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Why doesn't Sanger (fluorescent) DNA sequencing double count nucleotides?
My understanding is that PCR is carried out until a fluorescent nucleotide halts replication. The segments of DNA are fed through the capillary tube based on size, sifting through the segments from smallest to largest; subsequently, the sequence is read from one end to the other.
I'm confused as to how we know that each nucleotide in the sequence has been accounted for, or if a nucleotide has been counted twice. If two fragments of the same size, ending with the same ddNTP, pass through the capillary tube at slightly different times, how do we know if that specific nucleotide hasn't been double-counted?

In chain-termination sequencing, a population of molecules is detected as opposed to a single one. The readout looks like this:

[ http://seqcore.brcf.med.umich.edu/doc/dnaseq/trouble/badseq.html ]
The peaks represent intensity of the four different fluorophores at the detector. Every fragment that is terminated at the same spot will have the same fluorophore and the same length. Because capillary gel electrophoresis separates molecules by size, these fragments will pass through at approximately the same time. "Approximately the same time" is why you see broad-ish and overlapping peaks on the readout as opposed to sharp and distinct lines.
Ideally, the readout will appear like the left half of the image, where there's minimal overlap between peaks. However, often you will see overlapping peaks, as in the right half of the image. The link above explains many reasons for why this occurs. Whether or not a peak is correctly assigned is determined by Phred scores, which is a statistical analysis of the shape and resolution of each peak.

I would like to also add that this is precisely why we use a capillary tube. The small surface area  makes it ideal for resolution of small things like nucleotides. That is the whole idea behind chromatography. Trying to separate things that may only be modestly different in size (or charge) to separate. The more resolution something has, the farther each of those peaks will be from each other, and the sharper each peak will be, i.e. a very sharp line instead of a broad peak.

how do we know if a certain nucleotide hasn't been accounted for? (e.g., what if a fragment that terminated at nucleotide #70 was not produced?)

@Alzeon Statistically, that seems unlikely given that there is billions of DNA molecules in a sequencing reaction.


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H₂S as a source of electrons for plants
The first electron source for plants was H2S, but now most modern plants use H2O as an electron source.
What is the advantage of using H2O instead of H2S?

Water can dissolve minerals and nutrients what H2S not can as a gas.

I would guess the abundance of them is relevant to this. Also toxicity/corrosiveness of hydrogen sulphide.

You can look at some articles which hypothesize about early evolution. It is hypothesized that some of these habitats were rich in sulphide (early enzymes also had Fe-S catalytic centres. Some enzymes still do) . So I concur with @GriffinEvo that it is all a matter of abundance.

The major reason for this is because H20 can cause hydrogen bonding. Hydrogen bonding is what allows for plants to transport "this electron source" from their roots through their stems an further.
The stronger polarity of H20 also allows for stronger interactions. Such as ionic interactions (not fully bound but 2 polar atoms interacting). This kind of ionic interaction also allows for other types of material interactions such as cohesion and adhesion.
Overall, aside from the discussion of abundance as mentioned above (which is a very good point), it also allowed the plants to grow in directions that were more advantageous (darwinian) for their survival.

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What problems do invasive species cause ?
Why do we value species?  What is so bad about invasive species?  Why value biodiversity?

Here is a post that might interest you as well.

This is far to vague and broad, and all subquestions are large and opinion-based.

Biodiversity=ecosystem
system= more than one species
Advanced creatures such as us cannot live without other creatures, like plants and bacteria to support us. (yet)
If you want to see what invasive species can do watch this video, http://www.youtube.com/watch?v=Bk-9ndL3ykM it has some descriptions on what the invasive species homo sapiens and their domesticated cows do to their planet earth. Wasting resources basically. Displacing other animals and plants, monopolizing the earth. Monopoly or monoculture is not good. For if the monoculture fails all is lost. If you have diversity if one harvest goes bad it's not over yet. It's basically all about stability and sustainability. Without either advanced lifeforms cannot exist.

What do you mean by "non-natural"?  Human introduced?  Why does this make them bad?  Is this because we are responsible for the affects of our actions?  I've just never heard a teacher/proff/textbook set this logic out satisfactorily.  It seems like invasive species are, when it comes down to it, defined by what species cause economic damage - because there is no objective sense of bad.  So humans move fast... So??? What's so bad about upsetting the balance that was there before industrial- agricultural humans arrived?

It's not bad. Just inconvenient. That's all. If inconvenient = bad is up to you. ;) Balance = safe. No balance = unsafe. If unsafe is bad is again up to you.

Here is an attempt at a partial answer.

What is so bad about invasive species ?

Invasive species have been introduced to a new habitat by humans (or by natural means).
They usually do not have a predator in a new area nor are the pathogens in the area very adept at infecting them. So, they may proliferate rapidly and compete with the native species. They may also be ferocious predators as their preys do not have defenses against them.

But isn't this just how evolution and ecosystems work?  Things change.  Some are more virulent and they might monopolize a system for a while.  It's the nature of well, nature, to be in balance - but that balance is always changing and won't always be what it was before humans got there.

I don't know much about the field of conservation but I'm giving a try...
In the following, when I say conservation I mean: "Human decisions and actions in order to protect the ecosystems". It has not to be confused with the science of conservation biology.
I think that the question you're raising shows the paradox of conservation. The maintenance of Biodiversity occurs through a dynamic process of speciations and extinctions allowed thanks to mutations, selection, population structure and movements. Standard ideas of conservation is not to preserve these processes but to prevent extinctions.
Quite a lot of many in conservation is aimed to save some big and representative species. Species for which we, as humans, feel some tenderness, love and pity for their fate. I am not saying it is bad to protect this kind of species I just want to emphasize that if we conserve it is not only for economic issues (or for the survival of our species) but also because we have ethics,  because we feel compassion  and guiltiness with nature of with some species such as the panda, the deers, the lynx, the wolves or because we feel compassion.
I also think that our categorization of living things into species (which is quite an subjective categorization) might bring us to take some decisions that do not fit economic issues.
For those who speak french well enough, here is a serie of podcasts (follow: "La biodiversité - plus qu'une simple question de conservation/") that might interest you. Especially the one given by Pierre-Henry Gouyon, which pretty much explain (much better than I did) most of the ideas of the last two paragraphs.
The question of invasive species is particularly interesting I think because there are especially a lot of invasive species today, first because ecosystems of changing (mostly because of human's activities) but also because human means of transport allow species to travel very far and become invasive. I assume (although I have no reference!) that the current number of invasive species is particularly high and just like any other disturbance in ecosystem, we can hardly predict what will the consequences. So shouldn't we make sure to keep this number of invasive species to a level which is closer to what would be found in nature in absence of human?

I'm learning french so I will definitely attempt to listen to those, merci :)  I appreciate your attempt to answer these questions, especially because this answer seems - to me - more aware of the assumptions and contradictions inherent in the arbitrary definitions such as species, or invasive, and the need to pair words such as "Biodiversity" with the utility we plan for them.  Thanks!

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Why are human bones usually curved?
Is there any simple explanation as to why human bones are more curved than straight and are thicker at ends and thinner in the middle?

Can you explain what you mean by curved? Do you mean the surfaces of the bone are curved because of the greater width of the ends, or do you think the actual bone (i.e. the actual axis of the bone) is curved (one is true, the other may be an illusion, or present in disease.)

@anongoodnurse - I meant the axis.

Thanks. The anatomical axis of normal long bones is usually a straight line, but the outsides can be curved. Just clearing up terminology. Ribs are obviously curved, and quite commonly fractured as a result.  This might be rightly deleted as an answer in a comment.

The slight curve allows bone to absorb shocks better.
This curve allows the bone to act like a spring and flex a little bit. One issue as bone get older is that they become harder and, therefore, more brittle which leads to the elderly breaking bones for a fall that younger individuals just get a bruise. Young children often get stick or "splitting" breaks where the bone does not break but separates as the bone is still soft.
The ends tend to be thicker as that is where the joints are and there are forces that need to be absorbed.
Of course, if the load applied to the bone is just too much or it is a sharp shock then bones will break, but really the skeleton is nature's design for a suspension system to allow us to do what we need to do walk, run, stand, etc
This set of slides makes good reading, with things like "less ductile", "elastic behaviour" and "strength in compression" worth looking for:
Mechanics of bones by Phillipe GILLET
A quick search gave many results but of these two shown the first seems very interesting from an engineer's perspective:

shock absorbing "goo"
shock absorbtion

While I think you're right, you can improve your answer by adding literature that supports your thoughts.

@Arsak As an engineer, I wrote an answer explaining the function in layperson's terms, the OP did not ask for any formulae of how to calculate the maximum stress point or the maximum bending point for a given load. So, for the question asked I think the answer stands as sufficient. If you want to ask a question about stress calculations or whether a cylindrical structure is stronger or weaker than a solid structure you have that option.

I wasn't thinking about calculations or similar sophisticated level, rather about an introduction to biophysics for example that covers what you've written. And sorry if my comment reads like an attack, that wasn't my intention. I just know that the community prefers well referenced answers to maintain quality of the site.

While this sounds plausible, it is not correct. Long bones are not curved and they are not springs of any type. Furthermore, your sources do not support your assertions.

The two sources given are unrelated to the question asked and the answer given. Please provide appropriate references related to the specific question and answer asked, not unrelated trivia. I worry that the presence of unrelated citations appears to give an answer more credibility than it deserves - I find this worse than lack of citation and perceive it as a form of academic dishonesty.

@anongoodnurse please show me a perfectly straight bone.

Solar Mike, it is not the responsibility of the commenter to prove you wrong; it is the responsibility of the answerer to prove their answer is correct. Users are encouraged to point out wrong answers, not to argue with them.

As @BryanKrause pointed out, sources should address the question. Your added source, while long, does not discuss the axis (straight or curved?) of the bone. Again, it does not support your answer that bones are curved to provide a springlike advantage.

@anongoodnurse I did not choose it based on the length.... But words like ductile...

At this point, comments become discussion, so I will not press my point any further, Just looking for an answer based in fact, with proof if needed/challenged.

@anongoodnurse: After looking at a number of on-line pictures of human skeletons, I have to disagree.  The long bones ARE curved.  Sometimes, as with the femur & tibia, the curvature from end to end can be quite subtle, but it seems to be there. And of course there is a lengthwise curvature, with the ends being wider than the middle.

@jamesqf - The diaphyses of the long bones are not curved. Tthe anatomical axis (different from the mechanical axis) of the humerus is a straight line. I don't count the joints as curves. Joints are larger/oddly shaped because of their function. The radius/ulna, because of the rotatory function, are slightly  curved. The other long bones (tibia,  humerus, and shorter "long" bones (metacarpals/tarsals, phalanges, etc.) are not. Add all of them together, and the answer is that most bones are not curved. In any case, the answer does not support its assertions. (Bones are curved for springiness.)

@jamesqf - I don't want to promote an argument from authority, but as an ER doc, I have looked at literally many thousands of xrays over the decades, in addition to, well, studying human anatomy. I can see how someone would think they're curved. But if they are curved, there's something amiss (an old fracture, an early vitamin D deficiency, a musculoskeletal disorder, etc.)

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Can something like McDonalds be considered a life form?
"The current definition is that organisms are open systems that maintain homeostasis, are composed of cells, have a life cycle, undergo metabolism, can grow, adapt to their environment, respond to stimuli, reproduce and evolve." (Wikipedia)
Could McDonalds(or any other chain store) be considered a life form according to the current most accepted definition of Life? If not, what am i missing?
It evolves and changes over time; it reproduces by using excess Material to build new stores, it responds to outer stimuli by adapting to them; it grows to a point it is benefical; it starts to function sometime and will eventually stop; it autoregulates it self trying to maintain a stable state and it has a very complex metabolism
Thanks in advance

SE Biology is a question and answer site for real problems in Biology. It is not a philosophical discussion site. Please read the Introduction and Help for the site.

No. First of all, an "organism" is not automatically a "life form". And it is easy to see that McDonald's does not have an information repository in the form of a genome-like structure, where mutations are quantum-acausal, but still have causal consequences on the bearing reproductive units and they trace an evolutionary path all the way down to the ancestor. In your food stores there is no such a thing. Everything is just engineered and organized by us humans. This is "intelligent design" (although fast food is not really an intelligent thing to do) and has nothing to do with evolution in the biological sense.

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What Type of fly is this? its huge
I found this stunningly beautiful Fly in a graveyard in Point Lonsdale Australia.  Can someone tell my what type it is Please.
It was wide as my thumbnail about 3cm long.


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Are there examples of Apis mellifera of different colors?
Re: my previous species-identification question,  What species is this gray bee? I'm still curious: Are there any recorded/reported cases of either albino Apis mellifera, or at least with substantially different pigmentation/color? Is it possible that only part of a colony gets this trait?

In conjunction with your other question, I wanted to let you know that there is a huge variety of species of bees found in the wild, especially in more rural areas. See this link for example that has some bee genera found in Chile: https://www.yorku.ca/bugsrus/resources/galleries/bgoc I think your picture with that earlier question is too unclear to answer but I think the simplest answer is that you have found a bee of a species that is not Apis mellifera.

@BryanKrause Thanks! I really appreciate any info. If you could write that as an answer to the original question, I'd be grateful

I don't think it could really serve as an answer because your picture is too unclear to identify, and just providing a link to the first Google result for "bee species Chile" is not really enough research effort to warrant an answer, just wanted to help point you in the right direction for the future :)

I've been reading a little more, and found a partial answer.
Not sure about albinoes, but Wikipedia lists a few different colors, arguably substantially different:
Under Apis mellifera subsp. ligustica (the Italian honeybee),

Leather
Bright yellow (golden)
Very pale yellow

Under Apis mellifera caucasia (Caucasian honeybee),

Dark with brown spots at times

In fact, both photos below are reported as Apis mellifera, here and here respectively.


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Identify My Spider

I live in Littleton Colorado and caught this spider because I haven't seen it before. Any idea what it is?


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What species of tree is this?
We have this cute little tree in our front yard (Denver CO):

Unfortunately we have to get our water main replaced and this tree lies right in the path of destruction. Anybody know what species it is? And, in your opinion, is it worth saving?

Please add your location (country, state) and if possible where the tree comes from (wild or planted), that will make it much easier to id.

I am in Denver CO. The tree is planted. Its a residential area.

Looks vaguely apple-ish to me, but with a cultivated tree, it may be hard to tell (especially as other fruit trees also look similar). Take a look at the base of the trunk - is there any indication that the top portion has been grafted onto a different rootstock? If so, it's a strong indication it's a fruit tree, though without some sort of tag, telling which variety it is may be difficult/impossible.


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Is this European(western), Eastern(northern) or another Hedgehog?
Yesterday this little guy ambushed my bicycle, thankfully tire-hedgehog contact was avoided at the last moment. Now I am wondering which one is it. Going by wikipedia maps and photos it should be either European/Western (Erinaceus europaeus) or Northern (E. roumanicus).
Sadly due to nocturnal nature of Hedgehog, "smart"phone camera and general willingness of Mr. Spikey to quickly leave area of incident this is best photo I have:

Incident occurred in Poland, Europe, around 21:30 local time.

There are some field marks that can be used to make the distinction but you should have taken a picture of the foot and the nose more precisely. There is still the risk of some variations in colour, then the best would be a DNA analysis in my opinion.

What part of Poland is this? Both species occur in Poland, but they are geographically seperated.

@RHA It was about here, in Opole, Upper Silesia

I think the picture you have is not enough to make a proper distinction between the two species.
By this site, they found some morphological characteristics to make the distinction but:

You have to carefully take pictures of the animal parts
The study nearer Poland has been made in Estonia and those characteristics could be slightly different in other countries.

I did not find another documents about hedgehog populations in Poland but the wikipedia page says both species are living in the country.

Downvoters: please consider to leave a comment to explain what can be improved to this answer.


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Does adding milk to cereal make it harder for our body to absorb the vitamins and minerals from the cereal?
I add about 3/4 cups of Blue Diamond almond milk (unsweetened) every morning to a single serving of Cheerios. The milk contains filtered water, and I read that drinking water with food at the same time makes it harder for the small intestine to absorb the nutrients from the food. Has this been verified?

This topic is more appropriate for http://skeptics.stackexchange.com/

Do not migrate this to skeptics please. You've read it where? How does this apply when you're eating say a tomato, most of which consists of water. As do 90% of all foods you eat.

And by which way should water hinder the absorption?

Overall, no it doesn't. Cereal is made in a way that it's expected consumers will consume it with milk. Here's a list of some important fortifications added to cereal and milk effects on absorption.
Riboflavin: No. Affected most strongly by light.
Iron: Yes. Calcium can affect absorption. Milk causing a deficiency is rare unless it is being used as a breast milk substitute in babies.
Thiamin: No. Unless you are drinking alcohol with your cereal.
Folic acid: Milk is a source of this!

What about zinc?


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Looking for book or article that derives formula for estimating the "average heterozygosity"
An online lecture I need to watch on population genetics describes a formula for the "average heterozygosity" as follows:

...we can theoretically predict that the average heterozygosity in the population will simply be four times N, the size of the population,
  multiplied by the mutation rate.

The formula that appears on the screen as the lecturer says this does not match what he says (but it's hard to say; the typesetting is terrible).  Furthermore, I find this description too vague (I have a million questions about each of the words in it).  Also, I would like to see how this estimate is derived.  Finally, judging by the number of egregious typos I've found in this series of lectures so far, I'd like to get a second independent rendition of these ideas.
I thought that Google would make quick work of this question, but to my surprise, when I search for "heterozygosity" or "average heterozygosity" none of the hits I get mention this formula.
I imagine that this is textbook-level stuff (i.e. not something that I'd have to go to the current research literature to find).  Can someone point to a textbook that derives this estimate?  (I am interested only in textbooks that discuss the formula alluded to in the quote above, as opposed to general textbooks on population genetics.  I've already consulted several of the latter, and not been able to locate the formula in question.)

@Remi.b: I mean a formula that matches the verbal description I quoted in my question.  I.e. an expression involving the number 4, the size of the population, and the mutation rate.

Sorry, I did not read properly! $H=4N\mu$ is the formula you're trying to derive.

$H=4N\mu$ is the formula you're trying to derive.
It is an approximation coming from an infinite site model and applies to diploid populations only. For haploids, it becomes $H=2N\mu$. The value $4N\mu$ or $2N\mu$ is often also called $\theta$ as it is a value that appears in many places in the field.
There are a number of ways to derive it. It can be derived from coalescent theory or from classical fixation index stuff from Wright.
Any good intro book to population genetics should derive this formula. (see for example in Gillespie's book). You will find more book recommendation at Books on population or evolutionary genetics?.


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How do a particular arrangement of atoms become self aware?
At the simplest level, we're all just atoms, animals, plants and humans alike. But what I don't understand, is how a particular arrangement of atoms such as us can become self aware, and be able to not only understand our environment, but manipulate it to our will? How is that even possible?

well, we have to not think of the atoms themselves. It's the macrostructure that is more important, the cells themselves. It is the interaction of cells that make us self-aware, as they are able to communicate via Cell Signalling. It is like thinking of a computer, it is just a bunch of transistors really, and on their own they are not capable of calculating, but together they form a computer. You have to think of an object/organism as the sum of it's parts

this belongs in a philosophy forum :P

You are skipping too many steps.
$Atom \rightarrow \color{red}{molecule \rightarrow structure \rightarrow cell} \rightarrow organ \rightarrow organism$
The following is a proposed speculation regarding the steps in red on the above:

How life originated and how the first cell came into being are matters of speculation, since these events cannot be reproduced in the laboratory. It was first suggested in the 1920s that simple organic molecules could form and spontaneously polymerize into macromolecules under the conditions thought to exist in primitive Earth's atmosphere. At the time life arose, the atmosphere of Earth is thought to have contained little or no free oxygen, instead consisting principally of $CO_2$ and $N_2$ in addition to smaller amounts of gases such as $H_2$, $H_2S$, and $CO$. Such an atmosphere provides reducing conditions in which organic molecules, given a source of energy such as sunlight or electrical discharge, can form spontaneously. The spontaneous formation of organic molecules was first demonstrated experimentally in the 1950s, when Stanley Miller (then a graduate student) showed that the discharge of electric sparks into a mixture of $H_2$, $CH_4$, and $NH_3$, in the presence of water, led to the formation of a variety of organic molecules, including several amino acids.

Although Miller's experiments did not precisely reproduce the conditions of primitive Earth, they clearly demonstrated the plausibility of the spontaneous synthesis of organic molecules, providing the basic materials from which the first living organisms arose.
The next step in evolution was the formation of macromolecules. The monomeric building blocks of macromolecules have been demonstrated to polymerize spontaneously under plausible prebiotic conditions. Heating dry mixtures of amino acids, for example, results in their polymerization to form polypeptides. But the critical characteristic of the macromolecule from which life evolved must have been the ability to replicate itself. Only a macromolecule capable of directing the synthesis of new copies of itself would have been capable of reproduction and further evolution.
Of the two major classes of informational macromolecules in present-day cells (nucleic acids and proteins), only the nucleic acids are capable of directing their own self-replication. Nucleic acids can serve as templates for their own synthesis as a result of specific base pairing between complementary nucleotides. A critical step in understanding molecular evolution was thus reached in the early 1980s, when it was discovered in the laboratories of Sid Altman and Tom Cech that RNA is capable of catalyzing a number of chemical reactions, including the polymerization of nucleotides. RNA is thus uniquely able both to serve as a template for and to catalyze its own replication. Consequently, RNA is generally believed to have been the initial genetic system, and an early stage of chemical evolution is thought to have been based on self-replicating RNA molecules—a period of evolution known as the RNA world. Ordered interactions between RNA and amino acids then evolved into the present-day genetic code, and DNA eventually replaced RNA as the genetic material.
The first cell is presumed to have arisen by the enclosure of self-replicating RNA in a membrane composed of phospholipids.

Phospholipids are the basic components of all present-day biological membranes, including the plasma membranes of both prokaryotic and eukaryotic cells. The key characteristic of the phospholipids that form membranes is that they are amphipathic molecules, meaning that one portion of the molecule is soluble in water and another portion is not. Phospholipids have long, water-insoluble (hydrophobic) hydrocarbon chains joined to water-soluble (hydrophilic) head groups that contain phosphate. When placed in water, phospholipids spontaneously aggregate into a bilayer with their phosphate-containing head groups on the outside in contact with water and their hydrocarbon tails in the interior in contact with each other. Such a phospholipid bilayer forms a stable barrier between two aqueous compartments—for example, separating the interior of the cell from its external environment.
The enclosure of self-replicating RNA and associated molecules in a phospholipid membrane would thus have maintained them as a unit, capable of self-reproduction and further evolution. RNA-directed protein synthesis may already have evolved by this time, in which case the first cell would have consisted of self-replicating RNA and its encoded proteins.

Source: Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. The Origin and Evolution of Cells. Available from: http://www.ncbi.nlm.nih.gov/books/NBK9841/


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How does anadromous fish physiology "know" to switch from salt to freshwater and back?
What mechanism allows anadromous fish (like salmon) to switch from salt to fresh water and back?  How does the fish "know" to switch its physiology and do other fish possess the biochemical machinery for this?  How difficult would it be to genetically engineer salt tolerance into a freshwater fish?

Osmoregulation is a homeostasis regulation mechanism followed by salmons to adapt on both salt and fresh water.

Osmoregulation is the active regulation of the osmotic pressure of an organism's fluids to maintain the homeostasis of the organism's water content; that is, it keeps the organism's fluids from becoming too diluted or too concentrated. Osmotic pressure is a measure of the tendency of water to move into one solution from another by osmosis. The higher the osmotic pressure of a solution, the more water tends to move into it. Pressure must be exerted on the hypertonic side of a selectively permeable membrane to prevent diffusion of water by osmosis from the side containing pure water.

In order to reduce the dehydrating effects of salt water, salmons drink several liters of water per day, but in fresh water salmons doesn't drinks at all. The only water it consumes is that which goes down when it feeds. When an ocean-dwelling salmon drinks, it takes in a lot of salt(NaCl), which exacerbates the salt-loading problem.
In fresh water, the salmon's kidneys produce large volumes of dilute urine, while in the ocean , the kidneys' urine production rates drop dramatically and produce a very concentrated urine.

Salmon use to deal with the NaCl fluxes driven by the gradients between the salmon and its surroundings. In their gill epithelial cells, salmon have a special enzyme that hydrolyzes ATP and uses the released energy to actively transport both Na+ and Cl- against their concentration gradients. In the ocean, these Na+-Cl- ATPase molecules 'pump' Na+ and Cl- out of the salmon's blood into the salt water flowing over the gills, thereby causing NaCl to be lost to the water and offsetting the continuous influx of NaCl. In fresh water, these same Na+-Cl- ATPase molecules 'pump' Na+ and Cl- out of the water flowing over the gills and into the salmon's blood, thereby offsetting the continuous diffusion-driven loss of NaCl that the salmon is subject to in fresh water habitats with their vanishingly low NaCl concentrations.
Reference

Reference


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How to separate peptide on SDS PAGE?
I want to separate 1600 Da peptide on SDS PAGE, on 20% GEL I didn't get any band, How can I separate on PAGE? Can I use 25% SDS PAGE?

Didn't you get any bands because you sample run off the gel or because of other problems?

@Chris,yes,because of sample run off the Gel.

Well you could turn down the power or reduce the time. What are you trying to separate it from?

Then the answer is simple: Don't run the gel for too long. Sounds simple, but is not necessarily so. Your samples either run with or even before the blue line of the bromphenol blue. o if you run your gel only until 2/3, this should work.

"Can I use 25% SDS PAGE?" - I assume the protein is already saturated with SDS, so it would not make any difference...

@inf3rno I doubt it. 20% is already hard to handle as the high percentage gel get very brittle.

Image is of an 18% Tris-tricine small-peptide SDS-polyacrylamide gel stained with coomassie blue dye [source].

Your peptide is 1.6 kDa; it would not run off in 20% gel if you don't run it for a long time. Also, try to prevent heating up of the gel (you can run it in a cold room or in front of an A/C vent).  However, it is better to use other techniques such as chromatography. You can also try dialysis if other unwanted peptides are much larger.
Protocol for Tris-Tricine SDS-PAGE.

If band is below the dye front it might not stain very well.  Tricine gels are best for such small proteins, and you might might just run until dye front is only half way down the gel. It is also possible that your protein does not stain with conventional coomassie-based stains.  Maybe try a silver stain.


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positive and negative feedback
I want to know more about positive feedback in gene regulation and to know the similarity and differences between positive and negative feedbacks.

Do you have any specific genes in mind? The way you ask your question is really broad and hard tro answer.

I want to know about E.coli bacteria

Can you then edit your question and add the relevant information?

Positive and negative feedback are essential motifs that control transcriptional activity of genes. They may involve other genes, mRNA and/or proteins.
A classical pattern of negative feedback is where transcription of a gene results in mRNA and translation of this mRNA in a protein that represses the expression of the gene again. Feedback loops may involve much larger structures, e.g. if a gene codes for a hormone that stimulates the release of another hormone in a remote organ and if that other hormone represses the expression of the first gene again.
In general, negative feedback results in stable levels of certain products. Positive feedback leads to infinite growth (if not limited by a surrounding negative feedback loop or simply by lack of substrate).
It is easy to identify positive and negative feedback by counting the positive and negative correlations within the loop. Feedback loops are defined as positive or regenerative loops if there is at least one positive correlator and the number of negative correlators is even. If the number of negative correlators is odd than the loop is negative or degenerative.
See http://biomedicalcybernetics.wikia.com/wiki/Feedback for a more detailed explanation.

It is easy to identify positive and negative feedback by counting the positive and negative correlations within the loop.... Not that easy.. Correlations are not to be trusted blindly

A feedback loop is a network structure in which the gene is able to regulate itself via a single path.
$A\rightarrow B\rightarrow C\rightarrow A$
Interactions can be called positive or negative depending on their effect on the downstream gene. If a gene A represses another gene B, then it is a negative interaction; when it activates then the interaction is positive.
If you multiply the signs of all the interactions in the path from gene-A back to itself you will get the sign of the loop.
So a positive FBL will result (in the above example) if :

A activates (+) B; B activates (+) C; C activates (+) A
A represses (-) B; B activates (+) C; C represses (-) A
A activates (+) B; B represses (-) C; C represses (-) A
A represses (-) B; B represses (-) C; C activates (+) A

Any other combination of interaction will result in a negative feedback loop.
Differences are based on their properties. I'll mention two main unique properties of each.
PFBL

Switching circuits
Hysteresis

NFBL

Expression control (feedback control)
Oscillations

Similarity: well, nothing more that they both are called feedback loops and the topology is similar (just the nature of interaction is different).


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Need help with beetle identification and yellow stuff I am seeing
This beetle infested a kitchen in northeast USA.
enter image description here

Welcome Ken. Could you give us some idea of scale, also add any details about there in the house you found them (near wood, human food or maybe houseplants?). Were there any obvious traces of foodstuff, droppings or unusual dust? (Or even eggs?)

I can verify that this is a beetle - https://en.wikipedia.org/wiki/Beetle - the hard, wing cases are diagnostic - but until you provide more details about them I can't be any more specific.

Thanks @JiminyCricket. And Sir thinkalot.. I added more pics. Does that help identify? Although I can’t rule old boxed human food, I think they were attracted to or came from dog food and dog treats that were not sealed properly. Found ants in some dog food. Are attracted to light in kitchen and in general. Tiny ones sometime land on my cell phone screen at night. Also see dead ones around terrace door. All food now thrown out or in plastic containers.

I thought drugstore beetle but looks like furniture beetle to me. Thought about hyde beetle too. Can someone assist me? Thanks

@JiminyCricket. just trying to tag jiminycricket. Thanks

Hi. You've gotten my upvote - excellent pictures BTW. Before an answer appears, I am delighted to state with some certainty it's a beetle, but it's not a death-watch beetle.

@SirThinksalot. Thanks Jiminy. Trying to tag Sirthinksalot now.

We've this marvelous button the network developers put in, the follow facility. When activated, anyone interested automatically gets a ping when a comment/answer/edit happens. He probably knows.

Ok. Thanks @JiminyCricket.o thought drugstore beetle but someone else thought cigarette beetle.jfoakes Pheromone trap for pantry moths and “ beetle ( cigarette but not drugstore beetle I’m told) didn’t work.

My suspicion is furniture beetle (almost newly-formed adults), but I should wait for the experts, there are many related species and similar ones that aren't related at all.

For what it's worth, the two pictures of plastic (container?) don't contain any insect as far as I can tell.

@bob1 you may be right. I thought the white stuff may have been a nest. I vaccumed it so can’t get any more photos.

Also seeing brown stuff, I thought was dog food but now don’t think it is. Found something living in it. Photos attached. Any help would be appreciated.

Anybody out there? At very least I have merchant and cigarette beetles. Do they leave all this yellow stuff or do I have wood eating too?

I'm not sure who the entomologists here are, but there's quite a few members that pop-in on weekends and at odd times rather than every day. Just a thought, because tags act to ping people in some way or other on their feeds, it might be worth adding the [beetle] tag maybe the [insect] (or [insecta]) one too, if they exist.

@JiminyCricket. Not sure how to add a tag. To the title? Thanks

@JiminyCricket.sorry, how do I tag an existing post?

Click the [edit] button under the question (or the link in this comment) then look beneath the edit window, you'll see a horizontal box labeled "tags",  select it, just start typing - if the tag exists it should give you a drop-down of available tags that start with those letters.

@JiminyCricket.Thanks. Only insect is set up as a tag. Added it.thanks

Posted another pic. My question is whether the yellow stuff is consistent with Merchant and/or cigarette beetles or is this wood.

@JiminyCricket know of any other sites I can post my question? Thanks

I can't say I've used them myself, but there are several: Whatsthatbug and insectidentification seem to be up at present, not to mention there's almost certainly a Reddit thread or two out there.


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What kind of spider is this?
I spotted this spider in my garden (Northern UK). The body is about 20mm long, and it's made a sizeable (50cm) web on a wall.

There's another semi-identical one on a nearby hedge.

What kind is it?

Do you have any larger or clearer pictures of it?

@MattDMo - Larger, yes. Clearer, not especially. Hang fire while I go and get some more.

Thanks for the pictures! That's the European Garden Spider (Araneus diadematus)
They are most commonly seen from June to October, but they reach a peak around right now.  This species is all over UK, and is widespread in gardens, woodland, and meadows.  Here is another picture for reference:

Fun Fact: After laying their eggs in late autumn, the females die and only the eggs make it through winter.  Upon hatching, they look quite different from the adults:

Why have I never seen these little beasties before?

@Valorum - I'm truly shocked that you haven't, actually.  They seem to be one of the most common spiders around my parts (West Midlands) at the very least.  Although they do seem to have less of a tendency to end up indoors than most others.

@Jules - Never seen them. We get loads of house spiders, crane flies, daddy long-legs, wasps, ladybirds and the occasional bumble-bee but never one of these.


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what type of insect is this? is this a moth? (southeast asia - Malaysia)
i found this insect in the garden behind my house a few months ago.This is the first time i saw this insect.On that day the weather is very hot.I found the insect in the afternoon.I am from Kelantan,Malaysia.The climate in Malaysia is equatorial, hot and humid, heavy rain falls in the monsoon season between november and february.

Oleander Hawkmoth (Daphnis nerii)
Same fellow? (From oocities.org)

And a better picture from ukmoths.org.uk:

For more reading, here's a wiki article.


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What is this insect or lake dweller?

Found on my deck. We live next to a lake. Don’t know if a bird dropped it?  Not sure whether to save it?  Has scalloped front legs and a point from the end of what I think are wings. Antennae, mouthparts. Back legs either deformed or partly missing because can’t propel forward, just rolling side to side   I put it in a pen to keep it safe for now.

That is a mole cricket. Order Orthoptera, family, Gryllotalpidae https://en.wikipedia.org/wiki/Mole_cricket
I'm not surprised you live by a lake. They burrow in sandy soil or sand, often right up to the water's edge. They can fly, but spend most of their time underground. You do not need to save it, as it will find its way back to its home if you just let it go. They are not pests. They don't bite, or spread disease.


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What is the name of this tree with yellow flowers?
Location is South India,
Tree is very large, but leaves are very small.

Image: https://i.sstatic.net/CsSKp.jpg

For next time (because it has already been answered), it would be good to have a close-up on the flowers.

Looks like this one: https://en.wikipedia.org/wiki/Peltophorum_pterocarpum
Peltophorum pterocarpum or the Copperpod

How did you find it? which site helped you to identify this tree?

Honestly? https://en.wikipedia.org/wiki/Trees_of_India This right here.

Sorry, @AlwaysConfused should I find a new picture?

@AlwaysConfused is this better?


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What is this plant with pink flowers and maple tree shaped leaves?
This plant goes in my front yard in morning sun in the interior of British Columbia.

It has green leaves initially and then they curl brown and turn yellow. It gets water weekly but not lots. Is it okay to divide this plant to thin it out?

It's a Japanese Anemone (Anemone hupehensis); if I had to guess, I'd guess it was the cultivar "Robustissima".

I used to grow these when I had gardens. Absolutely you can divide them! Wait until the spring if you can; if you have to divide in the fall, wait as long as you can to do so.

I love them; they're easy to grow , they last long, the seedheads are charming, and they're hardy perennials. What's not to like? They're hardy in zones 4 - 8.

thanks so much for figuring it out for us.  It is beautiful and looks like the hot location in the garden means it needs more water so the leaves don't turn brown.


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Why is a butterfly actively looking for cool, dark spot, long before dark?
Here in Croatia, the Woodland grayling Hipparchia fagi flies constantly in the garden of my holiday home.
Yesterday, I observed that one of these bufferflies was actively looking for a cool/dark spot around 6 pm. First it hid at a wall in a shaded corner behind a bush. During the day these butterflies are very alert, but this specimen could be approached to a few cm. Finally it flew away, to take refuge inside the house, even more cool and dark. Again, it didn't move until I blew it away (couldn't lock it in, could I).
Now, my question is why this butterfly behaved like this.
I am convinced it did not seek shelter from the heat, because they keep flying during the hottest part of the day.
Was it already looking for a place to spend the night? That seems rather early. At 6 pm, the sun is going down a bit, but temperature is still around 30 degrees and it won't be dark for 3 or 4 hours. Other butterflies like Iphiclides podalirius are still active. Or has H. fagi a higher heat demand than other species? That seems inconsistent with its habitat (woodland). Any thoughts?


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On enhancers, strands, and zygosity
I came across a passage on enhancers that sounds out-of-whack to me:

...an enhancer sits on just one of DNA's two strands (usually the same strand as the protein-coding DNA gene itself).  This is unlike a protein-coding DNA gene, which might need to be on both DNA strands——in a so-called homozygous state, in order to surface as a phenotype——like the classic case of blue eyes.

This is what makes no sense to me, since, AFAICT, whether something is in one or two strands has nothing to do with zygosity.
The authors continue:

And this is [an] evolutionary advantage: an organism doesn't have to wait for a change on both DNA strands.  The bottom line is that evolutionary tinkering is in principle much easier with enhancers...

Is there a grain of truth in what the authors' write, despite their muddled explanation?  IOW: does the fact that enhancers "sit on just one of DNA's two strands" somehow facilitate "evolutionary tinkering"?

Firstly, the author is deviating from traditional jargon when he tries to represent different strands as paternally of maternally derived DNA. Finally does the author add some sort of example for his statement? More so, I would be very interested how you decide an enhancer sits on either the maternal or paternal DNA.

The two authors are a computer scientist and a linguist (from the Amazon description), which explains everything - they are not biologists, and don't know what they're talking about.

...an enhancer sits on just one of DNA's two strands (usually the same strand as the protein-coding DNA gene itself).

Yes and no. Enhancers are in fact sometimes palindromic, so they're mirrored on both strands of the DNA.

This is unlike a protein-coding DNA gene, which might need to be on both DNA strands

No. Protein-coding DNA is always on one strand only because transcription doesn't suddenly switch strands.

in a so-called homozygous state, in order to surface as a phenotype - like the classic case of blue eyes.

No. Homozygous means on both chromsomes and has nothing to do with strands or the need for an allele to be homozygous to produce its phenotype because it's recessive.

And this is [an] evolutionary advantage: an organism doesn't have to wait for a change on both DNA strands. The bottom line is that evolutionary tinkering is in principle much easier with enhancers...

This is completely all over the place and makes no sense to me. Either "strands" is used in the correct way, in which the previous statement is wrong, or "strand" is used as "chromosome", in which case there is no reason why an enhancer should only be on one chromosome. Just like the gene, it can be hetero- or homozygous. The statement about "having to wait for a change on both DNA strands" is more relevant to whether something is dominant or negative. Regardless, I don't think it's possible to make any statements here about enhancers allowing for evolution to progress faster.


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Why is insulin given in type 2 diabetes?

For this reason "insulin insensitivity", or a decrease in insulin receptor signaling, leads to diabetes mellitus type 2 – the cells are unable to take up glucose, and the result is hyperglycemia (an increase in circulating glucose), and all the sequelae that result from diabetes $^{(1)}$

Also

Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance. $^{(2)}$

So why don't we give people a medicine which just increases the number of receptors or increases the sensitivity of receptors? Isn't it illogical to give more of insulin for a deficit amount of receptors? So, what is the logic behind giving insulin?

Not all type-2 diabetics receive insulin. It depends on their HbA1C level in the beginning of treatment. See 2017 guidelines from the American Association of Clinical Endocrinologists and American College of Endocrinology.

Can you add reference for the two quotes in the question?

Isn't it illogical to give more of insulin for a deficit amount of receptors?
Seems like there is some confusion in the definition of type-2 DM itself. According to the American Diabetes Association:

If you have type 2 diabetes your body does not use insulin properly. This is called insulin resistance. At first, your pancreas makes extra insulin to make up for it. But, over time it isn't able to keep up and can't make enough insulin to keep your blood glucose at normal levels.

So the problem in type-1 DM and type-2 DM is quite same; both because of less insulin present than required, the difference being that in type-2 DM the cells need more insulin than normal. And that apparent deficiency of insulin is overcome by insulin injections. Also, the definition you cite doesn't say receptor deficiency anywhere, it just says decrease in receptor's response to insulin.
So why don't we give people a medicine which just increases the number of receptors or increases the sensitivity of receptors?
This is not quite possible yet. Increasing the number of receptors means increasing the gene expression for that receptor, something that is called 'upregulation'. Now, just to add, the cause of type-2 DM has been regarded to be downregulation of insulin receptors on cell surface by high concentration of insulin. See this article:

The process of downregulation occurs when there are elevated levels of the hormone insulin in the blood. When insulin binds to its receptors on the surface of a cell, the hormone receptor complex undergoes endocytosis and is subsequently attacked by intracellular lysosomal enzymes. The internalization of the insulin molecules provides a pathway for degradation of the hormone as well as for regulation of the number of sites that are available for binding on the cell surface. At high plasma concentrations, the number of surface receptors for insulin is gradually reduced by the accelerated rate of receptor internalization and degradation brought about by increased hormonal binding. The rate of synthesis of new receptors within the endoplasmic reticulum and their insertion in the plasma membrane do not keep pace with their rate of destruction. Over time, this self-induced loss of target cell receptors for insulin reduces the target cell's sensitivity to the elevated hormone concentration.

Now, coming back to the main point, it is not yet possible to inject transcription factors in every cell of body so that more and more receptors can be produced. It is possible in vitro, but not in vivo yet. However, it is possible to inject something else instead of insulin which might have similar effects on the body, something known as insulin agonist. Researchers are already trying to create insulin agonists, but haven't achieved much success. See this paper for example, in which they talk about a peptide S961. The problem here is that most of the molecules synthesized act as both agonist and antagonist based on different concentrations. That is why this field has not seen much success.
EDIT: As mentioned by @Don_S in comments, some drugs reportedly do increase insulin sensitivity and number of receptors in cells. Though they have indirect mechanisms for this, unlike insulin itself, but this works too (at least in vitro). One of them, thiazolidinediones, activates a nuclear receptor PPAR $\gamma$, which in turn increases transcription of proteins involved in glucose and lipid metabolism and energy balance. Another drug, pioglitazone, works even in vivo and has been suggested to work by activating receptor kinases and thus increase insulin sensitivity.
Thus, in future, it is very likely that type-2 DM patients would get prescriptions of such drugs instead of insulin injections, but not until there are more such drugs available and at an affordable cost.
References:

Type 2 — American Diabetes Association
Downregulation and upregulation — Wikipedia
Knudsen L, Hansen BF, Jensen P, Pedersen TÅ, Vestergaard K, Schäffer L, et al. (2012) Agonism and Antagonism at the Insulin Receptor. PLoS ONE 7(12): e51972. doi:10.1371/journal.pone.0051972
Hauner H. The mode of action of thiazolidinediones. Diabetes Metab. Res. Rev. 2002;18(Suppl. 2):S10–S15. doi: 10.1002/dmrr.249.
Kobayashi, M, Iwanishi, M, Egawa, K et al, Pioglitazone increases insulin sensitivity by activating kinase of insulin receptors. Diabetes. 1992;41:476–483.

Somewhere I have read that insulin induces more receptor formation.

@JM97 if it did so, then how would insulin resistance develop? Upregulation would mean increased sensitivity of cells towards insulin, but this quite the opposite of what happens.

then why do insulin overdose occurs?

I mean to say why then in patients with type 2 diabetes hypoglycaemia takes place when there is insulin overdose.

Thats the point with type 2 DM. Though pancreas are producing more and more insulin, body cells are just not able to respond to it & thus take up glucose from blood, due to which most of the glucose remains in blood and hyperglycemia occurs.

yes , but excess injection of insulin (exogenous) will lead to hypoglycaemia( in extreme cases may lead to death immediately) , which should not happen if the receptors are in same quantity on membrane.

OP: "So why don't we give people a medicine which just increases the number of receptors or increases the sensitivity of receptors?"

"This is not quite possible yet." Actually, it is. There is a group of anti-diabetic drugs called Thiazolidinediones which is said to increase the sensitivity of body cells to insulin. This rather old study (from when these drugs were new...) indicates that these drugs activate insulin receptor kinase. This is not glucose receptors upregulation, but it is an increase in the response to insulin.

Sorry, ran out of space, here's the link to this rather old study.

@Don_S thanks a ton for the references, added them in the answer :)

@JM97: insulin overdose causes hypoglycaemia because insulin's main function is to regulate blood sugar levels. Even if a patient is insulin resistant / has reduced number of receptors, sufficiently high levels of insulin will cause blood glucose levels to fall. This will be a higher amount than in a non-diabetic patient but it is still possible.

Why the downvote? Did I miss something or say anything wrong? Please add a comment so that I can improve my answer.

@Artelius it is possible, but its amount required for insulin resistant patients is quite high, mostly more than the capacity of pancreas.

This is true for the beginning of the disease. As a reaction to the reduced sensitivity of the cells in the body to insulin (and thus less uptake of glucose from the blood and a resulting hyperglycemia) the body produces more and more insulin to cope with this problem.
At some point the insulin producing beta cells cannot increase the production anymore and due to the insulin resistance this amount is not enough anymore. At this point insulin needs to be supplied to the body to ensure normal function and to combat hyperglycemia. See this figure for a schematic overview (from here):

For more details see this paper:

Defining and Characterizing the Progression of Type 2 Diabetes

Insulin is a "last resort" treatment for people with Type 2 diabetes—partly due to the unpleasantness of injections, but partly due to the fact that high insulin levels can worsen insulin resistance.
People with Type 2 diabetes are generally started on Metformin and/or advised on diet and exercise, and progress to other oral medication, before insulin is considered. However, the oral drugs can have significant side-effects, and since Type 2 diabetes is progressive, insulin can eventually become necessary.
That said, injected insulin carries the risk of hypoglycaemia (low blood sugar), and starting insulin treatment early, before pancreatic insulin production has been severely impacted, can help reduce this risk, as the pancreas can play more of a role in keeping blood sugars stable.
So, the simple answer is: insulin treatment is used because it works; reducing insulin resistance is preferable, but current drugs can only do this to a limited extent.


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How does sucrose protect bacterial cells in lysozyme solutions?
I have a microbiology question.
When we put bacterial cells in sucrose solution with concentration higher than 0.5M we observe plasmolysis - the cytoplasmic membrane detaches from the cell wall due to water loss in order to balance the osmotic gradient.
If after that we put some lysozyme in the solution, the cells become spherical as they turn into spheroplasts, but they are still alive.
If we put lysozyme in a solution that contains bacterial cells, but no sucrose, they die. So my question is how does sucrose protect cells from lysis?

What kind of bacteria did you use, gram positive or gram negative?

Gram positive, Bacillus megaterium.

hemolysis: this term is used with reference to RBCs

I beg your pardon. What I actually meant to say was plasmolysys, I always mistake those 2 words.

This is an interesting question and as often, it has been noted by someone before. In this case it has been a researcher named Claes Weibull, who did his research in the 1950s. He noted (as you did) that sucrose has a protective function on the generation of protoplasts from Bacillus megaterium) with lysozyme. He published the following figure (from the first paper below):

He did not really explain the phenomenon, but speculated about protective function of the sugar in solution when the bacterial cell wall is removed. This also works with PEG in solution (see the third paper below).
He published a number of papers on this (if you look him up in Pubmed, you will find more articles, but these seem most relevant):

The isolation of protoplasts from Bacillus Megaterium by controlled treatment with lysozyme
Characterization of the protoplasmic constituents of bacillus
megaterium.
Osmotic properties of protoplasts of Bacillus megaterium.

It seems also possible to cultivate these protoplasts on agar plates and let them form "normal shaped" bacteria again:

Morphological study of the reversion to bacillary form, of Bacillus
megaterium protoplasts.


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Calcium reabsorption from egg shell during embryogenesis, how is carbonate neutralized?
As the embryo reabsorbs calcium from the shell, it also reabsorbs an equal quantity of carbonate. Calcium is in quite high concentrations in the body, the same molarity for carbonate causes a very alkaline environment. Carbonate has a pKa near 10, seen in that the egg white in "food eggs" (non-incubated and non-impregnated) becomes alkaline as the egg ages, approaching pH 9 to 10.
Throwing some numbers in there, assuming 2.2 gram of CaCO3, 8% reabsorbed to cause the average 8% thinning documented here (this is also just day 3-5 I think. ) 2.2 gram*8% = 0.176 gram carbonate released. The molecular weight of carbonate is 61 g/mol, 0.176 g / 61 g/mol = 0.003 mol = 3 mmol. If newborn chicken weighs 85 gram, and is 70% fluid, 85 gram * 70% = 60 gram. 60 gram is 0.06 L water. 3 mmol carbonate equivalent to 3 mmol/0.06 L = 50 mmol/L. The solution gets a pH of 11, and if you add 25 mmol/L of hydrochloric acid it is still at pH 9.2.
How is that carbonate neutralized?
At least 1 carbonate ion in 5 can be neutralized by bone formation, since hydroxyapatite has a ratio of 5:1 calcium to hydroxide ions, and, 99% of calcium is in bone (assuming somewhat similar ratio in infant as well. ) What about the other 4?
EDIT: A user David emphasizes that Wikipedia's entry on Calcium carbonate gives a pKa of 9. I based pKa closer to 10 on equilibrium between carbonate and bicarbonate. 9 or 10 does not really change the question that much since its about the huge quantity of base, quite strong in either case. I used http://www.aqion.onl/ for pH calculations giving pH 11. Feel free to use the correct value.
EDIT: Carbonic acid from CO2 from cellular respiration was mentioned. Carbonic acid from cellular respiration is at least part of it. But I don't know if it is all of it or close to all of it. 3 mmol of calcium absorbed (see Crooks, 1973) if average egg volume is 50 mL, molarity is 60 mmol/L, and this is as carbonate which saturates pCO2/H2CO3/HCO3-/CO3^2- as well.
EDIT: Also quite a lot of uric acid created, 2.3 gram per L by day 13, jbc.org/content/70/2/535.full.pdf, molarity 14 mmol/L.
SUMMARY: Bone formation likely takes care of 1 in 5 carbonates. Carbonic acid from cellular respiration, uric acid from nitrogen excretion, both contribute. Other factors?

Comments are not for extended discussion; this conversation has been moved to chat.

Carbonic acid from cellular respiration, like Trond mentioned, and uric acid from nitrogen metabolism, and, bone mineralization, are large sources of acid, might be enough to neutralize 3 mmol (Crooks, 1973; Tuan, 1986) CO3.
Calculations
3 mmol CO3 in a chicken that weighs 45 gram when newly hatched, 45 gram * 60% = 27 g = 27 mL of water, is 3 mmol / 27 mL = 111 mmol/L. The carbonic acid is likely around 30 mmol/L, and shares an equilibrium with the carbonate ion which might reduce that number. Acid from bone mineralization is 1:5th of CO3, 111 mmol/L / 5 = 22 mmol/L. The upper bound for carbonic acid and mineralization is then 30 mmol/L + 22 mmol/L = 52 mmol/L. This leaves 111 mM - 52 mM = 59 mM. Uric acid is up to 14 mmol/L by day 13 (Fiske, 1926), and, could reasonably increase up to 59 mmol/L.
References
Crooks, R. J., & Simkiss, K. (1974). Respiratory acidosis and eggshell resorption by the chick embryo. The Journal of experimental biology, 61(1), 197–202.
Tuan, Rocky S., and Tamao Ono. ‘Regulation of Extraembryonic Calcium Mobilization by the Developing Chick Embryo’. Development, vol. 97, no. 1, Sept. 1986, pp. 63–74.
Fiske, Cyrus H., and Edward A. Boyden. ‘Nitrogen Metabolism in the Chick Embryo’. Journal of Biological Chemistry, vol. 70, no. 2, Jan. 1926, pp. 535–56.

I was asked by a little notification to provide references. The point is, everyone knows cellular respiration releases CO2, everyone knows uric acid is how uricotelic animals excrete nitrogen, and everyone knows hydroxyapatite is 5 Ca^2+ +3 PO4^3- + OH-, acid excreted during mineralization therefore. The reference I did provide, I can also include the whole APA citation for it, here:
Crooks, R. J., & Simkiss, K. (1974). Respiratory acidosis and eggshell resorption by the chick embryo. The Journal of experimental biology, 61(1), 197–202.

Obviously, reference standards from 20th century aren't ideal way to record information but so there you go.


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How spinal cord play its roles in human beings sex?
I know most people can't enjoy sex if their spinal cord injured.
How spinal cord play its roles in human beings sex?

can you add some background information or references germane to the question?

Assuming that the basis of your question is correct, maybe because ejaculation is controlled by parasympathetic nervous system.

One of the major functions of the spinal cord is to serve as a "highway" for signals to travel between the brain and the sensory (and motor) organs. Thus, sensory the signals that are generated on the body during sex must travel up through the spinal cord in order to get to the brain, where it will be processed into a pleasurable sensation. If the spinal cord is damaged, the signals will not be able to reach the brain and thus there will be no generation of pleasurable sensations.
Here's an image that shows the general sensory pathways. You can see they travel from the sensory organ to the spinal cord, and up it to the brain.


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When is it unacceptable to measure dry mass in an experiment to measure growth of plants?
I'm an A level student (British high school final year) and I was doing an exam question which asked for the design of an experiment to test the effect of light intensity on the growth of a certain type of plant. Here is the paper; it is question 2(c). The marking scheme can be found here.
As my measured dependent variable, I picked dry mass. However, the marking scheme specifically says to 'ignore dry mass' and asks for use of 'mass'. We were always taught that dry mass is the most accurate measure for experiments where we are trying to measure the effect of a certain parameter on the growth of plant. So now I am wondering - when is it unacceptable to use dry mass as a measured dependent variable in such experiments?
As far as my attempts extend, I tried determining what conditions we should use dry mass under, but I could not find any source that talks about detailed use of dry mass (when to use it and when to not use it).
Perhaps a different way to phrase this question is to ask: when do we use mass rather than dry mass? And when do we use dry mass rather than mass? As far as my knowledge extends, dry mass is the most accurate determinant of growth that there is, given that the plants are genetically identical. This is because it ignores the possible fluctuations that may be present due to fluid mass within the plants.

My guess is that because width and height of a plant are more greatly affected by light intensity, the dry mass has less relevance. If the plants were all the same size, and you wanted to know which plant is assimilating the greatest amount of substrate, then biomass would be okay. But,  you just want to know which plant is growing the fastest

Plus, do you really want to be the guy to dry an entire fir tree sapling? I think drying a flower might be easier

But the dry mass can also be used to determine which plants have had the largest amount of growth. If we start off with cloned plants of the same age (I learnt that this is always the correct way to start these experiments) and I know that I will end the experiment after around two weeks, why not use the dry mass? I am merely starting off with seedlings, so they will have grown to a fairly small size, hence we should be able to obtain their dry mass. Moreover, see my edit to the question.

It might depend on what we mean by "growth" though; actual production, or increase in vertical height ? In the latter case you could have some saplings growing faster than others due to different carbon allocation strategies and "dry mass" as a measure might not pick up on the differences.

@Rozenn Keribin, why do you say that dry mass may not pick up the difference in the rate at which the saplings are incorporating carbon? Isn't that NPP (the production of energy through biomolecules within the plants)? So it should indeed be picked up by dry mass.

@Mathematician I says that dry mass might not pick up the difference "in the latter case", i.e. if the variable of interest is increase in vertical height instead of production.


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Can i grow bacteria on potato dextrose agar?
I was wondering if potato dextrose agar was a suitable environment for bacteria. Does it have all the requirements bacteria need or is it limited? Specifically:
Escherichia coli,
Staphylococcus aureus,
Enterococcus faecium,
Pseudomonas aeruginosa.

We need to know which bacteria you want to grow in order to answer you

Without knowing specifics about the bacteria I question this will be kept vague.
Generally speaking though, yes, some bacterias can be cultured using a PDA plate. The plate contains potato starch agar and dextrose. Sometimes Tartaric acid is added to stop unwanted bacterial colonies from forming, which again highlights how possible it is for them to form on the plate. The mechanism of action of the Tartaric acid is to lower the pH, out of the physiological range of most bacteria.


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Is monogamy a human innate behaviour?
As the question states, got curious and I was wondering if monogamy is an innate human behaviour or is it because of how we built society (religion, traditions, etc.)?
Let's say we go back in time, would we see humans settling down with a single partner at a time and caring for their children as a couple for life or would they reproduce with several leaving the mothers with their children?
Thanks!

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Not at all... Humans are traditionally a warrior territorial tribal culture, that fight, that catch slaves as trophies, slaves are generally recorded in all human cultures, from roman, greek, north america, south american, papuan, african, oriental, chinese, vikings, slavery was the norm, as soon as the culture was a warrior culture... The female slaves did work for the owners, and they probably weren't nuns!!! I saw a papuan on TV say: my second wife, i ate the husband and buried his leg. the second one, I just ate the brain because i was not hungry and buried the rest. he had 3 wives.

How in the heck is this opinion-based? The are arguments on human monogamousness based on the differences in physiology between humans and other apes (whose sexual behaviour is known, and probably stems from biology rather than cultural expectations). There may be other arguments. Whether someone accepts any of those arguments is different, but then humans are very good at denying things they don't like, regardless of the subject. Even a possible lack of consensus doesn't make something opinion-based: "we don't know for sure but here's what we do know" is a valuable answer too.

@ilkkachu Quickly gain 2899 reputation and vote to reopen!

"leaving the mothers with their children?" I'm a big fan of promiscuity theory, but my question is: where would they leave? Men and women lived closely to each other, in large groups. There was no such thing as a private house.

Humans are believed to be mostly serial monogamists with a noticeable components of secret cheating. Serial monogamy means most will have a single partner at a time but  will likely have several partners throughout their life, there is however an under current (~15%) of hidden cheating in most studied populations. Also I say mostly becasue human behavior is plastic and nearly every possible combination exists, albeit in small numbers.  Males do have a stronger tendency to seek multiple partners at the same time, which makes biological sense.
 like many social species you really have several mating strategies coexisting, often in the same head. Our large brains allow for more flexible approach to strategies.
In other animals exclusive (one mate forever) monogamy is exceptionally, almost breathtakingly rare, (not counting animals that only ever mate once). The Azara's night monkey is one of the few that has been backed by genetic research. Almost every monogamous species ever studied either has some rate of cheating, or is serial monogamous.

Unlike other species humans also have an incredible ability to resist and skew objective studies of their behavior (from reality TV wannabes to lawsuits to crimes against humanity trials) so be mindful of how any such data has been collected.

Data collected from the Ache hunter gatherer tribe suggests that humans were somewhat promiscuous even when it could not be kept hidden. Relative testes size, which for humans are intermediate between highly promiscuous chimpanzees and the gorillas with their single sire harems, would tend to confirm an intermediate level of promiscuity.  The Ache data suggest that a moderate level of promiscuity was adaptive, with survival to adulthood maximized at about two potential fathers per child due to the significant chance of fathers dying from violence before their children reached adulthood.

I claim that humans have only one partner at a time only because they are too lazy to prove others that they do not live wrong if they choose to have several partners at once. Unless a date lasted for a few hours in prehistoric times.

The easy answer is simply, no.
The longer answer is that it depends on whatever cultural norms that are practiced in a given area at a certain time.
Often powerful men in history had multiple lovers, but had arranged marriages. Like wise open relationships were very normal in the 60's and 70's of the 20th century. Also polygamous relationships are practiced in certain religions today.
While in modern times, especially in the west, we seem to tend toward the monogamous relationships, it seems to be more dependent on culture rather than biology.

As a personal comment. If we were evolved to be monogamous it seems rather conflicting that we can be sexually attracted to other people besides our current partner.

@fredsbend: But many, if not most, humans actually act on those attractions without waiting for the death of the current partner.

@fredsbend my original comment was mostly focused on the cases were sexual attraction occur despite the partner being within a few meters. However if that increases the chance of passing on our genes, it is hardly surprising that we feel that way. From a simplified perspective; males being opportunistic while females seek stability and safety, would make good sense based on the hunter/gatherer theory. Males would then seek to pass on their genes as often as possible, while females would prioritize the safety of children by pursuing relationships with the males supplying food most often.

@fredsbend: True, but the problem is not with the many/most observation, but with your 15% statistic.

@Jeppe Nielsen: You do realize, don't you, that a good many of us engage in sex without any intention of passing on our genes?  Indeed, some of us spend time & money to avoid doing so.  Over $19 billon in the US, as of 2015, per this: https://www.gminsights.com/industry-analysis/contraceptives-market-report

@jamesqf, most certainly... but do you realise how few generations that have had that option. Also, sex in other species can be used in to build social cohesion. So sex doesn't have to be about having children.

@Jeppe Nielsen: I think it's always been an option (at least since humans recognized the connection between sex and procreation), it's just that current technology makes it much more convenient.  There are records of birth control techniques as far back as 1500 BCE: https://en.wikipedia.org/wiki/History_of_birth_control

@fredsbend 15% is definitely many people. Many enough to take them into account and explain their existence more argumentatively than "They exist only due to random useless mutations". Also, an average polyamorous human might be much more attractive/fertile than monogamous. This is another important factor. There is literally no sense in a completely unattractive person wanting to have multiple partners because it is insanely hard to get even one.

@JeppeNielsen That theory is flawed. Males do not seek as much partners as they can, otherwise they would be attracted to any female they see. Why so? Because societies where everyone had almost equal amount of offsprings could be better suited to survival than those where most offsprings belong to one or a few males. For a further support males wanting to have several partners are not often competitive. Also, females would not be only ones being interested to save their children, because if you pass genes to 100 females and all your children die you are less fit than an average male.

@jamesqf To pass your genes you don't actually need to have an intention of doing exactly that. Especially when there is no contraception. Most animals don't have a desire to become a parent.

No, they are not.
Polygyny, polyandry and group marriage are, or have been, practiced in various cultures. Polyamory and other forms of non-monogamy are practiced. There are estimates that four to five percent of Americans are involved in consensual non-monogamy (despite social pressure for monogamy).
A sizeable portion of what the porn industry is creating revolves around the subject of threesomes, group sex, cheating, cuckoldry etc. etc., so quite apparently there is a market for that. It turns people on, be that for the thrill of "breaking the taboo" or some underlying desire. (Excuse me for not posting a link to back this up. Use your favourite bookmark.)
There is nothing to indicate that non-monogamy in any of its forms is "unnatural" to humans. Tabooed in some cultures and / or religions, but not unnatural.

...over much of human prehistory, polygyny was the rule rather than the
  exception...

Dupanloup I, Pereira L, Bertorelle G, Calafell F, Prata MJ, Amorim A, Barbujani G (2003). "A recent shift from polygyny to monogamy in humans is suggested by the analysis of worldwide Y-chromosome diversity". J Mol Evol. 57 (1): 85–97 (quote from p. 94)

This paper puts that shift at about 18,000ya -- roughly the same time that agriculture became common, but much too recent to claim that Homo Sapiens as a species is now "naturally" monogamous.
It is rather something that developed culturally:

...an analysis of foragers in the Standard Cross-Cultural Sample reveals that male provisioning does affect the mating system. Societies with higher male contribution to subsistence are more monogamous.

Frank W. Marlowe. "The Mating System of Foragers in the Standard Cross-Cultural Sample". Cross-Cultural Research, Vol. 37 No. 3, August 2003 282-306 (quote from the abstract)

On page 147 of "The myth of monogamy. Fidelity and infidelity in animals and people" (ISBN 0-7167-4004-4), David P. Barash concludes that about 80% of human societies lived polygynous before they came into contact with the "Western" culture.

@fredsbend: At which percentage of current population living non-monogamous, or historic records of non-monogamy, do these so-called "exceptions" suffice in your eyes to indicate that we as a species are not "naturally" monogamous? It's a cultural / religious taboo, mostly.

@fredsbend: FWIW, lifting from WP, three representative studies in the USA found that "about 10–15% of women and 20–25% of men engage in extramarital sex". There are more numbers in there. That's a pretty large number of "exceptions" to uphold a claim that humans were "naturally" a monogamous species. (Be very aware when crossing the line where you're calling non-monogamous people "unnatural".)

@DevSolar: I think your numbers don't include what seems to be a very large majority of Americans/Western Europeans who engage in sex (often with multiple partners during the same time span), before marriage or in the intervals between marriages.  So maybe most are serial monogamists if you compress "serial" down to a day or so :-)

@fredsbend: I take "natural"/"innate" behaviour to mean "freak cases nonwithstanding". Tigers are natural carnivores. Horses are natural flight animals. Swans are naturally monogamous. Humans sometimes are, sometimes aren't monogamous, so saying they are "naturally" so is just false, and marginalizing a sizeable portion of the population. Also, you seem to confuse this with a discussion forum. Post a dissenting answer and downvote mine, if you like, but I woukd wellcome if you could get off my back about this.

@fredsbend: You're still confusing "mainstream culture" with "natural / innate" behaviour.

@fredsbend: These are the comments to my answer you're confusing with a chatroom, and I get notified when you post. And I challenged your closing statement, because it is assuming Western culture as "what's innate behaviour". Check the updates to the answer. Comments are for improving an answer, not discussing an alternative viewpoint or trying to change the poster's mind.

@fredsbend: If humans were "naturally" monogamous, the first person anyone has sex with would be the only one (barring death &c)  (Like some fish, where the male embeds himself in the female.)  But (per CDC statistics: https://www.cdc.gov/nchs/nsfg/key_statistics/n.htm ) the average is 4-6.   When you consider that many people either don't have the practical option of having multiple, frequent sex partners, or choose not to do so for religious/cultural reasons, the conclusion is that the majority aren't monogamous by nature.

@fredsbend: S. Fink, L. Excoffier, G. Heckel: Mammalian monogamy is not controlled by a single gene. In: Proceedings of the National Academy of Sciences of the United States. 103, Nr. 29, March 2006, S. 10956–10960. I think you will agree that 18kya is a bit on the short side to make Homo Sapiens come about full swing on a multi-gene trait...

@fredsbend: WRT monogamy as "one mate at a time", how short a time are we looking at?  Years, months, weeks, days?  Certainly when we get down to minutes, there are fairly obvious physical limitations :-)  Defining "mate" as procreational rather than recreational has difficulties, too.  There are people who choose not to procreate but who enjoy recreational sex; there are likewise half-siblings are by no means vanishingly rare.

I wouldn't call humanity polygynous as well. As you said: "group sex, cheating, cuckoldry etc. etc." This quite disproves this theory. As well as that many people (including men) do not have jealousy. I only suspect that many others are jealous because they are only complying to rules (like getting angry if you go to a theatre in shorts) which are not natural. Probably, we are the only primates with group sex (in particular gang bang) and that might explain our differences from other polygynandrous/with dispersed mating primates (like solid ejaculates, dimorphism and big testes).

I just read a book on the Evolution of Sex and  one of the questions was why primates have lost the estrous cycle. The thought was that the sexual desire of the female anytime rather then periodically tends to keep the male "at Home" ensuring survival of the female and offspring. This implies that males are genetically engineered for monogamy but since females can survive now without a male (as opposed to those living in a cave) some males at least in younger years practice polygamy as do females.


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Do cuttlefish know how to mimic animals since the moment they are born or do they learn by observing?
I can't seem to find information anywhere else so I hope somebody can help me out.
So, as the question states, I saw a cuttlefish mimicking a hermit crab the other day and I was wondering if cuttlefish carry information of what they can mimic as spiders carry information of how to make a web (innate behaviour) or if they learn how to mimic by observing other animals.

I am surprised a question with bounty has drawn no comments at all.

I haven't been able to find any definitive research/answers, but, based on the usage of their mimicry (camouflage and sexual), and some of its features (alteration of the surface texture of their skin, electric camouflage, development+change through lifetime), I'd hypothesise that it's most likely a mixture of the two. They likely have a large innate capacity to use the form of mimicry young cephalopods do, which is further developed socially/as a learned behaviour, which subsequently causes the change in the nature of their mimicry.
Cuttlefish texture change (Primary research article)
Transient sexual mimicry (Summary article (Nature))
Research has shown that cuttlefish mimicry develops and changes as they grow; it has also been shown to differ based on the location of the creature. There is also evidence of cephalopods learning socially, so it does indicate that their behaviour is at least partially learned. (Source + additional references- reed.edu ->Visual Mimicry in Cephalopods -> Ontogeny)


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Identify the pink mold infecting refrigerated lemons
I made lemon juice 6 month ago.

I just washed the lemon using brush and then cut them into pieces.
Then I put one layer of lemon in the bottle followed by one layer of
sugar
Again one layer of lemon and one layer of sugar.
Then I close the bottle and put it in the refrigerator.

When I opened it, I observed some pink colored mold on the lemon slices.
Can anyone can identify the mold or tell me how to identify it?
PS: in the 6 months, I never opened the bottle. The bottle was clean and I did not add water; just lemon and sugar.

Whatever it is, I would not consume the lemon juice. The chances of toxins being present are just too high.

It can be Neurospora crassa....cause the fungus is pink, can live in anaerobic conditions, & can survive on carbohydrates, like sugar...but it's only a wild guess.... The pickle in your case got spoiled because it got in contact with water, only a few drops, but enough to cause those scattered microbial infections...

The S.E is gradually becoming a "Show & Tell"-site...somebody or the other is watching a vid or a pic or something weird in their kitchens...& thinking " Let's-just-post-it-in-BiologyS.E-&-ask-for-an-answer"....

Additional details are necessary to answer this question. Can you please provide them?

I would say that it is very hard to impossible to identify a mold simply by photos. There are a number of different molds that can grow under the actual conditions.

I checked citrus diseases on wikipedia, then "ctrl+f" and typed in "pink mold". The result was Gliocladium roseum which is really a pink mold, but it is hard to find any image of it, where it is on fruits... So this is just a guess. Btw. I think it is rarely possible to identify microorganisms just by checking an image of them.

citrus disease refers to mainly diseases on live citrus trees or fruits still on trees...the q is talking about a dead, refrigerated citrus...

@souvikbhattacharya "It colonizes living plants as an endophyte, digests material in soil as a saprophyte and is also known as a parasite of other fungi and of nematodes." - according to wikipedia. So I think it can survive on a dead lemon as well and likes anaerob conditions. Before cutting into slices the lemon was pretty alive (like every other fruit). The freezing not necessary kills microbes. Btw. I think it is impossible to find out what it is without laboratory tests...

If the mold was already there before pickling it...then why pickle it in the 1st place???....neway the q is pretty frustrating...why don't she try it out to find what actually it is,"great 1st hand experience"..;)


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What are some places where biofilms could develop?
I'm trying to think of places where a biofilm could develop other than on medical equipment or food processing equipment such as stainless steel mechanized blades or knives. I'm thinking more along the lines of biofilms on typical house hold things such as the bottoms of shower curtains

Biofilm is sort of an organized bacterial colony. It can develop anywhere and depends on the kind of bacteria involved.

Try thinking about places that are not very often cleaned and disinfected such as the toilet. Not only that, but the bottoms of shower curtains and in drains. Plaque on teeth is a biofilm, catheters, in/on wounds.

They can certainly develop in the toilet. Just try not to disinfect for a week...
Another place is the surface of living organisms, e.g. dental plaque or the leaves of a plant, etc...

They will develop if you disinfect or not. Most disinfection processes are not done by qualified people and are too short, use the wrong disinfectants or have other failures. And it is usually not necessary to disinfect your toilet - clean it, yes, disinfect it, no.

@Chris Disinfectants and/or cleaning reduce the number of microorganisms in the biofilm (by killing or washing out them). Without the systematic usage of these methods the biofilm will grow and will be much more obvious that it is there...

The problem with biofilms is that they withstand a lot of disinfectants. It is really much less of a problem than commonly thought.

@Chris In toilet maybe, by diseases biofilms are a serious problem e.g. by Staphylococcus + Streptococcus biofilms.

I know. They are a serious problem in tubings in patients for example. And since it's a biofilm they are more resistant.

biofilms also form in almost all systems with water flow (e.g. water tap, central heating), which also include environments outside of the household such as rivers and the famous yellowstone park hot springs.


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Answer the questions in one word with help of clues and images given
Name the things associated with Antonie Van Leeuwenhoek - (6 pictures are given for help and four of them are associated with these clues)
a)Leeuwenhoek was the first to describe these and hence called the "Father of Microbiology"
b)He found many of these (rotifers) in the rainwater collected in ditches and canals
c)Leeuwenhoek was the first to describe plant vessels in this cross section of an ash tree
d)Leeuwenhoek used this to observe microorganisms.

Homework questions are off-topic unless you show some effort to solve them yourself.

How far did you come? What did you find out?

I found the following - A) Microorganism B) Rotifera C)Fraxinus D) Microscope

These answers look fine for me.

right click the image, "search google for this image"

Wanted to post this as an answer but can't since your question is on hold. So I'll post the links to the answers. 1) http://www.infection-research.de/perspectives/view/detail/23/shape_matters_why_bacteria_care_how_they_look/ 2) image of a rotifer http://upload.wikimedia.org/wikipedia/commons/2/2d/Bdelloid_Rotifer.jpg 3) ash tree cross-section http://en.wikisource.org/wiki/Popular_Science_Monthly/Volume_45/July_1894/Sunshine_Through_the_Woods 4) http://www.history-of-the-microscope.org/anton-van-leeuwenhoek-microscope-history.php  ... You go through these pages and you will get all your answers

Since you have apparently tried to answer the question here is my interpretation. I list the six pictures (numbered from top to bottom) and link four of them to an answer.
1 - yeast cells?
2 -  ash tree section (c)
3 - rotifer (b)
4 - muscle fibre??
5 - bacteria? (a)
6 - Leeuwenhoek's microscope (d)
According to the WP page on van Leeuwenhoek he did describe the banded pattern in muscle, but there is no mention of yeast (although he would have had no trouble seeing these cells if he could see bacteria).
It's a very odd question.


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Possibility of Human cloning
Technology has evolved so much as to clone animals. But, what about human cloning?
Is it really possible to create humans in lab? Or is it that technology has not advanced to that level..?
Why cant it be attempted..?

This is mainly not a technical, but a severe ethical problem.

As Chris said, it is possible to clone a human but there are ethical issues.

generally people are pretty scared of what science can do because they don't understand the risks and benefits properly - look at a lot of GM food and the sacremongering that goes on. I doubt we'll be able to convince many that cloning should be tried with humans any time in the next 50 years!

@AbhishekK I tend to differ. Not everything which is technically possible should be done from an ethical point of view. And ethics are clearly not hindering the scientific development.

I think even with a dedicated human cloning project one would be several years away from success, after all cloning tetra wasn't easy.  I agree with Chris that ethical concerns are not hindering research, but rather help focus it when used correctly.  I can think plenty of recombinant viruses that should not be made for ethical reasons as a less controversial example.

Cloning of animals typically involves:

Taking nucleus from healthy adult cell of animal to clone
Taking a healthy egg and replace the egg's nucleus with nucleus from source animal.
Implanting egg in female, stimulating the pregnancy process.

This same process should work on humans BUT:

"Is it really possible to create humans in lab?" No. Animal cloning doesn't work this way, so human cloning wouldn't either. Animals aren't "created" in lab. The one artificial step is the modifying the nucleus of the egg cell before the pregnancy process initiates. The rest of the egg->embryo->infant pregnancy process is traditional nature and there is no working lab process available to replace natural pregnancies.
Cloning animals is very high risk, it involves lots of trial and error, and involves lots of mistakes, botched pregnancies, abortions, and birth defects. The core concept of replacing the nucleus in an egg cell makes sense, but the practical reality of that procedure involves cell damage and pregnancy risks. With non-human animals, no one cares. With humans, purposefully causing lots of botched pregnancies, miscarriages, and birth defects will make most people squeamish.
Donor Eggs: If the process worked perfectly, a single donor egg would suffice. Since the process doesn't work perfectly, many donor eggs are required. Getting those donor eggs is a very invasive process that I would not want my wife, sisters, or daughters to subject themselves to. With lab animals, who cares, scientists can be as invasive as they want, and harvest all the eggs that they need. Humans have rights which really impedes this type of risky work.

Today, cloning humans is possible, but at prohibitively high cost and risk. It is inevitably going to happen, but the costs and risks will impede its popularity. Process improvements that deliver more safety and reliability will allow human cloning to become more popular.
UPDATE: "Why cant it be attempted..?" It definitely is being attempted. Panayiotis Zavos is one doctor who has been very public about his attempts to clone humans:
"In April 2009, he claimed to have cloned 14 human embryos and transferred 11 of those to wombs."
AFAIK, none of these efforts led to a live birth. I'm sure other doctors have attempted and even more are considering it and waiting until it's a little more practical and realistic.