text:
Why do we need to put phosphate fertilizers along with rhizobium?
Isn't phosphorous a macro nutrient? So it should be present in the soil in sufficient quantities... but still we add phosphate. Why?

But beware of what Sir Albert Howard called the "NPK mentality": it may help you now, but be a disaster on the long run.

Phosphorus (P) is a macronutrient and, after nitrogen (N), typically the limiting factor for plant growth. Potassium (K) is also often added in fertilizers.
P is an important plant macronutrient, making up about 0.2% of a plant's dry weight. It is a component of important compounds, including nucleic acids, phospholipids and ATP. Consequently, plants cannot grow without a supply of this nutrient. P is also involved in controlling key enzyme reactions and in the regulation of metabolic pathways (Schachtman et al., 1998).
Certain plant species actively increase root densities around phosphorus-rich patches (Snapp, 1995), because it is critical to optimize it's uptake.
References
- Schachtman et al., Plant Physiol (1998); 116(2): 447-45).
- Snapp, Plant and Soil (1995); 177(2); 211-21

Christiaan, either you mean Potassium, which is K or you mean for Potassium to be Phosphorus....

I've watched every Periodic Videos....

@Christiaan: yes it has :). one more question... is it difficult for plants to absorb phosphorous from the soil in general?

@AlexPrior - I am unsure, but I think it depends on the composition. CaPO4 for example is not soluble and plants will have a hard time extracting it. K2PO4 on the other hand dissolves well. Maybe worth a new question?

@Christiaan: Yes. If K2PO4 dissolves well wouldn't it go deep down by leaching and make its absorption difficult by the roots?

yep absolutely. some salts bind to soil particles and hence stay available, others wash away quickly.

Phosphorus is indeed a macronutrient!!! If you're wondering why it is insufficient in natural soils then read on. Phosphorus is, in fact, the most limited of the three primary macronutrients in most natural soils (being nitrogen, phosphorus and potassium). This is because it is released very slowly from insoluble phosphates (on rock surfaces) and rapidly becomes “fixed” after being released, making it difficult for plants to obtain their phosphate ions (intake form of phosphorus). Few unfertilized soils release phosphates fast enough to support the high growth rates of many plant species. Also, plants tend to only obtain their phosphate ions from the little “polyprotic phosphoric acid” in the soil, they are often very deficient in phosphorus and for this reason phosphate ions are used in high quantities than nitrogen and potassium in NPK fertilisers (N:P:K = 1:2:1).
P is found in natural compounds in soil (however this is very limited); it is more often found in NPK fertilisers in the forms of: Orthophosphates ( H2PO4- or HPO42- ) and Polyprotic phosphoric acid ( H3PO4 ).
The following reasons are why phosphorus is a primary macromolecule and why it is VERY essential to plant nutrition;

To build ATP (the energy currency of plants) from respiration ;
To build DNA and RNA (genetic information) ;
To build the cell membrane ;
To aid the growth of a plant in its early stages (seedlings and root development) ;
To perform phosphorylation ( the modification of the activity of various enzymes – this is responsible for cell signalling (which is the ability of cells to perceive and correctly respond to their microenvironments – aka tissue homoeostasis))

I'll try to give a wide answer, not only to why we have to add chemical fertilizers, but also to why this is not our best choice.
One thing is the isolated chemical compounds we add to the soil (like N, P and K), other is its natural fertility (which include a good part of the periodic table, and also many micro- and meso-organisms, what improves productivity and quality of products).
Sir Albert Howard, in his "An Agricultural Testament", reminded us about the danger of the specialization in the isolated chemicals, and warned us of the futile reasons why they came to be so widespread and dominant:

"The artificial fertilizers are being widely used. The characteristic
  of Western agriculture is the use of artificial fertilizers. The
  industries engaged in fixing atmospheric nitrogen for the production
  of explosives during World War I, had to find other markets; the use
  of nitrogen fertilizers in agriculture increased, and today most
  Western farmers based their fertilization programs in the cheapest
  forms of nitrogen (N), phosphorus (P) and potassium (K) available.
  What we might call the NPK mentality dominates the farms as well as
  research stations of agricultural research. Industrial vested
  interests in times of national emergency settled firmly and could no
  longer be dislodged."

(Sorry, it's been re-translated from a Portuguese translation.)
He also added that the only way to preserve the soil's original (and healthier) fertility is to keep animals along with the plants, like Indians and Chinese did for millennia and still do (whose farmers he used to call "my teachers"). The animals complete the natural cycle of the nutrients, and the high faunal diversity -- that exists when sufficient patches of native biomes are preserved -- helps fight against plagues. Both India and China are still countries of so-called "Megadiversity", even with more than a billion people each and such long history. We, Westerners, on the other hand, are destroying our fertile land in an alarming rate, as you can see with deforestation/desavannization in Brazil and many other countries in the Americas, places with far less people, and far less time of "civilization".
But, of course, all of this is only feasible in a world with a substantial peasantry, and not one who follows the machine-guided + urbanization philosophy that rules in Western world today.
Finally, some patches of land will naturally have more nutrients than others. That's why there has ever been "good lands" and "poor lands". And since we want to use them all to survive, we may end up using some chemical help here and there. But that should be seen as an exception, not as rule.


text:
What are the highest and lowest amplitude values in ECG for humans?
I'm currently trying to parse the records captured from an ECG device and display them on a mobile application. I am wondering what the highest and lowest possible amplitude values for ECGs are in humans? What may happen if they exceed those values?

Amplitudes are notoriously unreliable measures for biological potentials in general. They can vary widely from person to person and from test-to-test. What are you after? The uttermost limits possible? Note that recording artifacts may exceed the actual ECG. And what do you mean with they exceed those values? What is they? Which values?

@Christiaan, sorry, I'm referring to the amplitudes. English is not my primary language. So what are the possible limits of these amplitudes? We're developing a software that will display these amplitudes and knowing the possible limits will greatly help us in displaying them.

The QRS complex is the part of the ECG with the largest amplitude.

I scanned a dozen ECG traces across the web, and as far as I can see, the QRS complex has amplitudes of up to 4 mV in a normal ECG:

ECG trace. 1 mm corresponds to 0.1 mV on the y-axis
Amplitudes are relative peak-to-peak measures. If you are asking about absolute values then the minimal voltage versus maximal absolute voltages depend on your baseline value, i.e., the offset in your voltage potential measurement system. Further, artifacts and background noise may add signal amplitudes on top of the ECG proper.
As an absolute minimum estimate, the graphs here posted show that -1 mV would be a safe minimal voltage.

As you mentioned this is the case for healthy ECGs, old infarcted areas (e.g. post MI) regularly cause these values to be exceeded - often with very prominent Q waves which I think would go beyond your suggested minimum voltage.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Get Parent GO terms of GO term vector?
I have a vector of GOIDs that are specific GO IDs outputted from an enrichment analysis. I want to cluster my GOIDs by their parent GOID term. I used GOstats to do my enrichment analysis, and I have noticed there is an inducedTermGraph, which outputs a graphNEL object of direct children and direction parents of the GOIDs you query. If you set parents=TRUE and children=FALSE, your graph includes only parent nodes which relate to your GOID query.
However, how can I extract the node names of these parent nodes??? See code below:
gene.ids <- c(51141, 84968, 140850, 388289, 406994, 677828, 693217, 100287428,
             100505685, 100506540, 101926966, 101927244, 101928659)
require(RnBeads)
uids <- rnb.get.annotation("genes")
uids <- sort(unique(as.numeric(na.omit(unlist(sapply(unlist(uids)$entrezID,
        function(i) strsplit(i, split=";")))))))
params <- new("GOHyperGParams", annotation = "org.Hs.eg.db", geneIds = gene.ids,
             universeGeneIds = uids, ontology = "BP", conditional = TRUE,
             testDirection = "over")

res <- tryCatch({
    hyper.genes <- hyperGTest(params)
  }, error = function(ee) {
    print("Errorfests.")
  })
go.ids <- summary(hyper.genes)[,"GOBPID"]
result <- inducedTermGraph(hyper.genes, id=go.ids, children=FALSE, parents=TRUE)
nAttrs <- list()
z <- attributes(result)$nodes
    names(z) <- nodes(result)
    nAttrs$label <- z
plot(result, nodeAttrs=nAttrs)

What is this code? Is that formatting break supposed to be there? There are long winded solutions I can think of with Biopython. Could you make your input clear, and what you want your output to be.

If you just want to know the parent nodes of a list of GO terms, you can use GOBPPARENTS in the Bioconductor package GO.db (which you use when using GOstats). This may be a better way to manipulate this information programmatically.

@ddiez do you have a code example of what you mean? for example if I have:  terms = c("GO:0001071","GO:0005886") I can't just run this: GOMFPARENTS$terms or GOMFPARENTS(terms).

@RickBeeloo see my answer below with some code. First problem you are mixing ontologies (GO:0001071 is for MF and GO:0005886 for CC). 2) You cannot access GOMFPARENTS with $ and a variable like that. 3) GOMFPARENTS is not a function so using () doesn't work either.

To answer @RickBeeloo's comment above I decided to include an answer with some detailed code. Basically to obtain the ancestors of any Gene Ontology (GO) term using the Bioconductor package GO.db we need a call to the AnnDbBimap object for the adequate ontology. For example if we want it for Molecular Function (MF) we would use GOMFANCESTOR like in the example:
library(GO.db)

terms <- c("GO:0008022","GO:0001071")
as.list(GOMFANCESTOR[terms])

$`GO:0008022`
[1] "GO:0005515" "GO:0003674" "GO:0005488" "all"

$`GO:0001071`
[1] "GO:0003674" "all"

Similar objects can be used for Biological process (BP) and Cellular compartment (CC): GOBPANCESTOR and GOCCANCESTOR. The only limiation is that you cannot mix terms from different ontologies (i.e. all BP, MF or CC). There are similar options to obtain the children of any given GO term (e.g. GOCCCHILDREN). The description of each term can be obtained with:
Term(GOTERM[terms])
                   GO:0008022                                           GO:0001071
 "protein C-terminus binding" "nucleic acid binding transcription factor activity"

All available mappings can be listed calling GO():
GO()

Quality control information for GO:

This package has the following mappings:

GOBPANCESTOR has 28477 mapped keys (of 28477 keys)
GOBPCHILDREN has 16829 mapped keys (of 28477 keys)
GOBPOFFSPRING has 16829 mapped keys (of 28477 keys)
GOBPPARENTS has 28477 mapped keys (of 28477 keys)
GOCCANCESTOR has 3897 mapped keys (of 3897 keys)
GOCCCHILDREN has 1317 mapped keys (of 3897 keys)
GOCCOFFSPRING has 1317 mapped keys (of 3897 keys)
GOCCPARENTS has 3897 mapped keys (of 3897 keys)
GOMFANCESTOR has 10021 mapped keys (of 10021 keys)
GOMFCHILDREN has 2046 mapped keys (of 10021 keys)
GOMFOFFSPRING has 2046 mapped keys (of 10021 keys)
GOMFPARENTS has 10021 mapped keys (of 10021 keys)
GOOBSOLETE has 2012 mapped keys (of 2012 keys)
GOTERM has 42396 mapped keys (of 42396 keys)

Additional Information about this package:

DB schema: GO_DB
DB schema version: 2.1
Date for GO data: 20160305

Thankyou! I have one question you use: as.list(GOMFANCESTOR[terms]) this will give two lines of output. But which of these lines is the parent of both of the terms? @ddiez

The result is a named list, the names are what follows $ in the result (e.g. $GO:0008022``). The names are the ids of the original GO terms in the variable terms. Each line shows the ancestors of the corresponding id. For example, for GO:0008022 (first id in terms) you get: "GO:0005515" "GO:0003674" "GO:0005488" "all".

So you have to compare those by hand to get the common parent of both IDs? @ddiez

I posted a question about this topic: http://stackoverflow.com/questions/39879936/r-bioconductor-go-terms-output-interpretation mabye you are interested in answering it @ddiez

It turns out if you set the font.size in the graphNEL object, you can see the node names in the plot of the inducedTermGraph.
Setting font.size to >20 worked for me!

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text:
What happens to the mold spores we inhale?
What happens to the mold spores we inhale?
I'm guessing when we exhale, many of them are expelled back out to the environment.
But given that disease can be caused by mold exposure, I'm also guessing that we do not immediately expel a percentage of them.
Molds can colonize in the lungs, causing detrimental effects.  Can they colonize elsewhere in the body?
For mold spores that do not colonize inside the body, what happens to them?  Are they expelled?  If so, by what mechanisms?  Are they alive or dead when they are expelled?

I think spores can cause problems only in immunodeficienc individuals.

@OleksandrPapchenko You may think it, but if you research it, you will quickly learn that is not true!

Maybe I'm reading too much into this post, but I think there may be too many questions here. Like asking about other parts of the body? I also don't know why you ask, "are they dead or alive when expelled?" It's not like our lungs autoclave the air we exhale or bombard the spores with UV light or anything. How would simple inhalation/exhalation kill mold spores?

@anongoodnurse You're jumping to conclusions. We likely only expel some of the spores immediately via the air we exhale.  The question specifically asks by what mechanisms we expel the rest of the spores and if they are alive or dead at that point.  So to answer the question, you need to look at all mechanisms, not just the exhalation of air.

Mold spores are capable of landing and becoming dormant. Unless conditions are severe enough, mold spores will not just simply die off; they will essentially wait for conditions to improve and once those conditions do improve, they will take root and grow. When it comes to the human body, it all depends on the type of mold and the overall health of the host. The body is designed with natural defense mechanisms - mucous, enzymes, beneficial bacteria, filaments, etc. - against airborne particles and microorganisms. Basically, you'll never know if a sneeze or cough - other forms of defense - saved you from a miserable existence as a mold host.
As for whether or not mold spores are expelled from the body, that is not so easily answered. Mold spores can sometimes teem in the millions, especially around a dense infestation (such as grain silos or a house that has structural mold rot). Research has concluded that farmers (who make up 30% of victims who suffer respiratory illness in the U.S. alone), for example, inhale up to 750,000 mold spores per minute. The odds aren't exactly in their favor when it comes to expelling mold spores simply by exhaling.
(I write for MoldBlogger, by the way. If you have anymore questions or are curious about other mold-related scenarios, feel free to check it out.)
Edit:
Here are some of the sources where a lot of this information can be read about.
National Institute for Occupational Safety and Health. Agricultural Safety. Centers for Disease Control and Prevention website. https://www.cdc.gov/niosh/topics/aginjury/. Published June 19, 2014. Updated December 15, 2014. Accessed February 1, 2017.
Glen H. Hetzel, et al. Farmer’s Lung: Causes and Symptoms  of Mold and Dust Induced  Respiratory Illness. National Agriculture Safety Database website. http://nasdonline.org/1853/d001796/farmer-039-s-lung-causes-and-symptoms-of.html. Published 2005. Accessed February 1, 2017.
Dennis J. Murphy. Agricultural Safety and Health: Farm Respiratory Hazards. PennState Extension website. http://extension.psu.edu/business/ag-safety/health/e26. Published 2017. Accessed February 1, 2017
Also, please feel free to check out a simple post that summarizes this type  of information: Occupational Respiratory Diseases: The Farmer, His Lungs, and Mold

Great that you took the time to answer an old question +1. Could you add your sources to this answer to allow other users to background-read on your topics covered?

Thank you. Sources have been added. I will keep an eye out for more sources that I've used in my own research and return to edit again at some point.


text:
Do males ever produce the offspring?
Are there any non-asexual species in which the male of the species produces the offspring?
If so, why are they considered male and not female?

Yes the males of a group of bony fish Syngnathidae can bear offsprings or as you say produce offsprings. This group includes Seahorses and Pipefishes. In some species the male have either a brood pouch attached to the trunk or its tail while in others the egg is attached to the trunk or tail laid by the female.The fertilisation takes place in the pouch or in water before implantation.
Here are some pictures :
1.Male seahorse with brood pouch and a slender female without a brood pouch

2.Male seahorse giving birth to a baby seahorse

3.Male Syngnathus sp.(pipe fish) with the brood pouch

Inset image C shows eggs in pouch of pregnant male and Inset E shows Embryos in the pouch of pregnant male. (Images taken from researchgate.net and peaubleue.org)
Now coming to your question

why are they considered male and not female?

Though the males here bear the baby but the baby results from fertilisation of a sperm produced by the male (the same seahorse that is destined to bear the baby) and an ovum produced by the female (the other seahorse without a brood pouch).
The sperm / male gamete producing individual is a male and a ovum/female gamete producing individual is a female. The provision of being able to bear a child does not change the sex.
Note: Seahorse is an oviviviparous organism i.e they are organisms in which the fertilised eggs develop inside the parent's body until they are ready to hatch.
P.S. Brood pouch is a cavity outside the body of these fishes in which the eggs develop and hatch.
Source: Wikipedia

Good answer +1. Might be worth also going a tiny bit further in the definition of male vs female and define sperm vs ovum. Males produce small gametes while female produce large gametes. You might also want to say a word about species like yeast that have mating types and not gender as there are no difference in gamete size.

@Remi.b Thank you. I'm glad that you liked it. Its my third answer in this community. I was thinking about doing some research on the sex determination of seahorse/ fish in general and then adding it to the answer.

I stumbled upon two images of Syngnathus sp. and have merged it into one and added to my answer.

Thanks @SanjuktaGhosh; Great answer that perfectly combines knowledge and the pictures that transport the fascination that drives/drove (at least many of) us into biology. Looking forward to your additions. +1 anyways.

Parental care by the male parent is off course relatively common, especially in birds and mammals. Cases were the male actually does most of the 'breeding' are relatively rare. I think @Sanjuktaghosh gave a beautiful example, but there are a few more:

Mouthbreeders keep there offspring in the mouth for considerable amounts of time. In most mouthbreeders, the female takes the eggs, but Darwin's Frog is a notable example were the male does.
Biparental mouthbrooding occurs where both parents take some of the eggs. This is found in some fish species.
A different example is the Emperors penguin, where the female lays a single egg, which is incubated by the male while the female returns to the sea to feed. To keep it warm, he puts this egg on top off its feet, folding his belly over it. A picture of dad with the egg can be found here
A final example, with thanks to Sanjuktaghosh, is the Northern jacana

Like your Emperor penguin link to dailymail. Parenting by the male parent is also observed in a polyandrous bird Northern Jacana.


text:
How does a garlic clove thrive inside a closed refrigerator?
A garlic clove has been growing very well inside a closed refrigerator.
It has developed beautiful green stalks, which I think are the equivalent of leafs.  Since they are green, I assume they contain chlorophyll.
Without any source of sunlight (for photosynthesis) or soil (for nutrients), how can such a plant thrive so well?
Is it simply growing off the internal stored energy of the clove itself?
Will it continue to grow without sunlight and soil?

You called it, it is using stored energy to do this, and will continue for some time but will eventually run out of energy. An analogous but common example is when a tree or bush is cut down so it has no more branches/leaves and will re-sprout after some time.

Your garlic was likely purchased as a bulb, not seed, and stored in the fridge.  The garlic 'clove' is not frozen, so your fridge readily mimics underground conditions in the temperate late winter or spring season. The bulb is generally buried underground, and the subsequent initiation of plant development and growth uses the stored energy. In a garden, the garlic would, however, begin photosynthesizing soon thereafter. Bad news: in your fridge, the plant is certain to become etiolated, because the lack of light, and yes, eventually run out of the stored resources--and die. Good news: you can eat or transplant it.

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


text:
What biological process was taking place?
A tub of a side dish, either tomato salsa or baba ganoush (eggplant), was left in a plastic bag for several months.  The plastic bag was not airtight, but was wrapped somewhat tightly around the tub.  Although it was supposed to be stored refrigerated, it was not (it was stored at room temperature).  It also was not supposed to be stored for such a long duration.
When the bag with the tub inside was eventually handled, it was noticeably hot.
What biological reaction was taking place that would generate that kind of heat, especially after months of storage?

Exothermic bacteria such as routinely found in compost piles! http://compost.css.cornell.edu/physics.html

As outlined in my comment, I hypothesise it must have been the growth of exothermic bacteria. As the name suggests, these produce heat. An especially interesting phenomenon concerns the danger of fire erupting from moist hay, as the bacteria feed from it and dry it simultaneously! This is outlined here. A memorable quote from that article:

Dry hay (stored at 15 percent moisture or less) is safe for long-term storage. However, if the hay has become wet the quality has been permanently changed and the potential fire hazard from spontaneous combustion increased.

The same principle underlies the heating of compost, about which you can read in greater detail here.
Most astounding I found the post dealing with the possible contribution of exothermic gut bacteria to our thermoregulation.
As of now, I don't know about the basic mechanisms by which these bacteria generate heat, but the abstract of this article implies that heat absorbing bacterial growth is extraordinary.
I myself have forgotten everything about chemistry, but from the comments below I gathered that what happens is similar to the oxidations of sugar. You can read examples here, which demonstrate that these are exothermic.

The mechanism is that they are essentially "burning" the organic compounds for energy, just like your own cells do, it's just that they are doing so fast enough to create a lot of heat.

Why is it a tautology? I guess my point was that there isn't any special mechanism, it's just from metabolism. I suppose maybe what you mean is "what is the mechanism by which they can continue to generate so much heat without simply sterilizing themselves."

I meant burning in the sense that the end reactions are converting carbohydrates into CO2 and water. Although the path of reactions isn't the same (and much slower), the products and thermal output are the same as if you lit the pile of hay on fire. So yes, oxidation.

@BryanKrause ok that makes perfect sense!


text:
Are axons capable of endocytosis?
There is evidence for the uptake of toxic substances like prions from the cell bodies of neurons via endocytosis.  There is also evidence for prion deposition in white matter.  But I haven't been able to find a discussion of whether or not endocytosis is possible from axons.  Does anybody know if this is possible?

Are you asking specifically about the myelin sheathed region or are you also including the axon termini?

Short answer
In hippocampal neurons, endocytosis does occur in the axon, but only at the synapse and at varicosities.
Background
In cultured rat hippocampal neurons, Parton et al. (1992) showed that the cell body and dendritic regions are indeed capable of endyctosis. They used horse-radish peroxidase dissolved in an internalization medium. In the axon, endocytosis was only found to occur in the pre-synaptic region and in varicosities. Varicosities are points of synaptic release from the axon, outside the synapse proper.
Hence, axonal endocytosis is limited to regions where neurotransmitters are released. Presynaptic terminals often engage actively in neurotransmitter reuptake mechanisms to recycle released neurotransmitters.
Reference
- Parton et al., J Cell Biol (1992); 119(1): 123–37


text:
Can a color-blind person see color with filter glasses?
Why does color vision improve in color-blind persons using these filter glasses from Enchroma? Will a color blind person be able to see the same colors on a television? I'm asking, because the colors for every point on a TV screen are combinations of red, blue and green.

Short answer
Optical filters can optimize color contrast, but never restore color blindness. Filters remove colors, they can never add something. However, glasses like this can prove helpful for certain sub-populations of people that are partially color blind.
Background
First, the term color blindness is deceptive. It is better to talk about colour vision deficiency (CVD). This, because many people labeled as color blind in fact have all the red, green and blue cones like the normally-sighted. These people have protanomaly (abnormal, but still functional red cone photopigment), or deuteranomaly (abnormal green cone photopigment). These two conditions are mild and don't affect daily life too much (source: NEI / NIH).
The other two most common forms of CVD are protanopia and deuteranopia. Protanopes have no working red cone cells and deuteranopes have no green cones. These conditions are more severe and do affect daily life as color perception is compromised. These conditions can be coined color-blindness, as these folks miss one type of cone altogether (source: NEI / NIH).
The glasses of Enchroma target the first two conditions, namely the anomalies and not protanopia or deuteronopia. The Technology page of Enchroma explains why. Basically, protanomaly and deuteranomaly are characterized by the red and green pigments having a shifted spectral maxima. The end result is the same, namely more overlap between the spectral absorbance curves (shown for deuteranopia in Fig. 1). In normal vision, the overlap is already pretty extensive, meaning that green light activates a large portion of red cones and vice versa. In protanopia or deuteronopia this effect is further increased, resulting in a degraded capability to separate reds and grees. For example, protanopes perceive reds, oranges, and yellows as greener, and colors are not as bright. Deuteranopes perceive yellows and greens as more red and they have difficulty telling violet from blue (source: NEI / NIH).

Fig. 1. Left: normal cone spectral distribution vision, right: cone distribution in Deuteranopes. source: Enchroma
What Enchroma has come up with is actually really clever (!) - they've put a spectral notch filter in place and wedge it in-between the red and green spectral optima, thereby removing the large area of overlap. This reduces brightness, but it will enhance contrast when the glasses are worn (Fig. 2).

Fig. 2. Spectral notch filter to enhance green-red color contrast. source: Enchroma
And yes, above considerations hold for any colored object, including monitor pixels.

I am colourblind and own a pair of the enchroma glasses. For me (experiances seem to vary) the glasses certainly make colours look different however there is only limited improvement between difficult red-green differentiation. I've yet to try a colourblindness test wearing them!

I've been reading around a lot and I still don't understand how this is meant to work. Surely it just makes the wearer blind to wavelengths of light filtered out by the glasses? The wavelengths on either side of the notch (not being blocked) are going to excite the red and green cones about the same amount, just as they were before, and so will still be difficult to distinguish. I haven't found an explanation that feels sufficient yet.

The wavelengths on the side will excite as they did before, but the regions of high overlap are excluded by the notch. Imagine that the area on the left excites G 1 unit and R 0.2 units, while the are covered by the notch is 5 units G and 5 units R. With the notch, you have 1:0.2 or a contrast of 5. Without the notch you have (1+5):(5.2) or a contrast of 1.15. Contrast would be enhanced almost 5-fold.


text:
How can neurons divide without centrioles?
I have read in my studies that neurons lack centrioles. If that is so, then how is it possible that new neurons are added to our brain? Does this have anything to do with memory loss?

Neurons do not divide.

@WYSIWYG: in certain places in the brain, neuronal stem cells do.

@Christiaan  yes but they are not neurons.

You talk about memory loss. The hippocampus is involved in the formation and storage of memories and indeed one of the few places in the brain where new neurons are formed. The formation of new neurons here is indeed linked to the formation of memories (Coras et al., 2010).
Hippocampal neurons do not lack centrioles (Dotti & Banker, 1991; Poppov & Tsygunova, 1996). In fact, centrioles may not be necessary for cell division to occur (source: BSCB), although the lack of centrioles in cell models may result in aberrant cell division (Rodrigues-Martins et al., 2008).
In the hippocampus, however, it is not the neurons themselves that regenerate, but rather the resident neural stem cells and progenitor cells (Kirby et al., 2014).
References
- Coras et al., Brain (2010); 133(11): 3359-72
- Dotti & Banker, J Cell Sci (1991); S15: 75-84
- Kirby et al., PNAS (2014); 112(13): 4128–33
- Poppov & Tsygunova, Neuroscience Letters; 203(2): 135–8
- Rodrigues-Martins et al., Cell Cycle (2008); 7(1): 11-6


text:
Are drugs made bitter artificially to prevent being mistaken for candy?
All drugs I remember tasting (with the notable exception of Aspirin) have bitter taste. Is the taste due to the active substance, or is a bittering agent added to them, perhaps to prevent overdose?
Take Paracetamol for instance: adult pills taste bitter, while the syrup for babies is sweet without any noticeable bitterness. Or is the dosage simply so low that I couldn't distinguish the drug taste behind all that sugar they put in?

Why do you think aspirin doesn't taste bitter?

Not sure why Dmitry said it, but I know that some Ibuprofen (who many call "aspirin") are covered in a sort of 'candy shell' which is bit sweet to my senses as well. I've never had Acetaminophen that were coated, but I use the Ibuprofen that is coated specifically because I don't have to rush the chaser to get the taste out so fast.

Or perhaps he's only used that expensive coated brand, instead of the generic stuff.  So he's never actually tasted the aspirin.

I've seen paracetamol confused with aspirin, not ibuprofen with aspirin. Ibuprofen itself shouldn't be tasted, since it's usually either shelled or in a liquid-cap for good reason @coblr

@jamesqf Because I tasted it. Aspirin is an acid and has a typical sour taste.

@coblr, Not sure which part of my question you a referring to. The sweet paracetamol I was talking about was for babies, so it was certainly not in "candy shell", as babies cannot swallow pills without the risk of choking.

I’m voting to close this question because it is not about a problem in biology, but is solely about commercial/social marketing practice. It may possibly be relevant on SE Medical Sciences.

@Dmitry Grigoryev: Apparently your taste buds are more sophisticated, or perhaps I should say capable of greater discrimination, than mine are, because I certainly can't tell the difference.

@coblr you may be confusing Aspirin with Advil, which is a brand name for ibuprofen. Aspirin is acetylsalicylic acid

Sorry, I wasn't so much confusing it as I was just pointing out that many that don't know/could care less about the specific compound (including my wife) will call Advil an "Aspirin" in a similar way to how people call facial tissues a "Kleenexes", sodas "cokes" and vacuums, "Hoovers". I didn't realize that baby Aspirin had something extra or that, that's what was being referred to. It was just a reason I could think of for why a certain type of "Aspirin" may have been sweeter than expected. I didn't assume an adult was taking baby aspirin when it wasn't mentioned as such.

Short answer
A bittering agent may be applied to therapeuticals to prevent pediatric poisonings, but many drugs inherently taste bitter by themselves.
Background
Bitter taste is thought to have evolved as a way to decrease the risk of ingesting toxic substances, which may explain why many drugs taste bitter. In other words, classes of compounds that may harm the body often taste bitter (Menella et al., 2014). These include the often dangerous compounds like alkaloids and glycosides (source: University of Delhi). These include the familiar psychotropic compounds found in hallucinogenic plants, and the potentially deadly heart glycosides found in Digitalis species, respectively, among other classes of substances.
Paracetamol can be regarded as an alkaloid (Fig. 1), but not aspirin, as it lacks a nitrogen atom (Fig. 2). An alkaloid is defined as

any of a class of naturally occurring organic nitrogen-containing bases. Alkaloids have diverse and important physiological effects on humans and other animals. Well-known alkaloids include morphine, strychnine, quinine, ephedrine, and nicotine...

All of which are quite toxic. As cleverly noted in the comments, aspirin is not an alkaloid in its strictest sense, as it is not naturally occurring. However, it is chemically obtained by acetylation of salicylic acid (Mund et al., 2016), as shown in Fig. 2. Both of the reactants in themselves are naturally occurring; salicylic acid can  be sourced from willow bark, and acetylation is a widely occurring biochemical reaction (Gibbs, 2017).
I myself have never had the chance to taste aspirin, unfortunately (although I performed the acetylation shown in Fig. 2 for my Organic Chemistry class :-). Originally, aspirin was developed from salicylic acid (Fig. 3) just because the taste of salicylic acid was so bitter. Acetylation diminished the bitterness, yet the anti-inflammatory action remained (Wu, 2000)). Besides reducing bitterness by chemical modification, masking the bitterness of drugs with, e.g.., sweeteners, can help to overcome the aversion to the bitter taste. This can aid in helping patients, especially pediatric ones, to take their medicine and adhere to their treatment regime (Chauhan, 2017).
Reversely, coming back to your question, adding bitter-tasting additives to drugs indeed seem to be an effective way to reduce pediatric poisonings (Menella et al., 2014)
References
- Chauhan, J stem cell Bio transplant (2014); 1(2): 12
- Gibbs, Trends Plant Sci (2015); 20(10): 599–601
- Menella et al., Clin Ther. 2013 Aug; 35(8): 1225–1246
- Mund et al., J Occup Med Toxicol (2016); 11: 32
- Wu, Circulation (2000); 102: 2022–3

Fig. 1. Paracetamol, or acetaminophen. source: Wikimedia Commons

Fig. 2. Synthesis of Aspirin, or acetylsalycilic acid, from salicylic acid. source: Imperial College, UK

I recall an advert in the 90s advertising a form of aspirin "without the aspirin taste" - it showed a bunch of people taking aspirin dissolved in water, screwing up their faces.  I also recall experiencing the same.  I can't find the advert anywhere however, and I haven't taken aspirin in years.

Interesting read: The importance of taste in pharmaceutical development but that yummy chewable baby aspirin now seems somehow evil...

@RossPresser Notably, nowadays aspirin is the last thing you want to give to a kid because it might cause brain damage.

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


text:
What does the hominin phylogenetic tree look like?
I'm no biologist, but I'm curious what the rough phylogenetic tree looks like for Hominin.  Could you create a rough sketch that includes:

Homo rudolfensis
Homo ergaster
H. georgicus
H. antecessor
H. cepranensis
H. rhodesiensis
Homo neanderthalensis
Denisova hominin
Homo floresiensis
H. heidelbergensis
H. neanderthalensis
H. sapiens
H. erectus
H. habilus
any others I may have missed

Feel free to correct any incorrect assumptions I may have made here, or clarify anything that could be instructive.

Is this suitable? I am a novice so sorry if it is not: http://humanorigins.si.edu/evidence/human-family-tree                                              I Googled "Hominid tree" to find it.

Gonzalez-Jose et al. (2008) published the following cladograms, based on two analyses (parsimony versus maximum likelihood). The table shows the legend. The interesting case of Homo floriensis, among others are not included, likely because of their recent discoveries and limitations of the study cited.

Reference
- Gonzalez-Jose et al. Nature (2008); 453 775-79

Great answer, but one thing to note about the upper tree is that the Bremer support values are really really low (0.2 to 0.5) particularly within Homo. So basically there is no resolution at that point. They may as well have a large polytomy at that point. This is not a fault of the authors but of all these fossils being fragmentary.

@kmm - This is pretty much over the top of my head - Please advice, should I crop the image and only show the bottom tree instead? Piece of cake to do so. I simply pasted their complete figure in here without critically assessing their respective merits to the question.

No, it's fine as is. The tree is the tree and is (very likely) technically correct. It's just that the devil is in the details. I'm sure the bottom tree is equally poorly supported.


text:
Why is human vision restricted to 400-700 nm?
Across the electromagnetic spectrum, 400-700 nm is a narrow spectrum of frequencies and focused in the region of short wavelengths. For example, radio waves cover a large range of frequencies unexploited by the visual system. So what biological reason is there that evolved us to use such a small frequency bandwidth for vision?

We can only answer "how" or "how come"? "Why" actually is quite speculative and philosophical. Why human are the way they are? Why didn't humans evolve to swim naturally or run fast (very favourable attributes)? We can just guess the "why". :)

Short answer
The visible spectrum has the highest energy in sunlight at the earth's surface, explaining the gross location of the visible spectrum in life on earth. The specific frequency range varies across species and can be explained by species-specific survival strategies.
Background
When you look at the solar light spectrum at the earth's surface the visible spectrum has the highest intensity (fig. 1).

Solar irradiation. Source: University of California.
So it makes sense to use the range of frequencies that is represented most in sunlight as a starting point.
Then the question becomes, why do humans utilize approximately 400 to 700 nm, and not infrared or UV? That can be explained because we do not need it. Our range has been hypothesized to be related to foraging behaviors and our visual system is particularly sensitive in the frequency range of the coloring of (ripe) fruits, which is thought to have been of great benefit to our hominid ancestors (Osorio & Vorobyev, 1996).
Why then do animals extend their vision into UV? Many fish, amphibian, reptilian, avian, and some mammalian species use UV vision. Many birds can identify UV-reflected nectar and berries, and UV-reflecting plumages in birds, and scales in fishes are used for recognition (Shi & Yokoyama, 2003). Moreover, some arthropod species are know to use UV vision to reduce light-reflection distortions under water, such as in the mantis shrimp that features 12 photoreceptor types (as opposed to four in humans) (Thoen et al., 2014).
Why then do animals extend their dynamic range into the infrared? A notable beneficial effect of perceiving infrared is the detection of body heat. The generation of heat is accompanied by the generation of infrared light. The detection of this emitted light is highly useful for nocturnal predators, like the rattle snake (Hartline & Newman, 1982).
References
- Hartline & Newman, Sci Am (1982); 246(3): 116-27
- Osorio & Vorobyev, Proc Roc Soc B (1996); 263(1370)
- Shi & Yokoyama, PNAS (2003); 100(142003): 8308-13
- Thoen et al., Science (2014); 343(6169): 411-3
Further Reading
1. Is our color vision calibrated to sky, vegetation, and blood?
2. Is there a physical reason for colors to be located in a very narrow band of the EM spectrum?

Not that you said it was, but I'm not sure if snakes detecting IR light can be classified as vision. Anyways, nice answer +1

@canadianer - I classify vision as light perception. People classified as having ultra-low vision (near-blindness) sometimes have not much more than bare light perception (light on or off).

It's largely a semantics issue I think and I don't really know why I even brought it up ;) A plant can perceive light, thought I wouldn't say it has vision.

@canadianer - plus I never said that snakes had IR vision in my answer in the first place lol. I used perception

Most of the light from the sun doesn't actually reach the earth's surface due to the atmosphere.

[source]
So the light reaching earth includes near-UV, visible, near-IR and a band of radio waves. Seeing any other part of the spectrum would be impossible since it doesn't reach earth.
You asked why we only see in the visible light range; this is due to evolution. Birds, among other animals, can see UV light. In fact, all vertebrates have the potential for near-UV vision. Humans, as vertebrates, also have UV-sensitive photoreceptors. However, our lens is opaque to UV light:

[from Clinical Ocular Anatomy and Physiology via this website]
Just speculating, it would seem that the ability to see near-UV is an ancestral condition which we lost at some point; either it provided no significant advantage (neutral regression) or there was some advantage provided by a UV-opaque lens, either directly (such as protection from UVB light) or indirectly (through pleiotropic antagonism).
On the other hand, human photoreceptors cannot detect IR light. Again, this is a product of evolution.  These researchers hypothesize that the longer the wavelength of light detected, the more noise is produced. This noise is due to activation of the pigment molecule by heat. Or, it could just be that never happened. An IR-sensitive photoreceptor might be possible, but evolution doesn't lead to perfect adaptation. In other words, there isn't necessarily a reason why.
As for radio waves, they are too low energy to interact appreciably with matter, at least as far as vision is concerned.

Most photoreceptors, the way they work, cannot absorb IR because IR is too low in energy to cause electronic transitions. Regarding false alarms; yes heat can generate false alarms but that doesn't mean noisy (in fact IR scatterance is much less. Rayleigh scattering reduces with wavelength). I would reason that diurnal habit and temperate habitat of humans does makes IR sensing not very useful.

While it is true humans do have some marginal sensitively to UV (basically spillover) we have no UV focused receptors like many other animals. this is true of Mammals in general so the group as a whole seems ot have have lost UV sensitivity. A major problem with infrared is water is not very transparent to infrared, and what are eyes made of. this is why pit vipers have open air filled pits for infrared detection.

Its not really
That is only the human visible spectrum.
Humans actually have a reduced spectrum compared to many animals. Mammals in particular have a reduced spectrum compared ot non-mammals. Reptiles and birds have 4 color sensitive cell types (cones) and can see into the ultraviolet. Many invertebrates can see an even wider spectrum. Mammals lost two of these cells. Modern mammals are descended from early mammals who were nocturnal Thus color vision was less useful. Primates evolved a third cone, (a mutant variant of one of the two they had before) Primates did this because many are frugivores and color is excellent for determining when fruit is ripe.

This is my speculation, but there are no or few organic chemicals which can absorb radio waves having longer wave lengths. Eyes sense lights by absorbing light with organic chemicals, but to sense longer wave length, eyes might need more sophisticated devices like tuners.
In addition, less than 100nm radio waves from the outer space are absorbed by the atmosphere, so even if eyes could sense such radio waves, you don't see any signals on the earth.

This answer holds great potential, especially the radio wave part. Elaborating on that may get you your deserved upvotes.

"Visible light" is the wavelength of the light that we can see, if human beings could see UV or IR, those wavelengths had been included in the "visible light" definition.
Now, our Sun is brightest in yellow-green light, which (you guess?) is right in the midle of the "visible light" spectrum. So the only remaining question is: "Why can we only see that short spectrum?" The answer is EVOLUTION.
The same reason that made us to have only 5 fingers in our hands, only 2 eyes and only two kidneys.
The bandwith of the "visible spectrum" is enough to make the human beings (as specie) survive.

Every question can be answered by 'this is EVOLUTION'. I do acknowledge the inherent problematic nature of the why questions, but they nevertheless form an interesting class of questions in the light of speciation. Further, the capitalization should be used with caution as it implies yelling at OP. It is a legitimate question.

it is also a bad answer using evolution, since there are some pretty solid evolutionary artifacts that make human vision very limited.

These wavelengths happen to satisfy two conditions.
First, shorter wavelength photons (EM radiation) tend to be dangerous for biology. Even UV light (<350nm) is already can damage DNA. That is due to the fact that bond energies in biological molecules tend to have values close to energy of short-wavelength EM radiation. These is why high-energy particles called ionizing radiation. For reference, see this paper. ionization energy for DNA estimated in 4-5eV range, which is 300-250nm.
Secondly, on low-energy hand of spectrum, water absorbs a lot of IR radiation:

So, as you can see, what we see aka visible spectrum is sitting nicely in valley of water absorption but does not extend to area of harsh UV light that will damage chemicals of your body.
Now, why is that so? Because atoms have these masses and electrons around them have these energies. So bonds and molecular interactions have these values.
(In radio range of frequencies you, opposite to UV, have not enough energy to elicit any significant molecular changes, which is why you can't perceive WiFi)

The reasoning that UV shouldn't be visible because it is dangerous makes no sense. Along that reasoning the visual system should be filtering out predators, guys with guns etc. as well. Moreover, there are classes of critters that sense UV and use it for meaningful purposes.

Essentially none of the UV light that reaches the surface is ionizing. Lower wavelength UVB light can damage DNA, but this is hitting our body and eye whether we can see it or not. About 95% of UV light that reaches the surface is non-damaging UVA.

@AliceD My reasoning is following: UV is dangerous hence it is/should be filtered before it reaches anything sensitive. Animals don't really need retinal cancer.

Reasoning is one thing, claiming it to be so is another, especially since many species actually use UV. Oxygen is highly toxic. Should we therefore neutralize it before we breath?


text:
Is PCR a DNA cloning technique?
According to Genomes
PCR is

A technique that results in exponential amplification of a selected region of a DNA molecule [in test tube].

DNA cloning is

Insertion of a fragment of DNA into a cloning vector, and subsequent propagation of the recombinant DNA molecule in a host organism.

While, Molecular Biology of the Cell, Sixth Edition says in a summary:

DNA cloning (through the use of either cloning vectors or the polymerase chain reaction) in which portion of a genome (often an individual gene) is purified away from the remainder of the genome by repeatedly copying to generate many billions of identical molecules.

Here DNA cloning has been used to mean DNA replication in general.
Question: Which author's view is correct, or at least provides the most accepted definitions?

Short answer
The Oxford English Dictionary is quite clear on this. For the verb clone there are two meanings:
Biology To propagate (an organism or cell) as a clone.
Molecular Biology To make copies of (a DNA sequence or gene).
The latter definition clearly encompasses PCR.
History lesson
Most of the information below is taken from the Oxford English Dictionary.
The term clone has a long history, first as a noun and more recently as a verb. The evolution of the meaning and use of the word suggests that we shouldn't be too precious about this.

When I use a word,” Humpty Dumpty said, in rather a scornful tone, “it means just what I choose it to mean—neither more nor less.” “The question is,” said Alice, “whether you can make words mean so many different things.” “The question is,” said Humpty Dumpty, “which is to be master—that’s all.

The word is based on  a Greek word for twig and was originally used as a noun in the form clon.

1903 H. J. Webber in Science 16 Oct. 502/2 Clons..are groups of plants that are propagated by the use of any form of vegetative parts.

It soon gained the final e.

1905 C. L. Pollard in Science 21 July 88/1 I therefore suggest clone (plural clones) as the correct form of the word.

By 1930 it had become a verb...

1930 Jrnl. Ecol. 18 357 This is probably a record for the number of ‘individuals’ obtained at one time by cloning a herbaceous plant

...and, presumably because bacteria were considered to be plants at that time, it was used in microbiology too.

1929 Bibliographia Genetica 5 234 In Bacillus coli communis...a biotype was also found having lower motility than the remainder of the clone from which it came.

By the early 1960s it was extended to animals, probably as a direct result of Gurdon's experiments with Xenopus

1963 J. B. S. Haldane in G. Wolstenholme Man & his Future 352   Perhaps the first step will be the production of a clone from a single fertilized egg, as in Brave New World.

And finally the meaning  was extended to encompass DNA molecules, thus molecular cloning.

1974 Proc. National Acad. Sci. U.S.A. 71 3459/1 ColE1 has been shown to serve as an effective molecular vehicle for cloning and amplifying specific regions of unrelated DNA.

(Extra points if you have read this far AND you know what ColE1 is.)
This final quotation seems to me to show that the confusion over what molecular biologists mean by cloning arose very early. If cloning means “to make copies of”  then why is the word amplifying there? From the outset I think that molecular cloning carried the sense of purifying (by cutting and ligating). Or that's what I thought when I did it for the first time in 1980.
Update
Despite my reliance on dictionary definitions above, and prompted by Tyto alba's discovery of a contradictory definition in a different OUP publication (see comment) here's what I really think:
Anyone who has ever obtained a bacterial colony containing a plasmid with the inserted fragment that they wanted announced "I have cloned the gene!" and meant that they had made a recombinant plasmid AND got it into cells. On the other hand, if they started with a PCR amplification then ran a gel to check before ligating and saw a fragment of the expected size they did not say "I have cloned the gene!" And finally, the successful cloner, when streaking out their transformant colony, will rarely have referred to this step as cloning.

I found in 'A dictionary of genetics' (published by Oxford again) say it means creating genetically identical copies of recombinant cells, excluding the in vitro part (pg-182)?! Should OED be considered more precise when we are looking at words as this?

Short answer
All of your sources are correct as they are not mutually exclusive. PCR is used to isolate and amplify DNA to yield small quantities of pure target product. Gene cloning can subsequently be applied to scale the production of the fragment up. PCR thus can be part of the DNA cloning process.
Background
Cloning in general simply means duplicating. Cloning in Biology refers to

[Making] an exact copy of an animal or plant created in a laboratory from the
  animal’s or plant’s DNA

source: McMillan Dictionary
Gene cloning, as far as I understand refers specifically to the isolation of one single gene and inserting it into cells to amplify it:

The production of a lineage of cells all of which contain one kind of DNA fragment of interest derived from a population of many kinds of DNA fragments.

source: Northwestern University
PCR is a technique to amplify a specific strand of DNA that can be used to subsequently clone DNA into host cells (source: New England Biolabs). The cloning is done to upscale the quantity of DNA. PCR uses primers and can be used to isolate and amplify the DNA up to the scale it is easily clonable.


text:
What is the direction of current flow in myelinated nerve cells?
Is it correct to say electric current flows through the extracellular space, or cytosol of a nerve fiber during impulse conduction?
I know that an impulse is actually a change of membrane potential which is transferred along the length of a neuron through transfer of ions (by a series of ion channels and pumps).
In myelinated axons our professor told us the following:

When a nerve impulse propagates along a myelinated axon an electric
  current (carried by ions) flows through the extracellular fluid
  surrounding  the myelin sheath and through the cytosol from one node
  to the next.

How exactly does the current flow in myelineated nerve fibers?

@Christiaan It answered my question to some extent but I have a query, I have already posted it.

During an action potential current flows across the neuronal membrane. Basically, during depolarization, Na+ goes into the cell, during repolarization K+ goes out. This process for a myelinated axon is shown in Fig. 1.
Action potentials in myelinated neurons jump from node to node, a process called saltatory nerve conduction. These nodes, called nodes of Ranvier, lack myelin and contain Na+ and K+ channels. Outside these nodes there is insulating myelin wrapped around the axon and the axonal membrane lacks Na+ and K+ channels there.
What happens during an action potential at a node is the following: Na+ rushes in at the node. Because of the insulating myelin in the next axonal segment leading up to the next node in line, Na+ can run through the axon to the next node without much signal loss. This passive spread of depolarizing current is much faster than repeatedly generate a new action potential along the length of the axon.
To answer your questions now:

Question: Is it correct to say electric current flows through the extracellular space or cytosol of a nerve during impulse conduction?

Answer: Yes... and no. No, because electric current and notably Na+ and K+ flow perpendicular to the axonal membrane during action potentials. Yes, because the Na+ ions do move through passive current spread through the axon to the next node.

Question: How exactly does the current flow in myelineated nerve fibers?

Answer: Your professor was spot on. During depolarization, ions (notably Na+ in this case) are carried from the extracellular space through Na+ channels in the node of Ranvier to the intracellular space. From there it spreads through passive diffusion to then next node.

Fig. 1. Action potential generation in myelinated axons. source: Purves et al.(2001)
Reference
- Purves et al. (ed). Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates (2001)


text:
What happens to the hollow nerve cord?
The dorsal nerve cord of vertebrates is a hollow structure that develops into the nervous system. This embryonic tissue is hollow and I wonder what happens to this 'hollow' later?
Does it form the ventricles of brain?

The "hollow" i.e. the neural canal develops into the ventricles, the cerebral aqueduct and the spinal canal (Wikipedia; also see this site).
For a more authoritative reference, see this book by Haines and Ard† (page 82 onwards in google books; google book links are apparently transient and they expire; therefore I didn't provide one).

† Haines, Duane E., and M. D. Ard. Fundamental neuroscience for basic and clinical applications. Philadelphia, PA: Elsevier/Saunders, 2013. ISBN: 9781437702941


text:
How's the membrane potential restored to resting state after hyper polarisation?
I have known for so long that Na+/ K+ pump restores the membrane potential. But as it pumps in 2 K+ for every 3+ Na+ moving out how can it make the membrane potential less negative when the net result is one positive charged ion moving out?

If you see a normal AP curve, you would be able to appreciate that the membrane potential is generally brought back - which is around -70mV. So the potential doesnt matter much since its restored by the ion fluxes. What matters most is the ion composition on either side. You might see that after depolarization, Na+ came in (it generally satys out) and after hyperpolarization K+ came in. The potential is safe but the distribution is altered. This is what the pump takes care of, not the potential (although slightly electrogenic)

The Na,K-ATPase restores negative membrane potentials.  When a cell is hyperpolarized, leaky K+ channels take care of that. Leaky K+ channels are always open. Generally, K+ has the tendency to diffuse back out of the cell along its chemical gradient through leaky K+ channels, after been pumped in, making the cell's inside more negative. However, in the reverse situation, where the cell is hyperpolarized, they may flow inwards, along the electrical gradient.
Note that while the Na,K-ATPase is indeed the driving force behind the membrane potential, it is not the direct consequence of the ratio of Na+ being pumped out and K+ being pumped into the cell. It is the leaky K+ channels that determine the membrane potential largely, together with the Na+ channels being permanently closed, except when an action potential is generated.
Suggested further readings
- What keeps the resting potential of neurons constant at -70 mV?
- If the average resting potential of a neuron is -70 mV, why is there such a high ratio of potassium ions inside relative to out?


text:
Why does the intensity of an action potential once generated at the trigger zone remain undistured throught the axon?
What causes this consistency?
I read the previously asked questions on this site none of them carry an answer to this question.

If my / Thawn's post doesn't answer your question, then you should place a bounty on your question, and if it does answer, then please select it as correct answer. Don't just leave the question unanswered.

If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.

Actually, it would be better to say that action potential does not travel but is regenerated anew in a sequence along the axon.

I would like to elaborate how this happens and why this is the reason why the action potential stays constant:
In rest state, there is an ion gradient across the membrane of each cell. This causes a small voltage between the outside and the inside of the membrane, the so called transmembrane potential.
Once the cell membrane becomes permeable for ions (normally this occurs when an ion channel is opened), the potential causes ions to flow across the membrane, the membrane becomes depolarized.
In the axon, the membrane contains so called voltage-gated ion channels. As soon as the membrane is depolarized at the trigger zone, the depolarization of the adjacent membrane causes voltage gated ion channels to open in that adjacent memrane as well, causing ions to flow also across the adjacent piece of membrane. This process continues in a wave along the whole membrane, this is what we call the action potential. Because the ion gradient across the membrane and the density of ion channels is constant along the whole axon, the amplitude of the action potential stays constant along the whole length of the axon.

Your opening offers a very nice point of view +1

@Thawn Could we say that the ions (Na+) moving across the length of the axon cause conformational change in the voltage gated ion-channels and thereby opening adjacent ion channels, inducing a second action potential in new (adjacent) region of axon?

@SanjuktaGhosh Yes, that's how action potential reaches the adjacent areas. Na+ entered inside from one place diffuses to nearby region which causes voltage to rise (above -70mV), and as soon as that reaches threshold limit, action potential is generated in that region while the previous region is busy in repolarizing.

@another'Homosapien' I have just a small addition to your comment: while the influx of Na+ ions causes the depolarization of the membrane and initialized the action potential, the conduction of the potential along the length of the axon happens by the movement of any ion (K+, Na+ and even Cl-) since this is simply the conduction of a charge through a salty solution. Also, this movement is NOT simple diffusion but a directed motion driven by the difference in electric potential.

I am afraid I can't completely agree with you. Since action potential is largely governed by Na+, its movement through length of axon thus plays a major role in transmitting action potential (though other ions may have some effect too as you said). Also, it is indeed simple diffusion of Na+. It also reaches depolarized areas, but though it is already in recovery phase, so it cannot play its role there. But since polarized areas have (almost) no Na+ inside, so its diffusion qyickly generates action potential.

I would like to request someone to join this discussion. @Christiaan if you please, add your views.

@another 'Homo sapien' I was also wondering if the other ions could influence conformational changes.

@SanjuktaGhosh Simple answer- they cannot. I have put a diagram in my answer (first image) which clearly shows that ion channels are only for Na+ and K+. Other ions are either freely permeable (eg: Cl-) or impermeable (eg: amino acid/protein anions) through neural membrane, so they cannot cause conformational changes.

@another'Homosapien' You need to separate two ways that Ions move during signal transduction: 1) across the membrane. As you state correctly, there are specific channels for Na+ and K+ which only allow these ions to pass. 2) along the axon. This conduction is important for the action potential to reach neighboring voltage-gated ion channels and move along the length of the axon.This conduction is not limited by any membrane and therefore all availabel ions (mainly Na+,K+ and Cl-) take part in this conduction. Also the latter conduction is not driven solely by diffusion but also by the voltage.

@Thawn thanks for the suggestion, I added that part too in the answer :)

Descriptive Answer- A nerve impulse is the movement of an action potential as a wave through a nerve fibre. A wave of negative charge on the surface of an axon marks the position, at any moment, of the action potential. Action potentials are self-generated along the axon. The events that set up an action potential at one spot on the nerve fibre also transmit it along the entire length of the nerve fibre. The changes in membrane permeability at one site upset the normal membrane permeability at the adjacent area. The action potential then moves to the neighbouring region of the nerve fibre till it covers the whole length of the fibre. Action potential is propagated along a nerve fibre without any change in the amplitude. It is, thus, a nondecremental (not decreasing) phenomenon. Actually, it would be better to say that action potential does not travel but is regenerated anew in a sequence along the axon.
Explanation- To know why nerve impulse transmission is consistent, lets first know how it is transmitted, for which we should know how it is generated.
Generation-
At rest (no impulse), outside of neuron i.e. ECF (extra-cellular fluid) has more positive charge and inside of neuron has relatively less positive charge or more negative charge. This is maintained by keeping Na+ outside and allowing K+ to move freely between inside outside. It is done by action of voltage-gated ion channels like closing of Na+ channels and keeping K+ channels open, and through Na+/K+ ATPase which transports 3 Na+ outside for bringing 2 K+ inside, and K+ can again freely move outside down the concentration gradient. This results in a resting membrane potential of -70mV i.e. depolarization.
When neuron receives a stimulus, its Na+ channels open and K+ channels close which causes an influx of Na+ which results in more positive charge inside and negative charge outside. This is the action potential of neuron of about +30mV (value varies, I have taken from here, for variations in AP see this). It lasts for less than 1/1000 of a second as Na+/K+ pump  starts working again immediately and K+ channels open and Na+ channels close again to recover the resting potential of neuron i.e. repolarization.

Source
Transmission-
Breaking of resting potential i.e. action potential at one place stimulates action potential at the adjacent place. Actually, action potential is not transmitted through the neuron, it is regenerated at adjacent areas in a sequential manner from one point to another in the axon. Opening & closing of ion channels at one point causes opening & closing of ion channels at the next point by which action potential is transmitted through the axon.

Source
This also explains why nerve impulse does not travel in reverse direction i.e. due to repolarization state of neuron at the previous site during which it cannot transmit any impulse.

Source
Now, for why nerve impulse is consistent through the neuron i.e. why it does not decrease during its course through axon. This is because of equal charge throughout the length of axon. Resting potential is -70mV throughout the axon, and action potential is +30mV at any point in the axon, due to which no charge is dissipated and the nerve impulse remains consistent. For detail about it, refer to the all or none law of nerve impulse which states:

The all-or-none law is the principle that the strength by which a nerve or muscle fiber responds to a stimulus is independent of the strength of the stimulus. If that stimulus exceeds the threshold potential, the nerve or muscle fiber will give a complete response; otherwise, there is no response.

i.e. if a stimulus has the threshold potential (-40mV to -55mV), it will always generate nerve impulse of same action potential (+30mV) otherwise no action potential will be generated and transmitted i.e. it will be consistent everywhere.
Source- Pradeep's : A textbook of Biology for Class XI, chapter 22- Neural control and coordination.
Similar answer has been posted by @Thawn too. I have added some more explanation and citation to this answer.
EDIT 1- You may find an answer to How does a change in the potential across a neuron's membrane get turned into a signal that is sent down the axon? helpful which says:

the sodium gates open the more positive the voltage is, which in turn opens more sodium gates. If a patch of neural membrane is depolarized, the charge diffuses into the nearby patches of neural membrane. This will open the sodium channels of the nearby membrane patch. Now once enough sodium channels open, the neuron will fire a action potential, at this point potassium channels open and potassium rushes out of the cell repolarizing it(making it more negative). Furthermore the sodium gates close at positive voltages which further repolarizes the neuron and prevents back propagation.

EDIT 2- Thus propagation of ions in axon can be, as pointed out by @Thawn, categorised as:
1. Perpendicular to length- this type of movement is responsible for generation of action potential. It is perpendicular to length of axon i.e. through neuron's membrane. This type of movement of ions is governed by voltage-gated ion channels, which ensure charge difference between inside and outside of axon.
2. Along the length- this type of movement is responsible for transmission of nerve impulse through the axon. It is parallel to length of axon. Since there is no membrane in length of axon, this type of movement is thus governed only by diffusion. As Na+ enters cytoplasm of axon, it diffuses to adjacent areas. But since previous (depolarized) area already has high concentration of Na+, so its net movement is towards the next (polarized) area, which becomes the cause for depolarization of that area. This is similar for K+, Cl- and other ions (like protein-derived anions).


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What happens when our muscle tense?
Is the tensing of muscles equivalent to stretching them? I am trying to understand what tensing of the muscles means.

Do you mean to ask the sarcomeric state of the muscle while maintaining posture?

Stretching of muscle means muscle getting relaxed while "if you tense your muscles, or you or your muscles tense, they become tight and stiff, especially because you are not relaxed" (http://www.oxfordlearnersdictionaries.com/definition/english/tense_3). So, tensing can be called a consequence of stretching of muscle.

The course-work tag is nonexistent.  Please don't put it back.  Edits made by hi-rep users are often made for a reason.

@WYSIWYG et al; what is not clear in this question?

@Christiaan "Is the tensing of muscles equivalent to stretching them" What kind of equivalence is the OP referring to is unclear. Tensing is a standard English term and nothing specifically biological.

@WYSIWYG true, it's all about terminology. OP is likely trying to grasp what a regular word means in terms of the biological mechanism behind it. At least, that's what I understand and that's what I've answered. I don't think it should be closed. If it needs closure than the unclear what you are asking seems invalid to me.

@Christiaan That's the point. This question can have multiple interpretations. 1. what you said 2. whether tensing/extending involve same molecular mechanisms 3. whether they are mechanically equivalent... and many more so. That's why I VTCed this as unclear. Plus OP did not respond to comments requesting clarification, for more than a week. Moreover "What happens when our muscle tense" is basically a homework type of question.

Muscles are designed to contract i.e., when they tense they get shorter. Their stretch is a passive process, typically facilitated by antagonist muscles in case of skeletal (striated) muscles. Consider the biceps and triceps antagonists in the upper arm in Fig. 1:

Fig. 1. Left: The biceps actively contracts to bend the arm and is called the agonist. The triceps is inactive and is passively stretched by the biceps, called the antagonist. Right: To stretch the arm, the reverse happens, i.e. the triceps contracts and is now called the agonist. The biceps is now inactive and is called the antagonist and it is passively stretched by the triceps. Source: Pilates Studio
At the molecular level, the tensing of muscles can be readily seen as contraction, as opposed to stretching (Fig. 2):

Fig. 2. Muscle fibers contract actively and stretch passively. The passive stretched state is depicted in the upper panel. Under the influence of ATP (active part) the muscle fibers condense and the muscles contracts. source: Emaze Presentations.
Further Reading
- Do both ends of a muscle contract?


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What is the perisomatic region of a neuron?
In the scholarpedia page on interneurons I encountered the following passage:

The perisomatic domain is responsible for the summation of postsynaptic potentials arriving from all dendritic branches [...]. Thus, the perisomatic region - and particularly the axon initial segment [...] plays a crucial role in the generation of output.

The page, however, does not define what the perisomatic region really is. What comprises the perisomatic region of an interneuron?

Sure mate. If these edits are not to your liking feel free to roll it back. It's just that in the linked Scholarpedia page the term is not explained anywhere. Quoting the relevant section shows that to other users nicely.

In cortical GABAergic cells with local axonal projections, the perisomatic region is defined as that part of the plasma membrane including the proximal dendrites, the cell body and the axon initial segment (Zabó et al., 2010).
Reference
- Zabó et al., Eur J Neurosci (2010); 31(12): 2234–46

Now that I read your answer, maybe I should have deduced it from the name.. However I didn't so... Thank you!

@user135172 - No worries and happy to help - I had to look it up too. Nice question and well researched +1

'Peri' = 'in the region of'
'soma' = 'cell body'
so the perisomatic region is the area in the region of the cell body - I thought the breakdown might be useful in future as 'peri' is used a lot.


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Analysing the ERP (Event-Related Potential from EEG recordings) in terms of the P-300 wave
I am trying to understand how to analyze ERP (Event-Related Potentials) from EEG recordings in focus on P-300 waves.
I have come up with a few questions which I hope you might be able to help with:

I assume that the number of repetitions af the stimulus should give better results, but I am not sure why. On one hand, it should help because avaraged results are usually better in neurosciences. On the other hand, maybe there is an unwanted adaptation effect of the subject?
So, are repetitions wanted in this kind of experiment?
There are time points in which I didn't expect P300 but the brain activity was not 0. I understand that there is always a background activity in the brain, but maybe there is more to it? And if so, are there certain frequenciess that are more likely to happen under these conditions?
When I analyze the data using an avarage response, should I assume anything on the P300 response?
What is the recommended Sample Rate I should use. I guess there should be an advantage for high sample rate for more resolution bur I am not sure about that. Am I right, or maybe a lower sample rate has advantages thst I am not aware of?

So, are repetitions wanted in this kind of experiment?

Yes: repetitions reduce random noise and increase the chance to tell artifact from response. Adaptation is a serious issue, typically becoming apparent by decreasing amplitudes, or even skipped responses. Reading the existing literature and/or performing experiments with various stimulus intervals may help to identify adaptation effects, if any.

...there is allways a background activity in the brain...

Correct - if not, you are either not recording properly, or subject is brain dead.

are there certain frequencys that are more likey to happen under these conditions

If you repeat your recordings and average them out, this is not an issue. Otherwise, yes, FFT analysis shows several frequency bands, dependent on the state of the subject. For example, awake subjects show primarily fast beta activity (13-30 Hz), drowsy or sleeping subjects much slow-wave alpha (1-4 Hz).

should I assume anything on the P300 response?

In short: The P300 response is most commonly elicited in an "oddball" paradigm when a subject detects an occasional "target" stimulus in a regular train of standard stimuli. The P300 wave only occurs if the subject is actively engaged in the task of detecting targets (Picton, 1992).

What is the recommended sample Rate I should use. I guess there should be an advantage for high sample rate for more resolution bu[t] I am not sure about that. Am I right, or maybe a lower samp[le] rate has advantages th[a]t I am not aware of?

The higher the sample rate, the better. Downsampling can always be done later. Typically 1000 Hz is sufficient for fast responses. For a P300 this should already be kind of an overkill.
Reference
- Picton, J Clin Neurophysiol (1992); 9(4): 456-79


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Critical discussion: Gene expression and systems biology allows us to understand the control of complex traits
I'm having a bit of trouble tackling this question. Any help on what I should write about or the points I should mention would be much appreciated. I keep seeing articles about eQTL and QTL are these relevant as well?

What should be the question's title, is it theoretically or what?

In your question's current form, it may not receive many answers.
Please take a look at our homework policy faq.
Here you will find information on how to improve your homework question so your
fellow users will be more inclined to help. Thank you.

@ FloriOn it is Critically discuss

@cagliari2005 thank you im havin a look at the policy now

what's eQTL? Expression quantitative trait loci?

yes its Expression quantitative trait loci?

Turns to be too long for a comment.
If you are looking for explanation of the title/question, than it is following (roughly).
If we get information about gene expression from all different cell types, and extract also interactions between those genes (if a gets higher then b gets lower), this will allow studying multigene traits. E.g., life quality, height, mental disabilities, cardiovascular risks etc. Thing is that for most health problems that stem from single gene variation we already know named gene, or can easily find it out.
More complex issues are often hidden in statistics, links are not so clear. So, for example, autism is described by genetic variations (so far) only in less than 30% of cases or so. In other cases there is no genetic predisposition or strong evidence. Mainly that is so because many genes interact to produce final trait or illness. Looking with microscope one gene at a time will not provide information about it.
You should look into multi-gene traits, maybe pick your favourite illness (e.g. autism) and see how it is hereditary (tip: not fully). Whole-genome sequencing is important tool in tracing such issues because it gives wide overview and a lot of genetic information about patient.

"Looking with microscope one gene at a time will not provide information about it." Never saw a gene under a microscope. You should rephrase that to something like: "Studying one gene at the time will ..."

@cagliari2005 metaphor


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What is the significance of the amplitude of brain waves?
What does the amplitude of brain waves represent and to what neuronal activities is this amplitude related to?
For example, in a hypothetical situation, the frequency of brain waves is kept the same, but the wave amplitude is increased or decreased by some means. What would be the effect on human brain and its activities?
Can resonance related to waves effect human brain waves?

Brain waves are a colloquial term for EEG recordings. EEG recordings are gross potential recordings, in other words, they represent the responses of thousands of neurons together. Much of the background is stochastically determined, meaning it represents, basically, random activity. In other words, oftentimes neurons fire stochastically and they cancel out each others contribution to the EEG, resulting in random ('white') noise.
However, certain parts of the brain do exhibit synchronized activity in certain frequency bands (Fig. 1). Oftentimes a time-to-frequency analysis is necessary to visualize these activities, e.g. by FFT. Certain stages of sleep, most notably slow-wave deep sleep, is characterized by gross synchronized, slow-wave activities across the cortex, showing up in the raw EEG. In fact, simply closing ones eyes has marked effects on the cortical synchronization on the raw EEG. This is caused by the fact that certain swaths of the cortex become synchronized, resulting in more clear responses.
In general, to come to your question, gross potential recordings like EEG thus are plagued by background noise. Synchronized activity increases the amplitude of brain waves and hence increases their amplitude. Amplitude is hence directly related to the level of synchronization. This shows up as larger peaks on the FFT.
What synchronization exactly does to the brain boils down to down to is the classic interpretation of EEG frequency bands (Table 1).

Fig. 1. EEG waves. source: Neurosky

Table 1. EEG frequency bands and their associated mental state. source: Liang et al. (2016)
Reference
- Liang et al., J Sensors (2016), 1831742


text:
Asking for identification of biting insect

Inaturalist says it's a thrip, but my photo isn't very clear and inaturalist tries its hardest, but it can't positively identify everything, and I want to make sure it's not a flea or something else. I do know that thrips feed on the moisture of plants, and that if it is a thrip it likely mistook my bright yellow pants for a flower.
I have bites all over my legs, but mostly the left. Some bites on my midsection but surprisingly few. No bites on my arms. The bites on my legs are mostly clustered together. Anyway, when I pulled it off of my leg, it jumped out of my hand. I came back after showering to find it on the inside of my pants. At the cuffs?/bottom part of the legs of my pants, there were a lot of brown and red smears, and there weren't any bites on that part of my legs. I know that's indicative of bed bugs, so I'm worrying about that too. I need to check my mattress.
I'd argue this is still probably pretty funny.
The location is southern US. The bug is long and small. The light glints off of it. It would have been on me since this morning; I slept from probably 8 AM to 7 PM.
Mom gardens in the yard, though I haven't recently been out there. We also have a dog recovering from surgery, who went through some complications which caused her to bleed and get pus on the floor, which has only been spot cleaned, not bleached yet. She was given preventative flea meds like a month ago. I also cleaned my old beanie babies a few days ago, and while I was doing that a jumping bug landed on me, but it might have been coincidence, because I have been seeing jumping bugs on it long before that. They're dark, long, and the light glints off of them. Which means they're probably fleas, but I don't get a good look at them, so I don't know. Could still be thrips.
Thank you, in advance.
Edit:
The size is tiny. Smaller than a fingernail, but big enough to see. Mom works at an animal hospital; she said she could have definitely brought a flea home. I think it probably is fleas, but I'm still not sure. I'm used to them being smaller than this and thin. The ones I've seen are tiny and round and black

More bugs! On scenic my pants.

Fleas have a very characteristic shape, even when they are squashed they look quite round at the back end, sort of like a flat tear-drop shape. They are also quite thin  when looked at from the top, so I would guess that this is a flea. If you have one, you likely have many.

Does this answer your question? https://biology.stackexchange.com/q/56989/16866

Thrips fly; fleas jump.  The picture is certainly ambiguous, but I'd probably lean flea.


text:
How do muscles help erect the spine?
Muscles of the spine help to support it against gravity. For example, the multifidi interweave throughout the vertebrae and, as I understand, sort of reinforce the spine. So let's suppose muscles help to make the spine more stiff and rigid and this somehow helps it fight gravity.
What portion of support comes from the muscles? Would a spine by itself be able to support itself? In other words, to what extent is our ability to support our spine to remain upright due to muscles and how exactly do they help keep the spine erect in this capacity?

A biomechanical analysis can be done to determine how much support comes from the muscles vs other (skeletal) support structures. Assume the body is standing upright, in static equilibrium. Consider this (over simplified) free body diagram of the upper torso where the sum of the forces equals zero in static equilibrium.

Here the diagram over simplifies the analysis with one general equation: Fsupport = sum of all the weights. Since we are considering only how much weight muscle supports, we deduct Wbones from Fsupport.
A spine by itself would not be able to support itself because the sum of the forces do not equal zero in static equilibrium. (Wgravity + Wspine) > Fsupport.
In reality, each muscle, bone, and organ has many more forces with specific magnitudes in different directions that altogether equal the weight of the specific region of mass it supports. I imagine these forces as many vectors over an area/field. A more detailed analysis would require a program like MATLAB that uses triple integrals in calculus to visualize these forces in 3D. This kind of visualization can help us color code only the muscle vectors which answers your question, "to what extent is our ability to support our spine to remain upright due to muscles," as a percentage of the sum of all the forces input into the program. How the muscles keep the spine erect can be determined from such visualizations as descriptions of directional forces.
For an example of how this kind of analysis is done, see this paper on lumbar spinal support. http://www.uvm.edu/~istokes/pdfs/stab-model.pdf

I disagree on the interpretation, see my answer.

Spine is the only element between thorax and pelvis that can support compressive stress, and thus the weight of the upper body. So the spine needs to support all that.
However, the spine is not rigit enough, and would buckle without muscles. Muscles stabilize it by pulling in a coordinated manner, just as ropes can help stabilize an erected mast. The paper cited by Anna Lu, http://www.uvm.edu/~istokes/pdfs/stab-model.pdf, illustrates this, and states that muscles have both an active role (their relative tension can be tuned) and a passive role (they behave as elastic ropes).
Note however, that this is done at the price of exerting even more compressive stress on the spine!


text:
Are there calcium channel blocking neurotoxins?
I am learning about calcium ion channel blockers (CCBs) and am confused whether there are neurotoxins that are CCBs.

If they exist, what is an example of a CCB neurotoxin?
What animals use CCB neurotoxins as a weapon / defense tool?

This seems like it would be easy to Google. Have you tried?

I did. Several times. I found plenty on sodium. Potassium was easy too. But not CCBs. If you find it, paste the link in bio chat and I can delete this.

Just to clarify, they can be toxic, but it's not clear to me if they are a neurotoxin used by animals in the same way that, for example, tetrodotoxin is.

First hit: http://www.nature.com/nature/journal/v372/n6503/abs/372272a0.html

But they are cone snails. Is that OK?

Yes, my professor mentioned those, although I do not think that she necessarily specified that cone snails contained calcium blockers. Thanks! I can find a bunch of info now

That was so helpful! Thanks again. In future, should I post this sort of "I cant find blah blah" in chat?

You can do that, sure. That's probably a pretty good place to do that. :)


text:
How far can birds see?
I have heard that birds have exceptional eyesight. How far does this mean they can see? What's the resolution like? Are we talking about just vague shapes or something like, at 100 feet, seeing individual hairs on a dog's fur coat?
I've also read that, in general,  primates are the only mammals that have color vision. I know birds are not mammals. Is it common for birds to have color vision as well, like primates?

http://en.m.wikipedia.org/wiki/Bird_vision

This is a massive topic, with so many exceptions any short answer would probably pointless. Is there a specific kind of bird you had in mind? Even simply covering Raptors would fill a chapter of a textbook. Also, where did you get primates being a special case of colour vision? Thats false. Even dogs, famously colourblind, are thought to have two pigments for colour vision (not red, just blue and yellow).

primates are trichromats, many other animals (most mammals) are dichromats (can see color, but less well than primates). Birds, on the contrary, are tetrachromats and can see color better than we do. Hence your 2nd statement is incorrect. The first question needs refinement.


text:
How many different states can the femur and lower limb be in?
Often the knee can be thought of as a hinge joint. However, when it flexes, the knee permits the lower leg to rotate. So it is not a pure hinge joint in absolute sense because it permits more range of motion then a pure hinge joint.
Since the hip joint is a ball and socket joint, this means that, relative to the pelvis, the femur can also rotate.
In short, both have the capacity to rotate, to some extent independently.
Each leg has one femur and one lower leg. Each can be in one of three states.

Neutral
Inwardly rotated
Outwardly rotated

Basic math tells me that means 3^2 = 9 states
This seems like a small number, but if you then consider both legs that gives you 81 possible states.
I presume not all of these are possible. I assume that, if we exclude deformities, birth defects, or growth defects, in general there must be some kind of consistent patterns that humans tend towards.
What are the most common relative orientations (as defined above) for the femur and lower leg?
For example, if the femur inwardly rotates, does the lower leg automatically rotate inwards?

You have probably meant 18, not 81 states for both legs.

@Jan Stan mean 9^2, that is 81 possible combinations using his argument.

If one leg can be in 9 positions, wouldn't you say that both legs can be in 9 additional positions, so 18 in total? Anyway, if you say that one leg in one position and the other leg in another position make a new combined position, you can say 81.

In anatomy, the term movement usually applies to a specific bone in a specific joint, not to the limb. It is said "the flexion of the femur in the hip," and not "the flexion of the leg." So, if you rotate the femur in the hip inwards, your lower leg will also rotate inwards, but this does not "count" as an additional movement.
Possible movements in the hip joint include (TeachMeAnatomy):

Flexion
Extension
Inward rotation
Outward rotation
Abduction
Adduction

There are known possible movements in the knee joint and in the ankle. After all possible movements in these joints, your feet will be in different positions. It then depend on you what you consider a different position. You can have a flexed hip and flexed foot, or an extended hip and flexed foot - is your foot in the same or different position? From the anatomical viewpoint it is in one (flexed) position in both cases.


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When a muscle contracts, does it store potential energy like a spring that is released upon relaxation?
A colleague of mine who mainly focuses on clinical chiropractic work claimed recently in a book he wrote that muscles in the pelvic floor have "elastic recoil."
What he means by this is that a muscle behaves like a spring and, upon relaxation, releases potential energy somehow.
I am highly skeptical of this and want to verify if this is true or not.
When a muscle contracts, does it store potential energy like a spring that is released upon relaxation?


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Do secretomotor neurons activate for secretory cells due to the absence or presence of water and electrolytes? Why?
I read this passage in a book called Integrative Action of the Autonomic Nervous System by Wilfrid Jänig. In this book, he states

Reflex pathways involved in the regulation of secretory cells and/or local blood vessels (arterioles) have been much less explored than enteric reflex pathways that are involved in regulation of motility. This applies to the organization of the reflex pathways connected to the mucosa and mucosal blood vessels as well as to their coordination with the reflex pathways that are integrated into the regulation of motility. Activation of secretomotor neurons stimulates epithelial cells to secrete chloride ions into the intestinal lumen, taking with them sodium ions and water. The physiological stimuli that induce a reflex activation of the secretomotor neurons are mechanical stimulation of the mucosa (shearing stimuli) and chemical stimuli (e.g., glucose or proton ions). The most important activator of the reflexes is the absorption of water and electrolytes by nutrient transporters. For example, glucose transport involves the Na+-transporter and each molecule of glucose is accompanied by Na+, counterions and water. Absorption of 100 grams of glucose is accompanied by 1.8 liters of water (Furness 2006). The purpose of the secretomotor reflexes in vivo is therefore to preserve whole-body fluid balance. The intraluminal stimuli triggering secretion appear to be the same as those causing enteric motility reflexes in the intestine. The stimuli activate the IPANs via enterochromaffin cells (EC) in the mucosa, which release 5-HT and excite the IPANs, or possibly by other cells releasing CCK or motilin (Figure 5.13). The IPANs excite enteric neurons synaptically by release of acetylcholine and substance P. Intraluminal toxins, such as cholera toxin, lead to pathological activation of secretomotor neurons. This overwhelms the fluid-balance role of the reflexes, causes copious fluid loss and, if unchecked, death, because the fluid ultimately comes from the circulation. Secretomotor reflexes elicited by intraluminal physiological stimuli are always paralleled by enteric vasodilator reflexes mediated via the enteric neurons.

I am specifically confused by the sentence

The most important activator of the reflexes is the absorption of water and electrolytes by nutrient transporters.

Is he saying that the secretomotor neurons are triggered by the absorption of water and electrolytes? Or is he saying the absence of absorption triggers the reflex?

I read the text without having looked at your specific question, and I was confused in much the same way. I'm looking forward to the answers.


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Barr body. How does it work?
Barr's body is a spiral X chromosome. If I'm not mistaken, one random chromosome (a healthy woman) is inactivated in each cell. Which X chromosome is inactivated in a given cell is random. I've heard the example of a tricolor cat. The patched coloring is caused by the fact that  cells responsible for the color of each patch contain another inactivated X chromosome.
But what if a girl is a carrier of the Daltonism gene, why isn't she sick if a chromosome with this gene can be inactivated in some cells?

Hi silly school girl. There are 5 question marks in the question, that's about 4 too many. Try to post a targeted, clear question instead of stacking up a bunch of questions.

Thank you for your comment, I'll take it into account.

Get better? It was necessary to reduce a question a little. Thank you for your friendly attitude to young and naive students.

Like you said the sexual X chromosome inactivation is random in each different cell, this means women have some cells with the maternal x chromosome active and others with the paternal x chromosome active. Now if a woman carries the daltonism gene mutation (heterozygous for color blindness) she can actually manifest signs of the disease if the retinal cells randomly silenced the healthy x chromosome instead of the mutated one in more cells compared to the opposite pattern of silencing (meaning she can present daltonism out of pure bad luck).
It is worth mentioning that the magnitude of this disease will never be as strong as it presents itself in males since women (even the unlucky ones who present signs of daltonism) will always have the protection of a certain percentage of retinal cells with the healthy x chromosome active. The only way a woman could have classic daltonism to the same extent as a male is if she presents the color-blindness gene mutation in combination with Turner syndrome.
In conclusion recessive X-linked diseases aren't "everything or nothing" since woman could present signs in function to the number of cells that randomly inactivated the healthy X chromosome. They will fully express themselves in males all the time though.
References:
Scitable by nature education - Q&A
X chromosome inactivation - Nature education