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In vitro virus assembly
Are researchers able to assemble viruses in vitro?
For example, I imagine that a phage display library may be generated by throwing in a test tube the capsid proteins (or what have you) along with relevant DNA that will self assemble. Has this been done? If so, is it a technique readily applicable to a broad range of viruses?

Yes, and a quick search for viral in-vitro assembly will turn up tons of results. — it's a little more complicated than that! — but it's not usually done as such, which I will explain.  Basically, there are four things you might want to do:

You want to make large amounts of virus and study it. If so, then all you need to do is infect your cell culture with your virus and let it replicate.  Some are obviously easier than others — from my own experience, HIV is pretty easy but Hepatitis C is a real PITA — but that's essentially it.  This obviously presumes you already have some virus stock on hand for infection.  You could also transfect the culture with full-length viral plasmids, which leads me to...
You want to study some specific aspect of the virus.  That's cool!  Most people aren't just concocting virus.  Generally, for viruses that humans can get, it's generally recommended/heavily encouraged to only use what you need for safety reasons.  So, for example, you might transfect the one protein you think is important to see what it does by itself.  After that, you might transfect the cell culture with the full virus, but with one important gene knocked-out.  I used to make single-round HIV by using a plasmid for full-length HIV without a functioning envelope gene and another plasmid for VSV envelope; new HIV particles would be made infectious because of the VSV gene but after infecting they no longer had that gene anymore.  Basically, a limited version of the virus, which leads me to...
You want to make virus-like particles.  These are one of the better-named things in science and are just what they sound like — particles that look a lot like virus, but aren't.  Generally, they're empty shells.  We can use these for all sorts of things, from vaccine studies to other genes and diseases.  Techniques can vary, but generally it's similar to the above.
You want to introduce some other gene to a cell culture system, using a virus backbone for transduction; think "I want to fix these cells... permanently."  Generally, these viruses are usually based on adenovirus or lentivirus (aka HIV) because they will insert their genes into the cell's genome, so the gene will persist.

Item 4 is probably closest to what you specifically meant.  Here's a free review on the use and safety of retroviral vectors in humans, and here's a nifty one in fish.  As for which viruses it's applicable to, well, that varies a lot by virus, host, culture system, and so on.

Thanks, that was very helpful! I inadvertently googled de novo virus assembly, which was a dead end. With point 4, you touched on an interesting topic. Because as I understand, in order to apply gene therapy to living organisms using CRISPR (or other method), we would still need a way to deliver the corresponding genes to the organism. I guess in the future this may be done using viruses or virus-like particles .

Viral vectors can indeed insert genes into the host genome (this is one reason why HIV is so hard to beat) but they tend to do it in a random or stochastic fashion.  This is decidedly bad, from a therapeutic point-of-view.  Viruses like HTLV have a tendancy to cause cancer for that reason.


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Why do veins undergo vasoconstriction during physical activity?
How would this help increase blood circulation?

Do you have a citation for this claim?

"As physical activity increases, the veins undergo vasoconstriction, driving more blood back to the heart and increasing circulation." –http://www.biosbcc.net/doohan/sample/htm/vessels.htm

I believe that the answer is in the same cited source (BioSBCC).
Veins are considered a blood reservoir and undergo constriction to mobilize blood.

[...] the veins act somewhat like a blood reservoir, containing 60% of the total blood volume at rest. [...] When the body needs to mobilize more blood for physical activity, the sympathetic nervous system induces vasoconstriction of veins.

The result is an increase in circulating blood volume. This changes cardiac output and arterial blood pressure (CV Physiology: Blood Volume).
I also recommend reading on Biology.SE: Where does extra blood come from to fill your muscles during exercise?

There does not need to be a change in circulating blood volume during exercise; the role of vasoconstriction is more subtle than that.
Vasoconstriction increases the stiffness of venous vessels leading back to the heart. This makes them act more like stiff tubes than elastic reservoirs. As a result, any extra blood pumped by the heart is more likely to return to the heart rather than to be stored in the venous vasculature. The importance of regulating venous return in concert with cardiac function has been appreciated at least since the work of Guyton and colleagues in the 1950s.
In exercise the effective muscle pump arising from the combination of muscle contraction and valves in the veins preventing backflow is also important; both the muscle pump and venoconstriction promote venous return to the heart.

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How do eukaryotes terminate transcription? (clarification on Campbell Biology)
I'm having trouble understanding how eukaryotes terminate transcription. Studying Campbell Biology (pg. 342, 10th ed.), I read:

In eukaryotes, RNA polymerase II transcribes the polyadenylation signal sequence on DNA, which specifies a polyadenylation signal (AAUAAA) in the pre-mRNA. This is is called a "signal" because once this stretch of six RNA nucleotides appears, it is immediately bound by certain proteins in the nucleus.

The text continues with:

Then, at a point about 10-35 nucleotides downstream from the AAUAA, these proteins cut it free from the polymerase, releasing the pre-mRNA.

Does this mean pre-mRNA continues to be synthesized for 10-35 nucleotides after AAUAA is transcribed before finally being cut off?
Thanks so much.

According to Lewin's Genes XI - Krebs et. al on Eukaryotic Transcription, RNA Splicing, and Processing

It is not clear whether RNA polymerase II actually engages in a termination event at a specific site. It is possible that its termination is only loosely specified. In some transcription units, termination occurs more than 1000 bp downstream of the site, corresponding to the mature 3' end of the mRNA (which is generated by cleavage at a specific sequence) Instead of using specific terminator sequences, the enzyme ceases RNA synthesis within multiple sites located in rather long "terminator regions." The nature of the individual termination sites is largely unknown.

It does go on to say,

The site of cleavage/polyadenylation in most pre-mRNAs is flanked by two cis-acting signals: an upstream AAUAAA motif, which is located 11 to 30 nucleotides from the site, and a downstream U-rich or GU-rich element. The AAUAAA is needed for cleavage and polyadenylation because deletion or mutation of the AAUAAA hexamer prevents generation of the polyadenylated 3' end (though in plants and fungi there can be considerable variation from the AAUAAA motif).

I should add that the significance of 11 to 30, or as you said 10 to 35 nucleotides is that it is telling you the approximate size of the protein complex that is sitting on the RNA and where the active site of the protein is. The domain that recognizes the termination sequence is about 10 to 35 bases wide. It is likely that the variation is due to the RNA sequence following the termination sequence ability to form a stem loop structure.
Campbell takes a necessarily basic and less nuanced approach to the information that they provide on molecular biology. The approach is to provide some details and show the evolutionary commonalities between a diverse range of biological systems. The approach is okay as it gets you into the frame of mind of thinking about the interconnectedness of biological systems.
As you progress in your studies you will see that the reality and specifics are far more complex and exception based than was presented in introductory courses. But the more advanced courses spend an entire semester focused on what Campbell covers in one chapter. Campbell is accurate but incomplete out of necessity.

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How does a neuron change as you learn?
I am currently taking a course called "Introduction to Machine Learning with ENCOG 3", and I have a question about how well the Artificial Intelligence (AI) algorithm for a "neural network" corresponds with how an actual neuron works.
In the course, they model a neuron like this:
x1, x2, etc. are voltage inputs, the wij are weights.  The inputs are multiplied by these weights and summed up by the neuron.  The neuron then has an "activation function" which then takes the sum of weighted inputs and calculates an output, typically a value between 0 and 1 (or between -1 and 1). You can think of the wij as representing dendrites (a higher weight means a more dense and thus conductive dendrite), and the output of the activation function as the voltage that gets sent down an axon.
The AI neural network algorithm creates a kind of intelligence by modifying the weights (wij shown in the picture).
My first questions is: Is this a good approximation as to how neurons actually work?  That is, do our neurons "learn" by changing the weights (dendrite density, conductivity)?  Or, is there some other mechanism that is more important (e.g. do neurons learn by changing their activation or summation functions?)
My second question is: If neurons really do learn by changing the density of dendrites, then how fast does this happen?  Is this a fast process like DNA replication?  Does the neuron quickly generate (or decrease) dendrite density when it receives some kind of biochemical signal that it needs to learn now?
I understand that much of this might not yet be known, but would like to know how well the AI algorithm corresponds with current theories on biological neural networks.

have you tried googling and if so, what have you found? these questions are textbook/wikipedia level. for example, you might start with https://en.wikipedia.org/wiki/Hebbian_theory

Note that Hebbian model is quite a simplified one. More complex models of learning exist. There are several posts here that have dealt with similar topics: http://biology.stackexchange.com/a/3783/3340, http://biology.stackexchange.com/q/1198/3340, http://biology.stackexchange.com/q/11276/3340, http://biology.stackexchange.com/q/2595/3340, http://biology.stackexchange.com/a/31310/3340, http://biology.stackexchange.com/q/7762/3340.. Is your question about any topic that is not already addressed by these posts?

@WYSIWYG OP asked for a comparison of the above model to biology. Those posts don't address functional modelling at all.

With respect to your first question, that model isn't intended to take time into account, but is based on Hebbian learning with the goal of computability. It's generally used in simple pattern recognition situations where each case has no bearing on the next. The learning portion is performed ahead of time during the training phase. For example, a deterministic perceptron isn't permitted to change after training. In contrast, the Biological Neuron Model is much more complex, and uses a variety of ordinary differential equations to integrate the cumulative behavior of neurons over time. As such, those models are non-deterministic and don't see as much practical use outside of experimentation.
To address your second question, neurons themselves don't "learn." A single neuron is essentially meaningless. Learning is an emergent process created by the interaction of several systems at once. While one influencing factor is connectivity (zero for no connection, non-zero for the inhibitory or excitatory connection which emulates both synaptic and non-synaptic), what you might call short term learning can also be performed by existing clusters of neurons, without any change in connectivity. Biologically, this is what must occur before any of the comparably slow process of tissue remodelling can take place, and the computationally equivalent process is only possible in time-aware models like the aforementioned Biological Neuron Model.
Take, for example, someone who wishes to learn to play guitar. When they begin playing, existing clusters emulate the desired behavior as best as they can. These neurons act as the functional scaffold that initiates and drives the neuroplastic process. Playing becomes easier because this scaffold becomes more efficient as new connections (shortcuts) are created, existing connections are strengthened, and irrelevant connections are inhibited. The improved scaffold in turn allows further improvements. Newborn neurons may also migrate to the area, though the how, why, and when of that process is unclear to me. This "behavior emulation" or "short term learning" process used in practicing the guitar, or whenever a novel situation is encountered, must be primarily governed by excitatory and inhibitory neurons' influence. Otherwise the whole process cannot even begin.
Further reading

Parameter estimation of a spiking silicon neuron.
Synaptic plasticity, memory and the hippocampus: a neural network approach to causality
Signaling mechanisms in cortical axon growth, guidance, and branching

Do you have references for your second claim?

This model was a reasonable approximation when it was formulated. However, as we learn more about synaptic integration, it appears that neurons are best approximated by two-layer neural networks (1). In this way the active properties of individual dendrites are better taken into account. Each dendrite, or at least a group of dendrites, is viewed as capable of performing input summation from individual synapses, independently of the integration at the level of the soma.
Regarding your first specific question, mechanisms of plasticity other than modifying the individual weights have also been described, for example as you suggested, by modifying the intrinsic biophysical properties of neurons that lead to firing (2). These would be equivalent to altering the sigmoid function or all the weights collectively.
Regarding your second question, we do not think that changes in the weights happen through modification of the dendrite as a whole. Rather, they represent changes at the level of single synapses, what are termed 'synaptic weights'. The biological phenomenon underlying synaptic weight change is referred to as synaptic plasticity. It is thought to manifest through a variety of biophysical mechanisms, including incorporation of new receptors at the post-synapse, changes in those receptors' conductivity, increase in the number of pre-synaptic vesicles etc. These events can be quite fast, in the order of seconds to minutes (3). More long-term changes of the weights, referred to as long-term potentiation are thought to depend on protein synthesis which is a slower process.

References
1) Poirazi, P., Brannon, T., & Mel, B. W. (2003). Pyramidal neuron as two-layer neural network. Neuron, 37(6), 989–99. http://www.cell.com/neuron/fulltext/S0896-6273(03)00149-1
2) http://www.scholarpedia.org/article/Intrinsic_plasticity
3) Harvey, C. D., & Svoboda, K. (2007). Locally dynamic synaptic learning rules in pyramidal neuron dendrites. Nature, 450(7173), 1195–1200. https://doi.org/10.1038/nature06416


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Do we consume DNA and proteins of other organisms?
When we eat raw meat, e.g. chicken or fish, we are actually consuming the DNA, proteins etc. which are present in their cells.

Wouldn't this affect our cell functions as this DNA might enter our cells?
It is known that we get energy by eating them. Is it glucose or ATP or some other form of energy that is produced from them?

Or, to rephrase the question, why don't people who eat lots of sushi develop gills?

No, unless what we ate had the ability to infect our cells (viruses and some bacteria) 2. Proteins, complex carbohydrates, simple sugars, lipids, vitamins, ions...

We likely have the genes for making gills, however we do not express then in such a way during development as to have them form into functional gills. You won't develop new and novel organs after development and birth,.

While this is an obviously poorly phrased and researched question, it doesn't seem to be bad enough to warrant so many downvotes.

Yes, we are eating the DNA and proteins of an organism when we consume and digest its cells.
However, consuming the "raw flesh of hen or fish" in your example would not cause harm strictly due to the consumption of their DNA.
DNA has two basic components - a structural 'backbone' of alternating phosphate molecules and sugar molecules (called deoxyribose) and a nitrogenous base (a group of atoms that includes nitrogen) on each backbone unit. These basic components of DNA are common to the all organisms that contain DNA, like the hen and fish in your example.
When you digest the DNA in your food, specialized molecules (in this case nuclease, which digests DNA) produced by your digestive system break down DNA into its components. These components can then be rearranged to create 'human' molecules, such as human DNA.
In other words, you don't integrate fish or hen DNA directly into your human DNA; you break it down and rearrange it into human DNA, then integrate it into your body.
To answer your second question, we get energy by breaking down the proteins, carbohydrates, and fats (known as macromolecules) of other organisms. Much like DNA, these three macromolecules are broken down into their singular components. For carbohydrates, this would be glucose.
These components are then further broken down into energy (as a force) which powers cellular machinery to 'recharge' ADP (the 'discharged' version of ATP) back into ATP, a specialized molecule which can 'bring energy' to other parts of the body to power your body's processes.
ATP is not energy per se - energy is defined as the "capacity to cause change" (Campbell Biology, pg. 160) and do work. Energy is therefore a property rather than a distinct molecule.
Summary:

When we consume DNA of organisms, it does not inherently damage us as we break it down and rearrange it into completely 'humanized' molecules.
Glucose and ATP aren't energy per se - they are just molecules that contain lots of energy. ATP 'brings energy' to other parts of the body; glucose is broken down into energy to 'recharge' ATP. Energy is not a molecule - it is a property.

The second part of your question has been answered already, but you were right about your first point. I believe the previous answers are not completely correct concerning the total break down of nucleotide sequences.
It has been shown that RNA from ingested food (specifically rice miRNA) actually does enter mammalian cells and tissues and can influence gene expression [1].
A number of exogenous miRNAs from common foods where observed in Human blood plasma in this study [2].
I believe we still have to learn a lot about this kind of interaction with our food. It might be that miRNA is not the only component of our food that can survive digestion and influence human cells directly.

Nice find on miRNA!  From the two papers I think it's a bit early to hypothesize the same could be true for proteins or DNA though.

The lay summary of a newer paper says: "Experiments using mouse models show that the dietary uptake of microRNAs is barely significant, and certainly insufficient to affect physiological functions. Moreover, the microRNA molecules are broken down in the small intestine."

Please see also the even-newer paper, "Survey of 800 datasets from human tissue and body fluid reveals XenomiRs are likely artifacts", or its lay summary.

And some even newer papers: Chen et al 2021, PlosOne "Large-scale identification of extracellular plant miRNAs in mammals implicates their dietary intake", Li et al 2021 "A Timely Review of Cross-Kingdom Regulation of Plant-Derived MicroRNAs", Zhao et al 2018, PlosOne "Evidence for plant-derived xenomiRs based on a large-scale analysis of public small RNA sequencing data from human samples"

To add to adam's answer:
Protein and DNA molecules are simply too big to pass through cell membranes or through the wall of the gut.
In the process of digestion:
Proteins are broken down into amino acids.
Complex carbohydrates like starch are broken down into sugars.
Fats are broken down into fatty acids and glycerol.
These molecules are small enough to pass through the wall of the gut. These are essential food. Once through the wall of the gut, the body synthesizes "human" proteins, carbohydrates and fats from them.
DNA and RNA are broken down into nucleotides, which are small enough to pass through the wall of the gut. The mass of DNA is tiny compared to the mass of the above types of food. As far as I know nucleotides are not essential nutrients (that is to say, I believe our bodies can synthesize them from the above types of food.)
Incidentally one of the nucleotides of RNA, adenosine monophosphate (AMP) is the "discharged" form of ATP. According to https://en.wikipedia.org/wiki/Nucleotide all four of the nucleotides of RNA are used in monophosphate - triphosphate energy cycles, but the others are more specific.
It's important to remember that proteins, fats, sugars (and ATP) are not "energy" but simply molecules that are high in energy.
I would guess that there is far more of these RNA nucleotides free in the cell (involved in energetic pathways) than there is in the actual RNA used for protein transcription. And there is definitely more RNA than DNA.

"Protein and DNA molecules are simply too big to pass through cell membranes or through the wall of the gut." How about Prions? Kuru is the result of ingesting human tissue that carried the misfolded protein. Bovine Spongiform Encephalitis was transferred by eating affected cows. Our phagocytic cells are constantly taking in nucleic acids and processing them....

@AMR I was speaking in generalisations. Prions obviously do get through in small quantities (whether by passing through the gut membrane or through an open wound directly to the blood) but once through they are able to multiply. Calling me out on this is similar to calling someone out for the statement "sperm are too large to pass through condoms." The exceptions are rare, but the consequences are great.

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Evolution of endosymbionts?
Mitochondria and plastids in eukaryotes evolved through a process of endosymbiosis. How does an event like a eukaryote engulfing a bacteria, become a part of the genome? Some of these primitive eukaryotes could have been more predisposed to more vigorous endocytosis as a result of their DNA, but how could the physical event account for evolution of organelles?

What exactly are you asking here? Mitochondria still have their own DNA, it's not in the "parent" cell. They reproduce on their own, it's just that they wait for the cell reproduction signals to do so. In fact, this is exploited in mapping female genealogies, since mitochondrial DNA is transferred predominantly through the female line (egg cells tend to carry a lot more mitochondria than sperm cells).

I think you mean mitochondria and chloroplasts and are referring to the endosymbiont theory (Reference to the unedited question as it was originally asked).
The definition of symbiosis for the most part tells you how coevolution can be accounted for by this theory.
The larger Eukaryotes provided the protomitochondria with a protected environment for growth and the protomitochondria produced usable nutrients for their hosts from molecules that the eukaryotes were unable to process on their own.
The two organisms struck up a balance and the mutually beneficial relationship allowed both to prosper. As the Eukaryotes with protomitochondria were better able to utilize more of the chemicals from their environment than those that did not play host to the protomitochondria, they had a survival advantage that other early Eukaryotes did not.
As plant cells have both mitochondria and chloroplasts, it is believed that one of the eukaryotes with a mitochondria endocytosed a photosynthetic prokaryote. This event wasn't as much of an advantage as the first symbiotic relationship. Since all eukaryotes have mitochondria or evidence of ancestors that had mitochondria, but not all have chloroplasts, then it was beneficial enough that the photosynthetic organisms were also able to coevolve within the eukaryotes and alongside the mitochondria, but they were not beneficial enough so as to give those cells that hosted chloroplasts enough of an advantage that they took over all life on Earth.
Mitochondria also have their own DNA, so their complete genome is not found in the eukaryotic genome. Over evolutionary time, mitochondria have lost the genes that allowed them to live freely, so you could not extract them from eukaryotic cells today and expect them to grow external to the eukaryotic cell. They require substances that the eukaryotic cell makes. Whether there was recombination between the two genomes or just that both had the same function at one point and then through genetic drift caused the mitochondria to lose the homologous gene, I could not say.

If your question is about how the engulfed endosymbionts lost their genes and became dependent on the host cell then this is the answer.
The current theory (Limited Transfer Window hypothesis) says that at some point, injury or membrane rupture of the endosymbionts would have resulted in the leakage of their genomic DNA. The host genome would have acquired these genes by a lateral gene transfer mechanism. Now, because the endosymbionts that have lost these genes randomly, would have a lower cost of maintenance (as they can acquire these gene products from the host cell) compared to those who still maintain these genes themselves, the former will outgrow the latter at some point. Note that there is a constraint on the population size and therefore there is a good chance that the endosymbionts with full set of genes, could go extinct because of their additional growth cost.
This is a probable way by which the endosymbionts lost their genes and became dependent on the host. It has been observed the number of genes transferred to the host correlates with the number of endosymbionts present in the cell. The rationale behind the limited transfer window hypothesis is that if the number of endosymbionts is high, then the likelihood for the host to tolerate damage to a few endosymbionts is higher (note that damage was the first step in the endosymbiont to host gene transfer).
This is still a hypothesis and the exact mechanisms are yet to be elucidated.

References:

Timmis, Jeremy N., et al. "Endosymbiotic gene transfer: organelle
genomes forge eukaryotic chromosomes." Nature Reviews Genetics
5.2 (2004): 123-135.
Smith, David Roy, Kate Crosby, and Robert W. Lee. "Correlation between nuclear plastid DNA abundance and plastid number supports the limited transfer window hypothesis." Genome biology and evolution 3 (2011): 365-371.
Lane, Nick. "Plastids, genomes, and the probability of gene transfer." Genome biology and evolution 3 (2011): 372-374.
Gray, Michael W. "Mitochondrial evolution." Cold Spring Harbor perspectives in biology 4.9 (2012): a011403.

Thanks for the information. I have a great deal more information than when I started. Rupture of the membrane could explain acquisition of the foreign DNA.

@user17496 But you should bear in mind that it is just a hypothesis. This has not be explicitly proven.

@WYSIWYG Once the DNA is out of the symbiont, it would likely be like transfecting a Eukaryotic cell today, easier as the symbiont is already in the cytoplasm. The chromosome would need to get into the nucleus. It would need to be linearized, and there would need to be an area of complementarity that would allow for strand invasion. The rest would be handled by the cells own repair mechanisms. Genes are maintained through selective pressure, and as you said, if it costs less to have the product produced by the host, then sustaining deleterious mutations will not be under selective pressure.

@AMR Complementarity is not really essential. They can insert via a break and join mechanism. But as I said, we really do not know the mechanism yet. I don't think even the insertion hostpots have been studied in great detail. That reminds me; I should look for that.

No, not essential, but I was thinking along the lines that there would be more opportunity for homologous incorporation than going down the path of NHEJ, especially to get a productive insertion where the gene is downstream of an active promoter, unless the entire gene "cassette" was inserted. Anyhow, my crystal ball gets very fuzzy after looking about a billion years back.


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Virus-to-virus gene transfer via "sequences integrated into a common host organism"
From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese:

In addition to direct HGT between organisms as depicted in Figure 1, forms of indirect HGT have been observed, which involve an additional intermediary organism in gene transfer from a host organism to the final recipient organism. The most notable are virus mediated gene transfer (transduction) between bacteria (Weinbauer, 2004), retrotransfer of a plasmid to a second bacterium, acquiring host genes and returning to the original bacterium (Ronchel et al., 2000), the spread of donor genetic material between several different bacteria coexisting in complex communities or biofilms (Molin and Tolker-Nielsen, 2003; van Elsas et al., 2003; Wuertz et al., 2004); or from virus to virus via sequences integrated into a common host organism.

Does it mean that a viral gene or other DNA sequence gets integrated into the host's genome and then some other virus (that chanced to be in the same organism) manages to obtain this sequence and package it into its own DNA?
Keese's article has no reference for this statement, and perfunctory googling brought nothing to clear the matter for me.

Does it mean that a viral gene or other DNA sequence gets integrated
  into the host's genome and then some other virus (that chanced to be
  in the same organism) manages to obtain this sequence and package it
  into its own DNA?

Yup, that's what it means (although not all viral genomes are DNA-based).
A lot of genomes contain extensive content that is thought to arrive from viral transfer. Here's a reference to get you started:

Endogenous Viral Elements in Animal Genomes (by Aris Katzourakis , Robert J. Gifford; 2010; PLoS Genetics)

If much of an organism's genome originally derives from viral transfer, then any subsequent viral transduction represents a virus-to-virus transfer of genetic information.


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What is this tiny thing on the branch
I noticed a tiny spot with weird shape on the shoot of a plant (Variegata), and there are many others on other branches. I wonder what is it, this is a cropped picture of it, Thank you!

This is a female of yet another scale insect (Coccoidea). We have discussed one recently.
I guess we can identify this one rather precisely as Ceroplastes sinensis or its close relative. Species of this group are of South American origin, but Ceroplastes sinensis has today an extremely broad distribution. So, if you found this plant ("Variegata" is a specific epithet, by the way: it would be of some help if you provided the generic name as well) in Europe or Asia it's likely sinensis itself.

thank you very much for your answer, Very instructive,  I am not a botanist, I don't know the naming techniques, I just searched by leaf colors and I found Variegata as the closest plant, I think it's a Ficus benjamina 'Variegata'


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Why are there so many different humans yet chimpanzees are just chimpanzees?
There are two species belonging to the Pan genus (Pan troglodytes and Pan paniscus). That's just two.
I mean, humans have changed radically since we split from chimpanzees, we have Australopithecus afarensis, africanus, anamensis, Paranthropus robustus and boisei, Homo erectus, habillis and so on.
A chimpanzee fossil that is 2 millions years old should be pretty different from a modern one, why aren't they considered another species?

The rest you listed that are not Homo sapiens are evolutionary ancestors of humans. Not humans. Close to humans? Sure, some of them. But not humans.

@MCM Yeah, but my question stills stands even if they are not called humans.

Could you re-phrase your question? Are you asking why we don't find/identify more fossils of Pan ancestors?

There really is only one species "human" (Homo sapiens). I guess you want to know why "our" branch brought up a lot of species, whereas the "chimpanzees" branch remained nearly "untouched" since the last common ancestor? I'd say this is due to an greater expansion of our ancestors across a wide variety of different terrains.

@AstronAUT But what about those that stayed? Here's a modern Chadian (there are a lot of ethnic groups, but whatever), and heres a reconstruction of a Sahelanthropus Tchadensis/Toumai.

And to the wide variety of different terrains and climates, one might consider the possible impact of the genetic drift due to population bottlenecks that seem to have been significant in the history of human expansion.

I'd guess it is just sampling bias. Humans are dis-proportionally interested in humans so they spend more time looking for human fossils than Chimpanzee fossils. In addition there is the lure of declaring you found a new Homo species instead of declaring you found one weird-looking part of a known Homo-species.

There is an inherent flaw in your question. Humans did not split from chimpanzees. Humans and chimpanzees descended from a common ancestor. The modern chimpanzee lineage has made a similar number of evolutionary steps since the branching from the last common ancestor as the modern human lineage has. Australopithecus is an entirely different genus in the lineage that lead to modern human. Similar changes happened in the Chimpanzee, Bonobo, Orangutans, and Gorilla lines, until we reach the modern day lines that are examples of the survivors of the split millions of years ago.

The first chimpanzee fossils were found in 2005 http://www.nature.com/nature/journal/v437/n7055/full/nature04008.html and date back to ~500K years ago... the have been very few fossil finds for the chimp lineage, so unlike with Lucy which gets us back to about 3.3 million years ago for humans, we have not uncovered the same artifacts for Chimpanzees. It could be that the range of the Chimpanzees was not conducive to the fossilization and preservation of bones that the human lineage was afforded.

There's also a question of perception. As humans, our brain is very good at distinguishing other humans, so we see enormous variety whereas we are not good at seeing differences in chimpanzees, so they all look alike. In reality, present day humans are all one species; I don't know if the variability in humans is actually larger than in chimpanzees (or any other species), considering there are about 30000 times as many humans as chimps. There's a similar argument about human fossils if we classify them in far too many distinct species or if it's individual variability.

That's just two [species of chimpanzees]

C'mon!
There is a huge behavioral gap between the two species. I get your point that the human lineage had several, not just two, forms. Yet these two chimpanzee species are so brutally different that they make most of our "human diversity" seem so regularly the same.
About your question - it seems obvious to me the point brought by @Pete: That we, humans, came from the forests to the open land, which brought the seas and continents to us. Many different habitats would lead to wider variation.

A chimpanzee fossil that is 2 millions years old should be pretty
  different from a modern one

Why should it? The African Forests changed drastically in the last 2 million years? If not, then why should chimpanzees have changed? Take a look at the horseshoe crabs (Xiphosura, Limulidae): they've been that way for hundreds of millions of years! The punctuated equilibrium seems to be the norm, more than the exception, doesn't it? (I remember the horse evolution through the Mesozoic, apparently linear, but in a closer look there ain't some teeth in the line? Aren't there plateaus - long periods of stability - among the high precipices of sudden genetic/form/function change?

I think this is the first answer that looks like an answer, but it still needs to more clearly deconstruct the question. 1-The difference is greater than the species count suggests; we're missing chimp data. 2-Humans are more similar than you think, but they have had more dynamic geographical selection pressures to amplify their differences. 3-It's common for much less change to occur than what we see in both these examples.

For fossils the answer is simple chimps live in forests and forest are really bad at preserving fossils, we lived in savannah which include some floodplains which are really good at preserving fossils. Thus we find a lot more human fossils than chimp fossils.
Otherwise Chimps exhibit far more genetic diversity than humans. humans are just a weird branch of chimp.consider the genetic diversity below. If we were not so  morphologically biased we sould easily conclude all hominids as just one species based on genetics.Chimps actually have quite a wide morphological variation its just we as humans are far better at noticing human variation.

Can you please give the reference for this graph?

Its from this royal society publication http://rstb.royalsocietypublishing.org/content/366/1567/1080 a more detailed and updated version is available here http://ucsdnews.ucsd.edu/archive/graphics/images/Gagneux_et_al_PNAS_1.jpg

Cool +1 I am surprised there is really so little genetic diversity in humans despite our gigantic population size. I suppose we only very recently went through population expansion and still have the genetic diversity of a small population. But chimpanzees typically have rather small populations...

It could also be that humans keep killing of entire bloodlines and tribes, technology makes conquest easier. This is just an idea however.

Chimpanzees are relatively isolated and confined in so far as their environment, it's all much the same... forest. They haven't been subject to the environmental factors humans have... arctic, tropics, deserts, mountains etc. Therefore there hasn't been the need to change as much. Animals adapt to their environments, chimpanzees only have one, humans have hundreds.
If you have a look at the humans living in the same distribution area as compared to chimpanzees then you'll see that they don't have much variation either for that area.

Chimps haven't been subjected to tropics and mountains?

They certainly have

@AliceD I think Pete is trying to say that humans cover a much more varied ecological environment  due to our greater expansion. This is a good point.

Chimpanzees have only been subjected to a specific type of mountain and tropical environment. Humans have inhabited every type of mountain range and tropical environment there is... Hence our greater adaptive variations.

@Alex This is a good comment that Pete has made, but it's not an answer.


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Is there a genetic reason explaining the difference of the height of male and female?
The male and female height difference seems to be around 1.08 if all cultures are counted from these stats: https://en.wikipedia.org/wiki/Human_height
Can this ratio, 27/25, be explained by genetics and is there any research to explain how genes affect the growth of a man and woman? I assume there are a lot of factors that affect height and it might be very difficult to say if environmental and selective reasons or genetics are behind this factor.
ADDED:
GIANT study reveals a giant number of genes linked to height (October 6th, 2014)

“Height is almost completely determined by genetics, but our earlier studies were only able to explain about 10 percent of this genetic influence.”

https://www.broadinstitute.org/news/6119

The fact that only about 10% of the genetic influence can be accounted for suggests that height is definitely not completely determined by genetics.

Please note that the study, which you cite above,  studies growth variability across human populations. It does not (or at least not explicitly) state whether males tend to be taller because of some Y-chromosome specific genes (or possibly something else; - to expand your very intriguing initial question: e.g: silencing of certain growth genes in XX / female or XY / male ?- or non-genetic property of Y or Barr-bodies (silenced X)? -or specific social factors in nurturing? - ....)

@tsttst: The wood, the trees and the vision ... I forgot the genetic mechanism in my answer, but now added that to my discussion. Thanks for pointing that out!

One could say that the absence/presence of the Y chromosome is the major genetic difference, because males and females share all the genes on the 22 autosomes and the X chromosome.  Females enter puberty later, and their epiphyseal growth plates fuse, or close, earlier https://en.m.wikipedia.org/wiki/Epiphyseal_plate. Bones cannot grow longer after this happens.  Males do not enter puberty until later, and so their bones have more time to grow before the plates close. The Y chromosome regulates testosterone synthesis, and that increases growth hormone levels in males, as well.

@kmm the 10% figure is how well that study predicts. It says nothing about how heritable the trait is, which is determined via other methods. Imaging if you predicted height based on a GWAS with only 50 people; you'd explain 0% of the variance but that does not mean height is 0% genetic. In fact, genetic predictors of height now explain 82% of variation in height (by some estimates, this is near 100% of the genetic influence).

Short answer:
There is strong evidence that height is a heritable trait with a strong genetic component. The genetic mechanism could be higher expression of an X-chromosome gene that, expressed in high levels, inhibits cartilage development, perhaps causing lower height. The increased expression seems to be caused by incomplete X inactivation in females. Furthermore, there is differential selection for height between human males and females likely causing the differences we see in modern human populations.

Long Answer:
Genetic basis of height
The genetic variants analysed by Wood et al. (2014) account for ~29% of the phenotypic variance and 60% of the heritability of height.
Due to this high heritabilty (and the fact that there are still expected to be more unknown variants affecting height) there most likely is a genetic reason explaining the difference of height in human males and females. Thinking about the nature of this difference is a bit difficult. It is good to know that the trait has a high heritability and therefore a strong genetic component as this allows us to have a look at how natural selection affects height.

Selection on height
Height is a polygenic trait that is under recent and strong natural selection (Field et al., 2016 - preprint) leading to height increase in both human males and females (Fig. 3D in Field et al. (2016)):

What does this tell us in terms of the genetics underlying the height differences in human males and females? First, we have to understand that natural selection (at least mainly) affects individuals, not species. Then, we can understand that natural selection can affect males and females of a species differently. And Field et al. (2016) have shown exactly that for height. In their analyses, you can see that male and female height show (mildly) differing signals of natural selection (Fig. 4C in Field et al. (2016)):

But selection needs heritable genetic variation that allows this differentiation between the sexes. So what is the mechanism?

Genetic mechanism of height differences between human males and females
As pointed out by @tsttst in the comment differences between sexes are usually caused by genes on the X and Y allosomes. There is evidence that the height differences between human males and females are related to the X-chromosome (which also explains some of the missing heritability of the GWAS study by Wood et al. (2014)), reported by Tukiainen et al. (2014). They write

In one of these three associated regions, the region near ITM2A, we observed that there is a sex difference in the genetic effects on height in a manner consistent with a lack of dosage compensation in this locus. Further supporting this observation, ITM2A has been shown to be among those chrX genes where the X chromosome inactivation is incomplete.

They also give a molecular mechanism how this hypothesised increased expression of ITM2A can cause the height difference. They report that the ITM2A gene is
involved in cartilage development (van den Plas et al., 2004) and that the height-associated ITM2A variants change expression of the ITM2A protein. This is interesting as increased ITM2A expression in mesenchymal stem cells of adipose tissue seems to inhibit cartilage development (Boeuf et al., 2009). Tukiainen et al. (2014) conclude:

As the allele associated with shorter stature associated with increased expression of ITM2A (sic), this suggests the allelic effect to height could be mediated through the capacity to generate cartilage and bone.

Finally, how can this be interpreted from an evolutionary point of view?

Evolutionary interpretation of height differences in human males and females
Differences in height (but also other traits) between sexes of a species are refered to as sexual dimorphisms. Sexual dimorphism (at least in primates) in height is strongly related to differences in mating behaviour and a sign of aggression and/or dominance-based mating patterns (Wynn and Coolidge (2011, p.82), sorry for that poor referenc link). The counterpart to this is pair-bonding, or in human terms marriage: a primate example is our pretty close relative, the Gibbon, that is (at least socially) monogamous and as expected does not have a height-related sexual dimorphism. Great apes including humans do have this polymorphism even though pair-bonding in humans is widely spread. Therefore, it was not surprising to find a reduction in height dimorphism from Australopithecus over Homo erectus to Homo sapiens (Wynn and Coolidge, 2011, p. 83, see also this, especially the last paragraph of this chapter).

Update on the main source
One of the papers I mainly used for this answer - to illustrate selection on height - was a preprint. It is now published in Science: Field et al. (2016).


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How to troubleshoot islet isolation
I have been getting very low yield from islet isolations from rats.
My procedure is as follows:
Inject the pancreas with 5mL Liberase (1 wunch unit/ml) in HBSS + HEPES through the CBD (decent inflation, atleast of the frontal part of the pancreas) and excise it to an Erlenmeyer flask with 5mL Liberase in HBSS + HEPES on ice (takes ~10 minutes).
Once all animals have been processed, I incubate for 21 minutes at 37C.
After incubation, I shake for 5 seconds and stop digestion using HBSS + 10% FBS. I sediment for 20 minutes and homegenize again using a wide-tipped pipette.
The tissue is pelleted and dissolved in 20mL Histopaque gradient. Spun at 380g for 20min at RT.
Wash twice in culture media and handpick islets.
Can anyone flaw my procedure or give me some clues as to what might cause very low yields in general? I've read somewhere that blood and fat tissues might inhibit digestion. Does anyone have any experience with this?
My current concern is that the islets are over digested.
Thanks in advance.
Jesper


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Monocot stele in roots
Why do monocots have eustele in the roots instead of protostele like dicots? I thought the roots don't need the strength of eustele because the roots are supported by the soil. So what is the evolutionary reason for the eustele in the roots of monocots?

Possible duplicate of If a trait would be advantageous to an organism, why hasn't it evolved?


text:
Folding of bulliform cells
How do bulliform cells cause a leaf to fold in half when the leaf looses water? Also, how would these bulliform cells be arranged to cause the cell to instead curl up?

This is a really well written paper which answers at least your first question. As long as the curling up is concerned, they curl up when there is insufficient water and they curl in order to avoid excessive transpiration. There is something about this in the Discussion part, check it out. http://www.bio.uaic.ro/publicatii/anale_vegetala/issue/2010F2/01-2010F2.pdf

Curling up is due to turgor pressure. Quoting from wikipedia

Loss of turgor pressure in these cells causes leaves to "roll up" during water stress

More scientific reference , on morphology,  on mechanism, on development, some genetics and on physics.

Can I get a deeper explanation of the mechanism in layman's language?

In layman's term, According to this paper, these cells loose their water and reduces their volume in water scarcity. This osmotic flow of water creates pressure which pushes plasma membrane of cell to cell wall (which I think is causing 'curl up' phenotype') However same paper has also mentioned other hypothesis for this mechanism like use of 'pectin' as water reservoir.


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How can frogs tolerate freezing while humans cannot?
A wood frog can tolerate the freezing of their blood and other tissues. (wiki, news2), but human beings can not.
Some people plan to freeze their bodies/brains after death, and some of them have done that.
Can wood frogs help us learn how to freeze our brains safely?

@Dexter has the correct answer. Human cells are made mainly of water, it should be fairly obvious what the problem of freezing is. Water expands as it freezes, so the cells begin to rupture due to the expanding ice crystals. Cryoprotectants used to protect cells when they are frozen in Liquid Nitrogen in a lab setting are very toxic. You have a very short window of opportunity when thawing cells to exchange the cryoprotectant with growth medium before the cells start to die. Now multiply this a billion fold and you get an idea of what it would be like when unfreezing a whole body.

Generally frogs are cold blooded animals (more specifically ectothermic or poikilothermic) . Wood frogs can maintain their body temperature by production of cryoprotectants which a human body cannot produce from normal metabolic processes. Such molecules depress the freezing point of tissue and avoid ice formation. Here is a scientific report on the physiology of wood frogs and what helps them survive at freezing temperatures. There are also other mechanisms which cold blooded animals use to survive such conditions.
Now for the human part. Humans are warm blooded (more specifically endothermic). We always try to maintain their body temperature (our normal body temperature is $37^{o}$). That is why we cannot tolerate freezing temperatures, because our physiology does not have a means to avoid cell damage at that temperature. The company which you mentioned uses vitrification methods which uses various artificial cryoprotectants (which wood frog makes naturally).
There is research going on in this direction already. Researchers are using extremophiles and their metabolic products in cosmetics and medicine (like this, this and this).

how long can a wood frog keep frozen if they live in human-controlled cold environment?

No idea. I know for bacteria though. We can keep bacteria for many years in $-80^0$. I have recently used bacteria stored in $-80^0$ after 6 years!

It is  interesting to test how long can wood frogs keep frozen. For bacteria, Russian people are doing the similar things. [http://www.dailymail.co.uk/sciencetech/article-3243056/Is-key-elixir-life-3-5-million-year-old-eternal-bacteria-boosts-longevity-immune-scientists-claim.html]

You should specify that the body temperature provided is in Celsius to avoid a bit of confusion :P.

@JohnOdom $37^0$ F will be frog's body temperature during hibernation :P


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Why do some Brown Pelicans have orange or reddish parts on their bills?
I am doing research on Brown Pelicans and have photos/descriptions of the breeding and nonbreeding appearances of adults, esp. the California and eastern subspecies here on our southern Pacific, Gulf of Mexico, and southern Atlantic coasts.
One question is really puzzling me:
The birds are described as having long pale bills, some with some brown on them. The bill of the California subspecies is described as acquiring some orange or red during the breeding season (along with the gular pouch which turns bright red/orange/pink). But I see photos of nonbreeding birds (with completely white necks) with either a little or quite a bit of orange on their bills, usually on the lower half.
There are so many pictures like this that the orange cannot be just a breeding color.
Do some Brown Pelicans just have some or quite a bit of orange on their bills, even when they are not breeding? I have looked at just about every link that comes up under Brown Pelicans and no one explains the presence of orange in some of their bills (except during the California subspecies' breeding season). In the official descriptions of the appearances of nonbreeding adults, orange in the bill is never mentioned. I would like to know the answer to this detail in the appearance of some of them!

Maybe it's consequence of the Fukushima disaster?

After doing some reading at the Birds of North America webpage on Brown Pelicans.
It does mention orange on the bill outside of the breeding season.
Brown Pelicans have a greenish gray bill once they are older than 24 days which becomes gray-brown in their first year. At around 12 to 14 months of age, yellow will begin to appear at tip and on the sides. At 16 to 19 months of age, the bill becomes gray-green-yellow with some orange, the orange becomes more distinct at 29 to 37 months.
It is difficult to define the plumage of a Brown Pelican during their first 2 to 3 years; they acquire definitive plumage between the ages of 3 to 5 years old.
Here are the descriptions of their bill in Definitive Basic and Alternate plumages:

In Definitive Basic plumage, proximal end of upper mandible pinkish
orange, distal end buff yellow over pinkish orange, and nail at tip
buff yellow. Lower mandible pinkish orange, except middle section gray
or mottled gray. Proximal end of gular pouch reddish orange (P. o.
californicus) or green-gray (P. o. carolinensis); distal end dark
gray-green. As breeding season approaches, colors intensify; bill
becomes brightest 4–6 weeks before pouch.
In Definitive Alternate
plumage, upper mandible bluish pearl-gray and pinkish on proximal end,
buff-yellow-orange-red over bluish pearl-gray on distal end, and
bright buff-yellow on nail. Lower mandible pale yellow on proximal
third, bluish pearl-gray elsewhere; yellow at maximum intensity when
young being fed; may serve as target for begging nestlings.
Colors
fade with onset of incubation through prebasic molt; upper mandible
gray proximally, buff-yellow and orange over pearl-gray distally, and
buff-yellow on nail; distal two-thirds of lower mandible gray;
proximal end of gular pouch faded yellow-gray (P. o. californicus) or
gray-green (P. o. carolinensis); distal end dark green.

It appears their bill does retain the orange after breeding although it may begin to fade and it does mention how the colour intensifies during breeding.
Reference:
Shields, Mark.(2014).Brown Pelican (Pelecanus occidentalis), The Birds of North America (P. G. Rodewald, Ed.). Ithaca: Cornell Lab of Ornithology; Retrieved from the Birds of North America: https://birdsna.org/Species-Account/bna/species/brnpel

It reminds me of the red spot on the seagulls bills of the classic study by Niko Tinbergen.

In the mid-20th Century, Dutch scientist Niko Tinbergen studied nesting Herring Gulls. He noticed that newly hatched gull chicks were fed by their parents only after they pecked at the adults' bills. Tinbergen devised experiments that varied the shape and coloration of the adult's bill. It became clear that the red spot on the adult gull's bill was a crucial visual cue in a chick's demands to be fed, and thus its survival.

It may be that the same mechanism is used by the brown pelican to elicit a stimulation from the chick.


text:
How do we perceive acceleration?
Today me and my friend were coming on motor bike and I was sitting opposite direction because I was holding something in my hand (and it was fun :P). When he started bike I felt very high acceleration. I asked him to go slow however he said he is going with regular speed. Then out of curiosity, me and him tried different velocities and different accelerations while me sitting on either direction of acceleration and opposite to it. To my surprise I 'perceived' more acceleration when I was sitting opposite to direction of acceleration. While searching how we perceive acceleration, surprisingly it is not very well known. I found following explanations,

We overestimate arrival time ( ref: this )
Endolymph from Vestibular system ( ref: Wiki ) [Not exactly acceleration but rather balance]
Interpolated motion segments ( ref: this )

My question, Is it just visual perception or special mechanism for detection of acceleration? In any of these cases, why I was feeling more acceleration while siting opposite than in direction of acceleration? [ My initial guess is because I didn't have any support and visual cues were messed up ]
Update:
I found this post but I didn't get any satisfactory answer from book referred in answer.

Interesting question. However, it is unclear to me whether the question is on the perception of acceleration (a), the perception of velocity (v), or both. In  other words, did you perceive both a and v to be higher when sitting in reverse? Moreover, are you confident it has nothing to do with you being uncomfortable in reverse position on a bike? Personally, I would find it awkward and perhaps even scary to sit in reverse. Last, did you switch places with your friend? Any additional data, or is this an isolated anecdote?

I don't think we visually perceive acceleration. We just estimate it. However, we can perceive acceleration because of the vestibular system. Am I right @AliceD ?

@WYSIWYG - we most definitely obtain visual cues of acceleration visually. Ever sat in a train and the train besides you started moving? No inner ear involved, yet you felt you were starting to move away. You are correct that the inner ear is the end organ responsible for perceiving physical acceleration, but not velocity.

@AliceD but I don't think I can visually differentiate between acceleration and uniform velocity with reference to a stationary frame. Also, acceleration can be felt because it exerts force on mechanoreceptors.

@WYSIWYG - The latter example is pressure, not acceleration technically. The former depends I agree..

This book chapter talks something about visual perception of acceleration. Can't access it now. Also, it is quite old and I am not sure if it is very reliable.

@AliceD Yes, we switched positions. He also felt similar. Maybe you guys can also try :P. I did feel change in acceleration. It was hard to control precisely but we checked by changing bike speed from 0 to X in Y seconds.  Change in velocity was little bit crude. It was just checking (rather 'feeling') velocity when bike has achieved constant speed.

@WYSIWYG, to avoid bias from visual cues, We changed bike speed within certain time frame to keep acceleration same between observations.

@Dexter What if you close your eyes? Did you try that too? To eliminate visual contribution. Moreover I guess we would be more cautious towards backward acceleration because it may give a feeling of falling.

Oh, that is nice suggestion. We didn't try closing eyes. So unfortunately, there was always some visual cue. I will try sometimes tomorrow.

Personally I think the phenomenon is caused by higher cognitive processes, as I am unaware of the otoliths in the inner ear responding differently to various directions of acceleration. Instead, I think the novelty of the situation may be more important, which might even hold eyes closed.

The otolith detect linear acceleration (http://www.ncbi.nlm.nih.gov/books/NBK10792/). The semicircular canals detect angular acceleration.

My question, Is it just visual perception or special mechanism for detection of acceleration?

Acceleration is a synthesized conclusion from a multitude of systems.
Most prominent is the Endolymph system you already mentioned:

As you accelerate, the endolympth and the otoliths within (small, calcified deposits) pass over the hair cells and produce action potentials which travel to the brain. The higher the magnitude of acceleration, the more action potentials will be sent.
This is also where dizziness comes from, as the endolymph and otoliths do not come to rest at the same rate, momentarily giving the brain two different interpretations of what acceleration you're experiencing.
There is also the Doppler Effect:

Based in the cochlear system of the inner ear this time, instead of the vestibular system, the doppler effect is interpreted by the brain and gives a very rough interpretation of both velocity and acceleration (if the velocity of the object happens to be changing).
Then there is the entire visual side of things. Motion blur and the speed at which the perception of objects change size are large contributors to our sense of visual acceleration, but almost all of this is done via complex manipulation of visual data in the occipital and frontal lobes.
There are also countless minor contributors: skin and join tension (the sensation of weight due to acceleration), ease of breathing, sensory cells in your hair if your hair is exposed to the open air while acceleration, blood pressure sensors (and numbness when the body can't compensate), etc.

In any of these cases, why I was feeling more acceleration while siting opposite than in direction of acceleration?

My guess would be because your body is more visually attuned to facing the same direction as the acceleration, and when you were facing the opposing direction your mind overcompensated in an effort to protect you since you probably don't get a lot of opportunities to rapidly accelerate backwards over distances of more than a few feet.
Your brain might also have been panicking a bit because you couldn't see where you were going (usually very bad), and the heightened sensory state made the magnitude of the acceleration feel greater.
These are my best guesses, however. If someone has an academic source, please feel free to edit this answer!

I didn't get Doppler effect part .

@Dexter -- The doppler effect is the change in pitch of a sound due to the velocity of its source. If the source of a noise is moving, the sound waves in the direction of its velocity/acceleration are condensed (higher pitched), and those in the opposing direction are elongated (lower pitch). You can tell if something is heading towards or away based on that. A classic example are race cars or racing bikes, whose engine noises change pitch to an observer despite constant speeds: https://www.youtube.com/watch?v=qyxvPiOqEiE

Are I know what Doppler effect is. I was wondering how that is playing role in perception of acceleration ?

The otoliths are not responsible for dizziness. The moving endolymph is. The endolympoh in turn does not recognize acceleration, but direction of movement afaik.

@AliceD - "the endolympth and otoliths..." I specified both. The otoliths are partially responsible. The vestibular system is designed to track 3-axial movement (XYZ), and the frequency of action potentials changes depending on how many hairs are open and how "open" they are. Unless I'm very, very incorrect, the vestibular system tracks acceleration in addition to vector.

@Dexter -- The doppler effect comes into play with echoes made by your bike's motor, too, and other sounds as you passed by their origins.


text:
Plasmid with ITPG and pBR322 ori
I'm looking for suggestions as my internet searches aren't turning up much.
I'm trying to find a plasmid that has the pBR322 origin, as it's low(ish) copy number and can tolerate large inserts. Additionally I need the plasmid to be inducible with a system other than the pBAD setup (e.g. IPTG would be fine, but if there is one that is more tightly repressed that would be preferrable as IPTG is leaky).
Lastly, I could do with it having a potentially obscure resistance cassette, but this is less of a problem.
Any help appreciated.

You might want to check this https://www.embl.de/pepcore/pepcore_services/cloning/choice_vector/ecoli/vectorfeatures/

Gene 1985, Vol.40(2):183–190, doi:10.1016/0378-1119(85)90041-1 ‘ATG vectors’ for regulated high-level expression of cloned genes in Escherichia coli

The pET vectors family is what you are looking for.

Just to add, if you're worried about leaky expression you can select a strain expressing T7 lysozyme from pLysS.


text:
Is there a way to know how many sodium channels are active (conducting) at a given time in the brain?
I was doing some reading about anti-epileptic sodium channel blockers, then wondered how many sodium channels are actually conducting (actively passing ions) at any given time, that is, in an "average, awake" brain?

Welcome to Biology. What do you mean with "...but how many are active anyway?" As a side note, Na+ blockage is just one way of suppressing epileptic activity. Lamotrigine, as an example, has a host of other characteristics. In the case of carbamazepine, listed as a Na+ blocker and first-line treatment for generalized epilepsy in adults, it specifically blocks activated channels. So the number of channels blocked depends on brain activity. In a nut shell, I think your question needs specification (e.g., type of drug).

No, it is not on the blocker that I need an advice. I just tried to explain the way my reasoning went. What I mean is in the question : at a given time, in an "average, awake" brain, how many sodium channels are indeed conducting (actively passing ions).

I edited your question and retracted my close vote. Feel free to roll back, but I think it's quite clear now what you're after.

Unfortunately, there is no way to know how many sodium channels are active (or even present) in one person's brain due to the extremely high variability of channel and neuron density in a population and the lack of methodology around quantifying total number of healthy active synapses (1). Diseases like epilepsy can occur due various points of the sodium signaling process going wrong. It could be sodium channels are deformed and not accepting the proper signal, it could a low density of channel proteins, or it could be damage to the neuron themselves (2-4). No one has examined the "normal/healthy range" of sodium channels in the brain. When categorizing sodium channel deficiency scientists will often compare the number of sodium channels in a healthy brain vs. a disease brain using bioluminescence imaging or some other visualization technique. Bioluminescence specially quantifies the number of active sodium channels by binding causing healthy sodium channels light up and then quantifies density by the brightness of the synapse. This is not a direct quantification of the number of proteins, but I can not think of any technique that allows you to count the number of proteins on a cell without damaging the cell. I'm sorry this isn't technically an answer to your question, but hopefully it provides some helpful references to understand molecular brain protein imaging.

Principles of Neuroscience
Low Sodium Channel Density and    Epilepsy
Sodium Channel Mutations and Epilepsy/ Other Nervous    System Disorders
Neuropathy and Sodium Channel Related    Diseases

This is a difficult question because we are talking about properties of channels-molecules which can have stochastic opening and closing rates. The question is made even more difficult by the fact that there are multiple types of sodium channels. One can begin to quantify this by recording from many many cells in the awake animal using in-vivo electrophysiology by washing in sodium channel blockers and looking at sodium currents. Conversely you can start doing antibody staining for sodium channels in a brain area -- then take acute slices from that area and do single-channel recordings so you have some sense of number* probability of opening.


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What percentage of people today would likely be descendants a man born 4,000 years ago?
Assuming a particular man was born in  southern Mesopotamia, around 4,000 years ago, and was significant involved in a major religion.

To what degree (if any) of accuracy could his descendants be traced?
What percentage of the global population is likely a descendant of the man?

This question comes from a comment on sister site.

I don't think most people are really able to trace their entire family tree that far back. But Avraham is so many generations ago, I would expect that either nobody in the world is his descendant or nearly everybody in the world is

I'm voting to close this question as off-topic because it is not about biology.

If you are asking about any random person then it depends on a lot of factors and hence the question would be broad. If it is specifically about one person then it cannot be answered without having adequate and reliable archaeological evidences. Also, in that case the question is not really on-topic here.

To what degree (if any) of accuracy could his descendants be traced?

I don't really understand this question. To what degree can we trace its descendants given we know what from this man? Do we have a blood sample?

What percentage of the global population is likely a descendant of the man?

If $N_0$ was the population size 4,000 years ago and $N$ is the population today, then the expected number of descendent of any given person is simply $\frac{N}{N_0}$. However, there is a huge variance and this is where things get more complicated.
As coalescent processes are geometrically distributed (well approximated by an exponential distribution if we assume that the population is large; more info in this answer), then the variance in coalescent times is equal to the expected coalescent time.
The expected coalescent time in a diploid population of constant size $N$ is $2N$. Of course, the assumption of constant population size doesn't hold for humans due to the recent demographic explosion. When the population size is increasing the genealogy looks like a star as coalescent events are rarer and therefore, it is more likely for a given individual living in the past to live descendant today (Excoffier et al. 2009). However, I don't know how to calculate coalescent time in expanding populations.

Remi, You could start by ruling out Indigenous Americans, Australians (and associated islands), and sub Saharan Africans. Then the Y-Chromosome is pretty conserved. Genetic anthropologists could likely look at the distribution of Y-chromosomes native to that region of the Middle East and then determine the frequency of that Y-chromosome appearing in samples through out the rest of the word. I don't think that you can really look at today's Raw population, as we have had too many depopulation events over the last several thousand years. Plague, wars, famine, monastic orders, etc.

Working out the percentage of woman would be a total craps shoot. You don't have the option of using mitochondria, as the vast majority come from the mother, and with Meiotic recombination, working out the patrilineal X-chromosome would be near impossible.

Does the $N_0 / N$ formula make sense? Should it be the inverse? What if $N_0$ is very small, don't you expect a given person from the 4 k years ago population to have more descendants?

Yes, you are right. Thank you for noticing the small mistake. I fixed it.


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How good is the reproducibility of preclinical models?
Unofficially, biology researchers always complain how frequently fail to replicate results others have achieved. But of course, such failed experiments are underreported.
Is there data, or at least well-reasoned guesses, on what is the success rate of experiment replication in preclinical models? I don't mean translational research and the impossibility to replicate a mouse result in a human. My question is about failing to reproduce the results within the same model system, replicated at the detail level available in the original publication (e.g. same animal strain, same drug dosages, etc.)

Have you checked out https://www.plos.org/wp-content/uploads/2015/06/journal.pbio_.1002165.pdf yet? It may be a good place to start looking.

I searched for maybe an hour before posting, and while I found some papers declaring that reproducibility is a problem, none went into details. I'll look closer into the one you posted @BenS.

The Cochrane Collaboration has a great deal of this type of analysis. One of my favourite features of a Cochrane Review is the routine use of Funnel Plots, where there are sufficient data to produce them. Sensible interpretation of funnel plots can give some fairly strong hints about the reproducibility of published literature.
Funnel plots show datapoints of individual published studies which investigated the effectiveness of a technique when used for a specific purpose. The datapoints are plotted by estimated effect size (on the x axis) and an assessment of the quality of the trial, incorporating things like sample size and experimental design (on the y axis). A study with a small sample size and/or poor design (low on the y axis) would be expected to provide a relatively inaccurate estimate of the method's true effect size. As sample sizes increase and experimental methodology gets better (travelling up the y axis), you expect the studies to zero in on the true effect size, giving a pyramid or 'funnel' shape to the overall plot.
The reproducibility of trials affects where the points are in the pyramid in a couple of ways.
If there were a bunch of studies which looked for an effect of the method, and didn't find one, they might not be published because null results are considered boring by journal editors - the so-called 'file-drawer effect'. This would show up in a funnel plot as a pyramid that has a suspiciously low number of datapoints on the side of the pyramid that is close to the zero effect-size. The 'missing' datapoints are an indicator that this technique probably did not always reproduce an effect size as strong as the published effect sizes.
The other way that funnel plots can inform on the reproducibility of published studies is simply by looking at the width of the base of the pyramid. If it's wide, then with the experimental design methods of the studies at the bottom, the results aren't highly reproducible - different studies give very different results when looking at the same question.
It's a big job to synthesise this into a global assessment of 'the reproducibility of pre-clinical trials', but if you're interested, I'd recommend you spend some time trawling the Cochrane Library to get a hang of the sorts of variance you're dealing with.

PS: the fact that synthesising reproduction efforts into a combined analysis is a big job has not prevented it happening for high-profile psychology journals recently - with a fairly alarmingly low reproducibility rate.
http://www.sciencemag.org/content/349/6251/aac4716


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Can someone identify this ant?
This is one of seven ant queens I just collected yesterday morning (2015-09-21 9AM) around home.
I live in Hong Kong, at a hillside facing south. The weather was as follows (Hong Kong Observatory Daily Weather Summary, Hong Kong Observatory Daily Extract):

Mean Pressure (hPa): 1008.6
Max temp in my district: 24.2C
Min temp in my district: 28.0C
Mean dew point: 23.8C
Relative humidity: 66% - 95%
Rainfall: 16.9mm

Judging by the ridged head and the large mandibles, I'm guessing this is one of the Tetramoriums (Wikipedia, AntWeb).
The colour is dark brown. The total length from the tip of the mandibles to the tip of the abdomen is about 17mm. The length of the large wing is also 17mm. I don't know what habitat it lives in and I also don't know how the workers or soldiers look like, as I have never seen where these ant queens emerge from.
If anybody is fairly confident in identifying this species, I would also appreciate some tips about keeping it and starting a colony. I have a make-shift ant farm made out of two plastic bottles, one nested inside the other like a Russian doll. Out of the seven queens that I collected, three are already dying. A fourth one already show signs that she won't make it either.
More info
When I picked them up, they were not exactly "outdoors". The short but heavy rain was mostly over and these queens were "taking shelter" in the stairwell of my building, which is usually dim, slightly damper and cooler than outside.
Here are more pictures; these should be better because I just took these in natural daylight:

Somebody at The Ant Farm and Myrmecology Forum suggests that this is in the genus Carebara (previously Pheidologeton). After some more Google search of my own, and image comparing, I believe that this is indeed a Carebara affinis, which has previously been spotted in Hong Kong. Could somebody confirm?

I also want to commend you for providing a lot of information. However, even though I know very little about ant identification, I do know that the number/amount of bristles (setae) on head and legs, spines on the alitrunk/mesosoma and petiole as well as the number and shape of antennal segments are often used for genera and species determination, and these characters are difficult to see in your pictures. So it might be difficult to determine this to species, based on your pictures.

@fileunderwater Thanks for the tips! I'll try to get clearer pictures or count the setae, etc myself when I get home.

In my opinion you are pretty close to the exact identification.
I think it is Marauder Ant, which could be Pheidologeton diversus, but probably Carebara affinis as well.
The main feature I can gother from your pictures is Venation of wings which matches with Pheidologeton diversus venation (it would probably match with affinis as well, but I failed to find the picture):

Venation match: the combo picture of the wing from the post and the wing from the reference:

This ant is known as Hong Kong inhabitant -

Yes, I'm aware that it is also possibly a Pheidologeton diversus, renamed nowadays as Carebara diversa, if I'm not mistaken. Unfortunately, without successfully starting a colony and looking at all the different casts, it's rather hard to tell the C. diversa and C. affinis apart. IIRC from my research, the C. diversa has a more diverse range of worker sizes, ranging from super majors (with really big heads) to minors. C. diversa are also rarer than C. affinis, which makes the C. diversa highly prized as pet ants. There are even reports of sellers selling C. affinis as C. diversa knowingly.


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Are aquatic filter feeders effective at cleaning water to a safe level?
I've been raising Daphnia magna cultures over the last few months as feedstock for freshwater aquarium fish. From my reading, Daphnia feeds on bacteria and single-celled algae, as well as other small crud suspended in the water column.
Practically, yeast or soy flour can be suspended in water and poured into a tank containing a population of Daphnia, and the critters usually clear the water in a few days. The clarity of the resulting water is quite impressive. Which leads me to...
My question: How effective are these types of organisms at removing harmful bacteria and substances from a volume of water? Lets say you only needed a few gallons of clean water each day, could you have a tap that drew from a tank containing a dense culture of Daphnia, and use that water as drinking water?
I've not found information that studies the quantities of bacteria in the water column before and after introduction of Daphnia or other filter feeders.
P.S. I thought about posting this question in the Sustainability SE but figured I'd get more accurate information here.

Great question. +1. I slightly edited your post. It was great, but I thought to add a link to wikipedia and do some formatting. I removed the cooking part, because boiling water to cook typically kills all microorganisms in the water anyway. It's definitely on topic here.

My answer from the top of my head is that they will not be very effective at cleaning the water. One reason is that if the substances and organisms are harmful to the filter feeder as well, they will avoid eating them or they will die from them or have their health reduced. In either case they will be filtering less.
Another reason is that if you use the tap and replenish the water with new contaminated water regularly, the filter feeders will probably not filter all water in the tank, and the outflow from the tap will still contain the contaminant. This is certainly the case if the tank is also the culture vessel for your filter feeders. In this case, the tank has come close to being a continuous culture. There are decades of science (including R* theory) which show that resource levels in such systems settle at a positive level (and you propose that the harmful micro-organisms are used as resource or at least eaten in proportion to the resource if the filter feeder cannot be selective). This positive level will then thus also be present in the effluent from the tank (your tap water).
An alternative is to grow the filter feeders in a dedicated tank, and than add them later in high concentrations to your drinking water. This would not be efficient because you need to feed your filter feeders with something.
Finally, the harmful substances may be absorbed by the filter feeders, but also be excreted, in which case the will end up in your drinking water anyway.
For getting rid of the harmful micro-organisms, it is probably more efficient to boil your water!

Great links and information, thanks. I clearly have more reading to do. I suppose a common example of a functioning chemostatic continuous culture system would be a biofilter for a common aquarium, where ammonia-enriched water is fed into an environment full of bacteria that metabolize the ammonia into nitrites and nitrates?

Yes. Continuous cultures (e.g. chemostats) have a continuous supply of resources (nutrients/food), as opposed to batch cultures, in which resources are added in batches. Because continuous cultures are easier to model, lots of theory is derived from them. Batch cultures come close to continuous cultures if resources are added often in small batches, as opposed to rarely but in large batches. So chemostat theory may apply to batch cultures as well.


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How does life change when you dig deeper?
I've just realized that I have no idea what life / biotopes / soil looks like when you dig deeper than a few meters.
I know that in the first meter of soil you can find all sorts of live animals (like moles and rabbits), insects (like ants, but many more), plants, and single-celled organisms, of course.
But how does that change when you get to the depth of a metro station (below 30m)? When you plan to build a metro, do you have to consider that you might destroy a biotope?
I guess there is a point from which you will quite certainly not find animal/plant life in the soil anymore. This will, of course, depend on where exactly you are. But can you give a rough estimate of how deep we're talking? 50m? 100m? 1km?

With a quick search I found 'Subterranian worms from hell' in Nature. The worms were discovered in a gold mine over 1km deep.

Extremophile bacteria and archea are living very deep beyond our imaginations. This is what you need for general composition at different depths. And this and this is for the deepest living organism known ! Following is image from (Manson et al 2010) which shows at what depth you will get bacteria

Even more deeper, Wold's single species ecosystem, Desulforudis audaxviator which can be found 3 km below sea level.

"Soil horizon" was what I was looking for. Thank you!

First of all we must consider what the substrate is at 30 meters and deeper, either clay, anaerobic, impermeable or permeable substrates, everywhere that you find liquid water between 0-100 degrees you find life (Geogemma barossii reproduces at 120'C 250'F), even if the peak of everest is mostly under zero and has 270kph winds, algae grows there.
Plant life requires light, so you will only find roots underground, the deepest roots are an african fig that has a record of 120m 400ft. Most plants have roots that can go as deep as the tree is high in permeable ground while clay soil is very low on oxygen and voids for anything to infiltrate. Underground mining will rarely affect tree roots, or any other notable biotope, unless it encounters a rare cave system with fish and so on.
In very deep caves 200 meters deep there can be all kinds of insects and fish, although that doesnt qualify as ground.Krubera cave georgia has insects at 1.5 kilometers depth.
The solution of the question is that of matabolism, anaerobic versus aerobic, and it's effects on biotope richness. Funghi breathe and bacteria can be anaerobic, so they are the deepest, you can find some in oil wells and 1.6km under the sea floor.
The major concerns for drilling and damaging deep biotopes are from mining isolated aquifers with endemic animals, for example the deep lakes of antarctica that have been set apart from the rest of the world for 10's and 100's of thousands of years.
The ecosystem richness of zones without light and oxygen and flowing water is generally too low to foster much attention from any environmentalists and conservation organisations, it's also not a rare biotope.


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Why is squeezing not recommended after a needle prick?
I've read some interesting things about the risk of infection after a needle prick (30% - hepatitis B, 1.8% - hepatitis C and 0.3% - HIV), but I've also saw that the local squeezing is not recommended.
It's true that I've also found some articles that considered that there is no difference if you squeeze or not, but most of the articles I've read (in my native language) specified "Do not squeeze!!!". By squeezing I mean an act of extracting the blood by pushing the skin near the needle-prick.
Why?

If you've found relevant literature, don't just mention, cite!


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Are there nerves in the umbilical cord?
I have always imagined that cutting the umbilical cord after birth might be painful. But I have always been confused about who would feel the pain and why. It occurred to me that the mother or the infant could only feel pain if they had nerves connected to the umbilical cord.

Do either mother or infant have nerves running into the umbilical cord that carry nociceptive information?
If not, is there a reason why no pain receptors are present?

Short answer
There are no functional nociceptors present in the umbilical cord.
Background
Having had the opportunity to cut the umbilical cord of one of my kids, I can anecdotally confirm neither newborn nor mother gave any sign of pain during the procedure. That is, when cutting the umbilical after the birth of a full-term baby. The only person clenching his teeth was dad :)
In fetuses at gestational age of 18-36 weeks no stress response was noted after puncturing the umbilical (Teixeira et al., 1996), indicative of the absence of pain receptors connected to the baby's brain.
I couldn't find information about pain in the mother, but I cannot imagine that the maternal central pain centers are being connected to the umbilical, which would be pretty extraordinary. This, because long-distance neural connections are rarely, if ever, established in adult humans. Also, I haven't heard any reference to the mother feeling pain because of injury to the umbilical cord. For example, knots in the umbilical cord, or cords wrapped around the fetus' neck due to excessive movements of the fetus are never noticed by the mother, and are only revealed during ultrasounds.
Note, however, that the umbilical cord is innervated by cholinergic neurons that are thought to be involved in the control of blood transfusion to the fetus, but presumably do not carry sensory information to either fetus or mother (Ellison, 1971).
References
- Ellison, Am J Anat (1971); 132: 53-60
- Teixeira et al., The Lancet (1996), 347: 624

Yes there are
THE placenta and foetal membranes are usually described as being devoid of neural elements1,2. In other descriptions, the possibility of an innervation is not considered3,4. Nevertheless, reports of the presence of nerve elements in these foetal tissues continue to appear in the European literature5–7.
https://www.nature.com/articles/214103a0
They are especially small

a reference from within the last 50 years would be prefered.


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Introductory book on cell biology
I am studying the human circulatory and respiratory systems to develop tools for automated diagnosis of disease.
During the past year, I have read basic books about respiratory physiology, electrocardiography, etc.
At the moment, I feel that my lack of understanding of basic cell biology is prohibiting any further progress. I would like to find a very introductory book on cell biology, which would teach me

what kind of cells there are in humans, what are they made of, and what are their main components
basics of cell cycles, how cells are studied, how they look under the (various kinds of) microscopes
etc

The ideal text would probably be on the undergraduate level and not be much longer than 300 pages. Any suggestions? So I just want to find something to start with.

I would like to suggest the classic: Molecular Biology of the Cell, 5th Edition , ISBN-10: 0815341059

@LuizRobertoMeier MBOC now has a 6th edition, however, as Dexter pointed out, the 4th edition is available for search on the NCBI book shelf. I would almost suggest to the OP that you start by reading the relevant chapters of a recent edition of Campbell Biology, and then tackle MBOC. MBOC is a comprehensive and fantastic book, but if you don't have a basic understanding of the concepts it can be easy to struggle if you are trying to self-learn.

I just saw your final caveat... about 300 pages, MBOC clocks in around 1100... Start with the relevant chapters in Campbell. I believe that if you go to the Pearson website you are able to order by the chapter, which will make the book less expensive and leave out many of the sections you may not be interested in.

The Cell by Cooper is another option which I forgot to add in original list.

Lot of classic books available, most famous (at least in India) are

Molecular Biology of the Cell by Alberts et al [ Free Online | Amazon ] -- Simple language, good figures and my personal favorite
Molecular Cell Biology by Lodish et al [ Free Online | Amazon ] -- Very detailed with good examples
Gene IX by B Lewin [ Amazon ] -- Nice examples and figures. Lessons are in different order than most cell biology books.

If you want to just learn quick concepts, use online resources like Scitable by Nature. Pretty nice information with references and recommended reading.

Gene is far too advanced for an introduction to cell biology. MBOC is excellent.

Lewin 's series also contain a book called Cells. http://www.amazon.in/Lewins-Cells-Lynne-Cassimeris/dp/076376664X . It contains a good comparison of  cell biology of different domains.

All of these books are excellent about molecular biology and genetics. But that is not what the question asks for. They are completely inappropriate.

A basic book: Cell and molecular biology - concepts and experiments/ Gerald Karp/ Willey - Well explained.
For a detailed-concept - Cell Biology by Pollard and Earnshaw ... Perhaps it was the most mesmerizing textbook on cell-biology out-of whom I've gone through. A beauty of this book is, vast-number of proteins classified into certain groups, with using many tables, that easily help make the sense of their similarities and relationships.

@SanjuktaGhosh Yes there would be a D. It was a typing error I missed it Thank you


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DNA Replication And Primer
Why does nature rely on RNA primer for the start of DNA Replication? Why not simply use DNA primer and make life simple !

Biochemically none of the DNA-dependent DNA polymerases involved in DNA replication have the ability to begin elongation without a 5' to 3' primer.
The only DNA Polymerase that can catalyze elongation without a 5' to 3' primer is Reverse Transcriptase, however Reverse Transcriptase is an RNA-dependent DNA polymerase, and that accounts for the difference.
And if your next question is, but why, the answer is that that is how the systems evolved. Also DNA Polymerases have a much higher rate of fidelity due to error checking than RNA Polymerases do, and as the RNA primers get removed anyway and replaced with DNA, an error here or there in the primer will not matter.
The RNA-DNA duplex is also less stable than the DNA to DNA duplex, so it makes it easier for FEN1 to remove an RNA Primer than it would a DNA primer, assuming that the mechanism of primer removal and replacement after the complementary leading and lagging strands have been synthesized remained in place.

Main reason is that DNA pol needs template while RNA pol does not. Hence DNA pol need initial primer (which is made by RNA pol or primase ). That is why there is RNA primer not DNA.

@Dexter Did you read my answer? "... none of... have the ability... without a 5' to 3' primer. Third paragraph addresses your 2nd point.

I am still unclear from your answer. You gave fact not reason. I think reason should be "need of template" as question was asked why RNA primer not DNA. And how is error correction is contributing to RNA primer not DNA ? I think, error correction is output not reason.

@Dexter The reason is that is how the system evolved. But as to make the answer little more than a comment, the reason DNA Polymerase needs any primer is the answer that addresses the first question, "Why does nature rely on RNA primer for the start of DNA Replication?" And the reason is that the DNA-directed DNA Polymerases involved in DNA replication do not have the ability to begin elongation without a 5' to 3' primer. That answers the first question.

@Dexter, I will concede I could have been clearer, but the basic thing I was getting at with the third paragraph is that DNA-directed RNA primers are sloppy replicators, but as the primer is removed and replaced, you can sustain errors in the primers without detriment to the organism. I would guess that the energetic cost of using RNA primers is less and it works faster than an equivalently abled DNA polymerase could in laying down a primer, which is why we have Primase as an RNA Polymerase and not a DNA Polymerase.

@Dexter. The final paragraph just states that RNA-DNA is less stable, so that probably makes it easier (less energy required) for the enzymes to remove the primer, which, if that is why it evolved this way, would be another reason that nature uses RNA instead of DNA for primers.

Asking why question in evolution make life difficult :P
I doubt sloppy replicator is good explanation. See explanation of this phenomenon in Biochemistry by Stryer. On other point on energetic, some calculations have been done here. Going by that logic, I don't think it will matter if it is DNA or RNA. Nonetheless all these points are valid in light of "Evolution" :P


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Hydra immortality
Recent research on immortality ha been on an organism named Hydra. I have heard about it being related to some FoxO gene, which has been found in several other organisms but how does telomerase affect the immortality of this amazing species?

@Dexter No, hydra is specifically investigated for its (presumed) lack of senescence, not just its regenerative abilities — unlike, say, planaria.

Yes, I realized. Just searched. You are right @KonradRudolph . I had no idea about this FoxO. I will delete that comment .

Does this answer your question: http://biology.stackexchange.com/questions/6884/why-is-the-hydra-biologically-immortal?rq=1

@AliceD no i find it incomplete..

@TanMath what do you find incomplete about it? Please [edit] your answer and clearly state exactly what you're looking for, and how the answers to existing questions, as well as other online resources, don't completely address what you're looking for.


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Senescence in space
How is senescence of individual eukaryotic cells and tissues affected by gravity and zero-gravity environments? In other words, can eukaryotic cells live forever in space (given the appropriate nutrients)?

Why would you suspect this? There’s not really any good reason to think so.

@KonradRudolph I was thinking that the zero-gravity environment might lead to some cell signalling to for example create more telomerae.. something like that...

Wouldnt all the radiation be a factor too?

@RoSiv Yes it would