Does the leaves of papaya plant help in increasing platelets in a case of dengue? In Kolkata and nearby regions, due to sudden and huge amounts of rainfall, there has been an outbreak of dengue, a disease spread by female Aedes mosquitoes. The outbreak has been so dangerous that dozens have already died in the villages.

A problem of this disease is that, the platelets in blood are decreasing abnormally. For example, a patient had 120 thousand platelets when checked at night, but when checked on the morning, it drastically reduced to about 20 thousand. This particular patient could not be saved.

Many people say that the juice of papaya leaves (leaves of Carica papaya) helps in increasing the platelets in blood. Some doctors say it's wrong, while others say that it does effectively help. Even tablets and powders have been made, but the confusion persists as to whether they are effective or not.

I could not find any good information on the net. Can anyone, with scientific arguments, answer this question?

So With some digging, I found some articles/presentations that provide evidence that fresh papaya leaf extract does increase platelet counts. The first link tested this in a rodent model and found that in the test group treated with the leaf extract, there were significant increase in platelet count and red blood cells (RBCs) from the control group. Here is the summary of their results trend from the paper:

Additionally, I found a Multi-centric, Double-blind, Placebo-controlled, Randomized, Prospective Study and a meta-analyses that supports the observation that papaya leaf extract does in fact show statistically significant increase in platelet count than that of the control groups. (Dengue fever causes platelet counts to plummet). [#2-3]
Below is the image of platelet counts from the Multi-centric, Double-blind, Placebo-controlled, Randomized, Prospective Study (2):

Fig. 1: Comparison of platelet count between two groups during different
timepoint

A good criticism of the meta-analyses on Papaya leaf extract is that something being statistically significant does not equate to clinically significant. But, the placebo-controlled, double-blind prospective clinical trial provides some evidence that in this case, it is actually clinically significant.

However, the mechanism by which this occurs is not well understood. According to the 4th article, "The secondary metabolite of plants origin makes up a vast repository of compounds with a wide range of biological activities". The presentation (5) states some possible mechanisms by which the extract can inhibit the Dengue virus/vector.

Does Carica papaya leaf-extract increase the platelet count? An experimental study in a murine model
Efficacy and safety of Carica papaya leaf extract in the dengue: A systematic review and meta-analysis
A Multi-centric, Double-blind, Placebo-controlled, Randomized, Prospective Study to Evaluate the Efficacy and Safety of Carica papaya Leaf Extract, as Empirical Therapy for Thrombocytopenia associated with Dengue Fever.
Dengue fever treatment with Carica papaya leaves extracts
Role of Papaya in Dengue fever, an evidence based Answer


How do harsh conditions cause an increase in the male birth ratio? I've heard that in harsh conditions more human baby boys are born than girls because a bigger ratio of them will die before reproductive age. But in which aspects of the random gene combination while conception can harsh conditions (and which of their characteristics) actually can make a difference?

Issues with the post

Sexual selection is a mode of natural selection where members of one biological sex choose mates of the other sex to mate with (intersexual selection), and compete with members of the same sex for access to members of the opposite sex (intrasexual selection). This question has nothing to do with sexual selection.

What do you mean by random gene combination? More globally I don't understand the last sentence.

As a consequence, I don't understand the question. IMO, the post should be closed as unclear. However, I can imagine a question that I would consider interesting. I am answering to the question Is it possible that selection yield to a sex-ratio that deviates from 1:1 at equilibrium? How does it relate to environmental conditions?.

Fisherian scenario

Evolution of sex-ratio under a standard Fisherian scneario is often refered to as Fisher's Principle.

Basics

In the vast majority of strictly sexual species, every individual has exactly one mother and one father. It means that at equal sex-ratio the average relatedness of all offspring and all males in the previous generation is equal to the average relatedness of all offsprings and all females int he previous generation. When the sex-ratio is biased toward more females (for example), males have on average a higher reproductive success than females. As a consequence individuals that produce more males will increase their fitness and will increase in fecundity. As a consequence, the adult sex-ratio will always go back to 1:1 (fifty-fifty).

Adult vs baby sex-ratio

Now, it is important to understand that the adult sex-ratio is not necessarily the same as the babies sex-ratio. If typically, there is higher mortality in males than in females (could happen depending on the species and the environment), then selection would favour a bias sex-ratio toward males in babies. The adult sex-ratio will in any case be 1:1

Kin/group selection (non-fisherian scenario)

See for example the case of social spider Aviles (1993).

What is good for the population?

Thinking about the same problem but thinking about what is good for the population (rather than for the individual). For the population, the limiting factor in the number of babies produced are often the females. As a consequence, it would be good for the population if the sex-ratio were biased toward females.

When can alleles that are beneficial for the population overweight what is beneficial for the individuals

Under a standard fisherian scenario this cannot happen though selection will increase the frequency of alleles that spread the best and not the ones that are good for the population. However, typically when the relatedness within the population is high enough (you should read about group selection and kin selection) such trait that are good for the population may evolve.

Recommendation

I recommend that you take some time an introductory class to evolutionary biology such as Understanding Evolution for example. It is fast and you will learn more and faster than what you can learn here with your question. I think I already gave you this suggestion a number of times.


Could humans and chimpanzees hybridize? In some cases two species can hybridize. For example, Tigers and lions can hybridize to produce "Ligers".

Would it also be possible for humans and chimpanzees (or any other species) to hybridize ?
If not, what would be the likely cause of failure?

Why do some hybridization matings produce offspring, like the Liger, and some not? What mechanisms prevent hybridizations?

The concept of a human/chimp hybrid is called a humanzee. No humanzees have ever been recorded despite the fact that sexual intercourse between humans and chimps have been recorded on several occasions. This suggests that male-human/female-chimpanzee is not capable of producing viable offspring, at the very least.

As to why, several reasons will contribute: humans and chimps have a different number of chromosomes, making cross-fertility unlikely (although animals with different chromosome numbers can and do breed so this isn't absolute). Humans and chimps are anisomorphically quite different (i.e. the ratios of limbs are different and so on) so it's quite plausible that the growth patterns are not compatible. I'm not aware of any exhaustive studies into reasons why cross-breeding is impossible but it's also quite plausible that there are changes in the chemistry of fertilisation, etc. that will limit cross-breeding.

I'd note, finally, that there's evidence from the X chromosome that the human line continued to have some level of interbreeding with chimps for some million years after the initial split (Patterson et al, 2005†).

†  I see that there are some later publications that have disputed the claims made in that paper. So I'll leave you to judge the merits of the arguments.


Can elephants trumpet when they have water in their trunks? I am writing a fun story about elephants and want to know if elephants can trumpet or at least, make noises when they have water in their trunks, like when they are drinking water. Thanks for your help!

I think no. Because the elephant uses its trunk to make noise and if the trunk is filled with water then there is no chance the voice would come out.


Are There Rules for How Proteins Are Formed? Proteins are formed by stringing together different amino acids.  Different amino acids have different properties (such as being attracted to or repelled by water, positively or negatively charged, large, small, etc.).

What I would like to know is if there are any rules or principles which determine how amino acids are strung together to form proteins?  If so, what are those rules and can anyone recommend any resources where I can learn more about this subject?

Thanks.

MORE DETAILS

Let me try and explain what I am trying to ask.  I understand that there are rules of grammar that I need to follow in order to put together a well formed English sentence.  I am wondering if there is something akin to that for stringing together amino acids in order to create a 'well-formed' protein. (I am NOT referring to how DNA codes for amino acids).

For instance, imagine that I wanted to create a new protein and I had a pile of amino acids at my disposal.  It seems to me that if I understood the principles and rules by which amino acid chains work then I could know which amino acids to string together and the order in which to string them together in order to create the particular type of protein that I wish to create.

This is similar to how I can string together letters and words to form well formed sentences or how I can string together well-formed sentences to create logical arguments.  There's a logic to how to form a sentence and a different logic for how to form an argument -- and it is possible to discern that logic by studying syntax and reasonable arguments.

I assume the same is true for proteins.  There must be some sort of logic or system for how amino acids are strung together -- some sort of connection between the 3-dimension, functional protein and the nature of the properties of the individual amino acids and how they are organized together.  What I am wondering is whether or not we have any idea what that system of logic is.

It sounds like your question is "what are the rules to protein folding?"

That's not the only way to read your question.

Protein Folding is a unique problem - a 1D sequence maps to a 3D object.  Since proteins mediate nearly all biochemical transformations and therefore mediate life's processes, protein folding one of the great unsolved problems in science today.

You can see in the example folded structure above there are helices and flat sheets of connected strands.  You can see below in the schematic alpha beta barrel motif of triose phosphate isomerase (TIM) how elegant these structures can be.

Although the combinations and overall organization of the beta sheets and the alpha helices are boundless, there are some unifying motifs in these structures.

Long ago, a couple of researchers tabulated the amino acids probability of being in alpha helices or beta strands.  The Chou-Fasman model is important in that it has approximately ~70% chance of detecting alpha helices and beta strands.  Its not a great accuracy but what's really amazing about these algorithms is that they show that local forces - the interaction of amino acids near each other in the sequence have something to do with the formation of at least alpha-helices and beta strands.

There have been pounds worth of papers written since then.  In general, statistical surveys of protein sequences have been able to identify folds or motifs by a long list of string and machine learning algorithms.  Hidden Markov Models and Bayesian profiles are popular. Of course all these are similar to Chou-Fasman in that they work on the sequence in short segments more or less.

For a while it was thought that molecular dynamics and other discrete simulations might help to solve protein folding by allowing long distance interactions to be involved.  Just simulating the entire protein molecule in a computer program as it moves into a folded conformation, but this has not proven to be possible for a couple of reasons: (1) it takes a long time for a protein to fold relative to the length of a tractable simulation (2) the forces involved in protein folding and molecular size scales are not really easy to simulate - they do not precisely simulate the forces and behavior experienced by molecules and they involve many more solvent molecules than most computations can involve - even today's server farms would get clogged up with respectable protein folding simulation.

Since 1994 the Critical Assessment of Structure Prediction (CASP) have provided an open competition every 2 years where 3D structures that have been determined experimentally is held from publication.  While its well attended a new class of algorithms showed up around 2000.  These algorithms work on the assumption that local forces are important to protein folding, but often incorporating molecular dynamics.  Using MD or statistics based on protein structures (see the RCSB for the repository), segments of the protein sequence are tested for structural tendencies.  chaining these predictions together, initial protein folds are put together.  Once put together long term interactions can assemble a protein structure.

BTW that is not to say that Protein folding is solved - the solutions that come out often produce a structure that is really similar to the final structure, but often there are substantial differences.

Just looking at the individual sequence there are no simple rules to decide how the protein fold - ultimately molecular physics of the individual sequence determines where the fold will go.

This is incredibly terse, but it could get you started.  Study of protein without any helices or beta strands is a topic in itself - they can be treated the same way as above.  Then there are also proteins who do not have a single fold, but are dynamic and flop around all the time, or only have a shape when in contact with a surface of some kind.  So there's even more.


16S rRNA and 5S rRNA datasets I need 16S rRNA and 5S rRNA (Gammaproteobacteria - E.coli) Secondary structure files in ct format.

I tried looking for them in different RNA databases, could not find one. Can someone tell me where to find such datasets?

Thanks in advance.

RNA STRAND v2.0 - The RNA secondary STRucture and statistical ANalysis Database
http://www.rnasoft.ca/strand/

16S rRNA: secondary structure file in ct format

http://www.rnasoft.ca/strand/show_file.php?format=CT&molecule_ID=CRW_00111&check_out_the=View+the+RNA+sequence+and+secondary+structure+for+molecule+CRW_00111

5S rRNA: secondary structure file in ct format

http://www.rnasoft.ca/strand/show_file.php?format=CT&molecule_ID=CRW_00573&check_out_the=View+the+RNA+sequence+and+secondary+structure+for+molecule+CRW_00573


Are genes on the 5' to 3' strand only? I confused myself during studying, and wanted to confirm something. Since transcription via RNA polymerases only takes place in the 5'to 3' direction, that would mean that that 5' to 3' strand is the only one that contains the information to be translated later into a protein or mRNA or w/e.

So then the 3' to 5' strand would NOT contain any genes, but just the base pair complement to them? Or am I thinking of the concept of a gene wrong?

Both strands have a 5' and 3' end. Some genes will be on one strand and some on the other. The coding sequence will always be 5' to 3', but RNA polymerase reads the template 3' to 5' to polymerize mRNA.


Active & passive transport question If an element, ion or molecule is found in a cell is it possible to tell which method of transport was used? for example if a hydrogen or sodium ion was found in the cell could you tell if it got there by diffusion, or facilitated diffusion, or endocytosis, pinocytosis etc? If not could you at least narrow down the number of transport methods it could have used?

I'm very interested in which substances are let throught the cell membrane and by which method.

Welcome to BioSE! As @Chris mentioned, transported atoms and molecules don't typically retain a record of their past history, so just by looking at a molecule in the cell you can't in general tell how it arrived in the cell (an exception might be proteins that have some chemical modification on them that allows them to be imported via a specific mechanism, such as the mannose-6-phosphate enzyme re-uptake system). In order to infer if a molecule typically enters a cell by a particular method, you will have to do several different types of experiments. I'll list a few off of the top of my head. Note to other SE contributors: since this is not my area of expertise, I'm not sure how feasible some of these experiments are, or how they are typically done, so please edit my answer to be more accurate!

Diffusion If you want to know if something can diffuse across a membrane, then the easiest way would be to try it in vitro. One way I can imagine doing this is to use a phospholipid bilayer to separate two compartments: one with your molecule of interest, one without. By measuring the concentration of your molecule that transfers from one compartment to the other, you can see if your molecule can diffuse across a lipid bilayer. Note that this will only tell you if diffusion is possible for your molecule. It may be that cells have ways to actively prevent your molecule from diffusing across your membranes, which you wouldn't be able to know from this assay.
Endocytosis or pinocytosis One way to assess if your molecule is taken up by endocytosis or pinocytosis would be to knock out (genetically or with an inhibitory drug) these processes in your cell and see if your molecule of interest still ends up in the cell. Depending on the context of the molecule you're interested in, you might be able to simply place cells in solution with your molecule of interest and measure the concentration of the molecule outside the cells over time. You could compare how much of your molecule is lost from solution when cells can't endocytose and compare to when they can; if your molecule stays around when cells endocytose, you have some indication that process is necessary. Note that there would have to be a lot of other controls for this experiment as well: e.g. ensuring the effect you observe is specifically caused by endocytosis being inhibited. Since endocytosis and pinocytosis form vesicle intermediates containing your particle of interest, one check to see if endocytosis might be reasonable is to see if you can see vesicles containing your molecule of interest in the cell. Of course, this requires a method for being able to visualize your molecule of interest (maybe it's fluorescent, or can be modified with a fluorescent marker? Or maybe there is a fluorescent protein that binds your molecule and can change color on binding? These things all exist, they just depend on your particular molecule and context).
Transport channels: In a similar vein, how does the uptake of your molecule change when you inhibit or remove from the cell a particular type of channel? You could measure this in a similar way as the bullet point above.
Active vs passive transport: If you wanted to see if uptake of your molecule requires active transport, you could try inhibiting ATP synthesis with a drug and see if transport of your molecule decreases over time. Note that this is in general not good for the cell (really!), so you might also have to have some more controls for this, maybe showing that transport of a molecule known to travel by passive transport is not affected on the timescale you're looking at, for example.

This list is by no means exhaustive, but I hope it gives you a sense of the type of experiments and ways of thinking you might be able to use to figure this out. Some general thoughts:

This tends to be case-by-case. While the type of experiments you might do to determine the mode of transport for different molecules are similar, the controls you will have to do to shore up your conclusions will really depend on the system involved, what type of effect a molecule has on your cells, whether your cell imports and exports this molecule, under what circumstances you might expect the cell to take up this molecule (so you have a way to trigger the cells to take up this molecule for your experiment). I don't know of a completely generic method for resolving this type of question.

Being able to measure abundance of your molecule is important. All of the experiments above rely on being able to measure the concentration of your molecule, either outside of the cell, or inside of the cell. This is often easiest if you can modify your molecule to be visualizable in a microscope or spectrophotometer, but however you do it, you need a good, reliable, robust assay in order to make strong conclusions with this assay.

Controls are really important. Thinking up all the different alternative possibilities and trying to come up with ways to rule them out is the heart of experimental science. Fortunately, it also happens to often be rewarding and thought-provoking! I certainly had fun thinking about this.

Best of luck!


What percentage of twins has the same gender If 30% of all twins are identical twins, what percentage of twins has the same gender? I thought: all identical twins have the same gender so it’s at least 30%. And of the non-identical twins it’s about 50%. So 50+30=80%?? Correct me if I’m wrong..?

You stated:

30% of twins are identical
50% of non-identical twins have the same gender

Therefore 70% of twins are non-identical and 50% of those will have the same gender. I'll leave the rest of the calculation to you.


Richard Goldschmidt's “systemic mutations”? [TLDR] I dont understand the fault people had/have with Richard Goldscmidt's concept of systemic mutations [/TLDR]

As a preface, I am a undergrad biology student, so sorry if this is a "Stupid question".

How does Richard Goldschmidt's concept of systemic mutations, reject the classical gene concept, why were biologists so against it?

From what I  understand he used the concept of systemic mutations and developmental macromutations in his lectures to explain how macromutations could cause speciation(macroevolution?). The results of the developmental macromutations, if I understand him correctly would be then the Hopeful Monsters?

And from what I have read on a timeline of his work, systemic mutations describe the "large rearrangments of the chromosome", with a new arrangement meaning a new phenotype?

How is that wrong though? Do chromosomes not have rearrangements via cross over events during meiosis or via transposable elements? Or is he referring to something else, since I understand at the time, meiosis and TE's were not understood well.

The source i was reading from was:
(Richard Goldschmidt: hopeful monsters and other 'heresies' by Michael R. Dietrich) Available from http://www.dartmouth.edu/~dietrich/NRG2003.pdf

His notion of systemic mutations involved the postulation of massive chromosomal rearrangements (not mere recombination/crossing-over) as mediators of speciation in one-step. While whole genome duplications have been shown to induce speciation (see, for example, cryptic speciation in Hyla versicolor) they are not large scale rearrangements as he suggested. Additionally, while there is evidence for multiple large scale chromosomal arrangements at once in cancers (Chromothripsis) , there is no evidence of a similar process resulting in immediate reproductive isolation.


Why does increasing the space constant increase conduction velocity in myelinated neurons if nodes of Ranvier are constantly spaced? If depolarisation at one node of Ranvier triggers, by passive conduction, an action potential at the next node of Ranvier, why does increasing the space constant increase conduction velocity? Surely the locations of each action potential are pre-determined by the sites of the nodes of Ranvier? Is it simply the rate of the passive conduction that changes?

I think the simplest answer to your question is that you're correct in thinking passive flow would be what changes, but the reason behind it is important to understand.
I'd recommend looking at UT Health's neuroscience online resource where they break down action potential propagation in an understandable way. The main takeaway is that the space constant is determined by a number of different physical characteristics of the neuron/axon. You can find these characteristics at the link I provided, but the three parameters that define the length constant are diameter of the axon (d), membrane resistance (Rm), and axial resistance (Ra).
Starting with Rm (because you allude to myelin in the question), this is dramatically affected by myelination. An internode (the myelinated portion of an axon in between nodes of Ranvier) has an excessively high Rm, which just means that current doesn't readily flow across the membrane, so current doesn't "leak out" while it's passively flowing down the axon here. Therefore, increasing Rm by lengthening internodes would help increase the distance across which current can passively flow in the axon (which increases the space constant). Shortening internodes would have the opposite effect. However, you seem to be asking "All things with myelin remaining the same, why would a higher space constant increase conduction velocity?"  That's where d and Ra come in. I explain these below:
The values of d and Ra are somewhat linked. Basically, a high the value of d allows passive current to flow more easily along the axon, meaning it has a low value of Ra. So in the context of your question, if you had an axon and theoretically doubled the axon diameter (so from d to 2d), Ra is cut in half (so from Ra to Ra/2) and passive conduction can speed up. This would increase the space constant by its effect on passive conduction. The converse is true if you shrink the axon diameter. However, it's important to realize that Ra can also be affected by other factors like the contents of the cytoplasm in the axon. That is why both are used to calculate the space constant even though they relate to one another.


Measuring the Rate of Photosynthesis Update: I have just received a grant to pursue this research.  However, I must still perform the preliminary experiment described below before dipping into my very limited funds.  Thank you for any ideas.

What are some accurate methods to measure the rate of photosynthesis that can be performed without access to a professional laboratory?

I am a citizen scientist who is designing a experiment to measure the rate of photosynthesis under different conditions.  Although this idea stems from my interests as an amateur horticulturist, it has grown to into something of real scientific potential.  However, I must conduct this experiment on a low budget without access to a professional laboratory.

Furthermore, I should note that it is almost impossible to quantify photosynthesis by measuring gas emissions in this scenario. The only way to keep the plants in a stable environment with equipment that I can afford is in an open, climate controlled room, (as opposed to a closed testing chamber that could trap gasses).

Any ideas on how to measure the rate of photosynthesis would be greatly appreciated.

One of the simplest measures of photosynthesis is just measuring how much your plants grow (i.e., weigh them). Of course this technique is imperfect because of other influences on growth, the amount of time you have to wait to get a measurable change, and ideally you would want to use the dry mass of your plants to avoid water content differences, but you have opted to exclude the methods that get around those problems.


What is the term for "technical extinction" of yet alive animals? What is the term for an event in which a species is still alive, but has no chance of future reproduction and the species will be considered extinct once the current generation dies out?

For example a species of a tiger that has the last 5 surviving members left and which are all related and all male. Hence, even though they are still alive, there is no chance that the species will be able continue their bloodline and hence are already "technically" extinct.

This is technically called Functional extinction. With no viable reproducing population the species will almost certainly become extinct. Note that humans could potentially mess with this through the use of reproductive technologies.


Electron Transport Chain in Mitochondria I was researching cellular respiration, and this is a rather confusing part. I need help understanding the purpose of Complex II and how the ATP Synthase generates the energy to turn ADP to ATP.

The good ol'electron transport chain (ETC).

Before beginning let us begin by looking at the structure of a mitochondrion and the purpose of the ETC.

(source: tokresource.org)

Take of note four things:

The intermembrane space
The matrix
The electron transport chain proteins and
ATP Synthase

Now lets talk about the purpose of the ETC, essentially its job is to create a H+ (proton) gradient between the intermembrane space and the matrix it does this by taking protons from the matrix and "pumping" them out to the intermembrane space.

This creates a higher concertation in the intermembrane space and lower concertation in the matrix. This gradient will result in a process called chemiosmosis where these H+ ions (protons) will go through ATP synthase on the inner plasma membrane in order to return to the lower concentration in the matrix.

So the most important thing to note about this is that the flow of protons through the ATP Synthase is what gives it the energy necessary to create ATP.

Alright now that is out of the way lets discuss how the ETC goes about pumping these electrons out of the matrix into the intermembrane as well as how ATP Synthase works.

If you were to zoom into the area that is labeled electron transport chain proteins (that I told you to note) you would see something like this.

What we see here is that ETC is actually made up of a series of complexes (I, II, III, and IV) and a couple of "electron/reaction" carriers (ubiquinone and cyt c). These complexes and carriers are in charge of moving an electron via a series of redox reaction along resulting in the "pumping" of protons out the matrix at each complex.

*Note, understanding redox reactions help in understanding what is happening here.

The chemistry gets a little intense at this point, so I'm going to quote and link the Wikipedia article on this, which does a wondrous job explaining what occurs complex to complex.

  In Complex I, two electrons are removed from NADH [the electron carries from the previous steps] and transferred to a
  lipid-soluble carrier, ubiquinone (Q). The reduced product, ubiquinol
  (QH2), freely diffuses within the membrane, and Complex I translocates
  (pumps) four protons (H+) across the membrane, thus producing a proton
  gradient.

Note, that in Complex II no protons are pumped into the intermembrane.

  In Complex II additional electrons are delivered into the quinone pool (Q) originating from FAD [Again, electron carriers from previous steps].

Complex III receives the reduced ubiquinones from Complex I and II.

  in Complex III, two electrons are removed from QH2 at the QO site and sequentially transferred to two molecules of cytochrome c, a water-soluble electron carrier located within the intermembrane space. The two other electrons sequentially pass across the protein to the Qi site where the quinone part of ubiquinone is reduced to quinol. A proton gradient is formed by one quinol (2H+2e-) oxidations at the Qo site to form one quinol (2H+2e-) at the Qi site. (in total four protons are translocated: two protons reduce quinone to quinol and two protons are released from two ubiquinol molecules).

Finally

  In Complex IV, four electrons are removed from four molecules of cytochrome c and transferred to molecular oxygen (O2), producing two molecules of water. At the same time, eight protons are removed from the mitochondrial matrix (although only four are translocated across the membrane), contributing to the proton gradient.

NADH+H+ → Complex I → Q → Complex III → cytochrome c → Complex IV  → O2

Article here

So after all this beautiful chemistry we are left with a proton gradient. This is when ATP Synthase comes into play. Once the proton "flows" through it will bind ADP and inorganic phosphate together to form ATP.

energy + adp + pi → atp

More on how the ATP Synthase works here

This is water down in the actual chemistry portion of it but I feel like it will give you a better grasp on how it all works. If you have anyways especially regarding the series of reactions between complexes feel free to ask!


Synaptic pruning and selective elimination during adolescence How does Synaptic pruning occur during pre-adolescence, adolescence and post-adolescence, after there is blooming overproduction of synaptic connections until the years of late childhood, and how does during this stage of brain development, "selective elimination" of synaptic connections occur, which is depended on the activity of synapses which are involved in  primary functions?

Also, why, how and to what extent does the brain, after approximately age 6, receive the urge to cut back certain synapses?

Update 1: what exactly is triggered before and during adolescence, so that the brain receives the urge to perpetrate synaptic pruning? I know how synaptic pruning is carried out, I am however very intrigued in the specific processes that occur, from the signal that the brain receives to do it, to why exactly it occurs in such an early stage of life

An answer to this question could potentially be found in "Understanding Adolescent Brain Development and Its Implications for the Clinician"

  Thanks to research by Jay
  Giedd and colleagues at the National Institute of Mental Health, it has become
  clear that, during the adolescent years, the organization and functioning of the
  brain go through complex changes. Importantly, these changes seem to be unique
  to the adolescent years and not simply the trailing remnants of childhood brain
  development.

Changes in frontal lobes during adolescence

  Frontal lobe gray-matter volumes,
  which represent dense concentrations of neurons and their parts, increase
  throughout childhood and do not reach their peak until approximately the age of
  11 (girls) or 12 (boys), at which point they decline throughout the second decade
  of life and into young adulthood.

So why might frontal lobe gray-matter volumes go up during childhood and down
during adolescence?

  Recent data suggested that, during childhood, neurons in the
  frontal lobes are allowed to overgrow and form far too many points of communication,
  or synapses, with other neurons. As a result, gray-matter volumes
  increase. As childhood draws to a close and adolescence begins, the brain
  switches from overproduction mode to selection mode. Early in the second
  decade of life, the brain stops overproducing synapses in the frontal lobes and
  puts the synapses that exist on the chopping block. Hundreds of billions of points
  of communication will be sacrificed through the teenage years. Only those that
  form meaningful, useful points of contact will be kept. Guided by a teenager’s
  experiences, the frontal lobes are shaped and molded into a configuration that
  will carry the individual, for better or worse, through the adult years. As this
  pruning process unfolds, gray-matter volumes decrease.

Changes in other parts of the cortex (specifically temporal lobes)

  The temporal lobes, which are critical for memory formation as well as processing
  auditory information and seeing detailed patterns and shapes, do not reach
  their maximum levels of gray matter until the age of 16 to 17, at which point they
  plateau. The temporal lobes contain the hippocampus, a structure that is central
  to creating an autobiographical record of what one does and what one learns.

Sources:

White, Aaron M. "Understanding Adolescent Brain Development and Its Implications for the Clinician." Division of Medical Psychology, Department of Psychiatry, Duke University Medical Center, Box 3374, Durham, NC 27710, USA, 2009. Web. 7 Feb. 2016.
Steinberg, Laurence. "A Social Neuroscience Perspective on Adolescent Risk-Taking." Developmental Review : DR. U.S. National Library of Medicine, 28 Mar. 2008. Web. 07 Feb. 2016.


How many times have the cells in a human body divided? Every single cell in a multicellular organism can in principle trace its "ancestry" back to the zygote through a continuous chain of cell divisions. How many divisions have occurred in a typical cell in an adult human body since the zygote was fertilized?

Obviously the answer depends on the organism's age and on the type of cell (as different types of cells divide at different rates). To be concrete, what is the average number of cell generations from the zygote across all the cells in, say, a typical 25-year-old human?

(Or any other age, if that's more convenient to estimate. I'd also be curious about the approximate minimum and maximum number of divisions, and which types of cells they occur in. If it's too difficult to estimate these statistics over the whole organism, I'd be interested to know if there are any specific types of specialized cells for which it's possible to estimate the "generation number".)

To be clear, I'm not asking about the maximum number of times that a cell can divide. I'm asking about the average number of times it has divided at a given point in time.

The supplemental material of the paper that Dirigible references in a comment to my question gives a rough estimate of these values. If I understand their simple model correctly, then we can estimate the average number of times that the stem cells in various types of tissues have divided over an 80-year lifespan from Table S.1 by finding the row corresponding to a cancer of that tissue, and then calculating $\log_2(s) + d$, where $s$ and $d$ are given in the table. (For specialized cells, I guess you'd add 1 more to capture the final cell division that produces the specialized cell?)

I haven't done the math out, but glancing over the table, it looks like the generation number varies widely between tissues, from a low of about 27 for some brain cells to a high of almost 6000 for cells in the colon and rectum.


How can one accurately diagnose the cause of human hearing loss without surgery? In a human, if you were to avoid a tympanotomy (surgical examination of the middle ear), how could you distinguish between a blocked Eustachian tube, a ruptured eardrum, or a perilymph fistula?

For instance, take the situation where a young man (suffering from a common cold) blew his nose violently, became dizzy for 1 minute, and then reported loss of hearing in one ear of about 40%.  What would your diagnosis be, possible treatments, and expected outcome?

I am not an ENT doctor, but I think the following diagnoses would suffice to determine each of the conditions:

Blocked Eustachian tube: Complaints would be of sudden onset and likely associated with a common cold, or ear infection. Providing the patient with standard decongestant should provide quick relief.
Ruptured eardrum: Patient should have subtle hearing loss apparent on audiogram and it would be relatively easily identified by routine otoscopic examination.
Perilymph fistula: This condition is hard to diagnose and I quote from Vestibular Disorders Association:

  A physician can arrive at a presumptive diagnosis [of a perilymph fistula] through a thorough probing for events close in time to the onset of symptoms, along with a variety of tests. These tests can include hearing tests (audiogram, ECOG), balance tests (VNG, VEMP) and some form of a “fistula test.”

The periplymph fistula is by far the most severe condition and the one with the most prominent effects on the vestibular system (balance). Multiple tests and rigorous medical exam is necessary.

With regard to your presented case study: Again, I am not an ENT doctor but a ruptured ear drum can result in dizziness due to the fact that one inner ear is exposed to cold air due to a rupture and the other ear is not. Unilateral inner ear cooling can result in dizziness. However, blowing your nose is unlikely to cause a ruptured eardrum as it is generally caused by more serious barotrauma (diving accidents and in-air plane cabin pressure malfunctions) (Web MD).

Similarly, the fistula is most often caused by more serious traumatic injuries (Vestibular Disorders Association).

A blocked Eustachian tube sounds the most plausible, as it is associated with the common cold (Web MD). Violently blowing your nose can cause fluid to travel up the middle ear, and possibly cause subsequent infections.


Cis-AB phenotype verification I know that my blood type is AB. I wanted to know if I am cis-AB since cis-AB seems to have a different approach in blood transfusion.

Is there a lab test that can verify is a person is under cis-AB blood group phenotype?

First,do you have any probe that your type is AB chimera transferase? I discovered it because my mother is type AB and my brother type O. I have 2 sisters and my self cis-AB (my younger sister and me rh-). If you carried a cis-AB allele and another allele was  B1, surely you got A and B type compatible, but if you carried an A1 or O1 allele, surely you got O type compatible or worse luck. For example, I have a very rare multi-blood genotypes (rh D- C-G-, K1-, M+N-S+s+ and another unknown antigen). Actually, it doesn't matter if you are cis or trans AB phenotype, the most important thing is to know if another 34 blood groups and 200 minor groups and 600 blood antigenes have a rare combination that makes blood incompatibily or autologous like Bombay phenotype or autotransfusion like me.
If you want to be sure about your genotype, you must make dna test with SNPs of 10 cis-AB alleles


Longevity and extent of transfection after SARS-COV-2 vaccination with Janssen The Johnson vaccine, unlike the RNA vaccines from Pfizer & Moderna, uses a vector containing DNA encoding for the SARS-COV-2 spike protein. This vector DNA needs to enter the cell, allowing for transcription and translation into viral spike proteins to occur (Fig. 1). These spike proteins are then exposed on the cell surface by the host cells, thereby exposing the antigenic epitopes, creating the immune response.
Basically, this turns the immune cells against their own host, because they are expressing foreign proteins on the cell surface. In effect, I presume, those host cells are subsequently destroyed by the immune system.
Now I was wondering if there has been any research done revealing the consequences of this auto-immune response. In particular how long does it take to get rid of all the transfected cells (or 'vaccinated cells' as they tend to be called) and what is the extent (volume/area affected) of transfected cells? Basically you are genetically altering the host's cells  that are subsequently attacked by the immune system. So I am basically interested in the pharmacokinetics of the vaccine I guess.
This safety report from EMA says that in 1 animal (from how many?) there was still genetic material after 180 days to be detected. However, the report says nothing about the extent of transfected cells nor anything about the auto-immune damage after the host attacks its own cells. No references are to be found either; it all seems to be about internal safety studies.
In retrospect I'd rather not have had the Janssen vaccine; I bet mRNA vaccines are a lot more instable, guaranteeing safe removal of the foreign genetic material.
Anyway, I'm drifting... In short, (1) how long does it take to clear all signs of foreign DNA from the host after Janssen, and (2) what is the extent of the cells that are transfected and subsequently attacked and damaged/killed by the host?

Fig. 1. Schematic depiction of the DNA vaccine from Janssen. source: Livingstone et al. (2021)
References
- European medicines agency, Assessment report COVID-19 Vaccine Janssen
- Livingstone et al., JAMA (2021); 325(15): 1575

Both the AstraZeneca (AZ) and Janssen (J) vaccines against SARS-CoV-2 work by using what is known as a viral vector to generate an immune response. In both cases these vaccines use an Adenovirus as the vector (vector in this case means "carrier").
Adenoviruses are a family of double-stranded DNA viruses, most commonly known for being one of the causes of the illness known as the "common cold". There are about 88 human serotypes (how people's bodies react to the virus, different serotypes may not cross-protect by raising an immune response)  of the virus divided over the seven species: Adenoviruses A-G. Overall there are about 50 species from a wide range of animals. Because of the diversity and the abundance of the "common cold" most people will have some immune response to at least some of the human adenoviruses.
Adenoviruses are good vectors for vaccines and for other therapeutic uses such as oncolytic viral therapy because the genomes are easily modified and can be made replication incompetent very easily. To do this essential replication genes are removed and the viruses are replicated in cells that provide the essential proteins for the virus to complete its life cycle, so that you get a viral particle that no longer contains the full genome. These viruses are also tolerant of additions to the genome so they can be used to produce proteins that are not normally found in an adenovirus.
On the other hand the adenovirus component of these vectors can cause its own immune response, lowering effectiveness of the immune response to subsequent vaccines developed using the same or a similar sero-type virus.
The AZ vaccine is based on a chimpanzee adenovirus. The J vaccine on the other hand is based off serotype 26 (Ad26) of the human adenoviruses. In both cases the adenovirus is rendered replication incompetent by removal of essential replication genes.
For adenoviruses to work as vaccines they need to invade a cell and then insert their DNA into the nucleus (as seen in the diagram from OP), where cellular mechanisms produce lots of mRNA copies of the gene(s) and concomitantly produce proteins from these mRNA. These proteins are then translocated to the surface of the cell (this is a natural process).
However, in the process the viral DNAs and proteins are recognized by the cell as non self and trigger the innate immune system causing antigen presentation and activation of the adaptive immune system. This whole process is a natural response of the body to infection and does not result in "self recognition", so there is no auto-immune response to the cellular proteins.
Both the AZ vaccine and the J vaccine are administered intra-muscularly, which is very typical for vaccines. Intra-muscular injection is a good site for injection because it can tolerate a big volume and has a relatively high blood flow (both compared to sub-cutaneous (sub-skin)). However, once injected the virus doesn't necessarily stay in the muscle, it can travel in the blood and a portion will end up in other locations, particularly the liver and alveoli of the lung (places where there is a big blood supply and lots of small blood vessels). The adenovirus can infect any cell that expresses the cellular receptor called Coxsackievirus and Adenovirus Receptor (CAR) on its surface, which includes immune cells. There's a fairly comprehensive review of all the mechanisms and cell types here, but it is in written for the scientist. Here's a suitable quote about cell types:

The cell types present when vaccine is administered i.m. include myocytes, skeletal muscle cells, fibroblasts and endothelial cells, with APCs such as DCs or macrophages representing a minority when compared with the abundance of murine skeletal muscle cells

How long the viral genome persists depends on the paper, but not many people have looked. The data I could find seem to indicate that most protein expression is lost after about 3 weeks, but it may persist longer. e.g.:

Although Ag expression could no longer be detected 3 wk after immunization, examination of Ag presentation within the draining lymph nodes demonstrated that APCs were loaded with Ag peptide for at least 40 days postimmunization, suggesting that Ag remains available to the system for a prolonged period, although the exact source of this Ag remains to be determined.

However, the genomes seem to persist for a very long time, perhaps as much as a year or more:

By days 30 and 90, vector sequences remained detectable in most animals in these tissues but gradually declined 102 to 103-fold. After 1 year, relative copy numbers in liver and the injected muscles were comparable with those seen on day 90, whereas a further decline was seen in spleens.

Note that both of the quotes above are not about either the Janssen or AZ vaccines, but about adenovirus vaccines in general, and several Ad vectors were tested in both. It is highly likely that the AZ and J vaccines will have similar data.
Edited to add: I don't know why the DNA persists for so long, but it does not integrate into our genome. It seems that most replication deficient adenoviruses lack the E1A gene, which allows induction of the cell cycle and frees up resources for viral replication. However, the genes involved in viral DNA replication are E2A and E2B, so are not included in the deletion.
TLDR: Viral genome can persist for a very long time, but protein expression does not - possibly because the immune system deals with it quickly after a few weeks (effective vaccination...). The vectors can reach and infect many tissues in the body, particularly ones with high blood flow and lots of small blood vessels such as lungs and liver.


Estimation of cases with dominant inheritance I am reading [1] and I didn't understand this passage:

  All bilateral cases should be counted as hereditary because the proportion of affected offspring closely approximates the 50% expected with dominant inheritance.

Shouldn't the percentage be 75% with dominant inheritance?

[1]: Knudson, Alfred G. "Mutation and cancer: statistical study of retinoblastoma." Proceedings of the National Academy of Sciences 68.4 (1971): 820-823.

It depends on the genotype of P (parents). If only one parent carries the dominant allele, F1 will have the allele 50%.

D = dominant allele, d = recessive allele

P: dd x Dd

F1: Dd 50%, dd 50%


Difference between Category, Rank and Taxon Is there any differences between the terms Category, Rank and Taxon or they all are same?

I remember an explanation which goes on like this:

Category and Rank are the same and are the categories of taxonomic heirarchy whereas taxons are the organisms present in those.

Is this correct?

A taxon (plural taxa) is any taxonomic unit. For example, the class Mammalia is a taxon which includes all mammalian species. Similarly, a species is a taxon, Panthera tigris being the tiger. This taxon contains lower taxa, which are sub-species, such as Panthera tigris tigris (Bengal tiger) or Panthera tigris sumatrae (Sumatran tiger).

Rank is simply the level of a taxon in the taxonomic heirarchy. For example, the taxa Mammalia and Aves both have the same rank since they are both classes. Panthera tigris sumatrae is of a lower rank than Panthera tigris because the former is a sub-species and the latter a species. Use of the term rank is only truly meaningful when comparing two taxa.

Taxonomic category is usually – for better or worse – used interchangeably with the term taxonomic rank. A Dictionary of Biology (6 ed.) certainly indicates that the terms rank and category are equivalent. The major taxonomic categories are domain, kingdom, phylum, class, order, family, genus, and species. A category can contain one or more taxa.

Another example, to summarize:

Carnivora is a taxon, which contains many species including Vulpes
vulpes (red fox)
Carnivora is in the category of order
Carnivora (order) is a higher rank than Vulpes vulpes (species)


Gastric and intestinal gas exchange A very long time ago, I happened across research into using an oxygenated liquid in the stomach and or intestinal  cavity.  I wondered what further results came about of that research, and am having difficulty finding anything on it.   Is anyone aware of it and it and or  can point me to articles and or research papers done?

Intestinal gas consists of ingested air and gas formed during digestion. Stomach gas consists of  15% oxygen and 7% carbon dioxide approximately; the remaining is nitrogen.
The air that we breathe contains about 21% oxygen; thus some of the swallowed oxygen is absorbed through the blood capillaries present in stomach. Carbon dioxide is synthesized by digesting food using gastric juices. Nitrogen is not absorbed.
The small intestine absorbs some amount of carbon dioxide and oxygen. And the remaining gas is passed further to the large intestine. In the large intestine,  most of the oxygen is removed and carbon dioxide is increased. New gases are produced mainly hydrogen because of bacterial fermentation. And these gases are absorbed by blood and later released via lungs.
Check out following links:
https://katesalevelbiology.wordpress.com/2017/02/14/human-gas-exchange-the-digestive-system-and-breathing/
https://www.gastrojournal.org/article/S0016-5085(19)33654-6/pdf
https://journals.physiology.org/doi/abs/10.1152/ajplegacy.1926.76.1.92
https://nyaspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1749-6632.1968.tb19024.x


Why do some bacteria have an asymmetric replication? Our teacher said that Bacillus subtilis has an asymmetrical replication fork.

I know that this happens only in some strain of the bacteria . She asked us to find an explication for this mechanism , but all that I was able to find is that the chromosome is more compacted in some areas, therefore it slows the replication .

Are there other reasons?

The replication fork itself is always asymmetric. This is true for all organisms and is due to the fact that DNA polymerases can only add nucleic acids to the 3'-OH end of DNA. This leads to different mechanisms for the replication of the so called leading and lagging strands. You can find more details on wikipedia https://en.wikipedia.org/wiki/DNA_replication

Most Bacteria have circular chromosomes that they usually replicate using two replication forks. Both forks start from the origin of replication and progress in opposite directions to meet at the replication terminus which is opposite to the replication origin on the circular chromosome. Each replication fork replicates about half of the chromosome. We talk about the left replicore and the right replicore. I assume that your teacher was referring not asymmetry in the replication fork itself, but to asymmetry in the size of the replicores. In B. subtilis the left replicore is 196 kb longer than the right replicore (J Bacteriol. 1993 Feb; 175(3): 741–749.). I do not know whether there is any evolutionary explanation for this, but mechanistically it is caused by the fact that the terminus of replication is not placed opposite to the origin of replication on the circular chromosome.


Does dormant poison ivy contain urushiol in the above-ground portion of the plant? I recently had a run-in with poison ivy (late spring; Canadian shield).

The poison ivy plants had not yet leafed-out so I failed to identify them as a hazard.

I think I must have either trampled and broken the stems of the plants, or dug up and broke the roots (or both), and therefore was exposed to the poisonous sap.
While the plants had not leafed-out, they were also not truly dormant (it wasn't the middle of winter).

Question:

I'm wondering if there is a time of year when the above-ground portion of poison ivy plants would not contain urushiol.

In other words, in the dead of winter, when the plants are dormant, do poison ivy twigs contain the poisonous sap?

Let's tackle your second question first. Yes, leafless poison ivy still contains Urushiol, and still can give you a rash. Here are three sources supporting this statement: a first-aid sales company, a newspaper, and a non-peer reviewed infosheet from a university. Be careful with poison ivy all year.

Your first question has slightly more nuanced implications. To know if there is a time of year where above-ground poison ivy doesn't contain Urushiol, first we have to think about when and where the urushiol is produced in the plant cell, where it is stored, and how it degrades. Some studies have shown that Urushiol and like compounds are present throughout the plant. In this older article, they extract it from both the leaves and the twigs, but more current advances have been able to focus on urushiol in just the stem. I have seen no evidence that it reduces at any time of year, and very little publication on how it is produced biochemically, although people are working and have worked on the topic. I am interested to learn more about this aspect from other answers to this question.

(An aside: you can also pick up a Urushiol rash from some cheap furniture, so this compound can stay poisonous on a wood surface for quite a while. Unfortunately, I'm speaking from first-hand experience, which is backed up by this informative article about Urushiol!)


Can HIV be transmitted via breastfeeding? If a pregnant women is HIV positive and she is treated with medicines to deliver a normal child,can she transfer the HIV virus back to her normal HIV free child by colostrum?

Yes, it is possible and the chances are pretty high. According to the WHO paper linked below, the rate of partially or completely breastfed children which get infected by this route is about 20-35%, while the rate of children which are not infected and doesn't get breatfed is zero (no surprise here).

The mechanism by which this infection occurs is currently unknown, but it is hypothesized that the virus enters via the mucosa. See these two articles below for more information:

A review of HIV transmission through breastfeeding.
HIV transmission through breastfeeding : a review.


Why do peas change colour? I am doing an experiment on preservation of peas.

The first notable change to the peas over a period of one week is that they have changed colour from bright green to a dull colour... Why is this so?

The only test tube which did not have peas which changed colour was the one which was kept at 4 degrees Celcius in a fridge, so it probably has some relation to temperature...

Many thanks

N.B.: I know that the bacteria reproduce and could use the pea as their source of food, but how do they have any relation to the colour of the pea? I also put the tag "bacteria" and "thermodynamics" as I couldn't find any other related tags.

Chlorophyll is a dye that makes leaves green, it plays a key role in photosynthesis. It is present also in unripe fruits, young peas etc. Maybe I should say chlorophylls, because it is a group of similar chemicals. They get degraded by heat.

(No assistence of microbes needed).

Bonus: Chlorophyll contains magnesium at the molecule core, which facilitates the green color. There were some creative people, who were upset, that the canned cucumbers are not green enough, so they added some copper-containing molecule during canning. It replaced magnesium and was more stable, so beautiful bright green cucumbers were on the market for a while. However, they turned out to be slightly poisonous and are not sold anymore.

Bonus 2: Most varieties of peas change color also naturally as they rippen. The seeds become yellow. The chlorophyll gets degraded in plant metabolism. The chloroplasts, i.e. the cell organelles responsible for photosynthesis change function to become storage organelles called leucoplasts.

(Edit: Ooops, I first wrote that chlorophyll supposedly contains iron. That was wrong, it is magnesium. Iron is present in a similar die called heme, which makes blood red. Probably I am getting too old :-) )


What is this sand covered insect? I have found in a wooden house, in the mountains of central Spain this very curious insect:

I was wondering if that was its skin or whether it's decomposition or sand or saw-dust.  That particular region of Spain does have stink-bugs ... but this one doesn't look like anything I've seen before.  A google image search returns mostly arachnids ... but it seems to have only 6 legs.

It's a kind of assassin bug, specifically a Masked Hunter:

  The surface of an immature Masked Hunter is sticky and it attracts lint and dust which helps to camouflage this predator.

and

  The name refers to the fact that its nymph camouflages itself with dust.

Though they feed on small insects, they will bite defensively, and when they do, it's fairly painful.


What are different firing rates in different regions in the human brain? Could it for example be that neurons that are concerned with high-order thought and medium-term planning fire more slowly, or is it expected that all neurons rather fire more or less at the same rate?

Here is an article on the average firing rate: http://aiimpacts.org/rate-of-neuron-firing/

Is the assumption that the measurements tend to be biased by accounting only for visually responsive cells warranted?

The article, has a classical engineering approach (might be wrong I just skimmed it), not that it's a bad thing. The general criticism of bias against sparsely coding neurons is correct, don't know how they can say its a factor of 10 or anything else though.

Average firing rate of one neuron only makes sense in relation to a different condition. For example in sensory neuroscience studies, we say a neuron likes a stimulus if the average firing rate of this neuron while the stimulus is presented is higher than in an equal period in the absence of the that stimulus. Conversely a neuron dislikes a stimulus when the average firing rate goes down.

Average firing rate across all neurons also is a weird measure as neurons have different baseline firing, different morphologies, are part of different circuits and have different functions in these circuits. It would be like saying that the average of a normal distribution is enough to describe it ignoring its variance.

Regarding the question itself a couple of things should be better defined: what is higher order thought? and medium time planning of what?

Neurons certainly do not all fire at the same rate, however rate implies a time constant and most importantly when one averages across multiple neurons one must have a criterion of selecting them which begs the question: Which neurons? How does one defines an area of the brain? Morphologically? Functionally? Genetically? Furthermore, what is its relevant time constant? These seem like basic obvious questions however they don't seem to have a clear and defined answer yet.

You seem to have a particular architecture in mind with multiple areas that have different functions, I assume you are modeling it. All models are wrong (yeah yeah I know its a cliche) which is to say that every model has a particular set of more or less valid assumptions. You just have to know what these assumptions are and what you can conclude given these assumptions. So basically there isn't really an answer to your question from the biology side we're still blind scientists in a dark room looking for the brain dead cat that is hiding the light switch.

Once I figure out the function of an arbitrarily defined brain area I'll let you know its time constant, then again it is arbitrarily defined and I cannot possibly figure out its function in all possible conditions without having assumptions of my own of how things should work...


Do transcription factors block transcription entirely? Transcription factors bind to the DNA to block the transcription of a certain gene, right? But while they are bound to the DNA, do they completely block any transcription of this gene for as long as they stay there or can they also partially block transcription?

Of course it's never 100%. The protein still has a measurable Kd for the DNA, meaning that there's always some part that's not bound (or some time that it's not bound.

Besides that, you're talking about repressors. There are also activators, and they use many different mechanisms. The same regulator protein can even recognize different sequences of DNA and repress one gene more than another. Some can bind and actually recruit a RNA polymerase, some work only while they're binding small molecules.

https://en.wikipedia.org/wiki/Transcription_factor or your molecular biology textbook might be a good place to learn more.


Are the cytosol and extracellular fluids electrically neutral? I've found several sources that state that overall, the cytosol of a cell is electrically neutral. The extracellular fluid is also purportedly electrically neutral. How can that be when we have membrane potentials?

Also in that regard, how do the ion transporters that set up the membrane potential know when to stop pumping ions to get a certain potential set up?

Membrane potentials are caused by different concentrations of ions on opposite sides of membranes in micro-environments along the membrane. The membrane can be, overall,  electrically and chemically neutral with small areas that have differences in electrochemical gradients.

For cells to produce these potentials they have proteins embedded in the lipid membrane. Ion pumps are the main players in creating potentials and gradients; through active transport (the use of ATP) the protein moves ions from one side to the other. When the concentration of that area of membrane is at one concentration the proteins are held in one conformation (active or inactive) and when the gradient is changed or meets a threshold the protein changes conformation and becomes activated or inactivated. So the actual electrochemical gradient dictates when the proteins are transporting.

There are also other proteins/messengers that are produced which can interact with the transmembrane proteins that keep them in one configuration or another to facilitate the production of an action potential. Once again, when this specific concentration is met the signaling molecule/transporter will become inactivate or activated.

This is just stuff I recall from some classes. Honestly, wikipedia is a fine general knowledge source. And more detailed than my explanation.  http://en.wikipedia.org/wiki/Membrane_potential#Ions_and_the_forces_driving_their_motion


What equipment would one use to modify a virus? Would anyone be so kind as to give me a few examples of the equipment involved when modifying a virus? Otherwise my novel may end up reading

Eva entered the lab and modified a virus.

Not much back story there!

I'm no expert at this and I would welcome any changes to this post. First you need to decide, what your target organism which you want to infect is (e.g. mammalian cells, bacterial cells) and based on that you choose your viral vector as listed in this article. Generally for mammalian cell stable transfection (usually you want the genetic materials you introduced to persist between cell divisions hence stable transfection) and transformation (just a general statement about changing cells as you have introduced, usually foreign genetic material but transformation is not necessarily the same as making something immortalised, which means the cells won't stop dividing i.e. becoming cell lines or in lay term cancerous) scientists tend to use lentiviruses, which are retroviruses, similar to HIV and they can even infect non dividing cells (so this should allow your imagination to run wild!). Once you have decided what the best viral vehicle for targeting your cells of interest is then you essentially transfect the plasmid DNA (packaging vector), which produces the virus protein package, into cells, whose job becomes to produce the virus as those cells have the required cellular machinery for this purpose. These cells are often 293T packaging cells. Along with the plasmid (circular) DNA, which produces the virus package, you co-transfect the packaging (e.g. 293T) cells with another plasmid, called lenti-vector, which does whatever you want it do, such as express a particular protein or microRNA or whatever but the idea is that stuff produces by the lenti-vector should not be toxic to the target cell (i.e. the cells you intend to target), unless thats what you want it to do.

Now as you can see, you can play around with two things here, first the packaging vector, to change the behaviour of the virus if you wish. And second the lenti-virus vector, to produce whatever you want it to! Once the packaging cells made your viruses, containing your lenti-vector, the virus get secreted into the media, which the packaging cells are in so you have to extract the media, congaing the virus, and concentrate the virus using centrifugation. Once you got the virus then you can use it to transform the (target) cells you wish.

For the lab based procedure of how you make the virus and what equipments you use and how to concentrate the virus then please see this link, although its a little technical. In this case, the packaging vector is fuGENE 6 and the lenti-vector or just plasmids of interests are listed (please not that I do not endorse any products mentioned here and I'm just using it as an example).

Now for making the packaging plasmid (making the virus), you often use the genetic materials from a virus and change it through a procedure called polymerase chain reaction (PCR). Same goes for the lenti-vector/plasmid as they are derived from somewhere and then change through time using PCR and restriction digests, which is an equivalent of genetic material cut and paste, to make the vectors and products of interest. Once all is done the the virus can infect the target cells and effect it based on its designed function (defined by the two vectors I described).

If the above response does not answer you question, since it is currently very broad, please make further clarification to the question so that I can modify my response accordingly.


Looking for a database of plant features To perform some private data science experiments I am looking for accessible information on morphological plant features (tabular information would be best). Crawling the web I found many websites with limited more general description and a lot of information on location and population data.

Do you know a website, institute or person in possession of such data and willing to share it? Since I am located in Germany my main interest is in the local flora, but any other would also do the job.

-- Traits --

TRY

TRY is a Plant Trait Database. More formally, it's a network of vegetation scientists headed by DIVERSITAS/IGBP, and the Max Planck Institute for Biogeochemistry, providing a global archive of curated plant traits.

BioTraits

This is an online resource for empirical data on how biological traits respond to environmental drivers such as temperature, light, and salinity.

Nate Swenson

Nate and his collaborators have compiled a ton of traits for species all over the world (though focused on the tropics).

Coyle et al. 2014

Appendix 2 of their 2014 Ecography paper lists primary literature sources and publicly available trait databases they used to examine 3 traits: leaf nitrogen, seed mass, and wood density.

-- Images --

Morphbank

An international Web database that contains thousands of high-resolution photographs and other images of plant and animal specimens.

Botanical Images Databases

This site provides dozens of links to databases containing plant images. There are also regional databases provided (e.g., Pflanzenphotos.de).

Botany.ch

This site contains both text sources (e.g., lectures and essays) as well as links to morphology picture databases (e.g., Botanical Image Database of the University of Basel).

See also FAO Online Catalogues for a number of morphological sources in both English and German.


Why is blood pressure higher the more distal an artery is? Why is blood pressure generally higher in more distal arteries?

Because of reflected pressure waves and the stiffness of the blood vessel.  The forward pressure wave from the heart travels much faster than the blood itself and is reflected at areas of tapering and branching.  This backward wave slows the forward flow of blood, and at the same time, when it meets the next forward pressure wave, that forward pressure wave is augmented...so higher pressures distally...And now you know, and knowing is half the battle...


Why won't birds move an inch in total darkness? One day, a bird flew inside my house. I locked the door. It landed on my TV and then I turned off the light. Then I touched the bird and it didn't even to try to fly or move.

Then I went to the kitchen and turn on the light,  and suddenly it flew into the kitchen.

Why won't birds move an inch in total darkness?

Most birds are diurnal and have vision adapted for daylight. Vision is among the most important senses for most birds, so much so their eyes have evolved to be quite large -- much larger than human eyes, proportionally to body size. In order to have excellent daytime vision, many birds also sacrifice some of the cells in the retina that allow for dim lighting conditions. (These photoreceptor cells are called rods and cones; cones are responsible for color perception while rods are more sensitive in dim lighting. Diurnal birds can have a lower percentage of rods than other animals adapted for nocturnal activity.)

Falconers have been exploiting this trait for millennia, by using a hood, diurnal birds of prey calm down in darkness.

Owls are a great example of a bird that can see in very dim lighting conditions, though they can't necessarily see in total darkness. They also rely on acute asymmetrical hearing in order to pinpoint prey in extremely dark conditions.

Your avian visitor likely can't see in dim conditions in which you can still see. To avoid injury, birds will hold still and wait for light.


How much weight/volume do microbes occupy within the human body? Microorganisms constitute the bulk of all the biomass on Earth. I weighed myself yesterday, and wondered how much less I would weigh if I were completely free of bacteria and microbes, inside and out.

Approximately how much weight and volume do microbes occupy within the average human body? How were these values obtained?

@AlanBoyd's calculations are reasonable, I think the estimate is off though.  The human microbome includes other bacteria which are not necessarily E.coli equivalent.

The human microbome projects give estimates that microbes are 1-3% total body mass.  i.e. several pounds of bacteria.

The GI tract alone has most of the microbome mass - faeces is ~60% intestinal flora/fauna by dry weight, which for many adults alone must be hundreds of grams at any given moment.


Why is facial symmetry of the opposite sex attractive? Why do we give so much importance to the symmetry of face in the opposite sex? Why do we yearn to reproduce with a person with a beautiful face? How is it important for survival, if at all? Is there a biological explanation for this?

Facial symmetry is currently believed the be a sign of developmental stability and good health and thus good genes.  More precisely a sign of genetic diversity in a potential partner.


How can I learn about how cloning works in nature (twins)? I would like to learn about how the process of cloning works in nature - how are twins "created" after fertilization what genetic changes can occur in each of the twins.

Where should I start? What are some interesting books on the topic, as well as recent research papers (or just the most important research topics that I could use to start looking for more information)?

To learn about the process of how cloning works, you need to appreciate the underlying principles. A general bio textbook should suffice (most popular one is Alberts, where you should focus on chapter 21, but maybe read other chapters for background)

Nature Scitable is also a good source.

I'd discourage reading research papers at this stage, primary research paper are often very specialized, and reviews are aimed at other researchers in the field, that is unless you find one that is focused on communicating science to the public.


Comparing angles between population vectors of neural activity I am reading this paper on fear conditioning, where the following is given:

The n-dimensional population vector (activity of n neurons) evoked by the conditioned stimulus (CS+, auditory tone) before conditioning
The n-dimensional population vector (activity of n neurons) for the CS+ after conditioning

The authors write that: "[After conditioning] the CS+ population vector rotated out of the plane defined by the US [unconditioned stimulus] and the initial CS+". They conclude that this out-of-plane rotation corresponds to "new learning".
My question: Why is out-of-plane-rotation of neural activity vectors equated with a new representation/new learning?

They are not writing about "after conditioning" as you write, but, importantly, after extinction.
What they observe is that, during learning, the response to the conditioned stimulus (CS+) becomes more similar to the response to the US. In the n-dimensional space in which a population response lives, you can describe this as the population vector evoked by CS+ pointing closer to same direction as the population vector from the US.
We expect that during extinction, the CS+ vector will become different from the US compared to at the peak of conditioning. There are two general possibilities for how that could happen. The first possibility (perhaps the simplest one to expect) is that with extinction the CS+ vector returns to where it was initially, before the conditioned stimulus was paired with the US. You could describe this as merely forgetting what has been learned: responses to the US and CS go back to how they were before conditioning and it's as if nothing was ever learned.
However, that's not what these authors observe:

During within-session extinction, the CS+ representation did not revert and gained no more similarity to its initial representation before learning

Although they do observe that with extinction the CS+ vector moves away from the US, it doesn't move back towards the old response, it points in a new direction that is further both from the US response and from the original CS response. That can be described as an "out of plane" rotation, not towards either of the other vectors.
In case it's hard to think about these things in N-dimensional space, we can think of a more familiar situation in our own 3-dimensional world.
Let's say the US causes a response corresponding to "12 o'clock". The conditioned stimulus causes a response corresponding to "3 o'clock" before any training. As you do some conditioning training, pairing the US and CS, the CS response moves towards "1 o'clock", beginning to resemble the US response. During extinction, we might expect the CS response to move back towards "3 o'clock", maybe we'll find it at "2 o'clock". This would represent rotation in the "plane of the CS and US" made by the clock. Instead, the hand points out away from the wall, so it is further from both the original US at 12 and original CS at 3. That's the "new learning".


How does inbreeding depression cause infertility? My textbook states that repetitive self-pollination in the plants cause inbreeding depression which causes infertility thus plants develop techniques called outbreeding devices to encourage outcrossing. My question is how does inbreeding depression cause infertility?

One of the main contributors to inbreeding depression are recessive lethal alleles. Suppose you have an individual who has the genotype Aa, where A is the dominant, non-lethal allele and a is the recessive lethal allele. This recessive lethal allele is likely very rare in the population (selection would decrease the frequency of a recessive lethal allele), so our Aa individual can breed with almost any individual without consequence because most other individuals are AA, so the offspring of this individual will be either Aa or AA.

However, if the Aa individual breeds with itself or with a close relative who has the Aa genotype, its offspring will have a chance of inheriting the two aa alleles, which is lethal, decreasing the fitness of the Aa individual that bred with itself (or a close relative). This decrease of fitness resulting from self-breeding will cause selective pressure to outcross instead of self.

It is important to note that the recessive allele doesn't need to be strictly lethal for this effect to happen - if the recessive allele causes infertility (for isntance, failure to produce gametes or something similar) the same effect will happen.

In short, inbreeding can cause detrimental recessive alleles to become paired, causing lethality or infertility.


Can flow-FISH be used on metaphase cells? I know flow-FISH can be used on interphase cells but was wondering if it only works on interphase cells or can work on cells regardless of stage in the cell cycle.

Don't know if this will help but Maurizio Carbonari in cytometry A in 2016 published on methods which allow for cell cycle analysis.

The abstract

  Formamide has long been one of the most widely used reagents in the study of nucleic acids. However, the use of formamide for treating cells to be analyzed by flow cytometry is a recent development and is restricted to measuring telomere lengths by flow‐FISH. In this field, we have published several papers in order to observe the effects of formamide treatment on cells at room temperature. We therefore discovered that, with suitable modifications, a short and simple incubation in this ionizing solvent facilitates cell cycle analysis by flow cytometry, equivalent or superior to that obtained with treatments in alcohol, acetone or detergent in hypotonic solution. Even using a bulky and problematic stain (low quantum efficiency and G‐C base preference), such as 7‐aminoactinomycin D (7‐AAD) which, on the other hand, has the advantage of being excited at 488 nm and does not bind to the RNA, it is possible to obtain excellent coefficients of variation and (G2–M) mode/(G0–G1) mode ratios. These parameters, especially if stained cells are washed before acquisition, arrive at optimal values. It is noteworthy that the ability to wash the cells stained for DNA content analysis without affecting the stoichiometry of the staining has not been described elsewhere in the literature. With formamide treatment the doublets are practically absent, sample recovery is efficient, as well as the preservation of physical parameters, and the stained cells can be stored for at least 10 days at room temperature before acquisition.

As for Flow-FISH, it is a method used to measure telemore lengths.

Vyacheslav I Borisov et al. in Current Protocols in Cytometry. 2014
Published on applying flow-fish to look at M phases.


Difference between pipette and pipettor I've been translating a text listing some analytical laboratory equipment, and found that some fellow translators translate the Russian word "автоматическая пипетка" (avtomaticheskaya pipetka, which literally means "automatic pipette") as "pipettor".

I consulted the producer's website and found that the proper word for my particular model (thankfully the model code was mentioned) was indeed 'pipette'.

However, in case I come across a Russian 'pipetka' that really means "pipettor", how to distinguish between the two? Maybe the terms are largely synonymous?

Bear with me, I'm not a specialist in this sphere. I googled and found a discussion on Reddit that shed little light for me.

In my mind, pipette and pipettor are generally* synonymous in the life sciences. Pipetman, which is actually a trademark, is also commonly used to refer to these instruments.

Gilson UK
That being said, there are some other things that you need to differentiate between. A pipette tip is the (usually plastic) thingy that goes on the end of the pipette, shown in the image above as clear white plastic on the left end. There are also serological pipettes

Argos Tech
and volumetric pipettes

Pro Lab Supply
together also referred to as transfer pipettes. These can be made of plastic or glass, and are used in conjunction with an electrical or mechanical pipettor, or a bulb (not your mouth!). Just to be confusing, sometimes lab personnel will refer to serological pipettes as just pipettes, even though they refer to the things pictured above in image 1 as pipettes as well.
Some people, such as SeRe above, distinguish between pipettes (the first image above) and pipettors, such as those used with serological pipettes:

Drummond
These are also known as Pipet-Aids or by other brand names.

However, in case I come across a Russian 'pipetka' that really means "pipettor", how to distinguish between the two? Maybe the terms are largely synonymous?

So yes, the two terms can be synonymous, so just be consistent, whichever you choose. I would stick with pipette unless it's clear from the text that the authors are transferring larger volumes than 1 ml, in which case they're probably using a pipettor in conjunction with a transfer pipette. If it's unclear, sticking with pipette should be good enough. If your readers are familiar with lab techniques, they'll understand what's going on.


Comparative evolutionary study: is amino acid or nucleotide comparison more useful? I am a high school student and am currently learning about evolutionary relationship study in biology.

My teacher said that a comparative study of amino acid sequences is more useful than a comparative study of nucleotide sequences, because the genetic code is degenerate in nature — several codons may code for the same amino acid.

However, I just do not understand the logic.

Since several codons may code for the same amino acid, I (as a math person) consider the conversion of a nucleotide sequence to an amino acid sequence as a non-injective function, and thus is information-losing.

(Analogy: consider the function $f(x)=x^2$. Imagine that you have a number, and you plug it into $f(x)$ to get $1$ as the output. You would never know if the original number is $1$ or $-1$.)

Therefore I arrive at the exact opposite conclusion. Is my conclusion correct or not, and why?

Each has its own utility, depending on the time-frame you are looking at. For evolutionary studies, you need variation, but not so much variation that one substitution at the same position overwrites a previous substitution. So if you are looking at deep splits, over hundreds of millions of years, it may be that amino acids are more reliable. But you are correct in that since they are functionally more important than silent substitutions (nucleotide changes that don't change the amino acid), it is possible to have amino acids converge on the same state, independently. Nucleotides do this too. Both require statistical models (maximum likelihood) that accommodate the possibility of multiple changes at the same site. If you are looking at recent evolutionary splits, there may not be enough (or any) amino acid changes to compare, so in this case, nucleotides would be better. You would not measure continental drift with a stopwatch, or a 100-meter dash with radiometric dating.


Are there examples of human genes using meiotic drive? Meiotic drive is a type of intragenomic conflict, whereby one or more loci within a genome will affect a manipulation of the meiotic process in such a way as to favor the transmission of one or more alleles over another, regardless of its phenotypic expression. More simply, meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time.

But do humans have such genes?

Yes! Jeffrey and Neumann 2002 report evidence of meiotic drive at a recombination hot spot in the MHC.

Note that mtDNA could arguably be considered as an extreme case of sex-dependent meiotic drive. Mothers transmit mtDNA at rate of almost 1, while fathers transmit mtDNA at a rate of almost 0.


Can you disconnect sensation from the brain without destroying muscle functions? I want to know if it would be possible for a surgeon to "shut off" a person's senses without causing paralysis of any kind. The person would have to maintain their ability to speak and move, but not be able to hear their own voice or sense the physical world around them at all.

Even if it were possible to selectively destroy sensory (afferent) nerves alone, the individual would not be able to walk/move normally immediately afterwards, because there would be no environmental stimuli with which to orient one's actions.

Two of the senses people often overlook are balance (or spatial orientation) and proprioception (where the body parts are with respect to each other and the physical world). (Some people lump the two; it's easier to think of them independently, because they really do quite different things.)

Proprioception (and closely associated kinesthetics) is possible because of nerve signals from skin, tendons, muscles, and joints. This gives us the senses of limb position and movement, the sense of tension or force, the sense of effort, the sense of gravity.[1]

  Patients (lacking proprioceptive feedback) made large directional and amplitude errors when performing a reaching task without visual feedback....The errors were associated with differences in velocity and acceleration for movements in different directions.[2]

Basically, without proprioception, you could not touch your little finger to your thumb without visual input, let alone actually perform more complex voluntary movements successfully.

The vestibular system exists through input from three semicircular canals located in the inner ear on each side. The canals are oriented at (basically) 90° angles to each other so that we can maintain our balance no matter which position our head is in. These are also connected to one's ocular reflexes. Together they're called the vestibolo-occular system, which functions as a reflex (VOR).

  Three sensory systems, vestibular, visual, and somatosensory/proprioceptive, serve our sense of balance. Each of these systems provides unique sensory information to the brain where it is integrated (often in complex ways) to produce a final motor output to muscle groups for maintaining gaze, head and body posture, and controlling static and dynamic balance.[3]

Without these systems, we would be completely unable to get or stay in a standing position. We certainly could not walk.

So, long story short, the answer is no. Not only is it surgically impossible, but if it were, you would not have a coordinated, working body left. Eventually even speech would be affected (as proprioceptors on the mouth are involved in speaking).

[1] Proprioception From a Spinocerebellar Perspective
[2] mpairments of reaching movements in patients without proprioception. I. Spatial errors
[3] Anatomical and Physiological Considerations in Vestibular Dysfunction and Compensation


What's the role of SNP (Single Nucleotide Polymorphism) in a disease when there is no gene associated to that SNP I am quite new to the field of GWAS (genome-wide association studies), and I'm combining GWAS results and single cell analysis on type-1 diabetes (T1D), to see the role of cell specificity on the disease.
However, I don't understand one aspect about GWAS results. The GWAS results lists all the significant SNPs (low p-value) from a certain study on a particular disease. After that, those SNPs are mapped to genes using either positional mapping (using windows), eQTL mapping, or even both.
However, some SNPs do not map to any genes using both positional and eQTL mapping procedure. Some removed SNPs even have a lower p-value than those which are mapped to genes.
Here is my question: since all the listed SNPs are supposed to be significant (tiny p-value), how can those SNPs which are highly correlated to the disease also show no association towards any gene. How do these SNPs give rise to the disease?
I would like to thank you in advance. Sorry if I'm using wrong jargon or anything, and please let me know, if you want any further clarification.

SNPs do not signify anything about the functionality of a particular piece of DNA. You can think of a SNP as just a sign that says "hey, something in my neighborhood might be interesting!!" In this respect many GWAS SNPs are so-called "tag SNPs", that have been selected specifically to give the minimal number of SNPs that can be linked to all of the genome (e.g. every 1 centimorgan there is a SNP, or whatever).
So: SNPs do not say anything about biology, or about genes. The only thing that they signify is linkage to something that is possibly interesting.
Your issue seems to be that you are coming up with GWAS SNPs that do not show apparent linkage or statistical associations (e.g. eQTLs) to anything that you think should be interesting.
There are a lot of ways in which this could be the case:

There actually is a gene in that part of the sequence, and we just haven't annotated it properly.

The reference genome is wrong in that SNP's location, or is missing an interesting piece of sequence (i.e. a gene) that exists in your population.

That SNP has a population structure signal (i.e. it is more common in one population than another) that is associated with your trait of interest, which you have not properly corrected for.

That SNP is spuriously linked (for whatever reason) to a more distant part of the genome.

That SNP was mis-mapped and is actually in the wrong part of the genome somehow.

There is technical interference due to high similarity to some other part of the genome, which your procedure has not corrected for.

Sometimes frequentist p-values are not actually informative and a thing that looks interesting according to p-values is simply not interesting.

Though there are no genes, there is a long-range enhancer in the region of the SNP that affects a distant gene.

Though there are no genes, there is repetitive DNA linked to the SNP that leads to a complicated regulatory feedback that affects something about your character of interest.

Something about microRNAs?

Your SNP doesn't have any genes nearby, but it is linked to a TAD boundary that affects overall chromatin architecture.

There is a long non-coding RNA there.

Your eQTL significance threshold is too stringent.

Your eQTL association analysis missed an important isoform or transcript.

... and many other hypotheses! Many of these are very hand-wavey or unlikely, but sometimes biology is just weird.
However, in general I would default to an explanation in which there is some kind of technical or statistical artifact. Even when nothing is obviously wrong, there is usually some kind of technical problem in genomic datasets.


Possible calculations with temperature, humidity, images and VIS spectrum of a plant in an Integrating sphere I am currently working on a project which involves growing some plants in a integrating sphere made of foam. I have added temperature, humidity and soil moisture sensors as well as a Spectrometer (350 - 800nm) and a webcam which takes images of the plant every 30 minutes.

I thought of calculating the LAI (Leaf area index) from the webcam images.

Does anyone have any other suggestions/ideas on what I could calculate with the given data from these sensors?

With the images you could, perhaps, assess growth rate of the plant which can be plotted against spectral content of light to investigate effects of light quality on growth. Using moist and water and temperature the same can be done. Multivariate analysis can help to implement all the values, while ANCOVA may may help to correct for covariance.

A detailed experimental set up may help to answer this question. Not specifically the hardware, but how the effect of water stress is measured. E.g., are multiple plants tested under different watering conditions? In that case all the other measures (temperature, light) are probably used to check whether everything is constant across all specimens except water availability. This may limit the usefulness of analysis of these additional measures. I think the other parameters (light, water, temperature) may be not so interesting other than covariates for water stress as they are either not controlled or deliberately kept constant. Moreover, probably their effects on plants are pretty obvious too.


Difference between mutation and DNA damage What is the strict difference between mutation and DNA damage?  As far as I understand it, a mutation is an alteration in the genetic sequence, having "tricked" the repairing machinery and thus getting replicated in the future.  DNA damage, on the other hand, is any alteration of the DNA molecule including breaks, chemical alterations of the molecule, etc.

Then, are mutations considered a type of DNA damage?  I would thank the strict definition of both concepts.

Have you read the DNA repair article on Wikipedia?  The DNA damage and mutation section answers exactly what you're asking:

  DNA damages and mutation are fundamentally different. Damages are physical abnormalities in the DNA... [and] can be recognized by enzymes, and, thus, they can be correctly repaired if redundant information, such as the undamaged sequence in the complementary DNA strand or in a homologous chromosome, is available for copying.... In contrast to DNA damage, a mutation is a change in the base sequence of the DNA. A mutation cannot be recognized by enzymes once the base change is present in both DNA strands, and, thus, a mutation cannot be repaired.

Here's the entry from the NCBI MeSH Glossary saying the same thing:

  Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION... They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR).

And for mutation:

  Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.