text:
How do colds and flu not infinitely recur?
I'm in my third week of university, and a large number of people I know, including myself, still have "fresher's flu", which is probably just a cold and a cough. My lectures are constantly punctuated by the sound of violent coughing. What I don't understand is: how do colds ever go away, given these conditions? Surely by the time you've gotten rid of your cold you've passed it onto someone sitting near you in a lecture, who could then spread it back to you directly or indirectly later? Why don't we have an infinite recursion of colds, coughs and other minor infections throughout the year?

In one word, because of immunity (in particular adaptive immunity). Related question and answer with somewhat opposite reasoning here.

Atl LED says in that question that we can never develop immunity to the HRV. If that's so - and assuming, though I could of course be wrong, that HRV is the most common viral infection at this time and place - then why does the HRV not infinitely recur throughout the year? How do we ever have quiet, relatively healthy periods?

Short answer:
Because your immune system adapts to the virus causing the flu or the common cold and, thus, you become immune to it.

Longer answer:
When B cells first encounter an antigen (usually a protein on the surface of a pathogen), the antigen attaches to a receptor, stimulating the B cells. Some B cells change into memory cells, which remember that specific antigen, and others change into plasma cells. Plasma cells produce antibodies that are specific to the antigen that stimulated their production.
After the first encounter with an antigen, production of enough of the specific antibody takes several days. Thus, the primary immune response is slow and that's the reason you experience the symptoms of the disease.
But thereafter, whenever B cells encounter the antigen again, memory B cells very rapidly recognize the antigen, multiply, change into plasma cells, and produce antibodies. This response is quick and very effective.
This means that, theoretically, you shouldn't be able to become sick twice by the same virus.
However,
virus are very prone to mutations. If these mutations occur in the genes that code for antibody-binding sites, the antibodies produced by B Cells become less effective. This is called Antigenic drift and the reason you might catch the Flu every year (because, with enough time, the virus antigens become different enough to "fool" your immune system).

Also, there are a few explanations why the flu has a seasonal pattern, with a peak usually at winter. One of the theories postulates that in cold weather, people tend to stay indoor, favoring virus transmission.
Recently, an interesting article was published that found that:

transmission of influenza B viruses is enhanced at colder
temperatures, providing an explanation for the seasonality of
influenza epidemics in temperate climates

source


text:
Is it possible for a child to grow taller than their tallest parent?
I have heard that offspring can't grow taller than either of their parents but I've also heard that sometimes some gene activation can skip generations. Is it possible for a child to grow taller than their tallest parent?

Where did you heard that? Have you read it somewhere?

there are several examples of offsprings taller than their parents.

well, if that was true, primitive humans would have been a lot taller than us. And, eventually, humans would become hobbits, as far as height goes =P

Well.. I am taller than both of my parents. Phenotypic variance is the addition of the enviornmental variance and the genetic variance (and their covariance). In other words, the environment, not only the genes influence someone's height. This is one reason that may explain why an offsrping may be taller that their parents.

An easily visualized example of where even completely genetic traits don't simply average parent phenotypes is hair color: many dark haired parents have bright blond children when each parent has a recessive blond gene.

because people grow taller over generations this has to be true doesn't it :)

If it were true, wouldn't it likewise be true that no child could be shorter than their shorter parent?  Which would mean that eventually all humans would be the same height?

People can grow taller than their parents. Anecdotally: I'm 185 cm, my parents are 155 cm and 178 cm. Joakim Noah, an NBA basketball player is 211 cm, his dad was 193 cm and mother was 175 cm... how?
Genetics and environment play a role in determining height. First of all, a more nutritious environment during development can lead to increased height, this is one reason why more recent generations appear to be taller.
Height is also an example of a quantitative trait - this means many genes (or loci [singular is locus], locations in the DNA) affect the phenotype (the physical measurable result i.e. a persons height). It is infact how the vast majority of traits are determined. At each locus that affects height there may be polymorphism (when more than one allele, or variant of that gene, exists).
Example:
Suppose height entirely is determined by 2 additive loci, $A$ and $B$, and no environmental effect occurs, and there is diploidy (two of each locus, one from each parent, determines height in a person).
Each locus has two alleles denoted by $A_1$, $A_2$, $B_1 $ and $B_2$. Each copy of alleles $A_1$ and $B_1$ add 40 cm to a persons height, $A_2$ and $B_2$ add 50 cm to a persons height.
Now a man who is $A_1 A_1, B_1 B_2$ (remember, humans are diploid) and a woman who is $A_2 A_1, B_1 B_1$ have children. Both parents are 170 cm tall. The theoretical limits for the population would be 160 cm and 200 cm. The children will inherit one copy of $A_1$ from the father and $B_1$ from the mother, but they could inherit either $B_1$ or $B_2$ from the father and either $A_1$ or $A_2$ from the mother. If a child inherited both of the taller alleles then they would be taller than the parents ($A_1 A_2, B_1 B_2$ = 180 cm). Likewise some offspring could be shorter.
Of course the reality is much more complex; height is determined by many more than 2 loci, by the environment, and gene * environment interactions. This principle was a hugely important because it meant that reproduction did not necessarily remove variation from the gene pool (a fundamental problem with early evolutionary theory was the thought of "blending" - when offspring are the average of their parents)

Yes, people can definitely grow taller than their parents. Height is a polygenic quantitative trait (so affected by many genes), that is also strongly affected by environmental factors. You are also forgetting that there is a sex difference in height (~14 cm, Wright & Cheetham, 1999), so the height of the mother does for instance not set an absolute cap on the height of her sons ("....can't grow taller than either of their parents"), but her genetic background will influence their heights. If both parents are e.g. 180 cm tall, that is close to the population average for the father but considered tall for the mother, she is likely to carry genes that contribute to her offspring being tall.
That height is a polygenetic quantitative trait means that parental height will be a good predictor of offspring height, but with a wide scatter around the mean. Normally, 90% of children fall within 1.5 standard deviations of their midparental heights, after being sex-adjusted with +- 7cm for boys and girls (Wright & Cheetham, 1999). For simplicity, it is often said that 90% of children will fall within 10cm of the sex-adjusted mid-parental height. However, the deviations are smaller if the parents are unusually short or tall, representing "regression to the mean", and parental height is a poorer predictor for offspring height in these cases. Using the midparent mean as a predictor of offspring height is otherwise standard practice, as can be seen in online applications (e.g. http://medcalc3000.com/HeightPotential.htm). Using the same example as above, with both parents being 180 cm, will predict an offspring height of 186cm for sons and 174cm for daughters.
That height is strongly influenced by nutrition has been clearly shown in the general secular trend in body height in developed countries over the last centuries (Cole, 2003, where the average height of successive generations have been taller than their parents. For instance, the average height in the Netherlands have increased from 165 cm in 1860 to 181 cm in 1990 (numbers from Cole, 2003). Some of the online height calculators you see will also include a corrections for this, and add e.g. 1-2 cm to the mid-parent heights before correcting for sex.

Yes it is quite possible, recall nature vs nurture. I myself am slightly taller than both of my parents by about a head. As long as you have sufficient nutrition it should be quite possible.
And what you said about gene activation skipping generations is quite true- it can indeed happen, and if the gene responsible for height is not expressed in the parents but is in their offspring then it will also be more likely for the child to grow taller than their parent.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
True or False: Vaccines are designed to protect against invaders that are encountered rarely, not all the time
I read the following statement in this article:

Vaccines are designed to protect against invaders that are encountered
  rarely - not all the time

Is it true? If yes, why?

I think the idea behind this is not the frequency of the pathogen itself, but the frequency of exposure. If I am exposed to a pathogen frequently anyway, I have a chance to naturally develop immunity. If I never am exposed to it, one single exposure might be dangerous, if I am not vaccinated (exposed artificially). (Just to add, this is not necessarily true, but I tried to imagine what the author might have wanted to say.)

This analogy is not completely true. A lot of diseases were relatively common before the wide introduction of vaccinations. Measles, Diphteria, Smallpox and others where pretty dangerous although they were common.

Not true. Vaccines were initially made for the highly contagious diseases that used to cause epidemics (which obviously means they were not rare).
The efficacy of a vaccine depends on multiple factors which includes adaptability of the pathogen.
The all-the-time encountered pathogen that the article is talking about is HIV; the reason for why no effective vaccine exists for it is because it has high mutation rate.

The source article had several major errors in it. I wouldn't trust any of it.

Vaccines are designed to protect against invaders that are encountered rarely - not all the time.

This is one of the major errors. There is a vaccine for chicken pox now - an infection which affected approximately 4,000,000 cases per year in the US before the vaccine. That is a very high number of children.
The overall HPV prevalence was 26.8% among US females aged 14 to 59 years before the vaccine. (This vaccine refutes two major errors in the paper.)
Measles, mumps, German Measles, Influenza, Haemophilus influenzae, and Pneumoccocal pneumonia were all common before vaccines for them were developed. Those are just the ones I can think of off the top of my head.
Factors that influence the ability to make a vaccine against a pathogen include the mechanism of pathogenicity, the ability to render the vaccine less harmful than the wild-type illness (such as polio), the ability to mass produce easily, reliably, etc.

False.
Theoretically, a vaccine could be constructed for any pathogen, but the value of doing so if different. In business, this is called 'Return on Investment'. So, vaccines against serious common diseases are more valuable than ones against minor rare ones.
Polio, smallpox, whooping cough, rubella and typhoid are not rare. They are rare now.

A vaccine is not made because a pathogen is rare. It's made because a pathogen is so vicious that you're body does not have enough time to counteract it. Your body is always attacked by invaders, even now.
But usually the Innate immune responses are enough to rid you of the threat. And, when it isn't, it acts as a barrier until the adaptive responses fire up. This time gap is crucial, because the adaptive system needs antigenic presentation from the dendritic cells to differentiate B-cells into plasma and memory cells, then create antibodies and finally these antibodies will opsonize the pathogenic agent and then let the complement system or the CTLs take over.
This is where vaccines come in, Vaccines generally but not always stimulate the Adaptive responses, allowing the creation of Plasma B cells and memory cells. So next time when an invader arrives, the Adaptive response responds as soon as an antigen is encountered. Which is why, the diseases mentioned above have become such a rarity, but rest assured that if individuals choose not vaccinate then these diseases will re-emerge once again as they are doing now in the US.
I cannot post more than 2 links, so if you're interested read up. and If you're even more interested, pick up a copy of Kuby's Immunology, it helped me when I was in college and I'm sure it will help you out too.
http:// en.wikipedia.org/wiki/Antigen_presentation
  http:// en.wikipedia.org/wiki/Dendritic_cell
  http:// en.wikipedia.org/wiki/B_cell
  http:// en.wikipedia.org/wiki/Opsonin

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Localization of Protein Kinase-A
Is protein kinase-A located in the cytosol/cytoplasm of cells or in the plasma membrane?  Also, is it considered a receptor molecule since it is dependent on cAMP?
Any and all help is appreciated. Thanks!

The localization of the protein kinase A (PKA) cannot be explicitly answered, since the localization depends on the activation state of the protein. Lets have a look at the protein itself first, as this is important for the activation.
PKA consists of four subunits, two catalytic subunits and two regulatory subunits. See the image from the Wikipedia article on PKA:

Each regulatory subunit R is binding two cyclic AMP (cAMP) molecules and dissociates then from the protein complex. This sets the catalytic subunits free, which can then transfer phosphate groups from ATP to serine or threonine residues of target proteins. Among the target proteins is also the Phosphodiesterase (PDE) which gets activated by phosphorylation from PKA. Activated PDE hydrolyzes cAMP into AMP which reduces the amount of free cAMP which is necessary for PKA activation. PKA is also inactivated by phosphorylation.
In the cell you will find PKA almost everywhere. The traditional belief is that the protein is activated in the cytosol and enters the nucleus where it phosphorylates targets like CREB which then subsequently binds the the CRE sequence in gene promoters and activates this genes. Reference 1 shows that PKA is also activated in the nucleus, meaning that also the inactive form is present there. Reference 2 gives a nice summary of the article.
The regulatory subunit of inactive form of PKA binds to a special class of proteins: The A-kinase anchor proteins (AKAP). These are membrane bound and allow the association of PKA to membranes, although the protein itself is not directly binding to the membrane. The AKAP family is rather big (at least 50 family members are known today), which probably allows the localization of PKA at different membranes. Have a look at references 3-5 for details on the localization and the anchoring.

References:

Regulation of nuclear PKA revealed by spatiotemporal manipulation of
cyclic AMP.
Protein kinase A activated in the nucleus as well as the cytoplasm
The where's and when's of kinase anchoring
Localization of A-kinase through anchoring proteins.
The biological functions of A-kinase anchor proteins

It is present throughout the cytosol but can also be anchored to plasma membrane and mitochondria via indirect interactions. Can also be translocated to the nucleus. (See here).
It is not called a receptor for cAMP (though the mechanism is homologous).


text:
Does adding antibiotic after 5-10 mins of innoculation affect the protein yield or growth?
I've asked a lab colleague the same question. She said, it would loosen the bacterial cells in the LB medium and plasmids would come out. Is that true? and why?

That is not true. If you had forgotten to add the antibiotic before inoculation then you can add it before the bacteria starts growing. Make sure you add it when the bacteria is still in lag phase. If you add it later then it won't be effective as some non-resistant (non-transformed) bacteria would have already expanded their population. Ampicillin and kanamycin are best effective when the bacteria are growing. Even though these antibiotics are considered bacteriocidal, you would end up having unnecessary biomass in your culture.
So 5min delay for E.coli is not an issue. (I think this happens to all of us: forgetting to add antibiotic).

But isn't it still true that the plasmids will get lost if there are no antibiotics as they normally contain the resistance gene?

@TheGreenOne They would eventually but not so fast.


text:
Is Canine teeth enough evidence to prove that one is a Carnivore?
This question does not assume that we are meant to be carnivores in the first place; In fact I have no idea to which category we belong to anyway! There are several posts online indicating that classifying humans as carnivores and pointing to our canine teeth as evidence might be fallacious.
Also, the fact that Hippos, the largest canine teeth of any land mammal, are herbivores indicates there are exceptions to this view. A couple of other animals like the Gorilla are also herbivores with big and sharp canines. I have also read about the lack of cellulace production in humans as a counterargument to the above.
To what category would we fit in to? What evidence is required to support this idea? Do scientists agree upon a common theory?

We are pretty clearly omnivores.  Our teeth, and more importantly, our actual habits, confirm this.  It is possible for us to live an exclusively herbivorous or carnivorous lifestyle, of course.


text:
What is frank dehydration?
On Wikipedia article about Urine specific gravity we can read:

A specific gravity greater than 1.035 is consistent with frank dehydration.

What is frank dehydration? How it is different than regular dehydration?

A higher specific gravity means a higher concentration of salt. And a lower concentration of water. You can now think about reasons why the human body looses lots of water, the most likely is heat and not enough resupply of water. The Wikipedia article also states that the normal specific density is between 1.000 and 1.030, so you are beyond the normal range.

What about frank word, it's any special wording to indicate some kind of type of dehydration?

"Frank dehydration" is not really a regular medical term. You can suspect this by using Google search with "frank dehydration" in quotes and site:gov (only 3 websites showing up) and site:edu (2 websites) operators.
The term "frank dehydration" as an informal term can refer to "obvious," "actual," "test-confirmed" dehydration as opposed to feeling dehydrated or thirsty.
Tests to confirm dehydration include a combination of the body exam (dry mouth, prolonged skin turgor, decreased body weight), urine tests (dark urine, increased urine specific gravity, decreased urination frequency and 24-hour urine volume) and blood tests (increased sodium levels - hypernatremia).


text:
What is most ancestral: isogamy or anisogamy?
Sexual reproduction can be feasible with anisogamy (gametes of different sizes i.e. genders) or isogamy (gametes of same size i.e. mating types) or with undifferentiated gametes (i.e. true random mating; although I have to confess that I am not aware of such example).
De novo evolution of sexual reproduction happened several times independently. What seem to be the most ancestral states of gamete differentiation (isogamy or anisogamy)?. Does it differ between lineages?

It's not exactly what you're asking, but the recently published "Tree of Sex" might be relevant: http://treeofsex.org ; http://www.nature.com/articles/sdata201415

As stated here the first sexual reproduction seems to be isogamy, which's purpose was likely to repair the DNA, as a damaged cell could repair its' (DNA) strands via recombination with a "healthy" one.
As for lineages, the only thing I could find was also in this book at the very beginning, but there doesn't seem to be a difference as for which is the most ancestral.


text:
Ancestral states of sex determination system
Most (maybe all?) species that reproduce sexually have either genders (anisogamy) or mating types (isogamy). There exist today many different type of sexual determination system. There is a whole complicated continuum from species where the gender is exclusively determined genetically (genetic determination system, GSD) to those where the gender is determined by the environment (environment determination system, ESD).
Knowing that genders (and mating types) evolved several independently, what seem to be the ancestral states of sex determination system? Where the first sexually reproducing lineages GSD or ESD? Does it differ between lineages?

I saw a talk a couple of years back, many esd systems are strongly g*e. So there is a threshold of the environmental factor where all become one sex or the other. Then at intermediate environmental values you can develop males and females

Yes, as argued in Evolution of Sex Determination all liability factor (factor that define the sex relative to a threshold) follows a norm of reaction and therefore the concept of GSD makes sense only by defining the range of environmental condition where which the sex is only defined by the genes. But I think my question is still of interest even to the light of a more accurate definition of GSD and ESD.

Agreed. On another note,do you have that book? I nearly bought it this week -what do you think of it (assuming you do have it?)

No, I don't have it. I very often want to buy it but I stop right before doing so when I see its price! I read part of this book during my master degree, just before it got published for a class I attended at the University of Lausanne with Nicolas Perrin (one of the two authors) and I really appreciate it. It was for me a totally new subject and the book made a good job to introduce me into it. I also thought that the book makes a good job of providing both a good theoretical understanding and a rather impressive list of study cases separately into different paragraphs.

I bought the book, they printed the pages upside down...

@GriffinEvo Oh no! You got a defective copy. You can probably asked to be reimburse.


text:
Are there multicellular isogamous species?
Are there multicellular isogamous species?
Seeking through the examples of wikipedia I would tend to think that there are no multicellular isogamous species.

"Isogamy is common among algae, lower fungi, and many protozoans (Rhizopoda, Radiolaria, and lower Gregarinida) but absent in multicellular animals. In isogamy the copulating gametes differ in their biochemical and physiological properties." - but this is not from a scientific article...

Our knowledge about the sexual transmission of mitochondria and
  plastids (hereafter organelles) in isogamous eukaryotes comes mostly
  from studies of the yeast Saccharomyces cerevisiae and the green alga
  Chlamydomonas reinhardtii which are both unicellular species. To
  investigate organelle inheritance in a multicellular organism with
  morphological isogamy, we studied the filamentous brown alga
  Ectocarpus siliculosus, in which each gamete contributes one plastid
  and at least one mitochondrion to the zygote. ...

2004 - Inheritance of organelles in artificial hybrids of the isogamous multicellular chromist alga Ectocarpus siliculosus (Phaeophyceae)

So it is possible, but it seems like very rare.


text:
Gibson assembly - primer design with A and T rich regions
I have question about Gibson assembly. I have done it several times and it always worked okay for us, but now I want to assemble together a fragment which has sequence like this: 5'CTTTTTCTTCGTCGAAAAAGGCAATAAAAATTTTTATCACGTTTCTT3'.
Do you think a AA and TT repetitions will cause any problems? We usually used 30 bp of homology at both sides of sequence. Should I use more in this case? What are your experiences regarding this AT repetitive sequences?
thanks,
Martin Kavšček

Yes this is a very low-complexity sequence. Can you paste your entire sequence? There might be some trick to work it out.


text:
Gene duplication and subfunctionalization
I’ve been intrigued by gene duplication and want to learn more about it.
I’ve read the following from here:

several studies suggest that the proportion of duplicated genes
  retained in vertebrate genomes is much higher than is predicted by
  this model [4-6]. This has led to the suggestion of an alternative
  model whereby complementary degenerative mutations in independent
  subfunctions of each gene copy permits their preservation in the
  genome, as both copies of the gene are now required to recapitulate
  the full range of functions present in the single ancestral gene. This
  was formalized in the Duplication-Degeneration-Complementation (DDC)
  model [7] in a process referred to as subfunctionalization.

Can someone explain this?  What is meant by “both copies of the gene are now required to recapitulate the full range of functions present in the single ancestral gene”?
Can you suggest any other good articles on gene duplication?

I would interpret that to be a situation where a gene codes for an enzyme that does some necessary metabolic reaction that needs 2 steps, A -> B -> C. The gene gets duplicated, but in order to preserve both copies each copy needs to mutate. Let's say copy 1 can only do A -> B now, and copy 2 can only do B -> C. This means you need both copies to do A -> B -> C. Alternatively, copy 1 could still do A -> B -> C and copy 2 picks up a gain of function mutation that allows A -> B -> D or something. As long as D increases the odds of reproductive success the second gene copy is selected for.

Suppose a gene performs two distinct functions 1 and 2, both of which are essential. We'll call this gene A, for ancestral gene.
A duplication copies A to another locus. Now there are two genes, A and B, that perform the same two functions. At this point, if either A or B is deleted, the organism is fine.
Over evolutionary time, A and B undergo genetic drift to become A' and B', respectively. Let's say that B' loses function 1, and that A' loses function 2. This isn't a problem for the organism since A' still performs function 1, and B' still performs function 2. In other words, the two genes complement each other.
However, now A' can't be deleted without losing function 1, and, similarly, B' can't be deleted without losing function 2. The result is that both genes are fixed in the genome by evolution.
This means that now, after hundreds of millions of years of relevant evolution and genetic drift, we many duplications like A' and B'. The key to this is that through genetic drift with no selective pressure, it's very easy to lose function but extremely difficult to gain it.
As for your second question, I'll look for a paper on gene duplications that I think would be the most helpful, but there are many.


text:
Can connections between neurons be weakened?
Connections between neurons are said (by Wikipedia) to be strengthened as part of learning - can they also be weakened (below the original level)?
I understand the concept of the connections strengthening. After reading the article Ants Swarm Like Brains Think, my understanding is that positive feedback (I forget the words that I should use for positive vs negative action potentials) should strengthen the connection, and negative feedback should weaken it.
I'm interested to know whether neural connections can weaken below their original connection strength.
I'm curious about this so as to grasp the way that the human brain (or even simply the ant brain) learns good and bad. If I'm not completely wrong about what I'm asking, then I think I get it pretty well: The things that are good (like finding food) trigger positive feedback among the associated neuron groups, and the things that are bad (like pain or danger) trigger negative feedback in the associated neurons, and that's basically how brains learn good from bad.

see https://en.wikipedia.org/wiki/Long-term_depression

Have you forgotten anything you learned well at school at some point in the past? If so, you have your answer.

Short answer
Yes, neural connections can be weakened.
Background
Chemical connections between neurons (synapses) can certainly be strengthened or weakened, dependent on their input. Single synapses can undergo long term potentiation (LTP) or long term depression (LTD). As a typical example there are hippocampal neurons. High-frequency (tetanic) electrical stimulation in hippocampal neurons can result in long-term potentiation (strengthening) of synaptic connections in the hippocampus Moreover, when a synapse receives synchronous input from multiple incoming axons they can potentiate each other's responses (Purves et al, 2001). In contrast, low-frequency stimulation and  prolonged inactivity of synapses in the hippocampus can weaken them (Bear & Abraham, 1996).
The connection between learning, let alone good and bad as you ask for in your question, is far from clear. However, LTP and LTD do provide plausible mechanisms that could underpin these processes at the cellular level (Purves et al, 2001).
References
- Bear & Abraham, Ann Rev Neurosci (1996); 19: 437-62
- Purves et al., eds. Neuroscience, 2nd ed., Sunderland (MA): Sinauer Associates; 2001

What you are talking about called synaptic plasticity, and sure it is possible to weaken connection between neurons, that's why for instance you can forget things.

In neuroscience, synaptic plasticity is the ability of synapses to
  strengthen or weaken over time, in response to increases or decreases
  in their activity.1 Plastic change also results from the alteration
  of the number of neurotransmitter receptors located on a synapse.2
  There are several underlying mechanisms that cooperate to achieve
  synaptic plasticity, including changes in the quantity of
  neurotransmitters released into a synapse and changes in how
  effectively cells respond to those neurotransmitters.[3] Synaptic
  plasticity in both excitatory and inhibitory synapses has been found
  to be dependent upon postsynaptic calcium release.2 Since memories
  are postulated to be represented by vastly interconnected networks of
  synapses in the brain, synaptic plasticity is one of the important
  neurochemical foundations of learning and memory.

wikipedia - synaptic plasticity

neural connections can be weaken below their original connection strength. from neuroscience, new memories mean new neural connections, and the new neural connections require repeated activation. neurons that fire together, wire together, so it neurons or groups of neurons donot fire together often enough, new connections do not form.
i am not sure the relationship with ants, i think the neural connections is strength by frequently practice.

So are you saying rather than the strength of individual connections increasing, more connections form which in turn makes the over-all connection between the two neurons stronger?

yes. but i am not sure is there other thing or action can increase the strength of individual connection

It would be great if you provided some references for your response!

I DO not remember where i found that, i only remember it is about Recursive Hierarchical Recognition (RHR)


text:
How does the brain avoid feedback loops?
The article Ants Swarm Like Brains Think really helped me to understand the way that neurons which are pretty dumb on their own (like ants) can work together to create a pretty genius system (a brain or an ant-hive). The idea is that both the neurons and the ants function majorly via positive and negative feedback, which is really neat to understand.
However as shown in that article, sometimes groups of ants get caught in something called a feedback loop. They can repeat the same action over and over because the positive feedback is just being relayed from ant to ant to ant in a circle, and the ants can do something unhealthy such as walk in a circle for days. I don't know any examples of negative feedback loops but they would presumably also be unhealthy.
As noted in the comments, this is an analogy, but not without a good reason: The brain does work via positive and negative feedback. And that does create the potential for feedback loops.
So I'm curious about what biological features in neurons help to avoid these feedback loops in our brains. How does the brain avoid feedback loops?

The article is cool, but it's using an analogy. The brain doesn't really work, strickly speaking, as an ant swarm.

@Tivie of course, but the analogy is not without a good reason: The brain does work via positive and negative feedback. And that does create the potential for feedback loops.

Well, sometimes, it does enter a kind of feedback loop, Epilepsy.

@Tivie very true. So I'm even more curious now, about how most brains avoid them. Of course, Epilepsy may be far more complex than feedback loops, but it could be a good example of one.

I will try to post a simple answer

well balanced feedback loops create oscillations as well...

@jt0dd This is interesting. I just realized that feedback loop is not a common network motif in neural networks. Feed-forwards/bi-fan are very common. There should be a reason for this: something theoretical. I shall post when I get an answer to this

@WYSIWYG neat please explain

@jt0dd I was referring to the architecture of neural networks. I will have to look up for the reason to why FF is more common than FB

@jt0dd. I can think of a few reasons why FB is not preferred. It would take a long time to generate a FB. Therefore is is best to anticipate the fluctuation beforehand and correct/fix it.

Normally, after an excitatory neuron fires, it becomes more resistant to firing again for a period of time (refractory period). This is due to electrical changes within the excitatory neuron.
After depolarazing and reaching an action potential(firing), the neuron enters the refractory period, in which its charge will go back to normal (resting potential). This refractory period can be divided in two phases: Absolute and relative. During the Absolute refractory period, the neuron cannot be discharged again, since the sodium channels are inactive.
It's the relative refractory phase, however, that is more relevant to your question. During this period, the neuron enters a hyperpolarization states, meaning that it's resistant to firing again, unless it receives a greater stimulus.
So, basically, after firing and for a while, a neuron requires greater stimulus to be fired again. This works as a Feedback control, since even if you overstimulate a neuron it can fire only so often.
Inhibitory and excitatory neurons (and inhibitory and excitatory neurotransmitters) also play a role in the feedback control. Inhibitory neurons reduce the likelihood of a postsynaptic neuron to fire while excitatory neurons do the opposite.

However, sometimes these mechanism fail.
For instance, in Epilepsy, the resistance of excitatory neurons to fire during the refractory period is decreased. A group of neurons begin firing in an abnormal, excessive, and synchronized manner, resulting in a wave of depolarization known as a paroxysmal depolarizing shift, causing seizures.
In Parkinson disease, decreased dopamine causes increased inhibitory output (excess negative feedback) of the motor circuit, which leads to hypokinesia.
In contrast, excess dopamine and dopaminergic neuron activity seem to be related with Schizophrenia.

thank you for this explanation. Do you happen to know the relative timespan of neuron-neuron signal propagation and the refractory period? In other words, how many neurons would need to be in a positive feedback loop to moot the refractory effect. And is this much longer than a normal signal path?

@FullDecent has a great followup question here. Say the refractory period is 250ms. Then there could be a feedback loop as long as the time the signal takes to return to the starting node is at least 250ms.

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


text:
Can sealed epiphyseal growth plates theoretically be restored via epigenetic or genetic methods?
I know that epiphyseal growth plates seal up once people become young adults and that it is currently impossible to restore them to actively produce new bone growth but, is it theoretically possible via genetic or epigenetic means to reactivate them to produce new bone?

I don't know about bone length, that's one for science fiction. What about bone density?

bone density is something else I'd be interested in knowing about but this question is focused only on reactivating the epiphyseal growth plates.


text:
How can ingesting a prion "infect" someone?
That's something that's been bugging me for a while...
Our gastrointestinal tract produces proteases that degrade proteins. Prions are proteins. Shouldn't they be broken by proteases?
Also, how can a prion pass the gastrointestinal barrier? Shouldn't the intestine be able to absorb aminoacids only (instead of full proteins)?

Prions are misfolded proteins with abnormal tertiary or quaternary structures. That grants them resistance (to some extent, at least) to proteases (1).
Also researchers believe that prions are able to replicate (2), by changing the structure of other proteins.
Regarding the gastrointestinal barrier, that isn't exactly true. It has been shown that small quantities of intact proteins do cross the gastrointestinal tract in animals and adult humans (3), and that this is a physiologically normal process required for antigen sampling by subepithelial immune tissue in the gut

So, the resistance to the proteases and the ability to replicate in certain conditions might explain the odds of a prion crossing the gastrointestinal tract and infecting an individual.

References:

http://www.ncbi.nlm.nih.gov/pubmed/24338008
http://www.nejm.org/doi/full/10.1056/NEJM199609193351218
http://www.ncbi.nlm.nih.gov/pubmed/3060169

I think explaining the replication process here is worth including for a more complete answer.


text:
Why is coconut oil healthier when it has so much saturated fat?
I noticed that coconut oil has ~96% saturated fat, and I was under the assumption that saturated fats = bad for health.
Why is it that coconut oil is healthier to alternatives with much less saturated fat?

coconut oil is composed mainly of medium-chain triglycerides, 1)it is smaller than other long-chain triglycerides so that it can be digested easily, 2)the digestion of coconut oil does not involve in the Pancreatic digestive enzyme system, 3) liver prefer use medium-chain triglycerides as the fuel sources 4) medium-chain triglycerides will convert to monoglyceride and medium-chain fatty acid which have strong antibacterial


text:
How isolated are different areas of the brain?
I'm interested in understanding how isolated different parts of the brain are from each-other. I'm trying to understand the way that different sections of the brain work together.
More specifically, I'm interested in whether or not the different sections are all intertwined together into a wild mass, or work in a more isolated way:
Do different specialized areas of the brain have specific, consolidated connection areas where they exchange information (sort of like they do their job and pass on the necessary information to the other modules)?
Or do they instead mesh very thoroughly, connecting freely to other parts of the brain sort of like tangled string, with no obvious points of consolidated interaction?

Well, to answer your question, both your hypothesis are true, at least partially true.
The brain has several known specialized connections called neural pathways that connect specific areas of the brain and are responsible for determined functions.
For instance, when you move your leg, the stimulus starts at the motor cortex and travels through the pyramidal tract to your leg and then back.
However, one can argue that the stimulus didn't start at the motor cortex. Why? you thought about moving, then made the decision and only then perform the real action of moving your leg.
And here's a more complex (and maybe humorous) example:

You see a dog running ferociously at you.
The stimulus travels through your visual pathway to your visual cortex.
The image of a dog forms in your brain.
It then travels to your Hippocampus.
You realise that's a dog and also remember a traumatic childhood experience with a dog.
The stimulus travels to your amigdala.
You feel fear
The stimulus activates the sympathetic system.
You're now prepared to fight or flight
The frontal lobe is activated
You decide to kick the dog
The stimulus goes from your motor cortex to your cerebellum
Your cerebellum "remembers" the karate classes you had as a kid
The stimulus goes to your leg
You kick the poor dog. He runs.
Nucleus accumbens is activated
You feel good with yourself

So, in short, the brain has pathways that connect specific areas of the brain but, in a sense, all parts of the brain are connected either directly or indirectly. Like the saying "all roads lead to rome!"

DISCLAIMER: I do not endorse animal cruelty.

Poor dog... ;-(


text:
Is the brain functionally symmetrical?
I understand that each half of the human brain handles different parts of our thinking. Left brain, right brain, that whole topic.
But in pictures, the brain is always depicted as having symmetrical structure. I'm curious about that. I realize that it might be silly to expect such a complex tool to be truly symmetrical, so my question is:
Is the brain functionally symmetrical or not? By functionally, I'm referring to whether the specialized groups within the brain all exists on both sides or rather each side contains different components.

No. For instance, Broca's area exists only in the frontal lobe of one hemisphere, usually the left. (it's responsible for speech, btw)


text:
Can inverted microscope also be phase contrast microscope?
I've read somewhere that inverted microscope also allows phase contrast microscopy. Is that true? Do all inverted microscope have this ability? Do they have any other functions?
Many thanks in advance.

Definitely true, an inverted microscope is one where the optics are positioned below the specimen, and the light source above, providing an optimal situation for looking at a live culture. The Phase rings that shift the light come soon after the light source. For phase, the orientation doesn't matter, just the order:
Upright microscope
Orientation:
(top)eye--->objective--->specimen--->phase--->light source
order:
eye-->Phase compatible objective-->specimen-->phase disk-->light source
Inverted microscope
Orientation
(top)light source--->phase--->specimen---->Objective--->eye
order
eye-->phase compatible objective-->specimen-->phase disk-->light source
Not all microscopes have phase no, they are an important and expensive addition to a microscope. Adding phase not only required the phase disk but also a phase compatible objective.

i tried to start a microscopy SE in Area51, no one gave a @#$%


text:
Why is the ebola virus so intense now?
So i'm looking into the ebola crisis and it seems the death toll is really getting crazy.  I understand that it's a cytomegalovirus and that it basically overwhelms the immune system due to it's size and virulence but why is it so bad now?  What has changed about it?
The folks at the Dallas hospital were said to have 'broken protocol' but to me it seems the virus may be more infectious this time around.  Has it changed?  Mutated?

What do you mean by " that it's a cytomegalovirus"?  CMV is a herpes virus, while Ebola is a filovirus. CMV is also a double-stranded DNA virus, while Ebola is a single-stranded RNA virus.

What did the Ebola say to Cytomegalovirus? No mono!

I think what makes this outbreak so different from previous outbreaks is that it hit large cities. Previous outbreaks hit small villages, where it couldn't spread far and burned out fairly quickly. In dense urban areas there are plenty of people to spread to and easy access to transportation.

republicans, specifically George Bush

I don't think mutations are relevant in this case. It is very similar to previous strains. The main difference that it was recognized too late.

The answer here lies in epidemiology and the pathogenic nature of the virus. Humans infected with Ebola have a range of recovery rates of 5-75%, meaning that most of those infected will not survive infection. Given the combination of preparedness factors at first recognizing a true outbreak in Ebola and viral load which had already been spread by the point healthcare workers have organized an efficient response, it is not surprising that some outbreaks are worse than others. I think attempting to correlate the virulence to the type, size with the extent of the viral spread is not pertinent, but rather, as you mentioned breaking "protocol" can have more deleterious effect than simply explaining it by a mutation.
That is not to say that this strain of Ebola is not different from those detected in other outbreaks--in fact it is likely to be quite different and accumulated several mutations.


text:
What insect is this on the photos?
What insect is this on these photos?
Found in Russia in the living room.

I think I found it. It can be Lacewings:
https://en.wikipedia.org/wiki/Chrysopidae

Yes, it look like a lacewing. Many species in Chrysopidae overwinter as adults, and these are often found indoors in the autumn where they are looking for overwintering sites.

And given the state of genus-group classification of the family (for a slightly dated worldwide system see here) that's as far as anyone can go on the available evidence.


text:
Are some facial features more important than others in human facial recognition?
I'm often surprised by the human ability to correctly identify other individuals despite significant modifications due to ageing, hairstyle, injury, etc. But, sometimes the addition of a beard and a hat can radically increase the identification error.
I wonder whether all facial regions are equally important when we try to recognise human faces? Do we focus more on some regions than others? I doubt that this is the case, but I'm not certain.
Update:
So far I've read through the following:
1) http://en.wikipedia.org/wiki/Face_perception
2) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998394/
So far I haven't found an answer so I decided to try Biology.StackExchange.

Have you done any background research of your own? I'm pretty sure that there are quantitative research on this, e.g. on how humans scan faces (i.e. our eye movements) and the amount of time we focus on different facial features. I strongly suspect that the eyes + areas closeby are very important, so I would imagine that changes there will increase errors.

I have read through http://en.wikipedia.org/wiki/Face_perception and http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998394/ but so far I haven't found a conclusive answer to this question. Hopefully an expert on this stackexchange will be able to answer.

Look for facial recognition software algorithms. They seemed to have figured something out about it. Distance from pupil to pupil etc....

@rhill45 While interesting, this is something completely different. Even if we have identified software algorithms that are effective in identifying faces, this does not mean that we as humans (with behaviours molded by evolution) use the same cues/features when we recognize faces.

And for the record, I don't understand at all why this is closed as opinion-based. This an interesting Q, answerable by quantitative methods (brain activity when looking at facial features, eye scanning of faces etc), and on-topic for the site. It could be closed due to a lack of background research (@AidanRocke, you should add your summary of the Leipold & Rhodes paper to your Q, and what questions that remain after reading this), but I don't see why it would be opinion-based.

@MattDMo
Why is this question closed as opinion based? It appears that scientists are currently working on this question. Please explain.

@AidanRocke Your update is not including any new info, besides you saying that you've read something - not what you've learned and where you are stuck. Just by looking at the paper you've linked, there are several interesting papers/reviews to look into further (see section Components of face perception: identity).

The most important features are the eyes, followed by the nose and mouth, respectively.
An elaborate answer can be found on the duplicate question on Cognitive Sciences SE:
Are some facial features more important than others in human facial recognition?

Will format question link once I am off mobile

Hmm.. Chris did you check who posted that question on cogsci? It is the same OP and the Same Answerer too! lol

Good one Chris! Cross-site duplicates are not closed as a policy (from what I gathered in my stumbling through meta), though cross-posting is not encouraged. I think you should elaborate your answer in both sites. Even duplicating your answer is good

@Crags - thanks! What I understand is that a link to a cross-site is OK. Bio people not at CogSci can still find it that way. I will leave as is.

Link is definitely Ok. Just explain what you want in detail in one site and post the link with summary in the other! Yes, leave as is

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


text:
Why is it better to drink room temperature water instead of cold water?
My teacher told me that drinking water that is room temperature is better for you then drinking cold water, but she did not tell me why that is. I want to know because I often drink cold water (with ice), because I can't stand water that is room temperature or warm.

Are we even sure this is true? Countervailing attitudes to cold water exist.

Drink warm water, because calves choose the same! ;-) I don't think it has any significant effect on your health. You may get easier sore throat if you drink too cold, but that's all...

I think this would better fit to skeptics.sx.

I don't there is much difference. The only reason I can think of is that cold water lowers your temperature and therefore your body needs more energy.

better fitted for skeptics SE

http://www.jissn.com/content/pdf/1550-2783-9-44.pdf - this link may answer your q....partially, though...

Your teacher was passing on a myth.
This false belief might be related to the equally false belief that hot exerted horses should not be fed cold water. It could also be down to someone downing a big glass of ice-cold water in one go as a child, get a brief stomach ache and spin a health-advice on it.


text:
What (if anything) about tuberculosis makes producing a highly effective vaccine difficult?
What about tuberculosis makes it difficult to produce a safe vaccine that is effective at producing an immunogenic response in >99% of individuals against all strains of the bacteria?
I am aware of the BCG vaccine which has a variable efficacy depending on how it is measured and am aware of the 4 current vaccine candidates (MVA85A, rBCG30, 72F fusion protein, and ESAT6-Ag85b fusion protein). I am curious about the very specific question of aspects of the bacteria that make the TB vaccine difficult.
Many, many thanks.

The fact that it stays dormant for a while and resides in lungs, which makes it difficult for drugs to access it and diagnose its presence until its late!

Thats an interesting and complex question. First, Mycobacteria tuberculosis is present for a long time in the human population and evolved to evade our immune system. One of the keys are glycolipids and sugars which are part of the bacterial cell wall. These either help suppressing an immune response or help the bacteria to enter host cells in which they can stay without being identified by the immune system. See references 1-3 for details on this topic.
Then most tuberculosis infections are hold of by the immune system, mostly they come up, when the carriers immune system is compromised. M. tuberculosis can successfully hide inside macrophages and multiply there and start an infection from this hiding place. See references 4 and 5 for more details here.
One of the main problems with the development of new vaccines is that this takes quite a long time from successful experiments in the lab to the availability of a usable vaccine. Tuberculosis has been neglected here for decades. Then the market for such a vaccine wasn't deemed lucrative enough from the pharma companies, as this is mostly important for poor and developing countries. For use there, the vaccine needs to be cheap and easy to administer. Additionally humans are the main host for M.tuberculosis which makes chossing appropriate animal models for research and testing not an easy task.
The development of novel vaccine candidates follow different routes. First, there are live vaccinations, which mainly consist of modified strains of the BCG vaccine strain. Then there are vaccines in the development which are supposed to support the immune answer by BCG and finally, there are vaccines which are independent of BCG and are mostly composed from proteins of the outer bacterial cell wall. For an overview about this field, I can recommend the review articles 6 and 7, if you want to go deeper in the field, also the references 8-10.

References

Mycobacterium tuberculosis Cell Wall Glycolipids Directly Inhibit
CD4+ T-Cell Activation by Interfering with Proximal T-Cell-Receptor
Signaling
Divergent Effects of Mycobacterial Cell Wall Glycolipids on
Maturation and Function of Human Monocyte-Derived Dendritic Cells
Interactions between Mycobacterium tuberculosis and host cells: are
mycobacterial sugars the key?
Annulling a dangerous liaison: vaccination strategies against AIDS
and tuberculosis
Macrophages Play a Dual Role during Pulmonary Tuberculosis in Mice
Vaccines against Tuberculosis: Where Are We and Where Do We Need to
Go?
Vaccine against tuberculosis: what’s new
Tuberculosis vaccines: past, present and future.
Childhood tuberculosis: old and new vaccines.
Exploiting the mycobacterial cell wall to design improved vaccines
against tuberculosis


text:
Is there a known glucosepane cross-link breaker?
I read the following on wikipedia:

There is, however, no agent known that can break down the most common
  AGE, glucosepane, which appears 10 to 1,000 times more common in human
  tissue than any other cross-linking AGE.

(AGEs are related to oxidative stress, aging and chronic diseases.)
I was wondering maybe the article is out of date, and there is a glucosepane cross-link breaker available. Do you know anything of that, or a current research which aims to find that?

Unfortunately at this time, there are no known glucosepane breakers which can feasibly be used in a living organism.  There is a small (very small) amount of research being done on the topic by Yale university in cooperation with the SENS foundation, but the focus is extremely early stage - nothing more than synthesis and detection of artifical glucosepane and precursors.
It is a rather frustrating situation, as there are very good arguments indicating glucosepane as an almost universal 'bad thing that should be fixed', and the molecule itself isn't particularly complicated.  It seems that this would be a low effort/high reward research area.

Welcome to Bio SE and thanks for your interesting answer! Could you add some resources (web links, or preferably citations to articles) to this answer?

I accepted the answer, because I have found nothing after a few days of search either. You should add references to your answer especially about the research on Yale university you mentioned.

You may want to look at Chebulic Acid as a potential inhibitor of AGE cross linking AND a breaker of AGE cross-linking.
Review this article:  http://biofoundations.org/?p=1004

Thanks, it is interesting! :-) It is hard to find anything relevant, but according to this it is unlikely that CA breaks glucosepane. https://www.quora.com/Can-triphala-chebulic-acid-break-glucosepane-crosslinks-Can-it-increase-lifespan Ofc. there is still hope, I think we need more experiments.

The problem is the glucosepane bond is very strong, hence the molecules which would break this bond need be necessarily toxic and damaging to other molecules in the body.  Glucosepane breakers already exist, but they are too toxic, and perhaps all will necessarily be that way.  All hope is not lost however.  Other very effective medical drugs (like clot breaking agents) are extremely toxic although life saving if applied in a local fashion via angiography under controlled conditions.  My hunch is that the same will need to be done for the known glucosepane breakers.  Glucosepane is extracellular, so the problem is really to avoid liver and renal toxicity.  Animal studies should concentrate on delivering known glucosepane breakers under special conditions of renal, liver, and cardiovascular and respiratory support and though hyper-hydration, hypothermia, ECMO, dialysis, metabolic blocking agents, etc, to limit systemic toxicities.  It won't be easy, but it could be well worth the effort if such single shot therapies could be developed which might then have long lasting effects as glucosepane would take many years to decades to build up again.

I came across this new research from Yale University:

We are currently in the process of evaluating the enzyme’s mechanisms of action and identifying other metabolites generated. This is the first demonstration that glucosepane can be broken down enzymatically.

http://diabetes.diabetesjournals.org/content/67/Supplement_1/1229-P

The link is broken. Probably just server malfunction and they will restore later.


text:
Why is it called "Ebola virus disease", not just "Ebola" or "Ebola disease"?
Why do scientists (pretty consistently) call it Ebola virus disease, rather than just Ebola, or Ebola disease?
Many other diseases are caused by viruses, but they don't seem to have this detail of terminology.  Nor do you hear the analogous terminology for bacteria.
For example:

Rubella is caused by the rubella virus.
Influenza is caused by various influenza viruses (genus names Influenzavirus A/B/C).
Some strains of E. coli (pathogenic E. coli) cause disease, but you never hear E. coli bacteria disease.

I think there is no specific reason. It is probably simply a naming which got widely adopted.

This is now how new viral diseases are being named, possibly because one can have/carry a virus without having a disease (e.g. HIV, herpes simplex, etc.). It is not as uncommon as you think.
A bit of googling will turn up reputable sites which discuss the epidemiology of Hantavirus disease, Hendra Virus Disease, Powassan Virus Disease, Lake Victoria Marburgvirus disease, Lujo virus disease, Ross River virus disease, Nipah virus disease, respiratory syncytial virus disease, Kunjin virus disease, Chikungunya Virus Disease, Heartland virus disease, St. Louis encephalitis virus disease, West Nile virus disease, Eastern equine encephalitis virus disease, Western equine encephalitis virus disease, and California serogroup virus disease (includes infections with the following viruses: La Crosse, Jamestown Canyon, snowshoe hare, trivittatus, Keystone, and California encephalitis viruses) and others, but I'm stopping here.
Bacteria cause diseases, but many already had/have names: Typhus (Rickettsia typhi or Rickettsia prowazekii), Rocky Mountain Spotted Fever (Rickettsia rickettsii), Diptheria (Corynebacterium diphtheriae), Lyme disease (at least three species of bacteria belonging to the genus Borrelia), Pertussis/Whooping Cough (Bordetella pertussis), Tetanus (Clostridium tetani), etc.
Interestingly, I have started to see scholarly articles for Clostridium Difficile Disease, which was an entirely new name for what we used to call Antibiotic-Associated Diarrhea. So maybe there will be a shift in that direction as well; time will tell.
How diseases are named is another whole thing.

"Viral diseases" is also the term used in WHO reports on "International Nomenclature of Diseases", see e.g. "Viral Diseases: Infectious Diseases (International Nomenclature of Diseases)".

I notice that a lot of the examples you provide are geographical names. Maybe the convention is to use the name of the disease if there is one (encephalitis, chikungunya) and to use "[geographical place] virus disease" where it's a geographical term to avoid confusing it with the place name (St. Louis, Ross River, Ebola River, the town of Marburg, and so on).


text:
Do plants absorb toxins from the soil?
Consider a plant like Aloe Vera that grows up in a toxic environment where the concentration of pesticides, and materials like lead, mercury, cadmium, arsenic etc is very high(e.g. Marshland dumping yard ). Would that mean that the extract from these plants would contain all these toxic elements.

Yes that means, but every plant can contain heavy metals... Eat only meat! :D

This question is too vague to answer. It depends on the plant, it depends on the toxin.

Not "all of them". But yes, plants suck up water from the soil, with everything dissolved in this water - nutrients, heavy metals, poisons. And also they breathe air, and absorb stuff via this route.
There probably are some toxins which will not enter the plant, because their molecules are too large and/or fragile. For example, should a plant root come in contact with snake venom, I cannot imagine that any venom will end up stored in the plant leaves.
Plants also have their own metabolism, so they will change/deactivate some toxins. I've seen claims that some plants "purify" formaldehyde, although I don't trust the sources enough to be sure of that.
But the smaller the poison molecule, and the less similar to stuff which is usually digested in nature, the more likely that it will enter the plant and stick around instead of being broken down. The heavy metals you mentioned are prime candidates. If they are present in the groundwater - or also lead from air pollution, before we banned leaded gasoline - they end up in plants, including food plants. And mushrooms are even more at risk.
Growing food near waste dumps is a known problem in farming, and sometimes makes the news, for example here:
http://bigstory.ap.org/article/mafia-toxic-waste-dumping-poisons-italy-farmlands

Buckwheat is very efficiënt at taking up heavy metals from the soil and is even used for cleaning the soil, sometimes called phytoextraction. Try "Buckwheat heavy metals" on Google scholar.


text:
Cardiac Excitation Threshold - in C++ modelling
So I am trying to write a code in C++ about the cardiac excitation threshold.
I know that this excitation threshold is the shortest stimulus2 value at which it can conduct an action potential (known as the effective refractory period) at that stimulus1 value.
So my question is: In my code should I have: apply_stimulus1 for basic_cycle_length = 1000 and while you are applying this stimulus1 apply and a stimulus2 and print out the shortest value of s2 where I can have a potential? -> the way I am thinking this is apllying both stimulus simultaneously. If we say .... this is stimulus 1 and this is ,,,, stimulus2 at the end I will have ;;;;.
Or should I say when you finish applying that stimulus1 apply a stimulu2 and give me the shortest time where I get action potential? But here I will have stimulu1 .... || (meaning ends applying stimulus1) ,,,, apply stimulus2.
Is this how I am thinking it correct or I just got lost in my own thoughts and it is easier than I make it look?
My question is:
How do I get the cardiac excitation threshold using stimulus1 and stimulus2 and how can I incorporate the theory in my C++ code.

ok..i just wanted the biology part first so I can give it a try in C++ and then I will post in stackoverflow, if that is ok..

Please post your question on http://stackoverflow.com/ for help in C++ programming. And you need to edit your question for more clarity. The way it is now, it is confusing.

This doesn't seem like a programming question, however, the basic point of the question is unclear.

i just want to know how two different stimulus can create cardiac excitation threshold. As Devon replied below it would be applying stimulus1 for a certain time then wait and then apply stimulus2. So as this question is answered how can I incorporate this in my code. Is it more clear now or still confusing?

I'm not sure how this is off-topic. This is a subject covered in an intro undergrad neuroscience course. Aside from the programming aspect, I'd use a topic like this for an undergrad exam question (e.g., "design an experiment to demonstrate the concept of relative and absolute refractory periods"). This is just taking that and actually writing a program to do it.

neither do I, but anyhow.. thanks @Devon Ryan for your help.

You wouldn't normally apply the stimuli simultaneously. The idea is to apply stimulus1, which has a given amplitude and duration, and follow that with stimulus2, which also has a given amplitude and duration, after a variable lag. You'll then see that the effective refractory period is dependent on the amplitude of stimulus2 (at least until you hit the absolute refractory period).

so I will proceed with the way#2 -sort of. For example apply stimulus1 for 1000msec then wait for 5msec and then apply stimulus2? But should I got backwards in time such that I can create APs at my last AP created by Stimulus1?

Yes, you'll apply stimulus1 for 1sec and then wait, say, 5msec and then do stimulus2. Keep in mind that 1 sec is probably far too long...you normally just want to stimulate a single AP afterall, not a train. I have no idea what you mean by "go backwards" in this context.

i was thinking like if my variable lag is 5msec would be easier to generate an AP from 5msec decreasing to 1msec until it gets to the last AP of stimulus1 (is it clear now? :S ) also it is in 1D strand so isn't better to be a train of  APs?

Ah, got it. You'll want to use a minimum lag (say 1ms or so, depending on you AP duration). Otherwise, you end up just looking at a larger stimulus, which isn't informative. By a train of APs, I don't mean an AP traveling down the compartments of your model, unless you have to elicit a train in the first compartment to get propagation. Anyway, you certainly can use a train, I just wouldn't bother without reason. I should note that the last time I used/wrote a model like this I did it with skeletal muscle, so if I'm forgetting that cardiac models should show bursts then go with the train :)


text:
Why can't we smell our own bad breath?
Why can't we smell our own bad breath. Is there any way we can do that?

People can, and do, do this all the time. Some people have a decreased sense of smell, and may not taste/smell bad odors (e.g. people with sinus problems, smokers, etc.) but it is quite possible.

keep your hand in front of your mouth and blow on it.

What you might be experiencing is olfactory fatigue, the temporary, normal inability to distinguish a particular odor after a prolonged exposure to it.
It's a form of neural adaptation, a change over time in the responsiveness of the sensory system to a constant stimulus. This adaptative mechanism might prevent the overloading of the nervous system.
However, some people (maybe most of them?) are able to smell their own breath. At least, I know I do. I can't point you to any statistics, but it might be an interesting research project, figuring out how many people can smell their own breath.

authors: كلية الصيدلة 2198603307


text:
What are some of the general characteristics of the DH5 alpha strain?
I can not find some useful sources unfortunately.
Please tell me about some important characteristics of DH5 alpha.
What makes DH5 alpha suitable for the gene cloning?

There are two possible sources: One is the article from the Bethesda Research Laboratories (reference 1), which names a few, the other is the book "DNA cloning: A practical approach" (see reference 2)., which sits here in my bookshelf.
Taking both together, the DH5 alpha strain is derived from the DH5 strain with the introduction of a few additional features. The naming DH are the initials of Douglas Hanahan which developed the strain. The strain is easy to transform with high efficency.
The new features of DH5 alpha are the recA and the endA1 mutations:

The endA1 mutation inactivates an intracellular endonuclease that
degrades plasmid DNA.
The recA mutation eliminates homologous recombination. This reduces the chance for deletions and plasmid multimerization.

The DH5 strain also has the following features:

The hsdR17 mutation eliminates the restriction endonuclease of the
EcoKI restriction-modification system, so DNA lacking the EcoKI
methylation will not be degraded. DNA prepared from hsdR strains that
are wt for hsdM will be methylated and can be used to transform wt E.
coli K-12 strains.
Δ(lacZ)M15 is the alpha acceptor allele needed for blue-white
screening with many lacZ based vectors.

Of special interest are the references 3 and 4, which gives you all the details you want to know.

References:

Bethesda Research Laboratories. 1986. BRL pUC host: E. coli DH5α
competent cells. Focus 8(2):9. The article is on page 13 in this paper.
DNA Cloning: A Practical Approach. Glover, D. M. (ed.), 1985, Vol. 1, p. 109, IRL Press, McLean, Virginia
Choosing a Competent E.coli Strain
E. coli genotypes

Oh, I've forgotten about it. Sorry!


text:
Where do migratory birds go when it rains?
I was reading a comic from XKCD which inspired me to ask this question: "well, where do they go when it rains?" I know that when it rains you usually don't see any birds flying through the sky.
I imagine they normally hide in trees or under other kinds of cover. But for migratory birds, I don't think it is possible to hiding under cover until the rain passes. There might not be any cover (trekking across seas) or it might stay rainy for a very long time (and therefore cold...).

I did some research, but the answers are conflicting. Some people say they do stay in trees, others say they AVOID trees (because trees can snap in a storm, plus if there's lightning then sitting in a tree will net fried birds). Then there's people saying that birds have a waterproof coating... but that's a bit contradictory with me not seeing birds when it rains.
So where do birds go when it rains?
I assume that different bird species and groups of birds will behave in different ways. I am interested in the case of migratory birds because they are likely to encounter different climates and have perhaps devised strategies to be safe. I would appreciate any well-referenced examples.

Quick point, all birds aren't likely to do the same thing.  A duck, an ostrich, a pigeon, and an hawk are likely to have different reactions.  Example, pigeons are known to rain bathe on the ground.  Would examples for common flocking birds of US cities be sufficient?

@AtlLED I'm interested in trekking birds specifically. Birds in forests or urban regions have plenty of shelter, so I'd expect the obvious answer of "they get out of the rain and under the treetops/rooftops". But there's no shelter when you're trekking... I live in Europe and I don't know enough about birds to tell you what types they have here (sure we have geese, ducks, pidgeons, owls and hawks). If you NEED a focus, european "urban" trekking birds would be it.

Examples of specific birds are also welcome as I can see each bird having its own strategy.

Nominating to reopen, since nobody has stated clearly in the comments why it should be closed as opinion-based.

Also see discussion in Meta.

Obviously, as you point out, some birds, such as waterbirds (ducks, puffins, auks, sandpipers) are perfectly fine in the rain, as they spend much of their time in the water anyhow and have oil glands that waterproof their feathers.
For other birds, rain can increase heat loss. For instance, rain increases metabolism by up to 22% in eagles (Stalmaster & Gessaman, 1984), although the actual impact on average daily metabolism was 'negligible'. However, eagles were able to feed their offspring only half as much, and therefore had only half as many eaglets, when it rained (Elliott et al., 2005). (On the other hand, the authors point out that in the Tropics, eagles actually do better when it rains because there is more food available).
Migrating birds stop migrating, hide where they can, and wait until it dries up before they continue (Erdi et al, 2002); those that don't, often end up far away from where they should be and, eventually, dead. In short, some birds don't mind the rain (e.g. seabirds), others sit it out in misery (e.g. nesting eagles) and others hunker down wherever they can find shelter (e.g. migrating birds).

Interesting. Have there been cases of significant reductions in bird numbers because of a heavy storm during migration season?

Birds can easily cover enough distance flying that they can avoid short showers entirely by not sitting right below clouds, unless they have an actual reason to stick around. Birds move around a lot more than we do.

I've frequently seen rain clouds on weather radars that cover quite a big area. How do they dodge these?

@Pimgd presumably most clouds can't move faster than birds since they can ride the same currents. So to avoid big clouds the birds could fly with (or alongside or in front of) the cloud. This would help explain Kyle's answer on why the ones that continue flying end up far away: staying out of the cloud forces them to fly off course.


text:
Why can you not tickle yourself?
It's the age old question, why can't we tickle ourselves? If you rub your fingers along your skin, sure there's sensation but you don't break down into a laughing fit (at least I don't :P), if someone else does it to you, you're rolling around on the ground begging them to stop tickling you.
Why is it that other people can tickle us but we can't tickle ourselves by touch? (I'm aware that if you use a feather or foreign object on yourself you can be tickled by it so that doesn't count.)

Well, this is an interesting question... With a hole or two. I am able to tickle myself by attempting to itch my feet or my fingers.

Interesting, I suppose some folks are able to. The majority of the people I've talked to said they can't however :).

I count them lucky! :)

When one does it to oneself, the Braun knows it. Therefore, it isn't a sudden movement. When others tickle, sometimes people also get irritated instead of bursting out with a laugh. This is because the brain doesn't know when others do it so, it is a sudden action. Stimulus works differently in both situations.

Try tickling the roof of your mouth with your tongue. My understanding is that no one (realistically, very few people) will be able to avoid a tickling sensation

While one does not laugh the sensation of caressing by self's feet still might feel unpleasant.

In short, it's because your brain processes external and self-produced stimuli differently.
If someone tickles you, you feel that ticklish feeling, but when trying to tickle yourself, there is a reduction in the sensation. When you are tickled by someone, a part of your brain activates causing you to laugh, etc., but it seems that when you trying tickling yourself, your brain doesn't react the same way and that section of the brain does not activate as if someone were tickling you.

Blakemore, S.J., D.M. Wolpert, and C.D. Frith. 1998. Central cancellation of self-produced tickle sensation. Nature Neuroscience 1(7): 635–640. doi:10.1038/2870

You can't tickle yourself because your brain know that it's you. Your cerebellum knows that it's you, and so you don't feel it. Your cerebullum "predicts" that you are going to experience a tickling sensation (as you put, "a laughting fit"), and rushes to cancel out the other parts of the brain that is going to make you break down into laughter.
In other terms, tickling is 'controlled' by two part of the brain, the touch cortex (somatosensory) and the pleasure cortex (anterior cingulate). When you are tickling yourself, these two regions are fired less than when someone else is tickling you.
Basically, your brain is thinking "Why is this person hurting him/herself?" and rushes to cancel all the sensations you can feel. Only when someone else tickles you (and their brain is not connected to yours) can you start laughing. It is, in a way, unexpected when the tickle monster attacks you.
Sources: https://www.scientificamerican.com/article/why-cant-a-person-tickle/

Welcome. Can you add sources to your answer to allow other users to background read on your material?

Ok! Thanks! I added one source. Is that enough?

Oh yes, I love Sci Am :) Enough for me. Strictly spoken it's not peer-reviewed and may be frowned upon, but honestly, many folks simply cite wikipedia and that's the end of it. This is much better.

Ahh I see. Next time I'll use a more dependable source. Thanks!


text:
Exon skipping in mammals
I've heard from several sources that the predominant form of alternative splicing (at least in mammals) is exon skipping. However, my personal evidence is only anecdotal: I've heard it and read it, but have not seen references to literature. Is there a seminal paper or set of papers establishing this finding that I can cite?

You can see this review.

There are several different types of alternative splicing (AS) events,
  which can be classified into four main subgroups. The first type is
  exon skipping, in which a type of exon known as a cassette exon is
  spliced out of the transcript together with its flanking introns (see
  the figure, part a). Exon skipping accounts for nearly 40% of AS
  events in higher eukaryotes [17, 111] but is extremely rare in lower
  eukaryotes.


text:
Understanding intra and extracelullar concentrations (membrane potential)
I have 4 question (not homework)
What happens to the cells membrane potential if:
a) Na+ outside rises by 40mM
b) K+ inside rises by 10mM
c) K+ outside rises by 10mM
d) A- (impermeable ion) inside rises by 100mM
e) Na+ outside decline by 50mM
So my answers are:
a – hyperpolarisering (more negative)
b – Depolarisering (more positive)
c – Hyperpolarisering
d – Depolarisering
e - Depolarisering
I think it like this:
Membrane potential is the DIFFERENCE in electrical potential inside and outside the cell. When we say a cell has a resting potential of -60mV we mean that the cell has 60mV LESS than the extracellular space.
So when I am asked what happens if all of a sudden, the extracellular space increases in mV (first question) then I can say that the difference is now GREATER than 60 mV, it is now in fact 100 mV, as the extracellular space has increased by 40 mV, then plussing the already established 60 mV.
Is this the correct way to think about these problems?

Afaik you can describe the potentials between the two sides of the cell membrane using the Nernst-equation. Yepp wikipedia writes the same here.
Membrane potential is a very important thing, because human cells require stable internal concentrations of Na+, K+, Ca2+, etc... in order to work properly. These concentration can depend on species, for example plants cells work completely different than animal cells, they have higher Na+ than K+ in their cytoplasm. So every human cell has to maintain a membrane potential if they don't want to die. It requires a lot of ATP (energy) to do so... Human cells typically maintain this potential against the blood plasma. Cytoplasm has around 120mM K+ and 15mM Na+, while the blood plasma has about 5mM K+ and 140mM Na+. You can count the membrane potential from these concentrations using the Nernst equation (a short presentation about how). I don't remember the exact mV value, does not matter. So human cells are working hardly on keeping the Na+ outside and K+ inside, and they can possibly die because of membrane potential changes (e.g. when they require too much energy to maintain the internal concentrations and/or osmolarity).
Excitable cells, e.g. nerve cells or muscle cells are very special because they can change their membrane potential rapidly by sending out K+, Ca+ or sending in Na+. This can create small electric discharges, which can be used to send electric signals or contract muscles, etc... Different cells have different discharge diagrams, e.g. axons have something like this:

Figure 1 - axon electric discharge diagram - source

and muscles have something like this:

Figure 2 - muscle electric discharge diagrams - source

Summa summarum it can depend on the cell type what happens, but basicly you can count the new potential using the Nernst equation by the concentration changes you mentioned...

According to answers from the Nernst equation, I seem to have all my answers flipped...What am I misunderstanding about the basics of membrane potential? How is membrane potential explained if not the way I see it?

I mean if I put more POSITIVE ions in my cell, I should get a LESS negative membrane potential?! But it seems to be the other way around??

I put this into a new question as it is boggling me. Feel free to answer it if you like: http://biology.stackexchange.com/questions/23221/problems-understanding-membrane-potential


text:
Problems understanding membrane potential
I understand that membrane potential is the difference of the extracellular and intracellular ionic charges, due to their concentrations. We say that the extracellular space has a charge of 0 and then take the membrane potential with respect to the extracellular space. The intracellular space is normally around -60mV due to more negative charges being in the cell than the extracellular space.
This is how I understand membrane potential.
From this understanding, it is hard for me to see why I can't get this right:
We work with a regular cell with potassium 120mM inside and 4.5mM outside.
Say that we increase the intracellular concentration of potassium by 10 mM, a +1 valence ion which contributes to POSITIVE membrane potential.
What I envision is that as we put more positive ions in the cell, the cell is now more positive in regard to the extracellular matrix. However the Nernst equation states that the membrane potential actually gets MORE NEGATIVE!!
http://www.physiologyweb.com/calculators/nernst_potential_calculator.html
What is it that I am misunderstanding? Thank you.

An increase of the intracellular concentration of potassium decreases the membrane potential, i.e. makes it more negative. The Nernst equation provides the potential required 'to keep' the ions from flowing out of the cell, down their gradient. You shouldn't view those positively charged ions within the cell as positively contributing to the membrane potential. It's the contrary, the Nernst equation provides the potential to maintain the electrochemical equilibrium, as if it needs to stop the ions from flowing out of the cell (you need a negative potential to oppose + charged ions).

I think this question has more to do with kinetics / transport phenomenons than biology, but that's okay, everything is connected especially my computer to the internet. ;-)
The basic idea behind transport phenomenons is that there will always be a flux of quantitative properties (e.g. charges, particle number, entropy, volume, etc...) where the qualitative properties like (electrical potential, chemical potential, temperature, pressure, etc...) have a gradient in space (note that kinetics of chemical reactions can be described similarly without the space gradient part).
In this case we are talking about electrochemical potential gradient and ion flux. It is very important to recognize that the electrochemical potential is not the same as the electric potential. It has a chemical component, so the result will depend on both charge and concentration gradients. By a single ion channel system (e.g. Na⁺ channel only) you can count the potential of each side of the membrane using the Nernst equation, by a system with multiple ion channels it is more complicated, so in that case you have to use the Goldman equation. So at the end you can say something like one side has a potential of x[mV] and the other side has a potential of y[mV] and so the difference is:  d[mV] = x[mV] - y[mV]
The sign of d depends on x or y has a greater value. By single ion channel systems this expresses an x → y direction so by positive d the cation flow direction is x → y and by negative d it is y → x. By anion flow it is the opposite.
By cells we use the out → in direction by counting the membrane potential. We can count the potentials using the

Nernst equation:
$$E_m = \frac{RT}{zF} \times ln \left(\frac{c_{out}}{c_{in}}\right)$$ or the
Goldman equation:
$$E_m = \frac{RT}{F} \times ln \left(\frac{p_{K^+}.[K^+]_{out} + p_{Na^+}.[Na^+]_{out} + p_{Cl^-}.[Cl^-]_{in}} {p_{K^+}.[K^+]_{in} + p_{Na^+}.[Na^+]_{in} + p_{Cl^-}.[Cl^-]_{out}}\right)$$
where

$Em$ is the membrane potential
$z$ is the ion charge
$[X]$ is the ion concentration
$p_X$ is the relative membrane permeability for the actual ion

and so on...

So for example by an average human cell in blood plasma, assuming that the inside of the membrane has a small negative charge

the Na⁺ has a positive effect (positive charge, high out → in concentration gradient, low out → in charge gradient),
the K⁺ has a negative effect (positive charge, high in → out concentration gradient, low out → in charge gradient),
the Cl¯ has a negative effect (negative charge, high out → in concentration gradient, low in → out charge gradient)
the Mg⁺⁺ has a small positive effect (positive charge, low out → in concentration gradient, low out → in charge gradient)

on the membrane potential. It is hard to find an ion in this case which flow is charge gradient dominated instead of concentration gradient...

I understand that membrane potential is the difference of the
  extracellular and intracellular ionic charges, due to their
  concentrations.

The (sign and) value of the membrane potential is not determined by the charge gradient because the concentration gradients usually have a much bigger effect on it. The cells maintain these concentration gradients by using up energy.

We work with a regular cell with potassium 120mM inside and 4.5mM
  outside.
Say that we increase the intracellular concentration of potassium by
  10 mM, a +1 valence ion which contributes to POSITIVE membrane
  potential.

In your case K⁺ has a negative effect on the membrane potential, because of the high concentration gradient with reverse direction. So decreasing the concentration gradient will increase the membrane potential.
If you want to learn more about how to count membrane potentials, you should read this and its next section instead of wikipedia...

@WYSIWYG Thanks the edit, I did not know it is possible to use an equation description language.

yeah it is $\TeX$

So basically K has a negative effect because of its gradient. What if I'd put 100mM outside and only 5mM inside? Shouldn't the gradient now change and the effect be opposite?

Yes it will be then positive. ln a/b = - ln b/a

I can't seem to replicate this effect with the tool in the link you posted in another question: http://nernstgoldman.physiology.arizona.edu/using/
If I put 100mM outside and test the slider for inside around 100mM it still just goes one way.

@BjarniJóhannsson Then I am wrong or your counter is wrong, I don't know, I learned it this way... ;-)

I think I was misunderstanding the tool

I think inf3rno's answer is very complete, so I will just be adding some notes that might help OP understanding what's happening.

Say that we increase the intracellular concentration of potassium by
  10 mM, a +1 valence ion which contributes to POSITIVE membrane
  potential.

Let's say we do that, in an in vitro cell model, using a syringe with only K⁺ ions. What would happen?

What I envision is that as we put more positive ions in the cell, the
  cell is now more positive in regard to the extracellular matrix.

And that is true, at least instantly. However, due to the differences in concentration gradients, the K⁺ would quickly flow out until electrochemical balance was restored. This would lead to an increase in K⁺ concentration outside our cell model so, in the end, the net charge would decrease inside the cell.
So you can think of the Nernst equation as a mathematical model to the cell in equilibrium.

"However, due to the differences in concentration gradients, the K⁺ would quickly flow out until electrochemical balance was restored. ... So you can think of the Nernst equation as a mathematical model to the cell in equilibrium. " - Yes that's true.


text:
Book-recommendation: Biochemistry
I need to have a book which covers following topics two may also be fine:
(a) Structure and role of carbohydrates, fats, fatty acids and cholesterol, proteins and amino-acids, nucleic acids. Bioenergetics.
b) Glycolysis and the Krebs cycle, oxidation and reduction, oxidative phosphorylation, energy conservation and release, ATP cycle, cyclic AMP – its structure and role.
(c) Hormone classification (steroid and peptide hormones), biosynthesis and functions.
(d) Enzymes: types and mechanisms of action.
(e) Vitamins and co-enzymes
(f) Immunoglobulin and immunity.

I would say that the "usual suspects" aka Lehninger, Stryer and Voet should all be fine. Go into a bookstore, have a look in all three of them and then decide. They are a bit different in their approach.

http://www.typotex.hu/konyv/sarkadi_livia_biokemia_mernok_szemmel But it is in Hungarian... :D You don't necessary find all of these terms in one book, because hormones, vitamins, immunoglobulins are related to human physiology, immunology, etc...

Sorry but I don't know Hungarian, but thanks for your reply

Lehninger Principles of Biochemistry by Nelson and Cox is quite popular and covers everything you listed in great detail except for immunology.
I don't really have a recommendation for an immunology book; I think pretty well any of them will cover immunoglobulins (they're pretty integral). My university uses Kuby Immunology by Kindt et al. Molecular Biology of the Cell by Alberts et al. has a couple chapters (some 115 pages) on the subject. As a bonus, it's an amazing reference for cell biology (which you'll need, at least someday, if you're pursuing biochemistry).

Does the book Molecular Biology of the Cell also covers topics like:
1-Structure and function of cell and its organelles (nucleus, plasma membrane, mitochondria, Golgi bodies, endoplasmic reticulum, ribosomes, and lysosomes), cell division (mitosis and meiosis), mitotic spindle and mitotic apparatus, chromosome movements, chromosome type polytene and lambrush, organization of chromatin, heterochromatin, Cell cycle regulation.
2-Nucleic acid topology, DNA motif, DNA replication, transcription, RNA processing, translation, protein foldings and transport

@Ankit Yes, it does.


text:
What are the risks of elevating the legs too regularly and when tired?
I started to to think the pathophysiology of elevating legs high next to the wall too often and when you are tired.
I think possible manifestations

some damage to valves of the veins (No!)
because of collateral circulation, rhombus, heart damage, ... (No! Only in pathological situation but cannot be considered here. I think here that the risk of thrombus leaving legs is higher when you elevate your legs.)

Other side is when you should do this.
To do regularly like every evening - may not be the right way to go.
If you are tired and you do this, the vasomotor tonus is already lower so smooth muscles can less help to keep the blood so much more stress to the valves.
Cardiac output is also less because of tiredness so lymphatic drainage is less.
Elevating legs will move more lymph and blood to the middle of the body.
So less lymph and blood can be moved back to legs when you tired.
What are the risks of elevating legs for too long time in Short time and Long time?
Is there any advantage in elevating legs like increasing blood circulation of our body?
In what manner would elevating legs harm valves?
There should be no damage to valves because the direction of the blood circulation does not change.
Blood is only going from legs to heart.
I think the vasoconstriction of smooth muscles occurs first in the legs.
This returns some blood to the legs.
How is lymph made - -?
Lymph is made in lymph nodes.
After leaving the node, it is rich in lymphocytes.
After leaving digestive system, it is rich in triglycerides so called chyle.
I think after leaving legs it is also rich in triglycerides.
[W]hat is the danger of lymph leaving the legs?
I think the effective lymph (that one used in legs) is coming from the lymph nodes of the legs.
Some lymph can be made in lymph nodes of legs so no danger of lymph leaving legs.
However, some may come from the region of coxa.
How long distance can lymph travel as effective unit of immune system?
If all lymph nodes are working, there is no danger of lymph leaving the legs, I think.
If there are problems with lymph nodes of legs, then there may occur some constitutional symptoms of legs - but not sure about how fast.
Does the heart get tired like your head does, or like muscles after exercise?
No.

Valves in veins are one way. In what manner would elevating legs harm valves? How is lymph made and what is the danger of lymph leaving the legs? Does the heart get tired like your head does, or like muscles after exercise? I think if you examine these issues, you'll have a better understanding of what happens when you elevate your legs whether you're tired or not.

@anongoodnurse Thank you for your comment! I answered your questions. Do you have anything to add?

Nothing but an answer. I appreciate your improvements!

To answer your questions, one needs to address certain issues one at a time.
Veins do have valves, but they function to hold blood from settling in the legs. When you flex muscles, the blood flows towards the heart. Valve failure occurs when people stand (especially if they stand relatively still) for long periods of time every day over many years, dilating veins. You can see this on the surface of the legs as varicose veins. One way to treat varicose veins is with elevation. So, elevation does not harm vein valves.
Lymph is made at the arterial end of capillaries and is part of the interstitial fluid of tissues. It bathes cells, and returns to the circulation via the lymphatic system (which also has one-way valves), goes through lymph nodes, and returns to the blood via connections with the subclavian veins. The treatment for too much lymph in the lower extremities (also known as edema) is to elevate the legs. So, elevation does not harm the lymphatics system.
The heart was made to pump all day, every day, for many, many years. It doesn't get "tired" during a tiring day, and doesn't need to rest like we do. But it can get weak and pump inefficiently if injured (e.g. myocarditis, myocardial infarct), or if it pumps against high arterial pressure (hypertension).
As long as you have healthy arteries to the legs, I can't see how your legs can suffer by elevation.
The main effect that I can think of is on baroreceptors. The increased volume of blood in your upper body will cause an increased stroke volume from the heart, sensed by baroreceptors, and may cause smooth muscle dilation of the vascular system. In the short term, that means you will experience more pronounced orthostatic hypotension on standing (you will be dizzier). The long-term effect from elevation for a couple of hours a day are basically nil.
Since you asked about these parameters only, I won't elucidate on other possible effects.

Thank you for your answer! You can also include other possible effects. Just separate the body by "---" for clarity. I am very interested in about long-term effects because, sometimes, I hold my legs elevated more than a couple of hours - which you can feel then afterwards. I think it is a different feeling than holding for short-time. I must verify this again.  Assume you do this just before you go to sleep i.e. when your blood pressure is low, effect on baroreceptors low and also on smooth musculature.


text:
Does DNA replication in 5' to 3' (leading strand) need RNA primase?
https://www.youtube.com/watch?v=27TxKoFU2Nw
In the above video it shows that during DNA replication, the lagging strand require RNA primase to add 3' -OH group for further addition of nucleotides. However, it hasn't been shown that the above strand ( leading strand) require it.
Besides, RNA is needed to initiate the polymerization because it has the 3'-OH.
But when I look at the structure of deoxynucleotide, it also has the 3'-OH but it does not have the 2'-OH. So why DNA cannot initiate the polymerization?
Thanks for your answer!

The DNA polymerase also needs a RNA primer on the leading strand to be able to start polymerization. Afterwards this is not needed anymore, since the replication goes on without a break. On the lagging strand polymerization replication can only work between the replication fork and the next region of double-stranded DNA. See the figure (from here):

The reason for the need for RNA primers is located in the function of the enzymes. While the DNA polymerase can only work on a double stranded template (add nucleotides to the 3'OH-end of the strand) the DNA Primase (actually an RNA polymerase) can work on single stranded targets and thus add the RNA primer there.

I see! DNA primase cannot work in double stranded template. Thanks a lot.