text:
Why does this oxygen duration chart have increased times above 30,000 FT MSL?
This oxygen duration chart from an airplane shows the amount of time a pilot can be on oxygen at a specified altitude (in 1000s of feet).  For example, the chart shows two pilots able to cruise at a cabin altitude of 35,000 FT MSL for 182 minutes using a diluter demand system or 192 minutes using 100% oxygen.
I have one question.

Why does the oxygen duration chart show increasing times above 30,000 FT MSL?

“Why does using 100% oxygen provide greater time...” It does not, the bold numbers (for 100% oxygen) are all lower than the lighter face numbers - as explained at the bottom of the chart.

You're right.  I've updated the question.

I wonder if someone on the Physics stack would know. I can't think of a biological reason this would be the case, but maybe it has to do with the physical properties of the gas in the storage containers. Like, maybe at lower altitudes, more of the stored oxygen remain in the system because of the higher atmospheric pressure.

The bottle is regulated to output 75psi to all the passengers on the plane.  It could be the difference between PSIA and PSIG.  I'll ask them.  Thanks.

This might be worth asking on the aviation stack...

This is related to the diluter demand system, O2 present in the cabin, and tracheal pressure.

The diluter demand system is designed to compensate for the
short-comings of the continuous flow system. It   gives the user oxygen
on-demand (during inhalation) and stops the flow when the demand
ceases (during exhalation). This helps conserve oxygen. Additionally,
the incoming oxygen is diluted with cabin air and provides the proper percentage of oxygen, depending on the altitude. This system
is typically used at altitudes up to 40,000 feet.

Source: Oxygen Equipment: Use in General Aviation Operations - Federal Aviation Administration
When you get at altitudes higher than 35,000 feet you're more or less totally reliant on the oxygen provided by the diluter, that's why the diluter demand is very close to the cruise time. If there's low air pressure in the cabin above 35,000 feet there won't be enough oxygen for normal body function, and you run the risk of becoming hypoxic within half a minute.

Toe of Useful Consciousnees (TUC) per Effective Performance Time (EPT)

Look at the chart below:

Tracheal oxygen partial pressure starts at 149mm. Hg for sea level and can drop to 20 at 40,000 feet. If oxygen is given according to the % supplement O2 required for inspired air, the tracheal pressure stabilizes back to what it is at sea level. Above 30,000 feet, tracheal oxygen partial pressure cannot be maintained at 149mm. Hg. Therefore you need to use the diluter longer to at least maintain it close to 149mm. Hg. Or at level where the mm. Hg. isn't extremely low.
The required mean tracheal oxygen partial pressure can be different at the same altitude depending on the liters of O2 per minute BTPS (Body Temperature and Pressure Saturated) being inspired.
Source: Introduction to Aviation Physiology
Fore example, according to 14CFR 23.1443:

(ii) At cabin pressure altitudes above 18,500 feet up to and including
40,000 feet, a mean tracheal oxygen partial pressure of 83.8 mm. Hg
when breathing 30 liters per minute, BTPS, and with a tidal volume of
1,100 cc. with a constant time interval between respirations.
(2) For each flight crew member, the minimum mass flow may not be less
than the flow required to maintain, during inspiration, a mean
tracheal oxygen partial pressure of 149 mm. Hg when breathing 15
liters per minute, BTPS, and with a maximum tidal volume of 700 cc.
with a constant time interval between respirations.

So, at above 30,00 feet you will use most of the diluter demand oxygen to preserve tracheal pressure until the plane has stabilized. At lower altitudes the diluter demand is lower because you can reach safer altitudes faster.

Doesn't this mean you should use more oxygen above 30,000 FT MSL?

The % required O2 oxygen (inspired) needs to be 100%. That is because if you use the diluter system the air in the cabin is too thin to provide any meaningful O2. For the diluter system the incoming oxygen is diluted with cabin air and provides the proper percentage of oxygen. At 30,000 FT MSL oxygen in the air too thin and you're going to use more of O2 provided by the diluter.

Why then does the chart show in an increase in oxygen available time above 30,000 FT?

Oxygen in the air will be too little but the oxygen available from the diluter will increase above 30,000 FT. O2 is too thin at that level to maintain tracheal pressure and % saturated O2 in the blood the availability of O2 will increase. If you're flying at 35,000 for 182 minutes, you're going to need 182 minutes on diluter system and some extra so that the shift to lower altitudes minimizes the effects of altitude acclimatization.

I wonder if the physics stack had a different answer, or a better one. If they did and you could provide a link I would love to see what they answered with.

I don’t quite understand it all.  I’ll have to think about what you said.  Here is the link to the Physics question. https://physics.stackexchange.com/q/578377/274173.  I’ll probably ask in the aviation side too.

If you got time check the Introduction to Aviation Physiology I linked. It has extensive information which might help in elucidating some of your questions or confusions. It comes from the FAA.

Thanks.  I will do that.

Are you saying that since the tracheal pO2% is lower at 35,000 FT MSL (132 vs 149) we don't need as much O2?

Let us continue this discussion in chat.


text:
How is sexual selection evolutionarily stable?
It seems like in any population subject to evolutionary pressure, sexual attractiveness will inversely correlate with other kinds of reproductive fitness. If you see a peacock with a small tail feather, this is information that it is likely above average in other areas, because otherwise its genes would already have been wiped out. So intuitively, you would think that it would benefit individuals to find less conventionally attractive mates.
So far, I have encountered two possible explanations for this. One idea was that the things that make an animal attractive correlate with evolutionary fitness. I'm not an expert here, but it feels like the correlation here will diminish over time as soon as there is direct pressure to increase attractiveness.
The other, more convincing, explanation was that it is advantageous to produce attractive offspring. So, there might be a feedback loop here where if members of a population care about sexual attractiveness more, then attractiveness would confer a greater advantage, making attractive offspring more important, increasing the evolutionary pressure for individuals to choose attractive mates.
Can someone give an intuition (or better, the relevant math) for why these two latter effects dominate my original intuition? Or are there other effects at work here?

If your 3rd paragraph is true, isn't your 2nd paragraph also true?

Good point, I guess I meant that sexually attractive features (e.g. big muscles) might correlate with advantages in individual (i.e., not sexual) selection.

first off you are talking about runaway sexual selection, run away sexual selection works because attracting mates matters MORE than individual survival. An immortal survivally perfect creature that cannot mate is an evolutionary dead end and might as well not exist where its genes are concerned. A bright red neon sign on your back that draws  the attention of potential mates is an advantage as long as it attracts mates more often than it attracts predators. Coincidentally this is why so many sexual displays are things you can turn off, even a peacock can fold its tail fan down. These displays often exploit existing attention  factors, like eye shaped objects, bright contrasting colors, loud noises, ect, things organisms are already predisposed to pay attention to.  Of course once neon sign displays exist your second idea comes into play, once neon signs are in play a female is best served if her own male offspring and descendants also have neon signs, which makes attraction to the  neon signs (and thus the genes making them) an advantage.
For normal sexual selection both your ideas also come into play, likely more often. common attractive features are things like size, symmetry, health, or excess energy, direct signs of fitness.
Most of the time displays reaches a point of stability where the cost is balanced by the attractiveness, this is how most displays work.  But sometimes runaway selection can drive it past the point of no return, where the cost of reducing it is so high (lack of mates) the only winning strategy is to invest more and more, on and on until the cost is so high you never get a chance to mate.

You gave the example of a brightly colored male bird... and what about the females? The are well camouflaged and optimally fit to evade predation. So, even if 50% of males are caught and eaten due to theor bright colors, the demography stays the same.
The species as a whole is the same with or without the bright feathers.
The sexual display amplifies the pressure for fitness selection, to obtain more food, evade predators better, and invest more energy in sexual lures, horns, feathers, song.
You are right, if a predated population places sexual selection on the females, it is counter productive. Fish, birds, insects, frogs, they nearly always have super robust camouflaged females and males that fight and display their high fitness, except parrots and reef fish.
Birds are so good at evading predators and flying to food, that even the females are colorful in some species i.e. parrots, and thats a less easy example, why do female parrots risk having no camouflage? Perhaps their climate doesnt provide enough selection.
www.google.com/search?q=sexual+selection+graph+feathers+demography&tbm=isch&ved=2ahUKEwjN77n5lobsAhUPWBoKHSgGAcMQ2-cCegQIABAC&oq=sexual+selection+graph+feathers+demography

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text:
Probability of all alleles represented in a sample
I'm trying to wrap my head around some formulas presented in the 1992 paper from Chakraborty Sample Size Requirements for Addressing the Population Genetic Issues of Forensic Use of DNA Typing, but I have not been able to.
Specifically, the right hand side of formula (16) and it's relation with formula (13).
$1-\sum\limits_{i=1}^{k}(1-p_{i})^{2n}$ (13)
$[1-(1-p)^{2n}]^{r}\geqslant1-\alpha$ (16)
Formula 13 indicates the probability, for a locus with $k$ segregating alleles whose frequencies are contained in the vector $p$, that all alleles are represented in a given sample of size $n$, and the right hand side of formula 16 indicates the probability of $r$ alleles to be represented in a given sample of size $n$.
First of all, why, based on 13, the expression inside the summation indicates the probability of an allele of frequency p, to remain unobserved in a sample of size n?
I tried to understand this from the Hardy-Weinberg equation but did not have any success.
Second, Why to take the expression in (16) to the r'th power?
Which biological concepts am I missing?

I don't think there is any biology here, just concepts of probability

@BryanKrause Probability in this case is been used as a tool for a specific application, like in every other problem involving probability. The main issue here (for me) is to understand the underlying biological concepts to give sense to, for example, why is it that the power in (13) is 2n. Is not a problem related to solve for n in (16) or something of that nature, I'm more interested in understanding the concepts that dictate the reason(s) why the expressions adopt that form to estimate the probability of interest.

@BryanKrause, I absolutely agree that these are probability questions not pop gen questions per se. If I wanted to answer anyway, is it your opinion that (1) answering here would be harmless or (2) we should tell OP to go away, post it somewhere, leave a link here, and close it?

@BenBolker Grey area. I think if you want to answer the probability question here I'd appreciate if you narrate it with the biology, and I think that will overall be well received.

I'm going to strictly answer the questions, rather than step through the proof, because it involves a lot of formatting that I'm not familiar with.  Other folks are welcome to edit this!
Equation 13
This equation assumes a diploid genotype, given by the $2n$ power with $n$ individuals.  For anything with greater ploidy than mono-, it's mathematically simpler to determine the probability that an allele is not present.  As an example, see this calculation of a triploid Hardy-Weinburg equilibrium equation.  Using this simplification,
$P(single$ $allele$ $not$ $present)$ $= (1$ $- P(allele$ $present))$ ^ $(ploidy)$ ^ $(n)$
$= (1$ $- P(allele$ $present))$ ^ $(ploidy$ * $n)$
With $k$ segregating alleles, each allele has its own non-presence probability.  The probability of total non-presence is $1 - (sum$ $of$ $P(each$ $non$-$presence))$
Equation 16
In this equation, the author describes the probability that all alleles are present at a given frequency.  These allele presences are independent of each other and therefore multiplicative.  Since $P(allele$ $present)$ is vectorized, this product can be simplified to $^r$

Tip - to format equations, you should use the $ symbol rather than the grave accent.

Aha, thanks!  That's a lot better :)

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text:
What is it called when a dead flower is rotted away and only the veins remain?
I've spotted a flower that is dead:

It looks like most of the tissue has rotted away and only the veins remain.
(Sorry, I don't know the proper name for flower veins).
What is the technical term for this phenomenon?

Retting could be a valid term. But I think that the term "skeletonization" is more common. For instance here is a link to the University of Arizona showing how you would take a flower or a leaf and remove all components, leaving the veins:
Skeletonization
I think that "retting" is confined to the industrial harvesting of plants like flax. I would use the term "skeletonization" to include acts of botanical science in which the veins alone were sought. For instance in the above link the botanist Frederick Ruysch published a method of chemical skeletonization in his book Adversariorum Anatomico - Medico - Chirurgicorum Decas Tertia in 1723.
It also became a form of art and craft in the late 1800's in the United States; "Skeleton Leaves & Phantom Flowers" was published by E.Parrish. I would assume that the end result as a craft would be to display the skeletonized flowers or leaves on a display board.
As a natural, observed event the term skeletonization could be used. But if the  underlying causes such as fungus were considered then both rot, or fungal rot, and skeletonization might be used together in the same sentence. The wikipedia entry skeletonization considers animal decomposition. It's a reasonable and analogous step to use the same term for plants that decompose and leave fibres rather than bones.

I learned something new today! +1

Thats is great! I enjoyed researching it!

I have heard the process that leads to this called retting.


text:
Orange tipped plant found in Carden limestone plains of Ontario
What is species is this plant?
Found in the Carden limestone plains of Cameron Ranch (near Orillia, Ontario, Canada) on September 9th, 2017.
It is located in an old bog that seems to have sphagnum peat moss (to my untrained eye).

It's an odd angle, but I think the plant/flower is an Indian Paintbrush (Castilleja coccinea). It is found in Saskatchewan, Manitoba, Ontario, and Nova Scotia.

They're in Alberta, as well.

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text:
Spruce growing high up in a maple trunk: Can a partially rotted trunk completely sustain another tree?
I've come across a spruce tree that is growing 15ft up in the crotch of a sugar maple tree:

According to Google StreetView, the spruce has been there since before 2007 (over 10 years ago!).
I've seen other trees growing out of rotted stumps or in trunks near ground level before, but I've always just assumed that the roots of those trees reached down to soil -- in one way or another -- to get the nutrients they need for survival.
But with the subject tree, it's so high up that I would assume that that the roots do not have access to any soil. It's my guess that the spruce is getting all of its nutrients from decomposed wood in some rotten portion of the trunk.
I didn't know biology worked like this. I wouldn't have guessed that a live, partially decomposed trunk could contain 100% of the nutrients that a tree needs to survive for 10+ years. I know soil is made, in part, from decomposed wood, but it's my understanding that there are a lot more ingredients too.
Can the decomposed wood in a partially rotted trunk completely sustain a tree?

keep in mind the biggest nutrient it needs is water, which the tree will catch enough of as long as the spruce stays small, as it grows however this will cease to be true.

Is the maple rotting? It would be interesting if the spruce was parasitizing it somehow.

@canadianer I don't know for sure that the trunk of the maple is rotting. It's just a best guess, since the spruce needs to get food from somewhere, right? I'd probably get arrested if I drove up with a ladder, propped it up against this person's boulevard tree, and started rummaging around. Wish I could though!

@canadianer Since your name is canadianer, you might be interested that this tree is in the GTA.

Yes you'll need a flashlight and a diversion… ;)

Note  This answer makes the presumption that the crotch in the maple's trunk is indeed a breach through its bark, and does reach the inner woody tissues.

The heartwood of most trees consists of the dead connective tissues, xylem, which surrounded the cells that once formed the living layer of phloem under the protective bark.  That connective tissue itself mostly cellulose, and is a polymeric chain of glucose i.e. sugar molecules bonded and linked in such a way as to make them indigestible to most lifeforms.
Certain bacteria and fungi, among others, are able to do so, and they are among the first responders in the decomposition scene.  When these microbes, often present in the gut of various insects, are able to break down the woody fibers into forms that permit their re-use by other plants, the detritus is comprised mostly of carbohydrates, alcohols, carbonic acid, and water.  Phosphates and various other trace elements which were present in the cells of the woody tissues are released also.
Later, visiting birds and mosses will further augment the ecosystem, adding nitrates and various salts — potassium, sodium, chlorides, and the like.
Another thing that needs to be considered is the drainage.  Where does the excess water go?  Pressure on the capillaries inside the xylem of the maple should be able to channel some water downwards, but not much will exit through the roots.  I've never heard of such a thing.  The hole in the maple will widen and exacerbate, deepening the rotted area, but it will be acidic and somewhat saline due to the lack of drainage.
Can it completely sustain another tree?  As the ecosystem flourishes, probably; unless the new tree has special requirements for the pH or salinity of its soil which are not maintained by the rotten wood, then it should be able to gain enough nutrition in the form of nitrates, phosphates, and water, but not all of that will come from the other tree directly.
The branches of a tree will only grow so large as can be sustained by their root system, of course.  The limited space in which this little sapling has taken root will result in the less than maximal form that you see in the photographs.
So, in conclusion, that spruce will probably not thrive by any means, but it will manage to survive.  Spruces do favor more acidic soils — lower pH — than many other trees, so it has that going in its favor.
That much is obvious, I suppose:  ten years, and it no larger than a four–year shrub.
There is a problem if all this occurs inside a tree which has not fallen, however.  Usually, the outer bark of a tree protects it from such decompositional actions, because the inner woody tissues of most trees do not contain adequate chemicals to deter insects and fungi from chomping or ‘mycelizing’ their way through the heartwood.
Eventually, the maple will either need to be cut down or will be weakened enough that it will collapse.

Thorough and interesting answer. But please add some references to support your claims. Thanks.

Well, holes in rotting trees are not only going to contain rotten tree matter (aka compost :p), but they will also slowly gather fallen leaves, dead insects, dirt, dust and other debris. Even minuscule layers of these substances will essentially form a pile of "soil" with nutrients and minerals needed by the tree.

In fact, spruce trees are capable of growing on relatively thin soils and often grow with very shallow root systems[Source].
B/c so little of these substances can exist there, however, the tree will never grow large and will likely not live nearly as long as it's species' mean lifespan. But sometimes nature does funny things.

So it's not unheard of for plant to survive in these conditions.
Plants that grow (harmlessly) on other plants are called Epiphytes, and they derive moisture and nutrients from the air, rain and debris accumulating around them.

Though epiphytes are much more common and diverse in the tropics, common epiphytes that those of us living in less tropical places might recognize include mosses and lichens (and to some degree ferns).

It is true that many tropical epiphytes have modified biologies/anatomies to capture and mineralize nutrients from air and rain water (Yoon Lee,
 n.d.), but some epiphytic species do develop roots to take advantage of soil/debris/decomposed materials that have accumulated. (Cardelus & Mack, 2010)

Yoon Lee compared these accumulations of "arboreal soil" to terrestrial soil and found there were no significant differences in all primary nutrients between epiphytic and terrestrial soils, but that pH between the two soils differed significantly.

Citations:

Cardelús, C. L., & Mack, M. C. (2010). The nutrient status of epiphytes and their host trees along an elevational gradient in Costa Rica. Plant Ecology, 207(1), 25-37.
Lee, Yoon. n.d. Nutrient contentand biota of epiphytic and terrestrial soils in a tropical forest in Moorea, French Polynesia. unpublished. UC Berkeley.

In the Hoh Rainforest in Olympic National park, there are many "nurse trees" and "nurse logs"; the latter are trees that have fallen and now act as a nutrient source for smaller trees growing on them.

Some of the larger trees' roots find their way into the soil, which facilitates their growth, but some smaller trees do not.

...but it's my understanding that there are a lot more ingredients too.

I would not say 'a lot', but rather 'some', mostly water. The log provides most of the nutrients the new tree needs, the rest being supplied by rain, fungi, mosses, leaf litter, etc.

I think you should be more detailed with regards to the nutrients:  Fungi can't, so far as I know, obtain elemental nutrition except from their substrate; some mosses can, via symbiotic bacteria, fix nitrogen from the air; rain may contain in dissolved state whatever compounds were present in the raincloud where it formed — sulfur, nitrogen, halogens, et al.

@can-ned_food - I intended to say that these (fungi, mosses, leaf litter, etc.) can break down the tree and free as well as provide nutrients. If you're looking for halogens in my answer, you'll need to supply an answer of your own. I'm definitely not a botanist.

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text:
Green insects on gooseberry plants
I have green insects that eat the leaves of my gooseberry plants:

Location: Toronto, Ontario.
The insects seem to only eat the leaves of the plants (not the fruit).
They have been present since mid-May, and I expect that they'll be present until mid-June, based on past experience.
They do not have spots.

What is the name of this insect?

The species name of this insect is the gooseberry saw fly. There are three related species, I think this is the pale spotted gooseberry sawfly because it has a pale green head. They usually have black dots as well, but this might develop when the larvae grow. At least, this is what I observed once in my garden.


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Volunteer/seedling in Toronto garden
What species of plant is this?

Location: Toronto area (Ontario, Canada)
Date: July 7, 2022
Conditions: Acid soil in shade
Height: Approx. 11 inches
Description: Younger leaves resemble tomato leaves. Main leaves are serrated. Opposite.

August 25, 2022

September 6, 2022

I think the leaves are simple pinnate and alternating, though it is hard to tell from the photo. I want to say Dahlia, but the leaves don't look quite right.

@bob1 Thanks. If you click on the photo a couple of times in your browser, it should show the full photo, which is quite large. From there, you can zoom in. When we do that, I think it's a bit clearer that the leaves are opposite, not alternating.

Thanks. Opposite is correct. Not Dahlia - too hairy.

Can you post more photos of this plant? Closeups of the stem, roots (if you decide to kill or move it), and both surfaces of the leaves may help; however, flower photos are likely necessary for you to get a definitive identification (ideally from multiple angles).

Nice updates. Should help quite a bit.

I think that this is one of the beggarticks, in the genus Bidens. There are several possibilities in your area, including B. connata, B. frondosa, and B. vulgata. I think more detail would be needed for a finer identification.
The main features pointing me this way are the opposite, compound leaves, and the distinctive shape of the leaflets (ovate-lanceolate, serrated margins, attenuate tips).

Based on the number and type of bracts beneath the flowering head (aka "calyculus bractlets", about 8, not "foliaceous" but merely herbaceous), and the shape of the leaves (3-foliate), I think this is probably Bidens frondosa.


text:
What is atrial fibrillation?
I am wondering exactly what a-fib is (causes and symptoms).

I would really appreciate having a sample of an EKG with it (because in my limited research, I have found it nearly impossible to find just a sample piece of an EKG that has a-fib on it) with your answer, so I can actually get an idea of what it looks like. With the sample EKG, I would love to have a normal one beside it so I can kind of analyze the differences between the two.
Note: This is not and never was a homework question!

http://en.ecgpedia.org/wiki/Atrial_Fibrillation pretty much has exactly what you are after.

@jonsca How about linking one of the images here and make it an answer?

@Chris My point was more that this was answered quite well by the first hit on googling "atrial fibrillation ekg".  Wikipedia's chart is actually better, but I don't want to just copy large quantities of information from there.

I know this problem. But you can at least earn the reputation for that. Write a short answer, add a picture, reference to the Wikipage. I think this is perfectly fine.

@Chris I would not mind at all if you (or anyone else) wanted to take that opportunity.

This is NOT a homework question, guys! I was asking out of sheer curiosity.

A human heart can be viewed as 2 hearts, the left and the right heart, each consisting of an atrium and a ventricle. The atrium's function is to fill the ventricle with as much blood as it can and the ventricle then pump the blood away. Also there is a system of valves to control blood flow on each side. Basically this is how our heart works.
Now, to make this system work we need to have a coordinated movement of atrium and ventricle, that is, first atrium is filled, then it pumps blood into ventricle, valve closes and then ventricle compresses.
The movement of heart muscle causes currents that can be measured (this is the ECG pronounced EKG). These currents are representative of the movements of atrium and ventricles are expressed respectively as p waves (for atria) and qrs (for ventricles).
It is the case that atria are not very important and sometimes they can stop working properly. They now longer have coherent movement and stop helping to pump blood into the ventricles, but they still move. This event is called atrial fibrillation.
From this explanation one can expect that no longer p waves will be identifiable in the ecg, but instead a random noise overlapping with "normal" qrs representing normal ventricular movement. The movement is actually not exactly normal, because the ventricular contraction due to atrial fibrillation now occurs at random times, that is qrs complexes occur with random spaces between them. The explanation for this is rather more complex: there are bundles of specialized cardiomyocites with different frequencies of depolarization. The fastest ones are on SAN and basically guide the whole heart rhythm through specialized bundles. When you have atrial fibrillation, the depolarization signals no longer come from these preferential bundles, but from any part of the atria at random. This causes the ventricles to initiate motion at irregularly spaced intervals.
I've included a photo of a normal rhythm and a atrial fibrillation side by side, but I hope you can use this explanation to find better ones by yourself in the web.
Note: don't confuse atrial fibrillation with atrial flutter. Flutter is a faster paced regular (therefore organized) atrial movement. It will appear as a saw-tooth shaped wave with regularly spaced qrs complexes.

Hope this helps.
Causes of atrial fibrillation are numerous, bur mainly high blood pressure, vascular disease, heart and lung disease among others. It can be asymptomatic in most cases or presenting with the symptoms of its underlying cause.
Please refer to http://www.webmd.com/heart-disease/atrial-fibrillation/heart-disease-atrial-fibrillation-basics for a quick overview.

To add to your answer I think you mean P waves aren't visible in AF and also old age could be added as a cause in isolation - it's very very common in the elderly

Yes, thanks you are correct, it was a typo. I've corrected it now.

Good answer. I disagree only with this: It is the case that atria are not very important and sometimes they can stop working properly. Atrial kick contributes 15-35% to the volume of blood in the ventricle. This extra volume in turn increases cardiac output by a similar 15-35%. That can make the difference between living well and living with congestive heart failure.

The relationship between the HF and AF does exist, but is only partially understood (see http://circ.ahajournals.org/content/119/18/2516.full), and although atrial systole contributes to the loss of cardiac output, it is only one of the many possible reasons for it.


text:
How can I simulate heart electrical activity in a 2D plane?
I am not a biologist/medical student, I study software engineering. But I really like when medicine and engineering hold their hands together to achieve great things.
As a side/toy project, I was looking at creating a basic app that allows the simulation of the electrical conductivity of the heart (eg in the Left Atria), and to simulate some rotor drivers and fibrosis.

I got inspired by this Android App.
This app almost does what I want. Ideally I would like to extend this app to allow a more accurate model, allow fibrosis, allow pacing (i.e. manual intervalled stimulation of one point on tissue and see if it reveals rotors), and of course, allow manual ablation.
Unfortunately, this app has 2 issues for me:

I didn't find the source code of it, and I would not want to reverse engineer it and use it, even if just for fun, without any kind of consent. As a matter of principle, and I believe that all these kind of research should be open to the public by default, that's how Humanity evolves.

I don't know if this app is "too simplistic" in this simulation, I would like to use a more accurate model if possible (and still have this real-time simulation). I have seen tools such as OpenCARP, but they seem too heavy for a lightweight app, and I could not find a single tutorial showing how to make a 2D simulation of this kind of electrical activity, much less to do it in real-time and with user interaction. You can see that this app's rotors are not very accurate, as they do not depend on the tissue they conduct on, you can see as the simulation progresses, rotors are always generated at different spots, while in the real world rotors have a fixed location that corresponds to their core (which does not move constantly!), as depicted bellow:

So, it all boils down to: I will create my own app, inspired by that one, I will make its code publicly available, extend a few features and try to design it in a modular way such that other people can then easily extend it.
My ultimate question here regards the electrical physiology part of these simulators. And I need your suggestion: What is a good model for the electrical propagation, that I can use, that accounts for "fibrotic" obstacles, multiple rotors, etc.?
From a paper I have read regarding this topic, I found out they were using this model and obtaining some satisfactory results. Paper from that model.
I am still reading their paper, but their model seems complex to implement and probably will not result in any kind of real-time simulation (it seems it can take hours to simulate a single second of electrical activity).
So I would like to ask you what is the best model I could use for my app, that allows for a more real-time (not necessarily real, but at least allowing some 10fps, similar to the app), dynamic features (like different conductivity in different cells, fibrosis, manual pacing, rotors, etc.), being more accurate than what this app looks like?
Thank you!


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Besides hemoglobin, what proteins are present in red blood cells?
I knew that mature red blood cells (RBCs) lacked nuclei, but I wasn't aware until just now that they also lacked ribosomes and mitochondria. Most cells in the human body all contain a common laundry list of housekeeping proteins and RNAs (including mitochondrial proteins and ribosomal RNAs), but I guess RBCs lack a number of them. Do they still have all of the other organelles? Obviously hemoglobin (and to a lesser extent carbonic anhydrase) makes up a large portion of the dry weight of RBCs, but are other proteins still present? If so, what are their relative abundances?
For example, do red blood cells have any of the normal metabolic (i.e. ATP producing) proteins? Obviously they don't have any of the TCA cycle proteins, but do they still have the glycolysis ones?

Afaik they use mostly glycolysis to produce energy, so proteins of that pathway must be there...

Reticulocyte stage is when the ribosomes are still present and after that no new protein synthesis occurs. However RBCs have a lot of proteins and major proteins other than haemoglobin are cytoskeletal proteins and ion channels/pumps (In fact, cytoskeletal proteins are more abundant than haemoglobin). It is the Na+-K+-ATPase that consumes most ATP. As you correctly identified the RBCs produce ATP via glycolysis and glycolytic enzymes are also present. Note that deficiency of pyruvate kinase leads to haemolytic anaemia.
For a detail on the proteins present in human RBSs, see this paper. They have studied the RBC proteome by ion-trap MS. The top 5 proteins (from Table-1) are:
No.    Protein description              Molecular mass (Da)    Gi Number    Sequence     No. of identified
                                                                           coverage(%)      peptides
1      Spectrin α chain, erythrocyte         279,916.5          1174412       48.0           77*
2      Spectrin β chain, erythrocyte         246,468.1          17476989      48.0           76*
3      Ankyrin 1, splice form 2              206,067.9          105337        45.0           55
4      Ankyrin 1, isoform 4, erythrocytic    203,416.6          10947036      45.0           50
5      Ankyrin 1, isoform 2, erythrocytic    189,011.2          10947042      46.0           48
Although in this table you cannot find glycolytic enzymes other than GAPDH and Aldolase, but other enzymes are also present. They are perhaps not detected in this experiment because of overwhelming levels of structural proteins. You can check this old paper that shows a study of different glycolytic enzymes from erythrocytes. It is also to be noted that the glycolytic pathway flux is not as smooth as in other cells. So some accumulated metabolites are probably exported out of the cells to keep the flux smooth[ref Full text not found].


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How does the zygote divide much faster than other cells?
Normally a cell has a mechanism that controls its division. As far as I know, it checks surface area and stuff like that to decide to go for mitosis or not.
However, this is not the case for a zygote. A zygote, after around ~14 days starts to divide rapidly and forms the blastula. What mechanism controlls this "rapid division"?
Why can zygote divide rapidly when it has not reached a high surface area or doesn't have enough mitogens to induce the cell division? Does the zygotes mini-cells have a cell cycle like other cells but they are really fast? Or do they just copy the DNA and divide rightaway?
And when I first saw the video of this stage, I was surprised. The DNA is a one long molecule; how fast do those replicators work?

A zygote generally has a lot of nutrients, essential biomolecules like RNA and proteins and cytoplasmic organelles for rapid division. So the cell does not grow and divide but rather undergoes "cleavage" (there is no G1 phase of cell cycle). However, it still undergoes DNA replication. And yes, DNA replication is fast because it is initiated at once from several parts (origins of replication) of the long DNA (it still takes a few hours† ).

 † See:

Confusion about the duration of different phases of the cell cycle such as G1, G2 & S
Time spent in phases of cell cycle


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Do all animal cells have lysosomes?
I know that white blood cells have lysosomes but what about other body cells? I mean, any other cell such as cells in the respiratory system.

Well not red blood cells but that's cheating

You are probably referring to the process of phagocytosis, where macrophages engulf a pathogen by trapping it inside a vesicle called "phagosome", which then fuses with a lysosome, resulting in the digestion and disposal of the pathogen.
But in fact all eukaryotic cells have lysosomes. This is of course biology we are talking about, so there are many subclasses, different names, specializations and exceptions to the rule.
In plant and fungal cells, we find vacuoles, which serve a similar function as lysosomes in animal cells. There are also "lysosome-related organelles" with specialized functions in specific cell types (Marks et al. 2014).
The main role of lysosomes has been described in the recycling of macromolecular material. Their lumen has a low pH level (below 5) and contains a lot of enzymes specialized in degradation of e.g. proteins, nucleic acids etc. They can digest cellular waste products and material taken up by endocytosis. Nutrients can be reabsorbed into the cytoplasm.
Furthermore, research has proposed additional roles in nutrient sensing and metabolic homeostasis (Perera and Zoncu 2016).
That lysosomes play a crucial role in many cell types can also be seen in lysosomal diseases, which often result in severe effects in multiple organs (Ballabio and Gieselmann 2009, Saftig and Klumpermann 2009). In these diseases, lysosomes fail to degrade their targets, which impairs their ability to clean out cellular waste.
Here is a summary from the book "The Cell".


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Why do the RNAseq reads map to only a certain region of a viral genome?
I am looking at RNAseq data and mapping them to 3 RNA segments from Cucumber Mosaic Virus.
I trimmed the adapters from the fastq files and converted them to fasta, which I searched against a virus database using BLASTN.
The results were confusing:
The reads align to one RNA segment (RNA 1 segment) of this virus but not the other segments. I looked in my BLAST result file the qseqid of this RNA segment of this virus and compared with the ids in my fasta file.
I copied this sequence and I did a NCBI BLAST which gave to me the same result. These 3 segments are in the capsid together, so they should be together. I am sure that they are in this NGS file.
What parameters should do I change?

I have edited your question. Can you please confirm if this is what you meant? Add more details; for example, length of the reads, number of reads and percentage of reads mapping to your RNA 1 segment, where are other reads mapping etc.

Also, you do not generally use BLAST for aligning short RNAseq reads. Try other NGS aligners like Bowtie or STAR (since this is a viral genome you may not need splice site aligners like HISAT).


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Wim Hof Method claims Alkaline Blood is Good. Contradictions? Counterproof?
The Wim Hof Method claims, that it is beneficial to have alkaline blood.
On the other site there is the medical claim that if the pH-value is not within the
range of 7.36 – 7.42, enzyms are not functioning properly and their 3D structure could be broken (denaturation). The correct pH-value is also invaluable for exchange of gases/O2/CO2, proper function of muscle contraction and
nerve conductivity.
So: What is this all about and how can this method be so good? After all, they also have conducted medical studies, so there must be some truth in it?! Thanks!

Before anyone raises this flag: This is not spam (I've checked it).

The Wim Hof method unfolds its health effects by hormetic stressors, respiratory alkalosis is one of them (a minor one). The WHM does not follow the pH theory, even though Wim himself gave ambiguous statements in older interviews about this. There are many people who misinterpret the WHM breath work as plain hyperventilation, which is very wrong. It involves a hyperventilation phase in preparation of a hypoventilation phase. This is similar to apnea protocols. The hyperventilation phase itself can mediate minor health effects. As it is not a chronic practice but relates to a few minutes per day, the stress of respiratory alkalosis is very likely within the hormetic range, hence beneficial. The WHM does NOT advocate continuous hyperventilation, which is known to be linked to chronic disease (exceeding the hormetic window).
The clinical trials of the WHM are peer reviewed and well conducted. However, people tend to mix Wim's interviews with the clinical evidence, which is obviously bad. The major paper (group study with control group) is this one: https://www.pnas.org/content/111/20/7379.full.pdf
It clearly shows the anti-inflammatory effects and increased leukocytosis of the breath work (intermittent hypoxia) and also shows that blood pH correlates to the respiratory rate, more precisely blood CO2 levels as expected. Those are normal blood gas dynamics, nothing woo woo pH stuff and no serious scientist would attribute the health effects of the method to the temporary blood pH fluctuations seen from a short hyperventilation phase, especially not when far more dominant and better documented effects on hormonal adaptations can be discussed instead. Some practitioners get quite enthusiastic about urine pH measurements, which are VERY high after the breath work, however all this indicates is normal kidney function in response to temporary respiratory alkalosis, nothing fancy at all. The body increases bicarbonate outlet via the kidneys (renal compensation) when blood CO2 gets too low (hyperventilation) to maintain blood pH homeostasis. the pH strips measure this bicarbonate. Another misconception is that the reading would correlate to progress or health, while it actually just correlates with hyperventilation intensity/duration. It is quite annoying how many misconceptions about simple physiological details float around the web, primarily due to the success of the pseudoscientific pH theory and alkaline diet. I guess some people just got rich with that crap...
Understanding the WHM means understanding hormesis and the stress response in the first place. The whole idea is comparable to physical exercise: stress the body enough to become stronger but not so much to take damage.

It is true that the pH of blood does not normally vary very much and is near neutral pH, 7.36 – 7.42 is a good estimate. It is also true that very different pHs from this would denature proteins, slow down gas exchange and kill cells. The Wim Hof method has not passed peer-review and has common red flags of pseudoscience, such as claims of the method being a panacea and being promoted through pop-health sources instead of medical ones. That's not to say it's absolutely proven to be wrong, but the onus is definitely on them to prove their claims true to the greater scientific community, not the other way around.

After all, they also have conducted medical studies, so there must be some truth in it?!

No, that's not how scientific and medical testing works, we distinguish good medical science from bad by testing against placebos, blinding, repeating the studies, (to mitigate the effect of bias) and meta analysis of multiple studies, and if the studies can pass peer review they are considered scientific evidence. (though not proof, science is provisional.) Simply conducting studies doesn't mean the subject is scientifically sound.

What makes you think the studies are of bad quality? How scientific is your judgement here :) ?


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What is the difference between abundance and dominance in an ecosystem?
I was reading Hydroperiods of created and natural vernal pools
in central Ohio: A comparison of depth and duration
of inundation by Debra L. Gamble and William J. Mitsch (2008), and I came across this statement:

The dominant tree species in the vernal pool area were Acer saccharinum and Quercus palustris, while Ulmus americana, though smaller in diameter than the other trees listed, was the must abundant species...As at the New Albany, the most dominant tree species in the vernal pool area was Acer saccharinum, followed by Fraxinus pennsylvanica, while Fagus grandifolia was the most abundant species.

There seems to be a distinction between the terms dominance and abundance in the context of ecology. I've read some of the wikipedia articles on them, but I can't seem to find the difference in their meanings. They seem to both deal with the frequency that a species is in a population.
Any help is greatly appreciated.

There is a difference between dominance and abundance in vegetation science, and your citation is about vegetation.
Abundance is the relative representation of a species in a particular ecosystem. It is usually measured as the number of individuals found per sample.
Ecological dominance is the degree to which a taxon is more numerous than its competitors in an ecological community, or makes up more of the biomass.
In vegetation science, abundance is usually measured as the number of individuals or the percentage of coverage of that species in a plot. An abundant species would typically have a lot of individuals in the plot. A dominant species dominates the other species, so typically covers more than 50% (up to 100%) of the plot. Doing this, it also takes away space (and light!) for other plants.
Usually abundant species also cover a lot, but small species (for example grasses) can be abundant without becoming dominant while large species (like trees) can be dominant with relatively few individuals.

The terms are roughly the same, either is fine and you can choose depending on the audience or the nature of the topic and based on your preference.
A scientific journal examiner won't judge you for use of one or the other. Words outline ideas the same as color terms outline the rainbow, it's not very precise and two words can have similar and different meanings.
If you check the journal articles referring to species dominance and abundance, they are to similar to call a difference:
https://scholar.google.fr/scholar?as_ylo=2017&q=species+dominance&hl=en&as_sdt=0,5


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Moss Transportation System
In my biology textbook, it says that mosses are avasculer and do not have xylem like spermatophytes. So by what means do mosses transport nutrients ?

I am not sure if this answers your question, but mosses also have no roots (just rhizomes that do not take up nutrients). Mosses take up nutrients directly with there leafs. So many they have no need for a transportation system?

Mosses are able to transport water and nutrients internally through intercellular voids and cell-to-cell connections involving exchanges of cytoplasm, as well as externally across their surface. Labeling mosses as nonvascular plants is misleading because mosses in the Polytrichales order have highly specialized water and nutrient conducting systems which are reminiscent of xylem and phloem. But in general, a moss's main vascular system can be said to be its outer surface which is carefully designed to store and conduct water across the plant.
External Conduction
Moss cells absorb water and nutrients directly from their environment, so many of their nutritional needs can be met simply by ensuring water and its dissolved nutrients can spread across the entire surface of the moss plant. The water is able to spread through capillary action, aided by a carefully designed surface. Moss leaves are frequently appressed to the stem and have sheathed bases which create small places for water to climb along a stem. The leaves may also be covered in small bumps (papillae) which create capillary spaces. Rhizoids, which are somewhat like roots except typically only 1 cell thick, can also make good paths for water to flow across. Some mosses have their stems covered in rhizoids or paraphyllia to help conduct water. Sphagnum mosses have large cells across their leaves which exist mainly to absorb water like a sponge, and Leucobryum mosses have a layer of water holding cells on both sides of their leaves. Colonies of mosses often form compact mounds that allow for water to flow across the entire mound.
As far as I know, moss cells do not deliberately dump nutrients into the film of water on their surface in the hopes that it will be absorbed by other cells of the plant that need it more. But, when dessicated moss is rehydrated, solutes in the protoplasm may leak into the external film of water. These contents might be able to be reabsorbed by other cells of the moss, forming an incidental external nutrient transport pathway.
Internal Conduction
Water and nutrients are also able to flow through cells or spaces between cells from inside the moss. Experiments have shown that nutrients are relocated from old growth to new growth using cytoplasm-linked pathways in Sphagnum and Polytrichaceae mosses. Many moss stems and almost all seta (the stalk connecting a spore capsule to the main body of the parent moss plant) have special nutrient conducting parenchyma cells surrounding water conducting cells called hydroids. The central ribs of moss leaves also often show a similar pattern. Sometimes these chains of nutrient conducting cells in the leaves connect to the main conducting strands in the stem, but usually the leaf conducting strands come to an end somewhere in the stem cortex without connecting.
Mosses in the Polytrichales order have the most specialized nutrient and water conducting cells of all mosses. The nutrient conducting cells for mosses in this order are different enough from other mosses to be given a special name--leptoids. The vascular system in these mosses are not evolutionarily homologous to xylem and phloem, but serve the same basic transport purpose. In Polytrichum moss, water has been measured to flow 200 cm/h through the stem and organic compounds at 32 cm/h. These specialized hydroids and leptoids are what enables the tallest moss, Dawsonia superba, to grow up to 70 cm.
The water and nutrient transport architecture for mosses outside the Polytrichales is more variable and less specialized. Andreaeopsida, Andreaeobryopsida, and Sphagnopsida completely lack hydroids. Takkakia's hydroids are unique in that they are short instead of tall and transfer water through pores formed from plasmodesmata at their ends. Sphagnum has nutrient conducting cells, but they are not homologous to the nutrient transferring parenchyma cells of other mosses. Some mosses in families which typically have central conducting strands have lost that feature over time, and mosses which would normally have hydroids may fail to develop them if grown underwater.
Outside of the usual stem, seta, and leaf midrib conducting cells, it has been suggested that rhizoids and caulonemal cells also conduct nutrients due to similarities in cell organization to the nutrient conducting parenchyma cells. The cells that form the interface between the parent gametophyte and the sporophyte foot also transfer nutrients.
Sources
Chopra, R. N. Biology of Bryophytes. 2005. Chapter 11 "Conduction in Bryophytes".
Goffinet, B., and A. J. Shaw. Bryophyte Biology. 2009. Pages 60-70, 83, 301.
Ligrone, Duckett, and Renzaglia. Conducting tissues and phyletic relationships of bryophytes. 2000.


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What causes this acorn disease?
This year, many acorns in our area (Germany, Schartzwald) fell prematurely, plagued by some kind of warts or gall-nuts which I see for the first time:

Some of the acorns are covered by two or three warts at a time, so that the actual nut itself is practically non-existent.
Judging by the hole present in all the warts, I'm guessing those were houses for some insects or larvae. Unfortunately, warts on acorns available for inspection (those which already fell) are already abandoned by their hosts.
Does anyone know who those guys are and how they look like?

tiny vespids that lay an egg in the acorn, produce an enzymatic reaction by specific chemical release that mutates the acorn into a certain shape, depending on the species, it can be that shape, or a round ball of wood, and many other galls depending on species. if you cut it open you will see a small grub or it's silk cocoon, and a little tunnel where it lived and escaped from.

The structure on the oak nut is a knopper gall.

It is a distortion of growing acorns on pedunculate oak (Quercus robur L.) trees, caused by gall wasps(Andricus quercuscalicis), which lay eggs in buds with their ovipositor.

An Andricus quercuscalicis larva in an open gall of an acorn:
Link
Here's a video by BBC on the same you may find it interesting.


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Dawn simulation - does color change affect waking up?
just curious. Are there any works or research results related to the influence of light color used for dawn simulation? I mean those wake-up lights which try to simulate dawn to make waking up better for you.
The cheap ones only use one color - those "warm white" LEDs - and only change brightness. However the more expensive ones also change color like the sun during sunrise.
I am just curious how much important could be the color change. :-)
thanks


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Why do genitals feel frozen when freefalling?
I don't want to add much more about that. Since childhood I noticed a chilling effect, even when doing rollercoaster-type activities.

Is there evidence that what you are describing is a general phenomenon?

Probably because the blood would be forced, physically, that is, by inertia to move upwards during free-fall, thus causing the genital's blood supply to become obstructed thus reducing their temperature and thus leading to the sensation of them being frozen as you described. Plus you might feel cooler all over your body due to the air flow against it and since your genitals wouldn't be as biologically favoured when your body's survival instincts for low-temperature environments kicks in you're body would probably reduce the blood flow to your genitals and other extremities favouring your vital organs such as your heart, lungs, brain, etc. with a greater blood supply to keep them warm and working.

If it were blood flow, wouldn't your feet be cold as well?

Perhaps but perhaps as part of the person in question's biology the genitals are for some reason more prone to decreased blood flow. Different people have slightly different biologies and seeing  how from what I can tell this isn't a super common occurance in people this theory seems quite valid.

If it's not a general phenomenon, then I think the question is too narrow (i.e., applicable to only one person).

I kind of think you shouldn't be discussing that with me but rather with the asker under the question itself seeing how its more applicable to him/her. Put it to him/her that if they cannot find someone who experiences this too under those circumstances the question will be closed.

i think its all the ennervation in the region - they are quite sensitive compared to other ... regions


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

Previously frozen— thawed in refrigerator but not warmed
4 hours or less (ie the next feeding)
Store in refrigerator
24 hours
Do not refreeze

But in freezer the temperature is still below normal, still is there a probability of bacteria growth?
I wish to understand the reasons behind the warning. Answers with references will be appreciated.

This is just a guess, but I don't think this is a food safety issues, its more a case of 'this food is gross now' issue.
When I was a teenager I worked in a frozen food processing plant.  The freezers were giant boxes where freon was condensed on gigantic coils into a liquid and then the liquid freon would rain down on to the food passing under on a conveyer belt.  The vegetables were frozen instantly and it was quite tasty - frozen just a few minutes after being cleaned.
As industrial freezing is very quick and such flash freezing, the quality of the food is preserved in a pretty fresh state. [its horrible for the ozone in the atmosphere but this was in the 80s and I hope they changed the process].
Milk is a mixture of water based nutrients and globs of fat, which give the milk is homogeneous white color and its smooth texture.  Freezing milk in a typical refrigerator would take hours and ice crystals would form and separate out the two phases - the fatty portions would separate.  Try it with a glass of milk and see.   This is the same reason that you don't re-freeze ice cream, which has even heavier creme proportions (even fattier).  The texture is completely gone.

so how would fat separation effect health? Is harmful?

I don't think it would- it might be a bit more like skim milk.  The nutrients are still there and if its been frozen after only a short period there shouldn't be too much bacterial growth, but if you think food should be appetizing to be healthy you might not completely feel its as good as if it hadn't been refrozen.  On a molecular scale there could be some differences; if I was having lactovegans over for dinner I'd throw it out.  If I was starving and waiting for a check to come in I wouldn't think twice about drinking it.

oh breast milk - not sure why I didn't think of this.  We've actually refrozen breast milk and used it. This is not medical advice, but in our experience it wasn't a health hazard.

I think this recommendation is simply to be on the save side in terms of degradation. You don't want to feed babies with milk which is not ok anymore - so you take measures that exclude this for sure. Breast milk is a raw product, so if its not handled with care, it can be contaminated.

i agree @Chris .  if you refreeze how long can you keep the milk between freezings?  what temperature is the bottle?  how clean is it?  too complicated for a public guideline.

When I lived in the UK, most supermarket frozen foods came with a "Do not refreeze after opening pack" warning. This is only anecdotal, but I've never heard of anyone getting sick after ignoring this advice. I myself used to ignore that advice quite regularly.

I don't know why I can't comment, but this seems simple enough that you could do an experiment and freeze it and see what happens. One possibility that comes to mind is that fat globules formed during freezing will clog the nipple on the bottle and make it harder for the baby to drink. Breast milk isn't homogenized, so the fats are more likely to separate than normal cow milk from the store. It also isn't pasteurized, so it will spoil faster than store bought milk too, but if you keep it cold and don't let the experiment run for more than a couple days it should be ok. To be safe, don't feed the experimental sample to the baby.


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Why do we urinate more when we are nervous?
This question is a result of my personal experience... But I guess that is common for many of us.
My school timing is 8:00 am to 1:30 pm (usually). During normal school days I typically urinate one time - at most. Last month when we were having our practical exams. There was a fair amount pressure to score high marks and on top of that we did not have any experience with such exams.
On the day of the exam; I was a little nervous about it. The duration of the exam was 3 hours (from 9:00 am to noon) on this day I urinated 4 times.
Several of my friends also experienced the same thing.
I was nervous also because for two days before the exam I was afraid that I hadn't even touched any book. I was thinking that there was no way I could cover the whole book and so I didn't even touch them.
Now that I have final exams in about two weeks, I was revising my syllabus but for the last 4 days I'm not touching the books. Whenever I start solving problems from any chapter then I have to look back for the formulas. Questions in which reasoning is asked, I love to do that. I'm not very good at memorizing things and so when I compare myself to my classmates then I feel like I don't know anything and so I give up. I have never tried to memorize anything, but I understand the reasoning and the concepts.
Kindly give me the answer of the question.

Check this out http://www.ncbi.nlm.nih.gov/m/pubmed/11116129/

It's all about chemical reactions in your body triggered by your brain.
Lot's of researches and documents confirmed this is what happens when you face a stressful situation.
Stress -> hypothalamus -> sympathetic nerves -> Epinephrine (Adrenaline) -> more urine flow
Domino neural connectivity (Thinking) => Domino Chemistry (Body reaction = stress and anxiety)
Situations like thinking about exam and how hard it would be or how it could change opportunities and feelings in your life you are triggering a chain of neural and chemical responses.
If your thoughts (Activated neurons) end with unsolved vital problem, it activates parts of your brain that is related to anxiety and stress and these neurons activate hypothalamus.
Hypothalamus turns sympathetic nerves on.
The sympathetic nerves release adrenaline (epinephrine).
And adrenaline cause more urine flow.
This example shows two more kinds of polyuria
If you are interested in how increasing level of adrenaline results in more urine flow read this and this and this.

Your last two links both state that an increase in adrenaline causes renal flow rate to decrease. So how does an increasing level of adrenaline result in more urine flow?

Copy and paste exact part to approve your claim. You are wrong about decreasing of the urine flow by the higher blood pressure. It's almost 50 years that scientists confirmed adrenaline has direct effect on urine flow as I explained from sources. For more info read these two like below.
http://ajplegacy.physiology.org/content/192/1/131
AND
http://forums.studentdoctor.net/threads/blood-pressure-and-urine-production.920866/
The higher your blood pressure gets, the more urine flow

I can see easily that increased blood pressure increases renal flow. But is there not a second effect that decreases renal flow? Your newest link in your answer mentions "by acting directly on the kidney to decrease the output” and your first link mentions "Postganglionic neurotransmitter of the sympathetic nervous system norepinephrine causes particularly in the afferent arteriole vasoconstriction, thereby reducing the renal blood flow (and thus the GFR).” Also, my textbook (Campbell Biology) states that the sympathetic nervous system inhibits urination.

I found an interesting article that dealt with anxiety and micturition. There are no proven or accepted view on this. There are a few theories as to how this happens.
I am quoting it:

There are several beliefs for what causes frequent urination from anxiety, and the likelihood is that all of these factors play a role:
Muscle Tension – This is one of the most likely causes of frequent urination. When you have anxiety, your muscles get very tense. This tension puts pressure on your bladder, which in turn makes you feel like you need to urinate more than you would otherwise.
Evolutionary Adaptation – Another theory is that there is an evolutionary reason that frequent urination would be advantageous. Remember, anxiety is the misfiring of your healthy fight/flight system. In times of fear, urination may keep the body lighter by losing extra weight, making it easier to flee.
Light Overload – It's also possible that, because anxiety is a misfiring of the fight/flight system, your body may simply be lightly overloaded. The fear is not intense enough to cause immediate urination, but it may make it harder for you to feel like you can hold it back.
  Also, those with anxiety are more prone to focusing on different sensations unintentionally. There are often times when you may feel the need to urinate slightly but your body has no problem ignoring the feeling and holding it back. With anxiety, it's possible that your brain is focused on the sensation, potentially causing you to feel like you need to urinate more than you do.
Finally, anxiety can also change your body chemistry, altering your digestion and changing the way you process nutrients. That may cause more water to pass through your body.

Source:http://www.calmclinic.com/anxiety/signs/urination-problems


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What would happen if a person had the right side of their body totally removed (including the brain)?

What would happen (in reality or theoretically) if the entire right side of a human's body was removed?
Could they live (aside from all the probable infections and such)?
I would guess that humans can live without part of the liver or brain.
The left brain controls the right side of the body.
What do you think (or know) will happen?
Thank you very much in advance!

in the odd chance that the person survives, (s)he would be totally immobile as the right half of brain controls the left half of the body and vice-versa. The only part of the body that the person can control would be the upper half of face which is supplied by both halves of the brain!

This reminds me of a joke: Q. "What happens if a person has the left side of the body totally removed?"  A. "I think they'd be alright!"

They would die.
Let's imagine that we perfectly cut a person down the middle. That would mean cutting the spinal cord in half, probably damaging the tissue so much that the remaining half wouldn't work well. The liver would be gone. The intestines and bladder would just be open. The heart would have to be adjusted to the left. The surgery would probably cause so much blood loss that they wouldn't even survive to die of other organ failure.
And you already alluded to the mismatch between what side of the brain controls what side of the body, so if you kept the pseudocorpse "alive" on an IV, heart lung machine, and hemodialysis, they'd probably still be paralyzed.


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Why does a pacemaker have a negative pulse?
Why is the first phase of the pulse from a pacemaker cathodic?

Welcome to Stack Exchange Biology!

Do you have a reference to back this up? In general neural implants are tested to see what the most effective pulse phase is. Often one polarity will stimulate the system, while the other inhibits it.Starting with the stimulating phase is deemed best. Then the opposite phase follows to clear the system from the detrimental effects of charge injection.

Hello Chris, thank you for your answer. but still I could not understand why negative peak is important for the stimulation rather than positive peak. As I can understand from electrochemical reactions, for cathodic stimulation, the energy level of free electrons in the metal are raised. It allows to transfer of electrons from metal to reactant species in solution.

Jan - I don't know which phase is most important either - it depends on the implant system and importantly, on the location of the implant. For example, in retinal implants the active phase depends on whether it is placed sub-retinally (anodic phase most effective) or epi-retinally (cathodic phase most effective). I did a quick search on pace makers and couldn't find anything on it - so please provide me with a citation that says that cathodic-first stimuli are most effective and I'll have a look. Interesting topic!

BTW: My answer on a related question may be of help to you: http://biology.stackexchange.com/questions/22020/mechanisms-of-extracellular-stimulation-of-neurons

Can you give some background to the question and your reason for asking?


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Why not use lactase to aid the break down of lactose when making biofuels?
I did an experiment using nine different substrates (Lactose + lactase, corn, sugar cane, glucose control, wood, grass, no yeast control and yeast control) and observed their fermentation rates. Lactose + lactase had the highest fermentation rate. So now my question is: is there a usage of lactase in aiding the break down of lactose to make biofuels? I did a web search and all I could find was that lactase was used for helping lactose-intolerant people,etc.  And that the current whey-ethanol industry used special species of yeast that break down lactose directly instead of the enzyme lactase. There are other methods too, including the Carbery and the Bio-process Innovation (BPI) processes; all of which use yeast that can directly break down lactose. Does lactase play no role in the biofuel industry? And why don't people use lactase to aid them in making biofuels?

Lactase on its own doesn't ferment anything. Also, yeast produce lactase in response to lactose.

Cost, I imagine. Lactase is probably harvested from yeast exposed to lactose, so it seems a little odd to grow the yeast on lactose, harvest the lactase, then put that in a mixture with other lactose. Skip the middleman and put in the yeast directly, plus then it replicates.

I agree with you Resonating. I think adding extra lactase enzyme would be an extra step. And would be expensive...


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Why does uterus have to be prepared every month for fertilization?
I'm just curious why it has to happen every month when the uterus could have been prepared from the beginning and kept that way throughout life or till a certain point. But why make and break it every month? (The breaking of this preparation is the cause of menstrual pain, which is what I'm worried about).

Welcome to Biology S.E.! If you have additional questions please visit The Help Center

You may be interested in estrus

A quick search through the Internet, as well as any textbook, will reveal that the lining of the uterus (endometrium) created thickened during every menstruation cycle is rich in nutrients, and requires a constant blood supply, in order to accommodate a fetus.
Therefore, maintaining the lining would be more costly to the body than rebuilding it every month; in fact, as part of the lining is reabsorbed, rather than destroyed and expelled, thus conserving energy and nutrients. The reason a part of the endometrium is not reabsorbed is its thickness, which prevents its total reabsorption.
Also, the menstrual pain is, in fact, caused by the breaking down of the endometrium, although not directly, but by muscular contractions (cramps) and the contraction of blood vessels, which happen to prevent blood loss and help with the expelling of the endometrium.


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How to quantify the Abundance of a particular gene in Bacteria and Archaea?
For 16s rDNA metagenomic analysis, do I need to do the following steps?

DNA extraction-> Purification-> PCR amplification-> Clone -> Pick every single
  colony-> PCR amplify -> Sequence -> Phylogenetic Analysis

For the abundance of a particular gene abundance, what steps do I need to follow? Is it necessary to clone?
`

16S rDNA? You mean 16S ribosomal RNA, right? If yes then no you don't need to do a library in bacterial clones anymore. With next generation sequencing technologies the library is made In-Vitro followed by PCR-like step (e.g. Illumina Nextera XT kit). What you would do is RNA extraction -> Reverse-transcription -> PCR amplification -> library building using a kit -> Sequencing -> Phylogenetic analysis.


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Why does anxiety cause diarrhea or constipation?
Anxiety sometimes cause diarrhea, sometimes constipation, and sometimes both. It's interesting because it seems their underlying neurophysiology is somehow different. What are underlying physiological processes that lead to these two symptoms in anxious people? Particularly in terms of the activity of sympathetic and parasympathetic nervous system?

Do you have a citation for this claim?

Hraish is right about the relationship between emotions and gut-brain axis. Stress hormones released by the brain are responsible for the gut-brain reflexes. Anxiety is related to stress and stress hormones are released when anxiety is expressed by the individual.
Irritable bowel syndrome(IBS)  symptom-based diagnosis, which is having symptoms such as chronic abdominal pain, discomfort, bloating, alteration of bowel habits, diarrhea, constipation etc.

Irritable bowel syndrome (IBS) is a functional digestive disorder characterized by abdominal pain, bloating and altered bowel habits without any organic cause.
(Drossman 1999b; Mulak and Bonaz 2004).
In addition, stress is able to increase visceral sensitivity either at the central and/or peripheral level. (Mulak and Bonaz 2004; Larauche, et al. 2011).

Stress is enabled through the  corticotrophin-releasing factor (CRF) system (CRF, urocortins and their receptors CRF1,2), is a key factor involved in the pathophysiology of IBS.

Stress is able to modify visceral sensitivity as well as GI motility, permeability, intestinal microbiota, and immunity of the GI tract, all mechanisms that are involved in the pathophysiology of IBS. In addition, stress is able to modulate the hypothalamic pituitary adrenal (HPA) axis and the autonomic nervous system (ANS) which is the link between the gut and the CNS and an imbalance of the ANS is observed in IBS patients. The main brain areas involved in stress are the prefrontal cortex, the limbic system (e.g. the hippocampus and the amygdala) and the hypothalamus. Relations between the prefrontal cortex and the limbic system are important in the management of stress response.
  (Pellissier, et al. 2010a; Mazurak, et al. 2012)

One of the most common gut related conditions seen
  by GPs and Gastroenterologists is Irritable Bowel Syndrome (IBS), previously known as
  colitis,mucous colitis, spastic colon, and spastic bowel disease.Around 10-20% of adolescents and adults have symptoms consistent with IBS (with females twice as likely as males to report IBS symptoms).
  IBS is associated with 12 months of abdominal pain or discomfort which is (1) relieved with
  defecation; and/or (2) associated with change in stool frequency and/
  or form (i.e., constipation and/or diarrhoea). IBS is also associated with other gut-related symptoms including: bloating,nausea,and excessive gas. Non-gut related symptoms include fatigue, headaches, sleep problems,and pain conditions, such as fibromyalgia.
Individuals who experience IBS also identify that their gut problems increase doing times
  of stress.Itcan become a vicious cycle-IBS is exacerbated by stress and stress is inturn increased by symptoms of IBS.With anxiety comes increased muscle tension around the gut
  (affecting gutmotility) and activation of the flight fight response, reducing blood in the gut (this is what causes butterflies in the tummy!). These physical changes cause the
  gut-brain to send signals to the brain which in turn promote further stress and distress, most commonly in the form of anxiety.For individuals with IBS (or actually most gut conditions), the ongoing worry about their gut and unproductive patterns can be very
  debilitating. It can also be the starting point for their anxiety
  and/or depression.
  Reference

From the above definitions it is clear that anxiety and brain-gut relationships are valid and IBS is an important reason for gut related disorders when stress is been experienced by the person. Over 10-20 % of adults have symptoms related to IBS, which means a common type of disorder in the general public.

References
Stress Affects the Amygdala Activity
Anxiety and the Brain-Gut-Axis


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Neurology: spinal tract
I have had a few difficulties finding answers for the questions below. I have tried answering the first two myself; but, I am not sure they are correct or not. And I am not too sure about the third one.

In which structure of the brain does the axon from the spinocerebellum tract synapese? Is it the cerebellum?
Are the cell bodies of axon in the gracile tract located at the dorsal root, tectospinal tract located in cerebral cortex?
Which region  of spinal cord carries feed-forward information to help accommodate for upcoming motor movement?

Yes, the spinocerebellar tract ends in the ipsilateral cerebellum.
The gracile tract is a bundle of axon fibers in the dorsal root. The neural cell bodies are in the dorsal root ganglions. The tectospinal tract is part of extrapyramidal tract that connects midbrain (mesencephalon) with the spinal cord.
Didin't get exactly what you meant but: the lateral corticospinal tract (part of pyramidal tracts) controls fine movement of ipsilateral limbs, while the anterior corticospinal tract (part of the pyramidal tracts) conducts voluntary motor impulses from the precentral gyrus.

Source: Wikipedia: Tectospinal tract, Spinocerebellar tract, Dorsal root ganglion, Pyramidal tracts, Anterior corticospinal tract, Lateral corticospinal tract.


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Does every nerve ending send information to the brain separately?
Does every nerve ending send information to the brain separately? Is there a nerve path (I don't know their scientific name) from every nerve ending to the brain; or are they sent to brain from the same paths in the dorsal root ganglion? If not, how can we determine the (almost) exact location of pain in our hand?
I am not very familiar with the biology except the lessons I had taken in the high school. So please try to use daily language explaining this.

This depends on what you mean by a nerve ending. An entire nerve [bundle] such as the sciatic nerve? An individual neuron within the bundle? The dendritic branches at the terminal end of the neuron?

Nerve cells typically have many - sometimes thousands - of endings, called dendrites.  The inputs from these are integrated, and cause a spike to travel along the axon.  (This is a considerable oversimplification: look up "dendritic tree" for more info.)

sensory neurons often have a single dendrite, either synapsed to a sensory receptor cell, e.g. type I spiral ganglion neurons and inner hair cells in the cochlea. Or, the sensory neuron may have a specialised sensory dendrite, e.g. merkel's discs.

There are two main structures in the human nervous system:

The central nervous system, which includes the brain and spinal cord
The peripheral nervous system, which is all of the nerves in the rest of the body (fingers, arms, feet, etc.)

The signals taken by the peripheral nerves mainly travel to the brain through the spinal cord, and the brain sends signals back to the peripheral nerves through the central nervous system.
There are a lot more complex mechanisms and various exceptions, but essentially: the nervous system is a vast network of signals, and the majority of these signals travel through the spinal cord to the brain and from the brain to the target nerves.
The signals travel via different nerve "branches" — think of it like a tree of nerves, with the common root being the brain.
For more information please see:
Overview of the nervous system for dummies
Wikipedia (with strong references and lots of detailed information)

As commented, a nerve ending is really the ending of a neuron, some sensory neurons travel directly to the brain, some form synapses in the spinal cord (most touch and pain neurons from the body), then spinal cord neurons carry the information to the brain. (Note that facial sensation is carried by cranial nerves from the brain stem).
Some, e.g. in the retina undergo some quite intensive processing before ganglion cells carry any information to the brain.


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How do humans perceive time?
We can see length, and other physical quantities. We can perceive through our other senses like (temperature through thermoreceptors, weight through pressure receptors etc.). But how do we "sense" time?

Maybe better for http://cogsci.stackexchange.com/?

I think this is still under research. There is some hypothesis that hippocampus is involved.

It is not completely understood as far as I know, but circadian clock is a keyword for you to look into. http://en.wikipedia.org/wiki/Circadian_clock

On what time scales? Circadian is for longer time scales, but probably has little to do with perceptual time scales, which is on the order of hundreds of milliseconds. There you have research into duration perception, and temporal order perception as the main research areas. But also flutter (change stimulus rapidly in a sinusoidal way and determine what frequency we can detect) is a temporal perception bit as well. Flash lag illusion is an illusion of time perception wrt temporal order. This is a huge topic, like asking how we perceive space. Or 'what is mass' in a physics forum.

The nature of time has been discussed for millenia. We don't know exactly why or where time perception exists, but we do have some information on how it is perceived.
The circadian rhythm is basically in place to help us sleep, wake and perform tasks in a 24 hour cycle of light. Robbed of light, and the melatonin it's absence produces, the rhythm shifts considerably.
Vision is a powerful cue for the passage of time. Bees have an extremely sophisticated ability to predict the sun's location at a given moment (they can count the moments). While I doubt the same is true for humans, our eyes give us a great deal of information about the passage of time: the time in a 24 hour period (the position of the sun, moon, stars, shadows, etc), and the time in a year, the time in a lifetime. Witnessing the passage of time, according to physicist Paul Davies, we observe how the “later states of the world differ from earlier states that we still remember.”
Besides the important input from our eyes and memories, we also have internal timekeepers.  A study decades ago on short order cooks (I can't seem to find it) found that an experienced cook can keep internal time to the second, and can keep multiple "stopwatches" going in his head: the scrambled eggs, the toast, the pancakes, the grilled cheese sandwiches all take a certain amount of time, and short order cooks can tell when that time has passed with extraordinary precision.
The fact that the fluids flow at different rates tells us that we perceive time differently under different circumstances. Time perception is surprisingly prone to measurable distortions and illusions.

The importance of our temporal experiences for daily living is strikingly documented in individual neurological cases where patients report of an accelerated progression of time and, consequently, have troubles in adequately interacting with the environment, i.e. driving a car. Psychological research has shown that cognitive functions such as attention, working memory as well as long-term memory determine our temporal judgements. Moreover, drive states, moods and emotions, as well as factors of personality influence duration estimates. For example, time intervals are judged to be longer when we pay more attention to time and when the load of varying experiences stored in memory is higher. Our subjective well-being also strongly influences how time is experienced. Time speeds up when we are involved in pleasant activities, but it drags during periods of boredom. Thus, our sense of time is a function of the intricate interplay between specific cognitive functions and of our momentary mood states.[1]

Where exactly time is perceived by the brain is unknown, but several areas keep appearing, most prominently, the cerebellum, the right posterior parietal cortex, the right prefrontal cortex, as well as fronto-striatal circuits. All have been implicated as the neural substrates of a potential timekeeping mechanism. The inner experience of time[1] gives a broad overview. The conclusion is worth reading.
To further support that the where is not known, consider the following:

Studies done in humans also support the hypothesis that striatum and its afferents are involved in interval timing. Recent fMRI data showed that timing network could involve cortico-striatal loops, including premotor and supplementary motor areas, frontal operculum and dorsolateral prefrontal cortex, and temporal and parietal cortices, as well as the putamen. Imaging studies in humans, lesion studies in humans and rodents, and drug studies in rodents all point towards a central role of the basal ganglia in interval timing. The anatomy of the basal ganglia suggests that information is proceeded through cortico-striato-thalamic loops. Severe deficiencies in reproducing temporal intervals were also found in Parkinson’s patients, therefore, further supporting the hypothesis of basal ganglia involvement in interval timing. There are also lesions data suggesting that the timing network is much widely distributed. Lesions of the nucleus basalis magnocellularis, a cholinergic nucleus in the basal forebrain with projections to the frontal cortex, induced a progressive, proportional, delay in peak time response (memory pattern). This effect is believed to be related to altered temporal memories [42,43] due to change in acetylcholine (ACh) level. Lesions of the frontal cortex produce similar memory patterns, whereas lesions of the hippocampus or fimbria fornix, a basal forebrain cholinergic nucleus with projections to the hippocampus, result in memory effects translated into an advance of the peak time response. These experimental findings undoubtedly support the hypothesis of a distributed interval timing neural network.[2]

For a fun but non-scientific look at time, the NYT has written an understandable article.[3]
The final answer is that no one knows for sure.
The Experience and Perception of Time
1 The inner experience of time
2 Why noise is useful in functional and neural mechanisms of interval timing?
3 Where Did the Time Go? Do Not Ask the Brain
Time and the Brain: How Subjective Time Relates to Neural Time
Human time perception and its illusions

There is some hypothesis about "time cells" if I am not mistaken; for storing temporal memory (i.e. time of events, temporal order etc).

@WYSIWYG - I didn't see this 'til just now. I'm reading about it. Thanks! I'll amend my answer when I've read enough to understand.

Internal timekeepers are pretty controversial many people think time is kept implicitly just via the general dynamics of complex systems of neurons, without any explicit code for time. See eagleman for explicit coding of time, buonomo (sp?) for implicit coding. This is far from resolved, as the answer says.

Humans and many other organisms have a circadian clock, a biological system that oscillates every 24 hours (but is also sensitive to external stimuli). There are many components to the human circadian clock that are not known. On the molecular level, gene regulation, post-transcriptional and post-translational modification are all implicated. There is also evidence of a systemic network through which the oscillation propogates, probably via hormones or other intercellular signals.
Many of the molecular mechanisms are not well-understood (and to go into all of them would take all week), but I'll give an example of one fairly self-contained negative feedback loop mediated by the Period/Cryptochrome PER/CRY complex.
PER/CRY is a heterodimeric transcriptional regulator. During the day, it is located in the cytoplasm, unphosphorylated (and sometimes as independent subunits). However, upon phosphorylation, it enters the nucleus and negatively regulates many genes, including itself. This is a negative feedback loop, more PER/CRY in the nucleus means that less will be produced. Here's a hopefully simple figure to illustrate this (Belden et al. 2006):

Phosphorylated PER/CRY also regulates vasopressin, a hormone that helps the CNS regulate circadian rhythm (McGill University):

Hopefully this is clear. Remember that this is only part of the entire circadian clock system and that there is more detail even in relation to the PER/CRY complexes themselves (McGill University):

The molecular machinery for circadian clocks have even been found in single-celled organisms. These organisms can hardly be assumed to perceive time. Yet we can perceive time, and they don't.


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What makes cows stop being able to produce milk?
I'm writing a paper about cows and want to discuss why they stop producing milk. Is there a disease that causes them to stop producing milk?

OP noted that they had difficulty logging in - namely that it still treated them as a guest even though they were logged in.


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Is it necessary to remove a bullet from the body?
So here is the proof: William Lawis Pace lived with bullet in his head for many years & even hit 100.
However, both in real life and movies, we often see doctors struggling to remove bullets from the human body.
My Question: Is it necessary to take bullets out of a human?

I would think that this is somewhat dependent on what part of the body it has lodged in.

Of course it is. William Lawis Pace is clearly the exception (and suffered due to the wound). He was incredibly lucky to survive for so long. Also, I think the question is oversimplifying the gun-shot treatment (practical advice and academic references here). The aim is not to simply remove the bullet.

@James - it's not the bullet left in the body per se that causes the suffering; it is the damage the bullet does. If inert, it may not do further harm. In repairing the damage it has done (lacerating blood vessles, perforating bowel, etc.), the surgeon finds and removes the bullet, partly to make sure that's the end of the destructive trajectory, and partly because who wants a foreign body in their body? Please trust me when I say it's not extremely rare to have portions of bullets and shrapnel remain in the body after surgery. It depends on a number of factors, including risk of removal.

I'm voting to close this question as off-topic because the OP already has proof that removing a bullet is not necessary to life.

It depends on the size and the location. After both world wars plenty of people had odd bits of shrapnel wandering about inside them for years, because it would be too difficult or dangerous to get it out.
We had a dog who carried a few shotgun pellets inside her, shallowly enough for one to feel one of them under her skin. No point in subjecting the dog to the stress of an operation.
But with a bullet bullet, the size means that it would be almost certainly worth trying to get it out. Again, depending a bit on location and how much trouble it's causing. Abdominal cavity = one answer, muscle = another.


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Can human survive falling from 30,000 ft without a chute?
If someone falls 30,000 feet without a parachute; what are the chances of survival if they landed in the water?

I don't think it matters that 5000 or 30000 feet... As you descend the air will become more and more dense which will slow you down... Afaik. it is survivable, with severe injuries.

Summary: A fall from "any height" may be survivable, depending on what you hit, but with an expectation of severe injuries. A water impact at terminal velocity will in all likelyhood result in immediate death.
The Serbian Flight attendant Vesna Vulović holds the Guiness World Record for surviving a fall without a parchute with an estimated fall height 10,160 metres. However, some doubts have been cast on the accuracy of the record, with claims that the fall was actually only several hundred meters. Vulovic was found partly in the wreckage of the plane, so it can be discussed whether she had a truly "free fall" for the purposes of this question. However, several other persons have been known to survive completely "free" falls from great heights. Although it is hard to verify the exact altitudes, the WW2 aviators Alan Magee, Nicholas Alkemade and Ivan Chisov are reported to have survived falls of about 6700 m, 5500 m and 7000 m, respectively.
The exact altitudes are in any case not necessarily of interest, as it can be assumed that all persons falling from a height of more than about 500 meters will reach terminal velocity, the velocity where air resistance prevents the fall speed from increasing, before hitting the ground. As such, above a certain height, other factors become determining for the survivability of a fall. As has been demonstrated by the listed examples, it is clearly possible to survive a fall at terminal velocity. However, this requires favorable conditions at the site of impact, and will likely result in severe injuries.
Due to the flat surface and the surface tension of water, it is hard to imagine an unprotected impact with water being survivable at terminal velocity. The best chances for survival will likely be in areas with foliage, snow and/or a hilly landscape allowing the kinetic energy to be dissipated through rolling downhill. Of the listed aviators above, Nicholas Alkemade appears to have been the least injured. About him, it is reported that

His fall was broken by pine trees and a soft snow cover on the ground.
  He was able to move his arms and legs and suffered only a sprained leg

To put it simply... NOT GOOD!!!

US Coast Guard rescue swimmers will not do a free fall deployment from above 200 ft (actually, I think it is less, I cannot remember right now) into water, this is too dangerous.

I personally think you'd be better off trying to find about fifteen feet of soft snow to land in! In reading trying to find additional information with which to answer this question, I stumbled upon someone who said they knew of a pilot in Vietnam who's 'chute didn't open when he ejected. He survived with "only" broken bones and a ruptured spleen. I have included a link that I hope is helpful!

https://physics.stackexchange.com/questions/9059/jumping-into-water

isnt falling into water safer compared to concrete-pavement ?

@BeyondProgrammer Sure, it is safer, but, it is still going to feel about like hitting a concrete block if you're coming from 30,000 feet!

@BeyondProgrammer It's surprisingly little difference.


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What are genome wide functional linkages?
There are two types of interaction classifications used to describe Protein-protein interactions, namely physical and functional. Whilst physical interactions are obvious in nature and methodological determination, I was wondering what a functional interaction/linkage refers to, such as the one cited in the below paper, and is it purely inferred from genomic data?
"Visualization and interpretation of protein networks in Mycobacterium tuberculosis based on hierarchical clustering of genome-wide functional linkage maps."

did it!!!!!!!!!

It would be great if you show some of your workings! A simple google search would have provided you with your answer! I don't think the question should have been closed so once it opens I will answer it but please show what information you have found so far!

okay this is what I got to know, multiple proteins working together to attain a particular function can be termed as protein functional linkages. Am I correct?

Genome wide functional linkages refers to protein in a biochemical or signalling pathway. Inferences of functional interactions can be obtained from methods such as coexpression data from microarray analysis. Since experimental detection of genome-wide protein–protein interactions is costly and time-consuming a computational scope for essentially predictive genome-wide protein–protein interactions is created  [1], which is what the above paper is referring to. As obvious from the abstract of the paper, there are many ways of obtaining the linkages, which are often inferred by the Rosetta Stone, Phylogenetic Profile, Operon and Conserved Gene Neighbor computational methods [2].
Algorithms that identify genome-wide interactions between proteins mainly focus on coregulation of interacting proteins. These methods assume that the genes that are coregulated often occur close to each other on the genomes and show conserved gene order. Thus the genes, which are part of an operon, could be functionally linked.


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How can birds keep their eyes moist during flight?
Mammals have an upper lid and small mass  of tissue in the upper corner known as nictitating membrane. This helps keep the eyes clean; birds can moisten their eyes in flight using this membrane without blinking. How does this work?

Because the nictitating membrane secretes a fluid that is resistant to evaporation. Therefore, birds need not blink their eyes during flight.

Please do add some solid references.