text:
Are spores seeds?
It seems to me that the spores produced by bread mould are actually its seeds but my textbook says that they are not.
My rationale is that spores are seeds of bread mould because both spores and seeds perform similar functions: both of them develop into a new organism under favourable environmental conditions.
So, are spores seeds, or is there a flaw in my reasoning?

Don't forget that fungi are phylogenetically closer to animals than they are to plants.

It really is about language, and science uses precise terms. So although spores seem similar to seeds, "seed" is a specific term for a fertilized ovule that is restricted to conifers and seed plants, or gymnosperms and angiosperms. Moss and ferns, which are deeper on the phylogeny of plants, don't make seeds either, but reproduce with spores.

No as as a seed is a specific multicellular structure formed from a fertilised ovule found only in most spermatophytes
Furthermore a spore is at one stage produced within the ovule however it grows into a gametophyte without being dispersed

It mostly depends on what you define spores and seeds as, but according to the "official" definition, the answer is no. And just because two things do the same thing, doesn't mean they're the same. Pens and pencils do the same thing. They're different. See the Internet or something for the "official" definition.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Training Data for Secondary Protein Structure prediction using neural network
I am trying to find some training dataset for prediction of Secondary Structure of Protein. I am having problems finding them online.

The standard benchmark dataset is the one from Lindahl, which consists of 976 × 975 target-template protein pairs.

Lindahl, E. & Elofsson, A. Identification of related proteins on family, superfamily and fold level. Journal of molecular biology 295, 613–625 (2000).

It is for example used in the following articles:

Improving Protein Fold Recognition by Deep Learning Networks
Improving protein fold recognition by random forest

Another resource is SCOP: Structural Classification of Proteins.

Nearly all proteins have structural similarities with other proteins and, in some of these cases, share a common evolutionary origin. The SCOP database, created by manual inspection and abetted by a battery of automated methods, aims to provide a detailed and comprehensive description of the structural and evolutionary relationships between all proteins whose structure is known. As such, it provides a broad survey of all known protein folds, detailed information about the close relatives of any particular protein, and a framework for future research and classification.

source: Stack Exchange

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Why do fat people and thin people get hungry at the same time?
Say a fat person and a thin person take breakfast at the same time. Around lunchtime, they'll both be hungry. Why? After all, the fat person theoretically has lots of body fat the body can consume instead, so the fat person does not have to feel hungry.

Consider that part of it is simply social conditioning.  People in western cultures are generally trained to expect meals at certain times.

I am not sure your statement is true, fat and thin people may not always get hungry at the same time. You cannot simply compare these two categories as they contain subcategories including people "feeling hungry" because of disorders related to their mental health, physiology, diseases,...
The term you are looking for is "appetite regulation" and reading the wikipedia page will give you an overview of this subject and why your question is too broad to be answered. https://en.wikipedia.org/wiki/Appetite#Regulation

I accepted your answer because it tells me that my question is poorly formed: instead of asking "which body needs energy", I should be asking "what governs appetite".

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text:
DNA quantification in a high school bio lab
I'm working on a project in a high school bio lab (so limited resources), and I need a way to quantify the concentration of DNA in a PCR product. I can't use spectrophotometry (cheap spectrophotometers at school can't measure absorbance at 260nm), and any fluorescent dyes are out of the question as we don't have a transilluminator. Right now I'm looking at measuring absorbance change in a visible-light dye like crystal violet or methylene blue, but there isn't enough data on quantification using these dyes. Can anyone suggest anything?
Thanks.

Can you run a gel?

Yes, although gel extractions might be a little difficult.

If you are lucky, and you don't need many repeated measurements, and there is a university in your town, you can contact the administrative staff (note: not professors) of a fitting department (e.g.: genetics), who will usually put you in contact with a grad student of an experimental lab. Usually people are happy to help with "minor issues" like those - and having someone from a high school briefly visiting a lab will be good for any involved party, as it is a nice sign of community outreach.

I do know a guy at a nearby uni who might be willing to help, but because the project is officially graded I'd need a pretty good set of data with replicates so it would mean basically doing everything at the uni, which I'm trying to avoid for now. I'll keep it in mind for a backup option, though.

You can quantify DNA in a gel by comparing band intensity of the unknown sample to that of a known mass. I can elaborate if this seems like a reasonable strategy for you.

That sounds interesting, can you elaborate?

Within some linear range, the intensity of stained DNA bands in a gel is directly proportional to their mass. By making a standard curve from bands of known mass, the mass of unknown bands can be estimated. This process is called densitometry. I wrote briefly about its use in quantifying protein bands after SDS-PAGE in this answer, but I'll go into more detail on how this is done using the following ethidium bromide stained gel:

On the right is a molecular weight marker (BstEII digest of λ DNA) with bands of known mass. On the left are two bands of unknown mass (actually a double-cut plasmid).
I use a free program called ImageJ to estimate band intensities. They have a tutorial on measuring band intensity here. You can also get ImageJ packaged with Java (and bunch of other stuff) in the software Fiji.
Open the image in ImageJ and use the Rectangle tool to draw a box around the marker, then select Analyze > Gels > Select First Lane (or shortcut Ctrl+1). Next, drag the box over to surround the other lane and select Analyze > Gels > Select Next Lane (Ctrl+2). Now select Analyze > Gels > Plot Lanes (Ctrl+3) to plot image intensity as a function of position on the gel:

The area under each peak (minus the background noise) represents the some total of intensity for each band. To measure this area, use the line (Straight) tool to draw bounds on the base of each peak:

I've done it somewhat haphazardly here, but you get the idea. Now, using the wand tool, click inside each peak and ImageJ will tabulate the integrated intensity of each. Shown below are the intensities of the marker bands (with the top band being Band 1) as well as their masses (which are known):
          Mass (ng)    Intensity
Band 1    45           5319.891
Band 2    28           3816.234
Band 3    24           3256.406
Band 4    16           2298.749
Band 5    15           2074.749
Band 6    8            1084.991

Take this data into Excel (or similar) and plot intensity as a function of mass. Band 1 looks like it is outside the linear range and is underestimating the mass. This was actually expected since, if you look closely at the band in the gel image, there are red pixels indicating that it is oversaturated. Ignore this band and perform a linear regression on the rest.

The regression gives the equation $I = 134.74M + 53.988$ with $R^2 = 0.9975$. Rearranging for mass, we have $M = \frac{I - 53.988}{134.74}$. Get the intensity of the unknown bands as described above and calculate their mass with the preceding equation:
          Mass (ng)    Intensity
Band 1    27           3736.991
Band 2    15           2125.284

My experience is that this is a much safer method than using (for example) Nanodrop. I have to admit though, that I rarely ever did the quantification in ImageJ/FIJI; estimating by eye was usually close enough for most applications :)


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Why are fertilizers with polonium 210 used when growing tobacco?
Why are fertilizers with polonium 210 used when growing tobacco?
I'm thinking of pursuing a science fair in which I create my own fertilizer for tobacco that doesn't contain polonium or lead. However, I need more background research. Does anyone know why these fertilizers are used?

do you have a link to support your claim that fertilizer contains Po-210?

What brings you to the conclusion, that these fertilizers contain bigger amounts of lead and polonium?

Just wait a couple weeks for the Po 210 to turn into stable Pb 206.

According to RADIOACTIVITY IN CHEMICAL FERTILIZERS by Milica M. Rajačić, Nataša B. Sarap, Marija M. Janković, Jelena D. Nikolić, Dragana J. Todorović and Gordana K. Pantelić at the Institute for Nuclear Sciences "Vinča", University of Belgrade, Belgrade, Serbia, and the relatively short half-life of polonium, it appears that primordial metals are the only hazard in fertilizers:

Natural radioactivity results mainly from primordial radionuclides,
  such as 40K and the radionuclides from the 232Th, 238U and 235U series
  and their decay products. Terrestrial radioactivity and exposure due
  to gamma radiation depend primarily on the geological conditions and
  appear in different quantities in the soils of each region in the
  world. 1 [...]
Fertilizers usually employed in the agriculture contain traces of
  heavy metals and relatively high concentrations of naturally occurring
  radionuclides. Phosphate containing fertilizers have been used
  worldwide to increase the quantities of the micronutrients, which are
  being continuously taken off from the soil due to farming activities.
  At the same time, the use of such fertilizers is the main
  anthropogenic source of the uranium input in the environment (about 73
  % of the total input of uranium) 2. [...]
A total of 140 samples of different types of fertilizers were measured
  for their radioactivity content using gamma spectrometry technique in
  order to assess the implications of extended use of fertilizers on the
  concentrations of natural radionuclides in cultivated soil. The
  obtained data show that the activity concentration of naturally
  occurring radionuclides in fertilizer samples were 87 Bq/kg, 4860
  Bq/kg and 220 Bq/kg for 226Ra, 40K and 238U, respectively, which
  exceeds the activity concentration in soil by an order of magnitude.
  As it was shown in the paper, the use of fertilizers has a negligible
  effect on Raeq and D in soil due to dilution of fertilizer used on the
  large amounts of cultivated soil. However, the long term application
  of these fertilizers can have the effect of an accumulation of
  radioactivity in soils that can be harmful for the health of farmers
  and consumers of the products. [...]
1: Akhtar N. Radionuclide pollution due to fertilizer use in some
  saline soils of the Punjab and their potential risk assessment on
  human health. Department of Physics Bahauddin Zakariya University
  Multan, Pakistan, 2006. 2: Stojanović M, Stevanović D, Milojković J,
  Mihajlović M, Lopičić Z, Šoštarić T. Influence of soil type and
  physical–chemical properties on uranium sorption and bioavailability.
  Water Air Soil Pollut 2012;223:135-
  144.

Artificial fertilizer is cheaper than regular fertilizer that also contains long-term nutrients, but also contains Po-210:

Among all carcinogenic substances contained in tobacco smoke, Polonium
  210 (Po-210), with a half-life of 138 days, is one of the most
  dangerous, by exerting a devastating, chronic, slow and progressive
  carcinogenesis activity. The main source of Po-210 in tobacco is
  represented by fertilizers (polyphosphates) containing radium-226
  (Ra-222) which decades to plumb 210 (Pb-210). Through the thricomes
  Pb-210 is concentrated in the tobacco leaves, where it turns to
  Po-210, which at the cigarette combustion temperature (800-900 degrees
  C) reaches the gaseous state and it is absorbed by the micro particles
  released into tobacco smoke. Thus, smoke becomes radioactive in both
  its gaseous and corpuscular components and reaches the airways, where,
  particularly at the branches level and together with other substances,
  it exerts its carcinogenic activity, especially in those subjects with
  impaired respiratory mucosal clearance. The carcinogenic risk/one year
  lifetime of a smoker of 20 cigarettes per day is equivalent to that of
  undertaking 300 chest x-rays. It is calculated that Po-210 may be
  independently responsible of 4 lung cancers every 10,000 smokers.
  During cigarette's combustion, tobacco smoke is also released in the
  air, contributing to serious health risks for those exposed to passive
  smoke.


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Difference between bacteria and bacteroids?
During nodule formation Rhizobium is converted to bacteroids. What's the difference between them?

I edited your title: Bacteroides is a Genus of bacteria.

Bacteroids are the endosymbiotic forms of rhizobia (in the root nodules of leguminous plants).

Löhnis & Hansen (1921) J Agric Res 20: 543-556; emphasis mine:

It is not superfluous to emphasize once more that persistence in
  calling these forms "bacteroids" is by no means to be recommended.
  They are true bacteria, not foreign bodies looking like bacteria, as
  Frank's pupil Brunchorst erroneously believed. To speak of a
  "bacteroid" growth of bacteria is no less absurd than it would be to
  speak of a "fungoid" growth of fungi.

https://naldc.nal.usda.gov/download/IND43966363/PDF

Gerson & Patel (1975) Appl Microbiol 30: 193-198; emphasis mine:

Rhizobium is an aerobe, existing as a free-living bacterium in soil or
  as a partially anaerobic symbiont in the root nodules of leguminous
  plants. It is in the symbiotic form (bacteroid), which is frequently
  morphogenetically different, that nitrogen fixation takes place.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC365797/
MacKenzie et al. (1973) J Bacteriol. 113: 387-393; emphasis mine:

[C]hanges [accompany] the transformation from the free-living rod
  forms to the nitrogen-fixing bacteroid forms. (...) During the
  transformation into the bacteroidal state the wall decreased in
  thickness, became less rigid, and developed a particulate surface.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC251641/


text:
Don't understand how multiple replication bubbles work
I'm not exactly sure how multiple replication bubbles work, assuming were working with a linear, eukaryotic chromosome.
This is a diagram for reference:

It appears that the DNA is being synthesized "towards" the centre. What I mean is that in one replication bubble, the top strand is being replicated from left to right, whereas for the other replication bubble, the top strand is being replicated from right to left.
I don't understand why this is. Aren't the directions reversed? Isn't synthesis always supposed to be from 5' to 3'?
Thanks!

Take into consideration the helices.

You mistake replication direction with polymerase synthesis direction. Indeed, the polymerase synthesizes new strands 5' -> 3' but if the replication of each strand was continuous, there would be  no such structure as a replication bubble whatsoever. Take a good look at the drawings:

The thing is the direction of replication is consistent with the direction of leading strand synthesis, so the bubbles will "spread" outwards. Lagging strand is synthesized in the form of fragments 5' -> 3'. If you look closely fragments that are closest to the center of the replication bubble are synthesized first, then polymerase detaches and works on the next fragment which is actually closer to the 3' end of the lagging strand.
Here's an article on Wikipedia about those fragments: https://en.wikipedia.org/wiki/Okazaki_fragments
Hope this makes things clear.
Cheers and happy learning,
Krzysztof

That's a great explanation and also a great diagram. Thank you very much for your help.

Glad I could help ;)


text:
How many Endogenous Retroviruses do we share with other primates?
Is there a list of Endogenous Retroviruses that we share with other primates? I would like to map all (or most) of them into a hierarchy and see how it fits in our evolutionary branch.

Please do not use abbreviations in a title that may be unknown to many, and in your question only if you repeat it. This is a barrier to comprehension and indexing. I have made the changes for you.

There are several papers that cover this. Briefly, humans share the vast majority of their ERVs with other primates, but not all; and this is mainly because other primates have acquired ERVs that humans have not (rather than humans acquiring new ERVs themselves).  The third link, in particular, seems to cover your proposed reconstruction and concluded that in general "these sequences gave trees that were consistent with the well established phylogeny of the old world primates".

Divergent Patterns of Recent Retroviral Integrations in the Human and Chimpanzee Genomes: Probable Transmissions between Other Primates and Chimpanzees
The decline of human endogenous retroviruses: extinction and survival
Constructing primate phylogenies from ancient retrovirus sequences


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Are there animal species in which the females expend more energy attracting males than in their offspring?
In general, males of a species expend a lot of energy attracting females.  There are many instances where males utilize much of their nutrient intake to produce antlers, tusks, horns, etc. to either attract females or compete with other males for potential mates.  Are their any instances in animals in which the females do this to attract males or to compete with other females?  If so, what features have the females evolved to win over potential mates and fight off competitors and what advantage is there for the species?
I'm aware of a few animals, such as the seahorse and jacana where the males invest more energy in the offspring, but I'm not sure that the females of these species expend some of the energy saved in the offpring and put it into attracting males or competition with other females.

On the risk of being hilarious? Humans.

One thing to consider here is the definition of female. Females are not defined by their genitalia, but rather, the size of their gametes. The animal with the larger gametes is the female. As such, her gametes are more valuable as a resource. Sperm are cheap and expendable. Eggs are precious resources. So this explains the difference. I kind of agree with skymningen's comment about humans. Human females DO spend more effort to attract mates. But they are more selective than their suitors, while men spend more time "seeking"

The reason why, in most species, males are competing to access females and females are choosy is due to Bateman's principle.

Bateman suggested that, since males are capable of producing millions of sperm cells with little effort, while females invest much higher levels of energy in order to nurture a relatively small number of eggs, the female plays a significantly larger role in their offspring's reproductive success. Bateman’s paradigm thus views females as the limiting factor of parental investment, over which males will compete in order to copulate successfully.

But there are exceptions to this general rule.
Fish
In many fish species (e.g. pipefish, scissortail sergeant and seahorses), males are choosy and females are competing. In these species, females deposit their eggs in a special brooding pouch that the male possesses. The male then has the energy cost of raising the offspring, while the female does not provide any parental care. As a result, males in these species must choose among competiting females for mates( Vincent et al., 1992)
Birds
In many bird species, there is bi-parental care, leading to competition among mates in both species. See the interesting case of Jacana jacana (Emlen and Wrege, 2004).
Frogs
In poison-arrow frogs (Dendrobates auratus), the male spend more energy for raising the offspring than the females and the males are therefore choosy (Wells, 1978).

Related: Why are female not competitive for reproduction like males?

I'm looking at this as a total energy used by both sexes and am interested in how the female utilizes the saved energy when the male is using more of the total on the offspring.  So, if I'm reading the article correctly for the Jacana jacana, it appears that the females have greater development of fleshy facial ornamentation (attraction) and wing spurs (for competition) in exchange for the energy saved from raising offspring?


text:
Understanding Hodgkin-Huxley's model and activation variables
This question is about the Hodgkin-Huxley model as introduced in Eugene M. Izhikevich, Dynamical Systems in Neuroscience, p.33 ff.

I'm having trouble to understand and interpret the differential equation for the activation variable $m$:
$$\dot{m} = (m_\infty(V) - m)/\tau(V)$$
which enters via
$$p = m^a h^b$$
into the equation
$$I = \bar{g} p (V − E)$$
for the net current $I$ generated by a large population of identical
channels where $p$ is the average proportion of channels in the open state, $\bar{g}$ is the maximal
conductance of the population, and $E$ is the reverse potential of the current.
$m$ is the probability of one of $a$ activation gates to be open. Interchangeably: $m^a$ is the proportion of open activation channels (assuming all of its activation gates must be open simultaneously).
The differential equation might give us $m$ as an explicit function of time but it – explicitly – involves $V$ which is – implicitly – another function of time, which in turn depends on the number of open gates. Things are horribly complicated!
On the other hand — since it's about voltage-gated channels and there are "immediate" voltage-sensitive regions in the channel protein which presumably don't have memory ("the single channel has no memory about the duration of its own state"), but possibly a time lag — I expected the being-open-probability of an activation gate to be a "pure" (possibly time-lagged) function of $V$.
My question comes in two disguises
(1) Given two explicit functions $m_\infty(V)$ and $\tau(V)$ like these:

together with $m(0)$ and $V(0)$, how could we ever arrive at an explicit solution for $m(t)$, assuming that $V(t)$ depends somehow on $m(t')$ for $t'\leq t$, but possibly also on some injected currents.
(2) How can an intuitive and sensible interpretation of the terms in
$$\dot{m} = (m_\infty(V) - m)/\tau(V)$$
be given? What does the time constant $\tau(V)$ and its dependence on $V$ mean? In which respect and by which hypothesised mechanism is the gate "faster", when $\tau$ is smaller? How can the voltage-sensitive steady-state activation function $m_\infty(V)$ be intuitively explained other than by "giving the asymptotic value of $m$ when the potential $V$ is fixed (voltage-clamp)" or by some complicated description of experiments to determine it? What does $m_\infty(V) - m$ mean, i.e. "the deviation of the current activation from the steady-state activation"?

1) In practice, no one attempts to obtain explicit solutions for m(t), especially considering the presence of many other ion channel species, nor is there any need to. The standard of art is to use numerical simulations with a sampling interval dT that is sufficiently smaller than any relevant time constants.
2) I'm not sure what intuitive and sensible interpretation you are looking for; it may not make sense to come up with an intuitive explanation for each and every subset of terms. The use of time constants implies that the system is modeled as a linear time invariant system at a given voltage.

What does the time constant τ(V) and its dependence on V mean? In which respect and by which hypothesised mechanism is the gate "faster", when τ is smaller?

The time constant is a scalar that describes the rate at which the system approaches some equilibrium. You could think of the changes in channel state as chemical reactions of the form:
Open <=> Closed
which has some equilibrium and some rate constant - both the rate constant and equilibrium conditions can be a function of voltage, as depicted in the figure you provide. The physical meaning of a rate constant being voltage dependent would be that the activation energy for the transition between states is a function of voltage; when the activation energy is lower, the reaction can progress more quickly (in either direction).

How can the voltage-sensitive steady-state activation function m∞(V) be intuitively explained other than by "giving the asymptotic value of mm when the potential V is fixed (voltage-clamp)" or by some complicated description of experiments to determine it?

That's exactly what it means, and the descriptions are not complicated: the steady state value for a reversible reaction is the point at which the number of units moving from open to closed would be the same as the number moving from closed to open, so on average you see no more change: that's what steady-state means.

What does m∞(V)−m mean, i.e. "the deviation of the current activation from the steady-state activation"?

Yes, "the deviation of the current activation from the steady-state activation" is accurate. The equation is an equation for the change of m, and the change of m is proportional to the "distance from equilibrium" - this is a characteristic of any process that follows linear time invariant dynamics. Note that there are other ways to write this equation that involve a "forward rate", a "backward rate", and the concentration of units in each state (the Wikipedia Hodgkin-Huxley page you linked has these equations), but you can simplify these to the equation you show here because some proportion of the "forward rate" process is cancelled by the "backward rate": your equation is sufficient to describe the net change.

Thanks for your answer (which I edited slightly)! Please let me announce a reply to your answer which will show that it is definitely worth the effort to obtain explicit solutions for $m(t)$ (and to play around with them). Among other things: to see how action potentials happen to be created (beyond a not so well-defined threshold), or how being open (of a channel) cannot follow fast changing voltages.Please stay tuned!

With regard to $\tau(V)$: It's all about the inertia of gates, let it be activation, inactivation, or deactivation gates. I never found time constants being called "inertia coefficients" or the like, but in the case of ion channels, this would hit the nail on the head. (Note, how inertia has to do with delay.)

If you are interested in a preview: send an email to stricker@syspedia.de.

Thanks explicitly and especially for your link to Linear time-invariant theory, which was new to me.

"to see how action potentials happen to be created (beyond a not so well-defined threshold), or how being open (of a channel) cannot follow fast changing voltages" - all of these things can be answered with simulations.

That's what I am after, doing my own.  Or do you know some impressive and instructive simulations in the public?

I believe I've suggested the NEURON simulation environment to you several times.

Yes, you did, and yes, I had a look at NEURON, but unfortunately it's not a tool I could use out of the box: it needs a good understanding of terminology, theory and models (naturally!) but also of sensible variables and of the tool itself. Not so easy for someone like me (with not so much time). Thanks anyway.

https://senselab.med.yale.edu/modeldb/showModel.cshtml?model=5426 there are many premade models for NEURON like this one; frankly if you aren't willing to take the time then I feel a bit like I'm wasting my own time trying to answer your questions - it would take less time than I have spent answering questions to go through the tutorials and try out tweaking an existing simulation.

Since you seem particularly interested in ion channels lately, here is a whole list of models people have implemented in NEURON to demonstrate the effects of dozens of channels: https://senselab.med.yale.edu/ModelDB/ModelList.cshtml?id=3540

Let us continue this discussion in chat.


text:
Can you splice out the first and last exon from pre-mRNA?
I think the answer is no because there are no introns before the first exon or after the last exon, although I am not sure if this assumption is correct. Thanks!


text:
How does a trait become heritable?
How does a trait become associated with genetic loci?
It is possible for a previously negligible trait to become heritable.
For example, some phenotypes are under sexual selection, but clearly were not always under sexual selection (such as the Peacock's plumage).
How do traits like this become heritable?
If a parent favors offspring with traits that the parent shares, would this cause these traits to become heritable?

Ok, I see why this was closed, but this is a valid question. For example, see: https://en.wikipedia.org/wiki/Sexy_son_hypothesis https://en.wikipedia.org/wiki/Fisherian_runaway

The whole question is based on the assumption that it makes sense to talk about genetic trait, while it is actually a little bit undefined. The closest existing concept you might want to read about is the concept of heritability. Please see my comments in your text and especially the links on heritability.

Evolutionary psychology and genetics how does a trait become genetic

I don't understand why you are talking about evolutionary psychology in your title. The rest of the post seems unrelated.
As you have received a downvote which might be related to your title, I have now edited your title.

How does a trait become genetic?

It is unclear by what you mean here. But you should probably read about the post Why is a heritability coefficient not an index of how “genetic” something is?.

If a trait is passed down from parent to offspring how is it made that the trait is passed along as heritable.

Again, this is unclear. From the above link post, if at least part of the variation for a phenotypic trait is caused by genetic variation, then the trait is heritable (heritability differs from zero). If a trait is heritable, then parents and offspring will tend to look alike (see Why does the slope of parent-offspring regression equal the heritability in the narrow sense?).

If a woman is similar to her mother and she is sexually selected on this basis. Would this make the trait become genetic?

I don't understand why you are talking about sexual selection here.
Note that selection act on population, selecting specific genetic variants. Talking about an individual being selected just mean that the individual is carrying the genetic variant that is associated with higher fitness in the population.
Note also, that without heritability, there is no selection. You should have a look at Lewontin recipe, for example at the post How does Darwinian Evolution work?.

Parent favors Offspring with traits that they have that are similar to their own selves.

Do they? In humans? In other species? It would require a reference to really what process you are referring to and whether it is actually true.

Would this make it genetic?

Again, this is unclear unfortunately.

How a trait becomes heritable is a topic in evolutionary psychology, which is probably why they're mentioning it.

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text:
do tumour cells begin with abnormal characteristics?
At what point in the cell cycle do cells start to become tumorous? Do they have abnormal characteristics to begin with; if so what are they?

No, I recommend you look at the stages of tumour development. There are both environmental and genetic factors which contribute to this.

Cancer cells don't start to become cancerous at a specific stage of the cell cycle; you will find that while uncontrolled proliferation is a hallmark of cancer, different cancers acquire alterations in different phases of the cell cycle. BRCA-deficient cancers for example have a compromised G2-M checkpoint [1], while Rb deficient cancers have a compromised G1-S [2] checkpoint in the cell cycle.
The cell cycle is simply a property of proliferating cells and the same broad phases of the cell cycle are universal to both normal and malignant cells.
As for when abnormally growing cells actually become a cancer - this has nothing to do with phases of the cell cycle, and everything to do with the ability to break through the basement membrane of the original site (indicating the potential to be invasive/spread), because the ability to invade is a hallmark of cancer [3]
References
[1] http://cancerres.aacrjournals.org/content/67/13/6286
[2]  https://www.ncbi.nlm.nih.gov/pubmed/16936740
[3]  https://www.ncbi.nlm.nih.gov/pubmed/21376230

The question assumes that tumorigenesis is a cellular problem. My answer is a counter-question: Is tumorigenesis a cellular problem?
Sonnenschein & Soto (2018) Methods Mol Biol 1702: 15-26; emphasis mine:

[T]he tissue organization field theory (TOFT) (...) is based on the
  premises that cancer is a tissue-based disease and that proliferation
  and motility is the default state of all cells.

https://www.ncbi.nlm.nih.gov/pubmed/29119499

Sonnenschein & Soto (2016) Prog Biophys Mol Biol 122: 70-76; emphasis mine:

For a century, the somatic mutation theory (SMT) has been the
  prevalent theory to explain carcinogenesis. According to the SMT,
  cancer is a cellular problem, and thus, the level of organization where it should be studied is the cellular level.
  Additionally, the SMT proposes that cancer is a problem of the control
  of cell proliferation and assumes that proliferative quiescence is the
  default state of cells in metazoa. In 1999, a competing theory, the
  tissue organization field theory (TOFT), was proposed. In contraposition to the SMT, the TOFT posits that cancer is a
  tissue-based disease whereby carcinogens (directly) and mutations in
  the germ-line (indirectly) alter the normal interactions between the
  diverse components of an organ, such as the stroma and its adjacent
  epithelium.

https://www.ncbi.nlm.nih.gov/pubmed/27498170

In some ways this is simply a function of how we define 'tumorous'. We can trace the phylogeny of tumors in the same way we trace that of species, using DNA sequencing. In some tumors one sees a clear causative mutation at the root of the tree, so for these we might say that there was a single mutation which caused cells to become tumorous. Mostly though things are not so clear.
For instance, it's now believed that in many cancers, the rapidly dividing cells are descended from more slowly dividing 'cancer stem cells'. These cell cancer stem cells tend to survive therapies that target more rapidly dividing cells, such as radiotherapy or many chemotherapies. In such cancers we could talk about a mutation by mutation transition from non tumorous to tumorous cells.


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Why have certain plants evolved to contain psychoactive compounds?
Plants such as marijuana (Cannabis) and kratom (Mitragena speciosa) contain compounds that affect the human brain. Why have these plants evolved to incorporate substances like THC and mitragynine into their leaves/flowers?

The evolutionary history of different plants expressing psychoactive compounds can vary, and in many cases it's difficult if not impossible to pinpoint a particular origin. However, we can make some general observations:
Homology across wide ranges of species
Despite the differences between, say, a human versus a locust, animals share a lot of their physiology. Mammals and insects tend to use different neurotransmitters for different purposes, for example, but the actual neurotransmitters and their receptors are often homologous. A plant could therefore develop a compound that acts as a neurotoxin in certain insects, but also has some psychoactive effects in a human. Nicotine is an example of a psychoactive compound that has insecticidal effects: not only does nicotine protect a tobacco plant, but humans have even used nicotine as an insecticide. Plants could of course also develop toxins to protect them from other mammals, and those would be even more likely to have effects in humans.
There is even homology across kingdoms, such that plants could make compounds to prevent growth of competing plants, act as antibiotics/antifungals, etc, and all have a possibility to act on some homologous proteins that humans have.
Artificial selection
Once humans are aware of a plant's psychoactive or other medicinal properties, that plant can be cultivated and selected for desirable properties. In the case of a compound like THC, there is good evidence that this has occurred recently. In the case of plants that produce opiate compounds, many have been cultivated by humans for thousands of years, so they are a lot more prevalent than they would be if humans had not chosen to do so.
Selection bias
Maybe I should have opened with this one, because I think it's very very important to be aware of. I'm not talking about selection in evolutionary terms here, but in terms of cognitive biases. Selection bias happens when you focus on certain outcomes and not others. There are innumerable compounds produced by plants that can potentially have some biological activity in humans: thousands and thousands. Some do have psychoactive effects, others have effects on other body systems, and many have little effect at all besides dietary contributions. You notice all of the plants that do produce something "interesting" but ignore those that are benign or simply toxic.

WRT the last point, the function any particular compound performs in a plant might well have nothing at all to do with its psychoactive properties.

Indeed, that was the point I was trying to make with my first point, maybe it was unclear.


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Is Black mulberry always deciduous?
I have a black mulberry (Morus sp.) in my garden (or 2 actually). According to the information I could find it is a deciduous tree. The trees in my garden do indeed lose their leaves. However, as most native trees start to color yellow/brown/red in september and have lost all leaves by now, the mulberry doesn't. It remains green until the frost kicks in and only then drops its (still green) leaves. It almost looks like it doesn't want to drop its leaves, but is forced to so so. This can be seen at the picture below. Hence my question:
Is mulberry also deciduous in warm winters such as the mediterranean? And is it normal that leaves are still green when dropped?

The trees are generally deciduous in temperate regions, but trees grown in tropical regions can be evergreen.
According to wiki:
https://en.wikipedia.org/wiki/Morus_alba

Thanks, I thought as much but couldn't find a reference.

WARNING: This answer is very tangential to the question. Confused Morus sp. with Rubus frutticosa (don't use "common name in questions"! luckily I wrote the answer using scientific names). So, as addendum: some trees tend to lose some leaves later (in my region, such trees can recover easily with broken branches).
"Always" is "always" a strong word in biology.
You describe your mulberry (Rubus sp.) as deciduous: the leaves are changed every year.
Many plants (especially trees) lose leaves in autumn/winter and they get new one in late winter/spring, few plants are marcescent, e.g. various oaks (Quercus sp.), so the leaves dry in winter and the plant lose it just when the new leaves appeaers. Some plants lose the leaves in summer.
Mulberries, like various "small plants", tend to keep the leaves until they form the new one (eventually, replacing all the shot). In my zone mulberries tend to keep old leaves until the new one are already developing.
Why this habit? Mulberries lives at borders of forests, so they try to have more energy/sun when the tallest tree lose leaves. On the other hand, being shrub and tending to radicate easily, it keeps safer in case of frosts, and it is also not a long living organism (as "plant", not as clone).
Note some decidouos young trees have also the same habits: they keep their few leaves in winter, to try to catch up. Being young also means few investment for the original plant, so it could be still a gaining habit. Look this winter on undergrowth.
Not so different to strawberries and many grasses, which replace the leaves in springs. But they are not "decidouos", just because they doesn't have a trunk or just they replace the entire shot the shots.

I agree one should always use both names (added it to the question!). Still, I am not sure where your confusion comes from. If I say Mulberry and link to the wikipedia page on Morus sp., why do you think I am talking about Rubus sp.? Which BTW are called blackberry or raspberry, but never to my knowledge mulberry (do you have a source for this name?). Finally, Rubus sp. are always (small) shrubs, never trees. And finally: your entire answer lacks references.


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What is the difference between an alpha subunit and a non-alpha subunit in ACh receptors?
When reading about ACh receptors, it is frequently the case that a protein is described as (alpha) or (non-alpha).  However, I haven't really been able to find out what that means.  What is the difference, and why would it matter if a subunit is alpha or not?

Achetylcholine (ACh) receptor is a pentamer of two alpha chains, and one each of the beta, delta, and gamma (in immature muscle) or epsilon (in mature muscle) chains.

I see. So is it called alpha simply because there are always two when the others are only one?

an alpha subunit is alpha; a non-alpha subunit is beta, gamma, delta, or epsilon.

I fear that still doesn't clarify.  The subunits are different proteins, is that right?  That being the case, is there anything special about alpha?  I assume so, since the sub units are grouped as "alpha" and "non-alpha", implying that alpha has special status, doesn't it?

The alpha subunit contains the acetylcholine binding site. Lyddiatt et al. (1979) FEBS Lett 108: 20-24 (https://www.ncbi.nlm.nih.gov/pubmed/520545); Sumikawa et al. (1982) Nucl Acids Res 10: 5809-5822 (https://www.ncbi.nlm.nih.gov/pubmed/6183641).


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Do death rate and birth rate become equal at replacement fertility rate?

A population transitions from stage 3 to stage 4 when the fertility rate reaches the population replacement level of 2.1.
My question is that if the population replacement level reached, shouldn't the net growth rate be zero? i.e., birth rate = death rate? But in the figure, in stage 4, birth rate > death rate and there is still a population increase.
How is this so?

The transition to stationary populations is between stage 4 to stage 5 in all exemples of the DT model that I've seen. Not between stage 3 and 4. This is also what is being implied in the figure that you've included. In your link they also write:

Countries like India in the third phase of demographic transition have fertility rates that have declined significantly from previously high levels but have not reached the population-stabilizing "replacement level" of 2.1 children per woman.

This is not saying that countries reach the replacement level 2.1 at the end of stage 3.
The same stages are also described at the Wikipedia page on DT and at populationeducation.org.
So you are correct; at replacement levels, populations shouldn't increase and the net growth should be zero.


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Why do most plants reflect green and others other colors?
I have read that chlorophyll absorbs red and blue.

As shown in detail in the absorption spectra, chlorophyll absorbs light in the red (long wavelength) and the blue (short wavelength) regions of the visible light spectrum. Green light is not absorbed but reflected, making the plant appear green. Chlorophyll is found in the chloroplasts of plants.

It did not mention what the difference in chlorophyll between a red leafed plant and a green plant?
Does chlorophyll only come in green?
 So what in chlorophyll determines if other colors than green are reflected in plants that are naturally red? If chlorophyll needed can only be green would not the color green and the red from a " pigment" look brown?
Japanese Blood Grass

Blue Selaginella

Solenostemon scutellarioides

Plants contain many compounds that are not chlorophyll, for one.

Please provide some examples of plants that naturally - that is, not as a result of human selective breeding - have red leaves.

@jamesqf i made one working on more

@Procreator: The examples so far seem to be the result of human selective breeding.. Plants have other pigments in their leaves, as you can see when leaves change color in the fall.  That's caused by the breakdown of chlorophyll, allowing the other colors to show.  In the first two of your examples, you can see that there is clorophyll showing in parts of the leaves.  It's just that the intense pigment in the blood grass and the internal structure of the blue leaves masks the green of the chlorophyll.  I expect something similar would be true of the coleus.

Are you sure all the example are selective breeding? I didn't check either, but if there is presents of chlorophyll as in normal plants the color green and the red pigment would blend to make brown.

@Procreator: Fairly sure, as they're all garden plants.  The coleus, for instance, has been bred into many different cultivars with different colors & patterns in the leaves: https://plantcaretoday.com/colorful-coleus-plants.html  The best way to show that they do have chloroplasts would be to examine leaves under a microscope.  Can't do it myself, since I don't grow them (they're tender, and need more mosture than I have), and it's winter here anyway.  Google "coleus leaf chloroplast" for info.

@jamesqf then answer and i will up vote you

Here's an example of a plant (common to the mountains hereabouts) that doesn't have chlorophyll, the snow plant: https://www.fs.fed.us/wildflowers/plant-of-the-week/sarcodes_sanguinea.shtml  But it doesn't use the red pigment to photosynthesize, having become parasitic on soil fungi.

@jamesqf make sure to include what the pigments are composed of and what purpose they serve.

@jamesqf do you want me to compose an answer using your comments?

Tl;dr : Some plants reflect green while others don't simply because some plants are green while others are not.
Plants contain chlorophyll, but are not 100% made of it. Parts of the plant that contain a high amount of chlorophyll will look green, (Leaves, stem) while other parts that contain less chlorophyll and contain more of other pigments will look different. The flower looks red because it contains a lot more red pigment than any other pigments. The fruit looks yellow because it contains a lot more yellow than other pigments.
Carotene(orange) and Xanthophylls(yellow) are examples for pigments which absorb all colors except orange and yellow respectively, they reflect these colors. so it appears to be orange or yellow.
"Chlorophyll absorbs red and blue" is just another way of saying chlorophyll is green in colour.

I think the confusion is why some plants have a benefit to have less clorophyll and others more.

@MaDrung then it's not a physics question anymore. I'll wait for op to clarify.

This question is surely off topic here, but as long as you've answered in this way, it might just bear pointing out that different structures have different purposes.  A red flower may be intended to attract pollinators that wouldn't notice just another green thing.  A tree trunk (the purpose of which is support and transport) might be gray due to weathering or red due to the presence of protective tannins.

@Mike a red plant not flower.

Can you clarify what the pigments are made of?

All photosynthetic plants contain chlorophyll, and chlorophyll is green (leaving out various algae).  Plant leaves often contain other pigments, which can mask the chlorophyll's green, or be masked by it.
A common example of the latter is the color of autumn leaves.  The leaves contain various pigments such as xanthophylls, anthocyanins, and carotenoids that are generally masked by the green of the chlorophyll.  As the trees prepare to drop their leaves in the fall, the chlorophyll decomposes, allowing the other pigments to become visible.  Exactly what purpose(s) these other pigments serve isn't entirely clear.  Some are thought to make photosynthesis more efficient, others might have functions where the color is irrelevant.  See e.g. http://www.usna.usda.gov/PhotoGallery/FallFoliage/ScienceFallColor.html
Some plants may have a larger than average amount of other pigments, somewhat masking the chlorophyll's green, and giving rise to different shades of leaf color.  Human selective breeding can increase these differences, giving rise to e.g. the purple-leaf plum or the almost golden color of some honey locusts: https://www.thespruce.com/trees-and-shrubs-with-purple-leaves-3269731
Other plants, like the coleus, may have chloroplasts only in certain zones of the leaf, allowing other color combinations, which can be wildly amplified by human breeding:  plantcaretoday.com/colorful-coleus-plants.html
Sometimes the colors can be structural, as with the Blue Selaginella pictured in the question, or the grayish colors of desert plants that are produced by protective hairs: http://mojavedesert.net/plants/plant-adaptations.html
Finally, there are plants that don't have chlorophyll at all, but these don't photosynthesize.  An example (common to the mountains hereabouts) is the brilliant red snow plant:  fs.fed.us/wildflowers/plant-of-the-week/… But it doesn't use the red pigment to photosynthesize, having become parasitic on soil fungi.

Can you eat it?

@Procreator: Eat what?  The snow plant?  Supposedly yes, but they're illegal to pick.  Supposedly because they're rare, but they seem quite common in the mountains around here: https://www.scenicwonders.com/blog/rare-snow-plant-in-yosemite-west

In a survival situation.is why I was asking.


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What is the most readily usable form of nutrients/energy source for heterotrophic microorganism in general?
Consider a nutritious mixture containing abundant soluble sugars, soluble lipids and soluble protein etc. Would heterotrophic microbes preferentially use sugars first > lipids > proteins > insoluble polymer such as cellulose (please propose your own order if this is wrong)? If appropriate, you can further differentiate these compounds into e.g. sugars into monosaccharides and oligosaccharides. Is there a general trend or is it highly variable depending on the particular microbe concerned?

The generalization is not possible. For example, chemolithoautotrophic bacteria do not use organic molecules or polymers as the source of energy and carbon.

Thx, I edited the question


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Re-Plumping Dried Insects
I have begun to display some of my soft bodied insects and as I am trying to rehydrate some of them that were plump in the abdomen, they appear to have shrunk and the bodies have sunk into themselves.  Does anyone know how to avoid this or what can be done to plump the bodies back up?

using a serynge of silicone?

"Soft bodied" can come from a number of conditions, but generally, soft bodied insects are kept in ethanol. Adult insects should not need any kind of treatment before being pinned. Nymphs and immature insects should be in ethanol, and I suspect this is what you have. However, they can be freeze dried for a nice effect. One technique that works for females that are full of fatty eggs (such as Orthoptera) is to make an incision on the ventral side with an exacto-knife, and scrape out the contents of the abdomen. Then stuff with cotton, and close the incision. I think you likely have immatures, which should be in ethanol, but this technique would work if you are careful.

Sorry, I may have not fully explained what I am trying to do.
I have just re-hydrated, pinned and dry mounted some rather large bodied insects (spiders and soft bodied leaf cutters and the like) and their abdomens are beginning to dehydrate.  I believe I had seen that you could inject them with something  (not sure what) and it would dry and keep the body in shape.  I was hoping for some suggestions.
Nothing like a caved in body to show your friends!

Also, I have tried Purell for a few black widows that I got as a gift, but they are starting to look as if they are fuzzy. I do not normally use ethanol, is there another suggestion of something readily available.  Thank you again... Jenn B

I guess if I were you, and did not have access to a freeze drier, than I would use trial and error. Try injecting different things on some common spiders you don't care about. Like silicone (as suggested above), or even Elmer's glue.


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Validated Protein-Protein interaction database for cancer
I need to use validated PPI data in my research. Is there any database of such validated (like Mass Spectrometry) database for cancer?

One of the most popular databases of PPI data is STRING. It is not only for cancer though, but since many research is done in the field of cancer, you will find a lot of data derived from cancer research.

OncoPPi

This site provides a platform to facilitate discovery of new
  mechanisms to control tumorigenesis through the integration of
  genomic, pharmacological, clinical, and structural data with the
  network of cancer-associated protein-protein interactions
  experimentally detected in cancer cells.

Li et al. (2017) The OncoPPi network of cancer-focused protein-protein interactions to inform biological insights and therapeutic strategies. Nat Commun 16: 14356.


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How do trees grow?
A nail is inserted into a tree's trunk at a young stage of its development. At which height will we find the nail after some years? Will it be found higher or at the same height(What extent of accuracy?) as when it was inserted? I have two specific questions:

Doesn't the intercalary meristem, which is responsible for the
increase in internode length, affect the relative position of the
nail?
When plants are at a young stage their branches' position would be low but after some years they would have moved higher. How does this
happen if growth only happens in the apex? As an example, in the
following image the position of the branches changes with time. Why
wouldn't the same happen with a nail?

Welcome to Biology SE! I have suggested an edit of your question in an attempt to make it more cleear. Feel free to roll-back the changes if you do not think it was useful.

One cell at a time.

You will find the nail at the same height.  Trees grow by a) adding to the tips of their branches (sometimes sprouting new branches at nodes), and 2) adding to their diameter.  (Only a thin layer inside the bark actually grows, forming the annual growth rings.)
The branches changing position in your image is an illusion.  The branches do not actually move.  What happens is that the higher branches grow larger, shading out lower ones, which die (or become leafless support branches).  You can see this most obviously in many conifers, where the dead lower branches tend to remain on the trunks.  If you cut and split a trunk, say for firewood, you will find knots in the wood where the older, now dead, branches were once attached.

Nice answer. It would be even better if you included some references.

@RHA: If you want references, feel free to add some.  I don't have any, other than high school biology and spending a lot of time observing trees.  As for instance signs & wire fences nailed to trees.  Decades later, they're at the same height, but the tree bark has grown around them.


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Why is cancer more lethal than (hypothetical)infections?
I am a computer science student and I'm interested in algorithmic aspects of cancer! Once I heard that there exist more bacteria in human body than our own cells, I wondered that why bacteria, which divide faster than cell bodies, do not cause something like cancer in body? Isn't it evolutionary more probable for bacteria to gain aggressive properties and invade human tissues? Or maybe is it the case that bacteria really produce some lethal colonies like cancers in the body?
One difficulty with cancers is that cancer is a very complex disease  because of it's intra-tumor and inter-tumor heterogeneity. Isn't it more probable for bacteria to cause extremely heterogenous infections with regard to existing simple evolutionary models which are used to describe cancer?

Most of the bacteria you refer to live in the gut, and have evolved to coexist, not invade. Pathogenic bacteria are aggressive, and have evolved to invade human tissues, but our immune systems keep them in check. You would not call them "cancers" though.

@KarlKjer shouldn't it be that the pathogenic bacteria have not yet evolved to coexist with humans?

@Polisetty it's a common misconception that pathogens evolve toward "coexistence". Pathogens are selected for transmission, and while low virulence can sometimes help transmission, so can high virulence. So saying "not yet" implies an inevitability that isn't real.

@KarlKjer you are right but normal cells are evolved to help the whole organism but accidentally they become invasive! I think that bacteria according to their numbers and their higher rate of mutations are more prone to show such aggressive behaviors!

It's meaningless to suggest a bacterial tumor; tumors are by definition from the same organism as the host. If you have an overgrowth of bacteria you would just call that an infection, there's no need to reuse the term tumor in that context because an entire separate vocabulary exists to describe infections.

@BryanKrause you are completely correct! But the main point is why cancers are more lethal than infections? Cancer is very complex because of  it's intra-tumor and inter-tumor heterogeneity. Isn't it more probable for bacteria to cause extremely heterogenous infections in existing simple evolutionary models which are used to describe cancer?

@CharlesE.Grant You are right but the question is really that what is inherently different? Why something like anti-bacterial drugs do not exist for cancer! As far as I know one of the popular answers to this question is tumor heterogeneity and that cancer is not a single disease! The question is  why it is not the case in the bacteria scenario!

@Dandelion That's pretty similar.  Anti-bacterial drugs also kill good bacteria.  Likewise, there are drugs that kill cancer cells but also kill good cells.  Cancer cells, like bacteria, can be said to "evolve resistance" to drugs.

Cancer is not inherently more lethal than bacterial infections. That's simply an artifact of the time we live in. Broad spectrum anti-bacterial drugs we invented in the 1st half of the twentieth century. Before that, most folks died of infections. Cancer was relatively rare because most folks didn't live long enough for cancers to become apparent.
Why do we have generic drugs for bacteria and not for cancer?  Largely because bacteria are not eukaryotes and we are. The biology of bacteria and human cells are so different that it's relatively easy to find drugs that dramatically affect bacteria, but not people. I say relatively easy, but still took several thousand years of human history to figure it out.
Because cancer cells are just variations on our normal cells, it's very hard to find something that kills the cancer cells, but not the rest of us. That's why chemotherapy makes folks so sick: the chemotherapy agent is killing, or significantly impairing, fast growing healthy cells along with the cancer cells. The most successful cancer drugs have identified rare metabolic pathways that are important to specific types of cancer, but not so important to healthy cells.

Thank you but I think that extremely huge number of bacteria living in our body still seems unbelievably harmless! Almost all infections -as far as I know and of course I know just very little molecular biology and almost nothing else in the field of biology and bacteriology- have external sources!!!

All the bacteria in our bodies, not just the infections, come from external sources. You start collecting them as you path through the birth canal and never stop. As to being "unbelievably harmless":  there are lots of bacteria that are perfectly harmless when they are living in your gut, but potentially lethal if they start growing in your blood, your lungs, or your urinary tract. It's worth keeping in mind though that cooperation (symbiosis) can be a powerful evolutionary strategy.

Charle's E. Grant's answer, that bacteria are typically different from us and hence easier to kill, is most of the answer. Remember that this applies not only to drugs but to our immune system, which can have difficulty detecting cancers (while catching most of them) but is excellent at detecting foreign organisms like viruses or bacteria.
You do still ask a valid question however - shouldn't the enormous number of replicating cells in our gut mean that some bacteria occasionally arise which break the co-operation between bacterium and host, and cause problems (albeit problems mainly limited to the gut) ?
The answer seems to be - yes. We're only beginning to understand how people's microbiomes work, but it seems likely that they can be dysfunctional and this causes health problems. Sometimes this involves a single strain of bacterium overwhelming all others - this is in some ways analogous to a tumor.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315779/

Cancer cells are technically human cells and programming the immune system to recognize them can cause autoimmune problems. Some cancer mutations also fail to manifest on cell surfaces, making the cancer cells near impossible to medicate (without widespread friendly-fire on healthy cells) or immune-target.
Bacteria are plenty different enough that the immune system can target them with abandon and almost no risk of autoimmune problems. If they aren't resistant, you can shut them down with antibiotics (specifically designed against prokaryotes). A common approach includes interfering with bacterial ribosomes (which are fortunately different enough that the treatment doesn't significantly interfere with human ribosomes). If the antibiotic ever stops working, throw in some bacteriophages.


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Measuring Enzyme Kinetic constants
Is it possible to experimentally determine $k_1$ and $k_{-1}$ of the Michaelis Menten model:
$\ce{E + S <-->[k_1][k_{-1}] ES ->[k_{cat}] E + P}$,
or their ratio?


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CDK3 1 simple coding mutation/missense mutations (S106N) glioma
I found the below quotation in (Peyressatre, 2015)

CDK3   1 simple coding mutation/missense mutations (S106N)   glioma
  [135]

The author has cited a database but not a paper. I want to find the paper that talks about the above mentioned type of mutation in CDK3

Welcome to SE Biology. Two points about your question. 1 "Peyressatre, 2015" does not allow anyone who doesn't already know to find the paper your quotation comes from. Please include a proper journal reference, perferably with a link. (Also to the database). 2. What effort have you made to search for this yourself and with what results? This sounds a very specialized question for this list. You must help anyone who is interested in the area to help you.

Good question, if you check COSMIC and search for S106N, you'll find no hit with CDK3. So it isn't there (anymore?). One possibility is that it was present in 2014, when the paper was written, and the mutation is removed in the mean time by curation.
However, if you look at genecards and look for the variants, on top of the table you'll find a link to expasy. here they cite to a paper in Nature, and in the supplementary data of this paper you'll find your CDK3 S106N mutation.

UniProtKB: Cyclin-dependent kinase 3 (CDK3): Homo sapiens: Natural variant: 106 S to N in a glioblastoma multiforme sample; somatic mutation: 1 Publication [Greenman et al. (2007) Nature 446: 153-158].


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Which synamorphy evolved last
I know that if species are on the same height level, they existed at the same time and indicates extinction. Does that apply to synamorphy? Did hair and eggs with shells evolve at the same time or did one evolve last?

Your CAPS is on, it reads like you are yelling.

A cladogram does not indicate time. That would be a calibrated phylogram. We can tell from the above cladogram that the two synapomorphies "Hair" and "Eggs" with shells are the two most recent, and happened after all the other ones because cladograms do indicate the relative timing of events. However, knowing a bit about mammals, "Hair" is the more recent than eggs with shells. Actually, eggs with shells should be on the same internode as "Amniotic eggs" in this cladogram, because Montreme mammals had eggs with shells, which were lost in the most recent common ancestor of Marsupials and Eutherians (Primates and Rodents/Rabbits are both Eutherians). So "eggs with shells" came first.

Thank you very much Karl Kier. Lets say we didn't know which came frst (ignoring your explanation that hair is more recent than egg with shells). Would you be able to tell which came first, hair or eggs with shells, SOLEY, by looking at th cladogram (by comparing their respective heights on the cladogram)?

No. Cladograms are about relative relationships. So deeper in the tree is older, but by definition, sister groups (in this case Eutherians and Archosaurs) are of equal age. There is no estimate of branch lengths in cladograms. Its just not what they do. There are ways to estimate time with clock methods and models. But cladograms don't do that.

@KarlKjer I believe they are refeed to calcified eggs which synapids do not have.

@John Pelicosuars, and many if not all the extinct synapsid mammal-like reptiles (mammal ancestors) likely had calcified eggs, all of which are placed on this internode.

Do you have a source for that because I have never heard of calcified eggs for Pelycosaurs or synapsids. And that would be a pretty important discovery.

@John Interesting. I may have fallen prey to something I have always warned others against; assuming that pelycosaurs are like dinosaurs, when clearly they are not. However, it is safe to assume that they laid eggs on land. And turtles, crocs, and dinosaurs laid calcified eggs despite their phylogenetic distance. And Monotremes lay eggs. The cladogram said "eggs with a shell", which monotremes have. Why is calcification a critical part of that definition? I confess to not knowing if monotreme eggs are calcified.

calcification varies in reptiles, some including monotremes show none, others including turtles crocs and gekko show some calcification with varying degrees of thickness and structure, hard thick calcified eggs are likely unique to dinosaurs and their descendants birds. http://www.tandfonline.com/doi/abs/10.1080/08912963.2013.829824?src=recsys&journalCode=ghbi20


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The use of cytotoxic T-cells
The video below mentions whether the dendritic should call in a 'anti-virus force' or an 'army of bacteria killers'. The video goes on to talk about how bacteria is killed, using B-cells, but there's no mention of cytotoxic T-cells. Is the cytotoxic T-cells only for viral infections or is it for both?
https://youtu.be/zQGOcOUBi6s?t=2m42s   <-video is time stamped.
I don't study biology and the internet is confusing sometimes.

I didn't watch the video, but the answer you're probably looking for is that cytotoxic T cells are for intracellular infections -- that is, CTL target pathogens that grow inside one's own cells.  All viruses grow inside cells. Some bacteria also grow inside cells (e.g. tuberculosis, Listeria); those bacteria can (often) be effectively attacked by CTL. Many bacteria do not replicate inside cells, and for those, CTL aren't effective, but B cells (via antibody) and T helper cells (by recruiting other cell types and modifying inflammation) can still be effective.

This is all true. I would also add that an important function of cytotoxic T cells is to kill abnormal cells - such as cancers.


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Do strictly anaerobic organisms use metabolic reactions requiring oxygen?
When looking through genome annotations of strictly anaerobic organisms I see reactions featuring oxygen. I suspect these are likely an artifact of the annotation process. But I am wondering if it is possible for such organisms to have oxygen associated metabolism. Strict anaerobes are known to die in the presence of oxygen due to the lack oxidative stress pathways. So I cannot think of any reason for oxygen to be part of their metabolism.

Is it a molecular oxygen? Can you show some examples of reactions in anaerobes involving molecular oxygen?

Here is one of the reactions I came accross: Ferroxidase: 4 Fe2+ + 4 H+ + O2 = 4 Fe3+ + 2H2O

This is an aerobic oxidation of ferrous iron---impossible in strict anaerobes.

Strict anaerobes do not use molecular oxygen for oxidation reactions.
The oxidation of ferrous iron to ferric iron (viz. the example given by Septimus G) can be done anaerobically by anaerobic purple bacteria [eq. 2 in Ehrenreich & Widdel (1994) Appl Environ Microbiol 60: 4517-4526]:
4 FeCO3 + 10 H20 --> 4 Fe(OH)3 + (CH20) + 3 HCO3- + 3 H+

https://www.ncbi.nlm.nih.gov/pubmed/7811087


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What is the probability that there are no substitution between an ancestor and a modern individual?
What is the probability that there are no differences if you compare the DNA
of the ancient sample to a single DNA sequence from a modern individual? Assuming the individual was diploid and lived T generations ago.
How would you go about finding this probability? I would assume that drift and maybe selection would change the sequence and the probability of no change over time would be extremely low.

Expected number of substitutions
Let's assume a haploid mutation rate of $\mu$ and a population of constant size $N$. For simplicity, I will assume an absence of selection because otherwise, we would need to talk about what kind of selection you want to talk about.
There are therefore $2 N \mu t$ mutations since this last ancestor. A fraction of $\frac{1}{2N}$ of them drifted to fixation. Therefore, there were $\frac{2 N \mu t}{2N} = \mu t$ mutations fixed.
If we consequence a sequence with a mutation rate of $\mu = 10^{-4}$ (about 10 kilo bases if is a human genome) and $t = 10^5$ generations. Then, there were 10 substitutions (on average).
Of course, the assumption of no selection is likely wrong and violation of this assumption could well drastically affect this estimate. However, you would need to perfectly describe what type of selection pressures (and what selection coefficient and dominance coefficient) you want to consider for more calculations.
Probability of k substitutions
As events of substitutions are independent, the probability that exactly $k$ substitutions happen given the expected number of substitutions ($\mu t$) is given by the Poisson distribution with rate $\mu t$. The probability $P(k | \mu, t)$ of $k$ substitutions had happen in $t$ generations, given the mutation rate $\mu$ is therefore
$$P(k | \mu, t) = \frac{\left(\mu t\right)^k e^{-\left(\mu t\right)} }{k!}$$
Per consequence, the probability of no mutation is obtained by replacing $k$ to zero
$$P(k=0 | \mu, t) = e^{-\left(\mu t\right)}$$
Again, if $\mu = 10^{-4}$ (about 10 kilo bases if is a human genome), then the probability that zero mutation had happen in $t = 10^5$ generations is $e^{-10^{-4} 10^5} ≈ 5\cdot 10^{-5}$

Thanks, that makes sense. So would the probability there are no changes just 1-μt? I.e. 1-the probability of mutation,

@Frankfras I only gave you the expected number of substitutions. To compute the probability of $k$ substitutions, you need the Poisson distribution. See edit for more info.


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Do Vaccinium membranaceum plants need a minimum amount of darkness per 24 hours?
I have Vaccinium membranaceum (black huckleberry) seedlings growing in a greenhouse. I have the option of providing fluorescent light to the plants 24 hours a day.
However, it has occurred to me that plants like Vaccinium membranaceum might require a minimum amount of darkness per 24 hours.
What darkness requirements do Vaccinium membranaceum plants have?

This is likely to vary greatly given that some Vaccinium species grow under thick (shaded) canopies while others are capable of growing in clearings and forest gaps. So, they would experience different amounts of light to begin with. Are you instead thinking that perhaps temperature differentials or time spent respiring might impact the plants?  What research have you tried to do on this topic on yoru own?

Some plants are long day plants -- they require a certain number of days longer than a certain number of hours.
Some plants are long night plants -- they need nights that are longer than a certain number of hours.
See this for more details: http://www.biology-pages.info/P/Photoperiodism.html
Other plants are day neutral.  They bloom when triggered by other stimuli such as it being warm enough.
If you don't care if they bloom or not, then you can give them 24 hour light.  They should grow somewhat faster.
However, you may need to check what triggers them into dormancy.  E.g. Spruce start going into dormancy when days get shorter than about 10 hours (Varies by species, and provenance)  Reforestation growers trick them into going dormant in August with black tarps in mid afternoon.  They can then plant them with minimal stress, and they take off in the spring.

Please add citations or additional support to backup some of your claims. Thanks.

Can't.  First year botany lecture 45 years ago.

My old plant physiology textbook is at the office and it has been 15 years since I had the class so going a bit off memory here...  But yes, they do have a circadian rhythm and benefit from having a dark cycle.  There really isn't any need or extra benefit from having them under more than 16 hours of light.  I can dig out specifics from my textbook and old class notes later if someone else doesn't chime in with more info...

Recalling info from memory is much better reserved for a comment on this site. Answers should be complete. I recommend that you find your textbook and provide direct evidence (either a quote, citation, etc.) to support your claims. Thanks.

What's the title of the textbook? I'll order a copy.


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How lion can carry the cub without harming it?
We can see in the picture that lion is carrying its cub by the scruff of its neck without causing harm to it.

The skin of the felines has geneticaly evolved in such a way that the parent can do this.
Its strong and stretchy in the neck area.
Moreover, the cub enters into an obedient state.

Too complicated. I was going to answer but know I would get "dinged" because people on here seem to prefer the complex over the simple. The answer is "They don't bite down". Thats it. You can prove it to yourself. Put your finger in your mouth, and close your teeth around it. What keeps you from biting your finger off? : Intent.

@KarlKjer — Answer in answers or not at all. Comments are explicitly not for answers. It's a pretty naive question that demands a straightforward answer. If people 'ding' you just shrug it off.

just try to "ding" a human and see where is going :)


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Is there a way to determine how far and how fast an animal can run for based on geometry?
I was looking at research and finding that drastically different animals can fall under the same brackets for how far and how fast they can run, or that similar animals can fall under different brackets. For instance, a kangaroo could hop at 40mph for a couple miles, meanwhile an elephant can also run about 40mph but for only a couple miles. They're very differently shaped animals, and yet have a similar ratio of their sustained run to their stamina.
Conversely, humans can run for a very long time but maybe no more than 20mph for those in great shape, though they can do it for many miles, over 20 miles which is longer than an elephant can run for. Bears have very similar legs and feet to humans as they are both larger plantigrade mammals, but they can run at 35mph for their top speed and otherwise don't have as much stamina as humans.
Felines and canines are often thought to be similar in many ways. Wolves are known for being able to run and walk for long distances, often having more stamina than their prey and moving 10-30 miles in a day. But, their top speed is only somewhere in the range of 20-35mph. Lions have very similarly shaped bodies and yet are more adapted to run short distances at around 50mph. Similarly, dogs can run for long distances, but cats can jump much higher and not just in proportion to their body length but in terms of absolute length, despite having very similarly shaped bodies.
The reasons for these differences must have something to do with the combination of the geometry of their vertebral column, legs and feet over which their muscles are shaped as well as the weight of an animal. If an elephant was lighter, it would surely run much faster, probably comparable to a horse as its feet are already ovaloid and digigrade. And, if a dog was lighter, it would probably be able to jump higher than a cat. If humans were more massive, then they probably wouldn't be able to run as far, but would probably as fast or faster due to increased muscle mass that compensates. A horse and other horse-like animals seem to have a very good ratio of geometric features to mass that lets them run both very far and very fast.
With all this diversity in mind, what common denominators can be found to account for how the geometry of an animal determines its speed for its given mass?
For instance just as a very crude estimate, I would say animals with particularly long legs that are more closely aligned with the angle of their vertebral column have a tendency to run the farthest, but also the slowest. This might have something to do with how the elasticity of longer muscles and tendons is more efficient for repetitive motion, but not necessarily for propelling a body forward by keeping the force transferred from feet perpendicular to the ground up the leg and in the direction of motion.

Somewhat related: Why don't mammals have more than 4 limbs?

At first thought, I'd imagine that anatomical geometry & stature would most heavily influence the initial acceleration of the organism, as well as top speeds. From there, the predominant muscle type (slow vs. fast twitch) in the legs of the organism, coupled with a consideration of the organism's metabolic rate, would reveal how far it can travel. If you're wanting to study the kinesiology itself, then, a wholesome response to the OP would probably be too complex for this medium of Q&A. It is a good question though..

Is there anything about the anatomy of a given animal that would suggest it has more slow or fast twitch fibers?

It's not entirely a matter of geometry, but of differences in muscles, lungs, and circulation.  For a good example, read about the extreme endurance of sled dogs.

Couldn't those differences simply be attributed to training? I'm referring more to a purely elementary setting.

No, the differences between sled dogs and other breeds of dog are more basic than training.  They have better endurance &c than similar-sized dogs of other breeds that recieve the same training.


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What is the neural coding of rod and cone cells?
In Rushton's paper on the Principle of Univariance, he states:

Thus, though the rod input has two variables, wave-length and energy, the output differs only in one respect, namely 'brightness'.

However, as far as I understand, a photon can only vary according to one dimension, namely wavelength (vibrational energy), because the wavelength and energy of a photon are interdependent.
This suggests then that the input to a cone cell, for brightness to be perceived (i.e. the intensity of light), must be a beam of photons, so that the input can vary in wavelength and amplitude (does this equate to the number of quanta being absorbed by the photopigment per unit of time?).
My question, then, is how can a discrete event (the changing of shape of a photopigment) encode a continuous value (i.e. intensity)?

Indeed, brightness is a matter of photon count.
In any given rod, there are numerous photopigment molecules. There are about 1 billion rhodopsin molecules in any given rod, so although a change in conformation of any single rhodopsin molecule is a discrete event, you can consider the fraction of 11-cis- versus all-trans retinal (a photoreceptor's initial readout of brightness) to be effectively continuous, even more so because there is a <1 probability of a photon of light being absorbed by any rhodopsin molecule, so the discrete measure itself is an approximation of the 'actual' brightness/photon count.
Although it isn't perfectly analogous, because here we are talking about proportions rather than actual bitwise encoding, consider that computers are also able to represent fairly continuous values, but they are still always discrete approximations to those continuous values. A 24-bit computer monitor, for example, can actually only display 256 different intensities for each R, G, and B color stream (8 bits each).
The principle being discussed in the paper you describe is that once a rod (or cone) absorbs a photon, it loses any information about what the wavelength was, only that it was sufficient energy to activate the rhodopsin in that photoreceptor. There are several other questions and answers here on Biology.SE that discuss how wavelength (i.e. color) information can be extracted by differential activation of different cone types, for example:
Why can cones detect color but rods can't?
How do our eyes detect light at different frequencies?


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How much damage is caused by smoking 2-3 cigarettes on a healthy body?
I do not know how bad does 2-3  cigarettes on the average healthy body.
I do not want to include genetic factors on this issue.
So, maybe there is a study or something on this topic.
Does it cause a real damage, or to this quantities the body recovers.

2-3 cigarettes a day/week/year/life?

This question is way too broad, and, IMO, isn't well-suited for this site. Perhaps Health.SE would be better?

2-3 a day, right

I think it's suited for both of them, but i'll address it there as well.

http://tobaccocontrol.bmj.com/content/14/5/315
2-3 cigarettes could make difference absolutely.  It deals 5 points of damage exactly; just kidding.  Hopefully this study provides some insight.


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When did birds and mammals diverge?
Which was the most recent common ancestor between mammals and birds?
Form a rapid google research I could not find good answers. This site seems to imply it was at least 250 milions of years ago. This scientific article mentions 600 milion years but the sentence is a little unclear.

You can check it easily in the timetree website:
http://www.timetree.org/
Put a mammalian species as taxon 1 (Homo sapiens) and a bird as taxon2 (Gallus gallus) in the first pair of boxes and hit run.
You will see a compilation of studies, with their references, with different calculations about the time when the last common ancestor of both species lived. A median and a mean are also provided.
In this case the values are
Median Time:
320 MYA
Estimated Time:
312 MYA
CI: (297 - 326 MYA)

Useful tool for the timing! Any Idea about which one is so far the recognized  MRCA?

The Most Recent Common Ancestor (MRCA) of birds and mammals was the first amniotes.
Fossil record
The latest known fossil of amniotes are 312 million years old (Bentou and Donoghue, 2007).
Genetic data
From EOL, using data from The Paleobiology Database, the first amniote is in between 314.6 and 323.2 million years old. Those results are a little bit older than the latest known fossil which very much makes sense.
The (apparent) contradiction in the sources you found

This site seems to imply it was at least 250 milions of years ago.

They actually say 250 to 320 millions years. This broad estimates match the above studies and data.

This scientific article mentions 600 milion years but the sentence is a little unclear.

It is actually a news feature published by a science writer (former neuroscientist according to her twitter account), not a researcher. She indeed made the claim (Even so, 600 million years of evolution and radically different brain architectures separate birds from humans.). There is no reference for the claim and based on above evidences, it appears at first to be a mistake. It is not impossible though that she considered the evolutionary time in both branches in her statement but that would be very unusual If two lineages diverged $t$ years ago, then they both evolved for $t$ years and it could arguably be said that they are separate by $2 t$ years of evolution. If this is what she meant, then the claim is correct but quite misleading.

Scientists do not use the convention of measuring time on both branches, between endpoints, although maximum likelihood methods of estimating nucleotide states do measure both branches. So 600 million years is an error. Also, the first terrestrial ecosystems were little more than some plants surviving on the seashore, about 450 million years ago. The Earth was an inhospitable place with nothing to eat (Misof et al., 2014); no way could amniotes precede plant life.  The first tetrapods were much later, which preceded the first amniotes.

Also, the "first" amniote was not the MRCA of birds and mammals, as it is most likely that amniotes survived for a time, and diversified before branching off into synapsids and diapsids.


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Do Tardigrades preserve water or replace water?
If you find something funny in my argument, then please pardon me, as I lack knowledge of biology. I was reading an article titled as "Water Bears Can Replace All The Fluid In their Bodies With A Glass Matrix"
Being extremely new to biology, I am a bit confused. Do Tardigrades preserve water through this protein or entirely change their biological structure to flush away all the water present in their body and rely on these proteins? Does this mean that their bodies no longer contain water?
Thanks.

neither they are desiccating, some water remains but too little to sustain normal processes, the matrix just preventing all the normally destructive side effects of desiccation that would destroy the cellular machinery, the cellular processes are still essentially stopped.

Cellular processes are essential for living. You haven't clarified how Tardigrades survive without cellular processing taking place in them.

not really, if the proteins and other molecular structures are not degraded they can be interrupted and restarted, your own article discussed how the tardigrade proteins keep other proteins from degrading during dehydration. and tardigrades have other molecules to protect cellular membranes and nucleotides. Its just for 99% of all life the molecules degrade if   dessicated and wont function if rehydrated. Some single celled organisms and spores can survive suspended processeshttp://onlinelibrary.wiley.com/doi/10.1017/S095283690200078X/abstract;jsessionid=9D9B775F84753DB9AC7B12BCDFDD120D.f02t01


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Are there any bacteria, virus or mold that can withstand ozone?
Ozonation is often promoted as one of the most effective disinfection procedures. There are numerous reports on how ozone effectively kills bacteria and molds, and disarms viruses within seconds due to its exceptional oxidative activity and small size.
Still, there are examples of thermophilic bacteria existing in volcanoes, as well as viruses in arctic ice, so they both can adapt to extreme conditions. Are there any examples of bacteria, viruses or molds (not necessarily pathogens) that cannot be killed by ozone, or at least show significantly higher resistance to oxidation?

Bacteria resistant to ionizing  radiation (e.g., Deinobacterium chartae, Deinococcus spp., Desertibacter roseus, Geodermatophilus dictyosporus, Hymenobacter actinosclerus, Kineococcus radiotolerans, Methylobacterium radiotolerans, Microbacterium radiodurans, Paenibacillus darwinianus, Pseudomonas radiora, Rubrobacter radiotolerans, Spirosoma radiotolerans, Streptomyces radiopugnans; for links to the paper describing these species, see: Bacteria I. Names), can be expected to withstand higher doses of ozone compared to bacteria sensitive to ionizing radiation.
The sensitivity to ozone of different strains of the same bacterial species can differ markedly if the strains differ in the efficiency of DNA repair mechanisms.

Brinkman et al. (1964) Radiomimetic toxicity of ozonised air. Lancet 1: 133-136.
https://www.ncbi.nlm.nih.gov/pubmed/14074479

Hamelin & Chung (1976) Rapid test for assay of ozone sensitivity in Escherichia coli. Mol Gen Genet 145: 191-194.

ozone resistance is probably involved with DNA repair mechanism

https://www.ncbi.nlm.nih.gov/pubmed/778585


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What is the scientific name of this leaf?

Has anyone seen this before? I got it from India as a gift but I have no idea what it is called or how to take care of it. Thanks

If you use an Android device there're several plant identification apps available such as Pl@ntNet and there're some websites too which can help you.

Looks very similar to Naringi crenulata which is found in India.  More information can be found on this Encyclopedia of Life page.

Image source: https://commons.wikimedia.org/wiki/File:Naringi_crenulata_leaves_and_flowers.jpg

I believe that the scientific name of that leaf is Aegle marmelos. I think that a good place to start is by reverse searching the Google image and then seeing if there is a scientific name associated with it. If there is not a scientific name associated with it, you can search for the scientific name based on the organism's common name.

Following on from Kurt's response, there is a similar irregular margin version called
Hesperethusa crenulata which is perhaps apparently used as a beauty cream, Thanaka, unverifiably promoted as "skin whitening" i.e. bleaching by some sellers, antioxidant, antibacterial and moisturizing, mostly famous in Burma, and which can be bought around the world. So it's also a cultivated tree and you'll find a lot of common and cultivar names for it. the sources of information for it are confused, there seems to be Limonia Acidissima and Limonia crenulata which are closely related. Perhaps both are used medicinally.
Thanaka also appears as Thanaka tree with reference to Hesperethusa so it seems that it has some Natural remedy / Ayurveda properties from the same plant in Burma and India.
In depth page for it here: http://idtools.org/id/citrus/citrusid/factsheet.php?name=Hesperethusa+crenulata
one with bark havested


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How does the lymphatic system filter blood?
One of the main functions of the lymphatic system is to filter blood. How exactly is it done?
Its quite hard to find an exact answer.

Can you provide a reference? I've never heard of it being described as a blood filter before as it doesn't carry blood.

@OliverHouston My biology teacher told me 'how does the lymphatic system filter blood?' is there any filtering that takes place in the lymphatic system?

OK, I'd forgotten about the spleen being part of the lymph system... See the answer below.

The spleen is an integral part of the lymphatic system, and it is a major filter of blood.
The way this is done is by removing old, distorted, or antibody-coated red blood cells from circulation.
Interestingly, the spleen is enlarged with many leukemias and lymphomas.

Need more detail, just enough to know I'm on track.


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How do photoreceptors overcome the ambiguity of wavelength vs intensity to determine brightness?
I asked a similar question about the Principle of Univariance yesterday, but now I have another one.
According to the Principle of Univariance, the input to a photoreceptor differs along two dimensions (wavelength and intensity) but the output can only vary along one dimension (the cell's graded potential).
This means that there is inherent ambiguity in the output of the photoreceptor. What I do not understand then is how it is possible for a rod (or cone) to ever distinguish between intensities (or wavelengths) when each photopigment can absorb a range of wavelengths at different probabilities.
For example, say a rod cell absorbs $50\%$ of all photons at wavelength $x$ and $25\%$ at wavelength $y$.
If 100 photons reach the rod cell at wavelength $x$ we can roughly assume that $100*0.5=50$ isomerizations will occur. Equally, if 200 photons reach the rod cell at wavelength $y$ then we can roughly assume that $200*0.25=50$ isomerizations will also occur. From the perspective of the cell's synaptic activity, the two responses will be the same despite the large difference in intensity.
Clearly there are an infinite number of permutations to this basic pattern. It is thus unclear to me how the visual system is able to obtain any information about the intensity of light in rod cells.
The same issue also appears present to me in cone cells (the usual explanation is that the relative amount of excitation/inhibition can be compared between cone cells, but this does not seem to solve my overall question).


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Trying to extract DNA with an incomplete kit
I'm wanting to run a DNA extraction on soil and root samples using a 96-well plate kit.
My problem is that someone has gone through the kit and taken the Sealing Tape. This tape it used to seal the plates so they can be vortexed and centrifuged.
I have considered using a similar tape from our qPCR reactions, but this would be a very expensive last resort. I've tried filling a plate with water and covering it with strips of label tape, but the tape doesn't provide a good enough seal for the vortex.
I'm wondering if anyone has run into a similar situation, and if they were able to find a solution. This particular kit is this PowerSoil kit from MoBio, which no longer exists after being bought out by Qiagen. I called Qiagen and they do not sell the Sealing Tape individually.
Thank you

I use something like this for crystallography.

It is the vortex step that is causing you the trouble. But you can vortex manually, by pipetting up and down a few times in the well. Then seal the top of the plate with parafilm for centrifugation.


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A missing endogenous retrovirus in humans, but present in gorillas and chimpanzees?
I have read an article about an endogenous retrovirus called PtERV1. It is present in gorillas and chimps, but is missing in humans (original study here).
According to the article, this retrovirus is very similar to HIV. And all of us (gorillas, chimps and humans) have a protein called TRIM5α to fight against PtERV1.
Nearly at the end of the article the author says: currently, there is no explenation for why the endogenous retrovirus (PtERV1) has never entered the human genome.
Is that a typo? Isn't a missing endogenous retrovirus just basic heredity? Especially because humans have the TRIM5α protein against PtERV1 just like gorillas and chimps, which indicate that we used to have it, but we lost it due to how heredity works.
Or did the author meant something deeper that the average user would not understand without a lot of pre-knowledge about genetics?

I think your question boils down to:
Why do modern chimpanzees contain endogenous PtERV1 whereas humans do not?
This is discussed in the original research article:
Kaiser SM, Malik HS, Emerman M. 2007. Restriction of an Extinct Retrovirus by the Human TRIM5α Antiviral Protein. Science 316(5832):1756-1758.
PtERV1 was active after the phylogenetic split of humans and chimpanzees, so any infection would be from separate events. In other words, the endogenous virus was not inherited from a common ancestor:

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

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

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

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

Just to clarify, PtERV1 was not inherited to gorillas and chimps by their common ancestor. Gorillas and chimps got infected by PtERV1 separately. Correct?

@WatchHat Yes, that’s correct.


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Molecular genetics textbook (free?) suggestion for first time
I have never taken a molecular genetics course but want to prime myself for graduate school in the future. Does anyone have any suggestions or advice? A professor recommends "the molecular biology of the gene - latest edition" but I dont have too much money to spend on a text and simply prefer free/digital formats. ( less to carry)

Molecular Biology of the Gene is an excellent text that your university library may have.

Buy textbooks. Go without a meal or three if necessary, but buy books!

I can’t comment otherwise this would be a comment, not an answer, sorry...
If you can’t lay your hands on a cheap (legal) text book that is of quality and in digital format then  maybe check out course material from MIT open courseware or something similar. As a further alternative, you should be able to find decent pop science books which are applicable and may be more useful than you think. The Epigenetics Revolution, for example, provided me with a really solid grounding when first trying get to grips with the subject.