Are we "more evolved" than present-day bacteria? The common ancestor of humans and modern bacteria was most likely a prehistoric bacterium. Does this mean that humans are "more evolved" than today's bacteria?

This is a standard question. The whole problem boils down to what you mean by "more evolved"? Below I am answering the question considering a number of possible definitions. If you have other ("clearly defined") definitions in mind, let us know.

  Are [humans] "more evolved" than present-day bacteria?

If "more evolved" == "more evolution time"

Then, both bacteria and humans are exactly as evolved!

As all life on earth shares a common ancestor, all currently living creature has evolved for exactly the same amount of time (about 3.8 billion years).

If "more evolved" == "more generations"

Then, bacteria are more evolved.

Bacteria typically have a much shorter generation time than humans do, so with this metric, bacteria would be more evolved.

If "more evolved" == "more fixed mutations since the MRCA"

Then, it is a little more complicated and may depend upon which bacteria lineage you are considering.

If the genome-wide mutation rate is $\mu$ and the haploid population size is $N$, then there are $N\mu$ new mutations every generation. Given that each one of these mutations has a probability of fixing (fixing = reaching a frequency of 1 in the population) is $\frac{1}{N}$, the rate at which mutations fix is $\mu N \frac{1}{N} = \mu$ at each generation. If a species has $g$ generations per year, then over $t$ years, $\mu g t$ mutations would have accumulated.

The genome of bacteria is typically much smaller than the one of humans, but their mutation rate per nucleotide is much higher. Overall, the genome-wide mutation rate is rather higher in humans but that might well differ from species to species. However, again, bacteria have had more generations per year than humans and therefore bacteria species likely have fixed more mutations than humans have. So from this metric, bacteria are rather more evolved than humans.

If "more evolved" == "able to resist higher acceleration"

Then, bacteria are more evolved although that might among bacteria lineages

Some bacteria have been grown under 400,000 g (National Geographic), while a typical human can only tolerate about 5 g and for only a short period of time!

If "more evolved == more impact on the environment"

The term impact is a little hard to define but I think it is of interest to highlight that, even here, bacteria would probably win because cyanobacteria caused the great oxygenation event which is probably the largest planet-wide environmental change caused by biological organisms.

(thanks @Thawn for this definition he gave in the comments)

If "more evolved" == "having more lungs"

Then, humans are more evolved.

Bacteria have no lungs, humans have two.

If "more evolved" == "bigger genomes"

Then, humans are more evolved. Note also that corn would be more evolved than humans with this metric!

If "more evolved" == "higher fraction of the genome that is encoding for proteins"

Then, bacteria are more evolved.

If "more evolved" == "more protein coding sequences"

Then, humans are more evolved.

If "more evolved" == "more phenotypically different from the MRCA"

You would have to list specific phenotypes of interest. So, here the term "more evolved" still remained a little undefined.

Also, we do not have much information about the MRCA of these two highly distantly related lineages. The question could be more easily answered for more closely related lineages. For example, in mammals, if you consider the following traits and always ask what species is (likely) most different from the MRCA of all mammals

body mass -> blue whale
brain mass -> sperm whale (yes, sperm whales have a very big brain)
lips shape -> platypus (they have a beak)
time taken to type Hello\nWorld on a computer keyboard -> humans

Related posts

What is meant in biology by the term “evolved”?
Why have humans evolved much more quickly than other animals?


Is it possible to accurately measure micronutrient levels with the blood volume from a Dermal / Capillary puncture? I have not been able to find much information beyond what tests are normally done with Capillary puncture sampling, as opposed to what tests are possible.

Could we test for a single micronutrient, or maybe some subset of nutrients with the blood drawn in this way? Is the issue purely volume, or are there other factors?

Thanks!

Detection methods are constantly getting better, requiring lesser amounts of blood to make a determination. In newborns, a heel blood sample (of capillary blood) is used to detect up to 40 (sometimes more) disorders from maple-sugar urine disease and hypothyroidism to hemoglobinopathies and organic acid conditions. If such large molecules can be detected in capillary blood, smaller molecules should as well.

There are differences in central venous sampling and capillary blood sampling, but it could be argued that since the capillaries are the site of exchange of nutrients, this is the most accurate site to determine availability of micronutrients in blood.

One reason labs take more blood than required for the test is to run a second analysis if the first is abnormal. Although it's not done for every abnormal, clinicians often want to confirm significant abnormals before treating a possible lab error.

Newborn screening tests
Newborn Screening
Conditions Screened By State
A Layperson's Guide to Tandem Mass Spectrometry


Indian Snake Species Identification Location: southern India

Time: noon
Approx. Size:
Length: around 2 feet;
Size: extremely small, like a straw.
Diameter: less than 1 cm.
Was very fast in climbing aisle of mud bed/uphill like 90 degree accent.

Ashok's Bronzeback (Dendrelaphis ashoki).

This is a relatively small snake (typically 70 cm in length) that feeds on lizards, frogs and small rodents.

More information can be found here or here.

It's range is Southwestern India:

You can differentiate this species from closely related D. girii based on it having a longer "postocular" black line than D. ashoki -- in D. ashoki it stops shortly caudal to the eye (e.g., see here).


Why is there not an immune response to injected immunoglobulins? When you inject immunoglobulins as a treatment for certain diseases, the immunoglobulins are a foreign substance.
I can appreciate that maybe the constant region would be similar to the hosts as it is from another human and these don't change a lot.
However, in the variable regions, wouldn't there be the possibility that the antigen receptor region could be the complement to the patient's own antibodies? Wouldn't this trigger an immune response and destroy the injected Ig's? Yet we seem to do this procedure, so why doesn't this process occur?

If a head-to-head "match" between antibodies from two different people was to occur, a similar match would most likely have occurred already in the donor. People have the same tissues after all.
But in the donor; the B lymphocytes producing the antibodies had to go through the processes of "central tolerance" and "peripheral tolerance".
This would weed out the cells producing autoantibodies.
Theoretically, nasty autoantibodies in the recipient could react with innocent antibodies in the donor though.


Why Isn't mineral transport in xylem multi-directional? According to our textbook, Xylem transport is only unidirectional while transport through phloem is multi-directional.

But minerals are taken up by xylem from the surrounding tissues actively, and even though they flow along with the water column, they are actively unloaded near 'sink' sites. Sometimes, minerals are also taken up from aging parts and transported to growing areas of the plant. Then shouldn't mineral transport through xylem be multi directional?

Please Explain

Movement through the xylem is powered by transpiration of water through stomata in leaves and a sustained tension in the xylem itself due to water's cohesive properties.  See: https://en.wikipedia.org/wiki/Xylem#Cohesion-tension_theory

The "multi-directional" transport you are talking about does not actually occur in the xylem.  Minerals have to be transported OUT of the xylem before they can move other ways.  Transport THROUGH the xylem is uni-directional; transport OUTSIDE of the xylem can be multi-directional.


Does human brain store duplicate data? There are several answers and articles about how the brain stores data, but none specifically cover whether a human's brain stores duplicate data.

I was reading in this article that a human brain can have a capacity of 1 terabyte to 2.5 petabytes. But for example, if you read a book a dozen of times, will it be stored as data several times?

Let me put it this way. When we read a book a couple of times, we remember it better. Is that because it's stored in several synapses and then retrieved better while trying to remember, or is it because reading it over and over makes the missing parts be stored?

We do recognize a familiar phrase when reading a book, which means the brain can differentiate the unknown from known. What matters is that does it decide to store it again or not? Just like a computer who refuses to save a file if the file already exists.

The way neuroscientists currently think about storage in the brain, it doesn't make any sense to think about "duplicate" data but rather about the "robustness" of a given memory to interference or confusion, which increases with consolidation and reconsolidation of memories or can degrade over time.

Repeated exposure can contribute to the robustness of a memory, but so can other factors such as the emotional content of a memory (which, depending on the emotional state, can increase or decrease memory robustness, and this can also vary with the "jist" versus "detail" of a memory).

Note that there are also very different types of memory, so that repetition is very important for motor plans and "muscle memory" whereas episodic memory can get lost in the repetition of daily recurrent events, such as parking your car or eating lunch: you might remember where you parked or ate today, but if you have a routine this can blur into all one memory, where you have a notion of eating at a particular restaurant many times, but you would struggle to remember specifically eating there on December 14th, 2011, unless there was some other special event on that day.

In your example of reading a book, there would likely be two types of memory: 1) memory for the episodic event of reading the book, which would be a separate memory because it is a separate event, though it could be confused with other similar episodic events. 2) Semantic memory for the content of the book: this would be a single memory, reinforced with subsequent readings of the book, and supplemented with all your other semantic experience with the content of a book: discussing the characters of a fiction book with your friends, learning about molecular genetics from a textbook and from a lecture course, etc.

Note also that talking about the "data capacity" of a human brain compared to a computer is a bit silly, because data isn't stored in the nervous system in bits, and a "fair" accounting of human memory needs to consider the vastly multidimensional interactions that are easily coded in a nervous system but not at all easily in a binary system. Note that other papers have come up with estimates that diverge greatly from the numbers you cite, for example Wang et al 2003 which gives a value of 108432 bits based on the number of synaptic connections. That number is truly inconceivable to our conscious experience even if it is within the capability of our brain. Clearly there are other limiting factors not involved in a simple binary system, for example confusion with similar memories, and there are types of memory that computers excel at (such as the pixel values of an image) whereas human memory deals in abstractions and hierarchical representations.

References

LaBar, K. S., & Cabeza, R. (2006). Cognitive neuroscience of emotional memory. Nature Reviews Neuroscience, 7(1), 54-64.

Walker, M. P., Brakefield, T., Hobson, J. A., & Stickgold, R. (2003). Dissociable stages of human memory consolidation and reconsolidation. Nature, 425(6958), 616-620.

Wang, Y., Liu, D., & Wang, Y. (2003). Discovering the capacity of human memory. Brain and Mind, 4(2), 189-198.


Is every neurotransmitter receptor an ion channel? This is a rudimentary question--perhaps the answer is well known to biologists, but is every neurotransmitter receptor also an ion channel?

For example, NMDAR is a glutamate receptor and cation channel and GABA_A receptors are gated ion channels.  Is this true generally?  If not, is there a classification of neurotransmitter receptors according to abstract function (e.g. all gated ion channels would form one class, then perhaps there are others)?

Thank you in advance!  I am a mathematician just getting interested in some biology problems and trying to organize the basic knowledge in this area.  I appreciate any insights here!

is every neurotransmitter receptor also an ion channel?

No.

There are two general types of receptors for neurotransmitters, ligand gated ion channels and receptors that activate second messenger systems, for example, G protein coupled receptors. They are sometimes referred to as ionotropic and metabotropic receptors. This figure from Principles of Neural Science, Ch. 10 illustrates the difference nicely:


Why is Bcl2 a good target for cancer therapy? Bcl2 is a family of proteins that are involved in the inhibition of apoptosis in cells. My question is that what makes this anti-apoptotic protein useful in cancer therapies as opposed to focusing on pro-apoptotic proteins? Are Bcl2 proteins simply easier to work with as opposed to the pro-apoptotic proteins? Or Bcl2 proteins have some sort of other characteristic that has allowed them for be the target for cancer therapies?

Bcl2 is an anti-apoptosis protein, meaning that by inhibiting Bcl2 you will inhibit its anti-apoptotic effects. In other words, by inhibiting Bcl2 you actually induce apoptosis in cancer cells. This is one of those concepts in biology that can be hard to follow... that is, "by inhibiting an inhibitor you cause activation".

Cancer cells in particular seem to be resistant to the endogenous pathways in the cell leading to apoptosis, and the reasons for this phenomena are an area of active research. There are two major pathways of apoptosis within the cell, the extrinsic pathway the involves caspase proteins and the intrinsic pathway that involves Bcl2 and a number of other proteins associated with the mitochondria.

Bcl2 is part of a family of proteins that are involved in the intrinsic pathway of apoptosis - for a great and recent review see this recent review... or search on PubMed for a number of recent review articles.

Interestingly, cancer cells have a particular type of mitochondrial dysfunction that may be related to Bcl2, which is still incompletely understood. Cancer cells somehow inhibit the intrinsic apoptotic pathway, which involves the mitochondria. Additionally, cancer cells decrease aerobic metabolism by the mitochondria and preferentially use anaerobic metabolic processes instead - called the "Warburg Effect" by individuals in the metabolism and cancer fields. This was originally described by Otto Warburg almost 100 years ago - i.e. that cancer cells preferentially use anaerobic metabolism - but why this occurs is still unknown to present day.


Why is a hippo so big if it has round about the same genes as a mouse My science teacher told us that all mammals have round about the same number of genes. This confuses me, since there are very big and very small mammals. Where do genes come from and why do animals have such large differences in size between one another even if they have around the same amount of genes?

Genes are the "plans" for proteins in an organism; in turn, those proteins do all sorts of things, catalyzing chemical reactions and making up much of the structure of an organism.

A hippo is much bigger than a mouse, but it isn't that much more complex: both are going to have the same sorts of organs like a heart, lungs, kidneys, liver, brain. If you look at an individual cell from each animal from the same tissue, they will probably look almost identical! They are going to have similar metabolic pathways, etc. Their genes will be different, because some differences in proteins are necessary to build organisms of different structure and size, but the number of genes doesn't have to vary much, the hippo just needs to produce a lot more of the gene products, not have more plans.

A hippo will of course have way more genetic material, because it also has more cells and there is a copy of the DNA in every cell, but what your teacher is talking about is the number of genes within each cell.

Ultimately, genes come from evolution. You can read more about the basics of evolution somewhere like Berkeley's Evolution 101.


Are there any studies of epigenetic difference between twins during their lifespan? Are there any studies of epigenetic difference between twins during their lifespan ? I ask because I wonder if there exist phases during lifespan, when environmental factors plays major role (expecially in early adulthood) - twins study should allow to distinguish between changes in epigenetic  profile caused by external factors and that from "inner dynamics" of organism.

I would think there have to be, though do you mean collecting samples on a regular basis and plotting out the difference at each point? Or do you simply mean the total accumulated change. If it is the latter, the answer is certainly "yes". You have probably seen the Nova documentary "Ghost in Your Genes" (The US, not BBC one). In it they show comparison of accumulated epigenetic change between a pair of identical twin Spanish women. I'm guessing you are more looking at measuring this change on a regular basis and looking for points of rapid divergence.... I don't know if this has been done for individuals, but it appears that it has been done for sample sets (see the same documentary). They discuss accumulated genetic change in younger twins vs older ones...


How would homologous recombination and mutations affect speciation? I'm wondering how homologous recombination and mutations can affect how speciation can occur from one species (so that 2 will be created).

I'm doing research and I found that different mutations and genetic combinations occur in two geographically separated populations which can lead to speciation.

I know recombination can result in different genetic combinations, but how does that factor into a phylogenetic tree? Wouldn't recombination technically play no role in leading to evolution?

My (sort of) guess is that say recombination creates a population with a lot of AA genes and the other population, say by chance (genetic drift), has a population with a lot of aa genes.

We know A and a differ by perhaps a few SNPs, so on average, the two populations would become slightly different from one another due to genetic drift and geographic separation.

Do I have the right idea here? I'm not 100% sure how recombination during prophase I would affect recombination. Hoping someone can clarify this for me or provide some new insights.

Thank you!

Recombination occurs when homologous DNA sequences pair with each other and cross over, essentially swapping genetic material. Now, say that this crossover junction is in the middle of a gene, and we have some genetic differences in the top half and some in the bottom that distinguish the two alleles. If recombination occurs in the middle of the gene, then a new combination of alleles is created that didn't exist before. This new version of the chromosome can now be passed on as a single unit via sexual reproduction.

I left out a lot of details obviously, but this is the basic idea. The reason why recombination adds to genetic diversity and can lead to speciation is because it is essentially mixing and matching existing combinations to create new alleles.


I see various exposure limits for carbon monoxide, but what about one breath? I see exposure limits for carbon monoxide like 50 ppm over 8 hours. This would correspond to a total inspired volume of carbon monoxide on the order of a few hundred milliliters. This exposure is supposed to be far from fatal, but I'm unsure how to think about extrapolating long term exposure limits to acute limits, thus my questions:

What are the likely consequences if I breathed in the entire 200 ml of CO in a single breath, or even an entire lungful of pure CO?
If the answers to the above end up being "you would die", is there a reasonable way to estimate the maximum volume you could acutely breath in?

"In any high level CO environment, your exhaled breath CO level will gradually rise but remain lower than the ambient level because you always absorb some of the CO you inhale as long as the level in air is higher than the level in your blood.  As soon as you stop smoking or move to a lower CO environment, you start exhaling."

So I suspect a lungful of pure CO would indeed make you feel awful, but since that wouldn't be nearly enough to replace all the oxygen bound to your haemoglobin, I imagine it wouldn't be fatal in a healthy individual, especially if you were breathing air free of CO after that one lungful.

Apparently it takes 5 hours to eliminate half of your blood CO also.


Does mitochondrial eve have to exist? Suppose we took all living humans and found the set of their mothers, mothers' mothers, etc. and then traced down as far as possible. Is there a logical reason that this tree has to converge to one 'mitochondrial eve'?

Yes; she wouldn't necessarily have to be of the same species, but "mitochondrial Eve" must exist. The proof is pretty simple if you assume no one has more than one mother and that some mothers share a mother (and some other reasonable biological assumptions like the finite number of offspring).
Consider all living maternal lineages at any slice of time. This would effectively be a slice of all mothers, let's call it Generation N. In turn, these mothers all have mothers. We can call this Generation N-1. Not all women who have children in this generation are included: N-1 only contains mothers of the Generation N mothers. Generation N-1 must then be smaller than Generation N, because no mother has more than one mother. In practice, it's likely much smaller, since any mother who has more than one daughter who herself becomes a mother reduces the total possible by 1 more. You can recursively go through maternal generations N-2, N-3, etc this way and will find that every successive generation gets smaller. Eventually it will converge to 1 person, and that's your "Eve".
You can think about it similarly in the opposite direction, and find that as you go forward, extant maternal lineages can disappear but once a lineage disappears it cannot come back.
See also the Galton-Watson process.
A lot of "mothers" the same age as mitochondrial Eve have descendants today (in fact, they are likely to be either ancestors of everyone or ancestors of no one), but those lineages did not pass maternally. See also https://en.wikipedia.org/wiki/Pedigree_collapse


Which factors may affect a choice of an oviposition place in nocturnal moths? Winter Moth (Operophtera brumata) is a small brachypterous (females have stunned wings - unable to fly) moth which places eggs on thick branches.

I would like to know which abiotic and biotic factors may play a role in selection of place for oviposition. Taking into account that level of humidity is probably the same on whole tree (and probably whole forest) and the branches are so thick that they are not distinguishionable from surrounding environment (and there is no accumulated heat to identify their orientation (south, north etc.)

What other factors may play a role?

The winter moth's preferred host plants are mainly deciduous trees, oak being the main food plant and also many fruit trees, birch and hazel. Females generally deposit eggs in bark crevices, under bark scales, bark snags and under lichen along tree trunks of host species. Eggs are initially small and green but gradually change colour to orange and then red before hatching (reference 1 and reference 2).

Though the oak is preferred,

  There does not seem to be much discrimination in selection of host
  plant or oviposition site by the female (Wint 1983), as the choice of
  larval food plant depends on the female's pupation site and the
  direction she takes on emerging, as she just climbs up the nearest
  tree. So it might be fair to say that the larvae contribute more to
  host plant choice than the adults, as the larvae can balloon if the
  host plant is unsuitable. However there is the possibility that year
  after year each generation of females will climb up the same tree as
  their mother, and oaks (one of the most common host plants) can be
  hundreds of years old, so there could have been hundreds of
  generations of winter moth on the same tree (reference).

So that in effect means, that the thickness of branches or being indistinguishable should not be a factor. Regarding abiotic and biotic condition, the main abiotic conditions are precipitation, temperature and photoperiod.

An increase in temperature leads to more activity and a faster metabolism (reference) Since leaf buds open faster, there is a chance for eggs to be laid faster according because the larva needs to burrow into the buds before the leaf opens (bud-burst) Hatching is temperature dependant but I do not think that it effects the number of eggs much. Biotic factors like the presence of parasitic predators reduce population but does not seem to reduce the number of eggs.. (reference)


how can a pseudo coelomate like ascaris lay 200k eggs in a single day as per this site the dimensions of eggs of ascaris lumbricoides are 78-105 microns and as it is shown in the pic down here only half of the body cavity would be used for storage of all the stages of different sizes of eggs

and as we all know pseudo coelomates have very minute width of their body cavity
and rest of the body cavity is filled with mesoglea

so my question is how can a round worm accomodate $2$x$10^6$ eggs in its womb before its release

First of all, the statement that "pseudo coelomates have very minute width of their body cavity and rest of the body cavity is filled with mesoglea" is not correct at least for (large) nematodes and priapulids: they have quiet voluminous body cavity and no mesoglea. In small nematodes (to which Ascaris doesn't belong) the body cavity is indeed vestigial, but the "space" between the organs is filled with extracellular matrix.

Another point is that the eggs in nematodes develop not in the body cavity directly, but in the ovaries and uteri (as correctly shown in the picture you provided), which indeed occupy very large part of the body.

Now to the question about the counts: individual capacity of a single female 29 cm long was once (see also) estimated to be ca. 27 mln eggs contained in its ovaries and uteri, which is impressive, but reasonable given the extremely small size of the eggs and extremely large size of the worm.

If we very coarsely approximate the volume occupied by a single egg with a cube 70x70x70 µm3, we get ca. 9 ml for 27 mln of them, and not much imagination is required to see, how a female ascarid can find room for this volume of relatively loosely packed eggs in its genital system.

EDIT:
To check my statement about "quiet voluminous body cavity and no mesoglea" one can open any modern textbook on invertebrates (or attend a practical course of invertebrate zoology). This is how the nemotode body cavity is described in the monograph "Nematoda" by Vladimir Malakhov (the original I cite is in Russian, but there is also a translation of the book):

"The presence of a spacious body cavity is considered to be the most characteristic property of the whole class of nematodes".
"Schizocoel [= primary body cavity] doesn't have its own walls made of cellular material and is represented by spaces between organs filled with liquid".
"Nevertheless, it should be stressed, that the opinion of the schizocoel being a voluminous body cavity, appeared as a result of investigations on large parasitic nematodes."


Would a colony with only one male and female collapse? This is a thought experiment:

If we form a population with only a single founder pair, can this population survive? What would happen? Would this inbreeding cause the population to go extinct? Could such a population continue to exist indefinitely?

Populations founded by a single pair are quite common in the lab

The Drosophila Genetic Reference Panel, one such example of high artificial inbreeding, is a series of inbred lines where the researchers mated brother and sister flies for 20 generations to form the lines, which means they will be highly inbred. When you do these though you often lose many of the initial lines because of inbreeding depression. Inbreeding depression is reduced fitness as a result of increased homozygosity in the lines - deleterious mutations are more frequently expressed. I have tried to find the number of initial pairs they used to make the ~200 DGRP lines but come up unsuccessful, but I've heard it was around 1500 pairs, although that may be well off the mark*.

What would happen to your mice?

Just like the DGRP lines, there is a high risk that the population would collapse. However, if they do get through a few generations of inbreeding, and are kept in steady conditions (i.e. selection doesn't change once the lines are formed), then they have an ok chance of persisting. If you started with multiple founder pairs then there's a better chance you will still have some (very inbred) mice in a few generations. The success rate will depend on the frequency of deleterious mutations and strength of their effects.

What is inbreeding?

Inbreeding is increased homozygosity in the population than would be expected under random mating. For example, if the frequency of two alleles ($A_1$ and $A_2$) at a gene are $p = 0.1$ and $q = 0.9$ respectively, the expected frequency of $A_1A_1$ homozygotes is

$p^2 = 0.1^2 = 0.01$

the expected frequency of $A_2A_2$ homozygotes is

$q^2 = 0.9^2 = 0.81$

and the expected frequency of heterozygotes is

$A_1A_2$ is $2pq = 2 \times 0.1 \times 0.9 = 0.18$

If the true frequency of heterozygotes ($A_1A_2$) is less than 0.18, then there is inbreeding.

Is there a benefit to inbreeding?

Well inbreeding can be a good thing. Imagine all of those lines that did not collapse. It is possible that a population formed out of those would have higher fitness than the original population, because deleterious mutations may have been purged (lines carrying deleterious mutations are more likely to collapse). So a highly inbred population can prosper. However, that population would also have lower genetic variance. Genetic variance places limits on the potential for adaptation, low genetic variance means low potential to respond to selection. So, if selection is not constant, then inbred populations are more likely to go extinct as they are unable to adapt to novel scenarios.

Inbreeding in nature

One classical example of high inbreeding in nature is in cheetahs, where it is beleived they went through a strong genetic bottleneck ~10,000 years ago. The problems faced by cheetahs today really highlights the problems of high inbreeding because they are struggling to adapt. Genetic bottlenecking is a  serious long-term problem for many species including the Javan rhino, the Kakapo, Mountain Gorillas, and others; even if we can stop poaching and habitat loss wiping out these species in the short-term, they will struggle to adapt to changes in the climate etc..

  "As a species, cheetahs have famously low levels of genetic
  variation. This can probably be attributed to a population bottleneck
  they experienced around 10,000 years ago, barely avoiding extinction
  at the end of the last ice age. However, the situation has worsened in
  modern times. Habitat encroachment and poaching have further reduce
  cheetah numbers, consequently snuffing out even more genetic variation
  and leaving cheetahs even more vulnerable to extinction."

* Supporting material from the DGRP paper would suggest that it was indeed formed from 1500 isofemale lines.


Why do Centipedes always have an odd number of pairs of legs? Furthermore, centipedes are within the Myriapoda, a subphylum of arthropods which also contains millipedes. Do millipedes also have an odd number pair of legs?

Centipedes are part of the group of insects that utilize a short germ-band mode of embryonic development.1  One feature of this type of segmentation is that new segments are added sequentially to the end of the developing insect (the "posterior proliferative zone").  This is in contrast to insects that undergo long germ-band gastrulation, like Drosophila, where all segments are created simultaneously.
Additionally, Myriapoda demonstrate double segmental periodicity, meaning that segments are always added two at a time.  See the following informative figure from Damen 2004 2 --

Figure 2. Segmentation in the geophilomorph centipedes involves a phase of double segmental periodicity. The drawing shows a schematic model for segmentation in geophilomorphic centipedes. Segments are patterned in posterior tissue that does not show overt segmentation. Segments become molecularly defined in entities (coloured blocks) that eventually give rise to two segments each. Before morphological segments become visible, these two-segment entities are molecularly subdivided into segmental units
(dashed lines), which each eventually will give rise to one segment. For instance, at stage I C represents an entity that is refined into two units (C at stage II), which give rise to one segment each (C′ at stage III). This mechanism of segmentation provides a developmental constraint that only allows the addition of segments in bits of two and in this way only allows odd numbers of trunk segments in centipedes.

One would expect, then, to only see even numbers of leg pairs.  Arthur and Chipman explain this discrepancy in their 2005 essay 3 on Strigamia maritima, the most well-studied member of the Myriapoda subphylum.

Of course, if everything happens in twos, we would expect that there would always be an even, rather than odd, number of segments. But this apparent discrepancy is probably not real. It seems likely that the poison claw segment immediately anterior to the first pair of legs is really a modified trunk segment.

As for how Myriapoda add segments two at a time, I direct you to sources like Chipman and Akam 2008 4, though be prepared for some heavy reading on signaling cascades and morphogen gradients.

Citations

Hughes CL, Kaufman TC. Exploring myriapod segmentation: the expression patterns of even-skipped, engrailed, and wingless in a centipede. Dev Biol. 2002 Jul 1;247(1):47-61.
Damen WG. Arthropod segmentation: why centipedes are odd. Curr Biol. 2004 Jul 27;14(14):R557-9.
Arthur W, Chipman AD. The centipede Strigamia maritima: what it can tell us about the development and evolution of segmentation. Bioessays. 2005 Jun;27(6):653-60.
Chipman AD, Akam M. The segmentation cascade in the centipede Strigamia maritima: involvement of the Notch pathway and pair-rule gene homologues. Dev Biol. 2008 Jul 1;319(1):160-9.


Is a naive immune system equally able to handle new antigens as an educated one? This is a variation of the "does the immune system run out of memory" question.

Here's a (possibly imperfect) thought experiment: You take two twins. One of them lives in a bubble from birth. One of them is Mike Rowe from Dirty Jobs, and gets exposed to all sorts of antigens as well as vaccines. When they are 30 years old, you expose both of them to an antigen that neither has seen before. What happens?

PS: Note that while this example is illustrative, my question is really about whether there is any way at all in which the response of a naive immune system to a novel antigen is different from that of a very educated immune system (which has also not seen the antigen before). For instance, would the same amount of antigen be required to stimulate the immune system? Would the antibody count several months or years post-exposure differ?

They will both go through a primary and secondary immune response. So first low affinity antibodies will bind, the corresponding b cells will undergo affinity maturation, somatic hypermutation until high affinity (perfectly fitting) antibodies are available and these antibodies will finally undergo class switching.

Depending on the antigen an innate immune response will also be triggered as part of the first line of defense. There is no difference in the immune response between these two hypothetical brothers.


How do GPCRs transmit a signal across the plasma membrane? How do G-coupled protein receptors (GPCR) transmit signals through the plasma membrane?

Links containing information about this and pictures will be very helpful.

The G-coupled protein receptors (GPCR) transmit signals from outside of the cell into the cell and activate downstream signalling pathways. These change for example the expression of certain genes.

The whole process is a coorperation between the receptor, a G-protein, GTP as a co-factor and the ligand of the receptor (which starts the whole process). An extensive description (including much more images) is available in the Wikipedia, but in short, it looks like the images below (from the Wikipedia article on GPCR):

To answer how this signal is tranferred from the outside to the inside look at the first image: Upon ligand binding the conformation of the receptor changes its conformation and brings some of it transmembrane helices together so the G$\alpha$ subunit can bind here and activate downstream signalling.

The whole process happens in a few steps:

In the resting state the receptor has a trimeric G-protein (consisting of the subunits $\alpha, \beta$ and $\gamma$ bound on its cytosolic site. The G-protein also has a GDP molecule bound to it $\alpha$ subunit.
Upon binding of the ligand, the receptor changes its conformation, and G$\alpha$ exchanges the GD against GTP, which activates the complex.
The G-protein dissociates into the active G$\alpha$ the G$\beta\gamma$ subunits, which signal to downstream signal transduction pathways like the MAP-Kinase pathway.
Binding of RGS (regulator of G-protein signalling) to the g$\alpha$ subunit activates the intrinsic GTPase function of the subunit and hydrolyses GTP into GDP and P. The GDP stays bound to the G$\alpha$ subunit, which changes its conformation and forms the G-protein trimer at the receptor. At the receptor itself this induces also a change in conformation which makes the ligand dissociate from the receptor.

At the end of the fourth step the receptor has returned into its inactive form and stays there until the next ligand binding.


Why Do Healing Wounds Feel Warmer To The Touch? I fell over on my bicycle trying to avoid running over a rattlesnake, and ended up badly skinning my knee. It immediately began to bleed, but soon clotted.

It has been 2 days now and it has formed a thin scab and is healing well as far as I can tell. I was chilly from the air conditioning, and I noticed the wounded knee was much warmer than the healthy knee. It was very warm, while the other was rather cold to the touch.

I read here about skin healing, and thought, maybe it is because the blood rushed there to clot the wound. But, the wound is already clotted and sealed and the worst is over. So my question is:

Why is my wound and the area around it so much warmer days after the injury?

This is a normal part of the inflammatory process. Inflammation is your body's localised defensive response to tissue injury of any kind, and it is characterised by four cardinal signs- redness, swelling, heat and pain (severe inflammation involves a fifth, loss of function).

Your body is performing three main processes here:

Mobilisation of the body's defences.

Involves release of vasoactive chemicals, which cause the blood vessels to dilate and increase blood flow to the area. This causes the pain and heat, The blood vessels also produce cell-adhesion molecules which make immune cells (leukocytes) stick to the walls of the your blood vessels.
Containment and destruction of pathogens.

The immune system then goes to work clearing up any bacteria which have got into the wound. The leukocytes release chemicals called cytokines to attract more immune cells, to contain and destroy bacteria.
Tissue cleanup and repair.

Dead cells, cell fluid and other debris (pus) is then absorbed by the lymphatic system. Platelets and endothelial cells then secrete growth factors which stimulate cells called fibroblasts to multiply and produce collagen. The heat also increases metabolic rate and increases the rate of tissue repair.


Where in the nervous system are synapses chemical, and where are they electrical? Paraphrased from the Wikipedia article "Synapse":

There are two fundamentally different kinds of synapses:

Chemical synapses, which convert electrical activity in the presynaptic neuron into the release of neurotransmitters via the activation of voltage-gated calcium channels. The released neurotransmitters, which vary in type by cell, bind to receptors of the postsynaptic cell, giving rise to complex behaviors.
Electrical synapses, in which presynaptic and postsynaptic are connected by "gap junctions" or synaptic clefts capable of passing electrical current, resulting in rapid signal transduction.

Are there certain structures and locations in the nervous system that are mostly or exclusively chemical synapses, and certain ones that are mostly or exclusively electrical? Or, are they mixed throughout the nervous system?

For example, one might suppose that the neurons which transmit signals from brain to limbs might be electrical, due to the apparent advantage of fast transduction times in this scenario. On the other hand, it might be advantageous for the brain to be capable of more the dynamic, albeit slower, signal transmissions made possible by chemical synapses. Are these intuitions accurate?

Synapses are almost all chemical, the electrical synapses are more of a "special case".

The speed of transmission across limbs, etc, has very little to do with the speed of the actual synapse. The signal itself is conducted electrically inside a given cell (this is an "action potential"), aided in many cases by insulating myelination. The synapse is just the endpoint.

Some places where electrical synapses/gap junctions are present are:

Between cardiomyocytes, to synchronize heart contraction
Between certain networks of inhibitory interneurons in the CNS
In some (but not nearly all) reflex circuits


What bird is this (found at Alice Springs Desert Park in Australia)? I was reviewing photographs of the animals we found on our trip to Australia during the past September and I cannot find what is the bird in the picture. It was found inside Alice Springs Desert Park, so it has to be a native bird, same as all the others.

Could anyone please help me?

It is a Cisticola exilis as stated by @cezar
If someone has any objection please reopen this.


Are enhancers and silencers considered as epigenetic modifications? Are enhancers and silencers considered as epigenetic modifications? I am confused as it seems like enhancers and silencers are sequences on the DNA and how they work is through binding with proteins, while epigenetic changes seem to be changes made to the bases for instance adding a methyl group.

No.

Epigenetic information is (by definition) NOT included in the nucleotide sequence, but affects genetic expression.

Enhancers/silencers are themselves nucleotide sequences, and therefore not epigenetic information.

Methylation is an example of epigenetic information, but a DNA sequence itself is genetic information, even if it affects a gene.

CgATgCCAg= Genetic

Acetylation of a histone/DNA methylation= epigenetic

Hope that helps!

Further reading: http://www.whatisepigenetics.com/fundamentals/


Is there an advantage to having cellulite There are many ads nowadays advertising cellulite removal, and it causes me to wonder if there is an advantage to having cellulite or if it is just a result of too much fat unevenly spread?  Is it structurally more efficient at storing energy or providing insulation?

There's no advantage or disadvantage (beyond personal perception of attractiveness).

It's a benign condition that can occur with hormone changes, weight changes, and especially genetic predisposition.

It occurs in most women (up to 90% will have it at some point) and some men, and physicians consider it 'normal.'

http://www.mayoclinic.com/health/cellulite/DS00891


What plant is this? (Found in Southwest Germany in June) The picture was taken in Southwest Germany in June, and they covered the ground of a garden we were at...

I am almost sure this is Sedum reflexum (aka S. rupestre), in English prickmadam or crooked yellow stonecrop and in German Felsen-Mauerpfeffer. It usually grows at rocky or stony ground, not full of grass.

Distinctive features are the pointed leaves, which are not as round as in S. album and also the bended stem (flower stalks are always bend, hence the name reflexum). Its' flowers should be yellow.

These features can be seen well at the botanical drawing below (from wikipedia commons).

The reason I'm not completely sure is that in garden (and on roofs) exotic sedums are often planted.


1mm-long insect ID from Tennessee I live in east Tennessee. I went outside today (May 27.2017) and saw all these tiny insects all over my truck.

They are yellowish in color and have 6 legs, one solid body (including head). They move pretty quickly (like a chigger)

What are they?

The insects you have found must be of a species of thrips. This excerpt from Wikipedia fits your description well:

  Thrips (order Thysanoptera) are minute (1 mm long or less), slender insects with fringed wings and unique asymmetrical mouthparts. Different thrips species feed, mostly on plants although a few are predators, by puncturing and sucking up the contents. Approximately 6,000 species have been described.

I won't try to identify the exact species, but here is a photo of a yellowish-orange thrip I have found:

Image source:

https://6legs2many.files.wordpress.com/2012/04/thysanoptera_thrips_fringe_wings.jpg


Can someone identify this flowering bush from the US? This bush is in Tennessee, USA.:

Polygonum cuspidatum, common name Japanese knotweed. A notorious invasive species.

It's actually a herbaceous perennial (those stems grew in just one season, and will die back to the ground at the first hard freeze), not a shrub. The red things are ripening seeds, not flowers.


How much energy takes C4 photosyntesis to make glucose? Wikipedia has a kind of contradiction that I would like to understand:

According to this link

  The C3 pathway requires 18 ATP for the synthesis of one molecule of glucose while the C4 pathway requires 20 ATP. [...]

According to this other link:

  [...]. The C3 pathway requires 18 molecules of ATP for the synthesis of one molecule of glucose, whereas the C4 pathway requires 30 molecules of ATP.[...]

Also, I don't understand much of this, I was just curious. I found this link (not sure if reduction also means generate glucose):

  However, the C4 pathway of CO2 reduction expends more energy (5 ATP and 2 NADPH) than C3 pathway (3 ATP and 2 NADPH) (Hopkins 1999).

And this link:

  ATP consumed in C4 plants
  C4 cycle ( which involves regeneration of PEP from C3 acid) - requires 2 ATP per CO2 fixed.
  C3 cycle ( which is common in C2,C3,C4 cycle)- requires 3 ATP per CO2 fixed.
  Total - 5 ATP per CO2 fixed.
  Thus to form a hexose or to fix 6 CO2 6*5= 30 ATP

All emphasis mine.

So... Does C4 requires 20 or 30 ATP per molecule of glucose? I think I found more evidence over 30 than 20, is that correct?

Yes,C4 plants use 30 ATP molecules to make one molecule of Glucose.See since you have stated in your question that you know very less about biology and got some similar vibes from looking at your profile so I'll sum it up in a nutshell but hopefully this might help.In flowering plants,all of them follow a basic pathway know as the C3 cycle to make glucose from CO2.Now,in that process about 18  ATP is used.But apart from CO2, there's O2 also present in the atmosphere which interferes with the compounds taking part in C3 cycle and instead of CO2 participation O2 participates in the reaction and the consequence is that glucose is not produced and the plant wastes some energy in the form of ATP.

Now to prevent that from happening,some plants evolved themselves and made some chemicals which bind only with CO2.But the thing is that they also require energy to function and for each molecule of glucose produced they require 12 ATP this making net amount of ATP required to be 30 in a C4 plant.You can in a way visualise this C4 pathway that the plant placed some guards in the form of chemicals that combines with CO2 and makes sure it reaches its destination and to prevent traitor O2 molecules to disrupt plants from making glucose.But we all know that that guards would require some fee and so that fee is 12ATP.And visualise C3 pathway as some some sort of glucose making factory which makes glucose from CO2 and the production cost from raw materials is 18 ATP.


Why do depleted blood veins seem to appear near the surface (or skin) more frequently than blood vessels and arteries? I could be wrong, but it seems like blue veins generally exist closer to the surface of the body rather than red blood vessels and arteries. And I'm also wondering if this is evolutionary because during an injury, the outside gets damaged first, and I am just speculating that it's more important for muscle tissue to keep gaining blood from less damaged blood vessels than removing already depleted blood that simply bleeds anyway out due to the injury.

Or, if this is simply a trick of the color, that blue veins are just dramatically more noticeable and the first hypothesis is completely wrong.

Short Answer:

The veins you see are special veins right at the surface; major arteries are typically much deeper in the tissue.

Longer Answer:

Great question. Usually veins and arteries come in more or less one-to-one pairings, traveling side-by-side (often nerves accompany them as well). Both types of vessels tend to be fairly deep, because, as you note, damage to blood vessels can be quite problematic.

However, superficial veins, the ones you can typically see right under the surface of the skin, are different. They don't have a direct artery pairing, and they are not the only venous drainage from the areas distal to them.

Instead, superficial veins have a known purpose in temperature regulation. When core temperature is high, the superficial veins are relatively dilated to allow temperature exchange between the blood and outside. When core temperature is low, the superficial veins constrict to cause the blood to flow deeper and retain heat.

A nice side benefit to these superficial veins is that, because they aren't completely necessary for circulation, they can be harvested as surrogate vessels to divert around a blocked artery, like in coronary artery bypass grafting. The saphenous vein from the leg is often used. Superficial veins can also be removed for cosmetic reasons.

References

Webb-Peploe, M. M., & Shepherd, J. T. (1968). Responses of the superficial limb veins of the dog to changes in temperature. Circulation research, 22(6), 737-746.


Extending a small fragment of DNA Is there a way to extend a small fragment of DNA, say 150 bp, by making copies of itself and attaching each copy of that small fragment to the end of that 150 bp sequence?

For example, I want a 1 kbp+ DNA fragment made up of copies of that exact 150 bp sequence.

I am performing optical tests on DNA strands, but the issue is that the DNA fragments that I am targeting are too small.

However, if the DNA fragment is just a repeated sequence of the DNA fragment I am testing, the tests will yield the same results. For that reason, I am trying to create a long strand of DNA from just one DNA fragment copied over and over.

Is there a procedure that I can follow to accomplish this?

If what you trying to get is 1kbp of repetitive 150bp sequences, then synthesis as a large chunk might be better idea. It costs ~150-300$ but will potentially save tons of time. (see gBlock from IDT in US)

PCR and ligation with repetitive sequences is pain the butt. It might be true that you save money, but time and frustration could be more expensive.


Are there transposons which create homozygous genotypes in offspring? Transposons copy or cut and paste gene sequences. Alleles are passed down from parents and offspring may be heterozygous or homozygous for an allele (assuming diploidy).

Are there any transposons which ensure the frequency of a given genotype in a population by converting heterozygous zygotes into homozygous zygotes?

I study transposons for my PhD; I am not aware of any that preferentially insert through an active mechanism to an un-inserted allele.

There are tranposons such as R1/R2 which have a 'favorite' insertion site and will insert/compete for that sequence. That's kind of similar to your question but not generalizable.

The predominant factor I can think of which would cause such a thing to arise would be gene conversion in which the insert allele is used as a repair template for an un-inserted allele. Gene conversion is rare but can explain how the TE insertion is found on multiple haplotypes.

It's very unlikely that the alternative hypothesis occurs in which the same type of TE inserts at the exact same position in two different haplotypes and that TE doesn't have a preferred insertion site.


Can I do an MS in biotechnology after a bachelors degree in chemical engineering? I recently graduated from high school and now have to make a decision about my undergrad major. I am interested in biotechnology but my parents suggested that I should opt for a broad based degree and then specialize in my field of interest in grad school. So I read up about chemical engineering and I think it would be an interesting major, but my real interest probably lies in biotech.Is it possible to transition form chemical engineering to bio-related fields in grad school?

This will probably to a high degree depend on the (exact) curriculum and prerequisites of your chosen bachelor and master.
Also note that I'm not from the US and judging from the terms you are using, it seems that you are, so everything I say is also a bit speculative.

In general biochemistry and to some degrees also biotechnology will have a lot of overlap with many aspects of chemistry (or at least organic chemistry). Depending of the focus of each program this might, make it possible to switch over from one to the other. One thing you will definitely not learn in any chemical mayor is molecular biology, which may well be a requirement for studying in any biotech related field later on.

If both your majors focus more on the technological aspect and less on the biological or chemical you should probably be fine. The equipments used in (modern) biology and chemistry is in many cases similar, though biotech involves more equipment specialised for the handling and analysis of cells. The underlying principles are still the same though.

In your case I would recommend you to check the requirements of different MS or grad schools, that you'd be interested in first, and the see if you can meet these with a chemical engineering mayor (and maybe/probably some added courses like molecular biology).


Can anyone identify the worm in this video clip? My wife came across this youtube clip of a spider and a worm. Can anyone identify at least the phylum?

I think it's a Gordian worm or more accurately known as Spinochordodes tellinii . Good music for a parasitic event like that by the way. Nematomorpha is the phylum.

If your a molecular guy, check out Spinochordodes tellinii and the WNT pathway, pretty cool stuff.


How does beta branching stop alpha helices from forming? I am told that beta branching interferes with alpha helix formation.

Problem is that I don't see how beta branching has anything to do with alpha-helix formation. Beta-branches are on the outside of alpha helices and internal hydrogen bonding holds the helix together.

My book (Lehninger) also doesn't say anything about beta branching interfering with alpha helix formation.

The answer to this, as said by @canadianer in comment, is that beta branched amino acids are bulky and can sterically clash with neighbouring atoms, forcing the backbone to adopt torsion angles which don't favour helix formation.

I couldn't find reference for these exact words, but similar one here:

  amino acids such as Valine, Isoleucine, and Threonine all have branching at the beta carbon, this will cause steric clashes in an alpha helix arrangement... valine, threonine, and isoleucine will often destabilize the helix because of branching of the beta carbon. These three amino acid residues are more often found in beta-pleated sheets, where their side chains will lie in a separate plane than the main chain.

Also, for torsion angles, from same source:

  The torsion angle is the measure in degrees in bonds between atoms. Folding of proteins are influenced by the degree of rotation amino bonds can hold. There are two different types of torsion angles existing in polypeptide bonds. Psi, ψ is the angle between the α-carbon and the nitrogen atom of a peptide bond. The other bond is called phi, φ which is the angle between the α-carbon and the carbonyl group.

See this table for details of which amino acid prefers which configuration:

Source


Can we use Acetyl Phosphate instead of Acetyl CoA in TCA? I am thinking Citric Acid cycle and activation of the end parts of Acetyl and alfa-ketoglutarate.
Let's consider only now Acetyl to make things simpler.

I have tried to explain the thing by symmetry - phosphate tetrahedral, while coenzyme A seems to be mostly some V shaped.
However, it does not help.

Can human body use Acetyl Phosphate instead of Acetyl CoA in TCA in some situations?

I know that you can activate acetyl-CoA again by phosphate:

acetyl-CoA + phosphate <-> CoA + acetyl phosphate

Enzymes are usually specific to a greater or lesser extent for their substrates. In this case we are looking at citrate synthase which catalyses a condensation reaction in which the acetyl group from acetyl-CoA is added to an oxaloacetate molecule to form citrate. This is the entry point for carbon into the TCA cycle for energy production. The condensation reaction follows an ordered pathway: oxalocatetate binds first and this results in a conformational change which increases the enzyme's affinity for acetyl-CoA by a factor of 20.

Citrate synthase is highly specific for acetyl-CoA as a substrate. The cited reference discusses several aspects of this specificity. The enzyme has a well-defined binding site for CoA, with contacts from both the small and large subunits. This includes the recognition of the adenylyl portion of the molecule.

A relevant quotation from the review:

  "Citrate synthase is highly specific towards its substrates. The condensation reaction occurs only with the physiological substrates oxaloacetate and acetyl-CoA."

So, the answer is that citrate synthase cannot use acetyl-phosphate as a substrate because of its specificity for acetyl-CoA.

Wiegand,G and Remington, SJ (1986) Citrate Synthase: Structure, Control, and Mechanism. Ann. Rev. Biophys. 15: 97–117


Why does a cockroach not die even after decapitation? Why does a cockroach not die after its head is cut off?

Based on an article here, unlike humans, cockroaches have an open circulatory system. They don't have a huge network of blood vessels like that of humans, or tiny capillaries that you need a lot of pressure to flow blood through. Hence after you cut their heads off, very often their necks would seal off just by clotting.

According to the article cockroaches breathe through spiracles, or little holes in each body segment. Plus, the roach brain does not control this breathing and blood does not carry oxygen throughout the body. Rather, the spiracles pipe air directly to tissues through a set of tubes called tracheae. In addition cockroaches are poikilotherms, or cold-blooded, meaning they need much less food than humans do. Hence cockroaches can survive decapitation.


How many times can a human get chicken pox? How many times can a human get chicken pox?
For example: I got chicken pox, and recovered. If I was infected with HIV, and I am exposed to chicken pox again, can it infect me second time?, According to what I've heard, chicken pox comes only one time, because of the immune system of humans. But if I am infected with HIV and so definitely have immune system damage, will chicken pox come a second time, or will the immune system still protect the body from chicken pox?

Usually you get chicken pox only once in your life, the recurring form are usually shingles.  But: It can happen (also in people which are not immunocompromized). I know two persons which got chicken pox twice and which are otherwise normal in regards of their immune system.

Persons with an HIV infection are more at risk here. They can develop both forms and depending on how much their immune system is already affected by the HIV infection can develop severe forms of the infection. It might be necessary to treat them with antiviral drugs. So it is clearly recommended to ask a MD about this. See here for more details.


Why is metabolism of ethanol catabolism? Could it be also detoxification? Detoxification is the physiological or medicinal removal of toxic substances from a living organism, including the human body, which is mainly carried out by the liver. Additionally, it can refer to the period of withdrawal during which an organism returns to homeostasis after long-term use of an addictive substance. (Source: https://en.wikipedia.org/wiki/Detoxification)

Ethanol is metabolised in liver with ADH, which oxidises ethanol to acetaldehyde. The latter is a toxic substance and can cause tissue damage, therfore, it must be further oxidised by ALDH to form a non-toxic product, acetate.
Ethanol can be an addictive substance.

Why is ethanol metabolism catagorized as catabolism? Could it also be detoxification (according to the assumptions above)? Why not?

Is ethanol metabolism a catabolic metabolic pathway because it provides NADH and acetate (which can be activated to acetyl-CoA) for anabolic reactions? Or is there another reason?

These are somewhat loosely defined terms, but I would say catabolism is any metabolic process that extracts energy from a substrate. Ethanol conversion to acetate (via alcohol dehydrogenase; see this schematic) is an oxidative pathway which extracts energy in the form of NADH, so yes, it is a catabolic pathway.

I guess you can also call this process detoxification, since it removes a (mildly) toxic metabolite. Anyway, I think the "classification" of a pathway is less important than understanding the actual biochemistry.


Enzyme Assay, absorbance change to concentration change I have a few issues with this question.

An enzyme assay is performed and the kinetic data graphed. The y-intercept of a Lineweaver-Burk plot is 0.6 min/ΔA. The substrate being assayed has a molar absorbance coefficient (ε) of 4500 L/mol.cm.
What is the V max of the enzyme in mmol/L.min?

My working:

Vmax = 1 / 0.6min/ΔA = 1.66ΔA/min (the units switch back I believe?)

And then 1.66ΔA/min / 4.5L/mmol.cm to get 0.37 mmol/L.min?

see here.

y-intercept = $\frac{1}{V_{max}}$

To convert absorbance to concentration, plot the standard curve and get the linear relationship between the two quantities. Make sure that the line that you fit (for standard curve) passes through origin.


Why do Phobia exist if they aren't advantageous? A phobia is usually the irrational fear of something, and the individual experiencing it is often unable to justify whether there is such detestation of something which might not even be threatening.

I am aware that there are:

Agoraphobia
Social Phobia
Specific Phobias such as Arachnophobia (fear of spiders) or Ophidiophobia (fear of snakes)

My question is, why do some people have e.g. Arachnophobia but not something closely related such as Entomophobia (fear of insects)?
And why do phobias even exist at all? To me they don't seem to serve a purpose (protection), and do not seem to be of advantageous existence.
Furthermore, I am curious to why exactly a phobia exists – and in some cases manages to be  passed on from the parent to the offspring.

DISCLAIMER:

I am aware of there being several psychological processes involved in this such as events that occurred in early years, or if there is a relative with anxiety, the risk of you suffering of a phobia is significantly larger. I also heard there is a high incidence of people developing phobias after traumatic brain injuries.

However, I am interested in the biological aspect of a phobia, and that why if it isn't advantageous to us, why does it exist?

I think the fault in your reasoning is the assumption that phobias are not advantageous to us. As an example of a potentially useful phobia, consider the fear of heights. Now consider two different ancestors: one who was afraid of heights and one who was not. Generally speaking, the ancestor who was afraid of heights would likely avoid such environments and thereby reduce the likelihood of, say, falling off a cliff or high precipice. In evolutionary terms, we would say that natural selection confers an advantage to the phobia-possessing individual(s). This website in particular has some interesting reading:

  Others believe that phobias exist because of evolutionary development to avoid danger in order to improve survival. There are several stimuli that are shared by the most phobic people (heights, insects, crowds, etc.) These phobias, with a couple of exceptions, relate more closely to pre-technological societies. Thus, some scientists, such as Martin Seligman, believe that people are inherently "prepared" to fear certain objects. ((5))) In other words, our phobias relate closely to the perils of our ancestors, as through natural selection, those who feared the dangerous stimulus survived while those who didn't, died off. Prepared fears appear to be very easily conditioned. Some scientists, such as LeDoux, believe that preparedness and the ease of conditioning are the result of certain preexisting neurological connections that exist evolutionarily. These connections are turned on with relative ease.


What are the trajectories of flying insects? Many flying insects tend to have very jagged trajectories. For moves of a fruit fly looks like a random walk.

Is there any research on the properties of trajectories (e.g. their fractal dimension or mathematical models producing similar behaviour)?

Besides the path of a single insect, I am also interested in the interaction of a small number of insects (e.g. 2 or 3).

I am aware of the research in flocking and swarming (e.g. Tamas Vicsek, Anna Zafiris, Collective motion 2010) and of techniques of obtaining such trajectories (e.g. Danping Zou, Yan Qiu Chen, Acquiring 3D motion trajectories of large numbers of swarming animals or an open access pdf, 2009). However, I haven't found within them an answer to my particular question.

Dickinson (2005) has a good review of insect flight, including behavior, biomechanics, electrophysiology, and neural control with links to more of the primary literature. What follows is a general summary thereof.

The jagged trajectories you mention are called saccades in the insect flight literature. In Drosophila, saccades are ~90° turns accomplished in approximately 50 ms. Because flies can't move their eyes independently of their heads, saccades are though to allow a relatively constant visual field most of the time, interspersed with rapid reorientations during which the fly is "blind."

The actual turn begins with the generation of a torque, which starts the fly turning. Shortly thereafter, the halteres sense this change and a counter-torque is produces, which stops the turn.

Rather than random turns, Drosophila are turning away from visual expansion as they near objects. So as they move closer to an object, it expands in their visual field, and they turn away from it.


Is vermiform appendix no more a vestigial organ? The appendix has a role in the immune response.

So is it therefore recently removed from the list of vestigial organs?

Short Answer: No, the appendix is still considered a vestigial organ.

Long Answer: The idea that that vermiform appendix is vestigial originated when Kumar et al (1989) removed it from the body, but failed to find any side-effects. From then on, it got widely established that vermiform appendix is a vestigial organ and has lost all its functions during the course of evolution. The reason behind appendix becoming vestigial was given by Darwin himself in The Descent of Man, and Selection in Relation to Sex where he stated that appendix was used by early primates to digest leaves, and slowly became vestigial as ancient humans shifted towards foods like cereals and meat. This theory was also supported by presence of very long cecum in herbivores like koala and horse.

The only problem with this idea was that the role of appendix in only digestion was being considered. As appendix was connected to large intestine, so early scientists (kinda) presumed that it should be related to only digestion.

This theory got its first challenge when Parker et al (2007) suggested the appendix to be a safe-house of healthy bacteria when illness (such as diarrhea) flushes them out of the GI tract. It was based on the understanding, which came in 2000s by Sonnenburg et al (2004) and Everett et al (2004), about how the immune system supports the growth of beneficial intestinal bacteria. This was experimentally established when Dunn et al found that individuals without an appendix were four times more likely to have a recurrence of Clostridium difficile colitis.

After this, more functions of appendix were discovered, especially those related to immune system. It is because of the efforts of Zahid et al (2004) (the one you cite) and Rankin et al (2016) that appendix is now identified to be more related to immune system than digestive system in humans.

Also, research by Laurin et al (2011) and Smith et al (2013) concluded that during the evolutionary course, appendix has evolved about 38 times and lost as many as 6 times, suggesting that the cecal appendix has a selective advantage in many situations and argues strongly against its vestigial nature.

Conclusion:

Vermiform appendix is identified as Gut Associated Lymphoid Tissue (GALT) and important component in mammalian mucosal immune function, B-cell mediated immune response and extrathymically derived T-cells.
This structure helps in the proper movement and removal of waste matter in the digestive system, contains lymphatic vessels that regulate pathogens, and lastly, might even produce early defences that prevent deadly diseases.
It is thought that appendix may provide more immune defences from invading pathogens and getting the lymphatic system's B and T cells to fight the viruses and bacteria that infect that portion of the bowel and training them, so that immune responses are targeted and more able to reliably and less dangerously fight off pathogens.

Discussion: The problem is in the definition itself of vestigial organs. The point is that being vestigial is not equal to being useless. See this definition by Wikipedia (emphasis mine):

  In the context of human evolution, human vestigiality involves those traits (such as organs or behaviors) occurring in humans that have lost all or most of their original function through evolution. Although structures called vestigial often appear functionless, a vestigial structure may retain lesser functions or develop minor new ones. In some cases, structures once identified as vestigial simply had an unrecognized function.

Now, since vermiform appendix does not perform its (suggested) original function of digesting cellulose and other indigestible materials, and performs much less of its (possible) function in immune system, it is still officially considered as vestigial organ.

References:
 • Vermiform Appendix - Wikipedia
 • Human Vestigiality - Wikipedia
 • Kumar, Vinay; Robbins, Stanley L.; Cotran, Ramzi S. (1989). Robbins' pathologic basis of disease (4th ed.)
 • Darwin, Charles (1871) "Jim's Jesus". The Descent of Man, and Selection in Relation to Sex
 • Bollinger, R.R.; Barbas, A.S.; Bush, E.L.; Lin, S.S.; Parker, W. (21 December 2007). "Biofilms in the large bowel suggest an apparent function of the human vermiform appendix"
 • Sonnenburg J.L.; Angenent L.T.; Gordon J.I. (June 2004). "Getting a grip on things: how do communities of bacterial symbionts become established in our intestine?"
 • Everett M.L.; Palestrant D.; Miller S.E.; Bollinger R.R.; Parker W. (2004). "Immune exclusion and immune inclusion: a new model of host-bacterial interactions in the gut"
 • Dunn, Rob. "Your Appendix Could Save Your Life"
 • Zahid, Aliya (2004-04-01). "The vermiform appendix: not a useless organ"
 • Rankin, Lucille C.; Girard-Madoux, Mathilde J. H.; Seillet, Cyril; Mielke, Lisa A.; Kerdiles, Yann; Fenis, Aurore; Wieduwild, Elisabeth; Putoczki, Tracy; Mondot, Stanislas (2016-02-01). "Complementarity and redundancy of IL-22-producing innate lymphoid cells"
 • Laurin M.; Everett, M.L.; Parker W. (2011). "The cecal appendix: one more immune component with a function disturbed by post-industrial culture"
 • Smith H. F.; Parker W.; Kotzé, S. H.; Laurin, M. (2013). "Multiple independent appearances of the cecal appendix in mammalian evolution and an investigation of related ecological and anatomical factors"


Which Enzymes Catalyse the Deacetylation of Drugs in the Human Body? If you would like more specifics seeing how I realise that this question is very broad and may be difficult to answer in general then hopefully the following will help you out:

I am particularly interested in acetyl groups bound by carbon single bonds
Drug metabolism in the liver particularly interests me
The drug paracetamol's (acetaminophen) deacetylation to p-aminophenol is of particular interest to me.

Acetyl esters can be deacetylated by carboxylesterases.

In case of an acyl/aryl group attached to acetate group (e.g., benzoate), I guess it will first undergo ring opening and then beta oxidation (as in case of tyrosine).

Paracetamol -> p-aminophenol is a deamidation (I am not sure, but enzymes like ornithine decarboxylase can do that job... just a guess).


Why proteinase K doesn't degrade itself? Can anyone tell me why proteinase K doesn't degrade itself?

If possible please provide me the source.

According to invitrogen proteinase K does undergo autolysis, but that some leftover fragments still have protease activity. The solution should be stored at -20C, this low temperature is probably the best way to prevent autolysis. If you're using the enzyme to digest protein at 37C, you'll just have to deal with losing the proteinase k during the reaction and make sure you add enough to destroy the target protein before the proteinase is depleted.


What is indirect vs direction selection of genes? As the title suggests, what is the direct and indirect selection of genes. Couldn't find a straightforward answer. Is it the same as direct and indirect fitness?

Direct selection is when the fitness is directly associated with a certain gene. The beneficial alleles of this gene get selected.

When an allele gets selected not because of its direct effect on fitness but because of other reasons for e.g. strong linkage with other genes which in turn are being selected, then it is said to be undergoing indirect selection.

From Kirkpatrick and Barton (1997)

  Female preferences have caused the evolution of extreme male mating
  displays throughout the animal kingdom (1–3). One mechanism that might
  establish these preferences is indirect selection, which occurs when
  preference genes are associated (that is, in linkage disequilibrium)
  with other genes that are spreading under selection. Indirect
  selection is invoked by two types of theories (2). The first are “good
  genes” theories, which interpret male mating displays as indicators of
  high viability. In this view, the expression of the male display is
  correlated with the presence of alleles that increase viability.
  Because associations naturally develop between preference genes and
  male trait genes, as the high viability alleles spread by natural
  selection, preference alleles for extreme displays also spread. The
  second class of theories that postulates indirect selection involves a
  “runaway process.” Here alleles that exaggerate a male mating display
  decrease survival but nevertheless spread because they enhance male
  mating success. Genes for extreme preferences can then be established
  as the result of their associations with these spreading male trait
  genes.


How do tumor cells 'gravitate' towards each other? In a popular article it is mentioned that in centrifugal experiments with cancer cells that

  When subjected to microgravity-conditions, the cancer cells were unable to sense each other and therefore had a very hard time coming together.

which is because

  [...] the process through which cancer grows and spreads would seem to indicate that there is a means through which the cells are able to sense each other and gravitate together to form a tumor.

I would now be interested in the role of such fundamental forces in cell-signaling.

How does gravity interact with cell-signaling and lead to the 'gravitation' of tumor cells towards one another?

To my knowledge, cell signaling is a bunch of processes that involve the propagation of electrical signals by chemical means, so I am rather surprised that gravity would play any role in this.

It is reported that 99 genes are significantly upregulated in presence of normal gravity, whereas in absence of gravitational force no gene expression is seen in case of T cell activation. Research article attached concluded  that gravity is important for regulating various essential T-cell activation signalling pathways, which play key role in cell proliferation and apoptosis.

Transcription factors like NF-kB, CREB, ELK, AP-1, and STAT are responsible for tumor cell development. And NF-kB and CREB showed gravity-mediated gene expression. As, the PKA
signaling pathway regulates expression of these transcription factor, so it means that gravitational force moderates PKA signalling. And PKA signalling also mediates tumorigenesis. So, by regulating various cell signalling pathways, gravity controls the tumor cells.

Gravity also modulates the activity of Epidermal growth factor, which are implicated in tumor progression. (Via: https://www.ncbi.nlm.nih.gov/pubmed/7757250)


Activation of Glycogen Synthesis by Insulin - mechanism and cellular location? My textbook states the following...

Insulin activates enzymes that convert glucose to glycogen.

Does this conversion occur inside or outside the liver and muscle cells?

If it is inside, does the Insulin act as the primary messenger and activate an enzyme cascade that activates glycogen synthase?

Insulin, like glucagon, binds to receptors on the surface of muscle cells and illicits a response that is transduced to produce changes of phosphorylation in the enzymes controlling glycogen turnover. Unlike glucagon it does not initiate an enzyme phosphorylation cascade, but its binding to the receptor causes autophosphorylation on tyrosine residues, resulting in protein–protein interactions which lead to the activation of various enzymes through subsequent phosphorylations.

I would recommend you go to Berg et al. in NCBI Bookshelf online — rather than Wikipedia — for this kind of thing. It is a best-selling biochemistry textbook which is produced with great care (even if the edition online is out of date). Thus in Section 21.5.2 you will find:

  How is glycogen synthesis stimulated? As stated earlier, the presence of glucagon signifies the starved state and initiates glycogen breakdown while inhibiting glycogen synthesis. When blood-glucose levels are high, insulin stimulates the synthesis of glycogen by triggering a pathway that activates protein phosphatase 1 (Figure 21.20). The first step in the action of insulin is its binding to a receptor tyrosine kinase in the plasma membrane. Multiple phosphorylations again serve as the instigation for a regulatory wave of dephosphorylations. The binding of insulin to its receptor leads to the activation of an insulin-sensitive protein kinase that phosphorylates the RGl subunit of PP1 at a site different from that modified by protein kinase A. This phosphorylation leads to the association of the RGl subunit with PP1 and the glycogen molecule. The consequent dephosphorylation of glycogen synthase, phosphorylase kinase, and phosphorylase promotes glycogen synthesis and blocks its degradation.

I am assuming that you are familiar with the pathways of glycogen synthesis and breakdown. (If not, search for this in Berg et al.) At the risk of violating copyright, I reproduce Figure 21.20 below:

You can read more about the insulin receptor in Section 15.4.1 of Berg et al.

Addendum

Insulin also affects glycogen synthesis indirectly by stimulating/activating the glucose transporter, GLUT4. The mechanism by which this is accomplished is less well established than that described above.


what will be the effect of cockroach bite? I know the cockroaches are creepy for humans. But I want to know why humans are afraid of cockroaches and what will be the effect of there bite on my body. Can I touch them or if they walk over my foot is safe for me!

Are they toxic like snake or scorpion?
How they bite us?
What will be the effect if more than one cockroaches bite me?
Do I still get any disease if they don't bite me but present in my house?

There is already a question related to cockroaches bite on this form but it's about cockroaches lay eggs or not while biting and it doesn't explain the possible effects of the bite.

I have reared cockroaches by the thousands, for years. Three species, but mainly the infamous Periplaneta americana which I am sure everyone has at least heard about (see picture at the end).

First of all: Cockroaches do bite, and they have powerful mandibles. This is in the paper below:

https://doi.org/10.1371/journal.pone.0141226

Many people think they won't bite because they have never handled cockroaches. In fact, cockroaches are amongst the most common insects scavenging dead bodies, and they'll pester sleeping individuals when they're starving (e.g. in crowded infested buildings or ships).

In the case of large P. americana, males are way more prone to biting than females, especially when they're flying around. I have been bit three times by these cockroaches, and it hurts. Once I was wearing latex gloves and seized a large male, and it bit me through the glove. Because of the pinch, I pulled it off with my other hand, and the glove teared open. Last time, I was bit about 1.5 year ago on the shoulder in my sleep by an adult female P. australasiae. The pinch was enough to wake me up (so I could kill the bloody roach) and left a red mark that lasted for 2 days.

There are numerous reports of cockroach bites going infected, specially around lips. Linked paper is referenced as: http://dx.doi.org/10.1590/S1413-86702006000100006

Finally, they're not poisonous neither venomous insects, as they produce no relevant toxins. However they may carry many pathogenic microbes, so laster effects from contact with cockroaches may develop.

Hope this was clear enough!


In human anatomy / biomechanics, what is the motion called when the arm swings sideways so the elbow moves in an arc of 90 degrees? In human anatomy / biomechanics, what is the motion called when the arm swings sideways so the elbow moves in an arc of 90 degrees?
So e.g. if a person was to elbow somebody behind them , or if somebody had their arm out and then swung it keeping it parallel with the floor.
Like in this video
https://www.youtube.com/watch?v=IOh2-4WWzEE

It’s humeral retroversion at a 90 degrees abduction angle with extended elbow and slightly internally rotated shoulder.


What is the point at which abiogenesis is complete and evolution begins? Is the minimum criterion for life a single cell?  It seems that self-replicating RNA is not enough, but I don't know.

What would be the most basic cell that could fit this criterion and what cells today would be most similar?

I think it's a mistake to assume that there is such a point. All plausible seeming models of abiogenesis currently under consideration involve evolutionary processes long before they reach the stage we'd consider alive.

Evolution will occur whenever there is (a) replication-with-error and (b) selection (simplifying slightly). This is the case with a self-replicating RNA. It is replicating, but those replicates can be imperfect. Imperfections in replication that improve its ability to replicate will be favoured. That's evolution.


Blood samples in cell lysis I will be joining a team of field biologists on a trip to some uninhabited islands in the tropics. We will be collecting bird blood samples for some genetic research. We will be out there for two weeks. Will blood samples in lysis buffer last for two weeks with out refrigeration or freezing them? Or should we do our sampling closer to the day we leave so they have less time in tropical heat?

The exact answer to this greatly depends on the lysis buffer used, what you are lysing the cells for (DNA/RNA isolation, protein analysis, etc.) and how you intend to quantify your samples.
https://www.sigmaaldrich.com/content/dam/sigma-aldrich/docs/Roche/Bulletin/1/11814389001bul.pdf
This is a link to a standard red blood cell lysis buffer and handling recommendations. Note the following:

Lysis buffer must be stored at low temps prior to use
Use blood stored in EDTA, citrate or heparin anticoagulants
To obtain RNA use fresh blood only
For best results in DNA applications, use fresh blood or blood stored for less than 3 days.

Here is another paper describing the effects on DNA/RNA extracted from blood in ranging temperatures and storage methods
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0184692


Can aflotoxin presence be inferred from the mild discolorotion at the middle parts of a hazelnut? Can aflotoxin presence be inferred from the mild discolorotion at the middle parts of a hazelnut?
For instance, how likely is it that the hazelnuts pictured below contain Aflotoxin?

P.S.: these hazelnuts were fried before packaging in a vacuum sealed plastic bag. ( I am not sure whether the color change in the middle part comes from fungal activity (e.g., aflotoxins) or from the frying process?)

Depends on who you bought them from and how you stored them.
Molds can grow in nuts and nutmeats and produce mycotoxins (from toxin-producing strains such as aflatoxins by Aspergillus flavus). The mold is usually visible and below is picture of Aspergillus flavus growing on a nut product. Source

The amount of aflatoxin produced by the mold is dependent on weather conditions and storage. We can only account for or control the storage conditions. When food substances are not well preserved, fungal growth may occur, leading to the production of mycotoxins.
The pictures presented could also just be an improper storage (with no health risks). There's indication that storage of wet nuts in poorly ventilated silos increases the potential for developing kernel brown centers. Source
If these nuts were stored in improper conditions from farm to store and the farm has been associated with a breakout of Aspergillus flavus then there's chance, but slim. QA/QC and aflatoxin levels are regulated. Codex Standard 193-1995 mentions the maximum levels of aflatoxins and sampling plans.
If the nuts had mold on them and they were washed to get rid of the surface mold, they could have spores from Aspergillus flavus capable of producing alfatoxin. Aspergillus fungi can case discoloration of  certain grains (rice), but that implies that you're able to see them on the product (the mold growth). The nuts in the picture seem quite clear.
In terms of where you bought the product, street vendors are at higher risk of having their products present alfatoxin problems rather than commercial enterprises, because of the location the product is sold at. Source


Can an organism obtaining a part of its genome via horizontal gene transfer be called a "hybrid"? Wikipedia definition of "hybrid" offers many competing definitions. But most seem to be centered on sexual-reproduction gene transfer.

Is there an official (in a textbook or widely accepted peer reviewed work) definition of a "hybrid"/"hybridization" that would clearly include ANY genetic mixing, most specifically obtaining genes via horizontal gene transfer?

If not, is it specifically because "hybrid" requires sexual reproduction, or merely because it requires a certain minimal amount of inherited genetic material from both sides, and horisontal genetic transfer in practice involves significantly less genetic material being inherited?

As you point out, there isn't a singularly accepted biological defnition of 'hybrid.' The most basic would be a single organism that exhibits traits of two individual organisms, but that will find perfectly acceptable disagreement depending on who you talk to. You, for instance, are human - but a hybrid of your parents' genomes.

So I would personally say that horizontal gene transfer is equivalent to gene inheritance, and that as long as the organism exhibited traits of both 'parent' individuals - then yes, it is a hybrid. Some might include that even if it didn't exhibit traits and merely contained the genes in any inherited genomic data that the hybrid label would be appropriate.


How does activation of adenylcyclase lead to increased cAMP and diarrhea? I am trying find explanation for these mechanisms

  Tox plasmid -> exotoxin (enterotoxin) -> activation of adenylcyclase
  -> \up cAMP enterocytes -> release of H2O, electrolytes in gut lumen -> diarrhea.

Tox plasmid is a toxin generated by the genus enterobacteriaceae.
I read this as that exotoxin Tox activates adenilciclase enzyme (protein) which increases the amount of cyclic AMP in the enterocytes, and releases water and electrocytes into gut lumen consequently resulting in diarrhea.

How does the activation of adenylcyclase lead to increased cAMP heparis and diarrhea?

The crypt cells of the gut can actively secrete electrolytes (ions) via special channel which finally leads to water secretion. This is usually tightly controlled, since uncontrolled loss of water is obviously not good for the cells.
Have a look at this schematic figure, (from this webpage):

Sodium, Potassium and Chloride ions are co-transported into the cell,
sodium and potassium are transported back out via other channels.
If the adenyl cyclase is activated (for example by bacterial toxins,
cholera does this), then cAMP is made.
cAMP aktivates Protein Kinase A (PKA) which in turn phosphorylates the the Cystic fibrosis transmembrane conductance regulator
(CFTR)(this channel is also important for cystic fibrosis) which leads
to the secretion of chloride ions from the cell. This builds up a
negative potential across the membrane (positively charged ions are
missing).
This leads to the secretion of sodium ions through the tight
junctions, resulting in the netto secretion of NaCl.
The secretion of salt builds up and osmotic gradient across the
membrane, which leads to water secretion and can also lead to hyponatraemia.

To overcome this problems, the so called "oral rehydration therapy" is used. The solution contains of an isotonic solution of sodium chloride and glucose. This is taken up by the sodium-glucose symporter (a special class of transporter, that transports two molecules in the same direction) and builds up a gradient which is directed in the opposite direction of the diarrhoea, helping to fight dehydration.


How is histamine useful against allergies? Histamine is a chemical produced and stored within the body. It is a part of our immune response and is released during an allergic reaction.

Often histamine is responsible for hypersensitive response of the body towards certain specific compounds(allergens). It causes nasal congestion and pollen allergy. Also it acts as a powerful vasodilator, and causes inflammation. But is it really helpful against allergies?

I was wondering why antihistamines would be required to inhibit normal functioning of histamine, then realised that if histamine was not there, then perhaps we would not have allergies..

Histamine is produced in allergic reactions. - True

Histamine is produced against allergic reactions - False

Okay. Lets get a few things right here first. An allergy is an inappropriate immune hypersensitive response. It is something, we are not supposed to have. A small harmless pollen grain, in normal people shouldn't initiate an allergic reaction.

IgE antibodies are produced against an allergen. These attach their Fc ends to the mast cell. When these antibodies are cross linked by the antigen, degranulation of the mast cell ensues which release various mediators one of which is histamine. So there is a lot of histamine produced in allergic reactions and common antihistaminics like cetirizine and terbinafine act by blocking histamine receptors thereby reducing its biological effects.

So, allergy is a bad thing. The whole IgE, cross linking, degranulation and histamine release wouldn't have happened in a normal person. Histamine isn't going to protect from allergies. It is the cause of allergic effects. Hence the antihistaminics work. You might know that if you have taken a cetirizine during a rash or severe sneezing.

So if allergy is a bad thing, what is the normal physiological role of IgE?

IgE has a role to play in the immune response against parasites where a similar mast cell degranulation process happens.

And if histamines are causing the allergic effects and allergy is bad, what is the normal role of histamine?

Histamine has several roles to play. One is that it is produces as a part of immune response by basophils and mast cells. It also is a neurotransmitter and also is important is gastric acid secretion physiology. The various functions of histamine have important pharmacological considerations while talking of antihistaminics.

Reference : Kuby, Immunology 6th Ed.


Examples of biological turing machines Are there any examples of biological Turing machines? And what can they do?

There have been several Turing machines constructed using DNA computing. One of these machines has been used to solve the boolean satisfiability problem, another was used to solve the bounded post correspondence problem, both NP-hard combinatorial problems which are difficult for conventional computers to solve.
Also, a DNA computer was constructed that plays the optimal strategy in tic-tac-toe.

DNA computers store information in DNA sequences and perform calculations by DNA baseparing and other molecular biology strategies. In principle, DNA stores Information much denser than any modern hard drive and uses orders of magnitude less energy per calculation than a conventional computer ($10^{-22}$ vs $10^{-10} \frac{J}{operation}$) however, so far i/o is slow and calculations are comparatively error prone, limiting the practical use of DNA computing.

Also, a recent article has demonstrated that molecular motors can perform basic addition and solve the NP-complete subset sum problem by exploring nanolithographically fabricated networks. This could also, in principle, be used to construct a turing machine.


What is the probability of having a son with blood type O? So I was solving some biology questions, and this question left me confused. The response is supposed to be 22% according to the answers, but all the methods that I used did not lead me to it. I really hope that somebody can help me with it, the question sounds as follows:
Human ABO blood type is determined by two genes (H and I). First, the H gene codes
for the antigen precursor. The dominant allele (H) leads to expression of the precursor; the recessive
allele (h) does not. Second, the I gene has three allele forms, IA, IB and i, and determines blood type
(A, B, O or AB).
A male with blood type A and a female with blood type B marry. Each of them is heterozygous for
both the H gene and the I gene. What is the probability of having a son with blood type O? Give your
answer as a percentage (%) rounded to an integer (without any decimals).

7/16 for any child to be blood group O, half of that (21.875%) for a son with blood type O.
P  x  M
HA    HB
HO    HO
hA    hB
hO    hO
HA = 0/4 blood type O
HO = 2/4 blood type O (HO-HO, HO-hO)
hA = 2/4 blood type O (hA-hB, hA-hO)
hO = 3/4 blood type O  (hO-HO, hO-hB,hO-ho)
= 7/16 chance of type O
son = 1/2
Chance of blood group O = 7/16 * 1/2 = 7/32 = ~0.22
Edit: as it's not clear from the question, anyone who has genotype hh is not able to express either A or B antigens, so is always blood group O.


Why are dreams sometimes remembered and sometimes forgotten? Why is it that sometimes, when we wake up, we are able to remember what we were just dreaming, but sometimes we don't remember any of it?

Scientists say that people can have multiple dreams every night and the ones that are not very significant are easily forgotten. Only those experiences that elicit an emotional response (happy, frightened) seem to stick in memory. Suggestions have also been made that being anxious or depressed makes our dreams stick to memory too (reference). A study suggests that people woken up during REM sleep seem to recall their dreams more often (reference). Here is a link to some common questions about dreams.