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Fecundity per woman in early humans
The average fecundity per woman varies a lot from country to country. I call average fecundity per woman the average number of born children per woman. In Homo sapiens, what was the average fecundity per woman during the paleolithic age for example? Is it about 2 offspring per woman or about 12 offsprings per woman?

That goes back about 2.5 Ma - 12k am I right? I'm not an expert, and with all due respect, but my hunch is that the fossil record is very incomplete, and the geologic time frame pretty long. We don't know even how many species of humans there were, let alone reproductive rates during the period.

@ChrisStronks I edited my post to clarify that I talk about Homo sapiens when I say "humans". It is plausible that we don't have the tools to answer this question... But I hope that might be wrong and someone could come up with some rough estimate. An estimate can maybe be derived from the number of surviving kids that can itself eventually be inferred from the increasing population through time (itself inferred from genetic data or from the geographical range over which fossils are found).

Do you mean offspring as in individuals reaching reproductive age or as in born children? If the latter it was certainly not 2, since disease, violent death etc were common. If it was close to 2, H. sapiens would have been extinct and we wouldn't be here.

I meant offspring = born children. I edited my post. THanks

Infant mortality was high during the paleolithic, so the fecundity of females had to be quite a bit higher than 2 to sustain viable populations.
A recent paper by White (2014) that explores how the ratio of young and old individuals in a population relates to demographic rates compiles data on hunter-gatherer societies from previous studies that you will probably find useful. Among other statistics, that paper reports a range in total fertility of 2.6–8.0. One of the source papers (Hewlett, 1991, pdf here) has data for individual hunter-gatherer societies (along with data from other types of pre-industrial societies). Many populations lie in the range 4-7 offspring. Note however that most (all?) of these values are from current or recent hunter-gatherer societies and not paleolithic societies. However, to give a ballpark estimate they are probably useful and fairly accurate. Also note that the child mortality rate of these societies are often between 40-50% (infant mortality ~10-30%)


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What equipment is needed to perform simple plant electrophysiology?
What is the minimum needed equipment to perform simple plant electrophysiology? I am looking for some simple experiments that I could run at home for learning. Ideally, I would transfer the skills to stud neuroscience later on (the skills could be related to operating a microscope, doing recordings with microelectrodes, signal processing, statistics, etc). How expensive this would be?

I think it will be difficult to do at home. You would need to dissolve the cell wall first, to do electrophysiology. You would need cellulase+pectinase.

@WYSIWYG dissolve the cell wall? I don't know about plants, but the popular methods in neuroscience, such as patch clamp, measure the voltage between the plasma and the environment. The membrane has to stay intact so you can measure the current which depolarises (and sometimes hyperpolarises) the cell.

@rumtscho In neuroscience methods the clamp is fixed on the membrane. In this case there is an additional layer of cell wall that is quite permeable. IMO you won't be able to attach the clamp on the membrane properly.

Electrophysiology on plant cells means single-cell recordings, as there are no gross compound action potentials.  As you correctly say, this means micro-electrodes; this in turn means computerized manipulation of the pipettes, a decent microscope, signal amplifier, recording software, stimulator slash voltage/current control, Faraday cage, analysis software (Matlab), and not unimportantly a vibration-free workbench (whole departments have moved house due to micrometer vibrations in the building). I guess you should think anywhere between 10k - 100k (dollars, euros whatever) as a reasonable estimate.
A student internship would be advisable finance-wise, but especially because single cell recordings, and electrophysiological skills in general, are relatively difficult to master.

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Growing E. coli at room temperature?
If I were to do a blue/white selection of transformed E. coli on LB agar ampicillin plates at room temperature (23⁰C) for about 2 days and 18 hours, will I run into the issue of satellite colonies or any other issues?

Why do you do it this way and not use the classical overnight incubation followed by 1-2 hours in the fridge? Works usually pretty fine.

I normally incubate overnight at 37 C, but I was just curious if it's possible to achieve the same results at room temperature over the span of a weekend (when I am unable to come in to my lab and refrigerate the plates).

I have never tried this for blue/white selection, I have overexpressed protein a 18°C to have a higher yield of soluble proteins. I think it will not do harm, as the bacteria grow much slower. If you don't see a clear selection, you can still put them into the fridge.

ampicillin degradation is a real issue at room temperature for more than 1 day. YOu will see a ton of satellite colonies and false negatives

Yes, once I did it (pBR322's fault) and I did see some satellite colonies.

Since b/w screening is a means to  selection, you want maximum selection pressure. This will be obtained by incorporating all optimal conditions. The many enzymes of the lac operon are going to function best at their optimal temp.
Why would you do this? If it is because you can't go in the next day it's better to do it when you're available. You're only going to doubt your results when you get them.

Blue/White screening is not a selection step (unless you count picking the right colonies as selection).

@chris you are correct it's just a means to selection

You will definitely get satellite colonies. Ampicillin breaks down after about a day, especially exposed to light. Kan, keeps pretty well at room temp, but that does you no good :)

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Supercomputer and undergraduates
Is it common for an undergraduate to run their thesis (evolutionary genomics) in a supercomputer? In my country, few supercomputers exist, but I'm not sure how it is for bachelors in the US or Europe. I am writing my application to graduate school abroad and I want to know if it is a remarkable point I can use as hook to begin my statement.

This question would be better suited for academia SE.

If there are no pending jobs then you can use it. Why do you need supercomputer for. In any case this question is off-topic

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

IMO irrespective of country and level (undergrad/Masters), if you can run a job on a High Performance Computing cluster or a supercomputer, you should mention that on your resume. And sure, you can use that in your statement, especially given the fact that not many have access to it, you had the rare opportunity and made full use of it.
In my experience, I haven't seen many undergrads here in the US that can run a job on a HPC - not without prior computing experience!
All the best to you!


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Are there more true codes found in biology besides the central dogma?
I know each element of the central dogma is a code in the mathematical sense of finite-state machines. That is, DNA is transcribed into RNA, and RNA into proteins.  What other examples are there of codes that exist naturally in organisms?

Developmental patterning(?)

Stepwise polymerization of monomers, Operons for catabolism, operons for anabolism. Inducible and Repressible genomic expressions. Your question is very general. Also, besides methods of mathematical analysis, central dogma is mathematical in what sense exactly ?

@Macedona93 I am no expert. However, I believe FSM theories define a particular class of mathematical objects related to what are known as free monoids. I believe the conversion of DNA to RNA or vice versa follows FSM processing of this type. I think this is a well-established fact and is really the true definition for what we casually call a "code".

I see, perhaps im not enlightened in Finite State Machines and their philosophical relaton to cell and molecular biology. I just know that the rules of cellular biology follow those of physics, biological thermodynamics (Free energies and what have you) amongst others. Like the fact that DNA is coded in respects to monomerical polymerization. Regardless, i up-voted the question as i find it quite interesting. Seriously check out operons, they're quite amazing.

DNA is a code that occurs via stepwise polymerization, like all major macromolecules. In respects to DNA, it is Nucleic Acid sequences that polymerize to create the DNA. In eukaryotic cells this happens at multiple replicons (regions of replication). So you can look DNA as code for itself. You also have rRNA, mRNA, and tRNA. All of these code for and do specific things. rRNA facilitates the creation and movement of the ribosome, where mRNA and tRNA "code" for the final protein. tRNA serves as the principle code strand for the correct Amino Acids. This is read as a series of three N.A's (codons) One codon for a respective Amino Acid. mRNA actually guides the synthesis of these polypeptide chains. You also have something called operons. These are groups of genes with related functions that are clustered together. This allows for rapid initiation and termination of gene expression. Im sure there are a few others but these are those that come off the top of my head. The term "code" and molecular bio are very much intertwined.

I answered the question before his edit

Yea in respects to these situations rather than editing my answers I'll leave them as they are. And comment if I see fit. The only other situation where a "code" would represent its intrinsic definition would be with operons and genomic expressions.

I thought this was a nice answer for how I phrased the question previously. Your answer isn't what I had intended the original question to imply.  Hence I changed it immediately. But had I meant to ask that particular question, this answer would have been succinct and sufficient. I am new to SE, so if there is a better way to edit questions in the future I am open to suggestions. I would have liked to retain the information in how I phrased it originally so that your answer wouldn't seem so unrelated to the current phrasing.

wait, is the lac operon an operon of the type you mentioned? I don't remember much about it, but i remember learning about that in my intro bio class

Yep Lac Operon is a good introduction to the functioning and mechanisms behind operons. I also first heard of the Lac Operon in my Cell and molecular bio undergrad course

I am not very familiar with them, but I hear that bacterial non-ribosomal peptide synthases are made of catalytic modules, lined up in series, paralleling their product. My suspicion is that there is some promiscuity / ambiguity in the nonribosomal code.
Also, N-glycosylation in the ER / Golgi occurs in a defined series of events, but that includes backtracking (that is, sugar cleavage), which I am not sure would belong in a finite state machine.


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What species of eagle pushes their young to teach them flying?
There are many references to eagle pushing their young off the nest to make them know how to fly, for example this motivational video.
It is also described in this website:

Let me show you "the ways of an eagle" in the nest, and give you a picture of our lives as well. After the eaglets get to a certain size, or maturity, everything changes! One day the mother eagle comes back from being gone, but this time there’s no food in her beak, and she doesn’t land on the edge of the nest. Instead, she hovers over the nest.
You may not know this, but an eagle can do almost what a hummingbird can do. Even though they are great birds, they can remain almost motionless in midair with those great wings just undulating in the breeze. They do this about three feet above the nest. I’m sure if little eagles could talk to one another—and maybe they can—one would certainly say, "My, what strong wings Mommy has."
Why does the mother do this? She is demonstrating that those curious appendages on the babies’ backs have a useful function. Eagles, of course, were meant to fly, but they don’t know that. If we take an eagle and separate it at birth from its parents, it will never learn to fly. It will just grovel around in the dirt like a chicken. It might even look up and see eagles soaring overhead and never guess that it was meant to soar in the heavens.
Eagles have to be taught, and that’s the mother’s job. So first she just demonstrates.
The next thing she does is come down into the nest and surprise her young. One can imagine how warm it must normally be for the little eagles to snuggle with their mother and be enshrouded with her feathers, but this time she puts her head up against one of the little ones, and pushes that little one closer and closer to the edge of the nest. ("Hey mom, mom, what are you doing?")
All at once she pushes the little one out of the nest, and the eaglet falls down the face of the cliff, surely to be destroyed. But not so! In a flash the great mother eagle flies down, catches the little one on her back, and flies up and deposits it in the nest. ("Whew! Mom, that must have been an accident.") But it wasn’t an accident. The mother bird pushes the little one out again, and again, over and over.
Why would a mother do that to her young? Does she hates the little one? Not at all. It’s just that those little birds were made to fly, and they don’t know it, so she is going to push them out of the nest. She never lets them hit bottom, but she does let them fall, because they have to learn something they don’t know.
The next time the mother bird comes back she decides to clean house, and so she stands on the edge of the nest. The first things to go are the feathers inside; she drops them over the edge. Then the leaves go over the edge—heave ho! While this is going on, she’s not very talkative, either. ("Mom, what are you doing?") She pays no attention. Since she built the house, she knows how to take it apart.
Next she decides to take the sticks out of the middle of the nest, and with her great strong beak and feet, she’s able to break them off and stand them straight up. ("Mom, it’s not comfortable in here anymore.") Then she takes certain key sticks out of the nest and throws them over the edge. ("What are you doing, Mom? You are wrecking my room.")
She seemingly pays no attention to the concerns of her young as she prepares to pull the nest apart, for she is determined that those little ones will fly, and she knows something they don’t. She knows they will never fly as long as they remain in the nest.

However, looking at this very interesting documentary on white-tailed eagle, the young eagles don't learn to fly by getting pushed as described in the motivational video, but they learned flying by practicing their wings on good winds.
Looking from the nesting place (cliff), I read that it might be Golden Eagle. But the section describing the fledgling doesn't say anything about the parent eagle pushing the young, although it does say about "jumping off":

The first attempted flight departure can be abrupt, with the young jumping off and using a series of short, stiff wing-beats to glide downward or being blown out of nest while wing-flapping. The initial flight often includes a short flight on unsteady wings followed by an uncontrolled landing.

Does Golden Eagle really push their young to teach them flying? If not, which species is it?
In case it's not clear, I am also interested in references that describes the eagle behavior in more details. It would be good if there is a video documentary, but considering that capturing this moment on tape might be difficult, that's not my utmost concern.

I thought Eagles would push their babies off three times, and afterwards would let them fall if they didn't learn to fly.

I am pretty sure this doesn't happen with eagles, and I have no idea why this would be written.

But not so! In a flash the great mother eagle flies down, catches the little one on her back, and flies up and deposits it in the nest. ("Whew! Mom, that must have been an accident.") But it wasn’t an accident."

This is flight, alright: a pure flight of fancy.
There have been many hundreds of videocams set up in all kinds of remote locations so that behavior in the wild can be studied. Some of the most popular cams in recent years have been the eagle cams (e.g. at eagles.org). They are live during nesting season and record for all the behavior of eagles.
If the parents did not feed their young, as described in the fabrication above, the young would starve to death, as it takes time to learn to fly. If anything, the eagle parents must increase the feeding to keep up with the nutritional needs of the growing chicks, and the muscle building taking place. The parents don't stop feeding until a while after they're flying well.
Eagles don't learn "learn" why they have wings by observing the mother eagle hovering above them (pure anthropomorphizing). They leave the nest and start roaming on the branches, practicing hopping, landing, and building up their wing strength. Eventually flying, they still come back to the nest to feed. In this video from British Columbia (not the most exciting in the world) you can see exactly this happening with bald eagles. Eventually the young eagles scavenge and learn to hunt for themselves. It takes time. This page describes the fledgling feeding and flight behavior.
While I am not going to try to find an eagle that behaves in the bizarre manner you've found and asked about, I will say that eagles are eagles and more or less behave pretty similarly. The most common eagle in the world is the bald eagle. The Golden behaves like the Bald. Eagle behavior is influenced by habitat, etc. Wikipedia has a page listing 60 species of eagles. Picking a random eagle from another part of the world (in this case, the Sub-Saharan Martial eagle, this information seems to confirm that attentiveness of adult eagles and fledgling behavior is similar though not without species variation:

Martial eagles have a slow breeding rate, laying usually one egg (rarely two) every two years. The egg is incubated for 45 to 53 days and the chick fledged at 96 to 104 days. Despite increasing signs of independence (such as flight and beginning to practice hunting), juvenile birds will remain in the care of their parents for a further 6 to 12 months. Due to this long dependence period, these eagles can usually only mate in alternate years.

I'm sure I'm not the first to warn you not to believe everything you read on the internet.

I see. I like the knowledge about eagles that you share, but I sense a slight negativity in the sentiment. Perhaps we can try to discuss in more neutral manner. =)
Btw, can you point out the section in the story above where it describes "the parents did not feed their young"? As shown in the documentary I linked in my question (starts from 20:20), the parent eagle did still feed the young, but it also did limit the food given to the young, to encourage the young to find food themselves.

"One day the mother eagle comes back from being gone, but this time there’s no food in her beak, and she doesn’t land on the edge of the nest. Instead, she hovers over the nest." Yes, there is negativity. A lot of that passage is pure fabrication, which I do not like, and feel is an ethical violation, hence the sentiment you correctly picked up on. There is no reason at all to take a kindly attitude towards the spreading of falsehoods.

Can you confirm what I noticed in the documentary? I copy again here: "As shown in the documentary I linked in my question (starts from 20:20), the parent eagle did still feed the young, but it also did limit the food given to the young, to encourage the young to find food themselves." This is an observed behaviour, right?


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Dopamine and other neurotransmitter release during music listening
I'm looking for any studies that show a positive curve in respects to music sessions in humans and neurotransmitter release (specifically dopamine, epinephrine, and serotonin.) Any direct links would be great as I attempted googling and cannot find any at all for some reason.

Have a look at this question and answer: http://cogsci.stackexchange.com/questions/5627/is-there-evidence-to-suggest-that-music-can-trigger-release-of-a-particular-kind/15203#15203

It's a lot easier to measure brain electrodes for alpha wave activity, and MRI brain scans while listening to music, so those are more common studies.

Here is an article I found on google scholar. It links an increase in 5-HT a serotonin neurotransmitter when listening to pleasant music.
https://link.springer.com/article/10.1007/s004060070031

Thats pretty funny. 3 years later i randomly look at this question ive posted and you answered within the past hour. Ill take a look. Cheers

Since links die more frequently than you think, please provide a citation in your post as well as a summary in your own words. We want answers to be useful for the long-term. Thanks!


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Is probability for double crossing over included in distance cM? [task]
We got this task:
There are 3 genes (acb) on one chromosome (linked inheritance). Distance a-c = 12cM, a-b=16cM. Probability for double crossing-over (CO) is 0,6%. Find ratio of genotypes of descendants (AcB/acb X acb/acb).
I don't know whether the 0,6% for double CO is included in the 16% (16cM) probability.
I think it is not, so I got these ratios:
No CO and double CO: 42% AcB/acb, 42% acb/acb,
1x CO: 8% Acb/acb, 8% acB/acb

Centi-Morgan (cM) is based on observation not precise measurements. Now since double crossing-overs (and actually any arbitrary even number of crossing-overs) revert gene combination to the parental type, resulting lower recombinant frequency. So in your case since the chance (or the frequency if you wish) for double COs is 0.6%, you have to subtract this from parental genotypes and add it to the recombinants.


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When do the spindle fibers attach to the chromosome
At what phase does this occur in mitosis (or even meiosis); some text books say prophase while others say metaphase.

Would you like quoting which book said what?

Happens in prometaphase.

Your confusion comes from the inconsistent terminology in the literature. The attachement of the spindles to the chromosomes happens in the Prometaphase [1, 2]. The name already suggests that this is not one of the classical phases is cell division, but lies somewhere between Pro- and metaphase. Wikipedia states:

Prometaphase is sometimes simply included as part of the end of prophase and early metaphase.

If you really need to stick to the classical scheme of pro-, meta-, ana- and telophase, I would personally suggest to treat the attachement (not the formation!) of spindles as a part of the metaphase.


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How fallible are DNA paternity tests?
Is it possible to get either a false positive or a false negative from a DNA paternity test and what would be the likely mechanisms behind this?  For example, is it possible that a father's DNA could have changed during his lifetime enough to be unrecognisable to that of his children?

Only when the lab made a mistake and exchanged samples. Otherwise not.

Try to make the test again, in different place..

Thanks I we did take one mouth swap from one company then we did a blood test with another just to be sure. Both test came back negative.  Just confused with the similarities.

@lou It would be nice if you refrain from bringing your personal issues in the post. Just ask a neutral question.

I know. Just didn't know how to explain the situation for someone with knowledge about dna ect to help me with my question.

@lou hopefully that edit helps a bit

Discounting lab error and other kinds of human incompetence, there aren't very many things that can confound a paternity test. Normal DNA damage cannot, but there are kinds of genetic chimeras that get strange results.
Normal human DNA damage can't add up fast enough to change the results without killing you several times over, but there are a surprisingly large number of people who are chimeras.
The relevant particular flavor of chimerism is tetragametic chimerism, where essentially parts of your body are sibling-related to the rest. This occasionally is discovered during paternity testing, in one vivid instance when a woman was provably not the mother of the newborn that she had just given birth to. Technically I suppose the baby was her skin's niece.
The incidence of this was thought to be very low, but it's almost impossible to detect without DNA testing. We know the incidence is much higher than we thought, but we don't know how high.


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Why can blood group O be given to all blood groups?
The blood of persons of blood group O contains antibodies against antigens A and B. The red blood cells of persons of blood group A have A antigen on their surface. If someone with blood group A receives blood from a donor of group O, then anti-A antibodies in the donor blood should attack the A antigens on the recipient's red cells. Shouldn’t this be a problem?

Good question! Let's start with an overview and explanation of the ABO blood grouping system (Dean, 2005):

Blood groups, antigens and antibodies: Subjects with blood group A carry the A antigen on their red blood cells (RBCs) and have antibodies to antigen B; subjects with blood group B have the B antigen and anti-A antibodies, blood group AB carries both the A and B antigens and have no antibodies, and finally folks with group O have no antigens but both antibodies.
Blood groups and transfusion: Circulating antibodies in a person's blood will attack transfused RBCs from unmatching blood groups. These antibodies fix complement and cause rapid intravascular hemolysis, triggering an acute hemolytic transfusion reaction that can cause disseminated intravascular coagulation, shock, acute renal failure, and death (Dean, 2005). As people with blood group AB have no antibodies, they can receive all blood groups without issues. People with blood group O can only receive RBCs of blood group O, because they carry both antibodies. Blood group A can receive A and O, and blood group B can recive B and O. Hence, blood group O can be received by all other groups, and is therefore the universal donor.
Typically, literature on transfusion deals with the haplotyping the antigens of the donor RBCs. The question whether the antibodies in the donor's blood with blood group O would start attacking cells in recipient with blood group A, B and AB is, therefore, a very good question. And the answer is: yes, they will. Why then is O still the universal donor as they have both anti-A and anti-B antibodies?
First, whole blood is not used for "routine" blood transfusions (Torrens University Website). Instead, blood component therapy has largely replaced the use of whole blood (Patient.co.uk website). For routine transfusions, only the fraction containing packed red blood cells is transfused (Mayo Clinic website). Hence, in these cases, the blood plasma containing the antibodies is (virtually) removed after centrifugation. Since O-type red blood cells contain no antigens (Dean, 2005), and the plasma with the antibodies are not transfused, it can be donated to everyone, barred that the rhesus factor matches.
Secondly, even if plasma is transfused, antibodies in the donor's plasma are a minor problem, because of the small amount of antibody present in the donated plasma, which is further diluted on transfusion into the recipient's circulation (Dean, 2005).
Reference
- Dean (2005) Blood Groups and Red Cell Antigens. Chapter 5.The ABO Blood Group

Excellent overview of this concept. Also relevant, typically before transfusion (or a procedure that carries a risk of transfusion) we actually test a sample to make sure there won't be any hemolysis. So a recipient's blood is taken, typed (e.g., ABO group identified), and then mixed, or crossed with a sample from the donor pool before packed cells are given.

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What term describes insects that must eat protein to reproduce?
I know there is a specific term for insects that need to consume protein to produce viable eggs, as well as a term for those insects that don't need to consume protein to produce viable eggs.

I assume you are referring to species that needs to eat as adults before they can reproduce. Or are you only interested in species that specifically has to eat protein before they can reproduce (as adults or in general?)?

@fileunderwater I'm referring to a term that describes insect adults that must eat protein before they can reproduce.

The term I was looking for was anautogeny, or an anautogenous insect. I had slightly confused the definition, with the actual definition being; 'a gravid female insect that requires a blood meal before oviposition'.

Well, if you are satisfied with your own answer to the question, you might want to accept it. :)


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Can cfDNA testing distinguish results in the case of twins?
A fetus can now be screened for some of the more common genetic diseases and its sex determined from just a whole blood sample from the pregnant mother. Fetal DNA is abundant enough in the systemic circuit to be able to be purified and sequences analyzed. Question is, in the case of fraternal twins, could the procedure discern between the two fetus's...
As a clearer example, can it distinguish between:
Scenario 1: if one fetus was male and one fetus female
And scenario 2: both male?
It appears the test would just look for presence of Y chromosome using certain markers. But it could then look at SNP to distinguish individuals.
Looking for clarification here

I think you are overestimating how these cfDNA tests work.  Maybe I read the paper wrong, but from what I read of one technique (Sequenom's MaterniT21 test) there is no purification of fetal DNA.  They do restriction digests to assess the percentage of fetal DNA,  but I don't think they enrich for the fetal DNA when they sequence.  The library they make is mostly maternal, they are just looking for slight deviations in how many reads come from each chromosome, if too many come from chromosome 21, they conclude it's because the fetus has too many copies.
And as for SNPs, coverage is way to low for that.  We're talking about 40 million reads, even if that were mostly fetal DNA, which I don't think it is, that's not enough coverage to call SNPs.
So if there were two fetuses, and they were not identical, then the signal from each would be half what would be expected based on the restriction digests assay. So maybe you would have enough counts that you could tell that the Y chromosome counts were too low, and the X chromosome a bit too high, but since these tests almost certainly have not been clinically tested on multiple fetuses well enough for verify their accuracy, no company is going to report results.

http://www.qiagen.com/us/products/catalog/sample-technologies/rna-sample-technologies/dna-rna-protein/qiaamp-circulating-nucleic-acid-kit/

My wife just had this test done and we are having twins. So the test is largely performed. Y chromosome was detected in her peripheral blood sample. The question I'm asking here is how could test be modified to allow identification-we should be able to descent if we are having two boys or one boy and one girl

Like I said, the signal from each fetus would be less.  You'd need to boost that at least two fold, likely by increasing the real estate on the flow cell, which would cost more.  And if they appeared to be the same sex, there would be no way to know if you had enough signal from both.

I know they use that kit, its the rest of the protocol that matters.


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C1q attachment to antibodies
After reading about complement pathway and the complement components, I was wondering, does the C1q component attach to the Fab fragment or to the Fc fragment? The pictures in Janeway's Immunobiology are confusing and the text don't mention about this.

You said Fab fragment twice.

Can you please edit your question for clarity?  Right now it is unclear what you're asking.

I think voting for question closure based on a typo is a bit harsh. If journal referees would start rejecting manuscripts on that basis even Nature would have trouble filling its pages  =)

@ChrisStronks While I agree about the closing - an article in a bad grammatical style or with too much typos will never reach the reviewers. It will be sorted out by the editors when they do an initial review.

Complement factor c1q binds to the constant Fc portion of an antibody (Duncan & Winter, 1988). Indeed, the constant (Fc) tail of the antibody is where other proteins involved in immune responses typically bind, most notably the Fc receptors (e.g., Clynes et al., 2000) found on immune cells such as B lymphocytes. Fc receptors mediate the recruitment of immune cells to a site of infection. The primary role of the Fab region is antigen binding as it contains the highly variable antigen binding domain. See the following figure (from the site of Invivogen) for the Fab and Fc region showing the constant and variable regions of antibodies:

Figure legend from Invivogen): The Fc region mediates effector functions, such as antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). In ADCC, the Fc region of an antibody binds to Fc receptors (FcγRs) on the surface of immune effector cells such as natural killers and macrophages, leading to the phagocytosis or lysis of the targeted cells. In CDC, the antibodies kill the targeted cells by triggering the complement cascade at the cell surface. I

The constant regions of antibodies are located on the heavy chain (CH1,2,3) and the light chain (CL). These constant regions are potential binding sites for other immune molecules as they are constant between antibodies, irrespective of the variable region in Fab. Most of the constant regions are found on the Fc region explaining its major role in binding other molecules involved in the immune response, including complement factor c1q. However, the constant regions in Fab (CL) may also provide binding sites for other proteins and indeed some bacterial compounds are known to bind to this region (Bouvet, 1994). However, I have not found evidence of c1q binding the Fab region.

So Fab fragments can't activate the complement?

No, not as far as I am aware.


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How many cells does the smallest animal have?
Note: question rewritten to prevent misunderstanding and make it more answerable
I know that some small animals like C. elegans display surprising sophistication with a very small number of cells. But I wonder, among the animals with known/estimated cell count, which has the fewest cells?
To make the question answerable, please note these constraints:

I'm only asking about members of the kingdom Animalia, so single cell organisms and colonials like Vovox are excluded. If there are single cell organisms which are classified under Animalia (I think there aren't, but not 100% sure), I still want to know about the smallest multicellular animal.
I'm only asking about species where we can distinguish individuals. If some kind of polyp or sponge is just a bunch of cells which can merge with or separate from other cells and remain a viable organism, it's not interesting.
Please only consider species where the adult form reaches some size and stops growing. (Macroscopic) examples like the tapeworm, which continues building more proglottides throughout life, or fish which continue getting larger as they age, are excluded.
If the species consists of distinctive, stable "subgroups" of different sizes, the smallest size subgroup counts. For dogs, the size of the average chihuahua counts. For C. elegans, the size of the hermaphrodite (959 cells vs 1031 in the male) counts.
What counts is the number of cells in a healthy adult of the species or the relevant subgroup. For non-eutelic animals, make that the average healthy adult. Not the smallest ever observed exemplar, and also not amputated or stunted exemplars.
I am aware that we haven't discovered all microscopic animals yet, and haven't counted the cells of all discovered ones. Still, I'd like info on the current level of knowledge, including current known cell count, evidence that something has less than the current lowest known-for-sure count, and other relevant information.

What is an "actual animal"? This will be hard to define. Take a worm like C.elegans which has around 1000 cells (there are different numbers available here).

@Chris one officially classified in Animalia, the taxonomic kingdom. I know of C. Elegans, but I wonder if there are smaller ones.

I doubt that the number of cells has been estimated for many organisms, especially since most small animals are also usually poorly known (with C. elegans as a model organism being the exception). I therefore think you will have a better chance of getting accurate answers if "smallest animal" is framed in terms of actual body size (which is better known) instead of number of cells.

@fileunderwater but that would be boring :) and also an example of a tend which personally bugs me, as in "X, which interests us, is hard to measure, let's take the related Y and pretend we are talking about the same thing." I'm really interested in cell count, so I'd prefer to frame it as the smallest known, estimated or suspected cell count. I assumed that this is implicit, as we are unlikely to have discovered all microscopic animals anyway.

@rumtscho I'm not saying that its hard to measure, I'm saying that it is unknown for most animals. Therefore, any answer you get on cell count is most likely not the animal with the smallest cell count (just the smallest known cell count).

Also, I think that your last secondary question (cell count of small organisms fixed or not) should be posed as a separate quesion, since it's interesting on its own.

@fileunderwater thank you for the discussion. I realized that the original wording of the question wasn't so clear, so I rewrote it, including constraints on some of the factors you spoke of.

Rotifers are microscopic protostomes with around 1000 cells apiece.  This website claims the smallest rotifers have less than 100 cells, but I couldn't confirm this.  Most rotifers are eutelic — within a given species, each adult individual has the same number of cells (Encyclopeia of Life: Rotifers).

(Source)
Edit: Myxozoans might be even smaller.  These are microcsopic parasites that have been classified as cnidarians based on molecular studies.  They have complicated life cycles including a single-celled stage.

(Source)

About the edit: the single cell stage is probably not relevant. The Q is asking to adult stages. You've also had a single-celled stage - just after fertilization.

@fileunderwater Good point.  But it's hard to point to a single "adult" stage for myxozoans, they have two different hosts so they alternate between spores and infectious forms.

I don't know about all known animals, or actual cell count. However, males of the wasp Dicopomorpha echmepterygis are considered the smallest known insects with a body size of 139 μm. This should at least be a contender for smallest animal. As a reference point, C. elegans are usually about 1mm long.
However, given that we know only about 10% of the estimated number of species, and the ones we know are biased towards larger animal species, the smallest animal is most likely undescribed. In the case of parasitic wasps (or other insect parasites) these are extremely poorly known and new species are often described. Our knowledge of soil communities are also poorly known and includes many extremely small animals.
For the record, answers to a question like this depends alot on exactly what you include and how size is calculated. Could it be either sex or the average between sexes?

comments to downvotes are always appreciated...

Some of the smallest animals have only one cell. Paramecium Aurelia

Can you please indicate the species name and its position in the eukaryote phylogeny?

As far as I know, there are no single cellular animals. All single cellular organisms belong to other kingdoms. I admit that my taxonomy knowledge is not very good, so I may be mistaken. If there are single cellular animals please expand the answer, I'd like to learn more about them.

I just saw you have added the species name. I'm afraid a Paramecium is a member of the Chromalveolata kingdom, not of Animalia. Even in the early, not-so-clear worded version of the question, I specified "animal kingdom", and clarified in a comment that I mean the formal definition of an animal belonging to the taxonomic kingdom Animalia. So this doesn't give me the information I was asking about, even though it's related.

@rumtscho Agreed. Previously, many Protozoa (now obsolete) were considered animals, but they are not part of Animalia.

@fileunderwater the way I learned it, Protozoa were always considered separate from animals taxonomically, even though some of them were considered "animal like" and others "plant like" on an informal level.

@rumtscho Agreed, but in a loose/colloquial sense many labelled them animals.

@fileunderwater Chromaveolata is closer to plantae than to animalia; Chromaveolata and Plants fall under bikonta.

The classification of protozoa as animals (note "protozoa" means "first animals") dates back to a very old taxonomic system in which all living things were classified as plants or animals. I learned in high school that bacteria were plants. Really, this is just wrong and should be contradicted at every opportunity.


text:
How does steroid dependence occur?
I have seen on the internet that prolonged steriod treatment can result in the development of steroid drug tolerance leading to decreased hormone secretion. In turn this may lead to drug dependence, as you need to keep taking that drug to keep your body to function normally.
Can steroid treatment lead to drug dependency, and if yes, how?

I have made an edit to specify your question as your original question was unfortunately too broad for Biology SE to be acceptable as a valid question. Feel free to roll back if these edits are inappropriate

Your question on probiotic dependence, although unlikely to happen, could make a new separate question.

All classes of drugs react differently in the body. Some bind to receptors, some clean receptors, some drugs cause re-uptake inhibition in the brain, and others destroy viral and bacterial infections. Classifying drugs and how the human body would develop a tolerance to them in a post on this website would take pages upon pages to answer. When you say steroids, i'm assuming you are talking about anabolic steroids. That is the male sex hormone testosterone and its multitudes of derivatives. (DHT and non-DHT). Your body does not in fact develop a "dependance" on the drugs, rather it is a checks and balances system that your endocrine system establishes. Lets say you take a dosage of Testosterone Cypionate at 200mg a week for a 20 week interval from your G.P (common treatment for andropause). In laymans terms, your body senses the increase of testosterone and tells your Leydig Cells in the testes to stop signaling LH (responsible for testosterone production). Because it sees that there is already an abundance of the hormone. Now, once treatment stops, there are a series of protocols one could take to stimulate the natural production of testosterone again. Other forms of AAS are much harder on the HPTA than others however. (Trenbolone Acetate)

I edited and specified the question and it still fits your answer I think (it's not my area of expertise). Please check. If the OP doesn't roll back you could adapt your answer since the first part ("...would take pages to answer") is pretty much redundant then - thanks!

Yea it was definitely a needed edit. The title of his original question didn't really fit the breadth of what he was actually asking. Your edits are completely necessary in my opinion. As answering distinct drug dependencies would be outlandish here.

Steroid treatment with glucocorticoid drugs such as dexamethasone, prednisolone, hydrocortisone, etc. can lead to drug dependence, that is, an adaptive state formed after long-term administration. Drug dependence may cause withdrawal syndrome after stopping the drug abruptly.
Glucocorticoids are used to treat inflammatory, allergic, immune and malignant diseases. In the insufficiency of the adrenal cortex, the dose of glucocorticoid should mimic the physiological concentration and circadian rhythm of cortisol secretion to compensate for the inadequate production of natural cortisol. Even in the case of relatively low exposure to glucocorticoid therapy, long-term excessive replacement can lead to weight gain, glucose intolerance and abnormal bone metabolism, which can lead to osteoporosis.
In various conditions such as congenital adrenal hyperplasia, polycystic ovary syndrome and certain types of tumors, the body may produce too much androgens, male hormones. Such patients may not show signs of glucocorticoid deficiency. Women may experience symptoms such as hirsutism, oligomenorrhea, acne, infertility, and male pattern baldness. Men are usually asymptomatic, but acne, early baldness, and testicular adrenal gland resting tumors may occur. In this case, the use of glucocorticoids is prescribed to suppress excessive androgen production, rather than to compensate for the lack of cortisol. Here, the prescribed glucocorticoid acts in the following way through the hypothalamic-pituitary-adrenal (HPA) axis feedback loop: increased glucocorticoids suppress the release of adrenocorticotropic hormone (ACTH), thereby inhibiting the biosynthesis of pregnenolone from cholesterol. Pregnenolone is a steroid and the precursor of all other steroids, including glucocorticoids, mineralocorticoids, androgens and estrogens. Therefore, glucocorticoid drugs suppress excessive androgen production, but at a cost of suppressing all other steroid hormones as well.
The type of glucocorticoid drug prescribed depends on whether the goal is to compensate cortisol insufficiency or to suppress excessive androgen production. Hydrocortisone suppresses HPA least and dexamethasone most, with prednisolone in the middle.
When glucocorticoids are used in doses exceeding equivalent physiological production by a healthy organism, and the glucocorticoid treatment is suddenly stopped, HPA suppression prevents the adrenal glands from producing enough cortisol. Even lower but close to physiological doses of glucocorticoid drugs for long time may cause problems. Over a period of several weeks to several months or years, this may result in the gradual atrophy of cortisol producing cells in the adrenal glands, unable to respond to ACTH stimulation the HPA axis, leading to secondary adrenal insufficiency, i.e. the inability to produce normal levels of cortisol. Therefore, glucocorticoid withdrawal must not happen suddenly. Generally, patients taking glucocorticoid doses for less than two weeks are less likely to develop HPA axis suppression, and can stop treatment suddenly without gradual reduction, except patients receiving frequent "short-term" steroid therapy, such as in asthma.
In the case of chronic treatment that has been carried out for months or years, the goal is to gradually reduce the therapeutic dose to a physiological level, such as by reducing the dose step-by-step every 3-4 days for a few weeks, and then slowly withdrawing the drug for several months, to restore the HPA axis. Importantly, the adrenal suppression effect may last for a period of time, so after stopping glucocorticoid treatment, it may take more than a year for the HPA axis to fully recover.
Further reading:

Paragliola RM, Papi G, Pontecorvi A, Corsello SM. Treatment with
Synthetic Glucocorticoids and the Hypothalamus-Pituitary-Adrenal
Axis. Int J Mol Sci. 2017 Oct 20;18(10):2201. doi:
10.3390/ijms18102201. PMID: 29053578; PMCID: PMC5666882
Nicolaides NC, Pavlaki AN, Maria Alexandra MA, Chrousos GP. Glucocorticoid Therapy and Adrenal Suppression. 2018 Oct 19. In: Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dungan K, Grossman A, Hershman JM, Hofland HJ, Kaltsas G, Koch C, Kopp P, Korbonits M, McLachlan R, Morley JE, New M, Purnell J, Singer F, Stratakis CA, Trence DL, Wilson DP, editors. Endotext Internet. South Dartmouth (MA): MDText.com, Inc.; 2000–. PMID: 25905379


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What is the second phase of photosynthesis?
I really want to know what the second phase of photosynthesis (in the dark) is. I have a fair understanding of the first cycle where molecular oxygen is generated under the influence of light, but I don't understand the second cycle which can take place in the dark. It would greatly help to have a graphic of the second phase of photosynthesis.
Note: it is not for my homework, but for my own understanding. My textbook doesn't explain things very well.

I believe you are going to have to either elaborate on your question greatly and put forth some effort in specifics of what you are asking

photosynthesis has 2 phases.the first one is made in light,were oxygen is produced(i know this phase cause is easier and my teacher has it very good explained).The second phase is made in dark,were dioxide carbon is produced,but i don't know why and how.that's why i asked...

There are more than enough resources you can seek online to find the answer. Google the calvin cycle

actually i have,and i have found a lot of answers.but i posted here too,because i wanted even more answers. but thanks for your answer :)

I've voted to close because it seems like a homework question. What specifically is unclear to you about the second phase? Why does it confuse you more than the other phases?

well it is not for my homework,but it is for my school.I didn't know the calvin cycle,cause my book is a sh** book and doesn't explain it very well.and that's why i asked...

@user16901 What exactly do you want to know about Calvin cycle. Even after the edit the question is a little broad?

Here's an overview of both the Light and Dark cycles of photosynthesis, which looked particularly useful to me as it shows that the energy-carriers ATP and NADPH2 generated through solar energy are used in the dark cycle to generate sugars.
.
Here is another one that shows more details on the precursors involved in the Calvin cycle:

As commented by others, googling 'dark cycle' or its synonyms will give thousands of optional images to choose from if these don't suffice. The first one is taken from tutorvista.com the second one from users.rcn.com.

The dark reactions don't necessarily need to be in the dark; they're called that because they don't require light.

yes you are right


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Hamilton's derivation of direct fitness from his 1970 paper
In his 1970 paper "Selfish and Spiteful Behaviour in an Evolutionary Model", Hamilton uses Price's equation to derive his well-known rule $rb -c >0$. My question is about one of the steps in his derivation.
Hamilton considers a population of $n$ individuals. Let $s_{ij}$ be the effect of individual $i$ on the fitness of $j$. The fitness of an individual $j$ is defined as $w_j = 1 + \sum_i s_{ij}$, $w=1/n \sum_j w_j$ is the mean fitness in the population, and $q=1/n \sum_j q_j$ is the average frequency of a certain allele. Using Price's equation, we get
$w \Delta q = Cov (q_j, \sum_i s_{ij})$.
So far so good. But Hamilton then says that this equation can be rewritten as
$w\Delta q = \sum_i 1/n \sum_j (q_j - q)s_{ij}$
Based on the definition of covariance (i.e., $Cov (X,Y) = E((X-E(X))(Y-E(Y)))$, this seems to only be the case if $E(\sum_i s_{ij}) = 1/n \sum_j \sum_i s_{ij} = 0$. But this would imply that the average fitness wouldn't change over time, which sounds odd for me. In sum, I don't understand this step in Hamilton's paper. What am I missing?

Actually the derivation is pretty straightforward. It's easier to use the fact that $Cov(X,Y) = E(XY) - E(X)E(Y)$ to derive this result. Suppose
$x_{j} = \sum_{i} s_{ij}$.
\begin{align*}
  Cov (x_j, q_{j}) &= E (x_{j}q_{j}) - E (x_{j}) E (q_{j}) \\
                    &= \frac{1}{n}\sum x_{j} q_{j} - \frac{1}{n}\sum
                      x_{j} q \\
                    &= \frac{1}{n} \sum x_{j} (q_{j} - q)
\end{align*}


text:
What controls Fructose regulation in plants?
Sugars are found ubiquitously in plants and are regulated.
For sucrose it's pretty straightforward - it's basically kept at a low ish level, and put into storage or other intermediate compounds. These act to inhibit or promote other parts of the calvin cycle of sugar production (fructose 2,6 bisphosphate especially iirc).
Fructose is a bit more obscure. What are the regulatory feedback loops involved?

Preamble
In short, fructose kinases (like Fru6P,2-kinase) and fructose phosphotases (such as Fru2,6bisP) regulate and are in turn regulated by fructose (specifically Fru6P)  levels in plants. There are also several metabolites that regulate the rate at which those fructose enzymes function creating quite a complex fructose regulatory network. This phosphorylation can make fructose unavailable or available to proteins as well as providing energy in the process (and aparently the rate of this can be controlled effectively in vivo (Stitt, 1990)).
I haven't come across any cell uptake regulation, but remember plants are physiologically very different to humans and there may not be a like for like system in this case. Although I suspect there will be since in plants fructose can be concencentrated in fruiting bodies. Perhaps another answer, or a major edit to this answer can explain that.
Fructose is often referred to as a regulatory metabolite in plants i.e levels of fructose affect other pathways due to its phosphorylated state. However, there are lots of sugar regulating systems in plants. Although this article focuses more on glucose and galactose, it emphasises the idea of a regulatory web rather than a cycle when it comes to plants and sugar regulation. Below the studies are based on plants such as spinach and other leafy vegetation, not fruiting plants I'm afraid!
Kinase Control
3PGA, 2PGA, PEP, dihydroxyacetone P, and the 2-carbon intermediate glycollate-2-P are all metabolites that control phosphorylation that inhibit the kinase, whilst Pi activates the kinase. Interestingly PPi also inhibits the kinase by competing with ATP. As one can imagine, this causes sigmoidal ATP saturation kinetics and is clearly indicative of regulation.
Phosphorylation
Fru6P and Pi both inhibit Fru2,6bisP hydrolysis by FRU2,6PASE.
This article from 1996 has a figure showing just how complex sugar pathways can be. To expand on your question, we can see how fructose phosphorylation plays a role in regulating in Sucrose and Starch glycolysis (Plaxton, 1996).
Disclaimer: I haven't studied this since undergraduate level, so constructive comments are welcome and I encourage people to edit this answer to improve it and help it more aptly answer the question!


text:
How does the genetic material differ between dizygotic twins and ordinary siblings?
I am going to give a rough presentation on twin studies.
The terms heritability and concordance are included already, but I struggle with understanding the difference of the genetic material of dizygotic twins and ordinary siblings.
While ordinary siblings evolved from different sperm and egg cells, I only know that dizygotic twins form when two different sperm cells fertilize egg cells of the same cycle. However, I'm not sure if these cells are identical products of the same meiosis process.
I appreciate your help and time.

Differences in genetic material between dizygotic twins and siblings are likely to be very similar.

Dizygotic twins, or so-called fraternal twins, on the other hand, are no more genetically similar than any other set of siblings. - Utah.edu

Since all oocytes are all synthesized during fetal development, dizygotic twins are no more likely to come from a single mitotic division than siblings are.
Also note that in human females, only one egg comes from the a full mitotic division:


text:
How many mosquitoes would it take to "drain" enough blood to put a person into shock?
I'm just curious, how many mosquito "bites" (mosquitoes which have removed blood from a person) would it take to remove enough blood to put a person into shock? (Putting aside all reasons why it wouldn't happen, how many would it take?)

I don't have any mosquitos on hand to test this, but lets assume an average mosquito has a carrying capacity of 50uL of blood. If the average human has 8L of blood, 8 million uL / 50uL is 160,000 mosquitos. That's probably a decent first order approximation. I don't know how much blood a person has to lose before they go into shock, and that 50uL per mosquito estimate is based only on what I remember a full mosquito looking like, but I've never been good at measuring volumes by eye.

@user137 I don't know about your mosquito numbers, but 8l of blood sounds very unusual. I've always thought that the average is 4-5. Else, good starting point for the calculation.

@rumtscho You're probably right, I just remembered hearing somewhere that a human had 8 quarts of blood and 1 quart is about 1L.

@user137 Chris's approach sounds right - estimating the amount of blood based on body weight. Maybe you encountered the 8 quarts figure in a text on obese patients. I already thought after leaving the comment "wait, there's no way everybody has the same amount of blood".

@user137: maybe you saw "8 pints", a volume I've seen offered before. However, those are Imperial pints, a US pint is sufficiently smaller to matter. Even a "finger in the air" estimate in US pints should be 1 bigger than a UK estimate :-)

You might have to factor in blood loss after the Mosquitos leave due to the anticoagulants they inject. Unless we're talking 200k Mosquitos at exactly the same time... Great, that's my sleep gone for tonight.

This question falls into different subquestions:
1. How much blood does a mosquito take when feeding?
This is not so easy to answer, but there are publications which measure the volume of different mosquito species. Reference 1 lists volumes between 2.85 and 11.99µL per meal and mosquito. Reference 2 lists 3.07 and 5.71µL. To make the approximation a bit easier, let's assume that mosquitoes drink about 5µL per bite (which should be near enough).
2. How much blood does a human have?
According to Wikipedia, humans have around 77mL blood per kilogram of body weight. If we take a 70kg human, we get around 5L of blood.
3. How many mosquitos does it take to get a human into shock, and how many to suck him out completely?
According to the Medline, Hypovolemic shock occurs when a human loses about 1/5 (or more) of his blood volume. 1/5th of 5L is one litre. Since each mosquito sucks 5µL, this would take about 200.000 mosquitoes. To suck out all blood would take 1 million mosquitoes. (This is not possible since mosquitoes depend on an existing blood pressure, as reference 3 shows. If a capillary is empty due to massive blood sucking, they change to another.)
Besides this theoretical (but interesting) calculation, there are some real problems about getting biten by so many mosquitos. First, this is a question of available skin. The human skin is about 2 square meters in size, which would require 100.000 bites per square meter. To break this down further, a square meter has 10.000 square centimeters, so there would be 10 mosquitos which need to bite you per square centimeter. Rather unlikely.
Then each mosquito injects a mix of anti-coagulants, pain killers etc. prior to sucking to keep the blood from clotting and also to make sure you won't notice the bite immediately. As pointed out in the comments, this would already cause a lot of trouble and probably cause massive bleeding, since the effect of the anti-coagulants would sum up when biten by thousands of mosquitos. Additionally the body reacts by releasing histamines and since the amount would also be massive, this would cause real trouble and probably kill you.
References:

Regulation of blood meal size in the mosquito
La Crosse Virus Infection Alters Blood Feeding Behavior in Aedes
triseriatus and Aedes albopictus (Diptera: Culicidae)
Visualizing Non Infectious and Infectious Anopheles gambiae Blood
Feedings in Naive and Saliva-Immunized Mice

Great detective work Chris!

This reads like http://what-if.xkcd.com.

This question would clearly fit there. My drawing skills are less developed, though. :-)

I wonder whether the anticoagulants from 200K mosquito bites would cause more problems than the loss of blood.

@JeremyStein: indeed, it seems likely you'd be poisoned somehow before passing out from blood loss. The histamine system would be berserk, for example. Fortunately that's not the question ;-)

@JeremyStein I have been wondering about this myself, but had no time yet to follow this up.

there would be 10 mosquitos which need to bite you per square centimeter. Rather unlikely. Doesn't seem unlikely at all, assuming that they don't all have to be there at once. If a mosquito drinks for 5 minutes at a time, then one mosquito per hour per cm^2 would do it.  Images like this one from the Alaskan Arctic make that seem quite plausible.

Everyone seems to forget that the human body replaces blood that is lost quite rapidly. When I donate blood to blood bank they take half a liter or something and I was informed my body will replace it within 30 minutes, I just need to drink plenty of fluid after.
I think it would take a fairly concentrated effort by mosquitoes to do any damage from blood loss.

Nope, this is wrong. Otherwise blood transfusions would not be necessary, you would only have to supply enough liquids. It takes several days to weeks to fully replace it, see for example here.

It takes several weeks to replace the red/white/platelets yes, but the blood volume is replaced much faster as it is mostly comprised of water.

Hi welcome to Bio.SE! Please provide reputable sources to back up your claims. Anecdotal evidence should be reserved for comments or as supplement to claims supported by trustworthy citations. We ask that all answers on this site provide support, and failure to do so will result in your answer being downvoted or closed. Thanks!


text:
How would real-time blood glucose monitoring work?
Is it possible to perform real-time blood glucose monitoring using a wearable non-invasive device (similar to a fitness band measuring heart rate)? I'm aware that there are some devices in the market developed by medical companies but most of them require you to stick a needle in your body and it also requires you to switch needles and reapply it every few days.
How can blood glucose be measured in a non-invasive way?

Mark Arnold and other's have done work on using near infrared spectrophotometry to measure blood glucose non-invasively, but I'm not aware of any clinically approved methods available yet.

NIR spectrometers are relatively big and heavy and not cheap and this has been a hurdle in any wearable device, but perhaps there are MEMS type devices being developed. Luminous Medical, now out of business first proposed a monitor using NIR spectroscopy. But it was targeted for the hyperglycemia of the sick and injured (hospital use) rather than ambulatory diabetics. The cost of the technology is one of the factors that caused the company to fail.

If you browse the on-line patent data bases - either www.uspto.gov or www.freepatentsonline.com for "glucose monitor" you'll find there are at least half a dozen technologies that have been proposed including the most non-invasive technologies such as using light - similar to the pulse oximeters used in hospitals to measure the pulse and PaO2 through the skin to more invasive methods that periodically pump small samples of blood outside the body for chemical or optical analysis. But in terms of accuracy, the best way to measure BG is by some means that can analyze arterial blood in vivo.
Companies that are trying to develop these devices are shooting for accuracies better than 12 mg/dL, but that's very hard to do with the noninvasive methods. There is a very new technology that uses a contact lens as the sensor, measuring from the iris and transmitting to remote electronics for processing, but that's still probably year's away. I believe the best products that are available today may be those developed by Dexcom in San Diego, CA. See their website here: http://www.dexcom.com/
The journal Science just published its year end Breakthroughs and that includes an article that shows hope in restoring the B cells in the pancreas for type I diabetics see http://www.sciencemag.org/content/346/6216/1444.full . This of course is the best solution - a cure. I hold hope scientists are less than 5 years away from that goal.

Those are beta cells (B cells are a type of blood cell), and there are many more T2DM patients than T1DM. Beta-cells would do little for them.

http://news.sciencemag.org/chemistry/2015/01/temporary-tattoo-measures-blood-glucose-levels


text:
Do electromagnetic waves outside the visible spectrum have any role in photosynthesis?
Does photosynthesis occur only in the visible spectrum? If there is a way to completely remove all other electromagnetic bands from the sunlight, including infrared (IR), will photosynthesis continue to occur?
Is there any known plant (algae, fungi, bryophytes, pteridophytes, gymnosperms and angiosperms) that utilises the other wavelengths for photosynthesis?

Photosynthesis occurs at and around the absorption spectrum of chlorophyll, i.e. at green wavelengths, so in the visible spectrum. This does not mean that other wavelengths are not used, just less optimally.

@ChrisStronks Sorry, I started editing once I saw your comment. It seems your edit clashed with mine. Feel free to edit this version

Photosynthesis only occurs in the visible light.have a look at the absorption spectra of the different pigments involved in photosynthesis, you see that all these pigments absorb light between 400 and 700nm (from a diagram from here):

You see that the absorption spectra of chlorophyll a and b are located from 400 to 500nm and again from 630 to 700nm. The maxima for both molecules are different so that the light is used more efficiently.
The other three important light harvesting pigments involved in photosynthesis (in cyanobacteria and plants) are: Beta Carotene, Phycoerythrin and Phycocyanin. These use different parts of the visible spectrum (hence the different color of cyanobacteria), but they still only use the visible part of the light between 400 and 700nm.
The reason for this can be seen in the figure when you look at the intensity of the sunlight (plotted in black). All photosynthesis occurs in the area of the highest intensity. Wavelengths shorter than 350nm are efficiently blocked by our atmosphere, wavelengths much longer are not transporting much energy.
To shortly answer your question: If we could "switch off" all other wavelengths from the spectrum, there would still be photosynthesis on earth.

Don't we need some infrared to keep the plan warm enough, as otherwise most plants just shut down.

I'm curious, what software do you use to generate the graph?

I haven't made this myself, the source is named above the figure (in brackets).

@IanRingrose sort of? Infrared is more the mediator of heat than the provider. Warm things would emit it if it wasn't around, but a planet illuminated by only gamma rays would still be warm if it had an atmosphere to keep the heat in. It wouldn't exactly be a vacation spot.

Photosynthesis is nearly all visible light. There's usually not enough UV and thermodynamics more or less rules out infrared. Chris covered that pretty spectacularly, but that nearly is significant.
There is some evidence that certain kinds of fungi can use gamma rays or other ionizing radiation for energy, but they're not particularly common. Melanin is used instead of chlorophyll, but apparently 'tooling up' for radiosynthesis(is that a word?) is fairly hard on the cell. It was assumed the melanin was a protective pigment(like it is in humans) and produced only when necessary(also like humans), but these particular ones were discovered growing in the Chernobyl reactor and apparently evolved to continuously produce melanin and absorb ionizing radiation for food. They don't stop producing melanin even on the verge of starvation. Other melanized fungi live in high-radiation environments, like mountaintops and the poles, where there is more UV and cosmic rays and things.
Fun fact aside: Fossilized melanized fungal spores turn up at the K-T boundary when the earth had no magnetic field and therefore higher radiation flux at the surface (see paper linked above and Hulot & Gallet, 2003 for more).

+1 Interesting fact. The word is "radiotrophic" BTW.

I would use radiosynthesis to describe the process of absorbing ionizing radiation for energy, and things that primarily do that for food as radiotrophic, but my spellcheck underlines both as 'not real words' and I'd never heard radiosynthesis before. Chemo/photosynthesis, sure. radiosynthesis no.

You are right, I forgot about this part.

Do you have citation to the fun fact? Great additional answer.

Curiously enough, the paper about radiotrophic bacteria talks a little about that, but they cite in turn Hulot G, Gallet Y (2003) Do superchrons occur without any palaeomagnetic warning? Earth Planetary Sci. Lett. 210: 191–201.


text:
What is this insect in India?
I found this insect today in front of my room.
I am just curious to know what kind of insect it is? And, is it poisonous?
Location: India

Where do you live? It may help narrow the possibilities

Its a black Cricket .
Crickets, (family Gryllidae) are related to the Grasshoppers Family.
It should have grasshopper like hind legs .
Crickets usually emit  noise from its body.

I can't tell what its legs look like from that image, it's kind of blurry. But I think it's either a type of cricket or cockroach. If those are wings at the bottom of the insect I'd lean towards cockroach. And I swear I remember crickets and cockroaches as both being orthoptera, but now cockroaches are grouped with termites? When did that happen?

@user137 crickets were never grouped with cockroaches as far as I'm aware. Some scientists used to group together mantises, orthopterans, cockroaches, and stick insects together.


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Kinetic binding / unbinding constants of protein + mRNA ⇌ mRNP
I wish to find an order of magnitude for the binding/unbinding constants of mRNA and RNA-binding proteins.
Suppose molecules A and B reversibly associate to give the complex C. Assuming the diffusion is large enough such that no concentration gradient exist, the reaction equation at equilibrium is:

➕[A][B] — ➖[C] = 0
with ➕ the binding constant (units: concentration-1.time-1), ➖ the unbinding constant (units: time-1), and [A], [B], [C] the concentrations of the molecules.
I found many papers assessing the equilibrium constant K = + / ➖ but I am interested in + and ➖ independently.

It's hard to separate the on and off rates, but one approach I've heard of is affinity chromatography. You'd need a column of immobilized protein or RNA, then fluorescently labeled and unlabeled counterpart. You load the column with labeled compound, then pass unlabeled compound through and measure how the labeled compound comes off.

Thanks for your answer. I am not doing experiments so I was searching the literature for some order of magnitudes.

The keyword that you're missing is kinetic. You want the kinetic binding constants/rates. And @user137 is right, this type of data is sadly uncommon, but if all you're interested in is OOM it might be possible... maybe. I'll take a look.

@user137 for future reference, there are many experiments that can be used to determine kinetic rates. Surface plasmon resonance (SPR), stop flow spectroscopy, kinetic ELISA, and many others. There's even a lab in my department working on getting binding/unbinding rates from single-molecule microscopy data.

@tel The only reason I was aware of the affinity chromatography method was because my dad did that for his PhD in the 80's. He had to make his own FITC, label his own antibodies, pour his own column, then build his own fluorescence detector for their HPLC using an automobile halogen headlight bulb and then run hundreds of HPLCs at different protein concentrations and salt concentrations and pH. It makes me appreciate working in a lab with funding.

@user137 build his own fluorescence detector for their HPLC neat

Katsamba PS, Park S, Laird-Offringa IA. 2002. Kinetic studies of RNA–protein interactions using surface plasmon resonance. Methods 26(2):95-104
There are many methods for studying kinetics, I only mention this one because the lab I'm in has used it for studying protein-ligand interactions. That article has a good explanation of SPR and how it works, so I won't offer to much detail other than to say it basically measures the change of refractive index as one molecule binds to another, which is immobilized on a chip. This allows direct measurement of on- and off-rates.
The researches studied two RNA binding proteins: HuD and U1A, as well as several mutants. Here are their results (Table 1 in the article):

I really couldn't tell you if those rates are generally representative of RNA-protein interactions, but I suppose that's not what you're asking.

Ridgeway and coworkers designed a really neat microfluidic device for making these kinds of kinetic binding measurements on RNA and protein (Ridgeway et al. 2009). Their device works sort of like a stop-flow, and they used a FRET based scheme to detect binding and unbinding events. They took measurements for one particular rRNA/ribosomal protein pair and got (6 ± 0.4) × 105 M-1s-1 for the bimolecular on-rate kon and  (5 ± 0.9) × 10-3 s-1 for the unimolecular off-rate koff.
Ridgeway cites references 23,24,26, and 33 when talking about experiments with "similar constructs and buffer conditions", so those would probably be a good place to start looking if you want to assemble a diverse set of kon  and koff  values.


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Are pulp cells (in oranges) normal plant cells?
Does a pulp cell contain all the elements that a 'normal' plant cell contains?
I've searched for an hour to find more information about this but couldn't find anything useful. Is the pulp cell the exception from the general size range of most eukaryotic plant cells, normally between 10 - 100 µm?
Please include link to a reputable website.

They are not individual cells. In fact, the "juice sacs" (as they are known) are actually specialized, multicellular hairs:

Juice sacs originate as multicellular hairs in which the interior of the enlarged distal part breaks down and fills with liquid. The juice sacs constitute the fleshy, edible pulp of an orange and are the source of the sweet juice.

(Quote and image from Fruit Terminology, palomar.edu)
This is from a botany course; if for some reason that isn't reputable enough, check out the book Anatomy of Seed Plants by Katherine Esau (1960).

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


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Formation of Life
Originally, life evolved from non-living matter. Why is life only generated from other life nowadays, and why doesn't it evolve from inanimate matter, like it did originally billions of years ago, when life evolved on Earth?
Maybe I should reword this further. Living organisms reproduce other living organisms but the first living organism came from non living material or chemicals. So could life be created in a laboratory as it originally was ? Originally the process leading to a life form took one billion years, so would this be the answer to my question that it takes too long and that is why it is not being repeated again ?

Welcome to Biology SE and thanks for your interesting question! I edited your question slightly to improve readability. Please feel free to roll back.

Thanks Chris for finding my question interesting and for rewording it to improve it's readability. I am looking forward to reading answers to this question .

Szostack from Harvard in this video The Origin Of Life on Earth discusses various fundamentals to prebiotic biophysics that might provide insights although no definitive.

Abiogenesis, the development of living things from non living matter, is not something we know much about, since it happened about 4 billion of years before we were around and haven't reproduced it in the lab. My guess is that it's not easy. However, the Miller-Urey experiment and others have told us something about abiogenic production of organic compounds.
The first living organism on Earth ( Let's imaging some self-replicating RNA ) was probably very inefficient, copied itself slowly and made a lot of errors. At the time it could survive because there wasn't any competition. However, as time went on some of these copies were more efficient and copied themselves more quickly, outnumbering the original sequences and driving them into extinction. Wait another 3.5 - 4 billion years and you have modern life.
If abiogenesis were to occur on Earth today, the resulting organism would likely be inefficient like the first organism. However, now it would face immense competition from very efficient modern organisms and would probably be eaten.
This is speculation, but I assume that any new type of life on Earth would be carbon based, since organic carbon based building blocks are abundant. If anything, abiogenesis might be easier on modern earth than early earth because the starting materials (nucleotides, amino acids) are readily available, but competition from modern life and reactive oxygen in the atmosphere would hinder any new abiogenesis.

Interesting note about reactive oxygen there at the end — indeed, the Great Oxygenation Event, when oxygen began to be present in the atmosphere, was one of the most significant extinction events in the history of life on Earth.

@augurar I never thought oxygen would be that reactive until I started doing LC-MS and kept finding stuff 16 or 32 mass units too heavy, even after keeping them at -20 in the dark.

There are two questions here:

Why does life only generate life?
Why doesn't life continue to be generated on Earth?

The first one is easy. We don't only generate life. If that were true, it might be illegal to flush toilets. Life forms of some kind would occupy all the space in our atmosphere. Babies - or some living things - would rise up from our graves. Conceivably none of the millions/billions of people who have died from the beginning of history (and well before that) would be dead. Add to that animals, and everything in the other Kingdoms included in Life, and there would be nothing left perhaps except for life. To be honest, life generates heat, death and simple substances much more commonly than it generates life.
If you mean, why does like produce like (in your case, a life generates a similar life form*, that's because of genetic material. New life is based on the genetic material of the preceding life form. People don't give birth to zebras, zebras do. When the genetic material is damaged enough, we give birth to a non-viable or diseased child. If a mutation is favorable, it is (under the right circumstances) spread through an advantage. An example of this is the appearance of lactase, an enzyme which allows adults to derive continued nutrition from animal milk.
As to your second question: why doesn't life continue to be generated on Earth? Are you 100% sure that it isn't happening? How would you recognize a life form foreign to our own? How many different kinds of life can evolve under the same planetary conditions, the same planetary element ratios, etc.? If a very rudimentary silicon-based life form evolved in, say, the last 2,000,000 years, would you know how to look for it? In other words, are you defining life only as we now know it - a carbon based, DNA-propigated form?
Furthermore, if a non-carbon based life form could only evolve on this planet to a very basic, simple level, would you give credence to it as a newly evolved "life" form? Intelligent life is rare. I would guess that very simple life forms are far less rare in the Universe.
How would you classify (or explain) the chemosynthetic bacteria that oxidize sulfur instead of oxygen?
I realize that there are a lot of questions here and not many answers. But part of finding an answer is asking the right questions.
The Origins of Lactase Persistence in Europe

By question (1) I think the PO means why life is only generated by living organisms. In other words, there is only a single question I guess.

@ChrisStronks - I do tend to take people at their word...

Asking good questions is an art.

formulating good answers too - +1

I think this is mostly answering another question than what is being asked (especially looking at the original formulation by the original poster), and the second part of the answer, which is more relevant, is mostly speculation. LUCA is also an accepted and well-supported concept, and if you are challenging that all life on earth has a common ancestor you need to back this up by references (I'm not sure that you are though?).

You might also want to mention the theory that life didn't actually originate on Earth, but was seeded here by comets/meteors/whatever.

Chemosynthetic bacteria are a poor example.  All known life shares certain characteristics, in particular the same system of mapping DNA codons to amino acids (the genetic code).  In fact, almost all species use the exact same mapping from codons to amino acids, with minor exceptions.  If a life form were discovered that did not have DNA or transcribed it differently, that would be a good reason to suspect an independent origin.

Abiogenisis, where imperfect micelles (spheres) of hydrophobic carbon chain formatiions leads to potentials for capturing and mixing elements and molecules forming peptides, polypeptides and protiens that can then catalyze enzymes to patterns to the micelle to a cell of sorts.
Was it inside a terrestrial micelle that life formed or Did amazing spiraling symetry of life get help or even need it from galactic wave patterns, crystal energy of minerals or was it just a mixing up microscopic pieces of Pythogerian parts and geometry.
Either and anyway, given low energy potentials needed for effeciency of a new life form, unless it was non carbon based, it would have practically zero chance of survival where energetic mass of life that already exists just chews it up and mutates spin offs. Only a dynamic shift in genetics as we know it would allow us to detect divergent life.
That said, got to love the ugly waterbear.

It would be great of you added some references to support your response!

Check out iBiology playlist on Youtube to get you started Bez.


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How much does sleeping correlate with daily activity?
I'm a very lazy person. I spend most of my time in a chair, at a computer; I eat more than three meals a day. I don't do any sport, at all.
What I want to know is: why do I need to sleep 8-12 hours daily since I don't waste myself physically during the day?!
Wouldn't 3-5 hours be more reasonable? With an increase to 7-10 if I were a bodybuilder or a construction worker.. something that would actually deplete my body of energy?

Physical inactivity doesn't necessarily mean mental inactivity. Heavy mental exercise may also cause a need to sleep.

@ChrisStronks yes but why? Why does heavy mental and heavy physical labor produce equivalent global fatigue when they are fundamentally so very different, down to the actual organs under load?

@tel you seem to assume that 1) physical movement uses up lots of energy, and 2) sleep is there for muscle regeneration. Both assumptions are not very true. Your body heat production, viscera function and brain function use up by far more energy, and it is not known what sleep is for, but it's more likely to be about brain self-organisation without the meddiling of a wanton, energetically expensive consciousness, than for muscle relaxation.

@rumtscho Really, just like the OP I'm wondering why both a day of hard labor and a day of hard thinking leave me similarly tired. It's a curious symmetry.

Sleep helps organize what is learned during the day. It usually takes me two separate sleeps - two nights, or a nap and a night - for me to use material I have learned. I take a lot of naps because I do mental work, and it helps me learn faster. I also make faster progress in daily living learning than most people. Sleep early and often! It is productive!


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Does sample buffer require EDTA for protein separation on SDS PAGE?
In sample buffer preparation we add EDTA, but if SDS-PAGE is for protein then is it necessary to add EDTA in sample buffer? What is role of EDTA in sample buffer for protein separation for SDS-PAGE.

In my opinion EDTA is dispensable. Common proteases like serine proteases do not depend on metal ions. As the post in this page suggests, there are EDTA free loading buffers. This discussion in researchgate suggests that EDTA is excluded from protease inhibitor cocktails because it may interfere in downstream steps. I am commenting because I am not able to verify the dispensability of EDTA, from any reliable source.

I've never used EDTA in sample buffer. The combination of SDS and DTT (or β-ME), along with the boiling step, is enough to completely denature and inactivate pretty much every enzyme, including proteases.

EDTA is a complexing agent for bivalent cations and is usually used to inhibit enzymes (proteases, nucleases) which need these ions in their active center to work. Without it they do not attack the sample.
The presence of EDTA in the sample buffer is interesting, since Laemmli's original paper from 1970 ("Cleavage of structural proteins during the assembly of the head of bacteriophage T4.") doesn't use it and I think it is not necessary.
The reason for this is simple: Protein samples are usually generated in buffers which contain different protease inhibitors, which protects the samples. Additionally the purpose of the sample buffer is to denaturate (at least for the standard SDS gels) the protein sample completely, so it will run uniformly. Both steps ensure that proteases are either inhibited or completely denaturated, which will both protect the sample.
The only reason I can think of for using EDTA is that it can help to destabilize your target protein, when a co-factor which is important for the structure is complexed by EDTA and thus keep it in solution after the denaturation.
There are of course ressources which state that EDTA is necessary for protein integrity, but they only say it is there to inhibit proteases by complexing metal ions (see here for example).
As a 2x sample buffer, I use the following recipe (this can also be made 5x if necessary), which contains EDTA, but can also be done without. If you prefer β-Mercaptoethanol, you can use it in the same concentration as the DTT (which has the advantage of being less smelly):
2x sample buffer:

4% SDS
20% glycerol
2 mM EDTA (ethylene diamine tetraacetic acid) - can be made without
100 mM Tris-Cl, pH 6.8
200 mM DTT (dithiothreitol)
0.1 % (w/v) bromphenol blue dye

AFAIK only metalloproteases use metal ions (Zn and Co); these are not the most common proteases that one would encounter.

There are some calcium dependent proteases. You may also want to inhibit kinases or phosphatases.

There are very few of Ca dependent proteases. I am not sure kinases need metals as cofactors (activation is a different thing; that's signaling). Alkaline phosphatase needs Zn. But I guess this is not as common as the dependence of nucleases on metal ions. In any case we do use a protein inhibitor cocktail while doing extraction. Loading shouldn't require EDTA; you are just denaturing.

@WYSIWYG I looked into Laemmli's paper from 1970, and he doesn't mention EDTA at all. My guess for the moment is, that it has been added later for unknown reasons. I think since the concentration is not high anyways (1mM final), there will be no harm if it is removed. I'll check that later and edit the answer.

Yeah I guess it is like one of those occult biolab practices of putting every coloured substance including copper sulphate solutions, covered in aluminium foil at 4⁰. Not sure though.

It's not unlikely. Although the colored dye here make sense as it makes loading easier.

I agree with the other comments but want to add something.
EDTA works as a stabiliser for bME. If you have bME in your 5x sample buffer and want to store it for a long time period add EDTA, otherwise you have a big loss of activity.
https://www.sigmaaldrich.com/content/dam/sigma-aldrich/docs/Sigma/Product_Information_Sheet/1/m7154pis.pdf


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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