How do gain-of-function alleles help with problems caused by genetic redundancy? Genetic redundancy masks the gene functions (eg it masks diverse functions of the tumor suppressor gene). I have read on the internet that gain of function alleles can solve a such problem caused by genetic redundancy and would like to know how.

Genetic redundancy can be a problem when studying knockout or hypomorph mutations of genes, or analogues such as exogenous RNAi. The redundancy can consist either in incomplete knockout (the genome contains more than one copy of the gene but only one copy is mutated) or functional redundancy (different genes doing more or less the same thing). If you try to figure out what a gene does using a loss-of-function allele, the other copies or redundant genes may weaken or completely mask any phenotypic manifestation of the lost gene function.

Gain-of-function alleles can be useful in such a situation. A gain of function means the gene product does something different, or something additional to its normal function. Even if there are "healthy" other copies of the gene or redundant genes around, the modified function of the introduced allele will interfere with the normal behaviour of the molecular pathways it partakes in, and thus cause a phenotype.

A classic example are constitutively-active alleles. Imagine for example a tumour suppressor with a mutation that prevents it from being degraded (but imagine you don't know this gene is a tumour suppressor yet). Let's say there are other tumour suppressor genes around, so if you knock out your gene of interest, the cell behaves as normal - loss-of-function isn't useful to study what the gene does. Now, if you introduce this constitutively-active mutant variant that doesn't get degraded, it causes too much suppressive activity and drives the cell into complete cell cycle arrest, regardless of the other redundant genes being around. Based on this phenotype, you could infer that the gene is probably a tumour suppressor.


Are all cells organisms? As the title says, are all cells organisms? Why or why not?

As I understand, not every cell is an organism because some of them -those which aren't organism- require the rest of the organism to live. But arguing with someone about that, he says that, for that matter, every cell needs of others to live in some way or another, or that they can be kept alive and sometimes reproduce in a petri dish, without the need of the organism. So every cell, he says, even those which constitute larger organisms are organisms in themselves. I tell him that saying every cell is an organism is awkward, that would imply that every multi-cellular organism is really a colony, rather than an organism.

Is this only a philosophical question or can we say for sure, for example, that an epidermal stem cell or a lymphocyte are not organisms?

Your friend is incorrect. From Wikipedia:

  The word organism may broadly be defined as an assembly of molecules functioning as a more or less stable whole that exhibits the properties of life.

(Viruses are specifically excluded, as they depend on a host cell to fulfill all the functions of life.)

While cells extracted from a multicellular organism like a plant or a person may be able to be cultured in vitro for a time, they cannot survive independently - they require the intervention of humans (or very well-trained monkeys) to obtain nutrients and oxygen, and process/remove waste. A unicellular organism like a bacterium, for example, can handle these functions on its own - it can either synthesize or find a source for its own nutrients, and can reproduce on its own to create more organisms.

The key difference is being self-sustaining. An organism needs to be able to feed itself, take care of its waste, reproduce a full version of itself, respond to stimuli, etc. (see the "properties of life" link above). A single cell from a multicellular organism cannot do all that without assistance (kind of like a virus, actually), while a true unicellular organism can.


What is this Californian shrub? I spotted this shrub-like plant in California, USA.

Almost definitely not a CA native.

It looks like a coleus to me -- cultivars are pretty diverse but typically have variegated leaves with some amount of purple coloration.

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


What is the difference between Single Nucleotide Polymorphism (SNP), Mutation and Structural Variation(SV)? This is a question which plagues many people and today I was wondering it myself while writing a grant. Indeed, I've seen many people use the terms interchangeably, but they are all very different from each other.

So What is the difference between SNPs, Mutations and Structural Variations?

Lets state what a Mutation is first.

Mutation: A mutation is any change in an organism's genetic sequence which varies from that of the wild-type reference sequence (hg19/GrCH37 from 2009 or hg38/GrCH38 from 2013, which are the most current genome assembly).

Single Nucleotide Polymorphisms (SNPs): These are any single nucleotide base mutations which have been validated to be present in more than 1% of the population with the help of Genome-wide Association Studies.

Structural Variations: These are any mutations which cause a change in the organism's chromosome structure, such as Insertions, deletions, copy number variations, duplications, inversions and translocation.

For more please read Wiki Link here.

Thanks to WYSIWYG for his interesting question regarding SNPs.

This piqued my interest a bit, and to my surprise I found that the same actually applies to all other species for example chickens; This paper from way back in 2002 describes how EST mining was sometimes used to generate potential SNPs but also notes the possible false positives due to the possibility of RNA-Editing.

This paper describes the usage of SNPs to allocate bovine individuals to their source population. As does this paper which highlights the economic importance that SNPs may hold for identifying pure breeds and crossbreeds.

Apparently there are also SNP chips available for other animals as highlighted by this particular paper


How does vasoconstriction/vasodilation change blood pressure? Background: I am coming at this question from an electrical engineering background, and I feel like I am missing certain assumptions that are going into the statement found in my physiology textbook, "vasoconstriction increases blood pressure"."

Consider a simple series circuit and a parallel circuit run by a battery/heart [you will find the parallel and series circuit in any physiology book description of the vasculature, yet I can't find any exploration of the assumptions made when applying these circuit models]:

In the series circuit, if I have an increase in resistance across
one of my resistors, this will basically redistribute the pressure
drops across the resistors, but it will not alter the total pressure
drop across all the resistors [fixed by the heart].
In the parallel circuit, if I have an increase in resistance across
    one of my resistors, this will redistribute the flow to different
    branches, but the pressure drop will not change as again this is
    fixed by the heart.

This analysis seems to suggest that if the resistance across an organ [branch of parallel circuit] changes, the flow changes, not the pressure. The heart, I would assume, then responds by increasing the pressure to increase flow ie actually injecting energy into the system.

Here is the problem with the circuit model though:

it assumes that the battery/heart is the only source of energy in
the system, and the resistors are passive re distributors of that
energy.

the controllers of vascular resistance are smooth muscle which must actively put energy into the system to vasoconstrict. This could be
a source of pressure increase as the smooth muscle would be actively
constricting against an incompressible fluid, but I am really not
sure.
it does not account for the compliance of the vasculature.

-the tubing the heart is hooked up to modifies the blood pressure the heart has to generate to inject fluid into that tube. If the tubing was stiff, the heart would have to generate very high systolic pressures that would then rapidly decrease during the diastolic phase. The more compliant the tubing, the less pressure the heart has to generate to inject fluid into the tube. Intuitively though, there would seem to some relationship between the ability of a fluid to flow and vessel compliance. A highly compliant vessel with a fluid injection will simply expand and hold the fluid while a less compliant vessel will maintain a pressure necessary to push the fluid along.

Sparknotes in the form of questions:

Is the only source of energy in the cardiac circuit the heart? Or
does artiole smooth muscle actually inject energy into the system,
        and result in systemic increases in the pressure available in the
        closed circuit.
I don't think vascular compliance ie expansion of the artery walls
due to volume filling results in any active injections of
        energy into the system..it should simply transfer the energy
        available to push fluid to elastic energy in the connective tissue
        of the artery walls. Is this correct?
Does vessel compliance partly determine the pressure the heart has to inject into the system?
What is the relationship between compliance and flow if there is one?

The circulatory system is a dynamic system which cannot be adequately explained by your example (at least not by me). You need to understand it, not seek to make it fit your (especially) electrical circuits with resistors. Blood isn't electricity. At least try a fluid dynamics model.

Let's take this very simple model: Blow up a balloon four-fifths of the way, and put a wide inflatable cuff around its middle. Inflate the cuff so that the balloon bulges just a tiny bit at the ends, then stuff it all into a plexiglass box so that the balloon has no room to expand. The plexiglass box represents our body. Lets call the pressure inside the balloon now normal blood pressure. The air in the balloon represents your total blood volume. It can't change from moment to moment; it's fixed. The box can't change it's volume moment to moment either. It's fixed.

The cuff represents arterial smooth muscle. Vasoconstriction can be represented by inflating the cuff further. Constriction (inflation of the cuff) will increase the pressure throughout inside the balloon, because the same amount of gas now has to exist in a smaller space. Vasodilation (deflating the cuff) decreases the pressure inside the balloon, because the gas can now inhabit a larger amount of space.

That's it, really. If the same volume must inhabit a smaller, constricted space, the pressure exerted by blood in that space will be higher. If the blood vessles dilate, the pressure in the blood vessels falls.

Now add about 20 layers of complexity to that simple model, and you have a working model of the circulatory system.

Sparknote answers:

Arterial and arteriolar smooth muscle "injects energy into the system", resulting in systemic increases in the pressure existing in the vascular "circuit" (meaning somewhat elastic tubing) if resistance requires energy. (So I have misunderstood: see @Raoul's answer.)
Sorry, I didn't read this properly the first time around. Yes, the heart supplies the energy. The contribution of the elastic walls of the arteries is not active, but passive.
Absolutely. The more elastic/compliant the arteries are, the less work the heart must exert to pump the blood through the circuits. The stiffer and narrower the arteries are, the harder the heart must work to pump blood through the circuits. The result of that increased work is a thickening of the muscular walls of the heart, called ventricular hypertrophy, which is a sign of elevated pressure in the system.
I'm not sure I want to commit here to your lingo, but the answer should be inferable from numbers 1-3. Elastic vessels help (by rebound compression) to propel the blood through the circuits. Stiff vessels hinder it, making the heart do more of the work.

I am not an engineer, so I may be misusing some of the terms.

Edited to add: Please see @Raoul's answer for a better explanation.


Renal threshold for glucose Wikipedia in its article on 'Glycosuria' says that the renal threshold for glucose (RTG) reabsorption in the kidney is around 160-180 mg/dL. Beyond which the glucose starts to excrete in the urine. But in diabetic people blood glucose exceeds in range of 300-400 mg/dL is prevalent. How this is possible? What prevents the the excretion of excess glucose into urine?

Does it mean more glucose is reabsorbed in the nephrons above its threshold limit? Also, as the glucose is co-transported with sodium, does it mean that glucose reabsorption is tightly coupled with sodium reabsorption? Does sodium play any role in crossing the glucose threshold limit?

Or is it possible that the excess glucose (beyond RTG) is actually excreted out of blood in the kidney but the hyperglycemia is caused by the fresh gluconeogenesis of the body?

Or is it possible that both these mechanisms (RTG is exceeded as well as fresh gluconeogenesis) cause in furthering the hyperglycemia?

Is it possible to measure this state?

Thanks in advance.

Classic symptoms of untreated diabetes include excessive thirst and urination, and glycosuria. Think about the solute gradient. At some arbitrary number the level of glucose becomes saturated. The kidneys are forced to get rid of the extra glucose in urine. This increases the concentration of solutes in the urine, so where does the water go? Right? So that high blood glucose concentration translates into frequent trips to the bathroom, and frequent need to consume fluids. This can also lead to a fluid/electrolyte imbalance, which is potentially dangerous.

There's actually a limit to what can be reabsorbed, denoted the transport maximum,
but, you can only eliminate so much solute over time, so here's a figure from a Pearson physiology chapter:

Source

You've got your renal threshold around that 180 mg/dL but look at that excretion kinetic. It's known that the excretion rate increases linearly with the filtration rate above the renal threshold (ref). So say i'm an average male with 400 mg/dL plasma glucose and 50 dL of blood or 20 g of net plasma glucose. All other things held equal, it looks like it could take around 2 hours to clear that glucose on excretion alone, which doesn't typically happen. Clearance is also outlined in that Pearson chapter, and you can measure that by knowing the excretion rate, and the concentration of glucose in the urine and in the plasma.

Data shows, however, that the filtration/reabsorbtion process is maladapted in a diabetes model, and increased plasma glucose levels are maintained by an up-regulation in glucose transporters (thus an increase in the transport maximum), and an increase in the renal threshold (and thus the kidneys only begin to excrete glucose at a significantly higher level) (ref).


Is it possible to have a random un-mutation of genes? According to this article:

Gene mutations can be classified in two major ways:

Hereditary mutations are inherited from a parent and are present throughout a person’s life in virtually every cell in the body. ...

Acquired (or somatic) mutations occur at some time during a person’s life and are present only in certain cells, not in every cell in the body. These changes can be caused by environmental factors such as ultraviolet radiation from the sun, or can occur if a mistake is made as DNA copies itself during cell division. Acquired mutations in somatic cells (cells other than sperm and egg cells) cannot be passed on to the next generation.

The "random mutations in genes" appear to be called Somatic mutations. For the context of this question, these are the mutations I am asking about (not the hereditary mutations).
My question: Is it possible for there to be a random un-mutation of genes? Some sort of reverse-somatic mutation. If so, have there been any clinically proven instances of it?
After-thought: Or is it all a Somatic mutation, aka you can experience a mutation that makes you more susceptible to a particular disease, then another mutation that makes you less susceptible to the same disease... so not necessarily a reverse mutation, but a 'forward' mutation that negates the original ill effect of the first mutation.

A large part of the body of your question seems relatively unrelated to the main question which is a little confusing. I will focus on the question

  Is it possible for there to be a random un-mutation of genes?

Yes, these are usually called reversed mutation. It is quite common though that a second mutation at a distinct locus may reverse the phenotypic effect of a first mutation. This is called a compensatory mutation.


Consuming animals by slaughtering vs injecting barbiturates? In "Least painful way to die" we get an answer ...

Companion animals (e.g., dogs and cats): injected barbiturates are recommended
Laboratory animals (e.g., mice and rats): injected barbiturates are acceptable as are inhaled agents (isoflurane, carbon dioxide).

And assume the butcher guy as soon as he comes to know the animal is gone, he will do the following....

A very sharp knife is used in this process: the point of the knife cuts into the animal's throat and cuts through the dewlap, trachea, esophagus and jugular vein immediately below the jaw-line to allow the blood to flow out.........Animals are bled out before being dressed because it prevents blood from coagulating in the tissues and thus making the meat go rancid. (Source Slaughter Cattle commercial method - Step 6)

Here's my question... What if the animal was killed using 'barbiturates', then is that animal safe for eating by humans or the high levels of 'barbiturates' in that body cause unwanted results in humans too (if they consume it)?

I'm new to biology. :)

For many drugs, the animal cannot be slaughtered for consumption within a certain time. Here are the slaughter withdrawal periods for some common drugs when used on cattle. There are also withdrawal periods for lactating dairy cattle, but I won't list them for brevity.

flunixin (NSAID) - 6 days
florfenicol (antibiotic) - 36 days intramuscular, 55 days subcutaneous
penicillin G procaine (antibiotic) - 10-14 days
tilmicosin (antibiotic) - 28 days
oxytetracycline (antibiotic) - 28 days intramuscular, 48 days subcutaneous
enrofloxacin (antibiotic) - 36 days, do not use in veal calves

More importantly for your question, I have found this report on pentobarbital used for euthanizing cattle. It says:

  Adequate measures should be taken to ensure that carcasses of animals treated with this product and the by-products of these animals do not enter the food chain and are not used for human or animal consumption.

Barbiturates are more dangerous than many other drugs and, furthermore, dead animals cannot metabolize them and they can be quite heat stable (ie won't readily decompose during cooking).


NCBI-geo differences between platforms,series and samples This is the first time that I use NCBI-GEO and I've faced with 3 different categories inside it. They are platform, sample and series.

NCBI-GEO have GEO-Overview section to explain these terms to ones who are new to this website, however; although I read it a couple of times, I could not understand it totally.GEO-Overview page The terms are a bit complex for the ones who are not familiar with the concepts. Therefore, is there anyone who could explain them with simpler words ?

In my situation, I use NCBI-GEO to get RNA-seq data for the C. Elegans organism. I've downloaded the following SRA file : NCBI-geo C. Elegans sample

As far as I understood, a sample contains an individual organism's information.(In my case its a single C.elegans organism)

Series are somehow the collection of multiple samples I guess. I wonder what is the criteria to put different samples into same series?

And lastly, what is the differences between platforms and series ? I thought that each organism have a single platform, in other words, I thought I could find all the things about lets say C.elegans in its platform but I saw that a single organism type may have a lot of different platforms.

So, I'm seeking to learn these concepts and I think this website is the correct place to ask it. If my question is off topic, sorry about that I was not aware of it.

The platform at NCBI-GEO means the particular microarray that was used (because originally most of GEO was just microarrays), OR, more recently, it could mean the type of NGS machine that was used.  For example, every microarray manufacturer creates an ADF (array data file) that maps the DNA sequence at every position on the Chip to an accession ID. And this ADF mapping file gets registered at GEO as a GPLxxxxxx. This was presumably to facilitate direct comparisons between different experiments from various labs using identical Chips (e.g. Affymetrix, or Nimblegen).

With the advent of NGS the Platform has to be a name from an approved list of companies and devices: ILLUMINA, HiSeq, etc.

A series is constructed by the data providers and allows them to cluster the results from related samples. So, for example, in the modENCODE consortium, I believe all of the C. elegans RNA-Seq from Bob Waterston's lab/Project are clustered together under one overarching GSExxxxxxx. More details at www.modencode.org and links therein.


Trying to identify a bug that left a blood spot when killed Hi, this was flying around inside the car in northwestern Maryland, USA, yesterday. When I squished it with a tissue I was surprised to see a red spot that appeared to be blood. Cannot find a picture of this bug online and was hoping someone can identify it. Thanks in advance.

That looks like a species of syrphid fly (aka. hover fly, flower fly) — not sure about the red fluid, but it probably wasn't blood.  These flies are pollinators and the larvae eat pests such as aphids.

I don't know for sure what species that is, but it appears very similar to Toxomerus politus:

Other sources of information on this group of flies:

http://thingsupclose.com/syrphidae-hoverflies/
http://bugoftheweek.com/blog/2017/10/31/flies-that-mimic-wasps-masquerading-syrphid-fly-ihelophilusi-sp
http://bugoftheweek.com/blog/2016/10/19/a-flower-fly-grows-in-brooklyn-flowers-flies-syrphidae


How do developing neurons become tuned to fire only on receiving specific inputs? Research has uncovered neurons that seem to "listen" for specific inputs and fire only when these inputs are received. For example, neurons in the visual cortex may fire at a higher rate when visual stimuli of a particular orientation is presented, and may not fire for stimuli of other orientations.

Are there any good models on how neurons develop this tuning for specific inputs? Could anyone provide links to good papers or other resources?

The only "good model" I know of is hebbian plasticity* or hebbian theory, here's a link: https://en.wikipedia.org/wiki/Hebbian_theory

Usually what we mean by neurons "listen for" or are "tuned for" or even "like" a particular stimulus is that spiking activity in those neurons is significantly increased (or decreased) in the presence of that stimulus as compared to equal amount of time in the absence of it.

*Plasticity refers to the capacity of the brain to change both the strength of connection as well as number and configuration of connections.


Is evolution a means to an end? In "The Red Queen", Matt Ridley frequently argues that evolution is a means to an end, without providing much explanation for such a big statement.

Is this a fact in biology? Do species mutate their genes so they can reach an optimum state, like the coelacanth fish that (allegedly) remained unchanged for the last 300 hundred million years?

Good question--I think the first point to address is "a means to an end" seems to imply willful action. That is, evolution (according to Ridley) would be a conscious effort by a species to optimize the gene pool for survival of future generations; a rationalization for each species to mutate and diverge.

This is not the case, for a couple of reasons. First, evolution is largely due to environmental factors that exert much more control over the genetic drift of a species than any internal (i.e. willful) factors, such as sexual selection. Additionally, optimal performance is often sacrificed for the sake of reproduction (peacocks, now functionally flightless). All sexual selection happens in the context of the organism's environment--phentoypes can change, but if there's only one food source on your island, it's the limiting factor and will exert strong evolutionary pressure to maintain certain traits.

Second, no evolutionary trait is guaranteed to push the species towards a so-called optima. The influence of sexual selection on populations has left many species (again I lean on peacocks as an example) expending energy on developing traits that do not make them more viable or "optimized" as an organism, but instead make them more desirable mates and thus more likely to reproduce and pass on their genetic material. Peacocks could be much more resilient to predators without all that extra plumage, but they've traded off flight for mating success.

Finally, as an aside, evolution happens on such a large timescale that individual populations would barely be able to change their genetic makeup in the course of a single lifetime. This point is not as robust, but if general societal consensus was driving evolution, there would be extinct species littering the corners of the planet. Ridley seems to have missed the mark a little--nobody is doing anything to cause evolution; evolution happens to you over many years of mutations and environmental pressures.


Homology ratio comparison between different species I found the following homology ratio:

protein coding genes of the organism with an homolog in mouse / all protein coding genes in the organism

I have done this for all protein coding genes between several organisms and mouse using a phylogenetic-based approach. I have noticed that the ratio found between an organism and mouse is greater than the ratio between another organism and mouse! On the other hand the second is evolutionary closer to mouse than the first.So:

1.Is such an approach trying to quantify homology? Which i know is not correct as homology is qualitive measure.

2.Can we compare the ratio of homology between the above 2 couples od species or such a comparison is biased?

3.Shouldn't the ratio of homology be proportional to the evolutionary distance of the organisms (according to conservation)?

As you can understand, in the way i calculate the above ratio, i don't take into account the one-to-many or many-to many relationships! I just take into account the genes that have at least one homolog in mouse..is that the bias of my calculation?

1.Is such an approach trying to quantify homology? Which i know is not correct as homology is qualitive measure.

A common approach to identify orthologs (homology between two genes resulting from a speciation event) it 'best bidirectional match': if you blast gene A (in species 1) against all genes of species 2 the best match is gene B, and if you blast gene B against all genes of species 1 the best match is gene A.

2.Can we compare the ratio of homology between the above 2 couples od species or such a comparison is biased?
3.Shouldn't the ratio of homology be proportional to the evolutionary distance of the organisms (according to conservation)?

Not necessarly. The fact that two genes diverged a very long time ago does not prevent them from being homologous. Homology is about shared ancestry (here of two genes) and not about evolutionary distance.
Could you clarify how you get the homologies? Did you compute them yourself (if so how) or did you use a specific database?


How is receptor production (recycling) regulated? My understanding of receptor downregulation is that when activated, a receptor then gets absorbed into its cell, as shown in this weird video. It then gets either recycled or degraded. Tolerance presents when more degradation than usual happens.

Receptor activated (ligand binds to receptor)
Receptor-ligand complex internalized to cell
Some complexes recycled, others degraded
Tolerance = more degradation than usual, resulting in lower
receptor density at cell surface (called downregulation)

So, what is causing the higher degradation than usual? Is it the lack of the materials required to produce the receptor? If so, can this be compensated for via diet or supplementation (i.e. eating more dopamine precursors if you're trying to avoid dopamine receptor downregulation, for example?)

So, what is causing the higher degradation than usual? Is it the lack of the materials required to produce the receptor?

Lack of materials is almost never the reason. Receptor turnover is actively controlled by different mechanisms. Ubiquitylation is one of the common mechanisms. Ubiquitylated receptors are internalized; these internalized receptors can later on be sent back to the membrane (recycled) or be degraded depending on the conditions.

Receptor downregulation can also happen by stopping their production either at the level of transcription or translation (For an example see this).


What stimulates a nociceptor? For instance, when pressure is applied to the skin, what determines how much pressure results in nociceptor stimulation. And when a sharp object pierces the skin, why is pain, rather than simply touch, perceived? Also, what causes nociceptors to sometimes be stimulated when there is no painful stimulus present, such as during a migraine when the skin feels painful to touch and in chronic pain?

Thank you in advance :)

All of these are affected by specific characteristics of the nociceptors.

Nociceptors are only sensitive to high pressure. The low pressure stimulus would only stimulate mechanoresceptors which would not cause a perception of pain. Receptors like $TRPA1$ sense mechanical stimulus of a higher degree. $P2X/P2Y$ sense ATP which is released due to mechanical tissue injury, as mediated by high pressure or a sharp object injury. Further more, several cells die as a result of nociceptive mechanical stimuli releasing mediators the receptors to which also act as nociceptors.
Exaggerated response to a noxious stimuli is called Hyperalgesia. A sensation of pain in response to a normal stimulus is called Allodynia. Both of these are mediated by specific sensitizing receptors on the nerve endings sensitive to Bradykinin, %HT, Serotonin, Substance P etc. All these are commonly found in conditions where these two are observed, as in the case of burning on touching following sunburns, or increased pain adjacent to an inflammatory foci.

Source:- Ganong's Review of Medical Physiology


Calibrating Motic Camera to Stage Micrometer Whilst calibrating my Motic Microsope's camera, I am able to calibrate the 10x object lens against the stage micrometer accurately.  However when I calibrate (using the Motic 2.0 Plus software) the 40x object lens, it always sets the ratio incorrectly.

For example, in the calibration panel, I load a photo of the scale that I took and then I draw the circle so that it measures the pixels both in height and width and then I tell it that the circle is 10 µm.  But it doesn't seem to get the ratio correct.  When I did this for the 10x lens it worked perfectly.

So I took a photo of the scale with the 40x object lens and then went to calibrate that.

Here you can see how the calibration is performed: you position a circle over the photograph and tell it the size in µm (it's rather large, sorry):

Here you can see the measuring line out of whack.  It gives me 8 µm for a length that should only be 4 µm.

Am I missing something?

It looks like the shape is an ellipse rather than a circle. The ellipse has major and minor axes, which are described in terms of half-axes (177 and 175 pixels respectively). Is it possible the software is incorrectly using the half-axis measurements, whereas when you draw a perfect circle it will correctly use the diameter? This is consistent with the x and y scale numbers being different from each other.

So I would suggest re-calibrating with a perfect circle.

Hope this helps.


What creates the feeling of 'excess' blood pressure to an area of the body? If I hang upside down, and feel blood rushing to my head, what structures are actually responsible for me "feeling" this excess flow of blood? Baroreceptors? Mechanoreceptors? Something else?

Regardless, how does this process actually work? How do I "feel" excess blood pressure to a certain area of my body?

Arterial Baroreceptors felling the pressure.

Arterial blood pressure is normally regulated within a narrow range, with a mean arterial pressure typically ranging from 85 to 100 mmHg in adults. It is important to tightly control this pressure to ensure adequate blood flow to organs throughout the body. This is accomplished by negative feedback systems incorporating pressure sensors (i.e., baroreceptors) that sense the arterial pressure. The most important arterial baroreceptors are located in the carotid sinus (at the bifurcation of external and internal carotids) and in the aortic arch (Figure 1). These receptors respond to stretching of the arterial wall so that if arterial pressure suddenly rises, the walls of these vessels passively expand, which increases the firing frequency of receptor action potentials. If arterial blood pressure suddenly falls, decreased stretch of the arterial walls leads to a decrease in receptor firing.

The carotid sinus baroreceptors are innervated by the sinus nerve of Hering, which is a branch of the glossopharyngeal nerve (IX cranial nerve). The glossopharyngeal nerve synapses in the nucleus tractus solitarius (NTS) located in the medulla of the brainstem. The aortic arch baroreceptors are innervated by the aortic nerve, which then combines with the vagus nerve (X cranial nerve) traveling to the NTS. The NTS modulates the activity of sympathetic and parasympathetic (vagal) neurons in the medulla, which in turn regulate the autonomic control of the heart and blood vessels.

Of these two sites for arterial baroreceptors, the carotid sinus is quantitatively the most important for regulating arterial pressure. The carotid sinus receptors respond to pressures ranging from 60-180 mmHg (Figure 2). Receptors within the aortic arch have a higher threshold pressure and are less sensitive than the carotid sinus receptors. Maximal carotid sinus sensitivity occurs near the normal mean arterial pressure; therefore, very small changes in arterial pressure around this "set point" dramatically alters receptor firing so that autonomic control can be reset in such a way that the arterial pressure remains very near to the set point. This set point changes during exercise, hypertension, and heart failure. The changing set point (response curve shifts to right) explains how arterial pressure can remain elevated during chronic hypertension.

Baroreceptors are sensitive to the rate of pressure change as well as to the steady or mean pressure. Therefore, at a given mean arterial pressure, decreasing the pulse pressure (systolic minus diastolic pressure) decreases the baroreceptor firing rate. This is important during conditions such as hemorrhagic shock in which pulse pressure as well as mean pressure decreases. The combination of reduced mean pressure and reduced pulse pressure amplifies the baroreceptor response.

Although the baroreceptors can respond to either an increase or decrease in systemic arterial pressure, their most important role is responding to sudden reductions in arterial pressure (Figure 3). This can occur, for example, when a person suddenly stands up or following blood loss (hemorrhage). A decrease in arterial pressure (mean, pulse or both) results in decreased baroreceptor firing. Autonomic neurons within the medulla respond by increasing sympathetic outflow and decreasing parasympathetic (vagal) outflow. Under normal physiological conditions, baroreceptor firing exerts a tonic inhibitory influence on sympathetic outflow from the medulla. Therefore, acute hypotension results in a disinhibition of sympathetic activity within the medulla, so that sympathetic activity originating within the rostral ventrolateral medulla increases. These autonomic changes cause vasoconstriction (increased systemic vascular resistance, SVR), tachycardia and positive inotropy. The latter two changes increase cardiac output. Increases in cardiac output and SVR lead to a partial restoration of arterial pressure.

It is important to note that baroreceptors adapt to sustained changes in arterial pressure. For example, if arterial pressure suddenly falls when a person stands, the baroreceptor firing rate will decrease; however, after a period of time, the firing returns to near normal levels as the receptors adapt to the lower pressure. Therefore, the long-term regulation of arterial pressure requires activation of other mechanisms (primarily hormonal and renal) to maintain normal blood pressure.

This information from PhD Richard E. Klabunde lecture, that based on his book Cardiovascular Physiology Concepts (chapter 5, pages 93-123)


Do RNA molecules bind each other? I have a question, maybe a naive one.

Let's assume that we isolated some RNA from a tissue. Do RNA molecules can bind each other if they have the complementary sequence? I know that some small RNA molecules can bind other RNAs and regulate them but I do not know it is possible in this case? It is like 2 different mRNA can bind each other or not?

The difference between RNA and DNA is rather small, and both can form a double-helix structure. So if you had two sequences of RNA complementary to each other they would basepair and form a helix.

There were also some ideas to use this for therapeutic purposes, antisense RNA, an RNA oligo complementary to a messenger RNA, can theoretically be used to silence gene expression by base-pairing to the mRNA.


Why does dehydration lead to low blood pressure I understand that the two leading causes of death from dehydration is imbalance in electrolytes and loss of blood pressure. I'm trying to understand what role water is playing in these cases and how the loss of it causes these imbalances, focusing for now on the blood pressure angle.

While I understand that blood is made up heavily of water, I'm still a little confused why dehydration so quickly leads to drop in blood pressure.  Why can't the body continue to pump the already existing blood through the body, where is it using the water to keep the blood pressure up and what vital function is no longer being performed that causes that pressure to drop?

The blood pressure is the  exertion of force upon the blood vessels by the blood fluids. Thus having less fluids will results in decreased pressure.


Why do we do nested PCR? Wikipedia:

  Nested polymerase chain reaction (Nested PCR) is a modification of
  polymerase chain reaction intended to reduce non-specific binding in
  products due to the amplification of unexpected primer binding sites.

I understand that there are two steps and one of those steps involves a non-specific primer followed by a specific primer...

But this does not seem to have sense. What is the purpose of running a non-specific PCR just to hit it with a specific primer afterwards?

What do we gain when doing a nested PCR?

Practical example:
We are planning on sequencing human skin microbiome. Would the ratios of different bacterial species differ if we would use the nested PCR products for sequencing, as compared to standard PCR?

In the paper by K. Lily Therese, U. Jayanthi & H.N. Madhavan traditional PCR wasn't sensitive enough to allow for an accurate reading on what they were trying to study. By using nPCR they were able to amplify around the gene they were interested in and then amplify just the gene they were interested in for a more accurate and sensitive study. The successive PCR allowed them to amplify their specific gene even if there was only one copy in the sample.

I recall using this procedure in Molecular Genetics Lab, it was used to make sure that our sample was purer.


At what point during an action potential are the sodium potassium pumps working? I'm trying to understand how all of the potentials during an action potential are created. My question specifically is about the sodium potassium pumps, however I would also be grateful if someone could verify if I have grasped the concepts correctly.

From what I understand, the resting membrane potential is at around $-60\rm\,mV$, close to the equilibrium potential for potassium (from the Nernst equation) because the permeability of potassium is much greater than that of sodium, even though the permeability is low.

However, the resting potential is not as negative as the equilibrium potential for potassium because of some permeability of sodium and the permeability of potassium is very low so the tiny permeability of sodium has some impact in preventing the potential reaching the equilibrium potential of potassium.

When the threshold potential of $-50\rm\,mV$ is reached, the voltage gated $\ce{Na+}$ ion channels open, and sodium ions enter the cell, causing depolarisation. The potential rises to about $+40\rm\,mV$, which is close to the equilibrium potential for sodium (because the permeability for sodium is much greater than for potassium). However, it doesn't quite reach the equilibrium potential for sodium because of some potassium ions leaving the cell.

When the $+40\rm\,mV$ threshold is reached, sodium channels close and potassium channels open. Because of the now much higher permeability of potassium ions compared with when the membrane is at its resting potential, the potential becomes much closer to the equilibrium potential for potassium, which I think is about $-90\rm\,mV$, and therefore the cell hyperpolarises. Then the potassium channels close.

Now I'm unsure as to how the resting membrane potential is reached from the hyper polarised state, and I also do not see where the action of the sodium potassium pumps comes into this.

The Sodium-Potassium Pumps are always at work. One can think of them as a continuous process that maintains the equilibrium potential for the individual ions. They always are grabbing internal sodium and exchanging it with external potassium at the cost of ATP.

However a neuron's rest state (in your example -60 mV) is a combination of the equilibrium of the Sodium, Potassium, Chlorine, and other ions. Thus when the membrane hyperpolarizes beyond the rest potential, it is actually the leak potential that brings the membrane potential back up, not the Sodium-Potassium pump.

Leak potentials arise from ions (usually chorine) that pass through the membrane via channels that are always open. Furthermore, sodium channels reactivate and a small amount open to  sodium to enter. (Recall as a population there is usually a small amount of sodium channels open at rest. Another contributing factor is as the potassium channels close the other to factors dominate and slowly bring the membrane back to rest state. Remember that rest is defined as the balance of currents, there will always be small amounts of currents flowing. So even though the neuron is rest small amounts of sodium leak in and less potassium out. The sodium potassium pump maintains the equilbrium potential that allows these currents to flow.

The Sodium-Potassium pump is a slower process, so it usually can be ignored over a single spike. But If there is a high frequency spike train then the small amount of sodium that enters the cell and potassium that exits the cell can add up and effect the equilibrium potentials of the individual Ions. This of course changes the firing properties of the neuron.


Can anybody identify this kind of plant? Location: Low Tatras, Slovakia, elevation: 1800 m. Can anybody identify this plant from Slovakia mountains?

I think this is some kind of Hypericum.  In Costa Rica and the Andes there is a high altitude ecosystem called the paramo in which shrubby Hypericum are characteristic species.  The area in your photo looks to be covered with shrubby species, and you are at decent altittude.  Looking at your picture (at full size) the leaves look approximately decussate which is typical of the genus, and also, the stems are ridged which is also pretty characteristic.

There is a good paper here on Hypericum of the Mediterranean region.  It mentions some groups that are shrubby or dwarf but thus far I have not been able to find a species that looks just like your picture.

Update: Possibly it is Hypericum aegypticum which looks about right relative to your picture, esp, the leaf color and size.  Also known to grow at that altitude. Decent picture here plus the one at Wikipedia both look similar to yours.

Update 2: On fresh look, the bases of the leaves for Hypericum aegypticum don't compare well to your picture, but I still think it is a Hypericum.


In theory how fast could nerve signals travel if the nerve fibre was perfectly insulated? My question is purely theoretical and my main aim is to find out the maximum speed that a nerve signal can travel within a nervous system and and whether this speed represents the physical limit of how fast a nerve signal can travel. This could also extend to designs not seen in nature and possible artificially designed nerves i.e. synthetic biology. Apologies for an awkward question!! Any input is welcome!!

For some background on saltatory conduction: https://en.wikipedia.org/wiki/Saltatory_conduction

I feel that a "perfectly insulated" neuron couldn't actually allow the signal to travel. Insulation (which, in neurons, is basically layers of fat wrapped around axons so ions cannot pass) allows the electrical signal to move further along axons (less ionic leakage) and faster (due to decreased membrane capacitance-it takes less charge movement to generate the same potential difference across the membrane; see this question: How is membrane capacitance related to the increased speed of saltatory conduction?)

Also, you should check out wikipedia's page on cable theory of neurons:
https://en.wikipedia.org/wiki/Cable_theory

This is why myelination increases conduction speed, as you may or may not already know. The increased length of the ionic signal (due to the inhibited leakage) allows voltage-gated ion channels which are further away to be activated as a result of any given local membrane depolarization. This all happens faster due to the lower capacitance.

However, the only way the action potential can actually "travel" at all is due to the sequential activation of voltage-gated ion channels along the axon. This is the case in both myelinated and unmyelinated axons, it's just that the spacing is greater when myelinated. In the insulated, fat-wrapped regions of axonal membrane, there are no ion channels, voltage-gated or otherwise. If there were, the layers of fat would not allow ions to pass through anyway at this point. Thus, the "perfectly insulated" axon could never actually propagate a signal, because the signal still requires the chain reaction of voltage-gated ion channel activation and sodium influx at some point. Myelinated conduction is faster because the spacing is increased, but increasing the spacing to infinity would not allow the action potential to be passed on.

I suspect that there is a certain threshold in the extent of myelination where the spacing between nodes of Ranvier becomes to great to have effective propagation of action potentials. I wouldn't be surprised if evolution has resulted i a relatively optimal spacing of nodes. I suppose a better question might be: what is the speed of conduction between nodes?

I suppose it would be possible to send current through a perfectly insulated axon and potentially activate a voltage gated calcium channel at the terminal. However, This would be different than an action potential and would be effectively reducing the neuron to an electrical wire. Sometimes it's better to keep things simple.


Why not replace the human genome with it's decoy genome version? https://www.biostars.org/p/73100/
http://www.cureffi.org/2013/02/01/the-decoy-genome/

The decoy genome is an improved human genome from the regular reference. It's faster for mapping and it reduces false positive rate.
In this case, there shouldn't be any reason to use the regular human reference, because the decoy genome is simply better and faster. For instance, it has DNA sequence for common virus genomes presented in humans. It has everything in the regular reference.
Q: What's the point of the regular human reference (e.g. hg38) if the decoy version is more accurate and is a better representation for the human variation.

To clarify, when you say "decoy genome" you hopefully mean the decoy genome and the reference genome together; the decoy genome itself is not a complete reference, but a collection of contigs assembled from reads that didn't map to the current reference genome, but are known to be human sequence.

The decoy genome certainly seems to be a useful supplementary data set for speeding up read mapping to the human genome but it cannot be better than the reference because it is not comparable to the reference.


How much of the jejunum is bypassed during gastric bypass? There is both long and short limb gastric bypass surgeries (along with several other variations on intestinal bypass procedures). How much of the jejunum is bypassed with a long-limb and short-limb gastric bypass?

One of the most used surgical technique is Roux en-Y where the small intestine is divided approximately 40-50 cm below the lower stomach outlet and is re-arranged into a Y-configuration.

The portion of intestine (jejunum) from the upper stomach is called the "Roux limb". It has a total length of 80 - 150 cm.

So the Roux en-Y technique "bypasses" only the duodenum and a small portion of jejunum - no more than 50 cm, that's about 7-10% of total length of small intestine.

"Total gastrectomy with Roux-en-Y" by ignis - Own work. licensed CC BY-SA 3.0 via Wikimedia Commons.

Reference: Wikipedia contributors, "Gastric bypass surgery," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Gastric_bypass_surgery&oldid=606081291 (accessed June 27, 2014).


Is newly produced sperm healthy if there was previous DNA damage? I read that sperm cannot repair DNA damage. So does this mean that if your sperm has DNA damage, then all of your sperm (whether present or future) has DNA damage? Or does it just mean that the present sperm has DNA damage, but new sperm will be healthy?

Male gametes (aka sperm) is produced by meiosis of numerous germ cells (gametes precursors). It is unlikely that all germ cells have damaged DNA so the newly produced gametes should be healthy. This also implies that if the DNA inside the gametes was damaged after they were produced, then again, the new gametes will be healthy.

As a disclaimer, I am talking exclusively about damages to the DNA, it could very well be that gametes are unviable for other reasons than just spurious DNA (e.g. low mobility). In this case, viable gametes are unlikely to be produced unless the reason underlying the original production of unviable gametes is fixed (e.g. via medication).


I found this bug in my closet. Could someone help me identify? It looks like it recently died. The shell was shiny and smooth and fairly brittle. I've been having trouble identifying what it is because it doesn't quite look like any of your common house pests.

The bug is at most 4 mm. I live in a relatively old apartment in New York City and my best guess is that this guy crawled out of a crack in my closet wall.

The image you provided isn't the best of quality, but I really think it looks like a spider beetle. Anyone else agree?


Did animals evolve from plants? Did animals evolve from plants? Did animals' ancestors have chloroplasts in their cells?

See this paper "Divergence time estimates for the early history of animal phyla and the origin of plants, animals and fungi" for information on the divergence estimates (I'm not sure if there are more recent papers discussing this).

Plants, animals and fungi are eukaryotes, distinct from eubacteria and archaebacteria, which are prokaryotes. The difference being in the composition of the cell, particularly a nucleus contained within a membrane for eukaryotes, along with other membrane bound organelles, e.g. chloroplasts. They all share a common ancestor, according to this paper, that split 1.576 Bya (billion years ago) +/- 88 Mya (although it states the relationships are unresolved - it is often difficult to resolve relationships so deep in a tree). They form distinct groups known as Kingdoms under Linnaean based biological classification; the Fungi, Plantae and Animalia. Thus, in answer to your question, no, animals did not evolve from plants.

Plants have chloroplasts in their cells, which provide the ability to produce energy via photosynthesis. It is thought that the chloroplast resulted from a symbiotic relationship between early plants and a cyanobacteria in that they both relied on each other for survival and so coevolved. Animals don't contain chloroplasts and instead contain an organelle called the mitochondria (although most plants also have mitochondria), which is also thought to have been a bacterial endosymbiont, probably related to rikettsias.

Protists also contain chloroplasts. The protists are intermediate between all three groups and have been notoriously difficult to classify, being placed into a fourth Kingdom, the Protozoa, although this grouping has been contested. The current Cavalier-Smith system was proposed in 2004 and classifies life into 6 Kingdoms.

Chloroplasts are thought to have evolved from a single endosymbiotic event in Archaeplastida, although there are evidence to suggest some secondary endosymbiotic events. Check out this paper for more information; figure 1 shows the relationships between the different groups and the endosymbiotic events. The Opisthokonts are the origin of the Fungi and Animalia kingdoms.


Why aren't we allowed to refreeze previously thawed breastmilk in refrigerator? https://www.breastfeeding.asn.au/bf-info/breastfeeding-and-work/expressing-and-storing-breastmilk

  Previously frozen— thawed in refrigerator but not warmed

  4 hours or less (ie the next feeding)

  Store in refrigerator

  24 hours

  Do not refreeze

But in freezer the temperature is still below normal, still is there a probability of bacteria growth?

I wish to understand the reasons behind the warning. Answers with references will be appreciated.

This is just a guess, but I don't think this is a food safety issues, its more a case of 'this food is gross now' issue.

When I was a teenager I worked in a frozen food processing plant.  The freezers were giant boxes where freon was condensed on gigantic coils into a liquid and then the liquid freon would rain down on to the food passing under on a conveyer belt.  The vegetables were frozen instantly and it was quite tasty - frozen just a few minutes after being cleaned.

As industrial freezing is very quick and such flash freezing, the quality of the food is preserved in a pretty fresh state. [its horrible for the ozone in the atmosphere but this was in the 80s and I hope they changed the process].

Milk is a mixture of water based nutrients and globs of fat, which give the milk is homogeneous white color and its smooth texture.  Freezing milk in a typical refrigerator would take hours and ice crystals would form and separate out the two phases - the fatty portions would separate.  Try it with a glass of milk and see.   This is the same reason that you don't re-freeze ice cream, which has even heavier creme proportions (even fattier).  The texture is completely gone.


Required energy to metabolize fat Tl;dr: What is the net joule value of fat if used for energy provision, compared to e.g. carbohydrates. So does 1 Joule Fat intake result in 1 - X Joule energy provided to the cell, or does it work in a completely different way?

My understanding is that if I take in one Joule of fat, my body takes in the energy to move ~100g of mass up by one meter (Wikipedia).

Now for my body to use that energy, it needs to convert it to some sort of Glucose, right?

From the Lipid Metabolism Wikipedia Article I get that my fat needs to become a Triglyceride to serve as energy source.

There are some steps involved, roughly the following:

gastric peristalsis (basically muscle contractions to mix it all up)
peristaltic contractions in the gut (again, mixing is key)
lipase, also working in the gut to finally create Triglyceride
then the fat gets "packaged" in Chylomicrons and put into the bloodstream

releasing energy to the cell involves the following

Lipase unpacking the Chylomicrons
Splitting of the Triglyceride in Glycerin (the stuff we want) and fatty acids

Now this seems like a really cumbersome process to me, and I wonder what the net Joule Value is that arrives at the cell.
Is it significant, or is this process so efficient that it doesn't matter anyways?

So, what I was looking for, but was lacking the knowledge of, was the concept of "Thermic Effect of Food"
I really didn't know how to phrase my question well, due to the fact that I tackled the problem from the wrong angle.
Direct quote from the Wikipedia Article as it answers the question best:

The thermic effect of food is the energy required for digestion, absorption, and disposal of ingested nutrients. >Its magnitude depends on the composition of the food consumed:
Carbohydrates: 5 to 15% of the energy consumed [7]
Protein: 20 to 35% [7]
Fats: at most 5 to 15 %[8]


What happens if the Nematode epidermis becomes damaged? This animal has a hydrostatic skeleton which lets it move. If we damage the epidermis and fluids come out, can the nematode still move ?

Nematodes have external skeleton in the form of a cuticle. Their muscles are attached to this external skeleton and when a muscle cell contracts it moves a segment of the cuticle relatively to the other segments, which in turn allows the pushing of the environment and thus, motility. This is very similar to how we, humans, move.

Damaging the cuticle in nematodes results in motility impairment. For example, some C. elegans strains have a mutation that results in a non-normal cuticle formation which makes the animals roll instead of moving peristaltically (like a snake).

In addition, some muscles are not skeletal muscles, or body wall muscles in the case of nematodes. These muscles affect movement of an organ like the pharynx in nematodes or the heart in humans.

for further reading regarding the body wall muscles and cuticle interaction you can see wormatlas.org

References:

Labouesse, M. 2006. Epithelial junctions and attachments. WormBook, ed. The C. elegans Research Community, WormBook, doi/10.1895/wormbook.1.56.1


Effects of mushrooms on their hosts I learned that mushrooms are normally classified as either decomposers or symbiotes. I would like to know the differences between the two types and whether they are detrimental or beneficial to their host, often a tree.

It probably makes sense to classify mushrooms (fungi) in two separate ways:

symbiotic vs. free-living: symbiotic organisms are those that live in close association with a host (etymologically sym="with", biosis="life"), free-living organisms don't.  So a mycorrhizal fungus that lives within or on the surface of a plant root is a symbiote; a fungus that lives in the soil is free-living.
mutualistic (benefiting from and benefiting a host) vs. parasitic (benefiting from but harming a host) vs. saprotrophic (consuming already-dead material; these are your "decomposers"). (Commensalism [benefiting from, but neither hurting nor harming, a host] is  a fourth possibility.) Mycorrhizal fungi are generally mutualistic. Fungi like chestnut blight or the genus of phythophthora, which includes the organism that causes potato blight, are pathogens; so are the myco-heterotrophs. Fungi such as wood-decay fungi are saprophytic.

To answer your question, species of fungi that are associated with trees may be either mutualistic (e.g. mycorrhizal fungi) or parasitic (e.g. chestnut blight).

Parasitic fungi might also be called pathogenic (i.e., disease-causing)
In popular speech, "symbiotic" is synonymous with "mutualistic" (i.e., organisms that benefit each other); in biology, however, it may refer to either a parasitic or a mutualistic organism. An individual symbiotic organism is often called a "symbiont".
In general, saprotrophs would be free-living (since they don't get their resources from a host, it doesn't really make sense for them to live on a host)
Individuals of a some fungal species can switch lifestyles/categories depending on their environment: these are called facultatively mutualistic/commensal/parasitic, e.g. see Redman et al. 2001.

Redman, Regina S., David D. Dunigan, and Rusty J. Rodriguez. “Fungal Symbiosis from Mutualism to Parasitism: Who Controls the Outcome, Host or Invader?” New Phytologist 151, no. 3 (2001): 705–16. https://doi.org/10.1046/j.0028-646x.2001.00210.x.


Which beetle is this? I'm curious to find out what kind of beetle this is. Google lens search suggested a type of longhorn beetle, but I am not convinced.

The photo is taken in Karnataka, in India

Thanks!!

This is a beetle from the family of the "longhorned beetles", since you found this beetle in India, I think this is Acanthophorus serraticornis

See the images for comparision (from here and here):

There is not much information online, but some can be found here and especially  here in this scientific article. The larvae of this beetles are considered a pest, as the bore into wood.


How to interpret the simple sequence repeat (SSR) on the coding sequence, but not the related protein sequence? I have predicted some SSR repeat on the gene of interest using SSRLocator program, which the result creates a question for me. Please consider the below sequence, which is part of gene sequence of interest (coding sequence):

GGTGATGAGGTAGAGGAAGAGGCTGAGGAACCCTACGAAGAAGCCACAGA
GAGAACCACCAGCATTGCCACCACCACCACCACCACCACAGAGTCTGTGG
AAGAGGTGGTTCGAGAGGTGTGCTCTGAACAAGCCGAGACGGGGCCGTGC

The program reported CCA motif as a repeat; since this repeat located on CDS, I expected to find the related amino acid track (prolin), but I observed the Threonine track in the corresponding protein sequence.Threonine is coded by ACC. Now I would like to know which motif is really a repeat, CCA or ACC. Is it possible to consider CCA as a repeat, but just on the transcript level not protein sequence or the real repeat is ACC and the software didn't work well here? Please share me any your opinion in this regard.

Thanks so much for your help and participation.

SSR searching tools have generally no idea about CDSs: they consider DNA/RNA sequences as strings and search for tandemly repeated patterns, nothing else. It is also important to remember that in many real-life cases different programs with different settings will reports differing results.

[Knowing that you always have two strands in the genomic DNA, one has to bear in mind that also SSRs can be "read" in either direction, such that for a stretch ACCACCACC the unit can be reported as ACC or GGT. Some programs by default will report SSR units sorted according to alphabet: ACC in this case. Now with coding sequences the story is a bit different: RNA has only one strand, i.e. it has a direction, which means that you cannot "flip" RNA sequences.]

mRNA besides having a direction, codes for protein with the protein sequences sometimes showing their own repeated patterns. SSRs in mRNA are mostly tri-nucleotides or with unit lengths divisible by three and coincide with the tandem aminoacid repeats. So, from the functional point it is a ACC|ACC|ACC|ACC|ACC|ACC|ACA (note that the last element is ACA) repeat, which codes for the respective T|T|T|T|T|T|T aminoacid repeat. To formalize this idea you search for SSRs in the RNA sequence and in the protein sequence and try to find the overlap.

From the point of view of the DNA-polymerase [the enzyme which changes the SSR length] it is a perfect CCACCACCACCACCACCACCA repeat: within these limits the fragment is prone to slippage. But for an actual slippage event the unit boundary does not matter. Imagine that the polymerase "skipped" a CAC unit in the middle: CCACCAC[CAC]CACCACCACCA. The outcome for the protein sequence will be the same: minus one threonine.


Can the liver prioritize it's metabolizing potential? Let's assume we have two toxins - one of which is routinely metabolized by the liver, and the other is new to the organism (consider for example alcohol in a heavy drinker and any other drug that is taken for the first time) and they are administered at once.
Does the liver have any way to prioritize metabolizing either of these substances or does it happen simultaneously for both?

Aside from "toxins", the liver metabolizes a host of endogenous and exogenous compounds. Endogenous compounds are compounds that are normally present and produced within the body like ammonia and estrogens for example. Exogenous compounds are those like ethanol/alcohol, acetaminophen, and other drugs/etc that are not normally in the body but rather we take a mediations or recreational drugs, etc. Most of the compounds that the liver metabolizes are through a set of enzymes called the cytochrome P450 system, which includes numerous enzymes (too many to list here) that catalyze a number of reactions that help detoxify a substance and/or make it more likely to be excreted in the urine by the kidneys.

If the liver "sees" old and new compounds it doesn't differentiate between which it might metabolize first - that is based on concentrations within the liver. In fact, only if the compounds are metabolized by the same liver enzymes will they compete with one another. If they are metabolized by the same exact P450 enzymes, then the concentrations of each of these substances within the hepatocytes (liver cells) will determine which one gets metabolized more frequently. For example, if the concentration of substance A is much, much higher than substance B, then substance A is going to outcompete the other substance for the enzymes that metabolize it (similar to competitive inhibition in biochemistry). Most of the time, endogenous and exogenous compounds do not necessarily compete at the same P450 enzymes because there are so many different P450 enzymes within the liver.

The liver does not have any way of prioritizing different compounds, however, if the liver is exposed to a particular substance over a long amount of time then it may express more of a particular cytochrome P450 enzyme that metabolizes that particular substance. This is similar to alcoholics being able to metabolize a lot more alcohol than someone who has never drank alcohol previously.


Why does oxygen bind to hemoglobin in an specific angle? There is an specific angle of the bond between oxygen and hemoglobin in lungs, which I don't know, but what interests me more is the question, why is it specific?

summary:
O2 could form a linear complex with the Fe atom, but then it would start to look more like a mineral Fe=O...O bond - a linear bond would be like a transition state to an iron oxide (rust).   An Fe-O-O bent bond preserves more of the electronic character of the O2 molecule and promotes strong but reversible binding to Hemoglobin.

The oxygen molecule forms a partial covalent bond with the iron in the heme (the ringlike molecule in the picture below  ).  The lone pair of electrons of the oxygen atom which forms the bond to the iron has a 120 degree angle with respect to the oxygen molecule itself.  In chemistry we say it is sp2 hybridized.  This implies a slightly greater than 120 degree angle between the Fe-O and the O-O axis would be energetically preferred in oxygen binding.

You can see on the other end of the oxygen, there is a histidine sidechain nitrogen which interacts in a similar way - crooked at a similar angle to the oxygen molecule.

As @MattDMo points out in the comments, it would not be 120 degrees exactly in fact even freshman chemistry molecular orbital theory would say that the double bond would take up more 'space' than the sp2 orbitals, widening out the angle Fe-O=O angle to be greater than 120 degrees.  Then the protein has its own geometry - the histidine and the heme iron are fixed in space and probably have their own location, so this is just an approximate, qualitative bond angle..

The claims of superoxide formation is because the oxygen is diamagnetic the iron and he oxygen, which are both paramagnetic, somehow pair to eliminate their magnetic moment.  The PNAS paper cited here goes in depth on this issue.  The article curiously just says the highly reactive superoxide is kept from being chemically consumed by the hydrophobic pocket around it.

The oxygen almost makes a superoxygen the iron sort of oxidizes but doesn't quite. Its also due to the peroxide like character of the oxygen molecule, partially bonded at both ends.

Still the point is that hemoglobin holds onto the oxygen by making a partial covalent bond.  After all when the O2 unbinds, its just O2 again.  A later study does detect some paramagnetism at low temperatures. In the last word on this that I could find, Pauling does a review and concludes that the electronic state of the heme iron and oxygen complex is a combination of three different electronic states - partly superoxygen, partly oxy-iron and molecular oxygen.

The reference also gives the Fe-O-O angle as 117 degrees.

[Just a note that the reference page I got the picture from refers to rational design of the hemoglobin molecule...in this case they are engineers talking about how they could change the amino acids in the protein to get other properties out of the hemoglobin system - rationally.]


Can a virophage potentially be used to cure a viral disease? Wikipedia states "Virophages are satellite viruses that inhibit or impair the reproduction of the auxiliary virus."

Is it theoretically possible for a virophage that doesn't hurt the human body to attach itself to a more serious virus like the AIDS virus for example and be used to wipe out the virus, or at least inhibit it's reproduction?  I'm completely ignorant of the virophage relationship, so feel free to inform me as needed.

There are few enough virophages occurring in nature that I don't know if there's a clear and compelling case for them being potentially therapeutic.

In principle however, the answer is yes, though they may suffer from the same problems that bacteriophage treatments have suffered during their history - difficulty in preparation, extreme species specificity, and fairly daunting regulatory hurdles. While viral diseases don't have the "Or we could just use antibiotics, which work" out which made bacteriophages less popular, as far as I know there's not been a suggestion of widespread virophages against human pathogens.


Nucleotide sequence for STRING protein sequence I have protein sequences from STRING database:
The amino acid sequence files are like this:

  4932.Q0010 (Saccharomyces cerevisiae)
  MYYIMFLYNMLLIIILIFYSIVGVPIIIFNNNYYWDPDIFLFIIYYFIKFIIIFNLYLYYMINYIVYTPSGSPPGRGTYI
  LLYNMLYSYNMFIDYVMKFITCVTYMYLMFWLLSPTPSPYYVSEVPVS

I want the corresponding nucleotide sequence for the same protein ID.

  4932.Q0010

I tried emboss http://www.ebi.ac.uk/Tools/st/emboss_backtranseq/
But emboss is based on codon usage and backtranslate and it doesn't give me the original nucleotide sequence.

Then I tried DDBJ http://getentry.ddbj.nig.ac.jp/top-e.html
But DDBJ gives only amino acid sequences for corresponding Uniprot ID.

How do i get the original nucleotide sequence for the STRING protein sequences using STRING id or UniProt ID?

Any help in this regard is highly appreciated.

Google is not a bad resource for such a question.

In this case I find that the Yeast Genome site has a button which returns the nucleotide sequence. You can select the genomic sequence for the locus or the coding (CDS) sequence.

http://www.yeastgenome.org/cgi-bin/locus.fpl?locus=Q0010

They also give a link to NCBI at the bottom of the page.  I think the reason you were having such a hard time is that UniProt extracted the protein sequence from the mitochondrial genome record.  Like many genome ORF predictions, Q0010 does not seem to have a distinct nucleotide record assigned yet.

Summary:

In general  you can do a web search for the uniprot id to start.  In many cases, like this one you will find that the nucleotide seq is only a chromosomal sequence record.   Biodatabases are a bit of a maze - there are scores of them out there, you may find that someone has clipped the nucleotide sequence of the gene out, which is helpful if there are introns!


Do cockroaches have less health issues than humans? Cockroaches are known to live in very dirty places like sewers. Does this cause them to evolve to be stronger against parasites and bacteria? Recently I read online that cockroaches can sustain radioactive harm 6-15 more than humans, so does that mean that cockroaches are less likely to get cancer?

refernece for the radioactive exposure:

http://www.abc.net.au/science/articles/2006/02/23/1567313.htm?site=science/greatmomentsinscience

AndroidPenguin, where did you read that our immune systems are far better than those of 'a cockroach'? This seems pretty strange to me, but I'd be interested in reading a study that compared human and cockroach immune systems if you can provide a reference.

Victor, with respect to cockroaches, there are numerous species of cockroaches. Here's a page about cockroaches with a link to publications on cockroaches and a phylogenetic tree of the families and subfamilies.

http://www.bio.umass.edu/biology/kunkel/cockroach.html

All those species tend to occupy distinct niches with distinct traits. With respect to cockroach evolution, sewers are too new a phenomenon to have had an influence on cockroaches. Rather cockroaches have been successful in adapting to this novel 'habitat'. The same holds for rats and other denizens of sewers. Sewers are a very nutrient rich environment, and as in many nutrient rich environments, a few species tend to possess the right traits (whatever those may be) to survive and out-compete other species. To take an example from coral reefs, when coral reefs suffer from eutrophication, this leads to a growth in phytoplankton and a reduction of the euphotic zone that can lead to the death of all but the most resistant corals. Likewise in the terrestrial environment, only the most tolerant or opportunistic species tend to survive in highly perturbed and nutrient rich environments like sewers. With respect to cockroaches getting cancer, I've never read anything about insect cancer, but I imagine in theory that they could get cancer. I'm not sure, however, of the impact given the much shorter life spans of insects. It's an interesting question though.


How is there no limit to a human lifespan again? It's probably just misconstrued pop science, but I thought a read an article recently that said there's no known limit on how long humans can live. I could have sworn though that there were a few automatic processes that took place though, like that the chromosomes all shorten in length every time they're copied (is there any limit to that? Also, why does that matter?), the retinas in the eyes harden, the metabolism slows down, the heart muscles wears out, etc.
So, how could it be true?

You're probably reading about the recently-published responses to a publication that argued there is a limit to human lifespan.

The original article is Evidence for a limit to human lifespan, and in the June 29 issue of Nature there are five responses to it:

Contesting the evidence for limited human lifespan
Many possible maximum lifespan trajectories
Is there evidence for a limit to human lifespan?
Questionable evidence for a limit to human lifespan
Maximum human lifespan may increase to 125 years

Each of these responses has, in turn, a reply from the original authors.

The arguments turn on fairly intricate details of statistical analysis and database interpretation, and I think it's fair to say that outside experts remain unconvinced either way -- neither the original article, nor any of the five responses, nor any of the five responses to the responses, presents a slam-dunk case for or against a limit to human lifespan.


Transmission of HIV from Mother-to-Child Through Breastfeeding If a mother is HIV+ and was on medications which would help her deliver a HIV negative baby, can the baby contract the HIV through her breast milk?

In short, yes. Breast milk can contain virions which can be transferred from Mother-to-Child.

These are the guidelines from the National Institute of Health in the United States regarding the Prevention for Mother-to-Child Transmission of HIV and how the prevent Mother-to-Child Transmission of HIV After Birth

While the guidelines in the US are geared towards the fact that we have alternatives to breast milk, the World Health Organization has compiled evidence that suggests that Antiretroviral therapies along with exclusive breastfeeding may provide the most benefit for the health of the infant. This likely has to do with the access to suitable nutritional alternatives, clean water, and vaccines in developing countries, and in fact, it appears that mothers in wealthy countries that have HIV are advised not to breastfeed at all. This site outlines the different guidelines in place. The choice between breastfeeding and not in lesser developed countries has to do with the fact that the risk from waterborne illnesses and their impact on infant mortality rates is likely far greater than the risk of HIV transmission from mother to child through breastfeeding while both are on Antiretroviral therapy. The reason that exclusive breastfeeding is recommended is that it keeps the viral concentration in breast milk lower than if the baby was suckling only part of the time.

Italics in previous paragraph indicate an edit to the answer in order to clarify the reason why breastfeeding is recommended in lesser developed countries, even though it poses a risk for HIV transmission

Please note that these guidelines are in flux and as more evidence is obtained and as the virus mutates, things may change. It is always best to consult with a physician on the most current recommendations in the care of your infant if you are HIV+.


How do physics notions of fluid dynamics relate to pressure gradients in circulation? I'm having a hard time comprehending why sometimes physiology notions seem to contradict each other and contradict physics teachings.
More specifically I don't understand why aortic coarctation causes the pressure gradient to increase. In this condition the radius of the blood vessel decreases which should mean that pressure decreases too. According to Bernoulli theorem ΔP+Δvp/2=o
where v is velocity and p density. This theorem and the fact that velocity has to increase to maintain a stable flow through the coarctation should mean that the pressure gradient drops. Moreover in every textbook I've found it is said that tension on the aortic wall increases too but this seems even more counterintuitive, because if the radius decreases due to La Place T=Pr tension (T) should decrease too.
Then the most puzzling thing to me is the pressure drop when there vasoconstriction of  the arterioles, this is fine according to my reasoning so far (except it seems to contradict aortic coarctation) but resistance is supposed to increase too with vasoconstriction, and because of this equation: ΔP=Q*R (where Q is flow and R is resistance) the pressure gradient should go up. Now I think I understand that it increases because of the successive drop in pressure, correct? What am I missing with aortic coarctation? I'm sure it has to do with confusing the PTM in that specific place and the pressure gradient but I can't figure it out.

As far as we know so far, biology isn't able to break any laws of physics.
However, biology isn't passive: biological systems react to changing environments to maintain some level of homeostasis. Arguably this is one of the defining characteristics of life.
If you narrow the aorta, you will always get compensatory changes. Ultimately, the circulatory system is tasked with delivering sufficient blood to the body. It might be a bit of an oversimplification, but let's assume that blood flow stays constant, because flow is a good measure of the ability of circulatory system to deliver enough oxygen/nutrients to the periphery.
Blood flow is pulsatile, which also adds some challenges in understanding things simply, but let's simplify and think in terms of mean pressures. Again, this is wrong, but it's not terrible, kind of like when in a physics class you discuss a "uniform spherical cow" or something like that.
We can start with an equation you mentioned:
ΔP=Q*R
You write:

In this condition the radius of the blood vessel decreases which should mean that pressure decreases too

This is false. If we keep flow (Q) constant, but R increases due to a constriction, then ΔP, the change in pressure, must increase.
Consider:
ΔPaorta=Q*Raorta
If Q stays constant, but R (resistance) increases due to the decreased radius, then ΔPaorta must increase: there is a larger pressure drop. Perhaps you've confused the larger change in pressure with a "decrease in pressure" because there is this larger pressure drop?
Consider also that we can consider the rest of the parallel vasculature (all branches off the proximal aorta) in series with the aorta. If we think of the vasculature after the aorta as:
ΔPdistal=Q*Rdistal
then you can think of the whole system as:
(ΔPaorta + ΔPdistal) = Q*(Raorta + Rdistal)
If only the aorta is constricted and the distal vasculature keeps the same pressure and flow, then ΔPdistal must also not change. Therefore, the total pressure drop (equal to the difference in pressure between the aorta and great veins, the sum ΔPaorta + ΔPdistal) will be larger when ΔPaorta increases.

As far as Bernoulli:

This theorem and the fact that velocity has to increase to maintain a stable flow through the coarctation should mean that the pressure gradient drops. Moreover in every textbook I've found it is said that tension on the aortic wall increases too but this seems even more counterintuitive

Due to Bernoulli, if you go from large (A), to small (B), to large (C) diameter in some vessel, yes, you will have less outward pressure in the segment (B). You will also always have decreasing energy from A to B to C. However, think about what we were just talking about: if you want to keep the perfusion of the rest of the vasculature constant, that means you have to keep the energy at C (interchangeable with pressure in this context) constant, despite the constriction. You shouldn't be thinking about A B and C here when comparing a vessel with and without stenosis, you have to think about the non-stenosed case where you have large (X), large (Y), large (Z). In this case, you still have decreasing energy from X to Y to Z, but without the stenosis, you don't lose as much going through segment "Y". It is segment A that requires more energy/pressure/tension on the vascular wall compared to segment X.
There's some simplification here regarding vascular compliance, non-Newtonian fluids, and vascular permeability but these can be mostly ignored for these purposes. I think this website will help you a lot:
https://www.cvphysiology.com/Hemodynamics/H001
especially
https://www.cvphysiology.com/Hemodynamics/H012
for the part about Bernoulli's principle.


Why there aren't any pandemic diseases by prions? Learning biology in school, I became interested in the fact that there aren't any diseases by prions which are globally infectious (as far as I know), unlike diseases by viruses (ex. COVID-19, SARS etc.) or by bacteria (ex. plague, ...). Why is it?
cf. Here are some my hypothesis

Prions are not efficient pathogens because they don't have DNAs.
Such prions are not yet discovered or does not exist.
There exists lots of people who are immune to such diseases.

Are there any answers to the questions? Or is there any answers?

I think that you could argue that some prion diseases do form epidemics or outbreaks. In some cases it does appear that people have referred to BSE/vCJD as pandemics. There is even some journalism on the topic, and see also here.
Infection by prion from the environment does occur at some rate, and it is true that it is these prions are the more transmissible. See Table 1 in that linked paper for more information; it appears that the discovery of prion excretion through e.g. feces is relatively recent.
For less transmissible variants it is true that you usually have to directly ingest a fair amount of prion from (i.e. eat) an infected individual to be affected, which is a harder means of transmission because it implies cannibalism (which is not that uncommon biologically, but still).


Hemoglobin oxygen affinity curve I have a general understanding of the Bohr effect, and that Hemoglobin's affinity for oxygen will shift depending on the conditions of the lungs and tissues. However, I'm struggling with the following question; I feel as though I'm getting caught on the less-than-ideal answer choices, but I want to make sure I'm not missing a basic principle that could reason this answer more clearly.

Q) Which of the following best describes how a shift to the right in the dissociation curve results in more oxygen delivered to tissue?

A) The distance between the curves at 100 mmHg is less than the distance at 40 mmHg

B) The distance between the curves at 100 mmHg is more than the distance at 40 mmHg

C) On the right-shifted curve, Hb will pick up more O2 in the lungs

D) On the right-shifted curve, Hb will pick up less O2 in the lungs

My reasoning for choosing A is less-than-ideal: let me explain. First, I've been taught that a good rule-of-thumb for oxygen affinity is that Leftward shifts are related to the lungs, while Rightward shifts are related to the tissues. Therefore, because the answer choices C & D refer to right-shifted curves and the lungs, they can be eliminated. However, I'm not convinced this "rule" is so absolute - I can imagine that the curve can shift left & right within the tissues and the lungs. For the sake of argument though, I'll assume the rule works and eliminate answer choices C & D. Then, I can also eliminate answer choice B because it's not a true statement. As a result, I arrive at answer choice A. However, I don't feel as though it quite answers the question. Can anyone please provide some insights as to my reasoning, and/or perhaps what I'm missing? Thank you!

Comment: this question is a bit confusing, since none of the answers seems to directly explain how a shift to the right in the dissociation curve results in more oxygen delivered to tissue. Therefore, we'll try to choose the least wrong option...

This answer came out a bit long, so here's a TL;DR for you. I chose

   Option A

and here's why:

Although not stated explicitly, the pH in question is most probably the blood pH (this is a rather well-known graph from biochemistry undergrad studies). It shows that when blood pH drops or rises, the amount of %O2 saturation of hemoglobin deviates from the norm accordingly.

First of all, regarding your rule-of-thumb, it might be misleading in this context, since it may be true in both normal conditions and pathological conditions, depending on the site of measurement:

Under normal conditions, general blood pH is around 7.4 (7.35-7.45), blood pH in the tissues is around 7.2 (due to increased pCO2 resulting from cellular metabolism), and blood pH in the lungs is around 7.6 (due to the release of CO2 in the lungs for expiration, which results in lower pCO2 in the lungs) - see this reference and its references.
Under pathological conditions, general blood pH may rise above 7.45 (alkalosis) or fall under 7.35 (acidosis), regardless of the site of measurement [reference]. This means that a dissociation curve under abnormal blood pH value does not necessarily relate to normal conditions in a certain body site, but may also relate to a pathological condition in which blood pH is abnormal in general.

I believe the graph represents the latter situation, i.e. how hemoglobin behaves under the pathological states of acidosis (lower blood pH = right-shift) and alkalosis (higher blood pH = left-shift) compared to the normal state, since it depicts the change in %O2 saturation over the physiological range of pO2 and the curve is continuous (a depiction of blood pH only in the tissues or the lungs would not have resulted in a curve, since pO2 does not change significantly in each site, certainly not over the physiological range).

Now let us consider the possible answers:

Option A - The distance between the curves at 100 mmHg is less than the distance at 40 mmHg. This seems to be true in it's own right. However, other than describing the situation, it does not explain explicitly anything. It essentially says that the difference between oxygen release in the tissues is more pronounced than the difference in oxygen binding in the lungs, when comparing normal blood pH and acidosis. We can infer that if the right-shifted curve is below the normal and left-shifted curve, it means that less Oxygen is bound in the tissues (and also everywhere else, since this trend is consistent), i.e. Hemoglobin is less saturated, i.e. more Oxygen is released in the tissues in a state of acidosis than in any other state.
Option B - The distance between the curves at 100 mmHg is more than the distance at 40 mmHg. This is merely the opposite of A, and therefore is untrue by the same amount that A is true.
Option C - On the right-shifted curve, Hb will pick up more O2 in the lungs. This is a bit trickier. This option suggests that when pH is lower-than-normal (acidosis), more Oxygen will bond to Hemoglobin in the lungs. However, by observing the graph, we can see that the right-shifted curve is always below the other curves (both the normal and the alkalosis curves). This is also true in high values of pO2, which are present in the lungs. This renders this statement incorrect in itself, and it also does not explain why more oxygen is released in the tissues.
Option D - On the right-shifted curve, Hb will pick up less O2 in the lungs. Based on the analysis of option C, it should be rather evident that the opposite must be true. That is, if the right-shifted curve is always below the other curves, including in high pO2 values, then under this condition Hemoglobin is bound to pick up less oxygen in the lungs than in any of the other conditions. Therefore, this statement is correct, but it does not explain why more oxygen is released in the tissues.

According to the section titled The influence of pH on oxygen-hemoglobin binding in this excellent reference, "the presence of a low pH locks it [hemoglobin] in an unreceptive state, preventing it from binding oxygen molecules". This means that Hemoglobin's affinity to oxygen will be reduced, so that more oxygen will be released (in other words, less will be bound) in the tissues and less oxygen will be bound in the lungs. The two "less" in the previous sentence are in accordance with the curve of pH=7.2 being below the other two curves over the entire range of pO2. I highly recommend reading the above reference through and observing the figures.

To sum up, none of the possible options is satisfying enough, but option A seems to be the least wrong or unrelated to the situation described, so I would choose it.


What does breathing through the mouth have to do with cracked lips? https://www.healthline.com/health/mouth-breathing#symptoms3

Symptoms in children
Children who breathe through their mouths for most of the day may also have the following symptoms:
...
...
dry, cracked lips
...

Why can breathing through mouth result in dry, cracked lips?

You may notice waking up with chapped lips at times. It may be because of sleeping with your mouth open. So, of course you breathe through your mouth all night, leaving it exposed to continuous flow of your breath. Continuous airflow around the mouth region can cause chapped lips in many individuals.


Continuous EEG: Where does pronounced power peak at 38 Hz come from? I'm pretty new to EEG analysis. I measured EEG on six scalp positions over night. When I plot the power of the frequencies, I get the following:

What I want to explain (and didn't manage to) is the origin of the 38 Hz peak in my case.

The most important steps to arrive at my graph were (using Python-MNE):

band-pass filter of data (1 to 45 Hz)
resampling from 512 Hz to 200 Hz

Then for every of the six channels:

cut recording into consecutive segments of 2 sec duration

exclude segments if:

maximum allowed voltage step of 50 µV is exceeded
activity is lower than 0.5 µV
maximum and minimum amplitude exceed +/- 200 µV
maximum absolute difference of values in the segment > 200 µV

further:

retain only segments that are ok for all electrodes
randomly choose 15 such good segments (all electrodes) from every participant
calculate FFT for every 2 sec time segment for every electrode and participant
calculate mean of all these FFTs
plot

My question is: is someone familiar with such an artifact at 38 Hz? Where could it come from? These are the things I already checked:

it is pronounced in every participant
it is pronounced in every electrode
eye movements are unlikely since this peak is there after filtering out horizontal eye movements via ICA
electrical devises are unlikely since they should peak at 50 Hz
it is pronounced when segments are 6 sec instead of 2 sec
I also used a notch filter at 50 Hz instead of the bandpass filter, with the following result (here the individual 15 segments are shown, but the 38 Hz peak is still there):

Does someone have an idea where this feature could come from?

Someone taught me how to make a more informative plot without preprocessing the data. It thus seems like this artifact is 12.5 Hz apart from 50 Hz and therefore has something to do with the line noise from nearby electrical devices. The same pattern happens at 150 Hz.


What is the relationship between UV wavelength and penetration depth into human skin? Some background - Some recent research has strongly suggested that UVA penetration into the skin is far more dangerous than UVB, a very good example is this paper by Agar et al. (2004).

My query is, is there a measure that relates the UV wavelength with the penetration depth into human skin?  Related, is the answer to this related to skin types?

(I understand that this may be migrated to Biology.SE).

Solar UV radiation is broadly classified as UV- A,B and C (Decreasing order of wavelengths). Penetrating ability of UV is a not a direct function of its wavelength; lesser the wavelength lesser is the penetrating ability (But higher is the energy: a direct function of wavelength). Penetration ability is dependent on scattering and absorption. Most biomolecules in the skin, including melanin and proteins absorb at around 220-300nm range. Plus, scattering (esp Rayleigh scattering) is inversely proportional to wavelength.

Since UV B has higher energy compared to UV A, the former is more toxic to the cells. But a little UV B also does some good; conversion 7-dehydrocholesterol to Vitamin D. UV A doesn't have sufficient energy to directly cause DNA damage  but it can give rise to free radicals and cause DNA damage indirectly.

The paper that you mentioned says that the tissue that they studied has more of UV A mediated lesions. This could be because of higher availability of UV A to the cells. Ozone filters out a major chunk of UV B and C and melanin does little more. If these mechanisms didn't exist then high energy UVs would have burnt us.

To summarize, the inherent order of toxicity is C > B > A

References:

http://www.uio.no/studier/emner/matnat/fys/FYS3610/h04/undervisningsmateriale/Moan7.pdf
http://www.nature.com/jid/journal/v77/n1/abs/5615637a.html


What is the significance to life of the anomalous properties of water? I have heard that the anomalous properties of water - e.g the fact its solid form is less dense than its liquid form - is extremely important. In fact, some people have gone so far as to tell me it was crucial for the development of life.

What is the significance of the anomalous properties of water to life?

This is a brief treatment of your question, specifically:

  the fact its solid form is less dense than its liquid form - is extremely important. ...crucial for the development of life.

I can't speak to the importance of this property in the development of life (as I don't know the exact conditions of the world when life began, and therefore the role expansion of ice played in it) but life would not continue without it.

Water does not conduct heat very well, therefore water temperature fluctuates more near the surface of a body of water (say a lake, an ocean, or even a river) than in the deeper regions. In the winter, surface water freezes.

If water were denser on freezing, it would sink to the bottom, and liquid water would replace it. That liquid water would freeze, sink, be replaced, etc.

When it became warmer, the frozen water at the bottom would be less affected by surface temperature, i.e. it would be less likely to melt.

Even with summers, because of the failure of deep ice to melt, eventually you would be left with a mostly frozen body of water, and life doesn't carry on well in those conditions (freezing of the cells of plants and animals in the water would cause cell lysis, again, because of the expansion of water within), whereas life in a liquid under a frozen surface carries on much better. Life in the water would die.

If there were no life in water, then life on land would be most difficult. (Consider most of our oxygen comes from phytoplankton in the oceans. Even if the phytoplankton didn't happen to die from being trapped in frozen water, their nutrient supply would be cut off, frozen below.)

That's just the tip of the iceberg, really. The anomalous expansion of water also affects ocean currents and weather in ways that enrich life on earth.

Since you didn't ask about the other properties of water, this answer doesn't address surface tension, etc.

Edited to add: Corrected an error about the thermal conductivity (insulating properties) of ice. Ice does conduct heat more than water. It may be advantageous to the temperature of the water below possibly by holding snow (which does insulate well).

Source
Thermal Conductivity
Plankton: Ocean Drifters