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Confusion regarding the location of myelinated and unmyelinated nerve fibres
So, what I understand by neural system terms is

Central nervous system [CNS]- consist of brain and spinal cord

Peripheral nervous system [PNS] - consist of cranial and spinal nerves (all the nerves in the body)

A further classification of PNS is
I) Autonomous nervous system
II)somatic nervous system

(Here, my understanding is that both the system [somatic and Autonomous nervous  system] are made up of cranial and spinal nerve, and they are just classified based on the different organs that they are functioning upon [i.e for somatic it is skeleton muscles and for autonomous, it is heart, smooth muscles and involuntary organs] and not on composition ,since both systems consist of cranial and spinal nerves)
Now,i read the lines that are there (beside the red line) in picture below and I am highly confused now.

Now, it says that myelinated nerve fibers are found in cranial and spinal nerves i.e all the nerves in the body a.k.a Peripheral nervous system.
And on another note, it says unmyelinated nerve fibres are found in autonomous nervous system and somatic nervous system.
but isn't autonomous and somatic  nervous system makes up the peripheral nervous system?
so according to the first point (myelinated nerve fibres is present in peripheral nervous system.)
Therefore, It( somatic and autonomous nervous system i.e the peripheral system) should contain myelinated nerve fibres but here ,in just the next line ,it states that it contains unmyelinated nerve fibre?
By my understanding of the above mentioned terms......
My confusion here is.......
Does it contain both (myelinated and unmyelinated nerve fibre)?
or is there a printing mistake?
or is my understanding of terminology is wrong?
If so, please correct me.
Thank you so much

Where is this text from? Does it happen to be an Indian textbook? It's been a long time since I've seen one of these Indian textbook translation questions but I suspect this may be one...

@BryanKrause       Yes. This (confusing and unclear)text is from  "NCERT Biology" 11th std Indian Textbook. I will be highly grateful if you can clear this or anyone. Thank you so much

I don't know where these textbooks come from, but they aren't written by anyone who knows what they are talking about. I don't know why many Indian textbooks work this way. I'd highly recommend getting a different book or just learning from Wikipedia.


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How typhoid fever severe case's intestine perforation occur? (non trauma)
In typhoid severe case, intestinal perforation occurs. As stated here

[4, 6]. Intestinal perforation is a serious complication of typhoid fever

My question here is, how does the bacteria (Salmonella typhi) perforate intestine,like the process?
Does the bacteria somehow weakens the walls of intestine and the pressure cause it to rupture?(Guess)
OR
Due to the bacteria in the intestine, inflammatory reaction occurs which causes thickening of walls and pressure that leads to rupture? (Guess)
Even here, it doesn't state how the perforation occured by the the bacteria
Thank you.

source: Stack Exchange

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sort: votes


text:
Difference between sexual and asexual spore
This Wikipedia article on Spores mentions this:

In biology, a spore is a unit of sexual or asexual reproduction that may be adapted for ....

What is the difference between the sexual spore and asexual spore?
Are they any different on basis of formation, diploid or haploid, role in life cycle?
By Sexual Spores, I mean the spores that arise in the sexual reproduction process and similarly for Asexual Spores, i.e. spores which arise in asexual reproduction process.
To add to the context, this image shows the Sexual and Asexual spores in a certain fungi (Mycelium) life cycle.

I am curious - if this is for an assignment, are you not given sources that contain what your teacher thinks you should learn?  Or are students just turned loose on the internet now?

@Willk this is not an assignment given by anyone to me. I was in fact studying reproduction in organisms and dug into 'spores', eventually I ended up upon the Wikipedia page on Spore (link mentioned in the question). And was curious between their difference. [I have edited the question now]

In the same wikipedia page of spores you cited, you can find that they have said:

Fungi commonly produce spores, as a result of sexual, or asexual, reproduction. Spores are usually haploid..

Again,

Vascular plant spores are always haploid.

So, sexual and asexual spores have no difference in ploidy- both are haploid. (There are exceptions- zygospores in fungi are diploid)
Now, coming to mode of formation, they are different. For example, in Ascomycetes, sexual ascospores are produced endogenously whereas asexual conidiospores are produced exogenously.
Spores that are formed by the process of meiosis are sexual spores and when formed from mitosis are asexual. The term 'sexual' means meiosis is involved.

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What is meant by a muscle fiber being glycerinated?
I was popped this questions today, "what is a glycerinated muscle fiber, and what is required for its contraction," and had little idea. I'm assuming the question is "what's required for its contraction as compared to normal muscle tissue?"
There's a limited amount of information out there about this. It appears that it is a type of in vitro system requiring special preparation of typical muscle tissue. I was wondering if anyone here had a little more information. Is this something that's just used in teaching lab exercises?

From: http://www.acad.carleton.edu/curricular/BIOL/classes/bio126/Documents/Lab_5.pdf

Glycerination disrupts the membranes of the muscle cells, ruptures mitochondria, and leaches out soluble constituents such as ATP and inorganic ions. However, glycerinated muscle retains the organized structural array of myosin thick filaments and actin thin filaments, actin-associated proteins like troponin and tropomyosin which regulate contraction, and the functional capacity for contraction.

I would expect that because the sample has lost ATP and inorganic ions, you would need to supply ATP (the source of energy), $Mg^{2+}$ (which is necessary for ATP hydrolysis) and $Ca^{2+}$ (to induce the contraction).

this is the answer I was looking for. You may want to double check info the  Mg2+ though, I know free mg+ will inhibit  hydrolysis, while calcium alone can act as a cofactor. Your right though mg will help nucleophillic attack I just think Ca is ok alone, this is one of the reasons why the cell prefers the sarcoplasmic reticulum is quenched with ca2+.

I included the bit about magnesium based on the protocol linked to in the answer. Here is an article discussing myosin catalysed ATP hydrolysis which includes magnesium in the reaction mechanism (http://pubs.acs.org/doi/abs/10.1021/bi052433q). However, I have also found articles describing how magnesium inhibits myosin, so I don't know.

Calcium ions aren't needed (like normal muscle cells), because the glycerination process disrupts the troponin-tropomyosin complex so that the binding sites on the actin are exposed. However, glycerol makes the membrane permeable to small molecules, including ATP. That means that a glycerinated muscle requires addition of ATP so that the myosin heads can actually bind to the binding sites and create cross-bridges.
Magnesium ions aren't required, but they act as catalysts that help the muscle contract more.

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Why are cell lines frozen in vapor phase?
For most of the cell lines I've come across, ATCC recommends storing them in the vapor phase of liquid nitrogen. I'm taking that to mean any place above the level of liquid in the nitrogen storage tank. What is the reason for this? Under what conditions/requirements would one store cells/tissue submerged in liquid?

The storage itself can be done both in the liquid and also in the vapor phase in the liquid nitrogen. Both have their advantages and disadvantages. In my experience there are two main reasons why storage in the vapor phase (although there may be temperature fluctuations when the nitrogen gets low) is recommended.
First, you avoid cross contaminations of your cells lines with mycoplasma (and possible other contaminants) which can get transferred into the liquid nitrogen phase and then into your other cultures. This is not a theoretical danger, but pretty real. See the papers in the reference below.
Then liquid nitrogen will enter your cryotubes (which is also the cause for contaminations). If you use tubes which are not explicitly made for this kind of storage (which is not a problem for the vapor phase storage) then the liquid nitrogen which made it into the tube will expand upon thawing and can cause your tube to explode. This can cause injuries. For more details see here and here.
References:

Risk of contamination of germplasm during cryopreservation and
cryobanking in IVF units.
Microbial contamination of embryos and semen during long term
banking in liquid nitrogen

I don't think there can be any contamination issue with mycoplasma but is possible with viruses.

It can happen. Mycoplasma can survive in liquid nitrogen for very long periods of time and then cause contaminations. Been there, seen that. We had to discard a whole set of cells.

So how do the cellular membranes/viral proteins handle the liquid nitrogen? I assume nitrogen is a non-polar solvent, but would it be enough to disrupt a phospholipid bilayer?

It is indeed non-polar. But it will not disrupt the memnrane layers, as these have polar groups to the outside (the non-polar tails are directed to the inside of the membrane). Otherwise we couldn't store any cells in there. Additionally these cells survive as the other cells frozen in there. As they are more simple than an eukaryotic cell, they are more likely to survive.

Definitely right about the myco problems I've lost almost a thousand samples like this. I wish they made these dewers  able to hold more n2. Chris good answer here.

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Can cfDNA testing distinguish results in the case of twins?
A fetus can now be screened for some of the more common genetic diseases and its sex determined from just a whole blood sample from the pregnant mother. Fetal DNA is abundant enough in the systemic circuit to be able to be purified and sequences analyzed. Question is, in the case of fraternal twins, could the procedure discern between the two fetus's...
As a clearer example, can it distinguish between:
Scenario 1: if one fetus was male and one fetus female
And scenario 2: both male?
It appears the test would just look for presence of Y chromosome using certain markers. But it could then look at SNP to distinguish individuals.
Looking for clarification here

I think you are overestimating how these cfDNA tests work.  Maybe I read the paper wrong, but from what I read of one technique (Sequenom's MaterniT21 test) there is no purification of fetal DNA.  They do restriction digests to assess the percentage of fetal DNA,  but I don't think they enrich for the fetal DNA when they sequence.  The library they make is mostly maternal, they are just looking for slight deviations in how many reads come from each chromosome, if too many come from chromosome 21, they conclude it's because the fetus has too many copies.
And as for SNPs, coverage is way to low for that.  We're talking about 40 million reads, even if that were mostly fetal DNA, which I don't think it is, that's not enough coverage to call SNPs.
So if there were two fetuses, and they were not identical, then the signal from each would be half what would be expected based on the restriction digests assay. So maybe you would have enough counts that you could tell that the Y chromosome counts were too low, and the X chromosome a bit too high, but since these tests almost certainly have not been clinically tested on multiple fetuses well enough for verify their accuracy, no company is going to report results.

http://www.qiagen.com/us/products/catalog/sample-technologies/rna-sample-technologies/dna-rna-protein/qiaamp-circulating-nucleic-acid-kit/

My wife just had this test done and we are having twins. So the test is largely performed. Y chromosome was detected in her peripheral blood sample. The question I'm asking here is how could test be modified to allow identification-we should be able to descent if we are having two boys or one boy and one girl

Like I said, the signal from each fetus would be less.  You'd need to boost that at least two fold, likely by increasing the real estate on the flow cell, which would cost more.  And if they appeared to be the same sex, there would be no way to know if you had enough signal from both.

I know they use that kit, its the rest of the protocol that matters.


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condensed protocol for sequencing a portion of human DNA from buccal sample
Anyone have a short & sweet protocol for PCR amplifying a region of human DNA (chromosomal or mt, I don't care) extracted from a buccal sample: including validated primer sequences and preferred method of DNA isolation from a buccal swab. I'm looking for a new exercise to run in my classroom. We would be able to follow the amplification up with Sanger sequencing, done in-house.

Which possibilities do you have for the extraction? Would this be more "lab-like" or more "DIY-bio"-style?


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Asexual Reproduction Of sponges through endogenous or exogenous budding?
I was studying asexual reproduction in sponges and came across two website

Wikipedia of Gemmule and there is a line....

Only Endogenous Types of Buds develop into New Sponges.

Then as I was reading this Website Sponges there is a Section 9.1. iii) Budding, in which, there is Two Parts i.e (a) Exogenous Budding and (b) Endogenous Budding
So now, I am a bit confused..... if only Endogenous Bud can give rise to New Sponges then why there is a section of exogenous budding i.e reproducing through exogenous buds,in the reproduction section of sponges, in this website sponges ? ISN'T that Contradiction?

I would say that the quoted sentence from the Wikipedia gemmule article is wrong.  The first sentence of the containing paragraph says:

Asexual reproduction in sponges occurs via budding, either by external or internal buds.

At face value, the two sentences together imply that sponges can reproduce by external budding, but that the external budding "reproduction" does not produce "new sponges"(!). Note that the most recent edit to the article (on 10 March) was by an anonymous user who changed the sentence you quoted from "Both types" to "Only endogenous types", so this was a somewhat recent corruption.


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Why does the gravity of Earth appear in this formula estimating speed?
I'm currently reading the wonderful book The Dinosaurs Rediscovered by Michael J. Benton. It contains the formula
$$v = 0.25 * g^{0.5} * SL^{1.67} * h^{-1.17}$$
where $v$ denotes velocity, $SL$ is stride length in $m$, $h$ is hip height in $m$ and $g$ is the gravity of earth. Not being a biologist (in fact not being really familiar with any natural science), I don't quite understand why gravity appears in this formula. I can't imagine this would hold in any meaningful way in circumstances where gravity where different from earth's, so why not simply express the term $0.25 * g^{0.5}$ as $0.78 m^{0.5}/s$, which I assume stems from some fitting of terms to observed speeds given stride length and hip height.

I know nothing about this, but this formula appears to be the work of one Robert Alexander. If you can find some of his papers, he likely explains how this formula was developed. Alternatively, this website seems to go into the derivation.

Reading a little bit about the derivation of the formula as well as the corresponding wikipedia article, I would assume the g stems from the origin of the equation in Froude's number.

This question is about physics or engineering, not biology. The fact that the formula can be applied to biological movement is irrelevant.

Units
G is going to be different depending on what units you use, the original formula was derived using FEET not meters. As it stands the formula works both with metric and imperial units. With your change this would not be true. Paleontology is often uses both units so a formula that is not unit dependent is preferable.


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umbrella term for microtiter plate, petri dish, cell culture flask etc
I'm looking for a term I can use in a software user interface that includes anything that may carry cell cultures or similar biological imaging samples (ie that may conceivably go into an automated microscope).
Since it's for a user interface, the term should be short and intuitive.  It should not depend on context.
Examples:

vessel, carrier, dish --- often used for what I mean, but not intuitive out of context.
cell culture carrier --- too long, also potentially too specific.

A flask or petri dish do not go into a microscope. Can you specify what you are exactly after? Are you after containers to grow cells? Or are you after plates to do repetitive stuff with cells (add substrate, coloring agents etc), or are you after carriers that go under a microscope?

@AliceD: anything you might grow cells in, potentially adding reagents, potentially fixate, and then image, for example these plates.  And yes, we do image cultures in flasks like this one

Thanks for the clarification. I left the field some 20 years ago, so I'll not even bother trying to answer this question, but it may help others to answer your Q. Good luck programming!

This sort of question is not really about biology. It may be a better fit for English Language & Usage with the tag “technical” (or the like). There are technical people there who delight in this sort of thing (as well as people who know nothing about the subject but can’t stop themselves answering every question in a comment).

@AliceD No problem. Just a suggestion, anyway.

@David thanks for your understanding.

@David I know of EL&U (and I've posted there in the past), and you're right, this is a single-word-request (one of the tags there).  The reason I posted on biology SE is that I thought the chances of the right person seeing the question here are vastly higher.

Could be. You never know.


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How can I obtain a uniform bacterial sample?
I'm currently doing a research project wherein I will be testing the antibiotic resistance of a bacterial sample. Due to a risk of contamination during transport, I'm not allowed to request a uniform bacterial sample form a clinical laboratory. So, I have to produce my own sample. Then, I'm planning to identify the morphology of the bacteria to confirm the species or type.
The ideal scenario is obtaining a sample which is entirely one species of bacteria. However, taking a swab, either from somewhere in the lab or from the body will produce a sample with multiple bacterial species. What source of bacteria can provide the most uniform sample, i.e. a sample with a majority of one species of bacteria? Or, is there another way to obtain a uniform sample? Also, note: I will be conducting the experiment in a school laboratory, so I must be able to safely contain the pathogen.
Edit: I have recently updated my project to be specified towards testing on bacteria present in the throat. So, a bacteria present in this area or similar areas would be preferable.

Do you have a particular bacteria in mind? For safety, I have a link. Especially culture well below body temperature, and use common media e.g nutrient agar. https://www.riskassess.com.au/info/micro_issues

I have no specific species/strain in mind. However, I have recently updated my project to be specified towards bacteria in the throat. So, a bacteria which is present there or in similar areas would be preferable (I'll also update the question).

This is what streak plating is for.

You could inoculate your sample in a selective medium or an enrichment medium to kill off the unwanted species. Of course, you will need to do a literature search to find the optimum medium for the species of your interest.
Another option is to streak plates like so. With successive 'generations' of streaks, the inoculum gets diluted, so that you ultimately get separate colonies. Each colony is founded by a single bacterial cell: by picking up one such colony, you get a pure sample.
For even better results, combine both the methods described above by first growing in a selective medium and then streaking on a solid medium to get individual colonies.


text:
How Ants know about Earthquake?
How does an ant know about Earthquake is it because of an organ or due to other factors?

No, they may not sense Earthquake by an organ but due to other reasons. This may be any other physical factors which can be measured.

"...There is therefore
  little reason to believe that these ants react to earthquake
  precursors other, perhaps, than those that may affect colonies
  directly, by altering physical variables that can be directly measured
  by other means..."

Fascinating though the behavior and physiology of ants may be, they cannot be employed as reliable predictors or even sensors of earthquakes.
Source: Shaken, not stirred: a serendipitous study of ants and earthquakes

@Chris Is it better now?


text:
Standard Process Identification of New Disease outbreak Causing Pathogen
Is the any standard procedure or protocol followed for the identification of cause of new disease outbreak(or new pathogen)? Is it different for different countries?

I am not sure if there is any standard method for this. You find a patient with an unknown disease. Than you try to find out, what is going on. Isolate body fluids, analyze them and so on. Depending on the reason the methods are different.

I won't post it as an answer because of the 'human-biology' tag but this paper describes the process by which Schmallenberg virus was recently(ish) detected in Europe: syndromic surveillance picked up the disease, and NGS identified the agent. http://wwwnc.cdc.gov/eid/article/18/3/11-1905_article

Pathogen identification procedure is not necessarily standardised due to differences in resources available to each country but there are certainly several characterised and accepted approaches used to identify a disease causing pathogen. The predominant techniques used to identify pathogens relies upon conventional clinical microbiology-based approaches, which has been highlighted in the comments above. However these conventional techniques such as standard culture and susceptibility tests have many drawbacks such as time-consuption and lack of scalability in addition to lack of direct characterisation of virulence factors. Most pathogen (except prions) logically carry a unique DNA or RNA signatures that differentiate it from other organisms, which provides the basis for disease causing pathogen characterisation. According to this page there are two approaches used to detect a pathogen, once sampling has taken place.
1) qPCR based pathogen detection: allowing sensitive and real-time detection of genetic signatures, which is not currently matched by sensors such as immune-assay techniques (lagging in detection time, logistics and costing) and optical techniques (lacking specificity).
2) Microarray based pathogen detection: allowing combination of nucleic acid amplification (offered by PCR based techniques) combined with massive screening capability of microarray technology, resulting in high level of sensitivity, specificity, and throughput.
These techniques are obviously combined with powerful software technologies required to sieve through the data and allow for easing of experimental burden, minimising assay development as well as operational costs. Now clearly these techniques including sensors and conventional microbiology are used concurrently/synergistically to more efficiently identify a disease causing pathogen and strategies a treatment/preventative measure. This review nicely illustrates the molecular basis for pathogen identification and discusses general considerations (in this case for fungus detection) such as DNA extraction methods, sampling preparations and strategies and goes on to highlight some other sequencing independent methods such as FISH and macroarray.
This paper writes about sequencing based strategies and using the BLAST (NCBI) tool and talks about identification of variant strains of known species, identification of non-cultivatable pathogens and more importantly related to this question, identification of new species using (rDNA) phylogenetic trees of bacterial 16S gene and the fungal 18S gene, commonly used for this type of analysis. This is done in order to determine the phylogenetic position of a the suspected new species compared to a closely known related species, which is useful when there is a <98% of the sequence similarity with known species.

I was first thinking of voting to close the question because it was too broad, but in reconsideration I think the answer of showing why it is too broad would constitute a proper answer in this case.
First of all, the term disease is one of the most general terms for a problem in medicine.  The only term that could be higher up is "medical condition."  It could be an infectious disease, genetic disease, induced disease (think chemicals, tobacco, etc), or [insert organ here, ie heart] disease (which are not necessarily genetic).  There are attempts to distinguish between "diseases" and "disorders," but the difference is not always clear.  The term "disorder" is growing in usage and scope because it is seen as having fewer negative connotations than disease (think disease of the mind vs. disorder of the mind).
Thus each field has it's own ways of identifying new diseases.  As a general trend new diseases are found now by identifying greater specificity within a previously general disease.  For example, a person could be said to have an "adrenal cancer," but now we would want to know if they have an adrenocortical carcinoma.  In an infectious setting, we could think of all the particular pneumonia being specified out of interstitial lung diseases.
Diseases caused by external agents (pathogens, toxins, etc) can sometimes be more uniquely novel, in that they can change into something unpredicted (new compound or virus made by man for example).  Perhaps you meant to ask if there were standard ways for identifying new viruses or microbes?

Can you change your answer now?

@DevashishDas. Sorry to be slow on this.  My participation in the site is very intermittent, and I'm not checking anywhere for notices.  I think Benz has a good awnser, with my only additional thoughts being arrays currently under development to gage if the host response is to a viral or bacterial infection.


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Simulating Drug Entry in Protein and binding?
Is there any simulation protocol or paper which can simulate the dynamics of drug entry and  interaction with the target protein?

often there is no specific path of diffusion into the active site - it will tend to be a statistical ensemble of possible paths...

This is a tough topic, have a look at the following references and see, if they can help you:

Structural modelling and dynamics of proteins for insights into drug
interactions.
Ligand entry pathways in the ligand binding domain of PPARγ receptor
Pathway and mechanism of drug binding to G-protein-coupled receptors
Molecular Dynamic Simulation and Inhibitor Prediction of Cysteine
Synthase Structured Model as a Potential Drug Target for
Trichomoniasis

Absolutely, the two I've had the most success are working with a radiolabeled and a fluorescently labeled version of the drug. Many drugs autofluoresce as well and this can be easily tracked.
When it's labeled as mentioned above microscopy or a luminometer, spectrophomoter or a scintillation counter can evaluate fractions or whole cells, or purified binding substrates.


text:
When was it determined that Type 1 Diabetes is an autoimmune disease?
I just found out today that type 1 diabetes is an autoimmune disease.  When was this discovered?

It probably would help people answering the question if you could link or quote from the source where you found this out.

This question has two answers: The difference was first described in 1936 by Harold Percival Himsworth, which described it in this article.
At this time it was established that there are two forms of Diabetes, one sensitive to insuline while the other is not.
The terms Diabetes type 1 and 2 where established somewhere between 1974 and 1976, for details see the review "The discovery of type 1 Diabetes".

Thanks.  From the "discovery" article it appears the autoimmune theory really solidified around 1974.

It takes a while until such a concept is widely accepted.


text:
Dogs bark at familiar person in Santa costume. Why? Don't dogs trust smell over vision?
Last night 10 humans and 2 dogs spent Christmas together. At some point, one human dissappears for a few minutes and comes back wearing a full Santa outfit. Upon respawning, the dogs start barking aggressively until they are calmed down by non-Santa humans. They remained attentive of Santa until he left after a few more minutes.
Why is this? Did the dogs not recognize the human because of his fake full beard and altered body shape (pillow under coat for fattening)? The human didn't shower or put on perfume or anything. I'm stumped by this and I'd love to learn the reason for this odd behaviour.

Upon respawning, the dogs start barking aggressively until they are calmed down by non-Santa humans -  best sentence on the site

I like this question

I think this question would be a slightly better fit on pets.SE. Looking at the number of upvote and comments and answers of reputed users, it seems to also be on-topic here!

The dog was probably freaked out by the weird costume.  Humans do it all the time (I've been seeing Halloween decorations for sale since early August, which is terrifying) but we generally comprehend what's going on.  Dogs may not fully understand the idea of a costume, much as a human infant might be scared by masks or beards (or the sudden removal thereof).
Anyway, this 1997 article titled Canine fears and phobias; a regime for treatment without recourse to drugs is kind of a fun read and has some interesting tidbits about, go figure, canine fears and phobias.  One thing it discusses is the importance of the primary associations brought on by sight, smell, and hearing.

However with a fear of hot air balloons the dog will hear the propane burner and see the balloon but a primary (coming from the balloon), olfactory cue will be missing.

Missing out on that is enough to freak 'em out.  This research article from the 1950s is a little more exact/thorough and has what you want.  It's worth reading in more detail if this topic interests you, but the part that answers you is here (emphasis added):

Some at least of the test objects could not have been discriminated by smell, as with the bronze deer, or the mechanical turtle, and in the course of the work it was frequently clear that visual cues were affective before olfactory ones could have been. Vision also can dominate olfaction: fear of a modelled human head was observed although the model was completely wet with dog urine.*

Likely what happened was the dog saw a weird/scary/new person and, were upset that their vision and smell didn't match up, and continued being freaked out.
(*The urine experiment comes from this article out of 1944 Germany, in what is now known as Ethology, in case you feel like reading German.)


text:
How to monitor the use of Nootropics?
How do you monitor the use of nootropics?
What is a good process to measure both: side-effects and any improvements.
Where can I find resources with scientific and tested data of short and long term usage of various Nootropics? (I'm using google as well)
Thank you!

Have you tried PubMed?

The process of measuring the effect of nootropics would be the same as for any other drug: Do a double blinded placebo study and the follow the parameters you hope to influence. For example do "brain tests" if you want to test for enhanced brain function. If there is any function of your drug in the body, you will see a difference between the treatment and the control group. You could start by reading the Wikipedia article about Nootropics which is quite exhausting and also has quite a lot of references and go on with these two papers "Does taking vitamin, mineral and fatty acid supplements prevent cognitive decline? A systematic review of randomized controlled trials." and "Cognition enhancers between treating and doping the mind."

Thanks :) I think I asked the wrong question... should have asked which variables I should track. I've marked your question as correct anyway, as it answers what I asked. Thanks

Obviously, the choice of variables should depend on what the drug 'affects'. Anyway, you wrote a good answer to a poor question :)

About which drug effects are you thinking?


text:
How would you find out which gene is causing a specific phenotype in Drosophila through crosses only?
I'd recently attended an interview and was asked a question I've been trying to get to the bottom of. The question was that there is a mutation in which some smaller drosophila are only attracted to other smaller ones. This is activated at a specific temperature. Through drosophila crosses only, given that you have access to balancers and whatever else you need, how would you pinpoint which gene exactly is causing this mutation?
A test cross would tell you if it is genetic, and if it may be dominant or recessive, but how does one pinpoint a specific gene only through crosses (no using modern tech)?

I am not a geneticist, but I have some experience as an older (or perhaps just old) scientist in interviewing or examining younger scientists. So I suspect that the interviewer was trying to discover whether the original poster, whom we assume is familiar with modern techniques, was also familiar with the classic methodology of (drosophila) genetics. I therefore suggest that what the interviewers may have been after was simply Genetic Linkage.
Presumably in an interview one would say that one would test for linkage of the trait to a wide range of other traits (eye colour etc.) using the appropriate double mutants. Once having identified a gene showing linkage one would use the genetic map of drosophila (determined by classical methods) to test neighbouring genes, until one found almost ‘complete’ linkage to genes on either side of a candidate.
This answer may miss something that is obvious to a drosophila geneticist. At first sight it is difficult to see how if the gene had already been mapped its phenotype would not also have been described. I assume that it would have an additional phenotype that did not involve social behaviour — presumably just the smaller size. In this case any such genes would be candidates for testing for the more obscure phenotype of social behaviour at a specific temperature.

Not sure if this is what they'd be looking for, but if you were allowed to do research ahead of time you could select a few genes that you think might be involved in this behaviour, then use RNAi and GAL4/GAL80 to temporally knock down your genes of interest at high temperatures to see which genes give you the phenotype when knocked down

The question states: "no using modern tech".

Both of these techniques that I suggested were established and used consistently in Drosophila over 20 years ago, which is why I suggested them as they are specifically not "modern tech"

Of course we have no way of knowing what the interviewer was thinking of (or even if the OP remembered correctly). However I suspect traditional Drosophila geneticists regard anything after, say 1980, as modern. (Me too)


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What insects eat the inside of peanuts leaving the shells?
I put these peanuts in a mouse/rat trap and the insides of the peanuts were eaten leaving behind the shells. What insects can do these? Can ordinary ants do it?   What can I put that won't be eaten by insects, something not sweet enough to attract ants.


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What insect is this in photo? 1.5" size
What insect is this in photo? Saw this in outdoor table and wonder if it can bite and if it has venom. The size is about 1.5 inches and located in the Philippines.

You need to edit the question to give the regional location and approximate size of the insect.

Could be a longhorn beetle of some sort. Would need photos from other angles to get a more firm ID.

The other photo is so blurred. Its on the foot of table besides a swimming pool at condo. Good to know it is not dangerous so we can sit at the table again tnx

I would say this is some Hemiptera


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Examples for oscillatory behaviour in the human body
I'm looking for examples in the human body which show periodicity, more precisely, I'm looking for examples of oscillating reactions that occur in the human body which can be modelled using the Hamiltonian of the harmonic oscillator.
for example, as someone mentioned to me before, the circadian rhythm is controlled by the oscillation of protein concentration. I wanted to know if there are some examples from biologists perspective?
I want to read more about it, and I will be grateful to hear more examples so I can look for information about it online or if anyone could refer me to some reading material regarding this subject.
Thank you very much for your time and attention.

it would be helpful to know more about the hamiltonian of the harmonic oscillator, what it is traditionally used to model, why you would want to find such a mechanism, and any other relevant data. you don't normally start with a model and then go around looking for systems; you usually start with systems and try to figure out models that might match them.

@MaximilianPress thank you for your comment. I'm sorry for expressing myself so poorly, I edited my post, I hope it's more clear now.

This is a very broad question since a) periodic changes are not necessarily oscillations in Hamiltonian sense (like circadian rhythms, which is hard to describe as oscillations - just like roration of Earth around the sun), b) non-linear oscillations are not necessarily Hamiltonian and/or harmonic (like those describing the dynamics of a heart). It might be too technical to discuss in the biology community, but this is something you should keep in mind. Perhaps, you could post a parallel question on phsyics exchange, since it borders on biophysics.

Mathematical physiology by Keener could be one place to look at - the chapter on wave propagation certainly has oscillators in it, but there shoudl be more material spread over the book: https://books.google.fr/books/about/Mathematical_Physiology.html?id=xWBb7b5eEFoC&source=kp_book_description&redir_esc=y

@Vadim Thank you very much for your advice. I will look into it and I will try posting also on physics exchange.

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


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Is there species of mushrooms that grow in the wild in Mediterranean environment?
I'm looking for species of mushrooms which can grow wild (or with minimal human intervention) in Mediterranean environment (which is characterized by dry summers and mild, wet winters.), specifically in north and south Israel (I guess there are different kinds that are adequate to each area) and can spread over significant areas (in a scale of tens of kilometers)
Are there any known species that answer those characteristics? where can I read more about them, their abundance, and how to grow them? I found a-lot of unreliable information, and I'm looking for material with stronger scientific foundation.
Thank you.

Mediterranean is rather big: it includes the southern coast of Europe, Levant, and North Africa. E.g., this link claims 400 species known in Israel.

double posted https://earthscience.stackexchange.com/questions/22951/are-there-species-of-mushrooms-that-grow-in-the-wild-in-mediterranean-environmen

By spread do you mean that the "single" fungus spreads its mycelia that far or that it is capable of spreading via sporulation?


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Why do GPCRs pass exactly 7 times through the cell membrane?
7-transmembrane domain receptors or GPCRs are one of the most common receptors in biology.
They can be found in eukaryotic cells.
What is the significance of the number 7 here: why does it pass exactly 7 times through the cell membrane? What is so good about having it pass 7 times through it?
I can't find literature which goes deeper into this issue.

The Goldilocks effect? The magic number? There is no obvious functional reason, the structure works, but we don't know that some other would not have so any argument is circular and futile. The thing that interests experimental scientists, and can be answered by experiments, is how the binding of a hormone to the receptor transmits a signal into the cell. The details may be complex, but science seldom his simple answers, and you should be wary of people would provide them.


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Where is sialic group in gangliosides that form ABO blood groups?
A ganglioside is a molecule composed of a glycosphingolipid (ceramide and oligosaccharide) with one or more sialic acids (e.g. n-acetylneuraminic acid, NANA) linked on the sugar chain. (source: https://en.wikipedia.org/wiki/Ganglioside)
Gangliosides form ABO blood groups.
Do gangliosides always contain sialic acid? If true, then where is sialic acid in blood groups?
Structural formula of ganglioside GM1a:

Blood Group Antigens:

I suspect this is a product of differentialy expressed glycosyltransferases. Instead of adding a sialic acid, for example, if you're coding for Enzyme B which is an alpha 1-3-galactosyltransferase, you're going to add a Gal to the glycan chain forming B antigen, and so forth. Sialyltransferases can add sialic acid groups, but to the same structure it looks like there is competition between the glycosyltransferases to add sugar moieties that results in different structures getting produced from backbone structures. Source, pages 5-10

Type-1 units may be modified by glycosyltransferases that transfer sugars to either terminal galactose or subterminal GlcNAc, generating sialylated structures or blood group determinants. The synthesis of type-1 units and expression of the corresponding β1–3 galactosyltransferases are regulated in a tissue-specific manner...

Structures Common to Different Glycans
So that's to say there shouldn't be a sialic acid group on ABO antigens, though sialyltransferases are capable of forming Lewis Antigens (Source). In the anabolic pathway the backbone structure is simply getting attacked by glycosyltransferases and the pathway goes the direction whichever one wins out (level of protein vs level of substrate). Being said, I'm unsure it's proper to say ABO antigens are produced from gangliosides, but if anyone finds some faults in my explanation please let me know!
I'm looking into catabolic pathways that may produce ABO antigens by recycling gangliosides, probably resulting from some cleavages by other glycosyltransferases, I just haven't gotten there yet, I'll try to update if I find anything.


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Forensic genetics- why is mtDNA comparison sometimes better than nDNA comparison?
Why is (in forensic genetics) in some cases more appropriate comparison of nuclear DNA but in some other cases comparison of mitochondrial DNA?
Is it because geneticists are sometimes unable to find nDNA or if nDNA is too damaged? Also could it be because of the structure of mtDNA (it's more protected against degradation, which is good for identifying old biological material)? I can't see any other advantages, since mitochondrial DNA mutations occur frequently, due to the lack of the error checking, but are there any that I am missing?
Thank you in advance.

Degradation of mDNA is more difficult than nDNA as you said and it's present in more copies. But also, in some cases, when you just want to know the identity of the victim, and you already suspect who it might be, it can be compared the mDNA with the mother/brother/sister/grandmother. It can be useful as well to know the geographical ancestry.

mtDNA is present in a much higher copy number per cell than nuclear DNA.
According to this paper, there are approximately 4000 or so mitochondrial DNA copies per human muscle cell.

copy number of mtDNA per diploid nuclear genome in myocardium was 6970 ± 920, significantly higher than that in skeletal muscle, 3650 ± 620 (P = 0.006).

This makes it far more likely that a non-degraded copy of mtDNA exists, considering that there are normally only 2 or 4 copies of nuclear DNA per cell per locus for almost all kinds of cells.

Doesn't  a cell (or at least a human cell) usually have one copy of nDNA, only in phase S they can have two?
When would it have 4 copies?

@cherry8.8vanilla Humans are diploid, therefore "2 copies". Arguably if you consider the 2 alleles from each parent (which might be different) you can call it 1 copy as well.


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Is there any measure by which the Germans today could be called a genetically superior race?
The Nazi eugenics programs are well known. Despite their controversy, I cannot find any indication on their effectiveness. Were there ever and studies done on the (arguably subjective definition of) superiority of German genetics due to (or possibly in spite of) these programs?
Do we even have a way to objectively measure genetic superiority or fitness? In the case of a lack of such a measurement, the idea could be qualified for purposes of this question as:

Lower instances of genetic disease.
Lower instances of mental retardation, criminal tendencies, and mental illness.
Higher general academic achievement.
Healthier, longer lived population.

Note of course that I am not promoting or condoning eugenics in any way. I am only interested in knowing if the results were effective (i.e. achieved their goals), without comparing the programs' possible benefit against its obvious drawbacks. All contemporary discussion of the programs concentrate only on the drawbacks, unfortunately.
EDIT: Before anyone accuses me of bigotry or crimes against humanity, I will mention that my grandfather lost all seven of his siblings, his parents, and all the rest of his entire family to this same regime. My grandmother lost five of eight siblings, both parents, and all the rest of her entire family to this same regime. What these people did to Jews, Gypsies, and the feeble was terrible and I do not excuse it. This question is intended only to concentrate on the scientific issue of forced, deliberate genetic improvement, a form of "breeding" if you will.

There was already some discussion on the topic.

@har-wradim: Thank you, I'm surprised that I could not find that! Please mark this as a dupe (already answered), I don't have permissions to do so on the SE site.

That answer still has no answer, so I'm able to mark yours as a duplicate. You can close it yourself if you wish.

@har-wradim For me it is not a duplicate. This question is not about the efficiency of Nazi eugenic programs, but about the intrinsic genetical superiority of German race (or lack of thereof).

@PiotrMigdal I have nothing against this question, I'm even "glad" that this topic got a new chance.

But in any case there is some overlap, so I would suggest to edit this question to remove this 'effectiveness of eugenics' part (since it is a dup). And in any case, saying "Is it true that X because of Y?" is much harder than "Is is true that X?". See my answer - an I am trying to answer only the simpler variant.

To the extent this question means anything it could be asked without the inflammatory context. As it is, it is too broad and reflects badly on the site. It is also partly a dupe.

Why should they? This would imply that there is some "superiority" in some humans above others. This programme selected people by external criteria (tall, blonde, blue eyes), why should any of this lead to superiority? Genetics is much more complicated plus not everything that we are is inherited in our genes. A lot is society and behaviour. The question doesn't really make sense to me.

I think this is very much a duplicate of the question mentioned above & (despite the authors efforts) agree with Daniel that it reflects badly on the site - the underlying question is largely inoffensive but the concept of superiority is not necessary and likely to cause unnecessary deviation from the question itself. Personally I think that the essence of the question is "Has the eugenics program implemented by the Nazi regime left any real effects on genetics & genetically caused traits in the populations of the people it affected?"

I agree that the question as intended was a dupe, however the comments and Piotr's answer are terrific and the truth is, I find the direction that the question went in to be a valuable contribution. Thus I've edited the title to reflect the new direction in which the answer went and to keep it distinct from being a dupe. It is also less inflammatory. Thank you all for your wonderful contributions and insight.

I am leaving the word 'superior' aside (it's ill-defined and strongly valuing).
In any way - unlikely. If any ethnic group is 'superior' (at least, intellectually) - then, ironically, Nazi main victims - Ashkenazi Jews. But while there is some genetic component, it is impossible to disentangle it from societal and historical factors. Here are some links, is you are interested.
When it comes to Germans, as far as I remember, they are not a group genetically distinct from, say Poles. Yet Slavs were considered by Nazi also an inferior race, to be enslaved or eradicated.
In any case, culture and socioeconomic factors seem to be much stronger than (relatively small). In particular, for Germany itself, there was a huge difference between West and East Germany, prior to the fall of Berlin Wall. It can be hardly explained by 'genetical superiority' of West Germans. An excerpt from Race, IQ, and Wealth by Ron Unz:

Consider, for example, the results from Germany obtained prior to its 1991 reunification. Lynn and Vanhanen present four separate IQ studies from the former West Germany, all quite sizable, which indicate mean IQs in the range 99–107, with the oldest 1970 sample providing the low end of that range. Meanwhile, a 1967 sample of East German children produced a score of just 90, while two later East German studies in 1978 and 1984 came in at 97–99, much closer to the West German numbers.
These results seem anomalous from the perspective of strong genetic determinism for IQ. To a very good approximation, East Germans and West Germans are genetically indistinguishable, and an IQ gap as wide as 17 points between the two groups seems inexplicable, while the recorded rise in East German scores of 7–9 points in just half a generation seems even more difficult to explain.

See also The East Asian Exception to Socio-Economic IQ Influences and The Myth of American Meritocracy (on how ethnicity can affect admission) by the same author.

Thank you. As for being the same race as the Poles, I thought that the Germans are Aryans, genetically distinct from Slavs but rather the same people as the Persians / Iranians.

@dotancohen Then if you mean than, it is a duplicate of Did the eugenics program in Nazi Germany have a measurable effect? (with answer: WW II with all of its killings, migrations, changes in economy and politics had much stronger impact, and most likely it is impossible to separate it). And no, Germans are not closer to Persians/Iranians than to Poles. This Aryan thing is a myth, not supported by science.

I agree that as intended the question was a dupe, however the comments and your answer are terrific and the truth is, I find the direction that the question went in to be a valuable contribution. Thank you very much for your learned insight. I learned more than I expected to learn. Oh, and being an Ashkenazi Jew I find the linked Wikipedia article astounding, though I find it disturbing that the topic is notable enough to warrant a Wikipedia article.

@dotancohen In any case, SE has no-dupe policy. So I guess unless you edit question, it will be closed. If you like my answer, could you edit it to ask about superiority of Germans, without speculations or relations to effectiveness of any eugenics? (In short: if there was some truth in Nazi propaganda on the genetic superiority of Germans) BTW: I didn't note your surname. :) With respect to topic notability - it is hard to miss a great number of scientific and cultural achievements (especially in the 20th century) due to people of Jewish ancestry.


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Is Cas9 unique in it's ability to act in response to a specific DNA sequence?
As a computer scientist, I'm interested in the ability of the Cas9 protein to function as an if-gate for DNA. It opens up so many questions for me. Right now the protein works as "if the sequence matches, cleave", but perhaps you could customize it to do "if the sequence matches, [do arbitrary action]". However, I'd feel very dumb if I got all excited about this and it tuned out "no... there are plenty of things that function as [if sequence matches], the real revolution of CRISPR/Cas9 is... [something else]". Is my fear qualified?

There are two classes of proteins that I can think of off the bat that are DNA sequence-specific. First are restriction enzymes, which recognize a specific (usually short) sequence of DNA and cleave it, sometimes through both strands at the same spot (blunt ends) and sometimes leaving an overhang or "sticky end".
The other class is transcription factors. Instead of altering the DNA, these proteins bind to a consensus sequence and act as a gathering point for the transcription machinery to bind and begin transcribing the following gene into RNA.
What makes the CRISPR/Cas discovery unique is that the binding sequence can essentially be an arbitrary sequence, defined by the scientist, allowing for cuts just about anywhere. Transcription factors and restriction enzymes depend on the local sequence of the DNA itself, so they only bind in certain spots.
There are other sequence-specific technologies available, such as TALEN, but they are basically a combination of a site-specific transcription factor and a fairly non-specific restriction enzyme or nuclease fragment engineered into it that cuts at a specific, user-defined site, depending on which subunits are used. CRISPR is a much more powerful (and easier to implement in vivo) technology, though, so while TALEN still has a place in the molecular biology toolbox, CRISPR is rapidly eclipsing it.

Just a minor thing but the TALEN class of nucleases are actually transcription factors with a FokI nuclease domain attached to it. They resemble the old zinc finger nucleases in that they are DNA recognition proteins with a nuclease attached to it. CRISPR is unique in that it is a nuclease in its original form.

@mimat yes, you're right. I wrote that last section quickly, based off my reading on TALENs a little while back. I didn't remember that they actually have TF activities as well. I reworded that section a bit.

OK, if you want analogy, you can think of Cas9 as comparing device: if sgRNA (guide RNA) matches DNA, then cleave. You can pick this up from Wiki article or publications on CRISPR/Cas9
Read about DNA restriction enzymes. If in case of Cas9 template is provided by sgRNA (guide RNA), in case of restriction enzymes template is built-in this enzyme.
Cool thing about Cas9/CRISPR is that you can engineer guide RNA to match 20 bases of DNA for high specificity.


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Continuous (yeast) culture system satisfying multiple criteria
There are multiple ways yeast cells can be grown in liquid cultures.

Batch cultures are easy to prepare but cell density, medium composition and physiology change over time
Chemostats allow to maintain cells in physiological steady-state, but growth rate is limited by nutrient availability
With a turbidostat, cell density is kept constant and cells can grow at their maximal rate, with excess of nutrients, but medium composition changes over time
Cells in a microfluidics chamber can attain maximal growth rate with constant conditions, but with extremely low numbers.

I cannot think of a way to get (a) maximal growth rate, (b) constant medium composition, (c) constant cell density and (d) a decent culture volume (>50 mL). Am I missing something?

Unless I'm missing something, at steady state the cell density in a chemostat is constant and the specific growth rate is equal to the dilution rate. So you can keep density and specific growth rate at desired values.

Yes, you can keep them fixed, but what I am looking for is the maximal growth rate. In a chemostat there is at least one limiting nutrient that slows down cell division rate.

Im not sure I understand. Why not use media with excess nutrients? The specific growth will be equal to the dilution rate i.e. you can make the specific growth as high as you want (approaching the maximum growth rate) independent of nutrient levels.

Maybe I can approach maximal growth rate (for which I think I need a feedback mechanism to control the flow rate in order not to flush away the culture). However, I think I would not get constant medium composition anyway because each molecule in the chemostat is depleted/produced by the cells at a different rate. For example, if glucose is not limiting, it will be added to the culture faster that is consumed and thus will increase indefinitely. Multiple sources say that with chemostat you can get steady-state cultures, but to me it seems false. Where am I wrong?

A chemostat should satisfy your criteria.
The cell mass balance around a chemostat is the following (assuming no biomass in the feed):
$$F-FX+V_RX\mu_g-V_Rk_dX=V_R\frac{dX}{dt}$$
At steady state there is no change in parameters with respect to time so we set the derivative equal to zero. If we also assume that the death rate ($k_d$) is negligible (for example cells in exponential/log phase) and let:
$$D=\frac{F}{V_R}$$
Where $D$ represents the dilution rate (how quickly the volume in the tank is being replenished). Then rearranging the above equation you get:
$$D=\mu_g$$
This says that the growth rate will be equal to the dilution rate. In other words you can set how fast the cells grow by modifying the flow rate and/or volume of the tank. But there is a limit. Cells grow as fast as they can use the limiting nutrient ($S$) and this relationship is often modeled as:
$$\mu_g=\frac{\mu_mS}{K_s+S}$$
Where $\mu_m$ and $K_s$ are unique parameters for every cell type. $S$ is the concentration of the limiting substrate in the tank (which is also equal to the concentration of the substrate in the outlet stream). The maximum growth rate is $\mu_m$ and if the dilution rate is higher then this value, the cells get washed out of the chemostat. This can be troublesome if you need a flow rate higher than $\mu_m$. In this case a recycle is useful.
To answer your question in the comments regarding medium composition. You probably want to operate at steady-state. Steady state means that there is no change of parameters with respect to time. So if you write the substrate mass balance:
$$FS_0-FS-V_RX\mu_g\frac{1}{Y_{\frac{X}{S}}}--V_RXq_p\frac{1}{Y_{\frac{P}{S}}}=V_R\frac{dS}{dt}$$
And set the derivative to 0. Then you will find the outlet substrate concentration is a function of other constants (biomass, volume, product yield, etc.). You're right in that some substrates get used more than others, but when steady state is reached. They stop changing and the medium composition stays constant in the vessel.

Thanks for your help! Without stating what variables and constants are, the equations are a bit obscure though. And I still don't get why in a chemostat the medium composition would stay constant. In fact, a cell uses different compounds at different rates. However, the composition of the input medium is constant and is not adjusted to correct for these differences. Therefore, all input nutrients (except the limiting one) will increase their concentration in the vessel with time. But maybe I'd better open a new question to address this

I think you are confusing "constant" with "the same". If you feed 20 g/L glucose and 20 g/L uracil to the vessel then hypothetically you could have 1 g/L glucose leaving and 19 g/L uracil leaving, because they are used at different rates. But these rates would be "constant" in the sense that the levels stay at 1 g/L glucose and 19 g/L uracil because the system is at steady state. In other words the nutrients don't keep dropping to 0 because you are constantly add more nutrients in the feed.

I will try to update my answer but I was having issues logging on my computer and apparantly I made a new account so I can't edit at the moment.

Finally there is no "increase over time" for unused nutrients. Whatever isn't used leaves the vessel.


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Physiology of hyperpolarization
In my textbook, it is stated that after the closure of potassium voltage-gated channels and during hyperpolarization, potassium leakage channels allow potassium influx passively and this returns the cell to its normal polarised state. I don't understand why will potassium ions enter the cell against its electrochemical gradient ?
My textbook quote :

during Hyperpolarizatio: The Leakage K+ Channels tend to drive the membrane potential from hyperpolarized state to the resting state as they drive K+ ions inward

@BryanKrause and then comes another question if the stable membrane potential is for example -90 MV and potassium gated channels open why would potassium ions disrupt their original equilibrium (increase the inside negative charge) and move outside the cell more than before.

Which textbook is it? I think that phrase is completely wrong.

@BPinto  I think the phrase is correct and if it's wrong then what drives the membrane from hyperpolarization to normal resting membrane potential

When you`re in the hyperpolarized phase, the resting potential is closer to the K+ reversal potential.  When the voltage dependent K+ channels close the membrane permeability to potassium decreases and thus the resting potential shifts to more depolarized. @BrianKrrause answer should make it clear now

@BPinto thank you this answer made every clear

I don't get to say this on very many occasions with questions like this...
Your textbook is wrong.
A typical potassium reversal potential in a cell is ~-90 mV. Hyperpolarization through voltage-gated potassium channels can never go more negative than that reversal potential.
An experimenter with access to the cell through a patch clamp electrode could possibly set the voltage more negative than potassium reversal, in which case indeed, potassium would flow against it's concentration gradient into the cell due to the electrical potential. It is not possible to reach those very negative potentials using potassium channels alone.
For a typical cell, the resting membrane potential is more like -70 mV. This resting potential is due to the "leak conductance", which does include potassium but also includes other ions. The ratio of sodium to potassium permeability is typically around 1:20; potassium dominates but you can't just ignore the other ions. A more accurate replacement statement for your textbook would be:

The leakage conductances tend to drive the membrane potential from hyperpolarized state to the resting state as the net positive flow of ions is inward.

Even at rest, you will always find a slow potassium leak out of the cell. The reason that the cell is at equilibrium at rest is because this leak out of the cell is perfectly balanced by net positive charge flowing in to the cell; this is mostly sodium but can be other ions like calcium as well (note also that that chloride leaving the cell is also a net positive charge in).
Some of the sodium leak current is through specific sodium leak channels, but co-transporters that use the sodium concentration gradient also contribute.

Ren, D. (2011). Sodium leak channels in neuronal excitability and rhythmic behaviors. Neuron, 72(6), 899-911.

@Byran Krause what I understood from your answer is that due to the specific limited number of K+ channels (and not only the electrochemical gradient) the efflux of K+ ions is limited to a certain number and after increasing the conductance of membrane to K+ (causing hyperpolarization) ,the membrane conductance to K+ returns to normal slowing down its efflux .So, what causes the return from hyperpolarization to polarization is the normal flow of other cations with their electrochemical gradient (Na+) and the slowed down efflux of potassium not as was written by the influx of K+. Right?

@mohamed First think of each ion's reversal potential and the membrane voltage. Every ion will travel according to its own reversal potential. If potassium's reversal potential is -90mV, it will always be flowing out of the cell if the membrane is more positive than -90mV, and flowing in if the cell is more negative than -90mV. The rate of flow depends on the difference from -90mV. If the reversal potential for sodium is +60mV, it will always be flowing into the cell if the cell is more negative than +60mV. The membrane potential you actually observe, then, depends on a ratio of conductances.

and that's why the book is wrong K+ never enters the cells  and the  cell's membrane potential shifts towards sodium's potential stoping hyperpolarization ,but then the number of sodium inside the cell increases relative to before the action potential, so here comes the Na+-K+ in returning the original number of potassium ions inside the cell and expelling and excess sodium.


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reason for "not for diagnostic use" advice in protocols
I read "not for diagnostic use" in every protocol i saw. why is it so?
which differences have the kits and material that are used for diagnostic purposes?

the FDA has to approve diagnostics - a rigorous and expensive process.  Its a legal distinction, but also one which conveys a significant level of usefulness and reliability.

The quality controls (GMP, GLP and so on) which have to be implemented for diagnostic kits are also ways more complicated, what makes these kits more expensive.

Yes definitely - it takes years and $millions usually.  and its effectiveness has to be clear and reproducible.


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Smallest, specific RNA-binding protein - w/ sequence?
I'm looking to synthetically fuse an RNA-binding protein onto another protein, inside a viral vector which has a size-limit. I've considered some options, but I'm wondering what StackExchange will say. What is the smallest protein known that binds to a specific sequence of RNA, and what is that sequence?

This is Stack Exchange Biology. StackOverflow is the computing site.

@David - while in itself obviously true, I don't understand your comment in this context?

He has now corrected an initial mistake / typo.


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Why are there multiple sequences for the same segment for an individual "strain" of influenza?
I am looking at the genome of the influenza virus being used in the flu vaccine 2017-2018: A/Michigan/45/2015.
When I look below at the individual segments, there are 4 sequences for each segment - shouldn't there be only one for a single "strain"? Is this due to rapid mutation rates? Or is it that they are including both positive and negative sense of the virus?
Edit: sorry, link here:
https://www.fludb.org/brc/fluStrainDetails.spg?strainName=A/Michigan/45/2015(H1N1)&decorator=influenza

This is pretty typical for influenza, and reflects the ambiguity of "sequence" when talking about rapidly-mutating RNA viruses. Such viruses exist as a "cloud" of variable sequences; a single replication of influenza is likely to contain variants at every single site of the genome.  That also allows the virus to undergo extremely rapid natural selection, including during laboratory passages (which are obviously not performed using infected humans, but might be in various cell types, or very often in eggs).
A common scenario for an influenza isolate (especially one that, like MI/45, is used in vaccines) would be to swab someone's nose, use the swab to inoculate an egg to prepare a stock virus, send that stock to several other labs, grow a subset in cells, have another lab grow some in their cells or eggs, and so on. If it's used in vaccines, it might be made into a reassortant with a different (less virulent) backbone, but the surface genes would still be termed MI/45. Each lab would sequence the virus, often at multiple steps in the passage; and at each step, there's an opportunity for the virus to either undergo selection, or simply to drift, and change its sequence. Or, of course, if may not change, and identical sequences might be deposited into the databases, perhaps starting at slightly different points depending on each lab's sequencing protocol.
Many viruses are only sequenced once, perhaps as the original isolate or as an early passage, because there's no reason (or capacity) to look further at the tens of thousands of isolates that are taken every year, but where there's a reason to look at an influenza virus more than once, standard protocol is to re-sequence it each time it's used. I can guarantee that there are far more than just 4 sequences of MI/45 out there, probably there are more like 400 that have been done world-wide, it's just that there's no point in depositing all of them.

It looks to me that the website you're looking at is mostly taking publicly available data from Genebank (the NCBI repository for sequence data) an collects it to form an overview.
For your question this means that there are 4 available sequence datasets for the A/Michigan/45/2015 influenza strain - they are likely very similar but based on the reported segment length not quite identical.

Or is it that they are including both positive and negative sense of the virus?

If you mean the positive and negative strand of the DNA, then no - since the sequence of these two is always complementary the Genebank repositories only stores the forward sequence.
You can also see that the 4 different datasets have similar Acession numbers:
KY117020 - 27 (Passage M1/C3)
KU509700 - 07 (Passage E1)
KU933490 - 07 (Passage E3)
KY090607 - 14 (Passage M1/IR)
You can look up more details for these accessions on the genebank website:

It seems that all 4 datasets came from the same publication
... which apparently was never published (so it's not available online), but it might be part of some WHO program?
The main difference of the 4 datasets I can find is the passage of the strain. I'm no virologist, so I'm not quite sure what it means, but in cell biology passage describes the time a certain cell line has been in (in vitro) culture.


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Papers where protein oligomerization has been engineered away
I have a protein that acts as a monomer, but appears to have a relatively high self-affinity in vivo (measured using transient transfection of a plasmid coding for the protein), which is annoying because I'm trying to engineer conditional self-association like with FRB-FKBP w/ rapamycin. Have there been any papers where self-clumping of a protein has been engineered away?
My current approach is to use threading to identify a protein structure and a docking program to identify sites of self-interaction and mutate those sites away.

“Clumping” to mean means aggregation, but it sounds like you wish to change the oligomeric state. One approach I recall used in streptavidin was to introduce charged residues at the subunit interface to create a repulsive effect. I’ll find the paper when I have a moment.

Engineering Soluble Monomeric Streptavidin with Reversible Biotin Binding Capability

Stable, high-affinity streptavidin monomer for protein labeling and monovalent biotin detection

You should define your question properly. Does "self-clumping" means oligomerization or aggregation? You should also give more details about your preparation. How do you prepare your protein, is it recombinant, it is a known protein?

I have updated the question

The authors of the dronpa protein, mention that the initial WT protein they identified oligomerised and they introduced mutations to stop this. However, the explanation of how/why they chose the particular mutations (only shown in the supplements) is lacking.

You have not provided enough information to support your statements.  In what types of experiments does it behave as a monomer (and how can one determine whether it is acting as a monomer or a higher oligomer?)? What evidence do you base your assertion that in transient transfection assays it is clumping, or aggregating, or oligomerizing?  If the pure protein is soluble, you might be able to crosslink it to a matrix and construct a affinity column.  In a mixture of cellular proteins does this protein bind specifically to such a column?


text:
Egg sack identification
Can anyone identify this egg sack? It is on the underside of my organic poblano pepper leaf. No infestations, no bugs around that I can see. In case the picture is not clear, it has a smooth surface, is shiny-ish, and about an inch-inch 1/2 in length. This is in Southern California.

Looks somewhat similar to clutches of some treehoppers.


text:
Can axial myopia be caused by gravity?
I've been reading up on axial myopia and a few things struck me as odd.
This meta-analysis suggests that spending time outside decreases rates and severities of myopia. This makes me think that whatever is causing myopia might be inside, and after witnessing some school kids working on a test in a classroom, it hit me.
The schools' desk and chair setups around the world are far from ergonomic, so more often than not kids have to tilt their head or bend their bodies to read or write. While doing that, they align the front-back axis of their eyeballs with the vector of Earth's gravity. The acceleration caused by gravity exerts a constant force on the eyes that is normally not present along the front-back axis when we sit or stand upright. Combine the eyes being incredibly soft and prone to deformation more than other tissues with the general developmental stage of children's bodies making any kind of deformation and trauma more likely to be permanent in adult years, and you get a lot of myopic people in countries with high rates of formal education, especially among the most studious of people who are more likely to be bent over a book or writing something, and you get to where we are now.
Is this a new hypothesis or did someone already proposed and disproved it?
If that's the case, we could mitigate this by making reading/writing setups in schools more ergonomic, more like the ones from back in the day when we used quills to write. The one's I've seen have a more upright writing surface that's closer to the eye level so that the ink would flow down the page properly or some such


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Brain response frequencies while sleeping
I'm not sure if this is the right place to ask this but Biology seemed to fit best.
I'm trying to find out what frequencies the brain responds to best while sleeping.
The reason for this is recently I attended a lecture where it was stated that the brain hears low frequencies/deep noises better, meaning fire alarms for example might not be as effective as we think.
However I remember there was an episode of The Big Bang Theory where they said high pitch noises are heard better while sleeping as a built in response to, for example, a baby crying. Now I know this is just a TV show but I presume they must have some basis for the remark since they do have science advisors, it also just seems to make more sense.
Does anyone know which is correct or better yet can point me in the direction of some research to help.

Just to point out that the big bang theory episode states that women are more likely to respond to high pitched sounds such as a baby crying. I have no idea if it is true but it makes perfect evolutionary sense.

On a less serious sidenote: I know Francis Crick was an advocate of his brain@40Hz theory. / I would advocate for the Sceptics.SE site, which deals with scrutinizing notable sources...

Sleep as you may know is divided into 2 broad categories which are the REM (Rapid Eye movement) and NREM (non rapid eye movement). NREM is further divided into 3 stages (reference). You never know which stage of sleep you are in when you are subjected to a particular frequency of sound. Your response to different sounds differ in your different sleep cycles.
The present 3 stages in NREM sleep is an update by The American Academy of Sleep Medicine (AASM) in 2007 (reference).The original 4 stages in the Rechtschaffen and Kales (R&K) standardization of 1968 (reference) has been used to explain the effect of disturbances in different sleep cycles

Stage 1 is still the phase of sleep from which it is easiest to wake
  someone up.
People in Stage 2 sleep are unlikely to react to a light or a noise,
  unless it is extremely bright or loud.
During Stage 3, the muscles still have some tonus, and sleepers show
  very little response to external stimuli unless they are very strong
  or have a special personal meaning (for example, when someone calls
  your name, or when a baby cries within earshot of its mother).
Stage 4 is the stage of sleep that accomplishes most of the body’s
  repair work and from which it is most difficult to wake someone up (reference).

A study conducted to measure brain activity while sleeping subjects were subjected to varying degrees of sound found that some people did you wake up after being hit with 70db of sound while others woke up even at sounds between 40 - 50 db (reference). This could lead to new behavioral or drug therapies for people with sleep disorders.
A review on the affect of low frequency sound on sleep could not reach any significant conclusions warranting that more search needs to be conducted in the field.(reference).
You will be interested to know that different sounds have been found to wake up men and women. A list is available here. Differences between the sleep of men and women are listed in this article.


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A mathematician's confusion regarding parametric $t$ tests for gene expression data
I'm a mathematician trying to test some things on gene expression data, and I'm thus skimming over various articles such as Sotiriou et. al. to understand what is typically done with such data sets. Several things confuse me; in particular, a paragraph in Sotiriou et. al. reads:
"Clinical parameters such as ER status, [...] affect the behavior of breast
cancers. We asked whether these clinical/pathologic characteristics were
associated with differential gene expression. Parametric t tests identified 606
probe elements of 7,650 elements represented in our array that could segregate
ER+ and ER- breast tumors (P < 0.001)."
As segregation of ER+/- based on gene expressions is one of several things I'm
interested in attempting to achieve through novel methods, I have been trying
to understand what precisely is meant with the above paragrah. To recap the
article, there are 99 patients with 7,650 probe expression values, and one
ER+/- value each. The article sets out to determine which of those 7,650
probes successfully segregate the dataset into ER+ and ER-.
I've run the above paragraph by a nearby statistician, and he could not for
the life of him figure out what was done, and had not even heard of such a
thing as a "parametric t test". This leads me to suspect that the term is
specific to biology, so I ask: what is meant?  It is also unclear to me (and
him) what the P-value means in this context.
I hope the scope of this question isn't too broad. Of course I want to avoid
asking "explain this article to me, the outsider, please"; I do believe the
paragraph above is relatively self-contained in the context of gene
expression.
References:

Sotiriou et. al., Breast cancer classification and prognosis based on gene
expression profiles from a population-based study.

I understand this in the following way:
For each probe you have two sets of measurements, one for ER+ and one for ER-. What you do is a T-test (to my understanding is that the "parametric" just emphasizes that T-test is a parametric test) on these two sets, testing if their mean is significantly different (they refer to this as "separated"). You repeat this test for all 7650 probes, and you get a set of 7650 p-values. You then do some multiple testing correction, such as a Bonferroni correction (I haven't checked in the paper if they did it, but they obviously should). Finally, they find that 606 of the p-values are significant (for some choice of threshold), suggesting that they can "separate" ER+ from ER-.
As a computational biologist I would advise you to look specifically at bioinformatics papers if you are looking into developing new methods, since the analysis in "pure biology" papers can often be lacking and would not give you a good perspective of state-of-the-art analysis methods. Specifically for the question of separating groups from gene expression you should look into the field of Machine Learning, as it had been widely applied to this problem.

@leonardo sounds fishy... as I said, I wouldn't take this as an example of good data analysis. Although I believe that in the time since that paper was published some aspects of analysis in biology papers have become better, including multiple test corrections.

Thanks! Do any of you know of published clustering analysis of microarray data where the actual data that was fed into the big black box is available? As I am no biologist, processing "raw" data is quite difficult and seems to be a research area in its own.

This isn't the answer you're probably looking for, but I'd recommend not bothering with what they mean about their test in particular ... maybe they were really using a mann-whitney but their software (SPLUS) labeled it as a "non-parametric t test" for the non-formally-trained-statistical-end-user
[update]: I misread the text and thought you (and the paper) wrote "non-parameteric t-test" which is why I suggested a possible mann-whitney -- mistake on my part, sorry. The second part below still stands [/update]
Anyway, it has been nine years since that study has been published and the bioinformatics community has pretty much nailed down microarray analysis. Unless you have a specific reason not to, you should almost always prefer to use limma first for your analysis of such data (gene-level expression data). It has an extremely thorough user's guide to help you get started.
If you're looking for places to go to for follow up questions on your analysis, consider subscribing to the bioconductor mailing list, or head over to the biostars QA site.


text:
How can the symptoms of ovulation (pms or pmdd) occur if one is menstrating?
Even if your period is lasting overly long. Wouldn't starting to ovulate end menstrating?

Does this answer your question? Can ovulation and menstruation occur simultaneously?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources).  ——— Thank you for taking the  [tour], but please also go through the help pages starting with [Ask] questions effectively on this site. Thanks!


text:
Is there a nomenclature for human physiology?
Back when I studied botany in high school, the teacher taught us the nomenclature for botanical terms. I think there should be something similar for human physiology. Understanding how the name was formed helps a lot while reading about the human body. Can you please point me to any resources (books or websites) on this topic?

Hey yasouser, I’m not sure if this is the case, but I’m curious if you’re actually referring to etymology rather than nomenclature. Your point “Understanding how the name was formed helps...” makes it seem like that’s the case. If so, most medical terminology textbooks have this information on word roots, prefixes, etc. and might also delve into Latin origins (I can recommend some if I’ve understood your question correctly).

Yes etymology of the medical terminology is what I'm looking for. I used the term nomenclature because the names are formed with certain rules, right?

Des Moines University has an overview of medical terminology, for example:

Useful prefixes and suffixes
Word roots for organs
Some general terms
System-specific terms, for example, for circulatory system

The Free Dictionary has a Medical Dictionary, which shows results from various dictionaries with basic etymology included.
Etymonline is a detailed, general etymological dictionary, which includes a lot of medical terms.
Physiology as such may not have a lot of specific terms, but it is helpful to know basic anatomical and pathological terms when reading physiological texts.
Schulic Medicine & Dentistry has an one page glossary of ~400 medical terms.
BC Campus has basic anatomical terms with pictures on one page.

Thanks for the Des Moines University weblink. That's exactly what I was looking for.

The book I'm most familiar with is Medical Terminology: A Programmed Learning Approach to the Language of Health Care Second Edition by Marjorie Canfield Willis. This book is great for what you're looking for, and I believe you can get the 2nd edition pretty cheap from multiple vendors.


text:
Should consciousness be a defining property of living organisms?
High school students in India under the CBSE Board are taught that consciousness is a defining property of living organisms.
This question lies under the topic of 'What defines living organisms?'
Does that mean that if robots and other artificial intelligence have consciousness and can react to some external stimuli (just like plants), they are alive?
Also, what about the patients in coma or those who are 'brain-dead', are they alive or dead?
Then, how do we define living in terms of science?
A possible answer in my opinion to the second question above could be that life begins at conception and an organism is considered alive till the point where it has no differences with the dead; i.e. a person who is 'brain-dead' would still be considered alive because he/she still isn't the same as a dead person.
So should consciousness be a defining property of living organisms?

Edit: Defining Consciousness-
In the NCERT textbook which is used to teach the CBSE high school students in India, consciousness is explained as the ability to sense the surroundings or environment and respond to the environmental stimuli which could be physical, chemical or biological.

For reference: NCERT Class 11 Biology Textbook~ Unit 1: Chapter 1, Page 5 (second paragraph)
Link to book: 1http://ncert.nic.in/textbook/textbook.htm?kebo1=1-22

Define consciousness.  Is a bacterium conscious?  How about a potato?  Seems like an appropriate question for the (insert choice of religion) site.

@jamesqf It is mentioned in the textbook that, 'All organisms, from the prokaryotes to the most complex eukaryotes can sense and respond to environmental cues.' So this should mean that bacteria and potatoes are indeed conscious as they can react to external stimuli.
I've edited the answer and added the link to the book, you can check it out.

Someone in a coma doesn't respond consciously, but their body absolutely continues to sense and respond to stimuli. A brain-dead person can still maintain body temperature, metabolize nutrients, and maintain blood pH, none of which are possible without some kind of feedback loop that requires response to the environment. Consciousness could be a necessary condition of life, but it's certainly not sufficient - my TV isn't "alive" even though it responds to the stimuli of me pressing the buttons on the remote.

As someone who studies consciousness...that definition of consciousness would be a very unusual one in the field.

in my long-ago high school textbook this was defined as "irritability" (i.e., the capability of sensing and responding to changes in the environment). This is mentioned in the Khan Academy materials

@Roger Baker: But in aany semiconductor catalog, I can find a large number of  little pieces of doped silicon that sense environmental cues, and wire up circuits that will respond to them.  Heck, I'm writing this on one such thing: my computer senses the environmental cue of me pressing keys on my keyboard, and responds by drawing characters on the screen.  It senses the environmental cue of CPU temperature, and responds by turning on the CPU fan when it gets too warm,  Does that mean integrated circuits are alive?

@BenBolker Thanks for your input, the linked resource also comes up with the same conclusion: consciousness is not a defining property.

@jamesqf: I'm so glad that you have come to this conclusion because that exactly is my question too. Perhaps, consciousness is not the right property that can define living organisms as opposed to the non-living. Or maybe, we could come up with a better description of what's 'living' and 'non-living' to clear up the confusion.
And conclude that consciousness should NOT be a 'defining' property as mentioned in the textbook.

@Roger Baker: I think the problem is that the authors of that text are using the word consciousness in a way that's far different from general use.  Which is why I think it's really more of a religious question than a scientific one.

Hi and welcome to Bio.SE! No, consciousness should not be the threshold for being living since it only exists in animals, and even then it is very hard to define and measure. Behaviourism is one way of looking at this. I asked a question a while ago about why viruses don't meet the definitions of being alive here which might answer some of the things you are interested in.

I have to mirror Jamesqf here there are many very different definitions of consciousness, many with a lot of baggage attached. which is why a good definition would avoid the word entirely.

tl;dr this is an extremely unusual definition of "consciousness" (I'd be surprised if you can find it in any standard English dictionary). If you prefer, like Humpty Dumpty in Lewis Carroll's Through the Looking Glass, to define words (in this case "consciousness") in any way you want — i.e., as above ("ability to sense the surroundings or environment and respond to the environmental stimuli ..."), then consciousness is indeed one of the defining characteristics of life.
This property is (arguably) necessary, but not sufficient, for life — things can be 'conscious' (respond to stimuli) but not be alive, but they can't be alive if they don't respond to stimuli.
This property is more typically called irritability. The Khan Academy article on "What is Life?" gives this property under the section "Response" (along with the the other properties "Organization", "Metabolism", "Homeostasis", "Growth", "Reproduction", "Evolution"). (You can also find it in lots of biology textbooks in this Google Books search.) The text you refer to uses similar criteria (growth, reproduction, metabolism, cellular organization, 'consciousness').
As Khan Academy also says, it's hard to be precise:

Living organisms have many different properties related to being alive, and it can be hard to decide on the exact set that best defines life

So, to answer your specific examples:

robots respond to stimuli (and, arguably, have organization and metabolisms), but they don't grow or reproduce. If they did, we might call them living organisms.
people who are brain-dead or in a coma still exhibit some degree of response to the environment/irritability. So do dormant seeds, spores, and other "resting stages" of organisms.

There are always edge cases; is a sterile person (or indeed one who can't reproduce because they're in a coma) "alive"? The Khan Academy web page uses a similar example, the case of mules (the infertile hybrid offspring of horses and donkeys), along with several other examples that illustrate some of the more difficult cases (dieocious/gonochoric organisms that are isolated from members of the other sex [can't reproduce, but still considered alive]; fire ["reproduces" but not organized or homeostatic]; crystals [not homeostatic, don't evolve]).

And the edge cases can be even edgier.  Consider HeLa cells https://en.wikipedia.org/wiki/HeLa or women in comas who've been raped by their attendants and become pregnant.

I don't think this answers the question (which I doubt could be answered on stack exchange...). "Life" in biology typically do they have the biological machinery to replicate at the cellular level given enough resources. For almost all life, that comes down to does it have ribosomes.

@jamesqf This is not a fringe case at all. HeLa cells are universally considered an in vivo ("within life") experiment. I don't understand why the rape example would be a fringe case.

The title of the question is not "how do we define life?", but "should consciousness be a defining property of living organisms?" (to which the answer is, "yes, if you define 'consciousness' as ability to respond to changes in the environment)

@James: HeLa cells are a fringe case because they're living cells derived from a person who once was conscious, but who is now dead.  So are the cells "conscious"?  Likewise the brain-dead rape victims.  Not conscious by common definition, but still able to reproduce.

@BenBolker That definition is far too nebulous to be of much use in biology. Your roaring fire in a hearth will leap around when poked, whereas an oak tree wouldn't even flinch if I prodded it twice as hard! Being less pedantic, viruses respond in a very biological manner to their environment. Are they "conscious" in any meaningful way? A much more useful measurable and comparable classification for life is "does it have (active/translating) ribosomes in it"? There isn't really a need to drag any other qualifiers in.

@jamesqf This is starting to sound an awful lot like the definitions of a soul...

My final comment: as I say in my answer above (as do the various sources cited), (1) "response to the environment" is a necessary but not sufficient condition (i.e. 'fire responds to the environment' does not by itself imply fire is alive); (2) the particular environmental changes that organisms respond to vary enormously. Trees respond to changes in light, distribution of nutrients and water in the soil, etc.. I think my post is a reasonable answer to the OP's question; if you disagree you can downvote (if you haven't already); post your own answer; or vote to close the Q.

@BenBolker I think my overall point is that those irritability concepts are too soft, hard to define, and non-comparable between organisms without more qualifiers. I've voted to close the question. I agree that your answer is very reasonable. I just don't think any answer would completely answer this question. A more comprehensive essay on the topic of life is this Science editorial: The Seven Pillars of Life. It reframes the irritability as "adaptability" and "improvisation" I suppose.

@James: Exactly, which is why I say it's a question better suited to religion sites, or maybe philosophy, rather than biology.