Why are there so many sex determining systems in animals There are several sex determining systems in animals.

In mammals XY = male(except in rare cases where SRY crosses with genes on the X so that it is the reverse) and XX = female.

In  some birds it is just the opposite. That is XY(actually ZW) = fertile female and XX(actually ZZ) = fertile male.

In  some reptiles it is determined by temperature and has no genetic determination.

In lots of insects there is XX = female and X0 = male. This is usually accompanied by males being haploid and females being diploid like it is in bees.

In some insects and reptiles there is also the ZW/ZZ system but they are not dependent on it. In other words ZZW in some insects and reptiles can give rise to either sex but there is no temperature determination either.

Why are there so many sex determining systems? Why did animals evolve to not all have the familiar XY system? It must be so confusing as to which species has which sex determining system when biologists are trying to determine the gender of an animal.

Could not fit in a comment…

I don't quite know how to answer. I think that the only answer one could give is why not?. Various mechanisms may evolve under different life-history, different environment, different ecological strategy, different mutations occuring,..

In some species (including some amphibians) the evolution of sex determination system is highly dynamic and switch back and forth between one system and another.

I highly recommend the book: The Evolution of sex determination system (2014) that will give you a very good theoretical understanding of how sexual determination system evolve and make a complete review of empirical studies on the evolution and mechanisms of sex determination system. I think it is the only book existing on the subject.


What is the half-life of dNTPs at 95 °C? I'm looking for the half-life of dNTPs, either as a whole or broken into individual bases, at 95 °C (or similar). A titration would be great if that exists. I can provide more specifics if need be, but broadly the idea would be 'able to polymerize' vs. 'unable'.

Instead of searching for the stability of dNTPs, consider the stability of their constituent parts.
Caveat: ignoring the bonds between the different parts of dNTPs likely misrepresents the stability of the intact molecule, given that the covalent bonds between the nucleobase, sugar, and phosphate pieces each have their own relative stabilities.

Hydrolysis of Purines and Pyrimidines

In The stability of the RNA bases: implications for the origin of life,1 there is an Arrhenius plot showing the rate of decomposition of the most common nucleobases (A,T,C,G,U) at pH 7 in 50 mM phosphate buffer.  According to ThermoFisher, the pH of PCR buffer is between 8 and 9.5, though the authors of the paper linked above observe that the pH rate profile for the decomposition of purines (A,G) is relatively flat between pH 5 - 10.
At 95° C, the least stable nucleobase has a half life of 10-1 years, or about 1 month.

Fig. 2. Arrhenius plot for the decomposition of A, U, G, C, and
T, pH 7. ∆, data from Garret and Tsau (10). Equations are as follows:
log k(A) = -5902/T + 8.15; log k(U) = -7649/T + 11.76; log k(G) = -6330/T + 9.40; log k(C) = -5620/T + 8.69; log k(T) = -7709/T + 11.24. [red lines added for emphasis]

Decomposition of Pentose Sugars

The same research group investigated the stability of the sugar moieties of nucleic acids in Rates of decomposition of ribose and other sugars: implications
for chemical evolution.2  The analysis is slightly obscured by the use of deuterated water, though the authors observe that the rate of decomposition of ribose in H2O at 100° C and pH 7.0 is identical to that in D2O at 100° C and pD 7.4.
At 100° C and pD 7.4, ribose, the sugar component of RNA, has a half life of less than 2 hours.  Interestingly, the authors note that 2-deoxyribose, the sugar component of DNA, decomposes 2.6 times slower than ribose with a half life just shy of 4 hours.

Fig. 1. Rates of ribose decomposition as a function of pD.
The curves were fitted by assuming a functional form k = k0/(1 +
[H+]/Ka), where Ka and k0 are adjusted constants. [red lines added for emphasis]

Hydrolysis of Triphosphate

Getting to the heart of your question, i.e. at what point are dNTPs no longer "polymerizable", the stability of the triphosphate is vital, as the hydrolysis of the two distal phosphates and the creation of a phosphodiester bond with the remaining proximal phosphate is the rate-limiting step in DNA polymerization.
An older publication, The Hydrolysis of γ-Phenylpropyl Di- and Triphosphates,3 investigates the hydrolysis of nucleotide analogs at 95° C, over a pH range of 0.3 to 10.  For the ATP analog, the rate of spontaneous hydrolysis to ADP is very low, 17.5 × 10−5 s−1 at pH ~5.  Assuming first order kinetics, the half life of the triphosphate form is ~4000 seconds, or a little more than an hour at 95° C.  In a buffered solution closer to a neutral pH, we can expect triphosphate to be even more stable.

Table 5. A Comparison of the Rates of Hydrolysis of γ-Phenylpropyl Di- and Triphosphates and ADP and ATP at 95°

A PCR with one 2-minute initial melting and 20 cycles with 15-second melt steps will expose dNTPs to 420 seconds at 95° C.  Considering only the hydrolysis of triphosphate, which is the least stable component of the 3-component dNTP molecule outlined above, the equation for exponential decay can be used to calculate the proportion of unincorporated dNTPs that are still "polymerizable" at the end of cycling, using the rate constant provided in the "Hydrolysis" paper:
$N_{\text{final}} = N_{\text{initial}} × e^{-kt}$
$N_{\text{final}} = e^{(-17.5 × 10^{-5} s^{-1})(420 s)} = 0.929$
For some perspective, a 50 μL PCR with 0.2 mM dNTPs contains enough raw materials to create 1.51 × 1013 copies of a 200 bp dsDNA amplicon, ignoring the contribution of primers to the amplicon body, and assuming perfect fidelity of the polymerase and primers in excess.  A 20-cycle PCR with 106 molecules of template will yield 1.05 × 1012 amplicons, assuming perfect duplication at each cycle, meaning dNTPs are supplied in more than 10-fold excess and heat decomposition is unlikely to have an effect on PCR fidelity in this system.

References

Levy M, Miller SL. The stability of the RNA bases: implications for the origin of life. Proc Natl Acad Sci USA. 1998 Jul 7;95(14):7933-8.
Larralde R, Robertson MP, Miller SL. Rates of decomposition of ribose and other sugars: implications for chemical evolution. Proc Natl Acad Sci USA. 1995 Aug 29;92(18):8158-60.
Miller DL, Westheimer FH. Hydrolysis of Gamma-Phenylpropyl Di- and Triphosphates. Science. 1965 Apr 30;148(3670):667.


Can connections between neurons be weakened? Connections between neurons are said (by Wikipedia) to be strengthened as part of learning - can they also be weakened (below the original level)?

I understand the concept of the connections strengthening. After reading the article Ants Swarm Like Brains Think, my understanding is that positive feedback (I forget the words that I should use for positive vs negative action potentials) should strengthen the connection, and negative feedback should weaken it.

I'm interested to know whether neural connections can weaken below their original connection strength.

I'm curious about this so as to grasp the way that the human brain (or even simply the ant brain) learns good and bad. If I'm not completely wrong about what I'm asking, then I think I get it pretty well: The things that are good (like finding food) trigger positive feedback among the associated neuron groups, and the things that are bad (like pain or danger) trigger negative feedback in the associated neurons, and that's basically how brains learn good from bad.

Short answer
Yes, neural connections can be weakened.

Background
Chemical connections between neurons (synapses) can certainly be strengthened or weakened, dependent on their input. Single synapses can undergo long term potentiation (LTP) or long term depression (LTD). As a typical example there are hippocampal neurons. High-frequency (tetanic) electrical stimulation in hippocampal neurons can result in long-term potentiation (strengthening) of synaptic connections in the hippocampus Moreover, when a synapse receives synchronous input from multiple incoming axons they can potentiate each other's responses (Purves et al, 2001). In contrast, low-frequency stimulation and  prolonged inactivity of synapses in the hippocampus can weaken them (Bear & Abraham, 1996).

The connection between learning, let alone good and bad as you ask for in your question, is far from clear. However, LTP and LTD do provide plausible mechanisms that could underpin these processes at the cellular level (Purves et al, 2001).

References
- Bear & Abraham, Ann Rev Neurosci (1996); 19: 437-62
- Purves et al., eds. Neuroscience, 2nd ed., Sunderland (MA): Sinauer Associates; 2001


Confirmation of organoid's character with the respective organ How can we verify that the Organoid formed from culturing stem cells shows the exact characteristics of the organ it is developed for?

Verification of organoids is done by detecting the cellular proteins for particular tissue type using Immunofluorescence.

For verifying intestinal organoid, apical membrane markers  (villin or alkaline phosphatase) and basolateral markers (E-cadhehrin) are detected by immunofluorescence. Transporters present in intestinal membranes are also displayed on organoids.  The peptide transporter PEPT1 and the glucose transporter SGLT1 are located on apical membrane, and the glucose transporter GLUT2 is present on basolateral membrane. So, these proteins can also be used as markers for verifying intestinal cells.

Via:

https://www.nature.com/articles/srep16831
https://www.ncbi.nlm.nih.gov/pubmed/19329995


Comments on Experimental result regarding Anti-Bacterial soap After using soaps, we rinse our hands with water.

Do bacteria from the water attach themselves to our hands again?

If we wipe our hands to cloth after washing our hands, do bacteria from the cloth also attach to our hands?

Or, do antibacterial substances remain on our skin and, in a sense, 'protect' us from bacteria in a given amount of time?

After using soap, the pathogens that were previously present in hands are removed by the soap and water. But yes, bacteria from the water do attach themselves to our hands again, for that we should wash our hands with clean water, which may not be sterile but at least free from pathogens. Also if we wipe our hands to cloth after washing, the bacteria that may be present in the cloth adhere itself to human hands. The attachment of bacteria depends on the concentration of microbes, increase in microbial count increases the probability and risk of contamination. Unfortunately antibacterial soaps that use triclosan may kill more microorganisms while washing hands, but then they can't "protect us" from bacteria for some longer periods of time. Also it has been found that antibacterial soaps have the potential to create antibiotic-resistant bacteria, and some may even cause allergies.


Why are some berries poisonous? In my understanding, the evolutional function of berries is to be eaten and pood out somewhere else, so that the seeds of the plant spread. Is this so? Then why are some berries poisonous?

While poison affects not every organism equally, plants did develop some poisons to avoid being eaten. However, if you look at the great multitude of so-called secondary metabolites, most of them are poisonous to either viruses, bacteria, fungi or other microorganisms, or insects, or even other plants. Plant evolution just hasn't had time to adapt to humans.

So, if some substance from plants is a poison to us, it's accidentally so, and the target was another organism. Examples: nicotine is first and foremost an insecticide, nematistat, and herbicide; aconitine, atropine, caffeine are insecticides; many essential oils (causing allergies in human) are antimicrobial and so on.

This has also to do with the fact that nerve cell physiology has not much changed since they developed in the first multi-celled animals, and poisons for insect nerves have at least some effect on human nerves.


How do you increase eumelanin but not pheomelanin? Are Scientists currently looking into this?

I doubt that this will be really successful, since the synthesis is rather complex and can be influenced (positively and negatively) in many ways. First, the synthesis pathways looks roughly like this:

The first step is identical for both melanin forms, it is the conversion of the amino acid tyrosine into dopaquinone by the enzyme tyrosinase. The next steps are different for each process and only one of the possibilities can happen at any given time. The decision is done by the availibility of the necessary components. When the cysteine concentration in the cell is high, the pathway goes exclusively into the direction of pheomelanin, only when the cyteine concentration is lower than 0,76µM eumelanin is made (see here and here for details).

But this is not the only influence on the reaction. The availibility of dopaquinone is critical, and the activity of the tyrosinase can be influenced by the pH of the melanosome (the compartiment in which the pigment production takes place). The tyrosinase activity for people with dark skin is about 10 times higher than for people with pale skin (see here and here for details). The difference here is mainly the pH, which is neutral for dark skinned people and acidic for pale.

Then there is of course the availibity of tyrosine (which is less of a problem, as this amino acid is not essential) and also the availibity and activity of downstream enzymes for the eumelanin production as tyrosinase-related protein 1 and dopachrome tautomerase.


What's the exact species of this African Giant Snail? We've got an African Giant Snail a few years ago but failed to identify the exact species so far. When we got it, it's been about 20 % smaller than now, so it's probably not been an adult snail, but we don't know the exact age.
We only got this single snail, so there's no way to check for the eggs.
Here's a picture (small version, about 400 KiB) and a link to a bigger version. If you need more detailed pictures of certain parts, please let me know.

Bigger version: https://imgur.com/a/O9Bm2Tf (about 2.2 MiB)
This picture shows that the apex is about 12 centimeters (4.7") in length, while the foot is about 14 centimeters (5.5").

I am not sure how to handle this.
The answer is the content of this page, which (I guess) should not be entirely copy / pasted here for copyright reasons.
So based on the texture of the skin, you have a variety of Achatina.
If I receive advice about how to make this answer comply more with the rules of the site, I will edit my answer.


Would our body adapt to changes that are not in our DNA? If a person was to undergo a treatment or surgery at a very young age, that significantly reduced their final height, would the rest of their body adjust to the sudden change? If not; because our arms’ length is very similar to our height, would this give the person arms that weren’t proportional to the rest of their body?

It will be hard to discuss for the specific example you consider, mainly because it is unclear how would you treatment affect the person's height.

That being said, yes, our bodies can change in function of the environment. This is called phenotypic plasticity

  Phenotypic plasticity refers to some of the changes in an organism's behavior, morphology and physiology in response to a unique environment.

Here the term environment does not only refer to outside temperature or other obvious environmental factor. For example, one can ask whether the size of a vein can react plastically to the blood flow. Here, blood flow is the environmental factor toward which, the plastic response is mediated.

Note that some plastic responses are adaptive and some are not. Note also that there are a lot of related terms (developmental flexibility, acclimation, polyphenism, developmental selection, ...) in the field of plasticity and different authors sometimes use these terms with slightly different definitions which can make everything a bit confusing.


Splicing and “the dominance of RNA-world” This is a paragraph from my textbook.

  The significance of such complexities is now beginning to be
  understood. The split-gene arrangements represent probably an ancient
  feature of the genome. The presence of introns is reminiscent of antiquity,
  and the process of splicing represents the dominance of RNA-world. In
  recent times, the understanding of RNA and RNA-dependent processes
  in the living system have assumed more importance.

NCERT XII (pg. 111)

I am unable to understand the above sentence in bold. Can anybody explain. Thanks

This is a badly-worded phrase that means nothing in the context of the paragraph in which it occurs. There is no way the reader could be expected to understand it from this awful book on its own. Normally I would not think it the role of this site to remedy deficiencies in text books. However, as this involves some interesting questions I will try to read the author’s mind.

The author probably means something like:

  “splicing is a relic of the RNA world”

…although a more measured statement would be:

  “the existence of self-splicing supports the idea that the current DNA/protein world was preceded by an RNA world”

The author’s use of the word “predominance” is just incorrect English. (Sloppiness or deficient vocabulary.)

An RNA world?

So what is all this about an ‘RNA world’? The author refers to this on p. 104. He states as a categorical fact what it is important to realize is only a theory:

  RNA was the first genetic material…RNA used to act as a genetic material as well as a catalyst…

Why is splicing relevant to this? Some types of splicing are catalysed by the RNA itself — self-splicing — an example of an RNA enzyme (ribozyme). From the existence of these and other ribozymes it is argued that originally all enzymes may have been ribozymes, and protein enzymes only developed later, taking over most, but not all enzyme functions.

It is important to realize that RNA preceding DNA, and the first enzymes being RNA rather than protein, are two independent ideas. Although both these ideas are widely held, and I personally tend to favour them, certain scientists have argued strongly against them, as discussed by Harold S Bernhardt.


Bougainvillea flowering problem My bougainvillea plant hardly flowers and only at the tips. It has one very long vertically growing stem(if I may call it so).

Is this an example of apical dominance.
If so how is it to be corrected?
Do I have to cut the long step?

bougainvillea is a qualitative short day plant meaning that it needs long, uninterrupted nights to flower. Most flowring accours when it gets 8hrs of light (=16 hrs of night).
India is a huge country so you need to be more specific or tell us how many hours of light the plant gets. Note that if it's exposed to light from the house/street it may not flower as the light intensity for photoperiod is much smaller than that of photosynthesys.
Flowering requires a lot of energy, even if all conditions are met not enough sunlight might prevent flowering. bougainvillea loves sun, give it as much direct light as possible.
According to fao, Paclobutrazol shortens the time to flowering in long day conditions, meaning that GA might delay flowering. Another way to prevent GA synthesis is to stop watering the plant. Once the leaf start to fall give it water again.
Don't water too much:

these plants need full sun & well-drained soils. After establishing,
minimal watering is needed. Two or more irrigations with 3/4 – 1″ of
water per week would provide too much water for the bougainvillea to
bloom well.

What to do:

Give it more sun
Give it less water
Induce water stress to prevent GA synthesis
shorten the day, you may cover the plant with a dark cloth from the late afternoon to the morning


Black oyster of sweet water I have seen recently a documentary starting with introducing of the spectacular black oyster of sweet waters which imitate exactly like a prey fish in order to convey its eggs to predator fish's gills, while it had no eyes to see the form of prey fish favored by the predator fish.

The amazingness of what this creature do provokes me to ask some questions about this strange creature and know more about this odd phenomena and theories represented for evolving of such marvelous creature.

How the black oyster detect completely kind of prey fish which is favourite food of target predator fish ,and make a very detailed simillar image of it in order to deceive the target fish while it has no eyes to see?

I believe you're talking of the members of the families Unionidae and Margaritiferidae, which have a larval stage called glochidium. From the Wikipedia page linked here:

  This larva form has hooks, which enable it to attach itself to fish (for example to the gills of a fish host species) for a period before it detaches and falls to the substrate and takes on the typical form of a juvenile mussel. Since a fish is active and free-swimming, this process helps distribute the mussel species to potential areas of habitat that it could not reach any other way.

This interesting study about phylogeny of these species shows that lures mimics mainly fish, but also different prey species such as insect larvae. Some species display an aspecific lure, while others show fine mimicking in order to attract a precise set of host fish species.

As to how luring evolved:

  What drives the evolution of luring? Very little is known about what drives the evolution and diversification of luring, which has evolved independently multiple times. In Lampsilini mussels, luring appears to have arisen early, and the complexity of the lure has increased through the lineage. It is likely that diverse selection pressures govern the evolution of luring. One hypothesis is that luring increases the rate of prey encounter without incurring the metabolic costs associated with active search and pursuit. Alternatively, luring may present predators with an opportunity to exert control over a prey’s movement, reducing the risk of injury when hunting. Luring systems present a unique opportunity to understand signal design and evolution.

Do oysters need to see in order to evolve the lure?

No. Evolution of a body part does not require sight or will. From this blog post:

  Note that [...] the mussel can’t see the fish it’s parasitizing.  In this case natural selection is literally blind. Those mutations in the mussel that make its brood pouch look more fishlike will give it a reproductive advantage over its confrères, even if it can’t see the fish it’s deceiving. Note as well that selection has “acted” (I’m anthropomorphizing here: selection doesn’t really “act”, for it’s not an external force but a process of gene sorting) not just on the appearance of the mussel, but on its behavior.  It has genes that make it wiggle its brood pouch in a fishlike manner.

The mechanism is all here:

1st step: mutations that modify the coupling of fish bites and glochidia release/mantle shape/the movement of the mantle arise.
2nd step: The bearers of favourable mutations will have more progeny and the population will have more and more bearers as generations pass.

No need of being conscious about anything. :)


Significance of prostaglandins in semen? I am trying to figure out how prostaglandins in the semen relate to the female reproductive tract.
More specifically,
How does prostaglandins in semen help the female reproductive tract increase the chance for fertilization?

Nevermind. While writing out the question I found the answer on wikipedia.
Prostaglandin type PGF2α will act on the FP receptor to initiate uterus contraction which will help propel sperm further into the reproductive tract.


Do you have nerves on the outside of your skull? I have a spot on my skull that feels like a nerve or blood vessel. I know that there are many to the brain, however, it is the only one I have ever felt. So do we have nerves or blood vessels on the top or outside of the skull?

There are a number of nuerovascular bundles that exit the skull. Three involve branches of the trigeminal nerve.


What is the advantage of using plant-derived antibacterials rather than bacteria-derived antibacterials? So obviously we have a big problem with antibiotic resistance. Most of our antibiotics originate from bacteria themselves (or are synthetic variations on scaffolds which originate from bacteria). I have heard it asserted that using antibacterials derived from plants would lessen the problem.

One argument for the use of plants is that the bacteria from which we derive an antibiotic must themselves already be resistant to that antibiotic, meaning that the allele for resistance is already in the bacterial gene pool and when we exert a selection pressure by using the antibiotic, resistance will eventually appear among pathogenic species.

Another argument I have heard is that plants can provide a lot of structurally diverse metabolites from which we might discover new classes of antibacterials.

Is there anything else to this?

(I know I have answered my own question to an extent, but I am wondering whether there are any other good reasons to look to plants for the next generation of antibacterial drugs).

Thank you!

Bacterial isolates from ancient permafrost and isolated caves allow study of the resistome, or the collection of antibacterial resistance genes, in environments without exposure to modern antibiotics for medical and agricultural use. These samples have genes for resistance to antibiotics derived from a variety of sources, including fungal sources (penicillins, cephalosporins) and synthetic dyes (sulfonamides), as well as bacterial sources (macrolides, aminoglycosides, etc). This finding was surprising, but does help explain the rapid emergence of resistance in response to clinical use. The genes have been there all along.

The OP is correct that a great deal of our current armament of antibiotics were derived from bacterial products, but since fungal and wholly synthetic products don't solve the resistance problem, I don't believe plant products will either.


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

This question falls into different subquestions:

1. How much blood does a mosquito take when feeding?

This is not so easy to answer, but there are publications which measure the volume of different mosquito species. Reference 1 lists volumes between 2.85 and 11.99µL per meal and mosquito. Reference 2 lists 3.07 and 5.71µL. To make the approximation a bit easier, let's assume that mosquitoes drink about 5µL per bite (which should be near enough).

2. How much blood does a human have?

According to Wikipedia, humans have around 77mL blood per kilogram of body weight. If we take a 70kg human, we get around 5L of blood.

3. How many mosquitos does it take to get a human into shock, and how many to suck him out completely?

According to the Medline, Hypovolemic shock occurs when a human loses about 1/5 (or more) of his blood volume. 1/5th of 5L is one litre. Since each mosquito sucks 5µL, this would take about 200.000 mosquitoes. To suck out all blood would take 1 million mosquitoes. (This is not possible since mosquitoes depend on an existing blood pressure, as reference 3 shows. If a capillary is empty due to massive blood sucking, they change to another.)

Besides this theoretical (but interesting) calculation, there are some real problems about getting biten by so many mosquitos. First, this is a question of available skin. The human skin is about 2 square meters in size, which would require 100.000 bites per square meter. To break this down further, a square meter has 10.000 square centimeters, so there would be 10 mosquitos which need to bite you per square centimeter. Rather unlikely.

Then each mosquito injects a mix of anti-coagulants, pain killers etc. prior to sucking to keep the blood from clotting and also to make sure you won't notice the bite immediately. As pointed out in the comments, this would already cause a lot of trouble and probably cause massive bleeding, since the effect of the anti-coagulants would sum up when biten by thousands of mosquitos. Additionally the body reacts by releasing histamines and since the amount would also be massive, this would cause real trouble and probably kill you.

References:

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


How can I create a microcapillary for manipulation of single cells? i'm working as a diy bio. I'm finding a way to create a micro glass capillary for picking up single cells. I see this video on youtube and would like to know what is the minimum I/O diameter if I pull a capillary like this.
Can it be 10-50 µm at least ?

It is very difficult to establish what kind of tip you will get from pulling a capillary on a Bunsen burner.
There are many variables to consider, including the glass you are using, the temperature you reach before pulling, the pulling strenght, speed and time, whether you pull once or make multiple pulls etc.

If you do not want to invest into a micropipette puller (they are indeed VERY expensive) you could at least build some mechanism to obtain a constant pull in terms of time and force.

The following paper may be of help:

An Instrument for Controlled, Automated Production of Micrometer Scale Fused Silica Pipettes

It seems you would need a fairly high speed (0.8-1 m/s) to get a tip size of <50um.

I could not really find a specific reference for pulling over a Bunsen.


Are genes uniformly dispersed throughout the genome? I think that telomeres and centromeres are regions with a very low gene content (= regions that contain few genes). To the exception of telomeres and centromeres, are genes uniformly distributed throughout the genome or do they tend to clump together or to scatter as much as they can? Do genes tend to clumped or avoid specific regions such as regions with low mutation rate or low recombination rate?

No they are not. High gene density is correlated with GC content. Most genes are found in GC rich isochores, which are not distributed uniformly (as can be seen on any karyotype). It is also shown through direct sequence analysis (gene density shown in red, GC content in green):

Venter et al. go on to say:

This inhomogeneity, the net result of millions of years of mammalian gene duplication, has been described as the “desertification” of the vertebrate genome. Why are there clustered regions of high and low gene density, and are these accidents of history or driven by selection and evolution?

Desertification refers to this 1985 article by Ohno:

The net consequence of hundreds of millions of years of continuous gene duplication is the desertification of the euchromatic region of modern vertebrates; the average distance between still functioning gene loci becoming progressively longer.

This would seem to suggest that these deserts are the result of gene duplication and subsequent degeneration into pseudogenes, though this is surely not the only cause. I'm not sure that your last question or those posed by Venter et al. have an answer as of yet. This more recent paper offers some interesting ideas (references removed for brevity):

More than 20 years ago, Ohno (1985) postulated the desertification of the euchromatic region of the higher vertebrates’ genomes owing to continuous gene duplication events followed by degeneration of newly emerged gene copies in their evolutionary history. Only with the first release of the complete sequence of the human genome in 2001 was Ohno’s prediction of the existence of such deserts confirmed. Another mechanism to generate imbalance of gene deserts between chromosomes might be large intra-chromosomal duplications, from which some mammalian-specific gene deserts appear to have evolved. However, the functional or evolutionary significance of gene deserts is not yet fully understood. At first glance, gene deserts seem to be devoid of biologic functions because of their lack of protein-coding DNA. Despite this, some gene deserts have been shown to contain important regulatory and sometimes ultraconserved regions for neighboring genes that function over large distances. In addition, the observation of stable gene deserts with homologous flanking genes (often transcription factors), which are maintained for long evolutionary durations, as well as the existence of numerous conserved nongenic sequences in mammalian genomes suggest that gene deserts are not just genomic junkyards but instead might be of functional significance. However, some gene deserts can be deleted without noticeable phenotypic effects. Thus, it remains unclear whether the uneven accumulation of gene deserts in eutherian chromosomes, which appears to be the strongest causal agent for the observed relative lack of a NG/LC relation in the genomes of placental mammals, is simply a byproduct of their genome evolution and possibly the long-term decrease in population-size, as would be suggested by the enrichment of gene deserts along the evolutionary lineage leading to mammals. Upcoming detailed reconstructions of ancestral vertebrate genomes will help clarify these points.
Alternatively, this particular architectural feature of eutherian genomes might be linked to some of their morphologic, physiologic, neurologic, and cognitive evolutionary innovations, possibly by regulating genes with essential functions in development. It has recently been hypothesized that regulatory elements in gene deserts function in the regulation of core vertebrate genes. Furthermore, approximately 20% of conserved noncoding elements are eutherian-specific. Thus, the uneven distribution of gene deserts could itself be caused by an underlying pattern of uneven distribution of some core genes in placental genomes. This hypothesis should be tested in the future.


Healing rate of cut while suffering from a cold I recently cut my finger fairly deeply with a box cutter and had to have it stitched. During the healing process I contracted a strong cold/mild flu (a sore throat and runny nose with a high fever, aches and shivering). I doubt the two have anything to do with one another apart from happening to occur at the same time.

But they did occur at the same time. So I'm wondering: what is my body going to do?

If I recall my junior high biology, a cut is healed by platelets and [other stuff I can't recall], whereas a virus is fought with antibodies. Presumably in both cases it's a bit more complicated than just that. I'm also not sure if there is any crossover - are antibodies, for example, needed to protect the open wound from bacterial infection? Regardless, my question is:

Since the resources in the human body are finite, would having to fight off the cold have a detrimental effect on the healing of the cut?

If certain resources are needed for both tasks, would the body divide its resources or give one precedence over the other?

I'm guessing this is not something that is easy to measure, since it would be difficult to conduct a control experiment given the insane amount of variables. But presumably there is a consensus in the biological community on whether there would be an effect, even if it is not possible to determine the degree of said effect.

I should mention in closing that I am not remotely worried about any of this; it just piqued my curiosity.

First of all: No, there is no connection between these two incidents, correlation does not imply a causation. Cold and flu viruses affect the respiratory system and the infection route goes via it. A cut is a local wound, which does not affect the respiratory tract.

Then: Recovering from an infection is a task for the immune system (its both, the innate and the adaptive immune system, the last involves the antibodies), which is not doing much for wound healing. The wound attracts neutrophils and macrophages which are attracted by factors released by the wound and they react to bacterial infections (when they occur). See this Wikipedia article.

The ressources of a normally healthy person are quite big. This is demonstrated by the fact that many secondary infections only occur in a opportunistic fashion (for example viruses like Herpes or certain fungi) when the body is weakened by other infections. So there is a limit, but this will certainly not be reached with a severe cold.


Identification of protozoa under microscope I observed maybe Protozoa from standing FRESH water and from slowly flowing FRESH water. I am complete dilettante. Can you tell what these creatures are?

https://www.youtube.com/watch?v=6D5ck3zNJzA&t=474s

Thank you.

Added picture for to be more specific

At first glance, the organisms may hold the appearance of protozoans like ciliates. However, I am of the belief that these 'totally tubular' micro organisms are in fact diatoms.

The diatoms are a diverse range of eucaryotic microalgae which comprise a large percentage of the phytoplankton group. (Diatomaceous earth is the residual remains of their calcareous walls)

They are likely diatoms because of their apparent hard membrane, and slight brown-green pigment, typical of heterokont diatoms.

I would be unable to specify the organism to family level. However, you may wish to complete your investigation by looking under the order 'Pennales'.

For general information regarding the Diatoms, you may visit https://en.wikipedia.org/wiki/Diatom
Morphology and description available from: https://books.google.co.uk/books?id=xhLJvNa3hw0C&printsec=frontcover&source=gbs_ge_summary_r&cad=0#v=onepage&q&f=false

Good luck


If crocodiles are k-selected, why do they supposedly "not age," as in avoid senescence? I recently saw a few sources stating that Crocodiles do not biologically age, implying negligible senescence. Basically, a 70 year old crocodile is in the same physical/health condition as a 7 year old crocodile. However, crocodiles are K-selected, meaning that populations are generally close to their carrying capacity. If they do not exhibit natural senescence, isn't that evolutionarily disadvantageous, because the younger crocodiles with more slightly more fit genes will not necessarily replace the older generations, meaning that crocodile populations would adapt to environmental changes significantly slowly. Can someone please explain to me how this lack of senescence can apply for this type of species?

Comments

You seem to use the term evolutionary advantageous vs disadvantageous for the species rather than for individuals. It is a very common misconception from the general public. You might want to follow an introductory course to evolutionary biology such as Understanding Evolution (UC Berkeley) for example.

  younger crocodiles with more slightly more fit genes

"fit genes" does not mean much. Again an introductory course to evolutionary biology should help you there.

Answer

You'd right though that absence of senescence causes longer generation time and therefore lower response to selection pressure (such as those caused by an environmental change). But populations don't evolve in order to maximize the probability of the survival of this population (related to first comment above).

Those that live longer, leave more offspring and therefore long-lived individuals are expected to dominate the population in the long run. The evolution of senescence is not exactly that easy though otherwise no species would show any sign of senescence (see Why does evolution not make our life longer?).


Was the recent "conservation hunt" of a black rhino supported by science? CNN recently covered a sanctioned black rhino hunt in Namibia by Texan Corey Knowlton, who bid US$350,000 for the license. In the story, he claims that the hunt was actually supporting conservation of the critically endangered species, as they were looking to kill an older, non-reproducing male that was consuming resources and potentially threatening younger, breeding males. The Namibian government has a list of 18 rhinos in the country (out of a total population of about 2,000) that meet the criteria.

  Knowlton is targeting one of four black rhinos at the top of the government list, the ones considered "high priority threats to the herd."

Knowlton eventually caught up to and killed the animal he was targeting, and donated the meat to a local village.

CNN.com later published two opinion pieces, one in support of the hunt by Dr. Mike Knight, the Chairman of the International Union for Conservation of Nature (IUCN) Species Survival Commission's African Rhino Specialist Group (AfRSG) and the South African Development Community Rhino Management Group (SADC RMG), and one opposed to it by Jeffrey Flocken, the North America Regional Director of the International Fund for Animal Welfare (IFAW). Knight cites black rhino-specific data in his piece, arguing that in the case of this particular species, limited hunting is actually beneficial. Flocken instead uses a wider argument, citing hunting of polar bears, elephants, and lions, among other species, and claiming that the idea of "conservation hunting" as a whole is flawed. He does not, however, directly address the situation of black rhinos.

I have evaluated each side's argument, but have not yet formed a solid opinion, which is why I'm asking here. In the specific case of the black rhino, does the science support the notion of limited elimination of older males? Are there studies that show this has led to an increase in other types of conservation efforts? Does the money spent for licenses actually go towards conservation and assistance for locals?

As a second, optional question: Are the arguments posed by Flocken against "conservation hunting" in general supported by independent research? Just thinking logically I can imagine they are, as a lot of what he says makes sense in a broader context, if not necessarily in the case of the black rhino. Is there a scientific case for limited, situation-specific hunting, or should all forms of it be discouraged?

Note: I'm asking this here instead of Skeptics because I'm looking for a scientifically-supported answer. If you think it's better suited there, let me know and I'll move it.

Yes it is.  Besides Dr. Knights article which is very focused on the issue and describes numerous benefits, there are other sources of research that show this can be good not only for the animals but also the community.  And specifically that this has worked in Namibia (where the black rhino was hunted) extremely well.

Namibia has encouraged communities to see their local animals as resources to be protected and that they can profit from.  In cases of endangered species, the federal goverment abides by CITES and only allows so many to be killed. Other than that limitation communities are allowed to profit from their local animals both from trophy hunts but also tourism.  This has led to a reintroduction of many of these animals (endangered and not) onto private lands.  The survival and thrival of these animals is now an economic concern to the communities and land holders, and are protected as such.  This has worked for the recovery of many animals in Namibia.  In summary, the selling of a license to hunt one black rhino brings big profits to the community and therefore encourage the people to protect these resources.

The CITES articles are also a good resource when looking at this.  It's very clear in the resolutions to allow quotas for endangered animals that it is not harming the population.

And one other paper, though it's behind a paywall, describes how South Africa's white rhino population went from fewer than 100 to over 11,000 as privatization and legal hunting were legalized.

As a side note, the wildlife conservation department where I live receives almost half its funding from hunting licenses.  Since it has been in operation the deer population has gone from nearly wiped out in the state to over half a million animals.

Flocken's arguments are based on fact but are really targeted at examples of bad wildlife management rather than against the practice of conservation hunting.  There is some concern that allowing the legal killing of any endangered animals will lead to more poaching, but I haven't seen any evidence in the literature of that.


Calcium levels and nerve hyperexcitation Why does lower blood calcium levels (or lower calcium levels in ECF) cause nervous hyperexcitaton? Why does it cause over stimulation of nerves and muscles and spasmic contractions of muscles?
This is why undersecretion of parathormone causes parathyroid tetany.
I am aware of the role of calcium in opening the synaptic vesicles for transmission of impulses and the role of calcium in muscle contraction but fail to understand how that might hep me understand the overexcitation of nerves and spasmic contraction of muscles. It actually seems that higher calcium in ECF might cause over stimulation and spasms of muscles due to sustained contraction.

From Uptodate on Clinical Manifestations of Hypocalcemia:

  Acute hypocalcemia directly increases peripheral neuromuscular irritability [ 1 ]. As measured electromyographically, tetany consists of repetitive high-frequency discharges after a single stimulus. Hyperexcitability of peripheral neurons is probably the most important pathophysiologic effect of hypocalcemia, but hyperexcitability occurs at all levels of the nervous system, including motor end-plates, the spinal reflexes, and the central nervous system.

Guyton and Hall Textbook of Physiology:

  The concentration of
  calcium ions in the extracellular fluid also has a profound
  effect on the voltage level at which the sodium
  channels become activated. When there is a deficit of
  calcium ions, the sodium channels become activated
  (opened) by very little increase of the membrane potential
  from its normal, very negative level. Therefore, the
  nerve fiber becomes highly excitable, sometimes discharging
  repetitively without provocation rather than
  remaining in the resting state. In fact, the calcium ion
  concentration needs to fall only 50 per cent below
  normal before spontaneous discharge occurs in some
  peripheral nerves, often causing muscle “tetany.”This is
  sometimes lethal because of tetanic contraction of the
  respiratory muscles.

  The probable way in which calcium ions affect the
  sodium channels is as follows:These ions appear to bind
  to the exterior surfaces of the sodium channel protein
  molecule. The positive charges of these calcium ions
  in turn alter the electrical state of the channel protein
  itself, in this way altering the voltage level required to
  open the sodium gate.


Is there an advantage to antibacterial soap? There are plenty of different hand soaps out there, as well as hand sanitizers. Is there an advantage to soaps that claim that they're antibacterial vs soaps that just say soap?

In particular I'm looking at Softsoap who offers normal soap and antibacterial soap.

Examples:

Normal:

Antibacterial:

Short answer: There is no benefit for their use in households.

Long answer: These soaps (see here for the complete list) contain the so called quaternary ammonium compounds Benzalkonium chloride and Cetrimonium chloride which indeed have antimicrobial properties.

While they do not promote resistance to these compounds (see reference 1), their use is still not recommended, as their permanent use might dry out the skin, can cause contact allergies and the products released into the environment are also problematic.

There are two studies, which compared the use of normal soap (which has some antibacterial properties on its own) to antibacterial soaps in household environments and found no differences. See article linked in reference 2 for a summary and references 3 and 4 for details on the studies.

This doesn't mean that antibacterial soaps are useless at all, they simply make no sense in households. For hospitals or doctors they are an important tool to protect their patients before operations. But here detailed instructions for how long and how the hands have to be washed are provided. Hand washing is also followed by another disinfection step, which helps with efficiency. But this is very much different from the way people wash their hands at home. See reference 5 for some opinions here.

References:

Use of germicides in the home and the healthcare setting: is there a
relationship between germicide use and antibiotic resistance?
Plain soap as effective as antibacterial but without the risk
Consumer antibacterial soaps: effective or just risky?
Effect of antibacterial home cleaning and handwashing products on
infectious disease symptoms: a randomized, double-blind trial.
The Burning Question: Is It Safe to Use Antibacterial Soap?


Homologous structures under Lamarck I've read that Lamarck's theory doesn't explain homologous structures.

But, what about the following hypothetical under Lamarck's theories:

A population develops an adaptation to its environment
Part of the adapted population moves away
The adaptation is passed onto the population's offspring
All offspring of the original population have the adaptation, regardless of whether or not their ancestors moved away

Isn't this adaptation a homologous structure?

I agree with you that I can't see why Lamarck's hypothesis could not explain the presence of homologous structures.

The link you offer also claim that Larmarck's hypothesis would fail to explain "Biogeographical diversity patterns". While this expression is a little vague, I would fail to understand why Lamarck's hypothesis would fail to explain patterns of biogeographical diversity.

The phrasing of your scenarios (absence of the term allopatric speciation, usage of the term "develops" instead of "evolves" of just "adapts") suggests that you may take advantage of an intro course to evolutionary biology such as the short and good course by UC Berkeley called Understanding Evolution


Are there any scientifically based predictions or theories of future human evolution? Reading this question of the stack exchange got me thinking. I believe human evolution is an ongoing process and will not stop. Are there any predictions/theories about the phenotypes and genotypes of humans in the future? and how they may differ in a few thousand years compared to present day?

I remember watching a youtube video and in the video the user predicts that there will be two branches of human species; a short dwarf like species and a much taller species. I'm still skeptical about this claim. Is there any evidence to back it up?

One could argue that modern medicine is preventing natural selection. How will this effect human evolution?

Its pretty much impossible to predict what will happen in the evolution of species.  Evolution is a parallel search with millions (or in the case of humans 8+ billion) of threads.  Our adaptive capacities have never been fully understood and will always surprise us I think.

Of course that doesn't stop people from trying!  The prediction you mention is based on one man's ideas of dominant selection pressures on humanity now... for a men's TV show.  In Dr Curry's scenario, technology users, and economic disparity, producing Eloi and Morlock like dimorphism as in the HGWells book "Time Machine". This seems like hogwash to me.  All socioeconomic classes try to find high quality partners and height and attractiveness will be hard to stamp out in a large segment of humanity.

Economic elites breed slowly and even if they will try to skim the evolutionary cream of humanity off the top, there will be plenty of beautiful, tall and smart people who will lack economic opportunity in my opinion.

There have been more serious, IMHO, questions about whether medical technology, which lets the sick recover and may even compensate for genetically problematic traits.  There are no inoffensive examples I can think of so I'll take male pattern hair loss - apologies.  If medicine allows all men (and women) to grow a thick shock of hair regardless of our genes then the baldness traits might spread through the species.  Sure it could happen, but then most bald and balding people end up having children now anyway.

In fact since civilization has started feeding the hungry, making the hunting of wild beasts less important, causing the shrinkage of the male physique (we used to be much more muscular), inventing medicine and schools where smarts can be selected for, and giving us all more choice when it comes to mates, evolution has accelerated for human beings. The authors specifically cite social factors as being more important in our evolution now.


Can memory be improved with mental training? I am a man in his mid thirties, but I already have a pretty bad memory. (I have always had a bad memory.) I can remember certain kinds of facts and music very well, but when it comes to words or even random  stuff like how did I fix a particular issue when I last encountered it, my mind goes blank. Lack of sleep aggravates it even more. Lack of sleep also severely retards my language skills because I can't recall any vocabulary. Other than the memory issues I am a healthy person. Is there anything I can do to improve my memory?

You are not alone.
I think most people do not use the memory capacity of the brain optimally.
Some people use it more optimally than others though.

The researchers who wrote the book "Make it Stick" researched exactly this problem.

Of their many excellent findings, I think the most important was that most people did not convert the knowledge that they accumulated in working memory into long term memory because they did not do spaced repetition of recall practice.

When we learn something new those synaptic connections are weak unless we strengthen them.
The brain seems to let go of information that it deems to be less important in this fashion.

Everybody forgets a little.
But if you practice recalling what you've learned at spaced intervals, that seems to greatly improve the ability to convert working memory to long term memory.

Its important that recall involve actually struggling to recall the information.
Its the struggling that seems to strengthen the synaptic connections.
Just rereading some material wont work.

I put everything that I learn into Q&A documents that I use for recall practice.
This seems to have significantly improved my ability to commit new knowledge to long term memory.


Why do sneezes come in pairs or more? I very rarely sneeze just once, usually there's two coming in a row, and I've noticed the same thing in other people and even in animals.  Is there any reason for this?

The very simple answer is that the causal factor or trigger hasn't disappeared after the first sneeze. Sneezing is a reflex, partially autonomous, to clear the nasal cavity of particles that don't belong there. As long as the trigger is not removed, the reflex is repeated.

This is also one of the reasons that allergies that cause sneezing, such as hay fever, continue as long as the factor causing the allergy is present.


Can we taste electrons? Why does licking a 9-Volt battery elicits a taste sensation? Can taste be stimulated by electrical stimulation?

Short answer
Yes, taste sensations can be generated electrically. However, we cannot taste electrons themselves, as taste-receptor proteins on the taste receptor cells are not activated by electrons. Instead, electrical currents stimulate taste receptors directly by depolarizing the cell membrane, without the need of activation of the proteins that normally bind ions or molecules.

Background
There is a medical device called the BrainPort that electrically stimulates the tongue (Fig. 1.) The device is marketed as an electrotactile vision substitution device. Basically, it captures images of the outside world with a glasses-mounted camera and these images are translated into electrical stimuli presented on a 20 x 20 electrode array. That array is embedded in the tongue display unit (aka intra-oral device, IOD). The IOD is worn on the tongue.

Fig. 1. BrainPort V100. source: TuWindowsMundo

It typically generates electrotactile sensations, like champagne bubbles. However, some subjects do report metallic taste sensations when using the device. In fact, Lawless et al. (2005)* investigated the electrically evoked metallic-taste in response to anodic stimulation of the tongue directly and confirmed the anecdotal reports obtained with the BrainpPort device that electric stimuli evoke metallic-taste sensations.

Physiologically, taste receptor cells sense certain compounds (salts, acids etc.) due to activation of receptor molecules on the cell's surface. In turn, activation of receptor molecules depolarizes the cell membrane which eventually lead to neurotransmitter release and activation of secondary neurons that transmit the signal up to the brain (Fig. 2). Electrical stimuli bypass the receptor molecules and directly depolarize the taste receptor cells.

Given the anatomy of the taste receptor system in the tongue (Fig. 2), I am inclined to believe that the taste receptors are stimulated directly, and not the secondary neurons, because they are situated in deeper layers.

Fig. 2. Neural pathway of the taste buds on the tongue. Note that the secondary neurons transporting the taste information to the brain are situated in deeper layers than the taste buds. Source: Universe Review.

Note that taste receptors do not sense electrons. Rather, larger ions or molecules may stimulate them and cause a depolarization of the receptor cell, in turn activating the secondary neuron via a chemical synapse.

Reference
- Lawless et al., Chem Senses (2005); 30(3): 185–94

Acknowledgment
*Credits for the Lawless et al. (2005) reference go to @CMK


How is it possible to breathe perflurocarbon? I have heard of liquid breathing, where an organism, usually a person, would be breathing in perflurocarbon. Now I looked up perflourocarbon on wikipedia and I noticed, no oxygen at all, but fluorine that would rather bind to the molecules inside you and kill you. I mean, fluorine is electronegative enough to oxidize oxygen. So why doesn't perflurocarbon fluoridate every oxygen molecule in your body preventing your cells from working and form calcium flouride in your bones?

How would a person not be killed by breathing perfluorocarbon? Is oxygen more soluble in perfluorocarbon? Does perfluorocarbon not even get into the blood and instead stay in the lungs? And even then, why wouldn't the oxygen coming in be turned into oxygen fluoride? Is it simply because oxygen flouride has such a short half-life, especially at body temperature that it never forms in significant enough amounts? But even then you would still be breathing out fluorine gas of which some will come back in the next breath. Fluorine gas is toxic because it is such a powerful oxidizer that it will oxidize anything.

In liquid breathing systems the perfluorocarbons are simply an inert carrier for dissolved oxygen. It turns out that oxygen and other atmospheric gasses readily dissolve in perfluorocarbons without chemically reacting with them. Some perfluorocarbons can carry over 300 times as much oxygen as the equivalent amount of water. Perfluorocarbons are incredibly stable under conditions compatible with life, they aren't being broken down into free fluorine in you lungs or blood, or reacting with your tissues much at all. The perfluorocarbons don't cross the lung-blood interface in significant amounts.


Which is more susceptible to dehydration — extracellular and intracellular fluid? I want to ask in human body, there is intracellular and extracellular fluid that makes up the total body water of our body, which is drained first when we do activities? extra or intra? if I want to do a bioimpedance measurement, does measuring only the extracellular fluid good? Thankyou

You should understand that the body is an open system which is held at a steady state. Water can diffuse in and out of the cell such that the osmolarity is balanced on both sides of the membranes. If the water potential changes in either of these compartments (intra- and extra- cellular) because of addition or removal of water molecules, both the compartments would be affected such that finally the osmolarity is same in both the compartments. It may, however, take some time to achieve the steady state.

If you refer to sweating when you say "activity" then you should note that it is a complex process with extensive neurological control. The water that is secreted by the eccrine sweat gland primarily comes from the blood. However, profuse sweating will lead to water loss from both the intra- and extra- cellular compartments.

  Prolonged exposure to hyperthermic conditions and/or prolonged
  exercise in the heat can induce water deficits due to profuse
  sweating, resulting in hypohydration. This water deficit lowers both
  intracellular and extracellular volumes and results in plasma
  hyperosmolality and hypovolemia; both of which impair sweating.

  Shibasaki, Manabu, and Craig G. Crandall. "Mechanisms and controllers of eccrine sweating in humans." Frontiers in bioscience (Scholar edition) 2 (2010): 685-696.

So, for your experiment it is better to measure the osmolarity of the extracellular fluid or the blood plasma because:

It is easier to measure
It would not be sensitive to local and temporary effects


What is the energy produced by the mitochondria? I know that the mitochondria is basically the power house of the body,
it consumes amino acids, fatty acids, glucose, etc and oxygen.

When these molecules meet up in a enzyme, a series of reactions happen (Krebs
cicle) which end up in CO2, H20 and energy.

Then the enzyme and later mitochondria will release its energy which will be stored in ATP molecules.

My question is what is this energy?

The use of the energy in ATP is quite complex. Since my college days our knowledge of how ATP is used has broadened considerably.

Let's look first at the role of ATP in the sodium-potassium pump. This pump uses roughly 20% of the ATP your body produces, even more if you are a couch potato. ATP powers this process by attaching its terminal phosphate group to the pump. The phosphate group is highly charged. Its attachment pulls and tugs on some regions of the pump and repels other regions due to the fact that many of the amino acids comprising the pump are polar or charged. These electrical, magnetic-like, interactions change the shape of the pump. This causes sodium ions to be pumped outside the cell even though they are more plentiful there. When the phosphate is released, the pump returns to its original shape bringing in potassium ions and reloading sodium. It is this pumping action that, among other things, provides the energy for messages in nerve and muscle cells (action potentials).

Probably the important energy use of ATP is this. Many of the reactions your body needs are uphill battles. That is, there is more energy in the substances we wish to produce (products) than in the substances which we must use for raw materials (reactants). So, the ATP attaches its phosphate to the reactant. This raises the energy in the reactant making it now have more energy (more unstable) than the product we wish to produce. The reaction now becomes "downhill" and can proceed naturally ("spontaneously") without holding a bunsen burner under your bottom. This concept is termed "coupled reactions" where we take the "downhill" breaking down of ATP and use it to power the "uphill" production of a requires substance.

There are two principal reasons a molecule becomes more energetic when a phosphate is attached. It is now more complex. Complexity increases instability, a consequence of the laws of thermodynamics. Another reason is that the highly charged phosphate creates stress in the molecule due to electrical interactions with other parts of the molecule.

Here's an image (mine) to show the concept of coupled reactions:


How long does it take unused antibodies to clear the system? Say you have the flu and a normal immune system. Now you're all better but your antibody level is still elevated. How long does it take for those antibody levels to go back to a base value?

I agree that this question may be broader than a simple half-life question in theory, however, I think that it is still basically a half-life question. For instance, does the presence of the virus (using the flu example) contribute to opsionization and clearance? Possibly, but this would be variable and difficult to generalize about.

The question has been asked in a number of ways (for endogenous / exogenous antibody). For simplicity, Mankarious et al examined transferred antibody in IVIG therapy and found, "For total IgG, the half-life found was 25.8 days; for IgG1 it was 29.7 days; for IgG2 it was 26.9 days; and for IgG3 it was 15.7 days." - an answer in line with that proposed by canadianer, above.


Real Time PCR Test Chemistry I am working on building a real time PCR machine. Is there any chemistry set that I can purchase online to:

Identify if PCR amplification was successfully done.
Test fluorescence dyes that could be used to validate if the fluorescence detector optics worked; i.e. something I could excite with a specific wavelength and monitor for fluorescence.

I am looking for something that is not dangerous and only serves the single purpose of validating the real time PCR machine.

Mods please advise if I need to move to Chemistry StackExchange

There are two different ways to detect PCR product in real-time PCR: dyes which bind to DNA in general, such as SYBR Green I, or probes specific to your PCR product. There's a summary of the benefits of each here, with the following table:

You can buy either online; they'll be fairly expensive but I can't think of an obvious way to get them cheaper if you're interested in high-confidence validation.

[edit] forgot to mention that you will also need to normalise the reporter signal against a reference dye such as ROX (https://www.thermofisher.com/order/catalog/product/12223012).


what are the mechanics of sweating? The causes of sweating aside, i.e. I'm not interested in which and how nerve signals are transmitted to sweat glands. But I would like to read a detailed account on what a sweat gland consists of, what it does when not sweating, but esp. what happens when a sweat nerve signal arrives. Is there a good free review or can you give one?

Myoepithelial cell contraction initiates glandular release from most exocrine glands developed from the ectoderm. These are the cells that exist in the glandular epithelium.

At the distal end of the glanduar coil, an isotonic plasma filtrate gets actively transported into its lumen. As you move down the coil, close to where it connects to the duct, absorptive cells remove NaCl to make sure the sweat is hypotonic when it reaches the surface of the skin. If you view these cells where staining for alpha tubulin or beta actin, you will see they have abundant levels of myofillaments, something uncharacteristic of epithelial cells. Hence Myoepithelial.


Why are the no bioluminescent plants? There are bioluminescent creatures and some fungi too. As far as I can see there are no bioluminescent plants. Why is this?

I imagine it would make a good attraction for night pollinators, or even for carnivorous plants so there must be some reason why this hasn't evolved somewhere on our planet. My guess would be that it takes too much energy for the chemical reaction involved and it's not worth the pay out but that's just a guess.

Overall, bioluminescence has arisen over forty times in evolutionary history.[25]

There are bioluminescent funghi and bacteria.

Phosphorus is the 2nd most important nutrient for plants, so perhaps it's too expensive to use for bioluminescence, most plants don't live in phosphorus rich environments.

Bioluminescence also uses quite a lot of nitrogen, and most plants can't fix nitrogen.

there are 71 species of glowing funghi, perhaps to distribute spores, so plants with spores could have had the same strategy.

If two species of plants used light for night time insects, it can confuse the insects if they are plant specific, light is more confusing than scents.

A tree can potentially produce a lot of light, and it would turn into a forest lamp-post attracting lots of insects. It could be ecologically hazardous. perhaps a carnivorous plant could benefit from it.

It seems like plants and algea easily could have evolved bioluminscence easily, if bacteria and protists have, and that it wasn't profitable to the plants.

A crowdfunded project to make some failed because it was too difficult to put 6 animal genes into the plant.

land animals use light as an indicator of fitness, and plants don't need to indicate their individual fitness to others, and most bioluminescent animals have the option to switch things on and off very effectively, which difficult for trees.


Why must the alcohol decolorizer be used for 30 seconds or less for Gram staining? I had today a class in microbiology and my teacher said that the Decolorizer component is the critical one and cannot be more than 30 seconds.
The decolorizer has alcohol in high concentration, my lecturer says 95%.
I know that alcohol dissolves the lipid membrane, more exactly here for RBC which should be a similar situation here, not completely sure however.

What component is the critical one that you cannot keep alcohol on your bacteria samples more than 30 seconds?

The crystal violet stain will be removed if the decolorizer is left on too long.  I'm assuming that the crystal violet complexes that are retained in the gram positive bacteria's peptidoglycan layers end up being washed away (perhaps from overdehydrtation).


What would be the Hardy-Weinberg equilibrium condition for a population of haploid organism? What would be the Hardy-Weinberg equilibrium condition for a population of haploid organism?

Would it always be in Hardy-Weinberg equilibrium?

What is HW rule?

HW rule is a rule allowing one to compute genotype frequencies from allele frequencies and vice-versa. See Solving Hardy Weinberg problems and eventually Assumptions of Hardy-Weinberg rule for more information.

HWr in haploid organisms

In haploid individuals, the genotype frequencies and the allele (or haplotype) frequencies is the exact same thing! This is because the genotype is a simple haplotype. In other words, once you have the allele frequency, you necessarily have the genotype frequencies without need for any calculation. We can consider the haploid organism would display a special case of HW rule, where there is no assumption and where

$$p = f_{A}$$

$$q = f_{B} = 1 - f_{A}$$

, where $f_{A}$ is the frequency of the genotype carrying the allele A and $p$ is the frequency of the allele A. $f_{B}$ is the frequency of the genotype carrying the allele B and $q$ is the frequency of the allele B.


How are some people able to continue growing after reaching maturity? This is technically a cross-post of a question posted last year concerning gigantism and how certain people are able to grow far past expectations after it's assumed they've reached maturity.

How are some people still able to grow after reaching adulthood? Someone gave the answer in the old post that epiphyseal growth plate closure is caused by testosterone and not growth hormones. Is it a lack of testosterone, or an excess of testosterone? If it's a lack, why are women usually shorter than men and stop growing sooner? If it's an excess, does that mean basketball players produce less testosterone than average height people?

There are a number of cases of pituitary gigantism out there, but these are the best examples of what I'm asking:

Väinö Myllyrinne was 2.22m at the age of 21 but is described as having "experienced a second phase of growth in his late thirties", attaining a height of 2.51m by the time of his death at 54.
Adam Rainer at the age of 18, he was only 1.22m. However, he had a growth spurt in his 20's, reaching a height of 2.18m at the age of 30 and 2.34m by the time of his death at age 49.

What could have caused these men to grow so much after modern medicine tells us our growth plates have closed? Is there a possibility of replicating their late growth for people who suffer from hereditary short stature or other growth-related problems? And would it be safe?

EDIT: Although my question is different in many ways, here is the original question.

Usually the cause is 'acromegaly' but there are numerous possible causes.

It is impossible to start growing in length after your bones have matured too much. This is because of the 'Epiphyseal plate' this is a anatomical structure in bones that is necessary for length growth in bones and it degenerates at the start of adulthood.

The most common cause, although still not a common disease, for gigantism is acromegalia. It's cause is an abnormally high amount of growth hormone in the body which is most commonly caused by a hormone secreting tumor.

When the onset of this disease happens before the epiphyseal plates have degenerated it can cause them to stay active in which case the patient will continue growing.

Note: When the onset is after the degeneration of the disks it doesn't cause gigantism but it still causes a very recognizable change in appearance and the model for Shrek in the movie suffered from this illness.

Edit: Sorry, I didn't notice your subquestions initially. Yes, another possible cause in men is the lack of testosterone because this hormone is normally responsible for the degeneration of the plates in men.

Edit 2: In women estrogen is the hormone that is responsible for this, which explains why the length of men and women isn't dependent on testosterone in both cases


Do butterflies pass over migration patterns to their offspring? So, earlier, I read online (http://io9.com/butterflies-remember-a-mountain-that-hasnt-existed-for-509321799) that Monarch butterflies veer east during their southward migration to avoid a mountain that no longer exists. If this is true, how do butterflies know to continue avoiding the "mountain" after countless generations, and does it have to do with evolution? Do other animals have similar abnormalities in their migration routes?

If you think about it, monarchs must have a pretty strong genetic component to migration since often they only make one round trip at most in a lifetime. But its not as simple as passing a map in the DNA.

If a mountain springs up on the route, the 'common sense' of the butterflies are still operational and they will tend to find their way around it.

The paper discussed here is older.  More recent Monarch butterfly migration  of some genetics that have been done shows some traits that are related to migration patterns by sampling over many butterflies whose patterns vary tremendously.

Glancing over the paper, I'd say that there may be some 'muscle' memory in migration, but probably the mechanisms encoding the route of migration are not yet discernable.  This is far from something we understand well.

The insect is following patterns of behavior but doesn't turn into a robot just because its migrating.  Migration patterns are probably linked to a series of environmental cues.

Changes in climate or shifts in magnetic fields can change migration patterns. Butterflies would be very different than say migratory birds in terms of the social and environmental markers for migration.


Why does underwinding create topological strain of DNA? I am currently studying the supercoiling of DNA. I understand why overwinding would create additional strain for two attached strands of DNA, but I really don't get why underwinding would create strain and thus supercoiling. If anything it seems that the strands would just separate and strain would be relieved from any DNA helix. If someone would care to explain, that would be great!

The double helical structure of DNA with ~10.5 bp/turn is thermodynamically favorable. Any perturbation from this results in strain. Thus, if DNA is under wound, it is favourable for it to adopt a negative supercoil to return to ~10.5 bp/turn.

That said, negative supercoiling and DNA melting are in fact in some kind of equilibrium. This is important for processes such as transcription and replication which require ssDNA.


What level of cellular radiation is harmful for humans? What level of radiation at the frequencies used by the cellular network(1-2 Ghz) is harmful for human health?

Addition to the previous answer

First you need to understand how radiation causes cellular damage.

EM waves like γ-rays, X-rays and high-energy UV (in certain molecules even visible light) can knock out the electrons from the atom and create an ion and free radicals by breaking chemical bonds. This term — ionizing radiation is not used for low energy UV and visible light because these waves can only ionize a few types of molecules and are not ionizing in general. Moreover X-rays and γ-rays can dislodge even inner electrons which UV and visible light cannot (High energy γ-rays can also lead to the nuclear reaction of pair production). These ions that are formed are reactive and can attack other molecules (DNA/proteins etc) around them. DNA absorbs UV and this can cause DNA lesions such as dimerization of adjacent pyrimidines (via a cyclobutane bridge). Both reactive ions and pyrimidine dimers can cause cancer; the former is most frequent in melanomas which happen because of solar UV. Since UV cannot penetrate very deep, they affect mostly the skin (See here).

IR, with energy lower than visible light does not have sufficient energy to cause electronic transitions. But it can cause vibrational transitions such as bond stretching and bending. Microwaves have even lower energy and can only cause molecular rotation. Both IR and microwaves because of their property to make molecules move, generate heat.

Continuous usage of mobile phones can cause discomfort but only because of their heating effect. They can by no means cause cancer and even though mobile phone radiation is classified as a potential carcinogen (IARC Group 2B) perhaps because of the pressing allegations of certain factions, they do not have sufficient energy to cause DNA damage.

If you ask me if mobile phone radiation can be harmful to human health, then I would say yes, they can be potentially harmful with prolonged usage but in no way as harmful as to be causing cancer. I would say that it is as harmful as wine :P


Length of anopheles chromosomes? Where can I find the length of each anopheles chromosome? I've obtained data in which the length of each 2L chromosome for several anopheles is 39101648. I'm looking for an article that gives the length of 2L so I know my output is correct.

I came across this paper (Holt et al. 2002), does this answer your question? Look at Table 2 and 3. In this paper the lenght of 2L is  52393056 bp.


Potato with purple veins! Today while cooking with potatoes when I cut open a potato(raw) which was looking perfect from the outside showed purple veins. I threw it in my kitchen garden but than I wondered what it could be

Questions

Why did my potato developed these purple patterns?
What could be that purple pigment?
Are such potatoes Edible?

PS: The potato was not old. It was quite fresh.

The potato developed this pattern because it's (probably) natural to cultivar you're growing or due to cross-pollination.
Purple pigment is anthocyanin. It's perfectly normal and considered as more healthy (as those varieties of potatoes contain more antioxidants and vitamin C) and even 'gourmet'.


What kind of larvae are these. Lots of them in the basement in the summer, crawling around on the floor and the walls larvae crawl on basement floor.  Some are also found on the first floor of the house.  Lots of legs--I also thought they became "rolly polys"  but never knew for sure what they were either.

Those are not larvae, but adult millipedes. Myriopoda, Diplopoda. https://en.wikipedia.org/wiki/Millipede
Here is a good link from the U of Minnesota on common arthropods in the basement.
https://extension.umn.edu/insect-relatives/sowbugs-millipedes-and-centipedes


Is this in vivo or ex vivo? This question has probably been asked a few times but I get the concept I just dont know how to apply it for this paticular experiment

I aim to use cherry tomatoes and determine its glutamate content after drying for varying amounts of time.
This would involve putting the tomatoes into the centrifuge to extract its juice.
Due to this, I am 'preparing' the tomatoes in vivo (I think need clarification) but I am observing the Glutamate content outside of the organism (ex vivo)

I dont know how I should be classifying this experiment (between in vivo and ex vivo)

Help will be greatly appreciated !!!
Thank you!!

The classification usually applies to the experimental conditions. Are the experimental conditions applied to an organism, or to a less than whole organism (cells culture --> all the way to test tube chemistry reactions)?

This is somewhat subjective, but in your case, since the experimental conditions are drying time of the pretty much whole organism (the tomato), I would call it an in-vivo experiment.

Think of it this way, if you treat animals with X and examine Y, this is an in-vivo experiment regardless of whether you are isolating proteins, DNA, RNA etc... to examine afterward to characterize the change in Y.

Now if you isolated cells first from mice and plated them to grow in cell-culture, and then treated with X to examine the same endpoint, this has become more ex-vivo.

In-vitro would be to isolate a single enzyme from mouse cells, put into a test tube, and examine its ability to reduce some substrate after X treatment.

In your case, if you isolated enzymes from tomatoes and then used them in a test-tube to reduce some agent and measure activity before and after a given treatment, this would be more ex-vivo and have gone all the way to in-vitro.

EDITED: Matt pointed out I had confused in-vitro and ex-vivo on my continuum and he was correct.


Taxonomy problems on algae: Is Cryptophyta a Phylum or a Class rank? I  am currently interested in algae taxonomy (I am not an expert in the field).

I retrieved the taxonomy of my sequences with their NCBI access number via the taxonkit software (https://bioinf.shenwei.me/taxonkit/usage/).

I noticed that I get Cryptophyta at the Class rank level.

For me -phyta actually corresponds more to the phylum rank.

I checked on NCBI site and is actually tidy in Class rank ( https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=3027&lvl=3&lin=f&keep=1&srchmode=1&unlock) but for example on the algaebase database (http://www.algaebase.org/browse/taxonomy/detail/?taxonid=Xafa8c1d30aa53593), Cryptophyta is classified as Phylum.

Can you tell me why Cryptophyta is rank at the Class level on NCBI and not to the Phylum level ?

Conversely, I retrieve taxonomy with, for example, Phaeophyceae ranked at Phylum level (https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=2870&lvl=3&lin=f&keep=1&srchmode= 1 & unlock) while it is normally a Class on algaebase (http://www.algaebase.org/browse/taxonomy/detail/?taxonid=L8055ac0a94735f3e).

Do you have ideas being considered? I am very interested !

Thank you very much in advance for your answers.

Best regards

It is not possible to tell which one is "correct" and which one is "incorrect";
Actually "ranking" itself is a bigger problem with entire classification system.

After the "sexual species concept" we have somewhat a grasp that many (but not all) species fall on "same rank"; but for supra-specific ranks it is theoretically impossible to tell whether the  grass  (said to be "family" rank) and a  compositae (said to be "family" rank) fall exactly on same "rank" or not; similarly it is theoretically impossible to tell whether the animal (said to be kingdom rank) and plants (said to be kingdom rank) are exactly on same rank.

Practically; we forcefully assign the taxa from different lineages into similar ranks somewhat based on apparent perception, and in some cases we develop fine divisions of ranks and develop some criteria, that is also based on perception of 1 or a team op people; but that is not absolute.

What we can theoretically confirm, the taxon "Plant" is certainly higher than  (superset of) the taxon "grass" (a subset). I.e. hierarchies (superset-subset relationship) exist along a lineage. But the concept of "rank"; i.e. assigning 2 taxa from different lineage into "ranks" is a highly subjective and controversial.
(Personally I confess I don't know whether the ranking system have any real advantage other than arranging information)

A routine change of rank usually does not make anything correct or incorrect. (if within the single lineage you assigned a phylum into order and simultaneously an order into phylum; then it would be a clear false, or jumble-up the subset-superset relation). But when you just change a vague and confusing sort of
 "weightage" with respect to taxa on other lineages; keeping all subset-superset relations unaltered; nothing actually changes!

N.B. Additionally, if a taxon (set) is broken into adjacent or more taxa, or 2 adjacent taxa (set) is fused, (without cutting a taxon from one lineage to another) that is also a minor change in "refinement" or "resolution", not a change in correct-or-incorrect-ness.


Chemical methods to detect cell division So I have been working on a project for a while, and there is one mechanism that I need a little bit of advice about.

The project is chemical-biology based, so don't be deterred :)

Theoretically, by this point in the experiment:

I put cells (let's say lymphatic or endometrial) into stasis, through means of lyopreservation, and now, I have brought them out of stasis, through exposure to a sucrose (trehalose)-based medium.

Now I am attempting to chemically detect mitotic growth within the cells, how can I do this?

This is where the chemistry comes in: My first thought was to use a chromatic indicator that would fluoresce or irradiate in response to mitotic acceleration, but I have not yet found a suitable chemical. In research, I found that a similar experiment had been done in bacteria, and the chemical dimyristoylphosphatidylcholine (1,2-Dimyristoyl-sn-glycero-3-phosphocholine) had been used. Would this work in mammalian cells? Another idea was to use a chemical that detects the unnatural growth from the spindle fiber and centriole point of view, reacting when the centrioles entered the phase to replicate. I have been unable to find any chemicals that make use of the replication of centrioles, or the spindle fibers, so I need ideas.

To summarize: Does anybody know of any biochromatic indicators that react through detection of rapid, mammalian, mitotic growth? Not necessarily cancerous and uninhibited, but rapid meaning 'a speed of mitosis that is faster than the norm.' Preferrably, the indicator would be able to stay in stasis for extended periods of time.

If such an indicator is not available (or you do not believe so) then does there exist a biochromatic indicator that reacts in the presence of any sort of cell division?

Is there a way to chemically detect cell division?

I am welcome to all ideas.

The most common indicator for the growth of any kind of cell (population) I know of is the amount of DNA in that cell. There are a number of (fluorescent) dyes that bind to DNA in a stoichiometric fashion and can therefore be used to determine the (relative) amount of DNA inside a cell (is hope that's what you mean with 'biochromatic indicator'). The most common dye used in this way is probably DAPI.

In order to determine which cells are dividing, you'll obviously need a device that can measure the fluorescence of each cell individually- so either a microscope or a flow cytometer. Because growing mammalian cells (it seems to me that's what you want to look at) multiply their full set of diploid chromosomes in the S-phase of the cell cycle, you can discriminate growing cells from others by their relative DNA amounts:

A non-growing cell has only the diploid chromosomes (1x relative DNA)
A growing cell will have either the doubled set of chromosomes (2x relative DNA) if it sompleteded S-phase or an intermediate amount (1-2x relative DNA) if it's currently in S-phase

Figure 1 of this (really old) paper also shows, how DNA amounts can indicate at which point of the cell cycle a cell is (which tells you if its growing) works.

A note on cell viability:

Staining any kind of cell with DAPI (or most other dyes that bind to DNA) will most likely kill it or at least act as a very strong mutagen. Based on your answer to my comment this should not be a problem.

While not really part of your question, you mentioned that you want to preserve cells using lyopreservation, which basically means drying them. You should consider, that mammalian cells will most likely not to survive this process (unlike plants and some invertebrates there are no mechanisms in mammalian cells to protect them against the water loss). Without sorting the live cells from the dead ones first, your measurements may detect cells that were dividing prior to the preservation.


Requirements for ability to reproduce In my (albeit basic) biology classes in the past, we've learned about how, to reproduce, two organisms must have the same number of chromosomes. This has been verified by a few other websites I found. So- I've heard about various genetic disorders in which people can have fewer or more chromosomes than usual. For example, if a person had tetrasomy, they would have two extra chromosomes (48 in total). Chimpanzees also have 48.
Therefore:

If, hypothetically, a person with tetrasomy and a chimp's sex cells were combined, would it create anything?

If not, what are the other requirements for creating a baby organism besides the parents having the same number of chromosomes?

The ability to produce offspring has more to do with the compatibility of the chromosomes than the number. This is why hybrid species (such as mules) are able to survive (but are infertile). If you want to learn about why hybrids are infertile here is stackexchange question about.

Although, this would all be dependent on weather gametogenesis could occur with the tetrasomy. But as seen here with Down syndrome, it can be successful.


Is there a way to chemically detect the presence of Fungus in a sample? I would like to know if there is a way to chemically or somehow detect the presence of Fungus in a sample?

You could test for the presence of chitin, which is a fundamental component of fungal cell walls.  There is precedent for this: https://apps.dtic.mil/dtic/tr/fulltext/u2/a036986.pdf

Chitin is not only present in fungi though, it is also fundamental to insect and crustacean exoskeletons, and the occasional plant species (e.g. Aegagropila).


Predict if a given protein is recognized by antibodies Assume that i have a 3d-protein structure in a PDB file on a computer. Is there any bioinformatic method to predict if that protein is recognized by all known antibodies of human and cause an immune response or not?
If the answer is yes, how accurate of these method?

First of all: It is important to appreciate tha antibodies do not recognize antigens, they recognize epitopes borne on antigens.

There are several software (online) that allow to predict these epitopes with high accuracy. I´m going to describe some of them next:

Prediction of B-cell epitopes:
You have to be in mind that B-cell epitopes can be continuous and conformationals.

Continuous epitopes can be predicted using Bcepred. This prediction methods is based on physico-chemical properties on a non-redundant dataset. The dataset consists of 1029 B-cell epitopes obtained from Bcipep database and equally number of non-epitopes obtained randomly from Swiss-Prot database. The prediction accuracy for models based of various properties varies from 52.92% and 57.53%. Also It achived highest accuracy of 58.70% at threshold 2.38, when  combined four amino acid properties( hydrophilicity, flexibility, polarity and exposed surface).

Conformational epitopes can be predicted using DiscoTope 2.0. This method predicts discontinuous B cell epitopes from protein three dimensional structures. The method utilizes calculation of surface accessibility (estimated in terms of contact numbers) and a novel epitope propensity amino acid score. The final scores are calculated by combining the propensity scores of residues in spatial proximity and the contact numbers. Besides, Using the benchmark data set from the original DiscoTope paper, has been demonstrated that the updated method has a significantly increased predictive performance.

Important: Discotope allows to get a 3D structure of this epitopes.

I propose to use DiscoTope for prediction of discontinuous epitope residues for several reasons. First, I have shown on a data set of discontinuous epitopes that the average predictive performance of the DiscoTope is significantly higher than the Parker propensity scale and marginally higher than the surface localization score defined by the NACCESS RSA score. Second, several authors have shown that DiscoTope correctly predicts residues in epitopes that have been identified using different techniques such as phage-display, point mutation, and sequence analysis. Third, the DiscoTope prediction method is publicly available on www.cbs.dtu.dk/services/DiscoTope, and the output of the method is easily interpreted.

I would recommend you to check if this epitopes borne on the protein have possible allergenic sites that can contain experimentally proven IgE
epitope. For this you can use Algpred


Why are there no trees in Texas? In Texas, there is lot of grassland and many cotton fields, which need a great deal of water. However, I have not seen any forests or areas with many trees.

Why are there no forests or heavily-treed areas in Texas?

A quick google image search reveals that, indeed, Texas has quite lush forests. Remember that the state is extremely large (as compared to the Northeastern states, for example), and encompasses a huge variety of terrain, climates, rainfall amounts, etc. While the stereotypical view of Texas is rugged, dusty terrain:

From: http://texasmountaintrail.blogspot.com/2013/12/big-bend-landscape.html

The eastern part of the state borders Louisiana, and is definitely not dusty and dry:

From: https://www.flickr.com/photos/horwath/2488138213/

Rainfall varies across the state from east to west:

From: http://www.worldatlas.com/webimage/countrys/namerica/usstates/weathermaps/txprecip.htm

There are many different reasons why trees are not very likely to grow in certain regions, and these may vary from place to place. There may not be enough precipitation to support trees that are not adapted to a drier environment, while some species of grass could survive just fine. Temperature changes could be too severe between summer and winter (grasses just go dormant or die during harsh winters, and regrow in the spring). Fire is a big issue, as well - prairies often burn, and while grasses can regrow quite quickly, a tree that doesn't mature for 20 years may not make it between fires. Grasslands also have very deep, tightly-intertwined root networks, with some reaching 15 feet (~5m) or more below the surface:

(Click image for higher-resolution PDF)From: http://www.conservationresearchinstitute.org/educational-offerings.html

Tree species that survive the other challenges may not be able to penetrate deeply enough to adequately take root, sustain itself, and not fall over. Also, speaking of which, grasslands tend to be susceptible to tornadoes as well, and while grasses just bend before the wind, trees get uprooted or break. So, while any one or two of these issues may be overcome by a particular tree species, when added together it translates into a very inhospitable environment for trees.


How does hair grow and is it similar to how grass grows? If I recall correctly, nails (finger nails or toe nails) grow by adding matter at its base. So for instance, if you would draw a dot at the very bottom of your nail, it would end at the top in a couple of weeks.

I was wondering how this works with hair. Is new hair added at the bottom and the old hair 'pushed' away? Or does hair consist of layers that always try to get further and further (that would mean longer hair is thicker than shorter hair). And is this wayof growth similar to how grass grows?

In hair and nail growth new cells are added to the bottom. These cells are produced at the follicle. There are three stages called:

Anagen : active growth
Catagen : end of active growth
Telogen : total stop of follicular growth

I don't know what you mean by like grass but both nails and hair have a first in first out order.

Feathers present a contrasting case: the outermost portion is the most recent. Feather growth is relatively more complex. This article is a nice read on feathers.