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Blood become denser when you are dying of deshidration?
Blood become denser when you are dying of deshidration? I mean, when you are dying of deshidration does your body extract water from blood to survie more time?

Your reasoning is a bit off. You need "water" in your blood to survive. When you don't have enough water in your blood, you become thirsty. If you can't drink, water is extracted from your cells to survive. When there's not enough, you die.

Here is an abstract describing an experiment where they kept horses away from water.
Carlson GP, Rumbaugh GE, Harrold D. Am J Vet Res. 1979 Jul;40(7):982-5.
Physiologic alterations in the horse produced by food and water deprivation during periods of high environmental temperatures.

Eight normal horses were held without access to food or water for 72
  hours during a period of high environmental temperatures. During this
  period, the horses had an average weight loss of 51.6 kg (10.7% of
  body weight). Highly significant (P less than 0.001) decreases in
  extracellular fluid volume (18.6 L) and plasma volume (5 L) were
  observed during this period as compared with base-line values. Plasma
  protein, sodium, chloride, and osmolality progressively increased in
  response to the dehydration, whereas packed cell volume, plasma
  potassium, calcium, magnesium, and phosphate were not significantly
  altered. The dehydration and clinicopathologic alterations produced
  were similar to those observed in other species in which the principal
  problem was a water deficit. After the end of the experimental
  dehydration period, the horses replaced 62% of the weight loss during
  a 1-hour period with access to water only.

As the horses became dehydrated they took water from both plasma (the fluid component of blood) and extracellular spaces (tissue water).  "Packed cell volume" refers to red cells.  Red cells and cells in general do not readily give up their intracellular water.  They defend it with osmotically active solutes.  If cells gave up their water the packed cell volume would decrease - like a cup of grapes turning into raisins.
Increase in "Plasma protein, sodium, chloride, and osmolality" reflects to non-water components of blood, which increased in concentration as water was lost.  Like a soup cooking down and getting richer.
This all works the same with humans.

"As the horses became dehydrated they took water from both plasma..." I'm not understanding; how did 'they' 'take water' from plasma? Where did it go to?

@anongoodnurse: To meet their physiologic needs for water.  Ultimately out in urine, sweat, breath and feces.

Urine production stops. Sweat isn't a major problem Breathing is. Feces? They'll stay there and get hard as rocks. I'm not sure where you're getting your info.

@anongoodnurse - if there is any confusion, a fine question for this stack would be "Why do organisms like horses need water?"

I know why animals need water. I'm pointing out that your answer sounds like water in plasma is less important that urine, sweat, breathing and feces. Plasma osmolality increases because there is no external source of water.

Yes blood becomes denser on dehydration (water dilutes the blood, if there's no water in blood it becomes dense). No, body does not draw water from the blood. When you are dehydrated, blood is the first source to be depleted. Then blood pulls water from cells (there are various hormones acting on kidneys and blood vessels trying to preserve the remaining amount of water by increased reabsorption, decreased excretion and vasoconstriction to comparitively useless parts of the body) and on continued dehydration, heart is not getting enough blood to pump as liver is sacrificing all its blood to the brain and cells are being depleted of water and are dried up. So blood is dense and there is not enough amount to reach the brain and brain cells don't get enough glucose (ischemia) and build up of urea and BUN in blood on the other side. Brain Cells switch the metabolism as they try to keep the cells alive only to produce radical oxygen species as by-products which in turn destroys the cells. And hence. Death. Eventually.

It will be very useful if you'll add a few references to your answer.

Umm. You can refer to physiology of brain cells and pathophysiology of Ischemic brain diseases, endocrinology and haematology chapters dealing with excessive excretion of water and body's compensatory mechanisms. I don't want to quote any book titles. You can just refer to any good pathology book. My answer is merely a gist of one of the possibilities of the process and it is related to severe dehydration or medical conditions that are irresponsive despite drinking loads of water. It is more complex than my above explanation. There are so many other pathophysiology of dehydration.


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What is this bird?
I have found this bird in my house, I live in Haedo, Buenos Aires, Argentina. I tried to take a closer photo but it escaped flying. I am not sure how to describe it, but it's very big compared to normal birds.
This are the photos:

In the US , I would say it could be an osprey , especially if there is a body of water nearby. Or Caracas if in dry grasslands.

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How much energy takes C4 photosyntesis to make glucose?
Wikipedia has a kind of contradiction that I would like to understand:
According to this link

The C3 pathway requires 18 ATP for the synthesis of one molecule of glucose while the C4 pathway requires 20 ATP. [...]

According to this other link:

[...]. The C3 pathway requires 18 molecules of ATP for the synthesis of one molecule of glucose, whereas the C4 pathway requires 30 molecules of ATP.[...]

Also, I don't understand much of this, I was just curious. I found this link (not sure if reduction also means generate glucose):

However, the C4 pathway of CO2 reduction expends more energy (5 ATP and 2 NADPH) than C3 pathway (3 ATP and 2 NADPH) (Hopkins 1999).

And this link:

ATP consumed in C4 plants
  C4 cycle ( which involves regeneration of PEP from C3 acid) - requires 2 ATP per CO2 fixed.
  C3 cycle ( which is common in C2,C3,C4 cycle)- requires 3 ATP per CO2 fixed.
  Total - 5 ATP per CO2 fixed.
  Thus to form a hexose or to fix 6 CO2 6*5= 30 ATP

All emphasis mine.
So... Does C4 requires 20 or 30 ATP per molecule of glucose? I think I found more evidence over 30 than 20, is that correct?

Yes,C4 plants use 30 ATP molecules to make one molecule of Glucose.See since you have stated in your question that you know very less about biology and got some similar vibes from looking at your profile so I'll sum it up in a nutshell but hopefully this might help.In flowering plants,all of them follow a basic pathway know as the C3 cycle to make glucose from CO2.Now,in that process about 18  ATP is used.But apart from CO2, there's O2 also present in the atmosphere which interferes with the compounds taking part in C3 cycle and instead of CO2 participation O2 participates in the reaction and the consequence is that glucose is not produced and the plant wastes some energy in the form of ATP.
Now to prevent that from happening,some plants evolved themselves and made some chemicals which bind only with CO2.But the thing is that they also require energy to function and for each molecule of glucose produced they require 12 ATP this making net amount of ATP required to be 30 in a C4 plant.You can in a way visualise this C4 pathway that the plant placed some guards in the form of chemicals that combines with CO2 and makes sure it reaches its destination and to prevent traitor O2 molecules to disrupt plants from making glucose.But we all know that that guards would require some fee and so that fee is 12ATP.And visualise C3 pathway as some some sort of glucose making factory which makes glucose from CO2 and the production cost from raw materials is 18 ATP.

Thanks for your answer. Since it seems that you know about this, could I make a not much related question? Does CAM photosynthesis is the same as C4 but instead of absorbing CO2 during the day it does during the night to avoid competitors (other plants) and lose of water due transpiring?

See CAM pathway is found in xerophytic plants.Now,for eg: in deserts,there is a very high chances of water loss.So what they do is that they use some similar compounds as C4 plants and use it to store CO2 in the nighttime as there is chances of high water loss during daytime.Now in the day time,they use the stored CO2 to perform photosynthesis and manufacture glucose via the normal C3 pathway.

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Why are there no known photosynthetic archaea?
I'm taking a microbial physiology course and we noted that, while some archaea are phototrophic, there are no known photosynethetic archaea.  Are there any physiological characteristics that make archaea less suited for photosynthesis?  Or is it simply a matter of there likely being photosynthetic archaea, but they have not yet been found (which seems like it could easily be the case, given that there are many extremophilic archaea)?

There are photosynthetic archaea (such as Halobacterium) but the mechanism is different. They use rhodopsin-like ion pumps (bacteriorhodopsin and halorhodopsin) to move ions against the gradient and produce ATP via chemiosmosis (like mitochondria).

I was under the impression that this was distinct from photosynthesis.  At the very least, my professor emphasized that this was not the case, as rhodopsins do not utilize an electron transport chain in order to make a proton gradient, but photosynthesis does.

@Squirrel: Isn't this just a matter of definition?  That is, one could define photosynthesis in very general terms as using light to synthesize energy-bearing chemicals, or specifically as the clorophyll-based synthesis used by plants.  As for why no archaea use clorophyll, I don't know for sure, but would guess it's because plants evolved it after they split from archaea, and the identical process is unlikely to evolve twice.  But I'd certainly be interested in a more authoritative answer.

@Squirrel rhodopsins work just like electron transport chains and produce ATP with the help of F₀F₁ ATP-synthases.

@Squirrel If your professor said haloarchaea don't count, then (s)he probably wanted to ask for photoautotrophs instead. Both plants and haloarchaea are phototrophs, but haloarchaea are photoheterotrophs since they cannot fix carbon. Knocking out PSII in plants will also convert them into photoheterotrophs.

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What are the requirements for a spectrometer to be used in biological research?
Suppose one would do spectrophotometry on biological materials. What would be the minimum requirements for the measuring device so that the results could be published in a reputable journal? I suppose that two important properties are

resolution of the spectrum (would e.g. 25 nm be enough? 15 nm? 5 nm?)
measurement error (10%, 5%, 1%, ..?)

What else (if anything) should be taken into consideration?

This is very contextual. Can you give any specifics about your experiment (what is in the solution for example)?

I am in the process of buying such a device, so I was hoping to hear about general principles. User Mad Scientist gave a good answer.

For all the common uses of a spectrophotometer in biology, any commercial one should be sufficient. For all the routine stuff, the quality of the spectrophotometer is usually of negligible importance.
There are no general rules on what errors and resolution are acceptable, that always depends on what you're measuring. The error should be significantly smaller than size of the effect you're looking at, otherwise you get no useable data.
There are many sources of error with biological systems, the spectrophotometer is really one of the last ones you would think of. Simply the error of pipetting is likely far larger than the error of the spectrophotometer, and differences in the preparation of your biological samples might introduce an even larger error. Unless you're doing something beyond the routine uses of UV/Vis spectrometry, you probably don't need to worry about this.


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Why do dog's eyes glow green on a photo?
Taking my current profile picture as a prominent example:

This photo has been taken with flash. As I gather, this is the same effect that makes a human's eyes glow red on photos, namely the reflection of the flash at the choroid and then passing back through the retina.
The retina is full of bloodvessels and the blood inside them gives the reflected light it's reddish color.
If it's the same effect, why is the color different?

Come on that's photoshopped

Nope. Not at all

Then it's a star wars dog or you got some weird camera thing going on. Try  post another with a person looking at the camera and that will rule out the camera thing. User 137 is right below but I've never seen something like this.

Dogs, cats, and many other mammals have a Tapetum lucidum which reflects light back through the retina to help with night vision. Humans don't have this layer. The tapetum is probably reflecting green light that would have normally been absorbed.

The rod cells - cells used for night vision - are the most sensitive in the green region of spectrum. It does make sense for tapetum lucidum to reflect these preferentially

It's also interesting that different dogs can reflect different colors.  My Border Collie mix reflects greenish, but my (probably) Plott Hound reflects blue.  (This is with an LED headlamp at night, not camera flash.)

@jamesqf Sometimes 1 animal can do two colors at once.


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How can one determine how much of a region flanking an RNA sequence of interest to include in order to look for interfering secondary structures?
I have a set of RNA sequences, and I have been analyzing slices (i.e. target frames) of these sequences in order to determine whether they conform to certain structural criteria. One of these criteria requires that both the target frame of the RNA sequence and its flanking regions have as few secondary structures as possible, i.e. that the RNA nucleotides flanking the slice are as linear as possible.
Using Python and a number of standalone executables, I have been calculating the minimum free energy and optimal structural conformations of the RNA sequences and their flanking regions (see here for more details: http://math.mit.edu/classes/18.417/Slides/rna-prediction-zuker.pdf), but I realized that there is a slight hiccup in my current approach. Namely, I determine the secondary structures of the flanking regions as though they were sequences isolated from my target frame of interest. Now, given that the whole is more than just the sum its parts, I do not know if the secondary structures that are determined when the flanking region is examined on its own versus when the flanking region is examined including either a part or the whole target frame are the same.
Right now my code evaluates 20 nucleotides up and downstream of the target frame as the flanking regions, but should I instead, for example, evaluate 20 nucleotides up and downstream plus some nucleotides of my target frame? Right now, my target frame is 120 nucleotides long, so it might be worthwhile to consider 10 or 20 nucleotides of my target frame that are attached to the flanking regions. But I'm not sure how many nucleotides from my target length should be considered in order for the number of secondary structures to be consistent in the flanking regions. Or is this approach somehow faulty?


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Is our genetic evolution driven by what we catch?
When an environment changes, a multi celled organism can lose some cells without it producing an equal evolutionary change. But when a single cell organism experiences the same environmental pressure change, its life or death.
So single celled populations should evolve in direct relation to the environmental changes, while multi celled populations would evolve only in response to large scale environment changes.
If we are infected by the single cell organism, and it manages to insert highly evolved genes into one of our stem cells, then is it possible for these genes to insert in the correct place and upgrade our genetic code with new adaptions to the minor environmental changes?

Welcome to Biology.SE. The question is unclear to me. It is a little hard to pinpoint to what is unclear and there's little I understand. Here are two points. (1) lose some cells without it producing an equal evolutionary change I don't understand what you mean by evolutionary change here. (2) what do you mean by highly evolved genes. I think the start by saying that organisms of different size often face environmental variations at different scale (which is true). Then you seem to talk about parasitology but I am not sure what your question is.

As you are using terms and expression that are never used within the field of evolution biology (such as upgrade our genetic code or evolved genes), I think you might want to follow an introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

If the question is "do populations evolve in response to parasites", then the short answer is "yes".

But when a single cell organism experiences the same environmental
  pressure change, its life or death.

Do you understand that evolution is not about changes to individual organisms?  It's about changes to populations of organisms

So single celled populations should evolve in direct relation to the
  environmental changes, while multi celled populations would evolve
  only in response to large scale environment changes.

I have no idea what you mean here.  If you mean "A little DDT won't cause any changes to DDT resistance in a population of mosquitos", you are just wrong.  If you mean "A global climate temperature increase of 1 degree won't affect polar bear populations at all", that's wrong.

If we are infected by the single cell organism, and it manages to
  insert highly evolved genes into one of our stem cells,

Can you start with some evidence that this every happens?  Or any evidence that it happens often enough to be a common driver of evolution?  (Note that viruses are not organisms)


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How did we get self-aware?
Imagine being under a lot of stone age people and you are the only one who thinks something like "Hey I am a human being, and now I am thinking about this and that and maybe I change myself to become a better person". You would see the world in a totally different way. No one would understand your behaviour because nobody thinks about himself (self-aware) or sees the world as you do.
So my question is: How did we get self-aware? how did we develop this "feature"? And why did we develop this, how could the nature think that this would be an advantage?
There has to be a small "jump".
I mean, somebody has to be the first who thought about himself. Either you know (or think about) that you are a being or you don't. So you can't just be a little self-aware right?

There is no scientific consensus on this. The very nature of consciousness / sentience / self-awareness has been debated for centuries but is still not well understood. Some people argue like you do that self-awareness is a "jump", while others think that it is gradual. See https://en.wikipedia.org/wiki/Consciousness  for some more information.

Agree with Roland. I just want to add that you assume a first, remarkable jump toward self-awarness but there is eventually a gradient of self-awarness (as you suggested in  the last line of your question) and the position in any individual on this gradient also depends on social experience. Note also that there is no reason to think that such feature had been under direct effect of selection but may have evolved as a correlated side effect of some other trait.

The use of the term "feature" instead of "trait" and "develop" instead of "evolve" made me thing that you might eventually want to follow an very short introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

When talking about the evolution of self-awarness or other psychologic trait (evolutionary psychology), we often fall into a field where (1) empirical test of predictions are difficult to perform and (2) terms for which we have vague intuition need formal definition to be properly tackled and (2a) not everybody end up agreeing on a definition and (2b) there might not exist a natural category which corresponds closely enough to our vague intuitive understanding of a concept.

I think that through hunting all the time the ability of communication was more and more important. A failure of understanding could have ended in a disaster. Through communication they organised themselves and looked for the best way to hunt in group. Because of this they could have been thinking how to hunt better and, to work in a group the best way, how to be better in order to provide better understanding (social intelligence). Couldn't that be a possible way how this has evolved?


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What kind of an animal is that?

Found in Austria. At half past nine p.m. in the summer/autumn.


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Do pet animals and humans perceive good and bad smells differently
As the title says, just wondering if there is a difference in what animals like dogs and cats perceive as good smell vis a vis humans. Example : Smell of some flowers - great . Fart smells - bad.

When I see dogs and cows roaming in stinking garbage, I feel like the answer is no.

Humans perceive colours differently from each other, so why wouldn't the same be true of pets/dogs/animals in general, for smell? Even humans don't like the same smells. My mother despises the smell of daffodils. They make her gag, and if she is around them enough, vomit; But plenty of other people seem to love the smell.

Thank you for your comments. XaNaX, I understand your point. What do you think the reason for this difference is ? I am not an expert in understanding how the nose senses smell, but is this perception of good and bad smell physiological or is it psychological ? With eyes, the differences are the rods and cones right, so is the perception of good / bad  smell similar?

This article suggests that when we first smell something, we link it to the emotions we feel at the time. Those emotions are then associated with that smell, the article says, and depending on whether or not the original emotion/event was a positive or negative one, we then have a reaction that reflects the original emotion when we again smell that something.

TL; DR Mostly no.
On a molecular basis, cats' and dogs' noses look quite similar to ours. Most of what we know about smell comes from studies on non-human mammals, and is supposed to apply to humans too. So, big similarity, but...

Cats and dogs distinguish far more kinds of than humans. It's likely they know more kinds of bad smells and good smells, possibly including from things that we think lack odour.
Many animals also have a working vomeronasal organ, that is, a sensing organ similar to the olfactory mucosa we use for sensing common smells. The vomeronasal organ detects pheromones, the smell-like signals used for communication between animals. We, humans, are at least deficient, if not completely unable to use the vomeronasal organ and pheromone signals. It is debatable whether animals conflate regular smells with pheromones. Pheromones are very efficient in conveying information about potential sexual partners, rivals, and so on. So these are a completely different set of bad and good smells, available only to animals. That is, if we can call those sensations smells, a big if.
On the other hand, humans evaluate smells culturally. Some people learn to enjoy offensive smells that people from other cultures carry on disliking. Since dogs have limited ability to manipulate smells and to convey information to another dog, I doubt they can form these cultural constructs of smell. We sense sensuality in a perfume; the dog senses a bunch of pungent flowers, neither good, nor bad.

Thanks for the detailed answer Nick and also XaNaX for the link.

@VarunBKothamachu: On another side note regarding point 3: my cats absolutely dislike the new brand of antiperspirant I use. The old one seemed to be more okay to them. Additionally, one of my cats hates the smell of ginger and cumin (she even makes a sound that expresses her aversion and jumps away from it), while the other one clearly does not like it but is not really freaked out when she comes into contact. There must be a thousand anecdotes like that. :)


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Natural killers cells in insects/ arthropods
I'm wondering if someone knowns anything about Natural Killer cells in insects or other Arthropods. Do they exist or are their any similar cells of the innate immune system that someone knows of?
Thanks a lot!

should be easy to find some information on google for that straightforward question? where else have you tried looking?

I tried google and more specific scientific literature (concerning the immune system of insects, crustacea and drosophila), I find elaborate descriptions of the innate arthropod immune system, but NKcells (or cells that perform similar functions) were never mentioned

NK cells are desinated adaptive immune cells now. There was a discussion on this topic some while ago.


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Are there any viruses that have infected all humans in the past or present?
Are there any known viruses that have managed to infect all of humankind either in the past or presently, either benign or otherwise?

Could mitochondria, ancestrally the result of a bacterial infection, be included?

Quick answer: yes. Research human endogenous retroviruses for more information.

Do ERVs count? None of the HERVs are functional viruses(anymore). And they didn't need to infect 100% of humanity to cross over, so they may not have. On the other hand, does gut microflora count? There are lots of those, even if they don't infect human cells there's probably one that's inhabited 100% of humans at one time or another.

You mean to say some virus that everyone has got infected with at one point of time or the other. I don't understand the point of this question. Even for a common infection like viral cold, there can exist people who have not contracted the disease. @MattDMo are ERVs same as retrotransposons?

@WYSIWYG according to Wikipedia, yes, to an extent - HERVs are one class of retrotransposons.

This shouldn't be closed - I found the answer. The HHV-6 family of herpes viruses infects almost all humans by the age of 2. Thankfully, it's generally a commensal and negative health effects from it are rare. See https://hhv-6foundation.org/what-is-hhv-6

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Why is the nutritive value of grass to humans compared to alternatives?
Cows thrive on eating large amounts of grass. That's because they have specialized digestive processes, such as chewing a cud that maximizes the value of grass to her. Humans who don't have these processes, don't get as much a of a benefit.
Suppose a human being were "stuck" for food, and the most available food was grass. What percentage of the nutritive value of the grass would the human obtain, compared to what the cow would obtain? Also, how would the nutritional value of grass (for humans) compare to vegetables such as lettuce or spinach? And is the lack of nutritional value of grass one reason why humans prefer to eat beef rather than grass, even though 90% or so of energy is lost at every level of the food chain?

Grass has high silica contents. Chewing it would ruin your teeth. 2. We can't digest the cellulose and hemicellulose that are the major components of grass. Of most nutritional value would be the non-structural carbohydrates and sugars in grass. Their content depends on grass species, fertilization, environmental conditions, age, ... However, we are ill-equipped for extracting these sugars. The most probable outcome of eating larger quantities of grass is vomiting (which would make you lose nutrients in an emergency situation).

The exception would be sugarcane, which you could chew to extract the sugar.

Also, consider that cows do not much else than eating grass and digesting it, because this process is not very efficient. Human brains also need much more energy than cow brains. I don't think we could afford that and our usual level of activity if we were ruminants.


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Can different kinds of dogs mate?
This was inspired by a show in which two different kinds of dogs, who were neighbors, "dated," in order to bring their human neighbors together. This is a theme seen in Disney's "101 Dalmations" or "The Lady and the Tramp."
Can dogs of similar sizes, say Rotweilers or pitbulls actually interbreed? Can any of them mate with say, wolves? And under what circumances?
(I am "encouraged" by the fact that horses and donkeys can produce mules, and lions and tigers can produce "liger" or "tigons." Also of note is that dogs are of the same species as wolves, and "domestic dogs" are actually a subspecies.)

You don't need to restrict this to similar sizes. As long as the female is not much smaller than the male (making the uterus too small for successful pregnancy), it is possible (although it might require help for the mating act or even artificial insemination).

Yes, the vast majority of dogs out there are not pure bred. They are therefore a cross between two breeds. Consider cockapoos for example. The offsprings of a Cocker Spaniel and a poodle is called a cockapoo.

Yes, and domestic dogs can interbreed with both wolves and coyotes.  Also wolves and coyotes interbreed, producing the "coywolf", which is apparently becoming a significant predator in eastern North America: https://en.wikipedia.org/wiki/Coywolf


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Can elementary alternative splicing events be combined in more complex events?
I'm a computer scientist who is trying to understand alternative splicing. As the title says, I'm here to ask you if, from a biological point of view, elementary/basic alternative splicing events (such as exon skipping, alternative 3'/5' splice site...) can be combined into more complex alternative splicing events. If it is possible, how common is it?
Just to clarify my question, let A->B->C be a transcript made up by three exons (A, B and C). Biologically, is it possible to obtain a new transcript A'->C in which exon B has been skipped (exon skipping event) and exon A has been "cut" at a different splice site producing A' (for instance, alternative 5' splice site event)? Can I obtain also A->C' (exon skipping of B and alternative 3' splice site of C)? Another example could be the following one. Le A->B->-C->D be a transcript. Can I obtain a transcript A'->B'->D?
From a combinatorial point of view, I can combine all the events and all the exons in many different ways but from a biological point of view, are all the possible combinations plausible?
If so, can you please point me to some articles describing how alternative splicing events can be combined?
Thank you and sorry if this has been asked and answered already (but I didn't find anything regarding it).

This is a good question. I cannot see any biological mechanistic reason why the combination you suggest could not occur, but unfortunately I cannot provide you with an example. The literature on the subject looks very complex (e.g. see http://www.nature.com/nbt/journal/v22/n5/pdf/nbt964.pdf), so you really need help from someone in the field.


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Scientific name of a lizard's reproductive system
I need to find the scientific (latin) names of the reproductive organs of female and male lizards. So far the only result I've got is that male lizards have hemipenes inverso, but nothing on the female part.
Thanks for the help!

i'd recommend wiki and google images for that.


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What causes notches in elephants' ears?

What causes the elephants' ear to rip like this?
Is it a natural process as they get old, or it's injuries, like consequence of fighting with other elephants?


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Are there two varities of dandelion leaves?
This is in India. I noticed a dandelion plant which had the familiar leaves.

Right next to it there was another plant which had similar flowers and white tufts, but the leaves were different.

Is the second plant also dandelion? I'm asking because I was considering feeding the leaves to my budgies, but needed to know if it is a dandelion, to avoid having the birds consume a toxic plant species.
Did a Google search, but all of them show the arrow-style leaves only as dandelion.

I'm not familiair with the flora of India, but these both look like sonchus species to me, not taraxacum (dandelion).

Although the leaves are similar, these are both not Dandelions Taraxacum species, because:
1. Dandelions have leaves in a rosette, not distributed along a stem.
2. Dandelions have a stem with a single flower at the end, not multiple flowers.
3. The shape of the closed flower heads after flowering is too pointed.     Dandelions usually have the pappus (white hairs) sticking out a little.
These distinctions can be clearly seen in the picture below:

I am not familiair with the flora of India, but I think these could be Sonchus species. Sonchus is known to have  variable leaves.
For comparative purposes, see how Sonchus looks like

Very good answer! I hope you don't mind I added a Sonchus picture!

Dandelion is the commom name used to make reference mainly to Taraxacum officinale, but actually is also used to virtually any species of the genus Taraxacum. I mean, a lot of species are known as Dandelion, hence this name comprises a lot of morphologies.
Also, there is something called "Phenotypic plasticity", which refers to changes in the organism characteristics due to adaptation to environmental factors. (I.e. one species may have different morphologic and physiologic traits in response to environmental variation).
Regarding to the photos you posted, it's not safe to tell you if these are the same species or not, because one would need way more detailed images, mainly from flowers, to give you a more accurate identification.
There is a Fabebook group named DetWeb, where botanists identify plants if you post good enought photos... It's a brazilian group, but you can post in english, of course.

In my opinion, this doesn't really answer the question, which is if these are dandelions or not.

yes, you are right... but it's a brief explanatin on why it's not simple to tell if these are two dandelions.. Do you think I should have provided this information as comment instead of answer?

It is probably to long for a comment. And one can easily tell these are not Dandelions.


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Do homologous chromosomes have same rates of gene expression in a cell?
I was googling around and found only articles related to XY differences in expression. Can you please clarify if homologous genes/chromosomes have about the same levels of expression in a cell or one of them "stays silent" and another is "switched on" somehow?

It's a complicated subject. Try searching for "genetic imprinting" and also for "epigenetics" and for "gene regulation in cis and trans".

thanks for a feedback! Everything is a complicated subject, I'm a software engineer by the way ;)


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Is there a link between digestion and nightmares?
A common belief is that eating too much before going to sleep can cause to have nightmares. In fact, I often experience it: I systematically have nightmares after eating too much in the evening.
Then I was wondering: is there really a link between digestive system's activity and unconscious brain's activity?
If it actually exists,
- is the influence linked to the neurons we have in out gut?
- or is it linked to the augmentation of the concentration of a nutrient in our bloodstream (which can then reach our brain and)?
- or is the neuronal activity which control digestion that interferes with the process of dreaming?
If the influence is linked to the augmentation of the concentration of a nutrient in our bloodstream, does this mean what we eat actually controls our mood or level of anxiety, or any subconscious process? (regardless of compounds known for having a particular effect, like theobromine, etc...)

Although I haven't experienced this specific thing, it's reasonable to say that if someone is uncomfortable somehow when they're sleeping, that that would translate to bad things happening in dreams, as the brain tries to figure out a scenario that would account for the body's sensations. So my thought would be, maybe some stomach sensations are somehow uncomfortable, or maybe similar to how your stomach feels when you're scared. Or maybe this would be something totally different.

According to http://www.medicaldaily.com/bad-dream-more-just-dream-science-nightmares-327586 the extra energy from late night eating can increase brain activity and may contribute to nightmares.

Speaking from experience, I slept really well yesterday after my weekend lunch when I ate so much that I had trouble moving around. So, on a very light note I don't think overeating leads to nightmares. Rather, for me they would lead to a no dream sleep.

Thanks for you answers. I'll try to follow the lead of extra energy to figure out more precise processes.

I just wanted to note that I never felt any feeling of discomfort due to over eating in those situations, and I think this aspect of discomfort adds more complexity to the activity of the organism in its entirety, because it is a "violent" state compared to a normal digestion. Though, it could be interesting to study too.

A nightmare is basically an alarm; typically your subconcious mind trying to wake you. Nightmares often occur when you are experiencing pain or discomfort (like needing to use the bathroom).
Dreams are a way of sorting through questions in a "what if" sort of way. When it comes to a nightmare, you are in a panic-situation, often without a solution, or where a "logical" solution is unsuccessful.

Could you cite some sources for your claims regarding dreams and nightmares? While not implausible, the claims raise more questions than they answer without any supporting evidence.


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SRAP marker sequences
I am looking into SRAP markers and I have realized I am not sure if I need a reverse complement of the sequence given in the article or they are "ready to use" primers?

Can you add sources or links to your markers and explain what you are planning to do so that users can provide you with more accurate answers?

Which article are you talking about?


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Can one use dialysis tubing several times?
I would like to know, if one can use dialysis tubes multiple times. Or is there a risk of plugging the pores? I use the tubes for dialysis of a solution that contains a precipitated enzyme (183 kDa) and ammonium sulfate (132 Da). Thanks!

This is more of a long comment than an answer, since I don't know. It could be okay, but if you are unsure whether it will work, is it really worth the risk? Here are some thoughts:

With high AS concentration, there is an initial large influx of water which can stretch the tubing. If this is repeated several times you may stretch the pores to where they no longer retain your protein. You can determine yield after each dialysis to see if loss increases with use.
Clogging up the pores seems like it could plausibly happen. You could add some low molecular weight dye to monitor whether the membrane remains permeable with use.
Dialysis tubing costs like 5 ¢/cm. Unless you're using 10 meters at a time, it's really very cheap.


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Can dissolved aluminium from centrifuge tank deactivate enzymes?
I extract an enzyme called diamine oxidase with a tubular centrifuge. The centrifuge uses an aluminium tank to collect the liquide after centrifugation. I asked myself what would happen if some aluminium particles pell of from the tank due to the collision of liquid and got into the solution. Could this deactivate the enzyme?


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Degradation of PMSF in protein extract while dialysing - safe for feeding to animals?
I would like to use the protease inhibitor PMSF in enzyme isolation. The obtained enzyme diamine oxidase (or better the protein extract) is tested oral on dogs.
According to Wikipedia, PMSF has a lethal dose less than 500 mg/kg, but also degrades rapid in water, which would meet my application. (The half-life is short in aqueous solutions, 110 min at pH 7, 55 min at pH 7.5)
After roughly isolating the enzyme, I dialyse the protein extract for about 12 hours. Is this time sufficient, so that there are no or only small amounts of PMSF in the extract anymore?

Be careful with the toxic dose - it is not disclosed for which species this is valid. I would assume this is for humans and might be drastically different for dogs. So we can most like not give you an advice on a safe dose.

How much PMSF would you feed the dog if you used the initial prep? And do you want to use PMSF to be sure, or do you actually need a protease inhibitor?

@VonBeche How much PMSF would you feed the dog if you used the initial prep? -> Nothing, I want it to degrade in water while 12 hour dialysis. And do you want to use PMSF to be sure, or do you actually need a protease inhibitor? -> I am relatively sure that in the protein extract are proteases and I want to get the maximum yield of enzymes.

Please do / show some back of the envelope calculations to see how much would end up in the dog. Dialysis will approximate dilution for a small molecule like PMSF.


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Where occurs diamine oxidase in kidneys - in cells or in extracellular space?
I would be interested in where the enzyme diamine oxidase in kidneys of human/animals mainly occurs? In cells or in extracellular space? A literature reference if available would be great. Thanks!


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Do ants really find the shortest path to a food source?
There exist many computational intelligence algorithms based on the observation that ants deposit pheromones in such a way that they find the shortest path to food sources. This logic is used to optimize computer networks.
I cant really relate to that. I have seen ants take an extremely long path to food. This is not always for safety reasons either. What do biologists have to say about this?

Look on Wikipedia for "ant mill", or YouTube for "ant death spiral" and you will find they make paths that are not only sub-optimal, but are in fact invalid paths altogether.

Short answer

Do ants really find the shortest path to a food source?

No! But they can find a decent path
Longer answer
Optimization algorithms are used to search through a possibility space that is too large to explore every single possibility. Such algorithms attempt to find a good enough solution, often without necessarily knowing how 'good' the found solution is to the best possible solution. So optimization algorithms don't always find the best solution. Actually, most of the time, they do not find the best path but a good enough one in a reasonable amount of time.
Same holds true for ants. In the analogy, an ant colony is an agent based algorithm where agents leave pheromone trails. The concentration of the pheromone depends upon the length of the trail. By following the trails that smells the strongest and by regularly making small errors (so that they can keep exploring other paths), they end up with a decent solution. For more info, just google How do ants find their path?.

If we don't know how good the found solution compares to the best, then how do we know it is good enough?

@Ooker How do you judge what path to take to places? I think you'll find that you don't relate it to the "best" path (which you might not know) but to the situation instead, such as "is it okay to spend this amount of time".

Similarly, when you take your car to go to some place, the path you take is generally "good enough" and not the best. It is good enough because it  takes a reasonable time to go to destination...

@Charles Thanks, I brought a small modification to avoid stating that an optimization algorithm never know what the best solution is.

@Charles I don't agree. You can test the strength of a solution against other possible solutions. You don't need to know the distance of the best route possible to a location, if you work out 1,000 potential routes and then take the shortest of those

@Charles is there a way to calculate the confidence of the accuracy of the calculated path? Correct me if I'm wrong, but isn't that in statistics the confidence of a guess can be calculated independently with the correct value?

@ooker You cannot calculate the confidence in whether you have the best path from just sampling (trying solutions and seeing which ones work) unless you can brute force the entire state space.  However, if you know something about your state space, then you can use that problem-specific information to determine how good your solution is.  For example, if you know the space is differentiable, you can use any information you might know about the maximum derivatives to create an upper/lower bound.

@Charles: "If an optimization algorithm isn't aware of the true solution that it's trying to acheive, then it has no way of validating a potential solution." - That's not true - very often in real life the criterion is "Solution must cost less than X". If a solution is found that has a cost less than X, it is "good enough", and hence valid. If it is a lot less than X, so much the better. There's no need to know the absolute best achievable value. The value of X depends on the (external) constraints of the project, not on the parameters of the optimisation problem itself.

@Charles: I did read that comment, and it is different from what I'm saying. I'm not saying that you define an epsilon that gives an acceptable (proportional or absolute) difference between the true optimal value and the best found - that still requires a priori knowledge of the optimal value. I'm saying instead that you define a threshold X that's independent of the optimal value - i.e. you don't actually care at all how close you are to the true optimum, just whether you find a solution that "works" in whatever context you're operating in.

Comments are not for extended discussions. Please follow this up in the chat (and eventually on some CS SE site).

@Charles: You're confusing the algorithm with the problem domain, and specifically the problem's acceptability criterion (for the ants, perhaps: does the energy in the food at the end of this path exceed the energy expended taking the path by enough to ensure survival?) with the stopping criterion/heuristic of a particular algorithm ("OK we've spent enough time & energy checking out paths, now let's get on and eat."). The former will likely influence the choice of the latter, but it's important to be aware of the distinction. Good luck with your studies, your protein project sounds cool :)

@Pimgd https://xkcd.com/85/


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Why does inbreeding cause genetic defects, but cell division in one's own body does not?
I was watching a DNA transcription video when I realized that cells basically create copies of DNA all the time in our body. There may be a few mutations/errors, but it works out fine. However, when the haploid DNA in sperm combines with the one in the egg, there's so much extra work to be done to avoid errors. It's like if I write some software in one project and try to combine it the code I've written in another project, it's easier for me to do it because my coding style is similar and I know the code. But if I have to merge somebody else's code into my code, there would be a heck of a lot of merge conflicts and errors. Sure, I may learn better programming from the other person's efficient code, but the amount of bugs, testing etc. will be much more cumbersome.
Some research says:

Malformations or harmful traits can stay within a population due to a
  high homozygosity rate, and this will cause a population to become
  fixed for certain traits, like having too many bones in an area, like
  the vertebral column of wolves on Isle Royale or having cranial
  abnormalities, such as in Northern elephant seals, where their cranial
  bone length in the lower mandibular tooth row has changed. Having a
  high homozygosity rate is problematic for a population because it will
  unmask recessive deleterious alleles generated by mutations, reduce
  heterozygote advantage, and it is detrimental to the survival of
  small, endangered animal populations. When deleterious recessive
  alleles are unmasked due to the increased homozygosity generated by
  inbreeding, this can cause inbreeding depression.

But bed bugs for instance, have managed with inbreeding without any problem (goddamned creatures!).
The question I'm asking is from the perspective of how the DNA combination and copying happens. Since the regions chosen during meiosis is random, shouldn't a similar DNA from sperm and egg resulted in a more stable genetic code since they are similar? I'm not looking for simplistic answers like "because Nature wanted diversity" or "because recessive alleles are unmasked".
I'm looking for a more fundamental explanation about the property of DNA, or the process of copying/merging these complex structures. Why does merging two similar things cause more problems than merging two dissimilar things?

You are citing texts with terms "recessive alleles", "homozygosity" and "heterozygote advantage" but you not using them in your own questions makes me think you don't fully grasp them. Are you fully fammiliar with Mendels laws?

Homozygocity etc. are like telling grandma that the "internet" is a bunch of connected computers. My question is a more fundamental "why" about the genome.

Cell division involves mitosis primarily. In sexual reproduction there is meiosis. Genetic recombination occurs primarily when there is sexual reproduction. In short, your cells are simply multiplying, they do not have sex, and thus there is no novel genetic material (which there is with sexual reproduction). In sexual reproduction, there is a 'purging' effect: if there is a bad allele in some parental DNA, it could be masked by a good copy of the other parent. Your question stems from a misunderstanding of sexual reproduction and a mixup of inbreeding, very different to somatic cell divison.

I suspect your problem is grasping what is a deleterious recessive allele. Wikipedia and textbooks explain it much better but I will try to illustrate with respect to your question.

I have to merge somebody else's code into my code, there would be a heck of a lot of merge conflicts and errors.

Problem with this analogy is that when merging code both variants are written by people. People tend to write code that works on its own. This is not the case for DNA since mutations are usually random and more often than not result in gibberish. Better analogy would be maybe combining information from two coppies of the same data to overcome bit rot.

Since the regions chosen during meiosis is random, shouldn't a similar DNA from sperm and egg resulted in a more stable genetic code since they are similar?

Lets consider two made up genes A and B.

A is a dominant functional version of A gene involved in development of hand. In very abstract (code-like) way it could be read as: "If at the end of hand initiate 5 fingers"
a is a mutated nonfunctional version of A gene. In very abstract way it could be read as: "If at the end of hand initbzngers". It produces nonfunctional protein. In biological terms "a" is called deleterious recessive allele.
B is a dominant functional version of B gene involved in development of brain. In very abstract way it could be read as: "If in neuron keep junctions together"
b is a mutated nonfunctional version of B gene involved in development of brain. In very abstract way it could be read as: "If in geuron keep junctions together". It never produces the needed protein.

Now lets consider cross between two dissimilar individuals:
father AaBB X mother AABb
Following Mendel's laws they produce progeny:

AABB - has at least one functional copy A and B gene and thus develops fine.
aABB - has at least one functional copy A and B gene and thus develops fine.
AABb - has at least one functional copy A and B gene and thus develops fine.
aABb - has at least one functional copy A and B gene and thus develops fine.

now let's consider cross between two similar individuals:
father AaBB X mother AaBB
Following Mendel's laws they produce progeny:

AABB - has at least one functional copy A and B gene and thus develops fine.
AaBB - has at least one functional copy A and B gene and thus develops fine.
aABB - has at least one functional copy A and B gene and thus develops fine.
aaBB - fails to properly develop fingers.

cells basically create copies of DNA all the time in our body. ... Why does inbreeding cause genetic defects, but cell division in one's own body does not?

During normal cell division AaBB cells should produce only AaBB copies which have at least one functional copy A and B gene and thus are fine.
Big picture
In a real population imagine every individual has tens of thousands of genes and each of them can be made nonfunctional by random mutation. The nonfunctional copy often does not have effect since the individual has another functional copy. When two non-related individuals procreate, chances are mutations they carry are in different genes and their progeny are fine as illustrated above. When related individuals procreate chances are thay both have the same deterious mutation(s) and not all their progeny will be fine.

But bed bugs for instance, have managed with inbreeding without any problem (goddamned creatures!).

Species for which inbreeding is normal have much less recessive deleterious mutations prevalence in populations for simple reason. If new deleterious mutation appears the inbreeding leads in two generations to aa homozygots that die or fail to procreate and the "bad" mutations are selected out fairly fast. Inbreeding is normal state for some species. Today inbreeding-resistant species are descendants of individuals who have survived many generations of inbreeding.

You say

cells basically create copies of DNA all the time in our body. There may be a few mutations/errors, but it works out fine.

and

Why does merging two similar things cause more problems

Well, it doesn't, at least not in the way you seem to understand it. Cell division in the adult human leads to problems too. Every time a cell of yours divides, there is a chance that something goes wrong and the new cell receives an imperfect copy of the DNA. This is what is called a "somatic mutation" (the opposing term would be "germline mutation"). This is the reason people get cancer - when you are unlucky enough that a cell of yours gets all its anti-cancer mechanisms get mutated away, it can become the "granddaddy" of a tumor in your body. It (and its descendents) start multiplying exponentially. And of course, there is even more mutations in this large number of new divisions, which makes for subclonal tumors, complete with a perfidic kind of natural selection when exposed to some of the newer targeted therapies we have. So this kind of mutation happens frequently, and it does lead to quite large problems for individuals and for humanity as a whole.
The problems with inbreeding also exist, they are just a different kind of problem with a different cause and effect. Here, what you are afraid of is not a mutation. Rather, as explained in more depth in the other answers, if the father has one good and one malfunctioning copy of a gene, and the mother has one good and one malfunctioning copy of the same gene, you get very high chances of having a baby with two malfunctioning copies of that gene, without any transcription errors coming into play at all. And it is very rare for this to happen if you randomly select a mother and a father from the population, but if the two of them share a significant proportion of their genes (because they are related), it happens fairly frequently - enough for basically all human societies to have noticed it even in ancient times and to have created taboos around inbreeding.
A third thing can also happen, which is a de novo mutation in the very early stages of cell division of the zygote. It is not necessarily a result of merging the genomes of the mother and the father, but rather a cell division problem after this merging has happened. It is not necessarily more rare, per division event, than the somatic mutations (the first kind of problem). But it will affect all the cells emerging from that mutated cell, which will be a significant proportion of the baby's body. This is an event that is not very noticeable, since many of the problems at that stage will not result in a life birth - in fact the pregnancy/conception can end so early that the mother never realizes she conceived. It is also not as prominent in social norms, since it is not correlated to something obvious like inbreeding, so there are no traditional prohibitions for events that lead to it (actually, there are modern prohibitions, like warnings in situations which can cause mutations in a fetus or a zygote).
All three of these exist, and all of these lead to problems. So your wondering why one is a problem and the other isn't is based on a misunderstanding.

Why does inbreeding cause genetic defects, but cell division in one's own body does not?

Inbreeding does not cause genetic defects, it just makes already existing ones more likely to be problematic.

Why does merging two similar things cause more problems than merging two dissimilar things?

You have two copies of each gene, one from each parent.  For many possible defects all that matters is that you have at least one working copy, which can compensate for the other not working.  If you take two parents that each have a bad copy because they inherited from a common ancestor, there is a high likelihood that their children will receive two bad copies, and thus the previously hidden defect will be expressed.

I'm looking for a more fundamental explanation about the property of DNA, or the process of copying/merging these complex structures.

The fundamental part is just that you have two complete copies of your genome, one from each parent.  If you didn't, inbreeding would be much less of a problem.


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Do local field potentials (LFP) create waves on the surfaces of nerve cells?
Are waves created by the LFP on the surfaces of neurons cell bodies? Since the cells have a resting potential, do these waves create harmonic oscillation of the membranes at particular frequencies?
Are there studies available that look at electrical potential waves on the cell surfaces? I think that membranes should be sensitive to the LFP since they maintain a charge.

A LFP can be measured at any point in space and is just the sum of all the fields generated by nearby charges.  Conventionally, it's assumed to be some distance from a cluster of neurons, but you technically could measure the LFP near the external surface of a neuron (but that would bias your signal towards the reading of that one neuron).
LFP's are relatively weak, but have some small influence on the neighboring cells:
Modeling the coupling of single neuron activity to local field potentials


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Is there a way to remove hemoglobin from pig kidney homogenate without deactivating enzymes?
I would like to measure different enzyme activities in centrifuged pig kidney homogenate. I get out of range errors at 450 nm. The samples are still reddish after centrifugation. Is there a way to remove hemoglobin without deactivating / removing enzymes? Thanks!


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Sugars which are Carbohydrates and vice-versa?
Is it right that are all sugars are carbohydrates but not all carbohydrates are sugars?
If so, which carbohydrates are sugars and which aren't and why all sugars are carbohydrates?
If I had to answer I'd say there are carbohydrates of three kinds: sugars, starch, fiber and from which we can deduce that "not all carbohydrates are sugars".

there's also glucose and fructose i think...

Sugar is a common name for the scientific word carbohydrate. Carbohydrate are of four types basically on the basis of the number of units: Monosaccharide(1unit of sugar molecule), Disaccharide (2 units) Oligosaccharide (3-10 sugar units) and Polysaccharide(more than 10 units of sugar molecule).

@SanjuktaGhosh: Does that mean all carbohydrates are sugars?

@cpx I won't say that. I'd say sugar is another name for carbohydrate.

You need to make a distinction between polymers and monomers (or dimers).
Typically, sugars are monomers like glucose, maltose, or fructose. Sucrose (table sugar) is a dimer. These are all carbohydrates (made up of carbon, oxygen, and hydrogen).
Polymers of these sugars are also carbohydrates. For example, starch, glycogen, and cellulose.
Cellulose, which you called fibre, tends to be structural, and is only found in plants (think celery, or wood, or paper). Starch, is also synthesized by plants, and could be used for energy storage (as I recall). In animals, monomeric glucose is stored as glycogen in skeletal muscle, where it becomes available as energy for short bursts of energy.

Doesn't answer the question.

I'd edit your last sentence to stop after the first mention of the word glycogen. It is stored in liver and brain as well as muscle, and you must surely regret writing "energy for short bursts of energy".

The statement in your question is correct. All sugars are carbohydrates but not all carbohydrates are sugars.
In fact, sugars are by definition carbohydrates. Wikipedia defines sugars as :

Sugar is the generalized name for sweet, short-chain, soluble carbohydrates, many of which are used in food. They are composed of carbon, hydrogen, and oxygen

Not all carbohydrates are sugars. In addition to those you have named, there exist chemicals such as inositol, chitin, and various biologically important carboxylic acids.

Although one might naïvely imagine that the term carbohydrate is used for a molecule containing carbon, hydrogen and oxygen, this is not the case as, if so, it would include compounds like fatty acids. According to the Wikipedia entry it is more restricted, although still somewhat imprecise:

A carbohydrate is a biological molecule consisting of carbon (C), hydrogen (H) and oxygen (O) atoms, usually with a hydrogen–oxygen atom ratio of 2:1 (as in water); in other words, with the empirical formula Cm(H2O)n (where m could be different from n). Some exceptions exist; for example, deoxyribose, a sugar component of DNA has the empirical formula C5H10O4. Carbohydrates are technically hydrates of carbon; structurally it is more accurate to view them as polyhydroxy aldehydes and ketones.

By this definition all sugars are carbohydrates if one accepts the authoratitive definition of a sugar by Ron on SE Chemistry:

Simple sugars have the molecular formula Cn(H2O)n, where n is at least 3. They also have to be capable of forming an aldehyde or ketone carbonyl group.

He uses the qualifier of being able to form an aldehyde or ketone to exclude certain carbohydrates such as inositol from being classified as sugars:

…compounds in the inositol family [that] fit the molecular formula requirement, but are not considered to be sugars because they are incapable of forming a carbonyl.

So, yes, all sugars are carbohydrates, but not all carbohydrates are sugars. (Which, despite the unsatisfactory nature of the definitions, is what is generally accepted.)
Disclaimer
This answer describes the terminology used in biological sciences. Because it exists one has to work with it, but one should realize that it is not chemically exact, as illustrated by the following.
Chemists (and biochemists) refer to reducing sugars — and hence by implication there must be non-reducing sugars. The disaccharide sucrose — which is what most of us think of as sugar — is a non-reducing sugar. But the reducing property is a feature of the aldehyde or ketone group, which by Ron’s definition (which I emphasize is that accepted by biologists) would exclude sucrose from being a sugar! Clearly there is a conflict here.
The Wikipedia entry for Reducing Sugars includes the following:

A reducing sugar is any sugar that is capable of acting as a reducing agent because it has a free aldehyde group or a free ketone group. All monosaccharides are reducing sugars, along with some disaccharides, oligosaccharides, and polysaccharides.

and

Disaccharides are formed from two monosaccharides and can be classified as either reducing or nonreducing. Nonreducing disaccharides like sucrose and trehalose have glycosidic bonds between their anomeric carbons and thus cannot convert to an open-chain form with an aldehyde group; they are stuck in the cyclic form. Reducing disaccharides like lactose and maltose have only one of their two anomeric carbons involved in the glycosidic bond, meaning that they can convert to an open-chain form with an aldehyde group.

The way out of the dilemma available to chemists (but not to dieticians) would seem to be not to talk about sugars and carbohydrates at all, but refer to specific chemical types: monosaccharides, disaccharides etc. and their derivatives; and for other dietary/storage molecules refer to fatty acids, triglycerides etc.

Interesting, I had not heard of the aldehyde/ketone thing before, but it makes sense --- all sugars I know of are classified as either aldose (aldehyde forming) or ketose (ketone forming). Some refer to inositol (and sorbitol, mannitol, xylitol ... ) as sugar alcohols, as they form only alcohol (hydroxyl) gruops. Perhaps this distinction is important in that aldehyde and ketone groups permit certain reaction mechanisms?

@Roland I'm no expert (my chemistry degree was years ago, and I never 'practiced') but on thinking about the question was uncertain about the situation and googled a bit. However it all seems to be a bit of a 'fudge' as the term 'reducing sugar' suddenly welled up in my memory from the distant past. I'll add a footnote to my answer, but in brief the reducing sugars are the ones that are the aldehydes or ketones, so there must be non-reducing sugars, which then violate the definition. I think the get-out is to say that chemists would talk about monosaccharides and (in this case) disaccharides.


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Why the name coined for MARKUP LANGUAGE for SBML?
I'm get the confusion about  SYSTEM BIOLOGY filed.  SBML is refer to as SYSTEM BIOLOGY MARKUP LANGUAGE why we should called as MARKUP LANGUAGE? In HTML,XML and other field Mark up language mean particular function is declare into the Angular bracket like <H1> for Heading Tag this is displayed on the browser. Markup Language was actually developed for Wep application.
In other words, MarkUp language only displayed what we want., not display the simple mathematical function. Like, I need add function 1 + 1 which is display on the browser Markup language is not add, which is done by the CGI programming Like PERL,PYTHON, javascript.
So, in SBML(System Biology MarkUp language) Tools are not only display the what we want it? and It is not run on the browser? So why we called it is MarkUp Language?

I'm thinking you would do well to move this over to either the Computational Science or Programmers SE page. I down voted because of that. I think it is a good question. Just posted in the wrong location.

This question appears to be off-topic because it is not about biology.

SBML follows in the same vein as XML, in that it provides a standardized and flexible method for structuring information. XML and its ilk aren't just for making web pages, they're for sending structured datasets between systems and programs (in fact, XML is a fairly common configuration format). Why? Because the structure makes parsing simple (well, simple-ish).
BTW, markup languages were not invented for the web, HTML was far from the first one. The origin of markup languages is typesetting and in fact one of the most common uses these days is still in writing papers (ask a local math/physics/CS person what he/she uses to write papers and the answer will be Latex...a markup language).
Edit: BTW, this really has nothing to do with biology and you could have at least read the wikipedia page on what a markup language is.


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B-cell and T-cell activation by parasites
Parasitic infections lead to the production of parasite-specific IgE, but they also lead to the activation of nonspecific, polyclonal B-cells and T-cells. How do parasites trigger non-specific activation?

I've found a great article that says:

Mitogens   and   superantigens   have   been   described   to
  explain the strategy used by microorganisms to avoid the
  host specifc immune responses and to ensure persistence.
  These  moieties  are  responsible  for  the  initiation  of  non-
  specifc  (polyclonal)  immune  responses.

Mitogens are chemicals (usually proteins) that promote mitosis. Superantigens (sAg) form a subclass of antigens and are capable of inducing massive polyclonal T-cell activation and cytokine release (Cytokines crucial role in immune system mediation). Their ability to inflict massive T-cell activation comes from the fact that they bind directly to MHC-II without any pre-processing, and stimulate T-cell activation.
Source: https://escholarship.org/uc/item/47g8w51m
Also there are B-cell sAgs that stimulate B-cells, and their activation.
These altogether (mitogens cytokines, sAgs) result in rapid expansion of B-cells and T-cells.
Also this paper might help to understand why parasites trigger polyclonal T and B-cell activation. Namely to avoid host specific immune system, dilute the pathogen specific anti-bodies. It is important to note that chronic infections could lead to several auto-immune diseases.

Maybe we should attack the superantigens if they are so strong virulence factors, instead of developing antibiotics, which don't work.

Yepp, there is some research in the topic: http://www.mdpi.com/2072-6651/6/6/1724/htm http://informahealthcare.com/doi/abs/10.1517/14728222.2012.682573
Btw. afaik. superantigens are a subgroup of mitogens.

@inf3rno -  Well mitogen is a broad term, so I guess you can view it as such.


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Can pathogens enter the bloodstream if the epidermis has been scraped off?
Assume that the epidermis has been scraped off by a fall (not just scratched). Also assume that the dermis is completely untouched. Does this allow pathogens to enter the body more easily, or does the dermis still provide adequate protection?

Our epidermis is the first line defence against natural infections; it is also a part of the innate immune system. This is due to

it contains a layer of dead cells that separates the living cells of the deeper layers of epidermis and dermis from the environment.
This part of the epidermis is avascular and so pathogens can not easily enter into the bloodstream through it.
It contains natural bacterial flora (like in our gut) that kills a large number of pathogenic microorganisms with their toxins.
secretion of sebaceous gland contains some antimicrobial substances.

There are lots of other protective features of epidermis.
Dermis is richly supplied by blood vessels. So even if all the layers of dermis remain intact its high vascular nature will act as an open entrance of microorganisms. By definition abrasion involves only the epidermis or some parts of the dermis but still we need to take tetanus vaccine after getting an injury contaminated with soil. In diseases like Stevens-Johnson Syndrome (where epidermis separates from dermis) or in burn patients the skin is covered with antibiotics and dressings. The patient is also given high dose of antibiotics to fight those bacteria that still entered into the bloodstream.

Nice answer, I gather that bacteria would enter more easily, what about viruses?

This answer is a reply to the question asked in the comment of my answer given on 13th July 2016. The comment was, " Nice answer, I gather that bacteria would enter more easily, what about viruses?"
In my answer on 13th July 2016, I used the term "microorganisms" - this includes both bacteria and viruses. So the answer provided there can also be applied to viruses.
To specifically discuss on the susceptibility of the host towards viral infections after damage to the epidermis (dermis is intact) the following may prove to be helpful.
Viruses has evolutionarily developed specific surface molecules that either act as a ligand or a receptor being capable of interacting with the host surface-molecules. Example - Influenza virus contains Haemagglutinin that bind to Sialic acid  containing oligosaccharides found in almost every cell. Common entry route of a virus is usually determined by the surface molecules it possesses. Most common entry routes are respiratory system, gastrointestinal system, urogenital system and inoculation by bite of insects(via insect probosis). Viral infections after skin-damage are rather uncommon.
Intact skin is an effective barrier against viral infections. Dead cell layer of epidermis prevent viral growth. Viruses are non living particles outside leaving cells; so when they come in contact with the dead cellular layer of epidermis they behave in the same way as they were in outside environment. The requirement of blood or lymph supply for replication and spread of viruses meets when epidermis is removed. But in that case there occurs an inflammatory reaction causing accumulation of immune cells and antibodies. These antibodies neutralize the viral surface molecules, thus preventing viral attachment and entry into cells ( even in presence of living cells). Immune cells secret chemicals that disintegrate viral particles.
Most common mechanism of entry into the skin, for a viral pathogens are,
1. direct inoculation
2. systemic infection and
3.local spread from an internal focus

Direct inoculation is our topic. It uses two mechanisms -
(i) replication in endothelial cells and then spread into the bloodstream. Entry into endothelial cells are different for enveloped and non-enveloped viruses; enveloped virus fuses with the cell membrane, while non-enveloped viruses enter by endocytosis or receptor-mediated processes. Examples include warts, milker's nodules, primary herpes simplex etc.
(ii) Vectors may introduce the pathogen directly into the bloodstream
Systemic infections- Skin is infected during high viremia. Dermis is affected first followed by epidermis. Example- chicken pox.
Local spread from an internal focus-  Example, recurrent herpes simplex virul infection from dorsal nerve roots to specific skin dermatomes.

For further infomations you may read
1. Fitzpatrik's dermatology in general medicine, 8th edition,
2. Kuby Immunology, 7th edition.

The dermis provides some protection, and if it is removed the danger of deep tissue infection becomes extremely high. However, the epidermis provides an additional and important layer of antimicrobial protection. That is why first and second degree burns, opened blisters, and scrapes should be kept clean and isolated from the environment with bandages, and why antimicrobial ointments are often prescribed in such cases. The epidermis is an important waterproof barrier to environmental hazards, such as germs and dehydration, and its dryness is a natural inhibitor of microbial growth.    https://www.ncbi.nlm.nih.gov/pubmed/17621950  Also: http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0625.2008.00786.x/abstract

Welcome to Biology.SE! You've given some nice details, but additional references would be much more appreciated.

A couple of references added. Thanks for the suggestions.

And here's  your reward: +1! ;)

-1. This is incorrect. The epidermis provides protection, not the dermis (There are fatal diseases in people who have nothing more than occasional epidermal of parts of the epidermis. Your two references do not support your claim, but they do underline the importance of the epidermis.

I am in complete agreement with you that the epidermis provides essential protection, and that was my point and that is supported by the references. However, in areas where the epidermis is damaged or scraped off, the skin will heal completely. But when injury extends through the dermis,  such as with a third degree burn, the risk of infection, mortality, scarring, need for debridement, amputation, etc. goes up dramatically.

Mr. Gold, you are incorrect. A third degree burn forms an eschar, which is not associated with increased risk compared to second-degree burns. Skin healing has nothing to do with susceptibility to infection.

You may be a very good nurse, but you are wrong in this instance. "Because of the high risk of infection and septicemia from third-degree burns, these wounds must be carefully and scrupulously tended". http://www.consultantlive.com/articles/infection-secondary-third-degree-burn  I could get a lot more references if you like. How much time have you spent in burn units?

Sir, I am not a nurse, but a doctor, for over 40 years now. I have not spent any time in a burn unit, but as an Emergency Medicine specialist, I have a lot of experience with dermal injuries of all kinds. You? Of course there is a risk of infection with third degree burns, but it doesn't mean you're correct in your answer that the dermis stripped of the epidermis is still protective from invasion by bacteria.

I don't know why you're challenging my answer when I am agreeing with you. My answer stated that the epidermis is an "important layer of antimicrobial protection." Please let's leave it at that. I did spend a month in a burn unit. Full thickness injuries are a whole different horror altogether, and we don't need to discuss that here.


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If the liver can regenerate why can alcohol abuse permanently damage it?
The liver is a fairly unique organ in that it has the ability to regenerate itself even if parts of it are removed/damaged. It is a well known fact that continual alcohol abuse damages the liver and can lead to many liver problems.
Why is this the case? If alcohol does damage the liver, why can it not simply regenerate it's damaged cells from healthy cells?

I'd suggest starting your research by reading about cirrhosis, and following the links as you are interested.

I know what cirrhosis is. I should have been more specific. I meant what exactly is the mechanism which causes cirrhosis in the first place? What is the reason the liver cannot recover from cirrhosis when it does happen?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112892/


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anabolism in plants
The question is as following:
Which substance has the greatest contribution to the anabolism of glucose in plants. A- Oxygen (O2). B- Water (H2O). C- carbon dioxide (CO2).
The official answer given in this question was C, however I believe H2O and CO2 are equally important in their contribution, because glucose consists of 6 carbon atoms and 12 hydrogen atoms which respectively come from the 6 water molecules and the 6 carbon dioxide molecules needed for the light reaction and calvin cycle. Which step am I missing to the answer? This was by the way a high school biology national olympiad question in my home country, nl.
Kind regards, I'm looking forward to your response!

Water is not rate limiting in these reactions and is not actively consumed in these reactions, whereas carbon dioxide is fixed by an enzyme called rubisco. Have a look at the Calvin-Benson cycle.

But sir how is water not actively consumed, don´t the 12 hydrogen atoms in glucose come from hydrolysis of water? I just came up with the idea that carbon has a far higher mass and thus contributes more to the amount of bio mass, could that be a correct explanation?

I meant that water is in such high concentrations that it is neither considered a reactant nor a product. Its production or consumption does not affect its total concentration or any other rate of reaction where it is involved.

I think what they mean is that since water is split during the light reaction and oxygen is released, most of the mass of the glucose comes from carbon dioxide, because it contributes to the oxygen and carbon part of glucose whereas water only contributes to the hydrogen part which is only a small fraction of the mass


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Does human eye lens have a magnification of its own?
I have always wondered if the lens in our eyes have any sort of magnification by default. And if yes, if we're actually seeing everything around us bigger/smaller than what they actually are!
Has any research been done on this?

What do you mean, "bigger/smaller than what they actually are"? What is your definition for seeing a thing in an absolute size, because I can think of none that makes sense? (And no, the human eye does not work like a camera, so saying that when the image of a 2 mm worm hits a 2 mm stretch of neurons in the retina you have "actual size" doesn't make sense, because it doesn't matter for your visual perception).

The magnification by the lens of the eye is well understood.  This document, written by Dr. Glenn Chapman at Simon Frasier University in British Columbia, Canada, lays out some of the technical details.  The image below is taken from that document. I modified it slightly by enlarging the $s$ and $s'$ variables because they are important for this answer.

For a simple lens like that in our eyes, magnification, $m$, is calculated as
$$m= \frac{s'}{s}$$
where $s'$ is the distance between the lens and the retina at the back of the eye, and $s$ is the distance between the object and the lens. For the human eye, the distance $s'$ is about 24 mm, or just a bit under 1 inch.  For an object to have exactly 1:1 size ratio (no magnification or reduction), it would have to be exactly that same distance from the lens. That is, the object would have to be about 24 mm in front of our eye. The problem is that, unless you are myopic (nearsighted), you cannot focus on objects closer than about 25 cm (about 10 inches)
Most objects are much farther away from the lens than 24 mm. That means $s$ is a much larger value than $s'$, making $m$ a fraction less than 1. A value less than 1 means that our lens is not magnifying the object but instead is reducing or demagnifying the object.
As a simple experiment, hold your finger upright in front of your eyes at arms length.  Bring your finger closer and closer until you feel your eye lashes. Your finger looks smallest when it is farthest away from your eye. As you bring it closer ($s$ is getting smaller) your finger appears larger and larger. When your finger gets to about 24 mm, then $m=1$. When your finger touches your eye lashes, the distance is less than 24 mm, and the finger is magnified to larger than actual size ($s > s'$ and $m > 1$).
This also explains why distant objects appear smaller than closer objects. If you see a stop sign at 500 m and a stop sign at 100 m, the closer sign looks larger than the more distant sign.  But which is the actual size? Neither, because the lens changes the apparent size. The way to see the actual size is to stand with your eye about 24 mm away from the sign. Then, magnification will be exactly 1:1 and you'll know the true size of the sign. You just won't be able to focus on it.


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Why do we use DNA sequencing methods such as shotgun?
I am learning about DNA cloning for the first time. What I understand is that, in order to clone DNA, we break-up the original gene into shreds. Then try to piece it back together.
Why exactly do we do this? Instead wouldn't it be better to clone one base at a time? Basically in pseudo code:
old_dna_strand = 'ACTCATGCGAGCGTCAGTAGTACGTACTG'
new_dna = ""
for base in old_dna_strand:
    new_dna+=base

That looks a lot more easier and a lot less prone to errors. Why do we have weird methods such as shotgun?
Thanks in advance. Let me know if i should clarify or update anything in this question.

This is a technique from the "old time" of genome sequencing. The underlying method for sequencing is the Sanger chain termination method which can have read lenghts between 100 and 1000 basepairs (depending on the instruments used). This means you have to break down longer DNA molecules, clone and subsequently sequence them. There are two methods possible.
The first is called chromosome (or primer) walking and starts with sequencing the first piece. The next piece of DNA (which is  and then uses a specific primer from the end of the sequence. The next (contigous) piece of the sequence is then sequenced using a primer which is complementary to the end of the first sequence read and so on. This technique doesn't require much assembling, but you need a lot of primers and it is relatively slow.
To overcome this problem the shotgun sequencing method was developed. Here the DNA is broken into different pieces (not all broken at the same place), cloned and sequenced with primers specific for the vector used for cloning. The leads to overlapping sequences which then have to be assembled into one sequence on the computer. This method allows the parallelization of the sequencing (you can prepare a lot of sequencing reactions at the same time and run them) which makes the process much faster and also avoids the need for sequence specific primers. The problems are to sequence repetitive sequences, as overlaps are not as clear here. To resolve this problems a first draft is made and then critical regions are resequenced using other techniques as primer walking. Have a look at the Wikipedia page about shotgun sequencing if you want to read more details.

wow! thanks for the quick reply. Makes more sense now.

Primer walking will always give the exact replica of the original DNA. Shotgun sequencing can have potential mix-ups though (since we randomly cut-up the DNA). Is this problematic in most situations?

It can be, especially for repeat sequences. Generally a rough draft is created by shotgunning and it is then finished by filling gaps with multiple techniques (including chromosome walking).

@canadianer Thanks for filling in here. I'll add this to the answer as well.


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Is this a common garden spider?
Spotted this outside my window today. Looks like an orb-weaver, but I can't tell whether it's a regular garden spider or not. What species could this be?
This picture was taken in Bangalore, Karnataka, India.


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Do creatures exist which can stop their hearing at will?
Many people would love to have the ability to shut out noise while sleeping, in the same way that we have eyelids to shut out light. If this capability exists in nature, it could offer clues to researchers in the field of sound proofing.
Are there creatures which are capable of 'switching on or off' their hearing capabilities at will? At least partially?
I don't see why this cannot be evolutionarily possible. If perception of sound was necessary to know a predator was approaching while the creature slept, then according to evolution, creatures would not have had the ability to shut out vision either.

In what sense do you mean "not hearing"?  Physically shutting off the hearing mechanism (as with ecolocation), or not allowing the stimulus to propagate to higher brain areas?   That is, whether it's "not hearing" or "not paying attention".   My friend's dog seems to be able to do the latter, as can many children :-)

I think the "not paying attention" part is something that is a very pertinent concept that should be taken into account for any AI that processes sound and/or images.

A related subject is how we can give selective attention to some sounds while tuning out others, like picking out one conversation in a crowd, or tuning out background music.  Or pick out one instrument or line from a symphony...

Yes
Many echolocating bats use the stapedius muscle to separate the inner ear bones
when they emit their call so they are not deafened by their own call. Their ears are highly sensitive to the very frequency they are making so they need a way to protect against it. They are only deafened for 2-8ms but that is enough to protect their hearing while still being able to hear any echo.
Source

You can philosophically start arguing that bats see with their ears when echo-locating, and hence that they do not shut down hearing. +1 nonetheless, nice answer ;-)

Hmm...separating inner bones would reduce the sound. I was also considering that perhaps the true way of shutting out sound would be to block the signals that convey the message to the brain.


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Is there any current knowledge of how DNA polymerase is "motivated" to perform error corrections during transcription?
I was trying to understand the process of how polymerase performs error corrections on DNA. Every paper on this topic mentions what happens during the process, but there's no mention of how it happens. I even looked up the page on enzymes and it only explains enzyme binding sites, enzymes acting as catalysts and the types of reactions the enzymes perform.
It'd be reasonable to theorize that codons on DNA would have chemical properties that can attract certain enzymes to them to start the transcription process. But during transcription when the enzyme makes an error, what incentive does the enzyme have, to move backward to correct the error? I know that sometimes the error correction is performed only after the transcription, but the question is the same: How does the enzyme know what to do? Moreover, if enzymes were mere catalysts, does this mean that even without an enzyme, the DNA would get transcribed at an extremely slow rate? Could this mean that the "software code" that contains instructions of what to do during a transcription, is in the DNA itself?

Biologists look for mechanisms, not "motivations". No enzyme has "incentives" to do anything. Enzymes perform their functions because they have a chemical propensity to do it (encoded in their primary, secondary, tertiary or quaternary structure). Not because they feel any "obligation" to do so. Error-correcting mechanisms are just a type of propensity encoded in the enzyme's structure. It is a probabilistic event, whether they do or not, favored thermodynamically. Transcription involves many enzymes & proteins, not just polymerases; transcription would certainly not occur without enzymes.

Language and personification of enzymes aside, would you be satisfied with an answer to how does polymerase recognise it has made error as oposed to situation when it has integrated correct nucleotide? In other words what is the pysical stimul which triggers exonuclease activity of DNA polymerase? That would be answerable scientific question.

By motivation/incentive what I meant was the mechanism which makes it perform such a specific action. Codons showed us there was some kind of programming, so perhaps the way enzymes and proteins are folded are a kind of a programming that makes cellular bonds behave in a certain way. Anyway, from your replies it looks like we haven't figured this out yet. @ BagiM: I'd definitely like to know how the polymerase recognizes an error, but the answer would need to explain both the how and why of what happens. I reckon science doesn't yet have that answer.

There are no codons on DNA, only deoxribonucleosides.


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how can a recessive allele become represented in a significant number of individuals in a population
Darwin believed that individuals that are poorly adapted to their environment are less likely to survive and reproduce. This means that their genes are less likely to be passed to the next generation. Given enough time, a species will gradually evolve.
-individuals in a species show a wide range of variation
this variation is because of differences in their genes
-individuals with characteristics most suited to the environment are more likely to survive and reproduce. The genes that allow these individuals to be successful are passed to their offspring.
In genetic terms, evolution is any change in the allele frequency of a population.
A recessive allele can become represented in a significant number of individuals in a population, how?

A recessive allele is one whose phenotype can be masked by a dominant allele. A recessive allele is not necessarily deleterious, and the dominant allele does not necessarily have higher fitness than the recessive allele. Fitness and dominance are often confused, but they are not the same thing.
In some scenarios, the recessive allele indeed confers a fitness benefit, and when it does, it is predicted to increase in frequency rapidly because homozygous recessive individuals have higher fitness than both homozygous dominant genotypes and heterozygotes.
A recessive allele can also persist in a population if it is deleterious in homozygotes but confers a heterozygote advantage. The most famous example of this phenomenon is in Africa, where individuals heterozygous at the sickle cell locus have a fitness advantage because they are resistant to malaria. A higher prevalence of sickle cell phenotypes occur because selection for heterozygotes maintains a high frequency of recessive alleles in the population. For more, see Templeton (1982, http://www.indiana.edu/~curtweb/L567/readings/Templeton.pdf) and Allison (1954, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2093356/).

There is also effectively no selection pressure against recessive alleles that are deleterious when they are at a low frequency: selection pressure will only occur when mating two individuals that have the recessive allele. It isn't necessary to invoke heterozygote advantage to explain that part (though in some situations, like you point out, it does contribute).

@BryanKrause Perhaps you should put that in an answer since, well, it is the answer. The fitness of a homozygous dominant individual and a heterozygote is identical by definition.

@Nathan When it comes to fitness as the phenotypic trait of interest, then the sickle cell locus does not show a simple pattern of dominance. There is overdominance (aka heterozygote advantage).

@canadianer  The fitness of a homozygous dominant individual and a heterozygote is identical by definition. Yes, if you are talking about dominance for fitness. It is not uncommon to consider some other phenotypic trait though (coat color for example)

Dominance
Dominance explains the relationship between alleles in determining the phenotype. Consider two alleles A and a. If A is dominant, then individuals AA and individuals Aa present the same dominant phenotype while individual aa present the recessive phenotype.
Selection and dominance
When you ask

A recessive allele can become represented in a significant number of individuals in a population, how?

I am not sure why it seems unlikely to you. No one said that the recessive phenotype was less fit than the dominant genotype.
If the alleles a and A are present at the same frequency in the population, then most individuals will carry the dominant phenotype. But the alleles A and a may well not be at the same frequency. Selection (as well as other evolutionary processes that I won't talk about here) will affect the frequencies of these alleles. If the dominant phenotype has a higher fitness than the recessive phenotype, then the allele A will increase in frequency. If, on the other hand, the recessive phenotype has higher fitness than the dominant phenotype, then the allele a will increase in frequency.
From allele frequency to genotype frequency
Let $p$ and $q$ be equal to the frequencies of the allele a and A, respectively, such that $p = 1-q$ is necessarily true. Under a few assumptions (see here), the frequencies of the genotypes AA, Aaand aa are $p^2$, $2pq$ and $q^2$, respectively. For more information on why this is true, you can have a look at Solving Hardy Weinberg problems.
Let's imagine a scenario where, the recessive phenotype has a higher fitness. The allele a will increase in frequency in the population until eventually reaching a frequency of $p=0.95$. At such allele frequency, $0.95^2 = 0.902$ (or 90.2%) of the population will carry the recessive phenotype.
Note that at very low frequency of the recessive allele, the recessive phenotype is very rare (as it's frequency is the square of the frequency of the allele) and there is almost no selection acting on the locus of interest. But all of that is a story for another time.

My answer below demonstrates how recessive alleles can fixate and persist in potentially large numbers of the population.
 https://biology.stackexchange.com/a/61176/9771

If a question is a duplicate it should be closed as such. If it is not but the answer can be entirely found in an other answer, it is better IMO to partially copy-paste and re-adapt the answer to the current post than just providing a link. A link only is at best a comment, not an answer.

Ordinarily I'd have partially copied as you say, but as the other thread is figure heavy, I wasnt on my computer at the time, and there are other answers which will probably be accepted, I figured an answer was valid.

Ok. Note, that figures are included as links on each post and are stored independently of the post. So, if you just copy paste the whole thing (incl. the links) you don't have to bother about figures more than about any other piece of text. There is no need to download, re-upload the figures which would indeed be a pain without a computer.

Ah yeah good point! I did think SE would reformat the link to the title of the question though. I thought it usually happened automatically but i must be missing something.

Recessive diseases are insidious because most of the time the dominant (healthy) allele masks them. Then every once in a while, someone in the village gets a wide range of chronic, unexplainable symptoms that the local shaman explains as a random curse.
While these are a no-brainer in the developed world, they are a daunting problem for primitive cultures and third-world nations where superstition is much more commonly practiced than science and no one knows what a "genome" is.
With even distribution, a quarter of the population has the disease and half of the population have 1 allele for the disease.

I only read the first sentence. 1. Dominant does not necessarily mean healthy 2. By definition the heterozygote shows the dominant phenotype. It is always true when you have a pure dominance relationship. It is not only true "most of the time".