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How is an RT-PCR representative of the RNA contents in a cell?
For example, we first collect all the RNA contents from a mammalian cell line. Say, for instance, we collect 80 uL of RNA with a concentration of 150 ng/uL. Next, to make cDNA, we take 1,000 ng of the RNA. However, this 1,000 ng is a completely random sampling of the total RNA we had. How is that random sample of RNA representative of the RNA contents originally in our cells?

Are you asking if mRNA molecules that are present in only few copies may be distorted by random sampling?  That's certainly true.

It isn’t really clear exactly what the questioner is asking, but…
...one way of thinking about this is to ask how likely is it that a low-abundance RNA will be absent from the sample taken from the preparation of RNA. This would make the sample non-representative at the qualitative level.
The question states that 12,000 ng of RNA is isolated. Since nothing else is specified I assume this is total RNA. A rough estimate of total RNA per eukaryotic cell is 20 pg.
This means that the preparation came from 6 x 105 cells. (I’m assuming 100% yield, but this won’t really affect the conclusion.)
Now assume that a low-abundance mRNA is present at 10 copies per cell. The total RNA preparation therefore contains 6 x 106 copies of that low-abundance mRNA.
We take a sample of 1,000 ng from the total 12,000 ng. In other words we take 1/12th of the preparation of RNA. If that RNA preparation contains 106 copies of the low abundance mRNA how likely is it that we happen to take a sample which contains no copies of that low abundance mRNA? Here my maths fails me, but intuitively I say that the probability is very very small.
Now, if there are 1,000 different low-abundance mRNAs in the cell the probability of missing each of them is very very small, but the overall probability of missing one of them is 1000 x very very small, so maybe very small.
I'll continue thinking about how to calculate the value of very very small, but if anyone wants to help out - thanks in advance!

To add to my question, what if you are checking the inclusion of an exon and lets say if we assumed that the alternative exon shows up in 15% of gene X. However, if we take a random 12th, couldn't the 12th be non representative and show something like 60% inclusion when it should actually be much lower?

Yes, there are all kinds of ways in which, due to chance, the final cDNA mixture might be a rather skewed reflection of the original mRNA distribution, as Roland said in his comment.


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compute contact mixing matrix from partnership degree data
In a discussion of sexual partnering, we are given the following information on a momentary degree distribution (as percentages):
degree    0       1       2      3
men      32.3    53.2    12.4    2.
women    26.7    71.9     1.1    0.2

From this, the authors construct a "proportional mixing model", treating the data as providing the marginal effects.  (The rounding error is small, so I'm going to ignore it.)  I want to understand what this means.  I'll try to get started.
To begin, since this is heterosexual mixing, there cannot be the same number of men and women participating, since men and women must be in the same number of partnerships.  So if there are say 10000 individuals, we must have about 4707 men and 5923 women. From this (and the above percentages) we know the number men and women of each degree, and thereby how many total partnerships (3954).
degree    0          1         2        3
men    1520.36    2504.12    583.67    94.1399
women  1413.23    3805.67     58.22    10.586

I think (?) the challenge is first to find the number of partnerships of each type.  Obviously there are no partnerships with individuals of degree 0, so we are looking to fill a 3 x 3 matrix of partnership counts, so that each deflated row sums to a male total and each deflated column sums to a female total (as given by the table).  (By deflated, I mean divided by the degree.)  This does not seem too bad on the face of it: 9 variables with 6 equations looks to leave solutions to spare.  But the system appears to be inconsistent.  So, I must misunderstand.
I get the impression that this is very standard stuff, but I'm not finding it in the textbook I have at hand.  I'm happy to work through the math if pointed to a careful discussion.

source: Stack Exchange

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Can skeletal morphology change in adults?
I'm just a curious layman, so be gentle. I read around that things like the cranial1 and pelvic2 morphology change with age, but I also read seemingly contradictory information that bones are 'completely ossified' around age 25 (can't post a third link for reference) and that's often cited as meaning "done changing."
Wikipedia (my trusty friend) also describes 'bone remodeling' as a lifelong process, yet also describes ossification (not a lifelong process) as a key component.
So I'm confused. What actually changes in terms of bone morphology throughout an adult's life? Does bone tissue continue to form in adults? Do bones "bend" and flatten ever so slightly into new forms? Additional reading would be appreciated as well.
Thanks

+1 for writing a good question. Somebody competent will answer.

The statement "  bones are 'completely ossified' around age 25" means that all bones are now osseous i.e. there is no cartilage or membranous present after 25yrs. This doesn't mean that bone resorption and ossification doesn't take place. The term Ossifocation has different meaning in different context.

Bone never stops changing.
Your bones are constantly being broken down and reformed on a microscopic level. Your bones are done growing at a certain point but they continue to be reshaped. Remember bone exists to supply calcium (and to a lesser extent phosphorus), to your muscles, Your body needs to break down the surface of the bones for this calcium.*  So bone is dissolved and redeposited constantly, this regulated mineral levels but also allows the bone to slowly reshape itself.
Bone will slowly reshape itself to resist any stress it experiences, for instance if you build muscle the attachment point for the muscle will become more rugged to strengthen the attachment. A runner's leg bones will get thicker and denser to resist the greater stresses. Joint surfaces can even reshape with repetitive motion.
*bone originally evolved as armor but this has been lost in modern vertebrates. Vertebrate muscle requires calcium to function, Vertebrates have lost the armor but not the need for a calcium store, and have repurposed into a structural support. Vertebrates without structural bone need to have massive calcium levels in their body tissue instead.
for continued reading there is a whole series of books by R. Mcneill Alexander that cover bones in fascinating detail.

"bone exists first and foremost to supply calcium to your muscles" - What makes you so sure of claiming that? Bones certainly did not evolve for this reason. Also see: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3237026/

oops that was my bad, forgot to add phosphate, good catch. But if you read carefully that source supports my claim, calcium phosphate is resistant to the acidic conditions produced my active muscles creating a calcium and phosphate store that can be modulated. bone did evolve for that reason.

The structural use of bone (originally armor) could only occurred after the ability to deposit calcium phosphate had evolved.

@john What does 'joint surfaces can even respade' mean? Respade means to turn over(Wikitionary). Please can you explain,what do you mean by the above statement?

dyslexia plus a typo, "reshape" I'll fix that.

@adjan Bone evolved first just to rid the body of calcium, This was easily turned into external armor/skeleton. Bone then became biochemically important for how vertebrate muscles work. As armor was lost the calcium was still needed so it shifted to internal storage and reinforcing existing structural tissue. Out of the current uses of bone calcium regulation would be the most primitive. Structurally bone could be replaced but its calcium store function cannot.

@John - Bones are indeed the body's main repository for the critical-to-life element, Calcium. But to say that's why they evolved is a teleological argument. There's a difference.

no there are clear adaptations to make bone better calcium stores, I think you are confusing "evolved to" with "only evolved to"

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Number of elongating RNA polymerases on a gene
I'm interested in knowing how many Pol II molecules are simultaneously transcribing any given gene. There are RNA pol II ChIP-seq (phospho-S5) data for different cells but these come from pooled cell samples. So the different peaks on any given gene would be the average of the cell population. Single cell ChIP-seq data would help but I can't find any.
The other way to check this is to calculate transcription rates of different genes, normalize with copy number and divide by the elongation rate of the polymerase on that gene. However, elongation rate is not unique for all genes.
Is there any resource – paper or raw data, which would help me find the answer to the question?

Regulation of RNA polymerase II activation by histone acetylation in single living cells by Stasevich et al. provides detail on how they were able to determine the number of elongating RNA polymerase II for a given gene array. The issue I had with the paper is that they used a ~1.8Mbp tandem repeat as their target, so they really upped the probability of seeing activity. You may be able to do similar for your gene of interest, but there may not be enough signal to tease out your data.


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Limit of muscle atrophy
I read that lack of action leads to muscle atrophy , I experienced same when I had a cast for hand fracture. So how far this atrophy go, who decides minimum size of muscle due to lack of activity, for example in coma patients.
Which part to brain or body signals muscle atrophy and upto what limit it should go?


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Is prion a term used to describe the normal form of the protein as well as the disease causing form?
I've been reading my textbook and it refers to prions as a normal protein with a helpful function but it can turn into a disease causing form. However, I look in my other textbook and it refers to the word prion as solely being a disease causing protein.
I'd like to know which is the correct definition. Ie. Would I be correct in saying "The prion protein is normally involved in synaptic transmission but can turn into a disease causing form"?
Thanks in advance!

The normal isoform of the protein is called PrPC, which stands for cellular prion protein, while the infectious isoform is called PrPSC, which stands for scrapie prion protein.
According to Riesner (2003):

The biochemical properties of the prion protein which is the major, if not only, component of the prion are outlined in detail. PrP is a host-encoded protein which exists as PrPC (cellular) in the non-infected host, and as PrPSc (scrapie) as the major component of the scrapie infectious agent. (emphasis mine)

If you search for "cellular prion protein" you're gonna find several papers that use the name prion protein to the normal isoform. Some examples:

Prado, M., Alves-Silva, J., Magalhães, A., Prado, V., Linden, R., Martins, V. and Brentani, R. (2004). PrPc on the road: trafficking of the cellular prion protein. Journal of Neurochemistry, 88(4), pp.769-781.
Ramljak, S. (2008). Physiological function of the cellular prion protein (PrPc_1hnc). 1st ed. Berlin: Logos-Verl.
Pantera, B., Bini, C., Cirri, P., Paoli, P., Camici, G., Manao, G. and Caselli, A. (2009). PrPc activation induces neurite outgrowth and differentiation in PC12 cells: role for caveolin-1 in the signal transduction pathway. Journal of Neurochemistry, 110(1), pp.194-207.
Martins, V., Mercadante, A., Cabral, A., Freitas, A. and Castro, R. (2017). Insights into the physiological function of cellular prion protein.

And many others.
Therefore, following this nomenclature, the answer to your question ("Would I be correct in saying 'The prion protein is normally involved in synaptic transmission but can turn into a disease causing form'?") is yes. The difference is the adjective: cellular or scrapie.
Finally, pay attention to this: you have two different questions here. In the title you say "Is prion a term used...", but in the last paragraph you say ""Is the prion protein normally involved in...". As extensively discussed in the other answer, the term prion alone (instead of prion protein) is normally used only when referring to the abnormal isoform. More on that here: https://www.cdc.gov/prions/pdfs/public-health-impact.pdf
Source: Detlev Riesner; Biochemistry and structure of PrPC and PrPSc. Br Med Bull 2003; 66 (1): 21-33.

This is also a fairly good review that outlines some of the history of the research and how the naming came to be. THE PUBLIC HEALTH IMPACT OF PRION DISEASES

@AMR Thanks, I just linked that in the question.

If we are considering prions in general, I disagree with the answer supplied by Gerardo Furtado.
Here is a definition taken from an article by Susan Lindquist:

[Prions are]...self-perpetuating and heritable protein conformations that cause multiple phenotypes,
  represent an unusual mechanism of information transfer that occurs via protein instead of nucleic acid.

Compare Wikipedia:

Prions are infectious agents...

If a prion is self-perpetuating or infectious then the normal form of such a protein is not a prion. In yeast the term prion is used to refer to the infectious form of a protein in a formal genetic sense. For example the [PSI+] prion was discovered as a genetic element and  then subsequently found to be associated with the translation termination factor Sup35, a protein with a known cellular role. All yeast strains have Sup35 protein but only certain strains contain and transmit the prion form of this protein. So [PSI+] is referred to as the prion form of the protein.
The problem with interpreting the language used to describe the TSE prions is that they were discovered because of their prion activity so the normal form is referred to as prion protein (as far as I am aware the function of the normal form isn't known). This doesn't mean that this form of the protein IS a prion, merely that this protein is associated with the original prion phenomenon so is called 'prion protein'.

If you didn't truncate your Wikipedia quote: "Prions are infectious agents composed entirely of a protein material that can fold in multiple, structurally abstract ways"

And if you didn't truncate your Lindquist quote: "Prion proteins can assume at least two conformations"

I don't understand why you think that makes a difference. If a prion is the infectious form ('infectious agent') of a protein that can fold in different ways, that doesn't mean that the non-infectious form is a prion. A cell which contains only the normal form of a prion-forming protein doesn't contain any prions since it contains no infectious agents.

Yes, Lindquist refers to proteins that can form prions as 'prion proteins' but not as prions. Just like the cellular form  of the TSE agent is called 'prion protein'. But please, write your own answer.

I don't need to. I just need to upvote the correct answer and downvote the wrong one.

@OrangeDog I don't know why you're so emphatic that this answer is incorrect. The original definition from Prusiner states ...a new term "prion" is proposed to denote a small proteinaceous infectious particle.... Clearly that definition precludes its use for referring to normal proteins, especially since it predates any linkage between the infectious particle and it's normal, non-infectious variant. As Alan Boyd said, there is a distinction between prion and prion protein.

@GerardoFurtado The title also poses the following question (which is the one you answered yes to): Is prion a term used to describe the normal form of the protein as well as the disease causing form? The answer to this question should be no, which is presumably where the disagreement arises (though I can only speak for myself). Again, there is a distinction between a prion and what was later called the prion protein.

@canadianer OP is clearly not asking if the term alone is used to describe the normal isoform. Anyway, I'll edit my answer to make clear I'm answering his second question.

@GerardoFurtado There are two explicit questions and it seems that you answered one and this post the other. Anyways, you've got my upvote after your edit.

@canadianer is correct in referencing Prusiner, as he is credited with the nomenclature and usage.

@canadianer Ok, I'll edit my answer again (hopefully for the last time) to make it clear that the name cannot be used alone.

The Wikipedia definition of prions is quite clear I think:

Prions are infectious agents composed entirely of a protein material
  that can fold in multiple, structurally abstract ways, at least one of
  which is transmissible to other prion proteins, leading to disease in
  a manner that is epidemiologically comparable to the spread of viral
  infection.

Your definition: "The prion protein is normally involved in synaptic transmission but can turn into a disease causing form" it is misleading. First, it sounds like there is a protein called prion that is involved in synaptic transmission, which is not true. Prions are a subset of the group proteins. Moreover, not all the prions are derived from proteins involved in the synaptic transmission. Prions have been found in other organisms like bacteria and fungi, so there is little to do with synaptic transmission there. The wiki page I have linked is full of links to the related literature, start there your journey!


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How is omega 3 deficiency determined?
I read quite a bit online about omega 3 deficiency. How is this actually determined - that is, what happens in the lab to determine this ?
n-3 fatty acids have roles in many different human tissues, so does the definition of sufficiency vary depending upon which tissue is being studied ?


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How can heart disease cause excessive sweating?
According to google:

What can cause sudden sweating?
Excessive Sweating. A person with
  excessive sweating has a condition called hyperhidrosis. ... In
  adults, the most common cause of hyperhidrosis is emotional stress.
  However, excessive sweating is also caused by heart disease, lung
  disease, diabetes, and shock.

Sweating is seemingly unrelated to the heart conditions. By what mechanism can a heart disease cause excessive sweating?

I'm voting to close this question as off-topic because this is a medical not a biological question in terms of SE Biology.

@David I wonder why we have a pathophysiology tag then. Maybe you misunderstood what a "medical question" means here.

Tags do not define what is on topic, anyone can create them. The Tour and Help explicitly do so. Please read them.

I disagree that this is off-topic.

@David No thanks. I left these sites mostly because of self important admins who decide to close a question after 3 years and such things. I found that eventually every stack exchange sites turn this way. I rather go to forums, those are somewhat better.

The answer lies in compensation. Take myocardial infarction, for starters. MI, if large enough, severely weakens the heart, and hence, at the same level of stimulation, it can no longer pump blood effectively, causing what is called Heart Failure (inability to pump enough blood). This causes an excess stimulation of the sympathetic nervous system (or more technically, neurohumoral mechanisms) in an attempt to compensate, which by its effects on heart contractility and rate increases the amount of pumped blood to match the need. This sympathetic outflow also causes increased sweating, nervousness, dry mouth etc. Sweating, nervousness are cardinal signs of acute MI.
Additional point: This compensation can only work in certain cases, say for example where the heart failure is due to blood loss with a healthy heart. But in cases like MI, this compensation is not an optimal response, rather it worsens the case, since increasing the workload on an ischaemic heart (ischaemic levels of atherosclerosis being the commonest cause of MI), further damages the wall leading to chronic heart failure and disease. This is the Broken Compensation Model for chronic heart failure. This is why we use Beta Blockers to abrogate the sympathetic system's (or more technically, the neurohumoral mechanisms') unwanted compensatory efforts, and the observed efficacy and increased longevity substantiates the validity of the model.
References:
I added them in a bit of a haste. They might not be the best references available, but they are considerably credible. Pathophysiology of heart failure, ventricular remodelling and the involved neurohumoral mechanisms are well-studied, and you shall get several papers on it on pubmed or google scholar.

Books

Robbins and Cotran: Pathological Basis of Disease 9th Edition
Hutchison's clinical methods 23rd edition

Papers and links -Heart Failure pathogenesis

Kemp CD, Conte JV. The pathophysiology of heart failure. Cardiovascular Pathology. 2012 Oct 31;21(5):365-71. (General overview of the pathogenetic mechanisms underlying)
CVphysiology.com(A relatively less technical review)
Kırali K, Özer T, Özgür MM. Pathophysiology in Heart Failure. InCardiomyopathies-Types and Treatments 2017. InTech.
http://bestpractice.bmj.com/best-practice/monograph/61/basics/pathophysiology.html

Papers and links -Sweating as a symptom of MI

National Heart Lung and Blood Institute
Bruyninckx R, Aertgeerts B, Bruyninckx P, Buntinx F. Signs and symptoms in diagnosing acute myocardial infarction and acute coronary syndrome: a diagnostic meta-analysis. Br J Gen Pract. 2008 Feb 1;58(547):e1-8.
Gokhroo RK, Ranwa BL, Kishor K, Priti K, Ananthraj A, Gupta S, Bisht D. Sweating: A Specific Predictor of ST‐Segment Elevation Myocardial Infarction Among the Symptoms of Acute Coronary Syndrome: Sweating In Myocardial Infarction (SWIMI) Study Group. Clinical cardiology. 2015 Dec 1.
https://www.sciencedaily.com/releases/2005/11/051122183817.htm
http://www.webmd.com/heart-disease/news/20051115/sweating-prompts-heart-attack-care#1

Interesting answer. My educated guess would have been that blood transfers heat and this heat transfer is regulated with the speed of blood flow. So if the heart is not strong enough, then the heat transfer is not sufficient and the body overheats which results in excess sweating.

@inf3rno Sweating in this case is not because of temperature regulation. It is more of a side effect. The sympathetic effects on heart in MI is very well studied. Look up remodelling of the cardiac muscles.

Can you add some references about this to your answer?

@inf3rno Added.


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String-db locally downloaded
I need a ppi network of cancer and it should have 200k to 300k proteins (nodes)
As the web inteface don't allow more than 2000 proteins to be visualized . I have downloaded the protein_links of homosapiens from the download section .
It has 11353058 link which means 11353058 interaction .
The downloaded file is a .txt How do we do  to extract cancer interaction from this huge set ?
What are the different ways to manipulate this file .

I dare say it's outside of my realm to do network analyses, but I also don't believe it's possible to just say cancer and pull out a network. This is especially so since melanoma will differ widely from renal-cell carcinoma, lung cancer and so forth. Perhaps this paper will help you (ref).

Actually I don't really care about the type of cancer ,as far as I'm concerned with the data , the amount of data  I need a network of 200k of whatever type of cancer or any other disease from that file that's all I'm asking for And thank you for the paper @CMosychuk

It is more of data necessity than it is of biological , proteomics need


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Comprehensive biology or anatomy wordbank
I teach A&P for bio non majors. I have a special needs student whose accommodation requires a word bank for any anatomy identification questions I have on the exam. I would like to present the student with a 'master wordbank' (presumably hundreds of words in length) that would act as a word bank for all the exams in the course. I'm surprised to be unable to find much of anything online. Has anyone seen something like this?

The index of your textbook?

I agree that your textbook's index or glossary is probably your best bet. Because anatomy can be taught at so many different levels (breadth and depth) and you're teaching at a fairly basic level, you'd have a hard time finding  a list elsewhere that emphasizes/includes what you want but doesn't weigh you down with terms your class does not cover

this textbook has no such thing unfortunately

I've been trying to find something similiar so far all I have found is an academic headword  list. https://www.victoria.ac.nz/lals/resources/academicwordlist/awl-headwords/Headwords-of-the-Academic-Word-List.pdf

So I found a good list. Behold: wikipedia:
https://en.wikipedia.org/wiki/Glossary_of_biology

If you are teaching A&P, then this list will definitely not have all possible terms. For example, there are no named muscles in this list (or at least the first 5 most obvious I searched for were not), which normally would be included in an A&P exam.

@kmm this is not A&P at harvard medical college. However, that's not good regarding the muscles. When i did some random testing I didn't cross check any of those.. do you remember a muscle you queried?

Look for "rectus", "biceps" and "femur". None is on that list.

@kmm To be fair they are not really headwords but specific terms for an individual object. If you want to include ALL of those you would be better off with the entire biological dictionary.

You may want to look at some biological terminologies or ontologies. These can be browsed online using portals like the OLS or Bioportal. You can restrict your search to particular domains or sources, such as the FMA for adult human anatomy and Uberon for general metazoan and comparative anatomy. This may be overkill for your purposes, as these ontologies are intended for computational applications rather than as an educational reference source. For example, terms are linked to other terms via different relationship types. However, this extra information may turn out to be useful, and the developers of these ontologies may be interested in helping with educational use cases (I am the developer of Uberon and this is something I am interested in).
If you wanted to extract a table of terms from one of these, perhaps restricted to a domain (e.g. human muscles) then this may be possible with a bit of work with some of the online interfaces, or it's something that could be done by someone with programmatic skills. Someone on bioinformatics.stackechange.com could help with that task. Many of these are available via open and unrestrictive licenses so there should be no legal issue here.


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Would methamphetamine heal wounds, infections, and diseases?
Alright, so this sounds crazy but based on these research findings it is safe to assume that meth would allow wounds and diseases to heal faster by interleukin 6 . On the otherhand, using meth during illness would cause higher neurotoxicity due to extreme hyperthermia and fever.
Correct me if I'm wrong:
Firstly, dopamine increases interleukin 6 (IL-6) release and inhibits tumor necrosis factor release.
Interleukin-6 is the source of fevers and hyperthermia. Most importantly, IL-6 heals skin wounds. It's main goal is to regulate the immune system by raising and lowering temperature depending on if a person is sick or not. Raising body temperature will prevent a person from being sick and will make wounds heal faster, but will induce neurotoxicity, lowering it will prevent neurotoxicity but make someone vulnerable to infection. According to Wikipedia, IL-6 stimulates the inflammatory and auto-immune processes in many diseases such as diabetes, atherosclerosis, depression, Alzheimer's Disease (interestingly though, Alzheimer disease is reliant on dopamine depletion, and people with Alzheimer had significantly higher levels of IL-6, which is surprising. One possibility is due to the fact that dopamine increases interleukin 6 release, and without dopamine, IL-6 cant be released, meaning more IL-6 will be metabolized but not used).
IL-6 is also the main, and perhaps only, cause of meth-induced neurotoxicity. It is responsible for neurotoxicity by means including, but not limited to, cell death, ROS generation, and neuronal damage. Lowering enviromental temprature significantly prevents neurotoxicity. To verify this claim, I Googled "methamphetamine neurotoxicity interleukin-6", and came to this article, furthering the evidence that meth vastly potentiates IL-6 and IL-6 induced hyperthermia is the result of meth-induced neurotoxocity, as mice with a mutation for IL-6 blocked meth-induced neurotoxicity, which also means that these mice won't be able to reheal faster.
To bring an update to this post, I have found this paper that shows that happiness potentiates the immune system. But this is a very minor influence as meth produces >1000 "units" of dopamine, relative to 300 units which cocaine produces. Meth would be much more efficient.
To bring further updates, it seems that my assumptions were correct. By googling "site:nih.gov methamphetamine neuroprotective", I was led to the following: https://www.ncbi.nlm.nih.gov/pubmed/24333768 and https://www.ncbi.nlm.nih.gov/pubmed/25724762
Surprisingly it is neuroprotective following stroke.
So, putting all this into account, is it possible that meth actually heals wounds and diseases (while at the same time inducing neurotoxicity)?
This assumption came to me because I have an aggressive cat and whenever I'm high on meth I noticed how wounds from a cat scratch would heal within a day or two instead of a week.

I suggest performing an empirical experiment: make some kind of repeatable, standardized wound, and measure how long it takes to "heal" (you will have to define an endpoint) on 3-5 occasions, then do the same while the analyte chemical is present in the biological system of interest (it makes it hard for even the most open-minded scientists to take an investigation seriously when it includes the words "high on meth"). Compare the ~5 control trials and ~5 experimental trials and perform statistics to determine if there is a "statistically significant" difference.

Impact of methamphetamine on infection and immunity Methamphetamine alters blood brain barrier protein expression in mice, facilitating central nervous system infection by neurotropic Cryptococcus neoformans. There may be short term benefits but long term use would lead to more overwhelming negative effects.


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Gland defined based on morphology or hormone secretion?
Is a gland defined by a visible morphology, or is anything that secretes a hormone a gland?
The answer does matter for the definition of histamine. Based on the answer I can conclude whether it's an hormone or not.

Glands can be classified as endocrines or exocrines, and only endocrine glands secrete hormones. Thus, not all glands secrete hormones. Regarding your second paragraph ("The answer does matter for the definition of histamine. Based on the answer I can conclude whether it's an hormone or not.") I have absolutely no idea at all of what you tried to say here.

Thank you for your notes. Maybe I didn't explain myself well, so it would be better to see the place that the question came from... (kindly, look at "Wnt" things) https://en.wikipedia.org/wiki/Wikipedia:Reference_desk/Science#Histamine_is_considered_as_hormone_or_not.3F

Now I understand your question. You could actually go directly to the point, asking this in the title: "Is histamine an hormone or not?".


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Virus that can enter all cell types
As I understand, each virus type can enter a particular cell type. For example HIV can enter CD4 & CD8 cells, while HBV can enter liver cells, some other viruses can enter other cell types like brain cells and cause brain diseases.

Is there any kind of virus that can enter all mammalian cell type so it can be used as a general gene transfer method?

I have improved the English and removed title second unrelated question.

I don't know if there is any "universal" virus that really gets into every cell type, but lentiviruses come pretty close. Lentiviral transfection vectors have been developed for a wide range of human (or mammalian) cell types, including immune cells and terminally differentiated cell types such as neurons and skeletal muscle.
But these are of course experimentally modified viruses that have been optimized in various ways for transfection; typically, the naturally occurring virus is much less efficient. I would guess it's unlikely that a natural virus can enter any (human) cell type, because this capability would be expensive for the virus to maintain, and there is probably little pressure to do so --- as long as the virus has a working route of transmission, via the airways for example, there is probably little benefit in being able to transfect other tissues.

Unlikely. There are 2 ways for viruses to enter cells - mimic something the cell normally uses and trick the cell into "eating" the virus, or grabbing onto a structure on the cell membrane and forcing its way in. Either way, it's largely dependent on the target cell
Different cell types can have vastly different surface structures and receptors. Viruses that already thrive on infecting a specific type of cell have no need to develop the ability to infect other types of cells.
A virus that could enter every type of cell would look like a completely unfolded Swiss Army knife, requiring latches and grapples for each type of cell. The latches and grapples could interfere with each other, the end result being a virus that's ineffective at infecting any cell. This would actually discourage viral mutation for such multi-infection (as an intermediate form with new cell adapters could decrease its fitness on its main cell targets)

Why couldn't it attach to something fairly universal like the Na+/K+ ATPase, and trigger a calcium influx (e.g. by perforating the cell with a single MAC or similar, something a eukaryotic cell should be able to handle) to induce endocytosis-based membrane repair? AFAIK, virtually all cells have that mechanism.


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What is the mechanism by which passive immunity works?
My idea is that passive immunity can be used to cure an individual who is infected with a certain disease. For example, for someone infected by clostridium tetani, you would inject them with an antiserum. The antibodies give protection against bacteria, until the active immune response takes action. In this link (http://pmt.physicsandmathstutor.com/download/Biology/A-level/Notes/Edexcel-IAL/Unit-4/6-Infection-Immunity-and-Forensics/Set-A/Vaccines.pdf), page 3, the graph shows that the level of antibodies in the blood actually rises after injection! To me, this naturally begs the question, what is the mechanism by which passive immunity operates (because I want to know why the level of antibodies rise in order to understand the situation dynamically)?
[Note: would I be correct in saying that a short answer would be that the level of antibodies rises because the active immune system is stimulated due to the enhancement of phagocytosis by macrophages when the antibodies attach to the antigens? My book states that release of antibodies (by B-cells) that bind to the antigen is required to allow the macrophages to engulf the pathogen with the specific surface antigen.]

You seem to be overlooking the obvious answer, which is also spelled out in the linked document: "Sometimes actual antibodies are injected into people to give instant, short term, passive immunity." If you inject antibodies then yes, the level of antibodies in the blood rises immediately because that is what you injected.

No, that's not what the graph shows. The graph shows that after an initial injection you continue getting a rise over the subsequent weeks. I did not overlook the obvious answer. The sentence that you stated answers the question 'why use passive immunity'?

Yes, apologies, I understand now what is concerning you - I've posted an answer.

I'm voting to close this question as off-topic because it is not a question in the terms of SE Biology. SE Biology is a question and answer site, not a discussion site. Furthermore your titles seem to be an attempt to disguise the fact that your are not asking a question. I have already explained this in detail in relation to another of your questions I have voted to close, so will not repeat chapter and verse here.

Mr. David, I am not disguising not asking a question in this case. I see where you were coming from in the other case though. Apologies.

I commented on this question, but the OP's response prompted me to think again. Here is the graph from the document that the OP linked to:

Clearly what is confusing is that the parameter referred to as 'antibody level' rises quickly, but not as a step. In terms of the x-axis, vaguely labelled as weeks, it looks as if the level of antibody continues to rise over several days at least. The OP attempts to read into this an effect whereby the injected antibodies somehow stimulate the immune response in the recipient.
My knowledge of immunology isn't extensive enough to rule that out completely, but I don't think that is what this sketch graph is illustrating since the levels of these antibodies is shown as falling to zero due to destruction and excretion. This indicates that what is being graphed is just the injected antibodies.
In the absence of some real data for the time-course, my explanation for the rising phase illustrated is that this is showing levels of antibodies in the blood. However the prophylactic use of injected antibodies will often involve an intramuscular injection near the site of an injury. Here for example is a quotation from a recent review on the use of recombinant immunoglobulins (RIG) against rabies:

Because vaccination needs time to induce a humoral response, application of RIG immediately after exposure is important to inhibit viral spread, even when accelerated vaccination schedules are applied. As much of the RIG dose as anatomically feasible should be injected into the area around the wound, and the remaining volume then given intramuscularly at a site distant from rabies vaccine inoculation. Isotope-labelled HRIG, injected around simulated bite wounds, diffused readily into surrounding tissue and about 25% was still detectable around the injection site 24 h later.

Thus the level of antibodies in the blood will continue to rise as they slowly enter the circulation from the site of injection.

As Alan Boyd says, the relatively slow rise is due to gradual uptake of the injected antibody.
If you deliver the antibodies by intravenous injection or another mode that allows rapid uptake (I use intraperitoneal injection in mice) then the antibody levels peak rapidly, less than a day and probably a couple hours, and then drop off; there is no continued rise as shown in the chart, which shows that there's no effect on production of new antibodies.
If you deliver the antibodies via intramuscular injection, which is probably the most common mode in humans, they'll enter the circulation much less rapidly. According to Uptake and elimination of hepatitis B immunoglobulins after intramuscular application in man, following intramuscular injection of antibodies, most people showed peak serum antibody concentrations between 3 and 7 days after injection, and they note

The passive immunization via the intramuscular route does not accomplish an instantaneously available, maximum anti-HBs titer. There seems to be a great range of variation in uptake and elimination of the immunoglobulins in man.

The antibody levels go up, because you're adding more antibodies. The increase in antibodies isn't from the patient, it's from the injection of antiserum.
The half life of IgG (the most common antibody) is around 20 days. IgM and IgA last for 5-8 days.  Reference. So as you can see, the antibody levels increase due to the injection of antibodies into the patient.
The comment by Alan Boyd gave the answer I was just typing out, but I'll still put it as an answer.

Please see my reply. I disagree. This does not address my question.

I've edited my response. The injected antibodies survive for long and the injection of antibodies causes the subsequent increase.


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Why does yawning trigger tears?
I'm just wondering when I yawned, there are tears coming out from my eyes, which makes me look like I'm crying.
So my question is how does yawning give out tears?

When you yawn, the muscles surrounding the glands which are responsible for bringing tears, i.e. the Lacrimal glands get squeezed leading to teary eyes. This is the location of Lacrimal gland (it's present at the top left corner in this image):
https://upload.wikimedia.org/wikipedia/commons/c/cf/Gray896.png

These glands actually work all the time as they've the responsibility to coat the surface of our eyes (that's the reason our eyes appear glistening). When they get squeezed, due to the tightening of facial muscles surrounding the eye, or maybe because your closing eyelids too tightly while yawning, they release a small amount of "tears" they would have otherwise used at a later moment.

Also, as a side note, there are more than one type of tears, this specific type of tears are called reflex tears. Quoting a Wikipedia article as a reference (https://en.wikipedia.org/wiki/Tears#Types):

$\ldots$ It can also occur with bright light and hot or peppery stimuli to the tongue and mouth. It is also linked with vomiting, coughing and yawning. These reflex tears attempt to wash out irritants that may have come into contact with the eye.

Question: it was just me that genuinely yawned by reading this question/answer, or did somebody else experience the same? I'm not implying this question/answer is boring or something like this: I yawned just by reading about yawning! We learn in ethology that yawning, as a form of communication, is contagious, but I never thought that it could be started by reading about it!

@GerardoFurtado I've come across that before concept before (New Scientist article a few years back I think. Did you also know Dogs catch human yawns?

Oh, yes, I used to do this to my dogs all the time. Actually, when I studied ethology in the 90s, I liked testing (non scientifically, of course, just for fun)  communicative yawning with different mammals every time I could... People that saw me yawning at those animals probably thought "that one has a screw loose".

I'm pretty sure I've passed on yawns to my Uromastyx before. Could have been a coincidence too though. Maybe I'll yawn at her today and see what happens.

@Carcigenicate Nice! However, there is some debate regarding if reptiles (including birds, which are reptiles) do perform a genuine yawn. Konrad Lorenz, for instance, a huge specialist in birds, used to say that his geese didn't truly yawn, but were simply stretching their facial muscles. Maybe the same happens with your Uromastyx, sorry for being a killjoy.


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Stimulating an axon causes impulses to travel both ways?

A diagram is presented as such above.
The question given states What would be the effect of stimulation to cause a nerve impulse with a microelectrode at the middle of the axon?
I thought the nerve impulse only travels in one direction to the muscle fibres, but the book says "A nerve impulse would pass in both directions."
Why is that the case?

Allow me to do a silly analogy: think about the electric wire going from your outlet to your computer, conducting electricity. If you make two cuts in this wire, rotate it 180 degrees and weld it again at the cutting points, what will happen? It will conduct electricity just as it did before.
The same happens to an axon (but please have in mind that this is just an analogy, an action potential is not an electric current). That is, the axon doesn't determine or influence the direction of the action potential. If you cut a piece of that axon, rotate it 180 degrees and join it back in the cutting points, it will conduct the action potential the same way.
That being said, imagine that you stimulate that axon at a given point. There will be two action potentials, going to opposite ways:

unmyelinated (A) and myelinated (B) nerve cells
In your figure (given that is a motor neuron), if you stimulate that axon in the middle, the action potential going to the neuromuscular junction, which is the normal direction, is called orthodromic (from the greek orthos, "proper", and edramon, past of "run"), while the one going to the soma (the perikaryon) is called antidromic (from the greek anti, "against").
According to Oh (2003):

The sensory nerve conduction study measures the conduction of the nerve impulse along the sensory nerves. The routine method measures the conduction velocity of the large diameter sensory nerve fibers of the nerve being tested. There are two methods of obtaining sensory nerve action potentials (SNAP), orthodromic and antidromic. The orthodromic method includes recording of the sensory nerve action potential proximally and stimulating the nerve distally whereas in the antidromic method the location of the stimulating and recording electrodes is reversed. The latency and conduction velocities are identical with the orthodromic and antidromic methods if the recording and stimulating electrode positions are constant. (emphasis mine)

In a simplified scenario, the orthodromic impulse will reach the neuromuscular junction and stimulate the muscle contraction, while the antidromic impulse will be canceled by another orthodromic impulse or, if it can reach the dendrites, it will simply end, since there will be no neurotransmitter release.
Source: Oh, Shin J., 2002. Clinical Electromyography: Nerve Conduction Studies. Third. LWW.

I think Gerardo has given a very nice answer, there is just one think I would like to add:
The only reason it usually DOESN'T travel antidromically is because it is initiated at the axon initial segment at the soma. Once the action potential starts travelling (orthodromically) down the axon, it is directly followed by a section of the AP that is in the absolute refractory state. Thus, the action potential cannot turn around mid-way or start spreading into both directions.
However, when you stimulate the middle of an axon, there is (initially) no part of the axon in a refractory state which would keep the action potential from travelling in one direction or another. Both sides of the axon are ready to propagate the action potential, which is why it travels in both directions.
From the Wikipedia page on Action Potentials (under Propagation > Refractory period)

The absolute refractory period is largely responsible for the unidirectional propagation of action potentials along axons. At any given moment, the patch of axon behind the actively spiking part is refractory, but the patch in front, not having been activated recently, is capable of being stimulated by the depolarization from the action potential.


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Why would there be a spike in coverage within a gene in RNA seq data?
I'm looking at RNA seq data in Geneious for Salmonella typhimurium and I occasionally see a spike in coverage for a sequence of RNA within a gene. Why is there a section of the gene that seems to be transcribed much more often than any other part of it? The name of the gene in question is ftsI which is an essential cell division protein that may link upstream cytoplasmic cell division proteins with downstream periplasmic cell division proteins.

Welcome to SE Biology. Your question seems potentially acceptatble, however it needs some modification before you are likely to get an answer. In the meantime it risks removal as "unclear what you mean". First, I had no idea what geneious was. You should capitalize proprietary software and state what it is. More important you should include an image of the peak you are seeing and indicate what organism it is. We cannot be expected to know what ftsl is, and CDS is not the name of a gene but an acronym for "coding sequence". Please edit it.

Without knowing how your libraries have been prepared and sequenced it is hard to tell if that is due to a technical or biological source.
However, there are a few bias sources in RNA-seq (which aren't an issue in DNA-seq)
One of them is that if you used a "random-hexamer" protocol, they're known to not be so random after all. See: Hansen KD, Brenner SE, Dudoit S. Biases in Illumina transcriptome sequencing caused by random hexamer priming. Nucleic Acids Res. 2010;38: e131.
You might also have a contamination from other species that would present a sequence identity for that part more specifically.

Some regions might be more present than others in the sequencing data because some exons might be more often included in the mature transcript (alternative splicing). Check whether the peaks matches with exons. Edit: This will likely not be the case since you are dealing with a bacteria: as far as I know, splicing is very uncommon in bacteria
Another likely explanation could be that there are biases during library preparation or sequencing.
In both scenarios, the biases would be post-transcriptional.
Yet another possibility would be that other transcription units are present within your gene of interest. This sometimes happen, especially when dealing with compact genomes.

Salmonella would not have exons/introns.

@emilliman5 Indeed, I hadn't taken into account the fact that the poster's question involved a bacteria.


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haplotype data for 1000 Genomes
I need to get haplotype data for HapMap or 1000 Genomes for CEU, MKK, TSI, CHB and JPT for ± 1 Mb at LCT gene. I'm quite new in the area. Actually I don't know the meaning of "± 1 Mb". From which sites and how do I get the data? Do I need a program?
As far as I understand, LCT gene is on Chromosome 2. That's why I used following code:
wget -r --reject="index.html*" http://ftp.1000genomes.ebi.ac.uk/vol1/ftp/release/20130502/ALL.chr2.phase3_shapeit2_mvncall_integrated_v5a.20130502.genotypes.vcf.gz
Now I have a vcf file.
I also obtained a vcf file from Data Slicer ( http://grch37.ensembl.org/Homo_sapiens/Tools/DataSlicer ). I chosed populations and wrote 2:135,787,840-135,837,200 for region lookup. What does this file contain? How can I see the file content? What else do I have to do to get haplotypes? I will try to cluster and visualize haplotypes accorgind to populations. If you can guide me, I am very happy.
Thanks!

To obtain population related vcf files I created the respective (CEU, MKK, ...) samples list first using the samples file you can also download the 1000 genome ftp site.
grep CEU integrated_call_samples_v3.20130502.ALL.panel | cut -f1 > CEU.samples.list
Then I installed vcf tools (https://vcftools.github.io/index.html) and used the vcf-subset command.
I got the commands from this faq page:
http://www.internationalgenome.org/faq/how-can-i-get-allele-frequency-my-variant/
I did not compute haplotypes from the files, but I read in another post, that you can do that with PLINK. Have you checked that?

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


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How does a polymerized TruSeq adapter affect sequencing reads?
I am trying to build a NGS library on enriched DNA (DNA length = 93 bp).  I am using PCR amplification with two overhanging primers, both containing Illumina adapter sequences (Universal Adapter & TruSeq Adapter w/ barcode).  My final library should be (~182 bp):
Universal Adapter (-), Enriched DNA (+), TruSeq Adapter(=)
------------------++++++++++++++++++++++==================
After PCR amplification and QC by gel, I am seeing fragments of larger size.  Analysis by Bioanalyzer indicates that I am might be getting some polymerization of the TruSeq adapter on the library.  This is most likely due to bad primer design, with the primer containing two recognition sequences (21-nt), one at the 3' end and one at the 5' end of the TruSeq adapter
My question is:
How would the NGS analysis be affected if a library is submitting for sequencing, containing a mixture of single and dbl TruSeq adaptors?
Single:
Universal Adapter (-), Enriched DNA (+), TruSeq Adapter(=)
------------------++++++++++++++++++++++==================
Double:
Universal Adapter (-), Enriched DNA (+), TruSeq Adapter 1(=),  TruSeq Adapter 2(=)
------------------++++++++++++++++++++++==================\==================
Would the sequencing info from the "double library" be lost or would those fragments be read, just fine?
Thanks,

Remember to upvote answers you find useful. :-)

In short, you stand to lose information from your library due to the length of the fragments you're sequencing.
When you set up your sequencing run, you'll set the parameter for the number of sequencing cycles, which will determine the length of the reads to be sequenced. The longer the fragments contained in your library, the less they'll be fully sequenced.
A good idea would be to sequence your suspected polymerized fragments to verify that primer polymerization is really occurring. Just send your sample for normal sequencing, as you would for plasmids and PCR fragments.
If your primers are polymerizing because of inefficient design, you should fix this before loading your library into the Illumina device. If the primer-dimer effect comprises a significant portion of your library, this will only get amplified during the run and can definitely lead to a significantly less complex library. Sequencing a low-complexity library is a really expensive mistake whose one guaranteed result is to enrage your advisor and make him/her loudly question your competence. Trust me.


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If bortezomib, a cancer drug, inhibits cell proteasomes, wouldn't resulting protein aggregate in normal cells further increase the risk of cancer?
Bortezomib is an anti-cancer drug that inhibits the proteasomes of cancer cells, allowing proteins that stop cell growth to fold and perform their function.
However, wouldn't bortezomib also affect the proteasomes of normal cells? If the proteasomes of normal cells are inhibited, the major factor in the regulation of unfolded and damaged proteins is gone. The resulting protein aggregate would lead to cell damage and diseases such as cancer, Alzheimer's and Parkinson's.
What is stopping bortezomib from affecting normal cells? Does it?

Proteasome inhibitors do affect normal cells to some extent, but the whole point of using them as cancer treatments is that (some) cancer cells are far more sensitive to proteasome inhibitors than are normal cells.  For example, multiple myeloma cells (the first clinical targets of Bortezomib) that overproduce immunoglobulins are dependent on proteasome degradation to eliminate them and are therefore sensitive to Bortezomib.  There are many other aspects of cancer cells that may make them more dependent on proteasome; see for instance
Proteasome inhibitors in cancer therapy: Treatment regimen and peripheral neuropathy as a side effect for some examples.
But of course there are effects on normal cells as well, such as the peripheral neuropathy mentioned in that review.


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Exocrine system + endocrine system =?
What is the title name for endocrine system + exocrine system?
In another language that I speak they are called "secretion system" but in English the term secretion system is different and it is about proteins in Gram-negative bacteria.

Since it would be a collection of all glands I would call it as Glandular System same as vascular system which includes blood vessels.

Thank you for your comment. Based on this article, it seems that glandular system is a synonym for endocrine system. Isn't it? https://fmidr.com/glandular-system/

I don't think so because, in one of the heading it has written Endocrine system in a bracket beside glandular system, which can be interpreted as endocrine is a subset of glandular system. Thats my view. Try google ngram

Ok, after some searching and activation of my logic, I accept it. You can write it here as an answer of course.

"Glandular system" is not a valid name for that combination. There is not a single book on medical physiology (Guyton, Ganong, etc..) using that term.

We can coin our own term too.

As long as in any publication or communication you define your meaning of "glandular system",, it seems like a pretty reasonable term to use for convenience. As far as a conventional term already established in the literature, I'm not aware of any.


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Can immune cells be recruited to an area of inflammation, and later go on to a second?
With regards to innate or adaptive immune cells... can naive/immature cells such as neutrophils, monocytes, macrophage/dendritic cells or adaptive T-cells be recruited to an area of inflammation, for instance an infection in the gastric mucosa, then leave that area and be recruited to another different area of inflammation? Or once recruited to a site are they unresponsive to other events?


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Why the smell of sweat greatly varies across the body?
Having only two types of sweat glands (eccrine, apocrine) I would expect the sweat odor "spectrum" to be very "narrow". However, the smell of sweat greatly varies between scalp, arms, armpits, groin and feet. Why is that?

I think the odor is caused by bacteria, which vary in diversity across the body.

@canadianer why bacteria are so different between armpits vs. groin; hands vs arms; arms vs scalp?

Sweat is actually odorless regardless of what type of sweat gland it comes from, of which there are two types - apocrine and eccrine.
As suggested by canadianer, the odor comes from the mixture of bacteria and the resulting sweat. With regards to why your bacterial flora is so diverse is likely due to the different micro-environments found around your body.
In your armpits and feet (arguably where the strongest odor subsides), you'll find more anaerobic bacteria - bacteria that prefers low oxygen environments and sometimes, higher temperature, humid environments. Because they don't use oxygen to metabolize, their by-products in making energy are often organic acids, commonly lactic acid. Some anaerobic bacterias even have by-products containing sulfur.
Meanwhile, in less warm and damp environments on your body (i.e. face, hands), aerobic bacteria dominate. Oxygen is abundant and the temperature is just right for those strains of bacteria. Their by-products are much less putrid
EDIT: In addition, apocrine sweat is also high in the nutrients, such as lipids and proteins that bacteria can feed on. Once they metabolize the stuff in apocrine sweat, they start releasing the aforementioned by-products.

From what I understand from your answer, (1) aerobic vs. anaerobic explains why armpits and feet have the strongest odor, and (2) the variety of odors comes from the variety of bacteria. Could you please expand or add a link about how diverse are the bacteria across different micro-environments?

@Sparkler Here's a link to a good paper that explains the 3 different micro-environments found on skin and the bacteria flora that resides: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805064/
As shown in the paper, there are 3 types of environments. Sebaceous (oily), dry and moist. Here's an excerpt from a book that gives some examples of bacteria found in skin flora: https://www.ncbi.nlm.nih.gov/books/NBK7617/#A512


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Variations in action potential threshold and temporal coding
I would like to ask a few questions about things I'm not sure I understand in a paper Action potential threshold of hippocampal pyramidal cells (...).
(1) At the start the paper considers the possibility of irregular firing patterns of action potentials may be an argument to hold that the information processed by the CA1 neurons is a temporal code. I think it is hard to see the relation of final results (see the abstract) with these initial considerations. Do the results support the temporal coding hypothesis of CA1 neurons? How?
(2) At the end of the first page it says the following: "significant variations in action potential threshold would have implications for the precise timing of action potentials since the probability of initiating an action potential could not be predicted by only fluctuations in the membrane potential".
Does this mean that they aim to explain the irregular patterns by means of the fluctuations in the threshold?
I also don't see how from "the probability of initiating an action potential could not be predicted by only fluctuations in the membrane potential" follows that "significant variations in action potential threshold would have implications for the precise timing of action potentials".

It's very hard to read what you have written here. Can you take some time to edit your post?

@BryanKrause My apologies. I tried to rephrase it, I hope it's slightly more clear.

Hi,
For what I read, the objective of the paper is in fact to study the neural code using methods that study the membrane threshold changes (as you said). They mention both rate and temporal code in the introduction and they do give more emphasis to the temporal coding because it explains better the irregularities of the neuronal transmission.
They did find some correlations between changes in the threshold, which influences the iniciation of the action potential, and the timing and rate of the firing or the firing pattern. That means that the firing pattern influences the iniciation of the action potential even if in an indirect way (which is by influencing the membrane threshold). Saying that the pattern of firing is important it means that the timing is also important, instead of only the rate the firing. Because this is the major difference between both neural codes theory, it does support more the temporal code.


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Does the brain process sound in "clips" or "frames"?
I've always been under the impression that our brains process images (relayed to it via the eyes) at a particular frequency or "framerate"; this is supported by lots of sources, such as this one.
I'm wondering how close this compares to the way our brains process sounds:

Do we sample "snippets"/clips of sound? If so, is there any evidence as to how long (duration-wise) these "clips" are? Do we "sample" at the millisecond level? Microsecond?; or...
Do we actually sample "sound frames" (much like we do with visual images)? If so, how does our brain process a "frame" that contains multiple noises occurring at the same time (say a dog is barking at the same time the television is on)? After all, a frame is all the input for an instantaneous point in time, versus a clip, which is all the input over a period of time.

Any ideas?

It would seem that this 2014 publication adequately addresses your curiosity.
The abstract..

Does our perceptual awareness consist of a continuous stream, or a discrete sequence of perceptual cycles, possibly associated with the rhythmic structure of brain activity? This has been a long-standing question in neuroscience. We review recent psychophysical and electrophysiological studies indicating that part of our visual awareness proceeds in approximately 7–13 Hz cycles rather than continuously.

This confirms your statement regarding discrete visual processing. Continuing..
..

On the other hand, experimental attempts at applying similar tools to demonstrate the discreteness of auditory awareness have been largely unsuccessful. We argue and demonstrate experimentally that visual and auditory perception are not equally affected by temporal subsampling of their respective input streams: video sequences remain intelligible at sampling rates of two to three frames per second, whereas audio inputs lose their fine temporal structure, and thus all significance, below 20–30 samples per second.

This is saying that, (1) experimental methods for quantifying auditory  processing might not be so analogous to that of visual processing, and, (2) the minimum threshold sampling rate for auditory processing is much higher than auditory sampling rates. This second statement, however, is still no indication that audition processing is continuous (as will be stated next).
..

This does not mean, however, that our auditory perception must proceed continuously. Instead, we propose that audition could still involve perceptual cycles, but the periodic sampling should happen only after the stage of auditory feature extraction. In addition, although visual perceptual cycles can follow one another at a spontaneous pace largely independent of the visual input, auditory cycles may need to sample the input stream more flexibly, by adapting to the temporal structure of the auditory inputs.

And their conclusions..

Audition does not sample at a hierarchically early level in either an ongoing way (§3b and §4a) or an entrained (flexible) way (§3c and §4a). If it does sample, then it must be at a higher level, that is, a cortical level (§4b). Many reports of attentional control of phase entrainment [74,75,115] suggest that the sampling may also be attentional, as in the visual system. Can this high-level sampling be an ongoing process as in vision, or must it be entrained by the temporal structure of auditory inputs? The lack of ongoing EEG phase influence in audition (§3b) as well as the finding that phase entrainment strongly facilitates intelligibility [65,78,86] compels us to favour the latter alternative, just like other authors have recently argued [73,76,89].

..

To sum up, if perceptual cycles exist in audition, then they must be a relatively high-level or attentional phenomenon (as in vision), and they must proceed by stimulus entrainment (contrary to vision). Based on numerous studies of rhythmic entrainment and speech processing, we believe that the cycles are most likely to be observed in the theta-frequency range (though gamma-frequency sampling cannot be categorically ruled out). But the big ‘if’ lingers. Definite evidence for auditory perceptual cycles is still lacking.

So, it would seem that the verdict is still out as to whether or not auditory processing behaves similarly to visual processing, however, current consensus is that auditory processing is more continuous, and not as discrete, and, if perceptual cycles do occur for auditory processing, they occur at very specific frequency ranges, and not during conventional hearing.

Your summary of that paper omits all of the contradictory evidence they refer to and cherrypicks a bit... It's a big jump from "oscillatory activity might explain one perceptual illusion" to "all visual processing has a frame rate."

My summary omits pretty much the entire paper.. I'm not going to refactor the entire article when the OP can just read it. I gave the abstract and conclusion. The rest it too detailed and cumbersome to try and re-express as an answer (and is something that you personally have previously criticized me about). Hence, I provide their initial declaration (abstract) and end conclusion (results). As for "all of the contradictory evidence" that you refer to, can you be specific?

The article is making an argument that we should consider visual processing as discrete at the level of perception; that's fine. I feel like your post makes it sound like visual processing has been established to be discrete throughout, which is neither true nor what the authors of that paper are saying.

@BryanKrause I see your concern. So you're saying that I should explicitly address the hierarchical structure of sensory processing, and not just broad stroke describe it, as I may have led on to do by bolding that one statement in the abstract? If this is in fact the case, I'll make the appropriate edit. Thanks.

Please forgive my bluntness, but there is too much copy-paste here. "Copy-pasta" should not be the bulk of your answer. It should only be used to support your answer.

@anongoodnurse I agree, and will make the appropriate edits. Thank you. Just curious though, and forgive my bluntness too, but do you typically automatically downvote before giving the person a chance to edit their post? JW...

@Charles - Sometimes, if my objection to the answer is strong enough. If so, then when the edit is done (if it is), I can remove/reverse the DV. If I just think an answer is terrible, I'll DV without a comment. If I think it's wrong, I'll comment. I usually don't comment with a DV because people automatically assume I'm the down voter (as you did. Most often, I am not the DV. So if I comment, and you have a DV, it most likely didn't come from me for that very reason.)

@anongoodnurse Yeah, I only thought it was you due to the close time frame between the two actions. Sometimes is it good to know though that a DV came from someone who's a heavy user, because there's much more credibility to the DV, which would incline me more to consider an edit. Thanks again.

Y'all spend way too much time thinking about voting etiquette, go for a jog or something, get outside and away from the computer!

In your question, you ask about processing and sampling. I'd like to make a distinction between sampling, which in my view does not have a framerate, and perception which there is some evidence that there is sort of a framerate (though not as concrete as the framerate of a video display, for example). Processing is everything in between, and as such, whether it shows "framerate-like" behavior depends on the stage of processing.
Does vision really have a framerate?
The "framerate" depicted in those sources for vision is sort of a special case, talking about perception of a particular stimulus. There are no real "frames" in your vision, only temporal averaging (because phototransduction is quite slow on the timescale of neural processing in general). The article you link makes a mistake in logic in concluding that humans have a frame rate: the research they cite is about discriminating between separate flashes, which is an issue of temporal averaging rather than framerate. There is a separate issue, which is whether perception correlates with particular oscillatory frequencies; I'll get to this later in my answer.
If you flash a very bright 1 ms light, and record it with a video camera, you will often miss the light entirely (or it may appear only in part of the image, depending on the scanning pattern of the camera). With vision, though, you will always see the light, and for very brief flashes you will perceive changes in duration as changes in intensity.
The other contributor is the "magic" of perception: effectively, what you perceive is not directly the signals that come in through your eyes but rather the model your brain makes for the world based on that information. This process is the origin of all perceptual illusions; the appearance of "backward" images like with a spinning wheel is one example.
Our current model for how processing of sensory stimuli works in the brain is that there is a functional hierarchy with significant abstraction at higher levels of the hierarchy. As you get to higher order levels of processing, you will cease to see the "pixel information" and simple edge/feature detection, and begin to see more abstract representations like detection of particular visual objects or encoding of object velocity.
Okay but the question is about auditory stuff..
It's easiest to start with vision simply because, for better or worse, it is best studied historically. For auditory processing, there are a lot of similarities with vision even though the input stimuli start very different. At low levels of processing, auditory neurons are well described by spectro-temporal receptive fields. At higher levels of processing, you will instead see representations of whole features in sounds, such as phonemes.
Object segmentation is a very difficult problem in both vision and hearing (and a difficult task for computer/AI-based versions of those senses, as well). This is definitely an active field of research, but there is good evidence that some segmentation is present throughout the cortical hierarchy (for example, see here). There are no concrete answers for 'how' exactly segmentation works, just that it does, some evidence for where it might be happening, and some understanding of factors that make it harder to segment different sources. Sound localization is certainly one of the key factors, though segmentation can occur even when there are no localization cues. For example, if you have multiple speakers on the radio, or multiple musical instruments playing, there are some shared spectral characteristics of the speakers or instruments
Discrete signals in cortex
All that said, this does not mean that the brain is free from any discrete elements of processing (like "frames"), although it probably doesn't make sense to think of a frame rate but rather a type of "threading". There is recent strong evidence that activity in the neocortex can be organized into packets of activity that contain sensory or other information. So even though the auditory stream is sampled continuously, that continuous sample is most likely distilled into discrete auditory objects that reflect both the content and source of those stimuli.

Question about visual higher order. Do we have schemata for visuals? That's what I think of when you say "...more abstract representations like detection of particular visual objects or encoding of object velocity." but I'm not sure.

I would really love an explanation for the downvote...though I know how unlikely those requests are to actually produce an explanation.

@anongoodnurse, schemata looks like a psych term, haven't seen it used in (my area of) neuroscience. I'm not quite comfortable saying "yes" without understanding clearly what baggage that term might convey, but I'll say "probably" :). By abstract representations I mean to be a bit non-specific, I'm basically including anything that is not a pixel/edge representation. It could be a code for "dog" versus "cat" or simpler features like "triangular" versus "square" - those are things that all seem discrete in vision, the Necker cube being a great example.

A schema in learning theory is a concept (of information) we know in a matrix of such concepts (say it's a room among many millions of rooms). If the room has a label (e.g. "organelles"), we expend far less energy on learning new things about organelle-related subjects. If the room "organelle" is missing, we need to devote a lot of working memory in order to remember a new fact. Does that make sense? So, if I have a schema for "cat", it's easy to place new incoming info immediately where it belongs, cutting down on processing (or the use of working memory.)

DV not mine, but I had to read your answer twice. Maybe someone doesn't understand it and therefore thinks it's not useful?? Just a guess. I certainly disagree.

Yeah, I think I understand, I'm glad I didn't jump to say yes to schemas then, just because of all the additional implications. I would say that hierarchical representations are definitely a way to reduce complexity, and they are certainly related to schemas as you describe them. Where I want to distance them, though, is that having a representation of "cat" doesn't necessarily make all things easy to classify, it depends on the task: sometimes you have to group things, sometimes differentiate them.

For what it's worth, I've received a relatively high number of unexplained downvotes over the past week that didn't seem particularly warranted, so maybe there's someone with an axe to grind.


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Why does the ring finger not move independently?
Why is it that we need to move little finger in order to move ring finger with it? For example, put your palm on a table and fold your middle finger inside. You won't be able to move your ring finger unless you move your little finger along with it. Why? Paul Gilbert and Buckethead and various other guitarists are the only people that I'm aware of that use the ring finger and looks independent. Is it possible to have surgery to make the fingers independent or is it not functional to do that?

I'm not sure what you mean. Do you think piano players can't use their fourth and fifth fingers independently? Surgeons? (A surgical knot is performed primarily by the third and fourth fingers.) Other occupations requiring manual dexterity?

I'm no expert on the topic, so I'm not going to officially answer your question. But from what I know, all your finger extensions are controlled by a single extensor muscle - the extensor digitorum. However, only your index and pinky have an extra extensor muscle, making extension easier for those fingers. For flexing movements, you have 1 flexor muscle that controls a couple fingers and another flexor that controls the rest - the lack of flexors makes it harder to control. Getting surgery to alter your fingers' movement would probably be unnecessarily risky and probably not possible

It mainly because of Paul Gilbert who is the only person along with many others who uses his first, ring and pinky very well.

I have no problem moving my ring finger without moving my pinky...

indeed, here is another pic of the ulnar nerve. https://www.healthlinkbc.ca/sites/default/libraries/healthwise/media/medical/hw/h9991344_001.jpg

The reason for this phenomenon is in both the muscular structure and neural connections of the little and the ring finger. Lets start with the following diagram:

As you see (click on the image to see full version), the fingers contain extensor muscles for movement. However, the index finger and the little finger have separate extensors, because of which they can move more independently as compared to the middle finger and ring finger, which contain a common extensor muscle called extensor digitorum. Some people lack the interconnections between these extensors, and can thus move their ring finger quite easily. One can also achieve this through practice.
Now, as to why the ring finger moves easily when moved along with another finger, have a look at another image:

The fingers are connected to brain via two nerves:

radial nerve, which connects with thumb, index finger and one side of middle finger
ulnar nerve, which connects with little, ring and the other side of middle finger

As you see, the branching between these nerves is what causes dependence of the fingers on each other for movement. Since the nerves for ring finger and little finger are intertwined, it becomes difficult to move each of these fingers separately. Similarly, you may find it easier to move your ring finger along with your middle finger. But you can easily move your middle finger independently because it gets signals from radial as well as ulnar nerves.
Thus, it is the combined effect of muscular and neural anatomy of ring finger which causes this effect.
PS: Since the effect is due to the neural and muscular anatomy of the ring finger, I don't think surgery would help in this case.
References:

Wikipedia contributors. "Extrinsic extensor muscles of the hand." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 29 Jan. 2017. Web. 27 May. 2017.
Ross and Lamperti, 2006, p. 300
Flexor Tendon Anatomy - Medscape
Wikipedia contributors. "Median nerve." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 1 May. 2017. Web. 27 May. 2017


text:
Do animals with crypsis know where they should stay to save their lives?
For example, would a green lizard know it need to stay on a leaf, and avoid creeping on ground? Or in general, would animals with crypsis know what color they are and then hide on suitable place? Or they don't planned to do it and just be unlucky if they leave their suitable place and be seen by predators?

Is there any reason you are particularly interested in consciousness in animals that hide and not consciousness in general? Do you expect an answer that is any different from an answer to the question "Are animals conscious?" (Relevant: Wikipedia > Animal Consciousness)

@Remi.B I think this is not only about consciousness but also about awareness and perception.

I am not sure there is any commonly accepted difference between consciousness and awarness. At least I don't get the difference. It seems important that the OP make sure to define the relevant terms and explain why the question "Are animals conscious?"  would differ from the current one.

I think you can break this down into two sub-questions:

Will natural selection select animals whose crypsis and behavior align with each other? The answer here is definitely yes, but with a few caveats:

Crypsis might not be the best strategy in a particular situation: a green lizard crawling on a leaf might be outcompeted with a red-and-blue lizard that is poisonous, for instance.
Either behavior or crypsis might be easier to change over evolutionary time: you might see your green lizard evolving to spend more time in leaves (particularly if it's herbivorous or eats plant-dwelling insects), or you might see it evolving brown pigmentation to hide on the ground.
Natural selection isn't going to be concerned with individual actions but overall behavior. So a lizard might fall off a bush, get spotted on the ground and eaten. But it might dash from bush to bush without getting caught. But if a lizard spends most of its time on leaves, there might be selection towards it being well-camouflaged on leaves.

Does this require a conscious decision on the animal's part? I think the answer here is no, consciousness isn't necessary. Very simple animals show responses to their environment, such as bacteria swimming towards food. Your green lizard might be staying close to leaves that it feeds on, or near the insects it feeds on that itself feed on the leaves, and so stay near the green leaves that camouflage it by accident. Or its brain might be programmed to carry out a complex action to hide it better. Perhaps the most sophisticated examples of this is animals that reconfigure their body to match their surroundings, such as octopuses, cuttlefish (but not, interestingly enough, chameleons!)
This doesn't mean that the animals don't have consciousness or are not deliberately hiding by finding surroundings that match themselves. It just means that that's not necessary to explain why we find green lizards hanging out on leaves.


text:
What kind of tree is this (Seattle, WA)?
This tree is a volunteer and I am hoping to find out what kind of tree it is.
Young tree

Leaf sample

Below is a more recent photo showing flowering.

Could you provide more information? Are there veins on the leaves? If so, how do they run? How big are the leaves (perspective with the camera is hard to tell how big the tree is in general)? Are there flowers? Anything budding? The more information, the better someone can identify the tree for you

The kind of leaf is typical of Fabaceae (https://en.wikipedia.org/wiki/Fabaceae).

It looks like a Laburnum. Probably a Common Laburnum Laburnum anagyroides, also known as a Golden Chain Tree. It is from central and southern Europe.
The seeds are poisonous.
https://en.wikipedia.org/wiki/Laburnum_anagyroides
Here is a photo of the leaves

From http://www.saps.org.uk/trees/laburnum.htm
And the flower

http://wildflowerfinder.org.uk/Flowers/L/Laburnum/Laburnum.htm


text:
Spider identification Delaware
It looks like a wolf spider, but I've not seen these exact markings.

It could help if you gave indications of the size and environment.

That's a nice female Dolomedes tenebrosus - the upland Fishing Spider that lives in similar habitat to Wolf Spiders, and eats the same sort of foods.
The way it holds its long, stripey legs together (the front pair, anyway) is pretty standard for the Pisauridae, and the pattern on the body (while a bit variable in this species) is pretty distinctive.
https://bugguide.net/node/view/2011

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


text:
Is narrow sense heritability heritable?
I was wondering if narrow sense heritability $(h^2 = \frac{V_A}{V_p})$ was heritable itself. $(h^{2'} = \frac{V_A}{V_{h^2}})$

Would you explain what gave you this idea?

I would recommend looking into phenotypic robustness, which is to some degree heritable: https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1003041

Yes, it is, but you'd have to define heritability as heritability for a certain phenotype.

Heritability of heritability
Heritability is a property of a population (see here for more info), not of an individual. One can only calculate heritability for a trait if this trait can take a value for every given individual because you need variance among those individuals (as it is made clear from your equations). In other words, the trait you want to calculate the heritability from has to vary from individual to individual.
As we are looking for the heritability of heritability, then heritability would need to be defined at the individual level in order to calculate its heritability. But heritability is not defined at the individual level.
It makes no sense to talk about the heritability of heritability. Just like it makes no sense to talk about the heritability of the fitness variance or heritability of the species geographic range.
Phylogenetic signal for heritability
You might be interested of whether related lineages tend to share similar heritability (for a specific chosen trait). I do not know of any study on the subject, but it seems likely that related species are more likely to experience similar population size and structure and similar selective pressure on a given trait than more distantly related lineages. Per consequence, I would expect that heritability shows a phylogenetic signal. It would be wrong to say that heritability is heritable though.


text:
Do all parts of a plant contain the same type of cell?
I have only learned about the plant cell which is shown below. But plant stems alone are made up of different parts like xylem, phloem, parenchymatous cells, sclerenchymatous cells etc.
Are all the parts of a plant made up of cells like the one in this diagram or is the cell diagram changed for different parts of a plant?

The diagram shows an exemplary plant cell . Except for the raphide/druse crystals, which I do not know, all of these components are definitely present in every plant cell. Do note that this diagram is only an example and while it describes the basic components present in the cells, details can vary, since plants can have highly specialised vacuoles or plastids (like chloroplasts) in special cell types.
As @AlanBoyd pointed out, there are some specialised cases like the Sieve Tube cells, that do not have a nucleus. But in your average cell, you should find all of the components described in the diagram.
The differences between cell types are typically caused by the expression of different genes, that change the behaviour of each cell, and not directly by a change of how the cell is build up.

Do root hair cells contain chloroplasts?

Sieve tube elements (phloem) are anucleate https://en.wikipedia.org/wiki/Sieve_tube_element?wprov=sfsi1

@AlanBoyd True, must cells in the roots will not have Chloroplasts. They will, however, have Leukoplasts instead, which are very similar and so the diagram as 'base plant cell' still holds.
The Sieve tube's I didn't know about before (see edit)


text:
Where does the pain from headaches come from
I may be wrong but I have always thought that the brain doesnt have any nerve endings, so why is it we get headaches and where does this pain come from?
I have heard lack of sleep, hydration or stress can causes headaches but I am interested in why and where the pain comes from this.

I knew it would be somewhere, I just couldnt find it .. Thanks


text:
What is neuronal computation?
Can someone give me a good explanation of what is neuronal computation and some examples of its use in neuroscience investigation?

Hi Welcome to Bio.SE! What research have you done on your own? we ask that all question askers provide evidence that they've tried to answer their own question. Piccinini & Bahar (2013) seems like an ok start to get you some citations to explore...

The term neural computation is basically synonymous with computational neuroscience.  It is the science of studying how the brain processes information by creating realistic mathematical models. Unlike general study of artificial neural networks (ANNs), neural computation heavily relies on biological accurateness. However, it may use models from ANN research, and vice versa.
Also see this course description of the PhD level course "Neural Computation" at Carnegie Mellon University  (CMU) :

Neural Computation is an area of interdisciplinary study that seeks to
  understand how the brain computes to achieve natural intelligence. It
  seeks to understand the computational principles and mechanisms of
  intelligent behaviors and mental abilities -- such as perception,
  language, motor control, and learning -- by building artificial
  systems and computational models with the same capabilities. This
  course explores how neurons encode and process information, adapt and
  learn, communicate and compute at the individual level as well as at
  the levels of networks and systems. It will cover basic concepts in
  computational and neuronal modeling, information theory and coding,
  neural networks and learning, neural data analysis and decoding,
  signal processing and system analysis, statistical learning and
  probabilistic inference.

(Emphasis mine)


text:
Get Network Out of proteins of interest
I have generated a list of Proteins using oncogeenes and suppressor genes of cancer.
I have 5827 mapping identifier for 3916 interactions using STRINGdb R package  .
How do I build a network of 200k protein?
Identifiers.csv

"","mapping_identifier"
"1","9606.ENSP00000003084"
"2","9606.ENSP00000003100"
"3","9606.ENSP00000004921"
"4","9606.ENSP00000004982"
"5","9606.ENSP00000005178"

and these are the interactions
"","from","to","neighborhood","neighborhood_transferred","fusion","cooccurence","homology","coexpression","coexpression_transferred","experiments","experiments_transferred","database","database_transferred","textmining","textmining_transferred","combined_score"
"1","9606.ENSP00000163416","9606.ENSP00000240851",0,0,0,0,0,0,0,0,0,0,0,481,0,481
"2","9606.ENSP00000163416","9606.ENSP00000263967",0,0,0,0,0,0,0,0,0,0,0,195,0,195
"3","9606.ENSP00000163416","9606.ENSP00000270202",0,0,0,0,0,0,0,0,0,0,0,163,0,163

Have you tried biostars.org? I think they are far more suited to computational questions.

Or you could try https://bioinformatics.stackexchange.com/

What form is your data in, it would be helpful if you could post the first 10 lines of data.

@emilliman5     I edited the question  and I'll try bioinformatics.stackexchange


text:
Get protein annotation from Uniprot out of protein mappings
Having a file of for about 10k mapping identifiers how can I get the annotations of the proteins from Uniprot  ? As it is not possible to do It manually
My mappings are contained in a .csv file
They are from STRING database Example 9606.ENSP00000387699

Can you please expand on this. What format are your ID's in (csv, excel, etc.)? And what is a mapping identifier, a uniprot accession, some other id? Lastly, Uniprot has a batch download system here, which may suit your needs.

@emilliman5 I edited the question , they are contained in csv file , and they are  stringdb external identifier

This problem is discussed here. Apparently STRING IDs are in KEGG format but these can be mapped on to Uniprot IDs using information downloadable from here. I guess that it is either the protein.aliases data or the mapping_files data that you would need. The first link provides a Python script to extract useful info from the downloaded data. These are big downloads so I haven't actually tried this out myself.
Presumably once you have the STRING→Uniprot conversion done you can query Uniprot with the output as a batch request.
Good luck!

@AM please comment again when you know if it worked out. Or even write your own answer.

UniProt's batch download system, suggested by Alan Boyd above, also allows you to directly map identifiers, e.g. STRING to UniProtKB, or Ensembl to UniProtKB:
http://www.uniprot.org/uploadlists
Once you have your UniProtKB results, you can add or remove columns by clicking on "Columns", and once you are happy, you can download the results in tab-separated format (http://www.uniprot.org/help/customize).


text:
How much current is required to stimulate a neuron?
Extracellular stimulation of neural tissue is done using electrode. Amount of current determines neurons how far from the electrode will be excited. How much current is required to stimulate the neuron in immediate vicinity? Such information is not available on internet.

"Such information is not available on internet." - wrong, but okay, I understand it's hard to find. The problem with your question is it is ill-defined: what do you mean by immediate vicinity? That term is meaningless. It also doesn't say anything about the rest of the setup: how far apart are the electrodes, how big are they, what part of the neuron is nearby? If you really want to know the minimum current to make a neuron spike, all you need is the input resistance, resting potential, and threshold, but that's for current delivered directly across the membrane.

immediate vicinity means neurons in contact with the electrode. single electrode. how big? why? say 100 micron dia. axon is  in contact.

"If you really want to know the minimum current to make a neuron spike, all you need is the input resistance, resting potential, and threshold, but that's for current delivered directly across the membrane. " interesting.please tell me the calculation. rest potential -70mV, threshold -55mV and what is input resistance-  resistance of electrode wire? let us say it is 100 Ohms or R if you would like.

Because not all of the current will actually go through the membrane of the cell, especially if the ground is far away or not in the same direction. Input resistance is the input resistance of the cell. If you just want a ballpark estimate for some engineering project, typical extracellular stimulation intensities are in the microamp range, but the current you have to deliver across a membrane to make a cell spike is in the picoamp range, depending on cell type and other conditions.

To calculate for one cell, knowing the input resistance of the cell (not your wire), all you need is Ohm's law, knowing you want to change the voltage by, in your case, 15mV.

"the current you have to deliver across a membrane to make a cell spike is in the picoamp range" does this require electrode inside the neuron like the glass pipettte electrode.

"To calculate for one cell, knowing the input resistance of the cell (not your wire), all you need is Ohm's law, knowing you want to change the voltage by, in your case, 15mV. " For this, are two electrodes required,one inside cell and one outside? in that case why resistance  has to be known? just both electrodes should be at 15mV difference.

You always have two electrodes - in your case, your ground someplace is one of them. And yeah, I'm talking about inside the neuron with an electrode of some sort. For outside, you have to consider everything else, which is basically all the other places your current could flow. Imagine a massively parallel circuit where only one of the paths actually goes across the membrane you are interested in.


text:
What is the literal meaning of the scientific name for the cactus wren?
What does the scientific name Campylorhynchus brunneicapillum mean? I simply want to find a way to decipher the meaning of scientific names. In the past I had to translate the names syllable by syllable using an abbreviated Latin dictionary to get a rough idea of the meaning. I can not find an on-line Latin translator that works - and not all scientific names are Latin.

According to the Helm Dictionary of Scientific Bird Names:

Kampylos, καμπúλος (Greek): curved, bent;
Rhynchos, ῥύγχος (Greek): bill.

Also, for the specific epithet:

Brunneus (late Latin): brown;
Capillus (Latin): hair.

Page with the Genus name: https://books.google.com.au/books?id=-RfSBAAAQBAJ&lpg=PP1&pg=PA87#v=onepage&q&f=false
Page with the specific epithet: https://books.google.com.au/books?id=-RfSBAAAQBAJ&lpg=PP1&pg=PA78#v=onepage&q&f=false

PS: I already knew this by heart because I studied Ancient Greek (and Latin is quite obvious to me because I speak a Romanic language), but I linked that "birds names dictionary" so you can have another source to search. Also, have in mind that it's complicated to use a regular Latin or Greek dictionary as you use an English one because you have to know the declension and the nominative form of the word. For instance, androgen: if you look for andros in a Greek dictionary you're not gonna find it, because that's the genitive. You have to look for aner, which is the nominative.