text:
Central of Dogma? reverse transcriptase says No
I know what a reverse transcriptase is but I'm not sure why it is suggesting that the central dogma may be wrong -- RNA first then DNA instead of the well-known sequence of DNA -> RNA -> protein

Go to wikipedia and look reverse transcriptase. All your questions will be answered. But to answer your question, reverse transcriptase is an enzyme that uses RNA molecules as a template to make a DNA version of said RNA. ie the flow of information from DNA to RNA is reversed.
The central dogma... is a terrible name. It was an idea state in the 1950s that information flows one way from DNA to RNA to protein. The use of the word dogma is an ill choice to use. Because science does learn new things. And given that DNA was only just discovered in the 1950s....ie the same decade... the word dogma is a bad idea. SHould have waited a few more decades first
Anyhow... the discovery of reverse transcriptase allow information to flow back from RNA to DNA. The discovery of siRNA.. mean RNA can control DNA. The discovery of prions... lead to current work now where pre-existing proteins can be templates for the folding of newly synthesised protein. DNA methylation allows epigenetic inheritance. Ie changes of certain protein levels (say during starvation) in your body can leave inheritable marks on your DNA (which will then affect the behavior of those gene in your children).
The central dogma now (if it still is used) has a lot more lines leading up and down the chain.

You should probably read about the central dogma. Besides its poor naming, all that Crick said (and where he is still right) that no information goes back from the level of protein. Besides that, especially the existence of the reverse transcriptase proves its validity. When you take the wider formulation of it: DNA makes RNA (mRNA) to make proteins, then you see this. You prepare cDNA first, which is then transcribed and translated into proteins. Fits.

I still find the central dogma to be a useful starting place for introductory bio classes. As we go along additional elements are added to build up a more representative model. As a model, I equate it with bohr's atom cartoon- a good place to start.

Chris.... there are such things as RNA dependent RNA polymerases... where information from RNA is copies directly into another RNA molecule with no DNA intermediate. DNA can also be methylated by protein activity.. .changing the expression of the genes or the splice variants that the gene produces... and such changes are inheritable.

[https://biologydirect.biomedcentral.com/articles/10.1186/1745-6150-7-27/comments] This archived comment is informative.


text:
how did we breed after the fusion ? and why can't we bread with chimps?
after the chromosome fusion happened to one of our ancestors, how did he breed ? if he was allowed to breed because the chromosomal differences were still not very big back then, why can donkey and horse breed then ? ain't we supposed to be able to breed with chimps as well ?

There are plenty of people today with balanced Robertsonian translocations, they breed mostly fine, though Down's is more common than in the rest of the population, because meiosis is more likely to be messed up. If due to drift, people with those translocations became more common, eventually they could breed with each other, and make offspring with 22 pairs of chromosomes.  In theory, this drift could take over the whole human population.

Fusion of chromosome is not an absolute barrier. The two unfused chromosomes can pair up with the fused chromosome.
So long as all the genes are the same... offspring can be had.
However... a fused chromosome means that chromosome cross overs between the fused chromosome and its unfused chromosomes during meiosis will lead to unequal crossover of the chromosome, leading to massive lost or gain of genes... such germ cells if fertilized is usually lethal
Also if the fused chromosome is reassorted unequally with its unfused chromosomes during gamete formation.. will also lead to unbalanced genes for any fertilised embriyo... so again it is lethal.
So while there will be offspring... there will be few.
In effect... the fused chromosome creates a barrier.. not an absolute barrier... but one that makes free flow difficult.
So back to your question... the first individual with the fused chromosome could have reproduced by with a lower fitness with any member of the tribe. There will be children but it would be few. Those children with the fused chromosome can again reproduce with any member of the tribe but will have few children. However if two individuals with fused chromosome mate (sibling-sibling / parent-sibling) the pair will be fully fertile.
An interesting example
http://genetics.thetech.org/original_news/news124
Man with 44 chromosome instead of 46... Man has two chromosome composed of chr14-15 fusion. Produce of parents who are first cousin who both also have the Chr14-15 fusion.
Perhaps one day in the far future... this Man will be source of people with 44 chromosome.
Other example are families with balance translocation of chr21. They have a high incidence of down syndrome in the family.
As for Horse (2n=64) and Donkeys (2n=62).. not only is there chromosome fusion, but enough time has passed that changes in genes has occurred... ie specialization. As a result the reproductive cycles of jennies are affected.  Also Johns, are gelded as a matter of course. So no fertility to speak off. That being said, there have been instance of Jennies becoming pregnant and giving birth.. usually to a pure donkey (if sire is donkey) or pure horse (if the sire is horse)... an indication of some kind selective segregation of donkey and horse chromosomes... Perhaps donkey and horse centromeres do not play well together.

so you mean that we can't breed with chimps whilst donkeys can breed with horses because our speciation happened much earlier ? and not because of the number of chromosomes nor the differences of the genetic information ?

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What are these little creatures living inside a silk web?
They are found in Bangladesh. Some of my observations:

They are so small that their legs and appendages look transparent.
Their colour is brown and they have no wings.
My eye sight is not brilliant, but the don't look like spiders. Their head and mouthpart vaguely resemble that of the termite. When I tried to observe them closely, they looked bed-bug-shaped.
They are fragile: when I tried to grab them by pinching, they just squashed.
They seem like living in a big city made of silk strands. The can easily move in, out and within the structure which slightly bigger, potential predators could not.

Unfortunately my mobile camera is not good enough to capture a clear image of them. Click images for larger version.

Can you add where you took these photos? Also I can think of a couple of possible candidates but it would be purely speculative unless you can get a photo (or do a sketch?) of one. Any information on colour etc would also be useful.

it is from my backyard (Bangladesh). The silk structure is on old bamboo fence bordering a paddy field. Now it's raining so I can't go outside to make a stetch. so I'll try to describe it again. They are so small that it's legs and appedage look transparent. color is brown, has no wing. my eye sight is not brilliant but it didn't look like an spider. it's head and mouthpart vaguely resemble that of the termite,  my eyesight  is poor though so I can't fully gurantee this.
Please name all the candidate comes to your mind so I can compare with the images on the internet.

some sort of mites?

From the comments above (in particular, "it's head and mouthpart vaguely resemble that of the termite") it is possible that what is here is a Webspinner colony (Order Embioptera); if so you either have one of the few species in which the male is wingless, or the colony was without adults of that sex when your question was asked.  Webspinners are distantly related to termites, but have little or no economic importance (some species have been accidentally spread by man).  The Wikipedia article (https://en.wikipedia.org/wiki/Embioptera) has some basic information on the group (including photographs of both sexes and of nymphs), and references for further information; identification of species from Bangladesh will be problematic, as Edward S. Ross (the expert on this group from the mid-1940s, and not fully replaced--he has retired) had reportedly collected enough undescribed species to more than double the known diversity.

I didn't know this family so thanks for keying me into their existence. However...from the OP: "They looked like bed bug shaped" ; "They are so small that it's legs and appendage look transparent. color is brown, has no wing." The images of the embioptera I found do not match that description as they are too large and shaped incorrectly (even the wingless larva). Could you please comment about that in your answer. Thanks.

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What is this yellowish insect?
I found this insect inside of my shoe. It is approximately 1cm in length and less than half a centimetre wide. It was found in the Netherlands, in the province Gelderland.
Close shot

Distant shot

Upside down

What kind of insect is that?
Edit:
As @fileunderwater suggested: the question is "close" but not identical.
I think that the suggested duplicate will only provide an identification of the family of the insect, but nothing more precise and specific. Therefore, the answers for the 2 questions vary.

Possible duplicate of What insect is this? (Black body two orange lines in its back and six legs)

@rg255 Its probably reasonable to close this as duplicate, but strictly speaking these are probably two different species (I'm not into Coccinellidae larvae). So a more general question is to what extent we should close questions as duplicates if they are "close" but not identical (for species-id Qs, similar at what taxonomic level)? Here, the proposed duplicate will provide a family id, but that is all. So comparing to mammals, equal to answering "this is a deer" to a species-id Q with a picture of an Moose.

It is the larva of Harmonia axyridis (Asian lady beetle).

The image posted by timbernasley is more accurate because the larva you have shown is in its late instar ,a stage not an early as this one.

Here's the link: Wikipedia

Note that this is not the same as what is commonly called the "Lady Bug" in North America.

As we should all hopefully know, lady bugs/birds/beetles are a beneficial species, so try not to kill any larvae you see.  However, do be aware that larvae have been known to bite, so take care in relocating it.

@n_b although this is the Harlequin ladybird larvae which is a very aggressive invasive species currently wiping out the native population of the UK

@n_b No, this one is Harmonia, kill it on sight.

@Ilythya & Vladimir I stand corrected. I didn't know it was an invasive species. Kill these.

@n_b Good luck on killing them; this invasive species is now the most common ladybug in urban areas in the Netherlands. :-(

This is a ladybug larva:
google image search

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

authors: Vladimir F Героям слава


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How exactly apoptosis starts?
I read article about apoptosis on Wikipedia, but didn't understand, how exactly the organism learns that it is necessary to launch process of apoptosis in certain cell. In other words, on what signs the cell is marked as "necessary to destroy"? How exactly at the chemical/biological level process of apoptosis starts?
Also I am misled by the fact that apoptosis occurs by a row of strongly differing reasons - not only aging, functionality losing, chemical/radiation affection, but also process of apoptosis can start in absolutely normal cells (including just newly created ones - for example, during formation of an embryo). How in that case the embryo knows what cells need to be destroyed, and how exactly it does it?

Unfortunately, this question is far too broad. From the [help/dont-ask]: Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much.

Too bad for me.

Maybe just evolution through chance-events and natural-selections helped them to adopt a self-destructive process? especially in multicellular forms?  For an example, in plants, xylem (made mostly of dead-cells) was obtained probably because the death of some water-conducting cells (hydromes, as yet seen in bryophytes), made them empty, thus deceased friction and adhesion, that was advantageous.


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Mechanism of Myosin Head Bending in Cross Bridge Cycle Power Stroke Phase
What is the mechanism of bending of myosin head during the power stroke of the cross-bridge cycle of the muscle contraction? Does this have anything to do with the protein's 3-D structure i.e. folding of protein in space? I would prefer a physics explanation down to either the classical electrical dipole or quantum mechanical interaction amongst the proteins. I want to know what exactly produces the force that powers the bending. I am pretty sure that the force can only be electromagnetic. The question is how the force is manifested in the bending.
Any references for further reading are appreciated.

Introduction:
This is going to be quite a long answer. To have an introduction to the topic, you can have a look at articles from Wikipedia and RCSB Protein Data Bank.
The exact mechanism of physical interactions in myosin head during powerstroke cycle are not yet known. The only thing we definitely know about how release of Pi from myosin causes conformational changes (and hence, force) in it, as given at MJC website is:

This is a very basic description of the powerstroke cycle, so we'll move ahead for more detailed explanation of physical interactions during the cycle.
Details:
I have found three theories regarding physical interactions during the powerstroke cycle. Let's discuss them one by one.
THEORY 1: I could not find much explanation about physics of the cycle, the only thing I could find was at the JBC website (emphasis mine):

Mutation R759E in the myosin converter domain results in biochemical and biophysical defects as well as aberrant muscle structural and physiological properties. The central portion of the converter domain is encoded by exon 11e in indirect flight muscle (Fig., green), and the converter interfaces with the exon 9a-encoded relay domain (Fig., blue). Molecular modeling indicated that residues 508–511 in the relay loop are located near the converter residue 759 and defined weak and strong interactions of residues 509 and 511 during the rearrangements of the relay loop that are affiliated with the mechanochemical cycle. Furthermore, Ile508 can be cross-linked to Arg759 in Dictyostelium non-muscle myosin II when they are each substituted by cysteine. Therefore, we hypothesized that specific amino acids in the relay domain interact with converter residue 759 and that second site mutations in the relay residues may suppress the defects associated with converter mutation R759E.

They couldn't give much explanation of the physics involved in it. Maybe this is because I missed it or because there hasn't been much research on this because Dissecting the molecular mechanism of muscle myosin function in vivo has proved difficult. as said at JBC website.
THEORY 2: This theory, given at PNAS, provides a more detailed view of the physics, so we'll have a more thorough explanation of it:

Molecular motors produce force when they interact with their cellular tracks. For myosin motors, the primary force-generating state has MgADP tightly bound, whereas myosin is strongly bound to actin. We have generated an 8-Å cryoEM reconstruction of this state for myosin V and used molecular dynamics flexed fitting for model building. We compare this state to the subsequent state on actin (Rigor). The ADP-bound structure reveals that the actin-binding cleft is closed, even though MgADP is tightly bound. This state is accomplished by a previously unseen conformation of the $\beta$-sheet underlying the nucleotide pocket. The transition from the force-generating ADP state to Rigor requires a 9.5° rotation of the myosin lever arm, coupled to a $\beta$-sheet rearrangement. Thus, the structure reveals the detailed rearrangements underlying myosin force generation as well as the basis of strain-dependent ADP release that is essential for processive myosins, such as myosin V.

Just so that you know what it is, let me add a few points about Molecular Dynamics Flexible Fitting:

The molecular dynamics flexible fitting (MDFF) method can be used to flexibly fit atomic structures into density maps. The method consists of adding external forces proportional to the gradient of the density map into a molecular dynamics (MD) simulation of the atomic structure. For examples of MDFF applications, visit the websites on Mechanisms of Protein Synthesis by the Ribosome, Dynamics of Protein Translocation, Molecular Dynamics of Viruses, and Intrinsic Curvature Properties of Photosynthetic Proteins in Chromatophore.

Now, returning to the main point (results & discussion sections):

The equilibrium and rates of transition between the Strong-ADP and the Rigor states vary greatly among different myosin isoforms and predominantly determine how long a myosin motor can remain bound to actin in the absence of load. This kinetic tuning must be achieved by structural differences in the regions that we have seen to change in our Strong-ADP structure as well as regions involved in stabilizing the lever arm position...Our structures show that the Loop 1 conformation alters in the transition from Strong-ADP to Rigor. Thus, different sequences likely favor one conformation over the other, or promote the transition from the ADP-bound conformation to the Rigor conformation, providing a structural basis for this kinetic tuning.
For myosins, such as myosin V, that function in a cell as two-headed, processive motors, the length of processive runs and the initiation of processive runs are both enhanced by “gating” of the heads. For a two-headed molecule with both heads simultaneously attached to actin, gating refers to the fact that a lead head is essentially stalled in an ADP state strongly bound to actin, until the rear head is detached from actin by binding MgATP. This gating is attributable to the strain dependence of MgADP release. Although we do not know whether some of the subdomains of myosin may be deformed by strain, our Strong-MgADP actomyosin structure clearly reveals that strain must prevent the rearrangement of the $\beta$-sheet from the Strong-MgADP conformation to the Rigor conformation, based on the data presented in Results. Preventing this rearrangement is thus the basis of gating.

For better understanding, you should also see this video (same website) which shows animation of different conformations of myosin in different stages of the cycle:

The transitions are animated by direct morphing between the three structures Pre-Power Stroke (PPS), ADP state, and Rigor. Starting with the PPS conformation, myosin first rearranges to allow phosphate release without much change in its lever arm. Then, the first step of the powerstroke consists of a large swing of ∼58° of the lever arm toward the ADP state. The actin-binding cleft [between the U50 (blue) and L50 (white) subdomains] is closing for this transition, leading to the only state of the actomyosin cycle, which exhibits high affinity for both actin and the nucleotide. The second step of the powerstroke occurs upon ADP release and ends in the Rigor state after an additional lever arm swing of 9.5°.
THEORY 3: This theory gives even more detailed, but a bit different from the previous one, view about how the energy, released by ATP hydrolysis, is stored in myosin head. It is called Rotation-Twist-Tilt (RTT) energy storage mechanism. See this:

According to the mechanism, ATP hydrolysis in the catalytic site rotates the top of the regulatory domain, which, being connected to the coiled coils of the S-2 region, causes twist between them to increase, and leads to the twist in the myosin head. Since, at the time of hydrolysis, the myosin molecule is not bound to the actin filament, the head is free to rotate and tilt. The increase in twist is instrumental in storing the energy of ATP hydrolysis, while the rotation and tilt of the myosin head brings it sufficiently close to the actin so as to form the actomyosin complex. Untwisting of the coiled coils and the subsequent untilting and constrained reversal of rotation of the head cause the power stroke. This strain decreases the energy of interaction between actin and myosin and thus enables ATP to dissociate myosin from actin. The system is now in such a state that after the next ATP hydrolysis event, the myosin head can bind to actin, and thus, a new contractile cycle can be initiated.

The original paper of RTT mechanism (by Nath and Khurana, 2001) is available here. Since the detailed mechanism is too long, I am not posting it here. You can read the full process, just remember to have a pen and paper with you!

Conclusion:
All of the above theories provide an in-depth view of the powerstroke cycle. However, I'd still conclude that the exact physics behind the powerstroke cycle is not yet fully known, only the transitions in conformation of myosin head have been observed and interpreted to some extent.
References:

Myosin head: Wikipedia
Myosin: RCSB Protein Data Bank
Journal of Biological Chemistry: Mapping Interactions between Myosin Relay and Converter Domains That Power Muscle Function
Proceedings of the National Academy of Sciences of the United States of America: Force-producing ADP state of myosin bound to actin
Theoretical and Computational Biophysics Group: Molecular Dynamics Flexible Fitting
Cell Movements: From Molecules to Motility
Molecular mechanisms of energy transduction in cells: Biotechnology in India II
Molecular mechanism of the contractile cycle of muscle; Sunil Nath and Divya Khurana, March 2001

Thank you very much. As a matter of fact the Bonus part is most relevant to what I am most interested in, i.e. the more fundamental physical (classical electromagnetic or quantum) principle of how the force is generated of the myosin motor. Your quote in Bonus "for myosin motors, the primary force-generating state has MgADP tightly bound"only states the chemical compounds involved in the force generation but not how the force is generated. It also says "molecular dynamics flexed fitting". I suppose it refers to some physics model. But what is that physics model?

The Rotation-Twist-Tilt theory you added most recently hints at the more geometric and physical explanation of the myosin bending. I found the original paper on this theory cited by the book you linked to http://www.currentscience.ac.in/Downloads/article_id_081_01_0078_0082_0.pdf .

Yup, but since its just a theory (without any given evidences) I didn't go deeper into it. Also I was in a hurry so I couldn't look for the original paper. Thanks for finding that, I'll add it up in the answer :)

You seem to be quite knowledgeable and interested in the physics aspect of physiology. Would you mind taking a look at my other question http://biology.stackexchange.com/q/19725/8344, especially the question below the answer by James T. Fulton?


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Are there biochemical differences between the cell membranes of prokaryotes and eukaryotes?
I would like to know if there is any difference in chemical composition of cellular bilayer lipid membrane between eukaryotes and prokaryotes.
Specifically, I would like to know about the action of antimicrobial peptides on these bilayer membranes in context of the different membrane compositions.
It would be helpful if someone points me to some references.

I have given some references that let you discuss variations in membrane compositions. There are many more. I think for a more productive answer you need to talk about specific species.

Prokaryotes include archaebacteria.  Some archaebacteria shows ether-bridge (instead ester bridge) between glycerol and fatty-acid. Even in some cases in some archaebacteria, instead 2 layer of lipid there is 1 layer of lipid whose each molecule have 2 heads. Also, gram-negative eubacteria is wrapped with 2 membranes- the cell membrane and outer membrane.

But the basic-plan of cell-membrane of any-cell is the exact same... whatever it is prokaryote or eukaryote... exact same. Few scanty exceptional cases also, basically obey the physics rule of normal membranes of eukaryotes and prokaryotes.

There are differences. (Except mitochondrial eukaryotic membranes, which are indeed similar to bacterial membranes! (reviewed in van Meer et al., 2008)).
First, bare in mind that it is thought that even different eukaryotes, such as Fungi and Humans, have different cell membrane compositions and that this is reflected in the proteins (Sharpe et al, 2010). The outer membrane of Gram negative bacteria isn't even made of phospholipids, it's made of glycolipids (Kamio & Nikaido, 1976). Archean membranes have the most notable lipid compositions, including a bilayer-like monolayer, to adapt to the conditions they are found in (Oger et al 2013). My point being that saying "there are differences" is indeed an understatement.
This question has probably arisen because anti-microbial peptides seem to act with specificity, and that perhaps this specificity comes from direct peptide-lipid interaction. This is on the right lines. From wikipedia:

The cell membranes of bacteria are rich in acidic phospholipids, such as phosphatidylglycerol and cardiolipin[23][27]. These phospholipid headgroups are heavily negatively charged. Therefore, the outmost leaflets of the bilayer which is exposed to the outside of the bacterial membranes are more attractive to the attack of the positively charged antimicrobial peptides.

Notably, no such charge exists in eukaryotes since the negative charge is found on the inner leaflet of the plasma-membrane rather than the outer leaflet.
There is such a massive variation, even within bacterial membrane composition (Bogdanov et al 2014), that I cannot even really begin to list it here. Furthermore, there are variations in the glycocalyx, surface proteins, and lipid composition dynamics due to lipid rafts.


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How are Thyroid Stimulating Ab destroying thyroid tissues?
I was reading about Graves' disease, which is an autoimmune disorder. I read a few books, including Endocrinology by Hadley and Levine, and websites where they mentioned that the antibody named TSAb (Thyroid stimulating Antibody) binds to TSH receptors and stimulates synthesis and release of thyroid hormones from thyroid gland. This results in the symptoms of Exopthalmic goiter or Graves' disease.
My question is how are these antibodies actually attacking the healthy tissues (which I presume is the tissue of thyroid gland)?
I've so far found no website explaining this part of the autoimmune disorder. I'd appreciate any information or references in this regard.

Have you searched PubMed?

Thyroid stimulating antibodies (sTRAb) don't destroy thyroid tissue. To the contrary, they have a TSH-like effect on thyrocytes and therefore lead to hyperthyroidism and thyroid growth resulting in goiter. The exception is Graves' disease with Hashimoto component. Here, the thyroid is also affected by cytotoxic T cells and antibodies directed against thyroid peroxidase, which gives rise to destruction of the thyroid. But even in this case, it aren't the sTRAb, which destroy tissue.
Perhaps healthy tissues refers to extrathyroidal tissues. Due to unknown reasons several tissues including skeletal muscle, heart muscle, adipose tissue and skin have TSH receptors, and they are affected by sTRAb, too. Hypertrophy results from cross-talk of TSH receptors with IGF-1 receptors in Graves' disease.
References

Dietrich JW, Landgrafe G, Fotiadou EH. TSH and Thyrotropic Agonists: Key
Actors in Thyroid Homeostasis. J Thyroid Res. 2012;2012:351864. doi:
10.1155/2012/351864. Epub 2012 Dec 30. PMID 23365787.
Krieger CC, Neumann S, Place RF, Marcus-Samuels B, Gershengorn MC.
Bidirectional TSH and IGF-1 receptor cross talk mediates stimulation
of hyaluronan secretion by Graves' disease immunoglobins. J Clin
Endocrinol Metab. 2015 Mar;100(3):1071-7. doi: 10.1210/jc.2014-3566.
Epub 2014 Dec 8. PMID 25485727.
Krieger CC, Place RF, Bevilacqua C, Marcus-Samuels B, Abel BS, Skarulis MC, Kahaly GJ, Neumann S, Gershengorn MC. TSH/IGF-1 Receptor Cross Talk in Graves' Ophthalmopathy Pathogenesis. J Clin Endocrinol    Metab. 2016 Jun;101(6):2340-7. doi: 10.1210/jc.2016-1315. PMID 27043163.
Yoo WS, Chung HK. Recent Advances in Autoimmune Thyroid Diseases. Endocrinol Metab (Seoul). 2016 Aug 26. PMID 27586448.

In an autoimmune disorder body tissues are not necessarily damaged, the immune system can also cause

Altered organ growth
Altered organ function

Grave's disease is a result of altered organ function causing hyperthyroidism due to hypersensitivity reaction.
It is hypersensitivity Type-V.

Instead of binding to cell surfaces, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.

Wikipedia: Hypersensitivity


text:
The first species having circle of Willis (circulus arteriosus cerebri)?
I know mammals are not the only species that have this anatomical unit (i.e. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982101/).
But I was wondering what was the first species that had a similar structure in their brain (or brain-like organ). Do we know this?

it is interesting question


text:
How do bats manage lymph fluids?
We all know that bats hang upside down to sleep. I was watching some sleep for a while, and they don't move much while asleep.
If I fall asleep sitting in a chair my lower legs will swell. Lymph fluids in people are mostly moved by muscles in the limbs of the body.
It would seem like a sleeping bats lymph fluids would gather at or near the head, chest and lungs.
How do bats manage lymph fluids?


text:
Interpreting Allele frequency and allele count
In the following vcf file, the AF allele frequency of ALT allele  is 1.0. Does it mean that it is not a true SNP of interest? Does it also mean that ALT allele always occurs and REF allele never occurs in the population?
Also not sure how allele count AC=37 is being calculated.
Chr1 pos=565286, REF=C, ALT=T, Info AC=37; AF=1.0 Format GT:AC:AF:NC Child=1:11:1.0:+T=4,-T=7 mother=1:26:1.0:+T=8,-T=18,
Cheers,
Ambi.

Please let us know a bit more about your .vcf file. Spontaneously, I would say that all individuals in that file have a different allele (ALT) than the human reference (REF). It"s impossible to give an interpretation based on these information though. Allele count is defined as: "AC : allele count in genotypes, for each ALT allele, in the same order as listed" in the .vcf specification file. It is not really calculated, it is counted.


text:
Is it possible to genetically alter human beings to see parts of the infrared?
Most electron transitions take place in the infrared region,The ability to see this part of the electromagnetic spectrum without reliance on sophisticated technology would have tremendous advantages. Is it possible to manipulate human genes to see this part of the spectrum?

Our heads are warm, so the receptors that react to infrared radiation would be set off constantly by ambient radiation, not just radiation that comes in through the eye.  Note that the animals that do see infrared are cold blooded.
So it would be a massive genetic engineering project to get working infrared vision, to either make human heads be room temperature, or to thermally insulate eyeballs from the surrounding tissue.


text:
The smell of the shield bug (aka stink bug)
Every time a shield bug flies into my room I try to kill it. Unfortunately, they leave a strong smell after crushing them. Whenever I smell their odor, I always wonder what  the chemical compound is that the bug releases. Does anyone know what the smelly chemical is? If so, please help me out. I always wanted to know what that molecule was.

is this helpful?

bed bugs also have a very bad smell.

Some-how this question is locked for edit. (How?) . However tag add suggestion "identification" because this question basically seeking identification of a compound.

how did you locked your post from further edit? would you like to tell? however I wish keep my posts open to edit as per community guidelines, since all the edits yet done on my posts yet, were helpful to me.

If you don't like the smell,  you could always try to not kill it. Let it find it's own way out or help it on it's way with a glass and a piece of paper.

If an edit is already made and has not been approved then no further edits are allowed until the edit is approved/disapproved. @AlwaysConfused

Shield bugs (also known as stink bugs) are a group of insects in the superfamily Pentatomoidea. As summarized by this article from Rice University, the components of the chemical odor of these insects consist primarily of long chain alkanes, aldehydes, and esters. Esters are to be expected as they're the primary components of many odors. This article also includes other ecological info about the shield bugs' stink, as well as links to some references (including this peer reviewed journal article by Krall et all (1999)).
Another article mentions a 2006 study from Clemson University that identified 2 of the aldehydes in stink bug odor as trans-2-decenal and trans-2-octenal.


text:
How to write a palindrome sequence as-wish (create, theoretically) ? (self-answered)
There are specific examples from nature,  of palindromic sequences.
But without memorizing them, is there any way to randomly write or create or derive a palindromic sequence for a theoretical discussion?
by the way, Genetic palindromes are not an exact ditto of verbal-palindrome.

I once developed a method, but it is so-basic and simple that I'm pretty sure it is already discovered. Here I "shared my knowledge, Q&A-style"
Step-1
Write a small sequence randomly.
    5'... A T G C C

Step 2
Write the sequence in opposite-direction, on the next line. It will end at just at the next-place of last place of previous sequence, i.e.
         -------->

   5'... A T G C C

                        C C G T A ...5' .

                    <-------------

Step-3
Fill-in-the blanks following base-pair rule, and the sequence is now ready.
5'... A T G$\:$ C C$\:$ | G G C A T ...3'
3'... T A C G G | C C G T$\:$ A ...5'
Addendum (courtesy: user@Another'HomoSapien')
The previous method was similar way we usually read a verbal palindrome (though unlike a verbal palindrome, any reflection-symmetry was Not present ). But  there is a rotational-symmetry (2-fold), (rotational symmetry means it contains parts which are superposable on rotation).
So we could create a palindromic sequence using rotation also.

Or could rotate pre-filled up sequence (if exactly follow the user's instructions)

The brown dot indicates the axis of rotational-symmetry of the written-sequence, vertical to the plane of paper.

I use the same method, just the steps are different: create a sequence, write its complementary, turn it 180°, tada!

@another'Homosapien' Thanks but when Ii first came to me, no method was told so I developed one. Now I  thought about share, is there any problem doing that?

you could write an answer

Thanks for your sharing. I tried to find what is the secret so that the same strand pair with same strand. Whatever I try to create, become a non-palindromic. Then I found I can cut the pair-of strands into 2 non-palindromic half, that I create randomly, and join them.

ok on behalf of you I'll add your method already used in wikipedia.

basically it is yet an under-rated question so I thought there may be any objection from the community. It is also not specified to you

I don't think there's any objection, if there was, someone must have commented by now. sharing your knowledge is good, its just that this question has only 24 views yet. just have some patience ;)


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Could we tell that cancerous cells behave that way because-of their genetic machinery is work in a "primitive" way like Amoeba?
Amoeba sp. is unicellular, so can't form a tissue. It need not go through any apoptosis. It just continuously get doubled.
Could we compare them with cancer-cells?
or in-reverse,
could we tell that cancer-cells are a sort of mutated cell, that is behaving like Amoeba, or behaving in a primitive manner, and lost its later-upgrades?
It seemed to me when I came to know that,  mutation in many possible, separate genes, can cause mutation (probably that's why all environmental articles about different mutagens lead to the same disease... cancer). So I was wondering about there could be a common-cause behind all these cancers ... which maybe a loss in all latter-upgrades.

I don't think cancer cells are free-living. What do you mean by "later upgrades"?

Evolutionarily acquired characteristics to form a tissue and organ of particular shapes, that is absent in primitive organisms like Amoeba.

I didn't mean cancer cells if go to nature will behave like amoeba. I'm editing the question title. Thanks for your suggestion


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Is there any disease in adult human, other-than cancer, which-is resulted from mutation?
On all environmental articles I read about 3 impacts of mutagens (say Cigarette/ Naphthalene/ EtBr/ Colchicine/ ionizing radiation/ whatever )...
1. direct effect on tissues, other than mutation, such-as burns, choke, cirrhosis of liver, Lesion in lungs etc. (no direct relation with mutation)
2. Mutation affecting development of organs and intelligence, in youngs; and hidden mutation not affecting adults but showing expression (birth-defects) in future progeny.
and
3. Tumor and Cancer.
Now, my question is, if an adult become exposed to some mutagen; the only visible effect of mutation (not about burns etc, talking about genetic-mutation) ... on that affected-individual; whether cancer is the only-possible disease? or it is possible to occur some-other sort of genetic disease  (not about future but only to that particular affected-one)

anything else should happen ... say exact opposite thing... uncontrolled apoptosis that gradually kills whole affected person (for say).
or for say due to a genetic-damage a person became unable to perform cell-division, so no wound healing. If once part of body become cut, and it remain open forever, never seals. (I never heard or read anywhere).
instead of cell-death, they could perform some-other malfunctions, too. Like turning-off certain normal function, say stopped transport of certain molecule, or say stopped a function like color-vision, or start to secrete / accumulate some metabolites same-way as inborn error of metabolism?
But could anything such happen other-than cancer?

Are you asking about radiation poisoning?

@James Any mutagen. Radiation, Cigarettes, Naphthalene, EtBr, Colchicine, whatever

I cant recall anything else than cancer , that could affect an adult directly. That is quite bizarre. A malfunctuning gene should give rise to many-other problem... why cancer only???????

Cancer is a wide collection of different diseases with a huge variety of symptoms and physiological impacts. Another DNA damage based disease is acute radiation poisoning. I also have a feeling that sometimes DNA damage can lead to sclerosis... I'd have to look it up.

Hmm but basic phenomenon of cancer is uncontroled growth and proliferation of calls with some destructive activities without any apoptosis. But anything else could happen ... say exact opposite thing... uncontrolled apoptosis , but I never heard about that.

or , for say due to a genetic-damage a person became unable to perform cell-division, so no wound healing. I never heard or read anywhere.

Or for say after accidental consuming a poison, a person became color-blind due to DNA malfunction... could happen?

Once DNA is damaged the cell will be destroyed, it cannot replicate and the disease won't emerge. Healthy cells replace them. However in cancer the damaged cells are not killed because those were the mechanisms that were damaged; cancer will proliferate. This won't happen in cells that are damaged in other ways but still retain cell cycle control. With radiation sickness, DNA damage causes a lot of immediate symptoms because so many cells are damaged too badly to replicate and will be destroyed.

Let's use your examples. Say a cell gained the trait of uncontrolled apoptosis. What would happen? It would die and the damage is not passed on. If a cell becomes unable to divide, it will not be able to replicate and no disease will occur. You would need to instantly damage all the DNA of cells in the body in a very specific way to see disease states like that emerge. In a manner of speaking, this is what viruses aim to do - change host cell DNA in a specific way to do their bidding.

But instead of die, they could perform some-other malfunctions, too. Like turning-off certain normal function, say stopped transport of certain molecule, or say stopped a function like color-vision, or  start to secrete / accumulate some metabolites same-way as inborn error of metabolism?

If that sort of damage occurs, the cell cycle control mechanisms will target the cell for destruction, and the disease trait will not be passed onto another cell.

One answer from one of my teachers: Xeroderma pigmentosum.

I thought we were discussing somatic mutation diseases, not inherited mutations that cause disease. Xeroderma pigmentosum for example can be carried with relatively little effect because other alleles can pick up the slack of the defective allele. The disease only appears when a child inherits two defective copies of the gene.

In your question however, you ask about mutations that cause disease because of mutation agents such as tobacco radiation etc, not inherited defective genes.

@James Yes. You are on exact correct point. Not on other generation but the same individual organism who is taking the exposure such as consuming the cigarette smoke etc.

A previous comment mentioned radiation poisoning. An interesting thing to note is that most cells that suddenly develop a large number of mutations (e.g. through mutagen exposure) will automatically undergo apoptosis (an evolved sacrifice-self-to-save-the-body mechanism). If too many cells undergo apoptosis at once because of this (as can happen after a large dose of radiation), that can actually severly sicken or kill the person. Thus a person dies or is sickened from their body's reaction to numerous mutations.

Before answering your question, an important note. Not all neoplastic growth is malignant. A mutation may result in a benign growth, which is an outcome different from cancer. Not all of these change to cancers. Moreover, almost all genetic diseases may arise de novo as a germline mutation, and this mutation may be caused due to the environmental mutagen, and hence will be a non-neoplastic outcome of environmental mutation. The list of such genetic diseases is impossible to replicate here.
Assuming you are asking non-malignant diseases involving somatic (acquired) mutation as a pathogenetic event, here's a subset.
Some diseases with proven somatic mutation are:
Neurofibromatosis 1 & 2
McCune-Albright
Paroxysmal Nocturnal Hemoglobinuria
Incontinentia Pigmenti
For more details, have a look at this paper here.
Erickson RP. Somatic gene mutation and human disease other than cancer. Mutation Research/Reviews in Mutation Research. 2003 Mar 31;543(2):125-36.


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Are there examples of human genes using meiotic drive?
Meiotic drive is a type of intragenomic conflict, whereby one or more loci within a genome will affect a manipulation of the meiotic process in such a way as to favor the transmission of one or more alleles over another, regardless of its phenotypic expression. More simply, meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time.
But do humans have such genes?

Yes! Jeffrey and Neumann 2002 report evidence of meiotic drive at a recombination hot spot in the MHC.
Note that mtDNA could arguably be considered as an extreme case of sex-dependent meiotic drive. Mothers transmit mtDNA at rate of almost 1, while fathers transmit mtDNA at a rate of almost 0.


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largest bootstrap support
I was reading about bootstrap in phylogenetics and it got me wondering that amongst all of the methods (UPGMA, Maximum Likelihood, Parsimony, Neighbour joining method) which method generally provides the largest bootstrap support? Or does that vary from problem to problem?

For sequence data, UPGMA is not really accepted anymore. Maximum parsimony and Neighbour-joining are usually used because they are quite fast and they give you a relatively good idea about the phylogeny.
You should not decide based on which method gives you the highest bootstrap.
For publication, it is recommended to use either Bayesian consensus tree (MrBayes is popular program) or a maximum likelihood tree (RAxML or MEGA are popular for ML). For maximum likelihood bootstrap (BS) is used and the confidence is relatively high if at least reaches 80 (%). For Bayesian, instead of bootstrap Bayesian posterior probability (BPP) is used. For BPP it has to be at least 0.95 to be significant.

Any sources you could add?


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Constraint optimisation
I have been asked to talk about (constrained) optimisation like $$\max_{x,y} f(x,y)$$ $$\mbox{Constrained by } g(x,y) = 0$$
for high school students with applications to biology. However, I can not think of a single good example from biology that actually uses optimisation.
The existing application is proving what the optimal linear regression line is given by, but this is rather tedious to do and not really a fun exercise for high school students, which is why I hope you might have a great application that I can use.

Flux balance analysis involves constraint based optimisation and it is frequently used to study metabolic systems and drug effects. I think it's interesting but high school students may still find it tedious and interesting examples of it may be too complicated for them.

The most "naive" models of evolutionary biology are optimisation models. Otherwise, in bioinformatics, there is plentiful of optimization problems.

@Remi.b Would you by any chance have a link for those naive models for evolutionary biology?

The most famous are Hamilton's rule (original paper: Hamilton 1964 which is a bit hard to read because of a terrible notation) and Price's equation (wiki). I called them "naive" because they are simple in the sense that they don't make consideration of statistical genetics nor molecular genetics.

Are you looking of examples of usage of optimization models to model biological processes or of the usage of optimization algorithm for inference problems (or any)?

Nothing specific. I am going to present the topic of optimisation for biology interested high school students, so I need some examples that I can use to argue why it is relevant.


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Are there any chromosomal/molecular difference in following human reproductive- traits?
Are there any chromosomal/molecular difference in 5 following human traits?Klinefelter-syndrome, Transgender, Bisexual, intersex, hermaphrodite. Are all 5 terms synonymous?

Well..
Strictly speaking...
They are not the same.
Each of them has actually a different meaning and some of them such as hermaphrodite is used for lower animals while bisexual for plants animals etc.
Klinefelter's syndrome is totally different and has got nothing to do with the normal bisexual conditions.
Yeah...
sometimes we can use these words interchangeably.

+1'd and Accepted for "Each of them has actually a different meaning"


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Is the male bee's penis homologous to the female bee's stinger?
Considering that when a bee stings it loses its stinger and dies, this is similar to the male drone losing its penis and dying after copulation. It also seems similar that each event basically rips the abdomen open. Are the two structures a homologous pair?

Not sure why the downvotes. Is this question off topic here?

I didn't downvote it myself, rather I think this is already a good-question, but if properly edited it will be more clear. Are you sure, male-bee's copulation organs called 'penis'? (I don't know). If you know better anatomical terms you could use that.

Sting and stinger- same thing? Worker bees (modified females) contain sting surely. But does 'female' bees of popular use, i.e queen bees, contain sting?

Shouldn't be off topic. It actually is a very interesting question. +1 @AlwaysConfused: Of course it's a penis ... what else should it be?

I don't know terminology but of course bee's that structure is not homologous with mammals' pennis. I don't know exist  there any-other formal term or it is also called penis. Again it was a suggestion not criticism of any sort. I thought it would give the question more 'formal look' to collect upvotes

In more clear language, the question could be divided into 2 parts. 1. why some  activities kill the bees? 2. since death happens while stinging in worker bees, and copulation in male (drone) bees, could we corelate that these 2  organs (penis and sting) are homologous or not.

If an asker cannot use a formal term, it is not the asker's fault. It is the viewer's fault.

really it surprises me why bees need to die when they sting? is it of any benifit? I even fail to find an evolutionary significance.

@AlwaysConfused http://biology.stackexchange.com/q/45465/16433

@R.M. thanks for sharing an existing answer to MY question, btw however OP is not at all duplicate with it.

After a little bit of digging I was able to find a couple of facts that seem to verify that the drone bee's penis is in fact homologous to the worker bee's stinger:
This Wikipedia article about the stinger that says a honey bee's stinger is "a modified ovipositor as in other stinging Hymenoptera".
This book (actually about soil arthropods) states very specifically that, "The ovipositor, with which the female lays her eggs, is homologous to the male's penis.".

That is the very best explanation for why male bees do not have stingers (which I have been asking myself on several occasions). Thanks!


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Is this a bed bug? I found it crawling on me in hotel bed
Is this a bed bag? It doesn't have the stripes that I saw in other pictures. I'm traveling and for 5 days I was sleeping in different hotel rooms. What should I do if it is. I searched the bed and found no more.

Nope - it's a tick! If you can get a better photo I can tell you what species - dorsal and ventral surfaces, ideally.

Although probably an Ixodes, I suspect.

Since it's a tick, I would search on your skin, not in the bed. (Meaning: my first priority would be to make sure none of those beasts were attached to my body).

You should check that you haven't been bitten as some (not all) are know to carry Lime disease (http://www.nhs.uk/Conditions/Lyme-disease/Pages/Introduction.aspx)

Ticks and mites are allied to spider, which is an arachnid. Whereas bugs are a sort of insect

As already stated in the comments the animal you found is a tick (Wikipedia).
Since they are known to carry diseases you should make sure you have not been bitten or even still have one sucking your blood. So search your body. If you happen to find one still attached, do NOT squeeze it as this may stimulate fluids to flow from the tick into your body (bad). Instead get it out asap using tweezers or even better specialized tools. If you can't do it yourself ask another person preferably a doctor.
If you have been bitten watch for symtoms of an infection such as a red circle. If in doubt always see a doctor since you might require antibiotic treatment.
NOTE: usually nothing happens so don't worry too much but be alert for changes in skin around bites (if bitten that is).
EDIT: since hotel beds are not a typycal habitat of ticks you probably carried it there yourself.

I think it should be mentioned that hotel rooms are not their typical habitat. It's likely that the tick was transferred to the bed from OP's clothes.

Btw., the most dangerous infection would be tick-borne encephalitis which unlike Lyme disease can't be treated. So, prevention (i.e., apart from vaccination, early removal of the tick) is important.

Ticks need humidity to survive, they often just climb onto a leaf or some grass when it's 17-23C degrees and jump on animals passing by. An interesting biological fact is that young ticks that have had a lizard host absorb the lizards lyme antibodies and have far less lyme desease later when they bite a bigger animal.


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Are there hybrids that emerge as a new species?
We know a couple of hybride (mammal) animals (http://www.rantpets.com/2015/06/03/15-strangest-hybrid-animal-breeds-you-didnt-know-existed/) and perhaps even more and perhaps even insects like the Drosophila.
But are there animals which arise as a new species? And by species I mean animals who can't breed with the species of their parents but can interbreed succesfully with their own species ('brothers' and 'sisters'). Only leaving out pre-mating mechanisms in case they don't get offspring (so that only Post-mating isolating mechanisms counts)
See also: Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?
Have scientists ever produce a new species in laboratory by means of natural selection?

While it is an interesting question, since the operational definition of species is the inability to interbreed with other species, the fact that hybrids are viable suggests the two initial "species" are almost the same.  By post-mating I assume that you mean chromosomal problems during meiosis (e.g., aneuploid gametes)?

Yes, this is called hybrid speciation.

Hybrid speciation is a form of speciation wherein hybridization between two different species leads to a new species, reproductively isolated from the parent species

There has been a fair amount of work on hybrid speciation (see here). Hybrid speciation is often thought to be more frequent in plants than animals. In ferns for example, we estimate that 7% of species emerged through hybrid speciation (Otto and Whitton 2000). Typical cases of hybrid speciation include changes in ploidy levels (examples include sunflowers). Hybrid speciation also occurs in animals such as the lonicera fly to cite just an example.

In my initially question I asked (before it was edited) species created by human. Are new species created by human?

The post did not match the title (the post made absolutely no reference to humans). Now that the broad question of "is this a thing" has been answered I would recommend that you open a new post to ask specifically about humans. You will be able to use the term hybrid speciation which will make your post short and clear.


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Chemistry of the phosphodiester bond in RNA
I have been learning about the chemical structure of RNA, but I can't understand why all hydrogen atoms disappear in the phosophodiester bond between the riboses of RNA.
Phosphoric acid is $H_3PO_4$:

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

Where did the hydrogens go and why?

I have edited your question and corrected your diagrams in a way that should answer your question. The valency of the oxygen in the original diagram of the phosphodiester bond was incorrect. Addition of the negative charge — shown in any book or web page — makes it clear that a H ion has been lost. This is such a basic question of chemistry that I would regard it as off topic for Biology SE. As you have accepted the answer from @anotherHomoSapiens I will now vote for it to be closed.

@David good image resize edit.

Hydrogenation depends on pH

@Christiaan correct, I read somewhere that at cellular pH (~6.8) DNA easily loses H and acquires -ve charge.

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

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

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

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

If this solves your problem, click the tick mark, below the down symbol to the left of my answer, to select it as correct. If it doesn't, ask your query here or improve the question.

@AnisSouames If hydrogen is not shown, then there a negative charge is shown on oxygen, like HCl--->H+  +   Cl- ; the same way (H...PO4)---> H+ +  (-)OPO3 . Due to THAT hydrogen, DNA is an ACID after all... Deoxribo-Nucleic-Acid. As well it is a "base" at the same time due to presence of "nitrogenous" (N-containing) bases that can give a lone pair of electron (Lewis base). Biological nitrogen-containing bases are more popular in another name "Alkaloid".


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How does motor nerve innervation determine type of muscle fibre?
Muscle fibres are of two types - type I and type II. They differ from each other in various properties. Even the underlying biochemical processes are different to suit their function (slow vs fast)

In a normal muscle, on certain stains like ATPase and SDH, to differentiate between the types of fibres, a checkerboard pattern is seen. But in reinnervation following long standing denervation, there is a loss of the checkerboard pattern and fibre type grouping is seen.
This happens because, the the denervated fibres are reinnervated by other ones, which can change their type.
The question is, how can neural innervation lead to biochemical changes in muscle type?

'Slow' and 'fast' motor neurons differ in their firing patterns. This differentially affects intracellular calcium concentrations and energy usage of the innervated muscle fibers over time, and thereby influences their gene expression. The following review extensively covers this: http://www.ncbi.nlm.nih.gov/pubmed/22013216


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How does the ATPase stain for muscles revert on changing the pH?
Muscle sections are stained with ATPase to differentiate between types of fibres and to display the ckecerboard pattern. But it is done at two different pH. The staining is reversed at acidic/basic pH.
To quote this site

Acid preincubations inhibit the myosin ATPase activity in fast (mammalian type 2A, 2X, and 2B) fiber types, but not slow (mammalian type 1, see Figure 1A). Conversely, basic preincubations inhibit myosin ATPase in slow fiber types only (Figure 1B).

Why is this so? Isn't the ATPase same in both the fibres?

No, they contain different myosin ATPase isoforms. The myosin ATPases of slow fibers are more acid-resistant in their activity.

Does that ATPase act only on ATP? or it could work on some-other type of molecules?

@pbond thanks! Could you pls elaborate your answer so that I can mark it answered. I've understood it. Once the genes expressed changes, as you have mentioned in your previous answer, anything can change!


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Can low temperatures induce a withdrawal reflex?
I read in "Essentials of Pathophysiology: Concepts of Altered Health States
By Carol Porth" that

"The thermal pain receptors are stimulated only by extremes of temperature such as "freezing cold" below 5°C and "burning hot" above 45°C."

Also in "The Journal of Neuroscience, April 7, 2010 • 30(14):4933– 4942 • 4933" it states:

"In lightly anesthetized rats, hindpaw cooling with ethyl chloride, but not acetone, was sufficiently noxious to evoke withdrawal reflexes"

We know, 'burning-hot'-receptors induce a withdrawal reflex when we touch a very hot object, say hot frying pan.
But does this mean if we touch a very cold object (temperatures below 5°C), the 'freezing-cold'-receptors would induce a withdrawal reflex in humans?

The withdrawal reflex is a nociceptive flexor reflex and is a spinal reflex intended to protect the body from damaging stimuli.
In other words, activation of heat receptors is not the trigger of the withdrawal reflex, it is the activation of pain receptors at high, tissue-damaging temperatures.
Extreme cold is also damaging and causes skin lesions akin to heat-induced burn wounds. Again, at a certain tipping point extremeley low temperatures become damaging, and cause frost bites (Sachs et al., 2015). At this point tissue damage will activate pain receptors and these cause the withdrawal reflex to be initiated.
Reference
- Sachs et al., Dtsch Arztebl Intv; 112(44): 741–7

How cold does it have to be to cause harm? to cause withdrawal?

@DisplayName - I deliberately left that out as it depends on the duration of the exposure. It's hard to say.


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Charge distribution to neuron connections
How is charge generated by the action potential is distributed to all of the neuron connections? From what I understand the total charge transmitted by a neuron once it fires is same for every neuron. Is it divided based on synaptic weights?

The action potential is an active process, its mediated by voltage sensitive ion channels that shuffle ions around in order to create an electrical gradient that travels through the whole cell. When it reaches an axon, some of these positive ions bind to pockets of molecules (vescicles) that fuse with the cell membrane to release their neurotransmitters. Check out this very good answer to a similar question. Once these neurotransmitters bind to receptors in the post-synaptic membrane of the subsequent cell it produces an EPSP.
Each synapse is unique, meaning that although the action potential is the same synapses are changed depending on their activity some synapses might have more vescicles, more neurotransmitter, more sensitivity to the change in voltage. Postsynaptic membranes can also grow and increase the density of receptors in order to make the synapse more effective. The effectiveness or weight of a connection is just a measure of how good that connection is at eliciting a spike or action potential from the postsynaptic cell.
Once a cell fires it fires, but not all the connections count the same to elicit a response from the next cell down and there are a bunch of interesting sub-threshold dynamics.

I understand this much, but I am more interested in the mathematical side of the exchange in order to build a model. I wonder if it is safe to assume that every neuron produces same constant charge X when it fires, which is divided to all its output connections based on their weights?

Oh,well, I guess either a modeling tag or some indication in the question that it was a modeling issue would have saved me some time.

In this case the answer is yes, as I mentioned neurons either fire or not, once they do you go through all the connections and modify the input current by the weight of that connection, update the weight according to whatever rule and move on. I assume its a spiking model (https://en.wikipedia.org/wiki/Biological_neuron_model)?


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What animal / bird can be heard in this evening sound recording from Western Washington, USA?
We heard this animal outside in Western Washington (Port Townsend area) during the late evening. I think it is a bird, but it honestly sounds sort of like some creepy woman singing or something. The audio is linked below. The sound (in the audio) was repeated for a long time at random intervals averaging probably every ten seconds.
https://clyp.it/tzybty1w
Anyone know for certain?

If I exclude the humming noise, the call is quite clear. But do you have any more longer-records?

The sound is approx ranging 200 Hz to 2000 Hz with most-occurred components belong approx 500 to 600 Hz. seems so , when filtered with any media player's equalizer.

That is the only sound clip I have...

I asked the same question on another forum here: http://www.birdforum.net/showthread.php?p=3454684.
It looks like another possibility is a barred owl. It also sounds somewhat similar.

My guess is an owl, possibly a great horned owl, which are found in the area and can sound similar.
Alternatively, it could be a mourning dove, which sounds similar again, and is common throughout the USA.

Not a mourning dove; pattern wrong.  Owl is highly likely; Barred Owl suggested in other answer is better fit than Great Horned. Compare at Cornell site:allaboutbirds.org

@mgkrebbs I agree.

This does sound like the characteristic "who cooks for you" call of a distant barred owl (Strix varia). You can hear this call at All About Birds run by Cornell Ornithology Lab.

The recording by
Andrew Spencer is most similar to yours given the distance it was recorded (though, he suggests it's a subspecies out of range that was recorded).

You might also try Audobon's sound clips as they were recorded at farther distance than those at Cornell and so better represent what you're hearing.

You're in range of these owls in Port Townsend:

 Source: All About Birds

No question ; barred owl. There are a few in the subdivision and presently I hear them fairly often. I think it may be fledging practicing the call. I am in  E TX at the southern end of the range on the shown map.

It could be the Sri Lankan spot-bellied eagle-owl lost in America.
Link = [https://www.google.com/search?q=spot-bellied+eagle-owl&oq=spot-bellied+eagle-owl&aqs=chrome..69i57j46j0i22i30l7.931j0j7&sourceid=chrome&ie=UTF-8][1]

Welcome to the site!  It would be much better to embed the image in your post; the google query will change over time.  Please [edit] in the picture.  Thanks!

Given the similarity of the call to a bird known to live in the area this seems at best extremely speculative. You are also more likely to get a positive response if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated calls. Without this your answer is indistinguishable from opinion and thus off-topic. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!

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


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Is it possible to create DNA of a species that could be any animal
I was thinking about a fiction world in which all animal (at least vertebrate) could crossbred because they share same number and layout of chromosome but differ in hereditary detail (like human skin color) and/or using epigenetic modifications.
Is it actually possible? And how large of DNA it could be to code all vertebrate form and function?
I'm programmer so I just think DNA as a code. And it seem we could refactor and reuse most of DNA code between tetrapod species (also between arthropod-arthropod species)

I don't really understand your question. Are you asking something like "what is the Shanon's entropy of all vertebrates DNA put together?"

Cell fusions could be done in plants; don't know does it happen to animals or not. Usually animals can't support chromosomal aberration. They die.  But most plants can easily support chromosomal aberration.

I am voting to close as unclear. In addition of the post being unclear to me, my rough understand of the question in the post does not match the one in the title.

The very similarities in number and layout of chromosomes that allows animals to breed with each other are the same similarities that cause them to end up with reasonably similar phenotypes. As soon as the genomes are too different to breed with each other, the phenotypes of the animals are so different that we categorise them as different species (usually). Therefore, I believe the question that you're really asking is, "can epigenetic control alone result in phenotypes so different that they would seem like different species?"

(Because their genetic similarity is what makes them de facto the same species)

@Armatus That's right as my first question. What I meant is not just epigenetic but also hereditary like lactic tolerance. But on wider scale, such as same specie being ruminants herbivore in one area but carnivore in other place but still able to mate if they met. What I want to know is are there any impossible trait that can't be code in the same layout like that in DNA

"same specie being ruminants herbivore in one area but carnivore in other place" ... do you know any such example?

Probably the OP is asking "is it possible to write/formulate a general genetic-scheme for a group-of-organism (say all vertebrates)?". Is that?

Different species of Vertebrates do-not have same number of chromosome. even-if some have same number of chromosomes, it is just co-incidence... they are separate species. However, on chromosomes there are homologous sequences

@AlwaysConfused I press upvote at your right comment. As I was state that I am thinking about fictional alien (parallel) world, I just want it scientifically possible

@Thaina Please edit and improve your question because from its language it is creating so many possible meanings (ambiguous) to me.  btw for a virtual/theoretical "vertebrate" would behave like-to "real" vertebrates (otherwise we'll not use the term vertebrate for them). or if you write a  story then it is different thing. you could write a story about a human without no DNA... in story anything is possible. However, there are some technical mistakes in your question (or I had read them correctly). Write in simple way.

If I even could theoretically formulate a general formula for a large taxonomic group with some specific-portions (common for all them) and variable portions (that are different in different subset-taxa) ;  whenever I would practically   make one, there would nothing "variable". It will then become an individual with very specific genetic structure, that could not mate with so-many other kinds of organism.

Suppose genome A generates organism oA and genome B generates organism oB. Their phenotypes pA and pB are quite different from each other.
Because genome A and B are not similar enough, organism oA and oB cannot sexually produce viable offspring.
Your question seems to boil down to: "Would it be possible to generate oA/pA and oB/pB from genome A, or a genome similar enough to genome A such that it can still sexually reproduce with genome A?"
So you basically ask whether any genome A could simultaneously produce pA and pB under different external conditions.
Answer: Possibly? The genes involved in the development of organisms typically don't respond to external stimuli but to genes which were active before them (in time). Various genes produce proteins which sense temperature, osmotic pressure or particular chemical species or ions. If those were factored into very early developmental programs, feeding into transcription factors to modify gene expression according to external factors, the same genome could produce drastically different organisms.
To speculate more about this yourself, it would probably help to go away from a code-based understanding of DNA and think more about what it is physically and biologically. Unlike computer programs, DNA "programs" can modify themselves and other programs or the functions they execute.
Biologically, DNA is an information carrier that is transcribed into RNA, which can have functions of its own and/or be translated into proteins. DNA interacts very tightly (physically) with a lot of RNA and protein components, and most things that happen in cells and tissues around them end up modifying the way DNA is handled in some way. Keywords that you could look up are "gene expression", "gene regulation" and "developmental biology".


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Why would a flower evolve such that a particular pollinator cannot pollinate it?
I went on an interpretive trail today and came across a wild flower sign. It said that some flower species evolved such that they can not be pollinated by humming birds as they are shaped such that only an insect proboscis could get into it. Why would a flower evolve in such a way? Wouldn't it be advantageous to take any pollinator?
An interpreter in the visitor center suggested it might be that the flower wants to save it's limited pollen for pollinators most likely to visit other families of its species. I'm not completely sure I buy this, as a pollinator willing to visit one flower of a species is likely to visit another flower of the same species. That said, I think he might have been on to something. Alternatively, this link made me think perhaps certain pollinators might damage the flower and it would want to discourage them.
This question goes beyond a flower co-evolving such that a particular organism could specialize in pollinating it; I'm curious why a flower would specifically evolve such that it could not be pollinated by a particular organism.

Could you tell us specifically what species you are talking about. Otherwise this is an unclear question.

It's two sides of the same coin, by specialising to have one specific pollinator, you have to exclude others

Probability. A rare flower got a larger chance of successful pollen transfer if the pollinator searches specifically for other members of its species. The previous comment describes one option to achieve that. Typically, what we observe today is the result of coevolution. The pollinator gets access to a food source not accessible to others and the flower gets a specific pollinator.

The interpreter's explanation was also the one that immediately came to my mind. There is also some evidence that high specialization (and therefore low pollinator sharing) increases pollination probabilty: http://www.ncbi.nlm.nih.gov/pubmed/19909087

@James, I was afraid someone would ask that (: I looked a lot online and could not find the species. I believe it was a type of Elephant Flower indigenous to Utah but am not sure.

@rg255, thanks for the comment, but I'm specifically referring to a case where the flower adapted to exclude a pollinator where the adaptation did not benefit a preferred pollinator.

I think the explanation by the interpreter is most appropriate. The definition of species is a particular category of organisms capable of reproduction among themselves. Thus pollen of a particular species must fall on the stigma of the same species. But pollinators visit all species of flowers (as they never visit Biology Stock Exchange, thus ignorant of the definition of species) which bears nectar and the entrance is big enough to let them in.
The flowers in your question increase their chance of pollination by reducing the varieties of flowers a particular pollinator can visit. Lets make it simpler (or even more difficult for those who don't like mathematics!)...
Suppose there lives 4 humming birds and 4 bees in a oasis...both are too lazy to visit other oasis in search of nectar. One morning 4 flowers bloom in that oasis...2 wild flowers you mentioned and 2 wide mouthed flower of some other species.  Now 1 flower of the wild species can be visited by 4 bees (as humming birds can't enter the flower). One flower of the other species can be visited by 4 bees and 4 humming birds. This large number of pollinators for the second type of flower reduces its chance to be visited by a pollinator that visited a flower of the same species. Whereas for the wild type flower the possible number of pollinators are very few (only 4)...so the chance of one bee visiting two flowers of the same species is very common and so is the chance of it getting pollinated.
In this way these flowers increase their chance of pollination by modification of their shape.

I think the OP is asking why a flowering plant might evolve to exclude pollination by some species of pollinators, rather than why it might evolve to special adaptations to allow some specific pollinator

I answered by considering "species" of pollinator...humming birds and bees are examples of species only.

I think this is correct. To repeat but also perhaps flesh out your example, suppose a flower only has enough pollen to be visited by 5 pollinators each day. If a hummingbird only has a 10% chance of visiting another flower of the original flower's species but a bee has a 50% chance of visiting the original flower's species, it is advantageous for the flower to not "waste" pollen on the bird.


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Composition of EZ-Vision® DNA Dye?
I'm looking for the composition of the EZ-Vision DNA Dye for electrophoresis visualization. I could not find anything helpful on the web.
I would appreciate a lot your help :)

Presumably you're asking for safety reasons. Their safety data sheet is missing for that product on their website. You'd be justified in directly contacting the manufacturer on this topic.

Read the label of bottles. Find was there any datasheets or such provided with the bottle. Laboratories keeps various data-books and datasheets so ask for that. Ask your teachers/ guides about  its composition.  Googling is no difficult task.  If you are able to handle with DNA (for me it is enough difficult) why could you face difficulty in google search?

The MSDS does not specify which compound is actually present in the solution. A quick google search does not show what is composition of the solution, except for DMSO.

https://www.amresco-inc.com/media.acux?path=/media/products/dfu/dfu-N472.pdf  was it any helpful?

Sometimes companies keep some 'trade-secrets'; however I think main components should be mentioned. I  too feel discomfort in mind while working with something even if any 1 component  I do not know.

@Ashafix me too. I also could not found something helpful in Google within a short time.

@AlwaysConfused I found that info sheet as well, but sadly it doesn't provide the components. Thanks, anyway :)

Then you should write "I could not found anything helpful on web", than "I'm not very good in googling". That would help directly understand the research effort . (as well I'm not moderator), Moderation in stack websites is  done in tough way.

If a company keeps some trade-secret (I'm not sure if this the case), or even many well-popular facts are not available in web.

Contacted technical support and received the following response:
"Unfortunately, the information you requested is proprietary and we will not be able to share the images of excitation-emission spectra of EZ-Vision® Bluelight DNA Dye and the chemical structure of the dye. "


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Why do human females have permanently prominent breasts?
Humans seem to be the only animal whose females have breasts that permanently have a "full" appearance, ie a prominent amount of tissue even when not lactating, whereas other species' breasts seem to almost totally "deflate" when not longer lactating.
Why is that?
This feature has costs to the organism; significant biomass is dedicated and perhaps mobility is impacted. Given there are costs, for the feature to have come into existence, evolution/adaptation principles suggest there must have been some advantage.
Is there some biological advantage?
Are they vestiges of an adaptation that gave a significant advantage to some prior species or in some specific (presumably cold) prior environmental conditions?
Is there any credible research to support certain reasons?

My suspicion is that although genders can be distinguished easily enough, even from a distance, using other secondary characteristics, the answer may have an anthropological/social answer, rather than a biological one.

Are you sure, a cow's udder is not prominent, while not lactating?

@Always I have changed the question to "primates", but there seem to be very few. Hand on... when not lactating aren't bovine udders "empty"? Whereas human breasts stay "full" in appearance?

@Always I've retracted the edit and gone back to a more general statement, but clarified that they more or less appear as if lactating all the time. Other species' breasts enlarge when lactating, but basically almost totally "deflate" when not lactating. This is a serious question by the way. I think it is clear enough now.

Hmm but I've read in many places  that in humans, at time of lactating the tissues in mammary-gland grows. https://en.wikipedia.org/wiki/Lactation#Hormonal_influences

@AlwaysConfused Use comments only for requesting clarification or providing suggestions in the context of the post. Do not use comments for discussions. Some of your comments were not even directly related to the question.

there are tradeoffs and constraints in adaptive evolution, e.g. breasts swell substantially when breastfeeding, perhaps the non-lactating state represents a middle ground where it is easy to make swell when needed but keep them small at other times

You may be interested in Breast asymmetry, sexual selection, and human reproductive success.
Abstract:

Breasts of human females are large compared to those of closely related primate species,
  and they can thus be hypothesized recently or currently to have been subject to directional
  sexual selection. Here we show that (1) large breasts have higher levels of fluctuating
  asymmetry than small breasts, (2) breast fluctuating asymmetry is higher in women without
  children than in women with at least one child, (3) breast fluctuating symmetry is
  a reliable predictor of age-independent fecundity, and (4) breast fluctuating symmetry
  appears to be associated with sexual selection. These conclusions were similar in studies
  from two cultures differing in fecundity and brenstfeeding traditions (Spain; New Mexico,
  U.S.A.). Choosy males that prefer females with symmetrical breasts may experience a
  direct fitness benefit in terms of increased fecundity and an indirect benefit in terms of
  attractive or fecund daughters.

Some quotes from the text:

The size of breasts in human females is large compared to that of other primate
  species, and there has thus been a recent evolutionary change in breast size.
  Human breasts are characterized by their large size and rapid development prior
  to and during puberty, when growth of other body parts also reaches a high level.
  They can thus be considered costly structures in terms of energy use. …
  Heavy investment in breast development during puberty may seem puzzling
  because the functional significance of breasts is far from obvious. There is no
  or little relationship between breast size and production and composition of milk
  in current industrial societies (reviews in Anderson 1983; Cant 1981; Low et al.
  1987), and breasts have therefore been hypothesized to constitute a deceptive signal
  used by women to attract preferred mates (Low et al. 1987). In prehistoric
  human populations, conditions may have been different, when mother's milk
  was the sole source of nutrition for young children and when resources often
  may have been more limited than in present industrial societies. In this study
  we show that large breasts tend to be more asymmetric than small breasts. In
  prehistoric societies, where resources were likely to be less available or more unevenly
  distributed among women, breast asymmetries are likely to have been much
  larger than in present industrial societies with relatively easy access to resources. …
If the relationship between breast size and fluctuating
  asymmetry is robust, we hypothesize that a directional preference for large, symmetrical
  breasts, as apparently found in some cultures (Ellis 1954), can be maintained
  in the population because selection for large breasts will be balanced by
  selection against asymmetrical breasts
We also show that breast symmetry is a reliable predictor of age-independent
  fecundity, and that choosy males that use breast symmetry as a cue in their mate
  choice will experience an advantage in terms of reproductive success. Breast symmetry
  can thus be considered a reliable signal used in intersexual communication.

There are two theories that I find attractive regarding the prominence of the human breast. AS many have pointed out, human breast are really strange in mammals. Chimps are flat chested and have no problem nursing their young. And most of the female breast is fat tissue rather than milk glands (which grow during pregnancy and are mostly degraded after lactation stops)
theory 1
Human breast are under sexual selection. Men like big breast. So it gets selected for. There is much justification reported such as breast being a status of health (plenty of fat reserves) and estrogen levels, and thus a proxy for fertility.
However I have not seen any real data to back such an idea, such as A-B cup women being less attractive than C-D cup women. Nor data that women with small breast are less fertile than women with bigger breast.
theory 2
Anti smothering device. Human babies have no snout. So without a prominent breast to create an air space between the body of the mother and the nose of the baby, the baby would suffocate itself when nursing. And a chimp baby does have more of a snout than a human baby.
It is an intriguing idea. However it is also known that human breast does grow during pregnancy, becoming more prominent (particularly apparent for women with small breast). And such gains can be lost once lactation stops. So with that said... is there a reason why the female breast needs to be elevated all the time and not just after pregnancy. I have also not encountered any evidence that women with small breast are smothering their babies when breast feeding.
So at this moment I am leaning towards a hybrid idea...a hypothesis of my own.... that the human breast initially became more prominent for a biological reason.. perhaps a truly flat breast which chimps have really does smother babies without a snout. However once these small breast emerged, they came under the attention of men, and were sexual selected to a far larger size that we see today.

Even though human females' breasts appear full, they're only filled with milk after giving birth or parturition. Other times they're mostly made up of fat.
And they're full mostime probably only to signal the males that they're capable of raising a baby.

Tanvi- can you add some references to your answer? We generally appreciate references to external links/sources for all answers on this site. Thanks for your contribution!

Ya sure! Here are the links I referred: http://googleweblight.com/?lite_url=http://www.livescience.com/32745-why-do-women-have-breasts.html&ei=0AWhxY8O&lc=en-IN&s=1&m=890&host=www.google.co.in&ts=1474395463&sig=AKOVD66SUPVRn9NeVo3Cmq5drZDBoU-YGQ
https://www.quora.com/Is-there-an-evolutionary-reason-for-why-only-human-females-have-permanent-breasts-among-all-other-mammals                  Is this okay?

That does not answer why they are not annulled after menopause.

I think I remember reading once from Desmond Morris, and possibly from the Naked Ape, that (at least) one of the reasons that humans have large breasts is because they resemble to the buttocks.
It's definitely because of sexual selection, and apparently, it's also connected to the fact that lot of our body language messaging comes from our front side. (Contrary to some other apes that can have larger or swollen buttocks for sexual messaging).

Yes,  I recall many years ago some anthropologist postulating the signal of presented buttocks of a receptive female is more difficult with an upright posture, so breasts could have evolved to mimic this signal.


text:
Why do we like to touch fluffy things?
I read this article but it didn't explain much. Is the fact people like to cuddle pets with fur connected anyhow with our past when our ancestors had fur as well - and therefore could evolve an instict to enjoy hugging someone furry as an expression of friendship.

Not only touch... animals with furs looks far far more beautiful and 'cute' than bare animals.

http://psychclassics.yorku.ca/Harlow/love.htm, http://pages.uoregon.edu/adoption/studies/HarlowMLE.htm, https://www.pinterest.com/pin/377880224958982355/

"Overwhelmingly, the infant macaques preferred spending their time clinging to the cloth mother. Even when only the wire mother could provide nourishment, the monkeys visited her only to feed. Harlow concluded that there was much more to the mother/infant relationship than milk and that this “contact comfort” was essential to the psychological development and health of infant monkeys and children. " http://www.science20.com/eye_brainstorm/infants_monkeys_love_and_ai-99925

I've read about an epigenetics study on rats, though not same but similar to Harlow's experiments. http://learn.genetics.utah.edu/content/epigenetics/rats/

why this question is so under-rated yet?

You should include some more background from the linked article, to make this less "opinion-based" (since its currently being VTCed on these grounds now).

I wouldn’t touch a furry animal — its fur is probably crawling with insects carrying disease. Get a grip — fluffy things — are you a grown man or a child?

I'm voting to close this question as off-topic because it’s trivial and stupid.

An answer I got from Jan Kolář of Charles University:

I'm not sure that people prefer fluffy things just from the fact that
  they are fluffy. They like things that are soft to touch such like
  pillows. The popularity of fluffy things might have a simple
  explanation: There's no danger of getting cut.

So the fact we like to cuddle with dogs and cats has probably nothing to do with our furry past.

It's sensorily similar to "why do people love to eat crunchy things?". Shops contain thousands of the most crispy foods. Crunchy foods and fluffy material like velvet have a common attribute. that they can both generate thousands of complex nerve responses. https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1745-4603.1995.tb00782.x
Crispy foods generate nerve responses above 5KHz, and if you feel velvet with your fingers it has a similar effect. It's a kind of vibration, perhaps what they call vibrotactile.
Today they make haptic feedback with vibrotactile actuators, like a console gamepad, which is also designed to be pleasant.

Hi, thanks for your contribution. Have you got anything to base the hyporthesis fluffiness is similar?

Also, is there really no deeper explanation when it goes to crispiness? Is it something useless evolution just hasn't got ridden of yet?

Perhaps there is a social element that is common to mammals. It wouls be nice if there was a mechanical or physical explanation for nerve ending, synapse and cerebral effects, but science doesn't seem to have obvioys theories for it, it's even more mysterious than tickling.


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How can I test a germinating pea seed for the presence of maltose?
I need to do a simple experiment to test whether germinating pea seeds produce maltose for the breakdown of starch into simple sugars.

Iodine. Thre is a reputed classic experiment, wait for while

for breakdown they does not produce maltOse but they produce moltAse, also known as amylase. Alpha-amylase is common in seed, it helps supply food (simple sugar) to pre-photosynthetic seedling

Here it is, I can't remember the inventors right-now, if I could find them, I'll inform immediately. http://www.tankonyvtar.hu/en/tartalom/tamop412A/2011_0009_Levai_Laszlo_Veres_Szilvia-Applied_Plant_Physiology/ch13.html ; URL: http://www.tankonyvtar.hu/en/tartalom/tamop412A/2011_0009_Levai_Laszlo_Veres_Szilvia-Applied_Plant_Physiology/images/062.png. , and https://lh3.googleusercontent.com/sCX8V2iMGT47fmE4Xw-LNmBRjBUE4Edko3zPHhR6ii0y612AekZT14p9--C3Ce2h8mIWdw=s170 . In this website the inventors' name is not found

DNSA colorimetric assay is another popular method to test amylase activity.


text:
Why don't plants use radio waves?
I heard that the Earth's atmosphere is opaque at most wavelengths and only allows visible light and radio waves through, so why have plants evolved to only absorb visible light?

Probably because radio waves have super low energy.

Animals too don't use it (except human)

@AlwaysConfused even humans don't use it naturally. I ain't sure, but as Alex says, there is probably no molecule which can release electrons by getting energy in RF range.

Super low energy means super-low energy per single quantum. But even if we increase the intensity of radiation, i.e. higher rate of quanta-release at  unit time, as well more total energy; yet it will remain inefficient to create reaction directly.

@AlwaysConfused some of your questions can be researched by  googling. Also, comments on StackExchange are for discussing posted question, not other stuff like random ideas

Possible duplicate of Why do some bad traits evolve, and good ones don't?

@kmm No. this question is not a duplicate with http://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont   from any viewpoint.

@AlwaysConfused Comments are not for extended discussion. You can use the chat if you want.

Even if the atmosphere is mostly transparent in the radio domain, most of sunlight is visible light.
Also, to make photosynthesis work, you need photons of high energy (say: wavelength shorter than 700nm) in order to excite electrons in the reaction centres. Radio waves cannot do that.
The most widespread photosynthetic organisms make use of visible light and water, which are plentiful on Earth.


text:
Decoding animal language (dolphins etc)
I have this idea about how we perhaps could decode animal vocabularies that I would like to have some input on.
The idea is to design an experiment/challenge where we could predict roughly what has to be communicated between two individuals of a species in order to succeed with the challenge, for instance two dolphins.
An example could be a colored button that one dolphin has to push to give both dolphins a treat, but where only the other dolphin (the one that can't push it) gets to know which is the correct one. This should encourage them to communicate what to do and specifically what colored button to press. And by doing this kind of experiment several times we could perhaps extract what sounds represent for instance "red". And so on we could build up a basic vocabulary. What do you think about that? =)
The main idea is to in some way encourage two individuals to communicate something that we by design can infer from the outcome of the experiment. If first training one individual in solving a challenge and then letting it observe another individual that has no clue how to solve it, it should encourage it to communicate the solution, if it's sufficient intelligent that is.
Could it be done you think? I wish I had the resources to try this out myself but alas I don't. I'm all out of dolphins. I have asked a few researchers for input but they don't seem to think this is possible since no animal are intelligent enough and have any kind of language in the way we think about it. But personally I don't fully buy that. I still think a few animals would be possible subjects for a test like this, such as dolphins.

You know what? You ought to give it a shot!

All my dolphins have escaped!

Then you don't need such mechanisms to understand why they did so ;)

The design of scientific experiments is an art!

No, that's not really a good design. First, it is more than unlikely that dolphins have a "word" for "red". It would sound like a very advanced vocabulary word already. Second, it is unclear how you would determine that whatever sound you're hearing aren't meaning "I am distressed" or "I am excited to get food" or "I want sex" or whatever other meaning such sound could have. You would at least need a control.

If it's useful for dolphins to communicate a color in some way I assume their "language" should include some "representation" for this? Or do you suggest that no animal except human can communicate anything other than basic needs and states of mind? Perhaps that's true but have we really looked for it? Perhaps we are blinded by our preconceptions. Also, my idea is to repeat the same experiment many times to filter out the sounds that always turn up, to be able to exclude all non-essential sounds.


text:
Can dissolved aluminium from centrifuge tank deactivate enzymes?
I extract an enzyme called diamine oxidase with a tubular centrifuge. The centrifuge uses an aluminium tank to collect the liquide after centrifugation. I asked myself what would happen if some aluminium particles pell of from the tank due to the collision of liquid and got into the solution. Could this deactivate the enzyme?


text:
Do Type 1 (Slow Oxidative) muscle fibers also make use of glycolysis?
I'm aware that slow-twitch fibers make use of oxidative phosphorylation; however, I am unsure if this is done in conjunction with glycolysis and the krebs cycle? Do these muscle fibers go through all three stages of aerobic respiration, or just the final step? If not, where are they getting the precursors for oxidative phosphorylation (NADH, FADH2)? Would they use fatty acids and proteins as precursors in the krebs cycle (if applicable)?
Slow-twitch (Type IIB) seem to use glycolysis and then anaerobic respiration (forming lactate), right?
Any input is greatly appreciated!