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Is every part of a virus important for replication?
Is every component of a virus absolutely essential for its infection and replication in a host cell? Or can you just have parts of it to cause infection?

If you are a fan of Richard Dawkins (or at least like his reasoning), every gene in every organism supports replication.  Infection and replication are hard to separate in the case of HIV.  There are genes for which we have little or no clear understanding of how they might help the replication.  http://en.wikipedia.org/wiki/The_Selfish_Gene#Genes_and_selection

Unless you have a specific virus in mind, I can speak generally about viruses. It seems that the viral genome is reduced to just essential genes. Many viruses segregate their genome into periods of expression: early, mid and late. The early proteins are so-called because they encode for proteins that help their entry into cells (what is called infection). Middle and late genes tend to help the virus co-opt cellular machinery to aid in viral replication. Late genes are then useful for final stages of viral assembly and ultimtely their exit from the cell (lysis) and the newly made viral particles can go on and infect more cells. When viewed in this manner, it follows that removing even one coding region from the viral genome would inhibit the overall infection/reproduction/assembly process. In fact, if you remove the gene encoding for a viral envelope protein, purified virus added to cells in culture are able to infect cells, but not produce complete and functional viral particles. In this sense, they are infection-competent, but reproduction-incompetent.

Sorry I should have been more specific. I'm asking In regards to the HIV virus. Does that information still apply?

@Alan Boyd has given a detailed answer regarding HIV.

Thank you for your feedback! Okay, so not all of the genes are necessary but the genes are found within the RNA strands right? And you would need that genetic information in order to make more parts. So without RNA there is no information or instructions on how to make more of itself right? I'm sorry I just get soo confused with all of this!

That's correct. The RNA genome of HIV encodes genes for the 9 proteins mentioned above. These proteins each serve some function. These proteins together with the viral envelope, let the virus enter a susceptible cell, integrate with the host's genome and later replicate itself. For example, you couldn't just inject someone with the RNA genome and expect to see HIV virus production.

Ohh okay. So really, in order for HIV to replicate every part of the virus must be intact. The proteins, rna, enzymes etc..because each serve a function in the production process. If you take one away, the virus would not be able to replicate. Is that right? I just want to make sure I'm understanding.

That's right. Everything works together. What @Alan Boyd has pointed out is that 3 genes can be removed, and that HIV virus can still make more viral particles that are capable of replicating and reinfecting. Those 3 genes seem to play more nuanced roles in the dynamics of an HIV infection cycle.

HIV has nine genes. According to the paper cited below, three of these genes (vpu, vpr and nef) are not required for replication in cultured cells.

Gibbs JS et al. (1994) Construction and in vitro properties of HIV-1 mutants with deletions in "nonessential" genes. AIDS Res Hum Retroviruses 10: 343 - 50
Abstract
  Auxiliary genes that are not essential for viral replication in cell culture are found in all known lentiviruses. The "nonessential" auxiliary genes of HIV-1 are vif, vpr, vpu, and nef. Sequences within the upstream region of U3 in the LTR are also not required for virus replication in cell culture. We constructed a panel of 23 mutants with single and combination deletions in these regions in the wild-type HIV-1 infectious molecular clone NL4-3. Deletion of the vpu, vpr, and nef genes and the U3 upstream sequence (US), individually or in combinations, did not appreciably alter virus replication in either chimpanzee PBMCs, human PBMCs, or in the B/T cell hybrid line CEMx174. In contrast, deletion of the vif gene dramatically delayed virus replication in all three cell types. This collection of HIV-1 deletion mutants will be useful for elucidating the functions of these genes and for investigating antiviral immunity in animal models.

(PBMC = peripheral blood mononuclear cell)
As might be expected, none of these genes encodes a component of the virus - they are regulatory genes involved in co-ordinating the infective cycle of the virus. They are however implicated in HIV-associated disease symptoms. According to the Los Alamos National Laboratory HIV Sequence Compendium 2008:
vpu is an integral membrane protein which promotes extracellular release of viral particles and degrades CD4 in the ER.
vpr promotes nuclear localization of the preintegration complex, inhibits cell division, and arrests infected cells at G2/M
nef downregulates CD4 and class I MHC


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Neuroscience of temperature regulation and perception
The hypothalamus is known to be important in the regulation of body temperature, but I'm curious whether anyone knows about the neurocircuitry of perceived temperature. It seems like there could be a difference between how warm/cold someone feels and the temperature to which their body is trying to adjust. Intuitively, I'd imagine that any apparent difference in these  has to do with some sort of delayed feedback that is experienced before the autonomic nervous system can kick in. Does anyone know something more about this?

I've found a good resource for this--an open-access review by Nakamura, "Central Circuitries for Body Temperature Regulation and Fever." In it, the author provides a nice summary figure of the circuitry involved in temperature regulation (see below). As I suspected, the hypothalmus is pretty central to temperature regulation. I had forgotten about the involvement of the peripheral nervous system in responding to environmental temperatures, which, now that I think about it, makes some amount of sense, but is still pretty interesting. It appears that there's a difference in the specific circuitry and neurotransmitters used in responding to warm and cold temperature (especially GABA v. 5-HT), so I think a reasonable hypothesis regarding the basis of individual differences in the perceived temperature of an external environment might be differences in peripheral 5-HT systems (in addition to differences in body composition). Perhaps someone with a background in the peripheral nervous system could speak to this better than I can, but single nucleotide polymorphisms (SNPs) leading to differences in central 5-HT systems has been an active area of research in the neuroscience community of late (e.g., Nordquist & Oreland, 2010, Gonda et al., 2010), which I think lends some face validity to this idea.

Nice schematic!

@nico Thanks, I thought so too! Sadly, I cannot take credit for creating the figure!

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Simulating Cell differentiation
I'm a computer programmer deeply interested in Biology.
I wish to write a computer simulation for cell differentiation. I understand there will be seemingly impossible challenges in doing this. But first I am looking for  answers to some basic questions.

I've learned that a zygote turns into 'embryonic stem cells' which results in the organism. How does the zygote turn into embryonic cells ?
What are the factors that determine the specialization of embryonic stem cells into more specialized types of cells and how does this transformation take place physically ?
Where is the data stored which acts as the "guide" for all these processes ? Is it stored in the DNA ? If it's stored in the DNA , is it known how the cells interpret the information in the DNA?
What are some textbooks I should be referring for this project ?

PS : Pardon my ignorance if these questions sound stupid, but I'm willing to commit time for learning anything needed to do this. Also , I understand all these questions cannot be answered in a few lines. Please provide references/pointers . Thanks !

Basically to answer this question, people are devoting entire careers towards this goal. Even a simplified simulation can quickly become a PhD thesis if you so choose. I will assume you want a simulation which takes into account some level of biochemistry since the simple calculation of dividing cells is trivial. What you should decide on up front is to what depth of information do you want to simulate (eg, can you make some simplifications to make your model less realistic but more manageable)?

There is plenty of literature that shows information is stored in at least 3 major places. DNA is the lowest level of information (raw 'bits' of storage), then you have epigenetic modifications which can modulate the level of DNA accessibility and expresion (which are still not fully understood how these are inherited). The last important information encoding is at the level of protein and can be as trivial as a protein switched on/off, or embodied in the behaviour of a whole network of protein interactions. We are just starting to grasp the latter.

Trying to answer this question in a few lines is a tedious task. Mostly I'm not sure that as of today we know all there is to know about it.
I'll try to give you some hints though.

The process is called embryogenesis. The zygote (or ovum) undergoes rapid mitotic divisions with no significant size growth which will lead to the development of an embryo. This process is called cleavage. Blastomeres are created during this process. On the third day - time may vary but not significantly - cleavage reaches the state of 16 cells. Cell divisions always occurs by parallel division (1 -> 2, 2 -> 4, 4 -> 8, 8 -> 16). Study the links I gave you and come back with more specific questions.
Again that's kind of impossible question to answer without explaining the entire process from fertilization to fetal development, because creation of tissues (cells) and organs happens along the way, not at once. However, it's documented.
Not sure.
Start with the wikipedia links and try to come back with more specific questions. I have a couple of text-books but I'm afraid they are not as detailed as you would want :-)

Good luck!

The answers to most of your questions are under active research and there are many unknowns. Understanding this process is one of the main goals of developmental biology. So, try to set reasonable goals for your project, mainly by seeing where you have sufficient data to work with.
I would start with reading some basic textbook on developmental biology.
Regarding the flow of information: Remember that starting from the zygote and onwards to the whole organism, the DNA sequence is generally the same between all cells. As a computer scientist it might help you to think about it this way:
Think of the DNA as a very complicated mathematical function $f()$ acting on cellular states. The current cellular state $S_i$ will be the total molecular components of the cell and will yield the biological function of the cell. So, you start with an initial cell state $S_0$ (could be a vector, for example) and then the daughter cells will be: $S_1=f(S_0)$, their daughter cells will be $S_2=f(S_1)$. This is not a perfect representation of the process (since at time point 2 you may actually have both $S_0$ and $S_1$ cells), but it emphasizes the point that although the DNA sequence "computes" the next step it is in fact constant, and the point that each cellular state dictates the next state. Seems to me like a Markov chain could be appropriate. Of course you can also try more sophisticated models - but it is better to start simple.
Also, I would suggest starting with C. elegans as your modeled species. This is because the full differentiation fate of each of its 1031 somatic cells is known - a remarkable achievement and something you will not have in other species.

I would start with Developmental Biology, 9th Ed. It's not up to the absolute cutting edge, as it was published in 2010, but it has a lot of good stuff in it. Wikipedia is a decent resource to get very brief overviews on certain subjects, but a lot of the life science articles I've read tend to be lacking, as opposed to the physics and math articles, for example.
As for question 3, yes, the "data" is stored in DNA. For a thorough guide, one of my favorite books is Molecular Biology of the Cell, 5th Ed.. It's a little dated now (published in 2007), but if you want to understand how DNA, RNA, and proteins work, it's a great overview text.

Note that the data is actually stored not only genetically (in the DNA sequence) but also epigenetically (e.g. modified chromatin).

@Bitwise - yes, I know, but I figured a short, direct answer was the best here, as the questioner is obviously very new to this field. I could spend a long time talking about DNA sequences vs. DNA modifications, the contributions of histones and their post-translational modifications, and the overall structure and organization of the chromatin in general if you'd like :)

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Can allelopathy succesfully be used against algal blooms?
Algal blooms caused by man (harmful algal blooms) are a major ecological problem. An excessive amount of algae causes hypoxia and logically, most marine wildlife can't be sustained in hypoxic conditions.
Can't we use allelopathic plants to reduce the amount of algae significantly?

One problem I can see with this idea is that whereas in soil any allelopathic compound will be restricted to the immediate vicinity of the source plant, in an aqueous environment the allelopathic compound would diffuse away quickly, so that the source plant would have to produce a lot more to reach an effective concentration.

This has been tried and it sorta works.
Algae in general seems to be inhibited by rotting barley straw in the water.
There is also an observation (not universally accepted) that many plants in the water do not have as much algae.  This post is from April 2011, so it seems pretty current.

Here is a good review titled: Use of allelopathy of aquatic macrophytes for algal-bloom control.
Hu and Hung talked about Macrophyte species which have allelopathy effects on Algal-bloom.
This paper discussed the development and potential application of allelopathy of aquatic plants on algae, including the reported aquatic macrophytes having allelopathy on algae, their allelochemicals and potential modes of action on algae, possible ways for application and the prospect of using aquatic macrophytes to control algal bloom.
Plants which you want to use for allelopathy effects on algal bloom, must of course be marine.
But sometimes allelopathic agents of terresterial plants can be extracted and use for this purpose more commercial than marine planting.


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Possible to Gain More Weight than the Food You Eat
I was wondering if it's possible to gain more weight than the mass of the food you eat. At a first look, this is impossible because of the principle of mass conservation, but are there other things to take into consideration?
For example, fat contains carbon. Does the body use the carbon we breathe to produce the fat necessary to store any energy we don't use? And a relevant question: how efficient is human fat at storing energy, compared to what humans normally eat?

I don't know if you consider water as food, but you can easily gain weight by just drinking water. You might want to look into what can be absorbed through your skin as well.

No it is not possible.  Humans are heterotrophic organisms, which means that we use organic molecules (i.e., food) as a source of nutrients and energy.  We use the nutrients to add mass to our bodies.  These nutrients are the familiar carbohydrates, proteins, lipids (fats), etc...  During digestion food is broken down into simpler organic nutrient molecules that are then used to make our body tissues.
So even if we only used food for nutrients we could not gain more weight than the food we consume but note that the food is also used for energy. This means that some of the mass of the food that we eat is not used to add mass to the body but is "burned" as metabolic fuel.  The mass of the food used for energy is expelled from the body as waste in the $CO_2$ that we exhale and in the metabolic waste in the urine.
The carbon in the air is mainly $CO_2$, which is an inorganic molecule.  Only autotrophic organisms like plants can use inorganic molecules as a source of nutrients.  Since inorganic molecules usually contain less potential energy than organic molecules autotrophic organisms need a different source of energy.  Plants use sunlight.
Finally, fat contains about 9 Calories per gram whereas a Big Mac has about 2.4 Calories per gram so fat has almost 4 times the energy of a Big Mac.
(Calories are the amount of heat that is released if all of the energy in the organic molecules is released so it is an estimate of how much energy the body can get from food)

I think this is a good answer to a good question, and I've registered those feelings:  Nevertheless, I'm wondering when (if ever) a living human's body did not contain some autotrophic life, perhaps most commonly in the form of bacteria (which, at least in the time--decades ago--when I studied biology systematically, had or have usually been considered as microscopic relatives of plants).  As their activity would affect our state of mind, etc., I've usually considered us to be living partly in symbiosis with such forms of life (that might, consequently, not be easily distinguished from us).


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How much gas is exchanged in one human breath?
When we breathe, our lungs absorb a portion of the oxygen in the air, and replace it with some amount of carbon dioxide and water vapor.  Typically, how much $O_2$ (in grams, milliliters, or moles for instance) is absorbed and how much $CO_2$ and $H_2O$ are released in one breath of a healthy adult?
Of course, the exact amounts will vary from person to person and based on how deeply the person is breathing, lung health, etc.  I'm just looking for a ballpark figure.

Just as a side note, it's a common error to believe that you're just breathing out CO2 and H2O. You're also breathing out a fair amount of oxygen as well.

@Jeremy  Indeed.  This is why CPR includes breathing for the recipient.  If it was just CO2 and H20, you wouldn't be doing much good!

According to Wikipedia

"In a healthy, young adult, tidal volume is approximately 500 ml per inspiration..."

(tidal volume is the volume inspired/expired)
Using this figure, together with values for gas composition also taken from Wikipedia, I estimate that in each breath we take in 18 mg O2 (1.1 mmol) and we release 36 mg of CO2 (1.2 mmol) plus 20 mg H2O (1.1 mmol). These are, as you say, ballpark figures.
Sample calculation:
O2 inspired = 21% by volume; O2 expired = 16% by volume
O2 change = 5% by volume = 5*500/100 = 25 mL
1 mole gas = 22.4 L; 1 mmol gas = 22.4 mL
O2 change = 25/22.4 mmol = 1.1 mmol
MW O2 = 16
O2 change = 17.6 mg
The relative values are reassuringly close to what you might predict from the textbook equation for oxidation of carbohydrate: C6H12O6 + 6O2 -> 6CO2 + 6H2O

Thanks!  I guess all the figures I needed were on Wikipedia, but thanks for putting 'em together for me.  Fun fact: you lose about 1.5 pounds of weight per day just to breathing (since the CO2 and H2O are heavier than the O2; assuming 20K breaths/day).

@NathanReed, interesting point, but you have your numbers wrong. H2O is not heavier than O2. H2O is a single molecule of Oxygen with a couple of extra protons (H+). It will be lighter than O2.

@terdon I meant that the CO2 and H2O combined are heavier than the O2.

The textbook equation for respiration doesn't always hold. The molar ratios really depend on what is being metabolized by the organism, and that can depend on a number of factors including health and activity. For a more precise ratio you need to consider the respiratory quotient - see http://en.wikipedia.org/wiki/Respiratory_quotient


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Lateral, axional and temporal resolutions for imaging in vivo
What are the spatial (lateral and axional), and temporal resolutions that one is expected to get with the following optical imaging techniques?

Optical Bioluminiscence Imaging (BLI)
Optical Fluorescence Imaging (FLI)
Multiphoton Microscopy (e.g. 2-photon microscopy)

Are they any better than the  others in providing higher resolutions?

The lateral and axial resolution depends on the numerical aperture of your objective (lateral = lambda/2NA; axial = 2lambda/NA^2). You can improvee the axial resolution with FLI by using a confocal approach or with 2-photon microscopy (2PM). In 2PM you need absorption of two infrared photons to get emission. The probability of 2 infrared absorption depends quadratically on the excitation intensity. Therefore, fluorescence is restricted where the illumination beam is focused which give a better sectioning. An advantage of 2PM is the higher penetration depth and reduce phototoxicity. Indeed you can use 2 infrared photons to excite fluorophore which required visible excitation.
Temporal resolution depends on the area you want to measure and the integration time.
Resolution is limited by the diffraction. In the best case with the 3 imaging techniques you mentioned you can get ~200-300 nm in lateral resolution and 500 - 800 nm in axial resolution
Higher resolution can be achieved by using super resolution techniques. They are separated in two groups. The first one exploid the photo-physical properties of the fluorophore to excite and de-excite it. This allows to resolve sub-diffraction areas. This is the case STED (Stimulated emission depletion) microscopy or SSIM (saturated structured illimination microscopy). The second group use the fluctuation of the fluorophore emission to localize it better. It includes techniques such as STORM (STochastic Optical Reconstruction Microscopy, PALM (Photo-Activated Localization Microscopy) and SOFI (super-resolution optical ﬂuctuation imaging).


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Super-resolution imaging in vivo
Are there any microscopy modalities or techniques for in vivo imaging at higher resolutions than the diffraction limit?
I was looking at this list: Super resolution microscopy, but they don't talk about in vivo imaging.

Any superresolution techniques relying on stochastic sampling (e.g. PALM, STORM) is extremely difficult to accomplish in vivo, as the tissue would be moving (e.g. due to respiration) and this would hinder a lot the reconstruction of the image.
Apparently it may be possible to do it with STED but I could not find the related paper*, although the same authors recently published some interesting work on living brain slices.
* Note that the images in that article come from this paper, which is not done in vivo.
Thanks to @vkehayas for pointing out that in vivo STED has been done for instance here Nanoscopy in a living mouse brain

I beg to differ on the PALM/STORM point. While I'm a little biased as a co-author of Live-cell dSTORM with SNAP-tag fusion proteins, we had very good experience with live cells and dSTORM. After all, a dSTORM image can be taken in ten seconds, and many biological processes are slower.

@thiton: again, I reiterate that when speaking about in vivo (at least in physiology) one considers a living animal, not a cell culture, which is still considered in vitro (or, for living tissue I ex vivo). I doubt you had many problems of respiration with your cells...

The first paper published with STED in vivo was Nanoscopy in a living mouse brain.. Feel free to incorporate that in your answer if you'd like to.

@vkehayas Thank you! I had not seen that when I wrote the answer, I will add it.

There have been experiments with Live-cell dSTORM with SNAP-tag fusion proteins in Markus Sauer's lab in Würzburg. If you are using the physiology definition of in-vivo, I'm pretty sure some of my co-workers have measured on live organisms. However, this is work in progress and not fully published; if you are interested, you should ask Markus Sauer directly.
You can use the dSTORM-like techniques (STORM, dSTORM, GSDIM, RPM, etc.) in live cells because the chemical environment in the cell is favourable and the redox system of the cell works for you. The key problem is to get the fluorophores into the cell, but SNAP-tags can help you to do it.
As one of the co-authors, I can tell you that live cell was some pain, but considerably less than getting 3D localization microscopy to work.
PALM is a different story because you generally have longer acquisition times. STED is difficult: If the cell wasn't dead before, the STED beam will ensure it is, either through the intensity or by unbalancing the chemical environment sufficiently. You might have your image before the cell dies, or maybe not.

Since the question was asked, the field has seen tremendous growth and even a Nobel prize has been awarded for Super-resolution microscopy. Since other answers have already touched upon how STED, PALM, STORM could help, I would talk about Expansion Microscopy (ExM) and how it has been recently used to image intact zebrafish brain tissue and gastrulating zebrafish embryos [Freifeld et al].
Since the optical resolution is limited by the wavelength of light which gets diffracted if the object being imaged is smaller than the wavelength of light (~300 nm). In order to image small object, what if we could enlarge the object itself to cross the diffraction barrier? This has been done by a team of researchers at MIT who imaged mouse brain tissue in 2015 [Chen et al].

Chen et al. have solved this problem by digesting the mouse brain away after transforming it into a polymer gel but before inducing matrix expansion. But how can one study a brain in which all the neurons are gone? Here, a second idea came into play: For some questions, it would be enough to study a “shadow” of the brain in the polymer matrix. This was realized by first marking molecules of interest in neurons with antibodies. The antibodies then were labeled with fluorescent markers that bind both to the antibodies and the matrix. The brain was then digested away and the matrix expanded. The fluorescent neuronal shadows also expanded and could be studied in “superresolution.” Chen et al. could thus increase specimen size by about a factor of 5 while preserving general morphology, and could visualize cultured neurons and brain slices at 70-nm resolution. This allowed them to observe proteins localized to synapses.

The best part is that conventional confocal microscopes can be used to image these enlarged samples, so the imaging speed is also good.

Freifeld, L., Odstrcil, I., Förster, D., Ramirez, A., Gagnon, J. A., Randlett, O., ... & Martin-Alarcon, D. A. (2017). Expansion microscopy of zebrafish for neuroscience and developmental biology studies. Proceedings of the National Academy of Sciences, 114(50), E10799-E10808.
Chen, F., Tillberg, P. W., & Boyden, E. S. (2015). Expansion microscopy. Science, 347(6221), 543-548.

This question is asking about in vivo imaging but Expansion Microscopy is still performed in fixed samples. If you are claiming that Expansion Microscopy can be performed in vivo you are...stretching the definition of in vivo too much. For an example of true "super-resolution" imaging in vivo see https://www.nature.com/articles/s41598-017-18640-z.pdf.

Yes. A decade ago I've been working on a software for microscope that does what you want.
Here's how the product looks after 12 years of development.
It's optical, however it produces Z map instead if image, and has resolution is order of magnitudes below the diffraction limit:
http://www.amphoralabs.com/production/10404/10708

That does not work in vivo, does it (cell culture does not count as in vivo)?

Wikipedia thinks you're wrong. "In microbiology in vivo is often used to refer to experimentation done in live isolated cells"

well, when speaking about physiology, in vivo means on living animals, isolated cells are considered ex vivo.


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Atomic force microscopy: depth penetration?
What depth penetration can  one typically get with atomic force microscopes? (i.e. how far into the tissue can one image?). I have found numbers on acquisition times (minutes) and spatial resolutions (~nm), but what about depth?
Also, what is the sensitivity of AFM? (e.g. in moles)

I was under the impression that AFM works superficially on specimens.

Taken right from the Wiki page you linked to:
AFM only images the surface of a specimen, to a maximum depth of 10-20 µm and a maximum scan area of 150 µm x 150 µm. Compared with scanning electron microscopy, SEM has a much larger depth of penetration and scanning area (~1 order of magnitude greater). AFM is also a much slower scanning method.

AFM does not penetrate into the sample. It CAN give true topographic data from a sample however, with quantifiable heights (SEM cannot really do so). It also has the advantage of being usable in atmosphere or in liquid - on non-conductive samples (which are hard for SEM). High speed AFM can even record videos of proteins doing their thing, and probe the mechanics as well as topography of a cell's lipid membrane.
But it has no depth as such.

AFM is a surface technique, it has no depth. Spatial resolution can be far in excess of nm - there are publications wherein bonds -ewven hydrogen bonds- are shown.
Here is a popularized article which is not behind a paywall
https://www.chemistryworld.com/news/new-afm-tip-reopens-hydrogen-bond-imaging-debate/3008878.article
The sensitivity of AFM would not be measured in moles at all. How to measure it depends entirely on the mode you work with. Are you imaging the surface topography? Are you measuring the friction between the tip and the sample? Are you measuring magnetic domains? Surface hardness?

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Is it possible that the recipient of a heart transplant would display some of the donor's personality traits, as if the heart has memories?
I've read somewhere that after a person has a heart transplant, it is possible that his/her attitude, action or behavior would change slightly or significantly, as though he/she possesses some aspects of the organ donor's personality because he/she is using the donor's heart.
Anything to support this phenomenon? Does it suggest that there are actually memories 'stored' in the heart and these memories may be retrieved by the person that owns the heart even if he/she is not the original owner?

I would imagine most people's behaviour changes significantly after a heart transplant - these sort of things tend to change your outlook and approach to life!

It worked only once, but it was a dog ;)

Although there is clearly no feasible mechanism for such a phenomenon, there is good evidence that transplant patients can believe in some sort of transference of qualities from the donor. See for example (my emphasis):

Inspector, Y. et al. (2004) Another Person's Heart: Magical and Rational Thinking in the Psychological Adaptation to Heart Transplantation. The Israel Journal of Psychiatry and Related Sciences 41: 161-73.
Abstract
The goal of this study was to examine heart transplant recipients' psychological adaptation to another person's heart, with particular emphasis on recipients' attitudes toward graft and donor.
Thirty-five male heart recipients were examined by: the Symptom Distress Checklist (revised) (SCL-90-R); the Depression Adjective Checklist (DACL); a Post-Traumatic Stress Disorder Questionnaire (PTSD-Q); a Heart Image Questionnaire (HIQ); and a Semi-Structured Interview (SSI), aimed at eliciting attitudes and fantasies regarding the transplanted heart.
All instruments indicated high levels of stress even several years after the transplant, but, simultaneously, 73% of recipients felt that acquiring a new heart had had a dramatic influence on their lives with a new appreciation of the preciousness of life and a shift of priorities, toward altruism and spirituality. Sixty percent returned to work after the transplant but some had to adapt to a changed attitude from those around them who regarded them as anything from mystical creatures to vulnerable or still-sick individuals. While all recipients possessed a scientific knowledge of the anatomy and physiological significance of the heart (as revealed in the HIQ), many endorsed fantasies and displayed magical thinking: 46% of the recipients had fantasies about the donor's physical vigor and prowess, 40% expressed some guilt regarding the death of the donor, 34% entertained the possibility of acquiring qualities of the donor via the new heart. When asked to choose a most and least preferred imagined donor, 49% constructed their choices according to prejudices, desires, or fears related to ethnic, racial or sexual traits attributed to the donor.
This study confirms the intuitive idea that heart transplant involves a stressful course of events that produces an amplified sense of the precariousness of existence. Simultaneously, it gives rise to rejoicing at having been granted a new lease on life and a clear sense of new priorities, especially with regard to relationships. Less expectedly, this study shows that, despite sophisticated knowledge of anatomy and physiology, almost half the heart recipients had an overt or covert notion of potentially acquiring some of the donor's personality characteristics along with the heart. The concomitance of the magical and the logical is not uncommon in many areas of human existence, and is probably enhanced by the symbolic nature of the heart, and maybe, also, by the persistent stress that requires an ongoing, emotionally intense, adaptation process.

Another study is reported in:
Bunzel B, et al. (1992) Does changing the heart mean changing personality? A retrospective inquiry on 47 heart transplant patients. Qual Life Res. 1:251-6.
To actually investigate this further I suppose it would be necessary to set up experiments in which patients had transplant operations in which (unknown to the patient) no transplant actually took place, with the expectation that these individuals would display the same magical thinking. Grant application?

"To actually investigate this further I suppose it would be necessary to set up experiments in which patients had transplant operations in which (unknown to the patient) no transplant actually took place, with the expectation that these individuals would display the same magical thinking. Grant application?" ... Ha, yeah, I don't fancy the chances of getting past the ethics committee!

Alternately, they could be lied to about who their donor "was" to see if they manifest the memories and feelings of a 22 year old woman when their donor was actually a 35 year old man. Though I'm pretty sure an IRB would clobber that too.

There are neurons all over the body, not just in the brain.  The area with the most neurons, beside the brain, is the heart.  It's been theorized that some memory could reside in these cells.  I'm a big believer that if you keep an open mind people will throw garbage in it, but this particular phenomena seems worthy of further study.

Could you add citations for "It's been theorized that some memory could reside in these cells."?


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Are there known minimal marine ecosystems that are stable?
A more entertaining phrasing of the question would be "what would a marine ecologist put into a perfect aquarium?"
I was reading about Prochlorococcus, among other photoautotrophs, and found that they seem to get their nitrogen from ammonia, which must be produced by some other organism. This set me off wondering what different species I would need in a hypothetical aquarium (how big that would have to be is another question, I guess), such that a sustainable ecological equilibrium occurs (one different from everybody dead, I guess), only requiring sunlight and air from the outside.
I realize that I'll have to put other components like iron etc in the water, but let's say I only put some fixed amount in during setup. What exactly that would have to be is probably another can of worms, so let's keep that out of this question as much as possible.
Has there been research towards such model ecosystems, and are there known minimum configurations?
It's hard to give an authorative "no" to this answer. But maybe there's research that looked for such a system and failed, or maybe marine ecologists use model cultures in their labs that show instabilities (meaning the culture dies, you have to replace the water, or keep adding fertilizer, or keep removing some waste) which allow some generalizations.

This is the one I've heard of - Its a sealed acrylic globe that contains algae and brine shrimp.  There are quite a few references in the bibliography here to previous systems.
Of course, it needs sunlight, but all the elements are recycled.  Its really closed and has reasonable endurance.

The basic commercial version of his closed world -- sold under the label of "Ecosphere" -- is a glass globe about the size of a large grapefruit. My world #58262 was one of these. Completely sealed inside the transparent ball were four tiny brine shrimp, a feathery mass of meadowgreen algae draped on a twig of coral, and microbes in the invisible millions. A bit of sand sat on the bottom. No air, water, or any other material entered or exited the globe. The thing ate only sunlight.
The oldest living Hanson-world so far is ten years old; that's as long as they have been manufactured. That's surprising since the average life-span of the shrimp swimming inside was thought to be about five years. Getting them to reproduce in their closed world has been problematic, although researchers know of no reason why they could not go on replicating forever. Individual shrimp and algae cells die, of course. What "lives forever" is the collective life, the aggregate life of a community.

All of this is a real subject of research for those interested in creating entirely useful ecosystems.

It turns out that ecospheres scale up well. A huge commercial Ecosphere can weigh in at 200 liters. That's about the volume of a large garbage can -- so big you can't reach your arms around it. Inside a stunning 30-inch-diameter glass globe, shrimp paddle between fronds of algae. But instead of the usual three or four spore-eating shrimp, the giant Ecosphere holds 3,000. It's a tiny moon with its own inhabitants. Here, the law of large numbers takes hold; more is different. More individual lives make the ecosystem more resilient. The larger an Ecosphere is, the longer it takes to stabilize, and the harder it is to kill it. But once in gear, the collective give and take of a vivisystem takes root and persists.

Unfortunately larger systems that can support people have not been made yet.

Algae and man lasted a whole day. For about 24 hours, man breathed into algae and algae breathed into man. Then the staleness of the air drove Shepelev out. The oxygen content initially produced by the algae plummeted rapidly by the close of the first day. In the final hour when Shepelev cracked open the sealed door to clamber out, his colleagues were bowled over by the revolting stench in his cabin. Carbon dioxide and oxygen had traded harmoniously, but other gases, such as methane, hydrogen sulfide, and ammonia, given off by algae and Shepelev himself, had gradually fouled the air. Like the mythological happy frog in slowly boiling water, Shepelev had not noticed the stink.

Here is an academic reference you can use to start looking around if you like...

Very nice answer. And very interesting.


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Do siblings have a bias toward believing they look different from each other?
Anecdotally, I have observed (myself included) that siblings tend to think that they look less similar to each other than an unrelated observer would say. Is there any experimental data to back this up, or am I completely wrong?

if they did, I think it would be due to the fact that we don't look at ourselves so much as we see others.

Would this be better in http://cogsci.stackexchange.com

You are not completely wrong but not completely right either. Some siblings tend to think they are less similar to each other, even twins. It may or may not have scientific reason, but it has sociological reason behind it. Every people in our society want to have their own separate identity and they do not want themselves to be compared with others even with their siblings.It might be also due to the result of fact that, siblings pass times with each other so often that they notice distinct differences in both their characteristics and look while ordinary people, looking at them for the first time, can not notice the differences. This is related to the reason why we can not sometime recognize people from any particular race or ethnicity at first look.

Can you add references to support these statements?

+1 all familiar persons look distinctive does seem to relate to 'all foreigners look alike'.  In addition to wanting to be distinct, there may be some disconnect with indirect self-observation using photographs and mirrors--"is that really what I look like?"


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How long will norovirus live?
I hope this is the right place to ask. I subscribe to several Stack Exchange threads, and regard them as the best internet forum for genuine and credible answers.
I spent last evening talking to friend, at an Amateur Radio Club, who told me he has recently recovered from the norovirus. I was demonstrating an oscilloscope to him, and he also handled the handbook. All this is now in the holdall I used to carry it to the Club. I took all the precautions I could, like washing my hands and not getting them near my lips, nose etc. So, my question is: how long should I wait before opening my holdall, to be sure any infection there is dead?

Well, for him the virus is already likely at minimum levels within his body. If he's recovered (pass the fever phase) then his immune system has already dealt with the majority of the viral bodies in his system, since the peak of the immune response comes after the peak of the viral infection density (ignore B):

How much of the virus was left in his system to actually spread is hard to guess. Sometimes infections never truly go away, but merely become undetectable by conventional testing. However, if we're to assume that there's at least some norovirus left to transfer to you then you should realize that the greatest chance for exposure has already come and gone.
The moment you were in the same room together, talking in close proximity, shaking hands (if you did), or generally being close is the most likely source of any infection you could have picked up. However, while most virii don't survive well outside of the body, the norovirus notably bucks that trend. The Hawaiian Department of Health (PDF) notes that the virus can definitely survive outside the body for several days on hard surfaces (though it will not grow), can survive being frozen, and that it only takes about 100 viral units to cause an infection (which could fit a few thousand times over on a grain of salt). Scientific American also notes that norovirus can survive for months or years in sources of drinking water.
What you've already done is pretty much what you should do to avoid infection. You've washed your hands, refraining from mucous membrane contact, etc.
Ultimately how long you should wait depends on where the norovirus currently resides. A week should be sufficient if all of the norovirus is contained on the book or on other surfaces that you're not making contact with. However, if it's already had contact with your skin or mucous membrane, then you're either already fighting it off or you're about to become ill. Unfortunately it's a lot easier to expose yourself than contain something you can't see, as the Mythbusters have done a good job of showing (Video).
In all likelihood if he was still infected enough to transmit the virus to other people by the time you two started handling the same equipment and you didn't use gloves, you've probably been exposed. However, exposure doesn't automatically mean you get sick. If you're not sick within a week afterwards, you've successfully fought it off. So, congratulations, perhaps!

Thank you @MCM very much for that comprehensive answer. A bit reassuring, but it seems that really I must just wait and see. As a supplementary question: is my wife at risk (she did not come with me) assuming I do not show symptoms? Unfortunately I do not have enough "reputations" to vote your answer up, as I would like to do.

@HarryWeston - "Is my wife at risk if I don't show symptoms?" Yes. Whether or not you show symptoms after having contracted any infection depends on your immune system's response. If you've seen a similar strain (or the exact same strain) before, then there's every chance you won't show symptoms but still be a carrier. If your wife hasn't encountered the strain, she could still get sick and invoke the normal immune response. This is all contingent on whether or not the guy passed it on to you, though.

Thank you again @MCM, so it is just a question of wait and see, though much much better informed now.


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Are there inherent problems in simulating marine environments, as compared to terrestrial systems?
We cultivate a number of terrestrial organisms in greenhouses and stables where they live in completely artificial environments. This seems to extend far less to marine organisms, such as fish. Aquariums (especially the salt water variety) seem to be quite unstable and require a lot of maintenance, and commercial scale installations, like salmon farms, are set up in the ocean, rather than in a separate tank.
Are there inherent difficulties in cultivating marine organisms, or is it just that mankind has not tried as hard as with land species?

It probably depends on the type of marine organism you're referring to, some will be much more hardy than others and some will not be able to adapt to change at all. Due to the vast scale of the environment that marine fish come from it's likely that in their natural habitat the conditions they live in are not subject to drastic changes in water chemistry or temperature [1][2]. So recreating those exact conditions for them in man-made habitats, let alone maintaining them is going to be extrememly difficult.  Also, if you think about the conditions that most (there will be some exceptions) terrestrial animals and plants have to deal with on a day-to-day basis they have to be able to cope with some fluctuations in humidity, temperature, weather, light etc and therefore are highly adaptable by necessity.
Other issues can be supplying the correct feed. In artificial settings food may have to be a non-natural substitute and this will likely cause problems for species who require a highly specialised diet. The terrestrial animals we tend to cultivate extensively are omnivorous/herbivorous which are not difficult needs to meet. On the other hand a fish from the sea that requires a particular other kind of fish only found in a particular area and that needs very specific conditions to thrive is going to be problematic.
Check out this article http://www.vliz.be/imisdocs/publications/301.pdf , it might be for a specific fish but it highlights some of the general issues i think you are referring to.
[1] http://www.bestfish.com/saltg.html
[2] http://www.aquaticcommunity.com/marineaquarium/
(both general articles on keeping marine fish)
hope this helps!

Large numbers of marine animals are actually cultivated in large aquaria. They're just generally not as conspicuous as farms and farm animals and are often located in difficult to access areas around estuaries or close to ports. There are also a number of specialised journals that focus on aquaculture such as the journal aquaculture. In addition to being cultivated in aquaria, large numbers of animals are also cultivated in more natural settings such as the salmon you mentioned or shrimp in shrimp ponds, which are widespread in countries such as Indonesia. A major problem in aquaculture is disease, although this can also be a problem with terrestrial livestock raised in high densities. If you're interested in marine aquaculture, I suggest you browse the various aquaculture journals to get an idea of what's going on.

Yes there are some fundamental differences
Different types of water
the main challenge with aquariums compared with breeding terrestrial life, is that water differs a lot across the world, while the composition of air is virtually the same everywhere, whether over jungles, deserts, oceans or even cities.
Fish from the amazon rivers require slightly acidic water, with tannins but little minerals, while fish from the great african lakes need a higher pH and more dissolved minerals. Since saltwater is all about dissolved elements and its concentration is increased by evaporation, this becomes all the more critical with saltwater fish, which work to maintain their internal concentration of ions against that of the ocean around them.
Feces
Land animals drop their excrement on the ground, while fish swim in it, "breathe" the byproducts of bacterial breakdown of feces and suffer as the bacteria use up all the oxygen. Dealing with this while also maintaining "amazonian" or "tanganikan" water has kept many an aquarist busy. Land-animals are much simpler. The gecko dump its feces on the bottom of the cage and will happily breathe whatever air comes in your window.
On the microscopic scale, the difference between land and water is less pronounced. It is actually quite hard to breed in the lab many of the micro-organisms dwelling in soil. So much so that scientists has started sequencing DNA-fragments from soil to discover new species, never seeing them up front.


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Difference between Diffuse Optical Tomography and Optical Tomography
What are there the differences between these two modalities?

Diffuse Optical Tomography (DOT)
Optical Tomography (OT)

Are there forms of OT that are not DOT?


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Can jellyfish improve the Black Sea ecosystem?
According to this study, cited by many popular science magazines, jellyfish and other, smaller animals can contribute to the vertical ocean stir as much as currents do.
Black Sea chemistry and biodiversity is highly coupled with the lack of vertical currents, present in oceans or bigger seas. Some of the effects are low salinity in the top layers - many ocean fish species cannot tolerate the Black Sea salinity, and limited space for life (below 50 meters there is no oxygen)
Can the jellyfish population (which is exploding now) change the stratification of water layers enough that the highly saline waters from bottom go up, and oxygen goes to the deeper layers, allowing a completely new ecosystem here?
If yes, what are the outcomes of such prospects? Besides the potentially catastrophic release of hydrogen sulphide form the bottom, can it be an improvement for the biodiversity here?

At least they have an influence in the sense of butterfly effect. Which can be small, or huge. http://en.wikipedia.org/wiki/Butterfly_effect

To quote the PI from the BBC article:

But, Dr Dabiri explained, the jellyfish were unlikely to be the "primary ocean mixers".  "Crustaceans - like copepods and krill - are likely the primary biogenic mixers, because there are so many of them," he explained.
"But much of the open ocean is like desert," he added, "and the density of these animals is unlikely to be sufficient (to cause mixing)."

My guess therefore is no, jellyfish would not be sufficient to dramatically change the current structure of ocean layers.  Animals in general, as the paper and its references suggest, do contribute significantly, on-par with tides and wind.

While in the ocean they are not the primary mixers, their influence is not negligible. My questions is about their effect in a sea where other vertical movement vectors are missing. A change of 10% in water movement is not much in an ocean, but in a closed sea may mean a dramatic change.


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Do animal cells have vacuoles?
I overheard a rather heated argument about whether or not animal cells have vacuoles.
One person said that they do, but they're much smaller than vacuoles in plant cells.
The other person said they don't. While there is something there that acts similar to a vacuole, it's slightly different. The person also noted that the only websites that say that something as a vacuole aren't credible sites (ie. not University sites, etc...)
I'm really curious as to which it is: Do animal cells have vacuoles or not?

They are both right.
Animal cells do have vacuoles, but they are smaller, larger in number (plant cells usually have just one or a few large vacuoles) AND serve a somewhat different purpose than those of plants.
A vacuole is basically a membrane-covered compartment (vesicle) filled with molecules, that shouldn't, right now, be in the cytoplasm. For plants, this means long-term storage of water and waste products, which cannot be removed from the cell due to the cell wall. For animals it means mostly taking part in exocytosis and endocytosis - they are much more dynamic structures.
And about some half-professional sources, here is a bit from Molecular Biology of the cell which in fact calls plant vacuoles "a kind of specialized lysosome".

If their function and purpose are different, so we could not call them vacuoles.

Yes! As a matter of fact Animal Cells do have vacuoles.  Even though they are much smaller than the Large Central Vacuole of Plant Cells, they still do exist in Animal Cells.  Unlike the Large Central Vacuole of the Plant Cells, they do not take up 90% of the cells and instead there are multiple slightly smaller vacuoles.  Also in a Plant Cell, there is usually only one vacuole: the Large Central Vacuole.

can you provide some citations to reliable sources?

Yes, animal cells do have vacuoles. They just have a larger number of them and some sites call them with different names. In a plant cell there is just one vacuole. Pictures of cells in textbooks,online,etc should show you that they have vacuoles, despite contrary beliefs elsewhere.

Provide a reference for ur answer.


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Hearing system as in visual system: exists well also - in protecting the inner mechanical parts of both sensing systems - a similarity?
I prefer answers, not just discussing.
In the mechanical part of the human eye the control system to protect for overload of the diaphragm in the iris with a strong coupling to the light intensity that falls on the retina has his place in the visual system as close as possible to the light source in the chain of control devices of the human visual system. The iris is disk-shaped and consists of two muscles. Like a diaphragm for light, the iris regulates how much light comes into our eyes. In bright conditions, the muscles of the iris limit how much light comes in. In lowlit conditions, the muscles of the iris increase the amount of light comming in.
Basic hypotheses is that the protection device in mammalian human hearing system is based on similarity as in the visual system and therefore should well also be using similar protection tools as used in the visual system and should well also be placed in the chain of control devices as close as possible to the signal source, as an experienced system engineer will always place a protection device in the chain of control devices as close as possible to the signal source.
Exists such an continuous functioning simalarity analogue in the protection system for sound signals ?
Both the iris in the eye (two muscles) and eardrum+ossicular chain in the ear (two muscles): in protection.
Exists that similarity ?

I'm not sure what the question is, yes the ossicular chain is believed to have a function as 'overload protection' - but I feel you're aware of that already.  Could you clarify at all?

The cooperative functioning of the eardrum and ossicular chain attenuation can be regarded as in this schematic drawing of the ear as an externally activated spring-mass system. Fig. 2.
Ossicular chain and eardrum function, together operating as a continuous sound reduction mechanism for changes in the strength of the offered signal. The tympanic membrane and the ossicular chain can be seen as a spring-mass system with amplification facilities, like it is shown in this figure.
The combined action of the ossicular chain and the eardrum is hypothesized to provide for both permanent volume control of the input sound and for overload protection. The stapedius reflex, evoked by sudden strong sound signal, cannot be seen as anything else than an extreme manifestation of the very mechanism that the schematic drawing of the ear as an externally activated spring-mass system propose.


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Is the eyes' movement discrete?
When tired and it was dark, I noticed that if I focused on a dim light source and moved my eyes fairly rapidly sideways, the resulting images that lingered for a short while were not smoothly blurred together, but were discrete.
I assume this is not due to the brain's inability to process the data fast enough or the retinas not repairing fast enough when light breaks part of them down, so I am lead to the conclusion that eyes (if not generally, sometimes) move in very small sudden jolts rather than smoothly.
Is this correct? What is the reason for this (is it due to the eye muscles being unable to sustain motion for a long time, or something to do with the mechanics of the eye)? Was this result anomalous?

There are two types of eye movement: smooth pursuit and saccadic. As the name suggests the latter movement involves quick and discontinuous movements of the eyes. Saccadic movement is used most of the time as the eyes move around analysing the current scene.
According to Wikipedia, these saccades are the fastest movements produced by the human body: peak angular speed of 900 degrees of rotation per second (this would be 2.5 full rotations of the eyeball per second, were such a thing possible).
The processing of information by the eye-brain system during a saccade is complex, and may be responsible for the effect that you report: it causes the phenomenon of saccadic masking explained in this quote from Wikipedia:

A person may observe the saccadic masking effect by standing in front of a mirror and looking from one eye to the next (and vice versa). The subject will not experience any movement of the eyes nor any evidence that the optic nerve has momentarily ceased transmitting. Due to saccadic masking, the eye/brain system not only hides the eye movements from the individual but also hides the evidence that anything has been hidden. Of course, a second observer watching the experiment will see the subject's eyes moving back and forth. The function's main purpose is to prevent smearing of the image.

I assume the advantages of smooth pursuit and saccadic movement are that the image is continuous (so no information is lost) and that the angular speed is large, respectively, or am I oversimplifying?


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Why does human facial and head hair continue to grow?
Many people can grow extremely long head hair and facial hair. Are there evolutionary theories as to why this is the case? It seems like having long hair could be a disadvantage, and extremely long hair seems to be rare in other mammals.

Closely Related Question

Another closely related question

Yet non answer the question - how is longer hair advantageous.

Just want to point out that not everything can be explained in terms of advantage or disadvantage in evolution. Most of the characters are not directly selected or selected at all.

@nbubis: why has there to be an advantage? Maybe it's just that it is not disavantageous...

@nico, I agree, but that's the OP's question.

That is my question - it seems like it would be a disadvantage - it could get caught in things, takes energy to grow, clean, etc.

I think there may be some relation to the human skin biome. Long hair may act as a transmittor of beneficial skin flora through its potential for direct contact with soil-based organisms. We are only just now scratching the surface (pardon the pun!) of the complexity of the human macro and microbiome; hair is likely to play a role in skin ecology. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535073/

How humans evolved to have head / beard hair that continues to grow longer than other animals is a topic that many anthropologists & biologists are still not sure about & there is no general consensus as to "why" yet.
The three main views that I am aware of however are :
1) Evolution of the "Aquatic Ape." (Ingram, 2000: Morgan 1997; 1982)

Infants, in order to hold onto their mothers in the water, would latch onto her hair. Limiting separation from the mother & increasing chances of survivability
Longer hair meant that infants / small children would need to swim less in order to get to their mother
Believed to be supported even further when you consider that aquatic mammals are almost always hairless, indicating that at one point, humans were highly "aquatic" mammals.

2) No real benefit, but used as a tool for "mate selection." (Darwin, 1871; Cooper 1971)

The view held by many of the Darwin school of thought (I do not mean that as a derogatory), is that at first, "hairiness" was sexually attractive, but eventually "hairlessness" became more sexually attractive in most places (i.e. the face to see facial expressions & socialize better; Wong & Simmons 2001)
A sign of "virility" & "health" as can be seen in the mate-selection behavior of lions. Which is true even today as human diagnostic material for health (Klevay, 1972).

3) Practical evolutionary benefits for the human species specifically

A lot of body heat escapes from the head, probably the most important part of your body. Hair is a good insulator that can keep in heat. This increases survivability in colder climates. (Wong & Simmons 2001; Bubenick 2003). (A disputed but considered credible reason, especially when you compare hair length and types across different regions throughout history)
Protection against damaging UV rays (while still permitting adequate Vit.D3 to come through) & some protection from free-radicals or other harmful particles. Because we became bi-pedal, the head was the main area exposed to the sun (as well as some of our back). Extending hair's usefulness to even hot environments, while other body hair became less important with the development of sweat glands (Wheeler 1985).
Heightened "Situational Awareness" through "Touch sense." A concept that may seem silly at first but has some evidence to support the theory. Though the hair is not "alive," it is connected to the follicles & your nerves. In a nutshell, it may help to increase "sensory awareness" & "data gathering" of your environment, which would favor longer hair. This would be an asset in survivability (Kardong 2002; keratin.com 2010; Sabah 1974; washington.edu)
Though not a collegiate Journal article, if reasonably credible, this small article is an interesting case for supporting hair & "Touch sense" in "recent history" & in combat-survival : http://www.sott.net/article/234783-The-Truth-About-Hair-and-Why-Indians-Would-Keep-Their-Hair-Long.

I personally lean 90% "Evolutionary benefits" & 10% "Mate selection" as to reasons why humans' hair continues to grow longer than other animals. Beard & head.
Hope this info was a little helpful.
There are copious amounts of other respectable articles on each point, but I only referenced a few.

Does anyone have a link for the "Kardong 2002; keratin.com 2010; Sabah 1974; washington.edu" study? I can't find it. I have dreadlocks and raised a discussion with a group where I claimed I can sense touch on my hair even though the roots are not stimulated in any way. I couldn't find anything to support my claim but came across this by accident. Thank you.

The hair doesn't keep growing!
It's important to notice that there isn't a set point for the actual hair length. The hair doesn't know that it's been cut for example. Rather, there's a set point for time. A single strand of hair, in humans, on the scalp, will be in the growth phase for several years. The growth cessation takes a few weeks, and then the rest phase will last for another couple of months, until finally the hair strand is shed.
I don't think there's a natural advantage for hair of as long a length as many humans can grow it, it may just be little or not at all disadvantageous. The selective advantage, if there is one, probably emanates from sexual selection, similar to why lions grow manes. A display of health and surplus of resources. Hair has a pretty central role in beauty ideals. In some cultures, women even cover up their hair.
There are examples of traits that are disadvantageous to survival in the organism's environment, but shows advantages when it comes to reproduction, to a degree that the genes do not become extinct. I don't remember the name, so take it for what you will, but there's a fish species where the males are either small and stealthy, or they are very flashy. The females prefer the flashy males, but at the same time those males have a harder time avoiding getting eaten by other, larger fish. Thus both phenotypes are passed on to the next generation of fish.

"until finally the hair strand exits". What does "exit" mean here?

The fish you're thinking of is the goby.


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What percentage of human capillaries are located in the skin?
As in the subject line, what percentage of capillaries in a human (expressed in terms of total length, I suppose) are located in the skin, as opposed to internal organs?  Google scholar has not turned up anything obvious, but I'm an outsider so I may have missed the appropriate term.
Another followup question would be:  if we're considering the amount of energy expended by the heart in pumping blood throughout the body, what's the percentage of that energy that is devoted only to (1) transporting blood to the skin and (ii) circulating blood through the skin via capillaries?

really if capillaries are the tiniest blood vessels which oxygenate the tissue, the entire volume of the body has them  oxygen doesn't diffuse more than a few cells width from the blood vessels.

All but the first part of the second paragraph are not really answerable as you have written them, I think. I did a rough calculation for that one part.

I suggest all your questions can be answered in "Measuring the Skin" by Pierre Agache and Philippe Humbert ISBN 3-540-01771-2 Springer-Verlag 2004. This book, even in used condition, commands a high price.

The first part of your second question permits a rough calculation.
The second question ( i ): For humans the skin has been defined as ending at the hypoderm, which is 2-3mm deep. The average human skin has been estimated to cover an area of 1.5-2 m$^2.$ We can use 2.5 mm and 1.7 m$^2$, respectively. This gives a volume of 0.00425 m$^3$ or 4250 mL in fluid volume. The information for this calculation is at the Wiki site on human skin.
One estimate of the average total volume of fluid in a human body is 40L. Of that, 5L is blood. So roughly 1/8 of the body's fluid is blood. To a good approximation, the body is about 60% water by weight. This is presumably a little less than the percentage of fluids generally but since these are rough numbers we can use it. So 60% of the skin is fluid/water, and 1/8$th$ of this is blood.
Of the 4.250 L of skin, 60% is fluid, of which 1/8 $^{th}$ is blood, so $(4.25) \cdot (0.60) \cdot \frac{1}{8} = 0.3188$ liters of blood at any given moment in the skin, subject to considerable variation no doubt. This sounds a little low but the definition of skin sort of forces this--it is only skin-deep.
One source gives an estimate of the energy expended to pump blood in a normal adult heart as 0.5-1.0 Joule per beat which at 70 beats/minute amounts to 100.8 kJ/day using 1 Joule.
So the heart is handling about 5 L of blood of which 0.3188 L is blood in skin, so very roughly we could estimate that $0.3188/5 = 0.0638$ or 6.38% of the work above goes toward supplying skin, i.e. 6.43 kJ/day of energy.
As a sanity check, if someone burns 1200 [nutritional] calories a day, which is about 5 MJ, we can see that keeping skin supplied with blood represents a small fraction of daily energy expenditure.
The title question: Like you, I found no study on point but that does not mean one does not exist. I can't see why anyone would do/fund such a study as the answer is unlikely to inform further work, answer any current questions, or solve any problems.
The last part of your second question (ii) Transporting blood to the capillaries and circulating the blood through capillaries are aspects of the same job. Dividing the work of the heart into skin/non-skin was already artificial. To further divide the work into segments this way requires some motivation because any answer would be a bad approximation.


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What is the composition of human feces?
Are there any studies or general information on the composition of human feces?
I'd specifically like to know the percentage of carbohydrates and amino acids relative to the amount that was ingested in diets of various types and amounts.
Any additional facts are also welcome.

This is a bit hard because the usual composition statements are a combination of different types of molecules.
Most of faeces are, by dry weight, bacteria (30%), undigested food and fiber (30%), fat (10%-20%), inorganic matter( 10-20%), other protein(2-3%). (reference)
As you can see the bacterial portion contains proteins (amino acids) and other types of molecules.  the inorganic matter includes bilins which are part of the used up hemoglobin from red blood cells which have been retired.
There's also a lot of variation from one sample to the next - 10% seems pretty common here as you can imagine).  What makes faeces so dangerous is the bacterial portion, which can pose quite a health risk.


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Cell cycle selection
Is it possible to select from colonies only cells which are at a certain stage in the cell cycle? E.g. if I was trying to analyse expression of a number of genes during different stages of the cell cycle.
I could imagine that if this is possible, the selection mechanism might target cyclins, or use an artificial gene cassette controlled by them.
So for example, a method may attach some gene to a certain cyclin which protects against a substance that otherwise destroys the cell. We could then use that substance to destroy all cells which were not in the cell cycle stage that we want to look at, wash away their nucleic acids, and then extract the mRNA from remaining cells to analyse expression levels at this particular stage in the cell cycle. If we repeat that for the different stages, we should be able to get a nice picture of what is expressed when. Does any method like this exist or is commonly used?

see http://en.wikipedia.org/wiki/Cell_synchronization and http://en.wikipedia.org/wiki/Synchronous_culture

Depending on the stage of cell-cycle you are interested in, people often use the size/morphology of the cell as an indicator. Then you select cells with a cell sorter.
Another option is to specifically tag some cellular molecule that can give an indication as to the relevant stage and then sort the cells based on the tag. This does not necessarily have to be cyclins - for example if you are only interested in S/G2 you could tag the DNA or maybe histones.

You have correctly stated that we can monitor cell cycle stage by either monitoring protein (cyclin) levels or by following indirect methods such as green cassettes. One usually tries to monitor changing levels of:

G1 cyclins (D cyclins)
S-phase cyclins (cyclins E and A)
Mitotic cyclins (B cyclins)

Or one might try to modify the gene where these proteins are produced so that one can observe some unique behavior that highlights that particular stage of cell cycle is going on.

Thanks for the info! Though it doesn't quite answer what I wanted to know - I added more detail to my question as I can understand that I was a bit unclear.

The only strategy close to your suggested description is based on FUCCI sensors.
Fluorescent markers designed so that their presence informs of specific stages of the cell cycle, in principle without disrupting or perturbing cell progression.
So, although there is not a physical clean-up of pure cell sub-populations, these can be tracked by the abundance of these markers and even isolated by FACS.
I guess the issue of developing something selectively "lethal" (which does exist in the context of certain plasmids transformed in E.coli) lies partly in being able to retrieve those surviving cells in a timely fashion so that being halted at that particular stage is not detrimental. It does sound as an interesting analogy to Sanger Sequencing where 4 different terminators of each of the 4 bases render truncated fragments easily readable. In principle within the context you suggest, a single cycle would be allowed post genetic manipulation (eventual silencing of such genetic modification as representing an undesirable weight for the cell would be expected otherwise). As progression through each phase varies substantially in time, the idea in itself would require substantial refinement, and most likely the use of a conditional expression system. In this way a mix population transfected with the specific set of markers could be triggered for expression at a given time and then monitored for negative selection.
Commonly though, chemical synchronisation or perhaps more physiologically relevant methods of separation like elutriation, aim at enriching cell populations at specific stages of cell division. Mitotic cells are particularly problematic being rather scarce at any given time within an unperturbed population of growing cells. Mitotic shake-off followed by addition of hypotonic solutions have been suggested as methods of mitotic retrieval but yield is comprehensibly low.


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Parsimony (cladistics)
I don't understand how to sum the changes in a phylogenetic tree.
Here for example: http://www.med.nyu.edu/rcr/rcr/course/phylo-cladistic.html
How do you end up with 8 for the first and 9 for the second ?

It seems to me that they are not summing the changes correctly in this page.
They are summing the lengths of the paths to the root (and for the fig 2, they assume that the terminal branches, from left to right are of lengths 3, 2, 1 and 1). This doesn't make sense to me.
The correct way to count changes using parsimony is to consider each site in the alignment, and try to put the minimum number of mutations on the tree to explain the states observed at the terminal branches. Then, sum the number of mutations across alignment sites.
Here, for figure 1, I get:
site 1: 1 mutation, either on the left (T->A) or on the right (A->T) internal branch.
site 2: 1 mutation on the 4th terminal branch (T->C)
site 3: 0 mutations (all terminals have C)
site 4: 1 mutation on the 2nd terminal branch (G->C)
Total: 3
for figure 2:
site 1: 1 mutation on the branch leading to the most recent common ancestor of the two right-most terminals (A->T)
site 2: 1 mutation on the right-most terminal branch (T->C)
site 3: 0 mutations (same reason as for figure 1)
site 4: 1 mutation, either on the left-most branch (G->C) or on the branch leading to the most recent common ancestor of the 3 right-most terminals (C->G)
Total: 3
The trees are equi-parsimonious.
I hope I did not make any mistakes.
There exist algorithms to do this. For instance, Wagner parsimony.
Don't trust a course on phylogeny that resides on a medical center web page.


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Does regulate always mean suppress when it comes to heteroreceptors?
Do heteroreceptors always suppress the release of the neurotransmitter they regulate upon their (the heteroreceptor's) activation?


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Why are bacteria and archaea in different domains?
As I understand it, the main difference between the Bacteria and the Eucaryota domains are that eukaryotes have a nucleus and bacteria don't. I understand that bacteria and archaebacteria have enough of a genetic difference to be separate kingdoms, but why are they separate domains?

It is told that archaea (former archaebacteria) though showing prokaryotic cells like bacteria (former eubacteria) ; archaea have more evolutionary affinity with eukaryote (eukaryote's main cell, i.e. excluding chloroplast and mitochondria) instead bacteria(former eubacteria).

The reason that Archaea were determined to be a separate (and only the third) kingdom so late (1977 according to this reference) was because archaea often completely resemble eubacteria.  They are unicellular and have no organelles and appropriately they were grouped with other prokaryotes because of their morphology and cellular physiology.
But by the 1970s phylogeny becoming based on the sequence of DNA and RNA which were just becoming more available.  Based on a simple comparison of the sequences of 18S rRNA of 13 fungi, bacteria and archaea, Woese and Fox showed that the bacteria and the archaea were about as different from the eukaryotes than from the bacteria.  (see table 1).
Since then, the differences between bacteria and archaea have continued to be great.  The wikipedia diagram below is not to scale- the divergence of the three kingdoms is so far back that they pre-date the emergence of eukaryotes entirely. But you can see that fungi and other eukaryotes are more similar to archaea than the bacteria.
BTW, the idea that archaea are extremophiles is not entirely true - they are pretty much exclusively the only kingdom found in these conditions, but archaea have been found to coexist with bacteria and eukaryotes in the open sea and their detection heretofore in most environments may be only due to the fact that archaea are difficult to grow in the lab.
Just found this retrospective from Woese himself, who passed away recently.

I think the three kingdoms are prokaryotes/bacteria, eukaryotes and archaea...

Wikipedia entry for Archaea has a heading Relationship to other prokaryotes. Wikipedia entry for Prokaryote has: The division to prokaryotes and eukaryotes reflects two distinct levels of cellular organization rather than biological classification of species. Prokaryotes include two major classification domains: the bacteria and the archaea.


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Why are eggs "egg" shaped?
Is there a reason as to why chickens lay "egg" shaped eggs, as opposed to spherically shaped eggs (or a random shape)?
For extra points:

why do plant seeds often come in this same "egg" shape (e.g. avocado
seeds), as opposed to a sphere?  Is it a coincidence that avocado
seeds and eggs are the same shape?

There is variance in egg shape; sea-birds often use a more pear or conical shaped egg to prevent it from rolling off the cliff (where they nest) if it is disturbed. Some reptiles lay very spherical eggs (some turtles) whereas some reptiles lay very elongated ones (see black pine snake eggs).
I imagine that we don't see square eggs because they would be difficult to shape and difficult to lay. Shape may also influence strength.
Google your question (like I did after writing the above) and it will come up with this article which pretty much says what I just did. Here are some of the author's key points...

"If eggs were rectangular little boxes, they would be very strong on the corners, but very weak in the middle of the straight walls."
"The strongest shape of all is a ball, or sphere. But if you were to push or gently nudge a spherical egg, it would roll away downhill, never to be seen again."
"So one reason that eggs have an asymmetric tapered oval shape is that if you nudge them, they'll come back to you. They'll sweep out a circle around the pointed end, and come to a stop with the pointed end facing uphill. In fact, the eggs of birds that have their nests on cliffs are more oval than the eggs of birds that nest on the ground. This means the 'more-oval' eggs of these cliff-nesting birds will roll in a very tight little circle, and be less likely to roll out of the nest — and off the cliff."
"Another reason for eggs to be egg-shaped is that they fit together quite snugly in the nest, with only small air spaces between them. "
"Yet another reason that eggs are tapered is so that they can get pushed out of the hen."

An interesting study on egg shape: http://vis.sciencemag.org/eggs/

Wasn’t it Ken Dodd who said the ohh-argh bird laid square eggs?? :)

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


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Do octopuses have better eyes than humans?
I've read that unlike humans, octopuses have eyes "designed" the "right way", i.e. with the nerve fibers behind the retina, thus getting rid of the blind spot we humans have as well as theoretically improving eyesight.
Have there been tests to compare octopus sight with that of humans, and do they indeed have better vision than us?

I'd suggest adding the tag "cephalopods".

Why would removing the blind spot result in better vision?

the blind spot perhaps not, (although it could come in ahndy if the eyes are on the side of your head and not in front), but mostly one would think that the lack of nerve fibers would somehow improve resolution, vision in dim light, etc.

But octopus do not have fovea - so no more keen vision! They may have more photoreceptors , but they have no more complex brains than humans - the brain behind the eye is more important than eye itself.

monkey eyes can move so fast as to examine 10 branches and stems every second while they jump through the trees with awesome focus and positional mapping. chimps eyes have positional mapping for tree climbing that is 10x faster than human eye movement, so eyes have specializations for fine movement, distance, speed, narrow, wide, all very refined. eyes and ears are extremely advanced and perfected for the given environment. animal's primary senses are normally very near to perfection for their actions and needs. probably octopi trade range of eye movement for a more fixed structure.

There are a couple of advantages and disadvantages of possessing the eyes of octopuses.

The first advantage of the octopus eye is that it has no blind spot. This means that octopuses can see everything that is going on in their environment, and are more aware of predators and prey than some vertebrates. Also, they have many more photoreceptors than vertebrates, at roughly 20,000-50,000/mm2 which means that their vision is much better than that of any human.
The disadvantage of the octopus eye is that it can not see in colour. The eyes possess no cones, only the invertebrate equivalent of rods. This means that  octopuses can only distinguish between light and dark.

So if a diver and an octopus where to be threatened by a shark, the octopus would see the shark first?

Of course it depends, As I cleared above both have some advantages and disadvantages. So, It's completely depends. But In some manner of course the Octopus will see the Shark first because they didn't have blind spot so their field of view is more than a common person.

Nice answer, +1. Do you have a reference for the photoreceptor claim?

"Like other cephalopods, they can distinguish the polarization of light. Color vision appears to vary from species to species, being present in O. aegina but absent in O. vulgaris." - http://en.wikipedia.org/wiki/Octopus#Sensation

Would the blind spot matter? The respective blind spots of the two eyes don't overlap, so unless you are a pirate (I suppose a frequent victim of sharks), you will still see all the things in either of your blind spots, there will just be two small spots in your FOV where you don't have depth perception.

In terms of the number of photoreceptors; that may only benefit light sensitivity and not visual acuity dependent on the connections with the secondary neurons. The blind spot in humans is mitigated by binocular vision.

Adding to the answer above, another advantage of cephalopod eyes is the lower risk of retina detachment. (HumanEvolution)
Also, cephalopod eye focus image by moving the lense (like a camera or telescope), not by changing the lense's curvature, as in vertebrate eye (Wiki). Hence, I speculate that cephalopod would not experience either myopia or hyperopia. Cephalopod may still have problem with presbyopia at old age, affecting both near and far vision, however.
Furthermore, this article comparing human and cephalopod eyes might be of interest: QuarkPhysics

I thought presbyopia would not affect cephalopods. In vertebrates it's due to the lense becoming stiffer with age so it can't change shape, but as you say this is not how cephalopod eyes focus.

Ah, I mean if the muscles that move the eyes are not working properly when the animal ages, cephalopod would suffer presbyopia as vertebrates do.

Thanks, that's a good point (although I have no idea if old octopusses suffer a similar kind of muscle stiffness as humans, there's probably a lot more here that we don't know!).


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What is the difference between average and monoisotopic mass calculations of peptides?
I often have to calculate the mass of peptide sequences using calculators such as here.
I have the option of calculating the average and monoisotopic mass, but what is the difference?

The elements that typically make up peptides and proteins can be present in different isotopes. For example, carbon is present to 98.9% as $\ce{^12C}$, and to 1.1% as $\ce{^13C}$.
The monoisotopic mass assumes that every element is present in the most abundant isotope, the average mass uses the actual distribution of the isotopes in nature.
If you have sufficient resolution in your mass spectrum you can see multiple signals corresponding to different isotope compositions of your molecule.


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Can the mating of a couple with Rhesus positive and negative blood types result in miscarriage?
Can the combination of $+ve$ and $-ve$ blood groups of a couple be a cause of miscarriage in pregnancy?

I have added the qualification of Rhesus to the question, without which it is incomplete. Anyone can suggest an edit to a question. Please do so if you want to improve this SE.

I want to know can +ve and -ve blood group of a couple could be a cause of miscarriage in pregnancy?

Yes. In extreme cases, it can. You are talking about Rh Incompatibility, and can become a big issue when the mother has Rh(-) blood and the father has Rh(+) blood (such as the case with your cousin and his wife).
What could have happened (but definitely won't say for sure) is that your cousin's wife had a natural miscarriage which exposed her to the Rh proteins of the child, and then the subsequent pregnancy had complications due to the previous exposure and mother's development of antibodies which lead to the second miscarriage. However, I am not a licensed physician and you should consult a physician before pursuing any sort of treatments!!!
Rh factor is the presence of surface proteins on Erythrocytes (Red Blood Cells or "RBC"). If Leukocytes (White Blood Cells - most commonly reported as "T-cells") encounter Erythrocytes that do not share the Rh factor of their host, then they can develop antibodies to it - which help identify Antigens (foreign proteins and molecules). Once the Antibodies have been generated the Immune System can attack any foreign Erythrocytes.
In this way, the mother's Immune System can actually attack the RBCs of her child.
You can find out more here: http://kidshealth.org/parent/pregnancy_center/your_pregnancy/rh.html
And a few select quotations:

Rh incompatibility usually isn't a problem if it's the mother's first pregnancy because, unless there's some sort of abnormality, the fetus's blood does not normally enter the mother's circulatory system during the course of the pregnancy...
...Other ways Rh-negative pregnant women can be exposed to the Rh protein that might cause antibody production include blood transfusions with Rh-positive blood, miscarriage, and ectopic pregnancy...
...Rh antibodies are harmless until the mother's second or later pregnancies. If she is ever carrying another Rh-positive child, her Rh antibodies will recognize the Rh proteins on the surface of the baby's blood cells as foreign, and pass into the baby's bloodstream and attack those cells. This can lead to swelling and rupture of the baby's RBCs. A baby's blood count can get dangerously low when this condition, known as hemolytic or Rh disease of the newborn, occurs.*

And you are correct that there is a treatment via injection, but the Doctor is also correct in that administering it past the first pregnancy does little for future fetuses:

Today, when a woman with the potential to develop Rh incompatibility is pregnant, doctors administer a series of two Rh immune-globulin shots during her first pregnancy. The first shot is given around the 28th week of pregnancy and the second within 72 hours after giving birth. Rh immune-globulin acts like a vaccine, preventing the mother's body from producing any potentially dangerous Rh antibodies that can cause serious complications in the newborn or complicate any future pregnancies.

And the ultimate effects of missing the shots and having very unfortunate luck:

Rh incompatibility rarely causes complications in a first pregnancy and does not affect the health of the mother. But Rh antibodies that develop during subsequent pregnancies can be potentially dangerous to mother and child. Rh disease can result in severe anemia, jaundice, brain damage, and heart failure in a newborn. In extreme cases, it can cause the death of the fetus because too many RBCs have been destroyed.

Is there a cure? No. Once the antibodies have been developed, the Rh(+) protein is known to the mother's Immune System. Nothing short of wiping out the mother's Immune System would act as a cure.
However, in extreme cases, there are treatments:

If a doctor determines that a woman has already developed Rh antibodies, then the pregnancy will be closely monitored to make sure that those levels are not too high. In rare cases, if the incompatibility is severe and the baby is in danger, a series of special blood transfusions (called exchange transfusions) can be performed either while the baby is still in the uterus or after delivery.

But don't fret yet!
Rh surface proteins are determined by genetics, and each time a child is conceived there is a chance that the Rh protein will be (-) if the exact genotype of the (+) parent allows it. So if your cousin's wife were to get pregnant again (and each time she does) it's a chance that the Rh Incompatibility (aka - "Hemolytic Disease", aka - "Rhesus Disease") won't show up.
So there are some reasons to stay positive.

I would add one more thing - generally the longer they wait before trying again, the better chances fo a Rh+ foetus. Memory cells slowly die and in my country 5 years after last pregnancy with problems a Rh- woman's pregnancy is considered normal risk. Still - a specialist will tell you more and help your sister.

Ehh... Memory cells do slowly die, but they can last for up to 40 years. Though if the response wasn't strong to begin with, I suppose the level of CD4 cells could be relatively low.

As an addition it's worth pointing out that the timing and number of Anti-D antibody injections given to the mother varies, in the UK I believe it is at 28 and 34 weeks during pregnancy, soon after delivery then regular injections until the Kleihauer test comes back negative for foetal cells in the mother's bloodstream.

Sometimes If the pathology (Rh incompatibility) was diagnosed, the hormone progesterone is applied, functioning as a protection for the embryo and preventing pregnancy loss. Anyway, you should consult a physician first.

To add a more concise answer:
Yes, the conflict between positive and negative Rh (Rhesus) blood groups can cause miscarriage.
The genetic makeup decides whether red blood cells (RBC) carry a specific surface protein known as Rhesus factor (Rh). If your own RBCs do not carry this protein (Rh-), your body will consider it (or RBC carrying it) a foreign substance and treat it like anything foreign - the immune system will respond and eliminate it, just like an infection.
If a Rh- mother has a child whose RBC are Rh+ (which is possible even if only one parent was Rh+), the mother's body will develop an immune response against the baby's blood itself.
This includes the immune response's memory: just like it remembers the "fake" infection from a vaccine to protect against a real disease, the immune system will remember the Rhesus protein, so if future pregnancies develop babies with Rh+ blood, the reaction will be more severe.
See also Wikipedia on the Rh factor and Miscarriage due to Rh factor.


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Evolutionary explanation to why we have such large memory capacities?
The scientific consensus is that no one ever fills up their memory capacity by learning facts and so on, even in the information age.  My question is therefore, is there an evolutionary reason as to why we have evolved to have such large memory capacities, when we never come close to filling it up?

@Chris didn't you answer your own question in a way? if we did use our entire memory capacity, that might provide evolutionary pressure to select organisms with greater capacity. that's just speculation on my part though.

@JeffZemla, what you say makes sense, but we would evolve to have memory capacities that we would only just not be filling up.  But we evolved our memory capacities thousands of years ago when there was much less to remember than today, and even in the information age of today, we still don't come close to using it up.

See my comment here, increased memory (or at least brain and head size) has a cost. Vaguely, I think that the processes that led to our abnormal intelligence may have led to high memory as a side effect.

"But we evolved our memory capacities thousands of years ago"  RED FLAG

We don't have large memory capacities.
If anything I would have asked the opposite, why is our memory so bad and unreliable considering how large our brains are. Even with this gigantic brain we struggle to remember a few phone numbers. Here's how our short term memory compares to monkeys: https://www.youtube.com/watch?v=zsXP8qeFF6A&ab_channel=BBCEarth . I have no explanation as to why humans are so bad at this, this amount of data should be nothing for a brain of our size.
As for long term memory, I'm not really convinced it is that large really, it seems to me people in general in ten years.. have forgotten pretty much everything. Occational glitch.. occational stuff, and even that is usually vague and full of wrongs.
And when people cram for exams.. take the best students ten years later and see how much they still remember, it will be just a tiny fraction.
What do you mean by "filling up their memory capacity"?
Are you expecting some sort of a state where the persons hard disk is full and nothing.. nothing new can be learned? That state doesn't make any sense, the brain is always deleting from memory plus it would make more sense to have the memory slowly deteriorate, rather than fall off a cliff into no functionality at all.
We don't remember anything. We always feel like we are going to remember the now for so long and all but we don't. And we have this bias because we don't remember what we don't remember, which is nearly everything.

Can you summarize the contents of the youtube link? That video is not accessible (it's a good practice to summarize links even if this were not the case).