Did the eugenics program in Nazi Germany have a measurable effect? Did the killing or sterilisation of people considered as living a "life unworthy of life" in Nazi Germany have any measurable effect on the "average health" of Germany? Is there any statistical evidence that the rate of (a specific) mental or physical illness is lower in Germany compared to other countries that were not affected by the Nazis  (I guess you would need to have data on the rate of that illness from before the eugenics program as well)?

P.S. Please note, I'm neither interested in discussing the ethics of eugenics, nor in condoning what has happened in its name under the Nazis. I just want to know what the result on average health (if there is such a thing) was.

As most of the comment have pointed it out, It's nearly impossible to find out. This is my try:

Dr. L Alexander wrote in his paper, Medical Science under Dictatorship:

  Hitler issued the first direct order for euthanasia in Germany on
  September 1, 1939, as his Panzers moved on the Blitzkrieg of Poland.
  Organizations with humanitarian-sounding names were immediately set up
  to execute "health" programs, again, under deceptively, euphemistic
  terms. For example, questionnaires collected by a "Realm's Work
  Committee of Institutions for Cure and Care" gathered and reported
  information on patients who had been ill five years or more and who
  were unable to work. "On the basis of name, race, marital status,
  nationality, next of kin, whether regularly visited and by whom, who
  bore financial responsibility, and so forth," decisions were made at
  key universities about which patients should be killed by
  psychiatrists who had themselves never seen the patients.Likewise, the
  "Realm's Committee for Scientific Approach to Severe Illness Due to Heredity and Constitution" was exclusively devoted to the killing of
  children with congenital anomalies or chronic illnesses. In all,
  275,000 people were put to death in these killing centers before the
  Nazi Holocaust.

Law for the Prevention of Offspring with Hereditary Diseases (July 14, 1933)

  Anyone suffering from a hereditary disease can be sterilized by a
  surgical operation if, according to the experience of medical science,
  there is a high probability that his offspring will suffer from
  serious physical or mental defects of a hereditary nature.    Anyone
  suffering from any of the following diseases is considered
  hereditarily diseased   under this law:

  1. Congenital mental deficiency,

  2. Schizophrenia,

  3. Manic-depression,

  4. Hereditary epilepsy,

  5. Hereditary St. Vitus’ Dance (Huntington’s Chorea),

  6. Hereditary blindness,

  7. Hereditary deafness,

  8. Serious hereditary physical deformity.

  Furthermore, anyone suffering from chronic alcoholism can be sterilized.

If anyone is trying to get the statistical evidence that Eugenics have even remotely successful, have look at this table:

Current Top 50 death causes of Germany. (Rate = $\frac{death}{1000}$)

They have started various ways to brainwash people, one of them was movies.

$\text{Ich klage an}$

(source: filmportal.de)

Plot: A woman suffering from multiple sclerosis pleads with doctors to kill her

Current Scenario: Germany Rank $18^{th}$ in the world in death due to Multiple sclerosis

Source:

Alexander L. Medical science under dictatorship. N Engl J Med 1949;July 14.
http://www.life.org.nz/euthanasia/abouteuthanasia/history-euthanasia6
Table: WHO, World Bank, UNESCO, CIA and individual country databases for global health and causes of death.


Location of t tubule in muscle Why do mammalian skeletal muscles have t-tubules at the junction of the anisotropic and isotropic band, whereas non-mammalian muscles and cardiac muscles have it at Z-line? What could have been the functional significance?

If skeletal muscle would have it at the Z-line then I think it would have been more effective in contraction of muscle fibre. So which arrangement is more efficient?

Also, why is a common arrangement (the more efficient one) not seen in all those muscle types?

Interesting question. Indeed it is related to the working of cardiac muscles. First of all, lets have a look at the structure of a sarcomere of a cardiac muscle from here:

Here, what we can see is that the t-tubule is a depression formed in myocyte. It is important to know this fact here. Why? See this:

  In contrast to skeletal muscle, cardiac muscle requires extracellular calcium ions for contraction to occur. Like skeletal muscle, the initiation and upshoot of the action potential in ventricular cardiomyocytes is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, an inward flux of extracellular calcium ions through L-type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. The reason for the calcium dependence is due to the mechanism of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum that must occur during normal excitation-contraction (EC) coupling to cause contraction.

First, cardiac muscles don't work by external action potentials, they work on a cycle governed by themselves, known as the cardiac cell cycle.

Second, as is clear from above paragraph, these cells depend on extracellular Ca2+ ions for initiating contraction, a clear difference from skeletal muscles which need Ca2+ stored in SR. Hence, they require t-tubule at a place where a sarcomere ends. Obviously, having a depression in the middle of a sarcomere (i.e. between I- and A-band) would not work here.

Also, the structure of t-tubules is also different between the two. Compare my first image with the image below from here:

In the second one (from skeletal muscle), t-tubule seems like a mere little pit covering the muscle cell in 360° like a duct tape. In the first image, the t-tubule is more like a double wall dividing 2 sarcomeres. It is so because in skeletal muscles, t-tubules have to just transfer the action potential to SR while in cardiac muscle, they have to transfer calcium ions into the cell. So, at the end, the difference is not in efficiency, but in function.

If we look at non-mammalian muscles, then the cause of presence of t-tubules at z-lines couls be associated with presence of large amount of sarcoplasmic reticulum at z-lines. See this article:

  Electron microscopic examination of developing myofibrils in regenerating skeletal muscle of Rana pipiens tadpole tails reveals that SR is in regular and close association with Z-lines of young sarcomeres before t-tubules have formed alongside the myofibrils. SR is also associated with M-lines of young sarcomeres but on a less regular basis than with Z-lines...This suggests the formation of a specific bond between SR and Z- and M-lines...These observations support the conclusion that SR does not initiate formation of Z-line precursor elements, but rather associates with Z-lines as they condense from more diffuse Z-bodies.

Since SR is thought to be bonded with z-lines during their formation from z-bodies, hence large amount of SR should be present at the site of association. Hence, it might be beneficial for t-tubules to be present at z-lines to efficiently transfer action potential to SR. However, such association might be absent in mammalian muscles, which can partly answer your next question.

EDIT 1: As you asked in comments

what it would have been if duct like to tubules of skeletal muscle would were present at z line instead of a-i junction?

Now we head towards evolution aspect. Yes, it might have been more effective for skeletal muscles to have t-tubules at z-line instead of A-I junction, but it would not be effective enough to create an evolutionary pressure. Both of these could have same effectiveness too, but during the course of evolution, only those traits which have much greater and direct benefit to an organism's survival and fitness are selected. There is no specific answer for 'why we have 5 fingers instead of 6 or 4', the answer is just that there is no such benefit in having 6 or 4 fingers which would cause it to be selected against 5 fingers.

EDIT 2: Obviously, its exact cause can never be known, but following might also be partly helpful. In mammalian muscles, close communication between SR and mitochondria has been observed. Such so- called "through-space" communication is an important feedback system for effiecient muscle functioning. See this article:

  the SR and mitochondrial function in muscle are not independent as calcium uptake into the mitochondria increases ATP production by stimulating oxidative phosphorylation and mitochondrial ATP production and production/detoxification of ROS/RNS, in turn modulates SR calcium release and reuptake...The resultant anchoring of mitochondria to the Calcium Release Units provides a structural basis for maintaining bi-directional SR-mitochondrial “through-space” communication during vigorous contraction.

Now, for such critical communication, SR, t-tubule and mitochondrion need to be as close as possible for fastest & direct communication. Hence, SR & t-tubules need to be as near mitochondrion as possible.

  Ogata and Yamasaki used electron microscopy to provide the first detailed description of mitochondrial localization in adult mammalian skeletal muscle (Ogata and Yamasaki, 1985). These studies revealed that mitochondria are located within the I-band, adjacent to the CRU on either side of the Z-line. Precise localization of mitochondria adjacent to the CRU at the A-I band junction was subsequently confirmed in non-fixed rat skeletal and cardiac muscle (Vendelin et al., 2005). Juxtapositioning of mitochondria adjacent to sites of Ca2+ release that occur during EC coupling provides a structural basis for potential local or privileged communication between these two organelles (Rossi et al., 2009).

Thus, presence of mitochondrion at A-I junction and of a "through-space" communication also tend to answer this question.


What is the creature with the lowest neuron count that demonstrates cognition beyond reflexes? I'm under the impression that nematode worms just perform the same scripted actions over and over again in response to specific stimuli. They have 302 neurons. Chimpanzees display problem solving capabilities, as do other mammals with smaller brains (cats, for instance with ~ 1 billion neurons). You might say that bees demonstrate something more than reflexes when they communicate the location of nectar sources to the hive (~ 960,000 neurons).

What's the creature with the lowest number of neurons to demonstrate something more than mere scripted actions? I would imagine its somewhere between a bee and a nematode worm...

Indeed, C. elegans nematodes (which are the ones you are talking about) do not show cognitive responses. AFAIK, Drosophila melanogaster is also able to learn and display some quite complex behaviors, but no cognitive functions. I believe the "simplest" organism known to display what could be called "cognitive" functions is the honeybee (see for example this article).

But as to your question:

  to demonstrate something more than mere scripted actions

I would also ask "what is a scripted action?" and to what extend a complex, cognitive response from a monkey or a human isn't also scripted (though through many different interacting pathways)?


How long is DNA stable in a freezer? Inspired by the post about extracting pet DNA, how long would genomic DNA be stable for in a -20°C freezer? It is common practice to store DNA (double-stranded, plasmid) in a -20°C freezer in the lab, but would genomic DNA last longer in a -80°C freezer? With either method, how long would it be stable for?

If the DNA is pure, it should last quite a long time.  If there are enzymes and other biological molecules in there, -80C will work much better.

I think you could keep pure DNA at -20C practically indefinitely.

Purity is the main issue there, also pH stabilized, sealed properly, etc.  That makes all the difference.


How could this molecule affect the body? (Lysergic acid derivative) First of all, could you please help me name this molecule? I think the name of it is something like this: N,N-pentamethylene lysergic acid. Secondly, my main question is what could be the pharmacology / mechanism of action (eg the target receptors, etc.) of this molecule? I couldn't find any info on DrugBank, so I'm all ears to your ideas. Please help me on this; it is quite a burning question.

P.S.: If there are any mistakes in my English, please excuse me.

That is lysergic acid piperidide, an analog of lysergic acid diethylamide (LSD). According to Wikipedia, it is an agonist of the 5-HT2A receptor, but is much less potent than LSD.


Was 14,000+ year old DNA "laying around in cave dirt" protected from degradation, or is it just naturally this robust? In the NYTimes news article No Bones About It: Scientists Recover Ancient DNA From Cave Dirt I've read:

Although DNA sticks to minerals and decayed plants in soil, scientists did not know whether it would ever be possible to fish out gene fragments that were tens of thousands of years old and buried deep among other genetic debris.

I haven't read the original article yet, but I'd like to double check, this is bare DNA molecules, stuck to minerals or other detritus in 14,000 to 550,000 year old compacted dirt? Roughly speaking at least? In layman's terms, just laying around in some caves?
Has something protected the DNA from degradation, or is DNA just more environmentally stable and robust than I thought?
There is also discussion in the Science commentary No bones? No problem: DNA left in cave soils can reveal ancient human occupants.
The NYTimes article goes on to say:

The new study involved searching for ancient DNA in four caves in Eurasia where humans were known to have lived between 14,000 and 550,000 years ago.
Dr. Meyer and his colleagues figured out which DNA in the cave sediment was prehistoric by looking for telltale signs of degradation at the ends of the molecules.

What are the "telltale signs of degradation at the ends" of DNA molecules described in the paper?

To be clear they are not finding long DNA strands but short fragments. DNA becomes more robust the shorter it gets. Fragments can last millions of years. The local chemical conditions have a huge influence on how long DNA lasts the oldest being hundreds of millions of years old under ideal conditions.

The ones the archeologists are finding are not even close to enough to rebuild an intact strand but it can be used for matching. Of course contamination is a big problem, anything that dies leaves DNA in the soil. With humans it becomes especially problematic becasue the archaeologists themselves are a major source of contamination.

For an indepth look at contamination protocols, some of which as still questionable, can be found here. Sorry its behind a pay wall.

Likely they are referring to deamination cytosine substitution, which creates mismatched pairs of DNA and occurs more and more as DNA ages.


What is a "Valid Species"? I read in a reference book on Google Books (Biology of Termites: a Modern Synthesis, eds. Bignell, Roisin, and Lo) that the termite Heterotermes perfidus found on the South Atlantic island of St Helena is a "valid species":

  Gay states definitively that "there is no doubt now, however, that H. perfidus is a valid species ..." (p. 537)

I don't understand what "valid species" means.

"Valid" in this case is just emphasizing that the Heterotermes perfidus on this island are a different (real) species, and not just a variation of their closest relatives. You need not get bogged down with how we determine species, or define species. It just means that this taxon (named group) exists as a separate species: a "valid" species, based on differences that some taxonomist deemed important enough to describe and give a name. Others may disagree, and write a paper to synonomize it (sink it into another existing species), but that is part of the messy business of taxonomy.


Is aneuploidy/aneusomy only a problem for cell division? One of my textbooks states that:

  "recent studies suggest that aneuploidy can be seen in upwards of 10% of human brain cells without any noticeable effects"

I do know that trisomy 21 causes problems, specifically mental retardation by not allowing the brain to turn certain genes ON and OFF at certain protein levels, but I do not understand why plants are okay with aneuploidy?

Is it because plant cells are more "plastic" than animal cells that, they are okay with aneuploidy?

Because neurons never divide, do they never have to deal with aneuploidy?

Or is aneuploidy a problem of stress that results from failing to control gene expression?

or is it a problem strictly of mitosis?

I just want to understand WHY brain cells .... are okay with aneuploidy

Great question. The standard hypothesis has been that aneuploidy confers some kind of advantage to  the function of the organ (brain). After initial reports estimated a very high (>30% of brain cells) aneuploidy, it would be plausible that any potential negative effect would somehow have to be compensated. One hypothesis was that it increases the functional diversity of the neurons.

However, this notion is outdated. For instance, a recent study, which also nicely summarizes preceding literature, and has been published by Knouse et al. PNAS 2014 ( http://www.pnas.org/content/111/37/13409.full ), and has applied a more sensitive and accurate measurement, and also surveyed other tissues, found that the fraction of aneuploid cells in the brain is around 1-2%, and not higher than in most other tissues. One possible conclusion, which has also been drawn by the authors, is that for the brain aneuploidy is as much of a problem as for other organs, and that - given the low fraction of aneuploid cells, which is similar to other tissues - aneuploid cells in the brain do not contribute to some special organ-specific property. (Concerning your related questions to brain: the aneuploidy in brain is believed to result from cell division artifacts - also see paper mentioned above.)

  I just want to understand WHY ... plant cells are okay with aneuploidy

Although plants appear more tolerant against aneuploidy than humans, aneuploidy can be quite harmful to them, and can easily lead to phenotypic aberrations. While the basis of the increased resistance of plants over humans isn't known, or at least hasn't been known at the time of the publication listed below, it appears linked to some genetic factors as different strains can have a different robustness - see Henry et al. , Genetics, 2010 ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998307/ )

  Is aneuploidy/aneusomy only a problem for cell division?

No, aneuploidy can create further problems (e.g.: also see second paper). For instance, in plants, it can also change the activity of genes, or the spatial organization of chromosomes - as described in Huettel et al. Plos Genetics, 2008 ( http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000226 )


Is this maritime plant a species of zostera? This photograph was taken on the intertidal mudflats at Lindisfarne, Northumberland, UK today. It was about 40m from the shoreline at low tide. Is the green plant a species of zostera? Can anyone help with the identification?

It certainly looks like a Zostera species.  The ones that appear in the UK are Zostera angustifolia, Zostera noltii, and Zostera marina.  Its hard to tell exactly which species this one is without size information and knowing the conditions of the bay.  Z. marina has the broadest leaves at around 5 - 10 mm, whilst Z. angustifolia has leaves just 2 - 3 mm broad.  Is 40m around the mid-water mark?  If so I would hazard a guess this is Z. angustifolia.  Z. marina tends to stick to areas permanently covered by the sea (sub-littoral) whilst Z. noltii likes much more sheltered conditions than the middle of the bay, tending to stick to the upper shore.

Hope that helps!


What is this aquatic organism in Fiji? I found them under reefs in Fiji. The hand-like structures moved slowly. I was not sure if it was an animal or plant. I was not even sure if they were several individuals or it was a whole.
The part that was not hidden by the stone was about 50cm length. I did not touch them, since I was not sure if it was dangerous.

It is probably Holothuria leucospilota

Holothuria leucospilota is a medium-sized sea cucumber reaching a length of up to 40 centimetres (16 in) when relaxed but it can stretch to about a metre (yard) when extended.

Holothuria leucospilota is found in shallow water along the east coast of Africa and in much of the Indo-Pacific region. It is a common species on the north east coast of Australia where it is found on reefs and rocky coasts, often partly concealed under a boulder.

References
https://en.wikipedia.org/wiki/Holothuria_leucospilota


Simple diffusion of lipid-soluble molecules through phospholipid bilayer -- does anything get "stuck" in transit? It's a pretty elementary concept, and when I first learned of it I don't think I had the foundations to even think of such a question, but I found myself the other day thinking about the amphipathic nature of the phospholipids in the plasma membrane and why it might be that lipid-soluble molecules don't stay in between the layers (of the bilayer).

I know that simple diffusion is a response to a concentration gradient, but consider a case where equilibrium is being restored and lipid-soluble molecules are diffusing from whatever extracellular matrix through the membrane and into the cytosol. Towards the end of this process, when equilibrium is nearly restored and the last few molecules are making their way into the cell, the rate of diffusion for these last couple molecules will be slower than those that diffused when the concentration difference was greater. Since the polar heads on the outside and inside of the bilayer are hydrophilic but the inner part, where the fatty acid tails are, is hydrophobic, what drives a molecule to leave the cozy, accepting, lipophilic environment of the middle (of the bilayer) to cross through the cytosolic-side rejecting polar heads and enter the cytosol?

I understand that initially these molecules were moving into the cell in response to a difference in intracellular vs extracellular concentration, but I'm asking whether we would ever see a case where the gradient is nearly zero and a molecule in transit simply decides to reside in between the layers instead of crossing all the way into the cell; as if moving through the cytosolic polar head side is not worth the effort to reduce a nearly-zero gradient to zero.

Please ask me if I can clarify my question in any way -- I'm finding it difficult to phrase. I asked my professor (who has her doctorate in toxicology & pharmacology) and she understood what I was asking but didn't have an answer.

I interpret your question to refer to the movement of a lipid-soluble molecule that is therefore able to diffuse into cells down a concentration gradient. I think that you are asking whether as the gradient collapses, some of these molecules would "stay in the bilayer".

You are thinking about the diffusion process in the wrong way. There will always be a pool of these molecules in the bilayer, and these will be continually exchanging with molecules in the two aqueous phases on either side of the membrane. The net flux which results in diffusion in any particular direction will be the  movement that results from these equilibria. Diffusion isn't a directed process in the way you define your question.

My diagram shows on the left the progress towards equilibrium and on the right the situation where it has been reached. Note that at equilibrium, because it is lipid soluble, the molecule is at a higher concentration (larger typeface) than it is in either aqueous phase. And - importantly, molecules will still be moving into and out of the bilayer at both faces.

Added later:
A classic example of a lipid soluble molecule able to diffuse in this way is oxygen. According to this paper, at physiological temperatures, and at equilibrium, the concentration of oxygen in a bilayer will be approximately 3x that in the surrounding fluids.


Why is the ratio between action potential and threshold value called the 'safety factor'? "AllorNothing Principle. Once an action potential has been elicited at any point on the membrane of a normal fiber, the depolarization process travels over the entire membrane if conditions are right, but it does not travel at all if conditions are not right. This principle is called the all-or-nothing principle, and it applies to all normal excit- able tissues.

Occasionally, the action potential reaches a point on the membrane at which it does not generate sufficient voltage to stimulate the next area of the mem- brane. When this situation occurs, the spread of depolar- ization stops. Therefore, for continued propagation of an impulse to occur, the ratio of action potential to threshold for excitation must at all times be greater than 1. This “greater than 1” requirement is called the safety factor for propagation."

This might be a more basic, straightforward question but for some reason, there's not much info on it on the web.

I'm guessing its called the 'safety factor' because it means that not any stimulus can cause an action potential and that the cells remain at equilibrium/their un disturbed state for most of the time, but this is only a guess.

Source of Info: Guyton & Hall Medical Physiology textbook

Action potentials propagate by depolarization of one section of the membrane causing depolarization of an adjacent section.

It is necessary that this depolarization be greater than threshold. If the amplitude of the action potential were to drop below threshold, it would fail to propagate. Additionally, it would be quite slow and inefficient.

Therefore, the action potential amplitude is far greater than the threshold. This helps speed and builds in a "safety factor" to ensure the action potential propagates - that's what your book is saying.


How can DNA replication result in hair pin structures? My professor said that one of the reasons SSB proteins are so important was to prevent the formation of hair pin structures, I can't see how or why DNA would form hairpin structures and there's not much about it on the internet so can anybody explain this hair pin thing and how SSB proteins prevent it from happening ?

DNA Hairpins are formed when two regions in same single stranded DNA are complementary in nucleotide sequence but in the opposite directions (as represented in image below). These two sets of nucleotide sequences base-pair with each other by forming hydrogen bonds between adenine-thymine and guanine-cytosine respectively to form hairpin loop. Same structures can be seen in case of RNA.

(Figure via: https://brilliant.org/problems/dna-zipper/)

Single stranded binding (SSB) proteins bind to single DNA nucleotide sequences and prevent the breakdown of newly synthesized DNA because of nucleases and it also removes the secondary structure of the DNA  strands like hairpin loops so that other enzymes can bind to DNA strand and operate properly. As represented in figure below SSB bind to ssDNA through electrostatic interactions and prevent the bond formation within the nucleotides of single DNA strand, thus preventing formation of hairpin loops in DNA.

(Figure via: http://helicase.pbworks.com/w/page/17605582/Amanda-Kinney)

(via: https://proteopedia.org/wiki/index.php/Single_stranded_binding_protein)


Can stress and arousal be independent? I'm trying to figure out if it's possible to have a stress response without being initially, or simultaneously aroused. I'm defining stress to be physiological stress (ie. release of cortisol) and arousal to be activation of the sympathetic nervous system.

Every example I can think of, these two are not independent. In the case of "fight-or-flight," one initially activates the sympathetic nervous system, which is then followed by the release of cortisol. Or in individuals with major depressive disorder, their sympathetic nervous systems are constantly activated while cortisol is being secreted.

So, is it possible to experience cortisol release without activation of the sympathetic nervous system?

Stress response has 2 main components:

Quick response, within minutes, is by the Sympathomedullary Pathway (SAM): hypothalamus > sympathetic nervous system > release of adrenaline and noradrenaline from the adrenal medulla > stimulation of the heart, dilation of the muscle arteries, constriction of the gut and skin arteries, glcogenolysis (the breakdown of glycogen into glucose) > more glucose available as a fuel
Delayed response, within hours, is by the The Hypothalamic Pituitary-Adrenal (HPA) System: hypothalamus > pituitary gland > ACTH > release of cortisol from the adrenal cortex > gluconeogenesis (formation of glucose in the body from other substances) > more glucose available as a fuel

Cortisol secretion from the adrenal cortex can be stimulated by things other than stress, for example, hypoglycemia, but hypoglycemia will simultaneously activate the sympathetic nervous system, which will trigger the release of adrenaline (Neuroendocrine Response to Hypoglycemia).

Some cortisol is also secreted along with aldosterone in response to hyperkalemia or hyponatremia (Vivo.colostate.edu), for example in SIADH (A Case of Transient Hypercortisolism Simultaneously Occurring With the Syndrome of Inappropriate Antidiuretic Hormone Secretion Induced by Olanzapine).

Cortisol can be also increased without stimulation of the sympathetic system in Cushing syndrome due to a pituitary adenoma or, rarely, other tumors that secrete ACTH or in adrenal adenoma, which secretes cortisol.


In an ant (or bee) colony, what is the very approximate ratio of new breeders to workers? For example, out of every 1000 eggs laid, X mature into drones and/or virgin queens.  That seems impossibly precise but it illustrates the kind of number I want well.  I'll accept answers for any species and any number of species, even one, with any amount of precision or lack thereof, because right now I can't even feel confident saying that there are more workers or more breeders, though I obviously suspect more workers.

I would also be ecstatic to have any live count just before the nuptial flight, i.e. for this colony in this study there were X workers, Y drones, and Z virgin queens just before the nuptial flight, or X workers and (Y+Z) breeders, or X% of the colony was breeders, or for this species on average X% are breeders just before the nuptial flight.

Anything.  Any one thing and I can accept it as an answer.

I can find any number of studies that talk about the sex ratio between drones and virgin queens, so I know someone is counting.  Maybe I'm not reading closely enough, but they always seem to slip away from giving all the numbers I need to figure this out for myself.

So.

This answer is specific to the western honeybee, Apis mellifera, as there are massive amounts of data on them; more, possibly, than any other insect species. There has certainly been more data collected about them than any other hymenopteran.

At around the time of the nuptial flight, there may be as many as 60,000 workers in the hive, though likely number is more like 15,000 - 20,000. There will be either one (virgin) or two (one mated, one virgin) queens (the old queen will stay with the hive, if she is alive). There may be as many as 400 drones from the original colony (though usually the number is less, around 150 is typical; 10 - 50 of them will actually mate with the queen), and an equal number may join in the flight drawn from other colonies, especially in commercial beekeeping operations. Somewhere between 1000 - 6000 workers will take part in the nuptial flight with the virgin queen and the drones.

This means that in honeybees, the nuptial flight contains 1 queen:~5000 workers:~150 drones.

Data is drawn from many years working with bees and beekeepers. Opinions will vary somewhat depending on the beekeeper and the beekeeping methods. These are based, generally, on bees kept for clover and fruit pollination in the western USA.


To which distinctions does the term "hymenoptera" refer? Hymenoptera is an order of insects that includes bees, ants, and wasps. A quick search gives the following etymological analysis of the term hymenoptera.

  hymen (membrane) + pteron (wing)

Does the term hymenoptera have a firm basis in biology and physiology? In other words, what is different about membranes or wings (or membranous wings) in species of hymenoptera as opposed to species of other orders of insects?

I don't have a definitive answer, but I suspect Hymenoptera is "just a name," albeit a name that has lasted through the phylogenetic nomenclature revolution.

Hymenoptera was erected by Linnaeus in the 10th edition of Systema Naturae (1758). The description of Hymenoptera (membrane wing; p. 553 [hope your Latin is better than mine]) follows that of Lepidoptera (scale wing) and Neuroptera (net wing) and precedes Diptera (two wing).

Classical taxonomy, which Linnaeus was more or less inventing at the time, was based on shared similarities. Those insects which Linnaeus thought more similar to each other than to other insects (e.g., ants, wasps, bees) all shared the characteristic of having a membrane based wing. The scaly wings of moths and butterflies made them more similar to each other.

He needed names for these groups, so he chose logical ones based on outward appearance of the wings: scaly, netted, membranous, or paired. That fact that these major groupings have more or less stood the test of time suggests that Linnaeus picked a good characteristic on which to name his classification of the major groups of insects.


DNA replication - how many times and when does it occur? I’m currently learning about DNA replication in both prokaryotic and eukaryotic cells. And my lecturer has mentioned that replication is a once in a lifetime activity. And I’m not sure what this is implying because I’ve searched up that DNA replication occurs during cell division (cell cycles), which occur repetitively as organisms develop.

This sounds like a difference in perspective of when exactly cells "die". If you consider that, in a cell division, a mother cell "gives birth" to two daughter cells, you could argue that the mother cell has "died". It makes sense to think about cell division in this way because it puts both daughter cells in the same level, without one being "special" due to it being the mother cell itself while the other is considered the "new cell".

If you face cell division like this, any cell (eukaryote or procaryote) will only really duplicate their DNA once: they duplicate their DNA -> they split into daughter cells, in which they "die" -> (eventually) each daughter cell duplicate their DNA -> and so on.

Like I said this is just a particular POV we can adpot when we try to understand and describe cell cycle and cell division (although it is a common one for researchers in the field).


Why do specifically bananas go brown quicker in the fridge? Perhaps the title should be: Why don't all fruits containing phenol residues go brown quickly when left in the fridge?

Bananas go brown over time because of the oxidation of phenol residues.

Bananas go brown quicker in the fridge than left at room temperature. This seems to contradict the first point since the reaction should be slower at colder temperatures. Dialogue from the naked scientists briefly explains why my line of thinking might be wrong.

  Emily: Well it’s a good question and the answer is that they will
  brown faster in the fridge.  It’s mainly due to the formation of ice
  crystals, so if you put your banana in the fridge, the ice crystals
  grow, and they actually rupture the cells of the banana skin. This
  releases an enzyme called polyphenol oxidase and as the name suggests
  it acts to oxygenate phenols, which have a ring-like structure, into
  quinones, and these quinones can then all join together or polymerise
  and produce a black, brown, or red pigment called polyphenol and this
  is what gives it the brown colour. So, if you have your banana in the
  fridge, this will occur and you'll get a brown banana.  But another
  interesting thing about bananas is that if you have them in the fruit
  bowl, they'll release ethene and this will make the other fruits in
  the bowl ripen faster because it’s a ripening hormone.

  Chris:   So, the question is though, if this is a chemical reaction
  making this brown pigment, if you slow down the reaction by lowering
  the temperature, then it should happen more slowly, therefore, going
  in the fridge should make the bananas go black slower?

  Emily:   I can see why you're thinking that but actually, it’s more
  the rupturing of the cells.  So if you have a banana on your table,
  the cells are going to be intact, the enzymes contained, and the
  reaction is not happening at all whereas if you put in the fridge, the
  enzyme is released and the reaction can happen – although yes, it
  might happen slower.

At the risk of channeling people into a yes or no answer, could someone clarify for me if the following statement is true maybe with a peer-reviewed source, which I've had no luck finding:

  TLDR Bananas go brown quickly in the fridge because cell lysis, caused by ice crystal formation at cold temperatures in the fridge, releases Polyphenol oxidase (PPO) into the surrounding area which freely causes more browning.

This leads me to another seeming paradox and the question I would like answered: Why doesn't this rapid browning in cool temperatures happen for other fruits and vegetables? What is special about bananas?

What's interesting with this one is we don't really know very well the mechanism behind what's called chilling injury. It happens to a range of fruits, like bananas, peaches, avocado, or apples. The belief is that the chilling alters membrane permeability to storage vacuoles inside the plant cells. Try On Food and Cooking, pp.269, and Puig et al. (2015) for references here.

Now the membrane permeability to the storage vacuole changes (it gets leaky), and inside these vacuoles are phenolic compounds. In the cytoplasm of the plant cell, there's an active enzyme called polyphenol oxidase (PO). The reactions it catalyzes end up with a compound called melanin, a brown/black pigment:

Fig A. An overview of what a PO might do.

So the phenolic compounds leak out and PO goes to work catalyzing reactions that start building up the dark pigments associated with browning. Being said, I can't at this moment find a good paper that says "look, this is how the entire process happens," but I'll be attempting to read a little deeper into the matter.

Keywords: flesh browning, enzymatic browning, chilling injury, polyphenol oxidase, storage quality, storage conditions


Can DNA be used directly to determine the age of a mutation? I've studied that proteins found in a sample as biochemical evidences for evolution. Its variation in structure and configuration can be used to date the age when that mutation occured, effectively dating the sample. But can't DNA be directly used for the process? Proteins also require transcription and translation, increasing error. I think proteins make phylogenetic detection easier, but doesn't transcription and translation give more room for error?

Yes, you are right.  Proteins are specified by DNA sequences, so DNA sequencing is a more direct way to obtain essentially the same information.  Note that mutation dating via DNA or proteins is approximate.  It involves a lot of assumptions about continuous rates of mutation, but in fact mutation is a stochastic process and does not have a knowable continuous rate.  The sequence of mutations can be determined with high confidence, but the rate can only be determined approximately.


Kinetic Vs Potential Energy in Biochemical Contexts This question is causing great confusion in my head.

Which of the following is an example of potential rather than kinetic energy?
A) the muscle contractions of a person mowing grass

B) water rushing over Niagara Falls

C) light flashes emitted by a firefly

D) a molecule of glucose

E) the flight of an insect foraging for food

Answer:  D

A) Muscle contractions is caused by the use of potential energy in ATP used by actin and myosin.

B) This is a classic example of what potential energy means.

C) Bioluminescence is a process caused by the use of chemical (potential) energy.

D) Yes, the molecule of glucose does contain potential energy. BUT, it is not potential energy itself...

E) Flight is kinetic energy. However, you can still boil this down to ATP in actin and myosin.

How do I approach this problem? My teacher said this is the type of problem she would give us. But this is so ambiguous. Am I lost?

I think you are right and many examples are ambiguous.  Even D) is ambiguous as a molecule is always in motion due to entropy except, perhaps, at absolute zero (0 Kelvin). But normally, it does contain kinetic energy.

However, as you already identified the ambiguity, look at the best, or in this case least incorrect answer; The only option without any physical movement explicitly mentioned in the question description is D). All the others mention 'emit', 'flight', 'rushing down', etc.

Also ask your teacher :)


When did vision evolve for the first time? Today I wondered what the first organism to evolve vision would have been. I assume that it would have been kind of primitive and basic, but of course extremely innovative and eventually useful to a wide variety of beings.

It also makes sense that the evolution of vision would have accompanied the evolution of advanced brain functions in almost every case. So, do biologists have any idea as to what the first species to use vision would have been?

(By vision, I mean having some organ on your body that receives photons and has some signaling pathway that converts photons into a biochemical set of signals)

"To me, it also makes sense that the evolution of sight would have accompanied the evolution of advanced brain functions in almost every case."

Not necessarily! For instance, think of phototropism: the plant detects the presence of light and uses it to grow towards the light, but that's a very simple process regulated by auxins. Or the light-sensitivity (phototaxis) shown by Euglena, a single-celled protist, which reorients its entire body towards a light source. Really simple vision (is there a light, and if so, where is it?) can help organisms absorb more energy than rivals, giving them an evolutionary advantage.


Is there a database containing sequences of human cell lines? I'm looking for the whole genome sequences of several human cell lines, e.g., A549 or Ea.hy.926. Is there a database specifically dedicated to human cell lines?

As pointed out by @kmm (http://cancer.sanger.ac.uk/cancergenome/projects/cell_lines/) is an excellent database. Alternatively you can look at the broad institute page (http://www.broadinstitute.org/software/cprg/?q=data-resource) in the cancer cell line encyclopedia section, then go to the browse tab and select the cell line for a very comprehensive list of cell lines.


Why are sight and sound prerequisites for intelligence? Edward O. Wilson, in The Diversity of Life wrote (emphasis mine):

Ninety-nine percent of the animals find their way by chemical trails.  […]
Animals are masters of this chemical channel, where we are
idiots. But we are geniuses of the audiovisual channel, equaled in
this modality only by a few odd groups (whales, monkeys, birds). So we
wait for dawn, while they wait for the fall of darkness; and because
sight and sound are the evolutionary prerequisites of intelligence, we
alone have come to reflect on such matters […]

I'm getting this from an anthology (Dawkins' "Modern Science Writing") so I don't see how Wilson supports this statement, and my google-fu is bringin up nothing relevant-seeming.
My question is: why are sight and sound prerequisites for a species to evolve intelligence?

To answer your question, we must first ask the question What is defined as intelligence?

A googling will tell you that most people believe intelligence to be something related to apes or even more conservatively to humans. But, I find this to be a bit unpragmatic. The closest level of abstraction I find towards defining intelligence is this wiki on Animal Cognition. Having said so, I personally would define intelligence on a much more abstract level.

Intelligence can be broadly defined as a learned response towards an external stimulus, providing the organism with an increased fitness/survival within it's ecosystem.

So Intelligence can be broken down into two parts

Memory of a stimulus
A programmed response towards that stimulus

This is a very famous video showcasing intelligence in the animal world; Crow Intelligence test

But My objective is to state that sight and sound are are not at all prerequisites of intelligence.

This paper from way back in 2014 is I think the best that I can state

Memory and Fitness Optimization of Bacteria under Fluctuating Environments

In this particular paper the authors test the capacity of E coli to produce a response within fluctuating environments, and they find that as the generations progress the later generations take lesser time to produce a response towards the stimulus. They also note that what happens if the prior external environmental state is restored. In such a case later generations become optimised for that particular state.

This is a very good example of memory which is stored at the level of DNA, and a level of intelligence is manifested in a microbial system. So therefore, can you really state that "sight- and sound" are pre-requisites of intelligence. I would say No They are not, that would be an over-simplistic way of what intelligence really is.


Null hypothesis of Chi-square test for independence My understanding of null and alternate hypotheses :

The null hypothesis is a hypothesis whose plausibility is being tested by a test statstic and is denoted by H0. It assumes that observed data follows a standard scientific theory (and the variation/deviation is due to
chance).1 Alternative hypothesis is a hypothesis that contradicts null hypothesis. It assumes that the variation in the observed data is real, not due to chance.It is usually the hypothesis that a scientist is trying to establish.
(Source: Biostatistics by Lee & Forthofer & Statistics by David Freedman)

This1 holds good for Goodness-of-fit test but not chi-square test for independence as there is no theoretical data to compare the observed data with.

So my question is in a given problem of chi-square test for independence how to determine what the null should be?

When what the scientist is trying to establish is mentioned:

Q : In a study of effectiveness of an antipsychotic drug, patients are treated with the drug and were compared to those receiving a placebo. 698 of 1068 patients were released after taking the placebo while 639 out of 2,127 relapsed after taking the antipsychotic drug.
Test the prediction that the antipsychotic drug is significantly more effective in preventing relapse than placebo.

A:  Ho : Edrug = Eplacebo  Ha : Edrug > Eplacebo

(Reasoning: Ha is the hypothesis the scientist is trying to establish and so Ho should be something that opposes the Ha that he has to disprove.)
When what the scientist is trying to establish is not mentioned (at least not clearly):

Q: Among 60 males and 50 females, 25 males and 20 females were with attached ear lobes. Statistically prove whether or not the attached pinna has any relation with sex.

Not sure what the scientist wants to establish so unable to assume a null.

It might help if you first ask yourself what the independence test is for in plain English, you are testing to see if one categorical variable has
an influence on another. In other words, if a person (or whatever)with attribute X (for example, is bald) are they significantly more/less likely to have attribute Y (like being allergic to penicillin) than someone who does not have attribute X.

So in your example the alternative hypothesis would be (in words): the ratio of males with attached ear lobes compared to males without is equal to the ratio of females with attached ear lobes compared to those without.


What does 'direction' mean in the statement "mutations are non-directional"? I was reading the Mutation theory of De Vries; there I encountered this following statements

  Mutations are discontinuous, random & non-directional.This is in contrast to Darwinism where variations are continuous & unidirectional.

and

  [Hugo deVries] believed that it mutation that causes evolution and not the minor variations (heritable) that Darwin talked about. Mutations are random and directionless while Darwinian variations are small and directional. Evolution for Darwin was gradual while deVries believed mutation caused speciation and hence called it saltation (single step large mutation).

Could anyone please explain what direction means in the two statements above?

(I give an explanation to the statements, please understand that almost all  evolutionary changes are mutational in the basis).

Let's say the greater height is advantageous in one area, while in other area the smaller height is advantageous. In the former area, the direction of phenotypic changes will be to the individual with higher height, while in the latter the direction will be to smallest one. The evolution "seeks" example to follow, so you "can" find which one was an example to move towards to (who is the reference point).

In the case of mutations the is no apparent direction. These chaotic changes can be advantageous, or may be not - one cannot find a particular direction towards some "example" / reference model.


Can anyone ID this flower plant by the photo? Can someone identify this plant? It has big red flowers when it flowers! Not sure if it is native, but it is in my grandmothers garden in Vancouver, British Columbia, Canada.

It seems like it's either a Paeonia brownii or Paeonia californicus.  According to Wikipedia, these are the only peony trees native to North America, but there aren't any that are native to Canada specifically.  I guess these are the closest you can get.  I added some images to hopefully help you out a bit.

https://en.wikipedia.org/wiki/Paeonia_brownii

https://en.wikipedia.org/wiki/Paeonia_californica


Why do patients with type 2 diabetes not show the body wasting seen in type 1 diabetics? Type 1 diabetes results from the destruction of the cells in the pancreas that produce insulin, while type 2 diabetes is characterized by so-called "insulin resistance", presumably a reduced responsiveness of the body's tissues to the effect of insulin.  More succinctly, in type 1 diabetes, insulin is not produced at all, while in type 2 diabetes, insulin is produced, but it is ineffective.

Based on this description, one would expect that type 1 and type 2 diabetes would look similar, with maybe type 2 diabetes being a milder form of the condition.  This is not the case, however.  The diseases are markedly different, at least when it comes to their effect on body weight.

Type 1 diabetes results in wasting:

The images show a type 1 diabetes patient before and after insulin treatment.

In contrast, type 2 diabetes is associated with obesity, exactly the opposite scenario.

If the body does not respond to insulin in type 2 diabetes, why don't those afflicted waste away, in the way that (untreated) type 1 diabetes patients do?

The following is based on a conversation I had with a senior biochemist in my university who conducts grant-funded research on the relationship between diabetes and heart disease. It can be criticized for the paucity of external sources from which its veracity can be checked. However, although the question is based on a misconception I thought it should be addressed. Perhaps others could help improve the answer by supplying references etc.

The following points about Type 2 diabetes mellitus are relevant.

‘Type 2 diabetes’ refers to a disease which encompasses conditions
with a spectrum of severities.
This means that the description of it being “characterized by so-called ‘insulin resistance’” — alternatively expressed as cells being refractory to insulin — in fact means that there is a variation in the degree to which the cells are refractory. In many cases, although this leads to a higher blood sugar, it does not result in the complete breakdown of fat and muscle protein found in type 1 diabetes, where insulin is completely lacking.
Type 2 diabetes does not result in an increase in fat deposition and body weight. In many — but not all — cases it is caused by overweight.
In type 2 diabetes caused by overweight there is a gradual loss of fat. It is not apparent in a ‘snapshot’ of type 2 diabetics, many of whom have such large fat reserves that it will take a long time before these are broken down.
In severe type 2 diabetes the situation eventually becomes similar to type 1 diabetes as the beta cells of the pancreas can be destroyed. In these cases insulin injection is required.
Normally type 2 diabetes is controlled with drugs that reduce the glycemia — metaformin is currently the agent for the first line of treatment — and by lifestyle changes, especially in diet. (The treatment of type 2 diabetes was reviewed by Juan José Marín-Peñalver et al. in 2016 and considers their mechanisms of action etc..)


Choice of primers for PCR This exercise was given by my professor but I am struggling to understand the solution.

A PCR is performed on the following sequence (in order to replicate the chain and thus have a greater quantity of DNA so to be able to analyze it):

The main sequence belongs to a horse and differences are indicated below with dna belonging to a cow.

1) Choose appropriate primers in order to analyze some lasagna, which is suspected to contain both horse and beef.
Given Solution:
The primers should be:

I understand how these primers would work in this case, but why not just have the second pair of primers which would make it possible for the whole chain to be analyzed at once?

You do need two pairs of primers one unique to each species as you need a positive result to be confident that the thing you are looking for (cow or horse) is there.

There is no limitation on them being in the same place (with a different last base).

Usually this would be analyised by gel-electrophoresis and not by sequencing so you don't have to worry about getting the whole thing. This is because you are only looking for the presence or absence of PCR product.

When you do the PCR you will have 4 reactions, one which amplifies horse only, one which amplifies cow only and their negative controls (adding water instead of lasagna DNA extract). After the PCR you take a small amount of your PCR product and run it on a gel (gel-electrophoresis). If you see amplification in the negative controls then you have contamination and can't trust the result. Otherwise if you see amplification by the cow primers then cow is present in the lasagna and if you see amplification by the horse primers then you probably don't want to eat the lasagna. If you used both options for the first forward primer you suggested (blue) then all your bands would be the same size, if you used both the first (blue) and second (yellow) then you would get different band positions on the gel due to the different sized products which makes you feel more sure that you didn't make the mistake of adding the same primer pair to both tubes (it happens).

In the end it's simply a matter of style.


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.


Why can good music raise goosebumps? Listening to really good music right now, I was wondering why it raises goosebumps.

Is there any physiological reason for this reaction to specific wavelengths or something?

EDIT:
Due sometimes strong vibration, roadwork for example,  raise goosebumps too I reckon it's about the wavelengths but if someone could explain what is happening and why, that would be great.

CROSS-POSTED

It's a phenomenon called Frisson.  From the wikipedia page.

  Frisson (French for 'shiver') is a sensation somewhat like shivering, usually caused by stimuli. It is typically expressed as an overwhelming emotional response combined with piloerection (goosebumps). Stimuli that produce a response are specific to the individual.

  Frisson is of short duration, usually no more than 4–5 seconds, usually pleasurable.1 Typical stimuli include loud passages of music and passages that violate some level of musical expectation.[2]

There is some interesting research that shows it occurs when a sound contains certain chords or has certain notes because of how our biological setup reacts to those specific notes.  See the "crying chords" that were supposedly present in Adele's song "Someone Like You". npr article about crying chords


Concentration of caffeine in physiologically relevant setting Caffeine is known to overcome G2/M (and possibly other types of) cell cycle arrest through its effects on DNA repair machinery and is used as a positive control in studies of cell cycle arrest. In this paper, for example, researchers use concentrations of caffeine in the 1-4 mM range to overcome nocodazole-mediated arrest. Is this a physiologically relevant concentration?

I found a lot of interesting caffeine data including the LD50 (estimated to be around 150-200 mg/kg) but have not been able to turn up any good numbers on reasonable concentrations that might be found in a human.

Let's figure it out. Suppose an adult with an average blood volume of 5 L (5000 mL) drinks a cup of strong coffee with 100 mg of caffeine in it. Given caffeine's formula weight of 194.19 g/mol, and assuming 100% of the caffeine is in the blood stream, its concentration (from this awesome calculator page from Graphpad, the makers of Prism) would be approximately 103 µM, or 10-40 times less than what's being used in the experiments you cite.

Of course, this is overcoming drug-mediated cell cycle arrest, so its possible that a lower concentration is needed to jump-start physiologically-arrested cells.


Difference between Condensin and Cohesin proteins? The chromosomal DNA is stacked with help of cohesin and condensin protein in which particular manner? Can cohesin be said to form kinetochore? How would they vary exactly?
The terms are so narrowly windowed that they squeeze my brain through...!!! thank you for your kind help ^_^

Condensin

Condensin I: present in cytoplasm during interphase, has access to chromosomes after prophase. Contributes to condensed chromosome assembly during prometaphase and metaphase [1].

Condensin II: present in nucleus during interphase, involved in chromosome condensation. Contributes to condensed chromosome assembly during prometaphase and metaphase [1].

Cohesin

It keeps sister chromatids connected with each other during metaphase and ensures that each sister chromatid segregates to opposite poles. "It facilitates spindle attachment onto chromosomes. It facilitates DNA repair by recombination." [2]

References:

Wikipedia contributors, "Condensin," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Condensin&oldid=606814199 (accessed July 29, 2014).
Wikipedia contributors, "Cohesin," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Cohesin&oldid=617481362 (accessed July 29, 2014).


Is DNA replaced after organ donation? If an organ from person A is transplanted to a new human body B, is it possible that we can detect A's DNA in B?

How long until the organ's DNA is replaced by B's DNA so that we are no longer able to detect any signature of A?

DNA will be never replaced (unless you are speaking about something, where DNA might be only trash, like in the case of blood transplantation or in the case when "organ" would be slowly replaced itself by host regenerative power and "organ" transplantation would be only something temporary, but then we are probably speaking about wider definition of organs).

For further evidence, you may look at cases of chimerism. That is, when young embryos fuse together and create single one with two different cell-lines, which later differentiate to create different organs.
https://en.wikipedia.org/wiki/Chimera_%28genetics%29

Furthermore, rather more common but with less drastic effect can be somatic chimeras, that is when (usually) early, when embryo is formed only by small amount of cells, one of cell has a mutation, then later in life, this cell again can give rise to organ or several of them. In that case, those organs will carry this mutation while rest of the body will not. This can be potentially more common as this can happen in any single time during development and even after it (in fact, cancer cells are sort of product of that).
More interesting cases here:
https://en.wikipedia.org/wiki/Mosaic_%28genetics%29

So, from simple fact that these cases exists and are well-spread, and basically means that several different cell-lines can live in the same body, the answer on your question, if organ DNA will be replaced after transplantation is no.

edit: In the case of whole cell replacement, they can be from both donor and host. However, there are a few problems:

Most of cells that we have are not totipotent, not even pluripotent or multipotent (see: https://en.wikipedia.org/wiki/Cell_potency), most of our cells are plain and stupid. This means that highly specialized cells of some organ would probably be replaced only by other highly-specialized cells of that organ (or their precursor cells that are kept for this solo reason, keep regenerativ ability of particular organ, as quite a lot of highly-specialized cells can't divide any more). However, there are a few documented cases with regnancy, where a few cells (embryogenic, thus with bigger "healing" power) migrated through placenta to mother's body and healed her diabetes. So theoretically this is possible, as well as host getting cancer from donor's organ. But again, reason why we are transplanting organs is because human body is not particularly great in regenerating itself and those organs won't grow. So theoretically possible, but not great concern (except for cancer).


What is meant by clonal isolates? With respect to this website:
http://horfdb.dfci.harvard.edu/
what does the term clonal isolates mean?

Often genes or other DNA fragments are inserted into an expression vector and used to transform bacteria or other cells. When a mixture of vectors is used containing various DNA fragments (e.g. a chopped-up genome), then individual (bacterial) colonies need to be isolated to make sure they carry only one insert. This can be done, e.g., by plating the transformed cell culture such that individual colonies are obtained. Theoretically, one colony represents the offspring of one cell, hence the colony as a whole has one DNA insert and is a clonal isolate.


Same target receptor different mechanism of action? If different drugs have the same receptor as a target, does that imply that they have the same mechanism of action?

Not necessarily!

Biased agonism

It's reasonable to start with an expectation that agonists at the same receptor have the same effect, but that's not necessarily true due to biased agonism. Biased agonism occurs when binding of different agonists to the same receptor results in different downstream activation of second-messenger systems.

Psychedelics and serotonin receptors

A particular example I am familiar with (besides the Jarpe paper) involves the 5HT2a serotonin receptor. This receptor is a shared molecular target of several psychedelic drugs: LSD, psilocybin/psilocin, DMT and others. However, this receptor exhibits biased agonism (Berg et al 1998).

In fact, it seems like agonists at the 5HT2a receptor neatly segregate into those with psychedelic effects (eg: LSD/psilocybin) and without (eg: lisuride/ergotamine, also serotonin itself) based on the different downstream molecular signalling pathways that they trigger, despite binding to the same general site on the same receptor.

Other considerations

Drugs' mechanisms of action can also depend on concentration and on all the other possible targets for those drugs. Pharmaceuticals are often small molecule drugs and while they may have preference for certain receptors, they are rarely (probably never) purely specific.

For example, the NSAID class of anti-inflammatories all work through inhibition of cyclooxygenase enzymes, but they differ in their relative specificity for COX-1 and COX-2. If you are looking at two drugs that have the same effect on COX-2, but don't compare their effects at COX-1, you might be surprised to find they have different results.

For another class, SSRIs used as antidepressants also have effects on other monoamine transporters (dopamine and norepinephrine) but vary in how specific they are.

Berg, K. A., Maayani, S., Goldfarb, J., Scaramellini, C., Leff, P., & Clarke, W. P. (1998). Effector pathway-dependent relative efficacy at serotonin type 2A and 2C receptors: evidence for agonist-directed trafficking of receptor stimulus. Molecular pharmacology, 54(1), 94-104.

González-Maeso, J., Weisstaub, N. V., Zhou, M., Chan, P., Ivic, L., Ang, R., ... & Sealfon, S. C. (2007). Hallucinogens recruit specific cortical 5-HT2A receptor-mediated signaling pathways to affect behavior. Neuron, 53(3), 439-452.

Jarpe, M. B., Knall, C., Mitchell, F. M., Buhl, A. M., Duzic, E., & Johnson, G. L. (1998). [D-Arg1, D-Phe5, D-Trp7, 9, Leu11] Substance P acts as a biased agonist toward neuropeptide and chemokine receptors. Journal of Biological Chemistry, 273(5), 3097-3104.


Are SNPs or SSR copy number variation mutations more prominent? I'm trying to get a sense of the dominant way that mutations occur.  I have seen various numbers which seem at least at first glance to conflict, and I was curious if anyone had clarification on this.
According to Shastry, "SNP alleles in human disease and evolution" (Journal of Human Genetics 47:561–566, 2002),

In two randomly selected human genomes, 99.9% of the DNA sequence is identical. The remaining 0.1% of DNA contains sequence variations. The most common type of such variation is called a single-nucleotide polymorphism, or SNP.

However, according to Nevo, "Genetic Diversity" (Encyclopedia of Biodiversity, 2001),

Significantly, SSRs experience mutation at notably higher rates than do nonrepetitive sequences: $10^{-2}$ to $10^{-3}$ per locus, per gamete, per generation, which leads to their high polymorphism.

Additionally, according to Kashi and King, "Simple Sequence Repeats as Advantageous Mutators in Evolution", (TRENDS in Genetics 22(5):257),

Mutations that alter repeat number typically occur at rates orders of magnitude greater than single-nucleotide point mutations.

So, if variations in organisms is mostly due to SSRs, and this is mostly copy number variation, then would it be correct to say that copy number variants in SSRs is the dominant form of variation, or am I missing something?  Which one is correct, or which source is more authoritative, or is there a more up-to-date review I should be consulting?

It's not really clear to me what you're after when you ask about how prominent or dominant these two kinds of variations are. But let's look deeper.
Guichoux et al. (1) say:

There are two main differences between SSRs and SNPs. First, SNPs are more numerous than SSRs in the genome of most species. On average, in the human genome, there is one SNP every 100–300 bp (Thorisson et al. 2005), com-pared to one SSR locus every 2–30 kb (Webster et al. 2002), depending on how SSRs are defined (Kelkar et al. 2010).This can be important for genome-wide association studies but not necessarily for other applications. Second, the mutation rate per generation differs drastically between the two marker types. SSRs have mutation rates ranging from $10^3$ to $10^4$ per locus per generation (Ellegren 2000), compared to about $10^9$ for SNPs, i.e. several orders of magnitude lower. As a consequence, SNPs are typically diallelic: In humans, < 0.1% of SNPs are triallelic (Lai 2001).In contrast, SSR loci generally have high allelic richness, often in excess of 10 alleles.

Based on these numbers, SNPs occur perhaps 80 times as often as SSRs.  Is that more prominent?
An SSR is larger than an SNP, covering perhaps one hundred to several hundred bases versus one base (by definition).  An SSR locus also occurs in multiple variants, e.g. having a copy number from a wide range, versus only two possible variants that usually occur for an SNP locus.
The mutation rates are substantially different, apparently typically 5 orders of magnitude more frequent for SSRs than for SNPs.  Note, though, that mutation rate does not directly affect the frequency of variants seen in the genomes of extant organisms: the variants present are a result of the filtering of mutations by the forces of selection.
Note also that all bases are subject to mutation, thereby producing an SNP, but SSR mutations only occur where a repetitive sequence already exists.  (Also, the likelihood of mutation becomes significant only when the existing sequence has more than a few repeats, as the mechanism of mutation depends on this.)
A main question, though, is what is the significance of the variation?  Are you interested in variation just because they mark individual genomes within a population, or are you interested in the variation of the phenotypes of individuals?  Some genetic loci are irrelevant to phenotype and some can affect the phenotype to lesser or greater degree.  SNPs can occur anywhere so can be presumed to have a "fair" chance of affecting phenotype.  On the other hand SSRs can occur where only where repetitive sequences can occur (and persist where they survive selective forces). With SSRs, varying copy number in some contexts such as protein coding sequences, may have larger phenotype effects than an SNP, and thus be subject to stronger selection forces.
My view is that both SSRs and SNPs are important and it's not terribly productive to worry about general prominence or dominance of one over the other.
Reference:
(1) Guichoux, Erwan & Lagache, Lelia & Wagner, Stefanie & Chaumeil, Philippe & Léger, Patrick & Lepais, Olivier & Lepoittevin, Camille & Malausa, Thibaut & Revardel, Emmanuelle & Salin, Franck & Petit, Rémy. (2011). Current trends in microsatellite genotyping. Molecular ecology resources. 11. 591-611. 10.1111/j.1755-0998.2011.03014.x.


Why does meiotic recombination disrupt the independent assortment of genes on the same chromosome? There are many sources that say that genes that are "linked" by being on the same chromosome assort with each other -- that when an allele is passed on that the gamete containing said allele will also contain every allele from the chromosome rather than simple allowing everything to assort independently.

There are also many sources that say during meiosis there is recombination, hence, why aren't all genes completely random?

Recombination does not make any two genes completely independent because there will not systematically be a recombination event between two given loci (=position on the chromosome).

Distance between loci

Consider two scenarios that describe the position of two loci on a chromosome.

Tightly linked loci

Consider two very closely linked loci. Let's say that a recombination event occurs somewhere in the chromosome. It is very likely for this recombination event to occur somewhere else than between these two loci. These two loci are essentially linked and do not segregate independently

Distant loci

Consider now two loci on the same chromosome. Each locus (=singular of loci) is found at one end of the chromosome. If a recombination event occurs, it is pretty sure that it will occurs between the two loci. As a consequence, the two loci will segregate (quasi) independently.

Conclusion

As a conclusion, recombination allows to break down the linkage between two loci but it does so at a given rate that depends on the physical distance between the two loci and on the per nucleotide recombination rate.


What do the text annotations in an electron micrograph mean? I saw a photograph taken from an electron microscope, with some text.

I want to know what is the meaning of these numbers and letters?

Thank you! Regards.

The 1.40kX is the zoom (1400x), WD is the working distance (distance between the final lens and the object), 20kV is the voltage used to accelerate the electrons, 20μm is the scale.

I'm not aware of the other two.


Can Helicobacter pylori be eradicated naturally? This question is not to discuss whether substances that have anti-H. pylori activity work or not, or to discuss the pros and cons of such but from a medical perspective.

Assuming that one is able to control, reduce, or eliminate H. pylori via foods containing natural anti-bacterial activity targeted at H. pylori without the consumption of antibiotics, what is the possibility of reinfection or an overgrowth with H. pylori?

  In this study, the bactericidal activity of Korean and Japanese wasabi roots, stems and leaves against Helicobacter pylori were examined... All parts of wasabi showed bactericidal activities against H. pylori strain NCTC 11637, YS 27 and YS 50.

My questions are:

If this method was carried out in vivo and the results were found to be consistent with the research mentioned above, what is the chance of developing resistance to H. pylori?
Will developing resistance prevent recolonization of the stomach lining with H. pylori?

Bactericidal activity of wasabi (Wasabia japonica) against Helicobacter pylori

H.pylori is a bacteria that is a cause for Peptic ulcer disease of human being. It helps to create more acidic product and causes ulcer. But human body is naturally protected to H.pylore, but excess stress,irregular life style etc helps H.pylori to growth and causes ulcer. Simple measure can escape you from this infection. 1. Intake enough water 2. Maintain oral hygiene is very Imp, 3, at bed time gurgle by H2o2 ( Hydrogen per Oxyde) 3. If you are infected then triple therapy for 3 weeks is the choice of treatment


What does the spectrum of Chlorophyll fluorescence look like? I've just posted the question Which spacecraft can see plants "glow" during photosynthesis during the day, and what wavelength does it use? in a different SE site. I can't remember the details of which spacecraft this was or how exactly it worked.

My question here is simply about light produced by vegetation during photosynthesis. In this question I've shown a hodgepodge of absorption or sensitivity spectra of photosynthesis, but what I'm looking for is an emission spectrum and some details about where in the process this light is produced.

The Wikipedia article Chlorophyll_fluorescence covers the topic in general and mentions 735nm but I'd like to be able to see a fairly accurate spectrum in order to compare it against absorption lines in the Sun's spectrum.

NASA's OCO-3: Watching Plants Grow and Glow: https://youtu.be/_x-VzdEeq0c

I think for your purpose you should start, for example, with this link:
https://academic.oup.com/jxb/article/60/11/2987/533160

UPD:

Chlorophyllous tissues emit radiation of wavelengths approximately 680-760 nm. Source: Plant Physiological Ecolgy, Second edition, Hans Lambers, F.Stuart Chapin III and Thijs L. Pons, New York : Springer, c2008, p. 37, Box 2A.4 Chlorophyll Fluorescence


Do swarm of the same species attack each other? What happens when two swarms find each other?

For example: When a swarm of bats, of the same species, go through another bat swarm. Do the bats attack one another or they simply merge into a bigger swarm?

It will depend on the species and group you're talking about. If the species is territorial, one swarm will tend to chase the other away. If it's a locust, they'll merge until they get to trillions of tons...

A study on wasps (Vespidae) I've read years ago showed an interesting experience. One individual wasp was tied by the waist and put close to different nests. The violence demonstrated by the nest was greater in a different species, median in the same species with a greater genetic distance, and none to her own or related nests.

Some "solitary" bees are very interesting in this respect, because they show many different kinds of sociality in related or even the same species, like many Halictidae and Euglossina (Apidae).


Why is DNA replication  performed in the 5' to 3' direction? DNA replication goes in the 5' to 3' direction because DNA polymerase acts on the 3'-OH of the existing strand for adding free nucleotides. Is there any biochemical reason why all organisms evolved to go from 5' to 3'?

Are there any energetic/resource advantages to using 5' to 3'? Is using the 3'-OH of the existing strand to attach the phosphate of the free nucleotide more energetically favorable than using the 3'-OH of the free nucleotide to attach the phosphate of the existing strand? Does it take more resources to create a 3' to 5' polymerase?

Prof. Allen Gathman has a great 10-minutes video on Youtube, explaining the reaction of adding nucleotide in the 5' to 3' direction, and why it doesn't work the other way.

Briefly, the energy for the formation of the phosphodiester bond comes from the dNTP, which has to be added. dNTP is a nucleotide which has two additional phosphates attached to its 5' end. In order to join the 3'OH group with the phosphate of the next nucleotide, one oxygen has to be removed from this phosphate group. This oxygen is also attached to two extra phosphates, which are also attached to a Mg++. Mg++ pulls up the electrons of the oxygen, which weakens this bond and the so called nucleophilic attack of the oxygen from the 3'OH succeeds, thus forming the phospodiester bond.

If you try to join the dNTP's 3'OH group to the 5' phosphate of the next nucleotide, there won't be enough energy to weaken the bond between the oxygen connected to the 5' phosphorous (the other two phosphates of the dNTP are on the 5' end, not on the 3' end), which makes the nucleophilic attack harder.

Watch the video, it is better explained there.


Effect of the health of the male parent at the time of conceiving Does it matter at all in determining the traits of a baby what the current health of the father is? For example, let's say I got diabetes at the age of 40 because of the poor lifestyle choices. Will the baby be any different from how it would be if it was when I was say 26?

It can matter, though at this point we are just starting to understand how much.

Men can typically have children much later in life than women, but there are costs as time goes on.

Epigenetics has shown us that what happens to the parents in their lifetime can affect his offspring.  Obesity especially has been shown to affect the offspring, producing a higher risk of diabetes for two generations.

It is thought that this is not going to affect fathers who develop diabetes at a later age, but primarily those who are obese around 9-12 y.o. when the spermatogenic cells are produced in the testes.

What happens to men as they get older though is that their ability to produce healthy sperm starts to degrade.  They can lose fertility and produce more birth defects typically as early as age 35.  Given this there are probably a lot of habits or events that can adversely affect fertility.

Lifestyle choices as simple as tight underwear which might block blood flow to the testes is sometimes cited.

Given all this DNA or cellular damage from chemicals or diet or poor health certainly would also affect male fertility.


Primer design for Gibson assembly I'm trying to design a primer for Gibson assembly.  My gene of interest is on a plasmid, and I want to copy that gene, and put it into a different plasmid.

I am unsure how to design my primers for PCR. I know that I need 2 sets of primers (4 total).

Backward and forward primer to copy my gene out of the plasmid that holds it.
Backward and forward primer to copy the plasmid.

I also know that I need to create complementary regions of overlap between my gene and the plasmid I want to put it in.  How do I do this?

Here is the plasmid and the gene. I want to place the gene in between the biobrick prefix and suffix.

Here is what primers I think I need:

For the plasmid I want to put the gene in, my primers should be

Forward: ATTCGCGGCCGCTTCTAGAG
Reverse: CTGACGCGGCCGCTACTAGTA

Primers to copy gene and add overlap

Reverse: ATCATTTCAAATTCGTCCATCTCTAGAAGCGGCCGCGAAT
Forward: AATTAGAAAGAGATTATAATACTAGTAGCGGCCGCTGCA

Here is the gene

IodoY TyrRs

Here is the plasmid I want to put it in. I am using geneious, but I think for this purpose, word works just fine.

Disclaimer: I haven't ever done a Gibson assembly, but here is my theoretical understanding of how to design your primers. You need four 40mers each consisting of 20 bp segments derived from the vector and the insert and corresponding to the junctions that you are trying to create. In the diagram below the dotted lines represent the junctions between the two 20 bp segments of each 40mer.


Target cells of adrenaline? I have been thinking about how adrenaline increases blood sugar levels, but have not been able to find an answer to the target cells. Does it affect the hepatocytes and muscle cells, like glycogen?

Thank you in advance :)

Epinephrine is a hormone that works systemically and will activate any and all cells that express a hormone receptor with specificity for epinephrine.

As stated in the wikipedia article "It plays an important role in the fight-or-flight response by increasing blood flow to muscles, output of the heart, pupil dilation, and blood sugar. Epinephrine does this by its effects on alpha and beta receptors."


When collecting cell lysates for a Western blot, how do I induce di-sulfide bonds? I would like to conduct a simple dimerization experiment for some protein I'm collecting from a cultured cells. My thought is, that if I'm running a non-reducing, denaturing PAGE gel, then removing beta-mercaptoethanol/DTT from the sample buffer should be enough to allow di-sulfide bonds to form.

I have seen several authors incubate the cells first with a drug called BSS that diffuses across membranes and creates protein cross-links. I may be wrong, but the use of this drug seems more appropriate when trying to follow up with an immunoprecipitation or a pull-down assay.

If anyone has any experience with this, could you please enlighten me?

For the introduction of new cystine bonds, you will probably need to maintain an appropriate redox potential when dialyzing your cell-lysate to allow your cystine bonds to reform. To break the current di-sulfide bonds, we have been adding in Disulfide Bond Isomerases (DsBC to be precise) which will allow your lysate to get to an appropriate equilibrium.

As for examining for disulfide bond formation that has already occured between proteins in your lysate, removing reducing equivalents like DTT and beta-mercaptoethanol should do the trick. You can even denature your proteins by incubating them in LDS or Laemmli buffer at 90C as those components will not reduce your cystine bonds. In our experience the bands typically run at the expected molecular weight on a SDS-PAGE.


Is resource partitioning a type of character displacement? Question

Imagine two related species. They prey on the same species but avoid competition by feeding at different times of the day. Is this a type of character displacement?

Thought

On one hand I have the  Galapagos Finch example, which is typically used to illustrate character displacement. But since resource partitioning is more behavioral than anatomical, is resource partitioning a subset of character displacement or a rough overlap or none?

Does it look like character displacement?

By the fact that these two species feed at different moment of the day, they therefore have slightly different ecological niches. It is indeed the type of consequences brought about by character displacement. Yes, it looks like character displacement.

"Resource partitioning" is not necessarily more behavioural than anatomical and even if it was, a behaviour is a phenotype, just like any other phenotype, and it should not be disregarded. The character being displaced in a 'character displacement' scenario can be behavioural. So, yes if two species evolve to prey at different time of the day to avoid competition, then they have evolved so as to reduce the overlap between their ecological niche and we can call that character displacement.

Is it character displacement (highlight on a few missing information)?

It is possible (likely) that they evolved to feed at different times as a reaction of their competition and hence it would be called "character displacement" but technically speaking the question does not explain how these two species had been diverging in their feeding. It is possible that divergence in their feeding time happened long before being found in sympatry. In fact, the question does not even make clear that the two species are found in sympatry.


If a mother had a child with her own son, could a paternity test yield positive result for the son's father? Let's imagine a family composed of Mr A and Mrs B, who have a son named John.

Now, if for whatever twisted reason, John had a child with Mrs B, could a paternity test yield positive result for Mr A ?

Since John's genes all come from Mr A and Mrs B, the child's genes would all come originally from Mr A and Mrs B as well. Thus it seems to me like the test could suggest Mr A is the father of the child.

Or would there definetly be some "red flags" that suggest something wrong happened ?
Like, for example, if the child is a girl, that would mean both of her X chromosomes originally came from Mrs A (since John's X chromosome comes from his mother, as for all males), possibly even the same chromosome twice.

Let's consider that only Mr. A is tested, and not John. Would the child be considered genetically close enough to Mr. A that a test could attest that he is probably the child's father, granting there is no other test showing someone else as a much more likely candidate ?

Let's approach some different methods of distinguishing parents:

1: The Y chromosome. These are passed down from father to son. Therefore, if the baby is male, its Y chromosome will be the same as John's and his father's - it will be indistinguishable who it's from.

2: The X chromosome. A male baby always has one of the mother's X chromosomes. A female baby always has its father's X and one of the mother's X. A male baby of John and Mrs B would always end up with one of Mrs B's X chromosomes, meaning that this can't distinguish the father. A female baby would have two X chromosomes from Mrs B (because John's own X came from her), proving that it is the product of incest.

3: Mitochondrial DNA. mtDNA is passed on from mothers to their children, never from the father. Therefore regardless of whether John or Mr A is the father, the baby would have Mrs B's mtDNA - not useful.

4: DNA fingerprint. This is primarily based on stretches of the human genome that contain repeats of short DNA sequences (so-called STR/short tandem repeats, or VNTR/variable number tandem repeats). In both cases, the sequence is the same in individuals, but the number of repeats is extremely variable and each human therefore has a (possibly) unique combination across the different repeat locations in the genome. Because children inherit 50% of their DNA sequences from the father and 50% from the mother, John himself will have his mother's characteristic lengths in 50% of repeat locations and his father's in the remaining 50% of locations (roughly). A child of John and Mrs B would have MrA's repeat lengths in 25% of locations and Mrs B's in 75%. The fractions "100% Mr A" vs. "50% Mr A" vs. "25% Mr A" can be distinguished by this method.


What is contiguous premise culling and dangerous contact culling? I am reading this paper related to FMD (foot and mouth disease) epidemics which occurred in UK. It mentioned about terms like IP (infected premise culling), CP (contiguous premise) and DC (dangerous contact cull). IP is the mandatory slaughter of all livestock on an infected premise. But what is CP and DC?

Dangerous Contacts were defined as premises where animals have been in direct contact with infected animals or have, in any way, become exposed to infection
Contigous Premises are defined as a category of dangerous contacts where animals may have been exposed to infection on neighbouring infected premises

Tildesley, Michael J., et al. "The role of pre-emptive culling in the control of foot-and-mouth disease." Proceedings of the Royal Society B: Biological Sciences (2009): rspb20090427.


How was the diversity between ethanol fermentation and lactic acid fermentation evolved? Quite simply, some organisms metabolize glucose under anaerobic conditions via Glucose->(2) Pyruvic Acid->(2)Ethyl Alcohol. Some organisms, however, metabolize to lactic acid.

When did such a process (lactic acid) arise biochemically from its related (ethanol) fermentation, and how was it selected for? i.e What were the advantages?

Also, can someone create the glycolysis or fermentation tag?

First, it is not clear from the physiology or biochemical information alone to determine what evolved from what. The intermediate pyruvate is always there, so lactose dehydrogenase (LDH) and pyruvate decarboxylase (PDC) could have each evolved anytime, and there are good reasons for both:

LDH: the reaction pyruvate + NADH/H+ = lactate + NAD+ + 25 kJ/mol is highly exergonic, i.e. produces heat
PDC: the reaction pyruvate = acetaldehyde + CO2 (and with ALD present) acetaldehyde + NADH/H+ = ethanol + NAD+ where ethanol is poisonous to other species

Add to it that there are organisms like Sch. pombe that have both enzymes, so can do both reactions, your questions should be rather:

How has the enzyme LDH evolved?

The enzyme is similar to malate dehydrogenase, both form a family. They belong to a group of enzymes that all have a NAD(P) binding domain, so it's not too far-fetched to state that LDH and MDH evolved from another enzyme with NAD(P) binding domain.

http://www.ebi.ac.uk/interpro/IEntry?ac=IPR016040

How has the enzyme PDC evolved?

  Protein sequences of pyruvate decarboxylase (PDC) derived from cloned
  yeast (Saccharomyces cerevisiae) and bacterial (Zymomonas mobilis)
  genes were compared with each other and with sequence databases.
  Extensive sequence similarities were found between them and with two
  others: cytochrome-linked pyruvate oxidase from Escherichia coli and
  acetolactate synthase (ilvI in E. coli; ILV2 gene in S. cerevisiae).
  All catalyse decarboxylation of pyruvate using thiamine pyrophosphate
  (TPP) as cofactor. General overall similarity suggests common ancestry
  for these enzymes.

cited from abstract of

Green, Jeremy. "Pyruvate decarboxylase is like acetolactate synthase (< i> ILV2) and not like the pyruvate dehydrogenase E1 subunit." FEBS letters 246.1 (1989): 1-5. http://www.ncbi.nlm.nih.gov/pubmed/2651151?dopt=Abstract


"Oblong to Allantoids" .... Is it valid? I read on the text book:

The characteristic of Dinemasporium are: superficial, cupulate to Discoid conidiomata with brown satae, Phialid conidiogenous cells that give rise to hyaline, oblong to Allantoids, and Aseptate conidia with an appendage at each end.

My question:

the phrase "oblong to Allantoids"; Is the word oblong valid for this context? if not, what other word would associate?

Oblong is probably correct in this context, but "allantoids" should probably be "allantoid" to be the adjective form. It's describing translucent (hyaline), oval (oblong) to sausage-shaped (allantoid), undivided (aseptate) spore.


At which end does polymerization of microtubules occur? My book says that polymerization and depolumerization of microtubules occurs on the + end however, I've found a note that says that depolymerization occurs on the - end. I need help please :) thank you

From my Campbell's Biology textbook (Ninth Edition):

  Because of the orientation of tubulin dimers, the two ends of a microtubule are slightly different. One end can accumulate or release tubulin dimers at a much higher rate than the other, thus growing and shrinking significantly during cellular activities. (This is called the "plus end", not because it can only add tubulin proteins but because it's the end where both "on" and "off" rates are much higher.)

So in summary: polymerization and depolymerization occur on both the + and - ends. The "+" and "-" merely designate the speed/efficiency of polymerization and depolymerization.


Repopullation after a mass extinction Is it possible to restart the whole human species with less than 10 individual.
let say that the whole human species was wipe out of the surface of the earth by a catastrophe only 8 different couple survive the catastrophe could they restart the human species?

The estimate is probably going to depend on the source, but it's generally at least an order of magnitude more than that.

Back in 2002, John Moore, an anthropologist at the University of Florida, calculated that a starship could leave Earth with 150 passengers on a 2000-year pilgrimage to another solar system, and upon arrival, the descendants of the original crew could colonize a new world there—as long as everyone was careful not to inbreed along the way. [...]
A starting population of 40,000 people maintains 100 percent of its variation, while the 10,000-person scenario stays relatively stable too. So, Smith concludes that a number between 10,000 and 40,000 is a pretty safe bet when it comes to preserving genetic variation.

For the general concept see minimum viable population.


During the process of plasmid isolation, how can we be sure that only plasmid DNA has been isolated and there is no chromosomal DNA? We separate the membrane and all other cell components, but how is it that only plasmid DNA is isolated and not chromosomal DNA?

It comes down to the size of genomic DNA (relatively huge) compared to that of plasmid DNA (rather small).

Cell lysis for plasmid extraction involves an alkaline buffer that includes sodium hydroxide and SDS. Both plasmid and genomic DNA denature in this condition. When the alkaline reaction is neutralized with potassium acetate, the fairly short plasmid DNA can quickly re-anneal, while the much longer and more complex genomic DNA tends to become tangled up with itself, which prevents sister strands from properly aligning and often results in protein-DNA binding interactions.

DNA bound to protein will then get pulled down during centrifugation, while soluble plasmid DNA remains in solution.

Qiagen and BiteSize Bio both offer some more description of the process:
https://www.qiagen.com/us/resources/technologies/plasmid-resource-center/key%20steps%20in%20the%20plasmid%20purification%20protocols/

http://bitesizebio.com/1660/plasmid-v-genomic-dna-extractionthe-difference/


Is there any artificial species (in particular, an artificial species of animal)? Dogs were artificially selected from wolves, but a dog and a wolf can produce fertile offspring, and thus are of the same species. I had heard that the aurochs and cattle were different species, but I could not find this information anywhere. I had heard also that some artificially selected flies are considered to be a new species.

Is there any human-made species (especially a species of animal) which is not able to produce fertile offspring witch any other species, in particular with the one from which it evolved?

EDIT: (A similar question in different words.) Is there any human-made animal lineage which was conceived by artificial selection and which is broadly accepted as not being a race or subspecies, but a species on its own.

Artificial selection leading to new species - Domestication

As you talk about dogs in your intro, let's consider them.

You will fail to breed a great dane and chihuahua for obvious mechanical reasons. You will also fail to breed a chihuahua with a wolf. So, yes artificial selection have lead to reproductive isolation.

Artificial selection leading to new species - lab experiment

Artificial selection have also lead to reproductive isolation in non-domesticated species. See for example the post Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?

Concept of species

As a side note... Above, I consider the so-called 'biological species concept'. For a discussion on the definition of species, please have a look at this post.