Which algae grow fastest under optimal conditions? I'm interested in what the fastest growing microalgae are under optimal conditions for photoautotrophic growth (energy from photosynthesis only).  Fastest can be interpreted as either shortest doubling time, or maximum biomass yield per day per unit area.

Many of the algae investigated for biofuels are fast-growing, for example Nannochloropsis and Ankistrodesmus.  There are many publications that give yields in pond culture or in outdoor photobioreactor, for example Nannochloropsis at 20g/m^2/day (dry mass).  However it is not as common to see yields for lab photobioreactor (axenic, possibly with continuous illumination, and all other conditions optimized for fast growth).  I'm mainly interested in what family of algae would be evolved for fast growth, and where they may be found in nature.

EDIT As one of the answers pointed out, algae can grow heterotrophically as well and that may not be a fair comparison.  I changed the question to be about autotrophic growth (from photosynthesis) only.

The answer to your question depends on many variables. To narrow down the list of possible species it might be helpful to list under which conditions you intend to grow this algae and whether you want to give an additional carbon source such as glucose or acetate.

To give you an idea why this is important: the fastest growing alga I have ever worked with is Chlorella sorokiniana with double timings in the range of two hours. However this was in acetate containing medium and it would not have relied a lot on photosynthesis to grow nor would this make a lot of sense in open pond cultivation systems.

In terms of photoautotrophic algae, we have seen the most consistent quick growth (OD) in our system (Algem photobioreactor) for Dunaliella species. But this is based more on experience than rigorously testing a lot of species. In general there also seems to be a correlation between size and growth speed. Some cyanobacteria have a growth rate of around two hours Article


Why don't chilli peppers taste as hot in space? The following commentator writes:

  Chili peppers don’t taste as hot in space as they do on Earth. Nobody knows why.

We know that the 'hot' feeling of chilli peppers is caused by Capsaicin. We read:

  Capsaicin inside the pepper activates a protein in people’s cells called TRPV1. This protein’s job is to sense heat

There appears to be some question about the cause of the 'spicy' taste of chilli peppers.

My question is: What is the reason that chilli peppers don't taste as hot in space?

TL;DR

All food taste bland in space, not only chilli.

The claim in that tweet ("Chili peppers don’t taste as hot in space as they do on Earth") is not exactly correct because, the way it's worded, it gives the impression that only chilli peppers have a different taste. In fact, astronauts/cosmonauts use more chili and other spices than they regularly do on Earth, for a reason: they say that food in space (microgravity) taste bland. All food, not only chili.

Since the beginning of space flight, astronauts report that food taste different in microgravity. According to the Scientific American article When It Comes to Living in Space, It's a Matter of Taste (Romanoff and Romanoff, 2017):

  Many said that flavors are dulled and they crave fare that is spicier and considerably more tart than they would prefer on Earth.

So, due to the food tasting so bland, astronauts in fact use more chili and other spices than they normally do on Earth:

  It's possible that hot sauce and salsa could be key ingredients to the success of a manned mission to Mars. The kicked-up condiments already came close to causing a mutiny on the International Space Station (ISS) in 2002 when astronaut Peggy Whitson threatened to bar entry to the crew of the visiting shuttle Atlantis unless they came bearing a promised resupply of the spicy stuff. Only when shuttle commander Jeff Ashby announced that he had the goods did Whitson say, "Okay, we'll let you in then." Whitson was joking, but the need for astronauts to be able to  spice up their food while in orbit is no laughing matter.

However, it's still unknown why food taste bland in microgravity. Also, there is no consensus about that fact, to start with:

  There's little scientific data to back up astronauts' claims that taste changes in space, despite a number of studies since the 1970s on the effect of microgravity on the sense of taste and smell. In essence [...] study participants were split on the matter.

For those that report a change in the taste, some hypothesis were proposed:

  One of the most prominent physiological changes associated with spaceflight has to do with fluid shifting from the lower to the upper parts of the body because of weightlessness. This facial and upper-body swelling also creates significant nasal congestion, and because odor is essential to the sense of taste, a decrease in the perception of flavors would occur.

And also:

  The shuttle has a "sterile" smell, which when combined with other odors, such as the scent of their rinse-free shampoo, can be somewhat distracting.

However, there is little scientific evidence supporting this fluid-shifting hypothesis. According to Vickers et al. (2001), reproducing that fluid-shift in a simulated microgravity, where people had a head-down bed rest, has no effect on the threshold sensitivity of tastants. The same lack of changes in the taste and smell sensitivity under simulated microgravity was found by Olabi et al. (2002).

Despite that, this fluid-shifting hypothesis is supported by NASA (Nasa.gov, 2017) in an educational resource for kids:

  From the early 1960s, astronauts found that their taste buds did not seem to be as effective when they were in space. Why does this happen in space? This is because fluids in the body get affected by the reduced gravity conditions (also called fluid shift). On Earth, gravity acts on the fluid in our bodies and pulls it into our legs. In space, this fluid is distributed equally in the body. This change can be seen in the first few days of arriving in space when astronauts have a puffy face as fluid blocks the nasal passages. The puffy face feels like a heavy cold and this can cause taste to be affected in the short term by reducing their ability to smell.

The same source says:

  When food seems to lose its flavor, astronauts usually ask for condiments, such as hot sauces, to give food some intensity of taste. A variety of condiments are available for the crewmembers to add  to their food such as honey, and sauces like soy sauce, BBQ, and taco. (emphasis mine)

Conclusion

For reasons yet unknown, it seems that all food (not only chilli peppers) taste bland in microgravity. To cope with that, astronauts rely on chili and other hot spices.

Sources:

Romanoff, J. and Romanoff, J. (2017). When It Comes to Living in Space, It's a Matter of Taste. [online] Scientific American. Available at: https://www.scientificamerican.com/article/taste-changes-in-space/ [Accessed 26 Dec. 2017].
Nasa.gov. (2017) [online] Available at: https://www.nasa.gov/sites/default/files/files/Taste-in-space-TLA-FINAL.pdf [Accessed 26 Dec. 2017].
VICKERS, Z., RICE, B., ROSE, M. and LANE, H. (2001). SIMULATED MICROGRAVITY [BED REST] HAS LITTLE INFLUENCE ON TASTE, ODOR OR TRIGEMINAL SENSITIVITY. Journal of Sensory Studies, 16(1), pp.23-32.
Olabi, A., Lawless, H., Hunter, J., Levitsky, D. and Halpern, B. (2002). The Effect of Microgravity and Space Flight on the Chemical Senses. Journal of Food Science, 67(2), pp.468-478.


Darwin's views on Lamarckian Heredity? Currently I'm reading She Has Her Mother's Laugh: The Powers, Perversions, and Potential of Heredity, a fascinating book about heredity by the popular science author Carl Zimmer.
While reading this I came across this following passage, which bothers me.

It also meant that the inheritance of acquired traits - taken as a fact by Hippocrates, Lamarck, and Darwin alike - was impossible.
~ Chapter 2: Traveling Across the Face of Time

I've read Darwin's The Origin of Species, and a fair bit of other stuff on Evolutionary Biology, and as far as I know Darwin clearly opposed the idea of Lamarckian heredity. Which is why I was quite surprised to see this, from Zimmer, who's a very highly reputed author. How can he make such an obvious mistake, or is there something more to it than I know? Did Darwin ever agree with some form of Lamarckian heredity?
EDIT
Here's the passage of the book where it appears, for context.

I wrote to Carl Zimmer, and he replied within two hours. That's pretty cool!

So I thought I'd put everything I learned about this here as an answer with all the links, and if you guys have more to add, feel free to post more answers.

My Original Email:

Currently I'm reading She Has Her Mother's Laugh, which is a fascinating book, and I'm thoroughly hooked. However, while reading it, I came across this passage that troubled me. The bit in question is in Chapter 2: Traveling Across the Face of Time.

  "It also meant that the inheritance of acquired traits - taken as a
  fact by Hippocrates, Lamarck, and Darwin alike - was impossible."

From what I've read on the subject over the years, almost unanimously people agree that Darwin opposed the idea of Lamarckian heredity. I thought that Darwin's idea is that small modifications arising from random mutations (although he didn't know about DNA and genes at the time), if beneficial, were retained and accumulated over the generations resulting in new species. But is it not the case? Did actually Darwin subscribe to the idea of Lamarckian heredity?

I did a little bit of research on this, and found some conflicting and confusing information.

To start with, I've read Darwin's Origin of Species and though I remembered him opposing the idea, so I searched through the book again and found the following para.

  Thus, as I believe, the wonderful fact of two distinctly defined
  castes of sterile workers existing in the same nest, both widely
  different from each other and from their parents, has originated. We
  can see how useful their production may have been to a social
  community of insects, on the same principle that the division of
  labour is useful to civilised man. As ants work by inherited instincts
  and by inherited tools or weapons, and not by acquired knowledge and
  manufactured instruments, a perfect division of labour could be
  effected with them only by the workers being sterile; for had they
  been fertile, they would have intercrossed, and their instincts and
  structure would have become blended. And nature has, as I believe,
  effected this admirable division of labour in the communities of ants,
  by the means of natural selection. But I am bound to confess, that,
  with all my faith in this principle, I should never have anticipated
  that natural selection could have been efficient in so high a degree,
  had not the case of these neuter insects convinced me of the fact. I
  have, therefore, discussed this case, at some little but wholly
  insufficient length, in order to show the power of natural selection,
  and likewise because this is by far the most serious special
  difficulty, which my theory has encountered. The case, also, is very
  interesting, as it proves that with animals, as with plants, any
  amount of modification in structure can be effected by the
  accumulation of numerous, slight, and as we must call them accidental,
  variations, which are in any manner profitable, without exercise or
  habit having come into play. For no amount of exercise, or habit, or
  volition, in the utterly sterile members of a community could possibly
  have affected the structure or instincts of the fertile members, which
  alone leave descendants. I am surprised that no one has advanced this
  demonstrative case of neuter insects, against the well-known doctrine
  of Lamarck.

If you read the last few sentences, Darwin says "accumulation of numerous, slight, and as we must call them accidental, variations,..." which to me indicates he's referring to random mutations in genes even though he didn't know what genes were. Furthermore, a little later, "For no amount of exercise, or habit, or volition, in the utterly sterile members of a community could possibly have affected the structure or instincts of the fertile members, which alone leave descendants." and "I am surprised that no one has advanced this demonstrative case of neuter insects, against the well-known doctrine of Lamarck."

To me this clearly indicates he was opposed to the idea of Lamarckian heredity. Could you please explain a little bit more about your stance? I'd love to hear the different viewpoint and the reason(s) behind it.

Since I was curious about this, I posted the same question on StackExchange biology forum.

One of the users pointed me to an article by Michael T. Ghiselin who seems to be in agreement with you regarding the matter.

While some of his points about textbook authors misunderstanding Lamarckian heredity sounds fair and valid, I can't quite see how he came to the conclusion that Darwin agreed with Lamarck. The passage he points to (Lamarck was the first man whose conclusions ...") doesn't say anything about Darwin agreeing with Lamarck about acquired traits being passed down the generations.

In Wiki page about Pangenesis, the following is mentioned just as you have in your book.

  "Darwin thought that environmental effects that caused altered
  characteristics would lead to altered gemmules for the affected body
  part. The altered gemmules would then have a chance of being
  transferred to offspring, since they were assumed to be produced
  throughout an organisms life.2 Thus, pangenesis theory allowed for
  the Lamarckian idea of transmission of characteristics acquired
  through use and disuse. Accidental gemmule development in incorrect
  parts of the body could explain deformations and the 'monstrosities'
  Darwin cited in Variation."

Which indeed supports your viewpoint, but to me that seems like a direct contradiction to Darwin's own words in Origin of Species.

So which of it is true? Or, since Pangenesis theory came after he published Origin, did he change his mind later?

Carl Zimmer's reply:

  Thanks for your email. I've also had to struggle to work out Darwin's
  views about Lamarck--they were complicated and changed over his
  career. Basically, the more Darwin thought about heredity, the more he
  warmed up to the possibility of the inheritance of acquired
  characters. I've attached a few good papers that may be of interest.

  Best wishes, Carl Zimmer

Papers Referred by Carl Zimmer:

Gemmules and Elements: On Darwin’s and Mendel’s Concepts and Methods in Heredity.

Lamarck, Evolution, and the Inheritance of Acquired Characters.

orgThe Early History of the Idea of the Inheritance of Acquired Characters and of Pangenesis.

I haven't read those papers yet, will do so when I find time and hopefully it will shed some more light on it.

So, I'm still not quite sure about the issue, but I do think Carl Zimmer's point of view is fair enough, that it is possible Darwin's views evolved over time. Particularly, given that nobody knew what exactly even heredity means at the time, it's possible that Darwin thought it cannot just be ruled out. Besides doesn't seem like he was out campaigning for the idea, rather allowed for it with his Pangenesis hypothesis.

After all, Darwin's theory was about how small modifications accumulated over time leads to species change, not how those changes occurred in the first place. So, while it turned out to be untrue, if there was a mechanism in which experiences could be stored in the unit that transmitted heredity, you can probably incorporate that into Darwin's theory of evolution. That probably was a line of thought Darwin had.


Are there phage-eating bacteria? If phages (bacterium-eating viruses) prowl on bacteria, are there bacteria (or other micro-organisms) that hunt phages for food? They are rich in proteins anyway... Are there studies on this subject? Thanks

It's suspected that some protists (namely choanozoans and picozoans) are proper/direct "virus eaters" due to the size of their "eating apparatus" and scarcity of bacterial remains inside them (unlike viral remains), but the evidence is pretty recent; the (2020) study:

used modern single-cell genomics tools to sequence the total DNA from 1,698 individual protists in the water. Each of the resulting Single Amplified Genomes (SAGs) consists of the genome of a single protist, with or without associated DNA: for example, from symbionts, ingested prey, or viruses or bacteria sticking to its exterior. The technique is very sensitive, but doesn’t directly show the type of relationship between a protist and its associates.
The researchers found a range of protists including alveolates, stramenopiles, chlorophytes, cercozoans, picozoans, and choanozoans. Nineteen percent of SAGs from the Gulf of Maine and 48% of those from the Mediterranean were associated with bacterial DNA, suggesting that these protists had eaten bacteria. More common were viral sequences, found in 51% of SAGs from the Gulf of Maine and 35% of those from the Mediterranean, with a frequency of 1–52 virus types per protist. Most were from viruses known to infect bacteria – presumably representing parasites of the protists’ bacterial prey.
But choanozoans and picozoans, which only occurred in the Gulf of Maine sample, were different. These groups, neither of which have chloroplasts, are poorly known. Choanozoans (3–10 µm; also known as choanoflagellates), are of great evolutionary interest as the closest living relatives of animals and fungi. The tiny (up to 3 µ) picozoans were first discovered twenty years ago and originally known as picobiliphytes. Until now, their food sources were a puzzle, as their feeding apparatus is too small for bacteria – but ample for viruses, most of which are smaller than 150 nm.
Every single one of the choanozoan and picozoan SAGs were associated with viral sequences from bacteriophages and CRESS-DNA viruses, but mostly without any bacterial DNA, while the same sequences were found across a great diversity of species.
“It is very unlikely that these viruses are capable of infecting all the protists in which they were found,” says Dr Julia Brown, a researcher at the Bigelow Laboratory for Ocean Sciences and coauthor on the study.
The authors conclude that choanozoans and picozoans probably routinely eat viruses.

The news release also says that how these "virus eater" protists manage to protect themselves against viral infection isn't yet known/studied.
If this needs saying... protists (unlike bacteria) are eukaryotes. I haven't found any source suggesting that any prokaryotes (bacteria or archaea) manage to sustain themselves on viruses.


What actually are thoughts? The human brain consists of neurons that transmit impulses like wires that conduct electricity.I am confused about where are our thoughts stored and what really are thoughts? For example if I think about space, what is actually happening in my brain, and in what form is my memory that there are black holes in space, stored?

After doing a little bit of research I somehow came to the conclusion that thoughts are nothing but the electro-chemical reactions that are triggered by external stimuli and Hippocampus is responsible for storing long term memory. But I was unable to understand what the following paragraph means:

  "The hippocampus helps to solidify the pattern of connections that form a memory but the memory itself depends on the solidification of connections between the individual brain cells".

Please explain it. Am I correct so far? Please help.

The hippocampus helps to solidify the pattern of connections that form a memory but the memory itself depends on the solidification of connections between the individual brain cells".

This refers to the phenomenon called Long Term Potentiation which regulates synaptic strength between neurons. Certain patterns of firing (high frequency) causes the post synaptic neuron to strengthen the synapses. One way of doing that is by increasing the number of receptors (Usually NMDA receptors). Due to this, the response would be stronger in the next firing event. You can imagine its effects- more number of times you read a passage better will you remember it.

Hippocampus is involved in this process (it is one region where a lot of synaptic dynamics happens) but consolidation and long term storage of memories is handled by the cortex. Essentially what happens when a memory is formed is strengthening of synapses.


Can you be immune to a coronavirus? Can one be immune to the new coronavirus?

Another question is what is the exact definition of "being immune". Does it mean that even when the virus enters my system, it cannot multiply?

It is hypothesized that exposure to and recovery from SARS-CoV-2 (as with other coronaviruses in humans) would generally result in short-term immunity to this strain, but we do not yet have data on this:

However, according to Dr Stephen Gluckman, an infectious diseases physician at Penn Medicine and the medical director of Penn Global Medicine, who spoke to the outlet, it seems likely that having the disease once results in immunity in most individuals - as is seen with other coronaviruses.
“Coronaviruses aren’t new, they’ve been around for a long, long time and many species - not just humans - get them,” he explained. “So we know a fair amount about coronaviruses in general. For the most part, the feeling is once you’ve had a specific coronavirus, you are immune. We don’t have enough data to say that with this coronavirus, but it is likely.”
This means that people who initially recovered are more likely to relapse rather than get reinfected with the virus.
According to one study, people with mild infections can test positive for the virus by throat swabs “for days and even weeks after their illness”.
But, that doesn’t mean it isn’t possible to contract the disease again, especially in those who are immunocompromised.
“The immune response to Covid-19 is not yet understood,” the Centers for Disease Control and Prevention (CDC) explains. “Patients with MERS-CoV infection are unlikely to be reinfected shortly after they recover, but it is not yet known whether similar immune protection will be observed for patients with Covid-19.”

Coronavirus: Can You Get Covid-19 Twice Or Does It Cause Immunity?

It is also hypothesized (in humans) that previous exposure to coronaviruses may enable immunity to certain other highly related strains:

These data indicate that challenge immunity to coronaviruses is strong, but highly virus strain-specific.

Virus strain specificity of challenge immunity to coronavirus., Archives of Virology (1989)

But these are all examples of adaptive immunity - not innate.


Generate full dimer from monomer with C2 symmetry? I downloaded a PDB file of a dimer, but it only contains the monomer, and it says that the dimer can be obtained from C2 symmetry. For an example see here: http://www.rcsb.org/pdb/explore/explore.do?structureId=2PJY.

How can I generate the PDB for the full dimer?

I am comfortable with PyMol, so an answer using PyMol is preferred.

This article will probably be informative for you:
Looking at Structures: Introduction to Biological Assemblies and the PDB Archive

The PDB file contains the asymmetric unit found in a particular crystallographic study. The biological assembly is the quaternary structure known or predicted to be found in living systems. For many proteins (but not 2PJY), the biological assembly can be downloaded directly from RCSB. For other proteins, the PDB file may contain the transformation matrix used to create the biological assembly from the asymmetric unit. If you look at the file in a text editor, this information is found under remark 350:

REMARK 350 BIOMOLECULE: 1
REMARK 350 AUTHOR DETERMINED BIOLOGICAL UNIT: HEXAMERIC
REMARK 350 SOFTWARE DETERMINED QUATERNARY STRUCTURE: HEXAMERIC
REMARK 350 SOFTWARE USED: PISA
REMARK 350 TOTAL BURIED SURFACE AREA: 8880 ANGSTROM**2
REMARK 350 APPLY THE FOLLOWING TO CHAINS: A, B, C
REMARK 350   BIOMT1   1  1.000000  0.000000  0.000000        0.00000
REMARK 350   BIOMT2   1  0.000000  1.000000  0.000000        0.00000
REMARK 350   BIOMT3   1  0.000000  0.000000  1.000000        0.00000
REMARK 350   BIOMT1   2  1.000000  0.000000  0.000000        0.00000
REMARK 350   BIOMT2   2  0.000000 -1.000000  0.000000        0.00000
REMARK 350   BIOMT3   2  0.000000  0.000000 -1.000000        0.00000

Note that the actual biological assembly of 2PJY is a hexamer and the asymmetric unit in the PDB file is a trimer. You can see that the first matrix is identity (ie keeps the original asymmetric unit). The second matrix transforms the assymmetric unit to create the full hexamer. This matrix is both author and PISA predicted. You can actually go to the PISA website and have it predict the biological assembly of a particular PDB file, and it will spit out the coordinates of the hexamer (and other predicted assemblies) which you can then load into PyMOL.

PDB files may also contain a CRYST1 record, which gives information about the unit cell and space group of the crystal. Via the symexp command, PyMOL can use this information to recreate neighboring asymmetric units. By limiting the cut-off distance (and this requires trial-and-error), the biological assembly can be recreated. This script, for example, will generate the hexamer:

fetch 2PJY
symexp 2PJY, 2PJY, 2PJY, 2.5
hide everything
show cartoon


Can plants grow under extreme (>1%) carbon dioxide concentrations? Related to but distinct from this question due to the concentrations involved.

While small carbon dioxide concentration increases can positively impact plant growth under some circumstances and at the same time negatively affect it under other circumstances, these changes are relatively small (doubling CO2 from 0.04% to 0.08%).

Is there any research on plants grown at extremely high (>1%) carbon dioxide concentrations in the air, assuming Earth atomspheric pressure? For the purpose of this question, assume that the plants are supplied with pH modifiers such as limestone in the soil to prevent soil acidification.

Yes they can, but their normal growth is somewhat impaired. A study by Bugbee and collaborators showed that while the yield of rice and wheat increases with CO2 up to about 0.1% CO2, yield decreases sharply as CO2 climbs from 0.1% to 0.25%. There is a smaller loss in yield as CO2 is further increased from 0.25% to 2%.

One interesting thing to note about the study is that the above results turn somewhat on how "yield" is defined. Bugbee defines yield in terms of the mass of the parts of the plant that people can actually eat. They make a note in the study that the vegetative growth of the plants (the green leafy parts humans can't eat) was not affected by the jump from optimal to super-optimal CO2 levels.


Are clones less likely to be fertile? I know that hybrid animals like mules are infertile. What about clones? Do cloned animals show the same fertility as their original?

Cloned animals, at least in the first generation, are often subfertile and have lower viability than their progenitors. The reasons for this are complicated but often are related to epigenetic changes that lead to altered gene regulation.

Further reading:

  Although the technology of SCNT has been applied successfully by many research teams, some SCNT animals have abnormal or lethal phenotypes, including facial abnormalities, pulmonary hypertension [3], contracted tendons [9], low birth weight [10, 11], as well as distinct depigmentation of the skin and hair ... Based on previous studies, insufficient epigenetic reprogramming of somatic donor cells may result in phenotypic abnormalities in the offspring ...

--Dysregulation of genome-wide gene expression and DNA methylation in abnormal cloned piglets

  The epigenetic state of the ES cell genome was found to be extremely unstable. Similarly, variation in imprinted gene expression was observed in most cloned mice, even in those derived from ES cells of the same subclone. Many of the animals survived to adulthood despite widespread gene dysregulation, indicating that mammalian development may be rather tolerant to epigenetic aberrations of the genome.

--Epigenetic instability in ES cells and cloned mice.

  Because few clones survive to birth, the question remains whether survivors are normal or merely the least severely affected animals, making it to adulthood despite harboring subtle abnormalities originating from inadequate nuclear reprogramming ...  Our results suggest that many expression abnormalities are common to the NT procedure whereas some reflect the particular donor nucleus. These results further emphasize the severity of placental dysfunction and illustrate abnormalities in clones surviving to birth.

--Abnormal gene expression in cloned mice derived from embryonic stem cell and cumulus cell nuclei

  Although clone D had a poorer libido and entered puberty later than those of the other cloned male cats, he produced gonadal hormones within the average range. Four of the cloned male cats had normal fertility.

--Reproductive fertility of cloned male cats derived from adult somatic cell nuclear transfer.

(Note that this paper concluded that the cloned male cats had "normal fertility", but one of four (25%) had reproductive abnormalities (reduced libido and delayed puberty); the numbers are too small for anything definite but I would say this is evidence for abnormal fertility, not the reverse)

Some early papers do claim normal fertility of cloned mice, but those are simply based on the fact that the cloned mice could have offspring (i.e. were not completely infertile) and didn't actually compare fertility of cloned vs. "normal" laboratory mice.

Wakayama, T., Perry, A.C.F., Zuccotti, M., Johnson, K.R. & Yanagimachi, R. Full-term development of mice from enucleated oocytes injected with cumulus cell nuclei. Nature 394, 369–374 (1998).
Wakayama, T. & Yanagimachi, R. Cloning of male mice from adult tail-tip cells. Nature Genet. 22, 127–128 (1999).


Why does not the host produce any immune response to antiserum antibodies? When an antiserum is injected to a person to protect oneself from a certain disease, the antibodies in the antiserum come from another organism. The question is:

Why don't the injected antibodies cause an immune response in the individual?

That's a good question - because its certainly possible to get antisera against antibodies.

Sometimes antisera is actually human antisera, so there would be no rejection at all.  But that is for extreme cases, e.g. serum transfusions from convalescent Ebola survivors to current Ebola patients.

One would expect that you could only give an antiserum once and then it would be less effective each time you get it.  Since antisera to snakebites is the most common application, where its quite possible to be exposed to multiple bites over one's lifetime.

I found one reference to a horse antiserum treatment that's being used. It makes reference to a source of antiserum which sounds like its been designed to reduce the antibody antibody immune reaction:

  Horse-serum antivenin has been available since 1956; a purer antivenin with improved properties was released in 2000 (see Medication). With the reduced side-effect profile of antigen-binding fragment antivenom (FabAV) and the improvement in tissue injury with antivenin administration, the threshold for dosing is lower.

Even before the availability of these new treatments, its probable that most patients can endure multiple anti serum treatments from the same source animal.  Even goat, horse and rabbit antibodies are pretty similar to ours and the reaction will not be as strong, in addition to which, the immune system will tend to clear out the antigen-xenoantibody complexes from the blood.

I can't find references, but my guess is there must have been some cases of rejection and reaction otherwise they would not have bothered to improve the serum treatment.

Update: just read this little blurb in scientific american, that describes how venom antisera will occasionally cause deadly reactions, while most of the time simply disarming the venom.  The new generations of antivenoms described have the Fc portion of the antibodies removed.  This eliminates the adverse immune reaction but I also think also eliminates any immune resistance the patient might get out of the antisera.  The Fc portion of the antibody is the part which our immune cells bind to.  In this case the new antivenoms aren't anti sera exactly, but they do use the antibodies to deactivate the venom toxins and crosslink them to make them less effective.


Meiosis and combinations of chromosomes I was pondering about the genetics of siblings. It occured to me that a pair of biological brother and sister (not brothers or sisters) could inherit completely distinct sets of chromosomes from their parents, the mathematical probability being $\frac{1}{2^{46}}$.
This calculation is based on the assumption that each pair of chromosomes, upon meiosis, get separated independently of other pairs. Do you think I’m right about that? Has anyone looked into this matter? Could it be that a chromosome prefers to be accompanied by a specific chromosome (in a pair other than its own) during meiosis?

Edit: I only have a high school level understanding on this matter and I just realized that my speculation directly contradicts Mendel’s law of segregation. But as pointed out in the comment on the answer, some wiggly interaction might interfere with the assortment with some peculiar genes, although it doesn’t mean that some chromosomes are more fond of each other. Close the case.

It would be right if there were no recombination (see also crossing over) and no new mutations. However, there are crossover and there are mutations and hence the calculation is wrong.

Segregation

You have solved this problem yourself. You assumed that chromosomes segregate perfectly independently which is a rather sound assumption. The probability is $\frac{1}{2^{46}}$

Recombination

Assuming a genome-wide recombination rate of 22.8 (Wang et al. 2012) and assuming that the number of recombination is Poisson distributed, then the probability of no recombination is $e^{-22.8} ≈ 1.25\cdot 10^{-10}$.

Multiply this number by $\frac{1}{2^{46}}$ and you get about $1.8 \cdot 10^{-24}$. I would note however, that the assumption that the number of crossover is Poisson distributed might not hold (even if it is how it is typically modelled)

Mutation

Now assuming a genome-wide mutation rate of 45 (Rhabari et al. 2016), and assuming that the number of mutations is Poisson distributed, then the probability of no mutation to happen is $e^{-45} ≈ 2.9 \cdot 10^{-20}$.

Hence the probability becomes $\frac{1}{2^{46}} \cdot e^{-22.8} \cdot e^{-45} ≈ 10^{-44}$.

Note that we assumed that the number of mutations and the number of crossovers are independent which is definitely wrong. If we were to know the correlation, we could make better estimates. This would bring our estimate to some higher probability.


How to correctly and accurately identify a few species of trees from their leaves? I want to identify a tree from one of the 12 species listed based on observing their branch and leaves. Is there quick and neat way to do it?

Red Oak, White Oak, Red Maple, Striped Maple, Tulip Poplar, Black Cherry, White Pine, Virginia Pine, Dogwood, Hickory Species, Sourwood and Cucumber Magnolia.

Thank you!

A good first step is to pay attention to common differences between tree structure:

1. Alternate vs. Opposite structure

MADHORSE = your common eastern US opposite-leaved trees are Maple, Ash, Dogwood, and Horsechestnut (AKA buckeye).

2. Simple vs. compound leaves

3. Toothed ("entire") vs. untoothed leaves

4. Lobed vs. unlobed leaves

5. Differences in texture, hairiness, & color of leaves

both b/w species and b/w top/bottom of leaves of the same species

Generally when you come across a new tree in Eastern N. America I'd recommend going through these steps:

Is it alternate or opposite?
Is it simple or compound?
Is it toothed, doubly-toothed, or smooth along the edge?

If you can answer yes to (any or all of) those questions you typically SIGNIFICANTLY reduce your options.

You also want to make sure you're aware of large variations in some species (especially oaks and hickories). One good example is the difference in shape, texture, and color of sun leaves vs. shade leaves of many species.

Importantly, paying attention to WHERE the tree is located (and what else is growing around it) as this can really help narrow your choices. You'll also start recognizing common cohabitants of certain regions.

Finally, don't be afraid to use your many senses (smelling, feeling and even tasting) -- though get to know poison ivy well before you start licking plants!!

Ok, now for some useful hints:

Red Oak = stereotypical oak shape, smooth on both side of leaf, lobes are not deep. You'll find 'spikes' at the end of each lobe. Bark looks like it has vertical shiny stripes.
White Oak = rounded SMOOTH lobes. Bark light grey/white with flaking appearance when mature
Red Maple = OPPOSITE. Leaves serrated (toothed). Smooth grey bark (with few low-hanging branches)
Sugar Maple = OPPOSITE. Leaves NOT serrated. Smooth whiter grey bark.
Striped Maple = OPPOSITE. Maple-like shape, but with rounded/butt-shaped (cordate) base. Bark = very striped in appearance.
Tulip Poplar = Leaf-shape looks like a tulip flower. Tree tall and straight.
Black Cherry = Oval/round leaves with fine single-toothing along edge. Tuft of brown/white fur along mid-rib on underside of leaf. Bark = horizontal striping due to lenticels; gets flaky when mature. Bark/twigs have strong bad smell when scratched (cyanide).
White Pine = 5 relatively long wispy needles per cluster.
Virginia Pine = 3 Short, dense needles per cluster.  Bark has cornflake appearance.
Dogwood = OPPOSITE. round leaf with deep ribbing veins and drip tip. Leaves often look to be growing in pairs. If you pull a leaf apart carefully, you'll find some thin tissues dangling between the halves. The bark is cobblestone (mosaic bumpy) and the shape of the tree is typically flat-umbrella-esque.
Hickory Species = VERY DIFFICULT TO TELL SPECIES APART (though I can give you a bunch of hints to help). Fairly easy to tell apart from other species, though. Is ALTERNATE + COMPOUND with generally 5-9 leaflets per leaf. (unlike ash = opposite/compound or walnut = compound with MANY leaflets). Leaves often carry some odor and large seeds can be found nearby
Sourwood = Long, oval, tiny-toothed leaves that have strong sunken midrib and thin leaf texture. Tastes very sour. Bark is dark and ridged, and trunks very rarely grow straight (so look for crooked or leaning trees!).
Cucumber Magnolia = Look for LARGE, strongly veined leaves that are often drooping. Look for circular ring (stipule scar) beneath leaf petiole base.


Can you consider a human as alive, or is it the cells on the body that are alive? Sorry if this question seems strange, but in the recent time I have been interested in the question of what life is and how you can define life.

My question:
How long can individual cells live on a human body from the point the human dies? When a human dies, legally he is dead, but how is the medical explaination? Can a human be partly dead, that the heart and brain has stopped, but the cells on the body are still alive?

When you talk about a human life, is it one life or could you consider each cell on the body as a living piece and the whole human body itself including the consciousness is just a container for the cells?

The definition of life is the main issue here. That is one of the great philosophical questions in Biology (and not only Biology) and is way beyond the simple Q&A format of this site. However, most definitions of life can be boiled down to1:

  A self replicating entity that interacts2 with its environment.

Or, even more simply [1]:

  Life is self-reproduction with variations

In both cases, the answer to your question depends on which level you are focusing on, your resolution if you like. If you take a human cell and apply either of the definitions above, it is alive. A cell is capable of autonomous reproduction, and metabolizes substances harvested from its environment. The same holds true of you look at the human body. However, the definition will not hold for a part of the human body, for example an arm or kidney.

Consider also that a human cell is capable of making more copies of itself, more individual cells. A human body is also capable of making more copies of itself, more human bodies. They can, therefore, both be taken as alive.

There are even more complex examples like Dictyostelium discoideum an amoeba that can exist (and be alive) either as a single cell or as a colony sporting different cell types and rudimentary organization. However, the organism is alive in both of these stages. In one case, you would consider the cell to be the fundamental unit of D. discoideum life, and in the other you could consider the colony.

So, to answer your question both a human cell (as long as it is alive, actively metabolising and capable of reproducing) and the entire human body can be taken as alive. That my cells are alive does not lessen the fact that I am too. It is just a matter of perspective.

References

Trifonov EN., Vocabulary of definitions of life suggests a definition. J Biomol Struct Dyn. 2011 Oct;29(2):259-66.

1 Yes, I know this is a simplification, I just don't want to be drawn in to a long winded discussion on what the definition of life is. My answer is applicable to any of them really.
2 Metabolism can be seen as a form of interaction.


The effect of depth on net primary production in aquatic ecosystems The figure shows the relationship between the water depth and net primary production (=P-R). I want to know why the production (P) initially increases with water depth near the surface? I have seen similar relationships from other sources but never seen a clear explanation.

After a quick glance at the book "Light and Photosynthesis in Aquatic Ecosystems" by Kirk (2010), I think that the cause for the productivity dip towards the surface partially lies in photoinhibition, due to high light intensities at the surface. Here are a couple of relevant quotes from the book (Google books: p. 371):

  In this light saturated state, the electron transport and/or CO2 fixing enzymes (most likely, the latter) are working as fast as they are capable, and so any additional absorbed quanta are not used for photosynthesis at all. From the end of the linear region through to the light-saturated region ([i.e. close to the surface, my addition]), since photosynthetic rate does not increase in proportion to irradiance, (P/Ed steadily falls, see Fig. 10.3) the quantum yield and conversion efficiency necessarily undergoes a progressive fall in value. This is accentuated further if, at even higher light intensities, photoinhibition sets in. If the cells contain photoprotective carotenoids, in which absorbed light energy is dissipated as heat rather than being transferred to the reaction centre...

However, the suspended bottle methods often used to estimate these depth gradients might be part of the problem, by overestimating the effect of photoinhibition, by forcing plancton to stay at the same depth (p 358):

  Depth profiles of phytoplancton photosynthesis, such as those in Fig. 10.4, determined by the suspended bottle method, tend to overestimate the extent to which photoinhibition diminished primary production. In nature, the phytoplancton are not forced to remain at the same depth for prolonged periods. Some, such as dinoflagellates and blue-green algae, can migrate to a depth where light intensity is more suitable. Even non-motile algae will only remain at the same depth for extended periods under rather still conditions.

I hope I got the quotes right (quick manual retyping). There are many more relevant sections in the book as well, which seems to cover all kinds of aspects of aquatic photosynthetic efficiency and how this can be a function of depth.


What is the cell matrix? What is the matrix in the cell, and how does it connect cells together?

I read about this in my textbook. I know that a matrix is the material (or tissue) that connects other cells together. My book says:

  In biology, matrix (plural: matrices) is the material (or tissue) in animal or plant cells, in which more specialized structures are embedded, and a specific part of the mitochondrion that is the site of oxidation of organic molecules.

This wording feels very complex, and I'm having trouble picturing what it's trying to describe.

The quote (which you more likely got from Wikipedia) discusses multiple types of matrices.

Let's break down the quoted definition:

The general definition of a matrix would be "an environment or material in which something develops; a surrounding medium or structure." In biology, we think of a matrix as a material, tissue or area in which more specialized structures (molecules, cells, organisms, etc.) are embedded.

In animals or plants, the matrix is often describing a material or tissue.

The nail matrix is the layer of cells that your fingernail or toenail sits on that actually produces the nail.
The extracellular matrix (or ECM) consists of a collection of extracellular molecules secreted by cells that provides structural and biochemical support to the surrounding [more specialized] cells. One very familiar example of "matrix" tissue is connective tissue.

Here's a video from Khan  Academy's Youtube channel to walk you through this a bit.  And here's a more graphical walk-through explaining extra-cellular matrices.

The cytoplasmic matrix (aka cytosol) is the liquid found within cells in which organelles reside. It constitutes most of the intracellular fluid (ICF)

The mitochondrial matrix, a type of cytoplasmic matrix, is the fluid within the inner membrane of a cell's mitochondria that splits it into numerous compartments. This viscous "space" contains the mitochondria's DNA, ribosomes, soluble enzymes, small organic molecules, nucleotide cofactors, and inorganic ions; it is also the site in which oxidation of organic molecules occurs.

So whats this look like under a microscope? Here's an image of a mitochondria and surrounding cellular cytosol under an electron microscope:

In ecology, a matrix is the general area in which your population, community, or habitat "patch" exists within. In other words, Matrix is the "background ecological system" of a landscape with a high degree of connectivity.


What is a "monomeric polypeptide"? In the sentence: "Bacteriophage (viral) polymerases are typically monomeric polypeptides".

I know that polypeptides are chains of amino acids monomers. But what is a "monomeric polypeptide" and what other kinds of polypeptides are there?

Monomer in this context means the protein has only one polypeptide chain. In some  proteins, after the individual chains have folded into their 3D or tertiary structure, they associate (generally non-covalently) into a higher order or quaternary structure. A protein with a quaternary structure containing  two copies of the same chain would be called a homo-dimer. One with one copy of each of two different chains is a hetero-dimer.

Haemoglobin is a well-known example of a protein with quaternary structure — it has two copies of the alpha- and two of the beta- chain. Further elementary treatment can be found in Berg et al. and explanation of the nomenclature in this Wikipedia page.

Monomeric polypeptide is somewhat misleading in the sentence quoted. Monomeric protein would have probably been better as you wouldn't be likely to say ‘dimeric polypeptide’, given that polypeptide implies a single chain.


why did capacity of regeneration decreased in evolution? When we consider trend of evolution the ability of organisms to regenerate decreased as the complexity of body structure increased.

acetabularia-can regenerate whole body even if 1/100th part of body is left
small pieces of sponges can grow complete individual.
hydra-interstitial cells are totipotent.
planarians-neoblasts are omnipotent
crustaceans-heteromorphosis.
lizard-regenaratetail..........what is the reason you expect for this ?

Evolution made life more and more complex. The more complex the "bodyplan" of an organism became, the more different tissues and cell types it has, the more difficult it is to regrow them.
For example a sponge has about 3 different cell types. If you take a small piece of a sponge, these 3 cell types well still be present and once they grow they can form a whole new sponge.
The more complex you go, the more different cell types you need, and thus the harder it becomes for a few cells to represent a full organism.

It also has to do with symmetry. Sponges have none, cnidarians have radial symmetry, mammals bilateral. To put it simple: if you slice a piece out of a jellyfish like you would out of a pie, it's easy to imagine it can 'close' itself with new tissue coming out of the border tissue, because it's the same tissue as the one you removed. If however you cut of a foot of a human, the cells of the leg won't produce new foot cells, because they are (a lot of different) 'leg cells'.

As for the lizards, they can "regenerate" a tail but it is never the same tail as before, it will always be shorter than the one they lost. Also the tail is still pretty 'simple' (if you can put it that way). If you would cut of a lizards leg it would not regrow...

I hope this has somewhat answered your question!


Finding a template/oligo combination for my first PCR experiment I'm an information technology engineer. I love biology so I research biological topics and have an interest in PCR. That's why I have decided to create a PCR machine.

Everything is done now and I want to do my first experiment to see if it works or not. I would be very happy if someone could give me any suggestions for testing it at home. Which oligo should I use for testing in the easiest way? I mean a template DNA for testing that is easy to find and extract.

You need a genome that isn't too complex, which suggests something microbial. You also need a genome that is well-characterised : either fully- sequenced, or with lots of sequenced genes to allow you to design primers. And finally you need a readily accessible source of material for DNA extraction.

I would suggest either dried yeast, as a source of Saccharomyces cerevisiae DNA, or live yoghurt as a source of DNA from Lactobacilli. You could even try culturing something from yoghurt to get pure bacterial colonies: since these would be from a food source there should be minimal risk.

You might be tempted by one of the traditional plant sources of DNA (e.g. onions) , but it can be tricky to avoid copurifying polysaccharides which inhibit DNA-related enzymes.

Finally, if you do culture some bacteria, or even if you use dried yeast, you probably wouldn't need to actually prepare DNA at all. PCR direct from bacterial cells is widely used - the 95 C step will release sufficient DNA.

added later in response to comment by OP

I chose to follow up on Lactobacillus delbrueckii subsp. bulgaricus because I found this coming up over and over again with reference to yoghurt. If you were to test a range of yoghurts I think you could be fairly confident that this would be present.

There are 5 published genomes for different strains of the species Lactobacillus delbrueckii including subspecies bulgaricus (various strains) and lactis. How different are they? I decided to look at one gene, and lactate dehydrogenase seemed like a logical choice (it produces the lactic acid).

The complete nucleotide sequence for the lactate dehydrogenase gene from Lactobacillus delbrueckii subsp. bulgaricus ATCC 11842 is here. If you run a BLAST from that page limiting the search to Lactobacilli (taxid 1578) you do indeed find hits to the gene from several other genomes. Here is a representative selection from the sequence alignment to the least similar of the hits:

Query  99766   CCTTCCACGCTTCTGGAGGTACTGAATTCGCCCTGGCTCAACTGGGCAACGATGCCGGTA  99825
               ||||||||||||||| ||||||||||||||||||||| ||||||||||||||||||||||
Sbjct  90616   CCTTCCACGCTTCTGAAGGTACTGAATTCGCCCTGGCCCAACTGGGCAACGATGCCGGTA  90675

Query  99826   TGTACGGTGCCGTTAAGATGGTTCTGTAATTTTGAATGTAAAAAAGCACCAGGCTTTTAA  99885
               ||||||||||||||||||||||||||||||||||||| |||||||||||||| |||||||
Sbjct  90676   TGTACGGTGCCGTTAAGATGGTTCTGTAATTTTGAATATAAAAAAGCACCAGACTTTTAA  90735

Query  99886   AGTCTGGTGCtttttttGTTTATCCTAAAGAGTCCAGGGTTGCCTTTATCGTCGCGGCTG  99945
               |||||||||||| |||||||||| |||||||||||||||||||||| |||||||||||||
Sbjct  90736   AGTCTGGTGCTTATTTTGTTTATTCTAAAGAGTCCAGGGTTGCCTTCATCGTCGCGGCTG  90795

Query  99946   AGGCCCGCATCTTGGCCAATTCGCTGTCATTTAACGGCAATTCCAGTACGTGGCTGATCC  100005
               ||||| |||||||||||||||||||||||||||||||||||||||| ||||||||||| |
Sbjct  90796   AGGCCTGCATCTTGGCCAATTCGCTGTCATTTAACGGCAATTCCAGCACGTGGCTGATTC  90855

Query  100006  CTTGTCCGTTGATGATGGCCAGGGTGCCCAGGTAGATCTCATCCTTGATCCCGTATTCCC  100065
               |||| |||||||||||||||||||||||||| ||||||||||||||||||||||||||||
Sbjct  90856   CTTGCCCGTTGATGATGGCCAGGGTGCCCAGATAGATCTCATCCTTGATCCCGTATTCCC  90915

Query  100066  CGTGCAATGGTGCGGAAAGAGGCAGGGCCAGGTCGTTGTTTTCCAAAATGGCCGTCACGA  100125
               |||||||||| ||||||||||||||||||||||||||||||||||||||||||| |||||
Sbjct  90916   CGTGCAATGGCGCGGAAAGAGGCAGGGCCAGGTCGTTGTTTTCCAAAATGGCCGCCACGA  90975

Query  100126  TCTTGGCCAGCATCATGGCCACGCCATAGTAGGTTGCGCCCTTTTTGACGATAATCTCGC  100185
               |||||||||||||||||||||||||||||||||| |||||||||||| |||| |||||||
Sbjct  90976   TCTTGGCCAGCATCATGGCCACGCCATAGTAGGTCGCGCCCTTTTTGCCGATGATCTCGC  91035

As you can see, there are some differences, but there should be no problem designing primers matching both (again - this is just one part of the gene). Obviously you might wish to make an alignment for all 5 sequences, but I got the impression that at least some of the others were identical to the query, even though they are from different subspecies. These are very closely-related organisms.

In terms of your experiment, I suggest that you plan to use a range of yoghurts and/or starters as the source of template. You could even mix them, if there are constraints on your set-up.


Could an organism evolve to adaptively evolve? Besides chance mutations sticking around because of their utility towards survival and procreation, could an organism evolve the ability to aid this process by mutating more frequently in beneficial directions in response to the environment (e.g. based on some form of past higher order evolutionary experience)?

IMHO, the whole genome replication/recombination/mutation process and arrangement has evolved to increase the likelihood that changes will be beneficial or at least neutral.  In chromosome recombination, for example, new chromosome combinations are constructed from old, tested, gene sequences, while making sure that the new pieces are homologous to corresponding pieces in the parents' and grandparents' chromosomes.


How is the timing of gene expression controlled in developing embryo? I understand how cell differentiation works in general (gradients of homeobox proteins etc), but how is timing controlled? Why do some genes switch on at a very specific moment of development and then switch off.
I imagine that the timing could be enabled by the same homeobox proteins (genes are switched on as soon as the proteins diffuse far enough, and switched off as soon as the homeobox is used up), but perhaps there's some special mechanism of gene expression timing?

How can gene expression timing affect the formation of a developing embryo?

We should know that genetic imprinting is passed down. The formation of an embryo is not. Some takes on form when provoked, it is much like when oocytes are stimulated with a prod duplication
Happens automatically. The embryo is affected by the proximity of cells. Clusters, spread out, far apart. All make the cells behave automatically. But it's the first ignition of development that sets off growth. The cells have been through many phases and timing is not controlled by either proteins or genes.


Query from a ppt slide I came across this slide:

Now I haven't understood what the last two grey colored lines mean. Can't ORFS be of any size? What is overlapping frames here?

Can't ORFS be of any size?

I think the point being made is that in a random sequence of 64 amino acids, on average 3 out of 64 should be stop codons, because there are three possible nucleotide sequences for stop codons (UAA, UAG, UGA). ORFs could theoretically be any size but the longer the sequence the more likely you are to come across a stop codon purely due to probability.

What is overlapping frames here?

An example of overlapping frames is shown in the slide:

For instance, you can see that the first "CU" in the first frame produces an alanine (as GCU), while the "CU" in the second frame produces a leucine (as CUU).

They have the same nucleotide sequence, but are offset to produce different amino acids. Viruses have very "condensed" genomes and often can use the same nucleotide sequence for different genes, just starting at different points in that nucleotide sequence. This means they have functional overlapping frames.


Permeability of Plasma Membrane I’m having trouble grasping why small polar molecules can cross the hydrophobic region of the membrane and not ions. Won’t the polar molecules be attracted to the watery extracellular medium and not be inclined to move through the hydrophobic region? (This is my reasoning for why ions won’t go through.)

Also, why do lipid-soluble particles go through the membrane? I understand they have an affinity for the hydrophobic region, but won’t they want to stay there, sandwiched between the two watery layers? Isn’t that the point of the orientation of the bilayer? Why would the lipid-soluble particles move from the hydrophobic region into the watery interior of the cell? Furthermore, why are lipid molecules not repelled by the hydrophilic heads on the exterior of the membrane?

Passive diffusion.
This question specifically refers to passive diffusion.
Ill reiterate and clarify what was mentioned in the question.
Passive diffusion involves a molecule dissolving into the membrane, diffusing across it, and then dissolves in the aqueous solution on the other side.
The second part of your question can be answered briefly: this diffusion event occurs from time to time, and often at a high rate.

Importantly only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates. Thus, gases (such as O2 and CO2), hydrophobic molecules (such as benzene), and small polar but uncharged molecules (such as H2O and ethanol) are able to diffuse across the plasma membrane. Other biological molecules, however, are unable to dissolve in the hydrophobic interior of the phospholipid bilayer. Consequently, larger uncharged polar molecules such as glucose are unable to cross the plasma membrane by passive diffusion, as are charged molecules of any size (including small ions such as H+, Na+, K+, and Cl-).
-Cooper, 2000

Hydrophobic fatty acids repel charge.
The additional or missing electron gives the ion its charge. The hydrophilic head groups of the bilayer are charged, but the fatty acid chains are not, and these repel charge.
There are also repulsive forces between hydrophobic and polar residues (hence the bilayer exists in water), however polarity is essentially a spectrum. A small relatively non-polar polar molecule will not experience enough repulsion to stop diffusion, but a larger, or more polar molecule might.
Active and passive transport.
Although not mentioned in the question, these ions and other molecules can permeate the membrane via protein channels that allow, often with great specificity, ions and large molecules to traverse the membrane.


Can a brain process auditory signals at 18 weeks of human development? According to When a fetus hear , When a baby can hear in the womb and several other similar articles, a baby starts to hear sounds at week 18. And according to How hearing works. Hearing involves

  nerves communicate to the brain. The hearing nerve then sends the
  information to the brain with electrical impulses, where they are
  interpreted as sound.

Does this actually mean a brain is actually processing auditory signals at 18 weeks of human development, or is the brain at 18 weeks only processing sounds by a process that doesn't involve the brain? Perhaps the conclusion might seem obvious for some, but not for me considering the supposed inability of the brain to process several others (or any other?) kind of signals at that stage, such as pain At what stage is the nervous system developed enough to interpret neuronal signals as 'pain'? and being the hearing experience directly connected to pain sometimes.

According to a concise review by Graven & Brown (2008) the development of the auditory system (Fig. 1) in the human is as follows:

15 weeks gestational age*: structural parts of the cochlea and the middle ear are well formed;
20 weeks: middle ear and cochlea are anatomically functional;
Around 25 - 29 weeks: auditory system as a whole becomes functional, as the spiral ganglion cells in the cochlea connect inner hair cells to the brain stem
and temporal lobe of the cortex. In other words, only at this point, the peripheral end organ becomes connected to the central nervous system. At 25 to
26 weeks' gestation, a loud noise in utero will produce detectable changes in autonomic function.
28 - 30 weeks: neural connections to the temporal lobe of the cortex are functional. The development of tonotopic columns in the auditory cortex commences. They are needed to receive, recognize, and react to language, music, and meaningful environmental sounds.

* Gestational age is a measure of the age of a pregnancy which is taken from the beginning of the woman's last menstrual period (LMP), or the corresponding age of the gestation as estimated by a more accurate method if available. Gestational age can be obtained by adding 14 days to the point of fertilization.

Fig. 1. The adult auditory system. source: Graven & Brown, 2007

Reference
- Graven & Brown, Newborn Infant Nurs Rev (2007); 8(4): 187-93


Similarities Between Cells? Which of the following are usually identical between a lung cell and a brain cell, from the same person, assuming that they are normal (non-cancerous) cells?  Circle your choice(s).

a.  Size
b.  Shape
c.  Specific proteins found in the cell
d.  Specific genes in the cell’s genome
e.  Which genes are expressed
f.  Which parts of the DNA are methylated
g.  The specific DNA sequence of chromosome 12
h.  All of the above
i.  None of the above

I said only D and G because all cells have the full genome.  The difference between cells is how the these genes are expressed.  All of the other options are results of different amound of gene expression.  Is this the correct thinking?

I would also go for d and g. All the others may vary. Strictly speaking, you may even have random, point mutations that have changed the genomic sequence between two given cells so even d and g might not be true in some cases.

I would also like to point out that recent evidence implies that differential expression of non coding, regulatory RNA molecules may play as, or even more, important a role as differential expression of proteins. See the ENCODE papers or here for a recent review.


What is a group of tortoises called? This post at Mental Floss stated that a group of tortoises is called a 'Creep'. I had never heard of that before, and in trying to find the references for the name, I was surprised that I couldn't actually find anything.

Wikipedia showed no results in either of their lists for animal names.

http://en.wikipedia.org/wiki/List_of_animal_names
http://en.wikipedia.org/wiki/List_of_English_terms_of_venery,_by_animal

Neither did the Northern Prairie Wildlife Research Center: http://www.npwrc.usgs.gov/about/faqs/animals/names.htm

The closest I found was that a group of turtles is called a nest or a bale.

Is there an actual source for what a group of tortoises is called?

Creep is correct. I sent an email asking this question to The Tortoise Group, which is a non-profit organization whose mission statement is:

Improving the lives of wild and desert tortoises through education.

The Executive Director replied:

It's a bale for turtles and a creep for tortoises. I am sure they could have come up with a better name!

If you have additional questions, there's a wealth of scientific information on their website.


Lengthening muscles not good from evolutional perspective? Why do we do it with explicit stretching? Stretching has many advantages, among other things it helps us to be flexible in our movement (which is an advantage?!).

But why do we need to actively stretch, it seems that the body wants to shorten the muscles by evolution (e.g. when training often in fitness studio). This is the opposite of what we do when stretching.

It seems to be that there are advantages of being not stretched. So what are these advantages / what is the evolutional rationale?

Edit: Why this question is different from this question:

That question asks, why we automatically stretch sometimes after e.g. sleep. The answer is that we stretch the soft tissues because of transitions of high and low activities (especially after sleep, in which we ease the tension in our muscles [muscular antonia]).

This question asks something different. It asks about explicit stretching in sports and not about automatically stretching behavior. The aim is different. In sports we stretch because, we want to lengthen our muscular. The question is why lengthening doesn't seem to be a good thing from an evolutional perspective.

Edit 2: I'm not sure, if it is clear for everybody, what I mean, so I add a succinct example: Why would it be bad (evolutional rationale), if everybody could do a split (gymnastics) by nature (disadvantages?)? In our reality, the ability to do this is almost always an result of stretching. This is only one extreme example, mostly people don't strech to such extremes. Maybe this now  helps to understand, for what this question heads.

Muscles only ever work by shortening, as you say, but muscles in the human body tend to be found in antagonistic pairs.  These pairs of muscles act in opposite directions, one example being the biceps and triceps muscles - the biceps bends the arm (a flexor muscle) while the triceps straightens the arm (an extensor muscle), another example is the quadriceps-hamstring muscle pair in the upper leg.

If our muscles remained shortened, our mobility would be impaired.  If the biceps muscle remained too short, it would be impossible to extend our arms, for example.  Muscles do work by shortening, yes, but it's important for them to be able to stretch as well, and remain long enough for antagonistic muscles to have their full movement be possible as well.


Why don't rates of cancer increase generation to generation? As cells divide, they accumulate mutations that can sometimes cause cancer. Gametes have to divide like any other cell, and thus generation to generation mutations should accumulate in people's genomes. However, it doesn't appear to be the case that cancer rates increase as a species ages. Why isn't this the case? Is the process of development itself a filter that ensures that most of the cells in the body are "far from cancer"?

Species age

  However, it doesn't appear to be the case that cancer rates increase as a species ages

Species don't have an age. All lineages on earth are about 3.5 billions years old. No, lineage is younger or older than that. A lineage does not get its genetics magically reset when the lineage gets a new species name. For more information about the standard misunderstandings about the concept of species, please have a look at the post How could humans have interbred with Neanderthals if we're a different species?

In all cases, there is some equilibrium between the selection pressures brought about mutations that are linked to cancer (whether mutations on oncogenes or on tumor suppressor genes).

Individual age

Individual, do have an age though. Cells, within multicellular individual replicate in order to ensure the multicellular individual growth and maintenance. Those cell lineage can accumulate mutations that could be linked to cancer development. Within the individual, these mutations are not deleterious and are therefore not selected against. Actually, in case of a cancer, those mutations are, by definition, beneficial as cancerous cells proliferate (have a large fitness). As a result one should expect that old organisms are at greater risk of developing cancer than younger organisms. In humans, this correlation exists, however, the statistics are slightly more complex than that. Typically, different types of cancer seem to show different age associations. See this article from the NIH as a start for more information.


Does some form of self organizing map exist in the brain? Self organizing maps (SOM's) are an extremely interesting and powerful tool in the field of artificial neural networks. My question is: Does something similar exist in the brain? Or are these systems completely "man made"?
Also, if there are such things in the brain, how do they work?

These are great questions.  The SOM was absolutely biologically inspired.  Sure, there are many examples.

Examples of self-organizing topographical feature maps in the human brain include the the sensory homunculus, retinotopic maps, and the entorhinal cortex.  There are even maps such as these in the midbrain auditory nucleus of the barn owl as well as the auditory cortex of the mustache bat.

As to how they work and organize in nature, that is still an active area of research, and it seems like there are no experimental conclusions that suggest the existence of  universal rules for self-organization of sensory maps in the brain.  As far as I know, however, Kohonen's theory that these maps organize via a combination of lateral inhibition and Hebbian learning has not yet been displaced by a more modern idea.


How many times did endosymbiosis occur? According to the endosymbiont theory, mitochondria and chloroplasts originated as bacteria which were engulfed by larger cells. How many times is it estimated that this occurred in the past? Are there any examples of this process being observed directly?

Well, it seems quite obvious that it was not a single I-eat-you-but-you-survived act but rather a convergence of endosymbiotic and host species into a greater and greater cooperation.
Of course this leaves a question if there was one or more species of endosymbionts involved.

Mitochondria are a very primeval story forced by the oxygen catastrophe, so it is hard to say, although great majority of mitochondria seems to have a single origin.

Plastids are much more divergent, however it seems that they did originated from a single source, diverged into chloroplasts, cyanelles and rhodoplasts and were later mixed up by numerous acts of secondary and even tertiary endosymbiosis (plus a further evolution); this variety can be especially seen within Euglenas, and they are the main group investigated in this manner.


Why are there two replicase proteins translated from tobacco mosaic virus RNA? I’m trying to understand how TMV is expressed and have read (here) that there is a large and small form of the RNA-dependent RNA replicase. These are translated from the same region of the genome, the larger arising from read-through of a leaky stop codon.
Why are there two forms of the replicase? My first impression was that each might produce a sub-genomic RNA, one for the movement protein and one for the capsid protein, but can find no reports confirming this.

Very Short Answer
As of 2021 it does not appear to be known why Tobacco Mosaic Virus (TMV) produces two proteins from its replicase gene.
Relatively Short Answer
I have done a brief literature search on the topic, and found papers from 2008, and 2012 which relate to the replicase and studiously avoid the question of why there is a 126-kDa and 183-kDa form of the TMV RNA-dependent RNA replicase. I am therefore of the view that there has been no advance since the review by Buck (Phil. Trans. R. Soc. Lond. B (1999) 354, 613–627). From this I glean the following:

“…both the TMV-encoded 126-kDa and 183-kDa proteins are required for maximum efficiency of TMV RNA replication”. The full-length protein is absolutely required; preventing the production of the smaller protein reduces the replication rate to 20% of normal.
“The read-through portion of the 183-kDa protein contains amino-acid motifs characteristic of RNA- dependent RNA polymerases (RdRps) and hence the 183-kDa protein is likely to provide the catalytic activity for the synthesis of TMV RNA from NTP substrates.”
“The C-terminal domain of the TMV 126-kDa protein is helicase-like. Although helicase activity has not yet been demonstrated for the 126-kDa protein of any tobamovirus, these proteins contain six amino-acid motifs, which are highly conserved in known helicases, such as the translational initiation factor eIF-4A.”
“The TMV 126-kDa protein contains two domains. An N-terminal domain with amino-acid motifs and predicted secondary structure typical of S-adenosylmethionine binding proteins, methyltransferases and guanylyltrans- ferases is probably required for synthesis of the 5' m7GpppG cap structure. The TMV 126-kDa protein has been shown to have guanylyltransferase activity.”
There is some evidence in other viruses for association of two forms of replicase. However this is indirect, and there are no data for TMV. The implication in the original wording of the question that the two forms in TMV were two subunits of a replicase is not supported by any evidence and is not assumed to be the case.

The only suggestion that Buck makes is that as helicase activity is required for two separate purposes — to unwind double-stransded RNA during replication, and to remove secondary structure from single-stranded RNA when this is used as a template for multiple copies of the complementary strand —  the two forms of the replicase may have a different substrate specificity in their helicase activity.
[Updates welcome — I may have missed something recent.]


Can humans perceive sounds above 20 kHz? In the never-ending debate raging in the audiophile community about sound quality and what humans can or cannot hear, it is very very very very incredibly often cited that the upper-limit of the audible range of human hearing is 20 kHz, give or take. Some indicate that this is a conservative estimate, and that the actual upper-limit is actually lower than that (~18 kHz). While others suggest that sounds could be heard or otherwise perceived up to about 25 kHz-30 kHz:

  Sampling rates higher than about 50 kHz to 60 kHz cannot supply more usable information for human listeners.

And some others suggest that there is substantial variation between individuals around the upper limit:

  The human range is commonly given as 20 to 20,000 Hz, though there is considerable variation between individuals, especially at high frequencies

So is there any biological evidence whatsoever that young, healthy humans can hear or otherwise perceive (or sense) sound waves above 20 kHz? And what would be a conservative estimate of the absolute upper limit of the audible spectrum for humans (i.e. usable sound information for human ears and senses)?

Yes, we can. By means of bone conduction we can hear up to 50 kHz, and values up to 150 kHz have been reported in the young (Pumphrey, 1950). However, it is indeed generally agreed that 20 kHz is the upper acoustical hearing limit through air conduction. The reason for this is debated, but the transfer function of the ossicle chain in the middle ear is a suspected culprit in setting the upper frequency limit to 20 kHz (Hemila et al., 1995).

Hence, using normal speakers or headphones 20 kHz is a very reasonable absolute upper limit. Note that the Nyquist criterium necessitates higher sampling rates (at least 40 kHz), so your statement of using 50k-60k sound cards is correct. If you decide on using bone conduction aids, you might start to think on using higher sampling rates still.

Here is an example of a commercially available bone conduction head set (AfterShockz):

These devices have the potential to increase the upper limit because they bypass the middle ear and hence circumvent the limiting transfer function of the middle ear. They induce vibrations onto the temporal bone, that travel via the bone directly to the inner ear. See the following picture from The High Tech Society:

As a side note: when you grow older the hearing sensitivities at high frequencies  are severely reduced, and even the 6 kHz range is severely affected in the elderly (picture from John Perr's website):

Disclaimer: I haven't looked into the capabilities in terms of upper frequency limits of bone conduction head sets. I am just talking theoretical limits.

References
- Pumphrey, Nature 1950; 166:571
- Hemila et al., Hear Res 1995; 85:31-44


Chemistry of the phosphodiester bond in RNA I have been learning about the chemical structure of RNA, but I can't understand why all hydrogen atoms disappear in the phosophodiester bond between the riboses of RNA.

Phosphoric acid is $H_3PO_4$:

However, when it's connected to ribose the hydrogens disappear:

Where did the hydrogens go and why?

Generally hydrogen is not shown in DNA structure. I have made a simple diagram to show where all hydrogens go:

There are 3 hydrogens in phosphoric acid, each of them leaves as:

1 H joins with 3' -OH of previous nucleotide to form H2O during DNA replication.
1 OH joins with H of next nucleotide to form H2O during DNA replication.
1 H is released as H+ (remember it was phosphoric acid), hence giving rise to the acidic character of DNA (remember it is DeoxyriboNucleic Acid).

I think you should first study DNA replication (if you haven't, yet) to get more thorough knowledge about the topic.


HIV-RT nucleotide contact residues I'm investigating HIV-RT 3KLF and 1LWF trying to find a perfect pose of thymine. Which residues on HIV-RT is Thymine supposed to contact on 3KLF and 1LWF? Where exactly is the nucleotide binding domain on 3KLF and 1LWF?

Please provide a journal article as proof.

Thymine must make contact in two places on HIV-RT before being added to nucleotide strand. First contact is made with the fingers region then contact is made at the N-Site.
Allosteric Regulation of HIV-1 Reverse Transcriptase by ATP for Nucleotide Selection


Can skin be removed and replaced so that it maintains its original cellular structure? The cells in our body that form tissue, such as our skin, are interconnected. I would think that cutting out tissue or trying to repair/replace it, as is done in surgery, or after an injury, could not be accomplished without damaging this network and creating irreparable damage.

Am I mistaken and is it possible to remove and replace skin, close a wound without damaging the underlying cellular structure and having scar tissue form?

When it is healing, is the tissue that is healing in some way weaker than the tissue that remained intact, say just beyond the margin of the wound?

If someone has surgery, can their skin be repaired completely with the proper amount of healing time?

As pertains to skin, no. As pertains to your other fears, that's a different question.

Every cut that extends into the dermis significantly (and to remove skin, it must include the dermis) will leave a scar behind.

Cuts that extend only very superficially into the dermis may hit some capillaries and bleed, but these will usually not bleed much, and can heal "seamlessly". But anything that extends deeper will bleed more. Those are the cuts that often get stitches if they are long enough, won't stop bleeding, etc.

Lifting and replacing a piece of skin would necessitate the damage of many cells and the destruction of a lot of fine blood vessels, but even with the best microsurgical techniques, a scar will form. The best techniques combined with the best pre- and post-surgical care will only minimize scar formation; it can't be eliminated.

  In skin, the process of wound repair can be generalized into three cascading phases each with characteristic cellular events: 1) inflammation; 2) fibroplasia or proliferative phase; and 3) scar formation.

Wound Healing in Development


Is Urea excretion a shared ancestral trait of amphibians and mammals relative to synapomorphic Uric Acid excretion in living reptiles? Is the ancestral condition of prehistoric amphibians and early amniotes urea excretion? Would it follow then that the lineage leading to living reptiles went on to evolve uric acid excretion as a derived trait? Therefore urea excretion is a shared plesiomorphy of living amphibians and living mammals relative to a synapopmorphy of uric excretion in living reptiles?

There are reptiles that also use urea, and mammals that excrete uric acid.  it is likely that urea is the ancestral condition (compared to uric acid) as it occurs in adult amphibians and some fish. But ammonia is even more ancestral than that, occurring in young amphibians and most fish. It is likely uric acid developed alongside terrestrial eggs, as every egg laying amniote (including monotremes) uses uric acid at least during the embryonic stages. Uric acid is more metabolically costly so there is some incentive to switch to urea if you can, although there is a counter factor as urea requires significantly more water. so it comes down to which a group can afford more water or calories. It is notable that the few reptile to witch use urea only switch during their adult stage. It is possible to do both a few desert mammals produce uric acid and urea at the same time, producing more uric acid when water stressed.


Membrane Permeability to Pyruvate Pyruvate seems to pass easily through the outer membrane of the mitochondrion but has difficulty entering the inner membrane (and gets in by H+ symport). I have two questions: (1) what property of pyruvate disallows it from passing through the inner membrane? Is it its charge? and (2) what structural differences are there between the outer and inner membranes of the mitochondrion that create their disparate permeabilities to pyruvate?

Pyruvate is negatively charged and quite polar, which makes it unfavourable to diffuse directly through any membrane. The outer mitochondrial membrane contains porins, which allow small molecules, like pyruvate, to passively diffuse through. Specifically, pyruvate uses voltage dependent anion channels. The inner mitochondrial membrane lacks such channels and depends on active transport by the long anticipated but only recently discovered mitochondrial pyruvate carrier (Herzig et al. and Bricker et al., 2012).


Is it theoretically possible to restore the Tiger population to 100,000? The current global Tiger population is roughly 5100 according to Wikipedia. With habitat destruction and poaching continuing and no effective improvement in conservation, most likely the Tiger population will continue to decrease. I'm wondering what is the theoretical maximum population to which the Tiger species could be restored. Suppose poaching and habitat destruction stopped today and conservation efforts were increased drastically, so the only factors limiting population growth are the natural dynamics between the species and its prey. Could we then restore the global population of tigers to its pre-20th century level of 100,000?

I don't think your core question can be answered exactly, namely "...the theoretical maximum population to which the Tiger species could be restored", since there are too many variables to consider. However, the comment from @Remi.b is apt, in the sense that it shows that population growth rate per se (or reproductive rate) should not be the limiting factor. The bottleneck will probably be some concept of carrying capacity (the number of tigers that the current tiger habitats can sustain). This number will naturally depend on many factors, for instance whether all hunting of tigers and their prey is removed from the remaining habitats.

You could arrive at a ballpark estimate of the current "theoretical" maximum population size by finding the area of suitable tiger habitat and dividing this by the average size of tiger territories. However, the size of tiger territories differ quite a bit between males and females and between areas with different prey densities, and probably also between different tiger subspecies (which will covary with average prey density to some extent - Siberian tigers generally live in habitats with lower prey densities). Looking at estimates from the Smithsonian and wikipedia, territory sizes seems to range between 20 to 510 km2, with maybe even larger male territories in Siberia (so quite a big range). The IUCN Red list assessment of tigers state that the current tiger range is to 1.185 million km2 (from Sanderson et al. 2006 as "Tiger Conservation Landscapes"). It is however unclear whether this number corresponds to the total range extent or to the actual amount of suitable habitat (probably the former though). Nevertheless, lets say that the average territory size is 265km2 (probably way to high on average), that the estimated area from IUCN is correct, and lets assume that territories never overlap (which they do; male territories overlap with several female territories and female territories can also overlap to some extent). In that case, we will arrive at an estimated theoretical popultion size of ~4500 tigers. If we instead use a more modest territory size of 40km2 we will arrive at a population size of ~30000 tigers. Since territories can overlap, these estimates should be biased low, given their other assumptions.

Sanderson et al. (2006) however also includes a summary of "Effective Potential Habitat" of tigers, which sum to 5.65 million km2. If this number is used to calculate the estimated theoretical popultion size you will arrive at ~21300 or 141000 tigers, using the same territory sizes as above. However, this completely ignores issues such as landscape connectivity, and that tigers are completely missing from large parts of their former distribution (these factors, and others, were used to define the "Tiger Conservation Landscapes"). Also note that much of the potential habitat lies in low-productivity areas (Russia and parts of China), where territory sizes are relatively large.

Another perspective would be to use the historical population size pre-20th century and the amount of decrease in tiger habitat to estimate a theoretical population size. I don't know anything about the historical population size, but let's say that your 100000 is accurate (source?). Dinerstein et al (2007) state that current tiger ranges correspond to 7% of historical ranges. Using only these numbers, you could arrive at a current theoretical population size of 7000 tigers (100000*0.07), assuming that the tiger population should directly mirror the amount of available habitat. However, the current 7% of historical ranges include range contractions due to hunting, so this estimate should be biased low (maybe strongly so) with respect to the possible population size that could be obtained if all hunting stopped.

These calculations should show that the current Tiger populations could probably be increased quite a bit with strong and effective conservation efforts (in your words: if "poaching and habitat destruction stopped today and conservation efforts were increased drastically"), but that 100000 will probably be extremely hard to obtain, given that so much of the historical range has been lost. With reintroduction programmes and a long timeframe it doesn't appear to be impossible though, but this is ignoring potential future problems such as increased tiger-human conflicts. Also note that I don't know much about Tiger biology, that these are merely rough back-of-an-envelope calculations, and an expert could certainly give you a more detailed and accurate answer.

References:

Dinerstein et al. 2007. The Fate of Wild Tigers. Bioscience 57 (6): 508-514. doi: 10.1641/B570608
Sanderson et al. 2006. Setting Priorities for the Conservation and Recovery of Wild Tigers: 2005-2015. The Technical Assessment. WCS, WWF, Smithsonian, and NFWF-STF, New York – Washington, D.C.
The Smithsonian: Tigers
Wikipedia: Tiger
IUCN Red List: Panthera tigris


Transfer of antibodies in breast milk of humans Why isn't the IgA secreted in breast milk digested due to proteases of the digestive system in the baby?

Wikipedia says:

  The secretory component of sIgA protects the immunoglobulin from being
  degraded by proteolytic enzymes, thus sIgA can survive in the harsh
  gastrointestinal tract environment and provide protection against
  microbes that multiply in body secretions.

But what exactly does the secretory component do?  What is the secretory component?  Is IgA absorbed in the circulation of fetus? I remember reading it somewhere that it is not absorbed, at least in humans. Please answer these questions focusing more on humans. Though, information about other animals will be appreciated as well.

It is!  Here is an amazing review from 2011 that literally has all the answers.  I'm not kidding, all of them.  I would marry this review if I could.1  It also includes information on other animals.

The main takeaway is that IgA from milk is not readily absorbed by the infant body.  Secreted IgA is mainly to provide a protective coating for the mucosa while the infant is developing its own nascent immune system.  IgG passed along from the placenta (your other question) provides the main source of absorbed antibodies.  As it says in the review:

  Milk sIgA is not taken up by the infant’s intestinal mucosa. In fact, gut closure in humans occurs before birth and little immunoglobulin is absorbed intact in the intestine after birth. However, the presence of sIgA in the intestinal lumen is part of the protective function of the epithelial barrier in the intestine... Secretory IgA is considered to be the primary immunoglobulin responsible for immune protection of mucosal surfaces such as the intestine.

In terms of enzymatic activity, the digestive system will in indeed chomp up the antibodies; that's part of the reason breast feeding should continue as needed.  That's okay, because there's plenty to go around:

  Much of the immunoglobulin consumed in an immune milk can be expected to be partially or completely digested, however some portion of the immunoglobulin will remain intact or at least partially intact and capable of binding to an antigen.

It turns out that immunoglobulins are moderately resistant to digestion, at least more so than other milk proteins.  There's a section in there detailing some experiments where Ab was given to individuals:

  In adult humans consuming a bovine whey protein concentrate, approximately 59% of IgG and IgM was detected by radial immunodiffusion from effluents from the jejunum, while 19% was detected in the ileum. These estimates of digestion of immunoglobulin compare with estimates of digestion of milk proteins in adult humans which are approximately 42% complete at the end of the jejunum and 93% complete by the end of the ileum, again underscoring the relative resistance of immunoglobulins to digestion in the gastrointestinal tract.

Digestive enzymes vary as to which antibody they prefer to digest, but at least some of them will technically digest the antibody, but still leave functional Fab fragments, which are still immunologically active and useful to the infant immune system.

1: Did I mention I love this review?  I love it.


When is voltage generated across a membrane? I'm very confused so bear with me please.

Electrogenic pumps are carrier proteins that generate voltage through the movement of ions, right ?

When is a voltage generated ? When there's a net movement of ions ?

Doesn't that mean that when any ion passes through a channel protein, voltage is generated ? And energy is released ? Doesn't that make them electrogenic too ?

We need energy to move ions against their concentration gradient but if energy is released when ions move then why do we need energy ?

Is it that a voltage is generated when an ion moves towards the env with the same charge ? So when the movement enhances the overall seperation of charge , a voltage is generated ? And energy is released ?

In other words, the movement of Na+ through the Na+ channel protein down a concentration gradient doesn't release energy because the Na+ is moving towards the -ve environment but it being pumped outside does ? See that doesn't make sense either, because we need energy to pump and ion.

I'm very very confused

The main thing the sodium/potassium pump does is to move sodium and potassium ions, Na+ and K+. It technically generates a bit of charge separation in doing this, but you can ignore it for now.

What is important is that because of the operation of this pump, you now have two sides of membrane with different ion concentrations. One side is high in sodium ions (outside the cell), the other side is high in potassium ions (inside the cell).

So far, that doesn't really do anything electrical, but it does take a lot of energy to get this arrangement: the whole time, the pump is moving sodium ions to where sodium ions are high, and moving potassium ions to where potassium ions are high. Moving things against their concentration gradient costs energy. The sodium/potassium pump gets this energy from ATP.

Now, imagine you open some pores in the membrane (we call them leak channels), that are a particular size that only lets potassium ions through. The sodium ions can't move, but the potassium ions can. A few potassium ions move over to the high sodium side, down the concentration gradient for potassium. This doesn't take any energy, it just happens passively. It also doesn't involve very many ions, just a few, so the concentrations don't change much.

However, potassium ions have charge! These are positive charges, flowing out of the cell: that makes the inside more negative.

Also, because they are positively charged, potassium ions would tend to move towards more negatively charged spaces. So, as the inside of the cell gets more negative, potassium won't leave as quickly. There is an equilibrium, where the forces pulling potassium ions out to where potassium concentration is low equals the forces pulling potassium ions in to where the voltage is negative.

The voltage where this equilibrium occurs is called the resting membrane potential, and for many cells is somewhere between -100 and -40 millivolts: that's the voltage generated across the membrane, indirectly, by the sodium/potassium pump.

Purves' Neuroscience is a good general reference textbook for this sort of thing. The Goldman equation is a mathematical way to figure out what the voltage will be if you know the concentrations and permeability.


What is the best color for a PPG signal (photoplethysmography)? What is the best color for a PPG signal?
Red, green, blue or infra-red?

I'm asking because commercial oximeter sensors usually use a pair of red and infra-red LEDs. But recently, I've seen a lot of sensors using green LEDs.

Thanks.

The reason red and infra-red are used is the difference in absorbance at those two frequencies between oxygenated and unoxygenated hemoglobin. Using the difference in these two frequencies allows the concentration of oxyhemoglobin to be calculated. (The red LED is at the frequency where oxyhemoglobin and hemoglobin have identical absorbance).

As far as I know, there's no reason why a green LED wouldn't work. You would only be able to measure the PPG signal and not the oximetry data (unless you used two different LEDs and did some math).

Absorption curves.


Why does a tumour's genome change depending on the environment? According to the book "Primer of The Molecular Biology of Cancer" by Vincent, Theodore and Ateven, the tumour cell is changed depending on its environment.

  performed genome-wide analysis on three tumor samples: a patient's primary breast tumor; her metastatic brain tumor, which formed despite therapy; and a xenograft tumor in a mouse, originating from the patient's breast tumor. They find that the primary tumor differs from the metastatic and xenograft tumors mainly in the prevalence of genomic mutations

Why the tumour cell changing on different places?

why suddenly the breast tumour cells changes on the xenograft tumour and why the metastasis on the brain are now different from the place they came from?

How does this alteration obtained? in the DNA or microRNA or something else?

Tumor cells can have very unstable genomes, as much of the error repair machinery is damaged or missing. Since the cells are rapidly dividing and the DNA gets duplicated each time a cell splits, more and more mutations accumulate as the tumor grows and metastasizes. Just like in evolution as a whole, mutations that are either neutral or help the cell survive better in its environment are kept, whereas cells that develop deleterious mutations (perhaps killing the cell outright, making it more visible to the immune system, or just giving it a growth disadvantage as compared to neighboring cells) either die out or get outnumbered by other cells. This is why, over time, tumors can become resistant to therapies intended to kill them, as their cells accumulate mutations that help it evade the treatment and keep growing. There may be a disadvantage that the cells might grow more slowly than the original ones, but since the original ones were killed by the treatment, the resistant ones survive. So, this means that a tumor is rarely homogeneous, with all the cells having the exact same genome. Deep sequencing using next-generation methods is being used to gather information on all the different mutations throughout a tumor, which can help doctors learn which mutations are most common and prescribe patient-specific combination therapy which can kill all the various cell populations at once.

So why are metastatic and xenografted tumors different from the parent? Metastases can arise from single cells or very small clumps of cells, and xenografts are generally made with very small pieces of tumor, so both may start with a different set of mutations than is common in the original tumor. As they grow and divide, as described above, they will become different from their parents. The surrounding environment definitely affects this: the amount of oxygen present, degree of vascularization and blood supply, number and kind of immune cells present, etc. With all these and more factors, a metastasis or xenograft will evolve differently than its parents.