that, or you can compare Sample X untreated to treatments A, B, C and get data out that way.


What is the difference between rheobase and threshold?

Excellent question! The difference is the fact that the rheobase is an example of a threshold measure. The threshold, as you correctly suggest, is the minimal energy (typically current level and not voltage as you suggest) to excite neural tissue. The threshold applies only under the specific experimental parameter settings used. These parameters include the type of electric stimulus (for example, a biphasic current pulse), the electrode configuration (for example, bipolar stimulation) and the stimulus duration (for example 200 microseconds).

The rheobase is the minimal current level needed to excite a tissue when an infinitely long stimulus would be applied. The rheobase is typically found by plotting the threshold level (as defined above) as a function of stimulus duration. The reason for developing this measure is the fact that excitable membranes integrate the injected current, so charge builds up in the tissue. In other words, increasing the pulse duration decreases the threshold current level needed. Hence, the rheobase is a convenient threshold measure because it incorporates the duration parameter of the stimulus. It will still depend on things like electrode configuration and stimulus shape.

The function of the strength-duration relationship can be fitted with a decaying exponential:

I = Ith / ( 1-e(-t/Tsd) )

where I= Threshold current level;
Irh = rheobase
t = stimulus duration
Tsd = Tau = exponential

Here is a picture of a theoretical strength-duration curve copied from the wiki page on rheobase. [NB: I find the wiki page needlessly complicated].

The rheobase is the horizontal asymptote. An often used parameter to characterize the function is chronaxie, which is the pulse duration equivalent to two times the rheobase.

The explanation given here was adapted from the book "Cochlear Implants", chapter 5 "Biophysics and Physiology" by Abbas and Miller, two veterans in cochlear implant electrophysiology. Unfortunately I cannot give you a link to the pdf as I own the work in hard copy.


Which of the three is true for insulin receptors?

Signal recognition particle (SRP) receptor, also called docking protein, is a dimer composed of 2 different subunits that are associated exclusively with the rough ER in mammalian cells. The surface of the rough endoplasmic reticulum (often abbreviated RER or Rough ER) (also called granular endoplasmic reticulum) is studded with protein-manufacturing ribosomes giving it a "rough" appearance. so i don't think (3) is the right statement.
the insulin receptors is made up of two hormones, insulin and glucagon, are at the center of this signaling system. there is no such things as hydrophobic sequence in the middle of the protein i believe.
also, Insulin is a peptide hormone produced by beta cells of the pancreatic islets and and insulin receptors doesn't have an hydrophobic signal peptide. so i think (1) is the correct answer.
Edit :
https://en.wikipedia.org/wiki/Signal_recognition_particle_receptor
https://www.healthline.com/health/type-2-diabetes/insulin#Function1
www.news-medical.net/health/What-is-Insulin.aspx


Why don't the genetic similarities between ‘unrelated’ individuals of the same and different species outweigh the differences?

Relatedness measures a specific type of genetic similarity. In particular, it measures the genetic similarity relative to the rest of the population. When $r>0$, the recipient carries the actor's genes at a higher frequency than the population. When $r=0$ it doesn't mean that the actor and the recipient do not share genes; it only says that the recipient carries the genes of the actor at the same frequency as the population.


A tool to get annotation features by position in the reference genome

Well, after 2 weeks and several thousand lines of code I got a demo-version of my revamped annotator up and running, but then I was told to take a look at SnpEff. The tool makes everything I was to implement in my own one, so if anyone ever wants to annotate SNPs with regard to genomic features they hit and possible effects, give SnpEff a try. It's really fast.


Is there a surface or body cavity that does not have epithelium?

Short answer
Edit with credits to anongoodnurse: As far as I know, every bodily surface and cavity is covered by epithelia.

Background
Epithelial tissue is a sheet of cells that covers a body surface or lines a body cavity. There are two types of epithelium in the human body:

Covering and lining epithelium forms the outer layer of the skin; lines open cavities of the digestive and respiratory systems; covers the walls of organs of the closed ventral body cavity.
Glandular epithelium surrounds glandular tissue.

Hence, the entire the bodily surface is covered by some sort of epithelium. Even the eye is covered with squamous epithelia (thanks to anongoodnurse for pointing this out).

And while acknowledging that an absence of evidence is not evidence of absence, I believe that there is no surface on, or cavity in the body not lined with epithelium.

Fig. 1. Epithelial lining of bodily surfaces. source: Ternopil State Medical University


You are probably referring to the process of phagocytosis, where macrophages engulf a pathogen by trapping it inside a vesicle called "phagosome", which then fuses with a lysosome, resulting in the digestion and disposal of the pathogen.

But in fact all eukaryotic cells have lysosomes. This is of course biology we are talking about, so there are many subclasses, different names, specializations and exceptions to the rule.

In plant and fungal cells, we find vacuoles, which serve a similar function as lysosomes in animal cells. There are also "lysosome-related organelles" with specialized functions in specific cell types (Marks et al. 2014).

The main role of lysosomes has been described in the recycling of macromolecular material. Their lumen has a low pH level (below 5) and contains a lot of enzymes specialized in degradation of e.g. proteins, nucleic acids etc. They can digest cellular waste products and material taken up by endocytosis. Nutrients can be reabsorbed into the cytoplasm.
Furthermore, research has proposed additional roles in nutrient sensing and metabolic homeostasis (Perera and Zoncu 2016).

That lysosomes play a crucial role in many cell types can also be seen in lysosomal diseases, which often result in severe effects in multiple organs (Ballabio and Gieselmann 2009, Saftig and Klumpermann 2009). In these diseases, lysosomes fail to degrade their targets, which impairs their ability to clean out cellular waste.

Here is a summary from the book "The Cell".


Does cocaine bind competitively or non competitively to DAT?

Cocaine binds competitively to DAT, though not in precisely the same binding site, rather there is overlap, and many of the same amino acids are involved in binding of each.

Amphetamine and benztropines also bind in the same region.

Beuming, T., Kniazeff, J., Bergmann, M. L., Shi, L., Gracia, L., Raniszewska, K., ... & Loland, C. J. (2008). The binding sites for cocaine and dopamine in the dopamine transporter overlap. Nature neuroscience, 11(7), 780-789.


Why do house geckos take so long to react?

This is entirely behavioral and is quite widespread.

If they ran away everything something large passed by they would waste a lot of energy, many animals wait first to see if you are just moving through, and thus can be ignored, OR if you are going to hang around and thus are a potential threat (and in the case of camouflaged organisms have a much higher chance of spotting them).

It is seen in many animals gazelle are known for it for instance.  This paper on the behavior in other lizards should help with understanding the evolutionary pressures behind it.


What is the conical mouthpart of a soldier termite and what does it do?

This is actually the termite's labrum. Its quite big in termites. Does not have value in telling male from female.


Trying to answer this question in a few lines is a tedious task. Mostly I'm not sure that as of today we know all there is to know about it.

I'll try to give you some hints though.

The process is called embryogenesis. The zygote (or ovum) undergoes rapid mitotic divisions with no significant size growth which will lead to the development of an embryo. This process is called cleavage. Blastomeres are created during this process. On the third day - time may vary but not significantly - cleavage reaches the state of 16 cells. Cell divisions always occurs by parallel division (1 -> 2, 2 -> 4, 4 -> 8, 8 -> 16). Study the links I gave you and come back with more specific questions.
Again that's kind of impossible question to answer without explaining the entire process from fertilization to fetal development, because creation of tissues (cells) and organs happens along the way, not at once. However, it's documented.
Not sure.
Start with the wikipedia links and try to come back with more specific questions. I have a couple of text-books but I'm afraid they are not as detailed as you would want :-)

Good luck!


Does focusing on a certain part of the body increase electrical activity in that region?

Gut reaction, I don't think this is a solid thesis idea. If you attach an EMG to my finger, and then I concentrate on my finger, and then my finger moves (due to stray thoughts), there will of course be a whole bunch of action potentials firing. However, that's kind of trivial and not really that interesting.

If your theme is "weird EM effects in the human body", one possible decent idea (and one that's gotten some quantity of buzz in the recent past) would be to focus on the role of electric fields in wound healing. You could even add in an intentionality/focus angle, if you really wanted to.


Why does an autoclave need to pressurize steam?

An autoclave can sterilize both solids and liquids, whereas an oven with no pressure control is typically not suitable to sterilize liquids.

Not only do you need to heat the chamber to 121°C, but you also need to make sure that the things you are trying to sterilize are not degraded by the treatment.

For dry objects (e.g. glassware) you could heat the chamber up to 121°C at ambient pressure. In that case, the instrument you're using is called a "dry heat sterilizer" rather than an "autoclave" (REF)

So why use an autoclave at all, and not just a dry heat sterilizer? Quite often the things you would put in an autoclave are water-based solutions (for example, LB broth or buffers).
If you do not increase the pressure and try to heat to 121°C, the liquid in your bottles will first boil around 100°C until all the aqueous solvent is in the gas state (i.e. your solutions are going to evaporate) and then the temperature will increase to 121°C. However if the pressure is raised to stay at the liquid-gas phase transition, then the gas and the liquid are in equilibrium, therefore you neither lose or gain any volume in your solution.

So in theory, if you autoclave 1L of medium, then you get 1L back at the end. Note that in real life, the temperature and pressure of the autoclave are set based on the diagram for water, but for concentrated solutions these settings may be slightly off, meaning that the volume in the bottle at the end of the cycle is sometimes a little different from what you put in there at the beginning. See this illustrative diagram of how a solution behaves differently from the pure solvent:

(Copyright: Lumen Learning)


What are the benefits of elucidating the crystal structure of a protein?

Protein structures, which can be obtained from protein crystals or from concentrated solutions of pure protein via NMR, are arguably the primary source of knowledge that we have about how genes perform their function on the molecular level.

I've added a link to RCSB.org above - they write up a story on an important protein structure monthly(?) - its a great way to pick up some fascinating stories.

The precise atomic positions from a protein structure are indispensible for several reasons.  Since biological processes are all fundamentally chemical ones.  The specific positions of the atoms reveal how proteins, nucleotides, lipids, drugs and other biological molecules specifically interact.

Examples:

Protein structures broke the ground in biological inheritance (Watson / Crick / Franklin's DNA structure)
Protein structures of lysozyme and proteases were the first to show exactly how proteins bind their substrates and enzymatically catalyze chemical reactions.
Protein structure of hemoglobin in both oxy- and deoxy- forms (i.e. with and without oxygen bound). showed that proteins change their spatial arrangement to modulate their function.

This list goes on to more recent breakthroughs in how signals and molecules interact with the cell through the membrane.  There is literally no topic in cellular biology which has not substantially benefitted from having a protein structure revealed.

The advantages of working with protein crystals are that they can be larger proteins and certain kinds of difference experiments an be more easily performed when a protein crystal is obtained.  For instance if you have a crystal of a 100 kDa (~900 amino acid) protein, you can often find the binding pocket of the enzyme without a tremendous amount of work.

The disadvantage of working with protein crystals, as you probably know well is that getting crystals is often a quixotic effort soaking up months or years, often with little or no results.  Pretty demoralizing until you hit the target.

If you're astounded to think that proteins, which are often hundreds or thousands of times larger than a salt or mineral you usually find in crystals...you are dead on.  The crystals are often very tiny - a decent sized crystal measures about a millimeter on one side, but often are only a fraction of that size.  That's why protein crystals often are taken to synchrotrons, linear accellerators or other free electron X-ray sources which are millions (?) of times more intense than a dental x-ray. I would guess that most protein crystal structures are obtained using special beamlines created especially for biological crystallography.

That sort of tells you the funding priority science is willing to put into x-ray protein crystal structures.  Simply the idea that protein crystals might be easier to grow in microgravity (along with the low weight of the experiment) justified over a decade of protein crystal growth experiments on the shuttle and ISS.

Interesting note: The Guardian (which is based in the UK where crystallography, protein or otherwise started out) has posted a short video outlining highlights of crystallography's contributions over the past 100 years.  If you watch assiduously you will see protein crystallography cropping up with a litany of nobel prizes.

New thoughts:
There are signs that crystal structures are coming to an end.  Using an electron micrograph to simply take a picture of many thousands of individual proteins laying about can be digitally averaged to create low resolution structures they are gradually becoming higher resolution and are a lot less work than preparing and making a protein crystal - and it works well on larger proteins and protein complexes!


Resting membrane potential: K+ concentrations and charges on inside and outside of the neuron

Why is the interior negative despite the fact that there are more K+ ions inside than outside, and (2) What exactly causes the net negative charge?

It's because K+ isn't the only player in the game. Yes, there is a bigger concentration of K+ inside of the cell, however, there is also a higher concentration of Na+ outside of the cell, and also, there are other charged ions, such as Cl- or proteins.

One of the main reasons for the gradient is Na+/K+ ATPase, which transports 2 K+ ions to the inside of the cell, while 3 Na+ ions are pumped to the exterior of the cell. This generally yields in a higher concentration of + charge on the outside of the cell.

The final membrane potential depends on the permeability of the membrane to these ions. Higher the permeability for an ion, the closer is the actual potential to the equilibrium potential of this ion. (you can read about its calculation here.). Since the membrane in a normal state is not permeable to Na+ to a big extent, but is permeable to K+, the resting potential is similar to the equilibrium potential for K+, which is negative (the actual value depends on the specific cell type, generally we can say -70mV in neurons). (The K+ is driven to exit the cell because of the chemical and electrical gradient, which results in negative charge inside of the cell). The approximation of final potential can be calculated by using Goldman equation.

The principle is therefore in selective opening and closing of specific ion channels and functioning of transmembrane pumps.


Are prosauropods ancestors of all sauropods?

Welcome to Biology.SE! Your daughter asks interesting questions!

The question is debated. It is currently mostly thought that sauropods and pro-sauropods are sister lineages and therefore, one does not contain the other. In other words, the pro-sauropods are no more the ancestors of the sauropods than were the mammals are the dogs are the ancestors to the cats.

One of the most updated source of information for phylogenetic questions of the kind is tolweb.org. You should have a look. Here is the page for the Sauropodomorpha (which contains the sauropods and the pro-sauropods). You have a nice list of reference on this page including some from Sereno, who is the author who first defined the pro-sauropods.

I quickly sought through the literature. It seems indeed that all phylogenetic analysis were based on phenotypic comparisons and not on genetic comparisons. Citing from wikipedia:

  Evidence against sauropod ancestry within Prosauropoda comes from the fact that prosauropods had a smaller outer toe on their hind feet than the sauropods. Many maintain that it is easier for digits to be reduced or lost during evolution than the reverse, however there is no evidence for this. The lengthening, or gaining of extra digits is common in marine reptiles, and within the theropods digit lengthening occurred at least once. Therefore, using this as evidence against ancestral prosauropods is questionable.


As you have phrased it, the question can be understood in two ways.

The population size at t+1 is 350, after births, deaths and migration have taken place.
The population size is 350 after deaths, but you also have to take births and migration into account to calculate population size at t+1

For alternative 1 the growth rate is:

$pgr = \frac{(230+21)-(488+13)}{600} = -0.417$,

with $\Delta N=-250 \Rightarrow -250 = 230+21-deaths-13$

For alternative 2 the growth rate is:

$pgr = \frac{(230+21)-(250+13)}{600} = -0.02$


Let's firstly differentiate deafness - profoundly impaired ability to hear, and other states where the subjects can still hear at different degrees.

Secondly, differentiate the congenital deafness & infantile hearing loss and hearing loss in adults who previously had normal hearing.

The subjects with congenital and very early infantile hearing loss would have better sleep characteristics (this state will affect psychological state in a lesser degree than one acquired in more mature & "conscious" state), while persons who have lost their normal hearing would have abnormal sleep patterns at least in the period when they have just realized that they are going to lose their hearing. After this "preliminary" period, the sleep pattern should be dependent on the person's psychological status and other similar factors.

Many persons will mention that while using ear plugs they feel that their sleep is better comparing with "un-plugged" sleep.

sources

Characteristics of sleep in deafness. Rev Neurol. 1998 Jun;26(154).
Non-scientific source.

Please pay attention that scientific sources are scarce, thus take the answer as one of limited evidence.


Nanodrop may be fine for the volumes but as you rightly guessed it is not so easy to distinguish DNA from RNA (and primers). Qubit (invitrogen) is a sensitive, dye based quantification assay. You can use that for estimating cDNA yield. The kit contains different dyes for DNA, RNA and protein estimation.


Why have a placebo control group when testing a new drug if existing drugs can be used?

You are correct. For serious diseases, it would be unethical to withhold the existing treatment (Treatment A) for a placebo. Treatment A is called "standard of care", and new treatments are compared to this.


Why are there so many different humans yet chimpanzees are just chimpanzees?

For fossils the answer is simple chimps live in forests and forest are really bad at preserving fossils, we lived in savannah which include some floodplains which are really good at preserving fossils. Thus we find a lot more human fossils than chimp fossils.

Otherwise Chimps exhibit far more genetic diversity than humans. humans are just a weird branch of chimp.consider the genetic diversity below. If we were not so  morphologically biased we sould easily conclude all hominids as just one species based on genetics.Chimps actually have quite a wide morphological variation its just we as humans are far better at noticing human variation.


I think you are looking at other the wrong way around. There is no critical light period, there is a critical dark period. That long-day flower is also a short-night flower. As long as there is never any period of darkness that exceeds the critical dark period, it will flower.

In that second picture at the bottom, exactly that is the case. The dark period is not long enough to prevent the flowering.

And in the bottom example of the first picture, there is no uninterrupted dark period longer than the critical dark period, so the plant never flowers.


Does the brain process sound in "clips" or "frames"?

In your question, you ask about processing and sampling. I'd like to make a distinction between sampling, which in my view does not have a framerate, and perception which there is some evidence that there is sort of a framerate (though not as concrete as the framerate of a video display, for example). Processing is everything in between, and as such, whether it shows "framerate-like" behavior depends on the stage of processing.

Does vision really have a framerate?

The "framerate" depicted in those sources for vision is sort of a special case, talking about perception of a particular stimulus. There are no real "frames" in your vision, only temporal averaging (because phototransduction is quite slow on the timescale of neural processing in general). The article you link makes a mistake in logic in concluding that humans have a frame rate: the research they cite is about discriminating between separate flashes, which is an issue of temporal averaging rather than framerate. There is a separate issue, which is whether perception correlates with particular oscillatory frequencies; I'll get to this later in my answer.

If you flash a very bright 1 ms light, and record it with a video camera, you will often miss the light entirely (or it may appear only in part of the image, depending on the scanning pattern of the camera). With vision, though, you will always see the light, and for very brief flashes you will perceive changes in duration as changes in intensity.

The other contributor is the "magic" of perception: effectively, what you perceive is not directly the signals that come in through your eyes but rather the model your brain makes for the world based on that information. This process is the origin of all perceptual illusions; the appearance of "backward" images like with a spinning wheel is one example.

Our current model for how processing of sensory stimuli works in the brain is that there is a functional hierarchy with significant abstraction at higher levels of the hierarchy. As you get to higher order levels of processing, you will cease to see the "pixel information" and simple edge/feature detection, and begin to see more abstract representations like detection of particular visual objects or encoding of object velocity.

Okay but the question is about auditory stuff..

It's easiest to start with vision simply because, for better or worse, it is best studied historically. For auditory processing, there are a lot of similarities with vision even though the input stimuli start very different. At low levels of processing, auditory neurons are well described by spectro-temporal receptive fields. At higher levels of processing, you will instead see representations of whole features in sounds, such as phonemes.

Object segmentation is a very difficult problem in both vision and hearing (and a difficult task for computer/AI-based versions of those senses, as well). This is definitely an active field of research, but there is good evidence that some segmentation is present throughout the cortical hierarchy (for example, see here). There are no concrete answers for 'how' exactly segmentation works, just that it does, some evidence for where it might be happening, and some understanding of factors that make it harder to segment different sources. Sound localization is certainly one of the key factors, though segmentation can occur even when there are no localization cues. For example, if you have multiple speakers on the radio, or multiple musical instruments playing, there are some shared spectral characteristics of the speakers or instruments

Discrete signals in cortex

All that said, this does not mean that the brain is free from any discrete elements of processing (like "frames"), although it probably doesn't make sense to think of a frame rate but rather a type of "threading". There is recent strong evidence that activity in the neocortex can be organized into packets of activity that contain sensory or other information. So even though the auditory stream is sampled continuously, that continuous sample is most likely distilled into discrete auditory objects that reflect both the content and source of those stimuli.


What is the purpose of using two layers of gel in SDS- PAGE?

The stacking gel concentrates proteins loaded into the sample wells so that they are resolved as a unified "line" once they enter the stacking gel.  The reason for the lower pH is that this "lower ionic strength implies higher electrical resistance and consequently a higher electric field, provoking the faster movement of the proteins and of every other charged particle in the gel. Such a high electric field coupled with the glycine in the running buffer (that will not go into the resolving gel due to the pH), helps to clean the sample from the Cl- ions from the Tris-HCl buffer. That concludes in a stack of clean, denatured, and equally charged proteins in the boundary with the resolving gel; this will account for a good quality PAGE."

Bassically, in the stacking gel the pore size is larger so it gives a chance for the larger proteins and smaller proteins to equalize with each other.

"As the proteins are denatured and linearized by heating, SDS and dithiothreitol (if there is any di-sulfide bond), the proteins are loaded onto the wells on the stacking gel. The denatured proteins have a uniform mass to negative charge ratio. Since the current run from negative (top) to positive (bottom), the proteins move toward the bottom. When the electricity is turned on, the proteins and Tris-glycine enter the stacking gel. In stacking gel with pH 6.8, the N-terminal amino group of the proteins and amino acids are protonated at equilibrium which makes them less negative. The average electrophoretic mobility is very slow. A Gly-chloride ion boundary is formed since glycine moves slower than chloride ion. However, glycine still runs slightly faster than other proteins. As a result, the glycine keeps pushing the protein towards the chloride ion. In other words, the proteins are trapped between glycine and chloride ion. The proteins form a very tight band inside the stacking gel.

Once the protein reaches the resolving gel, the pH changes from 6.8 to 8.8 and the pores are smaller. As pH increases, the N-terminal amino groups are deprotonated. Amino acids and proteins are more negatively charged at equilibrium than in stacking gel. As a result, glycine moves faster than proteins. Glycine and chloride ions move ahead of the proteins. As the pores are smaller in the resolving gel, the size of the protein determines the mobility (speed). So the smaller the protein is, the faster it will reach the bottom."

SDS-PAGE stacking gel


Why doesn't water enter my body through my anus or genitals when swimming?

For the same reason that when you urinate or use the toilet, you have to exert pressure and urine or faeces just does not simply leak out when you stand up. The urethra seals shut when the urethral sphincter muscles relax. Similarly Sphincter ani externus muscle seals shut in the anal canal when there is no antagonistic force. So water can't just simply enter our body in such huge quantities that we die. It is possible to get more water through your anus with some pressure which is what happens when you get an enema.


How long does immunity to influenza last when contracting the disease vs vaccination

The effect on adaptive immunity are often stronger when contracting the flu than for getting the flu vaccination. The backside of this is that the flu is a quite dangerous disease which could end fatally, so getting the vaccine is always preferrable.

Getting infected by a specific flu strain (or receive a vaccination against it) generates specific immunity against this strain. If it mutates to strong or you get infected with another strain, you will have no immunity (and will have to develop a new immune response.

It seems that immunity against the flu can be livelong (against this strain) after you went through an infection and survived it. There are two studies showing long term response against antigens from the 1918 flu pandemic. The first (summarized in reference 1, the original article is reference 2) shows specific antibodies against the reconstructed haemagglutinin protein (H1) from the 1918 virus strain.

Serum from people born 1915 or before showed specific activity against this virus antigen, even more than 90 years after the infection.

The second study analyzes cross-reactivity of antibodies against the 2009 A/H1N1 pandemic flu strain. Here the cross reactivity of people born before 1930 was the highest - the 1918 strain (with which these people most likely had contact) was also a H1N1 virus. Although these viruses mutated between 1918 und 2009, there is still enough similarity that they are recognized by H1N1 specific antibodies (see reference 2).

A study which compared antibodies responses of people who contracted the 2009 flu against people who where vaccinated against it, showed that the antibody response was more longlasting in the people who got the infection (see reference 3).

So I think it is safe to say that the immune response is stronger after the infection compared to the vaccination, but the vaccination is much safer.

References:

How Long Does Flu Immunity Last?
Neutralizing antibodies derived from the B cells of 1918 influenza
pandemic survivors
Antibody Dynamics of 2009 Influenza A (H1N1) Virus in Infected
Patients and Vaccinated People in China


What is the number of DNA strands per cell?

Human cells contain 23 pairs of chromosomes (46 chromosomes in total).
Each chromosome is formed by 2 strands of DNA tied by hydrogen-bonds to each other making the classic  DNA double helix (double-stranded DNA). So, in total there are 46*2=92 strands of DNA in each diploid human cell! Gametes contain half of the chromosomes, so half of the strands as well.


Deep inhalation and deep exhalation are informal terms and cannot be defined by lung volumes, because saying deep by itself does not tell how deep.

In the first part of the question deep refers to maximal:

Deep inhalation that means inhaling the air with effort as much as possible = maximal inhalation
Deep exhalation that means exhaling the air with effort as much as possible = maximal exhalation

According to Physiology, Residual Volume (StatPerls):

The volume of air in the lungs after maximal expiration is called residual volume (RV).

  Residual volume (RV) is the volume of air that remains in the lungs
  after maximum forceful expiration. In other words, it is the volume of
  air that cannot be expelled from the lungs. This volume remains
  unchanged regardless of the lung volume at which expiration was
  started.

The volume of air in the lungs after maximal inspiration is called total lung capacity (TLC).

  TLC is the total volume of the lungs at maximal inspiration.

According to Merriam-Webster dictionary:

Expiratory reserve volume = the additional amount of air that can be expired from the lungs by determined effort after normal expiration.

Inspiratory reserve volume = the maximal amount of additional air that can be drawn into the lungs by determined effort after normal inspiration.

Lung volumes:

Image source: Wikipedia, Creative Commons License


Are facial 'cleansing' products 'effective' on human skin, and if so, what is their mechanism of action?

Do facial cleansing products actually do what they claim?

This dermatologist-tested cleansing gel formula lathers into a bubbly foam removing surface dirt, oil and makeup, while energizing exfoliators sweep away dead skin cells.

So essentially, they are claiming that it is a foaming soap.
Sodium Laureth Sulfate is a detergent, Lauryl glucoside is a surfactant, so it is a good bet that the product is effective as soap. There are a bunch of other compounds that modify how it forms films, so it probably also foams.
If so, what is their mechanism of action (i.e., how do the ingredients work)?
Similar to any other soap.  They make non-water soluble things on the surface of you skin (such as oil, make up, dead skin cells, etc) more water soluble so that it dissolves when you wash your face.
Some of the other you linked also have moisturizers, so they probably put another oil back in the place of the ones you removed to keep the skin from getting too dry.

I am unsure if any of these terms are reflective of a real problem, or if the products can even even help said issues.

Or do they work better than normal soap of comparable strength?  Probably not much, although having them labeled as use for your face is nice in that you have a reasonable idea that it won't be too harsh or irritating, whereas if you tried dish soap on your face that might not go so well.


Can the sulphur content of biological material be reliably calculated from fat, fibre and protein contents (Weender Analysis)?

I would say theoretically yes, if you know lots of other information, but practically no, because of all the unknowns.

According to this paper cysteine content and therefore sulfur content of proteins vary depending on what kind of organism your organic material is coming from. Animals have more, bacteria tend to have less.

The sulfur content as a fraction of protein content in a given animal or plant is constant or nearly constant across the entire animal/plant. If a sample's protein content is 50:50 corn protein:sheep protein it's possible to estimate the sulfur content of the protein fraction from the sulfur contents of the sources of the protein.

In addition the sulfur content can be affected by fermentation and sulfur/sulfate-reducing bacteria, many but not all of which are anaerobes. So figures for whatever the source of the feedstock is (as far as cysteine content) can be affected by whatever happens to it afterwards. Chicken waste with a high sulfur content allowed to ferment may give off fairly large amounts of hydrogen sulfide, lowing the sulfur content without necessarily affecting the bulk protein content. The reverse might also happen, where protein is digested and sulfur is released as sulfates but kept in the mixture.

Even if you know for certain the sources of all of the protein(and that no further biological activity has changed them), the unknown amount of organic acids is going to throw off your sulfur estimates if there are sulfur-containing organic acids in the N-free fraction.


What is the efficacy of an Ebola antibody response

Although there are a handful of papers suggesting that antibodies can enhance Ebola infection, in practice Ebola vaccines seem to be highly effective both in animal models (e.g. Aerosolized Ebola vaccine protects primates and elicits lung-resident T cell responses, VSV-EBOV rapidly protects macaques against infection with the 2014/15 Ebola virus outbreak strain, Vaccination With a Highly Attenuated Recombinant Vesicular Stomatitis Virus Vector Protects Against Challenge With a Lethal Dose of Ebola Virus) and, probably, in humans (Efficacy and effectiveness of an rVSV-vectored vaccine expressing Ebola surface glycoprotein: interim results from the Guinea ring vaccination cluster-randomised trial).

If antibodies can enhance infection, how could vaccines protect?  That's not as contradictory as it sounds.  In general, antibody-mediated enhancement of infection only works under specific conditions.  Even with Dengue, the poster child for ADE, it only occurs during a specific window of antibody titers and affinities.  Ebola is probably much less adapted to needing ADE than Dengue, so it's likely that you'd only get ADE in a very narrow range of antibody titers, affinities, and perhaps targets.  So if vaccines induce high titers, high affinities, and/or a particular set of antigenic targets, ADE may never kick in -- it may be a lab curiosity that isn't relevant in the real world.

(Alternatively, it may be an issue down the road, say if vaccine-induced immunity fades in a specific way that allows it. I don't know of any evidence suggesting this would happen, but I'm not an Ebola researcher.)


Enzyme kinetics; what happens at the peak of the Gibbs energy graph?

Enzymes are catalysts that lower a reactions activation energy (Ea), and thus increases the rate of the reaction. The diagram above is a Gibbs-Free energy landscape/pathway, where the top of the diagram is the transition state between the substrate and the product. Enzymes speed up chemical reactions by stabilising the transition state, and in effect, lowers the activation energy (Ea) required to transform the substrate into the product. The active site of enzymes are thus specifically 'designed' to be as energetically favourable as possible for the transition state.

To understand enzyme kinetics it could also be a good idea to look at (understand on a general level) the Arrhenius equation and reaction rate constants (k), to more completely understand what we mean by activation energy and reactions rate.
This whole topic is taught in basic biochemistry, and thus well described by many educational websites, all biochemistry text books, and even found in  educational youtube lectures (which is perfect for a basic understanding before you read more heavy theory). My earlier biology SE question Enzyme kinetics: recommended literature to grasp the concepts better also has some good book recommendations.
Following are also some webpages you can look at.
Khan Academy:

With the catalyst, the activation energy is lower than without. ...
That's because enzymes don't affect the free energy of the reactants
or products. Instead, enzymes lower the energy of the transition
state, an unstable state that products must pass through in order to
become reactant (...)

Chemistry LibreTexts: General transition state stabilisation is also a nice keyword that would give you a lot of information, e.g. from Chemistry LibreTexts:

Linus Pauling postulated long ago that the only thing that a catalyst
must do is bind the transition state more tightly than the substrate.
That this must be the case can be seen from the diagram (...)

Wikipedia: It could also be a good idea to generally read about catalysts, here from the wikipedia page where they use the classical example chymotrypsin and its oxyanion hole (active site that binds the substrate) that contains the Asp-His-Ser catalytic triad:

In the presence of chymotrypsin, (...), a nucleophile is used in the
form of the catalytic triad - Asp 102, His 57, Ser 195 side chains.
Moreover, the oxyanion hole, which consists of the backbone -NH-
groups of Gly 193 and Ser 195 of the enzyme, have the N-H groups
positioned in such a way that they will donate strong hydrogen bonds
to the substrate's C=O oxygen, given that the carbon atom is
tetrahedral as found in the transition state. This strains the bonds
of the trigonal planar C=O of the original substrate, helping the
reaction to proceed to the transition state. The hydrogen bonds also
stabilize the formal negative charge on the oxygen atoms. In this way,
the activation energy of the reaction is lowered and the rate of
reaction thus increases.


Why Do Most Humans & Cats Have Blue/Bluish Eyes At Birth?

The blue colour is an example of structural colour, caused by light interacting physically with something. Some examples of structural colour are the iridescence of insect wings and body surfaces (usually caused by repeating chitinous structures), and of certain birds feathers, as well as the non-iridescent colours of the blue and yellow macaw.

In the case of the eye it is the stroma of the iris that is responsible. This is a network of fibrous tissue which scatters light. When light is scattered in this way (Rayleigh scattering) it is the short wavelengths which are most scattered. So when you look at the sky (away from the sun) you are seeing diffuse blue light created by this scattering in the atmosphere. In the case of the iris what you are seeing is light reflected from the eye being scattered within the iris, creating the diffuse blue colour. As you say in the question, everything else is down to melanin.


Why is the hippocampus considered to be a cortical structure but not the amygdala?

You can't distinguish cortical from deep structures from a picture like the one you reference in Gray's Clinical Neuroanatomy. The hippocampus is a cortical structure because its cell bodies are in the outer layers of the cerebrum. The amygdala is a deep structure because its cell bodies are in nuclei. I'm not sure if your textbook has stained sections, but if it does, that should help clarify the difference between the two structures.

In this sagittal section you can see both. Notice the hippocampus (at both ends) follows the bumps and grooves of the cortex where the amygdala is a circular/almond shaped cluster of cells.


Does a plant have to be alive for its roots to prevent erosion?

The roots do actually continue to hold soil without being alie.  The stabilizing properties are structural in nature.  You begin to lose those though as the roots decompose, and the important roots against erosion, millions of fine root hairs, will go first. But leaving the roots in on a dead tree will help for a bit, but isn't a long term solution.


Does animal fat and meat contributes differently to our body?

Have you read the Wikipedia article on Fat?  It has literally all of the answers you are seeking.  However...

1: Every single thing is bad for you if you get too much of it.  Animal fat, sugar, water, you can over-do it on anything.  Fat can be bad for you but it is definitely required.  In particular, "Vitamins A, D, E, and K are fat-soluble, meaning they can only be digested, absorbed, and transported in conjunction with fats. Fats are also sources of essential fatty acids, an important dietary requirement."  Fat does a host of other things, as mentioned in the article.

2: Fat is indeed a concentrated store of energy, but there's more to life than just energy.  Protein, like other nutrients, are required for life.  Protein happens to be particularly important, providing the structure for all our cells, is required for muscle growth, and provides amino acids, which are needed to make other proteins in your body.  Proteins are used as hormones, cellular messengers, immune receptors, so on and so forth.  You couldn't live without protein.  Energy, while concentrated in fat, could come from elsewhere.

3: It worked just the same for them as for us.  I will add, however, that our ancestors did not necessarily use every part from every animal, and these days, we actually use every part of many animals, just not always for food.

4: Sure?  Energy is good, but protein is probably better.  "Athlete" is a vague term, as strength-training and endurance activities are very different from each other.  Protein is probably better for strength, carbohydrates are probably better for endurance.  But you can ask over at https://fitness.stackexchange.com/.


At what stage of meiosis does "first meiotic arrest of oogenesis" occur?

When females are in their mother's womb all their Oogonium (plural Oogonia) are being made, they they undergo mitotic divisions to become a primary oocyte. Then, the primary oocytes start to undergo meiosis I -  but meiosis I is arrested. This is the first meiotic arrest. Meiosis I continues when a female hits puberty, every month one or more primary oocytes undergo meiosis I and create secondary oocytes. These secondary oocytes will then  start the second meiotic division, but this second meiotic division is arrested as well. It is arrested for about 24 hours, waiting for a sperm to fertilise it in the Fallopian tubes. The only time an egg (or in medical terms - secondary oocyte) will complete meiosis II is if a sperm penetrates the egg, and then it is called an ovum, which develops into a zygote and a then foetus.

Therefore, the answer to your question will be - the first meiotic arrest in oogenesis will occur from the time the primary oocytes are created in the womb, until a female reaches  puberty. starting puberty until menopause every month one or more primary oocytes will mature and complete the first meiotic division.


What percent of genetic disease are preventable?

There is no simple answer to either of your questions.

There are many monogenic diseases where mutations in single genes result in disease phenotype.

There are far more diseases that have a genetic component where mutations in one or more gene increase the baseline risk of disease and this risk is then modified by the environment the individual encounters throughout their life-time (see Multiple Genes).

To get an overview of the functions of genes that have been so far identified, mutations within them and the diseases they have been linked to see Online Mendelian Inheritance in Man (OMIM).

If you want to get a feel for just how complex genetics is then a recently published paper on the genetics of hair colour would be worth reading...

Genome-wide study of hair colour in UK Biobank explains most of the SNP heritability


Do the individual claws of a bear have names?

I would be surprised if they do!

Bears have 5 clearly visible toes per paw. You could just name the claws based on the fingers it is on (thumb, index, middle, ring, pinky).


How long does it take for cancer to be detectable if it grows from a single cell?

The barriers you mention are outlined well in the classic Hallmarks of Cancer paper: http://www.cell.com/abstract/S0092-8674(11)00127-9

The main problem with finding a general answer to this question is the large diversity in cancers, and the resulting problem in defining what hallmarks are sufficient to call an individual cell cancerous. There are cancers that can't be detected by the immune system or blood tests and will hide for a very long time symptom-wise, and non-cancerous tumours that can be detected in various ways very early on.

Let's say for your timing reference you simply take the point of neoplasm diagnosis (for neoplasms that turn out to be cancers after testing). At this point, figuring out how much time this cancer has spent being cancerous is very difficult, and to my knowledge has never been done. It could be possible to determine:

The number of genetic or epigenetic malfunctions that made the difference between benign tumour and cancer for this particular neoplasm (once again, hard to define)
An approximate rate of acquiring those malfunctions. Conceptually, one could ex vivo culture the cancer and monitor the rate of aquisition of further mutations in cancer-related loci or epigenetic markers.

Depending on how that rate looks, it may be possible to reverse extrapolate the rate of acquisition before diagnosis, and thereby estimate an approximate timepoint of acquisition of the first proper cancerous malfunction.

Besides that, "it probably took more than a few days" is the only statement I can confidently make, although as far as biological theory goes, it's perfectly possible (though highly unlikely) for a cell to acquire a set of mutations sufficient to become cancerous in a single round of replication.


I believe that this white residue is starch. According to Wikipedia, Ginger is 17.7% carbohydrates by weight, or 14% excluding sugar and dietary fiber.

I let the residue settle and decanted the liquid. The residue behaved remarkably similarly to wet corn starch. From this, I have concluded that it is starch of some form.


Can anyone tell me what type of snake this is?

I believe this is a Barred Grass Snake, Natrix helvetica. There are only a few snakes naturally found in the UK, and the Grass Snake matches the size, color, and pattern (bars on the sides but not on the back). The "N. helvetica" designation is relatively new, 2017, following genetic testing that showed that the previous name of Natrix natrix was not correct. "The newly distinguished snake is grey, not olive green like the N. natrix and does not have the same bright yellow collar."

Youtube video
Stock photo from Alarmy
Publication describing geographical distribution: Phylogeography and taxonomy of the barred grass snake (Natrix helvetica), with a discussion of the subspecies category in zoology. Figure 1 (below) includes a photo

Smooth Snake is another possibility but seems much less likely to me.

  Smooth snakes are slender and normally grow to around 55 cm (2 ft). They are grey or grey-brown with darker markings along their back and usually a 'butterfly' shape on the top of their head. They are very rare in the UK but can be found in heathland habitats in Surrey. It would be very unusual to find a smooth snake in your garden. They are very secretive and would normally be found underneath objects.

--Which snake is it?
 (My emphasis)


What is this fruit found in a market in Uyuni, Bolivia at the end of December 2019? (orange skin, 4cm, white flesh)

I found the name: it appears to be Garcinia humilis, known commonly as achachairú or achach:

  Garcinia humilis, known commonly as achachairú or achacha, is a small, prolifically-fruiting tree related to the mangosteen. It grows in the southern part of the Amazon basin in the central area of Bolivia, but has recently been planted on a commercial scale in Burdekin, Australia.

That matches the area, appearance and season.


Can systemic venous congestion caused by tumor?

No. They increase the risk, but are not the causes.
There must be other factors involved which triggers the systemic venous congestion.


How do baby birds get fed when they are only a day or two old?

The hatchling's neck muscles are stronger than you think, because hatching from the egg requires strong neck muscles. Newly hatched songbirds and others do indeed open their mouths after they have had sufficient rest following hatching, though you don't seem to have witnessed this. They have little neck control and their heads wobble initially, but feeding is so important that they are born with this ability.

  Songbirds and most seabirds have altricial young, meaning that the newly hatched birds are blind, featherless, and helpless. Immediately after hatching, altricial birds can do little more than open their mouths to beg for food. They remain in the nest where the parents can feed and protect them while they continue to develop. For the first week of life, most altricial birds cannot control their own body temperature and must be constantly brooded (kept warm) by their parents.

This makes sense, as most altrical birds only spend about two to three weeks before flying off to start their own separate lives.

Newly hatched poultry chicks (precocial birds, which also include ducks and sea birds) can live for 48 hours on the last of the egg yolk that they take in just before the strenuous work of hatching out of the egg.

  Incubation periods are longer for precocial birds than altricial birds, allowing for increased embryonic development in the egg, and therefore they have relatively advanced motor and sensory functions at hatching.

Feeding poultry is actually not necessary during that time. The chicks are strong enough to stand, drink, and peck for food soon after birth, but it's not necessary for life. What they cannot do is regulate their body temperatures well.

Nesting Cycle


Genotypes in diploid/haploid cells under mitotic/meotic cell divisions

Though broad, here I provide a summary in graphical way.

Mitosis:

 .

MEIOSIS: 2 successive steps : Meiosis-1 and meiosis-2

Meiosis-1

Meiosis-2

So lets see what happens with cells given at question.

1. Cell with genotype Aa

(monohybrid or one-point cross-experiments; that means we are looking to gene-pair at 1 loci; not looking to any other genes):

1. A.  Mitosis:

Possible genotypes of their offsprings: All Aa.

1. B. Meiosis:

gametes will show 2-possibilities ; A, a.

2. Cell with genotype AaBb

(dihybrid or 2-point cross-experiments; that means we are looking on genes of 2 loci; not to any other cells):

2.A. Mitosis:

all offsprings AaBb.

2.B. Meiosis:

If given condition says the loci for A (or a) and B (or b) are on same chromosome (linked genes) and no crossing-over is there;

then We will get only 2 types of gamete AB and ab.

If crossing over(s) take place between the 2 loci; then we'll get 4 types of gamete AB, Ab, aB, ab; but their ocurring frequency will deviate from Mendel's independent assortment.

If the 2 loci are not-linked; i.e. they are located in distinct chromosome; then also we'll get 4 types of gametes AB, Ab, aB, ab; but they will follow Mendel's independent assortment pattern.

  Reference:

  Concepts of Genetics, 8th Edition (EBook) By William Klug, Michael Cummings, Charlotte Spencer / Pearson; chapter 2 (mitosis and meiosis)
  The science of Genetics, 6th edition, by George Burns and Paul Bottino, Macmillan.
  Genetics/ P.K. Gupta/ Rastogi Publication Meerut


I assume with EM you refer to electromagnetic?

You are right that the EEG (electroencephalogram) is a tiny signal. When about 50.000 neurons fire simultaneously, it possible to see a change in the measured signal. Typical EEG amplitudes are in the microvolt range.

Now, when the EEG is recorded, it is a function of time. You could for example collect data from 64 sensors, using a typical sampling frequency of 1000 Hz, and obtain 100000 samples from each sensor during a 100 second measurement.

So, what are alpha, beta, gamma, etc? When the recorded EEG signals are transformed into the frequency-domain (using the discrete Fourier transform), the signals become represented as a function of frequency. The obtained frequency range is half of the sampling frequency (according to the sampling theorem). So, with $f_s = 1 $ kHz you may observe frequencies from $0$ to $500$ Hz. Now, to make it easier to discuss about specific parts of the frequency range, they have been given names: delta refers to frequencies from 0-4 Hz, alpha to frequencies 7-15 Hz etc. So, these are just arbitrary names for different frequency ranges. (And yes, some processes do occur in quite exact ranges.)

So what effects what the EEG spectra will look like? Just about everything. From a short segment of data, it is rather impossible to say anything. This is why many paradigms do averaging: for example, you are presented a sound 100 times, and the repetitions are averaged to cancel uncorrelated noise. Have a look at the so called oddball paradigm, for example. Single-trial and continuous recording are also done today, but they are more difficult to analyse.

(Side note: since you asked about electromagnetic brain waves, have a look at magnetoencephalography too..)

For reference, see e.g. Luck (2005), An Introduction to the Event-related Potential Technique. Fourier transforms, sampling theorem, and signal averaging are well covered in Wikipedia.


It is possible for person with AIDS be negative for HIV antibodies?

Usually an antibody test against HIV is positive three month after the infection. Before this time a test can only be done with molecular biology methods as PCR. However, it is possible, that patients which have definitely been tested in an early phase using molecular biology methods and which afterwards receive a antiretroviral therapy (ART) that these patients do not develop high serum levels of antibodies, as the virus titer in the blood is not high enough for a sufficient reaction and thus stay undetected by the tests. This has been improved, so that the kits are supposed to have a higher sensitivity now. See these papers for more details:

Seroreversion in subjects receiving antiretroviral therapy during
acute/early HIV infection.
The effects of early antiretroviral therapy and its discontinuation
on the HIV-specific antibody response.

I haven't found any papers on the decline of HIV-antibodies in AIDS (which is the late stage of the disease), but if they do, this is probably due to the effects of the infection on the immune system.

Low counts in CD4 positive T cells (which are usually associated with an HIV infection) can also occur with other diseases. See these papers (especially the first, as this is a review which contains a lot of further references):

Idiopathic CD4 Lymphocytopenia: Spectrum of opportunistic infections,
malignancies, and autoimmune diseases.
Decreased CD4 and increased CD8 counts with T cell activation is
associated with chronic helminth infection.
Acquired immunodeficiency without evidence of HIV infection: national
retrospective survey.


If rabies always kills its hosts, must there be some animal that is an asymptomatic carrier?

This is an interesting question, and it's been subject to a fair amount of research. From an epidemiological perspective, most rabies outbreaks have been studied in dogs. Among domestic dogs, the R0, or basic reproduction number, of rabies is usually quite low—estimated to be around 1.2 in rural sub-Saharan Africa, and <2 in most historically observed cases [1] (though a particularly bad epidemic in Osaka had an R0 of ~2.42 [2]). This implies that, among dogs, it's quite possible for rabies to spread faster than it kills its hosts, but can be entirely eliminated in dogs by mass vaccinations (see [1] and [2]).

But your question is still valid—if, say, the virus infects all the dogs in an area, and they all die, shouldn't rabies disappear from that area? There's some debate as to where the virus keeps hanging out. For one, there is some circumstantial evidence [3] that the fatality rate in dogs is not 100%, but actually closer to 85%. However, this doesn't necessarily explain the reemergence of epidemics, since for the virus to spread, it needs to get to the dog's saliva, by which point the dog is likely exhibiting lethal symptoms [4][5]. Dogs sometimes being asymptomatic carriers is a tempting explanation, but remains a "highly speculative" possibility [6].

To answer your question, let's look at a place where rabies outbreaks can cause severe economic losses—the livestock farms of South America and sub-Saharan Africa. Vampire bats, the hematophagic suckers, can bite over half of the animals in at-risk zones [7], which house some 70 million head of cattle. Since bats are very well-known sources of infectious disease—in fact, they're known to be hosts of 10 out of 11 recognized Lyssavirus species, including the rabies virus [8]—they've been a tempting explanation since 1911, when a bat-borne rabies outbreak in Brazil was first diagnosed [9]. [9] continues to say this:

  An idea that vampire bats may be asymptomatic rabies carriers, shedding the virus in their saliva for months, was popular during initial studies of vampire bat rabies (16). However, in a well-documented experimental study by Moreno and Baer (17), the disease in vampire bats was similar to rabies observed in other mammals. The bats that developed signs of disease and excreted the virus via saliva soon died, whereas those that survived the inoculation without clinical signs never excreted the virus or had it in the brain as demonstrated upon euthanasia. More recently, the asymptomatic excretion of RABV in the saliva of experimentally infected vampire bats, which survived the challenge during at least 2 years of observation, was documented again (18). Clearly, this phenomenon requires additional investigation.

This is all I've been able to find so far. If I had to bet, I'd put my money on bats being the asymptomatic carrier that you're looking for, with a solid $n=14$ paper to back it up [13]. However, when it comes to established scientific consensus—well, I'm not sure there is one.


Difference between biological control and introducing species for conservation?

After talking to my teacher, he said that biological control is the introduction of species to control another species, however species may be introduced for other reasons (the "Introduced Species" method), such as to "assist an ecosystem cope, flourish or re-establish itself."

The example he gave was the introduction of South African veldt grass to Western Australia in order to stabilise sand dunes, so that they can later be built upon further (eg. plants which may not perform well in sandy, unstable soil can then be planted).

Hopefully this helps anyone else with the same problem.


Why do cockroaches and flying beetles survive high levels of radiation?

Cockroaches have slow cellular replication rates and radiation is known to be the most dangerous to replicating cells, thus making cockroaches (and several other insects) more resistant to radiation than us, but not immune.

This was the subject on a Discovery episode of MythBuster


Mesoporous silica particles as anti cancer drug delivery method

Though I totally agree with your views towards nanotechnology, There is always two sides of a coin.

According to this article THE BAD (of Nanotechnology):

  Health:

  Nanoparticles have been shown to be absorbed in the livers of research
  animals and even cause brain damage in fish exposed to them after just
  48 hours.   If they can be taken up by cells, then they can enter our
  food chain through bacteria and pose a health threat like mercury in
  fish, pesticides in vegetables or hormones in meat.  The
  increasingly-popular carbon nanotube (20x stronger and lighter than
  steel) looks very much like an asbestos fiber – what happens if they
  get released into the air?  Being carbon-based, they wouldn’t set off
  the usual alarms in our bodies, making them difficult to detect.

  Environmental:

  If nanomaterials really are as strong as diamonds, how decomposable or
  persistent are they?  Will they litter our environment further or
  present another disposal problem like nuclear waste or space litter?
  In the distant future, will self-replicating nanobots – necessary to
  create the trillions of nanoassemblers needed to build any kind of
  product – run amok, spreading as quickly as a virus, in the infamous
  “gray goo” scenario?

Not only that Each country have a different point of view on the topic of nanotechnology in Health(or nano-medicine).

Government Response on Nanotechnology:

United Kingdom

In its seminal 2004 report Nanoscience and Nanotechnologies: Opportunities and Uncertainties, the United Kingdom's Royal Society concluded that:

  Many nanotechnologies pose no new risks to health and almost all the
  concerns relate to the potential impacts of deliberately manufactured
  nanoparticles and nanotubes that are free rather than fixed to or
  within a material.

They want to change the existing regulation to be modified on a precautionary basis because they expect that the toxicity of chemicals in the form of free nanoparticles cannot be predicted from their toxicity in a larger form.

United States

Rather than adopt a new nano-specific regulatory framework, FDA convenes an 'interest group' each quarter with representatives of FDA centers that have responsibility for assessment and regulation of different substances and products. This interest group ensures coordination and communication. A September 2009 FDA document called for identifying sources of nanomaterials, how they move in the environment, the problems they might cause for people, animals and plants, and how these problems could be avoided or mitigated.

Berkeley, CA is currently the only city in the United States to regulate nanotechnology, which is still being opposed.

European Union

The European Union has formed a group to study the implications of nanotechnology called the Scientific Committee on Emerging and Newly Identified Health Risks which has published a list of risks associated with nanoparticles.
Consequently, manufacturers and importers of carbon products, including carbon nano-tubes will have to submit full health and safety data within a year or so in order to comply with REACH.

According to REACH(from Page 22, 4.2 Pharmaceutical regulation, PhD Thesis of Steffen Foss Hansen, DTU):

The application of engineered nanoparticles for medical use offers immense benefits
within areas like diagnosis, targeted drug delivery, and drug development and have been
marketed for more than 17 years (NanoRoad SME 2006, EGE 2007, Gaspar 2007).

Well-described and understood medicinal products containing nanoparticles in the form
of liposomes, polymer protein conjugates, polymeric substances or suspensions have
been given Marketing Authorizations within the EU under the existing regulatory
framework e.g. Regulation 726/2004 on authorization and supervision of medicinal
products for human and veterinary use, Directive 2001/83/EC on medicinal products for
human use, Directive 93/42/EEC concerning medical devices, Directive 90/385/EEC
relating to active implantable medical devices, and Directive 98/79/EC on in vitro
diagnostic medical devices (EP & CEU 2004, Council of the European Communities
1990, 1993, 1998, 2001).

There is no specific mentioning of nanomedicine in the EU legislation on medicinal
products and devices, tissue engineering and other advanced therapies. None of these
regulations or directives was written with nanomedicinal applications in mind and
although their scope covers nanomedicine they have been accused for being general and
non-specific and fraught with concerns and difficulties when it comes to dealing with
drugs more complex than traditional ones (Editorial 2007, D'Silva and Van Calster
2008).

The use of nanoparticles in nanomedicine has not been subject to much regulatory
scrutiny since existing laws and regulatory instruments are believed also to cover
medical products based on nanotechnology. The extensive testing requirements prior to
marketing of medicine may also contribute to the notion that the potentially negative
effects will be discovered prior to marketing, that patients are adequately informed
about negative side-effects, and that benefits outweigh the risks or the adverse effects,
should such be found to occur (EGE 2007, N&ET Working Group 2007) .


What percentage of the genetic variance is explained by the 'n'- most important loci?

From the statistical point of view, this question is rather vague. One would need a mathematical definition for the term "genetic variance".

In one extreme, if the "genetic variance" merely means the categorial variations of nucleotides (i.e. ACTG) in the pooled genomes of interest, then the distribution of total "genetic variance" vs. loci variation is uniform and only depends on the size of the locus.

In another extreme (among many dimensions of extremes), if the "genetic variance" is only manifest by the organism's immediate "fitness" and only has two values: life and death (on birth), then all the "essential genes" are "the most important" loci. If you're interested in the n most important loci where n > the number of essential genes, then you would first look at the binary genetic interactions in the database such as BioGrid where two non-essential genes would "interact" and change the organism's fitness (in life and death).

Of course none of the two extremes is very interesting in population genetics or evolution, but a statistical question is best phrased by statistical terms. I would try to find the mathematical definition for "fitness variance", too.

---EDIT---

For a semi-empirical/informatics study, I think you could start with the simplest organism whose genome is well studied.

Choose an organism (e.g. yeast)
Assume uniform inheritability
Choose a specific measurable phenotype/environment (e.g. the ability to grow on a specific sugar x)
Scan each gene in the yeast genome and see its quantitative impact on growth (They're documented in various database)
Ignore genetic interaction
(Or scan each gene pair/triplet/.../n-cluster to see its impact on growth on x)
Try to model your empirical distribution. It's only valid for that specific phenotype/environment
Define your "TOTAL genetic variance in fitness" meaningfully and rigorously. "Additivity" would be a very drastic assumption.

My guess as a non-geneticist is that, as rg255 suggested, for each phenotype as a function of the environment, the distribution would follow a power law. They would not have the properties that would allow you to use central limit theorem to "add them up". But for a specific phenotype, your empirical cumulative distribution function (cdf) would answer your question.


The motion after-effect (MAE) is believed to be primarily due to adaptation of direction sensitive cells in the middle temporal area (MT) (Fig. 1.). The directional cells in this area of the cortex are selectively sensitive to motion in one direction. Hence, looking at a waterfall will selectively cause adaptation in those cells tuned to the direction of the waterfall. When one looks away, the MT cells responsive to opposite directions will become dominant, as their counterparts are momentarily shut down and one will see the waterfall running in opposite direction.

Adaptation thus apparently weakens the opponent input to the adapted MT cells, enabling an enhanced response to motion balanced stimuli. However, the possibility of adaptation occurring in MT neurons themselves cannot be ruled out (Mather et al., 2008).

The MT area is one of the principal visual cortical areas devoted to motion sensing and hence a likely culprit for MAE. However, fMRI studies have indicated that a lot more visual areas in the brain may be involved, either directly, or indirectly, including V1, V2, V3, VP, V3A, V4, and also MT (Mather et al., 2008).

Fig. 1. Two visual streams dominate vision: the dorsal 'where" pathway (containing the direction-sensitive MT area), and the ventral 'what' pathway. source: InTech Open

Reference
-  Mather et al., Trends Cog Sci (2008); 12(12): 481-7


Just take a look at a potato and observe each of its eyes. You will see that each of them has two parts:

1) An "eyebrow" : this is a vestigial leaf

2) A small bud in the axil of that leaf

Thus, the two of them together form an eye + eyebrow

The eyes are not evenly distributed in a potato plant. One side may have just one or two but the other side will have lots of them. This is because that is the growing spot!

Examples:


It is of Phytolacca genus plant which could be toxic for mammals, DO NOT eat as is - it should be cooked properly to be usable/edible (the older, the more toxic leaves are).

Phytolacca acinosa:


Is reproduction intrinsically part of life?

Every species has the ability to reproduce.  Of course, individuals within a species can be born with a mutation that keeps them from reproducing, or lose the ability to reproduce at some point in life.  However, to say that once these individuals fail to meet that criteria they are no longer forms of life would be a fairly absurd semantics argument.  It might be useful to note in an evolutionary sense that those individuals can no longer pass on their genes, which is could select against whatever it was the resulted in that individual being sterile.

You could probably reword the characteristics of life to stress species instead of individuals, but then theres a problem with microbes which have very poorly, or non-existent species.  But in general, this is not something a biologist is going to lose sleep over.


Why haven't prey evolved the ability to always outrun their predators?

There are (at least) three important factors to consider here; evolution under selection requires genetic variation upon which to act, selection can act on covarying traits causing trade-offs, and adaptation also occurs in the predator. A lot of this is covered elsewhere on this site (including the effects of the other mechanisms of evolution), but little specific reference is made to predator-prey co-evolution.

Adaptation and genetic variance

One of the mechanisms of evolution is selection, and adaptation occurs when species evolve as a response to selection. For a response to selection to occur there must be genetic variation within the trait, such that the genes an individual carries affect the individuals fitness. For example, there may some genes which give the carrier better muscle structure for fast running, and this increases survival which, in turn, increases reproductive output. The importance of genetic variation is often overlooked, but is highlighted by the breeders equation. Genetic variance can arise by novel mutations, or can exist as standing genetic variance.

Selection on covarying traits

Selection is seldom, if ever, a univariate process. That means fitness is not determined by a single characteristic, so fitness in a prey species may be determined by the speed at which it can run, but also its metabolic rate, stamina, ability to acquire nutrients, the way it provisions nutrients for growth and repair etc.. Genetic covariance between traits (induced by linkage or pleiotropy) can impact the response to selection, because any selection acting on a covarying trait can cause affect the adaptation occurring in the focal trait (strengthening, weakening, neutralising, or even reversing the direction of response). Therefore, if running speed covaries with other traits it may be difficult for selection to increase running speed. Think about athletes, I doubt Usain Bolt could run 10,000 metres as fast as Mo Farah and vice versa, because there is a trade-off between speed and stamina.

Adaptation in other species

If selection did cause speed to increase in the prey species then that would strengthen selection for increased speed in the predator. This is called an evolutionary arms race, where the adaptive the evolution of two species interacts causing adaptation and counter-adaptation. For example, genes which allow faster running might spread through a population of gazelles (prey) because carriers are more likely to outrun the lion (or the other gazelles), but this will increase selection on lions (predator) to increase speed (or adopt other strategies) which will spread genes to make the lions faster (use other strategies); the result being adaptation and counter-adaptation between the gazelle and lion populations.

There is a little series here about Butch Brodie and his studies of coevolutionary arms races between garter snakes and toxic newts. It would be good to read on the Red Queen Hypothesis, which describes how species, under interaction with other species, must continue to evolve just to prevent extinction. Also worth noting that prey species often have more than one predator species (and predator species often have more than one prey); interaction and coevolutionary networks are complex. What may be adaptive in some interactions may also be maladaptive for other interactions (see specialist and generalist, and selection on covarying traits).


This is a good question as, although in higher eukaroyotes codon usage does not necessarily correlate with translational efficiency, it does to a large extent in Escherichia coli (see e.g. Boël et al., 2016). The answer is not simple, but the following may contribute.

To optimize the strength of base pairing

Although in particular circumstances ‘wobble’ allows one tRNA to decode more than one codon (see diagram in my answer to Redundancy and the Generic Code) the strength of base pairing will be less for the wobble base-pair:

It has been suggested this would generally disfavour (and hence reduce the incidence of) the degenerate codon that needs to be decoded by wobble. (In some cases a wobble interaction might be an advantage if the first two codon bases were G or C, so that the hydrogen bonding was not too strong.)

To utilize the spectrum of tRNAs able to decode degenerate codons

Although wobble enables a reduction in the total number of tRNAs necessary to decode the 61 amino-acid codons, additional tRNAs often exist that one might regard as unnecessary. Furthermore, where three codons are decoded by a tRNA with a 5'-I (inosine), the other tRNA sometimes has a 5'-G (rather than A) and can hence decode two codons. This is illustrated by the E.coli tRNAs for threonine:

Thus, the relative abundance of these three Thr-tRNAs could determine the codon usage, and Dong et al., 1996 reported that this is the case.

To reflect the overall GC-content of the genome

If the genome of a prokaryotic organism has a particular base composition, because there is so little non-coding genomic DNA the mRNA will necessarily reflect that base composition in its codon usage. Your might ask why doesn’t the base-composition of the genome just reflect that of the synonymous codons, but there are actually strong pressures on the GC-content of prokaryotic and viral genomes. In some bacteria this may reflect needs for thermal stability, but in others it seems to be random drift (see e.g. Biology SE questions on GC-content of genomes).


Understanding a Chromosomal formula in a karytope analysis

Cytogenetic nomenclature is standardized in the International System for Human Cytogenetic Nomenclature. Unfortunately it is not free and my institution does not have access. However, looking at a preview of the 2013 version in Google Books, it would seem that the number in square brackets is the number of cells scored with that karyotype.


Is the ACh receptor more permeable to sodium ions?

Short answer

No.

There are differences in Na+ versus K+ permeability, but you have it backward: potassium is actually slightly more permeable; however, these differences are not the only factors influencing the reversal potential, and also, the reversal potential for a nAChR need not be exactly 0 mV.

tl;dr to the long answer

You need to sum before taking ratios rather than take a difference of ratios when computing a reversal potential for multiple ions together.

Before we get into the weeds...

In most sources you will hear something like the reversal potential for a nonspecific ligand-gated channel like nAChR is "about 0 mV" - this is going to vary in different cell types, in different conditions, with different recent activity levels, with different versions of the receptor, etc.

What's important to remember in all this is that -14 mV is also about 0 mV... In the context of excitable cells, what is most important is the reversal potential relative to the threshold for firing a spike or activating other channels. That said, I'm not actually saying the reversal potential for nAChR is actually -14 mV, there are a couple other factors missing...

What you are missing

The big one you are missing is that the concentrations of the ions matter, not just their ratios. For the reversal potential of a single ion, all we really care about is the ratio inside and out, which is found in the Nernst equation.

Averaging the reversal potential for two major ion species, like you have done, gives you a pretty good ballpark estimate (afterall, -14 mV is also about 0 mV!).

To get the actual reversal, however, you'll need the Goldman Equation.

We can simplify the Goldman equation for just Na+ and K+ in fairly standard conditions to something like:

$61.5 \mathrm{mV} * log_{10}(\frac{P_{Na} [Na^+_{out}] + P_{K} [K^+_{out}]]}{P_{Na} [Na^+_{in}] + P_{K} [K^+_{in}]]}$)

If the permeabilities are both :=1, and the concentrations of Na and K are equal and opposite, then indeed you will get zero. However, if that was true, you would also have equal and opposite reversal potentials for Na and K alone in the cell: in the numbers you gave, that isn't the case.

I'm not sure what numbers you used exactly, but I'll use my own example. If potassium is 5mM out, 140 mM in, the reversal potential will be -85.6 mV for potassium. If sodium is 140 mM out, 12 mM in, the reversal potential will be 63.1 mV for sodium (you can check my math with the Nernst equation).

If you combine these numbers in the Goldman equation above, you will get -1.2 mV: closer to zero than your -14 mV estimate.

They are so close because the ratio (140+5)/(12+140) is a lot smaller than the difference of the ratios (5/140) and (140/12): order of operations matters.

This is assuming identical permeabilities

However, the permeabilities aren't actually identical

There are many papers measuring relative permeabilities in nAChRs, I just chose one randomly as an example (happened to be the first Google Scholar result).

Nutter and Adams 1995 found the relative permeability of several monovalent and divalent cations, with Na as a reference:

Therefore, potassium is actually slightly more permeable than sodium. However, there are also other important ions that could contribute, even if they are found at lower concentrations than either sodium or potassium, and the example ion concentrations you find in a textbook might not apply in the systems you are studying. A source that says nAChRs are only permeable to sodium and potassium really just means that they are not permeable to another other important high-concentration ion: chloride. They are also simplifying things a bit for you, which is okay.

If I use the Goldman equation quickly with these data, I get a reversal potential (with just Na and K, ignoring other ion species) of -5.9 mV: still "about 0 mV" and still closer than your original -14 mV estimate.

But how are different ions with the same charge showing different permeabilities?

This is better off as a separate question, and probably easier to address with a more extreme case, like in selective sodium or potassium channels. However, like in those channels, in channels that we call "non-specific", the particular arrangement of amino acid residues (especially charged ones) at the pore can favor particular ions because those ions differ slightly in size.

Nutter, T. J., & Adams, D. J. (1995). Monovalent and divalent cation permeability and block of neuronal nicotinic receptor channels in rat parasympathetic ganglia. The Journal of general physiology, 105(6), 701-723.


SARS-CoV-2 proteome: is the SPIKE protein not an issue for a hospitalized patient?

It is always a problem. "The virus" is not a single particle that only needs to enter a single cell, a single time. It is a population of millions of viral particles, that infect millions of cells. So, as long as there are more cells to infect, the viral population still needs a mechanism to enter the cell (i.e. it still needs all the proteins needed to function).


Which mountain range was formed first (historically) and which the pedigree is correct?

If mountain range 1 was formed first, pedigree 1 is correct.

If mountain range 2 was formed first, none of the two pedigree seem correct.

If mountain range 1 was formed first you would first have the split of the initial population into population P and the population Q+R. Then, the formation of mountain range 2 split the population Q+R into Q and R. Therefore, Q and R are more closely related than they both are to P. Therefore Pedigree 1 is correct.

You can apply the same kind of reasoning by guessing that mountain range 2 was formed first and you will realize that you would expect a pedigree different than Pedigree 1 and Pedigree 2. If mountain range 2 appeared first then, the correct Pedigree would display the population/species/lineages P and Q more closely related to each other than they both are to R.


How many generations between the first lifeform and humans are there?

The generations that preceded multicellular life will so vastly dominate the answer that the last 500,000,000 years don't even matter. So life is 3.5 billion years old, and for most of this time, life was prokaryotic, dividing every 20 minutes or so. Thats 26,000 generations per year. Multiply that by 3.5 billion and you get 9 trillion generations. That is likely an overestimate, based on optimal growing conditions of bacterial in exponential growth. But it is unlikely to be orders of magnitude off.


Do birds have quadriceps and thighs fused into their hips?

This is probably WAAAAY to late to be of any use to you but hey...
So the simple answer is:
Kinda.
You were actually correct to intuit that the femora of birds have a limited range of motion, with most of the limb motion being provided from the "knee"-down.
So you shouldn't animate bird legs the same way that you would the legs of other non-bird animals.
That's not to say that the femur doesn't move - it does but not my much (it typically doesn't extend posteriorly beyond the vertical). Much of the thicc thigh musculature is there for support.


C. elegans are either male or hermaphrodites, but why aren't there any females?

The evolution of self-fertile hermaphrodites is thought to be a specialization that occurred several times in the nematoda. For example, most of small, free-living soil nematode species related to C. elegans are male/female. C. briggsae, which last shared a common ancestor 80 myr ago is also male/hermaphrodite, but I believe their ancestor is thought to have been male/female.
At the developmental level, the first germ cells to mature in the somatic gonad develop as sperm and then the Germline switches over to make oocytes.


Kin selection Vs altruism (social biology)

how can kin selection be altruistic?

Part of you confusion is purely semantic.

Kin selection cannot be altruistic. Kin selection is an evolutionary process. Altruism is a behaviour. Saying "kin selection is altruistic" is like saying "natural selection is flying" (when thinking of selection for flying abilities in, say, flying squirrels).

Altruism

Altruism is a behaviour in which increases another individual fitness at the expense of its own fitness. However, this definition lead to confusion of whether one is talking to lifetime fitness or only to a contribution to one's fitness that will eventually be returned. For this reason people talk about True Altruism and False Altruism

True Altruism

True altruism is a behaviour in which the actors's (the one performing the altruistic behaviour) life time fitness is decreased while the recipient (the one benefitting from the altruistic behaviour) is increased.

True Altruism can only evolve via kin selection (or group selection for the few who still view these two processes as different).

It is the indirect component of the inclusive fitness that selects for altruism indeed.

False Altruism

False altruism refers to cases where the actor performs the behaviour because he is expecting (not necessarily consciously) a return later in life. False altruism can be seen as an investment.

Such false altruism can be selected by natural selection (no need to consider indirect fitness). "Return on investment" can be caused by direct reciprocity or indirect reciprocity. In case of indirect reciprocity, some populations can use a system of reputation, where individuals are more likely to help individuals that they have seen being helpful to others before.

Game theory

All types of interaction between individuals can be modelled in game theory. One can also investigate specific type of strategy in response to a a specific game. For example, Tit-for-Tat is one type of strategy in a multiple encounter between two individuals game.


Methylation Data for Erythrocytes (Red Blood Cells)?

The answer is relatively simple: Mature erythrocytes do not have a nucleus and thus you cannot study methylation patterns there. You can do this in young, developing erythrocytes which still have their nucleus.


How is Elysia chlorotica classified as an animal capable of photosynthesis?

Maybe you are familiar with the endosymbiotic theory which hypotetisays that the mitochondria (and chloroplast) was a little procrayote that got absorbed by larger organisme. At the beggining they were independent in an endosymbiontic relationship but in the process of evolution they merged to one organism from which all eukaryotes (plants). So yes, the process your describe is possible.
If it happens than the new organism is no longer E. chlorotica but a another which evolved from it, this creatue will likely still be clasified as an animal since there are non-photosynthetic plants and there are photosynthetic non-plants (algae, cyanobacteria), Therefore photosynthesys is not the definition of a plant.
The goal of the tree of life is to draw the "familiy tree" of all the living creatures. So, if we know one creature is an animal that gave rise to another one with a special ability we will still clasify it as an animal.


How do the High-Energy Electrons During Chemiosmosis Come from Water?

The light harvesting complexes use light energy to "lift" electrons to a higher energy state from which they can be used to reduce organic molecules (by way of an electron transport chain and NADPH), leaving a "hole" or cation behind in the LHC and thereby oxidizing it. If these complexes were not re-reduced by something, they would become non-functional after absorption of a single photon. So, they are re-reduced by removing electrons from water to generate molecular oxygen, which happens in photosystem II. So the photosystems I and II act as a series of "pumps" that make otherwise thermodynamically "uphill" (unfavorable) electron transfer from water to NADPH spontaneous, but they do not act as a net source of electrons--water does.


How many hairs per sq. cm. (or inch) do hamsters have on average?

According to Paul et al. (2007), shaved fur patches of male Siberian and Syrian hamsters had a mass of about 12 mg/cm2 dorsally and 3 mg/cm2  ventrally.
This search give me the page.

Fig 1 from Paul et al. (2007) compares mass of fur growth across time for 2 groups exposed to differing lengths of daylight (long, LD, and short, SD) to examine winter fur adaptation.

Paul, M.J., George, N.T., Zucker, I. and Butler, M.P., 2007. Photoperiodic and hormonal influences on fur density and regrowth in two hamster species. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 293(6), pp.R2363-R2369.


I deffinitly recomment to look at your calculations. But the abbility of cannot rolling tongue is recessive not dominant. And after all look at the Hardy-Weinberg equision p^2 + 2pq + q^2 = 1 (p*p=p^2). Try to extract the root of q^2 and you will get right sollution (because the 0.16 is squareroot).


You need to first build an initial protocol and then optimize it.

The most important to determine the conditions is the polymerase used. Some polymerases work at higher or lower temperatures and will work faster or slower. Find the default protocol from the polymerase seller and this will give you a good idea where to start.

The second most important is the primers used. Depending on the GC % in the primers and their length, the times or temperature of each step will change, or if you prefer will need to be Optimized.
The length of the DNA fragments will also determine the length of the cycles. Most polymerase sellers will includes steps to optimize the reaction depending on the quantity of DNA used, primer length and other parameters.

For more information:

Designing primers:

Taq DNA polymerase protocol example:

Optimizing PCR

PCR thermal profile, Deoxynucleoside Triphosphates and Primers are interesting paragraphs