texts: Safe parameters for external nerve stimulation using electrical impulses

texts:
Introduction

I've recently stumbled upon David Eagleman's TED talk on the concept of sensory substitution and addition. Being the most inspiring thing I've seen on the internet for the last few months I've decided to give it a try and mix it with some of my coding/electronics projects.

I've settled on using electrical impulses over electrode pads to feed sensory data onto a patch of skin, instead of vibro-motors as it is more energy efficient. That being said, when planning on running electrical current through me 24/7, safety obviously comes first.

[edit]
I am targeting the lower back or the side of the hips as these parts have the least contact with the environment and won't make you look goofy. In the long run this would probably have to run on dry skin to avoid the "wrinkling effect", caused when staying in water for too long.

Questions

Main unknowns I want to sort out are:

What is the range of perceivable voltage and current that can be safely  fed through the skin without causing any damage to the nerves or any other part of the body?
Is there a risk of permanent damage or reduction of sensitivity of nerves when exposed to an electrical current for a prolonged time? Any way to circumvent this problem?
What "resolution" or input density can I hope to achieve, before signal becomes "blurry" because of cross-talk?


texts: Discrepancy in time for genetic differences between human and chimpanzee to accumulate

texts:
Genetic differences between human and chimpanzee include ~50,000 amino acid changes, ~30,000,000 point mutations in non-coding sequences, and millions of insertions, deletions, inversions, genomic rearrangements, and transposable element movements [1]. The vast majority of these genetic changes are neutral [2] [3]. For neutral mutations, the expected number of generations required to reach fixation in the population is the reciprocal of the mutation rate per site per generation [4]. This holds irrespective of selection at other linked loci, changes in population size, or almost any other conceivable complication [4]. The human mutation rate, μ, is ~10-8 per site per generation [5]. Although μ can be orders of magnitude greater at certain sites, the fact that, as cited above, millions of neutral mutations occurred in the human line since its divergence from the chimpanzee line indicates that at least thousands of mutations occurred at the average rate of 10-8 per site per generation. Since the expected number of generations required for any one of these mutations to reach fixation in the population is the reciprocal of μ, this number equals ~108 generations. Since a generation is ~20 years for humans [5], the time required for any one of these thousands of neutral mutations to reach fixation is ~109 years.

According to the currently-known fossil record, the human line diverged from the chimpanzee line between 6 and 8 million years ago [7].

How is this major discrepancy between population genetics and the fossil record to be reconciled?

References

[1] Chimpanzee Sequencing and Analysis Consortium. Initial sequence of the chimpanzee genome and comparison with the human genome. Nature 437, 69–87 (2005)

[2] Harris, E. E. Non-adaptive processes in primate and human evolution. Am. J. Phys. Anthropol. 143 (Suppl. 51), 13–45 (2010)

[3] Vallender, E. J., Mekel-Bobrov, N. & Lahn, B. T. Genetic basis of human brain evolution. Trends Neurosci. 31, 637–644 (2008)

[4] Lanfear et al, Population size and the rate of evolution.  Trends in Ecology & Evolution, January 2014, Vol. 29, No. 1, Pages 33-42

[5] Kong, A. et al. Rate of de novo mutations and the importance of father’s age to disease risk. Nature 488, 471–475 (2012)

[6] Walker, R. et al. Growth rates and life histories in twenty-two small-scale societies. Am. J. Hum. Biol. 18, 295–311 (2006)

[7] Levin, N. Annual Review of Earth and Planetary Sciences, 43: 405-429 (2015)


texts: If sexuality is genetic, how did asexuality evolve?

texts:
If sexuality is genetic, then it stands to reason that evolution would strongly favor people who have children. In other words, heterosexuality & bisexuality should be favored, while homosexuality and asexuality should be disfavored and in fact eliminated by evolution. Why hasn't that happened?
I can find plenty of resources via Google for the evolution of homosexuality, such as this one, but not for the evolution of asexuality. Asexuality seems to pose a bigger challenge as well, since the lack of sexual attraction entirely should make it even less likely for asexual people to have children. Some of the explanations for the evolution of homosexuality can conceivably apply to asexuality too (such as "the genes for asexuality do other things"); still, I would like an authoritative paper/reference if there is one.


texts: Is there evidence to suggest that excessive consumption of Whey, or similar proteins will lead to acidification of the blood?


texts: Is it possible for a sex chromosome to be homologous?

texts:
I am following a great introductory biology course online, MITx: 7.00x on edX.

A question in the course assumes a cross between a pure-breeding male fly and a pure-breeding female fly:

  You are studying genetics in a hypothetical fly and you find a fly
  that has purple eyes. Assume that the purple eye phenotype is due to a
  mutation at a single locus. Use the notation E and e, where the upper
  case letter is used for the allele associated with the dominant
  phenotype and the lower case letter for the allele associated with the
  recessive phenotype.

  You cross a pure-breeding male fly with purple eyes to a pure-breeding
  female fly with normal eyes. All of the F1 offspring have normal eyes.
  From this experiment you determine that the purple eye phenotype is
  ______________ to the normal eye phenotype.

My question is this: how can a male fly be pure-breeding? The reason I wonder is that as far as I understand, pure-breeding implies a homozygote gene, yet the sex chromosome can not be homozygote because the Y chromosome is not homologous to the X chromosome. In other words, does it make sense to speak of homologous sex chromosomes?


texts: how to determine/ find the longest poly-purine tract in any genome  and this needs to be on the E. coli genome . is it to figure out the polypurine tract and then figure out the longest chain ? or is it to splice the introns and exons away from the DNA ? since E. coli's genome is 4.6 million BP long, i need some help in breaking this down ?


texts: Can humans eat a greater variety of things than other omnivores?

texts: One thing that I've always noted is that humans seem able to eat just about anything that isn't toxic (and many things that are). Even when compared to other omnivores, I have the impression that humans are capable of eating far more things without harm. Is this true?


texts: What does ΔC and ΔN mean with regards to a protein sequence?

texts:
I am reading a paper about the regulation of the nuclear export of the protein GSK3 and I have come across the following statement:

Full-length FLAG epitope-tagged mFrat1 (FLAG-Frat) and the
amino-terminal half of Frat (ΔC Frat) localized predominantly to the
cytoplasm of transfected MDCK cells (Fig. 1, A and B, i and iii).
Unexpectedly, the carboxyl-terminal half of Frat (ΔN Frat) accumulated
preferentially in the nuclei of transfected cells (Fig. 1B, iv).

I am not sure why the amino-terminal and carboxyl-terminal half of the Frat protein are referred to as ΔC Frat and ΔN Frat respectively. I know that the amino terminus of a protein is also referred to as the N-terminus, whilst the carboxyl terminus of a protein is referred to as the C-terminus. I am not sure why in this paper ΔC and ΔN are used to refer to the amino-terminal and carboxyl-terminal half of the Frat protein.
Any insights are appreciated.


texts: Can ncRNA convert to coding RNA/mRNA by mutations?

texts: DNA has transcribed into RNA (Non-coding). Can this RNA mutate and become a Protein-Coding one/mRNA? Have there been any such instances reported by scientists?


texts: Can anyone identify this tropical flower? It was found on a vine(?) in a garden adjacent to a rainforest in tropical north east Australia, however it may not be indigenous.


texts: Are pulp cells (in oranges) normal plant cells?

texts:
Does a pulp cell contain all the elements that a 'normal' plant cell contains?

I've searched for an hour to find more information about this but couldn't find anything useful. Is the pulp cell the exception from the general size range of most eukaryotic plant cells, normally between 10 - 100 µm?

Please include link to a reputable website.


texts: How is sexual selection evolutionarily stable?

texts:
It seems like in any population subject to evolutionary pressure, sexual attractiveness will inversely correlate with other kinds of reproductive fitness. If you see a peacock with a small tail feather, this is information that it is likely above average in other areas, because otherwise its genes would already have been wiped out. So intuitively, you would think that it would benefit individuals to find less conventionally attractive mates.
So far, I have encountered two possible explanations for this. One idea was that the things that make an animal attractive correlate with evolutionary fitness. I'm not an expert here, but it feels like the correlation here will diminish over time as soon as there is direct pressure to increase attractiveness.
The other, more convincing, explanation was that it is advantageous to produce attractive offspring. So, there might be a feedback loop here where if members of a population care about sexual attractiveness more, then attractiveness would confer a greater advantage, making attractive offspring more important, increasing the evolutionary pressure for individuals to choose attractive mates.
Can someone give an intuition (or better, the relevant math) for why these two latter effects dominate my original intuition? Or are there other effects at work here?


texts:
Would symptoms differ from eating virus contaminated food versus breathing in virus?

The COVID-19 causes respiratory symptoms and I guess that is because people are breathing in virus droplets in their lungs.
But if you would swallow COVID-19 contaminated food and avoid breathing in the virus would that cause other symptoms like stomach pain or diarrhea?


texts: Question about DNP derivatives of amino acids (specifically epsilon-DNP-lysine)

texts:
I have a pretty basic biochemistry question but am having trouble finding the answer to it:

Normally, 1-Fluoro-2,4-dinitrobenzene (DNFB) reacts with just the amino terminus of amino acids. However, with lysine, DNFB can react in two places (at the amino terminus and to the epsilon amino group). The DNP derivative of lysine is referred to as "epsilon-DNP-lysine".

Does "epsilon-DNP-lysine" refer to a product where the DNP is bound only to the epsilon amino group (but not to the amino terminus), or does it refer to a product where DNP is bound simultaneously to the epsilon amino group and to the amino terminus?

Also, can the same thing happen with other amino acids that have an amino group in the side chain? i.e. can there be epsilon-DNP-arginine, for instance, or is this behavior unique to lysine?


texts: Why does cholesterol need to attach to proteins to travel through the blood?

texts: I guess the deeper question is: what makes it possible for proteins like those part of HDL and LDL to move through the bloodstream?


texts: In what "space" does egg mature in Kiwi?

texts: This huge egg here, is it sort of tethered to the ovary, filling up the coelomic cavity, and then exiting out of the infundibulum, or, where is it in the bird exactly? What "space" does it occupy?


texts: Integration of several environmental signals

texts:
I am looking for examples of different functions that are good fit to how signals are computed in order to respond to the environment. Let's make my question more copmrehensible with an example...

One example

I have been told (I haven't found an article yet) that in plants, in order to know if it is overshadowed by a big tree, the plant computes that ratio of two signals (UV intensity over Infrared intensity or something similar) so that it can decide whether or not it should grow bigger leaves or other attributes.

This plant radiation example would be an example of a species that computes the function $\frac{S_1}{S_2}$ (where $S_1$ and $S_2$ are two types of signals) in order to take decisions about their response to the environment.

Question

Can you please give me examples (examples with a diversity different functions, with different numbers of different signals) of organism using environmental signals to adaptively respond to their environment?

For example, can you give me examples of the adaptive response to the environment is giving by the following functions of 2 signals:

Continuous traits:

$f(S_1, S_2)= S_1 + S_2$

Produce a trait value at $K_1 + K_2\cdot \left(S_1 + S_2\right)$

$f(S_1, S_2)= \frac{S_1}{S_2}$

Produce a trait value at $K_1 + K_2\cdot \frac{S_1}{S_2}$

$f(S_1, S_2)= S_1^2 \cdot S_2$

Produce a trait value at $K_1 + K_2\cdot \left(S_1^2 \cdot S_2\right)$

$f(S_1, S_2)= funA(S_1, S_2)$

Produce a trait value at $K_1 + K_2\cdot S_1$ iff $S_1$ is detected.

$f(S_1, S_2)= funB(S_1, S_2)$

Produce a trait value at $K_1 + K_2\cdot S_1$ iff $S_1 < S_2$.

Boolean traits:

$f(S_1, S_2)= OR(S_1, S_2)$

Iff signal 1 or signal 2 is detected, produce the trait

$f(S_1, S_2)= AND(S_1, S_2)$

Iff signal 1 and signal 2 are detected, produce the trait

$f(S_1, S_2)= FunA(S_1, S_2)$

Iff $S_1$ < $S_2$, produce the trait

, where iff means if and only if and $K_1$ and $K_2$ are constant values.

What I am NOT asking

I am NOT interested in the accurate description of the signal transduction (Description of the kinase cascade and names of the genes and transcriptions factors). I am interested in having examples of mathematical functions that are computed by the cell in order to take decision about which phenotype to produce (plasticity).


texts: I may be biased, and will delete if I'm wrong, but why are there so many more insects when compared to quad bugs?


texts: Kinetic Vs Potential Energy in Biochemical Contexts

texts:
This question is causing great confusion in my head.

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

B) water rushing over Niagara Falls

C) light flashes emitted by a firefly

D) a molecule of glucose

E) the flight of an insect foraging for food

Answer:  D

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

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

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

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

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

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


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

texts: Protein migrate differently in Bis-Tris and Tris-Glycine gels. I was curious about the actual reasons why. Do certain gel systems result in a tighter resolution than others?


texts: Where can I find a list of trees in the world?

texts:
I want to make an app for smartphones that list most common trees in the world.
Where can I find a list?
I would like to include if the tree is deciduous or perennial and geography/climatic location.
I can buy a book if it is complete, preferably with photos of tree leaves. If I had only the list I may find the rest of information on wikipedia or other sites.


texts: Functionality of vitamin A, Bx, C, D, E, K as used in cosmetics for the skin?

texts:
I was wondering if someone can compare the functionality of vitamin A, Bx (x means numbers, such as 1, 2, 3, ...), C, D, E, K in the skin?  They are used in cosmetics but what is their actual effect?

If there is some source that compares between them in particular, I think it will help me understand some important basics.

Some products:

GNC Vitamin C Moisturizing Cream

GNC Vitamins E, A & D Moisturizing Cream

Reviva™ Labs Alpha Lipoic Acid Vitamin C Ester & DMAE Cream

Reviva™ Labs Vitamin K Cream


texts: Why is the consumer/producer biomass ratio higher in the oceans?

texts:
According to Bar-on et al. (2018) (see figure 2), the terrestrial consumer/producer biomass ratio is 20/450  while the marine consumer/producer biomass ratio is 5/1 (in Gton of carbon).
Why is the consumer/producer ratio much higher in the oceans?
Is it perhaps because marine animals are more efficient? Or is terrestrial plant biomass underexploited by surface animals?
 Bar-On, Y.M., Phillips, R. and Milo, R., 2018. The biomass distribution on Earth. Proceedings of the National Academy of Sciences, 115(25), pp.6506-6511.


texts: Why are spiders afraid of flies caught in their web?

texts:
I recently noticed a fly got caught in a spider web in my house. The fly was very energetic and, even though caught, continued to flap it's one wing (which I think might have been partially free) with hyper-speed.

Initially I thought it was just trying to get free from the web but then I noticed that when the tiny spider (it was smaller than the fly) approached it to, presumably, try to inject its venom the fly started to again energetically flap it's wing and it scared the spider off.

I was wondering - why did the spider got scared? I know animals do not perceive threats quite like us and even a big lioness might give way to a tiny mongoose if the mongoose threatens with a fight (I'm guessing both because unnecessary fighting expends precious energy and any wound can be bad with no hospitals around) but still as far as I know the fly can't harm the spider in any way even if it is free and much less when it is bound and while it would be smarter for the spider to just sit and patiently wait for the fly to drop out of exhaustion he is also risking it getting free, eventually.

So why are spiders scared of flies caught in their web?


texts: What happens to the precursor protein's signal sequence after it is cleaved?

texts: Where does this signal sequence "go" after it has been cleaved by signal peptidase and what is its next function?


texts: The colors blue and golden (yellow-orange) and the human eye / brain

texts:
Many years ago I read a review in an article about why we love for example Lapis Lazuli so much. The article stated that there are two specific colors, yellow as golden (when it glows or shines) and a very certain type of blue (the one of Lapis Lazuli) or also a shiny dark blue. I think we are not talking about the way those are absorbed in the eye but rather which color has the biggest impact on our eyes. Like often we say red is a warning color and we see red as most 'aggresive' color this article stated that in fact this type of blue and gold is the one that causes the strongest respond in the human brain. They also added a chart back then where you could see this 'response' for each wavelenght.

I was unabled however to find anything related. I don't think it has to do with the absorption peaks of the human eye, the graph looked a bit different. Has anyone heard about this before?


texts: Methanol and brain damage -- special affinity for optic nerve or just really toxic?

texts:
Methanol is known for causing blindness. One explanation I have read is that the optic nerve is especially active and so methanol will be preferentially taken up by the cells there which then die.
But I assume methanol is also bad for neurons concerned with, for example, memory and cognition. But is this wrong? Could it be that methanol for some reason tends to cause temporary or permanent blindness but is no more toxic to other neurons than ethanol is?


texts: Natural enemies boost deep evolutionary fitness?

texts:
"Two species that reduce one another's fitness on microevolutionary
  (short-term) timescales can increase each other's macroevolutionary
  (long-term) fitness"

Opinions?

Intuitive Examples:

Body Size - Predator-prey relationships or interference relationships
(fighting, e.g. for territory) are often documented to put seletion
pressures to grow in body size, often a positive feedback loop. In
the short term the presence of the natural enemy in this case often
leads to decreased population fitness (probability of being
eaten/probability of fatal conflict over territory). But in the long
term such large body sizes acts as an advantage over potential future
enemies of the same kind. This is particularly relevant to marine
ecosystems - where the size of fish often determine where in the food
chain that fish is.
Speed/agility - Predators and prey that rely on speed/agility to
capture (predator) or escape (prey) undergo an evolutionary arms race
leading to positive feedback of speed/agility boosting morphologies.
In the short-term the natural enemy of the prey acts as a burden to
population fitness (probability of being eaten) but in deep time the
prey has acquired morphological advantages over potential future
natural enemies such as competitors for resources.
Venomousness -Why do venomous animals live in warm climates?


texts: Are there genes in humans from the common ancestor of all organisms?

texts: How long ago can human genes be traced? Are there any genes that go back unchanged to the beginning of life on Earth? And if so, how many?


texts: What determines if an allele is dominant or recessive?

texts:
Going back to my high school days we were taught about dominant and recessive genes. We were taught how to calculate the geneotype and pheneotype of potential offspring using a small table (forgotten the actual table name). But it never occurred to me then what determines if a gene is dominant or recessive and how this is carried out biologically.

Take my example below, there is a 50% change that an offspring will carry both the tall (T) and short (t) genes. What determines that the tall gene T has a dominant effect over the short gene t.

Now, I know that there is going to be differences between the different genes (i.e. eye colour), but is there a general description any one and provide which states how a gene becomes dominant and how the dominant effect is carried out biologically.


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

texts: At the very peak, the energy is in a state of activation energy. Here, is the substrate just attaching to the enzyme, or is is substrate already breaking?


texts: Why does sulfonamid not inhibit the growth of Rickettsia?

texts: Sulfonamid is an antimicrobial agent, why has it no effect on the growth of Rickettsia?


texts:
My 9 year old niece asked me this when I was explaining some stuff to her about the coronavirus. She asked "What does this virus taste like? Can I tell whether my sandwich is contaminated for example?"
That sounded like a silly question and I immediately responded by saying that they are too small to have any taste, and even if you manage to eat a whole lot of viruses it would taste like water.
The day after, I searched a bit just to make sure that I haven't fed the wrong information to the kid. As I expected, there wasn't a single page mentioning this question (except this quora post with a vague answer). Now it may sound like I am overthinking and the question is too naive and isn't worth the time, but then again, I thought what's the harm in asking?

Has there been any research on the likely taste or maybe smell of a specific virus or bacteria?


texts:
Last year I did my thesis in the field of a new method for DNA analysis.
Which I think is very interesting although I cannot seem to find any new methods in this field especially the SMRT sequencing method.

Do you maybe know a new method(s) which are introduced for DNA research in the area of SMRT sequencing ?


texts: What exothermic reaction distinguishes warm blooded animals?

texts: I would appreciate an answer specifically in the form of an exothermic chemical reaction. Namely, the one primarily responsible for generating heat in warm blooded animals that does not take place in cold blooded animals.


texts: Why is DNA replication not 100% accurate

texts: I've been reading about DNA mismatch repair (MMR) and how this process improves DNA fidelity. However, I was wondering, what is stopping MMR from correcting all mistakes in the daughter DNA with 100% fidelity? Why is the error rate still around 1 in 10^9 base pairs? Is it because the MMR proteins aren't present in cells in a high enough concentration? What would you have to change about this process to achieve 100% fidelity?


texts: How do we know the human species arose in Africa?

texts: I have heard (from multiple sources) that the current scientific opinion is that the human species arose in Africa. What are the reasons for this opinion? If possible, simple and non-technical explanations (as far as possible) would be appreciated.


texts: Hamilton's rule states that if $rB>C$ then a gene giving altruistic behaviour will increase in frequency in the population. What would happen if $rB=C$? Will an individual perform the altruistic act?


texts: Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics?

texts:
Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics, and why don't hospital acquired infections exist elsewhere ?

The infections that are caused in hospitals are usually a result of bacteria that are resistant to multiple antibiotics making them difficult to treat, but why are the bacteria resistant to all these antibiotics?
I realize that a lot of antibiotics are used in hospitals but the question that comes to my head whenever I read this is "So?".
To make my misconception clearer, I will use MRSA as an example .
I mean , for the Staphylococcus aureus bacterium to become resistant , the antibiotic has to be used on it , so how can the antibiotics used to treat different infections in difference people act as a selection pressure for  Staphylococcus aureus ( the Bacteria that causes MRSA )?


texts: Contact Inhibition of Cell Division: Signaling Pathway

texts:
The following article refers to contact inhibition of cell division in epithelial cells, specifically MDCK cells: Collective and single cell behavior in epithelial contact inhibition.

In their review of the literature, there are a number of possible signalling pathways implicated in contact inhibition of cell division. These pathways are outlined in the following quotes:

  It is widely accepted that contact inhibition requires establishment of E-cadherin-mediated cell-cell contacts and subsequent maturation of the adherens junctions (AJs) that link E-cadherin and F-actin in a synapse-like complex involving numerous other proteins

  One possible pathway involves β-catenin, a mediator of Wnt signalling, that, in addition to its function as a transcriptional cofactor, is associated with the AJs at the cell surface

  A contact inhibition role has been reported for NF2/Merlin, a tumor suppressor gene that encodes a membrane-cytoskeletal scaffolding protein, which most likely acts via the Hippo kinase pathway, controlling nuclear localization of the transcriptional activator YAP—itself a known regulator of cell proliferation.

  Contact inhibition is known to involve the MAPK pathway, which, in turn, promotes cell cycle entry by regulating the expression of cyclinD1. Also implicated are Nectins—a family of cell adhesion molecules that are involved, together with integrins and other proteins, in the regulation of cell motility and proliferation. Yet, this accumulated knowledge falls far short of a comprehensive picture of contact inhibition.

In the article, the findings were as follows:

  Our findings show that contact between cells is not sufficient for inhibition of mitosis in MDCK cells. Instead, inhibition of cell proliferation is a consequence of mechanical constraint that causes successive cell divisions to reduce cell area.

Where, in the discussion, they note the following:

  Our measurements also suggest that inhibition of cell division is a distinct single cell state rather than a global state induced by cell-cell signalling across the layer, as illustrated in Fig. 4E. In fact, confluent MDCK cell cultures with an average cell density corresponding to the morphological transition are often sufficiently heterogeneous in local cell density that highly motile cells and completely arrested cells coexist in the same colony. Thus contact inhibition is a local phenomenon...

Published later, the article Spatial constraints control cell proliferation in tissues showed that reducing the amount of space in a tissue prevented entry into S-phase. Actually stretching the tissue quickly reactivated the cell cycle, and compression leads quickly to arrest. More so, they found that cells had no memory of past constraint, and were able to suggest a model of growth in relation to the spatial constraint.

I'm editing my question because the way I posted it initially, to me, was unanswerable. Being said, I suspect that at this point cell volume and extracellular contacts are synergistic. This is probably going to need two separate questions, but:

1) How does the mitotic entry machinery roughly respond to cell volume? I'm currently reading into Cdc25/Wee1 regulation in addition to some stuff about internal fluidics that are influenced by water, ion channels, etc. but I still don't fully understand.

2) What's a relatively straightforward downstream pathway (core elements), starting at the adherens junctions, that illustrates how cell-cell signalling gets the STOP signal to the mitotic entry machinery (based on what we know)? This might require some much more in-depth knowledge about the field, however, but articles with some good figures are appreciated, too.


texts: Is it true reduction in sensitivity to dopamine due to over stimulation from addicting behaviors can be permanent, if yes how come?

texts:
I've read somewhat conflicting things.

General concept is this:

Addiction -> Over product of dopamine -> Reduction/Desensitization of dopamine receptors -> problems

And if you let go of addiction you go through period of withdrawl that can last from 90 days to a year.

BUT forever for some people... Why?


texts: What's the difference between naive and memory B cells?

texts: I understand that when naive B cells are exposed to antigens, they become memory B cells, but what is the functional difference between the two? I've looked at the quite a few article on B cells, but none of them stated the difference clearly enough for me to understand.


texts:
My aunt found this skull on the beach in Vancouver Canada. I believe it might be a type of bird, but I can’t place it.

It is about 5 inches (~13 cm) long and 2.5 inches (6.35 cm) wide.


texts: Repair of cloning vector nicks digested with antarctic phosphatase and ligated with T4 enzyme

texts: The vector product obtained by ligation between a vector previously digested with antarctic phosphatase lacks 5' phosphate groups. T4 ligase can ligate it to an insert with complementary sticky ends which provides 2 phosphate groups. But there are still 2 nicks in the vector product! How are these normally repaired ?


texts: What's the difference between growing cells in culture and cloning them?

texts:
The wikipedia page on Hela cells refers to George Gey being able "to isolate one specific cell, multiply it, and start a cell line." Later it says, "In 1955 HeLa cells were the first human cells successfully cloned."

What's the difference between multiplying the cells and cloning them? How is multiplying not cloning?


texts: Why do many people seem to prefer unhealthy compared to healthy foods?

texts:
I don't have any concrete statistics on this but many of us seem to love the taste of food that is unhealthy for us.

Over the centuries, wouldn't it have been a non negligible advantage to those who preferred (and hence ate) healthier food?

So, why don't most of us inherently find healthier food to also be tastier?

Apologies if this is a silly question or something that is frequently asked. I know very little about biology in general.


texts:
Is there any software that could be used to rapidly (quicker than humans) count the eggs laid by Drosophila on a substrate by placing them under a microscope with a camera attached? The eggs are laid on the surface of the food and have a fairly uniform shape - we regularly have to count the number of eggs in >200 vials, which can take a over 4-5 hours per 100 vials.

I wonder if there is some software which could be linked to a microscope with mounted camera connected to a computer, the software could then count from the live feed or a quickly taken photograph. It wouldn't have to be perfect but as long as it could be as accurate as humans (which is surprisingly low from our experience - we count up to a set amount then remove the rest, e.g. if I was aiming to leave 180 eggs I would be quite happy to get anywhere between 150-200 eggs). It would be using a stereo-microscope (aka dissection microscope) with a mounted camera.

The surface of the food with eggs looks something like this ->

purely for illustration, taken with iPhone - real images on microscope would be able to get closer (food surface could fill screen) and have more uniform lighting to give better contrast (this was taken to show in a talk so I wanted pretty rather than practical). The bottom two quarters of the food in this picture would be similar to the real result, just much closer...


texts: Why do I see purple stripes when moving a small source of light (flashlight) quickly in a dark room?

texts: I was playing with my phone's flashlight (white) in a dark room, Just moving it around quickly when I noticed that I could see thin stripes of purple in the same shape as my hand moved, they didn't disappear instantly rather I could see them like a net of thin purple strips, but vanished when I looked at them for more than 2 seconds. I don't understand why it happened and was curious.


texts: Transcription and translation of prokaryotic operons

texts:
I'm taking a molecular genetics course, and we're currently discussing prokaryotic operons. The lacZ operon came up frequently for me as an undergraduate as an example for teaching regulatory control of transcription, and the focus was always on determining whether the operon was transcribed under certain conditions (mutations, nutrients, etc). I don't remember much discussion about what happens after transcription. Today, however, I noticed something I had never seen before: three of the genes in the lacZ operon are transcribed simultaneously on the same transcript--I don't know how I missed this before!

My question is what happens post-transcription. Obviously there are 3 protein products. How are these products derived from the transcript? Is the transcript broken into 3 pieces, or does a single ribosome translate all 3 proteins from a single transcript substrate, or do ribosomes translate a single protein from a single transcript substrate at a time? Where could I find the relevant literature that elucidated the translation process?


texts:
In [1] it is stated that:

  the frequency of comutations in FGFR3 and KRAS or PIK3CA and KRAS was lower than predicted by chance, suggesting ... a lack of selective pressure for both mutations to occur

It is not clear to me how lack of selective pressure may produce a frequency of comutations that is lower than predicted by chance. I'd expect the frequency to be the one predicted by chance, if no selective pressure is applied. What am I missing?

[1]   S. E. Woodman and G. B. Mills, “Are oncogenes sufficient to cause human cancer?,” Proc. Natl. Acad. Sci. U.S.A., vol. 107, no. 48, pp. 20599–20600, Nov. 2010.


texts:
An inbred strain of plants has a mean height of 24cm. A second strain of the same species also has a mean height of 24cm. When these plants are crossed the F1 are also 24cm in height.However, when the F1 are crossed the F2 plants show a wide range of heights, the greatest number are similar to P1 and F1 but apprx. 4 out of 1000 are only 12cm tall and 4 of 1000 are 40cm tall. What fraction of the F2 plants will be apprx. 28cm in height ?

a)3/4

b)9/16

c)56/256

d)none

The answer given is c).


texts: What kind of worm is this? I’ve seen them in my bathroom and kitchen which are both ceramic tile. This morning I walked in the kitchen and this one just so happened to be dead.


texts: How can E. coli affect C. elegans expression?

texts:
Plasmids can be transferred to E. coli. These transformed E. coli can be fed to C. elegans to silence its gene expression by RNAi.

How can E.coli release RNAi to C. elegans? Even if we assume E. coli could enter cells of C. elegans for being intracellular Bacteria, it is hard to imagine that RNAi will exit E.coli directly and enter C.elegan's cells? Normally, no cells or bacteria will release RNA or genomic material outside of their cells?


texts: Self-replication in the genome in the seed

texts:
Is the genome in the seeds of the plant turned off?  That is, does the DNA in the seed not self-replicate?
My second question is, what are the cells feeding on inside the seed before it is planted?


texts: Why can't we call dog breeds different species?

texts:
I understand this question might fall into opinion based, but I'm trying to write it so that it meets the "Many good questions generate some degree of opinion based on expert experience" part and not get closed.

A closed creationist question about directly observing the evolution of new species made me think about just declaring dog breeds as new species just to provide an answer to that question. Turns out I'm not the first one to think of it, and to be honest I probably read that article and forgot about it.

That article quotes geneticist Jerry Coyne as saying:

  “If somehow the recognized [dog] breeds existed only as fossils,
  paleontologists would consider them not one species but
  many—certainly more than the thirty-six species of wild dogs that live
  in nature today.”

There is also this question about breeds of dogs being different enough they can't breed. The answer posted to that question discusses attempts to breed beagles with irish setters, and having great difficulty.

I'm aware that the commonly used definition of different species is individuals who can't interbreed and make a fertile offspring. However the Scientific American article I referred to above mentions that animals are often classified as separate species because they are separated by a geographical barrier, and if they could mingle they would make fertile hybrid offspring. The same articles mentions fruit fly research that bred two different species of fruit fly and made fertile offspring, even though they would never interbreed in the wild.

This is speculation, but let's imagine taking an island and putting several breeds of dogs on that island. Many of those breeds would easily interbreed and create mutts. But I'm pretty sure there would some sorting, the large dogs like st. bernards and great danes aren't going to easily interbreed with tiny dogs like chihuahuas. If we came back to this island after 50 or 100 years, we'd probably see small dogs and large dogs (assuming the island had decent ecological niches for both sizes of dogs to survive in)

Creationists like to ask why we haven't observed the evolution of a new species and don't want to listen to arguments about the fossil record or DNA sequences. If we just define some dog breeds as different species, we'd have an easy answer. I think some dogs would at least come close to meeting that definition for these reasons:

Dog breeds with large size differences would have great difficulty breeding.
Some pairs of breeds seem to have trouble interbreeding (Beagles + Irish Setter).
Some animals recognized as different species can create fertile hybrid offspring.

So why don't we recognize some dog breeds as different species?


texts: Can Programmable Cell Death (PCD) be engineered in a bacterium like E. coli?

texts:
I am reading a paper which says :
Messages not received after a certain time can be considered lost, as bacteria carrying them will suicide.
I even read some paper which says about PCD like this, but it just tells about a mechanism of Toxin and Anti-toxin.

My question: is there a reference which talks about genetically modifying E. coli bacteria (i.e. introducing a plasmid in it) which will cause cell death of the bacterium after a certain time. In short, we decide the life time of a bacterium after which it just commits suicide.


texts: Can mitochondria with "depleted" mtDNA reproduce?

texts:
Background

There's a popular group of antibiotics known as fluoroquinolones, abbreviated FQs. They're quinolone abx with a fluorine atom added at position 6 to increase cell permeability. Popular varieties of these drugs include ciprofloxacin, levofloxacin, norfloxacin, and many others. They also go by brand names Cipro, Levaquin, etc. They have a well known side effect of wreaking havoc on the body's mitochondria through numerous pathways.

This stunning image shows the in-vitro result of administering a clinically relevant dose of ciprofloxacin to human tissue for 24 hours (1). The study notes "short, swollen, fragmented mitochondria (smaller aspect ratio) with highly reduced branching (smaller form factor)"

Because the fluorine atom allows for deep tissue penetration, FQs can cross the double membrane of mitochondria, and because FQs are designed to target "double helix" DNA of some bacteria, they also appear capable of targeting the same double helix DNA structure in mitochondria. In bacteria, the FQs bind to the DNA-gyrase, causing breaks in the DNA that are fatal (2) to the bacteria.

Question

A study published in Molecular Pharmacology (3) shows that mtDNA is "depleted" by Cipro:

  Analysis of mtDNA from ciprofloxacin-treated cells revealed the presence of site-specific, double-stranded DNA breaks. These results suggest that ciprofloxacin may be causing cytotoxicity by interfering with a mitochondrial topoisomerase II-like activity, resulting in a loss of mtDNA.

The full text of this study is not available as far as I can tell. I can find scientific literature on depletion of mtDNA (4) but what does this mean for the long term health of the mitochondria / cell?

Can mitochondria with "depleted" mtDNA reproduce, passing on the damage from breaks in the DNA? Or is the mitochondria and cell doomed?
More open ended: Is there any literature suggesting mitochondria damaged by oxidative stress can recover (first image), or are they also doomed?

References

Bactericidal Antibiotics Induce Mitochondrial Dysfunction and
Oxidative Damage in Mammalian
Cells
Fluoroquinolones: Mechanisms of Action and
Resistance
Delayed cytotoxicity and cleavage of mitochondrial DNA in ciprofloxacin-treated mammalian cells
Mitochondrial DNA metabolism targeting drugs


texts: Homework question on chemically defined medium

texts:
Why would the following medium not be considered a chemically defined medium:

Glucose, 5 grams (g); NH4Cl, 1g; KH2PO4, 1g; MgSO4, 0.3g; yeast extract, 5g;
distilled water, 1 litre

I am unsure why it is not a chemically-defined medium considering all measurements and grams are given and such is required for it to be one. Therefore I am unsure why it would not be a chemically defined medium.


texts: Plant identification - variegated ivy-like

texts:
What plant is this? It's in the UK, grown in a pot, and looks like a variegated ivy.

Leaves are about 2 cm in diameter, and the full plant about 50 cm.


texts:
I'm translating a Russian text touching upon the IL-17 interleukin family, and it has a kind of typo in it. I'm not sure:

  As mentioned above, IL-17 was found to be expressed at the highest levels by CD3+ Th17 cells. However, subsequent studies showed that it may be produced as well by stimulated CD8+ memory T cells, γδ T cells, Th memory cells (?) and NKT cells.

The Russian text says "Th memory", there is no "cells" there. It might be a typo.

I've read a little about T cells and became curious. Are there T helper memory cells, or does being a T helper cell exclude the possibility of being a memory cell as well?

P.S. The original Russian sentence is

  Как уже было сказано выше, наибольшей экспрессией ИЛ-17 характеризуются CD4+ Th17 лимфоциты, однако последующие исследования установили, что стимулированные CD8+ Т-лимфоциты памяти, γδ Т-клетки, Th памяти и популяция NKT также способны к его продукции.


texts: Is there any plausible biological mechanism for "universally protective vaccines" via "MHC allotype-independent immune effector memory cells"?

texts:
Geert Vanden Bossche, who has recently gained some fame for dissing all current Covid-19 vaccines (and who is also asking the WHO to meet him so they can  be infused with his wisdom), has had the same poster at a couple of conferences/expos in 2015-2017. Quoting one of these (only the title seems to differ):

Universally protective vaccines: A revolution in modern vaccinology
Geert Vanden Bossche (University Leuven, Belgium; Univac NV, Belgium)
To eliminate safety risks related to infectivity, inactivated pathogens and more suitably, well-characterized pathogen-derived
antigens (Ags) have increasingly been used as immunogens in modern vaccines. The selection of these Ags is usually based on
their capacity to induce immune responses that correlate with natural protection. These Ags, however, are known to be antigenically
variable or conformation-dependent (e.g., B cell epitopes) and/or subject to immunogenetic restriction (e.g., linear, T-cell epitopes). In
addition, the immunogenicity of good vaccinal Ags is largely dependent on memory CD4+ T helper cells. However, activation of the
latter upon natural infection or foreign Ag exposure of genetically predisposed subjects can occasionally lead to immune pathology.
Priming of CD4+ T helper cells by adjuvanted vaccines is, therefore, increasingly raising safety concerns. On the other hand, Ags
that are highly conserved and vulnerable because of their exposure on the surface of infected or pathologically altered host cells are
either not immunogenic or subvert the host immune system. Hence, they are not used as vaccinal Ags in contemporary vaccines.
We consider that new technologies enabling immune targeting of these Ags by natural, MHC allotype-independent immune effector
memory cells is the new Holy Grail in modern vaccinology.

Basically, is this complete nonsense or is there any plausible biological basis for "universally protective vaccines"?
In his Covid-19 talk, he basically says that natural IgM is better than anything else, which actually seems dangerous crackpottery in the context of Covid-19 because patients with numerous but low potency antibodies are often among the dead.
But in his Covid talk he never mentions "MHC allotype-independent immune effector memory cells" which showed up as his punch line in these older posters that I'm asking about. So is this (older) concept (of his) phantasmagoric, or does it have any biological corresponded? I've looked through a review on memory T cells, which describes the effector memory as a rather problematic subset because it's apparently made of only seemingly connected further sub-types, but I can't tell if any of these could possibly have anything to do with what Bossche is saying. In particular, how would any effector memory cells be the basis for a universal vaccine?


texts: What is Mendelian Randomization, and how is it used to infer causality in epidemiology?

texts:
Studies of human traits and diseases are inherently confined to observational studies, known as epidemiological studies. This can make it very hard to determine what actually causes a particular disease or trait, and what is just a by-product or biomarker of the disease.

Mendelian randomization is a statistical technique used by genetic epidemiologists to determine causal effects, for instance whether a biomarker actually influences disease risk, or whether it is just a statistical association.

From basics, how can genetics be used to determine causal associations between traits (such as blood markers) and increased risk of disease, and on what assumptions is this based?


texts:
In this video on electro tonic potential, the tutor says that when the potassium channels open the potential drops from +40mV to -80mV, where the sodium channels have already closed at +40mV.

Now in that case,
wouldn't the sodium channels that usually open at -55mV open up again when the potential is on its way reaching -80mV from +40mV, thereby making changes in all the potential differences that are occurring normally(according to the video)?

Thanks for the help.


texts: Development of radial symmetry in starfishes and other animals

texts:
How does nearly perfect radial symmetry arise in an animal like the starfish? My confusion lies in the fact that cells are fluid & amorphous, & that these characteristics seem to make it difficult to form symmetric structures. Many of the sources I've read describe the formation of the blastula but not the development of the five arms following that. Also, at one point in the development it is bilaterally symmetric. Furthermore, some species of starfish can regrow from a single arm.
What process mediates the formation of radial symmetry in a developing organism? Is it that arms grow individually & there are cascades of cellular signaling that mediate the production of new arms until the desired amount is reached or is it something else? How do the arms of the starfish remain evenly spaced?


texts:
What is the best cut-off for e-value in BLAST?
Some say 0.01 ,others 0.0001?
Even BLAST tutorials don't give a very clear idea about which cutoff suits which purpose?
Could some experts give me a clear idea on this.
Why are we using 0.0001 and not 0.00011?


texts:
What does the total membrane current vs time plot of an action potential look like? I see that there are voltage vs time plots, but I can't seem to find the current plots.
Thanks


texts: How can soft tissue exist in dinosaur fossils?

texts:
In this article the author explains that they found soft tissues inside of 68-million-year-old dinosaur fossils. How can that be possible? It was believed that soft tissues cannot last more than a million years and that DNA degrades even sooner.

  Our findings challenged everything scientists thought they knew about
  the breakdown of cells and molecules. Test-tube studies of organic
  molecules indicated that proteins should not persist more than a
  million years or so; DNA had an even shorter life span.

What is the evidence that the fossils were real?


texts: Genomic distribution of tRNAs in eukaryotes

texts: The title says it all. I'm doing a literature search trying to see what is widely known and/or well established. I've found a couple of mentions that tRNAs are dispersed throughout the entire nuclear genome. Does this mean they are isolated from each other? Or do they occur in clusters? Is this true across eukaryotes? Or is any of this even well studied?


texts: How are there multiple varieties of the potato?

texts:
The potato appears to propagate by growing an 'eye'/'bud' which eventually grows into a new plant. So there would probably be single representative of the potato species in the world with all others being genetically identical.

Yet wikipedia indicates there are several closely related species of the potato; apparently as a result of selective breeding. To my understanding (which is probably wrong) there is only a single potato that grows the eyes without the need for a second parent - so there should probably only be the same genes repeated in each potato/plant.

What am I missing here? Why are there multiple varieties of the potato?


texts: What does completing the course of antibiotics accomplish?

texts:
This article from the WHO states:

If you stop treatment early, there is a risk the antibiotics won’t have killed all the bacteria that made you sick and that it will mutate and become resistant. This will not happen to everyone – the problem is that we don’t know who can safely stop treatment early.
By taking the full course prescribed by your doctor, even if you start to feel better earlier, you increase the chances of killing all of the bacteria and reduce the risk of resistance.

A clarification: When the WHO says “[bacteria] will mutate and become resistant,” they are implying that using antibiotics will create a selective pressure for bacteria with antibiotic resistance, arising most likely through mutations, correct? Bacteria don’t mutate into antibiotic resistant strains in direct response to a drug; rather, antibiotic resistance is a phenomenon of natural selection. I’ve seen so many articles about antibiotic resistance worded this way and I feel it’s simply wrong.
Presuming I am correct about my first point, here’s my true question: Say you’re prescribed a course of antibiotics. It kills the bacteria that are not resistant to the drug and leaves those that have developed resistance behind. What does it matter if you finish the whole course? Taking more of the drug is not going to affect the resistant strain. The only rationale I can think of is that it would kill off any residual non-resistant bacteria and prevent them from gaining resistance (via conjugation) from the resistant kind. However, is this the only mechanism whereby completing the course prevents the rise of antibiotic resistance? How effective is this at all at preventing the rise of antibiotic resistance in the bacterial population in general (i.e. beyond the host)?


texts: In centrioles, what type of fibers connect the triplet microtubules?

texts: In a centriole, each "arm" (a triplet microtubule) is attached from its A-tubule to the C-tubule of the adjacent arm. What is the type of fiber that connects each arm ("connecting fibrils" in the image below)?


texts: All-or-nothing-law: law or general principle?

texts:
The all-or-nothing principle indicates that a nerve cell fires at maximum potential or not at all, based on a threshold on the stimulus.

Is this a statement which is always true, or only mostly-always true?

In electrical engineering, a discipline I have studied, we have a similar rule, a logic signal is responded to as though it is either a high or a low.  However, in the middle are what are known as "metastable states," where the rules of thumb do not apply.  In fact, you can even theoretically lock up a logic circuit by presenting a steady stimulus in between two states.  Needless to say, designers of such circuits take great effort to ensure their logic is never exposed to such stimulus.

Do we have any evidence of neurons exhibiting behavior which defies the all-or-nothing law in some circumstances, or if not, what sorts of metastable behavior are seen when the stimulus is exceedingly close to that of the threshold?


texts: Identify these two large, colorful dragonflies in Taiwan?

texts:
Here are two dragonflies that I photographed today in Hsinchu county Taiwan. They are both quite large, with a body length of about 5 or 6 cm.
I often see them in the same pond or nearby marshy area. They seem pretty confident and are easy to photograph as long as you don't make a big commotion.
The arrows were drawn for my other question Why do dragonflies have these special little spots on their wings?
Is it possible to identify these two species? I can break them out as separate questions if necessary; I don't want to flood the site with "identify this dragonfly" questions.
The first is jet-black everywhere except for a robins-egg blue powdery coloration along the top side of the first two-thirds of it's abdomen. It's wings, like most but not all dragonflies, are transparent.
The second has some amount of red almost everywhere; its eyes and thorax are dull red and it has bright red patches on each segment of its abdomen. Notably its wings are solid opaque red, except for the furthers 1 cm which is transparent. The tiny "special spots" on the tips of each wing are a particularly bright shade of red!


texts: Gibson assembly - primer design with A and T rich regions

texts:
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


texts: Question about the DNA glycosylase enzyme assay/formamide gel loading buffer

texts: Often for the DNA glycosylase enzyme assay we can see that the DNA glycosylase is incubated with oligonucleotide in 37C and then reaction is stopped by addition of formamide gel loading buffer (80% formamide/1 mM EDTA, pH 8.0y0.1% bromophenol blue/0.1% xylene cyanol). How the reaction is stopped by this buffer?


texts: What would cause crows to be attracted to a human body?

texts:
On another SE site, there was a comment that told me something  about biology that I already know:

"A man left murdered in the fields would soon have a flock of crows mobbing his fragrant corpse."

But I don't quite understand why. Is it the "death" part,the fact that someone was injured/bleeding or just the fact the he was immobilized,that would attract the crows?

That is suppose you tied up someone and left him on the field. Would that attract the crows?
Suppose this person fell down, was bleeding, and immobile, but not seriously injured? Or is it the death part?


texts:
What plant species is this?

Its stalk looks like a grapevine, but the leaves & flowers not. It bloomed this week (Mid-June). I have found it in Turkey, Amasya.

If you want, I can add more shots of plant.


texts:
I saw there was another question about vitamin D; however, I do not believe this is a repeat.
What are some of the effects/side effects of having too much vitamin D in your body?


texts:
Recently, I found a few worms in my bathroom and I am wondering what kind of worms are they. They move slowly and they are about 6-9 millimetres long. It seems that they are not sensitive to water. Are they harmful parasites or harmless creatures? For your information, I live in Turkey.

Here are photos of a selected worm.

Thank you for your help.


texts: What is the term for awareness of or inclusion of real sounds within a dream?

texts:
I fell asleep while listening to a podcast, and I am sure I was dreaming but I could also still hear the podcast.

The podcast played an important role in the dream, I was searching for the source of the voice, wondering if others in the dream could hear the same voice. I started to feel a bit panicky and woke up as the podcast also happened to end. I rewound the show and confirmed that it was all there, exactly as I had heard in my dream!

I would like to read more about this type of experience, but I am having trouble finding the right words to search. Is there a name for this phenomenon? Is there anything that contributes to experiences like these? I know it wasn't lucid dreaming, because I wasn't aware of being asleep.


texts: What will happen if one keeps the photosynthesis plant active 24x7?

texts:
While reading this article online something said on it made me wonder.

Also, there have been suggestions and a Dawn / Dusk type of ramp up and down to simulate the slow changes in the sun have value, but we have not seen solid universal data in this regard to date...

It made me wonder if we are simulating the sun in a dark room for growing the plants with the help of red, blue, and a little bit of far-red light, what will happen to the plants if we keep the ideal conditions for which the plants carry out photosynthesis whole day? Does it affect its yield or the plants die out quick?
I am an engineering student working on indoor farming, my knowledge of botany is the same as a high school student. So if I am wrong please tell me.


texts: What are the methods of prophylaxis against exposure to radioactive isotopes?

texts: Potassium iodide is used as prophylaxis to prevent illness when one is likely to be exposed to Iodine-131 and other radioactive isotopes of iodine. Are there any other prophylactic treatments for exposure to other radioactive isotopes, such as Cesium-137, Tritium, Strontium-90, etc? If so, how do they work?


texts: What is the chance a given gene will end up in a given gamete?

texts:
Let us say a germ cell had a desired allele. This germ cell was replicated during interphase so that it had two of the desired allele. It then underwent meiosis.
My question then is, what is the chance a given allele will end up in a given gamete that will be involved in conception?
Firstly, there is a 50% chance a chromosome will be assigned to a given daughter cell. This is because of independent assortment. In addition, cross over occurs at chiasmata. Lets assume then that there was a 50% chance that an allele will be crossed over (although this probability may be far from true)
The process during meiosis is that cross-over occurs first. We have two desired alleles, each on one of two pairs of chromatid attached to each other. There is 50% chance for a given allele to cross over. For example, the chance for both desired alleles to cross over is 1/4 (1/2 x 1/2), the chance only one will cross over is 2/4 (since either of the two desired alleles can cross over).
Then there is the first independent assortment during meiosis I which produces the desired daughter cell. In this case there is a 50% chance that a given chromatid pair (containing the desired allele) will be assigned to the desired daughter cell. However, in the case where a desired allele is found in both homologs (2/4 of a chance), then the chance that at least one desired allele will be in the daughter cell is 100%.
Finally, during meiosis II, another independent assortment occurs which produces the desired gamete. The same rule applies with a 50% chance a given allele will be assigned to a given cell (in this case the gamete). However, if the desired daughter cell contains two of the desired alleles, then there is a 100% chance that the cell will have the desired allele.
In conclusion, the chance I estimated that the gamete will have at least one desired allele is 50%. Although, I'm not sure if this is correct. Anyone mind confirming this.


texts: How are monocytes larger than capillaries?

texts:
I have read that the average size of a capillary is about 8 micrometers. How is it possible that the 15 micrometer or so monocytes in blood do not block these vessels?

https://en.m.wikipedia.org/wiki/Blood_vessel#Vessel_size

https://www.britannica.com/science/monocyte


texts: If the flu vaccine is the exact same as last year, would it still offer protection this year?

texts: I understand why the flu shot changes and that's why we get an annual vaccine; however, if the vaccine is the same as last year, wouldn't people theoretically still have the same antibodies this year? Do antibodies disappear after a year?


texts: Other than Acetylcarnitine what other orally-bioavailable Acetyl donors exist to assist in the conversion of CoA to acetyl-CoA?

texts:
I asked a question on bio stackexchange a few days from which I was hoping to be able to arrive at an answer for this question myself but I have had no such luck so now I am going to just ask outright: other than acetyl-L-carnitine are there any orally-bioavailable compounds (in particular orally-bioavailable to humans)  that exists that can serve as an acetyl group donor for CoA?

My main motivation for asking this question is that I know that acetyl-L-carnitine indirectly promotes the acetylation of histones by serving as an acetyl donor for CoA by serving as a substrate for carnitine O-acetyltransferase and then this resulting acetyl-CoA then donates an acetyl group to histones by means of the enzyme histone acetyltransferase.


texts:
Is there a way to map smells to numerical values of different variables?

I.e. With RGB colours, each colour is made up of numerical values from 0-255. For example, red is (255,0,0), and yellow is (255,255,0). Is there a way to do this with smells. I.e, the smell of Candy is (140,70,255), and the smell of grass is (255,34,27)? How many different sets of numbers (like red, green and blue) would you need, and what would they represent?


texts: What kind of spider is this from Sydney, Australia?

texts:
I was cleaning the pool when this guy crawled on my foot. I hit him away and noticed a bite mark. I managed to snap a photo of him.

I went to the doctor because I was worried it was a funnel web and she told me to just keep an eye on it, ice it and take anti histamines if it itches.

I have a tiny bit of tenderness in my foot.


texts: Are all genes transcribed in differentiated cells?

texts:
My textbook tells me that it’s specific transcription factors that allow for a different set of genes to be expressed in different cells (differential gene expression). My book gives the example of liver and lens cells—liver cells contain the specific transcription factors (STFs) to activate the enhancer for the albumin gene, while lens cells contain the STFs to activate the enhancer for the crystallin gene. Liver cells do not have the STFs to activate the crystallin gene, and lens cells cannot activate the album gene.

However, my book also tells me that there is a basal level of transcription that arises from the binding of general transcription factors. Enhancers only increase the rate of transcription on top of that basal rate. Does this mean that in differentiated cells, all genes are indeed transcribed? I.e. a lens cell does transcribe the gene for albumin and the liver cell does transcribe the gene for crystallin?

(The wording of my book dissuades me: "Liver cell: The albumin gene is expressed, and the crystallin gene is not. Lens cell: The crystallin gene is expressed, and the albumin gene is not.”)


texts:
Humans (and other humanoid mammals) have five fingers in each hand.

Curious to know, why five? Wouldn't more fingers be more useful?

Is there any evidence that it used to be different and natural selection caused those with five fingers to survive?


texts:
Yesterday I thought about a question and asked it to my friend.  The question was
which gene is completely the same for a male cell that made meiosis 1 recently.

My answer was the gene that starts meiosis 2, but he said he thought that there is no such gene - only a gene to start meiosis and meiosis 1 and 2 are just parts that scientists named.

My question is is there any gene that starts meiosis 2?


texts: Are there any primary structure sequences that strongly suggest b-sheet or alpha helix?

texts: Is there a particular sequence of amino acids that we know will take on a beta-sheet or an alpha helix or is it essentially random?


texts: Why is the 5′ end of DNA a monophosphate?

texts:
According to my textbook:

While the 5′ end of a DNA strand is typically a monophosphate, the 5′
end of an RNA molecule is typically a triphosphate.

Source: Biology: How Life Works, 3rd Edition
How do we know the 5′ end of DNA a monophosphate? I understand that...

DNA and RNA synthesis cleaves nucleoside triphosphates into nucleoside monophosphates to form the sugar-phosphate backbone.
Necessarily, the first nucleotide will have three phosphates intact.

What I don't understand is why DNA doesn't have a triphosphate on the 5′ end like RNA. How does that happen?


texts:
I have another question regarding cystic fibrosis.

I understand that gene therapy is currently being talked about in the cure for cystic fibrosis. I know that Eric Alton at imperial college London is working on delivering genes using liposomes and viruses like lentiviruses but I am confused over the advantages and disadvantages of those two methods.

In addition, is there an alternative 3rd method for injecting genes that don't involved viruses or liposomes. (An alternative type of vector) ?

Thanks


texts:
I have received this question during a recent discussion about pet birds and cats. We know that birds evolved from the dinosaurs before the mass extinction that happened about 66 million years ago.
However, I could not find such clear information about the most prolific creature on the Internet.
This article suggests Felis attica (reclassified to Pristifelis attica) as an ancestor which seems to have lived about 12 million years ago.
I am interested in filling the gap between the mass extinction and Felis attica to have an answer for my question, but I cannot find an article diving even further in cats history.
Question: What did (domestic) cats evolve from?


texts: Is it possible for any impurities to get through the apple peel?

texts:
My parents always told me not to eat from the apple trees near the  road, because some kind of bad toxic dirt might get through.

This sounds to be physically possible but not really probable in my view. In the time apples grow on the tree they never rot. The rotting procces starts as the apple falls down and damages - the wound will quickly change its colour and it begins to decay - from this I assume the peel is almost perfect defense against bacteria & toxic penetration.

I think the only danger may come from the dust microparticles spread by the cars - which can be easily washed by water or wiped off with a piece of cloth. Am I right? What about other types of fruit?


texts: Is there a realtime molecular clock within the genome to co-ordinate the developmental sequences in an embryo?

texts:
It is difficult to assume that the massive number of co-ordinated developmental sequences in a developing embryo is controlled by molecular signalling alone. Is anyone aware of a molecular or developmental clock within the genome which control the on off states of the genes concerned with developmental sequences? If it has not been reported is it likely to exist? (This is not about the molecular clock in evolution.)

Assuming there is a molecular clock, is it possible that the clock is switched on at the time of fertilization, and the zygote transfers the elapsed time to the progressive generations of the cells?


texts: Why do we have two of some organs, but not all?

texts:
We have two eyes, but we don't have two hearts.
Why do humans have two of some organs, but not all?


texts:
In my text book there is an example of a 18 carbon long fat and it says that it can run 8 laps of oxidation. I don't understand why it doesn't run 9? 2 are removed each cycle?

Thanks.


texts: I was curious about a fact given in my biology textbook as to why the Japanese have  3 pairs o floating ribs unlike the rest who have just two?


texts: The Effects of Large Static Magnetic Fields on the Human Nervous System

texts:
How do static magnetic fields impact the nervous system?
I imagine with sufficiently intense magnetic fields the Lorentz force is going to change the behavior of nerve impulses, but at what field intensity do these issues occur? Which parts of the nervous system are most impacted by these fields? What specifically does the magnetic field interfere with? Are motor nerves more impacted than sensory nerves?
The WHO has some guidelines which suggest that fields of high intensity cause nerve issues, but this seems more related to MRI tech safety and doesn't really go into the biophysics of the situation. Additionally, they talk about issues which appear while moving through the fields, which seems to imply they're talking about low frequency field variation because an MRI field isn't spatially uniform.


texts:
I am currently reading "The Chemistry of Life" by Rose. It's a great book (to me as a lay reader at least) and an interesting topic so I am interested in pursuing some of the further reading he suggests.

The first book he mentions in the bibliography is Alberts' "Molecular Biology of the Cell". Looking at the description and the reviews it seems that this is a pretty advanced bio-sciences graduate level text, and I am very much not that. I see that Alberts has also written "Essential Cell Biology" which looks more accessible. Before I buy this I wondered if anyone can explain the difference, which would be a better read for an enthusiastic amateur?

If it helps at all I am a science grad and I typically read authors such as Dawkins and Matt Ridley, but I'm looking for something a little bit more rigorous to expand my knowledge in cell biology.


texts: Do any non-human species have juveniles that cannot communicate with adults?

texts:
Human babies take 1+ years to begin learning how to speak (though sign language can be learned a bit earlier1).

I know that cries, yells, and other non-linguistic sound are a simple form of communication, but they don't actually get across a specific point (e.g., what is causing a cry).

I understand that no other species use language, per se, and that linguistic development is complex and therefore requires time.

However, I'm wondering if other species have similar periods in which the adults "don't understand" the babies/juveniles.

In other words, do any other animals have a period of communication development early on in life before which the juvenile's cannot communicate with adults?

Boughman & Moss (2003) mentions the development of call types in some birds based on exposure to parents or certain social groups, but it doesn't quite address how these individuals communicate prior to the development of these calls (if at all). The paper also discusses individualization of sounds and recognizing variations to identify individuals, but again, this doesn't quite capture my question about a period of ontogenetic communication incompatibility.

1. Fitzpatrick, E.M., Thibert, J., Grandpierre, V. and Johnston, J.C., 2014. How HANDy are baby signs? A systematic review of the impact of gestural communication on typically developing, hearing infants under the age of 36 months. First Language 34(6):486-509. pdf

2. Boughman, J.W. and Moss, C.F., 2003. Social sounds: vocal learning and development of mammal and bird calls. In Acoustic communication (pp. 138-224). Springer, New York, NY. pdf


texts: Where does the fate map of a human embryo end?

texts: I'm confused about the fate map of a human embryo. Is it just a particular part of the embryo development or does it include everything, from the conception (germinal stage) to the day the baby is born?


texts: How to avoid air bubbles while pipetting?

texts: I get air bubbles while pipetting small volumes. How can I avoid them ?


texts: What kind of bonds are there between a Transcription Factor and its DNA binding site?

texts: I want to know what kind of bonds are there between a Transcription Factor and its DNA binding site when the complex is created. This information will be used to determine the method for a molecular Dynamics simulation, which intends to predict/calculate the binding energy/Gibbs free energy.


texts: What is the prehistory of amino acids in cells?

texts:
As a followup to Why 20 amino acids instead of 64? and What is the smallest number of amino acids required for life?, I am trying to understand the prehistory of amino acids in cells.

All living cells now use 20 (or 22 if you include selenocysteine and pyrrolysine) amino acids. Perhaps in the past there were fewer amino acids used in cells, especially if the theory of a 2-nucleotide codon is to be believed.

Is there any theory as to the order in which these amino acids were incorporated into cells?

This paper (by Akanuma, Kigawi, Yokoyama, "Combinatorial mutagenesis to restrict amino acid usage in an enzyme to a reduced set", http://www.pnas.org/content/99/21/13549.full) suggest that the full complement of 20 amino acids are not strictly necessary by reducing the number of amino acids in a certain enzyme to 13, yet still retain functionality.


texts: Spruce growing high up in a maple trunk: Can a partially rotted trunk completely sustain another tree?

texts:
I've come across a spruce tree that is growing 15ft up in the crotch of a sugar maple tree:

According to Google StreetView, the spruce has been there since before 2007 (over 10 years ago!).

I've seen other trees growing out of rotted stumps or in trunks near ground level before, but I've always just assumed that the roots of those trees reached down to soil -- in one way or another -- to get the nutrients they need for survival.

But with the subject tree, it's so high up that I would assume that that the roots do not have access to any soil. It's my guess that the spruce is getting all of its nutrients from decomposed wood in some rotten portion of the trunk.

I didn't know biology worked like this. I wouldn't have guessed that a live, partially decomposed trunk could contain 100% of the nutrients that a tree needs to survive for 10+ years. I know soil is made, in part, from decomposed wood, but it's my understanding that there are a lot more ingredients too.

Can the decomposed wood in a partially rotted trunk completely sustain a tree?


texts: In DNA sequencing, is "mate pairs" synonymous with "paired ends"? If not, how do they differ?

texts:
By just looking at Roach et al's paper I get the impression that they are the same thing, and the Wikipedia URL for the former is a redirect to the latter.

However, I suspect they are not exactly the same - for starters, they wouldn't have two different words for the same thing, right?

Can anybody shed some light and suggest some references?

Thanks.


texts:
I was not sure if this question is more appropriated to be here or in Pets Exchange. I'm posting here first.

I accidentally broke a thermometer in my bedroom and, by my lack of attention, have spread mercury along the house. I cleaned the most part before the spread, so what I found after was only really tiny drops of mercury. However, I have four cats and I'm afraid that one of these tiny beads could possible be stuck in them paws while they are walking and they possible lick it, swallowing the beads.

I'm maintain the house ventilated most part of day (except when I go sleep) to minimize mercury vapors and I already search for possible symptoms of mercury intoxication in cats and found weakness, vomiting, diarrhea and difficult walking. Until now, I didn't observe any of these symptoms, but I would like to know what I should to if I notice some of them.

Because COVID-19, reach my veterinarian maybe will be difficult.

PS: I live in a country which doesn't have a service to come to my house to check the mercury amount in the ar neither get rid of it.


texts: What's the name of this bug from Toronto, Canada?

texts: It's about 3 millimetres in length. Found on September 10, 2015.


texts: Are there any non-pathogenic gram-positive bacteria in human gut?

texts:
I wish to know if there are any non-pathogenic (not even opportunistic pathogen) gram-positive bacteria in the human gut? Is there any reference that shows there exists a non-pathogenic gram-positive bacterium in the human gut?

I searched the internet but was unable to find anything conclusive.


texts: Why does yeast react the way it does to water combined with sugar?

texts:
I almost wanted to ask this in Cooking SE, but thought it would be better fit here.

So I understand than when you mix yeast with sugar and warm water, you get CO2. When using baking powder, it's a standard redox reaction, but what is it with yeast? Is the yeast still present after whatever reaction happens there? I don't think so, because that would mean that the reaction would go on forever. But what evolutionary sense is there for yeast to evaporate into CO2 when confronted with sugar and warm water?


texts: Are there any situations in which phenylephrine is preferred to pseudoephedrine?

texts:
In the mid 2000s in the US, due to issues of drug enforcement, pseudoephedrine containing medications were brought behind the pharmacy counter and in most cases require ID, and phenylephrine was substituted in most over-the-counter products.

Pseudoephedrine increases the amount of endogenous norepinephrine, whereas phenylephrine works on α1-adrenergic receptors directly.

There are numerous cases where experts have spoken out about the effectiveness of phenylephrine, so it likely is a less effective substitute for pseudoephedrine in its main role as a decongestant.

What I'm curious about is whether there are clinical indications for which the phenylephrine is actually preferred (so situations where the α1-agonist nature without the increase of endogenous NE is sought after)?


texts: Does cooking or ripening reduce the concentration of solanine in nightshade?

texts:
I recall a story from one of my Botany professors where he encountered a woman picking Solanum dulcamara (nightshade) berries. When he asked her what she was doing with them, she responded that her husband had her make a pie from them every year.

As her husband was presumably still alive, and since I regard this particular professor as reliable, what would have removed enough solanine from the berries to avoid ill effects? Does the concentration decrease upon ripening, or would cooking destroy the toxin? Would that also be why we fry green tomatoes?

(As a disclaimer, no-one should eat plants that are known to be poisonous. Even though some people don't react to poison ivy, it is still a bad idea to rub it all over your body.)


texts: Workspace preparation and cleanup for DNA work

texts: What steps should be taken in a molecular lab environment to help ensure that DNA samples/stocks are not contaminated, or contaminate other objects in the lab?


texts: Can the human body survive in a zero sugar diet strictly through gluconeogenesis?

texts: I read an article a while back about athletes (I believe cyclists) being exposed to a 0 sugar diet and their blood sugar levels stayed relatively constant, which prompted the question whether people could survive strictly off a no sugar diet.


texts: If what we eat can be seen in our hair, then to what degree can our food affect the "look and feel" of our hair?

texts:
It looks like most things (or everything?) that we consume, whether it is a food, drink, or something we smoke (like e.g. some drug like marijuana) ends up in some amounts in our hair.

If this is the case, is it theoretically possible that there exists some compound that, when ingested, could affect the color of our hair?

Or alternatively, would it be possible for an ingested chemical to weaken or strengthen the disulfide bonds present in hair structure?


texts: Universal clock for humans contained in the telomeric sequences?

texts:
I don't know if this would make sense, but imagine that we could only suffer from natural aging (not diseases whatsoever involved). Is there an estimate of what is our natural maximum lifespan that a human can have?

I learned that the telomeric sequences protect sensible information in DNA, and that somatic cells suffer from a cut of these sequences in each replication. So I wonder if this is a natural clock, and if it has been estimated how much time do we have naturally.


texts:
Is it better to say 0 chromatids or 46 Chromatids in a human cell?

Because most of the webpages I have seen say 46 chromatids and some clarified that it is infact according to the definition 0 but 46 is more commonly used


texts: Turning publicly available genome data into proteins

texts:
I'm a computer scientist who is starting to dabble with biology. My eventual goal is to model different kinds of cells with a computer program. As of right now, I'm just trying to take some smaller steps.

First, I downloaded a complete human genome from http://hgdownload.cse.ucsc.edu/downloads.html#human  There is a FASTA file for each chromosome.

Then, I wrote a java program which can convert FASTA DNA sequences into the appropriate amino acid chain.

Next, I made my program look for the "start" code (ATG) and "stop" codes (TAA, TAG, TGA).

So, now I have sequences of amino acids which might theoretically end up folding into proteins. But, before I start diving into protein folding, I wanted to try to verify that the steps I took so far were done correctly. I looked up some important human genes in an online database and found their amino acid sequences. I then searched through my program's data for those sequences and confirmed that they were there. However, the gene was in a different base-pair location than the database said that it should be in.

This led me to some questions, which, so far I have been unable to answer and hopefully people here will be able to help shed some light.

I know there are a lot of different publicly available genomes. Maybe the UCSC one that I downloaded is different from the one used by the gene database. How much does each genome vary from each other genome and in what ways do they vary?
In attempting to answer that first question, I was going to download a bunch of genomes from the 1000genomes website and do some comparisons, but I wasn't sure which files to download. Each of the files begins with either ERR or SRR and I'm not sure what that means. This is the folder I'm currently looking in ftp://ftp-trace.ncbi.nih.gov/1000genomes/ftp/data/HG00239/sequence_read/
Lets say I'm trying to model a white blood cell. How do I know which parts of the genome get turned into proteins for that type of cell?

Sorry if anything I said doesn't make sense. As I said, my expertise lies in programming, not biology/genetics.


texts: What does it mean to "write an image and GIF into the DNA of bacteria"?

texts:
BBC News recently published an article saying that:

  An image and short film has been encoded in DNA, using the units of inheritance as a medium for storing information ...
  The team sequenced the bacterial DNA to retrieve the gif and the image, verifying that the microbes had indeed incorporated the data as intended.

The news article shows an image of a hand (shown above) and a short film (not shown here) of a horse rider that was encoded into the DNA "using a genome editing tool known as Crispr [sic]".

My question is, what does this mean? Did the scientists break down an image into 0's and 1's and (install?) it into bacteria?  How does a scientist (download?) an image into bacteria and then (redownload?) the image later?  How does DNA hold information of a picture that can be (downloaded)?


texts:
Why would the expression of an ancestral gene and comparing the product to a modern protein give misleading conclusions about heredity?

Update:
By ancestral gene I mean a gene which was used by an ancestor but than changed slightly through evolution, though it still serves the same purpose. And by the misleading conclusion I mean that using this similarity between the product of the ancestral gene and the modern protein as evidence that the organism is descended from the ancestor.


texts: Why does non-continuous sleep makes you feel tired?

texts: Let's say, hypothetically, that you fell asleep at 10PM, and you were woken up by a noise at 1AM. If you went back to sleep immediately and woke up at 6AM, you will feel tired even though you had slept for 8 hours. However, if you sleep for 8 hours straight , your body will feel rejuvenated. Is it because of REM sleep being cut off and restarting again?


texts: How do animals perform detailed active camouflage?

texts:
We often see videos of octopuses and chameleons changing their color to suit their surroundings. If it was a simple color change from white to red, it'd be understandable, but some of these animals can change colors while incorporating a lot of detail.

How do they process so much information and mimic it. Is this a subconscious action, or do they actually draw a picture in their head and then 'print' it on their bodies? Does this ability come from birth or does it get better over time?


texts: Are pheromones capable of activating changes to the Phenotype of a complex organism?

texts: I know that pheromones are means of communication between the same species, but are they capable of changing the phenotype of an organism, may be influencing the expression of the genes of a said organism.


texts: Why does uterus have to be prepared every month for fertilization?

texts: I'm just curious why it has to happen every month when the uterus could have been prepared from the beginning and kept that way throughout life or till a certain point. But why make and break it every month? (The breaking of this preparation is the cause of menstrual pain, which is what I'm worried about).


texts: What is the role of gills in terrestrial Crustaceans?

texts: Why do Crustaceans that live on land have maintained their gills? In aquatic species, the gills play a pivotal role in respiration, but terrestrial crustaceans have tracheal lungs. So why do they have gills?


texts: What's the determinant of the male-biased birth sex ratio in humans?

texts:
Will the baby be male or female? If it was a random biological switch then, with a huge sample number, the sex ratio at birth would be exactly 50-50. But it isn't; the ratio is about 51-49 in favour of males. So how does this inequality arise?

Further to @Remib's comments. I was specifically thinking of the sex ratio in humans. Would it be true to say that the genetic determinant of the sex ratio would be exactly 50:50 M/F? If the disparity is environmental, then how does it work, and wouldn't an environmental effect be more variable than the 51:49% that we see?


texts:
The electron transport chain in aerobic bacteria functions by pumping H+ out of the cell to establish a concentration gradient.
So if the bacteria are placed in a buffer solution having pH equal to the cytosolic pH of the bacteria, will they still be able to establish the required concentration gradient? Will the increase in pH of cytosol(due to loss of H+) alone be enough to drive ATP synthesis even in the absence of a pH change in the medium? i.e.Will obligate aerobic bacteria die if placed in a buffer solution even in the presence of oxygen?


texts:
I understand that the imidazole ring in histidine is aromatic. I also realize that it retains it's aromaticity when protonated.
I am wondering why it is not mentioned at all in basic text books such as Lehninger? Also, across the web there are a number of places claiming that histidine isn't aromatic in all cases.
Another reason I am a little confused is, if protonation doesn't harm the aromatic nature, then why is histidine such a weak base?
Am I missing something?


texts: Pituitary giants - is the fusing of growth plates dependent on amount of growth hormone in blood?

texts:
I wanted to ask a couple questions related to pituitary giants (people who are giants because of some anomaly, such as a tumor, in their pituitary gland).

Some of these giants seem to keep growing and growing until the tumor (or the gland) is removed. Is this because the fusing of the growth plates is controlled by the amount of growth hormone in blood?

The reason for this question is that many of the giants have been described to grow past when the growth plates should probably have fused. For example (all heights in meter, m):

Bernard Coyne This giant is described as having been 2.36m at the age of 20, but 2.54m at the time of his death at the age of 23.
Edouard Beaupré At the age of 17, this giant was measured as 2.16m tall and at the age of 21, he was measured at 2.50m tall. At the time of his death, at the age of 23, he was listed (in his death certificate) as having been 2.51m tall and "still growing".
Väinö Myllyrinne This giant was 2.22m at the age of 21 but is described as having "experienced a second phase of growth in his late thirties", attaining a height of 2.51m by the time of his death at 54.
Adam Rainer This giant was, unusually enough, a "dwarf" at the age of 18, reaching a height of 1.22m. However he had a growth spurt afterwards, reaching a height of 2.18m at the age of 30 and 2.34m by the time of his death at age 49.

Also, in some cases the giant individuals facial (bone) structure changes as he/she ages. Considering that the human skull does not have any growth plates, or anything that would (as far as I know) put a stop to the skull bones response to growth hormone, can changes in face structure also happen to "regular" people who take growth hormones?


texts: What evolutionary advantages are provided by ovoviviparity?

texts: I read that some sharks are ovoviviparous.  What advantages and disadvantages are provided by this type of reproduction as opposed to egg laying and live birth?


texts: Scoring matrices (BLOSUM & PAM) in BLAST and other sequence-comparison programs

texts:
The Wikipedia page on BLAST states that:

  The scores are created by comparing the word in the list in step 2* with all the 3-letter words. By using the scoring matrix (substitution matrix) to score the comparison of each residue pair, there are 203 possible match scores for a 3-letter word. For example, the score obtained by comparing PQG with PEG and PQA is 15 and 12, respectively with the BLOSUM62 weighting scheme.

I do not understand how they got a score of 15 for PQG v. PEG. What is a scoring matrix, how is it computed, and how is it used?

Step 2 on that page is Make a k-letter word list of the query sequence: “Take k=3 for example, we list the words of length 3 in the query protein sequence (k is usually 11 for a DNA sequence) sequentially, until the last letter of the query sequence is included”.


texts: Should I use RNAseZAP on my bench and pipettes before RNA extraction?

texts: Should I spray RNAseZAP on my bench and pipettes before working with RNA? I am regularly using RNase at my bench and would like to work with RNA as well. Could traces of RNase on my equipment degrade my RNA?


texts: Simplest known form of aerobic glycolysis

texts:
What is the simplest known way that an organism performs aerobic glycolysis? In other words, what is the simplest known way known to convert glucose into $\ce{H2O}$ and $\ce{CO2}$, other than by burning it?

In general, the (relatively conserved) pathway is glycolysis $\ce{->}$ pyruvate decarboxylation $\ce{->}$ citric acid cycle $\ce{->}$ oxidative phosphorylation, but perhaps there exist simpler pathways with possibly a lower energy yield.

I am interested in a way to convert glucose into water and carbon dioxide under (near-)physiological conditions, with a reaction timeframe of 12 hours, give or take. Specifically, I'd like to get rid of sugar as tidily as possible, disregarding energetic benefits. In that sense, I am interested in the (bio-)chemistries of organisms, not in the energy yield.

I am aware, of course, that sugar is used as an energy source by organisms, and they generally want to accumulate it, or at least, decompose it as efficiently as possible. It may well be that the "shortcut" I'm looking for is not known.

Several publications sort of address this topic, but I haven't found a fitting answer so far. In fact, the closest research to what I'm looking for I've found is a publication from 1931 by Degering and Upson; they describe iron pyrophosphate as a catalyst for sugar oxidation. However, they work with far higher reaction times (up to about 3 weeks) and somewhat high temperatures (around 40-90 °C as opposed to 0-35 °C) than I'd like.

I've also tried looking for shortcuts within the pathways using KEGG database. Glucose is COMPOUND C00031 and is referenced in 32 pathways; I've looked at the Glycolysis pathway (map00010) and have found no pathway other than the generally known one.


texts: I am working on an enzyme activity assay using NADPH as a cofactor. The MSDS for NADPH Tetrasodium Salt, tells to store it in a place away from heat and light. Does this include UV light or just visible light? I was told that a pure NADPH stock solution (with pH 7 phosphate buffer as solvent) could be re-used after absorbing UV light at 340 nm, but based on my understanding of the MSDS it seems that shouldn't be the case. So my question is: could I reuse a sample of pure NADPH stock solution that was exposed to UV for my enzyme activity assay?


texts: Can telomere length maintenance be an answer to increased life span of human beings?

texts: Telomere shortening may prevent the development of cancer in human aged cells by limiting the number of cell divisions. However, shortening of telomeres impairs immune function and thus might also increase susceptibility to cancer.Hence if length of telomere is kept constant, wouldn't it lead to development of cancerous cells rather than increase of life span?


texts: RMSD during conformational transition in proteins

texts:
When I was investigating the differences between protein structures obtained by X-ray crystallography and NMR spectroscopy, I found the paper [1] compairing structures of several proteins resolved both with X-ray and NMR. The average root-mean-square deviation (RMSD) between NMR and Xray structures is 1.4Å (max. 3.6Å), and the average RMSD between different NMR structures for same protein is 0.4Å (max. 1.3Å). I've checked some proteins studied in this paper, and they are mostly within 100–200 residues long.

However, there are plenty of papers (e.g. [2], [3], dealing with similarly sized proteins) that base their statements about conformational transitions on structures with RMSD difference 1–2Å.

I wonder what is considered reliable RMSD between two structures to draw any solid conlusions about conformational transitions (e.g. upon ligand binding) as opposed to simple thermal fluctuations or perturbance caused by the method to obtain structure?

Of course, the best way (at least in my opinion) to distinguish actual conformational transition from thermal fluctuations is to measure its lifetime, but it is often not an option.

 Andrec M, Snyder DA, Zhou Z, Young J, Montelione GT, Levy RM. 2007. A large data set comparison of protein structures determined by crystallography and NMR: statistical test for structural differences and the effect of crystal packing. Proteins 69: 449–65.
 Grant BJ, Gorfe AA, McCammon JA. 2009. Ras conformational switching: simulating nucleotide-dependent conformational transitions with accelerated molecular dynamics. PLoS Computational Biology 5(3): e1000325.
 Kumaraswami M, Newberry KJ, Brennan RG. 2010. Conformational plasticity of the coiled-coil domain of BmrR is required for bmr operator binding: the structure of unliganded BmrR. Journal of Molecular Biology 398: 264–75.